Physiology Exam 1 Notecards

Front 1

cardiovascular disease

Back 1

is the leading cause of death in the country and elsewhere (>40% of all deaths can be attributed to CVD), is the most costly component of health care delivery in this country (about 1/3 of total health care budget), is the leading cause for acute hospital bed occupancy

Front 2

functioning of the heart

Back 2

functions as a pump moving blood through the circulatory system, must have an orderly sequence of electrical and mechanical events that are accomplished through the initiation of the cardiac action potential in the sinus node and conduction of this signal throughout the heart

Front 3

importance of the action potential in cardiac muscle

Back 3

it is the trigger that initiates contraction of individual cardiac muscle cells and synchronizes the contraction of the heart as a whole

Front 4

arrhythmia

Back 4

a disruption of the normal electrical rhythm of the heart, compromises mechanical performance and can lead to life-threatening DEC in cardiac output, may lead to a DEC in blood pressure, usually due to problems from SA node not firing fast enough

Front 5

internodal atrial conduction tracts

Back 5

three of them that INC excitation by the SA node, allows for rapid activation of the AV node

Front 6

Bachmann’s bundle

Back 6

helps in excitation of the left atrium, allows for rapid activation of the left atrium

Front 7

purpose of the AV node

Back 7

delays the electrical transmission to the ventricle (which allows for the proper filling of the ventricular chambers) and receives the signal from the SA node, from the AV node, electrical transmission goes to the bundle of His (where cardiac cells are much larger compared to the SA and AV node) and look more like myocytes equipped for fast conduction

Front 8

left and right bundle branches

Back 8

penetrate the ventricle as Purkinje fibers and branch out into 1/3 of the ventricular mass and via gap junctions and can transmit the action potential into the ventricle, activation occurs in the septum and transmission occurs via Purkinje fibers

Front 9

Purkinje fibers

Back 9

composed of large cells specialized for the very rapid transmission of the electrical impulse to the ventricular cells allows for the synchronous contraction of the two ventricles

Front 10

types of muscle cells in the heart (myocytes)

Back 10

1. those that are specialized for conduction of the electrical impulse
a. SA node cells
b. Cells of the internodal conduction track
c. AV nodal cells
d. cells of the bundle of Hiss
e. Purkinje cells
2. those that are specialized for contraction and relaxation
a. atrial cells
b. ventricular cells

Front 11

SA node (primary/dominant pacemaker)

Back 11

is an ellipsoid strip of muscle ~3 mm in diameter, 15 mm long and 1 mm thick, located in the upper lateral portion of the right atrium, near the SVC, composed of relatively small cells which contain few contractile proteins, spontaneously discharge electrical impulses which initiate the normal cardiac contraction and is called the primary pacemaker

Front 12

conduction times through the heart

Back 12

impulse from SA node takes about 30 ms to reach AV node, reaches left atrium in about 70 ms, from AV node impulse reaches bundle of His in about 120 ms, from the bundle of His impulse reaches the base of the heart in about 20 ms

Front 13

escape pacemakers

Back 13

are the secondary pacemakers, can be from the AV node (40-60/min), bundle branches (30-40/min) or the Purkinje network (30-40/min), not all cells in the AV node generate electrical activity, if there is no SA node activity, the AV node cells will take over, can survive SA nodal block

Front 14

what determines heart rate

Back 14

determined by the pacemaker triggering impulses at the fastest rate

Front 15

SA nodal cells

Back 15

continuous with surrounding atrial cells and transmit the electrical impulse to initiate atrial contraction

Front 16

AV node

Back 16

small compact tissue located at the junction between the right atrium and interventricular septum

Front 17

action potentials in different excitable cells

Back 17

motor neurons and skeletal muscle have short action potential duration, all cells have a negative resting potential, cardiac muscles have longer action potential durations, since there is one single cardiac muscle, all the cells are coupled together electrically, INCing the duration and elevating the plateau, changes force of contraction

Front 18

when does the peak of contraction occur

Back 18

during repolarization because there is a delay in contraction activity after the AP, ventricular AP activates a phasic contraction

Front 19

morphology of the AP in different regions of the heart

Back 19

cells of the SA (-60 mV) and AV (-65 mV) nodes are more depolarized at rest and generate an action potential exhibiting a relatively slower upstroke than atrial (-80 mV), Purkinje (-90 mV) and ventricular (-80 mV) cells, their unique cellular electrical properties largely determine their role in the propagation of the electrical impulse through the different regions of the heart

Front 20

properties of the cardiac AP

Back 20

duration exceeds 150 ms, displays a prominent plateau in the range of -20 to +20 mV

Front 21

phase 0 of AP in non-pacemaker cells

Back 21

the upstroke phase, non-stoppable phase, self-regenerating, all-or-none response, change of potential from negative to positive values, generated by Na+ channels, from ~-80 mV (resting potential) becomes depolarized to a value of ~+20 to +30 mV

Front 22

overshoot

Back 22

period where the potential is positive

Front 23

phase 1 of AP in non-pacemaker cells

Back 23

quick repolarizing phase that immediately follows the peak of the action potential, this phase is not apparent in nodal tissues, beginning of the repolarization phase

Front 24

phase 2 of AP in non-pacemaker cells

Back 24

plateau phase, long event, lasts about 150-200 ms, represents a period in which membrane potential remains relatively stable at a depolarized level, characteristic of cardiac muscle versus other excitable cells such as nerve and skeletal muscle, its duration and potential level are important determinants of the amount of force developed by the muscle, it is also not prominent in nodal tissues

Front 25

phase 3 of AP in non-pacemaker cells

Back 25

final phase of repolarization, its maximum velocity is a few orders of magnitude slower than phase 0

Front 26

phase 4 of AP in non-pacemaker cells

Back 26

resting potential, very stable, very polarized (very negative), diastolic phase
(i) pace-maker tissues capable of self-generating rhythmicity: slow depolarizing phase that ends when membrane potential reaches threshold for firing an AP
(ii) non pace-maker tissues (ventricles, atria): membrane potential is constant during this phase and is defined as the resting membrane potential of the cell

Front 27

how can one slow down SA node activity

Back 27

cholinergically, changes membrane potential to more negative so it takes longer to elicit an AP, can also change slope to slow down SA node activity

Front 28

K+ concentration and E

Back 28

if have [K+] of 0.1 M in one container and 0.01 M in another, then E = -60 mV

Front 29

Nernst Equation

Back 29

Eion = RT/zF log [X]o / [X]i, E ion is the equilibrium potential of the ion, R is the gas constant, T is temp, z is the charge or valence of the ion, F is faraday constant, Rt/zF is equal to 61.5 mV at 37C

Front 30

why is resting potential for SA nodal cells and smooth muscle cells not too polarized?

Back 30

because of an INC permeability to other ions

Front 31

ion distributions in most types of cells

Back 31

1. Na+ (extracellular: 145, intracellular 10, equilibrium potential +50)
2. Cl- (extracellular: 130, intracellular 20, equilibrium potential -47)
3. K+ (extracellular: 4, intracellular 150, equilibrium potential -90)
4. Ca2+ (extracellular: 2, intracellular 10^-7, equilibrium potential +140)
5. H+ (extracellular: 0.0001, intracellular 0.0002, equilibrium potential -18)

Front 32

Goldman-Hodgkin-Katz Equation (GHK)

Back 32

Em = 61.5 log (([K]o + PNa/Pk [Na+]0) / ([K]i + PNa/Pk [Na+]i)), this modified version uses the relative membrane permeabilities as opposed to the absolute, this is what determines where the resting potential will lie, gives a value for membrane potential

Front 33

membrane permeability

Back 33

responsible for setting the value of the resting membrane potential, more permeable to K+ compared to Na+, Ca2+ and Cl-, as opposed to skeletal muscle, the cardiac membrane permeability to Cl- is very low, Ca2+ also seem to contribute little, there is a significant permeability to Na+ which explains the small deviation of RMP from Ek

Front 34

non-pacemaker cell ratio of Pk/PNa

Back 34

Pk/PNa = 100

Front 35

pacemaker cell ratio of Pk/PNa

Back 35

Pk/PNa = 10

Front 36

resting potential vs. log [K+]o

Back 36

there is a straight line for Nernst potential for K+ if the membrane is completely permeable to K+, for ventricular cells, there is a deviation of the straight line (at low [K+], because the relative permeability is about 1% (1 Na+ / 100 K+), there is a much larger deviation form the E for K+ in SA nodal cells because the relative permeability is about 10% (1 Na+ / 10 K+), nodal cells have a much higher permeability ratio for Na:K at rest than ventricular cells

Front 37

what happens during a heart attack

Back 37

heart has its own vascular system, if one of the coronary arteries is blocked, then downstream low O2, DEC in ATP, consumed quickly, generation of lactic acid, Na+ and K+ movement across membrane will equilibrate, no ATP for the pump

Front 38

Na+/K+ pump

Back 38

is electrogenic and participates in determining the resting potential, can participate by as much as -10 mV to the resting potential of cardiac cells

Front 39

what determines the cardiac resting potential

Back 39

determined by an electrodiffusion potential generated by the presence of transmembrane ionic gradients and the relative permeability of the membrane to Na+ and K+, and by a small potential generated by the Na-K pump

Front 40

non-pacemaker cells vs. pacemaker cells

Back 40

non-pacemaker cells exhibit a high permeability ratio of K:Na and are thus more polarized (more negative RP) than pacemaker cells which display a relatively lower permeability ration of K:Na (~10)

Front 41

classes of ion channels

Back 41

1. ligand-gated channels: Ach-induced K+ channel in SA node cells
2. voltage and time dependent channels: Na+ channels (Phase 0 in non-pacemaker cells), normally have an aqueous pore, have a voltage sensor coupled to a gate, the pore has a selectivity filter that allows it to differentiate between the different ions
3. voltage and time independent channels: background channels (leak channels), voltage independent, movement depends on concentration

Front 42

voltage dependent channels

Back 42

have an aqueous pore, have a voltage sensor, sensor coupled to a gate, pore has a selectivity filter that allows it to differentiate between the different ions

Front 43

leak channels

Back 43

voltage independent, movement depends on concentration

Front 44

overdrive suppression

Back 44

related to the Na/K pump, per cycle there is one + charge moving out of the cell causing a hyperpolarizing current, if have high frequency stimulation in a Purkinje fiber (overdrive part), SA node may stop firing, if stops firing then hyperpolarization occurs due to Na+ channels until they close, when it closes then returns back to level, when back at level then Purkinje fiber can fire again starting action potential, suppression is when the pacemaker dies, stops firing, then go to secondary pacemakers

Front 45

what happens if you drop extracellular levels of Na+ to a lower level

Back 45

hyperpolarization of the resting potential more towards Ek, if drop Na+ to 0, then potential is at Ek

Front 46

Na+ current and phase 0 in non-pacemaker cells

Back 46

is a depolarizing current, + charge moves into the cell, Na+ current system is very large, -50 nA, huge density of sodium channels, caused by a regenerative INC in Na+ conductance, huge relative to all other currents (almost 50 times larger), open and inactivate quickly

Front 47

Long QT syndrome

Back 47

caused by an incomplete inactivation of the channels, leads to longer APs which favor the development of early after depolarizations (EADs)

Front 48

EADs

Back 48

dangerous electrical abnormalities that often result in severe ventricular arrhythmias such as torsades de Pointes, ventricular tachycardia and fibrillation

Front 49

maximum upstroke velocity

Back 49

the rate of depolarization during phase 0, aka Vmax, proportional to number of sodium channels that open, cells with high Vmax have high conduction velocities (e.g. Purkinje fibers)

Front 50

what happens to the number of available Na+ channels for activation as the membrane potential is depolarized

Back 50

the number of available Na+ channels decrease, more are inactivated

Front 51

Na+ channel gates

Back 51

m=activation gate, h=inactivation gate, at resting m is closed and h is open (inactivated inactivation gate), once threshold is release both the m and h gates are open, when repolarization occurs, the inactivation gate closes (activating the inactivation gate) while m remains opened (but Na+ cannot flow through because h is closed), then goes back to the rested state after the refractory period

Front 52

states of the Na+ channels

Back 52

rested->activated->inactivated->rested (after a recovery period)

Front 53

transient outward K+ channel (Ito)

Back 53

responsible for phase 1, voltage dependent channel, has some inactivation ability to it, if have no transient outward K+ channel then phase 1 is absent and only phase 2 is present, activate quickly once the threshold of -30 mV is reach, inactivate relatively quickly

Front 54

Ca2+ channels and phase 2 (Ica)

Back 54

responsible for phase 2, have slow inactivation, voltage gated, activation threshold of ~-40 mV, balances a slowly INC efflux of K+ ions through delayed rectifier K+ channels, d gate is the activation gate, f gate is the inactivation gate

Front 55

delayed rectifier K+ channel (Ik)

Back 55

activation threshold of -20 mV, helps maintain phase 2 with the help of Ca2+ channels and also responsible for phase 3, caused by a reduction in Ca2+ influx due to time and voltage dependent activation, and an INC in K+ mediated by Ik, as time goes on and repolarization continues, Ik closes, when below -20 mV then Ik1 (inward rectifier K+ channel) opens finishing repolarization and causing the AP to enter phase 4

Front 56

inward rectifier K+ channel (Ik)

Back 56

voltage and time independent, the only channel that is, a leak channel, magnitude varies with the driving force of the ion, if at Ek then there is no flux, if block this channel then cause membrane potential to move towards Ena and Eca (depolarization)

Front 57

regulation of inward rectifier K+ channel

Back 57

physiologically regulated by internal Mg2+ and the polyamines spermine and spermidine (+ charged organic molecules), during depolarization, Mg2+ and the polyamines are pushed into the internal side of the Ik1 channel pore and obstruct K+ permeation, block is relieved by membrane repolarization allowing Ik1 to terminate membrane repolarization and stabilize the resting potential during phase 4

Front 58

Ik1 and phase 4

Back 58

the stable resting membrane potential is caused by a high K+ permeability across Ik1 channels

Front 59

depolarizing currents and their channels

Back 59

1. Na+ channel-voltage dependent, -65 threshold, fast time dependent activation, fast time dependent inactivation, role is phase 0
2. Ca2+ channel-voltage dependet, -40 threshold potential, medium time dependent activation, medium time dependent inactivation, role is phase 2

Front 60

repolarizing currents

Back 60

1. Ik1 channel-voltage independent, no threshold potential, no time dependent activation, not time dependent inactivation, role is phase 4
2. Ito channel-voltage-dependent, -30 threshold, medium time dependent activation, medium time dependent inactivation, role is phase 1
3. Ik channel-voltage dependent, -20 treshold, slow time dependent activation, no time dependent inactivation, role is phase 3

Front 61

steady state activation and inactivation of Na+ and Ca2+ channels

Back 61

Ca2+ channels are slower than the Na+ channels and require more voltage change to become active or inactive, Na+ starts to become active at -60ish and is fully active at -50ish, Ca2+ channels become active at -40ish and are fully active at -10ish, in terms of inactivation Na+ channels begin inactivation at -90 and become fully inactive at about -60 mV, Ca2+ channels begin inactivation at -30 mV and become fully inactive at about 10 mV

Front 62

AP and ionic conductance in SA node cells

Back 62

ionic currents display a rhythmic oscillatory behavior, never stable in time as seen in ventricular and Purkinje fiber cells that are stable during the resting membrane potential during diastole

Front 63

phase 0 of the SA nodal AP

Back 63

is initiated from a much more depolarized membrane potential than that of non-pacemaker cells

Front 64

activation of the AP in SA nodal cells

Back 64

activated at a threshold of -50 to -40 mV, activation of two Ca2+ channels, one being activated at slightly more negative potential than the other, Na+ channels do not contribute to any of the phases of the SA nodal AP, Ca dependent phase 0 cells are slow, displaying a max upstroke vel. of 12-20 volts/sec., has slow onset of the voltage activated delayed rectifier K+ current which opposes the depolarizing influence of Ca2+ influx through Ica channels causing phase 3, repolarization causes activation of I funny

Front 65

I funny

Back 65

instead of being activated by depolarization, it is stimulated by hyperpolarization below -40 mV, also, when open the channel is non-selective allowing Na+ and K+ to flow through its pore relatively equally, when below -40, produces an inward current by Na+ influx depolarizing the membrane

Front 66

phase 4 diastolic depolarization in SA nodal cells

Back 66

repolarization caused by Ik leads to activation of If which opposes repolarization until a minimal potential point (maximum diastolic potential, MDP) is reached, the slow time and voltage dependent closure of IK combined with the slow onset of activation of If ends repolarization and initiates phase 4, Ik continues to decline and If grows until it reaches its threshold potential

Front 67

excitability

Back 67

the capacity of a cardiac cell to initiate an AP in response to an external stimulus, in non-pacemaker cells, related to INC in gna in pacemaker cells, related to INC in gca

Front 68

threshold potential

Back 68

critical level of membrane potential at which an all-or-none (propagating) response will be initiated

Front 69

maximum diastolic potential (MDP)

Back 69

most negative membrane potential achieved during diastole in cardiac cycle

Front 70

what happens when K+ INC outside as seen in cardiac ischemia

Back 70

if INC to about 8mM, has an effect on AP, causing inactivation of Na+ channels in the steady state, upstroke reduced because lower level of Na+ channels available (partially inactivated Ina), classified as a fast depressed response

Front 71

what happens if K+ is INC even further

Back 71

if INC to about 12mM, then lose even more Na+ channels, are classified as fast depressed response since Na+ channels still contribute to the response, but at a depressed level, becomes biphasic, has two phases, an initial and faster component still determined by Ina and a slower delayed component produced by opening of Ca2+ channels

Front 72

why is the Ca2+ current not effected by the INC in K+

Back 72

there is no inactivation of Ca+ channels until high levels of voltage change, start to inactivate at -40

Front 73

slow response

Back 73

occurs when the extracellular K+ levels reach 17 mM, occurs when Na+ channels become completely inactivated, found in heart attacks caused by coronary blood flow interruptions

Front 74

availability of voltage gated Na+ channels

Back 74

determined by the resting potential, membrane depolarization in the steady-state favors inactivation of these channels which diminishes their availability when a propagating depolarizing wavefront reaches a cell, if for any reason the resting potential becomes more +, Na+ channels will become gradually inactivated until membrane potential reaches a level where they are completely inactivated

Front 75

membrane depolarization and its effect on response

Back 75

depolarization reduces Vmax and the overshoot, a biphasic upstroke appears as well at intermediate resting potential levels, partial depolarization prior to stimulation causes the same stimulus to produce a small, slowly rising AP, these changes in the AP upstroke reflect the voltage-dependent closing of the inactivation gates of the Na+ channels

Front 76

refractory period

Back 76

takes some time for the Na+ channesl to become active again, eventually the upstroke is depressed because some will be unable to go back to its resting state to allow for entrance of Na+, depends upon relationship between the sodium conductance gna and membrane potential, recovery of gna from inactivation and magnitude of outward K+ current during repolarization

Front 77

what happens when a stimulus reaches threshold slowly

Back 77

produces a small, slowly rising AP, reflects the voltage-dependent inactivation of the Na+ channels, add stimulation before reaching the threshold, you have already started to inactivated Na+ channels so have a depressed response

Front 78

syncytium

Back 78

where multiple cells act as a single cell, cardiac muscles do act as this, interconnected by intercalated disks (form the basis of the electrical conduction between cells)

Front 79

gap junctions

Back 79

low resistance pathway for passage of currents between cells, formed by connexon proteins

Front 80

propagation

Back 80

passage of the AP along cells, velocity INC when size INC or when resting membrane potential INC

Front 81

absolute or effective refractory period (ARP or ERF)

Back 81

time following an AP in which it is not possible to elicit a second propagated response

Front 82

relative refractory period (RRP)

Back 82

interval following ERP during which only a supranormal stimuli can elicit a propagated response

Front 83

full recovery time (FRT)

Back 83

time following an AP after which the threshold for excitation returns to normal

Front 84

supernormal period (SNP)

Back 84

interval following ERP during which a subnormal stimuli can elicit a propagated response

Front 85

automaticity

Back 85

ability of cardiac cell to spontaneously depolarize and initiate propagated response

Front 86

conductance velocity

Back 86

the rate at which the wave of excitation spreads through the functional syncitium of the heart, depends upon the fiber diameter, maximum upstroke velocity of the AP and overshoot of the AP

Front 87

decremental conduction

Back 87

in most cardiac fibers, conduction spreads without decrement (constant conduction velocity, however in some areas conduction spreads with decrement (DEC in conduction velocity), a good example of decremental conduction is through the AV nodal region to the bundle of His, bundle of His has fast depolarization because has high density cells compared to other areas, has more gap junctions

Front 88

arrhythmia

Back 88

any disorder of rate, rhythm, origin or conduction of impulses within the heart

Front 89

normal sinus rhythm

Back 89

is the regular response of the heart to electrical impulses originating in the SA node and conducted normally through the atria and after a short delay through the AV node, ot the His-Purkinje system and finally activating the ventricular myocardium

Front 90

occurrence of arrhythmias

Back 90

1. acute myocardial infarction-80-90% incidence, when you have blockage in the heart, leads to ventricular arrhythmias
2. general anesthesia-20-50% incidence, some arrhythmias may be harmful affecting K+ channels everywhere
3. digitalis usage-drug used in heart failure, can be toxic, 10-20% incidence

Front 91

consequences of arrhythmias

Back 91

1. compromised mechanical performance (especially with tachycardias, extrasystoles, bradycardias, AV block, fibrillation)
2. triggers for more serious arrhythmias
3. formation of thrombi-may form stagnation of the heart, precursor of clots in the heart

Front 92

precipitating factors of clinical arrhythmias

Back 92

1. ischemia with pH and electrolyte abnormalities (reduction in blood flow, low O2 delivery, low evacuation of waste (CO2 products), accumulation of lactic acid, associated with changes in pH and electrolytes
2. excessive myocardial fiber stretch
3. excessive discharge or sensitivity to autonomic neurotransmitters
4. exposure to foreign chemicals (e.g. digitalis)

Front 93

sinus tachycardia

Back 93

atrial rate of 100-200, ventricular rate of 100-200, regular rhythm

****how to measure heart rate-use the pneumonic 300-150-100-75-60, start at QRS and measure how many solid lines pass before next QRS, if pass two then less than 150, if pass three, then less than 100...

