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321 Cards in this Set

  • Front
  • Back
semilumar valves prevent backflow by structure. AV valves prevent backflow by chordae tendonae
right AV is tricuspid
left AV is bicuspid
aortic and pulmonary semilunar valves have 3 lobes
right atrium get blood from inferior and superior vena cava
Cardiac pacemakers depolarize in response to an influx of Ca++
Contractile cells depolarize due to an influx of Na+
Ca++ plays a role in the prolonged depolarization of contractile cells.
Plateau period of cardiac cells is vital for complete pumping and allows ventricles to fill.
6 regions of autorhythmic cells in elec cond. system: SA node, internodal pathway, interarterial pathway, AV node, bundle of His, and Purkinje fibers
SA node
right atrium, normal pacemaker of heart.
Interatrial pathway
goes from SA node in right atrium to the left atrium to make sure both depolarize together.
Internodal pathway
conducts action potential from SA to AV node.
AV node
small bundle of cells at the junction of the atria and ventricles. Only point where action potential from SA node can spread to ventricles.
Bundle of His
goes from AV node down the interventricular septum and transfer action potential to Purkinje fibers
Purkinje fibers
go from bundle of His to ventricles
AV nodal delay makes sure ventricles fill.
Whatever cell has the fastest inherent rate of depolarization is the pacemaker because if it goes off it will set everything else off. SA has fastest rate so it is the pacemaker.
Inherent SA pacemaker
70-80bpm
Inherent AV pacemaker speed
40-60 bpm
Inherent bundle of His pacemaker
20-40 bpm
If AV node is damaged
Atria go at 70 bpm. Purkinje fibers make ventricles go much slower about 30 bpm.
Ectopic focus
A normally slower functioning tissue becomes ecvited and sets a faster pace.
P wave
atrial depolarization
PR segment
AV nodal delay
QRS complex
ventricular depolarization (atria repolarizing as well)
ST segment
ventricles contracting and emptying
T wave
ventricular repolarization
TP interval
Time ventricles relaxing and filling
end diastolic volume
about 135 mL
Isovolumetric ventricular contraction
none of the valves are open and ventricles are contracting. It lasts until the pressure of the ventricles and
end systolic volume
about 65 mL
dicrotic notch
closing of the aortic vessel which makes the second heart sound.
Frank starling law of the heart
Increased venous return results in increased strength of contraction and increased stroke volume.
stenotic valve
narrowed valve that does not close completely
heart failure
inability of the cardiac output to keep up with demand
epicardium
thin external membrane covering the heart.
endocardium
lines entire circulatory system
CHF
inability for cardiac output to keep pace with need and blood dams up in the veins behind the failing heart
diameter of systemic cappilaries
7-10 microns
venous blood is 60-70 in venules and small veins.
arterial blood is 10 % of total blood.
What buys time for the ventricles to fill
slow conduction at the AV node
myogenicity
fluxuation in membrane potentials independent of neural or hormonal influence. This happens with the sm muscle in arterioles and contributes to tone.
timing of sequential activitaion is a fxn of the ability of one group of cells to depolarize adjacent cells
arterioles
resistance vessels + controls distribution blood flow
Venules & Small Veins
capacitance vessels
Large Veins
collecting vessels that return blood to the heart.
His Bundle & Bundle Branch System
Composed of Purkinje Fibers. Specialized Ventricular Conducting System. – Purkinje Fibers can develop pacemaker
Neural input can change heart rate, change activation, and change force of muscle contraction, but neural input not required
Parameters that Determine Spread of Activation through Cardiac Tissue
1. Rate of Rise and Amplitude of the Action Potential of Cells within a Tissue 2. Electrical Coupling among Cells – Presence and # of Low Resistance Junctions 3. Geometric Relationship among Cells with the Tissue 4. Refractory Properties of the Inward, Depolarizing, Current Channels
Study slide 8 about different action potentials in the heart.
Basic Principles in Understanding Ionic Generation of Cardiac Action Potentials
1. Affect of inward and outward ionic current flow on the membrane potential referenced to the resting membrane potential (inside the cell negative). 2. For our purposes, current flow represents movement of + charge. • Inward ionic Current Flow Depolarizes the Cell – makes the inside of the cell less negative or more positive. • Outward ionic Current Flow Repolarizes the Cell – makes the inside of the cell less positive or more negative. 3. Depolarization occurs when there is net movement + charge into cell. 4. Repolarization occurs when there is net movement + charge out of cell.
