Transcript Congestive Heart Failure

Heart Failure (CHF)
Brunner, ch. 30, pp. 795-812
Chronic Heart Failure
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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
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Impairment of ventricles from damage or overstretching
(Starling’s Law) makes them unable to fill with and
effectively pump blood.
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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
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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
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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
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Preload and Afterload
Frank Starling Law
Compensatory Mechanisms cont’d
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Decreased CO and renal perfusion stimulates the
Renin-Angiotensin-Aldosterone System creating a
rock-slide effect (RAAS cascade)
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Angiotensin stimulates aldosterone
Antidiuretic hormone is released
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 with Heart
Failure
Pathophysiology:
Decompensation—ADHF
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Occurs when these mechanisms become exhausted
and fail to maintain the CO needed for adequate
tissue perfusion.
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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
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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
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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
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Long standing CAD—creates prolonged ischemia
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Previous MI—weakens muscle
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HTN—increases afterload in great vessels, causes
LV hypertrophy
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Hx of pericarditis—scar tissue causes constriction
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Dysrhythmias—affect pump action
Etiology cont’d
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Anemia—increases HR
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Thyroid disease—increases HR and BP
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Lyte imbalances—affects regularity, contractility
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COPD—increases afterload in PA
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Diabetes—constricts small arteries
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Valvular disorders—causes leakage
Classifications of Heart Failure:
Right and Left
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Right-sided
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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
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Congestion in left
chambers
Increase in size of LV
Backflow to
pulmonary veins
Congestion in lungs
Systolic and Diastolic Heart
Failure
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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
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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
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Systolic Failure (Forward Failure)—poor cardiac
contraction results in poor CO and decreased EF. Kidneys
suffer the most.
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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
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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 (796):
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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
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Wet means the patient has fluid overload
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Dry means the patient does not.
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Warm means the patient has good perfusion
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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
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Collaborative Management: Core
Measures
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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
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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
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O2 sat < 89
Weight gain > 3 lb/2d
Edema of extremities
Management of ADHF
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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
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Meds:
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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
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Management cont’d
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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
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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