PubMed Health⌕ Search

Biomedical subjects

I Mayers

Publications and source records attributed to I Mayers.

At least 19 recordsLinked to original sources
PubMed2001

Matrix metalloproteinase 2 in tumor cell-induced platelet aggregation: regulation by nitric oxide.

A correlation exists between the ability of tumor cells to aggregate platelets and their tendency to metastasize. Tumor cell-induced platelet aggregation (TCIPA) facilitates the embolization of the vasculature with tumor cells and the formation of metastatic foci. It is well documented that matrix metalloproteinases (MMPs) play an integral part in tumor spread and the metastatic cascade. Therefore, we have examined the role of MMPs during TCIPA and its regulation by nitric oxide (NO) in vitro. Human HT-1080 fibrosarcoma and A549 lung epithelial cancer cells induced TCIPA in a concentration-dependent manner that was monitored by aggregometry. This aggregation resulted in the release of MMIP-2 from platelets and cancer cells, as measured by zymography. HT-1080 cells released significantly more MMP-2 than A549 cells and were more efficacious in inducing TCIPA. Inhibition of MMP-2 with phenanthroline (1-1000 microM), a synthetic inhibitor of MMPs, and by neutralizing anti-MMIP-2 antibody (10 microg/ml) reduced TCIPA induced by HT-1080 cells. TCIPA was abolished by simultaneous inhibition of platelet function with acetylsalicylic acid (100 microM; thromboxane pathway inhibitor), apyrase (250 microg/ml; ADP pathway inhibitor), and phenanthroline. NO donors such as S-nitroso-n-acetylpenicillamine and S-nitrosoglutathione (both at 0.01-100 microM) inhibited TCIPA and MMP-2 release from platelets and tumor cells. The inhibitory actions of S-nitroso-n-acetylpenicillamine and S-nitrosoglutathione were reversed by 1H-[1,2,4]oxadiazole[4,3]quinoxalin-1-one (0.01-30 microM), a selective inhibitor of the soluble guanylyl cyclase. We conclude that (a) human fibrosarcoma cells aggregate platelets via mechanism(s) that are mediated, in part, by MMP-2; (b) NO inhibits TCIPA, in part, by attenuating the release of MMP-2; and (c) these effects of NO are cGMP-dependent.

Adenosine Diphosphate↗
PubMed2001

Multiple organ dysfunction syndrome: a narrative review.

PURPOSE: To review multiple organ dysfunction syndrome with respect to: 1) clinical measurement systems; 2) molecular mechanisms; and 3) therapeutic directions based upon molecular mechanisms. METHODS: The Medline, Cochrane, and Best Evidence databases (1996 to 2000), conference proceedings, bibliographies of review articles were searched for relevant articles. Key index words were multiple organ failure, multiple system organ dysfunction, sepsis, septic shock, shock, systemic inflammatory response syndrome. Outcomes prospectively defined were death and physiological reversal of end organ failure. RESULTS: Multiple organ dysfunction/failure (MODS) is the most common cause for death in intensive care units. The recognition of this syndrome in the last 30 yr may be due to advances in early resuscitation unmasking these delayed sequelae in those that would have died previously. Multiple organ dysfunction occurs after shock of varied etiologies and may be the result of unbridled systemic inflammation. As yet, therapy directed to prevent or improve MODS has not dramatically altered outcomes. CONCLUSION: Multiple organ dysfunction may serve as useful measure of disease severity for risk adjustment and outcome marker for quality of care and therapy provided. Anesthesiologists treating shock patients will note the subsequent development of MODS in the critical care unit and may be required to provide anesthetic support to these patients.

Humans↗
PubMed2001

Cardiac surgery increases the activity of matrix metalloproteinases and nitric oxide synthase in human hearts.

