Hemorrhagic Shock: Pearls and Pitfalls for the Resuscitation Room

Authors: Anthony DeVivo, DO (EM Resident Physician, Mount Sinai St. Luke-West) and Jenny Beck-Esmay, MD (EM Attending Physician, Co-director, Medical Student Clerkship, Mount Sinai St. Luke-West) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)


A 55 y/o male with a past medical history of hypertension and alcohol abuse is triaged to your Emergency Department team for 1 day of multiple episodes of bloody vomitus.  Patient denies any abdominal pain, fever, chills, chest pain, syncope, or change in stools.  Patient denies any history of similar symptoms in the past. Patient reports poor compliance with his hypertension medications and affirms that he drinks 1.5L of vodka per day for the past several years. Upon initial assessment, he is pale appearing, but in no pain or respiratory distress.

Vitals include BP 110/80, HR 102, RR 18, Sat 98% on RA, and T 98.7 F.

How sick is this patient?  Do these vitals reassure you? Should he be in a resuscitation bay? What clues are there in this middle-aged male’s history that might guide you in your initial resuscitation?

While the brief information provided seems superficial, it may be all you have to answer the quintessential ER question of “sick or not sick” and direct your immediate resuscitation of this patient.


Hemorrhagic shock is a state of systemic hypoperfusion secondary to acute blood loss which may have either traumatic or atraumatic etiologies.  While gastrointestinal and traumatic etiologies are some of the most common causes of hemorrhagic shock, other causes such as ruptured aneurysms and post-partum hemorrhage may also cause rapid intravascular depletion. Systemic shock from acute intravascular volume loss will subsequently lead to decreased cardiac output, impaired tissue oxygenation, end organ dysfunction, and without intervention, death.1  At the microvascular level, systemic hypoperfusion leads to cell death which causes a release of intracellular substrates that induce peripheral vasodilation similar to the pathophysiology of distributive shock.  The pathophysiologic effects of intravascular depletion, in conjunction with systemic peripheral vasodilation, can lead to rapid vascular collapse.1,2

In order to counteract the pathophysiologic effects of massive hemorrhage, several homeostatic compensatory mechanisms enable the body to maintain adequate perfusion to vital organs.  As part of these mechanisms, the heart will compensate for a lack of volume by increasing the rate of cardiac contraction in order to maintain adequate cardiac output (CO = HR X SV).2,3  In addition, the body will begin to shunt blood from visceral organs via systemic peripheral vasoconstriction induced by the release of catecholamines in order to provide the heart with adequate volume to perfuse vital organs.  While these compensatory mechanisms can be lifesaving, if left unassisted, they can also lead to significant end organ dysfunction such as ischemic bowel, shock liver, and acute kidney injury.1,2

The compensatory mechanisms enacted by the body during hemorrhagic shock inevitably fail without intervention.  As these mechanisms become overwhelmed, acidosis will begin to worsen due to decreased perfusion.  This will be reflected by the progressive increase in lactate and base deficit. These two levels can be evaluated as point-of-care test in the emergency department and may be utilized as rough estimations for impending failure of physiologic compensatory mechanisms, and thus vascular collapse.3,4

The remainder of this article will be focused on resuscitation bay pearls for early detection, intervention, and prevention of rapid deterioration in hemorrhagic shock.

Resuscitation Bay History and Physical Exam

In the resuscitation bay, critical decisions are made with frequently limited history and physical exams. That being said, it is vital that whatever history is obtained is focused and assists in guiding resuscitation.

History Pearls:

  • Use every possible resource when obtaining a history.
    • Get all possible information from people presenting with the patient, be they EMS, family, or friends.
    • Patients frequently keep medication and problem lists with them that can provide superficial but also vital information that may direct resuscitation.
    • A quick chart search can be invaluable in resuscitation. Knowing a patient had a transjugular intrahepatic portosystemic shunt 1 week ago or was seen for an MVC 1 day ago can completely alter management.
    • A home health aide can change the clinical picture from 1 day of AMS to 1 week of black stool which will guide resuscitation.
    • Calling available family can seem cumbersome, but they can provide necessary information. If there are extra staff available, delegate this task to them.  Additionally, in certain situations, it may be an opportune time to discuss code status.

