<i>Alveolar Dead Space as an Index of Distribution of Blood Flow in Pulmonary Capillaries</i>

Severinghaus, John W.; Stupfel, M

doi:10.1152/jappl.1957.10.3.335

Cited by 257 publications

(56 citation statements)

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“…In normal subjects anatomical and physiological dead spaces are equal but in patients with lung disease physiological dead space is enlarged, which means that more of each breath is useless for the purpose of gas exchange. The difference between physiological and anatomical dead space is called the alveolar dead space and is an index of ventilationperfusion imbalance in the lung (Severinghaus & Stupfel, 1957 (Finucane, Egan & Dawson, 1972;Cotes, 1975). …”

Section: Theoretical Problemsmentioning

confidence: 99%

Ventilation.

Sterling¹

1979

Brit J Clinical Pharma

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Section: Theoretical Problemsmentioning

confidence: 99%

Ventilation.

Sterling¹

1979

Brit J Clinical Pharma

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“…In an experimental study involving glass-bead embolization, alveolar dead space increased proportionate to the degree of pulmonary vascular obstruction in mechanically ventilated goats 15 . Other animal studies have suggested that an increase in the alveolar dead space occurs simultaneously with the onset of pulmonary vascular occlusion 15,16 . Measurement of alveolar dead space in humans has been examined as a method of screening for acute pulmonary embolism 7,19 .…”

Section: Risk Of Postoperative Pulmonary Dysfunctionmentioning

confidence: 99%

“…A large bolus of embolized marrow can block perfusion to a portion of the well-ventilated lung, resulting in a high ventilation-to-perfusion ratio or increased alveolar dead space [7][8][9][10][11][12][13][14][15][16][17] . The method used to prepare the medullary canal may determine the amount of bone marrow extrusion during intramedullary nailing 3,[18][19][20] .…”

mentioning

confidence: 99%

“…However, few patients had an adverse pulmonary outcome, limiting the conclusions of the study. Measurement of alveolar dead space provides a clinical measure of pulmonary vascular occlusion, regardless of the etiology, because it accurately reflects the difference between measurements of alveolar and arterial carbon dioxide 8,[10][11][12][14][15][16]23 . In healthy patients, the ratio should approach 1.0, as carbon dioxide rapidly debonds from the hemoglobin molecule at the alveolar level.…”

mentioning

confidence: 99%

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Pulmonary Dysfunction in Patients with Femoral Shaft Fracture Treated with Intramedullary Nailing

Norris¹,

Patton²,

Rudd

et al. 2001

The Journal of Bone and Joint Surgery-American Volume

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Background: This study was undertaken to determine whether alveolar dead space increases during intramedullary nailing of femoral shaft fractures and whether alveolar dead space predicts postoperative pulmonary dysfunction in patients undergoing intramedullary nailing of a femoral shaft fracture. Methods: All patients with a femoral shaft fracture were prospectively enrolled in the study unless there was evidence of acute myocardial infarction, shock, or heart failure. Arterial blood gases were measured at three consecutive time-periods after induction of general anesthesia: before intramedullary nailing and ten and thirty minutes after intramedullary nailing. The end-tidal carbon-dioxide level, minute ventilation, positive end-expiratory pressure, and percent of inspired and expired inhalation agent were recorded simultaneously with the blood-gas measurement. Postoperatively, all subjects were monitored for evidence of pulmonary dysfunction, defined as the need for mechanical ventilation or supplemental oxygen (at a fraction of inspired oxygen of >40%) in the presence of clinical signs of a respiratory rate of >20 breaths/min or the use of accessory muscles of respiration. Results: Seventy-four patients with a total of eighty femoral shaft fractures completed the study. Fifty fractures (62.5%) underwent nailing after reaming, and thirty fractures (37.5%) underwent nailing with minimal or no reaming. The mean alveolar dead-space measurements before canal opening and at ten and thirty minutes after canal opening were 14.5%, 15.8%, and 15.2% in the total series of seventy-four patients (general linear model, p = 0.2) and 20.5%, 22.7%, and 24.2% in the twenty patients with postoperative pulmonary dysfunction (general linear model, p = 0.05). Of the twenty-one patients with an alveolar dead-space measurement of >20% thirty minutes after nailing, sixteen had postoperative pulmonary dysfunction. According to univariate and multivariate analysis, the alveolar dead-space measurement was strongly associated with postoperative pulmonary dysfunction. Conclusions: According to our data, intramedullary nailing of femoral shaft fractures did not significantly increase alveolar dead space, and the amount of alveolar dead space can predict which patients will have pulmonary dysfunction postoperatively.

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“…(2). However, an alveolar deadspace exists that arises due to causes distal to the alveolar-bronchiolar junction, which must be taken into consideration when determining _ V I 1 : 5,21 This comprises the effects due to both the mismatch of ventilation and perfusion within the poorly ventilated compartment, and uneven distribution of ventilation and perfusion between the healthy and unhealthy compartments. This is captured by the inclusion of a constant correction term, d s , that models the volume of gas that remains in the deadspace (see Fig.…”

Section: Ventilationmentioning

confidence: 99%

Modeling Alveolar Volume Changes During Periodic Breathing in Heterogeneously Ventilated Lungs

Dunn

Whiteley

2010

Ann Biomed Eng

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Abstract-A simplified model of periodic breathing, proposed by Whiteley et al. (Math. Med. Biol. 20:205-224, 2003), describes a non-uniform breathing pattern for a lung with an inhomogeneous gas distribution, such as that observed in some subjects suffering from respiratory disease. This model assumes a constant alveolar volume, and predicts incidence of irregular breathing caused by small, poorly ventilated regions of the lung. Presented here is an extension to this work which, by allowing variable lung volume, facilitates the investigation of pulmonary collapse in poorly ventilated compartments. A weakness of the original model is that a very small alveolar volume is required for periodic breathing to occur. The model presented within, which removes the assumption of constant compartment volume and allows alveolar volume to vary with time, predicts periodic breathing at higher, more realistic alveolar volumes. Furthermore, the predicted oscillations in ventilation match experimental data more closely. Thus the model that allows for alveolar collapse has improved upon these earlier results, and establishes a theoretical link between periodic breathing and atelectasis.

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Alveolar Dead Space as an Index of Distribution of Blood Flow in Pulmonary Capillaries

Cited by 257 publications

References 0 publications

Ventilation.

Ventilation.

Pulmonary Dysfunction in Patients with Femoral Shaft Fracture Treated with Intramedullary Nailing

Modeling Alveolar Volume Changes During Periodic Breathing in Heterogeneously Ventilated Lungs

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