Pharmacology Flashcards
(211 cards)
Heparin
[half-life elimination time]
1 -2 hours
2-Chloroprocaine
[rapid onset]
able to use high concentrations due to its low systemic toxicitiy
- unlike normally, does not depend on PKa, which is about 9 and thus more pronated (less likely to cross cell membrane) at physiologic pH
5-HT3
[receptor]
serotonin on platelets and GI tract
Adrenergic Agonists
[which 2 have the greatest increase on CO]
isoproterenol and dobutamien
Adrengergic Agonists
[which 2 cause a large decrease in renal blood flow]
phenylephrine and norepinephrine
Agents
[effect on SA node]
depresses SA node automaticity
- only modest effects on AV node; explains the occurrence of junctional tachycardia when administering an anticholinergic during inhalation anesthesia
Agents
[effects on blood pressure]
decrease
- Des, Sevo, and Iso decrease blood pressure due to a decrease in systemic vascular resistance
- halothane depression is due to decreases in myocardial contractility and cardiac output
Agents
[effects on cardiac output]
minimal decrease
Agents
[effects on CVP]
slight increase except for Sevoflurane
- However, around 1.5 MAC, sevo will show an increase in CVP, then drop again
Agents
[effects on heart rate]
increase heart rate
- Sevoflurane only increases HR when MAC > 1.5
- halothane has no effect on heart rate
Agents
[effects on minute ventilation]
decrease
- increase respiratory rate while decreasing tidal volume
- except for Isoflurane
Agents
[effects on pulmonary vascular resistance]
little to no effect
Agents
[effects on systemic vascular resistance]
decrease SVR
Agents
[ventilatory response]
decrease response to incrasing PaCO2
- Desflurane above 1 MAC has the greatest effect
Agents
[best for ablative procedures]
Sevoflurane
- no effect on AV conduction
- Isoflurane increases the refractoriness of accessory pathways
Alpha Blockers
[examples]
prazosin
phentolamine
phenoxybenzamine
Alpha-1 Agonists
[cardiovascular effects]
vasoconstriction
leading to an increase in peripheral vascular resistance, left ventricular afterload, and atrial blood pressure
Alpha-1 Agonist
[mechanism of action]
increase intracellular [Ca2+] leading to contraction of smooth muscles
Alpha-2 Agonists
[cardiovascular effects]
reduction of sympathetic outflow
peripheral vasodilation and lower blood pressure
Alpha-2 Agonists
[mechanism of action]
inhibits adenylate cyclase activity
- decreases the entry of calcium ions into neuronal terminal, which limits exit of norepinephrine
anesthetic agent with low potency and poor blood solubility
Desflurane
(and N2O)
Anti-Arrhythmic Agents
[Class I - type]
Na+ channel blocker
- blocks voltage-gated Na+ channels and decreases the slope of phase 0 (Vmax)
Anti-Arrhytmic Agents
[Class III - examples]
amiodarone and sotalol