6 Hypertension Nursing Care Plans

Risk for Decreased Cardiac Output

Blood pressure is the product of cardiac output multiplied by peripheral resistance. Hypertension can result from an increase in cardiac output (heart rate multiplied by stroke volume), an increase in peripheral resistance, or both.

Nursing Diagnosis

• Risk for Decreased Cardiac Output
• Other possible nursing diagnoses include:
  • Risk for Impaired Cardiovascular Function
  • Decreased Cardiac Output
  • Risk for Decreased Cardiac Tissue Perfusion

Risk factors may include

The following are the common related factors for the nursing diagnosis risk for decreased cardiac output secondary to hypertension:

• Increased vascular resistance, vasoconstriction
• Myocardial ischemia
• Myocardial damage
• Ventricular hypertrophy/rigidity

Possibly evidenced by

• Not applicable. Existence of signs and symptoms establishes an actual nursing diagnosis.

Goals and desired outcomes

Below are the common expected outcomes for decreased cardiac output secondary to hypertension:

• Patient will participate in activities that reduce BP/cardiac workload.
• Patient will maintain BP within individually acceptable range.
• Patient will demonstrate stable cardiac rhythm and rate within patient’s normal range.
• Patient will participate in activities that will prevent stress (stress management, balanced activities and rest plan).

Nursing Assessment and Rationale

Here are the nursing assessments for the nursing diagnosis risk for decreased cardiac output secondary to hypertension.

1. Review clients at risk as noted in Related Factors and individuals with conditions that stress the heart.
Persons with acute or chronic conditions may compromise circulation and place excessive demands on the heart.

2. Check laboratory data (cardiac markers, complete blood cell count, electrolytes, ABGs, blood urea nitrogen and creatinine, cardiac enzymes, and cultures, such as blood, wound, or secretions).
To identify contributing factors.

3. Monitor and record BP. Measure in both arms and thighs three times, 3–5 min apart while the patient is at rest, then sitting, then standing for initial evaluation. Use correct cuff size and accurate technique. Comparison of pressures provides a complete picture of vascular involvement or the scope of the problem. Severe hypertension is classified in adults as a diastolic pressure elevation of 110 mmHg; progressive diastolic readings above 120 mmHg are considered first accelerated, then malignant (very severe). Systolic hypertension is also an established risk factor for cerebrovascular disease and ischemic heart disease when elevated diastolic pressure. See updated guidelines for classifying hypertension above. 

4. Note presence, quality of central and peripheral pulses.
Bounding carotid, jugular, radial, and femoral pulses may be observed and palpated. Pulses in the legs and feet may be diminished, reflecting effects of vasoconstriction (increased systemic vascular resistance [SVR]) and venous congestion.

5. Auscultate heart tones and breath sounds.
S₄ heart sound is common in severely hypertensive patients because of atrial hypertrophy (increased atrial volume and pressure). Development of S₃ indicates ventricular hypertrophy and impaired functioning. The presence of crackles, wheezes may indicate pulmonary congestion secondary to developing or chronic heart failure.

6. Observe skin color, moisture, temperature, and capillary refill time.
The presence of pallor; cool, moist skin; and delayed capillary refill time may be due to peripheral vasoconstriction or reflect cardiac decompensation and decreased output.

7. Note dependent and general edema.
May indicate heart failure, renal or vascular impairment.

8. Evaluate client reports or evidence of extreme fatigue, intolerance for activity, sudden or progressive weight gain, swelling of extremities, and progressive shortness of breath.
To assess for signs of poor ventricular function or impending cardiac failure.

Nursing Interventions and Rationales

Here are the therapeutic nursing interventions for the nursing diagnosis risk for decreased cardiac output secondary to hypertension.

1. Provide calm, restful surroundings, minimize environmental activity and noise. Limit the number of visitors and length of stay.
It helps lessen sympathetic stimulation; promotes relaxation.

2. Maintain activity restrictions (bedrest or chair rest); schedule uninterrupted rest periods; assist patient with self-care activities as needed.
Lessens physical stress and tension that affect blood pressure and the course of hypertension.

3. Provide comfort measures (back and neck massage, the elevation of head).
Decreases discomfort and may reduce sympathetic stimulation.

4. Instruct in relaxation techniques, guided imagery, distractions.
Can reduce stressful stimuli, produce a calming effect, thereby reducing BP.

