The triad of hypotension, elevated jugular venous pressure (JVP) and clear lung fields is found in only a few conditions - most notably right ventricular myocardial infarction (RVMI), pulmonary embolism (PE), tension pneumothorax and cardiac tamponade. The absence of pulsus paradoxus and lack of muffled heart sounds make cardiac tamponade less likely. In general, clinical signs and symptoms do not allow confirmation or exclusion of PE. However, the presence of deep venous thrombosis (DVT), a history of recent major surgery or presence of a malignancy might raise the suspicion of this diagnosis. In addition, the associated chest pain is typically pleuritic in nature. Patients with tension pneumothorax are typically severely dyspneic, while examination may show absent breath sounds on one side, tracheal deviation or hyper-resonant lung fields. However, absence of these signs does not exclude this diagnosis. RVMI may be suspected in a patient with a history of ischemic heart disease, or with risk factors like diabetes, hypertension or smoking. Note also that isolated RVMI is uncommon - there is often a concomitant inferior myocardial infarction. The ECG in this patient demonstrates the presence of ST segment elevations in the inferior leads and lead V4R, thus giving the diagnosis of a combined inferior and right ventricular ST segment elevation myocardial infarction (STEMI). If he had a PE, the ECG might have shown sinus tachycardia, an S1-Q3-T3 pattern (i.e. a S wave in Lead I, Q wave in Lead III and T inversions in Lead III) and also evidence of RV strain or a right bundle branch block (although none of these findings need be present). The normal chest x-ray excludes a tension pneumothorax. RVMI is usually not associated with x-ray changes, while the findings in PE are highly variable - the x-ray may even be normal. Note that if tension pneumothorax had been the probable clinical diagnosis, empirical treatment should have been initiated immediately, as even the small delay associated with obtaining a chest x-ray may prove lethal. The AHA guidelines mention that patients with a STEMI should have a portable chest X-ray, although this should not delay implementation of re-perfusion therapy. He needs immediate resuscitation with IV fluids (and inotropes if necessary). Supplemental oxygen should be commenced, aspirin should be administered and re-perfusion therapy (PCI or Thrombolysis) should be commenced as soon as possible.
Isolated RVMI is a rare event. However, RVMI in the setting of an acute inferior MI is much more common and may be found in 30 to 50% of such patients. RVMI results from acute occlusion of the right coronary artery proximal to the right ventricular branches. Infarction of the right ventricle leads to decreased right ventricular compliance, reduced filling, and diminished right-sided stroke volume with concomitant right ventricular dilation. These hemodynamic changes cause a reduction in left ventricular filling and contractile function, causing a concomitant fall in cardiac output. Thus, the left-sided end diastolic volume is below normal even though the clinical signs are suggestive of increased right sided pressure. The triad of hypotension, elevated JVP and clear lung fields is highly specific for RVMI, but has a sensitivity of less than 25%. Note however that elevated JVP alone is 88% sensitive and 69% specific. Other associated clinical findings include atrioventricular dissociation, tricuspid regurgitation and a right sided gallop rhythm. The presence of ST-segment elevation >1 mm in lead V4R is highly suggestive of RVMI. However, it should be kept in mind that the ST segment elevation may be transient - thus the importance of recording an ECG as soon as possible. Note that lead V4R is equivalent to the V4 chest lead but is instead positioned on the right side of the chest in order to assess the electrocardiographic state of the right ventricle. Echocardiography is also of use in confirming the diagnosis, and may demonstrate abnormal right ventricular free wall motion, right ventricular dilatation, and reversed septal curvature (due to increased right ventricular end-diastolic pressure). Echocardiography may also demonstrate interatrial septal bowing indicating a concomitant right atrial infarction, which is an important prognostic marker predictive of more hypotension and atrioventricular blocks, and higher mortality. The chest x-ray is not particularly helpful in the diagnosis of RVMI, although right ventricular and right atrial dilation may be seen. However, x-rays may be of use in excluding alternative diagnoses. The principles of treatment of RVMI are reversal of the decreased filling, restoration of the right-sided stroke volume and improvement of right ventricular function. Patients with RVMI who have a low cardiac output should be given isotonic saline, which enhances right ventricular filling pressures by raising the central filling pressure. When fluid resuscitation proves insufficient, inotropic support with dobutamine should be started - this will increase forward flow and augment cardiac output. Note also that certain drugs which are frequently used in the setting of a myocardial infarction like nitrates, diuretics and vasodilators cause reduction of right ventricular preload. Given that the right ventricular output is preload dependent, this results in worsening of the haemodynamic status. Thus, these drugs should be avoided in the setting of a RVMI. If severe concomitant left ventricular dysfunction causing pulmonary congestion is present, the right ventricle is further compromised by increased afterload. In such a circumstance, sodium nitroprusside or an intra-aortic counterpulsation device may be used to reduce the afterload. Patients with RVMI are prone to develop bradyarrythmias - especially high degree atrioventricular blocks, which occur in up to 48% of patients. Given that the ischemic right ventricle has a relatively fixed stroke volume and is thus dependent upon heart rate to maintain output, bradyarrythmias can cause severe hemodynamic compromise and should be corrected with either pacing or pharmacological agents like atropine. Early re-perfusion is the definitive treatment and should be attempted with either primary PCI or thrombolysis. Note that GTN should be avoided as it causes vasodilation, which reduces venous return and cardiac preload. Pericardiocentesis is indicated in cardiac tamponade. An intercostal tube would be indicated in tension pneumothorax.