Shock Management - Traumatic shock
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Diagnosis And Management Of Shock In The Emergency Department

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Table of Contents
 
Table of Contents
  1. Abstract
  2. Case Presentation
  3. Introduction
  4. Critical Appraisal Of The Literature
  5. Pathophysiology
    1. Hypovolemic Shock
    2. Distributive Shock
    3. Cardiogenic Shock
    4. Obstructive Shock
  6. Emergency Department Evaluation
    1. Initial Stabilization
    2. History
    3. Physical Examination
  7. Diagnostic Studies
    1. Laboratory Studies
      1. Base Deficit
    2. Imaging
      1. Ultrasound
    3. Chest X-Ray
    4. Computed Tomography
    5. Echocardiography
    6. Other Diagnostics
  8. Treatment
    1. Cardiovascular Monitoring
    2. Fluid Resuscitation
      1. Goals Of Fluid Resuscitation
      2. Fluid Selection
    3. Central Venous Lines
      1. Arterial Lines
      2. Pulmonary Artery Catheters
    4. Vasopressors
    5. Clinical Course In The Emergency Department
      1. Deterioration
  9. Special Circumstances
    1. Shock In Pregnancy
    2. Traumatic Shock
    3. Septic Shock
    4. Anaphylactic Shock
    5. Cardiogenic Shock Due To Myocardial Infarction
  10. Controversies And Cutting Edge
    1. Early Goal-Directed Therapy
    2. Pulmonary Embolism
    3. Noninvasive Hemodynamic Monitors
  11. Disposition
  12. Summary
  13. In The March/April Issue of EM Practice Guidelines Update
  14. Pitfalls To Avoid In The Diagnosis And Management Of Shock
  15. Case Conclusion
  16. Clinical Pathway For Diagnosing And Managing Shock
  17. Tables
    1. Table 1. Categories Of Shock
    2. Table 2. Etiologies Of Cardiogenic Shock
    3. Table 3. Causes Of Shock In The Trauma Patient
    4. Table 4. Early Goal-Directed Therapy Protocol For Patients With Severe Sepsis And Septic Shock
  18. References

Abstract

Shock is a state of acute circulatory failure leading to decreased organ perfusion, with inadequate delivery of oxygenated blood to tissues and resultant end-organ dysfunction. The mechanisms that can result in shock are divided into 4 categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive. While much is known regarding treatment of patients in shock, several controversies continue in the literature. Assessment begins with identifying the need for critical interventions such as intubation, mechanical ventilation, or obtaining vascular access. Prompt workup should be initiated with laboratory testing (especially of serum lactate levels) and imaging, as indicated. Determining the intravascular volume status of patients in shock is critical and aids in categorizing and informing treatment decisions. This issue reviews the 4 primary categories of shock as well as special categories, including shock in pregnancy, traumatic shock, septic shock, and cardiogenic shock in myocardial infarction. Adherence to evidence-based care of the specific causes of shock can optimize a patient’s chances of surviving this life-threatening condition.

Case Presentation

You are working in the ED late one evening when an 82-yearold man is brought in by his son. His son reports that earlier today, his father had been in his usual state of health, but this evening he found his father confused, with labored breathing. On arrival, the patient has the following vital signs: temperature, 38°C; heart rate, 130 beats/min; blood pressure, 110/60 mm Hg; respiratory rate, 34 breaths/min; and oxygen saturation, 89% on room air. He is delirious and unable to answer questions. A focused physical examination demonstrates tachycardia without extra heart sounds or murmurs, right basilar crackles on lung auscultation, a benign abdomen, and 1+ lower extremity pitting edema. You establish intravenous access with a peripheral catheter and send basic labs. A further history obtained from the son reveals that his father has congestive heart failure with a low systolic ejection fraction, as well as a history of several prior myocardial infarctions that were treated with stent placement.

As you consider this case, you ask yourself whether this patient is in shock, and if he is, what are the specific causative pathophysiologic mechanisms? You review which diagnostic tests are indicated to assist with the differential diagnosis of shock and you consider options for the initial management of this patient.

Introduction

Shock is a state of acute cardiovascular or circulatory failure. It leads to decreased delivery of oxygenated blood to the body's organs and tissues or impaired oxygen utilization by peripheral tissues, resulting in end-organ dysfunction.1 The physiologic mechanism of oxygen delivery to peripheral tissues (DO2) is described in the formula in Equation 1.

Equation 1

DO2=(cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2 x 0.003)

Abbreviations: DO2, oxygen delivery; PaO2; partial oxygen pressure; SaO2, arterial oxygen saturation.

