SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Patients with respiratory failure should be approached in a systematic way, with emphasis both in diagnosis and treatment on arterial blood gases. The intelligent assessment of oxygenation, ventilation and acid-base balance, based on physiologic principles, can make the management of these patients very rewarding. The physiologic principles outlined here should be well understood by anyone entrusted with the care of these patients. They provide the cornerstone of diagnosis and management, and will remain valid long after current clinical dogma has been revised.
Patients with acute respiratory failure who have high mortality risk can be analyzed according to the methods outlined above. Some (but not all) of the high mortality risk patients can be identified early in the course of respiratory failure. Temporary support with ECMO is indicated in these patients if there are no signs of irreversible damage.
Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.
Two obese patients with acute respiratory failure are described. Both required mechanical ventilation to reverse the respiratory acidosis. On recovery, the major abnormality was failure of ventilatory response to inhaled carbon dioxide. After oral progesterone (100 mg/day and 20 mg/day, respectively) the slope of the carbon dioxide response line increased from 0,02 to 1,14 I min-1 mmHg-1 and from 0,04 to 1,14 I min-1 mmHg-1, respectively. This was associated with sustained clinical remission in 1 patient.
Three young adults with respiratory failure as a first or early manifestation of acute leukemia were hospitalized. Aggressive support with mechanical ventilation, high fractions of inspired oxygen, and positive end-expiratory pressure provided time for appropriate chemotherapy to be used. One patient was alive, with the disease controlled, 18 months after these events. The other two patients responded to therapy but died subsequently from other aspects of their disease. With the advent of effective specific chemotherapy, the onset of acute respiratory failure in the presence of certain malignancies in young adults should not be considered a terminal event when no other organ is involved.
Both short and longterm effects of positive end-expiratory pressure (PEEP) on oxygenating capacity (OC) were investigated in three groups of patients with acute respiratory failure following multiple trauma (MT). Group A consisted of six patients with "uncomplicated" MT; Group B, eight patients with MT and generalized sepsis; Group C, nine patients with MT and lung contusion. OC was evaluated in terms of PaO2/FIO2 and P(A-a)DO2 on FIO 2 = 1.0. OC was markedly and equally reduced in the three patient groups before use of PEEP. The use of a mean PEEP of 6-7 cm H2O resulted in an initial improvement in mean PaO2/FIO2 of 152.5, 36.1, and 59.2 mm Hg, and an overall improvement of 196.8, 57.5, and 107.0 mm Hg in Groups A, B, and C, respectively. There was a similar improvement in both the initial and the overall effect of PEEP on P(A-a)DO2 in the three groups. The difference in the improvement in OC due to PEEP was statistically significant between Groups A and B. It is concluded that acute respiratory failure following MT includes a wide spectrum of clinical syndromes, and that the improvement in OCT due to PEEP depends on the clinical sydrome that is responsible for the respiratory failure associated with MT.
PEEP is the most important therapeutic intervention in the management of acute respiratory failure. Transitory PEEP disconnection to perform clinically relevant maneuvers is often necessary, but its effect upon PaO2 and physiological shunt in patients requiring high-level PEEP is not clear from the literature. Nine adult patients in severe respiratory failure requiring high-level PEEP therapy were studied. The elimination of PEEP decreased the PaO2 and increased the physiological shunt. Maximum values were reached in about 4 min. Restoration of PEEP after 7.4 min in zero and end-expiratory pressure caused an increase in the PaO2 and decrease in the physiological shunt. Baseline values were restored in about 5 min. In 4 patients having endotracheal suction under hand ventilation with 100% oxygen, the continuous PaO2 recording showed an increase in PaO2 during the maneuver. Therefore, necessary manipulations can be accomplished without fear of negating the salutory effects gained by high-level PEEP therapy.
Patients requiring respiratory support may have normal lungs but inadequate ventilation, or they may suffer from defective pulmonary gas exchange despite adequate ventilation. In the first group some form of mechanical ventilatory support is called for, either pressure-cycled or volume-cycled, used first with an endotracheal tube and only later with a tracheostomy. Weaning the patient from the apparatus requires special care. In cases of pulmonary insufficiency the use of positive end-expiratory pressure has been a major advance. Hemoglobin concentration, cardiac output and renal function must receive attention. Open lung biopsy is of the greatest value when the diagnosis is open to question. Resort to a membrane oxygenator to provide extracorporeal oxygenation of blood can sustain for a time the patient in whom hypoxia is critical in degree.
Eight patients with multiple fractures were all treated for acute respiratory failure. The investigation included catheterization of the right side of the heart, determinations of alveolar-arterial oxygen gradients and studies of serum lipid and coagulation and of water and protein balance. The magnitude of respiratory failure correlated well with the number of fractures, the duration and degree of hypotension, the quantity of fluids and blood administered for resuscitation, the magnitude and duration of positive water balance, and the degree of serum hypoalbuminemia. In three patients, the pulmonary-artery pressures were normal at the onset of respiratory failure. The essential aspects of successful therapy included the early institution of assisted ventilation and the achievement of early negative negative water balance.
