Transmural Pulmonary Artery Pressure Research Articles

Physiological and symptom effects of changing posture from sitting to supine, and vice versa, in stable chronic heart failure

Objective The current study aimed to evaluate the effects of supine position in stable chronic heart failure (CHF) patients with systolic dysfunction, their relationship with dyspnoea and differences in NYHA classes.Methods In 17 CHF male patients (61 ± 8 y, NYHA class II 8 NYHA classes III and IV 9) admitted to hospital for clinical stabilization and rehabilitation scopes we measured oxygenation, respiratory mechanics, dynamic lung volumes, haemodynamics, and dyspnoea in sitting vs supine posture (randomized order) when in stable state condition.Results Compared to sitting, supine posture decreased oxygenation and maximal oesophageal swing, increased oesophageal pressure swing, respiratory drive normalized for maximal inspiratory strength, pressure time index, pulmonary artery pressure, transmural pulmonary artery pressure (TM-PAP) and transmural pulmonary artery occlusion pressure (TM-PAOP) (all P< 0.01). The decline in TM-PAP (P =0.0195) and TM-PAOP (P =0.0421) was significantly greater in New York Heart Association class II than III-IV patients. Delta variation in dyspnoea related only with supine value of TM-PAOP and delta change of TM-PAOP (R = - 0.53 and P< 0.0277 ; R = 0.56 and P< 0.0175, respectively).Conclusions In stable CHF patients with systolic dysfunction, supine position is associated with a worsening of oxygenation, respiratory mechanics and haemodynamics but not dyspnoea; patients with less severe heart failure show a greater worsening of transpulmonary pressures. Sensation of dyspnoea seems, at least in part, independent of worsening of cardiac and pulmonary functions.

Relationship of pulmonary arterial pressure to pulmonary haemorrhage in exercising horses

Exercise-induced pulmonary haemorrhage (EIPH) is characterised by blood in the airways after strenuous exercise and results from stress failure of the pulmonary capillaries. The purpose of this experiment was to establish a threshold value of transmural pulmonary arterial pressure at which haemorrhage occurs in the exercising horse. Five geldings, age 4-14 years, were run in random order once every 2 weeks at 1 of 4 speeds (9, 11, 13, 15 m/s); one day with no run was used as a control. Heart rate, pulmonary arterial pressure and oesophageal pressure were recorded for the duration of the run. Transmural pulmonary arterial pressure was estimated by electronic subtraction of the oesophageal pressure from the intravascular pulmonary arterial pressure. Within 1 h of the run, bronchoalveolar lavage was performed and the red and white blood cells in the fluid were quantified. Red cell counts in the lavage fluid from horses running at 9, 11 and 13 m/s were not significantly different from the control value, but after runs at 15 m/s, red cell counts were significantly (P<0.05) higher. White cell counts were not different from control values at any speed. Analysis of red cell count vs. transmural pulmonary arterial pressure indicated that haemorrhage occurs at approximately 95 mmHg. Red cell lysis in the lavage fluid was also apparent at transmural pulmonary arterial pressures above 90 mmHg. We conclude that, in the exercising horse, a pulmonary arterial pressure threshold exists above which haemorrhage occurs, and that pressure is often exceeded during high speed sprint exercise.

Atrial natriuretic peptide levels and pulmonary artery pressure awake, at exercise and asleep in obstructive sleep apnoea syndrome.

Elevated nocturnal plasma atrial natriuretic peptide (ANP) levels were found in patients with obstructive sleep apnoea (OSA). The purpose of our study was to examine the secretion of ANP during the night and to measure changes in oxygen saturation, pulmonary artery pressure and intrathoracic pressure swings in patients with OSA. Moreover, we analysed the secretion of ANP and the pulmonary artery pressure in different behavioural states, e.g. awake, at exercise and asleep. Consecutive apnoeas in non-rapid eye movement (NREM) sleep at the beginning, middle and end of the sleep study were analysed in six patients with obstructive sleep apnoea. In addition, we measured the plasma levels of ANP. The apnoea duration was significantly longer (P< 0.05) at the middle of the sleep study than at the beginning or end. Correspondingly, the end-apnoeic oxygen saturation and end-apnoeic oesophageal pressure were both significantly lower (P< 0.05) in the middle of the sleep study than at the beginning or end. No significant differences were found in the end-apnoeic systolic transmural pulmonary artery pressure (P(PATM)) and the levels of ANP. Evaluation of the ANP levels during different behavioural states revealed that the asleep levels were slightly, but not significantly, higher than the awake levels (0.235+/-0.088 vs. 0.207+/-0.057 nmol/L). However, the highest levels were found during exercise (0.334+/-0.170 nmol/L) with a significant difference compared with the awake and asleep levels. These data suggest that volume effects may be a potent factor in liberating ANP during exercise, but the role of OSA in ANP secretion when asleep is questionable.

