Sweetums 24% Sucrose

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Combined use of nonnutrative sucking and oral sucrose helps calm
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Why 24% sucrose solution?
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Source: http://www.sandboxmedical.com/sweetums_pro...

Pulmonary Function Testing Symposium 2017

Pulmonary Function Testing Symposium 2017

Canadian Association of Cardio-Pulmonary Technologists

Friday, 22 September 2017 at 7:45 AM - Saturday, 23 September 2017 at 4:00 PM (EDT) Toronto ON

sponsored by the Canadian Association of Cardiopulmonary Technologists, Novus Medical Inc. and MGC Diagnostics.  Goto https://www.eventbrite.ca/e/pulmonary-function-testing-symposium-2017-tickets-33394162840?ref=ecount to register for this world class educational symposium for PFT and CPET.  

The Pulmonary Function Testing Symposium 2017 is a 2 day event involving presentations and workshops on topics in the field of Pulmonary Function Testing.  It is open to Pulmonary Function Technologist, Registered Cardio-Pulmonary Technologist, Respiratory Therapist and any other alllied health professional.  Great opportunity to meet others in the field, to have group discussions and to network.  

Hotel Information: for discounted rate contact Laura Seed – lseed@hotmail.com


Friday September 22, 2017

07:45 – 08:35 Registration and Continental Breakfast

08:35 – 08:45 Opening Remarks – Laura Seed RCPT(p), SickKids

08:45 – 09:30 Pulmonary function assessment of the COPD patient with a focus on rehabilitation - Dr. Chris Allen

09:30 – 10:15 Clinical Practice Parameters and Facility Standards. The Ontario model - Dr. Gottschalk, Hamilton & Lori Davis RCPT(p)

10:15 – 10:30 Refreshment Break

10:30 – 11:15 New inhalers for COPD and asthma: a user’s guide – Dr. Stanbrook, Toronto Western

11:15 – 12:00 Infection Prevention and Control - Angela Thomas, RN, SickKids

12:00 – 12.45 Lunch

12:45 – 14:15Technical Workshop A: Spirometry – Ontario Lung Association, Provider Education Program. (Accredited with the College of Family Physicians)
Technical Workshop B: Mapping your QC program – Susan Blonshine, RRT, TechEd Inc

14:15 – 14:30 Break

14:30 – 16:00Technical Workshop A: Mapping your QC program - Susan Blonshine, RRT, TechEd Inc
Technical Workshop B: Spirometry – Ontario Lung Association, Provider Education Program. (Accredited with the College of Family Physicians)

19:00 PFT Social – Monarch’s Pub, Chelsea Hotel.

Saturday September 23, 2017

08:00 – 08:30 Continental Breakfast

08:30 – 09:15 Spirometry: The Good, the Bad and the Ugly – David Wilson RCPT(p), SickKids

09:15 – 10:00 The ABCs of plethysmography – Dr. Allan Coates, SickKids

10:00 – 10:15 Refreshment Break

10:15 – 11:00 Predicted Values – Looking at confounding factors – Andrea White-Markham, RRT

11:00 – 11:45 Methacholine Challenge: What do we know now? – Dr. Myrna Dolovich, McMaster & Tony Kajnar RRT, Sault Area Hospital

11:45 – 12:00 Closing Remarks before workshops.

12:00 – 12:45 Lunch

12:45 – 14:15Technical Workshop C: Cardiopulmonary exercise testing – Jane Schneiderman, PhD & Susan Iori, R.Kin, SickKids
Technical Workshop D: Plethysmography workshop – Tony Kajnar, RRT, Sault Area Hospital

14:15 – 14:30 Break

14:30 – 16:00Technical Workshop C: Plethysmography workshop – Tony Kajnar, RRT, Sault Area Hospital
Technical Workshop D: Cardiopulmonary exercise testing – Jane Schneiderman, PhD & Susan Iori, R.Kin, SickKids

Have questions about Pulmonary Function Testing Symposium 2017? Contact Canadian Association of Cardio-Pulmonary Technologists

CSRT 2017 Highlights

Novus Medical Inc. sponsors the CSRT banquet entertainment for a second year

Novus Medical Inc. has sponsored the entertainment for a second year.  After a stepping in at the last minute to provide the entertainment for the banquet in 2016, Novus Medical Sales Manager and resident DJ, Dan Pinard was asked back to provided the musical entertainment for the 2017 banquet.  DJ Danny P kept the Respiratory Therapists letting loose and dancing until 1 am when it was time to close the banquet hall.  

In the exhibit hall, Novus Medical launched their new "Novus Green" Converse Chuck Taylors.   The bright green shoes contrasted by the black trousers was definitely a way to get noticed.  But seriously, the highlights of the Novus Medical booth had to the new Resmon PRO FOT from MGC Diagnostics and the new 17.3 inch Bellavista 1000e from IMT Medical.  The booth staff were busy doing demonstrations of these devices during exhibit hall hours for the duration of the conference.  For more information on the Resmon PRO and how it can add value to your PFT department email us at info@novusmedical.ca.  For more information about the iPad® of ventilators with the most advanced synchronization and forward thinking software, the Bellavista 1000e, please email info@novusmedical.ca.  For more information about the Novus Green Chuck Taylors ....well you should be able to find them at any fine sporting shoe stores in your area.  

Seeya next year in Vancouver.


PITSI Harness, a seat belt for transport incubators

The PITSI harness has been re-introduced into Canada, and is now distributed by Novus Medical Inc.  The PITSI was developed in conjunction with the Quebec EVAQ transport team, to secure infants being transported in the Draeger Transport Isollette.  The PITSI harness is a seat belt of sorts, that secures the infant at the shoulders and legs similar to a 5 point harness seen in race cars.  The PITSI has been specifically designed to allow access to the infant for procedures, blood work and invasive lines. 

The PITSI is a must for transporting infants in a transport incubator.  email Novus at info@novusmedical.ca for more information and pricing.  

CSRT 2017 Halifax and the launch of the Bellavista 1000e 17 inch

Novus Medical Inc. is looking forward to demonstrating Canada's newest and most sophisticated mechanical ventilator, the bellavista by IMT Medical.  The Swiss made bellavista ventilator features neonatal to adult ventilation, NIV, nCPAP, HFOT (high flow oxygen therapy) and lung recruitment tools.  One of bellavista's greatest advantages, is it's automated synchrony tools, especially important for NIV and pressure support ventilation.  

Novus will also be displaying the brand new bellavista 1000e with a 17 inch Gorilla Glass display.  

Come to the Novus Medical booth to get a demonstration of the bellavista and receive a ballot for a chance to win a UE Boom portable speaker valued at $250.00.  

Breath Test May Soon Detect Pneumonia-Causing Bacteria in ICU Patients on Ventilation

Breath Test May Soon Detect Pneumonia-Causing Bacteria in ICU Patients on Ventilation

MARCH 21, 2017



A non-invasive test that relies only on collecting gases from a person’s breath may soon help doctors detect a potentially aggressive species of bacteria that causes pneumonia in intensive care unit (ICU) patients needing mechanical ventilation.

The new test may lead to more judicious use of antibiotics — a huge consideration given the ever-increasing rates of antibiotic resistance worldwide.

The study, Breath analysis for noninvasively differentiating Acinetobacter baumannii ventilator-associated pneumonia from its respiratory tract colonization of ventilated patients,” appeared in the Journal of Breath Research.

