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Step 1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Truncus arteriosus

A

Ascending aorta and pulmonary trunk

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2
Q

Bulbus cordis

A

Smooth parts (outflow tract) of left and right ventricles

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3
Q

Endocardial cushion

A
  • Atrial septum, membranous interventricular septum

- AV and semilunar valves

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4
Q

Primitive atrium

A

Trabeculated part of left and right atria

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5
Q

Primitive ventricle

A

Trabeculated part of left and right ventricles

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6
Q

Primitive pulmonary vein

A

Smooth part of left atrium

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7
Q

Left horn of sinus venosus

A

Coronary sinus

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8
Q

Right horn of sinus venosus

A

Smooth part of right atrium (sinus venarum)

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9
Q

Right common cardinal vein and right anterior cardinal vein

A

Superior vena cava

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10
Q

Heart begins to beat spontaneously at

A

Week 4 of development

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11
Q

Cardiac looping

A
  • Primary heart tube loops to establish left-right polarity
  • Begins in week 4 of gestation
  • Defect in left-right dynein (involved in L/R asymmetry) can lead to dextrocardia, as seen in Kartagener syndrome (primary ciliary dyskinesia)
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12
Q

Conotruncal abnormalities associated with failure of neural crest cells to migrate

A
  • Transposition of great vessels
  • Tetralogy of Fallot
  • Persistent truncus arteriosus
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13
Q

What causes a patent foramen ovale

A
  • Caused by a failure of septum primum and septum secundum to fuse after birth
  • Most are left untreated
  • Can lead to paradoxical emboli, similar to those resulting from ASD
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14
Q

Where do ventricular septal defects usually occur

A
  • Usually occurs in membranous septum

- Most common congenital cardiac anomaly

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15
Q

Allantois → urachus

A
  • Median umbilical ligament

- Urachus is part of allantoic duct between the bladder and umbilicus

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16
Q

Ductus arteriosus

A

Ligamentum arteriosum

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17
Q

Ductus venosus

A

Ligamentum venosum

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18
Q

Foramen ovale

A

Fossa ovalis

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19
Q

Notochord

A

Nucleus pulposus

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20
Q

Umbilical arteries

A

Medial umbilical ligaments

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21
Q

Umbilical vein

A
  • Ligamentum teres hepatis

- Contained in falciform ligament

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22
Q

3 layers of pericardium

A
  • Fibrous pericardium
  • Parietal layer of serous pericardium
  • Visceral layer of serous pericardium
  • Pericardial cavity lies between parietal and visceral layers
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23
Q

CO during exercise

A
  • EARLY: CO is maintained by ↑ HR and ↑ SV

- LATE: CO is maintained by ↑ HR only (SV plateaus)

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24
Q

With ↑ HR, what becomes preferentially shortened

A
  • Diastole is preferentially shortened with ↑ HR

- Less filling time → ↓ CO (eg ventricular tachycardia)

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25
Q

Conditions that ↑ pulse pressure

A
  • Hyperthyroidism
  • Aortic regurgitation
  • Aortic stiffening (isolated systolic hypertension in elderly)
  • Obstructive sleep apnea (↑ sympathetic tone)
  • Exercise (transient)
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26
Q

Conditions that ↓ pulse pressure

A
  • Aortic stenosis
  • Cardiogenic shock
  • Cardiac tamponade
  • Advanced heart failure
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27
Q

Ejection fraction in diastolic vs systolic heart failure

A
  • ↓ in systolic HF

- Normal in diastolic HF

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28
Q

How does the left ventricle compensate for ↑ afterload

A

LV compensates for ↑ afterload by thickening (hypertrophy) in order to ↓ wall tension

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29
Q

Force of contraction is proportional to

A

End diastolic length of cardiac muscle fiber (preload)

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30
Q

What do AV shunts do to total peripheral resistance and cardiac output

A

AV shunts ↑ CO and ↓ TPR

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31
Q

Which phase of the cardiac cycle consumes the most O2

A

Isovolumetric contraction is the period of highest O2 consumption

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32
Q

S1

A
  • Mitral and tricuspid valve closure

- Loudest at mitral area

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33
Q

S2

A
  • Aortic and pulmonary valve closure

- Loudest at left upper sternal border

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34
Q

S3

A
  • Early diastole during rapid ventricular filling phase
  • Associated with ↑ filling pressures (eg mitral regurgitation, HF)
  • More common in dilated ventricles (can be normal in children and young adults)
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35
Q

