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Flashcards in CV and ANS Deck (242)
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1
Q

Thin filaments in myocytes are made of (3 things):

A

Actin, tropomyosin, troponin

2
Q

Thick filaments are made of:

A

myosin heavy and light chains

3
Q

The interaction of thick and thin filaments in the contraction of heart cells is called the _______ theory.

A

sliding filament

4
Q

When Ca++ binds to troponin, what happens to tropomyosin?

A

It moves off of the actin chain, exposing a site for cross-bridging with the myosin head

5
Q

Is the heart electrically excited by neurons?

A

No

6
Q

Ach binds to […] receptors in motor end plate for skeletal muscle to initiate the muscle action potential

A

Ach binds to nicotinic cholinergic receptors in motor end plate for skeletal muscle to initiate the muscle action potential

7
Q

There is a flux of [ion name] ions through Ach receptors to initiate the skeletal muscle action potential.

A

There is a flux of Na+ ions through Ach receptors to initiate the skeletal muscle action potential.

8
Q

If you do not have Ca++ surrounding a heart cell will it continue to beat?

A

No (classic result by Sydney Ringer in 1883 w/ frog heart)

9
Q

Does skeletal muscle contraction require a Ca++ influx?

A

No. In skeletal muscle all the Ca++ for contraction is released from the sarcoplasmic reticulum.

10
Q

What happens to skeletal muscle during a series of action potentials at high frequency?

A

Tetanus (sustained contraction)

11
Q

Label the lines and bands in this diagram

A
12
Q

In smooth muscle are actin and myosin structured into sarcomeres?

A

No, therefore it appears histologically “smooth”

13
Q

Does smooth muscle contain troponin? What must happen to the myosin light chain so that it can interact with actin in smooth muscle?

A

No; the myosin light chain must be phosphorylated to interact with actin in smooth muscle

14
Q

In smooth muscle, can you have a contraction without an action potential?

A

Yes

15
Q

Which two boundaries does the Ca++ in smooth muscle cross to create a contraction event?

A
  • membrane Ca++ channels (voltage-gated and not)
  • Ca++ is released from sarcoplasmic reticulum
16
Q

What enzyme phosphorylates the myosin light chain in smooth muscle cells? What is it activated by?

A

Myosin light chain kinase (MLCK); activated by Ca++ bound to calmodulin

17
Q

Does β-adrenergic stimulation relax or contract smooth muscle, in general?

A

Relax

18
Q

Does nitric oxide contract or relax smooth muscle, in general? What is a drug that participates in this functionality?

A

Relax; Viagra

19
Q

Does α-adrenergic stimulation usually contract or relax smooth muscle?

A

Contract

20
Q

In which zone of the sequence of cardiac electrical activation does the impulse travel slowest?

A

The AV node (creates the delay between atrial and ventricular contraction)

21
Q

Are the Purkinje fibers more similar to the ventricles or the atria in terms of the shape and timing of the action potential during a contraction cycle?

A

The ventricles; the atria correspond more closely with the SA and AV node.

22
Q

What is happening during stage 3 of this action potential in the ventricles?

A

Repolarization.

23
Q

Would this be a ventricular or an SA node myocyte? How can you tell?

A

SA node; it’s skinny and there are no striated fibers. Compare with ventricular:

24
Q

Do healthy ventricular cells fire spontaneously?

A

No, they will stay at the resting potential of -85mV indefinitely.

25
Q

Is this an SA node or ventricular action potential? What’s the easiest way to know?

A

SA node; the depolarization phase would be much faster in ventricle

26
Q

In this experiment, electrical stimuli are delivered at the points shown in part a. What is the name of the period between the dash-dotted lines in part b?

A

The RRP or Relative Refractory Period; a strong stimulus can trigger a weak action potential in this period.

27
Q

What is the name of the period during which it is impossible to trigger a second action potential in a cardiac myocyte?

A

Absolute Refractory Period. This is the reason the heart cannot go into tetanus (prolonged contraction) the way skeletal muscle can.

28
Q

Which ion moves into the cell during the rapid depolarization of a ventricular action potential? Immediately afterward? How about during the plateau and repolarization?

A

Na+ in during depolarization, Ca++ in right afterward, K+ out during repolarization

29
Q

What ion is influxing during phase 0 of this SA nodal action potential?

A

Ca++

30
Q

What is the EK for a cardiomyocyte?

A

Approx -89mV.

31
Q

If V across the membrane is greater than EX, does the positive ion X move into or out of the cell?

A

Positive current; ion moves out.

32
Q

Based on this experiment measuring Na+ current at different test potentials across the membrane of a cardiomyocyte, at what membrane potential do Na+ channels begin to open?

A

-60mV

33
Q

Which EX is the cardiomyocyte closest to at resting potential?

A

EK (around -85mV)

34
Q

As Na channels open at -60mV, and current begins to flow, does the current increase or decrease the voltage across the membrane?

A

Increase, thus driving more Na current, and creating a positive feedback system

35
Q

What is the current (which ions) described by the black and top red curves here?

A

INa and ICa

36
Q

After the transient [direction] K+ current in an action potential in the cardiomyocyte, there are delayed rectifier currents [direction].

A

After the transient outward K+ current in an action potential in the cardiomyocyte, there are delayed rectifier currents inward.

37
Q

If you block delayed rectifier currents for K+ with a drug, what would happen to the action potential?

