Targeted case finding for OSA within the primary care setting.

STUDY OBJECTIVES: The aim was to determine the feasibility of using an unattended 2-channel device to screen for obstructive sleep apnea in a population of high-risk patients using a targeted, case-finding strategy. The case finding was based on the presence of risk factors not symptoms in the studied population. METHODS: The study took place from June 2007 to May 2008 in rural and metropolitan Queensland and New South Wales. Family doctors were asked to identify patients with any of the following: BMI > 30, type 2 diabetes, treated hypertension, ischemic heart disease. Participants applied the ApneaLink+O2 at home for a single night. The device recorded nasal flow and pulse oximetry. Data were analyzed by proprietary software, then checked and reported by either of two sleep physicians. RESULTS: 1,157 patients were recruited; mean age 53 ± 14.6, M/F% = 62/38, mean BMI = 31.8, obesity = 35%, diabetes = 16%, hypertension = 39%, IHD = 5%, Mean Epworth Sleepiness Scale score (ESS) = 8.3. The prevalence of unrecognized OSA was very high: 71% had an AHI > 5/h, 33% had an AHI > 15/h, and 16% had an AHI > 30/h. The ApneaLink+O2 device yielded technically adequate studies in 93% of cases. CONCLUSION: The study shows that a "real world" simple low cost case finding and management program, based on unattended home monitoring for OSA, can work well in a population with risk factors and comorbidities associated with OSA, independent of the presence of symptoms. The prevalence of unrecognized OSA was very high.

Subject specific effects of hyperpnea but not hypocapnia on airway conductance.

We investigated the effects of hypocapnia in normal subjects on airway tone while controlling airway cooling and drying. We hypothesized that airway tone is positively related to the degree of hypocapnia. Participants (8; 2 women) underwent 3 protocols consisting of 20 min of hyperpnea (breathing frequency = 20 breaths min-1; tidal volume = 2.5 L) and 10 min recovery. End-tidal PCO2 was maintained at +1 Torr above rest (ISO; 37.9 ± 1.2 Torr), 8 Torr below resting values (H-8; 29.2 ± 1.7 Torr) or 15 Torr below resting values (H-15; 23.2 ± 2.9 Torr). Breath-by-breath lung conductance (GL) was calculated from flow, volume, and esophageal pressure. GL responses to hyperpnea varied widely across subjects. However, individual responses during ISO correlated highly with responses during H-8 (r = 0.976, p < 0.001) and H-15 (r = 0.952, p < 0.001), with the magnitude of change inversely related to basal GL (r = -0.555, p = 0.006). Thus, inter-subject variation in GL was due to hyperpnea, with no detectable effect of hypocapnia.

Volume loading reduces pulmonary vascular resistance in ventilated animals with acute lung injury: evaluation of RV afterload.

During mechanical ventilation, increased pulmonary vascular resistance (PVR) may decrease right ventricular (RV) performance. We hypothesized that volume loading, by reducing PVR, and, therefore, RV afterload, can limit this effect. Deep anesthesia was induced in 16 mongrel dogs (8 oleic acid-induced acute lung injury and 8 controls). We measured ventricular pressures, dimensions, and stroke volumes during positive end-expiratory pressures of 0, 6, 12, and 18 cmH(2)O at three left ventricular (LV) end-diastolic pressures (5, 12, and 18 mmHg). Oleic acid infusion (0.07 ml/kg) increased PVR and reduced respiratory system compliance (P < 0.05). With positive end-expiratory pressure, PVR was greater at a lower LV end-diastolic pressure. Increased PVR was associated with a decreased transseptal pressure gradient, suggesting that leftward septal shift contributed to decreased LV preload, in addition to that caused by external constraint. Volume loading reduced PVR; this was associated with improved RV output and an increased transseptal pressure gradient, which suggests that rightward septal shift contributed to the increased LV preload. If PVR is used to reflect RV afterload, volume loading appeared to reduce PVR, thereby improving RV and LV performance. The improvement in cardiac output was also associated with reduced external constraint to LV filling; since calculated PVR is inversely related to cardiac output, increased LV output would reduce PVR. In conclusion, our results, which suggest that PVR is an independent determinant of cardiac performance, but is also dependent on cardiac output, improve our understanding of the hemodynamic effects of volume loading in acute lung injury.

Diagnosis of sleep apnoea: some critical issues.

Rather than describing a method for determining which patients should be labelled as having a disease, sleep apnoea, this review describes assessment as a process for deciding whom to investigate, what degree of sleep apnoea they have, how important their symptoms are, whether symptoms are likely attributable to sleep apnoea, and what sort of treatment to offer, if any. Beginning with identifying patients at risk and use of clinical prediction rules, the review covers (i) measurement and implications of the apnoeahypopnoea index; (ii) distinguishing central from obstructive apnoeas; (iii) significance of associated periodic limb movements; (iv) the controversy about the use of portable monitors instead of laboratory polysomnography; (v) evaluation of symptoms associated with sleep apnoea; and (vi) the important role of trials of treatment.

