The Ketamine induction dose of anaesthesia is, 1 to 2 mg/kg IV or 4 to 8 mg/kg IM. Injection of ketamine IV does not produce pain or venous irritation. Consciousness is lost in 30 to 60 seconds after IV administration and in 2 to 4 minutes after IM injection. Unconsciousness is associated with maintenance of
Etomidate induces loss of consciousness rapidly (5—15 seconds) and recovery occurs in 5 to 15 minutes. The elimination Etomidate half life is 4.6 +1- 2.6 hours and total apparent volume of distribution, 4.5 +/- 2.2 L/kg. The volume of distribution of etomidate half life is large, suggesting considerable tissue uptake. The plasma clearance is 879
The foregoing discussion is in the situation of a normal blood brain barrier about blood brain barrier crossing drugs. In a brain lesion, where the integrity of BBB varies according to the severity of damage, the control of fluid molecules is further complex. The osmotic/oncotic gradient will not be effective in areas of complete blood
The most commonly used barbiturate is pentobarbital. Induced coma with use of barbiturates like thiopentone sodium or pentothal is called barbiturate coma or pentobarbital coma . High-dose barbiturates have been used for more than 60 years in critically ill neurologic patients. The most common application has been to lower elevated intracranial pressure (ICP) in patients
Ketamine respiratory depression is considered to be the ideal anesthetic for asthmatic patients because it decreases the risk of bronchospasm during induction of anesthesia and preserves the pulmonary vasoconstriction reflex to hypoxia. It does not produce significant depression of ventilation. The ventilatory response to carbon dioxide is maintained during ketamine respiratory depression anesthesia. The respiratory
For the Barbiturate therapy , High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Barbiturates decrease ICP by decreasing cerebral blood volume through drug-induced cerebral vascular vasoconstriction and an associated decrease in cerebral blood flow. This therapy in used either as a anti seizure medication
Propofol mechanism of action exerts its sedative hypnotic effects through a GABA receptor interaction. GABA is the principal inhibitory neurotransmitter in the CNS. When GABAA receptors are activated, transmembrane chloride conductance increases, resulting in hyperpolarization of the postsynaptic cell membrane and functional inhibition of the postsynaptic neuron. The interaction of propofol mechanism of action also
The mechanisms for ketamine induced cardiovascular effects are complex and also Ketamine effect on blood pressure characteristics. Direct stimulation of the CNS leading to increased sympathetic nervous system outflow seems to be the most important mechanism for cardiovascular stimulation. One of the characteristic of Ketamine is related to blood pressure and is therefore termed as
Barbiturates mechanism of action is described here. Barbiturates most likely produce their sedative hypnotic effects through an interaction with the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the CNS. Barbiturates cause reversible depression of all excitable tissues, the CNS being exquisitely sensitive. They bind to beta subunit of the inhibitory GABA-A receptor, a site distinct from
Flumazenil or Anexate is an imidazo benzodiazepine that binds competitively to BDZ receptors and antagonizes many of the actions of benzodiazepines. Flumazenil is a benzodiazepine antagonist. It does not block the pharmacologic effects of GABA or all GABA mimetic but it specifically antagonizes the actions of benzodiazepines. Given alone, it has minimal effect on the