A

It is prolonged

38
Q

[loss or gain of function] mutations in K+ channels or [loss or gain of function] mutations in Na+, Ca2+ channels can cause “Long QT” syndrome.

A

Loss-of-function mutations in K+ channels or gain-of-function mutations in Na+, Ca2+ channels can cause “Long QT” syndrome.

39
Q

During the plateau of the action potential, which ion current mirrors Ca++?

A

K+ in the opposite direction (outward)

40
Q

[ion] links electrical activation to mechanical contraction in heart cells.

A

Calcium links electrical activation to mechanical contraction in heart cells.

41
Q

During each heartbeat, calcium both enters the cell through […] and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

A

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

42
Q

During each heartbeat, calcium both enters the cell through membrane channels and is released from the […]. Most of the calcium is released from the latter.

A

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

43
Q

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the [former or the latter].

A

During each heartbeat, calcium both enters the cell through membrane channels and is released from the sarcoplasmic reticulum. Most of the calcium is released from the latter.

44
Q

[cellular structure] in heart cells allow for calcium to rise uniformly throughout large myocytes.

A

Transverse tubules in heart cells allow for calcium to rise uniformly throughout large myocytes.

45
Q

In the resting state for a cardiomyocyte, is more Ca++ in the extracellular space, within the cytosol, or in the sarcoplasmic reticulum?

A

Extracellular space.

46
Q

Is contraction of the heart cell during, before, or after the Ca++ influx? Is the action potential during, before or after the Ca++ influx?

A

Contraction is after, action potential is before.

47
Q

What is the structure pointed to by the huge black arrow in this diagram of a cardiomyocyte?

A

transverse tubule (T-tubule)

48
Q

What is the spacing between T-tubules in a cardiomyocyte?

A

2μm

49
Q

What is the purpose of having T-tubules spaced every 2μm in the ventricular myocyte?

A

It places all locations in the ventricular myocyte within 1μm of the cell membrane so that Ca++ can reach them quickly

50
Q

Do Purkinje fibers need to contract in order to ensure proper heart function?

A

No, they main function is electrical propagation. But they do contract somewhat.

51
Q

The following shows changes in Ca++ concentration along the longitudinal axis of two different kinds of cardiomyocytes, over the time course of a contraction cycle. Based on this picture, what can you say about T-tubules in Purkinje cells?

A

Purkinje cells usually don’t have T-tubules, so Ca++ must diffuse in from the periphery.

52
Q

Ca++ can be pumped out of the cardiomyocyte using active transport channels that transfer the ions in one direction, but how else can it enter and leave the cell?

A

Sodium-calcium exchangers (NCXs), which symport 3 Na+ ions in one direction in exchange for one Ca++. These can act much quicker than other modes of transport.

53
Q

Do sodium-calcium exchanges (NCXs) change the membrane potential? Do they require ATP?

A

Yes, there is a net transfer of +1 charge into the cell. They do not require ATP, but the Na+ gradient is usually created by a different ATP-consuming symporter, the Na+/K+ ATPase.

54
Q

T-tubules may alter their shape from state E to state F, shown below. Would this change enhance or detract from heart function?

A

Detract; it is more difficult to initiate Ca++ release from the sarcoplasmic reticulum if the T-tubules are unevenly spaced

55
Q

What does inotropy mean? What is an inotrope?

A

Intropy: contractility, the force of muscle contraction. Inotrope: an agent that changes this. Greek: Inos, fiber. Trope, turning.

56
Q

The following is the treatment strategy for Digitalis, intended to increase inotropy. What is the problem with this strategy?

A

Cardiotoxicity, because: not only are you knocking out Na+/K+ ATPases somewhat nonspecifically, but increased intracellular Ca++ can cause spontaneous Ca++ release from the sarcoplasmic reticulum, which produces uncontrolled cardiac contractions.

57
Q

What does SERCA (sarco-endoplasmic reticulum Ca++-ATPase) do? What happens if it is inhibited?

A

It transfers Ca++ from the cytosol to the lumen of the sarcoplasmic reticulum (SR) during muscle relaxation, in preparation for its release from the SR during muscle contraction. Inhibition of SERCA impairs muscle contraction.

58
Q

[sympathetic or parasympathetic] stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

A

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

59
Q

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in [cell type in heart] cells.

A

Parasympathetic stimulation decreases heart rate (negative chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

60
Q

[sympathetic or parasympathetic] stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

A

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

61
Q

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in [cell type in heart] cells.

A

Sympathetic stimulation increases heart rate (positive chronotropy) due to effects on several ion transport pathways in sinoatrial nodal cells.

62
Q

What does chronotropy mean?

A

Heart rate (Greek: chronos, time. Tropo, turning.)

63
Q

Sympathetic stimulation […] ventricular contractility ([…] inotropy) due to phosphorylation of multiple targets and increased intracellular calcium

A

Sympathetic stimulation increases ventricular contractility (positive inotropy) due to phosphorylation of multiple targets and increased intracellular calcium

64
Q

Increased heart rate leads to […] ventricular contractions ([…] inotropy) through […] intracellular calcium

A

Increased heart rate leads to stronger ventricular contractions (positive inotropy) through increased intracellular calcium

65
Q

Heart failure leads to [shorter or longer] action potentials, weaker contractions, and an altered response to sympathetic stimulation

A

Heart failure leads to longer action potentials, weaker contractions, and an altered response to sympathetic stimulation

66
Q

Heart failure leads to longer action potentials, weaker contractions, and an altered response to [sympathetic or parasympathetic] stimulation

A

Heart failure leads to longer action potentials, weaker contractions, and an altered response to sympathetic stimulation

67
Q

What does dromotropy mean?