OBJECTIVES: Heart function is variably impaired after cardiopulmonary bypass. We hypothesized that, similar to other myocardial injury states, cardiopulmonary bypass leads to enhanced activity of nitric oxide synthase and matrix metalloproteinases. METHODS: We obtained right atrial biopsy specimens and plasma samples at the onset and termination of cardiopulmonary bypass in 10 patients. Biopsy specimens were analyzed for nitric oxide synthase activity by using a citrulline assay, whereas plasma and tissue were analyzed for matrix metalloproteinase-9 and matrix metalloproteinase-2 activity by using zymography. Tissue inhibitor of metalloproteinase-4 was analyzed by means of Western blotting. The cellular expression of inducible nitric oxide, endothelial nitric oxide synthase, matrix metalloproteinase-2, and matrix metalloproteinase-9 was determined in right atrial biopsy samples from 3 additional patients by using the appropriate conjugated antibodies. RESULTS: Nitric oxide synthase activity increased from the beginning to the end of bypass (4.46 +/- 1.07 vs 16.77 +/- 4.86 pmol citrulline/mg of protein per minute, respectively; P =.018). Pro-matrix metalloproteinase-9 activity increased in hearts (199 +/- 41 vs 660 +/- 177 density units/mg protein; P =.008) and plasma (14.1 +/- 4.6 vs 52.2 +/- 5.9 density units/mg protein; P =.008). Pro-matrix metalloproteinase-2 activity increased in the heart (201 +/- 23 vs 310 +/- 35 density units/mg protein, P <.05) but not in plasma. Tissue inhibitor of metalloproteinase-4 expression in the heart decreased (1574 +/- 280 vs 864 +/- 153 density units, P =.014). CONCLUSIONS: Cardiopulmonary bypass activates enzymes mediating acute inflammation and organ injury (ie, nitric oxide synthase, matrix metalloproteinase-9, and matrix metalloproteinase-2). Decreased tissue inhibitor of metalloproteinase-4 expression allows relatively unopposed increases in matrix metalloproteinase tissue activity. We postulate that these changes play a role in the pathogenesis of heart dysfunction after bypass surgery.

Aged↗
PubMed2001

Safety and dose relationship of recombinant human activated protein C for coagulopathy in severe sepsis.

OBJECTIVES: To assess the safety and effect on coagulopathy of a range of doses of recombinant human activated protein C (rhAPC). To determine an effective dose and duration of rhAPC for use in future clinical trials. DESIGN: Double-blind, randomized, placebo-controlled, multicenter, dose-ranging (sequential), phase II clinical trial. SETTING: Forty community or academic medical institutions in United States and Canada. PATIENTS: One hundred thirty-one adult patients with severe sepsis. INTERVENTIONS: Intravenous infusion of rhAPC (12, 18, 24, or 30 microg/kg/hr) or placebo for 48 or 96 hrs. MEASUREMENTS AND MAIN RESULTS: No significant differences in incidence of serious bleeding events (4% rhAPC, 5% placebo, p >.999) or incidence of serious adverse events (39% rhAPC, 46% placebo, p = 0.422) between rhAPC- and placebo-treated patients were observed. One of 53 rhAPC-treated patients with suitable immunogenicity samples had a low level, transient, non-neutralizing anti-APC antibody response not associated with any clinical adverse event. Significant dose-dependent decreases in both D-dimer (p <0.001) and end of infusion interleukin 6 levels (p =.021) were demonstrated. No statistically significant effects on fibrinogen or platelet counts were observed. A nonstatistically significant 15% relative risk reduction in 28-day all-cause mortality was observed between rhAPC- and placebo-treated patients. CONCLUSIONS: rhAPC was safe and well-tolerated and demonstrated a dose-dependent reduction in D-dimer and interleukin 6 levels relative to placebo. The dose of 24 microg/kg/hr for 96 hrs was selected for use in future clinical studies.

Critical Care↗
PubMed2000

Regional citrate anticoagulation in continuous venovenous hemodiafiltration.

Over the past several years, continuous venovenous hemodiafiltration (CVVHDF) using pump-driven devices has gained wide acceptance as a form of renal replacement therapy for critically ill patients with acute renal failure. More recently, regional citrate anticoagulation has proven useful as a method of anticoagulating CVVHDF circuits, particularly in those patients at high risk for bleeding. However, an easy and convenient method for guiding the dose of citrate infusion has not previously been described. We describe the use of an algorithm using posthemofilter levels of ionized calcium to guide the dose of administered regional citrate on the survival time and urea and creatinine clearances of 24 Hospal AN69HF hemofilters. Nine patients with acute and chronic renal failure requiring CVVHDF were studied. The median filter survival time when using the postfilter ionized calcium algorithm was 3.4 days, with a survival probability of 46% (95% confidence interval [CI], 17 to 71). Random-effects linear regression analysis did not show a significant decline in blood-side urea clearance (P = 0.041) or creatinine clearance (P = 0. 308). Moreover, definite bleeding complications occurred with an incidence rate of 0.045/person-day on citrate anticoagulation (95% CI, 0.006 to 0.16), and occult bleeding occurred with an incidence rate of 0.091/person-day on citrate anticoagulation (95% CI, 0.03 to 0.23). Guiding regional citrate anticoagulation through the use of posthemofilter ionized calcium levels is a safe and effective method of prolonging filter life during CVVHDF.

