Beta-Blocker Poisoning
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Basics
Description
Normal Physiology- Cardiovascular: β1-receptors:
- ATP converted to cAMP by adenyl cyclase with stimulation of β-receptors
- cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasmic reticulum
- Sarcoplasmic reticulum releases calcium
- Excitation–contraction coupling occurs
- Effects of β-blockers:
- Cardiovascular:
- Decreased excitation/contraction
- Membrane stabilizing activity
- Sodium channel blockade causes a prolongation of the QRS complex (with some agents)
- Prolongation of QTc interval leading to ventricular dysrhythmias (with some agents)
- Intrinsic sympathomimetic activity
- Partial agonist properties (with some agents)
- Neurologic:
- CNS effects with the lipophilic agents (propranolol, metoprolol, labetalol)
- Cardiovascular:
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Basics
Description
Normal Physiology- Cardiovascular: β1-receptors:
- ATP converted to cAMP by adenyl cyclase with stimulation of β-receptors
- cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasmic reticulum
- Sarcoplasmic reticulum releases calcium
- Excitation–contraction coupling occurs
- Effects of β-blockers:
- Cardiovascular:
- Decreased excitation/contraction
- Membrane stabilizing activity
- Sodium channel blockade causes a prolongation of the QRS complex (with some agents)
- Prolongation of QTc interval leading to ventricular dysrhythmias (with some agents)
- Intrinsic sympathomimetic activity
- Partial agonist properties (with some agents)
- Neurologic:
- CNS effects with the lipophilic agents (propranolol, metoprolol, labetalol)
- Cardiovascular:
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