Distribution Of Pulmonary Perfusion Research Articles

Modulation by endogenous opioids of pulmonary vasoconstrictor response to acute lung injury.

The effects of endogenously generated opioids on distribution of pulmonary perfusion (as assessed by radiolabeled microspheres) and overall gas exchange in acute acid-induced lung injury were studied. In 14 anesthesized dogs, sufficient acid was given to one lung to double shunt fraction (Qs/Qt) from 14.2 +/- 0.8 to 32.4 +/- 2.6% (SE). This resulted in a significant decrease in Po2 from 495 +/- 9 to 136 +/- 21 Torr, cardiac output from 2.47 +/- 0.27 to 1.46 +/- 0.15 1/min, and blood pressure from 139 +/- 3 to 116 +/- 5 mmHg and a significant rise in pulmonary arterial pressure from 9.6 +/- 0.8 to 14.9 +/- 0.8 mmHg. After acid instillation, microsphere distribution to the injured lung segments decreased to 50% of the base-line value. At the same time, microsphere distribution in the normal segments increased to 160% of base line. In 7 of the 14 dogs the effects of naloxone (1 mg/kg) given after lung injury were compared with the other 7 animals that were given saline. Naloxone administration caused a significant redistribution of regional pulmonary perfusion such that microsphere distribution in the injured lung segments increased by a factor of 2 at 35 min compared with the animals given saline. Consistent with this finding, Qs/Qt in the naloxone group increased to 34.7 +/- 5.0% at 35 min, whereas that of the saline group decreased to 28.2 +/- 2.5%. The difference between the two groups was significant at 35 min. These changes occurred without further alterations in cardiac output, pulmonary arterial pressure, or systemic blood pressure in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Elevated pulmonary artery systolic storage volume associated with redistribution of pulmonary perfusion.

The possibility that an increased pulmonary arterial systolic storage volume (PASSV) correlates with a significant redistribution of pulmonary perfusion was examined in 30 surgical patients. Right ventricular stroke work index (RVSWI) was used as an index of distribution of pulmonary perfusion. The systolic storage volume was calculated from the pulmonary arterial compliance and mean pulmonary arterial distending pressure. Pulmonary arteriolar pressures were computed by Fourier analysis. Pulmonary arterial compliance was derived from the pulmonary arterial time constant and pulmonary arterial resistance. There was a linear relationship between PASSV and RVSWI (r = .81, p less than .001). Also, a direct correlation was found between RVSWI and pulmonary arterial time constant (r = .45, p less than .01). When the patients were divided into three groups according to the severity of pre-existing disease, linear relationships between PASSV and RVSWI were present in all groups, and the slopes were not different among the three groups. The patients were also divided into two groups based on a storage volume fraction of stroke volume index, to evaluate the effect of other hemodynamic data on the PASSV. Comparison of the two groups revealed that pulmonary arterial pressure and pulmonary arterial compliance were significantly higher in the group with a high storage volume fraction (p = .05 and p = .01, respectively). RVSWI and time constant were also significantly different between the groups (p less than .01 and p less than .01, respectively). We conclude that the pressure work generated by the right ventricle improved the distribution of pulmonary perfusion by increasing PASSV.

Changes in Distribution of Lung Perfusion and Ventilation at Rest and during Maximal Exercise*

A new method for evaluation of changes in the distribution of pulmonary perfusion and ventilation during exercise was applied to normal male volunteers. Ventilation and perfusion scans were done with the subjects seated on a bicycle ergometer. The resting studies utilized krypton 81 (81mKr) for ventilation and technetium 99m (99mTc) macroaggregate albumin intravenously for perfusion. Exercise studies were done when 80 percent of maximum predicted heart rate was maintained for five minutes and utilized 81mKr for ventilation and a tenfold dose of 99mTc for perfusion. Higher dose of 99mTc would minimize the effect of radioactivity left over from the resting study. This method allowed us to assess changes in ventilation and perfusion in normal subjects induced by exercise, but may also be applicable in a variety of cardiopulmonary conditions that affect pulmonary ventilation and perfusion or both.

