Peter Lindholm

The physiology and pathophysiology of human breath-hold diving

This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hemorrhage postdive. However, a remarkable, and so far poorly understood, variation in individual disposition for such problems exists. Mortality connected with breath-hold diving is primarily concentrated to less well-trained recreational divers and competitive spearfishermen who fall victim to hypoxia. Particularly vulnerable are probably also individuals with preexisting cardiac problems and possibly, essentially healthy divers who may have suffered severe alternobaric vertigo as a complication to inadequate pressure equilibration of the middle ears. The specific topics discussed include the diving response and its expression by the cardiovascular system, which exhibits hypertension, bradycardia, oxygen conservation, arrhythmias, and contraction of the spleen. The respiratory system is challenged by compression of the lungs with barotrauma of descent, intrapulmonary hemorrhage, edema, and the effects of glossopharyngeal insufflation and exsufflation. Various mechanisms associated with hypoxia and loss of consciousness are discussed, including hyperventilation, ascent blackout, fasting, and excessive postexercise O(2) consumption. The potential for high nitrogen pressure in the lungs to cause decompression sickness and N(2) narcosis is also illuminated.

Pulmonary edema and hemoptysis after breath-hold diving at residual volume

To simulate pressure effects and experience thoracic compression while breath-hold diving in a relatively safe environment, competitive breath-hold divers exhale to residual volume before diving in a swimming pool, thus compressing the chest even at depth of only 3-6 m. The study was undertaken to investigate whether such diving could cause pulmonary edema and hemoptysis. Eleven volunteer breath-hold divers who regularly dive on full exhalation performed repeated dives to 6 m during a 20-min period. The subjects were studied with dynamic spirometry, video-fibernasolaryngoscopy, and single-breath diffusion capacity of carbon monoxide (Dl(CO)). The duration of dives with empty lungs ranged from 30 to 120 s. Postdiving forced vital capacity (FVC) was reduced from mean (SD) 6.57 +/- 0.88 to 6.23 +/- 1.02 liters (P < 0.05), and forced expiratory volume during the first second (FEV(1.0)) was reduced from 5.09 +/- 0.64 to 4.59 +/- 0.72 liters (P < 0.001) (n = 11). FEV(1.0)/FVC was 0.78 +/- 0.05 prediving and 0.74 +/- 0.05 postdiving (P < 0.001) (n = 11). All subjects reported a (reversible) change in their voice after diving, irritation, and slight congestion in the larynx. Fresh blood that originated from somewhere below the vocal cords was found by laryngoscopy in two subjects. Dl(CO)/alveolar ventilation (Va) was 1.56 +/- 0.17 mmol.kPa(-1).min(-1).l(-1) before diving. After diving, the Dl(CO)/Va increased to 1.72 +/- 0.24 (P = 0.001), but 20 min later it was indistinguishable from the predive value: 1.57 +/- 0.20 (n = 11). Breath-hold diving with empty lungs to shallow depths can induce hemoptysis in healthy subjects. Edema was possibly present in the lower airways, as suggested by reduced dynamic spirometry.

Aggravated hypoxia during breath-holds after prolonged exercise

Hyperventilation prior to breath-hold diving increases the risk of syncope as a result of hypoxia. Recently, a number of cases of near-drownings in which the swimmers did not hyperventilate before breath-hold diving have come to our attention. These individuals had engaged in prolonged exercise prior to breath-hold diving and it is known that such exercise enhances lipid metabolism relative to carbohydrate metabolism, resulting in a lower production of CO2 per amount of O2 consumed. Therefore, our hypothesis was that an exercise-induced increase in lipid metabolism and the associated reduction in the amount of CO2 produced would cause the urge to breathe to develop at a lower P O2, thereby increasing the risk of syncope due to hypoxia. Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest in the supine position and then 5 or 6 additional breath-holds during intermittent light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on two different days: control (C) and post prolonged sub-maximal exercise (PPE), when the breath-holds were performed 30xa0min after 2xa0h of sub-maximal exercise. After C and before the prolonged submaximal exercise subjects were put on a carbohydrate-free diet for 18xa0h to start the depletion of glycogen. The respiratory exchange ratio ( RER) and end-tidal P CO2, P O2, and SaO2 values were determined and the data were presented as means (SD). The RER prior to breath-holding under control conditions was 0.83 (0.09), whereas the corresponding value after exercise was 0.70 (0.05) ( P <0.01). When the three apnoeas of the longest duration for each subject were analysed, the average duration of the dynamic apnoeas was 96 (14)xa0s under control conditions and 96 (17)xa0s following exercise. Both P O2 and P CO2 were higher during the control dynamic apnoeas than after PPE [PO2 6.9 (1.0)xa0kPa vs 6.2 (1.2)xa0kPa, P <0.01; P CO2 7.8 (0.5)xa0kPa vs 6.7 (0.4)xa0kPa, P <0.001; ANOVA testing]. A similar pattern was observed after breath-holding under resting conditions, i.e., a lower end-tidal P O2 and P CO2 after exercise (PPE) compared to control conditions. Our findings demonstrate that under the conditions of a relatively low RER following prolonged exercise, breath-holding is terminated at a lower P O2 and a lower P CO2 than under normal conditions. This suggests that elevated lipid metabolism may constitute a risk factor in connection with breath-holding during swimming and diving.

