Category Archives: Physiology

Hyperventilation Syndrome

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While reviewing a CPET I noticed the patient had a low PETCO2 throughout exercise and an elevated Ve-VCO2 slope. In addition the patient’s minute ventilation was on the high side (75% of predicted) at peak exercise. This is something you might expect to see in association with pulmonary vascular disease but the subject had a normal DLCO; normal spirometry; their oxygen saturation was normal at all times; and they had a normal maximum VO2 and a normal VO2 at anaerobic threshold. Since there didn’t seem to be any clinical reason for the low PETCO2 I had to wonder whether it was due to hyperventilation syndrome (HVS).

Hyperventilation syndrome is something that everybody “knows” about but is still somewhat ill-defined and this is at least partly because it is most often diagnosed solely by patient-reported symptoms. My lab does not have any diagnostic criteria for hyperventilation syndrome and for this reason I decided to review the literature on the subject.

Hyperventilation syndrome is usually suspected when a patient has rapid, shallow breathing with an irregular breathing frequency and with frequent sigh breaths. Common complaints are dizziness, dry mouth, tingling sensations in the hands and feet and often in combination with chest pain. These symptoms may raise the suspicion that a patient has hyperventilation syndrome and the classic way to diagnose HVS is has to have the patient perform a Hyperventilation Provocation Test (HVPT). During this test a patient voluntarily hyperventilates for three minutes and is then asked whether they felt the symptoms they had been complaining of occurred while they were hyperventilating.

The causes of HVS are considered to be primarily psychosomatic and the majority of articles written on the subject primarily explore this aspect. There are surprisingly few articles on the physiology of HVS and for this reason the physiological causes and consequences of HVS are poorly understood. Of note, I reviewed a couple dozen textbooks on pulmonary function testing and pulmonary diseases that I have on hand and found hyperventilation syndrome to be mentioned in only one (Cotes) where it merited one relatively small paragraph.

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Vocal cord dysfunction

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Recently I reviewed a set of completely irreproducible spirometry results. The patient had made eight attempts and the FVC, FEV1 and Peak Flow were different every time. In particular, there were frequent stops and starts during exhalation. I’ve always wondered why some patients have so much difficulty with what should be a simple test and although in this particular case it could simply be glottal closure I wondered if it could be Vocal Cord Dysfunction (VCD). For this reason I spent some time reviewing the literature.

Vocal Cord Dysfunction is defined as the paradoxical closure of the vocal cords with variable airflow obstruction that often mimics asthma and in fact VCD is often mistaken for refractory asthma. Unfortunately, for this reason individuals with VCD are often treated with corticosteroids and bronchodilators for years without any improvement of their symptoms.

The gold standard for diagnosing VCD is direct visualization of the vocal cords with a laryngoscope. Characteristically, the anterior (frontal) two-thirds of the vocal cords are closed with a narrow posterior glottal chink. The difficulty with this is that VCD symptoms are often transitory and a large number of patients that are suspected to have VCD are asymptomatic when a laryngoscopy is performed.

Since most PFT labs are not equipped with laryngoscopes nor are they prepared to perform a laryngoscopy at a moment’s notice we have to rely on the tests that measure airflow. Although the wheeze and shortness of breath that accompanies VCD mimics asthma the most common problem associated with VCD is inspiratory obstruction. The flow-volume loop pattern is therefore that of a variable extrathoracic airway obstruction.

VCD_FVL

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The effects of Obesity on lung function

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Obesity has become far more commonplace than it was a generation ago. The reasons for this are unclear and have been attributed at one time or another to hormone-mimicking chemicals in our environment, altered gut biomes, sedentary lifestyles or the easy availability of high calorie foods. Whatever the cause, obesity affects lung function through a variety of mechanisms although not always in a predictable manner.

Spirometry:

Many investigators have shown a relatively linear relationship between an increase in BMI and decreases in FVC and FEV1. These decreases are small however, and FVC and FEV1 tend to remain within normal limits even in extreme obesity. The decreases in FEV1 and FVC tend to be symmetrical which is shown by the fact that the FEV1/FVC ratio is usually preserved in obese subjects without lung disease. Several studies have shown that the decreases in FVC and FEV1 are reversible since a decrease in weight showed a corresponding increase in FVC and FEV1.

In one study a 1 kg increase in weight correlated with a decrease in FEV1 of approximately 13 ml in males and 5 ml in females. The same increase in weight correlated with a decrease in FVC of approximately 21 ml in males and 6.5 ml in females. The greater change in FVC and FEV1 in males than females has been attributed to the fact that males tend to accumulate extra weight primarily in the abdomen.

The notion that abdominal weight has a disproportionate effect on lung function is seconded to some extent by studies that have shown that decreases in FVC and FEV1 correlated better with increases in waist circumference and the waist to hip ratio than with BMI. One study showed a 1 cm increase in waist circumference caused a 13 ml reduction in FVC and an 11 ml reduction in FEV1 across a range of elevated BMI’s.

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