3 | Discussion
H2S is considered to be a mitochondrial poison. It
inhibits cytochrome C oxidase, blocks the activity of the mitochondrial
electron transport chain, disrupts the aerobic metabolism of cells,
hinders the production of ATP, and ultimately leads to reduced oxygen
use of cardiomyocytes and myocardial damage.2 Besides,
H2S poisoning can also rapidly reduce cardiac
contractility and cardiac output, leading to cardiogenic shock even
cardiac arrest within a few minutes, possibly due to the blocking of the
L-type calcium channel of myocardial cells.3
Several autopsies showed that the skin and internal organs of these
patients had green discoloration with pulmonary
edema.4 Our report supplements that their myocardial
tissue experienced sarcolysis and hypertrophy with increased
intracellular vacuoles, irregular nuclei and swelling mitochondrial.
Delayed myocardial damage can occur in a few days after exposure, and
clinical manifestations include ST-segment elevation, increased
myocardial markers, decreased ventricular wall motion, myocardial
infarction , arrhythmia, etc.5 It can develop within a
few weeks and most of them died of circulatory failure caused by acute
inhibition of myocardial contractility. We successfully helped the
patient go through this acute stage with the support by combination of
IABP and VA-ECMO. As we know, this case is the first report of using
IABP and VA-ECMO in cardiogenic shock caused by H2S
successfully.