Nutrient stimulation of mesenteric blood flow - implications for older critically ill patients

Abstract

Nutrient ingestion induces a substantial increase in mesenteric blood flow. In older persons (aged ≥ 65 years), particularly those with chronic medical conditions, the cardiovascular compensatory response may be inadequate to maintain systemic blood pressure during mesenteric blood pooling, leading to postprandial hypotension. In older ambulatory persons, postprandial hypotension is an important pathophysiological condition associated with an increased propensity for syncope, falls, coronary vascular events, stroke and death. In older critically ill patients, the administration of enteral nutrition acutely increases mesenteric blood flow, but whether this pathophysiological response is protective, or precipitates mesenteric ischaemia, is unknown. There are an increasing number of older patients surviving admission to intensive care units, who are likely to be at increased risk of postprandial hypotension, both during, and after, their stay in hospital. In this review, we describe the prevalence, impact and mechanisms of postprandial hypotension in older people and provide an overview of the impact of postprandial hypotension on feeding prescriptions in older critically ill patients. Finally, we provide evidence that postprandial hypotension is likely to be an unrecognised problem in older survivors of critical illness and discuss potential options for management.

Keywords: Aged; Critical care; Enteral nutrition; Mesenteric ischaemia; Postprandial hypotension.

Figure 1

Factors involved in the regulation of postprandial blood pressure. (1) ingestion of a meal, with a greater carbohydrate load results in a greater postprandial hypotensive response; (2) Meal-induced gastric distension from the meal triggers stretch receptors in the stomach wall, increasing sympathetic nerve outflow; (3) gastric content is emptied into the small intestine, and, in response to the nutrient in the small intestine; (4, 5) gastrointestinal peptides are secreted from the small intestine (e.g., GLP-1 and GLP-2, glucagon-like peptide-1 and 2; GIP, glucose insulinotropic polypeptide); (6) gastrointestinal peptides stimulate mesenteric vessel dilation; (7) this results in reduced circulating blood volume and the reduction in blood pressure is detected by baroreceptors; (8a) the “gastrovascular” and baroreceptor reflexes stimulate sympathetic activity to increase heart rate (HR), stroke volume (SV) and thus cardiac output (CO) to maintain postprandial blood pressure; (8b) skeletal vasculature constricts to decrease peripheral blood flow. ¹These factors are affected by age and have been identified as potential pathophysiological mechanisms of postprandial hypotension. Figure drawn by Ms. T. Nguyen. GIP: Glucose-dependent insulinotropic peptide; GLP: Glucagon-like peptide.