To function adequately, the nurse knows that the heart valves need to open simultaneously.

This nursing care plan guide contains 18 nursing diagnoses and some priority aspects of clinical care for patients with heart failure. Learn about the nursing interventions and assessment cues for heart failure, including the goals, defining characteristics, and related factors for each nursing diagnosis.

Heart failure (HF) or Congestive Heart Failure (CHF) is a physiologic state in which the heart cannot pump enough blood to meet the body’s metabolic needs following any structural or functional impairment of ventricular filling or ejection of blood.

Heart failure results from changes in the systolic or diastolic function of the left ventricle. The heart fails when, because of intrinsic disease or structural, it cannot handle a normal blood volume or, in the absence of disease, cannot tolerate a sudden expansion in blood volume. Heart failure is a progressive and chronic condition managed by significant lifestyle changes and adjunct medical therapy to improve quality of life. Heart failure is caused by various cardiovascular conditions such as chronic hypertension, coronary artery disease, and valvular disease.

Heart failure is not a disease itself. Instead, the term refers to a clinical syndrome characterized by manifestations of volume overload, inadequate tissue perfusion, and poor exercise tolerance. Whatever the cause, pump failure results in hypoperfusion of tissues, followed by pulmonary and systemic venous congestion.

Heart failure can affect the heart’s left side, right side, or both sides. Though, it usually affects the left side first. The signs and symptoms of heart failure are defined based on which ventricle is affected—left-sided heart failure causes a different set of manifestations than right-sided heart failure.

Because heart failure causes vascular congestion, it is often called congestive heart failure, although most cardiac specialists no longer use it. Other terms used to denote heart failure include chronic heart failure, cardiac decompensation, cardiac insufficiency, and ventricular failure.

Nursing care plan goals for patients with heart failure include support to improve heart pump function by various nursing interventions, prevention and identification of complications, and providing a teaching plan for lifestyle modifications. Nursing interventions include promoting activity and reducing fatigue to relieve the symptoms of fluid overload.

NOTE: This nursing care plan is recently updated with new content and a change in formatting. Nursing assessment and nursing interventions are listed in bold and followed by their specific rationale in the following line. Still, when writing nursing care plans, follow the format here.

Decreased Cardiac Output

The heart fails to pump enough blood to meet the metabolic needs of the body. The blood flow that supplies the heart is also decreased; therefore decrease in cardiac output occurs. Blood then is insufficient and making it difficult to circulate the blood to all parts of the body, thus may cause altered heart rate and rhythm, and weakness.

Nursing Diagnosis

• Decreased Cardiac Output

Common related factors for this nursing diagnosis:

• Altered myocardial contractility/inotropic changes
• Alterations in rate, rhythm, electrical conduction
• Structural changes (e.g., valvular defects, ventricular aneurysm)
• Poor cardiac reserve
• Side effects of medication
• Generalized weakness.

May be evidenced by

The common data cues that could serve as defining characteristics or part of your “as evidenced by” in your diagnostic statement.

• Increased heart rate (tachycardia), dysrhythmias, ECG changes
• Changes in BP (hypotension/hypertension)
• Extra heart sounds (S3, S4)
• Decreased urine output (oliguria)
• Diminished peripheral pulses
• Cool, ashen skin; diaphoresis
• Orthopnea, crackles, JVD, liver engorgement, edema
• Chest pain

Desired goals and outcomes

Common goals and expected outcomes:

• Patient will demonstrate adequate cardiac output as evidenced by vital signs within acceptable limits, dysrhythmias absent/controlled, and no symptoms of failure (e.g., hemodynamic parameters within acceptable limits, urinary output adequate).
• Patient will report decreased episodes of dyspnea, angina.
• Patient will participate in activities that reduce cardiac workload.

Nursing Assessment and Rationales

The following is a nursing assessment guide for heart failure nursing care plans.

1. Auscultate apical pulse, assess heart rate.
Tachycardia is an early sign of heart failure. An increase in heart rate is the body’s first response to compensate for reduced cardiac output (CO). Initially, this compensatory response has a favorable effect on cardiac output, but over time, persistent tachycardia is harmful and may worsen heart failure. Appropriate heart rate control has been associated with better clinical outcomes, including decreased hospitalizations and mortality (Yancy et al., 2017).

