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USMLE Step 1. > Cardiology > Flashcards

Cardiology Flashcards

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USMLE® Step 1 flashcards
1
Q

Truncus arteriosus gives rise to:

A

Ascending aorta and pulmonary trunk

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2
Q

Bulbous cordis gives rise to:

A

Smooth parts (outflow tract) of L and R Ventricles

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3
Q

Primitive atrium gives rise to:

A

Trabeculated part of L and R atria

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4
Q

Primitive ventricle gives rise to:

A

Trabeculated part of L and R ventricles

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5
Q

Primitive pulmonary vein gives rise to:

A

Smooth part of the L Atrium

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6
Q

Left horn of Sinus Venosus gives rise to:

A

Coronary Sinus

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7
Q

Right horn of Sinus Venosus gives rise to:

A

Smooth part of R A Atrium (Sinus Venarum)

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8
Q

Right common cardinal vein and Right anterior cardinal vein give rise to:

A

Superior Vena Cava (SVC)

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9
Q

When does the heart start beating?

A

Week 4 - first functional organ in vertebrate embryos

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10
Q

Kartagener Syndrome

A

Defect in L-R dynein (involved in L/R asymmetry) can lead to dextrocardia as seen in this disease.

Messes up embryological cardiac looping

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11
Q

Where does VSD commonly occur?

A

in the membranous septum

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12
Q

Patent Foramen Ovale

A

caused by failure of septum primum and septum secundum to fuse after birth

Most are left untreated

Can lead to paradoxical emboli (venous thromboemboli that enter systemic ARTERIAL circulation) - similar to those resulting from ASD

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13
Q

What are 3 common conotruncal abnormalities?

A

Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosus

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14
Q

Sites of erythropoiesis

A

Yolk Sac (3-8 wks)
Liver (6 wks - birth)
Spleen (10-28 wks)
Bone marrow (18 wks to adult)

Only bone marrow is doing this ish after birth

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15
Q

What are 3 important shunts in fetal blood flow?

A

Ductus venosus
Foramen ovale
Ductus arteriosus

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16
Q

Allantois/urachus becomes…

A

Meidan umbilical ligament (urachus is part of allantoic duct btw bladder and umbilicus)

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17
Q

Ductus arteriosus becomes…

A

Ligamentum arteriosum

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18
Q

Ductus venosus becomes…

A

Ligamentum venosum

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19
Q

Foramen ovale becomes…

A

Fossa ovalis

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20
Q

Notochord becomes…

A

Nucleus pulposus

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21
Q

Umbilical arteries become…

A

Medial umbilical ligaments

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22
Q

Umbilical vein becomes…

A

Ligamentum teres hepatis (contained in falciform ligament)

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23
Q

What the most common coronary artery blockage?

A

LAD

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24
Q

Left coronary artery branches

A

LCX - supplies lateral and posterior walls of LV, anterolateral papillary muscle

Left Marginal (Obtuse) Artery

LAD - supplies anterior 2/3 of interventricular septum, anterolateral papillary muscle, and anterior surface of LV

PDA (rarely, but can happen) - If it does happen it would be a branch of LCX

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25
Q

Right coronary artery branches

A

Right marginal (Obtuse) Artery - supplies RV

PDA (usually) - supplies posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle.

RCA also supplies AV node most of the time

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26
Q

Cardiac output formula

A

CO = SV x HR

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27
Q

Fick’s principle

A

CO = [rate of O2 consumption]/[arterial O2 content - venous O2 content]

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28
Q

Mean arterial pressure (MAP) formula

A

MAP = 2/3(diastolic) + 1/3(systolic)

MAP = CO x TPR

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29
Q

Pulse pressure formula

A

PP = systolic - diastolic

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30
Q

Stroke volume formula

A

SV = EDV - ESV

SV = CO/HR

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31
Q

Wall Tension formula (Laplace’s Law)

A

Wall tension = (pressure x radius)/(2 x wall thickness)

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32
Q

Ejection Fraction formula

A

EF = SV/EDV = (EDV=ESV)/EDV

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33
Q

Resistance, Pressure, Flow formulas

A

Change in P = QR

R = P/Q = 8NL/Pi r^4

TR in series = R1 + R2..

TR in parallel: 1/TR = 1/R1 + 1/R2

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34
Q

Conditions that exhibit wide splitting of heart sounds

A

Pulmonic stenosis
R Bundle branch block

Conditions that delay RV emptying

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35
Q

Conditions that exhibit fixed splitting of heart sounds

A

ASD

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36
Q

Conditions that exhibit paradoxical splitting of heart sounds

A

Aortic stenosis
L Bundle branch block

Conditions that delay aortic valve closure

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37
Q

What is best heard over Aortic area?

