Risk for Decreased Cardiac Output | Nursing Diagnosis for Chronic Renal Failure

Nursing diagnosis: risk for decreased Cardiac Output

Risk factors may include
Fluid imbalances affecting circulating volume, myocardial workload, and systemic vascular resistance (SVR)
Alterations in rate, rhythm, cardiac conduction (electrolyte imbalances, hypoxia)
Accumulation of toxins (urea), soft tissue calcification (deposition of calcium phosphate)

Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will
Circulation Status
Maintain cardiac output as evidenced by blood pressure (BP) and heart rate within client’s normal range; peripheral pulses strong and equal with prompt capillary refill time.

Nursing intervention with rationale:
1. Auscultate heart and lung sounds. Evaluate presence of peripheral edema, vascular congestion, and reports of dyspnea.
Rationale: S3/S4 heart sounds with muffled tones, tachycardia, irregular heart rate, tachypnea, dyspnea, crackles, wheezes, and edema or jugular distention suggest heart failure (HF).

2. Assess presence and degree of hypertension: Monitor BP and note postural changes, such as sitting, lying, and standing.
Rationale: Significant hypertension can occur because of disturbances in the renin-angiotensin-aldosterone system caused by renal dysfunction. Although hypertension is common, orthostatic hypotension may occur because of intravascular fluid deficit, response to effects of antihypertensive medications, or uremic pericardial tamponade.

3. Investigate reports of chest pain, noting location, radiation, severity (0 to 10 scale), and whether or not it is intensified by deep inspiration and supine position.
Rationale: Although hypertension and chronic HF may cause myocardial infarction (MI), approximately half of CRF clients on dialysis develop pericarditis, potentiating risk of pericardial effusion and tamponade.

4. Evaluate heart sounds for friction rub, BP, peripheral pulses, JVD, capillary refill, and mentation.
Rationale: Presence of sudden hypotension with paradoxical pulse, narrow pulse pressure, diminished or absent peripheral pulses, marked JVD, pallor, and a rapid mental deterioration indicate tamponade, which is a medical emergency.

5. Assess activity level and response to activity.
Rationale: Weakness can be attributed to heart failure and anemia.

6. Monitor laboratory and diagnostic studies, such as the following: Electrolytes—potassium, sodium, calcium, magnesium; BUN/Cr
Rationale: Imbalances can alter electrical conduction and cardiac function.

7. Collaborate in treatment of underlying disease or conditions, where possible.
Rationale: Delaying or halting progression of CRF in early stages can be aided by interventions, such as controlling BP, managing diabetes, treating hyperlipidemia, and avoiding toxins such as NSAIDs, intravenous (IV) contrast dye, aminoglycosides, and so on.

8. Administer medications, as indicated, for example: Antihypertensive drugs, such as prazosin (Minipress), captopril (Capoten), clonidine (Catapres), and hydralazine (Apresoline)
Rationale: Aggressive treatment of hypertension is needed to reduce SVR or renin release to decrease myocardial workload and aid in prevention of HF and MI.

9. Administer oxygen, as indicated.
Rationale: Cardiac function can be improved with use of oxygen if client is severely anemic or metabolic acidosis and electrolyte abnormalities are causing dysrhythmias.

10. Prepare for renal replacement therapy, such as hemodialysis.
Rationale: Reduction of uremic toxins and correction of electrolyte imbalances and fluid overload may limit or prevent cardiac manifestations, including hypertension and pericardial effusion.

Risk for Decreased Cardiac Output | Nursing Diagnosis for Renal Failure

Nursing diagnosis: risk for decreased Cardiac Output

Risk factors may include
Fluid overload—kidney dysfunction or failure, overzealous fluid replacement
Fluid shifts, fluid deficit (excessive losses)
Electrolyte imbalance (potassium, calcium), severe acidosis
Uremic effects on cardiac muscle, oxygenation

Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will
Circulation Status
Maintain cardiac output as evidenced by BP and HR and rhythm within client’s normal limits and peripheral pulses strong and equal, with adequate capillary refill time.

