Acute Cor Pulmonale

Report:

Supraventricular tachycardia, probably sinus, 160/min

Right axis deviation +95o

Small voltage

Right bundle branch block

Borderline T wave changes

Comment:

The rhythm strip from a later trace is superimposed over the original one to show the position and shape of the sinus P waves: they were probably merged with T waves during the initial tachycardia.

Transient complete or incomplete RBBB is quite frequent in acute pulmonary embolism; it tends to confuse the significance of the associated S1Q3T3 (McGinn-White) pattern. In this trace, there are small Q waves in all three inferior leads, a pattern that may be seen in pulmonary embolism (although only Q3 is well known). RBBB too can cause inferior Q waves, but they are generally absent from Lead 278. Neither embolism nor RBBB cause truly infarctional-looking Q waves, however. The mechanism of RBBB in pulmonary embolism may be neuropraxia of the RBB caused by high RV pressures.

A general diminution of voltage may accompany, for unknown reasons, acute pulmonary embolism; this serves to differentiate it from LPHB (where such differential diagnosis is entertained) since the latter is associated with increased voltages79.

Below (Fig 109a) is the following day’s trace, without the RBBB. Most of the S1Q3T3 pattern remains, but the striking change is the anteroseptal T wave inversion, a sign of extensive embolisation. This V-leads’ T wave pattern usually comes after the frontal plane changes and takes longer to resolve. Its genesis is unknown; I think it reflects a partial LPHB developed at the height of the hæmodynamic stress and “remembered” analogously to T wave inversion following LBBB or pacemaker rhythm80.

109a. 110. 66 year old lady with advanced COAD, admitted with resistant respiratory failure and shock. She died the same day