Step-Up: Cardiovascular

Front 1

CAD can have the following clinical presentations:

Back 1

Asymptomatic, stable angina pectoris, unstable angina pectoris, MI, sudden cardiac death.

Front 2

Risk factors for stable angina pectoris:

Back 2

DM, LDL, HTN, smoking, men > 45, women > 55, 1st degree relatives with CAD/MI before m45/w55, low HDL, homocysteine.

Front 3

Prognostic indicators of CAD:

Back 3

Decrease prognosis: EF < 50%, L main coronary, 2 or 3 vessel CAD

Front 4

1. What is the sensitivity of a stress ECG?
2. What is a positive stress ECG?
3. What drugs should be withheld?
4. Next step in management for a positive stress ECG?

Back 4

1. 75% sensitivity if HR reaches 85% of maximum for predicted age.
2. ST segment depression, chest pain, hypotension, arrhythmias.
3. Withhold beta-blockers 12-24 hrs before, with hold digoxin and other antiischemic drugs.
4. Cardiac catheterization.

Front 5

Advantages of stress echo over ECG:

Back 5

More sensitive, assess LV size and function, diagnose valvular disease.

Info on hemodynamics, intracardiac pressures, cardiac output, oxygen saturation...

Front 6

What is the purpose of IV administration (thallium 201) during exercise stress test?

Back 6

Viable myocardial cells extract the radioisotope. No uptake means no blood flow. Helps determine ischemia (perfused over time) versus infarction. Reversible ischemia can be rescued with PTCA or CABG.

Front 7

Alternative to exercise stress test:

Back 7

IV adenosine, dipyramidole, or dobutamine. Adenosin/dipyramidole cause generalized coronary vasodilation (less blood to areas of need) = coronary steal.
Dobutamine: B1>B2 agonist.

Front 8

Medical therapy for CAD? Which Rx decrease morbidity or mortality?

Back 8

Aspirin - decreases morbidity (reduce MI risk).
Beta-blocker - reduce frequency of coronary events.
Nitrates - symptomatic relief.
Calcium channel blockers - secondary treatment to beta-blockers.
If CHF present: add ACEi +/or diuretic.

Front 9

Indications for revascularization versus medical management of CAD:

Back 9

Severe disease (decreased EF, severe angina, 3 vessel, left main, or LAD disease).
Revascularization does NOT reduce incidence of MI but does result in significant improvement in symptoms.

Front 10

Revascularization: PTCA w/ stent vs. CABG. Indications?

Back 10

PTCA: 1 or 2 vessel disease, proximal lesions. Restenosis up to 40% in first 6 months.
CABG: high-risk disease; left main, 3 vessel w/ reduced LV function, 2-vessel with proximal LAD stenosis, or severe ischemia for palliation of symptoms.

Front 11

10 yr patency of CABG:
1. LITA
2. RITA
3. Radial A.
4. Saphenous V.

Back 11

1. 95%
2. 90%
3. 80%
4. 50%

Front 12

Pathophysiology of unstable angina:

Back 12

Unstable angina = acute coronary syndrome = clinical manifestation of atherosclerotic plaque rupture and coronary occlusion. Oxygen demand is unchanged, alternatively, coronary flow is reduced.

Front 13

What is the diagnostic work up for unstable angina?

Back 13

1. Work up for MI: ECG, cardiac enzymes.
2. Stabilize with medical management before stress testing or undergo cardiac catheterization initially.

Front 14

1. Initial treatment of acute coronary syndrome:
2. Medical management:
3. Drugs not proven to be beneficial in unstable angina:

Back 14

1. Admit, monitor, IV access, oxygen, pain control with morphine and nitrates.
2. Aspirin, beta-blockers, LMWH (enoxaparin is drug of choice), nitrates, consider abciximab/tirofiban if PTCA/stenting
3. Calcium channel blockers and thrombolytic therapy.

Front 15

In conservatively treating unstable angina when should revascularization take place after medical therapy fails?

Back 15

If medical therapy fails to improve symptoms and/or ECG changes indicative of ischemia persist after 48 hours.

Front 16

Explain the findings of the CARE trial regarding MI.

Back 16

Statins reduce the risk of death, stroke and need for CABG or coronary angioplasy in patients with history of MI.

Front 17

Prinzmetal's angina:
1. Whats the hallmark sign on ECG?
2. Whats the definitive test?
3. What's the treatment of choice?
4. Are atherosclerotic lesions involved?

