Airway occlusion pressure correlates with central respiratory drive. The airway occlusion pressure (P0.1) may be an excellent predictor of the ability of patients with obstructive lung disease to wean from mechanical ventilation. We describe a new method for measuring P0.1 using digitized signals generated from standard respiratory equipment and a computer program to automatically determine P0.1 values. The accuracy of this new method was tested by comparison with standard analog recorder methods using a mechanical lung model, in ventilated patients in an intensive care unit, and in normal volunteers. In all settings, excellent correlation was obtained between P0.1 measurements by the digital Servo and standard analog methods (r = 0.99). This new method permits accurate and automatic determination of P0.1 in ventilated patients using standard respiratory equipment. The rapid response and ease of use of this method should enable evaluation of a number of physiologic variables involved in respiratory control in ventilated and nonventilated patients.

The purpose of this study was to determine the relationship between recruitment of the DI and SM muscles measured as EMG signal amplitudes, the pattern of respiratory muscle recruitment measured with inductive plethysmography, and the intensity of the sensation of dyspnea, measured with 100 mm VAS. Eighteen normal subjects between the ages of 33 and 47 breathed under two conditions: normal controlled breathing and breathing against an inspiratory resistance at 60 percent of their maximal inspiratory pressure (MIP). The PM, RR, duty cycle (TI/TTOT, and VT were held constant. During resistance breathing, VAS dyspnea was increased when EMG-DI decreased; EMG-SM increased in association with the sensation of dyspnea. During inspiratory resistance breathing, dyspnea markedly increased and rib cage and accessory muscle recruitment was the predominant pattern of breathing. These data suggest that dyspnea may be associated with the recruitment of the accessory respiratory muscles rather than the recruitment of the diaphragm.

Pulmonary nocardiosis is a well-described infection in immunocompromised patients; however, it is less well documented in patients with AIDS. The pulmonary manifestation in 21 HIV-positive patients who developed pulmonary infection with Nocardia asteroides is described. The radiographic picture included lobar or multilobar consolidation (52 percent [11/21]), solitary masses (24 percent [5/21]), reticulonodular infiltrates (33 percent [7/21]), and pleural effusion (33 percent [7/21]). Cavitation was common (62 percent [13/21]), and upper lobes were more commonly involved (71 percent [15/21]). Although the radiographic picture is variable, nocardiosis should be suspected in an HIV-positive patient who has subacute pulmonary disease with an unexplained lung mass or cavitary lesions.

Intensive management of patients with severe head injury offers the best hope of minimizing death and functional disability in a young, working population. Secondary neurologic insult can be decreased by cardiorespiratory support and ICP control from the outset. Rapid neurologic assessment, airway management, and support of circulation are the basis of emergency management for head injury. Patients with severe head injury require intensive care management for two major reasons: management of ICP and management of organ system dysfunction. Care should not be withheld because of initially grim (and inaccurate) prognostic assessment. Newer techniques for assessing the adequacy of cerebral circulation may allow refinement of management strategies in the future.

We evaluated bronchial responsiveness to inhaled albuterol (salbutamol), ipratropium bromide, methacholine, and propranolol in eight heart-lung transplant (HLT) recipients 2.3 +/- 1.5 months (mean +/- SD) (range, 1 to 4.5 months) after HLT. All patients had a restrictive ventilatory defect but none had airflow limitation (FEV1/FVC = 0.93 +/- 0.05) (range, 0.86 to 0.97). Specific airway conductance (sGaw) improved significantly with both albuterol (p less than 0.01) and ipratropium bromide (p less than 0.01) but FEV1 did not. Only one HLT patient had bronchoconstriction with propranolol, whereas all but one were hyperresponsive to methacholine. Prior inhalation of ipratropium bromide blocked the response to methacholine (p less than 0.005). Serial methacholine provocation tests performed in seven long-term survivors of HLT 24.6 +/- 16.0 months (range, 12 to 51 months) after HLT revealed no time-dependent evolution of bronchial hyperresponsiveness to methacholine. Limited maximal airway narrowing to methacholine was seen in five HLT recipients who showed a 29 +/- 4 percent (range, 23 to 35 percent) fall in FEV1 compared with two patients who did not achieve a plateau with a 47 percent and 63 percent fall in FEV1, respectively. These results further our understanding of bronchial responsiveness in the denervated transplanted lung. The findings of stable hyperresponsiveness to methacholine over a prolonged time interval, limited maximal airway narrowing to methacholine, and blockade of methacholine hyperresponsiveness by ipratropium bromide support the concept of denervation hypersensitivity of muscarinic receptors.

