Norepinephrine (B1, Alpha 1 Agonist) Flashcards
What is the correct intravenous push dose for Norepinephrine?
A. 2-4 mcg
B. 5-10 mcg
C. 10-20 mcg
D. 25-50 mcg
A. 2-4 mcg
What is the standard concentration for Norepinephrine when used for intravenous push?
A. 16 mcg/mL
B. 4 mcg/mL
C. 10 mcg/mL
D. 8 mcg/mL
B. 4 mcg/mL
4 mcg/mL concentration
(5 mL of Levo bag with 15 mL NS to quarter the concentration from 16 mcg/mL to 4 mcg/mL)
Which of the following correctly describes the Norepinephrine infusion rate for IV drip?
A. 1-20 mcg/min
B. 2.5-40 mcg/min
C. 5-50 mcg/min
D. 10-60 mcg/min
B. 2.5-40 mcg/min
16 mcg/mL concentration (4 mg/250mL)
**NOTICE THIS IS MCG/MIN IN THE PUMP
What is the onset time for Norepinephrine when administered via IV infusion?
A. 5-10 minutes
B. 2-3 minutes
C. <1 minute
D. 15-30 minutes
C. <1 minute
What is the peak effect time for Norepinephrine following administration?
A. <1 minute
B. 1-2 minutes
C. 3-5 minutes
D. 10-15 minutes
B. 1-2 minutes
What is the duration of action (DOA) of Norepinephrine after administration?
A. 1-2 minutes
B. 5-10 minutes
C. 15-20 minutes
D. 30-60 minutes
B. 5-10 minutes
What is the primary effect of Norepinephrine on blood flow distribution?
A. Redistribution of blood flow to the liver and kidneys
B. Redistribution of blood flow to the skin and muscles
C. Redistribution of blood flow to the brain and heart due to vasoconstriction of other vascular beds
D. Redistribution of blood flow to the gastrointestinal tract
C. Redistribution of blood flow to the brain and heart due to vasoconstriction of other vascular beds
MOA: ↑SVR…higher doses ↑HR
Redistributes blood flow to brain & heart bc all
other vascular beds are constricted
- At low doses, Norepinephrine primarily activates which receptors, and what are the resulting cardiovascular effects?
A. Alpha-1 receptors, causing vasoconstriction and increased systemic vascular resistance (SVR)
B. Beta-1 receptors, leading to increased heart rate, cardiac output, contractility, and conduction
C. Beta-2 receptors, resulting in vasodilation and decreased heart rate
D. Alpha-2 receptors, leading to decreased heart rate and cardiac output
B. Beta-1 receptors, leading to increased heart rate, cardiac output, contractility, and conduction
Low dose: B1
● ↑ HR, CO, CTX, Conduction
What is the primary mechanism of action (MOA) of Norepinephrine at high doses?
A. Vasodilation with increased heart rate
B. Increased systemic vascular resistance (SVR) and minimal change in heart rate due to Beta-1 receptor counteractions
C. Decreased SVR with increased heart rate
D. Decreased SVR with decreased heart rate
B. Increased systemic vascular resistance (SVR) and minimal change in heart rate due to Beta-1 receptor counteractions
High dose: B1 + Alpha1
● Systemic Vasoconstriction (except coronaries)
● ↓HR (minimal change d/t counteractions of B1)
How does vasoconstriction caused by Alpha-1 stimulation affect heart rate?
A. It leads to reflex bradycardia via the baroreceptor reflex, which is generally not fully compensated for by Beta-1 activity.
B. It leads to reflex tachycardia due to increased Beta-1 activity.
C. It causes no significant change in heart rate.
D. It results in a significant decrease in heart rate, with full compensation by Beta-1 activity.
A. It leads to reflex bradycardia via the baroreceptor reflex, which is generally not fully compensated for by Beta-1 activity.
What is the effect of Norepinephrine on cardiac output at high doses, considering the combined effects of Alpha-1 and Beta-1 stimulation?
A. Cardiac output significantly increases due to dominant Beta-1 effects.
B. Cardiac output decreases or stays the same despite Beta-1 agonism, due to reflex bradycardia and increased afterload.
C. Cardiac output increases with a minimal impact on heart rate.
D. Cardiac output increases significantly, overcoming any adverse effects from Alpha-1 stimulation.
B. Cardiac output decreases or stays the same despite Beta-1 agonism, due to reflex bradycardia and increased afterload.
* Vasoconstriction secondary to alpha1 stimulation can result in reflex bradycardia via the baroreceptor reflex, which is generally not compensated for by the beta1 activity. The overall result is that cardiac output may decrease, or at most stay the same, despite beta1 agonism. At the same time, the increase in SVR increases the work of the heart by increasing afterload, thereby increasing myocardial oxygen demand.*
Why should caution be exercised when using Norepinephrine in patients with right ventricular failure (RVF)?
A. Norepinephrine can decrease venous return, worsening RVF.
B. Norepinephrine can increase venous return, leading to elevated pulmonary artery pressure (PAP) and worsening RVF.
C. Norepinephrine directly improves right ventricular function, making it safe for RVF patients.
D. Norepinephrine has no impact on venous return or PAP in RVF patients.
B. Norepinephrine can increase venous return, leading to elevated pulmonary artery pressure (PAP) and worsening RVF.
CAUTION:
*Pts w/ RVF: ↑Venous return ⇒ ↑PAP
What are potential risks of using Norepinephrine in patients with volume depletion and ischemic damage?
A. Increased myocardial oxygen demand and worsening ischemic damage
B. Decreased myocardial oxygen demand and improved ischemic damage
C. No impact on myocardial oxygen demand or ischemic damage
D. Improved myocardial oxygen demand and reduced ischemic damage
A. Increased myocardial oxygen demand and worsening ischemic damage
CAUTION:
*Pts w/ RVF: ↑Venous return ⇒ ↑PAP
*R/F Vol depletion + Ischemic damage
*Not useful in HOCM
In which condition is Norepinephrine NOT recommended due to its potential to exacerbate the issue?
A. Hyperdynamic septic shock
B. Hypovolemic shock
C. Hypertrophic obstructive cardiomyopathy (HOCM)
D. Cardiogenic shock
C. Hypertrophic obstructive cardiomyopathy (HOCM)
CAUTION:
*Pts w/ RVF: ↑Venous return ⇒ ↑PAP
*R/F Vol depletion + Ischemic damage
*Not useful in HOCM
