Pharm- Volatile Anesthesia

Front 1

Stage of analgesia

Back 1

Patient experiences analgesia. Later amnesia.

Front 2

Stage of excitement

Back 2

patient appears to be dilerious, amnesic, and irregular respiration.

Front 3

Stage of surgical anesthesia

Back 3

Apnea, analgesia, hemodynamic depression. Generally you can get hypothermia and emesis.

Front 4

Stage of medullary depression

Back 4

Circulatory and respiratory depression.

Front 5

What are characteristics of ideal drug.

Back 5

Loss of consciousness smoothly and rapidly. Prompt recovery after withdrawal. Wide margin of safety.

Front 6

When GABA binds to the GABA receptor, what is the result.

Back 6

The receptor opens and chloride passes through allowing for inhibition to take place.

Front 7

Minimal anasthetic concentration (MAC)

Back 7

Minimal alveolar concentration at 1 a.t.m. that produces immobility of 50% of subjects exposed to noxious stimulus.

Front 8

How can we decrease MAC

Back 8

Additive drug like Nitrous oxide, age, hypertension, hypercarbia, alcohol intoxication, sympathetic decrease

Front 9

How is MAC increased.

Back 9

Young age (6 months highest). Chronic alcohol abuse, cocaine influence.

Front 10

What are the three variables to remember during uptake and distribution of volatile anesthetics

Back 10

Solubility. Cardiac output. Alveolar to venous partial pressure difference. If any go up, you get higher uptake. The more lipid soluble it is though, the slower brain effects will take place. That's because it has a wider distribution in the body and can't get to the brain as quick.

Front 11

With the development of new anesthetics, what has happened to the metabolism and solubility of the drugs?

Back 11

They have both gone down. Halothane is one of the older drugs with around 40% metabolism going down to Desflurane being the new drug with almost no metabolism by the liver.

Front 12

What is the relationship between solubility and recovery time.

Back 12

The more soluble the longer the recovery time.

Front 13

Halothane

Back 13

Depress CV function by being directly cardio-depressive. Lowers HR. Reduce myocardial oxygen consumption and act against myocardial reperfusion injury.

Front 14

Enflurane

Back 14

Direct cardio depressive. No HR effect. Reduce myocardial oxygen consumption and act against myocardial reperfusion injury. May cause spike and wave pattern and mild generalized muscle twitching at high doses.

Front 15

Sevoflurane

Back 15

Depress CV function by reduction in systemic vascular resistance. No HR effect. Reduce myocardial oxygen consumption and act against myocardial reperfusion injury.

Front 16

Desflurane

Back 16

Depress CV function by reduction in systemic vascular resistance. Increase HR. Reduce myocardial oxygen consumption and act against myocardial reperfusion injury.

Front 17

Isoflurane

Back 17

Depress CV function by reduction in systemic vascular resistance. Increase HR. Reduce myocardial oxygen consumption and act against myocardial reperfusion injury. Coronary steal-phenomenon which is dilation of only healthy artery in CHD patients. This is bad.

Front 18

Volatile anesthetics effect on respiratory system.

Back 18

Increase the apneic threshold and decrease hypoxic drive. Depress mucociliary function in the airway )atelectasis and postop infections), bronchdilatory properties (good). No effect on hypoxic reflex of vessels in lung.

Front 19

Volatile effect on kidneys

Back 19

May reduce RBF and GFR. Impair autoregulation of renal blood flow.

Front 20

Volatile effects on liver.

Back 20

Reductino of blood flow.

Front 21

Volatile effects on brain.

Back 21

Reduction in metabolic rate of brain. Increase in blod flow because of reduction in Cerebral vascular resistance. Different from what you would think. Nitrous oxide has analgesic and amnestic affects.

Front 22

Halothane-hepatitis

Back 22

Metabolite of halothane is trifluoroacetyl chloride binds to hepatocytes which can cause inflammatory response. Next metabolite is trifluoracetic acid (TFAA)

Front 23

Sevoflurane metabolism effects

Back 23

During CO2 absorption with sevoflurane you get compund A which is a major degradation product that can cause nephrotoxicity.

Front 24

Fluoride induced nephrotoxicity

Back 24

Sevoflurane is biggest culprit. has seven fluoride atoms. They build up over time and cause damage.

Front 25

What potentially lethal substance is produced by anesthetic metabolism.

Back 25

CO. They interact with strong bases in the CO2 absorbents.

Front 26

Malignant hyperthermia

Back 26

Hypercarbia, sinus tachycardia, masseter spasm. Temperature abnormalities Respiratory acidosis and muscular abnormalities. All can cause this. Succinylcholine can trigger as well as stress and temp.

Front 27

How does malignant hyperthermia occur.

Back 27

Dihydropyridine receptor on transverse tubule couples the ryanodine receptor on SR. Ryanodine receptor opens to let Ca flow into myoplasm allowing contraction. Mutation on ryanodine receptor can get uncontrolled flow of Ca with constant contraction and all of the other symptoms.

Front 28

How would you treat MH

Back 28

Discontinue triggering agents and give 100% oxygen. Then give dantrolene.