Cardiology

Question 1

Difference between MI and stable angina?

Answer 1

MI persists >30 mins and is NOT relieved by rest.

Question 2

Findings for acute MI?

Cardiac auscultation finding with Acute MI? (2)

Answer 2

Chest pain (heavy, squeezing, crushing pain localized to the retrosternal area or epigastrium sometimes radiating to the arm, lower jaw or neck)

S4 - myocardial noncompliance
S3 - severe systolic dysfunction

Question 3

ECG signs of Acute MI (4 Stages)

Answer 3

1. Earliest: hyperacute T-waves (in the ischemic vascular territories)
2. ST elevation
3. Over hours to days: T-wave inversions
4. Diminished R-wave amplitudes = Q-waves - significant myocardial necrosis and replacement of scar tissue

Question 4

When does ST elevation occur?

ST depression?

Answer 4

ST elevation - Acute transmural ischemia

ST depression - Acute subendocardium ischemia

Question 5

Definition of STEMI?

Answer 5

ST-segment elevations more than 1 mm (0.1 mV) in 2 or more contiguous leads (i.e. same vascular territories)

Question 6

Elevations in Leads II, III, aVF

Answer 6

Inferior surface of the heart supplied by RCA

Question 7

Elevation in V2 to V4

Answer 7

Anterior surface of the heart supplied by the Left Anterior Descending (LAD)

Question 8

Elevation to Leads I, aVL, V5, V6

Answer 8

Lateral surface of the heart supplied by the LCX (Left circumflex coronary artery)

Question 9

Rise and fall of:
1. Creatine Phosphokinase (CK)
(while CK is found in skeletal muscles and other tissues, CK-MB is not found in significant amounts outside of heart muscle)
2. Cardiac specific troponin I and troponin T (cTnI, cTnT) - more specific to heart muscle and preferred markers for myocardial injury.

Answer 9

CK: rise within 4-8hrs. return to normal 48-72 hrs.

cTnI, cTnT: rise within 3-5 hours after infarct. cTnI remain elevated for 7-10 days. cTnT remain elevated for 10-14.

Question 10

Other Dx with chest pain made worse with anticoagulants.

Answer 10

Aortic Dissection - unequal pulses or pressures in the arms, new murmur of aortic insufficiency, widen mediastinum

Acute pericarditis - pericardial friction rub, diffuse ST elevations

Question 11

What is the management for Acute MI?

Answer 11

Antiplatelet agents: Aspirin, heparin
Beta-blockers - decrease myocardial oxygen demand
Nitrates - increase coronary blood flow
Morphine - pain, tachycardia
O2

Percutaneous Coronary Intervention (preferred for most) or Thrombolytics

Question 12

What criteria are met for thrombolytic therapy? (5)

Answer 12

1. Chest pain consistent with ischemia
2. No contraindications to thrombolytics
3. Age < 75 y.o.
4. ST segment elevations more than 1 mm in at least 2 anatomically contiguous leads
5. MI within 2-6 hours or within 12 hours with persistent chest pain + ST elevations

Question 13

What criteria are met for PCI? (3)

Answer 13

Preferred method

1. <1 hour-90 mins to reperfusion and/or
2. contraindications to lytic therapy and/or
3. hypotensive or in cardiogenic shock

Question 14

Sinus Bradycardia is often seen with MI to which heart wall?

Answer 14

Inferior. RCA supplies the inferior wall of the left ventricle and the sinoatrial node.

Question 15

What steps are taken for secondary prevention after a myocardial infarction to prevent recurrent cardiac events and death?

Answer 15

Smoking cessation
Anti-platelets: Aspirin and clopidogrel
Beta-blockers
Ace-inhibitors 
Statins

Question 16

Cardiogenic shock

Answer 16

Hypotension with systolic BP < 80mmHg
Reduced cardiac index less than 1.8 L/min/m^2
Elevated LV filling pressure (pulmonary wedge pressure >18mmHg)
Due to left ventricular pump failure
Evaluated via Swan-Ganz catheterization

Question 17

What mechanical complications can occur within 1 week of a MI? (4)

Tx?

Answer 17

1a. Papillary muscle dysfunction - cause mitral regurgitation that is hemodynamically significant
1b. Papillary muscle rupture - acute mitral regurgitation
1c. Ventricular septal rupture

2. Rupture of ventricular free wall - filling of the pericardium, cardiac tamponade develops rapidly with sudden pulselessness hypotension. Always fatal.

Use Doppler echocardiography to distinguish.
Tx: Intravenous nitroglycerin or nitroprusside (after load reduction) or aortic balloon until definitive surgical repair can be done.

Question 18

What late complications can occur after an MI?

Answer 18

1. Ventricular aneurysms - if ST elevations persists weeks after the event
2. Dressler’s syndrome - immune –> pericarditis, pleuritis, and fever

Question 19

What is mortality in MI caused by?

Management?

Answer 19

Ventricular arrhythmia (VT, VF), pump failure –> cardiogenic shock.

Direct current (DC) cardioversion or defibrillation followed by intravenous antiarrhythmics such as amiodarone

If bradycardia –> atropine

Symptomatic bradycardia –> pacemaker

Question 20

Diastolic dysfunction

Symptoms

Answer 20

Impaired diastolic relaxation and decreased ventricular compliance, but with preserved ejection fraction > 40% to 50%

Dysnea, peripheral edema, ascites

Question 21

Systolic dysfunction

Symptoms

Answer 21

Low cardiac output by impaired systolic function ( EF < 40%)

Fatigue, lethargy, hypotension

Question 22

Therapy for Congestive Heart Failure

Answer 22

Decrease mortality:
ACE inhibitors - Reduce preload and afterload so reduce right atrial, pulmonary pressures along with systemic vascular resistance and prevent remodeling.
Beta Blockers - prevent and reverse adrenergically mediated intrinsic myocardial dysfunction and remodeling
Aldosterone Antagonist

Salt restriction
Diuretics - decrease preload
Nitrates (vasodilators) - reduce preload, and clear pulmonary congestion
Digoxin - improve cardiac contractility

Question 23

What devices are useful in heart failure?

Answer 23

If widen QRS > 120 ms, dysynchronous ventricular contraction –> Cardiac resynchronization therapy (CRT), a biventricular pacemaker.

Patients with EF Implantable cardiac defibrillator (ICD)

Question 24

Most common symptomatic valvular abnormality in adults? Underlying etiology for 70y.o..

Answer 24

Aortic Stenosis

< 30 y.o. - congenital bicuspid valve
30-70 y.o. - congenital stenosis or rheumatic heart disease
>70 y.o. - degenerative calcific stenosis