Effects of extrathoracic airway obstruction on intrathoracic pressure and pulmonary artery pressure in exercising horses

Abstract Objective To determine whether dorsal displacesment of the soft palate (DDSP) results in pulmonary artery hypertension and leads to increases in transmural pulmonary artery pressure (TPAP); to determine whether pulmonary hypertension can be prevented by prior administration of furosemide; and to determine whether tracheostomy reduces pulmonary hypertension. Animals 7 healthy horses. Procedure Horses were subjected to 3 conditions (control conditions, conditions after induction of DDSP, and conditions after tracheostomy). Horses were evaluated during exercise after being given saline (0.9% NaCI) solution or furosemide. Results Controlling for drug, horse, and speed of treadmill, DDSP-induced increase in intrathoracic pressure was associated with a significant increase in minimum (36 mm Hg), mean (82 mm Hg), and maximum (141 mm Hg) pulmonary artery pressure, compared with values for control horses (30, 75, and 132 mm Hg, respectively). Increases in pulmonary artery pressure did not induce concomitant increases in TPAP. Tracheostomy led to a significant reduction of minimum (53 mm Hg), and mean (79 mm Hg) TPAP pressure, compared with values for control horses (56 and 83 mm Hg, respectively). When adjusted for horse, speed of treadmill, and type of obstruction, all aspects of the pulmonary artery and TPAP curves were significantly decreased after administration of furosemide, compared with those for horses given saline (0.9% NaCI) solution. Conclusions DDSP was associated with increases in pulmonary artery pressure but not with increases in TPAP. Clinical Relevance Expiratory obstructions such as DDSP are likely to result in pulmonary hypertension during strenuous exercise, but may not have a role in the pathogenesis of exercise-induced pulmonary hemorrhage. (Am J Vet Res 1999;60:485-494).

The role of intra-abdominal pressure on splanchnic and pulmonary hemodynamic and metabolic changes during carbon dioxide pneumoperitoneum

Background and Methods: To find an intra-abdominal pressure (IAP) range for laparoscopic procedures that elicits only moderate splanchnic and pulmonary hemodynamic and metabolic changes, including hepatic and intestinal tissue pH and superficial hepatic blood flow, we installed an IAP of 7 and 14 mm Hg each for 30 minutes in 10 healthy pigs (30 ± 4 kg). Results: In parallel with the increase of IAP, the mean transmural pulmonary artery pressure increased (from 25 ± 3 to 27 ± 4 at 7 mm Hg IAP and 30 ± 6 mm Hg at 14 mm Hg IAP, p < 0.05); the pulmonary artery–to–pulmonary capillary wedge pressure gradient also increased (from 17 ± 2.7 to 21 ± 3 mm Hg at 7 mm Hg IAP and 24 ± 4.2 mm Hg at 14 mm Hg IAP, p < 0.01), and the arterial oxygenation decreased ( p < 0.005). Relevant changes at an IAP of 14 mm Hg were observed in right atrial pressure during inspiration (from 7 ± 2 to 12 ± 3 mm Hg, p < 0.0001) and in abdominal aortic flow (from 1.43 ± 0.4 to 1.19 ± 0.3 L/min, p < 0.01). However, transmural right atrial pressure and cardiac output remained essentially unchanged. Portal and hepatic venous pressure increased in parallel with the IAP (portal: from 12 ± 3 to 17 ± 3 at 7 mm Hg IAP and 22 ± 3 mm Hg at 14 mm Hg IAP, p < 0.01; hepatic venous: from 8 ± 3 to 14 ± 6 at 7 mm Hg IAP and 19 ± 6 mm Hg at 14 mm Hg IAP, p < 0.005), but the transmural portal and hepatic venous pressures decreased ( p < 0.01), indicating decreased venous filling. Portal flow was maintained at 7 mm Hg but decreased at 14 mm Hg from 474 ± 199 to 395 ± 175 mL/min ( p < 0.01), whereas hepatic arterial flow remained stable. Hepatic superficial blood flow decreased during insufflation and increased after desufflation. Tissue pH fell together with portal and hepatic venous pH (intestinal: from 7.323 ± 0.05 to 7.217 ± 0.04; hepatic: from 7.259 ± 0.04 to 7.125 ± 0.06, both p < 0.01) at 14 mm Hg. Conclusion: The hemodynamic and metabolic derangement in the pulmonary and splanchnic compartments are dependent on the extent of carbon dioxide pneumoperitoneum. The effect of low IAP (7 mm Hg) on splanchnic perfusion is minimal. However, higher IAPs (14 mm Hg) decrease portal and superficial hepatic blood flow and hepatic and intestinal tissue pH. (Gastrointest Endosc 1999; 49:84-91.)

