Hypertension is the term used to describe high blood pressure. Hypertension is repeatedly elevated blood pressure exceeding 140 over 90 mmHg. It is categorized as primary or essential (approximately 90% of all cases) or secondary, which occurs as a result of an identifiable, sometimes correctable pathological condition, such as renal disease or primary aldosteronism.
Here are 6 hypertension nursing care plans.
- Hemoglobin/hematocrit: Not diagnostic but assesses relationship of cells to fluid volume (viscosity) and may indicate risk factors such as hypercoagulability, anemia.
- Blood urea nitrogen (BUN)/creatinine: Provides information about renal perfusion/function.
- Glucose: Hyperglycemia (diabetes mellitus is a precipitator of hypertension) may result from elevated catecholamine levels (increases hypertension).
- Serum potassium: Hypokalemia may indicate the presence of primary aldosteronism (cause) or be a side effect of diuretic therapy.
- Serum calcium: Imbalance may contribute to hypertension.
- Lipid panel (total lipids, high-density lipoprotein [HDL], low-density lipoprotein [LDL], cholesterol, triglycerides, phospholipids): Elevated level may indicate predisposition for/presence of atheromatous plaques.
- Thyroid studies: Hyperthyroidism may lead or contribute to vasoconstriction and hypertension.
- Serum/urine aldosterone level: May be done to assess for primary aldosteronism (cause).
- Urinalysis: May show blood, protein, or white blood cells; or glucose suggests renal dysfunction and/or presence of diabetes.
- Creatinine clearance: May be reduced, reflecting renal damage.
- Urine vanillylmandelic acid (VMA) (catecholamine metabolite): Elevation may indicate presence of pheochromocytoma (cause); 24-hour urine VMA may be done for assessment of pheochromocytoma if hypertension is intermittent.
- Uric acid: Hyperuricemia has been implicated as a risk factor for the development of hypertension.
- Renin: Elevated in renovascular and malignant hypertension, salt-wasting disorders.
- Urine steroids: Elevation may indicate hyperadrenalism, pheochromocytoma, pituitary dysfunction, Cushing’s syndrome.
- Intravenous pyelogram (IVP): May identify cause of secondary hypertension, e.g., renal parenchymal disease, renal/ureteral calculi.
- Kidney and renography nuclear scan: Evaluates renal status (TOD).
- Excretory urography: May reveal renal atrophy, indicating chronic renal disease.
- Chest x-ray: May demonstrate obstructing calcification in valve areas; deposits in and/or notching of aorta; cardiac enlargement.
- Computed tomography (CT) scan: Assesses for cerebral tumor, CVA, or encephalopathy or to rule out pheochromocytoma.
- Electrocardiogram (ECG): May demonstrate enlarged heart, strain patterns, conduction disturbances. Note: Broad, notched P wave is one of the earliest signs of hypertensive heart disease.
- Maintain/enhance cardiovascular functioning.
- Prevent complications.
- Provide information about disease process/prognosis and treatment regimen.
- Support active patient control of condition.
- BP within acceptable limits for individual.
- Cardiovascular and systemic complications prevented/minimized.
- Disease process/prognosis and therapeutic regimen understood.
- Necessary lifestyle/behavioral changes initiated.
- Plan in place to meet needs after discharge.
1. Decreased Cardiac Output
- Cardiac Output, risk for decreased
Risk factors may include
- Increased vascular resistance, vasoconstriction
- Myocardial ischemia
- Ventricular hypertrophy/rigidity
Possibly evidenced by
- Not applicable. Existence of signs and symptoms establishes an actual nursing diagnosis.
- Participate in activities that reduce BP/cardiac workload.
- Maintain BP within individually acceptable range.
- Demonstrate stable cardiac rhythm and rate within patient’s normal range.
- Participate in activities that will prevent stress (stress management, balanced activities and rest plan).
|Review clients at risk as noted in Related Factors as well as individuals with conditions that stress the heart.||Persons with acute or chronic conditions may compromise circulation and place excessive demands on the heart.|
|Check laboratory data (cardiac markers, complete blood ell count, electrolytes, ABGs, blood urea nitrogen and creatinine, cardiac enzymes, and cultures, such as blood, wound or secretions).||To identify contributing factors|
|Monitor and record BP. Measure in both arms and thighs three times, 3–5 min apart while patient is at rest, then sitting, then standing for initial evaluation. Use correct cuff size and accurate technique.||Comparison of pressures provides a more complete picture of vascular involvement or scope of problem. Severe hypertension is classified in the adult as a diastolic pressure elevation to 110 mmHg; progressive diastolic readings above 120 mmHg are considered first accelerated, then malignant (very severe). Systolic hypertension also is an established risk factor for cerebrovascular disease and ischemic heart disease, when diastolic pressure is elevated.|
|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.|
|Auscultate heart tones and breath sounds.||S4 heart sound is common in severely hypertensive patients because of the presence of atrial hypertrophy (increased atrial volume and pressure). Development of S3 indicates ventricular hypertrophy and impaired functioning. Presence of crackles, wheezes may indicate pulmonary congestion secondary to developing or chronic heart failure.|
|Observe skin color, moisture, temperature, and capillary refill time.||Presence of pallor; cool, moist skin; and delayed capillary refill time may be due to peripheral vasoconstriction or reflect cardiac decompensation and decreased output.|
|Note dependent and general edema.||May indicate heart failure, renal or vascular impairment.|
|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.|
|Provide calm, restful surroundings, minimize environmental activity and noise. Limit the number of visitors and length of stay.||Helps lessen sympathetic stimulation; promotes relaxation.|
|Maintain activity restrictions (bedrest or chair rest); schedule periods of uninterrupted rest; assist patient with self-care activities as needed.||Lessens physical stress and tension that affect blood pressure and the course of hypertension.|
|Provide comfort measures (back and neck massage, elevation of head).||Decreases discomfort and may reduce sympathetic stimulation.|
|Instruct in relaxation techniques, guided imagery, distractions.||Can reduce stressful stimuli, produce calming effect, thereby reducing BP.|
|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 as well 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.|
|Administer medications as indicated:|
|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.|
|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.|
|Potassium-sparing diuretics: spironolactone (Aldactone); triamterene (Dyrenium); amiloride (Midamor);||May be given in combination with a thiazide diuretic to minimize potassium loss.|
|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).|
|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.|
|Adrenergic neuron blockers: guanadrel (Hylorel); guanethidine (Ismelin); reserpine (Serpalan);||Reduce arterial and venous constriction activity at the sympathetic nerve endings.|
|Direct-acting oral vasodilators: hydralazine (Apresoline); minoxidil (Loniten);||Action is to relax vascular smooth muscle, thereby reducing vascular resistance.|
|Direct-acting parenteral vasodilators: diazoxide (Hyperstat), nitroprusside (Nitropress); labetalol (Normodyne);||These are given intravenously for management of hypertensive emergencies.|
|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.|
|Implement dietary sodium, fat, and cholesterol restrictions as indicated.||These restrictions can help manage fluid retention and, with associated hypertensive response, decrease myocardial workload.|
|Prepare for surgery when indicated.||When hypertension is due to pheochromocytoma, removal of the tumor will correct condition.|