Back 17

1. S-T segment elevation.
2. Coronary angiography (when given IV ergonovine).
3. Calcium channel blockers and nitrates.
4. 75% of the time.

Front 18

MI:
1. Mortality rate?
2. Which patients can present asymptomatic?
3. Symptoms.

Back 18

1. 30% mortality (1/2 prehospital).
2. Postoperative, elderly, diabetic, women.
3. Substernal chest pain (>30 mins is a stronger indicator), diaphoresis, dyspnea, fatigue, nausea/vomiting, impending doom.

Front 19

Antithrombin III (thrombate III, Atnativ)

Back 19

-anticoagulant, protease inhibitor, heparin cofactor I
-inhibits thrombin and factors IXa, Xa, Xia, XIIa and plasmin
-for pts w/ antithrombin III deficiency

Front 20

When monitoring a patient with an acute MI, what is the importance of PVC's?

Back 20

PVC's can lower stroke volume and coronary artery filling time. PVC's may predict VFib or VT.

Front 21

1. How should cardiac enzymes be drawn?
2. What can falsely elevate Troponin I?

Back 21

1. Once on admission and every 8 hours for a total of three. CKMB (onset 4-8, peak 24, normal at 48-72). Troponins (3-5, 24-48, 5-14 days).
2. Renal failure.

Front 22

In MI:
1. What agents are shown to reduce mortality in MI?
2. What agent reduces risk of further coronary events?
3. What agent that prevents progression of thrombus has not been shown to decrease mortality (but given to all patients with MI)?

Back 22

1. B-blockers (CAPRICORN - reduce risk of death in patients with post MI LV dysfunction), ACEi (HOPE), aspirin.
2. Statins.
3. Heparin.

Front 23

Revascularization (PTCA or tPA) after MI:
1. Most important principle.
2. Indications
3. GUSTO trials says...
4. Contraindications of thrombolytics?
5. PAMI trials says...

Back 23

1. Time more important than method. Best within 6 hrs (up to 24).
2. ST elevation in two contiguous ECG leads in symptomatic patient refractory to nitroglycerin.
3. Use tPA + IV heparin over streptokinase.
4. HTN 180/110, head trauma, active PUD, Hx of stroke, surgery, dissecting aortic aneurysm.
5. PTCA > tPA.

Front 24

After treating an MI with percutaneous transluminal coronary angioplasty, what anticoagulants are indicated?

Back 24

Aspirin and clopidogrel (12 mo for NSTEMI or 20 days for post-PCI)

Front 25

What is the appropriate treatment for AV block after an MI?

Back 25

1st and 2nd (type I) degree: no treatment.
2nd (type II) and 3rd degree: prognosis is dire in the setting of anterior MI - emergent pacemaker. If inferior MI, IV atropine initially then pacemaker if needed.

Front 26

Name the complications of acute MI:
1. 7 days post ant.-MI patient develops PEA, muffled heart sounds.
2. New onset systolic murmur.
3. Fever, malaise, pericarditis, pleuritis, 4 weeks post MI.
4. Treatment consists of aspirin to prevent myocardial scar formation.

Back 26

1. Free wall rupture leading to tamponade.
2. Papillary muscle rupture.
3. Dressler's syndrome.
4. Acute pericarditis.

Front 27

Causes of high-output heart failure:

Back 27

Chronic anemia, pregnancy, hyperthyroidism, AV fistulas, Wet beriberi (B1 def.), Paget's, mitral regurgitation, aortic insufficiency.

Front 28

CHF:
What NYHA class may experience diaphoresis and cool extremities at rest?

Back 28

This occurs in desperately ill patients - NYHA IV: symptoms at rest.
NYHA III: symptoms occur with acitivites of daily living.
NYHA II: symptoms occur with prolonged/moderate exertion.
NYHA I: symptoms occur with vigorous activities.

Front 29

1. Signs of left-sided heart failure?
2. Signs of right-sided heart failure?

Back 29

1. Displaced PMI (cardiomegaly), S3 (specific), S4, crackles/rales, dull percussion, rusty sputum.
2. Peripheral pitting edema, nocturia, JVD, hepatomegaly, ascites, RV heave.