Nursing intervention with rationale:
1. Monitor BP and heart rate.
Rationale: Fluid volume excess, combined with hypertension, which often occurs in renal failure, and effects of uremia increase cardiac workload and can lead to cardiac failure. In ARF, cardiac failure is usually reversible.

2. Observe ECG or telemetry for changes in rhythm.
Rationale: Changes in electromechanical function may become evident in response to accumulation of toxins and electrolyte imbalance. For example, hyperkalemia is associated with a peaked T wave, wide QRS complex, prolonged PR interval, and flattened or absent P wave. Hypokalemia is associated with flattened T wave, peaked P wave, and appearance of U waves. Prolonged QT interval may reflect calcium deficit.

3. Auscultate heart sounds.
Rationale: Development of S3/S4 is associated with congestive HF. Pericardial friction rub may be only manifestation of uremic pericarditis, requiring prompt intervention and, possibly, acute dialysis.

4. Assess color of skin, mucous membranes, and nailbeds. Note capillary refill time.
Rationale: Pallor may reflect vasoconstriction or anemia—common in ARF, whether associated with actual blood loss or abnormalities in life of RBCs. Cyanosis is a late sign and is related to pulmonary congestion or cardiac failure. A long capillary refill time is associated with hypovolemic states.

5. Note occurrence of slow pulse, hypotension, flushing, nausea or vomiting, and depressed LOC—central nervous system (CNS) depression.
Rationale: Magnesium is typically decreased with ARF. If client is also using drugs (e.g., antacids) containing magnesium, the result can be significant hypomagnesemia, potentiating neuromuscular dysfunction and risk of respiratory or cardiac arrest.

6. Investigate reports of muscle cramps, numbness or tingling of fingers, with muscle twitching and hyperreflexia.
Rationale: These are symptoms of hypocalcemia. Calcium levels are typically somewhat decreased with ARF. If phosphorus levels are also high, hypocalcemia can become severe, which can also affect cardiac contractility and function.

7. Maintain bedrest or encourage adequate rest and provide assistance with care and desired activities.
Rationale: Reduces oxygen consumption and cardiac workload.

8. Administer and restrict fluids as indicated. (Refer to NDs: excess Fluid Volume.)
Rationale: Cardiac output depends on circulating volume—affected by both fluid excess and deficit—and myocardial muscle function.

9. Administer medications, as indicated, such as: Inotropic agents
Rationale: May be used to improve cardiac output by increasing myocardial contractility and stroke volume.

10. Prepare for and assist with dialysis, as necessary.
Rationale: May be indicated for persistent dysrhythmias and progressive HF unresponsive to other therapies.

Risk for Decreased Cardiac Output | Nursing Care Plan for Hyperthyroidism

Nursing diagnosis: risk for decreased Cardiac Output

Risk factors may include
Uncontrolled hyperthyroidism, hypermetabolic state
Increasing cardiac workload
Changes in venous return and systemic vascular resistance (SVR)
Alterations in rate, rhythm, conduction

Possibly evidenced by
(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will
Circulatory Status
Maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.

Nursing intervention with rationale:
1. Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.
Rationale: General and orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects compensatory increase in stroke volume and decreased SVR.

2. Monitor central venous pressure (CVP), if available.
Rationale: Provides more direct measure of circulating volume and cardiac function.

3. Investigate reports of chest pain and angina.
Rationale: May reflect increased myocardial oxygen demands and ischemia.

4. Assess pulse and heart rate while client is sleeping.
Rationale: Provides a more accurate assessment of tachycardia.

5. Auscultate heart sounds, noting extra heart sounds and development of gallops and systolic murmurs.
Rationale: Prominent S1 and murmurs are associated with forceful cardiac output of hypermetabolic state; development of S3 may warn of impending cardiac failure.

6. Monitor ECG, noting rate and rhythm. Document dysrhythmias.
Rationale: Tachycardia greater than normally expected, with fever and increased circulatory demand, may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac function and output.