Acidosis↗
PubMed1999

Systemic thermal injury in anesthetized rabbits causes early pulmonary vascular injury that is not ablated by lazaroids.

PURPOSE: To study the effects of a systemic thermal injury on the pulmonary vasculature with and without inhibitors of lipid peroxidation (U74389G). METHODS: In a prospective, placebo control, randomized, and blinded multi-group study, burn shock was induced by scalding thermal injury (65C) to 35% body surface area in rabbits (n = 28). Hemodynamics and gas exchange were followed for 240 min post burn in four groups: No Burn, Burn-Control, Burn-U74 (10 mg.Kg-1 U74389G), No Burn-U74 (10 mg.Kg-1 U74389G). RESULTS: Scald resulted in early pulmonary injury as measured by increased pulmonary vascular resistance in the pooled Burn group compared with the No Burn groups (942 +/- 358 vs 605 +/- 255 dynes.sec-1.cm-5 respectively, P < 0.05). These pulmonary changes were associated with alveolar sequestration of leukocytes (4.8 +/- 2.9 vs 17.7 +/- 6.0 cells x 10(9).L-1, P < 0.05) in the No Burn and Burn groups respectively. Histological evidence of decreased neutrophil sequestration after scald injury was present in U74 treated animals (3+ vs 2+, P < 0.05 in the Burn and No Burn groups respectively and 2+ vs 2+, P > 0.05 in the Burn-U74 and No Burn-U74 groups respectively) although bronchial alveolar lavage still demonstrated neutrophil sequestration (5.3 +/- 2.5 vs 12.2 +/- 3.3 cell 10(9).L-1, P < 0.05 in No Burn-U74 and Burn-U74 groups respectively). Similarly, circulating white blood cells were increased in the Burn group but not Burn-U74 group four hours post burn. The increase in pulmonary vascular resistance after burn was not altered by administration of U74. CONCLUSIONS: Systemic burn results in early pulmonary vascular changes associated with leukocyte sequestration. After scald injury administration of lazaroids (U744389G) did not lessen pulmonary vascular resistance changes but did reduce neutrophil sequestration.

Analysis of Variance↗
PubMed1999

Increased nitric oxide synthase activity after canine cardiopulmonary bypass is suppressed by s-nitrosoglutathione.

OBJECTIVES: Hemodynamic instability and generalized organ dysfunction are common after cardiopulmonary bypass in human beings. Previous studies have suggested that alterations of nitric oxide metabolism may be associated with this impaired function. Using a canine model we tested whether nitric oxide synthase activity is increased after cardiopulmonary bypass. We also tested whether administration of a nitric oxide donor can influence nitric oxide synthase activity after cardiopulmonary bypass. METHODS: After induction of anesthesia, dogs were randomized to receive cardiopulmonary bypass (n = 12) or to serve as controls (n = 12). They were further randomized to receive a continuous infusion of a nitric oxide donor, S-nitrosoglutathione, or an equivalent volume of placebo. Cardiopulmonary bypass was maintained for 90 minutes, and then 4 hours later dogs were put to death. Cardiac and coronary artery sections were frozen in liquid nitrogen immediately after death for later determination of nitric oxide synthase activity using a citrulline assay. RESULTS: After cardiopulmonary bypass, 4 of 6 placebo-treated but only 2 of 6 S-nitrosoglutathione treated animals required phenylephrine infusion (3.1 +/- 3.1 microgram/min and 0.2 +/- 0.4 microgram/min, respectively, P =.05) to maintain a predetermined blood pressure. Furthermore, after cardiopulmonary bypass, Ca2+-dependent nitric oxide synthase activity in the left ventricle, atrium, and coronary artery did not increase compared with activity in the control animals, but Ca2+-independent nitric oxide synthase activity did increase (P =.005): left ventricle (+28.0% +/- 9.0%), atrium (+45.0% +/- 12.0%) and coronary artery (+17.0% +/- 12.0%). CONCLUSIONS: We have found that (1) cardiopulmonary bypass results in increased activity of Ca2+-independent nitric oxide synthase, (2) S-nitrosoglutathione can prevent the increase of Ca2+-independent nitric oxide synthase after cardiopulmonary bypass, and (3) Ca2+-independent nitric oxide synthase may contribute to hemodynamic dysfunction after cardiopulmonary bypass.

