Pathophysiology of Hypertension
Although hypertension is usually treated in a community setting, management of stages III and IV with symptoms of complications/compromise may require inpatient care, especially when TOD is present. The majority of interventions included here can be used in either setting.
- Cerebrovascular accident/stroke
- Myocardial infarction
- Psychosocial aspects of care
- Renal failure: acute
- Renal failure: chronic
- Patient Assessment Database
May report :
- Weakness, fatigue, shortness of breath, sedentary lifestyle
- May exhibit:
- Elevated heart rate
- Change in heart rhythm
- Tachypnea; shortness of breath with exertion
History of intermittent or sustained elevation of diastolic or systolic blood pressure; presence of atherosclerotic, valvular, or coronary artery heart disease (including myocardial infarction [MI], angina, heart failure [HF]) and cerebrovascular disease (reflecting TOD)
Episodes of palpitations, diaphoresis
Elevated blood pressure (BP) (serial elevated measurements are necessary to confirm diagnosis) Note: Postural hypotension, when present, may be related to drug regimen or reflect dehydration or reduced ventricular function.
Bounding carotid, jugular, radial pulsations; pulse disparities, e.g., femoral delay as compared with radial or brachial pulsation; absence of/diminished popliteal, posterior tibial, pedal pulses
Point of maximal impulse (PMI) possibly displaced and/or forceful
Tachycardia, various dysrhythmias
Accentuated S2 at base; S3 (early HF); S4 (rigid left ventricle/left ventricular hypertrophy)
Murmurs of valvular stenosis
Vascular bruits audible over carotid, femoral, or epigastrium (artery stenosis); jugular venous distension (JVD) (venous congestion)
Discoloration of skin, cool temperature (peripheral vasoconstriction); capillary refill possibly slow/delayed (vasoconstriction)
Pallor, cyanosis, and diaphoresis (congestion, hypoxemia); flushing (pheochromocytoma)
History of personality changes, anxiety, depression, euphoria, or chronic anger (may cerebral impairment)
Multiple stress factors (relationship, financial, job-related)
Mood swings, restlessness, irritability, narrowed attention span, outbursts of crying
Emphatic hand gestures, tense facial muscles (particularly around the eyes), quick physical movement, expiratory sighs, accelerated speech pattern
Past or present renal insult (e.g., infection/obstruction or past history of kidney disease)
- Food preferences, which include high-salt, high-fat, high-cholesterol foods (e.g., fried foods, cheese, eggs); licorice; high caloric content; low dietary intake of potassium, calcium, and magnesium
- Nausea, vomiting
- Recent weight changes (gain/loss)
- Current/history of diuretic use
- Normal weight or obesity
- Presence of edema (may be generalized or dependent); venous congestion, JVD
- Glycosuria (almost 10% of hypertensive patients are diabetic, reflecting TOD)
- Fainting spells/dizziness
- Throbbing, suboccipital headaches (present on awakening and disappearing spontaneously after several hours)
- Episodes of numbness and/or weakness on one side of the body, brief periods of confusion or difficulty with speech (transient ischemic attack [TIA]); or history of cerebrovascular accident (CVA)
- Visual disturbances (diplopia, blurred vision)
- Episodes of epistaxis
- Mental status: changes in alertness, orientation, speech pattern/content, affect, thought process, or memory
- Motor responses: decreased strength, hand grip, and/or deep tendon reflexes
- Optic retinal changes: from mild sclerosis/arterial narrowing to marked retinal and sclerotic changes with edema or papilledema, exudates, hemorrhages, and arterial nicking, dependent on severity/duration of hypertension (TOD)
- Angina (coronary artery disease/cardiac involvement)
- Intermittent pain in legs/claudication (indicative of arteriosclerosis of lower extremity arteries)
- Severe occipital headaches as previously noted
- Abdominal pain/masses (pheochromocytoma)
(Generally associated with advanced cardiopulmonary effects of sustained/severe hypertension)
- Dyspnea associated with activity/exertion
- Tachypnea, orthopnea, paroxysmal nocturnal dyspnea
- Cough with/without sputum production
- Smoking history (major risk factor)
- Respiratory distress/use of accessory muscles
- Adventitious breath sounds (crackles/wheezes)
- Pallor or cyanosis
- Impaired coordination/gait
- Transient episodes of numbness, unilateral paresthesias
- Light-headedness with position changes
- Postmenopausal (major risk factor)
- Erectile dysfunction (medication related)
- Familial risk factors: hypertension, atherosclerosis, heart disease, diabetes mellitus, cerebrovascular/kidney disease
- Ethnic/racial risk factors, e.g., more prevalent in African-American and Southeast Asian populations
- Use of birth control pills or other hormones; drug/alcohol use
Discharge plan considerations:
- DRG projected mean length of inpatient stay: 3.5 days
- Assistance with self-monitoring of BP
- Periodic evaluation of and alterations in medication therapy
- Refer to section at end of plan for postdischarge considerations.
- 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 plaquing.
- 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.