Heart failure is a syndrome characterized by myocardial dysfunction that leads to impaired pump performance or to frank heart failure and abnormal circulatory congestion. Congestion of systemic venous circulation may result in peripheral edema or hepatomegaly, congestion of pulmonary circulation may cause pulmonary edema. Pump failure usually occurs in damaged left ventricle (left-sided heart failure) but may occur in the right ventricle (right-sided heart failure). Heart failure affect about 2 of every 100 people between ages 27 and 74. It has become more common with advancing age. Advances in diagnostic and therapeutic techniques have greatly improved the outlook of patients with heart failure, but prognosis still depends on the underlying cause and its response to treatment.
Nursing Care Plans
Here are 6 heart failure nursing care plans.
- ECG: Ventricular or atrial hypertrophy, axis deviation, ischemia, and damage patterns may be present. Dysrhythmias, e.g., tachycardia, atrial fibrillation, conduction delays, especially left bundle branch block, frequent premature ventricular contractions (PVCs) may be present. Persistent ST-T segment abnormalities and decreased QRS amplitude may be present.
- Chest x-ray: May show enlarged cardiac shadow, reflecting chamber dilation/hypertrophy, or changes in blood vessels, reflecting increased pulmonary pressure. Abnormal contour, e.g., bulging of left cardiac border, may suggest ventricular aneurysm.
- Sonograms (echocardiography, Doppler and transesophageal echocardiography): May reveal enlarged chamber dimensions, alterations in valvular function/structure, the degrees of ventricular dilation and dysfunction.
- Heart scan (multigated acquisition [MUGA]): Measures cardiac volume during both systole and diastole, measures ejection fraction, and estimates wall motion.
- Exercise or pharmacological stress myocardial perfusion (e.g., Persantine or Thallium scan):Determines presence of myocardial ischemia and wall motion abnormalities.
- Positron emission tomography (PET) scan: Sensitive test for evaluation of myocardial ischemia/detecting viable myocardium.
- Cardiac catheterization: Abnormal pressures are indicative and help differentiate right- versus left-sided heart failure, as well as valve stenosis or insufficiency. Also assesses patency of coronary arteries. Contrast injected into the ventricles reveals abnormal size and ejection fraction/altered contractility. Transvenous endomyocardial biopsy may be useful in some patients to determine the underlying disorder, such as myocarditis or amyloidosis.
- Liver enzymes: Elevated in liver congestion/failure.
- Digoxin and other cardiac drug levels: Determine therapeutic range and correlate with patient response.
- Bleeding and clotting times: Determine therapeutic range; identify those at risk for excessive clot formation.
- Electrolytes: May be altered because of fluid shifts/decreased renal function, diuretic therapy.
- Pulse oximetry: Oxygen saturation may be low, especially when acute HF is imposed on chronic obstructive pulmonary disease (COPD) or chronic HF.
- Arterial blood gases (ABGs): Left ventricular failure is characterized by mild respiratory alkalosis (early) or hypoxemia with an increased Pco2 (late).
- BUN/creatinine: Elevated BUN suggests decreased renal perfusion. Elevation of both BUN and creatinine is indicative of renal failure.
- Serum albumin/transferrin: May be decreased as a result of reduced protein intake or reduced protein synthesis in congested liver.
- Complete blood count (CBC): May reveal anemia, polycythemia, or dilutional changes indicating water retention. Levels of white blood cells (WBCs) may be elevated, reflecting recent/acute MI, pericarditis, or other inflammatory or infectious states.
- ESR: May be elevated, indicating acute inflammatory reaction.
- Thyroid studies: Increased thyroid activity suggests thyroid hyperactivity as precipitator of HF.
- Improve myocardial contractility/systemic perfusion.
- Reduce fluid volume overload.
- Prevent complications.
- Provide information about disease/prognosis, therapy needs, and prevention of recurrences.
- Cardiac output adequate for individual needs.
- Complications prevented/resolved.
- Optimum level of activity/functioning attained.
- Disease process/prognosis and therapeutic regimen understood.
- Plan in place to meet needs after discharge.
1. Decreased Cardiac Output
- Decreased Cardiac Output
May be related to
- Altered myocardial contractility/inotropic changes
- Alterations in rate, rhythm, electrical conduction
- Structural changes (e.g., valvular defects, ventricular aneurysm)
Possibly evidenced by
- Increased heart rate (tachycardia), dysrhythmias, ECG changes
- Changes in BP (hypotension/hypertension)
- Extra heart sounds (S3, S4)
- Decreased urine output
- Diminished peripheral pulses
- Cool, ashen skin; diaphoresis
- Orthopnea, crackles, JVD, liver engorgement, edema
- Chest pain
- Display vital signs within acceptable limits, dysrhythmias absent/controlled, and no symptoms of failure (e.g., hemodynamic parameters within acceptable limits, urinary output adequate).
