Heart Failure (CHF)

1. Heart Failure (CHF) Lewis, ch. 35

2. Pathophysiology • Impairment of ventricles makes them unable to fill with and effectively pump blood. Ventricles have become impaired by either damage or from overstretching (Starling’s Law). • 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.

3. Pathophysiology-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 • Results in increased myocardial workload and O2 demand.

4. Compensatory Mechanisms cont’d • Decreased CO and renal perfusion stimulates the renin-angiotensin system creating a rock-slide effect: • Angiotensin stimulates aldosterone • Antidiuretic hormone is released • Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are released leading to……………………..

5. Compensatory Mechanisms • Vasocontriction • Increased BP • Salt and water retention • Increased vascular volume • Water excretion inhibited—then ANP & BNP kick in resulting in vasodilation and diuresis • Decreased perfusion to other organs

6. Compensation vs. Decompensation • Cardiac compensation occurs when compensatory mechanisms succeed in maintaining adequate CO needed for perfusion. • Cardiac decompensation occurs when these mechanisms become exhausted and fail to maintain the CO needed for adequate tissue perfusion.

7. Etiology • 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

8. 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

9. 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

10. Classifications cont’d • Systolic failure (AKA forward failure)—poor cardiac contraction results in poor CO and decreased EF. Kidneys suffer the most. • Diastolic failure (AKA 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.

11. Classifications cont’d • Acute decompensated failure—lung 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

12. 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 Functional Classifications

13. 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

14. 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

15. 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

16. 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, BUN, creatinine, BNP • Stress testing

17. 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

18. 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

19. 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