Lecture 19 Flashcards
(20 cards)
Difference between LV and RV
Wall of LV much thicker than RV as distance that it takes for blood to travel from heart to lungs is less than from heart to rest of body. More force generated by LV
Cardiac muscle cells
Myocardiac contractile and autorhythmic cells. Both excitatory. Autorhythmic don’t contain many contractile fibres and no sarcomeres as they are involved in generating electrical current, not contraction. CM has intercalated discs which have desmosomes (force conduction can initiate contraction in adjacent cells) and gap junctions (ion channels that allows the conduction of APs to continue along the tissue) which allows the heart cells to beat in unison.
Autorhythmic cells
Generate own AP without innervation from NS therfore AKA pacemaker cells. There is no resting membrane potential, they have pacemaker potential which always increases until it reaches the threshold and fires. It has a temporary resting potential (~60mv), but, it drifts upwards. Unstable membrane potential caused by funny channels (IF) which remain open at very - MP. This causes an influx of Na+ = allows increase in MP until ~30mM = IF shut = Ca2+ channels open = Ca2+ influx = depolarisation ~ 60mV and repeat. Pacemaker potential sets heartbeat. If slope of PP increases = increase of AP and vice versa.
Sinoatrial node
Only on RA. Where pacemaker cells are. When they start to fire, AP travels down a network of nerves. When the AP leave SA, it travels down internodal pathways across the atriums and culminate in AV nodes.
Atrial ventricular node
Base of RA near septum.
Bundle of His (AV bundle)
After AV node, reach AVB which travels through septum and up the apex through Purkinje fibres.
Electrical conduction steps
- SA node depolarises, simulating AP to travel down L and R atria causing them to contract.
- AP travels down atria until it reaches AV node where it experiences AV node delay (as atrium contract, you want them to finish before the ventricles contract)
- After delay, AP sent down AV bundle through septum.
- Travels from apex up to Purkinje fibres depolarising the ventricles causing them to contract.
- Cycle begins after ventricles repolarise.
Electrocardiogram (ECG)
Placement of electrodes to pick up electrical activity. Leads are the perspective of electrical activity across the chest. It generates a waveform that generates atrial depolarisation and repolarisation of atrium and ventricles.
Waves
Single repolarisation or depolarisation event (P, QRS and T).
Segment
Period between waves
P wave
atrial depolarisation
PQ/PR segment
Time where AP to AV node and bundle
QRS complex
Ventricles depolarise and atrial repolarisation.
ST segment
Ventricles begin to repolarise
T wave
ventricular repolarisation
Contractile cells
Similar to neurons and skeletal muscle except it is elongated to have a plateau phase. In the heart, you don’t want to compound APs to generate an increase force. Overlap of plateau and muscle tension period = one heartbeat per cell per AP. There are mechanisms that increases force generated by heart, but, that still ensures 1 HB per AP. If this didn’t occur, heard would always be strained muscle contraction state where it wouldn’t fill or eject blood properly.
Contractile cells steps
- AP stimulates contractile cell causing Na+ channels to open (increase charge)
- Instead of quick repolarisation where there’s an influx of K+, fast K+ channels open that causes. immediate decline in charge. This triggers Ca2+ channels to open causing Ca2+ influx which keeps elevating the membrane potential.
- Ca2+ channels close, slow K+ channels open and cell repolarises
refractory period
Elongated period that stimulates contraction in myocardiac contractile cells.
Cardiac cycle
- Late diastole: Heart at rest where heart passively filled with blood
- Atrial systole: SA node fires, causing a small volume of blood to be pushed into the ventricles.
- Isovolumetric ventricular contraction: Ventricles have filled and they begin to contract. As they do, the pressure that builds in ventricles contract but volume doesn’t charge.
- Ventricular ejection: As pressure increases, semilunar valves are forced open allows volume to change and blood to enter pulmonary/systemic circulation.
- Isovolumic ventricular relaxation: Ventricles repolarise, pressure decrease and semilunar valves close but AV valves open. Cycles repeat.
Heart sounds
Result of valve closure where blood hits them. First sound is when AV valve shuts during isovolumeric ventricular contraction and blood slams into it causing turbulent flow (1st heart sound). After ventricular contraction, SL valves shut 2nd heart sound.
