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89 Cards in this Set

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Stable chest pain that arises with exertion or emotional stress; represents reversible injury to myocytes (no necrosis)

Cause of angina

atheroslcerosis of coronary arteries with >70% stenosis; decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion

How does angina present?

chest pain (lasting >20 min) that radiates to left arm of jaw, diaphoresis, and shortness of breath; relieved by rest or nitroglycerin

What does EKG show in angina?

ST-segment depression due to subendocardial ischemia

Unstable angina

Pain that occurs with rest; usually due to rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery

Prinzmetal angina

episodic chest pain unrelated to exertion; due to coronary artery vasospasm; relieved by nitroglycerin or calcium channel blockers

What is found on EKG in prinzmetal angina?

ST-segment elevation due to transmural ischemia

Clinical features of MI

severe, crushing chest pain (lasting > 20 min) that radiates to left arm of jaw, diaphoresis, dyspnea; symptoms not relieved by nitroglycerin

Which part of the heart does MI usually involve?

Left ventricle

Right ventricle and atria are generally spared

Most commonly involved artery in MI

LAD; which leads to infarction of anterior wall and anterior septum of LV

2nd most commonly involved artery in MI

RCA; leads to infarctino of posterior wall, posterior septum, and papillary muscles of LV

Which area of the heart becomes infarcted with occlusion of the left circumflex artery?

lateral wall of LV

EKG finding with MI

Initially, ST-segment depression (subendocardial infarction) but ST-segment becomes elevated with transmural infarction

Lab tests to detect MI

  • Troponin I is most sensitive and specific
  • CK-MB is useful for detecting re-infarction

Treatment for MI

1. Aspirin/heparin to limit thrombosis

2. Supplemental O2 to minimize ischemia

3. Nitrates to vasodilate

4. Beta blocker to slow HR and decrease demand

5. ACE inhibitor to decrease LV dilation

6. Fibrinolysis or angioplasty to open blocked vessel

Complications within four hours of MI

Cardiogenic shock (massive infarction), congestive heart failure, arrhythmia

4-24 hrs post infarction

  • Dark discoloration
  • Coagulative necrosis
  • Arrhythmia

1-3 days post infarction

  • Yellow pallor
  • Neutrophils
  • Fibrinous pericarditis

4-7 days post infarction

  • Yellow pallor
  • Macrophages
  • Rupture of ventricular free wall (leading to cardiac tamponade), IV septum (leading to shunt), or papillary muscle (leading to mitral insufficiency)

1-3 weeks post infarction

  • Red border emerges as granulation tissue enters from edge of infarct
  • Granulation tissue with plump fibroblasts, collagen, and BVs

Months post infarction

  • White scar
  • Fibrosis
  • Aneurysm, mural thrombus, or Dressler syndrome

Dressler syndrome

exposure of heart antigens to body leads to production of autoimmune antibodies, leading to autoimmune pericarditis

Sudden cardiac death

Unexpected death due to cardiac disease, usually due to fatal ventricular arrhythmia due to acute ischemia (less common causes include mitral valve prolapse, cardiomyopathy, cocaine abuse)

Causes of Left-sided Congestive Heart Failure

Ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, restrictive cardiomyopathy

Clinical features of Left-sided Congestive Heart Failure

1. Pulmonary congestion leads to pulmonary edema resulting in dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles

2. Small congested capillaries may burst, leading to intraalveolar hemorrhage; marked by hemosiderin-laden macrophages ('heart-failure cells')

3. Decreased flow to kidneys lead to activation of RAAS leading to fluid retention that exacerbates CHF

Treatment of Left-sided Congestive Heart Failure


Cause of Right-sided Congestive Heart Failure

Most commonly due to left-sided heart failure; other causes include left-to-right shunt and chronic lung disease (cor pulmonale)

Clinical features of Right-sided Congestive Heart Failure

1. Jugular venous distension

2. Painful hepatosplenomegaly with 'nutmeg' liver; may lead to cardiac cirrhosis

3. Dependent pitting edema (due to increased hydrostatic pressure)

Which type of shunt, left-to-right or right-to-left, will present as cyanosis shortly after birth? (as opposed to the type of shunt that may be asymptomatic initially)

right to left

Most common congenital heart defect

Ventricular septal defect

Which defect is associated with fetal alcohol syndrome?

