a physiologic state in which the heart cannot pump enough blood to meet the metabolic needs of the body (Black & Hawks).
The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients (Brunner & Suddarth).
a general term used to describe a pathophysiological state in which abnormal cardiac function results in a heart that can no longer pump an adequate supply of blood in relation to the venous return and to the metabolic needs of the tissues (Patrick and Rokowsky).
Myocardial failure - refers specifically to abnormalities in myocardial function; myocardial failure commonly leads to heart failure. Circulatory failure – refers to inability of the cardiovascular system to adequately perfuse the tissues. Congestive heart failure (CHF) – is the state of circulatory congestion resulting from heart failure and its compensatory mechanisms.
Etiology and Risk Factors The performance of the heart depends in four essential components:
Contractility of the muscle
Contractility – is the force of contractions generated by the myocardium under given loading conditions.
Preload – amount of blood in the ventricle at the end of diastole
The stretch of the ventricular myocardial fibres just before ventricular contractions.
Afterload – the pressure against which the left ventricle ejects
The amount of tension the heart must generate to overcome systemic pressure and allow ventricular emptying.
The causes of the heart failure can be divided into three subgroups: Abnormal loading conditions Abnormal muscle function Conditions or disease that limit ventricular filling
Etiology of Heart Failure
Conditions that Precipitate Heart Failure Physical or emotional stress Dysrhythmias Atherosclerotic Heart Disease Infection Nutritional Deficiency Hypervolemia Anemia Thyroid Disorder
Forms or Classification of Heart Failure Backward versus Forward Failure
Backward Failure – used to refer to the venous congestion arising from the damming of blood behind the failing chamber.
Forward Failure – refers to the problems of inadequate perfusion. It results when reduced contractility produces a decrease in stroke volume and cardiac output.
High Output versus Low Output Failure
High Output Failure – occurs when the body’s need for oxygen are excessively increased: the heart increases output but is still unable to meet the body’s needs.
Causes of high output failure include sepsis, Paget’s disease, beri-beri, anemia, thyrotoxicosis, and pregnancy.
Low Output Failure – occurs when the heart is unable to pump an adequate supply of blood to the body.
Low output failure results in hypoperfused tissue cells because of the heart’s inability to pump an adequate supply of blood to the body. It occurs when the myocardium is so damaged that it cannot maintain adequate cardiac output; it is the failure of the heart as a pump. Right and left-sided heart failure are sometimes referred to as low output failure.
Left versus Right Ventricular Failure
Left ventricular failure (left-sided heart failure) – results from the failure of the left ventricle to maintain adequate cardiac output.
In LSHF, basic fault lies in the heart muscles itself. Practically always result from damage to the left ventricular myocardium. Precipitating factors: 1. MI 2. Hypertension 3. Aortic & mitral valve disease 4. Dysrhythmias
Failure of the left ventricle to eject its quota of blood Increased workload & end-diastolic volume CO .↑HR .Tingling in the extremities Enlargement of the left ventricle .↓BP . ↓urine output .fatigue .cool, clammy skin Diminished left ventricular function Blood pools in the ventricle & atrium & back up into the pulmonary veins & capillaries .dyspnea on exertion .confusion .dizziness .cyanosis .↓ peripheral pulses .postural hypotension Pulmonary circulation becomes engorged Left Ventricular Failure
Capillary pressure rises Sodium & water are pushed into the interstitial space Pulmonary edema .cough .crackles .↑Pco2 .↓PO2 .rapid, weak pulse .orthopnea Impaired gas exchange & hypoxia .tachypnea .confusion .restlessness .pulsus alternans .Pulmonary effusion
Right Ventricular Failure (Right-sided heart failure) – occurs when the right pump fails.
