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3D printing and pulmonology. COVID-19. Lung volume measurements. Pulmonary hypertension.


 

Pulmonary Physiology, Function, and Rehabilitation

Controversies and the clinical value of lung volume measurements

Lung volumes are often measured by body plethysmography or gas dilution. Their clinic importance in decision making is unclear. Though measured differently, predicted sets obtained by plethysmography from Caucasian populations are often used for gas dilution measurements (Ruppel GL. Respir Care. 2012 Jan;57[1]:26). Recently the GLI felt lung volume data were insufficient to develop universal reference equations (Cooper B, et al. Breathe (Sheff). 2017 Sep;13[3]:e56-e64). ERS/ATS guidelines recommend adjusting Caucasian predicted values depending on race, without advising how to adjust the confidence limits. Their algorithms show if the VC is normal, lung volumes are unnecessary, though it is not unusual to see a normal VC with reduced TLC. Does this suggest the VC is more important than the TLC, even if lacking predicted volume equations for non-Caucasians? Because combined obstructive and restrictive abnormalities occur simultaneously, recommendations state severity of impairment be determined by the FEV1 percent of predicted rather than TLC (Pellegrino R, et al. Eur Respir J. 2005;26:948). The value of quantifying other volumes such as FRC and ERV in conditions such as obesity and musculoskeletal defects is also not clear. In obstruction, volumes can indicate air trapping or hyperinflation measuring RV and RV/TLC. Though cutoffs of <80% and >120% of predicted are often used, guidelines discourage this practice, recommending using predicted equations based on age, race, height, and sex, with statistical limits of normal (Ruppel GL. Respir Care. 2012 Jan;57(1):26).

Dr. Said A. Chaaban

Dr. Said A. Chaaban

Further research is needed to define comprehensive racially appropriate predicted equations for lung volumes to support their clinical applicability in decision making, as well as if predicted values by plethysmography are applicable to values obtained from gas dilution.

Dr. Zachary Q. Morris

Dr. Zachary Q. Morris

Said A. Chaaban, MD

Steering Committee Member

Zachary Q. Morris, MD

NetWork Member

Pulmonary Vascular Disease

Pulmonary hypertension associated with atrial septal defect in adults: closing time?

Up to 10% of adults with atrial septal defects (ASDs) can develop pulmonary arterial hypertension (PAH) according to European Guidelines on pulmonary hypertension (PH) (Galie, et al. Eur Heart J. 2016;37[1]:67). If ASD closure is considered, they propose a pulmonary vascular resistance index (PVRi) <4 Wood units (WU) m² as a safe cutoff. Higher PVRi carries a higher operative risk, warranting evaluation in specialized PH centers.

American guidelines (Stout, et al. Circulation. 2019 Apr 2;139[14]:e698) recommend closure in symptomatic patients with a net shunt (Qp/Qs) of >1.5:1. Closure appears safe if pulmonary artery (PA) systolic pressure is <1/2 systemic blood pressure, and PVR / systemic vascular resistance is <0.3. They recommend specialized evaluation for higher pressures and to avoid closure once a net right to left shunt is present (Qp/Qs <1.0).

However, in severe cases, experienced centers have reported some success with a “treat-and-close” approach if post-therapy PVR reaches <6.5 WU (Bradley, et al. Int J Cardiol. 2019;291:127).

Dr. Francisco J. Soto

Dr. Francisco J. Soto

Finally, consider the following when evaluating ASD-associated PAH: 1. A thermodilution cardiac output method should not be used to calculate PVR/PVRi because of confounding recirculation from the intracardiac shunt (Kwan, et al. Clin Cardiol. 2019;42[3]:334). Qp is used instead and is calculated using Fick equation, requiring accurate oxygen saturation measurements. 2. Mixed venous saturation (MvO2) is needed to determine Qs, and PA saturation cannot be used as MvO2 surrogate. MvO2 must be calculated using superior and inferior vena cava saturations. 3. Some patients with idiopathic PAH may have a small coexisting ASD that is not responsible for the abnormal hemodynamics. Closing the ASD in those cases would be contraindicated. 4. Patients may have more than one type of coexistent congenital heart defect.

Francisco J. Soto, MD, MS, FCCP

Steering Committee Member

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