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Succinylcholine is a short-acting depolarizing neuromuscular blocker that is approved by the United States Food and Drug Administration (FDA) as an adjunct to other sedatives or hypnotics. It blocks the action of acetylcholine, disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. This results in skeletal muscle paralysis and can be beneficial during certain surgical procedures. However, it is important to understand the potential risks and side effects of succinylcholine, particularly its impact on muscle function and health.
| Characteristics | Values |
|---|---|
| Mechanism of action | Succinylcholine is a depolarizing neuromuscular blocker. It blocks the action of acetylcholine (ACh) and adheres to post-synaptic cholinergic receptors of the motor endplate, disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. |
| Effects | Transient fasciculations or involuntary muscle contractions, followed by skeletal muscle paralysis. |
| Therapeutic use | Preventing involuntary patient movement, e.g. during surgical procedures or electroconvulsive shock therapy. |
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What You'll Learn
How does succinylcholine work?
Succinylcholine is a short-acting depolarizing neuromuscular blocker. It is the only therapeutically used depolarizing neuromuscular blocker. It blocks the action of acetylcholine (ACh), disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. It is a more stable agonist than acetylcholine and lasts longer, causing a more stable depolarization. This means the process of repolarization is blocked and the muscles relax.
During this period, muscles that cause fine movement (ocular, facial, neck) are the most sensitive and are blocked first, followed by muscles of the extremities, and finally the most stable respiratory muscles. Restoration occurs upon completion of drug action.
Succinylcholine binds to the post-synaptic cholinergic receptors found on motor endplates, inducing first transient fasciculations or involuntary muscle contractions, followed by skeletal muscle paralysis. This paralysis continues until there is sufficient disassociation of succinylcholine from the acetylcholine neuromuscular receptor sites and consequential pseudocholinesterase hydrolyzation, permitting baseline neuromuscular receptor function and, thus, normal motor endplate activity.
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How does succinylcholine affect the body's muscles?
Succinylcholine is a short-acting depolarising neuromuscular blocker. It blocks the action of acetylcholine, disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. It is the only therapeutically used depolarising neuromuscular blocker.
As a neuromuscular receptor site-specific drug, succinylcholine is ineffective for the smooth and cardiac muscles of the body. Instead, it causes a prolonged period of membrane depolarisation, which induces transient fasciculations or involuntary muscle contractions, followed by skeletal muscle paralysis. The muscles that cause fine movement (ocular, facial, neck) are the most sensitive and are blocked first, followed by the muscles of the extremities, and finally the most stable respiratory muscles.
The skeletal muscle relaxation provided by succinylcholine is beneficial during certain surgical procedures, specifically when abdominal wall muscle disruption is necessary, mechanical ventilation is difficult or defied, or in surgical cases where spontaneous respiration of the patient is counterproductive to the procedure. It is also used as an adjunct therapy in patients undergoing electroconvulsive shock therapy to control muscle contractions induced by the electrical impulses delivered during the procedure.
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How does succinylcholine affect the body's nervous system?
Succinylcholine is a short-acting depolarising neuromuscular blocker. It blocks the action of acetylcholine (ACh), disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. It is the only therapeutically used depolarising neuromuscular blocker.
Succinylcholine is not a competitive antagonist; it is a more stable agonist than acetylcholine. It lasts longer, causing a more stable depolarisation. This means the process of repolarisation is blocked and the muscles relax.
During this period, muscles that cause fine movement (ocular, facial, neck) are the most sensitive and are blocked first, followed by muscles of the extremities, and finally the most stable respiratory muscles. Restoration occurs upon completion of drug action.
Therapeutic use of succinylcholine consists of preventing involuntary patient movement. It is often used as an adjunct therapy in patients undergoing electroconvulsive shock therapy to control muscle contractions induced by the electrical impulses delivered during the procedure.
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How does succinylcholine affect the body's respiratory system?
Succinylcholine is a short-acting depolarising neuromuscular blocker. It blocks the action of acetylcholine, disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. This causes a prolonged period of membrane depolarisation, which results in skeletal muscle paralysis.
Succinylcholine is used to prevent involuntary patient movement during certain surgical procedures, specifically when abdominal wall muscle disruption is necessary, mechanical ventilation is difficult or defied, or in surgical cases where spontaneous respiration of the patient is counterproductive to the procedure. It is also used as an adjunct therapy in patients undergoing electroconvulsive shock therapy to control muscle contractions induced by the electrical impulses delivered during the procedure.
During the period of muscle relaxation, muscles that cause fine movement (ocular, facial, neck) are blocked first, followed by the muscles of the extremities, and finally the most stable respiratory muscles.
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How does succinylcholine affect the body's cardiac system?
Succinylcholine is a short-acting depolarising neuromuscular blocker. It blocks the action of acetylcholine, disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems. It is ineffective for the smooth and cardiac muscles of the body.
Succinylcholine is often used as an adjunct therapy in patients undergoing electroconvulsive shock therapy (ECT) to control muscle contractions induced by the electrical impulses delivered during the procedure. It can also be used to expedite rapid endotracheal intubation, facilitate surgical procedures, and aid in mechanical ventilation by relaxation of skeletal muscles.
Succinylcholine is the only therapeutically used depolarising neuromuscular blocker. It differs from acetylcholine only in duration—it lasts longer, causing a more stable depolarisation. Thus, the process of repolarisation is blocked and the muscles relax. During this period, muscles that cause fine movement (ocular, facial, neck) are the most sensitive and are blocked first, after which muscles of the extremities are blocked, and finally the most stable respiratory muscles. Restoration occurs upon completion of drug action.
Therapeutic use of succinylcholine consists of preventing involuntary patient movement. Succinylcholine doses require calculation following a thorough patient assessment and evaluation. Dosing is patient-specific and calculated based on current total body weight and overall physical condition.
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Frequently asked questions
Succinylcholine is a depolarizing neuromuscular blocker, meaning it causes a prolonged period of membrane depolarization in order to exert its therapeutic effects. It blocks the action of acetylcholine (ACh), disrupting all cholinergic receptors of the parasympathetic and sympathetic nervous systems.
The skeletal muscle relaxation provided by succinylcholine is beneficial during certain surgical procedures, specifically when abdominal wall muscle disruption is necessary, mechanical ventilation is difficult or defied, or in surgical cases where spontaneous respiration of the patient is counterproductive to the procedure.
Succinylcholine adheres to post-synaptic cholinergic receptors of the motor endplate, inducing continuous disruption that results in transient fasciculations or involuntary muscle contractions and subsequent skeletal muscle paralysis.
