Diaphragm Fibers in Mechanically Ventilated Humans

Rapid Disuse Atrophy of Diaphragm Fibers in Mechanically Ventilated Humans

Mechanical ventilation is a critical component of modern intensive care medicine, but the process of discontinuing mechanical ventilation can be difficult.Laboratory studies have shown that the combination of diaphragmatic inactivity and mechanical ventilation for prolonged periods (more than 18 hours) is associated with atrophy of myofibers in the rat diaphragm. 
  We hypothesized that similar changes occur in the human diaphragm and that disuse atrophy of human diaphragm myofibers could be a major contributor to the weaning problems that occur in some of our patients.
We evaluated the diaphragms of brain-dead organ donors, who show respiratory-muscle inactivity and undergo mechanical ventilation for prolonged periods, to determine whether disuse atrophy of the diaphragm occurs in ventilated humans. We compared intraoperative biopsy specimens obtained from the costal diaphragms of 14 brain-dead organ donors before harvest (case subjects) and compared them with intraoperative biopsy specimens obtained from the diaphragms of 8 patients who were undergoing surgery for either benign lesions or stage 1 lung cancer (control subjects). Case subjects with diaphragmatic inactivity underwent mechanical ventilation for 18 to 69 hours, whereas in control subjects, the combination of diaphragm inactivity and mechanical ventilation was limited to 2 to 3 hours.

Methods

Subjects

Our protocol for case subjects was approved by the Gift of Life Donor Program (http://www.donors1.org), and our protocol for control subjects was approved by the University of Pennsylvania institutional review board; the protocols appear in the Supplementary Appendix, available with the full text of this article at www.nejm.org. All biopsy specimens were obtained with appropriate written informed consent.

Biopsies

Full-thickness biopsy specimens (about 20 to 24 mm by 6 to 8 mm in size) were obtained from the same region of the right anterior costal diaphragm in all case and control subjects, frozen in isopentane after 3 to 5 minutes for length equilibration, and then transferred to liquid nitrogen and stored at −80°C until used. Specimens from case subjects were obtained before circulatory arrest or removal of any organs, and specimens from control subjects were obtained during the surgery for their lung lesions. In addition, to determine whether our hypothesis regarding atrophy was limited to the diaphragm or primary respiratory muscles, we obtained specimens of the pectoralis major muscle at the level of the third interspace in six subjects from each group. (These subjects were the only ones for whom appropriate consent was obtained for these biopsies.) To avoid surgical trauma to this superficial muscle, these specimens were obtained immediately after the skin incision and processed in the same manner as the diaphragm specimens.

Measurements

We carried out histologic, biochemical, and gene-expression measurements on diaphragm specimens. Only histologic data were obtained from the pectoralis specimens.
We measured fiber-type proportions, fiber-type cross-sectional areas, and area fractions to characterize fiber atrophy in diaphragm-biopsy specimens. We also measured the concentrations of glutathione, active caspase-3, and procaspase-3. Glutathione-concentration analyses were used to assess the presence of oxidative stress; we used active caspase-3 and procaspase-3 as indicators of caspase activity. Active caspase is known to dissociate proteins from the myofibrillar lattice, which is a critical step in muscle proteolysis.
We quantitatively assessed the number of messenger RNA (mRNA) transcripts for atrogin-1 and MuRF-1 relative to MBD4, a housekeeping gene, using real-time reverse-transcriptase polymerase chain reaction. Atrogin-1 and MuRF-1 are ubiquitin ligases that are key components of the ubiquitin–proteasome pathway for proteolysis.
Histologic studies were carried out using previously described immunohistologic methods, and a minimum of 400 fibers were studied in each specimen. Biochemical and gene-expression studies were performed in triplicate on each specimen. Glutathione was measured using an enzyme-recycling assay kit (glutathione assay kit, Cayman Chemicals). Caspase measurements were conducted using sodium dodecyl sulfate–polyacrylamide-gel electrophoresis, followed by immunoblotting with monoclonal antibodies specific for the 32- and 17-kD fragments. We used the relative standard curve method to compute the gene-expression level in each of our diaphragm samples. Complete details for all methods are available in the Supplementary Appendix.

Statistics

Means (±SD) and medians are presented for all continuous data. Demographic, histologic, biochemical, and gene-expression variables were compared between case and control groups using t tests for normally distributed continuous data, Mann–Whitney tests for non-normally distributed data, and Fisher's exact tests for categorical variables.

Results

Characterization of Experimental Cohort

Demographic information, reason for inclusion in the study, and medical history for case and control subjects are summarized in Table 1 
Table 1Summary of Demographic Characteristics, Reason for Surgery, and Medical History for Control and Case Subjects.; ventilator settings, measurements of arterial blood gases, and vital signs are summarized in Table 2


Table 2Summary of Ventilator Settings, Arterial Blood Gas Measurements, and Vital Signs for Control and Case Subjects.

Clinical data for each of the case subjects are presented in the Supplementary Appendix in Table S1; Tables S2 and S3 contain histologic data for case and control subjects; and Table S4 contains usual laboratory measurements. Case subjects were younger than control subjects (mean age, 35±16 years vs. 57±18; P=0.008). The two groups did not differ with respect to proportions of men and women or to body-mass index. After brain death, case subjects' diaphragms were inactive for 18 to 69 hours, whereas inactivity in control subjects' diaphragms was limited to 2 to 3 hours; the mean inactivity time for case subjects' diaphragms was appreciably greater — more than 10 times that of control subjects' diaphragms (2.4±0.5 vs. 34±16, P<0.001).

Analysis of Diaphragm-Biopsy Specimens

Histology

A comparison of Figure 1A and 1B
 Figure 1Comparison of Representative Case and Control Diaphragm-Biopsy Specimens with Respect to Fiber Size. indicates that the fibers in the diaphragm-biopsy specimens from case subjects were appreciably smaller than those from control subjects.

Figure 1C, 1D, 1E, and 1F show that both slow-twitch and fast-twitch fibers in the case specimens were affected by atrophy. Importantly, all panels in Figure 1 indicate that fiber atrophy in case specimens was not accompanied by an inflammatory-cell infiltrate.
In case specimens, the mean cross-sectional areas of slow-twitch and fast-twitch fibers were 2025±745 and 1871±589 μm², respectively, whereas in control specimens these cross-sectional areas were 4725±1547 and 3949±1805 μm², respectively. Therefore, in case specimens, the cross-sectional area of slow-twitch fibers decreased 57% (P=0.001) as compared with control values, and the cross-sectional area of fast-twitch fibers decreased 53% (P=0.01) (Figure 2A
 Figure 2Group Comparisons of Case and Control Diaphragm-Biopsy Specimens with Respect to Histologic Features.).


Case and control specimens did not differ with respect to the numerical proportions or area fractions of slow-twitch and fast-twitch fibers (Figure 2B and 2C). In addition, in an age-matched subgroup of five case and five control subjects, the cross-sectional areas of both slow-twitch and fast-twitch fibers did not differ statistically from those of the full groups; in this subgroup, slow-twitch and fast-twitch fibers in case specimens exhibited mean decreases in cross-sectional areas of 39% (P=0.004) and 41% (P=0.02), respectively, as compared with controls.

Biochemistry

Total glutathione concentration in diaphragm-biopsy specimens from case subjects was 1.03±0.17 mM, whereas that in control specimens was 1.35±0.21 mM; therefore, case specimens exhibited a decrease of 23% (P=0.01) from that noted in controls (Figure 3A
 Figure 3Group Comparisons of Case and Control Diaphragm-Biopsy Specimens with Respect to Measurements of Glutathione, Active Caspase, and Procaspase.).


Figure 3B and 3C show immunoblots and a quantitative comparison of case and control specimens with respect to the expression of the active 17-kD caspase-3 fragment and the 32-kD inactive procaspase fragment. Figure 3C shows that active caspase-3 in case specimens had a value of 1.52±1.15 optical-density units, whereas that in controls had a value of 0.66±0.45 optical-density unit; therefore, the diaphragm-biopsy specimens from case subjects showed an increase of 154% above controls (P=0.05). In addition, Figure 3C shows that procaspase in case specimens measured 0.72±0.40 optical-density unit, whereas that in control specimens was 1.13±0.51 optical-density units; this higher value of procaspase in the control specimens approached but did not reach statistical significance (P=0.07).

Gene Expression

Expression of MBD4 was used to normalize the number of transcripts of atrogin-1 and MuRF-1 (the two ubiquitin ligases of interest), since its expression in the diaphragm-biopsy specimens from case and control subjects did not differ (data not shown). Control specimens contained 72±19 arbitrary normalized copy units (ANCU) of atrogin-1, whereas case specimens contained 216±67 ANCU. In addition, control specimens contained 128±51 ANCU of MuRF-1, whereas case specimens contained 885±294 ANCU. Therefore, the case specimens showed 3.0 times as much expression of atrogin-1 mRNA transcripts (P=0.002) and 6.9 times as much expression of MuRF-1 mRNA transcripts (P=0.001) as control specimens (Figure 4 
Figure 4Group Comparisons of Case and Control Diaphragm-Biopsy Specimens with Respect to mRNA Expression for Atrogin-1 and MuRF-1 Normalized to a Housekeeping Gene.).

Histology of Pectoralis Major–Biopsy Specimens

The cross-sectional areas of slow-twitch and fast-twitch fibers in the biopsy specimens from the pectoralis major in case subjects were 3084±796 and 2933±1343 μm², respectively, whereas the cross-sectional areas of these fiber-types in the control specimens were 3325±1256 and 3418±1281 μm², respectively. These data show that the pectoralis fibers from case and control subjects did not differ with respect to cross-sectional area of any fiber type (see Figure S1 in the Supplementary Appendix). Likewise, these case and control specimens did not differ with respect to the numerical proportion or area fractions of slow-twitch and fast-twitch fibers (Table S7 in the Supplementary Appendix).

