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Physiology Review Q's Flashcards

1. Physiology humoral and nonhumoral factors (1-26) 2. seminar arterial pulse (27-69) 3. cardiac muscle action potentials (70-129) ---- 4.ECG seminar 1 (130-149) 5. ECG seminar 2 (150-165) 7. pathophysiology of arrhythmias (166-185) 8. cardiac cycle (186-216) 9. regulation of cardiac volume (217-252) 10. regulation of contraction of cardiac muscle (253-292) 11. regulation of cardiac output (293-322)

1
Q

Describe the relationship between blood pressure and volume?

a. directly proportional
b. inversely proportional

A

a. directly proportional

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2
Q

Where are two locations that arterial baroreceptors are found?

A

aortic arch and carotid sinus (the wider area before the internal carotid artery splits)

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3
Q

What two nerves are the afferent pathway of baroreceptors?

A

CN X and IX

(CN X for the aortic arch and CN IX for the carotid sinus)

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4
Q

Describe action potentials of baroreceptors during low pressure vs high pressure?

A

more firing during high pressure and less during low pressure

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5
Q

Describe the relationship between compliance and pressure

A

inversely proportional

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6
Q

During low blood pressure, how will baroreceptors act on vasopressin, sympathetic, and parasympathetic activity?

A

increase vasopressin

increase sympathetic activity

decrease parasympathetic activity

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7
Q

What is the effect of the setpoint atrial blood pressure on sympathetic activity?

A

ABP at setpoint inhibits sympathetic activity

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8
Q

During high blood pressure, how will baroreceptors act on vasopressin, sympathetic, and parasympathetic activity?

A

decrease vasopressin

decrease sympathetic activity

increase parasympathetic activity

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9
Q

Which body reflex prevents pulmonary edema?

A

the atrial mechanoreceptor reflex

(AKA Bainbridge reflex or cardiopulmonary reflex)

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10
Q

During pulmonary congestion, how will baroreceptors act on vasopressin, sympathetic, and parasympathetic activity?

A

decrease vasopressin

increase sympathetic activity

decrease parasympathetic activity

(Atrial mechanoreceptor reflex)

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11
Q

In which of the following can tachycardia be found? explain.

a. brain ischemic reflex
b. cushing reflex

A

a. brain ischemic reflex

(this reflex is associated with hypotension, so the tachycardia is used to compensate; the cushing reflex has hypertension, so the baroreceptor reflex is used to compensate)

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12
Q

Which (one or more) of the following inhibits parasympathetic/ vagal activity?

a. brain ischemic reflex
b. crushing reflex
c. baroreceptor reflex
d. atrial mechanoreceptor reflex
e. atrial chemoreceptor reflex

A

d. atrial mechanoreceptor reflex

AKA bainbridge reflex

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13
Q

Which of the following is both sympathetic and parasympathetic activity activated?

a. brain ischemic reflex
b. crushing reflex
c. baroreceptor reflex
d. bainbridge reflex
e. atrial chemoreceptor reflex

A

e. atrial chemoreceptor reflex

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14
Q

How does angiotensin 2 affect blood pressure? explain.

A

it increases BP by vasoconstriction and helping release aldosterone and vasopressin/ADH which then reabsorb Na and water

(it also indirectly enhances sympathetic activity by increasing NA release and by increasing reactivity to adrenergic stimulation)

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15
Q

How do ANP and BNP affect BP and how?

(atrial natriuretic peptide (ANP); B-type natriuretic peptide (BNP))

A

decrease BP by promoting vasodilation and natriuresis

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16
Q

What degrades natriuretic peptides?

A

Neprilysin

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17
Q

What is used as a biomarker of heart failure? Why?

A

proteolytic fragments of B-type natriuretic peptide (BNP)

(WHY? Natriuretic Peptides are high in heart failure. They’re r_eleased when the atrial pressure is high_ and its dilated, they act to reduce the BP- by natriuresis= the excretion of sodium by the kidneys)

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18
Q

How can we reduce mortality in heart failure patients?

A

sacubitril (neprilysin inhibitor) and valsartan (angiotension II receptor blocker)

** this combo is called ARNI

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19
Q

Which of the following does vasopressin use to increase systemic vascular resistance?

a. cAMP
b. IP3

A

b. IP3

(vasopressin uses cAMP to increase blood volume)

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20
Q

Which cells produce nitric oxide? What stimulates their synthesis?

A

endothelial cells; blood flow shearing forces and NO-dependent vasodilators stimulate synthesis.

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21
Q

What is a potential issue that may develop after endothelial destruction?

A

Atherosclerosis

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22
Q

Give me four vasodilators/activators of NO synthase.

A

Acetylcholine (usually)

Adenosine

Bradykinin

Substance-P

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23
Q

When does acetylcholine do vasoconstriction/dilation?

A

causes constriction when directly related to vascular smooth muscle

causes dilation when endothelium present

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24
Q

Which second messenger does NO use to mediate vasodilation?

A

cGMP

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25
Q

How do thrombocytes work?

A

they circulate and check if there’s endothelial damage. if damage is present, they’re activated and cause thrombosis.

(** NO acts to counteract this, so if NO is not present, the thrombosis is uncontrolled)

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26
Q

Which of the following is NOT a function of NO?

a. antiproliferative
b. antithrombotic
c. antiinflammatory
d. they’re all NO functions

A

d. they’re all NO functions

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27
Q

LVEPD (Left ventricular end-diastolic pressure) shows a change in blood pressure that’s known as an atrial kick. explain it.

A

the atrial kick occurs when the ventricle is 80% filled with blood and its relaxed. The rest of the 20% of blood is added in when the atrium contracts (forcing the blood in the relaxed ventricle). This is the atrial kick

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28
Q

What is the ventriculo-aortic pressure gradient and what does it cause?

A

Its the pressure difference between the ventricle and the aorta, it causes the blood to move out of the ventricle and into the circulation.

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29
Q

The arterial pressure slope of the ascending limb is determined by

A

the ejection speed (the stroke volume)

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30
Q

Which of the following makes the arterial pressure slope of the ascending limb LESS steep?

a. anemia
b. aortic insufficiency
c. aortic stenosis

A

c. aortic stenosis

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31
Q

The arterial pressure slope of the descending limb is determined by

A

systemic vascular resistance (SVR)

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32
Q

What does it mean when the arterial pressure slope of the ascending limb is not steep (slowly rising pressure)?

