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195 Cards in this Set

  • Front
  • Back
define stressed volume
the blood volume contained in the arteries
where is the site of highest ressitance in the cardiovascular system?
what are the smooth muscle walls of arterioles innervated by?
autonomic nerves
where are a_1 adrenergic receptors found?
arterioles of skin, splanchnic and renal circulation
where are b_2 adrenergic receptors found?
arterioles of skeletal m
which component of the vasculature has the largest total cross sectioanl and surface area?
describe the morphology of capillaries
single layer of endothelial cells surrounded by basal lamina
what are venules?
merged capillaries
which component of the cardiovascular system comtains the highest proportion of blood?
define unstressed volume
blood volume contained in the veins
how are veins innervated?
a_1 adrenergic receptors
give the equation for blood velocity
v = Q/A
give the equation for blood flow
Q = dP/R = CO

CO = (MAP-right atrial pressure)/TPR
give the eqn for resistance
R = 8nl/(pi*r^4)

- l = length of blood vessel
- n = viscosity of blood
is systemic resistance in parallel or in series?
in parallel
where do you find resistance in series?
arrangement of blood vessels in an organ
- the largest resistance is contributed by the arterioles
what does reynolds number predict?
whether blood flow is laminar or turbulent
what does a large reynolds number mean?
turbulence --> bruits
list factors that decrease blood viscosity
decreased hematocrit
what increase blood velocity
narrowed vessel
define capacitance
distensibility of vessel
inverse of capcitance
give the equation for capacitance
C = V/P
do arteires or veins have more blood in them? (and why?)
veins, since the capacitance is greater in the 'unstressed' volume of veins
where is the largest pressure gradient found?
arterioles because they are the sites of highest resistance
what is the MAP in the aorta?
what is the MAP in the arterioles?
what is the MAP in the Capillaries?
what is the MAP in the vena cava?
define pulse pressure
systolic pressure - diastolic pressure
what is the most important determinant of pulse pressure?
stroke volume
- because diastolic pressure remains unchanged during systole, the PP increases proportionally to systolic pressure
what is the equation for MAP?
diastolic pressure + 1/3 Pulse pressure
what is a measure of L. atrial pressure?
pulmonary wedge pressure
what does the p wave represent?
atrial depolarization
where is atrial repolarization?
buried in the QRS complex
what does the PR interval represent?
how long it takes for the beginning of ventricular depolarization
- varies with the conduction velocity through the AV node
what happens to the PR interval with heart block?
what happens to the PR interval if you have stimulation of the sympathetic nervous system?
(increased AV node conduction velocity)
what happens to the PR interval if you have stimulation of the parasympathetic nervous system?
(decrease AV node conduction velocity)
what is the QT interval?
the entire period of depolarization and repolarizatino of the ventricles
what is the ST interval?
ventricles are depolarized
what is the T wave?
ventricular repolarization
what is the resting potential of the ventricles, atria and prukinje system?
-90mV (close to K eq potential)
how long do action potentials in the ventricles, atria and purkinje system last?
the purkincje fibers are particularly long (300msec)
Phase 0
- Na current
- at the peak, membrane potential reaches Na equlibrium potential
Phase 1
- initial repolarization
- K+ conductance favored by both chemical and electrical gradients
- decrease in Na conductance
Phase 2
- plateau
- transient increase in Ca2+ conductance inwards
- increase in K conductace outwards
- inward and outward currents are equal
Phase 3
- repolarization
- Ca conductance decreases
- large outward K current (I_K)
- hyperpolarization of membrane
Phase 4
resting membrane potential
- inward and outward currents (I_k1) are equal
- both delayed rectifier channels and leak channels`
SA node
- normal pacemaker of the heart
- has an unstable resting potential
- automaticity (phase
name the latent pacemakers
AV node and His-purkinje system
what is the relative rates of phase 4 depolarization?