Front 94

sinus bradycardia

Back 94

atrial rate of 40-60, ventricular rate of 40-60, regular rhythm

Front 95

atrial flutter

Back 95

atrial rate of 240-350, ventricular rate of 80-150, regular rhythm

Front 96

atrial fibrillation

Back 96

atrial rate of 300-600, ventricular rate of 140-175, very irregular rhythm

Front 97

paroxysmal atrial tachycardia

Back 97

atrial rate of 150-250, ventricular rate of 150-250, regular rhythm

Front 98

AV nodal tachycardia

Back 98

atrial rate of 100-180, ventricular rate of 100-180, regular rhythm

Front 99

ventricular tachycardia

Back 99

atrial rate of variable, ventricular rate of 100-250, regular/irregular rhythm

Front 100

ventricular fibrillation

Back 100

atrial rate of variable, ventricular rate of >300, no pulse or irregular rhythm

Front 101

mechanisms responsible for arrhythmias

Back 101

all arrhythmias are believed to result form either disorders of impulse formation, disorders of impulse conduction or both

Front 102

disorders of impulse formation (automaticity)

Back 102

there are those that lead to no change in pacemaker site (sinus bradycardia and sinus tachycardia) and those that do have changes in pacemaker site (ectopic pacemakers), leads to the emergence of latent pacemakers, automaticity resulting form injury current, oscillatory after-depolarizations

Front 103

disorders of impulse conduction

Back 103

there are those that have slowed conduction without re-entry and those that have slowed conduction with re-entry

Front 104

AV node primary and secondary pathways

Back 104

can have one pathway slower and the fast one is gone, leads to delayed conduction, can also have lengthened refractory period in AV node when the next impulse cannot make AP

Front 105

unidirectional conduction block

Back 105

favors re-entry, doesn’t go through in one direction, but it does in the other direction, when impulse goes on the right side, it can loop back and reexcite the structure

Front 106

bidirectional conduction block

Back 106

no looping as seen in the unidirectional conduction block, can’t reexcite

Front 107

requirements for re-entry

Back 107

1. unidirectional block (absolute requirement)
2. conduction time around alternative pathway must exceed the effective refractory period of the tissue

Front 108

factors that will favor development of re-entry

Back 108

1. long re-entrant pathway
2. slow conduction
3. short effective refractory period (could be due to ischemia or vagus nerve which slows down the refractory period)

Front 109

first degree AV block

Back 109

conduction velocity through AV node is slowed but all impulses reach ventricles, prolonged PR interval

Front 110

second degree AV block

Back 110

not all impulses reach ventricles and hence some P waves are not followed by QRS complexes

Front 111

third degree AV block

Back 111

complete block of all impulses through AV node, total dissociation of P waves and QRS complex

Front 112

determinants of conduction velocity

Back 112

1. factors-fiber diameter, rate of rise of phase 0 (upstroke) of AP, AP amplitude
2. AP types-fast responses, depressed fast responses, slow response

Front 113

influence of K+ on arrhythmias

Back 113

1. direct effect on resting membrane potential (hyperkalemia->depolarization)
2. indirect effects on upstroke velocity and hence conduction velocity (hyperkalemia -> DEC upstroke velocity and conduction velocity)
3. direct effects on automaticity

Front 114

hypokalemia

Back 114

can accelerate automaticiy leading to a very arrhythmogenic cell (especially ectopic pacemakers)

Front 115

hyperkalemia

Back 115

can depress automaticity (especially ectopic pacemakers)

Front 116

arrhythmias and long QT syndrome

Back 116

a single point mutation in a gene encoding for a channel can lead to arrhythmias, a long QT syndrome has an INC in QT interval, the AP is prolonged, can be three types
1. long QT type 1-caused by K+ channel mutation causing a reduced expression
2. long QT type 2-caused by delayed rectifier K+ channel mutation
3. long QT type 3-Na+ channel inactivation, slower inactivation of Na+ channel leading to a sustained current that remains during the inactivation of Na+ channel, causes a lengthening of the AP

Front 117

EKG

Back 117

records extracellular potential as a function of time, syncytium in heart allows for the measurement of the potential through an EKG, since it is extracellular the polarity sensed by the electrodes is reversed

Front 118

heart as a dipole

Back 118

a dipole is an asymmetrical distribution of electrical charges within a given volume conductor which creates an oriented electrical field, magnitude of voltage depends on both the distance to the dipole (the V DEC to the square of the distance to the dipole) and the position of the electrode

Front 119

unipolar recordings

Back 119

a sensing electrode is placed near the preparation, measures a potential difference relative to an indifferent electrode placed far away from the source, at resting state, electrode measures 0, not a lot of information can be obtained from a single recording (concerning velocity), need to measure between two different points,

Front 120

bipolar recordings

Back 120

uses two electrodes placed over the cardiac preparation and both will be influenced by changes in surface potentials, records a relative potential difference, can measure difference between the two electrodes, never sure if 0 means if the cells are all repolarized or depolarized, can measure conduction velocity, know distance between the two electrodes and time taken to reach from first electrode to second

Front 121

advantages of bipolar over unipolar recordings

Back 121

1. they can determine the direction of propagation as dipolar signals will be highest in the direction of propagation, this can be done by analyzing recordings from electrodes placed at different positions
2. conduction velocity can be measured

Front 122

why is there no recording from bundle of His, SA node and other such structures?

Back 122

mass is not that great compared to ventricles

Front 123

ST cycle and cells

Back 123

during the ST cycle all the cells are depolarized

Front 124

P wave

Back 124

caused by electrical potentials generated when the atria depolarize before atrial contraction begins, positive deflection, there is a delay between the P wave and the QRS complex and that is due to the fact that there is very slow conduction through the AV node, allows for pumping of blood through the atria into the ventricles, duration of 0.06-0.11 seconds

Front 125

length of P-R interval

Back 125

0.12-0.21 seconds

Front 126

QRS complex

Back 126

caused by potentials generated when the ventricles depolarize before their contraction, as the depolarization wave spreads through the ventricles, duration of 0.03-0.10 seconds, Q and S wave are small negative deflections that are due to the initial depolarization of the septum (on the LV side) and late activation of the base, R wave caused by activation of most of the ventricular mass

Front 127

formation of the Q wave

Back 127

caused by initial depolarization of the left side of the septum before the right side which creates a weak vector from left to right for a fraction of a second before the usual base-to-apex vector occurs

Front 128

T wave

Back 128

caused by potentials generated when the ventricles recover from the state of depolarization, repolarization, the atrial T wave is not seen because it fires when the QRS complex is being produced, duration varies

Front 129

duration of Q-T (measured from onset of Q to end of T)

Back 129

0.26-0.49 seconds

Front 130

duration of the ventricular AP

Back 130

0.25 to 0.35 seconds

Front 131

isoelectric segments

Back 131

waveforms on the EKG that are electrically silent, have no potential difference

Front 132

calibrations of the EKG paper

Back 132

Y-axis: thick lines or boxes (0.5 mV, each thin line is equivalent to 0.1 mV)
X-axis: thick lines (200 msec, each thin line is equivalent to 40 msec)

Front 133

what is the potential when the EKG is either completely polarized or depolarized

Back 133

there is no potential present, only when the muscle is partly polarized does current flow from one part of the ventricles to another part, and therefore some current flows to the surface of the body to produce the EKG

Front 134

how long does the ventricle remain contracted

Back 134

the ventricles remain contracted until a few milliseconds after repolarization has occurred at the end of the T wave

Front 135

P-Q interval

Back 135

the interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles, can also be called the P-R interval since the Q wave is often missing, about 0.16 seconds

Front 136

Q-T interval

Back 136

contraction of the ventricle, lasts from the beginning of the Q wave to the end of the T wave, about 0.35 seconds

Front 137

S-T interval

Back 137

is isoelectric segment, due to the fact that most ventricular cells are in the plateau phase

Front 138

why is the repolarizing T wave in the same direction as the depolarizing R wave

Back 138

have differences in repolarization mechanisms in the heart between the epicardium and endocardium, there is deflection because in space there is a difference in voltage between the epicardium and endocardium, endocardium activation occurs first, followed by the epicardium, in terms of repolarization, the epicardium repolarizes more quickly than the endocardium (answers question above)

Front 139

average current flow

Back 139

occurs with negativity toward the base of the heart and with positivity toward the apex, depolarization spreads from the endocardial surface outward through the ventricular muscle mass to the epicardium

Front 140

why is a gel added to the electrodes

Back 140

to lower the electrical resistance through the skin

Front 141

lead 1

Back 141

the negative terminal of the EKG is connected to the right arm and the positive terminal to the left arm, therefore, when the right arm is electronegative and left is electropositive, then the EKG records +, if vice versa, then records –, provides an index of impulse propagation in the horizontal direction of the frontal plane (0 degrees)

Front 142

lead 2

Back 142

negative terminal of the EKG is connected to the right arm and the positive terminal to the left leg, so if right arm is negative compared to left leg, then EKG is +, provides an index of impulse propagation of 60 degrees

Front 143

lead 3

Back 143

negative terminal is connected to the left arm and the + terminal is connected to the left leg, EKG is + when left arm is negative and left foot is +, provides an index of impulse propagation of 120 degrees

Front 144

Einthoven’s triangle

Back 144

drawn around the area of the heart, apices are the two arms and the left leg, right arm is always -, left arm is + or – and left leg is always +

Front 145

Einthoven’s law

Back 145

states that if the electrical potentials of any two of the three bipolar limb electrocardiographic leads are known at any given instant, the third one can be determined mathematically from summing the first two, to measure the lead voltages, take the differences of the instantaneous potential differences at each of the three spots, the sum of the voltages in leads I and III equals the voltage in lead II

Front 146

precordial chest leads

Back 146

set of six leads (V1-V6), unipolar recordings as the voltage recorded from them are measured relative to a common ground obtained by connecting the three limb electrodes together, useful to obtain information on patterns of ventricular activation in the transverse or horizontal plane (can pinpoint where in the ventricular chambers an abnormality is arising)

Front 147

leads V1, V2…V6

Back 147

six standard chest leads that are recorded from the anterior chest wall (+ electrode), negative electrode is connected through equal electrical resistances to the right arm, left arm, and left leg all at the same time, measures the electrical potential of the cardiac musculature immediately beneath the electrode

Front 148

V1 and V2

Back 148

the QRS recordings of the normal heart are mainly negative because the chest electrode in these leads is nearer to the base of the heart than to the apex

Front 149

V4, 5, and 6

Back 149

the QRS complex is mainly + because the chest electrode in these leads is nearer the apex, which is the direction of electropositivity during most of the depolarization

Front 150

positions of the precordial chest leads

Back 150

` V1-fourth intercostal space just to the right of the sternum
V2-fourth intercostal space just ot the left of the sternum
V3-midway between V2 and V4
V4-fifth intercostal space at the left midclavicular line
V5-left anterior axillary line horizontally to the left of V4
V6-midaxillary line horizontally to the left of V4 and V5

Front 151

augmented unipolar limb leads

Back 151

two of the limbs are connected through electrical resistances to the negative terminal of the EKG (acts as an indifferent electrode) and the third limb is connected to the positive terminal, makes aVR, aVL and aVF leads

Front 152

aVR lead

Back 152

when the + terminal is on the right arm, recording is inverted, negative depolarization, provides an index of impulse propagation at an angle of 210 degrees

Front 153

aVL lead

Back 153

when the + terminal is on the left arm, provides an angle of impulse propagation at an angle of 330 degrees

Front 154

aVF lead

Back 154

when the + terminal is on the left leg, provides an index of impulse propagation of 90 degrees from the horizontal plane

Front 155

use of vectors to represent electrical potentials

Back 155

an arrow that points in the direction of the electrical potential generated by current flow, with the arrowhead in the positive direction, the length of the arrow is drawn proportional to the voltage of the potential

Front 156

mean QRS vector

Back 156

the average direction of the vector in a normal heart during the spread of the depolarization wave through the ventricles, is about + 59 degrees

Front 157

axis of the lead

Back 157

the direction from the negative to the positive electrode, lead I has an axis of 0, lead II has an axis of about +60 degrees, lead III has an axis of 120 degrees, aVR is 210, aVL is 90 and aVF is 330 (-30)

Front 158

hexagonal reference system

Back 158

a diagram that shows the axes of all the bipolar and unipolar leads as well as their polarities, from 0 to 360 the axes and polarities are (I, avR, II, aVF, III, aVL) (+, -, +, +, +, -, -, +, -, -, -,+)

Front 159

vectorial analysis of potentials in different leads

Back 159

basically take the vector for the instantaneous potential in the ventricle and connect a perpendicular line from the tip of that vector to the line of the axis of the lead, the vector that runs from the base of the vector for potential to the perpendicular line is how much potential (and its sign) will be detected by the EKG, therefore when the vector in the heart is in a direction almost perpendicular to the axis of the lead, the voltage recorded in the EKG of this lead is very low, conversely when the heart vector has almost exactly the same axis as the lead, essentially the entire voltage of the vector will be recorded

Front 160

which side of the heart depolarizes faster

Back 160

the right side of the heart depolarizes faster than the left side of the heart, therefore the vector for the instantaneous potential progressively moves to the lefts side

Front 161

repolarization of the heart

Back 161

after the ventricular muscle has become depolarized, about 0.15 seconds elapses before sufficient repolarization begins for it to be observed in the EKG, it is complete at about 0.35 seconds after the onset of the QRS complex

Front 162

so what is the order of muscles in the heart in terms of repolarization for the ventricle

Back 162

the greatest portion of ventricular muscle to repolarize first is that located over the entire outer surface of the ventricles (epicardium) and especially near the apex of the heart, then the septum (endocardium) is repolarized

Front 163

why is this the order for repolarization

Back 163

high blood pressure inside the ventricles during contraction greatly reduces coronary blood flow to the endocardium, thereby slowing the repolarization process in the endocardial areas

Front 164

direction of the vector during repolarization

Back 164

the direction of the vector through the heart during repolarization of the ventricles is from base to apex, the same as the direction during depolarization, as a result the normal T wave in the three bipolar limb leads is positive, first small then grows then shrinks

Front 165

how long is the duration of repolarization

Back 165

0.15 seconds, that is how long the T wave lasts

Front 166

what is the order of muscles in the heart in terms of repolarization of the atria

Back 166

spread of depolarization is slow in atria, the area in the atria that also becomes repolarized first is also the sinus nodal region, therefore the vector for atrial repolarization is backwards to the vector of depolarization

Front 167

mean electrical axis of the venctricular QRS

Back 167

the direction of the electrical potential is from the base of the ventricles toward the apex during most of the cycle, mean value is 59 degrees, in pathological conditions, this direction is changed

Front 168

what causes variations in the mean electrical axis

Back 168

the causes of the normal variations are mainly anatomical differences in the Purkinje distribution system or changes in the musculature itself of different hearts, a number of abnormal conditions can causes axis deviation even beyond these normal limits

Front 169

changes in the position of the heart and the mean electrical axis

Back 169

if heart angulates to the left, the mean electrical axis of the heart also shifts to the left, seen at the end of deep expiration, when a person lies down and in fat, stocky people whose diaphragms normally press upward against the heart, angulation can also occur to the right as seen at the end of deep inspiration, when a person stands up or in tall lanky people whose hearts hang downward

Front 170

ventricular hypertrophy and the mean electrical axis

Back 170

when one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle for two reasons, (1) a far greater quantity of muscle exists on the hypertrophied side allowing for excess generation of electrical potential on that side and (2) more time is required for the depolarization wave to travel through the hypertrophied venctricle than through the normal ventricle

Front 171

left axis deviation due to hypertrophy of the left ventricle

Back 171

may see a prolonged QRS complex, can be due to INC in blood pressure, aortic valcular stenosis or aortic valvular regurgitation

Front 172

right axis deviation due to hypertrophy of the right ventricle

Back 172

can be caused by congentital pulmonary valve stenosis, but can also occur in other congenital heart conditions that cause hypertrophy of the right ventricle, such as tetralogy of Fallot and interventricular septal defect

Front 173

bundle branch block and axis deviation

Back 173

if have bundle branch block then depolarization spreads through the normal ventricle long before it spreads through the blocked one leading to axis deviation

Front 174

left bundle branch block and axis deviation

Back 174

the right ventricle becomes electronegative whereas the left ventricle remains electropositive during most of the depolarization process and a strong vector projects from the right ventricle toward the left ventricle, great prolongation of the QRS complex

Front 175

right bundle branch block and axis deviation

Back 175

the left ventricle becomes electronegative far before the right ventricle does, get intense right axis deviation

Front 176

causes of INC voltage in the limb leads

Back 176

if sum of three leads is greater than 4 mV, then considered high, usually due to INC muscle mass of the heart (usually due to hypertrophy of the heart)

Front 177

causes of DEC voltage in the limb leads

Back 177

usually due to a series of old myocardial artery infarctions with resultant diminished muscle mass, also causes depolarization wave to move slowly leading to prolongation of the QRS complex, may also be caused by fluid in the pericardium acting as a short circuit to the potential (pleural effusion, pulmonary emphysema (leads to excessive air in the lungs which slows down conduction))

Front 178

prolonged QRS

Back 178

cause is always prolonged conduction of the impulse through the ventricles, may be caused by hypertrophy or dilation

Front 179

Purkinje system block and prolonged QRS

Back 179

if blocked then the cardiac impulse must be conducted by the ventricular muscle, DEC velocity to about 1/3 to ¼ normal

Front 180

bizarre QRS

Back 180

due to either (1) destruction of cardiac muscle in various areas throughout the ventricular system with replacement of this muscle by scar tissue and (2) multiple small local blocks in the conduction of impulses at many points in the Purkinje system

Front 181

current of injury

Back 181

occurs when the current flows between the pathologically depolarized and the normally polarized areas even between heartbeats, the injured part of the heart is negative because this part is depolarized and emits negative charges into the surrounding fluids, whereas the reaminder of the heart is positive

Front 182

causes of current of injury

Back 182

1. mechanical trauma-makes the membranes remain so permeable that full repolarization cannot take place
2. infectious processe-damage the muscle membranes
3. ischemia of local areas of muscle caused by local coronary occlusions-most common, not enough nutrients from the coronary blood supply are available to the heart muscle to maintain normal membrane polarization

Front 183

effect of slow conduction of the depolarization wave on the T wave

Back 183

slow conduction in say the left ventricle can cause the mean axis of the T wave to deviate to the right, opposite to the mean electrical axis of the QRS complex, T wave is opposite polarity to that of the QRS complex when slow conduction is the problem

Front 184

mild ischemia and the T wave

Back 184

most common cause of INC duration of depolarization of cardiac muscle, and if it occurs in only one area then changes in the T wave may take place

Front 185

digitalis and the T wave

Back 185

digitalis is a drug that can be used during relative coronary insufficiency to INC the strength of cardiac muscle contraction, also INC the duration of depolarization of cardiac muscle by about the same proportion in all or most of the ventricular muscle, if overdosed then may lead to T-wave inverstion and even to current of injury, use EKG to prevent from overdosage of digitalis

Front 186

SA node abnormalities

Back 186

sinus bradycardia, sinus tachycardia, sinus arrest, sinus tachycardia

Front 187

sinus bradycardia

Back 187

an SA node abnormality, reduced firing rate originating from the SA node

Front 188

sinus tachycardia

Back 188

an SA node abnormality, enhanced firing rate originating from the SA node

Front 189

abnormalities originating from the atria themselves

Back 189

premature contractions, atrial tachycardia, atrial flutter, atrial fibrillation

Front 190

arrhythmias of junctional origin (AV node, bundle of Hiss, Purkinje Fibers)

Back 190

first, second and third degree AV blocks, premature junctional contractions, junctional escape rhythm, junctional tachycardia

Front 191

ventricular arrhythmias

Back 191

premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, ventricular asystole

Front 192

determination of mean axis deviation

Back 192

a left or right axis deviation may be a sign of cardiac hypertrophy

Front 193

example of right axis deviation

Back 193

this could be a consequence of right ventricular hypertrophy possible caused by obstructive lung disease or pulmonary hypertension, such conditions would chronically INC the afterload imposed on the right ventricle

Front 194

example of left axis deviation

Back 194

this could be a consequence of left ventricular hypertrophy which might be physiological (training athletes) or pathological due to an increased afterload (e.g. systemic hypertension, aortic stenosis etc.)

