scholarly journals Lowering Pulmonary Wedge Pressure after Heart Transplant: Pulmonary Compliance and Resistance Effect

Author(s):  
Nádia Moreira ◽  
Rui Baptista ◽  
Susana Costa ◽  
Fátima Franco ◽  
Mariano Pêgo ◽  
...  
1990 ◽  
Vol 68 (4) ◽  
pp. 1688-1695 ◽  
Author(s):  
A. Nahum ◽  
L. D. Wood ◽  
G. Crawford ◽  
R. Ripper ◽  
L. Segil ◽  
...  

To examine the role of central nervous system injury in the pathogenesis of pulmonary edema, we injected Escherichia coli endotoxin (5 mg/kg) into the cisterna magna of six dogs (group E) and compared, over 4 h, both the pulmonary edema and cerebrospinal fluid (CSF) abnormalities with those in six control dogs (group C). In group E, intracisternal endotoxin raised intracranial pressure from 21 +/- 6 to 38 +/- 8 cmH2O (P less than 0.001), CSF total protein from 18 +/- 6 to 54 +/- 19 mg/dl (P less than 0.001), and CSF malondialdehyde from 0.12 +/- 0.11 to 0.61 +/- 0.35 nmol/ml (P less than 0.05); all were unchanged in group C. When the pulmonary wedge pressure was maintained at 10 mmHg by fluid infusion, extravascular thermal volume in group E increased from 7.2 +/- 1.2 to 12.0 +/- 2.7 ml/kg (P less than 0.005) at 4 h when the excised lungs weighed 13.6 +/- 1.5 g/kg; in group C, extravascular thermal volume did not increase, and the excised lungs weighed less (10.8 +/- 1.3 g/kg, P less than 0.05) than those in group E. The dry weights of the lungs were not different between groups, and the alveolar lining fluid-to-plasma albumin ratio in both groups remained low, 0.1-0.2. Fluid infusion in group E (9.2 +/- 2.9 liters) caused colloid oncotic pressure to decrease 4.5 +/- 2.8 mmHg; colloid oncotic pressure fell less (0.8 +/- 1.9 mmHg, P less than 0.001) in group C as less fluid (2.2 +/- 1.5 liters, P less than 0.001) was required to maintain pulmonary wedge pressure.(ABSTRACT TRUNCATED AT 250 WORDS)


1968 ◽  
Vol 24 (5) ◽  
pp. 640-644 ◽  
Author(s):  
W A Droszcz ◽  
F LaTorre ◽  
J T Reeves

1994 ◽  
Vol 76 (2) ◽  
pp. 750-755 ◽  
Author(s):  
A. Frans ◽  
E. Lampert ◽  
O. Kallay ◽  
B. Nejadnik ◽  
C. Veriter ◽  
...  

We hypothesized that the decrease in single-breath diffusing capacity of CO (DLCO) as observed in patients with Raynaud's phenomenon (P.J. Fahey et al. Am. J. Med. 76:263–269, 1984) may be present in normal subjects. Therefore, we examined 31 healthy subjects in two different laboratories. Two series of experiments were performed. In the first series DLCO was measured in 22 volunteers before (twice) and 5, 10, and 30 min after a cold pressor test (CPT), which consisted of immersing both hands in a 12 degrees C water bath for 2 min. In the second series right heart catheterization was performed in nine healthy seated subjects. Cardiac output, mean pulmonary arterial pressure, heart rate, and pulmonary wedge pressure were measured before, during, and 10, 20, and 30 min after the CPT. In every volunteer the CPT induced a decrease in DLCO that was still present 30 min after the test. In the nine catheterized subjects DLCO increased above control values during the CPT and then decreased below control values for 30 min. The CPT had no effect on cardiac output, heart rate, or pulmonary wedge pressure. In contrast, pulmonary arterial pressure and pulmonary vascular resistance increased during the CPT and then became lower than the control values for at least 30 min. In summary, the CPT induced a biphasic evolution of DLCO in normal subjects, being increased during the CPT and decreased after it. Our data are best explained by the West model of the lung. Our data suggest that the pulmonary Raynaud's phenomenon is not specific to patients with primary Raynaud's phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
Bryan J. Taylor ◽  
Thomas P. Olson ◽  
Chul-Ho-Kim ◽  
Dean Maccarter ◽  
Bruce D. Johnson

We determined whether a non-invasive gas exchange based estimate of pulmonary vascular (PV) capacitance [PVCAP = stroke volume (SV) x pulmonary arterial pressure (Ppa)] (GXCAP) tracked the PV response to exercise in heart-failure (HF) patients. Pulmonary wedge pressure (Ppw), Ppa, PV resistance (PVR), and gas exchange were measured simultaneously during cycle exercise in 42 HF patients undergoing right-heart catheterization. During exercise, PETCO2 and VE/VCO2 were related to each other ( r= -0.93, P < 0.01) and similarly related to mean Ppa (mPpa) ( r = -0.39 and 0.36; P < 0.05); PETCO2 was subsequently used as a metric of mPpa. Oxygen pulse (O2 pulse) tracked the SV response to exercise (r = 0.91, P < 0.01). Thus, GXCAP was calculated as O2 pulse x PETCO2. During exercise, invasively determined PVCAP and non-invasive GXCAP were related (r = 0.86, P < 0.01), and GXCAP correlated with mPpa and PVR (r = -0.46 and -0.54; P < 0.01). In conclusion, noninvasive gas exchange measures may represent a simple way to track the PV response to exercise in HF.


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