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Brian P Kavanagh

Publications and source records attributed to Brian P Kavanagh.

At least 19 recordsLinked to original sources
PubMed2007

Atelectasis in the perioperative patient.

PURPOSE OF REVIEW: To report the impact of atelectasis on perioperative outcomes. Atelectasis occurs in the dependent parts of the lungs of most patients who are anesthetized. Development of atelectasis is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance and development of lung injury. Here, we examine the etiology, contributing factors, consequences, diagnosis and treatment of atelectasis. RECENT FINDINGS: Atelectasis describes the state of absent air in alveoli attributable to collapse, but recent findings suggest that alveoli are filled with foam and fluid. It is now known that atelectasis plays an important role beyond abnormal gas exchange and that prevention or reversal of atelectasis in some populations of postoperative patients may improve outcome. SUMMARY: Atelectasis in the presence of preexisting lung disease or limited cardiopulmonary reserve may have significant consequences. Increasing understanding of the underlying nature of atelectasis and its contribution to acute lung injury will improve our approach to the prevention and management of atelectasis.

Aging↗
PubMed2006

Incidence, risk factors and consequences of ICU delirium.

OBJECTIVE: Delirium in the critically ill is reported in 11-80% of patients. We estimated the incidence of delirium using a validated scale in a large cohort of ICU patients and determined the associated risk factors and outcomes. DESIGN AND SETTING: Prospective study in a 16-bed medical-surgical intensive care unit (ICU). PATIENTS: 820 consecutive patients admitted to ICU for more than 24 h. INTERVENTIONS: Tools used were: the Intensive Care Delirium Screening Checklist for delirium, Richmond Agitation and Sedation Scale for sedation, and Numerical Rating Scale for pain. Risk factors were evaluated with univariate and multivariate analysis, and factors influencing mortality were determined using Cox regression. RESULTS: Delirium occurred in 31.8% of 764 patients. Risk of delirium was independently associated with a history of hypertension (OR 1.88, 95% CI 1.3-2.6), alcoholism (2.03, 1.2-3.2), and severity of illness (1.25, 1.03-1.07 per 5-point increment in APACHE II score) but not with age or corticosteroid use. Sedatives and analgesics increased the risk of delirium when used to induce coma (OR 3.2, 95% CI 1.5-6.8), and not otherwise. Delirium was linked to longer ICU stay (11.5+/-11.5 vs. 4.4+/-3.9 days), longer hospital stay (18.2+/-15.7 vs. 13.2+/-19.4 days), higher ICU mortality (19.7% vs. 10.3%), and higher hospital mortality (26.7% vs. 21.4%). CONCLUSION: Delirium is associated with a history of hypertension and alcoholism, higher APACHE II score, and with clinical effects of sedative and analgesic drugs.

Delirium↗
PubMed2006

Therapeutic hypercapnia prevents chronic hypoxia-induced pulmonary hypertension in the newborn rat.

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO(2)) may have beneficial effects on the pulmonary circulation. We tested the hypothesis that exposure to CO(2) would protect against chronic pulmonary hypertension in newborn rats. Atmospheric CO(2) was maintained at <0.5% (normocapnia), 5.5%, or 10% during exposure from birth for 14 days to normoxia (21% O(2)) or moderate hypoxia (13% O(2)). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries, and distal arterial muscularization. Exposure to 10% CO(2) (but not to 5.5% CO(2)) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals (P < 0.05), whereas both concentrations of CO(2) normalized right ventricular performance. Exposure to 10% CO(2) attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO(2) on the lung and consequent modulating effects on the endothelin pathway.

Animals↗
PubMed2006

Atelectasis causes alveolar injury in nonatelectatic lung regions.

RATIONALE: Many authors have suggested that the mechanism by which atelectasis contributes to injury is through the repetitive opening and closing of distal airways in lung regions that are atelectatic. However, neither the topographic nor mechanistic relationships between atelectasis and distribution of lung injury are known. OBJECTIVES: To investigate how atelectasis contributes to ventilator-induced lung injury. METHODS: Surfactant depletion was performed in anesthetized rats that were then allocated to noninjurious or injurious ventilation for 90 min. MEASUREMENTS: Lung injury was quantified by gas exchange, compliance, histology, wet-to-dry weight, and cytokine expression, and its distribution by histology, stereology, cytokine mRNA expression, in situ hybridization, and immunohistochemistry. Functional residual capacity, percent atelectasis, and injury-induced lung water accumulation were measured using gravimetric and volumetric techniques. MAIN RESULTS: Atelectasis occurred in the dependent lung regions. Injurious ventilation was associated with alveolar and distal airway injury, while noninjurious ventilation was not. With injurious ventilation, alveolar injury (i.e., histology, myeloperoxidase protein expression, quantification, and localization of cytokine mRNA expression) was maximal in nondependent regions, whereas distal airway injury was equivalent in atelectatic and nonatelectatic regions. CONCLUSIONS: These data support the notion that lung injury associated with atelectasis involves trauma to the distal airways. We provide topographic and biochemical evidence that such distal airway injury is not localized solely to atelectatic areas, but is instead generalized in both atelectatic and nonatelectatic lung regions. In contrast, alveolar injury associated with atelectasis does not occur in those areas that are atelectatic but occurs instead in remote nonatelectatic alveoli.

