Chapter 46. Classification of Shock

Critical illness is defined as “any patient who is physiologically unstable, requiring constant and minute-to-minute titration of therapy according to the evolution of the disease process.”1 It is a continuum often culminating in rapid decline, shock, organ failure, and, frequently, patient demise. Traditionally, shock is defined as a clinical diagnosis identified through physical manifestations observed by medical staff.2 Complementing clinical acumen is the recognition of accumulating oxygen debt due to perturbations of microvascular circulation. Early phases of evolving shock may manifest through biochemical markers with minimal physical alterations.3–5 Although typically considered an intensive care unit (ICU) ailment, shock develops well before ICU admission with patients often initially presenting to the emergency department (ED). Effective, timely shock treatment requires a continuum of care beginning with prehospital providers, continuing within the ED, and concluding within the ICU.6,7 Thus, shock treatments should be defined by level of care rather than location of care.8

With the ever-increasing incidence of the critically ill and injured initially presenting through the ED, active emergency medicine participation in the continuum of care is essential. The number one reason for ED overcrowding is reported as a severe lack of accessible ICU beds.9 Lambe et al noted a 59% increase of ED critical care volume with an 8% decrease in nonurgent patients10 (Figure 46-1). This is mirrored nationally with 23% of ED patients triaged as requiring immediate or emergent (within 15 minutes) care. One of every 10 patients hospitalized from the ED is directly admitted to the ICU.11 Underscored is the clinical reality that emergency medicine physicians are seeing a higher volume of patients, with more patients severely ill than in the past.

ED epidemiology of shock remains speculative as it is typically veiled within other diagnoses. However, shock is a significant contributor to ED critical care volume; an estimated 1.1 million patients present to the ED with potential shock each year.12 From 1999 to 2002, the prevalence of patients requiring emergent resuscitation increased from 17% to 22%.11,13 Mortality is high, ranging from 23% to 80%, depending on the type of shock, patient age, and comorbidities.14–17 As Americans age, the incidence of shock is expected to increase with estimates of one half of patients initially presenting to the ED.15

Traditionally, the diagnosis of shock is made based on clinical signs and symptoms such as hypotension, tachycardia, weak pulse, and cold, clammy skin. Unfortunately, due to diverse circumstances, many of these signs and symptoms—or their absence—prove to be unreliable gauges of the presence and/or degree of shock. Furthermore, different etiologies of shock often result in differing degrees of signs and symptoms. For instance, due to pathologic vasodilatation and excessive organ dysfunction, sepsis will account for a much more complicated array of signs and symptoms than those attributed to hemorrhage. Moreover, otherwise healthy individuals possess the ability to sustain a considerable loss of volume before exhibiting such obvious signs and symptoms, while a less healthy patient, or one with significant preexisting comorbidities, may not be able to endure even a small volume loss without demonstrating serious signs and symptoms. In short, depending on the patient's age, comorbidities, and clinical circumstances, shock may exist prior to the onset of evident signs and symptoms.

Therefore, shock is not defined by clinical condition, but rather by biochemical outcome resulting from ineffective tissue perfusion, that is, inadequate delivery of oxygen and substrates for normal cellular function.18,19

Understanding shock requires understanding the concepts of oxygen delivery. Oxygen delivery (DO2) is the total amount of oxygen bound to hemoglobin (Hg) and delivered to the peripheral tissues per minute. It is calculated as follows (see Figure 46-2):

DO2 = CO × CaO2 × 10

Cardiac output (CO) is the most important determinant of oxygen delivery. As illustrated in Figures 46-3, 46-4, 46-5, 46-6, CO has the ability to compensate for increases in metabolic needs or decreases in O2-carrying capacity. However, CO is a product of both heart rate and stroke volume (SV), and SV is affected by a multiplicity of factors. Thus, CO can be difficult to predict and manipulate.

Hg is another significant contributor to oxygen delivery. As Hg is easily manipulated through transfusion, it becomes an important factor in regulating oxygen delivery. A schematic of a train may represent the impact of these components on the DO2 system. How much oxygen is delivered to the tissues through the microvasculature depends on how many oxygen-carrying units (Hg) are present, how many of those Hb units are effectively carrying oxygen, and how effectively the heart is working to transport the oxygenated units. In cases with accumulating oxygen debt, demonstrated through elevated lactate and/or decreased central venous oxygen saturation (ScvO2), individual patient requirements must be assessed by considering the previously discussed components of oxygen delivery (DO2 = CO × CaO2 × 10):

1. Is there sufficient oxygenation?

2. Is there sufficient preload—does the patient require further fluid resuscitation?

3. Is there sufficient afterload for end-organ perfusion?

4. Is the concentration of oxygen-carrying units optimal? This is best assessed via a postresuscitation Hb, as the initial value may be significantly hemoconcentrated.