Front 195

detection of ischemic heart disease

Back 195

chronic (e.g. atherosclerosis) or acute (e.g. acute myocardial infarcation) stoppage of blood flow or ischemia may lead to reversible or irreversible damage to the myocardial cells irrigated by the impaired coronary artery, Such a depression will impair the metabolic, electrical and mechanical properties of the underperfused area of the heart. Action potentials generated in these areas may be depressed exhibiting a lower resting membrane potential and reduced duration. Electrical disparities between damaged and normal well perfused areas can create injury currents flowing across these during both diastole and systole. The ECG waveform, in particular the S-T segment (depressed or elevated) and T wave (amplitude, shape and polarity) are very sensitive to such electrical inhomogeneities. As a clinician, you will rely heavily on interpretation of the ECG to assess whether a patient suffered from a heart attack and determine the site of injury (precordial leads are particularly useful in that respect).

Front 196

why is the ST segment isoelectric?

Back 196

all cells are depolarized, currently in phase 2, thus there is no electrical potential difference between the two electrodes

Front 197

to which electrical waveform is the diagram beside corresponding to? (the waveform is where depolarization is almost complete but not yet, instantaneous potential pointing up and left)

Back 197

the S wave

Front 198

for a normal heart, the polarity of the signal in aVr…aVf…lead III

Back 198

negative, positive, positive

Front 199

ventricular AP with a short delay

Back 199

delay caused by process of excitation-contraction coupling, not possible to induce tetanus in the muscle because it is impossible to sum the contractions, always phasic contractions in the heart, peak of contraction is during phase 3 of AP

Front 200

Ca2+ transient

Back 200

the temporal change in the concentration of free intracellular Ca2+ concentration during one cardiac beat

Front 201

membrane in skeletal muscle

Back 201

has a plasma membrane (sarcolemma) that produces invatinations inside the cell, contiguous with the plasma membrane into T-tubules

Front 202

membrane in the heart

Back 202

has a dyad, not a triad, will find a saccule of SR on one side and a T-tubule on the other

Front 203

T-tubules

Back 203

if no T-tubules are present then only the surface myofibrils would be activated, by having the T-tubules it allows for a powerful contraction, T-tubules narrower in skeletal muscle than in cardiac muscle, bifurcate to follow the longitudinal axis of the cell, continuous with the extracellular space

Front 204

SR

Back 204

an extensive intracellular membrane network, portion that takes part in formation of the dyad is the subsarcolemmal cisternae (other portion is the sarcotubular network), contains large amounts of stored Ca2+ which are released during EC-coupling

Front 205

triad

Back 205

comes from a unit of SR-T-Tubule-SR

Front 206

cardiac mycocytes

Back 206

polynucleated cells, have striations, lots of mito (occupy ~35%), use a lot of O2 to contract

Front 207

I band

Back 207

isotropic, is mainly formed of thin filaments (actin)

Front 208

A band

Back 208

thick, dark area of the muscle (anisotropic), ordered overlap between thick filaments (mainly composed of myosin)

Front 209

ATP in the cardiac myocyte

Back 209

ATP utilized for contraction (~65-70%) and maintanence of the ionic gradients necessary for cellular excitability and excitation-contraction coupling

Front 210

an isolated rat ventricular myocyte shortening

Back 210

monitor contraction via phase contrast, when have 1 mM extracellular Ca2+ and switch to one with no Ca2+, immediately lose contraction, have definitive dependence on extracellular calcium, when get it back then get full blown contraction again, not caused by depletion of stores

Front 211

single frog skeletal fiber

Back 211

measure tension, have ringer solution, contraction is even higher when calcium is absent, EGTA is used (makes sure that the Ca2+ is not involved, is a Ca2+ chelating agent), extracellular Ca2+ is not directly involved in excitation-contraction coupling in skeletal muscles

Front 212

heart muscle

Back 212

absolutely requires Ca+ in the extracellular fluid to contract

Front 213

mechanism for the generation of the Ca2+ transient

Back 213

AP propagates along the sarcolemma and T-tubule triggering Ca2+ release from the SR, voltage and time-dependent Ca2+ channels open, maintains the long plateau phase of the AP, Ca2+ enters from the extracellular space (Ca from this method accounts for only about 5-10%, rest from SR)

Front 214

dihydropyridine receptors (DHP)

Back 214

the Ca2+ channels used in Ca2+ entrance, compounds of this class (e.g. nifedipine) are inhibitors of these channels

Front 215

Ca2+ release at the dyads

Back 215

there is large amounts of Ca2+ stored in the SR, released by Ca2+-induced Ca2+ release (CICR), dyadic regions of the T-tubules act as an amplification system to enhance the magnitude and kinetics of the Ca2+ transient

Front 216

CICR

Back 216

occurs because of the preferential juxtaposition of Ca2+ channels in the T-tubules with a different class of Ca2+ channels present in the SR called ryanodine receptors (RyR)

Front 217

RyR

Back 217

activated by Ca2+ entering the cell through the T-tubule Ca2+ channels, Ca2+ binding to specific sites through to be located at the surface of the RyR protein triggers the opening of this large multi-barreled channel allowing intracellular Ca2+ release due to the steep chemical gradient between the inside of the SR and cytoplasm, the rat of release initially INC until it reaches a max, after which it declines due to a DEC driving force for Ca2+ and an intrinsic inactivation mechanism which closes the RyR, there are fast and slow types, also allows for lateral movement of Ca2+

Front 218

relationship between intracellular Ca2+ and force in cardiac muscle

Back 218

there is a sigmoidal relationship between [Ca2+] and force, at 50% force at a normal beat to beat cardiac cycle, can add more Ca2+ intracellularly to build more force (a major pathway for the cardiac muscle cell to INC force), 50% force at about 600 nm [Ca2+]

Front 219

roles of Ca2+ current in cardiac excitation-contraction coupling

Back 219

responsible for maintaining the long plateau of the AP, triggers the release of Ca2+ from the SR (amplification of the plasma membrane signal), refills the SR Ca2+ stores to be used in subsequent beats

Front 220

relaxation of the Ca2+ transient

Back 220

inactivation of RyR is one form, also promoted by Ca2+ transporters present in the sarcolemma, T-tubules and mito, major one is the Ca2+-ATPase present in the SR membrane, also a Na+/Ca2+ exchanger

Front 221

Ca2+-ATPase

Back 221

accounts for 70-80% of rate of relaxation of the Ca2+ transient, pump is activated by Ca2+ on the cytoplasmic side of the membrane and uses the energy liberated from ATp hydrolysis to drive Ca2+ back into the SR against its steep electrochemical gradient

Front 222

Na+/Ca2+ exchanger

Back 222

present in the T-tubules and sarcolemma, does not require ATP, uses the energy provided by the inwardly-directed Na+ gradient to drive Ca2+ out of the cell, 3 Na+ are transported in for each Ca2+ transported out of the cell, accounts for 25-30% of the overall rate of relaxation of the Ca2+ transient, responsible for more than 95% of Ca2+ transport out of the cell, major mechanism for balancing Ca2+ entry although it plays a lesser role than the SR Ca2+-ATPase in determing the overall rate of relaxation of the Ca2+ transient

Front 223

digitalis toxicity

Back 223

uses the Na+/Ca2+ exchanger system for toxicity, if partially block the Na/K leads to accumulation of Na+ and this reverse the exchanger

Front 224

regulation of contractility by changes in the morphology of the AP

Back 224

the actual shape of the AP has an effect on contractility, due mostly to Ca2+ channels, injection by an electrode inside the cell

Front 225

premature systole

Back 225

caused by a unit time when more Ca2+ enters the cell, extra Ca2+/time is stored in SR, then next AP makes larger reaction

Front 226

staircase phenomenon

Back 226

after a sudden INC in freq. of stimulation, there is a slow build up of contraction which will reach new steady state level w/ higher tension strength, due to more Ca2+ refilling the SR, more and more reaching a new steady state level at a higher freq., without the influence of the ANS, can INC force of contraction by INC freq., phasic not summation, the additional Ca2+ influx through Ca2+ channels is not readily available to activate Ca2+ release but is rapidly captures by the SR Ca2+-ATPase

Front 227

importance of the AP morphology and Ca+ current

Back 227

determinant of the magnitude of the Ca2+ transient is the duration and morphology of the AP, lengthening the AP leads to enhancement of the Ca2+ transient and contraction, elevation of plateau phase also INC Ca2+ transients of subsequent beats, these happen bec. the voltage and time dependent properties of the Ca2+ channels change in such a way that more or less Ca2+ enters the cell per unit time

Front 228

importance of internal Na+ in determining contractility

Back 228

Na+ plays a role in overall Ca2+ balance, have an influence on the Na+/Ca2+ exchanger

Front 229

cardiac glycosides

Back 229

e.g. digitalis, improve the mechanical performance of the heart, influence the Na+/Ca2+ exchanger, inhibitors of the Na+/K+ pump, leads to accumulation of Na+, yields reduced Ca2+ extrusion, Ca2+ accumulates and is reuptaken by the SR INC its Ca2+ content, this Ca2+ is then available for relased during an AP through CICR

Front 230

the heart chamber and muscle mechanics

Back 230

when the heart chamber shortens, the thickness of the wall INC relieving some of the tension across the ventricular wall, generates pressure instead of tension, causes ejection of blood rather than a decrease length, changes in tension and length are transformed into changes in pressure and volume, V = (4*pi*r^3)/3, when there is a 50% reduction in the radius, this would lead to an 87.5% decrease in V, when there is a smaller change in the radius there is a bigger change in volume (DEC in volume), impact on pumping blood through the circulation

Front 231

Laplace’s Law

Back 231

T = (P * R) / h (wall stress = pressure * radius / wall thickness), during a contraction there is enormous development of pressure on the wall causing an INC in thickness in heart chamber alleviating the tension that is on the heart, force applied to surface of the heart will INC greatly and this can be alleviated by the wall thickness during contraction, can alleviate tension by a decrease in radius in chamber during contraction

Front 232

pressure vs. wall stress

Back 232

pressure is the amount of force/unit surface applied perpendicularly to the heart wall, wall stress is the shear force exerted around the circumference of the cardiac chambers

Front 233

the heart and applying Laplace’s Law

Back 233

the cells forming the ventricular wall allows individual ventricular cells to share the burden of wall stress by a distribution over several layers, endocardial cells undergo greater changes in wall stress during systole than epicardial cells

Front 234

heart failure and Laplace’s Law

Back 234

heart failure is characterized by a marked enlargement of the ventricular chamber (ventricular dilation) and thinning of the heart wall,

Front 235

systole and types of contractions

Back 235

during systole the heart contracts through a cycle of isometric and isotonic contractions followed by isotonic and isometric relaxation, goes from isometric contraction -> isotonic contraction -> isotonic relaxation -> isometric relaxation

Front 236

isometric contraction

Back 236

muscle contracts, force develops but there is no change in length until it exceeds the load
isotonic contraction

Front 237

isotonic contraction

Back 237

when the muscle undergoes a force larger than the weight, the muscle undergoes shortening and the load is displaced

Front 238

isotonic relaxation

Back 238

occurs when muscle relaxation just begins and the load is still suspended but moving down with gravity

Front 239

isometric relaxation

Back 239

occurs once the load reaches the support

Front 240

tension vs. length graph

Back 240

for a skeletal muscle, makes an upside down L shaped graph with isometric contraction occurring at a longer length, INC in tension, then DEC in length during an isotonic contraction, is a square if the load is removed at the end of the isotonic contraction (this is the model for how the heart works), if this is the case then isometric relaxation occurs before isotonic relaxation

Front 241

what causes the removal of weight that causes the heart to act like a box and not an L?

Back 241

when the pressure in the aorta is greater than in the ventricle, this leads to closure of the valve due to difference in pressures, this causes isometric relaxation, this is just like taking off weight, the muscle then undergoes isotonic relaxation

Front 242

active tension

Back 242

follows a bell curve when looking at a tension vs. length graph, INC to max at lmax, then starts to decline as INC length even more, there is no difference in active tension in skeletal vs. cardiac muscle because the sarcomere length is relatively the same

Front 243

passive tension

Back 243

AKA resting tension, has nothing to do with any contractile properties of the heart, just the structure, these are non-active elastic components of the muscles that have their own compliance to being stretched, when this structure is stretched then one gets tension (like a rubber band), keeps INC with an INC in length (doesn’t stop INC), passive tension curve in skeletal muscle starts at lmax, in heart starts at active tension, this is what causes the big difference, relates to starlings law of the heart, if stretch ventricular chamber then leads to larger force development

Front 244

index of contractility

Back 244

the rate a muscle contracts and relaxes per unit time (dP/dt), when heart is stimulated with epinephrine, the pressures INC a little bit but get a large INC in max dP/dt

Front 245

velocity vs. force relationship

Back 245

Vmax is inversely proportional to afterload, higher velocity with smaller force, P0 is the pressure where there is no contraction in the blood (no pumping)

Front 246

ANS role on velocity vs. force graph

Back 246

during interventrion of the ANS (beta-agonist), the curve is shifted to the right producing a more powerful contraction against a larger load

Front 247

congestive heart failure role on velocity vs. force graph

Back 247

smaller power is present shifting the curve to the left, Vmax is also reduced

Front 248

Pressure-Volume loop

Back 248

done by taking one cardiac cycle and measuring the pressure developed by the heart and the heart’s volume (shows the changes in intraventicular pressure as a function of blood volume), the two thin lines (upper and lower lines) define the limits of pressure changes that the heart can develop at any given volume of blood

Front 249

end-diastolic pressure volume

Back 249

the bottom thin line on the pressure-volume loop, defines the properties of the relaxed hart (lusitropic properties), defines the forces emanating form the circulation that tend to fill the heart with blood

Front 250

end-systolic pressure volume

Back 250

the top thin line on the pressure-volume loop, good index of myocardial contractility (inotropy) and its relationship with the circulation (aortic pressure)

Front 251

pre-load

Back 251

how much blood there is before a contraction, end of diastole, found on the corner of the A and D segment, occurs before there is isovolumic/isometric contraction, because the pressure within the left ventricle exceeds the left atrial pressure the mitral valve is closed, heart builds up pressure because blood is filling and valves are closed

Front 252

isovolumic contraction of the heart

Back 252

when the ventricles are filling with blood, INC pressure with constant volume, once the pressure within the ventricle exceeds that in the aorta, the aortic valve opens bringing a start to the ejection phase

Front 253

afterload

Back 253

pressure at which the ejection phase begins, is where the force against which the heart must contract and exceed to get an ejection phase)

Front 254

ejection phase

Back 254

pressure continues to rise and then falls until the end-systolic pressure is reached

Front 255

end-systole

Back 255

break point, caused by the valve closing because the pressure inside the ventricles become lower than in the aorta and there is isovolumic relaxation of the heart before filling starts again, this is why there is no filling in this phase and why volume stays constant, relaxation phase

Front 256

isovolumic relaxation of the heart

Back 256

relaxation at a constant volume as pressure decreases, aortic valve is closed, pressure drops quickly because the ventricle is disconnected from its load, pressure continues to fall until it drops below the left atrial pressure which opens the mitral valve, then pressure rises slowly as the ventricle fills with more blood and volume INC

Front 257

what happens to passive curve during hypertrophy

Back 257

have much thicker walled heart, compliance is much less, stiffer, greatly impacts contraction of the heart in terms of the pressure that needs to be produced, have enhancement of the slope of the passive curve, need more pressure to eject blood, usually caused by high BP, causes chronic changes in heart remodeling

Front 258

Starling’s Law of the heart

Back 258

the heart has an ability to INC its contractility in reponse to an INC in blood volume, systolic pressure is top line and diastolic is bottom line, INC volume augements both the end-diastolic and systolic pressure, by subtracting the end-diastolic pressure and systolic pressure, forms the starling curve, law states how the heart balances out changes in blood volume in different compartments of the vascular system

Front 259

starling curve

Back 259

reflects the net contractility of the heart, has a ascending and descending limb

Front 260

ascending limb of starling curve

Back 260

represents the normal range of blood volumen changes that occur physiologically, the heart is able to modify its ejection volume in the face of the changing preload imposed by venous return

Front 261

descending limb of starling curve

Back 261

at very high volumes, the performance of the heart declines, due to (1) a DEC in the compliance of the heart and (2) the volume limit imposed by the pericardium, descending limb helps to protect the ventricle from the serious consequences of overfilling

Front 262

What is the cardiac cycle?

Back 262

the series of electrical and mechanical events taking place during one heart beat, measures aortic pressure (which is a direct measure of BP), atrial pressure, ventricular pressure, ventricular volume, EKG and phonocardiogram

Front 263

What accounts for the first heart sound?

Back 263

occurs when both AV valves close due to the ventricular pressure exceeding the atrial pressure

Front 264

When does maximum ejection occur

Back 264

occurs during the phase when there is continued rise of the ventricular and aortic pressure until a peak is reached, the rate of ejection of blood is equal to the rate of evacuation of blood from the aorta

Front 265

What accounts for the second heart sound?

Back 265

occurs when the aortic valve closes due to ventricular pressure falling to a level below that of the aortic pressure

Front 266

What accounts for the AV valves opening?

Back 266

when the semilunar valves close, ventricular pressure continues to decline until the atrial pressure exceeds it, this causes the AV valves to open, the ventricles then rapidly fill with blood, this rapid filling may cause a 3rd weaker sound, atria then contract which slightly INCs both atrial and ventricular pressures and provides additional priming for ventricular filling, may make a 4th weaker sound

Front 267

what is cardiac output?

Back 267

it is the quantity of blood pumped into the aorta each minute by the heart

Front 268

what is venous return?

Back 268

it is the quantity of blood flowing from the veins into the right atrium each minute

Front 269

What is the average cardiac output (CO) at rest and why must it match venous return (VR)?

Back 269

~5 L/min, must be matched to venous return to adequately supply the needs of the body in oxygen and nutrients, this is controlled by Starling’s law (stroke volume INC when more blood fills the heart and vice versa)

Front 270

What factors directly affect CO?

Back 270

the level of body metabolism, whether the person is exercising, the person’s age and the size of the body

Front 271

What is an equation for calculating cardiac output?

Back 271

CO = arterial pressure/total peripheral resistance, so that way when afterload INC, CO DEC

Front 272

What is the cardiac index (CI)?

Back 272

it is a value that normalizes CO with respect to body mass and the fact that CO changes with age, is the CO per square meter of body surface area and therefore has units of L/min/m^2

Front 273

what is a normal CI value for a young male adult?

Back 273

3 L/min/m^2

Front 274

what effect does age have on CO?

Back 274

rises rapidly to about an age of 10 years (~4.5 for CI), then declines to about 2.4 at age 80

Front 275

Describe Frank-Starling in terms of mechanics.

Back 275

when INC quantites of blood flow into the heart, the INC blood stretches the walls of the heart chambers, as a result of the stretch the cardiac muscle contracts with INC force and empties from the expanded heart chambers the blood that has entered from the systemic circulation, therefore the extra blood that came in is excrete out with no delay

Front 276

What effect does right atrial pressure have on cardiac output?

Back 276

CO INC in a sigmoidal fashion as a function of right atrial pressure, normal CO can be INC by ~2.5 fold to a max of ~13 L/min (where it then plateaus, this is the point at which the heart becomes the limiting factor) in a heart that pumps better than normal or drop just as much in a hypoeffective heart that pumps less than normal

Front 277

What is the cardiac function curve?

Back 277

it expresses CO as a function of right atrial pressure, also important in analyzing what the limit is of the amount of blood that the heart can pump

Front 278

Why does the curve start at a negative right atrial pressure?

Back 278

right atrial pressure depends on intrapleural pressure, under normal conditions that pressure is -4 mm Hg

Front 279

How does breathing influence intrapleural pressure?

Back 279

during normal breathing, intrapleural pressure oscillates by +/- 3 mmHg, this can INC to about +/- 50 mmHg during strenuous exercise, this negative pressure in the chest has an impact on CO and VR because it determines the pressure in the right atrium

Front 280

How is the cardiac function curve shifted up (made hypereffective)?

Back 280

1. sympathetic stimulation (which INCs heart rate and cardiac contractility) as well as parasympathetic inhibition-causes an INC in heart rate and strength of contraction (INC contractility)
2. cardiac hypertrophy or INC cardiac mass through growth (as in marathon runners, CO can reach 30-35 L/min)-

Front 281

How is the cardiac function curve shifted down (made hypoeffective)?

Back 281

these all causes DEC in the heart’s ability to pump blood
1. inhibition of nervous excitation
2. conditions leading to irregular heart rhythms
3. valvular heart disease
4. hypertension
5. congenital heart disease
6. myocarditis
7. cardiac anoxia
8. diphtheria or other types of myocardial damage or toxicity

Front 282

What is the role of the nervous system in controlling CO?

Back 282

the nervous system gives pressure control, without pressure control, arterial pressure falls and the CO rises very little when the heart is stimulated metabolically, leads to vasodilation of vessels that causes a fall in arterial pressure

Front 283

What does dinitrophenol do?

Back 283

it is a metabolic stimulant that INCs CO greatly

Front 284

How does the nervous system INC the arterial pressure during exercise?