It almost always follow LSHF, it develop as a result of the stress placed upon the right ventricle as it attempts to pump blood against resistance into the patient’s congested lungs. Occasionally, RSHF develops independently of LSHF. Some causes are: 1. Pulmonary diseases (COPD & Corpulmonale) 2. Constrictive pericarditis 3. Tricuspid and pulmonic valve disorders 4. Infarction of the right ventricle (rare)
↑ pressure in the pulmonary system ® ventricle become stressed because it’s pumping against greater pulmonary resistance & because vascular pressure has risen & cardiac function has declined Stressed ® ventricular hypertrophies & dilate .↑ HR .cool skin .cyanosis .↓ CO .dyspnea .dysrhythmias Blood pools in the ® ventricle & atrium Engorgement of venous system that extends backward Right Ventricular Failure
Venous congestion Sluggish blood flow Enlargegement of liver & spleen Lowered output of the heart’s left side .anorexia .nausea .abdominal pain .palpable liver & spleen .weakness .elevated CVP .jugular vein distension Hepatojugular reflux ↑ capillary pressure
Forces excess fluid from the capillaries into the interstitial space .unexplained weight gain .abdominal distension .pitting edema .nocturia .weakness .dyspnea on exertion
Cardiac Compensatory Mechanism When cardiac output is not sufficient to meet the metabolic needs of the body, compensatory mechanisms, including neurohormonal responses become activated. These mechanisms initially help to improve contraction and maintain integrity of the circulation, but if continued lead to abnormal cardiac muscle growth and reconfiguration (remodeling) of the heart.
Ventricular Dilation - refers to lengthening of the muscle fibers that increases the volume in the heart chambers.
Clinical Manifestations Clinical Manifestations of Right and Left Ventricular Failure
Assessing for Heart Failure
- Pale, cyanotic skin - Dependent edema - Decreased activity tolerance - Unexplained confusion or altered mental status
- Apical impulse, enlarged and left lateral displacement - Third heart sound - Murmurs - Tachycardia - Increased jugular venous congestion (JVD)
- Decreased urinary frequency during the day - Nocturia
- Dyspnea on exertion - Orthopnea - Paroxysmal nocturnal dyspnea - Bilateral crackles that do not clear with cough - Cough on exertion or when supine
Diagnostic Evaluation Echocardiography-two-dimensional with Doppler flow studies – may show ventricular hypertrophy, dilation of chambers, and abnormal wall motion. ECG (resting and exercise) – may show ventricular hypertrophy and ischemia. Chest x-ray may show cardiomegaly, pleural effusion, and vascular congestion. Cardiac catheterization – to rule out CAD. ABG studies may show hypoxemia due to pulmonary vascular congestion. Liver function studies may be altered because of hepatic congestion.
Human B-type natriuretic peptide (BNP, triage BNP, N-terminal probrain NP, or proBNP) As volume and pressure in the cardiac chambers rise, cardiac cells produce and released more BNP. This test aids in the diagnosis of heart failure. A level greater than 100/mL is diagnostic for heart failure. In addition, the higher the BNP, the more severe the heart failure. BNP is used in emergency department to quickly diagnose and start treatment.
Stages of Heart Failure Stage A
Represents the patient who are at a higher risk for developing heart failure, but do not have any structural disorder of the heart
these could include persons with hypertension, CAD, Diabetes, alcohol abuse, or family history of cardiomyopathy. Stage B
Represents those patients who have a structural problem with their heart but who have not developed any symptoms of heart failure.
Patients in this category may have left ventricular hypertrophy, previous MI, or valvular heart disease
Represents the patients who have or have had symptoms of heart failure and who also have a basic underlying structural heart disorder
These patients exhibit fatigue and dyspnea as a result of left ventricular dysfunction, or have these symptoms but are currently receiving treatment for heart failure. Stage D
Represent patient who have end-stage heart failure and whose care may entail the use of mechanical circulatory support, heart transplantation of end-of-life care.
Functional and Therapeutic Classification of Heart Disease Class I No limitation on physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain. Class II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
Class III Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain. Class IV Unable to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.
Dyspnea on exertion
Shortness of breath
Crackles (rales) in lung bases
Activity in tolerance
S3S4 heart sounds
Elevated central venous pressure
Neck vein distentions
Sudden Cardiac death
Right upper quadrant pain
Decreased urine output
Pallor or cyanosis
Increased risk for tissue breakdown
Multisystem Effects of Heart Failure
The overall goals of management of HF are to:
Relieve patient symptoms Improve functional status and quality of life Extend survival
Medical management is based on the type, severity, and cause of heart failure.
Specific objectives of medical management include the following:
Eliminate or reduce any etiologic contributory factors especially those that may be reversible. Reduce the workload on the heart by reducing afterload and preload. Optimize all therapeutic regimens. Prevent exacerbations of heart failure.