A

Cell-to-cell conduction; Greek: dromos, running. Tropos, turning.

68
Q

Are the cardiac effects of parasympathetic inhibition greater OR less than the effects of sympathetic inhibition? What does this tell you about the tone of cardiac muscle?

A

Parasympathetic is greater. This means cardiac muscle has parasympathetic tone.

69
Q

A heart transplant patient has decreased “default” innervation of the heart–therefore, what would the change in heart rate be compared with typical patients?

A

It would be faster, due to less basal vagal stimulation.

70
Q

Which has faster effects, parasympathetic or sympathetic stimulation of the heart?

A

Parasympathetic is faster

71
Q

Are parasympathetic effects on the heart due to nicotinic, muscarinic, or adrenergic receptors?

A

Muscarinic receptors (M2 to be specific)

72
Q

Parasympathetic stimulation affects the SA node via 1) [activation or inhibition] of acetylcholine-sensitive K current, 2) inhibition of funny current If, and 3) decreased sarcoplasmic Ca++ release by inhibiting SERCA.

A

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current If, and 3) decreased sarcoplasmic Ca++ release by inhibiting SERCA.

73
Q

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) [activation or inhibition] of funny current If, and 3) decreased sarcoplasmic Ca++ release by inhibiting SERCA.

A

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current If, and 3) decreased sarcoplasmic Ca++ release by inhibiting SERCA.

74
Q

What parts of the heart express the funny current?

A

Mostly the spontaneously active regions, like the SA node, AV node, and Purkinje fibers.

75
Q

Does increasing cAMP levels increase or decrease the open probability of f-channels, the channels that convey the funny current?

A

Increase

76
Q

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current If, and 3) [increased or decreased] sarcoplasmic Ca++ release by inhibiting SERCA.

A

Parasympathetic stimulation affects the SA node via 1) activation of acetylcholine-sensitive K current, 2) inhibition of funny current If, and 3) decreased sarcoplasmic Ca++ release by inhibiting SERCA.

77
Q

What region of the heart is mediated by sympathetic effects but not parasympathetic effects?

A

The ventricles

78
Q

Where are ryanodine receptors located? What do they do?

A

Sarcoplasmic reticulum membrane; they control release of intracellular Ca++ stores.

79
Q

Are ryanodine receptors more likely or less likely to release Ca++ in the sarcoplasmic reticulum if the concentration of Ca++ on the cytosolic side is higher? Is this a positive or negative feedback system?

A

More likely to release Ca++ with higher cytosolic levels; this is positive feedback

80
Q

What controls the open or closed state of an L-type calcium channel? Where are they located and why are they important to muscle cells?

A

They are voltage gated, so at a certain membrane potential they open. They are located in the cellular membrane. In muscle cells, they control Ca++ influx from the extracellular space.

81
Q

What kind of receptor are L-type calcium channels coupled to in striated muscle and what membrane are those receptors embedded in?

A

The L-type calcium channel in the cytoplasmic membrane is coupled to a ryanodine receptor (RyR) in the sarcoplasmic reticulum, facilitating simultaneous flow of Ca++ from both compartments into the cytoplasm

82
Q

Do ECG electrodes detect intracellular or extracellular voltages?

A

Extracellular

83
Q

Which histological structure stains strongly for connexin 43 protein in cardiomyocytes, the main constituent of cardiac gap junctions?

A

Intercalated disks

84
Q

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage […]. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

A

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

85
Q

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only [location] potential over a distance.

A

An ECG doesn’t look like an action potential because the ECG doesn’t measure absolute voltages, it measures voltage differences. The action potential occurs between the inside and outside of the cell; the ECG measures only extracellular potential over a distance.

86
Q

A signal minus a time shifted version of itself is a rough [mathematical function] of the signal. This is why the ECG signal is roughly proportional to the [mathematical function] of the the action potential.

A

A signal minus a time shifted version of itself is a rough derivative of the signal. This is why the ECG signal is roughly proportional to the derivative of the the action potential.

87
Q

Depolarization moving towards a positive electrode gives an [up or down] deflection.

A

Depolarization moving towards a positive electrode gives an upward/positive deflection.

88
Q

What kind of deflection does an orthogonal waveform produce as measured by two electrodes?

A

No deflection/signal.

89
Q

The T-wave appears as a positive deflection because the endocardium is activated [before or after], but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant Vendo-Vepi looks like a T wave.

A

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant Vendo-Vepi looks like a T wave.

Note how the black line is above the red during the repolarization (tail end) of the action potentials, and that subtracting red from black would result in an upward bump. That is the T-wave.

90
Q

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes [before or after] the epicardium. When the differences in signal and time are taken into account, the resultant Vendo-Vepi looks like a T wave.

A

The T-wave appears as a positive deflection because the endocardium is activated before, but repolarizes after the epicardium. When the differences in signal and time are taken into account, the resultant Vendo-Vepi looks like a T wave.

Note how the black line is above the red during the repolarization (tail end) of the action potentials, and that subtracting red from black would result in an upward bump. That is the T-wave.

91
Q

Why do you not see a signal for atrial repolarization on an ECG? (The T wave is the signal for ventricular repolarization).

