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195 Cards in this Set
- Front
- Back
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define stressed volume
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the blood volume contained in the arteries
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where is the site of highest ressitance in the cardiovascular system?
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arterioles
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what are the smooth muscle walls of arterioles innervated by?
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autonomic nerves
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where are a_1 adrenergic receptors found?
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arterioles of skin, splanchnic and renal circulation
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where are b_2 adrenergic receptors found?
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arterioles of skeletal m
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which component of the vasculature has the largest total cross sectioanl and surface area?
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capillaries
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describe the morphology of capillaries
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single layer of endothelial cells surrounded by basal lamina
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what are venules?
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merged capillaries
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which component of the cardiovascular system comtains the highest proportion of blood?
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veins
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define unstressed volume
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blood volume contained in the veins
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how are veins innervated?
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a_1 adrenergic receptors
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give the equation for blood velocity
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v = Q/A
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give the equation for blood flow
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Q = dP/R = CO
CO = (MAP-right atrial pressure)/TPR |
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give the eqn for resistance
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R = 8nl/(pi*r^4)
- l = length of blood vessel - n = viscosity of blood |
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is systemic resistance in parallel or in series?
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in parallel
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where do you find resistance in series?
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arrangement of blood vessels in an organ
- the largest resistance is contributed by the arterioles |
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what does reynolds number predict?
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whether blood flow is laminar or turbulent
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what does a large reynolds number mean?
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turbulence --> bruits
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list factors that decrease blood viscosity
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decreased hematocrit
anemia |
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what increase blood velocity
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narrowed vessel
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define capacitance
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distensibility of vessel
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inverse of capcitance
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elastance
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give the equation for capacitance
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C = V/P
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do arteires or veins have more blood in them? (and why?)
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veins, since the capacitance is greater in the 'unstressed' volume of veins
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where is the largest pressure gradient found?
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arterioles because they are the sites of highest resistance
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what is the MAP in the aorta?
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100mmHg
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what is the MAP in the arterioles?
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50mmHg
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what is the MAP in the Capillaries?
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20mmHg
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what is the MAP in the vena cava?
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4mmHg
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define pulse pressure
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systolic pressure - diastolic pressure
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what is the most important determinant of pulse pressure?
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stroke volume
- because diastolic pressure remains unchanged during systole, the PP increases proportionally to systolic pressure |
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what is the equation for MAP?
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diastolic pressure + 1/3 Pulse pressure
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what is a measure of L. atrial pressure?
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pulmonary wedge pressure
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what does the p wave represent?
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atrial depolarization
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where is atrial repolarization?
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buried in the QRS complex
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what does the PR interval represent?
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how long it takes for the beginning of ventricular depolarization
- varies with the conduction velocity through the AV node |
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what happens to the PR interval with heart block?
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increased
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what happens to the PR interval if you have stimulation of the sympathetic nervous system?
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decreased
(increased AV node conduction velocity) |
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what happens to the PR interval if you have stimulation of the parasympathetic nervous system?
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increased
(decrease AV node conduction velocity) |
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what is the QT interval?
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the entire period of depolarization and repolarizatino of the ventricles
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what is the ST interval?
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ventricles are depolarized
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what is the T wave?
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ventricular repolarization
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what is the resting potential of the ventricles, atria and prukinje system?
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-90mV (close to K eq potential)
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how long do action potentials in the ventricles, atria and purkinje system last?
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long.
the purkincje fibers are particularly long (300msec) |
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Phase 0
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- Na current
- at the peak, membrane potential reaches Na equlibrium potential |
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Phase 1
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- initial repolarization
- K+ conductance favored by both chemical and electrical gradients - decrease in Na conductance |
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Phase 2
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- plateau
- transient increase in Ca2+ conductance inwards - increase in K conductace outwards - inward and outward currents are equal |
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Phase 3
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- repolarization
- Ca conductance decreases - large outward K current (I_K) - hyperpolarization of membrane |
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Phase 4
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resting membrane potential
- inward and outward currents (I_k1) are equal - both delayed rectifier channels and leak channels` |
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SA node
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- normal pacemaker of the heart
- has an unstable resting potential - automaticity (phase |
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name the latent pacemakers
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AV node and His-purkinje system
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what is the relative rates of phase 4 depolarization?
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SA node > AV node > His-purkinje system
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AV node Phase 0
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Ca conductance
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AV node Phase 1-2
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no such thing
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AV node Phase 3
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- repolarization
- outward K current |
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AV node Phase 4
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slow depolarization
- accounts for pacemaker activity of SA node (automaticity) - inward Na current: I_f |
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what is I_f turned on by?
