Kaplan Cardiology

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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

Typical duration of angina sxs:

more than 15 seconds, less than 15 minutes

Three findings on physical exam in pt with angina:

Diaphoresis (sweating), tachycardia; S4 gallop

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 aortic dissection:

1) CT, 2) TEE, 3) aortography

3 ways to confirm diagnosis of esophageal reflux or spasm mimicking angina:

1) upper GI series; 2) endoscopy; 3) esophageal manometry

To confirm diagnosis of pneumothorax:

CXR

Definition of stable angina:

occurs during exertion; same amt of exercise reproduces pain; relieved by rest

Definition of unstable angina:

new onset CP; worsening pattern in frequency, duration or intensity

Work up for angina:

ECG, stress test, cardiac catheterization

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].

What are the 2 main criteria for bypass?

three vessel disease, left main dz

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

JNC7 guidelines for LDL in pts with CAD or equivalent

LDL <100

Effect of nitrates in low doses

increase venous dilatation --> decrease preload

Effect of nitrates in moderate doses

increase venous and arterial dilatation --> decrease both preload and afterload

Effect of nitrates in high doses

increase coronary artery dilatation --> increase O2 supply

3 Effects of beta blockers that make them useful in treating angina

Decrease
1) HR, 2) BP; 3) contractility --> decrease O2 demand of heart

Contraindication of BBs

1) Severe asthma (BBs cause bronchoconstriction)
2) Prinzmetal angina
3) Pregnancy
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

Which pts s/p acute MI will continue to receive statin therapy?

Those with LDL >70

4 equivalents of CAD

1) DM
2) Peripheral Arterial Disease (PAD);
3) Carotid dz;
4) Aortic dz

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

1) vasculitis;
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

Which cardiac region is most susceptible to ischemia?

Left ventricular subendocardium

Duration of chest pain in acute MI:

Usually longer than 20 minutes

4 cardiac (not equipment) factors that would make ECG interpretation of MI difficult:

1) LBBB;
2) Previous MI;
3) Pacemaker;
4) Digoxin use

What blood enzymes remain elevated 1-2 wks after acute MI?

Troponins

Which vessel supplies the inferior wall of the left ventricle?

(PDA) Posterior Descending Artery of the RCA

Which vessel supplies the lateral wall of the left ventricle?

Left Circumflex A

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

Posterior MIs generally occur in association with what other MI?

Lateral or inferior

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

2 complications of thrombolysis:

1) Bleeding;
2) Reperfusion arrhythmias

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

Contraindications to BB in acute MI

1) Bradycardia;
2) AV block;
3) hypotension;
4) COPD or asthma

What Beta blocker do you give in acute MI?

Metoprolol IV q5min or propranolol

Maximum benefit of ACE inhibitors have been shown in what 3 clinical situations?

CLAM
1) CHF;
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

RV infarct is associated with what other MI area?

Inferior wall

Treatment for right ventricular infarction

IV fluids

Indications for IABP (intra-aortic balloon pump)

1) recurrent or persistent MI; 2) severe left or biventricular failure +/- shock

Indications for ACE inhibitors post-MI

Low EF or LV dysfunction

Most common cause of CHF

MI or ischemia

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

4 tests used to make diagnosis of CHF

1) BNP screening -- >100 has 95% sensitivity
2) CXR;
3) Echo;
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

3 indications for digoxin

1) CHF;
2) A-fib;
3) Paroxysmal atrial tachycardias

Effect of hyperkalemia on digoxin

Decrease digoxin activity

Effect of hypokalemia on digoxin

Digoxin toxicity

Drugs to avoid in treatment of CHF secondary to diastolic dysfunction:

1) Positive inotropics -digoxin!;
2) Vasodilators nitrates!

Rx tx for diastolic dysfunction:

Negative inotropic agents:
1) BBs;
2) verapamil;
3) cardizem

Etiology of interstitial edema with elevated PCWP (pulmonary arterial wedge pressure)

Cardiac disease

Etiology of interstitial edema with normal to low PCWP (pulmonary arterial wedge pressure)

Noncardiac cause

Cardiac causes of pulmonary edema

1) Left CHF
2) Arrhythmias;
3) MI
4) Valvular heart dz

Noncardiac causes of pulmonary edema

1) Adult respiratory distress syndrome -ARDS;
2) Uremia;
3) Pulmonary embolism
4) Aspiration;
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

1) Tachypnea;
2) Cough with pink frothy sputum;
3) Cyanosis;
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

Work up for pulmonary edema

1) CXR; 2) ABG; 3) ECG

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?

