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NURS 310
Winter 2016
ANSWERS – CV Case
John Kale, a 68 year-old hypertensive patient, is being treated for congestive heart failure
and has been taking Digoxin (Lanoxin) for the last 3 years. Over that time, he has gained
approximately 20 kg. Over the last year, he reports he has been ‘getting real tired real easy’
when he goes out for walks or shopping, and so he’s basically stayed home to watch TV or
read the papers, but can easily do things for himself around the house or when he goes out.
At the time you see him in the physician’s office, BP is 170/110, heart rate is 110 and regular,
and respiratory rate is 22. His ankles are puffy, his jugular veins distended, and his belly
protruding and “full”. He can’t lie flat on his bed to sleep; he sleeps in a semi reclining
position with three pillows under his head.
Do you want to decrease or increase afterload in J. K.? Why?
Make sure you can define afterload.
You would want to decrease afterload to decrease the work of the heart in pumping
blood to the body.
Remember – what is the primary determinant of afterload?
Do you want to decrease or increase preload in J. K.? Why?
Make sure you can define preload.
You would want to decrease preload to decrease blood volume and thereby decrease the
work of the heart in pumping blood to the body.
Remember – what is the primary determinant of preload?
Why would an ACE inhibitor be beneficial in this case?
An ACE inhibitor would be beneficial in this case and works by inhibiting conversion of
angiotensin I to angiotensin II thereby inhibiting the Renin/Angiotensin system resulting
in: arteriolar dilation (decreases afterload), venous dilation (decreases preload), and
enhanced excretion of sodium and water (decreased preload via suppression of
aldosterone). Don’t forget to look at the diagram from your lecture notes on the reninangiotensin system.
After being seen in the clinic, John is to continue to take Digoxin (Lanoxin). However,
Captopril (Capoten), Furosemide (Lasix) and a beta blocker are added to his pharmacologic
treatment plan.
What does Furosemide (Lasix) add to the treatment of congestive heart failure in this
patient?
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NURS 310
Winter 2016
John likely has a fluid overload evidenced by his significant weight gain and edema.
Diuretics are first-line drugs for patients in HF. Furosemide (Lasix) is a diuretic that
will reduce fluid volume and thus decrease the work of the heart by decreasing preload.
But (and I know that you have not had this yet) Lasix causes loss of K+ which is of
note.
Why would a beta blocker be beneficial in this case?
The role of beta blockers in treating heart failure is complex. Beta blockers may be
useful in patients with heart failure by protecting against cardiac dysrhythmias and
protecting the heart from excessive sympathetic stimulation and subsequent
downregulation of beta receptors (remember the speakers example when she used her
hands to explain downregulation).
Also, beta blockers will decrease renin release which (if you look at the diagram) should
decrease the vasoconstriction (resulting in vasodilation) which will help in HF.
Interesting note: BB have been shown to decrease mortality from HF and are standard
of care.
Cardiac selective beta blockers are indicated in HF as well as drugs which have both
alpha1 and beta blocking actions.
Consider that John also has diabetes. Explain the reasons that propranolol (Inderal)
would not be a good choice for a beta blocker drug?
Propranolol (Inderal) is a nonselective beta blocker and, therefore, in addition to
blocking beta1 receptors in the heart (the desired therapeutic outcome) Propranalol
blocks beta2 receptors in the muscle and liver which suppresses glycogenolysis.
Glycogenolysis in the muscle and liver is an important mechanism for correcting
hypoglycemia. Blocking this function may be extremely detrimental, particularly in
diabetics who take insulin as they may be at an increased risk for developing
hypoglycemia. In addition, propranolol (and all other beta blockers) suppresses
tachycardia, an important early warning sign of hypoglycemia.
Shortly after beginning Captopril (Capoten), John reports the onset of a bothersome
symptom and does not want to continue taking the drug. What side effect is most likely
to have occurred? AND What causes this side effect?
Persistent, dry cough is a common side-effect of all ACE inhibitors and is caused by
accumulation of bradykinin due to the inhibition of ACE. What could we use instead?
