Hemodynamic Tolerance and Plasma Volume Variations during Plasma Exchange

1987 ◽  
Vol 10 (5) ◽  
pp. 325-330 ◽  
Author(s):  
B. Guidet ◽  
L. Luquel ◽  
C. De Labriolle Vaylet ◽  
G. Offenstadt

Little is known about mechanisms of systemic hypotension frequently reported during plasma exchange (PE). Type of substitution fluids may interfere with hemodynamic tolerance. In a prospective study, right heart catheterization was performed during 18 PE by filtration with isovolumic substitution. Blood volume was measured with 51Cr tagged erythrocytes and plasma volume (PV) calculated from hematocrit. Substitution fluids were either albumin (A; n = 9) or A + gelatin (A + G; n = 9). In both groups, PE induces significant (p < 0.01) decreases of mean arterial pressure: group A: - 21 ± 14%; group A + G: - 23 ± 15%; of pulmonary wedge pressure: group A: - 41 ± 33%; group A + G: - 36 ± 22%; of cardiac index: group A: - 38 ± 18%; group A + G: - 25 ± 15%. Plasma volume also decreases after PE: group A: - 13.5 ± 4%; group A + G: - 18.5 + 4%. None of the variations are significantly different between the two groups. So we think that substitution with albumin alone has no advantage for hemodynamic tolerance.

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Noa Markovitch ◽  
Shmuel Rispler ◽  
Yair Feld ◽  
Amir Solomonica ◽  
Sergey Yalonetsky ◽  
...  

Introduction: An increase in the pulmonary wedge pressure (PCWP) is associated with an increase in the respiratory effort and the sensation of dyspnea. Hypothesis: We investigated the inverse cause and effect relationship, whether an increase in the respiratory effort can by itself aggravate the hemodynamic congestion. Methods: We scrutinized the cardiopulmonary interactions by simultaneously measuring hemodynamic and respiratory indices in heart failure (HF) patients undergoing right heart catheterization. The immediate effects of the respiratory effort on the hemodynamic indices were analyzed by asking the patients to perform short events of apnea and intentional vigorous breathing. The cardiac waves are superimposed on the respiratory waves in the PCWP. To quantify the respiratory effort, the PCWP was decomposed into cardiac and respiratory waves. The respiratory effort (PRESP) was defined as the peak to peak swing in the respiratory wave that modulated the PCWP. Results: HF patients (n=38) exhibited a high PRESP of 9.0±3.2 mmHg, ~3.5-fold higher than the reported normal respiratory effort. The end-expiratory PCWP rose with PRESP, by 0.83±0.06 mmHg for every 1 mmHg of PRESP (p<0.01). The pulmonary artery pressure (PAP) rose with PRESP by 1.40±0.09 mmHg for every 1 mmHg of PRESP. The changes in the respiratory effort had immediate effect on PCWP, within a single breathing-cycle (t =1.67±0.40 s) in all patients. Interestingly, similar changes in the PCWP with PRESP were obtained in all the patients, independently of the HF etiology. Conclusions: An increase in the respiratory effort is not just a result of cardiac decompensation. The respiratory effort has immediate detrimental effects on the PCWP, PAP and the workloads of the heart. The results highlight the existence of a cardiopulmonary vicious cycle the can lead to progressive decompensation, where the respiratory effort plays a pivotal role.


2019 ◽  
Vol 15 (4) ◽  
pp. 499-502
Author(s):  
Grzegorz Kubiak ◽  
Michał Zakliczyński ◽  
Michał Hawranek ◽  
Michał Zembala ◽  
Piotr Przybyłowski ◽  
...  

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.


2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Michael C. Viray ◽  
Eric L. Bonno ◽  
Nicholas D. Gabrielle ◽  
Bradley A. Maron ◽  
Jessica Atkins ◽  
...  

2020 ◽  
Vol 10 (4) ◽  
pp. 204589402092915 ◽  
Author(s):  
Shelsey W. Johnson ◽  
Alison Witkin ◽  
Josanna Rodriguez-Lopez ◽  
Richard Channick

To describe the frequency with which pulmonary capillary wedge pressure measurements, obtained during right heart catheterization, are falsely elevated and to educate operators on techniques to improve accuracy of pulmonary capillary wedge pressure reporting. Failure to completely occlude pulmonary artery branch vessels during balloon inflation can lead to falsely elevated, “incomplete” pulmonary capillary wedge pressures. Balloon deflation prior to catheter retraction may result in catheter advancement into smaller branch vessels, yielding an inadvertent but more accurate alternative pulmonary capillary wedge pressure. We hypothesized that this phenomenon can be identified on retrospective review of right heart catheterization tracings, which occurs commonly and goes unrecognized by operators. We conducted a retrospective study of patients undergoing right heart catheterization or right heart catheterization and left heart catheterization with computer-generated pulmonary capillary wedge pressure ≥20 from January 2015 to June 2017. Alternative pulmonary capillary wedge pressures were defined as a pulmonary capillary wedge pressure trace during balloon deflation ≥3 mmHg lower than the reported pulmonary capillary wedge pressure. Inter-rater reliability of tracing reviewers was also evaluated. Results showed that, of the 182 tracings reviewed, an alternative pulmonary capillary wedge pressure was identified in 26 or 14.3% of cases. Eleven of these alternative pulmonary capillary wedge pressures were ≤15 mmHg with a calculated pulmonary vascular resistance ≥3 Wood units in 10 patients, re-classifying the etiology of pulmonary hypertension from post-capillary to pre-capillary in 38.5% of cases. For the eight patients for whom left heart catheterization data were available, left ventricular end-diastolic pressure aligned with the alternative pulmonary capillary wedge pressure. In conclusion, inadvertently obtained, but likely more accurate, alternative pulmonary capillary wedge pressures were identified in almost 15% of procedures reviewed from a busy academic institution. As wedge pressures often drive diagnosis and treatment decisions for patients with cardiac and pulmonary pathology, operators should be attuned to balloon deflation as a time when alternative pulmonary capillary wedge pressures may be identified as they are likely more reflective of left ventricular end-diastolic pressure. Additional tools to ensure accuracy of pulmonary capillary wedge pressure reporting are reviewed.


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