Systemic to Pulmonary Bronchial Blood Flow in Heart Failure

Agostoni, Piergiuseppe; Doria, Elisabetta; Bortone, Franco; Antona, Carlo; Moruzzi, P

doi:10.1378/chest.107.5.1247

Cited by 16 publications

(10 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However the results of several studies provide indirect evidence that changes in bronchovascular conductance may be related to changes in pulmonary function and symptoms of congestion in HF (Cabanes et al 1992; Lockhart et al 1992; Wetzel et al 1993; Agostoni et al 1995; McIlveen 2000). In an early study of anesthetized mini-pigs, Wetzel and colleagues (1993) demonstrated that intravascular volume loading resulted in bronchial mucosal engorgement and decreased airway cross sectional area.…”

Section: Introductionmentioning

confidence: 99%

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

Ceridon

Morris

Hulsebus

et al. 2011

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

The aim of this study was to determine the relationship between airway blood flow (Q̇aw), airway conductance (Gf-aw) and pulmonary function in patients with stable HF. 12 controls (CTRL: age=63±9yr, FVC=98±15%pred, LVEF=61±6%) (all data presented as mean±SD), 16 patients with mild HF (HF-A, NYHA I–II: age=64±9yr, FVC=90±17%pred, LVEF=28±6%), and 14 patients with moderate/severe HF (HF-B, NYHA III–IV: age=65±6yr, FVC=84±12%pred, LVEF=26±6%) were studied. Q̇aw was assessed using soluble gas measurements; perfusion pressure across airway bed (ΔPaw) was estimated from systemic and pulmonary pressure measurements; Gf-aw was calculated as Q̇aw/ΔPaw; PF was assessed by spirometry. While Q̇aw was not significantly different between CTRL (61.3±17.9 μL·min−1·ml−1), HF-A (70.1±26.9 μL·min−1·ml−1) and HF-B (56.2±14.9 μL·min−1·ml−1) groups, Gf-aw, was elevated in HF-A (1.1±0.4 μL·min−1·ml−1·mmHg−1, p<0.03) and tended to be elevated in HF-B (1.2±0.6 μL·min−1·ml−1·mmHg−1, p=0.07) when compared to CTRL (0.8±0.3 μL·min−1·ml−1·mmHg−1). Significant positive correlations were found between Gf-aw and RV/TLC for HF-A (r=0.63, p<0.02) and HF-B (r=0.58, p<0.05). These results support the hypothesis that increased bronchial conductance and bronchial congestion may be related to greater small airway obstruction and as such may play a role in the PF abnormalities and symptoms of congestion commonly observed in HF patients.

show abstract

Section: Introductionmentioning

confidence: 99%

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

Ceridon

Morris

Hulsebus

et al. 2011

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

show abstract

“…A major redistribution of bronchial venous return could modify the VO 2 difference. Agostoni et al [19] have demonstrated high bronchial blood flow in patients with heart failure (89 ml.min )1 : 2.1% of cardiac output) and mitral stenosis (76 ml.min )1 : 2.1% of cardiac output). We cannot exclude this possibility, although our patients did not have any pre-existing clinical pathology.…”

Section: Discussionmentioning

confidence: 99%

Estimation of pulmonary oxygen consumption in the early postoperative period after thoracic surgery

et al. 2007

View full text Add to dashboard Cite

SummaryLung injury, including pneumonia, can occur in the early postoperative period following thoracic surgery. Pulmonary oxygen consumption is thought to increase in patients with pulmonary infection. This study measured oxygen consumption in relationship to lung injury in the early postoperative period after thoracic surgery. Thirty-five patients who underwent thoracoabdominal oesophagectomy for oesophageal cancer were studied. Measured oxygen-consumption was obtained by indirect calorimetry and calculated oxygen-consumption was simultaneously determined by the reverse Fick method. The difference in oxygen consumption was attributed to pulmonary oxygen consumption. The difference in oxygen consumption increased to 23.1 ml.min .m )2 on postoperative day 2. In patients with pneumonia the difference in oxygen consumption increased significantly to 39.0 ml.min )1 .m )2 the day before clinical onset of pneumonia, and it increased further to 65.7 ml.min )1 .m )2 on the day that pneumonia became clinically apparent. These findings suggest that the difference in oxygen consumption may be useful for estimating the extent of lung injury and for predicting pulmonary complications in the postoperative period. In recent years, there has been increasing interest in the measurement of oxygen consumption (VO 2 ) in critically ill patients as VO 2 is related to the clinical outcome of this population. VO 2 can be measured either by indirect calorimetry, using analysis of respiratory gas exchange, or with the reverse Fick method, as the product of thermodilution cardiac output and arterial-venous oxygen content difference. Lung tissue and a considerable part of the bronchial tree are metabolically active and consume oxygen. Theoretically, the difference in oxygen content between arterial and venous blood does not include the effect of pulmonary tissue and bronchial tree oxygen uptake. Thus lung VO 2 (VO 2pulm : including that from part of the bronchial tree) should be reflected as a difference between VO 2 measured by gas exchange (VO 2meas ) and that derived using Fick's principle (VO 2Fick ). Despite this sound theoretical basis, methodological limitations can make this small difference undetectable under clinical conditions. Under carefully controlled experimental conditions, however, a constant difference between VO 2meas and VO 2Fick has been demonstrated. In previous studies [1][2][3][4][5], the difference was widely variable and some of the measurements indicated greater values with reverse Fick than with indirect calorimetry. Errors and variation of gas exchange, thermodilution cardiac output, haemoglobin and saturation measurements may accumulate, and the difference between VO 2meas and VO 2Fick may be less than the cumulative methodological error. Previous studies have demonstrated that the difference between VO 2meas and VO 2Fick , taken to represent VO 2pulm , increases once pneumonia develops [1,2,[5][6][7][8][9][10]. Accordingly, VO 2pulm might be one of the indices reflecting the extent of lung injury.In the ear...

