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 Pharmaco kinetics &dynamics of local anesthetics

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كاتب الموضوعرسالة
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عدد الرسائل : 171
العمر : 39
العمل/الترفيه : Anesthesiologist
تاريخ التسجيل : 09/07/2010

مُساهمةموضوع: Pharmaco kinetics &dynamics of local anesthetics   الخميس أبريل 11, 2013 4:20 pm

Pharmaco kinetics &dynamics of local anesthetics:
Absorption and distribution:

Local anesthetic drugs are administered to the areas around the nerves to be blocked which include skin, subcutaneous tissues, intrathecal and epidural spaces.

The distribution of the drug is influenced by the degree of tissue and plasma protein binding of the drug. The more protein bound the agent, the longer the duration of action as free drug is more slowly made available for metabolism
.
Metabolism and excretion:

Ester and amide anesthetics differ in their metabolism
.
Esters (except cocaine) are broken down rapidly by plasma esterases to inactive compounds and consequently have a short half life. Cocaine is hydrolysed in the liver.
Ester metabolite excretion is renal
.
Amides are metabolized hepatically by amidases. This is a slower process, hence their half-life is longer and they can accumulate if given in repeated doses or by infusion. Prilocaine is also metabolized extra-hepatically
.
Effects on organ systems:

A-Neurological

The central nervous system is the site of premonitory signs of overdose in awake patient

Early symptoms are circumoral numbness, tongue paresthesia and dizziness.
Sensory complication may include tinnitus and blurred vision. Excitatory signs (eg, restlessness, agitation, nervousness, paranoia) often precede central nervous system depression (eg, slurred speech, drowsiness, and unconsciousness),muscular twitching heralds the onset of tonic-clonic seizures
.
B-Respiratory

Apnea may result from phrenic and intercostal nerve paralysis or depression of the medullary respiratory center following direct exposure to local anesthetic agents

Local anesthetics relax bronchial smooth muscle. Intravenous lidocaine (1.5 mg/kg) may be effective in blocking the reflex bronchconstriction, sometimes associated with intubation

C-Cardiovascular

In general local anestheticsdepress myocardial automaticity and decrease the duration of refractory period. These effects result from direct cardiac muscle membrane changes (i.e., cardiac sodium channel blockade) and inhibition of the autonomic nervous system

Major cardiovascular toxicity usually requires about three times the concentration of blood that produce seizures.

Cardiac arrhythmia or circulatory collapse is therefore the usual presenting sign of local anesthetic overdose during general anesthesia.

Unintentional intravascular injections of bupivacaine during regional anesthesia produce severe cardiotoxic reactions, including hypotension, atrioventricular heart block, idioventricular rhythm and life threating arrhythmias such as ventricular tachycardia and fibrillation. Pregnancy, hypoxemia, and respiratory acidosis are predisposing risk factors. Young children may also at increased risk of toxicity. The R (+) isomer of bupivacaine blocks cardiac sodium channels. At high doses calcium and potassium channels may be also blocked. Resuscitation from bupivacaine-induced cardiac toxicity often requires high doses of vassopressors and prolonged therapy.

D-Immunological

The hypersensitivity reactions to local anesthetic agents are quite uncommon.

E-Musculoskeletal

When directly injected into skeletal muscle local anesthetics are myotoxic
(Bupivacain>lidocaine>procaine).

F-Hematological

It has been demonstrated that lidocaine decrease coagulation (prevention of thrombosis and decrease platelet aggregation) and enhances fibrinolysis of whole blood as measured by thromboelastography
.

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