Approach to Shock

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Author Credentials

Author: Benjamin J. Sandefur, MD, Mayo Clinic College of Medicine and Science

Editor: Todd A. Guth, MD, MHPE, University of Colorado School of Medicine:

Updated: September, 2019

Original Author: Jennifer Avegno, MD, Louisiana State University School of Medicine

Original Editor: David Manthey, MD, Wake Forest University School of Medicine

Created: 2008

Case Study

A 63 year old female patient is brought to the emergency department by pre-hospital providers. The patient’s family called 911 after they noticed her to be confused this morning. Paramedics found her to be oriented to person and place, though not oriented to time or event. Vital signs were notable for a temperature of 37.8 ° C, heart rate 132 beats per minute, blood pressure 88/48, and an oxygen saturation of 98% on room air. She was given 1 liter of intravenous normal saline during transport to the emergency department. On arrival, she appears ill and remains hypotensive, tachycardic, and confused.

Objectives

Upon completion of this module, the student will be able to:

Define shock
Describe a clinically relevant categorization for mechanisms of shock
Develop a diagnostic plan for a patient with shock of undifferentiated etiology
Discuss empiric management strategies for a patient with shock, directed by the presumed etiology of illness

Introduction

Shock is a pathophysiologic state in which the oxygen supply to body tissues inadequately meets metabolic demands, resulting in dysfunction of end-organs. Shock may arise by impaired delivery of oxygen to tissues, impaired utilization of oxygen by tissues, increased oxygen consumption by tissues, or a combination of these processes. While circulatory failure and hypotension is the most common and readily identified clinical presentation of shock, the manifestations of shock exist along a continuum of illness severity, thus a patient with initially normal vital signs may still be in shock.

Initial Actions and Primary Survey

Early recognition of shock and institution of empiric treatment is of utmost importance. Some patients in shock present with a readily identifiable etiology (i.e. gunshot wound to the abdomen), while others may be undifferentiated. A rapid and accurate assessment of the airway, breathing, and circulation, followed by a focused history and physical examination should be performed. Particular attention should be directed to neck veins (± jugular venous distention), cardiopulmonary examination, abdominal examination, and extremity examination (± signs of hypoperfusion or abnormal vasodilatation). A rectal examination is often indicated to assess for melena or hematochezia. Robust intravenous access (i.e. two large-bore IVs, intraosseous access, or central venous catheter) should be established. The patient should be placed on continuous telemetry, noninvasive blood pressure monitoring, and pulse oximetry. An ECG and chest radiograph should generally be obtained. Bedside ultrasonography (i.e. FAST examination) can provide valuable information to narrow the differential diagnosis. Initiation of intravenous fluid resuscitation is usually indicated, and is rarely harmful, to a patient in shock.

Presentation

The many causes of shock maybe categorized based on etiology. While various categorizations for shock exist, a commonly utilized and clinically relevant categorization is depicted in the following table.

Table 1.Categorization of Shock

Category	Physiology	Examples
Hypovolemic	Decreased intravascular volume resulting in decreased preload, stroke volume, and cardiac output	Hemorrhagic (major trauma, gastrointestinal bleeding, ruptured ectopic pregnancy, etc.) Non-hemorrhagic (vomiting, diarrhea, burns, etc.)
Cardiogenic	Impaired cardiac output secondary to cardiac pump function, rhythm aberrancy or structural defect	Arrhythmogenic (brady- or tachydysrhythmia) Cardiomyopathic (myocardial infarction, heart failure, etc.) Cardiotoxicity from medication Structural (valvular insufficiency, ventricular septal wall defect, etc.)
Distributive	Pathologic vasodilatation leading to relative intravascular volume depletion	Anaphylactic (IgE mediated allergic reaction) Septic (pneumonia, pyelonephritis, etc.) Neurogenic (spinal cord injury) Toxicologic (vasodilatory medication)
Obstructive	Impaired cardiac output due to pulmonary vascular or mechanical obstruction	Pulmonary vascular obstruction (pulmonary embolism, venous air embolism, etc.) Mechanical obstruction (tension pneumothorax, pericardial tamponade, left ventricular outflow tract obstruction, etc.)
Mixed / Other	Any of the above may be present concurrently	Cellular poisons (carbon monoxide, cyanide, etc.) Endocrinologic (adrenal insufficiency, myxedema coma, etc.) Environmental (hypothermia, etc.) Toxicologic etiology with cardiac and vasoplegic manifestations (calcium channel blocker, etc.)

Signs and symptoms of shock may be subtle or exceedingly clear. A history may be challenging or impossible to obtain in the shock patient, thus collateral history (i.e. from family, EMS, nursing facility, etc.) and a focused physical examination is of importance.