Back 284

brain activity that fires signals to the peripheral muscles that cause exercise also sends simultaneous signals into the autonomic nervous centers of the brain to excite circulatory activity causing a rise in heart rate and contractility, INC pressure causes more blood flow to the active muscles

Front 285

What peripheral factors can cause a DEC in CO and subsequently in VR?

Back 285

1. DEC blood volume-most common, results from hemorrhage
2. acute venous dilation-results when the sympathetic nervous system becomes inactive, this causes a DEC in the filling pressure of the vascular system, blood pools in the vessels and cannot fill the heart
3. obstruction of the large veins-means blood can’t get back into the heart

Front 286

How does external pressure outside the heart effect CO?

Back 286

if external pressure rises (say from -4 to -2 mm Hg), then the CO curve moves to the right because in order to fill the cardiac chambers with blood requires an extra 2 mm Hg right atrial pressure to overcome the INC pressure on the outside of the heart

Front 287

How does a reduction in intrapleural pressure (breathing against a negative pressure) and cardiac contractility affect the cardiac function curve?

Back 287

will lower the maximum CO and shift the curve to the left towards lower right atrial pressures

Front 288

How does an elevation of intrapleural pressure (positive pressure breathing) and myocardial contraction affect the cardiac function curve?

Back 288

it elevates the curve shifting it to the right towards elevated right atrial pressures

Front 289

What is cardiac tamponade?

Back 289

is the accumulation of a large quantity of fluid in the pericardial cavity around the heart with resultant INC in external cardiac pressure and shifting of the curve to the right

Front 290

What is the venous return curve?

Back 290

is the volume of blood returning from the large veins into the heart as a function of right atiral pressure, has a broad plateau at negative atrial pressures, venous return is favored by the suction exerted by the negative pressure, at pressures below -4, it does not INC because veins collapse, then starts to decline towards 0 (at the mean systemic filing pressure)

Front 291

what factors affect the VR curve?

Back 291

1. right atrial pressure-it exerts a backword force on the veins to impede flow of blood from the veins into the right atrium
2. degree of filling of the systemic circulation, measured by the mean systemic filling pressure, which forces the systemic blood toward the heart
3. resistance to blood flow between the peripheral vessels and the right atrium

Front 292

what causes the plateau phase in the VR curve?

Back 292

caused by collapse of the large veins entering the chest when the right atiral pressure falls below atmospheric pressure, VR is zero when the right atrial pressure rises to equal the mean systemic filling pressure

Front 293

what is the mean systemic filling pressure and what is its value when all reflexes are inhibited?

Back 293

it is the steady-state intravascular pressure that one would measure if the heart was arrested, ~7 mm Hg, is when there is equilibrated pressure levels everywhere in the circulation (could be due to the heart from stopping the flow of blood)

Front 294

what is the effect of blood volume on mean circulatory filling pressure (Psf)?

Back 294

the greater the volume the greater the mean circulatory filling pressure because extra blood volume stretches the walls of the vasculature, slope of the mean circulatory filling pressure vs. volume graph is steep, so even slight changes can have large effects on the mean circulatory filling pressure

Front 295

How does INCing or DECing the Psf affect the VR curve?

Back 295

INCing Psf moves the VR curve to the right, DECing moves it to the left, basically says that the greater the system is filled, the easier it is for blood to flow into the heart, the less the filling, the more difficult it is for blood to flow into the heart, also the greater the differene between the Psf and right atrial pressure, the greater becomes the venous return

Front 296

what factors influence venous return?

Back 296

1. right atrial pressure
2. the degree of filling of the systemic circulation (blood volume)

Front 297

How does venous return (similar to changing blood volume) affect CO?

Back 297

1. an INC in venous return will INC CO because of starlings law of the heart
2. a DEC in venous return will negatively impact CO, due to reduced filling pressure and end-diastolic volume

Front 298

How does cardiac contractility affect venous return or CO?

Back 298

1. INCing cardiac contractility augments CO (by shifting the graph up and left) but also venous return due to larger ejection volumes which will tend to DEC left atrial pressure and thus INC the pressure gradient for venous return
2. DECing cardiac contractility (such as in myocardial disease) will result in poor emptying of the ventricular chambers which will dam up blood on the venous side and thus reduce venous return, CO graph is shifted down and to the right

Front 299

What is the effect of heart rate on CO?

Back 299

INCing HR is the main mechanism responsible for the INC in CO observed during exercise, but there are limits to how HR can influence CO, slow rates can lead to DEC CO because the heart cannot compensate by INC stroke volume because the peak of the Starling curve is already reached, at extremely high rates, diastolic phase is incomplete and stroke volume DEC yielding to reduced CO

Front 300

What is resistance to venous return?

Back 300

the resistance against blood entering the heart, when resistance INC blood begins to be dammed up in all parts of the systemic circulation, but the venous pressure rises very little because the veins are highly distensible, venous return thus DEC

Front 301

How does one calculate venous return?

Back 301

VR = (Psf-PRA)/RVR where PRA is right arterial pressure and RVR is resistance to venous return, normal values are VR of 5 L/min, Psf of 7 mm Hg, PRA of 0 mm Hg, and RVR of 1.4 mm Hg/L

Front 302

What is the effect of resistance to venous return to the venous return curve?

Back 302

a DEC in this resistance to ½ normal allows twice as much flow of blood and therefore rotates the curve upward to twice as great a slope, an INC in this resistance to twice normal rotates the curve downward to one half as great a slope, the Psf stays constant (at 7), the highest level to which the right atrial pressure can rise is equal to the mean systemic filling pressure

Front 303

How does one analyze CO and VR curves on one graph?

Back 303

superimpose the two lines on one graph, where they intersect is the equilibrium point, where the heart and the systemic circulation operates together as well as where the right atrial pressure is the same for both the heart and the systemic circulation

Front 304

Define hemodynamics.

Back 304

it is the scientific field concerned with the relationship among the physical principles governing pressure, flow, resistance, and compliance as they relate to the cardiovascular system

Front 305

What are the basic principles of circulation?

Back 305

1. circulation is a complete circuit-it starts and stops at the heart, this is important because if there is a change in one part of the circulation, it affects all parts of the circulation, if there is vasodilation in one part, there has to be vasoconstriction in another
2. circulation features a branching pattern-blood takes many parallel pathways from the left heart to the right heart, in most cases blood flows through a single capillary bed, whereas in other cases, the blood flows through two capillary beds in series

Front 306

What parts of the circulation can only take a single pathway?

Back 306

blood flow from the right heart to the left heart can only take a single pathway, across a single capillary bed in the lungs

Front 307

what parts of the circulation can take multiple pathways?

Back 307

most of the body systems involved in systemic circulation including skin, digestive track, and muscle

Front 308

What is the most important innervation in blood vessels?

Back 308

is sympathetic innervation, INCing sympathetic stimulation INCs vasoconstriction

Front 309

Describe arteries.

Back 309

1. deliver oxygenated blood to the tissue
2. transport the blood under high pressure to the tissues (with the aorta having the highest pressure because it takes all the pressure spit out by the heart)
3. have strong vascular and muscular walls, thick and composed of elastic and smooth muscle
4. have rapid pulsatile blood flow
5. are densely sympathetically innervated

Front 310

Describe arterioles.

Back 310

1. are the smallest branches of the arteries (5-100 micron diameter)
2. are major resistance vessels of the whole peripheral circulation, have the highest resistance in the CV system, maintaining arterial blood pressure, resistance maintained by the ANS
3. have thick smooth muscle layer
4. have endothelial cell layer
5. are very densely innervated
6. regulated blood flow to capillary beds
7. biggest pressure drop (stopcocks of the circulation)
8. the smooth muscle is partially contracted under normal conditions (basal tone)
9. regulate regional blood flow to the capillary beds (strong muscular walls, densely innervated)

Front 311

What types of receptors are found on arterioles?

Back 311

1. alpha-adrenergic receptors are found on the arterioles of the skin, splanchnic and renal circulations
2. beta-adrenergic receptors are found on arterioles of skeletal muscle

Front 312

Describe the basal tone in arterioles.

Back 312

blood flow to capillaries is controlled by vasoconstriction and vasodillation, vasoconstriction needs a vessel that is not fully constricted while vasodilation needs a vessel that is not fully relaxed, the smooth muscle surrounding the resistance vessels therefore have some basal tone (some level of tonic contraction), have this with no neural input, basal tone probably comes from intrinsic and local factors

Front 313

Describe capillaries.

Back 313

1. are even smaller with no smooth muscle (5-10 micron diameter)
2. have very thin walls consisting of a single layer of endothelium permeable to small molecule substances
3. are the major exchange vessels between the blood and interstitial fluid
4. have the largest total cross-sectional area
5. have low flow velocity
6. there is no innervation in true capillaries

Front 314

Describe venules

Back 314

1. are small vessels (20 microns) with thin walls
2. collect blood from capillaries
3. also participate in exchange
4. gradually coalesce into progressively larger veins
5. the total cross-sectional area diminishes and the velocity of blood flow INC
6. form from merging of capillaries

Front 315

Describe veins.

Back 315

1. progressively merge to form larger veins
2. transport blood from tissues back to the heart
3. are major capacitance vessels acting as a major controllable reservoir, they are the major collection and storage site for blood
4. have thin but muscular walls
5. are under low pressure because they are getting the blood from the slow capillaries
6. are densely innervated, even more than arteries
7. contain the highest proportion of the blood in the CV system
8. have alpha-1 and 2 adrenergic receptors that mediate vasoconstriction

Front 316

What is the first system affected by a hemorrhage?

Back 316

since the venous system is controllable, the venous system is the first system affected by a hemorrhage

Front 317

What is the distribution of blood in the different parts of the circulatory system in the resting individual?

Back 317

systemic veins (60-68%), lungs (10-12%), systemic arteries (10-12%), heart (8-11%), capillaries (4-5%), about 84% of entire blood is in the systemic circulation

Front 318

How does cross-sectional area and velocity relate in the different parts of circulation?

Back 318

smaller area leads to larger velocity and larger area leads to smaller velocity, can see area INC from aorta -> arteries -> capillaries then taper and shrink from capillaries -> veins -> vena cava, note particularly the much larger cross-sectional areas of the veins than of the arteries (explains the large storage of blood in the venous system in comparison to the arterial system

Front 319

What is the cross sectional area of the aorta compared to the capillaries?

Back 319

aorta has an area of 2.5 cm^2 while capillaries have area of 2500 cm^2

Front 320

What is the fundamental law of vessel branching

Back 320

at each branch point, the combined cross sectional area of daughter vessels exceeds the cross sectional area of the parent vessel

Front 321

How does one measure the velocity of blood flow

Back 321

v = q/A, where v is velocity, q is blood flow and A is cross-sectional area

Front 322

Where in circulation does pulsatile blood flow occur?

Back 322

it occurs in the arteries as well as in the pulmonary circulation

Front 323

describe blood pressure.

Back 323

1. is the force exerted by the blood against any unit area of the vessel wall
2. the contractions of the heart produce hemodynamic pressure in the aorta
3. intravascular pressure stretches blood vessels in proportion to their compliance

Front 324

What happens to blood pressure as it flow through the systemic circulation? where is it highest, lowest?

Back 324

pressure decrease progressively because of the resistance to blood flow, the pressure is highest in the aorta and large arteries and lowest in the vena cava, the largest decrease in pressure occurs across the arterioles because they are the site of the highest resistance

Front 325

What are the mean pressures in the different parts of the systemic circulation?

Back 325

1. aorta (100 mm Hg), but can fluctuate at a systolic pressure of 120 and a diastolic of 80 because of pulsatile pumping
2. arterioles (50 mm Hg)
3. capillaries (20 mm Hg)
4. vena cava (4 mm Hg)

Front 326

Describe Grave’s disease in terms of circulation.

Back 326

1. hyperthyroidism
2. elevated basal metabolism
3. often associated with arteriolar vasodilation
4. reduced arteriolar resistance
5. the dampening effect on the pulsatile arterial pressure is diminished
6. pulsatile flow in the capillaries is observed in the finger nailbeds

Front 327

Describe the pulsatile pressure in the pulmonic arteries.

Back 327

the pressure is pulsatile but the pressure level is far less, at a systolic of 25 mm Hg and a diastolic of 8 mm Hg, with a mean pulmonary arterial pressure of 16 mm Hg

Front 328

What is systolic pressure?

Back 328

it is the highest arterial pressure during a cardiac cycle and is measured after the heart contracts (systole) and blood is ejected into the arterial system

Front 329

What is diastolic pressure?

Back 329

is the lowest arterial pressure during a cardiac cycle and is measured when the heart is relaxed (diastole) and blood is returning to the heart via the veins

Front 330

What is the pulse pressure?

Back 330

it is the difference between the systolic and diastolic pressure, most important determinant is stroke volume, as blood is ejected, systolic pressure INC because of the low capacitance of the arteries, diastolic pressure remains unchanged, pulsatile pressure INC to the same extent as the systolic pressure

Front 331

What dampens pulse pressure over the course of the arterial wall tree?

Back 331

1. compliance of the arterial vessel wall-DEC in compliance (such as with the aging process) causes INC in pulsatile pressure
2. resistance to flow as vessel diameter becomes smaller

Front 332

What is the affect of congestive heart failure or severe hemorrhage on arterial pulse pressure?

Back 332

individuals with either of these are likely to have very small arterial pulse pressures because their stroke volumes are abnormally small

Front 333

what is the affect of aortic regurgitation on arterial pulse pressure?

Back 333

individuals with aortic regurgitation have large stroke volumes and thus are likely to have INCd arterial pulse pressure, this is similar to well-trained athletes that have large stroke volumes because there heart rates are usually low, the prolonged ventricular filling times in these individuals induce the ventricles to pump a large stroke volume and hence their pulse pressures are large

Front 334

what is mean arterial pressure and how is it calculated

Back 334

mean arterial pressure is the average arterial pressure with respect to time, it can be calculated using one of three equations
1. MAP = 1/3 pulse pressure + diastolic pressure
2. MAP = 1/3 (systolic pressure – diastolic pressure) + diastolic pressure
3. MAP = (1/3 systolic pressure + 2/3 diastolic pressure)

Front 335

describe venous pressure.

Back 335

it is very low because the veins have a high capacitance and can hold large volumes of blood at lower pressure

Front 336

describe atrial pressure

Back 336

is even lower than venous pressure, left atrial pressue is estimated by the pulmonary wedge pressure

Front 337

what is the pulmonary wedged pressure and how is it measured?

Back 337

a catheter is inserted into the smallest branches of the pulmonary artery, it makes contact with the pulmonary capillaries, the measured pulmonary capillary pressure is approximately equal to the left atrial pressure

Front 338

what are the basic principles of the circulatory function?

Back 338

1. the blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue needs, when active need up to 20-30 times more blood than at rest, if need more blood flow usually done at local blood vessels dilating or constricting them to control the local blood flow, nervous control also exists
2. the cardiac output is controlled mainly by the sum of all the local tissue flows (Starling law)
3. in general, the arterial pressure is controlled independently of either local blood flow control or cardiac output control (it is controlled by nervous reflexes, release of pressure controlling hormones and regulation of blood volume)
4. the needs of the individual tissues are served by the circulation

Front 339

Define blood flow.

Back 339

it is the quantity of blood that passes a given point in the circulation in a given period of time, overall blood flow at rest for an adult is 5000 ml/min, this is called cardiac output because it is the amount of blood pumped by the heart each time

Front 340

How is blood flow calculated?

Back 340

Q = deltaP/R where Q is flow or cardiac output, deltaP is pressure gradient, R is the resistance or total peripheral resistance, the equation for blood flow is analogous to Ohm’s law for electrical circuits, this equation holds at any instant of time, regardless of how simple or how complicated the circuit

Front 341

what drives blood flow

Back 341

the pressure gradient (not the absolute pressure) drives blood flow, thus blood flows from high pressure to low pressure

Front 342

What is compliance (capacitance)

Back 342

it is the total quantity of blood that can be stored in a given portion of the circulation for each mm Hg pressure rise, capacitance is much greater for veins than for arteries, describes the distensibility of blood vessels, blood vessels are elastic, and they expand when the blood in them is under pressure, determined in large part by the relative proportion of elastin fibers versus smooth muscle and collagen in the vessel wall, elastin offers the least resistance whereas collagen offers the greatest resistance, capacitance is much greater for veins than for arteries (so more blood volume is contained in the veins (unstressed volume))

Front 343

How is compliance calculated?

Back 343

C = dV/dP, where C = capacitance or compliance, V = volume, P = pressure

Front 344

What is the effect on aging on vascular compliance?

Back 344

on a volume vs. pressure curve, see that as age INC the slope of the volume/pressure DEC, in older aortas because of decreased compliance, as a person ages, the arteries become stiffer and less distensible

Front 345

What effect does atherosclerosis have on compliance?

Back 345

atherosclerosis is caused by the formation of multiple plaques within the arteries, arteriosclerosis (“hardening of the artery”) results from a deposition of tough, rigid collagen inside the vessel wall and around the atheroma, this INC the stiffness, DEC the elasticity of the artery wall

Front 346

What is the relationship between resistance and flow

Back 346

lower resistance has higher flow

Front 347

What is the relationship between pressure and tissue flow

Back 347

INC pressure INC the tissue flow, an INC in arterial pressure not only INC the force that pushes the blood through the vessel but also distends the vessels at the same time, which DECs vascular resistance, when have sympathetic stimulation (vasoconstriction) the line shifts to the right, vasodilation moves it to the left

Front 348

What is resistance in terms of blood flow?

Back 348

it is the impediment to blood flow in a vessel, it cannot be measured by any direct means

Front 349

How is resistance calculated?

Back 349

using Poiseuille’s equation, R = (8*n*l) / (pi*r^4) where R is the resistance, n is the viscosity of the blood, l is the length of the blood vessel and r is the radius of the blood vessel, normally the viscosity of normal blood is about three times as great as the viscosity of water (which is 1), plasma is about 1.5

Front 350

How does one INC viscosity

Back 350

by INC hematocrit, this will also INC resistance and DEC blood flow, in the body it is difficult to change the viscosity from moment to moment

Front 351

What is hematocrit and what is its average in men and women?

Back 351

hematocirt is the percentage of the blood that is cells, it is mainly the large numbers of suspended red blood cells in the blood, each of which exerts frictional drag against the adjacent cells and against the wall of the blood vessel that makes the blood so viscous, in men that is ~42 while in women it is ~38

Front 352

How is hematocrit altered in polycytemia vera?

Back 352

causes the apparent viscosity to INC more than twofold, tends to exert a proportionate effect on the resistance to blood flow

Front 353

Describe parallel resistance in terms of blood vessels.

Back 353

it is illustrated by the systemic circulation, each organ is supplied by an artery that branches off the aorta, parallel vessels DEC total vascular resistance, each artery in parallel receives a fraction of the total blood flow, when an artery is added in parallel, the total resistance DEC, in each parallel artery, the pressure is the same

Front 354

How does one calculate the total resistance of blood vessels in parallel?

Back 354

1/Rtotal = 1/Ra + 1/Rb + 1/Rc + …, the total resistance is less than the resistance of any of the individual arteries

Front 355

Describe series resistance in terms of blood vessels.

Back 355

it is illustrated by the arrangements of blood vessels within a given organ, each organ is supplied by a large artery, smaller arteries, arterioles, capillaries, and vein arranged in series, each blood vessel or set of blood vessels in series receives the same total blood flow, Pressure DEC as blood flows through the series of blood vessels

Front 356

How does one calculate the total resistance of blood vessels in series.

Back 356

Rtotal = Rarteries + Rarterioles + Rcapillaries, largest portion of resistance is contributed by the arterioles

Front 357

Define total peripheral resistance

Back 357

the complete resistance that blood encounters as it flows from the arterial to the venous side of the circulation

Front 358

What is conductance in terms of blood vessels

Back 358

it is a measure of the blood flow through a vessel for a given pressure difference, is the reciprocal of resistance (conductance = 1/resistance)

Front 359

What is venous resistance?

Back 359

the resistance that the blood encounters as it flows form the capillaries back to the heart

Front 360

What is the relationship between viscosity and hematocrit?

Back 360

viscosity depends on hematocrit, at low hematocrits, viscosity INC compared to plasma because of the stickiness of red blood cells, at higher hematocrits, viscosity INC because of cell deformation

Front 361

What is laminar flow?

Back 361

states that as flow rate INC, red blood cells move toward the center of the blood vessels (performing axial streaming) when velocity is highest, flow is proportional to driving pressure only under laminar flow conditions

Front 362

What is turbulent flow and how does it affect laminar flow?

Back 362

turbulent flow opposes laminar flow, turbulent flow is characterized by blood flowing in all directions and mixing within the vessel, occurs when Ng (Reynodls Number) exceeds a critical value of 2000, also occurs until a critical velocity is reached, when INC there is greater tendency for turbulence, causing buits (auditory vibrations)

Front 363

How is Reynodl’s Number calculated

Back 363

Ng = V*d*density / n, where Ng is Reynold’s Number, d is diameter, and n is fluid viscosity, Ng and therefore turbulence, is INC by DEC blood viscosity (e.g. reducing hematocrit, anemia) or INC blood velocity (e.g. narrowing of a blood vessel)

Front 364

How is viscosity affected by radius

Back 364

blood viscosity is relatively insensitive to changes in vessel radius for large vessels but decreases steeply with DEC in radius for smaller vessels

Front 365

What are the functions of arteries?

