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Congestive Heart

Failure

(Kozier, “Nursing Management: Heart


Failure and Cardiomyopathy,” chp.34)

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Heart Anatomy

Preload
Contractility
Afterload
CO

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Congestive Heart Failure
Definition

• Abnormal condition involving


impaired cardiac pumping.

• CHF is not a disease.

• Ventricular dysfunction caused by


cardiac and non-cardiac
dysfunctions.

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Definition (Cont’d)
• Cardiac diseases:
long-standing hypertension
coronary artery disease (CAD)
• Characteristics:
ventricular dysfunction
↓ exercise tolerance
↓ quality of life
shortened life expectancy

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Definition (Cont’d)

• incidence for men = women


• High rate of mortality and morbidity
• 1 in 100>65yrs

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ETIOLOGY & RISK
FACTORS
– CAD
– Age
– Hypertension
– Obesity, high cholesterol level
– Smoking
– DM
– African American descent

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Manifestation of Ventricular
Failure
• low BP,
• low CO
• poor renal perfusion,
• poor exercise tolerance,
• ventricular arrhythmias

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PATHOPHYSIOLOGY
• CO depends on:

– Preload

– Afterload

– Myocardial contractility

– Heart rate

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Compensatory
Mechanisms
1. Ventricular dilatation
2. Ventricular hypertrophy- in
chronic CHF
3. Sympathetic nervous system
stimulation
4. Neurohormonal responses:
>Kidneys: angiotensin
aldosterone
>Brain: antidiuretic
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(ADH)
Types of CHF

• One-sided failure eventually leads


to biventricular failure
– Left sided failure
– Right sided failure

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Left Sided Failure

– Most common form (LV


dysfunction)
– Blood backs up through the LA
into the pulmonary veins
Pulmonary congestion and
edema
– Causes: HTN, CAD, rheumatic
heart disease (streptococcus
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Lt Sided Failure Symptoms
• dyspnea, orthopnea & paroxysmal
nocturnal dyspnea
• adventitious sounds: crackles at bases of
lungs --- throughout lungs
• moist, hacking productive cough w/frothy
sputum
• restlessness & anxiety, fatigue
• Nocturia

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Right Sided Failure

– Backward flow to the RA and


venous circulation
– Results from diseased RV
– Leads to venous congestion in
systemic circulation peripheral
edema, etc..
– Causes: Lt sided failure, Cor
Pulmonale, Rt ventr. infarction
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Rt sided Failure Symptoms
• jugular vein distention
• ascities: hepatomegaly
• Anorexia, nausea, GI bloating
• weight gain
• Dependant edema
• Peripheral edema
• fatigue

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Acute CHF
• Manifestation: Pulmonary edema.
• Cause: Lt ventricular failure secondary to CAD
• Symptoms:
-Pale or cyanotic, Cold, clammy skin-
secondary to vasoconstriction from
sympathetic nervous system response
-Agitation
-Severe dyspnea-use of accessory
muscles, orthopnea
-Tachypnea , wheezing, crackles,
coughing
-Nocturia
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CHRONIC CHF
• Fatigue.
• Dyspnea, orthopnea (key symptom)
-Paroxysmal nocturnal dyspnea
• Dry hacking cough.
• Tachycardia- (compensatory mechanism)
• Edema-pitting edema, dependant edema
(sacral edema).
• Sudden weight gain
• Nocturia (6-7 x/night)
• Skin changes
• Behavioral changes

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Complications of CHF
1. Pleural effusion: collection of
fluid in pleural space.
2. Arrhythmias: alteration normal
electrical pathway.
3. Left ventricular thrombus:
enlarged LV and decrease CO
can increase chance of clot.
4. Hepatomegaly (RV failure)
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CLASSIFICATION OF CHF
by the NY Heart Association

– Class 1: No limitation of physical


activity

– Class 2: Slight limitation

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CLASSIFICATION (cont’d)

– Class 3: Marked limitation

– Class 4: Inability to carry on any


physical activity without
discomfort

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Diagnostic Studies

• Primary goal is to determine


underlying cause
– Physical exam
– Chest x-ray
– ECG
– Hemodynamic assessment

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Diagnostic studies (cont’d)

– Echocardiogram-measures ejection
fraction.
– Stress testing
– Cardiac catheterization
– Ejection fraction (EF)

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Collaborative Care

• Treat underlying cause


• Maximize CO
• Alleviate symptoms

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Drug Therapy
Goal: improve symptoms, minimize side effects
of treatment, prevent morbidity and prolong
survival
• ACE inhibitors
• Diuretics
∀β-Adrenergic blockers
• Inotropics agents
• Vasodilators
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ACE Inhibitors