History: Patients in shock may complain of lethargy or weakness, or they may present because of altered mental status (i.e. CNS end-organ damage). Symptoms are frequently nonspecific, such as chest pain or dyspnea, and may be due to the primary insult (i.e. ACS, PE) or a result of end-organ tissue ischemia secondary to shock.

Hypovolemic shock due to hemorrhage is suggested by the report of trauma or bleeding from other source (melena or hematemesis from a gastrointenstinal source, vaginal bleeding from a gynecologic source, etc.).
Non-hemorrhagic hypovolemic shock may be suggested by decreased oral intake, diarrhea, vomiting or high ostomy output.
Cardiogenic or obstructive shock may be suggested by chest pain, shortness of breath, recent leg swelling, or syncope.
Anaphylactic shock may present as the sudden onset of pruritus, hives, or swelling following exposure to an inciting trigger.
Septic shock may be associated with signs of infection such as fever, cough, dysuria, abdominal or flank pain, or rigors.

In many cases, non-focal, vague complaints such as weakness, altered mental status, or malaise may be the only presenting symptoms of shock.

Physical Exam: A comprehensive physical examination provides important information to assist in narrowing a differential diagnosis for the patient in shock. Hypotension alone should not be used as the sole determinant of shock, as early shock may present with normal or even elevated blood pressure, and normal heart rate. Without prompt treatment of the patient in early shock, hypotension and tachycardia frequently follow. Altered mental status is common. Thready pulses, tachycardia and tachypnea are frequently present. Patients in shock often exhibit cool, pale or ashen skin with decreased capillary refill and dry mucous membranes; however, in distributive shock states the extremities may be inappropriately warm. In cardiogenic shock, arrhythmias, dependent edema, or new murmurs may be present, while jugular venous distention is seen in both cardiogenic and obstructive shock states.

Focused bedside ultrasonography is beneficial to assess for intraperitoneal hemorrhage, pneumothorax, or pericardial tamponade, and to assess global cardiac function and intravascular volume status. Vascular catastrophes such as abdominal aortic aneurysm with rupture may also be identified on bedside ultrasonography.

While physical examination findings may vary, a generalization of classic findings according to shock category is depicted below in Table 2. Understanding the how the pump, the tank, and the pipes are functioning when determining the category of shock is present. The pump refers to cardiac function as measured by cardiac output in terms of cardiac contractility and heart rate (HR). The tank refers to the amount of preload present, often measured by central venous pressure (CVP), and the pipes are assessed by systemic vascular resistance (SVR).

Table 2. Hemodynamic Paramaters in Various Categories of Shock

Category	HR	CVP	Contractility	SVR
Hypovolemic	↑	↓	±↑	↑
Cardiogenic	↑ or ↓ (tachy- vs. brady-)	↑	±↓	↑
Distributive (Sepsis)	↑	↓	±↑	↓
Obstructive	↑	↑	±↑	↑

Diagnostic Testing

Although a wide array of studies are generally ordered for the patient in shock, the suspected etiology and differential diagnosis should guide diagnostic testing. Studies should be focused on identifying the underlying etiology of shock and determining if end-organ damage is present. Serum lactate, a marker of anaerobic metabolism and the degree of tissue oxygen supply and demand imbalance, is particularly useful in the initial assessment and assessing response to therapeutic interventions. However, no isolated diagnostic test is sensitive or specific for shock. The following tests should be considered:

CBC with differential
Electrolytes, BUN, creatinine, glucose
Lactate
Coagulation studies
Hepatic function panel
Calcium
Urinalysis
ECG
Chest radiograph
Pregnancy test (blood or urine)
Blood gas

If a particular etiology of shock is suspected, further studies may be indicated:

Hemorrhagic etiology – type and screen
Infectious etiology – blood and urine cultures; CSF studies; focused CT or ultrasound
Cardiogenic – cardiac enzymes (ACS, myocarditis); echocardiogram (heart failure or structural etiology)
Obstructive – CT (PE); echocardiogram (pericardial tamponade)

The decision to transport a patient in shock outside of the ED to obtain a radiographic study (i.e. CT) must be carefully considered. Often, deferring imaging in favor of empiric management in the ED and critical care setting is advisable until the patient’s condition has stabilized.

Treatment

Timely empiric treatment for the shock patient is crucial to minimize morbidity and mortality. Critical findings involving the airway, breathing, and circulation (i.e. “the ABCs”) should be emergently addressed. Ensuring proper oxygenation is critical for all of the etiologies of shock, and arterial oxygen saturation should be maximized. Intubation should be strongly considered for airway protection, optimization of oxygenation and ventilation, and reducing the metabolic load incurred from work of breathing. However, it is important to consider that some induction and sedative medications used to facilitate intubation, as well as positive pressure ventilation itself, can reduce preload and have negative hemodynamic effects. This is of particular importance in patients with conditions in which preload is impaired, such as some obstructive or distributive shock states. In these circumstances, interventions to optimize hemodynamics (i.e. needle decompression in tension pneumothorax; rapid fluid bolus in septic shock) prior to intubation may be indicated before intubation, if feasible.

