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Sudden Cardiac Arrest and Cardiopulmonary Resuscitation (CPR)

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  1. Introduction to sudden cardiac arrest and resuscitation
    4 Chapters
  2. Resuscitation physiology and mechanisms
    2 Chapters
  3. Causes of sudden cardiac arrest and death
    2 Chapters
  4. Cardiopulmonary Resuscitation
    10 Chapters
  5. Special Circumstances
    11 Chapters
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Cardiac arrest due to trauma

In cases of traumatic cardiac arrest, addressing reversible etiologies takes precedence over chest compressions. If trauma is not definitively established as the cause of cardiac arrest, cardiopulmonary resuscitation (CPR) should be performed per standard guidelines.

Cardiac arrests due to trauma are characterized by very low survival rates. In the nationwide Swedish Registry for Cardiopulmonary Resuscitation, the 30-day survival for traumatic cardiac arrest is 2.5%. As per data from the registry, only suicide attempts have lower survival outcomes. Nonetheless, prompt interventions can reverse cardiac arrest and survivors of traumatic cardiac arrest often exhibit favorable neurological outcomes (Rawshani et al).

Traumatic cardiac arrests typically result from mechanisms that render chest compressions ineffective. For instance, a traumatic hemorrhage can deplete intravascular volume to such an extent that chest compressions fail to generate stroke volumes. Consequently, addressing reversible causes of cardiac arrest becomes more critical than performing chest compressions. Hemorrhages, either manifesting externally or concealed internally, account for approximately half of all traumatic cardiac arrests. In the absence of evident hemorrhage, potential etiologies to consider include tension pneumothorax, traumatic asphyxia, and cardiac tamponade, each implicated in roughly 10% of cases.

Potentially reversible causes of traumatic cardiac arrest (Salomone et al):

  • Hypovolemia: Hypovolemic shock is common in both penetrating and blunt-force trauma. Loss of blood volume renders chest compressions futile.
  • Hypoxia: Hypoxia is common in traumatic cardiac arrest and can arise from a range of injuries. Any trauma impairing ventilation or gas-exchange can cause hypoxia. Such traumas include cerebral, facial, airway and thoracic injuries.
  • Tension pneumothorax: Tension pneumothorax increases intrathoracic pressure, which subsequently compresses larger thoracic veins and thus inhibits venous return to the heart. Pneumothorax can be treated successfully in many instances.
  • Cardiac tamponade: Tamponade in trauma patients is due to blood accumulation in the pericardial sack. This impairs atrial and ventricular filling, such that stroke volumes are severely reduced.

Commotio cordis

Commotio cordis occurs as a result of a blunt, non-penetrating blow to the chest, typically over the precordium. The mechanical impact can induce ventricular fibrillation, even if the force seems relatively minor. It is believed that commotio cordis occurs if the impact coincides with the T wave apex (the peak of the T wave), which represents an electrically vulnerable phase during the cardiac cycle (see R on T phenomenon). While commotio cordis is caused by trauma to the chest, it is managed as a non-traumatic cardiac arrest (i.e. standard CPR, as per guidelines).

Contusio cordis

Contusio cordis refers to a contusion of the myocardium, greater vessels or valves, due to a direct, non-penetrating traumatic blow to the chest. Unlike commotio cordis, contusio cordis implies actual structural injury to the tissues. Manifestations of contusio cordis include:

  1. Arrhythmias: Ventricular or supraventricular arrhythmias (bradyarrhythmia or tachyarrhythmia).
  2. Atrial or ventricular rupture: In severe cases, there can be a rupture of the atria or ventricles.
  3. Myocardial infarction: The contusion can cause coronary artery dissection, atherothrombosis or rupture, resulting in myocardial infarction.

Initial rhythm in traumatic cardiac arrest

The initial rhythm in traumatic cardiac arrests comprises PEA in 60% of instances, asystole in 30%, and VF/VT in 5%.

