The evaluation and treatment of shock in the prehospital environment presents unique challenges to the EMS physician. Decisions regarding the balance between sophisticated field treatment and minimizing transport time to definitive care must continually be evaluated. The benefit of advanced care in the field has been questioned.1–3 Some studies have demonstrated that the addition of the physician on the scene may increase scene time in certain scenarios, while other studies have not observed this effect.3 This is likely related to the prehospital training and experience of the physician. Balancing physician intervention with scene time is an important part of the care of the patient in shock and must be explored during the EMS education of residents and fellows.
Describe the identification of shock in the field.
Describe the initial management of shock in the field.
Analyze the causes of shock.
Examine how to treat specific causes of shock while in the prehospital setting.
Present the use of advanced vascular access and pressors in the field.
Discuss the use of tourniquets and hemostatic agents for severe hemorrhage.
Physician participation in the field is routine in the Franco-German model of prehospital care and is becoming more common in the United States. Participation in the field also allows the physician to gain a first-hand perspective on how the system works. The physician is often in a position to have an effect on protocols, provider education, and operational matters that affect patient care. For those in training, participation in the field provides them with critical insight into the challenges and limitations of caring for patients in the out-of-hospital setting. Without an understanding of the differences inherent in the provision of prehospital emergency care, it is often less than productive to apply in-hospital evaluation and treatment techniques in the field environment. To treat a patient in shock effectively in the field environment requires a knowledge base specific to EMS.
Shock is a state of decreased perfusion resulting in inadequate delivery of oxygen to the tissue. Typically, the body has exhausted its ability to compensate for the stressors it is experiencing. The principles for management of shock include the maintenance of perfusion while supporting ventilation and oxygenation. The precise degree of resuscitation of the patient depends on a number of factors and has been the topic of significant discussion in the literature.4 The prehospital environment presents unique challenges when treating a patient in shock. Equipment and supplies are typically limited in the field environment. Austere conditions such as temperature extremes, darkness, and precipitation may hamper care of the patient in shock. Temperature control is a significant factor. Initial studies indicated that therapeutic hypothermia may have beneficial effects on patients after return of spontaneous circulation (ROSC), although further evaluation of this is required.5 Alternatively, trauma patients requiring massive transfusion with a core temperature less than 34°C is associated with a mortality rate >85%. Maintaining an adequate environment in the ambulance may be challenging. Factors as simple as opening the doors to the back of the ambulance on a cold day may have a significant effect on the cabin temperature. Warmed saline may not be as readily available in the field. For hypothermic patients, interventions such as invasive warming may not be practical or even possible in the field environment. This is to say nothing of the patient who cannot be removed from the elements such as is the case with vehicle entrapment or patients in remote locations.
Identification of the patient in shock may not be as apparent in the field environment as it may be in the hospital. Equipment is limited and environmental factors such as temperature and vibration may affect the accuracy of that equipment. Skin color and temperature that is consistent with shock may be difficult to differentiate from a normal response to outdoor environmental factors. Peripheral vasoconstriction in colder environments may render distal SaO2 monitors useless. Other equipment such as EtCO2 detectors and prehospital ultrasound, which can indicate poor ventilatory exchange and ventricular collapse respectively, may not be available to assist in the diagnosis of shock.
Shock is generally divided into four main categories: hypovolemic, cardiogenic, obstructive, and distributive. While the overarching goal of shock management is to support adequate perfusion, specific interventions tailored to each type of shock are important.
Hypovolemic shock results from decreased intravascular volume. Decreased preload leads to a compensatory increase in both cardiac output and systemic vascular resistance. Etiologies may include hemorrhage or other fluid losses such as gastrointestinal, insensible losses, burns, and third spacing.
Cardiogenic shock is secondary to a failure of the cardiac pump itself. Systemic vascular resistance increases to compensate for diminished cardiac output. Etiologies include arrhythmias, cardiomyopathies, and mechanical abnormalities such as valve dysfunction. In all of these cases the ability of the heart to maintain adequate cardiac output is overwhelmed, leading to inadequate systemic perfusion.
Obstructive shock is sometimes classified as a type of cardiogenic shock as the heart is unable to maintain output due to an extracardiac etiology. This type of shock is secondary to mechanical impedance of forward flow such as saddle pulmonary embolism (PE) or tension pneumothorax.
In distributive shock, systemic vascular resistance is compromised. Cardiac output is increased in an effort to compensate for the vasodilatory effects that cause distributive shock. Distributive shock includes septic shock, anaphylaxis, and other systemic inflammatory processes. Neurogenic shock may fall into this broader category.
In addition to the broad categories above, a particular process may produce different types of shock simultaneously. Sepsis is an excellent example of this. In addition to the vasodilatory effects of the inflammatory mediators (distributive shock), the septic patient may also have a component of hypovolemic shock secondary to decreased oral intake, insensible losses, and GI losses. Myocardial irritability may also result in cardiac arrhythmias inducing a component of cardiogenic shock.
