Htn--ch. 32

~Maria Vogel’s Chapt 32 HTN—Med/Surg Page1~

Coronary arteries:  Originate inside aorta  Fill during diastole  RCA—Supply Rt atrium and ventricle and AV node and Bundle of His.  LCA—supply the left atrium and ventricle.  Coronary arteries empty into the coronary sinus (venous flow), which empties into the Rt. Atrium. HTN—Chapter 32 Increased HR = Increased Oxygen demand BP = CO x SVR Systemic Vascular resistance—force opposing the movement of blood within the blood vessels. CO = SV X HR (total blood flow through the systemic or pulmonary circulation in one minute) SV--blood pumped out from Lf. Ventricle each beat (aprox. 70 mL) Normal CO = 4-8 L/min 1) Regulation: a) Sympathetic nervous system Stimulation  Increases HR  Vasoconstriction  Release of rennin  Causes Angiotension I and II  Release of aldosterone from adrenals –conserves Na and H2O—Increases fluid vol. b) Parasympathetic Nervous System—Rest and digest  Decreases HR  Vasodilation—via vagus nerve (Vaso vagal response Dec. HR and dec. BP)

~Maria Vogel’s Chapt 32 HTN—Med/Surg Page2~

 Baroreceptors—specialized nerve cells located in the carotid arteries and arch of aorta. They are sensitive to stretch. When BP increases it sends inhibitory impulses to the sympathetic vasomotor center of the brain. c) Vascular Endothelium  Produces vasoactive substance  Dilation  Constriction  Produces—endothelin (ET) an extremely potent vasoconstrictor.  Nitric oxide and endothelium-derived relaxing factor (EDRF)—Causes vasodilation --inhibits platelet aggregation --Intact endothelium, non-reactive to platelets. d) Kidneys—rennin-angiotensin-aldosterone system. e) Endocrine System—releases aldosterone which causes Na retention and water retention— increases BP by increasing CO. f) Increased Na+ stimulates release of ADH—increases fluid and increased BP. Stages of HTN: 2) HTN—sustained BP of >140/90 3 + readings a) Stage I –140-159/90-99 b) Stage II—160-179/100/109 c) Stage III-->180/110 Types of HTN: a) Primary HTN  95% of case  Cause unknown b) Secondary HTN  5% of cases

~Maria Vogel’s Chapt 32 HTN—Med/Surg Page3~

 can identify cause—usually renal disease, sleep apnea, medications, estrogen and NSAID, and Coarctation aorta. 3) Pathophysiology— ~ Increased SNS stimulation = Increased HR and Increased CO Increased vascular resistance and Increased BP. ~ hyperinsulinemia or insulin resistance prevents nitricoxide release—prevents vasodilation. 4) Manifestations—Signs and Symptoms ~ Asymptomatic—no symptoms—SILENT KILLER ~ fatigued—nonspecific ~ Dizziness ~ Palpitations ~ Angina—advanced. 5) Complications of HTN Evidence of target organ damage: a) CAD—coronary artery disease b) Left ventricular hypertrophy—most muscle mass in heart works harder it enlarges. Starling’s law—it can’t stretch anymore. Detected with chest x-ray and EKG c) Heart failure d) Stroke e) Peripheral vascular disease f) retinopathy g)End stage renal failure.

6) Diagnostics: a) H and P b) Kidneys—UA BUN and creatinine signal kidney problems c) chest x-ray d) EKG e) CBC f) Lipids—cholesterol g) Blood sugar

~Maria Vogel’s Chapt 32 HTN—Med/Surg Page4~

1. Treatment Stage I <159/99 treat with lifestyle modification Stage II and III lifestyle modification and drug therapy. Lifestyle modifications cont. for one year: a) dietary change: reduce Na, and fat. Maintain Ca, Mg and K. Increase K. b) Exercise—activity c) Limit ETOH consumption d) Quit smoking—smoking release epi and norepi = Inc. HR. Vasoconstriction, release of CO2 in system competes with O2. Dec. O2 in system. Changes endothelial lining— becomes reactive to platelet aggregation over time. 2. Medications—Stage II and III I) Diuretics—Increase urinary output and dec. volume. A) Thiazides—K wasters Diuril and hydrodiuril NORMAL K LEVELS 3.5 – 5 B) Loop Diuretics Lasix and Bumix SE: Orthostatic Hypotension C) K Sparing Diuretics Aldactone and spironalactone II. ACE inhibitors—vasocdilation, dec. fluid vol. Inhibits aldosterone release Lotensin and Prinivil SE: Hyperkalemia 3 Most common SE with antiHTN: a) orthostatic hypotension b) Dry mouth and frequent voiding c) Sexual dysfunction DAMAGE FROM HTN happens OVER TIME.

~Maria Vogel’s Chapt 32 HTN—Med/Surg Page5~

3. HTN Crisis: --Not over time It is a severe and abrupt elevation with elevation of > 130 Diastolic. Causes—Failure to comply, inconsistently taking medications ~ Response to cocaine, crack and LSD ~ Eclampsia. VASOCONSTRICTION triggers endothelial damage, which leads to MI, Stroke, and seizures. Treatment: Dec. Mean arterial pressure by 10-20% in first 1-2 hours. MAP = Diastolic and 1/3 of pulse pressure Pulse Pressure—difference between diastolic and systolic Medications: Nitroprusside/Hyperstat Apressoline Given IV Rx titrated for effect Pt should be in intensive care because we don’t have an expected outcome. Adrenegic Blockers—NORMADINE—Alpha Beta adrenergic blocking properties—produces peripheral vasodilation, dec. HR which reduces CO, SVR, and BP. ? Add an oral Rx—vasotec (ACE inhibitor)