Ionic Current Carried by 3 ions and their ion Channels
1. K ionic current through a number of K channels 2. Na ionic current through a few Na channels 3. Ca ionic current through a few Ca channels
Depolarization of cardiac tissue
Activation of Na and Ca Channels and Current Flow
Repolarization of cardiac tissue uses what ion.
Activation of K Channels and Current Flow
Eq Ca++
+30 mv
Eq K
-95 mv
P – R Interval
Atrial – Ventricular Conduction time.
Sympathetic stimulation of cardiac tissue
increases the slope of the pacemaker potential
Parasympathetic (vagal) stimulation of cardiac tissue
Increases the maximum diastolic potential and decreases the slope of the pacemaker potential.
ANS Affects on Conduction through the AV Node
Effective refractory period
The tissue behaves as if it is unexcitable. Action potential will not spread through the tissue.
Relative refractory period
Tissue is excitable but conduction velocity slowed & conduction time prolonged because time course for cell to cell spread of activation is prolonged
If a cardiac cell is rel refract. it does not need a stronger stimulus to get it to depolarize.
Absolute refractory period
cell cannot be stimulated to produce an action potential. 2/3 of the time of the ventricular contraction the cells are in ARP.
Maximum diastolic potential
How far below the threshold for an action potential will go before it starts to depolarize again as seen in cardiac pacemaker cells.
What determines Systolic Blood Pressure?
What determines Diastolic Blood Pressure?
Why is Systolic Blood Pressure higher than Diastolic Blood Pressure?
If there is less volume of blood on the arterial side than on the venous side of the circulatory system, why is arterial pressure higher than venous pressure?
Why are the arterioles considered the resistance elements within the circulatory system and not the capacitance elements?
Why are the venules and small veins considered the capacitance elements within the circulatory system and not the resistance elements?
If the capillaries are the smallest diameter blood vessels, why are they not the principle site of resistance to flow through the circulatory system?
The outputs of the right and left hearts are equal over time. Why is the pressure in the pulmonary vascular system about 1/5 to 1/4 that of the systemic vascular system?
Static Hemodynamic Properties
Parameters that determine Pressure
Pressure Function of
1. Capacitance or Compliance of the vessels or chamber 2. & Volume contained within the capacitance or compliance Specifically, Pressure = Volume/Capacitance
Dynamic Hemodynamic Properties
Parameters that determine Flow (Vol/min)
Flow Function of
1. Pressure Gradient (P1 – P2) 2. & Resistance (Function of Length, Viscosity & Radius) Specifically, Flow = Pressure Gradient /Resistance
Diagram the pressure wave associated with contraction
1/3 is systole, 2/3 is diastole - half way through is dicrotic notch associated with closing of aortic valve
Mean Circulatory Pressure
average pressure for flow through Total Vascular System. dictated by the capacitance of the total vascular system and the total volume of blood contained within this capacitance
What determines arterial and venous pressure when there is flow from the venous side to the arterial side of the vascular system?
capacitance
compliance - holding capacity
resistance is a fuction of
length, viscosity, radius.
average resting pressure
1/3 of 120 and 2/3 of 80
What determines arterial and venous pressure when there is flow from the venous side to the arterial side of the vascular system?
What do you predict will happen to venous pressure with decreases in volume as volume is transferred to the arterial side?
What do you predict will happen to arterial pressure with the addition of this volume to the arterial side?
What would you predict will happen to the relative magnitudes of pressure changes in the arterial and venous components with the transfer of a volume from the venous to the arterial components?
Why, with the heart pumping, doesn’t the pressure in the vascular system return to the mean circulatory pressure between cardiac contractions & ejections of volume?
Poisseulle’s Law
Quantifies parameters that determine flow through a tube. Flow = Π/8 [(P1 – P2)R4]/Lη
Contractility
pressure generating capacity, the rate of cycling, of each Actin – Myosin Cross-Bridge.
review page 315 - 318
How does parasympathetic stimulation decrease heart rate
Reduces spontaneous AP by SA node by increasing K+ permeability which hyperpolarizes the cell taking it farther from threshold and decreasing the rate (slope) of depolarization.
