📘 Cardiac Drugs & Key Exam Pearls

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 📘 Cardiac Drugs & Key Exam Pearls

1. Statins

  • Use: First-line for patients with ASCVD or diabetes (≥40 y).

  • Mechanism: HMG-CoA reductase inhibitors → ↓ hepatic cholesterol synthesis → ↑ LDL receptor expression → ↓ LDL.

  • Benefits: ↓ MI & ischemic stroke risk.

  • Side Effects:

    • Myopathy (myalgia → rhabdomyolysis, rare).

    • Mild ↑ LFTs.

  • Notes:

    • If muscle symptoms occur → switch to another statin (eg, pravastatin, pitavastatin, fluvastatin have lower risk).

    • Check TSH (hypothyroidism ↑ risk of statin myopathy).

  • Second-line: Ezetimibe, PCSK9 inhibitors (alirocumab, evolocumab) if statin inadequate/tolerated poorly.

2. PCSK9 Inhibitors (Alirocumab, Evolocumab)

  • MOA: Inhibit PCSK9 → prevent LDL receptor degradation → ↑ LDL clearance.

  • Effect: ↓ LDL by ~50–60%.

  • Indications:

    • Familial hypercholesterolemia.

    • ASCVD with uncontrolled LDL despite maximal statins ± ezetimibe.

  • Side Effects: Injection site reactions, mild myalgias, rare cognitive effects.

3. Phentermine

  • MOA: Sympathomimetic → ↑ NE/Dopamine release → ↓ appetite.

  • Use: Short-term weight loss if lifestyle change fails.

  • Problems:

    • ↑ BP, tachycardia, insomnia.

    • Little long-term efficacy.

    • Abuse potential.

4. ACE Inhibitors (eg, Lisinopril)

  • Benefits: ↓ mortality in HF, CAD, diabetes with proteinuria.

  • Adverse Effects:

    • Dry cough (↑ bradykinin, substance P → bronchial irritation).

      • Can start early or months after initiation.

      • Not influenced by asthma/COPD.

    • Angioedema (rare, 0.1–0.7%).

  • Management of cough/angioedema: Switch to ARB.

5. Beta Blockers

  • Use: Angina, MI, CHF, arrhythmias, hyperthyroidism, aortic dissection.

  • Side Effects:

    • Bradyarrhythmias, worsening CHF, bronchospasm (esp. nonselective).

    • Fatigue, depression, sexual dysfunction.

    • Metabolic: can impair glucose control, ↑ weight gain.

  • Overdose: Bradycardia + hypotension ± hypoglycemia, bronchospasm, seizures.

    • Tx: Airway + fluids + atropine → IV glucagon if refractory.

    • Other: IV calcium, vasopressors, high-dose insulin/glucose, lipid emulsion.

  • Angina: HR goal = 55–60 bpm.

6. Aminophylline (Theophylline)

  • Class: Methylxanthine.

  • MOA: PDE inhibition → ↑ cAMP → bronchodilation; adenosine antagonist.

  • Effects: Bronchodilator, positive inotropy/chronotropy.

  • Uses: Rare now (toxic); experimental in beta-blocker toxicity.

  • Toxicity: Seizures, tachyarrhythmias, GI upset.

7. Calcium Channel Blockers (CCBs)

a) Dihydropyridines (Amlodipine, Nifedipine)

  • Potent vasodilators → ↓ BP.

  • Side Effects: Peripheral edema (arteriolar dilation ↑ capillary hydrostatic pressure), headache, flushing, dizziness.

  • Edema risk ↓ if combined with ACEi/ARB (post-capillary venodilation).

b) Non-DHP (Verapamil, Diltiazem)

  • MOA: Block L-type Ca²⁺ channels in myocardium & AV node.

  • Effects: ↓ HR, ↓ contractility, ↓ conduction (negative inotropy & chronotropy).

  • Uses: Rate control in AF, angina, HCM (if β-blockers not tolerated).

  • Side Effects:

    • Constipation (esp. verapamil).

    • Bradycardia, AV block.

    • Worsen CHF (contraindicated in HFrEF).

8. Hydralazine

  • MOA: Arteriolar vasodilation → ↓ SVR.

  • Adverse Effects:

    • Reflex tachycardia & palpitations.

    • Fluid retention → edema (give with diuretic).

    • Orthostatic hypotension.

    • Drug-induced lupus-like syndrome (esp. slow acetylators).

9. Digoxin

  • Use: Rate control in AF, HF with reduced EF (symptomatic relief).

  • MOA: Inhibits Na⁺/K⁺ ATPase → ↑ intracellular Ca²⁺ → ↑ contractility.

  • Toxicity:

    • Acute: Nausea, vomiting, abdominal pain, weakness, confusion.

    • Chronic: Neurologic (confusion, lethargy), visual (yellow/green vision changes, scotomas).

    • Arrhythmias (AV block, ventricular ectopy).

10. Amiodarone

  • Thyroid:

    • Hypothyroidism: Wolff-Chaikoff effect + ↓ T4→T3 conversion.

    • Hyperthyroidism:

      • Type 1 = iodine-induced hormone synthesis (Jod-Basedow).

      • Type 2 = destructive thyroiditis.

  • Other Toxicities:

    • Pulmonary: interstitial pneumonitis, ARDS, hemorrhage.

    • Hepatic: hepatocellular injury.

    • Cardiac: conduction abnormalities.

    • Neurologic: neuropathy.

    • Skin: blue-gray discoloration.

  • Note: ~50% develop significant side effects; 20% discontinue.

11. Norepinephrine

  • Receptors: α1 (↑ SVR, ↑ MAP), β1 (↑ contractility, HR).

  • Net Effect: ↑ BP, ↑ CO; HR unchanged or ↓ (reflex bradycardia).

  • Uses: First-line vasopressor in septic shock.

  • Adverse: Limb/mesenteric ischemia, tissue necrosis (extravasation).

12. Other Key Pearls

  • HCM Tx: β-blockers first-line → if intolerant, use NDHP CCBs (verapamil, diltiazem). Disopyramide sometimes added.

  • Peripheral edema is not caused by statins, HCTZ, β-blockers, or ACE inhibitors (instead: CCBs, hydralazine).

  • CCB + ACEi helps reduce edema.

  • AICD (not pacemaker) prevents sudden death in HCM patients at risk for ventricular arrhythmia.


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