Chapter 33 Hypertension

OBJECTIVE: Describe the pathophysiology, clinical manifestations, and nursing and collaborative
management of patients with primary hypertension, secondary hypertension, and hypertensive crisis.

Blood pressure: the force exerted by the blood against the walls o f the blood vessel and must be
adequate to maintain tissue perfusion during activity and rest.
Arterial blood pressure = Cardiac output X Systemic vascular resistance.

Cardiac output (CO): the total blood flow through the systemic or pulmonary circulation per minute.

Stroke volume: the amount of blood pumped out of the left ventricle per beat (approximately 70ml)
multiplied by the heart rate for 1 minute.

Systemic vascular resistance (SVR): is the force opposing the movement of blood within the blood
vessels. If SVR is increased and CO remains constant or increases than BP will increase.

Sympathetic Nervous System

1. Increased SNS activity increases HR and cardiac contractility, produces widespread
vasoconstriction in the peripheral arterioles, and promotes the release on rennin from the kidneys.
2. The net effect of SNS activation is to increase arterial pressure by increasing both CO and SVR.
3. Baroreceptors: specialized nerve cells that sense changes in BP. Changes are transmitted to the
vasomotor centers in the brainstem.
a. Baroreceptors are located in the carotid arteries and the arch of the aorta.
b. A fall in BP, sensed by the baroreceptors, leads to activation of the SNS.
4. BP may be reduced by withdrawal of SNS activity or by stimulation of the parasympathetic
nervous system, which decreases the HR via vagus nerve and thereby decreases CO.
5. In the presence of long-standing hypertension, the barorecpetors become adjusted to elevated
levels of BP and recognize this level as “normal”. The baroreceptor reflex is less responsive in
some older adults.

Vascular Endothelium
1. A single cell layer that lines the blood vessels. Has the ability to produce vasoactive substances
and growth factors.
2. Nitric oxide, an endothelium-derived relaxing factor(EDRF) helps maintain low arterial tone at
rest, inhibits growth of the smooth muscle layer, and inhibits platelet aggregation.
3. Endothelin(ET) extremely potent vasoconstrictor. 3 subclasses ET-1, ET-2, ET-3.

Renal System
1. Kidneys to contribute to BP regulation by controlling sodium excretion and extracellular fluid
volume.
2. Water retention increases ECF, which increases venous return to the heart, increasing the stroke
volume, which elevates the BP through an increase in CO.
3. Renin is an enzyme that convertse angiotensinogen to angiotensin 1. Angiotesin-converting
enzyme(ACE) converts angiotensin I into angiotensin II.
 4. AII is a potent vasoconstrictor and increases vascular resistance, resulting in immediate BP
increases. AII increases increases bp indirectly by stimulating the adrenal corte to secrete
aldosterone, which causes NA+ and H2O rentention by the kidneys resulting in increased blood
volume and increased CO.
5. Prostoglandins secreted by the renal medulla have a vasodilator effect on systemic circulation,
resulting in decreased systemic vascular resistance and lowering of BP.

Endocrine System
1. Epinepherine increases CO by increasing HR and myocardial contractility.
2. Epinepherine activates B2-adrenergic recptors in peripheral arterioles of skeletal muscle, causing
vasodilation. In peripheral arterioles with only a1-adrenergic receptors(skin and kidneys),
epinephrine causes vasoconstriction.
3. Adrenal cortex is stimulated by A-II to release aldosterone. Increasing BP by increasing CO.

Sympathetic Nervous System Receptors influencing blood pressure

1. a1- found in vascular smooth muscle. Response when activated is vasoconstriction. Heart response
isIncreased contractility.
2. a2 – found in the presynaptic membrane. Response when activated is inhibition of norepinephrine
release. Found in vascular smooth muscle is vasoconstriction.
3. b1 – found in the heart. Response when activated is increased contractility(positive isotropic
effect). Increased heart rate(positive chronotropic effect). Increased conduction (positive
dromotropic effect). Found in the Juxtaglomerluar cells and the response is increased rennin
secretion.
4. b2 – found in the smooth muscle of peripheral blood vessels in skeletal muscle and coronary
arteries. Response is vasodilation.
5. Dopaminergic receptors – Primarily renal and mesenteric blood vessels. Response is vasodilation.

Hypertension
Sustained elevation in BP. In adults, hypertension exists when systolic blood pressure(SBP) is equal to or
greater than 140mmHG or diastolic blood pressure(DBP) is equal to or great than 90mmHG for extended
periods of time.

Cultural and Ethnic Considerations of Hypertension

1. African Americans, Puerto Ricans, Cubans, and Mexican Americans have a higher incidence of
hypertension than whites.
2. African Americans have the highest incidence of hypertension.
3. African Americans develop hypertension at a younger age than whites.
4. African American women have a particularly high incidence of hypterension.
5. Hypertension is more aggressive in African Americans and results in more severe end-organ
damage.
6. African Americans have a higher mortality rate related to hypertension than whites.
7. African Americans and whites living in the southeastern united states have a higher incidence of
hypertension than similar ethnic groups living in other parts of the united states.
8. African Americans produce less rennin and do not respond as well to angiotensin inhibitors.
Primary Hypertension: is elevated BP without an identified cause and accounts for 90-95% of all cases
of hypertension. Risk factors include age, alcohol, smoking, diabetes mellutis, Elevated serum lipids,
excess dietary sodium, gender, family history, obesity, ethnicity, sedentary lifestyle, socioeconomic status,
stress.

