Ronald L. Holliday

The Trendelenburg position: hemodynamic effects in hypotensive and normotensive patients.

The effect of the Trendelenburg position on systemic and pulmonary hemodynamics in critically ill patients is not generally appreciated. This study examined the hemodynamoc effect of 15-20 degrees head-down tilt in 61 normotensive and 15 hypotensive patients with acute cardiac illness or sepsis. In normotensive patients, the head-down tilt increased the preload of both right and left ventricles, increased cardiac output slightly, decreased systemic vascular resistance, and did not change the mean arterial pressure. This effect was probably mediated by baroreceptor stimulation. In hypotensive patients, the Trendelenburg position did not increase preload, slightly increased afterload, and decreased cardiac output. This study failed to document any beneficial hemodynamic effect of the Trendelenburg position in critically ill normo- or hypotensive patients.

Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury.

Myocardial dysfunction may result from severe trauma. Therefore, left (LV) and right ventricular (RV) function were prospectively assessed by ECG-gated blood pool radionuclide (RN) angiography in 25 consecutive patients who had sustained severe trauma including blunt chest injuries. Focal abnormalities of RV and LV wall motion were defined in 17 patients; 12, RV; two, LV; and three, biventricular. In two patients traumatic tricuspid insufficiency was also demonstrated, and subsequently verified by contrast angiography. Other means to detect myocardial contusion (enzymatic, electrocardiographic, and Tc-99m pyrophosphate scintigraphy) proved to be insensitive when compared to RN angiography. Two of the five deaths in the group were attributed to refractory arrhythmias. Surgical or post-mortem evidence of traumatic myocardial injury was obtained in five instances when RN angiography indicated contusion. Of the 13 patients available for followup examinations, 11 showed complete or partial resolution of the abnormality and two were unchanged. Comprehensive cardiopulmonary monitoring revealed an inverse relationship between right ventricular ejection fraction (RVEF) and pulmonary vascular resistance (PVR) (R2 = 0.42; p < 0.01) and between the PVR and left ventricular ejection fraction (LVEF) (R2 = 0.48; p < 0.01) and left ventricular end-diastolic volume (LVEDV) (R2 = 0.69; p < 0.01). Further, as right ventricular end-diastolic volume (RVEDV) was increased in trauma, left ventricular function and compliance were reduced. In blunt chest trauma RV contusion occurs more frequently than previously recognized and positive RN angiography constitutes prima facie evidence of direct myocardial injury. Further, LV function remains preload dependent, but may be depressed by elevated PVR impeding the blood flow from RV to LV and/or decreases in LV compliance.

Frequency of myocardial injury after blunt chest trauma as evaluated by radionuclide angiography

Seventy-seven patients who had sustained multisystem trauma, including severe blunt chest injury, were prospectively evaluated to assess the frequency of associated traumatic myocardial injury. Traumatic injury to either the right or left ventricle was defined by the presence of discrete abnormalities of wall motion on electrocardiographically gated cardiac scintigraphy in patients without a clinical history of heart disease. Forty-two patients (55%) (Group 1) had focal abnormalities of wall motion; 27 involved the right ventricle, 7 the left ventricle, 7 were biventricular, and 1 involved only the septum. Both the right and left ventricular ejection fractions were significantly (p less than 0.01) lower (31 +/- 11% and 47 +/- 14%, respectively) than those in the 35 traumatized patients without wall motion abnormalities on scintigraphy (Group 2) (49 +/- 8% and 58 +/- 11%, respectively). Repeat scintigraphic examination in 32 Group 1 patients at a time remote from initial injury showed improvement or resolution of previously defined focal wall motion abnormalities in 27 of 32 patients (84%). The electrocardiogram and serum enzyme tests were insensitive indexes of traumatic myocardial injury when defined by the scintigraphic abnormalities. Thus, severe blunt chest trauma results in a higher frequency of traumatic myocardial injury than heretofore recognized, and frequently involves the anteriorly situated right ventricle.

Accuracy of technetium‐99m SPECT‐CT hybrid images in predicting the precise intraoperative anatomical location of parathyroid adenomas

This study evaluated the accuracy of single photon emission computed tomography (SPECT)‐CT imaging for the preoperative localization of parathyroid adenomas.

Concepts in the Pharmacologic and Nonpharmacologic Support of Cardiovascular Function in Critically Ill Surgical Patients

The critically ill surgical patient requires close clinical, biochemical, and hemodynamic monitoring to define the right timing as well as the proper type of therapeutic intervention. Although many factors are available for monitoring, O2 delivery and extraction are two of the most important, since the enhanced metabolic demands of the stressed patient dictate a need to maintain greater than normal values to ensure survival. In other situations, primary therapy of the blood pressure, the PCWP, or other indices may take temporary precedence in the choice of therapeutic agents. Regardless of the means used to optimize O2 delivery, scrutiny of the consequences of therapy is equally important. Above all, any therapeutic intervention does not negate the need to treat the primary underlying process expeditiously.