Acinetobacter (A.) baumannii is one of many bacterial species that can cause pneumonia in patients on mechanical ventilation. This so-called ventilator-associated pneumonia (VAP) can be the tipping point that kills already severely ill ICU patients. But A. baumannii presents a challenge for physicians trying to diagnose and treat ventilator-associated pneumonia. The bacteria resist nearly all available antibiotics; making matters even more complicated, it can exist in two different forms.

One form causes pneumonia, while the other simply colonizes the lung harmlessly. But so far, there has been no way for physicians to tell if a detected bacteria is causing disease or not. This, in turn, makes it more likely they’ll prescribe antibiotics unnecessarily.

To get around this situation, researchers at China’s Zhejiang University School of Medicine first analyzed volatile organic compounds, or gases, present in patients’ breath. Using the 52-bed ICU of the school’s Sir Run Run Shaw Hospital, they compared 20 patients with VAP caused by A. baumannii to 20 whose lungs had been colonized by the bacteria without apparent disease. In addition, they selected 20 patients who were ventilated but had neither pneumonia nor A. baumannii in their lungs as controls.

The team then compared the identified compounds to those emitted by the bacteria and kept in a lab dish. After a thorough analysis, they isolated four compounds present in both patients and lab-grown bacteria” 1-undecene, decanal, longifolene and tetradecane.

The test could discern not only between patients with no A. baumannii infection and those with the bacteria in their lungs, but also between infectious and colonizing forms of the bacteria. The 24-month study lasted from February 2014 to February 2016.

Researchers admit that the new method needs further testing and validation before being introduced as a routine tool. But they say it shows great promise in improving the diagnosis and treatment of pneumonia among already critically ill patients.

Source: https://pneumoniaresearchnews.com/2017/03/...

IMT Medical - the bellavista gateway


Enhancing the clinical use of the advantages

of Internet of things (IoT):


bellavista gateway, the new, innovative cloud service from imtmedical ag, increases the safety

of ventilated patients in ICU, high care, home care

and during transport.

bellavista gateway is our youngest brain child. The cloud-based respiratory care ventilation monitoring system allows medical staff to access the current monitoring and measurement data directly from the ventilator via a cloud solution, irrespective of the location, enabling them to monitor the ventilated patient as closely as required. This gateway allows a response with the necessary immediate medical assistance in an emergency at any time.

A clear improvement of the current situation
Until now, the safety of ventilated patients has been critically dependent on the monitoring cycle of the support staff. Enhancedpatient monitoring and an improvement in patient safety has only been possible with considerably higher costing solutions. In the event of an acute risk to the ventilated patient, the physician responsible for the ventilated patient either has to attend to or delegate ventilation changes.

Debunking myths in pulmonary function testing

to see the full article on the CJRT website, please go to http://www.cjrt.ca/article/20175301-05/

Jeffrey M Haynes, RRT, RPFT, FAARC

Author Affiliations

Pulmonary Function Laboratory, St Joseph Hospital, Nashua, NH

Correspondence: Jeffrey Haynes, Pulmonary Function Laboratory, St Joseph Hospital, 172 Kinsley St, Nashua, NH 03060, e-mail: gro.hnhjs@senyahj

This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) (http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact moc.trsc@rotide

Can J Respir Ther 2017;53(1):7–11


The goal of evidence-based medicine is to move away from practices based on theory and replace them with practices based on robust scientific evidence. Unfortunately, many clinicians performing and interpreting pulmonary function tests dogmatically adhere to ideas based on theory despite evidence to the contrary. This paper will highlight examples of myths dressed up as science in the realm of pulmonary function testing. The goal of this paper is not just to inform but to also stimulate healthy debate and introspection about what we believe to be true and how these beliefs impact our practice and patient care.


Caffeine should be withheld prior to pulmonary function testing

As a member of the methylxanthine family, caffeine has been thought to possess bronchodilator properties. Because of this, the 1999 American Thoracic Society (ATS) guideline for methacholine and exercise testing recommended that caffeine-containing products be withheld on the day of testing [1]. While the 2005 ATS/European Respiratory Society guidelines for pulmonary function testing do not prohibit caffeine prior to testing [2], many laboratories continue to prohibit caffeine use prior to testing. It has been my experience that many patients are unhappy that they must withhold their morning coffee or tea prior to testing. Yurach et al [3] assessed the effect of caffeinated coffee on patients undergoing spirometry, methacholine challenge, and exhaled nitric oxide testing. The investigators found that a 16-ounce cup of coffee (~330 mg caffeine) had no effect on FEV1, methacholine responsiveness, or mean exhaled nitric oxide (Table 1). Precluding patients from ingesting usual amounts of caffeine prior to pulmonary function testing is unwarranted.


Note: Data are expressed as mean with standard deviation. FEV1,= forced expiratory volume in the first second; PC20, provocative concentration of methacholine causing a 20% decline in FEV1;FENO = fraction of expired nitric oxide; ppb, parts per billion. Table produced with data from Yurach et al [3].

*p > 0.05.

†Measured after decaffeinated coffee.

Patients are usually the cause of poor quality data

Numerous studies have documented a high prevalence of poor-quality spirometry testing in both the pulmonary function laboratory and office settings [4, 5]. This has occurred at a time when spirometer accuracy and reliability appears to be much better than in the past [6]. It is therefore not surprising that most technologists can be expected to blame poor patient effort and cooperation for poor test quality [7]. However, the literature clearly indicates that most patients, even children [8] and the elderly [9], are capable of producing high-quality pulmonary function data. The key to higher quality pulmonary function data is technologist performance monitoring and feedback [7]. In the Lung Health Study, Enright et al [10] documented a reduction in spirometry test quality after initial technologist training, which improved with retraining, but could only be sustained with a program of on-going technologist performance monitoring. Borg et al [4] evaluated the effect of technologist monitoring and feedback in two clinical pulmonary function laboratories. Prior to the intervention, lab #1 and lab #2 had poor test acceptability and reproducibility rates, 61% and 59%, respectively. Lab #1 implemented a technologist performance monitoring and feedback program and lab #2 did not. In response to the intervention, lab #1’s test quality rates rose to 92% while the quality of lab #2 remained poor at 65% (Figure 1). The unfortunate truth is that it is the technologist, and not the patient, who is usually the cause of poor quality testing. Pulmonary function laboratories should include technologist training and performance monitoring in their quality assurance programs.



FIGURE 1. The percentage of quality spirometry tests from two clinical laboratories. Baseline data from 2004 is compared to 2008 after lab #1 instituted an on-going technologist performance monitoring and feedback program. Figure produced with data from Borg et al [4].

Only high-quality spirometry tests are meaningful

As stated above, high-quality test results should be the goal of every pulmonary function laboratory. However, there are always going to be some patients, albeit a minority, that will not be able to produce high-quality spirometry. When spirometry quality is not perfect, many technologists reject sub-optimal tests to avoid reporting spurious data. While the practice of discarding less-than-perfect spirometry data is well intentioned, it may frequently discard clinically useful data. Using an A-B-C-D-F scoring strategy, Hankinson et al [11] found that only quality scores of D or F affected test interpretation. While we must always strive for maximum quality, technologists and physicians should exercise caution when discarding data.