Back 365

1. distribute blood to capillary beds
2. a hydraulic filter in the systemic circulation (since the arterioles are high-resistance vessels that regulate the distribution of flow to the capillary bends, its an elastic conduit and high resistance terminal)
3. store some of the ejected blood during systole to secure continuous flow through the capillaries

Front 366

What are the functions of veins?

Back 366

1. they act as conduits for transport of blood from the tissues back to the heart since they are capable of constricting and enlarging
2. is a major controllable reservoir of blood
3. it helps to regulate cardiac output

Front 367

What are the three layers that make up the walls of the blood vessel?

Back 367

1. tunica intima-composed of endothelium, may have internal elastic lamina deep to it
2. tunia media-composed of smooth muscle, collagen, elastin, may have an external elastic lamina deep to it
3. tunica adventitia-composed of collagen, fibroblasts, vasa vasorum and nerves

Front 368

Which of these layers are present in capillaries?

Back 368

have only an intimal layer of endothelial cells resting on a basal lamina

Front 369

What are the major structural elements that make up the vessel wall?

Back 369

endothelial cells, elastic fibers, collagen fibers, vascular smooth muscle cells (VSMCs) and nerve terminals

Front 370

Why are the venous walls in the venous system so thin?

Back 370

venous walls are thin because the pressure in the venous system is very low, but they are still very muscular, contain even more smooth muscle than arteries, have less elastic fiber but more collagen fiber

Front 371

What are the differences between arteries and veins in terms of structural components?

Back 371

arteries contain more elastic fibers, have a smaller radius (cross-sectional area) but thicker wall, and have less smooth muscle and collagen fibers compared to veins

Front 372

Describe the structural composition of the endothelial cells.

Back 372

form a single, continuous layer that lines all vascular segments

Front 373

Describe the use of the elastic fibers in blood vessels.

Back 373

they are a rubber-like material that accounts for most of the stretch of vessels at normal pressures, as well as the stretch of other tissues, in arteries are arranged as concentric, cylindrical lamellae, abundant everywhere except in true capillaries and venuls

Front 374

Describe the use of the collagen fibers in blood vessels.

Back 374

consititue a jacket of far less extensible material than the elastic fibers (like the fabric woven inside the wall of a rubber hose), present throughout the circulation except for in the capillaries

Front 375

Describe where VSMCs can be found in blood vessels.

Back 375

present in all vascular segments except the capillaries

Front 376

What are the characteristics of conducting or elastic arteries and what are some examples?

Back 376

include the aorta, subclavian and pulmonary arteries, large, have strong elastic walls, must withstand an enormous head of pressure to pump against the peripheral resistance, have lots of elastic fibers (for springiness) and collagen (for rigidity preventing over-stretching)

Front 377

What are the characteristics of distributing or muscular arteries and what are some examples?

Back 377

include the femoral, facial, brachial, celiac arteries, have well-distinguished internal elastic lamina, wall is mostly tunic media composed almost entirely of smooth muscle (which are circumferentially arranged forming a spiral or helix with a low pitch)

Front 378

Describe the tunica intima, media and adventitia of veins.

Back 378

consists of endothelium alone because internal elastic lamina is missing, tunic media consists of concentrically arranged smooth muscle cells widely separated by thick bundles of collagen fibers, adventitia is thick and consists of collagen bundles longitudinally arranged elastic fibers and fibroblasts

Front 379

How important is the level of resistance in the arterioles?

Back 379

resistance is the force that impedes blood through the system, comes from compression by the surrouding tissues, the arterioles are high-resistance vessels that regulate the distribution of flow to the various capillary beds, large veins have very little resistance, pressure in large veins is 4-7 mmHg higher than the pressure in the right atrium

Front 380

What is the importance of distensibility in blood vessels?

Back 380

veins are the most distenislbe of all the blood vessels, this gives veins their ability to act as a reservoir storing large quantities of blood, veins more distensible because walls of arteries are far stronger (can withstand larger transmural pressure differences)

Front 381

Define compliance (capacitance).

Back 381

it is the total quantity of blood that can be stored in a given protion of the circulation for each mm Hg pressure rise, vascular compliance = INC in volume/INC in pressure

Front 382

How is compliance calculated in terms of distensibility?

Back 382

Compliance = distensibility X volume
can also calculate Compliance = dV/dP, then D = C/V or D = dV/(dP * V)

Front 383

How do the values for distensiblity, volume and compliance compare between veins and arteries?

Back 383

vein is 8 times as distensible as the corresponding artery, the volume is 3 times as great as the corresponding artery, and the vein is 24 times the compliance of the artery

Front 384

What does aging do to compliance?

Back 384

aging diminishes the compliance of the arteries, the less compliant the arteries the more work the heart must do to pump a given cardiac output

Front 385

Describe delayed compliance in blood vessels.

Back 385

1. a vessel exposed to INC volume (blood transfusion) will at first exhibit a large INC in pressure, there is delayed stretch in the vessel wall which allows the pressure to return back to normal
2. if a vessel is exposed to a sudden removal of blood (hemorrhage), pressure falls to a very low value, smooth muscle readjusts their tension back to their initial values restoring the normal vascular pressure

Front 386

What happens when an artery is compliant (normal)?

Back 386

when the arteries are normally compliant, blood flows through the capillaries throughout the cardiac cycle

Front 387

what happens when an artery is rigid?

Back 387

when the artery is rigid, blood flows through the capillaries only during systole, but flow ceases during diastole

Front 388

What are the normal volumes of blood in the arterial and venous systems?

Back 388

in arteries, when filled with 700 mm blood, MAP is 100 mm Hg, when have 500 mm blood, MAP is 0, in veins, normally have blood volume of 2500 mm with a pressure of 20 mm Hg, tremendous changes in volume are required to change the venous pressure only a few mm Hg

Front 389

How are veins able to control cardiac output?

Back 389

veins hold a large amount of blood, when there is an INC in vascular tone throughout the systemic circulation, this excess blood is pushed into the heart, INC pumping by the heart

Front 390

How do the pressure-volume curves change as one ages?

Back 390

the curves of the arterial systems shift downward and the slopes diminish, so compliance DEC with age, changes in compliance is due to an INC rigidity (artherosclerosis) of the system caused by progressive changes in the collagen and elastin contents of the arterial walls

Front 391

What is more responsive to sympathetic nerve stimulation, arteries or veins?

Back 391

capacitance vessels (veins) are more responsive than resistance vessels (arteries), release more NE, have stronger contractions

Front 392

What are the effects of sympathetic stimulation or inhibition on the volume-pressure curves?

Back 392

INC in vascular smooth muscle tone caused cy sympathetic stimulation INC the pressure at each volume thus moving the curve to the left, sympathetic inhibition DEC pressure at each volume

Front 393

What is the importance of having a strong sympathetic reaction in veins?

Back 393

causes veins to constrict leading to large volumes of blood shifting into the heart, this leads to an INC in pumping by the heart

Front 394

Define hydrostatic pressure.

Back 394

it is the pressure that results from the weight of the water, occurs in the vascular system because of the weight of the blood in the vessels, due to this pressure, a standing person has a pressure of 100 mm Hg at the level of the heart and at the same time 190 mm Hg at the level of the legs

Front 395

What is Toricceli’s law

Back 395

states that in any body of water, the pressure at the surface of the water is equal to the atmospheric pressure but the pressure rises below the surface, the pressure rises 1 mm Hg with each 13.6 mm change in the heart, therefore there is a +90 mm Hg pressure in the leg compared to at the heart

Front 396

Define venous pressure.

Back 396

it is the average blood pressure within the venous compartment

Front 397

How does one INC peripheral venous pressure?

Back 397

by INC volume of blood in veins or INC venous tone

Front 398

define central venous pool

Back 398

corresponds roughly to the volume enclosed by the right atrium and the great veins in the thorax, blood leaves this pool into the right ventricle at a rate equal to the cardiac output

Front 399

define central venous pressure.

Back 399

it is the pressure in the thoracic vena cava near the right atrium, basically right atrial pressure, it is the filling pressure of the right heart, is a major determinant of the preload of the right ventricle, which regulates stroke volume through Frank-Starling, dCVP = dV/Cv (venous compliance)

Front 400

How does one INC central venous pressure?

Back 400

CVP is INC by either an INC in venous blood volume or a DEC in venous compliance

Front 401

What happens mechanically when CVP INC?

Back 401

1. right ventricular stroke volume INC via Starling’s law.
2. this causes INC CO of right heart
3. right heart output temporarily exceeds that of the left heart
4. as long as this imbalance exists, blood accumulates in the pulmonary vasculature and rise pulmonary venous and left atrial pressure
5. INC left atrial pressure INC left ventricular stroke volume via Starling’s law
6. very quickly a new steady state will be reached when left atrial pressure has risen sufficiently to make left ventricular stroke volume exactly equal to the INC right ventricle stroke volume

Front 402

What does INC blood volume do?

Back 402

it causes INCs in mean systemic pressure, venous return, right atrial pressure, and cardiac output

Front 403

define venous return.

Back 403

the rate at which blood returns to the thorax from the peripheral vascular beds and thus is the rate at which blood enters the central venous pool, in any stable situation, venous return equals cardiac output

Front 404

What factors affect venous return?

Back 404

primary factors include systemic pressure while secondary factors include movements of the skeletal muscles, respiratory diaphragm, venous valves, suction of relaxed atrium, and venous tone

Front 405

Define mean systemic filling pressure

Back 405

the pressure measured everywhere in the systemic circulation after blood flow has been stopped by clamping the large blood vessels so that the systemic circulation can be measured independently from those in the pulmonary circulation

Front 406

How does one INC mean systemic pressure?

Back 406

INCed by an INC in blood volume or DEC in venous compliance, reflected as a shift of the vascular function curve to the right

Front 407

How does one DEC mean systemic pressure?

Back 407

DEC in blood volume or INC in venous compliance, a DEC in mean systemic pressure is reflected in a shift of the vascular function curve to the left

Front 408

What is a normal value for the right atrial pressure?

Back 408

0 mm Hg which is about equal to atmospheric pressure, can rise to 20-30 mm Hg at serious heart failure, lower limit is -3 to -5

Front 409

What facilitates the return of blood flow to the heart?

Back 409

facilitated by the large diameter of the veins, one-way valves, skeletal muscle contraction and respiration

Front 410

what is the right atrial pressure in individuals with CHF or massive blood transfusion?

Back 410

4-6 to 20-30 mm Hg

Front 411

what is the right atrial pressure in individuals with a hemorrhage

Back 411

-3 to -5 mm Hg

Front 412

what is the pressure in the chest cavity

Back 412

-3 to -5 mm Hg

Front 413

what is the pressure in the peritoneal cavity

Back 413

6 mm Hg, can rise to 30 mm Hg in pregnancy, people with ascites or abdominal tumor

Front 414

what is the pressure in the peripheral small veins

Back 414

4 to 7 mm Hg

Front 415

How long does blood remain in the capillaries?

Back 415

1 to 3 seconds, this is surprising since all diffusion of nutrient food substances and electrolytes that takes place through the capillary walls must occur in this short time

Front 416

Where do capillaries come from and where do they drain?

Back 416

arterioles give rise to metarterioles which give rise to capillaries, capillaries drain via short collecting venules, there are scattered smooth muscle cells in the metarterioles and venules that guard the opening of capillaries by muscular precapillary sphincters

Front 417

What are the different sizes of capillaries?

Back 417

1. there are large ones called preferential channels
2. there are smaller ones called true capillaries (lack smooth muscle, consist of a single layer of endothelial cells surrounded by a basement membrane on the outside), thickness of wall is only 0.5 um

Front 418

What allows for passage between endothelial cells in the capillaries?

Back 418

clefts (pores) between the endothelial cells allow passage of water-soluble substances, has a width of about 6 to 7 nm (slightly smaller than albumin), vesicle formation and diffusion (which is by far the most important means of transport between plasma and interstitial fluid) of lipid-soluble molecules through the endothelial cell are other pathways for exchange

Front 419

What regulates blood flow through the capillaries?

Back 419

blood flow is regulated by contractions and relaxations of the arterioles and the precapillary sphincters (vasomotion), flow is intermittent, concentration of O2 is the most important factor that affects the degree of opening and closing

Front 420

What are the three types of capillaries?

Back 420

1. continuous capillary-this is the most common form of capillary, it has inter-endothelial junctions, clefts are absent in the blood-brain barrier whose capillaries have narrow tight junctions
2. fenestrated capillary-in these capillaries, the endothelial cells are thin and perforated with fenestrations, these capillaries most often surround epithelia (small intestine, exocrine glands, renal glomeruli)
3. discontinuous (sinusoidal) capillary-have fenestrae as well large gaps, found in sinusoids (liver, spleen, bone marrow)

Front 421

What determines the net movement of substances across the capillary wall?

Back 421

net movement of substance is in response to either a hydrostatic pressure gradient (bulk flow) or a diffusion gradient, there is tremendous numbers of water molecules and dissolved particles that diffuse back and forth though with no net movement

Front 422

What are the four mechanisms of exchange found in capillaries?

Back 422

diffusion, bulk flow, vesicular transport, active transport

Front 423

Describe the diffusion of lipid-soluble substances across a capillary wall.

Back 423

1. cross the membranes of the capillary endothelial cells by simple diffusion without going through the pores
2. include O2 and CO2
3. because these substances can permeate all areas of the capillary membrane, their rates of transport through the capillary membrane are many times faster than the rates for lipid-insoluble substances such as Na+ and glucose

Front 424

Describe the diffusion of small water-soluble substances across a capillary wall.

Back 424

1. cross via the water-filled clefts between the endothelial cells
2. include water, glucose and amino acids
3. generally, protein molecules are too large to pass freely through the clefts
4. in the brain, the clefts between endothelial cells are exceptionall tight
5. in the liver and intestine, the clefts are exceptionally wide and allow passage of protein (these capillaries are called sinusoids)

Front 425

Describe the diffusion of large water-soluble substances across a capillary wall.

Back 425

they can only cross by pinocytosis

Front 426

Describe the movement of water across the capillary wall

Back 426

water freely moves across the capillary wall

Front 427

Define bulk flow.

Back 427

bulk flow of water and dissolved substances out of the capillary through endothelial pores in response to a hydrostatic pressure gradient, hydrostatic pressure inside the capillary is always greater than the pressure of the interstitial fluid surrounding the capillary

Front 428

What is osmotic pressure and what generates it?

Back 428

pressure caused by the fact that water but not large proteins crosses the capillary wall, since large proteins (like albumin) are only found in the vessel and not in the interstitial space, then the conc. gradient is for the protein to leave the blood, however it cannot cross the capillary wall, water is thus drawn into the blood and blood proteins are classified as osmotic particles that produce an osmotic pressure, osmotic pressure generated is opposed by the capillary blood pressure

Front 429

What is the normal value of osmotic pressure?

Back 429

25 mm Hg

Front 430

What is capillary blood pressure?

Back 430

capillary blood pressure forces water out of the capillary (similar to water out of a hose), this pressure opposes the osmotic pressure produced by blood proteins, when capillary blood pressure is greater than osmotic pressure, then filtration occurs, reabsorption occurs if the opposite is true

Front 431

How does blood pressure change along the length of the capillary?

Back 431

it declines from about 35 mm Hg to about 15 mm Hg due to resistance of the capillary, so therefore at the arterial end of the capillary, the force driving the water out of the blood is > the force at the venous end of the capillary, so at the arteriole end, net filtration occurs and at the venous end net reabsorption occurs

Front 432

How does the balance between blood and osmotic pressure compare in the kidney and lungs?

Back 432

in the kidney, only filtration occurs (renal capillary blood pressure (~55 mm Hg) is greater than capillary osmotic pressure) and in the lung only reabsorption occurs (happens because pulmonary capillary pressure (~15 mm Hg) is normally less than capillary osmotic pressure so fluid is always drawn into the blood)

Front 433

How do local changes in vascular resistance that does not alter systemic BP produce local changes in capillary blood pressure?

Back 433

if resistance INC upstream from a capillary, capillary BP DEC while if resistance INC downstream from a capillary, capillary BP INC

Front 434

What does an INC in arteriolar resistance do?

Back 434

it will lower capillary BP, DEC filtration and INC reabsorption

Front 435

What does an INC in venular resistance do?

Back 435

it will INC capillary BP, INC filtration and DEC reabsorption

Front 436

How are transcapillary water movement and BP related?

Back 436

during times of low arterial BP, reabsorption predominates, which INC blood volume and BP

Front 437

What produces edema?

Back 437

excess filtration produces INC interstitial volume or edema, elevated capillary BP produces edema, reduced blood osmotic pressure produces edema

Front 438

What problems with blood osmotic pressure are caused by protein deficiency and malnutrition?

Back 438

protein deficiency leads to DEC in blood osmotic pressure and edema, malnutrition leads to a DEC in albumin in the blood which lowers blood’s osmotic pressure, therefore capillary BP exceeds osmotic pressure for a longer distance across capillary and filtration exceeds absorption, will appear as a swollen abdomen

Front 439

What are normal values for bulk flow over 24 hours?

Back 439

cardiac output = 8000 L/day
filtration = 20 L/day
re-absorption = 16-18 L/day
lymphatics = 2-4 L/day

Front 440

What is the Starling equation for fluid movement?

Back 440

Jv = Kf [(Pc-Pi) – (pi c – pi i)] or Jv = Kf [(Pc + pi i) – (Pi + pi c)] where Jv is fluid movement, Kf is hydraulic conductance, Pc is capillary hydrostatic pressure, Pi is interstitial hydrostatic pressure, pi c is capillary oncotic pressure and pi i is interstitial oncotic pressure

Front 441

What do the values of Jv stand for?

Back 441

Jv is fluid flow, if Jv is +, there is net fluid movement out of the capillary (filtration), when it is -, there is net fluid movement into the capillary (absorption)

Front 442

What do the values for Kf stand for?

Back 442

it is the hydraulic conductance (water permeability) of the capillary wall

Front 443

What do the values of Pc stand for?

Back 443

an INC in Pc favors filtration out of the capillary, determined by arterial and venous pressures and resistances, an INC in either of these pressures produces an INC in Pc, INC in venous pressure have a greater effect, Pc is higher on the arteriolar end (except in glomerular capillaries where it is nearly constant)

Front 444

What do the values of Pi stand for?

Back 444

an INC in Pi opposes filtration out of the capillary, it is normally close to 0 mm Hg (or it is negative)

Front 445

What do the values of pi c stand for?

Back 445

depends on the concentration of plasma proteins, an INC in pi c opposes filtration out of the capillary, pi c INC by INC in protein conc. in blood (dehydration), pi c is DEC by DEC in protein (nephritic syndrome, protein malnutrition, liver failure), small solutes do not contribute to pi c

Front 446

what do the values of pi i stand for?

Back 446

an INC in pi i favors filtration out of the capillary, pi i is dependent on the protein conc. of the interstitial fluid, which is normally quite low because very little proteins is filtered

Front 447

what factors INC filtration?

Back 447

an INC in Pc or pi i, or a DEC in Pi or pi c

Front 448

Describe the anatomy of the lymphatic vessels.

Back 448

they are the safety valve that normally balances out any net differences between hydrostatic and oncotic forces, have a special structure that permits passage of substances of high MW into the lymph, the wall of collecting lymphatics has smooth muscle cells

Front 449

What is the function of lymphatic capillaries?

Back 449

the contraction-relaxation cycle of lymph bulbs is the fundamental process that removes excess water and plasma proteins from the interstitial spaces, lymphatic pressures along the lymphatic vasculature are generated by lymphatic vessel contraction and organ movements

Front 450

What is the function of lymph?

Back 450

normally, filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries, excess filtered fluid is returned to the circulation via the lymph, also returns any filtered protein to the circulation

Front 451

Describe the unidirectional flow of lymph.

Back 451

vessels have one-way flap valves that permit interstitial fluid to enter, but not leave the lymph vessels, flow through larger lymphatic vessels is also unidirectional, and is aided by the one-way valves and skeletal muscle contraction

Front 452

What is edema?

Back 452

occurs when the volume of interstitial fluid exceeds the capacity of the lymphatics to return to the circulation, can be caused by excess filtration or blocked lymphatics

Front 453

What are some causes and examples of edema?

Back 453

1. INC Pc, examples include arteriolar dilation, venous constrction, INC venous pressure, heart failure, extracellular volume expansion, standing
2. DEC pi c, examples include DEC plasma protein conc., severe liver disease, protein malnutrition, nephritic syndrome
3. INC Kf, examples include burn, inflammation

Front 454

How can an INC in volume affect pressure in vessels?

Back 454

tissue pressure is normally slightly negative, but an INC in volume can cause the pressure to be positive, if the interstitial volume exceeds the safe range, high hydrostatic pressure will exist and edema will be present, dehydration of the tissue can cause very negative hydrostatic pressures

Front 455

What are some factors affecting lymphatic return?

Back 455

1. peristaltic contractions
2. one way valves
3. movements by skeletal muscles
4. respiratory diaphragm (DEC intrapleural pressures)

Front 456

Describe what the blood brain barrier is.

