How do you make diagnosis of prinzmetal's angina?
cardiac catheterization: shows no atherosclerosis, but ergonovine can precipitate spasm
Name 5 precipitating factors for acute coronary syndrome:
1) physical exertion; 2) emotional/ mental stress; 3) anxiety; 4) cold exposure; 5) post large meal
How can u differentiate pericarditis from angina from the history?
pericarditis pain is sharper, worse with lying down, relieved with sitting up
3 ways to confirm diagnosis of esophageal reflux or spasm mimicking angina:
1) upper GI series; 2) endoscopy; 3) esophageal manometry
Definition of stable angina:
occurs during exertion; same amt of exercise reproduces pain; relieved by rest
Name 3 indications for exercise stress test:
1) to confirm diagnosis of angina; 2) to determine severity of dz; 3) post MI evaluation
Contraindications to stress testing:
1) unstable angina; 2) aortic stenosis; 3) IHSS; 4) severe COPD; 5) acute CHF; 6) acute ischemia on ECG; 7) aortic dissection; 8) severe uncontrolled HTN
Name 3 indications for cardiac catheterization in pt with angina:
1) sxs poorly controlled with rx; 2) + stress test --> determine need for revascularization; 3) determine presence of main criteria for bypass sx
JNC7 guidelines for controlling BP in pts with and without DM
without DM = <140/90; with DM = <130/80
JNC7 guidelines for controlling total cholesterol and LDL in pt with very high cardiac risk profile
T.chol <190; LDL <70
Effect of nitrates in moderate doses
increase venous and arterial dilatation --> decrease both preload and afterload
3 Effects of beta blockers that make them useful in treating angina
decrease 1) HR, 2) BP; 3) contractility --> decrease O2 demand of heart
Name 6 treatment options for angina
1) nitrates; 2) BBs; 3) lipid lowering agents (i.e. statins); 4) antiplatelet agents (aspirin +/- plavix); 5) CCBs (only for prinzmetal's); 6) revascularization
In a pt with one or no risk factors, at what LDL level do u institute dietary modification? medication?
LDL >130; LDL >160
In a pt with more than one risk factor, at what LDL level do u institute dietary modification? medication?
LDL >160; LDL >190
3 questions to ask to determine whether chest pain is typical, atypical or nonanginal:
1) is the pain retrosternal? 2) is the pain brought on by stress? 3) is the pain relieved with rest or NTG?
5 general causes of non-atherosclerotic MI
1) vasculitis; 2) congenital anomaly of coronaries; 3) coronary spas (i.e. cocaine); 4) coronary artery embolus (i.e. atrial thrombus); 5) hypercoagulable states
Name 4 factors that would make ECG interpretation of MI difficult:
1) LBBB; 2) previous MI; 3) pacemaker; 4) digoxin use
Sign of posterior infarction on initial 12-lead ECG
in leads V1-V2: 1) tall, broad R waves; 2) ST depression; 3) tall peaked T wave
Indications for thrombolytic therapy for acute MI
within 12 hrs of onset of chest pain plus one of following ECG findings: 1) >1mm ST elevation in 2 contiguous leads; 2) new LBBB
Contraindications to thrombolytic therapy:
1) dissecting AA; 2) uncontrolled HTN (>180/110); 3) active PUD; 4) recent head trauma; 5) recent invasive procedure or sx; 6) previous CVA; 7) traumatic CPR; 8) proliferative diabetic retinopathy; 9) active internal bleeding; 10) intracranial malignancies; 11) recent IV puncture at noncompressible site
Maximum benefit of ACEI have been shown in what 3 clinical situations?
