Table 2.

MODS and cardiac dysfunction

Determinants	Description	Mechanism of myocardial damage
Myocardial ischemia-reperfusion injury [66]	Happens when tissue O2 supply is unable to meet the cardiac oxygen demand (e.g., acute myocardial infarction, circulatory arrest, hypovolemic shock)	Ischemia results in ATP depletion, lactic acidosis, intracellular sodium overload, and cell edema. Myocardial calcium overload leads to the stimulation of cellular apoptosis pathways, with impaired diastolic relaxation and susceptibility to arrhythmias. Consequent to reperfusion, there is a paradoxical amplification in cardiac injury due to the disparity between reactive oxygen species production and the inability of cells to detoxify.
Systemic inflammation response syndrome (SIRS) [67]	Recurrent among ICU patients. Distinguished by increased oxidative stress and deregulated inflammatory response.	TNF-α, IL-1, and IL-6 myocardial depressants. Nuclear factor κB provokes an inflammatory response within the myocardium. Mitochondrial damage and self-intensifying cycles of reactive oxidative species may be triggered by inflammation-produced oxidative stress.
Catecholamine induced cardiac dysfunction [68]	Stress reaction to critical illness is distinguished by increased catecholamine levels in plasma, autonomic dysfunction, and increased sympathetic initiation.	Catecholamine- mediated myocardial damage occurs through calcium overload, ATP depletion, mitochondrial dysfunction, and reactive oxidative species overproduction.
Effects of treatments given on CVS [69]	Norepinephrine – to maintain organ perfusion pressure and sufficient vascular tone.	May combine with the endogenous adrenergic response and contribute to myocardial damage
	Sedative (Propofol)	Direct cardiac decline along with hypotension and vasodilation resulting in an increased requirement of vasopressors.
	Mechanical Ventilation	Positive end expiratory pressure (PEEP) and positive pressure ventilation reduce the venous return and cardiac output. Higher PEEP may cause an overall decrease in the oxygen delivery due to the decline in carbon dioxide in spite of an induced increase in arterial blood oxygenation.
	Dobutamine– ↑ cardiac output and myocardial contractility.	May result in cardiac ischemia because of its association with ↑ myocardial O2 demand.