Preoperative assessment of the thoracic surgery patient: pulmonary function testing.

Tests of pulmonary function before thoracic surgery can help to assess the risk of perioperative morbidity and mortality, and are the basis for estimating remaining lung function after resection of lung tissue. Testing has evolved over the past 50 years from reliance on the maximum breathing capacity to a range of studies including spirometry, and measurement of lung volume, diffusing capacity, and arterial blood gases, and the interpretation of these in conjunction with radionuclide scanning. The surgeon must consider both the early postoperative decrement in function and the level to which the patient is expected to recover. Although it is difficult to establish absolute limiting values, and current surgical techniques are blurring the boundary further, the reported experience underlying current guidelines is reviewed.

Clinical aspects of pulmonary embolism.

Pulmonary embolism is a common disease in the United States, affecting as many as 500,000 persons annually. Unfortunately, this disorder is commonly undiagnosed, resulting in significant excess morbidity and mortality. The clinical symptoms and signs caused by pulmonary embolism are nonspecific and may be confused with a variety of other cardiopulmonary disorders having similar presentations. However, accurate diagnostic tests are available for diagnosing pulmonary embolism, even in the face of coexistent cardiopulmonary disorders. This article describes the clinical characteristics of pulmonary venous thromboembolism, reviewing its typical symptoms and signs, its routine laboratory tests, and chest radiographic abnormalities.

Systemic gas embolism complicating mechanical ventilation in the adult respiratory distress syndrome.

Most forms of barotrauma related to mechanical ventilation are known to occur in both adult and pediatric patients. The pressure-driven transfer of gas from the alveolar compartment to the systemic circulation, a devastating complication of ventilatory support in infants, is not generally recognized as a consequence of ventilatory support in adults. Two young adult patients who received ventilatory support with high levels of positive pressure for pneumonia and the adult respiratory distress syndrome developed massive sub-pleural air cysts, interstitial emphysema, and tension pneumothoraces. Despite receiving appropriate treatment for these problems, the patients had recurrent episodes of cerebral infarction, myocardial injury, and a characteristic pattern of livedo reticularis. This distinctive triad of findings, otherwise unexplained and occurring in the setting of cystic barotrauma, is highly suggestive of systemic gas embolism. Although our patients presented with dramatic clinical features, we believe that patients with ventilator-related gas embolism may present more commonly with subtler signs, such as puzzling disturbances in heart rhythm or mental status, seizure activity, hypotension, localized pain, or other embolic manifestations readily ascribed to other causes in critically ill patients.

Humid air increases airway resistance in asthmatic subjects.

Eight persons with asthma were exposed to seven air conditions varying in temperature (37 degrees C to 49 degrees C [98.6 degrees F to 120.2 degrees F]) and water content (44 mg H2O per liter to 79 mg H2Oper liter) . Normocapnic hyperventilation for three minutes at 40% maximal voluntary ventilation was carried out for each condition. A constant-volume body plethysmograph measured the functional residual capacity and specific airway conductance (SGaw), followed by two forced expiratory manuevers. Measurements were taken before and 1, 5, 10, and 20 minutes after each challenge. Air conditions with 100% relative humidity caused a fall in the SGaw that was maximal in 1 minute. Air conditions at 100% relative humidity caused a greater fall in both the forced expiratory volume in 1 second (FEV1) (P<.05) and the SGaw (P<.005) than did conditions of the same temperature but less water content. At 44 degrees C and 100% relative humidity, the mean percent change in FEV1 and SGaw was -2% and -40%, respectively, at 1 minute after challenge. Of the conditions examined, the optimal temperature was 44 degrees C, and we speculate that the optimal water content is less than 44 mg H2O per liter. Inhaled water concentrations exceeding 44 mg H2O per liter should probably not be used in patients with asthma.

Independently measured oxygen consumption during reduction of oxygen delivery by positive end-expiratory pressure.

