The goal of this article is to provide nurses with information regarding hypertension and its management, with the main emphasis on nursing management.
Hypertension is the most common primary diagnosis in the United States. It is one of the most common diseases worldwide that affects humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is a major public health challenge.
Hypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or more, or a diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication.
General classification of BP: This classification is based on the average of two or more accurate blood pressure measurements taken during two or more contacts with a health care provider.
|CLASSIFICATION OF HYPERTENSION|
|Category||SBP (mm Hg)||DBP (mm Hg)
|Normal||less than 120||and less than 80
|Hypertension, stage 1||140-159||or 90-99|
|Hypertension, stage 2||≥160||or ≥100|
|Isolated systolic hypertension||≥140||and|
Source: Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), retrieved from www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf.
But in the new guidelines by ACC/AHA (2017), the category of prehypertension is eliminated and the patients are categorized as having either Elevated (120-129 and less than 80) or Stage I hypertension (130-139 or 80-89).
While in the previous guidelines 140/90 mm Hg was classified as Stage 1 hypertension, this level is classified as Stage 2 hypertension under the new guidelines.
|NEW CLASSIFICATION OF HYPERTENSION (2017 GUIDELINES)|
|Category||SBP (mm Hg)||DBP (mm Hg)
|Normal||less than 120||and less than 80|
|Elevated||120-129||and less than 80|
|Hypertension, stage 1||130-139||or 80-89|
|Hypertension, stage 2||≥140||or ≥90|
|Hypertensive crisis||≥180||and /or|
Classification based on etiology:
- Primary Hypertension: Primary (essential or idiopathic) hypertension is elevated BP without an identified cause (accounts for 90% to 95% of all cases of hypertension).
- Secondary Hypertension: Secondary hypertension is elevated BP with a specific cause that often can be identified and corrected (accounts for 2-10% of cases).
- Pregnancy induced: (over 15 mm Hg above normal pressure during the first trimester) precursor to toxemia.
White coat type: hypertension in individuals who have normal blood pressures except at clinical visits.
Hypertensive crises: BP of more than 180/120 mm Hg. Further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by evidence of impending or progressive target organ dysfunction. Hypertensive urgencies are those situations without progressive target organ dysfunction.
In hypertensive emergencies, the BP should be aggressively lowered within an hour by no more than 25%, and then lowered to 160/100-110 mm Hg within the next 2-6 hours. Acute end-organ damage that may occur in the setting of a hypertensive emergency includes the following:
- Neurologic: hypertensive encephalopathy, cerebral vascular accident, subarachnoid hemorrhage, intracranial hemorrhage
- Cardiovascular: myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, aortic dissection, unstable angina pectoris
Other: acute renal failure, retinopathy, eclampsia, microangiopathic hemolytic anemia
- Hypertension is a worldwide epidemic. According to the American Heart Association, approximately 86 million adults (34%) in the United States are affected by hypertension.
- Data from the Centers for Disease Control and Prevention’s (CDC) National Center for Health Statistics (NCHS)-2017 shows that 30% of adults have prehypertension, and approximately 8% have undiagnosed hypertension.
- Globally, around 972 million people (26% of the world’s population) has hypertension, and the prevalence is expected to increase to 29% by 2025.
- Gender differences:
- Before age 45, hypertension is more common in men than in women.
- From age 45 to 64 years, the percentages are nearly equal between men and women.
- Hypertension is more common in women than in men after the age of 64, (attributed to menopause-related factors such as estrogen withdrawal, overproduction of pituitary hormones, and weight gain).
Race: primarily among blacks; twice the incidence of whites.
Etiology and Pathophysiology
Primary hypertension: exact cause is unknown (may develop as a result of environmental or genetic causes). There are several contributing factors. These include:
- Increased activity of the sympathetic nervous and renin-angiotensin-aldosterone systems (RAAS)
- Overproduction of sodium-retaining hormones and vasoconstricting substances
- Increased sodium intake
- Diabetes mellitus
- Tobacco use
- Excessive alcohol consumption.
Secondary hypertension: has multiple etiologies.
