Ear Oximeter Research Articles

P070 Rheum to Empower: Home Spirometry and Oximetry Monitoring in Connective Tissue Related Interstitial Lung Disease

Abstract Background/Aims Interstitial lung disease (ILD) is a common cause of morbidity and mortality in connective tissue diseases (CTDs). Distinct challenges arise for individuals with impairments from rheumatic diseases, especially when coupled with respiratory symptoms. While home spirometry monitoring is valuable for patients with idiopathic pulmonary fibrosis (IPF), its applicability in CTD related ILD (CTD-ILD) is relatively unexplored. This study examines the feasibility and acceptability of home spirometry and oximetry monitoring in CTD-ILD patients compared with those with IPF. Methods Patients with CTD-ILD and IPF were recruited prospectively in a tertiary hospital. A portable handheld spirometer (MIR Spirobank Smart) and a Nonin finger oximeter linked to a smartphone app were provided, and patients were educated on its use. Spirometry and oximetry results were collated. At six months, a survey was conducted to assess patients’ perception of home monitoring. Results Fourty-one patients with CTD-ILD and 51 with IPF were recruited. The median ages were 66 and 71 years respectively (Table 1). 2946 FVC and 2787 oximetry readings were captured in the CTD-ILD cohort compared with 4984 FVC and 4778 oximetry readings in the IPF cohort. Among the 41 patients, 12 experienced Raynaud’s phenomenon. Only 7.32% (3/41) of CTD-ILD patients required an ear oximeter due to inaccurate oxygen saturation measurement caused by Raynaud’s phenomenon. Among the CTD-ILD cohort, 16.67% (6/36) experienced difficulty using the devices due to hand problems, while none of the IPF cohort encountered such issues. In the survey, patients reported barriers to long-term remote monitoring usage included forgetting to use, coughing or breathlessness. Less than one-third of patients indicated that spirometry and oximetry results contributed to health anxiety. A majority of patients found home monitoring useful and insightful, and would recommend this to others. Conclusion Our findings suggest the practicality of remotely monitoring FVC and oximetry in CTD-ILD patients, even with challenges like Raynaud’s phenomenon and impaired hand function. This not only underscores feasibility but also empowers patients through continuous monitoring despite physical limitations. Incorporating remote monitoring into standard care should be regarded as an essential approach for this understudied population, enhancing both clinical management and patient empowerment. Disclosure W. Ng: Grants/research support; StAR MD Scholarship, ISR Rheumatology Patient Initiative Fund. D. Howard: None. L. Durcan: None. K. Hurley: Grants/research support; Health Research Board, Ireland, Emerging Clinical Scientist Award (ECSA-2020-011).

Noninvasive Assessment Of Cardiovascular Hemodynamics During Exercise Using Systolic Time Intervals

Noninvasive Assessment Of Cardiovascular Hemodynamics During Exercise Using Systolic Time Intervals

P005 The effect of alcohol on the motor control of the genioglossus muscle

Abstract Rationale Alcohol is recognised to worsen snoring and obstructive sleep apnea (OSA). This effect is thought to be due to alcohol’s depressant effect on upper airway dilator muscles such as the genioglossus, but how alcohol reduces genioglossus activity is unknown. The aim of this study was to investigate alcohol’s effect on genioglossus single motor units (SMUs). Methods Healthy individuals visited the lab on two days (Alcohol: breath alcohol concentration ~0.08% or Placebo). They were instrumented with a nasal mask, 4 intramuscular genioglossus SMU EMG wires and an ear oximeter. They were exposed to 8–12 hypoxia trials (45-60s of 10%O2 followed by one breath of 100%O2) while awake. The SMUs were sorted according to their firing patterns with respect to respiration and were quantified during baseline, hypoxia, hyperoxia and recovery. Results The total number of SMUs recorded at baseline (68 and 67 respectively) and their distribution (ET: 29 vs 22, IP: 5 vs 10, IT: 8 vs 20 and TT: 26 vs 15 respectively) was similar between conditions. The discharge frequency did not differ between conditions (21Hz vs 22.4Hz, p>0.08). There was no difference between placebo and alcohol in the number (101 vs 88 respectively) and distribution (ET: 35 vs 32, IP: 22 vs 16, IT: 14 vs 22 and TT: 30 vs 17 respectively, p<0.05) of SMUs during hypoxia. Afterdischarge following hypoxia was also not different between conditions. Conclusion Alcohol has little effect on genioglossus SMUs and afterdischarge. OSA following alcohol may be related to increased upper airway resistance/nasal congestion.