Front 30

Diagnosis of CHF:
1. Initial test of choice?
2. What determines systolic dysfunction?
3. What are Kerley B lines?
4. BNP > ____ correlates strongly with CHF.

Back 30

1. Echocardiogram.
2. EF < 40%
3. Lines near periphery of the lung near the costophrenic angles and indicate pulmonary congestion secondary to dilatation of pulmonary lymphatic vessels.
4. BNP > 100 pg/mL

Front 31

Treatment of CHF:
1. NYHA I or II?
2. NYHA II to III?
3. NYHA III to IV?

Back 31

1. Salt < 4g; loop if pulmonary congestion; ACEi .
2. Loop and ACEi; add B-blocker.
3. Add digoxin; IV - spironolactone.

Front 32

CHF (systolic):
1. Do diuretics reduce mortality or improve prognosis?
2. Do ACEI reduce mortality?
3. Do B-blockers decrease mortality in post MI CHF?

Back 32

1. NO.
2. YES (CONSENSUS, SOLVD).
3. YES (COMET).

Front 33

Premature beats:
1. Treatment for asymptomatic PAC's? Symptomatic?
2. treatment for asymptomatic PVC's? Symptomatic?

Back 33

1. None, b-blockers.
2. None, b-blockers. PVC's + underlying heart disease = consider implantable cardioverter defibrillator (ICD).

Front 34

1. Diagnosis of AF?
2. What constitutes a hemodynamically unstable AF patient?

Back 34

1. ECG - irregularly irregular rhythm. Atrial rate - 400bpm, ventricle rate - 75-175.
2. Systolic BP < 90, chest pain, dyspnea, hypoperfusion.

Front 35

Treatment of acute AF?

Back 35

Hemodynamically:
Unstable: electrical cardioversion (90% successful).
Stable: treat rate: CCB > BBlocker (or amiodarone if LV systolic dysfunctin; treat rhythm: electrical > chemical; anticoagulate.

Front 36

What are the anticoagulation strategies in treating acute AF?

Back 36

If AFib > 48 hours: anticoagulate for 3 weeks before and 4 weeks after cardioversion.
INR: 2-3.
Alternatively do TEE, if no thrombus present, start IV heparin and cardiovert + 4 weeks anticoagulation.

Front 37

When would a patient with chronic AFib not be anticoagulated?

Back 37

"Lone" AFib (absence of heart disease or other cardiovascular risk factors) under age 60. Aspirin only.

Front 38

AFlutter:
1. Common associations?
2. Atrial rate? ventricle rate?
3. Affect of carotid pressure?

Back 38

1. COPD (most common), ASD, CHF, CAD.
2. 250, 125.
3. 2:1 flutter to 3:1 flutter.

Front 39

Paroxysmal Supraventricular Tachycardia (PSVT):
1. Pathophysiology?
2. Causes?

Back 39

1. Reentry circuits: AV nodal or Orthodromic AV. Initiated by PACs or PVCs.
2. IHD, digoxin (w/ 2:1 block)), AFlutter, caffeine, EtOH

Front 40

PSVT:
1. Acute treatment?
2. Prevention?
3. Recurrent symptomatic treatment option.

Back 40

1. Adenosine (or DC cardioversion if unstable/refractive).
2. Digoxin is drug of choice.
3. Cardiac ablation.

Front 41

WPW:
1. ECG changes?
2. Avoid what drug?

Back 41

1. Short PR, delta wave, tachy
2. Avoid digoxin.

Front 42

Patient presents with palpitations, dyspnea, and near-syncope. Signs include hypotension, cannon a-waves, S1 that varies in intensity, and HR of 150 pbm for 40 seconds. Diagnosis?

Back 42

Sustained VT (> 30 seconds): repetitive firing of 3+ PVC in a row and rate 100-250. Prognosis depends on sustained (worse) or unsustained and underlying heart conditions (MI, LV dysfunciton).

Front 43

Treatment of sustained VT:
1. If hemodynamically stable?
2. Hemodynamically unstable?
3. Nonsustained VT?

Back 43

1. Pharm: IV amiodarone, procainamide, sotalol over lidocaine or bretylium. Lidocaine increases risk of asystole.
2. DC cardioversion then amiodarone.
3. Nil.

Front 44

What is the most effective treatment for a patient with underlying heart disease and nonsustained VT?

Back 44

Implantable defibrillator.