2. Note heart sounds.
An extra heart sound S3 or ventricular gallop may be heard during auscultation (S3 mixtape here). This is caused by a large volume of fluid entering the ventricle at the beginning of diastole (Drazner et al., 2003). S1 and S2 may be weak because of decreased pumping action. Murmurs may reflect valvular incompetence.

3. Assess rhythm and document dysrhythmias if telemetry is available.
Both atrial and ventricular dysrhythmias are common. Myocardial stretch, fibrosis, and chamber dilation all alter the electrical paths of the heart. Atrial fibrillation (AF) is common in patients with HF, and occurrence increases with HF severity (Maisel et al., 2003; Yancy et al., 2007). Atrial fibrillation promotes thrombus formation within the atria. Other common dysrhythmias associated with HF include premature atrial contractions, paroxysmal atrial tachycardia, PVCs, multifocal atrial tachycardia, ventricular tachycardia, and ventricular fibrillation.

4. Assess for palpitations or irregular heartbeat.
Palpitations can occur due to dysrhythmias secondary to chronic heart failure. Atrial fibrillation is the most common dysrhythmia in HF. It can also be a compensatory mechanism as the failing heart tries to accommodate for the lack of flow with a faster HR (Kemp et al., 2012). Patients may report fast or irregular heartbeat.

5. Palpate peripheral pulses.
Decreased cardiac output may be reflected in diminished radial, popliteal, dorsalis pedis, and post tibial pulses. Marked diminution or absence of peripheral pulses can indicate severely depressed stroked volume or the presence of severe occlusive vascular disease (Leier, 2007). Pulses may be fleeting or irregular to palpation, and pulsus alternans (strong beat alternating with a weak beat) may be present.

6. Monitor blood pressure (BP).
In acute heart failure, BP may be elevated because of increased systemic vascular resistance (SVR). BP is often used to determine interventions (e.g., vasodilators, vasopressors, etc.). In chronic heart failure, BP is used as a parameter to determine the adequacy or excess dosage of pharmacological therapy (e.g., administration of ACE inhibitors).

7. Inspect the skin for mottling.
Low cardiac output can results in decreased perfusion to the skin of the extremities and may result in mottling – a blue or gray coloring of the skin (Albert et al., 2010). Because of increased tissue capillary oxygen extraction in chronic HF, the skin may appear dusky.

8. Inspects the skin for pallor or cyanosis.
Cool or clammy feeling to touch can occur with diminished perfusion; hypoperfusion in the limb will render pallor (Leier, 2007; Bolger, 2003). This finding, along with other signs of systemic hypoperfusion, will assist the primary care provider to choose proper pharmacotherapy and interventions needed to manage the patient’s condition.

9. Monitor urine output, noting decreasing output and concentrated urine.
Urine output may be decreased due to decreased renal perfusion – kidneys react to reduced cardiac output by retaining water and sodium. The patient may also develop resistance to diuretics, resulting in decreased urinary output (De Bruyne et al., 2003). Urine output is usually low during the day because fluid shifts into tissues and increases at night (nocturia) due to increased renal perfusion during supine position (Redeker et al., 2012).

10. Note changes in sensorium: lethargy, confusion, disorientation, anxiety, and depression.
Cerebral hypoperfusion occurs because of hypoxia to the brain from the decreased cardiac output. The patient may report this as confusion, forgetfulness, restlessness. Through assessment is necessary to evaluate for possible related conditions, including psychologic disorders. Depression is common among patients with heart failure and can lead to poor adherence to treatment plans. Studies have shown depression is 4 to 5 times more common in patients with heart failure and confers a twofold risk of mortality and higher readmission rates (Joynt et al., 2004; Rutledge et al., 2006).

11. Monitor results of laboratory and diagnostic tests.
Signs and symptoms of heart failure are not highly specific and may mimic many other medical conditions (Yancy et al., 2017). The goal in diagnosis is to find the underlying cause of HF and the patient’s response to treatment.

