Cause Of Hypoxemia Research Articles

Pulmonary hypertension following hepatopulmonary syndrome in a patient with cirrhosis

We report the case of a patient with liver cirrhosis who successively developed hepatopulmonary syndrome and portopulmonary hypertension. Initially, the patient presented with severe dyspnea and hypoxemia at rest. Technetium-99 macroaggregated albumin lung perfusion scan demonstrated right-to-left shunt, and hemodynamic study revealed a hyperdynamic state with low pulmonary vascular resistance, thus confirming the diagnosis of hepatopulmonary syndrome. More than 2 years after the onset of pulmonary symptoms, a marked improvement in dyspnea and gas exchange was observed. Lung perfusion scan did not disclose any right-to-left shunt and right-sided heart catheterization showed evidence of severe pulmonary hypertension. We conclude that hepatopulmonary syndrome and portopulmonary hypertension are not mutually exclusive. We hypothesize that, by reversing the phenomenon of intrapulmonary vasodilatation, the development of portopulmonary hypertension interfered with each of the potential causes of hypoxemia in hepatopulmonary syndrome (ventilation-perfusion inequalities, intrapulmonary shunting, oxygen diffusion limitation) and, as a result, led to a correction of hypoxemia.

Tension pneumothorax complicating diagnostic upper endoscopy: a case report

Hypoxemia is common during various endoscopic procedures and may result from a variety of causes. These causes range from benign and otherwise easily reversible events like oversedation to potentially life threatening complications such as pneumothorax. Although pneumothorax has been reported secondary to gastrointestinal perforation as a complication of various therapeutic endoscopic procedures, there has been no report of pneumothorax without perforation. We report a case of a patient who developed severe hypoxemia and hemodynamic instability during diagnostic upper endoscopy as a result of pneumomediastinum and tension pneumothorax in the absence of any signs of gastrointestinal perforation and comment on various possible mechanisms. Immediate endotracheal intubation and bilateral chest tube placement resulted in prompt return of the patient’s oxygenation and vital signs back to normal. This report enlarges the list of possible causes of hypoxemia during endoscopy and shows the importance of early and prompt recognition, which allowed directed therapy with a good outcome.

An unusual cause of hypoxemia during aortic reconstruction

An unusual cause of hypoxemia during aortic reconstruction

Effect of high-intensity exercise on arterial blood gas tensions and upper airway and cardiac function in clinically normal Quarter Horses and horses heterozygous and homozygous for hyperkalemic periodic paralysis

Abstract Objective To determine the effect of exercise on arterial blood gas tensions and upper airway and cardiac function in clinically normal Quarter Horses and horses heterozygous and homozygous for hyperkalemic periodic paralysis (HYPP). Animals and Procedure 5 clinically normal Quarter Horses, and 5 heterozygous and 2 homozygous HYPP-affected horses were examined before, during, and after exercise on a high-speed treadmill. Arterial blood gas tensions, ECG, and echocardiogram were obtained prior to exercise. Upper airway endoscopy, collection of arterial blood samples, and continuous electrocardiography were performed during a high-intensity stepwise exercise test. An ECG was obtained within 1 minute after completion of the final step. Results None of the horses homozygous or heterozygous for HYPP had signs of weakness or muscle fasciculations before, during, or after exercise. Horses homozygous for HYPP had intermittent laryngospasm, dynamic pharyngeal collapse, and appreciable hypoxemia, hypercapnia, and ventricular premature contractions during exercise. Heterozygous and clinically normal horses did not have any abnormalities. Potassium concentration increased significantly above the baseline reference range during exercise in all groups of horses. Conclusions Horses homozygous for HYPP had laryngospasm and dynamic pharyngeal collapse associated with exercise, most likely secondary to increase in potassium concentration. Upper airway dysfunction is the most likely cause of hypoxemia and hypercapnia. Cardiac arrhythmias were most likely caused by a combination of hypoxemia and hyperkalemia. (Am J Vet Res 1998;59:615–618)

Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients

Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients

Hepatopulmonary syndrome

Hepatopulmonary syndrome (HPS) is now recognized as a cause of hypoxaemia in patients without intrinsic cardiopulmonary pathology who have chronic liver disease. It is estimated to affect 30% of patients with end-stage liver disease. The hypoxaemia is secondary to intrapulmonary vascular dilatations which result in intrapulmonary shunting and gross V/Q mismatch. It may pass unnoticed until assessment for orthotopic liver transplantation occurs and arterial blood gases are analysed. Clinical features include hyperventilation and exertional dyspnoea. Orthodeoxia (arterial deoxygenation upon standing and relieved by the supine position) and platypnoea (dyspnoea upon standing) are strongly suggestive of HPS. This hypoxaemia, even if severe, is not a contraindication to liver transplantation, and there is evidence that the pulmonary vasculature can return to normal following successful transplantation.

Physiology of One-Lung Ventilation

The understanding of the physiology and management of one-lung ventilation (OLV) has advanced over the last two decades. OLV induces an obligatory shunt through the nonventilated lung that causes varying degrees of arterial hypoxemia. Shunt may also occur in the venti lated lung. The optimal mode of ventilation of the dependent lung has not been well defined. The optimal tidal volume, respiratory rate, inspired oxygen concen tration, and positive end-expiratory pressure (PEEP) during OLV are not known. Functional residual capacity (FRC) of the ventilated lung can be lower than during two-lung ventilation, causing atelectasis and arterial hypoxemia. Patients who desaturate might be expected to show improvement in oxygenation with dependent lung PEEP, because of increased FRC and reduced V/Q mismatch. Not all patients have low lung volumes, and not all patients who have low lung volumes will desatu rate. Therefore, prophylactic PEEP is not usually neces sary or appropriate. Because the predominant cause of hypoxemia during OLV is shunt in the nondependent lung, therapies to improve arterial oxygenation during OLV should be primarily directed toward the nondepen dent lung. Partial reinflation of the nondependent lung with O2will reduce the physiological shunt fraction of the lung. Continuous positive airways pressure (CPAP) is an effective prophylactic and therapeutic treatment for hypoxemia. All studies examining CPAP have found it to be effective, provided it is preceded by lung reinflation.

Difficult Airway Management in a Patient with Traumatic Asphyxia

Difficult Airway Management in a Patient with Traumatic Asphyxia

V̇ a/Q̇ abnormalities during gram negative sepsis

Hypoxemia in bacterial sepsis develops by mechanisms which are incompletely understood. In this study, we measured pulmonary gas exchange in eight baboons to determine the causes of hypoxemia after infusion of live Escherichia coli (1 × 10 10 CFU/kg) followed by resuscitation with intravenous fluid. V̇ a/Q̇ distributions were measured periodically using the multiple inert gas elimination technique until death or for a maximum of 42 h. After E. coli infusion, dispersion of perfusion (logSDq) increased rapidly and a transient rise in dead space was observed at 6 h coinciding with systemic hypotension and acidosis. The intrapulmonary shunt developed later and reached 27 ± 6% at 24 h. Pa o 2 began to decrease at 12 h and correlated with increases in intrapulmonary shunt and logSDq. There was no evidence of diffusion limitation. Lung edema was mild despite aggressive fluid resuscitation. Morphometric analysis of postmortem lungs revealed dramatic intravascular accumulation of granulocytes. There were increases in arithmetic mean thicknesses of epithelium and interstitium. These data indicate that gram negative sepsis with fluid resuscitation causes progressive hypoxemia, primarily due to the development of intrapulmonary shunt and very low V̇ a/Q̇ regions in the lung. The V̇ a/Q̇ abnormalities occur early and likely reflect ongoing cellular responses in pulmonary vasculature and smaller airways in sepsis.

