Mean Pulmonary Artery Occlusion Pressure Research Articles

Response to Fluid Boluses in the Fluid and Catheter Treatment Trial

Recent emphasis has been placed on methods to predict fluid responsiveness, but the usefulness of using fluid boluses to increase cardiac index in critically ill patients with ineffective circulation or oliguria remains unclear. This retrospective analysis investigated hemodynamic responses of critically ill patients in the ARDS Network Fluid and Catheter Treatment Trial (FACTT) who were given protocol-based fluid boluses. Fluid responsiveness was defined as ≥ 15% increase in cardiac index after a 15 mL/kg fluid bolus. A convenience sample of 127 critically ill patients enrolled in FACTT was analyzed for physiologic responses to 569 protocolized crystalloid or albumin boluses given for shock, low urine output (UOP), or low pulmonary artery occlusion pressure (PAOP). There were significant increases in mean central venous pressure (9.9 ± 4.5 to 11.1 ± 4.8 mm Hg, P < .0001) and mean PAOP (11.6 ± 3.6 to 13.3 ± 4.3 mm Hg, P < .0001) following fluid boluses. However, there were no significant changes in UOP, and there were clinically small changes in heart rate, mean arterial pressure, and cardiac index. Only 23% of fluid boluses led to a ≥ 15% change in cardiac index. There was no significant difference in the frequency of fluid responsiveness between boluses given for shock or oliguria vs boluses given only for low PAOP (24.0% vs 21.8%, P = .59). There were no significant differences in 90-day survival, need for hemodialysis, or return to unassisted breathing between patients defined as fluid responders and fluid nonresponders. In this cohort of critically ill patients with ARDS who were previously resuscitated, the rate of fluid responsiveness was low, and fluid boluses only led to small hemodynamic changes.

The Role of Transesophageal Echocardiography in Optimizing Resuscitation in Acutely Injured Patients

The goal of resuscitation is to correct the mismatch between oxygen delivery and that of cellular demands. The pulmonary artery catheter (PAC) is frequently used to gauge the adequacy of resuscitation and guide therapy based on ventricular filling pressures. Transesophageal echocardiography (TEE) has emerged as a potential tool in assessing adequacy of acute hemodynamic resuscitation. The purpose of this study was to evaluate the role of TEE in assessing preload during ongoing volume resuscitation in trauma patients. A retrospective review was conducted of acutely injured patients undergoing TEE during resuscitation from hemorrhagic shock from January 2002 to 2004 at a Level I trauma center. The indication for TEE was persistent hemodynamic instability in the absence of ongoing surgical hemorrhage. Variables included hemodynamic and PAC parameters, pre-TEE resuscitation volume, and vasopressor requirements. The impact of TEE findings on therapeutic decisions was evaluated. Twenty-five patients underwent TEE, 18 (72%) had an indwelling PAC with a mean pulmonary artery occlusion pressure of 19.3 mm Hg (range, 12-29 mm Hg) and mean cardiac index of 2.9 L/min/m2 (range, 1.6-4.6 L/min/m2). Twelve patients (48%) were receiving inotropes and/or vasopressors for hypotension at the time of TEE. Resuscitation volume within 6 hours before TEE included a mean of 6.5 L of crystalloid and 12.2 units of blood products (packed red blood cells, fresh frozen plasma, and platelets). TEE revealed left ventricular hypovolemia in 13 patients (52%) and altered therapy in 16 patients (64%), including additional volume (n = 13), addition of an inotrope (n = 4), and addition of a vasodilator (n = 1) in one patient with ventricular overdistention. Comparison of the abnormal and normal TEE groups revealed that only cardiac index was significantly different (2.6 L/min/m2 in the abnormal group vs. 3.9 L/min/m2 in the normal group; p = 0.005). Significant mitral valve regurgitation leading to valve replacement was identified in one patient. No clinically relevant pericardial effusion was identified. TEE altered resuscitation management in almost two thirds of patients. Many patients with "acceptable" pulmonary artery occlusion pressure parameters may in fact have inadequate left ventricular filling. In addition, TEE offers the advantage of direct assessment of cardiac valve competency, myocardial wall contractility, and pericardial fluid.

