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Flashcards in Cardiac Deck (57):

Stable Angina

Chest pain that arises with exertion or emotional stress.
Atherosclerosis of coronary arteries >70% stenosis leads to decreased blood flow that cannot meet metabolic demand of myocaridum during exertion.
Reversible injury to myocytes
Presents with chest pain (<20mins) that radiates to L arm or jaw, diaphoresis, and SOB
ST segment depression due to subendocardial ischemia
Relieved with Nitro or rest


Unstable Angina

Chest pain that occurs at rest usually due to rupture of an atherosclerotic plaque with thrombosis (clot formation) that results in INCOMPLETE occlusion of coronary artery
Reversible injury to myocytes
ST segment depression
Relieved by Nitro
High risk of progression to MI since clot can grow to occlude entire artery


Prinzmetal Angina

Episodic chest pain not associated with exercise and due to coronary artery vasospasm
Reversible injury to myocytes
ST segment elevation due to transmural ischemia (entire wall is denied O2)
Relieved by nitro or calcium channel blockers (relieve vasospasm)



Vasodilates arteries and veins
Main mechanism is that venodilation leads to decreased venous return to heart, leads to decreased preload, so decreased stress on the myocardium


Myocardial Infarction: Mechanisms and Clinical Presentation

Necrosis of cardiac myocytes (irreversible)
Usually due to rupture of an atherosclerotic plaque with thrombosis and COMPLETE occlusion of coronary artery. Can also be caused by coronary vasospasm (persistent prinzmental angina or cocaine use), emboli, and vasculitis (kawasaki disease in children)
Clinically appears with severe, crushing chest pain (>20mins) that radiates to L arm or jaw, diaphoresis, and dyspnea
NOT relieved by Nitro or rest


Occlusion of Left Anterior Descending

Infarction of anterior wall and anterior septum of Left Ventricle
Most common


Occlusion of Right Coronary Artery

Infarction of posterior wall, posterior septum, and papillary muscles of the left ventricle
2nd most common


Occlusion of Left Circumflex

Infarction of lateral wall of the left ventricle


Cardiac Enzymes

Troponin I = most sensitive and specific marker of MI.
Rise in 2-4hrs-->Peak at 24hrs-->Return to normal 7-10 days

CK-MB = useful for detecting reinfarction cus drops to normal quickly
Rise in 4-6hrs-->peak at 24hrs-->return to normal by 72hrs


Treatment of MI

Aspirin or Heparin = limits thrombosis
O2 = minimizes ischemia
Nitrates = vasodilate veins and arteries (mainly decreases stress on LV)
Beta blockers = slows heart rate, decreasing O2 demand and risk for arrhythmia
ACE inhibitor = decreases LV dilation by decreasing aldosterone release that decreases retention of water that would increase blood volume
Fibrinolysis or Angioplasty = opens blocked vessel


Reperfusion Injury

Reperfusion allows for:
1) Calcium influx that leads to hypercontraction of myofibrils ="contraction band necrosis"
2) O2 influx that can form free radicals and further damage myocytes and further elevate cardiac anzymes


Initial phase vs late phase of MI

1) Initially see subendocardial necrosis involving <50% of myocardial thickness and see ST segment depression
2) Continued severe ischemia leads to transmural infarction that results in ST segment elevation


<4hrs after MI

Can get cardiogenic shock, CHF, and arrhythmia if conduction system was damaged


4-24hrs after MI

dark discoloration, coagulative necrosis (removal of nucleus) and can get arrhythmia


1-3 days after MI

Yellow pallor, neutrophil infiltration, and can get fibrinous pericarditis that presents as chest pain and friction rub (only seen with trasmural infarction)


4-7 days after MI

Yellow Pallor, macrophage infiltration, and can see rupture of ventricular wall and subsequent cardiac tamponade, rupture of intraventricular septum, or papillary muscle that can lead to mitral insufficiency


1-3 weeks after MI

Red border emerges as granulation tissue enters edge of infarct and see plump fibroblasts, collagen, and blood vessels


Months after MI

White scar, fibrosis that is not as strong as original wall so can get ventricular aneurysm, mural thrombosis, dessler syndrome


Dessler Syndrome

Transmural infarction and inflammation within the pericardium which can expose pericardial antigens to immune system, can form antibodies against own pericardium and get pericarditis 6-8 weeks after MI


Sudden Cardiac Death

Unexpected death due to cardiac disease, occurs without symptoms or <1hr after symptoms arise. Usually due to ventricular arrhythmia
Usually due to acute ischemia from severe atherosclerosis
Also can be caused by mitral valve prolapse, caridomyopathy, and cocaine abuse


Chronic Ischemic Damage

Poor myocardial function due to chronic ischemic damage, progresses to CHF


Left Sided Heart Failure

Causes include ischemia, hypertension (L concentric ventricular hypertrophy leads to thick heart muscle that is hard to oxygenate and get ischemia), dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy.

