Halothane anesthesia?

Question

do you know how halothane sensitizes the heart to epinephrine?

Answer 1

Epinephrine (adrenaline) regulates the heart's speed, some people are sensitive to the effects of halothane and the stimulation of epinephrine can throw the heart rate out of balance.  After its use epinephrine slows down the heart as it clears the body, with a sensitivity to halothane the person won't recover and the heart will continue to slow possibly to the point of death.  The halothane is also slowing down the rate of circulation and it can stimulate a sudden demand in the skeletal muscles.  If you get the slow down rate after the epinephrine wears off occurring while the halothane is forcing the body to demand more oxygen then the lack of oxygen can starve organs.  If the brain is one of those organs then death is likely.

The heart is suddenly forced to overwork itself, then after the effects wear off it slows then the body's demand for oxygen can suddenly increase before the heart can speed up enough to keep pace with the demand.  This sudden flux in the heart rate can cause it to stutter.

According to Wikipedia:  

"Halothane vapour (or Fluothane) is an inhalational general anaesthetic. Its IUPAC name is 2-bromo-2-chloro-1,1,1-trifluoroethane. It is the only inhalational anaesthetic agent containing a bromine atom; there are several other halogenated anesthesia agents which lack the bromine atom & do contain the fluorine & chlorine atoms present in halothane. It is colourless and pleasant-smelling, but unstable in light....

Adverse effects

Halothane hepatitis, while rare, led to gradual abandonment of halothane anesthesia in adults in the 1980's, as safer halogenated volatile anesthetics, such as isoflurane, were developed. Cardiac side-effects can occur. All volatile anaesthetics such as halothane can trigger malignant hyperthermia in genetically susceptible individuals. The caffeine-halothane contracture test was developed to directly test muscle biopsy specimens for this susceptibility. This test may be replaced by genetic testing in the future."

According to Wikipedia:  

"Malignant hyperthermia (MH or MHS for "malignant hyperthermia syndrome", or "malignant hyperpyrexia due to anaesthesia") is a rare life-threatening condition that is triggered by exposure to certain drugs used for general anaesthesia (specifically all volatile anaesthetics), nearly all gas anaesthetics, and the neuromuscular blocking agent succinylcholine. In susceptible individuals, these drugs can induce a drastic and uncontrolled increase in skeletal muscle oxidative metabolism which overwhelms the body's capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly."

According to Wikipedia:  

"Epinephrine (usually referred to as adrenaline; see Terminology) is a hormone and neurotransmitter. It is a catecholamine, a sympathomimetic monoamine derived from the amino acids phenylalanine and tyrosine. The Latin roots ad-+renes and the Greek roots epi-+nephros both literally mean "on/to the kidney" (referring to the adrenal gland, which sits atop the kidneys and secretes epinephrine). Epinephrine is often shortened to epi or to EP in American medical jargon...

Epinephrine is used as a drug to treat cardiac arrest and other cardiac dysrhythmias resulting in diminished or absent cardiac output; its action is to increase peripheral resistance via α1-adrenoceptor vasoconstriction, so that blood is shunted to the body's core, and the β1-adrenoceptor response which is increased cardiac rate and output (the speed and pronouncement of heart beats). This beneficial action comes with a significant negative consequence—increased cardiac irritability—which may lead to additional complications immediately following an otherwise successful resuscitation...



Epinephrine synthesis is solely under the control of the central nervous system (CNS). Several levels of regulation dominate epinephrine synthesis."

Answer 2

It's not completely clear, but the most convincing theory I've read about is this:

"Volatile anesthetics alter tissue excitability by decreasing the extent of gap junction–mediated cell-cell coupling and by altering the activity of the channels that underlie the action potential."  It affects certain gap junctions more than others, creating an effect where some conduction pathways conduct faster than others, causing dissynchrony.

The basic effect is an increased sensitivity of the ventricle to sympathetic stimulation, which can be blocked by sympathetic blockade (by epidural anesthesia, beta-blockers, and calcium channel blockers).