SA node > AV node > His-purkinje system
AV node Phase 0
Ca conductance
AV node Phase 1-2
no such thing
AV node Phase 3
- repolarization
- outward K current
AV node Phase 4
slow depolarization
- accounts for pacemaker activity of SA node (automaticity)
- inward Na current: I_f
what is I_f turned on by?
the repolarization of the membrane potential during the preceding action potential
What is the upstroke of the AV node action potential caused by?
inward Ca current
what is the conduction velocity proportional to?
the size of the inward current during the upstroke
were is conduction velocity fastest and slowest? why?
fastest: purkinje system
slowest: AV node (allowas time for ventricular filling)
define excitability
ability of cardiac cells ot initiate action potentials in reposne to inward, depolarizing current
- changes over the course of the action potential (refractory period)
define absolute refractory period
- begins at upstroke
- ends after plateau
- no action potential generated
define effective refractory period
- a conducted action potential cannot be elicited
define relative refractory period
action potential can be elicited, but more than usual inward current is needed
(less excitability)
what is a negative chronotropic effect?
decreases HR by decreasing SA node firing
what is a negative dromotropic effect?
decreases conduction velocity through the AV node, increases the PR interval, and increases the time that ventricles have to fill
what parts of the heard have parasympathetic vagal innervation?
- SA node
- atria
- AV node
NOT ventricles
what is the NT for vagal stimulation of the heart?
ACh on mACh
what are the effects of vagal stimulation on chronotropic and dromotropic effects?
neg chronotropic effect
- decreased HR b/c of decreased phase 4 depolarization (decreasded I_f)
neg dromotropic effect
- decreased inward Ca current and increased outward K current --> decreased conduction velocity through AV node
- increased PR interval
what is the NT and receptor for sympathetic innervation of the heart?
Norepi at B_1 receptor
define intercalated disks
necessary for cell-cell adhesion at the ends of myocytes
- runs perpendicular to directin of fibrils
what do gap junctions do in the heart?
allow the heart ot behave like an electrical syncytium
what has more mitochondria: skeletal or cadiac muscle?
cardiac muscle
what do T tubules do?
carry action potentials into the cell interior
where are T tubules well developed?
in the ventricles, but not in the atria
what do T tubueles form?
dyads in the SR
during excitation-contraction coupling, what regulates Ca release?
during the plateau, Ca conductance is increased. This Ca entry triggers more Ca release from the SR (Ca-induced Ca release)
** Amount of Ca released depends on the amount of Ca previously stored and on the sized of the inward Ca current during the plauteau phase
what happens after Ca is released from the SR
Ca binds to troponin C --> tropomyosin is moved out of the way, removing inhbition of actin and myosin binding
what is the magitude of the tension created by the myocardial contraction proportional to?
intracellular [Ca]
define contractility
intrinsic ability of cardiac muscle to develop fore at a given muscle lengh
whats another name for contractility?
what is contractility proportional to?
the intracellular Ca concentration
how can you estimate the contractility?
by ejection fraction (stroke volume/end-diastolic volume)
what is the normal value for stroke volume?
what do positive ionotropic agents do?
increase contractility
name three factors that increase contractility
1. HR
2. sympathetic stimulation
3. cardiac glycosides (digitalis)
explain how increased HR increases contractility
when more action potentials occur per unit time, more Ca enters the myocardial cells during the plateau --> more Ca is released from the SR --> greater tension during contraction
what is the positive staircase?
aka bowditch staircase (or Teppe)
- increased HR increases force of contraction in a stepwise fasion as the intracellular Ca increases cumulatively over several beats
what is postextrasystlic potentiation?
the beat that occurs after an extrasysstolic beat has increased force of contraction b/c extra Ca entered the cells during the extrasystole
what does vesamicol do?
targets the H-ACh antiporter so ACh cannot be packaged into vessicles
describe the receptor for muscarinic receptors
7 transmembrane domain G protein coupled receptor
describe the receptor for nicotinic receptors
5 subunit ligand gated channels`
describe the signal cascade for mAChR
G_i inhibits adenylyl cyclase and stimulates PLC (both effects are mediated by the alpha subunit)
the Betagamma subunit binds to potassium channels (GIRK- inwardy rectifying K channes) and hyperpolarize the cell
what is M1 associated with?
cortical neurons
autonomic ganglia
what is M2 associated with?
cardiac muscle
what is M3 associated with?
smooth muslce
glandular tissue
how does the AChR undergo desensitization?
continuous binding of ACh to the receptor causes it to undergo a conformational change where the channel is locked closed
what are the two cholinesterases?