Front 45

AV BLOCK:
1. Where is the site of block in Mobitz I?
2. Where is the site of block in Mobitz II?
3. Treatment of I and II?

Back 45

1. Progressive prolongation. Block within AV node.
2. P wave (and QRS) drop suddenly. Block within His-Purkinje.
3. I - none. II - pacemaker.

Front 46

Cardiomyopathy:
1. Most is the most common cause of the most common type of cardiomyopathy?
2. Causes of this type of cardiomyopathy?

Back 46

1. CAD (w/ prior MI) is most common cause of dilated cardiomyopathy.
2. EtOH, doxorubicin, thiamine deficiency, uremia, infectious, peripartum, thryroid disease, catecholamine-induced, collagen vascular disease (SLE, scleroderma).

Front 47

Standing, the Valsalva, and leg raise maneuvers increase the intensity of which murmurs?

Back 47

MVP and HCM. These maneuvers decrease left ventricular volume. Squatting decreases the intensity.
Sustained handgrip (increase systemic resistance) increases the intensity of MVP murmur, but diminishes HCM.

Front 48

What is the treatment for symptomatic HCM?

Back 48

Beta-blockers (increase duration of diastole). Surgery (myomectomy of the myocardial septum).

Front 49

Patient presents with severe, pleuritic chest pain (pain on inspiration) which is mildly relieved by leaning forward. The patient recalls having a sore throat last week. Exam: pericardial friction rub.
1. What could be apparent on ECG?
2. Duration of disease?
3. Tx?

Back 49

Acute pericarditis: postviral is a common cause.
1. ECG: diffuse ST elevation and PR depression.
2. Resolves in 2-6 weeks.
3. NSAIDs. Glucocorticoids if required.

Front 50

Patient presents very ill, hepatomegaly, ascites, and over the next couple days develops a cough and orthopnea. The patient's JVD fails to decrease during inspiration. Pericardial knock present.
1. Initial diagnostic test?
2. Treatment?

Back 50

Constrictive pericarditis.
1. Echocardiogram.
2. Surgical: resection of pericardium.

The patient's JVD fails to decrease during inspiration (Kussmaul's sign).

Front 51

CXR shows a patient with an enlarged heart without pulmonary vascular congestion. Patient has muffled heart sounds.
1. Imaging procedure of choice?
2. ECG may show?
3. Treatment?

Back 51

1. Echo - can see as little as 20 mL of fluid (CXR shows 250 mL).
2. Low QRS voltage, electrical alternans (if massive).
3. Repeat echo in 1 to 2 weeks. Drain if hemodynamically unstable.

Front 52

Tamponade:
1. More important: volume or rate?
2. Whats pulsus paradoxus?
3. Most common finding?

Back 52

1. Rate.
2. Decrease in arterial pressure during inspiration (> 10 mm Hg drop).
3. Elevated JVP. Prominent x descent with absent y descent.

Front 53

Mitral stenosis:
1. Normal valve area is 4-5 cm2. When do patients become symptomatic?
2. Murmur?
3. ECG?
4. Most important test?

Back 53

1. When area is reduced by 1.5 cm2.
2. OS, diastolic rumble. Increased severity brings OS closer to S2. Loud S1.
3. Bifid P-wave if LAH. AFib in long standing stenosis.
4. Echo.

Front 54

1. Aortic valve area at which CO fails to increase with exertion, leading to angina?
2. Three classic symptoms and associated average survival?

Back 54

1. 0.7 cm2.
2. Angina - 3 yr survival; syncope - 2 yr; heart failure - 1.5 yr.

Front 55

Diagnosis criteria for acute Rheumatic Fever:

Back 55

2 major or 1 major/2minor
Major: migratory polyarthritis, erythema marginatum, cardiac involvement, chorea, subcutaneous nodules.
Minor: fever, ESR, arthralgia, hx of RF, prolonged PR interval, evidence of streptococcal pharyngitis infection.

Front 56

Endocarditis - name the common causative organism:
1. Acute
2. Subacute
3. Prosthetic valve
4. Bowel cancer
5. HACEK
6. IV drug (2x)

Back 56

1. S. aureus
2. S. viridans
3. S. epidermidis
4. S. bovis
5. Haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
6. S. aureus, enterococci.

Front 57

Name the condition associated with these valvular lesions:
1. Small warty vegetations on both sides of valve leaflets.
2. Sterile deposits of fibrin along the closure line of leaflets.

