Arterial blood gases in bronchial asthma

Miyamoto, Tomofumi; Mizuno, Kenta; Furuya, Koji

doi:10.1016/0021-8707(70)90135-8

Cited by 24 publications

(5 citation statements)

References 9 publications

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“…If airflow obstruction is severe and unrelieved, there may be progression to hypercapnia and metabolic acidosis, the former as a result of muscle fatigue and inability to maintain adequate alveolar ventilation, and the latter a result of lactate production by the respiratory muscles exceeding clearance mechanisms. Analysis of blood gases in three published reports [33][34][35] showed that only 13% of patients had Paco 2 between 45 mm Hg and 60 mm Hg and 4% had values Ͼ 60 mm Hg. Studies 36 -38 of patients with respiratory failure secondary to acute severe asthma using multiple inert gas-elimination techniques have shown that bimodality of V /Q distributions with little shunt is a characteristic feature of their gas exchange; these studies demonstrated a substantial fraction of perfusion is associated with areas of lung with low V /Q ratio.…”

Section: Gas Exchangementioning

confidence: 99%

Acute Asthma in Adults

Rodrigo

Rodrigo²,

Hall

2004

Chest

242

139

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Section: Gas Exchangementioning

confidence: 99%

Acute Asthma in Adults

Rodrigo

Rodrigo²,

Hall

2004

Chest

242

139

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“…Raimondi et al performed a case series study exploring acid-base patterns in patients admitted for acute severe asthma, in correlation with forced expiratory volume in 1 s (FEV 1 ) values [8]. Airway obstruction severity did not seem to correlate significantly with PaO 2 values, a finding also reported in several other studies in the past [18,20,21] and thought to be due to V A /Q mismatch not being connected to air flow rates; moreover, treatment with β-agonists may lead to further widening of V A /Q mismatch. A statistically significant reverse correlation was demonstrated between FEV 1 and PaCO 2 levels.…”

Section: Respiratory Acidosismentioning

confidence: 87%

Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology

Vasileiadis

Alevrakis

Ampelioti

et al. 2019

JCM

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Asthma is a common illness throughout the world that affects the respiratory system function, i.e., a system whose operational adequacy determines the respiratory gases exchange. It is therefore expected that acute severe asthma will be associated with respiratory acid-base disorders. In addition, the resulting hypoxemia along with the circulatory compromise due to heart–lung interactions can reduce tissue oxygenation, with a particular impact on respiratory muscles that have increased energy needs due to the increased workload. Thus, anaerobic metabolism may ensue, leading to lactic acidosis. Additionally, chronic hypocapnia in asthma can cause a compensatory drop in plasma bicarbonate concentration, resulting in non-anion gap acidosis. Indeed, studies have shown that in acute severe asthma, metabolic acid-base disorders may occur, i.e., high anion gap or non-anion gap metabolic acidosis. This review briefly presents studies that have investigated acid-base disorders in asthma, with comments on their underlying pathophysiology.

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“…[ 311 ] Hypercarbia occurs in the presence of arterial oxygen desaturation, severe obstruction and/or ventilatory depression. [ 312 313 314 315 ] Room air oxygen saturation ≥92% is uncommonly associated with complications. [ 316 317 318 ] Patients classified as having a severe asthma attack are best managed in a hospital setting [ Figure 1 ], while those classified as having non-severe asthma exacerbations can be safely managed on an outpatient basis.…”

Section: F Management Of Acute Exacerbations Of Asthmamentioning

confidence: 99%