Pulmonary vascular effects of furosemide on gas exchange in pulmonary edema.

To test the hypothesis that pulmonary vasoactivity of furosemide redistributes blood away from edematous lung, thus improving gas exchange, we studied two groups of 10 dogs each with unilobar oleic acid edema, treating one group with 1 mg/kg furosemide 2 h after the oleic acid. Pulmonary perfusion distribution was determined with radio microspheres. Shunts of the injured lobe, measured from O2 contents of lower lobar pulmonary venous blood, increased significantly (P less than 0.05) at 2 h after injury in both groups. Within 0.5 h after furosemide the lobar shunt decreased in the treated animals from 40.1 +/- 20.6 to 28.6 +/- 20.1% and increased from 21.4 +/- 14.0 to 53.8 +/- 26.9% in the control group (P less than 0.05). Mean fractional lobar perfusion to the injured lobe increased from 18.2 +/- 4.8 to 21.6 +/- 6.4% (P less than 0.05) in the furosemide group but decreased from 20.1 +/- 3.5 to 16.1 +/- 4.4% (P less than 0.05) in the controls. Wet lung-to-body weight ratios of the edematous lobes did not differ between the two groups. Our data suggest the possibility that, before decreasing edema, furosemide improved shunt through pulmonary vascular effects by preferential perfusion of nonflooded alveolar units.

Effect of posture on inter-regional distribution of pulmonary perfusion and V̇aQ̇ ratios in man

Using a gamma camera regional pulmonary perfusion per unit alveolar volume (Q̇ Va and ventilation-perfusion ratios ( V̇aQ̇ were measured in fourteen normal male volunteers in upright, supine, lateral decubitus, prone and prone suspended postures with inhalation and intravenous infusion of radioactive 81Kr m (half-life 13 sec) and inhalation of radioactive 85Kr m (half-life 4.4 h). In the vertical axis, Q̇ Va increased from upper to lower lung regions in upright, lateral decubitus, prone and prone suspended postures but was uniform in supine and within the dependent lung in decubitus postures. Horizontally, Q̇ Va decreased from cranial to caudal in lateral decubitus, prone suspended, and near the diaphragm in supine. Vertically, V̇aQ̇ decreased from upper to lower in all postures except in supine and within the dependent decubitus lung where it increased. V̇aQ̇ tended to increase from cranial to caudal in horizontal postures. The effects of gravity on Q̇ Va and V̇aQ̇ vertical distributions are modified when FRC is low (supine, lower decubitus lung) because perfusion is more funiformly distributed. Horizontal gradients of Q̇ Va and V̇aQ̇ are more pronounced under conditions of high local lung volume but also occur in postures where FRC is low.

Right Ventricular Stroke-Work: An Index of Distribution of Pulmonary Perfusion in Acute Respiratory Failure

To evaluate the possibility that an elevated right ventricular stroke-work index observed in acute respiratory failure correlates with less dead space ventilation, 20 patients requiring mechanical ventilation were studied. Ratio of physiologic dead space to tidal volume was used as an index of distribution of pulmonary perfusion. An inverse linear relationship was found between right ventricular stroke-work index and dead space ratio (r = -0.74, p less than 0.001). No correlation was present between cardiac index and dead space ratio. To evaluate the effects of other hemodynamic data on the distribution of pulmonary perfusion, the patients were divided into two groups based on a dead space ratio. Comparison of the two groups revealed right ventricular stroke-work index was significantly higher in the low dead space ratio group (p less than 0.001). There were no differences in cardiac index, pulmonary-artery pressure, or right atrial pressures. These data suggest that elevated right ventricular stroke-work index in acute respiratory failure is associated with more even distribution of pulmonary perfusion, and that patients with a high dead space ratio were characterized by right ventricular dysfunction when compared to patients with a low dead space ratio.

Effect of nitroglycerin on pulmonary perfusion distribution and gas exchange of normal subjects.