Technologists must scream at patients to obtain quality spirometry results

A typical lesson in spirometry testing includes stressing the importance of using a loud voice, to the point of yelling or screaming test instructions, to obtain maximum effort and quality data. This practice has no basis in science and in most situations is completely unnecessary. Yelling or screaming spirometry instructions can be frightening to children, annoying to teens, and less audible to those with hearing deficits. Demonstrating the maneuver to the patient prior to testing and using suggestive body language during testing is more effective than yelling or screaming instructions at the patient. Studies should be conducted to investigate the best way to communicate pulmonary function test instructions to patients.

FEF25–75% aids in test interpretation

The forced expiratory flow over the middle half of the vital capacity (FEF25–75%) is believed by many to be representative of small airways function. A common interpretation of a “low FEF25–75%” is that the test results are “compatible with small airways disease.” The problem with this interpretation is that FEF25–75% has a very wide normal range [12]. Indeed, after age 70 years, one can have an FEF25–75% less than 50% of predicted and still be above the 5th percentile [13]. Quanjer et al [13] examined the impact of FEF25–75% on test interpretation, they found the incidence of FEF25–75% falling below the lower limit of normal as an isolated finding (i.e., normal FVC, FEV1, and FEV1/FVC) was only 2.75%. FEF25–75% adds virtually nothing to the information provided by FVC, FEV1, and FEV1/FVC.

DLCO/VA can normalize an abnormal DLCO

For many clinicians, the interpretation of diffusing capacity (DLCO) is based on both DLCO and the DLCO to alveolar volume ratio (DLCO/VA). While it is undeniable that DLCO and lung volume are directly related, this relationship is both complicated and difficult to predict [14, 15]. A common mistake is to declare an abnormal DLCO normal if the DLCO/VA is within the normal range. This implies that the DLCO is low due exclusively to a lack of lung volume, not alveolar–capillary pathology. A recently published study by Pastre et al [16] shows that DLCO/VA can often be within the normal range even in patients with significant parenchymal lung disease. Therefore, DLCO/VA is not a reliable parameter for inverse modeling (i.e., predicting structure from function) [17].

80% of predicted is a reliable lower limit of normal

The interpretation of pulmonary function data requires knowledge of expected values in subjects without respiratory disease. To this end, reference or “predicted” equations are generated. The mean or median value for a pulmonary function value is referred to as the “predicted value.” If the measured value is identical to the predicted value, the measured value is declared “100% of predicted.” If the data are normally distributed, the predicted value will be found at the center of a symmetrical bell curve. In other words, there are an equal number of normal values above and below the predicted value. A long-standing and fundamentally flawed technique to define the lower limit of normal (LLN) of pulmonary function values is to multiply the predicted value by 0.80. The so-called “80% of predicted” rule declares any value below 80% as abnormal and vice versa. In 1979, Sobol and Sobol [18] commented that “nowhere else in medicine is such a naïve view taken of the limit of normal.” The “80% rule” is statistically invalid for a number of reasons. Firstly, the normal ranges for different pulmonary function values are not identical. In addition, the normal variance around any value is affected by age, race, and gender [19]. As previously mentioned, after age 70 years, an FEF25–75% value less than 50% of predicted can still be normal [13]. Quanjer et al [20] found that using the “80% of predicted” rule and 0.70 as the LLN for FEV1/FVC misclassified >20% of patients. Wesolowski et al [21] documented that 14% of surgical lung cancer patients had pulmonary function values which were both <80% of predicted and above the LLN. This difference proved to be clinically important because having lung function below the LLN was a better predictor for perioperative complications than lung function <80% predicted but also ≥ LLN. Pulmonary function data should not be interpreted using 80% of predicted as the LLN (Figure 2, [22]).



FIGURE 2. The percent of predicted lower limit of normal as a function of age in males and females. The red horizontal dashed line represents 80% of predicted. LLN, lower limit of normal; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity. From Quanjer et al [22] (open access material under CC-BY-NC license).

A positive methacholine challenge confirms asthma

Methacholine challenge tests (MCT) are performed to test for the presence or absence of airway hyper-responsiveness (AHR) [23]. AHR is clearly a feature of asthma; however, AHR is not exclusive to asthma. For example, Leone et al [24] found that 46% of patients with non-allergic rhinitis with eosinophilia syndrome and no respiratory symptoms demonstrated AHR to methacholine. AHR is also a feature of COPD [25], sarcoidosis [26], and allergic rhinitis [27]. In addition, some subjects with no signs or symptoms of asthma demonstrate AHR to methacholine (asymptomatic AHR) [28, 29]. In patients with an intermediate pre-test probability of asthma, AHR in response to MCT may significantly increase the post-test probability of asthma. When the post-test probability of asthma is higher than the pre-test probability of asthma, a working diagnosis can be made. However, it is prudent to document an improvement in symptoms and lung function in response to therapy before making a working diagnosis of asthma official.

A negative methacholine challenge excludes asthma

As mentioned above, MCTs are performed to test for the presence or absence of AHR [23]. A lack of demonstrable AHR in response to MCT may significantly decrease the post-test probability of asthma; however, the sensitivity of MCT is not 100%. Indeed, Anderson et al [30] found that 45% of children with a positive exercise challenge had a negative methacholine challenge. In a study of elite athletes, the sensitivity of MCT to identify a positive response to eucapnic voluntary hyperventilation was only 36% [31]. The failure of MCT to identify asthma with perfect sensitivity is multi-factorial including both physiologic and technological considerations.

From a physiologic standpoint, phenotypic differences among asthmatics may affect the response to MCT [32]. In addition, the response to methacholine may be affected by seasonal variations in AHR. For example, Sposato et al [33] found a greater prevalence of AHR to methacholine in the spring and fall than during the summer months. Fruchter and Yigla [34] also found a higher incidence of AHR to methacholine in winter and spring when compared to summer. It is probably not uncommon for a patient to experience respiratory symptoms during the height of spring pollen season but not have their MCT scheduled until months later, after their allergen exposure has waned.

There are also technologic and methodological factors that can affect the results of a MCT. Methacholine dose, nebulizer type, inhalation method (e.g., dosimeter versus tidal breathing), and the threshold for a “positive test” can all affect MCT interpretation [1].

The impact of the bronchodilatory and bronchoprotective effect of deep inhalation on MCT has received a lot of attention. Cockcroft and Davis [35] have shown that using the full inhalation dosimeter method can significantly reduce the response to MCT and may result in false negative tests in patients with mild AHR.

In addition, relying solely on FEV1 as a MCT outcome measure may reduce MCT sensitivity for AHR. An example of a patient with respiratory symptoms, markedly reduced specific conductance (sGaw), yet little to no change in FEV1 during MCT is shown in Figure 3 [36]. Khalid et al [37] evaluated sGaw and FEV1 in 138 patients undergoing a MCT. The researchers found that a 51–52% reduction in sGaw was a more appropriate cut-off point for a positive MCT than the 45% reduction recommended by the ATS [1]. A remarkable finding was that 32 patients with an FEV1 decline <20% had a reduction in sGaw >50% (Figure 4). In a similar study, Parker and McCool [38] measured FEV1 and sGaw following MCT in 248 consecutive patients with asthma-like symptoms. Forty patients showed a response to methacholine as assessed by sGaw (≥ 40% reduction) without a significant decline in FEV1 (<20%). A negative MCT reduces the post-test probability of asthma; however, clinicians should be mindful that a negative MCT cannot rule out asthma with 100% certainty.



FIGURE 3. sGaw and FEV1 in a symptomatic patient during a MCT. (A) Baseline testing before methcholine challenge test (MCT). (B) Post MCT. (C) Post BD administration. sGaw, specific airway conductance; FEV1. forced expiratory volume in 1 second; MCT, methacholine challenge test; BD, bronchodilator). From Haynes [35] with permission.



