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Biomedical subjects

W J Sibbald

Publications and source records attributed to W J Sibbald.

At least 163 records · Page 9Linked to original sources
PubMed1983

Clinical correlates of the spectrum of lung microvascular injury in human noncardiac edema.

We measured the clearance from blood to pulmonary edema fluid of a small molecular weight hydrophilic radiotracer, Indium-111-DTPA (In-DTPA) and a larger molecular weight radiotracer, Iodine-125-HSA (I-HSA), in patients with pulmonary edema on either a cardiac or noncardiac (permeability) basis. In previous investigations, we had noted an apparent relationship between the magnitude of clearance of I-HSA across the alveolocapillary membrane and the severity of noncardiac pulmonary edema. In this study, we were able to distinguish at least 2 distinct groups of patients with noncardiac pulmonary edema. Patients with the greatest damage to the alveolo-capillary exchanging membrane, defined by the flux of I-HSA from blood to edema fluid, were significantly differentiated from those with a lesser microvascular injury on the basis of higher mean heart rate (HR), temperature, cardiac index (CI), pulmonary artery pressures, right ventricular stroke work index (RVSWI), and a lower mean total white blood cell count (WBC), among others. Therefore, noncardiac pulmonary edema is characterized by a spectrum of permeability injury to the pulmonary microvasculature which seems to parallel other measurable indices of the severity of the systemic response to the illness.

Cell Membrane Permeability↗
PubMed1983

Right ventricular function in acute disease states: pathophysiologic considerations.

In critically ill patients, alterations in pulmonary vasomotor tone profoundly influence right ventricular (RV) function. An increase in end-diastolic volume (EDV) follows elevations in the RV afterload, this increase in preload probably subserving the increased RV stroke work (SW) required to ensure unchanged RV pump function. The maintenance of a normal left ventricular (LV) preload is essential in the cardiovascular adaptation to an acute illness. With volume overload of the RV consequent upon pulmonary artery hypertension (PAH), leftward septal shift occurs and reduces LV diastolic compliance. With extremely high levels of RV loading conditions, a depression in RV contractility and reduced RV pump function are eventually seen, both of which then become partially responsible for LV pump failure. Hence, abnormalities in RV function will have a marked clinical influence on the circulatory response seen in critically ill patients. Future investigation should be directed toward the effects of augmenting or improving RV function with pharmacologic agents in this patient population.

Blood Pressure↗
PubMed1983

Phentolamine in low cardiac output states: an assessment with ECG-gated cardiac scintigraphy.

We examined the effect of parenteral phentolamine in 11 critically ill patients with a low cardiac output state and a high systemic resistance. Because vasodilators often affect left ventricular end-diastolic pressure-volume relationships (compliance) in acute cardiac disease, changes in the pulmonary capillary wedge pressure (WP) may conceivably not reflect the true effect of vasodilators on left ventricular preload. Hence, we measured left ventricular ejection fraction (LVEF) with ECG-gated cardiac scintigraphy and stroke volume by thermodilution before and during phentolamine infusion. We then calculated left ventricular end-diastolic volume index (LVEDVI). Phentolamine infusion was associated with an increase in the mean cardiac index (CI) (1.96 +/- .53 [mean +/- SD] to 2.45 +/- .69 L/min X m2; p less than .0025) whereas the mean WP fell (19.5 +/- 7.5 to 13.5 +/- 7.3 mm Hg; p less than .05). There was no simultaneous change in the mean LVEDVI (100 +/- 48 to 110 +/- 40 ml/m2; p = NS), implying that one of the effects of phentolamine infusion was to improve left ventricular diastolic compliance. Multiple regression analysis suggested that the major effect of phentolamine on stroke volume was mediated by concomitant changes in the LVEDVI (r2 = .64). Therefore, benefit from phentolamine in low cardiac output states is multifactorial and phentolamine likely improves left ventricular compliance in some patients.

Aged↗
PubMed1983

Clinical studies of measuring extravascular lung water by the thermal dye technique in critically ill patients.

