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STEP 1 (2) > Cardiovascular- Anatomy and Physiology > Flashcards

Cardiovascular- Anatomy and Physiology Flashcards

1
Q
A
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2
Q

What artery supplies the right ventricle?

A

right (acute) marginal artery

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3
Q

What artery supplies the SA and AV node?

A

the right coronary a. (note that RCA infarct can cause complete heart block)

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4
Q

What are the main branches of the left main coronary a.?

A
  • left circumflex coronary a. (LCX)
  • left anterior descending a. (LAD)
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5
Q

What does the LCX supply?

A

the lateral and posterior walls of the left ventricle and the anterolateral papillary muscles

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6
Q

What does the LAD supply?

A

the anterior 2/3rds of the interventricular septum, anterolateral papillary muscle, and the anterior surface of the left ventricle

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7
Q

The majority (85%) of people are ‘right-heart dominant’. What does this mean?

A

the PDA (posterior descending a.) arises from the RCA

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8
Q

What does left-heart dominant mean?

A

the PDA arises from the LCX (co-dominant= arises from the LCX and the RCA)

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9
Q

Coronary artery occlusion most commonly occurs where?

A

LAD

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10
Q

When does coronary artery blood flow peak?

A

early diastole

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11
Q

Enlargement of what part of the heart is associated with dysphagia due to compression of the esophagus or hoarseness due to compression of the left recurrent laryngeal nerve?

A

the most posterior part, the left atrium

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12
Q

What is the eqn for CO?

A

HR X SV or via the Fick principle:

CO= rate of O2 consumption/ (arterial O2 content- venous O2 content)

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13
Q

What is the eqn for mean arterial pressure?

A

CO x TPR, or

MAP= 2/3 diastolic pressure + 1/3 systolic pressure

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14
Q

What is pulse pressure?

A
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15
Q

What is the eqn for SV?

A

end diastolic volume - end systolic volume

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16
Q

How does SV and HR change during exercise?

A

during the early stages of exercise, both HR and SV increase, and eventually SV plateaus

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17
Q

What are some things associated with increased pulse pressure?

A
  • hyperthyroidism
  • aortic regurg
  • aortic stiffening
  • obstructive sleep apnea
  • exercise (transient)
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18
Q

Isolated increased systolic pressure in the elderly suggests what?

A

aortic stiffening

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19
Q

What are some things associated with decreased pulse pressure?

A
  • aortic stenosis
  • cardiogenic shock
  • cardiac tamponade
  • heart failure
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20
Q

What are the three variables that affect stroke volume?

A
  • contractility
  • preload and afterload
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21
Q

What things increase contractility?

A
  • catecholamines (increase the activity of SR Ca2+ pumps)
  • increased intracellular Ca2+
  • decreased extracellular Na+ (via decreased activity of the Na/Ca2+ pump)
  • Digitalis
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22
Q

How does digitalis increase contractility?

A

by blocking Na/K pumps leading to increased intracellular Na+, decreasing Na/Ca exchanger activity, and thus leading to elevated levels of Ca2+

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23
Q

What are some things that decrease contractility?

A
  • B1-blockade (decreased cAMP)
  • acidosis
  • acidosis
  • hypoxia/hypercapnia
  • non-dihydropyridine CCBs
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24
Q

What are some things that increase myocardial oxygen demand?

A
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25
Q

What is the eqn for cardiac wall tension (aka thickness)?

A

WT= (pressure*radius)/(2*wall thickness)

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26
Q

Venodilators such as nitroglycerin ______ preload

A

decrease

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27
Q

How does the left ventricle compensate to increased afterload?

A

by thickening to decrease wall tension

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28
Q

Vasodilators such as hydralazine ______ afterload

A

decrease

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29
Q

How do ACEIs and ARBs affect pre- and afterload?

A

they decrease both

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30
Q

What is the eqn for equation fraction?

A

SV/EDV= (EDV- ESV)/EDV

Normal EF = 55+%

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31
Q

How is EF affected by systolic HF? diastolic HF?

A

systolic HF: decreased

diastolic HF: normal

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32
Q

What is inotropy?

A

An inotrope is an agent that alters the force or energy (aka contractility) of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents (e.g. digoxin) increase the strength of muscular contraction.

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33
Q

Contractility is proportional to what?

A

the end-diastolic length of cardiac muscle fibers (aka preload)

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34
Q

How does organ removal affect TPR and CO?

A

it increases TPR and decreases CO

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35
Q

_______ account for most of TPR

A

Arterioles

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36
Q

What is the period of heart contraction with the highest O2 consumption?

A

isovolumetric contraction

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37
Q

What is S1?

A

mitral and tricuspid valve closure. Loudest at the mitral area

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38
Q

When does S1 occur?

A

at the start of isovolumetric contraction

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39
Q

What is S2?