S4

A
  • Late diastole (“atrial kick”)
  • Best heart at apex with patient in left lateral decubitus position
  • High atrial pressure
  • Associated with ventricular noncompliance (eg hypertrophy)
  • Left atrium must push against stiff LV wall
  • Considered abnormal, regardless of patient age
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36
Q

Order of jugular venous pulse

A

a wave → c wave → x descent → v wave → y descent

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37
Q

a wave

A
  • Atrial contraction

- Absent in atrial fibrillation

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38
Q

c wave

A

RV contraction (closed tricuspid valve bulging into atrium)

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39
Q

x descent

A
  • Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
  • Absent in tricuspid regurgitation
  • Prominent in tricuspid insufficiency and right HF
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40
Q

v wave

A

↑ right atrial pressure due to filling against closed tricuspid valve

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41
Q

y descent

A
  • RA emptying into RV
  • Prominent in constrictive pericarditis
  • Absent in cardiac tamponade
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42
Q

Normal splitting

A
  • Inspiration → drop in intrathoracic pressure → ↑ venous return → ↑ RV filling → ↑ RV stroke volume → ↑ RV ejection time → delayed closure of pulmonic valve
  • ↓ pulmonary impedance (↑ capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
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43
Q

Wide splitting

A
  • Seen in conditions that delay RV emptying (eg pulmonic stenosis, right bundle branch block)
  • Causes delayed pulmonic sound (especially on inspiration)
  • An exaggeration of normal splitting
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44
Q

Fixed splitting

A
  • Heard in ASD
  • ASD → left to right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
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45
Q

Paradoxical splitting

A
  • Heard in conditions that delay aortic valve closure (eg aortic stenosis, left bundle branch block)
  • Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound
  • Therefore, on inspiration, P2 closes later and moves closer to A2, therby “paradoxically” eliminating the split (usually heard on expiration)
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46
Q

Effect of inspiration

A

↑ intensity of right heart sounds

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47
Q

Effect of hand grip

A
  • ↑ afterload
  • ↑ intensity of MR, AR, VSD murmurs
  • ↓ hypertrophy cardiomyopathy murmurs
  • MVP: later onset of click/murmur
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48
Q

Effects of valsalva (phase II), standing up

A
  • ↓ preload
  • ↓ intensity of most murmurs (including AS)
  • ↑ intensity of hypertrophic cardiomyopathy murmur
  • MVP: earlier onset of click/murmur
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49
Q

Effect of rapid squatting

A
  • ↑ venous return, ↑ preload, ↑ afterload
  • ↓ intensity of hypertrophic cardiomyopathy murmur
  • ↑ intensity of AS murmur
  • MVP: later onset of click/murmur
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50
Q

How is cardiac muscle different from skeletal muscle

A
  • Cardiac action potential has a plateau, which is due to Ca2+ influx and K+ efflux
  • Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from SR (Ca2+ induced Ca2+ release)
  • Cardiac myocytes are electrically coupled to each other by gap junctions
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51
Q

Why are voltage gated Na+ channels permanently inactivated in pacemaker action potential

A

Due to less negative resting potential of these cells

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52
Q

Which phases are absent in pacemaker action potential

A

1 & 2

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53
Q

What determines heart rate

A

Slope of phase 4 in SA node

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54
Q

Rank speed of conduction

A

Purkinje > atria > ventricles > AV node

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55
Q

Treatment of torsades de pointes

A

Magnesium sulfate

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56
Q

Congenital long QT syndromes

A

Inherited disorder of myocardial repolarization typically due to ion channel defects

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57
Q

Romano-Ward syndrome

A
  • Congenital long QT syndrome
  • AD
  • Pure cardiac phenotype (no deafness)
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58
Q

Jervell and Lange-Nielsen syndrome

A
  • Congenital long QT syndrome
  • AR
  • Sensorineural deafness
59
Q

Brugada syndrome

A
  • AD
  • Asian males
  • ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3
  • ↑ risk of ventricular tachyarrhythmias
60
Q

Wolf-Parkinson-White syndrome

A
  • Most common type of ventricular pre-excitation syndrome
  • Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node → ventricles begin to partially depolarize earlier → characteristic delta wave with widened QRS complex and shortened PR interval on ECG
  • May result in reentry circuit → supraventricular tachycardia
61
Q

