To assess the effects of crystalloid and colloid resuscitation on hemodynamic response and on lung water following thermal injury, 79 patients were assigned randomly to receive lactated Ringer's solution or 2.5% albumin-lactated Ringer's solution. Crystalloid-treated patients required more fluid for successful resuscitation than did those receiving colloid solutions (3.81 vs. 2.98 ml/kg body weight/% body surface burn, p less than 0.01). In study phase 1 (29 patients), cardiac index and myocardial contractility (ejection fraction and mean rate of internal fiber shortening, Vcf) were determined by echocardiography during the first 48 hours postburn. Cardiac index was lower in the 12- to 24-hour postburn interval in the crystalloid group, but this difference between treatment groups had disappeared by 48 hours postburn. Ejection fractions were normal throughout the entire study, while Vcf was supranormal (p less than 0.01 vs. normals) and equal in the two resuscitation groups. In study phase 2 (50 patients), extravascular lung water and cardiac index were measured by a standard rebreathing technique at least daily for the first postburn week. Lung water remained unchanged in the crystalloid-treated patients (p greater than 0.10), but progressively increased in the colloid-treated patients over the seven day study (p less than 0.0001). The measured lung water in each treatment group was significantly different from one another (p less than 0.001). Cardiac index increased progressively and identically in both treatment groups over the study period (p less than 0.01). These data refute the existence of myocardial depression during postburn resuscitation and document hypercontractile left ventricular performance. The addition of colloid to crystalloid resuscitation fluids produces no long lasting benefit on total body blood flow, and promotes accumulation of lung water when edema fluid is being reabsorbed from the burn wound.

A B S T R A C T The purpose of this study was to examine the dynamics of left ventricular ejection in patients with obstructive and nonobstructive hypertrophic cardiomyopathy (HCM). 30 patients with HCM and 29 patients with no evidence of cardiovascular disease were studied during cardiac catheterization. Using a single multisensor catheter, electromagnetically derived ascending aortic flow velocity and high fidelity left ventricular and aortic pressures were recorded during rest (tl = 47) and provocative maneuvers (it = 23). Dynamic ventricular emptying during rest was also analyzed with frame-by-frame angiography (n = 46). Left ventricular outflow was independently derived from both flow velocity and angiographic techniques. The HCM patients were subdivided into three groups: (I) intraventricular gradients at rest (n = 9), (II) intraventricular gradients only with provocation (n = 12), and (III) no intraventricular gradients despite provocation (n = 9). During rest, the percentage of the total systolic ejection period during which forward aortic flow existed was as follows (mean+ 1 SD): group I, 69+17% (flowv), 64±6% (angio); group II, 63 +14% (flow), 65±+6% (angio); group III, 61+16% (flow), 62±+4% (angio); control group, 90±o5% (flow), 86±+9% (angio). No significant difference was observed between any of the HCM subgroups, but compared with the control group, ejection was completed much earlier in systole independent of the

The generation of abnormal gradients between the apical cavity and the subaortic valvular region of the left ventricle in patients with hypertrophic cardiomyopathy (HCM) has traditionally been equated to a dynamic obstruction to left ventricular outflow. To examine this concept in more detail, left ventricular ejection dynamics were studied during cardiac catheterization in 30 patients with HCM and 29 patients with no evidence of cardiovascular disease. Using multisensor catheterization techniques, ascending aortic flow velocity and micromanometer left ventricular and aortic pressures were simultaneously recorded during rest (n = 47). Dynamic left ventricular emptying was also analyzed with frame-by-frame angiography (n = 46). The temporal distribution of left ventricular outflow was independently derived from both flow velocity and angiographic techniques. The HCM patients were subdivided into three groups: I, intraventricular gradients at rest (n = 9); II, intraventricular gradients only with provocation (n = 12); III, no intraventricular gradients despite provocation (n = 9). Expressed as a precentage of the available systolic ejection period (%SEP), the time required for ejection of the total stroke volume was (mean +/- 1 S.D.): Group I, 69 +/- 17% (flow), 64 +/- 6% (angio); Group II, 63 +/- 14% (flow), 65 +/- 6% (angio); Group III, 61 +/- 16% (flow), 62 +/- 4% (angio); control group, 90 +/- 5% (flow) 86 +/- 10% (angio). No significant difference was observed between any of the three HCM subgroups, but, compared with the control group, ejection was completed much earlier in systole independent of the presence or absence of intraventricular gradients. The presence of coexisting mitral regurgitation in 12 of the HCM patients did not alter these results. This study demonstrates that 'outflow obstruction', as traditionally defined by the presence of an abnormal intraventricular pressure gradient and systolic anterior motion of the mitral valve, does not impede left ventricular outflow in HCM. In a pure fluid dynamic sense, we believe that outflow obstruction does not exist in this disease entity.