A

high afterload (slow ejection ex/ arterial stenosis)

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33
Q

What is the incisura? (whats its other name?)

A

the incisura (aka the dicrotic notch) is a lowering in the arterial pressure due to the closure of the aortic valve (occurs at the beginning of diastole)

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34
Q

T/F: the higher the slope of the arterial ascending limb pressure, the slower the heart rate

A

false, the opposite is true (higher slope with higher heart rate)

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35
Q

How does vascular resistance affect the slope of the descending limb of the arterial pressure?

A

more vascular pressure, less steep slope

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36
Q

T/F: the lower the heart rate, the lower the diastolic pressure

A

true (lower heart rate gives more time for the blood to run off)

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37
Q

Aortic stenosis results in? (3 things)

A

reduces stroke volume

a slow rising arterial waveform

late peaks in systole

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38
Q

What is pulasus parvus?

A

its a small amplitude of arterial pressure

(Pulsus parvus et tardus is the physical exam finding in aortic valve stenosis-The term “parvus” means weak and “tardus” means late, thus the pulse is weak and late.)

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39
Q

How does the anacrotic notch affect arterial blood pressure?

A

distorts the pressure upstroke

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40
Q

describe the stroke volume and vascular resistance thats relates to a small and slow pulse.

A

stroke volume = low

vascular resistance = high

(small and slow pulse=Pulsus parvus et tardus=aortic stenosis- due to the stenosis the resistance is high and the stoke volume is low-blood cannot easily get through)

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41
Q

Which disease is characterized by low diastolic pressure, no incisura, and large stroke volume

A

aortic insufficiency also known as aortic regurgitation

(low diastolic pressure because the blood is leaking into wrong compartments. the large stroke volume because of the stretching due to the extra blood. incisura missing because the aortic valve isn’t closing)

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42
Q

Which of the following peaks in systole?

a. bispheriens pulse
b. dicrotic pulse
c. pulsus alternans
d. A and B
e. B and C

A

c. both

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43
Q

Which of the following peaks in systole and diastole?

a. bispheriens pulse
b. dicrotic pulse
c. both
d. neither

A

b. dicrotic pulse

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44
Q

What causes the double peak in systole in bispheriens pulse?

A

anterior motion of mitral valve

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45
Q

Which of the following is the diagram a representation of? explain.

a. bigeminal pulse
b. pulsus alternans

A

a. bigeminal pulse

the pulses in pulsus alternans is regular while the pulses in bigeminal pulse occur irregularly (not the same distance between each pulse)

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46
Q

What causes dicrotic pulse?

A

low cardiac output and high vascular resistance

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47
Q

Describe the diastolic pressure if the heart rate and vascular resistance are high.

A

diastolic pressure would be high. The high heart rate wouldn’t give enough time for the blood to run off to the periphery; the vascular resistance is also high, so it would make it hard for the blood to run off into the circulation. -> high diastole

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48
Q

Why is the flow of blood to the body continuous if the heart ejects blood in a pulsatile manner?

A

The elastic recoil of the aorta is what makes blood flow smooth. It stretches to accommodate the blood then pushes it out continuously until the next pulse occurs.

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49
Q

Which of the following is the diagram a representation of? explain.

a. bigeminal pulse
b. pulsus alternans

A

a. bigeminal pulse

pulsus alternans is regular while the pulses in bigeminal pulse occur irregularly (not the same distance between each pulse)

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50
Q

The aortic pressure is described as rising in a “tardus” manner, what does this mean? What condition could this be an indicator or?

A

tardus means slow; the pressure of the aorta would be rising slowly, which could indicate aortic stenosis

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51
Q

Describe the diastolic pressure if the heart rate and vascular resistance are low.

A

diastolic pressure would be low. The low heart rate would give the blood plenty of time to run off to the periphery; the vascular resistance is also low, so it would make it easier for the blood to run off into the circulation. -> low diastole

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52
Q

What is this called?

a. anacrotic notch
b. dicrotic notch

A

a. anacrotic notch

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53
Q

What is the third elevation called?

A

incisura (or dicrotic notch)

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54
Q

What kind of pulse is this? What does it indicate?

A

bispheriens pulse

occurs in hypertrophic cardiomyopathy

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55
Q

What kind of pulse is this? What does it indicate?

A

Dicrotic pulse (2 peaks in once cycle, one in systole and one in diastole)

indicates heart failure /shock

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56
Q

What kind of pulse is this? What does it indicate?

A

pulsus internans

found in aortic stenosis and is a sign of severe left ventricular dysfunction

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57
Q

What kind of pulse is this?

A

Bigeminal pulse

(rhythm of heart is disrupted, variable cycle length, and thus variable filling of the heart with blood)

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58
Q

Describe an anacrotic pulse

A

slow rise, later peak, and less stroke volume

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59
Q

Describe the systolic and diastolic pressure in aortic insufficiency/regurgitation

A

systolic pressure high and diastolic pressure low

(the aortic valve not closing means that blood can go in two directions- the circulation and back to the ventricle- and this causes the diastolic pressure to be lowered)

(the systolic pressure is high because more volume goes in the ventricle, causing it to stretch and eject blood harder)

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60
Q

Which is associated with Watson’s water hammer?

a. aortic stenosis
b. aortic insufficiency

A

b. aortic insufficiency

(Watson’s water hammer AKA bounding pulse AKA Corrigan’s pulse)

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61
Q

Which of the following patients experience a higher increase in heart rate after standing up after laying down?

a. normal patient
b. patient with autonomic dysfunction
c. patient with venous insufficiency

A

c. patient with venous insufficiency

(because they have a larger amount of blood pooling in the veins, so the compensation is greater)

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62
Q

Which of the following may activate baroreceptors?

a. epinephrine
b. norepinephrine

A

b. norepinephrine

(it has a high affinity to alpha one receptors, they increase the vascular resistance, increasing both systolic and diastolic pressure, this leads to an increase in mean arterial pressure, which baroreceptors compensate for)

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63
Q

Which two of the following adrenergic receptors does epinephrine have a higher affinity for?

a. alpha 1
b. alpha 2
c. beta 1
d. beta 2

A

c. beta 1

+

d. beta 2

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64
Q

Which of the following decreases diastolic pressure?

a. epinephrine
b. norepinephrine

A

a. epinephrine

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65
Q

Which two of the following adrenergic receptors does norepinephrine have a higher affinity for?

a. alpha 1
b. alpha 2
c. beta 1
d. beta 2

A

a. alpha 1

+

c. beta 1

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66
Q

What causes transient tachycardia that’s caused by norepinephrine release?