Animals↗
PubMed1998

The nonspecific inflammatory response to injury.

PURPOSE: The role of the nonspecific inflammatory response in causing injury related to surgery has become better understood over the last decade. There are complex interactions between neutrophils, cytokines and nitric oxide metabolites that may cause organ injury following surgery. The purpose of this review is to summarize some of the processes causing injury through these nonspecific pathways. METHODS: A review of the medical and anaesthetic literature related to inflammation, neutrophils and pro-inflammatory cytokines were performed using Medline. Bibliographies of relevant articles were searched and additional articles were then selected and reviewed. RESULTS: Pro-inflammatory cytokines, such as tumour necrosis factor, are released in response to a variety of noxious stimuli (e.g. burns, sepsis, or CABG surgery). These cytokines cause activation of neutrophils with increased upregulation of adhesion complexes on neutrophils and vascular endothelium. Nitric oxide synthase activity is also increased with a resultant increased production of nitric oxide. The increased nitric oxide concentration in the presence of superoxide free radicals secreted by activated neutrophils forms peroxynitrite, a more reactive and toxic molecule. Once this process is initiated, diffuse organ injury can result. Although some information related to specific anaesthetics is available, firm recommendations related to clinical practice cannot be made. CONCLUSIONS: There is a complex interplay of inflammatory mediators that can cause injury. Although specific clinical applications for manipulating these pathways are not yet generally available, this area holds promise to develop new techniques to improve outcomes following surgery.

Cell Adhesion Molecules↗
PubMed1997

Depletion of activated neutrophils by a filter during cardiac valve surgery.

PURPOSE: To determine whether inclusion of a neutrophil-specific filter into the extracorporeal circuit during open heart valve surgery alters postoperative outcomes. METHODS: Convenience sampling of 24 patients undergoing elective open heart valve surgery between July 1993 and June 1994. Patients were randomized to a neutrophil-specific filter (n = 11) or to a standard blood filter (n = 13) during cardiopulmonary bypass. RESULTS: Neutrophil-specific filter diminished (P < 0.02) the expression of CD18, a neutrophil surface adhesion molecule, at I (84.5 +/- 4.2 vs 94.8 +/- 3.8%), 4 (80.0 +/- 4.2 vs 95.1 +/- 3.9%) and 24 hr (75.2 +/- 4.2 vs 98.2 +/- 3.9%) post-operatively compared with standard filter. Total white blood cell count, neutrophil count, and pro-inflammatory cytokines (IL-6, IL-8) were similar between groups at all times. Measured outcomes including: PaO2 cardiac index, ejection fraction, haemodynamic variables, use of inotropes, spirometry (FEV1, FVC), and hospitalization duration were similar between groups. CONCLUSIONS: Inclusion of the neutrophil filter during open heart valve surgery selectively depletes activated neutrophils. There were no other detectable differences between the two groups and the use of a neutrophil-specific filter in routine clinical practice for patients undergoing open heart valve surgery is not supported.

Adult↗
PubMed1997

Respiratory outcomes with early extubation after coronary artery bypass surgery.