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the repolarization of the membrane potential during the preceding action potential
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What is the upstroke of the AV node action potential caused by?
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inward Ca current
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what is the conduction velocity proportional to?
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the size of the inward current during the upstroke
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were is conduction velocity fastest and slowest? why?
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fastest: purkinje system
slowest: AV node (allowas time for ventricular filling) |
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define excitability
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ability of cardiac cells ot initiate action potentials in reposne to inward, depolarizing current
- changes over the course of the action potential (refractory period) |
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define absolute refractory period
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- begins at upstroke
- ends after plateau - no action potential generated |
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define effective refractory period
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- a conducted action potential cannot be elicited
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define relative refractory period
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action potential can be elicited, but more than usual inward current is needed
(less excitability) |
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what is a negative chronotropic effect?
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decreases HR by decreasing SA node firing
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what is a negative dromotropic effect?
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decreases conduction velocity through the AV node, increases the PR interval, and increases the time that ventricles have to fill
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what parts of the heard have parasympathetic vagal innervation?
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- SA node
- atria - AV node NOT ventricles |
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what is the NT for vagal stimulation of the heart?
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ACh on mACh
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what are the effects of vagal stimulation on chronotropic and dromotropic effects?
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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 |
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what is the NT and receptor for sympathetic innervation of the heart?
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Norepi at B_1 receptor
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define intercalated disks
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necessary for cell-cell adhesion at the ends of myocytes
- runs perpendicular to directin of fibrils |
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what do gap junctions do in the heart?
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allow the heart ot behave like an electrical syncytium
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what has more mitochondria: skeletal or cadiac muscle?
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cardiac muscle
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what do T tubules do?
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carry action potentials into the cell interior
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where are T tubules well developed?
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in the ventricles, but not in the atria
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what do T tubueles form?
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dyads in the SR
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during excitation-contraction coupling, what regulates Ca release?
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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 |
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what happens after Ca is released from the SR
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Ca binds to troponin C --> tropomyosin is moved out of the way, removing inhbition of actin and myosin binding
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what is the magitude of the tension created by the myocardial contraction proportional to?
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intracellular [Ca]
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define contractility
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intrinsic ability of cardiac muscle to develop fore at a given muscle lengh
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whats another name for contractility?
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inotropism
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what is contractility proportional to?
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the intracellular Ca concentration
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how can you estimate the contractility?
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by ejection fraction (stroke volume/end-diastolic volume)
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what is the normal value for stroke volume?
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55%
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what do positive ionotropic agents do?
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increase contractility
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name three factors that increase contractility
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1. HR
2. sympathetic stimulation 3. cardiac glycosides (digitalis) |
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explain how increased HR increases contractility
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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
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what is the positive staircase?
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aka bowditch staircase (or Teppe)
- increased HR increases force of contraction in a stepwise fasion as the intracellular Ca increases cumulatively over several beats |
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what is postextrasystlic potentiation?
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the beat that occurs after an extrasysstolic beat has increased force of contraction b/c extra Ca entered the cells during the extrasystole
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what does vesamicol do?
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targets the H-ACh antiporter so ACh cannot be packaged into vessicles
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describe the receptor for muscarinic receptors
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7 transmembrane domain G protein coupled receptor
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describe the receptor for nicotinic receptors
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5 subunit ligand gated channels`
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describe the signal cascade for mAChR
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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 |
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what is M1 associated with?
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cortical neurons
autonomic ganglia excitatory |
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what is M2 associated with?
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cardiac muscle
inihibitory |
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what is M3 associated with?
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smooth muslce
glandular tissue excitatory |
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how does the AChR undergo desensitization?
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continuous binding of ACh to the receptor causes it to undergo a conformational change where the channel is locked closed
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what are the two cholinesterases?
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1. acetylcholinesterase
2. butyrylcholinesterase |
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what is the positive feedback loop associated with ACh?
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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
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how does sympathetic stimulation (catecholamines) increase contractility?
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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 |
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how do you increase activity of the Ca2+ pump of the SR?
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by phosphorylation of phospholamban
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how do cardiac glycosides (digitalis) increase contractility?
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inhibits the Na,K,ATPase system --> Na gradient diminishes --> Na/Ca exchange is diminshed --> increase in intracellular Ca
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what decreases cardiac contractility?
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Parasympathetic stimulation via mAChR
- decreases force of contraction in atria Mech: decreases inward Ca current during plateau phase |
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define preload
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EDV, which is proportional to right atrial pressure
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what is oubain?
