1. Heart Failure
NURS 241
Chapter 35 (p.797)

2. Heart Failure Impaired cardiac pumping and/or filling
Often caused by chronic HTN, CAD, MI
Increasing in prevalence d/t increased post-cardiac event survival & increasing age of population
High morbidity & mortality rates, long length of stays, frequent readmissions (expensive)

3. Systolic vs. Diastolic Failure
Systolic Failure
Inability to effectively pump
*Hallmark- *decrease in LV EF
Causes: Impaired contractile function, increased afterload, cardiomyopathy, mechanical abnormality (valve disease)
LV becomes dilated & hypertrophied
Inability of ventricles to relax & fill during diastole
*Hallmarks- *Normal EF, pulmonary congestion & HTN, ventricular hypertrophy
Decreased filling = decreased SV = decreased CO
High filling pressures d/t non-compliant valves/ventricles

4. Mixed Failure
Dilated Cardiomyopathy- poor systolic function further compromised by dilated LV walls
Patients typically have very low EFs (less than 35%), high pulmonary pressures, & biventricular failure

5. Compensatory Mechanisms
SNS Activation- first response, least effective, initially increases CO, eventually tires heart
Neurohormonal Response- RAAS cascade = water/Na retention, vasoconstriction (again becomes detrimental in time)
Dilation- muscle fibers stretch w/ increase volume= increases contractility & initially increases CO (Starling’s Law)
Hypertrophy- initially good, but poor contractility, increased myocardial O2 demands, prone to dysrhythmias

6. Counter-regulatory Mechanisms
Natriuretic peptides
-Produced by heart
-Venous & arterial vasodilation (reduces preload & afterload)
-Inhibit development of hypertrophy
Nitric Oxide
-Produced by vascular endothelium
-Vasodilation of arteries (decreased afterload)

7. Types of Failure Right-Sided Failure Left-Sided Failure
LV dysfunction causes backup of blood into left atrium & pulmonary veins
Increased pulmonary pressure = fluid leaks into alveoli = pulmonary edema
Backup of blood into right atrium & venous circulation
Venous congestion = JVD, hepatomegaly, splenomegaly, peripheral edema

8. Acute Decompensated Heart Failure (ADHF)
Manifests as pulmonary edema (frothy pink sputum)
Low PaO2, progressive respiratory acidosis
Anxious, pale, cool & clammy skin (vasoconstriction), tachycardia
Severe dyspnea- tachypnea, use of accessory muscles, crackles, wheezes, rhonchi

9. Forrester Subsets Congestion (wet or dry) Low perfusion (cold or warm)
Acute Decompensated Heart Failure (ADHF)-most commonly present warm & wet
Worst subset cold & wet
Pg. 801 (Table 35-3)

10. Chronic HF Manifestations
Fatigue
Dyspnea
Paroxysmal nocturnal dyspnea and/or nocturia- reabsorption of fluid in dependent spaces when pt. in recumbent position
Tachycardia
Edema
Skin Changes- shiny, swollen lower extremities
Behavioral Changes d/t potential impaired cerebral circulation
Chest Pain
Weight Changes

11. HF Complications Pleural Effusion
Dysrhythmias- d/t stretching of muscle, EF <35% highest risk for fatal dysrhythmias
Left ventricular thrombus- d/t enlarged LV & decreased CO
Hepatomegaly
Renal Failure- decreased CO = decreased renal perfusion

12. Drug Therapy for HF Patients
Diuretics (i.e. Lasix, Bumex) = ↓ preload
Vasodilators (i.e. NTG) = decrease preload & afterload, increase myocardial O2 supply
Morphine- dilates pulmonary & systemic vessels
Positive Inotropes (i.e. digoxin) = increase contractility
ACE Inhibitors, Angiotensin II Receptor Blockers, Beta Blcokers