ABSTRACT
This study investigated improvements in pre-hospital care for patients with acute exacerbated chronic obstructive pulmonary disease (aeCOPD) achieved by using a standard operating procedure (SOP). An SOP for pre-hospital treatment of patients with aeCOPD was designed based on valid national guidelines. A total of 1000 Emergency Medical Service patient care reports were analysed prospectively: 500 before and 500 after introduction of the SOP. Overall guideline adherence was 34.6% before and 53.8% after introduction of the SOP; this increase was not statistically significant. After SOP introduction, the administration of ß(2) mimetics by inhalative, intravenous and subcutaneous routes increased significantly. The level of knowledge of the national guidelines was rated at 67% by emergency physicians during self-assessment, but was only 33% when physicians were asked specific questions during interview. Introducing the SOP for patients with aeCOPD did not significantly improve adherence to valid national guidelines, but did help to improve specific elements of therapy.
Subject(s)
Adrenergic beta-2 Receptor Agonists/therapeutic use , Emergency Service, Hospital/standards , Guideline Adherence/standards , Practice Guidelines as Topic/standards , Practice Patterns, Physicians'/standards , Pulmonary Disease, Chronic Obstructive/therapy , Adrenal Cortex Hormones/therapeutic use , Bronchodilator Agents/therapeutic use , Drug Administration Routes , Drug Administration Schedule , Germany , Humans , Inpatients , Oxygen/administration & dosage , Pulmonary Disease, Chronic Obstructive/diagnosis , Self-Assessment , Surveys and QuestionnairesABSTRACT
AIM: This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage. METHODS: Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1 plus ETA blockade. RESULTS: In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (-40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols. CONCLUSIONS: Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output--but not MAP--was similar in all protocols.
