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. 2020 May 4;17(2):539–562. doi: 10.1007/s13311-020-00856-z

Table 1.

Three hemodynamic stages following resuscitation

Hyperemia (0–30 min) Hypoperfusion (30 min–12 h) Restoration of blood flow (12–72 h)

• Hyperemia linked to cerebral vasoparalysis [35]

• Vasoparalysis linked to increasing lactic acid from anaerobic respiration [36], NO [37], and adenosine [38]

• Loss of vascular tone is independent of changes in BP or reactivity to CO2, which is preserved [19, 21]

• CBF decreases by 50% [39, 40]

• Hypoperfusion linked to intravascular stasis (no-reflow phenomenon) [24] and vasoconstriction [27]

• Imbalance of vasodilators (e.g., NO) [41] and vasoconstrictors (e.g., endothelin-1) [28] contributes to hypoperfusion

• In survivors, large vessel blood flow exhibits gradual return to near-baseline, along with increased metabolism [42]

• Increases in large vessel blood flow observed in nonsurvivors [29]

Following resuscitation, three stages of hemodynamic alteration have been observed in patients and preclinical models. The first stage (hyperemia) is marked by increased blood flow. The second phase (hypoperfusion) is characterized by a reduction in blood flow. The third stage involves the recovery of near-normal CBF. Each box highlights specific pathophysiologic mechanisms linked to these hemodynamic changes

NO = nitric oxide, BP = blood pressure, CBF = cerebral blood flow