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The first is the use of beta-blockers, which reduce portal pressures. Non-selective beta blockers (such as propranolol and nadolol) have been used to decrease the pressure of the portal vein in patients with esophageal varices, and have been shown to regress portal hypertensive gastropathy that has been worsened by medical treatment of varices. [5]
It may worsen the symptoms of asthma. [2] Propranolol may cause harmful effects for the baby if taken during pregnancy; [7] however, its use during breastfeeding is generally considered to be safe. [8] It is a non-selective beta blocker which works by blocking β-adrenergic receptors. [2]
Beta blockers are only indicated in cases of compensated, stable congestive heart failure; in cases of acute decompensated heart failure, beta blockers will cause a further decrease in ejection fraction, worsening the patient's current symptoms. [citation needed] Beta blockers are known primarily for their reductive effect on heart rate ...
Portosystemic shunts, Nonselective beta-blockers [2] Portal hypertension is defined as increased portal venous pressure , with a hepatic venous pressure gradient greater than 5 mmHg . [ 3 ] [ 4 ] Normal portal pressure is 1–4 mmHg; clinically insignificant portal hypertension is present at portal pressures 5–9 mmHg; clinically significant ...
However, non-selective β-blockers do not prevent the formation of esophageal varices. [8] When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed. [9]
Carvedilol is a nonselective beta blocker and alpha-1 blocker. [5] How it improves outcomes is not entirely clear but may involve dilation of blood vessels. [5] Carvedilol was patented in 1978 and approved for medical use in the United States in 1995. [5] [8] It is on the World Health Organization's List of Essential Medicines. [9]
Nadolol is a non-selective beta blocker; that is, it non-selectively blocks both beta-1 and beta-2 receptors. It has a preference for beta-1 receptors, which are predominantly located in the heart, thereby inhibiting the effects of catecholamines and causing a decrease in heart rate and blood pressure.
Toxicity of beta-1 blocker will contribute to symptoms including bradycardia, hypotension, due to its extensive blockage of beta-1 receptor. [5] Moreover, overdose of beta-1 blocker may lead to the loss of their selectivity and bind to beta-2 receptor, causing bronchopulmonary symptoms. [5]