1) CHF; 2) LV dysfunction (EF <40%); 3) anterior wall MI
Indications for temporary transvenous pacing in acute MI:
1) 2nd degree heart block, type II or greater; 2) sinus bradycardia despite atropine; 3) junctional or idioventricular rhythm w/ slow ventricular rate and hypoperfusion; 4) LBBB in acute MI; 5) bifascicular block with 1st degree AV block; 6) new bifascicular block
Indications for IABP
1) recurrent or persistent MI; 2) severe left or biventricular failure +/- shock
Precipitating causes of CHF
1) increased salt intake; 2) inappropriate reduction in drug regimen; 3) excess exertion or stress; 4) arrhythmias; 5) systemic infection; 6) cardiac depressants; 7) fluid overload; 8) renal failure; 9) MI
3 tests used to make diagnosis of CHF
1) CXR; 2) echo; 3) MUGA scan or radionuclide ventriculography
3 main therapeutic objectives in management of CHF:
1) reduce cardiac workload; 2) improve cardiac performance; 3) control excess salt and water
Mechanism of action of digoxin
inhibition of Na/K ATPase --> --> increase intracellular Ca --> inotropic effect
Cardiac causes of pulmonary edema
1) arrhythmias; 2) MI; 3) severe systemic HTN; 4) PE; 5) valvular heart dz
Noncardiac causes of pulmonary edema
1) ARDS; 2) uremia; 3) aspiration; 4) head trauma; 5) allergic reaction to rx; 6) alveolar capillary leak
CXR findings in pulmonary edema
1) prominent pulmonary vessels; 2) enlarged cardiac silhouette; 3) Kerley B lines; 4) effusion
Signs and sxs of pulmonary edema
1) tachypnea; 2) cough with pink frothy sputum; 3) cyanosis; 4) nocturnal dyspnea; 5) rales, rhonchi and wheezing
Name 4 CXR findings in pulmonary edema
1) prominent pulmonary vessels; 2) cardiomegaly; 3) kerley b lines; 4) pleural effusion
Treatment for pulmonary edema
1) morphine; 2) lasix (to reduce preload); 3) dobutamine; 4) sit pt upright; 5) O2 with PEEP; 6) NTG to reduce preload; 7) digoxin if afib; 8) IV ACEI
Pathophys in mitral stenosis
MS --> impedes LV filling --> increased LA pressure --> pulmonary congestion --> secondary pulmonary vasoconstriction --> RV failure
What is the murmur of mitral stenosis?
mid to late low pitched diastolic murmur preceded by opening snap
Name 3 findings of ECG consistent with mitral stenosis:
1) LA enlargement; 2) RV hypertrophy; 3) +/- afib
What findings on CXR suggest left atrial enlargement?
1) double-density right heart border; 2) posterior displacement of esophagus; 3) elevated left mainstem bronchus
4 causes of acute mitral regurgitation
1) ruptured chordae tendineae; 2) papillary muscle rupture; 3) endocarditis; 4) trauma
What is the effect of chronic mitral regurgitation on preload?
increases preload (MR --> decreased CO --> RAAS --> fluid retention
What is the effect of chronic mitral regurgitation on afterload?
decreased afterload as a portion of stroke volume is ejected retrograde into LA
What are the 2 goals of treatment for mitral regurgitation?
relieve sxs by 1) increasing forward output; 2) reducing pulmonary venous hypertension
4 classes of drugs used to treat MR
1) digitalis; 2) diuretics; 3) arteriolar vasodilators; 4) anticoagulants
Indication for surgical repair of MR
severe MR with significantly limiting sxs despite optimal medical management
Papillary muscle rupture with acute MR is associated with which infarct?
inferoposterior infarcts (posterior papillary muscle involvement)
Palpable precordial thrill associated with rupture of papillary muscle or ventricular septum?