Exam Pearls:

  • Aside from the assessment of obvious external signs of trauma, there are also subtle findings that may indicate significant intravascular volume loss.
    • Confusion or altered mentation is a means of assessing end organ dysfunction without any lab results.2,5
    • Anxiety or agitation
    • Generalized pallor, conjunctival pallor, or jaundice
    • Poor skin turgor
    • Cool extremities
    • Mottled skin
    • Diminished peripheral pulses

Exam Pitfalls:

  • Physiologic compensation in early hemorrhagic shock may make initial assessment and recognition difficult.
    • Beware of reassuring heart rates. A normal heart rate, in some circumstances, may be reassuring as it would imply the patient is not requiring physiological compensation for a lack of cardiac output.  But, a patient on beta blockers may NOT have compensatory tachycardia and still be critically ill.
    • Beware of reassuring blood pressures. Patients in hemorrhagic shock with normal or borderline blood pressures may also be reassuring, but be sure to take into account the patient’s past medical history.  Patients with a history of uncontrolled hypertension may present in hemorrhagic shock with a “normal” blood pressure that, for them, is functionally hypotensive.

POC lab interpretation and utility

Until recently, laboratory results have not been readily available for early decision making during initial resuscitation of critically ill patients. Over the last several years, point of care testing has become more readily available within emergency departments, allowing certain laboratory results to guide early resuscitation.

  • Lactate may be utilized as a nonspecific means of assessing degree of shock and peripheral ischemia. Generally, a lactate >4.0 mmol/L indicates significant hemorrhage.3,4
  • Base deficit is another means of assessing systemic perfusion. A base deficit > – 4.0 mEq/L indicates significant circulatory compromise.3,4
  • Hemoglobin and/or hematocrit levels are now more readily available during initial resuscitation. However, these values should be interpreted with caution as they may not yet reflect the quantitative repercussions of the patient’s condition.  When massive acute hemorrhage occurs, the fluid lost is isotonic to the remaining intravascular fluid. Thus, the concentration or percentage of red blood cells in a blood sample taken from a patient who is acutely bleeding may not reflect the acute blood loss sustained and should be interpreted with caution.3
  • Lab values indicative of end organ dysfunction:
    • Creatinine
    • LFTs
    • Troponin

POC Lab Pearl:

  • Consider lactate, base deficit, creatinine, LFTs, and troponin as markers of significant hemorrhage and/or end organ damage.

POC Lab Pitfall:

  • Beware of a reassuring hemoglobin or hematocrit in the setting of acute blood loss.


Resuscitation of patients in hemorrhagic shock, as in all patients, begins with addressing and continued reassessment of the ABCs. Once the airway is stabilized, adequate large bore access is obtained, and fluid resuscitation is initiated. Further management revolves around maintaining appropriate intravascular repletion and attaining rapid hemostasis. Also, after exposure, make sure to cover the patient to avoid hypothermia.

Airway: Patients presenting in hemorrhagic shock will likely require a definitive airway at some point during resuscitation. If upon presentation the airway is obviously compromised, whether secondary to altered mentation, trauma, or hematemesis, it is likely intubation will need to be a first priority.  The procedure and medications involved in rapid sequence intubation may inadvertently lead to the suppression of the adrenergic compensation that is maintaining cardiac output and systemic perfusion. If airway intervention must be pursued before volume resuscitation, then hemodynamic augmentation with vasopressors may be considered as a means of maintaining adequate systemic perfusion during intubation. High dose paralytics and lower dose induction agents (1/4 to 1/2 the normal induction dose) are recommended for patients in shock. Patients able to maintain their airway should receive fluid resuscitation prior to intubation in order to mitigate risk of cardiovascular collapse.6,7

Circulation: After the airway is either secured or deemed stable at the moment, the next priority is the establishment of large bore IV access, preferably bilaterally.  Due to volume depletion, patients in hemorrhagic shock may have limited peripheral access and so central access should be pursued early if necessary.  In the event that there is a delay in both peripheral and central access, an IO may be established for initial resuscitation.5

Resuscitation Pearls

  • Whenever possible volume resuscitate a hemodynamically unstable patient prior to intubation.
  • Obtain intravascular access quickly. If peripheral or central access is delayed, establish an IO to start resuscitation while continuing to work on further access.