Arterial oxygen saturation (SvO2), measured as blood is ejected from the left side of the heart, is approximately 100%. As oxygenated blood circulates through the microvasculature, an estimated 25% of delivered oxygen is extracted by the peripheral tissues. This is best measured by evaluating the SvO2 through a pulmonary artery catheter. However, because of efficacy and safety questions surrounding pulmonary artery catheters,20 the measurement of ScvO2 has been proven a functional surrogate,19 and because of logistics, ScvO2 is a more practical and less morbid alternative in the ED and even ICU setting.

ScvO2 is measured through a central line placed into the superior vena cava (SVC). This translates into the oxygen saturation report from a venous blood gas taken from the distal port of a typical internal jugular (IJ) or subclavian (SC) central line, or from an electronic readout from a central line with an appropriate sensor. ScvO2 provides a measurement of global tissue hypoxia. For patients in shock, ScvO2 is typically 5–7% higher than SvO2. Thus, ScvO2 measurements below 70% may represent significant unresolved oxygen debts.19 ScvO2 can be measured by individual blood draws from a typical SVC central line or one may use a central line that allows continuous monitoring of ScvO2.

Clinical Implications of Shock Pathophysiology

Traditionally systolic blood pressure (SBP) or mean arterial pressure (MAP) is used to denote shock (<90 or 65 mm Hg, respectively). This is based on the misconception that peripheral blood pressure universally equates to end-organ perfusion. Traditionally, shock has been defined or diagnosed at the point at which it could easily be identified via vital sign aberrations. However, shock does not commence when blood pressure deteriorates; blood pressure deteriorates when the body can no longer compensate physiologically for oxygen debt not yet identified and/or addressed. Cryptic shock, also described as normotensive shock, refers to a physiologic state at the microvascular level resulting in accumulating oxygen deficit. Cryptic shock confers a high risk of morbidity and/or mortality.21–24 Biomarkers, in conjunction with vital signs and physical exam, assist in early identification. If developing shock is arrested prior to decompensation, significant mortality benefit is achieved. This concept is already established in hemorrhagic/traumatic,25–28 cardiovascular,29–32 septic,21,33–35 and general critical shock presenting to the ED.36–37

The presenting signs and symptoms of specific types of shock are presented elsewhere in this text. As with any emergent patient, whether in the ED, ICU, or deteriorating in a less monitored setting, airway, breathing, and circulation should be quickly assessed on presentation and intervened upon as necessary.

Vital signs should be checked frequently. This is a reality that cannot be overstated; in a scenario in which the patient is unstable, vital signs are, by definition, changing unpredictably. In the presence of such a dynamic situation, the repeated monitoring of vital signs may often translate into the difference between recovery and significant morbidity and/or mortality.

An initial set of vital signs should include blood pressure, temperature, heart rate, respiratory rate, oxygen saturation, fingerstick glucose, and ECG. The patient should be placed onto a cardiac monitor with frequent reassessments. A rectal temperature should be considered in all patients. Any vital sign abnormality is a clear indicator that further workup is warranted.

Any patient with clear or suspected shock requires a thorough physical exam, including the often omitted skin, back, urogenital system, and all orifices. Potential etiologies of shock should be considered during each component of the physical exam. Other chapters will discuss specific elements; the following list is only a general reminder of elements to include or consider:

1. General appearance—“How does the patient look when I walk into the room?” The patient's general appearance will direct the immediate plan of action.

2. Mental status and full neurologic exam—Altered mental status refers to a wide spectrum from confusion to coma. Mild, new confusion may be an early indicator of an ominous process, especially in the elderly. A complete neurologic exam should be performed. When the neurologic exam is limited, radiographic assessment may be required.

3. Head, ears, eyes, nose, and throat—An oral process is a potential septic source frequently overlooked.

4. Neck—Hypotension with full neck veins requires consideration of a cardiac etiology, and hypotension with flat neck veins may indicate a systemic origin. Furthermore, consideration should be given to an infectious or traumatic process contributing to the presentation. Swelling that causes tracheal deviation may be due to a pharyngeal abscess. In the setting of trauma, tracheal deviation may be due to hemorrhage, and crepitus may be due to a laryngeal fracture. Furthermore, a cervical spine fracture may lead to neurogenic shock.