Ventilatory patterns differ between maximal running and cycling

To determine the effect of exercise mode on ventilatory patterns, 22 trained men performed two maximal graded exercise tests; one running on a treadmill and one cycling on an ergometer. Tidal flow-volume (FV) loops were recorded during each minute of exercise with maximal loops measured pre and post exercise. Running resulted in a greater VO2peak than cycling (62.7±7.6 vs. 58.1±7.2mLkg−1min−1). Although maximal ventilation (VE) did not differ between modes, ventilatory equivalents for O2 and CO2 were significantly larger during maximal cycling. Arterial oxygen saturation (estimated via ear oximeter) was also greater during maximal cycling, as were end-expiratory (EELV; 3.40±0.54 vs. 3.21±0.55L) and end-inspiratory lung volumes, (EILV; 6.24±0.88 vs. 5.90±0.74L). Based on these results we conclude that ventilatory patterns differ as a function of exercise mode and these observed differences are likely due to the differences in posture adopted during exercise in these modes.

Anesthesiology: From Patient Safety to Population Outcomes

Anesthesiology: From Patient Safety to Population Outcomes

Takuo Aoyagi: Discovery of Pulse Oximetry

In the 1930s and 1940s, photo cells permitted German, English, and American physiologists to construct ear oximeters with red and infrared light, requiring calibration. In 1940 Squire recognized that changes of red and infrared light transmission caused by pneumatic tissue compression permitted saturation to be computed. In 1949 Wood used this idea to compute absolute saturation continuously from the ratios of optical density changes with pressure in an ear oximeter. In 1972 Takuo Aoyagi, an electrical engineer at Nihon Kohden company in Tokyo, was interested in measuring cardiac output noninvasively by the dye dilution method using a commercially available ear oximeter. He balanced the red and infrared signals to cancel the pulse noise which prevented measuring the dye washout accurately. He discovered that changes of oxygen saturation voided his pulse cancellation. He then realized that these pulsatile changes could be used to compute saturation from the ratio of ratios of pulse changes in the red and infrared. His ideas, equations and instrument were adapted, improved and successfully marketed by Minolta about 1978, stimulating other firms to further improve and market pulse oximeters worldwide in the mid 1980s. Dr. Aoyagi and associates provided a detailed history for this paper.

Effect of Altitude on the Heart and the Lungs

This review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the high-altitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. ### Circulation The major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors.1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Figure 1. Effects of hypoxia on systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues2,3; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs …

An Early Example of Evidence-based Medicine

Diffusion anoxia. By Bernard Raymond Fink. Anesthesiology 1955; 16:511-14. In 1955, Dr. Bernard Raymond Fink published his findings that described the mechanism by which hypoxemia occurred when nitrous oxide-oxygen anesthesia was discontinued and room air breathing commenced. Using an ear oximeter and brachial artery blood gases, he measured oxygen saturation in eight healthy patients who had received 75% nitrous oxide-25% oxygen for gynecologic surgery. He showed that oxygen saturation decreased from 5% to 10% and often reached a value below 90% when the patient began room air breathing after the nitrous oxide-oxygen was discontinued. The effect was seen over a 10-min period. He concluded that "anoxia arises because the outward diffusion of nitrous oxide lowers the alveolar partial pressure of oxygen." This phenomenon can become a causative factor of cardiac arrest in patients with impaired pulmonary or cardiac reserves.

