Cardiac Output and Cerebral Blood Flow

Abstract

Cerebral blood flow (CBF) is rigorously regulated by various powerful mechanisms to safeguard the match between cerebral metabolic demand and supply. The question of how a change in cardiac output (CO) affects CBF is fundamental, because CBF is dependent on constantly receiving a significant proportion of CO. The authors reviewed the studies that investigated the association between CO and CBF in healthy volunteers and patients with chronic heart failure. The overall evidence shows that an alteration in CO, either acutely or chronically, leads to a change in CBF that is independent of other CBF-regulating parameters including blood pressure and carbon dioxide. However, studies on the association between CO and CBF in patients with varying neurologic, medical, and surgical conditions were confounded by methodologic limitations. Given that CBF regulation is multifactorial but the various processes must exert their effects on the cerebral circulation simultaneously, the authors propose a conceptual framework that integrates the various CBF-regulating processes at the level of cerebral arteries/arterioles while still maintaining autoregulation. The clinical implications pertinent to the effect of CO on CBF are discussed. Outcome research relating to the management of CO and CBF in high-risk patients or during high-risk surgeries is needed.

Cerebral blood flow alteration following acute myocardial infarction in mice

“…Although LV remodeling starts at the onset of MI, clinical manifestation of chronic heart failure may not develop for years in humans given the progressive maladaptive remodeling that may continue for a lifetime [20]. Multiple studies revealed the association between CO and CBF in both healthy and cardiac impaired individuals linking heart failure mediated low CO to CBF reduction [4,6–10]. However, no studies assessed the impact of early (day 1) till late stages (30 days) of acute cardiac injury post MI, on CBF.…”

“…These data suggest that in the first and second stages of cardiac remodeling post-MI, regulatory mechanisms limit the impact of CO on CBF. In fact, CBF is an integrative and complex process combining the function of multiple systems including pulmonary gas exchange, cardiovascular function, and intracranial cerebrovascular regulators [3,4]. MI impact on cerebral perfusion is multifaceted and not only mediated through CO alteration.…”

“…Distinct amongst other organs, the brain requires a constant supply of oxygen and nutrients due to its limited substrate storage capacity and high metabolic activity [3]. Despite the fact that the brain contributes only 2% to total body weight, it receives approximately 12% of the CO [4]. …”

“…Cerebral blood flow (CBF) regulation is an integrative and multifaceted process that combines the function of multiple processes including pulmonary gas exchange, cardiovascular function, and intracranial cerebrovascular regulators [3]. Although CO and mean arterial pressure (MAP) are interrelated hemodynamic parameters that could exert simultaneous effects on CBF [4], multiple studies have revealed that the strongest correlation with CBF belonged to CO, especially in conditions with low CO such as heart failure disease [4,6,7]. In addition, several studies reported that therapies targetted at improvement of CO, including pharmacological interventions, cardiac transplantation, and cardiac resynchronization therapy, exerted a positive effect on improvement of CBF [8–10].…”

“…In addition to direct alteration of CO through myocardial mechanical injury and LV remodeling [19,21,22], MI induces a systemic inflammation and an elevated renin–angiotensin–aldosterone system (RAAS) activation affecting the remote organs including kidneys and the brain, and have been directly linked to brain perfusion impairment [4,23–26]. Although a strong correlation between chronic heart failure and CBF alteration has been established, no existing data link CO to CBF post-MI through the main phases of MI-induced cardiac remodeling including the inflammatory, granulation, and wound-healing phases [27].…”