Oxygen consumption (VO2) is often assumed to be fixed by metabolic demand, but some investigators have found VO2 linearly dependent on O2 delivery (QT-CaO2) during positive end-expiratory pressure (PEEP) trials for the adult respiratory distress syndrome. However, in those studies VO2 was calculated using the same cardiac output (QT) and O2 content measurements used to calculate the O2 delivery to which it was being compared. We therefore obtained independent measurements of VO2, QT, and oxygen contents under 3 conditions in 21 dogs: 14 normal dogs, each receiving varying degrees of PEEP or central venous obstruction, and 7 dogs receiving PEEP after developing pulmonary edema from intravenously infused oleic acid. In all groups, VO2 measured from expired gas analysis remained unchanged until QT-CaO2 was reduced to below 13 ml/kg/min. The VO2 was then linearly dependent on QT-CaO2. We conclude that this reduction in VO2 is due to severe QT-CaO2 reduction and not to any special effect of PEEP or lung injury.

Transmission of airway pressure to pleural space during lung edema and chest wall restriction.

To investigate the influence of positive end-expiratory pressure (PEEP) on hemodynamic measurements we examined the transmission of airway pressure to the pleural space during varying conditions of lung and chest wall compliance. Eight ventilated anesthetized dogs were studied in the supine position with the chest closed. Increases in pleural pressure were similar for both small and large PEEP increments (5-20 cmH2O), whether measured in the esophagus (Pes) or in the juxtacardiac space by a wafer sensor (Pj). Increments in Pj exceeded the increments in Pes at all levels of PEEP and under each condition of altered lung and chest wall compliance. When chest wall compliance was reduced by thoracic and abdominal binding, the fraction of PEEP sensed in the pleural space increased as theoretically predicted. Acute edematous lung injury produced by oleic acid (OA) did not alter the deflation limb pressure-volume characteristics of the lung, provided that end-inspiratory volume was adequate. With the chest and abdomen restricted OA was associated with less than normal transmission of airway pressure to the pleural space, most likely because the end-inspiratory volume required to restore normal deflation characteristics was not attained. Together these results indicate that the influence of acute edematous lung injury on the transmission of airway pressure to the pleural space depends importantly on the peak volume achieved during inspiration.

Flow resistance of exhalation valves and positive end-expiratory pressure devices used in mechanical ventilation.

We studied the flow-impeding characteristics of the exhalation valves and PEEP attachments commonly used in mechanical ventilation. To characterize these devices, the pressure difference across each mechanism was measured at a series of constant flows (5 to 160 L/min), and resistance-related energy dissipation was measured using mechanical models of passive and active exhalation. At ambient end-expiratory pressure, an inflatable diaphragm (mushroom) design commonly used to valve exhalation presented resistance comparable to that of an endotracheal tube with an internal diameter of 5 mm. The valve's energy dissipation increased further as PEEP was applied. By comparison, the servo-actuated scissor valve we tested presented less resistance during the passive deflation experiment but impeded the early phase of active exhalation. Spring-loaded PEEP attachments were prohibitively resistive in comparison with alternative methods using an underwater tube, a water column, a weighted spirometer, or an inflatable diaphragm to raise end-expiratory pressure. We conclude that the exhalation valves and PEEP attachments currently available for clinical use present significant impedance to air flow. Such resistance within the exhalation pathway may be clinically important for patients supported by mechanical ventilation during the hyperpneic or weaning phases of their illness.

The inspiratory work of breathing during assisted mechanical ventilation.

We quantified the mechanical work of breathing in six normal subjects during assisted mechanical ventilation. Using two volume-cycled ventilators of different design, we investigated the influence of minute ventilation (VE) and machine settings of trigger sensitivity and flow during CO2-driven hyperventilation to moderate and high levels (12-24 L/min). Work estimates were derived from plots of esophageal and airway pressure against inflation volume. Peak flow and trigger sensitivity were important determinants of the energy expended, and for each combination of machine settings the work done by the subject per liter of ventilation increased with VE. During assisted ventilation the subject expended energy equivalent to 33-50 percent of the work of passive inflation, even under the most favorable conditions of VE, sensitivity and flow. Under the least favorable conditions of VE, sensitivity and flow, the subject's inspiratory work of breathing substantially exceeded the energy needed by the ventilator to inflate the passive thorax. These observations imply that exertion of the respiratory muscles continues throughout inflation during assisted mechanical ventilation and call attention to the possibility that inappropriate selection of ventilatory mode or machine settings may contribute to respiratory muscle fatigue and dyspnea.