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a cardiac glycoside (digitais)
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define afterload
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LV: aortic pressure
RV: pulmonary artery |
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on the chest exam, which valves are you listening to?
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1. aortic
2. pulmonic 3. tricuspid 4. mitral |
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what does the sarcomere length tell you?
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1. number of cross-bridges between actin and myosin
2. maximum tension/force of contraction |
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what is the Frank Starling relationship?
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when there is an increase in venous return or EDV, there is a compensatory increase in stroke volume
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what is mean systemic pressure?
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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 |
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how do you increase the mean systolic pressure?
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- increase blood volume
- decrease venous compliance seen as a right shift in the venous return curve |
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how do you decrease the mean systolic pressure?
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- decrease blood volume
- increase venous compliance seen as a left shift in the venous return curve |
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what determines the slope of the venous return curve?
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- smaller slope: decrease in total peripheral resistance (TPR)
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what does the point at which the venous return curve and the cardiac output curve intersect mean?
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it's the equilibrium point- when cardiac output equals venous return
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how do you increase the cardiac output curve?
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positive inotropic agents
this is actually pretty cool: increase CO --> equlibrium point moves up and left --> decrease EDV/right atrial pressure, and increased SV |
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equilibrium point: for increased blood volume or decreased venous compliance
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increased venous return curve
- increased CO - increased Right atrial pressure |
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equilibrium point: for hemorrhage or increased venous compliance
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- decreased CO
- decreased right atrial pressure |
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Describe the changes to the venous return and CO for an increase in TPR
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- decrease in both CO and VR curves
- new equilibrium point: both CO and venous return are decreased - atrial pressure is UNCHANGED |
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Describe the changes to the venous return and CO for an decrease in TPR
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- increase in both CO and VR curves
- new equilibrium point: both CO and venous return are increased - atrial pressure is UNCHANGED |
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Stroke Volume
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SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
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Cardiac Output equation
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CO = SV * HR
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Ejection Fraction
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- proportional to contractility
- normally: 55% EF = SV/ EDV |
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Stroke Work
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- the work the heart performs in each beat
= pressure x volume SW = Aortic pressure x SV |
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what is the primary energy source for stroke work?
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fatty acids
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what increases Oxygen consumption?
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- proportional to the tension developed by ventricles
Increased by: 1. inc. afterload 2. inc. heart size 3. inc. contractility 4. inc. HR |
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why does an increase in heart size cause an increase in the tension generated by the ventricles?
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Laplace's law: tension is proportional to the radius of a sphere
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Fick equation
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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) |
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how is the pulmonary artery O2 concentration taken?
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measured in systemic mixed venous blood
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What are the two main mechanisms for regulating arterial pressure?
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1. baroreceptor (fast, neurally mediated)
2. renin-angiotensisn-aldosterone (slow, hormonally mediated) |
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where are the barorecptor stretch receptors found?
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1. in the walls of the carotid sinus, near the bifurcation of the common carotid arteries
2. in the aortic arch |
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what does decreased streatch on the walls of the carotid sinus cause?
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decreased firing rate of the carotid sinus nerve: Hering's nerve (CN IX)
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what is the set point for mean arterial pressure?
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100mmHg
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what 4 modulators control arterial pressure? What can you do to autoregulate set point?
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increase HR
increase contractility and SV increase vasoconstriction of arterioles increase vasoconstriction |
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how do you test the baroreceptor mechanism?
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valsava maneuver
increase in intrathoracic pressure --> decrease in venous return --> decrease in CO and arterial pressure --> sensed by baroceptor --> increase sympathetic output |
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which form of angiotensin is the active form?
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angiotensin II
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what degrades angiotensin II?
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angiotensinase. angiotensin III, one of the peptide fragments, has some activity
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captopril
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ACE inhibitor: blocks conversion of angiotensin I to II --> decreases BP.
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losartan
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angiotensin receptor (AT1) antagonists: blocks angiotensin at its receptor --> decrease BP
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what are the 4 effects of angiotensin II?
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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 |
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what does aldosterone do?
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increase Na absorption by the renal distal tubule
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how can you get contraction alkalosis from angiotensin?
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stimulation of Na-H exchange in the proximal convoluted tubule
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where is a decrease in renal perfusion pressure sensed?
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at the juxtaglomerular cells of the afferent arteriole. They will then secrete renin
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what are other regulators of arterial BP?
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1. cerebral ischemia
2. chemoreceptors in the carotid and aortic bodies 3. vasopressin (ADH) 4. Atrial natriuretic peptide (ANP) |
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how does cerebral ischemia regulate BP?
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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 |
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what is the cushing reaction?
