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Exertional heat stroke is a medical emergency that uncommonly results in severe cardiac dysfunction. The military physician diagnosed a 19-year-old military recruit from an elite unit to have exertional heat stroke. Immediate treatment in the field with rapid ice water cooling and vigorous fluid administration resulted in pulmonary edema. Transthoracic echocardiography on admission to the emergency department revealed moderate reduction in left and right ventricular function. After treatment, within a few days, rapid myocardial recovery was noted and persisted after 6 months of follow-up. Possible mechanisms of cardiac dysfunction in exertional heat stroke and treatment strategies are discussed. It is suggested that intravenous fluid administration to patients with suspected exertional heat stroke should preferably be done with appropriate hemodynamic monitoring and after cardiac dysfunction has been ruled out.

Background and Aims: Nitrate therapy improves hemodynamics in patients with heart failure, but the chronic effects of oral nitrates on exercise performance and clinical status have not been well studied., Methods: Oral isosorbide-5-mononitrate (ISMN) (50 mg once daily) or placebo was administered to 136 patients (NYHA Class 2-3) treated for heart failure, all receiving captopril and most also furosemide. Endpoints were treadmill exercise time at 12 weeks by modified Naughton protocol (primary), with an additional 12-week follow-up period. Secondary endpoints included left ventricular dimensions, ejection fraction, cardiothoracic ratio, functional class, quality of life, hospitalizations and plasma norepinephrine and atrial natriuretic peptide in a four-center substudy., Results: Intention-to-treat analysis showed that mean change in treadmill exercise duration tended to be greater in patients receiving ISMN than placebo (treatment difference +42 s, 95% CI -5, +90 s at 12 weeks and +21 s, 95% CI -25, +74 s after 24 weeks) (NS). Treatment difference was greater in the prespecified subgroup with ejection fraction 31-40% (+55 s, 95% CI -11, +136 s at 12 weeks and +65 s, 95% CI +3, +147 s) (p = 0.035) at 24 weeks. No deleterious effects (i.e. hypotension) were observed with ISMN, although headache was reported in 19% of the active treatment group (p = 0.0001)., Conclusions: ISMN added to captopril increased treadmill exercise time in patients with heart failure and a lesser reduction in baseline ejection fraction, although for the group as a whole, the increase in treadmill time was not significant.

We compared the acute hemodynamic effects of captopril and nitrates in 11 patients with severe congestive heart failure and grade IV cardiac disability. Pressures were measured using a Swan-Ganz catheter system; cardiac output and stroke index were measured by thermodilution, and left-ventricular (LV) volumes and ejection fraction were calculated simultaneously with the hemodynamic measurements from radionuclide ventriculography. Measurements were made in each of 4 treatment states: control, sublingual isosorbide dinitrate (ISDN; 5 and 15 mg), oral captopril (50-200 mg daily) and during combined therapy with captopril and ISDN. Captopril produced a fall in mean arterial pressure (p < 0.01) from 81 +/- 14 to 72 +/- 13 mm Hg and a rise in stroke index from 30 +/- 5 to 35 +/- 91/min/m2 (p < 0.05), while LV ejection fraction increased from 18 +/- 5 to 21 +/- 7% (p < 0.05). ISDN reduced mean arterial, pulmonary arterial, right-atrial and wedge pressure. The combination of captopril and ISDN produced a greater fall in mean arterial pressure, a further rise in ejection fraction to 22 +/- 8% (p < 0.05), a fall in systemic (p < 0.05) and pulmonary vascular resistance (p < 0.01) and a rise in cardiac (p < 0.01) and stroke work index (p < 0.01), while the beneficial effects of ISDN on right-atrial, pulmonary arterial and wedge pressure were again achieved. LV contractility, assessed from end-systolic stress-shortening relations, was essentially unaltered or decreased very slightly. The study showed that combined therapy with captopril and nitrates produced acute hemodynamic benefits superior to those achieved by treatment with captopril or nitrates alone.

The effects of captopril on cardiovascular dynamics and left ventricular (LV) contractility were studied in 11 patients with severe congestive heart failure and very poor global LV function. Pressures were measured using a flow-guided catheter, cardiac output by thermodilution, and LV contraction and ejection fraction by simultaneous radionuclide angiography. Ventricular loading conditions were altered by sublingual isosorbide dinitrate to facilitate construction of LV pressure-volume and stress-shortening curves. Captopril decreased mean arterial pressure (p less than 0.02) and systemic vascular resistance, while stroke and cardiac index increased in most patients. Left ventricular ejection fraction increased from 18 +/- 5 to 22 +/- 7% (p less than 0.05), but contractility, assessed from end-systolic pressure-volume and end-systolic pressure-shortening relations, was unchanged or decreased slightly. Heart rate and double product also tended to decrease. In contrast, arteriovenous oxygen difference widened and calculated total oxygen consumption increased during captopril therapy (p less than 0.05). The study showed that captopril improved forward blood flow, total oxygen extraction, and LV ejection fraction following the decrease impedance to LV emptying but not at the expense of an increase in ventricular contractility. This makes captopril an attractive drug for patients with end-stage cardiac failure and a severely damaged myocardium.