A

Systolic murmur:
Aortic Stenosis
Flow murmur
Aortic valve sclerosis

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38
Q

What is best heard of left sternal border?

A

Diastolic murmur:
Aortic regurgitation
Pulmonic regurgitation

Systolic murmur:
Hypertrophic cardiomyopathy

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39
Q

What is best heard over left infraclavicular region?

A

Continuous murmur:

PDA

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40
Q

What is best heard over Pulmonic Area?

A

Systolic ejection murmur:
Pulmonic stenosis
Flow murmur (physiologic murmur)

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41
Q

What is best heard over Tricuspid Area?

A

Pansystolic murmur:
Tricuspid regurgitation
VSD

Diastolic murmur:
Tricuspid stenosis
ASD

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42
Q

What is best heard over Mitral Area?

A

Systolic murmur:
Mitral regurgitation

Diastolic murmur:
Mitral stenosis

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43
Q

What murmurs are systolic?

A 
Aortic Stenosis
Pulmonic Stenosis
Mitral Regurgitation 
Tricuspid Regurgitation 
VSD
MVP
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44
Q

What murmurs are diastolic?

A

Aortic Regurgitation
Pulmonic Regurgitation
Mitral Stenosis
Tricuspid Stenosis

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45
Q

Aortic stenosis findings

A

Crescendo-decrescendo systolic ejection murmur.

LV&raquo_space; aortic pressure during systole

Loudest at heart base - radiates to carotids. “Pulsus parvus et tardus” - pulses are weak with a delayed peak.

Can lead to syncope, angina and dyspnea on exertion (SAD)

Often due to age-related calcification or early-onset calcification of bicuspid aortic valve.

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46
Q

Mitral/Tricuspid regurgitation findings

A

Holosystolic, high-pitched “blowing murmur”

Mitral - loudest at apex and radiates to axilla. MR is often due to ischemic heart disease (post MI), MVP, LV dilation

Tri - loudest at tricuspid area and radiates to right sternal border. TR commonly caused by RV dilation

Rheumatic fever and infective endocarditis can cause either MR or TR

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47
Q

MVP findings

A

Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae).

Most frequent valvular lesion.

Best heard over apex. Loudest just before S2.

Usually benign.

Can predispose to infective endocarditis. Can be caused by myxomatous degeneration ( primary or secondary to connective tissue disease such as Marfan or Ehlers-Danlos), rheumatic fever, chordae rupture.

48
Q

VSD findings on auscultation

A

Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.

49
Q

Aortic regurgitation findings

A

High-pitched blowing early diastolic decrescendo murmur.

Long diastolic murmur and signs of hyperdynamic pulse when severe and chronic. Often due to aortic root dilation, bicuspid aortic valve, endocarditis, RF. Progresses to left HF.

50
Q

Mitral stenosis findings

A

Follows opening snap (OS - due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips).

Delayed rumbling late diastolic murmur (smaller interval between S2 and OS correlates with increased severity).

LA&raquo_space; LV pressure during diastole. Often occurs secondary to RF. Chronic MS can result in LA dilation

51
Q

PDA findings on auscultation

A

Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity.

Best heard at left infraclavicular area

52
Q

P wave

A

atrial depolarization

Atrial repolarization is masked by QRS

53
Q

PR interval

A

time from start of atrial depolarization (start of P wave) to start of ventricular depolarization (start of QRS).

Normal = less than 200 ms

54
Q

QRS complex

A

Ventricular depolarization

Normally less than 120 ms

55
Q

QT interval

A

ventricular depolarization, mechanical contraction of the ventricles. ventricular repolarization. From start of QRS to end of T.

56
Q

T wave

A

ventricular repolarization

T wave inversion may indicated recent MI

57
Q

J point

A

junction between end of QRS complex and start of ST segment

58
Q

ST segment

A

isoelectric, ventricles depolarized

59
Q

U wave

A

caused by hypokalemia, bradycardia

60
Q

Torsades de pointes

A

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to VFib.

Long QT interval predisposes to torsade de pointes. Caused by drugs, decreased K, decreased Mg, other abnormalities.

Tx = magnesium sulfate

61
Q

Congenital long QT syndrome

A

Inherited disorder of myocardial repolarization, typically due to ion channel defects.

Higher risk of sudden cardiac death (SCD) due to torsades de pointes. Includes:

1) Romano-Ward Syndrome: autosomal dominant, pure cardiac phenotype (no deafness)
2) Jervell and Lange-Nielson Syndrome: autosomal recessive, sensorineural deafness

62
Q

Drug-induced long QT caused by:

A

ABCDE

anti Arrhythmics (class 1A, III)
anti Biotics (macrolides)
anti "C" ychotics (haloperidol)
anti Depressants (TCAs)
anti Emetics (ondansetron)
63
Q

Brugada Syndrome

A

Autosomal dominant disorder most common in Asian males

ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.