Effects of airway obstruction on transmural pulmonary artery pressure in exercising horses

Abstract Objective To determine whether laryngeal hemiplegia would increase transmural pulmonary artery pressure (TPAP). Animals 6 horses. Design Horses were studied under 5 conditions: control conditions, after induction of left laryngeal hemiplegia, during obstruction of the left nostril, after placement of an instrumented tracheostomy, and after placement of an open tracheostomy. Horses were evaluated after being given saline solution and after being given furosemide. Procedures Horses were exercised on a high speed treadmill, using a maximum speed of 13 m/s. During each exercise, airway pressures, airflow, esophageal and pulmonary artery pressures, and blood gas partial pressures were measured. Results When adjusted for horse, speed, and obstruction condition, mean TPAP (pulmonary artery pressure – esophageal pressure) and minimum TPAP were significantly lower after administration of furosemide than after administration of saline solution. In horses given saline solution, respiratory obstruction that increased intrapleural pressure significantly increased mean TPAP, and respiratory obstruction that decreased intrapleural pressure significantly decreased minimum TPAP. Conclusions Changes in intrapleural pressure appear to play an important role in pulmonary artery pressure and TPAP. Clinical Relevance Because induction of laryngeal hemiplegia did not increase TPAP, laryngeal hemiplegia is unlikely to contribute to development of exercise-induced pulmonary hemorrhage. (Am J Vet Res 1997;58:897–903)

Pulmonary haemodynamics in obstructive sleep apnoea.

The time course of right ventricular output (RVO) and transmural pulmonary artery pressure (PAP) changes, detected beat-by-beat, were analysed in a sample of obstructive sleep apnoea (OSA) episodes recorded in six patients with OSA syndrome. RVO showed a trend to a decrease during apnoeas, due to a decrease in heart rate, and decreased further in the immediate post-apnoeic period, due to a decrease in right ventricular stroke volume [post-apnoeic RVO = 82.6 +/- 9.3 (SD) % of the value in the immediate pre-apnoeic period; P < 0.01]. Both systolic and diastolic transmural PAP showed a progressive increase throughout apnoeas (from 23.7 +/- 7.3 to 29 +/- 6.9 and from 9.1 +/- 4.4 to 14.3 +/- 3.3 mmHg, respectively, from early to late apnoeic period; P < 0.01), and similarly high values in the late apnoeic and in the immediate post-apnoeic period. Therefore, cardiac output and arterial pressure in the pulmonary circulation undergo simultaneous inverse changes in OSA, similar to what was previously shown in the systemic circulation. Although these data cannot define accurately the behaviour of pulmonary vascular resistance, they suggest that pulmonary vascular resistance could also undergo continuous oscillations in OSA, with recurring peaks detectable between apnoea termination and the immediate post-apnoeic period.

Intrathoracic pressure changes and cardiovascular effects induced by nCPAP and nBiPAP in sleep apnoea patients.

