Comparative Study between Norepinephrine and Dopamine in the management of septic shock using noninvasive cardiac output monitoring
Heba Abdel Azim Labib;
Abstract
Septic shock requires early, vigorous resuscitation. An integrated approach directed at rapidly restoring systemic oxygen delivery and improving tissue oxygenation hasbeen shown to improve survival significantly in septic shock.
When fluid administration fails to restore an adequate arterial pressure and organ perfusion, therapy with vasopressor agents should be initiated. The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalizecellular metabolism.
The precise blood pressure goal to target in septic shock remains uncertain. Mostexperts agree, largely on the basis of the animal studies cited previously and on physiologicreasoning, that in septic patients with evidence of hypoperfusion, mean arterialpressure should be maintained above 60 or 65 mm Hg.
There has been longstanding debate about whether one catecholamine vasopressoragent is superior to another.the arguments tend to focus on the agents themselves when the therapeuticstrategy isactually what differs. Different catecholamine agents have differenteffects on α- and β-adrenergic receptors. The hemodynamicactions of these receptors are well known, with a-adrenergic receptors promoting vasoconstriction, β1-adrenergic receptors increasing heart rate and myocardial contractility, and β2-adrenergic receptors causing peripheral vasodilation.
Dopamine, the immediate precursor of norepinephrine and epinephrine is a less potent vasopressor than norepinephrine with dose-varying receptor binding. Although less potent, dopamine is very effective at increasing systemic blood pressure.Dopamine increases mean arterial pressure and cardiac output, primarily by anincrease in stroke volume, and to a lesser extent by an increase in heart rate.
Norepinephrine, the endogenous mediator of the sympathetic nervous system, isa potent α-adrenergic agonist with less pronounced β-adrenergic agonist effects. Norepinephrine increases mean arterial pressure by vasoconstriction, with a small(10%–15%) increase in cardiac output and stroke volume.
The more recent trend in monitoring of septic shock focuses on monitoring the variables that have a direct influence on the outcome of septic shock such as ,Systolic and mean arterial pressure (SBP and MAP), Systemic vascular resistance index (SVRI) ,Cardiac index (CI).
These variables may be monitored either invasively or non-invasively. Impedance cardiography, the non-invasive method of cardiac output monitoring, has been found to be a satisfactory substitute for invasive monitoring as it provides essentially similar information and is easier, quicker, cheaper and much safer to use .
Thisstudy was carried out in Ain Shams university hospitals.After medical ethical committee approval and informed written consent, 80 patients diagnosed as septic shock wereenrolled in this study. The age of all patients ranges between 18-65years.
When fluid administration fails to restore an adequate arterial pressure and organ perfusion, therapy with vasopressor agents should be initiated. The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalizecellular metabolism.
The precise blood pressure goal to target in septic shock remains uncertain. Mostexperts agree, largely on the basis of the animal studies cited previously and on physiologicreasoning, that in septic patients with evidence of hypoperfusion, mean arterialpressure should be maintained above 60 or 65 mm Hg.
There has been longstanding debate about whether one catecholamine vasopressoragent is superior to another.the arguments tend to focus on the agents themselves when the therapeuticstrategy isactually what differs. Different catecholamine agents have differenteffects on α- and β-adrenergic receptors. The hemodynamicactions of these receptors are well known, with a-adrenergic receptors promoting vasoconstriction, β1-adrenergic receptors increasing heart rate and myocardial contractility, and β2-adrenergic receptors causing peripheral vasodilation.
Dopamine, the immediate precursor of norepinephrine and epinephrine is a less potent vasopressor than norepinephrine with dose-varying receptor binding. Although less potent, dopamine is very effective at increasing systemic blood pressure.Dopamine increases mean arterial pressure and cardiac output, primarily by anincrease in stroke volume, and to a lesser extent by an increase in heart rate.
Norepinephrine, the endogenous mediator of the sympathetic nervous system, isa potent α-adrenergic agonist with less pronounced β-adrenergic agonist effects. Norepinephrine increases mean arterial pressure by vasoconstriction, with a small(10%–15%) increase in cardiac output and stroke volume.
The more recent trend in monitoring of septic shock focuses on monitoring the variables that have a direct influence on the outcome of septic shock such as ,Systolic and mean arterial pressure (SBP and MAP), Systemic vascular resistance index (SVRI) ,Cardiac index (CI).
These variables may be monitored either invasively or non-invasively. Impedance cardiography, the non-invasive method of cardiac output monitoring, has been found to be a satisfactory substitute for invasive monitoring as it provides essentially similar information and is easier, quicker, cheaper and much safer to use .
Thisstudy was carried out in Ain Shams university hospitals.After medical ethical committee approval and informed written consent, 80 patients diagnosed as septic shock wereenrolled in this study. The age of all patients ranges between 18-65years.
Other data
| Title | Comparative Study between Norepinephrine and Dopamine in the management of septic shock using noninvasive cardiac output monitoring | Other Titles | دراسة مقارنة بين الدوبامين والنورايبينيفرين في علاج الصدمه التسمميه باستخدام مراقبة النتاج القلبي غير الهجوميه | Authors | Heba Abdel Azim Labib | Issue Date | 2016 |
Attached Files
| File | Size | Format | |
|---|---|---|---|
| G12532.pdf | 245.7 kB | Adobe PDF | View/Open |
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