Cardiac Glycosides Flashcards
Cardiac Glycosides
Digoxin, Digitoxin, Digitalis, Ouabain
Used in CHF and AFib
Digoxin used widely due to short half-life and availability of antidote
Structure of Cardiac Glycosides
Lactone Ring- functional
Steroid Nucleus- functional
Sugar Residues- PK properties affecting absorption, metabolism and half-life
MOA of Digoxin
Inhibits Na/K ATPase which reverses Ca/Na pump
Ca rises in cell and enters SR
Increased contractility at next depolerisation
Effects on Myocardium
Increase force of contraction
Increase cardiac automaticity and excitability
Effects on Conducting System
Slows Heart Rate
Deceases automaticity of AV node
Prolongs refractory period
Increase automaticity of His-Purkinje system
Mechanism of Increased Automaticity/ Excitability
Depolerisation of membrane potential
An increase in slope of phase 4
Effects on Autonomic System
Increase Parasympathetic tone: decrease HR, decrease AV node conduction velocity, increase AV node refractory period
Decrease Sympathetic tone: Augments vagal effects on SA and AV node, counteracts vasoconstriction
Sensitises baroreceptors
Other Effects
Vessels: Vasoconstriction
CNS: Fatigue, drowsiness, confusion
GI: Anorexia, Nausea, Vomiting
Glycoside Interactions
Loop Diuretics and Potassium: In hypokalaemia, Digoxin will be hyperactive- arrhythmia
Calcium: Hypercalcaemia will cause DADs
Chronic Renal Failure: Requires dose adjustment
Digoxin Toxicity and Treatment
Therapeutic Window: 1-2ng/ml to 2.5 ng/ml
Signs and Symptoms are similar to CHF: tachyarrhythmia, Conduction Block, fatigue, nausea
Treatment: Reduce Dose, Antidote, Lignocaine(anti-arrhythmatic)
Phosphodiesterase Inhibitors
Milrinone
Ionodilator
Inhibits degredation of cAMP and cGMP
Long-term use increases risk of mortality
