Background: Sudden Infant Death Syndrome (SIDS) mechanisms of death remains obscured. SIDS' Triple Risk Model assumed coexistence of individual subtle vulnerability, critical developmental period and stressors. Prone sleeping is a major risk factor but provide no clues regarding the mechanism of death. The leading assumed mechanisms of death are either an acute respiratory crisis or arrhythmias but neither one is supported with evidence, hence both are eventually speculations. Postmortem findings do exist but are inconclusive to identify the mechanism of death. What does the proposed hypothesis based on?: 1. The stressors (suggested by the triple risk model) share a unified compensatory physiological response of decrease in systemic vascular resistant (SVR) to facilitate a compensatory increase in cardiac output (CO). 2. The cardiovascular/cardiorespiratory control of the vulnerable infant during a critical developmental period may be impaired. 3. A severe decrease in SVR is associated with hyper-dynamic state, high output failure and distributive shock. The hypothesis: Infant who is exposed to one or more stressors responds normally by decrease in SVR which increases CO. In normal circumstances once the needs are met both SVR and CO are stabilized on a new steady state. The incompetent cardiovascular control of the vulnerable infant fails to stabilize SVR which decreases in an uncontrolled manner. Accordingly CO increases above the needs to hyper-dynamic state, high output heart failure and hyper-dynamic shock. Conclusions: The proposed hypothesis provides an appropriate alternative to either respiratory crises or arrhythmia though both speculations cannot be entirely excluded.
- Cardiac output (CO)
- Distributive shock
- Mechanism of death
- Sudden Infant Death Syndrome (SIDS)
- Systemic vascular resistant (SVR)