Long QT Syndrome and Antiarrythmic Drugs
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Long QT Syndrome and Antiarrythmic Drugs

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Questions and Answers

Which class of antiarrhythmics decrease heart contractility by causing a blockade of calcium channels in the SA and AV nodes?

  • Class V
  • Class II
  • Class IV (correct)
  • Class I
  • What is the primary indication for Amiodarone?

  • Long QT syndrome
  • Ventricular tachycardia (correct)
  • Ventricular fibrillation
  • Atrial fibrillation
  • What is the mechanism of action for Class I antiarrhythmics?

  • Sodium channel blockade (correct)
  • Potassium channel blockade
  • Beta-adrenergic receptor blockade
  • Calcium channel blockade
  • Which of the following is a major risk associated with Class 1A sodium channel blockers?

    <p>All of the above</p> Signup and view all the answers

    What is the mechanism of action for Adenosine?

    <p>Potassium channel opening</p> Signup and view all the answers

    What is the effect of Amiodarone on the QT interval?

    <p>Prolongation</p> Signup and view all the answers

    What is the mechanism of action for Anticoagulants?

    <p>Inhibiting Vitamin K</p> Signup and view all the answers

    Which of the following is a Class III antiarrhythmic?

    <p>Amiodarone</p> Signup and view all the answers

    What is the standard form of heparin?

    <p>Unfractioned heparin</p> Signup and view all the answers

    What is the MOA of heparin?

    <p>Activates antithrombin to inactivate clotting factors Xa and thrombin</p> Signup and view all the answers

    What are the two main uses of heparin?

    <p>Prophylactic and treatment of existing clots</p> Signup and view all the answers

    Can heparin be taken orally?

    <p>No, it can't be absorbed through the digestive system</p> Signup and view all the answers

    What is the reason to avoid heparin via the IM route?

    <p>Risk of hematoma formation</p> Signup and view all the answers

    What is the reversal agent for heparin toxicity?

    <p>Protamine sulfate</p> Signup and view all the answers

    What is Heparin-induced Thrombocytopenia (HIT)?

    <p>A condition where platelets are too low</p> Signup and view all the answers

    What is the class of drugs that promotes the lysis of fibrin and the dissolution of thrombi?

    <p>Thrombolytics</p> Signup and view all the answers

    What is the MOA of thrombolytics?

    <p>Promote the lysis of fibrin and the dissolution of thrombi</p> Signup and view all the answers

    What is the difference between anticoagulants and thrombolytics?

    <p>Anticoagulants prevent clot formation, while thrombolytics break up existing clots</p> Signup and view all the answers

    In a patient with Long QT syndrome, which medication should be avoided?

    <p>Procainamide</p> Signup and view all the answers

    What is the sensation felt by a patient experiencing Torsedes De Pointes?

    <p>Near-syncope</p> Signup and view all the answers

    Which of the following antiarrhythmic classes does NOT decrease heart contractility?

    <p>Class III</p> Signup and view all the answers

    What is the primary mechanism of action of beta blockers?

    <p>Blockade of beta receptors</p> Signup and view all the answers

    Which of the following antiplatelet drugs is a prototype?

    <p>Aspirin</p> Signup and view all the answers

    What is the mechanism of action of thrombolytics?

    <p>Dissolution of thrombi</p> Signup and view all the answers

    Which of the following is NOT a risk associated with Class 1A sodium channel blockers?

    <p>Bradycardia</p> Signup and view all the answers

    What is the primary effect of Adenosine on the heart?

    <p>Slows heart rate</p> Signup and view all the answers

    What is the primary function of anticoagulants?

    <p>To prevent the formation of new clots</p> Signup and view all the answers

    Which of the following is a side effect of beta blockers?

    <p>Bradycardia</p> Signup and view all the answers

    What is the mechanism of action of Class II antiarrhythmics?

    <p>Decreases the automaticity of the SA node</p> Signup and view all the answers

    Which of the following is a route of administration for heparin?

    <p>IV</p> Signup and view all the answers

    What is the primary indication for Class III antiarrhythmics?

    <p>Ventricular tachycardia</p> Signup and view all the answers

    What is a common side effect of amiodarone?

    <p>Pulmonary toxicity</p> Signup and view all the answers

    What is the mechanism of action of thrombolytics?

    <p>Promote the lysis of fibrin</p> Signup and view all the answers

    What is the primary indication for thrombolytics?

    <p>Breaking up existing blood clots</p> Signup and view all the answers

    What is the reversal agent for heparin toxicity?