We measured extravascular lung water (EVLW) by the thermal-dye technique in a broad group of critically ill patients who had either acute cardiac or noncardiac illnesses. A portable AP supine chest roentgenogram, reviewed blindly, was used to classify patients as to the presence or absence of pulmonary edema; by clinical history we categorized patients into either a cardiac or noncardiac (ie, ARDS) group. With a normal chest roentgenogram, the mean EVLW was 5.6 +/- 1.8 ml/kg, and the pulmonary capillary wedge pressure (PCWP) was 11.3 +/- 5.3 mm Hg (mean +/- SD). In contrast, patients with pulmonary edema on a cardiac basis had a mean EVLW of 10.2 +/- 3.1 ml/kg (mean PCWP, 20.5 +/- 8.2 mm Hg), while patients with clinically defined noncardiac pulmonary edema and a normal PCWP (11.6 +/- 5.7 mm Hg) had a mean EVLW of 15.8 +/- 4.6 ml/kg, significantly higher than in the cardiac group (p less than 0.001). On a severity system of 014, the EVLW increased in parallel to the severity of the chest radiologic appearance of edema in both the cardiac (r2 = .44; p less than 0.001) and noncardiac (r2 = .59; p less than 0.001) patients. This study defined a normal range of thermal-dye EVLW in critically ill patients without radiologic evidence of pulmonary edema. We further demonstrated the increased pulmonary microvascular permeability of noncardiac pulmonary edema compared with cardiac edema by the greater EVLW at normal microvascular hydrostatic pressures in the former group.

Adult↗
PubMed1983

Biventricular function in the adult respiratory distress syndrome.

We examined biventricular function in patients with the adult respiratory distress syndrome (ARDS) by a combination of invasively determined pressures and flows and concomitant radionuclide angiography. Right (RVEF) and left (LVEF) ventricular ejection fractions were measured; right and left ventricular end-diastolic (EDVI) and end-systolic (ESVI) volume indices were calculated from the respective ejection fraction and measured thermodilution stroke volume. With an increase in the outflow pressure load on the right ventricle, measured as the mean pulmonary artery pressure (PAP), the RVEF fell (Y = 66.25 -1.01X; r2 = .42; p less than .001) and both the RVEDVI (y = 13.39 + 3.66X; r2 = .33; p less than .001) and RVESVI (Y = 23.9 + 3.57X; r2 = .41; p less than .001) increased. Progressive increases in the PAP also seemed associated with a change in left ventricular end-diastolic pressure-volume relationships: without pulmonary artery hypertension (PAP less than 20 mm Hg) the mean LVEDVI was 87.2 +/- 31.3 ml/m2 (mean +/- SD) and the mean PCWP was 5.0 +/- 2.8 mm Hg; with a mean PAP exceeding 30 mm Hg, the LVEDVI remained constant (90.4 +/- 26.9 ml/m2) although the PCWP was greater than previous (18.5 +/- 5.7 mm Hg; p less than .01). Analysis of right ventricular peak-systolic pressure end-systolic volume ratios implied a concurrent depression in right ventricular contractility at high levels of PAP. However, right ventricular "pump" function to maintain an adequate left ventricular preload remained unaltered regardless of the presence of pulmonary artery hypertension.

Adult↗
PubMed1983

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension.

To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15 degrees, 30 degrees, and 60 degrees. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15 degrees (a fall of -4.5 +/- 1.6 mm Hg, p less than 0.001) and 30 degrees (a fall of -6.1 +/- 3.5 mm Hg, p less than 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60 degrees, the mean ICP increased to -3.8 +/- 9.3 mm Hg of baseline, while the CPP decreased -7.9 +/- 9.3 mm Hg (p less than 0.02), and the cardiac index also fell -0.25 +/- 0.28 liters/min/sq m (p less than 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15 degrees or 30 degrees) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0 degrees) or higher (60 degrees) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.

Blood Pressure↗
PubMed1983

The short-term effects of increasing plasma colloid osmotic pressure in patients with noncardiac pulmonary edema.