Higher risk of ventricular tachyarrhtymias and SCD. Prevent SCD with implantable cardioverter-defribrillator (ICD)

64
Q

Wolff-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

This leads to ventricles beginning to partially depolarize earlier leading to characteristic delta wave with widened QRS complex and shortened PR interval on ECG.

May result in reentry circuit leading to supraventricular tachycardia

65
Q

AFib on ECG

A

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes.

Associated with: (7)
HTN
CAD
Rheumatic heart disease
Binge drinking (holiday heart)
HF
Valvular disease
Hyperthyroidism

Can result in atrial stasis and lead to cardioembolic events.

Tx includes antithrombotic therapy (warfarin), rate control (B blockers, non-dihydropyridine Ca channel blockers, digoxin), rhythm control (class 1C or 3 antiarrhtymics) and or/ cardioversion (pharm or electrical)

66
Q

Atrial flutter on ECG

A

A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.

Management similar to Afib (rate control, anticoagulation, caridoversion). Definitive treatment is catheter ablation

67
Q

VFib on ECG

A

A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation

68
Q

1st degree AV block on ECG

A

The PR interval is prolonged (greater than 200 ms). Benign and asymptomatic. No Tx required

69
Q

2nd degree AV block - Mobitz type 1 (Wenckebach) on ECG

A

Progressive lengthening of PR interval until a beat is “dropped” ( a P wave not followed by a QRS complex).

Usually asymptomatic.

Variable RR interval with a pattern (regularly irregular)

70
Q

Mobitz type II on ECG

A

Dropped beats that are not preceded by a change in the length of PR interval (as in type 1). May progress to 3rd degree block.

Often treated with pacemaker

71
Q

3rd degree (complete) AV block on ECG

A

The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. Atrial rate faster than ventricular rate.

Usually treated with pacemaker.

Lyme Disease can result in 3rd degree block

72
Q

Atrial natriuretic peptide

A

Released from atrial myocytes in response to increased blood volume and atrial pressure.

Acts via cGMP.

Causes vasodilation and lower Na reabsorption at the renal collucting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism

73
Q

B-type (Brain) naturietic peptide

A

Released from ventricular myocytes in response to increased tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosing HF (very good negative predictive value)

Available in recombinant form (nesiritide) for treatment of HF

74
Q

Cushing reaction triad

A

Hypertension
Bradycardia
Respiratory depression

75
Q

Right to Left Shunts

A

Congenital heart defects

Early cyanosis - “blue babies.” Often diagnosed prenatally or become evident immediately after birth. Usually require urgent surgical correction and/or maintenance of a PDA.

5 T’s

1) Truncus arteriosus (1 vessel)
2) Transposition (2 vessels)
3) Tricuspid atresia (3 = tri)
4) Tetralogy of Fallot (4 = tetra)
5) TAPVR (5 letters)

76
Q

Persistent Truncus arteriosus

A

Congenital heart defect

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

77
Q

D-Transposition of great vessels

A

Congenital heart defect

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior). This leads to separation of systemic and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (e.g. VSD, PDA, or patent foramen ovale)

Due to failure of the aorticopulmonary septum to spiral

Without surgical intervention, most infants die within the first few months of life.

78
Q

Tricuspid atresia

A

Congenital heart defect

Absence of tricuspid valve and hypoplastic RV - requires both an ASD and VSD for viability

79
Q

Tetralogy of Fallot

A

Congenital heart defect

Caused by anterosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis.

1) Pulmonary infundibular stenosis (most important determinant for prognosis)
2) Right ventricular hypertrophy - boot shaped hear on CXR
3) Overriding aorta
4) VSD

Pulmonary stenosis forces R-L flow across VSD leading to early cyanotic “tet spells,” RVH.

Squatting: Increases SVR, lowers R-L shunt and improves cyanosis

Tx = early surgical correction

80
Q

Total anomalous pulmonary venous return (TAPVR)

A

congenital heart defect

Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc): associated with ASD and sometimes PDA to allow for R-L shunting to maintain CO.

81
Q

Left-Right shunts

A

LATE cyanosis - blue kids

VSD
ASD
PDA

Frequency: VSD > ASD > PDA

82
Q

Ventricular septal defect

A

Most common congenital cardiac defect. Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life. Most self resolve; larger lesions may lead to LV overload and HF

83
Q

Atrial septal defect

A

Defect in interatrial septum; loud S1; wide, fixed split S2.

ostium secundum defects are most common and usually occur as isolated findings.

Ostium primum defects are rarer yet usually occur with other cardiac anomalies.

Symptoms range from none to HF. Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.