Initial management of the patient in shock follows the typical mantra of critical care patient management. Consideration of the primary survey with the establishment of high flow oxygen administration, cardiac monitoring, and establishment of IV access, typically two large bore IVs, is compulsory in the field as it is in the hospital. Limitations of equipment, space, or personnel may limit interventions to those that have the highest priority, but, in general, all of these are critical initial steps in the general field management of the patient in shock. While the necessity of establishing two large bore IVs has been challenged, it warrants consideration that in the chaotic scene environment one should anticipate that a single IV may become inadvertently dislodged by a combative patient or patient moving mishap.6 With any advanced procedure the understanding of when not to perform an intervention is often as critical as knowing when to perform one. Any intervention must be weighed against scene time, provider safety, and issues of sterility.
Initial interventions need not be advanced to have a significant beneficial effect on the patient in shock. It is important not to overlook or underestimate the effect of basic life support (BLS) intervention on a critical patient. Simple positioning of a patient in supine or slightly elevating the feet can be beneficial to maintaining perfusion. The importance of BLS care is amplified in an environment where advanced equipment is limited. Aggressive basic hemorrhage control with direct pressure and tourniquets, when needed, can have a profound effect on patient outcome. Other BLS maneuvers, such as proper basic stabilization of a pelvic fracture, are essential. Overlooking basic interventions such as these could prove fatal during transport if not properly implemented.
Normal saline solution is a satisfactory choice for initial resuscitation. Lactated Ringer’s has also been suggested in the treatment of trauma- induced shock. Lactated Ringer’s fails to show significant benefit over normal saline in the immediate phases of resuscitation and may not be available in the field.4 Rapid administration of fluid must be tempered with the risks of volume overload which may result in pulmonary edema and hemodilution. In addition, the cooling effect of unwarmed saline administration may compound hypothermia in a patient in shock. According to the Hagen-Poiseuille equation of fluid dynamics flow is inversely proportional to length and exponentially proportional to diameter (Figure 35-1). Rapid instillation fluids are best administered via a short, large bore line. Hence, shorter peripheral IVs are preferable to longer central lines for rapid volume administration. The question whether to administer large quantities of fluid rapidly or to delay fluid administration continues to be unanswered. There is no definitive evidence for or against the use of rapid or high-volume administration of fluid in patients with uncontrolled hemorrhage in trauma.4 Many practitioners will titrate fluid hydration in trauma to various end points such as maintenance of the patient’s mental status or an arbitrary systolic blood pressure such as 90mm Hg or mean arterial pressure of 60 mmHg.
The determination of colloid versus crystalloid infusion in the treatment of shock has long been discussed. Albumin and hetastarch are two common examples of colloids. Initially, there were theoretical advantages of colloid infusion including less risk of pulmonary edema and faster volume expansion. A number of studies failed to demonstrate that colloids provided any significant benefit over crystalloid.7 The use of colloid in trauma resuscitation has fallen out of favor due to poor efficacy and higher cost compared to crystalloid.
The decision regarding when and how to administer vasopressors in the field to a patient in shock depends, in part, on the cause of the shock itself (Table 35-1). Patients who are fluid overloaded, for example, may require vasopressors sooner than those who can tolerate volume resuscitation. Pressor choices are often limited in the field and relatively infrequently used. This coupled with cost and other factors such as shelf life or need for temperature control further contribute to limit the choices of pressors in most advanced life support (ALS) ambulances. There may be additional choices, however, in critical care transport units or in EMS physician vehicles. These units may handle a higher proportion of critical calls and cover a wider geographic area. Vasopressors are often recommended to be administered via a central line. This is mainly because of the sclerotic complication should extravasation of the pressor occur in the periphery. In the prehospital environment placement of a central line is often not practical for a number of reasons. Space is limited and, in an uncontrolled environment, it may be difficult to maintain sterility. This is not to mention the potential for injury to the providers from the sharps required to perform this procedure. In the field vasopressors are often started peripherally until after arrival to the hospital, when a central line can safely and more practically be placed. The choice of vasopressor agents used in EMS may vary. In most cases, the choice is often limited to one or perhaps two agents. While no individual agent has been determined to be superior to another, there are some differences among the available agents8 (Table 35-2). In addition, certain agents may be associated in a greater number of adverse events such as increase incidence of arrhythmias with dopamine compared with norepinephrine.9
Common Vasopressors
Drug | Dose |
---|---|
Dopamine | • Low dose: <5μg/kg/min • Moderate dose: 5-10μg/kg/min • High dose: >10μg/kg/min |
Dobutamine | 2.0-20μg/kg/min |
Epinephrine | • For refractory hypotension • Typical dosing is 1-4μg/min (1:10,000 solution) • For anaphylaxis, the dose and route change, based on the presence of shock: • Without evidence of shock: 0.3-0.5mg (300-500μg) IM q 5-10min (1:1000) • With evidence of shock: 0.1mg (100μg) IV, which is 1.0mL of 1:10,000 dilution IV given slowly over 3-5 min or infused at 5-15μg/min |
Norepinephrine | 0.03-3.0μg/kg/min |
Vasopressin | • 0.04U/min • Not titrated |
Phenylephrine | • 0.5-8μg/kg/min • 100-180μg/min IV drip |
Isoproterenol | 2-10μg/min |
Milrinone | 50μg/kg bolus, and then 0.25-1μg/kg/min |