Back 456

a barrier between the systemic circulation and the brain circulation, it severely restricts the movement of large molecules and highly charged ions from the blood into the brain and spinal cord, substances that want to enter the neurons and glial cells must pass through the cell membrane

Front 457

What are some functions of the BBB?

Back 457

1. helps to maintain controlled environment, spinal cerebral fluid: low K+ and Ca2+ due to carrier-mediated transport-helps maintain electrical excitability in neurons
2. prevents circulating neurotransmitters like ACh, NE, dopamine, glycine from entering the brain
3. fluid cushions brain within the cranial vault, protection against blows to the head

Front 458

What constitutes the blood brain barrier?

Back 458

the choroid plexus and the arachnoid membrane since is stands between the blood and CSF

Front 459

Describe what the function of the ventricles is.

Back 459

a series of spaces found in the tissue of the brain and spinal cord, filled with CSF

Front 460

what is the function of CSF?

Back 460

it cushions the brain and regulates the extracellular environment of neurons, formed largely from the choroid plexuses (which is lined with specialized ependymal cells), each ventricle (lateral, third and fourth) contains a choroid plexus

Front 461

What is the course of CSF?

Back 461

once it escapes from the ventricular system, CSF enters into the subarachnoid space through three apertures (two lateral foramina of Luschka and a single foramen of Mgendie) in the roof of the fourth ventricle, eventually it drains into blood in the superior sagittal sinus

Front 462

What is the anatomy of the BBB that allows it to be such a strong barrier?

Back 462

for certain brain capillaries (choroid plexus) several factors restrict the diffusion of water-soluble substances:
1. there are tight junctions and fewer clefts between adjacent endothelial cells
2. there are fewer pinocytoctic vesicles
3. fibrous astrocytes (a type of brain glial cells) send processes which extensively surround the brain capillaries

Front 463

What are the leaky regions of the BBB?

Back 463

in these regions (subfomical organ, pineal gland, posterior pituitary, OVLT, median eminence, area postrema) the neurons are directly exposed to the solutes of the blood plasma (OVLT-organum vasculoum laminae terminalis)

Front 464

Describe the permeability of the BBB?

Back 464

1. high permeability to water, CO2, O2, lipid-soluble substances (greatest effect on a substance’s capacity to pierce the BBB)
2. slight permeability to electrolytes
3. low permeability to water-soluble substances, plasma proteins, large organic molecules
4. certain molecules needed for brain metabolism cross the barrier more readily than their lipid solubility would suggest, such compounds (d-glucose, L-DOPA, phenylalanine) are carried across the barrier by specialized transport systems

Front 465

Describe the transporters that allow molecules to cross the BBB better than they should.

Back 465

some transporters facilitate osmotic diffusion while others are active, some are found on both membranes of the endothelial cells (D-glucose and phenylalanine) allowing for entrance and exit, some are only on one side (K+ and other small neutral amino acids (glycine)) and move only from brain to blood, pumped out by transporters found on the antiluminal membrane, glycine coupled with Na+ while K+ is coupled with ATP

Front 466

Describe the process of L-DOPA entering the brain.

Back 466

L-DOPA enters and leaves the brain by means of a carrier for large neutral amino acids, once in the endothelium, 1-DOPA may be converted into dopamine and DOPAC in successive steps, neither of these two can cross the antiluminal membrane into the brain, thus enzyme conversion can serve as a means of controlling how much 1-DOPA reaches the brain

Front 467

Describe the brain’s metabolism.

Back 467

brain is 2% of body mass but 15% of cardiac output/metabolism, can actually double brain metabolism, most activity is aerobic, no significant place to store O2 (few sec. supply) or glucose (2 mins. supply), result in that a break in blood supply to brain causes unconsciousness in 5-10 mins.

Front 468

What is some pathology of BBB?

Back 468

1. brain tumors can impair BBB leading to hydrocephalus
2. brain edema can cause + feedback, compressed vasculature DEC blood flow causing ischemia, ischemic arteriolar dilation causes INC capillary pressure and further edema
3. dysfunction of BBB may lead to, or contribute to, neurological disorders associated with paranoia, AD, AIDS, multiple sclerosis

Front 469

How does circulation being a complete circuit affect blood flow?

Back 469

any change in flow in a single part of the circuit alters flow in other parts, constriction in one part must be accompanied by opposite dilation of another part

Front 470

How is blood flow calculated?

Back 470

Q = deltaP/R, so therefore blood flows only when pressure exceeds resistance (pressure gradient is the driving force for flow, also Q = (deltaP*pi*r^4)/(8*viscosity*length)

Front 471

What is vascular resistance and how is it calculated?

Back 471

the force that impedes blood flow through the system, R = (8*viscosity*length)/(pi*r^4), therefore changes in the radius are the primary means by which resistance is regulated

Front 472

What are the basic principles of circulatory function?

Back 472

1. each tissue has the ability to control its own local blood flow in proportion to its metabolic needs
2. in general, the greater the metabolism in an organ, the greater its blood flow
3. the blood flow to each tissue is usually regulated at the minimum level that will supply its requirements, no more, no less

Front 473

What do tissues need from blood flow?

Back 473

1. delivery of O2
2. delivery of other nutrients (i.e. glucose, amino acids, fatty acids)
3. removal of CO2
4. removal of H+
5. maintanence of proper concentration of other ions in the tissues
6. transport of various hormones and other specific substances to different tissues

Front 474

What are the 4 regulatory mechanisms in the control of circulation?

Back 474

1. adjustment of pump output (heart)
2. changes in diameter of resistance vessels (arterioles)
3. alterations in the amount of blood pooled in the capacitance vessels (veins)
4. changes in total extracellular fluid volume and its osmolatlity

Front 475

Describe the control of peripheral circulation.

Back 475

under dual control, centrally through the nervous system and locally by the conditions in the immediate vicinity of the blood vessels, which type dominates a certain tissue varies from different areas of the body, blood flow is regulated by the arterioles

Front 476

Which parts of the body does neural regulations dominate? locally?

Back 476

skin and splanchnic regions, neural regulations dominate, in heart and brain neural regulations play only a minor role

Front 477

Describe the vasodilator theory for local blood flow regulation (release of vasodilators)

Back 477

a type of acute local control, the greater the rate of metabolism or the less O2 available the greater the rate of formation of a vasodilator substance (release from the tissue), vasodilator diffuses back to the precapillary sphincters, metarterioles and arterioles to cause dilation

Front 478

What are some examples of vasodilator substance?

Back 478

adenosine, CO2, lactoid acid, ATP, histamine, K+, H+, c-type natriuretic peptide, NO, EDRFs

Front 479

Describe the oxygen demand theory for local blood flow regulation (altered ability of the vascular smooth muscle to contract).

Back 479

since O2 is required to maintain vascular muscle contraction, vasodilation can be caused by O2 deficiency, glucose deficiency, amino acid deficiency, fatty acid deficiency, vitamin deficiency

Front 480

What is beriberi?

Back 480

it is deficiency of vita B (thiamin, niacin, riboflavin, leads to diminished smooth muscle contractile ability and therefore to local vasodilation

Front 481

What are some examples of metabolic control of local blood flow?

Back 481

reactive and active hyperemia

Front 482

How does reactive hyperemia control local blood flow?

Back 482

impacts flow above control level upon release of an arterial occlusion, more compatible with the release of a vasodilator metabolite from the tissue than with a direct effect on PO2 on the vascular smooth muscle

Front 483

How does active hyperemia control local blood flow?

Back 483

INC blood flow caused by enhanced tissue activity, possible causes, especially in the initial stage of active hyperemia during skeletal muscle contraction, are K+ ions, phosphorous and osmolarity, role of adenosine and prostaglandins should also be considered

Front 484

What are some examples of active hyperemia?

Back 484

1. INC in metabolic activity (e.g. strenuous exercise) leads to INC in demand for O2 and INC in production of vasodilator metabolites (which cause arteriolar vasodilation, INC blood flow and INC O2 delivery to the tissue to meet demand)
2. if blood flow to organ INC due to INC in arterial pressure, then INC O2, INC in flow also washes out vasodilator metabolites, this causes arteriolar vasoconstriction occurs, resistance INC and blood flow is DEC to normal

Front 485

Describe autoregulation of blood flow.

Back 485

the acute return of the flow back to normal shortly after the arterial pressure changes from normal, in other words, changes that occur in perfusion pressure (arterial blood pressure) at constant levels of tissue metabolism are met with changes in vascular resistance that tend to maintain a constant blood flow

Front 486

Why is autoregulation important?

Back 486

it offers a tissue the ability to maintain a relatively constant blood flow over a wide range of arterial pressures, it is a constant blood flow in the face of change in perfusion pressure

Front 487

What is the metabolic theory that explains autoregulation?

Back 487

based on the observation that the tissue supply of O2 is matched to the tissue demand for O2, any intervention that results in an O2 supply that is inadequate for the requirements of the tissue prompts the formation of vasodilator metabolites, these vasodilators are CO2, H+, K+, lactate and adenosine

Front 488

What is the myogenic theory that explains autoregulation?

Back 488

invokes a role for arteriolar wall tension, rather than blood flow, as the controlled variable in the vasculature, stretch of the small blood vessels will cause the smooth muscle of the vessel wall to contract in response to an INC in pressure difference across the wall of a blood vessels and relax in reponse to a DEC in transmural pressure, vasoconstriction will maintain a constant flow

Front 489

How does autoregulation deal with a change in the mean arterial pressure?

Back 489

at pressures above 160 mm Hg vascular resistance DEC since the pressure forces dilation to occur, at pressures below 60 mm Hg, the vessels are fully dilated and resistance cannot be appreciably further decreased

Front 490

What are the systemic effects of local regulation?

Back 490

it is a cascade effect, vasodilation produced by autoregulation produces INC blood flow to the needy tissue at the expense of other tissues in the body, the possible fall in blood pressure due to generalized vasodilation is prevented by autonomic nervous system control

Front 491

What are the three mechanisms for the long-term regulation of local blood flow.

Back 491

1. change in tissue vascularity-final degree of response is much greater in younger tissue than in older, O2 is important for acute control and long-term control
2. growth of new vessels (angiogenesis)-angiogenic factos include endothelial cell growth factor, fibroblast growth factor, angiogenin, released from ischemic tissues, tissues that are growing rapidly or tissues that have excessively high metabolic rates
3. development of collateral circulation-when an artery or vein is blocked, a new vascular channel usually develops around the blockage allowing partial resupply, first stage is dilation of vascular loops around the point of blockage (along with metabolic relaxation of the muscle fibers of the small vessels)

Front 492

What agents are used in the systemic mechanisms for humoral regulation.

Back 492

vasoconstrictor agents, vasodilator agents, ions

Front 493

What are some examples of vasoconstrictor agents?

Back 493

norepinephrine, epinephrine, angiotensin, vasopressin, endothelins

Front 494

How does norepinephrine and epinephrine work in humoral regulation of systemic circulation?

Back 494

norepinephrine causes vasoconstriction that is mediated primarily by alpha adrenoreceptors, epinephrine can cause vasodilation that is mediated by beta adrenoceptors, local effect, systemic effects, adrenal medulla is involved

Front 495

How does angiotensin work in humoral regulation of systemic circulation?

Back 495

is local (Ang II direct vasoconstriction, release of ET fromendothelium) and systemic (renin-angiotensin system)

---angiotensinogen -> angiotensin I -> angiotensin II -> ADH and aldosterone which causes kidneys to DEC Na+ and H2O excretion, this INC blood volume and BP

Front 496

How does vasopressin (ADH) work in humoral regulation of systemic circulation?

Back 496

a potent vasoconstrictor that is actively secreted by the posterior pituitary gland in response to hemorrhage, water reabsorption, a small peptide nine amino acids in length

Front 497

How does endothelins work in humoral regulation of systemic circulation?

Back 497

there are ET-1, ET-2, ET-3, functions as a local, paracrine regulator of a vascular tone, mechanism involves ETA and ETB receptors, vasoconstriction via ET receptor/Gq protein/PLC/IP3/intracellular Ca2+ pathway

Front 498

What are the effects of endothelin-1?

Back 498

vasoconstriction (veins > arteries), initial depressor response (PgI2 mediated) followed by sustained pressor effect, positive inotropic and chronotropic effect, INC plasma levels of ANP, renin, aldosterone, and catecholamins, modulates sympathetic transmission, produces bronchoconstriction, DEC glomerular filtration rate, renal blood flow, INC Na+ reabsorption, stimulates cell growth in numerous cell lines

Front 499

What are some examples of vasodilator agents?

Back 499

bradykinin, natriuretic peptides, serotonin, histamine, prostaglandins

Front 500

How does bradykinin work in humoral regulation of systemic circulation?

Back 500

causes powerful arteriolar dilation and INC capillary permeability, INC filtration and edema, related with the rennin-angiotensin systems (the enzyme that degrades kinins is the same enzyme that converts the inactive angiotensin I into the active angiotensin II)

Front 501

How do natriuretic peptides work in humoral regulation of systemic circulation?

Back 501

DEC blood pressure, DEC responsiveness of vascular wall to vasodilator agents, acts in the neural regulation of the CV system, INC cGMP levels

Front 502

How does serotonin work in humoral regulation of systemic circulation?

Back 502

present in chromaffin tissue of the intestine and other abdominal structures, also in plateltes, can have a vasodilator or a vasoconstrictor effect, causes arteriolar constriction and is release in response to blood vessel damage to help prevent blood loss, has been implicated in the vascular spasms of migraine headaches

Front 503

How does histamine work in humoral regulation of systemic circulation?

Back 503

released in every tissue when it becomes damaged or inflamed or in the allergic reaction, causes arteriolar dilation and venous constriction, this causes INC Pc and filtration out of the capillaries resulting in local edema

Front 504

How do prostaglandins work in humoral regulation of systemic circulation?

Back 504

there is protacyclin(a vasodilator in several vascular bends, including coronary circulation), E-series (vasodilators) and F-series (vasoconstrictors) prostaglandins) and thromboxane A2 (vasoconstrictor)

Front 505

How does Ca2+ work in humoral regulation of systemic circulation?

Back 505

is a vasoconstriction, an INC in Ca2+ causes vasoconstriction, results from the general effect of calcium to stimulate smooth muscle contraction

Front 506

How does K+ work in humoral regulation of systemic circulation?

Back 506

is a vasodilator, cause hyperpolarization of the membrane potential

Front 507

How does Mg2+ work in humoral regulation of systemic circulation?

Back 507

a vasodilator that inhibits smooth muscle generally, competes with Ca2+

Front 508

How does Na+ work in humoral regulation of systemic circulation?

Back 508

a mild arteriolar vasodilator mainly from an INC in the osmolarity of the fluids

Front 509

How do citrate and acetate anions work in humoral regulation of systemic circulation?

Back 509

they are vasodilators

Front 510

How does H+ ion (decreased pH) work in humoral regulation of systemic circulation?

Back 510

a slight DEC in H+ causes vasoconstriction, but an intense DEC leads to vasodilation

Front 511

How does CO2 work in humoral regulation of systemic circulation?

Back 511

a direct vasodilator (especially in the brain) and indirect vasoconstrictor (acting on the brain vasomotor center)

Front 512

What effect does nervous control have on blood vessels (extrinsic factors)?

Back 512

mainly affects more global functions as opposed to local tissue blood flow control, it redirects the blood flow to different areas of the body, INCing the pumping activity of the heart and provides rapid control of arterial pressure

Front 513

What is the SNS and PNS role in circulation regulation?

Back 513

SNS regulates circulation while PNS regulates the heart

Front 514

What vessels get sympathetic innervation?

Back 514

all the vessels except the capillaries and most of the metarterioles are innervated, SNS stimulation in small arteries and arterioles INC resistance and DEC rate of flow through tissues, stimulation of large vessels DEC volume in veins and alters the volume of the peripheral circulatory system

Front 515

What does sympathetic innervation to vascular smooth muscle do?

Back 515

INC in sympathetic tone cause vasoconstriction, DEC in tone cause vasodilation, skin has greatest innervation whereas coronary, pulmonary, and cerebral vessels have little innervation

Front 516

What do sympathetic fibers to the heart do?

Back 516

INC the activity of the heart both INCing the heart rate and enhancing the strength of pumping

Front 517

What role does parasympathetic innervation play in heart function?

Back 517

controls heart rate via the vagus, cause DEC in rate and heart muscle contractility

Front 518

What role does norepinephrine play in global control of circulation?

Back 518

acts directly on the alpha adrenoreceptors of the vascular smooth muscle to cause vasoconstriction

Front 519

What role does the adrenal medulla play in global control of circulation?

Back 519

makes NE (vasoconstriction) and epinephrine (alpha is vasoconstriction, beta is vasodilation)

Front 520

aWhat do sympathetic fibers to skeletal muscle do?

Back 520

they carry both vasodilator and constrictor fibers, release epinephrine and controlled by the anterior hypothalamus, at the onset of exercise the sympathetic vasodilators cause initial vasodilation even before muscles require INCd nutrients

Front 521

What type of factors (extrinsic or intrinsic) in regulation of peripheral blood flow dominates in the brain, heart and contracting skeletal muscle?

Back 521

intrinsic flow regulating mechanisms are dominant

Front 522

What is vascular smooth muscle responsible for?

Back 522

responsible for the control of total peripheral resistance, arterial and venous tone and the distribution of blood flow throughout the body

Front 523

What are some of the characteristics of the vascular smooth muscle?

Back 523

graded changes in membrane potential associated with INC or DEC in force, contain large number of actin and fewer myosin, contraction controlled by [Ca2+], lacks troponin and fast Na+ channels, pharmaco-mechanical coupling is the predominant mechanism for eliciting contraction of vascular smooth muscle

Front 524

What is the principle intracellular signal transduction mechanism for vasoconstriction?

Back 524

1. activation of receptor/Gq protein/PLC/IP3/DAG/PKC pathway, alpha1 adrenoceptors, Ang II receptors, ET receptors, 5HT receptors, H1 receptors, TxA2 receptors, NPY Y1 receptors
2. inhibition of cAMP/AC pathway (Gi receptor-mediated), alpha2 adrenoceptors, A1 adenosine receptors

Front 525

What is the principle intracellular signal transduction mechanism for vasodilation?

Back 525

1. activation of cAMP/AC/PKA pathway (Gs receptor-mediated), beta adrenoceptors, A2 adenosine receptors, PgI2 receptors
2. activation of cGMP/GC/PKG pathway, NO, ANP receptors

Front 526

Describe endothelium-mediated regulation.

Back 526

endothelium lines all blood vessels, so it experiences the shear stress associated with flow, with INC flow and shear stress endothelium releases factors in particular EDRF (endothelium-derived relaxing factor)

Front 527

Describe EDRF (one form of which is NO).

Back 527

causes local relaxation of vascular smooth muscle, activates cystolic guanylate cyclase and produces cGMP, production can be stimulated by circulating ACh causing vasodilation, NO production stimulated by bradykinin and substance P from nitroglycerin, nitroprusside and other nitrovasodilator drugs, NO used in penile erection and inhibition of platelet aggregation

Front 528

What is the percent of total cardiac output that reaches the liver and kidneys at rest?

Back 528

receives about 50% of total cardiac output

Front 529

What is the percent of total cardiac output that reaches the heart at rest?

Back 529

receives 5% of CO but accounts for more than 10% of total O2 consumption

Front 530

Describe autoregulation.

Back 530

it is an example of local (intrinsic)control of blood flow, blood flow to an organ remains constant over a wide range of perfusion pressures, organs that exhibit autoregulation are the heart, brain and kidney, for example if perfusion pressure to the heart is suddenly DEC, compensatory vasodilation of the arterioles will occur to maintain a constant flow

Front 531

Describe active hyperemia

Back 531

an example of local (intrinsic)control of blood flow, states that blood flow to an organ is proportional to its metabolic activity, for example, if metabolic activity in skeletal muscle INC as a result of strenuous exercise, blood flow to the muscle will INC proportionately to meet metabolic demands

Front 532

Describe reactive hyperemia

Back 532

an example of local (intrinsic) control of blood flow, is an INC in blood flow to an organ that occurs after a period of occlusion of flow, the longer the period of occlusion, the greater the INC in blood flow above preocclusion levels

Front 533

Describe the myogenic hypothesis.

Back 533

a mechanism that tries to explain local control of blood flow, explains autoregulation, but not active and reactive hyperemia, is based on the observation that vascular smooth muscle contracts when is stretched

Front 534

What is an example of myogenic hypothesis?

Back 534

if perfusion pressure to an organ suddenly INC, the arteriolar smooth muscle will be stretched and will contract, the resulting vasoconstriction will maintain will maintiain a constant flow (without vasoconstriction, blood flow would INC as a result of the INC pressure)

Front 535

Describe metabolic hypothesis.

Back 535

a mechanism that tires to explain local control of blood flow, is based on the observation that the tissue supply of O2 is matched to the tissue demand for O2, vasodilator metabolites are produced as a result of metabolic activity in tissue, these vasodilators are CO2, H+, K+, lactate and adenosine

Front 536

What are examples of the metabolic hypothesis?