show abstract

“…These include 1) left heart stretch which has been shown through reflex mechanisms to increase bronchial conductance [26], 2) a rise in left atrial pressure and pulmonary vascular pressures that may cause a reduction in flow from the bronchial vascular bed, through an increased resistance to forward flow, leading to fluid stasis and possible vascular distension due to an increased volume [15, 27], 3) a rise in circulating inflammatory mediators may cause further increases in conductance in the bronchial circulation [28, 29], 4) the release of other vasoactive substances (e.g., atrial natriuretic peptide, ANP, brain natriuretic peptide, BNP, bradykinin, angiotensin II) that influence vascular tone and overall fluid handling [30, 31] (Figure 1). Furthermore, the chronic hyperventilation (cooling) and hypocapnia (low CO 2 ) associated with HF may further alter flow in this vascular bed [32–34].…”

Section: Altered Control Of the Bronchial Circulation In Hfmentioning

confidence: 99%

Section: Bronchial Blood Flow In Human Heart Failure Patients During mentioning

confidence: 99%

“…Only one study has examined directly how bronchial blood flow is altered in an HF patient population [27]. This study examined bronchial blood flow in subjects undergoing procedures requiring total cardiopulmonary bypass [27]. Patients were divided into 3 groups: those with HF (EF<40%) for less than 2 months (acute HF), patients with conditions and a history of HF (EF#x0003C;40%) lasting longer than 6 months (chronic HF), those undergoing surgical procedures with no conditions or history of HF (non-HF, EF#x0003E;60%).…”

Section: Bronchial Blood Flow In Human Heart Failure Patients During mentioning

confidence: 99%

See 1 more Smart Citation

Does the bronchial circulation contribute to congestion in heart failure?

2009

View full text Add to dashboard Cite

Summary Pulmonary congestion is a hallmark feature of heart failure and is a major reason for hospital admissions in this patient population. Heart failure patients often demonstrate restrictive and obstructive pulmonary function abnormalities; however, the mechanisms of these functional declines remain controversial. It has been suggested that the bronchial circulation may play an important role in the development of these pulmonary abnormalities and in the symptoms associated with pulmonary congestion. Congestion may occur in the bronchial circulation from either a marked increase in flow or an increase in blood volume but with a reduction in flow due to high cardiac filling pressures and/or high pulmonary vascular pressures (a stasis like condition). Either may lead to thickened bronchial mucosal and submucosal tissues and reduced airway compliance resulting in airway obstruction and restriction and a lack of airway distensibility. These structural changes may contribute to “cardiac asthma” and dyspnea, characteristic features common in HF patients. Thus the bronchial circulation may be a potential target for therapeutic interventions. The aim of this paper is to review factors governing the control of the bronchial circulation, how bronchial vascular conductance may change with HF and to pose arguments, both supporting and in opposition to the bronchial circulation contributing to congestion and altered pulmonary function in HF. We ultimately hypothesize that the engorgement of the bronchial circulatory bed may play a role in pulmonary function abnormalities that occur in HF patients and contribute to symptoms such as orthopnea and exertional dyspnea.

show abstract

Systemic to Pulmonary Bronchial Blood Flow in Heart Failure

Cited by 16 publications

References 20 publications

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

Estimation of pulmonary oxygen consumption in the early postoperative period after thoracic surgery

Does the bronchial circulation contribute to congestion in heart failure?

Contact Info

Product

Resources

About