84
Q

Patent ductus arteriosus

A

In fetal period, shunt is R-L (normal). In neonatal period, lower lung resistance leads to shunt becoming L-R leading to progressive RVH and/or LVH and HF

Associate with a continuous, “machine-like” murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)

Indomethacin ends patency of PDA; PGE keeps it open (may be necessary to sustain life in conditions such as transposition of the great vessels).

PDA is normal in utero and normally closes only after birth

85
Q

Eisenmenger syndrome

A

Uncorrected L-R shunt (VSD, ASD, PDA) lead to increased pulmonary blood flow leading to pathologic remodeling of vasculature leading to pulmonary arterial HTN. RVH occurs to compensate leading to shunt becoming R-L.

Causes late cyanosis, clubbing, and polycythemia. Age of onset varies.

86
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.

HTN in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay). With age, collateral arteries erode ribs (notched appearance on CXR)

87
Q

Alcohol exposure in utero (fetal alcohol syndrome) leads to what congenital heart defects?

A

VSD
PDA
ASD
Tetralogy of Fallot

88
Q

Congenital rubella leads to what congenital heart defects?

A

Septal defects
PDA
Pulmonary artery stenosis

89
Q

Down Syndrome leads to what congenital heart defects?

A

AV Septal defect (endocardial cushion defect)
VSD
ASD

90
Q

Infant of diabetic mother leads to what congenital heart defects?

A

Transposition of great vessels

91
Q

Marfan Syndrome leads to what congenital heart defects?

A

MVP
Thoracic aortic aneurysm and dissection
Aortic regurgitation

92
Q

Prenatal lithium exposure leads to what congenital heart defects?

A

Ebstein anomaly

93
Q

Turner Syndrome leads to what congenital heart defects?

A

Bicuspid aortic valve

Coarctation of aorta

94
Q

Williams Syndrome leads to what congenital heart defects?

A

Supravalvular aortic stenosis

95
Q

22q11 syndromes lead to what congenital heart defects?

A

Truncus arteriosus

Tetralogy of Fallot

96
Q

Anteroseptal infarct (LAD) on ECG

A

V1-V2

97
Q

Anteroapical (distal LAD) infarct on ECG

A

V3-V4

98
Q

Anterolateral (LAD or LCX) infarct on ECG

A

V5-V6

99
Q

Lateral (LCX) infarct on ECG

A

I, aVL

100
Q

Inferior (RCA) infarct on EKG

A

II, III, aVF

101
Q

Dressler Syndrome

A

Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI)

102
Q

Acute bacterial endocarditis - organisms

A

S. aureus (high virulence)

Large vegetations on previously normal valves. Rapid onset.

103
Q

Subacute bacterial endocarditis - organisms

A

strep viridans (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.

104
Q

Bacterial endocarditis - organism present in colon cancer

A

S. bovis

105
Q

Bacterial endocarditis - organism present on prosthetic valves

A

S. epidermidis

106
Q

bacterial endocarditis - culture is negative

A

Coxiella burnetii
Bartonella

HACEK

Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
107
Q

Bacterial endocarditis signs

A

FROM JANE

Fever
Roth spots
Osler nodes
Murmur

Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli

108
Q

Beck triad for cardiac tamponade

A

Hypotension
Distended neck veins
Distant heart sounds

109
Q

Angiosarcoma

A

a vascular tumor

Rare blood vessel malignancy typically occurring in the head, neck, and breast areas. Usually in elderly, on sun-exposed areas. Associated with radiation therapy and chronic postmastectomy lymphedema.

Hepatic angiosarcoma associated with vinyl chloride and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.

110
Q

Bacillary angiomatosis

A

vascular tumor

benign capillary skin papules found in AIDS patients. Caused by bartonella henselae infections. Frequently mistaken for Kaposi sarcoma, but has a neutrophilic infiltrate

111
Q

Cherry hemangioma

A

Vascular tumor

Benign capillary hemangioma of the elderly.

Does not regress. Frequency higher with age

112
Q

Cystic hygroma

A

Vascular tumor

Cavernous lymphangioma of the neck

Associated with Turner Syndrome

113
Q

Glomus tumor

A

Vascular tumor

Benign, painful, red-blue tumor under fingernails.

Arises from modified smooth muscle cells of the thermoregulatory glomus body

114
Q

Kaposi Sarcoma

A

Vascular tumor

Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract.

Associated with HHV-8 and HIV.

Frequently mistaken for bacillary angiomatosis, but has lymphocytic infiltrate

115
Q

Pyogenic granuloma

A

Vascular tumor

Polypoid capillary hemangioma that can ulcerate and bleed

Associated with trauma and pregnancy

116
Q

Strawberry hemangioma

A

Vascular tumor

Benign capillary hemangioma of infancy

Appears in first few weeks of life (1/200 births): grows rapidly and regresses spontaneously by 5-8 years old

USMLE Step 1. (19 decks)

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