Practitioner Updates

Cardiac Trauma

A photo of people moving in a veterinary lab

Several mechanisms and types of cardiac injury exist. Because the term cardiac or myocardial contusion is considered non-specific and lacks a clear definition, some authors replace it with blunt cardiac injury (BCI) as a catch-all term used to describe non-penetrating trauma to the heart.1

In humans, cardiac injury following blunt thoracic trauma has been reported in up to 76% of patients.1 The incidence of BCI in dogs and cats is unknown. The clinical presentation of a dog, cat or human with BCI is extremely variable in terms of injury severity, cardiac consequences and clinical consequences.1,2,3 Some patients with BCI seem unaffected; others show minimal clinical consequences, despite evidence of cardiac injury; others present in various states of clinical compromise, including death.1,2,3

Importantly, trauma affects the whole body. In the traumatized patient with tachycardia, arrhythmias, or other possible signs of cardiac injury, it is important to consider the whole patient – i.e., treat shock, haemorrhage, pain, etc. – rather than hyper-focussing on the heart.

Mechanisms of cardiac trauma

  1. Direct impact to the chest wall is a common cause of BCI in humans.2 Kinetic energy is directly transferred to the heart. The right heart is more frequently injured than the left, due to its anterior location.1,2 This may not be the case for animals, due to different morphologies. The timing of the impact affects the degree of injury: impacts that occur at the end of diastole, when the ventricles are maximally filled, result in more serious injury.1,2,3
  2. Indirect injury refers to a massive increase in preload due to the trauma. Trauma to the abdomen, for example, can compress capacitance vessels leading to a large increase in blood volume pushed toward the heart.1,3 This leads to an abrupt increase in intracardiac pressure and overdistension.
  3. Bidirectional forces is a term used to describe compression of the heart between two walls (for example, the right and left rib cages or the sternum and the spine).
  4. Deceleration injuries are frequently encountered in humans in car accidents.2 With deceleration, two things can occur:
    • Tissues decelerate at different rates (for example, the heart versus the great vessels), leading to shearing between these structures.
    • The tissues can thump to a sudden stop, i.e., a direct impact injury. In people, the “seatbelt sign” is bruising to the chest due to constriction by the seatbelt, which heightens doctors’ awareness to a possible BCI due to deceleration.2
  5. Blast injury can have a variety of meanings. According to the United States CDC, there are four categories of blast injury: primary injuries, due to compression and over pressurization of gas-filled structures (for example, the lungs); secondary injury, resulting from flying debris; tertiary injuries occur when a body is thrown by the blast wind; quaternary is anything not primary, secondary, or tertiary (e.g., burns).4 Over-pressurization of the heart can occur, particularly at end-diastole (see direct impact above).1,2,3 Kinetic energy transfer can also cause shear-related injury (acceleration/deceleration).5 Spallation can occur when kinetic energy waves travel between materials of high and low acoustic impedance, resulting in fragmentation of the high impedance material into the low impedance material.5
  6. Penetrating injury is caused by anything penetrating the heart. This is reported with rib fractures in humans. Sticks, porcupine quills and metallic foreign bodies (airgun pellets) have been reported in dogs and cats.6,7,8,9