Blood pressure is not included in this formula; while shock is frequently associated with hypotension, patients may present with “cryptic shock” in which they have a blood pressure typically considered to be within normal ranges, yet they have pathophysiologic signs of shock (particularly early in their clinical course). Many patients in shock ultimately develop hypotension, but a high index of suspicion is necessary to identify patients with shock and normal blood pressures during their initial presentation.

Equation 2 demonstrates the influence that cardiac output has on blood pressure (as evidenced by mean arterial pressure). A mean arterial pressure that decreases below a critical threshold will result in decreased cardiac output and, thereby, decreased DO2.

Equation 2

MAP=CO x SVR

Abbreviations: CO, cardiac output; MAP, mean arterial pressure; SVR, systemic vascular resistance.

As noted in Equation 3, cardiac output is determined by stroke volume and heart rate, and stroke volume is affected by preload, afterload, and contractility. The concept of preload influencing stroke volume (and thereby affecting cardiac output and DO2) is a core physiologic aspect of the assessment and management of patients in shock.

Equation 3

CO=HR x SV

Abbreviations: CO, cardiac output; HR, heart rate; SV, stroke volume.

Changes in preload, stroke volume, system vascular resistance, and cardiac output can result in impaired tissue and organ perfusion. The impaired delivery of oxygen to peripheral cells that occurs in shock results in a transition from aerobic to anaerobic cellular metabolism. Anaerobic metabolism generates lactate via metabolism of glucose to pyruvate, and lactate can be used as a surrogate marker for tissue hypoxemia and the severity of shock. Cells can engage in anaerobic metabolism for a limited time, but persistent cellular hypoxia results in cell death and tissue necrosis, leading to multiorgan system dysfunction and failure. The saturation of venous oxygen measured from central vessels (such as the superior vena cava), is another biochemical marker of peripheral oxygen uptake and can be used diagnostically to help with prognosis in the comprehensive assessment of patients presenting in shock.

The pathophysiologic mechanisms that can result in shock are divided into 4 separate (but potentially overlapping) categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive.2 Definitive treatment for patients in shock depends on the specific etiology; however, this may not be immediately clear on initial presentation to the emergency department (ED). As with much of emergency medicine, the initiation of therapy and patient stabilization may occur simultaneously with evaluation. The goals in treating patients in shock are restoring adequate organ perfusion and oxygen delivery while considering/treating the possible cause(s) of shock.

In early shock, compensation occurs by modulation of cardiac output and vascular tone by the autonomic nervous system.1 Carotid baroreceptors respond to decreased blood pressure by triggering increased sympathetic signaling. This autonomic nervous system-mediated sympathetic response results in an increase in contractility and heart rate, thereby increasing cardiac output. (See Equation 1 and Table 1). In addition, increased sympathetic signaling results in alpha-1 receptor activation and systemic vascular resistance. This issue of Emergency Medicine Practice analyzes the pathophysiology of the 4 types of shock and provides best practice recommendations on the diagnosis and management in the ED.

Critical Appraisal Of The Literature

A literature search was performed using Ovid MEDLINE ® and PubMed from 1950 to December 2013. Areas of focus were shock, emergency management of shock, and emergency diagnosis of shock. Specific searches were performed for types of shock including the terms: hypovolemic, hemorrhagic, distributive, septic, neurogenic, anaphylactic, cardiogenic, obstructive, pulmonary embolism, and cardiac tamponade. Highquality review articles were noted and provided the foundation for additional primary literature review. Over 300 articles were reviewed, which provided background for further literature review.

The Cochrane Database of Systematic Reviews and the National Guideline Clearinghouse (www. guideline.gov) were also consulted.

Literature from emergency medicine journals was assessed. Although studies from the critical care or intensive care literature do not necessarily include ED patients, clinical lessons from these studies are often reasonable to apply to the ED population. Studies from cardiology literature were also included.

Randomized controlled trials were included in this review whenever possible. Due to the acute nature of patients presenting to the ED in shock, randomization in the ED can be difficult, thereby limiting the availability of these studies. Randomized controlled trials are more prevalent in the critical care and cardiology literature. Where randomized controlled trials are not available, prospective observational studies and retrospective studies were used.