Animals↗
PubMed2006

Epinephrine increases mortality after brief asphyxial cardiac arrest in an in vivo rat model.

Epinephrine may be detrimental in cardiac arrest. In this laboratory study we sought to characterize the effect of epinephrine and concomitant calcium channel blockade on postresuscitation myocardial performance after brief asphyxial cardiac arrest. Anesthesized rats were disconnected from mechanical ventilation, resulting in cardiac arrest. Resuscitation was attempted after 1 min with mechanical ventilation, oxygen, chest compressions, and IV medication. In experimental series 1 and 2, animals were allocated to 10 or 30 microg/kg epinephrine or 0.9% saline. In series 3, animals received 30 microg/kg of epinephrine and were randomized to 0.1 mg/kg of verapamil or to 0.9% saline. In series 1 and 3, left ventricular function was assessed using transthoracic echocardiography. In series 2, left atrial pressure was measured. Epinephrine was associated with increased mortality (0/8 [0%] in controls, 4/12 [33.3%] in 10 microg/kg animals, and 16/22 [72.8%] in 30 microg/kg animals; P < 0.05), hypertension (P < 0.001), tachycardia (P = 0.004), early transient left atrial hypertension, and dose-related reduction in left ventricular end diastolic diameter (P < 0.05). Verapamil prevented mortality associated with large-dose epinephrine (0% versus 100%) and attenuated early diastolic dysfunction and postresuscitation hypertension (P = 0.001) without systolic dysfunction. Epinephrine appears to be harmful in the setting of brief cardiac arrest after asphyxia.

Animals↗
PubMed2005

The effect of global hypoxia on myocardial function after successful cardiopulmonary resuscitation in a laboratory model.

Most laboratory studies of cardiac arrest use models of ventricular fibrillation, but in the emergency room, operating room or intensive care unit, cardiac arrest frequently results from asphyxia. We sought to investigate the effect of different durations of asystole secondary to asphyxia on myocardial function after resuscitation. In a laboratory based experimental series, anaesthetized rats received either 4 or 8 min of asphyxial cardiac arrest, and following standardized resuscitation, serial transthoracic echocardiography was performed. Severe depression of left ventricular fractional shortening occurred in both groups with partial recovery only in the 4-min arrest group, while left ventricular end-diastolic diameter was increased in the 4-min group. The pH, HCO3(-) and SBE were reduced in both groups after resuscitation, but the degree of acidosis was greater in the 8-min group. In this model, transthoracic echocardiography demonstrated both systolic and diastolic impairment following asphyxial cardiac arrest, and a clear dose-effect relationship between duration of asphyxia and degree of impairment. A shorter duration of asphyxia was associated with a lesser increase in left ventricular end-diastolic dimension, compared with more protracted asphyxia; the shorter arrest was associated with better recovery of contractile function and acidosis. Increased duration of asphyxia causes increased systolic and diastolic dysfunction. These findings may have significant implications for resuscitative therapeutics. ECHO assessment may permit specific targeting of therapy directed towards systolic or diastolic function during CPR.

Animals↗
PubMed2005

Continuous positive airway pressure causes lung injury in a model of sepsis.

Continuous positive airway pressure, aimed at preventing pulmonary atelectasis, has been used for decades to reduce lung injury in critically ill patients. In neonatal practice, it is increasingly used worldwide as a primary form of respiratory support due to its low cost and because it reduces the need for endotracheal intubation and conventional mechanical ventilation. We studied the anesthetized in vivo rat and determined the optimal circuit design for delivery of continuous positive airway pressure. We investigated the effects of continuous positive airway pressure following lipopolysaccharide administration in the anesthetized rat. Whereas neither continuous positive airway pressure nor lipopolysaccharide alone caused lung injury, continuous positive airway pressure applied following intravenous lipopolysaccharide resulted in increased microvascular permeability, elevated cytokine protein and mRNA production, and impaired static compliance. A dose-response relationship was demonstrated whereby higher levels of continuous positive airway pressure (up to 6 cmH(2)O) caused greater lung injury. Lung injury was attenuated by pretreatment with dexamethasone. These data demonstrate that despite optimal circuit design, continuous positive airway pressure causes significant lung injury (proportional to the airway pressure) in the setting of circulating lipopolysaccharide. Although we would currently avoid direct extrapolation of these findings to clinical practice, we believe that in the context of increasing clinical use, these data are grounds for concern and warrant further investigation.

