Chapter 7 Ronald N. Roth, Raymond L. Fowler, and Francis X. Guyette Shock is a life-threatening physiological state characterized by decreased tissue perfusion and end-organ tissue dysfunction, and is a significant predictor for complications including death [1]. The presence of shock must be recognized and therapeutic interventions must be started early to prevent progression. Unfortunately, the identification and treatment of shock in the out-of-hospital setting are fraught with many difficulties and potential pitfalls. Patient assessment is often limited by the challenging out-of-hospital environment and lack of diagnostic and therapeutic options. The tools available for the diagnosis and treatment of shock in the field are limited. Even when shock is properly identified, the most appropriate out-of-hospital management is often unknown or the subject of great debate. In the out-of hospital setting, the identification of shock relies primarily on the recognition of signs and symptoms, including tachycardia, poor skin perfusion, and altered mental status. Note that hypotension, arbitrarily defined at a systolic blood pressure of less than 90 mmHg, is not an adequate definition of shock and may not adequately reflect the onset of tissue hypoperfusion [2]. Unfortunately, the early stages of compensated shock, with only subtle alterations in physical findings, are easily overlooked or misinterpreted by out-of-hospital care providers. Physiological changes associated with age, pregnancy, or treatment for medical conditions, such as beta-blockers for hypertension, may also mask or alter the body’s compensatory responses. As a result, the patient with severe shock may present with near-normal vital signs. Shock is a complex physiological process defined as the widespread reduction in tissue perfusion leading to cellular and organ dysfunction and death. In the early stages of shock, a series of complex compensatory mechanisms act to preserve critical organ perfusion [3]. In general, the following relationships drive this process. Blood pressure = Cardiac output × Peripheral vascular resistance Cardiac output = Heart rate × Stroke volume Any condition that lowers cardiac output and/or peripheral vascular resistance may decrease blood pressure. Alterations of heart rate (very low or very high) can lower cardiac output and hence blood pressure secondary to decreased cardiac filling. Also, decreasing stroke volume may lower cardiac output with a possible reduction in perfusion, as well. Stroke volume may be reduced by lower circulating blood volume (e.g. hemorrhage or dehydration), by damage to the heart (e.g. myocardial infarction or myocarditis), or by conditions obstructing blood flow through the thorax (e.g. tension pneumothorax, cardiac tamponade, or extensive pulmonary embolism). To aid in the evaluation and treatment of shock, it is often useful for the physician and EMS personnel to categorize the etiology of the shock condition [4]. Most EMS providers are familiar with the “pump-fluid-pipes” model of the cardiovascular system, with the pump representing the heart, pipes representing the vascular system, and fluid representing the blood [5]. Thus, categorizing shock into four categories may help prehospital providers and EMS physicians organize their assessments and approaches (Table 7.1). Accurate physical assessment is vital for the EMS provider to determine the etiology of the shock state (Box 7.1). Table 7.1 Categories of shock The diagnosis of shock depends on a combination of key historical features and physical findings in the proper clinical setting. For example, tachycardia and hypotension in an elderly patient with fever, cough, and dyspnea may represent pneumonia with septic shock. Hemorrhagic shock should be suspected in a middle-aged man with epigastric pain, hematemesis, melena, and hypotension. Hypotension, tachycardia, and an urticarial rash in a victim of a recent bee sting strongly suggest distributive shock secondary to anaphylaxis. Obstructive shock precipitated by a tension pneumothorax should be suspected in a hypotensive trauma patient with unilateral decreased breath sounds and tracheal deviation to the opposite side. An important problem in the prehospital diagnosis of shock is the frequent inaccuracy of field assessment. For example, Cayten et al. found an error rate of more than 20% for vital signs obtained by emergency medical technicians (EMTs) in a non-emergency setting [6]. The researchers suggest that when critical medical decisions will be based on the data gathered in the field, multiple assessments should be performed. Emergency medical services providers should look for the signs and symptoms of system-wide reduction in tissue perfusion, such as tachycardia, tachypnea, mental status changes, and cool, clammy skin (see Box 7.1). When