HYPERVENTILATION IN PATIENTS WHO HAVE SUSTAINED MYOCARDIAL-INFARCTIONAFTER A WORK INJURY

Patients who present with acute myocardial infarction after a work inj ury (AMI-WI) often report symptoms consistent with chronic hyperventil ation 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 hyperve ntilation significantly contributes to the symptoms of AMI-WI patients . The prevalence of hyperventilation was assessed by clinical capnogra phy in 12 AMI-WI patients, 20 normal controls, 15 AMI patients whose A MI 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 h yperventilation (FHPT), after recall of the relevant stressor (Think) and when the breathing was felt to be normal (MBIN). PetCO2 levels aft er FHPT were: 29.0+/-1.5 (mean+/-SD) mmHg for AMI-WI; 26.7+/-1.9 mmHg for PTSD; 32.1+/-4.1 mmHg for AMI-C and 33.7+/-1.4 mmHg for the contro ls (P < 0.05 and P < 0.01 for AMI-WI and PTSD, respectively, versus co ntrols). 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 fo r normals (P < 0.05 and P < 0.01 for AMI-WI and PTSD, respectively, ve rsus 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 posit ive for hyperventilation versus four AMI-C patients and four controls (P < 0.01). The implications for rehabilitation, compensation and path ophysiology of AMI-WI are discussed, both from a medical-scientific pe rspective and in terms of admissible legal evidence.