OBJECTIVE: Aortocoronary bypass surgery has undergone recent changes, promoting the concept of "fast tracking," in which patients are extubated and discharged postoperatively at an accelerated pace compared with previous historic patterns. Postoperative respiratory function and complications have not been previously studied in patients selected for "fast tracking." DESIGN: Matched retrospective cohort study. SETTING: Referral university teaching hospital. PATIENTS: Thirty-one patients who were compared with a retrospective matched cohort of 112 patients. Matching was based on forced vital capacity, age, and gender. INTERVENTIONS: Respiratory physiological outcomes defined as pneumonia, postoperative pulmonary spirometry, chest x-ray atelectasis or lobar collapse, and gas exchange were compared. MAIN RESULTS: The increase in atelectasis score compared with preoperative (0 = no atelectasis, 4 = lobar collapse) was higher (p < 0.01) on the day of extubation in the late extubation group (4.1 +/- 1.4) compared with the early extubation group (2.6 +/- 1.3). These chest radiographic findings were not related to pain (0 to 10 visual analog scalei, which were equivalent between groups (4.0 +/- 2.3 v 4.2 +/- 1.6). The decreases in spirometry on postoperative day 5 (FVC 1.15 +/- 0.42 v 0.86 +/- 0.54 liters; FEV1 0.92 +/- 0.38 v 0.59 +/- 0.50 liters) were greater (p < 0.001) in the late extubation group. A significantly (p < 0.001) greater decrease in FEV1/FVC ratio in the late extubation group (3.25 +/- 0.87 v -1.6 +/- 1.11%) was indicative of greater airway obstruction. Fluid balance until extubation was greater in the late extubation group (4.0 +/- 2.1 v 1.4 +/- 1.2 liters). CONCLUSIONS: Differences in chest radiographs in the late extubation group at the time of extubation may be related to greater use of fluids or increased airway obstruction. The rationale of early extubation is based on cost minimization to decrease hospital duration. This article suggests that respiratory physiological outcomes are not worsened in patients who are extubated and discharged early after elective aortocoronary bypass surgery.

Airway Obstruction↗
PubMed1997

Inhaled nitric oxide reduction in systolic pulmonary artery pressure is less in patients with decreased left ventricular ejection fraction.

OBJECTIVE: To assess whether inhaled nitric oxide decreases pulmonary artery pressure in patients with depressed left ventricular ejection fraction. DESIGN: Randomized, blinded, crossover clinical trial. SETTING: Tertiary care university referral hospital. PATIENTS: Thirty-three patients with pulmonary hypertension and left ventricular dysfunction or valvular heart disease were recruited by convenience. INTERVENTIONS: Systolic pulmonary artery pressure was measured by Doppler echocardiography during randomized inhalation of either 20 ppm or 40 ppm nitric oxide in 30% oxygen as well as during control periods without nitric oxide. MAIN RESULTS: Systolic pulmonary artery pressure was significantly (P < 0.05) decreased with 20 ppm nitric oxide (53.4 +/- 13.9 mmHg) and 40 ppm nitric oxide (53.1 +/- 14.4 mmHg) compared with either initial control (55.8 +/- 15.3 mmHg) or terminal control (56.3 +/- 15.2 mmHg) values. The regression equation for the change in systolic pulmonary artery pressure (y) as predicted by the left ventricular ejection fraction (x) alone for 20 ppm nitric oxide was y = 13.8x-2.9; R2adj = 0.30, P < 0.0001. For 40 ppm nitric oxide alone, the regression equation was y = 16.3x-3.3; R2adj = 0.25, P < 0.0001. Left ventricular ejection fraction was the most explanatory independent variable in the multivariate equation for nitric oxide-induced change in systolic pulmonary artery pressure (R2 = 0.61, P = 0.0000). The change in systolic pulmonary artery pressure was -5.1 +/- 5.2 versus 0.8 +/- 4.9 mmHg (P < 0.0000) in patients with left ventricular ejection fractions greater than 0.25, and 0.25 or less, respectively. CONCLUSIONS: These data imply that in patients with left ventricular ejection fraction of 0.25 or less, nitric oxide may not decrease systolic pulmonary artery pressure. Nitric oxide inhalation may result in a paradoxical increase in systolic pulmonary artery pressure in patients with severely depressed left ventricular ejection fraction. This effect would significantly limit the therapeutic role of nitric oxide in patients with severe heart failure.

Administration, Inhalation↗
PubMed1996

Augmentation of hypoxic pulmonary vasoconstriction by N(G)-L-methyl-arginine in a rabbit model of thermal injury.

We tested deeply anesthetized rabbits to determine if a burn acutely diminished the strength of hypoxic pulmonary vasoconstriction (HPV) and if this could be augmented by L-NMMA, a nitric oxide synthase inhibitor. We induced a burn using water heated to 75 degrees C and assessed the strength of HPV as the difference in pulmonary vascular resistance during 100% and 13% O2 ventilation. The rabbits then were randomized to receive 10 mg/kg L-NMMA (n = 8) or a placebo (n = 8). The strength of HPV decreased from 0.42 +/- 0.11 mm Hg/mL/min preburn to 0.22 +/- 0.11 mm Hg/mL/min postburn (P <.05). L-NMMA administration augmented HPV to a postburn value of 0.48 +/- 0.014 mm Hg/mL/min (P <.05). We speculate that the loss of HPV following a burn could worsen ventilation to perfusion mismatch and thereby aggravate the hypoxia associated with burns. Augmentation of HPV might be a short-term goal during the acute stabilization of hypoxic burn patients.

