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- 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
Cardiac Pump Effectiveness (NOC)
- 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.
Nursing Interventions & Rationale
|Auscultate apical pulse; assess heart rate, rhythm||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 (S3 and S4), produced as blood flows into noncompliant/distended chambers. Murmurs may reflect valvular incompetence/stenosis.|
|Palpate peripheral pulses.||Decreased cardiac output may be reflected in diminished radial, popliteal, dorsalis pedis, and posttibial 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/irreversible 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 dark/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, e.g., 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 medical/nursing management; help patient avoid stressful situations; listen/respond to expressions of feelings/fears.||Psychological rest helps reduce emotional stress, which can produce vasoconstriction, elevating BP and increasing heart rate/work.|
|Provide bedside commode. Have patient avoid activities eliciting a vasovagal response, e.g., 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/output.|
|Elevate legs, avoiding pressure under knee. Encourage active/passive exercises. Increase ambulation/activity as tolerated.||Decreases venous stasis, and may reduce incidence of thrombus/embolus formation.|
|Check for calf tenderness; diminished pedal pulse; swelling, local redness, or pallor of extremity.||Reduced cardiac output, venous pooling/stasis, and enforced bedrest 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/ischemia.|
|Administer medications as indicated:
Diuretics, e.g., furosemide (Lasix), ethacrynic acid (Edecrin), bumetanide (Bumex), spironolactone (Aldactone);
Vasodilators, e.g., nitrates (Nitro-Dur, Isordil); arteriodilators, e.g., hydralazine (Apresoline); combination drugs, e.g., prazosin (Minipress);ACE inhibitors, e.g., benazepril (Lotensin), captopril (Capoten), lisinopril (Prinivil), enalapril (Vasotec), quinapril (Accupril), ramipril (Altace), moexipril (Univasc);
Angiotensin II receptor antagonists, e.g., eprosartan (Teveten), ibesartan (Avopro), valsartan (Diovan);
Inotropic agents, e.g., amrinone (Inocor), milrinone (Primacor), vesnarinone (Arkin-Z);
Beta-adrenergic receptor antagonists, e.g., carvedilol (Coreg), bisoprolol (Zebeta), metoprolol (Lopressor);
|A variety of medications may be used to increase stroke volume, improve contractility, and reduce congestion.
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 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 (e.g., Nitropress) are reserved for patients with severe HF or those unable to take oral medications.
ACE inhibitors represent first-line therapy to control heart failure by decreasing venticular filling pressures and SVR while increasing cardiac output with little or no change in BP and heart rate.
Antihypertensive and cardioprotective effects are attributable to selective blockade of AT1 (angiotensin II) receptors and angiotensin II synthesis.
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.
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.
Useful in the treatment of HF by blocking the cardiac effects of chronic adrenergic stimulation. Many patients experience improved activity tolerance and ejection fraction.
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.
Promote rest/relaxation, reducing oxygen demand and myocardial workload.
|Administer IV solutions, restricting total amount as indicated. Avoid saline solutions.||May be used prophylactically to prevent thrombusembolus formation in presence of risk factors such as venous stasis, enforced bedrest, cardiac dysrhythmias, and history of previous thrombolic episodes.|
|Monitor/replace electrolytes.||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 serial ECG and chest x-ray changes.||Fluid shifts and use of diuretics can alter electrolytes (especially potassium and chloride), which affect cardiac rhythm and contractility.|
|Measure cardiac output and other functional parameters as indicated.||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.|
|Monitor laboratory studies, e.g., BUN, creatinine;
Liver function studies (AST, LDH);Prothrombin time (PT)/activated partial thromboplastin time (aPTT) coagulation studies.
| 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.Elevation of BUN/creatinine reflects kidney hypoperfusion/failure.
May be elevated because of liver congestion and indicate need for smaller dosages of medications that are detoxified by the liver.
Measures changes in coagulation processes or effectiveness of anticoagulant therapy.
|Prepare for insertion/maintain pacemaker, if indicated.||May be necessary to correct bradydysrhythmias unresponsive to drug intervention, which can aggravate congestive failure/produce pulmonary edema.|
|Prepare for surgery as indicated, e.g., valve replacement, angioplasty, coronary artery bypass grafting (CABG);Cardiomyoplasty;Transmyocardial revascularization.||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, 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.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/maintain 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.|