A

Atrial repolarization is too slow with respect to time, and the atrial mass is too small; the signal is not significant enough to be visualized on the ECG

92
Q

The strength of a given signal depends not only on propagation direction, but also on the [physical property] of tissue contributing to the signal

A

The strength of a given signal depends not only on propagation direction, but also on the mass of tissue contributing to the signal

93
Q

Which part of the PQRST wave on an ECG corresponds with atrial depolarization?

A

The P wave

94
Q

Why aren’t there any ECG signals from conducting tissues, e.g. the AV node or Purkinje fibers?

A

Not enough mass.

95
Q

As the ventricles depolarize, what is the motion of the vector representing the averaged direction of propagation of the action potential through the tissue?

A

A counterclockwise circle

96
Q

When reading a paper ECG, how many large boxes indicate a second?

A

5.

97
Q

What’s going on in this ECG? Hint, look at the red lines.

A

The P-R interval is too long (240 ms, should be <200ms), this indicates first degree AV block. First degree means delayed, not blocked.

98
Q

What’s wrong with this ECG?

A

There’s a P wave without a QRS! This is 2nd degree AV block

99
Q

What is this waveform called?

A

Atrial fibrillations: P waves are random and indistinct, R-R intervals are irregular

100
Q

What are the large weird waveforms in this ECG? (Assume nobody is bumping the leads) How many ectopic foci are there?

A

These are premature ventricular contractions, or PVCs. There are multiple ectopic foci since the PVCs have different shapes.

101
Q

What is this heart rhythm called?

A

Monomorphic ventricular tachycardia. Monomorphic because all complexes are similar

102
Q

What does ventricular tachycardia reflect?

A

Either ventricular focus, or reentry

103
Q

What is cardiovascular reentry mean?

A

When signals are propagated from a Purkinje twig to muscle, if they propagate much faster through one branch than another, they can start circling back through other branches and re-stimulate ventricular tissue

104
Q

What is this heart rhythm called? Without intervention, how long does the patient have to live?

A

Ventricular fibrillation; patient could die in minutes

105
Q

How do you convert mMol/L to mEq/L?

A

Multiply it by the valence of the ion and then by the relative number of the ion from the empirical formula.

106
Q

How do you convert from mMol/L to mOsm/L?

A

Multiple by the number of ions in the molecule

107
Q

What’s the typical total body fluid volume? How much is intracellular? How about extracellular?

A

40L total, intracellular 25L, extracellular 15L

108
Q

What’s the typical blood volume, and how much of it is plasma?

A

5L blood, 3L plasma

109
Q

What’s the primary ion in extracellular fluid? How about intracellular fluid?

A

Na+ extracellular, K+ intracellular

110
Q

What does the Morse equation calculate?

π = gCRT

A

Osmotic pressure

111
Q

When using Morse’s equation, typically a correction factor σ is added to correct for a small permeability of capillaries to certain proteins. What is the range of this correction factor?

π = σgCRT

A

0 to 1, depending on the capillary boundary in question

112
Q

Does water move toward high osmotic pressure or away from it?

A

Toward it, as it is defined as the amount of (hydrostatic) pressure needed to keep the fluid out in this experimental setup:

113
Q

Are GI secretions hypertonic, hypotonic, or isotonic?

A

Isotonic except for saliva which is hypotonic

114
Q

Is sweating hypertonic, hypotonic, or isotonic

A

Hypotonic. It tastes salty because it evaporates quickly.

115
Q

What are Starling’s forces?

A
  1. Hydrostatic pressure.
  2. Oncotic (osmotic) pressure.
116
Q

What is the primary neurotransmitter of the parasympathetic system?

A

Acetylcholine

117
Q

What is the primary neurotransmitter at neuromuscular junctions, excluding muscles with sympathetic tone? What are the receptor types for smooth vs. skeletal muscle?

A

Acetylcholine; nicotinic receptors at skeletal, muscarinic at smooth

118
Q

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is […].

A

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

119
Q

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter […] which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

A

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

120
Q

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates […] receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

A

Sympathetic fibers for cardiac and smooth muscle release the neurotransmitter norepinephrine which activates adrenergic receptors; in renal vascular smooth muscle, the neurotransmitter is dopamine.

121
Q

Does parasympathetic stimulation cause bronchoconstriction or bronchodilation? Via what receptor?

A

Bronchoconstriction, via M3 (muscarinic) receptors

122
Q

Sympathetic innervation uses noradrenaline as the primary neurotransmitter at the end organ or gland with two exceptions. What are they?

A

1) Sweat glands: acetylcholine –> muscarinic receptor
2) Renal vascular smooth muscle: dopamine –> dopamine receptor

123
Q

What is the primary neurotransmitter and receptor at ganglia for both the sympathetic and parasympathetic nervous system?

A

Acetylcholine, nicotinic receptor

124
Q

Blood flow through the circulatory system is driven by gradients in blood pressure. Blood vessels exhibit both […] and compliance.

A

Blood flow through the circulatory system is driven by gradients in blood pressure. Blood vessels exhibit both resistance and compliance.

125
Q

Connecting blood vessels in [series or parallel] decreases the overall system resistance; conversely,
connecting blood vessels in [series or parallel] increases the overall system resistance.

A

Connecting blood vessels in parallel decreases the overall system resistance; conversely,
connecting blood vessels in series increases the overall system resistance.

126
Q

The resistance of a blood vessel is determined primarily by its [physical property].

A

The resistance of a blood vessel is determined primarily by its radius.

