Introduction: Aluminum phosphide (ALP) is a pesticide that is highly toxic. It is a mitochondrial toxin that causes death by cardiac and metabolic toxicity. The most ominous effect is cardiac toxicity, which may range from minor electrocardiographic abnormalities to severe depression of cardiac contractility secondary to toxic myocarditis. There is no documented report of the use of Intra-aortic Balloon Pump (IABP) for toxic myocarditis from ALP poisoning, although it has been used effectively for toxic myocarditis due to other toxins.Case Report: We are reporting a young female who presented with ALP poisoning, in cardiogenic shock due to myocarditis. We used an IABP for cardio-circulatory support until the effects of ALP resolved. She is the only reported survivor of ALP poisoning, presenting with cardiogenic shock.Discussion: Several reports describe the use of IABP for cardiogenic shock due to toxic myocarditis. There is no report in the medical literature using IABP for cardiogenic shock caused by ALP toxin-induced myocarditis. Our patient presented with cardiocirculatory shock, necessitating the use of inotropes and mechanical ventilation. As she did not improve despite ventilation and maximal doses of inotropes, IABP was used for cardio-circulatory support until the effects of ALP resolved.

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The studies of pulmonary venous flow-pattern in mitral stenosis (MS) have given conflicting data about the type of abnormality. This study was undertaken to assess the pulmonary venous flow-pattern in severe MS and to study the changes occurring after balloon mitral valvuloplasty (BMV). There were 51 patients of MS with sinus rhythm with the mean age of 32.5+/-9.35 years, 18 males and 33 females. Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were performed before and after BMV. Pulmonary venous flow was recorded by TEE from left upper pulmonary vein (PV). Peak velocities (V) and velocity time integrals (VTI) of systolic wave (S), diastolic wave (D), and atrial reversal wave (A) were measured. The S(v)/D(v) and S(VTI)/D(VTI) were calculated. Mitral valve area (MVA) increased from 0.81+/-0.18 cm(2) to 2.02+/-0.46 cm(2), left atrium (LA) mean decreased from 28.55+/-6.68 mmHg to 13.88+/-4.89 mmHg, and cardiac output increased from 3.1+/-0.86 L/min to 3.7+/-1.02 L/min. The S, D, and A velocities increased from 33.84+/-13.55 cm/s, 37.24+/-11.55 cm/s, and 20.53+/-6.7 cm/s to 59.86+/-18.25 cm/s, 48.43+/- 12.55 cm/s, and 24. 94+/-9.14 cm/s, respectively. The VTIs of S, D, and A waves increased from 4.88+/-2.24 cm, 6+/-2.45 cm, and 2+/-0.88 cm to 10.46+/-4.23 cm, 8.82+/-3.61 cm, and 2.34+/-1.29 cm, respectively. MS leads to reduction in pulmonary flow velocities during all the phases. Successful BMV resulted in improvement of all these velocities, with improvement in systolic fraction being the maximum. These improved flows after BMV appear to be secondary to reduction in LA pressure and improved cardiac output.

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