1. Following A. Electrolyte status.norepinephrine (Levophed) administration, it is essential to the
nurse to assess:
A. Electrolyte status.
B. Color
... [Show More] and temperature of toes and fingers.
C. Capillary refill.
D. Ventricular arrhythmias.
Correct Answer: B. Color and temperature of toes and fingers.
Because decreased perfusion is a side effect of norepinephrine (Levophed), the nurse must check
circulation frequently. 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 isthat cardiac output may decrease, or at moststay the same, despite beta1 agonism. Electrolytes
and ventricular arrhytmias are not specific for norepinephrine.
Option A: Blood pressure requires close monitoring whenever vasopressors such as
norepinephrine are in use; thisis possible via invasive or non-invasive measurement techniques.
If following non-invasive measurements, then it is recommended to obtain values every 2 to 3
minutes during initial titration and then at least every 5 minutes following the determination of
the appropriate maintenance dose.
Option C: Capillary refill is not a reliable indication of perfusion in a shocking state.
Option D: At the same time, the increase in systemic vascular resistance increases the work of
the heart by increasing afterload, thereby increasing myocardial oxygen demand. Because of
these phenomena, the benefits of norepinephrine for cardiogenic shock are still unclear but
merit consideration under certain conditions.
2. ACEs participate in the renin-angiotensin-aldosterone system to have which of the following
physiologic effects?
A. Inhibit conversion of angiotensin II to angiotensin I.
B. Vasoconstriction and sodium depletion.
C. Promote sodium and water retention.
D. Stimulate vasodilation and inhibitsodium depletion.
Answer: C. Promote sodium and water retention.
Angiotensin is a potent vasoconstrictor that stimulates the release of aldosterone. Aldosterone release
promotes sodium and water retention. The renin–angiotensin–aldosterone system (RAAS) is a critical
regulator of blood volume and systemic vascular resistance. While the baroreceptor reflex respondsin a
short-term manner to decreased arterial pressure, the RAAS isresponsible for more chronic alterations.
It is composed of three major compounds: renin, angiotensin II, and aldosterone.
Option A: The conversion of angiotensin I to II is not inhibited. The conversion of angiotensin I to
angiotensin II is catalyzed by an enzyme called angiotensin-converting enzyme (ACE). ACE is
found primarily in the vascular endothelium of the lungs and kidneys. After angiotensin I is
converted to angiotensin II, it has effects on the kidney, adrenal cortex, arterioles, and brain by
binding to angiotensin II type I (AT) and type II (AT) receptors.
Option B: Aldosterone promotes sodium retention, not depletion. Aldosterone is a steroid
hormone that causes an increase in sodium reabsorption and potassium excretion at the distal
tubule and collecting duct of the nephron. Aldosterone works by stimulating the insertion of
luminal Na channels and basolateral Na-K ATPase proteins. The net effect is an increased level of
sodium reabsorption.
Option D: The effect of angiotensin II on vasoconstriction takes place in systemic arterioles.
Here, angiotensin II binds to G protein-coupled receptors, leading to a secondary messenger
cascade that results in potent arteriolar vasoconstriction. This acts to increase total peripheral
resistance, causing an increase in blood pressure.
3. Which of the following vitamins may not be absorbed properly when giving bile acid
sequestrants?
A. Vitamin B
B. Vitamin [Show Less]