Nasraway SA. Renal effects of norepinephrine used to treat septic shock patients. Effect of norepinephrine on the outcome of septic shock.
Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: Does dopamine administration in shock influence outcome? A comparison of epinephrine and norepinephrine in critically ill patients. Intensive Care Med. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock: the VANISH randomized clinical trial. Impact of norepinephrine weight-based dosing compared with non-weight-based dosing in achieving time to goal mean arterial pressure in obese patients with septic shock.
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Vasopressin versus norepinephrine infusion in patients with septic shock. Interaction of vasopressin infusion, corticosteroid treatment, and mortality of septic shock. The effects of vasopressin on acute kidney injury in septic shock. Vasopressin versus norepinephrine in patients with vasoplegic shock after cardiac surgery: the VANCS randomized controlled trial. A selective V 1A receptor agonist, selepressin, is superior to arginine vasopressin and to norepinephrine in ovine septic shock.
Crit Care. Crit Care Resusc. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters.
Safety of peripheral intravenous administration of vasoactive medication. J Hosp Med. Safety of the peripheral administration of vasopressor agents. J Intensive Care Med. Review of vasopressor therapy in the setting of vasodilatory shock. Adv Em Nurs J. Allen JM. Understanding vasoactive medications: focus on pharmacology and effective titration. J Infus Nurs. Discontinuation of vasopressin before norepinephrine increases the incidence of hypotension in patients recovering from septic shock: a retrospective cohort study.
Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension. Relationship between intraoperative hypotension, defined by either reduction from baseline or absolute thresholds, and acute kidney and myocardial injury after noncardiac surgery: a retrospective cohort analysis. Intraoperative mean arterial pressure variability and day mortality in patients having noncardiac surgery.
Takotsubo cardiomyopathy: a review. Acute Card Care. Forgot Username? Become a Member Renew or Upgrade. Congress On Demand.
Research Grants. Research Surveys. ICU Management. Choosing Wisely in Critical Care. Surviving Sepsis Campaign Sepsis Definitions. Search for:. Phenylephrine is about ten times less potent than norepinephrine i.
Phenylephrine is generally supplied as a fairly dilute solution, which can make this logistically problematic for patients requiring high-dose vasoconstriction. Thus, phenylephrine monotherapy is largely restricted to patients with mild to moderate vasodilatory shock due to logistic constraints. Increases blood pressure and may increase urine output. Tends to cause cardiac output to increase or remain stable depending on how responsive the heart is to preload, afterload, and inotropy.
Clinical use Widely popular first-line agent for a variety of shock states septic shock, cardiogenic shock with severe hypotension. How to titrate: Typically, against blood pressure. Physiology Causes chronotropy and inotropy, thereby increasing the cardiac output. Increases systemic vascular resistance and also causes venoconstriction increasing preload.
Stabilizes mast cells, blocking the pathophysiology of anaphylaxis. Beta-2 agonist stimulation causes bronchodilation, decreases potassium levels, and stimulates the generation of aerobic lactate production by the liver. This is often feared, but lactate may be used as a metabolic fuel by the heart, so this mechanism of action is probably beneficial in the absence of profound pre-existing metabolic acidosis.
Clinical uses 1 Bradycardia and bradycardic shock given inotropic effects. Epinephrine is generally a good choice for the nearly-dead patient. Note that epinephrine may be indicated for treatment for anaphylaxis even if the hemodynamics are stable see IBCC anaphylaxis chapter.
How to titrate: depends on clinical application. The main concern is that at high doses for long periods of time, it may promote a stress cardiomyopathy. It causes lactate production which isn't dangerous may be physiologically beneficial. However, practitioners must be aware of this issue; otherwise they may senselessly chase lactate values. Epinephrine causes a small decrease in potassium, which is generally not a problem. It's often difficult to figure out what it is doing to your patient.
For example, low-dose dopamine can actually cause hypotension due to a predominant effect of vasodilation , which can make it difficult to wean off the dopamine. Reasons dopamine should be abandoned: Dopamine increases mortality in RCTs: Dopamine increased mortality compared to norepinephrine in the subgroup of patients with cardiogenic shock De Backer It also increased mortality compared to epinephrine among septic children Ventura It's often impossible to figure out what dopamine is doing given the variety of different effects at different doses in different patients.
This makes it impossible to titrate in any rational fashion up-titration may cause dopamine to function via a different mechanism entirely. Dopamine has unique adverse endocrine effects. Dopamine may directly stimulate diuresis via action on dopamine-receptors, thereby falsely suggesting that renal perfusion is adequate. There is a relatively high risk of tissue necrosis if it extravasates.
Dopamine may cause greater malperfusion of the gut compared to norepinephrine. Thus, peripheral vasopressors should be started immediately if the blood pressure or perfusion is inadequate.
Norepinephrine is safe for short periods of time through a large peripheral vein. Ongoing peripheral infusion also appears safe, but this should ideally be done within the context of a well-designed protocol involving frequent monitoring of the extremity and preparation for management of extravasation reaction more on this here.
Ongoing infusion should be avoided in deep ultrasound-guided peripheral IVs, where it may be impossible to monitor the tissue surrounding the end of the IV cannula. Phenylephrine and epinephrine have not been reported to cause tissue necrosis.
Peripheral infusion of these agents appears to be generally safe, although this should still ideally be done via a well-functioning cannula proximal to the wrist more on this here. Vasopressin should arguably be avoided for peripheral administration, because if it extravasates there is no vasodilatory agent which can counteract its action.
Discontinuation of vasopressin before norepinephrine may result in clinically significant hypotension. Methods: This retrospective, cohort study compared discontinuation of norepinephrine and vasopressin in medically, critically ill patients in the recovery phase of septic shock from May to June Linear regression was performed, examining the effect of agent discontinuation on clinically significant hypotension.
Results: Vasopressin was discontinued first or last in 62 and 92 patients, respectively.
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