Action of atrial natriuretic peptide

A
  • Acts via cGMP
  • Causes vasodilation and ↓ Na+ reabsorption at the renal collecting tubule
  • Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism
  • B-type natriuretic peptide has a longer half-life, is used for diagnosing HF, and is available in recombinant form (nesiritide)
62
Q

Normal pressure of right atrium

A
63
Q

Normal pressure of right ventricle

A

25/5

64
Q

Normal pressure of pulmonary artery

A

25/10

65
Q

Normal pressure of left atrium

A
66
Q

Normal pressure of left ventricle

A

130/10

67
Q

Normal pressure of aorta

A

130/90

68
Q

Autoregulation of heart

A

Local metabolites (vasodilatory): adenosine, NO, CO2, ↓ O2

69
Q

Autoregulation of brain

A

Local metabolites (vasodilatory): CO2 (pH)

70
Q

Autoregulation of kidneys

A

Myogenic and tubuloglomerular feedback

71
Q

Autoregulation of lungs

A

Hypoxia causes vasoconstriction

72
Q

Autoregulation of skeletal muscle

A

Local metabolites during exercise: lactate, adenosine, K+, H+, CO2 →→ “CHALK”

At rest: sympathetic tone

73
Q

Autoregulation of skin

A

Sympathetic stimulation most important mechanism: temperature control

74
Q

What causes ↑ interstitial fluid colloid osmotic pressure

A

Lymphatic blockage

75
Q

Right-to-left shunts

A
  1. Truncus arteriosus (1 vessel)
  2. Transposition (2 switched vessels)
  3. Tricuspid atresia (3 = tri)
  4. Tetralogy of Fallot (4 = tetra)
  5. TAPVR (5 letters in name)
76
Q

Cause of persistent truncus arteriosus

A
  • Truncus arteriosus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation
  • Most patients have accompanying VSD
77
Q

Cause of D-transposition of great vessels

A
  • Due to failure of the aorticopulmonary septum to spiral

- Not compatible with life unless a shunt is present to allow mixing of blood (eg VSD, PDA, or patent foramen ovale)

78
Q

Cause of tetralogy of Fallot

A
  • Anterosuperior displacement of the infundibular septum

- Most common cause of childhood cyanosis

79
Q

Cause of Ebstein anomaly

A
  • Displacement of tricuspid valve leaflets downward into RV, artificially atrializing the ventricle
  • Associated with tricuspid regurgitation and right HF
  • Lithium exposure in utero
80
Q

VSD vs ASD O2 saturation

A
  • VSD: O2 saturation ↑ in RV and pulmonary artery

- ASD: O2 saturation ↑ in RA, RV and pulmonary artery

81
Q

How do ASD and patent foramen ovale differ

A

With ASD, septa are missing tissue rather than unfused (patent foramen ovale)

82
Q

Uncorrected PDA results in

A

Late cyanosis in the lower extremeties (differential cyanosis)

83
Q

Eisenmenger syndrome

A
  • Uncorrected left-to-right shunt (VSD, ASD, PDA) → ↑ pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arterial hypertension
  • RVH occurs to compensate → shunt becomes right to left
  • Causes late cyanosis, clubbing and polycythemia
  • Age of onset varies
84
Q

Coarctation of the aorta

A
  • Aortic narrowing near insertion of ductus arteriosus (“juxtaductal”)
  • Associated with bicuspid aortic valve, other heart defects, and Turner syndrome
  • Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay)
  • With age, intercostal arteries enlarge due to collateral circulation → arteries erode ribs → notched appearance on CXR
  • Complications: HF, ↑ risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis
85
Q

Is endocarditis a possible complication of coarctation of the aorta

A

Yes, along with HF, ↑ cerebral hemorrhage (berry aneurysms), aortic rupture and possible endocarditis

86
Q

Alcohol exposure in utero (fetal alcohol syndrome)

A
  • VSD
  • ASD
  • PDA
  • Tetralogy of Fallot
87
Q

Congenital rubella

A
  • PDA
  • Pulmonary artery stenosis
  • Septal defects
88
Q

Down syndrome

A
  • AV septal defect (endocardial cushion defect)
  • VSD
  • ASD
89
Q

Infant of diabetic mother

A

Transposition of great vessels

90
Q

Marfan syndrome

A
  • MVP
  • Thoracic aortic aneurysm and dissection
  • Aortic regurgitation
91
Q