The effect of nasal continuous positive airway pressure (nCPAP) and nasal bi-level positive airway pressure (nBiPAP) on intrathoracic pressure and haemodynamics during wakefulness was studied in a group of nine patients with severe sleep apnoea. No patient took cardiovascular medication. Patients were studied with a Swan Ganz catheter, an arterial line and an oesophageal balloon. nCPAP and nBiPAP were applied in the following pressure sequence: 5, 10 and 15 cm H2O of CPAP and 10/5 and 15/10 cm H2O of nBiPAP. Measurements were made at the end of a 5-min period at each pressure level. Intrathoracic pressure was noted to increase to a level of approximately 50% of the pressure delivered at the mask. At a CPAP of 10 cm H2O and above, as well as at BiPAP of 10/5 or higher, there was a decrease in cardiac output (CO) and cardiac index (CI). CI fell below the normal value in two of the patients. Transmural pulmonary artery pressure (PPAtm) decreased at a CPAP of 15 cm H2O and at both BiPAP levels. Transmural right atrial pressure (PRAtm) decreased at both BiPAP levels. There were no differences in CO, CI, PPAtm and PRAtm between nCPAP and nBiPAP at equal inspiratory pressures. SaO2 increased during BiPAP 15/10 cm H2O, whereas heart rate and arterial blood pressure did not change significantly. The data presented here are consistent with the literature on positive end-expiratory pressure (PEEP) applied via intratracheal tube and are likely to be due to a reduced venous return. It is concluded that nasally applied positive pressure may have acute negative effects on cardiac function in patients with sleep apnoea.

Continuous Negative Extrathoracic Pressure and Positive End-Expiratory Pressure: A Comparative Study in Escherichia coli Endotoxin-Treated Neonatal Piglets

Recent clinical studies have suggested that improvement in pulmonary gas exchange with the use of continuous negative extrathoracic pressure (CNEP) in conjunction with intermittent mandatory ventilation (IMV) may be due to increased pulmonary blood flow. Accordingly, we investigated the effects of CNEP vs positive end-expiratory pressure (PEEP) in ventilated neonatal piglets after Escherichia coli endotoxin was administered to induce pulmonary hypertension. Two experimental groups of piglets with six in each, were subjected to three 30-min alternating periods--6 cm H2O CNEP with 6 cm H2O PEEP, beginning 2 h after endotoxin infusion. End-expiratory lung volume (EELV) increased similarly from baseline (13 +/- 2 mL/kg) with both CNEP (28 +/- 2 mL/kg) and PEEP (29 +/- 2 mL/kg). In addition, the increase in PaO2 from baseline with CNEP (106 +/- 9 to 135 +/- 7 mm Hg) was similar to that with PEEP (114 +/- 11 to 132 +/- 6 mm Hg). Further, no differences were found in dynamic lung compliance, EELV, lung resistance, blood gas indexes, or hemodynamics, including transmural pulmonary artery pressure and pulmonary vascular resistance between CNEP and PEEP. With transpulmonary pressure and transrespiratory pressure equal, CNEP in tandem with IMV is physiologically equivalent to PEEP and IMV.

Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea.

Our purpose was to assess how pulmonary artery pressure changes in relation to hypoxia and oesophageal pressure during obstructive sleep apnoeas. Transmural systolic pulmonary artery pressure (Ppa,STM), oxyhaemoglobin saturation (SaO2) and oesophageal pressure were analysed in two samples of consecutive obstructive apnoeas in each of four patients. In the first samples (samples A; probably recorded during non-rapid eye movement (NREM) sleep), SaO2 swings were small and repetitive. In the second samples (samples B; probably recorded during rapid eye movement (REM) sleep), they were large and more variable. Oesophageal pressure oscillated similarly in the two groups of samples. In all cases, transmural systolic pulmonary artery pressure progressively increased throughout apnoeas, and subsequently decreased in the interapnoeic periods. However, both early and end-apnoeic transmural systolic pulmonary artery pressure, remained stable in samples A; whilst they progressively increased in samples B. Transmural systolic pulmonary artery pressure at the beginning of each apnoea was inversely correlated with SaO2 at the end of the preceding apnoea. These results suggest that transmural systolic pulmonary artery pressure is influenced by SaO2, but does not vary at the same speed as SaO2. In all cases, beat-by-beat analysis showed, as expected, that the lower the oesophageal pressure, the higher the transmural systolic pulmonary artery pressure however, at each oesophageal pressure level, transmural systolic pulmonary artery pressure was more variable and higher, in samples B. In conclusion, transmural systolic pulmonary artery pressure in obstructive apnoeas shows rapid changes, which reflect oesophageal pressure variations, and slower changes, which are likely to be caused by SaO2.

Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury

The present study was designed to evaluate if continuous positive airway pressure (CPAP) augments the effect of nitric oxide (NO) inhalation on matching between ventilation and perfusion (VA/Q) during acute lung injury. Prospective, randomized study. A research laboratory at a university medical center. Ten anesthetized mongrel dogs with oleic acid-induced lung injury. Zero or 40 parts per million of NO in the inspiratory gas, with and without 10 cm H2O CPAP in random order. Gas exchange was assessed by estimating the VA/Q distributions using the multiple inert gas elimination technique. Application of CPAP decreased blood flow to shunt units by 26 +/- 2 percent (mean +/- SD) and increased the fraction of cardiac output to normal VA/Q units (VA/Q ratio of 0.1 to 10) by 26 +/- 2 percent (p < 0.05). Inhalation of NO during CPAP accounted for a further 10 +/- 2 percent decrease in the blood flow to shunt units and an 8 +/- 2 percent increase in the fraction of the cardiac output to normal VA/Q units (p < 0.05). Inhalation of NO alone had no significant effect on the VA/Q distributions. Inhalation of NO decreased mean transmural pulmonary artery pressure (Ppatm) both without (Ppatm from 30 +/- 2 to 23 +/- 2 mm Hg; PVR from 323 +/- 44 to 228 +/- 43 dynes.s .cm-5; p < 0.05) and with CPAP (Ppatm from 25 +/- 2 to 20 +/- 2 mm Hg; PVR from 255 +/- 30 to 173 +/- 31 dynes.s.cm-5; p < 0.05). Although pulmonary vascular resistance can be lowered with NO inhalation alone, recruitment of gas exchange units with CPAP is necessary to produce a beneficial effect of NO inhalation on VA/Q matching and oxygenation. When recruitment of gas exchange units with CPAP brings gaseous NO in contact with enough pulmonary blood vessels, NO-induced vasodilation will augment VA/Q matching by a steal mechanism.

Radiographic Inversion of Pulmonary Blood Flow in Acute Asthma

Chest radiographs are obtained routinely in children hospitalized with asthma but are considered to be of low utility. We describe a previously unreported radiographic inversion of pulmonary artery flow patterns in the chest films of a majority of children and young adults hospitalized for asthma. Seventy-five hospital records of 65 patients aged 2 to 25 years (mean 9.2) admitted for asthma during the calendar year 1991 were reviewed. As compared with the normal pattern, patients with inverted vascularity were younger (mean age 6.75 years), tended to be admitted through the emergency department, and had significantly more signs of labored breathing, such as tachypnea, retractions, nasal flaring, and tachycardia. We propose that the exaggerated respiratory effort in these children raises the transmural pulmonary artery pressure, impeding pulmonary blood flow. This results in distension of the right ventricle, which then compresses the left ventricle in the confines of the pericardium by posterior displacement of the interventricular septum. The resultant loss of left-sided compliance raises the left atrial and pulmonary venous pressures, leading to inversion of vascular markings through the same mechanism as seen in left-heart failure. We conclude that attention to this easily recognized sign will detect presence of the hemodynamically significant respiratory obstruction in asthmatic patients.

Pulmonary edema associated with upper airway obstruction in dogs.