Discussion

In our case subjects, the combination of 18 to 69 hours of diaphragmatic inactivity and mechanical ventilation was associated with marked atrophy of both slow-twitch and fast-twitch fibers of the diaphragm. Muscle inactivity is known to effect oxidative stress and increase cytosolic calcium concentration, perturbations known to elicit increases in the activity of proteases (e.g., caspases) that cause increased dissociation of the myofibrillar lattice, the critical initial step in proteolysis. In case subjects, the decrease in diaphragmatic glutathione concentration is consistent with oxidative stress, and the increases in active caspase-3 suggest an increased rate of protein release from the myofibrillar lattice.
After release from the lattice, the major route of proteolysis for muscle proteins is the ubiquitin–proteasome pathway, which consists of the following sequential steps: activation of the small protein cofactor ubiquitin (76 amino acid residues), formation of activated ubiquitin-chain moieties catalyzed by specific ubiquitin-conjugase enzymes (i.e., E2 enzymes), attachment of ubiquitin chains to specific proteins by ubiquitin-ligase enzymes (i.e., E3 enzymes such as atrogin-1 and MuRF-1), and recognition of specific ubiquitin-protein chains by the 26S proteasome, followed by release of ubiquitin residues and degradation of proteins to small peptides (8 to 11 amino acid residues) by the 20S catalytic core of the proteasome. In conditions characterized by degradation of muscle protein, there is an up-regulation of mRNAs coding for atrogin-1 and MuRF-1; therefore, the marked increases in these transcripts noted in the diaphragm-biopsy specimens from case subjects are consistent with increased proteolysis.
Since our data are histologic or biochemical, we can only speculate on the functional significance of our findings. One report re-emphasized the idea that weaning patients from ventilators is closely linked to diaphragm force generation (usually assessed clinically as transdiaphragmatic pressure). The question then becomes how measurements of fiber atrophy in our case subjects relate to force generation. If the findings in our samples occurred throughout the diaphragm, the degree of atrophy we observed would predict an approximately 55% decrease in transdiaphragmatic pressure (i.e., to 45% of control values). Therefore, we believe that fiber atrophy of the magnitude noted in case specimens could have clinical significance.
There are limitations to our study. We recognize that the decreases in fiber cross-sectional area — noted in the diaphragm-biopsy specimens from case subjects — can be explained by either artifactual increases in mean sarcomere length due to improper fixation or actual functional decreases in mean fiber volume. To distinguish between these possibilities, we used both longitudinal and transverse sections of case specimens and determined a mean sarcomere length of 2.0±0.2 μm for both slow-twitch and fast-twitch fibers. This value is very similar to that noted for the diaphragm fibers from control subjects. On the basis of these observations, we conclude that the decrease in cross-sectional area of diaphragm fibers from case subjects could be attributed entirely to atrophy.
Another limitation is that our case subjects were younger than the control subjects. Although the preferred method for analyzing this type of data is a matched-pair design, we lacked a sufficient number of subjects to allow matching for both age and sex. The results from our previous study as well as the present data strongly suggest that sex is not a determinant of cross-sectional area in diaphragm fibers. Therefore, since we found no statistically significant differences in cross-sectional area between the age-matched (5 subjects) and full case (14 subjects) groups, we reason that the difference in age between case and control subjects does not account for the atrophy of diaphragm fibers from case subjects.
There are other possible causes of atrophy in the diaphragm fibers from case subjects. One or more of the following conditions may have played some role in eliciting the atrophy: systemic inflammatory response syndrome (SIRS) or sepsis, barotraum–volutrauma, brain death, or unmeasured humoral substances. Current concepts suggest that diaphragm atrophy associated with SIRS, sepsis, or barotrauma–volutrauma should be associated with an inflammatory-cell infiltrate or increased proinflammatory cytokines. Neither of these findings, however, was evident in the diaphragm fibers from case subjects (Figure 1A, and Table S5 in the Supplementary Appendix).
To assess the possibility that noncytokine humoral substances or other factors associated with brain death accounted for the diaphragm-fiber atrophy, we compared biopsy specimens from the pectoralis major muscle of six case subjects and six control subjects. The specimens from the two groups did not differ with respect to cross-sectional area of either slow-twitch or fast-twitch fibers (Figure S1 in the Supplementary Appendix). These observations suggest that neither brain death nor unmeasured humoral factors played a role in effecting fiber atrophy in case subjects' diaphragms.
There are factors affecting fiber atrophy in disuse states that could influence our results. Our data do not elucidate the complex relationships between conditions present in the diaphragms of case subjects — inactivity, level of phrenic motoneuron activity, diaphragm muscle lengths, and perhaps additional factors — and the marked atrophy of both slow-twitch and fast-twitch fibers in the diaphragms. The orthopedic literature indicates that limb muscles that are used frequently show appreciably more inactivity-associated fiber atrophy than muscles used less frequently. Because the diaphragm is active in most people 24 hours a day, one might expect it to show a greater rate of atrophy than limb muscles that are rendered inactive by interventions such as spinal cord injury, microgravity, or bed rest.
In summary, our study indicates that the combination of 18 to 69 hours of diaphragm inactivity and mechanical ventilation is associated with marked atrophy of both slow-twitch and fast-twitch fibers in the human diaphragm. Since our observations strongly suggest that increased proteolysis accounts for the fiber atrophy noted in the diaphragm-biopsy specimens from case subjects, we speculate that blocking or attenuating diaphragm proteolytic pathways in patients on mechanical ventilation might mitigate the weaning problems that occur in some patients.

 

Mechanical Ventilation

Basic Principles

The indications for mechanical ventilation, as derived from a study of 1638 patients in eight countries, are acute respiratory failure (66 percent of patients), coma (15 percent), acute exacerbation of chronic obstructive pulmonary disease (13 percent), and neuromuscular disorders (5 percent). The disorders in the first group include the acute respiratory distress syndrome, heart failure, pneumonia, sepsis, complications of surgery, and trauma (with each subgroup accounting for about 8 to 11 percent of the overall group). The objectives of mechanical ventilation are primarily to decrease the work of breathing and reverse life-threatening hypoxemia or acute progressive respiratory acidosis.
Virtually all patients who receive ventilatory support undergo assist-control ventilation, intermittent mandatory ventilation, or pressure-support ventilation; the latter two modes are often used simultaneously. With assist-control ventilation, the most widely used mode, the ventilator delivers a set tidal volume when triggered by the patient's inspiratory effort or independently, if such an effort does not occur within a preselected time.
Intermittent mandatory ventilation was introduced to provide graded levels of assistance. With this mode, the physician sets the number of mandatory breaths of fixed volume to be delivered by the ventilator; between these breaths, the patient can breathe spontaneously. Patients often have difficulty adapting to the intermittent nature of ventilatory assistance, and the decrease in the work of breathing may be much less than desired.
Pressure-support ventilation also provides graded assistance but differs from the other two modes in that the physician sets the level of pressure (rather than the volume) to augment every spontaneous respiratory effort The level of pressure delivered by the ventilator is usually adjusted in accordance with changes in the patient's respiratory frequency. However, the frequency that signals a satisfactory level of respiratory-muscle rest has never been well defined, and recommendations range from 16 to 30 breaths per minute.
New modes of mechanical ventilation are often introduced. Each has an acronym, and the jargon is inhibiting to those unfamiliar with it. Yet each new mode involves nothing more than a modification of the manner in which positive pressure is delivered to the airway and of the interplay between mechanical assistance and the patient's respiratory effort. The purpose of a new mode of ventilation may be to enhance respiratory-muscle rest, prevent deconditioning, improve gas exchange, prevent lung damage, enhance the coordination between ventilatory assistance and the patient's respiratory efforts, and foster lung healing; the priority given to each goal varies.

Coordinating Respiratory Effort and Mechanical Ventilation

Probably the most common reason for instituting mechanical ventilation is to decrease the work of the respiratory muscles. The inspiratory effort expended by patients with acute respiratory failure is about four times the normal value, and it can be increased to six times the normal value in individual patients. Critically ill patients in whom this increased level of effort is sustained indefinitely are at risk of inspiratory-muscle fatigue, which can add structural injury to already overworked muscles. It is sometimes thought that the simple act of connecting a patient to a ventilator will decrease respiratory effort. Yet unless the settings are carefully selected, mechanical ventilation can actually do the opposite.
With careful selection of ventilator settings, inspiratory effort can be reduced to the normal range. But eliminating inspiratory effort is not desirable because it causes deconditioning and atrophy of the respiratory muscles. Surprisingly, researchers have not attempted to determine the desirable target for reducing inspiratory effort in patients with acute respiratory distress. To reduce effort markedly requires that the ventilator cycle in unison with the patient's central
respiratory rhythm 








 Flow, Airway Pressure, and Inspiratory and Expiratory Muscle Activity in a Patient with Chronic Obstructive Pulmonary Disease Who Received Pressure-Support Ventilation at an Airway Pressure of 20 cm of Water.).

