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.