available, adjunctive technologies can provide improved recognition and assessment of shock by demonstrating reductions in expired CO2, hypovolemia, obstruction, or poor contractility on ultrasound, and elevated serum lactate levels. Vital signs that fall outside of expected ranges must be correlated with the overall clinical presentation. Vital signs have a broad range of normal values and must be interpreted in the context of the individual patient. A petite 45 kg, 16-year-old female with lower abdominal pain with a reported blood pressure of 88 mmHg systolic by palpation may have a ruptured ectopic pregnancy, or may just be at her baseline blood pressure. An elderly patient with significant epistaxis may be hypertensive due to catecholamine release and vasoconstriction despite being relatively volume depleted. Consideration should be given to patient age, comorbid conditions, and medications that may affect the interpretation of vital signs. In the noisy field environment, providers often measure blood pressure by palpation rather than auscultation. Blood pressure by palpation provides only an estimate of systolic pressure [7]. Without an auscultated diastolic pressure, the pulse pressure (difference between systolic and diastolic pressure) cannot be calculated. A pulse pressure less than 30 mmHg or 25% of the SBP may provide an early clue to the presence of hypovolemic or obstructive shock. Conversely, a wide pulse pressure may be indicative of distributive shock [3]. Dividing the pulse rate by the systolic pressure typically produces a ratio of approximately 0.5 to 0.8, which is called the “shock index.” When that ratio exceeds 1.0, then a shock state may be present [8]. Previously healthy victims of acute hypovolemic shock may maintain relatively normal vital signs with up to 25% blood volume loss [3]. Sympathetic nervous system stimulation with vasoconstriction and increased cardiac contractility may result in a normal blood pressure in the face of decreasing intravascular volume, especially in the pediatric population. In some patients with intraabdominal bleeding (e.g. ruptured abdominal aneurysm, ectopic pregnancy), the pulse may be relatively bradycardic despite significant blood loss [9]. Emergency medical services personnel may equate “normal” vital signs with normal cardiovascular status [5]. The field team may be lulled into a false sense of security initially if the early signs of shock are overlooked, only to be caught off guard when the patient’s condition dramatically worsens during transport. Following trends in the vital signs may also help identify shock before patients reach abnormal vital sign triggers. Early recognition and aggressive treatment of shock may prevent progression to the later stages of shock that can result in the death of potentially salvageable patients [10]. Prehospital hypotension may predict in-hospital morbidity and mortality in both trauma and medical patients [11–13]. Jones et al. noted a 30% higher mortality rate for medical patients with prehospital hypotension [11]. Other studies have shown similar findings in trauma patients with prehospital hypotension, even with subsequent normotension in the emergency department [12,13]. Therefore, hospital providers should consider any episode of prehospital hypotension as evidence of significant shock and the presence of a critical illness. Despite their questionable value, orthostatic vital signs are often evaluated in the emergency department, and occasionally in the field. A positive orthostatic vital sign test for pulse rate would result in a pulse increase of 30 beats per minute after 1 minute of standing [14]. Symptoms of lightheadedness or dizziness are considered a positive test. Occasionally, orthostatic vital signs are performed serendipitously by the patient who refuses treatment while lying down, then stands up to leave the scene, and suffers a syncopal episode. This demonstration of orthostatic hypotension is often helpful in convincing the patient to allow treatment and transport. However, rescuers should not equate absence of orthostatic response with euvolemia. Capillary refill, an easy test to perform in the field setting, is not a useful test for mild-to-moderate hypovolemia [15]. Moreover, environmental considerations, such as cold temperatures and adverse lighting conditions, also affect the accuracy of this technique for shock assessment. On-scene estimates of blood loss by EMS providers may influence therapeutic interventions, including fluid administration. However, studies suggest that providers are not accurate at estimating spilled blood volumes [16]. Hypoxia is a common manifestation of shock states. Patients in various stages of exsanguination may not have sufficient blood volume to adequately perfuse the body with oxygen. Unfortunately, pulse oximetry alone cannot