Heart failure (HF) is an abnormal clinical condition involving impaired cardiac pumping that results in the characteristic pathophysiologic changes of vasoconstriction and fluid retention.
HF is characterized by ventricular dysfunction, reduced exercise tolerance, diminished quality of life, and shortened life expectancy.
Risk factors include coronary artery disease (CAD) and advancing age. Hypertension, diabetes, cigarette smoking, obesity, and high serum cholesterol also contribute to the development of HF.
TYPES OF CONGESTIVE HEART FAILURE
Right Ventricular Failure, Left Ventricular Failure
Because the two ventricles of the heart represent two separate pumping systems, it is possible for one to fail alone for a short period.
Most heart failure begins with left ventricular failure and progresses to failure of both ventricles
Acute pulmonary edema, a medical emergency, results from left ventricular failure.
If pulmonary edema is not treated, death will occur from suffocation because the client literally drowns in his or her own fluids
Forward Failure, Backward Failure
In forward failure, an inadequate output of the affected ventricle causes decreased perfusion to vital signs.
In backward failure, blood backs up behind the affected ventricle, causing increased pressure in the atrium behind the affected ventricle.
Low Output, High Output
In low-output failure, not enough cardiac output is available to meet the demands of the body.
High-output failure occurs when a condition causes the heart to work harder to meet the demands of the body.
Systolic Failure, Diastolic Failure
Systolic failure leads to problems with contraction and ejection of blood.
Diastolic failure leads to problems with the heart relaxing and filling with blood.
HF can have an abrupt onset or it can be an insidious process resulting from slow, progressive changes. Compensatory mechanisms are activated to maintain adequate CO.
Cardiac compensation occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion.
Cardiac decompensation occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.
The most common form of HF is left-sided failure from left ventricular dysfunction. Blood backs up into the left atrium and into the pulmonary veins causing pulmonary congestion and edema. HF is usually manifested by biventricular failure.
Acute decompensated heart failure (ADHF) typically manifests as pulmonary edema, an acute, life-threatening situation.
Clinical manifestations of chronic HF depend on the patient’s age and the underlying type and extent of heart disease. Common symptoms include fatigue, dyspnea, tachycardia, edema, and unusual behavior.
Pleural effusion, atrial fibrillation, thrombus formation, renal insufficiency, and hepatomegaly are all complications of HF.
CAUSES OF CONGESTIVE HEART FAILURE
Congenital heart disease
Valvular heart defects
Chronic obstructive pulmonary disease
Blood volume excess/polycythemia
SIGNS AND SYMPTOMS OF CONGESTIVE HEART FAILURE Left-sided Congestive Heart Failure Right-sided Congestive Heart Failure
Signs of pulmonary congestion
Crackles in the lungs
Paroxysmal nocturnal dyspnea
Increased BP (from fluid volume excess)
Dependent edema (legs and sacrum) Jugular vein distention Abdominal distention Hepatomegaly Splenomegaly Anorexia and nausea Nocturnal diuresis Swelling of the fingers and hands Increased BP (from fluid volume excess)
Assessment Findings of Acute Pulmonary Edema
Severe dyspnea and orthopnea
Expectoration of large amounts of blood-tinged, frothy sputum
Wheezing and crackles on auscultation
Acute anxiety, apprehension, restlessness
Cold, clammy skin
Use of accessory breathing muscles
The primary goal in diagnosis of HF is to determine the underlying etiology of HF.
A thorough history
laboratory- (serum chemistries, liver function studies, thyroid function studies, and complete blood count)
Major therapy for CHF
Has positive inotropic (strengthens force of cardiac contractility) and negative chronotropic effects (decreases heart rate)
DOC: Lanoxin (Digoxin)
Antidote for Toxicity: Digibind
Assess heart rate before administration; if below 60 bpm or above 120 bpm, withhold the drug.
Monitor serum potassium
Assess for signs of Digitalis toxicity
GI manifestations (anorexia, nausea, vomiting and diarrhea)
Altered visual perceptions
In males: gynecomastia, decreased libido and impotence
To decrease cardiac workload by reducing circulating volume and thereby reduce preload
Commonly used diuretics:
Thiazides: Chlorthiazide (Diuril)
Loop diuretics: Furosemide (Lasix)
Potassium-Sparing: Spironolactone (Aldactone)
Assess for signs of hypokalemia when administering loop and thiazide diuretics.
Give potassium supplement and potassium-rich foods.
Administer early in the morning or early in the afternoon to prevent sleep pattern disturbance related to nocturia.
To decrease afterload by decreasing resistance to ventricular emptying
Commonly used vasodilators:
Diet: sodium-restricted diet to prevent fluid excess
Activity: balanced program of activity and rest
Oxygen Therapy: to increase oxygen supply
Administer oxygen therapy per nasal cannula at 2-6 LPM as ordered
Evaluate ABG analysis results
Semi-Fowler’s or High-Fowler’s position to promote greater lung expansion
Promoting Rest and Activity
Bed rest or limited activity may be necessary during the acute phase
Provide an overbed table close to the patient to allow resting the head and arms
Use pillows for added support when in High-Fowler’s position
Administer Diazepam (Valium) 2-10 mg 3-4x a day as ordered to allay apprehension
Gradual ambulation is encouraged to prevent risk of venous thrombosis and embolism due to prolonged immobility
Activities should progress through dangling, sitting up on a chair and then walking in increased distances under close supervision
Assess for signs of activity intolerance (dyspnea, fatigue and increased pulse rate that does not stabilize readily)
Allow verbalization of feelings
Identify strengths that can be used for coping
Learn what can be done to decrease anxiety
*** Anxiety causes increased breathlessness which may be perceived by the client as an increase in the severity of the heart failure and this in turn increases anxiety.
Facilitating Fluid Balance
Control of sodium intake
Administer diuretics and digitalis as prescribed
Monitor I and O, weight and V/S
Dry phlebotomy (rotating tourniquets)
Providing Skin Care
Edematous skin is poorly nourished and susceptible to pressure sores
Change position at frequent intervals
Assess the sacral area regularly
Use protective devices to prevent pressure sores
Provide bland, low-calorie, low-residue with vitamin supplement during acute phase
Frequent small feedings minimize exertion and reduce gastroistestinal blood requirements
There may be no need to severely restrict sodium intake of the client who receives diuretics.
“ No added salt” diet is prescribed. No processed foods in the diet.
Advise to avoid straining at defecation which involves Valsalva manoeuvre.
Administer laxative as ordered
Encourage use of bedside commode
Teach the client and his family about the disorder and self-care
Monitor signs and symptoms of recurring CHF (weight gain, loss of appetite, dyspnea, orthopnea, edema of the legs, persistent cough and report these to the physician)
Avoid fatigue, balance rest with activity
Observe prescribed sodium restrictions
SFF rather than 3 large meals a day
Take prescribed medications at regular basis
Observe regular follow-up care as directed
If acute pulmonary edema occurs in the client with CHF, the following are the appropriate management:
Morphine Sulfate 10-15mg/IV as ordered to allay anxiety, reduce preload and afterlaod
Oxygen therapy at 40-70% by nasal cannula or face mask
Aminophylline IV to relieve bronchospasm, increase urinary output and increase cardiac output
Monitor serum potassium. Diuresis may result to hypokalemia.
The prognosis depends on the patient's age, the severity of the heart failure, the severity of the underlying heart disease and other factors.
When congestive heart failure develops suddenly and has a treatable underlying cause, patients can sometimes return to normal heart function after treatment.
With appropriate treatment, even individuals who develop congestive heart failure as a result of long- standing heart disease can often enjoy many years of productive life.