Increased Pulmonary Venous Resistance in Morbidly Obese Patients without Daytime Hypoxia

Her, Charles; Cerabona, Thomas; Baek, Sun‐Yong; Shin, Sang‐Wook

doi:10.1097/aln.0b013e3181e4f706

Cited by 13 publications

(11 citation statements)

References 37 publications

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“…The patients in this group were divided into two groups, those patients with a PAD-PCWP gradient of 6 mmHg or higher and those with a PAD-PCWP gradient less than 6 mmHg, to determine the effect of pulmonary venous resistance (PvR) on PASS and other hemodynamic variables. This is because in patients with morbid obesity, increases in PvR contribute to increases in PAD-PCWP gradient, according to a previous study [6]. A PAD-PCWP gradient higher than 6 mmHg has been considered to indicate pulmonary hypertension [17,18].…”

Section: Measurements Of Pulsatile Gas Flowmentioning

confidence: 91%

“…To derive PvR, PA output pressure was computed from the harmonic form of the recorded PA pressure by applying an attenuating factor to its phasic components, for which Fourier analysis was used. The data calculation and Fourier analysis have been described previously in detail [5,6,9]. Since the relationship between PvR/TPVR ratio and PAD-PCWP gradient in morbid obesity [6] is the same as that in ARDS [9], we compared our data in the present study on obesity with those in the previous study on ARDS.…”

Section: Measurements Of Pulsatile Gas Flowmentioning

confidence: 92%

“…We also examined the possibility that a too much increased PBV may actually decrease PASS by decreasing distensibility of PA. We performed this study in patients with morbid obesity without daytime hypoxia. Patients with morbid obesity have been shown to have an increased pulmonary artery diastolicpulmonary capillary wedge pressure (PAD-PCWP) gradient, which reflects an increased pulmonary venous resistance [6]. Since obesity is associated with a low-grade endotoxemia [7], it has been suggested that the mechanism of pulmonary venous vasoconstriction in morbid obesity is similar to that in patients with endotoxemia [8].…”

Section: Introductionmentioning

confidence: 99%

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Change in pulmonary blood volume changes pulmonary artery systolic storage

Her

Kim

Jeon

2013

Journal of Surgical Research

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Section: Measurements Of Pulsatile Gas Flowmentioning

confidence: 91%

Section: Measurements Of Pulsatile Gas Flowmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Change in pulmonary blood volume changes pulmonary artery systolic storage

Her

Kim

Jeon

2013

Journal of Surgical Research

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“…For example, morbidly obese patients have increased pulmonary venous pressure even in the absence of overt pulmonary disease symptoms, such as daytime hypoxia or uncontrolled systemic hypertension [94]. Although there are no clinical trials of the effects of weight loss in obese patients with PH-LHD, such data, taken together with the multiple positive effects of weight loss in terms of hypertension, diabetes, sleep apnoea, exercise capacity etc., should encourage weight management in obese patients with PH-LHD.…”

Section: Review: Ph In Left Heart Diseasementioning

confidence: 99%

Pulmonary hypertension in left heart disease

Guazzi

Galiè

2012

Eur Respir Rev

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Pulmonary hypertension (PH) is a frequent complication of left heart disease arising from a wide range of cardiac disorders. In the clinical classification, PH associated with left heart disease is classified as Group 2, which includes left heart systolic dysfunction, left heart diastolic dysfunction and left heart valvular disease. In the past, rheumatic mitral valve disease was the most common cause of PH in left heart disease; however, today it is more likely to be associated with hypertensive and/or ischaemic heart disease.As the incidence of these conditions is increasing, the number of patients presenting with PH is also increasing and, today, left heart disease represents the most frequent cause of PH. The development of PH in patients with left heart disease is associated with poor prognosis. However, despite the increasingly large number of patients affected and the impact of PH on outcome, there are currently no specific treatment options for these patients.This review gives an overview of the pathophysiology and epidemiology of PH associated with left heart disease, and discusses the challenges associated with its management and treatment.

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“…11 mm for a diagnosis of PAH. [13][14][15][16] Patients with PVH had no other cause of PH identifi ed after evaluation and had a PAOP . 15 mm Hg at rest, increased PAOP .…”

Section: Setting and Populationmentioning

confidence: 99%

End Tidal CO 2 Tension

Hemnes

Pugh

Newman

et al. 2011

Chest

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Background: CO 2 excretion is impaired in pulmonary arterial hypertension (PAH) due to underlying vascular obstruction and increased dead space. Our aim was to determine whether resting end tidal CO 2 (E TCO 2 ) could differentiate patients with PAH from those with pulmonary venous hypertension (PVH) or patients without pulmonary hypertension (PH) and whether successful treatment of PAH resulted in higher E TCO 2 values. Methods: We performed E TCO 2 measurements for fi ve breaths at rest and after a 6-min walk test (6MWT) in patients seen at our pulmonary vascular center. Mean E TCO 2 values were correlated with 6-min walk distance and right-sided heart catheterization data. Results: We enrolled 84 patients with PAH, 17 with PVH without left ventricular systolic dysfunction, and seven with no PH and no severe alterations in pulmonary function testing. E TCO 2 was signifi cantly lower in patients with PAH than in those with no PH and PVH ( P , .0001 PAH vs both groups). E TCO 2 correlated with the pulmonary artery diastolic pressure-to-pulmonary artery occlusion pressure gradient ( r 5 2 0.50, P 5 .0002) and pulmonary vascular resistance ( r 5 2 0.44, P 5 .002). E TCO 2 after 6MWT correlated with walk distance ( r 5 0.34, P 5 .003). In patients with prostaglandin therapy escalation, E TCO 2 increased in those who had clinical improvement, whereas in patients who did not improve clinically, E TCO 2 failed to rise ( P 5 .04). Conclusions: E TCO 2 is a promising tool to differentiate patients with PAH from those with PVH or no PH, correlates with diagnostic and prognostic hemodynamic indicators, and may increase with successful treatment of PAH. CHEST 2011; 140(5):1267-1273Abbreviations: 6MWT 5 6-min walk test; E tco 2 5 end tidal CO 2 ; mPAP 5 mean pulmonary artery pressure; PAd 5 diastolic pulmonary artery pressure; PAH 5 pulmonary arterial hypertension; PAOP 5 pulmonary artery occlusion pressure; PH 5 pulmonary hypertension; PVH 5 pulmonary venous hypertension; PVR 5 pulmonary vascular resistance; RHC 5 right-sided heart catheterization

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Increased Pulmonary Venous Resistance in Morbidly Obese Patients without Daytime Hypoxia

Abstract: A strong correlation between PvR/TPVR ratio and PAD-PCWP gradient suggests that the increased PvR contributes to increased PAD-PCWP gradient in obese patients without daytime hypoxia.

Cited by 13 publications

References 37 publications

Change in pulmonary blood volume changes pulmonary artery systolic storage

Change in pulmonary blood volume changes pulmonary artery systolic storage

Pulmonary hypertension in left heart disease

End Tidal CO 2 Tension

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