Hypertension

commonly used veins for IV tx:

External jugular,
median cubital,
median antebrachial
ulnar

What is the most common form of cardiovascular disease

Hypertension

BMR=

10 cal/lb

blood pressure=

perfusion

3 elements of BP

Blood vol
Peripheral resistance/diameter of arterioles
cardiac output

how will your body try to correct high bp

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

normal MAP

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

Co=

SVx HR
normal ejection fraction 70%

CPP=

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

normal ICP

5-15 mmHg

arterial pressures at aorta=

SBP

capillary pressures @ arteriole=

35mmHg

Capillary ‘hydrostatic pressure’ (CHP)=

35-18mmHg
-declines throughout the capillary bed

Venous pressure=

18mmHg

RA pressure=

5mmHg

what SBP is considered hypertension

>135

3 types of hypertension

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

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

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

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

Who is at risk for orthostatic hypotension

Elderly
dehydrated or fluid restricted patients antihypertensive medication patients

Secondary HTN

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

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

TX for gestational HTN

sodium restriction, antihypertensive meds

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

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

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

what synthesizes Nitric Oxide?

Arginine

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

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

S/E Diuretics

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

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)

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

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)

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

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

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

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

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

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

what drug is produced when combing Thiazide diuretic + ARB?

Hyzaar, Cosart

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

2 vascular selective Calcium channel blockers
DIPINE

Nifedipine (Alalat), Amlodipine (Norvasc)

2 cardio selective calcium channel blockers

verapamil (Isoptin), Diltiazem (Cardizem)

overall how do calcium channel blockers effect the heart?

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

ex of a herbal calcium channel antagonist

Ginseng
-therapeutic dose: 20-30mg/day

what body parts are only innervated by SNS

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

Adrenergic antagonists aka blockers

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

Alpha 1 receptors

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

Alpha 2 receptors

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

what antagonist drug binds to just alpha 1

Prazosin

what antagonist drugs binds to alpha 1 + 2

Phentolamine

beta 1 receptors

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

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

What antagonist drug binds just to beta 1

Atenolol

What antagonist drug binds to Beta 1 + 2

Propranolol

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

metoprolol

Beta blockers end in

OLOL

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

Lopressor HCT

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!