Electrical properties of the heart Flashcards
things that make cardiac muscle in functional syncytium:
- electrical connections via gap junctions –> passing APs to the neighbouring cells, resulting in them depolarising at more or less the same time.
- physically connected via desmosomes –> prevent the cells from pulling apart from one another during contraction and instead contract together.
*desmosomes interspersed with gap junctions = intercalated discs
differences between skeletal muscles and cardiac muscles
- cardiac muscles in functional syncytium
- AP in skeletal muscle 2 msec while in cardiac muscle 200-250 msec and therefore cannot exhibit tetanic contraction.
- some cells in cardiac muscles called pacemakers have unstable membrane potential and can depolarise easily
similarities between skeletal and cardiac muscles
- made from the same components: actin, myosin, Z-line, surrounded by sarcolemma, invagination called T tubles, have sarcoplasmic reticulum for Ca storage
what makes the AP of cardiac muscle longer and what benefit does this have?
- note that AP and contraction are different things.
- longer because Ca2+ not only comes from sarcoplasmic reticulum but also flows in from outside. Also because Ca2+ does not saturate the troponin and strength of contraction can be purely determined by how much Ca2+ is present
- this means that it also has longer refractory period and therefore does not suffer from tetanus (sustained contraction) unlike skeletal muscles.
describe the depolarisation of normal cardiac cells
- leaky K+ channels are open like and have membrane potential of -90mV like in normal skeletal muscle cells
- cells depolarise when neighbouring cells depolarise and the V gated Na+ channel opens quickly and closes quickly afterwards (strong and short depolarisation)
- this is where normal AP would end, but in cardiac muscle, there is also another set of Ca2+ gated channels called L type channels that open much slower than Na+ gated channels but stay open for much longer, resulting in sustained depolarisation and AP
- during sustained depolarisation, leaky K+ channels permeability would decrease because it would just be a waste of K+ and energy
- during repolarisation, there will be decrease in Ca2+ channels and increase in leaky K+ channels
describe depolarisation in pacemaker cells
- like normal cardiac cells, during depolarisation there would be a decrease in leaky K+ channels
- a funny type of V gated Na+ channels will open (triggered by repolarisation phase of the previous AP)
- increased permeability of Ca2+ channels come later on. This is T type (transient) channels that involves very little Ca2+ can cannot generate AP on its own, only contributes to depolarisation.
- after that, there will be increase in L type V gated Ca2+ channels, this is the main contribution to AP
*since AP is mainly due to L type Ca2+ channels and not Na+, it takes much slower to rise to threshold than normal cardiac cells, but the threshold is lower.
modulators of electrical activity:
- para/sympathetic NS
- drugs: Ca channel blockers reduces the amount of open Ca channels –> weak contraction, cardiac glycosides increases amount of Ca being released –> increased contraction
- temperature: increased in 1 C increases by 20 bpm
- hyperkalemia (excess K+): will depolarise the cells towards threshold –> fibrillation and heart block
- hypkalemia: will hyperpolarise a little in the beginning and then return to depolarisation –> fibrillation and heart block
- hypercalcemia: more Ca flowing when channel opens –> increased contraction and HR
- hypocalcemia: less concentration gradient –> decreased contraction and HR
when do pacemaker cells and normal cardiac cells depolarise?
pacemaker: when threshold is reached
normal cells: when neighbouring cells do
how does signal pass from atrium to venticles?
Sinoatrial node (in right atrium), transmission 0.5m/sec –> atrioventricular node (this is the only connection, the rest are blocked by annulus fibrosus), transmission 0.05m/sec–> Bundle of his –> right and left bundle branches –> purkinje fibers, transmission 5m/sec
- all of the above are cardiac muscle fibers except annulus fibrosus
- quick transmission of SA node and purkinje fibers makes all of the RA and ventricles contract at the same time, but the slower transmission of the atrioventricular node means that atrium and ventricle contracts at different times.
what does an ECG tell you?
- disorders of electrical conduction in the heart
2. the rhythm
first, second, third degree heart block
1st degree: electrical impulses move slower than normal but each signal still conducted (lengthened P interval but QRS present)
2nd degree:
- type I: electrical signal goes slower and slower until the heart skips a beat (progressively lengthening P interval and a drop in QRS complex, then start over)
- type II: some electrical signals do not reach the ventricles and there are random drops in QRS
3rd degree: no electrical signal sent, ventricles beat steadily from specialised pacemakers in the ventricles but is completely out of sync with atrium
atrial flutter, atrial fibrillation, ventricular fibrillation
atrial flutter: no prob with electrical conduction, but atrial depo happens right after ventricular repo, conduction happening too quickly (P wave sitting almost on top of the previous T wave)
AF: no atrial contraction and random and uncoordinated ventricular depo (no P waves detected, random QRS)
ventricular fibrillation: no ventricular depo (no QRS complex, the heart is quivering but not pumping)
treatment of fibrillation?
defibrillator:
gives current that will depolarise all of the cells in the heart and make it enter refractory period at the same time and start everything over again normally.