1. acetylcholinesterase
2. butyrylcholinesterase
what is the positive feedback loop associated with ACh?
there is a presynpatic cholinergic receptor. When triggered by ACh, it facilitates the mobilization fo synpatic vesicles from the RESERVE pool to the DEPOT pool
how does sympathetic stimulation (catecholamines) increase contractility?
via B1 receptors
1. increases inward Ca current
2. increases SR Ca pump --> more Ca is accumulated in the SR --> more Ca can be released
how do you increase activity of the Ca2+ pump of the SR?
by phosphorylation of phospholamban
how do cardiac glycosides (digitalis) increase contractility?
inhibits the Na,K,ATPase system --> Na gradient diminishes --> Na/Ca exchange is diminshed --> increase in intracellular Ca
what decreases cardiac contractility?
Parasympathetic stimulation via mAChR
- decreases force of contraction in atria
Mech: decreases inward Ca current during plateau phase
define preload
EDV, which is proportional to right atrial pressure
what is oubain?
a cardiac glycoside (digitais)
define afterload
LV: aortic pressure
RV: pulmonary artery
on the chest exam, which valves are you listening to?
1. aortic
2. pulmonic
3. tricuspid
4. mitral
what does the sarcomere length tell you?
1. number of cross-bridges between actin and myosin
2. maximum tension/force of contraction
what is the Frank Starling relationship?
when there is an increase in venous return or EDV, there is a compensatory increase in stroke volume
what is mean systemic pressure?
the point at which the vascular function curve intersects the x-axis
- is the right atrial pressure when there is no flow, and all pressures throughout the CV systems equalize
how do you increase the mean systolic pressure?
- increase blood volume
- decrease venous compliance
seen as a right shift in the venous return curve
how do you decrease the mean systolic pressure?
- decrease blood volume
- increase venous compliance
seen as a left shift in the venous return curve
what determines the slope of the venous return curve?
- smaller slope: decrease in total peripheral resistance (TPR)
what does the point at which the venous return curve and the cardiac output curve intersect mean?
it's the equilibrium point- when cardiac output equals venous return
how do you increase the cardiac output curve?
positive inotropic agents
this is actually pretty cool: increase CO --> equlibrium point moves up and left --> decrease EDV/right atrial pressure, and increased SV
equilibrium point: for increased blood volume or decreased venous compliance
increased venous return curve
- increased CO
- increased Right atrial pressure
equilibrium point: for hemorrhage or increased venous compliance
- decreased CO
- decreased right atrial pressure
Describe the changes to the venous return and CO for an increase in TPR
- decrease in both CO and VR curves
- new equilibrium point: both CO and venous return are decreased
- atrial pressure is UNCHANGED
Describe the changes to the venous return and CO for an decrease in TPR
- increase in both CO and VR curves
- new equilibrium point: both CO and venous return are increased
- atrial pressure is UNCHANGED
Stroke Volume
SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
Cardiac Output equation
CO = SV * HR
Ejection Fraction
- proportional to contractility
- normally: 55%

Stroke Work
- the work the heart performs in each beat
= pressure x volume

SW = Aortic pressure x SV
what is the primary energy source for stroke work?
fatty acids
what increases Oxygen consumption?
- proportional to the tension developed by ventricles
Increased by:
1. inc. afterload
2. inc. heart size
3. inc. contractility
4. inc. HR
why does an increase in heart size cause an increase in the tension generated by the ventricles?
Laplace's law: tension is proportional to the radius of a sphere
Fick equation
VO2 = O2 consumption per minute
Cv= O2 concentration in pulmonary vein
Ca= O2 concentration in pulmonary artery
VO2 = (CO x Ca) - (CO x Cv)
CO = VO2/(Cv- Ca)
how is the pulmonary artery O2 concentration taken?
measured in systemic mixed venous blood
What are the two main mechanisms for regulating arterial pressure?
