Drugs (s/e, dosing, MOA, onset, peak, etc) & some cardiac Flashcards
Trade name for Succinylcholine?
Anectine
Trade name for Mivacurium?
Mivacron
Trade name for Atracurium?
Tracurium
Trade name for Cisatracurium?
Nimbex
Trade name for Vecuronium?
Norcuron
Trade name for Rocuronium?
Zemuron
Trade name for d-Tubocurarine?
Tubarine
Trade name for Pancuronium?
Pavulon
Name the following (ultrashort, short, intermediate, or long):
1) Succinylcholine
2) Pancuronium
3) Mivacurium
4) Cisatracurium
5) d-Tubocurarine
6) Rocuronium
7) Atracurium
8) Vecuronium
1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate
Name the onset time for the following:
1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate
1) Succinylcholine: 0.5-1.5 min
2) Pancuronium: 2-4 min
3) Mivacurium: 3-4 min
4) Cisatracurium: 5-7 min
5) d-Tubocurarine: 2-4 min
6) Rocuronium: 1-1.5 min
7) Atracurium: 3-4 min
8) Vecuronium: 3-4 min
Name the duration to 25 % recovery for the following:
1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate
1) Succinylcholine: 6-8 min
2) Pancuronium: 60-120 min
3) Mivacurium: 15-20 min
4) Cisatracurium: 35-45 min
5) d-Tubocurarine: 60-120 min
6) Rocuronium: 30-40 min
7) Atracurium: 35-45 min
8) Vecuronium: 35-45 min
Name the ED95 for the following:
1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate
1) Succinylcholine: 0.30 mg/kg
2) Pancuronium: 0.06 mg/kg
3) Mivacurium: 0.08 mg/kg
4) Cisatracurium: 0.05 mg/kg
5) d-Tubocurarine: 0.50 mg/kg
6) Rocuronium: 0.30 mg/kg
7) Atracurium: 0.20 mg/kg
8) Vecuronium: 0.05 mg/kg
Name the primary route of elimination of the following:
1) Succinylcholine
2) Pancuronium
3) Mivacurium
4) Cisatracurium
5) d-Tubocurarine
6) Rocuronium
7) Atracurium
8) Vecuronium
1) Succinylcholine: metabolism (plasma cholinesterases)
2) Pancuronium: 85% RENAL/ 15% BILIARY
3) Mivacurium: metabolism
4) Cisatracurium: metabolism (HOFFMAN ONLY)–> nonspecific esterases are NOT involved
5) d-Tubocurarine: primary renal, secondary biliary
6) Rocuronium: 80% Biliary/ 20% renal
7) Atracurium: metabolism (2/3 by hydrolysis–> nonspecific esrterases, 1/3 by Hoffman elimination)
8) Vecuronium: 60% BILIARY/ 40% RENAL/ some metabolism
* *the termination of atracurium, cisatricurium, vec, and roc is by redistribution
Place the following NMB’s into the appropriate category:
vec, roc, pancuronium, atracurium, cisatracurium
1) monoquaternary aminosteroids
2) bisquaternary aminosteroids
3) bisquaternary benzylisoquinolines
1) monoquaternary aminosteroids: vec, roc
2) bisquaternary aminosteroids: panc
3) bisquaternary benzylisoquinolines: atrac, cisatra
* *aminosteroids= “curonium”
* *benzylisoquinolines= “curium”
* *ALL are quaternary ammonium compounds
Which NMB’s produce autonomic ganglionic blockade? (2)
d-tubocurarine and metocurine block nicotinic receptors at the autonomic ganglia
Which NMB’s elicit the release of histamine? (5)
sux, mivacurium, atracurium, d-tubocurarine, and metocurarine
Which NMB’s produce bradycardia and why? (1)
succinylcholine mimics the action of acetylcholine and directly stimulates muscarinic receptors of the sinoatrial node
Which NMB’s produce tachycardia and why? (5)
- atracurium, d-tubocurarine, metocurine produce reflex tachycardia
- pancuronium and gallamine competitively antagonize acetylcholine, which are referred to as direct vagolytic, or more specifically antimuscarinic, actions
Which NMB’s produce significant hypotension? (3)
succinylcholine, d-tubocurarine, metocurarine
Which NMB’s produce significant hypertension? (2)
pancuronium and gallamine
The acronym “M-SAC” is my way to remember NMB’s that are primarily eliminated by METABOLISM. What does it stand for?
M- mivacurium S- succinylcholine ** BOTH of the above are by plasma cholinesterase A- atracurium 2/3 hydrolysis, 1/3 Hoffman C- cisatricurium ALL by Hoffman
I am a long acting non-selective alpha adrenergic antagonist used to control blood pressure in patients with pheochromocytoma.
phenoxybenzamine
* another non-selective alpha adrenergic antagonist is phentolamine
I am a selective alpha 2 adrenergic antagonist used to treat impotence.
yohimbine
How is prazosin different from other alpha adrenergic antagonists?
unlike non-selective alpha blockers, prazosin (a selective alpha 1 adrenergic antagonist) lowers BP without increasing release of NE from postganglionic sympathetic nerve terminals b/c it doesn’t block alpha 2
Name one of the primary non-selective beta antagonists, and why it isn’t usually used for with irritable airways.
propanolol–> beta 2 adrenergic receptor blockade can induce bronchoconstriction
I am a competitive antagonist of beta 1 adrenergic receptors. I am also very short acting and am metabolized in the _______ by __________ of the red blood cell.
