Myocardial Contusion

Chapter 40 Myocardial Contusion



Adam J. Reiss, DVM, DACVECC



KEY POINTS



• Myocardial injuries often are overlooked in the trauma patient.

• The most common physiologic consequence of myocardial injury in dogs and humans is arrhythmias.

• Arrhythmias associated with myocardial injury may be delayed in onset up to 48 hours.

• Holter monitoring or continuous electrocardiographic (ECG) monitoring should be considered in high-risk patients.

• Troponins, cardiac-specific proteins, are an effective biomarker of myocardial injury in dogs.

• Normal ECG findings and cardiac troponin I levels on admission in traumatized human patients are an efficient way to rule out myocardial injuries and arrhythmias associated with trauma.

• Management of myocardial injuries is aimed toward maintaining optimal cardiac output and suppressing life-threatening arrhythmias.

• The class I antiarrhythmic agents, including lidocaine and procainamide, are used commonly to manage ventricular ectopy associated with myocardial injury.


INTRODUCTION


Traumatic myocarditis is a controversial subject. Much of the controversy in human studies revolves around a lack of consistent evidence that this injury has any effect on patient outcome and the expense associated with diagnostic testing, cardiac monitoring, and prolonged hospital stays.1 Additional controversies associated with this injury revolve around its name, incidence, and how it is diagnosed. What appears to be agreed on consistently in the literature is the basic definition of this injury and that there is lack of an antemortem diagnostic gold standard. Direct visualization of the heart or histologic examination of damaged myocardium are considered the current diagnostic gold standard.2


The term traumatic myocarditis has been used frequently in veterinary literature to describe an assumed myocardial injury associated with arrhythmias in patients suffering from blunt thoracic trauma.3 This term is used interchangeably with myocardial injury in this chapter.



INCIDENCE


Blunt thoracic trauma has been reported to result in myocardial injuries in 8% to 95% of human patients.3-10 Reported variations in the frequency of myocardial injuries of dogs are similar to those described in humans. Several studies (three prospective, two retrospective) have examined the prevalence of traumatic myocarditis in the dog and report a range from 10% to 96%.4,11-14 Variations in study design as well as disagreements regarding terminology, diagnostic modalities, and criteria used to identify myocardial injuries in humans and dogs contribute to the wide range in the reported frequency of this type of injury in both the human and veterinary literature.2,3,7,13-21 The authors of these studies do agree, however, that myocardial injuries are easily overlooked.18



ETIOLOGY, MECHANISM OF INJURY, AND PATHOPHYSIOLOGY


Thoracic trauma is common in dogs injured by automobiles, animal attacks (bites, kicks), and falls from a height.2,3,11-13,19-21 Because of the elastic nature of the thoracic cage, blunt trauma may subject the myocardium to compressive and concussive forces.13,14,22-24 The most common mechanism of myocardial injury in the dog is that secondary to lateral chest compression.22,24 In addition to potential concussive injury from forceful contact with the ribs, sternum, and vertebrae when rapid acceleration or deceleration occurs, it has been proposed that distortion of the thoracic cage results in a rise in intrathoracic and intracardiac pressures, causing shearing stresses within the myocardium powerful enough to result in contusions.6


In vivo studies performed in dogs to mimic blunt chest trauma have correlated histopathologic areas of myocardial injury with areas of injury found during echocardiographic examination. Experimental trauma delivered to the left side of the chest resulted in abnormalities that were located primarily in the craniolateral wall of the left ventricle, and right-sided chest trauma produced septal and right ventricular wall damage.6


Gross pathologic findings in the traumatized heart have been characterized by localized edema, ecchymosis, and intramyocardial hematoma formation. Myocardial injuries were often transmural, with the epicardial surface being more severely affected.6


Arrhythmias and conduction defects are the most commonly reported consequences of myocardial injuries in humans and dogs.7,11,22-27 One proposed proarrhythmic mechanism of myocyte trauma is the lowering of the ratio of effective refractory period to action potential duration and an increase in the resting membrane potential (less negative) in damaged myocardial cells. Additionally it is proposed that myocyte injury results in alterations of sodium and calcium currents across cell membranes, increasing the availability of intracellular calcium, resulting in increased sensitivity to depolarization.3 These proposed intracellular derangements secondary to trauma can potentiate arrhythmogenesis.3 Arrhythmias become apparent when the injured myocardium becomes the site of the most rapid impulse formation, overcoming the sinus node as the dominant (overdrive) pacemaker. The injured myocardium becomes the new overdrive pacemaker, propagating the arrhythmia by depolarizing the sinus node before it has a chance to fire and recapture the cardiac rhythm.3


Isolated rabbit hearts have been subjected to injury during high-resolution mapping of epicardial excitation to identify the origin of arrhythmias in injured myocardium. The results of this study identified reentry as the mechanism of arrhythmia due to myocardial contusion. The authors found that the site of impact became electrically silent (temporarily), resulting in a fixed and functional conduction block that caused reentry initiation.28


Traumatized patients may also develop arrhythmias associated with metabolic acidosis, hypoxia, electrolyte imbalance, intracranial injuries, and catecholamine release.23,25-27,29 These physiologic aberrations all promote alterations in membrane transport and permeability of cations (sodium, potassium, and calcium), which lead to a decrease in resting membrane potential, as described earlier, contributing to aberrant depolarization and arrhythmias.3,23,25


The most frequently reported arrhythmias secondary to canine myocardial injuries include premature ventricular contractions, ventricular tachycardia, and nonspecific ST segment elevation or depression.6,22-27,29 Less commonly reported arrhythmias reported in dogs with chest trauma include atrial fibrillation, sinus arrest with ventricular or junctional escape complexes, and second-degree and third-degree atrioventricular block.7,12,22,27

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Pulmonary Contusions and Hemorrhage

Stay updated, free articles. Join our Telegram channel
Tags:
Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Myocardial Contusion

Full access? Get Clinical Tree
Get Clinical Tree app for offline access