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Shock

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Last Update: October 27, 2018.

Introduction

Shock is a life-threatening manifestation of circulatory failure.  Circulatory shock leads to cellular and tissue hypoxia resulting in cellular death and dysfunction of vital organs. Effects of shock are reversible in the early stages and a delay in diagnosis and/or timely initiation of treatment can lead to irreversible changes including multiorgan failure (MOF) and death.

Etiology

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic and obstructive.[1] The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

1. Distributive Shock

Characterized by peripheral vasodilatation. 

Types of distributive shock include:

Septic shock

Sepsis is defined as a life-threatening organ dysfunction resulting from dysregulated host response to infection.[2] Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion, manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)

Most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus.

Systemic inflammatory response syndrome

Systemic inflammatory response syndrome (SIRS) is a clinical syndrome of vigorous inflammatory response caused by either infectious or noninfectious causes. Infectious causes include pathogens such as gram-positive (most common) and gram-negative bacteria, fungi, viral infections (e.g., respiratory viruses), parasitic (e.g., malaria), rickettsial infections. Noninfectious causes of SIRS include but are not limited to pancreatitis, burns, fat embolism, air embolism, and amniotic fluid embolism

Anaphylactic shock

Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm. The immediate hypersensitivity reactions can occur within seconds to minutes after presentation of the inciting antigen. Common allergens include drugs (e.g., antibiotics, NSAIDs), food, insect stings, and latex.

Neurogenic shock

Neurogenic shock can occur in the setting of trauma to the spinal cord or to the brain. The underlying mechanism is the disruption of autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.

Endocrine shock

Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.

2. Hypovolemic Shock

Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension. Hypovolemic shock can be divided into two broad subtypes: hemorrhagic and nonhemorrhagic.

Common causes of hemorrhagic hypovolemic shock include

  • Gastrointestinal bleed (both upper and lower gastrointestinal bleed (e.g., variceal bleed, portal hypertensive gastropathy bleed, peptic ulcer, diverticulosis) trauma.
  • Vascular etiologies (e.g., aortoenteric fistula, ruptured abdominal aortic aneurysm, tumor eroding into a major blood vessel).
  • Spontaneous bleeding in the setting of anticoagulant use (in the setting of supratherapeutic INR from drug interactions).

Common causes of nonhemorrhagic hypovolemic shock include:

  • GI losses - the setting of vomiting, diarrhea, NG suction or drains.
  • Renal losses - medication induced diuresis, endocrine disorders such as hypoaldosteronism.
  • Skin losses/insensible losses - burns, Steven Johnson syndrome, Toxic epidermal necrolysis, heat stroke, pyrexia.
  • Third-space loss - in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.

3. Cardiogenic Shock

Due to intracardiac causes leading to decreased cardiac output and systemic hypoperfusion. Different subtypes of etiologies contributing to cardiogenic shock include:

  • Cardiomyopathies - include acute myocardial infarction affecting more than 40% of the left ventricle, acute myocardial infarction in the setting of multi-vessel coronary artery disease, right ventricular myocardial infarction, fulminant dilated cardiomyopathy, cardiac arrest (due to myocardial stunning), myocarditis.
  • Arrhythmias - both tachy- and bradyarrhythmias.
  • Mechanical - severe aortic insufficiency, severe mitral insufficiency, rupture of papillary muscles, or chordae tendinae trauma rupture of ventricular free wall aneurysm.

4. Obstructive Shock

Mostly due to extracardiac causes leading to decrease in the left ventricular cardiac output

  • Pulmonary vascular - due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.[3]
  • Mechanical - impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.

Epidemiology

Distributive shock is the most common type of shock followed by hypovolemic and cardiogenic shock. Obstructive shock is relatively less common. The most common type of distributive shock is septic shock and has a mortality rate between 40% to 50%.

Pathophysiology

Hypoxia at the cellular level causes a series of physiologic and biochemical changes, resulting in acidosis and a decrease in regional blood flow which further worsens the tissue hypoxia.[4] In hypovolemic, obstructive, and cardiogenic shock there is a decrease in cardiac output and decreased oxygen transport. In distributive shock, there is decreased peripheral vascular resistance and abnormal oxygen extraction. Excitement is a spectrum of physiologic changes, ranging from early stages which are reversible to final stages which are irreversible with multiorgan failure and death. Generally, shock has the following three stages:

  1. Pre-shock or compensated shock - As the name suggests, this stage is characterized by compensatory mechanisms to counter the decrease in tissue perfusion, including tachycardia, peripheral vasoconstriction, and changes in systemic blood pressure
  2. Shock - During this stage, most of the classic signs and symptoms of shock appear due to early organ dysfunction, resulting from progression of the pre-shock stage as the compensatory mechanisms become insufficient.
  3. End-organ dysfunction - This is the final stage, leading to irreversible organ dysfunction, multiorgan failure, and death