Septic shock in coccidioidomycosis.

To describe the clinical and laboratory parameters of patients with septic shock following infection with Coccidioides immitis, estimate the incidence of septic shock from coccidioidomycosis, and outline clues that may be helpful in early diagnosis of this syndrome. Retrospective, descriptive case series. A 250-bed general public hospital in Kern County, CA. Eight patients diagnosed with septic shock from infection with C. immitis from September 1991 to December 1993. Five were Hispanic, two were Filipino, and one was African-American. The diagnosis of C. immitis was made by microscopic examination and culture of the organism from sputum or other sites. Septic shock was diagnosed using criteria formulated by the American College of Chest Physicians Consensus Conference/Society of Critical Care Medicine. No patient had traditional immunocompromising conditions. All patients had pulmonary symptoms and were symptomatic for a mean duration of 19.4 +/- 19.8 days before admission. One patient presented with septic shock and the remaining seven developed shock during their hospital course. Serology for coccidioidomycosis was positive in six patients. The mean cardiac index was 5.8 +/- 1.9 (SD) L/min/m2, the mean arterial pressure was 71.0 +/- 16.7 mm Hg, the mean pulmonary artery occlusion pressure was 16.9 +/- 3.5 mm Hg, and the mean systemic volume resistance index was 846.6 +/- 224.1 dyne-sec/cm5xm2. All patients developed acute respiratory distress syndrome. Coccidioidomycosis was recognized or considered in only five of eight patients before they developed septic shock. Despite therapy with amphotericin B, all patients died. One patient died of progressive pulmonary disease, two patients suffered an acute arrest, and five patients developed progressive multiple organ system failure and died with additional organ involvement. Septic shock following infection with C. immitis is an ominous yet underrecognized condition. Hemodynamic parameters and cytokine concentrations were not significantly different from values seen in gram-negative septic shock. Clinical clues to the diagnosis include duration of illness and conspicuous pulmonary involvement. Patient outcome in this series was poor but may improve with increased recognition of septic shock in infections from C. immitis.

Systemic and Pulmonary Haemodynamic Effects of Intravenous Infusion of Non-Ionic Isoosmolar Dimeric Contrast Media

The systemic and pulmonary haemodynamic effects of i.v. infusion (1 ml/s) of high doses (4 ml/kg) of 2 non-ionic, isoosmolar dimeric contrast media (CM) were investigated in 17 female pigs. The 2 CM were iodixanol and iotrolan. Both CM induced a significant increase of the following parameters: mean arterial, mean right atrial, mean pulmonary arterial, mean pulmonary arterial occlusion pressure, cardiac output, stroke volume, and diuresis. The plasma concentration of atrial natriuretic peptide was significantly increased following infusion of the 2 CM. A significant decrease was seen in the systemic and pulmonary vascular resistance.

Systemic and Pulmonary Haemodynamic Effects of Intravenous Infusion of Non-Ionic Isoosmolar Dimeric Contrast Media

The systemic and pulmonary haemodynamic effects of i.v. infusion (1 ml/s) of high doses (4 ml/kg) of 2 non-ionic, isoosmolar dimeric contrast media (CM) were investigated in 17 female pigs. The 2 CM were iodixanol and iotrolan. Both CM induced a significant increase of the following parameters: mean arterial, mean right atrial, mean pulmonary arterial, mean pulmonary arterial occlusion pressure, cardiac output, stroke volume, and diuresis. The plasma concentration of atrial natriuretic peptide was significantly increased following infusion of the 2 CM. A significant decrease was seen in the systemic and pulmonary vascular resistance.

Systemic and Pulmonary Haemodynamic Effects of Intravenous Infusion of Non-Ionic Isoosmolar Dimeric Contrast Media

The systemic and pulmonary haemodynamic effects of i.v. infusion (1 ml/s) of high doses (4 ml/kg) of 2 non-ionic, isoosmolar dimeric contrast media (CM) were investigated in 17 female pigs. The 2 CM were iodixanol and iotrolan. Both CM induced a significant increase of the following parameters: mean arterial, mean right atrial, mean pulmonary arterial, mean pulmonary arterial occlusion pressure, cardiac output, stroke volume, and diuresis. The plasma concentration of atrial natriuretic peptide was significantly increased following infusion of the 2 CM. A significant decrease was seen in the systemic and pulmonary vascular resistance.