4 diagnostic tests to confirm diagnosis of papillary muscle rupture
1) 2-d echo; 2) doppler flow study; 3) PA cath; 4) LV angiography
Murmur of mitral valve prolapse
mid to late systolic click and a late systolic murmur heard best at the apex
Effect of maneuvers on murmur of mitral valve prolapse
improves with squatting (increased venous return); worsens with valsalva (decreased venous return)
3 most common causes of AS
1) degenerative (aging); 2) calcification and degeneration of a congenital bicuspid valve; 3) rheumatic heart dz
What heart sound is associated with AS
S4 (forceful atrial contraction augments filling of thick, noncompliant ventricle)
3 mechanisms which contribute to angina in AS
1) LV hypertrophy; 2) high intramyocardial wall tension; 3) decreased diastolic coronary blood flow
Pulsus parvus et tardus
upon palpation, the pulse is weak/ small (parvus) and late (tardus) in relation to contraction of the heart
3 possible findings on CXR in pt with AS
1) cardiomegaly; 2) calcified aorta; 3) pulmonary congestion
6 conditions that may affect the ascending aorta and cause AR
1) syphillis; 2) ankylosing spondylitis; 3) marfan's syndrome; 4) systemic htn; 5) aortic dissection; 6) aortic trauma
Pathophys of chronic AR
AR --> volume overload of LV (increased LVEDV) --> LV dilatation --> dilated cardiomyopathy and volume overload
Cause of increased pulse pressure in AR
AR --> initial decrease in stroke volume --> compensatory decrease in SVR to maintain CO --> drop in diastolic BP; compensatory LV dilation --> increase in SV --> increased systolic BP
2 factors which affect pulse pressure
1) stroke volume (proportional) ; 2) compliance of aorta (inversely proportional)
Murmur of AR
diastolic decrescendo murmur OR systolic flow murmur (secondary to greatly increased stroke volume)
systolic and or diastolic thrill or murmur heard over the femoral arteries; related to high pulse pressure
Austin Flint murmur
a mid-diastolic, low pitched rumbling murmur best heard at the cardiac apex; seen in AR
Pathophys of austin flint murmur
the result of mitral valve leaflet displacement along with turbulent mixing of antegrade mitral flow and retrograde aortic flow
Treatment for AR
treat like CHF secondary to systolic dysfxn: 1) preload reduction (salt restriction and diuretics); 2) digitalis; 3) afterload reduction (ACEI)
Effect of Hypertrophic cardiomyopathy on stroke volume and ejection fraction
stroke volume: normal to increased; ejection fraction: increased
Clinical manifestations of dilated cardiomyopathy:
same as those for left and right ventricular failure
4 DDx for dilated cardiomyopathy
1) acute myocarditis; 2) valvular heart disease; 3) CAD; 4) hypertensive heart dz
Treatment for dilated cardiomyopathy
same as for systolic dysfxn CHF: 1) decrease preload (salt restriction, diuretics); 2) digoxin; 3) decreased afterload (ACEI, hydralazine); 4) ventricular remodeling (BB) PLUS 5) anticoagulants (high freq of pulm and systemic embolism)
Why does a reduction in preload increase obstruction in HCM?
decreased venous return --> decreased size of the heart --> mitral valve brought closer to the septum
Name 3 mechanisms that increase obstruction in HCM:
1) increase in contractility; 2) reduction in preload; 3) reduction in afterload
3 factors that decrease obstruction in HCM:
1) decrease in contractility; 2) increased preload; 3) increase in afterload
Rx Tx for HCM
negative inotropes: 1) BB; 2) CCB (verapamil, diltiazem); 3) disopyramide (sxs benefit for severely limited pts)
What is the preferred treatment in nonobstructive HCM?
goal is to improve LV relaxation; tx with CCBs
What is the preferred tx in latent obstructive HCM?
goal is to prevent provocation of obstruction; tx with BBs
What is the preferred tx in resting obstructive HCM?
goal is relief of obstruction to LV outflow; tx with disopyramide
How to auscultate for pericardial friction rub?
with diaphragm, as pt sits forward at forced-end expiration
ECG findings in acute pericarditis:
diffuse ST segment elevation, absence of reciprocal changes, upright T waves
A transudative pericardial effusion can be seen in what 3 cases?
1) CHF; 2) hypoproteinemia; 3) overhydration
decrease in systolic BP of more than 10mmHg with normal inspiration; palpated as weakened pulse with inspiration along with more heart contractions to pulse beats
How to differentiate btw constrictive pericarditis and restrictive CM on cardiac catheterization:
in constrictive pericarditis, end-diastolic pressures are equal in all 4 chambers, while in RCM, LVEDP > RVEDP
What initiates torsades de pointes?
ventricular premature beat in the setting of abnormal ventricular repolarization characterized by prolonged QT
What 2 electrolyte disturbances are associated with torsades de pointes?
1) hypokalemia; 2) hypomagnesemia
Treatment for torsades de pointes:
1) magnesium sulfate; 2) isoproterenol infusion; 3) cardiac pacing; 4) cardioversion if hemodynamically unstable
What is the most commonly missed cause of syncope in the elderly? How do you make diagnosis?
subclavian steal; diagnosis by 1) measuring both L and R sided BP (difference of more than 25 mmHg = supports diagnosis); 2) confirmed by doppler US of neck vessels
What is the second most commonly missed cause of syncope in the elderly?
carotid hypersensitivity; make daignosis by carotid massage --> bradycardia
Name 3 common but often missed causes of syncope in the elderly:
1) subclavian steal; 2) carotid hypersensitivity; 3) L main or severe 3 vessel disease