- Report decreased episodes of dyspnea, angina.
- Participate in activities that reduce cardiac workload.
|Auscultate apical pulse, assess heart rate, rhythm. Document dysrhythmia if telemetry is available.||Tachycardia is usually present (even at rest) to compensate for decreased ventricular contractility. Premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), PVCs, multifocal atrial tachycardia (MAT), and atrial fibrillation (AF) are common dysrhythmias associated with HF, although others may also occur. Note: Intractable ventricular dysrhythmias unresponsive to medication suggest ventricular aneurysm.|
|Note heart sounds.||S1 and S2 may be weak because of diminished pumping action. Gallop rhythms are common (S3and S4), produced as blood flows into noncompliant chambers. Murmurs may reflect valvular incompetence.|
|Palpate peripheral pulses.||Decreased cardiac output may be reflected in diminished radial, popliteal, dorsalis pedis, and post tibial pulses. Pulses may be fleeting or irregular to palpation, and pulsus alternans (strong beat alternating with weak beat) may be present.|
|Monitor BP.||In early, moderate, or chronic HF, BP may be elevated because of increased SVR. In advanced HF, the body may no longer be able to compensate, and profound hypotension may occur.|
|Inspect skin for pallor, cyanosis.||Pallor is indicative of diminished peripheral perfusion secondary to inadequate cardiac output, vasoconstriction, and anemia. Cyanosis may develop in refractory HF. Dependent areas are often blue or mottled as venous congestion increases.|
|Monitor urine output, noting decreasing output and concentrated urine.||Kidneys respond to reduced cardiac output by retaining water and sodium. Urine output is usually decreased during the day because of fluid shifts into tissues but may be increased at night because fluid returns to circulation when patient is recumbent.|
|Note changes in sensorium: lethargy, confusion, disorientation, anxiety, and depression.||May indicate inadequate cerebral perfusion secondary to decreased cardiac output.|
|Encourage rest, semirecumbent in bed or chair. Assist with physical care as indicated.||Physical rest should be maintained during acute or refractory HF to improve efficiency of cardiac contraction and to decrease myocardial oxygen demand/ consumption and workload.|
|Provide quiet environment: explain therapeutic management, help patient avoid stressful situations, listen and respond to expressions of feelings.||Psychological rest helps reduce emotional stress, which can produce vasoconstriction, elevating BP and increasing heart rate.|
|Provide bedside commode. Have patient avoid activities eliciting a vasovagal response (straining during defecation, holding breath during position changes).||Commode use decreases work of getting to bathroom or struggling to use bedpan. Vasovagal maneuver causes vagal stimulation followed by rebound tachycardia, which further compromises cardiac function.|
|Elevate legs, avoiding pressure under knee. Encourage active and passive exercises. Increase activity as tolerated.||Decreases venous stasis, and may reduce incidence of thrombus or embolus formation.|
|Check for calf tenderness, diminished pedal pulses, swelling, local redness, or pallor of extremity.||Reduced cardiac output, venous pooling, and enforced bed rest increases risk of thrombophlebitis.|
|Withhold digitalis preparation as indicated, and notify physician if marked changes occur in cardiac rate or rhythm or signs of digitalis toxicity occur.||Incidence of toxicity is high (20%) because of narrow margin between therapeutic and toxic ranges. Digoxin may have to be discontinued in the presence of toxic drug levels, a slow heart rate, or low potassium level.|
|Administer supplemental oxygen as indicated.||Increases available oxygen for myocardial uptake to combat effects of hypoxia.|
|Administer medications as indicated:||A variety of medications may be used to increase stroke volume, improve contractility, and reduce congestion.|
|Diuretics: furosemide (Lasix), ethacrynic acid (Edecrin), bumetanide (Bumex), spironolactone (Aldactone).||Diuretics, in conjunction with restriction of dietary sodium and fluids, often lead to clinical improvement in patients with stages I and II HF. In general, type and dosage of diuretic depend on cause and degree of HF and state of renal function. Preload reduction is most useful in treating patients with a relatively normal cardiac output accompanied by congestive symptoms. Loop diuretics block chloride reabsorption, thus interfering with the reabsorption of sodium and water.|
|Vasodilators: nitrates (Nitro-Dur, Isordil); arterial dilators: hydralazine (Apresoline); combination drugs: prazosin (Minipress);||Vasodilators are the mainstay of treatment in HF and are used to increase cardiac output, reducing circulating volume (venodilators) and decreasing SVR, thereby reducing ventricular workload. Note: Parenteral vasodilators (Nitropress) are reserved for patients with severe HF or those unable to take oral medications.|
|ACE inhibitors: benazepril (Lotensin), captopril (Capoten), lisinopril (Prinivil), enalapril (Vasotec), quinapril (Accupril), ramipril (Altace), moexipril (Univasc).||ACE inhibitors represent first-line therapy to control heart failure by decreasing ventricular filling pressures and SVR while increasing cardiac output with little or no change in BP and heart rate.|
