CardiooAll 437 Terms

8/3/2019 CardiooAll 437 Terms

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All 437 terms

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Terms Definitions

cardiac catheterization: shows noatherosclerosis, but ergonovine can

precipitate spasm

How do you make diagnosis of prinzmetal's angina?

calcium channel blockers and

nitratesTreatment for prinzmetal's angina?

1) physical exertion; 2) emotional/

mental stress; 3) anxiety; 4) cold

exposure; 5) post large meal

Name 5 precipitating factors for acute coronary syndrome:

more than 15 seconds, less than 15

minutesTypical duration of angina sxs:

1) diaphoresis; 2) tachycardia; 3)

transient S4Three findings on physical exam in pt with angina:

pericarditis pain is sharper, worse

with lying down, relieved with sitting

up

How can u differentiate pericarditis from angina from the history?

1) tachypnea; 2) dyspnea; 3) cough;

4) pleuritic chest pain; 5) hemoptysisName 5 sxs of PE:

1) CT, 2) TEE, 3) aortography 3 ways to confirm diagnosis of aortic dissection:

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

esophageal manometry

3 ways to confirm diagnosis of esophageal reflux or spasm

mimicking angina:

CXR How do you confirm diagnosis of pneumothorax?

occurs during exertion; same amt of

exercise reproduces pain; relieved

by rest

Definition of stable angina:

new onset CP; worsening pattern in

frequency, duration or inteDefinition of unstable angina:

1) ECG; 2) stress test; 3) cardiac

catheterizationWork up for angina:


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1) to confirm diagnosis of angina; 2)

to determine severity of dz; 3) post

MI evaluation

Name 3 indications for exercise stress test:

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

Contraindications to stress testing:

1) sxs poorly controlled with rx; 2) +

stress test --> determine need for

revascularization; 3) determine

presence of main criteria for bypass

sx

Name 3 indications for cardiac catheterization in pt with angina:

1) three vessel disease; 2) left main

dzWhat are the 2 main criteria for bypass?

without DM =


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agents (i.e. statins); 4) antiplatelet

agents (aspirin +/- plavix); 5) CCBs

(only for prinzmetal's); 6)

revascularization

LDL >130; LDL >160 In a pt with one or no risk factors, at what LDL level do u institute

dietary modification? medication?

LDL >160; LDL >190In a pt with more than one risk factor, at what LDL level do u

institute dietary modification? medication?

those with LDL >70 Which pts s/p acute MI will continue to receive statin therapy?

1) DM; 2) PVD; 3) carotid dz; 4)

aortic dzName 4 equivalents of CAD

1) ACS; 2) CAD + DM or smoker Who has very high cardiac risk?

1) is the pain retrosternal? 2) is the

pain brought on by stress? 3) is the

pain relieved with rest or NTG?

3 questions to ask to determine whether chest pain is typical,

atypical or nonanginal:

1) vasculitis; 2) congenital anomaly

of coronaries; 3) coronary spas (i.e.

cocaine); 4) coronary artery

embolus (i.e. atrial thrombus); 5)

hypercoagulable states

5 general causes of non-atherosclerotic MI

left ventricular subendocardium Which cardiac region is most susceptible to ischemia?

usu longer than 20 minutes Duration of chest pain in acute MI:

1) LBBB; 2) previous MI; 3)

pacemaker; 4) digoxin useName 4 factors that would make ECG interpretation of MI difficult:

1-2 wks For how long do troponins remain elevated after acute MI?

PDA of the RCA Which vessel supplies the inferior wall of the left ventricle?

left circumflex a Which vessel supplies the lateral wall of the left ventricle?

in leads V1-V2: 1) tall, broad R

waves; 2) ST depression; 3) tall

peaked T wave

Sign of posterior infarction on initial 12-lead ECG

lateral or inferior Posterior MIs generally occur in association with what other MI?


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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

Indications for thrombolytic therapy for acute MI

1) bleeding; 2) reperfusion

arrhythmiasName 2 complications of thrombolysis:

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

Contraindications to thrombolytic therapy:

1) bradycardia; 2) AV block; 3)

hypotension; 4) COPDContraindications to BB in acute MI

metoprolol IV q5min What BB do you give in acute MI?

1) CHF; 2) LV dysfunction (EF


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MI or ischemia Most common cause 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

Precipitating causes of CHF

1) CXR; 2) echo; 3) MUGA scan or

radionuclide ventriculography3 tests used to make diagnosis of CHF

1) reduce cardiac workload; 2)

improve cardiac performance; 3)

control excess salt and water

3 main therapeutic objectives in management of CHF:

inhibition of Na/K ATPase --> -->

increase intracellular Ca -->

inotropic effect

Mechanism of action of digoxin

1) CHF; 2) afib; 3) paroxysmal atrial

tachycardias3 indications for digoxin

decrease dig activity Effect of hyperkalemia on digoxin

dig toxicity Effect of hypokalemia on digoxin

1) digoxin; 2) vasodilatorsDrugs to avoid in treatment of CHF secondary to diastolic

dysfunction:

negative inotropic agents: 1) BBs; 2)

verapamil; 3) cardizemRx tx for diastolic dysfunction:

cardiac cause Interstitial edema with elevated PCWP

noncardiac cause Interstitial edema with normal to low PCWP

1) arrhythmias; 2) MI; 3) severe

systemic HTN; 4) PE; 5) valvular

heart dz

Cardiac causes of pulmonary edema

1) ARDS; 2) uremia; 3) aspiration;

4) head trauma; 5) allergic reaction

to rx; 6) alveolar capillary leak

Noncardiac causes of pulmonary edema

1) prominent pulmonary vessels; 2) CXR findings in pulmonary edema


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enlarged cardiac silhouette; 3)

Kerley B lines; 4) effusion

1) tachypnea; 2) cough with pink

frothy sputum; 3) cyanosis; 4)

nocturnal dyspnea; 5) rales, rhonchi

and wheezing

Signs and sxs of pulmonary edema

1) prominent pulmonary vessels; 2)

cardiomegaly; 3) kerley b lines; 4)

pleural effusion

Name 4 CXR findings in pulmonary edema

1) CXR; 2) ABG; 3) ECG Work up 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

Treatment for pulmonary edema

MS --> impedes LV filling -->

increased LA pressure -->

pulmonary congestion --> secondary

pulmonary vasoconstriction --> RV

failure

Pathophys in mitral stenosis

mid to late low pitched diastolicmurmur preceded by opening snap

What is the murmur of mitral stenosis?

1) ECG; 2) CXR; 3) echo What 3 tests help make diagnosis of mitral stenosis?

1) LA enlargement; 2) RV

hypertrophy; 3) +/- afibName 3 findings of ECG consistent with mitral stenosis:

1) double-density right heart border;

2) posterior displacement of

esophagus; 3) elevated left

mainstem bronchus

What findings on CXR suggest left atrial enlargement?

decrease preload: 1) diuretics; 2)

sodium restrictionGoals of medical treatment of mitral stenosis

1) rheumatic fever; 2) dilation of left

ventricle2 most common causes of mitral regurgitation


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1) ruptured chordae tendineae; 2)

papillary muscle rupture; 3)

endocarditis; 4) trauma

4 causes of acute mitral regurgitation

holosystolic murmur heard best at

apex and radiating to axilla

Murmur of mitral regurgitation

increases preload (MR -->

decreased CO --> RAAS --> fluid

retention

What is the effect of chronic mitral regurgitation on preload?

decreased afterload as a portion of

stroke volume is ejected retrograde

into LA

What is the effect of chronic mitral regurgitation on afterload?

1) ECG; 2) CXR; 3) Echo; 4) Cath Name 4 diagnostic tests to confirm presence of MR

1) LV hypertrophy; 2) LA

enlargement2 findings on ECG consistent with MR

1) VSD; 2) HCM; 3) AS Name 3 entities that mimic mitral regurgitation on physical exam

relieve sxs by 1) increasing forward

output; 2) reducing pulmonary

venous hypertension

What are the 2 goals of treatment for mitral regurgitation?

1) digitalis; 2) diuretics; 3) arteriolar

vasodilators; 4) anticoagulants4 classes of drugs used to treat MR

severe MR with significantly limiting

sxs despite optimal medical

management

Indication for surgical repair of MR

anterior wall Ventricular septal rupture is associated with which infarct?

inferoposterior infarcts (posterior

papillary muscle involvement)

Papillary muscle rupture with acute MR is associated with which

infarct?

septal perforators of the PDA Blood supply of the posterior papillary muscle

PDA (85% from RCA; 15% from

LCA)Blood supply of the inferior wall of the left ventricle

marginal branch of the left

circumflex aBlood supply of the posterior wall of the left ventricle

ventricular septum Palpable precordial thrill associated with rupture of papillary muscle


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or ventricular septum?

1) 2-d echo; 2) doppler flow study;

3) PA cath; 4) LV angiography4 diagnostic tests to confirm diagnosis of papillary muscle rupture

mid to late systolic click and a late

systolic murmur heard best at the

apex

Murmur of mitral valve prolapse

improves with squatting (increased

venous return); worsens with

valsalva (decreased venous return)

Effect of maneuvers on murmur of mitral valve prolapse

calcification and degeneration of a

congenitally normal valveMost common cause of AS

1) degenerative (aging); 2)


congenital bicuspid valve; 3)

rheumatic heart dz

3 most common causes of AS

S4 (forceful atrial contraction

augments filling of thick,

noncompliant ventricle)

What heart sound is associated with AS

1) LV hypertrophy; 2) high

intramyocardial wall tension2 causes of increased O2 demand in AS

1) LV hypertrophy; 2) high

intramyocardial wall tension; 3)

decreased diastolic coronary blood

flow

3 mechanisms which contribute to angina in AS

1) angina; 2) syncope; 3) dyspnea

secondary to CHFClassic triad of AS

AS Pulsus parvus et tardus is a classic findng in which disease?

upon palpation, the pulse is weak/small (parvus) and late (tardus) in

relation to contraction of the heart

Pulsus parvus et tardus

LV hypertrophy Findings of AS on ECG

1) ECG; 2) CXR; 3) echo 3 diagnostic tests which can be used to support diagnosis of AS


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1) cardiomegaly; 2) calcified aorta;

3) pulmonary congestion3 possible findings on CXR in pt with AS

2.5 to 3.5 cm What is the normal aortic valve orifice?


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6) aortic trauma

AR --> volume overload of LV

(increased LVEDV) --> LV dilatation

--> dilated cardiomyopathy and

volume overload

Pathophys of chronic 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

Cause of increased pulse pressure in AR

1) stroke volume (proportional) ; 2)

compliance of aorta (inversely

proportional)

2 factors which affect pulse pressure

dyspnea What is the most common presenting sxs in AR?

diastolic decrescendo murmur OR

systolic flow murmur (secondary to

greatly increased stroke volume)

Murmur of AR

systolic and or diastolic thrill or

murmur heard over the femoral

arteries; related to high pulsepressure

Duroziez sign

aortic regurgitation Duroziez sign is present in what valvular disease?

a mid-diastolic, low pitched rumbling

murmur best heard at the cardiac

apex; seen in AR

Austin Flint murmur

the result of mitral valve leaflet

displacement along with turbulent

mixing of antegrade mitral flow and

retrograde aortic flow

Pathophys of austin flint murmur

AR Austin flint murmur is associated with which valvular disease?

continuous (throughout cardiac

cycle)Murmur of PDA


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decreases murmur Effect of amyl nitrate on austin flint murmur

treat like CHF secondary to systolic

dysfxn: 1) preload reduction (salt

restriction and diuretics); 2) digitalis;

3) afterload reduction (ACEI)

Treatment for AR

stroke volume: normal to increased;

ejection fraction: increased

Effect of Hypertrophic cardiomyopathy on stroke volume and

ejection fraction

decreased Effect of dilated (congestive) cardiomyopathy on ejection fraction

dilated cardiomyopathy What is the most common cause of heart transplants?