detect the adequacy of oxygen delivery. Pulse oximetry may fail to detect a pulse when blood flow is reduced [17,18]. Like pulse oximetry, capnography may also serve as an important tool in the evaluation and treatment of shock in the prehospital setting [19–22]. Capnography is the measurement of the exhalation of carbon dioxide from the lungs. Exhaled end-tidal carbon dioxide (EtCO2) levels vary inversely with minute ventilation, providing feedback regarding the effect of changes in ventilatory parameters [23,24]. Additionally, changes in EtCO2 are virtually immediate when the airway is obstructed or the endotracheal tube becomes dislodged [25]. EtCO2 concentration may be influenced by factors other than ventilation. For example, EtCO2 levels are reduced when pulmonary perfusion decreases in shock, cardiac arrest, and pulmonary embolism [26–28]. EtCO2 is most useful as an indicator of perfusion when minute ventilation is held constant (e.g. when mechanical ventilation is applied) [20,26]. 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. Use of portable ultrasound in the field can facilitate the recognition of immediately life-threatening causes of shock including intraabdominal hemorrhage, cardiac tamponade, or an abdominal aortic aneurysm. Many EMS agencies, primarily air medical services, have deployed ultrasound for field evaluations, including the focused assessment by sonography in trauma (FAST) examination [29]. Ultimately, the EMS medical director must determine if the cost and time of acquiring equipment, training, and performing the 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 basic skills (e.g., airway maintenance). There is growing interest in the use of biomarkers that can be used to identify, monitor, and predict the outcome in shock [30]. Point-of-care testing devices make measurement of biomarkers in the field an attractive option. Elevation of the serum lactate may reflect anaerobic tissue metabolism in acute sepsis and shock [30–32]. In the emergency department, elevated lactate in the setting of infection indicates septic shock and the need for early sepsis therapy. Elevated point-of-care venous lactate is associated with increased mortality risk and the need for resuscitative care in trauma patients. Indeed, recent work by the RESUSCITATION OUTCOMES CONSORTIUM in prehospital trauma research indicates that lactate levels may rise before blood pressure drops, and that an elevated lactate level in the setting of trauma may be a useful predictor of a patient that will require aggressive resuscitation. Serial lactate measurements may indicate the progress of ongoing resuscitation [33]. In summary, although technology may offer future value, the current evaluation of the potential shock victim in the out-of-hospital setting is challenging due both to limited assessment capability in this environment as well as fewer diagnostic tools. Both the provider and the medical oversight physician must be cautioned on placing too much emphasis on a single set of vital signs or a limited assessment. All treatment approaches to shock must include the following basic principles. 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 IV fluids. The treatment of cardiogenic shock in an unresponsive elderly patient with ventricular tachycardia (VT) 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 out-of-hospital setting (primarily fluids, inotropic agents, and vasopressors), field treatment may be individualized for the four categories of shock: hypovolemic, distributive, obstructive, and cardiogenic.
Hypotension and shock
Introduction
Pathophysiology
Type of shock
Disorder
Examples
Comments
Hypovolemic
Decreased intravascular fluid volume
Hypovolemic shock states, especially hemorrhagic shock, produce flat neck veins, tachycardia, and pallor
Distributive
Increased “pipe” size: peripheral vasodilation
A. Drug or toxin induced
B. Spinal cord injury
C. Sepsis
D. Anaphylaxis
E. Hypoxia/anoxia
Distributive shock states usually show flat neck veins, tachycardia, and pallor. Neurogenic shock due to a cervical spinal cord injury tends to show flat neck veins, normal or low pulse rate, and pink skin
Obstruction
Pipe obstruction
A. Pulmonary embolism
B. Tension pneumothorax
C. Cardiac tamponade
D. Severe aortic stenosis
E. Venocaval obstruction
Obstructive shock states tend to produce jugular venous distension, tachycardia, and cyanosis
Cardiogenic
“Pump” problems
A. Myocardial infarction
B. Arrhythmias
C. Cardiomyopathy
D. Acute valvular incompetence
E. Myocardial contusion
F. Myocardial infarctionG. Cardiotoxic drugs/poisons
Cardiogenic shock states tend to produce jugular venous distension, tachycardia, and cyanosis
Evaluation
Future technologies in the assessment of shock
General approach to shock
Hypovolemic shock
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