Recall the 4 main types of adrenergic receptors: alpha-1, alpha-2, beta-1, beta-2.
Beta-1 receptors are normally responsible for increasing the heart rate and contractility when activated. Beta-2 receptors are normally responsible for bronchodilation and vasodilation.
Beta-2 receptors are in direct opposition to alpha-1 receptors. Alpha-1 receptors when stimulated cause vasoconstriction. Beta-2 receptors when stimulated cause vasodilation.
There are 3 main classes of beta blockers:
- Cardioselective (only block beta-1 receptors which are found primarily in the heart) [A – N]
- Bisoprolol
- Metoprolol
- Atenolol
- Non-cardioselective (block beta-1 and beta-2 receptors) [N – Z]
- Nadolol
- Timolol
- Propanolol
- Non-cardioselective with alpha blocking action (potent vasodilators)
- Carvedilol
- Labetelol
In cirrhosis, patients develop portal hypertension due to the stiff and fibrotic nature of the cirrhotic liver. Portal hypertension can lead to the formation of portosystemic shunts which lead to 3 main pathological consequences: esophageal varices which can burst resulting in massive upper GI bleed, caput medusae, and hemorrhoids.
If these patients have esophageal varices or a prior bleed due to an esophageal varix then they are usually put on a beta-blocker – specifically a non-cardioselective beta blocker. Why specifically non-cardioselective?
Well the answer is simple, because we need both beta-1 and beta-2 receptors blocked, but why though? Anything that decreases the blood flow into the portal system will decrease the pressure at the varices.
- Blocking the beta-1 receptor results in decreased cardiac output and lower contractility of the heart. This results in decreased blood flow to the splanchnic circulation, ultimately resulting in less stress on the esophageal varices.
- Blocking the beta-2 receptor results in vasoconstriction of the splanchnic circulation due to unopposed alpha-1 activity. This ultimately also reduces the amount of blood that reaches the esophageal varices.