Shock in the Operating Room 

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Key points in the management of shock in the operating room (OR) include the following:

Shock is the life-threatening condition caused by a failure of the circulatory system that results in a mismatch between oxygen supply and demand. Cellular hypoxia can arise from a multitude of causes, including decreased oxygen delivery, increased oxygen consumption, or inadequate oxygen utilization at the tissue level. The goal of management is early recognition in order to restore tissue perfusion and thereby prevent progression to multisystem organ failure and death.

In the OR, the differential diagnosis for hypotension and tachycardia is broad and multifactorial. A patient in shock may be hypotensive, normotensive, or hypertensive. It is important to arrive at the correct diagnosis because the initial stages of shock can be reversible. This review aims to facilitate accurate diagnosis of shock in the OR; different types of shock require different forms of expeditious treatment.

Distributive shock

Distributive shock occurs when there is inappropriate peripheral vasodilation leading to hypoperfusion of vital organs.

Septic shock, a form of distributive shock, is the most common type of shock observed in the ICU. [1]  In 2016, the Society for Critical Care Medicine (SCCM) and the European Society of Intensive Care Medicine (EISCM) published new definitions for sepsis and septic shock, according to which sepsis was defined as a “dysregulated host immune response to infection” and septic shock as “a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.” [2]

Mortality in septic shock has been estimated to be in the range of 10-40%. The most common of the organisms that cause sepsis include Escherichia coli, Staphylococcus aureus, Klebsiella pneumoniae, and Streptococcus pneumoniae. (For a fuller review of the pathophysiology of septic shock, see Septic Shock.)

Neurogenic shock, another form of distributive shock, usually results from a cervical or high thoracic spine injury (above T6) leading to the sudden loss of sympathetic tone. The loss of sympathetic tone, in turn, leads to unopposed parasympathetic response.

Clinically, patients with neurogenic shock may present with temperature dysregulation, bradycardia, and hypotension that is not responsive to volume resuscitation. Vertebral fractures and dislocations may cause a disruption of descending sympathetic tracts, so that the patient is unable to activate sympathetic responses from the baroreceptor reflex. There is usually primary spinal cord injury (SCI) that occurs within minutes of the original insult. Hours to days after the insult, there may be secondary SCI from edema, ischemia, and electrolyte shifts.  

Less common causes of neurogenic shock include spinal anesthesia, transverse myelitis, Guillain-Barré syndrome, and autonomic nervous system toxins.  

Cardiogenic shock

Cardiogenic shock is shock due to cardiac pump failure. Reduction in myocardial contractility results in decreased cardiac output, hypotension, systemic vasoconstriction, and cardiac ischemia. The body attempts initially to improve coronary and peripheral perfusion through peripheral vasoconstriction; however, this produces increased afterload that causes further cardiac stress and damages myocardium.

Cardiac pump failure may be due to cardiomyopathic, arrhythmic, or mechanical reasons. Clinically, patients may present with hypotension that is unresponsive to volume resuscitation, with signs of end-organ hypoperfusion. Although not all myocardial infarctions (MIs) result in cardiogenic shock, acute MI accounts for 81% of patients in cardiogenic shock. [3]   

Hypovolemic shock

The most common type of shock in trauma patients is hypovolemic shock—specifically, hemorrhagic shock. Clinically, patients present with hypotension, tachycardia, and a narrowed pulse pressure.

The baroreceptor reflex and the hormonally regulated renin-angiotensin-aldosterone mechanism are the most important mechanisms for regulating arterial pressure. A decrease in mean arterial pressure (MAP) due to acute blood loss will lead to decreased stretch on carotid sinus baroreceptors. Decreased stretch decreases the firing rate of the carotid sinus nerve (Hering’s nerve), a small branch of cranial nerve IX (the glossopharyngeal nerve). This is transmitted to the vasomotor center of the brainstem. As a result, parasympathetic outflow to the heart is decreased, and sympathetic outflow to the heart and vasculature is increased.

In a trauma patient, blood loss can be estimated on the basis of vital signs and symptomatology according to the classification of hemorrhagic shock (see Table 1 below). In the OR, it is important to keep the trauma patient in hemorrhagic shock warm and adequately resuscitated in order to avoid the lethal triad of acidosis, hypothermia, and coagulopathy.

Table 1. Classification of Hemorrhagic Shock* (Open Table in a new window)

BP = blood pressure; HR = heart rate; RR = respiratory rate.

*Values based on 70-kg man. Adapted from American College of Surgeons Committee on Trauma.