Animals↗
PubMed2005

12-hour versus 24-hour creatinine clearance in critically ill pediatric patients.

Measurement of renal function is important to optimize drug dosing in critically ill pediatric patients and to prevent dose-related toxicities caused by medications that are eliminated or metabolized by the kidney. In clinical practice, the 24-h creatinine clearance (CrCl) is used as a surrogate marker of renal function. However, a 24-h urine collection period delays the availability of the result and increases the potential for collection errors. This prospective, observational study was performed to determine whether a 12-h CrCl is comparable to the traditional 24-h CrCl and to assess whether CrCl could be reliably predicted by the Schwartz equation, which mathematically estimates a child's GFR. A 24-h urine sample was collected in two 12-h aliquots from 60 catheterized critically ill children (age 2 d to 18 y). CrCl and Schwartz glomerular filtration rate (GFR) estimates were determined for each 12- and 24-h period. Agreement between 12- and 24-h CrCl and between CrCl and Schwartz GFR estimates was assessed using intraclass correlation coefficients (ICCs). An ICC > or =0.8 was considered to indicate excellent agreement. The ICC between the first 12-h CrCl and 24-h CrCl was 0.9605. The ICC between the second 12-h CrCl and 24-h CrCl was 0.9602. The ICC between the 24-h CrCl and Schwartz GFR was only 0.7046. All comparisons of 12- and 24-h CrCl indicated excellent agreement. In summary, the Schwartz equation was not a reliable estimate of renal function in critically ill children, and a 12-h CrCl is just as accurate as the standard 24-h CrCl to assess renal function and guide drug dosing.

Adolescent↗
PubMed2005

Lung development and susceptibility to ventilator-induced lung injury.

RATIONALE: Ventilator-induced lung injury has been predominantly studied in adults. OBJECTIVES: To explore the effects of age and lung development on susceptibility to such injury. METHODS: Ex vivo isolated nonperfused rat lungs (infant, juvenile, and adult) were mechanically ventilated where VT was based on milliliters per kilogram of body weight or as a percentage of the measured total lung capacity (TLC). In vivo anesthetized rats (infant, adult) were mechanically ventilated with pressure-limited VTs. Allocation to ventilation strategy was randomized. MEASUREMENTS: Ex vivo injury was assessed by pressure-volume analysis, reduction in TLC, and histology, and in vivo injury by lung compliance, cytokine production, and wet- to dry-weight ratio. MAIN RESULTS: Ex vivo ventilation (VT 30 ml.kg(-1)) resulted in a significant reduction (36.0 +/- 10.1%, p < 0.05) in TLC in adult but not in infant lungs. Ex vivo ventilation (VT 50% TLC) resulted in a significant reduction in TLC in both adult (27.8 +/- 2.8%) and infant (10.6 +/- 7.0%) lungs, but more so in the adult lungs (p < 0.05); these changes were paralleled by histology and pressure-volume characteristics. After high stretch in vivo ventilation, adult but not infant rats developed lung injury (total lung compliance, wet/dry ratio, tumor necrosis factor alpha). Surface video microscopy demonstrated greater heterogeneity of alveolar distension in ex vivo adult versus infant lungs. CONCLUSION: These data provide ex vivo and in vivo evidence that comparable ventilator settings are significantly more injurious in the adult than infant rat lung, probably reflecting differences in intrinsic susceptibility or inflation pattern.

Animals↗
PubMed2005

Hypocapnia attenuates mesenteric ischemia-reperfusion injury in a rat model.

PURPOSE: Hypocapnia, a recognized complication of high frequency oscillation ventilation, has multiple adverse effects on lung and brain physiology in vivo, including potentiation of free radical injury. We hypothesized that hypocapnia would potentiate the effects of mesenteric ischemia-reperfusion on bowel, liver and lung injury. METHODS: Anesthetized male Sprague-Dawley rats were ventilated with high frequency oscillation and were randomized to one of four groups, exposed to either mesenteric ischemia-reperfusion or sham surgery, and to either hypocapnia or normocapnia. RESULTS: All animals survived the protocol. Ischemia-reperfusion caused significant histologic bowel injury. Bowel 8-isoprostane generation was greater in ischemia-reperfusion vs sham, but was attenuated by hypocapnia. Laser-Doppler flow studies of bowel perfusion confirmed that hypocapnia attenuated reperfusion following ischemia. Plasma alanine transaminase, reflecting overall hepatocellular injury, was not increased by ischemia-reperfusion but was increased by hypocapnia; however, hepatic isoprostane generation was increased by ischemia-reperfusion, and not by hypocapnia. Oxygenation was comparable in all groups, and compliance was impaired by ischemia-reperfusion but not by hypocapnia. CONCLUSION: Hypocapnia, although directly injurious to the liver, attenuates ischemia-reperfusion induced lipid peroxidation in the bowel, possibly through attenuation of blood flow during reperfusion.