How does sympathetic stimulation increase heart rate
generally speeds up depolarization of SA node. Norepi decreases K+ permeability by accelerating inactivation of K+ channels. Symp stimulation also increases rate of conduction by enhancing slow Ca2+ channels which speeds up spread of AP in conduction pathway. Increases force of contraction in contractile cells by increasing Ca2+ channels.
diagram action potential of cardiac muscle and all the steps. page 309
stays at -90 until excited by elec. 1) elec. excite then fast Na+ channels (steep up slope) 2) plateau maintained by slow L-type Ca+ channels mostly in the T tubules (the #1 factor in plateau) and decrease in K+ permeability. 3) Rapid falling phase - inactivate Ca+ channels and delayed activation of volt. gated K+ channels.
cardiac muscle contraction lasts 300 ms and the action potential for 50 ms. The contraction of the cell lasts 50 ms longer than the action potential
what is the effect of arteriolar resistence
establishes pressure differential that encourages flow from heart downstream and converts pulsatile pressure to nonfluctuating pressure for capillaries.
2 things accomplished by adjusting arteriole diameter
change where blood is sent, and regulate arterial blood pressure.
vascular tone and causes
baseline arteriolar resistance, caused by regular myogenic activity by the smooth muscle and constant releasee of noradr. by sympathetic fibers. Without it no possibility for vasodilation.
pressure gradient for entire systemic circulation
mean arterial pressure - difference between beginning and end of circ system.
no parasympathetic stimulation to arterioles
velocity of flow is inversly proportional to total cross sectional area of a region
total cross section of the capillaries is 1300 times greater than that of the aorta.
4 causes of edema
1) Reduced plasma protein 2) increased capillary permeability 3) increased venous pressure (as in CHF) 4) blockage of lymph
review page 369
Kf – Filtration Coefficient (Surface Area, Thickness, Permeability of Membrane to Water)
Pcap – Capillary Hydrostatic (Blood) Pressure
Pinterst – Interstitial Hydrostatic (Fluid) Pressure
πcap – Capillary Oncotic Pressure
πinterst – Interstitial Oncotic Pressure
Veins Sympathetic stimulation to venules and small veins generates a very small constriction over a large cross-sectional area.
• Hyperventilation 
Increasing Ventilation over Metabolic Rate  Increase in Alveolar Po2 and a Decrease in Alveolar Pco2
• Hypoventilation
Decreasing Ventilation over Metabolic Rate  Decrease in Alveolar Po2 and an Increase in Alveolar Pc02.
active hyperemia
local arteriolar vasodilation to increase blood flow
Local metaboilic influences of arteriolar radius
increased: CO2, acid, K+, osmolarity, adenosine release, prostaglandins Decrease in:O2
angiotensin 2
important in maintaining salt balance. and a potent vasoconstrictor.
Immediate response to loss of much blood
release of angiotensin 2 and vasopressing which causes vasoconstriction increasing blood pressure and preserving blood volume.
what controls flow of blood through capillaries
precapillary sphincters which have no direct innervation but are sensitive to local metabolic changes.
percent of body fluid that is plasma
only 20%. the rest is interstitial fluid.
bulk flow
ultra filtration out of capillaries followed by reabsorption into them.
respiratory quotient
ratio ofCO2 produced to O2 consumed. When carbos are being used it is 1
transmural pressure gradients in the lung
760 torr in alveolar air and 756 in inrapleural space which forces lungs to the edge of thoracic cavity.
elastic properties of the lung
elastic connective tissue and alveolar surface tension
alveolar interdependence
one collapsing alveolus stretches others close by and helps keep the collapsing one from getting smaller.
alveolar ventilation
amount they get per minute = (tidal volume - dead space) * resp rate.
if alveolus gets too little ventilation compared to perfusion
CO2 increases in alveolus and tissue which stims vasodilation of bronchiolar smooth muscle which dilates airway.
Too much O2 in alveolus
causes vasoconstriction in alveolar bronchioles.
Partial pressures of O2 and CO2 in normal atmosphere
O2 - 160 torr. CO2 0.23 Torr
effect of H2O humidification to alveolar partial pressures
dilutes partial pressures so at beginning of inspiration O2 - 150 torr. CO2 0.23 Torr
Average P-O2
100 torr
Average P-CO2
40 torr
P-O2 of deoxy blood leaving the heart to the lungs
40 torr
P-O2 of deoxy blood leaving the heart to the lungs
46 torr
rate of diffusion of a gas
proportional to diffusion coefficient which is related to solubility in tissue and molecular weight. Diffusion coefficient of CO2 is 20 times that of O2 because it is more soluble.
