scholarly journals SWAN-GANZ AND INTRA-PERICARDIAL PRESSURE GUIDED PERICARDIOCENTESIS IN SCLERODERMA-ASSOCIATED PAH

CHEST Journal ◽  
2021 ◽  
Vol 160 (4) ◽  
pp. A2210-A2211
Author(s):  
Marianna Weaver ◽  
Matthew Taylor ◽  
Karim El-Kersh
Keyword(s):  
1991 ◽  
Vol 17 (2) ◽  
pp. A50
Author(s):  
Jean-Paul Lethor ◽  
Shawn McGlew ◽  
J.Luis Guerrero ◽  
Arthur E. Weyman ◽  
Michael H. Picard

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.


1981 ◽  
Vol 61 (3) ◽  
pp. 34P-34P
Author(s):  
P.J. Oldershaw ◽  
M. St. John Sutton ◽  
P. Kay ◽  
D.G. Gibson
Keyword(s):  

1989 ◽  
Vol 257 (3) ◽  
pp. H726-H733
Author(s):  
G. J. Crystal ◽  
M. R. Salem

Experiments were performed on 14 anesthetized, open-chest dogs to assess myocardial and systemic responses to cardiac tamponade alone (TAMP) and combined with arterial hypoxemia (HYP). Regional blood flow (RBF) was measured with radioactive microspheres and used to compute regional O2 supply. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption (MVO2) was calculated with Fick equation. An increase in pericardial pressure, sufficient to reduce mean aortic pressure (MAP) by 20%, caused proportional decreases in myocardial RBF and MVO2 but had no effect on endo-to-epi flow ratio or on myocardial lactate extraction. TAMP alone decreased RBF and O2 supply in kidney, splanchnic organs, skeletal muscle, and skin, but it had no effect in brain. HYP (arterial PO2, 35 +/- 2 mmHg) during TAMP restored MAP and caused transmurally uniform increases in myocardial RBF that were adequate to maintain MVO2 and lactate extraction. RBF increased sufficiently in brain to maintain regional O2 supply, whereas unchanged or inadequate increases in RBF in other tissues accentuated reductions in O2 supply. During combined TAMP and HYP, local vasodilator mechanisms were capable of maintaining adequate oxygen supply in myocardium and brain but not apparently in the nonvital tissues where these mechanisms were antagonized by reflex vasoconstriction.


1989 ◽  
Vol 66 (1) ◽  
pp. 481-491 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown ◽  
K. G. Warner ◽  
S. Khuri

In 12 dogs, we examined the correspondence between esophageal (Pes) and pericardial pressures over the anterior, lateral, and inferior left ventricular (LV) surfaces. Pleural pressure was decreased by spontaneous inspiration, Mueller maneuver, and phrenic stimulation and increased by intermittent positive pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). To separate effects due to blood flow, we analyzed beating and nonbeating hearts. In beating hearts, there were no significant differences between changes in Pes and pericardial pressures. In arrested hearts, increasing LV pressure by 8 Torr increased pericardial pressures by only 3.6 Torr. With IPPV and PEEP, increases in Pes and pericardial pressures were equal in live hearts and in low-volume arrested hearts (LV pressure = 4 Torr). In high-volume arrested hearts (LV pressure = 12 Torr), the increase in pericardial pressure over the anterior LV surface was less than Pes, whereas that over the lateral and inferior LV surfaces was the same as Pes. At high LV volume, in arrested hearts pericardial pressures decreased less than Pes during negative pressure maneuvers. In another six dogs, external LV configuration and volume were measured. In beating hearts during spontaneous inspiration, Mueller maneuver, and phrenic stimulation (endotracheal tube open), septal-lateral dimension and LV volume decreased by approximately 3% (P less than 0.05). This was also true for PEEP. In arrested hearts, septal-lateral dimension and LV volume decreased only with PEEP. We conclude that 1) the relationship between Pes and pericardial pressures is complex and depends on LV volume, local pericardial compliance, and the means by which Pes is changed, 2) changes in measured pericardial pressures did not completely explain changes in LV configuration, and 3) during different respiratory maneuvers, different forces account for the same observed changes in LV volume and configuration.


