A novel hypothesis comprehensively explains shock, heart failure and aerobic exhaustion through an assumed central physiological control of the momentary cardiovascular performance reserve

Background: Heart failure (HF) and shock are incomprehensively understood, inconclusively defined and lack a single conclusive test. The proceedings that preceded and triggered clinical manifestations are occult. The relationships in between different shock and HF types and between each HF type and its matched shock are poorly understood. The assumed hypothesis: We suggest that HF and shock are attributed to a momentary cardiovascular performance reserve - "the reserve". The reserve is controlled through an assumed central physiological mechanism that continuously detects and responds accordingly - "the reserve control". The assumed reserve is maximal at rest, and decreases with aerobic activity. When it decreases to a given threshold the reserve control alerts by induces manifestations of dyspnea and fatigue enforcing activity decrease, follow which the manifestations dissolve. HF is a condition of low reserve at baseline; hence, fatigue and dyspnea are frequently experienced following mild activity. Shock is assumed to occur when the cardiovascular reserve deteriorates below a sustainable limit where the reserve control induces a salvage-sacrifice response, preserving vital organ perfusion while impairing microcirculation effective perfusion in non-vital organ in which it causes cellular hypoxia followed by the familiar devastating cascade of events seen in shock. Discussion and conclusions: The hereby hypothesis may comprehensively explain the heart failure - shock puzzle as no alternative theory had ever succeeded. It provides the missing link between the different types of HF as of shock and in between. The hypothesis poses a great prove challenge but opens new research and clinical possibilities.