Review Of Hemodynamics, Raas, Calcium Channel Blockers, Vasodilators, Drugs For Htn

Front 1

components of the circulatory system

Back 1

-arteries transport blood to tissues under high pressure
-arterioles control valves that regulate local blood flow
-capillaries are sites for exchange of oxygen, fluid, nutrients, hormones, wastes, etc.
-venules collect blood from capillaries
-veins transport blood back to the heart

Front 2

mechanisms that ensure venous return

Back 2

1) negative pressure in right atrium helps "suck" blood towards the heart
2) smooth muscle constriction in venous wall increases venous pressure
3) most important--combination of venous valves and skeletal muscle contraction creates a "VENOUS PUMP"

Front 3

primary (essential) hypertension

Back 3

-no identifiable cause
-chronic and progressive
-treated but not cured

Front 4

secondary hypertension

Back 4

-identifiable cause
-possible to treat the cause directly
-some individuals can actually be cured

Front 5

consequences of HTN

Back 5

-heart disease such as heart failure, MI, and angina pectoris
-kidney disease
-stroke

Front 6

antiHTNsive drug therapy

Back 6

-dosage should start low and gradually increase
-lack of adherence is major cause of treatment failure
-usually no symptoms
-slow progression
-treatment is complex and
sometimes expensive

Front 7

METHYLDOPA

Back 7

-drug of choice for pregnant women
-HTN most common complication of pregnancy
-chronic hypertension
-preeclampsia and eclampsia

Front 8

RAAS drugs

Back 8

-angiotensin-converting enzyme inhibitors (ACE inhibitors)
-angiotensin II receptor blockers (ARBs)
-aldosterone antagonists

Front 9

ACEI mechanism of action

Back 9

-reduces levels of angiotensin II by inhibition of ACE
-increases level of bradykinin through inhibition of kinase II
-vasodilation and blood volume reduction through effects on kidneys

Front 10

ACEI pharmacokinetics

Back 10

-almost always taken orally (except for Enalaprilat)
-almost all can be administered with food (except for captopril and moexipril)
-administered once or twice a day (except for captopril, which is bid or tid)
-undergo conversion to active form in small intestine and liver (except for lisinopril)
-all excreted renally

Front 11

ACEI indications

Back 11

-HTN
-heart failure
-MI
-diabetic neuropathy

Front 12

RAMIPRIL (Altace)

Back 12

ONLY ACEI approved for prevention of MI, stroke, and death in high-risk cardiac patients

Front 13

ACEI side effects

Back 13

-"first dose hypotension"
-COUGH
-hyperkalemia
-renal failure
-angioedema (very rare)
-fetal injury (2nd and 3rd trimesters)

Front 14

ACEI drug interactions

Back 14

-diuretics
-antihypertensives
-drugs that raise potassium
-lithium
-NSAIDs

Front 15

angiotensin II receptor blockers (ARBs)

Back 15

-decrease influence of angiotensin II by blocking its action, not its production (like ACEIs)
-DO NOT cause cough or hyperkalemia
-not interchangeable with ACEIs
-usually given to patients who don't tolerate ACEIs

Front 16

ARB indications and mechanism of action

Back 16

indications:
-HTN
-MI
-diabetic neuropathy
-heart failure
mech of axn:
vasodilation due to angiotensin II inhibition, less aldosterone so more excretion of water and sodium

Front 17

ARB pharmacokinetics

Back 17

all taken orally

Front 18

LOSARTAN (Cozaar)

Back 18

stroke prevention

Front 19

ARB side effects and drug interactions

Back 19

side effects:
-angioedema
-fetal harm
-renal failure
drug interactions:
-antihypertensives

Front 20

EPLERENONE

Back 20

-aldosterone antagonist
-approved in 2002
-indications: HTN and heart failure
-administered orally
-generally well-tolerated (greatest risk is hyperkalemia)

Front 21

EPLERENONE drug interactions

Back 21

-erythromycin
-verapamil
-fluconazole
-ketaconazole

Front 22

SPIRONOLACTONE

Back 22

-much older than eplerenone
-binds with steroid hormone receptor sites--interferes with hormones

Front 23

SPIRONOLACTONE side effects

Back 23

-HYPERKALEMIA
-gynecomastia
-menstrual irregularities
-impotence
-hirsutism
-deepening of voice

Front 24

sympatholytics (antiadrenergic drugs)

Back 24

suppress the influence of the sympathetic nervous system on heart, blood vessels, & other structures

Front 25

categories of sympatholytics

Back 25

1) beta-adrenergic blockers
2) alpha1 blockers
3) alpha/beta blockers
4) centrally-acting alpha2 agonists
5) adrenergic neuron blockers

Front 26

beta-adrenergic blockers

Back 26

-less effective in blacks
-most widely-used antihypertensives
-exact mechanism of action is unknown

Front 27

beta-adrenergic blocker mechanism of action

Back 27

-block cardiac beta1 receptors, which causes decreased heart rate and contractility
-suppress reflex tachycardia caused by vasodilators
-block beta1 receptors in kidneys so less renin is produced--inhibits RAAS
-reduce peripheral vascular resistance