Back 536

1. if the metabolic activity of a tissue INC (strenuous exercise), both the demand for O2 and the production of vasodilator metabolites INC, these metabolites cause arteriorlar vasodilation, INC blood flow, and an INC O2 delivery to the tissue to meet demand
2. if blood flow to an organ suddenly INC as a result of a spontaneous INC in arterial pressure, then more O2 is provided for metabolic activity, at the same time, the INC flow washes out vasodilator metabolites, as a result of this washout, arteriolar vasoconstriction occurs, resistance INC and blood flow is DEC to normal

Front 537

Describe sympathetic innervation of vascular smooth muscle as a means of hormonal (extrinsic) control of blood flow.

Back 537

INC in sympathetic tone cause vasoconstriction, DEC in sympathetic tone cause vasodilation, the density of sympathetic innervation varies widely among tissues, skin has the great innervation, whereas coronary, pulmonary and cerebral vessels have little innervation

Front 538

What are the different levels of response in organs to vasoconstriction in response to the sympathetic neurotransmitter norepinephrine?

Back 538

skin > muscle > kidney >>> brain and coronary

Front 539

What are some examples of vasoactive substances?

Back 539

histamine, bradykinin, serotonin, angiotensin II, endothelins, natriuretic peptides, NO, CO2, prostaglandins (has been implicated in the vascular spasms of migraine headaches, serotonin)

Front 540

How does the rate of oxidative metabolism compare between the gray and white matter?

Back 540

gray matter has a very high rate of oxidative metabolism and its flow rate is up to 6 times higher than that of white matter

Front 541

How sensitive is gray matter to hypoxia?

Back 541

the brain, particularly gray matter, is exquisitely sensitive to hypoxia and consciousness is lost in humans after as little as 10 min of ischemia, with irreversible cell damage occurring within minutes

Front 542

Describe the vascular anatomy of the brain.

Back 542

the cerebral circulation is surrounded by nearly incompressible brain matter and is encased in the rigid skull, blood comes to the brain mostly from the carotid arteries (only a minor amount from vertebral arteries, vertebral arteries unite to form basilar artery, basilar artery joins the carotid arteries to form the circle of Willis, which supplies the cerebral cortex and upper brain stem, branches of the vertebral arteries supply the medulla, pons, occipital lobe and cerebellum

Front 543

What happens if there is reduced blood flow in either carotid?

Back 543

will cause ipsilateral ischemia and brain damage

Front 544

What is the location of the small cerebral arteries?

Back 544

lie on the surface (pial vessels) or penetrate the substance of the brain (parenchymal vessels)

Front 545

Describe the structure of the cerebral capillaries.

Back 545

they are tight with no fenestrations or clefts

Front 546

What is the primary function of the cerebral circulation?

Back 546

it is to ensure an uninterrupted supply of O2 to the brain, it is controlled almost entirely by local metabolic factors, exhibits autoregulation, exhibits active and reactive hyperemia, the most important local vasodilator for the cerebral circulation is CO2, INC in PCO2 cause vasodilation of the cerebral arterioles and INC blood flow to the brain, sympathetic nerves play a minor role, vasoactive substances in the systemic circulation have little or no effect on cerebral circulation because such substances are excluded by the BBB

Front 547

What is the average cerebral blood flow (CBF)?

Back 547

average CBF in adults = 50 mL/100g/min (~15% of CO), average brain weight = 1400 g), for whole brain, average blood flow is 760 mL/min

Front 548

Describe the innervation of the cerebral circulation.

Back 548

1. postganglionic sympathetic neurons (cell bodies in superior cervical ganglion), NE (alpha and beta-2), NPY (vasoconstriction), remember sympathetic nerves play a minor role in the innervation (presumably reflecting a low density of adrenergic receptors on cerebral arteioles)
2. cholinergic neurons (originate in sphenopalatine ganglia)-weak vasodilatory responses, ACh, VIP, polypeptides
3. sensory nerves (cell bodies in trigeminal ganglia)-weak responses, SP, CGRP (calcitonin-gene related peptide)

Front 549

How sensitive are cerebral arterioles to changes in PCO2 and PO2?

Back 549

unlike the heart, cerebral arterioles appear to be more sensitive to changes in arterial blood PCO2 than to changes in PO2

Front 550

Describe cushing reflex.

Back 550

1. INC cranial pressure
2. compression of cerebral arteries + bradicardia due to compress-induced activation of the cardioinhibitory center
3. DEC cerebral blood flow
4. ischemia
5. stimulates vasomotor center
6. peripheral vasoconstriction
7. INC systemic arterial pressure (potential problem, high systemic pressure -> high pulmonary arterial pressure -> edema in the lung
8. restoration of CBF

Front 551

What does reduced CBF cause in cardiovascular pressor centers?

Back 551

causes stimulation of the cardiovascular pressor center, this causes peripheral vasoconstriction and restoration of CBF, however, the problem is that INC systemic pressure (afterload) leads to high pulmonary arterial pressure-causing edema in the lungs, the Cushing reflex also comes in to play after severe hypotension and circulatory shock

Front 552

Describe the coronary arteries.

Back 552

the right and left coronary arteries originate from the root of the aorta, the right coronary artery supplies the right ventricle and atrium, the left coronary artery divides into the left circumflex artery and the left anterior descending artery

Front 553

what does the left circumflex artery supply?

Back 553

supplies the left lateral portion of the ventricle and the left atrium

Front 554

what does the left anterior descending artery supply?

Back 554

supplies the free wall of the left ventricle and the septum

Front 555

describe the coronary capillaries.

Back 555

every muscle fiber has at least one supplying capillary, maximum diffusion distance about 10 microM

Front 556

What does cardiac hypertrophy cause?

Back 556

it INC the diameter of fibers, but may not be accompanied by INC vascularization, enlarged hearts are more vulnerable to circulatory insufficiency

Front 557

describe the coronary venous system.

Back 557

1. superficial system-drains left ventricle, ends in coronary sinus and anterior cardiac veins
2. deep system-drains rest of heart into chambers (arteriosinusoidal vessels, arterioluminal vessels, thebesian veins)

Front 558

How does systole relate to subendocardial pressure and occlusion?

Back 558

systole = high subendocardial pressure = occlusion of arteries = no flow

Front 559

Where are compression forces greatest?

Back 559

compressive forces are particularly high in the left ventricle, compression is greatest in the endocardium (making it more susceptible to ischemic injury) and lessens in the direction of the epicardium, compressive forces are less in the right ventricle, but the same endo- to epicardial gradient exists

Front 560

What happens to blood flow when there is an INC in myocardial contractility?

Back 560

INC in myocardial contractility are accompanied by an INC demand for O2, to meet this demand, compensatory vasodilation of coronary vessels occurs and both blood flow and O2 delivery to the contracting heart muscle INC (active hyperemia)

Front 561

Is there collateral circulation between major coronary branches?

Back 561

in normal individuals, there is little collateral circulation between major coronary branches, generally, coronary arteries are end arteries, sudden occlusion of one artery will cause ischemia and/or infarction, if occlusion is slow (atherosclerosis) then anastomoses will form and become functional, these are called collateral arteries, this is usually not enough to completely restore blood flow

Front 562

What are normal levels of O2 consumpation? what are they during exercise?

Back 562

normally about 8-10 mL/min/100g heart, during exercise, O2 consumption can INC many-fold, INC in coronary blood flow mediated by autoregulatory mechanisms, close link between metabolic rate and coronary blood flow

Front 563

Describe what coronary steal is.

Back 563

the coronary vasculature in the normal heart has a great capacity to DEC resistance (INC flow) in response to exercise, in disease states, e.g. atherosclerosis, vessels may already be maximally dilated to ensure flow under resting conditions, thus, coronary reserve is already used up, additionally, because normal areas neighboring one with low reserve can dilate, blood flow may be further diverted away (this is called coronary steal)

Front 564

How is skeletal muscle circulation controlled?

Back 564

is controlled by the extrinsic sympathetic innervation of blood vessels in skeletal muscle and by local metabolic factors

Front 565

Describe the sympathetic innervation of the skeletal muscle circulation.

Back 565

is the primary regulator of blood flow to the skeletal muscle at rest, arterioles of the skeletal muscle are densely sympathetic, are alpha1 (vasoconstriction) and beta1 (vasodilation) receptors

Front 566

Describe the local metabolic control of the skeletal muscle circulation.

Back 566

blood flow in skeletal muscle exhibits autoregulation and active and reactive hyperemia, demand for O2 varies with metabolic activity and flow is regulated by demand, local metabolic mechanisms are dominant during exercise

Front 567

What are the local vasodilator substances for local metabolic control of skeletal muscles?

Back 567

lactate, adenosine, K+

Front 568

What happens to skeletal muscle circulation during exercise?

Back 568

mechanical effects during exercise temporarily compress the arteries and DEC blood flow, during postocclusion period, reactive hyperemia INC blood flow to repay the O2 debt, exercise can elicit a profound INC (20-fold) in skeletal blood flow that is mediated by vasodilator metabolites

Front 569

What types of innervation does skin circulation have?

Back 569

has extensive sympathetic innervation, under extrinsic control, skin areas are under direct CNS control

Front 570

What causes blushing?

Back 570

caused by CNS inhibition of sympathetic fibers

Front 571

What causes blanching?

Back 571

caused by CNS excitation of sympathetic fibers

Front 572

What role do vasodilator fibers have in cutaneous tissue?

Back 572

there are no known vasodilator fibers in cutaneous tissue except for sympathetic vasodilator fibers, which innervate sweat glands, stimulation causes release of kinins and subsequent dilation of cutaneous blood vessels, most vasodilation is due to inhibition of sympathetic tone

Front 573

Describe the role of ateriovenous anastomoses in the cutaneous tissue.

Back 573

shunt blood from arterioles to venules and bypass capillary bed, found primarily at fingertips, palms, ears, nose and lips, is heavily innervated by sympathetic nerves causing them to close, smooth muscle sphincters of these shunts are controlled by temperature (cold = vasoconstriction, heat = vasodilation), allows direct flow from arteries to venules and greatly INC blood flow when dilated

Front 574

Describe temperature regulation as a principal function of the cutaneous sympathetic nerves.

Back 574

INC temp leads to cutaneous vasodilation allowing dissipation of excess body heat, thus initial response to exercise is vasoconstriction but as temp rises there is a reflex inhibition of sympathetic activity (leads to dilation of skin vessels and INC heat loss, as core temp rises, so does skin temp and flow, this is a withdrawal of sympathetic tone and vasodilation due to bradykinin release from sweat glands

Front 575

What response does trauma to skin produce?

Back 575

the triple response, a red line, a red flare and a wheal (local edema that results from the local release of histamine, which INC capillary filtration)

Front 576

Describe the innervation of the skin vasculature.

Back 576

composed of a plexus of large arterioles and venules in the deep dermis which send branches to the superficial plexus of smaller arterioles and venules, capillary loops into the dermal papillae beneath the epidermis are perfused and drained by microvessels of the superficial dermal vasculature

Front 577

What is the control of blood flow to the skin concerned with?

Back 577

temperature regulation (neural control) and response to injury (paracrine control)

Front 578

What is the metabolic rate of the skin and how does it relate to its blood flow?

Back 578

skin has a low metabolic rate, so unless there is some severe pathology, blood flow is adequate for metabolic needs

Front 579

Describe the axon reflex.

Back 579

is neurovascular response conducted through the C nociceptive nerve fibers, important mechanism for regulating the microcirculation, antidromic stimulation of the C fibers releases vasodilating substances such as substance P, bradykinin, ATP and calcitonin gene related peptide, diabetic neuropathy can lead to microcirculatory problems by damaging this reflex

Front 580

What causes the pale, cold skin found in patients with hypovolemic shock?

Back 580

it reflects a rise in cutaneous vascular resistance that appears to help support arterial blood pressure, during WWI, it was noticed that men rescued quickly and warmed in blankets (producing cutaneous vasodilation) were less likely to survive than men who could not be reached for some time and who retained their natural cutaneous vasoconstriction, therefore patients in shock should not be warmed to the point that their body temp rises

Front 581

What are the two circulations in the lung?

Back 581

1. bronchial circulation
2. pulmonary circulation

Front 582

Describe bronchial circulation

Back 582

this is blood flow for meeting the metabolic needs of the lung tissue, its only about 1% of cardiac output, bronchial arteries are branches of the thoracic aorta, they divide down to arterioles and capillary bed, same type of vascular architecture as the systemic vessels, bronchial veins and azygous vein for drainage back to the right atrium

Front 583

Where do the lungs (in terms of pulmonary circulation) receive there cardiac output from?

Back 583

receive 100% from the right heart, thus flow to the lungs is the same as to the periphery, CO of right ventricle is pulmonary blood flow and is equal to CO of left ventricle

Front 584

Describe the pulmonary vessels.

Back 584

they are very thin, short and distensible, therefore have very low resistance

Front 585

Describe the pressure found in the pulmonary vessels.

Back 585

pressure is much lower than in the systemic circulation (pulmonary arterial pressure is 15 mm Hg, compared to 100 mm Hg), although low, still sufficient to pump CO because resistance of the pulmonary circulation is relatively low

Front 586

Describe the resistance found in the pulmonary vessels.

Back 586

is also much lower than in the systemic circulation, the resistance is low and constant (even during exercise)

Front 587

What is the blood flow throughout the lung when the patient is supine, standing?

Back 587

when supine nearly uniform throughout the lung, when standing blood flow is unevently distributed because of the effect of gravity, blood flow and pressure is lowest at the apex of the lung and highest at the base of the lung

Front 588

What does hypoxia cause in the lung?

Back 588

vasoconstriction, this response is opposite of that in other organs (i.e. brain) where hypoxia causes vasodilation, local vasoconstriction redirects blood away form poorly ventilated, hypoxic regions of the lung and toward well-ventilated regions, this hypoxic vasoconstriction maintains the optimal ventilation-perfusion ratio, hypoxia is the most important regulator of pulmonary flow in pulmonary circulation

Front 589

Describe the splanchnic circulation to the GI tract, liver, spleen and pancreas.

Back 589

supplied by a series of parallel circuits whereas the liver receives blood from the hepatic artery and the portal vein

Front 590

What happens to GI blood flow after a meal?

Back 590

it INCs with digested nutrients, metabolic factors and GI hormones and neuropeptides mediating the active hyperemia

Front 591

What is the blood supply to the intestines?

Back 591

supplied by a series of parallel circulation via branches of the superior and inferior mesenteric arteries, neural regulation is almost exclusively sympathetic (alpha receptors mediate vasoconstriction, beta receptors mediate vasodilation), autoregulation caused by adenosine, functional hyperemia is found in food ingestion which causes an INC in intestinal blood flow

Front 592

How is blood flow to the intestine regulated?

Back 592

Ingesting food increases intestinal blood flow, This is due to a combination of factors., Paracrine regulation includes the release of vasodilators including bradykinin, CCK, VIP, gastrin, and secretin, Metabolic regulation includes PO2 and adenosine production, Sympathetic stimulation directly decreases GI blood flow in order to increase the circulating blood volume (e.g., during exercise), Splanchnic blood flow is profoundly reduced during sympathetic activation and with increased blood levels of angiotensin II and vasopressin.

Front 593

What is the blood supply to the liver?

Back 593

is normally about 25% of total CO, ¾ of blood supply is from portal vein, rest from hepatic artery, ¾ of O2 used by liver supplied hepatic artery (since O2 in portal vein is low), blood flow between the hepatic artery and portal vein are inversely related helping to maintain a constant hepatic blood flow, innervated by sympathetic vasoconstrictors, flow influenced by systemic venous pressure

Front 594

How is blood flow to liver regulated?

Back 594

The liver receives about 25% of cardiac output, This comes from the portal vein (draining the intestinal circulation; 75% of flow) and the hepatic artery (25% of flow). The liver is a blood reservoir (15% of total blood volume), and sympathetic stimulation can divert this blood to the systemic circulation (e.g., in response to hemorrhage or exercise). The portal venous and hepatic arterial flows vary reciprocally. The portal system does not autoregulate, but the arterial side does.

Front 595

What are the basic components of a typical neural control system?

Back 595

1. a signal (change in arterial pressure)
2. detectors or sensors (arterial baroreceptors)
3. afferent pathways that translate the signal to a coordinating center
4. a neural network (CNS; coordinating center) which compares a signal from the sensors with a command signal which originates in CNS
5. a neural output which connects the nervous system to the target cells in the effector organs (efferent pathways)
6. the target organs themselves (heart and peripheral blood vessels.

Front 596

What are baroreceptors and where are they located?

Back 596

stretch receptors that are located within the walls of the carotid sinus near the bifurcation of the common carotid arteries, they detect changes in intravascular pressure and volume by sensing vascular wall tension, there are high and low pressure classes

Front 597

What pressures do the carotid baroreceptors work? aortic baroreceptors

Back 597

1. carotid baroreceptors monitor arterial pressure within the range of 50-200 mm Hg
2. aortic baroreceptors monitor pressure between 100 and 200 mm Hg

Front 598

How is baroreceptor stimulation related to magnitude and rate of change of blood pressure?

Back 598

degree of high-pressure baroreceptor stimulation is directly related to magnitude and rate of change of blood pressure, respond to the absolute level of BP but also how rapidly it changes

Front 599

Do baroreceptors contribute to the long-term regulation of arterial pressure?

Back 599

NO, adapt to INC in arterial pressure after 1-2 days only

Front 600

When are high-pressure baroreceptors activated?

Back 600

under normal levels of BP and volume, the receptors are still under some degree of stretch and so are continuously sending a constant number of APs to the brain

Front 601

Describe what the low-pressure baroreceptors are and where they are located.

Back 601

they are bare ends of myelinated nerve fibers, located at strategic low-pressure sites including the pulmonary artery, the junction of the atria with their corresponding veins, the atira and monitor venous volume

Front 602

How are the low-pressure baroreceptors activated?

Back 602

distension of these receptors depends largely on venous return to the heart, small changes in pressure produce large changes in volume, and so the body interprets changes in the activity of the low-pressure baroreceptors as changes in blood volume, help control blood volume through the reflex release of antidiuretic hormone, A-type receptors found in the body of the right atrium while B-type are found in the IVC and SVC

Front 603

What role does the right atrium play in pressure regulation?

Back 603

sends info about blood volume to brain and also releases natriuretic hormone when that volume INC, this hormone acts on the kidney to stimulate excretion of salt and water, which acts to return blood volume toward normal

Front 604

What role does the medullar cardiovascular center play in pressure regulation?

Back 604

integrates sensory information about the status of the cardiovascular system and initiates adjustments to maintain an appropriate systemic arterial blood pressure

Front 605

What is the medullar cardiovascular center produced from?

Back 605

it is a collection of neurons in the medulla forms vasoconstrictor (C-1), cardioinhibitor and vasodilaotr (A-1) centers, receives sensory information from a variety of sources, compares the info to the set point for systemic arterial BP

Front 606

Where does the medullar CV center receive info from?

Back 606

CV systems as well as info from higher areas in the brain such as hypothalamus, limbic and cerebral cortex, the higher areas can override the homeostatic activity of the CV system (as seen when BP rises during extreme events in life)

Front 607

What is the speed of the baroreceptor reflex and what type of system is it?

Back 607

it includes fast, neural mechanisms and acts as a negative feedback system that is responsible for the minute-to-minute regulation of arterial blood pressure

Front 608

What are the steps in the baroreceptors reflex when there is a DEC in arterial pressure?

Back 608

1. a DEC in arterial pressure DEC stretch on the walls of the carotid sinus (with rapidly DECing pressure producing the greatest response), aortic arch also plays a role but only responds to INCs, not DECs in pressure
2. DEC in stretch DEC firing rate of the carotid sinus nerve (CN IX, Hering’s nerve) which carries info to the vasomotor center in the brain stem
3. if less than set point of 100 mm Hg then changes in autonomic response will occur to attempt to INC blood pressure toward normal
4. the vasomotor center responds by DECing parasympathetic (vagal) outflow to the heart and INC sympathetic outflow to the heart and blood vessels

Front 609

What are some effects that attempt to INC the arterial pressure to normal?

Back 609

1. INC heart rate-results from DEC parasympathetic tone and INC sympathetic tone to SA node
2. INC contractility and stroke volume-results from INC sympathetic tone to the heart, with INC in heart rate, the INC in contractility and stroke volume produce an INC in cardiac output that INC arterial pressure
3. INC vasoconstriction of arterioles, results from the INC sympathetic outflow, as a result, TPR and arterial pressure will INC
4. INC vasoconstriction of veins (venoconstriction)-results from the INC sympathetic outflow, constriction of the veins causes a DEC in unstressed volume and INC in venous return to the heart, the INC in venous return causes an INC in cardiac output by the Frank-Starling mechanism

Front 610

How does the baroreceptor reflex respond to acute blood loss?

Back 610

acute hemorrhage -> DEC in mean arterial pressure -> DEC stretch on carotid sinus -> DEC in firing rate of carotid sinus nerve -> two things
1. DEC in parasympathetic outflow of heart which INC heart rate and INC mean arterial pressure to normal
2. INC sympathetic outflow of heart and vessels which INC rate, contractility and constriction of arterioles, this INC constriction of veins, venous return and mean systemic pressure to INC mean arterial pressure toward normal
3. can also result in a DEC renal perfusion pressure which in turn INC release of renin

Front 611

How does the baroreceptor respond to an acute INC in arterial blood pressure?