Monitoring of Ventilation on and off Cardiopulmonary Bypass

Monitoring of Ventilation on and off Cardiopulmonary Bypass

Cardiopulmonary manifestations of hantavirus pulmonary syndrome

To describe the clinical characteristics of a group of patients infected with the newly recognized hantavirus in the Southwestern United States. Case series. Tertiary referral center. All patients with confirmed hantavirus infection admitted to the University of New Mexico Hospital between May 1, 1993 and January 1, 1994. Records of patients with hantavirus infection were reviewed to collect all pertinent clinical data. Pulmonary disease in these patients was characterized by hypoxemia covering a wide range of severity. The cause of hypoxemia was an increased permeability (noncardiac) pulmonary edema which could be differentiated from hydrostatic (cardiac) pulmonary edema by its association with low pulmonary artery occlusion pressures and increased protein content of edema fluid. Hemodynamic measurements in severe cases showed a shock state characterized by a low cardiac index (range 1.6 to 3.0 L/min/min2), a low stroke volume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997 dyne.sec/cm5.m2). Progression to death was associated with worsening cardiac dysfunction unresponsive to treatment and causing oxygen debt and lactic acidosis. The two major life-threatening pathophysiologic changes in Hantavirus Pulmonary Syndrome are increased permeability pulmonary edema, and an atypical form of septic shock caused by myocardial depression and hypovolemia.

ASA AWARD

Robert Dunning Dripps Professor and Chair, Department of Anesthesia, University of Pennsylvania, 4 North Dulles Building, 3400 Spruce Street, Philadelphia, Pennsylvania 19104-4283.THERE are rare occasions in any field when the time, the environment, and a special person converge to produce an outstanding result. Fortunately, the time and the environment were right for Bryan E. Marshall, and the result will have a lasting impact on our specialty. (Figure 1).Dr. Bryan E. Marshall was born in London, England, in 1935, and educated at Ravenswood and Daunteys Schools. His interest in anesthesia, which began while a student at the Leeds University Medical School, was solidified during a general medical internship, when he undertook his first research into the incidence of muscle pains after outpatient surgery. He became a registrar in anesthesia at the United Cambridge Hospitals and, after qualifying as a specialist in Anaesthesia and in General Medicine, was awarded an Elmore Research Scholarship at Cambridge University. Under the encouragement of Dr. Ronald Millar, his first major work concerned the factors influencing postoperative hypoxemia. A report of this work was awarded the prestigious Research Prize of the Association of Anaesthetists in 1964. Soon after, Dr. Marshall, his wife, Carol, and their two children, Leisa and David, moved to the University of Pennsylvania for what was intended to be 2 yr of research training.At the University of Pennsylvania, Dr. Robert Dripps had assembled an extraordinary group of clinician-scientists that included James Eckenhoff, Henry Price, Harry Wollman, Craig Alexander, Peter Cohen, Ted Smith, Stanley Deutsch, and others, and Dr. Marshall thrived under their guidance. He joined the University of Pennsylvania faculty in 1967; by 1973, he was appointed a full Professor of Anesthesia in the School of Medicine and Professor of Comparative Anesthesia in the School of Veterinary Medicine. In 1983, the Horatio C. Wood Professorship was endowed to support his continued research activities.Although a skilled clinician, teacher, scientific reviewer, and research administrator, the majority of his career has been committed to anesthesia research, where he has brought an extraordinary combination of dedication, brilliance, and expertise to questions of real importance to the specialty. His investigations have been devoted to understanding the causes of hypoxemia in the perioperative period, but this terse description does not capture his flair as a scientist. He has demonstrated a knack for seeing what others have missed and a willingness to learn whatever methods are required to advance a difficult scientific area. In the process, he has studied mitochondrial respiration, lung water balance, and shock, and his contributions have brought order and quantitation to areas previously dominated by opinion, conflict, and uncertainty. His publications, which span more than a quarter century of work in the area, represent the scientific basis that guides much of our current practice, teaching, and research regarding perioperative hypoxemia. His work of the last decade on hypoxic pulmonary vasoconstriction began with a paper that demonstrated why disparate data from different laboratories were entirely consistent when looked at from a new viewpoint, an approach typical of his vision and insight in research matters. From there, his laboratory embarked on a series of studies to identify and quantitate the important factors that influence hypoxic pulmonary vasoconstriction. Dr. Marshall created a computer model that combined this new understanding of the active regulation of pulmonary blood flow with existing concepts of gas exchange as a distribution of ventilation-perfusion ratios. The model is both powerful and realistic and is being tested as a bedside clinical assistant. Simultaneously, his research team began to focus on the basic mechanisms by which the pulmonary arteries sense local oxygen tension, and it is my understanding that they are close to a successful outcome here also.Not surprisingly, Dr. Marshall has attracted a succession of outstanding collaborators and visiting scientists from some 15 countries to his laboratory. None have been more important than his wife, Dr. Carol Marshall, who, in 1979, brought her research talents to join those of her husband to evaluate the importance of hypoxic pulmonary vasoconstriction in perioperative pulmonary function, a collaboration that has been extraordinarily productive.The enthusiasm, energy, and analytical approach that Dr. Marshall brings to his work have influenced many who have gone on to successful careers in anesthesiology and the basic sciences, including several who now hold leadership positions in the specialty. His interest in the scientific basis of our specialty continues unabated, and he serves as an excellent role model for future investigators in our discipline.David E. Longnecker, M.D., Robert Dunning Dripps Professor and Chair, Department of Anesthesia, University of Pennsylvania, 4 North Dulles Building, 3400 Spruce Street, Philadelphia, Pennsylvania 19104-4283.

