cardiac action potentials and contraction excitation coupling Flashcards
what are the three pacemakers of the heart and its corresponding frequencies
- primary pacemaker SAN (100/min)
- secondary pacemaker AVN (40-60/min)
- tertiary pacemaker purkinje fibres (20-30/min)
what is the structure of the action potential in the SAN
- phase 4- resting phase slight increase in membrane potential
- phase 0 depolarisation phase
- phase 3 repolarisation phase
what are the main ionic currents in each phase of the action potential in the SAN
- phase 4 includes I_funny (slow na channel), I_CaL and I_CaT and acetylcholine sensitive potassium channels
- phase 0- I_CaL
- phase 3- I_Ks and I_Kr (delayed rectifier potassium channels)
what is the structure of an action potential in the ventricular myocardium
- phase 4 (resting phase is stable)
- phase 0- depolarisation
- phase 1- slight depolarisation
- phase 2- plateau phase
- phase 3- repolarisation
what is the different ionic currents involved in each phase of the ventricular myocardium action potential
- phase 4- I_Ki (inward rectifier pottasium channels), leaky pottasium channels and Na/K Atpase
- phase 0- I_Na
- phase 1- closing of I_Na and I_to (pottasium)
- phase 2- I_CaL and I_Kr/I_Ks (delayed rectifier pottasium channels)
- phase 3- I_Kr I_Ks
compare and contrast the two action potentials in the SAN and ventricle
- SAN is spontaneous and slow
- ventricle is induced and fast
what is the starting membrane potential of a SAN action potential
-65/-60
what is the resting membrane potential of a ventricular action potential
- 90
how is the frequency of the action potential in the SAN regulated
- change threshold potential
- change resting potential
- change slope of depolarisation (phase 4)
what is the excitation-contraction coupling
- action potential leads to opening of calcium voltage gated channels (I_CaL)
- this causes the ryanodine receptors in the sarcoplasmic reticulum to open allowing flow of calcium from its store to the sarcoplasmic reticulum
- this increase in calcium thus leads to contraction
what happens when the calcium ions are re pumped in the sarcoplasmic reticulum and also out of the cell
- muscle relaxation
- repolarisation
what is the refractory period and what can it be divided into
- absolute refractory period- action potential can not be triggered no matter how strong the stimuli is
- relative refractory period- action potential most likely would not be triggered, needs a very strong stimuli to trigger one, new action potential would have a low amplitude
what is the characteristic of cardiac muscle
- striated
- sarcomeres made of actin and myosin making a banding pattern
- during contraction sarcomere decrease in lengthen
- nuclei in centre of cell with one per cell
- interrelated discs are sites of attachments between cells
how does calcium ions cause muscle contraction
- myosin binding site on actin is blocked by troponin
- troponin has 3 structures a calcium binding site, a site blocking the myosin binding site and a structural domain
- binding of calcium causes a conformational change in shape resulting in the myosin binding site to be exposed
where are the sources of calcium
- intracellular from sarcoplasmic reticulum
- extracellular sarcolemma
how does an action potential cause muscle contraction
- action potential goes along the t tubule of the muscle
- causes calcium voltage gated L channels to open
- causes calcium influx into myocyte
- causes the ryanodine receptors to open which allows influx of calcium into sarcoplasm from the sarcoplasmic reticulum
- this causes binding of calcium to troponin which results in muscle contraction
what happens during muscle relaxation
- Ca ATPase found in membrane of sarcolema which pump out calcium ions from the cell
- Ca/Na exchanger- 3 sodium ions into cell, one calcium ion out of cell
- Ca2+ pump in membrane of sarcoplasmic reticulum to pump calcium back into its store
how does parasympathetic nervous system decrease heart rate
- parasympathetic NS releases Ach which binds to M2 muscarinic (Gi receptors)
- inhibition of adenylate cyclase and decreased levels of cAMP
- reduced protein kinase activity less activation of I_funny and I_Ca currents
- activation of M2 receptors also directly activate acetylcholine sensitive pottasium channels
- this results in hyperpolarisation making it longer to reach the action potential threshold thus reducing heart rate
how does sympathetic activation lead to increased heart rate
- release of noradrenaline from sympathetic fibres derived from paravertebral of sympathetic trunk
- binds to B1 adrenergic receptors in SAN- increased adenylate cyclase activity- increased cAMP
- activation of phosphokinase A, phosphorylates I_funny and I_Ca channels
- more influx of sodium and calcium into cells during phase 4 and action potential threshold met quicker
how does sympathetic innervation cause increased contractility of the heart
- noradrenaline binds to B1 receptors in myocardium
- activation of adenylate cyclase= increased cAMP+activation of phosphokinase A
- phosphorylates calcium L channels and ryanodine receptors causing more calcium to enter sarcoplasm of cell
- increased contractility
- calcium influx also results extended plateau phase of phase 2 meaning contraction happens longer
- PKA deinhibtis phospholamban meaning more calcium is uptake by Ca pump into their store during relaxation
what is channelopathies
- mutations in ion channels (mostly K and Na) responsible for AP generation
- usually no apparent problem but is responsible for 85% of sudden death syndrome (unexpected cardiac arrest in seemingly healthy individuals due to underlying cardiac arrhythmias)
what is long QT syndrome
- due to channelopathies
- mutation in sodium channel
what is idiopathic ventricular fibrillation
- ventricular fibrillation in patients with no underlying heart condition or genetic condition
what is the effect of calcium channel inhibition on hear Tate and contractility
- decreased frequency
- reduced contraction
what are the three effect of antihypertensive and antiarrhythmic drugs
- inhibit spontaneous AP generation- reduced frequency
- inhibit ventricular contraction- reduced cardiac output and cardiac work
- vasodilation- decrease in bp
action potentials arising from the relative refractory period can cause what type of condition
arrhythmias
how does an ECG work
- galvanometer
- measures potential changes on surface of heart which is measured by electrolytes