Pulse Oximeters 101

Pulse Oximeters 101

History of Pulse Oximetry in Neonatal Medicine

Although pulse oximetry in neonatal medicine was introduced fewer than 25 years ago, today it is the principal form of oxygen monitoring around the world in nearly all clinical situations that require measurement of oxygen in neonates. It has become, in fact, the fifth vital sign in neonatal medicine. For the near future, it holds center stage as the primary form of oxygen monitoring for a large international commitment to determine, after more than 50 years of mistakes, mistrials, and misunderstandings, the appropriate level of oxygen supply and blood oxygenation in preterm infants. Hopefully, these studies and the unique advantages of pulse oximetry will help to eliminate, or at least diminish, the adverse effects of too much oxygen, such as retinopathy of prematurity (ROP), without increasing the incidence of complications of hypoxia, such as patent ductus arteriosus (PDA) and pulmonary hypertension. The purpose of this review is to look back at how oximetry began, how “pulse” oximetry was developed, and how this new technology has revolutionized oxygen monitoring in neonatal medicine. Oximetry, or the use of light to measure the amount of oxygen carried in the blood, began in about 1874, when Karl von Vierordt attempted to measure blood saturation in the human hand. Quantitative oximetry began with Krogh in Copenhagen just after World War I in 1918. In the 1930s, Millikan and Wood developed the two-wavelength ear oximeter that later was modified in 1935 by Matthes into the first oxygen saturation meter using red and green filters (personal communication, W. Clifford, 2004). Squire developed an instrument for measuring the quantity of blood and its degree of oxygenation in the web of the hand in 1940, and Goldie developed a device for continuous indication of oxygen saturation in circulating blood in adults in 1942. (1)(2)(3) …

Arterial Oxygen Desaturation after Induction of Anesthesia

Royal Infirmary, Edinburgh, United Kingdom. g.b.drummond@ed.ac.ukNaguib et al. 1have presented a clinically relevant study of arterial saturation values after preoxygenation and different doses of suxamethonium, and discuss their results using the extensive reports relevant to this topic. Unfortunately, they perhaps did not search the published work back to times before the pulse oximeter was introduced. Before the pulse oximeter, the Hewlett Packard ear oximeter (Waltham, MA) was used to measure arterial oxygen saturation continuously. Although clumsy, it was accurate and gave reliable results.2We used this device to be the first to report changes in oxygen saturation, measured continuously, at induction of anesthesia. We recorded arterial oxygen saturation in patients who were given thiopental and suxamethonium (although in greater doses than those used by Naguib et al. ) and described the effects of preoxygenation.3We showed convincingly that desaturation was more likely in obese patients and that even a small mask leak markedly impaired the efficacy of oxygenation.Naguib et al. suggested “shunting” as a reason for the hypoxemia they found, particularly in obese patients. This is not the most probable explanation. As they acknowledge, in anesthetized obese subjects, functional residual capacity is small, often close to residual volume, as shown in the study by Damia et al. 4In these circumstances, oxygen stores are small, and desaturation occurs more quickly as the small alveolar oxygen content decreases. This effect is shown clearly in the model predictions of Hardman et al. 5This model, which was more complete than the model studies considered by Naguib et al. , showed much more rapid desaturation with a small functional residual capacity than with a greater pulmonary shunt.Royal Infirmary, Edinburgh, United Kingdom. g.b.drummond@ed.ac.uk

Exercise‐induced arterial hypoxemia is not different during cycling and running in triathletes

