Pharmacology: Test 3: Clinical Aspects Of Congestive Heart Failure Lec 54

Front 1

4 stages of CHF based on sx

Back 1

1. Prevention of heart failure

2. treatment and prolonging life

3. treatment and reducing sx

4. Endstage considerations

Front 2

2 Major consequence of abnormal functin of LV?

Back 2

Decreased CO: 'forward failure'. decreased excercise tolerance, fatigue, decreased renal perfusion, hypotension.

2. Venous Congestion: 'backward failure'. less blood pumped out so more left behind... causes activation of neurohormonal response (to hypoperfusion) causing Na/fluid retention, edema, hypoxemia, dyspnea, hyopxia.

Front 3

Improving Left Ventricular Fxn: Four Independant Factors

Back 3

Preload, Afterload, Contractility (Systolic and Diastolic dysfunction), and HR and Rhythm.

Front 4

Improving Preload in CHF

Back 4

Preload: Use loop diuretics (i.e. furosemide) plus a K-sparing diuretic (spironolactone). Drugs that improve 'forward flow' (i.e. by enhancing contraction) such as digoxin, ACE-i are also useful.

Front 5

Improving Afterload in CHF

Back 5

largely determined by systolic blood pressure, and hence reduced CO., which then causes neurohormonal compensation, increasing afterload further, worsening the Afterload (a vicious cycle).

use ACE-i and Ang-R-blockers to break this cycle.

Front 6

Contractility: Systolic Dysfunction

Back 6

results in reduced EF, mostly due to MI, dilated cardiomyopathy etc.

Digoxin, beta-agonists (DA, dobutamine increase systolic function BUT ONLY DIGOXIN used b/c the others increase mortality despite improving sx.

Goal is to reduce afterload, and minimize cardiac workload.

Beta blockers in LONG Term, INCREASE EF, and adding ACE-i to it reduces total mortality over ACE-i alone.

Ca Ch blockers CONTRAINDICATED in Systolic Dysfunction (excepto for amlodipine) b/c they reduce contractility.

Front 7

Contractility: Diastolic Dysfunction

Back 7

abnormally INCREASED contractility, commonly seen in concentric LV hypertrophy or hypertrophic cardiomyopathy. Most common cause is HYPERTENSION 'little old lady's heart'.

Smaller chamber requires higher preload (diastolic pressure) to achieve adequate Stroke Volume (hence CO).

Therapy: Neg inotropes like beta blockers and Verapamil used. Small doze diuretics also used to decrease afterload. Excessive reduction in afterload may cause "cavity obliteration" and reflex bradycardia causing syncope.

Digoxin is contraindicated.

Front 8

HR and Rhythm

Back 8

chronic bradycardia: permanent pacemaker indicated,

Amiodarone: drug for maitaining Sinus rhythm is heart failure, also Beta blocker or its combo.

Control Ventricular Rhythm with Digoxin. (or surgical ablation of AV node if no response to Rx).

Front 9

Dealing with abnormal neurohumoral response?

Back 9

heart failure > poor perfusion> increase sympathetic tone (NE) and renin-ang activation > peripheral vasculature, Increased CO and preload with water and Na retention.

This is beneficial short term but long term cardiac workload increase can make progressive heart failure worst.

Use Beta-blockers, ACE-i combined or use ARB (Valsartan) instead of ACE-i. Using all 3 at once causes excessive symp NS depression that's undesirable.

Front 10

4 classes of NYHA

Back 10

based on effort intolerance

NYHA Class I:No sx
II: Sx w/ ordinary activity
III: sx w/ less than ordinary activity.

IV: Sx at rest.

Excercise capacity improved with Digoxin. Also, improves with exercise itself.

Front 11

Fluid retention

Back 11

Early on: ACE-i
Digoxin also helpful

With progression, use loop diuretic like Furosemide (but watch out for hypokalemia). use of K-sparing diuretics would eliminate hypokalemia BUT WATCH OUT FOR INTERACTION WITH ACE-i (lethal hyperkalemia).

End stage: use low dose DA (improve fwd flow and renal perfusion) and morphine (a venodilator).

Front 12

Drugs that reduce risk of sudden death?

Back 12

ACE-i (class 2 and 3), Sprironolactone, most importantly BETA-BLOCKERS.

AVOID unnecessary NSAIDS with ACE-i.