12. Monitor oxygen saturation and ABGs.
Baseline oxygen saturation is useful in establishing the diagnosis and severity of heart failure in acute settings (Masip et al., 2012; Milo-Cotter et al., 2009). Additionally, this provides information regarding the heart’s ability to perfuse distal tissues with oxygenated blood.

Nursing Interventions and Rationales

Here are the nursing interventions for this heart failure nursing care plan.

1. Give oxygen as indicated by the patient’s symptoms, oxygen saturation, and ABGs.
Supplemental oxygen increases oxygen availability to the myocardium and can help relieve symptoms of hypoxemia, ischemia, and subsequent activity intolerance (Giordano, 2005; Haque et al., 1996). The need is based on the degree of pulmonary congestion and resulting hypoxia. Ongoing pulse oximetry monitors the need for and effectiveness of oxygen supplementation.

2. Provide a restful environment and encourage periods of rest and sleep; assist with activities.
Minimizing controllable stressors and unnecessary disturbances reduces cardiac workload and oxygen demand (Rogers et al., 2015). Physical and emotional rest allows the patient to conserve energy. The degree of rest depends on the severity of HF. Patients with severe HF may need to rest in bed, while those with mild to moderate HF can be ambulatory with limited activity.

3. Encourage rest, semirecumbent in bed or chair. Assist with physical care as indicated.
During acute or refractory HF, physical rest should be maintained to improve cardiac contraction efficiency and decrease myocardial oxygen demand/ consumption and workload. Enforce complete bed rest when necessary to decrease the cardiac workload on acute symptomatic attacks of HF.

4. Provide a quiet environment: explain therapeutic management, help the 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.

5. Assist the patient in assuming a high Fowler’s position.
Allows for better chest expansion, thereby improving pulmonary capacity. In this position, the venous return to the heart is reduced, pulmonary congestion is alleviated, and pressure on the diaphragm is minimized. Additionally, heart failure with pulmonary congestion can cause a chronic nonproductive cough worsening in the recumbent position (Platz et al., 2017; Picano et al., 2010).

6. Check for calf tenderness, diminished pedal pulses, swelling, local redness, or pallor of extremity.
The risk for thrombophlebitis increases with enforced bed rest, reduced cardiac output, and venous pooling.

7. Elevate legs, avoiding pressure under the knee or in a position comfortable to the patient.
Decreases venous return and preload and may reduce the incidence of thrombus or embolus formation.

8. Reposition patient every two (2) hours.
For patients under bed rest, prolonged immobility should be avoided because of its deconditioning effects and risk such as pressure ulcers, especially in patients with edema. Decreased circulation in edematous areas also increases the risk of pressure ulcers.

9. Provide bedside commode, provide stool softeners as ordered. Have patient avoid activities eliciting a vasovagal response (straining during defecation, holding breath during position changes).
Using a bedside commode decreases work of getting to the bathroom or struggling to use a bedpan. Patients with HF have autonomic dysfunction. Valsalva maneuver or similar behaviors reduces mean arterial blood pressure and cerebral blood flow, leaving patients vulnerable to hypoperfusion, ischemia, and stroke (Serber et al., 2014).

10. Encourage active and passive exercises. Increase activity as tolerated.
For acute HF, bed rest may be temporarily indicated. Otherwise, a total of 30 minutes of physical activity every day should be encouraged (Yancy et al., 2017).

11. Administer medications as indicated:

11.1. Diuretics
Diuretics are first-line drugs for all patients with signs of volume overload. Diuretics work by reducing blood volume, therefore, decreasing venous pressure, arterial pressure, pulmonary edema, peripheral edema, and cardiac dilation (Ellison et al., 2017; Brater, 2000). Administering diuretics relieves symptoms quickly and controls fluid retention. Data from several small controlled trials show that conventional diuretics appear to reduce the risk of death and worsening heart failure compared to a placebo in patients with CHF. About 80 deaths may be avoided for every 1000 people treated. Diuretics also increase the ability to exercise by about 28% to 33% more than other active drugs (Faris et al., 2012). Commonly used diuretics include:

