Question

Patient chart reads.

Patient is a 65-year-old male weighing 65 kg recovering stroke patient.

Past Health history (+) Hypertension since 2000 (+) CAD since 2015 (+) history of asthma (-) DM

Home Medications:

Aspirin 80 mg/tab 1 tab once a day

Atorvastatin 80 mg/tab 1 tab at bedtime

Budesonide/Formoterol (Symbicort) 160/4.5 mcg 1 puff twice a day Digoxin 0.5 mcg/tab 1 tab once a day

Metoprolol 25 mg/tab 1 tab twice a day

Furosemide 20 mg/tab twice a day

Lactulose 30 ml at once a day, hold if BM >2/day

He was brought to the local community hospital due to difficulty of breathing and expiratory wheezes; diagnostic exams show Chest X-ray is clear and CBC shows platelet count= 145,000 and WBC= 5.0. Blood chemistry further shows SGPT=80 and CBG= 160 mg/dL. Additional orders were made as follows:

Salbutamol nebulization, 1 nebule every 8 hours Prednisone 40mg/tab twice a day

Esomeprazole 40mg once a day Monitor CBG every 4 hours

Start Regular Insulin using the following sliding scale: <180= none 181-200= 2 units/SC 201-220= 4 units/SC 221-240= 6 units/SC 241-260= 8 units/SC >280=refer

Develop a nursing care plan for Decreased cardiac output due to Insufficiency of the heart to pump blood in order to meet metabolic demands related to increased blood pressure

Answer 1

Nursing Assessment

Assessment is required in order to distinguish possible problems that may have lead to Decreased Cardiac Output as well as name any episode that may happen during nursing care.

Assessment	Rationales
Note skin color, temperature, and moisture.	Cold, clammy, and pale skin is secondary to compensatory increase in sympathetic nervous system stimulation and low cardiac output and oxygen desaturation.
Check for any alterations in level of consciousness.	Decreased cerebral perfusion and hypoxia are reflected in irritability, restlessness, and difficulty concentrating. Aged patients are particularly susceptible to reduced perfusion.
Assess heart rate and blood pressure.	Most patients have compensatory tachycardia and significantly low blood pressure in response to reduced cardiac output.
Check for peripheral pulses, including capillary refill.	Weak pulses are present in reduced stroke volume and cardiac output. Capillary refill is sometimes slow or absent.
Inspect fluid balance and weight gain. Weigh patient regularly prior to breakfast. Check for pedal and sacral edema.	Compromised regulatory mechanisms may result in fluid and sodium retention. Body weight is a more sensitive indicator of fluid or sodium retention than intake and output.
Assess heart sounds for gallops (S3, S4).	S3 indicates reduced left ventricular ejection and is a class sign of left ventricular failure. S4 occurs with reduced compliance of the left ventricle, which impairs diastolic filling.
Note respiratory rate, rhythm, and breath sounds. Identify any presence of paroxysmal nocturnal dyspnea (PND) or orthopnea.	Shallow, rapid respirations are characteristics of decreased cardiac output. Crackles indicate fluid buildup secondary to impaired left ventricular emptying.
Assess beta-type natriuretic peptide (BNP).	BNP is elevated with increasing filling pressure and volume in left ventricle. It aids in differentiating cardiac from noncardiac cause of dyspnea.
If hemodynamic monitoring is in place, assess CVP, pulmonary artery diastolic pressure (PADP), pulmonary capillary wedge pressure (PCWP), as well as cardiac output and cardiac index.	CVP provides information on filling pressures of the right side of the heart; PADP and PCWP reflect left-sided fluid volumes. Cardiac output provides an objective number to guide therapy.
Assess oxygen saturation with pulse oximetry both at rest and during and after ambulation.	An alteration in oxygen saturation is one of the earliest signs of reduced cardiac output. Hypoxemia is common, especially with activity.
Check symptoms for chest pain.	Low cardiac output can further decrease myocardial perfusion, resulting in chest pain.
Assess for reports of fatigue and reduced activity tolerance.	Fatigue and exertional dyspnea are common problems with low cardiac output states. Close monitoring of the patient’s response serves as a guide for optimal progression of activity.
Monitor electrocardiogram (ECG) for rate, rhythm, and ectopy.	Cardiac dysrhythmias may occur from low perfusion, acidosis, or hypoxia. Tachycardia, bradycardia, and ectopic beats can further compromise cardiac output. Older patients are especially sensitive to the loss of atrial kick in atrial fibrillation.
Ascertain contributing factors so an appropriate care plan can be initiated.	Specific causes guide treatment.
Assess patient for understanding and compliance with medical regimen, including medications, activity level, and diet.	This promotes cooperation of patient in his or her own medical situation.
Identify emergency plan, including use of CPR.	Decreased cardiac output can be life threatening.