Stage A – focuses on eliminating risk factors by initiating therapeutic lifestyle changes and controlling chronic diseases, such as hypertension and diabetes. Beta-adrenergic blockers, ACE inhibitors, and diuretics are useful during this stage. Stage B – treatment is similar to Stage A, with emphasis on use of ACE inhibitors and beta-adrenergic blockers. Stage C – same as A and B, but with closer surveillance and follow up. a. Digoxin is typically added to the treatment plan in the stage.
b. Drug classes to be avoided due to worsening of heart failure symptoms include antiarrhythmic agents, calcium channel blockers, NSAIDS. 4. Stage D – may need mechanical circulatory support, continuous inotropic therapy, cardiac transplantation, or palliative care. a. Treatment aimed at decreasing excess body fluid. b. May not tolerate other classes of drugs used in previous stages.
1. Angiotensin Converting Enzyme (ACE) Inhibitors - plays a vital role in the management of HF due to systolic dysfunction. - ACE inhibitors promotes vasodilation and diuresis by decreasing afterload and preload. - decrease the secretion of aldosterone, a hormone that causes the kidneys to retain sodium and water. - stimulate the kidneys to excrete sodium and fluid thereby reducing left ventricular filling pressure & decreasing pulmonary congestion. - started at a low dose that is increased every 2 weeks until the optimal dose is achieved and the patient is hemodynamically stable.
Patients receiving ACE inhibitors should be monitored for hypotension, hypovolemia, hyperkalemia, and alteration in renal function, especially if they are also receiving diuretics. Example: Captopril, enalapril, fosinopril, quinapril, lisinopril, moexipril, and trandolapril. 2. Angiotensin II Receptor Blockers (ARBs) - blocks the effects of angiotensin II at the angiotensin II receptor. - ACE inhibitors and ARBs have similar hemodynamic effects: ↓BP, ↓systemic vascular resistance, improved cardiac output. - used in patients who cannot tolerate ACE inhibitors due to cough or angioedema.
3. Diuretics - eliminate excess body water and decrease ventricular pressures. - a low-sodium diet and fluid restriction complement this therapy. - some diuretics may have slight venodilator properties. 4. Positive Inotropic Agents - increase the heart’s ability to pump more effectively by improving the contractile force of the muscle. a. Digoxin (Lanoxin) may only be effective in severe cases of failure. b. Dopamine (Intropin) improves renal blood flow in low does range.
c. Dobutaime (Dobutrex) d. Milrinone (Primacor) and amrinone (Inocor) are potent vasodilators. 5. Vasodilator therapy - decreases the workload of the heart by dilating peripheral vessels. By relaxing capacitance vessels (veins and venules) , vasodilators reduce ventricular filling pressures (preload) and volumes. By relaxing resistance vessels (arterioles), vasodilators can reduce impedance to left ventricular ejection and improve stroke volume. a. Nitrates such as NTG, isosorbide (Isordil), NTG ointment (Nito-Bid) – predominantly dilate systemic veins.
b. Hydralazine (Apresoline) – predominantly affects arterioles; reduces arteriolar tone. c. Prazosin (Minipress) – balanced effects on both arterial and venous circulation. d. Sodium nitroprusside (Nipride) – predominantly affects arterioles. e. Morphine (Duramorph) – decreases venous return, decreases pain and anxiety. 6. Beta-adrenergic blockers - decrease myocardial workload and protect against fatal dysrhythmias by blocking norepinephrine effects of the sympathetic nervous system.
a. Metoprolol (Lopressor) are commonly used. b. Carvedilol (Coreg) is a nonselective beta and alpha adrenergic blocker. Patients may actually experience in general malaise for a 2 to 3 week period while they adjust to the medication. 7. Aldosterone Antagonist - decrease sodium retention, sympathetic nervous system activation and cardiac remodeling. a. Spironolactone (Aldactone) is most commonly used.
8. Human B-type Natriuretic Peptide (Nesiritide) - used in patients with decompensated heart failure. - It produces smooth muscle cell relaxation, diuresis, and a reduction in afterload.
1. Restricted sodium 2. Restricted fluids
Mechanical Circulatory Support
- may be used in Stage D heart failure. Intra-aortic balloon pump Enhanced external counterpulsations– pneumatic cuffs are wrapped around the calves, thighs, and buttocks and inflated in rhythm with the patient’s ECG. The cuffs push venous blood back to the heart during diastole and decrease afterload. Continuous positive airway pressure – decreases sleep apnea (which worsens heart failure), slows ventricular remodeling, improves hemodynamics, and reduces irritability. The mechanism is unknown.
