Inhaled And Local Anesthetics

Front 1

what is anesthesia (inhaled)?
how start? how end?

Back 1

a reversible absence of sensation from a painful stimulus and have amnesia
start with an agent that causes unconsciousness
end with an opiate/painkiller

Front 2

Chemically, what are their structures like?

Back 2

alkane derivaties that are small, non-polar and hydrophobic

Front 3

What is the difference in uptake between an insoluble anesthetic (NO) vs a soluble one (isoflourane)? Discuss equilibrium dynamic in a soluble gas? Also, depends on rate of ventilation!!!

Back 3

more rapid uptake for NO (insoluble gas)
Equilibrium- gradient between lungs and blood stream is established and gas flows from lung to bloodstream much quicker if none gets into blood (insoluble)..think LeChatlier's principle and that areas with greatest cardiac output get hit first (brain/heart)

Front 4

What is the minimum alveolar concentration (MAC)of an inhaled anesthetic?

Back 4

analagous to the EC50. The concentration whereby 50% of patients WONT make a movement in response to a surgical incision.

Front 5

Elimination: where does it take longest for the inhaled anesthetic to clear?

Back 5

From fat and other low perfused areas; remember, route of excretion is in exhalation

Front 6

What occurs first; lost of consciousness or [] needed to make a surgical incision? What happens to BP, HR, and ventilation rate under anesthesia?

Back 6

loss of consciousness happens right away, but need to wait until surgery can start.
CNS depressant- get decreased BP, HR, and peripheral resistance. Also, get decreased ventilation rate. Hence, keep oxygenated during procedures.

Front 7

Are anesthetics neurotoxic? Carcinogenic? What is one major side effect that you must watch for with inhaled anesthetics?

Back 7

Isoflurane may be neurotoxic
NOT carcinogenic/mutagenic
Malignant Hyperpyrexia- rapid temp increase, hr increase, muscles get rigid

Front 8

Mechanism of local anesthetics?

Back 8

reversible blockage of local nerve conduction by blocking Na+ permeability and keeping it in inactive state

Front 9

Are local anesthetics weak acids or weak bases? Lipophilic or hydrophilic components? Which stereoisomer is more cardiotoxic; R or S?

Back 9

weak bases with both lipophilic and hydrophilic components
R is 40X more cardiotoxic

Front 10

Amides vs Ester..how tell name apart? (# of I's) Which has short T 1/2 and which has long (hence toxicity)? Where is each metabolized? which contains the allergin PABA?
How do both travel in blood?

Back 10

Amide = 2 I's
Ester = 1 I's
Esters- very short half lives and contain PABA- highly allergic, metabolized in plasma
Amides- long half lives, hence more toxic!, in liver
Both travel on albumin in the blood.

Front 11

What determines the potency, duration, onset of local anesthetics, and CNS toxicity? What to do in CNS toxic situation?

Back 11

potency- the more lipid sol, the more potent
Duration- the more lipid soluble, the longer it will last
Onset- the closer the pKa is to the PH, the quicker the onset
CNS toxicity- the more lipid soluble, the more toxic it will be

Front 12

Local anesthetics and cardiovascular toxicity? How treat CV toxicity? Effects on vascular smooth muscle (except cocaine)?

Back 12

decreased ionotropic effect, decreased contractility, and decreased conduction velocity

Make more lipid environment- will become soluble- IV lipids

Vasodilates, except cocaine vasoconstricts

Front 13

What are the symptoms of methemoglobinemia (i.e. when Hb exists in ferric form and can't bind O2?

Back 13

become blue (cyanotic) and your tongue goes numb