We compared the acute hemodynamic effects of captopril and nitrates in 11 patients with severe congestive heart failure and Grade IV cardiac disability. Pressures were measured using a Swan-Ganz catheter system; cardiac output and stroke index were measured by thermodilution, and left-ventricular (LV) volumes and ejection fraction were calculated simultaneously with the hemodynamic measurements from radionuclide ventriculography. Measurements were made in each of four treatment states: control, sublingual isosorbide dinitrate (ISDN) (5 and 15 mg), oral captopril (50 to 200 mg daily) and during combined therapy with captopril and ISDN. Captopril produced a fall in mean arterial pressure (P less than 0.01) from 81 +/- 14 to 72 +/- 13 mm Hg, and a rise in stroke index from 30 +/- 5 to 35 +/- 91/min per m2 (P less than 0.05), while LV ejection fraction increased from 18 +/- 5 to 21 +/- 7% (P less than 0.05). ISDN reduced mean arterial, pulmonary arterial, right-atrial and wedge pressure. The combination of captopril and ISDN produced a greater fall in mean arterial pressure, a further rise in ejection fraction to 22 +/- 8% (P less than 0.05), a fall in systemic (P less than 0.05) and pulmonary vascular resistance (P less than 0.01) and a rise in cardiac (P less than 0.01) and stroke work index (P less than 0.01), while the beneficial effects of ISDN on right-atrial, pulmonary arterial and wedge pressure were again achieved. LV contractility, assessed from end-systolic stress-shortening relations, was essentially unaltered or decreased very slightly. The study showed that combined therapy with captopril and nitrates produced acute hemodynamic benefits superior to those achieved by treatment with captopril or nitrates alone.

10 patients suffering from refractory heart failure were treated with an oral angiotensin converting enzyme inhibitor captopril. The etiology of heart failure in 9 patients was related to ischemic heart disease, and to valvular heart disease in 1 patient. All patients experienced subjective improvement and feeling of well-being. The functional capacity improved to class II-IIB. Serial chest X-ray films showed improvement in pulmonary congestion. The time course of the hemodynamic effect appeared to 0.5-1.5 h after intake, and tended to disappear about 6 h later. The optimal dose of the drug achieving maximal hemodynamic benefit without excessive hypotension was 50 mg. Some of the patients exhibited a triphasic response. The cardiac index increased from 1.99 +/- 0.1 to 2.69 +/- 0.151/min/m (p less than 0.001), while pulmonary capillary wedge pressure decreased from 25.3 +/- 5.86 to 13.67 +/- 4.14 mm Hg (p less than 0.001). Mean peripheral arterial blood pressure decreased from 90.06 +/- 3.7 to 71.4 +/- 2.7 mm Hg. The total peripheral resistance decreased from 1,942 +/- 169 to 1,170 +/- 109 dyn X s X cm-5. The total pulmonary resistance decreased from 272.6 +/- 42.9 to 142.34 +/- 13.76 dyn X s X cm-5. Heart rate decreased from 83.4 +/- 10.9 to 70.8 +/- 10.14 bpm (p less than 0.01). During a 6-month follow-up period the beneficial clinical effects of captopril were sustained, without late vasodilator tolerance. 1 death, unrelated to captopril, occurred. 2 patients developed transient rash, and 1 experienced transient dysgeusia.

Gunshot wounds and traumatic injuries are the main causes of acquired arteriovenous fistulas. The high cardiac output associated with such fistulas depends mainly on the size of the pathological communication and the degree of reduction in the systemic vascular resistance that results. Since the findings on cardiac examination in these patients may mimic those of valvular heart disease or dilated cardiomyopathy, careful attention should be paid to noncardiac physical findings, such as thrill and/or continuous murmur over the traumatic or surgical scar. We describe a 64-year-old man who developed severe left heart failure 39 years after a gunshot injury in the left lower quadrant of the abdomen. This had led to an acquired arteriovenous fistula between the left internal iliac artery and the left common iliac vein.