Nursing Interventions

The following are the therapeutic nursing interventions for Decreased Cardiac Output which you can use for writing your nursing care plans (NCP):

Interventions	Rationales
Record intake and output. If patient is acutely ill, measure hourly urine output and note decreases in output.	Reduced cardiac output results in reduced perfusion of the kidneys, with a resulting decrease in urine output.
For patients with increased preload, limit fluids and sodium as ordered.	Fluid restriction decreases extracellular fluid volume and reduces demands on the heart.
Closely monitor fluid intake including IV lines. Maintain fluid restriction if ordered.	In patients with decreased cardiac output, poorly functioning ventricles may not tolerate increased fluid volumes.
Auscultate heart sounds; note rate, rhythm, presence of S3, S4, and lung sounds.	The new onset of a gallop rhythm, tachycardia, and fine crackles in lung bases can indicate onset of heart failure. If patient develops pulmonary edema, there will be coarse crackles on inspiration and severe dyspnea.
Closely monitor for symptoms of heart failure and decreased cardiac output, including diminished quality of peripheral pulses, cold and clammy skin and extremities, increased respiratory rate, presence of paroxysmal nocturnal dyspnea or orthopnea, increased heart rate, neck vein distention, decreased level of consciousness, and presence of edema.	As these symptoms of heart failure progress, cardiac output declines.
Note chest pain. Identify location, radiation, severity, quality, duration, associated manifestations such as nausea, and precipitating and relieving factors.	Chest pain/discomfort is generally suggestive of an inadequate blood supply to the heart, which can compromise cardiac output. Patients with heart failure can continue to have chest pain with angina or can reinfarct.
If chest pain is present, have patient lie down, monitor cardiac rhythm, give oxygen, run a strip, medicate for pain, and notify the physician.	These actions can increase oxygen delivery to the coronary arteries and improve patient prognosis.
Place on cardiac monitor; monitor for dysrhythmias, especially atrial fibrillation.	Atrial fibrillation is common in heart failure.
Examine laboratory data, especially arterial blood gases and electrolytes, including potassium.	Patient may be receiving cardiac glycosides and the potential for toxicity is greater with hypokalemia; hypokalemia is common in heart patients because of diuretic use.
Monitor laboratory tests such as complete blood count, sodium level, and serum creatinine.	Routine blood work can provide insight into the etiology of heart failure and extent of decompensation. A low serum sodium level often is observed with advanced heart failure and can be a poor prognostic sign. Serum creatinine levels will elevate in patients with severe heart failure because of decreased perfusion to the kidneys. Creatinine may also elevate because of ACE inhibitors.
Administer medications as prescribed, noting side effects and toxicity.	Depending on etiological factors, common medications include digitalis therapy, diuretics, vasodilator therapy, antidysrhythmics, angiotensin-converting enzyme inhibitors, and inotropic agents.
Review results of EKG and chest Xray.	EKG can reveal previous MI, or evidence of left ventricular hypertrophy, indicating aortic stenosis or chronic systemic hypertension. Xray may provide information on pulmonary edema, pleural effusions, or enlarged cardiac silhouette found in dilated cardiomyopathy or large pericardial effusion.
Maintain adequate ventilation and perfusion as in the following:
Position patient in semi-Fowler’s to high-Fowler’s.	Upright position is recommended to reduce preload and ventricular filling when fluid overload is the cause.
Place patient in supine position	For hypovolemia, supine positioning increases venous return and promotes diuresis.
Administer oxygen therapy as prescribed.	The failing heart may not be able to respond to increased oxygen demands. Oxygen saturation need to be greater than 90%.
During acute events, ensure patient remains on bed rest or maintains activity level that does not compromise cardiac output.	In severe heart failure, restriction of activity often facilitates temporary recompensation.
Monitor blood pressure, pulse, and condition before administering cardiac medications such as angiotensin converting enzyme (ACE) inhibitors, digoxin, and beta-blockers such as carvedilol. Notify physician if heart rate or blood pressure is low before holding medications.	It is necessary for the nurse to assess how well the patient is tolerating current medications before administering cardiac medications; do not hold medications without physician input. The physician may decide to have medications administered even though the blood pressure or pulse rate has lowered.
Monitor bowel function. Provide stool softeners as ordered. Tell patient to avoid straining when defecating.	Decreased activity can cause constipation. Straining when defecating that results in the Valsalva maneuver can lead to dysrhythmia, decreased cardiac function, and sometimes death.
Advise patient to use a commode or urinal for toileting and avoid use of a bedpan.	Getting out of bed to use a commode or urinal does not stress the heart any more than staying in bed to toilet. In addition, getting the patient out of bed minimizes complications of immobility and is often preferred by the patient.
Apply music therapy to decrease anxiety and improve cardiac function.	Music has been shown to reduce heart rate, blood pressure, anxiety, and cardiac complications.
Associate patient to heart failure program or cardiac rehabilitation program for education, evaluation, and guided support to increase activity and rebuild life.	A thoroughly monitored exercise program can improve both functional capacity, and left ventricular function.
Educate family and patient about the disease process, complications of disease process, information on medications, need for weighing daily, and when it is appropriate to call doctor.	Early recognition of symptoms facilitates early problem solving and prompt treatment.
Aid family adapt daily living patterns to establish life changes that will maintain improved cardiac functioning in the patient.	Transition to the home setting can cause risk factors such as inappropriate diet to reemerge.
Explain importance of smoking cessation and avoidance of alcohol intake.	Smoking cessation advice and counsel given by nurses can be effective, and should be available to patients to help stop smoking.
Educate patient the need for and how to incorporate lifestyle changes.	Psychoeducational programs including information on stress management and health education have been shown to reduce long term mortality and recurrence of myocardial infarction in heart patients.