Clinical manifestations of primary hypertension

1. Often called the silent killer and is frequently asymptomatic until it becomes sever and target
organ disease has occurred.
2. Other symptoms include fatigue, reduced activity tolerance, dizziness, palpitations, angina, and
dyspnea, headache, and nosebleeds.

Complications of primary hypertension

1. Most common are target organ diseases occurring in the heart (hypertensive heart disease),
brain(cerebrovascular disease), kidney(nephrosclerosis) and eyes(retinal damage)

Manifestations of Target Organs

1. Cardiac: Clinical, electrocardiographic, or radiologic evidence of coronary artery disease. Left
ventricular hypertrophy or “strain” by ectrocardiography or left ventricular hypertrophy by
echocardiography. Left ventricular dysfunction or cardiac failure.
2. Cerebrovascular: Trans ischemic attack or stroke.
3. Peripheral vascular: Absence of one or more major pulses in the extremities(except for dorsalis
pedis) with or without intermittent claudication, aneurysm.
4. Renal: Serum creatinine greater than or equal to 1.5mg/dl.
5. Retinopathy: Hemorrhages of exudates, with or without papilledema.

Diagnostic Studies
Routine urinalysis, BUN, and serum creatinine levels are used to screen for renal involvement and to
provide baseline information about kidney function.

Creatinine clearance, the rate at which creatinine is cleared from the circulation, reflects the glomerular
filtration rate.

Measurment of serum electrolytes especially potassium is important to detect hyperaldosteronism which

causes secondary hypertension.

ECG provides baseline information about cardiac status. It is helpful in identifying the presence of LVH
and cardiac status.

CBC, Serum lipid profile, EKG. ECHO.

Secondary Hypertension: is elevated BP with a specific cause that often can be identified and corrected.
This type of hypertension accounts for 5-10% of hypertension in adults and more than 80% of
hypertension in children.
Collaborative Care
Periodic monitoring of BP. Nutritional therapy, low sodium, reduce weight, restrict cholesterol, maintain
adequate potassium, smoking cessation, moderate alcohol intake, antihypertensive drugs.

BP elevation should usually be assessed carefully over several months before initiating treatment.

High normal blood pressure 130-135/35-89

Stage 1 hypertension 140-159/90-99
Stage 2 hypertension greater than or equal to 160/greater than equal to 100.

Nursing Management
**Nursing Assessment: past health hx, meds, functional health patterns, cardiovascular (bp consistently
>140mmHg systolic or 90 mmHg diastolic, orthostatic change in BP and pulse; retinal vessel changes,
abnormal heart sounds, laterally displaced , sustained, forceful, apical pulse, sminished or absent
peripheral pulses, carotid, renal, Ischia, or femoral bruits, presence of edema). Musculoskeletal, possible
findings (electrolytes, increased BUN, creatinine, glucose, cholesterol, tryglyceride levels).

**Planning: The overall goals for the pt with hypertension are that the pt will(1) achieve and maintain the
individually determined target BP; (2) understand, accept, and implement the therapeutic plan(3)
experience minimal or no unpleasant side effects or therapy; and (4) be confident of ability to manage and
cope with this condition.

Patient and family teaching

* provide the numerical value of the pts BP and explain what it means
*inform the pt that HTN is usually asymptomatic and symptoms do not reliably indicate BP lvls.
*Inform pt of side effects of meds.
* Caution about potentially high-risk OTC meds, such as high sodium antacids, appetite suppressants, and
cold and sinus med. Advise to read warning labels and to consult with pharmacist.

Evaluation
The overall expected outcomes are that the pt with hypertension will achieve and maintain desired BP as
defined for the individual, understand/accept/implement the therapuetic plan, and experience minimal or
no unpleasant side effects of therapy.

Isolated systolic hypertension(ISH)

Defined as a sustained elevation in SBP equal to or greater than 160mmHg with a DBP less than
90mmHg.
Older adults often have ISH caused by loss of elasticity in large arteries from atherosclerosis.
Treating ISH reduces risk of stroke and cardiovascular morbidity and mortality.

Psuedohypertension (false hypertension)

Can occur with sclerosis of the large arteries.
Suspected if arteries feel rigid or when few retinal or cardiac signs are found relative to the pressures
obtained by cuff.
Olster’s sign is a palpable radial artery after the blood pressure cuff is inflated above peak SBP. Has a low
sensitivity and specificity to pseudo hypertension and is not recommended.

Hypertensive crisis: is a severe and abrupt elevation in BP, arbitrarily defined as a diastolic BP of above
120 to 130mmHg.
Occurs most commonly in pts with a hx of hypertension who have failed to comply with their prescribed
meds or who have been undermedicated.
Classified by degree of organ damage and the rapidity with which the BP must be lowered.
Can develop over hrs to days and is situational.

Causes of hypertensive crisis

Exacerbation of chronic HTN, Renovascular HTN, Preeclampsia, eclampsia, pheochromocytoma, MAIO
taken with tyramine, Rebound HTN, Necrotizing vasculitis, head injury, acute aortic dissection.