1) A-fib;
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

Treatment of mitral stenosis & rationale

Decrease preload:
1) diuretics;
2) sodium restriction

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;
3) endocarditis;
4) trauma

Murmur of mitral regurgitation (MR)

Holosystolic murmur heard best at apex and radiating to axilla

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

4 diagnostic tests to confirm presence of MR

1) ECG; 2) CXR; 3) Echo; 4) Cath

Echo findings consistent with MR

1) LV hypertrophy;
2) LA enlargement
3) Papillary muscle or chordae tendonae damage

3 entities that mimic mitral regurgitation on physical exam

1) VSD; 2) HCM; 3) AS

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

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

Ventricular septal rupture is associated with which infarct?

Anterior wall

Papillary muscle rupture with acute MI is associated with which infarct?

Inferoposterior infarcts (posterior papillary muscle involvement)

Blood supply of the posterior papillary muscle

Septal perforators of the PDA

Blood supply of the inferior wall of the left ventricle

PDA (85% from RCA; 15% from LCA)

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?

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

Classic triad of AS

1) angina;
2) syncope;
3) dyspnea secondary to CHF

Pulsus parvus et tardus is a classic finding in which cardiac pathology?

Aortic stenosis

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 diagnostic tests which can be used to support diagnosis of AS

1) ECG; 2) CXR; 3) echo

3 possible findings on CXR in patient with Aortic Stenosis

1) Cardiomegaly; 2) Calcified aorta; 3) Pulmonary congestion/edema

What is the normal aortic valve orifice?

2.5 to 3.5 cm

At what diameter is aortic stenosis considered to be critical or severe?

<0.8cm

4 DDx whose murmurs mimic AS

1) aortic valve sclerosis of the elderly; 2) Hypertrophic Cardiomyopathy; 3) Mitral Regurgitation; 4) Pulmonary Stenosis

Maneuvers which increase preload

1) squatting; 2) leg raising; 3) inspiration

Maneuvers which decrease preload:

1) valsalva; 2) standing

Maneuvers which increase afterload:

1) hand grip; 2) phenylephrine

Maneuvers which decrease afterload:

1) amyl nitrate

Effect of hand grip on Ventricular Septal Defect murmur

increase SVR-- systemic vascular resistance; increase murmur

Effect of hand grip on MR

increase SVR-- systemic vascular resistance; increase murmur

Effect of valsalva on HCM

decrease preload; increase murmur

Effect of valsalva on Aortic Stenosis

decrease preload; decrease murmur

Effect of squatting on HCM

increase preload; decrease murmur

Effect of squatting on AS

increase preload; increase murmur

Effect of inspiration on Tricuspid Regurgitation

increase preload; increase murmur

Effect of valsalva on Mitral Valve Prolapse

Decrease preload; so "Opening Snap" is later, closer to S2

Effect of hand grip on AS

increase SVR; decrease murmur

Effect of handgrip on HCM

increase SVR; decrease murmur

2 common bacterial causes of aortic regurgitation:

1) rheumatic fever from GA = group A strep; 2) infective endocarditis from Strep viridans, staph, or other.

What is the most common cause of aortic regurgitation?

rheumatic heart dz

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)

What is the most common presenting sxs in AR?

dyspnea

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

Duroziez sign

systolic and diastolic thrill (double murmur) heard over the femoral arteries; related to high pulse pressure in Aortic Regurgitation (insufficiency)

Becker's sign

Visible pulsations of the retinal arterioles

Corrigan's "water hammer" pulse

Abrupt distention and collapse of the peripheral arterial pulse;

Austin Flint murmur

a mid-diastolic, low pitched rumbling murmur best heard at the cardiac apex; seen in AR

de Musset's sign

Bobbing of the patient's head with each heartbeat

Hill sign

SBP with Popliteal cuff is 40 mm Hg higher than SBP at brachial cuff

Quinke's sign

Visible pulsations of the fingernail bed with light compression of nail

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 amyl nitrate on austin flint murmur

decreases murmur

Murmur of PDA Patent ductus arteriosus

continuous "machine-like" murmur throughout cardiac cycle

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.

Beta blockers
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.

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