D.K, a 72-year-old man, had a myocardial infarction (MI) 5 years ago. He has been diagnosed with classic (stable) angina. D.K is prescribed a beta blocker. His baseline vital signs are blood pressure 108/58; pulse 56 (at times irregular); and respirations 28. His past medical history includes asthma.
How do beta blockers work to manage angina? (USLO 5.3)
What assessments should be made while D.K is taking a beta blocker? (USLO 5.3, 5.6, 5.8)
Select 3 other antidysrhythmics prototypes and explain how each works. (USLO 5.2, 5.3, 5.4)
Case Context
Patient: D.K, 72-year-old male
Condition: Classic (stable) angina, history of MI
Medication: Beta blocker prescribed
Baseline Vitals: BP 108/58, pulse 56 (irregular), respirations 28
Past Medical History: Asthma
1. How Beta Blockers Work to Manage Angina (USLO 5.3)
Mechanism of Action:
Beta blockers inhibit beta-adrenergic receptors (primarily β1 receptors in the heart).
This reduces the effects of catecholamines (epinephrine and norepinephrine).
Results:
Decreased heart rate (negative chronotropic effect)
Reduced myocardial contractility (negative inotropic effect)
Lower myocardial oxygen demand
Prolonged diastole, improving coronary perfusion
Clinical Benefit in Angina:
By lowering oxygen demand and improving perfusion, beta blockers reduce frequency and severity of angina attacks.
They also improve survival post-MI by reducing arrhythmias and sudden cardiac death.
2. Assessments While D.K Is Taking a Beta Blocker (USLO 5.3, 5.6, 5.8)
Vital Signs:
Monitor heart rate (hold if <60 bpm or irregular).
Monitor blood pressure (risk of hypotension).
Monitor respiratory status, especially since D.K has asthma (non-selective beta blockers can cause bronchospasm).
Cardiac Assessment:
Watch for signs of worsening bradycardia or heart block.
Assess for symptoms of heart failure (edema, dyspnea, weight gain).
Respiratory Assessment:
Monitor for wheezing, bronchospasm, or increased respiratory distress due to asthma history.
Patient Complaints:
Fatigue, dizziness, or shortness of breath may indicate adverse effects.
Laboratory/Diagnostic Monitoring:
ECG monitoring for arrhythmias or conduction abnormalities.
3. Three Other Antidysrhythmic Prototypes and How They Work (USLO 5.2, 5.3, 5.4)
a) Amiodarone (Class III – Potassium Channel Blocker)
Mechanism: Prolongs repolarization by blocking potassium channels.
Effect: Increases action potential duration and refractory period.
Clinical Use: Effective in treating atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
Note: Has multiple toxicities (thyroid, pulmonary, hepatic).
b) Lidocaine (Class Ib – Sodium Channel Blocker)
Mechanism: Blocks sodium channels, shortening action potential duration in ischemic tissue.
Effect: Suppresses ventricular arrhythmias, especially post-MI.
Clinical Use: Used IV for acute ventricular arrhythmias.
Note: Not effective for atrial arrhythmias.
c) Verapamil (Class IV – Calcium Channel Blocker)
Mechanism: Blocks calcium channels in the AV node.
Effect: Slows conduction, prolongs refractory period, reduces contractility.
Clinical Use: Supraventricular tachycardias (SVT), rate control in atrial fibrillation/flutter, angina, hypertension.
Note: Can cause hypotension and bradycardia; avoid in severe heart failure.
Summary
Beta blockers reduce myocardial oxygen demand and improve perfusion, making them effective in managing stable angina.
Assessments include monitoring heart rate, blood pressure, respiratory status (especially with asthma), and signs of heart failure.
Other antidysrhythmics:
Amiodarone (potassium channel blocker) prolongs repolarization.
Lidocaine (sodium channel blocker) suppresses ventricular arrhythmias.
Verapamil (calcium channel blocker) slows AV node conduction.