1. baroreceptor (fast, neurally mediated)
2. renin-angiotensisn-aldosterone (slow, hormonally mediated)
where are the barorecptor stretch receptors found?
1. in the walls of the carotid sinus, near the bifurcation of the common carotid arteries
2. in the aortic arch
what does decreased streatch on the walls of the carotid sinus cause?
decreased firing rate of the carotid sinus nerve: Hering's nerve (CN IX)
what is the set point for mean arterial pressure?
what 4 modulators control arterial pressure? What can you do to autoregulate set point?
increase HR
increase contractility and SV
increase vasoconstriction of arterioles
increase vasoconstriction
how do you test the baroreceptor mechanism?
valsava maneuver
increase in intrathoracic pressure --> decrease in venous return --> decrease in CO and arterial pressure --> sensed by baroceptor --> increase sympathetic output
which form of angiotensin is the active form?
angiotensin II
what degrades angiotensin II?
angiotensinase. angiotensin III, one of the peptide fragments, has some activity
ACE inhibitor: blocks conversion of angiotensin I to II --> decreases BP.
angiotensin receptor (AT1) antagonists: blocks angiotensin at its receptor --> decrease BP
what are the 4 effects of angiotensin II?
1. stimulates secretion of aldosterone by adrenal cortex (slow- requires protein synthesis)
2. increase Na-H exchange in the proximal convoluted tubule
3. increase thirst
4. vasoconstriction of arterioles
what does aldosterone do?
increase Na absorption by the renal distal tubule
how can you get contraction alkalosis from angiotensin?
stimulation of Na-H exchange in the proximal convoluted tubule
where is a decrease in renal perfusion pressure sensed?
at the juxtaglomerular cells of the afferent arteriole. They will then secrete renin
what are other regulators of arterial BP?
1. cerebral ischemia
2. chemoreceptors in the carotid and aortic bodies
3. vasopressin (ADH)
4. Atrial natriuretic peptide (ANP)
how does cerebral ischemia regulate BP?
increase PCO2 in brain tissues is detected by the vasomotor center --> increase in sympathetic outflow to the heart and blood vessels --> peripheral vasoconstriction (severely reduced renal perfusion too)
- cushing reaction
what is the cushing reaction?
increase in intracranial pressure --> compressure on cerebral blood vessels --> cerebral ischemia --> increase in sympathetic output from vasomotor center
how do the chemoreceptors in the carotid and aortic bodies regulate BP?
sense decreases in PO2 --> activate vasomotor centers --> vasoconstrction
how is ADH released?
- invovled in regulation of BP in response to hemorrhage, but not to min-to-min reg
- atrial receptors sense decrase BP and cause vasopressin release from the p. pit
how does ADH regulate BP?
1. potent vasoconstrictor by activating V1 receptors on the arterioles
2. increase water reabsoprtion by the renal distal tubules and collecting ducts by activating V2 receptors
how is ANP released?
- increase in blood volume and atrial pressure --> atria releases ANP
how does ANP regulate BP?
1. causes vascular SM relaxation, dilation of arterioles, and decreased TPR
2. increases excretion of Na and water by kidney
3. inhibits renin secretion
what is at the junction of the arterioles and capillaries?
precapillary sphincter
do capillaries have smooth muscle?
no. have a single layer of endothelial cells surrounded by a basement membrane
Starling Equation
Jv = Kf([Pc − Pi] − σ[πc − πi])

* Kf is the proportionality constant/hydraulic conductance
* Jv is the net fluid movement between compartments.
what does it mean when J_v is positive?
net fluid movement out of the capillary (filtration)
what does it mean when J_v is negative?
net fluid movement into the capillary (absorption)
what is the normal value of P_i (interstitial fluid hydrostatic pressure)
define edema
volume of interstitial fluid exceeds the capacity of lymphatics to return it to circulation
Endothelium derived relaxing factor (EDRF)
- made by endothelial cells
- causes local relaxation fo vascular smooth muscle
- mech: increase production of cGMP
name one form of EDFR
why does circulating ACh cause vasodiation?