In eight healthy subjects we assessed the effects of 3 mg sublingual nitroglycerin on lung distribution of ventilation and perfusion using 133Xe (sitting, supine and lateral decubitus) and on alveolo-arterial O2 and CO2 partial pressure differences [(PAO2-PaO2), (PaCO2-PACO2)] and physiological dead space to tidal volume ratio (VD/VT) (sitting). In all studied positions, nitroglycerin induced a significant decrease in uppermost perfusion indices, and a significant increase in dependent perfusion indices, without changing the distribution of ventilation. Significant increases in (PaCO2-PACO2) and VD/VT were observed up to 60 min after nitroglycerin. No changes in (PAO2-PaO2) occurred, except for a transient decrease due to transient hyperventilation following nitroglycerin. The redistribution of pulmonary perfusion after nitroglycerin may be attributed to the passive effects of lowered pulmonary vascular pressures, and to possible action on extra-alveolar vessels. The evolution of the indices of pulmonary gas exchange is compatible with the observed redistribution of ventilation/perfusion relationships.

The effect of unilateral PEEP on gas exchange and pulmonary perfusion in canine lobar pneumonia.

Positive end-expiratory pressure (PEEP) has little beneficial effect in improving gas exchange in canine left lower lobe (LLL) pneumonia. This is true because while PEEP improves lobar gas exchange, it also increases relative perfusion (QL) to the diseased lobe. The authors hypothesized that PEEP administered to only the diseased lung would avoid the increased QLLL. Six dogs with LLL pneumonia in which PEEP was applied only to the left lung were observed. The dogs were studied supine and each lung was ventilated separately with 100 per cent O2. Measurements of arterial oxygen tension (PaO2), shunt (Qs/Qt) and lobar distribution of pulmonary perfusion were made before, during, and after 12 cm H2O PEEP. Changes in QLLL expressed as per cent of cardiac output were determined using radiolabeled microspheres. PEEP improved PaO2 from 310 +/- 86 to 532 +/- 58 torr and Qs/Qt from 29 +/- 5 per cent to 12 +/- 5 per cent, returning after PEEP to 337 +/- 84 torr and 26 +/- 5 per cent, respectively. QLLL per cent did not increase during PEEP. These results suggest that unilateral PEEP improves regional gas exchange within the pneumonia lobe, probably by ventilating units which were previously perfused but not ventilated. Further, this improvement in regional gas exchange occurred without the diversion of blood flow towards consolidated lung that occurs with whole-lung PEEP, and so resulted in a substantial net improvement in overall gas exchange.

Pathophysiology of gas exchange and pulmonary perfusion in pneumococcal lobar pneumonia in dogs

We placed an inoculum of Streptococcus pneumoniae type III into a left lower lobe bronchus of six dogs (group P), and in six other dogs (Group C) a sterile control inoculum was used. Measurements of shunt (Qs/Qt) and venous admixture (Qva/Qt) were made immediately before (day 1) and 48 h after (day 3) inoculation. All dogs in group P had extensive lobar pneumonia confirmed radiologically and at autopsy, whereas Group C had only small sterile lesions at the site of inoculation. In group P, mean Qs/Qt and Qva/Qt increased significantly to 0.15 and 0.21, respectively. Mean lobar Qs/Qt, calculated using blood samples from lobar veins at thoracotomy on day 3, was markedly increased in the pneumonia lobe (0.69) compared with the contralateral lower lobe (0.08), and alveolar ventilation of that lobe approached zero. Perfusion of the infected lobe determined by radioactive microspheres showed a variable and statistically nonsignificant decrease between control and infected states that was not affected by oxygen breathing. In group C there was no change between days 1 and 3 in gas exchange or in distribution of pulmonary perfusion. We conclude that hypoxemia in pneumonia was due to both increased shunt and venous admixture in the infected regions, and that local hypoxic vasoconstriction was in most instances ineffective in directing blood flow away from the consolidated lobe.

Effect of isoproterenol on regional pulmonary perfusion and its blockade by propranolol.