Animals↗
PubMed1996

Anti-CD18 antibodies improve cardiac function following cardiopulmonary bypass in dogs.

PURPOSE: Cardiopulmonary bypass is associated with activation of neutrophils, which may adhere to vascular endothelium causing lung, heart, and brain injury. We tested whether blocking neutrophil adherence would improve organ function following cardiopulmonary bypass in dogs. MATERIALS AND METHODS: All dogs received a standard anesthetic, and then one group (n = 6) received 2 hours of cardiopulmonary bypass followed by 4 hours of observation. A second group (n = 6) received a monoclonal antibody (6 mg/kg) to CD18, a neutrophil adherence factor, immediately before cardiopulmonary bypass. A third group (n = 6) did not receive cardiopulmonary bypass or antibody. RESULTS: Using flow cytometry we found that the antibody bound essentially all neutrophil CD18 sites. All three groups had similar gas exchange and hemodynamics. Lung and heart histology results were similar between groups. By echocardiography, five animals receiving cardiopulmonary bypass alone showed regional wall abnormalities, whereas only one receiving antibody showed wall motion abnormality (P < .05). Following cardiopulmonary bypass, intracellular myocardial pH was higher (P < .05) in the antibody-treated group compared with the group that had cardiopulmonary bypass alone (7.23 +/- 0.05 v 7.07 +/- 0.07 respectively). CONCLUSION: Monoclonal antibodies to CD18 can prevent the deterioration in cardiac function routinely observed following cardiopulmonary bypass.

Analysis of Variance↗
PubMed1996

Respiratory function after cardiac surgery.

STUDY OBJECTIVE: Cardiac surgery is complicated by decreased postoperative respiratory muscle strength and spirometry with accompanying increased atelectasis. The specific respiratory symptoms attributable to these physiologic changes are unknown, and this study looked at the symptoms and underlying physiology. DESIGN: Convenience sampling of observational cohort. SETTING: Tertiary care university hospital. PATIENTS: One hundred thirty-eight patients undergoing elective surgery were enrolled. INTERVENTIONS: Changes from admission to 8-week postoperative values in atelectasis, pleural effusions, spirometry (forced vital capacity and forced expiratory volume in one second), and respiratory muscle strength (negative inspiratory pressure) were measured. These physiologic changes were compared with changes in respiratory symptoms of cough, wheeze, phlegm, and dyspnea on walking up a slight hill noted from admission to 8-week follow-up by stepward logistic regression. MEASUREMENTS AND RESULTS: Spirometry and negative inspiratory pressure decreased and atelectasis increased from admission to discharge. These disturbances had only incompletely resolved at 8-week follow-up. Some patients reported fewer symptoms of cough (11%), phlegm (9%), wheeze (35%), and dyspnea (46%) at 8 weeks follow-up. Other patients reported increased symptoms of cough (15%), phlegm (10%), wheeze (6%), and dyspnea (4%) at 8 weeks follow-up. Residual atelectasis at 8 weeks was predictive of fewer symptoms of dyspnea (odds ratio [OR] 0.335, p = 0.199; 95% confidence interval [CI] 0.188, 0.597), increased symptoms of dyspnea (OR 855, p = 0.006; 95% CI 6.6, 11052), and increased symptoms of cough (OR 260, p = 0.023; 95% CI 2.13, 31829). Negative inspiratory pressure at 8 weeks was predictive of fewer symptoms of dyspnea (OR 1.05, p = 0.032; 95% CI 1.02, 1.09) and increased symptoms of wheeze (OR 0.7, p = 0.45; 95% CI 0.533, 0999). Forced vital capacity at 8 weeks was predictive of increased symptoms of wheeze (OR 0.005; p = 0.015; 95% CI 0.0060, 0.775). CONCLUSIONS: Postoperative changes in respiratory muscle strength and spirometry can persist up to at least 8 weeks postoperatively. Many patients report a change in respiratory symptoms of cough, phlegm, dyspnea, or wheeze. The change in respiratory symptoms at 8 weeks is correlated with residual respiratory muscle weakness, decrease in spirometry, and residual atelectasis.

