Hypertension

External jugular, median cubital, median antebrachial ulnar

Hypertension

10 cal/lb

perfusion

Blood vol Peripheral resistance/diameter of arterioles cardiac output

vasodilation, decrease stroke vol, decrease heart rate, decrease cardiac output

70-100mm Hg Used to measure adequacy of blood getting to vital tissues and organs Systolic pressure +2 (diastolic pressure) % 3

SVx HR normal ejection fraction 70%

MAP-ICP cerebral perfusion pressure (brain requires constant flow) min: 55-60mmHg

5-15 mmHg

SBP

35mmHg

35-18mmHg -declines throughout the capillary bed

18mmHg

5mmHg

135

1. Essential (Idiopathic) 2.Secondary (organ disease) 3.Sudden onset

-Age -ethnicity/genetics -gender -lifestyle: diet sedentary smoking excess alcohol TX: collect data, focus on modifiable risk fxs, tx BP PRN & TITRATE TO EFFECT; BW BW: glucose, electrolytes, creatinine, cholesterol, lipids

Decreases: elasticity of vessels= increases PVR renal blood flow sensitivity to baroreceptors TX: titrate meds to effect, Monitor for ORTHOSTATIC hypotension => risk for falls

drop of SBP > 20 mmHg or DBP > 10 -caused by Venus pulling in lower extremities transient (compensated once baroreceotors intervene- slowed intervening in elderly) S/S: faintness/ dizzy, decreased CNS perfusion TX: titrate drugs, adrenergic agonists if ER

Elderly dehydrated or fluid restricted patients antihypertensive medication patients

-Organ disease eg: diabetes, renal, adrenal, congenital defects -prego- TX: BW, tx the cause, tx BP

normal prego BV: increases by 50% ->20 weeks gestation -inflammatory etiology (immune) theory -=>inflammatory cytokines release=> endothelial changes => at risk for clotting to fix damage=> organ damage + placental flow compromise + risk for DIC: clotting & thrombocytopenia

sodium restriction, antihypertensive meds

sudden change of > 20mmHg -assess patient for cause: Pain? Infection? Compensation for changes? Hypervolemia? Drug induced? e.g. stimulants: cocaine, sympathomimetics,… TX: treat the cause; tx BP PRN

SBP >180 ‘Malignant HTN’ = medical emergency TX: medications

-Brain: stroke or hypertensive encephalopathy -Arteries: acute aortic syndromes -Retina: Grade III-IV Keith wagner barker -Kidney: acute renal insufficiency or thrombotic microangiopathy -Heart: acute heart failure, pulmonary edema

DIRECT ACTING VASODILATORS drugs: NIPRIDE (nitroprusside) IV/ET, HYDRALAZINE PO/IV IV t1/2- 2 mins

MOA: stimulates endothelial cell-produced NITRIC OXIDE S/E: reflex tachycardia: hypotension, syncope, headache

Arginine

-Direct acting vasodilators -Diuretics (decrease blood volume) -Renin angiotensin drugs- ACE inhibitors (vasodilate and decrease blood volume) Angiotensin II receptor blockers (vasodilate and decreased blood volume)

-Calcium channel blockers (decrease CO) -Adrenergic agents (decrease vasoconstriction) & CO)

Drug combos -synergy effect

increase urine output -deceases circulating blood vol = lowers BP Decreases H20 & ELECTROLYTES 1ST line in HTN tx 4 types:

1. loop diuretics

2. thiazides

3. potassium sparing

4. osmotic

Dehydration hyponatraemia hypokalemia (thiazide, loop) hyperkalemia (potassium sparing diuretics) nocturia

loop of Henle -blocks NA, Cl, K+ re-absorption => increased Na, K, Cl out => w/ H20 Drug: FUROSEMIDE (lasix) -1ST LINE TX FOR HTN -potent, IV,PO S/E: HYPOKALEMIA, ototoxicity (this is reversible), drug interactions(High PPB)

Distal convoluted tubule -decrease in reabsorption of NA, Cl , K => increased NA, K , Cl out w/ H20 Drug: HYDROCHLOROTHIAZIDE (HZTZ) CHLOROTHIAZIDE (diuril) METOLAZONE (ZAROXOLYN) S/E: HYPOKALEMIA

Collecting distal tubule: ANTAGONIZES renal aldosterone => increases NA out and KEEPS K in normally aldosterone causes Na retention Drugs: Spironolactone (Aldactone) S/E: HYperkalemia long t1/2 (1-2 days)

Aldactazide -Used very frequently -Balances out K+ -PO administration -Excellence maintenance therapy for HTN

Drugs: MANNITOL (osmitrol), ISOSORBIDE -high solute, travel unchanged -pulls water into circulation and into renal tubules (proximal tubule and loop of Henle) -inhibit renin release TX: cerebral edema i Intraocular hypertension low use for CV

Liver produces Angiotensinogen in plasma=> renin then comes and transforms forms it to Angiotensin 1 in plasma=> ACE turns that into Angiotensin II in plasma

-Inhibit ACE => vasodilate -potent, titrate to effect

• 1ST line drugs in heart failure- high efficacy Drugs: PRILS Enalpril (vasotec) Captopril Monopril Ramipril (altace) S/E: severe hypotension

MOA: angiotensin I I receptors antagonized -decrease afterload = >decreased preload -slow onset of action (a few weeks to take full effect) Drugs: Losartan (Cozaar); Ibesartan (Avapro) S/E: hypotension

Hyzaar, Cosart

Muscle contraction regulated by calcium (Ca 2 enters the cell = contraction initiated) -MOA: Ca 2+ influx blocked => muscle relaxation specificity Drugs:

1. Vascular selective: smooth muscle Nifedipine (aldalat), Amlodipine (norvasc)

2. cardio-selective: Cardiac muscle verapamil (Isoptin); Diltiazem (Cardizem) tx: of arrhythmias: atrial Fibrillation

Nifedipine (Alalat), Amlodipine (Norvasc)

verapamil (Isoptin), Diltiazem (Cardizem)

-decrease HR -decrease CO -optimize cardiac contractions -decrease BP (smooth)

Ginseng -therapeutic dose: 20-30mg/day

adrenal medulla, arrector pili muscles, sweat glands, some blood vessels

MOA: antagonize the sympathetic NS @ various adrenergic receptors => decrease catecholamine activity

Cause vasoconstriction! (increase peripheral resistance) -Pupil dilation -Increased closure of the internal urinary sphincter -Secretions

-vasoconstriction of arteries plus veins! -Decreased G.I. motility -Decreased smooth muscle motility -Contraction of male genitalia during ejaculation

Prazosin

Phentolamine

CARDIAC muscle- increases myocardial activity & increased HR -AV node conduction

-Smooth muscles in blood vessels, bronchi in the periphery -Stimulation leads to vasodilation/bronchodilation!!!! -Increased muscle and liver breakdown of glycogen and increased release of Glucagon from the alpha cells in the pancreas

Atenolol

Propranolol

metoprolol

OLOL

Lopressor HCT

MOA: stimulate (agonise) CNSs neg feedback mechanism @ alpha 2 receptors (vasomotor center) => inhibits release of norepinephrine (NE) => decreased sympathetic tone Drugs: CLONIDINE; METHYLDOPA TX: resistant HTN S/E: hypotension, headache!