Cardiology

Question 1

What elements of the history and physical steer you away from a diagnosis of MI?

Answer 1

Wrong age (under 40 without known heart disease, family history)
Lack of risk factors
Physical characteristics of pain (reproducible by palpation? sharp? well-localized? related to eating?)

Question 2

What findings on EKG should make you suspect an MI?

Answer 2

Flipped or flattened T waves, ST-segment elevation (depression means ischemia; elevation means injury) and/or Q waves in segmental distribution

Question 3

Describe the classic pattern of chest pain in an MI

Answer 3

Classically crushing or pressure sensation; poorly localized substernal pain that may radiate to the shoulder, arm, or jaw
Usually NOT reproducible on palpation and does not resolve with nitroglycerin (as it does in angina)
Lasts at least half an hour

Question 4

What tests are used to diagnose an MI?

Answer 4

EKG, CK-MB, troponin I or T, or myoglobin (usually drawn Q8 3x before MI is ruled out)
Elevated LDH uncommonly used for late MI presentation (troponin stays elevated more than 24 hrs)
AST can be elevated but not used clinically
Radiographs - cardiomegaly +/- pulmonary congestion
Echo - ventricular wall motion abnormalities

Question 5

Describe the classic physical exam findings in patients with MI

Answer 5

Diaphoretic, anxious, tachycardic, tachypneic, pale, may have nausea/vomiting
Large heart attacks causing HF: bilateral pulmonary rales, distended neck veins, S3 or S4 heart sound, new murmurs, hypotension, +/- shock

Question 6

What historical points should steer you toward a diagnosis of MI?

Answer 6

History of angina or previous chest pain, murmurs, arrhythmias, risk factors for CAD, HTN, diabetes

Question 7

What medications do you administer for an MI?

Answer 7

Morphine (pain control)
Aspirin
Nitroglycerin
Beta blocker (reduce mortality rate of MI and incidence of second MI)
Clopidogrel
Unfractionated or LMW heparin
ACEI or ARBC within 24 hrs
HMG-Coa reductase inhibitor

Question 8

When is reperfusion therapy indicated for an MI?

Answer 8

Reperfusion is indicated if the time from onset of symptoms is less than 12 hours. Early reperfusion (less than 4-6 hrs) is preferred to try to salvage myocardium.
Can be accomplished by fibrinolysis or percutaneous coronary intervention (i.e. balloon angioplasty/stent), coronary artery bypass grafting may be required.

Question 9

True or false: With good management, patients with an MI will not die in the hospital.

Answer 9

False. Even with the best management, patients may die from an MI. May also have a second MI during hospitalization. Watch for sudden deterioration!

Question 10

When is heparin indicated in the setting of chest pain and MI?

Answer 10

Heparin should be started if unstable angina is diagnosed, if the patient has a cardiac thrombus, or if severe congestive HF is seen on echo.
Do NOT give heparin to patients with contraindications to use (e.g. active bleeding)

Question 11

What clues suggest GERD/peptic ulcer rather than MI chest pain?

Answer 11

Relation to certain foods (spicy, chocolate), smoking, caffeine, or lying down
Pain relieved by antacids or acid-reducing meds
Positive H. pylori test

Question 12

What clues suggest chest wall (e.g. costochondritis, bruised or broken ribs) rather than MI chest pain?

Answer 12

Pain is well localized and reproducible on chest wall palpation

Question 13

What clues suggest esophageal problems (e.g. achalasia, nutcracker esophagus, spasm) rather than MI chest pain?

Answer 13

Difficult differential!
Negative MI work-up or lack of atherosclerosis risk factors
Barium swallow abnormalities or esophageal manometry

Question 14

What clues suggest pericarditis rather than MI chest pain?

Answer 14

Viral URI prodrome
EKG with diffuse ST-segment elevation, ESR elevated, low-grade fever
Pain relieved by sitting forward!
Most common cause is coxsackievirus (but also consider TB, uremia, malignancy, SLE)

Question 15

What clues suggest pneumonia rather than MI chest pain?

Answer 15

Chest pain is due to pleuritis
Patients also have cough, fever, +/- sputum production
Ask about sick contacts

Question 16

What clues suggest aortic dissection rather than MI chest pain?

Answer 16

Associated with severe tearing or ripping pain that may radiate to the back
Look for HTN or evidence of Marfan’s (tall, thin, hyperextensible joints)
Blunt chest trauma can cause aortic laceration and pseudoaneurysm

Question 17

How can you recognize stable angina?