    <p>Protamine sulfate</p> Signup and view all the answers

    What is Heparin-induced Thrombocytopenia (HIT)?

    <p>A blood disorder characterized by low platelet count</p> Signup and view all the answers

    Study Notes

    Medications for Long QT Syndrome

    • In an acute setting, magnesium sulfate is given to patients with Long QT syndrome.

    Antiarrhythmic Drugs and QT Prolongation

    • Class I (Sodium channel blockers, e.g., Quinidine) and Class III (Potassium Channel Blockers, e.g., Amiodarone) antiarrhythmic drugs increase the risk of QT prolongation.
    • Other medications associated with increased risk of QT prolongation include antipsychotics, antidepressants, and antibiotics.

    Torsedes De Pointes

    • A patient experiencing Torsedes De Pointes feels skipped beats, palpitations, racing heart, and chest discomfort/pain/pressure.
    • QT prolongation occurs when repolarization takes longer than depolarization, causing the heart to relax and then receive another beat during that relaxation period.

    Antiarrhythmic Drug Classes

    • Class I: Sodium channel blockers (e.g., Quinidine) decrease heart contractility by blocking sodium channels in the SA node and AV node.
    • Class II: Beta blockers (e.g., Propranolol) decrease heart contractility by blocking beta receptors in the SA node and AV node.
    • Class III: Potassium Channel Blockers (e.g., Amiodarone) decrease heart contractility by blocking potassium channels in the SA node and AV node.
    • Class IV: Calcium Channel Blockers (e.g., Verapamil) decrease heart contractility by blocking calcium channels in the SA node and AV node.
    • Class V: Others (e.g., Adenosine) decrease heart contractility by blocking various channels in the SA node and AV node.

    Beta Blockers

    • Beta blockers belong to Class II antiarrhythmics.
    • Mechanism of action: decrease the automaticity of the SA node and slow conduction through the AV node, helping to control tachyarrythmias.
    • Clinical uses: antihypertension, heart failure, angina, myocardial infarction, arrhythmias.
    • Types:
      • Non-selective (e.g., Propranolol): cause bradycardia, hypotension, and broncospasms.
      • Beta 1 selective (e.g., Metopralol, Atenelol): slow down heart rate, preferred for patients with respiratory issues.
      • Non-selective with additional actions (e.g., Carvedilol, Labetalol): also block alpha 1, helping with hypertension.

    Class III Antiarrhythmic: Amiodarone

    • Prototype drug for Class III antiarrhythmics.
    • Mechanism of action: blocks potassium channels, preventing efflux of potassium from the cell, leading to delayed repolarization of the cardiac cell membrane.
    • Uses: primarily indicated for ventricular arrhythmias.
    • Side effects: pulmonary toxicity, thyroid dysfunction, hepatotoxicity, optic neuropathy, blue-gray skin color changes, hypotension, bradycardia, and QT prolongation.
    • Can accumulate in tissues due to its lipophilic nature, leading to toxicity.
    • Crosses the blood-brain barrier.

    Anticoagulants

    • Mechanism of action: disrupt the coagulation cascade, ultimately suppressing the production of fibrin.
    • Do not break up existing clots, but rather prevent the development of future clots.
    • Classes:
      • Heparin and its derivatives (e.g., Enoxaparin)
      • Warfarin
      • Direct Oral Anticoagulants (DOACs): Dabigatran, Rivaroxaban, Apixaban

    Antiplatelet Drugs

    • Mechanism of action: inhibit platelet aggregation, preventing platelets from clumping together to form clots.
    • Prototype drugs: Aspirin, Clopidogrel, Ticagrelor

    Thrombolytics

    • Mechanism of action: promote the lysis (breaking) of fibrin and the dissolution of thrombi.
    • Prototype drug: tPA alteplase
    • Uses: break up existing clots.

    Heparin

    • Standard form: unfractionated heparin.
    • Lower molecular form: Enoxaparin.
    • Mechanism of action: activates antithrombin, which inactivates clotting factors Xa and thrombin, preventing the conversion of fibrinogen to fibrin.
    • Routes of administration: subQ, IV.
    • Not absorbed through the digestive system, so cannot be taken orally.
    • Should be avoided via the IM route to prevent hematoma formation.
    • Uses: prophylactic (prevents clots from forming in those with risk of clots, such as Afib) and prevents current clots from getting bigger (those with DVT).
    • Side effects: bleeding, bloody stool, vomiting that looks like coffee grounds, petechiae.
    • Reversal agent: Protamine Sulfate.
    • Can cause Heparin-induced Thrombocytopenia (HIT), an immune response against heparin.

