Tips on Heart failure for undergraduate clinical pharmacy students

1. Clinical pharmacy I
Cardiovascular diseases
Dr. Dalia K. Zaafar
Lecturer of clinical pharmacology

2. 
It is a chronic, progressive condition in which the
heart muscle is unable to pump enough blood to
meet the body’s needs for blood and oxygen
What is heart failure

3. 
 At first the heart tries to make up for this by:
 Enlarging: The heart stretches to contract more strongly
and keep up with the demand to pump more blood. Over
time this causes the heart to become enlarged.
 Developing more muscle mass. The increase in muscle
mass occurs because the contracting cells of the heart get
bigger. This lets the heart pump more strongly, at least
initially.
 Pumping faster. This helps increase the heart’s output.
What is heart failure

4. 
 The body also tries to compensate in other ways:
 The blood vessels narrow to keep blood pressure up,
trying to make up for the heart’s loss of power.
 The body diverts blood away from less important
tissues and organs to the heart and brain.
What is heart failure

5. 
What is heart failure

6. 
 Types of heart failure
 Left-sided heart failure: the most common type of heart failure.
 The left heart ventricle is located in the bottom left side of your
heart. This area pumps oxygen-rich blood to the rest of your
body.
 Left-sided heart failure occurs when the left ventricle doesn’t
pump efficiently. This prevents your body from getting enough
oxygen-rich blood. The blood backs up into your lungs instead,
which causes shortness of breath and a buildup of fluid.
What is heart failure

7. 
 Types of heart failure
 Right-sided heart failure: right heart ventricle is responsible for
pumping blood to lungs to collect oxygen. Right-sided heart failure
occurs when the right side of the heart can’t perform its job
effectively. It’s usually triggered by left-sided heart failure. The
accumulation of blood in the lungs caused by left-sided heart failure
makes the right ventricle work harder. This can stress the right side of
the heart and cause it to fail.
 Right-sided heart failure can occur as a result of other conditions, such
as lung disease. It is marked by swelling of the lower extremities. This
swelling is caused by fluid backup in the legs, feet, and abdomen.
What is heart failure

8. 
 Types of heart failure
 Diastolic heart failure occurs when the heart muscle
becomes stiffer than normal, due to heart disease, as the
heart doesn’t fill with blood easily. This is known as
diastolic dysfunction. It leads to a lack of blood flow to the
rest of the organs
What is heart failure

9. 
 Types of heart failure
 Systolic heart failure: occurs when the heart muscle loses its ability to
contract. The contractions of the heart are necessary to pump oxygen-rich
blood out to the body. This problem is known as systolic dysfunction, and
it usually develops when your heart is weak and enlarged.
 Both diastolic and systolic heart failure can occur on the left or right sides
of the heart.
 Diastolic heart failure occurs when the heart muscle becomes stiffer than
normal, due to heart disease, as the heart doesn’t fill with blood easily.
This is known as diastolic dysfunction. It leads to a lack of blood flow to
the rest of the organs
What is heart failure

10. 
 Types of heart failure
 Systolic heart failure: occurs when the heart muscle loses its ability to
contract. The contractions of the heart are necessary to pump oxygen-rich
blood out to the body. This problem is known as systolic dysfunction, and
it usually develops when your heart is weak and enlarged.
 Both diastolic and systolic heart failure can occur on the left or right sides
of the heart.
 Diastolic heart failure occurs when the heart muscle becomes stiffer than
normal, due to heart disease, as the heart doesn’t fill with blood easily.
This is known as diastolic dysfunction. It leads to a lack of blood flow to
the rest of the organs
What is heart failure