In order to evaluate the effect of acute upper airway obstruction upon pulmonary edema (PE) formation, we studied seven dogs that were subjected to inspiratory obstruction for three hours. Hypoxia was avoided by the administration of supplemental oxygen during the study period. Six dogs developed pulmonary vascular congestion, and four developed histologic findings of PE. Inspiratory intrapleural pressure decreased to -28 +/- 4 mmHg in dogs that developed PE and to -23 +/- 2 mmHg in dogs that did not. Transmural pulmonary artery pressure and pulmonary artery wedge pressure did not increase significantly. Central venous pressure during inspiration (CVPi) increased in all dogs, and CVP at end expiration (CVPe) was significantly higher in dogs with PE. Dogs that developed PE experienced a decrease in cardiac output and an increase in systemic vascular resistance. Furthermore, alveolar ventilation declined in dogs with PE, ultimately resulting in ventilatory failure. Pulmonary edema formation was not preceded by an increase in pulmonary vascular pressures but was associated with higher CVP, pulmonary vascular congestion, and hypercarbia.

Acute Effects of Oxygen Administration on Transmural Pulmonary Artery Pressure in Obstructive Sleep Apnea

In order to investigate the role of hypoxia on the cyclic oscillation of transmural pulmonary artery pressure (PAP) in obstructive sleep apnea, oxygen was administered during one half of the night to six patients affected by obstructive sleep apnea syndrome during a nocturnal polysomnographic study. In each patient, transmural PAP measurements were performed on 15 randomly selected apneas recorded while breathing room air, and on 15 during O2 administration. During O2 administration in all patients, apneas were associated with a higher oxyhemoglobin saturation (SaO2), a smaller SaO2 swing, and a higher transcutaneous PCO2. The mean highest level of transmural PAP in the apneic episodes, commonly reached at their end, was significantly lower than while breathing room air in only two patients; however, due to a decrease in the mean lowest PAP level (at the beginning of apneas), the extent of the PAP increase within apneas did not differ between air and O2 breathing; these patients showed the smallest increase in transcutaneous PCO2 in our sample. End-apneic transmural PAP during O2 administration was significantly higher in one subject (for systolic values) and was not significantly different in the remaining three subjects. The extent of the increase in transmural PAP within apneas was greater in one patient; it was smaller in another one, but only for the diastolic values; and it did not differ significantly with respect to the value observed while breathing room air in all of the other subjects. The results suggest that hypoxia in obstructive apneas, at least in some patients, may lead to a steady increase in PAP, detectable both at the beginning and at the end of the episodes; conversely, the increase in PAP within apneas does not seem to be influenced by the simultaneous decrease in SaO2.

Increased right ventricular compliance in response to continuous positive airway pressure.

The right ventricular hemodynamic effects of incremental continuous positive airway pressure (CPAP) were assessed in 16 studies in nine unanesthetized, spontaneously breathing sheep. In seven sheep, studies were performed before and after the induction of sepsis. CPAP was applied in four increments of 4 mm Hg via a cuffed tracheostomy tube. Cardiac output, right ventricular ejection fraction (RVEF) and right ventricular end-diastolic volume (RVEDV) were assessed by thermodilution. In this model, incremental CPAP produced similar effects in septic and nonseptic studies. Cardiac output was preserved by a progressive increase in heart rate (106 +/- 25 to 126 +/- 29, p less than 0.05) in spite of a significant decline in stroke volume index (49 +/- 7 to 43 +/- 7, p less than 0.05). Transmural pulmonary artery pressure and pulmonary vascular resistance index increased with incremental CPAP whereas RVEF declined (0.38 +/- 0.05 to 0.31 +/- 0.05, p less than 0.05). Transmural right atrial pressure declined significantly (7.7 +/- 1.7 to 4.8 +/- 2.9, p less than 0.05) whereas RVEDV was unchanged. In this study incremental CPAP was associated with an enhancement of right ventricular compliance. Further, right ventricular preload was preserved in spite of the measured increase in intrathoracic pressure and cardiac output was maintained in the face of a CPAP-related increase in right ventricular afterload by compensatory increases in heart rate and right ventricular work.

Compliance of the main pulmonary artery during the ventilatory cycle.