For perfect synchronization, the period of mechanical inflation must match the period of neural inspiratory time (the duration of inspiratory effort), and the period of mechanical inactivity must match the neural expiratory time.Difficulties in synchronization can arise at the onset of inspiratory effort, at the onset of flow delivered by the ventilator, during the period of ventilator-induced inflation, and at the switch between inspiration and expiration.
Almost all patients who undergo mechanical ventilation receive some form of assisted ventilation, with the patient's inspiratory effort triggering the ventilator. To ensure that the ventilator does not cycle too often, the clinician sets a threshold for airway pressure that will trigger the ventilator. This threshold, referred to as set sensitivity, is usually –1 to –2 cm of water. To reach this threshold, the patient must initiate an inspiratory effort. But when the threshold is reached, inspiratory neurons do not simply switch off. Consequently, the patient may expend considerable inspiratory effort throughout the machine-cycled inflation.
The display of airway pressure and flow tracings on ventilator screens has increased awareness that inspiratory effort is frequently insufficient to trigger the ventilator. At high levels of mechanical assistance, up to one third of a patient's inspiratory efforts may fail to trigger the machine. Surprisingly, unsuccessful triggering is not the result of poor inspiratory effort; indeed, the effort is more than a third greater when the threshold for triggering the ventilator is not reached than when it is reached. Breaths that do not reach the threshold for triggering the ventilator have higher tidal volumes and shorter expiratory times than do breaths that do trigger the ventilator. Consequently, elastic-recoil pressure builds up within the thorax in the form of intrinsic positive end-expiratory pressure (PEEP), or auto-PEEP. To trigger the ventilator, the patient's inspiratory effort first has to generate a negative intrathoracic pressure in order to counterbalance the elastic recoil and then must reach the set sensitivity. The consequences of wasted inspiratory efforts are not fully known, but they add an unnecessary burden in patients whose inspiratory muscles are already under stress.
The inspiratory flow rate is initially set at a default value, such as 60 liters per minute. If the delivered flow does not meet the patient's ventilatory needs, inspiratory effort will increase. Sometimes the flow is increased in order to shorten the inspiratory time and increase the expiratory time, especially in patients with inspiratory efforts that are insufficient to trigger the ventilator. But an increase in flow causes immediate and persistent tachypnea, and as a result, the expiratory time may be shortened. In one study, for example, increases in inspiratory flow from 30 liters per minute to 60 and 90 liters per minute caused increases in the respiratory rate of 20 and 41 percent, respectively.
In studies of interactions between the patient's respiratory effort and mechanical ventilation, remarkably little attention has been paid to the switch between inspiration and expiration. With the use of pressure-support ventilation, ventilatory assistance ceases when the patient's inspiratory flow falls by a preset amount (e.g., to 25 percent of the peak flow). Air flow changes more slowly in patients with chronic obstructive pulmonary disease than in other patients, and patients often start to exhale while the ventilator is still pumping gas into their chests. In 5 of 12 patients with chronic obstructive pulmonary disease who were receiving pressure support of 20 cm of water, expiratory muscles were recruited during ventilator-induced inflation.

Improving Oxygenation and Preventing Lung Injury

A primary goal of mechanical ventilation is to improve arterial oxygenation. Improvement is achieved partly through the use of endotracheal intubation to ensure the delivery of oxygen to the airway and partly through an increase in airway pressure. Satisfactory oxygenation is easily achieved in most patients with airway obstruction. The main challenge arises in patients with alveolar-filling disorders, especially the acute respiratory distress syndrome — a form of noncardiogenic pulmonary edema resulting from severe acute alveolar injury. It has long been recognized that arterial oxygenation can be achieved at a lower inspired oxygen concentration by increasing airway pressure. The goal of using the lowest possible oxygen concentration to achieve an arterial oxygen saturation of approximately 90 percent has not changed in decades. What has changed is how this goal is viewed in relation to other factors, particularly ventilator pressures. In recent years, there has been a growing tendency to be more concerned about high airway pressures than about oxygen toxicity, although this shift has been based on a consensus of opinion rather than on data from studies in patients and animals.
From the outset, clinicians recognized that mechanical ventilation could rupture alveoli and cause air leaks. In 1974, Webb and Tierney showed that mechanical ventilation could also cause ultrastructural injury, independently of air leaks.Their observations went largely unnoticed until a decade later, when several investigators confirmed and extended them. Alveolar overdistention causes changes in epithelial and endothelial permeability, alveolar hemorrhage, and hyaline-membrane formation in laboratory animals.
Diffuse infiltrates on chest radiographs originally led clinicians to infer that lung involvement was homogeneous. But computed tomography (CT) reveals a patchy pattern: about one third of the lung is unaerated, one third poorly aerated, and one third normally aerated. A ventilator-induced breath will follow the path of least impediment, travelling preferentially to the normally aerated areas. As a result, these regions are vulnerable to alveolar overdistention and the type of ventilator-induced lung injury found in laboratory animals.Figure 2



  

Lung Injury Caused by Mechanical Ventilation in a 31-Year-Old Woman with the Acute Respiratory Distress Syndrome Due to Amniotic-Fluid Embolism.).


A new era of ventilatory management began in 1990, when Hickling et al.reported that lowering the tidal volume caused a 60 percent decrease in the expected mortality rate among patients with the acute respiratory distress syndrome. In a subsequent trial, Amato et al. randomly assigned patients to a conventional tidal volume (12 ml per kilogram of body weight) or to a low tidal volume (less than 6 ml per kilogram). Mortality was decreased by 46 percent with the lower tidal volume. In a recent study of 861 patients, the Acute Respiratory Distress Syndrome Network confirmed this benefit: mortality was decreased by 22 percent with a tidal volume of 6 ml per kilogram as compared with a tidal volume of 12 ml per kilogram. Lowering the tidal volume, however, failed to improve the outcome in three controlled trials. The discrepant findings can be explained by differences in trial design. Increased survival was demonstrable only when the patients undergoing conventional ventilation had a mean pressure during an end-inspiratory pause (the so-called plateau pressure, a surrogate for peak alveolar pressure) that exceeded 32 cm of water.
The pressures pertinent to ventilatory management are the peak inspiratory pressure, plateau pressure, and end-expiratory pressure. Patients with airway obstruction may have a very high peak pressure without any increase in the plateau pressure. Indeed, the gradient between the two is directly related to the resistance of the airway to airflow. An increase in the peak inspiratory pressure without a concomitant increase in the plateau pressure is unlikely to cause alveolar damage. The critical variable is not airway pressure itself but transpulmonary pressure — airway pressure during the end-inspiratory pause minus pleural pressure. The normal lung is maximally distended at a transpulmonary pressure between 30 and 35 cm of water, and higher pressures cause overdistention. Patients with stiff chest walls, such as those with the acute respiratory distress syndrome due to a nonpulmonary disorder (e.g., abdominal sepsis), have an elevated pleural pressure. In such patients, the airway plateau pressure may exceed 35 cm of water without causing alveolar overdistention.
Clinical decisions based on plateau pressure must take into account the relation between lung volume and airway pressure in the individual patient. The pressure–volume curve in patients with the acute respiratory distress syndrome typically has a sigmoid shape with two discrete bends, called inflection points


 


Respiratory Pressure–Volume Curve and the Effects of Traditional as Compared with Protective Ventilation in a 70-kg Patient with the Acute Respiratory Distress Syndrome.).

Some investigators believe that a plateau pressure above the upper bend causes alveolar overdistention. Reducing the tidal volume lowers the plateau pressure, but at the cost of hypercapnia. In a study in which 25 patients with the acute respiratory distress syndrome underwent mechanical ventilation with a tidal volume of 10 ml per kilogram, 20 had a plateau pressure that was 2 to 14 cm of water above the upper bend of the pressure–volume curve. Lowering the plateau pressure to a value that fell below the upper bend required a 22 percent decrease in the tidal volume, causing the partial pressure of carbon dioxide to increase from 44 to 77 mm Hg. The partial pressure of carbon dioxide, in turn, can be decreased by as much as 28 percent by removing tubing and thus decreasing dead space and increasing the frequency of ventilator-induced breaths. By virtue of their stiff lungs, patients with the acute respiratory distress syndrome who do not have an underlying airway obstruction can tolerate a frequency of 30 breaths per minute without gas trapping. Severe hypercapnia can have adverse effects, including increased intracranial pressure, depressed myocardial contractility, pulmonary hypertension, and depressed renal blood flow. The view that these risks are preferable to the higher plateau pressure required to achieve normocapnia represents a substantial shift in ventilatory management.
Lowering the tidal volume is not without hazards. In addition to the potential harm of hypercapnia, the volume of aerated lung may be decreased, with a consequent increase in shunting and worsening oxygenation. One means of minimizing the loss of lung volume is the use of sighs (i.e., single breaths of large tidal volume). In one study, increasing the plateau pressure by at least 10 cm of water during sighs, applied three times a minute over a period of one hour, caused a 26 percent decrease in shunting, with a 50 percent increase in the partial pressure of oxygen. It is unknown whether sighs used at this low frequency cause injury from alveolar overdistention.
The more usual way of improving oxygenation is through the use of PEEP with the intention of recruiting previously nonfunctioning lung tissue. Selecting the right level of PEEP for a given patient with the acute respiratory distress syndrome is difficult, because the severity of injury varies throughout the lungs. PEEP can recruit atelectatic areas but may overdistend normally aerated areas. In a study involving six patients with acute lung injury, for example, the use of PEEP at 13 cm of water resulted in the recruitment of nonaerated portions of lung, with a gain of 320 ml in volume, but three patients had overdistention of already aerated portions of lung, with an excess volume of 238 ml.
Overall, about 30 percent of patients with acute lung injury do not benefit from PEEP or have a fall in the partial pressure of oxygen. With the patient in the supine posture, PEEP generally recruits the regions of the lung closest to the apex and sternum. Conversely, PEEP can increase the amount of nonaerated tissue in the regions close to the spine and the diaphragm. Among patients in the early stages of the acute respiratory distress syndrome, those with pulmonary causes, such as pneumonia, are less likely to benefit from PEEP than are those with nonpulmonary causes, such as intraabdominal sepsis or extrathoracic trauma. This distinction may be related to the type of morphologic involvement: pulmonary causes of the syndrome are characterized by alveolar filling, whereas nonpulmonary causes are characterized by interstitial edema and alveolar collapse. In the later stages of the acute respiratory distress syndrome, remodeling and fibrosis may eliminate this distinction between pulmonary and nonpulmonary causes.
To select the right level of PEEP, some experts recommend bedside calculation of the pressure–volume curve. With the ventilators currently used in the United States, calculating the pressure–volume curve is logistically difficult and technically demanding. Yet many ventilators have a computer screen, and minor software modifications would make it feasible to calculate the curve in as little as two minutes — as with the ventilators available in France. Providing this option on ventilators would increase clinicians' experience with the use of pressure–volume curves in ventilatory management.
Even if the pressure–volume curve is not calculated at the bedside, it is useful to select the PEEP level according to this conceptual framework. A level above the lower bend in the pressure–volume curve is thought to keep alveoli open at the end of expiration and thus prevent the injury that can result from shear forces created by the opening and closing of alveoli. This level of PEEP may also prevent an increase in the amount of nonaerated tissue and, thus, atelectasis. However, the notion that the lower bend signals the level of PEEP necessary to prevent end-expiratory collapse and that pressures above the upper bend signal alveolar overdistention is a gross oversimplification. The relation between the shape of the pressure–volume curve and events at the alveolar level is confounded by numerous factors and is the subject of ongoing research and debate. An understanding of this relation is also impeded by the difficulty in distinguishing collapsed lung units from fluid-filled units on CT.
Most patients with the acute respiratory distress syndrome have an increase in the partial pressure of oxygen when there is a change from the supine to the prone position. In a study of 16 patients, for example, 12 had an increase of 9 to 73 mm Hg in the partial pressure of oxygen, and 4 had a decrease of 7 to 16 mm Hg. The mechanism responsible for the improvement in the partial pressure of oxygen is not clear. The attribution of this improvement to lung recruitment has not been proved. It is now posited that a prone position causes ventilation to be distributed more evenly to the various regions of the lungs, improving the relation between ventilation and perfusion.

