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Flashcards in Cardiovascular Deck (144):
1

Truncus arteriosus

Ascending aorta and pulmonary trunk

2

Bulbus cordis

Smooth parts (outflow tract) of left and right ventricles

3

Endocardial cushion

- Atrial septum, membranous interventricular septum
- AV and semilunar valves

4

Primitive atrium

Trabeculated part of left and right atria

5

Primitive ventricle

Trabeculated part of left and right ventricles

6

Primitive pulmonary vein

Smooth part of left atrium

7

Left horn of sinus venosus

Coronary sinus

8

Right horn of sinus venosus

Smooth part of right atrium (sinus venarum)

9

Right common cardinal vein and right anterior cardinal vein

Superior vena cava

10

Heart begins to beat spontaneously at

Week 4 of development

11

Cardiac looping

- 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)

12

Conotruncal abnormalities associated with failure of neural crest cells to migrate

- Transposition of great vessels
- Tetralogy of Fallot
- Persistent truncus arteriosus

13

What causes a patent foramen ovale

- 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

14

Where do ventricular septal defects usually occur

- Usually occurs in membranous septum
- Most common congenital cardiac anomaly

15

Allantois → urachus

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

16

Ductus arteriosus

Ligamentum arteriosum

17

Ductus venosus

Ligamentum venosum

18

Foramen ovale

Fossa ovalis

19

Notochord

Nucleus pulposus

20

Umbilical arteries

Medial umbilical ligaments

21

Umbilical vein

- Ligamentum teres hepatis
- Contained in falciform ligament

22

3 layers of pericardium

- Fibrous pericardium
- Parietal layer of serous pericardium
- Visceral layer of serous pericardium

- Pericardial cavity lies between parietal and visceral layers

23

CO during exercise

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

24

With ↑ HR, what becomes preferentially shortened

- Diastole is preferentially shortened with ↑ HR
- Less filling time → ↓ CO (eg ventricular tachycardia)

25

Conditions that ↑ pulse pressure

- Hyperthyroidism
- Aortic regurgitation
- Aortic stiffening (isolated systolic hypertension in elderly)
- Obstructive sleep apnea (↑ sympathetic tone)
- Exercise (transient)

26

Conditions that ↓ pulse pressure

- Aortic stenosis
- Cardiogenic shock
- Cardiac tamponade
- Advanced heart failure

27

Ejection fraction in diastolic vs systolic heart failure

- ↓ in systolic HF
- Normal in diastolic HF

28

How does the left ventricle compensate for ↑ afterload

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

29

Force of contraction is proportional to

End diastolic length of cardiac muscle fiber (preload)

30

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

AV shunts ↑ CO and ↓ TPR

31

Which phase of the cardiac cycle consumes the most O2

Isovolumetric contraction is the period of highest O2 consumption

32

S1

- Mitral and tricuspid valve closure
- Loudest at mitral area

33

S2

- Aortic and pulmonary valve closure
- Loudest at left upper sternal border

34

S3

- 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)

35

S4

- 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

36

Order of jugular venous pulse

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

37

a wave

- Atrial contraction
- Absent in atrial fibrillation

38

c wave

RV contraction (closed tricuspid valve bulging into atrium)

39

x descent

- Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
- Absent in tricuspid regurgitation
- Prominent in tricuspid insufficiency and right HF

40

v wave

↑ right atrial pressure due to filling against closed tricuspid valve

41

y descent

- RA emptying into RV
- Prominent in constrictive pericarditis
- Absent in cardiac tamponade

42

Normal splitting

- 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

43

Wide splitting

- 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

44

Fixed splitting

- 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

45

Paradoxical splitting

- 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)

46

Effect of inspiration

↑ intensity of right heart sounds

47

Effect of hand grip

- ↑ afterload
- ↑ intensity of MR, AR, VSD murmurs
- ↓ hypertrophy cardiomyopathy murmurs
- MVP: later onset of click/murmur

48

Effects of valsalva (phase II), standing up

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

49

Effect of rapid squatting

- ↑ venous return, ↑ preload, ↑ afterload
- ↓ intensity of hypertrophic cardiomyopathy murmur
- ↑ intensity of AS murmur
- MVP: later onset of click/murmur

50

How is cardiac muscle different from skeletal muscle

- 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

51

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

Due to less negative resting potential of these cells

52

Which phases are absent in pacemaker action potential

1 & 2

53

What determines heart rate

Slope of phase 4 in SA node

54

Rank speed of conduction

Purkinje > atria > ventricles > AV node

55

Treatment of torsades de pointes

Magnesium sulfate

56

Congenital long QT syndromes

Inherited disorder of myocardial repolarization typically due to ion channel defects

57

Romano-Ward syndrome

- Congenital long QT syndrome
- AD
- Pure cardiac phenotype (no deafness)

58

Jervell and Lange-Nielsen syndrome

- Congenital long QT syndrome
- AR
- Sensorineural deafness

59

Brugada syndrome

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

60

Wolf-Parkinson-White syndrome

- 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

Action of atrial natriuretic peptide

- 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

Normal pressure of right atrium

63

Normal pressure of right ventricle

25/5

64

Normal pressure of pulmonary artery

25/10

65

Normal pressure of left atrium

66

Normal pressure of left ventricle

130/10

67

Normal pressure of aorta

130/90

68

Autoregulation of heart

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

69

Autoregulation of brain

Local metabolites (vasodilatory): CO2 (pH)