Back 611

INC aortic pressure leads to INC afferent nerve activity from the baroreceptors, which results in reciprocal changes in efferent sympathetic and parasympathetic nerve activity to the heart and blood vessels with a resultant DEC in aortic blood pressure back to normal

Front 612

What role does the sympathetic nervous system play in the rapid control of arterial pressure?

Back 612

responsible for vasoconstriction and cardioacceleration

Front 613

What are the three major changes that occur simultaneously when wantgin to INC BP?

Back 613

1. almost all arterioles of the body are constricted greatly INCing total peripheral resistance
2. the large vessels (especially veins) are constricted forcing blood into heart INCing the force of the heart beat and to pump INC quantities of blood to INC BP
3. direct stimulation of the ANS further enhancing cardiac pumping, most rapid of all mechanisms for pressure control, often INC it by two times normal in 5 to 10 secs

Front 614

Describe the players in the renin-angiotensin-aldosterone system.

Back 614

1. renin is an enzyme
2. angiotensin I-inactive
3. angiotensin II-active
4. angiotensin III-active, has some of the biological activity of angiotensin II since it is a peptide fragment of angiotensin II when it is cleaved by angiotensinase

Front 615

What is the speed of the renin-angiotensin-aldosterone system and how does it affect BP regulation?

Back 615

it is a slow, hormonal mechanism, is used in long-term BP regulation by adjustment of blood volume

Front 616

What are the steps involved in the renin-angiotensin system with a DEC in renal perfusion pressure?

Back 616

1. a DEC in renal perfusion pressure causes the juxtaglomerular cells of the afferent arterioles to secrete renin
2. renin catalyzes the conversion of angiotensinogen to angiotensin in plasma
3. ACE (angiotensin-converting enzyme) catalyzes the conversion of angiotensin I to angiotensin II primarily by the lungs

Front 617

What effects does angiotensin II have?

Back 617

1. stimulates the synthesis and secretion of aldosterone by the adrenal cortex, this INC Na+ reabsorption by the renal distal tubule thereby INCing extracellular fluid volume, blood volume and arterial pressure, this action of aldosterone is slow because it requires a new protein synthesis
2. causes vasoconstriction of the arterioles, thereby INCing TPR and mean arterial pressure

Front 618

What do ACE inhibitors due in regulating BP?

Back 618

block the conversion of angiotensin I to angiotensin II to DEC BP

Front 619

How does cerebral ischemia cause a change in arterial BP and how is it regulated?

Back 619

when brain is ischemic, PCO2 is INC, chemoreceptors detect this and INC sympathetic outflow to the heart and blood vessels, vasoconstriction happens, INCs TPR and preserves blood flow to brain by reducing blood supply to other organs

Front 620

What is the Cushing reaction in terms of cerebral ischemia

Back 620

it is an example of the responses to cerebral ischemia, INCs in intracranial pressure causes compression of cerebral blood vessels, leading to cerebral ischemia and INC cerebral PCO2, the vasomotor center directs an INC in sympathetic outflow to the heart and blood vessels which causes a profound INC in arterial pressure

Front 621

What role do chemoreceptors in the carotid and aortic bodies have in regulating BP?

Back 621

they are located near the bifurcation of the common carotid, have very high rates of O2 consumption and are very sensitive to DEC in PO2, DEC in PO2 activate vasomotor center that produce vasoconstriction, an INC in TPR and an INC in arterial pressure, DEC in PO2 < 60 mm Hg causes hyperventilation, in CV system only plays a role in severe hypoxia, not a powerful arterial pressure controller in the normal BP range (only when below 80 mm Hg), INC in PCO2 and [H]+ stimulate breathing resuling in hyperventilation which retruns the arterial PCO2 toward normal, bradycardia exists when ventilation is fixed or held and tachycardia exists when ventilation is sped up

Front 622

What role does vasopressin (antidiuretic hormone (ADH)) play in regulating BP?

Back 622

regulates BP in response to hemorrhage, but not in minute-to-minute regulation of normal BP, atrial receptors respond to a DEC in blood volume and cause the release of vasopressin from the posterior pituitary, vasopressin has effects to INC BP to normal:
1. a potent vasoconstrictor that INC TPR by activating V1 receptors on the arterioles
2. it INCs water reabsorption by activating V2 receptors

Front 623

What role does atrial natriuretic peptide (ANP) play in regulation of BP?

Back 623

is it relased from the atria in response to an INC in atrial pressure, causes relaxation of vascular smooth muscle, dilation of the arterioles and DEC TPR, causes INC excretion of Na+ and water, reduing blood volume and bring BP down, inhibits renin secretion as well

Front 624

Describe the essential (primary) type of hypertension.

Back 624

it occurs in 90% of the patients with hypertension, has unknown etiology

Front 625

What is the mechanism involved in essential hypertension?

Back 625

there has been no identification of a primary abnormality in essential hypertension, CO is usually normal so that the sustained BP is probably a result of an elevation in peripheral resistance

Front 626

What are some possible mechanisms for INC in peripheral resistance?

Back 626

1. autoregulation hypothesis-overreaction of the resistance vessels to random changes in BP, genetic susceptibility, structural alterations in resistance vessels
2. hormonal hypothesis-existence of a circulating hormone or chemical which causes INCd tone in vascular smooth muscle
3. sympathetic hypothesis-INCd sympathetic vasoconstrictor drive in early stages
4. membrane alteration hypothesis-membrane alterations which either directly (myogenic control) or indirectly (neurogenic or humoral control) INC vascular tone

Front 627

Describe the secondary type of hypertension.

Back 627

occurs in 10% of all cases, can be renal, endocrine, or other:
1. renal-due to tumors of JG cells, narrowing of renal arteries or renal disease
2. endocrine-due to hyperaldosteronism (Conn's syndrome), Cushing’s syndrome (glucocorticoid hypersecretion), pheochromocytoma (tumor of adrenal gland, NE and epinephrine hypersecretion)
3. other-due to oral contraceptives and narrowing of the aorta

Front 628

What is preload?

Back 628

is the venous pressure that results in filling of the heart in diastole

Front 629

What is afterload?

Back 629

is the pressure against which the heart must work to pump blood (how much pressure is needed to overcome aortic pressure)

Front 630

What is cardiac output?

Back 630

is the volume of blood ejected from the heart per unit time, determined primarily by the status of the heart, CO = stroke volume X heart rate

Front 631

What is stroke volume?

Back 631

is the blood ejected from the heart per each beat, it equals end-diastolic volume minus end-systolic volume

Front 632

What does tissue perfusion (flow) depend on?

Back 632

arterial pressure and local vascular resistance (Q (flow) = MAP / R)q

Front 633

What does arterial pressure depend on?

Back 633

it depends on cardiac output and total peripheral resistance (TPR), CO = MAP/TPR

Front 634

What determines systolic pressure?

Back 634

stroke volume, aortic distensibility, ejecting velocity

Front 635

What determines diastolic pressure?

Back 635

systolic pressure, aortic distensibility, heart rate, peripheral resistance

Front 636

What is total peripheral resistance (TPR)

Back 636

the total resistance to the flow of blood from the aorta back to the right atrium, determined primarily by the status of the resistance vessels

Front 637

What factors help determine the long-range regulation of BP?

Back 637

1. the control of fluid balance by the kidney
2. adrenal cortex
3. CNS with maintenance of a constant blood volume

Front 638

How do non-circulatory systems interact with the CV system?

Back 638

ANS, respiratory, hepatopoietic organs and liver, urinary and GI systems, endocrine system and temperature control system all effect the CV system and its subsystems (CO, MAP, TPR, blood volume, systemic circulatory reflexes, local vasomotor control

Front 639

What pressures exist when one is in the supine position?

Back 639

aorta-90 mm Hg, right atrium-0-5 mm Hg, driving pressure-85-90 mm Hg

Front 640

What is the effect of gravity on pressure?

Back 640

it INC the pressure of any blood vessel below the level of the heart and DEC the pressure of any blood vessel above the level of the heart

Front 641

What happens to an individual in terms of pressure when one moves from a supine position to a standing position?

Back 641

1. a significant volume of blood pools in the lower extremities because of the high compliance of the veins (muscular activity would prevent this pooling), causes INC in local venous pressure
2. Pc in the legs INC and fluid is filtered into the interstitium, edema will occur if net filtration exceeds the ability of the lymphatics to return it to circulation
3. blood volume and venous return DEC, therefore stroke volume and CO DEC
4. arterial pressure DEC because of the reduction in cardiac output, fainting may occur if cerebral BP DECs low enough
5. compensatory mechanisms will attempt to INC BP to normal

Front 642

What are the compensatory mechanisms that will occur to INC BP in an individual shifting from a supine to standing position?

Back 642

carotid sinus responds to DEC in arterial pressure by DECing the firing rate of the cartodi sinus nerve, vasomotor center then INC sympathetic outflow to the heart and DEC parasympathetic outflow, this INC heart rate, arterial constriction and venoconstriction, and restores venous return, CO and BP, also INC renin and aldosterone levels, cerebral adjustments also occur

Front 643

What are the cerebral adjustments that are made to INC BP in an individual shifting from a supine position to a standing one?

Back 643

consists of cerebral dilation due to autoregulatory mechanisms (pH, PO2, PCO2) and INC O2 extraction that will keep O2 consumption constant

Front 644

What is orthostatic (postural) hypotension?

Back 644

a condition where sudden standing causes a fall in BP, dizziness, and fainting associated with autonomic insufficiency, may occur in individuals with impaired baroreceptors reflex (individuals treated with sympatholytic agents)

Front 645

What is the CV response to prolonged standing?

Back 645

with prolonged standing, capillary BP INC in the leg INCing filtration and reducing blood volume, contraction of skeletal muscle helps pump blood toward the heart reducing capillary blood pressure and filtration

Front 646

What are the steps to the compensatory response to acute blood loss?

Back 646

1. A decrease in blood volume produces a decrease in mean systemic pressure. As a result, there is a decrease in both cardiac output and arterial pressure.
2. The carotid sinus baroreceptors detect the decrease in arterial pressure. As a result of the baroreceptors reflex, there is increased sympathetic outflow to the heart and blood vessels and decreased parasympathetic outflow to the heart, producing:
↑ heart rate
↑ contractility
↑ TPR (due to arteriolar constriction)
3. Vasoconstriction occurs in skeletal, splanchnic, and cutaneous vascular beds. However, it does not occur in coronary or cerebral vascular beds, ensuring that adequate blood flow will be maintained to the heart and brain.
4. Chemoreceptors in the carotid and aortic bodies are very sensitive to hypoxia. They supplement the baroreceptor mechanisms by increasing sympathetic outflow to the heart and blood vessels.
5. Cerebral ischemia (if present) causes an increase in PCO2, which activates chemoreceptors in the vasomotor center to increase sympathetic outflow.
6. Arteriolar vasoconstriction causes a decrease in Pc. As a result, capillary absorption is favored, which helps to restore circulating blood volume.
7. The adrenal medulla releases epinephrine and norepinephrine, which supplement the actions of the sympathetic nervous system on the heart and blood vessels.
8. The renin-angiotensin-aldosterone system is activated by the decrease in renal perfusion pressure. Because angiotensin II is a potent vasoconstrictor, it reinforces the stimulatory effect of the sympathetic nervous system on TPR. Aldosterone increases NaCl reabsorption in the kidney, increasing the circulating blood volume.
9. ADH is released when atrial receptors detect the decrease in blood volume. ADH causes both vasoconstriction and increased water reabsorption in the kidney, both of which tend to increase blood pressure.

Front 647

How long does the compensatory response last?

Back 647

a temporary response that sacrifices the immediate needs of some tissues to maintain those of other, more critical tissues such as heart and brain

Front 648

How are other systems involved in regulating BP during acute blood loss?

Back 648

try to INC BP and blood volume by having kidneys DEC urine output, angiotensin II and aldosterone are released and there is an INC sense of thirst, urine output is reduced and the kidney forms angiotensin II

Front 649

What is the treatment of choice for a hemorrhage?

Back 649

blood transfusion, it is an effective way of returning the system to normal, INC total blood volume by INCing the end-diastolic volume of the heart

Front 650

What are some of the changes to the capillary system during hemorrhage?

Back 650

MAP and venous pressure are reduced due to the hemorrhage, capillary pressure is also reduced, plasma protein concentration has not changed to reabsorption is favored and interstitial fluid is transferred to the blood, may take as long as 12-24 hours to reach completion, more prolonged response than the compensatory response, does allevate the hemodynamic crisis, it cannot account for complete recovery

Front 651

What is necessary for complete restoration of total body water?

Back 651

involves the control of fluid ingestion and kidney function

Front 652

What is necessary for complete restoration of blood?

Back 652

requires stimulation of erythropoesis to INC the hematocrit and synthesis of plasma proteins

Front 653

What is circulatory shock?

Back 653

the progressive deterioration of cardiovascular function due to greater losses of blood that can lead to severe tissue damage, irreversible circulatory collapse and death

Front 654

What is reperfusion injury?

Back 654

the events that occur following restoration of blood flow to any tissue that has experienced a prolonged episode of ischemia, immune cells release molecular free radicals that cause cellular damage by oxidation of proteins, lipids and nucleic acids

Front 655

How can the body be protected from the effects of reperfusion injury?

Back 655

these effects can be partially protected against by the use of free radical scavengers and antioxants, natural antioxidants present in the body include Vita C and E

Front 656

Define exercise in terms of skeletal muscle activity and the CV changes associated with it.

Back 656

exercise is an INC in the rate and extent of contraction of skeletal muscle, CV changes are opposite those occurring during hypotension and hemorrhage, they consist of a combo and integration of neural and local factors

Front 657

What are the neural factors involved in regulation of BP during exercise?

Back 657

originate in the motor cortex or from reflexes initiated in muscle proprioceptors

Front 658

What role does central command play in BP regulation during exercise?

Back 658

cerebrocortical activation of the SNS leading to cardiac acceleration, INC cardiac contractile force (positive inotropic effect) and peripheral vasoconstriction, also have DEC in parasympathetic outflow, CO is INC, venous return is INC, arteriorlar resistance in the skin, splanchnic regions, kidneys and inactive muscle is INC, blood flow to organs is DEC

Front 659

What role do reflexes originating in the contracting muscle play in regulation of BP during exercise?

Back 659

reflexes initiated by stimulation of mechanoreceptors and chemoreceptors, impulses travel centrally via small myelinated (group III) and unmyelinated (group IV) afferent nerve fibers, group IV may represent muscle chemoreceptors, the central connection of this limb is unknown but ht efferent limb consists of sympathetics to the heart and blood vessels

Front 660

What are the local (metabolic) factors found during exercise?

Back 660

include vasodilator metabolites (lactate, K+ and adenosine) which accumulate because of INC metabolism of the exercising muscle, local mechanisms are the most important for maintaining high blood flow during exercise

Front 661

What purpose do the vasodilator metabolites have?

Back 661

cause arteriolar dilation in the active skeletal muscle, INCing skeletal muscle blood flow, INCing O2 delivery, number of perfused capillaries is INC to DEC diffusion distance for O2, DEC in TPR

Front 662

Why does TPR DEC during exercise?

Back 662

1. INC sympathetic activity to splanchnic, renal and non-exercising muscle arterioles
2. cutaneous vasodilation in response to a rise in blood temperature

Front 663

What are the two points insured due to a DEC in peripheral resistance during exercise?

Back 663

1. MAP will not rise too high in spite of the INC in CO and
2. an adequate portion of the INC in CO will reach exercising muscle

Front 664

what happens to the pressure volumes during moderate to intense exercise?

Back 664

MAP INC with 15 % response to moderate exercise and 25% in response to intense exercise, TPR INC by 50% during moderate and 60% during intense exercise, CO by 120% and 240%, heart rate by 100% and 200%, skeletal muscle blood flow INC by 175% and 1000%

Front 665

What does anticipation of physical activity do to get ready for exercise?

Back 665

leads to simultaneous inhibition of parasympathetic areas and activation of sympathetic areas of the medulla and this results in INC heart rate and myocardial contractility, tachycardia and enhanced contractility INC CO, SNS changes vascular resistanc to periphery by vasoconstriction diverting blood away from skin (which then gets more blood later as temp elevates), kidney, splanchnics and inactive muscle, this INC CO and blood flow to active muscles, blood flow to myocardium INC, flow to brain stays the same, all this is done to maintain a normal arterial blood pressure for adequate perfusion of the active tissues

Front 666

How is the level of arterial pressure during exercise relate to the severity of the exercise performed?

Back 666

they roughly parallel each other, the INC in CO is proportionally greater than the DEC in TPR

Front 667

What happens to systolic, diastolic and pulse pressure during exercise?

Back 667

systolic usually INC more than diastolic, thus INCing pulse pressure, larger pulse pressure is attributable to a greater stroke volume and a more rapid ejection of blood by the left ventricle

Front 668

What is heart failure?

Back 668

is the result of the inability of the heart to maintain adequate CO and the tissues of the body are not adequately perfused so that the metabolic demands of the body for oxygen and nutrients are not met

Front 669

What mechanisms lead to heart failure?

Back 669

1. abnormalities of the heart muscle (cardiomyopathies)
2. abnormal valvular function
3. abnormal heart rhythms
4. congential structural abnormalities

Front 670

How do abnormalities of the heart cause heart failure?

Back 670

1. poor contractile function (systolic dysfunction)
2. abnormal filling of the ventricle or abnormal ventricular relaxation (diastolic dysfunction)
3. hyptertrophy (abnormal thickening of the ventricle) that is associated with obstruction of flow

Front 671

How does a reduction in cardiac contractility cause heart failure?

Back 671

leads to INCd end-diastolic volume and DEC CO and stroke volume and BP, how does this work with the Frank-Starling law intact, kidneys respond to DEC in blood pressure by INC retention of water and Na+, INC in blood volume causes INC in cardiac output, but with progressive heart failure, additional INC in volume stretch the muscle beyond its optimal length, once this happens, further INC in heart volume actually reduce the ability of the heart to pump blood, leads to congestive heart failure

Front 672

What are the causes of systolic dysfunction?

Back 672

1. coronary artery disease (myocardial ischemia, MI)
2. infection (virus, bacteria, protozoa)
3. toxicity (alcohol, cobalt, lead)
4. idiopathic
5. metabolic conditions (diabetes mellitus)
6. altered loads (valvular abnormalities, long-lasting hypertension)

Front 673

What happens in failure of the left heart?

Back 673

it leads to an accumulation of blood in the pulmonary circulation

Front 674

What happens in failure of the right ventricle?

Back 674

leads to an accumulation of blood in the right heart and the venous system, the INC volume in either the pulmonary or systemic veins leads to INC capillary pressure and loss of fluid to the interstitial space (edema)

Front 675

What is diastolic dysfunction?

Back 675

give symptoms of heart failure due to abnormal filling of the left ventricle, this abnormal filling is commonly due to reduced compliance of abnormal distensibility of the left ventricle, this is associated with an INC pressure for a specific volume during diastole, if venous return is kept constant, the end-diastolic pressure is elevated, which in turn causes elevated left atrial pressure in the same manner described for systolic dysfunction, elevated end-diastolic pressure is the pathophysiologic basis for the similar symptoms observed in heart failure resulting from diastolic dysfunction and systolic dysfunction

Front 676

What are the causes of diastolic dysfunction?

Back 676

1. coronary artery disease (myocardial ischemia)
2. infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis)
3. hypertrophy in response to an abnormal load (aortic stenosis, hypertension)
4. primary or genetic conditions (hypertrophic cardiomyopathy)

Front 677

What symptoms are associated with diastolic dysfunction?

Back 677

dyspnea (shortness of breath), pulmonary edema, fatigue (due to inadequate delivery of O2 to peripheral tissues), protrusion of jugular veins due to elevated jugular venous pressure

Front 678

What are some treatment options for diastolic dysfunction?

Back 678

diuretics, inotropics (digitalis), vasodilators (venodilators, arteriodilators), neurohormonal antagonists, others (anticoagulants, antiarrhythmics)

Front 679

How and what does digoxin do?

Back 679

INC CO, INC ejection fraction, DEC LVEDP, INC exercise tolerance, INC natriuresis, DEC neurohumoral activation

Front 680

How and what does nitrates do?

Back 680

are venous vasodilators (venodilation), DEC preload (by DEC pulmonary congestion, DEC ventricular size, DEC ventricular wall stress), coronary vasodilation, INC myocardial perfusion (arterial vasodilators), DEC afterload (by DEC CO and BP)

Front 681

How and what do ACE inhibitors do?

Back 681

arterio-venous vasodilation, no change in heart rate/contractility, INC renal, cerebral and coronary blood flow, diuresis and natriuresis

Front 682

How and what do diuretics do?

Back 682

DEC volume and preload (improve symptoms of congestion), no direct effect on CO, but excessive reduction in preload may reduce CO, improve arterial distensibility

Front 683

How and what do beta-blockers do?

Back 683

DEC neurohormonal activation, reduced heart rate, anti-hypertensive and antianginal, antiarrhythmic

Front 684

What are the treatment options for hypertension?

Back 684

1. Lower body Na+ and water:
diuretics
restricting salt intake

2. Lower smooth muscle tone
in arterioles:
vasodilators
Ca channel antagonists
alpha-adrenoceptor antagonists

3. Decrease levels of ANG II, potentiate effects of bradykinin:
ACE inhibitors

4. Decrease heart rate and stroke volume:
beta-blockers