Back 57

1. Libman-Sacks endocarditis (SLE).
2. Marantic endocarditis (mucin-producing tumors).

Front 58

Define:
1. Hypertensive emergency
2. Hypertensive urgency

Back 58

1. SBP > 220 and/or DBP > 120 in addition to end-organ damage (papilledema, mental status, renal failure/hematuria, angina/MI/CHF/aortic dissection, pulmonary edema).
2. No end-organ damage.

Front 59

60 yr old patient with known longstanding HTN presents with interscapular tearing pain, hypertension, diaphoresis and new onset aortic regurgitation.
1. What will CXR show?
2. Whats the best bedside test?
3. What is the treatment?

Back 59

Aortic dissection.
1. Widened mediastinum (> 8 mm).
2. Transesophageal echocardiogram.
3. IV B-blockers, IV nitroprusside, surgical management for type A (asc. aorta) dissection.

Front 60

What are the progressive symptoms of peripheral vascular disease? What are the signs?

Back 60

1. Intermittent claudication: REPRODUCED by same walking distance. (ABI < .7)
2. Rest pain (especially at night). (ABI < .4)
3. Gangrene.
Signs: absent pulse, muscular atrophy, hairless, thicken toe nails, cool, ulceration (over toes), pallor on elevation, rubor on dependency.

Front 61

Patient had an MI 4 days ago. Now presents with pain, pallor, pulselessness, and coolness in his leg.
1. Diagnosis?
2. Treatment?
3. Complication of treatment?

Back 61

Acute arterial occlusion (other causes: Afib, endocarditis, myxoma, athteromatous plaque).
1. Arteriogram
2. Anticoagulate - IV heparin, surgical embolectomy (Fogarty balloon).
3. Reperfusion, rhabdomyolysis (arrythmia, ARF)

Front 62

1. Is anticoagulation appropriate in the setting of cholesterol embolization syndrome?
2. Common cause of mycotic aneurysm? Fungal? Bacterial?

Back 62

1. No.
2. Fungal - aspergillus, candida, mucor.
2. Bacterial - B. fragilis, P. aeruginosa, Salmonella.

Front 63

Complications of DVT:

Back 63

1. PE
2. Chronic venous insufficiency - damaged valves leading to ambulatory venous HTN resulting in edema and indurated, pigmented skin (extravasation of fluid, proteins and RBCs).
3. Phlegmasia cerulea dolens - severe leg edema compromising arterial supply: pain, cyanosis.

Front 64

Explain the treatment for DVT:

Back 64

1. Anticoagulation: IV heparin for 48 hrs at aPTT 1.5-2x and begin warfarin when aPTT is therapeutic. Aim for INR 2-3 for 3-6 months.
2. Thrombolytic therapy for massive PE, RHF, unstable pt.
3. Greenfield filter - if contraindications for anticoag
4. Mechanical: PEDs, elevation, compression.

Front 65

1. Whats the consequence of long standing chronic venous insufficiency (CVI)?
2. Treatment?

Back 65

1. Reduced capillary flow - hypoxic tissue - ulcer/tissue death (m. malleolus).
2. LEG ELEVATION.

Front 66

Superficial thrombophlebitis
1. Cause of migratory ST?
2. MCC of upper extremity ST?
3. Symptoms?
4. Anticoagulation?

Back 66

1. Malignancy (pancreas).
2. IV infusion. (in lower limb - associated with varicosities).
3. Pain, tenderness, erythema, INDURATED vein (cellulitis more diffuse, no induration of vein).
4. NO. NSAIDs only.

Front 67

Cardiogenic shock
1. Quantitative definition?
2. MCC?
3. Unique clinical feature (vs. other forms of shock)?
4. What surgical intervention improves survival?

Back 67

1. SBP < 90 with urine output < 20 mL/hr.
2. Acute MI.
3. Elevated JVP/PCWP.
4. IABP: decreases afterload, increases CO, decreases oxygen demand of myocardium.

Front 68

Hemodynamic changes in hypovolemic shock and % of loss?
1. Class I
2. Class II
3. Class III
4. Class IV

Back 68

1. 10-15% - none changes.
2. 20-30% - tachycardia, tachypnea, 20-30 ml/hr of urine.
3. 30-40% - weak pulse, decrease SBP, confusion, 20ml/hr.
4. > 40% Coma, no urine.