Discontinuing Mechanical Ventilation

Because mechanical ventilation can have life-threatening complications, it should be discontinued at the earliest possible time. The process of discontinuing mechanical ventilation, termed weaning, is one of the most challenging problems in intensive care, and it accounts for a considerable proportion of the workload of staff in an intensive care unit.
When mechanical ventilation is discontinued, up to 25 percent of patients have respiratory distress severe enough to necessitate the reinstitution of ventilatory support. Our understanding of why weaning fails in some patients has advanced considerably in recent years. Among patients who cannot be weaned, disconnection from the ventilator is followed almost immediately by an increase in respiratory frequency and a fall in tidal volume — that is, rapid, shallow breathing



 
Tidal Volume, Pleural Pressure, and Pulmonary-Artery Pressure in a Patient Undergoing Assist-Control Ventilation and at the Start and End of a Failed Trial of Spontaneous Breathing.).

As a trial of spontaneous breathing is continued over the next 30 to 60 minutes, the respiratory effort increases considerably, reaching more than four times the normal value at the end of this period. The increased effort is mainly due to worsening respiratory mechanics. Respiratory resistance increases progressively over the course of a trial of spontaneous breathing, reaching about seven times the normal value at the end of the trial; lung stiffness also increases, reaching five times the normal value; and gas trapping, measured as auto-PEEP, more than doubles over the course of the trial.
 Before weaning is started, however, the respiratory mechanics in such patients are similar to those in whom subsequent weaning is successful. Thus, unknown mechanisms associated with the act of spontaneous breathing cause the worsening of respiratory mechanics in patients who cannot be weaned from mechanical ventilation.
In addition to the increase in respiratory effort, an unsuccessful attempt at spontaneous breathing causes considerable cardiovascular stress. Patients can have substantial increases in right and left ventricular afterload, with increases of 39 and 27 percent in pulmonary and systemic arterial pressures, respectively, most likely because the negative swings in intrathoracic pressure are more extreme. At the completion of a trial of weaning, the level of oxygen consumption is equivalent in patients who can be weaned and in those who cannot. But how the cardiovascular system meets the oxygen demand differs in the two groups of patients. In those who are successfully weaned, the oxygen demand is met through an increase in oxygen delivery, mediated by the expected increase in cardiac output on discontinuation of positive-pressure ventilation. In patients who cannot be weaned, the oxygen demand is met through an increase in oxygen extraction, and these patients have a relative decrease in oxygen delivery. The greater oxygen extraction causes a substantial decrease in mixed venous oxygen saturation, contributing to the arterial hypoxemia that occurs in some patients.
Over the course of a trial of spontaneous breathing, about half of patients in whom the trial fails have an increase in carbon dioxide tension of 10 mm Hg or more. The hypercapnia is not usually a consequence of a decrease in minute ventilation. Instead, hypercapnia results from rapid, shallow breathing, which causes an increase in dead-space ventilation. In a small proportion of patients who cannot be weaned, primary depression of respiratory drive may be responsible for the hypercapnia.
The discontinuation of mechanical ventilation needs to be carefully timed. Premature discontinuation places severe stress on the respiratory and cardiovascular systems, which can impede the patient's recovery. Unnecessary delays in discontinuation can lead to a host of complications. Decisions about timing that are based solely on expert clinical judgment are frequently erroneous. Several functional measures are used to aid decision making. The level of oxygenation must be satisfactory before one attempts to discontinue mechanical ventilation. Yet in many patients with satisfactory oxygenation, such attempts fail. The use of traditional predictors of the success or failure of attempts — maximal inspiratory pressure, vital capacity, and minute ventilation — frequently has false positive or false negative results. A more reliable predictor is the ratio of respiratory frequency to tidal volume (f/V_T). The ratio must be calculated during spontaneous breathing; calculating it during pressure support markedly impairs its predictive accuracy. The higher the ratio, the more severe the rapid, shallow breathing and the greater the likelihood of unsuccessful weaning. A ratio of 100 best discriminates between successful and unsuccessful attempts at weaning. In a case of clinical equipoise — that is, a pretest probability of 50 percent — an f/V_T of 80, which has a likelihood ratio of 7.5, is associated with almost a 95 percent post-test probability of successful weaning. If the f/V_T is higher than 100, the likelihood ratio is 0.04 and the post-test probability of successful weaning is less than 5 percent.
Several groups of investigators have evaluated the predictive value of f/V_T. Its positive predictive value — the proportion of patients who are successfully weaned among those for whom the ratio predicts success — has generally been high (0.8 or higher). The negative predictive value — the proportion of patients who cannot be weaned among those for whom the ratio predicts failure — has sometimes been reported to be low (0.5 or less). Low negative predictive values have often been reported for patients with a high likelihood of successful extubation — for example, patients undergoing routine postoperative ventilatory assistance and patients who have tolerated initial trials of weaning.
There are four methods of weaning. The oldest method is to perform trials of spontaneous breathing several times a day, with the use of a T-tube circuit containing an enriched supply of oxygen. Initially 5 to 10 minutes in duration, the trials are extended and repeated several times a day until the patient can sustain spontaneous ventilation for several hours. This approach has become unpopular because it requires considerable time on the part of intensive care staff.
The two most common approaches, intermittent mandatory ventilation and pressure support, decrease ventilatory assistance gradually by respectively lowering the number of ventilator-assisted breaths or the level of pressure. When a minimal level of ventilatory assistance can be tolerated, the patient is extubated. The minimal level of assistance, however, has never been well defined. For example, pressure support of 6 to 8 cm of water is widely used to compensate for the resistance imposed by the endotracheal tube and ventilator circuit. A patient who can breathe comfortably at this level of pressure support should be able to tolerate extubation. But if the upper airways are swollen because an endotracheal tube has been in place for several days, the work engendered by breathing through the swollen airways is about the same as that caused by breathing through an endotracheal tube. Accordingly, any amount of pressure support overcompensates and may give misleading information about the likelihood that a patient can tolerate extubation.
The fourth method of weaning is to perform a single daily T-tube trial, lasting for up to two hours. If this trial is successful, the patient is extubated; if the trial is unsuccessful, the patient is given at least 24 hours of respiratory-muscle rest with full ventilatory support before another trial is performed.
Until the early 1990s, it was widely believed that all weaning methods were equally effective, and the physician's judgment was regarded as the critical determinant. But the results of randomized, controlled trials clearly indicate that the period of weaning is as much as three times as long with intermittent mandatory ventilation as with trials of spontaneous breathing. In a study involving patients with respiratory difficulties on weaning, trials of spontaneous breathing halved the weaning time as compared with pressure support; in another study, the weaning time was similar with the two methods. Performing trials of spontaneous breathing once a day is as effective as performing such trials several times a day but much simpler. In a recent study, half-hour trials of spontaneous breathing were as effective as two-hour trials. However, this study involved all patients being considered for weaning, not just those for whom there were difficulties with weaning.
A two-stage approach to weaning — systematic measurement of predictors, including f/V_T , followed by a single daily trial of spontaneous breathing — was compared with conventional management in a randomized trial. Although the patients assigned to the two-stage approach were sicker than those assigned to conventional weaning, they were weaned twice as rapidly. The rate of complications and the costs of intensive care were also lower with two-stage management than with conventional management.
When patients can sustain spontaneous ventilation without undue discomfort, they are extubated. About 10 to 20 percent of such patients require reintubation. Mortality among patients who require reintubation is more than six times as high as mortality among patients who can tolerate extubation. The reason for the higher mortality is unknown; it is not clearly related to the development of new problems after extubation or to complications of reinserting the tube. Indeed, the need for reintubation may simply be a marker of a more severe underlying illness.
In a controlled trial involving patients who could not sustain spontaneous ventilation, the patients who were extubated and then received noninvasive ventilation through a face mask had a shorter mean overall period of ventilatory support (10.2 days) than those who remained intubated and were weaned by decreasing pressure support (16.6 days). Although this result is promising, it is not clear how many such patients or which ones could benefit from this approach.

