McKenna's Pharmacology for Nursing, 2e

704

P A R T 8  Drugs acting on the cardiovascular system

Sodium level equalises

The risk of bleeding effects of these drugs increases if they are combined with oral anticoagulants; people receiving this combination should be monitored closely and have their anticoagulant dose reduced as needed. Check individual drug monographs for specific inter­ actions associated with each drug. Prototype summary: Lignocaine Indications: Management of acute ventricular arrhythmias during cardiac surgery or MI. Actions: Decreases depolarisation, decreasing automaticity of the ventricular cells; increases ventricular fibrillation threshold. Pharmacokinetics: Route Onset Peak Duration IM 5–10 mins 5–15 mins 2 hours IV Immediate Immediate 10–20 mins T 1/2 : 10 minutes, then 1.5 to 3 hours; metabolised in the liver and excreted in urine. Adverse effects: Dizziness, light-headedness, fatigue, arrhythmias, cardiac arrest, nausea, vomiting, anaphylactoid reactions, hypotension, vasodilation. ■■ Antiarrhythmics are drugs that alter the action potential of the heart cells and interrupt arrhythmias. The CAST study found that the long-term treatment of arrhythmias may actually cause cardiac death, so these drugs are now indicated only for the short-term treatment of potentially life-threatening ventricular arrhythmias. ■■ Class I antiarrhythmics block sodium channels, depress phase 0 of the action potential and generally prolong the action potential, leading to a slowing of conduction and automaticity. ■■ Class I antiarrhythmics are membrane stabilisers; the adverse effects seen are related to the stabilisation of cell membranes, including those in the CNS and the GI tract. C lass II antiarrhythmics The class II antiarrhythmics are beta-adrenergic blockers that block beta-receptors, causing a depression of phase 4 of the action potential (Figure 45.7). Several beta- adrenergic blockers, such as esmolol ( Brevibloc ) and pro- pranolol ( Deralin , Inderal ), are used as antiarrhythmics. Therapeutic actions and indications The class II antiarrhythmics competitively block beta- receptor sites in the heart and kidneys. The result is a KEY POINTS

Effects of Class Ic antiarrhythmics: markedly slow phase 0 Effects of Class Ia antiarrhythmics: block sodium channels Sodium and potassium leave cell

phase 1

phase 2

0 –20 +20

Calcium enters cell

phase 3

phase 0

Sodium enters cell

phase 4

–80 –100

Effects of Class Ib antiarrhythmics: slower phase 0 of action potential, rapid repolarisation

Resting membrane potential

FIGURE 45.6  The cardiac action potentials, showing the effects of class Ia, Ib and Ic antiarrhythmics.

breastfeeding. Another method of feeding the baby should be chosen. Adverse effects The adverse effects of the class I antiarrhythmics are associated with their membrane-stabilising effects and effects on action potentials. Central nervous system (CNS) effects can include dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech, vision changes and tremors that can progress to convulsions. GI symptoms include changes in taste, nausea and vomiting. Cardiovascular effects include the proarrhyth- mic effects that lead to the development of arrhythmias (including heart blocks), hypotension, vasodilation and the potential for cardiac arrest. Respiratory depression progressing to respiratory arrest can also occur. Other adverse effects include rash, hypersensitivity reactions, loss of hair and potential bone marrow depression. Flecainide is a class Ic drug that was found to increase the risk of death in the CAST study. Clinically important drug–drug interactions Several drug–drug interactions have been reported with these agents, so the possibility of an interaction should always be considered before any drug is added to a regimen containing an antiarrhythmic. The risk for arrhythmia increases if these agents are combined with other drugs that are known to cause arrhythmias, such as digoxin and the beta-blockers. Because quinidine competes for renal transport sites with digoxin, the combination of these two drugs can lead to increased digoxin levels and digoxin toxicity. If these drugs are used in combination, the person’s plasma digoxin level should be monitored and appro- priate dose adjustment made. Serum levels and toxicity of the class Ia antiarrhythmics increase if they are combined with cimetidine; extreme caution should be used if people are receiving this combination.