Prenatal lithium exposure

A

Ebstein anomaly

92
Q

Williams syndrome

A

Supravalvular aortic stenosis

93
Q

22q11 syndromes

A
  • Truncus arteriosus

- Tetralogy of Fallot

94
Q

Hypertensive urgency vs emergency

A

Hypertensive urgency → severe (>180/>120 mmHg) hypertension WITHOUT acute end-organ damage

Hypertensive emergency → severe hypertension with evidence of acute end-organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia)

95
Q

Xanthoma

A

Plaques or nodules composed of lipid-laden histocytes in skin, especially the eyelids (xanthelasma)

96
Q

Tendinous xanthoma

A

Lipid deposit in tendon, especially Achilles

97
Q

Corneal arcus

A

Lipid deposit in cornea. Common in elderly (arcus senilis) but appears earlier in life in hypercholesterolemia.

98
Q

Location of atherosclerosis

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery

99
Q

Progression of atherosclerosis

A

Endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF and FGF), proliferation and extracellular matrix deposition → fibrous plaque → complex atheromas

100
Q

Difference in association of thoracic vs abdominal aortic aneurysms

A

Abdominal aortic aneurysm → atherosclerosis

Thoracic aortic aneurysm → cystic medial degeneration, hypertension, bicuspid aortic valve, connective tissue disease, tertiary syphilis

101
Q

0-24 hours after MI

A
  • Early coagulative necrosis, release of necrotic cell contents into blood
  • Edema, hemorrhage, wavy fibers
  • Neutrophils appear
  • Reperfusion injury, associated with generation of free radicals, leads to hypercontraction of myofibrils through ↑ free calcium influx
  • COMPLICATIONS: ventricular arrhythmia, HF, cardiogenic shock
102
Q

1-3 days after MI

A
  • Extensive coagulative necrosis
  • Tissue surrounding infarct shows acute inflammation with neutrophils
  • COMPLICATIONS: postinfarction fibrinous pericarditis
103
Q

3-14 days after MI

A
  • Macrophages
  • Granulation tissue at margins
  • COMPLICATIONS: free wall rupture → tamponade; papillary muscle rupture → mitral regurgitation; interventricular septum rupture due to macrophage-mediated structural degradation; LV pseudoaneurysm (risk of rupture)
104
Q

2 weeks to several months after MI

A
  • Contracted scar complete

- COMPICATIONS: Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus)

105
Q

ST elevation or Q wave in V1-V2

A

Anteroseptal (LAD)

106
Q

ST elevation or Q wave in V3-V4

A

Anteroapical (distal LAD)

107
Q

ST elevation or Q wave in V5-V6

A

Anterolateral (LAD or LCX)

108
Q

ST elevation or Q wave in I, aVL

A

Lateral (LCX)

109
Q

ST elevation or Q wave in II, III, aVF

A

Inferior (RCA)

110
Q

ST elevation or Q wave in V7-V9, ST depression in V1-V3 with tall R waves

A

Posterior (PDA)

111
Q

Cardiac arrhythmia

A

Occurs within first few days after MI. Important cause of death before reaching the hospital and within the first 24 hours post-MI.

112
Q

Postinfarction fibrinous pericarditis

A

Occurs 1-3 days after MI. Friction rub.

113
Q

Papillary muscle rupture

A

Occurs 2-7 days after MI. Posteromedial papillary rupture ↑ risk due to single blood supply from posterior descending artery. Can result in severe mitral regurgitation.

114
Q

Interventricular septal rupture

A

Occurs 3-5 days after MI. Macrophage mediated degradation → VSD.

115
Q

Ventricular pseudoaneurysm formation

A

Occurs 3-14 days after MI. Contained free wall rupture. ↓ CO, risk of arrhythmia, embolus from mural thrombus.

116
Q

Ventricular free wall rupture

A

Occurs 5-14 days after MI. Free wall rupture → cardiac tamponade.

117
Q

True ventricular aneurysm

A

Occurs 2 weeks to several months after MI. Outward bulge with contraction (“dyskinesia”), associated with fibrosis.

118
Q

Dressler syndrome

A

Occurs several weeks after MI. Autoimmune phenomenon resulting in fibrinous pericarditis.

119
Q

LV failure and pulmonary edema

A

Can occur secondary to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation.

