Increased pulmonary vascular resistance and reduced stroke volume in association with CO2retention and inferior vena cava dilatation

2006 ◽  
Vol 101 (3) ◽  
pp. 866-872 ◽  
Author(s):  
Darija Baković ◽  
Davor Eterović ◽  
Zoran Valic ◽  
Žana Saratlija-Novaković ◽  
Ivan Palada ◽  
...  

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO2and O2were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO2increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (∼4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO2retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Temistocle Taccheri ◽  
Francesco Gavelli ◽  
Jean-Louis Teboul ◽  
Rui Shi ◽  
Xavier Monnet

Abstract Background In patients ventilated with tidal volume (Vt) < 8 mL/kg, pulse pressure variation (PPV) and, likely, the variation of distensibility of the inferior vena cava diameter (IVCDV) are unable to detect preload responsiveness. In this condition, passive leg raising (PLR) could be used, but it requires a measurement of cardiac output. The tidal volume (Vt) challenge (PPV changes induced by a 1-min increase in Vt from 6 to 8 mL/kg) is another alternative, but it requires an arterial line. We tested whether, in case of Vt = 6 mL/kg, the effects of PLR could be assessed through changes in PPV (ΔPPVPLR) or in IVCDV (ΔIVCDVPLR) rather than changes in cardiac output, and whether the effects of the Vt challenge could be assessed by changes in IVCDV (ΔIVCDVVt) rather than changes in PPV (ΔPPVVt). Methods In 30 critically ill patients without spontaneous breathing and cardiac arrhythmias, ventilated with Vt = 6 mL/kg, we measured cardiac index (CI) (PiCCO2), IVCDV and PPV before/during a PLR test and before/during a Vt challenge. A PLR-induced increase in CI ≥ 10% defined preload responsiveness. Results At baseline, IVCDV was not different between preload responders (n = 15) and non-responders. Compared to non-responders, PPV and IVCDV decreased more during PLR (by − 38 ± 16% and − 26 ± 28%, respectively) and increased more during the Vt challenge (by 64 ± 42% and 91 ± 72%, respectively) in responders. ∆PPVPLR, expressed either as absolute or as percent relative changes, detected preload responsiveness (area under the receiver operating curve, AUROC: 0.98 ± 0.02 for both). ∆IVCDVPLR detected preload responsiveness only when expressed in absolute changes (AUROC: 0.76 ± 0.10), not in relative changes. ∆PPVVt, expressed as absolute or percent relative changes, detected preload responsiveness (AUROC: 0.98 ± 0.02 and 0.94 ± 0.04, respectively). This was also the case for ∆IVCDVVt, but the diagnostic threshold (1 point or 4%) was below the least significant change of IVCDV (9[3–18]%). Conclusions During mechanical ventilation with Vt = 6 mL/kg, the effects of PLR can be assessed by changes in PPV. If IVCDV is used, it should be expressed in percent and not absolute changes. The effects of the Vt challenge can be assessed on PPV, but not on IVCDV, since the diagnostic threshold is too small compared to the reproducibility of this variable. Trial registration: Agence Nationale de Sécurité du Médicament et des Produits de santé: ID-RCB: 2016-A00893-48.


1993 ◽  
Vol 264 (1) ◽  
pp. H14-H20
Author(s):  
S. Gelman ◽  
S. E. Curtis ◽  
W. E. Bradley ◽  
C. T. Henderson ◽  
D. A. Parks ◽  
...  

An earlier study has shown that angiotensin and catecholamines were responsible for the vasoconstriction observed in the isolated hindlimb preparation during aortic cross-clamping. That study also demonstrated that when vasoconstriction was blocked with an alpha-adrenergic antagonist, phenoxybenzamine, vasodilation was elicited by aortic cross-clamping. The present study tested the hypothesis that this vasodilation was mediated via beta-adrenergic receptors. Eighteen dogs had their hindlimb denervated, vascularly isolated, and pump perfused with blood drained from the inferior vena cava, after passing through a gas-exchanging membrane where oxygen and carbon dioxide tensions were normalized. Left and right thoracotomies were performed, and the aorta and inferior vena cava were cross-clamped. The cross-clamping was associated with 29-37% increase in limb vascular resistance in control dogs (n = 6), in animals pretreated with propranolol (2 mg/kg, n = 6), and in dogs pretreated with a combination of phenoxybenzamine (3 mg/kg) and propranolol (2 mg/kg, n = 6). In animals pretreated with a combination of phenoxybenzamine, propranolol, and enalaprilat (2 mg/kg, n = 6), an angiotensin-converting enzyme inhibitor, limb vascular resistance did not change. This study has confirmed that aortic cross-clamping is associated with vasoconstriction induced by angiotensin and activation of alpha-adrenoceptors and has further demonstrated that vasodilation is attributable to beta-adrenoceptor activation.


1983 ◽  
Vol 54 (6) ◽  
pp. 1585-1589 ◽  
Author(s):  
J. B. Philips ◽  
R. K. Lyrene ◽  
M. McDevitt ◽  
W. Perlis ◽  
C. Satterwhite ◽  
...  