Other Approaches to Mechanical Ventilation

Noninvasive ventilation, an approach that is becoming more widespread, was reviewed in the Journal in 1997. Two new approaches under investigation are liquid ventilation and proportional-assist ventilation; they have not yet been approved for general clinical use.

Conclusions

Since my previous overview of mechanical ventilation in the Journal, we have gained a better understanding of the pathophysiology associated with unsuccessful weaning and have learned how to wean patients more efficiently. We have also learned how ventilator settings influence survival in patients with the acute respiratory distress syndrome. Less progress has been made in determining how the ventilator can best be used to achieve maximal respiratory-muscle rest, which is the most common reason for providing mechanical ventilation. Although further research may lead to unexpected new insights, an important challenge for researchers is to identify elements of our current knowledge that can be incorporated into a clinical management scheme to improve the outcome for patients who require ventilatory assistance.

Ventilation for Building Products

In light of the new Building Regulations, Lee Nurse, Marketing Director at Vent-Axia, reviews what impact the changes will have for the specification of ventilation in new housing developments.

The new Approved Documents Part F (Means of Ventilation) and Part L (Conservation of Fuel and Power) of the Building Regulations have changed the outlook on the choice of ventilation solution for specifiers in the new build sector.

They feature a number of major revisions that include minimum energy efficiency levels for all ventilation systems.

The launch of Part L’s new Domestic Building Services Compliance Guide highlights ventilation performance levels. Here, a specific fan power requirement of less than 0.5 watt/sec is now included to cover intermittent fans which are used in new build developments.

The Regulations also require that homes are increasingly air tight to further lower dwelling emission levels, but not at the expense of good air quality. So, Part F offers guidelines for airtight properties with infiltration rates tighter than 5m3h/m2 at 50pa. For Intermittent System 1 and Passive Stack System 2 approaches, in airtight dwellings the guidance increases background ventilation rates by up to 50%. Since this level is difficult to achieve with trickle ventilators in windows, this new demand will increase the uptake of continuous ventilation solutions at the expense of intermittent fans. Continuous ventilation performs better in SAP, is easier to specify and easier to standardise.

The result will be a growth in the specification of whole house and decentralised Mechanical Extract Ventilation systems (MEV and dMEV) plus Mechanical Extract Ventilation systems with Heat Recovery (MVHR).

Meanwhile, for the first time Part F requires post-completion testing of ventilation equipment. Part F’s new Domestic Ventilation Installation and Commissioning Compliance Guide has been introduced to ensure ventilation not only delivers the required airflow, but does it efficiently and quietly. The guide includes sign-off procedures and paperwork completion to ensure performance and efficiency are met. Post-installation performance policing is critical to ensure air quality in increasingly air tight homes. This is especially important with the increased adoption of highly efficient ventilation systems, like MVHR, which require trained competent installers.

It’s at this point that leading players, like Vent-Axia, have an important role to play. That’s why we have introduced a dedicated and comprehensive Vent-Axia Lo-Carbon™ ventilation range which meet the approved document’s specific fan power requirements of less than 0.5watt/sec for all applications. Our ventilation is also supported by unrivalled access to extensive technical advice, design and ventilation applications expertise to help understand low carbon ventilation issues, advising on how best to reduce energy consumption and cut emissions on a diverse range of projects. At Vent-Axia we are constantly pushing the boundaries to create innovative solutions to meet the changing requirements of the industry and to comply and stay ahead of current legislation.

For example, the latest solutions on the market, such as Vent-Axia’s Lo-Carbon™ Centra dMEV, comply with Building Regulations Part F for continuous mechanical extract ventilation (System 3) and are capable of achieving ventilation at only 1.4 watts, thus meeting the requirements of the Regulations as far as specifiers are concerned but also offering homeowners not only literal peace and quiet, but also peace of mind electrical bills won’t hit the roof. Offering virtually silent operation, a fresh design and a reduction in the requirement for trickle ventilators potentially to zero, these energy efficient systems fit discreetly in modern homes and are simple to install.

Meanwhile, residential mechanical ventilation with heat recovery (MVHR) systems, such as the Sentinel Kinetic, offers a SAP Appendix Q eligible ventilation solution capable of up to 92% heat recovery. This will help reduce the DER (Dwelling Emission Rate) of new build properties and deliver points to meet Level 3 and Level 4 of the Code for Sustainable Homes.

Indeed, together, the Code for Sustainable Homes and the Building Regulations map out the journey towards the zero carbon homes target in 2016. As homes become inevitably more airtight to meet the demands of the new Building Regulations, so it will become key to specify more energy efficient ventilation solutions, such as MVHR. But meeting the challenge of zero carbon homes is about more than just making a product selection, we need to work together to consider correct specification, installed performance of products, ongoing maintenance and system design, which are all necessary to meet our shared goal of achieving good, low carbon ventilation.

Ventilation That You Need in Your House

How to Get the Ventilation That You Need in Your House

 The old farmhouses where people lived several generations ago had little resistance to air. They were drafty, uncomfortable and very dry in winter due to high air-change rates. Modern housing restricts air entry through good air barriers and sheet materials, such as plywood, oriented strand board (OSB) and drywall. In fact, new Canadian houses and many retrofitted existing houses are so airtight that you cannot count on incidental leakage for good indoor air quality. You must induce or augment the house air-change rate using mechanical ventilation, a requirement in the National Building Code for new houses since 1990.

What Does This Mean to You?

Figure 1 — Infiltration and exfiltration of air in a house

If your house is stuffy, odours linger, or humidity is high in fall and winter, it is likely that your house does not have adequate fresh air. If you or your children have respiratory conditions, such as asthma, bronchitis or chronic colds, getting the proper amount of fresh air is even more important. Opening windows can be part of the solution, but open windows can be a security risk (in some neighbourhoods), can cause comfort problems and can increase heating and cooling costs. Furthermore, opening windows may not improve indoor conditions under all circumstances. Using a mechanical ventilation system, such as an exhaust fan or a heat recovery ventilator (HRV), can be more effective.

Ventilation

Ventilation is often defined as a means of providing fresh air. However, the word “ventilation” can describe several different types of air movement.

Infiltration

Figure 2 — Distribution of air throughout a house

We get some fresh air from natural infiltration. This is the amount of fresh air that comes into your house through leaks, and is sometimes shown as house air changes per hour (ACPH). An air-change rate of 0.5 ACPH means that half the house air is changed every hour, or that the amount of fresh air that enters the house every two hours equals the volume of the house. Exfiltration, or the amount of air that exits the house, always equals infiltration — if it didn’t, the house would either implode or explode.

Distribution

The fresh air needs to be moved around the house, particularly to rooms with closed doors (such as bedrooms). This distribution usually requires fans and ducting systems. Imagine a two-storey house with all the fresh air infiltrating or being delivered into the basement where the clothes dryer is running. Without distribution, the fresh air would be removed from the house by the clothes dryer before it reached the occupants on the floors above. Only the basement would receive fresh air.

Circulation

Figure 3 — Circulation of air in a house

Even if fresh air is introduced to a room, it will often need some help to be circulated to all parts of the room. Rooms with lots of furniture or stored items are susceptible to having under-ventilation in some parts of the room. Fans can help here, too.

Is Ventilation Necessary?

Ventilation and good air quality are sometimes under-appreciated. If your furnace breaks down in the winter and the house starts getting cold, you will notice that problem within a couple of hours at the most. Insufficient ventilation will generally not be noticed as quickly as it takes time for symptoms, such as stuffy air, to develop.

A good time to check your indoor air quality is when you enter your house, before you get accustomed to the indoor air. Does it have a distinctive odour? Is it fresh and neutral? People moving to a house with good ventilation from a house with bad ventilation will recognize that the indoor air quality in their previous residence was not as good as in their new home.

People need fresh air all the time, but the need for additional ventilation will change. In the middle of winter, when it is very cold or windy outside, the natural air-change rate of the house will be highest and you may not require additional mechanical ventilation.

However, most times in fall, winter and spring, having some mechanical ventilation may make sense. Mechanical ventilation is beneficial for mid-summer if you are using an air conditioner and do not open windows for extended periods of time. In fact, summer is when houses have the lowest natural air change rate. Figure 4 shows the results of recent research that monitored air change rates in an Ottawa home during the summer. Most of the time, the house air change rate was below 0.3 air changes per hour — a recognized threshold for good indoor air quality.

Providing Good Ventilation

All houses can be provided with good ventilation. It is easier to do so when you have ducted air-moving equipment. Here is advice for a variety of houses, starting from the most difficult.

 

Figure 4 — Summer natural air infiltration rates for an Ottawa home not using its mechanical systems and with its windows closed

Older Houses with No Ducts or Fans

Intentional ventilation was a foreign concept to homeowners of houses built 60 or more years ago. Open windows could sometimes induce a breeze in hot summer periods. Open windows were also the standard ventilation for most bathrooms. Houses were so air leaky that the common goal was to reduce ventilation, rather than to promote it.