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic iso-osmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic iso-osmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Systemic, Pulmonary and Renal Haemodynamic Effects of Intravenously Infused Iopentol

The central, peripheral and renal haemodynamic effects after intravenous infusion (1 ml/s) of high doses (4 mg I/kg) of two low osmolar, chemically and physically similar non-ionic contrast media (iohexol and iopentol) were investigated in 16 pigs. Both contrast media induced a significant increase of mean arterial, mean right atrial, mean pulmonary arterial and mean pulmonary arterial occlusion pressure along with an increase in cardiac output. The systemic vascular and pulmonary vascular resistances were decreased. Renal venous blood flow and renal vascular resistance were not significantly changed after infusion of contrast media. There were no differences in haemodynamic effects between the two media studied.

Systemic, Pulmonary and Renal Haemodynamic and Renal Morphologic Effects of Intravenously Infused Iodixanol

The systemic, pulmonary and renal haemodynamic effects following an intravenous infusion (1 ml/s, 4 ml/kg) of a non-ionic isoosmolar contrast medium (iodixanol) were investigated in 8 pigs. Histopathologic changes occurring after infusion of iodixanol were studied by repeated renal biopsies. Iodixanol caused a significant increase of cardiac output, mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary arterial occlusion pressure and mean arterial pressure. There was a decrease of the systemic and pulmonary vascular resistances. Most renal biopsies showed no pathologic findings after infusion of iodixanol but in 3 specimens proteinaceous content was observed 15 min after infusion.

Systemic, pulmonary and renal haemodynamic effects of intravenously infused iopentol

The central, peripheral and renal haemodynamic effects after intravenous infusion (1 ml/s) of high doses (4 mg I/kg) of two low osmolar, chemically and physically similar non-ionic contrast media (iohexol and iopentol) were investigated in 16 pigs. Both contrast media induced a significant increase of mean arterial, mean right atrial, mean pulmonary arterial and mean pulmonary arterial occlusion pressure along with an increase in cardiac output. The systemic vascular and pulmonary vascular resistances were decreased. Renal venous blood flow and renal vascular resistance were not significantly changed after infusion of contrast media. There were no differences in haemodynamic effects between the two media studied.

Cardiopulmonary effects of oleic acid-induced pulmonary edema and mechanical ventilation: Henning RJ, Heyman V, Alcover I, et al. Anesth Analg 65:925, 1986

Changes in intrathoracic pressure can influence cardiac performance by altering ventricular loading conditions. Since ventricular loading, both from systemic venous return (preload) and from left ventricular wall stress (afterload), varies during the cardiac cycle, we reasoned that appropriately placed, phasic, cardiac cycle-specific (synchronous) increases in intrathoracic pressure might augment ventricular ejection in acute ventricular failure. Recent studies in animals suggest that synchronous increases in intrathoracic pressure during systole increase ejection. We compared the hemodynamic effect of synchronous increases in intrathoracic pressure with similar increases delivered at random in the cardiac cycle in patients with congestive cardiomyopathy (n = 9). Intrathoracic pressure was estimated by measuring esophageal pressure. High-frequency jet ventilation (HFJV) synchronized with the electrocardiogram (synchronous HFJV) was compared with HFJV at a fixed frequency within 15 percent of the heart rate (asynchronous HFJV) and with intermittent positive-pressure breathing (IPPB) (tidal volume = 10 ml/kg; f = 15). All forms of ventilation resulted in the same mean airway pressure and esophageal pressure. Mean pulmonary arterial occlusion pressure and arterial pressure were constant in all conditions. Cardiac output was greater with synchronous HFJV than with either IPPB or asynchronous HFJV (4.5±0.7 L/min compared with 3.5±0.7 and 3.4±0.6 L/min [mean±SE], respectively; p<0.05). Mixed venous oxygen saturation covaried with cardiac output (p<0.05), such that calculated oxygen consumption remained constant for all conditions. We conclude that synchronous HFJV augments cardiac output more efficiently than do similar increases in intrathoracic pressure delivered randomly in the cardiac cycle.

