No abstract

Two types of pulmonary edema occur in clinical medicine: cardiogenic pulmonary edema (or hydrostatic pulmonary edema) and noncardiogenic pulmonary edema, better known as acute lung injury or acute respiratory distress syndrome (ARDS). Their clinical manifestations are very similar, so the differentiation between them, based only on clinical grounds, may be very difficult, and knowing the precise etiology of the episode of acute pulmonary edema has major implications in the treatment plan. Cardiogenic pulmonary edema is usually due to systolic and/or diastolic left ventricular dysfunction and is typically treated with diuretics, nitrates, and afterload reduction medications such as angiotensin converting enzyme inhibitors, although some cases also require coronary revascularization. Noncardiogenic pulmonary edema is usually secondary to a more systemic severe medical or surgical pathology that triggers the event, and the treatment should be directed to treat that pathology. Oxygen supplementation in the form of mechanical ventilation (invasive or non-invasive) is always required. A rapid diagnosis of the cause of the episode of acute pulmonary edema facilitates a timely and appropriate therapeutic intervention.Electroconvulsive therapy (ECT) is recognized as a well-established, highlyeffective, safe psychiatric treatment. It is estimated that 100,000 patients per year receive a course of ECT across the United States, with an average of 8 to 10 treatments per course of therapy. Severe complications are very infrequent and generally reported as transitory cardiac arrhythmias and severe transitory Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.

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We present a case of atrial repolarization waves from an ectopic atrial rhythm mimicking inferior ST segment elevation myocardial infarction in a 78-year-old male patient who presented with left sided chest wall and shoulder pain. His ischemic workup was negative, and the ST elevations completely resolved upon the resumption of sinus rhythm before discharge.

Atrioventricular block; Parodoxical; Ventriculophasic arrhythmiaVentriculophasic arrhythmia is a phenomenon commonly seen in patients with complete atrioventricular (AV) block. The usual observation is that the PP intervals containing the QRS complex are shorter in duration than the PP intervals without an intervening QRS complex. And also an inverse relation is seen between the QP interval and the subsequent PP interval without a QRS complex. We report a case of paradoxical ventriculophasic arrhythmia in an 85-year-old patient presenting with 2:1 AV block, wherein the PP intervals containing the QRS complex are longer than the PP intervals without a QRS complex. CASE REPORTAn 85-year-old woman was admitted to our facility with a 4-day duration of fatigue and progressive worsening of shortness of breath on exertion. She denied any chest pain, palpitations, and syncope. She was not on any medications. On admission, she was registering a blood pressure of 160/68 mmHg, heart rate of 40 beats per minute, and oxygen saturation of 95% on 2 liters of oxygen. The 12-lead electrocardiogram ( Fig. 1) showed sinus rhythm, left bundle branch block, and second-degree AV block with 2:1 AV conduction. The PP intervals containing the QRS complex are longer (800 milliseconds) than the PP intervals without a QRS complex (720 milliseconds) which is the paradox of ventriculophasic arrhythmia. Also to be noted that the QP interval is also quite prolonged at 620 milliseconds. She received a dual-chamber pacemaker for symptomatic high-grade AV block. DISCUSSIONVentriculophasic arrhythmia is most commonly observed in patients with complete heart block. It has been also reported in patients with seconddegree heart block, paroxysmal atrial tachycardia with block and ventricular paced rhythms. The usual observation is that the PP intervals containing the QRS complex are shorter in duration than the PP intervals without an intervening QRS complex. This phenomenon was first observed and described by Erlanger and Blackman in an animal study on chronic AV block. 1 Further studies reported 40-50% incidence of this phenomenon in patients with complete heart block and paced rhythms. 2-4 A paradoxical effect in which PP intervals containing the QRS complex are longer than the PP intervals without a QRS complex has been seen in 3.5% of cases with complete heart block.Dadu and McPherson proposed a quantitative definition of ventriculophasic phenomenon based on a study on ventriculophasic response and its clinical correlations in complete heart block patients with pacemaker. 4 They observed that the shortening of PP interval mainly occurred when the interposed QRS occurs in the first 60% of the anticipated PP interval. They defined ventriculophasic response as being present during heart block when an interposed QRS occurring in the first 60% of the anticipated PP interval results in a greater than 3% shortening of % PP interval surrounding the QRS compared to the preceding PP interval. The exact mechanism of this phenomenon is still unclear. The prop...