• Thiazide diuretics [hydrochlorothiazide (Microside)] are oral agents that produce moderate diuresis and are used for long-term therapy of heart failure when edema is moderate (Sica et al, 2011; De Bruyne et al, 2003). Thiazides are ineffective when the GFR is low and if the cardiac output is severely reduced. Adverse effects of thiazides include hypokalemia (thereby increasing risk of digoxin-induced dysrhythmias).
• Loop diuretics [furosemide (Lasix), ethacrynic acid (Edecrin)] promote fluid loss even when GFR is low, in contrast with thiazides. Loop diuretics are the drug of choice for patients with severe heart failure (Felker, 2012). Other than hypokalemia, loop diuretics can also cause severe hypotension due to excessive fluid volume loss.
• Potassium-sparing diuretics [spironolactone (Aldactone)] are used to counteract potassium loss caused by thiazide and loop diuretics, thereby reducing the risk of digoxin-induced dysrhythmias (Gao et al, 2007). Hyperkalemia is the principal adverse effect of these drugs (Brater, 2000).

11.2. Vasodilators, arterial dilators, and combination drugs.

Vasodilators treat heart failure by increasing cardiac output, reducing circulating volume, and decreasing systemic vascular resistance – ultimately reducing ventricular workload. Commonly used vasodilators include:

• Isosorbide dinitrate (ISDN) [Nitro Dur, Isordil] causes selective dilation of veins. For patients with severe refractory HF, ISDN can reduce congestive symptoms and improve exercise capacity (Ziaeian et al, 2017; Nyolczas et al, 2017; Cohn et al, 1991). Watch out for adverse effects such as orthostatic hypotension and reflex tachycardia.
• Hydralazine [Apresoline] causes selective dilation of arterioles therefore can help improve cardiac output and renal blood flow (Herman, 2017; Jacobs 1984). Hydralazine is always used in combination with ISDN (e.g., BiDil – a fixed-dose combination of hydralazine and ISDN).
• Nitroglycerin when given intravenously is a powerful venodilator that produces a dramatic reduction in venous pressure. It is also used to relieve acute severe pulmonary edema (Levy et al, 2007). Hypotension and reflex tachycardia are its main adverse effects.
• Sodium nitroprusside [Nitropress] rapidly dilates arterioles and veins. Arteriolar dilation reduces afterload and thereby increasing cardiac output. Venodilation reduces venous pressure thereby reducing pulmonary and peripheral congestion. Note: Blood pressure must be monitored continuously when taking this drug.
• Nesiritide administration leads to a rapid and balanced vasodilatory effect, which results in a significant decrease in right and left ventricular filling pressures and systemic vascular resistance and at the same time in an increase in stroke volume and cardiac output without a change in heart rate. (Elkayam et al, 2002). Nesiritide treatment significantly increased left ventricular ejection fraction, cardiac index, and 24- and 72-hour urine volumes. The drug safely improves global cardiac and systemic function for patients with heart failure (Zhao et al, 2020).

11.3. Angiotensin-converting enzyme (ACE) inhibitors [ benazepril (Lotensin), captopril (Capoten), lisinopril (Prinivil), enalapril (Vasotec), quinapril (Accupril), ramipril (Altace), moexipril (Univasc)] blocks the renin-angiotensin-aldosterone-system (RAAS) by inhibiting the conversion of angiotensin I to angiotensin II. They decrease mortality, morbidity, hospitalizations, and symptoms in patients with heart failure (Yancy et al., 2017). These drugs also decrease the release of aldosterone and suppressing the degradation of kinins. As a result, they improve hemodynamics and favorably alter cardiac remodeling. Additionally, observe for symptomatic hypotension, hyperkalemia, cough, and worsening renal function.

11.4. Angiotensin II receptor blockers (ARBs) [ eprosartan (Teveten), irbesartan (Avapro), valsartan (Diovan)] are for patients who are unable to tolerate ACE inhibitors (usually owing to intractable cough). They prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. ARBs promote afterload reduction and vasodilation, improve LV ejection fraction, reduce heart failure symptoms, increase exercise tolerance, decrease hospitalization, enhance the quality of life, and reduce mortality (Yancy et al., 2017). Monitoring is the same as ACE inhibitors.

