Pharmacology of Heart

Failure
Raditya Weka Nugraheni
Definition
• Cardiac output < the needs of O2 in the body
Pathophysiology
Classification
• Chronic
According to New York Heart Association (NYHA):
- Class I failure is associated with no limitations on ordinary activities and symptoms that occur only with greater than
ordinary
exercise.
- Class II is characterized by some limitation of ordinary activities, which results in fatigue and palpitations.
- Class III presents with no symptoms at rest, but fatigue and other clinical manifestations appear
with less than ordinary physical activity.
- Class IV is associated with symptoms even when the patient is at rest.

• Acute
In contrast, acute heart failure manifests as the fairly rapid (hours ro days) development of worsening
peripheral edema, respiratory distress with exertion and later at rest, and diaphoresis and cyanosis; acute
failure requires urgent medical intervention.
Goal of Therapy
• Primary goal: Prevention of heart failure i.e. in Hypertension and
Arterial problems
• If myocardial dysfunction already happened:
1. Prevents the worsening of cardiac functions  ACE inhibitor and β-
blocker
2. Decrease the symptoms of heart failure  diuretics, vasodilators,
inotropics
 inotropics

Β-blocker
vasodilators

diuretics
Drug mechanism
Vasodilators
• decrease preload and afterload  decrease heart workload
• ACE inhibitors (captopril and enalapril)
Lower arterial resistance
Inhibit the increase of Angiotensin II
Adverse effects: Cough (because of bradykinin production)
Sympathetic Effect inhibition
• Continuous symphathetic activation via RAAS could lead to myocardial
hypertrophy due to peripheral vasoconstriction. Coronary
vasoconstriction could also lead to myocardial ischemia.
 β-blocker
However, the use of this drug should be very cautious  high risk
Only Bisoprolol, carvedilol, and metoprolol.
Inotropic drugs
is a medicine that alters the force or strength of the heart's muscular
contractions (heartbeats).
Digoxin
Mechanism: inhibit Na+/K+-ATPase pump  [Na+] intracellular increase  inhibit
Na+/Ca2+ exchange  Ca2+ stays at Reticulum Sarcoplasmic inside the myocardial
cell contractility increase
Adverse effects: Digoxin compete with receptor of K+  dangerous in hypokalemia.
β-agonist – dobutamine
Mechanism: stimulate adrenoreceptor β  increase contractility
Diuretics
• Drug of choice for acute heart failure  liquid overload  pulmonary
congestion and peripheral edema.
• Should not be prescribed for asymptomatic patient and no liquid
overload.
Example: furosemide, thiazide
Physiotherapist considerations
• Orthostatic hypotension may cause patients to faint when transferring from a sitting or supine
position to standing, exiting from warm aquatherapy area, or if aerobic exercise is terminated
without an appropriate cool-down period.
• Dyspnea may decrease the aerobic capacity of patients.
• Cardiac output may be depressed during aerobic activities
• Altered plasma potassium levels can cause paresthesia, decrease skeletal muscle function, and
increase cramps.
• Effective therapy improves cardiac function and reserve in many patients with heart failure,
allowing them to participate in aerobic activities associated
with rehabilitation.