Heart Failure (CHF) Lewis, ch. 35 Concept 22.6, pp. 1404-1421
Pathophysiology • Impairment of ventricles from damage or overstretching (Starling’s Law) makes them unable to fill with and effectively pump blood. • As a result, cardiac output falls (decreased ejection fraction), leading to decreased tissue perfusion, making the heart unable to meet the metabolic demands of the body.
Physiology-Compensatory Mechanisms • Decreased CO stimulates SNS to release catecholamines • This increases HR, BP, peripheral resistance, and venous return • This decreases ventricular filling time and decreases CO leading to decreased organ perfusion • Results in increased myocardial workload and O2 demand.
Compensatory Mechanisms cont’d • Decreased CO and renal perfusion stimulates the renin-angiotensin system creating a rock-slide effect (RAAS cascade) • Angiotensin stimulates aldosterone • Antidiuretic hormone is released leading to……………………..
Compensatory Mechanisms cont’d • Vasoconstriction • Increased BP • Salt and water retention • Increased vascular volume • Causing atrial natriuretic and b-type natriuretic peptides (ANP & BNP, heart hormones) and nitric oxide to kick in resulting in vasodilation and diuresis……. Compensation successful!
Pathophysiology: Decompensation • Occurs when these mechanisms become exhausted and fail to maintain the CO needed for adequate tissue perfusion. • Alveoli become filled with serosanguineous fluid from congestion and the fluid leaks into interstitial spaces. Lung tissue becomes less compliant and airways constrict (AKA: Pulmonary Edema)
S/S of Acute Decompensated Heart Failure (ADHF) • Severe dyspnea, tachypnea, orthopnea • Dry hacking cough, wheezing, hemoptysis • Lungs with crackles, wheezes, rhonchi • <SBP, >DBP, <PP, tachy, S3 gallop rhythm • Anxious, pale, cyanotic • Cold, clammy skin
S/S of Chronic Heart Failure • Wt gain, edema • JVD • Hepatomegaly • Oliguria, nocturia • DOE, PND, orthopnea • Fatigue, anorexia • Restlessness, confusion, decreased attn span • Skin changes in extremities
Etiology of Heart Failure • Long standing CAD—creates prolonged ischemia • Previous MI—weakens muscle • HTN—increases afterload in great vessels, causes LV hypertrophy • Hx of pericarditis—scar tissue causes constriction • Dysrhythmias—affect pump action
Etiology cont’d • Anemia—increases HR • Thyroid disease—increases HR and BP • Lyte imbalances—affects regularity, contractility • COPD—increases afterload in PA • Diabetes—constricts small arteries • Valvular disorders—causes leakage
Right-sided Congestion in right chambers Increase in CVP Increase in size of RV Backflow to vena cava Congestion in jugular veins, liver, lower extremities Left-sided Congestion in left chambers Increase in size of LV Backflow to pulmonary veins Congestion in lungs Classifications of Heart Failure: Right and Left
Classifications: Forward and Backward • Systolic Failure (Forward Failure)—poor cardiac contraction results in poor CO and decreased EF. Kidneys suffer the most. • Diastolic Failure (Backward Failure)—ventricles are stiff and thick and will not relax enough during the resting phase to receive adequate amount of blood to maintain good CO. Also causes backflow into lungs and systemic circulation.
According to activity tolerance: 1: no limitations 2: slight limitations 3: marked limitation 4: inability to tolerate without discomfort According to risk and symptoms: A: risk but no sx B: HD but no sx C: HD with sx of CHF D: Advanced HD with severe sx Classifications: Functional
Classifications: Wet/Dry; Warm/Cold • Wet means the patient has fluid overload • Dry means the patient does not. • Warm means the patient has good perfusion • Cold means the patient does not.
Diagnostic Assessment • CXR—fluid and heart enlargement • ECG—can reveal hx of heart problems • Echo or TEE—enlargement, valvular function, condition of great vessels, ejection fraction • ABGs, O2 sat, cardiac markers, BMP • Liver functions, thyroid functions, BUN, creatinine, BNP • Stress testing
Collaborative Management: Core Measures • Discharge Instructions • Evaluation of Left Ventricular Systolic (LVS) Function • ACEI or ARB for LVSD (angiotension converting enzyme inhibitor or angiotensin receptor blocker for left ventricular systolic dysfunction) • Adult Smoking Cessation Advice
Collaborative Management—ADHF • Hi-Fowlers • O2 by mask or BiPAP. Intubation and mechanical ventilation is possible if needed • VS, Pulse ox, UOP hourly • Telemetry • Daily wt • Meds: diuretics (Lasix), vasodilators (NTG), inotropics (dobutamine), MS, (BNP) Natrecor • Hemodynamic monitoring—CVP, PAWP • Circulatory assistive devices—VAD, IABP
Collaborate Management of Chronic HF • Meds: digoxin, Lasix, ACEIs (Vasotec), ARBs (Cozaar), beta-blockers (Lopressor) • 6 small meals of NAS diet with >calories, protein • Fowler’s position • O2 by NC 3-6 L/min • Rest-activity schedule, stress reduction • I&O, daily wts, possible fluid restriction • Circulatory assistive device • Long-term: cardiac transplantation
Complications • Pleural effusion from pulmonary congestion • Dysrhythmias caused by stretching of the chambers particularly the atria (a-fib) and especially if EF < 35% • LV thrombus from atrial fib and poor ventricular function. Need anticoagulant therapy. • Liver dysfunction—can result in cirrhosis • Renal failure from poor renal perfusion
Patient Education • Disease process • Meds • Balancing rest and activity • Low Na diet; fluid restriction if indicated • Monitoring of fluid status—daily wt • S&S to report—chest pain, palpitations, dyspnea, hemoptysis, wt gain, increase in edema, fatigue • Emotional support—high level of anxiety and depression