- Renal disease (e.g., renal artery stenosis, glomerulonephritis, Polycystic kidney disease)
- Endocrine disorders (e.g., Cushing syndrome, thyroid disease, pheochromocytoma)
- Neurologic disorders (e.g., traumatic brain injury, brain tumors, quadriplegia)
- Coarctation or congenital narrowing of the aorta
- Pregnancy-induced hypertension
- Sleep apnea
- Drug-related: oral contraceptives, corticosteroids, nonsteroidal antiinflammatory drugs (e.g., cyclooxygenase-2 inhibitors), sympathetic stimulants (e.g., cocaine, monoamine oxidase)
Pathophysiology of Primary Hypertension
Abnormalities in any of the mechanisms involved in the maintenance of normal blood pressure can cause hypertension. Blood pressure is the product of cardiac output multiplied by systemic vascular resistance. Hypertension can result from increases in cardiac output, increases in systemic vascular resistance (constriction of the blood vessels), or both.
Pathophysiological mechanisms involved includes:
- Increased Sympathetic Nervous System Activity
- Alteration in Renin-Angiotensin-Aldosterone mechanism
- Sodium and water retention
- Insulin Resistance and Hyperinsulinemia
- Endothelium Dysfunction
Increased Sympathetic Nervous System Activity: Increased Sympathetic Nervous System stimulation produces vasoconstriction, increased HR, and increased renin release. Increased rennin activates the RAAS, leading to elevated BP.
Altered Renin-Angiotensin-Aldosterone Mechanism: High plasma renin activity (PRA) results in the increased conversion of angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II in the lungs by angiotensin converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor and thus causes a rise in blood pressure.
Sodium and water Retention: Angiotensin II stimulates the release of aldosterone from the adrenal gland, which results in sodium and water retention. This further raises BP.
Insulin Resistance and Hyperinsulinemia: Insulin resistance, along with lipoprotein metabolism abnormality, is a risk factor in the development of hypertension and cardio vascular diseases. High insulin levels can cause increased renal sodium reabsorption. Also high insulin levels causes vasoconstriction by Sympathetic Nervous System stimulation and impairment of nitric oxide mediated vasodilation.
Endothelium Dysfunction: Vascular endothelial cells produce a number of potent local vasoactive agents, including the vasodilator molecule nitric oxide and the vasoconstrictor peptide endothelin. Dysfunction of the endothelium can cause vasoconstriction (due to either reduced response to nitric oxide or high levels of endothelin) and thus contribute to development of primary hypertension.
The clinical manifestations and laboratory findings are mainly referable to involvement of the target organs: brain, heart, kidneys, eyes, and peripheral arteries.
- Asymptomatic or vague symptoms: Mild to moderate primary hypertension may be asymptomatic for many years.
- The most frequent symptom is morning headache.
- Patients with severe hypertension may experience a variety of symptoms including fatigue, dizziness, palpitations, angina, and dyspnea.
- Accelerated hypertension is associated with somnolence, confusion, nose bleeds, visual disturbances, nausea and vomiting (hypertensive encephalopathy).
- Hypertensive Heart Disease
- Coronary Artery Disease
- Left Ventricular Hypertrophy (LVH)
- Heart Failure
- Hypertensive Cerebrovascular Disease
- Cerebro vascular Disease
- Hypertensive encephalopathy
- Vascular complications
- Peripheral Vascular Disease
- Aortic dissection
- Hypertensive Kidney Disease
- Retinal Damage
- Hypertensive retinopathy
- History and physical examination, including an ophthalmic examination
- Series of resting BP measurements
- Tests and examinations to check for other organ involvement
|Basic Laboratory Tests for Initial Evaluation|
|Renal||Microscopic urinalysis, albumin excretion, serum BUN and/or creatinine|
|Endocrine||Serum sodium, potassium, calcium, TSH|
|Metabolic||Fasting blood glucose, total cholesterol, HDL and LDL cholesterol, triglycerides|
|Cardiac||Hematocrit, electrocardiogram, echocardiography|
|Secondary Hypertension and Screening Tests|
|Chronic kidney disease||Estimated glomerular filtration rate|
|Coarctation of the aorta||CT angiography|
|Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy||Dexamethasone suppression test|
|Drug-induced/drug-related hypertension||Drug screening|
|Pheochromocytoma||24-hour urinary metanephrine and normetanephrine|
|Primary aldosteronism, other states of mineralocorticoid excess||Plasma aldosterone to renin activity ratio (ARR). If abnormal, refer for further evaluation such as 24-hour urinary aldosterone level, and specific mineralocorticoid tests|
|Renovascular hypertension||Doppler flow ultrasonography, MRI, CT angiography|
|Sleep apnea||Sleep study with oxygen saturation|
|Thyroid/parathyroid disease||TSH level, serum parathyroid hormone level|
Treatment of Hypertension
- Lifestyle Modification
|Lifestyle Modifications to Manage Hypertension|
|Weight reduction||Attain and maintain BMI|
|Dietary salt reduction||less than 6 g NaCl/day|
|Adapt DASH-type dietary plan||Diet rich in fruits, vegetables, and low-fat dairy products with reduced content of saturated and total fat|
|Moderation of alcohol consumption||For those who drink alcohol, consume
≤2 drinks/day in men and
≤1 drink/day in women
|Physical activity||Regular aerobic activity, e.g., brisk
walking for 30 min/day
Abbreviations: BMI, body mass index; DASH, Dietary Approaches to Stop Hypertension, > greater than, < less Than , > greater than or equal to
- Pharmacologic Therapy
GOAL: The goal for treating hypertension is a BP less than 140/90 mm Hg. A lower goal of 130/80 mm Hg may be appropriate for persons with high risk for CVD (e.g., diabetes mellitus, kidney disease, tobacco use).