11. 
 Classification of heart failure according to NYHA
Classification of heart
failure
Stage Functional class
A At high risk of HF
(uncontrolled risk
factors) but without structural
heart
disease or symptoms of HF
none
B Structural heart disease but
without signs
or symptoms of HF
I Asymptomatic HF; no
limitations in physical
activity caused by HF symptoms
C Structural heart disease with
prior or
current symptoms of HF
I No limitations in physical
activity caused by HF
symptoms
II Slight limitation of physical
activity; asymptomatic
at rest, but symptoms of HF
with normal level
of activity
III Marked limitations in physical
activity because of
HF symptoms; asymptomatic at
rest
IV Symptoms of HF at rest or
unable to carry out any
physical activity
D Refractory HF requiring
specialized
interventions
IV Symptoms of HF at rest

12. 
 Goals of therapy
a. Modify or control risk factors (e.g., HTN, obesity, DM)
b. Manage structural heart disease
c. Reduce morbidity and mortality
d. Prevent or minimize Na and water retention
e. Eliminate or minimize HF symptoms
f. Block compensatory neurohormonal activation caused by
reduced cardiac output (CO)
g. Slow progression of worsening cardiac function
Heart failure

13. 
 NON-PHARMACOLOGICAL THERAPY
1- Prevent further cardiac injury by
a. Discontinue smoking. b. Reduce weight if obese.
c. Control HTN (goal BP < 130/80 mm Hg per the 2017 ACC/AHA/Heart Failure Society of
America Focused Update of the HF guidelines) d. Control DM.
e. Decrease alcohol intake to 2 or fewer drinks per day for men and 1 or fewer drinks per day for women.
Eliminate alcohol intake if cardiomyopathy is alcohol induced.
f. Limit Na intake to 1500 mg/day for stages A and B; consider less than 3 g/day for stages C and D.
g. Treat sleep apnea. h. Educate patient about appropriate self-care.
Heart failure

14. 
 NON-PHARMACOLOGICAL THERAPY (continued)
2- Restricting fluid intake to 1.5–2 L/day is reasonable in stage D if serum Na is low.
3- Modest exercise program benefits
4- Influenza and pneumococcal vaccines
5- Monitor and appropriately replace electrolytes (to minimize risk of arrhythmias).
6- Monitor for thyroid disease: as hypothyroidism can be masked by HF symptoms and
hyperthyroidism will worsen systolic dysfunction.
7- Screen for and treat depression.
Heart failure

15. 
 Inclusion criteria:
 Patients suffering from moderate HTN and DM,
 their HbA1c ≥ 7 and
 age range between 40-60 years,
 treatment with diet alone, or any combination of oral anti-
diabetic agents and/or insulin before admission
Patients and Methods

16. 
 A- ACE Inhibitors
Place in therapy: Recommended in all patients with HFrEF and current or prior symptoms, unless contraindicated (class I indication)
 Benefits
Decreased mortality (about 25%–50% relative risk reduction compared with placebo depending on severity of HF)
Decreased hospitalizations (about 30% relative risk reduction compared with placebo)
Symptom improvement
Improved clinical status
Improved sense of well-being
 Mechanism of action
Blocks production of angiotensin II: Decreases sympathetic stimulation, decreases production of aldosterone and vasopressin, Decreases
vasoconstriction (afterload and preload)
Increases bradykinins by decreasing their metabolism: Increases vasodilatory prostaglandins, may attenuate myocardial remodeling
Pharmacological therapy

17. 
 A- ACE Inhibitors
• Avoid use in patients who have experienced angioedema as the result of previous ACE inhibitor use or those
who are pregnant or plan to become pregnant.
• Use with caution if SBP is less than 80 mm Hg, SCr is greater than 3 mg/dL, K is greater than 5.0 mEq/L, or the
patient has bilateral renal artery stenosis.
• Ninety percent of people tolerate ACE inhibitors.
1- Angioedema (less than 1%): Can switch to angiotensin II receptor blockers (ARBs cross-reactivity is 2.5%) or
hydralazine–isosorbide dinitrate
2- Cough (20%): Can switch to ARBs (less than 1%)
Pharmacological therapy

