Cardiovascular Effects of Norepinephrine in Septic Shock

  • X. Monnet
  • J.-L. Teboul
Part of the Annual Update in Intensive Care and Emergency Medicine book series (AUICEM, volume 2012)


Septic shock is characterized by numerous cardiovascular abnormalities including absolute and relative hypovolemia, vascular tone depression, myocardial dysfunction, derangements in regional blood flow distribution and microcirculation disorders. The degree of severity of each of these abnormalities is variable from patient to patient. Although volume resuscitation is the most urgent therapy, current international guidelines recommend administering a vasopressor early to sustain life and maintain perfusion in the face of life-threatening hypotension, even when hypovolemia has not yet been resolved [1]. Indeed, if the mean arterial pressure (MAP) is markedly reduced, the perfusion pressure of critical organs (e.g., kidney, brain, myocardium, liver) may be lower than the lower threshold of autoregulation so that the ability of autoregulation to maintain vital organ blood flow may be lost. This can result in organ ischemia and eventually in organ failure, even if the systemic blood flow is high. The decrease in organ blood flow may be particularly marked in those patients with pre-existing renal, carotid, coronary or mesenteric atherosclerotic lesions as well as in those with pre-existing hypertension. In these conditions, increasing MAP above a certain critical level can restore organ perfusion even in the absence of an increase in cardiac output. Clinical evidence of such a pressure effect has been provided in the context of septic shock in studies where correction of severe hypotension with a vasoconstrictor was associated with improved renal function in the absence of any change in cardiac output [2–4].


Cardiac Output Septic Shock Septic Patient Venous Return Septic Shock Patient 
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© Springer-Verlag Berlin Heidelberg 2012

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  • X. Monnet
  • J.-L. Teboul

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