Clinical features are pulmonary congestion that leads to pulmonary edema. See dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles. Small capillaries in alveoli might burst and see hemosiderin-laden macrophages.

Decreased flow to kidneys leads to activation of renin-angiotensin system that leads to fluid retention that exacerbates CHF. Therefore treatment is often ACE INHIBITORS


Right Sided Heart Failure

Usually due to left sided heart failure, or left to right shunt and chronic lung disease.
Clinically see JVD, painful hepatospleenomegally with characterisitc "nutmeg liver" leading to cardiac cirrhosis. Also can get pitting edema from increased hydrostatic pressure


Hemosiderin-laden macrophages

Sign of left sided heart failure. Occurs when congested capillaries burst and have intraalveolar hemmorhage.


Nutmeg Liver

Sign of right sided heart failure that can cause cardiac cirrhosis


Eisenmenger Syndrome

Increased pulmonary resistance develops over time when there is a L to R shunt and therefore the pressure builds and the shunt is reveresed. Get late cyanosis, R ventricular hypertrophy, polycythemia, and clubbing


Ventricular Septal Defect (VSD)

Defect in the septum that divides the L and R ventricle.
Most common congenital heart defect
Associated with fetal alcohol syndrome
L to R shunt but can reverse to get Eisenmenger Syndrome


Atrial Septal Defect

Defect in the septum that divides the L and R atria. Most common is ostium secundum but ostium primum is associated with down syndrome
L to R shunt and split S2 on auscultation (increased blood in R heart delays closure of pulmonary valve)
Can get paradoxical emboli. DVT get into arterial circulation rather than causing a PE


Patenet Ductus Arteriosus

Failure of the ductus arteriosus to close. Associated with congenital rubella.
L to R shunt between the aorta and pulmonary artery
Asymptomatic at birth with continuous holocystolic "machine like" murmur.
May get Eisenmenger Syndrome
Treat with indomethacin that decreases the PGE which has been keeping the PDA open.


Tetralogy of Fallot

1)Stenosis of R ventricular outflow
2) R ventricular hypertrophy
3) VSD
4) An aorta that overrides the VSD
R to L shunt leads to early cyanosis. Degree of stenosis determines the extent of the shunt.
See little kids that run around and then turn blue but then go into a squatting stance to remove cyanotic spell
Boot shaped heart on x-ray


Transposition of the Great Vessels

Characterized by the pulmonary artery arising from the L ventricle and Aorta from R Ventricle
Associated with Maternal Diabetes
Early cyanosis
Need to create a shunt (possibly by giving PGE to keep PDA) until surgery can be performed
Get hypertrophy of the R venttricle and atrophy of the L ventricle


Truncus Arteriosus

Single large vessel arsing from both ventricles.
Presents with early cyanosis, from mixing of blood


Tricuspid Atresia

Tricuspid valve orifice fails to develop so get hypoplastic R venticle. Often associated wit ha ASD resulting in R to L shunt. Present with early cyanosis


Infantile Coarctation of the Aorta

Assoicated with a PDA, coarctation lies after the aortic arch but before the PDA. Presents as lower extremity cyanosis in infants at birth.
Associated with Turner Syndrome


Adult Coarctation of the Aorta

Coarctation lies after the aortic arch.
Presents as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities
Collateral circulation develops across the intercostal arteries. Engorged arteries cause "notching" of ribs on x-ray
Associated with a bicuspid aortic valve


Acute Rheumatic Fever

Systemic complication of pharyngitis 2-3weeks after a child is infected with Abeta hemolytic due to MOLECULAR MIMICRY.
Jones Criteria = Joint, O (looks like heart) Nodules on skin, Errythema marginatum, Syndeham Choreas
1)Evidence of Abeta hemolytic (elevated ASP pr DNase B-titers)
2) Fever and elevated ESR
3) migratory polyarthritis
4) Pancarditis - endocarditis (mitral valve more common than aortic). Myocarditis (aschoff bodies = chronic inflammation, reactive histiocytes with slender ,wavy nuclei, giant cells, fibrinoid , pericarditis (frictional rub and chest pain)
5) subcutaneous nodules
6) Erythema marginatum
7)Syndeham chroea