Obstructive shock

Obstructive shock results from physical obstruction of circulation into or out of the heart. It is the rarest form of shock. Examples of conditions that can give rise to obstructive shock include tension pneumothorax, cardiac tamponade, air embolism, and pulmonary embolism (PE). The pathophysiology of obstructive shock depends on the location of the obstruction in the vascular system in relation to the heart.  

To determine the cause of shock, one must initially look for diagnostic clues in the patient history and physical examination. In the OR, it is also useful to take note of the surgical procedure being performed. Additional tests, such as laboratory studies, electrocardiography (ECG), imaging, and heart function tests, though helpful, should not delay resuscitation. 

In all cases of shock, intravascular access is important, whether via large-bore peripheral intravenous (IV) lines or via a central venous catheter, especially if central venous oxyhemoglobin saturation (ScvO2) will be used to guide therapeutic intervention. Anyone under general anesthesia should have standard American Society of Anesthesiologists (ASA) monitors (five-lead ECG, noninvasive blood pressure [BP] monitoring, pulse oximetry, end-tidal carbon dioxide [ETCO2] monitoring, and temperature).

Pulmonary artery catheters should not be routinely placed in patients in shock, because this has not been shown to improve outcome. Hemodynamic profiles of different types of shock on pulmonary artery catheters are listed in Table 2 below.

Table 2. Hemodynamic Profiles of Shock Types on Pulmonary Artery Catheter (Open Table in a new window)

BP = blood pressure; CO = cardiac output; CVP = central venous pressure; PAOP = pulmonary artery occlusion pressure; PAP = pulmonary arterial pressure; SVR = systemic vascular resistance.

*In cardiac tamponade, there is equalization of right atrial pressure (RAP), right ventricular end-diastolic pressure (RVEDP), and PAP.

Septic shock (distributive)

The quick Sequential (Sepsis-related) Organ Failure Assessment (qSOFA) score enables rapid identification of patients with infection who are at risk for clinical deterioration. The score takes into account a respiratory rate (RR) of 22 breaths/min or higher, a systolic BP of 100 mm Hg or lower, and altered mental status (Glasgow Coma Scale [GCS] score < 15). Those with qSOFA scores of 2 or higher are at risk for poor outcomes. The expanded Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score (see Table 3 below) requires laboratory tests and thus cannot be used as easily for frequent assessment of patients. However, it has been found to have a greater predictive value for poor outcomes.

Table 3. Sequential (Sepsis-Related) Organ Failure Assessment Score (Open Table in a new window)

MAP (mm Hg)

or

vasopressor dosage (μg/kg/min)

Dopamine < 5

or

dobutamine (any dosage)

Dopamine 5.1-15

or

epinephrine ≤ 0.1

or

norepinephrine ≤ 0.1

Dopamine >15

or

epinephrine >0.1

or

norepinephrine >0.1

FiO2 = fraction of inspired oxygen; GCS = Glasgow Coma Scale; MAP = mean arterial pressure; PaO2 = arterial oxygen tension.

Adapted from Singer et al. [2]

To find the source of infection, blood cultures, urine cultures, and sputum cultures (if applicable) should be obtained before broad-spectrum antimicrobial therapy is started. Response to antibiotics should be monitored on the basis of the white blood count (WBC) and the fever curve and deescalated appropriately. Lactate levels should be monitored to guide fluid resuscitation. Procalcitonin may be used to determine whether the infection is from a bacterial or a viral cause.

Neurogenic shock (distributive)

The diagnosis of neurogenic shock is made through a combination of clinical examination, hemodynamic monitoring, and radiologic imaging. It is a diagnosis of exclusion in the trauma patient, made when hemorrhagic shock has been ruled out. It is most commonly associated with blunt cervical and high thoracic spine injuries.

Classic signs include hypotension, bradycardia, and flushed, warm skin. Computed tomography (CT) and magnetic resonance imaging (MRI) of the spine aid in diagnosis. Neurogenic shock must not be confused with spinal shock, which is the reversible acute loss of sensory, motor, and reflex functions below the level of the spinal injury.

Cardiogenic shock

The classic presentation of patients with cardiogenic shock falls into the “cold and wet” category, where there is a reduced cardiac index (CI), an increased systemic vascular resistance index (SVRI), and an increased pulmonary capillary wedge pressure (PCWP). Patients who fall into the “wet and warm” category typically have a reduced CI, a low-to-normal SVRI, and an increased PCWP. These patients have a higher incidence of sepsis and mortality.  