4. Cardiac resynchronization therapy or biventricular pacing - helps to restore synchronous ventricular contractions , improves ventricular left ventricle filling, and improves CO. 5. Left ventricular assist device 6. Partial left ventriculectomy (reduction ventriculoplasty or Batista procedure) - a triangular section of the weakened heart muscle is removed to reduce ventricular wall tension. This procedure is not commonly used. 7. Endoventricular circular patch plasty or the Dor procedure - removal of diseased portion of septum or left ventricle
7. Endoventricular circular patch plasty or the Dor procedure - removal of diseased portion of septum or left ventricle with a synthetic or autologous tissue patch, thus providing a more normal shape and size of the heart, which improves hemodynamics. 8. Acorn cardiac support device - a polyester mesh, custom-fitted jacket is surgically placed on the epicardial surface, providing diastolic support. Over time, it decreases or halts remodeling. 9. Heart transplant
Complications Intractable or refractory heart failure Cardiac dysrhythmias Myocardial failure and cardiac arrest Digoxin toxicity Pulmonary infarction, pneumonia, and emboli
Nursing Diagnoses Decreased cardiac output related to impaired contractility and increased afterload and preload. Impaired gas exchange related to alveolar edema due to elevated ventricular pressures. Excess fluid volume related to sodium and water retention. Activity intolerance related to oxygen supply and demand imbalance.
Nursing Interventions Maintaining Adequate Cardiac Output 1. Place patient at physical and emotional rest to reduce work of heart. Provide rest in semi-recumbent position or in armchair in an airconditioned environment – reduces work of heart, increases heart reserve, reduces BP, decreases work of respiratory muscles and oxygen utilization, improves efficiency of heart contraction; recumbency promotes diuresis by improving renal perfusion. Provide bedside commode – to reduce work of getting to bathroom and for defecation.
Provide for psychological rest – emotional stress produces vasoconstriction, elevates arterial pressure, and speeds the heart. - promote physical comfort - avoid situations that tend to promote anxiety and agitation - offer careful explanations and answers to the patient’s questions. 2. Evaluate frequently for progression of left-sided heart failure. Take frequent BP readings. Observe for lowering of systolic pressure. Note narrowing of pulse pressure. Note alternating strong and weak pulsations
3. Auscultate heart sounds frequently and monitor cardiac rhythm. 4. Observe for signs and symptoms of reduced peripheral tissue perfusion: cool temperature of skin, facial pallor, poor capillary refill of nail beds. 5. Administer pharmacotherapy as directed. 6. Monitor clinical response of patient with respect to relief of symptoms (lessening dyspnea and orthopnea, decrease in crackles, relief of peripheral edema). NURSING ALERT: WATCH FOR SUDDEN UNEXPECTED HYPOTENSION WHICH CAN CAUSE MYOCARDIAL ISCHEMIA AND DECREASE PERFUSION TO VITAL ORGANS.
Improving Oxygenation Raise head of bed 8 to 10 inches (20 to 30 cm) – reduces venous return to heart and lungs; alleviates pulmonary congestion. Support lower arms with pillows – to eliminate pull of their weight on shoulder muscles. Sit orthopneic patient on side of bed with feet supported by a chair, head and arms resting on an over-the-bed table, and lumbosacral area supported with pillows. Auscultate lung fields at least 4 hours for crackles and wheezes in dependent lung fields. Observe for increased rate of respirations (could be indicative of falling arterial pH).
Observe for Cheyne-stokes respirations. Position the patient every 2 hours (or encourage the patient to change position frequently) – to help prevent atelectasis and pneumonia. Encourage deep breathing exercises every 1 to 2 hours – to avoid atelectasis. Offer small, frequent feedings – to avoid excessive gastric filling and abdominal distention with subsequent elevation of diaphragm that causes decrease in lung capacity. Administer oxygen as directed. Restoring Fluid Balance 1. Administer prescribed diuretic as ordered.
