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A further occupational history was sought at this time, and the patient was reviewed by an occupational lung disease specialist physician. Prior to his current employment, he had worked in a number of different jobs; none had involved any significant occupational exposures. Following this, he had been off work sick for 2 months and had been redeployed by the company to an office job. He was managed with inhaled corticosteroids and bronchodilators, which continued to have some symptomatic benefit; he was advised to seek prompt treatment of any respiratory infections and to keep up-to-date with influenza and pneumococcal vaccinations. Due to his young age and severe airflow obstruction, an assessment for lung transplantation was also undertaken. Discussion A complete, thorough, and detailed occupational history should be taken in all cases of newly diagnosed respiratory disease and, in particular, where no other identifiable cause is present. The timing of symptoms relative to any employment changes (this can include job change, increased hours or intensity, differences in exposures and environment) is particularly important. Identification of any occupational factors that may be causal is vital; this can be very difficult in rare diseases. A lifetime job history should be recorded, including the nature of the jobs, all reported exposures, the size of the organization (workforce, output), and the availability of environmental controls and whether personal protective equipment is worn. Access to company occupational health can be invaluable, but this should only be undertaken after gaining consent from the patient; smaller employers are less likely to have formal occupational health provision. Removal of exposure is often key, although, in some cases, disease progression appears to continue. Long-latency Case 13 Occupational lung disease 163 diseases are particularly hard to attribute to occupational causes, as the relevant exposures may have occurred over 40 years previously; a frequently quoted example is the relationship between asbestos exposure and mesothelioma. Prognosis, irrespective of the underlying aetiology, is poor, and, whilst the rate of decline is variable, most patients will deteriorate slowly and develop respiratory failure over the course of months to years. Various management strategies have been employed; these commonly include systemic corticosteroids, sometimes in combination with other immunosuppressive treatment. Long-term macrolide therapy has been used, with some success (possibly due to an immunomodulatory effect), but has not been tested in randomized clinical trials. Secondary bacterial infection often leads to irreversible deterioration, so prevention is a key priority, with vaccination, physiotherapy, and prophylactic or prompt antibiotic therapy. A subsequent workplace survey at this plant found irreversible obstructive lung function at three times the rate expected in population controls; when limited to non-smokers, the rate was ten times that of a referent population. These studies showed a dose dependence, with a greater prevalence of disease in factories using larger quantities of diacetyl. Whilst other agents were considered as potentially causative agents, the available data suggested that the relationship between exposure and disease was strongest for diacetyl-with a further four cases identified in a diacetyl manufacturing company [32].
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This results in an overall ventricular rate that is less than the programmed rate. The P wave is difficult to identify on the bedside monitor recording at such a rapid rate. In panel (B), marker channels are shown to illustrate the atrial sensed-ventricular paced rhythm at a rate that just exceeds the upper tracking rate of the pacemaker. As the P wave rate increases, there will be 2:1 pacemaker block when the P wave rate exceeds the total atrial refractory period. Depending on the P-P coupling interval, the paced rhythm may go to 2:1 or 3:1 sensing block. Automatic mode switch algorithms Mode switching is an upper rate behavior that allows an algorithm to smooth the paced upper rate during an atrial arrhythmia. Some devices have the capability of being programmed for a higher mode switch rate than the lower rate during dual chamber programming. This occurred when internal components of the pacemaker generator failed and the pacemaker produced an inappropriate rapid rate. Far-field ventricular signals seen on the atrial electrogram should be assessed during pacemaker lead implantation. Atrial tracking of the tachycardia can result in ventricular pacing at or near the maximum tracking rate. Ventricular pacing (Vp) is followed by a retrograde P wave which is seen on the atrial sensing channel as an atrial sensed event (As). This triggers a ventricular paced beat and results in inappropriate rapid pacing (endless loop tachycardia). If the interval between a ventricular paced beat to the following atrial sensed event is shorter than a pre-determined value. In this situation, a ventricular paced beat is followed by a retrograde atrial beat. If the lower rate limit is sufficiently high, an atrial paced event occurs but finds the atrium refractory (functional atrial non-capture). In panel A, ventricular pacing (Vp) is performed at a rate faster than the intrinsic atrial rate. In panel B, dual chamber pacing is performed to assure an atrial paced (Ap) and ventricular paced (Vp) rhythm. This results in a ventricular paced event followed by retrograde conduction to the atrium (As). The atrium is no longer refractory because of the loss of atrial capture on the previous beat. The resultant rhythm of ventricular pacing with retrograde atrial activation can lead to symptoms of pacemaker syndrome.
