From the Guidelines
Levophed (norepinephrine) is not the indicated vasopressor in cardiogenic shock, instead, norepinephrine is the recommended vasopressor. The typical starting dose is 0.1-0.2 mcg/kg/min, titrated to maintain a mean arterial pressure of 65-70 mmHg, with careful monitoring via arterial line if possible. Norepinephrine works primarily through alpha-1 adrenergic receptor stimulation, causing peripheral vasoconstriction that increases systemic vascular resistance and blood pressure without significantly increasing myocardial oxygen demand. This is particularly beneficial in cardiogenic shock where the heart's pumping ability is compromised. Unlike other vasopressors like dopamine, which can increase heart rate and arrhythmia risk, or pure vasoconstrictors like phenylephrine, which lack inotropic effects, norepinephrine provides a balanced hemodynamic profile. It also offers mild beta-1 effects that provide some inotropic support without the pronounced chronotropic effects seen with agents like dopamine. When administering norepinephrine, it should be given through a central line whenever possible to prevent tissue necrosis from extravasation, and patients require continuous cardiac monitoring, frequent blood pressure checks, and assessment of peripheral perfusion, as recommended by the European Society of Cardiology 1.
Some key points to consider when using norepinephrine in cardiogenic shock include:
- The importance of careful monitoring and titration to maintain adequate blood pressure and perfusion
- The potential benefits of combining norepinephrine with other agents, such as dobutamine or levosimendan, in certain cases
- The need to consider alternative agents, such as vasopressin or phenylephrine, in patients who do not respond to norepinephrine
- The importance of addressing the underlying cause of cardiogenic shock, such as myocardial infarction or heart failure, in addition to providing supportive care with vasoactive agents, as discussed in the literature 1.
Overall, the use of norepinephrine as a vasopressor in cardiogenic shock is supported by the available evidence and should be considered a key component of the management strategy for these patients.
From the FDA Drug Label
CLINICAL PHARMACOLOGY LEVOPHED functions as a peripheral vasoconstrictor (alpha-adrenergic action) and as an inotropic stimulator of the heart and dilator of coronary arteries (beta-adrenergic action). The FDA drug label does not answer the question.
From the Research
Vasopressor Use in Cardiogenic Shock
- The use of vasopressors in cardiogenic shock is a common practice to restore adequate tissue perfusion 2, 3.
- Norepinephrine is often recommended as a first-line vasopressor agent due to its lower risk of adverse events compared to other catecholamine vasopressors 2, 3, 4.
- However, recent studies have suggested that norepinephrine use in cardiogenic shock patients may be associated with increased 30-day mortality 5.
- Other vasopressors, such as vasopressin, may be used as an adjunctive therapy to catecholamines, particularly in patients with right ventricular failure and pulmonary hypertension 3, 4, 6.
- The use of vasopressin has been associated with lower mortality in patients with cardiogenic shock, particularly amongst those requiring high-dose vasopressors 6.
Levophed (Norepinephrine) as a Vasopressor
- Levophed, also known as norepinephrine, is a commonly used vasopressor in cardiogenic shock 2, 3, 5, 4.
- It is often used as a first-line agent to restore adequate arterial pressure and tissue perfusion 2, 3, 4.
- However, its use has been associated with increased short-term mortality in cardiogenic shock patients 5.
Alternative Vasopressors
- Other vasopressors, such as epinephrine and dopamine, may be used in certain situations, but their use is limited due to the risk of adverse events 2, 3.
- Vasopressin may be a suitable alternative to norepinephrine in certain patients, particularly those with tachycardia or pulmonary hypertension 3, 4, 6.
- The choice of vasopressor should be individualized and based on the patient's hemodynamic response and underlying condition 3.