Answer 17

Begins with exertion or stress and remits with rest or calming down. Described as pressure or squeezing pain in substernal area and may radiate to shoulders, neck, and/or jaw.
Often accompanied by SOB, diaphoresis, +/- nausea. Usually relieved by nitroglycerin.
EKG - ST-segment depression during acute attack, otherwise normal
Pain lasts less than 20 minutes

Question 18

Define unstable angina

Answer 18

Change from previously stable angina. If pt used to experience angina once a week and now has it once a day, technically that is unstable angina.
EKG shows ST depression, minimally elevated cardiac enzymes, prolonged chest pain that does not respond to nitro initially. Pain often begins at rest.

Question 19

How do you treat unstable angina?

Answer 19

Similar to MI
O2, aspirin, nitro, beta-blocker, clopidogrel, heparin, glycoprotein IIb/IIIa receptor inhibitor, ACEI or ARB
Consider emergent PTCA if pain does not resolve

Question 20

Describe variant (Prinzmetal angina)

Answer 20

Pain at rest (unrelated to exertion) and ST elevation; cardiac enzymes are normal.
Cause is coronary spasm.
Usually responds to nitro and it treated long-term with calcium channel blockers (reduce arterial spasm)

Question 21

Define silent MI. How common is it?

Answer 21

Patients with silent MI do not develop chest pain
Present with CHF, shock, or confusion and delirium (esp. elderly patients)
Up to 25% of cases (esp. in diabetics with neuropathy)

Question 22

What physical exam findings are associated with mitral stenosis?

Answer 22

Late diastolic blowing murmur (best heart at apex)

Opening snap, loud S1, a. fib, L atrial enlargement, pulmonary HTN

Question 23

What physical exam findings are associated with mitral regurgitation?

Answer 23

Holosystolic murmur (radiates to axilla)
Soft S1, L atrial enlargement, L ventricular hypertrophy, pulmonary HTN

Question 24

What physical exam findings are associated with aortic stenosis?

Answer 24

Harsh systolic ejection murmur (best heard in aortic area, radiates to carotids)
Slow pulse upstroke, S3/S4, ejection click, L ventricular hypertrophy, cardiomegaly
*syncope, angina, HF

Question 25

What physical exam findings are associated with aortic regurgitation?

Answer 25

Early diastolic decrescendo murmur (best heard at apex) | Widened pulse pressure, L ventricular hypertrophy, L ventricular dilatation, S3

Question 26

What physical exam findings are associated with mitral prolapse?

Answer 26

Midsystolic click, late systolic murmur | *panic disorder

Question 27

Who should receive endocarditis prophylaxis?

Answer 27

Cardiac conditions for which prophylaxis with dental procedures is recommended includes prosthetic cardiac valve, previous infectious endocarditis, congenital heart disease, and cardiac transplant recipients who develop valvulopathy No longer recommended for GU or GI procedures.

Question 28

Describe the protocols for endocarditis prophylaxis

Answer 28

Should be administered in single dose before procedure. Amoxicillin is preferred choice for oral therapy. Cephalexin, clindamycin, azithromycin, or clarithromycin may be used for penicillin allergies. Ampicillin, cefazolin, ceftriaxone, or clindamycin may be used if unable to take orals.

Question 29

What is Virchow's triad?

Answer 29

3 findings associated with DVT: * endothelial damage * venous stasis * hypercoagulable state

Question 30

Common clinical scenarios for development of DVT

Answer 30

Surgery (esp. orthopedic, pelvic, abdominal, or neurosurgery), malignancy, trauma, immobilization, pregnancy, birth control pills, DIC, thrombophilias

Question 31

Describe the physical signs and symptoms of DVT. How is it diagnosed?

Answer 31

Unilateral leg swelling, pain or tenderness, +/- Homan sign (pain on dorsiflexion, present in 30%) Best diagnosed by compression ultrasonography or impedance plethysmography of veins of extremity. Gold standard is venography but this is invasive, reserved for situations in which diagnosis is not clear.

Question 32

True or false: Superficial thrombophlebitis is a risk factor for pulmonary embolus.

Answer 32

False. Superficial thrombophlebitis (erythema, tenderness, edema, palpable clot in superficial vein) affect superficial veins and does not cause PEs. It is considered a benign condition though if recurrent can be marker of malignancy (e.g. Trousseau syndrome - migratory thrombophlebitis - is classic marker for pancreatic cancer)

Question 33

How should you treat patients with superficial thrombophlebitis?

Answer 33

NSAIDs and warm compresses

Question 34

How is DVT treated? For how long?