7. Auscultate breath sounds, noting adventitious sounds such as crackles.
Rationale: Early sign of pulmonary congestion, reflecting developing cardiac failure.

8. Monitor temperature, provide cool environment, limit bed linens and clothes, and administer tepid sponge baths.
Rationale: Fever, which may exceed 104°F (40.0°C), can occur as a resultof excessive hormone levels increasing diuresis and dehydration, causing increased peripheral vasodilation, venous pooling, and hypotension.

9. Observe for signs and symptoms of severe thirst, dry mucous membranes, weak and thready pulse, poor capillary refill, decreased urinary output, and hypotension.
Rationale: Rapid dehydration can occur, which reduces circulating volume and compromises cardiac output.

10. Record intake and output (I&O). Note urine specific gravity.
Rationale: Significant fluid losses through vomiting, diarrhea, diuresis, or diaphoresis can lead to profound dehydration, concentrated urine, and weight loss.

Nursing Care Plan Cardiac Surgery

Nursing diagnosis: risk for decreased Cardiac Output

Risk factors may include

Altered myocardial contractility secondary to temporary factors, such as ventricular wall surgery, recent MI, response to certain medications and drug interactions

Altered preload (hypovolemia) and afterload (systemic vascular resistance)

Altered heart rate or rhythm (dysrhythmias)

Possibly evidenced by

(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will

Tissue Perfusion: Cardiac

Display hemodynamic stability, such as stable blood pressure, cardiac output.

Report and display decreased episodes of angina and dysrhythmias.

Demonstrate an increase in activity tolerance.

Participate in activities that maximize and enhance cardiac function.

Nursing intervention with rationale:

1. Monitor and document trends in heart rate and BP, especially noting hypertension. Be aware of specific systolic and diastolic limits defined for client.

Rationale: Tachycardia is a common response to discomfort, inadequate blood or fluid replacement, and the stress of surgery. However, sustained tachycardia increases cardiac workload and can decrease effective cardiac output. Hypotension may result from fluid deficit, dysrhythmias, heart failure, and shock. Hypertension can occur (fluid excess or preexisting condition), placing stress on suture lines of new grafts and changing blood flow or pressure within heart chambers and across valves, with increased risk for various complications.

2. Monitor and document cardiac dysrhythmias. Observe client response to dysrhythmias, such as drop in BP, chest pain, and dyspnea.

Rationale: Life-threatening dysrhythmias can occur because of electrolyte imbalance, myocardial ischemia, or alterations in the heart’s electrical conduction. Atrial fibrillation and atrial flutter are the most common dysrhythmias occurring around the second or third day after CABG (older clients or presence of right coronary artery disease increases risk). Decreased cardiac output and hemodynamic compromise that occur with dysrhythmias require prompt intervention. Note: This is the most frequently occurring postoperative complication, often prolonging hospital stay.

3. Observe for bleeding from incisions and chest tube (if in place).

Rationale: Helps identify bleeding complications that can reduce circulating volume, organ perfusion, and cardiac function.

4. Observe for changes in usual mental status, orientation, and body movement or reflexes, such as onset of confusion, disorientation, restlessness, reduced response to stimuli, and stupor.

Rationale: May indicate decreased cerebral blood flow or oxygenation as a result of diminished cardiac output—sustained or severe dysrhythmias, low BP, heart failure, or thromboembolic phenomena.

5. Record skin temperature and color and quality and equality of peripheral pulses.

Rationale: Warm, pink skin and strong, equal pulses are general indicators of adequate cardiac output.

6. Measure and document intake and output (I&O) and calculate fluid balance.

Rationale: Useful in determining fluid needs or identifying fluid excesses, which can compromise cardiac output and oxygen consumption.

7. Schedule uninterrupted rest and sleep periods. Assist with self-care activities as needed.

Rationale: Prevents fatigue or exhaustion and excessive cardiovascular stress.

6. Monitor graded activity program. Note client response; vital signs before, during, and after activity; and development of dysrhythmias.