127
Q

Is the vascular pressure in the aorta higher or lower than in the vena cava?

A

Higher

128
Q

Water flow can be related to current (from electromagnetism). What is the pressure difference analogous to?

A

Voltage. Q = ΔP/R ⇔ I = V/R

129
Q

Velocity is [relationship operator] to flow and inversely proportional to cross-sectional area of the vessel.

A

Velocity is proportional to flow and inversely proportional to cross-sectional area of the vessel.

130
Q

Velocity is proportional to flow and [relationship operator] to cross-sectional area of the vessel.

A

Velocity is proportional to flow and inversely proportional to cross-sectional area of the vessel.

131
Q

Blood vessel resistance is inversely proportional to the [N]th power of vessel radius.

A

Blood vessel resistance is inversely proportional to the 4th power of vessel radius.

132
Q

Does increased hematocrit increase, decrease, or not change blood viscosity?

A

Increase

133
Q

When vessels are more “stretchy”, are they more compliant or less compliant? Given constant volume, is what is the relationship between compliance and pressure?

A

More compliant. Inversely. C = V/P.

134
Q

Are arteries more compliant or less compliant than veins? How can compliance be estimated from the following curves?

A

Arteries are less compliant; Compliance is equivalent to the slope of these curves

135
Q

Capillaries are very small, so they are extremely high resistance (resistance is inversely proportional to the 4th power of radius). Why isn’t the capillary bed the area of greatest resistance in the circulatory system?

A

The ~3 billion capillaries are in parallel, which knocks out their overall contribution of resistance to the system

136
Q

Which section of the vasculature presents the greatest resistance? How do we know this?

A

Arterioles: we know this because there is the greatest pressure drop across this segment

137
Q

Is the greater resistance of arterioles due to their smooth muscle?

A

No, it is purely the geometry of connectivity; the smooth muscle does mean that the resistance can be regulated by arterioles, redirecting flow.

138
Q

Cardiac valves open and close in response to changes in [physiological variable] in cardiac chambers and blood vessels

A

Cardiac valves open and close in response to changes in blood pressure in cardiac chambers and blood vessels

139
Q

From tracings of pressure and volume versus time, loops of pressure versus volume can be created. Changes in [physiological variable] can be understood from changes in pressure-volume loops.

A

From tracings of pressure and volume versus time, loops of pressure versus volume can be created. Changes in cardiac output can be understood from changes in pressure-volume loops.

140
Q

The [name] relationship describes the fact that increased filling of the ventricle will increase cardiac output.

A

The Frank-Starling relationship describes the fact that increased filling of the ventricle will increase cardiac output.

141
Q

Increased filling pressure (preload) leads to [increased or decreased] cardiac output.

A

Increased filling pressure (preload) leads to increased cardiac output.

142
Q

Increased pressure in arteries (afterload) leads to [increased or decreased] cardiac output.

A

Increased pressure in arteries (afterload) leads to decreased cardiac output.

143
Q

Increased afterload will decrease the degree of muscle shortening.

Increased preload will [increase or decrease] the degree of muscle shortening.

A

Increased afterload will decrease the degree of muscle shortening.

Increased preload will increase the degree of muscle shortening.

144
Q

What is the name of this kind of diagram?

A

The classic “wiggers” diagram

145
Q

In this wiggers diagram, what does the top red line correspond to? What is happening during the “bump”? Which valve is opening and closing on either side of it?

A

The aortic pressure; ejection is occuring during the bump, and the aortic valve opens and closes on either side of it.

146
Q

Why would the mitral valve close at this point of the Wiggers diagram? Keep in mind the blue line is the left ventricular pressure and the pink is left atrial pressure.

A

The left atrial pressure drops below the left ventricular pressure, so there can be no forward flow through the valve; retrograde flow closes the mitral valve.

147
Q

When the mitral valve opens at this point, what starts happening to ventricular volume?

A

It rises, this is when the heart fills.

148
Q

At each corner of this curve, what is the valve that is opening or closing?

A
149
Q

What is the stroke volume represented in this diagram? How about the systolic blood pressure?

A

~65 mL and 115 mmHg

150
Q

Why is the diastolic blood pressure at this corner of the PV loop?

A

This is when the aortic valve opens during systole; in other words, when ventricular pressure has just exceeded aortic pressure. Aortic (and blood) pressure is at a minimum just before ejection begins and therefore, this pressure is the diastolic blood pressure.

151
Q

The end-diastolic pressure volume relationship is measure by tracking which corner of the PV curve?

A

The bottom right.

152
Q

The end diastolic pressure and volume are in which corner of the PV loop?

A

The bottom right corner.

153
Q

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the […] relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

A

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

154
Q

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a [greater or smaller] slope.

A

The end-systolic elastance of the ventricles, an index of myocardial contractility, is represented by the slope of the end systolic pressure volume relationship, which is a linear relationship. A stronger heart has a greater (steeper) slope.

155
Q

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume [increases or decreases] and thus cardiac output [increases or decreases] with increased preload.

A

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

This indicates a weaker heart or risk of heart failure.

156
Q

If the end-systolic pressure volume relationship has a [high or low] slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

A

If the end-systolic pressure volume relationship has a low slope, indicating low myocardial contractility, stroke volume decreases and thus cardiac output decreases with increased preload.

This indicates a weaker heart or risk of heart failure.

157
Q

What physiological perturbations alter preload?