The assessment of maximal respiratory mouth pressures in adults.

Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) are simple, convenient, and noninvasive indices of respiratory muscle strength at the mouth, but standards are not clearly established. We review recent literature, update the 2002 American Thoracic Society/European Respiratory Society statement, and propose as the best choice using a flanged mouthpiece for reference values and lower limit of normal (LLN) values as a function of age for adults age up to about 70 years. Because male pressures are higher than female and MEP exceeds MIP, we present 4 linear regression reference equations as a function of age for adults age up to approximately 70 years: Male MIP=120-(0.41xage), and male MIP LLN=62-(0.15xage). Male MEP=174-(0.83xage), and male MEP LLN=117-(0.83xage). Female MIP=108-(0.61xage), and female MIP LLN=62-(0.50xage). Female MEP=131-(0.86xage), and female MEP LLN=95-(0.57xage). (Pressure in cm H2O and age in years.) We discuss normal values in older subjects, estimation of LLN values, and the relationship between vital capacity and respiratory muscle strength, and offer a guide to interpretation of maximal pressure measurements. The approach should allow direct implementation of MIP and MEP in a pulmonary function laboratory.

Wave intensity analysis and the development of the reservoir-wave approach.

The parameters of wave intensity analysis are calculated from incremental changes in pressure and velocity. While it is clear that forward- and backward-traveling waves induce incremental changes in pressure, not all incremental changes in pressure are due to waves; changes in pressure may also be due to changes in the volume of a compliant structure. When the left ventricular ejects blood rapidly into the aorta, aortic pressure increases, in part, because of the increase in aortic volume: aortic inflow is momentarily greater than aortic outflow. Therefore, to properly quantify the effects of forward or backward waves on arterial pressure and velocity (flow), the component of the incremental change in arterial pressure that is due only to this increase in arterial volume--and not, fundamentally, due to waves--first must be excluded. This component is the pressure generated by the filling and emptying of the reservoir, Otto Frank's Windkessel.

Differences between middle cerebral artery blood velocity waveforms of young and postmenopausal women.

OBJECTIVE: We characterized middle cerebral artery (MCA) blood flow velocity waveforms measured by transcranial Doppler ultrasonography in premenopausal (26.6 +/- 6.1 years, mean +/- SD) and postmenopausal (54.0 +/- 3.6 years) women, of whom six were receiving hormone therapy (PM-HT) and seven were not (PM-non-HT). We hypothesized that feature points on MCA waveforms are altered in postmenopausal women compared with those in young women. DESIGN: A short protocol involved maintaining end-tidal PO2 at euoxia (88 mm Hg) and end-tidal PCO2 at 1.5 mm Hg above eucapnic values using a dynamic end-tidal forcing system. Doppler data for the velocity spectral outline (Vp) were collected every 10 ms, and velocity waveform analyses were done on a beat-by-beat basis. Waveform features were identified over each cardiac cycle, including the average Vp (VCYC), maximum acceleration (AMAX), and the ratio of the velocity at the reflected wave and the velocity at peak systole (VR:VMAX). RESULTS: VCYC was unchanged between premenopausal and postmenopausal women (69.4 +/- 9.6 and 67.5 +/- 11.1 cm/s, respectively). AMAX was significantly higher (P = 0.007) in premenopausal women (987.9 +/- 280.7 cm/s) compared with postmenopausal women (743.1 +/- 100.3). Conversely, VR:VMAX was significantly smaller (P < 0.001) in premenopausal women (0.90 +/- 0.09) compared with postmenopausal women (1.11 +/- 0.05). In postmenopausal women, the reflected wave is higher than the maximum velocity at peak systole, suggesting the presence of a shoulder in the MCA waveform. CONCLUSIONS: Further investigations are required to assess whether this waveform analysis can provide insight into pathophysiologic changes in cerebral hemodynamics with aging.

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation.

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs.

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.

Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea.

The practical purpose of diagnostic assessment in most cases of obstructive sleep apnea is to predict which patients have symptoms that will improve on treatment. We measured the accuracy with which clinicians make this prediction using polysomnography compared with oximeter-based home monitoring. Patients referred to a sleep center with suspicion of symptomatic obstructive sleep apnea were randomized to have polysomnography or home monitoring. Patients with comorbidity or physiologic consequences of sleep apnea were excluded. Sleep specialists estimated the likelihood of success of treatment as greater than 50% (predicted success) or less than 50% (predicted failure) on the basis of clinical data and test results. All patients were treated for 4 weeks with autoadjusting continuous positive airway pressure. Success was defined as an increase greater than 1.0 in Sleep Apnea Quality of Life Index. Correct prediction rates were compared. Two hundred eighty-eight patients were enrolled. Initial patient characteristics, compliance, and improvement in quality of life at 4 weeks were not different in the two groups. The correct prediction rate was 0.61 with polysomnography and 0.64 with home monitoring (not significant). We conclude that the ability of physicians to predict the outcome of continuous positive airway treatment in individual patients is not significantly better with polysomnography than with home oximeter-based monitoring.