AHF and ACS RW Exam 3

Common causes of HFrEF

Coronary artery disease (myocardial infarction or ischemia)

Dilated cardiomyopathies (drug-induced, viral infections, postpartum)

Pressure overload (systemic or pulmonary HTN, aortic or pulmonic valve stenosis)

Volume overload (valvular regurgitation, shunts, high-output states)

Common causes of HFpEF

Increased ventricular stiffness

Ventricular hypertrophy (hypertrophic cardiomyopathy, HTN)

Infiltrative myocardial diseases (amyloidosis, sarcoidosis, endomyocardial fibrosis)

Myocardial infarction or ischemia

Mitral or tricuspid valve stenosis

Pericardial disease (pericarditis, pericardial tamponade)

What LVEF defines HFrEF

LVEF ≤ 40%

What LVEF defines HFpEF

LVEF ≥ 50%

Calculation of cardiac output (CO)

CO = HR x SV

What is cardiac output (CO)

Volume of blood ejected per unit of time (L/min)

Major determinant of tissue perfusion

What are the categories of precipitating factors for ACF

Cardiac

Metabolic

Patient-related

Cardiac precipitating factors for ACF

Acute ischemia

Arrhythmia

Endocarditis

Myocarditis

Pulmonary embolus

Uncontrolled HTN

Valvular disorders

Metabolic precipitating factors for ACF

Anemia

Hyperthyroidism/thyrotoxicosis

Infection

Pregnancy

Worsening renal function

Patient-related precipitating factors for ACF

Dietary/fluid nonadherence

HF therapy nonadherence

Use of cardiotoxins (cocaine, chronic alcohol, amphetamines, sympathomimetics)

Offending medications (NSAIDs, COX-2 inhibitors, steroids, lithium, BBs, CCB, antiarrhythmics, alcohol, thiazolidinediones)

What are the drug mechanisms that may precipitate or exacerbate HF

Negative Inotropic Effects

Cardiotoxic

Sodium and Water Retention

Uncertain mechanisms

What are medications with mech. of negative inotropic effects that may precipitate or exacerbate HF

Antiarrhythmics (disopyramide, dronedarone, flecainide, propafenone, sotalol)

B-blockers (propranolol, metoprolol, carvedilol)

Ca-channel blockers (verapamil diltiazem)

Itraconazole

What are medications with mech. of cardiotoxic that may precipitate or exacerbate HF

Doxorubicin, daunorubicin, epirubicin, idarubicin

Daunomycin, Cyclophosphamide

Amphetamines (cocaine, methamphetamines)

What are medications with mech. of Na and water retention that may precipitate or exacerbate HF

NSAIDs

COX-2 inhibitors

Rosiglitazone and pioglitazone

Glucocorticoids

Androgens and estrogens

Salicylates (high dose)

Sodium-containing drugs (eg, pipercillin/tazobactam)

What are medications with uncertain mech.'s that may precipitate or exacerbate HF

TNF-a (adalimumab, infliximab, etanercept)

Dipeptidyl peptidase-4 (DPP-4) inhibitors (Saxagliptin)

Subsets of AHF

Subset I: Normal (Warm & Dry)

Subset II: Pulmonary Congestion (Warm & Wet)

Subset III: Hypoperfusion (Cool & Dry)

Subset IV: Pulmonary congestion & Hypoperfusion (Cool & Wet)

What does a cardiac index (CI)

Inadequate perfusion (cool skin)

What does a cardiac index (CI) >2.2 indicate

Normal/well-perfused (warm skin)

What does a PCWP >18 indicate

Volume overload (wet)

What does a PCWP

Normal volume/euvolemic (dry)

Subset 1 of AHF presentation

Normal (warm + dry)

CI >2.2 (warm), PCWP

Subset 1 (normal) of AHF treatment

No immediate intervention needed

Optimize oral meds and monitor pt.