Suspicion for cardiogenic shock should be high in patients who have had MIs and a history of recent or distant percutaneous coronary intervention (PCI). Important in the diagnosis of cardiogenic shock is to carry out a thorough history and physical examination, including cardiac auscultation and examination of extremities. Laboratory studies (eg, cardiac biomarkers, complete blood count [CBC], and renal function panel) are vital as well. If transesophageal echocardiography (TEE) is not available, focus-assessed transthoracic echocardiography (FATE) will suffice.  

Hemorrhagic shock (hypovolemic)

In a hemodynamically unstable trauma patient, suspicion for hemorrhagic shock should be high. In looking for sources of bleeding, one must remember the saying “blood on the floor plus four more.” “Four” refers to four possible compartments of bleeding: chest, abdomen/pelvis, retroperitoneum, and thigh.

On the basis of the patient’s vital signs and physical examination, blood loss may be estimated by using the classes of shock (see Table 1 above). Focused assessment with sonography for trauma (FAST) may be performed to evaluate for bleeding in the abdomen. Laboratory studies such as hematocrit, lactate levels, arterial blood gas (ABG) values, and thromboelastography may help guide resuscitation.    

Obstructive shock  

Suspicion for obstructive shock in the OR should be high if the patient has a history of hypercoagulability, recent cardiac surgery, trauma, mechanical ventilation with high positive end-expiratory pressure (PEEP), or a mediastinal mass. Unfortunately, the symptoms of obstructive shock can be nonspecific. As with other types of shock, it is important to carry out a thorough history and physical examination. Point-of-care ultrasonography (POCUS) to assess for lung sliding may be useful in diagnosing tension pneumothorax. TEE may be useful in assessing for PE and cardiac tamponade.

For the induction of anesthesia, it is important to minimize the use of agents that confer hemodynamic instability. Caution should be exercised with the use of propofol because this agent causes dose-dependent venous and arterial dilation, as well as decreased cardiac contractility. It is also important to reduce the dosage because the volume of the central compartment is smaller in patients with shock. It may be prudent to administer a vasopressor bolus before or concurrently with induction.

The goals of septic shock management are (1) source control and (2) maintaining an MAP of 65 mm Hg or higher through fluid resuscitation or use of vasopressors. A number of studies have been published that are useful for helping guide management of patients with septic shock.

A retrospective multicenter study from 2006 found that delaying antimicrobial therapy in septic shock led to significant increases in mortality. [4] Each hour of delay was associated with a 12% increase in mortality over that seen in the previous hour.  

Jansen et al compared standard early goal-directed therapy (EGDT) with EGDT combined with early lactate-guided therapy in ICU patients with increased lactate levels. [5] Early lactate-guided therapy included reduction of lactate levels by at least 20% every 2 hours during the first 8 hours of admission. Lactate-guided therapy significantly reduced in-hospital mortality and led to shorter periods of time on mechanical ventilation and in the ICU.

Rivers et al showed that EGDT in ICU patients with severe sepsis and septic shock (according to the 2001 definitions) significantly reduced the incidence of organ dysfunction and lowered mortality as compared with standard therapy. [6] EGDT target goals included maintaining a central venous pressure (CVP) of 8-12 mm Hg, an MAP 65 mm Hg or higher, a urine output of 0.5 mL/kg/hr or greater, and a mixed venous oxygen saturation (SmvO2) of 70% or higher.  

The Saline versus Albumin Fluid Evaluation (SAFE) trial found no significant difference in 28-day mortality when comparing albumin with normal saline for fluid resuscitation in the ICU. [7] Albumin also was not found to yield significant benefits in terms of length of ICU or hospital stay and duration of supportive treatment measures.  

The Vasopressin And Septic Shock Trial (VASST) trial showed that in comparison with norepinephrine, low-dose vasopressin did not reduce mortality in patients with septic shock who were treated with vasopressors. [8]   

The Corticosteroid Therapy of Septic Shock (CORTICUS) study showed no significant difference in mortality between patients with septic shock who received low-dose hydrocortisone and those who received placebo. [9] Although treatment with hydrocortisone reversed shock more quickly, it also resulted in more cases of superinfection.

For effective treatment of neurogenic shock, it is important to treat the cause. The patient should be resuscitated with fluids. Vasopressors should be administered to restore vascular tone. Phenylephrine should be given for its vasoconstrictive effect on alpha1 receptors, but one should watch for bradycardia. Norepinephrine is also a good choice for its action on alpha1 receptors and positive inotropic effects. Steroids have not been found to be helpful and may increase the risk of infection. Maintaining MAP at 85-90 mm Hg is prudent for spinal cord perfusion. If warranted, emergency spinal cord decompression may prevent further SCI.