Animals↗
PubMed2005

Pulmonary atelectasis: a pathogenic perioperative entity.

Atelectasis occurs in the dependent parts of the lungs of most patients who are anesthetized. Development of atelectasis is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance, and development of lung injury. The adverse effects of atelectasis persist into the postoperative period and can impact patient recovery. This review article focuses on the causes, nature, and diagnosis of atelectasis. The authors discuss the effects and implications of atelectasis in the perioperative period and illustrate how preventive measures may impact outcome. In addition, they examine the impact of atelectasis and its prevention in acute lung injury.

Aging↗
PubMed2005

Oxygen attenuates atelectasis-induced injury in the in vivo rat lung.

BACKGROUND: Atelectasis results in impaired compliance and gas exchange and, in extreme cases, increased microvascular permeability, pulmonary hypertension, and right ventricular dysfunction. It is not known whether such atelectasis-induced lung injury is due to the direct mechanical effects of lung volume reduction and alveolar collapse or due to the associated regional lung hypoxia. The authors hypothesized that addition of supplemental oxygen to an atelectasis-prone ventilation strategy would attenuate the pulmonary vascular effects and reduce the local levels of vasoconstrictor eicosanoids. METHODS: In series 1, anesthetized, atelectasis-prone mechanically ventilated rats were randomly assigned to one of six groups based on the inspired oxygen concentration and ventilated without recruitment. Series 2 was performed to determine the cardiac and pulmonary vascular effects of 21% versus 100% inspired oxygen. In series 3, computed tomography scans were performed after ventilation with a recruitment strategy (21% O2) or no recruitment strategy (21% O2 or 100% O2). In series 4, functional residual capacity was measured in animals where the gas was 21% or 100% O2. RESULTS: The partial pressure of arterial oxygen increased with increasing inspired oxygen, but the alveolar-arterial oxygenation gradient was also greater with higher inspired oxygen. Ventilation with 21% O2 (but not with 100% O2) was associated with progressive pulmonary vascular impedance and increased pulmonary vascular permeability. Prostaglandin F2alpha was increased by mechanical ventilation, especially without supplemental oxygen. Computed tomography scans demonstrated no atelectasis in recruited lungs, and atelectasis in nonrecruited lungs that was greater with supplemental oxygen. Increased atelectasis with 100% O2 (vs. 21% O2) was demonstrated by measurement of functional residual capacity. CONCLUSIONS: Although supplemental oxygen worsened atelectasis in this model, it prevented the pathologic effects of atelectasis, including microvascular leak and pulmonary hypertension. Atelectasis-induced lung injury seems to be mediated by hypoxia rather than by the direct mechanical effects of atelectasis.

Animals↗
PubMed2005

Airway management in the lateral position: a randomized controlled trial.

UNLABELLED: It may be required to ensure patency of the airway in the lateral position in certain circumstances. We performed a prospective randomized clinical trial investigating the effects of left lateral patient positioning on airway anatomy and subsequent airway management. Laryngoscopic airway examination was performed in anesthetized patients, in the supine and left lateral positions, and in the presence and absence of cricoid pressure. Patients were randomized to airway management via an endotracheal tube or laryngeal mask airway (LMA). The left lateral position resulted in a deterioration of laryngoscopic view in 35% of patients and improvement in none. In the lateral position, failure of airway management occurred in more patients with the endotracheal tube versus LMA (8 of 39 versus 1 of 30; P = 0.03), and the mean time to successful completion of airway management was longer with tracheal intubation compared with the LMA (39 +/- 19 s versus 26 +/- 12 s; P = 0.002). LMA use results in more reliable airway control compared to tracheal intubation in the lateral position. The LMA should be considered as the primary airway device when instituting airway management in this position. IMPLICATIONS: Inadequate airway management may be fatal. There are recommendations for airway difficulties, but the evidence favoring any specific strategy is limited. This study suggests that, in the lateral position, a laryngeal mask airway more rapidly and reliably establishes airway control than attempts at endotracheal intubation. It further suggests that placing a patient with an inadequate airway into the lateral position will hinder, not help, airway management.

Female↗