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Mosul Anesthesia & ICU

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Mosul Anesthesia & ICU

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Mosul Anesthesia & ICU

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    Pharmaco kinetics &dynamics of local anesthetics

    ashdom
    ashdom


    عدد الرسائل : 149
    العمر : 44
    العمل/الترفيه : Anesthesiologist
    تاريخ التسجيل : 2010-07-08

    Pharmaco kinetics &dynamics  of local anesthetics Empty Pharmaco kinetics &dynamics of local anesthetics

    Post by ashdom Thu Apr 11, 2013 11:20 am

    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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