Esmolol. in the plasma by non-selective esterases of the red blood cells
What are some uses of esmolol?
1) treat intraop SVT
2) treat intraop HTN
3) blunt reflex cardiovascular responses to DL and produce controlled hypotension
What receptors does labetalol competitively antagonize?
alpha 1, beta 1, beta 2
Name 2 uses of labetalol?
1) treat HTN emergencies
2) produce controlled hypotension
* decreases HR, myocardial contractility, and SVR
What is the alpha to beta ratio of the block produced by labetalol?
7:1 beta to alpha (so stronger beta than alpha)
What drugs can be used to treat excess myocardial depression induced by beta antagonists?
1) Atropine (incremental doses of 7mcg/kg)
2) Dobutamine (selective beta 1)
3) Calcium Chloride (250 to 1000mg IV)
4) Glucagon (1-10 mg IV, followed by 5 mg/hr IV)
5) transvenous artificial cardiac pacer
* Isoproterenol not good d\t its beta 1 and beta 2 effects, could cause vasodilation
* Dopamine NOT recommended
Why is Ketamine not normally recommended for use with beta blockers?
b\c it promotes SNS stimulation and with beta blockade it promotes increased SVR–> not able to be compensated by increased myocardial contractility (b\c the heart is beta blocked)–> heart failure may ensue
*same thing can happen with pheochromocytoma if beta blockade is produced prior to alpha blockade
What alpha adrenergic blocker could you use to control HTN during a pheo case?
phentolamine (regitine)
What drugs should you avoid in the asthmatic patient?
1) beta 2 blockers like propanolol and labetalol
2) drugs that stimulate histamine release (trimethaphan, d-tubocurarine, atracurium, and mivacurium)
Order MOST to LEAST on sedation: atropine, scopolamine, robinul.
scopolamine, atropine, glyco
Order MOST to LEAST on antisialogogue: atropine, scopolamine, robinul.
scopolamine, glyco, atropine
Order MOST to LEAST on increased HR: atropine, scopolamine, robinul.
atropine, glyco, scop
Order MOST to LEAST on relax smooth muscle: atropine, scopolamine, robinul.
atropine and glyco, scop
Order MOST to LEAST on mydriasis: atropine, scopolamine, robinul.
scop, atropine, glyco
Order MOST to LEAST on motion sickness prevention: atropine, scopolamine, robinul.
scopolamine, atropine, glyco
What antimuscarinic LEAST crosses the BBB?
glyco, b\c it has a charged quaternary ammonium group (ions DO NOT like to cross lipid membranes)
What is the treatment for anticholinergic syndrome?
physostigmine (an acetylcholinesterase inhibitor) 15-60mcg/kg IV
T/F? Decreased tone of the lower esophageal sphincter is a disadvantageous feature of antimuscarinics.
TRUE
What is the action of milrinone?
well… cAMP is normally cleaned up by phosphodiesterase…… so, milrinone is a PDA blocker–> causing a buildup of cAMP
When administering terbutaline… what receptor does it agonize? Is it metabotropic or ionotropic? Why?
works on beta 2–> terbutaline is a 1st messenger (Gs protein)–> the substrate ATP combines with enzyme adenylyl cyclase to activate 2nd messenger cAMP (the product)–> activates protein kinase–> bronchodilation
When looking at bronchiole smooth muscle, the presence of Ca+ indicates _______.
constricition…. absence of Ca+ = dilation
How does nitric oxide (NO) work?
it is a 1st messenger that crosses the lipid membrane (lipid soluble, so no receptor needed)–> acts with GTP–> cGMP (2nd messenger inside the cell)–> bronchodilation
What is the 2nd messenger of terbutaline in bronchiole smooth muscle?
cAMP
What is the 2nd messenger of nitric oxide in bronchiole smooth muscle?
cGMP
What is the 2nd messenger of atropine and ipratroprium in bronchiole smooth muscle?
IP3 and Ca+; AcH binds to muscarinic receptor–> phospholipase C cuts the head off… that is IP3–> IP3 helps release Ca+–> both are second messengers–> bronchoconstriction
cAMP and cGMP are “cleaned up” by _________.
phosphodiesterase; but different kind called isoform
Name the phosphodiesterase isoform for: cAMP
PDE III
Name the phosphodiesterase isoform for: cGMP
PDE V
What is aminophylline?
a phosphodiesterase inhibitor–> so causes buildup of cAMP–> promote bronchodilation as cAMP accumulates
How does nitroglycerin and nitroprusside (nitric oxide donors) promote bronchodilation?
by increasing the concentration of cGMP
How do atropine and ipratropium (atrovent– an inhaled antimuscarinic) promote bronchodilation?
competitively inhibit muscarinic 3 receptors
What 4 second messengers are at work in bronchial smooth muscle cells?