|Angiotensin II receptor antagonists: eprosartan (Teveten), irbesartan (Avapro), valsartan (Diovan);||Antihypertensive and cardioprotective effects are attributable to selective blockade of AT1(angiotensin II) receptors and angiotensin II synthesis.|
|Digoxin (Lanoxin)||Increases force of myocardial contraction when diminished contractility is the cause of HF, and slows heart rate by decreasing conduction velocity and prolonging refractory period of the atrioventricular (AV) junction to increase cardiac efficiency /output.|
|Inotropic agents: amrinone (Inocor), milrinone (Primacor), vesnarinone (Arkin-Z);||These medications are useful for short-term treatment of HF unresponsive to cardiac glycosides, vasodilators, and diuretics in order to increase myocardial contractility and produce vasodilation. Positive inotropic properties have reduced mortality rates 50% and improved quality of life.|
|Beta-adrenergic receptor antagonists: carvedilol (Coreg), bisoprolol (Zebeta), metoprolol (Lopressor);||Useful in the treatment of HF by blocking the cardiac effects of chronic adrenergic stimulation. Many patients experience improved activity tolerance and ejection fraction.|
|Morphine sulfate.||Decreases vascular resistance and venous return, reducing myocardial workload, especially when pulmonary congestion is present. Allays anxiety and breaks the feedback cycle of anxiety to catecholamine release to anxiety.|
|Antianxiety agents and sedatives.||Promote rest, reducing oxygen demand and myocardial workload.|
|Anticoagulants: low-dose heparin, warfarin (Coumadin).||May be used prophylactically to prevent thrombus and embolus formation in presence of risk factors such as venous stasis, enforced bed rest, cardiac dysrhythmias, and history of previous thrombotic episodes.|
|Administer IV solutions, restricting total amount as indicated. Avoid saline solutions.||Because of existing elevated left ventricular pressure, patient may not tolerate increased fluid volume (preload). Patients with HF also excrete less sodium, which causes fluid retention and increases myocardial workload.|
|Monitor and replace electrolytes.||Fluid shifts and use of diuretics can alter electrolytes (especially potassium and chloride), which affect cardiac rhythm and contractility.|
|Monitor serial ECG and chest x-ray changes.||ST segment depression and T wave flattening can develop because of increased myocardial oxygen demand, even if no coronary artery disease is present. Chest x-ray may show enlarged heart and changes of pulmonary congestion.|
|Measure cardiac output and other functional parameters as indicated.||Cardiac index, preload, afterload, contractility, and cardiac work can be measured noninvasively by using thoracic electrical bioimpedance (TEB) technique. Useful in determining effectiveness of therapeutic interventions and response to activity.|
|Monitor laboratory studies:|
|BUN, creatinine.||Elevation of BUN or creatinine reflects kidney hypoperfusion.|
|Liver function studies (AST, LDH).||May be elevated because of liver congestion and indicate need for smaller dosages of medications that are detoxified by the liver.|
|Prothrombin time (PT), activated partial thromboplastin time (aPTT) coagulation studies.||Measures changes in coagulation processes or effectiveness of anticoagulant therapy.|
|Prepare for insertion and maintenance of pacemaker, if indicated.||May be necessary to correct bradydysrhythmias unresponsive to drug intervention, which can aggravate congestive failure and/or produce pulmonary edema.|
|Prepare for surgery as indicated:|
|valve replacement, angioplasty, coronary artery bypass grafting (CABG).||Heart failure due to ventricular aneurysm or valvular dysfunction may require aneurysmectomy or valve replacement to improve myocardial contractility/ function. Revascularization of cardiac muscle by CABG may be done to improve cardiac function.|
|Cardiomyoplasty.||Cardiomyoplasty, an experimental procedure in which the latissimus dorsi muscle is wrapped around the heart and electrically stimulated to contract with each heartbeat, may be done to augment ventricular function while the patient is awaiting cardiac transplantation or when transplantation is not an option.|
|Transmyocardial revascularization.||Other new surgical techniques include transmyocardial revascularization (percutaneous [PTMR]) using CO2 laser technology, in which a laser is used to create multiple 1-mm diameter channels in viable but underperfused cardiac muscle.|
|Assist with mechanical circulatory support system, such as IABP or VAD, when indicated.||An intra-aortic balloon pump (IABP) may be inserted as a temporary support to the failing heart in the critically ill patient with potentially reversible HF. A battery-powered ventricular assist device (VAD) may also be used, positioned between the cardiac apex and the descending thoracic or abdominal aorta. This device receives blood from the left ventricle (LV) and ejects it into the systemic circulation, often allowing patient to resume a nearly normal lifestyle while awaiting heart transplantation. With end-stage HF, cardiac transplantation may be indicated.|