FIGURE 4. Change in sGaw versus FEV1 in patients undergoing MCT. The red square includes subjects with a >50% reduction in sGaw with a <20% reduction in FEV1. The black line is the linear regression line. sGaw, specific airway conductance; FEV1, forced expiratory volume in 1 second; MCT, methacholine challenge test. From Khalid et al [36] with permission.

A negative exercise challenge test excludes exercise-induced bronchospasm

Exercise challenge tests are commonly performed to identify or exclude exercise-induced bronchospasm as the source of exercise limitation and symptomatology [1, 39]. An obvious limitation of exercise challenge tests is that they are not performed under the same circumstances as those from where the patient’s symptoms originate. This is perhaps no more true than patients involved in cold-weather athletics. Rundell et al [40] performed field exercise challenge testing in elite cold-weather athletes; 78% of athletes with a positive field exercise challenge test had a negative exercise challenge test in a clinical laboratory. Differences between field and laboratory testing may be due to differences in exercise pattern and intensity as well as environmental factors such as ambient humidity and air quality. Anderson et al [41] performed two exercise challenge tests within four days in 373 subjects with asthma-like symptoms associated with exercise. While most subjects had either two positive or two negative tests, 23.9% of subjects had conflicting results (i.e., one positive, one negative). Exercise intensity could not explain the differences in test outcome. For these reasons, a single negative exercise challenge test cannot by itself exclude the possibility of exercise-induced bronchoconstriction.

Normal spirometry excludes emphysema

An irreversible obstructive spirometry test in a patient with COPD risk factors defines the disease [42]. However, over the past several years it has become known that COPD has many phenotypes [43]. Some of these phenotypes refute the paradigm that normal spirometry precludes COPD pathology. For example, the COPDGene investigators found that 24% of current or former smokers with normal spirometry and a GOLD 0 classification had computed tomography evidence of emphysema [43]. Another poorly appreciated syndrome associated with cigarette smoking is combined pulmonary fibrosis emphysema (CPFE). Patients with CPFE have radiologic evidence of upper lobe emphysema and lower lobe fibrosis [44]. Patients with CPFE typically have a low diffusing capacity, elevated alveolar–arterial oxygen gradient, but normal spirometry and lung volumes [45]. Relying solely on spirometry to diagnose or exclude disease in symptomatic smokers can be expected to misdiagnose many patients with emphysema and CPFE.

Delta FEV1 effectively assesses bronchodilator response in COPD

As mentioned above, spirometric indices such as FEV1 are widely relied upon to make a diagnosis of COPD. As a consequence, many clinicians use ∆FEV1 to assess bronchodilator response/benefit in COPD patients. While patients with COPD can demonstrate significant increases in FEV1 after bronchodilator, many do not. A not so uncommon yet mistaken conclusion is that an insignificant ∆FEV1 indicates a lack of therapeutic efficacy. However, it is important to keep in mind that COPD patients seek medical care for dyspnea, not a recalcitrant FEV1. Bronchodilators reduce dyspnea on exertion by reducing the rate of dynamic hyperinflation [46], which may not be accompanied by an arbitrarily agreed upon “significant” ∆FEV1. O’Donnell et al [47] studied acute bronchodilator response in COPD patients who did not show improvement in FEV1. These patients showed significant reduction in hyperinflation (i.e., increased inspiratory capacity, reduced residual volume) despite no change in FEV1. Similar findings were recently shown by McCartney et al [48]. In their study, many COPD patients showed marked reduction in residual volume after bronchodilator despite little change in FEV1. Judging bronchodilator response in COPD patients solely on ∆FEV1 may lead to an under-appreciation of clinically important improvements in lung function, exercise capacity, and quality-of-life.


Evidence-based medicine has revolutionized both diagnostics and therapeutics. However, the age of evidence-based medicine has not made pulmonary function laboratories immune from policies, procedures, and mistaken beliefs borne of myth and unproven theory. Indeed, pulmonary function guidelines contain recommendations based on both scientific data and unproven expert opinions. Pulmonary function technologists should be on the forefront of incorporating evidence-based practices in pulmonary function laboratories.


1.  Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. Am J Respir Crit Care Med 2000;161(1):309–29. doi: 10.1164/ajrccm.161.1.ats11-99.

2.  Miller MR, Crapo R, Hankinson J, et al. General considerations for lung function testing. Eur Respir J 2005;26(1):153–61. doi: 10.1183/09031936.05.00034505.

3.  Yurach MT, Davis BE, Cockcroft DW. The effect of caffeinated coffee on airway response to methacholine and exhaled nitric oxide. Respir Med 2011;105(11):1606–10. doi: 10.1016/j.rmed.2011.06.006.

4.  Borg BM, Hartley MF, Bailey MJ, Thompson BR. Adherence to acceptability and repeatability criteria for spirometry in complex lung function laboratories. Respir Care 2012;57(12):2032–8. doi: 10.4187/respcare.01724.

5.  Leuppi JD, Miedinger D, Chhajed PN, et al. Quality of spirometry in primary care for case finding of airway obstruction in smokers. Respiration 2010;79(6):469–74. doi: 10.1159/000243162.

6.  Skloot GS, Edwards NT, Enright PL. Four-year calibration stability of the EasyOne portable spirometer. Respir Care 2010;55(7):873–7.

7.  Haynes JM. Comprehensive quality control for pulmonary function testing: It’s time to face the music. Respir Care 2010;55(3):355–7.

8.  Gochicoa-Rangel L, Vargas-Domínguez C, García-Mujica ME, et al. Quality of spirometry in 5-to-8-year-old children. Pediatr Pulmonol 2013;48(12):1231–6. doi: 10.1002/ppul.22765.

9.  Haynes JM. Pulmonary function test quality in the elderly: A comparison with younger adults. Respir Care 2014;59(1):16–21. doi: 10.4187/respcare.02331.

10.  Enright PL, Johnson LR, Connett JE, Voelker H, Buist AS. Spirometry in the lung health study. 1. Methods and quality control. Am Rev Respir Dis 1991;143(6):1215–23. doi: 10.1164/ajrccm/143.6.1215.

11.  Hankinson JL, Eschenbacher B, Townsend M, Stocks J, Quanjer PH. Use of forced vital capacity and forced expiratory volume in 1 second quality criteria for determining a valid test. Eur Respir J 2015;45(5):1283–92. doi: 10.1183/09031936.00116814.

12.  Quanjer PH, Stanojevic S, Cole TJ, et al. Multi-ethnic reference values for spirometry for the 3–95-yr age range: The global lung function 2012 equations. Eur Respir J 2012;40(6):1324–43. doi: 10.1183/09031936.00080312.

13.  Quanjer PH, Weiner DJ, Pretto JJ, Brazzale DJ, Boros PW. Measurement of FEF25–75% and FEF75% does not contribute to clinical decision making. Eur Respir J 2014;43(4):1051–8. doi: 10.1183/09031936.00128113.

14.  Hughes JM, Pride NB. In defence of the carbon monoxide transfer coefficient KCO (TL/VA. Eur Respir J 2001;17(2):168–74. doi: 10.1183/09031936.01.17201680.

15.  Cotes JE. Carbon monoxide transfer coefficient KCO (TL/VA): A flawed ndex. Eur Respir J 2001;18(5):893–4. doi: 10.1183/09031936.01.00246701.

16.  Pastre J, Plantier L, Planes C, et al. Different KCO and VA combinations exist for the same DLCO value in patients with diffuse parenchymal lung diseases. BMC Pulm Med 2015;15:100. doi: 10.1186/s12890-015-0084-1.

17.  BatesJHT. Lung mechanics, an inverse modeling approach. New York: Cambridge University Press; 2009. p. 9–14.

18.  Sobol BJ, Sobol PG. Per cent of predicted as the limit of normal in pulmonary function testing: A statistically valid approach. Thorax 1979;34(1):1–3. doi: 10.1136/thx.34.1.1.

19.  Culver BH. How should the lower limit of normal range be defined? Respir Care 2012;57(1):136–45. doi: 10.4187/respcare.01427.

20.  Miller MR, Quanjer PH, Swanney MP, Ruppel G, Enright PL. Interpreting lung function data using 80% predicted and fixed thresholds misclassifies more than 20% of patients. Chest 2011;139(1):52–9. doi: 10.1378/chest.10-0189.

21.  Wesolowski SP, Boros PW, Orlowski TM, Quanjer PH. Use the lower limit of normal, not 80% predicted, in judging eligibility for lung resection. Respiration 2016;92(2):65–71. doi: 10.1159/000447974.

22,  PhilipH.Quanjer, Sanja Stanojevic,TimJ.Cole, Janet Stocks. GLI-2012 – All-Age Multi-Ethnic Reference Values for Spirometry. Global Lung Function Initiative. Avaialable at: http://www.ers-education.org/lrmedia/2012/pdf/266696.pdf.

23.  Cockcroft DW. Direct challenge tests: Airway hyperresponsiveness in asthma: Its measurement and clinical significance. Chest 2010;138(2 Suppl):18S–24S. doi: 10.1378/chest.10-0088.

24.  Leone C, Teodoro C, Pelucchi A, et al. Bronchial responsiveness and airway inflammation in patients with nonallergic rhinitis with eosinophilia syndrome. J Allergy Clin Immunol 1997;100(6 Pt 1):775–780. doi: 10.1016/S0091-6749(97)70273-2.

25.  van den Berge M, Vonk JM, Gosman M, Lapperre TS, Snoeck-Stroband JB, Sterk PJ, et al. Clinical and inflammatory determinants of bronchial hyperresponsiveness in COPD. Eur Respir J 2012;40(5):1098–1105. doi: 10.1183/09031936.00169711.

26.  Young LM, Good N, Milne D, Zeng I, Kolbe J, Wilsher ML. The prevalence and predictors of airway hyperresponsiveness in sarcoidosis. Respirology 2012;17(4):653–659. doi: 10.1111/j.1440-1843.2012.02137.x.

27.  Sin BA, Yildiz OA, Dursun AB, Misirligil Z, Demirel YS. Airway hyperresponsiveness: A comparative study of methacholine and exercise challenges in seasonal allergic rhinitis with or without asthma. J Asthma 2009;46(5):486–491. doi: 10.1080/02770900902855936.

28.  Boulet LP, Prince P, Turcotte H, et al. Clinical features and airway inflammation in mild asthma versus asymptomatic airway hyperresponsiveness. Respir Med 2006;100(2):292–9. doi: 10.1016/j.rmed.2005.04.026.

29.  Haynes JM. A positive methacholine challenge test in the absence of symptoms. Respir Care 2007;52(6):759–62.

30.  Anderson SD, Charlton B, Weiler JM, et al. Comparison of mannitol and methacholine to predict exercise-induced bronchoconstriction and a clinical diagnosis of asthma. Respir Res 2009;10:4. doi: 10.1186/1465-9921-10-4.

31.  Holzer K, Anderson SD, Douglass J. Exercise in elite summer athletes: Challenges for diagnosis. J Allergy Clin Immunol 2002;110(3):374–80. doi: 10.1067/mai.2002.127784.

32.  Shim E, Lee E, Yang SI, et al. The association of lung function, bronchial hyperresponsivenss, and exhaled nitric oxide differs between atopic and non-atopic asthma in children. Allergy Asthma Immunol Res 2015;7(4):339–45. doi: 10.4168/aair.2015.7.4.339.

33.  Sposato B, Scalese M, Pammolli A, Scala R, Naidi M. Seasons can influence the results of the methacholine challenge test. Ann Thorac Med 2012;7(2):61–8. doi: 10.4103/1817-1737.94521.

34.  Fruchter O, Yigla M. Seasonal variability of the methacholine challenge test. J Asthma 2009;46(9):951–954. doi: 10.3109/02770900903265796.

35.  Cockcroft DW, Davis BE. The bronchoprotective effect of inhaling methacholine by using total lung capacity inspirations has a marked influence on the interpretation of the test result. J Allergy Clin Immunol 2006;117(6):1244–8. doi: 10.1016/j.jaci.2006.02.038.

36.  Haynes J. A positive methacholine challenge based on specific airway conductance: A case report. Can J Respir Ther 2016;52(2):53–5.

37.  Khalid I, Morris ZQ, DiGiovine B. Specific conductance criteria for a positive methacholine challenge test: Are the American Thoracic Society guidelines rather generous? Respir Care 2009;54:1168–74.

38.  Parker AL, McCool FD. Pulmonary function characteristics in patients with different patterns of methacholine airway hyperresponsiveness. Chest 2002;121:1818–23. doi: 10.1378/chest.121.6.1818.

39.  Parsons JP, Hallstrand TS, Mastronarde JG, et al. An official American Thoracic Society clinical practice guideline: Exercise-induced bronchoconstriction. Am J Respir Crit Care Med 2013;187(9):1016–27. doi: 10.1164/rccm.201303-0437ST.

40.  Rundell KW, Wilber RL, Szmedra L, Jenkinson DM, Mayers LB, Im J. Exercise-induced asthma screening of elite athletes: Field versus laboratory exercise challenge. Med Sci Sports Exerc 2000;32(2):309–316. doi: 10.1097/00005768-200002000-00010.

41.  Anderson SD, Pearlman DS, Rundell KW, et al. Reproducibility of the airway response to an exercise protocol standardized for intensity, duration, and inspired air condition, in subjects with symptoms suggestive of asthma. Respir Res 2010;11(1):120. doi: 10.1186/1465-9921-11-120.

42.  Qaseem A, Wilt TJ, Weinberger SE, et al. Diagnosis and management of stable chronic obstructive pulmonary disease: A clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med 2011;155(3):179–91. doi: 10.7326/0003-4819-155-3-201108020-00008.

43.  Han MK, Agusti A, Calverley PM, Celli BR, Criner G, Curtis JL, et al. Chronic obstructive pulmonary disease phenotypes: The future of COPD. Am J Respir Crit Care Med 2010;182(5):598–604. doi: 10.1164/rccm.200912-1843CC.

44.  Regan EA, Lynch DA, Curran-Everett D, et al. Clinical and radiologic disease in smokers with normal spirometry. JAMA Intern Med 2015;175(9):1539–49. doi: 10.1001/jamainternmed.2015.2735.

45.  Jankowich MD, Rounds SI. Combined pulmonary fibrosis and emphysema syndrome: A review. Chest 2012;141(1):222–31. doi: 10.1378/chest.11-1062.

46.  O’Donnell DE, Lam M, Webb KA. Spirometric correlates of improvement in exercise performance after anticholinergic therapy in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999;160(2):542–9. doi: 10.1164/ajrccm.160.2.9901038.