5. Chest/heart/lungs—Potential etiologies that may manifest acutely as shock include but are not limited to acute myocardial infarct, pericardial tamponade, myocarditis, tension pneumothorax, and/or pneumonia.

6. Abdominal exam—An extensive evaluation in conjunction with the history for physical manifestations of multiple diseases is important. Considerations include but are not limited to vascular insufficiency, bowel perforation, cholangitis, hemorrhage, and perforated stomach ulcer. Radiographic exam is often necessary. Notably an unimpressive abdominal exam does not rule out a significant insult; notoriously, the elderly may present with a seemingly unimposing exam while harboring significant pathophysiology.

7. Urogenital exam—A complete urogenital exam will prevent missing important causes of toxic shock syndrome such as intrauterine devices and tampons, or sepsis due to Fournier's gangrene in a diabetic patient.

8. Back—If the back has not been evaluated, only half of the patient has been examined. In patients using intravenous drugs, consider an epidural abscess.

9. Rectal exam—Evaluation may include but should not be limited to perirectal abscess, blood, and foreign body.

10. Skin—Septic shock may be from an unrecognized infected joint, decubitus ulcer, or endocarditis. Especially in obese patients in whom heart sounds can be difficult to auscultate, it is even more important to check hands, feet, and nail beds.

Classification of Shock

The clinical utility of the differential diagnosis of shock is based on understanding differences in effective tissue perfusion. Shock can be divided into four categories: hypovolemic, distributive, cardiogenic, and obstructive shock. Poor venous return is the base etiology of hypovolemic (absolute reduced intravascular volume) and distributive (ineffective vasomotor tone, relative reduced intravascular volume) shock. Cardiogenic shock is due to pump failure, so while there may be adequate intravascular volume, there is inadequate circulating volume. Finally, obstructive shock is due to a structural impediment of blood flow through the cardiac circuit. Additionally, there are mixed forms of shock with various overlaps of the above categories.2,18

Hypovolemic Shock

Hypovolemic shock is due to decreased intravascular volume, leading to decreased preload and therefore CO, resulting in reduced oxygen delivery. Potential etiologies include dehydration, hemorrhage, vomiting, severe burns, and iatrogenic sources such as diuretics and vasodilators. Hypovolemic shock can be recognized clinically by tachycardia, tachypnea, hypotension, narrow pulse pressure, altered mental status, decreased venous pressure, decreased urine output, and capillary refill. These signs and symptoms are derived from the lack of baroreceptor activation, which tends to increase heart rate and contractility coupled with a lack of stretch receptor activation in the atria leading to reduced release of atrial natriuretic peptide. Other acute changes that occur include activation of the renin–angiotensin–aldosterone system, mediated by the kidney. Angiotensin causes two main responses: vasoconstriction of the arteriolar smooth muscle and secretion of aldosterone, which promotes sodium reabsorption and water retention that results in extreme thirst. Often, these clinical symptoms are not recognized until 10–20% of whole blood volume has been lost. Importantly, it is possible for children to compensate for loss of volume for a longer period of time than adults (blood pressure maintenance despite hypovolemia). However, when decompensation commences, clinical decline is extremely rapid, often with poor outcomes. Fluid replacement and blood transfusions are the ultimate treatments for hypovolemic shock.

Cardiogenic Shock

Cardiogenic shock results from significant “pump failure” that may occur due to valvular pathology, myocardial insult, or pericardial pathology.18 Depending on patient reserve, for myocardial etiologies, cardiogenic shock may occur when 40% of the myocardium is compromised, due usually to toxins, ischemia, immune, or inflammatory processes.38 The reduction in effective CO results in decreased DO2. The clinical manifestation may appear similar to hypovolemia (see above), except the patient may have jugular venous distension (due to increased jugular venous pressure) and a pulmonary exam consistent with edema (due to fluid backup resulting from inefficient pumping of the heart). Additionally, there may be cardiac sounds such as a new murmur or ECG changes that may guide resuscitation. Diagnosis of cardiogenic shock can be made by clinical findings (as above); radiologic findings, which may show poor ventricular function or ventricular septal rupture on echocardiography; or ECG findings, which may demonstrate arrhythmias or signs of ischemia.