History and Physical

A focused history should be obtained from the patient (if feasible) and/or patient's relatives. Also, a review of the patient’s outpatient medical records (information regarding risk factors, medications, and trend of baseline vital signs including blood pressure), as well as hospital medical records, could give valuable clues regarding the patient's risk for shock and potential etiology. Clinical features and symptoms can vary according to the type and stage of shock. Most common clinical features/labs which are suggestive of shock include hypotension, tachycardia, tachypnea, obtundation or abnormal mental status, cold, clammy extremities, mottled skin, oliguria, metabolic acidosis, and hyperlactatemia.[5][6] In addition, features pertaining to the underlying cause of the shock can also be present.

Patients with hypovolemic shock can have general features as mentioned above as well as evidence of orthostatic hypotension, pallor, flattened jugular venous pulsations, may have sequelae of chronic liver disease (in case of variceal bleeding).

Patients with septic shock may present with symptoms suggestive of the source of infection (example-skin manifestations of primary infection such as erysipelas, cellulitis, necrotizing soft-tissue infections), and cutaneous manifestations of infective endocarditis.

Patients with anaphylactic shock can have hypotension, flashing, urticaria, tachypnea, hoarseness of voice, oral and facial edema, hives, wheeze, inspiratory stridor, and history of exposure to common allergens such as medications or food items the patient is allergic to or insect stings.

Tension pneumothorax should be suspected in a patient with undifferentiated shock who has tachypnea, unilateral pleuritic chest pain, absent or diminished breath sounds, tracheal deviation to the normal side, distended neck veins and also has pertinent risk factors for tension pneumothorax such as recent trauma, mechanical ventilation, underlying cystic lung disease).

In a patient with undifferentiated shock, diagnostic clues to pericardial tamponade as the etiology include dyspnea, the Beck triad (elevated jugular venous pressure, muffled heart sounds, hypotension), pulses paradoxus, and known risk factors such as trauma, the recent history of pericardial effusion, and thoracic procedures. 

Cardiogenic shock should be considered as the etiology if the patient with undifferentiated shock had chest pain suggestive of cardiac origin, narrow pulse pressure, elevated jugular venous pulsations or lung crackles, and significant arrhythmias on telemetry or EKG.

Evaluation

Resuscitation should not be delayed while investigating the etiology of undifferentiated shock. Physicians should have a high clinical suspicion for the presence of shock and an attempt to stratify the severity of the shock should also be done to assess the need for emergent or early interventions. Evaluation of undifferentiated shock should begin with a thorough history and physical examination.

Besides telemetry monitoring, a 12-lead electrocardiogram should be obtained. ECGs might show evidence of acute coronary syndrome, arrhythmias or provide diagnostic clues suggestive of pericardial effusion or pulmonary embolism.

Laboratory tests in a patient with undifferentiated shock should include a CBC and differential, renal and liver function tests, serum lactate level, cardiac biomarkers, D-dimer level, coagulation profile, type and screen for a possible blood transfusion if appropriate (if concern for hemorrhagic shock), blood and urine cultures, and blood gas analysis. Initial imaging studies recommended in patients with undifferentiated shock and hypotension include chest x-rays to look for the source of infection such as pneumonia, complications of shock such as ARDS, clinical findings supporting the diagnosis of pulmonary edema in cardiogenic shock, widened mediastinum in aortic dissection. CT scans can also assist in unmasking the etiology of shock in appropriate clinical scenarios. Point of care ultrasonography or focused cardiac ultrasound is also a useful bedside diagnostic tool.[7]

Treatment / Management

The initial approach to management is stabilization of airway and breathing with oxygen and oral mechanical ventilation when needed. Peripheral IV or intraosseous infusion (IO) access should be obtained. Central venous access may be needed in the setting of shock if there is difficulty securing peripheral venous access or the patient needs prolonged vasopressor therapy or large volume resuscitation. Immediate treatment with intravenous (IV) fluid should be initiated followed by vasopressor therapy, if needed, to maintain tissue perfusion. Depending on the underlying etiology of shock, specific therapies might also be needed.

Septic shock - initial aggressive fluid resuscitation with IV isotonic crystalloids 30 mL/kg within 3 hrs with additional fluid based on frequent reassessment, empiric antibiotic therapy within one hr. [8] For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mmHg. The first choice of vasopressor is a norepinephrine with the addition of vasopressin if refractory.[9]

Anaphylactic shock - aggressive IV fluid resuscitation with 4 to 6 L of IV crystalloids. Stop the offending agent, intramuscular epinephrine, antihistamines, corticosteroids, nebulized albuterol.