70

Autoregulation of kidneys

Myogenic and tubuloglomerular feedback

71

Autoregulation of lungs

Hypoxia causes vasoconstriction

72

Autoregulation of skeletal muscle

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

At rest: sympathetic tone

73

Autoregulation of skin

Sympathetic stimulation most important mechanism: temperature control

74

What causes ↑ interstitial fluid colloid osmotic pressure

Lymphatic blockage

75

Right-to-left shunts

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

Cause of persistent truncus arteriosus

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

77

Cause of D-transposition of great vessels

- 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

Cause of tetralogy of Fallot

- Anterosuperior displacement of the infundibular septum
- Most common cause of childhood cyanosis

79

Cause of Ebstein anomaly

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

80

VSD vs ASD O2 saturation

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

81

How do ASD and patent foramen ovale differ

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

82

Uncorrected PDA results in

Late cyanosis in the lower extremeties (differential cyanosis)

83

Eisenmenger syndrome

- 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

Coarctation of the aorta

- 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

Is endocarditis a possible complication of coarctation of the aorta

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

86

Alcohol exposure in utero (fetal alcohol syndrome)

- VSD
- ASD
- PDA
- Tetralogy of Fallot

87

Congenital rubella

- PDA
- Pulmonary artery stenosis
- Septal defects

88

Down syndrome

- AV septal defect (endocardial cushion defect)
- VSD
- ASD

89

Infant of diabetic mother

Transposition of great vessels

90

Marfan syndrome

- MVP
- Thoracic aortic aneurysm and dissection
- Aortic regurgitation

91

Prenatal lithium exposure

Ebstein anomaly

92

Williams syndrome

Supravalvular aortic stenosis

93

22q11 syndromes

- Truncus arteriosus
- Tetralogy of Fallot

94

Hypertensive urgency vs emergency

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

Xanthoma

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

96

Tendinous xanthoma

Lipid deposit in tendon, especially Achilles

97

Corneal arcus

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

98

Location of atherosclerosis

Abdominal aorta > coronary artery > popliteal artery > carotid artery

99

Progression of atherosclerosis

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

Difference in association of thoracic vs abdominal aortic aneurysms

Abdominal aortic aneurysm → atherosclerosis

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

101

0-24 hours after MI

- 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

1-3 days after MI

- Extensive coagulative necrosis
- Tissue surrounding infarct shows acute inflammation with neutrophils
- COMPLICATIONS: postinfarction fibrinous pericarditis

103

3-14 days after MI

- 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

2 weeks to several months after MI

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

105

ST elevation or Q wave in V1-V2

Anteroseptal (LAD)

106

ST elevation or Q wave in V3-V4

Anteroapical (distal LAD)

107

ST elevation or Q wave in V5-V6

Anterolateral (LAD or LCX)

108

ST elevation or Q wave in I, aVL

Lateral (LCX)

109

ST elevation or Q wave in II, III, aVF

Inferior (RCA)

110

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

Posterior (PDA)

111

Cardiac arrhythmia

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

112

Postinfarction fibrinous pericarditis

Occurs 1-3 days after MI. Friction rub.

113

Papillary muscle rupture

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

Interventricular septal rupture

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

115

Ventricular pseudoaneurysm formation

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

116

Ventricular free wall rupture

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

117

True ventricular aneurysm

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

118

Dressler syndrome

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

119

LV failure and pulmonary edema

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

120

Dilated cardiomyopathy - systolic or diastolic dysfunction

Systolic dysfunction

121

Hypertrophic cardiomyopathy - systolic or diastolic dysfunction

Diastolic dysfunction

122

Restrictive/ infiltrative cardiomyopathy

Diastolic dysfunction

123

Etiologies of dilated cardiomyopathy

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

What type of cardiomyopathy is associated with Friederich ataxia

Hypertrophic cardiomyopathy

125

Etiologies of restrictive/ infiltrative cardiomyopathy

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

What is special about the ECG of restrictive/ infiltrative cardiomyopathy

Low voltage ECG despite thick myocardium (especially amyloid)

127

Findings of dilated cardiomyopathy

- HF
- S3
- Systolic regurgitant murmur
- Dilated heart on echocardiogram
- Balloon appearance of heart on CXR

128

Treatment of dilated cardiomyopathy

- Na+ restriction
- ACE inhibitors
- β blockers
- Diuretics
- Digoxin
- ICD
- Heart transplant

129

Findings of hypertrophic cardiomyopathy

- S4
- Systolic murmur
- May see mitral regurgitation due to impaired mitral valve closure

130

Treatment of hypertrophic cardiomyopathy

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

131

Obstructive hypertrophic cardiomyopathy

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

132

HF with systolic dysfunction

- Reduced EF
- ↑ EDV
- ↓ contractility often secondary to ischemia/MI or dilated cardiomyopathy

133

HF with diastolic dysfunction

- Preserved EF
- Normal EDV
- ↓ compliances often secondary to myocardial hypertrophy

134

When should β blockers not be used in patients with HF

Acute decompensated HF

135

Hypovolemic shock

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

136

Cardiogenic shock

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

137

Obstructive shock

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

138

Distributive shock caused by sepsis and anaphylaxis

- Skin is warm
- ↓ PCWP/ preload
- ↑ CO
- ↓↓ SVR/ afterload
- Treat with IV fluids and pressors

139

Distributive shock caused by CNS injury

- Skin is dry
- ↓ PCWP/ preload
- ↓ CO
- ↓↓ SVR/ afterload
- Treat with IV fluids and pressors

140

Nonbacterial endocarditis

- Marantic/ thrombotic
- Secondary to malignancy, hypercoaguable state, or lupus

141

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

Cardiac tamponade

142

Beck triad

- Associated with cardiac tamponade
- Hypotension
- Distended neck veins
- Distant heart sounds

143

Pulsus paradoxus is associates with

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

- Cardiac tamponade
- Asthma
- Obstructive sleep apnea
- Pericarditis
- Croup

144

Kussmaul sign

- ↑ 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