Effects of isoproterenol and propranolol on regional pulmonary perfusion were assessed in the dog. In each experiment the right upper lobe was isolated in vivo by a balloon catheter and artificially ventilated with nitrogen, air or 60% oxygen in nitrogen before and after administration of the medicaments listed above. The rest of the lungs kept breathing air spontaneously. Following administration of isoproterenol regional pulmonary perfusion increased in the hypoxic right upper lobe induced by artificial ventilation with nitrogen, but the increase was not observed when isoproterenol was administered following pretreatment with propranolol. Administration of propranolol alone did not induce any change in regional pulmonary perfusion distribution. When artificial ventilation was done in the right upper lobe either with air or 60% oxygen in nitrogen, thus inducing regional less hypoxia or hyperoxia, no change in regional perfusion was observed with any of the medication. Thus isoproterenol reversed regional hypoxic pulmonary vasoconstriction, but its action was blocked by pretreatment with propranolol. Propranolol per se, however, showed no effect on pulmonary vascular responses to the different alveolar oxygen tensions.

Effects of contusion and flail chest on pulmonary perfusion and oxygen exchange.

Localized pulmonary contusions were produced in the right lower lobes (RLL) of 12 anesthetized ventilated dogs, 6 of which had a flail segment in the chest wall over the RLL. Pulmonary oxygen exchange during ventilation with air and oxygen, and the lobar distribution of pulmonary perfusion by radioactive microsphere techniques were measured before and 3 h after contusion, and again after thoracotomy. These were compared to 12 noncontused dogs, 6 of which had a flail segment. Contusion produced an average decrease of 20 Torr in Pao2 during air breathing and an average increase in Qs/Qt of less than 5%, surprisingly small given the doubled weight and average 44% shunt calculated in the contused lobe after thoracotomy. No significant effect of flail or thoracotomy was found, indicating that the presence of an intact chest wall and lung-chest wall interdependence was not a major factor preventing a larger increase in intact whole-animal shunt of contused dogs. Rather, the small effect of this severe lobar injury on whole-animal shunt was due to a 30% decrease in RLL relative perfusion. This reduction was demonstrated to be localized to a smaller hemorrhagic subsection of the contused lobe.

Pulmonary Perfusion Defect and Bronchial Artery Collateral Blood Flow

A five-year-old child with severe congestive heart failure following repair of tetralogy of Fallot was examined for correction of a suspected left-to-right shunt. Lung scan and selective bronchial angiographs demonstrated greatly diminished perfusion to the right upper lobe, which was supplied by a large bronchial artery. Technetium microspheres were injected into the artery for quantification. Subsequently, the artery was occluded by injection of the tissue-adhesive bucrylate. During the following year, radionuclide scans showed improvement in the uniformity and percentage distribution of pulmonary perfusion by way of the pulmonary artery. The child has become asymptomatic following closure of the bronchial vessel.

Pulmonary Function after Uncomplicated Myocardial Infarction

Derangement of pulmonary function following myocardial infarction is related to the severity of hemodynamic dysfunction. Abnormalities of pulmonary function appear even in patients without clinical or radiologic evidence of congestive failure. There is a reduction in vital capacity and rates of air flow. There is evidence for dysfunction of "small airways" and diminished ventilation to dependent parts of the lung. Total lung capacity may be normal or reduced, and residual volume may be increased slightly in uncomplicated myocardial infarction. Residual volume falls with more pronounced pulmonary congestion and edema. Distribution of pulmonary perfusion is altered after myocardial infarction, with a shift of perfusion away from the dependent parts of the lung (bases) towards the apices. Pulmonary gas exchange is impaired, with hypoxemia (due to both ventilation-perfusion inequality and increased shunting); and the diffusing capacity for carbon monoxide is diminished. Dead space is increased. The basic pathophysiologic mechanism responsible for abnormalities of pulmonary function is increased pulmonary water, which may be very minimal with uncomplicated myocardial infarction and stay primarily in the pulmonary interstitial space, but becomes progressively more severe with eventual alveolar flooding and marked impairment of pulmonary function.

Hypertensive pulmonary vascular disease in children. Detection by radioactive nitrogen (13N) inhalation and injection.