However, ventilation should be considered if these houses have been tightened as a result of renovations and energy retrofits. While opening windows will still play a part in a ventilation strategy, people are reluctant to leave them open long enough to ensure adequate air quality control. At the very least, bathroom or kitchen fans vented to the outside can be installed to control moisture in these areas. Sometimes, ducting can be retrofitted into chases or installed on the basement ceiling, if the homeowners want the benefits of an air distribution system. Do not install ducting systems in the attic, as the temperatures in Canadian attics are inappropriate for ducting in both the summer and winter. Cross-ventilation, through windows on either side of the house, can contribute to an increased ventilation rate.

Houses with Bathroom Fans and Forced-Air Furnaces

This is the basic system for older houses. The bathroom fan vents air from the house. Infiltration matches the rate at which the exhaust fan vents air outdoors, and outdoor air enters through various leaks in the house envelope. The furnace fan and ducting system can mix this fresh air with house air and distribute it around the house. In new houses in some parts of the country, the “ventilation” fan switch is located by the thermostat so that the furnace distribution fan can be turned on at the same time as the ventilation fan to ensure ventilation air is distributed and circulated evenly throughout the house.

Is this the best way to run a ventilation system? Probably not, but it can be made to work. First, install a good bathroom fan vented to the outside. Make sure that it is highly energy efficient (less than 50 watts) and quiet (1.5 sones or less), so you can use it without getting annoyed. Make it small (25 L/s or 50 cu. ft./min.), or ensure that you can control the speed. Leave it running all the time, or at least when the house is occupied. That ensures that some fresh air is entering the house. If your furnace or air conditioner is running frequently, then the fresh air is being distributed. You can leave your furnace fan on to ensure distribution, but that will usually cause high electrical consumption. New furnaces can be purchased with DC motor fans that can be controlled to run at under 100 W at low speed. Older furnace fans have power consumption of 400 – 600 W.

If you have an inefficient furnace fan and need to use the furnace fan for distribution, consider getting a fan-cycling control device. This controller can be used to turn the furnace fan on for 20 minutes per hour, for instance, to reduce the fan motor electrical consumption. Even 20 minutes an hour should ensure adequate circulation. Having the ventilation fan electrically linked to the furnace fan will ensure that when you turn your ventilation system on the furnace fan comes on too and the fresh air gets to where it is needed.

Heat Recovery Ventilators (HRV) Connected to the Furnace Ducting System

HRVs are efficient devices that provide good ventilation without a big energy cost for heating the outside air. The HRV uses the air being exhausted to preheat incoming air. They are able to recover 60 – 80% of the heat in the outgoing air which means, in winter, the incoming air will be much warmer than outside air (but still cooler than house air). The balanced ventilation provided by an HRV does not usually create house depressurization that could effect the proper and safe functioning of fuel fired appliances in the home.

Since the HRV in this case uses the furnace ductwork, the furnace fan has to be on, or at least cycling on and off, for the fresh air to get distributed around the house. The same considerations apply about getting a furnace with an efficient fan motor or a furnace-fan cycling controller. Note also that all HRVs need maintenance and cleaning.

See CMHC’s About Your House fact sheet Maintaining Your HRV for advice.

Separately Ducted HRVs

This system is the most efficient way to ventilate your house, as the HRV does the air preheat and the HRV fan motor distributes the fresh air and collects the stale air through its own ducting system. This means that the furnace fan motor does not need to run as part of the ventilation distribution system which represents significant energy savings.

The HRV should be used anytime the house is normally closed up. Run it continuously at low or medium speed, and switch to “high” for parties or other times when you want more ventilation. If you are buying an HRV, pick one that has been independently certified (e.g. choose one with a Home Ventilating Institute or HVI certification sticker). Choosing one with a high “sensible recovery efficiency” and a fan motor with low energy consumption will ensure lowest operating costs.  Also ensure that the contractor installing the HRV has been certified to do so through an organization such as the Heating, Refrigeration and Air Conditioning Institute of Canada (HRAI).

As mentioned in the previous section, make sure that the HRV is regularly maintained.

Running the Ventilation System

Ventilation is not as critical when the house is unoccupied, although some houses require ongoing mechanical ventilation to keep the windows from fogging up in winter and to prevent the subsequent damage to window frames, trim and walls. It is especially important to have high ventilation rates for:

• The first fall and winter for a new house, to get rid of construction moisture.
• Houses with high numbers of occupants, either temporary or permanent.
• Houses in which renovation activities (drywalling, painting, floor re-finishing and so on) or new furniture may be creating high concentrations of pollutants.
• Houses in which bedroom doors are generally closed during sleeping hours. Open doors help ensure that the bedroom air has the same quality as the air in the rest of the house. Closed-door bedrooms require higher ventilation rates or good distribution systems.
• Houses whose residents have respiratory problems (people allergic to outdoor pollutants require filtered outdoor air).

Summary

Most Canadian houses will benefit from the fresh air supplied by mechanical ventilation. In new houses, that fresh air is most efficiently delivered by a separately ducted HRV. In existing houses, quiet and efficient bathroom and kitchen fans, or HRVs when practical, can improve air quality. Using efficient furnace fan motors or furnace fan cycling controls will help to distribute fresh air to all rooms of the house at a reasonable cost.

 

Mechanical Ventilation for Medical Students

Patients may require mechanical ventilation for chronic or acute respiratory failure.  When a patient is intubated and placed on ventilation, there are several settings a physician may have to manage on the mechanical ventilator.  These ventilator settings include the positive end expiratory pressure (PEEP), the fraction of inspired oxygen (FiO2), the respiratory rate and the tidal volume.

As a medical student in the ICU, you will surely get asked several basic questions on mechanical ventilation.  Wrong answers to these questions will bore your attending, amuse your residents, and feed that desperate fear you have of accidentally killing your future patients through your own ineptness.

With that being said, correctly answering questions on the mechanical ventilation of your ICU patients could make your team nod proudly, yes, proudly.  The simplified basics of mechanical ventilation are described below.  Once you get the basics, move on to the second article in this series, “How to determine the initial settings for mechanical ventilation”.

There are two aspects medical students must understand about ventilation control settings:

1. Oxygenation and pH. 

2. Volume and Pressure

The reason we want to control inspiratory volume and pressure is because we are trying to walk a fine line between assisting the patient with breathing without allowing their respiratory muscles to atrophy or drastically decreasing the cardiac preload.

We want to control the oxygen levels and pH of our patient’s bodies to sustain healthy tissues and metabolic function.  The pH is reflected in our carbon dioxide and bicarbonate balance.  So we adjust oxygen and carbon dioxide levels as needed.

Oxygenation:

In the ICU, an oxygen concentration on the arterial blood gas (pO2) can be as low as 70 and still be considered acceptable.  How do we keep the pO2 at or above 70 mmHg?  Adjust the FiO2 and PEEP on the ventilator settings. Altering the patient’s pO2 can be just that simple- FiO2 and PEEP

The FiO2 is the fraction of inspired oxygen, while PEEP is the positive end expiratory pressure.

Carbon dioxide and pH:

The blood pH in your patient should be 7.4 plus or minus 0.5 and the carbon dioxide levels on the arterial blood gas (pCO2) should read 40 mmHg plus or minus 5.  How do we keep the pH and CO2 at safe levels? Adjust the respiratory rate and tidal volume.  Again, it’s just that simple.  You can alter the pH and pCO2 for your patient by adjusting the respiratory rate and the tidal volume on the ventilator. 

[Remember: The rate multiplied by the tidal volume will give you the minute ventilation (in units of L/min).  You may or may not get pimped on minute ventilation but it’s easy enough to remember: tidal volume x respiratory rate.]

So in short, the two basic goals of mechanical ventilation are to get the oxygen and carbon dioxide on the arterial blood gas close to perfect, and to do this with a pressure and volume that is appropriate for the medical situation the patient is in.  Alter the oxygen with the FiO2 and PEEP.  Alter the carbon dioxide (and thus pH) with the respiratory rate and tidal volume

MECHANICAL BELT

A belt is a looped strip of flexible material, used to mechanically link two or more rotating shafts. They may be used to move objects, to efficiently transmit mechanical power, or to track relative movement. Belts are looped over pulleys. In a two-pulley system, the belt may either drive the pulleys in the same direction, or the belt may be crossed so that the shafts move in opposite directions. A conveyor belt is built to continually carry a load between two points.

Power Transmission

Belts are the cheapest utility for power transmission between shafts that may not be parallel. Power transmission is achieved by specially designed belts and pulleys. The demands on a belt drive transmission system are large and this has led to many variations on the theme. Belts run smoothly and with little noise, and cushion motor and bearings against load changes, albeit with less strength than gears or chains. However, improvements in belt engineering allow use of belts in systems that formerly allowed only chains or gears.

Pros and cons

A belt drive is simple, inexpensive, and does not require parallel shafts. It helps protect a car from overload and jam, damping it from noise and vibration. Load fluctuations are shock-absorbed (cushioned). They need no lubrication and only little maintenance. They have high efficiency (90-98 percent), higher tolerance of misalignment, and are relatively inexpensive. Clutch action is activated by releasing belt tension. Different speeds can be obtained by step or tapered pulleys.

However, the angular-velocity ratio is not constant or equal to that of the pulley diameters, due to slip and stretch. Heat accumulation is present, and speed is limited to approximately 7000 feet per minute (ft/min), and a power of only 500 horsepower (hp). Temperatures ranges from -31 to 185°F. Adjustment of center distance or addition of an idler pulley is crucial for balancing the wear and stretch. To install endless belts, the relevant assembly must be dismantled first.

Flat belts

Belts on a Yanmar 2GM20 marine diesel engine.