A fluoroscopic and laryngoscopic study of glossopharyngeal insufflation and exsufflation.

Glossopharyngeal breathing, frequently performed by elite breath-hold divers, relies on muscles of the mouth and pharynx to move air into (glossopharyngeal insufflation, GI) and out of the lungs (glossopharyngeal exsufflation, GE). GI has also been used by patients with weak respiratory muscles. Fluoroscopic and endoscopic examinations were performed on four divers (three of whom were world record holders) during both GI and GE maneuvers. A detailed pictorial description of both GI and GE, with online video material that includes external, endoscopic and fluoroscopic examinations, is provided in this publication. Both GI and GE are accomplished with a coordinated series of contractions by glossopharyngeal muscles and they rely on a piston pump-like action of the larynx. In particular, the larynx moves extensively and repeatedly up and down, to either inject air into (GI) or extract it from the lungs (GE), with the vocal cords functioning as a valve. During both maneuvers, when the larynx is in its highest position, the epiglottis does not fold back, unlike what happens during swallowing.

Effects of dietary inorganic nitrate on static and dynamic breath-holding in humans

Inorganic nitrate has been shown to reduce oxygen cost during exercise. Since the nitrate-nitrite-NO pathway is facilitated during hypoxia, we investigated the effects of dietary nitrate on oxygen consumption and cardiovascular responses during apnea. These variables were measured in two randomized, double-blind, placebo-controlled, crossover protocols at rest and ergometer exercise in competitive breath-hold divers. Subjects held their breath for predetermined times along with maximum effort apneas after two separate 3-day periods with supplementation of potassium nitrate/placebo. In contrast to our hypothesis, nitrate supplementation led to lower arterial oxygen saturation (SaO(2), 77 ± 3%) compared to placebo (80 ± 2%) during static apnea, along with lower end-tidal fraction of oxygen (FETO(2)) after 4 min of apnea (nitrate 6.9 ± 0.4% vs. placebo 7.6 ± 0.4%). Maximum apnea duration was shorter after nitrate (329 ± 13 s) compared to placebo (344 ± 13 s). During cycle ergometry nitrate had no effect on SaO(2), FETO(2) or maximum apnea duration. The negative effects of inorganic nitrate during static apnea may be explained by an attenuated diving response.

Transient ischemic attacks from arterial gas embolism induced by glossopharyngeal insufflation and a possible method to identify individuals at risk

Breath-hold divers report transient, severe neurological symptoms that could be caused by arterial gas embolism after glossopharyngeal insufflation. This technique is often used to overinflate the lungs and stretch the chest prior to breath-holding and can increase the transpulmonary pressure to around 7–8xa0kPa, so introducing risk of pulmonary barotrauma. Airway pressure, blood pressure and static spirometry (nitrogen dilution) were measured simultaneously in ten subjects attempting to identify individuals at risk. Compared to baseline, total lung capacity (TLC) after glossopharyngeal insufflation increased by 19xa0% along with increased vital capacity (23xa0%) and residual volume (6xa0%) (Pxa0<xa00.05), while mean relaxed airway pressure (Paw) at TLC increased from 3.62xa0±xa00.93 to 7.26xa0±xa02.04xa0kPa as a result of performing glossopharyngeal insufflation (Pxa0=xa00.0001). Blood pressure fell during glossopharyngeal insufflation and attained relaxed airway pressure correlated positively to baseline mean arterial pressure in the subjects. Two of the subjects had glossopharyngeal insufflation-related accidents before the study and two subjects (with the highest Paw during GI; 9 and 10.3xa0kPa respectively) suffered glossopharyngeal insufflation-related accidents within 6xa0months after our study, with one suffering a non-fatal drowning accident. The principal finding of this study was that some subjects were able to use GI to reach Paw high enough to suggest a risk of pulmonary barotrauma, while other subjects would lose consciousness due to hypotension while still within safe limits of pulmonary pressure. This mechanism could offer an alternative explanation to drowning in breath-hold divers, and indicates that glossopharyngeal insufflation should be avoided or done with extreme caution.