Initial treatment for cardiogenic shock often consists of carefully chosen combinations of vasopressors and inotropic agents. Vasopressors cause vasoconstriction while inotropic agents increase the force of cardiac contraction, depending on which receptors are stimulated by these medications. The goal is to increase perfusion of the ischemic myocardium. In the particular case of cardiogenic shock, however, extreme heart rates must be avoided due to increased myocardial oxygen consumption, which may further impair cardiac function and worsen the cardiogenic shock. In addition, there is the potential for increasing permanent damage to the heart (by increasing infarction size or causing valvular dysfunction). Short-acting inotropes, such as dobutamine, dopamine, or norepinephrine, should be considered, while longer-acting agents such as milrinone should be used with caution. (Please refer to Chapter 16 for further details.) Cautious fluid administration might be considered as required to maintain preload and thereby CO, but must be monitored carefully. In cases of myocardial infarction, rapid definitive treatment of coronary artery reperfusion should be sought. When rapid transport to a cardiac catheterization laboratory is not possible, chemical thrombolysis and/or mechanical device support such as an intra-aortic balloon pump (IABP) should be considered. Additionally, in appropriate cases a left ventricular assist device (LVAD) may be a necessary bridge to cardiac transplant.

Obstructive Shock

Obstructive shock is an extracardiac obstruction resulting in decreased diastolic filling or decreased ejection fraction. Usually both diastolic filling and decreased ejection are involved, with one predominating. Decreased CO occurs from decreased diastolic filling such as occurs in restrictive pericarditis and cardiac tamponade. Decreased CO is also seen—immediately—with large pulmonary emboli. A large pulmonary embolus (or multiple smaller ones) decreases the cross-sectional area of blood flow from the right ventricle to the left atrium causing right ventricular overload and leading to right ventricular failure. The clinical presentation is similar to that of cardiogenic shock with hypotension and IJ distension but without pulmonary edema.

Distributive Shock

Distributive shock is due to significant vasodilatation that causes decreased preload. In the arterial bed, it manifests through decreased arterial resistance, causing hypotension. Distributive shock may arise from circumstances such as sepsis, anaphylaxis, adrenal insufficiency, and neurogenic shock.

Despite the various etiologic agents, sepsis is the most prominent example.

Initially, septic shock typically presents as hypovolemia due to both vasodilatation (distributive shock) and leaking capillary membranes (hypovolemic shock). However, a distinguishing clinical feature is significantly more intravenous fluid requirement. It is not uncommon for distributive shock patients to have a 6- to 10-L fluid deficit and still require vasopressors to maintain a reasonable mean arterial blood pressure (MAP ≥65mm Hg).39 Once the fluid deficit is abated, the typical manifestations of distributive shock, such as high CO, low systemic vascular resistance (SVR), and hypotension, emerge.

Interestingly, although the patient in distributive shock exhibits a high CO, it is paradoxically in conjunction with depressed myocardium. Inflammatory mediators cause myocardial depression so that the heart pumps less efficiently. The myocardial depression results in a depressed biventricular ejection fraction. In response to volume loading, the stroke work index is further reduced. However, it appears that simultaneously the ventricles dilate. The dilatation, in conjunction with an increased heart rate, provides the increased cardiac index (CI). This may actually be protective, as nonsurvivors who were unable to attain left ventricular dilatation have been observed to die from a cardiogenic form of septic shock.40

Although distributive shock manifests with a normal or increased CO, it is functionally ineffective due to maldistribution of blood flow caused by shunting either from or within an organ, such that the organ, either in part or whole, may be compromised. A common clinical example is a septic patient who has normal or increased CO but is in acute renal failure. Clinically, distributive shock may manifest as a hyperdynamic, high-flow state with hyperdynamic heart sounds, prominent and rapid pulses, quick capillary refill, and a wide pulse pressure.

Mixed Shock

Although it would be helpful if all patients presented in a specific isolated type of shock, frequently there is significant overlap requiring solid clinical acumen. The most challenging clinical example is septic shock, which may manifest with multiple components of the various forms of shock listed above.