Flat belts were used early in line shafting to transmit power in factories. It is a simple system of power transmission that was well suited to its time in history. It delivered high power for high speeds (500 hp for 10,000 ft/min), in cases of wide belts and large pulleys. However, these drives are bulky, requiring high tension leading to high loads, so vee belts have mainly replaced the flat-belts (except when high speed is needed over power). The Industrial Revolution soon demanded more from the system, as flat belt pulleys need to be carefully aligned to prevent the belt from slipping off. Because flat belts tend to slip towards the higher side of the pulley, pulleys were made with a slightly convex face (rather than flat) to keep the belts centered. The flat belt also tends to slip on the pulley face when heavy loads are applied. In practice, such belts were often given a half-twist before joining the ends (forming a Möbius strip), so that wear was evenly distributed on both sides of the belt (DB). A good modern use for a flat belt is with smaller pulleys and large central distances. They can connect inside and outside pulleys, and can come in both endless and jointed construction.

Round belts

Round belts are a circular cross section belt designed to run in a pulley with a circular (or near circular) groove. They are for use in low torque situations and may be purchased in various lengths or cut to length and joined, either by a staple, gluing or welding (in the case of polyurethane). Early sewing machines utilized a leather belt, joined either by a metal staple or glued, to great effect.

Vee belts

The Vee belt (also known as V-belt or wedge rope) provided an early solution to the slippage and alignment problem. It is now the basic belt for power for the transmission. It provides the best array of traction, speed of movement, load of the bearings, and longer service life. It was developed in 1917 by John Gates of the Gates Rubber Company. They are generally endless, and their general cross-section shape is trapezoidal. The "V" shape of the belt tracks in a mating groove in the pulley (or sheave), with the result that the belt cannot slip off. The belt also tends to wedge into the groove as the load increases—the greater the load, the greater the wedging action—improving torque transmission and making the vee belt an effective solution, needing less width and tension than flat belts.

V-belts trump flat belts with their small center distances and high reduction ratios. The preferred center distance is larger than the largest pulley diameter but less than three times the sum of both pulleys. Optimal speed range is 1000-7000 ft/min. V-belts need larger pulleys for their larger thickness than flat belts. They can be supplied at various fixed lengths or as a segmented section, where the segments are linked (spliced) to form a belt of the required length. For high-power requirements, two or more vee belts can be joined side-by-side in an arrangement called a multi-V, running on matching multi-groove sheaves. The strength of these belts is obtained by reinforcements with fibers like steel, polyester or aramid (e.g. Twaron). This is known as a multiple-belt drive.

When endless belts do not fit the need, jointed and link vee-belts may be used. They are, however, weaker and speed up to only 4000 ft/min. A link v-belt is a number of rubberized fabric links held together by metal fasteners. They are length adjustable by dissasembling and removing links when needed.

Film belts

Though often grouped with flat belts, they are actually a different kind. They consist of a very thin belt (0.5-15 millimeters or 100-4000 microns) strip of plastic and occasionally rubber. They are generally intended for low-power (ten hp or seven kW), high-speed uses, allowing high efficiency (up to 98 percent) and long life. These are seen in business machines, tape recorders, and other light-duty operations.

Timing Belts

Timing belts, (also known as Toothed, Notch or Cog) belts are a positive transfer belt and can track relative movement. These belts have teeth that fit into a matching toothed pulley. When correctly tensioned, they have no slippage, run at constant speed, and are often used to transfer direct motion for indexing or timing purposes (hence their name). They are often used in lieu of chains or gears, so there is less noise and a lubrication bath is not necessary. Camshafts of automobiles, miniature timing systems, and stepper motors often utilize these belts. Timing belts need the least tension of all belts, and are among the most efficient. They can bear up to 200 hp (150 kW) at speeds of 16,000 ft/min, and there is no limit on speed.

Timing belts with a helical offset tooth design are available. The helical offset tooth design forms a chevron pattern and causes the teeth to engage progressively. The chevron pattern design is self-aligning. The chevron pattern design does not make the noise that some timing belts make at idiosyncratic speeds, and is more efficient at transferring power (up to 98 percent).

Disadvantages include high starting price, grooving the pulleys, less protection from overload and jam, no clutch action, and backlash.

Specialty Belts

Belts normally transmit power on the tension side of the loop. However, designs for continuously variable transmissions exist that use belts that are a series of solid metal blocks, linked together as in a chain, transmitting power on the compression side of the loop.

"T belts" that simulate rolling roads for wind tunnels can be made to reach speeds of up to 250 km/h.

WE KNEW ABOUT VENTILATION

I have never failed to register my dislike of ‘small lofts’ particularly those mean and undersized structures which dictatorial, bureaucratized urban district councils sometimes permit their unfortunate tenants to erect in their back gardens. Believe it or not, these bureaucrats actually specify the size the loft is to be, yet they know nothing about racing pigeons or their permitted habitat nor about the hygiene without which animals cannot be kept as they should be. For instance, what do those form-filling bureaucrats know about ventilation and its affect on animals? Sweet Fanny Adams!

At the same time, what do fanciers know about ventilation and its effect on hygiene in the loft? I regret to have to say that the majority of fanciers have no idea at all! They think you can bung racing pigeons into any old shed, or disused barn, and then proceed to monopolize the prizes. Such thinking is so wide of the mark as to be laughable.

The first product of inadequate ventilation in a loft is the production of gases. What I want you all to understand is that gases have the facility of diffusion, a function which does not apply to everything.

It is in order for me to give you a further example, this time of non-diffusion. Let us help ourselves to a large glass jar and fill a third of its capacity with mercury, which is an extremely heavy metallic liquid. We now take up a can of water and pour this into the glass container until the liquid has taken up its third of the accommodation. Finally, we fill the remaining third of the glass jar with oil. So, we have oil, water and mercury stacked up inside the jar and wonder of wonders! Each liquid stays in its own space forbearing to mix with the other liquids in the jar. Even if we shake the contents of the glass jar in an attempt to make the contents diffuse, the three elements sort themselves out and stratarise with a third of the jar occupied by the mercury at the bottom, then the water, and finally the oil occupying a layer on top of the water. So, we have demonstrated the fact that certain elements won’t diffuse or, to put it another way, they won’t mix, representing a perfect case of class distinction!

Let us carry out another experiment which is as simple and informative as the non-diffusion demonstration. Once again we help ourselves to a capacious glass jar and into ft we pour a comparatively heavy gas, such as oxygen. Next, we pour into this jar a light gas, such as hydrogen. Right, we have two gases corked up in the Jar, a heavy one and a light one, and we leave them alone for a while. Soon, by chemical examination (because we cant see these gases which are invisible) we test the contents of the jar to discover if the two gases we put in it are infact not still separate and we find that the two gases had, in fact, diffused (mixed). This mixture would be the same throughout the jar, a perfect mixture of the two gases. This property (the mixing together of several gases) has a considerable bearing on ventilation, as we shall see. In fact, we have seen that one gas, which is sixteen times heavier than the other, has diffused with ft without difficulty!

Let us now tackle the aspect of loft ventilation by using the owner as a guinea pig. So, you are sitting in the corner of a room which has been sealed up, with you inside. You are breathing, of course, taking in air and exhaling carbonic acid gas. Although you are using up the air and replacing it with a poisonous gas, the latter gas does not work on you at once to affect your inhalement of air. This is because the carbonic acid gas you exhale from your lungs tends to diffuse with the air in the room, mixing freely with it. This process could continue for a long time before breathing became difficult or laboured because the air in the whole room would not deteriorate to a state where it affected breathing until the foul air given off by the lungs had practically exhausted the oxygen content of the gases.

We know, because we were taught at school, that air expands with heat and contracts with cold. When heat is put to air it tends to become lighter and because it is less dense than colder air it is forced upwards by the cool air which continues to press against it. Thus, we define the well-known statement that ‘hot air rises’ for the simple reason that it is being pressurised by the cooler air round about and below it. We note how air moves in a room ‘under pressure’ and it is a fact that winds are caused the same way viz under cooler pressure.

If we were naive and simple (which we most definitely are not) we would kid ourselves that all we need in a loft are inlets along the lower sections of walls to allow the cooler air to pass into the loft and outlets at higher altitudes to permit the cooler air to pressurise the hotter air and force it out of the loft, the hotter air being the carbonic acid gas breathed out by the pigeons in the loft after they had inhaled the cooler, purer air. As I have said, we are far too clever to fail for that idea because your ‘Old Hand’ knows very well that you can’t change the air efficiently in one large compartment (or in one small one) more than three times per hour without setting up unwanted draughts which could be of a harmful nature. The last thing we wish to do is put your birds in jeopardy but you can be quite sure that your old preceptor has far more sense than to commit an elementary error of this kind.

Let us bear In mind that gases, including harmful ones, freely mix together, thereby diffusing impurities as well as purities, so we must get to know more about the art of ventilation before we can hope to provide our bird with a safe and proper home. Perhaps we had better take the example once again of a man sitting in a seated room, breathing the air in it. We know from our tables and statistics that a man can turn out enough carbonic acid gas from his lungs and his skin, each hour, sufficient to render about 3,000 cu.ft. of air unfit for further respiration. A simple calculation will show that this person must be provided with a room l2ft x l0ft x 8ft as an alternative to being the target of nasty draughts. So, we now come to the inescapable basic fact of all schemes of ventilation viz that an animal must be given sufficient room viz ample air space.