Intrapulmonary injections of prostaglandin D2 (PGD2) reduce pulmonary arterial pressure and resistance in fetal and hypoxic neonatal lambs without affecting systemic arterial pressure. This apparently specific pulmonary effect of PGD2 could be explained by inactivation of the agent during passage through the pulmonary capillary bed. We therefore studied the effects of both pulmonary and systemic infusions of PGD2 on the acute vascular response to a 1-min episode of hypoxia in newborn lambs. Since PGD2 has been reported to be a pulmonary vasoconstrictor in normoxic lambs, we also evaluated its effects during normoxemia. Pulmonary vascular pressures were not affected by either 1- or 10-micrograms . kg-1 . min-1 infusions into the left atrium or inferior vena cava during normoxia. Infusion of 1 microgram . kg-1 . min-1 PGD2 into the inferior vena cava decreased pulmonary vascular resistance and increased systemic arterial pressure. These two parameters were unchanged with the other three infusion regimens. Mean pulmonary vascular resistance rose 83% with hypoxia and no PGD2. PGD2 prevented any change in pulmonary vascular resistance with hypoxia, while systemic arterial pressure increased (1-microgram . kg-1 . min-1 doses) or was unchanged. Thus PGD2 specifically prevents hypoxic pulmonary vasoconstriction while maintaining systemic pressures, regardless of infusion site. PGD2 may be indicated in treatment of persistent pulmonary hypertension of the newborn and other pulmonary hypertensive disorders.


2019 ◽  
Vol 8 (5) ◽  
pp. 717
Author(s):  
Hee-Sun Park ◽  
Sung-Hoon Kim ◽  
Yong-Seok Park ◽  
Robert H. Thiele ◽  
Won-Jung Shin ◽  
...  

The aim of this study was to analyze whether the respiratory variation in electrocardiogram (ECG) standard lead II R-wave amplitude (ΔRDII) could be used to assess intravascular volume status following inferior vena cava (IVC) clamping. This clamping causes an acute decrease in cardiac output during liver transplantation (LT). We retrospectively compared ΔRDII and related variables before and after IVC clamping in 34 recipients. Receiver operating characteristic (ROC) curve and area under the curve (AUC) analyses were used to derive a cutoff value of ΔRDII for predicting pulse pressure variation (PPV). After IVC clamping, cardiac output significantly decreased while ΔRDII significantly increased (p = 0.002). The cutoff value of ΔRDII for predicting a PPV >13% was 16.9% (AUC: 0.685) with a sensitivity of 57.9% and specificity of 77.6% (95% confidence interval 0.561 – 0.793, p = 0.015). Frequency analysis of ECG also significantly increased in the respiratory frequency band (p = 0.016). Although significant changes in ΔRDII during vena cava clamping were found at norepinephrine doses <0.1 µg/kg/min (p = 0.032), such changes were not significant at norepinephrine doses >0.1 µg/kg/min (p = 0.093). ΔRDII could be a noninvasive dynamic parameter in LT recipients presenting with hemodynamic fluctuation. Based on our data, we recommended cautious interpretation of ΔRDII may be requisite according to vasopressor administration status.


Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 179-192 ◽  
Author(s):  
Matthew J. Kaptein ◽  
John S. Kaptein ◽  
Christopher D. Nguyen ◽  
Zayar Oo ◽  
Phyu Phyu Thwe ◽  
...  

2013 ◽  
Vol 29 (7) ◽  
pp. 471-475 ◽  
Author(s):  
Emily A Wood ◽  
Rafael D Malgor ◽  
Antonios P Gasparis ◽  
Nicos Labropoulos

Background Perforation of the inferior vena cava by filters struts is a known complication. The goal of our review is to assess the impact of inferior vena cava perforation by filters based on an open, voluntary national database. Methods We reviewed 3311 adverse events of inferior vena cava filters reported in Manufacturer and User Facility Device Experience database from January 2000 to June 2011. Outcomes of interest were incidence of inferior vena cava perforation, type of filter, clinical presentation, and management of the perforation, including retrievability rates. Results Three hundred ninety-one (12%) cases of inferior vena cava perforation were reported. The annual distribution of inferior vena cava perforation was 35 cases (9%), varying from seven (2%) to 70 (18%). A three-fold increment in the number of adverse events related to inferior vena cava filters has been noted since 2004. Wall perforation as an incidental finding was the most common presentation ( N = 268, 69%). Surrounding organ involvement was found in 117 cases (30%), with the aorta being the most common in 43 cases (37%), followed by small bowel in 36 (31%). Filters were retrieved in 97 patients (83%) regardless of wall perforation. Twenty-five (26%) cases required an open procedure to remove the filter. Neither major bleeding requiring further intervention nor mortality was reported. Conclusions Inferior vena cava perforation by filters remains stable over the studied years despite increasing numbers of adverse events reported. The majority of filters involved in a perforation were retrievable. Filter retrieval, regardless of inferior vena cava wall perforation, is feasible and must be attempted whenever possible in order to avoid complications.


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