47.  O’Donnell DE, Forket L, Webb KA. Evaluation of bronchodilator responses in patients with “irreversible” emphysema. Eur Respir J 2001;18(6):914–20. doi: 10.1183/09031936.01.00216501.

48.  McCartney CT, Weis MN, Ruppel GL, Nayak RP. Residual volume and total lung capacity to assess reversibility in obstructive lung disease. Respir Care 2016;61(11):1505–12. doi: 10.4187/respcare.04323.

PITSI Neonatal Transport Harness Now Available for Sale in Canada

Novus Medical is proud to announce the re-launch of the PITSI Neonatal Transport Harness in Canada.  Originally designed and developed in Montreal PQ, the PITSI Harness disappeared from the Canadian market when the developer and manufacturing was re-located.  The PITSI is used to safely secure infants in a transport incubator.  The PITSI's uniques design provides a secure hold while allowing access to the infant for care and invasive lines.  

"This is the only product of it's kind and is a necessary accessory for transport incubators, to keep the infants safe during transport", said Robert Simms, Marketing Manager of Novus Medical Inc.  Please contact Novus Medical Inc. at info@novusmedical.ca for pricing and more information or visit www.novusmedical.ca for a complete listing of products.  

New MGC Diagnostics PFT machine at CVHC can help identify lung problems

If you have a lung disease such as asthma or COPD, or are having symptoms of lung problems, your doctor may order a Pulmonary Function Test (PFT) and set you up with an appointment to see Mary Curtis, the Certified Respiratory Therapist at Clearwater Valley Hospital and Clinics.

In order to make these tests easier for patients and to deliver more accurate results CVHC recently acquired a new PFT machine.

“The new machine checks how the patient is breathing, how they are able to take air into and out of their lungs, how well the oxygen is able to transfer into the blood stream when it is into the lungs, and also the lung volumes,” says Curtis. “The machine also measures lung volumes and it will tell us if a patient is air trapping (difficulty exhaling completely) or not.”

These tests are commonly ordered by a patients Primary Care Provider, the VA, a cardiologist, or a pulmonologist. PFT tests are typically scheduled Monday - Friday between 10 a.m. and 3 p.m. and they usually take about an hour to complete.

If you haven’t been to see Mary Curtis recently, know that she moved into the old radiology area in the hospital building. If patients need to speak with radiology now they will need to check in with the outpatient receptionist.

The PFT machine is located in Mary’s new office and is designed to be easy for Mary to use (and even easier for patients). The machine’s benefits include faster set-up, minimal analysis time, and unprecedented patient comfort.

“If you have any additional questions, or think you might benefit form a PFT test, please talk to your primary care provider at CVHC,” says Curtis.

Dynamic driving pressure associated mortality in acute respiratory distress syndrome with extracorporeal membrane oxygenation

The survival predictors and optimal mechanical ventilator settings in patients with severe acute respiratory distress syndrome (ARDS) undergoing extracorporeal membrane oxygenation (ECMO) are uncertain. This study was designed to investigate the influences of clinical variables and mechanical ventilation settings on the outcomes for severe ARDS patients receiving ECMO. 


Methods: We reviewed severe ARDS patients who received ECMO due to refractory hypoxemia from May 2006 to October 2015.


Serial mechanical ventilator settings before and after ECMO and factors associated with survival were analyzed. 


Results: A total of 158 severe ARDS patients received ECMO were finally analyzed. Overall intensive care unit (ICU) mortality was 55.1%.


After ECMO initiation, tidal volume, peak inspiratory pressure and dynamic driving pressure were decreased, while positive end-expiratory pressure levels were relative maintained. After ECMO initiation, nonsurvivors had significantly higher dynamic driving pressure until day 7 than survivors.


Cox proportional hazards regression model revealed that immunocompromised [hazard ratio 1.957; 95% confidence interval (CI) 1.216–3.147; p = 0.006], Acute Physiology and Chronic Health Evaluation (APACHE) II score (hazard ratio 1.039; 95% CI 1.005–1.073; p = 0.023), ARDS duration before ECMO (hazard ratio 1.002; 95% CI 1.000–1.003; p = 0.029) and mean dynamic driving pressure from day 1 to 3 on ECMO (hazard ratio 1.070; 95% CI 1.026–1.116; p = 0.002) were independently associated with ICU mortality. 


Conclusions: For severe ARDS patients receiving ECMO, immunocompromised status, APACHE II score and the duration of ARDS before ECMO initiation were significantly associated with ICU survival. Higher dynamic driving pressure during first 3 days of ECMO support was also independently associated with increased ICU mortality.

Noninvasive Breathing Support Device Seen to Help DMD Patient Live to Mid-50s in Case Report

A Duchenne muscular dystrophy (DMD) patient who is now in his 50s gained the notice of researchers, who say his case could illustrate the benefits of noninvasive mechanical ventilation in patients with well-maintained cardiac function.

It is the first report of a patient living into his sixth decade.

The report, “New Survival Target for Duchenne Muscular Dystrophy,” was published in the American Journal of Physical Medicine & Rehabilitation.

DMD patients’ life expectancy has improved significantly, in part because of improvements in ventilation support systems.
“Without ventilatory support, DMD survival did not extend much beyond teen years,” the team wrote. “However, with advances in cardiorespiratory care, life expectancy has increased into the late 20s for patients using continuous tracheostomy ventilatory support and is approximately 40 years for patients using continuous noninvasive ventilatory support.”

The patient in the case report was 53 when evaluated by researchers (he was born in September 1962). He was diagnosed with a typical phenotype and clinical history of DMD.

“Because of improvements in cardiopulmonary care, there has been a great improvement in survival and preservation of quality of life for many of these patients. Whereas it is no longer rare to find patients with Duchenne muscular dystrophy living into their fifth decade, this is the first report of a patient in his sixth decade of life,” the authors wrote.

The man has been able to maintain cardiac function, which is notable because cardiac dysfunction is common in DMD patients. (An unrelated study showed that, in a population of DMD patients, 96% had cardiomyopathies, or abnormalities in their heart muscles.)

“The reason why this patient with typical phenotypic Duchenne muscular dystrophy has preserved cardiac function is unclear. It may be partly because dystrophin has different functions in skeletal and cardiac muscle, or quite possibly, because of his particular point mutation in the dystrophin gene that we have been unable to find reported elsewhere,” the team wrote.

“We believe his survival is due to well-preserved cardiac function along with continuous noninvasive mechanical ventilation,” they wrote. Noninvasive mechanical ventilation is a modality that supports breathing without the need for intubation or surgical airway,” they wrote.

Altogether, this case report suggests that noninvasive mechanical ventilation may be particularly beneficial in enhancing survival of patients with preserved cardiac function.

One-third of Adults Diagnosed with Asthma Don't Have the Disease, Canadian Study Finds

A new research study revealed that 33 percent of adults in Canada who were diagnosed with asthma in the last five years do not have active asthma after all.

The study, “Re-evaluation of Diagnosis in Adults With Physician-Diagnosed Asthma,” was published in the Journal of the American Medical Association.

Lead author of the study was Dr. Shawn Aaron, a senior scientist and respirologist at Ottawa Hospital in Canada. In 2008 he had suggested that about 30 percent of asthma patients had been misdiagnosed. These findings confirm his suspicions.

Of the 613 randomly selected patients from 10 Canadian cities who participated in the study, 33 percent were found to not have asthma. Of those patients, about 90 percent were able to stop their medication and stay off it for at least one year with no threat to their health.

