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NURS 310
Winter 2015
ANSWERS – CV Case
 Case Info #1: 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.
Make two lists: What do we know?.(green)..........
What do we need or want to know? Completed in class discussion
What do you suspect is happening to JK?
 This pt experienced a worsening of his heart failure… John likely has a fluid
overload evidenced by his significant weight gain and edema.
 It would have been better if he had come in when he started to get tired more easily:
he would have benefited from a medication adjustment sooner.
Do you want to decrease or increase afterload in J. K.? Why?
You would want to decrease afterload to decrease the work of the heart in pumping
blood to the body.
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Make sure you can define afterload.
Afterload is the “work” that the ventricle has to overcome in order to eject
blood. (Systemic vascular resistance, aortic pressure and compliance, aortic stenosisif present)
Remember – what is the primary determinant of afterload?
o Systemic vascular resistance, ie arterial “tone” (relative degree of dilation
vs constriction)
Do you want to decrease or increase preload in J. K.? Why?
You would want to decrease preload to decrease blood volume in the ventricles and
thereby decrease the work of the heart in pumping blood to the body.
Make sure you can define preload.
Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction.
Preload, therefore, is related to muscle sarcomere length. Because sarcomere length cannot be
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Winter 2015
determined in the intact heart, other indices of preload are used such as ventricular end-diastolic
volume or pressure.
Remember – what is the primary determinant of preload?
Ventricular filling, stretch of the sarcomeres due to volume of blood in the heart
chamber
Would an ACE inhibitor be beneficial in this case?
An ACE inhibitor would be beneficial in this case. ACE-inhibitors work by inhibiting conversion
of angiotensin I to angiotensin II thereby inhibiting the Renin/Angiotensin/Aldosterone
System. Inhibiting RAAS results in:
 arteriolar dilation (decreases afterload)
 venous dilation (decreases preload)
 and enhanced excretion of sodium and water (decreased preload and ECF
reduction via suppression of aldosterone).
 Case Info #2: After being seen in the clinic, John is to continue to take Digoxin
(Lanoxin). However, three additional medications are added to his pharmacologic
treatment plan: Furosemide (Lasix), a beta blocker, and Captopril (Capoten).
1. What does Furosemide (Lasix) add to the treatment of congestive heart failure in
this patient? (see below)
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, Lasix causes loss of K+ which is of note.
2. 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).
 Beta blockers will also decrease renin release which (if you look at the
diagram, lecture handout pages 17 - 18) should decrease the
vasoconstriction (resulting in vasodilation) which will help in HF.
 BB have been shown to decrease mortality from HF and are standard of
care.
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 Cardiac selective beta blockers are indicated in HF as well as drugs which
have both alpha1 and beta blocking actions.
3. Is hyperkalemia a potential problem for J. K. given that he is taking Captopril
(Capoten)? Why or why not?
 Yes, there is a potential risk of hyperkalemia because inhibition of
angiotensin II production causes (in turn) 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.
These opposite effects on potassium will- to some effect- cancel each
other out. Nonetheless, potassium levels must be closely monitored in this
patient; especially of concern as John is also taking digoxin.
 Case Info #3:
Consider that John also has diabetes.
Explain the reasons that propranolol (Inderal) would not be a good choice for a beta
blocker drug?
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Propranolol (Inderal) is a nonselective beta blocker
Therefore, in addition to blocking beta1 receptors in the heart (the desired
therapeutic outcome) Propranalol also 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) suppress tachycardia, an
important early warning sign of hypoglycemia.
 Case Info #4:
Shortly after beginning Captopril (Capoten), John reports the onset of an annoying,
bothersome symptom and does not want to continue taking the drug.
What side effect is most likely to have occurred? 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, Angiotensin Receptor Blockers)
 Case Info #5:
Losartan (Cozaar) is prescribed instead of Captopril (Capoten).
What is the pharmacologic class of losartan? Of captopril?
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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.
 Case Info #6: John’s health care provider is considering prescribing an aldosterone
blocker or a calcium channel 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?
Under normal conditions, aldosterone reabsorbs Na+ and water from the collecting duct
in exchange for excreting a K+ … this effect increases preload.
Preventing the effects of aldosterone by using an Aldosterone Receptor Antagonist will
decrease the work of the heart which is crucial for a patient with heart failure.
FYI cardiac effects: Under normal conditions, aldosterone 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 a calcium channel blocker such as Verapamil (Calan) is useful in both
hypertension AND as an antidysrhythmic.
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.
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What are the beneficial effects of Digoxin (Lanoxin)?
What is important to know before administering digoxin?
AND why is the serum potassium level so important to monitor during therapy?
Digoxin’s primary indication is heart failure. 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: overall, digoxin leads to an increase in cardiac
output, and slightly extend time for perfusion of the myocardium. This is very helpful in
patients with HF.
Digoxin 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 be 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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