The drugs currently used for treating hypertension have two main actions:
- Decrease the volume of circulating blood and
- Reduce SVR.
The drugs used in the treatment of hypertension include: diuretics, adrenergic (SNS) inhibitors, direct vasodilators, angiotensin and renin inhibitors, and calcium channel blockers.
- Diuretics: promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines.
- Adrenergic-inhibiting agents: act by decreasing the Sympathetic nervous system effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit Norepinephrine release or to block the adrenergic receptors on blood vessels.
- Direct vasodilators: decrease BP by relaxing vascular smooth muscles and reducing Systemic vascular resistance.
- Calcium channel blockers: increase sodium excretion and causes vasodilation by preventing the movement of extracellular calcium into cells.
- Angiotensin-converting enzyme (ACE) inhibitors: ACE inhibitors prevent the conversion of angiotensin I to Angiotensin -II and thus reduce – Angiotensin II-mediated vasoconstriction and sodium and water retention.
- Angiotensin -II receptor blockers (ARBs): ARBs prevent Angiotensin -II from binding to its receptors in the blood vessel walls.
|ANTIHYPERTENSIVE DRUGS||MECHANISM OF ACTION|
|Thiazide and Related Diuretics|
|• Inhibit NaCl reabsorption in the distal convoluted tubule.
• Increase excretion of Na+ and Cl−.
• Initial decrease in ECF. Sustained decrease in SVR.
• Lower BP moderately in 2-4 wk.
|Loop Diuretics |
|• Inhibit NaCl reabsorption in the ascending limb of the loop of Henle.
• Increase excretion of Na+ and Cl−.
• More potent diuretic effect than thiazides, but shorter duration of action.
|Potassium-Sparing Diuretics |
|• Reduce K+ and Na+ exchange in the distal and collecting tubules.
• Reduce excretion of K+, H+, Ca+, and Mg+.
|Aldosterone Receptor Blockers |
|• Inhibit the Na+-retaining and K+-excreting effects of aldosterone in the distal and collecting tubules.|
|Central-Acting α-Adrenergic Antagonists |
|• Reduce sympathetic outflow from CNS.
• Reduce peripheral sympathetic tone, produces vasodilation, decreases SVR and BP.
|Peripheral-Acting α-Adrenergic Antagonists|
|• Prevents peripheral release of norepinephrine, resulting in vasodilation.
• Lowers CO and reduces SBP more than DBP.
|α1-Adrenergic Blockers |
|• Block α1-adrenergic effects, producing peripheral vasodilation (decreases SVR and BP).|
|• Cardioselective agents block β1-adrenergic Receptors.
• Reduce BP by blocking β-adrenergic effects.
• Decrease CO and reduce sympathetic vasoconstrictor tone.
• Decrease renin secretion by kidneys.
|• Nonselective agents block β1- and β2-adrenergic receptors.
• Reduce BP by blocking β1- and β2-adrenergic effects.
|Mixed α- and β-Blockers |
|• α1-, β1-, and β2-adrenergic blocking properties producing peripheral vasodilation and decreased heart rate.
• Reduce CO, SVR, and BP.
Sodium nitroprusside (Nipride)
|• Relaxes arterial and venous smooth muscle, reducing preload and SVR.
• At low dose, venous dilation predominates; at higher dose, arterial dilation is present.