Answer 34

Systemic anticoagulation is necessary. Use IV heparin or subcutaneous LMW heparin initially, followed by crossover to oral warfarin. Should be maintained on warfarin for at least 3-6 months - possibly for life if more than one episode of clotting occurs.

Question 35

What is the best way to prevent DVT in patients undergoing surgery?

Answer 35

Early ambulation for low risk patients. LMW heparin, low dose unfractioned heparin, or fondaparinux for moderate risk patients. LMW heparin, fondaparinux, or oral vitamin K antagonist for high risk patients. Moderate or high risk + high risk of bleeding = pneumatic compression stockings

Question 36

In what clinical settings does PE occur? Describe the signs and symptoms.

Answer 36

Commonly follows DVT, delivery (amniotic fluid embolus), or fractures (fat emboli). Tachypnea, dyspnea, chest pain, hemoptysis (if lung infarct occurred), and hypotension, syncope, or death in severe cases. Rarely, CXR shows wedge-shaped defect due to pulmonary infarct.

Question 37

True or false: DVT can lead to a stroke.

Answer 37

False - with one rare exception. Embolization of L-sided heart clots (e.g. a. fib, ventricular wall aneurysm, severe CHF, endocarditis) causes arterial infarcts (stroke and renal, GI, or extremity infarcts) - NOT pulmonary emboli. DVT (or R-sided heart clots) that embolize cause pulmonary emboli - NOT arterial emboli. RARE Exception: Patient with R-to-L shunt (e.g. patent foramen ovale, atrial or ventricular septal defects, or pulmonary AV fistula)

Question 38

How is PE diagnosed?

Answer 38

V/Q scan or CT pulmonary angiogram to screen. If test is positive, PE is diagnosed and treatment is started. If indeterminate, conventional pulmonary angiogram is used. Conventional pulmonary angiography is gold standard but is invasive and carries high risk.

Question 39

How is PE treated?

Answer 39

Initially with LMW heparin or IV unfractioned heparin to prevent further clots and emoboli. Then switch to oral warfarin, which must be taken for at least 3-6 months. Recurrent clots on anticoagulation or contraindications to anticoagulation, IVC filter should be used. Rare patients with massive PE, surgical embolectomy or pharmacologic thrombolysis (e.g. t-PA) may be attempted.

Question 40

What is the most important side effect of heparin?

Answer 40

Thrombocytopenia that may be associated with arterial thrombosis. Measure CBC to monitor for this, usually occurs on days 3-7 of heparin administration. Discontinue heparin immediately if platelet counts begin to fall.

Question 41

How are the effects of aspirin, heparin, and warfarin monitored?

Answer 41

Heparin - partial thromboplastin time (PTT), a measure of the internal coagulation pathway Warfarin - prothrombin time (PT), a measure of the external coagulation pathway Aspirin - bleeding time, a measure of platelet function

Question 42

How are the effects of LMW heparin monitored?

Answer 42

LMW heparin does NOT affect any of the coagulation parameters and its effect is not clinically monitored. Rarely, a special type of factor X assay (anti-Xa) is used to measure the effect.

Question 43

In an emergency, how can you reverse the effects of heparin, warfarin, and aspirin?

Answer 43

Heparin and LMW heparin - reversed with protamine Warfarin - fresh frozen plasma (contains clotting factors; immediate effect) and/or Vitamin K (takes a few days to work) Aspirin - platelet transfusions

Question 44

How does Hemophilia A affect coagulation tests?

Answer 44

Prolongs PTT Low levels of factor 8 Normal PT and bleeding time X-linked

Question 45

How does Hemophilia B affect coagulation tests?

Answer 45

Prolongs PTT Low levels of factor 9 Normal PT and bleeding time X-linked

Question 46

How does vWF deficiency affect coagulation tests?

Answer 46

Prolongs bleeding time and PTT Normal or low levels of factor 8 Normal PT Autosomal dominant

Question 47

How does DIC affect coagulation tests?

Answer 47

Prolongs PT, PTT, bleeding time Positive D-dimer or fibrin degradation products Postpartum, infection, malignancy Schistocytes and fragmented cells on peripheral smear

Question 48

How does liver disease affect coagulation tests?

Answer 48

``` Prolongs PT Normal or prolonged PTT All factors EXCEPT 8 are low Stigmata of liver disease NO correction with vitamin K ```

Question 49

How does Vitamin K deficiency affect coagulation tests?

Answer 49

``` Prolongs PT, PTT (slight) Normal bleeding time Low levels of factors 2, 7, 9, and 10 Low levels of protein C and S Look for neonate who did not receive vitamin K shot, malabsorption, alcoholism, prolonged antibiotic use (kills Vitamin K producing flora) ```

Question 50

How does uremia affect platelets?

