Case Files Flashcards
When is direct current cardioversion indicated post-MI?
When ventricular contraction is not coordinate w/ the SA node, such as in sustained VT (over 30 sec) and VF
Amiodarone
Antiarrhythmic
What is an inferior MI?
Inferior MI = ST segment elevation in the inferior leads (II. III. aVF) = RCA territory
Complications of an inferior MI that may required atropine
Inferior MI is MI involving the RCA (leads II, III, aVF are the inferior leads), RCA Is what supplies the SA node => inferior MI can cause bradycardia
-usually this bradycardia doesn’t require tx, but if HR falls low enough for CO and BP to fall, give IV atropine (ACh receptor blocker)
Mobitz I vs. Mobitz II second-degree AV Block
Mobitz I = Gradual prolongation of the PR interval before a nonconducted P wave (dropped beat)
Mobitz II = nonconducted P waves (dropped beat) NOT preceded by PR prolongation
-AV nodal dysfunction (ex: nodal ischemia from inferior MI)
Criteria for cardiogenic shock
Hypotension w/ systolic BP under 80 mmHg
- markedly reduced cardiac index less than 1.8 L/min/m2
- elevated LV filling pressure
Clinical appearance of pt in cardiogenic shock
- hypotensive
- cold extremities due to peripheral vasoconstriction
- pulmonary edema (due to high left sided filling pressures)
- elevated jugular venous pressure (due to high right sided filling pressures)
Development of acute heart failure w/ new holosystolic murmur after MI
Complication of MI = ventricular septal rupture => holosystolic murmur
-stabilize w/ afterload reduction (IV nitroglycerin)
Most catastrophic and lethal complication of MI
Rupture of the ventricular free wall
- as blood fills the pericardium, cardiac tamponade develops => sudden pulselessness, hypotension, LOC
- nearly always fatal
Dressler syndrome
(a) Tx
Dressler syndrome = post-MI immune phenomenon characterized by pericarditis, pleuritis, and fever
(a) Tx = anti-inflammatory, mainly NSAIDs and sometimes prednisone
Most important risk factor to prevent cardiac events
Smoking cessation
Medicines for secondary prevention of ischemic heart disease
- aspirin
- clopidogrel
- beta-blocker
- statin
- ACEi
59 yo diabetic F had acute anterior wall MI 5 days ago, is complaining of CP
- current EKG shows no ischemic changes
- troponin levels are mildly elevated
Next best step?
Next best step = serial EKGs and obtain CK-MB
(not PCI)
- tropnonins remain elevated 5-14 days after event => shouldn’t be used to diagnose reinfarction
- new EKG findings or rising CK-MB can be used to dx reinfarction
EKG leads
(a) Anterior
(b) Lateral
(b) Inferior
EKG leads
(a) Anterior leads = LAD territory = V2,3,4
(b) Lateral leads = Left circ territory = I, aVL, V5, V6
(c) Inferior leads = RCA territory = II, III, aVF
How to ACEi reduce mortality in heart failure?
ACEi reduce preload and afterload => decreasing atrial, pulmonary arterial, pulmonary capillary wedge pressures and systemic vascular resistance => prevents remodeling
Use of diuretics in HF
To reduce preload
Most probable cause of aortic stenosis in
(a) Pts under 30
(b) Pts 30-70 yoa
(c) Pts over 70 yoa
Aortic stenosis cause in
(a) Pts under 30 = congenital bicuspid aortic valve
(b) 30-70 yoa: congenital bicuspid aortic valve or acquired rheumatic disease
(c) Over 70 yoa: degenerative calcific stenosis
Gives examples in each of the categories for causes of CHF
(a) Myocardial injury
(b) Chronic pressure overload
(c) Chronic volume overload
(d) Infiltrative Diseases
Causes of CHF
(a) Myocardial injury
- acute rheumatic fever
- ischemic cardiomypathy from atherosclerotic CAD
- alcohol and cocaine use
- viral myocarditis
- chemo drug: adriamycin
(b) Chronic pressure overload from HTN (high SVR) and aortic stenosis
(c) Chronic volume overload from mitral regurg
(d) Infiltrative disease
- amyloidosis
- hemochromatosis
55 yo M w/ CHF and DOE
-EF 47%
Diastolic or systolic dysfunction?
W/ EF over 40%- more likely to be diastolic dysfunction (stiff ventricles that do not readily accept blood)
Signs of aortic stenosis
(a) pulse pressure
(b) type of murmur
- best heard where?
Aortic stenosis
(a) Narrow pulse pressure
- narrow reading btwn systolic and diastolic
(b) harsh, late-peaking systolic murmur
- late-peaking crescendo-decrescendo ejection systolic murmur
- heard best at right 2nd intercostal space, radiates up to carotids
Pulsus parvus et tardus
Delayed slow-rising carotid upstroke- indicative of aortic stenosis
Parvus = weak/small b/c upon palpation pulse is weak Tardus = late b/c upon palpation pulse is late
What is the most common cause of CHF in the US?
Myocardial injury due to ischemic cardiomyopathy (atherosclerotic coronary artery disease)
-so basically CAD so basically HTN/HLD
How to distinguish HF from systolic vs. diastolic dysfunction
Ejection fraction
HF due to impaired systolic fraction has EF under 40%
HF due to diastolic dysfunction will have preserved EF
What determines CHF functional class?
Exercise tolerance
-best predictor of mortality and often guides therapy
