HEART
FAILURE
Treatments and
Intervention
Mabel Joy M. Tagud, RPh, CPh.
STRUCTURE OF THE HEART
HEART FAILURE
➢ A state in which the heart is unable to pump sufficient
blood to meet the metabolic needs of the tissues
➢ Ventricles may become stiff and not fill properly
between beats
➢ Heart muscles may be damaged and weakened and
ventricles dilate to the point where the heart cannot
pump blood efficiently
HEART FAILURE
➢ Types Ejection Fraction:
A. HFrEF: Heart Failure with reduced Ejection Fraction
(<40%)
B. HFpEF: Heart Failure with preserved Ejection Fraction
(≥50%)
➢ Causes: Ischemic heart disease, hypertension,
cardiomyopathy, valvular disease.
➢ Symptoms: Dyspnea, fatigue, edema, orthopnea.
TYPES OF HEART FAILURE by
Ventricular Dysfunction
A. RIGHT SIDED HEART FAILURE
B. LEFT SIDED HEART FAILURE
C. HIGH OUTPUT HEART FAILURE
RIGHT SIDED HEART
FAILURE
Inability of the right ventricle to pump effectively.
RESULT:
•Blood builds up in your veins, vessels that carry
blood from the body back to the heart.
•This buildup increases pressure in your veins.
•The pressure pushes fluid out of your veins and
into other tissue.
•Fluid builds up in your legs, abdomen or other
areas of your body, causing swelling.
LEFT SIDED HEART
FAILURE
Inability of the left ventricle to pump effectively.
Result:
• Blood backs up into the pulmonary veins.
• Increased pressure in these veins pushes fluid
into the lung tissue.
• Fluid accumulation in the lungs causes
pulmonary congestion.
• Leads to symptoms such as shortness of breath,
orthopnea, and paroxysmal nocturnal dyspnea.
HIGH OUTPUT HEART
FAILURE
Heart failure with elevated cardiac output due to
increased metabolic demand or decreased
systemic vascular resistance.
Result:
• The heart pumps more blood than normal but
still fails to meet the body’s metabolic needs.
• Increased demand or reduced resistance
causes persistent strain on the heart.
Pathophysiology
➢Neurohormonal activation:
RAAS (Renin-Angiotensin-Aldosterone System)
SNS (Sympathetic Nervous System)
➢ Consequences:
Vasoconstriction
Sodium and water retention
Cardiac remodeling.
CARDIAC TROPIC EFFECTS
➢ Cardiac drugs are often described by their effect on
heart rate, force of contraction, and conduction. These
effects are described using the suffix “-tropic.”
INOTROPIC EFFECT
➢ Effect on the force of myocardial contraction.
➢ Positive Inotropic (+): Increases contraction strength →
improves cardiac output.
➢ Negative Inotropic (–): Decreases contraction strength
→ reduces myocardial workload.
CHRONOTROPIC EFFECT
➢ Effect on the heart rate via changes in the SA node
impulse formation.
➢ Positive Chronotropic (+): Increases heart rate.
➢ Negative Chronotropic (–): Decreases heart rate.
DROMOTROPIC EFFECT
Effect on the conduction velocity of electrical impulses
through the heart, especially the AV node.
Positive Dromotropic (+): Increases conduction speed.
Negative Dromotropic (–): Slows conduction.
Pharmacologic Goals
➢ Remove or mitigate underlying cause.
➢ Relieve symptoms & improve cardiac function.
➢ Slow disease progression.
➢ Improve survival.
Non
Pharmacologic
DIETARY CHANGES
pOTASSIUM INTAKE
STRESS MANAGEMENT
ALCOHOL REDUCTION PHYSICAL ACTIVITY
SMOKING CESSATIONT SLEEP QUALITY
WEIGHT MANAGEMENT
PHARMACOLOGIC
INTERVENTIONS
Digitalis Glycosides
(+ Inotropic): Inhibits Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → promotes Ca²⁺
influx via Na⁺/Ca²⁺ exchanger → ↑ contractility.
(– Chronotropic): Increases vagal tone → slows AV node conduction → lowers
heart rate.
Example: Digoxin (Lanoxin®)
Therapeutic Benefits:
1. Improves CO, reduces preload and pulmonary congestion.
2. Symptom improvement in HF with atrial fibrillation.
DIURETICS
Promote Na⁺ and water excretion → reduce preload.
Therapeutic Benefits:
Rapid relief of congestion, edema, pulmonary symptoms.
Examples:
Loop: Furosemide, Bumetanide, Torsemide.
Thiazide: Hydrochlorothiazide, Metolazone.
K⁺-Sparing: Spironolactone, Eplerenone, Amiloride.
Dopaminergic & Beta-Adrenergic Agonists
Dopamine (dose-dependent):
Low doses → renal vasodilation; moderate doses → β₁ stimulation (↑
contractility);
high doses → α stimulation (vasoconstriction).
Dobutamine: β₁ agonist → ↑ inotropy with minimal HR change.
Therapeutic Benefits:
Short-term use in acute decompensated HF to improve CO.
Examples:
Dopamine, Dobutamine, Isoproterenol, Fenoldopam.
Vasodilators
Arteriolar dilation (↓ afterload) and/or venodilation (↓ preload).
Therapeutic Benefits:
Symptom relief, mortality benefit in certain groups.
Examples:
Hydralazine, Isosorbide dinitrate, Nitroglycerin.
Beta Blockers
Block β₁ receptors → ↓ HR, ↓ contractility, ↓ sympathetic activation.
Therapeutic Benefits:
Reverse remodeling, ↓ mortality, ↓ arrhythmia risk.
Examples:
Carvedilol, Metoprolol succinate (Toprol XL®), Bisoprolol.
SGLT2 Inhibitors
Inhibit SGLT2 in kidneys → ↑ glucose & Na⁺ excretion → osmotic diuresis.
Therapeutic Benefits:
↓ HF hospitalizations & mortality, works even in non-diabetics.
Examples:
Dapagliflozin (Farxiga®), Empagliflozin (Jardiance®).
Natriuretic Peptides
Bind natriuretic peptide receptors → ↑ cGMP → vasodilation, natriuresis,
diuresis.
Therapeutic Benefits:
Reduce preload & afterload, relieve dyspnea in acute HF.
Examples:
Nesiritide (BNP analog), Ularitide (ANP analog).
End of Lecture