Coached efforts at diaphragmatic breathing were assessed as a means of increasing diaphragmatic movement in postoperative patients. Inductive plethysmography was used to measure compartmental tidal volumes of the abdomen (Vab) and the chest (Vc) in eight women (aged 41 +/- 16 years) who had no history of cardiovascular or pulmonary disease. These patients were studied before and after (POD1,3) elective cholecystectomy. In preoperative studies, DB increased the supine value of Vab. The corresponding increase on POD1 represents a similar proportion of the resting value. The postoperative fall in resting and stimulated values of Vab is attributed to the known effects of abdominal surgery on diaphragmatic movement. Hence, DB warrants investigation as a method of prophylaxis against the pulmonary complications of surgery, because diaphragmatic movement is largely responsible for ventilation of the lower lung fields, where atelectasis and infection occur most often.

The long-term CVC allows patients with a variety of diseases to lead a more normal and pain-free life. The use of these catheters has become commonplace in most hospitals, and the physician caring for patients in the ICU will be caring for increasing numbers of patients with an indwelling long-term CVC. Infections of these catheters can be manifested in many different ways: tunnel infections, exit site infections, catheter-related bacteremia, and septic thrombophlebitis. The overwhelming majority of these infections are caused by coagulase-negative staphylococci, but physicians should be aware of the wide variety of organisms that can infect the long-term CVC. The diagnosis of long-term CVC sepsis can be difficult, but the use of quantitative blood cultures for catheters left in place and the Maki method for culturing those catheters that are removed will aid physicians in their quest for diagnostic certainty. The great majority of catheter infections will resolve with antibiotic therapy alone without the need for catheter removal, but there are important exceptions to this general rule. Tunnel infections and fungal long-term CVC infections often require catheter removal for their resolution; septic thrombophlebitis and CR-SCVT require the addition of anticoagulation or fibrinolytic therapy to antibiotic regimens for resolution of the infection, and surgical debridement may be warranted if these modalities fail to resolve the infection.

Although commonly found at autopsy, leukemic infiltration of the lung is rarely recognized as a cause of respiratory symptoms or roentgenographic densities. Previously reported cases of patients who had symptomatic or roentgenographic acute leukemic lung diseases invariably presented with diffuse pulmonary infiltrates. We describe three patients with leukemic involvement of the lung who presented with cough, fever, and localized roentgenographic infiltrates suggestive of bacterial pneumonia. In each case, the diagnosis was made by transbronchial biopsy specimen and confirmed by complete response to chemotherapy. In common with the other reported cases, all of our patients had peripheral blast counts above 40 percent (greater than 6,000 blasts per ml3) at the time the pulmonary diagnosis was made. Leukemic invasion of the lung should be considered in patients with acute leukemia who develop lung infiltrates--whether diffuse or focal--in association with a high peripheral blast count.

Chronic bronchitis is characterized by mucociliary dysfunction resulting from structural and functional defects of cilia and the secretory apparatus. The combination of hypersecretion and ciliary impairment leads to disruption of mucociliary interaction and hence the accumulation of secretions in the lower airways. Cigarette smoke appears to play a critical role in the pathogenesis of chronic bronchitis-associated mucociliary dysfunction. While the excessive lower airway secretions may have only minor effects on the natural course of airflow obstruction, they could transiently compromise airway function during acute exacerbations. In addition, altered aerosol deposition in the airways resulting from excessive airway secretions could influence the airway responses to inhaled irritants and pharmacologic agents. There are currently no direct, non-invasive methods available to assess the quantity and distribution of airway secretions in vivo. Indirect indices such as cough frequency, sputum volume, respiratory function, and mucociliary clearance are nonspecific and subject to misinterpretation. The clinical utility of mucotropic pharmacologic agents and of physical maneuvers directed at removing excessive lower airway secretions is therefore difficult to evaluate objectively.