1) idiopathic (familial 20-30%); 2)

alcoholic2 most common causes of dilated cardiomyopathy

dilated CM Beriberi disease results in which type of cardiomyopathy?

"i can't i can't" in Singalese What does Beriberi mean?

thiamine (vitamin B1) Beriberi is secondary to what vitamin deficiency?

same as those for left and right

ventricular failureClinical manifestations of dilated cardiomyopathy:

1) acute myocarditis; 2) valvular

heart disease; 3) CAD; 4)

hypertensive heart dz

4 DDx 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)

Treatment for dilated cardiomyopathy

1) ECG; 2) CXR; 3) echo; 4) cath; 5)

stress test 5 diagnostic tests used to diagnose dilated CM

autosomal dominant What is the heritance pattern of HCM?

unexplained myocardial hypertrophy

with thickening of the interventricular

septum

Hallmark of HCM


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80-90% Typical EF in pts with HCM

decreased venous return -->

decreased size of the heart -->

mitral valve brought closer to the

septum

Why does a reduction in preload increase obstruction in HCM?

1) increase in contractility; 2)

reduction in preload; 3) reduction in

afterload

Name 3 mechanisms that increase obstruction in HCM:

1) decrease in contractility; 2)

increased preload; 3) increase in

afterload

3 factors that decrease obstruction in HCM:

negative inotropes: 1) BB; 2) CCB

(verapamil, diltiazem); 3)

disopyramide (sxs benefit for

severely limited pts)

Rx Tx for HCM

1) septal myomectomy; 2)

aortotomy; 3) etoh ablation3 surgical procedures for HCM

goal is to improve LV relaxation; tx

with CCBsWhat is the preferred treatment in nonobstructive HCM?

goal is to prevent provocation of

obstruction; tx with BBsWhat is the preferred tx in latent obstructive HCM?

goal is relief of obstruction to LV

outflow; tx with disopyramideWhat is the preferred tx in resting obstructive HCM?

with diaphragm, as pt sits forward at

forced-end expirationHow to auscultate for pericardial friction rub?

diffuse ST segment elevation,

absence of reciprocal changes,

upright T waves

ECG findings in acute pericarditis:

1) TB; 2) neoplasmSerosanguinous pericardial effusion is classic sign in what 2

diseases?

1) CHF; 2) hypoproteinemia; 3)

overhydrationA transudative pericardial effusion can be seen in what 3 cases?

echo What is the best diagnostic test for pericardial effusion?


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water bottle configuration of the

cardial silhouetteCXR finding in pericardial effusion

1) fluid aspiration; 2) manage

etiologyTreatment for pericardial effusion:

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

Pulsus paradoxus

1) pericardiocentesis; 2) subxiphoid

surgical drainageTreatment for cardiac tamponade:

in constrictive pericarditis, end-

diastolic pressures are equal in all 4

chambers, while in RCM, LVEDP >

RVEDP

How to differentiate btw constrictive pericarditis and restrictive CM

on cardiac catheterization:

CT Procedure of choice for constrictive pericarditis:

conservative: salt restriction and

diureticsRx tx for constrictive pericarditis:

pericardiectomy Sx tx for constrictive pericarditis

atropine Rx tx for symptomatic sinus bradycardia

ventricular premature beat in the

setting of abnormal ventricular

repolarization characterized by

prolonged QT

What initiates torsades de pointes?

recurrent dizziness or syncope Sxs of torsades de pointes:

1) hypokalemia; 2)

hypomagnesemia

What 2 electrolyte disturbances are associated with torsades de

pointes?

1) magnesium sulfate; 2)

isoproterenol infusion; 3) cardiac

pacing; 4) cardioversion if

hemodynamically unstable

Treatment for torsades de pointes:

failing cardiac output during What is pulsus paradoxus a signal of?


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inspiration

1) amiodarone; 2) lidocaine 2 Medical treatment options for stable, monomorphic v.tach

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 most commonly missed cause of syncope in theelderly? How do you make diagnosis?

carotid hypersensitivity; make

daignosis by carotid massage -->

bradycardia

What is the second most commonly missed cause of syncope in the

elderly?

1) subclavian steal; 2) carotid

hypersensitivity; 3) L main or severe

3 vessel disease

Name 3 common but often missed causes of syncope in the elderly:

1) decreased libido; 2) pain

mimicking DJD of the hipName 2 sxs of PVD of the internal iliac system:

Beta Blockers

-target two receptors, beta 1 receptors, to decrease heart rate and

beta 2 recpetors to bronchoconstrict

Decrease:

1.Heart Rate

2. Force of contraction

3. Renin Secretion(lessening the activity of RAA system**especially useful in younger patients with hyperadrenergic states

Hypertension

Systolic blood pressure>140mmgHg or diastolic blood pressure >90

mmHg

*Ideal is


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-Weight Loss->specify a target weight

-Sodium restrictions

-Alcohol reduction

3 mechanisms to lower blood

pressure

1. lower heart rate

2. Decrease stroke volume

3. Decrease peripheral vascular resistance

The Kidney

-Renin released from renal juxtaglomerular celss activates RAA

system

-regulation of blood volume

-when blood pressure rises for any reason, the kidney should ideally

secrete more sodium... which will lower blood volume

-lowering blood volume tends to decrease cardiac output and

restore pressure toward normal

Sympathetic Nervous system

major role in regulating CO and TPR

**elevated sympathetic nervous system activity may result in

transient or sustained HTN

Diuretics

-used to get rid of excess water.

