Anti anginals Flashcards
(12 cards)
Pharmacodynamics of GTN
Causes release of NO in vascular smooth muscle, which increases cGMP causing smooth muscle relaxation and vasodilation
Affects arteries and veins, veins first / at lower concentrations
At lower doses, venodilation leads to decreased preload and stroke volume
At higher doses, arterial dilation leads to reduced blood pressure, which reduces CO and myocardial oxygen demand. Also causes dilation of coronary arteries
Decreases LV volume, therefore decreases LV wall tension and subsequent myocardial oxygen demand
Also decreases platelet aggregation (clinically insignificant)
Pharmacokinetics of GTN
Bioavailability 10-20%
Half life 2-8 mins
Liver metabolism to 1,2-dinitro derivative (significant vasodilator), excreted by kidney
Sublingual route, onset in 1-3 minutes, duration of action 15-30 mins
Tachyphlaxis occurs with continuous use due to a decrease in tissue sulfhydryl groups:
Smooth muscle develops tolerance to effects, especially with continuous IV infusion or long acting preparation
“Drug-free” interval of 8 hours between doses may reduce this
Clinical use of GTN
Angina
Acute coronary syndrome
Hypertensive emergencies
APO
Aortic dissection (with beta-blockade)
Precautions with GTN
Hypotension
Inferior and posterior MI / RV infarct
Fixed cardiac output e.g. aortic stenosis, tamponade
Significant tachycardia or bradycardia
Mechanism of action of Propanolol
Non selective beta blocker
also has membrane-stabilizing activity (MSA), which refers to sodium channel blockade—a secondary property relevant at high doses
Cardiovascular effects of Propranolol
↓ Chronotropy (↓ HR)
↓ Inotropy (↓ contractility)
↓ Dromotropy (↓ AV node conduction)
↓ Renin → ↓ Angiotensin II → vasodilation
Electricophysiological effects of Na channel blockade with Propranolol
Reduces slope of phase 0 in non-nodal (fast-response) tissues
May contribute to:
- QRS widening at high doses
- Proarrhythmic potential in overdose
Contraindications of propranolol
Asthma / COPD (due to β₂ blockade)
Bradycardia
AV block
Decompensated heart failure
Severe depression (relative)
Pharmacokinetics of propranolol
Oral bioavailability: ~25–35% (first-pass metabolism)
Half-life: ~3–6 hours (longer with extended release)
Metabolized by liver
Crosses BBB (→ CNS side effects)
Why is propranolol used in thyroid storm?
Beta blockade - Reduces adrenergic symptoms of thyrotoxicosis: tachycardia, palpitations, tremor, anxiety, heat intolerance
Inhibits peripheral conversion of T₄ to T₃
Why is propranolol used in essential tremor
Tremor arises from β₂ activation in skeletal muscle (enhancing muscle spindle sensitivity) → propranolol blunts this effect
Why is propranolol contraindicated in asthma
Propranolol blocks β₂ receptors in the lungs, which are normally responsible for bronchodilation. Blocking them can lead to bronchoconstriction, potentially triggering life-threatening bronchospasm in asthmatic patients.