Answer 50

Causes QUALITATIVE platelet defect

Question 51

How does Vitamin C deficiency and chronic corticosteroid therapy affect coagulation tests?

Answer 51

NORMAL coagulation tests but still have bleeding tendency

Question 52

What are the general symptoms and signs of CHF?

Answer 52

Fatigue, ventricular hypertrophy on EKG, dyspnea, S3 or S4 on cardiac exam, cardiomegaly on CXR

Question 53

Signs and symptoms of left-sided HF?

Answer 53

Orthopnea (SOB when lying down, pt sleeps on more than 1 pillow or even sitting up), paroxysmal nocturnal dyspnea, pulmonary congestion (rales), Kerley B lines on CXR, pulmonary vascular congestion and edema, bilateral pleural effusions

Question 54

Signs and symptoms of right-sided HF?

Answer 54

Peripheral edema, jugular venous distention, hepatomegaly, ascites, underlying lung disease (cor pulmonale)

Question 55

How is chronic CHF treated?

Answer 55

Sodium restriction, ACEI (first-line agents that reduce mortality), beat blockers (counter-intuitive but work), diuretics, spironolactone, digoxin (not for diastolic dysfunction, usually reserved for moderate-to-severe CHF with low EF or systolic dysfunction), vasodilators (arterial and venous)

Question 56

How is acute CHF treated?

Answer 56

Inpatient basis with oxygen, diuretics, and positive inotropes. Digoxin may by used if patient is stable. IV sympathomimetics (dobutamine, dopamine, amrinone) are used for severe CHF.

Question 57

What factors precipitate exacerbations in previously stable patients with CHF?

Answer 57

Most commonly noncompliance with diet or meds, but watch for MI, severe HTN, arrhythmias, infections and fever, pulmonary embolus, anemia, thyrotoxicosis, and myocarditis

Question 58

Define cor pulmonale. With what clinical scenarios is it associated?

Answer 58

Right ventricular enlargement, hypertrophy, and failure due to primary lung disease. Common causes are COPD and PE. In young woman with no other history/risk factors think of idiopathic pulmonary HTN (treat with prostacyclins - parenteral epoprostenol, antiendothelins - bosentant, PDE5 inhibitors, Ca channel blockers) Sleep apnea (look for obese snorer who is sleepy during the day) *Tachypnea, cyanosis, clubbing, parasternal heave, loud P2, and R-sided S4 in addition to pulmonary disease signs/symptoms

Question 59

What causes restrictive cardiomyopathy?

Answer 59

Problem with the ventricles and usually is due to amyloidosis, sarcoidosis, hemochromatosis, or myocardial fibroelastosis. Ventricular biopsy is abnormal in all these conditions. S4 (indicates stiff ventricles) and signs of R-sided HF (JVD and peripheral edema)

Question 60

How is restrictive cardiomyopathy different from constrictive pericarditis?

Answer 60

Constrictive pericarditis can be fixed by removing an abnormal pericardium; look for pericardial knock on exam, calcifications of the pericardium, and a normal ventricular biopsy. Both conditions can have S4 (indicates stiff ventricles) and signs of R-sided HF (JVD and peripheral edema).

Question 61

What is the most common kind of cardiomyopathy? What causes it?

Answer 61

Dilated cardiomyopathy, most commonly caused by chronic CAD or ischemia, though by strict definition is not a true cardiomyopathy. Watch for alcohol, myocarditis, or doxorubicin as the cause.

Question 62

Which cardiomyopathy is likely in a young person who passes our or dies while exercising and has a family history of sudden death?