A

activation of beta 1 adrenergic receptors

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67
Q

compare and contrast the effect of epinephrine and norepinephrine on systemic vascular resistance

A

norepinephrine has a high affinity to alpha 1, which causes constriction of vascular smooth muscles, and thus increases SVR

epinephrine (low concentration) has a high affinity to beta 2, which causes relaxation of vascular smooth muscles, and thus decreases SVR

epinephrine (high concentration) has a high affinity to alpha 1, which causes constriction of vascular smooth muscles, and thus increases SVR

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68
Q

compare and contrast the effect of epinephrine of high VS of low concentrations on diastolic and systolic pressure

A

at low concentrations= increases systolic + decrease diastolic

at high concentrations= increases systolic + increase diastolic

(because at high concentrations it also starts affecting the alpha receptors, not just the beta)

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69
Q

Describe the relationship between pressure and heart rate while undergoing the Valsalva maneuver (in a normal patient)

A

inversely proportional

(because high mean arterial pressure, the baroreceptors see this and decrease heart rate)

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70
Q

What is the primary pacemaker of the heart? Why?

A

the SA node is the primary pacemaker because it depolarizes at a more rapid pace than the others (60-100bpm)

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71
Q

What’s the intrinsic rate of the AV node?

A

40 to 55 beats/min

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72
Q

What’s the intrinsic rate of Tawara branches & Purkynje?

A

25 to 40 beats/min

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73
Q

Which results from ventricular repolarization?

a. P wave
b. T wave
c. QRS complex

A

b. T wave

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74
Q

Which results from ventricular depolarization?

a. P wave
b. T wave
c. QRS complex

A

c. QRS complex

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75
Q

What’s the electrical connection that links the atria and ventricles?

A

the AV node and AV bundle

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76
Q

Which results from artrial depolarization?

a. P wave
b. T wave
c. QRS complex

A

a. P wave

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77
Q

What is the last place to be activated in the heart?

A

posterobasal areas of the ventricles (the outflow tracts)

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78
Q

Where does depolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

a. endocardium

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79
Q

Describe the ion flow in stage 2. What causes the plateau

A

Ca influx is balancing K efflux

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80
Q

Does this represent the AP in the antiarrhythmic cells or the AP in cardiac muscle?

A

In cardiac muscle

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81
Q

During stage 4, what is the cell permeable to?

A

Na and K (more to Na; as stage four continues the K movement decreases)

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82
Q

Where does repolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

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83
Q

At which stage can another AP form?

A

At the latter part of stage 3, deformed AP can be generated with stronger than normal stimuli

(relative refractory period is end of stage 3)

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84
Q

Describe the action potential that occurred in stage 3

A

They’re abnormal (upstroke is slower, amplitude is lower, duration is shorter)

The sodium channels aren’t fully activated, but the calcium channels are fully activated.

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85
Q

Explain cardiovascular syncope

A

Fear causes a strong activation of the vagus nerve, which hyperpolarizes the AV node. Due to this hyperpolarization, the threshold cannot be reached.

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86
Q

Action potentials last shorter in which of the following? Why?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

they have stronger Ito current (outward potassium current) which acts to repolarize

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87
Q

How does the positive chronotropic effect work?

A

opens more HCN-channels and L-type calcium channels to make the depolarization more rapid (so we reach threshold faster-> heart rate increases)

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88
Q

Explain how Parasympathetic stimulation causes a slower heart rate. What mechanisms are used?

A

reduces iHCN and iCa2+ channels (these channels act to depolarize)

opening of the acetylcholine regulated K+-channels (these channels hyperpolarize)

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89
Q

T/F: the smaller the radius, the more vulnerable the nodal cell is to conduction block (AV block)

A

true

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90
Q

Why is the AV-node delay important?

A

ensures that the ventricles are relaxed at the time of atrial contraction and permits optimal ventricular filling during the atrial contraction

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91
Q

What does negative dromotropic intervention cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

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92
Q

What determines absolute refractory period?

A

The refractory period lasts as long as the inactivation gates are closed

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93
Q

What does the conduction speed of the AV node depend on?

A

diameter of node

the amplitude

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94
Q

Which of the following does hyperkalemia cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

(Negative dromotropic intervention)

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95
Q

Conduction velocity is called

A

dromotropy

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96
Q

How do Sympathetic stimulation & catecholamine speed up dromotropy?

A

phosphorylation of Ca-channels and HCN channels

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97
Q

Which of the following use the sympathomimetic effect to change dromotropy?

a. hyperkaliemia
b. thyroxine
c. ischemia
d. inflammation

A

b. thyroxine

(sensitizes sympathetic receptors)

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98
Q

How does hyperkaliemia effect dromotropy?

A

decrease it by inactivating calcium channels (-> inhibit AP generation and block conduction)

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99
Q

How does Parasympathetic stimulation slow down the conduction velocity?

A

hyperpolarization via opening of acetylcholine regulated K-channels

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100
Q

What is the primary pacemaker of the heart? Why?

A

the SA node is the primary pacemaker because it depolarizes at a more rapid pace than the others (60-100bpm)

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101
Q

What’s the intrinsic rate of the AV node?

A

40 to 55 beats/min

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102
Q

What’s the intrinsic rate of Tawara branches & Purkynje?

A

25 to 40 beats/min

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103
Q

Which results from ventricular repolarization?

a. P wave
b. T wave
c. QRS complex

A

b. T wave

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104
Q

Which results from ventricular depolarization?

a. P wave
b. T wave
c. QRS complex

A

c. QRS complex

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105
Q

What’s the electrical connection that links the atria and ventricles?

A

the AV node and AV bundle

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106
Q

Which results from artrial depolarization?

a. P wave
b. T wave
c. QRS complex

A

a. P wave

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107
Q

What is the last place to be activated in the heart?