-lower blood pressure by decreasing CO

-Very effective as anti-HTN with AA's

-used in pts. with concomittant conditions such as edema or CHF

-

SE of Diuretics

-Hypokalemia/hyponatremia

-Hyperuricemia

-Hypercalcemia(thiazide)

-Glucose intolerance

-Hypercholesterolemia/ hypertriglyceridemia

**important to monitor pottasium levels when on a diuretic

Indications for Beta Blocker use

-CAD/angina pectoris/MI

Tachyarrythmia(atrial fib, flutter, v-tach

-PVC's/PAC's

-Dissecting aortic aneurysm

-perioperative cardioprotection

-non-cardiac indications:

1. migraine prophylaxis

2. stage fright

3. hyperthyroidism


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4. senile tumor

Contrainications for Beta-Blockers

1. Over CHF(pulmonary edema present)

2. Severe bradycardia

3. 2nd or 3rd degree AV block

4. Asthma/bronchospasm

5. severe depression(lipophilic agents)

6. Diabetics that are prone to hypoglycemia

7. Active peripheral artery disease(pain at rest)

Side Effects of Beta-Blockers

-Fatigue/lethargy

-Depression

-Impotence

-Nightmares

Cardioselective Beta Blockers

-greater affinity for beta-1 receptors(heart), less likely to

bronchospasm

-less vasoconstriction

-less interference with insulin therapy

Alpha-Beta BlockersProvide benefits of beta blockade with additional benefit of

vasodilation by blocking apha-1 recpetors

Beta Blockers with ISA-reduce resting heart rate and CO less than traditional beta blockers

-NOT to be used in CAD and MI patients

Lipid Solubility

How readily the drug crosses the blood-brain-barrier-Incidence of CNS side effects may be exacerbated with higher lipid

solubility

**Beta blockers should not be stopped abruptyl...There is a

withdrawal syndrome and they should be weaned off!

Calcium Channel Blockers(CCB's)

Block intracellular entry of calcium in cardiac and vascular tissue in

particular

-this action leads to arteriolar smooth muscle relatxation and

decrease TPR

-Well tolerated

-contraindicated in CHF with exception of amlodopine

-ideal in elderly with increased TPR

-used in CAD/Angina in patients that are unable to use beta

blockers(asthma/COPD)

Side Effects of CCB's -Peripheral Edema


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-Constipation

-HA, flushing, palpitation

Dihydropyridine CCB's

Typically pure vasodilators(but with the exception of amlodopine,

may have some negative inotropic effects

-should NOT be used during acute MI WITHOUT a beta

blocker.(Reflex Tachacardia!)

Non-Dihydropyridine CCB's

These drugs vasodilate, but also have a more prominent negative

inotropic effects

-negative chronotopic effect by decreasing: Sinus rate and AV node

conduction

**Ideal for pts. with HTN and atrial arrhythmias

-should be used with caution in conjuction with Beta blockers as

they may lower HR too much

-Avoid in 2nd and 3rd degree AV block

Angiotensin Converting(ACE)

Inhibitors

-block conversion of Angiotensin I to Angiotensin II

-Angio II is a potent vasoconstrictior and indirect facilitator of

sympathetic NS

Ace Inhibitors MOA

Decrease blood pressure by:

1. Reducing TPR

2. Suppressing aldosterone secretion(decreases BV and CO)

Side Effects of ACE Inhibitors Cough

Contraindications of ACE Inhibitors

1. Pregnancy(2nd or 3rd trimester)

2. Renal artery stenosis(may precipitate ARF)

3. hyperkalemia(particularly in renal insufficiency)

4. Angioedema with intial doses

* serum BMP(creatinine, potassium) should be measure before

and during therapy

*potassium sparing diuretics/ potassium supplements should be

avoided unless specifically indicatied, in which case potassium

should be monitored closely.

Concomittant uses of ACE inhibitors

along with HTN

-Diabetes(slows diabetic nephropathy

-CHF( slows progression of LV systolic dysfunction

-Post MI(reduces mortality)

-Mitral Regurgitation(afterload reduction promotes forward flow)

Angiotensin II Receptor Blockers - does not inhibit the enzyme


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(ARB's) -blocks effect of angiotensin II on specific tissue receptors

-well tolerated and NO cough

Alpha-1 Blockers

-Lower blood pressure by antagonism or post synaptic Alpha-1

adrenergic receptors resulting in potent arterial and venous dilation.

-NOT effective in CHF

-USed with pts. with BPH

-Have a favorable effect on lipid profiles(raise HDL)

Side effects Alpha-1 blockers

-1st dose syncope/orthostatic hypotension

-Nasal congestions

HA

-Depression

-Start with low dose in the evening

Central Alpha Agonists

Reduce sympathetic vasoconstriction and decrease TPR

**very effective but their use is limited due to SE's

Side effects of CAA's

Sedation

Drowsiness

*Extreme dry mouth

Clonidine

Catapres

Available as pill/patch

*abrupt discontinuation results in rebound HTN

Mehthyldopa Aldomet*primary indication is HTN in pregnancy

2.4 grams/dayWhat is the current recommendation of dietary sodium intake for the

DASH diet?

Diuretic and ACEIWhat is the first-line antihypertensive treatment therapy for heart

failure?

Beta blocker and ACEI What is the first-line antihypertensive treatment therapy for post MI?

Beta blocker

What is the first-line antihypertensive treatment therapy for a high

coronary disease risk patient?

ACEI or ARBWhat is the first-line antihypertensive treatment therapy for a patient

with diabetes mellitus?

ACEI or ARBWhat is the first-line antihypertensive treatment therapy for a patient

with CKD?


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Diuretic and ACEIWhat is the first-line antihypertensive treatment therapy for recurrent

stroke patient?

