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Questions and Answers
What type of channel is responsible for the slow depolarization of the pacemaker cell membrane towards the action potential threshold?
What type of channel is responsible for the slow depolarization of the pacemaker cell membrane towards the action potential threshold?
The influx of sodium ions is responsible for the upstroke of the slow pacemaker action potential.
The influx of sodium ions is responsible for the upstroke of the slow pacemaker action potential.
False (B)
Early After Depolarizations (EADs) occur at increased heart rates.
Early After Depolarizations (EADs) occur at increased heart rates.
False (B)
The intrinsic rate of firing of SAN cells is approximately ______ APs per minute.
The intrinsic rate of firing of SAN cells is approximately ______ APs per minute.
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What is the specific name for the slow depolarization phase of the pacemaker potential, often referred to as the 'funny current'?
What is the specific name for the slow depolarization phase of the pacemaker potential, often referred to as the 'funny current'?
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The threshold potential for the action potential formation in a sinoatrial node pacemaker cell is approximately ______ mV.
The threshold potential for the action potential formation in a sinoatrial node pacemaker cell is approximately ______ mV.
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Which of the following is a drug used to treat bradycardias?
Which of the following is a drug used to treat bradycardias?
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Match the following drug with its primary action or effect:
Match the following drug with its primary action or effect:
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Match the phases of the sinoatrial node pacemaker potential with their corresponding events:
Match the phases of the sinoatrial node pacemaker potential with their corresponding events:
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Increased K+ efflux hyperpolarizes the membrane.
Increased K+ efflux hyperpolarizes the membrane.
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Which ion channels are responsible for the rapid depolarization of the ventricular myocyte?
Which ion channels are responsible for the rapid depolarization of the ventricular myocyte?
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Sympathetic nerve activation leads to the release of ______, which binds to ______ receptors on the cardiac pacemaker cells.
Sympathetic nerve activation leads to the release of ______, which binds to ______ receptors on the cardiac pacemaker cells.
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What is the primary indication for using Lidocaine?
What is the primary indication for using Lidocaine?
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Amiodarone is used to treat asystole.
Amiodarone is used to treat asystole.
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Class 1a antiarrhythmic drugs, such as Quinidine, Procainamide, and Disopyramide, ______ the action potential duration and refractory period.
Class 1a antiarrhythmic drugs, such as Quinidine, Procainamide, and Disopyramide, ______ the action potential duration and refractory period.
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What is the primary mechanism of action of Class 1 antiarrhythmic drugs?
What is the primary mechanism of action of Class 1 antiarrhythmic drugs?
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Match the following drug classes to their corresponding effects on the action potential:
Match the following drug classes to their corresponding effects on the action potential:
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Which of the following is a non-selective beta blocker?
Which of the following is a non-selective beta blocker?
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Lidocaine's effect on the heart is dependent on the rate of depolarization, meaning it has a use-dependent effect.
Lidocaine's effect on the heart is dependent on the rate of depolarization, meaning it has a use-dependent effect.
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What is the primary adverse effect of Lidocaine?
What is the primary adverse effect of Lidocaine?
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Which of the following are potential adverse effects of Class 2 drugs?
Which of the following are potential adverse effects of Class 2 drugs?
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Amiodarone, a Class 3 drug, can prolong the QT interval on an ECG.
Amiodarone, a Class 3 drug, can prolong the QT interval on an ECG.
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What type of drug is Verapamil classified as?
What type of drug is Verapamil classified as?
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Dihydropyridines, such as Nifedipine and Amlodipine, predominantly exert their effects on the ______.
Dihydropyridines, such as Nifedipine and Amlodipine, predominantly exert their effects on the ______.
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Match the following drugs with their respective drug classes:
Match the following drugs with their respective drug classes:
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What is the effect of acetylcholine on HCN channels in pacemaker cells?
What is the effect of acetylcholine on HCN channels in pacemaker cells?
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Increased potassium efflux from the cell leads to hyperpolarization of the membrane.
Increased potassium efflux from the cell leads to hyperpolarization of the membrane.
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What is the name of the phase in a ventricular myocyte action potential where the sodium current is inactivated and fast potassium channels open?
What is the name of the phase in a ventricular myocyte action potential where the sodium current is inactivated and fast potassium channels open?
