| Abstrakt: |
Patients who present with acute myocardial infarction after a work injury (AMI-WI) often report symptoms consistent with chronic hyperventilation which date back as far as the work injury itself, rather than to the AMI. The aim of the study was to test the hypothesis that hyperventilation significantly contributes to the symptoms of AMI-WI patients. The prevalence of hyperventilation was assessed by clinical capnography in 12 AMI-WI patients, 20 normal controls, 15 AMI patients whose AMI was conventional and not subsequent to a work injury (AMI-C) and 14 patients with post-traumatic stress disorder (PTSD). End-tidal carbon dioxide partial pressure (PetCO2) was measured at rest, after 1 min hyperventilation (FHPT), after recall of the relevant stressor (Think) and when the breathing was felt to be normal (MBIN). PetCO2 levels after FHPT were: 29.0±1.5 (mean±SD) nmiHg for AMI-WI; 26.7 ±1.9 nunHg for PTSD; 32.1 ± 4.1 mmHg for AMI-C and 33.7±1.4 mmHg for the controls (P< 0.05 and P< 0.01 for AMI-WI and PTSD, respectively, versus controls). After Think, the levels were 25.8±1.6 mmHg for AMI-WI, 24.6±1.4 mmHg for PTSD, 31.2 ±4.1 mmHg for AMI-C and 31.2±1.5 mmHg for normals (P< 0.05 and P< 0.01 for AMI-WI and PTSD, respectively, versus controls). For MBIN, values of PetCO2 were 26.8±1.7 mmHg and 26.7±1.5 mmHg for AMI-WI and PTSD versus 33.8±1.2 mmHg for normals, (P< 0.01 for both versus controls). Ten AMI-WI and 12 PTSD were positive for hyperventilation versus four AMI-C patients and four controls (P< 0.01). The implications for rehabilitation, compensation and pathophysiology of AMI-WI are discussed, both from a medical-scientific perspective and in terms of admissible legal evidence. [ABSTRACT FROM AUTHOR] |