Beta BlockerWhat should be added to a heart failure patient's therapy if their

blood pressure is not controlled with a diuretic and ACEI?

Aldosterone antagonistWhat should be added to a post MI patient's therapy if their blood

pressure is uncontrolled with a beta blocker and ACEI?

Loop What is the preferred diuretic for a patient with significant edema?

4 weeks How long does it take to see the effects of eplerenone?

False True or false: There are few interactions likely with eplerenone.

Carvedilol, bisoprolol and

metoprolol

What three beta blockers may have benefit in some patients with

heart failure?

Carvedilol, labetalol What two beta blockers have alpha blocking activity?

Increase TG, decrease HDL What can beta blockers cause in regards to lipid panels?

Captopril What ACEI needs to be dosed most frequently? (BID or TID)

ARB Which is less likely to cause angioedema: ARB or ACEI?

Diltiazem and verapamil What are the two nondihydropyridine calcium channel blockers?

decreased risk of stroke What is the major benefit for calcium channel blockers in HTN?

FalseTrue or false: Alpha-1 blockers are notorious for causing reflex

tachycardia and significant edema.

True True of false: Alpha-1 blockers do not effect lipids and glucose.

First dose hypotension What is the major side effect of alpha blockers?

Clonidine, guanabenz, guanfacine,

methyldopaWhat are the four central alpha-2 agonists used in HTN?

Hydralazine and minoxidil What are two direct vasodilators used in HTN?

TrueTrue or false: Reserpine is an inexpensive once daily regiment for

hypertension.

TrueTrue or false: Methyldopa, labetalol, atenolol and hydralazine could

all be options in treating hyptertension in a pregnant women.

False True or false: Pindolol is common to give in hypertensive patients


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with coronary artery disease.

True True or false: Alpha-blockers decrease LDL and increase HDL.

Morning What time of day should you take thiazides?

Thiazide What is the first line treatment for uncomplicated hyptertension?

FalseTrue or false: Thiazides do not effect total peripheral vascular

resistance.

Furosemide and Metolazone What two diuretics are great for use in severe heart failure?

FalseTrue or false: Loop diuretics that are dosed twice daily should

always be separated 12 hours apart.

False True or false: Both thiazides and loops can cause hypocalcemia.

TrueTrue or false: There can be a significant drug interactions between

loops/thiazides and digoxin.

True True or false: Diuretics at high doses can cause ototoxicity.

FalseTrue or false: A dose of atenolol 400 mg per day still has

cardioselectivity.

TrueTrue or false: Beta blockers lower the afterload pressure on the

heart.

Propranolol What beta blocker can be used for migraines due to its lipophillicity?

AmlodipineWhat is the only dihydropyridine calcium channel blocker that

doesn't increase the heart rate?

VerapamilWhich calcium channel blocker has significant CYP3A4 drug

interactions, significant chance of edema and constipation?

Hypertensive emergency When is intravenous nitroprusside used in hypertension?


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FalseTrue or false: Resistant hypertension occurs when a patient's blood

pressure is uncontrolled with 2 or more antihypertensive agents.

Category X What pregnancy category are statins?

thrombin

the most powerful clotting factor in the clotting cascade. combines c

fibrinogen to form fibrin.

Low Molecular Weight Heparin

Lovenox. this medication binds to antithrombin II and the

preferential effect is on Factor Xa. is not very good at inhibiting

thrombin formation. sub Q route only. less risk involved, but 5x more

expensive.

D-dimer a diagnostic study for clots. this will tes for a fragment of fibrin.

Unfractioned Heparin (UFH)

Tx and prevention of thromboembolism. dependent on the ability to

bind and catalyze antithrombin III....this anticoagulant neutralizes

the activities of several clotting factors. Inactivates thrombin and Xa.

this halts growth and propogation of thrombi.

Protamine Sulfate the antidote for someone with blood that is too thin.

Warfarin

inhibits factors II, VII, IX, X, protein C and S. used to prevent

recurrent thromboembolic events. highly protein bound, has a

narrow therapeutic range. desired anticoag. effect achieved in 3-4

days. oral use only.

Vitamin K the antidote for warfarin

International normalized ratio

a more consistant measure of coagulation. normal range is 0.75-

1.25, but therapeutic range is 2-3 for most depending on their

condition.

Aspirinan antiplatelet medication. this medication is used to prevent platelet

aggregation, there is no interruption of the clotting cascade.

Glycoprotein IIb/IIIa Inhibitor

this is a potent antiplatelet agent. produces antithrombotic effect by

direct inhibition of the binding of fibrinogen to the glycoprotein IIb/IIIa

receptor.

thrombolyticsthis medication targets the red tail of clots (fibrin and blood vessels).

these have a huge risk associated with taking them.

S1 heart sound made from the closure of the mitral and tricuspid valves

S2 heart sound made from the closure of the pulmonic and aortic


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valves

S3heart sound occuring in early diastole caused by fluid overload.

"sloshing in, sloshing in"

S4

heart sound occuring in late diastole caused by rigidity and

decreased elasticity. "a stiff wall"

diastolic the filling pressure when the heart is relaxed.

Risk factors for HTN

smoking, dyslipidemia, sedentary lifestyle, obesity, diet, DM, and

microalbumiuria (protein coming through the urine). age/gender,

family Hx, ethnicity, alcohol, and socioeconomic status.

Target Organ Damage from HTNHeart, LVH; brain, chronic kidney disease, peripheral arterial

disease, retinopathy

thiazide diuretics

a HTN pharmacological tx that inhibits Na and water reabsorption.

K+ wasting. the initial drop in BP is from a decreased CO followed

by decreased peripheral resistance. SE: hypokalemia, dehydration,

hyperglycemia, hyperuricemia.

loop diureticsa HTN pharmacological tx that is shorter-acting and more potent for

emergent fluid overload. SE: hypokalemia

K+ Sparing Diureticsa HTN pharmacological tx that acts as an aldosterone antagonist.