Answer - (ARBs)
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NURS 310
Winter 2016
Is hyperkalemia a potential problem for J. K. given that he is taking Captopril (Capoten)?
Why?
Yes, there is a potential risk of hyperkalemia because inhibition of angiotensin II
production causes an inhibition of aldosterone release which, in turn, leads to potassium
retention by the kidney. However, John is also taking Lasix which can cause loss of
potassium. Potassium levels must be closely monitored in this patient; especially of
concern as John is also taking digoxin.
Losartan (Cozaar) is prescribed instead of Captopril (Capoten). How is the mechanism of
action of Losartan (Cozaar) the same and how is it different from Captopril (Capoten)?
Both ACE inhibitors (captopril) and ARBs (losartan) reduce the action of angiotensin II.
ACE inhibitors block the conversion of angiotensin I to angiotensin II, whereas ARBs
block angiotensin II receptors.
John’s health care provider is considering prescribing an aldosterone blocker. Why might
John prefer to take an SARA rather than a nonselective aldosterone blocker such as
spironolactone (Aldactone)?
SARAs (selective aldosterone receptor antagonists) block the aldosterone receptor
without some of the side-effects of spironolactone such as gynecomastia and sexual
dysfunction (less androgen binding when using SARAs).
Why does blocking aldosterone help in heart failure?
Aldosterone (in the normally functioning system) promotes excretion of K+ and retention
of Na+ and water which increases preload.
Overall, blocking aldosterone will decrease the work of the heart which is crucial for a
patient with heart failure.
FYI cardiac effects - Aldosterone (in the normally functioning system) also stimulates
the SNS (predisposing the heart to dysrhythmias), contributes to the ventricular
remodeling seen in heart failure and stimulates the release of endothelin which is a
vasoconstrictor that increases afterload.
Explain how Verapamil (Calan) is useful in both hypertension AND as an antidysrhythmic.
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NURS 310
Winter 2016
Verapamil reduces hypertension by blocking calcium channels primarily in the heart (very
little effect on peripheral blood vessels) which leads to decreased contractility and
decreased CO (which will decrease BP) but also has the following effects - increased
coronary perfusion, reduced HR, and decreased AV nodal conduction. Please note the
two categories of CCBs – Verapamil is used primarily for the effects on the heart (has
little effect peripherally) while drugs ending in ‘pine’ have the primary action on the
peripheral blood vessels causing vasodilation.
Verapamil is useful as an antidysrhythmic because of its ability to suppress impulse
conduction through the AV node which slows ventricular rate in patients with atrial
flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia.
What are the beneficial effects of Digoxin (Lanoxin), what is important to know before
administering AND why is the serum potassium level so important to monitor during
therapy?
Digoxin (class of drug – cardiac glycoside; we did not cover this and you do not need to
know this but please know M of A and benefits of use) increases the force of
ventricular contraction (positive inotropic effect) and also slightly decreases heart rate
which leads overall to an increase in cardiac output. This is very helpful in patients with
HF.
Although Digoxin’s primary indication is heart failure, it is also used to treat
supraventricular dysrhythmias. Digoxin suppresses dysrhythmias by decreasing
conduction through the AV node and by decreasing automaticity in the SA node.
However dysrhythmias are also the most serious side effect of Digoxin. Therefore, all
patients on digoxin should be evaluated for changes in heart rate and rhythm throughout
treatment. Routine monitoring includes checking for HR prior to giving Digoxin and
holding administration for a HR less than 60 beats/min (remember that it will decrease
HR).
Digoxin has a narrow therapeutic range: Drug levels only slightly higher than
therapeutic greatly increase the risk of toxicity. We want to super vigilant about
interactions with other drugs because of impacts on potassium levels (diuretics; ACEI;
ARBs) because of potential for Digoxin toxicity.
FYI (you do not have to know but you may be intrigued to know . . .) Potassium ions
compete with digoxin for binding to Na+/K+ ATPase. There is increased binding of
digoxin when potassium levels are low which leads to augmentation of contractile force
and toxicity. Conversely, when potassium levels are high, there may be a decreased
therapeutic response of the drug because there are less binding sites.
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