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Heart Failure (CHF) Brunner, ch. 30, pp. 795-812 Chronic Heart Failure Has exacerbations and remissions. Acute phase is called acute decompensated heart failure. Most common hospital admission in pts over 65 Second most common office visit ER visits and readmissions are common. Prevention and early intervention are important health initiatives. Pathophysiology Impairment of ventricles from damage or overstretching (Starling’s Law) makes them unable to fill with and effectively pump blood. Starling’s Law: The greater the stretch of cardiac muscle the greater the degree of shortening. Pg.660. SV increases with increased bld V. filling heart 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. Physiologic Compensatory Mechanisms Decreased CO stimulates SNS to release catecholamine's 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. Cardiac Output CO = SV times HR CO = total amt of blood ejected by one ventricle in L/min (4-8 L) SV= total amt of blood ejected by one ventricle per heartbeat (60-130 ml) HR= 60-100/min For Example: CO = 100 times 75 = 7500ml or 7.5 L Preload and Afterload Frank Starling Law Compensatory Mechanisms cont’d Decreased CO and renal perfusion stimulates the Renin-Angiotensin-Aldosterone 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 with Heart Failure Pathophysiology: Decompensation—ADHF 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 ADHF; AKA: Pulmonary Edema Severe dyspnea, tachypnea, orthopnea Dry hacking cough, audible wheezing and moist sounds, hemoptysis, Lungs with crackles, wheezes, rhonchi <SBP, >DBP, <PP, tachy, S3 gallop rhythm Anxious, pale, cyanotic, dropping O2 sat 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 Classifications of Heart Failure: Right and Left 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 Systolic and Diastolic Heart Failure Systolic failure: The left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation Diastolic failure (also called diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can't properly fill with blood during the resting period between each beat 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. Right Sided Heart Failure Left Sided Heart Failure Classifications: Functional According to activity tolerance: 1: no limitations 2: slight limitations 3: marked limitation 4: inability to tolerate without discomfort According to risk and symptoms (796): A: risk but no sx B: HD but no sx C: HD with sx of CHF D: Advanced HD with severe sx 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 (see Pt Ed slide) Evaluation of Left Ventricular Systolic (LVS) Function (ejection fraction). Must be documented on the chart. ACEI or ARB for LVSD (ejection fraction less than 40%). Adult Smoking Cessation Advice Admission Criteria Left-sided O2 sat < 89 BUN or creatinine 1½ times upper limits of normal Change in mental status Failed OP tx (2 vs/7d) Sustained HR 100-120 Right-sided O2 sat < 89 Weight gain > 3 lb/2d Edema of extremities Management of ADHF Hi-Fowlers O2 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), morphine, (brain (B-type) natriuretic peptide) Natrecor Hemodynamic monitoring—CVP, PAWP Circulatory assistive devices—VAD, IABP Management of Chronic HF Meds: Digoxin Lasix ACEIs (Vasotec) ARBs (Cozaar) Renin inhibitor (Tekturna) Beta-blockers (Lopressor) Nitrates (isosorbide initrate) Be mindful of potential dangerous side effects (837) Ending Tell The Drug Calcium Channel Blockers = pine Beta Blockers = lol Angiotensin = pril Angiotensin Receptor Blockers = tan Management cont’d 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—indications, SEs Balancing rest and activity Low Na diet; fluid restriction if indicated Monitoring of fluid status—daily wt—same time, same clothes S&S to report—chest pain, palpitations, DOE, PND, orthopnea, hemoptysis, wt gain (>3 lb/2d or >5 lb/wk), increase in edema, fatigue, cough, anorexia Emotional support—high level of anxiety and depression Keep appts