The Hepatopulmonary Syndrome

To review current knowledge about the hepatopulmonary syndrome, including definition and clinical features, methods for diagnosing it, pathophysiologic mechanisms of the associated vascular dilatations, and considerations in treatment, with emphasis on potential reversibility of the syndrome after liver transplantation. The MEDLINE database from January 1986 to December 1993 and bibliographies of selected articles. Case studies and series reporting results from patients with the hepatopulmonary syndrome were reviewed. Clinical reviews and animal studies relevant to the hepatopulmonary syndrome were examined. Outcomes, including survival and the frequency of reversibility of the hepatopulmonary syndrome, were extracted from available clinical reports. Mild hypoxemia is multifactorial and occurs in approximately one third of all patients with chronic liver disease. The hepatopulmonary syndrome is one cause of hypoxemia that may also cause dyspnea, platypnea, and orthopnea. Intrapulmonary vascular dilatations and the resulting right-to-left intrapulmonary shunt are characteristic of the syndrome. Pharmacologic treatment with almitrine bismesylate, somatostatin analog, and indomethacin and treatment with plasmapheresis have been disappointing. The underlying cause and the predictors of reversibility of the hepatopulmonary syndrome remain unknown, but it has recently been shown that such reversibility is possible and that contrast-enhanced echocardiography appears to be the most sensitive diagnostic test for detecting intrapulmonary vascular dilatations. In the context of persisting uncertainty about the cause and treatment of the hepatopulmonary syndrome, future studies must focus on better understanding the pathophysiology of the hepatopulmonary syndrome, predicting reversibility after liver transplantation, and identifying other treatment options.

Postoperative Tracheal Extubation

Postoperative Tracheal Extubation

Postoperative Tracheal Extubation

Postoperative Tracheal Extubation

High-Altitude Pulmonary Edema in Partial Anomalous Pulmonary Venous Connection of Drainage with Intact Atrial Septum

Partial anomalous pulmonary venous drainage may be the cause of hypoxemia and overperfusion of the lungs and therefore an important factor in the pathogenesis of high-altitude pulmonary edema (HAPE). Partial anomalous pulmonary venous drainage may be the cause of hypoxemia and overperfusion of the lungs and therefore an important factor in the pathogenesis of high-altitude pulmonary edema (HAPE).

The Anesthesiologist's Response to a Low-Output State After Cardiopulmonary Bypass: Etiologies and Remedies

Artifacts or mechanical problems may cause data which suggest poor myocardial performance during emergence from cardiopulmonary bypass (CPB). Transducer and monitoring equipment malfunctions, damping of the arterial blood pressure tracing, effects of drugs, hypercarbia, inordinately high intrathoracic pressure, cardiac tamponade, and others are all possible culprits. It is important to have a systematic plan for evaluating and interpreting the signs and data that are evident. Causes of hypotension after CPB include low hematocrit, hypercarbia, sympathetic inhibition, vasodilator action, anaphylaxis or anaphylactoid reactions, protamine reactions, and impaired myocardial performance. Impaired myocardial performance can be attributable to rate and rhythm disturbances, inadequate ventricular preload, inappropriately elevated right and left ventricular afterload, and decreased myocardial contractility. Common causes of hypoxemia include a malfunctioning ventilator system, pulmonary problems such as atelectasis and shunt, anemia, and inordinately high utilization of oxygen.