Chest compressions in traumatic cardiac arrest

In the context of cardiac tamponade, increased pressure within the pericardial sac impedes venous return to the right atrium. Similarly, in tension pneumothorax, the elevated intrathoracic pressure obstructs the venous return via the superior and inferior vena cava. Under these circumstances, chest compressions are ineffective, and they may exacerbate the situation by further increasing thoracic pressure, further compromising venous return. Similarly, in hypovolemic shock, compressions may also impede venous return (Luna et al, Jeffcoach et al, Watts et al). The efficacy and appropriateness of intrathoracic compressions in such situations remain debated (Endo et al).

Spinal shock in trauma

Spinal shock may complicate restoration of perfusion and ROSC. Traumatic spinal shock occurs in case of cerebral or spinal lesions, and leads to hypotension with paradoxical warm periphery and bradycardia. Vasopressors are required to correct spinal shock.

FAST (Focused Assessment with Sonography for Trauma)

Bedside ultrasound with FAST can be done if an experienced examiner is present. FAST protocols and findings are not discussed here.

Management of traumatic cardiac arrest

  1. Hypovolemia
    • Immediate administration of fluids and blood products, including plasma, erythrocytes, and platelets, is recommended upon suspicion of hypovolemia.
    • Administer 1 g of tranexamic acid intravenously if hemorrhage is suspected.
  2. Hemorrhage control
    • Visible external sources of bleeding should be promptly managed with compression or other immediate interventions.
  3. Permissive hypotension
    • In the context of trauma, permissive hypotension might be adopted, permitting a certain level of hypotension to minimize hemorrhage until the bleeding can be controlled.
  4. Aortic occlusion techniques
    • Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) and Resuscitative Thoracotomy (RT) are methods to occlude the aorta and might be utilized as lifesaving measures in cases of infra-diaphragmatic hemorrhage.
  5. Ventilation management
    • Ventilation with elevated intrathoracic pressures can be deleterious as such pressures can inhibit venous return, particularly in the presence of conditions such as pressure pneumothorax, hypovolemia, or cardiac tamponade. Excessive ventilation pressures might escalate a non-complicated pneumothorax to a tension pneumothorax. Employing lower tidal volumes could enhance perfusion under these circumstances.
  6. Tension pneumothorax
  7. Tamponad:
  8. Criteria to withhold initiation of CPR (as per ERC, ILCOR, AHA guidelines):
    • Absence of vital signs for the 15 minutes preceding the initiation of CPR.
    • Injuries that are incompatible with survival, such as decapitation or extensive damage to vital organs like the heart or brain.
  9. Criteria to terminate ongoing CPR (as per ERC, ILCOR, AHA guidelines):
    • Failure to achieve return of spontaneous circulation (ROSC) after all reversible causes have been addressed.
    • Lack of echocardiographic evidence of cardiac activity, even during PEA, following the management of reversible causes.


Traumatic Cardiac Arrest (TCA): Maybe We Could Do Better? Prehospital trauma care and outcomes have improved little in the past 50 years, the authors write. It’s time to change that. Bryan E. Bledsoe, DO, FACEP, FAEMS, Jeffrey P. Salomone. JEMS (2023).

Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamic effects of external cardiac massage in trauma shock. J Trauma 1989;29:1430-3.

Jeffcoach DR, Gallegos JJ, Jesty SA, et al. Use of CPR in hemorrhagic shock, a dog model. J Trauma Acute Care Surg 2016;81:27-33.

Watts S, Smith JE, Gwyther R, Kirkman E. Closed chest compressions reduce survival in an animal model of haemorrhage induced traumatic cardiac arrest. Resuscitation 2019;140: 37-42.

Endo A, Kojima M, Hong ZJ, Otomo Y, Coimbra R. Open-chest versus closed-chest cardiopulmonary resuscitation in trauma patients with signs of life upon hospital arrival: a retrospective multicenter study. Crit Care 2020;24:541.

Ebo DG, Clarke RC, Mertes PM, et al. Molecular mechanisms and pathophysiology of perioperative hypersensitivity and anaphylaxis: a narrative review. Br J Anaesth 2019;123:e3849.

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