Types of Cardiac Trauma

  1. Myocardial contusion is a non-specific term for bruising of the heart. Histopathologically, it is characterized by haemorrhage (ruptured vessels), inflammation and/or necrosis, and oedema.1,2 This is the most common type of BCI and can be variably compromising. Most humans with mild contusions or intramural haematomas recover.1,2 In the 20th century “contusion” was defined as elevated myocardial band creatine kinase (a cardiac biomarker) with echocardiographic evidence of injury versus “concussion”, where there were no echocardiographic abnormalities. Modern authors suggest BCI replace contusion or concussion when referring to patients with cardiac injury following blunt trauma.1 Other authors use “cardiac contusion” to refer to less severe primary injuries.3
  2. Myocardial rupture is the loss of integrity of the myocardium. It often results in death prior to emergency room presentation in humans2 and animals.10 Patients presenting to the emergency room are expected to have haemorrhagic pericardial effusions.2,11 If the pericardium is also ruptured, pericardial effusion may not be seen.3
  3. Septal injury can occur directly due to trauma, or days after the trauma with necrosis of the septal tissue.1 Severity varies from minor tears to major compromise of the septum. New inter-chamber communications can cause a new heart murmur. Three reports of traumatic Gerbode defects (communications between the left ventricle and the right atrium) have been published in dogs.12,13,14
  4. Valvular trauma can occur. Like septal injuries, the haemodynamic consequences may be immediate (for example, sudden, massive regurgitation) or delayed (for example, with later rupture of a papillary muscle due to necrosis). New valvular insufficiencies (often indicated by heart murmurs) should raise suspicion for septal and/or valvular injuries. Heart failure may occur acutely or be delayed.3
  5. Pericardial laceration can occur with or without rupture of the myocardium.3 Some authors suggest pericardial laceration concurrent with myocardial rupture may improve survival to presentation, as tamponade physiology is less likely to ensue.2 However, massive haemothorax is then a concern. Herniation of cardiac structures out of the pericardium, or extra-cardiac structures into the pericardium, is possible and might result in strangulation.3
  6. Commotio cordis is sudden cardiac death without an identified pathology. It has been demonstrated in a pig model.15 When a precordial impact occurs immediately before the peak of the T wave, it triggers ventricular fibrillaton.3 Commotio cordis is reported in young people playing sports with low-energy impacts and no previous heart disease.15

Tools for Emergency Evaluation

  1. The physical examination is paramount. Significant cardiac trauma uncommonly occurs in isolation: standard approaches to the traumatized patient, including ABC (airways, breathing, circulation…), are recommended.
    • Cardiac trauma can occur in any traumatized patient. Patients with thoracic injuries are obvious candidates; however, BCI can occur with extra-thoracic injuries too (see “indirect injury” above).
    • Shock, tachycardia and hypotension can occur due to BCI; however, similar signs occur in the general trauma patient and not all shock is cardiogenic.
    • Muffled heart sounds might indicate pericardial haemorrhage; however, other pathologies, such as pneumothorax and haemothorax, are more common.
    • Relocation of the apex beat or auscultation of the heart in an unusual location can occur with cardiac herniation out of the pericardium.
    • A new or worsened cardiac murmur might indicate injury to the septum or valvular apparatus.
    • Human literature suggests jugular venous distension as an indicator of pericardial tamponade.1,2 This is harder to evaluate in dogs and cats, especially with haemorrhage, hypotension and polytrauma.
  2. Electrocardiography (ECG) should be considered in all traumatized patients. An arrhythmia does not necessarily represent serious cardiac injury, as other causes may exist (shock, haemorrhage, pain, acidosis, brain injury, etc. …). A normal admission electrocardiogram does not necessarily rule out an arrhythmia, as some arrhythmias are intermittent and others may develop during hospitalization.1,3 However, a normal admission ECG in dogs suggests that compromising cardiac arrhythmias are unlikely to develop in the first 24 hours.16
  3. Cardiac biomarkers are used to demonstrate cardiac injury. Cardiac troponin I (cTnI) seems to be most useful. In dogs, a normal cTnI level had a 100% negative predictive value for ruling out development of clinically significant arrhythmias in the first 24 hours.16 In humans, a normal ECG and normal troponin level supports discharge from the emergency room in an otherwise stable patient.1 However, some cardiac injuries, such as septal rupture, may be delayed and might not be associated with an elevated admission troponin level.
  4. Point of care ultrasound (POCUS) is a powerful tool when used correctly. Focused cardiac ultrasound (FCU) can be used to investigate pericardial effusions, overt left ventricular systolic dysfunction and marked right heart pressure or volume overload (which may be pre-existing). The caudal vena cava can be assessed, along with other metrics, such as the caudal vena cava-to-aorta ratio. The practitioner is reminded that POCUS techniques are intended to be quick to implement and answer binary (yes/no) style questions, for example “is there pericardial effusion?” FCU is better suited to assessing volume tolerance as opposed to fluid responsiveness.
  5. Critical care echocardiography (CCE) may be performed by an appropriately trained practitioner (for example, a cardiologist). CCE generally focuses on instantaneous haemodynamic assessments in critically ill patients. With cardiac trauma, the sonographer may identify valvular regurgitations, loss of septal integrity and cardiac chamber collapse (with tamponade physiology).
  6. Advanced imaging such as cardiac CT and MRI are generally not performed emergently in dogs and cats. Formal echocardiography is important for any patient with a new onset murmur, refractory hypotension or persistent haemodynamic instability. If considering pericardiocentesis, it is recommended to obtain an echocardiogram first, though this is not always possible. Intracardiac thrombi, myocardial infarction and cardiac volume overload can all occur with BCI and require echocardiography.3
  7. Exploratory thoracotomy can facilitate diagnosis and treatment. Emergency room thoracotomy is discussed below.

