Halothane Cerebral effects include cerebral vasodilatation and increases cerebral blood flow (CBF). A concentration of I MAC doubles CBF and 1.6 MAC quadruples the CBF. Cerebral autoregulation may be abolished and cerebrospinal fluid (CSF) production reduced by 30%. The cerebral oxygen consumption (CMRO,) may be reduced by 25%. There is no epileptiform activity in the […]
Halothane neuromuscular junction effect produces moderate muscle relaxation, it increases the degree and duration of relaxation produced by nondepolarizing muscle relax- ants. The action is at the postjunctional membrane. There is relaxation of the uterine muscle, which is useful in podalic version procedure but may hinder uterine contraction postpartum. Halothane neuromuscular junction effect may produce
One of the most dreaded Halothane Complications is hepatic injury. There are two types, the first which is a transient sub clinical type with increases in liver enzymes. Halothane Complications may occur due to decreased hepatic blood flow and reductive biotransformation. Secondly, fatal hepatic necrosis may occur up to one month after exposure. The National Halothane
Halothane Malignant hyperthermia syndrome may be triggered by halothane, it is an autosomal dominant inherited condition. There is a massive release of intracellular calcium from the sarcoplasm of the muscle. An increased metabolism results in rise in temperature of 2°C per hour, severe acidzsis, rhabdomyolysis, with associated hyperkalaemia. Mortality is 70%. Treatment is by active
Desflurane cardiovascular effects are mentioned here. There is a decrease in systemic vascular resistance and peripheral vasodilatation. Cardiac depression, a dose-dependent tachycardia and fall in blood pressure are seen. Along with N20 this effect is minimal. Splanchnic and renal blood flow is preserved. Desflurane is a direct coronary vasodilator. A rapid increase in concentration of
Sevoflurane metabolic effects are seen when approximately 5% of the dose is metabolized by the liver, catalyzed by cytochrome P450 (2E1) enzyme. While Sevoflurane metabolic effects are studied we see that, it is broken down to hexafluoro isopropanol (HFIP) and fluoride ions. Hexafluoro isopropanol is conjugated with glucuronic acid to form HFIP glucuronide and excreted
The metabolism of Sevoflurane complications yields fluoride ions, which if greater than 50 tmol/Iit is toxic. However, there are no reports of renal toxic effects. Compound A which is a degradation product when exposed to sodalime is also nephrotoxic, however this has not been clinically reported. It is safer to use flows greater than 2
Functioning of Isoflurane cerebral blood flow is discussed here. Isoflurane reduces cerebral metabolism and so the oxygen consumption is reduced. At 1 MAC there is a 23% reduction in CMRO2. Isoflurane cerebral blood flow is not associated with seizure activity as opposed to Enflurane. The EEG shows progressive development of slow waves after an initial
A rapid Isoflurane inhalation induction is possible with isoflurane because of low blood/gas solubility coefficient. It has a pungent odour, patients complain of burning sensation in the airway though there is no increase in airway reflexes or secretions. So a smoother induction is seen with halothane or sevoflurane which are preferred for inhalational induction. Recovery:
Isoflurane renal effects are minimal, only 0.2% metabolites are excreted in the urine and fluoride excretion is minimal. In patients for renal transplantation where there is a risk of arrhythmia, due to alteration in plasma electrolyte concentration, release of renin and catecholamines; there is hemodynamic stability. Skeletal muscle tone is reduced to a greater extent