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increase in intracranial pressure --> compressure on cerebral blood vessels --> cerebral ischemia --> increase in sympathetic output from vasomotor center
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how do the chemoreceptors in the carotid and aortic bodies regulate BP?
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sense decreases in PO2 --> activate vasomotor centers --> vasoconstrction
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how is ADH released?
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- 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 |
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how does ADH regulate BP?
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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 |
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how is ANP released?
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- increase in blood volume and atrial pressure --> atria releases ANP
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how does ANP regulate BP?
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1. causes vascular SM relaxation, dilation of arterioles, and decreased TPR
2. increases excretion of Na and water by kidney 3. inhibits renin secretion |
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what is at the junction of the arterioles and capillaries?
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precapillary sphincter
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do capillaries have smooth muscle?
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no. have a single layer of endothelial cells surrounded by a basement membrane
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Starling Equation
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Jv = Kf([Pc − Pi] − σ[πc − πi])
where: * Kf is the proportionality constant/hydraulic conductance * Jv is the net fluid movement between compartments. |
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what does it mean when J_v is positive?
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net fluid movement out of the capillary (filtration)
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what does it mean when J_v is negative?
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net fluid movement into the capillary (absorption)
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what is the normal value of P_i (interstitial fluid hydrostatic pressure)
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0
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define edema
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volume of interstitial fluid exceeds the capacity of lymphatics to return it to circulation
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Endothelium derived relaxing factor (EDRF)
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- made by endothelial cells
- causes local relaxation fo vascular smooth muscle - mech: increase production of cGMP |
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name one form of EDFR
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NO
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why does circulating ACh cause vasodiation?
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stimualates productin of NO in vascular smooth muscle
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active hyperemia
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blood flow is proportional to its metabolic activity
e.g exercise and increased flow to skeletal muscle |
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define hyperemia
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increase perfusion to an organ
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reactive hyperemia
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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 |
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Name 2 theories on the mechanisms that control local blood flow
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1. myogenic hypothesis
2. metabolic hypothesis |
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myogenic hypothesis
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- vascular smooth muslce contracts with it's stretched.
- explains autoregulation - stretched arteriolar smooth muscle wil contract, and thereby autocorrect the vasodilation |
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metabolic hypothesis
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- 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 |
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name 5 vasodilators
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CO2
H K Lactate adenosine |
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what happens to vascular sm with increase sympathetic innervation?
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vasoconstriction
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what happens to vascular sm with decreased sympathetic innervation?
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vasodilation
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name in order of decreasing density, the sympathetic innervation in different tissues
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skin- a lot
coronary, pulmonary, and cerebral vessesl- little |
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name some vasoactive hormones
|
- histamine
- bradykinin - 5-HT - Prostaglandins |
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histamine and vasoactivity
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- arteriolar dilation and venous constriction --> increased capillary pressure --> increased filtration out of capillaries --> local edema
- released in response to trauma |
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bradykinin and vasoactivity
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- causes arteriolar dilation and venous constriction --> local edema
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serotonin and vasoactivity
|
- arteriolar constriction
- released during vessel damage - implicated in vascular spasms of migrane headaches |
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prostaglandings and vasoactivity
|
prostacyclin
E-series prostaglandins F-series prostaglandins Thromboxane A2 |
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prostacyclin
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vasodilator
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E-series porstaglandins
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vasodilator
|
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F-series prostaglandins
|
vasoconstrictor
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Thromboxane A2
|
vasoconstrictor
|
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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) |
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what are the most important local metabolic factors for coronary circulation?
|
hypoxia
adenoside |
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do sympathetic nerves play a role in coronary circulation?
|
minor
|
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how is cerebral circulation controlled?
|
primarily by local metabolic factors
- autoreg, active and reactive hyperemia |
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what is the most important vasodilator for the cerebral circulation?
|
CO2
|
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do vasoactive substances in systemic circulation eeffect cerebral circulation?
|
no. doesn't cross BBB
|
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how is skeletal muscle circulation controlled?
|
1. extrinsic sympathetic innnervation
- regulator of blood flow to skeletal m at REST 2. local metabolic factors |
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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 |
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what does a1 stimulation do to blood vessels?
|
vasoconstriction
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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 |
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how is skin circulation controlled?
|
- extensive sympathetic innervation
- trauma causes: 1. red line 2. red flare 4. wheal |
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what is a wheal?
|
local edema that results from local release of histamine
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what happens during exercise?
|
increased arteriolar resistance in:
skin, splanchnic regions, kidneys, and inactive muscles |
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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 |
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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
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what is my name
|
fan
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