Short, large-bore intravenous allows for rapid volume infusion and medication delivery. If peripheral IV access is unable to be established, intraosseous access or a percutaneous introducer catheter may be inserted. Generally, volume expansion with crystalloid fluids (normal saline or Ringer’s lactate) should be administered as rapid bolus infusion. However, fluid administration to the patient in cardiogenic shock has potential to worsen the hemodynamic state and precipitate pulmonary edema. Blood products may be indicated in hemorrhagic shock, particularly in the trauma patient, in whom crystalloid infusion should be minimized to reduce clotting factor dilution and hyperchloremic acidemia. If volume resuscitation does not improve the patient’s hemodynamic state, initiation of vasopressor medications such as norepinephrine or epinephrine may be indicated.

The underlying etiology of shock should be aggressively treated:

Hypovolemic shock due to hemorrhage may warrant source control via surgical intervention or radiographically guided percutaneous intervention (IR).
Distributive shock due to sepsis should be treated with goal-directed therapy (i.e. lactate clearance, accurate hemodynamic monitoring), appropriate antibiotic treatment, and infection source control if indicated. Vasopressors such as norepinephrine may be required.
Distributive shock due to anaphylaxis should be treated with intramuscular epinephrine.
Cardiogenic shock may necessitate synchronized cardioversion, cardiac pacing, emergent angiography, or surgical procedures (i.e. valve repair). Use of an intra-aortic balloon pump or extracorporeal membrane oxygenation (ECMO) may be beneficial in some circumstances.
Obstructive shock due to pulmonary embolism may require systemic thrombolysis, whereas cardiac tamponade requires pericardiocentesis and tension pneumothorax requires pleural decompression (i.e. needle thoracostomy followed by thoracostomy tube).

Adequate resuscitation of a shock state is not indicated by any specific end point or parameter. However, indications of appropriate resuscitation and resolution of a shock states include:

Normalization of hemodynamic parameters (i.e. BP, HR, and urine output)
Lactate clearance with reduction in lactate concentration below 2 mmol/L
Volume status restored
Resolution of acidosis and return to normal metabolic parameters

Patients in shock usually require admission to a critical care setting under the care of an intensivist and other consulting services as needed. The mortality rate from shock states depends upon the underlying etiology, and range from exceedingly low (distributive shock due to anaphylaxis) to 50% (distributive shock due to sepsis).

Pearls and Pitfalls

While shock is generally associated with ill-appearing, hypotensive and tachycardic patients, the clinical picture can be subtle and vary widely.

Shock is a true emergency and should be treated promptly and aggressively in the ED to decrease morbidity and mortality. Do not wait until diagnostic studies return to begin resuscitation.

An understanding of the different categories of shock and recognition of their pathophysiologic features can guide appropriate empiric treatment.

Case Study Resolution

The emergency medicine team rapidly recognized the clinical presentation of shock, and established two large-bore IVs. A broad differential diagnosis was considered, and the focused physical examination revealing of flat neck veins and warm extremities was suspicious for a distributive shock state. A treatment and a diagnostic plan was initiated in parallel, with crystalloid volume expansion and attainment of a chest x-ray and laboratory studies including lactate, blood cultures and urine studies. The lactate was elevated at 4.5 mmol/L, and urine studies revealed pyuria and gram negative bacilli on gram stain. Empiric antibiotics were initiated followed by norepinephrine infusion, given persistent hypotension despite fluid resuscitation. The patient was admitted to the ICU, where she experienced gradual improvement, discontinuation of vasoactive medications, and was subsequently transferred to the general medical floor.

References

Nicks, B.A. and Gaillard, J. (2016). Approach to Shock. In J.E. Tintinalli, et al (Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill. http://accessmedicine.mhmedical.com/content.aspx?bookid=1658&sectionid=109384946
Puskarich, M.A. and Jones, A.E. (2018). Shock. In R.M. Walls et al (Eds.), Rosen’s Emergency Medicine: Concepts and Clinical Practice (pp.68-76). Philadelphia, PA: Elsevier.
Weingart, S.D. and Meyers, C.M. (2011). The Patient with Undifferentiated Shock. In M.E. Winters et al (Eds.), Emergency Department Resuscitation of the Critically Ill (pp.1-4). Dallas, TX: American College of Emergency Physicians.