• Direct arterial vasodilation reduces SVR and BP.
|Trimethaphan||• Interrupts adrenergic control of arteries, results in vasodilation, and reduces SVR and BP.|
|Angiotensin-Converting Enzyme Inhibitors |
|• Inhibit ACE, reduce conversion of angiotensin I to angiotensin II (A-II).
• Inhibit A-II–mediated vasoconstriction.
|Angiotensin II Receptor Blockers |
|• Prevent action of A-II and produce vasodilation and increased Na+ and water excretion.|
|Aliskiren||• Directly inhibits renin, thus reducing conversion of angiotensinogen to angiotensin I.|
|Calcium Channel Blockers|
|• Inhibit movement of Ca2+ across cell membrane, resulting in vasodilation.
• Cardioselective resulting in decrease in heart rate and slowing of AV conduction.
|• Cause vascular smooth muscle relaxation resulting in decreased SVR and arterial BP.|
Combination Therapy in the Management of Hypertension
- Once antihypertensive therapy is started, patients should return for follow-up and adjustment of medications at monthly intervals until the goal BP is reached.
- More frequent visits are necessary for patients with stage 2 hypertension or with co-morbidities.
- After BP is stable, follow-up visits can usually be at 3- to 6-month intervals.
The frequency of visit is influenced by the presence of co-morbidities (e.g., heart failure), associated diseases (e.g., diabetes mellitus), and the need for ongoing monitoring (e.g., laboratory testing).
Severe elevation of BP with evidence of end-organ damage (CNS, retinal, CVS, renal, GI)
- Blood work: CBC, electrolytes, BUN, Cr
- Peripheral blood smear: to detect microangiopathic hemolytic anemia
- CXR: if shortness of breath or chest pain
- ECG, troponins, CK: if chest pain
- CT head: if neurological findings or severe headache
- Toxicology screen if sympathomimetic overdose suspected
- In general, strategy is to gradually and progressively reduce BP in 24-48 hrs
- Lower BP by 25% over the initial 60 min by initiating antihypertensive therapy (usually nitroprusside and labetatol)
- If preeclampsia, immediately consult OB/GYN.
- Establish arterial line; transfer to ICU for further reduction in BP under monitored setting
- In case of ischemic stroke: do not rapidly reduce BP, maintain BP >150/100 for 5 days
- In case of aortic dissection: rapid reduction of SBP to 110-120mm Hg (do not resuscitate with IV fluids)
- In case of excessive catecholamines: avoid beta-blockers (except labetalol)
- In case of ACS: address ischemia initially, then BP
Definition: severely elevated BP (usually sBP >180, dBP >110) with no evidence of end-organ damage
Cause: most often caused by non-adherence to prescriptions
Treatment: re-initiate antihypertensive therapy, acute BP reduction not indicated
Goal: differentiate hypertensive emergencies from hypertensive urgencies
- Carefully monitor blood pressure at frequent intervals and then at routinely scheduled intervals.
BLOOD PRESSURE DETERMINATION
- Measure the BP of the patient under the same conditions each time.
- Avoid taking BP readings immediately after stressful or taxing situations. Wait 30 minutes after patient has smoked.
- Place the patient in a position of comfort and have him or her remain silent. Make sure feet are on the floor or otherwise supported.
- Support the bared arm; avoid constriction of arm by a rolled sleeve.
- Use a BP cuff of the correct size.
- The bladder within the cuff should encircle at least 80% of the patient’s arm.
- Many adults will require a large cuff.
- Two or more readings separated by 2 minutes should be averaged.
- Be aware that falsely elevated BPs may be obtained with a cuff that is too narrow; falsely low readings may be obtained with a cuff that is too wide.
- Auscultate and record precisely the systolic and diastolic pressures based on Korotkoff sounds.[/su_box]
- A complete history should be obtained to assess for other cardiovascular risk factors and for signs and symptoms that indicate target organ damage.
- Assess heart rate and palpate peripheral pulses; determine respirations.
- Determine mental status by asking patient about memory, ability to concentrate, and ability to perform simple mathematical calculations.
Nursing diagnoses and collaborative problems for the patient with hypertension include, but are not limited to, the following.
- Acute Pain related to increased cerebrovascular pressure, possibly evidenced by verbal reports (throbbing pain located in suboccipital region, present on awakening and disappearing spontaneously after being up and about), reluctance to move head, avoidance of bright lights and noise, increased muscle tension.
