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Vascular Disorders: Hypertension. Brunner, ch 31. Physiology of Blood Pressure. SBP—force of blood against artery walls during systole DBP—force of blood during diastole
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Vascular Disorders: Hypertension Brunner, ch 31
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
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
Regulation: Arterial Vessel Walls • Vascular endothelium (inner layer) releases nitric oxide and endothelin and adrenomedullin 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
Regulation: Kidneys • Control Na+ excretion and ECF volume; less sodium and water excretion leads to increased venous return to heart • Secretion of renin converts angiotensinogen to A-I; ACE converts A-I to A-II. • A-II causes vasocontriction and changes to the vessel walls and stimulates adrenal cortex to release aldosterone, causing increase Na+ and water retention.
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.
Regulation: Other factors • Temperature—environmental or local application • Meds—affect CO, vessel reaction • Nicotine • Alcohol
Compensatory Mechanisms • Prostaglandin release from kidneys causes vasodilation, decreasing BP. • Atrial and b-type naturietic peptides from atria and ventricle walls antagonize the effects of aldosterone and ADH and cause loss of sodium • This results in reduced blood volume and decreased blood pressure.
Terminology • SBP > 140 and DBP > 90 at least 3 times on separate occasions. • Hypertensive crisis-DBP > 120. • Malignant HTN-rises rapidly. 180/120 • White coat HTN-increased BP when patient goes to MD.
Classifications and F/U Guidelines • Normal—less than 120/80—recheck 2 yrs • Prehypertension—120/80-139/89—recheck 1 yr • Stage 1—140/90 to 159/99—recheck 2 mo • Stage 2— > to 160/100—recheck 1 mo or within 1 week if > 180/100
Etiology • 90-95% of patients have primary or essential HTN (probably due to malfunction of regulatory mechanisms) • 5-10% have secondary, meaning there is a disease process or condition causing it (thyrotoxicosis, renal dz, adrenal disorders and tumors, pregnancy, ICP, coarctation (narrowing) of aorta
Risk Factors • Nonmodifiable: • Genetics, age, race, family hx • Modifiable: • Diet • Obesity • Excess ETOH • Insulin resistance • Meds • Stress • Smoking
Manifestations • Usually absent unless severe or advanced • If symptoms they include morning occipital HA, blurred vision, dizziness, nosebleeds • BP > 140/90 • S4 gallop rhythm • Retinal changes—constricted arterioles, hemorrhages, and papilledema
Diagnostics • BP readings • Labs: CBC, UA, BMP, and liver functions (includes lipid profile) 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 • Secondary would require more extensive testing acc’d to suspected cause
Management of HTN • Wt reduction, heart healthy diet (low Na+ < 2.4 g/d, low fat) • No nicotine • Moderate, regular exercise • DASH diet—Dietary Approaches to Stop Hypertension—more fish, fiber, fruits and veggies, water • Limit alcohol intake
Pharmacologic Management • Algorithm approach (865). BP goal for people with compelling indications is lower • May start with diuretic & BB if Stage 1. However, most pts need 2 meds or combo drug • ACEIs are preferred (except Blacks) for compelling indications such as diabetes • Stepped approach using diuretics, BBs, direct vasodilators, ACEIs, ARBs, CCBs.
Management of HTN cont’d • Treat complications: • Angina, MI • CHF (from LV hypertrophy) • Chronic renal failure (CRF) • Cerebrovascular accident (CVA-stroke) • Retinal hemorrhages
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
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
Patient Education—Meds • Don’t stop suddenly (rebound HTN, edema, angina) • OTC meds including herbals • Keep list of meds • Interacting meds—BCPs, steroids, NSAIDs, some antidepressants, antihistamines, nasal decongestants