The team concluded that 80 percent of the patients who didn’t have asthma had been taking medication unnecessarily for over a year, and 35 percent of them had been taking medication every day.

“It’s impossible to say how many of these patients were originally misdiagnosed with asthma, and how many have asthma that is no longer active,” Aaron said in a press release. “What we do know is that they were all able to stop taking medication that they didn’t need – medication that is expensive and can have side effects.”

“Doctors wouldn’t diagnose diabetes without checking blood sugar levels, or a broken bone without ordering an x-ray,” he said. “But for some reason many doctors are not ordering the spirometry tests that can definitely diagnose asthma.”

To determine how these study participants had been diagnosed in the first place, investigators looked at all the medical records of patients they could access (530 in total). They found that in 49 percent of the cases, physicians had not ordered the airflow tests needed to confirm a diagnosis and had based their decision on their own observations and their patients’ self-reported symptoms.

In total, 28 percent of the participants did not have anything wrong with their health, and only 2 percent actually suffered from a serious condition like pulmonary hypertension or heart disease. Patients found to be disease-free stopped taking their asthma medication, while the remaining patients began taking the correct medicine right away.

“It wasn’t a surprise to most patients when we told them they didn’t have asthma,” Aaron said. “Some knew all along that their puffer wasn’t working, while others were concerned that they might have something more serious. Thankfully, the majority of the conditions were mild and easily treated.”

“We need to educate physicians and the public to get the diagnosis right in the first place,” he added. “Patients who have difficulty breathing should ask their doctor to order a breathing test (spirometry) to determine if they might have asthma or even chronic obstructive pulmonary disease (COPD).”

And, if patients think they may have been misdiagnosed or no longer have the disease, they should ask their doctor for a spirometry test, he said. “Asthma can be deadly, so patients should never go off their medication without speaking to a doctor first,” Aaron said.

COPD Diagnosis with Lung Function Test Linked to Decreased Mortality, Fewer Hospital Admissions - COPD News Today

https://copdnewstoday.com/2016/11/17/copd-diagnosis-lung-function-test-linked-decreased-mortality-fewer-hospital-admissions/ https://copdnewstoday.com/2016/11/17/copd-diagnosis-lung-function-test-linked-decreased-mortality-fewer-hospital-admissions/

COPD Diagnosis with Lung Function Test Linked to Decreased Mortality, Fewer Hospital Admissions Confirmation of a diagnosis of chronic obstructive pulmonary disease (COPD) using pulmonary function testing is associated with not only a decreased risk of death, but fewer admissions to the hospital due to COPD.

The study reporting the findings, “Outcomes of patients with chronic obstructive pulmonary disease diagnosed with or without pulmonary function testing http://www.cmaj.ca/content/early/2016/11/14/cmaj.151420.full.pdf+html,” was published in the Canadian Medical Association Journal http://www.cmaj.ca/.

COPD is the third leading global cause of death, a leading cause of hospital admission, and affects more than 10 percent of adults. Pulmonary function testing plays a fundamental role in COPD diagnosis by confirming persistent airflow obstruction and ruling out other diseases.

However, pulmonary function testing is underused, with only about 30 to 50 percent of people with a COPD diagnosis undergoing testing.

“Given low rates of testing, these findings point to an opportunity to improve patient outcomes, reduce health services use and decrease healthcare costs by increasing rates of testing for suspected COPD,” the study’s first author, Dr. Andrea Gershon, from the Sunnybrook Research Institute and the Institute for Clinical Evaluative Sciences (ICES), wrote in the study, according to a news release http://medicalxpress.com/news/2016-11-lung-function-copd-patients-health.html.

The research team conducted a longitudinal population study of 68,898 patients with physician-diagnosed COPD from 2005 to 2012 using health administrative data from Ontario, Canada. From these, 16,798 patients had recently been diagnosed with the disease.

The researchers assessed whether having pulmonary function testing around the time of diagnosis was associated with the composite outcome of admission to the hospital for COPD or all-cause mortality.

The team found that from the overall patient population, only 41 percent of the patients had received pulmonary function testing. They also found that these patients were more likely to be younger, to have seen a specialist, and to have seen a primary care physician who followed the clinical guideline recommendations for COPD. These patients were also less likely to have other diseases.

Patients who underwent testing were 10 percent less likely to die or be admitted to the hospital for COPD, and were more likely to be prescribed an inhaled long-acting bronchodilator (medications that are used to treat COPD over a longer period of time) than patients who did not undergo testing.

The study results validate current guideline recommendations that encourage pulmonary function testing for diagnosis in all patients with suspected COPD.

“Our results support the commonly held understanding that pulmonary function testing is key to the accurate diagnosis and quality care of people with COPD,” the authors wrote.

The researchers suggest that a more frequent use of pulmonary function testing to diagnose suspected cases of COPD, can help improve patient outcomes, as well as promote a better use of healthcare services and decrease costs.

Robert Simms / Business Manager Novus Medical Inc. mobile +1- 905-407-3005 / office +1-866-926-9977 2333 Wyecroft Rd., Unit 9, Oakville, Ontario, L6L 6L4 Canada

visit novusmedical.ca http://novusmedical.ca/ for more medical innovation.

Bellavista 1000e ICU with 17 inch monitor

Last week at Medica, the worlds largest medical trade show in the world held in Dusseldorf Germany, IMT Medical launched their new model of Bellavista, the Bellavista 1000e with a 17 inch monitor.  The e in 1000e stands for everything included.  The Bellavista 1000e differs from it's previous models, only in size.  "The number one piece of feedback we received about the Bellavista was that it looked too small to be an ICU ventilator, even though it was fully featured and had a 13.3 inch monitor.  Well, if size matters, IMT Medical only needed to repackage the Bellavista with a large 17 inch Gorilla Glass display" said Robert Simms, Business Manager for Novus Medical Inc. in Canada.  "The large colour touch display looks and feels beautiful adding to the ease of use of the Bellavista."  

In addition to the 17 inch display, the Bellavista 1000e comes standard with neonatal, paediatric and adult ventilation, advanced modes of mechanical ventilation, the worlds best non-invasive ventilation package on the market, respiratory diagnostics, high flow oxygen delivery, an internal turbine, and 6 hour back up battery.  Call today to book a demonstration of what's latest and greatest in mechanical ventilation by emailing info@novusmedical.ca or calling 1-866-926-9977.

Trend in Ventilator-Associated Pneumonia Rates, 2005-2013 | Critical Care Medicine | JAMA | The JAMA Network

http://jamanetwork.com/journals/jama/fullarticle/2583369 http://jamanetwork.com/journals/jama/fullarticle/2583369

Trend in Ventilator-Associated Pneumonia Rates Between 2005 and 2013 <>From 2006 to 2012, the incidence of ventilator-associated pneumonia (VAP) reported to the Centers for Disease Control and Prevention National Healthcare Safety Network (NHSN) decreased.,2 In medical and surgical intensive care units, between 2006 and 2012, the reported incidence of VAP per 1000 ventilator-days decreased from 3.1 to 0.9 (71% decline) and 5.2 to 2.0 (62% decline), respectively. Whether the decrease was attributable to better care or stricter application of subjective surveillance criteria is unclear. The Medicare Patient Safety Monitoring System (MPSMS) has independently measured VAP rates since 2005, using a stable definition of VAP. Trends in MPSMS VAP rates from 2005 through 2013 were analyzed.