Partial pressure gradients for CO2 and O2
CO2 - 6 torr O2 60 torr
Length of the pulm. capillaries it takes for blood to equilibrate
about 1/3 the length usually. Which lets you pump it faster and still have room to equilibrate.
what percent of blood O2 is transported dissolved
1.5 percent (3mL/L) is dissolved in plasma and 98.5% is transported connected to Hb. Blood connected to Hb does not contribute to partial pressure so it is a reserve for O2 partial pressure.
Most important factor in determining % sat of Hb
The PPressure of O2 in the blood.
Law of mass action
Just another way of saying Le Chatellier's principle.
Importance of the steep part of the curve
25% is dropped off in from 100-40 torr. From 40-20 another 35% is dropped off. If tissues are using lots of O2 the steep part allows a dramatic increase in flow rate of oxygen to a tissue, requiring less of a rate of the heart. Without that there would be more of a linear curve to heart rate and metabolic demand. This acts as a buffer to HR.
What can affect the curve
Increased: P-CO2, acid, temperature or 2,3-bisphosphoglycerate - right shift the curve meaning it dumps off more O2 earlier.
What does left shifting the curve do
makes it harder to dissasociate oxygen and hemoglobin
What does right shifting the curve do
makes it easier to dissasociate oxygen and hemoglobin
Bohr effect
both CO2 and H+ can combine with Hb reversibly which changes the molecular structure making it have less of an affinity for O2.
Biphosphoglycerate
produced by red blood cells during metabolism and will right shift the curve. It is produced in en masse when blood cells are chronically unsaturated like at high altitude. Problem with this is it is continuously present even in the lungs so it decreases the amount of O2 that can be picked up in the lungs.
3 ways CO2 is transported in the blood
1) dissolved - 10% 2) bound to hemoglobin - 30% 3) as bicarbonate - 60%.
Production of bicarbonate
Happens slowly in plasma but really fast in RBCs because of carbonic anhydrase.
4 types of hypoxia
Hypoxic hypoxia - not enough P-O2 in arterial blood due to either suffocating environment, or decreased diffusion across respiratory membranes. Anemic hypoxia - not enough O2 carrying capacity due to not enough Hb, not enough RBCs, or CO poisoning. Circulatory hypoxia - Too little blood to tissues. Histotoxic hypoxia - O2 gets to the tissues but it. eg. cyanide poisoning.
Control of breathing
does 3 things: generates alternating insp./expir. rhythm, regulate magnitude of breath, and other stuff like sneezing or conscious control. Controlled mostly by medullary respiratory center, but also affected by 2 centers in the pons: the pneumotaxic and apneustic centers.
nerves for breathing
phrenic and intercostal nerves have cell bodies in the spine. Impulses from medullary center end on those motor neurons and cause inspiration.
Medullary respiratory center
2 neuronal clusters. Dorsal Respiratory Group - works for normal quiet breathing. Ventral Respiratory Group - is the overdrive system. Activates expiratory muscles in increases rate of inspiration when active.
pneumotaxic center
from pons and shuts off inspiration from DRG cutting it short.
apneustic center
in pons and keeps the pneumotaxic center from shutting off DRG and thus boosts inspiration.
apneusis
abnormal breathing charictarized by prolonged inspiratory gasps abruptly interrupted by brief expirations
Hering Breuer reflex
tidal volume is greater than 1 L (like during exercise) pulmonary stretch receptors in smooth muscle of the airways activated by stretching of the lungs send action potentials to medullary center and inhibit the inspiratory neurons. Keeps them from being overinflated • Stretch receptors in the small bronchioles that fire as the airways and lung expand.
carotid and aortic bodies
peripheral chemoreceptors lie at fork of common carotids and on both sides of the arch of the aorta. If there is a large decrease in P-O2 (below 60) they send info to med. insp. neurons which increases respiration. The P-O2 has to drop below 60 which only happens at high altitude or during disease so does not usually effect respiration.
Why do the chemoreceptors not go off during CO poisoning
P-O2 levels are normal in the arteries, it is only Hb that is affected, and this does not change P-O2.
What is the usual regulator of ventilation?
CO2 cause acid.
Why does it make more sense to regulate through P-CO2 rather than P-O2
Metabolic influences show up directly with CO2 but Hb buffers the P-O2.
