title: Increasing mean arterial pressure in cardiogenic shock secondary to myocardial infarction: effects on hemodynamics and tissue oxygenation.
abstract: There are very few data regarding the effects of norepinephrine uptitration on global and regional hemodynamics in cardiogenic shock. We studied 25 patients with shock secondary to myocardial infarction successfully treated with percutaneous coronary intervention. Before the inclusion, 16 of 25 patients presented a cardiac arrest in the presence of medical staff. Norepinephrine was titrated to increase mean arterial pressure (MAP) from 65 to 85 mmHg during 1 h. Swan-Ganz variables, arterial and mixed venous blood gases, lactate, and thenar near-infrared spectroscopy variables (muscle tissue oxygen saturation [StO2] and its changes during a vascular occlusion test) were measured before, 1 h after norepinephrine uptitration, and 1 h after norepinephrine downtitration. To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.6 (0.28-1.2) to 1.53 µg · kg · min (0.76-2.6 µg · kg · min) (P < 0.00001) (median and interquartile range), with no change in heart rate. Norepinephrine uptitration significantly increased cardiac index (2.3 ± 0.5 to 2.8 ± 0.1 L · min · m), cardiac power index (0.40 ± 0.1 to 0.55 ± 0.1 W/m), mixed venous oxygen saturation (69% ± 9% to 73% ± 9%), and coronary perfusion pressure (32 ± 3 to 43 ± 4 mmHg). Lactate level decreased from 2.6 ± 1.7 to 1.6 ± 0.4 mmol/L (P < 0.05). Pulmonary artery occlusion pressure remained unchanged. Regarding near-infrared spectroscopy variables, all values except StO2 were significantly pathological when compared with healthy volunteers. The StO2 recovery slope and delta StO2, respectively, increased from 3.0% ± 1.3%/s to 3.6% ± 1.3%/s and 10% ± 3% to 14% ± 4%, whereas StO2 did not change (83% ± 6% to 83% ± 7%). After H1, norepinephrine was decreased to basal values, and all variables returned to baseline. In conclusion, a short-term increase in MAP with norepinephrine in resuscitated cardiogenic shock complicated by postreperfusion disease is associated with better cardiac performance and improved microcirculatory variables.
authors: *CHU Nancy, Service de Réanimation Médicale Brabois, Pole Cardiovasculaire et Réanimation Médicale, Hôpital Brabois; and †INSERM, Groupe Choc, U1116, Faculté de Médecine, Vandoeuvre-les-Nancy; and ‡Université de Lorraine, Nancy, France.
authors: Pierre
authors: P
authors: Perez
authors: Antoine
authors: A
authors: Kimmoun
authors: Vincent
authors: V
authors: Blime
authors: Bruno
authors: B
authors: Levy
mesh_terms: D000328:Adult; D000368:Aged; D062186:Arterial Pressure / Q000187:drug effects / Q000502:physiology; D004334:Drug Administration Schedule; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000628:therapy; D009638:Norepinephrine / Q000008:administration & dosage / Q000627:therapeutic use*; D010101:Oxygen Consumption / Q000187:drug effects* / Q000502:physiology; D062645:Percutaneous Coronary Intervention; D011446:Prospective Studies; D012770:Shock, Cardiogenic / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D019265:Spectroscopy, Near-Infrared / Q000379:methods; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D055815:Young Adult
chemical_list: D014662:Vasoconstrictor Agents; D009638:Norepinephrine