A

Increased venous return, which is affected by venous tone and the volume of circulating blood.

158
Q

Should the slope of the end-systolic pressure volume relationship change under typical physiological variations throughout the day, e.g. ingestion of a meal or physical activity? If not, what does affect the slope?

A

No. It’s a reflection of the limits of the contractility of heart tissue, which (generally) does not respond to changes in preload or afterload. This is why it is a reliable diagnostic indicator. Inotropic drugs can affect contractility, however.

159
Q

Under normal physiological conditions, which vasculature system affects afterload?

A

Arterial system

160
Q

Does increased peripheral vascular resistance increase or decrease afterload?

A

Increase

161
Q

What sort of pharmacological agents or endogenous regulators would affect afterload?

A

Vasoconstrictors and vasodilators: agents that affect peripheral vascular resistance.

162
Q

If contractility of a heart increases given the same preload and afterload, what happens to cardiac output?

A

It increases (dramatically)

163
Q

What physiological perturbations can affect contractility?

A

1) Sympathetic stimulation of the ventricles
2) Increased circulating Ca++
3) Myocardial hypertrophy (growth of heart muscle)

164
Q

Why is ejection fraction used to measure contractility in heart patients instead of the end systolic pressure volume relationship (ESPVR)?

A

To get the ESPVR you need to measure left ventricular pressure and volume accurately while subjecting the heart to different loads. Measuring ventricular pressure is fairly invasive so it is usually only done in animal studies.

165
Q

How do you calculate ejection fraction from a pressure volume loop? How is it related to the slope of the end systolic pressure volume relationship (ESPVR)?

A

Ejection fraction = stroke volume / end diastolic volume. It roughly correlates with ESPVR slope, but as you can see in the following curve it will be a very rough correlation.

166
Q

Is preload or afterload a greater confounding variable for the clinical use of ejection fraction to measure contractility of heart muscle?

A

Afterload is a worse confounder. As can be seen in the following curves, increasing afterload can decrease the ejection fraction. (remember, EF = SV/EDV) Increasing the preload can change ejection fraction, but generally not as much (it depends on the EDPVR curve).

167
Q

When […] receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

A

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

168
Q

When nicotinic receptors on the adrenal medulla are activated by […], epinephrine and norepinephrine are released into the blood.

A

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

169
Q

When nicotinic receptors on the [organ part] are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

A

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

170
Q

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, [hormone] and [hormone] are released into the blood.

A

When nicotinic receptors on the adrenal medulla are activated by acetylcholine, epinephrine and norepinephrine are released into the blood.

171
Q

Cholinergic transmission occurs in three primary sites; what are they?

A

1) Pre-ganglionic fibers in the sympathetic and parasympathetic systems
2) Post-ganglionic fibers in the parasympathetic system
3) Somatic nerves at the neuromuscular junction

172
Q

What is taken up via a sodium-dependent transporter in order to be synthesized into acetylcholine via a reaction with acetyl coenzyme-A (AcCoA) and what enzyme performs this reaction?

A

Choline; the enzyme is choline acetyltransferase

173
Q

Acetylcholine is stored in synaptic vesicles by what transporter?

A

Vesicle Associated Transporter (VAT)

174
Q

In the synapse, what enzyme breaks down acetylcholine? What happens when this enzyme is inhibited?

A

Acetylcholinesterase; inhibitors would prolong the action of acetylcholine.

175
Q

Why would there be acetylcholine receptors on the presynaptic terminal of a cholinergic synapse?

A

Regulation of neurotransmitter release

176
Q

What two classes of membrane proteins coordinate synaptic vesicles to the synaptic membrane for release?

A

SNAPs and VAMPs

177
Q

What amino acid is the precursor for dopamine, norepinephrine, and epinephrine synthesis?

A

Tyrosine

178
Q

What transporter stores noradrenaline, adrenaline, and domaine into vesicles within presynaptic terminals?

A

Vesicular Monoamine Transporter (VMAT)

179
Q

What transporter facilitates reuptake of catecholamines into the presynaptic terminal?

A

Norepinephrine transporter (NET)

180
Q

What is the class of molecules that adrenergic receptors respond to?

A

Catecholamines, which look like catechol + a chain that terminates in an amine. This is catechol:

181
Q

What is the primary function of α1 adrenergic receptors? What is their primary location in the periphery?

A

Smooth muscle contraction; blood vessels of the skin and GI tract, so the result is vasoconstriction in these areas

182
Q

What are the primary functions of β1 adrenergic receptors in the heart?

A

Increases heart rate, cardiac contractility and conduction

183
Q

What does activation of β2 adrenergic receptors do in blood vessels?

A

Small muscle relaxation; Vasodilitation

184
Q

Does acetylcholine have a higher affinity for muscarinic receptors or nicotinic receptors?

A

Muscarinic

185
Q

If blood pressure increases, baroreceptors sense this, and [increase or decrease] their firing to [increase or decrease] parasympathetic and [increase or decrease] sympathetic input to the heart. This [increases or decreases] heart rate.

A

If blood pressure increases, baroreceptors sense this, and increase their firing to increase parasympathetic and decrease sympathetic input to the heart. This decreases heart rate.

186
Q

What is the primary tone of blood vessels?

A

Sympathetic

187
Q

What is the primary adrenergic receptor type in bronchiolar smooth muscle and the blood vessels of skeletal muscle?

A

adrenergic β2

188
Q

What is the primary receptor for parasympathetic signals to the heart?