SE: hyperkalemia

Angiotensin Converting Enzyme

Inhibitor

causes a suppression of angiotensin II and potentiates bradykinin

(vasodilation). causes the syppression of aldosterone secretion.

decreases LV mass. SE: cough, increased K+, angioedema,

hypotension, teratogenic. pril

angiotensin II receptor blockers

a HTN pharmacological tx that blocks the effects of angiotensin II

with no effect on bradykinin. there is limited vasoconstriction and

aldosterone secretion. this may cause dilation of arterioles and

veins....which would decrease the SVR and decrease the BP.

typcially there is no cough or hyperkalemia. sartan

renin inhibitor

a HTN pharmacological tx that works very early in the angiotensin

cycle and decreases the ability of the renin to work. SE:

hypotension, diarrhea, terratogenic. ie. tekturna

beta-blockersa HTN pharmacoloical tx that has a lower risk of morbidity and

mortality. decrease HR, myocardial contractility, and conduction


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velocity...which reduces the CO. this inhibits renin release and

reduces sympathetic NS activity. this reduces LVH. need to taper

dose when discontinuing. SE: bradycardia, AV Heart Block, postural

hypotension, sexual dysfunction, bizarre dreams. -olol

Calcium Channel Blockers

a HTN pharmacological tx that blocks inward movement of calcium

ions across cell membranes and causes smooth muscle relaxation.

causes a decrease in systemic vascular resistance. SE: peripheral

edema, dizziness

alpha blockersa HTN pharmacological tx that blocks sympathetic activity leading to

vasodilation. SE: orthostatic hypotension

vasodilators

a HTN pharmacological tx that is the second or third line treatment.

hydrolizine. this is sometimes used during pregnancy because it is

not contraindicated.

HMG-CoA reductasethe enzyme that is needed to synthesize cholesterol in the liver

naturally.

Angiojet devicethis device is a thrombectomy device that rotates and aspirates any

emboli

lipoproteins the vehicles that move the fat. not water soluble.

apoliproteins

the proteins that are found on the surface of lipoproteins. if the

metabolism of these proteins is impaired, there is an increased risk

for athrosclerosis.

HDL cholesterol

the good cholesterol. recommended to have greater than 40 mg/dl.

this type represents cholesterol reurning from the cells to the liver.

the high level is desirable for preventing CHD.

VLDL

this type of lipoprotein contains most of the TG. high levels may

increase the risk of premature atherosclerosis in persons with DM,

HTN, and smoking. optimal level is less than 151 mg/dl

LDL

this type of lipoprotein is best if less than 100 mg/dl. the higher the

level, the greater the risk for coronary heart disease.

Framingham risk scorethis screening estimates the 10 year risk of having a CHD event.

Includes factors like age, total cholesterol, smoking hx, HDL, SBP,

Adult Treatment Panel IIIthis creates an overall tx plan for people c high cholesterol. aims to

create/encourage therapeutic lifestyle changes in LDL-lowering


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therapy. TLC diet, weight management, increased physical activity

monounsaturated fatthe best kind of fat to have....up to 20% of your total intake. second

is polyunsaturated fat.

HMG-CoA Reductase Inhibitors

(statins)

a hyperlipidemiapharmacological tx that decreases plasma

cholesterol and LDL levels by 20-60%. HDLs increase 5-15%.

reduces TG by 10-30%. these are selective inhibitors of the enzyme

which is required in cholesterol synthesis. SE: headache, GI

symptoms, myalgia, hepatotoxicity. need to monitor liver function

labs, and the creatine kinase levels. ie. lipitor.

Bile acid resins

a hyperlipidemiapharmacological tx that binds bile salts in exchange

for chloride ions in the intestines. bile-acid drug complex prevents

reabsorption of bile acids; liver then increases the production of bile

acid, which is able to increase the uptake of LDLs....thereby

decreasing the circulating LDL. lowers the LDL by 15-2030%,

increases HDL by 3-5%, and no change/increase in TG. SE:

bloating, nausea, indigestion, gas, constipation, fat in stool, elevated

TG. Advantages: synergistic c statins and non-systemic. dispensed

in powder form.

fibric acid derivatives

a hyperlipidemiapharmacological tx that causes an alteration in the

rate of synthesis of specific lipoproteins c activation of extra hepatic

lipoprotein lipase. this increases formation of HDLs and reduces TG

production. primarily used for treatment of hyperTG. SE: GIdisturbances, gallstones, fatigue, headache, rash, eczema,

hepatotoxic, myopathy.

nicotinic acid

a hyperlipidemiapharmacological tx that decreases the production of

VLDLs, thereby decreasing LDLs. decreases TG 20-50%, increases

HDL 15-35%, and reduces LDL by 5-25%. need to monitor the

fasting plasma glucose. SE: flushing of the face, pruritis, nausea,

vomiting an diarrhea, hepatotoxicity, gout, ulcer. ie. Niacin

Ezetimibe (Zetia)

a hyperlipidemiapharmacological tx that blocks the cholesterol from

being absorbed from our diet. decreases LDL, decreases TG, and a

small increase in HDL. SE: hypersensitive rxn, angioedema,

pancreatitis, hepatitis, cholecystitis, thrombocytopenia.

estrogena hyperlipidemiapharmacological tx that naturally lowers LDLs and

raises HDLs. but it raises TGs


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Omega-3 Fatty Acids (fish oil)

a hyperlipidemiapharmacological tx that is used in the tx of elevated

TG levels. inhibits VLDL and apo B-100 synthesis. ingestion of large

amounts can cause prolonged bleeding times. ie. Omacor

angina

chest pain resulting from myocardial ischemia (inadequate blood

supply). the vessels are unable to dilate. caused by inadequate

blood supply through coronary vessels to meet the metabolic needs.

characteristics: quick onset, substernal, radiate to neck, jaw,

shoulders, arms, lasts usually less than 5 minutes, feels like

squeezing/burning/pressing/choking, mild/mod severity, dyspnea,

pallor, diaphoresis, faintness, palpitations, dizziness, GI

ST segment depression the EKG results of a chronic stable angina.

