Congestive Heart Failure
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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.
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
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
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.
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:
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
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