Ventricular septal defect

Eisenmenger syndrome

Any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis. The previous left-to-right shunt is converted into a right-to-left shunt secondary to elevated pulmonary artery pressures and associated pulmonary vascular disease.

Clinical features associated with Eisenmenger syndrome

Right ventricular hypertrophy, polycythemia, clubbing


a disease state in which the proportion of blood volume that is occupied by red blood cells increases; can be due to an increase in the number of red blood cells or to a decrease in the volume of plasma

Most common type of atrial septal defect

ostium secundum

Which clinical syndrome is ostium primum associated with?

Down syndrome

What is heard on auscultation in atrial septal defect?

split S2

In which condition are paradoxical emboli an important complication?

atrial septal defect

Which congenital defect is associated with congenital rubella?

PDA; left to right shunt between aorta and pulmonary artery

How is PDA treated?

indomethacin, which decreases PGE, resulting in PDA closure (PGE maintains patency of ductus arteriosus)

Characteristics of tetralogy of fallot

1. Stenosis of right ventricular outflow tract

2. Right ventricular hypertrophy

3. VSD

4. Overriding aorta

Leads to right-to-left shunt & cyanosis

What do patients with tetralogy of fallot learn to do in response to a cyanotic spell?


What is characteristic of tetralogy of fallot on x-ray?

'boot-shaped' heart

Which congenital defect is associated with maternal diabetes?

Transposition of the great vessels

How is transposition of the great vessels treated?

1. Creation of shunt (allowing blood to mix) after birth is required for survival

2. PGE can be administered to maintain PDA until definitive surgical repair is performed

Truncus arteriosus

Characterized by a single large vessel arising from both ventricles (truncus fails to divide); presents with early cyanosis

Tricuspid atresia

tricuspid valve orifice fails to develop; right ventricle is hypoplastic; often associated with ASD resulting in R to L shunt; presents with early cyanosis

Coarctation of aorta (infantile form)

  • Associated with PDA
  • Coarctation lies after aortic arch but before PDA
  • Presents as lower extremity cyanosis
  • Associated with Turner Syndrome

Coarctation of aorta (adult form)

  • coarctation lies after aortic arch
  • presents as HTN in upper extremities and hypotension with weak pulses in lower extremities
  • associated with bicuspid aortic valve

What is commonly seen on x-ray in coarctation of aorta (adult form)?

collateral circulation develops across the intercostal arteries; engorged arteries cause 'notching' of ribs on x-ray

acute rheumatic fever

systemic complication of pharyngitis due to group A beta-hemolytic strep; affects children 2-3 weeks after episode; caused by molecular mimicry (bacterial M protein)

Jones criteria for diagnosing acute rheumatic fever

  • J oint - migratory polyarthritis
  • O (circle resembles heart) - pancarditis
  • N odules - subcutaneous
  • E rythema marginatum - rash
  • S ydenham chorea - rapid, involuntary movements

Pancarditis as seen in acute rheumatic fever

  • Endocarditis: mitral valve (and sometimes aortic valve) develop small vegetations leading to reguritation
  • Myocarditis: Aschoff bodies with Anitschkow cells; most common cause of death
  • Pericarditis: friction rub & chest pain

Aschoff bodies

foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material

Chronic rheumatic heart disease

Valve scarring (usually mitral, sometimes aortic) that arises as consequence of rheumatic fever; results in stenosis with 'fish-mouth' appearance

What usually causes aortic stenosis?

  • 'Wear and tear'; presents >60 years
  • Bicuspid aortic valve increases risk and hastens disease onset

What kind of murmur is heard in aortic stenosis?

Systolic ejection click followed by crescendo-decrescendo murmur

Complications of aortic stenosis

1. Concentric left ventricular hypertrophy

2. Angina and syncope with exercise

3. Microangiopathic hemolytic anemia

Tx: valve replacement

Cause of aortic regurgitation

Aortic root dilation (eg syphilitic aneurysm & aortic dissection) or valve damage (eg infectious endocarditis); most common cause is isolated root dilation

Clinical features of aortic regurgitation

1. Early, blowing diastolic murmur

2. Hyperdynamic circulation due to increased PP (bounding pulse, pulsating nail bed, head bobbing)

3. Results in LV dilation and eccentric hypertrophy

Mitral valve prolapse

Ballooning of mitral valve into left atrium during systole

What causes mitral valve prolapse?

myxoid degeneration (accumulation of ground susbstance) of valve, making it floppy

*may be seen in Marfan/Ehlers-Danlos syndrome

What is heard on auscultation in mitral valve prolapse?