A

posterobasal areas of the ventricles (the outflow tracts)

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108
Q

Where does depolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

a. endocardium

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109
Q

Describe the ion flow in stage 2. What causes the plateau

A

Ca influx is balancing K efflux

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110
Q

Does this represent the AP in the antiarrhythmic cells or the AP in cardiac muscle?

A

In cardiac muscle

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111
Q

During stage 4, what is the cell permeable to?

A

Na and K (more to Na; as stage four continues the K movement decreases)

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112
Q

Where does repolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

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113
Q

At which stage can another AP form?

A

At the latter part of stage 3, deformed AP can be generated with stronger than normal stimuli

(relative refractory period is end of stage 3)

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114
Q

Describe the action potential that occurred in stage 3

A

They’re abnormal (upstroke is slower, amplitude is lower, duration is shorter)

The sodium channels aren’t fully activated, but the calcium channels are fully activated.

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115
Q

Explain cardiovascular syncope

A

Fear causes a strong activation of the vagus nerve, which hyperpolarizes the AV node. Due to this hyperpolarization, the threshold cannot be reached.

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116
Q

Action potentials last shorter in which of the following? Why?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

they have stronger Ito current (outward potassium current) which acts to repolarize

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117
Q

How does the positive chronotropic effect work?

A

opens more HCN-channels and L-type calcium channels to make the depolarization more rapid (so we reach threshold faster-> heart rate increases)

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118
Q

Explain how Parasympathetic stimulation causes a slower heart rate. What mechanisms are used?

A

reduces iHCN and iCa2+ channels (these channels act to depolarize)

opening of the acetylcholine regulated K+-channels (these channels hyperpolarize)

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119
Q

T/F: the smaller the radius, the more vulnerable the nodal cell is to conduction block (AV block)

A

true

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120
Q

Why is the AV-node delay important?

A

ensures that the ventricles are relaxed at the time of atrial contraction and permits optimal ventricular filling during the atrial contraction

121
Q

What does negative dromotropic intervention cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

122
Q

What determines absolute refractory period?

A

The refractory period lasts as long as the inactivation gates are closed

123
Q

What does the conduction speed of the AV node depend on?

A

diameter of node

the amplitude

124
Q

Which of the following does hyperkalemia cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

(Negative dromotropic intervention)

125
Q

Conduction velocity is called

A

dromotropy

126
Q

How do Sympathetic stimulation & catecholamine speed up dromotropy?

A

phosphorylation of Ca-channels and HCN channels

127
Q

Which of the following use the sympathomimetic effect to change dromotropy?

a. hyperkaliemia
b. thyroxine
c. ischemia
d. inflammation

A

b. thyroxine

(sensitizes sympathetic receptors)

128
Q

How does hyperkaliemia effect dromotropy?

A

decrease it by inactivating calcium channels (-> inhibit AP generation and block conduction)

129
Q

How does Parasympathetic stimulation slow down the conduction velocity?

A

hyperpolarization via opening of acetylcholine regulated K-channels

130
Q

The ECG line is made by comparing which of the following?

a. inside and outside of cell
b. outside of cells from different locations

A

b. outside of cells from different locations

131
Q

During Lead III, we use two electrodes- a negative one on the left arm and a positive one the left leg. From which angle are we monitoring the heart?

a. upper angle
b. lower angle
c. side angle

A

b. lower angle

the positive electrode is the one recording

132
Q

During Lead I, we use two electrodes- a negative one on the righ arm and a positive one the left arm. From which angle are we monitoring the heart?

a. upper angle
b. lower angle
c. right side angle
d. left side angle

A

d. left side angle

133
Q

Describe a depolarization wave if we are viewing it from a perpendicular view

A

biphasic wave

134
Q

The green arrow is the sum of all dipoles of a normal patient. Your patient’s arrow is red, which is the most likely diagnosis?

a. hypertension
b. right ventricular hypertrophy
c. myocardial infarction

A

b. right ventricular hypertrophy

135
Q

The green arrow is the sum of all dipoles of a normal patient. Your patient’s arrow is red, which is the most likely diagnosis?

a. hypertension
b. right ventricular hypertrophy
c. myocardial infarction

A

a. hypertension

136
Q

Which ECG wave represents septal depolarization?

A

Q wave

137
Q

Which ECG wave represents depolarization of the ventricular base?

A

S wave

138
Q

What does the U wave of an ECG represent?

A

repolarization of purkinje fiber remnants

139
Q

What does the ST segment of an ECG represent?

A

plateau phase of AP

140
Q

What is the amplitude of the QRS complex?

A

0.7mV

(7 tiny boxes X 0.1 mV per box= 0.7mV)

141
Q

Calculate the PR interval.

A

0.12sec

(3 tiny boxes X 0.04 sec per box= 0.12sec)

142
Q

Calculate the heart rate

A

60bpm

300/5=60bpm

143
Q

Diagnose this patients ECG. Does he have any symptoms? (if yes, list them)

A

The PR segment is prolonged, but no QRS complexes are missing, this means first degree AV block.

*First-degree heart block often does not cause symptoms*

144
Q

Is this Atrial flutter or atrial fibrillation? What is the difference between the two conditions?

A

atrial fibrillation

both conditions are abnormal heart rhythms. In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles, so you may have four atrial beats to every one ventricular beat.

145
Q

diagnose

A

ventricular fibrillation

146
Q

diagnose

A

independent atrial and ventricular rhythms, so complete (third degree) AV block

147
Q

What is this ECG describes as? Diagnose it.

A

Sawtooth appearance

atrial flutter (regular but fast)

148
Q

In which direction is the septum of the heart depolarized?

A

from left to right

149
Q

What is occuring in the heart if the PR segment (also called PQ segment) is elongated?

A

AV block

150
Q

diagnose

A

Sinus tachycardia

151
Q

diagnose. Is the pause compensatory or noncompensatory? Is the SA node affected?

A

Premature ventricular complex (PVC)

The pause is compensatory and SA nose not affected (beat time didn’t change)

152
Q

How many ectopic foci are present?

A

one (atrial flutter)

153
Q

How many ectopic foci are present?

A

many foci in the atrium

154
Q

diagnose

A

Second degree heart block Type II, Mobitz II

(PR interval constant + a QRS missing)

155
Q

diagnose

A

Second degree heart block type I, Mobitz I

(PR interval prolonging + QRS missing)

156
Q

diagnose

A

2:1 block, second degree AV block

(2p waves then one QRS complex)

157
Q

diagnose

A

Third degree complete heart block

158
Q

How many ectopic foci are present?

