Cardiac

Question 1

Stable Angina

Answer 1

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

Question 2

Unstable Angina

Answer 2

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

Question 3

Prinzmetal Angina

Answer 3

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)

Question 4

Nitroglycerin

Answer 4

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

Question 5

Myocardial Infarction: Mechanisms and Clinical Presentation

Answer 5

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

Question 6

Occlusion of Left Anterior Descending

Answer 6

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

Question 7

Occlusion of Right Coronary Artery

Answer 7

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

Question 8

Occlusion of Left Circumflex

Answer 8

Infarction of lateral wall of the left ventricle

Question 9

Cardiac Enzymes

Answer 9

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

Question 10

Treatment of MI

Answer 10

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

Question 11

Reperfusion Injury

Answer 11

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

Question 12

Initial phase vs late phase of MI

Answer 12

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

Question 13

<4hrs after MI

Answer 13

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

Question 14

4-24hrs after MI

Answer 14

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

Question 15

1-3 days after MI

Answer 15

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

Question 16

4-7 days after MI

Answer 16

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

Question 17

1-3 weeks after MI

Answer 17

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

Question 18

Months after MI

Answer 18

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

Question 19

Dessler Syndrome

Answer 19

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

Question 20

Sudden Cardiac Death

Answer 20

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

Question 21

Chronic Ischemic Damage

Answer 21

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

Question 22

Left Sided Heart Failure

Answer 22

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

Question 23

Right Sided Heart Failure

Answer 23

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

Question 24

Hemosiderin-laden macrophages

Answer 24

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

Question 25

Nutmeg Liver

Answer 25

Sign of right sided heart failure that can cause cardiac cirrhosis

Question 26

Eisenmenger Syndrome

Answer 26

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

Question 27

Ventricular Septal Defect (VSD)

Answer 27

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

Question 28

Atrial Septal Defect

Answer 28

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

Question 29

Patenet Ductus Arteriosus

Answer 29

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.

Question 30

Tetralogy of Fallot

Answer 30

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

Question 31

Transposition of the Great Vessels

Answer 31

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

Question 32

Truncus Arteriosus

Answer 32

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

Question 33

Tricuspid Atresia

Answer 33

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

Question 34

Infantile Coarctation of the Aorta

Answer 34

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

Question 35

Adult Coarctation of the Aorta

Answer 35

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

Question 36

Acute Rheumatic Fever

Answer 36

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

Question 37

Jones Criteria

Answer 37

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

Question 38

Chronic Rheumatic Heart Disease

Answer 38

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

Question 39

Aortic Stenosis

Answer 39

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

Question 40

Aortic regurgitation

Answer 40

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)

Question 41

Mitral Valve Prolapse

Answer 41

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

Question 42

Mitral Regurgitation

Answer 42

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

Question 43

Mitral Stenosis

Answer 43

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

Question 44

Endocarditis

Answer 44

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

Question 45

Nonbacterial Thrombotic Endocarditis

Answer 45

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

Question 46

Libman Sacks Endocarditis

Answer 46

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

Question 47

Subacute Endocarditis

Answer 47

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

Question 48

Acute Endocarditis

Answer 48

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

Question 49

Endocarditis of Prosthetic valves

Answer 49

Usually due to Staph Epidermidis

Question 50

Endocarditis of patients with colorectal carcinoma

Answer 50

strep bovis

Question 51

Endocarditis with negative blood cultures

Answer 51

``` HACEK organisms Haemophilius Actinobacillus Cardiobacterium Eikenlla Kingella ```

Question 52

Dilated Cardiomyopathy

Answer 52

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

Question 53

Hypertrophic Cardiomyopathy

Answer 53

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

Question 54

Restrictive Cardiomyopathy

Answer 54

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

Question 55

Myxoma

Answer 55

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

Question 56

Rhabdomyoma

Answer 56

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

Question 57

Metastasis to heart

Answer 57

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