Pharmacology Flashcards
volatile agents - arrhythmias
sevo > des = iso
volatile agents - coronary steal
- dilates healthy coronary vessels which takes blood away from the diseased vessels which were already dilated
- iso
volatile agents - systemic vasculature
-reduces resistance by activating endothelial nitrous oxide synthase which releases nitrous oxide
volatile agents - pulmonary blood flow
- NO and des increase pulmonary vasculature resistance
- iso inhibits hypoxic pulmonary vasoconstriction
desflurane - rule of 24
-take des % times flow
>24 = sympathetic response and tachycardia <24 = hypotension
volatile agents - avoid in cardiac surgery
- des
- NO
volatile agents - baroreceptor reflex
-suppresses at all parts (afferent, control center, efferent)
volatile agents - anesthetic pre-conditioning
- protective mechanism to reduce the size of infarcts
- acts indirectly
- two times: 1-3 hrs, 2-3 days
volatile agents - cardiac effects
- dose-dependent cardiac depression which is amplified in diseased tissue
- suppress L-type Ca channels in sarcoplasmic reticulum which prolongs isovolumetric relaxation and decreases contractility
- maintain CO, effects due to reduction in SVR
intravenous agents - preconditioning
- do not offer benefits
- ketamine may block the body’s innate response
Propofol
- negative inotrope: blocks L-type Ca channels
- antioxidant
- affects are more pronounced in patients with high sympathetic tone (shock, CHF)
Midazolam
- 0.05-0.2 mg/kg
- does not provide analgesia, need to combine with Fentanyl or Ketamine
Etomidate
- cardiostatic
- may see changes in patient’s with valvular heart disease
Ketamine
-dual affect in myocardium: positive inotrope and impairs sarcoplasmic reticulum function
Dexmedetomidine
-bolus can produce profound hypotension: give over 10 minutes
opioid receptors
- mu, delta, kappa
- inhibit G-coupled protein receptors, closing N-type, voltage-gated Ca channels and open CA dependent inwardly rectifying K channels resulting in hyperpolarization
opioid - cardiac affects
- reduce sympathetic outflow
- bradycardia (except Demerol which produces tachycardia)
- promotes ischemic preconditioning
- negative inotropic (need high doses, so clinically irrelevant)
drugs for ischemia - do what? newer drugs do what?
- alter oxygen demand or oxygen supply
- new drugs increase the efficiency of oxygen utilization
NO - how is it made
-breaking down arginine by the enzyme nitric oxide synthase (NOS) into citrulline and NO
NO - where is it stored
-NO is not stored, has to be made when it is needed
NO - effects; low and high
- low doses: venous dilation that reaches a ceiling
- high doses: arterial dilation, preferentially dilates coronary arteries
NO donors - mechanism of action
-requires sulfhydryl groups that can become depleted leading to tolerance, giving the patient N-acetylcysteine (Mucinex) stops the deficiency
NTG - drug interactions
- causes resistance to heparin
- avoid phosphodiesterase 5 inhibits
NO - mechanism of action
- guanylyl cyclase
- GTP
- cyclic-GMP
- cGMP-dependent protein kinase
- lowers Ca
- smooth muscle relaxation