Transmural pulmonary arterial pressure (Ppa), diameter (D), and length (L) of a segment of the main pulmonary artery (MPA) were measured simultaneously in anesthetized open-chest dogs. The instantaneous volume was calculated from D and L. Pulmonary arterial elasticity for diameter (EpD) was calculated as the ratio of the amplitude of Ppa to D oscillation normalized by the mean D. Similar indexes were calculated for L (EpL) and V (Epv). Compliance per unit length was calculated from the dimensions and elasticity of the MPA. Under control conditions with 5 cmH2O positive end-expiratory pressure, EpD, EpL, and Epv at cardiac frequency were 175 +/- 27, 147 +/- 27, and 55 +/- 7 cmH2O, respectively. EpD increased with positive end-expiratory pressure, but EpL decreased and Epv was unaffected. EpD, EpL, Epv, and compliance per unit length were not significantly different between the start of inspiration and the start of expiration. In addition, there were no significant phase differences between the oscillations of Ppa and V at respiratory frequency. We conclude that the previously reported time variation of pulmonary arterial compliance during the ventilatory cycle is not due to time-varying properties of the MPA.

Effects of PEEP on pulmonary hemodynamics in intact dogs with oleic acid pulmonary edema

The effects of positive end-expiratory pressure (PEEP) on the pulmonary circulation were studied in 14 intact anesthetized dogs with oleic acid (OA) lung injury. Transmural (tm) mean pulmonary arterial pressure (Ppa)/cardiac index (Q) plots with transmural left atrial pressure (Pla) kept constant were constructed in seven dogs, and Ppa(tm)/PEEP plots with Q and Pla(tm) kept constant were constructed in seven other dogs. Q was manipulated by using a femoral arteriovenous bypass and a balloon catheter inserted in the inferior vena cava. Pla was manipulated using a balloon catheter placed by thoracotomy in the left atrium. Ppa(tm)/Q plots were essentially linear. Before OA, the linearly extrapolated pressure intercept of the Ppa(tm)/Q relationship approximated Pla(tm). OA (0.09 ml/kg into the right atrium) produced a parallel shift of the Ppa(tm)/Q relationship to higher pressures; i.e., the extrapolated pressure intercept increased while the slope was not modified. After OA, 4 Torr PEEP (5.4 cmH2O) had no effect on the Ppa(tm)/Q relationship and 10 Torr PEEP (13.6 cmH2O) produced a slight, not significant, upward shift of this relationship. Changing PEEP from 0 to 12 Torr (16.3 cmH2O) at constant Q before OA led to an almost linear increase of Ppa(tm) from 14 +/- 1 to 19 +/- 1 mmHg. After OA, Ppa(tm) increased at 0 Torr PEEP but changing PEEP from 0 to 12 Torr did not significantly affect Ppa(tm), which increased from 19 +/- 1 to 20 +/- 1 mmHg. These data suggest that moderate levels of PEEP minimally aggravate the pulmonary hypertension secondary to OA lung injury.

Plasma Levels of Atrial Natriuretic Factor, Renin Activity, and Aldosterone in Patients with Chronic Obstructive Pulmonary Disease: Response to O2Removal and to Hyperoxia

To examine the interrelations between humoral systems involved in the circulatory and body fluid volume homeostasis of patients with chronic obstructive pulmonary disease (COPD), we measured plasma levels of renin activity (PRA), aldosterone (Aldo), and atrial natriuretic factor (ANF) in 14 patients with stable COPD who used continuous O2 therapy. Hemodynamics, blood gases, and plasma hormone levels were measured (1) while patients received supplemental O2; (2) after 30 min O2 discontinuation; and (3) after a 30-min period of 96% O2 breathing. Plasma immunoreactive ANF concentrations were 196 +/- 50 pg/ml during O2 breathing and were positively related to transmural pulmonary arterial wedge pressure (tPpaw, r = 0.90, p less than 0.001) and to PaCO2 (r = 0.57, p less than 0.02). Compared to normal subjects matched for age and sex, patients had higher plasma ANF levels (196 +/- 52 versus 72 +/- 6 pg/ml, p less than 0.01), similar PRA (2.1 +/- 0.5 versus 1.3 +/- 0.3 ng/ml/h, NS), and slightly lower plasma Aldo (98 +/- 17 versus 156 +/- 19 pg/ml, p less than 0.05). Discontinuation of O2 while decreasing PaO2 from 70 +/- 3 to 50 +/- 3 mm Hg resulted in a significant increase in pulmonary arterial pressure (Ppa) from 29 +/- 2 to 32.5 +/- 3 mm Hg (p less than 0.01) and cardiac index (Cl) from 3.6 +/- 0.1 to 3.9 +/- 0.1 L/min/m2 (p less than 0.01) and a decrease in systemic arterial pressure (Psa) from 96 +/- 3 to 91 +/- 2 mm Hg (p less than 0.05); transmural cardiac filling pressures and pulmonary vascular resistance (PVR) were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular performance during bronchospasm in dogs.