Rationale: Regular exercise stimulates circulation and promotes feeling of well-being. Progression of activity depends on cardiac tolerance.

7. Evaluate presence and degree of anxiety or emotional duress. Encourage the use of relaxation techniques such as deep breathing and diversional activities.

Rationale: Excessive or escalating emotional reactions can negatively affect vital signs and systemic vascular resistance, eventually affecting cardiac function.

8. Inspect for JVD, peripheral or dependent edema, congestion in lungs, shortness of breath, and change in mental status.

Rationale: May be indicative of acute or chronic heart failure.

9. Investigate reports of angina or severe chest pain accompanied by restlessness, diaphoresis, and ECG changes.

Rationale: Although not a common complication of CABG, perioperative or postoperative MI can occur.

10. Investigate and report profound hypotension and unresponsiveness to fluid challenge, tachycardia, distant heart sounds, and stupor or coma.

Rationale: Development of cardiac tamponade can rapidly progress to cardiac arrest because of the heart’s inability to fill adequately for effective cardiac output. Note: This is a relatively rare, life-threatening complication that usually occurs in the immediate postoperative period but can occur later in the recovery phase.

Nursing Diagnosis for Dysrhythmias | Decreased Cardiac Output

Nursing care plan | NCP Dysrhythmias

Risk factors may include

Altered electrical conduction

Reduced myocardial contractility

Possibly evidenced by

(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will

Cardiac Pump Effectiveness

Maintain or achieve adequate cardiac output as evidenced by BP and pulse within normal range, adequate urinary output, palpable pulses of equal quality, and usual level of mentation.

Display reduced frequency or absence of dysrhythmia(s).

Participate in activities that reduce myocardial workload.

Nursing care plan intervention with rationale:

1. Palpate radial, carotid, femoral, and dorsalis pedis pulses, noting rate, regularity, amplitude (full or thready), and symmetry. Document presence of pulsus alternans, bigeminal pulse, or pulse deficit.

Rationale:Differences in equality, rate, and regularity of pulses are indicative of the effect of altered cardiac output on systemic and peripheral circulation.

2. Auscultate heart sounds, noting rate, rhythm, presence of Specific dysrhythmias are more clearly detected audibly than by palpation.

Rationale: Specific dysrhythmias are more clearly detected audibly than by palpation. Hearing extra heartbeats or dropped beats helps identify dysrhythmias in the unmonitored client.

3. Monitor vital signs. Assess adequacy of cardiac output and tissue perfusion, noting significant variations in BP, pulse rate equality, respirations, changes in skin color and temperature, level of consciousness and sensorium, and urine output during episodes of dysrhythmias.

Rationale: Although not all dysrhythmias are life-threatening, immediate treatment may be required to terminate dysrhythmia in the presence of alterations in cardiac output and tissue perfusion.

4. Provide calm and quiet environment. Review reasons for limitation of activities during acute phase.

Rationale: Reduces stimulation and release of stress-related catecholamines, which can cause or aggravate dysrhythmias and vasoconstriction, increasing myocardial workload.

5. Demonstrate and encourage use of stress management behaviors such as relaxation techniques; guided imagery; and slow, deep breathing.

Rationale: Promotes client participation in exerting some sense of control in a stressful situation.

6. Investigate reports of chest pain, documenting location, duration, intensity (0 to 10 scale), and relieving or aggravating factors. Note nonverbal pain cues, such as facial grimacing, crying, changes in BP and heart rate.

Rationale: Reasons for chest pain are variable and depend on underlying cause. However, chest pain may indicate ischemia due to altered electrical conduction, decreased myocardial perfusion, or increased oxygen need, such as impending or evolving MI.

7. Be prepared to initiate cardiopulmonary resuscitation (CPR), as indicated.

Rationale: Development of life-threatening dysrhythmias requires prompt intervention to prevent ischemic damage or death.

Nursing Diagnosis for Myocardial Infarction | Decreased Cardiac Output

Nursing diagnosis: risk for decreased Cardiac Output.