11.5. Digitalis (Lanoxin)
Digoxin is a cardiac glycoside that increases the myocardial contractile force (positive inotropic action). By increasing contractile force, digoxin can increase cardiac output. It also slows the conduction of the heart through the AV node. Unfortunately, digitalis does not result in decreased mortality rates in patients with HF though effective in preventing hospital readmission and decreasing symptoms of systolic HF (Alkhawam et al., 2019; Qamer et al., 2019). Digitalis is considered a second-line agent for heart failure and was widely used in the past. Monitor the renal function and serum potassium levels of patients taking digitalis.

11.6. Inotropic agents [amrinone (Inocor), milrinone (Primacor), vesnarinone (Arkin-Z)].
These medications are useful for short-term or acute treatment of HF unresponsive to cardiac glycosides, vasodilators, and diuretics to increase myocardial contractility and produce vasodilation. They are given intravenously. Positive inotropic properties have reduced mortality rates by 50% and improved quality of life.

11.7. Beta-adrenergic receptor antagonists [carvedilol (Coreg), bisoprolol (Zebeta), metoprolol (Lopressor)].
Beta-blockers directly block the negative effects of the SNS on heart failure. Caution must be taken for patient’s volume overload as they can reduce myocardial contractility. Careful control of the dosage of beta-blockers can improve patient status by improving LV ejection fraction, increasing exercise tolerance, slowing HF progression, reducing the need for hospitalization, and prolong survival (Butler et al., 2006; Barrese et al., 2013). Side effects to look out for include worsening HF symptoms, hypotension, fatigue, and bradycardia.

11.8. Morphine sulfate
Decreases vascular resistance and venous return, reducing myocardial workload, especially when pulmonary congestion is present. The use of morphine should be reserved for patients with myocardial ischemia who are refractory to drugs that favorably alter myocardial oxygen supply and demand. Morphine should not be used in patients whose chest pain syndrome has not been treated with nitrates and beta-blockers (Conti, 2011). Additionally, morphine can help allay anxiety and break anxiety’s feedback cycle to catecholamine release to anxiety.

11.9. Antianxiety agents and sedatives.
Promote rest, reducing oxygen demand and myocardial workload. Patients with HF are likely to be restless and anxious and may feel overwhelmed by breathlessness due to their difficulty maintaining adequate oxygenation (Hinkle et al., 2017). Emotional stress can stimulate the SNS, ultimately increasing cardiac workload. By decreasing anxiety, the patient’s cardiac workload also decreases (De Jong et al., 2011). Additionally, patients with HF have a high incidence of depression and is linked with increased morbidity and mortality (Joynt et al., 2014). (see: Anxiety nursing diagnosis)

11.10. Anticoagulants: low-dose heparin, warfarin (Coumadin).
Prescribed to patients with a history of atrial fibrillation or thromboembolic event. Anticoagulants are used prophylactically to prevent thrombus and embolus formation in the presence of risk factors such as venous stasis, enforced bed rest, cardiac dysrhythmias, and history of previous thrombotic episodes (Kim et al., 2018; Amin et al., 2019).

12. Withhold digitalis preparation as indicated, notify the physician if marked changes occur in cardiac rate or rhythm or signs of digitalis toxicity occur.
The incidence of toxicity is high (20%) because of the 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.

13. Administer IV solutions, restricting total amount as indicated. Avoid saline solutions.
Because of existing elevated left ventricular pressure, the patient may not tolerate increased fluid volume (preload). The amount of fluid administered should be monitored closely (Bikdeli et al., 2015; Albert, 2012). Patients with HF also excrete less sodium, which causes fluid retention and increases cardiac workload.

14. Monitor for signs and symptoms of fluid and electrolyte imbalances.
Fluid shifts and the use of diuretics can lead to excessive diuresis and may lead to electrolyte imbalances such as hypokalemia (Oh et al., 2015). Signs of hypokalemia include ventricular dysrhythmias, hypotension, and generalized weakness. Hyperkalemia can occur with the use of ACE inhibitors, ARBs, or spironolactone.