Regional lung function has been studied in 16 children with intracardiac shunts and a variety of associated cardiac anomalies using radioactive nitrogen (13N) and a gamma camera-computer system. The distribution and washout of inhaled 13N were usually normal. The distribution of intravenously injected 13N was often abnormal and could be related to local anatomy. The most important finding was delayed clearance by ventilation of intravenously injected 13N in children with an abnormally raised pulmonary/systemic vascular resistance ratio (Rp/Rs) at cardiac catheterisation. The regional localisation of this ventilation-perfusion imbalance could be related in several children to the probable distribution of hypertensive pulmonary vascular disease, predicted either from local anatomy shown at cardiac catheterisation or from the abnormal distribution of pulmonary perfusion. Abnormalities present on breathing air may be partially reversed on breathing 100 per cent oxygen.

Arterial hypoxemia and distribution of pulmonary perfusion after uncomplicated myocardial infarction.

To assess the consequences of myocardial infarction on the lung, pulmonary gas exchange and distribution of pulmonary perfusion and ventilation were studied after uncomplicated myocardial infarction in 35 patients in whom no clinical or radiographic evidence of congestive failure was apparent. Studies were performed in some of the patients during the first and third weeks after infarction and in 7 patients 2 to 6 months later. During the first week, the mean arterial oxygen tension was decreased to 72 mm Hg and the mean alveolar-arterial oxygen tension gradient increased to 47 mm Hg; both values improved in the convalescent phase. The mean arterial oxygen tension was 447 mm Hg and the mean alveolar-arterial oxygen tension gradient was 203 mm Hg while breathing 100 per cent oxygen during the first week after infarction; both values returned to normal in the 2- to 6-month follow-up studies. Distribution of pulmonary perfusion was abnormal in the first week. There was diminution of the normally occurring ver...

Distribution of pulmonary blood flow during the valsalva and Müller maneuvers.

During the Valsalva and Muller maneuvers, the effect of different levels of superatmospheric and subatmospheric alveolar pressures on the distribution of pulmonary perfusion was studied with the 133Xe method in 14 healthy subjects in the sitting position. Significantly increased unevenness was found to attend alveolar pressures of +20 and +40 mm Hg, whereas negative alveolar pressures (-5 to -40 mm Hg) resulted in significantly decreased unevenness of perfusion. The results are interpreted as due mainly to alterations in venous return.

Pulmonary diffusing capacity for carbon monoxide and topography of perfusion during changes in alveolar pressure in man.

Breathholding carbon monoxide diffusing capacity (DlCO) and the topographic distribution of pulmonary perfusion (xenon 133 distribution) were measured in normal seated men before and during graded changes in airway pressure. When airway pressure increased, the preponderance of flow distribution shifted downward in the lung; DlCO varied linearly with airway pressure in the range of −20 to +60 mm Hg. These results confirm, in man, previous observations using isolated lungs, and they show the normal dependence of pulmonary flow topography on alveolar pressure. The associated changes in DlCO suggest that increases in alveolar pressure compress the pulmonary capillary net and make less blood available for CO absorption.

Changes in regional pulmonary function following bronchography.

Spirometric and blood gas studies have shown that pulmonary function is significantly impaired during the course of bronchography but improves rapidly once the patient is allowed to expectorate (1–3). The decrease in the measured lung volumes indicates that the impaired pulmonary function is due, at least in part, to obstruction of the bronchi with contrast material. In addition, it has been demonstrated experimentally that perfusion of a segment of lung will diminish if its alveolar oxygen is depleted (4–6). Also, in acute and perennial asthma, marked abnormalities in the distribution of pulmonary perfusion develop, as indicated by perfusion lung scans (7, 8). This is associated with, and probably secondary to, airway narrowing. Since experimental hypoxia as well as bronchial disease can disrupt the distribution of pulmonary perfusion, it appears reasonable that any material which accumulates in the bronchial tree impairing ventilation also can alter the distribution of perfusion. A perfusion lung scan, ...

Vertical gradient of alveolar size in lungs of dogs frozen intact.

Vertical gradient of alveolar size in lungs of dogs frozen intact.

Distribution of pulmonary perfusion in erect man.

Distribution of pulmonary perfusion in erect man.