Nitroglycerin or rest recommendations to relieve the sx of chronic stable angina.

short-acting nitrates

this group of medications will dilate the peripheral blood vessels,

dilate coronary arteries and coronary vessels. these are vary fast

and effective at relieving the sx of chronic stable angina. SE:

hypotension and headache. ie. SL absorption

long-acting nitratesthis group of medication will treat the sx of chronic stable angina for

3-6 hours. can be oral or transdermal.

beta-blockers

a chronic stable angina pharmacological tx that decreases cardiac

contractility, HR, SVR, and BP. decreases morbidity and mortality in

patients c CAD...especially p MI. SE: bradycardia, HPO, wheezing,GI complaints, weight gain, depression, sexual dysfunction. do not

stop tx abruptly

Calcium channel blockers

a chronic stable angina pharmacological tx that decrease SVR,

decrease contractility, and cause coronary vasodilation. these drugs

are not ideal for angina...more so for HTN...but complement the

action of nitrates and BB.

Dobutamine

the chemical stressor used in a stress echocardiogram. this

monitors the heart's response....this method is used when a

traditional excercise stress test isn't feasible.

ST elevated myocardial infarction STEMI.... or non-STEMI. two types of acute coronary syndromes.

unstable anginachest pain is new in onset, occurs at rest or has a worsening

pattern. one type of acute coronary syndrome

myocardial infarction irreversible cardiac cell death. described based on the location of


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damage. the mechanisms of injury can be: ischemia, injury, or

infarction. Sx: severe/unrelieved chest pain;

heaviness/pressure/burning/constriction/crushing; may radiate; c

rest or activity; substernal, retrosternal, epigastric; common in early

morning hours; increased Sympathetic NS stimulation (skin ashen,

clammy, cool to touch); BP and HR high initially but c decreasing

CO comes a drop in BP; crackles, JVD, drop in UO; S3 and S4,

murmurs; nausea and vomiting; fever

CK-MB Band

an isoenzyme that can be used to diagnostically be aware if the

myocardial cells have been stressed. useful within 48 hours. Dx

window ends 72 hours p MI.

C-reactive protein

this protein can indicate a MI becasue cardiac cell death will

stimulate the inflammatory response. but may get a false positive if

there is an inflammatory process anywhere else in the body.

myoglobinthis protein can will rapidly rise after a MI. it is a very sensitive

indicator, ends 24 hours p MI.

Cardiac Troponin I

the is a very sensitive and specific diagnostic indicator of a MI or

unstable angina. This is not affected by other types of muscle

damage. the levels will rise 3-12 hours p onset of MI. the window

ends 5-7 days p MI.

Coronary artery bypass graft

(CABG)

this recommendation is for patients with acute coronary syndrome

who have failed medical management, OR have disease in the L

main coronary artery or 3 vessels, OR are not candidates for

Percutaneous Coronary Intervention, OR have failed PCI c ongoing

chest pain. the mammary artery or the saphenous vein from the leg

are commonly used.

drug therapy after MInitroglycerin, BB, ACEI, antidysrrhythmics, cholesterol lowering

drugs, stool softeners.

Heart failure

main causes: HTN and CAD. other contributors: valvular disease,

dilated cardiomyopathy, congenital heart disease, dysrrhythmias,

aging. Sx: early stages asx, dyspnea, fatigue, limited exercise

tolerance, fluid retention (peripheral and pulmonary edema)

systolic heart failureinability of the ventricles to contract. causes a decrease in the LV

ejection fraction

diastolic heart failure impaired ability of the ventricles to fill, results in a decreased SV.


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more than 15 seconds, less than 15

minutesTypical duration of angina sxs:

1) diaphoresis; 2) tachycardia; 3)

transient S4Three findings on physical exam in pt with angina:

pericarditis pain is sharper, worse

with lying down, relieved with sitting

up

How can u differentiate pericarditis from angina from the history?

1) tachypnea; 2) dyspnea; 3) cough;

4) pleuritic chest pain; 5) hemoptysisName 5 sxs of PE:

1) CT, 2) TEE, 3) aortography 3 ways to confirm diagnosis of aortic dissection:

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

esophageal manometry

3 ways to confirm diagnosis of esophageal reflux or spasm

mimicking angina:

CXR How do you confirm diagnosis of pneumothorax?

occurs during exertion; same amt of

exercise reproduces pain; relieved

by rest

Definition of stable angina:

new onset CP; worsening pattern in

frequency, duration or inteDefinition of unstable angina:

1) ECG; 2) stress test; 3) cardiac

catheterizationWork up for angina:

1) to confirm diagnosis of angina; 2)

to determine severity of dz; 3) post

MI evaluation

Name 3 indications for exercise stress test:

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

Contraindications to stress testing:

1) sxs poorly controlled with rx; 2) +

stress test --> determine need for

revascularization; 3) determine

presence of main criteria for bypass

sx

Name 3 indications for cardiac catheterization in pt with angina:


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1) three vessel disease; 2) left main

dzWhat are the 2 main criteria for bypass?

without DM =


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1) is the pain retrosternal? 2) is the

pain brought on by stress? 3) is the

pain relieved with rest or NTG?

