heart Doctor in Sahakaranagar Cor pulmonale Cor pulmonale is simply heart disease secondary to lung disease. In a sense, the example in is cor pulmonale too: RVH (heart disease) from pulmonary hypertension (lung disease) from mitral stenosis (heart disease again). The term tends to be used mostly for heart disease due to primary lung disease, which may be vascular or parenchymal. It is often described as acute or chronic, but the distinction is more clinical than electrocardiographic. shows an ECG taken on the ward for a patient with stable COPD, yet the V1 morphology shows acute right ventricular ‘strain’. A 61-year-old man with ‘cardiac asthma’ due to mitral stenosis. His LAA is a real P mitrale. He had proven RVH from pulmonary hypertension and eventually came to mitral valve replacement. The frontal plane axis is about +160°, but should perhaps be best described as indeterminate, with all six leads more or less equiphasic. A 76-year-old woman with obvious cor pulmonale with RVH of uncertain age. The lack of sinus tachycardia suggests that it is chronic, but the patient may have chronotropic incompetence (the sinus node is diseased and unable to increase its rate when required). RAA is diagnosed because the P wave axis is +78° and there is a qR complex in V1, even though the actual P wave looks like LAA. The QRS LAD (–60°) is due to the position of the heart rather than to LAHB. The S wave in L2 is larger than the S wave in L3, which is the opposite to what is seen in LAHB and is typical of COPD. This hypotensive, hypoxic and breathless 39-year-old man had extensive thrombophlebitis and a clear chest X-ray. He would easily have been diagnosed with pulmonary embolism even without the typical ECG shown. The pattern can be caused by any acute respiratory failure and the clinical context remains paramount. Note the superficial resemblance to acute inferior myocardial infarction, including the slight ST elevation in L3. However, there are no reciprocal changes and L2 shows ST depression, partly produced by a marked shift of the atrial repolarisation often seen in sinus tachycardia of this magnitude. The same patient in a day later. The original S1Q3T3 pattern has almost resolved. The right precordial T inversion implies extensive embolism, but this was obvious from the patient’s clinical course. The clinical picture also rules out anteroseptal ischaemia as the cause of the ECG changes. The prototype acute cor pulmonale is pulmonary embolism that classically produces the S1Q3T3 (McGinn-White) pattern—a deep S wave in L1, and Q wave and T wave inversion in L3—followed by right precordial T wave inversion ). Electrocardiographically, cor pulmonale is quite pleomorphic. As expected, the effects are mostly right-sided (new or chronic RAA, RBBB, rightward axis shift), but the coexistence of hypoxaemia and acidosis may cause left ventricular ST/T changes suggesting severe ischaemia. Massive embolism may cause bradycardia rather than tachycardia. Atrial tachyarrhythmias may impose a haemodynamic burden of their own and mask the ‘causal’ underlying condition.