120
Q

Dilated cardiomyopathy - systolic or diastolic dysfunction

A

Systolic dysfunction

121
Q

Hypertrophic cardiomyopathy - systolic or diastolic dysfunction

A

Diastolic dysfunction

122
Q

Restrictive/ infiltrative cardiomyopathy

A

Diastolic dysfunction

123
Q

Etiologies of dilated cardiomyopathy

A

Often idiopathic or familial. Other etiologies include chronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy.

“ABCCCD”

124
Q

What type of cardiomyopathy is associated with Friederich ataxia

A

Hypertrophic cardiomyopathy

125
Q

Etiologies of restrictive/ infiltrative cardiomyopathy

A

Sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (although dilated cardiomyopathy is more common)

126
Q

What is special about the ECG of restrictive/ infiltrative cardiomyopathy

A

Low voltage ECG despite thick myocardium (especially amyloid)

127
Q

Findings of dilated cardiomyopathy

A
  • HF
  • S3
  • Systolic regurgitant murmur
  • Dilated heart on echocardiogram
  • Balloon appearance of heart on CXR
128
Q

Treatment of dilated cardiomyopathy

A
  • Na+ restriction
  • ACE inhibitors
  • β blockers
  • Diuretics
  • Digoxin
  • ICD
  • Heart transplant
129
Q

Findings of hypertrophic cardiomyopathy

A
  • S4
  • Systolic murmur
  • May see mitral regurgitation due to impaired mitral valve closure
130
Q

Treatment of hypertrophic cardiomyopathy

A
  • Cessation of high-intensity athletics
  • Use of β blockers or non-dihydropyridine Ca2+ channel blocker
  • ICD for high risk patients
131
Q

Obstructive hypertrophic cardiomyopathy

A
  • Subset of hypertrophic cardiomyopathy
  • Asymmetric septal hypertrophy and systolic anterior motion of mitral valve → outflow obstruction → dyspnea, possible syncope
132
Q

HF with systolic dysfunction

A
  • Reduced EF
  • ↑ EDV
  • ↓ contractility often secondary to ischemia/MI or dilated cardiomyopathy
133
Q

HF with diastolic dysfunction

A
  • Preserved EF
  • Normal EDV
  • ↓ compliances often secondary to myocardial hypertrophy
134
Q

When should β blockers not be used in patients with HF

A

Acute decompensated HF

135
Q

Hypovolemic shock

A
  • Caused by hemorrhage, dehydration and burns
  • Skin is cold and clammy
  • ↓↓ PCWP/preload
  • ↓ CO
  • ↑ SVR/ afterload
  • Treat with IV fluids
136
Q

Cardiogenic shock

A
  • Caused by acute MI, HF, valvular dysfunction, arrhythmia
  • Skin is cold and clammy
  • ↑ PCWP/ preload
  • ↓↓ CO
  • ↑ SVR/ afterload
  • Treat with inotropes and diuresis
137
Q

Obstructive shock

A
  • Caused by cardiac tamponade, pulmonary embolism
  • Skin is cold and clammy
  • ↑ PCWP/ preload
  • ↓↓ CO
  • ↑ SVR/ afterload
  • Treat by relieving obstruction
138
Q

Distributive shock caused by sepsis and anaphylaxis

A
  • Skin is warm
  • ↓ PCWP/ preload
  • ↑ CO
  • ↓↓ SVR/ afterload
  • Treat with IV fluids and pressors
139
Q

Distributive shock caused by CNS injury

A
  • Skin is dry
  • ↓ PCWP/ preload
  • ↓ CO
  • ↓↓ SVR/ afterload
  • Treat with IV fluids and pressors
140
Q

Nonbacterial endocarditis

A
  • Marantic/ thrombotic

- Secondary to malignancy, hypercoaguable state, or lupus

141
Q

In what condition do you see equilibration of diastolic pressures in all 4 chambers

A

Cardiac tamponade

142
Q

Beck triad

A
  • Associated with cardiac tamponade
  • Hypotension
  • Distended neck veins
  • Distant heart sounds
143
Q

Pulsus paradoxus is associates with

A

↓ amplitude of systolic BP by > 10 mm Hg during inspiration

  • Cardiac tamponade
  • Asthma
  • Obstructive sleep apnea
  • Pericarditis
  • Croup
144
Q

Kussmaul sign

A
  • ↑ JVP on inspiration instead of normal ↓
  • Inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into vena cavae → JVD
  • Constructive pericarditis
  • Restrictive cardiomyopathies
  • Right atrial or ventricular tumors

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