• Hypovolemic shock—Septic shock patients presenting with a lactate ≥4 commonly have a 6- to 10-L fluid deficit. Aggressive fluid administration is a mainstay of initial treatment, underscoring the importance of measuring central venous pressure (CVP) on presentation and using this measurement to guide the amount of fluid resuscitation.
• Distributive shock—Bacterial-derived mediators such as endotoxin, along with components of the inflammatory cascade, cause distributive shock with low SVR early in the disease presentation and normal to high CO in later stages.
• Cardiogenic shock—Although the typical description of septic shock is high CO in the face of a low SVR, early septic shock frequently manifests as a low CO/CI state consistent with hypodynamic, cardiogenic shock. In the early goal-directed therapy (EGDT) study of Rivers et al, the average time to enrollment was 1 hour with the CI ranging between 1.7 and 2.9.21 Depressed myocardium persisted even after fluid resuscitation, implying myocardial dysfunction rather than a factor of decreased preload as the etiology of a low CI. The high CO state arises after the compensatory dilatation of the ventricles as described earlier in the section “Distributive Shock.”40,41

The inflammatory response of any of these forms of shock, especially distributive, may result in multiple organ dysfunction syndrome (MODS). Often at this time, the only therapeutic options left are supportive with many patients refractory to the support.

Interventions and procedures are based on the type of shock suspected. All require confirmation that oxygen delivery is meeting demand. However, not all facilities are equipped to deal with patients in shock. Thus, transfer to an ICU or to an ED that has more resources may be necessary.

Noninvasive tests depend on the type of shock suspected. Most cases will require ECG, x-ray, pulse oximetry, and continuous vital sign monitoring. The role of ultrasound is rapidly expanding beyond the standard extended focused assessment for trauma (EFAST), which is sensitive and reliable in the assessment of trauma patients. Ultrasound applications such as the ability to look at the ventricle size, estimate the ejection fraction, and determine the collapsibility of the inferior vena cava are sensitive in cases of differentiated and undifferentiated shock.42–49 If the patient is sufficiently stable to leave the department, further noninvasive diagnostic testing is based on suspected shock etiology such as CT for blunt trauma or PE.

Laboratory testing should also be based on the type of shock but generally includes chemistry, complete blood count (CBC), coagulation profile, troponin, lactate, arterial blood gas, central venous blood gas (if continuous ScvO2 monitoring is not available), urinalysis, and cultures of blood and urine. Additional labs may include liver function tests, thyroid function tests, base deficit, toxicology screening for medications or drugs of abuse, and an ethanol level.

Depending on the cause of the shock, potential invasive procedures include:

• General practice for all forms of shock:

  1. Central line placement for administration of vasopressors, measurement of CVP, measurement of ScvO2 (preferably SC line or IJ line), need for multiple ports, or an inability to establish sufficient peripheral intravenous accesses.

  2. Arterial line placement for continuous arterial blood pressure monitoring should be considered in all hypotensive patients requiring vasopressors.

• Cardiogenic shock should be considered for rapid transfer to the cardiac catheterization lab; however, these patients may additionally require a balloon pump as a bridge to percutaneous cardiac intervention or bypass surgery if not readily available.
• Obstructive shock interventions are based on potential etiology:

  1. Pericarditis or cardiac tamponade: Pericardiocentesis, traditional or guided by real-time cardiac ultrasound or echocardiography.

  2. Massive pulmonary embolus: Thrombectomy, emergent thoracotomy, and cardiopulmonary bypass.

Cryptic Shock: Support for Early Recognition and Treatment

Shock must be recognized before it can be treated. Fulminant or late forms of shock manifesting with hypotension are not difficult to identify. Diagnosing shock before physiologic deterioration is a far greater challenge. However, significant improvements in morbidity and mortality can be achieved with early recognition of biochemical or cryptic shock that manifests as physiologic deterioration on a microvascular level, prior to deterioration of global parameters such as blood pressure (Figure 46-7).

• Cryptic shock in severe sepsis and septic shock: The EGDT trial demonstrated an absolute mortality benefit of 16% when septic patients who were hypotensive after a fluid bolus OR and had a lactate ≥4 mmol/dL were treated under a protocol that normalized CVP, blood pressure, ScvO2, and lactate. The authors then sought to evaluate what happened to patients who “looked good” with a normal blood pressure at presentation but had abnormal biomarkers. A subgroup analysis of EGDT trial showed that for patients who were normotensive (MAP >100 mm Hg) with abnormal biomarkers (lactates ≥4 mm Hg and ScvO2 <70%) but for whom practitioners were able to achieve biomarker normalization within 6 hours, the mortality benefit was 40%.48