Jones Criteria

O (looks like heart)
Nodules on skin,
Errythema marginatum,
Syndeham Choreas


Chronic Rheumatic Heart Disease

Valve scarring that arises as a consequence of rheumatic fever. Get stenosis with a "fish mouth" appearance (usually mitral but sometimes aortic)
Complications include infectious endocarditis


Aortic Stenosis

Usually due to fibrosis and calcification from "wear and tear" that presents in late adulthood. (with rheumatic can get FUSION of valve commisures)
More likely in people with a bicuspid aortic valve
Systolic ejection click followed by a CRESCENDO-DESCRENDO murmur
Complications include 1) concentric LV hypertrophy 2)angina and syncope with exercise 3)Microangiopathic hemolytic anemia


Aortic regurgitation

Back flow of blood from the aorta into the LV during diastole.
Arises due to aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)
Get early, blowing diastolic murmur, hyperdynamic circulation due to increased pulse pressure(see bounding pulse, pulsating nail bed, and head bobbing) and LV dilation and eccentric hypertrophy (from volume overload)


Mitral Valve Prolapse

Balooning of Mitral Valve into left atrium during systole from myxoid degeneration of the valve making it floppy.
Seen in marfan and ehlers-danlos syndrome
Incidental mid-systolic click followed by a regurgitation murmur that become softer with squatting
Complications are rare but include infectious endocarditis, arrhythmia, and severe mitral regurg


Mitral Regurgitation

Reflux of blood from LV to LA during systole
Seen in mitral valve prolapse, LV dilation, infective endocarditis, ACUTE rheumatic heart disease, and papillary muscle rupture following an MI
Notice a "holosystolic blowing" murmur that is LOUDER with squatting and expiration
Results in volume overload and left-sided heart failure


Mitral Stenosis

Narrowing of the mitral valve orifice usually due to CHRONIC rheumatic valve disease.
Notice an opening snap followed by a diastolic rumble
volume overload leads to dilation of LA resulting in pulmonary congestion with edema and alveolar hemmorhage, pulmonary hypertension and eventual R sided heart failure, a fib with increased risk of mural thrombi



inflammation of endocardium that lines the surface of cardiac valves.
Presents with fever, murmur, Janeway lesions (erythematous nontender lesions on palms and soles), Osler nodes (ouch/tender lesions on toes and fingers), splinter hemmorhages in nail beds, and anemia of chronic disease


Nonbacterial Thrombotic Endocarditis

Sterile vegetations that arrise in association with hypercoaguable state or underylying ADENOCARCINOMA. Vegetations arise on mitral valve along lines of closure


Libman Sacks Endocarditis

Sterile vegetations that arise on BOTH sides of mitral valve in association with SLE


Subacute Endocarditis

Usually due to step viridans which is a low virulent organism that infects previously damaged valves.
Get small vegetations that do not destroy the valve.
Damaged valves develop thrombotic vegetations that trap transient bacteremia


Acute Endocarditis

Usually due to Staph aureus in IV drug abusers. Highly virulent and can attack even healthy valves.
Get large vegetations that destroy the valve


Endocarditis of Prosthetic valves

Usually due to Staph Epidermidis


Endocarditis of patients with colorectal carcinoma

strep bovis


Endocarditis with negative blood cultures

HACEK organisms


Dilated Cardiomyopathy

Dilation of all four chambers of the heart results in systolic dysfunction (ventricles cant pump) leading to biventricular CHF. Can get mitral and tricuspid valve regurg and arrythmia
Usually idiopathic but result from genetic mutation, myocarditis (cocksackie virus with lymphocytic infilitrate) , alcohol abuse, doxorubicon/cocaine, pregnancy (late or soon after birth) and hemochromatosis


Hypertrophic Cardiomyopathy

Massive hypertrophy of the Left Ventricle usually due to genetic mutations in sarcomere proteins.
Get decreased CO Ileft ventricle cannot fill), Sudden death due to ventricular arrythmias, syncope with exercise.
Biospy shows myofiber hypertrophy with dissaray


Restrictive Cardiomyopathy

Decreased compliance of the ventricular endomyocardium that restricts filling during diastole.
Causes include amyloidosis, sarcoidosis, endocardial fibroelastosis (children) and Loeffler syndrome (fibrosis with eosinophilic infiltrate)
Presents with CHF and LOW VOLTAGE EKG with diminished QRS complex



Benign mesenchymal tumor with gelatinous appearance and abundant ground substance.
Pendunculated mass in L atrium can cause syncope when it blocks mitral valve



Benign hamartoma of cardiac muscle
CHILDREN and associated with tuberous sclerosis
Usually in a ventricle


Metastasis to heart

Breast and lung carcinoma, melanoma, lymphoma are common sources
Usually involve the pericardium and result in pericardial effusion