Regional blood flow during cardiopulmonary resuscitation in dogs using simultaneous and nonsimultaneous compression and ventilation.

We studied regional blood flow (QR) using radiolabeled microspheres and measured hemodynamic variables in 20 anesthetized dogs in normal sinus rhythm and during ventricular fibrillation treated with cardiopulmonary resuscitation (CPR). Nonsimultaneous compression and ventilation CPR (NSCV-CPR) was performed in seven dogs with a pneumatic piston that gave 50 chest compressions/min with an open airway with 10 ventilations at an airway pressure of 33 mm Hg interposed between each fifth and sixth compression. Simultaneous compression and ventilation (SCV-CPR) was performed in seven dogs with the piston and in six other dogs with a circumferential pneumatic vest. Both devices gave 30 compressions/min simultaneously with 30 ventilations that elevated airway pressure to 80 mm Hg., The abdomen was bound during SCV-CPR. Regional blood flow (mean +/- SD) to the cerebral hemispheres, cardiac ventricles, and kidneys, expressed as ml/min/100 g tissue, was 3.1 +/- 4.0, 3.4 +/- 3.3 and 1.5 +/- 1.5, respectively, during NSCV-CPR; 11.5 +/- 5.9, 4.9 +/- 4.7 and 2.7 +/- 2.7 during SCV-CPR (vest); and 16.2 +/- 7.2, 11.0 +/- 4.0 and 20.1 +/- 20.2 during SCV-CPR (piston) (all p less than 0.05 compared with NSCV-CPR). These results indicate that QR to all organs studied is reduced below normal sinus rhythm levels during CPR for ventricular fibrillation, QR to the brain is proportionately greater than QR to the heart and kidneys, and QR to the brain is greater with both forms of SCV-CPR than with NSCV-CPR.

Estimation of transmural cardiac pressures during ventilation with PEEP.

Assessment of ventricular performance during positive end-expiratory pressure (PEEP) requires accurate measurement of transmural cardiac pressures. We investigated the influence of PEEP on the atrial and juxtacardiac pressures estimated by different methods in eight dogs. Left atrial pressure was measured by hydraulic and transducer-tipped catheter systems. Juxtacardiac pressure was estimated by an esophageal balloon and by air- and fluid-filled mediastinal wafer sensors. The supine canine heart was observed radiographically to lift and tilt during PEEP subjecting the left atrial catheters and the fluid-filled mediastinal wafer to a hydrostatic pressure increase. The esophageal balloon seriously underestimated the pressure increment occurring during the application of PEEP in the supine (but not prone) position, perhaps because mediastinal weight was lifted from the esophagus during lung distension. Similar phenomena were also observed in three human subjects. We conclude that lung distension lifts and tilts the heart in a supine preparation causing a hydrostatic increase of intracavitary pressure and attenuation of the esophageal pressure increment. These effects help to account for the apparent alterations of ventricular compliance and performance previously attributed to PEEP.

Effect of positive end-expiratory pressure on canine ventricular function curves.

Recent observations have been interpreted to suggest altered ventricular function during ventilation with positive end-expiratory pressure (PEEP), apart from the effect of reduced preload. We constructed ventricular function curves in 14 anesthetized dogs as PEEP was varied under closed- and open-chest conditions. The systemic venous flow of the animal was diverted through an external circuit so that blood return to the right atrium could be varied stepwise from 1--4.5 l/min before and after 15 cmH2O PEEP was applied to the airway. Pressures adjacent to the heart were measured with thin fluid-filled water sensors to enable estimation of transmural pressure. Alterations in ventricular function were assessed by comparing tangential slopes as well as the atrial pressure differences separating the curves at high and low stroke volumes. Sensitivity of this method to cardiac depression was demonstrated by similar comparisons made before and after propranolol. Curves using transmural pressure on and off PEEP were statistically indistinguishable. We conclude that hemodynamic changes resulting from PEEP are attributable to the combined effects of reduced preload and raised juxtacardiac pressure, without ventricular dysfunction.

