Session 7 Flashcards
What does initial polarisation in ventricular cells cause?
Voltage gated sodium channels open and depolarise the membrane rapidly
What occurs after immediately depolarisation of a ventricular cell?
- Outward flow of potassium causes brief repolarisation
Why is there a delay in repolarisation of ventricular cells?
Voltage gated calcium channels take time to activate so the repolarisation is delayed
What does initial influx of calcium into a ventricular cells due to the opening of voltage gated calcium channels cause?
- Further calcium is released from cellular stores in the mitochondria and SR
- Calcium causes contraction of the ventricular cells, producing contraction
What repolarises ventricular cells to their resting membrane potential?
Potassium efflux from the cell
Why is the membrane potential of pacemaker cells persistently less negative than the membrane potential of ventricular muscle cells?
To ensure fast sodium channels remain inactivated
What is the funny current in pacemaker cells?
Spontaneous, gradual depolarisation caused by the movement of sodium ions through slow sodium channels which open during repolarisation when potential reaches its most negative values
What occurs in pacemaker cells when the cell reaches threshold voltage?
Calcium channels open to create a relatively slow depolarisation
How do pacemaker cells repolarise?
After calcium channels close, potassium efflux repolarises the cell
What happens to the membrane potential changes in pacemaker cells if heart rate increases?
Interval between contractions, and therefore depolarisations, shortens so the funny current becomes steeper
What effect does activating baroreceptors have on the membrane changes in pacemaker cells?
If stretch sensitive baroreceptors are activated (due to increased arterial blood pressure) they send signals to the medulla oblongata to increase parasympathetic innervation to the heart so the funny current becomes shallower and heart rate slows
What can cause cardiac arrhythmias?
- Ectopic pacemaker activity
- Abnormal depolarisations following an action potential (after-depolarisations)
- Re-entry loop
What causes ectopic pacemaker activity?
Damaged areas of myocardium can become spontaneously active when depolarised so a latent pacemaker region is activated and dominates over the SA node causing abnormal pacemaker activity
What causes after-depolarisations?
High intracellular calcium levels
What causes a re-entry loop in the heart?
Damaged area of the myocardium prevents normal spread of excitation so there is a delay in conduction
What are class 1 anti-arrhythmic drugs?
Voltage gated sodium channel blockers: blocks sodium channels that are open or inactive and rapidly dissociates so normal firing isn’t prevented, only over-firing is prevented
Give an example of a type 1 anti-arrhythmic drug
Lidocaine
What is a class 2 anti-arrhythmic drug?
Beta-receptor antagonist: blocks sympathetic action by acting on beta1 receptors so funny current slope is decreased and inotrophy is decreased
Give an example of a type 2 anti-arrhythmic drug
Propranolol or atenolol
Why are type 2 anti-arrhythmic drugs used after a MI?
To combat increases in sympathetic activity and reduce oxygen demand of the heart
What are type 3 anti-arrhythmic drugs?
Drugs which block potassium channels: prolongs the action potential and lengthens the absolute refractory period so further action potentials are delayed
Why are type 3 anti-arrhythmic drugs not generally used?
They can also be pro-arrhythmic
What are class 4 anti-arrhythmic drugs?
Drugs which block calcium channels: decreases the slope of the funny current at the SA node; decreases AV node conduction and decreases force of contraction of the heart. Also causes some coronary and peripheral vasodilation
Give an example of a class 4 anti-arrhythmic drug
Verapamil