Massive Transfusion Protocol

Patients who have sustained massive hemorrhage have lost plasma and platelets in addition to red blood cells. While the loss of red blood cells leads to a deficit in oxygen carry capacity, the deficiency in platelets and clotting factors will make obtaining hemostasis in an actively bleeding patient significantly more difficult. Thus, the replacement of large volumes of red blood cells also requires supplementation with plasma and platelets.8 Massive transfusion is defined as replacement of 1 total blood volume in 24 hours or the replacement of 50% of total blood volume in 4 hours.2  As a means of mobilizing all blood products necessary for hemorrhaging patients, Massive Transfusion Protocol (MTP) was developed.8 MTP designates a balanced ratio of red blood cells:plasma:platelets.  While there is still some debate over ratio of blood products, current literature supports utilizing a 1:1:1 ratio.9-10,12-13 This ratio has been designed as a means of transfusing the appropriate amount of plasma and platelets to red blood cells in order to maintain the physiologic hemostasis of blood.  This design can effectively maintain hemostasis and assist in mitigating the risks of developing the “triad of death” consisting of coagulopathy, hypothermia, and acidosis.3,9,10,11  In addition, current literature suggests that early, aggressive resuscitation may reduce total blood requirements, making early recognition and intervention of hemorrhagic shock vital in resuscitation bay management.12

Complications of MTP

  • Respiratory compromise due to the rapid infusion of large volumes in intravascular fluid.
  • Transfusion associated circulatory overload (TACO) can develop secondary to rapid large volume resuscitation.2
  • Dilutional coagulopathy is seen more commonly in patients resuscitated with crystalloid or isolated red blood cells. The risk of this is reduced by the transfusion of plasma and platelets as dictated by MTP.2,8-10
  • Abdominal compartment syndrome secondary to the development of interstitial edema due to fluid shifts during MTP.2
  • Transfusion Related Acute Lung Injury (TRALI).
  • Hyperkalemia may develop throughout MTP administration due to hemolysis and acidosis from peripheral tissue hypoxia.13
  • Acidosis which develops due to peripheral ischemia may worsen during massive transfusion due to the acidic pH of previously stored red blood cells.2,13
  • Hypothermia may worsen due to the temperature of blood products in conjunction with decreased peripheral perfusion secondary to hemorrhagic shock.13
  • Hypocalcemia and hypomagnesemia develops from the large amount of citrate within packed red blood cells.13

MTP Pearls

  • In order to mitigate many of these complications, frequent reassessment of vitals, core body temperature, fluid status, and electrolytes should be performed.
  • Blood can be run through an IO while large peripheral or central access is established.
  • Avoid hypothermia.
  • Initiate MTP early if clinical impression indicates impending hemodynamic collapse.

Tranexamic Acid (TXA)

While we will not be discussing definitive means of hemostasis for specific etiologies of hemorrhagic shock in this article, there are interventions which may be utilized in all hemorrhaging patients to facilitate cessation of hemorrhaging. A source of much interest as of late is the use of Tranexamic Acid (TXA) in the setting of acute hemorrhage as an adjunctive means to attaining hemostasis.  TXA is an antifibrinolytic agent which facilitates clot formation and hemostasis that is given as 1g IV over 10 minutes. This is to be followed by an additional infusion of 1g IV over 8 hours.14  While data supporting the use of TXA in hemorrhagic shock is primarily from trauma literature, it is being studied and utilized for additional etiologies of hemorrhagic shock as well.14  It is typically recommended within the first 3 hours of injury, and improved outcomes are associated with earlier administration. Due to the relative low risk of adverse effects, TXA is being investigated and utilized for many common etiologies of hemorrhagic shock. This emDocs post contains great information on TXA use.

TXA Pearl

  • While investigation into the use of TXA for atraumatic etiologies of hemorrhagic shock is still underway, the evidence for its use in traumatic shock may be theoretically extrapolated to patients such as the one in the case at the beginning of this article.
  • TXA can be provided via IV and IO access.