Risk factors may include

Changes in rate, rhythm, electrical conduction

Reduced preload and increased systemic vascular resistance (SVR)

Infarcted or dyskinetic muscle, structural defects—ventricular aneurysm, septal defects

Possibly evidenced by

(Not applicable; presence of signs and symptoms establishes actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will

Cardiac Pump Effectiveness

Maintain hemodynamic stability, such as BP, cardiac output within normal range, adequate urinary output, decreased frequency or absence of dysrhythmias.

Report decreased episodes of dyspnea and angina.

Nursing intervention with rationale:

1. Obtain BP readings. Compare both arms and obtain lying, sitting, and standing pressures when able.

Rationale: Hypotension may occur related to ventricular dysfunction, hypoperfusion of the myocardium, and vagal stimulation. However, hypertension is also a common phenomenon, possibly related to pain, anxiety, catecholamine release, and preexisting vascular problems. Orthostatic (postural) hypotension may be associated with complications of infarct, such as heart failure.

2. Evaluate quality and equality of pulses, as indicated.

Rationale: Decreased cardiac output results in diminished, weak, or thready pulses. Irregularities suggest dysrhythmias, which may require further evaluation and monitoring.

3. Auscultate heart sounds: Note development of S3 and S.

Rationale: S3 is usually associated with heart failure, but it may also be noted with the mitral insufficiency (regurgitation) and left ventricular overload that can accompany severe infarction. S4 may be associated with myocardial ischemia, ventricular stiffening, and pulmonary or systemic hypertension.

4. Note presence of murmurs and rubs.

Rationale: Indicates disturbances of normal blood flow within the heart, such as incompetent valve, septal defect, or vibration of papillary muscle and chordae tendineae (complication of MI). Presence of rub with an infarction is also associated with inflammation, such as pericardial effusion and pericarditis.

5. Auscultate breath sounds.

Rationale: Crackles reflect pulmonary congestion; may develop because of depressed myocardial function.

6. Monitor heart rate and rhythm. Document dysrhythmias via telemetry.

Rationale: Heart rate and rhythm respond to medication, activity, and developing complications. Dysrhythmias, especially premature ventricular contractions or progressive heart blocks, can compromise cardiac function or increase ischemic damage. Acute or chronic atrial flutter or fibrillation may be seen with coronary artery or valvular involvement and may or may not be pathological.

7. Note response to activity and promote rest appropriately.

Rationale: Overexertion increases oxygen consumption and demand and can compromise myocardial function.

8. Provide small, easily digested meals. Limit caffeine intake, such as coffee, chocolate, and cola, as indicated.

Rationale: Large meals may increase myocardial workload and cause vagal stimulation, resulting in bradycardia or ectopic beats. Caffeine is a direct cardiac stimulant that can increase heart rate, but may not be a problem for everyone, such as for some clients with regular daily caffeine intake.

9. Have emergency equipment and medications available.

Rationale: Sudden coronary occlusion, lethal dysrhythmias, extension of infarct, and unrelenting pain are situations that may precipitate cardiac arrest, requiring immediate life-saving therapies or transfer to CCU.

Collaborative Management:

1. Administer supplemental oxygen, as indicated.

Rationale: Increases amount of oxygen available for myocardial uptake, reducing ischemia and resultant cellular irritation and dysrhythmias.

2. Measure cardiac output and other functional parameters as appropriate.

Rationale: Cardiac index, preload and afterload, contractility, and cardiac work can be measured noninvasively with thoracic electrical bioimpedance (TEB) technique. Useful in evaluating response to therapeutic interventions and identifying need for more aggressive or emergency care.

3. Maintain IV and saline-lock access, as indicated.

Rationale: Patent line is important for administration of emergency drugs in presence of persistent lethal dysrhythmias or chest pain.

4. Review serial ECGs.

Rationale: Provides information regarding progression or resolution of infarction, status of ventricular function, electrolyte balance, and effect of drug therapies.