Once cardiogenic shock has been diagnosed, it is important to maintain coronary perfusion. Vasopressors should be titrated to a MAP goal of greater than 65 mm Hg. Norepinephrine is usually the most commonly employed first-line agent for cardiogenic shock. For patients in cardiogenic shock who have acute right ventricular (RV) failure, vasopressin is a first-line vasopressor because it causes less pulmonary vasoconstriction than norepinephrine does.

An intra-aortic balloon pump (IABP) may help in improving coronary perfusion pressure. If the patient continues to deteriorate, it may be necessary to provide mechanical circulatory support (eg, with extracorporeal membrane oxygenation [ECMO] [10] or ventricular assist devices [VADs]). Emergency cardiac catheterization can help with diagnosis of the problem and guidance of therapeutic intervention.

Once the source of bleeding has been identified, attempts should be made to control it by means of pressure, application of a tourniquet, a pelvic binder, embolization, or hemostatic agents. Perfusion pressure should be restored by increasing circulating volume through the use of crystalloids, colloids, blood products, or blood salvage. One may need to activate massive transfusion protocol early, mindful of the need to administer calcium when large volumes of packed red blood cells (RBCs) have been transfused.  

As noted above, the SAFE trial found no significant difference in 28-day mortality when comparing albumin and normal saline for fluid resuscitation in the ICU, nor was albumin found to yield significant benefits in terms of length of ICU or hospital stay or duration of supportive treatment measures. [7]   

The Transfusion Requirements In Critical Care (TRICC) study, a randomized controlled trial, showed that a restrictive transfusion strategy in critically ill patients did not significantly increase 30-day mortality when compared with a liberal transfusion strategy. It also showed that a restrictive transfusion strategy was associated with significantly lower mortality in patients younger than 55 years and with Acute Physiology and Chronic Health Evaluation (APACHE) II scores of 20 or lower. [11]   

The Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 2 (CRASH-2) trial found that early administration of tranexamic acid, an antifibrinolytic agent, improved survival in trauma patients with known or suspected significant bleeding. [12]

Management of the patient with obstructive shock depends on the location of the obstruction. If the patient has an air embolism in the OR, he or she should immediately be placed in a left lateral decubitus or Trendelenburg position. The surgeon should flood the surgical field. Attempts should be made to withdraw air from the right atrium if patient has a central line in place. If the patient has a PE, anticoagulation should be started, or the patient should be sent for emergency thrombectomy. If the patient has cardiac tamponade, he or she should be sent for emergency pericardiocentesis. If there is a tension pneumothorax, needle thoracostomy should be performed, with eventual tube thoracostomy.       

A 63-year-old woman with a history of obesity, sleep apnea, hypertension, diabetes mellitus type 2, and chronic kidney disease is recovering in the postanesthesia care unit (PACU) after an emergency exploratory laparotomy for perforated diverticulitis. She suddenly complains of crushing chest pain, and new T-wave inversions are seen on lead II on telemetry. Her vital signs are as follows: HR, 51 beats/min; BP, 85/65 mm Hg; oxygen saturation, 92% on 4 L by nasal cannula. On physical examination, the patient is diaphoretic and has cold, clammy extremities.       

Cardiac troponin levels and a renal function panel were ordered. Chest x-ray was pending. A 12-lead ECG confirmed acute T-wave inversions in leads II, III, and aVF. The patient developed worsening hypoxemia and increased work of breathing and was reintubated in the PACU. Bedside transthoracic echocardiography (TTE) showed regional wall-motion abnormalities in the inferior wall. The patient was rushed to the cardiac catheterization suite, where the right coronary artery was found to have 90% stenosis. A drug-eluting stent was placed, and the patient was admitted to the ICU.

The diagnosis is cardiogenic shock secondary to a postoperative non-ST-elevation MI (NSTEMI).

A 25-year-old man is taken to the hospital after multiple gunshot wounds to the abdomen. He is unable to provide his medical history. He is tachycardic and hypotensive, with a GCS score of 9 (eye, 2; verbal, 3; motor, 4). FAST is positive for free fluid in Morison’s pouch (the area between the liver and the kidney). The patient undergoes emergency intubation via rapid sequence induction and is brought to the OR.