If you care to look at ft in another way, you can say that ‘air space’ is really ‘lung space’. We must understand that if there is insufficient room, or air space, the metabolism must suffer from toxic gases which quickly put impurities into the bloodstream. How can any fancier hope to excel when racing pigeons whose blood has been poisoned by carbonic acid gas through loft overcrowding? You can feed your birds on the finest food money can buy and change the drinkers every few minutes, but without benefit to birds who are living in overcrowded accommodation. They would be steadily gassed every day and every night which, though not killing them immediately, would exert a subtle but lethal effect on them. Perhaps now you will realise why I detest ‘small lofts’ and in particular those heartless bureaucrats who are probably the country’s main contributors to the poisoning of racing pigeons.

If I lived in a ‘council house’ and was therefore at the mercy of dictatorial bureaucrats I would not erect a loft at all! Instead, I would construct an aviary with four walls of wire mesh. Then I would drape some transparent polythene sheeting over it. Incidentally, I’m not quite sure about modern council regulations governing the erection of ancillary buildings but I know that up to recent times the council had no Jurisdiction over property that is transparent. In other words, I hold the opinion that anyone could build an aviary with a transparent roof without needing permission from the local authority but please don’t act on this advice without getting good legal opinion, or an opinion from the RPRA, which probably knows the ins-and-outs of modem local by-laws.

I would then insert a wire-mesh floor some 12in above ground level so that birds could not reach the ground below the wire-mesh floor. One could stick a wooden rod or two through both wails of the mesh to provide perches. Nestboxes could be put in the aviary in the proper season and I maintain that birds living in this structure would be healthier and fitter than any birds kept in a loft or structure with wooden or solid walls.

It would be almost impossible for birds living in this way to contract respiratory disease, or anything like it. They would have to be healthy to live, anyway.

The only birds I lost in such conditions were some Belgian squeakers which I suspected of suffering from respiratory disease. I wasn’t sure so decided to take no chance. There were thirteen of them and they went into the aviary one November night. Four of them toppled from their perches so they were indeed affected, but the remaining nine stayed to thrive and prosper. If the four had contracted the disease so had the other nine but the healthy conditions in which they were compelled to live cleared up the trouble once and for all.

As we have seen, a cubic air space of about 3000 cu.ft. is necessary for the well-being of one human but the average quota for animals is 25 cu.ft. for each pound of body weight. As the average racing pigeon weighs only l6oz (1-1 lb) altogether then 9 cu.ft. would appear to be quite sufficient. On the basis of a pigeon requiting about one third of the 25 cu.ft. of air, a small loft 9ft x 9ft x 6ft high would accommodate about 54 pigeons. So much for theory!

However, as pigeon fanciers we know that we are not just beset by the production of carbonic acid gas through pigeon respiration but there are other sources of obnoxious loft gas build up. For instance, what about the pigeons’ droppings? These fall onto the loft floor where they build up all through the night, giving off ammonia.

This brings me back to what I was saying about the diffusion of gases. No matter how much individual gases weigh, they mix freely and instantly, to produce yet another type of gas, some productions being worse than others. In a pigeon loft, where perched birds spend the night building up a floor or perch layer of wet droppings, the said droppings give off ammonia gas which diffuses (mixes freely) with the carbonic acid gas to create an entirely but even more obnoxious gas, known as carbamate gas. This additional hazard militates against the sums we have just been doing in respect to air space per bird. Therefore, a much more liberal amount of air space must be provided if we are to counteract this inevitable drawback.

How is a fancier to know if the production of obnoxious gas to generate atmospheric impurity has reached a dangerous level, affecting the general loft ventilation system? Well, nature fitted him with a very reliable obnoxious gas detector - his nose! If you can smell impurities in the air, then the ventilation is inadequate, in fact, it is downright dangerous. No one should be able to smell ‘pigeons’ in a pigeon loft, nor should any nose be assaulted by the abominable stink of ammonia from droppings. If you can smell either pigeons or droppings, or both, the loft ventilation system should be overhauled at once. To delay the work is to inflict respiratory disease on all the loft’s inmates.

Take your own home for example. If you can sniff unpleasant odours, by way of a general mustiness, two possibilities are imminent: (1) The ventilation system is inadequate; (2) There is ‘rising damp.’ The risk of (2) above is inherent in every pigeon loft which has been erected without adequate damp-proofing, which is to say that a waterproof-course has not been laid between the piers which support a structure on the ground and the loft Itself. Before standing the loft on anything one should first cover the pier or prop with slate, lead impregnated damp course, polythene, or some material which is waterproof and has lasting qualities. Otherwise, rising damp will reach up into the loft and begin to poison the internal air.

Fanciers should know that rising damp’ is not merely moisture moving up the wall of the loft through capillary attraction but it is a living, seething vile bacteria, which destroys as it progresses, with its single task of multiplying its spores (cells) in its course of encroachment on the structure. No good racing pigeons should be exposed to this damnable risk.

The ‘nose detection’ of obnoxious gas can only operate when one is on the point of entering a loft. After some time spent in the loft’s interior the nose stales in its quest for odours and tends to get used to the vitiated air. Therefore, practice sniffing when you enter the loft and if you can smell atmospheric impurities decide to do something about the situation immediately.

As I said, it is necessary for us to do our sums again by taking into consideration not merely the carbonic acid gas exhaled by perched pigeons but also the ammonia gas exuded by the damp droppings. According to the standard adopted by scientists, a loft 9ft x 9tt x 6ft high (486 sq.ft.) would accommodate 24 pigeons. Judged by what I have seen on my past travels most fanciers are keeping double that number of birds in their lofts, thereby Indulging In blatant overcrowding with the worst possible results. Indeed, most of the birds in these lofts will be suffering from respiratory disease which, in most cases, will have escaped the notice of the owner.

When calculating air space in order to arrive at figures which show there is sufficient air to ventilate the structure there is a limit to how high we can go inside the loft. For instance, if we supposed that the loft roof was some 18ft above the floor, the air in the upper layer of some lift would not be deemed air that was available for respiratory purposes to the inmates of that loft. Although the actual accommodating air space height is somewhat of an arbitrary nature (science poses pros and cons) I think we can discount air that stacks up more than 7ft from the floor. This requirement Indicates, in no uncertain manner that floor area is of the greatest factor, not height. This means that loft designers and builders should be encouraged to provide depth (or width) as an important provision towards the ventilation problem.

Air space in buildings which contain chimneys is less critical than buildings which do not contain chimneys, such as pigeon lofts. The chimney does not merely discharge the smoke from fires, it also has the effect of sucking out the used air so that new, fresh air can penetrate the rooms and replace the vitiated air which is being extracted via the flue. I saw ducted ventilation (square wooden ducts installed) in the loft of Van Den Bosche of Ghent. Although the loft was in the attic (loft) of a house which peaked up to a considerable height to the centre ridge, the partners had installed the duct to bring fresh air down from the height to a level some 6ft above floor level. I complimented them on their cleverness and pointed out the remarkable condition of their birds as their response to the purer air they were breathing. It is a fact which so few fanciers will subscribe to, that pigeons in most lofts would react to Improvement made to the ventilation system by assuming a high level of ‘Condition’ of a kind few fanciers have ever seen. I hereby invite my reader to take his nose to his loft and, if he is not entirely satisfied with what he encounters, he sets about the introduction of a system of ventilation which can bestow real benefits on his pigeons.

My own birds occupy loft sections which are 8ft deep, 5ft wide and 6ft 61n high. In a section of this size I allow six pairs of birds to breed, no more. However, it should be borne in mind that apart from the above dimensions I have also installed fittings which I have proved definitely assist the ventilation by helping to keep the fresh air moving through the loft. I will not permit any air inside the loft to ‘dwell’ viz remain static. I require the air to flow into the loft and keep moving until it passes out to give perfect ventilation.

I know there are those who will cry out against this system by pointing out that I have already said that when a loft’s internal air is changed more than three times in an hour draughts are created. Well, what are draughts? A draught is a stream of cold air which is playing into an interior containing warm air. But there is no warm air in my loft! Like those other fanciers who have created ‘east wind pigeons’, I deliberately built my loft to face east and it is wide open to this cold wind. The result is that the air inside my loft is of the same temperature as that of the coldest which is found outside it, therefore no draughts are possible. I wish my reader to understand that you can’t create an ‘east wind’ family of racing pigeons if you pamper your birds and give them heated or ‘protected’ interiors. Why not? Because an ‘east wind’ strain of pigeons can only become so if it develops the kind of plumage which can be guaranteed to keep its body temperature at the correct level (107’F) in the coldest of conditions but no pigeon is going to grow such a thick plumage unless its environment demands growth of that kind. Hence the exposure to east winds.

The secret of keeping the air moving in the loft is to install louvers at floor level and a 4in gap running the length of the rear wall at the position where it meets the roof. In a loft fitted up in this way the air streams from the front and both ends (like the front, the end walls of the loft must also be louvered at floor level) Incidentally the gap in the rear wail must not be louvered but be covered with fine mesh wire.

If this kind of ventilation is installed (and it is the best) the fancier should again use his nose as an air impurity detector, especially when he has nestlings in the nest. Obviously, the hatching out of nestlings means something like a doubling of those sources of supply of carbonic acid gas and the ammoniac gases from the droppings. Can you still smell pigeon and/or ammonia when you enter the loft? If so there is only one thing for it and that is to increase the number of louvers in front and side wails until enough air is streaming through the loft, from front to rear, to keep the air clean and sweet.

In the past, few fanciers were willing to consider the effect of bad ventilation on racing pigeons. They tended to blame a number of other external ponderables for their sad lack of success. Fortunately, more and more fanciers have seen the light and are taking notice of loft design as an influential factor in pigeon racing success. Some things one can ignore in the hope that they will go away but no amount of indifference will relieve a loft of the burdens it imposes on its inmates because of its bad design and lack of real ventilation.