15. Monitor serial electrocardiogram (ECG) and chest x-ray changes.
Can indicate the underlying cause of HF. ST-segment depression and T wave flattening can develop because of increased myocardial oxygen demand, even if no coronary artery disease is present. A chest x-ray may show an enlarged heart and pulmonary congestion.

16. Measure cardiac output and other functional parameters as indicated.
Cardiac index, preload, afterload, contractility, and cardiac work can be measured noninvasively using the thoracic electrical bioimpedance (TEB) technique. Useful in determining the effectiveness of therapeutic interventions and response to activity.

17. Monitor laboratory studies as indicated: 

• 17.1. Blood urea nitrogen (BUN) and creatinine.
  Elevation of BUN or creatinine reflects decreased renal perfusion – may be caused by HF or medications (e.g., diuretics, ACE inhibitors).
• 17.2. Liver function studies (AST, LDH).
  May detect alterations in liver function which can demonstrate possible cause or effect. May also be elevated because of liver congestion and indicate need for smaller dosages of medications.
• 17.3. Prothrombin time (PT), activated partial thromboplastin time (aPTT) coagulation studies.
  Helps in identifying patients at risk for excessive clot formation and measures changes in coagulation processes or effectiveness of anticoagulant therapy.
• 17.4. Atrial natriuretic peptide (ANP).
  ANP is a. hormone secreted from the right atrial cells when pressure increases. It is increased in congestive HF.
• 17.5. Beta-type natriuretic peptide (BNP).
  BNP is secreted from the cardiac ventricles as a response to ventricular volume and fluid overload (Cowie & Mendez, 2002). BNP levels in the blood increases when symptoms of HF worsen.

18. Prepare for insertion and maintenance of pacemaker, if indicated.
It may be necessary to correct bradydysrhythmias unresponsive to drug intervention. This can aggravate congestive failure and/or produce pulmonary edema.

19. Assist with mechanical circulatory support systems such as the placement of a ventricular assist device (VAD).
A battery-powered ventricular assist device (VAD) is 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 the patient to resume a nearly normal lifestyle while awaiting recovery, transplantation, or waiting for a decision (Yancy et al., 2017).

20. Recognize that some patients may need an intra-aortic balloon pump (IABP), provide assistance.
An intra-aortic balloon pump (IABP) may be inserted as temporary support to the failing heart in the critically ill patient with potentially reversible HF (Reid et al., 2005). When caring for a patient managed with IABP, the nurse must continually assess and measure the often subtle changes in patient condition. This requires expert knowledge of the cardiovascular system, therapeutic effects of IABP, and potential adverse events (Lewis et al., 2009). With end-stage HF, cardiac transplantation may be indicated.

21. Prepare for the surgery as indicated: 

• 21.1. 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.
• 21.2. Cardiomyoplasty.
  Cardiomyoplasty, an experimental procedure in which the latissimus dorsi muscle is wrapped around the heart and electrically stimulated to contract with each heartbeat. It may be done to augment ventricular function while the patient is awaiting cardiac transplantation or when transplantation is not an option. Benefit of cardiomyoplasty in treatment of HF remains unclear (Bocchi, 2001). The challenge for clinical application of cardiomyoplasty is that it is a major surgical procedure and the benefits obtained are limited. Cardiomyoplasty is usually not recommended due to unfavourable results.
• 21.3. 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.

22. Teach the patient the pathophysiology of the disease, medications
Patient education is key to the successful management of HF. Provide the patient with the needed information about the management of the disease (see: Deficient Knowledge)

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy.

Recommended journals, books, and other interesting materials to help you learn more about heart failure nursing care plans and nursing diagnosis:

Originally published on July 14, 2013. 

Which set of valves are involved with the second heart sound quizlet?

How should a nurse assess a client for pulse rate deficit?

What causes normal heart sounds?

What causes the heart sounds heard with a stethoscope quizlet?