Electrical Activation Of Heart Flashcards
Describe features of the membrane of heart muscle cell?
Normally only permeable to K+
Potential determined only by ions that can cross membrane
Explain negative membrane potential in the heart
K+ ions diffuse outwards (high to low conc)
Anions cannot follow
Excess of anions inside the cell
Generates negative potential inside the cell
What does the myocyte membrane pump?
IN – K+
OUT – Na+ and Ca2+
Against electrical and concentration gradients
Therefore requires active transport (Na+-K+ pump)
Requires ATP for energy
What happens in Phase 0 of action potential?
Rapid Depolarisation
Due to Na+ inflow
What happens in Phase 1 of action potential?
Partial repolarisation
Due to K+ outflow and Inflow of Na+ stops
What happens in Phase 2 of action potential?
Plateaus
Due to Ca2+ slow inflow
What happens in Phase 3 of action potential?
Repolarisation
Due to K+ outflow
Inflow of Ca2+ stops
What happens in Phase 4 of action potential?
Pacemaker potential
Due to Na+ inflow
Slowing of K+ outflow
What are antiarrhythmic drugs?
Medications that prevent and treat a heart rhythm that’s too fast or irregular.
What is a Ia antiarrythmic drug?
Na+ channel blocker
(Prolong conduction + repolarisation)
E.g. Quinidine,Procainamide,Disopyramide
What is a Ib antiarrythmic drug?
Na+ channel blocker
(No effect on conduction + repolarisation)
E.g. Lignocaine
What is a Ic antiarrythmic drug?
Na+ channel blocker
(Prolong conduction)
E.g. Flecainide
What is a II antiarrythmic drug?
Beta blocker
E.g. Atenolol, Sotalol
What is a III antiarrythmic drug?
K+ channel blocker
Prolong repolarisation
E.g. Amiodarone, Sotalol
What is a IV antiarrythmic drug?
Ca2+ channel blocker
E.g. Verapamil
Compare the contraction of skeletal muscle to cardiac muscle
Contraction of cardiac muscle lasts longer than skeletal muscle
Up to 15 times longer duration
Due to slow calcium channels
Decreased permeability of membrane to potassium after action potential
What happens in propagation of action potential?
Action potential spreads over cell membrane
Positive charge from Na+ affects adjacent cells
Causes depolarisation
Newly depolarised cells also cause depolarisation
Ions can travel directly via gap junctions
Explain the speed in conduction in the heart
Velocity of conduction faster in specialised fibres
Atrial and ventricular muscle fibres: 0.3 to 0.5 m/s
Purkinje Fibers: 4m/s
What is the Sinus Node?
Normally determines the rate the heart beats
Resting membrane potential of -55 to -60 mV
Related to slow Na+ inflow
Gradually drifts towards threshold for discharge
Fast Na+ channels closed (inactivating gate closed)
Action potential driven by slow Ca2+ channels
Explain Automaticity
Sinus node potential drifts towards threshold for discharge
Steeper the drift, faster the pacemaker
Spontaneous discharge rate of heart muscle cells decreases down the heart
What is the AV Node?
- Transmits cardiac impulse between atria and ventricles
- Delays impulse
Allows atria to empty blood into ventricles
Fewer gap junctions
AV fibres are smaller than atrial fibres
What is His-Purkinje System?
- AV node - ventricles
- Rapid conduction
To allow coordinated ventricular contraction
Very large fibres
High permeability at gap junctions
What is the Refractory Period?
- Heart muscle
Refractory to further stimulation during the action potential
Fast Na+ +/- slow Ca2+ channels closed (inactivating gates) - Normal refractory period of ventricle approx 0.25s
Less for atria than for ventricles - Prevents excessively frequent contraction
- Allows adequate time for heart to fill
What is the Relative Refractory Period?
- After absolute refractory period
Some Na+ channels still inactivated
K+ channels still open - Only strong stimuli can cause action potentials
- Affected by heart rate
What is Sympathetic Stimulation?
Increases heart rate (positively chronotropic)
Increases force of contraction (positively inotropic)
Increases cardiac output
Controlled by
Adrenaline and noradrenaline + type 1 beta adrenoreceptors
Increases adenyl cyclase increases cAMP
Increased sympathetic stimulation
Increases heart rate (up to 180-250 bpm)
Increases force of contraction
Large increase in cardiac output (by up to 200%)
Decreased sympathetic stimulation
Decreases heart rate and force of contraction
Decreases cardiac output (by up to 30%)
What is Parasympathetic Stimulation?
Decreases heart rate (negatively chronotropic)
Decreases force of contraction (negatively inotropic)
Increases cardiac output
Controlled by:
Acetylcholine
M2 receptors – inhibit adenyl cyclase reduced cAMP
Increased parasympathetic stimulation
Decreased heart rate (temporary pause or as low as 30-40 bpm)
Decreased force of contraction
Decreased cardiac output (by up to 50%)
Decreased parasympathetic stimulation
Increased heart rate
When do Ryanodine receptors (RyR) open?
When they detect high calcium levels
What effect do drugs have on action potential?
Calcium channel blockers (E.g. Verapamil) prolong the refractory period of cardiac tissues (AV Node)
Other classes of drugs
Potassium channel-blockers (E.g. Amiodarone)
Beta-blockers (E.g. Bisoprolol)
Sodium channel-blockers (E.g. Lignocaine)
What is Long QT Syndrome?
Abnormality of (usually) K+ channel causes loss of function
Slower outward K+ current delays repolarization (hence prolongation of the QT interval)
Delayed repolarization increases the risk of Early Afterdepolarizations (EADs).
What can Long QT Syndrome cause?
Risk of syncope / sudden cardiac death