3 questions to ask to determine whether chest pain is typical,

atypical or nonanginal:

1) vasculitis; 2) congenital anomaly

of coronaries; 3) coronary spas (i.e.

cocaine); 4) coronary artery

embolus (i.e. atrial thrombus); 5)

hypercoagulable states

5 general causes of non-atherosclerotic MI

left ventricular subendocardium Which cardiac region is most susceptible to ischemia?

usu longer than 20 minutes Duration of chest pain in acute MI:

1) LBBB; 2) previous MI; 3)

pacemaker; 4) digoxin useName 4 factors that would make ECG interpretation of MI difficult:

1-2 wks For how long do troponins remain elevated after acute MI?

PDA of the RCA Which vessel supplies the inferior wall of the left ventricle?

left circumflex a Which vessel supplies the lateral wall of the left ventricle?

in leads V1-V2: 1) tall, broad R

waves; 2) ST depression; 3) tall

peaked T wave

Sign of posterior infarction on initial 12-lead ECG

lateral or inferior Posterior MIs generally occur in association with what other 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

Indications for thrombolytic therapy for acute MI

1) bleeding; 2) reperfusion

arrhythmiasName 2 complications of thrombolysis:

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

Contraindications to thrombolytic therapy:


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IV puncture at noncompressible site

1) bradycardia; 2) AV block; 3)

hypotension; 4) COPDContraindications to BB in acute MI

metoprolol IV q5min What BB do you give in acute MI?

1) CHF; 2) LV dysfunction (EF

-->

increase intracellular Ca -->

inotropic effect

Mechanism of action of digoxin

1) CHF; 2) afib; 3) paroxysmal atrial 3 indications for digoxin


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tachycardias

decrease dig activity Effect of hyperkalemia on digoxin

dig toxicity Effect of hypokalemia on digoxin

1) digoxin; 2) vasodilators Drugs to avoid in treatment of CHF secondary to diastolicdysfunction:

negative inotropic agents: 1) BBs; 2)

verapamil; 3) cardizemRx tx for diastolic dysfunction:

cardiac cause Interstitial edema with elevated PCWP

noncardiac cause Interstitial edema with normal to low PCWP

1) arrhythmias; 2) MI; 3) severe

systemic HTN; 4) PE; 5) valvular

heart dz

Cardiac causes of pulmonary edema

1) ARDS; 2) uremia; 3) aspiration;

4) head trauma; 5) allergic reaction

to rx; 6) alveolar capillary leak

Noncardiac causes of pulmonary edema


enlarged cardiac silhouette; 3)

Kerley B lines; 4) effusion

CXR findings in pulmonary edema

1) tachypnea; 2) cough with pink

frothy sputum; 3) cyanosis; 4)

nocturnal dyspnea; 5) rales, rhonchi

and wheezing

Signs and sxs of pulmonary edema


cardiomegaly; 3) kerley b lines; 4)

pleural effusion

Name 4 CXR findings in pulmonary edema

1) CXR; 2) ABG; 3) ECG Work up for pulmonary edema

1) morphine; 2) lasix (to reducepreload); 3) dobutamine; 4) sit pt

upright; 5) O2 with PEEP; 6) NTG to

reduce preload; 7) digoxin if afib; 8)

IV ACEI

Treatment for pulmonary edema

MS --> impedes LV filling --> Pathophys in mitral stenosis


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increased LA pressure -->

pulmonary congestion --> secondary

pulmonary vasoconstriction --> RV

failure

mid to late low pitched diastolic

murmur preceded by opening snapWhat is the murmur of mitral stenosis?

1) ECG; 2) CXR; 3) echo What 3 tests help make diagnosis of mitral stenosis?

1) LA enlargement; 2) RV

hypertrophy; 3) +/- afibName 3 findings of ECG consistent with mitral stenosis:

1) double-density right heart border;

2) posterior displacement of

esophagus; 3) elevated left

mainstem bronchus

What findings on CXR suggest left atrial enlargement?

decrease preload: 1) diuretics; 2)

sodium restrictionGoals of medical treatment of mitral stenosis

1) rheumatic fever; 2) dilation of left

ventricle2 most common causes of mitral regurgitation

1) ruptured chordae tendineae; 2)

papillary muscle rupture; 3)

endocarditis; 4) trauma

4 causes of acute mitral regurgitation

holosystolic murmur heard best at

apex and radiating to axillaMurmur of mitral regurgitation

increases preload (MR -->

decreased CO --> RAAS --> fluid

retention

What is the effect of chronic mitral regurgitation on preload?

decreased afterload as a portion of

stroke volume is ejected retrograde

into LA

What is the effect of chronic mitral regurgitation on afterload?

Name 4 diagnostic tests to confirm

presence of MR1) ECG; 2) CXR; 3) Echo; 4) Cath

1) LV hypertrophy; 2) LA

enlargement2 findings on ECG consistent with MR

1) VSD; 2) HCM; 3) AS Name 3 entities that mimic mitral regurgitation on physical exam


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relieve sxs by 1) increasing forward

output; 2) reducing pulmonary

venous hypertension

What are the 2 goals of treatment for mitral regurgitation?

1) digitalis; 2) diuretics; 3) arteriolar

vasodilators; 4) anticoagulants

4 classes of drugs used to treat MR

anterior wall Ventricular septal rupture is associated with which infarct?

septal perforators of the PDA Blood supply of the posterior papillary muscle

marginal branch of the left

circumflex aBlood supply of the posterior wall of the left ventricle

ventricular septumPalpable precordial thrill associated with rupture of papillary muscle

or ventricular septum?

1) 2-d echo; 2) doppler flow study;

3) PA cath; 4) LV angiography4 diagnostic tests to confirm diagnosis of papillary muscle rupture

Murmur of mitral valve prolapsemid to late systolic click and a late systolic murmur heard best at the

apex

improves with squatting (increased

venous return); worsens with

valsalva (decreased venous return)

Effect of maneuvers on murmur of mitral valve prolapse


congenitally normal valveMost common cause of AS

1) degenerative (aging); 2)


congenital bicuspid valve; 3)

rheumatic heart dz

3 most common causes of AS

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