Transcript Congestive Heart Failure

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.
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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.
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Compensatory Mechanisms
cont’d
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Decreased CO and renal perfusion
stimulates the renin-angiotensin system
creating a rock-slide effect (RAAS cascade)
Angiotensin stimulates aldosterone
 Antidiuretic hormone is released
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leading to……………………..
Compensatory Mechanisms
cont’d
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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)
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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
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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
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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
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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
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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.
Classifications: Functional
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According to activity
tolerance:
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1: no limitations
2: slight limitations
3: marked limitation
4: inability to tolerate
without discomfort
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According to risk and
symptoms:
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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.
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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
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
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Collaborative Management—
ADHF
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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
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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
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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
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