Central chemoreceptors
Two populations in Brainstem • Adjacent to the 4th Ventricle & influenced by BBB • Population neurons in Brainstem adjacent to permeable capillaries (permeable gases and ions)They are in the medulla and measure H+ levels in the ECF produced by CO2 in the ECF. H+ does not pass the BBbarrier but CO2 does.
Large increases in PCO2 does what?
Past 80 torr P-CO2 depresses respiration which would be fatal without intervention. It also causes a decrease in the sensitivity to it. HCO3- will pass through in enough quantity to buffer the excess H+. The problem is the patients have abnormally low respiration rates and low O2 sat.
Things that contribute to increase of respiration during exercise
Joint and muscle receptors - will be triggered if a machine moves your body. Increased temp - we also see increased respiration with fevers. Epinephrine - stimulates ventilation Impulses from cerebral cortex - motor part of cerebral cortex stim Med. Respiratory neurons
dyspnea
mental anguish associated with unsatiated desire for more adequate ventilation.
Efferent info
REVIEW SLIDE 32 ON VERY THOROUGHLY
Minimum production of the kidneys
500 mL/day
nephron
functional unit of kidney. Held together by connective tissue. ~ 1 million. Made up by renal medulla, and cortex.\
glomerulus
ball of capillaries through which fluid is filtered. These don't supply blood to the tissue.
Afferent arterioles
go in. 1 to each nephron.
efferent arterioles
go out
peritubular capillaries
supply the renal tissue with blood and important in exchanges between the tubular system and the blood while making urine. Entertwined around the tubular system.
Bowmans capsule
start of tubes
start at beginning go to end of tubes in kidneys
Bowman's capsule - Prox. tube. - loop of henle - distal tubule
juxtaglomerular apparatus
cortical nephrons
most abundant, 80% - glomerulus lies in outer layer of cortex - hairpin loop dips only slightly into medulla
juxtamedullary nephrons
20% of all nephrons - lie in inner layer of cortex. Loop goes through the entire medulla and are accompanied by vasa recta.
vasa recta
peritubular capillaries of juxtamedullary nephrons
what gives medulla striated appearance
parallel arrangement of everything
What layers does filtered fluid pass through
glomerular capillary wall, basement membrane, inner layer of bowman's capsule made out of podocytes
Glomerular capillary wall
single layer of cells with large pores making it 100 X more permeable
basement membrane
acellular gelatinout layer of collagen and glycoproteins between glomerulus and bowmans capsule. Albumin is small enough to get through the wall but the glycoproteins are neg. charged and repel albumin
inner layer of bowman's capsule
made of podocytes that interlock and form filtration slits
Glomerular capillary blood pressure
55 torr. High because afferent art. is wider than efferent
Plasma colloid osmotic pressure
30 torr.
Bowman's capsule hydrostatic pressure
15 torr
Net filtration pressure
55 - (30+15) = 10 torr
GFR
125 mL / minute.
2 factors controlling autoregulation in nephron
myogenic mechanism and juxtaglomerular feedback.
myogenic mechanism
smooth muscle contracts in response to stretch due to increased BP.
juxtaglomerular feedback
juxtaglomerular apparatus has macula densa containing sensors for salt in fluid flowing past them. If macula densa sense salt they release adenosine as a paracrine which constricts sm musc. in afferent arteriole next to it.
layers reabsorbed materials must pass through
Luminal membrane - cytosol - basolateral cell membrane - instititial fluid - capillary wall
sodium atpase pump
in basolateral membrane and is important for Na+ absorption. 80% of cell energy used for this.
Where is Na+ reabsorbed
PCT - 67% loop of henle - 25% 8% in DCT
Na+ reabsorption in PCT
important in reabsorbing glucose, AA, H2O, Cl- and urea.
Na+ reabsorption in ascending loop of henle
important in concentration urine
Na+ absorption in DCT.
Under hormonal control and important in regulating ECF volume and thus blood volume.
Where is Na+ not absobed
descending limb of loop of henle.