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Match the following phases of the SA node pacemaker potential with their corresponding events:
Match the following phases of the SA node pacemaker potential with their corresponding events:
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Study Notes
Cardiac Arrhythmias
- Cardiac arrhythmias are irregular heartbeats
Sinoatrial Node Pacemaker Potential
- Pacemaker cells contain HCN-gated channels
- Hyperpolarization activates the channels
- This causes slow depolarization toward the AP threshold
- Phase 4: Prepotential enables automaticity
- HCN channels trigger a "funny current"
- Simultaneously, potassium efflux and sodium influx occur
- Reaches the threshold, upstroke, then inactivates HCN channels
- Phase 0: Upstroke of slow pacemaker action potential initiated at the threshold potential (-55 mV)
- Ca2+ movement increases into the cell
- Phase 3: Ca2+ channels inactivate, delayed K+ efflux leads to membrane hyperpolarization
- Phase 4: Pacemaker Na+ influx (If), Ca2+ channels recover, ion gradients restored
- The SA node firing rate establishes the heart rate, initiating the cardiac cycle
Sympathetic Nerves and Heart Rate
- Activation releases norepinephrine (NE) onto B1 adrenoreceptors on cardiac cells
- Opening of HCN channels increases
- Increased Na+ influx
- Opens Ca2+ channels; increased Ca2+ influx
- Increases slope of prepotential (phase 4)
- Heart rate increases
Parasympathetic Nerves and Heart Rate
- Activation releases acetylcholine (ACh) onto muscarinic receptors
- Decreases opening of HCN channels; decreased Na+ influx
- Slows opening of Ca2+ channels, decreased Ca2+ influx
- Opens additional K+ channels; increased K+ efflux
- Hyperpolarization reduces prepotential slope and heart rate
Ventricular Myocyte Action Potentials
- Phase 0: Rapid depolarization, membrane potential reaches the critical firing threshold (-60 mV) due to inward Na+ current
- Phase 1: Partial repolarization (Na+ channels inactivate; fast K+ channels open)
- Phase 2: Calcium channels open; fast K+ channels close
- Phase 3: Ca2+ channels inactivate; slow K+ channels activated
- Phase 4: Resting potential
Vagal Tone
- Intrinsic rate of firing of SAN cells is ~100–110 APs per minute
- Constant tonic activation of some parasympathetic nerves on the SA node
Early After Depolarizations (EADs)
- Occurs when heart rate is low, suppressed by high HR
- AP is prolonged; some Ca channels inactivated during an earlier part of the AP
- Reactivate to give EAD
- Ca L channels – end phase 2
- Ca T channels – mid phase 3
- Need different drugs to treat
Delayed After Depolarizations (DADs)
- Seen at increased HRs
- Associated with elevated Ca2+
- Ca2+ activation of Na/K channels (depolarizing)
- Na/Ca exchange 3:1 = electrogenic
- Toxic doses of cardiac glycosides
Drugs to Treat Bradycardias
- Atropine: Switches to vagus nerve
- Isoproterenol (Isoprenaline): Activates beta receptors
- Pacing
Atropine
- Naturally occurring antimuscarinic alkaloid (from deadly nightshade)
- Blocks vagal inhibition of sinus and AV nodes
- Given intravenously (IV)
- Predominantly metabolized by the liver
- Short half-life (~3 hours)
- Anticholinergic effects (e.g., dry mouth, mydriasis, postural hypotension)
Adenosine
- Used to treat, primarily re-entry supraventricular tachycardia
- Action on AV node, slows rate of pacemaker potential rise
- Usually administered intravenously (IV) to terminate paroxysmal SVTs
- Action lasts 20-30 seconds; patient returns to sinus rhythm
- Side effects: chest pain, shortness of breath, dizziness, nausea
Drug Treatment for Cardiac Arrest
- Asystole: No cardiac stimulation; give adrenaline
- Ventricular fibrillation: Electric activity, but ventricles don't contract together; give amiodarone and lignocaine
Drugs to Treat Tachycardia
- Class 1 Na channel blockers (blocks phase 0)
- Class 2 Beta blockers (affecting SA node)
- Class 3 K channel blockers (block phase 3)
- Class 4 Ca channel blockers (block phase 2)
Class 1 Antiarrhythmic Drugs
- Divided into 3 groups based on action potential duration effects
- Class 1a: Lengthen action potential duration and refractory period (e.g., Quinidine, Procainamide, Disopyramide.)
- Class 1b: Shortens action potential duration and refractory period (e.g., Lignocaine/Lidocaine)
- Class 1c: No effect on action potential duration and refractory period; delays conduction velocity in Purkinje fibers (e.g., Flecainide)
Lidocaine
- Blocks fast sodium channels, slows phase 0 depolarization, shortens action potential duration
- Used for ventricular arrhythmias
- Indications: Treating specific diseases or conditions
- Short half-life; given intravenously (IV)
- Adverse effects: Hypotension, heart block, neurotoxicity, seizures
Class 2 Drugs (Beta Blockers)
- Beta blockers, either non-selective (affects both B1 and B2) or cardio selective (affects only B1)
- Reduces intrinsic rate of sinus and AV nodes; reduces HR and BP, cardiac work, renin secretion
- Examples: Propranolol. Atenolol, Metoprolol
- Useful in treating supraventricular and atrial fibrillation
Adverse Effects of Class 2 Drugs
- B1 effects: Bradycardia and heart failure
- B2 effects: Exacerbation of asthma, peripheral cooling, muscle aches, intermittent claudication
- Other severe effects: Fatigue, nightmares, sleep disturbances, angina, MI, unawareness of hypoglycemia
- Beta blockers can cross the blood-brain barrier
Class 3 Drugs
- Amiodarone prolongs AP duration & refractory period, lengthening QT interval
- Indicated for ventricular and supraventricular tachycardia, first-line therapy for ventricular fibrillation
- Long half-life; hepatic metabolism
- Adverse effects: Thyroid disturbances, pulmonary fibrosis , pro-arrhythmia, torsades de pointes
Class 4 Drugs
- Dihydropyridines (e.g., Nifedipine, Amlodipine): Primarily arterial vasodilation
- Benzothiazepines (e.g., Diltiazem): Mixed vascular and cardiac effects
- Phenylalkylamines (e.g., Verapamil): Primarily cardiac effects (negative inotrope and chronotrope, antiarrhythmic)
Verapamil
- A Ca2+ channel blocker that slows phase 4 Ca2+ entry
- Reduces rate and contraction velocity in sinus and AV node
- Indications: Supraventricular arrhythmias
- Pharmacology: Acts on the heart, oral and IV use; first pass hepatic metabolism
- Adverse effects: Heart failure, hypotension, constipation, vasodilation, edema, flushing
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Description
Explore the intricacies of cardiac arrhythmias and the pacemaker potential of the sinoatrial node. This quiz focuses on the mechanisms of heart rate regulation, including the effects of HCN channels and sympathetic nerve activation. Understand how these processes contribute to the cardiac cycle and overall heart function.