1967 ◽  
Vol 20 (1) ◽  
pp. 65-77 ◽  
Author(s):  
NATALIO BANCHERO ◽  
WILHELM J. RUTISHAUSER ◽  
ANASTASIOS G. TSAKIRIS ◽  
EARL H. WOOD
Keyword(s):  

2000 ◽  
Vol 60 (1) ◽  
pp. 28-36 ◽  
Author(s):  
Z. Yuan ◽  
B. Boulanger ◽  
M. Flessner ◽  
M. Johnston

1983 ◽  
Vol 244 (6) ◽  
pp. G604-G612 ◽  
Author(s):  
G. B. Bulkley ◽  
P. R. Kvietys ◽  
M. A. Perry ◽  
D. N. Granger

The local hemodynamic response of the innervated but vascularly isolated colon to decreased systemic perfusion induced by cardiac tamponade was studied in anesthesized dogs as a model of nonocclusive mesenteric ischemia. Increasing levels of pericardial pressure caused progressive decreases in colonic blood flow associated with substantial increases in colonic vascular resistance. These increases in local colonic resistance were proportionately larger than concurrent increases in systemic resistance. The disproportionate response of the colonic resistance vessels was not diminished by colonic (sympathetic) denervation. Reductions of blood flow to 30 ml . min-1 . 100 g-1 resulted in compensatory increases in colonic oxygen extraction such that colonic oxygen consumption remained constant (flow independent) at about 1.5 ml . min-1 . 100 g-1. At blood flows below 30 ml . min-1 . 100 g-1 colonic oxygen consumption was markedly dependent on blood flow. This fundamental relation of colonic oxygen consumption to blood flow was the same whether ischemia was induced by cardiac tamponade, partial mechanical arterial occlusion, or vasoconstrictor (norepinephrine or digoxin) infusion. Furthermore, this relationship was not altered by vasodilation with isoproterenol after the induction of ischemia by any of the above means.


1991 ◽  
Vol 261 (6) ◽  
pp. H1693-H1697 ◽  
Author(s):  
N. W. Scott-Douglas ◽  
M. Traboulsi ◽  
E. R. Smith ◽  
J. V. Tyberg

Pericardial pressure measurement with a balloon transducer requires opening and reapproximating the pericardium. If this instrumentation significantly compromises pericardial volume, the heart may be constrained, exaggerating the magnitude of pericardial pressure and thus altering the left ventricular end-diastolic pressure-volume relationship. In open-chest dogs, we studied the effects of opening the pericardium, inserting a pericardial balloon transducer and myocardial sonomicrometer crystals, and reapproximating the pericardium on the left ventricular end-diastolic pressure-strain relationship (LVEDPSR). After a thoracotomy, sonomicrometer crystals were inserted through small holes (less than 3 mm) in the pericardium to measure LV segment length. A micromanometer with a reference lumen was used to measure LV pressure. LVEDPSRs were recorded in the following situations: 1) before the pericardium was opened (but after the crystals were inserted); 2) after the pericardium was opened, the heart was instrumented (4 pairs of crystals and 1 balloon), and the pericardium was reapproximated with interrupted sutures; and 3) after the pericardium was removed. For each dog, a cubic regression equation was fitted to the data obtained before opening the pericardium, and the 95% confidence intervals for the individual data points were determined. In each case, the LVEDPSR obtained after instrumentation was similar to the LVEDPSR described before opening the pericardium. Furthermore, data obtained after instrumentation were uniformly located within the confidence intervals of the LVEDPSR obtained before opening the pericardium and instrumenting the heart.(ABSTRACT TRUNCATED AT 250 WORDS)


Heart ◽  
1977 ◽  
Vol 39 (1) ◽  
pp. 1-6 ◽  
Author(s):  
J Sutton ◽  
D G Gibson
Keyword(s):  

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