Na load
total amount in body cluids (not concentration in body fluids)
in prox tube. and loop a const. % of Na is reabsorbed
What secretes renin
Granular cells of the juxtaglomerular apparatus
what stims secretion of renin
granulosa cells themselves as intrarenal baroreceptors secrete when there is a fall in BP. Macula densa cells in tub. portion of JGA in response to fall in NaCl moving past in tube lumen. Sympathetic stim of granular cells in response to baroreceptor reflex causes release
Effect of renin release
sets cascade which tells DCT to absorb more Na+ back into blood
Renin angiotensin pathway
Renin acts as an enzyme to activate angiotensinogen (protein made in liver and always in blood in high conc.) turning it into angiotensin 1 Angiotensin 1 is converted into angiotensin 2 in lungs angiotensin 2 stims release of aldosterone from adrenal cortex Aldosterone stimu reabsoption of water by distal collecting tubules by the addition of extra Na+ channels into luminal membrane and extra pumps into basolateral membranes of distal and collecting increasing
Atrial Natriuretic Peptide
Hormone from special cells in atria that release it when stretched due to increased plasma volume. It promotes Na+ loss by inhibiting collection in DCT. It also inhibits secretion of aldosterone and renin
reabs. of glucose
secondary active transport across the luminal membrane coupled to Na in prox. conv. tubules. Not regulated by the kidneys. Normal filtered load is 125 mg/minute. Tubular maximum is 375 mg/minute
Tubular maximum
Limit of what the memb. transport prot. can move. Anything filtered past this point will be excreted in the urine.
filtered load
quantitiy filtered per minute = GFR * plasma concentration.
amount of glucose in blood needed to see it in the urine
300mg/100mL
Control of Cl-
controlled by amount of Na+ active reabsor.
Control of potassium
High plasma K+ directly stims aldosterone from the adrenal cortex. it is actively absorbed in the prox. so it must be actively excreted in the distal and collecting tubules. K+ excretion is coupled to Na+ absorption using a pump taking Na from lateral space into cell and K vice versa. High intracellular K+ favors passive movement into lumen. From peritubular capillaries because the interstitial fluid has low K+ it leaks out of the capillaries in to then be pumped into the tubular cell. The distal and collecting tubules have passive channels on the luminal membrane and the previous ones have them on the basolateral surface so K+ just leaks back into the interstitial fluid to be recycled so the pumps can be used.
2 ways to stimulate aldosterone secretion
high K+ stims directly, or RAAS due to low Na+
how is excretion of H+ and K+ related
the basolateral pump can secrete either K+ or H+ and high conc. of one will decrease secretion of the other.
importance of regulating plasma K+
need for sm. musc. action potentials, cardiac and sk. muscle.
proximal tubule secretory carriers
one for organic anions and one for organic cations
Medullary Countercurrent System
juxt. med nephrons long loop establish vert osmotic grad. - Vasa Recta preserve gradient - all nephrons use the gradient in conjunction with vasopressin
How are the descending and ascending limbs of the loop of henle diff
Descending 1) highly permeable to water 2) no active reabsorb (only part to not) Na+. Ascending - 1) actively transport NaCl out of lumen into interstitial 2) impermeable to water
action of vasopressin
distal and collecting tubules have vasopressin receptors which produce cAMP which stims production of aquaporins.. These vessels carry hypotonic soln and are impermeable to water unless vasopressin stims production of aquaporins in the luminal membrane which allows it to leave passively across basolateral membrane.
How does the body remove H+ without losing HCO3- as well
Proximal tubule cells produce NH3 from metabolism of glatamine NH3 diffuses into tubular fluid where it binds with H+ and is excreted as NH4+.
6 regions of autorhythmic cells in elec cond. system:
SA node, internodal pathway, interarterial pathway, AV node, bundle of His, and Purkinje fibers
Interatrial pathway
goes from SA node in right atrium to the left atrium to make sure both depolarize together.
Inherent SA pacemaker
70-80bpm
Inherent AV pacemaker speed
40-60 bpm
Inherent bundle of His pacemaker
20-40 bpm
If AV node is damaged
Atria go at 70 bpm. Purkinje fibers make ventricles go much slower about 30 bpm.
Ectopic focus
A normally slower functioning tissue becomes ecvited and sets a faster pace.
P wave
atrial depolarization
PR segment
AV nodal delay
QRS complex
ventricular depolarization (atria repolarizing as well)
ST segment
ventricles contracting and emptying
T wave
ventricular repolarization
TP interval
Time ventricles relaxing and filling
end diastolic volume
about 135 mL
Isovolumetric ventricular contraction
none of the valves are open and ventricles are contracting. It lasts until the pressure of the ventricles and
end systolic volume
about 65 mL
dicrotic notch
closing of the aortic vessel which makes the second heart sound.