Authors who stratified infected ED patients by lactate found that an initially elevated lactate was associated with ICU admission from the ED, transfer to the ICU after admission to the floor, and increased in-hospital mortality.49

Another study evaluated infected patients presenting to the ED with lactate ≥4 mmol/dL. Twenty-nine percent of this population was normotensive, yet mortality, if lactate was not normalized within 6 hours, was 55%. For every 10% decrease in lactate, there was a corresponding 11% decrease in mortality.33

• Cryptic shock in congestive heart failure (CHF): In another study, patients with end-stage CHF with an ejection fraction ≤30% presenting in decompensated CHF were stratified by lactate. They were then treated by protocol using ScvO2 as a real-time guide to management instead of traditional use of vital signs alone. The treatment group was compared with a control group of clinic patients with known, stable, end-stage CHF (EF <30%) for 3 months. There was no statistical difference in vital signs, or Killip and New York Heart Association criteria, among the three groups.

The authors found that 50% of their patient population with normal vital signs (as designated by the control group) had evidence of ongoing biochemical shock with significantly lower presenting ScvO2 and higher lactate. Both values significantly improved with protocol-directed treatment based on ScvO2 and lactate rather than vital signs alone.32,50

• Cryptic shock in general shock patients: Rady and Rivers evaluated patients presenting to the ED in shock. After triage, the patients were resuscitated to an MAP >70 mm Hg and CVP ≥15 mm Hg. After achieving MAP and CVP goals, ScvO2 and lactate were measured. They found 50% of patients with an MAP >70 mm Hg and SBP >100 mm Hg had an ScvO2 <65% and a lactate >2. This level of anaerobic metabolism supported a continued process of biochemical shock in the face of traditionally “normal” blood pressure. Additional resuscitation led to a significant increase of ScvO2 (52–65%; P < .05) and decreased lactate (4.6–2.6; P < .005) while MAP and SBP remained unchanged.36
• Cryptic shock in trauma patients—The Golden Hour and Silver Day25: Occult shock in trauma patients has been extensively studied. Scalea et al demonstrated that biochemical markers of hypoxia were present in trauma patients with “normal” vital signs. Thirty-nine percent of patients with normal vital signs had evidence of tissue hypoxia (ScvO2 <65%, lactate >2.5 mmol/dL). The occult hypoxia group had more extensive injuries and greater blood loss, and required significantly more transfusions.23

Another study evaluated lactate clearance in critically injured trauma patients who had an elevated lactate, SBP greater than 100, pulse rate less than 120, and urine output greater than 1 mL/kg/h. Sixty-eight percent of patients had occult hypoperfusion (elevated lactate with normal blood pressure) during the first 24 hours. Of those with occult hypoperfusion, if the lactate was cleared within 24 hours, multisystem organ failure, respiratory compromise, and mortality were significantly reduced (P < .05). The authors concluded that early identification and aggressive resuscitation based on biomarker normalization improved survival and reduced morbidity in the critically injured patient.25 Other studies have since confirmed the concept of resuscitation to normalization of biomarkers in trauma patients.51–60

Primary Survey

As with all ED patients, especially those who present as critically ill or injured, the first step is assessing airway, breathing, and circulation. Simultaneously, large-bore IV access should be established, oxygen should be administered, and continuous vital sign monitoring and pulse oximetry are applied. With establishment of IV access, blood can be drawn and held for laboratory and point-of-care testing. Laboratory evaluation should be targeted to the type of shock suspected but should include lactic acid. (Note: Lactate is metabolized by the liver. A patient with liver insufficiency or failure may have an elevated lactate due to reduced clearance rather than oxygen debt. Furthermore, due to shunting, liver failure patients frequently demonstrate an elevated ScvO2. Therefore, a high lactate and high ScvO2 may not provide information about oxygen debt. However, a high lactate and low ScvO2 may signify the presence of oxygen debt.)

• Airway: If in doubt, secure the airway. A patient in shock usually has multiple reasons for intubation and mechanical ventilation. Ventilatory failure should be recognized early through the clinical presentation. In shock, the decision to intubate is made by the clinician, not the lab. Thus, a blood gas is not required. The decision to intubate may fall into one of the following four categories:

  1. Respiratory failure: Respiratory muscle fatigue may manifest as inability to speak in complete sentences, labored breathing, either rapid or slow respiratory rate, diaphoresis, pale or cyanotic skin, paradoxical abdominal breathing, or the use of accessory muscles.

