Hypertension

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commonly used veins for IV tx:

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1

commonly used veins for IV tx:

External jugular, median cubital, median antebrachial ulnar

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2

What is the most common form of cardiovascular disease

Hypertension

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3

BMR=

10 cal/lb

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4

blood pressure=

perfusion

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5

3 elements of BP

Blood vol Peripheral resistance/diameter of arterioles cardiac output

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6

how will your body try to correct high bp

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

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7

normal MAP

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

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8

Co=

SVx HR normal ejection fraction 70%

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9

CPP=

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

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10

normal ICP

5-15 mmHg

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11

arterial pressures at aorta=

SBP

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12

capillary pressures @ arteriole=

35mmHg

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13

Capillary ‘hydrostatic pressure’ (CHP)=

35-18mmHg -declines throughout the capillary bed

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14

Venous pressure=

18mmHg

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15

RA pressure=

5mmHg

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16

what SBP is considered hypertension

135

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17

3 types of hypertension

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

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18

Essential HTN

-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

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19

How does age impact HTN

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

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20

orthostatic hypotension

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

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21

Who is at risk for orthostatic hypotension

Elderly dehydrated or fluid restricted patients antihypertensive medication patients

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22

Secondary HTN

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

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23

Gestational HTN (preeclampsia)

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

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24

TX for gestational HTN

sodium restriction, antihypertensive meds

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25

sudden on set HTN

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

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26

How does malignant HTN effect the body

-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

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27

what drugs and drug class tx for ER malignant HTN

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

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28

what synthesizes Nitric Oxide?

Arginine

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29

HTN tx med classes

-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

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30

Diuretics=

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

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31

S/E Diuretics

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

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32

Loop Diuretics

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)

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33

Thiazide Diuretics

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

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34

Potassium sparing diuretics AKA aldosterone antagonists

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)

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35

what drug is produced when combing Thiazide & K+ sparing combo?

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

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36

Osmotic diuretics

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

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37

Normal mechanism of Vasoconstriction

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

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38

Angiotensin converting enzyme inhibitors aka ACE inhibitors

-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

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39

Angiotensin II receptor blockers (ARBs)

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

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40

what drug is produced when combing Thiazide diuretic + ARB?

Hyzaar, Cosart

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41

Calcium channel blockers

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

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42

2 vascular selective Calcium channel blockers DIPINE

Nifedipine (Alalat), Amlodipine (Norvasc)

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43

2 cardio selective calcium channel blockers

verapamil (Isoptin), Diltiazem (Cardizem)

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44

overall how do calcium channel blockers effect the heart?

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

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45

ex of a herbal calcium channel antagonist

Ginseng -therapeutic dose: 20-30mg/day

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46

what body parts are only innervated by SNS

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

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47

Adrenergic antagonists aka blockers

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

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48

Alpha 1 receptors

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

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49

Alpha 2 receptors

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

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50

what antagonist drug binds to just alpha 1

Prazosin

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51

what antagonist drugs binds to alpha 1 + 2

Phentolamine

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52

beta 1 receptors

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

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53

Beta 2 receptors

-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

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54

What antagonist drug binds just to beta 1

Atenolol

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55

What antagonist drug binds to Beta 1 + 2

Propranolol

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56

What antagonist drug binds to beta 1 and in high doses beta 2

metoprolol

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57

Beta blockers end in

OLOL

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58

What drug will be produced when you combine diuretic thiazide with adrenergic antagonist

Lopressor HCT

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59

Centrally acting alpha-2 adrenergic agonists

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!

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