We infused hyperoncotic albumin (25 or 50 gm of a 50% solution) into patients with noncardiac pulmonary edema (adult respiratory distress syndrome [ARDS]) to evaluate its effect on the transmicrovascular flux from blood to pulmonary edema fluid of two radiotracers--111In-DTPA (mol wt 504) and 125I-human serum albumin (HSA) (mol wt 69,000). Two groups of patients were studied--one with a modest increase in permeability of the pulmonary alveolocapillary membrane to 125I-HSA (group 1) and another with a large increase in permeability to 125I-HSA (group 2). We used furosemide, when necessary, to minimize the effect of albumin infusion to increase the pulmonary microvascular hydrostatic pressure (Pmv), measured clinically as the pulmonary capillary wedge pressure (PCWP). Therapy significantly increased the mean colloid osmotic pressure (COP) in both groups, but not the mean PCWP or calculated Pmv. Albumin had no significant effect on the mean pulmonary transmicrovascular flux of the radiotracers in either group, despite the increase in COP. In individual patients, a change in the Pmv in response to albumin infusion was directly correlated with the change in flux of 111In-DTPA [group 1: delta In-DTPA (%) = 8.66 + 1.4 delta Pmv (%) r = 0.51, P less than 0.02; group 2: delta In-DTPA (%) = -3.43 + 1.6 delta Pmv (%) r = 0.67, P less than 0.01]. A change in the transmicrovascular flux of I-HSA also correlated with a change in the intravascular Starling forces in both groups. We conclude that albumin infusion in patients with ARDS will not augment the pulmonary transmicrovascular flux of low or high molecular-weight solutes when the effect of albumin to increase the Pmv is minimized; nor, however, does an increase in plasma COP significantly reduce the flux of such solutes.

Albumins↗
PubMed1982

Pulmonary accumulation of polymorphonuclear leukocytes in the adult respiratory distress syndrome.

The polymorphonuclear leukocyte (PMN) plays an integral role in the development of permeability pulmonary edema associated with the adult respiratory distress syndrome (ARDS). This report describes 3 patients with ARDS secondary to systemic sepsis who demonstrated an abnormal diffuse accumulation of Indium (111In)-labeled PMNs in their lungs, without concomitant clinical or laboratory evidence of a primary chest infection. In one patient, the accumulation of the pulmonary activity during an initial pass suggested that this observation was related to diffuse leukoaggregation within the pulmonary microvasculature. A 4th patient with ARDS was on high-dose corticosteroids at the time of a similar study, and showed no pulmonary accumulation of PMNs, suggesting a possible reason for the reported beneficial effect of corticosteroids in human ARDS.

Acute Disease↗
PubMed1982

Patterns of urinary protein excretion in patients with sepsis.

Urine protein excretion patterns have been studied in 42 patients with sepsis and compared with that in 21 healthy controls. Patients with sepsis were shown to have highly significant increases in fractional clearances for beta 2-microglobulin, albumin, amylase and immunoglobulin G as compared with the controls. Analysis of the pattern of protein excretion demonstrates that the proteinuria is of the tubular rather than the glomerular type. There was no evidence that administration of aminoglycoside antibiotics contributed to the production of tubular proteinuria, and in particular these drugs did not appear to affect the excretion of beta 2-microglobulin.

Albuminuria↗
PubMed1981

Does the pulmonary capillary wedge pressure predict left ventricular preload in critically ill patients?

The construction of a Frank-Starling myocardial function curve relating heart work to left ventricular preload is clinically utilized to assess therapeutic protocols in critically ill patients. The pulmonary capillary wedge pressure (PWP) is the index of left ventricular filling pressure most frequently utilized as representative of left ventricular preload. The authors assessed the relationship between left ventricular preload measured as the left ventricular end-diastolic volume (LVEDV), and the PWP, in acutely ill patients with sepsis and cardiac disease. Within each group, no relationship was found between the LVEDV and the PWP; however, when omitting the effect of PEEP, a modest correlation was noted (r = 0.302; p less than 0.01). Of the left ventricular ejection fraction, LVEDV and PWP, the PWP accounted for less than 5% of the explained variance in the stroke volume index. The PWP is a poor predictor of left ventricular preload, probably because of abnormalities of left ventricular compliance in critically ill patients.

Aged↗
PubMed1981

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.

Adolescent↗
PubMed1981

Pulmonary microvascular clearance of radiotracers in human cardiac and noncardiac pulmonary edema.

We examined the integrity of the alveolocapillary membrane in human cardiac (hydrostatic) (group 1) and noncardiac (permeability) (group 2) edema by measuring the clearance of two intravenously administered radiotracers from the blood to suctioned bronchoalveolar secretions (BAS), representing pulmonary edema fluid, and compared the clearances to simultaneously measured pulmonary capillary wedge pressure (PCWP) and colloid osmotic pressure (COP), representing the intravascular Starling forces, Pmv and pimv. 111In-labeled diethylenetriamine pentaacetic acid (DTPA), mol wt 504, a hydrophilic radiotracer that equilibrates with extracellular water, and 125I-labeled human serum albumin (HSA), mol we 69,000, were injected intravenously. Samples of blood and BAS were then collected hourly for 405 h, and clearances were calculated. We found the clearance of both radiotracers to be greater in group 2 than in group 1 patients, despite a low mean PCWP-COP gradient, indicating greater alveolocapillary membrane permeability membrane in noncardiac, than in cardiac edema. Furthermore, 111In-DTPA clearance was linearly correlated with the PCWP-COP gradient in both groups (group 1, R2 = 0.726, P less than 0.001; group 2, R2 = 0.879, p less than 0.001 as was the clearance of 125I-HSA in group 2 (R2 = 0.35, P less than 0.027). Clinically, the data suggest that in cardiac and noncardiac pulmonary edema the transmicrovascular flux of small and large solutes may be favorably influenced by therapeutic alterations aimed at widening the intravascular PCWP-COP gradient. However, the greater permeability of the alveolocapillary membrane in noncardiac edema would prohibit any major resolution of edema by simple therapeutic alterations of this gradient.

Capillary Permeability↗
PubMed1981

Positive end-expiratory pressure (PEEP) does not depress left ventricular function in patients with pulmonary edema.

We evaluated the effects of positive end-expiratory pressure (PEEP) on left ventricular function in 15 patients with acute respiratory insufficiency secondary to pulmonary edema with invasive (pressure; flow) measurements and radionuclide angiography (RA). Using RNA allowed a definition of the left ventricular ejection fraction (LVEF), and then calculation of the left ventricular end-diastolic volume (LVEDV), both before and after PEEP. With a mean PEEP of 14.2 +/- 1.8 cm H2O (mean +/- SD) (range, 10 to 15), a fall in the cardiac index (4.34 +/- 1.5 to 3.84 +/- 1.4 L/min/M2; p less than 0.001) was accompanied by a significant decrease in the stroke volume index (42 +/- 13 to 39 +/- 12 ml/beat M2; p less than 0.01) and pulse rate (103.4 +/- 14.3 to 98 +/- 13.5 beats/min; p less than 0.01). The decrease in the stroke volume index was primarily due to a significant decrease in left ventricular preload (LVEDV) from 85.9 +/- 19 to 71.4 +/- 21.4 ml/m2 (p less than 0.01). Simultaneously, the mean LVEF increased from 0.47 +/- 0.10 to 0.53 +/- 0.08 (p less than 0.05), despite a significant increase in the systemic vascular resistance (1,619 +/- 575 to 1,864 +/- 617 dynes . s. cm-5/M2; p less than 0.01). We concluded that the use of PEEP in patients with acute pulmonary edema, to the degree used in this study, may depress cardiac output by simply decreasing left ventricular preload. We were unable to produce any evidence that would support a change in the contractile state of the left ventricle as a cause of depressed forward flow with the use of PEEP.

Angiography↗