This study examined the effect of running and cycling on exercise-induced arterial hypoxemia (EIAH) in individuals well trained in each modality. Thirteen male triathletes (X+/-SD: age=36+/-5 years, mass=69+/-8 kg, body fat=12+/-1%) performed progressive exercise to exhaustion during cycle ergometry and treadmill running. Gas exchange was determined, while oxyhemoglobin saturation (SaO(2)) was measured with an ear oximeter. At maximal exercise, the respiratory exchange ratio (1.15+/-0.06 vs. 1.10+/-0.05) and the ventilatory equivalent for oxygen uptake (37.6+/-3.8 vs. 34.2+/-2.7) were greater during cycling vs. running (P<0.05). However, there were no differences at maximal exercise in oxygen uptake (64.4+/-3.2 vs. 67.0+/-4.6 mL kg(-1) min(-1)), SaO(2) (93.4+/-2.8% vs. 92.6+/-2.2%), or the ventilatory equivalent for carbon dioxide (V(E)/VCO(2); 33.1+/-3.1 vs. 31.0+/-3.1), during cycling vs. running, respectively. During submaximal exercise, the V(E)/VCO(2) was less for cycling (26.0+/-1.0) compared with running (29.1+/-0.4; P<0.05), but this had no apparent effect on the SaO(2) response. In conclusion, EIAH was not significantly different during cycling and running in athletes who were well trained in both exercise modalities.

The desaturation response time of finger pulse oximeters during mild hypothermia*

Pulse oximeters may delay displaying the correct oxygen saturation during the onset of hypoxia. We investigated the desaturation response times of pulse oximeter sensors (forehead, ear and finger) during vasoconstriction due to mild hypothermia and vasodilation caused by glyceryl trinitrate. Ten healthy male volunteers were given three hypoxic challenges of 3 min duration under differing experimental conditions. Mild hypothermia increased the mean response time of finger oximeters from 130 to 215 s. Glyceryl trinitrate partly offset this effect by reducing the response time from 215 to 187 s. In contrast, the response times of the forehead and ear oximeters were unaffected by mild hypothermia, but the difference between head and finger oximeters was highly significant (p < 0.0001). The results suggest that the head oximeters provide a better monitoring site for pulse oximeters during mild hypothermia.

The Legacy of Albert Faulconer Jr

The Legacy of Albert Faulconer Jr

From control of airway and breathing to cardiopulmonary-cerebral resuscitation. 1958.

Background: For respiratory resuscitation without devices, the author hypothesized that providing upper airway patency requires lifting the base of the tongue off the posterior pharyngeal wall and that artificial ventilation with intermittent positive pressure using exhaled air, i.e., direct mouth-to-mouth ventilation (MMV), is more effective than back or chest pressure with or without arm lift. MMV leaves the operator's hands free for backward tilt of the head, forward displacement of the mandible, or both. Methods: The author studied 25 sedated, nonintubated adult human volunteers under neuromuscular blockade with succinylcholine for 1-3 h each. One hundred sixty-seven untrained lay persons performed various direct MMV methods after one demonstration. Eighteen trained ambulance rescuers performed back or chest pressure arm-lift methods. Ventilation volumes were recorded during MMV from a calibrated pneumograph and during the manual methods from a taped face mask on a spirometer. Arterial oxygen saturation was monitored by an ear oximeter, and end-tidal carbon dioxide was measured by an infrared analyzer. Results: With the head in the mid position or flexed, airway obstruction occurred in all volunteers, equally in the supine or prone position. With the head tilted backward and the mouth held open, one half to two thirds of the volunteers had an open airway; the remaining volunteers required additional forward displacement of the mandible or a pharyngeal tube. Ninety percent of the lay persons performed MMV effectively. Moderate hyperventilation by the operator achieved normoxemia and normocapnia in the volunteer and moderate hypocapnia in the operator. Apnea-induced moderate hypoxemia was reversed with 5-9 MMVs. In the majority of volunteers, the manual methods caused no ventilation (mostly because of neck flexion), and in others, it caused progressive airway obstruction. In some volunteers, there was valve-like nasopharyngeal obstruction. Conclusions: In coma without a tracheal tube, direct MMV is effective because of the ability of the rescuer to support the head and jaw for upper airway patency and because of controllable high inflation pressures and volumes, whereas manual methods frequently fail to ventilate, mainly because of upper airway obstruction. The author recommends that backward tilt of the head plus exhaled air inflation methods be taught for general use in adults and children.

