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Biomedical subjects

W J Sibbald

Publications and source records attributed to W J Sibbald.

At least 145 records · Page 8Linked to original sources
PubMed1985

The immediate effects of isosorbide dinitrate on right ventricular function in patients with acute hypoxemic respiratory failure. A combined invasive and radionuclide study.

We administered 20 mg of isosorbide dinitrate sublingually to 16 patients with acute hypoxemic respiratory failure (ARF) complicated by pulmonary artery hypertension (PAH) and evaluated its effects 20 to 30 min later using a combination of invasively measured pressures and flows and ECG-gated cardiac scintigraphy. We measured the right and left ventricular ejection fractions and a simultaneous thermodilution stroke volume index; we then calculated respective end-diastolic (EDVI) and end-systolic (ESVI) volume indexes. An initially depressed mean right ventricular ejection fraction (RVEF) increased modestly after the administration of isosorbide dinitrate (35 +/- 10 to 41 +/- 10%; p less than 0.02), whereas both the mean right ventricular end-diastolic (-27 +/- 50 ml/M2; p less than 0.04) and end-systolic (-27 +/- 44 ml/M2; p less than 0.03) volume indexes fell. The RVEF increased in 11 of 16 patients: within this subgroup, a decrease in the RVEDVI and RVESVI was associated with a decrease in both cardiac index (delta 0.3 L/min/M2) and LVEDVI (delta -15 +/- 21 ml/M2; p less than 0.01); hence, O2 delivery also fell (delta -36 +/- 56 ml/min/M2; p less than 0.05). In some patients with ARF complicated by PAH, sublingually administered nitrates may improve right ventricular systolic function when globally depressed. However, left ventricular "pump" function appears to be depressed when a concurrent depression in right ventricular "pump" function ensues.

Acute Disease↗
PubMed1985

Thermal dye measurements of extravascular lung water in critically ill patients. Intravascular Starling forces and extravascular lung water in the adult respiratory distress syndrome.

To assess the concurrent influence on extravascular lung water (EVLW) content of the intravascular Starling forces, the pulmonary capillary wedge pressure (PCWP), and the colloid osmotic pressure (COP), we measured EVLW by the thermal green dye technique in 174 patients with and without radiographically defined pulmonary edema; in the former group, patients with cardiac (CPE) and noncardiac (NCPE) causes of pulmonary edema were compared (study A). In 119 patients, EVLW was again measured one to three days later (study B). Patients with CPE demonstrated a significantly lower EVLW (9.3 +/- 3.9 ml/kg) (mean +/- SD) than patients with NCPE (14.5 +/- 4.9 ml/kg; p less than 0.05), despite a higher mean PCWP in the former group (20 +/- 7 mm Hg) than in the latter (12 +/- 6 mm Hg; p less than 0.05). In patients potentially with only a hydrostatic cause of pulmonary edema in study A, regression analysis demonstrated the following: EVLW = 3.2 + 0.30 PCWP (r2 = 0.38; p less than 0.005); and in patients with NCPE, EVLW = 10.9 + 0.304 PCWP (r2 = 0.17; p less than 0.01). In study B the change (delta) in EVLW between the two studies was described as follows: delta EVLW = 0.25 + 0.173 delta PCWP (p less than 0.01) + 0.663 group NCPE (p, not significant) + 0.236 group NCPE X delta PCWP (p less than 0.01). This latter equation indicated that the EVLW content manifested a greater change with concurrent alterations in the PCWP in patients with NCPE than was found in patients with only a hydrostatic influence to EVLW formation. Therefore, NCPE is characterized by a greater measurable thermal green dye EVLW than is observed in CPE at any given PCWP, and the PCWP synergistically influences EVLW accumulation in both CPE and NCPE.

Adult↗
PubMed1985

Assisted ventilation in patients with preexisting cardiopulmonary disease. The effect on systemic oxygen consumption, oxygen transport, and tissue perfusion variables.