5. Review chest x-ray.

Rationale: May reflect pulmonary edema related to ventricular dysfunction.

6. Monitor laboratory data, such as cardiac enzymes, arterial blood gases (ABGs), and electrolytes.

Rationale: Enzymes monitor resolution or extension of infarction. Presence of hypoxia indicates need for supplemental oxygen. Electrolyte imbalances, such as hypo- or hyperkalemia, adversely affect cardiac rhythm and contractility.

7. Administer medications, as indicated: Antidysrhythmic drugs.

Rationale: Dysrhythmias are usually treated symptomatically. Early inclusion of ACE inhibitor therapy, especially in presence of large anterior MI, ventricular aneurysm, or heart failure, enhances ventricular output, increases survival, and may slow progression of heart failure.

8. Antiemetics and stool softener

Rationale: Vomiting (vasovagal reflex) or bearing down to pass stool (Valsalva’s maneuver) can result in bradycardia, temporarily reducing cardiac output followed by rebound tachycardia.

9. Assist with insertion and maintain pacemaker or automatic internal cardiac defibrillator (AICD) when used.

Rationale: Pacing may be a temporary support measure during acute phase or may be needed permanently if infarction severely damages conduction system, impairing systolic function. Use of AICD is currently advocated in client who has had ventricular fibrillation or tachycardia resulting in arrest. Strong supporting data document the benefits of ICDs for the primary prevention of sudden cardiac death.

Nursing Diagnosis for Angina Pectoris | Decreased Cardiac Output

Nursing Diagnosis: Decreased cardiac output related to inotropic changes, such as transient or prolonged myocardial ischemia and effects of medications; alterations in rate, rhythm, and electrical conduction.

Possibly evidenced by

(Not applicable; presence of signs and symptoms establishes an actual diagnosis)

Desired Outcomes/Evaluation Criteria—Client Will

Cardiac Pump Effectiveness

Demonstrate increased activity tolerance.

Report or display decreased episodes of dyspnea, angina, and dysrhythmias.

Participate in behaviors and activities that reduce the workload of the heart.

Nursing care plan intervention with rationale:

1. Maintain bedrest or chair rest in position of comfort during acute episodes.

Rationale: Decreases oxygen consumption and demand, reducing myocardial workload and risk of decompensation.

2. Monitor vital signs and cardiac rhythm.

Rationale: Tachycardia and changes in blood pressure (hypotension or hypertension) may be present because of pain, anxiety, hypoxemia, and reduced cardiac output. ECG changes reflecting ischemia and dysrhythmias indicate need for additional evaluation and therapeutic intervention.

3. Auscultate breath sounds and heart sounds. Listen for murmurs.

Rationale: S3, S4, or crackles may occur with cardiac decompensation or some medications, especially beta blockers. Development of murmurs may reveal a valvular cause for chest pain,

such as aortic or mitral stenosis or papillary muscle rupture.

4. Provide for adequate rest periods. Assist with or perform self-care activities, as indicated.

Rationale: Conserves energy and reduces cardiac workload.

5. Stress importance of avoiding straining and bearing down, especially during defecation.

Rationale: Valsalva’s maneuver causes bradycardia, which may be followed by rebound tachycardia, both of which may impair cardiac output.

6. Encourage immediate reporting of pain for prompt administration of medications, as indicated.

Rationale: Timely interventions can reduce oxygen consumption and myocardial workload and may prevent or minimize cardiac complications.

7. Monitor for and document effects of and adverse response to medications, noting BP, heart rate, and rhythm (especially when giving combination of calcium antagonists, beta blockers, and nitrates).

Rationale: Desired effect is to decrease myocardial oxygen demand by decreasing ventricular stress. Drugs with negative inotropic properties can decrease perfusion to an already ischemic

myocardium. Combination of nitrates and beta blockers may have cumulative effect on cardiac output.

8. Assess for signs and symptoms of heart failure.

Rationale: Angina is only a symptom of underlying pathology causing myocardial ischemia. Disease may compromise cardiac function to point of decompensation.

