Acute Heart Failure, 90-Day Mortality, and Gravitational Ischemia in the Brain.

During the 90 days following hospitalization for acute heart failure, the ejection fraction and type of discharge medications have been shown in clinical trials to have little effect on mortality. We examined the recent literature addressing brain-related etiologies of sudden death following heart failure. Two mechanisms of sudden unexpected death have been suggested to possibly result from four significant influences on pathophysiology in the brain. The two causes of sudden death are (1) severe cardiac arrhythmia and (2) neurogenic pulmonary edema. They are both mediated through the brainstem autonomic nuclei generally and executed specifically through the dorsal motor nucleus of the vagus nerve. The four significant influences on pathophysiology, all contributing to ischemia in the brainstem autonomic nuclei, are: (1) Hyper-stimulation of neurons in the solitary tract nucleus, increasing their metabolic requirements; (2) Inadequate blood flow at a vascular watershed terminus, perfusing the autonomic nuclei; (3) Additionally decreased blood flow, globally throughout the brain, following vasoconstriction related to relative hyperventilation and decreased pCO2 levels; (4) Gravitational ischemia in the brainstem caused by the weight of the cerebral hemispheres sitting above the brainstem. Changes in head tilt release gravitational ischemia in the brain. There is no specific head position relative to gravity that is considered favorable or unfavorable for an extended period of time, longer than 24 h. Even a small degree of head elevation, used in managing pulmonary congestion, may increase gravitational ischemia in the posterior fossa and brainstem. In this paper, we suggest a new and important research avenue for intervening in cardiac arrhythmias and preventing their occurrence through the non-invasive use of head-tilting and other head repositioning maneuvers. This could potentially help many geriatric patients with heart failure, who have decreased mobility in bed, and who tend to stay in one position longer, thereby increasing gravitational ischemia in the brain.

CO2-related vasoconstriction superimposed on ischemic medullary brain autonomic nuclei may contribute to sudden death.

INTRODUCTION: In 2015, a multinational randomized controlled phase IV clinical trial of adaptive servoventilation for the management of heart failure with central sleep apnea was halted in progress because more patients in the study group were dying than in the control group. One year later, another large clinical trial reported results on the effectiveness of continuous positive airway pressure (CPAP) in preventing sudden death and other cardiovascular events such as heart attack and stroke in patients with preexisting vascular disease as well as obstructive sleep apnea. BACKGROUND: Sudden unexpected death has been associated with many types of small and nonmalignant medullary brain lesions, like demyelination plaques - largely asymptomatic until they caused sudden death. Many such medullary lesions, typically without hemorrhage or mass effect, have in themselves been previously considered relatively harmless - in cases where they have been known to be present. DISCUSSION: Why did not the improved pulmonary ventilation and subsequently improved gas exchange provided during the CPAP and servoventilation clinical trials help to resolve any ischemic lesions that may have been present both in the heart and in the medulla, thereby tending to normalize interactions between the vagal neural structures and the heart? CO2 is a potent dilator of brain vasculature, thereby increasing blood flow to the brain. When ventilation is increased, even if only to improve it back toward normal from a depressed steady-state level, the alveolar partial pressure of carbon dioxide is decreased, likely resulting in a converse relative vasoconstriction in the brain, thereby reducing blood flow in the brain, especially in watershed areas like the solitary tract nucleus. In normal physiology, this is demonstrated impressively by the ability of hyperventilation to induce loss of consciousness. CONCLUSIONS: The findings of several clinical trials recently reported, taken together with neuropathology case studies reported elsewhere, suggest that additional research is warranted in regard to the mechanisms by which focal medullary autonomic brain ischemia may be related to sudden death in general medical illnesses - and how it may additionally be influenced by changes in arterial CO2 levels.