Effects of Slow Deep Breathing at High Altitude on Oxygen Saturation, Pulmonary and Systemic Hemodynamics

Om hvordan sakte pust øker oksygennivå når man er på høyfjellet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495772/

Study variables, including SpO2 and systemic and pulmonary arterial pressure, were assessed before, during and after 15 minutes of breathing at 6 breaths/min. At the end of slow breathing, an increase in SpO2 (Study A: from 80.2±7.7% to 89.5±8.2%; Study B: from 81.0±4.2% to 88.6±4.5; both p<0.001) and significant reductions in systemic and pulmonary arterial pressure occurred. This was associated with increased tidal volume and no changes in minute ventilation or pulmonary CO diffusion

From the point of view of oxygen gas exchange, human lungs are highly inefficient, as suggested by the 50–60 mmHg PO2 gap between atmosphere and arterial blood observed at sea level. Indeed, some animal species can reach much higher altitudes than humans without supplement O2 due to several reasons including a lower PO2 gap between atmosphere and arterial blood

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In turn, hypoxemia activates a chemoreflex response leading to increased ventilation, which results in hypocapnia and respiratory alkalosis. Exposure to HA is also associated with pulmonary hypertension and lung fluid accumulation, both of which further contribute to hypoxemia and, in some cases, lead to high altitude pulmonary edema (HAPE)

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Efficiency of ventilation for oxygen may be improved by changing the respiratory pattern in order to optimize the partitioning between alveolar ventilation and airway ventilation, being that the latter useless in terms of gas exchange. This has been reported by Yoga practice

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Destroy user interface control[4] or by regular breathing as obtained during regular rosary praying

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Controlled breathing with low rate and high tidal volume, the so called “slow deep breathing”, has also been shown to improve the efficiency of ventilation by increasing alveolar and reducing dead space ventilation

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Destroy user interface control[6]. Slow deep breathing may also improve arterial oxygenation by increasing alveolar volume and gas exchange at the alveolar capillary membrane level. The latter particularly increases when interstitial lung fluids are increased. Indeed, it has been reported that paced slow deep breathing improves blood oxygenation in subjects chronically exposed to HA

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Destroy user interface control[7] and in patients with congestive heart failure or with chronic pulmonary obstructive disease

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Destroy user interface control[10]. Slow deep breathing might also counteract some hemodynamic effects of hypobaric hypoxia at HA, including the increase in systemic blood pressure

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Destroy user interface control[11], given the evidence that device-guided slow deep breathing reduces elevated blood pressure in hypertensive patients

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495772/bin/pone.0049074.g002.jpg

Our main result is that in healthy subjects exposed to HA, i.e. to a low ambient-air PO2, the change in breathing pattern from a spontaneous rate to a paced frequency of 6 breaths per minute was associated with an improvement of ventilation efficiency, as shown by the significant increase in blood oxygen saturation. This was the case both for acute (Study A) and prolonged (Study B) exposure to HA hypoxia. This increase occurred rapidly and was maintained throughout the slow deep breathing period. Most of the improvement of blood oxygenation was lost within 5 minutes after restoration of spontaneous breathing pattern, and no differences compared with baseline were evident after 30 minutes.

In the present study, we showed for the first time the time course of the response to slow deep breathing, showing that the maximum effect is reached after about 5 minutes and is subsequently maintained. Moreover, we reported for the first time data on the recovery period. In Study B, we extended the recovery period to 30 minutes, which allowed us to observe a progressive reduction of slow deep breathing effects, which are at their highest after 5 minutes, but some continue up to 30 minutes after its termination.

However, the reduction of PtCO2 during slow deep breathing exercise in Study A and the SpO2increase in both studies suggest that slow deep breathing improves the efficiency of ventilation. The lack of reduction of PetCO2 in Study B (table 1) is not in contrast with this interpretation of our findings but merely a technical consequence of the measurement technique.

Indeed, PetCO2 pressure, due to the shape of the CO2 curve during expiration, is higher with lower respiratory frequency. Therefore, a reduction in PaCO2 may actually have occurred during slow deep breathing in both studies.

Moreover, because slow deep breathing is associated to a reduction of sympathetic tone (see below), the improvement of ventilation/perfusion matching may also originate by more respiratory sinus arrhythmia

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Destroy user interface control[22]. Finally, the reduction of sympathetic tone could lead to a reduction in metabolic rate, which, possibly combined with an increase of cardiac output, may lead to an increase of mixed venous PO2 and thus less admixture. All together, our data suggest that the benefits from slow deep breathing exercise are due to an improvement in ventilation mechanics, in pulmonary perfusion and in ventilation/perfusion matching, and possibly to a reduction of the metabolic rate.

This acute blood pressure lowering effect of slow deep breathing may be related to the ability of this manoeuvre to increase baroreflex and reduce chemoreflex sensitivity

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Destroy user interface control[23], resulting in a sympathetic inhibitory action, as recently directly shown by Oneda et al.

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The blood pressure reduction observed in our study is in line with data obtained in previous studies that proposed regular and repeated performance of slow deep breathing exercise at sea level as a nonpharmacological approach to the treatment of hypertension

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Destroy user interface control[14]. These studies have also emphasized that this effect may originate from an enhanced sensitivity of the baroreflex and/or a reduced sensitivity of the chemoreflex

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In conclusion, slow deep breathing induced a significant improvement in ventilation efficiency as shown by SpO2 increase in healthy subjects exposed to HA. This improvement was most likely due to a reduction of dead space ventilation and an increase in alveolar ventilation, and was associated to a reduction of both pulmonary and systemic BP levels, both elevated at HA. This intervention is easy and cheap.

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