1) cAMP
2) cGMP
3) IP3
4) Ca+
In bronchial smooth muscle, which first messenger does NOT bing to a cell membrane receptor?
nitric oxide (NO)
Name two common xanthines.
aminophylline and theophylline–> competitively antagonize adenosine receptors
CNS: nervousness, anxiety, n/v
RESP: bronchodilation
Does aminophylline readily cross the placenta?
YES
How do antimuscarinics cause bronchodilation?
atropine & ipratropium (atrovent); they antagonize AcH–> cause bronchodilation because less inositol triphosphate IP3 is produced, so less calcium is available for contractile proteins
What second messenger promotes bronchoconstriction?
Ca+ and IP3
Anti HTN: Name the trade name and action: hydralazine
Apresoline–> arterial vasodilator
Anti HTN: Name the trade name and action: diazoxide
Hyperstat–> arterial dilator (can cause hypoglycemic coma)
Anti HTN: Name the trade name and action: nitroglycerin
venodilator
Anti HTN: Name the trade name and action: nitroprusside
Nipride–> arterial and venous dilator
CCB: Name the trade name and action: verapamil
Calan, Isoptin–> arterial dilator and decreased HR
CCB: Name the trade name and action: diltiazem
arterial dilator and decreased HR
CCB: Name the trade name and action: nifedipine
Procardia–> arterial dilator (causes reflex increase in HR)
ACE INH: Name the trade name and action: captopril
Capoten–> arterial dilator
ACE INH: Name the trade name and action: enalapril
Vasotec–> arterial dilator
PDE INH: Name the trade name and action: inamrinone
Inocor–> block breakdown of cAMP= inc. myocardial contractility= dec. SVR (relaxes vascular smooth muscle)
PDE INH: Name the trade name and action: milrinone
Primacor–> block breakdown of cAMP= inc. myocardial contractility= dec. SVR (relaxes vascular smooth muscle)
What is the action of Adenosine?
it is an endogenous nucleotide occurring in all cells of the body…. can be administered to:
1) slow conduction of impulses through the AV node
2) interrupt reentry pathways through AV node
3) restore NSR in pt’s with paroxysmal SVT, including the associated WPW syndrome
What is the dose of Adenosine?
6-12 mg IV as rapid injection
What is the elimination half time of Adenosine?
< 10 seconds owing to rapid metabolism
“Fast, Full, and Forward” applies to ______.
regurgitation; you want a faster HR so you spend LESS time in systole
What is the mneumonic to remember what will increase or decrease an outflow obstruction?
Old Cats Pee Alot
Obstruction: up down (increased or decreased)
——————————————-
Contractility: up down
Preload: down up
Afterload: down up
Is ephedrine good to give a patient with a valve obstruction?
No! increases HR (you want to maintain)
Is digitalis good to give a patient with a valve obstruction?
No! increases contractility and worsens obstruction
Is increasing PEEP good for a patient with a valve obstruction?
No! decreases venous return= Not good, worsens obstruction
Aortic regurgitation can either be congenital or from ______.
rheumatic fever–> causes valvular problems
Aortic annulus dilation can cause regurgitation. What are causes of aortic annulus dilation?
syphilis, rheumatoid and psoriatic arthritis, ankylosing spondylitis, cystic medial necrosis, annuloaortic ectasia
What happens when there is aortic regurgitation and eccentric LV hypertrophy?
ventricles experience a large increase in volume with a small increase in pressure… left ventricular compliance is large–> fluid backs up into LV and starts to dilate it
Where is the coronary “take-off” located?
right after the aortic arch
Patients with acute aortic regurgitation present with the sudden onset of _______ and _______.
pulmonary edema and HTN typically the 3 things seen are: 1) severe dyspnea 2) hypotension 3) weakness
Chronic aortic regurgitation normally presents as _______. Symptoms are minimal when the regurgitant volume are < _____, and severe if > ______ of SV.
CHF; 60%
Can remembers rule of 1/2’s:
1/2 SV= severe
Chronic aortic regurgitation can be heard as a ______ murmur, best heard at the _______.
diastolic murmur, best heard at the left sternal border (b\c blood is flowing anterograde
* other manifestations: widened pulse pressure, bounding peripheral pulses, mitral regurg
Arterial waveform of a pt with IHSS may be ____.
bifid…. bisferiens pulse
What is the pressor of choice with aortic and mitral regurgitation?
Ephedrine… keep it fast full and forward.. phenylephrine would increase the afterload
Chronic mitral regurgitation is usually d\t _______. (3)
rheumatic fever, incompetent valve, or destruction of mitral valve annulus
What is the rule to remember when comparing the symptomatic progression of mitral regurgitation?
rule of 1/3rds
60= severe
Chronic mitral regurgitation is heard as a ________ murmur, best heard at the _____.
holosystolic murmur best heard at the apex
