Effects of norepinephrine on static and dynamic preload indicators in experimental hemorrhagic shock.
OBJECTIVE
To investigate the effect of norepinephrine on static (right atrial pressure, pulmonary artery occlusion pressure ) and dynamic (pulse pressure variation and arterial systolic pressure variation) preload indicators in experimental hemorrhagic shock.


METHODS
Prospective controlled experimental study.


METHODS
Animal research laboratory.


METHODS
Six anesthetized and mechanically ventilated dogs.


METHODS
Dogs were instrumented for measurement of arterial blood pressure, pulmonary artery catheter derived variables including right atrial pressure, pulmonary artery occlusion pressure, and cardiac output. Simultaneously, pulse pressure variation and systolic pressure variation were calculated. Pulse pressure variation is the difference between the maximal and the minimal value of pulse pressure divided by the mean of the two values and is expressed as a percentage. Systolic pressure variation is the difference between the maximal and the minimal systolic pressure and is expressed as an absolute value. After baseline measurements, hemorrhagic shock was induced by a stepwise cumulative blood withdrawal of 35 mL.kg of body weight. A second set of hemodynamic measurement was made 30 mins after bleeding. The third set was made 30 mins later under norepinephrine.


RESULTS
Mean arterial pressure and cardiac output decreased after hemorrhage (p < .05), whereas right atrial pressure and pulmonary artery occlusion pressure remained unchanged. Baseline pulse pressure variation and systolic pressure variation increased significantly with hemorrhage, from 12% (9%) to 28% (11.5%) (p < .001) and from 12.5 (6.5) to 21 (8.2) mm Hg (p < .05), respectively. Norepinephrine induced a significant increase of cardiac output and a significant decrease of pulse pressure variation and systolic pressure variation but did not significantly change right atrial pressure or pulmonary artery occlusion pressure values. Stroke volume was correlated to pulse pressure variation and systolic pressure variation but was not correlated to right atrial pressure or pulmonary artery occlusion pressure.


CONCLUSIONS
Our study confirms the superiority of dynamic variables (pulse pressure variation and systolic pressure variation) over static ones (right atrial pressure and pulmonary artery occlusion pressure) in assessing cardiac preload changes in hemorrhagic shock. However, norepinephrine could significantly reduce the value of these dynamic variables and mask a true intravascular volume deficit possibly by shifting blood from unstressed to stressed volume.
Nouira
Semir
S
Medical Intensive Care Unit, Fattouma Bourguiba University Hospital, Monastir 5000, Tunisia. Semir.nouira@rns.tn
Elatrous
Souheil
S
Dimassi
Saoussen
S
Besbes
Lamia
L
Boukef
Riadh
R
Mohamed
Boussarsar
B
Abroug
Fekri
F
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002496:Central Venous Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D004285:Dogs; D009638:Norepinephrine / Q000494:pharmacology*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013318:Stroke Volume / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
D014662:Vasoconstrictor Agents; D009638:Norepinephrine