A

one ventricular foci

(Monomorphic ventricular tachycardia)

159
Q

How many ectopic foci are present?

A

many ventricular foci

Polymorphic ventricular tachycardia

AKA Torsades de pointes

160
Q

diagnose. How many ectopic foci are present?

A

Ventricular fibrillation

many ventricular foci

161
Q

diagnose. How many ectopic foci are present?

A

Ventricular flutter

one ventricular ectopic focus

162
Q

diagnose. Is there an ectopic foci? if yes, where is it located?

A

Premature atrial complex (PAC)

ectopic foci is next to the SA node (R atrium), if it was in any other place the extra beat would be inverted

163
Q
A

couplet

164
Q
A

trigeminy

165
Q
A

bigeminy

166
Q

What is the normal resting potential of myocardial cells? What occurs to the cells when it increases to -60mV? how about -50mV?

A

normal resting potential is -85mV, the more positive the resting potential becomes the less functional the cell gets. Thats because channels get blocked.

resting potential→ -60 = less Na channel available

resting potential→ -50 = all Na channels unavailable

167
Q

Why do patients with heart disease experience arrhythmias more often?

A

Heart conditions can cause myocardial death. When the cell dies, it releases all its contents, including the potassium. That leads to a region that’s hyperkalemic, which causes the nearby myocytes to contract- thus cause arrhythmias.

(when the K increases extracellularly, the gradient between K inside and outside decreases, that causes less K from leaving the cell- and that makes it more + = partial depolarization)

168
Q

A 30 year old cannot get his heart rate to 160. What is this called?

A

Chronotropic incompetence = sinus rate does not adequately increase in response to stress or exertion (< 85% of age appropriate HR during exercise testing)

His maximum should be 190. 85% of that is 161.5

169
Q

How do you calculate the age appropriate heart rate?

A

220 - age

(if patient is 20, maximum heart rate is 200)

170
Q

What is it called when the SA node stops generating electrical impulses. How would it present in an ECG?

A

sinus arrest

No P wave in ECG

171
Q

What occurs to QRS complex when the pacemaker is in the ventricles? Why?

A

wide QRS

it’s wide because its not going through the fast Purkinje fibers

(supraventricular/arterial orgin= narrow QRS because Purkinje fibers are fast)

172
Q

When the SA node stops pacing the heart, junctional escape beats take over. Where is the focus located?

A

located in the AV junction

173
Q

The SA node of a patient stopped pacing the heart, but his heart rate is 100. How is this possible?

A

Accelerated idioventricular rhythm, a ventricular rhythm with a rate of between 40 and 120 beats per minute.

Idioventricular = ventricle alone

174
Q

suppression of all pacemaker activity occurs during

A

cardiac arrest

175
Q

What are Escape rhythms and how are they activated?

A

Normally, overdrive suppression occurs and all cells besides the SA are suppressed from exhibiting normal spontaneous depolarization. However, when the SA node is defective these cells are released from this suppression and we will get “Escape rhythms”.

(it’s a protective mechanism; ex/ Atrial escape and ventricular escape)

176
Q

Early afterdepolarizations occur due to which of the following?

a. Na/Ca exchanger
b. Ca-channels

A

b. Ca-channels

(delayed afterdepolarizations -> because of Na/Ca exchanger)

177
Q

Describe the relationship between heart rate and QT interval. What does it mean if the QT interval is too long?

A

inversely proportional

If QT is too long, means repolarization is not coming in the correct time, myocytes remain depolarized for longer time.

178
Q

How does the Na/Ca exchanger cause delayed afterdepolarization?

A

The calcium is high in the cell so the Na/Ca exchanger on plasma membrane will bring in Na and take Ca out. This exchanger is electrogenic, that is they will take 3 Na in and 2 Ca out, and this will lead to cell becoming more positive and lead to depolarization, causing the condition.

179
Q

Which gene mutation causes long QT syndrome?

A

LQT 1-17

180
Q

What is the direction of a reentry impulse coming from the atria to the ventricles via accessory pathways (bundle of Kent)? What does this type of reentry result in?

A

It moves in a counter-clockwise direction

This type of reentry results in supraventricular
tachyarrhythmia

181
Q

What is the most important thing that allows reentry impulses to occur?

A

Retrograde conduction must be slow enough to allow for the recovery of excites regions (1st degree block)

182
Q

Which of the following AV node electrical pathways has a longer refractory period?

a. fast pathway
b. slow pathway

A

a. fast pathway

183
Q

How can an atrial premature atrial beat use to create a sustained reentrant supraventricular tachycardia?

A

The impulse cannot go through the fast pathway because its still in the refractory period, so it goes to the slow pathway. It then reenters the fast pathway after the refractory period ended and retrogradely activates it.

184
Q

How do we prevent reentrant supraventricular tachycardia?

A

increase refractory period

(or restore the accessory bypass tract)

185
Q

Which of the following AV node electrical pathways conducts normal sinus beats?

a. fast pathway
b. slow pathway

A

a. fast pathway

186
Q

Which condition causes murmurs to start at the beginning of systole and continues throughout diastole?

A

Patent ductus arteriosus

187
Q

In which stage are the semilunar valves open?

a. diastole
b. systole

A

b. systole

188
Q

In which stage does the blood flow out of the ventricles?

a. diastole
b. systole

A

b. systole

189
Q

T/F: blood flow from the ventricles is continuous

A

false, its pulsatile

190
Q

T/F: blood flow to the body is continuous

A

true, this is due to aortic storage

191
Q

When do the atria contract?

A

at the end of ventricular filling, phase 1 in the cardiac cycle

192
Q

How long does the cardiac cycle last? (in 75bpm) and how is it divided into systole and diastole?

A
  1. 8sec per cycle
  2. 5 diastole and 0.3 systole
193
Q

How do you calculate stroke volume?

A

EDV - ESV=SV

EDV= end diastolic volume (the max amount of blood in the heart)

ESV= end systolic volume (the one third of blood left in the ventricle after ejection)

194
Q

When does ventricular ejection begin?

A

When the left ventricle pressure is higher than the aortic pressure

195
Q

When do the semilunar valves close?

