Flashcards in Antihypertensives (slides) Deck (42):
pre htn. values
stage 1 htn. values
stage 2 htn. values
essential htn. is
idiopathic and is 90% of all htn.
secondary htn. is caused by a specific
etiology. 10% of all htn.
specific htn. etiologies.
coarctation of the aorta, pregnancy (primary htn.) kidney disease, hyperthyroidism, cushing syndrome (hyper adrenal)
hyper secretion of ACTH
natural bp control
arterioles, venules, heart, renin/angiotensin
external bp control
the pump , anesthetic depth, drugs
anti hypertensive work to alter bp by
decreasing CO or decreasing SVR
CO SVR are generally controlled by
SNS and baroreceptor feedback, or renin/angiotensin system
first line Rx for HTN.
110% OF NORMAL BV can cause
profound htn. in patients with stiff arteries. while 95% can mean normotensive
diuretics are superior for treatment in
b blocker decrease bp by
decreasing CO, SNS TONE, RENAL RENIN RELEASE
angiotensin receptor blockers
beta 1 selective are being
used more and more because of less side effects
nebivolol b1 selective and potent vasodilator.
results of ace inhibitors
decrease sym. activity, aldosterone secretion, tubular nacl/water reabsrorption, k excretion, vasocontriction, adh secretion
rate limiting factor of ace inhibitors
the inhibition of bradykinin degradation. vasodilator but causes problems
commonly used as a first line drug post-MI for HTN
ace inhibitors cannot be used
in pregnant women
problems from bradykinin from ace inhibitors
dry heaving because they get caught in lungs
ARBs advantage over ACE inhibitors
don't cause bradykinin release. fewer respiratory problems
why ARBs more effective then ACE
ore effective than ACE-Inhibitors in blocking Angiotensin since there are other chemicals that also convert Angiotensin-I into Angiotensin-II (understand?)
A2 AGONIST WORK BY
decrease sympathetic firing from CNS, decrease vascular tone, used with other drugs because of sedative side effect
(catapres,duraclon) dilates peripheral vessels but not renal arteries. useful in HTN. complicated with renal disease
like clonidine but less tranplacental passage
#1 to control bp on bypass
more anesthetized the
lower the bp
when giving drugs on bypass its different because
there is no cardiac reflex, urgent, reversal agents
apresoline. arterial and arteriole effect > venous effect. causes endothelial cell to releases NO (vasodilator muscle relaxant) can be used in pregnant girls
• Used for treatment of angina for > 100 years! • At lower doses venous dilation>arterial • At higher doses arterial dilation>venous
forms of NTG
NTG tablets, Nitro Bid ointment, translucent NITREK patch,
NTG in body
• Converted to nitric oxide by mitochondrial enzymes.
• Commonly used as a bolus (what’s this?) or IV drip on CPB to treat “HTN”.
• Decreases B.P., pulmonary capillary wedge pressure, and SVR.
• decreases myocardial O2 demand during ischemia while leaving contractility unaffected.
two ways to blow air out of coronaries
changes in EKG indicates injury or MI. half of surgeons will want to increase BP. some will give NTG to dilate
NIPRIDE OR NITROPRESS. *Potent arterial & capacitance dilator.
...so it decreases both preload and afterload (explain) which helps increase C.O. in patients with heart failure.
nitroprusside must be
*Very commonly used to control BP on CPB (both bolus and IV drip) Breaks down in the blood stream into nitric oxide...
• and cyanide
nitroprusside half life
• Although nitroprusside has a half-life of 1-2 minutes...
• It’s toxic metabolite thiocyanate has a half- life of many days. babies susceptible
***Normal adult dosage is 0.5-10.0 μg/kg/min (peds receive the low end of this dose
DO NOT give at higher dosages for more than ten minutes or toxicity can result!!!
*Cyanide “shuts down” cellular metabolism. Why would this be problematic on bypass??
you can poison a patient because you are flying blind on bypass. because if you keep giving it and no decrease in BP