Fatal intrapulmonary arteriovenous shunting in cirrhosis — diagnosis by radionuclide lung perfusion scan

Intrapulmonary arteriovenous shunting is an important cause of hypoxaemia in patients with chronic liver disease. We describe an unusual case of a patient with haemochromatosis who died as a result of severe hypoxaemia which was due to this disorder. The shunt was demonstrated by radionuclide lung perfusion scanning.

Hypoxemia During Hemodialysis: A Critical Review of the Facts

The literature describing the fall in PaO2 during dialysis is intensively and critically reviewed. This phenomenon is related to both the type of membrane used (cellulosic v noncellulosic membrane), and to the composition of the dialysate (acetate v bicarbonate). It appears that a ventilation/perfusion mismatch due to pulmonary leukostasis can, in part, explain hypoxemia in patients dialyzed with cellulosic membranes. This phenomenon is especially apparent in patients with preexisting pulmonary abnormalities. However, hypoventilation remains the major cause of hypoxemia. This hypoventilation is mainly due to CO2 consumption during acetate metabolism (acetate dialysis), or alkalinization of the blood (bicarbonate dialysis). The metabolic consequences of acetate metabolism, and of bicarbonate and CO2 losses through the dialyzer are critically analyzed. The cause for the increment in oxygen consumption during acetate dialysis is examined. Finally, the respective role of these combined factors are described and used to explain the changes in VCO2, VO2, respiratory quotient (RQ), and PaO2 reported in the literature during dialysis against acetate and/or bicarbonate.

4 Polycythaemia and thrombocythaemia in the elderly

The investigation of elderly patients presenting with raised PCV values has been described. Suitable clinical and laboratory investigation enables the separation of those with a raised red cell mass (RCM) into three groups: primary proliferative polycythaemia (PPP), secondary polycythaemia and idiopathic erythrocytosis. Those patients with a raised PCV but normal RCM either have apparent polycythaemia (normal plasma volume) or relative polycythaemia (low plasma volume). PPP is a clonal disorder with a peak incidence in the elderly. It commonly presents with vascular occlusive symptoms/signs involving larger vessels, both arterial and venous. The microvasculature may also be involved, particularly when there is associated thrombocythaemia. Effective treatment is required to minimize the future vascular occlusive incidence and diminish the complication rate of surgery if it is ever required. Both the PCV and the platelet count, if elevated, should be adequately controlled. 32P is probably the simplest treatment and is very effective, but venesection and intermittent low-dose busulphan is equally satisfactory in the co-operative patient with good peripheral veins. Secondary polycythaemia may arise from a variety of causes, particularly from arterial hypoxaemia and renal lesions. Occasionally, more than one pathology is identified in the elderly patient. Lung disease is the most common cause of hypoxaemia. Venesection may be indicated in those patients with excessively raised PCV values. The term idiopathic erythrocytosis should only be used for patients who have been adequately investigated. These patients most commonly present with ischaemic or vascular occlusive symptoms/signs. Relative polycythaemia may be caused by fluid loss, but generally the origin of the low plasma volume is not established. Apparent polycythaemia may represent a physiological variant or a stage before the development of a definitely raised RCM. The management of idiopathic erythrocytosis, and relative and apparent polycythaemia, should initially involved removal of known risk factors if present (e.g. hypertension) with the addition of venesection in selected patients. Reactive thrombocytosis in the elderly is most commonly due to malignant disease of chronic infection. The high platelet count is usually asymptomatic, and antiplatelet therapy is rarely required. Primary thrombocythaemia (PT) is a clonal myeloproliferative disorder similar to PPP. The finding of splenomegaly, abnormal platelet morphology or function helps to separate PT from reactive thrombosis. PT most commonly presents with digital or transient cerebral ischaemia or haemorrhage.(ABSTRACT TRUNCATED AT 400 WORDS)