A

Muscarinic, M2

189
Q

Does sympathetic activity open or close the iris? Which muscle does it use? Which receptor?

A

Open; iris radial muscle; adrenergic α1 receptor

190
Q

What is the action of parasympathetic stimulation of the iris (dilation or constriction)? Which muscle(s) does it contract? Which receptor is involved?

A

Constriction; iris circular muscle and ciliary muscle; muscarinic M3 receptor

191
Q

Why are postsynaptic receptors often ligand-gated channels?

A

Upon binding of the ligand (the neurotransmitter) ions rush through the channel, starting a postsynaptic action potential

192
Q

If acetylcholine receptors line the edges of junctional folds within a neuromuscular junction, what lines the depths of the folds and why?

A

Acetylcholinesterase, to break down the neurotransmitter and terminate stimulation of the muscle

193
Q

What receptor family do the β-adrenergic receptors belong to? Via which enzyme do they act to increase intracellular cAMP?

A

G-protein coupled receptors; adenylyl cyclase

194
Q

Which part or layer of the adrenal gland releases epinephrine?

A

The medulla

195
Q

When epinephrine binds to β2 adrenergic receptors, what happens? Which tissues carry this receptor?

A

The smooth muscle in bronchioles and a subset of blood vessels (mostly to skeletal muscle) relax.

196
Q

For which adrenergic receptor does norepinephrine significantly lack agonist activity? How does this make its effects different from those of epinephrine?

A

β2 adrenergic receptors; therefore, it does not cause dilation of blood vessels in some skeletal muscles

197
Q

What are the targets of isoproterenol? Is it an antagonist or an agonist?

A

Adrenergic β-receptors (both β1 and β2). It is an agonist.

198
Q

Which receptors are targeted by phenylephrine? What are its physiological effects?

A

Adrenergic α1 and α2 receptors. It causes vasoconstriction in many blood vessels, and lowers heart rate.

199
Q

What are the series of events leading to phenylephrine’s effect of lowered heart rate?

A

Phenylephrine causes vasoconstriction, which causes baroreceptors to detect an increase in SBP. They fire more frequently, leading to increased (vagal) parasympathetic and decreased sympathetic stimulation of the heart, decreasing heart rate.

200
Q

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex [heart response].

A

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

201
Q

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a [increase or decrease] in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

A

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

202
Q

Phentolamine is a reversible, nonspecific [drug target and agonism]. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

A

Phentolamine is a reversible, nonspecific adrenergic α-receptor competitive antagonist. It causes a decrease in peripheral resistance, and may cause a baroreceptor-mediated reflex tachycardia.

203
Q

Beta blockers can be selective or non-selective.

  • Metoprolol is a [selective or non-selective] beta blocker that targets [type(s)] receptors.
  • Propanolol is a [selective or non-selective] beta blocker that targets [type(s)] receptors.
A

Beta blockers can be selective or non-selective.

  • Metoprolol is a selective beta blocker that targets β1 receptors.
  • Propanolol is a non-selective beta blocker that targets β1 and β2 receptors.
204
Q

In the steady state, venous return must [be greater than, equal, be less than] cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

A

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

205
Q

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve [geometric relationship].

A

In the steady state, venous return must equal cardiac output. Thus steady-state cardiac output occurs where the Frank-Starling curve and the venous return curve intersect.

206
Q

The venous return curve can be constructed by considering the following: (a) arterial […], (b) arterial compliance, (c) venous compliance

A

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

207
Q

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial […], (c) venous compliance

A

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

208
Q

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) […] compliance

A

The venous return curve can be constructed by considering the following: (a) arterial resistance, (b) arterial compliance, (c) venous compliance

209
Q

Why does the venous return curve in a Frank-Starling relationship fall with increasing venous/atrial pressure?

A

Increased atrial pressure makes it harder for venous blood to return to the heart

210
Q

What are the two curves in a Frank-Starling relationship chart?

A

One is cardiac function, or cardiac output (volume) vs. right atrial pressure; the other is vascular function, or venous return (volume) vs. right atrial pressure

211
Q

What would a decrease in blood volume do to the Frank Starling relationship—what is the predicted effect on right atrial pressure and cardiac output?

A

Both would fall.

212
Q

What are the two major classes of direct-acting cholinoreceptor stimulants?

A

Alkaloids and choline esters

213
Q

Where are M1 receptors principally located? How about M2 receptors? M3 receptors?

A

M1: nerves;

M2: Heart, nerves and smooth muscle;

M3: Glands, smooth muscle and endothelium

214
Q

Which muscarinic receptor acts through activation of K+ channels instead of a IP3/diacyl glycerol cascade?

A

M2

215
Q

Nicotinic receptors can be sorted into NM and NN type receptors, which are located in skeletal muscle neuromuscular junctions and […], respectively.

A

Nicotinic receptors can be sorted into NM and NN type receptors, which are located in skeletal muscle neuromuscular junctions and post-ganglionic cell bodies, respectively.

216
Q

Nicotinic receptors can be sorted into NM and NN type receptors, which are located in […] and post-ganglionic cell bodies, respectively.

A

Nicotinic receptors can be sorted into NM and NN type receptors, which are located in skeletal muscle neuromuscular junctions and post-ganglionic cell bodies, respectively.

217
Q

Which muscarinic receptor type is targeted by vagus stimulation of the heart?

A

M2

218
Q

What physiologic effects on the heart would be expected from a parasympathetic agonist?