    Medications for Long QT Syndrome

    • In an acute setting, magnesium sulfate is given to patients with Long QT syndrome.

    Antiarrhythmic Drugs and QT Prolongation

    • Class I (Sodium channel blockers, e.g., Quinidine) and Class III (Potassium Channel Blockers, e.g., Amiodarone) antiarrhythmic drugs increase the risk of QT prolongation.
    • Other medications associated with increased risk of QT prolongation include antipsychotics, antidepressants, and antibiotics.

    Torsedes De Pointes

    • A patient experiencing Torsedes De Pointes feels skipped beats, palpitations, racing heart, and chest discomfort/pain/pressure.
    • QT prolongation occurs when repolarization takes longer than depolarization, causing the heart to relax and then receive another beat during that relaxation period.

    Antiarrhythmic Drug Classes

    • Class I: Sodium channel blockers (e.g., Quinidine) decrease heart contractility by blocking sodium channels in the SA node and AV node.
    • Class II: Beta blockers (e.g., Propranolol) decrease heart contractility by blocking beta receptors in the SA node and AV node.
    • Class III: Potassium Channel Blockers (e.g., Amiodarone) decrease heart contractility by blocking potassium channels in the SA node and AV node.
    • Class IV: Calcium Channel Blockers (e.g., Verapamil) decrease heart contractility by blocking calcium channels in the SA node and AV node.
    • Class V: Others (e.g., Adenosine) decrease heart contractility by blocking various channels in the SA node and AV node.

    Beta Blockers

    • Beta blockers belong to Class II antiarrhythmics.
    • Mechanism of action: decrease the automaticity of the SA node and slow conduction through the AV node, helping to control tachyarrythmias.
    • Clinical uses: antihypertension, heart failure, angina, myocardial infarction, arrhythmias.
    • Types:
      • Non-selective (e.g., Propranolol): cause bradycardia, hypotension, and broncospasms.
      • Beta 1 selective (e.g., Metopralol, Atenelol): slow down heart rate, preferred for patients with respiratory issues.
      • Non-selective with additional actions (e.g., Carvedilol, Labetalol): also block alpha 1, helping with hypertension.

    Class III Antiarrhythmic: Amiodarone

    • Prototype drug for Class III antiarrhythmics.
    • Mechanism of action: blocks potassium channels, preventing efflux of potassium from the cell, leading to delayed repolarization of the cardiac cell membrane.
    • Uses: primarily indicated for ventricular arrhythmias.
    • Side effects: pulmonary toxicity, thyroid dysfunction, hepatotoxicity, optic neuropathy, blue-gray skin color changes, hypotension, bradycardia, and QT prolongation.
    • Can accumulate in tissues due to its lipophilic nature, leading to toxicity.
    • Crosses the blood-brain barrier.

    Anticoagulants

    • Mechanism of action: disrupt the coagulation cascade, ultimately suppressing the production of fibrin.
    • Do not break up existing clots, but rather prevent the development of future clots.
    • Classes:
      • Heparin and its derivatives (e.g., Enoxaparin)
      • Warfarin
      • Direct Oral Anticoagulants (DOACs): Dabigatran, Rivaroxaban, Apixaban

    Antiplatelet Drugs

    • Mechanism of action: inhibit platelet aggregation, preventing platelets from clumping together to form clots.
    • Prototype drugs: Aspirin, Clopidogrel, Ticagrelor

    Thrombolytics

    • Mechanism of action: promote the lysis (breaking) of fibrin and the dissolution of thrombi.
    • Prototype drug: tPA alteplase
    • Uses: break up existing clots.

    Heparin

    • Standard form: unfractionated heparin.
    • Lower molecular form: Enoxaparin.
    • Mechanism of action: activates antithrombin, which inactivates clotting factors Xa and thrombin, preventing the conversion of fibrinogen to fibrin.
    • Routes of administration: subQ, IV.
    • Not absorbed through the digestive system, so cannot be taken orally.
    • Should be avoided via the IM route to prevent hematoma formation.
    • Uses: prophylactic (prevents clots from forming in those with risk of clots, such as Afib) and prevents current clots from getting bigger (those with DVT).
    • Side effects: bleeding, bloody stool, vomiting that looks like coffee grounds, petechiae.
    • Reversal agent: Protamine Sulfate.
    • Can cause Heparin-induced Thrombocytopenia (HIT), an immune response against heparin.

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    Test your knowledge on Long QT syndrome and its association with antiarrythmic drugs. Learn which medications increase the risk of QT prolongation and how to manage acute settings.

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