Term
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Definition
Inability of heart to pump sufficient CO to meet body's demands due to structural or functional impairment of ventricular filling or ejection of blood.
Systolic HF: reduced contractility = decreased ejection fraction (LVEF <40%)
Diastolic HF: incomplete ventricular filling = reduced CO, preserved LVEF
> 45% |
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Term
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Definition
Cardiomyopathy
Hypertension
Type 2 DM
MI
Valvular Disease
Congenital heart disease
Atherosclerotic Artery Disease |
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Term
| Clinical Presentation of CHF |
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Definition
Dyspnea
Cyanosis
Peripheral Edema
Pulmonary Edema
Ascites (peritoneal fluid)
Fatigue
Weight gain
Jugular venous distension |
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Term
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Definition
Stage A: high risk for HF but no structural heart disease or HF Sx
Stage B: structural heart disease w/out s/s of HF
Stage C: structural heart disease w/prior or current Sx of HF
Stage D: refractory HF |
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Term
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Definition
ACE inhibitors
ARB's
Statins |
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Term
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Definition
ACE inhibitors
ARB's
Statins
ADD BETA BLOCKERS (lolz) selective B1 |
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Term
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Definition
Spironolactone
Loop diuretics (if edema present)
Hydralazine + isosorbide (AA patients)
Digoxin (short periods of time) |
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Term
| CHF Treatment Short Term Meds |
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Definition
Phosphodiesterase inhibitors and Inotropic agents such as Digoxin.
Both increase contractility of the heart. only to be used for short periods of time |
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Term
| Most common med regimens for CHF |
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Definition
Loop diuretics
ACE inhibitors or ARBs
Beta Blockers
Spironolactone
Hydralazine + isosorbide
Digoxin |
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Term
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Definition
Decreased energy levels
SOB
Edema |
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Term
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Definition
Abnormal Ischemic events
hypoxia
scarred tissue
drug toxicity
electrolyte imbalance |
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Term
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Definition
Phase 0: Rapid depol (Na+ influx)
Phase 1: Brief repol (outflow of K+)
Phase 2: Plateau phase (K+ current balanced by influx of Ca++)
Phase 3: Repolarization
Phase 4: resting potential |
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Term
| Antiarrhythmic Drug Classification |
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Definition
Class I: Na+ channel blocking agents
Class II: beta-blockers
Class III: cardiac action prolongation
Class IV: calcium channel blockers |
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Term
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Definition
Moderate slowing of AP's by blocking K+ currents, prolonging refractory period.
- Minimize premature ventricular beats
- minimize recurrent vent tachycardia
Agents: Quinidine, disopyramide, procainamide.
ADE's: nausea, vomiting, diarrhea
"start low (dose), go slow"
-minimize premature ventricular beats and recurrent vent tachycardia
Quinidine, Disopyramide, Procainamide
ADE's: Nausea, vomiting, diarrhea
may worsen arrhythmias so start low go slow |
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Term
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Definition
Block Na+ channels (minimally), slowing depol but also decreasing AP duration by shortening refractory period and suppressing conduction.
- used to inhibit vent tachycardia
Agents: Lidocaine (Xylocaine), mexiletine, and tocainide
ADE's: drowsiness, slurred speech, confusion |
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Term
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Definition
Markedly slow phase 0 depolarization
- used in Tx of refractory ventricular arrhythmias
Agents: Flecainide (Tambocor) and Propafenone (Rythmol)
ADE's: Dizziness, blurred vision and headaches. |
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Term
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Definition
Depress sinus node automaticity and prolong AV nodal conduction
- most commonly used in atrial flutter and atrial fibrillation
Agents: Beta-blockers |
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Term
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Definition
Prolong repolarization and refractory period by blocking K+ channels on the heart.
Agents: amiodarone, sotalol (Betapace), Ilbutilide, and dofetilide (Tikosyn)
ADE's: interstitial pulmonary fibrosis, GI problems, blurred vision, dizziness, liver toxicity, neuropathy |
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Term
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Definition
Inhibit Ca++ transport thru membrane channels resulting in depression of contractility.
Agents: CCB's - Verapamil and Diltiazem |
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Term
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Definition
ADE's may affect therapy (could be due to drug toxicity)
- faintness
- dizziness
- visual disturbances
All antiarrhythmic agents can produce arrhythmias haha
Negative inotropic effects impair exercise performance (weaken force of muscle contractions) |
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