Enalapril & Capoten


• Action: -Block production of
angiotensin II
decrease aldosterone
-Dilate arterioles and veins,
decrease SVR, afterload and increase
CO.
• Adverse effects -hypotension
- hyperkalemia
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DIURETICS
• Action:

-Reduce blood volume and decrease


preload

-Mobilize edematous fluid

-Decrease venous pressure and afterload

-Decrease pulmonary edema, peripheral


edema, cardiac dilation
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Diuretics (cont’d)

3 Types:

• Thiazide-Hydrochlorothiazide:
Inhibit Na/H2O resorption of distal
tubule
2. Loop Diuretics- Lasix
-Acts on ascending loop of Henle
-Na, CL, H2O excretion.
-SE: hypokalemia, ototoxicity,
severe hypotension.
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DIURETICS (cont’d)

3. K sparing diuretics: Spironolactone


(aldactone)
>Improves survival of CHF pts by
blocking effects of aldosterone in
heart.
>Excretion of Na,H2O

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Beta Adrenergic
Carvedilol, Metoprolol, Bisoprolol
• Action:
-Blocks the sympathetic nervous system
(high HR)
-improve L ventricular ejection fraction,
increase exercise tolerance, slow progression
of CHF,
• Adverse effects: fluid retention from
worsening CHF, fatigue, hypotension,
bradycardia, MI

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INOTROPIC AGENTS
1.DIGOXIN(LANOXIN)
• cardiac glycoside, anti-arrthymic
(digitalis)
• used CHF & arrthymias
• functions in 2 ways:
– increases force of myocardial
contractility
– slows conduction from AV node 
slows HR  ventricular emptying
>inhibits K Intracellular levels uptake
>increase intracellular Na, Ca---
increase contractility
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Digoxin (cont’d)
• NRSG:
– take AP for full minute
– note rate & rhythm (if AP < 60, HOLD)
– monitor K+ levels
– educate client & family to assess
pulse for rhythm & rate
– educate & monitor for signs of digoxin
toxicity *(sign of toxicity??)*

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Digoxin (cont’d)
• SE:
-Therapeutic range: 1.54 +/- 0.5 mmol /L
-First sign is arrthymia
-anorexia, N & V, malaise (mild)
-vision disturbances: “yellow”
-changes in HR & rhythm through
palpation, auscultation or on ECG
-monitor K+ levels: hypokalemia may
predispose to toxicity

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INOTROPIC AGENTS

2.sympathomimetics:
• Dopamine
• Dobutamine
• Hydralazine (APRESOLINE)
 Increases CO and renal blood flow.

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INOTROPIC AGENTS (cont’d)

3.Phosphodiesterase inhibitor
• Inamarinone lactate(INOCOR):
-increases contractility (increasing ca
entry)
-Vasodilator, increases CO and
decreases afterload (lower BP)

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Vasodilators

• Sodium Nitrate: (Nitroprusside)


-IV vasodilator for pulmonary
edema
• Nitrates:
-decrease preload
-beneficial in MI: increase
vasodilatation of arteries

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POTENTIAL COMPLICATIONS
• Electrolyte imbalances due to use of
diuretics & digoxin
• Hypokalemia: (low K+)
– weakens cardiac contractions
– leads to digoxin toxicity
– Signs of hypokalemia: weak pulse,
hypotension, muscle flabbiness, generalized
weakness & diminished deep tendon reflexes
• K supplements(K-Dur) if not on ACE
inhibitor or K sparing diuretics. Give with
meals.

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POTENTIAL COMPLICATIONS
(cont’d)

• Hyponatremia: low Na+

– due to prolonged diuretic therapy


– signs: apprehension, weakness, fatigue,
muscle cramps & twitching, rapid,
thready pulse

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Nutritional Therapy for CHF
• Fluid restrictions not commonly prescribed
only for severe CHF
• Na restriction in order to decrease
circulating volume and decrease workload
of heart
– 2 g sodium diet for mild CHF
– 500-1000mg for severe CHF
• Daily weights

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Nursing and Collaborative
Management

- Goal: Improve LV function by:


- Action demands:
– Decreasing intravascular volume
– Decreasing venous return
– Decreasing afterload
– Improving gas exchange and
oxygenation

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Nursing and Collaborative
Management (Cont’d)
Action demands:
– Improving cardiac function
– Reducing anxiety
– Promote skin integrity
– Promote activity tolerance
– Provide client & family education:
self care at home

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