Pitfalls To Avoid In The Diagnosis And Management Of Shock

  1. “His blood pressure is normal. He can’t be in shock.” Focusing on blood pressure alone as an indicator of shock can lead to missing signs of occult shock. Impaired organ perfusion, as evidenced by acute renal failure, altered mental status and/ or increased serum lactate concentration, is a sign of shock pathophysiology and obligates early, aggressive clinical management.
  2. “Let’s get the chest CT scan before deciding whether to give antibiotics or not.” Failure to give antibiotics within 1 hour of presentation for all cases of possible septic shock may result in increased mortality. Early empiric antibiotic coverage is indicated for suspected septic shock with a target of administering (not just ordering) antibiotics within 1 hour of presentation.
  3. “Her ejection fraction is 30%, so let’s start norepinephrine instead of giving a second liter of fluid.” Adequate volume resuscitation for hypovolemic patients is critical. Markers of tissue perfusion such as lactate clearance, ScvO2, pulse pressure variation with passive leg raise, and ultrasonographic measures of intravascular volume are appropriate determinants of the need for further volume resuscitation. A history of a low ejection fraction or other hypothetical concerns may lead clinicians to underresuscitate hypovolemic patients and may result in inappropriate initiation of vasopressors.
  4. “It could be a myocardial infarction, but let’s wait for the troponin to come back before calling cardiology.” Time-to-revascularization is one of the primary determinants of survival in patients with cardiogenic shock due to acute coronary syndromes. Delaying time to catheterization and revascularization will increase patient morbidity and mortality. When cardiogenic shock is possible, early consultation with cardiology and activation of the catheterization laboratory are necessary to optimize patient outcomes.
  5. “Let’s give a fifth liter of saline and see if her mean arterial pressure comes up to at least 60 mm Hg…” Starting vasopressors without adequately volume resuscitating a patient while following markers of tissue perfusion and intravascular volume status is inappropriate (see pitfall #3); however, not recognizing that vasopressors need to be started for patients who are not volume responsive is also inappropriate. Patients with a pathologically decreased systemic vascular resistance may require vasopressors to maintain mean arterial pressure even after volume resuscitation and normalization of intravascular volume status. Continuing to administer fluids and not recognizing the need for vasopressors can result in perpetuating complications of shock.
  6. “She has a fever and hypoxemia. Her hypotension is probably due to sepsis from pneumonia.” Failure to consider obstructive shock on the differential diagnosis can lead to inappropriate clinical management, such as treating a pulmonary embolism with antibiotics. Maintaining a broad differential diagnosis and considering obstructive pathophysiologic causes of shock, when clinically appropriate, can lead to more rapid diagnosis and treatment.
  7. “I read that a hemoglobin of 7 gm/dL is the evidence-based transfusion trigger, so let’s hold off on giving this hypotensive trauma patient blood.” While conservative transfusion thresholds are appropriate for critically ill patients without active hemorrhage, prompt resuscitation with blood products is critically important for patients presenting with hemorrhagic shock. Furthermore, the hemoglobin concentration will not reflect the degree of blood loss early in such a patient’s presentation, obligating the emergency clinician to identify possible acute hemorrhage based on the patient’s clinical circumstances.
  8. “Her mean arterial pressure of 50 mm Hg is probably just because she’s pregnant.” Numerous physiologic changes occur during pregnancy, including increased cardiac output, increased heart rate, and decreased systemic vascular resistance. The decrease in systemic Pitfalls To Avoid In The Diagnosis And Management Of Shock (Continued from page 16) vascular resistance usually results in a drop in the mean arterial pressure of 5 mm Hg to 10 mm Hg from normal prepregnancy levels. Mean arterial pressures < 60 mm Hg, however, should raise awareness of the possibility of pathophysiologic processes contributing to hypotension.
  9. “Let’s try bilevel positive airway pressure and see if his pneumonia gets better after antibiotics.” Recognition of multiorgan system failure and hypotension from septic shock that requires early intubation and mechanical ventilation is critically important. Failure to intubate early in the course of care for critically ill patients in septic shock can perpetuate the cycle of impaired oxygen uptake, deficient oxygen delivery to peripheral tissues, and increased metabolic demand from increased work of breathing. Furthermore, recognizing that a patient’s disease process will take days, rather than hours, to resolve prioritizes intubation above noninvasive mechanical ventilation.
  10. “I know how to treat sepsis: antibiotics, fluids and pressors. I don’t need a protocol.” Aggressive, protocolized, and bundled clinical management of patients in septic shock results in improved initial resuscitation and improved patient outcomes. Adherence to institutional guidelines for the initial treatment of septic shock is an important component of the acute care of severe sepsis and septic shock.

Tables

Table 1. Categories Of Shock

Table 2. Etiologies Of Cardiogenic Shock

References

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study will be included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.

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Publication Information
Authors

Jeremy B. Richards, MD, MA; Susan R. Wilcox, MD

Publication Date

March 2, 2014

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