Front 28

alpha1 blockers

Back 28

-not first-line
-block vascular alpha1 receptors, preventing sympathetically-mediated vasoconstriction
-e.g. terazosin, doxazosin,
-orthostatic hypotension

Front 29

alpha/beta blockers

Back 29

-e.g. carvedilol, labetalol
-promote dilation of arteries and veins; decrease heart rate and contractility
-can exacerbate asthma and postural hypotension

Front 30

centrally-acting alpha2 agonists

Back 30

-act in brainstem to reduce sympathetic outflow to heart and blood vessels
-cause vasodilation and reduced cardiac output
-SEs: dry mouth and sedation

Front 31

types of centrally-acting alpha2 agonists

Back 31

-methyldopa (pregnancy)
-clonidine, which can cause rebound hypertension if abruptly discontinued

Front 32

adrenergic neuron blockers

Back 32

inhibit NE release and decrease sympathetic stimulation of heart and blood vessels
-guanethidine and guanadrel can cause severe orthostatic hypotension
-reserpine can cause depression

Front 33

calcium channel blockers (CCBs)

Back 33

-prevent calcium ions from entering cells, preventing contraction
-help regulate myocardium, SA and AV nodes, beta1 adrenergic receptors
-AKA calcium antagonists, slow channel blockers

Front 34

VERAPAMIL and DILTIAZEM

Back 34

(class IV)
BLOCK CALCIUM CHANNELS AT:
1) peripheral arterioles - dilation and reduction in arterial pressure
2) cardiac arteries and arterioles - increased coronary perfusion
3) SA node - negative chronotropic
4) AV node - decreased AV node conduction
5) myocardium - negative inotropic

Front 35

VERAPAMIL and DILTIAZEM pharmacokinetics

Back 35

-administered orally or IV
-well absorbed orally, but hepatic metabolism preserves only 20% of dose
-effects begin in 30 minutes and peak in 5 hours
-elimination is primarily hepatic

Front 36

VERAPAMIL and DILTIAZEM indications

Back 36

(class IV)
-angina pectoris
-essential HTN
-supraventricular dysrhythmias such as afib, atrial flutter, and SVT

Front 37

VERAPAMIL and DILTIAZEM side effects, drug interactions, and toxicity

Back 37

(class IV)
side effects: constipation (verapamil) and cardiac effects, but generally well-tolerated
drug interactions: digoxin, beta-adrenergic _______
toxicity: sever hypotension
treatment of toxicity: IV calcium gluconate and IV norepinephrine

Front 38

NIFEDIPINE

Back 38

-very little blockage of calcium channels
-vasodilation and reflex cardiac stimulation
-angina and HTN
-high doses of rapid-acting can be very dangerous

Front 39

NIFEDIPINE side effects, drug interactions, toxicity

Back 39

side effects:
-dizziness
-flushing
-headache
-peripheral edema
-gingival hyperplasia
drug interactions:
-beta adrenergic blockers
toxicity: loses selectivity, so increased doses can affect heart and blood vessels

Front 40

vasodilators

Back 40

-differ from one another based on which blood vessels they act on
-selectivity determines hemodynamic effects

Front 41

vasodilator indications

Back 41

-essential HTN
-hypertensive crisis
-angina pectoris
-heart failure
-MI
-PVD
-pulmonary arterial hypertension
-production of controlled hypotension during surgery

Front 42

adverse effects related to vasodilation

Back 42

-postural hypotension
-reflex tachycardia
-expansion of blood volume

Front 43

HYDRALAZINE (Apresoline) indications and mechanism of action

Back 43

indications:
-essential HTN
-heart failure
-hypertensive crisis
mechanism of action:
-selective dilation of arterioles (exact mech is unknown)

Front 44

HYDRALAZINE (Apresoline) side effects and drug interactions

Back 44

side effects:
-reflex tachycardia
-increased blood volume
-systemic lupus erythematosus-like syndrome
drug interactions: other antihypertensive agents

Front 45

MINOXIDIL (Loniten) indication and mechanism of action

Back 45

indication: severe HTN
mechanism of action: selective dilation of arterioles

Front 46

MINOXIDIL (Loniten) side effects

Back 46

reflex tachycardia
sodium and water retention
hypertrichosis
pericardial effusion

Front 47

SODIUM NITROPRUSSIDE (Nitropress)

Back 47

-causes venous and arteriolar dilation
-fastest-acting antiHTNsive agent for HTNsive emergencies
-given IV for immediate onset
-side effects: excessive hypotension, cyanide poisoning, thiocyanate toxicity

Front 48

DIAZOXIDE (Hyperstat IV) indication and mechanism of action

Back 48

indication: hypertensive emergency
mechanism of action: selective dilation of arterioles

Front 49

DIAZOXIDE (Hyperstat IV) side effects and drug interactions

Back 49

side effects:
-reflex tachycardia
-salt and water retention
-hyperglycemia
-hyperuricemia
drug interactions:
-diuretics
-antihypertensive drugs