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 âhydrostatic pressureâ (CHP)=
35-18mmHg -declines throughout the capillary bed
Venous pressure=
18mmHg
RA pressure=
5mmHg
what SBP is considered hypertension
135
3 types of hypertension
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 âMalignant HTNâ = 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:
loop diuretics
thiazides
potassium sparing
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:
Vascular selective: smooth muscle Nifedipine (aldalat), Amlodipine (norvasc)
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!