5. Monitor response to medications to control blood pressure.
Response to drug therapy (usually consisting of several drugs, including diuretics, angiotensin-converting enzyme [ACE] inhibitors, vascular smooth muscle relaxants, beta and calcium channel blockers) is dependent on both the individual and as the synergistic effects of the drugs. Because of side effects, drug interactions, and patient’s motivation for taking antihypertensive medication, it is important to use the smallest number and lowest dosage of medications.

6. Administer medications as indicated:

• 6.1. Thiazide diuretics: chlorothiazide (Diuril); hydrochlorothiazide (Esidrix/HydroDIURIL); bendroflumethiazide (Naturetin); indapamide (Lozol); metolazone (Diulo); quinethazone (Hydromox).
  Diuretics are considered first-line medications for uncomplicated stage I or II hypertension and may be used alone or in association with other drugs (such as beta-blockers) to reduce BP in patients with relatively normal renal function. These diuretics potentiate the effects of other antihypertensive agents as well, by limiting fluid retention, and may reduce the incidence of strokes and heart failure.
• 6.2. Loop diuretics: furosemide (Lasix); ethacrynic acid (Edecrin); bumetanide (Bumex), torsemide (Demadex).
  These drugs produce marked diuresis by inhibiting resorption of sodium and chloride and are effective antihypertensives, especially in patients who are resistant to thiazides or have renal impairment.
• 6.3. Potassium-sparing diuretics: spironolactone (Aldactone); triamterene (Dyrenium); amiloride (Midamor).
  May be given in combination with a thiazide diuretic to minimize potassium loss.
• 6.4. Alpha, beta, or centrally acting adrenergic antagonists: doxazosin (Cardura); propranolol (Inderal); acebutolol (Sectral); metoprolol (Lopressor), labetalol (Normodyne); atenolol (Tenormin); nadolol (Corgard), carvedilol (Coreg); methyldopa (Aldomet); clonidine (Catapres); prazosin (Minipress); terazosin (Hytrin); pindolol (Visken).
  Beta-Blockers may be ordered instead of diuretics for patients with ischemic heart disease; obese patients with cardiogenic hypertension; and patients with concurrent supraventricular arrhythmias, angina, or hypertensive cardiomyopathy. Specific actions of these drugs vary, but they generally reduce BP through the combined effect of decreased total peripheral resistance, reduced cardiac output, inhibited sympathetic activity, and suppression of renin release. Note: Patients with diabetes should use Corgard and Visken with caution because they can prolong and mask the hypoglycemic effects of insulin. The elderly may require smaller doses because of the potential for bradycardia and hypotension. African-American patients tend to be less responsive to beta-blockers in general and may require increased dosage or use of another drug (monotherapy with a diuretic).
• 6.5. Calcium channel antagonists: nifedipine (Procardia); verapamil (Calan); diltiazem (Cardizem); amlodipine (Norvasc); isradipine (DynaCirc); nicardipine (Cardene).
  May be necessary to treat severe hypertension when a combination of a diuretic and a sympathetic inhibitor does not sufficiently control BP. Vasodilation of healthy cardiac vasculature and increased coronary blood flow are secondary benefits of vasodilator therapy.
• 6.6. Adrenergic neuron blockers: guanadrel (Hylorel); guanethidine (Ismelin); reserpine (Serpalan).
  Reduce arterial and venous constriction activity at the sympathetic nerve endings.
• 6.7. Direct-acting oral vasodilators: hydralazine (Apresoline); minoxidil (Loniten).
  Action is to relax vascular smooth muscle, thereby reducing vascular resistance.
• 6.8. Direct-acting parenteral vasodilators: diazoxide (Hyperstat), nitroprusside (Nitropress); labetalol (Normodyne).
  These are given intravenously for management of hypertensive emergencies.
• 6.9. Angiotensin-converting enzyme (ACE) inhibitors: captopril (Capoten); enalapril (Vasotec); lisinopril (Zestril); fosinopril (Monopril); ramipril (Altace). Angiotensin II blockers: valsartan (Diovan), guanethidine (Ismelin).
  The use of an additional sympathetic inhibitor may be required for its cumulative effect when other measures have failed to control BP or when congestive heart failure (CHF) or diabetes is present.

7. Implement dietary sodium, fat, and cholesterol restrictions as indicated.
These restrictions can help manage fluid retention and, with the associated hypertensive response, decrease myocardial workload.

8. Prepare for surgery when indicated.
When hypertension is due to pheochromocytoma, removal of the tumor will correct the condition.