A

When the atrial pressure is higher than ventricular pressure

196
Q

When do the AV valves open?

A

when ventricular pressure is bellow atrial pressure

197
Q

What sound is made when the AV valves close?

a. lub
b. dub

A

a. lub

(S1)

198
Q

During isovolumic/isovolumetric contraction, what occurs to pressure and volume?

A

increase in pressure

no change in volume

199
Q

During rapid ejection of the ventricles, what is happening in the atria?

A

the pressure begins to rise as blood fills it

200
Q

What heart sounds can be heart in children?

A

S1, S2, S3 (S3 because their ventricles are smaller and more compliant, not due to pathology)

201
Q

Why does the S3 heart sound (aka ventricular gallop) occur?

A

The S3 sound is produced by a large amount of blood striking a very compliant left ventricle.

S3= often a sign of systolic heart failure

Heard in: congestive heart failure+dilated cardiomyopathy

(it’s also heard normally in children and well-trained athletes because of the compliance of the ventricles)

202
Q

Why does the S4 heart sound (aka atrial gallop) occur?

A

If the left ventricle is noncompliant, and atrial contraction forces blood through the AV valves, S4 sound is produced by the blood striking the left ventricle.

S4 = sign of diastolic heart failure

Heard in: left ventricular hypertrophy or any condition that makes the ventricles stiffer

(very rarely occurs in normal conditions, unlike S3)

203
Q

Which phase of the cardiac cycle does the AV valves close?

A

phase 2

(Isovolumic contraction)

204
Q

Which phase of the cardiac cycle do the semilunar valves open?

A

phase 3

205
Q

What causes the blood flow to continue from the ventricle to the aorta?

A

Kinetic energy (this occurs during reduced ejection- which is phase 4- not rapid ejection)

206
Q

Which phase of the cardiac cycle do the AV valves open?

A

phase 6

207
Q

What conditions cause holosystolic (pansystolic) murmurs?

A

mitral/tricuspid regurgitation + ventricular septal defect

holosystolic= high amplitude throughout systole

208
Q

Which condition causes mid-systolic murmurs?

A

aortic or pulmonic stenosis

mid-systolic murmurs= starts softly and become loudest near mid-systole then decrease

211
Q

What percent of the ventricular filling is due to the atrial kick when patient is at rest VS during exercise?

A

At rest, the atrial kick is responsible to 20% but during exercise it does up to 40%

212
Q

Which 2 areas reach maximum systolic pressure?

A

aorta and pulmonary artery

213
Q

When does isovolumetric relaxation occur?

A

at the beginning of diastole, phase 5

214
Q

Systolic murmurs versus Diastolic murmurs

A

Systolic murmurs= occur between S1 and S2

Diastolic murmurs= occur after S2

215
Q

Which of the following causes a mid/ late diastolic murmur?

a. aortic stenosis
b. pulmonic stenosis
c. mitral stenosis

A

c. mitral stenosis

(A&B cause mid-systolic murmur)

216
Q

Which of the following causes a diastolic murmur?

a. mitral regurgitation
b. aortic regurgitation
c. tricuspid regurgitation

A

b. aortic regurgitation

(A&B= Holosystolic murmur)

217
Q

Describe the relationship between preload and stroke volume

A

directly proportional

218
Q

Describe the relationship between afterload and stroke volume

A

inversely proportional

wide aorta→ high afterload → low aortic pressure → low stroke volume

narrow aorta→low afterload→high aortic pressure→high SV

219
Q

How is the force of contraction determined?

A

preload and inotropy

220
Q

When does preload = end-diastolic volume?

A

right before contraction, the start of systole

221
Q

What increases VS decreases preload?

A

increase= fluids (they increase ventricular stretch)

decrease= diuretics (less water, less volume, less stretch)

222
Q

relationship between venous return and preload

A

directly proportional (duh)

223
Q

Describe what occurs to stroke volume when the aorta is more compliant.

A

the stoke volume increases

SV= EDV - ESV (original)

↑SV= EDV - ↓ESV

(the SV increased by decreasing the end-systolic volume, which is the volume of blood in a ventricle at the end of contraction/systole. The ventricle was able to push more blood out since the aorta is compliant, so it had less blood left at the end)

224
Q

Describe the effect of increased venous return on the stroke volume.

A

increased venous return → increase stretch of cardiomyocytes → increases the preload → increase SV

225
Q

explain why the stroke volume is unable to make a remarkable increase after a certain point?

A

the pericardium that acts to protect the heart stops in from stretching further. (stops the linear relationship between SV and preload)

227
Q

How can stroke volume increase without EDP or preload increase?

A

the contractility of the ventricles (inotropy) may change and directly increase the SV, while the preload and EDP remain unchanged.

***length independent SV increase***

228
Q

T/F: more overlap between myosin and actin always means stronger contraction

A

false, when there’s complete overlap or no overlap the contraction power will be decreased

230
Q

Using what mechanism does contractility change?

A

via Ca channels

Ca comes in from extracellular space (in phase 2)

Ca increases when it comes from the sarcoplasmic reticulum

troponin C sensitivity to Ca is increased

231
Q

Describe the relationship between afterload and stroke volume

A

inversely proportional

(more afterload more resistance against ejection, less stroke volume)

232
Q

Which of the following points is when the aortic valve closes?

A

1

233
Q

Which of the following points is when the mitral valve opens?

A

3

234
Q

In of the following intervala is when ventricular filling occurs?

A

D

235
Q

In of the following intervals is when isovolumic contraction occurs?

A

C

236
Q

Which of the following points is preload?

A

4

237
Q

Which of the following points is afterload?

A

2

238
Q

What occurs when the pressure-volume loop is shifted to the left?

A

reduced end systolic volume

increased SV

increased inotropy

239
Q

What occurs when the pressure-volume loop is shifted to the right?

A

increase end-systolic volume

increase end-diastolic volume

increase afterload

(this heart is a failing/dilated heart)

240
Q

How does increasing afterload decrease stroke volume?

A

by increasing the end-systolic volume (it increases because of higher resistance, lower shortening speed, more energy needed to open aortic vales, etc.)