Liver cell membrane alterations during hemorrhagic shock in the rat

Previous studies using the Ling-Gerard microelectrode to measure membrane potential and a muscle biopsy technique to determine water and electrolyte content have established a skeletal muscle cell membrane defect in hemorrhagic shock. The present study was undertaken to compare and contrast changes occurring on a cellular level in the liver and skeletal muscle of the rat during sustained hemorrhagic shock. The liver has been suggested as a possible primary site of organ failure during prolonged shock with a loss of normal liver processes and important hepatic metabolic functions. Thirty-four experiments were performed in rats with 11 experiments in the control group. Skeletal muscle membrane potential as well as liver cell membrane potential was measured after opening the abdomen through a midline incision. The ventral lobe of the liver was exposed and placed on a suspension apparatus to decrease respiratory interference and the liver was impaled with a Ling-Gerard microelectrode. Muscle cell resting membrane potentials were measured in exposed skeletal muscle in the leg of the animals. Biopsy samples were obtained at intervals in both the liver and skeletal muscle. Twenty-three experiments were conducted by producing hemorrhage with the withdrawal of blood over a 5- to 15-min period of time and maintaining a systolic blood pressure of 60 mm Hg for 115 ± 40 min. The distribution of water and electrolytes in intra- and extracellular space in the muscle biopsies as well as in the liver on the basis of chloride distribution was considered to be a passive phenomenon related to the resting cell membrane potential as predicted by the Nernst equation. Correction of the measured water and electrolyte content of the biopsies for residual blood was carried out with the use of chromium-51-tagged red blood cells. The control group of rats did not demonstrate any significant change in membrane potential of either muscle or liver cells during the experiment. The membrane potentials were maintained at normal levels in the muscle −91.4 ± 2.2 mV; and in the liver at a mean of −40.3 ± 3.3 mV. The hemorrhagic shock group of animals demonstrated significant changes. Muscle membrane potential decreased to −80.99 ± 6.3 mV (P < 0.01) while at the same time period the liver membrane potential decreased to −24.1 ± 4.6 mV (P < 0.001). The results of these experiments give further evidence of a cellular membrane defect in hemorrhagic shock. The liver cell membrane potential changes and accompanying water and electrolyte shifts occurred before any significant changes in the muscle tissue. The data indicate the existence of a major alteration in rat liver cell membrane function early in the shock state.

Hemodynamic adaptation to acute myocardial contusion complicating blunt chest injury

Abstract The immediate hemodynamic sequelae of blunt chest injury complicated by acute myocardial contusion were examined in multiply traumatized patients. Focal defects of ventricular wall motion defined by gated cardiac scintigraphy identified acute myocardial contusion In 28 of 43 patients, involving the right ventricle alone in 18 (group 1A), the left ventricle In 4 (group 1B) and both ventricles in 6 (group IC). Qualitatively normal ventricular wall motion was found in the 15 patients (group 2). Although there was no difference between groups 1A and 2 in mean systemic oxygen transport (620 ± 189 vs 627 ± 105 ml/min/m2), left ventricular ejection fraction (52 ± 14% vs 60 ± 9%) or calculated left ventricular end-diastolic and end-systolic volumes, mean right ventricular (RV) ejection fraction was significantly lower in group 1A (29 ± 9%) than In group 2 (47 ± 7%, p 2 ) but not in group 2 (RV end-systolic volume, 50 ± 21 ml/m 2 , p 2 ) than in group 2 (RV end-diastolic volume 93 ± 26 ml/m 2 , p

Wedged balloon catheter angiography in the critical care unit.

In order to visualize pulmonary vascular drainage and to assess its influence on measurements obtained by Swan-Ganz catheters in the wedge position, 75 patients were examined with a portable chest x-ray after injection of water soluble contrast medium into a Swan-Ganz catheter in the wedge position. In normal patients and patients with left-sided cardiac failure, the pulmonary vein draining the wedged segment was easily visualized. However, in many patients with sepsis and ARDS, the pulmonary vein was poorly visualized or not visualized. In some of these patients, there was a high pulmonary wedge pressure. It is hypothesized that in some of these patients, the competitive flow system between the pulmonary and bronchial circulation is upset due to a decrease in flow through pulmonary vessels and either relative or absolute increase in bronchial flow in the segment distal to the balloon. This increase in the ratio of bronchial to pulmonary blood flow results in dilution of the contrast medium by the nonopacified bronchial blood. The decreased pulmonary blood flow may be due to a vasospastic factor in either the small pulmonary arterioles or venules as, in two cases, the pulmonary vein was visualized after injection of vasodilators. In order to eliminate these misleading false high wedge pressures (WP) in these types of patients, the authors recommend that wedged Swan-Ganz catheter angiograms be performed in selective cases. If the pulmonary vein is not visualized and there is elevation of the pulmonary WP, this must not be taken as a sign of elevated left-sided cardiac pressure. If the pulmonary vein is visualized, the WP measured can be considered to reflect the left-sided cardiac pressure.