Ventricular Assist by Cardiac Cycle-Specific Increases in Intrathoracic Pressure

Changes in intrathoracic pressure can influence cardiac performance by altering ventricular loading conditions. Since ventricular loading, both from systemic venous return (preload) and from left ventricular wall stress (afterload), varies during the cardiac cycle, we reasoned that appropriately placed, phasic, cardiac cycle-specific (synchronous) increases in intrathoracic pressure might augment ventricular ejection in acute ventricular failure. Recent studies in animals suggest that synchronous increases in intrathoracic pressure during systole increase ejection. We compared the hemodynamic effect of synchronous increases in intrathoracic pressure with similar increases delivered at random in the cardiac cycle in patients with congestive cardiomyopathy (n = 9). Intrathoracic pressure was estimated by measuring esophageal pressure. High-frequency jet ventilation (HFJV) synchronized with the electrocardiogram (synchronous HFJV) was compared with HFJV at a fixed frequency within 15 percent of the heart rate (asynchronous HFJV) and with intermittent positive-pressure breathing (IPPB) (tidal volume = 10 ml/kg; f = 15). All forms of ventilation resulted in the same mean airway pressure and esophageal pressure. Mean pulmonary arterial occlusion pressure and arterial pressure were constant in all conditions. Cardiac output was greater with synchronous HFJV than with either IPPB or asynchronous HFJV (4.5 +/- 0.7 L/min compared with 3.5 +/- 0.7 and 3.4 +/- 0.6 L/min [mean +/- SE], respectively; p less than 0.05). Mixed venous oxygen saturation covaried with cardiac output (p less than 0.05), such that calculated oxygen consumption remained constant for all conditions. We conclude that synchronous HFJV augments cardiac output more efficiently than do similar increases in intrathoracic pressure delivered randomly in the cardiac cycle.

Plasma Colloid Oncotic Pressure—Pulmonary Artery Occlusion Pressure Gradient

Because Starling's equation contains four factors that theoretically influence fluid movement across the pulmonary capillary bed, we prospectively examined the relationship between the plasma colloid oncotic pressure (PCOP) minus the mean pulmonary artery occlusion pressure (PAOP) (the only two presently available clinically for measurement) and pulmonary edema determined in terms of percent venous admixture (Qs/Qt) and roentgenographically in 17 consecutive patients in a surgical intensive care unit to determine whether this PCOP-PAOP gradient could accurately predict the presence of pulmonary edema. The PCOP-PAOP gradient proved to be a poor predictor of pulmonary edema determined by these means. We believe this resulted from the inherent insensitivity of the PCOP-PAOP gradient as an estimate of the net intravascular filtration pressure, and Qs/Qt and roentgenograms as measurements of lung edema, as well as the multiplicity of variables involved in the genesis of pulmonary edema in the clinical situation.

Albumin Treatment Following Major Surgery

The effects of i.v. infusion of 5% albumin and balanced salt solutions were investigated in a prospective study on 18 patients subjected to reconstruction of the abdominal aorta. The same schedules for blood replacement and intraoperative fluid therapy were followed for all patients. Postoperatively, the amounts of fluid administered were adjusted with the aim of keeping the mean pulmonary arterial occlusion pressure (MPAOP) close to the preoperative level. Immediately after operation, there was a decrease in cardiac filling pressures, indicating a blood volume deficit, in both groups. Less fluid was needed for adequate haemodynamic restitution in the albumin group. Postoperatively, the mean plasma oncotic pressure (POP) in the albumin-treated patients remained steady at 2.4-2.5 kPa (86-88% of preoperative value). In the control group, POP fell to a mean minimum of 1.8 kPa (64% of preoperative value) 8 h after operation. The difference between POP and MPAOP decreased significantly in both groups, but the difference between the groups was not significant at any time. There was no significant correlation between venous admixture, on the one hand, and POP, MPAOP, POP-MPAOP difference, total sodium intake or net supply of non-colloid fluids, on the other. No clinically important differences in haemodynamic or lung function variables were found between the groups.