Frank starling law of the heart
Increased venous return results in increased strength of contraction and increased stroke volume.
stenotic valve
narrowed valve that does not close completely
heart failure
inability of the cardiac output to keep up with demand
epicardium
thin external membrane covering the heart.
endocardium
lines entire circulatory system
CHF
inability for cardiac output to keep pace with need and blood dams up in the veins behind the failing heart
What buys time for the ventricles to fill
slow conduction at the AV node
myogenicity
contraction is initiated by the cell itself
Talk about neural input to heart. What nerves? What do they do?
Parameters that Determine Spread of Activation through Cardiac Tissue
1. Rate of Rise and Amplitude of the Action Potential of Cells within a Tissue 2. Electrical Coupling among Cells – Presence and # of Low Resistance Junctions 3. Geometric Relationship among Cells with the Tissue 4. Refractory Properties of the Inward, Depolarizing, Current Channels
Ionic Current Carried by 3 ions and their ion Channels
1. K ionic current through a number of K channels 2. Na ionic current through a few Na channels 3. Ca ionic current through a few Ca channels
Eq Ca++
+30 mv
Eq K
-95 mv
P – R Interval
Atrial – Ventricular Conduction time.
Sympathetic stimulation of cardiac tissue
increases the slope of the pacemaker potential
Parasympathetic (vagal) stimulation of cardiac tissue
Increases the maximum diastolic potential and decreases the slope of the pacemaker potential.
Diagram pressure volume loop in association with EKG. Where in the loop is the heart absolutely refractory?
What determines Systolic Blood Pressure?
What determines Diastolic Blood Pressure?
capacitance
Why is Systolic Blood Pressure higher than Diastolic Blood Pressure?
Increase in volume during systolic, decrease in volume in diastolic.\
If there is less volume of blood on the arterial side than on the venous side of the circulatory system, why is arterial pressure higher than venous pressure?
Less on arterial. Arterial pressure is higher because it has a lower capacity and pushes the same volume.
Why are the arterioles considered the resistance elements within the circulatory system and not the capacitance elements?
They contract and decrease flow of blood to
Why are the venules and small veins considered the capacitance elements within the circulatory system and not the resistance elements?
When smooth muscle in the veins is affected by symp. stim. capacitance is decreased, not resistance since it is over a long area so diameter is effected very little.
If the capillaries are the smallest diameter blood vessels, why are they not the principle site of resistance to flow through the circulatory system?
The outputs of the right and left hearts are equal over time. Why is the pressure in the pulmonary vascular system about 1/5 to 1/4 that of the systemic vascular system?
Capacitance of the vein is greater
Static Hemodynamic Properties
Parameters that determine Pressure
Pressure Function of
1. Capacitance or Compliance of the vessels or chamber 2. & Volume contained within the capacitance or compliance Specifically, Pressure = Volume/Capacitance
Dynamic Hemodynamic Properties
Parameters that determine Flow (Vol/min)
Flow Function of
1. Pressure Gradient (P1 – P2) 2. & Resistance (Function of Length, Viscosity & Radius) Specifically, Flow = Pressure Gradient /Resistance
Diagram the pressure wave associated with contraction
1/3 is systole, 2/3 is diastole - half way through is dicrotic notch associated with closing of aortic valve
Mean Circulatory Pressure
average pressure for flow through Total Vascular System. dictated by the capacitance of the total vascular system and the total volume of blood contained within this capacitance
capacitance
compliance - holding capacity
resistance is a fuction of
length, viscosity, radius.
average resting pressure
1/3 of 120 and 2/3 of 80
What determines arterial and venous pressure when there is flow from the venous side to the arterial side of the vascular system?
Arterial pressure is regulated by flow in, resistance to flow out and capacitance within (which is not changed much), Venous is controlled by amount flowing out, resistance to flow in, and capacitance of vessels which is adjusted by smooth muscle.
What do you predict will happen to venous pressure with decreases in volume as volume is transferred to the arterial side?
Venous pressure goes down
What do you predict will happen to arterial pressure with the addition of this volume to the arterial side?
Arterial pressure goes up
What would you predict will happen to the relative magnitudes of pressure changes in the arterial and venous components with the transfer of a volume from the venous to the arterial components?
Arterial increases more than venous decreases.
