Introduction
Traumatic cardiac arrest (TCA) is a condition that results from stoppage of the heart due to blunt and/or penetrating trauma. It remains the leading cause of death for persons 1-44 years of age in industrialized countries (unintentional injuries, homicide, suicide).1 The most common cardiac rhythm in TCA is pulseless electrical activity (PEA). PEA may manifest as an electrical pattern on the ECG, that varies significantly between bradycardia and tachycardia, without a palpable pulse. In contrast, persons who suffer medical cardiac arrest (MCA) often have a detectable dysrhythmia such as ventricular fibrillation.2 However, TCA is often treated in a similar or identical fashion to MCA (compressions, epinephrine, fluids) despite the known differences in pathophysiology. The overall survival of victims of TCA remains dismal. A recent study of the United States National Trauma Data Bank (NTDB) for the nine-year period of 2007 to 2015 examined patients with blunt and penetrating torso trauma without vital signs in the emergency department (patients with head injuries, transfers from other hospitals, or those with missing values were excluded). There was a total of 24,191 patients evaluated. Of these, 96.6% were declared dead on arrival (DOA). Only 246 (1%) survived to admission and only 73 (0.3%) were discharged alive. Based on these findings, a trauma center would have to attempt over 100 resuscitations of TCAs to save one patient.3
Pathophysiology
The pathophysiology of TCA is highly variable depending on the mechanism of injury and body structures affected. Some injuries are clearly mortal. Trauma patients lose effective cardiac output because of a loss of preload, hypoxia, massive neurological injury, direct cardiac damage to an otherwise healthy heart, or a combination of these.4 However, there are several causes of TCA that are potentially reversible:
- Hypoxia. Hypoxia is common in TCA and can result from various injuries. Any injury or injuries that adversely affects respiratory gas exchange can result in hypoxia. These include facial and airway injuries, thoracic trauma affecting the lungs and surrounding structures, and interference with the bellows function (expansion/contraction of the chest wall).
- Tension Pneumothorax. The presence of air or fluid in the pleural space with resultant loss of respiratory capacity, sometimes called obstructive shock, is common in trauma and reversible in many cases. Increased intrathoracic pressure decreases venous blood return to the heart (preload). Early decompression of the chest can potentially improve respiratory function and venous return until damage control surgery.
- Cardiac Tamponade. Compression of the heart by the presence of fluid collecting in the pericardial sac thus inhibits adequate ventricular filling of the heart during diastole. This also affects preload and is a form of obstructive shock.
- Hypovolemia. The loss of blood volume (hypovolemic shock) is common in both penetrating and blunt trauma. This adversely affects tissue perfusion causing shock.
There are a few exceptions (although rare). Sometimes trauma, even minor trauma, can bruise the heart (contusio cordis) or disturb the electrical conductive system of the heart (commotio cordis). The mechanism of injury in these two conditions is typically relatively minor and can cause dysrhythmias or impaired cardiac function. While these are, by definition, of a traumatic cause, the treatment is more akin to that provided in MCA (CPR, defibrillation). However, contusio cordis is more apt to cause cardiac structural damage such as valvular damage and pericardial tamponade.5
Management Changes
Management Changes
1. Should we change how we manage TCA? As stated, the pathophysiology of TCA is markedly different than MCA. Treating these two conditions in the same fashion is non-sensical. There is no evidence that any of the following conditions improves outcomes in TCA:
a. Epinephrine and other medications. The loss of perfusion in TCA is considerably slower than in most cases of MCA. As the trauma patient deteriorates, catecholamine release (epinephrine, norepinephrine) will increase causing widespread vasoconstriction until it reaches maximum levels. Giving additional vasopressors (e.g., epinephrine) may actually worsen the patient’s condition.6,7 Other medications, such as sodium bicarbonate and calcium salts, are often given despite any evidence of benefit.
b. Chest compressions may be harmful in TCA. There is no role for chest compressions in TCA—especially when the cause of the TCA is profound hypovolemia. Animal studies have shown worsened survival when chest compressions were provided.8 The use of chest compressions in TCA is highly associated with poor survival. A recent study compared prehospital TCA patients who received prehospital chest compressions with those who did not receive prehospital chest compressions and who were transported for emergency thoracotomy. There were no survivors in the cohort that received prehospital chest compressions (100% mortality versus 94% mortality for those who went straight to emergency thoracotomy). Statistically there was no difference in overall survival in either group).9 TCA death is caused by hypoxia and/or inadequate preload (hypovolemia, tension pneumothorax, pericardial tamponade). Compressing an empty heart is futile as the heart contains nothing to pump! Furthermore, chest compressions may worsen existing thoracic trauma and also cause dislodgement of a beneficial clot. Also, an emphasis on chest compressions may distract or interrupt more effective treatment strategies (ventilation, chest decompression, blood product administration).
c. Do not give fluids (unless blood products are available). The administration of crystalloid IV solutions has limited role in trauma resuscitation (with the exception of burn injury). The literature has clearly shown that administration of crystalloid solutions in trauma worsens outcomes. The prehospital administration of blood products may be beneficial although no study to date has shown any significant improved long-term survival with the prehospital administration of blood products.10,11,13 Various studies of plasma and whole blood are ongoing. It is unlikely whole blood products would be widely available (because of logistical and cost issues). Despite lacking oxygen carrying capacity like red blood cells, plasma may have a beneficial effect. Despite this, the administration of blood products seems intuitive.