Adult↗
PubMed1996

The effect of physical therapy on respiratory complications following cardiac valve surgery.

STUDY OBJECTIVE: To determine whether higher personnel intensive chest physical therapy can prevent the atelectasis that routinely follows cardiac valve surgery. DESIGN: Randomized, controlled trial. SETTING: Tertiary care hospital. PATIENTS: Seventy-eight patients undergoing elective cardiac valve surgery between October 1991 and April 1993 were enrolled. INTERVENTIONS: Patients were randomized in an unmasked fashion to receive early mobilization and sustained maximal inflations (lower-intensity treatment) or to receive early mobilization, sustained maximal inflations, and single-handed percussions (higher-intensity treatment.) MEASUREMENTS AND RESULTS: Clinical efficacy was determined by extent of atelectasis, length of ICU stay, total length of hospital stay, and personnel costs. The extent of postoperative atelectasis was similar in both groups on the fifth postoperative day. Postoperative values of FVC and FEV1 were reduced to a similar extent in both groups. Hospital stays and ICU stays were similar regardless of treatment. Physical therapy costs were highest in the higher-intensity therapy group. CONCLUSIONS: Postoperative respiratory dysfunction is common but does not usually cause significant morbidity or prolong hospital stay. The routine prescription of high-intensity physical therapy does not improve patient outcomes but does add significantly to patient costs.

Aged↗
PubMed1995

Postoperative physical therapy after coronary artery bypass surgery.

Coronary artery bypass surgery is frequently complicated by postoperative atelectasis. Although routinely prescribed, the efficacy of any specific chest physical therapy is not well established. We studied patients at a university center undergoing elective coronary artery bypass surgery. Based upon chest X-ray criteria at extubation, patients (n = 228) were classified as demonstrating greater or lesser degrees of atelectasis. Those with a lesser degree of atelectasis were randomized to receive either early mobilization or sustained maximal inflations (SMI). Those with greater a degree of atelectasis were separately randomized to receive either SMI or single-handed percussions (SSP). We found the extent of atelectasis at extubation did not predict the risk of developing pneumonia. Hospital stays and intensive care unit stays were similar regardless of treatment. Physical therapy costs were highest in the most labor-intensive therapy group (SSP). We conclude that postoperative respiratory dysfunction is common but does not commonly cause significant morbidity or prolong hospital stay. Adding SMI to patients with minimal atelectasis at extubation does not improve clinical outcomes. Similarly, adding SSP to patients with marked atelectasis does not improve outcomes over those obtained with SMI and early ambulation.

Aged↗
PubMed1995

Depletion of neutrophils by filter during aortocoronary bypass surgery transiently improves postoperative cardiorespiratory status.

STUDY OBJECTIVE: To determine whether inclusion of a leukocyte specific filter into the extracorporeal circuit during aortocoronary bypass surgery alters postoperative cardiopulmonary function. DESIGN: Randomized, double-blinded control trial. SETTING: Tertiary care hospital. PATIENTS: Convenience sampling of patients undergoing elective aortocoronary bypass between October 1992 and June 1993. INTERVENTIONS: A total of 32 patients were randomized to a leukocyte specific filter (n = 16) or to a standard blood filter (n = 16) during the surgical procedure. MEASUREMENTS AND RESULTS: White blood cell count in the standard filter group (12.2 +/- 3.6 10(9)/L) was higher (p = 0.047) than in the leukocyte filter group (9.9 +/- 2.6 10(9)/L) at 4 h postoperatively but counts were similar (p = 0.063) at 24 h (10.8 +/- 2.7 vs 8.9 +/- 2.6 10(9)/L, respectively). Leukocyte activation assessed by chemiluminescence was similar between groups at all measurement periods. We noted transient improvements (p < 0.05) in intrapulmonary shunt (19 +/- 50% vs 24 +/- 9%) and mean blood pressure (85 +/- 8 vs 76 +/- 9 mm Hg, respectively) in the leukocyte filter group compared with the standard filter group, respectively. Otherwise there were no differences noted between groups. CONCLUSIONS: Inclusion of a leukocyte filter during cardiopulmonary bypass caused transient cardiorespiratory improvement that was lost within 24 h and did not offer any significant clinical benefits.

Aged↗