Cardiology Flashcards
(143 cards)
Difference between MI and stable angina?
MI persists >30 mins and is NOT relieved by rest.
Findings for acute MI? Cardiac auscultation finding with Acute MI? (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 noncomplianceS3 - severe systolic dysfunction
ECG signs of Acute MI (4 Stages)
- Earliest: hyperacute T-waves (in the ischemic vascular territories) 2. ST elevation 3. Over hours to days: T-wave inversions4. Diminished R-wave amplitudes = Q-waves - significant myocardial necrosis and replacement of scar tissue
When does ST elevation occur?ST depression?
ST elevation - Acute transmural ischemiaST depression - Acute subendocardium ischemia
Definition of STEMI?
ST-segment elevations more than 1 mm (0.1 mV) in 2 or more contiguous leads (i.e. same vascular territories)
Elevations in Leads II, III, aVF
Inferior surface of the heart supplied by RCA
Elevation in V2 to V4
Anterior surface of the heart supplied by the Left Anterior Descending (LAD)
Elevation to Leads I, aVL, V5, V6
Lateral surface of the heart supplied by the LCX (Left circumflex coronary artery)
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.
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.
Other Dx with chest pain made worse with anticoagulants.
Aortic Dissection - unequal pulses or pressures in the arms, new murmur of aortic insufficiency, widen mediastinum
Acute pericarditis - pericardial friction rub, diffuse ST elevations
What is the management for Acute MI?
Antiplatelet agents: Aspirin, heparin
Beta-blockers - decrease myocardial oxygen demand
Nitrates - increase coronary blood flow
Morphine - pain, tachycardiaO2
Percutaneous Coronary Intervention (preferred for most) or Thrombolytics
What criteria are met for thrombolytic therapy? (5)
- Chest pain consistent with ischemia
- No contraindications to thrombolytics
- Age < 75 y.o.
- ST segment elevations more than 1 mm in at least 2 anatomically contiguous leads
- MI within 2-6 hours or within 12 hours with persistent chest pain + ST elevations
What criteria are met for PCI? (3)
Preferred method
- <1 hour-90 mins to reperfusion and/or
- contraindications to lytic therapy and/or
- hypotensive or in cardiogenic shock
Sinus Bradycardia is often seen with MI to which heart wall?
Inferior. RCA supplies the inferior wall of the left ventricle and the sinoatrial node.
What steps are taken for secondary prevention after a myocardial infarction to prevent recurrent cardiac events and death?
Smoking cessation Anti-platelets: Aspirin and clopidogrel Beta-blockers Ace-inhibitors Statins
Cardiogenic shock
Hypotension with systolic BP < 80mmHg
Reduced cardiac index less than 1.8 L/min/m^2Elevated LV filling pressure (pulmonary wedge pressure >18mmHg)Due to left ventricular pump failureEvaluated via Swan-Ganz catheterization
What mechanical complications can occur within 1 week of a MI? (4)Tx?
1a. Papillary muscle dysfunction - cause mitral regurgitation that is hemodynamically significant
1b. Papillary muscle rupture - acute mitral regurgitation1c. Ventricular septal rupture
2. Rupture of ventricular free wall - filling of the pericardium, cardiac tamponade develops rapidly with sudden pulselessness hypotension. Almost 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.
What late complications can occur after an MI?
- Ventricular aneurysms - if ST elevations persists weeks after the event
- Dressler’s syndrome - immune –> pericarditis, pleuritis, and fever
What is mortality in MI caused by? Management?
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
Diastolic dysfunction
Symptoms
Impaired diastolic relaxation and decreased ventricular compliance, but with preserved ejection fraction > 40% to 50%
Dysnea, peripheral edema, ascites
Systolic dysfunction
Symptoms
Low cardiac output by impaired systolic function ( EF < 40%)Fatigue, lethargy, hypotension
Therapy for Congestive Heart Failure
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
What devices are useful in heart failure?
If widen QRS > 120 ms, dysynchronous ventricular contraction –> Cardiac resynchronization therapy (CRT), a biventricular pacemaker.
Patients with EF Implantable cardiac defibrillator (ICD)
Most common symptomatic valvular abnormality in adults? Underlying etiology for 70y.o..
Aortic Stenosis
< 30 y.o. - congenital bicuspid valve
30-70 y.o. - congenital stenosis or rheumatic heart disease
>70 y.o. - degenerative calcific stenosis