How do you make diagnosis of prinzmetal's angina?
cardiac catheterization: shows no atherosclerosis, but ergonovine can precipitate spasm
Treatment for prinzmetal's angina?
Calcium channel blockers (diltiazem/verapamil) and nitrates (nitrostat, sorbitrate)
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
5 sxs of pulmonary embolism:
1) tachypnea; 2) dyspnea; 3) cough; 4) pleuritic chest pain; 5) hemoptysis
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
3 indications for exercise stress test:
diagnosis of angina, determine severity of dz, post MI evaluation
Contraindications to stress testing:
Unstable angina, aortic stenosis, IHSS (Idiopathic hypertrophic subaortic stenosis, severe COPD, acute CHF, acute ischemia on ECG, aortic dissection, severe uncontrolled HTN
3 indications for cardiac catheterization in angina patient:
1) symptoms poorly controlled with tx,
2) to determine need for revascularization;
3) to determine presence of main criteria for bypass [3 vessel disease or left main disease].
JNC7 guidelines for controlling BP in pts with and without DM
With DM = <130/80;
Without DM = <140/90
JNC7 guidelines for controlling total cholesterol and LDL in pt with very high cardiac risk profile
Total cholesterol <190; LDL <70; HDL >40
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
1) HR, 2) BP; 3) contractility --> decrease O2 demand of heart
Contraindication of BBs
1) Severe asthma (BBs cause bronchoconstriction)
2) Prinzmetal angina
4) Heart block
6 treatment options for angina
nitrates, Beta Blockers, statins, antiplatelet agents (aspirin +/- plavix), Calcium channel blockers for prinzmetal's, revascularization
In a pt with one or no risk factors, at what LDL level do u institute dietary modification? medication?
LDL >160; LDL >190
In a pt with more than one risk factor, at what LDL level do u institute dietary modification? medication?
LDL >130; LDL >160
Who has very high cardiac risk?
1) Acute coronary syndrome (ACS); 2) Coronary artery disease (CAD )+ DM or smoker
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 nitro?
5 general causes of non-atherosclerotic MI
2) congenital anomaly of coronaries;
3) coronary spasm (i.e. cocaine);
4) coronary artery embolus (i.e. atrial thrombus 2/2 A-fib);
5) hypercoagulable states
4 cardiac (not equipment) factors that would make ECG interpretation of MI difficult:
2) Previous MI;
4) Digoxin use
Which vessel supplies the inferior wall of the left ventricle?
(PDA) Posterior Descending Artery of the RCA
Sign of posterior infarction on initial 12-lead ECG
1) Tall, broad R waves in leads V1-V2;
2) ST depression in V3, V4; (V5)
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
Mark's list: SAD & HAPPY Stroke, Active Bleed; HTN above 180, Anticogulants, Pregnant, PUD, Year over 75
Maximum benefit of ACE inhibitors have been shown in what 3 clinical situations?
2) LV dysfunction [EF <40%];
3) Anterior MI
Indications for temporary transvenous pacing in acute MI:
1) 2nd degree heart block, type II or greater;
2) Brady despite Atropine;
3) Junctional or idioventricular rhythm w/ hypoperfusion or slow ventricular rate;
4) LBBB in acute MI;
5) Bifascicular block with 1st degree AV block;
6) New bifascicular block
Indications for IABP (intra-aortic balloon pump)
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;
4 tests used to make diagnosis of CHF
1) BNP screening -- >100 has 95% sensitivity
4) 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
Drugs to avoid in treatment of CHF secondary to diastolic dysfunction:
1) Positive inotropics -digoxin!;
2) Vasodilators nitrates!