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists.

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O(2) = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O(2) consumption (VO(2 max)) and arterial oxyhemoglobin saturation (Sa(O(2)), Ohmeda Biox ear oximeter) under normoxic (VO(2 max) = 4.88 +/- 0.43 l/min and Sa(O(2)) = 90.2 +/- 0.9, means +/- SD) and hypoxic (VO(2 max) = 4.24 +/- 0.49 l/min and Sa(O(2)) = 75.5 +/- 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO(2 max), under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO(2) (Pa(O(2))), arterial PCO(2), and Sa(O(2)) were determined, and the alveolar-arterial difference for PO(2) (A-aDO(2)) was calculated. Measurements of Pa(O(2)) and Sa(O(2)) were significantly lower and A-aDO(2) was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for Pa(O(2)), Sa(O(2)) and A-aDO(2) (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.

CYTOKINES DO NOT CONTRIBUTE TO ELEVATED RESTING METABOLIC RATE IN ALPHA-1 ANTITRYPSIN DEFICIENCY

1853 Cytokine spillover leads to increased resting metabolic rate (RMR) in many disease states. Increased RMR in lung disease has been attributed to an increased metabolic cost of breathing. Loss of protease inhibition in alpha-1 antitrypsin deficiency (A1AD) results in lung damage. Indirect calorimetry and blood chemistries were used to determine if RMR is elevated in A1AD, as in other obstructive lung disease, and to explore the possibility of cytokine presence in blood. Individuals with A1AD (FEV1.0/FVC: 31.7±5.8%, n=19) and controls (C, n=7) were fitted with a two-way mouthpiece and ear oximeter, and rested supine. Calorimetry data were collected for 30 min; the mean of the last three min were analyzed. Tests were performed in a dim, thermoneutral (23±1.2 °C, 69±1.0% humidity) room. Subjects were similar in age (A1AD: 49±11.2 yrs; C: 43±3.9 yrs) and height (A1AD: 170.2±7.4 cm; C: 171.9±11.7 cm), but C had greater body weight (A1AD: 70.9±13.7 kg; C: 82.0±26.2 kg). RMR (V̇O2) was elevated in A1AD (A1AD: 5.26±1.71 ml-kg−1-min−1; C: 3.5±0.71 ml-kg−1-min−1). Ventilation (V̇E) was higher in A1AD (A1AD: 14.2±4.67 L/min; C: 8.7±1.9 L/min), but increased ventilatory equivalents for O2 (V̇E/V̇O2, A1AD: 34.9±7.3; C: 28.2±3.3) and CO2 (V̇E/V̇CO2C: 30.9±3.4; A1AD: 40.8±6.3) and lower SaO2 (C: 96.7±1.6%; A1AD: 94.2±2.7%) suggests hyperventilation in A1AD. Tumor necrosis factor and Interleukin-1α were not detected in plasma of either group (ELISA system). It appears that elevated RMR associated with AlAD is due to increased cost of breathing and defense of SaO2 without apparent cytokine involvement. Supported in part by the Alpha-1 Foundation, Miami, FL.

Modafinil decreases hypersomnolence in the English bulldog, a natural animal model of sleep-disordered breathing.