  2. Mental status change: If the patient is obtunded with a GCS <8, or is combative or uncooperative, intubation should be considered.

  3. Potential for decline or unsupervised location: If the patient is hypermetabolic or has potential to decline, early intubation is the best course of action. This includes the necessity to send the patient out of the department for diagnostic testing or for transfer to another unit or hospital. Additionally, if the physician is in a low-coverage, high-acuity situation in which other patients require significant time, this should be considered similar to an unsupervised or low supervision state, and the patient should be intubated.

  4. Significant oxygen debt, multisystem organ failure or insufficiency: The increased metabolic demand of failing respiratory muscles consumes a disproportionate component of “whole-body oxygen delivery.” Thus, supporting ventilation assists in oxygen delivery to other high-need areas.2

• Breathing: During the primary survey, an assessment of breathing only involves auscultation. Adventitious breath sounds may suggest cardiogenic or obstructive shock, absent breath sounds in the face of shock may suggest a tension pneumothorax and therefore obstructive shock, and an area of decreased breath sounds may suggest a consolidation and therefore pneumonia in septic shock. For patients intubated during the primary survey, it is important to confirm endotracheal placement by ensuring that the endotracheal tube (ETT) was seen passing through the vocal cords, auscultation, appearance of condensation in the ETT, end-tidal CO2 detection, maintenance of oxygen saturation with manual or ventilator-delivered breaths, and CXR. Other methods such as bronchoscopy, ultrasound, or esophageal detector devices may be used as well. Direct visualization, however, remains the “gold standard” for confirming tube placement.
• Circulation: Specific causes of shock may be suggested by findings such as muffled heart sounds and electrical alternans (pericardial tamponade), or murmurs (valve pathology, papillary muscle rupture). Furthermore, injuries such as flail chest or penetrating wounds may also suggest certain injuries or, more likely, the need for definitive treatment in an OR. Pulses in all extremities should be checked for quality and symmetry. Vital signs should be rechecked frequently.
• Neurologic exam, including neurologic assessments of the extremities as deficits, may indicate a neurogenic cause of the shock.
• Full-body exposure with special attention given to clues to the etiology of the shock.

With hypotensive patients, although early consideration should be given to administering a vasopressor, it is important to remember that for a vasopressor to be effective, there must be sufficient intravascular volume “to press.” Fluid is the fundamental component for the initial therapy for shock. With appropriate volume resuscitation, the CI may improve by 25–40%,61 and up to half of patients presenting with hypotension due to distributive shock may resolve with fluid replacement alone.62 How much fluid and how fast it may be given are based on shock etiology and individual patient response. Cardiogenic shock due to an ischemic left ventricle will require smaller, frequent boluses such as 250 cm3 every 30 minutes while monitoring for inotropic failure and treating with vasopressors or inotropic agents as needed. However, cardiogenic shock due to right ventricular failure will need significantly more fluid at a faster rate, though again dependent on patient response. Starting fluid resuscitation at 500 cm3 every 30 minutes for hypovolemic or distributive shock is a reasonable starting point, but it should be increased or decreased based on patient conditions or response.

Optimally, adequate fluid resuscitation occurs prior to administering vasopressors or inotropes. In extreme cases, the physician may choose to administer vasopressors in conjunction with giving fluid and then titrating down the pressor dose as volume is replenished. Note that oxygen debt and end-organ perfusion can be worsened in underresuscitated patients receiving vasopressors.

Secondary Survey

Obtain history from any available source. If the patient is unable to give an adequate history, speak with the EMTs and any friends or family.

Do a complete physical exam.

Assess results from interventions done in the primary survey; decide on further interventions and formulate a differential diagnosis.

Airway: If the patient has been intubated and placed on mechanical ventilation, or even if the patient has been placed on noninvasive ventilation with a rate, consider the following:

• Tidal volume: Traditionally, tidal volumes of 15 cm3/ kg were used. Recent data support the use of 6 cm3/kg in acute respiratory distress syndrome (ARDS).63 Because many emergently intubated patients are at high risk for ARDS, this recommendation is a good starting point for all respiratory failure patients.
• Weaning: Since mechanical ventilation is not a therapy in and of itself but is, instead, a support therapy, consideration should be given to weaning, as soon as mechanical ventilation is initiated. An initial blood gas should be checked for pH and PCO2, checking for carbon dioxide retention. Minute ventilation can then be titrated by adjusting the tidal volume, rate, and pressure support (for patients with spontaneous breaths). FiO2 can be weaned by pulse oximetry. If the patient is unstable and in current oxygen debt, wean the oxygen as permitted keeping the SaO2 100%. When oxygen debt has been resolved, wean as permitted keeping SaO2 ≥93%. Goal FiO2 is 30–40%.
• If intubated, consider an oral gastric tube for gastric decompression and a Foley catheter for bladder decompression pending urologic exam.