During the past nine years 10 patients with the adult form of acid maltase deficiency have been observed at the Mayo Clinic. Three of the adults presented with respiratory failure. In all three the respiratory manifestations dominated the clinical picture and the cause of the respiratory failure (muscle weakness) and the underlying myopathy (glycogen storage disease) were initially unsuspected. Careful evaluation of the respiratory function tests, including the maximal static respiratory pressures, electromyographic examination and histochemical and biochemical studies of muscle biopsy specimens eventually led to the correct diagnosis.
Described are two patients whose initial symptom was acute respiratory failure requiring mechanical ventilation. Initially, the cause of the respiratory failure in each patient was obscure, but diaphragmatic paralysis was subsequently demonstrated fluoroscopically in each case. Further neurologic evaluation then supported the diagnosis of amyotrophic lateral sclerosis. Postmortem examination corroborated this diagnosis.
Acute respiratory failure can be diagnosed using clinical judgment and simple bedside measurement of physiologic function. Respiratory support is based on the pathophysiology of the disorder. Initial therapy is directed at correcting life-threatening hypercapnia, hypoxia, and acidosis. The final outcome is positively influenced by skillful intensive care and a team approach.
Nine medical centers collaborated in a prospective randomized study to evaluate prolonged extracorporeal membrane oxygenation (ECMO) as a therapy for severe acute respiratory failure (ARF). Ninety adult patients were selected by common criteria of arterial hypoxemia and treated with either conventional mechanical ventilation (48 patients) or mechanical ventilation supplemented with partial venoarterial bypass (42 patients). Four patients in each group survived. The majority of patients suffered acute bacterial or viral pneumonia (57%). All nine patients with pulmonary embolism and six patients with posttraumatic acute respiratory failure died. The majority of patients died of progressive reduction of transpulmonary gas exchange and decreased compliance due to diffuse pulmonary inflammation, necrosis, and fibrosis. We conclude that ECMO can support respiratory gas exchange but did not increase the probability of long-term survival in patients with severe ARF.
A modification is proposed to the well-known hypothesis which explains the development of progressive carbon-dioxide retention in patients with acute exacerbations of chronic respiratory failure when they are given supplementary oxygen to breathe. It is suggested that, in these patients, increased production of lactic acid by the brain, due to profound hypoxia, leads to a central hypoxic drive to breathing which is absent in remission when the arterial oxygen tension is higher. Evidence from the literature in support of this modification is sought by comparing the respiratory response to oxygen of patients in an acute exacerbation of respiratory failure with the response of patients in a chronic stable state. Three patients are described in whom the response to oxygen during an acute infective episode was very different from their response when in remission.
A patient with miliary blastomycosis had acute fulminating respiratory failure requiring prolonged external ventilatory support. Treatment consisted of antifungal chemotherapy with two drugs and administration of corticosteroids. Restrictive ventilatory impairment and exercise-induced hypoxemia persist at one year after completion of therapy.
Respiratory failure is a frequent complication of acute pancreatitis. Two clinical studies of this association have demonstrated a high incidence of concomitant hypertriglyceridemia. Experimental studies were carried out using an ex vivo, isolated, perfused, ventilated, canine pulmonary lobe to evaluate the effects of triglyceride elevations on pulmonary mechanics and gas exchange. Control lobes perfused for a four hour period remained stable. When 5g and 10g of triglyceride were added to the perfusate, the lobes became grossly edematous and hemorrhagic. Intrapulmonary shunting developed (23 and 46%), weight gain occurred (130 and 189g), effective compliance decreased, and the pressure-volume deflation curves became abnormal. Free fatty acid (FFA) levels increased markedly during the perfusion periods. When small quantities of FFA were infused directly into the pulmonary artery, similar changes, but less severe, occurred. These studies demonstrate that triglyceride elevations are capable of adversely affecting pulmonary gas exchange and mechanics. Such changes probably occur secondary to FFA release. These data thus add support to the concept that the respiratory insufficiency that is seen in acute pancreatitis could be mediated through triglyceride elevations.
In an 18-month period, we treated 561 patients with mechanical ventilation. Fifty-four (10 percent) of these patients had acute respiratory failure, requiring treatment with positive end-expiratory pressure (PEEP) in excess of 20 mm Hg (range, 20 to 40 mm Hg). All patients were allowed to breathe spontaneously between volume-limited mechanical breaths delivered at a rate sufficient to maintain an arterial pH greater than or equal to 7.35. PEEP was applied until calculated pulmonary venous admixture was minimized. Forty-three (80 percent) of these 54 patients were alive and asymptomatic three months after dischage from the hospital, and tests of pulmonary function were performed on ten patients within one year after hospitalization. Abnormalities in pulmonary function appeared to be reversible, and pulmonary function gradually approached normal within one year. It appears that neither acute respiratory failure nor exposure to high airway pressures caused significant permanent pulmonary damage in the ten patients studied.