We have evaluated systemic oxygen consumption (VO2), systemic oxygen transport, and tissue perfusion variables in 30 patients with preexisting cardiac and underlying pulmonary disease during continuous positive-pressure ventilation and positive end-expiratory pressure [PEEP], during intermittent mandatory ventilation (IMV and PEEP), and during spontaneous ventilation (continuous positive airway pressure [CPAP]), with end-expiratory pressure held constant during all ventilatory modes. Using radionuclide angiography together with invasive determinations of pressure and flow, we also measured left and right ventricular ejection fractions and calculated the end-systolic (ESVI) and end-diastolic (EDVI) volume indices of both ventricles. We found that oxygen transport was significantly greater during CPAP (583 +/- 172 ml/min/M2)(mean +/- SD) than during either IMV and PEEP (543 +/- 151 ml/min/sq; p less than 0.01) or CPPV and PEEP (526 +/- 159 ml/min/M2; p less than 0.01); however, we found no significant change in systemic VO2 with conversion from CPPV and PEEP to CPAP. The increase in oxygen transport was related to a greater cardiac index and, more specifically, to a higher heart rate during CPAP (CPAP, 106 +/- 16 beats per minute; CPPV and PEEP, 97 +/- 14 beats per minute) (p less than 0.01). Enhanced oxygen transport during CPAP was also associated with an increase in mixed venous oxygenation and a decrease in arterial lactate. Although neither the mean left ventricular EDVI nor ESVI changed from CPPV and PEEP to CPAP, the mean pulmonary capillary wedge pressure increased (CPPV and PEEP, 12 +/- 5 mm Hg; CPAP, 14 +/- 7 mm Hg) (p less than 0.01), suggesting the possibility of a decrease in left ventricular compliance with the spontaneous ventilatory mode. This study suggests that in the absence of ventilatory failure, spontaneous ventilation provides for better systemic oxygen transport and overall tissue perfusion than either controlled ventilation or IMV; however, this benefit of enhanced oxygen delivery with spontaneous ventilation may potentially be offset by a decrease in left ventricular compliance.

Aged↗
PubMed1985

Myocardial function in the critically ill: factors influencing left and right ventricular performance in patients with sepsis and trauma.

Myocardial performance in critically ill patients is primarily responsive to the need to supply O2 to the periphery. An increase in CO is the common finding in an acute illness characterized by an increase in systemic VO2 (for example, sepsis and trauma), since acute variations in flow are the most efficacious mode of augmenting systemic O2t to match the VO2. The lower systemic VO2 of a patient with an acute cardiac illness explains why the CO in this disease is not as elevated as that found in the acutely ill patient with sepsis or trauma. Endogenous compensatory mechanisms used to vary flow according to the need for O2t include heart rate, ventricular preload, contractility, and afterload. An increase in LV contractility and a reduction in afterload facilitate LV stroke volume, hence O2t. Conversely, pulmonary hypertension may result in a restriction of LV preload if RV pump failure ensues. Other factors relevant to the care of the critically ill that will decrease LV preload--and thus reduce the heart's left-sided adaptation to maintain O2t--include the presence of underlying cardiac disease, which will limit any necessary increase in contractility, and the use of PEEP, which will restrict venous return to the RV. Therapeutic intervention is required when O2t does not balance systemic VO2 and arterial lactate levels rise. The use of resuscitative fluid to improve flow by the Frank-Starling (preload) mechanism may be limited by the compliance properties of either ventricle, but it is a reasonable first choice, with guidelines for administration determined by the PCWP, which influences fluid flux across the pulmonary microvascular exchanging membrane. Vasodilators may be used to increase CO by reducing impedance to ventricular ejection; they may also improve LV compliance, thereby allowing the administration of more fluid (that is, increasing preload) without an untoward rise in the PCWP. If vasodilators are without effect or are potentially dangerous because of concomitant hypotension, inotropic support to increase O2t is required. A brief summary of interventional pharmacologic support in acute illness is depicted in Figure 8.

Acute Disease↗
PubMed1985

Noninvasive clinical investigation of the cardiovascular system in the critically ill.

An understanding of fundamental principles of various modes of noninvasive cardiovascular monitoring is important in the investigation and management of acute cardiac illnesses found in the critically ill. The clinical application of electrocardiography, radiology, echocardiography, and nuclear medicine will be discussed as it applies to investigation and management of the cardiovascular system in these patients.

Cardiovascular System↗
PubMed1985

Blunt traumatic myocardial injury.

This article reviews the cardiac sequelae of blunt chest injury. Major cardiac injuries of blunt chest trauma involve damage to the myocardium, although pericardial disease, valvular heart disease, and coronary artery disease may result. Recognition of the various syndromes associated is discussed, and a synthesis of diagnostic and management strategies for speculation is provided.

Contusions↗
PubMed1985

Renal and cardiovascular response to nonhypotensive sepsis in a large animal model with peritonitis.

We studied the functional effects of intraperitoneal sepsis on systemic hemodynamics in general, and on renal function in particular, in sheep in whom bacterial peritonitis was induced by cecal perforation. In the first group of seven sheep (group 1) fluid was administered throughout the period of sepsis to maintain pulmonary capillary wedge pressure as close to presepsis values as possible. These sheep exhibited hemodynamic changes known to be associated with sepsis in man: increased cardiac output and decreased systemic vascular resistance. In a second group of seven sheep (group 2) fluid intake was restricted; compared with group 1, these sheep demonstrated a smaller increase in cardiac output that did not persist and that was associated with an increase in the systemic vascular resistance during the septic period. Plasma renin levels increased fivefold in group 2 but were unchanged in group 1. Serial renal biopsies during the septic period revealed that all sheep had evidence of tubular cell damage on electron microscopy: cell swelling, loss of the microvillous brush border, and cell necrosis. Both groups of sheep also demonstrated marked tubular proteinuria similar to that found in humans with generalized sepsis. Despite this, sheep in group 1 exhibited no functional renal changes: creatinine clearance levels rose slightly from control values, urine concentrating ability was unimpaired, and fractional excretion of sodium increased appropriately in response to a sodium load. In contrast, group 2 sheep exhibited a fall in creatinine clearance levels but fractional sodium excretion did not fall as would have been expected were renal function entirely normal. The results suggest that generalized "hyperdynamic" sepsis induces tubular cell damage and tubular proteinuria by an unknown mechanism. However, this does not necessarily produce renal impairment since the glomerular filtration rate does not fall unless volume contraction is also allowed to occur.

Animals↗
PubMed1985

Acute pulmonary hypertension, leucopenia and hypoxia in early haemodialysis.

A sheep model is described which produces acute pulmonary hypertension, leucopenia and hypoxia after blood, previously placed in contact with a Cuprophan hollow fibre artificial kidney, re-enters the circulation. Relationships between these manifestations (acute pulmonary hypertension, leucopenia and hypoxia) were examined in normal leucopenic and Indomethacin pre-treated sheep. The degree of pulmonary vascular response, and severity of leucopenia and hypoxia were all directly interrelated and were dependent upon the volume of blood injected. The induction of leucopenia did not affect the pulmonary hypertension or hypoxia. Pre-treating the animals with the cyclo-oxygenase inhibitor, Indomethacin, abolished both the pulmonary hypertension and the hypoxia without any effect on the development of neutropenia. These results suggest that leucocytes do not play a role in the haemodynamic response nor in the hypoxia; activation of the cyclo-oxygenase system is necessary for the development of acute pulmonary hypertension which causes hypoxia subsequent to alterations in ventilation perfusion relationships.

Animals↗
PubMed1985

Acute renal failure and tubular damage due to sepsis in an animal model.

Generalised sepsis was induced in sheep by caecal perforation. Serial measurement of haemodynamic parameters revealed that the subsequent generalised sepsis induced increased cardiac output and decreased systemic resistance comparable to that known to occur in man. Glomerular filtration rate in these animals fell significantly 48 hours after induction of sepsis and there was evidence of tubular damage in the finding of low molecular weight proteinuria and increased clearance of lysozyme. Pathological examination of the kidney revealed normal glomeruli, no consistent changes in tubular cells on light microscopy, negative immunofluorescence, but structural changes in proximal tubular cells on EM. In this model, non-hypotensive sepsis predictably produces damage to proximal tubular cells accompanied by reduction in GFR.

Acute Kidney Injury↗
PubMed1984

The synergistic influence of the intravascular starling forces on pulmonary microvascular solute flux in human ARDS.

To assess the importance of the intravascular Starling forces on the pulmonary microvascular flux of solutes in ARDS, the clearance from blood to pulmonary edema fluid of a small-molecular-weight hydrophilic radiotracer, indium-111-DTPA, and a large-molecular-weight radiotracer, iodine-125-HSA, in patients with noncardiac pulmonary edema was measured. Since permeability changes of the pulmonary microvessels in ARDS are likely not homogeneous, the severity of the permeability lesion according to the magnitude of I-HSA flux was predefined. A significant positive correlation between the clearance of In-DTPA and the Pmv-pi mv gradient was found both in patients with a "moderate" (R2 = 0.46, P less than 0.01) and "severe" (R2 = 0.45 P less than 0.01) increase in microvascular permeability. The clearance of I-HSA from blood to edema fluid was also positively correlated with the Pmv and the Pmv-pi gradient. Therefore, even though ARDS is primarily characterized by a spectrum of change in permeability within the pulmonary microvasculature, the flux of both small- and large-molecular-weight solutes remains synergistically modulated by the measurable intravascular Starling forces.