9. Evaluate mental status, noting development of confusion and disorientation.

Rationale: Reduced perfusion of the brain can produce observable changes in sensorium.

10. Note skin color and presence and quality of pulses.

Rationale: Peripheral circulation is reduced when cardiac output falls, giving the skin a pale or gray color depending on level of hypoxia and diminishing the strength of peripheral pulses.

11. Assess lung for adventitious sounds, such as crackles.

Rationale: Respiratory system may become decompensated with anginal attack.

Collaborative Intervention:

1. Administer supplemental oxygen as needed.

Rationale: Increases oxygen available for myocardial uptake to improve contractility, reduce ischemia, and reduce lactic acid levels.

2. Monitor pulse oximetry or arterial blood gases (ABGs), as indicated.

Rationale: Oxygen saturation may decrease as oxygen demands increase for heart muscle and systemic circulation. Monitoring determines adequacy of respiratory function and O2 therapy.

3. Measure cardiac output and other functional parameters, as indicated.

Rationale: Cardiac index, preload and afterload, contractility, and cardiac work may be measured noninvasively through various means, including TEB technique, and is useful in evaluating response to therapeutic interventions and identifying need for more aggressive emergency care. Note: Evaluation of changes in heart rate, BP, and cardiac output requires consideration of client’s circadian hemodynamic variability. These measurements are normally expected to be lower at night in clients who are active during the day.

4. Administer medications, as indicated, for example: Calcium channel blockers, such as diltiazem (Cardizem), nifedipine (Procardia), verapamil (Calan), bepridil (Vascor), amlodipine (Norvasc), felodipine (Plendil), and isradipine (DynaCirc).

Rationale: Although differing in mode of action, calcium channel blockers play a major role in preventing and terminating ischemia induced by coronary artery spasm and in reducing vascular resistance, thereby decreasing BP and cardiac workload.

5. Beta blockers, such as atenolol (Tenormin), nadolol (Corgard), propranolol (Inderal), and esmolol (Brevibloc).

Rationale: These medications decrease cardiac workload by reducing heart rate and systolic BP. Note: Overdose produces cardiac decompensation.

6. Antiplatelets, such as aspirin (ASA), clopidogrel (Plavix), ticlopidine (Ticlid), tirofiban (Aggrastat), and eptifibatide (Integrilin).

Rationale: Aspirin is proven beneficial in primary and secondary prevention of coronary artery disease. For clients with major gastrointestinal intolerance, alternative drugs may be indicated. Newer antiplatelets, especially Plavix, are frequently used in conjunction with angioplasty and stent placement for relief of angina.

7. IV heparin.

Rationale: Bolus followed by continuous infusion is recommended to help reduce risk of subsequent MI by reducing the thrombotic complications of plaque rupture for clients diagnosed with intermediate or high-risk unstable angina. Note: Use of low-molecular-weight heparin is increasing because it is more efficacious and predictable and has fewer adverse effects, such as less risk of bleeding and longer half-life. It also does not require anticoagulation monitoring.

8. Monitor laboratory studies, such as PTT and aPTT.

Rationale: Evaluates anticoagulation therapy needs and effectiveness.

9. Discuss purpose and prepare for stress testing and cardiac catheterization when indicated.

Rationale: Stress testing provides information about the health or strength of the ventricles.

10. Prepare for surgical interventions such as angioplasty with or without intracoronary stent placement, valve replacement, and coronary artery bypass grafting (CABG), if indicated.

Rationale: Angioplasty, also called percutaneous transluminal coronary angioplasty (PTCA), increases coronary blood flow by compression of atheromatous lesions and dilation of the vessel lumen in an occluded coronary artery. Intracoronary stints may be placed at the time of PTCA to provide structural support within the coronary artery and improve the odds of long term patency. This procedure is preferred over the more invasive CABG surgery. Drug-coated stents may be considered for clients at high risk for thrombosis, acute closure, and for diabetics.

