in the prehospital setting [18–21]. Exhaled end‐tidal carbon dioxide (EtCO2) levels vary inversely with minute ventilation, providing feedback regarding the effect of changes in ventilatory parameters [22, 23]. Additionally, changes in EtCO2 are virtually immediate when the airway is obstructed or the endotracheal tube becomes dislodged [24]. EtCO2 concentration may be influenced by factors other than ventilation. For example, levels are reduced when pulmonary perfusion decreases in shock, cardiac arrest, and pulmonary embolism [25–27]. EtCO2 is most useful as an indicator of perfusion when minute ventilation is held constant (e.g., when mechanical ventilation is applied) [19, 25]. Under these conditions, changes in EtCO2 levels reliably indicate changes in pulmonary perfusion. In any patient suffering from a potential shock state, diminished EtCO2 should be a warning of the critical nature of the patient’s problem.
Additional Modalities to Assess Shock
Use of portable ultrasound in the field can facilitate the recognition of immediately life‐threatening causes of shock including intra‐abdominal bleeding and cardiac tamponade. Many EMS agencies, primarily air medical services, have deployed point‐of‐care ultrasound for field evaluations, including the focused assessment by sonography in trauma (FAST) examination, the EFAST incorporating a lung assessment for pneumothorax, and various shock protocols to assess volume status, a limited cardiac exam, or reversible causes of shock [28]. Ultimately, the EMS medical director must determine if the cost and effort required to acquire the equipment, training, and performance of these skills translates into improved patient outcomes. The use of field ultrasound has the potential to worsen patient outcome if the procedure delays the time to definitive care, does not influence patient destination or care, or interferes with maintenance of critical parameters such as airway, ventilation, and hemorrhage control.
There is growing interest in the use of biomarkers that can be employed to identify, monitor, and predict the outcome in shock [29]. Point‐of‐care testing devices make measurement of biomarkers in the field an attractive option. Elevation of serum lactate may reflect anaerobic tissue metabolism in acute sepsis and shock [29, 30]. In the setting of infection, elevated lactic acid may indicate septic shock and the need for early goal‐directed therapy. Elevated venous lactate is associated with increased mortality risk and the need for resuscitative care in trauma patients. Prehospital trauma research indicates that an elevated lactate level in the setting of trauma predicts the need for aggressive resuscitation [31]. Serial lactate measurements may indicate the effectiveness of ongoing resuscitation [32].
Prehospital telemedicine holds the promise of providing access to the highest levels of care to patients and field clinicians by using EMS as a “telemedicine facilitator” (see Chapter 73). In the event that the patient is in profound shock or extremis, EMS clinicians can engage a wide range of expertise to help manage the patient [33].
Artificial intelligence technology (“assisted intelligence”) is also uniquely suited to prehospital medicine. Diagnostic algorithms can interpret trends in data and identify patients who are in compensated shock prior to clinical deterioration [34]. Further recognition of those patterns may lead to individualized care in the form of direct decision support informing EMS clinicians in how to best care for their patients.
Treatment
All treatment approaches to shock must include the following basic principles:
1 Perform the initial assessment.
2 Deal with issues identified during the initial assessment such as airway, breathing, and circulation issues, including active external bleeding.
3 Determine the need for early definitive care:hemorrhage control and volume resuscitationneedle thoracostomyelectrical therapy for dysrhythmiainvasive airway management.
4 Maintain adequate oxygen saturation (SaO2 greater than 94%).
5 Ensure adequate ventilation without hyperventilating.
6 Monitor vital signs, ECG, oxygen saturation, capnography, and lactate (if available).
7 Prevent additional injury or exacerbation of existing medical conditions.
8 Protect the patient from the environment.
9 Determine the etiology of the shock state and treat accordingly.
10 Notify and transport to an appropriate facility.
Often the etiology of the patient’s shock state and the initial management options are clear from the history. For example, the out‐of‐hospital treatment of a young, previously healthy college student with hypotension secondary to severe vomiting and diarrhea includes intravenous (IV) fluids. The treatment of cardiogenic shock in an unresponsive elderly patient with ventricular tachycardia requires prompt cardioversion. Occasionally, the primary problem may be strongly suspected but not readily diagnosable or treatable in the field (e.g., pulmonary embolism). Less frequent, but most difficult to manage, is the patient in shock without an obvious cause. With the understanding of the limited treatment options in the prehospital setting (primarily fluids, inotropic agents, and vasopressors), field treatment may be individualized for the four categories of shock: hypovolemic, distributive, obstructive, and cardiogenic.
Hypovolemic Shock
Hypovolemic shock is the result of significant loss of intravascular volume resulting in hypotension. The many etiologies of hypovolemic shock include external fluid loss and shifting of fluids from the vascular system to a nonvascular body compartment. The treatment of hypotension and shock caused by hypovolemia is relatively straightforward. External bleeding should be controlled. Fluid replacement via vascular access is the mainstay of treatment. Unfortunately, the ideal fluid for the resuscitation of hypovolemic shock and the amount of fluids that should be provided remain controversial [35–37].
Distributive Shock
Distributive shock, characterized by a decrease in systemic vascular resistance, is associated with abnormal distribution of microvascular blood flow [38]. Causes of distributive shock include sepsis, anaphylaxis, medication overdose, and acute neurological injury. The treatment of distributive shock involves the combination of vasoactive medications, which constrict the dilated vasculature, and fluids, which fill the expanded vascular tree. Commonly used vasoactive medications for distributive shock in the field include epinephrine, norepinephrine, and dopamine. Although epinephrine is easily administered via several routes (e.g., intramuscular, intravenous bolus, or infusion), the drug has significant adverse effects. Norepinephrine infusions are associated with a lower incidence of cardiac dysrhythmias than either dopamine or epinephrine [39]. In addition, studies of cardiogenic shock suggest increased mortality associated with dopamine [40]. However, continuous infusions may be difficult to maintain without special infusion pumps.
Anaphylaxis is a serious, generalized allergic or hypersensitivity reaction that can be of rapid onset (minutes to hours) and is potentially fatal. Mediators that have been implicated in the pathophysiology of anaphylaxis target the skin, digestive, respiratory, and cardiovascular systems (see Chapter 21) [41]. With respect to the cardiovascular system, these mediators can precipitate hypotension, tachycardia, vasodilatation, and increased vascular permeability. These effects result in a decrease in peripheral vascular resistance and an expanded vascular tree, precipitating distributive shock. In reality, mediators also contribute to decreased cardiac inotropic and chronotropic effects and fluid loss via edema, contributing to components of cardiogenic and hypovolemic shock, respectively [41].
