Cardiac coherence brainn injury8/8/2023 Studies in comatose resuscitated patients have shown that both the cerebral metabolic rate of oxygen, and the cerebral oxygen extraction fraction also decreased 24–72 h after cardiac arrest, suggesting that the coupling between CBF and oxygen demand was maintained. The role of delayed hypoperfusion as a cause of PCABI is unclear. In patients with PCABI, CBF may decrease by more than 50% during this phase. In animal models, return of spontaneous circulation (ROSC) is followed by a transient (15–30 min) increase in global CBF (global hyperaemia), after which delayed hypoperfusion occurs. The number and extent of these perfusion defects increase with the duration of ischaemia, while their distribution coincide with anatomical locations where PCABI is most commonly detected (striatum, hippocampus, amygdala, and thalamus ). This phenomenon is called no-reflow and histologically appears as multifocal perfusion defects of the brain tissue. In the experimental setting, reperfusion of the brain after transient global ischaemia is incomplete and inhomogeneous. Leukocyte migration is facilitated by an increased permeability of the blood–brain barrier, which also leads to vasogenic oedema.įull size image Cerebral perfusion changes in PCABI No-reflow Additional release of cytokines from activated leukocytes further amplifies the inflammatory response. This is initiated both by resident macrophages, known as microglia, and by circulating leukocytes which adhere to the endothelial cells of the cerebral microvasculature and migrate into the neuronal tissue. Ca ++ dependent mitochondrial dysfunction also ensues, leading to cell energy failure, release of pro-apoptotic proteins and reactive oxygen species, with resulting further neuronal damage.Ī further component of reperfusion injury is activation of the innate immune system and subsequent tissue inflammation (Fig. Subsequent activation of Ca ++-dependent lytic enzymes (proteases, phospholipases) exacerbate neuronal damage. The intracellular Ca ++ increase caused by the primary injury leads to release of glutamate, an excitatory neurotransmitter that binds to the cell membrane causing further intracellular Ca ++ influx and cytoplasmic accumulation from the endoplasmic reticulum (Fig. With return of spontaneous circulation (ROSC), CBF is restored, but reperfusion of the ischemic cerebrovascular bed triggers a series of mechanisms leading to secondary brain injury. Upon initiation of cardiopulmonary resuscitation (CPR), CBF is partially restored (low-flow), but it remains suboptimal to sustain neuronal integrity as CPR generates approximately 25% of normal CBF, substantially below the 40–50% of normal CBF needed to maintain cellular integrity and avoid additional ischemic injury. Experimental evidence shows that signs of brain oedema on MRI develop already during cardiac arrest and resuscitation. Potassium efflux and membrane depolarisation also ensue shortly thereafter, leading to the opening of voltage-sensitive Ca ++ channels and intracellular Ca ++ influx. ATP depletion results in dysfunctional energy-dependent Na +/K + ion exchange pump action, which leads to massive influx of sodium and water and intracellular cytotoxic oedema. At the cellular level, ischaemia results in cessation of aerobic metabolism with consequent depletion of high-energy substrate adenosine triphosphate (ATP) (Fig. ĭue to their lack of inherent energy stores, neurons are particularly vulnerable to ischaemia and cellular damage starts immediately upon absence of CBF. Human studies demonstrate that consciousness is lost between 4 and 10 s of absent CBF, while the electroencephalogram (EEG) becomes isoelectric after 10–30 s of asystole. Brain tissue viability strongly depends on consistent supply of oxygen and energy substrates, namely glucose, and cessation of cerebral blood flow (CBF) results in an immediate interruption of brain activity. This no-flow phase starts upon the onset of cardiac arrest and lasts until partial reperfusion is established by cardiopulmonary resuscitation (CPR).ĭespite accounting for only 2% of body weight, the brain receives 15–20% of total cardiac output to maintain tissue homeostasis. Primary injuryĬardiac arrest results in cessation of both cardiac output and oxygen delivery to all vital organs. PCABI pathophysiology is encompassed by primary (ischaemic) and secondary (reperfusion) injury which occur sequentially during cardiac arrest, resuscitation, and the acute post-resuscitation phase.
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