Cardiac tamponade is usually a consequence of increased pericardial pressure with accumulation of pericardial effusion. Pericardial effusion may be caused by acute pericarditis, tumor, uremia, hypothyroidism, trauma, cardiac surgery, or other inflammatory/noninflammatory conditions. In this article we describe four scenarios illustrated by case reports where a small or apparently small pericardial effusion may produce cardiac tamponade. The first scenario illustrates how a small pericardial effusion can cause clinically significant cardiac tamponade when it accumulates rapidly. The second scenario exhibits how an apparently small pericardial effusion on transthoracic echocardiogram (TTE) turned out to be a small amount of unclotted blood and an echogenic hematoma. The third scenario details how an apparently small pericardial effusion on TTE was actually a large loculated effusion in an unusual location seen only by transesophageal echocardiogram (TEE). The fourth scenario demonstrates how the combination of a large pleural effusion and a small pericardial effusion can result in cardiac tamponade. The role of echocardiography in the diagnosis and management of these scenarios is discussed here. Although many clinicians depend on the amount of pericardial effusion to suspect cardiac tamponade, it is important to suspect cardiac tamponade when patients have hemodynamic compromise regardless of the amount of pericardial effusion.
contributed to the smaller difference in peak VO 2 between diabetics and nondiabetics in the Guazzi et al. (5) study. Glycosylated hemoglobin was Ͻ7% in every one of the Guazzi et al. (5) patients, whereas it averaged 7.5% in our patients. Insulin therapy improves peak VO 2 in patients with diabetes and CHF (6,7). Diabetes is associated with cardiac, vascular, metabolic, and skeletal muscle alterations that all tend to reduce peak VO 2 (8). High-energy phosphate metabolism is impaired in skeletal muscles from patients with diabetes in the absence of CAD or LV dysfunction (2). Phosphocreatinine loss, pH decline, and deoxygenation occur sooner in exercising skeletal muscles of diabetics than in controls. Alterations in energy metabolism contribute to reduce peak aerobic capacity in CHF (9,10). The coexistence of diabetes and CHF may further alter skeletal muscle energy metabolism and reduce peak aerobic capacity. A major limitation of our study is the absence of longitudinal data with tighter diabetes control.In summary, diabetes negatively impacts on and is an independent determinant of peak aerobic capacity in patients with CHF. Diabetes needs to be taken into consideration when evaluating functional capacity in patients with CHF.
Amit S. Tibb, MD
A novel ultrasound transducer developed in our laboratory (CONTISON) was used for monitoring catheter balloon commissurotomy (CBC). The transducer was placed at the cardiac apex to obtain an apical four-chamber view and attached to the chest wall using an adhesive ring. During the procedure, the tip of the needle was imaged first in the right atrium and was seen to traverse the interatrial septum and enter the left atrium. Mitral valve gradients were measured before and after CBC.
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