The English bulldog is a natural model of sleep-disordered breathing (SDB). This condition is marked by 1) hypersomnolence and 2) disordered breathing episodes that are most frequent and severe during rapid eye movement (REM) sleep. Modafinil has been found to increase arousal levels in animals and decrease excessive daytime sleepiness in humans. Therefore, in this study we focused mainly on the effects of the drug on total sleep time and sleep latency and secondarily assessed its effect on REM SDB. Five English bulldogs were implanted with subcutaneous electroencephalographic/electrooculographic (EEG/EOG) electrodes and instrumented with respiratory oscillation belts to measure abdominal and rib cage movements and an ear oximeter to measure saturation. The dogs were studied for approximately 8 hours each subsequent day on two consecutive days. On the first day, they received the vehicle dimethyl sulfoxide (DMSO) i.v. as a control. On the following day they received 10 mg/kg body weight of modafinil i.v. dissolved in the DMSO vehicle. Our findings indicate that modafinil significantly alleviates hypersomnolence (p < 0.05) in the bulldog, as evidenced by dramatically decreased mean total sleep time (from a control value of 50.5% to 8.3% with the drug) and increased mean sleep latency (from a control value of 71.0 minutes to a value of 346.6 minutes with the drug). We obtained limited data on the effect of modafinil on SDB because the drug either greatly diminished or entirely eradicated REM sleep in all five dogs.

Near-Infrared spectroscopy: Theory and applications

In conclusion, NIRS appears to offer both a new monitoring modality and new information about cerebral oxygenation. Technical problems in the application of this technology persist, most notably determination of pathlength and the volume of tissue interrogated. Those familiar with the history of pulse oximetry will recall that although Millikan developed an ear oximeter in 1947, it was not until Aoyagi combined recognition of the pulse signal with spectroscopy in the 1970s that oximetry was transformed into a clinically applicable monitor. In much the same way, NIRS may find the same tremendous usefulness as a noninvasive monitor of cerebral oxygen utilization, pending resolution of the remaining technical problems.

Pathogenesis of Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Relationship to Arterial Pco2

In order to determine which patients with congestive heart failure (CHF) develop Cheyne-Stokes respiration (CSR) during sleep, we compared the cardiorespiratory profiles of CHF patients with CSR to those of CHF patients without CSR. Overnight polysomnography and continuous transcutaneous PCO2 (tc PCO2) monitoring, estimation of left ventricular ejection fraction (LVEF), pulmonary function tests, and chest radiograph were performed on 16 consecutive patients with chronic, stable CHF. The tc PCO2 monitor (Kontron 7640) was calibrated so that measurements reflected arterial PCO2 values. A mean value was calculated for wakefulness (W) and total sleep time (TST). Circulation time (CT) from the lung to the carotid body was estimated from the end of an apnea or voluntary breath-hold to the nadir of oxygen desaturation recorded on an ear oximeter. The duration of CSR was expressed as a percent of TST. Nine patients developed CSR during sleep (52.5 +/- 31.6 percent TST) (group 1) and 7 did not (group 2). All patients were male and both groups were a similar age (64 +/- 8 vs 63 +/- 4 years) and weight (body mass index, 28.1 +/- 3.5 vs 25.4 +/- 3.4 kg/m2). There were no significant intergroup differences between LVEF (22 +/- 5.2 vs 24.1 +/- 5.2 percent), CT (19.1 +/- 3.6 vs 15.9 +/- 6.7 s), SaO2 (W) (94 +/- 1.2 vs 92.4 +/- 2.1 percent), and SaO2 (TST) (90.8 +/- 2.7 vs 92.4 +/- 2.1 percent). The tc PCO2 (W) was lower in group 1 (34.4 +/- 3.5 vs 38.1 +/- 1.9 mm Hg), increased during sleep by a similar amount in both groups (1.6 +/- 1.5 vs 2.1 +/- 2.2 mm Hg), and was significantly lower during sleep in group 1 (36.1 +/- 3.4 vs 40.2 +/- 2.2 mm Hg). We conclude that CHF patients with CSR hyperventilate during sleep and wakefulness and that CHF patients with awake hypocapnia are more likely to develop CSR during sleep. These findings indicate that arterial PCO2 is important in determining which CHF patients develop CSR.