Etiology of interstitial edema with elevated PCWP (pulmonary arterial wedge pressure)
Etiology of interstitial edema with normal to low PCWP (pulmonary arterial wedge pressure)
Noncardiac causes of pulmonary edema
1) Adult respiratory distress syndrome -ARDS;
3) Pulmonary embolism
5) Head trauma;
6) Drug allergies;
7) Alveolar capillary leak, example: Goodpasture's vasculitis
CXR findings in pulmonary edema
1) Prominent pulmonary vessels;
2) Enlarged cardiac silhouette;
3) Kerley B lines;
4) Effusion (transudate- check LDH and protein levels)
Signs and symptoms of pulmonary edema
2) Cough with pink frothy sputum;
4) Nocturnal dyspnea;
5) Rales, rhonchi and wheezing
4 CXR findings in pulmonary edema
1) prominent pulmonary vessels; 2) cardiomegaly; 3) kerley b lines; 4) pleural effusion
Treatment for pulmonary edema
1) Sit pt upright; 2) O2 with PEEP; 3) NTG (reduces preload & HTN); 4) Morphine (reduces vascular resistance); 5) Lasix (Furosemide, loop diuretic that is 1st line CHF, reduces preload); 6) Dobutamine (positive inotrope, sympathomimetic, used to treat systolic CHF); 7) IV ACEI 8) Digoxin if A-fib present
Progression 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
What 4 findings help make diagnosis of mitral stenosis?
2) ECG with notched P in lead II & right axis deviation = cor pulmonale;
3) CXR shows LA enlargement & RV hypertrophy;
4) Echo verifies
3 findings of ECG consistent with mitral stenosis:
1) LA enlargement;
2) RV hypertrophy;
3) A-fib may be present
What findings on CXR suggest left atrial enlargement?
1) Double-density right heart border;
2) Posterior displacement of esophagus;
3) Elevated left mainstem bronchus
2 most common causes of mitral regurgitation
1) Rheumatic fever;
2) Dilation of left ventricle (LVH, usually 2/2 CHF)
4 causes of acute mitral regurgitation (MR)
1) ruptured chordae tendineae;
2) papillary muscle rupture;
What is the effect of chronic mitral regurgitation (MR) on preload?
Increases preload because regurgitation results in decreased Cardiac Output, so the RAAS increases aldosterone leading to fluid retention
What is the effect of chronic mitral regurgitation on afterload?
Decreases afterload, because a portion of stroke volume is ejected retrograde into LA
Echo findings consistent with MR
1) LV hypertrophy;
2) LA enlargement
3) Papillary muscle or chordae tendonae damage
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 Mitral Regurgitation
3) arteriolar vasodilators;
Indication for surgical repair of MR
Severe MR with significantly limiting sxs despite optimal medical management
Papillary muscle rupture with acute MI is associated with which infarct?
Inferoposterior infarcts (posterior papillary muscle involvement)
Blood supply of the posterior wall of the left ventricle
Marginal branch of the left circumflex artery
Your patient has a palpable precordial thrill. Is it associated with the rupture of a papillary muscle or of the ventricular septum?
4 diagnostic tests to confirm diagnosis of papillary muscle rupture
1) 2-d echo; 2) doppler flow study; 3) PA cath for wedge pressure; 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, which increases venous return; and worsens with valsalva or standing, which both decrease venous return.
Most common cause of AS
1) calcification (often a bifid valve)
2) degeneration of a congenitally normal valve
3 most common causes of AS
1) degenerative (aging); 2) calcification and degeneration of a congenital bicuspid valve; 3) rheumatic heart dz
What "Gallop" is associated with AS
S4: a forceful atrial contraction augments filling of thick, noncompliant left ventricle
Three signs of AS on physical exam
1) Narrow pulse pressure;
2) Harsh, late-peaking systolic murmur at the right second intercostal space; and
3) A delayed, weak carotid upstroke (pulsus parvus et tardus).
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 is defined as?
upon palpation, the pulse is weak/ small (parvus) and late (tardus) in relation to contraction of the heart
ECG indicators of Aortic Stenosis
LV hypertrophy is indicated by 1) S in V1 + R in V5 or V6 ≥ 35 mm; or, 2) R in Lead I is > 14 mm
3 possible findings on CXR in patient with Aortic Stenosis
1) Cardiomegaly; 2) Calcified aorta; 3) Pulmonary congestion/edema
4 DDx whose murmurs mimic AS
1) aortic valve sclerosis of the elderly; 2) Hypertrophic Cardiomyopathy; 3) Mitral Regurgitation; 4) Pulmonary Stenosis
Effect of hand grip on Ventricular Septal Defect murmur
increase SVR-- systemic vascular resistance; increase murmur
Effect of valsalva on Mitral Valve Prolapse
Decrease preload; so "Opening Snap" is later, closer to S2
2 common bacterial causes of aortic regurgitation:
1) rheumatic fever from GA = group A strep; 2) infective endocarditis from Strep viridans, staph, or other.
