Contents



Foreword on Shock

Shock, defined as a state of insufficient perfusion and impaired tissue oxygen delivery, is a life-threatening condition of varied etiologies that requires prompt recognition, diagnosis, and resuscitation [1, 2]. Prehospital shock is associated with a 33–52% in-hospital mortality rate [1]. While trends in frequency and mortality of undifferentiated shock in the emergency department (ED) are under-explored, in-hospital mortality rates of 23–24% have been reported in Danish [1] and US ED settings [3, 4], with 90-day mortality approaching 41% [1]. Moreover, mortality rates for some subtypes of shock may be higher (e.g., trauma patients with hemorrhagic shock) [5]. Mortality further increases with any associated end-organ dysfunction or failure [6], as well as with increased comorbidity burden as measured by the

Despite technical improvement in diagnostics and advances in treatment, shock remains a critical finding in acute medical care. Reducing time to recognition and targeted treatment are critical aspects of patient care. Shock's clinical recognition is traditionally based on vital sign abnormalities (blood pressure, heart rate), and it may be defined as the presence of hypotension (systolic blood pressure ≤ 100 mmHg) and ≥ 1 organ failures [1]. The Shock Index (SI; systolic blood pressure/heart rate)

Traditionally shock has been classified into four categories: cardiogenic, distributive, hypovolemic, and obstructive. However, although the circulatory system is complex and depends on a multitude of variables, some find it helpful to simplify it to three main components: cardiac function ("the pump"), intravascular volume ("the tank"), and systemic vascular resistance ("the pipes") [2]. In shock, dysfunction occurs within one or more of the three components – the pump, tank, or pipes – such that tissue perfusion and oxygen delivery are impaired [2]. Acute pump malfunction can be caused by arrhythmias, conditions that result in a sudden decrease in cardiac contractility (e.g., myocardial infarction, myocarditis, valvular insufficiency) or by extracardiac conditions that obstruct cardiac output (e.g., pericardial tamponade, pulmonary embolus). Acute tank malfunction primarily results from a decrease in intravascular volume due to hemorrhage, volume loss, or impaired venous return and impaired left ventricular preload (e.g., tension pneumothorax). Pipe malfunction may be observed with processes that alter vascular tone including anaphylaxis, neurogenic (e,g., spinal cord injury), sepsis, and processes that disrupt pipe integrity (e.g., aortic dissection, abdominal aortic aneurysm). Importantly, some entities (e.g., burns, trauma, etc.) may compromise more than one system (pump, tank, pipes). Regardless of the underlying mechanism of shock, if impaired perfusion and oxygen delivery are not recognized and reversed, organ dysfunction, tissue necrosis, and

may further be used as a measure of cardiovascular failure (≥ 1) [7].

Significant regional disparities in evidence-based care have been reported, and in-hospital mortality remains high. This book goes beyond the basics of epidemiology, pathophysiology, and recognition, and targets the difficult, and at times confusing, management decisions that clinicians treating shock are faced with including resuscitation fluid (or blood product) selection, mechanical ventilation,

Charlson comorbidity index [1].

death may ensue.

*Ranjan Matthias and Muna Al Musalmani*