Detection of pulmonary embolism using repeated MRI acquisitions without respiratory gating: a preliminary study

Background Pulmonary embolism (PE) is a severe medical condition with non-specific clinical findings. Computed tomography angiography (CTA) using iodinated contrast agents is the golden standard for diagnosis, but many patients have contraindications for CTA. Purpose To investigate the diagnostic accuracy of repeated acquisitions of magnetic resonance imaging (MRI), without respiratory gating or breath holding, in diagnosing PE using CTA as the reference standard. Material and Methods Thirty-three patients with clinically suspected PE underwent MRI within 48u2009h after diagnostic CTA. A control group of 37 healthy participants underwent MRI and was matched with an equal number of negative CTA exams. The MRI protocol was based on free-breathing steady-state free precession producing 4.5u2009mm slices in axial, sagittal, and coronal planes. Instead of respiratory or cardiac gating five repetitive slices were obtained in each anatomical position to compensate for movement and artifacts. Clinical assessment including d-dimer and Well’s score was performed prior to imaging. One radiologist reviewed the CTA exams and two radiologists reviewed the MRI scans. Results All 70 MRI exams were of diagnostic quality and the total acquisition time for each MRI scan was 9u2009minu200934u2009s. On CTA, 29 patients were diagnosed with PE and the MRI readers detected 26 and 27 of those, respectively. Specificity was 100% for both readers. Sensitivity was 90% and 93%, respectively. Inter-reader agreement using Cohen’s kappa was 0.97. Conclusion Our unenhanced MRI protocol shows a high sensitivity and specificity for PE, but further studies are required before considering it as a safe diagnostic test.

Aerobic efficiency is associated with the improvement in maximal power output during acute hyperoxia.

This study investigated the relationship between aerobic efficiency during cycling exercise and the increase in physical performance with acute hyperoxic exposure (FiO2 ~31%) (HOX) and also tested the hypothesis that fat oxidation could be increased by acute hyperoxia. Fourteen males and four females were recruited for two sessions, where they exercised for 2 × 10 min at 100 W to determine efficiency. HOX and normoxia (NOX) were administered randomly on both occasions to account for differences in nitrogen exchange. Thereafter, a progressive ramp test was performed to determine VO2max and maximal power output (Wmax). After 30 min rest, workload was set to 80% of maximal power output (Wmax) for a time to exhaustion test (TTE). At 100W gross efficiency was reduced from 19.4% during NOX to 18.9% during HOX (P ≤ 0.0001). HOX increased fat oxidation at 100 W by 52% from 3.41 kcal min‐1 to 5.17 kcal min‐1 (P ≤ 0.0001) with a corresponding reduction in carbohydrate oxidation. Wmax increased by 2.4% from 388.8 (±82.1) during NOX to 397.8 (±83.5) during HOX (P ≤ 0.0001). SaO2 was higher in HOX both at the end of the maximal exercise test and TTE. Subjects with a high level of efficiency in NOX had a larger improvement in Wmax with HOX, in agreement with the hypothesis that an optimum level of efficiency exists that maximizes power production. No association between mitochondrial excess capacity and endurance performance was found; increases in oxygen supply seemed to increase maximal aerobic power production and maintain/increase endurance capacity at the same relative workload.

Acute effects of glossopharyngeal insufflation in people with cervical spinal cord injury

Objectives: To evaluate acute effects of glossopharyngeal insufflation (GI) on lung function, airway pressure (Paw), blood pressure and heart rate (HR) in people with cervical spinal cord injury (CSCI). Design: Case-control design. Setting: Karolinska Institutet, Stockholm, Sweden. Participants: Ten participants with CSCI suffering from lesions between C4 and C8, and ASIA classification of A or B were recruited. Ten healthy particpants familiar with GI were recruited as a reference group. Outcome measures: Spirometry, mean arterial blood pressure (MAP), Paw, and HR were measured in a sitting and a supine position before, during, and after GI. Results: GI in the study group in a sitting position increased total lung capacity (TLC) by 712 ml: P < 0.001, vital capacity (VC) by 587 ml: P < 0.0001, Paw by 13u2005cm H2O: P < 0.01, and HR by 10 beats/min: P < 0.001. MAP decreased by 25 mmHg, P < 0.0001. Significant differences were observed between groups comparing baseline with GI. The reference group had a higher increase in; TLC (P < 0.01), VC (P < 0.001), Paw (P < 0.001) and HR (P < 0.05) and a higher decrease in MAP (P < 0.001). With GI in a sitting compared to a supine position, TLC, MAP, HR, Paw remained unchanged in the study group, while residual volume decreased in the supine position (P < 0.01). Conclusion: There was a difference between the groups in the increase in TLC; VC; Paw, HR and in the decrease in MAP with GI, however MAP, HR and Paw responded in similar way in both groups in a sitting as well as a supine position. If performed correctly, the risks of GI resulting in clinically significant hemodynamic changes is low, although syncope may still occur.