Subset 2 of AHF presentation

Pulmonary congestion (warm + wet)

CI >2.2 (warm), PCWP >18 (wet)

Subset 2 (Pulmonary congestion) of AHF treatment

Loop diuretics and vasodilators

Subset 3 of AHF presentation

Hypoperfusion (cool + dry)

CI

Subset 3 (hypoperfusion) of AHF treatment

Positive inotropic agents and/or replace intravascular fluids

Subset 4 of AHF presentation

Pulmonary congestion and hypoperfusion (cool + wet)

CI

Subset 4 (pulmonary congestion + hypoperfusion) of AHF treatment

Diuretics, vasodilators, and inotropic agents

Vasopressors may be needed to maintain BP

Diuretics of choice for AHF

Furosemide, Bumetanide, and Torsemide

Dosing of IV loop diuretics

1-2.5x the oral dose

Monitoring for Dopamine

BP, HR, urinary output and kidney function, ECG,

Extremity perfusion (higher doses only)

Monitoring for Dobutamine

BP, HR, urinary output and function, ECG

Monitoring for Milrinone

BP, HR, urinary output and function, ECG,

Changes in ischemic symptoms (chest pain),

Electrolytes

Monitoring for Nitroprusside

BP, HR, liver and kidney function,

Blood cyanide and/or thiocyanate concentrations if toxicity suspected (nausea, vomiting, altered mental function)

Monitoring for Nitroglycerin

BP, HR, urinary output and kidney function,

Blood BNP/NT-proBNP concentrations

ACS classification based on ECG changes

STEMI: ST-segment elevation

NSTEMI: non-ST-segment elevation (ST-segment depression, T-wave inversion, no ECG changes)

When to perform ECG in ACS

Within 10 minutes of first medical contact (FMC)

Key findings on ECG associated with ACS

ST-segment elevation (STE)

ST-segment depression

T-wave inversion

(indicate myocardial ischemia or infarction)

How long till troponin is released into the blood after an MI

Troponins released into blood about 1-4 hours after an MI

Peak around 18-24 hours

How long does troponin stay elevated in the blood after an MI

Troponins can stay elevated for up to 2 weeks

How often should biochemical markers be repeated in ACS pt.'s

Measured at presentation and repeated in 1-2 hours

Other reasons why troponin may be elevated in the bloodstream

Pulmonary embolus,

Tachyarrhythmias,

Pericarditis,

Myocarditis,

Sepsis

What therapies should all ACS patients receive as early treatment

Morphine or fentanyl

Oxygen

Nitroglycerin

Aspirin + P2Y12 (ADP-receptor antagonists) + Anticoagulant

B-blockers + GPIIb/IIa inhibitors (Eptifibatide)

(MONA3 2B)

What TIMI score indicates low risk

0-1

What TIMI score indicates intermediate risk

2-4

What TIMI score indicates high risk

5-7

Which criteria count for 1 point in the TIMI risk score for ACS

Age 65 years or older

Three or more CAD risk factors: smoking, hypercholesterolemia, HTN, DM, family history of premature CAD death/events

Known CAD (50% or greater stenosis of at least one major coronary artery on coronary angiogram)

Aspirin use within the past 7 days

Two or more episodes of chest discomfort within the past 24 hours

ST-segment depression 0.5 mm or greater

Positive biochemical marker for infarction

Ideal timing of PCI therapy for patient initially presenting with a STEMI

Within 90 minutes of first medical contact

In STEMI patients who present within 12 hours of symptom onset

Ideal timing of fibrinolytic therapy for patient initially presenting with a STEMI

Within 30 minutes of hospital arrival

In STEMI patients who present within 12 hours of symptom onset

Long-term therapies recommended for all patients after MI for secondary prevention of death, stroke, or recurrent infarction

Aspirin

P2Y12 inhibitor

B-Blocker

ACE-inhibitor or ARB

Statin

Pharmacologic and nonpharmacologic recommendations for secondary prevention for patients following MI

Antiplatelet agents (Aspirin, clopidogrel)

ACE/ARB

B-Blocker

Cholesterol management (statin)

Diabetes management

Dietary modifications (weight loss)

HTN management

Nitrates (short acting)

Smoking cessation

(ABCDHeadline NewS)

Metoprolol brand name

Lopressor

Primary route of administration of Enoxaparin

Subcutaneous

Available formulations of Aspirin

Tablet + suppository

Primary indication for use of tPA

Blood clot dissolution

MOA of Clopidogrel

P2Y12 antagonist

How does SL nitroglycerin relieve chest pain

Dilates blood vessels

Major contraindication to use of tPA

Active bleeding

Med with BBW for bleeding risk

Ticagrelor

Major ADR of Aspirin

GI bleeding

How is Enoxaparin excreted

Renal elimination