Considerations for Treatment

  1. Shock management takes priority. This might include crystalloids, blood products and, in select cases, vasopressors. Thoracocentesis may be necessary (for example, tension pneumothorax). Repeating FCU during resuscitation is recommended, as increasing circulating volume (thus intracardiac pressures) may increase intrapericardial haemorrhage if the myocardium is ruptured.2 Refractory shock and destabilization following initial stabilization require immediate investigation, including ECG and POCUS/FCU (or ideally formal CCE/formal echocardiography). In humans, atrial rupture can be delayed.2
  2. Arrhythmias often occur in traumatized patients. Not all arrhythmias require immediate intravenous treatment, for example sinus tachycardia and isolated atrial or ventricular ectopies may resolve with stabilization and analgesia. A consistent pulse and a reasonable blood pressure might be reasons to prioritize treating the patient rather than the arrhythmia. Immediate treatment is indicated for compromising ventricular tachycardia (for example, intravenous lidocaine) or ventricular fibrillation (defibrillation).
  3. Pericardiocentesis can be lifesaving with pericardial tamponade. Specific to acute haemorrhagic pericardial effusion, as is the case with trauma, pericardial decompression may permit continued haemorrhage through the ruptured myocardium, resulting in re establishment of tamponade or death by exsanguination. A indwelling pericardial catheter (for example, using the modified Seldinger technique) may be used and can be a useful bridge to surgery.
  4. Emergency room thoracotomy can be effective, particularly in the arrested or periarrest patient with pericardial or pleural space occupying lesions (i.e., pericardial effusion, intrapericardial herniations, pneumothorax, haemothorax, diaphragmatic hernia). ER thoracotomy is controversial in humans, though authors recommend considering it.1,2 The morphology of some dogs makes this procedure relatively straight forward, whilst other dogs and cats may be more challenging. When opening a chest with intrapleural haemorrhage, visibility can be obscured. If removing the pericardium (for example, to relieve tamponade), expect marked, rapid haemorrhage and obscured visibility. Digital pressure can temporarily stem the haemorrhage. Definitive repair of the ruptured myocardium includes suturing or haemostasis patches.2,11,17
  5. Pain and other comorbidities should be treated as appropriate. Pure mu-agonist opioids are recommended. Fentanyl can be titrated to effect and is relatively short acting.
  6. Antifibrinolytics may have a role with cardiac haemorrhage. Benefits to using tranexamic acid have been demonstrated in humans undergoing cardiac surgery and when administered early following trauma.18 It is unclear how these data translate to the canine patient with BCI and cardiac haemorrhage.
  7. Cardiac dysfunction occurs with BCI. Mild cardiac dysfunction likely needs no specific treatment. Systolic failure may be managed with inotropic (for example, dobutamine) or ino-pressor (for example, low dose noradrenaline) medications. The practitioner is reminded that pushing the injured heart to work is potentially deleterious and medications with inotropic properties may be proarrhythmogenic. Pimobendan, an ino-dilator, may be considered. There is concern using pimobendan in the traumatized heart, due its mechanism of action (calcium sensitization).19 This has not been studied in dogs or cats with BCI. Different to other inotropes, pimobendan does not increase intracellular calcium content, so this concern may be unfounded.20 This use of pimobendan would be off-label. Measuring cardiac output via CCE/echocardiography should be considered to avoid overworking the injured heart.
  8. Treatment of congestive heart failure and volume overload may be necessary acutely (for example, due to valvular rupture) or later. Judicious use of fluids is recommended in a patient with a new heart murmur or evidence of new valvular insufficiency. Intracardiac thrombosis can occur21, which may warrant anticoagulant therapy: formal echocardiography is recommended to assist in decision making.