<>To track the national frequency of safety events in hospitalized patients, the MPSMS abstracted a random selection of acute-care hospital records from 2002-2013, except 2008 (because of a 1-year lapse in federal funding). Between 18 000 and 34 000 records were abstracted from between 730 and 4000 randomly selected hospitals across the nation each year. Detailed MPSMS methods have been previously reported. This analysis included MPSMS VAP rates during calendar years 2005 through 2013 among Medicare patients 65 years and older with principal diagnoses of acute myocardial infarction (AMI), heart failure, pneumonia (including a primary diagnosis of sepsis or respiratory failure and a secondary diagnosis of pneumonia), and selected major surgical procedures.

<>Determination of VAP required all of the following beginning 2 or more days after initiation of mechanical ventilation: chest radiograph with a new finding suggesting pneumonia, physician diagnosis of pneumonia, and an order for antibiotics to treat pneumonia. The denominator included all patients who received invasive mechanical ventilation for 2 or more consecutive days without a physician diagnosis of pneumonia prior to the onset of mechanical ventilation.

<>MPSMS was reviewed by Solutions IRB and determined not to be research involving human participants.

<>The cohort was divided into 4 periods (2005-2006, 2007 and 2009, 2010-2011, and 2012-2013). Because the proportions of patients with AMI, heart failure, pneumonia, and major surgery varied from year to year, the 2005-2006 condition-specific proportions served as a baseline. Then, a sample of patients with each condition was randomly selected (with replacement; 10% AMI, 15% heart failure, 20% pneumonia, 55% surgical) for each subsequent period to align the proportions in each period with the condition-specific proportions in 2005-2006. To reduce resampling variability, bootstrap resampling was performed, calculating VAP rates for each period 10 000 times, deriving means and 95% CIs. A mixed model with an ordinal time variable was fit, ranging from 0 to 7, corresponding to years 2005 (time = 0) to 2013 (time = 7), except 2008, to represent the annual change in VAP rates. Analyses were performed using SAS version 9.2 (SAS Institute Inc).


<>The VAP rate was studied among 1856 patients. Numbers and characteristics of patients included in the sample during each period are reported in the Table. MPSMS VAP rates were stable over time (Figure), with an observed rate of 10.8% (95% CI, 7.4% to 14.4%) during 2005-2006, 9.7% (95% CI, 5.1% to 14.9%) during 2012-2013, and an adjusted average annual change of 0.00 (95% CI, −0.05 to 0.07).


<>From 2005 through 2013, MPSMS VAP rates remained stable and substantial, affecting approximately 10% of ventilated patients. Persistently high VAP rates bolster concerns that most interventions purported to reduce VAP are supported by limited evidence.

<>The data have limitations. The VAP rates were not measured in all hospitalized patients, just the subset included in the MPSMS (patients ≥65 years with 4 specific conditions).

<>The discordance between these findings and the significant declines in VAP rates reported by the NHSN,2 could in part be due to differences in MPSMS and NHSN measure definitions, hospitals or patient groups, changes in characteristics of hospitals reporting to the NHSN over time, or preferential declines in VAP rates among hospitals reporting to the NHSN.

<>Nonetheless, the dichotomy between VAP rates reported to the NHSN and measured in the MPSMS supports the concern that surveillance using traditional definitions may be unreliable. The ongoing risk to patient safety represented by VAP supports the NHSN’s decision to explore more objective surveillance targets.

<>Back to top Article Information

Section Editor: Jody W. Zylke, MD, Deputy Editor.

<>Corresponding Author: Mark L. Metersky, MD, Division of Pulmonary and Critical Care Medicine, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, CT 06030-1321 (Metersky@uchc.edu ).

Published Online: November 11, 2016. doi:10.1001/jama.2016.16226 http://jamanetwork.com/article.aspx?doi=10.1001/jama.2016.16226 Author Contributions: Dr Metersky had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Metersky reported that he has worked on various quality improvement and patient safety projects with Qualidigm, the Centers for Medicare & Medicaid Services (CMS), and the Agency for Healthcare Research and Quality (AHRQ). His employer has received remuneration for this work. No other authors reported disclosures.

Funding/Support: This work was supported by contract HHSA290201200003C from the Agency for Healthcare Research and Quality, United States Department of Health and Human Services, Rockville, Maryland. Qualidigm was the contractor.

Role of the Funder/Sponsor: AHRQ employees were involved with the design and conduct of the study; analysis and interpretation of the data; preparation, review, and approval of the manuscript; and decision to submit the manuscript for publication.

Disclaimer: The content of the publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government. The authors assume full responsibility for the accuracy and completeness of the ideas presented.

Additional Contributions: We thank all the previous and current MPSMS team members for their contributions to this work, with a special thanks to the abstractors and other team members at the CMS Clinical Data Abstraction Center.


  1. <> Edwards JR, Peterson KD, Andrus ML, et al; NHSN Facilities. National Healthcare Safety Network (NHSN) Report, data summary for 2006, issued June 2007. Am J Infect Control. 2007;35(5):290-301. PubMed http://www.ncbi.nlm.nih.gov/pubmed/17577475Article http://dx.doi.org/10.1016/j.ajic.2007.04.001
  2. <> Dudeck MA, Weiner LM, Allen-Bridson K, et al. National Healthcare Safety Network (NHSN) report, data summary for 2012, device-associated module. Am J Infect Control. 2013;41(12):1148-1166. PubMed http://www.ncbi.nlm.nih.gov/pubmed/24274911Article http://dx.doi.org/10.1016/j.ajic.2013.09.002
  3. <> Klompas M. Is a ventilator-associated pneumonia rate of zero really possible? Curr Opin Infect Dis. 2012;25(2):176-182. PubMed http://www.ncbi.nlm.nih.gov/pubmed/22248978Article http://dx.doi.org/10.1097/QCO.0b013e3283502437
  4. <> Wang Y, Eldridge N, Metersky ML, et al. National trends in patient safety for four common conditions, 2005-2011. N Engl J Med. 2014;370(4):341-351. PubMed http://www.ncbi.nlm.nih.gov/pubmed/24450892Article http://dx.doi.org/10.1056/NEJMsa1300991
  5. <> O’Grady NP, Murray PR, Ames N. Preventing ventilator-associated pneumonia: does the evidence support the practice? JAMA. 2012;307(23):2534-2539. PubMed http://www.ncbi.nlm.nih.gov/pubmed/22797453Article http://dx.doi.org/10.1001/jama.2012.6445
  6. <> Magill SS, Klompas M, Balk R, et al. Developing a new, national approach to surveillance for ventilator-associated events. Crit Care Med. 2013;41(11):2467-2475. PubMed http://www.ncbi.nlm.nih.gov/pubmed/24162674Article http://dx.doi.org/10.1097/CCM.0b013e3182a262db

Win a MacBook Air by visiting the new IMT Medical Website

Hey RT’s, Visit the New IMT Medical new website and win a Mac Book Air

Visit our new website https://www.imtmedical.com/ - browse through our world of advanced ventilation and high-precision test equipment - we are giving away one Apple MacBook Air 1.4GHz i5 13.3 silver, worth USD 1'150.- to a lucky winner.

How can you participate?

Find and fill out the contact form on our new website https://www.imtmedical.com/. Answer the following question and hit send: "What's the dimension of the screen diagonal of the glass touch screen of our bellavista 1000e, first presented at Medica?"

Good luck!