In 8 anesthetized mongrel dogs, we studied the effects of carbachol-induced bronchoconstriction (BC) on the cardiovascular system. Inhalation of carbachol in an amount sufficient to produce at least a 50% decrease in lung conductance (GL) did not lead to significant changes in cardiac output, mean transmural left atrial (Pla) or right atrial pressure, end-diastolic left ventricular septal-lateral dimension, left ventricular apex to base dimension, or in end-diastolic right ventricular septal to lateral dimension during expiration. Mean transmural pulmonary arterial pressure rose and mean transmural aortic pressure (Pao) fell during BC. During inspiration, there were significant increases in transmural left atrial pressure, Pla, associated with decreases in end-diastolic left ventricular septal-lateral and apex-base dimensions. End-diastolic right ventricular septal-lateral dimension increased during inspiration. Beat-to-beat aortic flow (Qao) decreased during inspiration, while pulmonary arterial flow increased. There were no changes in transmural Pao during inspiration measured at the nadir of aortic flow. During BC, these changes were exaggerated, but remained qualitatively the same. The magnitude of the inspiratory decrease in pleural pressure (Ppl) was shown to be linearly related to the magnitude of the change in GL, and the magnitude of the inspiratory decrease in Pao and Qao (pulsus paradoxus) was shown to be linearly related to the magnitude of the inspiratory swing in Ppl. Although vagotomy significantly altered the pattern of respiration such that tidal volume increased and respiratory rate decreased, it did not substantially alter the responses of the cardiovascular system to breathing during BC. We conclude: the inspiratory decrease in Pao and Qao (pulsus paradoxus) is associated with a decrease in left ventricular end-diastolic filling, and a stiffening of the left ventricle; these changes are exaggerated during BC as a result of the exaggerated inspiratory swings in Ppl; the effects on left ventricular dynamics are mediated only in part through increases in right ventricular end-diastolic filling operating through the mechanism of ventricular interdependence; changes in left ventricular afterload appear to play little role in determining the responses seen.

Hemodynamics in dogs with pulmonary hypertension due to emphysema

We examined hemodynamic parameters in a canine model of pulmonary emphysema in which the lesion was severe enough to increase transmural mean pulmonary artery pressure (\(P\bar a\bar ptm\)) to about 10 mmHg higher than a control group of dogs. Pulmonary emphysema was produced in 6 dogs (Group E) by the repeated weekly instillations of the enzyme papain administered into their lobar bronchi. In 5 control dogs (Group C), a normal saline solution was used. Pulmonary hemodynamics and gas exchange measurements were obtained after 7 doses of the enzyme were administered when, relative to the prepapain value, total lung capacity had increased by 40% in Group E. Hemodynamic measurements were performed before and after plasma volume expansion to elevate the mean transmural wedge pressure (\(P\bar w\bar ptm\)) to approximately 15 mmHg. At similar cardiac outputs and\(P\bar w\bar ptm\),\(P\bar a\bar ptm\) in Group E were higher than in Group C in both the pre (mean ±SD; 7.3 ± 1.4 mmHg vs 18.5 ± 5.5 mmHg,P < 0.01) and volume-loaded (21.7 ± 2.2 vs 27.9 ± 4.7 mmHg,P < 0.01) conditions. Compared with Group C, arterial blood oxygen tension and diffusing capacity for carbon monoxide were reduced in Group E. Left ventricular performance was normal in Group E, whereas right ventricular performance appeared slightly depressed. The latter finding was explained in terms of a relatively increased right ventricular afterload in Group E, which impeded right ventricular ejection.