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Hypertension

Hypertension. Lewis, ch 33. Physiology of Blood Pressure. SBP—force of blood against artery walls during systole DBP—force of blood during diastole Systemic vascular resistance (SVR)—tension in arteries against which force is pushing—most important in small arteries and arterioles.

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Hypertension

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  1. Hypertension Lewis, ch 33

  2. Physiology of Blood Pressure • SBP—force of blood against artery walls during systole • DBP—force of blood during diastole • Systemic vascular resistance (SVR)—tension in arteries against which force is pushing—most important in small arteries and arterioles

  3. Regulation of Blood Pressure—SNS • Responds within seconds to a drop in BP thru messages from baroreceptors (carotid and aortic arch). • Releases catecholamines, affecting alpha and beta receptors • This leads to increased HR, contractility, vasoconstriction, and release of renin from kidneys

  4. Regulation—Arterial Vessel Walls • Vascular endothelium (inner layer) releases nitric oxide and endothelin that partially control relaxation and constriction of the artery, affects growth of arterial muscle, and inhibits and attracts cellular component to the wall of the artery. • Dysfunction of this system may contribute to atherosclerosis and HTN

  5. Regulation--Kidneys • Control Na+ excretion and ECF volume; less sodium and water excretion leads to increased venous return to heart • Secretion of renin converts angiotensin to A-I; ACE converts A-I to A-II. • A-II causes vasocontriction and remodeling of the vessel walls and stimulates adrenal cortex to release aldosterone, causing increase Na+ and water retention.

  6. Regulation—Endocrine System • Release of aldosterone causes Na+ and water retention • Stimulates release of ADH causing more retention and increasing CO and BP • Insulin resistance and hyperinsulinemia stimulate SNS activity, impairs vasodilation, and causes Na+ retention.

  7. Compensatory Mechanisms • Prostaglandin release from kidneys causes vasodilation, decreasing SVR and BP. • Atrial and b-type naturietic peptides from atria and ventricle walls antagonize the effects of aldosterone and ADH and cause naturesis • This results in reduced blood volume and decreased blood pressure.

  8. Definitions • SBP > 140 and DBP > 90 at least 3 times. • Hypertensive crisis-DBP > 120. • Malignant HTN-rises rapidly. • White coat HTN-increased BP when patient goes to MD.

  9. Classifications • Normal—less than 120/80 • Prehypertension—120/80 to 139/89 • Stage 1—140/90 to 159/99 • Stage 2— > or = to 160/100

  10. Etiology • 90-95% of patients have primary or essential HTN (unknown etiology—although there is debate and theory as to the effect of malfunction of regulatory mechanisms) • 5-10% have secondary, meaning there is a disease process causing it (thyrotoxicosis, renal artery stenosis, pheochromocytoma).

  11. Manifestations • Usually absent unless severe or advanced • If symptoms they include HA, blurred vision, dizziness, nosebleeds • BP > 140/90 • S4 gallop rhythm

  12. Diagnostics • BP readings • Labs: CBC, UA, BMP, and liver functions to monitor for anemia, kidney and liver damage • ECG—to detect LVH, ischemia, previous damage • CXR—to detect fluid and heart size • Echo—evaluate heart size, valvular function, afterload, ejection fraction

  13. Management of HTN • Algorithim p. 769, Table 33-6. • Lifestyle changes include wt reduction, heart healthy diet (low Na+, low fat), no nicotine, moderate ETOH, regular exercise • DASH diet—Dietary Approaches to Stop Hypertension—more fish, fiber, fruits and veggies, water

  14. Pharmacologic Management • May start with diuretic if Stage 1. However, most pts need 2 meds. • ACEIs are preferred for compelling indications. • Stepped approach using diuretics, BBs, direct vasodilators, ACEIs, ARBs, CCBs.

  15. Management of HTN cont’d • Treat complications: • Angina, MI • CHF (from LV hypertrophy) • Chronic renal failure (CRF) • Cerebrovascular accident (CVA-stroke) • Retinal hemorrhages

  16. Nursing Management of HTN • History: assess for all risk factors • Physical assessment: • VS, heart sounds, pulses • Lungs—crackles, wheezes • Carotids—bruit • Retina—hemorrhages • Thyroid—enlargement, nodules • Abd—liver enlargement, aortic bruit • Neuro—unilateral weakness, confusion

  17. Patient Education • Lifestyle modifications • Teach patients how to monitor BP and daily wts and importance of keeping a record • Let HCP know if BP or P are out of range • Keep F/U appointments • Safety—hot showers and environments, orthostatic BPs • Take meds as ordered

  18. Patient Education—Meds • Don’t stop suddenly (rebound HTN, edema, angina) • OTC meds • Keep list of meds • Interacting meds—BCPs, steroids, NSAIDs, some antidepressants, antihistamines, nasal decongestants

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