13.09.2016 | Understanding the Disease
Understanding patient-centredness: contrasting expert versus patient perspectives on vasopressor therapy for shock
Erschienen in: Intensive Care Medicine | Ausgabe 7/2017
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In septic shock, we use vasopressors under the assumption that they improve organ perfusion. The vasoconstricting effect should be limited in intensity, only enough to compensate for excessive arterial vasodilatation or to mobilize blood pooled in venous capacitance vessels. In other types of shock, vasopressors are used as bridge therapy for profound hypotension to induce vasoconstriction predominantly in ‘less vital organs’, redistributing blood flow to ‘more vital’ organs [1]. Thus, when we administer vasopressors, we postulate that we control the intensity and the distribution of the vasoconstrictive effect. Poiseuille’s law suggests that we might frequently be wrong as vasoconstriction is more likely to reduce blood flow despite higher blood pressure values. However, even when we are not wrong, a number of unavoidable trade-offs may be associated with short- and long-term adverse effects (Table 1).
Primary objective of vasopressor therapy
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Underlying assumptions
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Underlying uncertainty
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Potential detrimental effects on tissue perfusion
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Other potential detrimental effects on patient-centred outcomesa
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Treat underlying pathological pathway: excessive vasodilation
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Intense vasodilatation causes severe hypotension which, in turn, reduces perfusion in all organs
Vasoconstriction induced by vasopressors is controlled to avoid excessive vasoconstriction and iatrogenic reduction of organ perfusion
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Even with severe hypotension, blood flow may be normal or high
We have no means to titrate vasopressor doses in function of flow (i.e. controlling vasoconstriction)
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Uncontrolled vasoconstriction may worsen organ failure and trigger more intense resuscitation (including more intense vasopressor therapy) leading to a downward spiral and death
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Myocardial injury, arrhythmia, pulmonary oedema (short-term consequences of arrhythmogenic effects and increased afterload)
Sensorimotor deficits and reduced functional autonomy (long-term consequences of shunting blood away from nerves and muscles for prolonged periods)
Skin breaks, infectious risks, visible scars (long-term consequences of shunting blood away from skin for prolonged periods)
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Redistribute blood flow from non-vital to vital organs
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Vasopressors selectively vasoconstrict skin, muscles and nerves more than gut, kidneys, liver, heart, lung and brain
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We have no means of comparing blood flow between vital organs and non-vital organs (i.e controlling the distribution of vasoconstriction)
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