2. We should embrace the evolving science and guidelines.
Updated guidelines for the treatment of cardiac arrest have been published by the European Resuscitation Council (ERC) and prehospital treatment of TCA should focus on limiting blood loss and addressing reversible causes.13 These are often referred to as the H’s and T’s (see Table 1). Based on this, the ERC has published the following guidelines (U.S.) derivation based on the evolving evidence (Table 1).
Table 1.
Problem | Intervention |
Hypoxia | Airway, oxygenation, ventilation |
Hypovolemia | External hemorrhage control/pelvic binder/blood products (if available) |
Tension Pneumothorax | Bilateral thoracostomies |
Tamponade | Ultrasound-directed pericardiocentesis/emergency thoracotomy* |
- Hypoxia: It is often difficult to identify all causes of hypoxia in the trauma patient. Do not await pulse oximeter readings before treating possible hypoxia. Care should be directed at immediately establishing an airway (not necessarily endotracheal intubation—perhaps a supraglottic airway), ventilation (BVM) and providing supplemental oxygenation. Ventilation and oxygenation are the primary treatment for asphyxia and high spinal cord injuries.
- Hypovolemia: The first strategy in treating hypovolemia in the prehospital setting is controlling external hemorrhage. This can be accomplished with pressure dressings (created with an elastic bandage), wound packing, tourniquets, and pelvic binders. Internal hemorrhage requires trauma center care. Administration of crystalloid solutions can worsen survival. Blood products (whole blood, plasma, packed red blood cells) may be of benefit but are not widely available. Patients should not be held on scene awaiting blood products. Rapid trauma center transport should be initiated.
- Tension Pneumothorax: Tension pneumothorax should be decompressed if suspected. In the past, bilateral needle decompression of the chest was recommended. However, this was largely ineffective and the size of the needle bore is small limiting the amount of air that can pass. Also, the population has become more obese and some needles are not long enough to reach the pleural space. Several studies have recommended bilateral finger thoracostomy to decompress the chest. It appears to be a safe and effective intervention although further research is needed.14,15
- Pericardial Tamponade: The presence of blood or fluid in the pericardial sac can limit ventricular filling during diastole. Pericardial tamponade can occur in both blunt and penetrating trauma. When emergent surgical intervention is not immediately available, decompression of the pericardium can be life-saving. However, successful placement of a needle into the pericardium in the prehospital setting is difficult even with point-of-care ultrasound (POCUS). In almost all instances, pericardial tamponade is decompressed with a resuscitative thoracotomy in the trauma center. However, if trained and credentialed, prehospital pericardiocentesis might be considered.
3. Utilize Termination of Resuscitation (TOR) protocols.
Field termination of resuscitation (TOR) protocols and recommendations by the American College of Surgeons (ACS) have been recommended since 2003.16 Other organizations, such as the National Association of EMS Physicians (NAEMSP), have had position papers on field trauma TOR available for some time.17 Despite this, many EMS systems have been hesitant to use or enforce these. In one study, more than half of cardiac arrest patients meeting criteria for termination of resuscitation were transported anyway.18 It is incumbent on EMS systems to embrace and use these validated protocols—especially in the setting of emergency department crowding and hospital closures. Some advocate transport of TCA patients for possible organ donation. However, organ retrieval and donation from non-heart beating cadaveric donors is very uncommon.19
4. Transport to the closest appropriate trauma center.
Trauma centers are highly specialized and equipped specifically to manage injured patients. Trauma is a surgical disease and prompt transport to a trauma center for prompt surgical intervention is essential for patient survival. Numerous studies have shown improved outcomes and survival of trauma patients treated in designated trauma centers.20 Rapid transport to a trauma center is essential to improved survival. Most of the prehospital interventions detailed herein can and should be provided during transport.21
Summary
Although the origins of modern EMS are vague, much of the impetus for EMS system development were based on trauma mortality. In 1967, Dr. J.D. Farrington pointed this out in his paper Death in a Ditch.22 The historic white paper, Accidental Death and Disability: The Neglected Disease of Modern Society, published in 1966 by the National Academy of Sciences, focused primarily on the disease of trauma.23 Over 50 years following the publication of this landmark paper, prehospital trauma care and outcomes have improved little.24 National and International trauma organizations should develop or update prehospital TCA guidelines/protocols to reflect the evolving science. Also, increased emphasis on injury prevention can oftentimes prevent many injuries.
References
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