Circulation: If the patient remains hypotensive after appropriate fluid boluses:

• Fluid optimization: For patients who remain hypotensive despite sufficient IV fluid, there are additional considerations. First, it is important to consider how much fluid has been given. Certainly, for patients who have received <20 mL/kg, absent signs of fluid overload, it is prudent to continue administering IV fluid. However, at some point the question must be asked as to whether sufficient fluid has been administered or should vasopressors be initiated. If vasopressors have been started and the patient remains hypotensive, should they be increased, or a second agent added, or does the patient have an unmet fluid requirement? Volume status is very difficult to assess clinically in the critically ill patient and often is inaccurate. Currently the most clinically practical and dynamic bedside method of monitoring fluid requirement in the ED is through CVP. While central access is being obtained, crystalloid or colloid equivalent should continue to be administered peripherally as a 500-cm3 bolus every 30 minutes, depending on patient dynamics, until a goal CVP of >8 mm Hg is achieved.64 CVP measurements can be determined from femoral, IJ, or SC central lines. In the supine patient, a femoral line is almost as accurate as an IJ or SC central line, although this is not true if the head of the bed is placed at 30°. Furthermore, ScvO2 measurements are also more accurate when taken from an IJ or SC central line since they include venous drainage from the head. However, ScvO2 values can be obtained from a femoral central line. While not as accurate, the trend can be monitored and monitoring the trend can be as accurate as monitoring the trend of an IJ or SC central line. However obtained, the CVP and ScvO2 values will be critically important in optimizing therapy if initial fluid boluses are not sufficient, and therefore an SC or IJ line is preferable when possible.
• MAP optimization: If a patient remains hypotensive (MAP <65 mm Hg) after receiving adequate volume resuscitation (CVP >8 mm Hg), a vasopressor should be added to titrate the MAP ≥65 mm Hg. The MAP may be measured via a standard arterial line in either a femoral or radial location. An arterial line is recommended in hypotensive patients, especially if vasopressors are required, as noninvasive BP monitoring in hypotensive or tachycardic patients may be less accurate.39,64–68
• After CVP and MAP have been optimized, ScvO2 and serum lactate must be reassessed. If the values have normalized, treatment goals are complete. If they remain abnormal, oxygen debt and shock persist. To optimize DO2, the components of oxygen delivery must be reevaluated:

DO2 = CO × (Hb × SaO2 × 1.38)

CO = SV × HR

If SaO2, preload (CVP >8 mm Hg), and afterload (MAP >65) have been addressed, attention can be turned to Hg and CO. A repeat hematocrit (HCT) should be evaluated, as the pre-resuscitation analysis may be hemoconcentrated, and the administration of IV fluids may not yield a low HCT. If the HCT <30%, the patient should be transfused red blood cells until an HCT goal of ≥30% is achieved. If the goal CVP, MAP, and HCT have been achieved and the ScvO2 remains <70%, an inotropic agent should be considered to enhance forward flow and tissue oxygenation. The physician may choose to evaluate myocardial function by direct observation such as with a pulmonary artery catheter or echocardiography if immediately available. However, if there is any significant delay, inotropes should be initiated empirically.

Due to the short half-life, dobutamine is the most readily available and most commonly used inotropic agent. It should be considered if the CVP, MAP, and HCT goals have been met and the ScvO2 remains <70% despite resuscitation and vasopressor support. It is not advocated in tachycardic patients (HR >120).

At the end of the secondary survey, the patient should be reevaluated, checking all endpoint parameters and labs. This should be repeated as often as necessary.

Disposition

As soon as a shock patient is identified, the ICU should be notified and admission or transfer should be initiated. However, due to stressed ICU resources, the critically ill or injured patient may reside in the ED longer than optimal or appropriate. The emergency physician should have a clear understanding of the care required, balanced with the resources available for optimal patient care and disposition.