By Christopher R. Kennedy, BVetMed, DACVECC, DECVECC

References

  1. Singh S., Heard M., Pester J.M., et al. Blunt cardiac injury. StatPearls [Internet] [Accessed February 28, 2023]
  2. Nair L., Winkle B. and Senanayake E. Managing blunt cardiac injury. J Cardiothorac Surg 2023;18(1):71.
  3. Oldach M.S. Blunt cardiac injury. In: Silverstein D.S., Hopper K, editors. Small animal critical care medicine, 3rd edition. St. Louis, USA, Elsevier, Saunders; 2022: 266-270.
  4. Center for Disease Control Injury Prevention. Explosions and blast injuries. Center for Disease Control [Internet] [Accessed February 28, 2023].
  5. Scott T.E., Kirkman E., Haque M., et al. Primary blast lung injury – a review. Br J Anaesth 2017;118(3):311-316.
  6. Pelosi A., Hauptman J.G., Eyster G.E., et al. Myocardial perforation by a stick foreign body in a dog. J Vet Emerg Crit Care (San Antonio) 2008;18(2):184-187.
  7. Nucci D.J.S. and Liptak J. The diagnosis and surgical management of intracardiac quill foreign body in a dog. J Am Anim Hosp Assoc 2016;52(1):73-76.
  8. Elliot J.M. and Mayhew P.D. Diagnostic challenges and treatment options of a suspected pericardial metallic projectile foreign body in a dog. J Vet Emerg Crit Care (San Antonio) 2011;21(6):684-91.
  9. Bomassi E. Corps étranger intramyocardique chez un chat. Pratique médicale et chirurgicale de l’animal de compagnie 2010;45:89-92.
  10. Piegari G, Prisco F., De Biase D., et al. Cardiac laceration following non-penetrating chest trauma in dog and cat. Forensic Sci Int 2018;290:e5-e8.
  11. Witt A.L., Mathews K.A. and Holmberg D.L. Successful management of traumatic right atrial rupture. J Vet Emerg Crit Care (San Antonio) 2000;10(2):85-89.
  12. Hezzell M.J., Dennis S., Lewis D.H., et al. Gerbode defect associated with blunt trauma in a dog. J Vet Cardiol 2011;13(2):141-6.
  13. Cunningham S.M., Lindsey K.J and Rush J.E. Acquired Gerbode defect and third-degree atrioventricular block secondary to vehicular trauma in a dog. J Vet Emerg Crit Care (San Antonio) 2003;23(6):637-642.
  14. Gardener L., Silva J. and Novo Matos J. Spontaneous closure of a traumatic acquired Gerbode defect in a dog. J Vet Cardiol 2022;41:194-198.
  15. Link M.S, Wang P.J, Pandian N.G, et al. An experimental model of sudden death due to low-energy chest-wall impact (Commotio Cordis). N Engl J Med 1998;338:1805-1811.
  16. Biddick A.A., Bacek L.M., Fan F., et al. Association between cardiac troponin I concentrations and electrocardiographic abnormalities in dogs with blunt trauma. J Vet Emerg Crit Care (San Antonio) 2020;30(2):179-186.
  17. Romero-Velez G., Kaban J.M., Chao E., et al. Use of the EVARREST patch for penetrating cardiac injury. Trauma Case Rep 2020;28:100324.
  18. Ockerman A., Vanassche T., Garip M., et al. Tranexamic acid for the prevention and treatment of bleeding in surgery, trauma and bleeding disorders: a narrative review. Thrombosis J 2021;19(1):54
  19. Choi Y.H., Cowan D.B., Wahlers T.C.W., et al. Calcium sensitization impairs diastolic relaxation in post-ischaemic myocardium: implications for the use of Ca(2+) sensitising inotropes after cardiac surgery. Eur J Cardiothorac Surg 2010;37(2):376-83.
  20. Stern J.A. and Walker A.L. Pimobendan. In: Silverstein D.S., Hopper K, editors. Small animal critical care medicine, 3rd edition. St. Louis, USA, Elsevier, Saunders; 2022: 872-876.
  21. Ballocco I., Parpaglia M.L.P., Corda F., et al. Left atrial thrombosis secondary to blunt cardiac injury in two dogs. Vet Rec Case Rep 2019;7:e000803.