The patient is a 28 year old male with no known history of heart disease. He is being treated with sodium valproate for epilepsy.
0715: He was the driver of a car that was hit on driver’s side by another car. The patient was wearing a lap-sash set belt. His car did not have air bags. There was intrusion of the side panel into driver’s compartment, and he was trapped in the car
0739: Ambulance arrived at the accident scene. Their initial findings were:
- Heart rate (HR): 160 beats per minute (bpm)
- Systolic blood pressure (SBP): 150-160 mm Hg
- Respiratory rate: 24 breaths per minute
- Glasgow coma score (GCS): 14 (E 4, V 4, M 5). There were no signs of head injury, but the patient had no recollection of the accident,
- ECG monitor: narrow complex tachycardia at a rate of 160-180 bpm. A Valsalva manoeuvre had no effect onthe tachycardia.
- Examination of chest, shoulders and arms was normal. The abdomen was soft and not tender to palpation.
- There were abrasions to the right thigh, and pain and swelling in the right leg.
0739-0800: Pillar and car door cut away, and patient put onto spinal board
The patient received a total of 1.5 L of crystalloid intravenously (IV) and 7.5 mg of morphine IV before reaching hospital.
EMERGENCY DEPARTMENT MANAGEMENT
0825: Patient arrived at the Emergency Department (ED).
The vital signs were:
- GCS: 15
- Pulse oximetry (SaO2): 97%
- SBP: 80 mm Hg
- HR: ~ 300 beats per minute
- ECG monitor: broad complex tachycardia
0827: The findings on the primary survey were:
- Head & Neck: No facial injuries; cervical collar in place
- Chest: Bruising over left lower chest and under left costal margin; auscultation of the heart and lung was normal
- Abdomen: Normal examination
- Chest Xray/pelvis Xray - normal
- ECG (at 0828) - Broad complex tachycardia (BCT) with a ventricular rate of 300 bpm (Figure 1)
- Bedside ultrasound examination (FAST - focused assessment with sonography for trauma) of the heart and abdomen was normal
Figure 1. Twelve lead ECG of C_0008, The ventricular rate is 300 bpm, and the rhythm is regular. The QRS complexes are widened with a right bundle branch block (RBBB) pattern. There are small notches on the downstroke of the QRS complexes in Lead II, and just before the upstroke of the QRS complexes in Leads II and aVR. These could be retrograde P waves. There is a 1:1 relationship between the QRS complexes and the notches. There is marked right axis deviation. The morphology of the complexes in Lead V1 (monophasic and broadR ) and in Lead V6 (rS) favours ventricular tachycardia.
Analysis of the morphology of Lead aVR using the criteria proposed by Vereckei et al (1) is complicated by the presence of a small upright deflection just before the upstroke of each QRS complex. If this deflection is regarded as part of the QRS complex then the morphology of aVR (rsR') does not favour ventricular tachycardia, but the Vi/Vtratio is > 1 which favours supraventricular tachycardia with aberrant conduction. If thisdeflection is not part of the QRS complex then the morphology of aVR (R) favours ventricular tachycardia (although the Vi/Vtratio continues to favour supraventricular tachycardia with aberrant conduction)
Conclusion: Analysis of ECG morphology using published criteria for determining the likely mechanism of the BCT produced conflicting results
Figure 3. Analysis of Lead aVR from the ECG of C_0008 taken at 0827. Small notches (mauve arrows) precede the QRS complex- these could be caused by atrial depolarisations (retrograde P waves or atrial flutter waves) or could be part of the QRS complexes. Two QRS complexes are shown enclosed by vertical blue lines; in the first complex the preceding notch is assumed to be part of the complex, so this complex has a rsR' configuration. In the second complex the notch is assumed to originate from the atria, so the second complex has a R configuration. Vi is the amplitude of the complex during the first 40 msec of ventricular depolarisation, and Vt the amplitude during the last 40 msec. The Vi /Vt ratio of2.3 favours the diagnosis of supraventricular tachycardia.
Further management was as follows:
One litre ofnormal saline IV statim
0831: Adenosine (12 mg) IV: no effect on the BCT
0835: SBP was 50 mm Hg and HR was 300 bpm. After 0.5 mg of metaraminol IV the SBP increased to 120 mmHg
0839: Adenosine 18 mg IV: transient slowing of the ventricular rate showing a possible underlying atrial flutter. The HR then returned to 300 bpm
Blood test results: normal haemoglobin concentration; normal serum electrolyte concentrations apart from a slightly reduced serum potassium concentration of 3.3 mmolL; normal cardiac enzymes; arterial blood gases: pH 7.29, pCO2 37 mm Hg, pO2 81 mm Hg, bicarbonate 17 mmol/L
0845: Amiodarone 300 mg IV: no effect on the BCT
0846: Metaraminol 0.5 mg IV (pre-intubation)
0848: Rapid sequence intubation with suxamethonium 100 mg IV and thiopentone 425 mg IV
0851: BCT changed spontaneously to a narrow complex tachycardia at a rate of about 150 beats per minute (Figure 4) as the patient was about to be cardioverted
An ECG taken at 0853 is shown on Figure 5, and one taken at 0923 is shown in Figure 6.
FOLLOW UP INVESTIGATIONS
The results of other investigations were:
CT scans of the brain and cervical spine were normal
CT scans of the chest, abdomen and pelvis were norma apart from patchy atelectasis at lung bases
Radiology of limbs:
- Bilateral tibial plateau fractures
- Fracture of proximal left fibula
- Fractures involving the left mid-talar joints
- Fractured fourth left metatarsal
- Dislocation of the left 3rd to 4th metatarso-phalangeal joints
An echocardiogram study (Figure 7) was normal
Stay tuned for Part 2 - "One Algorithm to rule them all"....