Cheyne-Stokes respiration is characterized by crescendo-decrescendo fluctuations in tidal volume and respiratory rate interrupted by central apneas. It has long been associated with cardiac disease and has often been cited as a poor prognostic indicator, yet the incidence and immediate significance of CSR in the setting of acute cardiogenic PE is not well defined. Therefore, we studied 95 patients who required MVS because of PE. Breathing patterns were monitored by continuous respiratory inductive plethysmography for a minimum of 12 hours of spontaneous respiration after recovery from PE; CSR was noted in 42 patients (44 percent). There were no significant differences between patients with PE and CSR and those with only PE in regard to LVEF (mean +/- SD, 36 +/- 18 percent vs 33 +/- 16 percent; p = 0.55), reinstitution of MVS within 48 hours (4.8 percent vs 17.0 percent; p = 0.065), or in-hospital mortality (16.7 percent vs 26.4 percent; p = 0.255). We conclude that CSR is a relatively common breathing pattern in patients who required MVS because of cardiogenic PE and does not portend a poor immediate prognosis in this population.

Carbon monoxide poisoning is a major cause of illness and death in the United States. Most cases result from exposure to the internal combustion engine and to stoves burning fossil fuels. Most cases of accidental exposure are preventable if proper precautions are taken; however, when cases arise, their presenting signs and symptoms are nonspecific and often lead to a misdiagnosis resembling a flu-like viral illness. As a result, the incidence of acute CO poisoning is underestimated. The effects of CO poisoning are due to tissue hypoxia, with the CNS and the heart being the most susceptible target organs due to their high oxygen needs. Prolonged hypoxia due to high CO levels may lead to cardiac arrhythmias or arrest (or both) and a variety of neurologic sequelae. Treatment is directed toward the relief of tissue hypoxia and the removal of CO from the body. Severity of poisoning can be divided into three levels based on CO levels in the blood. Administration of normobaric 100 percent oxygen is the therapy of choice for most cases, while hyperbaric oxygen therapy is reserved for severe poisonings.

Silent ischemia is a common finding in coronary artery disease and occurs more frequently than painful episodes in the total ischemic burden. Since painless ischemia places limits on the history, it can encourage physicians to spend more time studying and treating the electrocardiogram and less time with patients, potentially leading to a deterioration in doctor-patient relationship and care. Silent ischemia should be considered only in patients 35 years of age or older who: (a) have a strong family history of early coronary artery disease, or (b) have two major coronary risk factors. Verification is made by performing an electrocardiographic exercise stress test and followed by a thallium-201 electrocardiographic stress test when the electrocardiograms are equivocal. In females it is best to proceed directly to a thallium-201 electrocardiographic stress test because of the frequency of false positives on the exercise electrocardiograms. The results will help determine the indications for further studies and subsequently the need for drug or interventional management. Frequently a history in which symptoms of lower esophageal disorders, hiatal hernia, gastric disease and arthritic pains mimic angina or in fact coexist with ischemic heart disease makes the clinical diagnosis of angina more elusive and difficult. However, a careful unhurried history and an exercise stress test can often differentiate the etiology of the chest pains. A 24-hour ambulatory electrocardiographic recording aids in measuring the total ischemic burden. When the diagnosis and severity of the ischemic syndrome is established, a course of medical therapy tailored to the symptoms and with defined end points is initiated. Since silent ischemia and angina frequently coexist, suppression of the frequency and severity of the anginal episodes will also reduce the episodes of silent ischemia. Symptomatic improvement is thus a guide in the treatment of the total ischemic syndrome. Drug management will usually consist of two or more of the following drugs: a nitrate, beta blocker, calcium channel blocker, and aspirin. A 24-hour ambulatory electrocardiographic recording is helpful in assessing the efficacy of medical management of silent ischemia. Failures in drug management should proceed with coronary angiography, and when indicated, followed by percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery.