Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

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Heart Failure (CHF) Brunner, ch. 30, pp. 824- 840

Transcript of Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

Page 1: Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

Heart Failure (CHF)

Brunner, ch. 30, pp. 824-840

Page 2: Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

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.

Page 3: Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

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.

Page 4: Heart Failure (CHF) Brunner, ch. 30, pp. 824-840.

Physiologic 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.

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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……………………..

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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!

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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)

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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

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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

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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

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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

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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

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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.

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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 (826): A: risk but no sx B: HD but no sx C: HD with sx of CHF D: Advanced HD with

severe sx

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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.

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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

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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

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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

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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

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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)

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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

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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

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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