Trauma & the Heart Case 2 - "One Algorithm to Rule Them All"


The most likely mechanism of the tachycardia in the previous case is atrial flutter with an initial 2:1 atrioventricular (AV) conduction, followed by 1:1 AV conduction that produced the BCT (because of aberrant conduction). Alternative diagnoses are ventricular tachycardia or pre-excited supraventricular tachycardia.

The possible causes of the tachycardia are a "direct" effect of the chest trauma on the heart (stretching or cardiac contusion or other mechanism) or a "secondary" effect due to the increased sympathetic discharge that accompanies multiple injuries. This may have occurred in a normal heart, but it is possible that the patient could have a undiagnosed pre-existing paroxysmal supraventricular tachycardia or accessory pathway. It is also possible that the tachycardia began before the accident.



The patient's General Practitioner provided the following information that was not available at the time of the accident. About 11 months earlier the patient had an episode of palpitation, with a ventricular rate of 196 beats per minute. Carotid sinus pressure restored sinus rhythm. Blood tests (electrolyte concentration and CK-MB concentration) were normal. The chest Xray was normal, and the ECG showed incomplete right bundle branch block.

The response to carotid sinus massage makes it unlikely that this rhythm was due to atrial flutter.



The immediate management of the patient was based on the working diagnosis of atrial flutter with 1:1 AV conduction. This initially involved increasing AV block with IV adenosine - this caused transient slowing of the ventricular rate.

Metaraminol was used to maintain the SBP - larger doses could have been given to produce hypertension and cause increased vagal discharge via baroreceptor stimulus, but this was potentially dangerous if there was an associated arterial injury. 

The examination of a trauma victim involves a log roll to examine the thoracic spine and lumbar spine, and often includes a rectal examination. In this case rectal examination with digital rectal stimulation was not done, but would have beena safe and non invasive way to increase AV block by vagal stimulation (2). 

The next step was rapid sequence endotracheal intubation prior to cardioversion.  Amiodarone was given shortly before intubation.

Shortly after endotracheal intubation the ventricular rate suddenly halved to 150 bpm and the QRS complexes narrowed. The underlying atrial rhythm was atrial flutter. The decrease in AV conduction that resulted in 2:1 AV block was presumed to be due to increased vagotonia caused by intubation, although amiodarone and possibly suxamethonium (which can cause bradycardia or heart block [3]) may have contributed. 



Determining the underlying mechanism in a case of BCT (or Wide Complex Tachycardia [WCT]) can be challenging and frustrating, and various algorithms have been proposed to help with this task (See Figure 8). The number of these is greater than the number of commandments handed to Moses. This case illustrates that there is no single "Lord of the Algorithms".

Figure 8. Published algorithms for determining the mechanism in BCT


"Go to a good engineering firm and ask them to make you a reliable, compact, automatic pump about 1/250 of a horsepower, as big as a man's fist and weighing rather less than a pound (about 450 grams). It must have an output which can be varied from one gallon to 8 gallons (5 to 35 litres) of thickish fluid per minute. For the most part it must idle smoothly along at the lower rate, beating about 40 million strokes a year. It will work usually against a head equivalent to 6 feet (2 metres) of water, but at times this may be doubled, and then it must automatically increase its force. Similarly it must be sensitive to any increase or decrease in the pool of fluid from which it is pumping, responding immediately by acceleration or deceleration, or by increased or decreased stroke as the case may be. It must also accept signals which may reach it electrically from other pieces of machinery or from control centres elsewhere. It must react, too, to signals in the form of dissolved substances reaching it in the fluid being pumped. Its valve closures must not damage millions of suspended cells which will form almost half the volume of this fluid. It must never stop in an average run of 60 to 80 years, during which time each of its chambers will pump 65 million gallons (about 300 million litres) of blood" (4).

"The human heart is nearly all muscle, a hollow lump of red meat expanding and contracting with each beat about as much as a half-opened and re-clenched fist"(4). 

This muscle is remarkably resilient: there is a very low incidence of significant structural damage or rhythm disturbance despite the battering that the thorax receives during a boxing match or the intra-thoracic forces that are generated by a blow or a high velocity acceleration-deceleration event.

In a previous blog on trauma and the heart (Trauma and the Heart Case 1) we presented a case of blunt thoracic trauma producing a myocardial contusion. In this blog we present a case of atrial flutter with 1:1 AV conduction that followed blunt trauma to the torso and major fractures to the legs. 

The following ECGs show some other aspects of ECG changes after a blow to the chest.

Case 1. Cardioversion of presumed supraventricular tachycardia in a haemodynamically unstable trauma case. 

This middle aged patient presented with multiple injuries after a motor vehicle accident. There was a significant head injury that had resulted in the patient being intubated. On arrival the systolic blood pressure was 90 mm Hg, and the ECG monitor showed a narrow QRS complex tachycardia that appeared regular, with a ventricular rate that was about 300 bpm, with occasional slowing to 150 beats per minute. A diagnosis of supraventricular tachycardia (? atrial flutter) was made and the patient received three synchronised cardioversions (Figure 9). There was no effect on the ventricular rate. Review of the rhythm strip showed that the underlying rhythm was atrial fibrillation, and review of the patient's past history confirmed they had pre-existingatrial fibrillation. The ventricular rate slowed to 110 bpm following rapid IV fluid administration, increasing sedation and increasing the dose of analgesia.

Figure 9. Sequential rhythms strips showing atrial fibrillation with a very rapid ventricular rate that persists despite three synchronised cardioversions (DCCS).

Commotio cordis is "mechanical stimulation of the heart by non-penetrating (impulse-like) impact to the praecordium that, via intrinsic myocardial mechanisms, gives rise to rhythm disturbances of varying type, duration and severity (including sudden death) in the absence of any structural damage that would explain the observed electro-physiological effect" (5-9). 

Case 2 is an experiment in a anaesthetised pig where a blow over the heart produced ventricular fibrillation (experimental commotio cordis)(8) (Figure 10).

Figure 10. Experimental commotio cordis

Case 3 is the ECG of a 25 year old man who developed palpitations after he was hit in the sternum while playing basketball (clinical commotio cordis)(Figure 11)

Figure 11. There is a regular BCT with a ventricular rate of about 250 bpm. Theinitial diagnosis is ventricular tachycardia, but the morphology of the complexes is suggestive of a pre-excited supraventricular tachycardia.

Figure 11. There is a regular BCT with a ventricular rate of about 250 bpm. Theinitial diagnosis is ventricular tachycardia, but the morphology of the complexes is suggestive of a pre-excited supraventricular tachycardia.

Case 4. The use of a precordial thump to (possibly) convert ventricular tachycardia or ventricular fibrillation to sinus rhythm is no longer recommended because there is no definite evidence that it improves the outcome. This last case shows the restoration of sinus rhythm following a precordial thump in a case of ventricular tachycardia.

Figure 12. Consecutive rhythm strips. The upper strip shows an episode of torsades de pointes that reverts spontaneously. The bottom strip shows monomorphic ventricular tachycardia that is converted to sinus rhythm by a precordial thump.