2. Give diuretic early in the morning. – nighttime diuresis disturbs sleep. 3. Keep input and output record – patient may lose large volume of fluid after a single dose of diuretic. 4. Weigh patient daily – to determine if edema is being controlled: weight loss should not exceed 1 to 2 lb (0.5 to 1 kg)/day. 5. Assess for signs of hypovolemia caused by diuretic therapy – thirst, decreased urine output, orthostatic hypotension, weak, thready pulse, increased serum osmolality, and increased urine specific gravity. 6. Be alert for signs of hypokalemia, which may cause weakness of cardiac contractions and may precipitate digoxin toxicity in the form of dysrhythmias, anorexia, nausea & vomiting, paresthesias, & confusion.
7. Give potassium supplements as prescribed. 8. Be aware of disorders that may be worsened by diuretic therapy including hyperuricemia, gout, volume depletion, hyponatremia, magnesium depletion, hyperglycemia, and diabetes mellitus. 9. Watch for signs for bladder distention in elderly male patients with prostatic hyperplasia. 10. Administer IV fluids carefully through an intermittent access device to prevent fluid overload. 11. Monitor for pitting edema of lower extremities and sacral area. Use convoluted foam mattress and sheepskin to prevent pressure ulcers. (poor blood flow and edema increase susceptibility). 12. Observe for the complications of bedrest – pressure ulcers, phlebothrombosis, pulmonary embolism.
13. Be alert to complaints of right upper quadrant abdominal pain, poor appetite, nausea, and abdominal distention (may indicate hepatic and visceral engorgement). 14. Monitor patient’s diet. Diet may be limited in sodium – to prevent control or eliminate edema; may also be limited in calories. 15. Caution patients to avoid added salt in food and foods with high sodium content. Improving Activity Tolerance Increase patient’s activities gradually. Alter or modify patient’s activities – to keep within the limits of his cardiac reserve. a. Assist patient with self-care activities early in the day (fatigue sets in as day progresses).
b. Be alert to complaints of chest pain or skeletal pain during or after activities. 2. Observe the pulse, symptoms, and behavioral response to increased activity. a. Monitor patient’s, symptoms, and behavioral response to increased activities. b. Allow heart rate to decrease to preactivity level before initiating a new activity Note time lapse between cessation of activity and decrease in heart rate (decreased stroke volume causes immediate rise in heart rate.) Document time lapse and revise patient care plan as appropriate (progressive increase in time lapse maybe indicative of increased life-sided-heart failure).
Relieve nighttime anxiety & provide for rest and sleep-patients with heart failure have a tendency to be restless at night because of cerebral hypoxia with superimposed nitrogen retention. Give appropriate sedation to relieve insomnia and restlessness.
Patient Education and Health Maintenance Explain the disease process; the term failure have terrifying implications. Explain the pumping action of the heart- to move blood through the body to provide nutrients and aid in the removal of waste material. Explain the difference between heart attack and heart failure. Teach the signs & symptoms of recurrence. Watch for Gain weight Swelling of ankles, feet, or abdomen Persistent cough Tiredness, loss of appetite Frequent urination at night
Review medication regimen Label all medications Give written instructions. Make sure the patient has a check-off system that will show that he has taken medications. Teach the patient to take and record pulse rate and BP. Inform the patient of adverse drug effects. If the patient is taking oral potassium solution, it maybe diluted with juice and taken after a meal. Tell the patient to weight self daily and log weight if on diuretic therapy.
Review activity program. Instruct the patient as follows: Increase walking and other activities gradually, provided they do not cause fatigue & dyspnea. In general continue, at whatever activity level can be maintained without the appearance of symptoms. Avoid excesses in eating and drinking. Undertake a weight reduction program until optimal weight is reached. Avoid extremes in heat and cold, which, increase the work of the heart, air conditioning may be essential in a hot, humid environment.
Restrict sodium as directed. 1. Teach restricted sodium diet and the DASH (Dietary Approaches to Stop Hypertension) diet. 2. Give patient a written diet plan with lists of permitted and restricted food. 3. Advise patient to look at all labels to ascertain sodium content. 4. Teach patient to rinse the mouth well after using tooth cleansers and mouthwashes – some of these contain large amounts of sodium. 5. Teach patient that sodium is present in cough remedies, laxatives, pain relievers, estrogens, and other drugs.
EVALUATION: EXPECTED OUTCOMES Normal BP and heart rate Respiratory rate 16 to 20, ABG levels within normal limits, no signs of crackles of wheezes in lung field. Weight decrease of 2.2 lb daily, no pitting edema of lower extremities and sacral area. Heart rate within normal limits, rests between activities.