classic presentation of anaphylaxis – urticaria, shortness of breath, and hypotension precipitated by a bee sting, medication injection, or ingestion of a previously known allergen (e.g., peanut ingestion) – is rarely missed in the field. However, anaphylaxis presenting with hypotension but without a rash or an identifiable precipitant would be difficult to identify.
Epinephrine is a nonselective agonist of all adrenergic receptors. These receptors are present within organ systems affected by anaphylaxis [42, 43]. By increasing peripheral resistance via α‐1 receptors and increasing cardiac output via β‐1 receptors, epinephrine helps to reverse the distributive shock state.
The treatment of anaphylaxis is the administration of epinephrine as soon as the condition is recognized. The initial dose is typically injected intramuscularly in the lateral thigh as additional monitoring and intravenous access are obtained. The administration of antihistamines and steroids should never delay the administration of epinephrine. Prompt prehospital epinephrine injection is associated with a lower risk of hospitalization and fatality [41, 44].
Obstructive Shock
Blood pressure is dependent on the maintenance of cardiac output. Any condition that inhibits venous return can be anticipated to decrease cardiac output and induce shock. A number of clinical conditions exist in which venous return to the thorax and heart are reduced. These conditions include tension pneumothorax, cardiac tamponade, and massive pulmonary embolism.
Obstructive causes of shock are often difficult to diagnose and treat. Clinical signs of decreased venous return include neck vein distension and cyanosis, often in the setting of shock. Identifying these signs requires the clinician to complete an efficient, organized assessment. Shock in the setting of neck vein distention and cyanosis should lead the EMS clinician to suspect an obstructive condition as the cause.
If possible, the obstruction should be resolved, such as by decompression of a tension pneumothorax. However, when the primary problem cannot be treated successfully in the field (e.g., massive pulmonary embolus or cardiac tamponade), intravenous fluids may be helpful in increasing preload and temporizing the condition.
Cardiogenic Shock
Causes of cardiogenic shock include arrhythmias, valvular heart disease, infection, cardiotoxic agents, and most commonly myocardial infarction. As a result, cardiogenic shock requires individualized treatment. Early revascularization among patients with myocardial infarction improves long‐term survival [45]. Cardiogenic shock from severe dysrhythmias should be treated with appropriate electrical or pharmacological therapy. “Pump failure” is often difficult to diagnose and to treat without invasive monitoring. Adult patients without obvious pulmonary edema may benefit from fluid challenges of approximately 200‐300 mL of crystalloid. An improvement in the patient’s condition suggests that enhancing preload would be beneficial. A worsening of the patient’s condition with a modest fluid challenge, or the presence of obvious pulmonary edema on initial evaluation, suggests that fluid therapy would not be helpful. In such settings, treatment with inotropic agents or vasopressors, such as dobutamine or norepinephrine, would be more appropriate. Intravenous infusions are often difficult to manage in the field without an infusion pump and must be monitored closely.
Less common causes of cardiogenic shock include beta‐blocker and calcium channel blocker toxicity. Such agents block sympathomimetic receptors, impairing the body’s normal compensatory responses. These patients present with profound bradycardia and shock, often refractory to sympathomimetic treatment and fluid challenges due to the receptor blockade. Additional therapies may include IV glucagon or calcium, which facilitate heart rate stimulation and vasoconstriction through alternative cellular receptors. EMS agencies carry them for the treatment of hypoglycemia and hyperkalemia, respectively.
Shock of Unclear Etiology
In some clinical scenarios, the primary etiology for the patient’s shock state may be difficult to determine despite careful history taking and physical examination. Focused ultrasound may be helpful identifying hypovolemia (inferior vena cava), hemorrhage (FAST, aortic exam), obstructive shock (pneumothorax, cardiac tamponade, right heart strain consistent with pulmonary embolus), or cardiogenic shock (hypokinetic wall, valvular dysfunction), providing additional information for consideration of the cause of the condition.
The primary treatment decision is whether to give fluids. In hypovolemic, distributive, and obstructive shock, fluids are an appropriate initial treatment for hypotension or other signs of shock. The caveat is that indiscriminate administration of large volumes of IV fluids may not improve patient outcomes. Some cases of cardiogenic shock may respond to fluids. However, fluids should not be given to patients in cardiogenic shock with pulmonary edema. When fluids are contraindicated, or they fail to improve the patient’s response, vasopressors or ionotropic agents may be indicated. The EMS clinician should exercise caution with respect to worsening cardiogenic shock when using vasopressors that increase afterload. Ionotropic agents (i.e., dobutamine) may also precipitate hypotension through afterload reduction. Fluids are also not appropriate when cardiogenic shock has been precipitated by a treatable arrhythmia. Response to fluid challenges (where appropriate) should dictate whether additional fluid challenges should be given or whether a trial of a sympathomimetic agent should be used.
Some patients with shock may remain refractory to initial attempts at resuscitation. This response may reflect the need for definitive care in the hospital (e.g., thoracotomy, laparotomy). If, after vigorous field treatment, the patient remains hypotensive, it is prudent to consider other etiologies for the hypotension, including adrenal suppression, hypothyroidism, or various toxic agents. In some cases, patients with profound acidosis will not respond to vasopressors or inotropic agents, as their receptors are pH dependent. Administration of sodium bicarbonate, 1 mEq/kg IV, may improve perfusion by buffering acidosis and improving sensitivity to vasopressor activity. Use of vasopressin to supplement other vasopressors may also improve perfusion as it increases systemic vascular resistance even during acidosis. In cases of refractory shock or adrenal suppression, administration of steroids may also be of benefit. Hydrocortisone is ideal for this purpose, as patients may benefit from both mineralocorticoid and glucocorticoid properties. Methylprednisolone is far more widely available in the prehospital environment and may have some limited utility in refractory shock. Patients exposed to potent cellular toxins such as cyanide or hydrogen sulfide may present with refractory shock, requiring therapy with agent‐specific antidotes. Consider transport to a facility capable of mechanical support for patients with refractory shock.
Pediatric Shock
Recognition and management of shock in the pediatric population follow the same general principles as in adults, with a few notable exceptions [46]. Children in shock more commonly present with a low cardiac output and a relatively high systemic vascular resistance (SVR). This has been described as “cold shock,” as opposed to the low‐SVR state or “warm shock” frequently seen in adults. Children presenting in distributive shock usually require more aggressive fluid resuscitation with volumes of 60 cc/kg or more [47]. If children fail to respond to the initial fluid resuscitation, epinephrine is preferred as the first‐line vasopressor to counter the relatively low cardiac output seen in pediatric shock. Additional support for patients with low SVR and wide pulse pressure may be provided with norepinephrine or vasopressin. Dobutamine may provide inotropic and chronotropic support in patients with very low cardiac output and improve delivery of oxygen to tissues.
Following initial treatment with fluids and vasoactive agents, pediatric patients may also benefit from adjunctive therapies for shock [46]. Early airway management should be considered, as children may use up to 40% of their cardiac output to support the work of breathing. Ketamine is the preferred induction agent, as it preserves cardiac output and will not result