18. 
 B- ANGIOTENSIN RECEPTOR BLOCKERS
 Place in therapy: Recommended in patients with HFrEF with current or prior symptoms who are unable to take an ACE inhibitor
(class I indication). Have not been proven superior to ACE inhibitors at target HF dosages.
 Benefits
Decreased HF-related hospitalizations and decreased death from CV causes.
 Mechanism of action
Selectively block the binding of angiotensin II to the angiotensin I receptor
Deters vasoconstriction and aldosterone-secreting effects
Does not affect ACE or inhibit kinin catabolism
Pharmacological therapy

19. 
 C- BETA BLOCKERS
 Place in therapy: Recommended in all patients with HFrEF with current or prior symptoms unless contraindicated (class I
indication)
 Benefits (when added to an ACE inhibitor)
Decreased mortality (about 35% relative risk reduction compared with placebo)
Decreased hospitalizations (about 25% relative risk reduction compared with placebo)Symptom improvement
Improved clinical status
 Mechanism of action
Blocks the effect of norepinephrine and other sympathetic neurotransmitters on the heart and vascular system: Decreases ventricular
arrhythmias, decreases cardiac hypertrophy and cardiac cell death, Decreases vasoconstriction and HR
Carvedilol also provides α1-blockade: Further decreases SVR (afterload), Results in greater reduction in BP than metoprolol succinate
Pharmacological therapy

20. 
 C- BETA BLOCKERS
 Notes
Only bisoprolol, carvedilol, and metoprolol succinate are recommended in HFrEF
Avoid abrupt discontinuation; can precipitate clinical deterioration
Should be considered even in patients with reactive airway disease or asymptomatic
bradycardia
Pharmacological therapy

21. 
 D- DIURETICS
Place in therapy: Indicated in patients with evidence of fluid retention (class I indication)
 Benefits
Decreased jugular venous distension
Decreased pulmonary congestion
Decreased peripheral edema
Decreased daily symptoms
Increased exercise tolerance
No benefit on mortality
 Mechanism of action
Inhibit reabsorption of Na in the ascending limb of the loop of Henle
(loops) or in the distal tubule (thiazides)
Pharmacological therapy

22. 
 D- DIURETICS
Notes
Should be combined with an angiotensin-converting enzyme (ACE) inhibitor, β-blocker, and
aldosterone receptor antagonist (ARA)
A loop diuretic can be combined with another diuretic class (e.g., thiazide diuretic) for synergy, if
needed.
Loop diuretics are preferred because of their greater diuretic capabilities and also for retaining
efficacy with decreased renal function
Pharmacological therapy

23. 
 E- ALDOSTERONE RECEPTOR ANTAGONIST
 Place in therapy: Recommended in patients with NYHA class II–IV with an LVEF of 35% or
less to reduce morbidity and mortality unless a contraindication exists.
 Should be added to ACE inhibitor (or ARB) and β-blocker therapy
 Benefits
Decreased mortality (30% relative risk reduction compared with placebo)
Decreased hospitalizations for HF (35% relative risk reduction compared with placebo)
Improved symptoms
Pharmacological therapy

24. 
 E- ALDOSTERONE RECEPTOR ANTAGONIST
 Mechanism of action
Blocks effects of aldosterone in the kidneys, heart, and vasculature
Decreases K and magnesium loss; decreases ventricular arrhythmias
Decreases Na retention; decreases fluid retention
Eliminates catecholamine potentiation; decreases BP
Blocks direct fibrotic actions on the myocardium
 Notes
Decrease dose by 50% or discontinue if K is greater than 5.5 mEq/L.
In case of Spironolactone administration, gynecomastia is reported at a rate of 10% in clinical trials, so Eplerenone can be considered
as an alternative to spironolactone if gynecomastia is present
Pharmacological therapy