In order to maintain adequate peripheral perfusion during hemorrhagic shock, we transfuse large volumes of blood products into patients while simultaneously attempting to obtain hemostasis in order to prevent further exsanguination.2,5 However, there are scenarios where compensatory mechanisms are failing, resuscitation efforts are inadequate, and additional hemodynamic support is required.  This may be confounded by peripheral ischemia causing the release of proinflammatory constituents leading to a systemic response similar to the vasodilatory shock seen in severe sepsis.2  The use of vasopressors in hemorrhagic shock is a longstanding point of controversy, as some have postulated that vasopressors may compromise peripheral perfusion thereby increasing the potential for ischemia.  While in certain clinical scenarios vasopressor use may be required for hemodynamic temporization during initial resuscitation, there is no evidence to support any mortality benefit.  Further investigation will be required in order to ascertain whether or not there is any utility in use of vasopressors in hemorrhagic shock.15  Please see these emDocs posts (Part 1 and Part 2) for more on vasopressors.

Vasopressor Pearls

  • Vasopressors such as norepinephrine or phenylephrine may be utilized for hemodynamic temporization but should not replace adequate fluid resuscitation.
  • Temporary vasopressor use or push-dose vasopressors may be of particular use during intubation in the hemodynamically unstable hemorrhagic shock patient.

References / Further Reading

  1. Rosen, Peter, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Elsevier, 2018.
  2. Tintinalli, Judith E. Emergency Medicine: a Comprehensive Study Guide. McGraw-Hill, 2011.
  3. Marino, Paul L. Marino’s the ICU Book. Wolters Kluwer Health/Lippincott Williams & Wilkins, 2014.
  4. Dunham, C. Michael, et al. “Oxygen Debt and Metabolic Acidemia as Quantitative Predictors of Mortality and the Severity of the Ischemic Insult in Hemorrhagic Shock.” Critical Care Medicine, vol. 19, no. 2, 1991, pp. 231–243.
  5. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) student course manual. 9th ed. Chicago: American College of Surgeons, 2012:69.
  6. Heffner, Alan C., et al. “The Frequency and Significance of Postintubation Hypotension during Emergency Airway Management.” Journal of Critical Care, vol. 27, no. 4, 2012.
  7. Ferrada, Paula, et al. “Circulation First – the Time Has Come to Question the Sequencing of Care in the ABCs of Trauma; an American Association for the Surgery of Trauma Multicenter Trial.” World Journal of Emergency Surgery, vol. 13, no. 1, 2018.
  8. Cannon, Jeremy W., et al. “Damage Control Resuscitation in Patients with Severe Traumatic Hemorrhage.” Journal of Trauma and Acute Care Surgery, vol. 82, no. 3, 2017, pp. 605–617.
  9. Holcomb, John B., et al. “The Prospective, Observational, Multicenter, Major Trauma Transfusion (PROMMTT) Study.” JAMA Surgery, vol. 148, no. 2, 2013, p. 127.
  10. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA 2015; 313:471.
  11. Cotton, Bryan A., et al. “Predefined Massive Transfusion Protocols Are Associated With a Reduction in Organ Failure and Postinjury Complications.” The Journal of Trauma: Injury, Infection, and Critical Care, vol. 66, no. 1, 2009, pp. 41–49.
  12. Kautza, Benjamin C., et al. “Changes in Massive Transfusion over Time.” Journal of Trauma and Acute Care Surgery, vol. 72, no. 1, 2012, pp. 106–111.
  13. Sihler, Kristen C., and Lena M. Napolitano. “Complications of Massive Transfusion.” Chest, vol. 137, no. 1, 2010, pp. 209–220.
  14. Shakur H, 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.” The Lancet, vol. 376, no. 9734, 2010, pp. 23–32.
  15. Gupta, Babita, et al. “Vasopressors: Do They Have Any Role in Hemorrhagic Shock?” Journal of Anaesthesiology Clinical Pharmacology, vol. 33, no. 1, 2017, p. 3.

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