A

Negative chronotropy (lower heart rate), inotropy (decreased contractility in the atria), and dromotropy (decreased conduction velocity).

219
Q

Alkaloids are structurally recognizable by what feature?

A

Nitrogen containing rings.

220
Q

What are the sites of action of a nicotinic agonist?

A

1) gangia of both arms of the ANS
2) skeletal muscle neuromuscular junctions

221
Q

What is the structural difference between scopalamine and atropine? What is their targeted receptor(s) and physiological activity?

A

Scopalamine has an additional oxygen molecule as indicated in this diagram. They are both competitive antagonists for all muscarinic acetylcholine receptors, suppressing parasympathetic stimulation.

222
Q

What is the pharmacological function of atropine? What receptor do they target?

A

Muscarinic competitive antagonist; they target muscarinic receptors

223
Q

Would atropine cause vasodilation or vasoconstriction? Why or why not?

A

It causes neither, because although there are muscarinic receptors in blood vessels there are no parasympathetic innervators

224
Q

What is meant by orthostatic hypotension?

A

A sudden drop in blood pressure when a person stands, by at least 20 mmHg (usually causes some dizziness)

225
Q

What does a ganglionic blocking agent do? What is the classical prototype of these agents?

A

They blockade both sympathetic and parasympathetic input to organs by acting as a nicotinic antagonist. The classical prototype is hexamethonium, but it is not used clinically because it causes orthostatic hypotension

226
Q

What is the pharmacological mechanism of physostigmine?

A

It is a carbamylating acetylcholinesterase inhibitor, and it is reversible.

227
Q

How does a neuromuscular blocker like tubocurarine (curare) work at the molecular level?

A

They are competitive antagonists at skeletal muscle cholinergic nicotinic receptors, preventing opening of the Na+/K+channels and skeletal muscle contraction.

228
Q

All membrane cotransporters and counter-transporters move ions from [higher or lower] to [higher or lower] electrochemical potential

A

All membrane cotransporters and counter-transporters move ions from higher to lower electrochemical potential

229
Q

How many ATP does the Na+/K+ ATPase consumer per cycle? What is the net charge movement (amount and direction)?

A

One; +1 charge moves out of the cell

230
Q

What are the two transporters that are primarly responsible for maintaining a Ca+ gradient between the cytosol and the sarcoplasmic reticulum/extracellular space in a cardiomyocyte?

A

SERCA (Sarco/Endoplasmic Reticulum Ca++ ATPase) and NCX (Na+-Ca++ exchanger)

231
Q

Is plasma membrane Ca++ ATPase (PMCA) important for maintaining the Ca++ gradient in cardiomyocytes?

A

Quantitatively, not really

232
Q

How much of a cardiomyocyte’s ATP is used for myosin movement (contraction)? How about for maintaining ionic homeostasis?

A

70% for myosin; 30% for maintaining the gradient (via Na+/K+ ATPase and SERCA)

233
Q

Can the Na+-Ca+ exchanger (NCX) operate in reverse?

A

Yes, if the Na+ gradient is reversed and there is sufficient Ca+ outside the cell, it can reverse direction

234
Q

At equilibrium, the voltage across the membrane will be closest to the Nernst potential of the ion that the membrane is [least or most] permeable to.

A

At equilibrium, the voltage across the membrane will be closest to the Nernst potential of the ion that the membrane is most permeable to.

235
Q

If contractions of a cardiomyocyte are quickly paced, what happens to the Ca++ release over the course of ~20 beats?

A

It increases

236
Q

What effect would a clinical dosage of norepinephrine have on BP and HR and why?

A

Increased BP, because of direct effect on α1 receptors. Norepinephrine has a weak effect on β1 and barely any effect on β2 receptors. Usually, the indirect effect of baroreceptor-mediated increased parasympathetic and decreased sympathetic input to heart wins out over the direct β1 agonism of NE, and HR decreases.

237
Q

What effect does isoproterenol have on HR and BP, and why?

A

Isoproterenol is a β1 agonist, increasing heart rate, and a β2 agonist, vasodilating blood vessels to skeltal muscle and causing a drop in BP.

238
Q

What is the mechanistic difference between β-adrenergic stimulation, as opposed to α-adrenergic stimulation?

A

β-adrenergic activates adenylyl cyclase, increasing cAMP production; cAMP inhibits MLCK, causing smooth muscle relaxation. α-adrenergic produces IP3 which increases intracellular Ca++, promoting smooth muscle constriction.

239
Q

Of K+, Na+, and Ca++ in the cardiomyocyte, which ion is least affected by digitalis treatment?

A

K+

240
Q

What does phospholamban do? What changes when it is phosphorylated? What phosphorylates it and what upstream branch of the autonomic nervous system controls this?

A

Phospholamban inhibits the action of SERCA, slowing Ca++ uptake into the sarcoplasmic reticulum. When phosphorylated by PKA, this action is inhibited. Increased cAMP and activation of the β2 adrenergic receptor will activate PKA, phosphorylate phospholamban, and increase Ca++ uptake.

241
Q

What is the Nernst equation? What is the approximate value of RT/F in mV? What is z?

A

RT/F = 25mV

z is the valence of the ion

242
Q

Which ion current does endogenously produced acetylcholine modulate in order to decrease the heart rate?

A

It increases the amount of repolarizing K+ current that opposes membrane depolarization during phase 4 of the SA nodal action potential.