In the OR, the patient remained hypotensive and tachycardic. In addition to standard ASA monitors, a right internal jugular venous catheter and an intra-arterial catheter were placed. Massive transfusion protocol was initiated. Temperature regulation was maintained through forced-air warming. ABG values and lactate levels were monitored frequently.

Intraoperatively, the patient was found to have a grade 3 liver laceration. The anesthesiologist requested that the trauma surgeon perform the Pringle maneuver to stop bleeding from the liver. As this maneuver was performed, the patient’s BP improved slightly. No other injuries were found, and the patient’s abdomen was closed. The patient was transferred to the trauma ICU.

The diagnosis is hypovolemic shock secondary to a gunshot wound with subsequent liver injury and hemorrhage.

A 57-year-old man with ankylosing spondylitis is a victim in a motor vehicle collision involving his tour bus and an 18-wheeler truck. Upon arrival, his BP is 70/40 mm Hg, his HR is 45 beats/min, and he is unable to move any of his extremities.

With manual in-line stabilization, the anesthesiologist proceeds to intubate via video laryngoscopy but is unable to see the epiglottis. A laryngeal mask airway (LMA) is placed, but the patient still cannot be ventilated. The decision is made to perform an emergency surgical cricothyroidotomy. X-rays of the cervical spine show traumatic subluxation of C5-6 resulting in complete transection of the spinal cord. FAST is negative. There are no immediate signs of exsanguination.

The patient’s hypotension and bradycardia were attributed to neurogenic shock from his cervical SCI with loss of sympathetic tone. His pulse pressure was narrowed. He was resuscitated with IV fluids and started on norepinephrine for a MAP goal of 85-90 mm Hg. The patient was then taken to the OR on an emergency basis for decompression. His postoperative course included admission to the ICU and formalization of his tracheostomy on postoperative day 2.  

The diagnosis is neurogenic shock (distributive category) secondary to spinal cord transection.

A 38-year-old male ironworker is brought into the trauma bay after falling 20 ft at work. He is conscious, with a GCS score of 14, and is able to state that he has no medical problems. He reports brief loss of consciousness and claims to have landed on his feet. He complains of extreme pain in his left leg. His vital signs are stable, except for an HR of 107 beats/min. He has an open left lower leg fracture with protruding bone.

In view of the severity of the patient’s injury, CT scans of his head, chest, spine, abdomen, and pelvis are obtained, but no acute abnormalities are found. An x-ray of the patient’s left lower extremity shows a comminuted fracture of his tibia and fibula.   

The patient was brought to the OR on an emergency basis for external fixation of his open left tibial-fibial fracture. He arrived with a 22-gauge peripheral IV line, which enabled induction of anesthesia and intubation. There had been three failed attempts at large-gauge peripheral IV cannulation; therefore, the decision was made to place a central venous catheter. The surgical intern volunteered to place a left subclavian venous catheter. It took three attempts to cannulate the left subclavian vein, but the intern was eventually able to place the line.  

About 40 minutes into this otherwise uneventful case, the patient suddenly became hypotensive, tachycardic, and hypoxemic. The peak inspiratory pressure (PIP) suddenly climbed to 45 mm Hg. The anesthesiologist noted absent breath sounds in the left lung with tracheal deviation to the right. A clinical diagnosis of tension pneumothorax was made, and a needle thoracostomy was performed at the second intercostal space in the midclavicular line. The patient’s BP normalized, and the PIP decreased. A chest tube was placed in the left chest. The patient was extubated and admitted to the ICU.

The diagnosis is obstructive shock secondary to a tension pneumothorax.

A 72-year-old woman who lives in a nursing home and has a history significant for obesity, hypertension, diabetes mellitus type 2, chronic kidney disease, and stroke is transferred to the emergency department (ED) for fever and altered mental status. Before becoming obtunded, she was complaining of pain in her genitals. Her BP is 89/34 mm Hg, her HR is 135 beats/min, and her temperature is 38.4ºC.  

Upon examination, the patient has disproportionate pain in her perineal area. She undergoes CT of her abdomen and pelvis, which shows the presence of gas in soft-tissue planes in the upper thigh and peroneal area. Blood cultures are obtained before broad-spectrum antibiotics are started. The patient’s WBC count is 24,000/μL, her creatinine is 2.2 mg/dL, her glucose is 430 mg/dL, and her lactate is 4.8 mmol/L.