Answer 62

``` Hypertrophic cardiomyopathy, which may be autosomal dominant. Causes an asymmetric ventricular hypertrophy that reduces cardiac output (diastolic dysfunction). Treat with beta-blockers, or disopyramide (to allow ventricle more time to fill). Competitive sports should be avoided. Positive inotropes (e.g. digoxin), diuretics, and vasodilators are CONTRAINDICATED because they worsen the condition. ```

Question 63

How does atrial fibrillation look on EKG? How is it treated?

Answer 63

Erratic ventricular rate and atrial waves are not identical from segment to segment In symptomatic patients, first slow ventricular rate with beta-blocker, Ca channel blocker, or digoxin: - If acute (onset <24 hrs), cardiovert with amiodarone, procainamide, or DC cardioversion - If chronic, first anticoagulate, then cardiovert; if this fails leave patient on rate control meds and warfarin

Question 64

How does atrial flutter look on EKG? How is it treated?

Answer 64

Atrial waves are identical ("sawtooth") | Treat like atrial fibrillation. May try to stop arrhythmia with vagal maneuvers (e.g. carotid massage)

Question 65

How does first-degree heart block look on EKG? How do you treat it?

Answer 65

PR interval prolonged (more than 0.20 seconds) | No treatment, avoid beta-blockers and Ca channel blockers, both of which slow conduction

Question 66

How does second-degree Mobitz type I heart block look on EKG? How do you treat it?

Answer 66

Progression of PR interval before impulse is completely blocked Treat with pacemaker or atropine only in symptomatic patients

Question 67

How does second-degree Mobitz type II heart block look on EKG? How do you treat it?

Answer 67

Every alternate P wave is blocked | Treat with pacemaker

Question 68

How does WPW look on EKG? How is it treated?

Answer 68

Shortened PR interval and delta wave (slurred upstroke of QRS complex) Treat with procainamide or quinidine; avoid digoxin and verapamil

Question 69

How does WPW syndrome classically present?

Answer 69

Child becomes dizzy or dyspneic or passes out after playing, then recovers and has no other symptoms. The cause is a transient arrhythmia via the accessory pathway.

Question 70

How is ventricular tachycardia treated?

Answer 70

If pulseless, treat with immediate defibrillation followed by epinephrine, vasopressin, amiodarone, or lidocaine If pulse is present, treat with amiodarone and synchronized cardioversion

Question 71

How is ventricular fibrillation treated?

Answer 71

Immediate defibrillation

Question 72

How are premature ventricular complexes treated?

Answer 72

Usually not treated; if severe and symptomatic, consider beta-blockers or amiodarone

Question 73

How is sinus bradycardia treated?

Answer 73

Usually not treated; use atropine if severe and symptomatic (e.g. after MI) Avoid beta-blockers, Ca channel blockers, and other conduction-slowing medications

Question 74

How is sinus tachycardia treated?

Answer 74

Usually not treated; correct underlying cause | Use beta-blocker or Ca channel blocker if symptomatic

Question 75

What endocrine disease is suggested when a patient presents with sinus tachycardia or atrial fibrillation?

Answer 75

Hyperthyroidism, check TSH level as screening test

Question 76

Describe patent ductus arteriosus

Answer 76

Constant, machine-like murmur in upper L sternal border Dyspnea and possible CHF Close with indomethacin or surgery (if indomethacin fails) Keep open with PGE1 Associated with congenital rubella and high altitudes

Question 77

Describe ventricular septal defect

Answer 77

Holosystolic mumur next to sternum Most cases resolve on their own Watch for fetal alcohol, Down syndrome, or TORCH

Question 78

What is the most common congenital heart defect?

Answer 78

Ventricular septal defect

Question 79

Describe atrial septal defect

Answer 79

Often asymptomatic until adulthood Fixed, split S2, and palpitations Most defects do not require correction (unless very large)

Question 80

Describe Tetralogy of Fallot

Answer 80

Four anomalies: VSD, RVH, pulmonary stenosis, overriding aorta Look for "tet" spells (squatting after exertion)

Question 81

What is the most common cyanotic congenital heart defect?

Answer 81

Tetralogy of Fallot

Question 82

Describe coarctation of aorta

Answer 82

Upper extremity HTN only, radiofemoral delay, systolic murmur heard best over mid-upper back Rib notching on CXR Associated with Turner syndrome

Question 83

What is most important to remember about tachycardia in children?

Answer 83

Heart rates over 100 bpm may be noral in a child, as may respiratory rates greater than 20 per minutes

Question 84

In the fetal circulation, where is the highest and lowest oxygen content?

Answer 84

Higher oxygen content in umbilical vein (blood coming from the mother) Lowest in umbilical arteries Remember that oxygen content is higher in blood going to the upper extremities than in blood going to lower extremities

Question 85

What changes occur in the circulation as an infant goes from intrauterine to extrauterine life?

Answer 85

First breaths inflate lungs and cause decreased pulmonary vascular resistance, which increases blood flow to pulmonary arteries. This and clamping of cord increases L-sided heart pressures, causing functional closure of foramen ovale. Increased oxygen concentration shuts off prostaglandin production in ductus arteriosus, causing gradual closure.