A

closure of the aortic and pulmonary valves

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40
Q

When does S2 occur?

A

at the end of systolic ejection when the aortic pressure generated becomes higher than that of the left ventricle

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41
Q

Where is S2 best heard?

A

left upper sternal border

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42
Q

When is S3 heard (pathologic)?

A

in early diastole during the rapid ventricular filling phase

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43
Q

What things cause an S3?

A

associated with increased filling pressure (e.g. mitral regurg, HF) and more common in dilated ventricles (but normal in children and pregnant women)

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44
Q

When is S4 heard (pathologic)?

A

in late diastole (aka atrial kick)

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45
Q

Where is S4 best heard?

A

at the apex with the pt. left lateral decubitus

46
Q

What things cause an S4?

A

high ventricular pressure/hypertrophy

47
Q
A
48
Q

What causes the ‘a’ wave of jugular venous pulse?

A

atrial contraction (absent in a fib)

49
Q

What causes the ‘c’ wave of jugular venous pulse?

A

RV contraction (closed tricuspid valve bulging into the atrium)

50
Q

What causes the ‘x’ descent of jugular venous pulse?

A

atrial relaxation and downward displacement of the closed tricuspid valve during ventricular contraction (absent in tricuspid regurg)

51
Q

What causes the ‘v’ wave of jugular venous pulse?

A

increased right atrial pressure due to filling against a closed tricuspid valve

52
Q

Splitting pg 277

A

Splitting pg 277

53
Q

Describe the murmur of aortic stenosis

A

It is a crescendo-descrendo systolic ejection murmur (between S1 and S2) caused by LV pressure being higher than aortic pressure during systole

54
Q

Where is aortic stenosis best heard?

A

at the heart base; radiates to the carotids

55
Q

A common finding with aortic stenosis is ________

A

pulsus parvus el tardus (pulses are weak and delayed)

56
Q

What is the most common cause of aortic stenosis?

A

age-related calcification or early-onset calcification of bicuspid aortic valves

57
Q

Describe the murmur of mitral/tricuspid regurg

A

It is a holosystolic, high-pitched ‘blowing’ murmur

58
Q

Where is a mitral regurg murmur best heard?

A

at the apex and radiates toward the axilla

59
Q

What commonly causes mitral valve regurg?

A

ischemic heart disease (post-MI) or LV dilation

60
Q

Where is a tricuspid mumur best heard?

A

the tricuspid area- 5th right intercostal space at the sternal border

61
Q

_________ and ________ can cause either MR or TR

A

Rheumatic fever and infective endocarditis

62
Q

Describe the murmur of mitral valve prolapse

A

it is a late systolic crescendo (building) murmur with a midsystolic click (this is the most common valvular lesion)

63
Q

What causes the midsystolic click in mitral valve prolapse?

A

sudden tensing of chordae tendineae

64
Q

Where is MVP best heard?

A

over the apex

65
Q

What are some common causes of MVP?

A

-myxomatous degeneration (primary or secondary to CT disease such as Marfan or Ehlers-Danlos syndrome)

rheumatic fever

chordae rupture

66
Q

Describe the murmur of a VSD

A

It is a holosystolic, harsh-sounding murmur

67
Q

Where is a VSD murmur best heard?

A

the tricuspid area

68
Q

Describe aortic regurg murmurs

A

it is a high-pitched, ‘blowing’ early diastolic (right after S2) descrescendo murmur

69
Q

What is the other murmur heard in diastole (after S2) besides aortic regurg?

A

mitral stenosis

70
Q

Describe a mitral stenosis murmur

A

It follows opening snap after S2 with a delayed rumbling late diastolic murmur

71
Q

T or F. Decreased interval between S2 and OS in mitral stenosis correlates with increasing severity

A

T.

72
Q

Describe the murmur of a PDA

A

It is a continuous (systolic and diastolic- only one) machine-like murmur loudest at S2

73
Q

Where is a PDA murmur best heard?

A

the left infraclavicular area

74
Q

A PDA murmur commonly arises after what?

A

congenital rubella or prematurity

75
Q

What is the resting potential of a myocardial cell?

A

-85 mV

76
Q

Describe Phase 0 of the myocardial action potential

A

rapid upstroke and depolarization as voltage-gated Na+ channels open and Na+ influx into the cell

77
Q

Describe Phase 1 of the myocardial action potential

A

Initial reploarization caused by inactivation of voltage-gated Na+ channels and opening of some K+ channels

78
Q

Describe Phase 2 of the myocardial action potential

A

plateua phase, in which Ca2+ influx balances K+ efflux / Ca2+ influx riggers additional Ca2+ release from the SR and myocyte contraction

79
Q

Describe Phase 3 of the myocardial action potential

A

Padily repolarization due to massive K+ efflux

80
Q

Describe Phase 0 of SA/AV node action potentials

A

initial depolarization/upstroke once the nodes reach a potential of -40mV due to opening of voltage-gated Ca2+ channels

81
Q

Why are fast volatge-gated Na+ channels inactive in the SA/AV nodes?

