Pharmacology Flashcards

1
Q

volatile agents - arrhythmias

A

sevo > des = iso

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2
Q

volatile agents - coronary steal

A
  • dilates healthy coronary vessels which takes blood away from the diseased vessels which were already dilated
  • iso
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3
Q

volatile agents - systemic vasculature

A

-reduces resistance by activating endothelial nitrous oxide synthase which releases nitrous oxide

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4
Q

volatile agents - pulmonary blood flow

A
  • NO and des increase pulmonary vasculature resistance

- iso inhibits hypoxic pulmonary vasoconstriction

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5
Q

desflurane - rule of 24

A

-take des % times flow

>24 = sympathetic response and tachycardia
<24 = hypotension
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6
Q

volatile agents - avoid in cardiac surgery

A
  • des

- NO

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7
Q

volatile agents - baroreceptor reflex

A

-suppresses at all parts (afferent, control center, efferent)

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8
Q

volatile agents - anesthetic pre-conditioning

A
  • protective mechanism to reduce the size of infarcts
  • acts indirectly
  • two times: 1-3 hrs, 2-3 days
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9
Q

volatile agents - cardiac effects

A
  • 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
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10
Q

intravenous agents - preconditioning

A
  • do not offer benefits

- ketamine may block the body’s innate response

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11
Q

Propofol

A
  • negative inotrope: blocks L-type Ca channels
  • antioxidant
  • affects are more pronounced in patients with high sympathetic tone (shock, CHF)
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12
Q

Midazolam

A
  • 0.05-0.2 mg/kg

- does not provide analgesia, need to combine with Fentanyl or Ketamine

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13
Q

Etomidate

A
  • cardiostatic

- may see changes in patient’s with valvular heart disease

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14
Q

Ketamine

A

-dual affect in myocardium: positive inotrope and impairs sarcoplasmic reticulum function

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15
Q

Dexmedetomidine

A

-bolus can produce profound hypotension: give over 10 minutes

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16
Q

opioid receptors

A
  • 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
17
Q

opioid - cardiac affects

A
  • reduce sympathetic outflow
  • bradycardia (except Demerol which produces tachycardia)
  • promotes ischemic preconditioning
  • negative inotropic (need high doses, so clinically irrelevant)
18
Q

drugs for ischemia - do what? newer drugs do what?

A
  • alter oxygen demand or oxygen supply

- new drugs increase the efficiency of oxygen utilization

19
Q

NO - how is it made

A

-breaking down arginine by the enzyme nitric oxide synthase (NOS) into citrulline and NO

20
Q

NO - where is it stored

A

-NO is not stored, has to be made when it is needed

21
Q

NO - effects; low and high

A
  • low doses: venous dilation that reaches a ceiling

- high doses: arterial dilation, preferentially dilates coronary arteries

22
Q

NO donors - mechanism of action

A

-requires sulfhydryl groups that can become depleted leading to tolerance, giving the patient N-acetylcysteine (Mucinex) stops the deficiency

23
Q

NTG - drug interactions

A
  • causes resistance to heparin

- avoid phosphodiesterase 5 inhibits

24
Q

NO - mechanism of action

A
  • guanylyl cyclase
  • GTP
  • cyclic-GMP
  • cGMP-dependent protein kinase
  • lowers Ca
  • smooth muscle relaxation