HTN and CAD

hypertension

BP greater than 140/90 or over 130/80 if comorbid conditions exist; includes primary, secondary, and malignant types

primary hypertension

occurs on over 90% of hypertension cases; idopathic with no known cause

secondary hypertension

hypertension caused by other disorders ex. cushing’s disease, brain tumour, primary aldosteronism; or by medications ex. stimulants, corticosteroids, estrogen replacements, NSAIDs

malignant hypertension

a hypertensive emergency in which the BP spikes over 180/120, causing acute damage to target organs

nonmodifiable risk factors for HTN

gender: male; age: over 55 for males, over 65 for females; family history

modifiable risk factors for HTN

sedentary lifestyle, high alcohol consumption, obesitym hyperlipidemia, excessive sodium intake, smoking

ACE inhibitors

drugs ending in -pril; prevents conversion of angiotensin I → angiotensin II, causing vasodilation; prevents proatglandins that cause vasodilation; also inc renin and dec aldosterone

ACE inhibitors adverse effects

angioedema → swelling of face, mouth, tongue with dyspnea due to strong vascular inflammatory reaction; also dry cough, hypotension, kidney function problems; may also inc blood glucose levels

ACE inhibitors lab values

serum K+: drug may cause hyperkalemia by promoting K+ resorption in kidneys

serum Na+ may be decreased

creatinine clearance may be decreased; serum creatine may be increased

BUN may increase

angiiotensin receptor blockers (ARBs)

drugs ending in -sartan; blocks angiotensin II receptors in vasc smooth muscle and adrenal glands → blocks vasocinstriction and aldosterone production → vasodilator

ARBs adverse effects

loss of taste, anemia, upper respiratory tract infections, headache

ARBs lab values

increased BUN

increased creatinine

increased serum K+

calcium channel blockers (CCBs)

drugs ending in -dipine; also including verapamil and diltiazem; blocks Ca2+ from entering muscle, resulting in muscle relaxation and vasodilation

CCBs adverse effects

peripheral edema, bradycardia, dizziness, hypotension

CCBs monitoring

must monitor BP because drug causes systemic vasodilation; do not adminoster if BP is below 90/50

beta blockers

drugs ending in -lol; blocks beta 1 receptors in heart → dec HR, dec contractility → dec BP; also blocks beta 2 receptors → vasoldilation

beta blockers adverse effects

bradycardia, hypoglycemia, fatigue, weakness, erectile dysfunction, makes asthma worse, cold hands and feet

beta blockers lab values

increased BUN

increased serum lipoproteins and triglycerides

increased K+

increased urid acid levels

increased blood glucose

increased liver enzymes

beta blockers monitoring

prior to administering: auscultate apical pulse for full min. do not administer if apical pulse is less than 60 BPM

monitor for asthma; do not give if client has asthma as it may induce bronchospasm

thiazde diuretics

diuretic that inhibits Na+, K+, and Cl- resorption at DCT → Na+, K+, Cl- loss in urine, with water following → dec BP; also relaxes arterioles → dec afterload → dec BP

thiazide and loop diuretics adverse effects

hypokalemia → lethargy, nausea, vomiting, anorexia, muscle weakness, mental confusion, weak pulsem hypotension

thiazide and loop diuretics lab values

may cause low K+ levels: narrow reference range → hypokalemia

lower but still normal Na+ and Cl-; even though it is excreted, it has a wide reference range → still in normal range

potassium sparing diuretics

diuretic that blocks aldosterone receptors in collectind ducts and DCT; also excretes Na+ and water while retaining K+ → inc urine output and dec BP

potassium sparing diuretics adverse effects

hyperkalemia → fatigue, muscle weakness changes, paralysis, paresthesia (lack of sensation), confusion, dyspnea, cardiac arrythmias

potassium sparing diuretics lab values

may cause high K+ levels → narrow reference → hyperkalemia

avoid potassium rich foods

loop diuretics

diuretic that blocks Cl-, Na+, and K+ reabrosption on loop of henle → water follows as these are excreted → dec BP; also reduces SVR due to activation of prostaglandins

coronary artery disease (CAD)

lipid deposition of plaques from blood to damages coronary arteries resulting in the hardening and narrowing of the artery; alters normal blood flow to heart resulting in ischemia and infarct

ischemia

decreased blood flow to an organ

infarct

complete blockage of blood flow to an organ resulting in tissue death

CAD risk factors

similar to those of HTN; also includes high LDL cholesterol (bad fat), low HDL cholesterol (good fat), high BP, family history, diabetes, smoking

saturated fats

“bad” fat; made up of H+, carbon, and O2; can accomodate large amounts of cholesterol, includes dairy foods such as butter, cream, ghee, reg-fat milk, cheese; meats such as fatty cuts of beef, pork, and lamb, also processed meats

monosaturated fats

“good” fat; molecular make up; can accomodate less cholesterol; includes olive oil, nuts, canola oil, avocados, nut butters, olives, peanut oil

polyunsaturated fats

“better'“ fats; can accomodate even less cholesterol; includes walnuts, sunflower seed, flax seeds or flax oil, fish, corn oil, soybean oil, safflower oil

HMG CoA reductase inhibitors

includes statins; very common for CAD treatment; lowers LDL and increases HDL triglyceride; better to give at night due to fat buildup at night; may cause muscle pain due to muscle inflammation

bile aced sequesterants

includes cholestyramine; not common due to drug interactions; decreases LDL; give other drugs 1 hr before or 4 hr after administration; may cause rhabdomyolysis

niacin

vitamin that decreases LGL and triglycerides; used as adjunct with cholestyramine or fibrates; may cause hyperglycemia, facial flushing, feeling warm, tingling feet and hands, diarrhea

cholesterol absorption inhibitor

includes ezetemibe; common for CAD treatment; inhibits cholesterol and decreases LDL; may cause rash or nausea

fibrates

decreases trigylcerides by inhibiting triglyceride synthesis

dyslipidemia

imbalance of any lipid, including HDL, LDL, or TG

ASA

used for treatment of CAD, also proven to decrease mortality and prevent MI

angina

chest pain cause by decreased blood flow to the heart; may feel tightness, pain, squeezing sensations