Incidental mid-systolic click following by a regurgitation murmur

Clinical features of mitral regurgitation

1. Holosystolic 'blowing' murmur; louder with squatting and expiration

2. Results in volume overload and left-sided heart failure

What does mitral stenosis sound like on auscultation?

Opening snap followed by diastolic rumble

Consequences of volume overload in mitral stenosis?

  • pulmonary congestion with edema and alveolar hemorrhage
  • pulmonary HTN and eventual right-sided heart failure
  • atrial fibrillation with associated risks for mural thrombi

Most common cause of endocarditis

Strep. viridans; low virulence organism that infects previously damaged valves (eg chronic rheumatic heart disease and mitral valve prolapse); results in small vegetations that do not destroy the valve (subacute endocarditis)

Most common cause of endocarditis in IV drug users

Staph. aureus; high virulence organism that infects normal valves (often tricuspid) resulting in large vegetations that destroy valve (acute endocarditis)

Which organism is associated with endocarditis of prosthetic valves?

Staph. epidermidis

Which organism is associated with endocarditis in patients with underlying colorectal carcinoma?

Strep. bovis

Which organisms are associated with endocarditis with negative blood cultures?

HACEK organisms:






Clinical features of bacterial endocarditis

1. Fever

2. Murmur

3. Janeway lesions, osler nodes, splinter hemorrhages in nail bed and Roth spots (on fundoscopy)

4. Anemia of chronic disease

Lab findings in bacterial endocarditis

1. Positive blood cultures

2. Anemia of chronic disease (↑ferritin, ↓Hb, ↓MCV, ↓TIBC, ↓serum Fe, ↓%saturation)

3. Transesophageal echocardiogram useful for detecting lesions on valves

Nonbacterial thrombotic endocarditis

due to sterile vegetations that arise in association with a hypercoaguable state or underlying adenocarcinoma; vegetations arise on mitral valve along lines of closure and results in regurgitation

Libman-Sacks endocarditis

due to sterile vegetations that arise in association with SLE

Dilated cardiomyopathy

Dilation of all four chambers of the heart; most common form of cardiomyopathy; results in systolic dysfunction leading to biventricular CHF

Causes of dilated cardiomyopathy

1. Genetic mutation

2. Myocarditis (usually due to coxackie A or B)

3. Alcohol abuse

4. Drugs (eg doxorubicin, cocaine)

5. Pregnancy

6. Hemochromatosis

Tx: heart transplant

Cause of hypertrophic cardiomyopathy

Usually due to genetic mutations in sarcomere proteins; most common form is autosomal dominant

Clinical features of hypertrophic cardiomyopathy

1. Decreased cardiac output

2. Sudden death due to ventricular arrhythmias (young athletes)

3. Syncope with exercise

What is seen on biopsy in hypertrophic cardiomyopathy?

Myofiber hypertrophy with disarray

Restrictive cardiomyopathy

Decreased compliance of ventricular endomyocardium that restricts filling during diastole

Causes of restrictive cardiomyopathy

  • Amyloidosis
  • Sarcoidosis
  • Endocardial fibroelastosis
  • Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia)

How does restrictive cardiomyopathy present?

Congestive heart failure; classic finding is low-voltage EKG with diminished QRS amplitude


Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology; usually forms a pedunculated mass in L atrium that causes syncope due to obstruction of mitral valve

Most common primary cardiac tumor in adults



Benign hamartoma of cardiac muscle; usually arises in ventricle; associated with tuberous sclerosis

Most common primary cardiac tumor in children


Common metastases to heart

breast/lung carcinoma, melanoma, lymphoma

Which species make up the Viridans strep group that cause endocarditis?

S. mutans

S. Sanguinis

S. oralis

S. mitis