SV= EDV - ESV (original)

↓SV= EDV - ↑ESV

(the ESV increases along with afterload, decreasing SV)

241
Q

T/F: increasing the afterload decreases the cardiac output of every heart equally

A

False; cardiac output (CO) of a healthy heart isn’t as affected as the CO of a heart with dysfunction

(more dysfunction in heart = more CO decrease when afterload increases)

250
Q

What occurs to cardiac efficiency with less oxygen uptake?

A

increased efficiency

CE = CW/O2uptake

(CE= cardiac efficiency)

(CW= cardiac work)

251
Q

Which ventricle has higher cardiac work?

A

left ventricle

252
Q

How does aortic stenosis affect cardiac efficiency?

A

aortic stenosis increases the pressure, and that increases the stroke work. Stroke work is directly proportional to O2 consumption. Higher O2 consumption decreases cardiac efficiency.

↑SW = SV x ↑MAP

↑ SW= ↑ O2 demand

↓CE = CW/ ↑O2uptake

253
Q

Dihydropyridine channels are also known as

A

L-type calcium channels

254
Q

T/F: pacemaker cells don’t have sarcomeres

A

true

255
Q

What induces Ca release from ryanodine receptor channels?

A

Ca entering from outside the cell via voltage gates Ca channels

256
Q

Where are gap junctions of myocytes located?

A

at the intercalated disc

257
Q

How can the autonomic nervous system release hormones to increase heart rate?

A

they release epinephrine and norepinephrine, which activate beta 1 adrenergic receptors and act to increase the rate and strength of contractility (HOW? by increasing Ca current, release and reuptake)

258
Q

What two things determine contractile force?

A

intracellular Ca concentration

sarcomere length

259
Q

What are the three factors that control the number of cross-bridge activation?

(number of cross-bridge activation determines…?)

A

Ca concentration

troponin C to Ca affinity

Number of sarcomeres present

(number of cross-bridge activation determines the force of contraction)

260
Q

What controls the troponin C to Ca affinity?

A

the autonomic nervous system

the stretch (of cardiac muscle)

261
Q

Why is the force of contraction reduced in the cardiac muscle of older patients?

A

the force of contraction depends on the number of active cross bridges, and the number of cross-bridges depend on the number of sarcomeres present. Older patients have fewer sarcomeres due to apoptosis.

262
Q

We stated that the stretch of cardiac muscle gives the optimal overlap between actin and myosin, this causes the length-dependent change in troponin sensitivity. What law/mechanism does this showcase?

A

frank-starling law

263
Q

How does the frank starling law explain the lower resting heart rate observed in athletes?

A

they have longer sarcomeres, so each contraction produced is stronger and results in higher stroke volume. (so the heart doesn’t have to work as hard)

264
Q

Explain the link between end-diastolic volume and contractility

A

When EDV is high, the heart is maximally filled, which stretches the heart and increases contractility

265
Q

Explain the relationship between increased heart rate and…

1- filling time

2- stroke volume

3- cardiac output

A

When heart rate increases, the filling time decreases (not enough time for blood to go in maximally)

Because there’s not enough blood inside the heart when it contracts, the stroke volume decreases. HOWEVER, the stroke volumes per minute increase (less stroke volume, but more of them… quantity over quality).

This explains how cardiac output increases, due to the increase in number not the increase in volume. **this is true when when heart rate is 80-150bpm**

266
Q

Explain how age and stroke volume are related.

A

the greater the age the lower the stroke volume. This is due to the arteries losing their compliance and not being able to hold as much blood. This causes the venous return to decrease, which decreases stretch and stroke volume.

267
Q

How does high end systolic volume (ESV) change stroke volume in normal hearts versus in failing hearts?

A

when ESV is high (more blood left over in heart after contraction) the normal heart stretches, which increases contactility and thus stroke volume.

when ESV is high in a failing/dilated heart, the contractility and stroke volume are unchanged because the overlap in actin and myosin is decreased.

(remember= dilated/failing/systolic failure heart decreases contractility)

268
Q

What does inotropy depend on?

A

The entry of external calcium by L-type Ca-channels

Calcium release from sarcoplasmic reticulum (CICRC)

TnC affinity to calcium

269
Q

T/F: sympathetic activity speeds up the hearts contraction and slows down its relaxation

A

false, it speeds up both contraction and relaxation, that’s how it increases heart rate

(Ca release from L type channels and ryanodine receptors and Ca reuptake from SERCA is sped up)

270
Q

How does systolic failure and increased afterload affect inotropy?

A

systolic failure = heart cannot contract well so it lowers inotropy

increased afterload = increased pressure makes the heart push harder to counteract it, so increased inotropy

271
Q

Which most accurately describes positive inotropy changes the ventricle curve shift?

A

B

Higher stroke volume without a change in diastolic pressure

272
Q

Explain the Staircase phenomenon aka Treppe effect

A

As the time interval between each beat gets shorter, the Ca has no time to decrease (go to SR) so it builds up. That means the higher the heart rate increases, the calcium builds up (higher tension) until it hits a plateau.

(with each beat, the calcium levels get higher and higher- stair case/treppe- until maximum heart rate is reached)

273
Q

What is it called when the heart skips a beat? Explain why the force of the beat after the pause is greater than the rest.

A

heart skips beat= potentiation

the force is increased because of both frank starling mechanism and inotropy. frank s because during the missed beat, the blood filled the heart more, which caused increase in length. inotropy because the calcium levels accumulated causing a higher contractility.

274
Q

What mechanism/law causes the change from point A to point B?

A

higher inotropy

(or lower afterload?)

275
Q

What mechanism/law causes the change from point A to point B?

A

frank starling

276
Q

After an increase in venous pressure, where would the operational point be?

A

Point B, EDP would increase. Frank starling law.

283
Q

Which has a lower efficiency? explain.

a. inotropy
b. frank starling

A

b. frank starling

because it causes a larger ventricular volume, and that would cause an increase in oxygen consumption = lower efficiency

284
Q

Which has a greater effect on heart rate, parasympathetic or sympathetic system?

A

parasympathetic. When we block the parasympathetic effect with atropine, there’s much more of a drastic change than when we block the sympathetic system with propanolol.

285
Q

Which increases stroke volume by decreasing the end systolic volume?

a. inotropy
b. frank starling

A

a. inotropy

286
Q

Which has beat to beat adjustments?

a. inotropy
b. frank starling

A

b. frank starling

287
Q

Explain how inotropy makes adjustments/adaptations.