25. 
F- DIGOXIN
 Place in therapy: Can be beneficial in decreasing hospitalizations in patients with HFrEF
(class IIa indication); should be added after ACE inhibitor (or ARB) and β-blocker therapy
 Benefits
Improved symptoms
Improved exercise tolerance
Decreased hospitalizations (28% relative risk reduction compared with placebo)
No effect on mortality
Pharmacological therapy

26. 
F- DIGOXIN
 Mechanism of action (in HF)
Inhibits myocardial Na-K adenosine triphosphatase
Decreases central sympathetic outflow by sensitizing cardiac baroreceptors
Decreases renal reabsorption of Na
Minimal increase in cardiac contractility
Pharmacological therapy

27. 
F- DIGOXIN
 Dosing and administration considerations
For most patients, 0.125 mg/day is adequate to achieve the desired serum
concentration.
Consider dosing 0.125 mg every other day in patients older than 70 years, those with
impaired renal function, or those with low lean body mass.
Avoid abrupt discontinuation; can precipitate clinical deterioration
Pharmacological therapy

28. 
F- DIGOXIN
 Drug interactions: Digoxin concentrations are increased with concomitant:
Clarithromycin, erythromycin, Amiodarone, Dronedarone, Itraconazole, posaconazole, Cyclosporine, tacrolimus,
Verapamil
 Monitoring
Serum concentrations should be less than 1 ng/mL; in general, concentrations of 0.5–0.9 ng/mL are suggested.
Minimizes the risk of adverse effects and ventricular arrhythmias associated with increased concentrations.
Risk of toxicity increases with age and renal impairment, presence of hypokalemia, hypomagnesemia, or hypercalcemia.
Signs of toxicity generally include nausea, vomiting, vision changes.
SCr should be monitored because the drug is primarily cleared renally
Pharmacological therapy

29. 
G- HYDALAZINE/ ISOSORBIDE DINITRATED
 Place in therapy: Recommended in addition to ACE inhibitors and β-blockers to reduce morbidity and mortality (NYHA class
III or IV), May be useful in patients with current or prior symptoms of HFrEF who are unable to tolerate an ACE inhibitor or an
ARB.
 Benefits
Decreased mortality Reduced pulmonary congestion and improved exercise tolerance
 Mechanism of action
Hydralazine
Arterial vasodilator (reduces afterload)
Increases effect of nitrates through antioxidant mechanisms
Isosorbide dinitrate
Stimulates nitric acid signaling in the endothelium
Venous vasodilator (reduces preload)
Pharmacological therapy

30. 
H- Sacubatril / Valsartan (Entresto)
 A combination drug for use in heart failure.
 It consists of the neprilysin inhibitor (sacubitril) and angiotensin receptor blocker (valsartan).
 It is recommended for use as a replacement for an ACE inhibitor or an angiotensin receptor blocker
in people with heart failure with reduced ejection fraction
 Potential side effects include angioedema, kidney problems, and low blood pressure.
 The combination is can be described as an "angiotensin receptor-neprilysin inhibitor" (ARNi)
Pharmacological therapy

31. 
H- Sacubatril / Valsartan (Entresto)
Pharmacological therapy

32.  Anticoagulation
Recommended for HF with permanent, persistent, AF with or without an additional risk
factor for stroke (no preference on agent)
 Statins
Not recommended solely on the basis of HF diagnosis
 Antiarrhythmics
Given the neutral effects on mortality, the preferred antiarrhythmics in patients with
HFrEF are dofetilide and amiodarone.
Other medication therapy

33.  Non-dihydropyridine calcium channel blockers
Have negative inotropic effects can be harmful in patients with a low EF and should be avoided (class III
recommendation: harm).
 Dihydropyridine calcium channel blockers:
no proven benefit on morbidity or mortality in HF. Use of amlodipine can be considered for HTN or ischemic
heart disease management in HF patients because of its neutral effects on morbidity and mortality.
 In addition to non-pharmacological and pharmacological treatment there is also device therapy
Implantable cardioverter defibrillator
Chronic resynchronization therapy
Other medication therapy

34. 