Autonomic Drugs Flashcards
acebutolol
B-1 selective beta blocker: partial agonist
membrane stabilizing: block fast Na channels
SE: tachycardia and HTN
atenolol
B-1 selective beta blocker
betaxolol
B-1 selective beta blocker
Ca block
mod. long T1/2
lipid soluble
carvedilol
non-selective alpha and B blocker
Ca block, antioxidant
lipid soluble
membrane stabilizing: block fast Na channel
esmolol
B-1 selective beta blocker
short T1/2
labetalol
non-selective alpha and B blocker
use: HTN in pregnancy
metoprolol
B-1 selective beta blocker
lipid soluble
nadolol
non-selective beta blocker
long T1/2
nebivolol
B-1 blocker + B3 stimulation leading to NO synthase
antioxidant
long T1/2
pindolol
non-selective beta blocker: partial agonist
SE: tachycardia and HTN
propranolol
non-selective beta blocker
highly lipid soluble
membrane stabilizing: block fast Na channels
SE: seizure and coma
timolol
non-selective beta blocker
mod. lipid solubility
B-1
accelerates SA node, ectopic pacemakers
increases heart contractility and rate
release of renin from juxtaglomerular cells: angiotensin to angiotensin I and II (potent vasoconstrictor)
B-2
relaxes skeletal muscle vessels. glycogenolysis, glucagon release
alpha-1
vasoconstriction of skin and splanchnic vessels
NSAID effect on kidneys
inhibit PGs and AE on renal perfusion by preventing vasoconstrictor actions instigated through renin release
isoproterenol
parenteral or aerosol non-selective beta agonist use: AV/heart block, bradycardia effect: increase CO, decrease diastolic AE: palpitations, tachycardia, headache, flushing
epinephrine
IV, inhale, IM, SC
alpha-1,2 and beta-1,2 agonist
low dose: B, widened pulse pressure
high does: alpha, no widened pulse pressure
use: anaphylaxis, cardiac arrest, hypotension, with local anesthetic
AE: angina, ventricular arrhythmia
CI: nonspecific beta blockers (fatal HTN and cerebral hemorrhage)
effects: increase systolic pressure, decrease diastolic pressure (B2), increase HR (accelerated depol), CO, SV; renin release, decrease renal blood flow
norepinephrine
IV
alpha-1,2 and beta-1 agonist
low dose: cardiac stimulant
high dose: vasoconstrictor
use: hypotension (but with decreased renal perfusion)
effects: decrease CO, increase BP, SV, coronary BF, MAP
AE: necrosis, decreased blood flow to organs, HTN
use: increase BP, arrhythmia
Class II anti-arrhythmics
Beta blockers that also block fast Na channels
intrinsic sympathomimetic activity
partial agonist B blockers
can prevent profound bradycardia or neg. entropy in a resting heart
DON’T use in secondary prevent MI
inverse agonists
bind to inactive from of receptor and shift the conformational equilibrium in to the inactive state
in systems not constitutively active behave like competitive antagonists
Use of B blockers
HTN (block renin and inhibition of presynaptic B receptors)
ischemic heart disease
atrial flutter and fibrillation arrhythmias (increase AV node refractory period)
CHF
Non-cardiac: tremor, thyrotoxicosis, anxiety, migraine prophylaxis, esophageal varicies prophylaxis (nonspecific), glaucoma
B blocker AE
taper to discontinue to avoid rebound effect
bradycardia, bradyarrhythmia, hypotension, hypoglycemia
bronchospasm and dyslipidemia (increase TG and decrease HDL)- less likely with B-1 selective or partial agonist
CNS depression and vivid dreams (lipophilic)
CI: CV or pulmonary disease patient at increased risk of lethal outcome, diabetics (mask tachycardia that is a sign for insulin-induced hypoglycemia)
Tx of beta blocker overdose
glucagon or high dose insulin/glucose
can’t use B agonist because receptors are blocked
sotalol
B blocker and K blocker
SE: prolong QT, torsade de pointes, ventricular fibrillation