Why, with the heart pumping, doesn’t the pressure in the vascular system return to the mean circulatory pressure between cardiac contractions & ejections of volume?
takes time for blood to leave arterial side
What determines capillary pressure
volume of blood, which is determined largely by the constriction or relaxation of arterioles
What is the effect of sympathetic stimulation to venules and small veins
Decreases capacitance of the vessels without restricting flow, which increases venous pressure which increases blood return to the heart which increases stroke volume.
preload
cardiac fiber length. This is set by end diastolic volume which is controlled by end systolic volume + passive filling + active filling.
afterload
pressure left over from last cycle (pressure at the end of isovolumetric contraction) in the aorta that the heart has to overcome to expel contents. Directly proportional to HR and vascular (arteriolar) resistance.
cardiac output formula
HR * Stroke volume
Stroke Volume determined by
• Changes in Venous Pressure & Venous Return (Cardiac Filling & Preload) • & Changes in Contractility (increase cont. and decrease end volume because the extra was squirted out.
HR increased by
• Increasing Sympathetic Activity SA Nodal Pacemaker Cells • &/or decrease Parasympathetic Activity SA Nodal Pacemaker Cells
What changes venous capacitance
sympathetic stimulation decreases capacitance and increases pressure. If you decrease stim it increases capacitance. Products of metabolism also effect capacitance.
Factors effecting venous volume
Increase arteriolar pressure increases P-gradient and increases filling. Inversely prop. to resistance of arterioles. Proportional to total circulating blood volume.
Venous limit to HR
venous filling cannot keep up with venous emptying of the heart. Over 200 BPM decreases output. Output limit by only increasing rate is between 30 and 35 LPM.
What change occurs in arteriolar resistance for skin in going from rest to exercise?
What change occurs in arteriolar resistance for GI Tract in going from rest to exercise?
What change occurs in arteriolar resistance for skeletal muscle in going from rest to exercise?
Control of the arteriole sphincters
• Sympathetic Neural Activity – Constricts (local not direct control) • Local Metabolites (K+, CO2, Decr O2, H+ - All Vasodilate) • Endothelial Derived Vasoactive Substances – some Dilate (Nitric Oxide (NO), dominant) & a few Constrict.
Where does each type of substance diffuse accross capillaries?
• Gases diffuse across endothelial cell membranes and through junctions between cells. • Solutes diffuse through channels in cell membranes and through junctions between cells. • Water osmotically moves through Aquaporins (water channels) in cell membrane or through spaces at cell junctions.
The exchange of fluid determined by
1. Capillary Blood and Interstitial Fluid Pressures (Hydrostatic Pressures of the blood and interstitial fluid), 2. & Oncotic Pressures generated by plasma proteins, and any proteins in the interstitial fluid compartment
Filtration =Kf [(Pcap – Pinterst) – (πcap –πinterst)]
Kf
Filtration Coefficient (Surface Area, Thickness, Permeability of Membrane to Water)
Pcap
Capillary Hydrostatic (Blood) Pressure
Pinterst
Interstitial Hydrostatic (Fluid) Pressure
πcap
Capillary Oncotic Pressure
πinterst
Interstitial Oncotic Pressure
Baroreceptors & Volume Receptors
Stretch occurs through changes in the Transmural Pressure (Pressure inside – Pressure outside)
baroreceptor reflex
aortic arch vagus and carotid sinus nerves - cardio area of medulla - symp and parasymp efferents - heart and vascular
Vascular Volume Reflex
stretch receptors pulmonary veins and left atrium. Activation inhibits release of ADH (Antidiuretic Hormone)
baroreceptor reflex to a fall in blood pressure
1. Aortic Arch and Carotid Sinus Baroreceptors – stretch
receptors.
2. Afferents – vagus (aortic arch) and carotid sinus nerves
(carotid sinus baroreceptors)
3. Central Integration in Medulla – Cardiovascular Area
Medulla
4. Efferents – Sympathetic and Parasympathetic
5. Effectors – Heart and Vascular System
baroreceptor reflex to an increase in blood pressure
volume receptor reflex to decrease or increase in volume
What changes would you observe in the Po2 and Pco2 in the alveoli and blood leaving the pulmonary capillaries if there were (1) a decrease in ventilation, (2) an increase in ventilation, (3) a decrease in metabolism, (4) an increase in metabolism?
What are the partial pressures for O2 and CO2 in systemic arterial blood?
PO2 = 100 torr. PCO2 = 40 torr
TV
Tidal volume - 500
IRV
Inspiratory reserve volume - 3000
IC
Inspiratory capacity - 3500
ERV
expiratory reserve volume - 1000
FRC
functional residual capacity - 2200
VC
vital capacity - 4500
TLC
total lung capacity - 5700