A

it adapts based on large hemodynamic changes. So, after a strong contraction, the ESV decreases and thus increases SV. Over time, the stroke volume goes through the body and comes back to the heart and (slightly) increases the ESV. In exercise, this becomes more apparent (because the changes would be bigger).

288
Q

A 140-150 bpm, describe the relationship between heart rate and cardiac output. Why?

A

directly proportional

from 80-150bpm: when the heart rate increases, the stroke volumes decreases (cuz less filling time) BUT the stroke volume per minute increase and compensate for that fact… so CO increases

(more SV’s > less volume in the SV’s)

289
Q

A 150-170 bpm, describe the relationship between heart rate and cardiac output.

A

inversely proportional

from 150bpm and above: when the heart rate increases, the stroke volumes decreases (cuz less filling time) AND the stroke volume per minute increase but cannot compensate for that fact… so CO decreases

(more SV’s

290
Q

At which heart rate does the atrial pressure start to increase?

A

at 150bpm, there isn’t enough time for the ventricles to fill up with blood between each contraction (decreased filling time), that means that the extra blood gets stuck in the atria and increase their pressure

292
Q

How does the heart rate get affected by Ca concentrations, K concentrations, and pH?

A

↑Ca= ↑HR (hypercalemia)

↑K= ↓HR (hyperkalemia)

↑pH=↑HR (alkalosis)

293
Q

T/F: a hypertrophic heart is hypoeffective

A

false; this is not always the case. A physiologically hypertrophic heart is hyperreflective while a pathologically hypertrophic heart is hypoeffective

295
Q

T/F: cardiac output of elders is decreased mainly due to the increase stiffness of vessels

A

false, its mainly due to the higher surface area

296
Q

How do you correct the cardiac output to body size?

A

divide it by body surface area

CO/BSA = cardiac index (the corrected CO)

297
Q

Which two reflexes are located on the aortic arch and carotid sinus?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

a. Baroreceptor reflex

+

c. Chemoreceptor reflex

298
Q

Which reflexes detect stretch?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

a. Baroreceptor reflex

+

b. Cardiopulmonary reflex

299
Q

Which reflex detects CO and O2 levels?

a. Baroreceptor reflex
b. Cardiopulmonary reflex
c. Chemoreceptor reflex

A

c. Chemoreceptor reflex

300
Q

How does the expiration affect venous return?

A

Exhaling increases intrathoracic pressure (abdominal pressure low in comparison) so the venous return is lowered

301
Q

Explain how increased resistance decreases stroke volume

A

more resistance means less venous return. less venous return means less CO, and that means less stoke volume.

(keep in mind that the area where CO and venous return cross is SV)

302
Q

What’s the relationship between total peripheral resistance and stroke volume

A

inversely proportional

(EX/ patient has hypertension, that increases resistance and decreases SV)

304
Q

When contractility increases, what occurs to SV, EDV, and ESV?

A

SV increases

EDV increases

ESV decreases

305
Q

How does the heart adjust to increased peripheral resistance?

A

↑ resistance

↓ SV

↑ EDV

↑stretching

↑force

306
Q

What occurs to stoke volume and venous return when central venous pressure increases?

A

the central venous pressure increases, pushing the blood to both sides: the heart and the periphery.

↑ stroke volume

↓ venous return

307
Q

How do you calculate venous return?

A

(peripheral venous pressure - central venous pressure)/venous resistance

308
Q

Describe the relationship between central venous pressure and venous return

A

inversely proportional

309
Q

What is the normal level of central venous pressure, cardiac output, and venous return?

A

CVP= 2

CO/venous return=5

(CO/venous have to be equal for no change to occur)

310
Q

Explain the events that must occur for central venous pressure to go from a high pressure back to a normal pressure.

A

high CVP means that venous return is low and cardiac function is high. The CO would work hard to push the blood out harder until the pressure is evened out, leading the venous pressure is to get back to normal (=to CO)

changes in central venous pressure go to an automatical adjustment

311
Q

What is cardiac tamponade? Which phase of the cardiac cycle does it affect? What can it lead to?

A

cardiac tamponade is when blood fills the pericardial sac. This compresses the heart and reduces the filling/stretching of the left ventricle (diastole affected). The right heart is also compressed so atrial pressure increases, which causes the blood to back up into the veins (blood in veins increase, distended jugular vein). Because the L ventricle isn’t taking enough blood, so the blood stagnates in the lung and causes pulmonary edema.

312
Q

Assuming the red point is the normal intersection point, which point represents what occurs in heart failure? explain.

A

point A

When heart failure occurs, ↓SV and ↓CO, which would drag the cardiac function curve downwards. This change increases the central venous pressure.

313
Q

Which point would the red dot shift to when the sympathetic stimulation increases? explain.

A

point H

The sympathetic stimulation increases contractility and CO, so the cardiac function curve increases.

(now it gets confusing) Venous constriction is also activated by the sympathetic stimulation, and that decreases compliance and increases CVP (it looks like it decreases in the graph? and in class he said CVP doesn’t change)

314
Q

Where does the red point shift during hemorrhage?

A

point B

↓CO because ↓venous return, so ↓CVP

315
Q

What occurs when you breathe against a closed glottis?

A

Valsalva maneuver. The intrapleural pressure increases and reduces ventricular return. Less venous return leads to less SV and CO.

316
Q

During cardiac failure, how does the body compensate?

A

by increasing blood volume via vasoconstriction. This decreases compliance and increases venous resistance

(point C moves to point D, decreasing the right arterial pressure and central pressure.)

317
Q

Explain how the therapeutic interventions given improve cardiac function (in heart failure) work.

EX/ beta adrenergic receptors blockers, ANG II receptor blockers, ACE inhibitors and aldosterone receptor antagonists.

A

they function by increasing the venous resistance and decreasing central venous pressure to maintain the venous gradient.

** moves shifts the venous curve to the right **

318
Q

What two things increase venous pressure?

A

higher blood volume

vasoconstriction

322
Q

Explain how expiration affects SV

A

when we expire, the diaphragm rises and the pressure in the thorax increases. This compresses the right atrium and ventricle, decreasing CO+SV.

The venous return decreases because the pressure gradient between the peripheral venous pressure and central venous pressure has decreased

CVS (13 decks)

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