Several different drugs are available to help decrease restenosis after insertion of stents or

angioplasty. Stent placement may also be effective for the variant form of angina where periodic vasospasms impair arterial flow. Note: A recent innovation in thrombolytic therapy associated with angioplasty and use of stents is the Anjiojet (a device approved for removing blood clots from coronary arteries), which can reduce risk of heart attack or death. CABG is the recommended treatment when testing confirms myocardial ischemia due to left main coronary artery disease or symptomatic three-vessel disease, especially in those with left ventricular dysfunction.

11. Prepare for transfer to critical care unit if condition warrants.

Rationale: Profound or prolonged chest pain with decreased cardiac output reflects development of complications requiring more intense or emergency interventions.

Nursing Diagnosis for Heart Failure: Decreased Cardiac Output

Nursing Diagnosis: Decreased Cardiac Output related to altered myocardial contractility, inotropic changes, alterations in rate, rhythm, electrical conduction, structural changes, such as valvular defects and 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 and diaphoresis

Orthopnea, crackles, JVD, liver engorgement, edema

Chest pain

Desired Outcomes/Evaluation Criteria—Client Will

Cardiac Pump Effectiveness

Display vital signs within acceptable limits, dysrhythmias absent or controlled, and no symptoms of failure, for example,

hemodynamic parameters within acceptable limits and urinary output adequate.

Report decreased episodes of dyspnea and angina.

Cardiac Disease Self-Management

Participate in activities that reduce cardiac workload.

Nursing Care Plan Intervention with Rationale:

1. Auscultate apical pulse; assess heart rate, rhythm, and document dysrhythmia if telemetry available.

Rationale: 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 AF are common dysrhythmias associated with HF, although others may also occur. Note: Intractable ventricular dysrhythmias unresponsive

to medication suggest ventricular aneurysm.

2. Note heart sounds.

Rationale: 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 and stenosis.

3. Palpate peripheral pulses.

Rationale: 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 may be present.

4. Monitor BP.

Rationale: 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 or irreversible hypotension may occur. Note: Many clients with HF have consistently low systolic BP (80 to 100 mm Hg) due to their disease process and the medications they take, and most

tolerate these BPs without incident (Wingate, 2007).

5. Inspect skin for pallor and cyanosis.

Rationale: 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.

6. Monitor urine output, noting decreasing output and dark or concentrated urine.

Rationale: 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 client is recumbent.

7. Note changes in sensorium, for example, lethargy, confusion, disorientation, anxiety, and depression.

Rationale: May indicate inadequate cerebral perfusion secondary to decreased cardiac output.

8. Encourage rest, semirecumbent in bed or chair. Assist with physical care, as indicated.

Rationale: Physical rest should be maintained during acute or refractory HF to improve efficiency of cardiac contraction and to decrease myocardial oxygen consumption and workload.

9. Provide quiet environment, explain medical and nursing management, help client avoid stressful situations, listen and respond to expressions of feelings or fears.

Rationale: Physical and psychological rest helps reduce stress, which can produce vasoconstriction, elevating BP and increasing heart rate and work.

10. Provide bedside commode. Have client avoid activities eliciting a vasovagal response, for instance, straining during defecation and holding breath during position changes.

Rationale: 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 and output.

11. Elevate legs, avoiding pressure under knee. Encourage active and passive exercises. Increase ambulation and activity as tolerated.

Rationale: Decreases venous stasis and may reduce incidence of thrombus and embolus formation.

12. Check for calf tenderness; diminished pedal pulse; and swelling, local redness, or pallor of extremity.

Rationale: Reduced cardiac output, venous pooling and stasis, and enforced bedrest increases risk of thrombophlebitis.

13. Withhold digoxin, as indicated, and notify physician if marked changes occur in cardiac rate or rhythm or signs of digoxin toxicity occur.

Rationale: 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.

Risk for Impaired Gas Exchange

Excess Fluid Volume

Activity Intolerance

Risk for Chronic Pain