Mechanical effect of lung distention with positive pressure on cardiac function.

To investigate the contribution of local mechanical factors to the alteration in ventricular function that occurs during ventilation with positive end-expiratory pressure (PEEP), the hemodynamic effects of increasing end-expiratory pressure with both lungs ventilated, and with the upper lobes, lower lobes, right and left lungs selectively ventilated, were examined in 20 anesthetized open-chest dogs. The rise in pressure between the lungs and heart exceeded that of the ipsilateral atrium. Increasing PEEP with both lungs ventilated caused atrial and mediastinal (juxtacardiac) pressures to increase and stroke volume to decrease more than with ventilation of smaller lung volumes. Patterns causing distention of lung tissue adjacent to the right heart were associated with the greatest decrease of stroke volume. Decreasing stroke volume related more closely to increasing right atrial than to left atrial pressure. We concluded that juxtacardiac pressure increases markedly as the lungs distend, even in an open-chest preparation, and that preload reduction on this basis, not ventricular impairment, best explains diminished cardiac output during ventilation with PEEP.

Lung volume and pleural pressure effects on ventricular function.

To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.

Respiratory distress syndrome from lymphangiography contrast medium.

Adult respiratory distress syndrome (ARDS) has been reported as a rare complication of lymphangiography with ethiodized oil. We report 2 patients who developed otherwise unexplained pulmonary edema after lymphangiography, and describe an animal model of pulmonary injury after an injection of ethiodized oil. We injected 0.25 ml/kg of body weight intravenously into 45 rabbits, and followed arterial blood gases and/or killed the rabbits randomly at various intervals for morphologic lung examination by light and electron microscopy. Within 24 h after injection, there was moderate hypoxemia from oil embolization, but only minimal lung edema. However, by 2 to 4 days after injections, hypoxemia was most severe and was accompanied by extensive alveolar and interstitial inflammation, hemorrhage, and edema. After 4 days, there was gradual blood gas and morphologic recovery, with complete restoration of normal anatomy by 6 wk. Our data showed that in rabbits, ethiodized oil can reproducibly cause delayed, severe pulmonary injury, thus supporting the clinical reports that ARDS may occur several days after lymphangiography.

New developments in cardiopulmonary resuscitation.

The traditional concept of cardiopulmonary resuscitation (CPR) is that the heart is squeezed between the sternum and the spine during external cardiac massage to create a pressure gradient that forces blood from the heart to the periphery. Although the heart may actually be squeezed in some persons by this maneuver, a newer view of CPR holds that closed-chest compression produces a generalized rise in intrathoracic pressure that is applied to the pulmonary vascular bed as well as the heart. Thus, the heart does not serve primarily as a pump during external cardiac massage but instead acts as a conduit for blood from the lungs. Furthermore, flow into extrathoracic vessels depends on their tendency to remain open or to collapse: forward flow occurs across the head during CPR because a pressure gradient is developed between the carotid artery and the more compressible jugular vein. These ideas have potential clinical implications and greatly increase our understanding of the physiology of CPR.

Pressure outside the extrapulmonary airway in dogs.

We have measured the static and dynamic transmural pressures of extrapulmonary airways during positive pressure lung inflation in anesthetized dogs suspended in the standing position. Thin, fluid-filled catheters measured pressures within and on the anterior surface of the airways in the mediastinum and neck. The change from mediastinal to cervical static extra-airway pressures (Pea) was not abrupt but occurred through the thoracic outlet and the root of the neck. The static Pea in the mediastinum was more positive than pleural pressure when lung volume was increased with positive pressures. During forced deflation equal pressure points (EPP) were in labor bronchi from which airway narrowing extended towards the mouth. Under these conditions, the dynamic mediastinal Pea mouthward of the EPP remained close to pleural pressures even at high volumes. This suggested that forces of restitution generated in the surrounding tissues by the narrowing of the airways did have a small effect in reducing the pressure affecting their anterior surface.