- Deficient Knowledge related to the disease process, its consequences, and treatment, related to lack of effective teaching as manifested by verbal acknowledgement of a deficiency in knowledge, expressions of an inaccurate perception of health status, or incorrect performance of the desired or prescribed health behavior.
- Ineffective management of therapeutic regimen: noncompliance, related to knowledge deficit, failure to follow a prescribed regimen, inadequate support system, or lack of involvement in the treatment plan.
- Anxiety related to complexity of management regimen
- Sexual dysfunction related to side effects of antihypertensive medication
- Risk for decreased Cardiac Output related to increased afterload (vasoconstriction), fluid shifts, hypovolemia, myocardial ischemia, ventricular hypertrophy and rigidity.
- Risk for ineffective cerebral tissue perfusion
- Risk for ineffective renal perfusion
- Risk for fluid volume deficit related to abnormal fluid loss due to use of diuretics
- Potential complication: stroke
- Potential complication: MI
- Reduce symptoms of high BP and enhance comfort
- Stabilize hemodynamic status
- Improve cardiac output
- Prevent/reduce anxiety
- Increase clients knowledge of disease process/prognosis, diagnostic measures and treatment regimen
- Development of a treatment plan acceptable to the patient
The overall goals for the patient with hypertension are that the patient will
- Achieve and maintain the goal BP;
- Understand and follow the therapeutic plan;
- Experience minimal or no unpleasant side effects of therapy; and
- Be confident of the ability to manage and cope with this condition.
Nursing Care Plan of Hypertension
- Nursing Care Plan for Hypertension – Risk for decreased cardiac output
- Hypertension Nursing Care Plan and Management
- Myocardial Infarction Nursing Care Plan
Nursing Diagnosis: Acute pain
- Increased cerebral vascular pressure
As evidenced by
- Verbalization of throbbing pain in suboccipital region, present on awakening and disappearing spontaneously after being up and about
- Rubbing head, avoidance of bright lights and noise, wrinkled brow, clenched fists
Outcome Criteria: The patient will report relief of pain/discomfort.
|Assess the location, characteristics, intensity, onset and duration of pain. Note nonverbal cues.|
Instruct the patient to avoid activities that may aggravate headache (straining at stool, bending over, prolonged coughing etc).
|Facilitates diagnosis of problem and initiation of appropriate therapy. Helpful in evaluating effectiveness of therapy.
May accentuate the headache in the presence of increased cerebral vascular pressure.
|Instruct the patient to take bed rest during acute attacks.||Minimizes stimulation and promotes relaxation.|
|Provide non pharmacological measures for pain relief (massage, cold application to forehead) ; quiet, dimly lit room;||These measures are effective in relieving headache and associated complications.|
|Teach relaxation techniques (guided imagery, distraction); and provide diversional activities.|
|Provide a calm, quiet, low stimuli environment( dimly lit room)|
|Administer analgesics and anxiolytics as prescribes||Analgesic drugs helps to reduce or control pain and decrease stimulation of the sympathetic nervous system. Anxiolytics helps to reduce tension and discomfort that is intensified by stress.|
Nursing Diagnosis: Deficient Knowledge
- The disease process, its consequences, and treatment
- Lack of effective teaching
As manifested by
- Verbal acknowledgment of knowledge deficit
- Inaccurate perception of health care status
- Failure to perform the desired or prescribed health behaviors
Outcome Criteria: The patient will be able to
- Describe the disease process and the causes and factors contributing to the course of the disease
- Describe the procedure for hypertension control
- Actively participate in health behaviors prescribed or desired
- Experience less anxiety related to fear of loss of control, misconceptions, or misinformation
- Blood pressure will be maintained within normal limits
|Assess the level of knowledge, emotional readiness for learning and health beliefs||Assessment before developing a teaching plan ensures greater efficiency, appropriateness, and success of teaching and learning process.|
|Provide patient with additional information regarding pathology, general well-being (dietary habits, weight control, alcohol, exercise, caffeine, smoking, stress management), and risks of uncontrolled high blood pressure.||Enables patient to make choices about lifestyle changes and adherence to medical regimen.|
|Develop an individualized teaching plan based on patient's knowledge, habits, and experience.||Ensures greater efficiency, appropriateness, and success of teaching and learning process.|
|Have the patient recognize that hypertension is chronic and requires persistent therapy and periodic evaluation.||Effective treatment improves life expectancy; frequent follow ups are necessary|
|Initiate behavior modification methods|
• Have patient keep written diary of activities, diet, and medication over a week's time.
• Ask patient to recall activities, dietary intake, and medication over a 2-day period.
• Teach patient to take and record own blood pressure, and to record factors of concern.
|Patient education and opportunities to make voluntary adaptions of behavior will improve or maintain health. This implies active involvement of the patient in his or her own care and assumes that the patient takes responsibility for learning|
|Discuss drug actions, interactions, and side effects.||Knowledge, attitudes, and skills of the four critical patient behaviors are essential to taking medication and ultimately to achievement of long-term blood pressure control.|
Nursing Diagnosis: Potential ineffective management of therapeutic regimen: noncompliance to long-term disease management
- The chronic nature of the disease
- Knowledge deficit
- Inability to follow treatment regimens
- lack of social support
- Lack of active involvement in self-care
As manifested by
- Verbalization of nonparticipation
- Missed appointments
- Partially used or unused medications
- Persistence of symptoms
- Progression of the disease process
Outcome Criteria: The patient will
- Assume responsibility for self-care as able
- Develop personal and health care goals that contribute to following the treatment plan and control of high blood pressure
|Assess patient's perception of his illness and its treatment.||Misunderstandings of the nature and seriousness of the illness and susceptibility to complications can greatly affect compliance.|
|Encourage the patient to express any fears or frustrations he or she has related to health needs.||Fears and frustrations about prescribed treatment (whether valid or not) can interfere with following the treatment plan and must be discussed openly for effective problem solving to take place.|
|Provide written instructions on medication dosage, schedule side effects, and goals of therapy. |
Schedule medication taking in association with daily activities.
Stress not stopping or changing medication without calling clinician.
|Improves compliance to the treatment regimen and promotes satisfaction|
|Instruct the patient the proper method BP measurement at home and at work. Inform patient of desired range of BP and the readings that need to be reported.||Improves compliance to the treatment regimen and promotes satisfaction|
Nursing Diagnosis: Risk for decreased Cardiac Output
- Increased afterload (vasoconstriction)
- Fluid shifts
- Myocardial ischemia
- Ventricular hypertrophy and rigidity
Outcome Criteria: The patient will
- Maintain BP and heart rate within individually acceptable limits.
- Free from signs of heart failure
|Assess heart rate, rhythm, quality of central and peripheral pulses.||Bounding carotid, jugular, radial, and femoral pulses may indicate increased cardiac workload. . Pulses in the legs and feet may be diminished, reflecting effects of vasoconstriction (increased systemic vascular resistance).|
|Observe skin color, temperature, capillary refill time and diaphoresis.||Peripheral vasoconstriction may result in pale, cool, clammy skin, with prolonged capillary refill time.|
|Monitor BP every 1-2 hours, or every 5 minutes during actve titration of vasoactive drugs.||Changes in BP may indicate changes in patient status requiring prompt attention.|
|Monitor ECG for dysrrhythmias, conduction defects and for heart rate.||Decrease in cardiac output may result in changes in cardiac perfusion causing dysrhythmias.|
|Instruct the patient to decrease intake of caffeine, cola and chocolates.||Caffeine is a cardiac stimulant and may adversely affect cardiac function.|
|Administer medications to control blood pressure and monitor response.||To assess for response to drug therapy and possible side effects.|
Expected patient outcomes may include:
- Maintains blood pressure at acceptable level
- Reports increased comfort, decreased anxiety
- Reports knowledge of disease process diagnostic measures, prevention and management
- Adheres to the self-care program
- Adheres to the dietary regimen as prescribed: reduces calorie, sodium, and fat intake; increases fruit and vegetable intake
- Exercises regularly
- Takes medications as prescribed and reports any side effects
- Measures blood pressure routinely
- Abstains from tobacco and excessive alcohol intake
- Keeps follow-up appointments
- Has no complications
- Reports no changes in vision
- Maintains pulse rate and rhythm and respiratory rate within normal ranges
- Maintains urine output consistent with intake
- Has renal function test results within normal range
- Demonstrates no motor, speech, or sensory deficits
- Reports no headaches, dizziness, weakness, changes in gait, or falls
- Hypertension Pathophysiology & Disease Process (Diagram)
- Pregnacy Induced Hypertension (PIH) Case Study
- Preeclampsia Pathophysiology and Schematic Diagram
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