In adrenal crisis - judicious fluid resuscitation, IV dexamethasone.

Hypovolemic shock - obtain two large-bore IVs or central line. Place the patient in the Trendelenburg position. Aggressive IV fluid resuscitation with 2-4 L of isotonic crystalloids. PRBC transfusion if ongoing bleed. Appropriate medical or interventional strategies to treat the underlying etiology. Continue with isotonic crystalloids and use vasopressors if needed

Obstructive shock - the judicious use of IV crystalloids. If shock persists, early initiation of vasopressors-norepinephrine is the first choice and add vasopressin if refractory. Continue IV fluids but monitor very closely. 

If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has paradoxical worsening of hypotension; it may develop due to severe right ventricular dilatation and septal bowing compromising left ventricle filling. 

If tension pneumothorax - needle thoracotomy followed by tube thoracotomy. If cardiac tamponade-pericardiocentesis, significant clinical improvement is possible, even with minimal fluid removal).

Cardiogenic shock - if unstable tachyarrhythmia or bradyarrhythmias, initiate ACLS protocol and cardioversion. Judicious use of IV fluids in the absence of pulmonary edema. Consider inotropes (dobutamine is the most commonly used agent) or intra-aortic balloon pump (IABP), if refractory shock, and vasopressor (norepinephrine) with inotropes.

If STEMI - consider a thrombolysis or coronary revascularization procedures and or IABP.

Differential Diagnosis

Uncovering the etiology of undifferentiated shock is very important. In a patient presenting with undifferentiated shock, the differential diagnosis includes a wide variety of etiologies which falls under the four major categories of shock as outlined above. Also, sometimes patients can have a combination of shock syndromes. Another differential is "pharmacological shock" which results from vasodilatation or myocardial depression from medications (e.g., benzodiazepines, beta-blockers, calcium channel blockers, opiates, anticholinergics, and sildenafil).

Prognosis

Sepsis and septic shock, in general, are associated with long-term morbidity and mortality, with many of the survivors requiring placement into long-term acute care facilities or post-acute care centers.[10][11] Septic shock has a mortality rate between 40% and 50%. Cardiogenic shock has a mortality rate ranging from 50% to 75%, an improvement over prior mortality rates. Hypovolemic and obstructive shock generally have much lower mortality and respond better to timely treatment. 

Pearls and Other Issues

Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.

There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.

An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.

Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.

Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.

Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.

Questions

To access free multiple choice questions on this topic, click here.

References

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Vincent JL, De Backer D. Circulatory shock. N. Engl. J. Med. 2014 Feb 06;370(6):583. [PubMed: 24499231]
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Angus DC, van der Poll T. Severe sepsis and septic shock. N. Engl. J. Med. 2013 Aug 29;369(9):840-51. [PubMed: 23984731]
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Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc. Res. 2000 Oct;48(1):23-33. [PubMed: 11033105]
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Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May;4(2):161-7. [PubMed: 8774792]
5.
Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS, Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):762-74. [PMC free article: PMC5433435] [PubMed: 26903335]
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Kraut JA, Madias NE. Lactic acidosis. N. Engl. J. Med. 2015 Mar 12;372(11):1078-9. [PubMed: 25760366]
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Shokoohi H, Boniface KS, Pourmand A, Liu YT, Davison DL, Hawkins KD, Buhumaid RE, Salimian M, Yadav K. Bedside Ultrasound Reduces Diagnostic Uncertainty and Guides Resuscitation in Patients With Undifferentiated Hypotension. Crit. Care Med. 2015 Dec;43(12):2562-9. [PubMed: 26575653]
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Hylands M, Moller MH, Asfar P, Toma A, Frenette AJ, Beaudoin N, Belley-Côté É, D'Aragon F, Laake JH, Siemieniuk RA, Charbonney E, Lauzier F, Kwong J, Rochwerg B, Vandvik PO, Guyatt G, Lamontagne F. A systematic review of vasopressor blood pressure targets in critically ill adults with hypotension. Can J Anaesth. 2017 Jul;64(7):703-715. [PubMed: 28497426]
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Howell MD, Davis AM. Management of Sepsis and Septic Shock. JAMA. 2017 Feb 28;317(8):847-848. [PubMed: 28114603]
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Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M., Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. [PMC free article: PMC4910392] [PubMed: 26903336]
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Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet. 2018 Jul 07;392(10141):75-87. [PubMed: 29937192]
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Bookshelf ID: NBK531492PMID: 30285387

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