stimualates productin of NO in vascular smooth muscle
active hyperemia
blood flow is proportional to its metabolic activity
e.g exercise and increased flow to skeletal muscle
define hyperemia
increase perfusion to an organ
reactive hyperemia
increase in blood flow that occurs after a period of occlusion of flow
- the longer the period of occlusion, the greater the increase in blood flow
Name 2 theories on the mechanisms that control local blood flow
1. myogenic hypothesis
2. metabolic hypothesis
myogenic hypothesis
- vascular smooth muslce contracts with it's stretched.
- explains autoregulation
- stretched arteriolar smooth muscle wil contract, and thereby autocorrect the vasodilation
metabolic hypothesis
- tissue supply of O2 is matched to the tissue demand for O2
- vasodilator metabolites are made as a result of metabolic activity in the tissue
name 5 vasodilators
what happens to vascular sm with increase sympathetic innervation?
what happens to vascular sm with decreased sympathetic innervation?
name in order of decreasing density, the sympathetic innervation in different tissues
skin- a lot
coronary, pulmonary, and cerebral vessesl- little
name some vasoactive hormones
- histamine
- bradykinin
- 5-HT
- Prostaglandins
histamine and vasoactivity
- arteriolar dilation and venous constriction --> increased capillary pressure --> increased filtration out of capillaries --> local edema
- released in response to trauma
bradykinin and vasoactivity
- causes arteriolar dilation and venous constriction --> local edema
serotonin and vasoactivity
- arteriolar constriction
- released during vessel damage
- implicated in vascular spasms of migrane headaches
prostaglandings and vasoactivity
E-series prostaglandins
F-series prostaglandins
Thromboxane A2
E-series porstaglandins
F-series prostaglandins
Thromboxane A2
how is coronary circulation controlled?
entirely by local metabolic factors
- autoregulation, active and reactive hyperemia
- increase in myocardial contractility --> increased demand --> compensatory vasodilation (active hyperemia)
- systole --> compression of coronary vessels --> blood flow increases afterwards (reactive)
what are the most important local metabolic factors for coronary circulation?
do sympathetic nerves play a role in coronary circulation?
how is cerebral circulation controlled?
primarily by local metabolic factors
- autoreg, active and reactive hyperemia
what is the most important vasodilator for the cerebral circulation?
do vasoactive substances in systemic circulation eeffect cerebral circulation?
no. doesn't cross BBB
how is skeletal muscle circulation controlled?
1. extrinsic sympathetic innnervation
- regulator of blood flow to skeletal m at REST
2. local metabolic factors
describe sympathetic innervation on skeletal muscle
- primary regulator of blood flow at REST
- arterioles are densely innervated
- veins innervated too (but less densely)
- a1 stimulation --> vasoconstriction
- b2 stimulation --> vasodilation
what does a1 stimulation do to blood vessels?
describe local metabolic control on skeletal muscle
- autoreg, active and reactive hyperemia
- during exercise, arteries are compressed --> reactive hyperemia
- local vasodilators: lactate, adenosine, and K
how is skin circulation controlled?
- extensive sympathetic innervation
- trauma causes:
1. red line
2. red flare
4. wheal
what is a wheal?
local edema that results from local release of histamine
what happens during exercise?
increased arteriolar resistance in:
skin, splanchnic regions, kidneys, and inactive muscles
what happens when you place increased metabolic demand on skeletal muscle?
vasodilator metabolites increase (lactate, K and adenosine) b/c of increased metabolic demand
- overall decrease in TPR
NOTE: activation of sympathetic nervous system alonew would cause an INCREASE in TPR
describe the interplay between chemoreceptors in the carotid and aortic bodies and the baroreceptor mechanism
chemoreceptors in the carotid and aortic bodies are very sensitive to hypoxia. they supplement the baroreceptors mech by increasing sympathetic outflow to the heart and blood vessels
what is my name