In the ED, the patient was intubated and a central line placed. She was started on vasopressors and broad-spectrum antibiotics to cover gram-positive, gram-negative, and anaerobic organisms. She underwent fluid resuscitation with crystalloid and was given insulin for her hyperglycemia. The patient was then taken to the OR on an emergency basis for wide excisional debridement of her perineal area. She was admitted to the ICU on insulin and vasopressor infusions. She was scheduled for serial debridements in the OR.  

The diagnosis is distributive shock secondary to sepsis.

Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013 Oct 31. 369 (18):1726-34. [Medline].

Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23. 315 (8):801-10. [Medline].

Harjola VP, Lassus J, Sionis A, Køber L, Tarvasmäki T, Spinar J, et al. Clinical picture and risk prediction of short-term mortality in cardiogenic shock. Eur J Heart Fail. 2015 May. 17 (5):501-9. [Medline].

Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006 Jun. 34 (6):1589-96. [Medline].

Jansen TC, van Bommel J, Schoonderbeek FJ, Sleeswijk Visser SJ, van der Klooster JM, Lima AP, et al. Early lactate-guided therapy in intensive care unit patients: a multicenter, open-label, randomized controlled trial. Am J Respir Crit Care Med. 2010 Sep 15. 182 (6):752-61. [Medline].

Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8. 345 (19):1368-77. [Medline].

Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004 May 27. 350 (22):2247-56. [Medline].

Russell JA, Walley KR, Singer J, Gordon AC, Hébert PC, Cooper DJ, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl J Med. 2008 Feb 28. 358 (9):877-87. [Medline].

Sprung CL, Annane D, Keh D, Moreno R, Singer M, Freivogel K, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008 Jan 10. 358 (2):111-24. [Medline].

Kelly B, Carton E. Extended Indications for Extracorporeal Membrane Oxygenation in the Operating Room. J Intensive Care Med. 2020 Jan. 35 (1):24-33. [Medline].

Hébert PC. Transfusion requirements in critical care (TRICC): a multicentre, randomized, controlled clinical study. Transfusion Requirements in Critical Care Investigators and the Canadian Critical care Trials Group. Br J Anaesth. 1998 Dec. 81 Suppl 1:25-33. [Medline].

CRASH-2 trial collaborators., Shakur H, Roberts I, Bautista R, Caballero J, Coats T, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010 Jul 3. 376 (9734):23-32. [Medline].

BP = blood pressure; HR = heart rate; RR = respiratory rate.

*Values based on 70-kg man. Adapted from American College of Surgeons Committee on Trauma.

BP = blood pressure; CO = cardiac output; CVP = central venous pressure; PAOP = pulmonary artery occlusion pressure; PAP = pulmonary arterial pressure; SVR = systemic vascular resistance.

*In cardiac tamponade, there is equalization of right atrial pressure (RAP), right ventricular end-diastolic pressure (RVEDP), and PAP.

MAP (mm Hg)

or

vasopressor dosage (μg/kg/min)

Dopamine < 5

or

dobutamine (any dosage)

Dopamine 5.1-15

or

epinephrine ≤ 0.1

or

norepinephrine ≤ 0.1

Dopamine >15

or

epinephrine >0.1

or

norepinephrine >0.1

FiO2 = fraction of inspired oxygen; GCS = Glasgow Coma Scale; MAP = mean arterial pressure; PaO2 = arterial oxygen tension.

Adapted from Singer et al. [2]

Noreen E Tiangco, MD, MA Resident Physician, Department of Anesthesiology, Temple University Hospital

Noreen E Tiangco, MD, MA is a member of the following medical societies: American Medical Association, American Society of Anesthesiologists, International Anesthesia Research Society, Society for Education in Anesthesia

Disclosure: Nothing to disclose.

Jessica M Reardon, DO Associate Program Director, Director of Experiential Learning, Chair of Clinical Competency Committee, Department of Anesthesiology, Temple University Hospital

Jessica M Reardon, DO is a member of the following medical societies: American Osteopathic Association, American Society of Anesthesiologists, Society for Education in Anesthesia, Society of Critical Care Anesthesiologists, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Richard Lindsey Staff Editor, Medscape Reference

Disclosure: Nothing to disclose.

Sheela Pai Cole, MD Clinical Associate Professor of Cardiothoracic Anesthesiology and Critical Care Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine

Sheela Pai Cole, MD is a member of the following medical societies: American Medical Association, American Society of Anesthesiologists, American Society of Echocardiography, California Society of Anesthesiologists, International Anesthesia Research Society, Pennsylvania Society of Anesthesiologists, Society of Cardiovascular Anesthesiologists, Society of Critical Care Anesthesiologists, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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