Heart Failure NURS 241 Chapter 35 (p.797)

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)

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

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

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

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)

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

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

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)

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

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

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