A

because of the less negative resting voltage of these cells. This results in a slow conduction velocity that is used by the nodes to prolong transmission from the atria to the ventricles

82
Q

Phases 1 and 2 are absent in the SA/AV nodes. Describe Phase 3

A

inactivation of Ica2+ channels and activation of K+ channes causes K+ efflux and repolarization back to a potential around -65mV

83
Q

Describe Phase 4 of the AV/SA action potential

A

this is a slow spontaneous diastolic depolarization as Na+ conductance increases due to If channels (aka ‘funny current channels’)- this accounts for the autmaticity of the nodes

84
Q

What determines HR?

A

the slope of phase 4 in the SA node

85
Q
A
86
Q

What is occurring during the P wave of the EKG curve?

A

atrial depolarization

87
Q

Why is atrial REpolarization not seen on an EKG curve?

A

it is masked by the QRS complex

88
Q

What does the PR interval represent?

A

the time from the start of atrial depolarization to the start of ventricular depolarization, normally less than 200 ms

89
Q

What does the QRS complex represent and what is the normal length?

A

ventricular depolarization; 120msec

90
Q

What does the QT interval represent?

A

the time for:

ventricular depolarization, contraction, and repolarization

91
Q

What does the T wave represent and what would an inverted T wave suggest?

A

ventricular repolarization; recent MI

92
Q

What would an additional ‘U’ wave after the T wave suggest?

A

caused by hypokalemia or bradycardia

93
Q

What is the conduction pathway of the heart?

A

SA node -> atria -> AV node -> common bundle -> bundle branches -> fascicles/Purkinje fibers -> ventricles

94
Q

What parts of the conduction pathway move the fastest?

A

Purkinje > atria > ventricles > AV node

95
Q

What is the blood supply to the AV node?

A

RCA

96
Q

What is this?

A

Torsades de pointes- venticular tachycardia (can progress to v. fib)

97
Q

What predisposes to TDP?

A

long QT interval

98
Q

What drugs can cause an elongated QT interval?

A

ABCDE

AntiArrhythmics (clas IA, III)

AntiBiotics (e.g. macrolides)

Anti”C“ychotics (e.g. haloperidol)

AntiDepressants (e.g. TCAs)

AntiEmetics (e.g. ondansetron)

99
Q

What is Congenital long QT syndrome?

A

inherited disorder of myocardial reploarization, typically due to ion channel defects. Includes:

Romano-Ward Syndrome and Jervell and Lange-Neilson Syndrome

100
Q

What is the difference between Romano-Ward Syndrome and Jervell and Lange-Neilson Syndrome?

A

Romano-Ward Syndrome is AD with no deafness

Jervell and Lange-Neilson Syndrome is AR with sensorineural deafness

101
Q

What is Brugada Syndrome?

A

an AD disorder that presents with an ECG pattern of pseduo-right bundle branch block and ST elevation in V1-V3

102
Q

Brugada syndrome is particularly common in _______

A

Asian males

103
Q

What is this?

A

Wolff-Parkinson-White Syndrome

104
Q

What causes Wolff-Parkinson-White Syndrome?

A

Abnormally fast accessory conduction pathway from the atria to venticles through the bundle of Kent, which bypasses the slow V node, causing the venticles to begin partially depolarizing earlier giving rise to the characteristic DELTA WAVE

105
Q

The worst potential sequelae of WPW is _______

A

may result in a reentry circuit causing supraventicular tachycardia

106
Q

Changes in BP are sensed by a series of chemo, baro, and mechanoreceptors in the periphery. How do the aortic arch receptors work?

A

they transmit via the vagus nerve to the solitary nucleus of the medulla in response to changes in BP

107
Q

How does the carotid sinus transmit to the solitary nucleus of the medulla in response to changes in BP?

A

via the glossopharyngeal n.

108
Q

How do baroreceptors (like those found on the aortic arch and the carotid sinus) work?

A

they sense hypotension which decreased baroreceptor firing while increasing sympathetic firing to cause vasoconstriction, increased HR and contractility.

109
Q

What occurs during a ‘carotid massage’?

A

pressure on the carotid sinus increased afferant baroreceptor firing, which increased the AV node refractory period, decreasing HR

110
Q

What is the classic triad of a Cushing rxn?

A

HTN, bradycardia, and respiratory depression

111
Q

What causes a Cushing rxn?

A

increased intracranial pressure constricts arterioles leading to cerebral ischemia and increased pCO2 (leading to acidosis). This causes the central CNS to increase sympathetics causing HTN which then causes a peripheral-reflex baroreceptor-induced bradycardia

112
Q
A

STEP 1 (2) (16 decks)

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