Herein lies the predominant secret of the regulation of the amount of oxygen consumed by the whole organism, determined only by the cell itself … arterial oxygen content, aortal pressure, velocity of blood stream, mode of respiration are all incidental and subordinate, they all combine their actions in the service to the cell. —Pfluger 18721
Shock clinically manifests as tissue hypoperfusion but fundamentally originates from inadequate cellular oxygen delivery or utilization. Phenotypically, the degree of “inadequacy” can vary among patients or even within the same patient. The clinical spectrum of hypoperfusion can be transient (i.e., vasovagal syncope), persistent with compensation (i.e., normotensive and tachycardic with small volume loss), or persistent and decompensated with cardiovascular collapse, multiorgan failure, and death.
Clinically, health care providers are alerted to intervene emergently when patients are hypotensive or are “not looking right.” Because shock is a time-sensitive diagnosis, recognizing and managing it early and closest to the onset of hypoperfusion portends the best prognosis.2–8 In general, definitive shock etiologies and their treatments are easier to classify retrospectively as more time and investigation unfold. Unfortunately, there are other times, acutely, when the exact etiology of shock may be multifactorial or undifferentiated thereby leaving providers to act with incomplete information. Regardless of circumstance, high-risk decisions need to be made to ensure acute stabilization and resuscitation, optimization, and prevention of organ dysfunction and death. The intent of this chapter is to serve as a framework for providers to build on or refresh their confidence in understanding, diagnosing, and managing a wide array of shock states.
Mortality from shock can be high and highly variable, ranging from 10% to 87%, depending on the type of shock, patient age, and comorbidities.9–12 There is no consensus definition for refractory shock although clinical trials often use 0.5 mcg/kg/min of norepinephrine or epinephrine as a threshold.13 Nearly 6% of critically ill patients will develop refractory shock, which accounts for 18% of deaths in intensive care units.13 Recent studies have examined this patient population. In a recent study, those patients requiring high-dose (≥1 mcg/kg/min norepinephrine equivalent) vasopressor (HDV) (n = 443) had significant 90-day mortalities (83%) with greater than half (58%) undergoing withdrawal of care.14 Of the few surviving to 90 days (n = 76), many (82%) went on to survive to 3 years and were younger than those who died before 3 years (53.1 vs. 64.8).15 When compared to other ICU illnesses, surveyed HDV survivors (n = 36) had similar rates of depression (19%), anxiety (39%), disability (36%), and full time employment (17%), and had lower post-traumatic stress disorder (8%).15 Taxonomically, shock etiologies have appeared similar between HDV survivors (sepsis 62%, cardiogenic 13%, cardiac arrest 7%, overdose 5%, hemorrhagic 3%, neurogenic 1%, pulmonary embolism 1%)14 and HDV patients who died (sepsis 54%, cardiogenic 11%, cardiac ...