Cell Membrane Permeability↗
PubMed1984

Blood--dialyzer interactions: hemodynamic manifestations in an animal model.

A sheep model is described that reliably produces acute pulmonary hypertension after blood, previously in contact with a number of different dialysis membranes including Cuprophan, enters the animal's circulation. This hemodynamic manifestation is associated with myocardial ischemia and arrhythmias and coincides in time with neutropenia but precedes maximal hypoxemia. The resulting pulmonary vascular response occurs following both exposure of flowing blood to a dialyzer in an extracorporeal circuit and reinjection of blood previously in static contact with a number of different devices for varying periods of time. Increasing volumes (1-15 ml) previously in static contact (10 min) with regenerated cellulose, saponified cellulose ester, and Cuprophan (hollow fiber and sheet form) caused varying increments in mean pulmonary artery pressure. Contact with either polyacrylonitrile or cellulose acetate resulted in little response. This effect was magnified with all the surfaces, even polyacrylonitrile and cellulose acetate, by prolonging the duration of contact up to 30 min. The hemodynamic events that occurred with this model are similar to those reported in the clinical entity of "dialyzer hypersensitivity." This model may be of value in the quest for elucidation of the mechanisms involved in this syndrome.

Acrylic Resins↗
PubMed1984

Polyneuropathy in critically ill patients.

Five patients developed a severe motor and sensory polyneuropathy at the peak of critical illness (sepsis and multiorgan dysfunction complicating a variety of primary illnesses). Difficulties in weaning from the ventilator as the critical illness subsided and the development of flaccid and areflexic limbs were early clinical signs. However, electrophysiological studies, especially needle electrode examination of skeletal muscle, provided the definite evidence of polyneuropathy. The cause is uncertain, but the electrophysiological and morphological features indicate a primary axonal polyneuropathy with sparing of the central nervous system. Nutritional factors may have played a role, since the polyneuropathy improved in all five patients after total parenteral nutrition had been started, including the three patients who later died of unrelated causes. The features allow diagnosis during life, and encourage continued intensive management since recovery from the polyneuropathy may occur.

Adult↗
PubMed1984

The effect of an infusion of zymosan-activated plasma on hemodynamic and pulmonary function in sheep.

To assess the integrated cardiopulmonary response to acute microvascular lung injury, we infused zymosan-activated plasma (ZAP) into mature, awake sheep. ZAP infusion resulted in an immediate increase in the mean pulmonary artery pressure (PAP) from 17.5 +/- 4.5 mm Hg to a maximum of 33.0 +/- 5.4 mm Hg by 5 min (p less than 0.01) of a 90-min infusion. The pulmonary artery hypertension (PAH) was sustained throughout ZAP infusion, and for up to 30 min after infusion was completed (p less than 0.05). Lung lymph flow increased immediately, but lymph to plasma total protein ([L/P]) ratios remained unchanged, suggesting increased pulmonary microvascular permeability. The PaO2 fell to a minimum by 5 min (106.9 +/- 17 to 88.3 +/- 14 mm Hg; p less than 0.01), but recovered toward preinfusion values in the final 60 minutes of ZAP infusion. The cardiac index (CI) and stroke volume index (SVI) also fell significantly for 15 minutes (p less than 0.01), and then recovered to levels not different from baseline by 30 min. In parallel with all of these changes, the polymorphonuclear leukocyte count (PMN) in arterial blood fell immediately [baseline to 5 min, delta 4.9 +/- 2.5 (X 10(3))/mm3; (p less than 0.01)] due to sequestration within the pulmonary microvasculature, since a baseline PMNs were being released from the lung, -6.0 +/- 19%, while by 15 min the PMNs were being sequestered, +58.4 +/- 31% (p less than 0.01). Therefore, ZAP infusion reproduced the clinical picture of acute microvascular lung injury in humans, specifically acute PAH and increased pulmonary microvascular permeability. These two changes were due to a cascade of events associated with the pulmonary microvascular trapping of PMNs.

Animals↗
PubMed1983

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.

Adolescent↗
PubMed1983

Overwhelming pneumococcal infection in a hyposplenic adult.

In a woman with an atrophic, apparently nonfunctioning spleen pneumococcal septicemia led to death within 72 hours of admission. As in five previously described adults, the patient's presentation and subsequent clinical course were identical to those of the syndrome of overwhelming postsplenectomy infection, except that there was no history of splenectomy. Patients without spleens may be given penicillin prophylaxis for an indefinite period, vaccinated against pneumococci or both.

Atrophy↗
PubMed1983

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.

Blood Circulation↗