6 diseases/conditions that may affect the ascending aorta and cause Aortic Regurgitation
1) Ankylosing spondylitis; 2) Aortic trauma 3) Hypertension, 4) Marfan's syndrome; 5) Aortic dissection; 6) Syphillis
ASTHMA & syphillis: Ankylosing Spondylitis, Trauma, Hypertension, Marfan's, Aortic dissection & Syphillis!
Pathophys of chronic AR
AR --> volume overload of LV (increased LVEDV) --> LV dilatation --> dilated cardiomyopathy and volume overload
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)
Eponymous signs of Aortic regurgitation
1) Becker sign -
2) Corrigan pulse ("water-hammer" pulse)
3) de Musset sign
4) Hill sign
5) Duroziez sign
6) Quincke sign
systolic and diastolic thrill (double murmur) heard over the femoral arteries; related to high pulse pressure in Aortic Regurgitation (insufficiency)
Austin Flint murmur
a mid-diastolic, low pitched rumbling murmur best heard at the cardiac apex; seen in AR
Treatment for Aortic Regurgitation
Treat like CHF secondary to systolic dysfunction: 1) pre-load reduction by salt restriction and diuretics; 2) digitalis; 3) afterload reduction by ACE inhibitor
Austin flint murmur is associated with which valvular disease?
Aortic Regurgitation = aortic insufficiency
Pathophys (cause!) of austin flint murmur
Regurgitant blood from the aortic valve strikes the anterior leaflet of the mitral valve, causing turbulent mixing.
Effect of Hypertrophic cardiomyopathy on stroke volume and ejection fraction
stroke volume: normal to increased; ejection fraction: increased
What drugs are used in treatment of Hypertrophic Cardiomyopathy, and what drugs should be avoided.
Calcium channel blockers
Amiodarone is used rarely
Avoid inotropic drugs especially digitalis
Avoid nitrates and sympathomimetic amines, except in concomitant coronary artery disease
Use diuretics with caution
Effect of dilated (congestive) cardiomyopathy on stroke volume and ejection fraction
Decreased stroke volume and ejection fraction
What is the most common cause of heart transplants, and what are it's 2 main etiologies?
Dilated cardiomyopathy is the most common cause of transplant. It is either familial/ idiopathic or alcohol induced.
Strategy & Treatment for dilated cardiomyopathy
Srategies are same as for CHF w/systolic dysfunction: Preload reduction, Afterload reduction and Diuresis:
Treatment includes 1) Decrease preload = salt restriction & diuretics; 2) Positive inotrope = digoxin; 3) Decrease afterload with ACE inhibitors & hydralazine; 4) ventricular remodeling with Beta Blockers PLUS 5) Anticoagulants to protect against high frequency of pulmonary and systemic embolisms.
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
Why does a reduction in preload increase obstruction in HCM?
decreased venous return --> decreased internal volume of the heart --> mitral valve brought closer to the septum
3 mechanisms that contribute to obstruction in HCM:
1) increased muscle mass & contractility; 2) reduced preload; 3) reduced 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 Non-obstructive HCM?
The goal is to improve LV relaxation; treat with Calcium Channel Blockers
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
Pulsus paradoxus description
a 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 between constrictive pericarditis and restrictive cardiomyopathy on cardiac catheterization:
in constrictive pericarditis, end-diastolic pressures are equal in all 4 chambers. In restrictive cardiomyopathy, left ventricular end diastolic pressure is greater than right ventricular end diastolic pressure.
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
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
2 sxs of Peripheral Vascular Disease of the internal iliac system:
1) decreased libido; 2) pain mimicking DJD of the hip
WHY does valsalva accentuate the murmur of mitral regurgitation?
Reduces preload reduces chordae tendonae pressure, so prolapse can occur sooner.
HOW does the valsalva maneuver affect heart rate and murmurs?
Valsalva reduces preload by decreasing venous return to the heart.
HOW can mitral regurgitation and hypertrophic cardiomyopathy be distinguished?
BOTH have murmurs accentuated by valsalva, but HCM is improved by hand grip maneuver.