Cardiac muscle cells contract spontaneously, independently, regularly and continuously. Autorhythmic fibres generate action potentials that trigger heart contractions repeatedly, acting as the natural pacemaker of the heart throughout the electrical activity of the heart.
SA Node a.k.a. Sinoatrial Node is the pacemaker of the heart, exactly where cardiac excitation begins. It fires 60-100 electrical impulses per minute (approx. one every 0.8 secs). The SA Node cells DEPOLARISE repeatedly to threshold spontaneously; SPONTANEOUS DEPOLARISATION = PACEMAKER POTENTIAL.
AV Node a.k.a. gatekeeper of the heart acts as an electrical gateway to the ventricles. It fires 40-60 electrical impulses per minute (approx. one every 0.5 secs), evidently having slowed down due to having thinner myocytes with fewer gap junctions over which signals are transmitted. This delay allows the ventricles to fill up with blood before contracting.
The Bundle of His a.k.a. AV Bundle is where action potentials can conduct from the atria to the ventricles, entering both the right and left bundle branches.
Here the Purkinje Fibres conduct the action potential from the apex of the heart up to the rest of they ventricular myocardium, causing the ventricles to contract at the fastest speed of the whole conduction system (4m/s), pushing blood towards the semilunar valves.
Ventricular Myocyte Action Potential
Cardiac myocytes have a stable resting membrane potential of -90mV, depolarising only when stimulated. Ventricular Myocytes’ action potential has 3 phases:
DEPOLARIZATION – a stimulus opens voltage-gated Na+ channels, causing depolarisation as they enter the cells. The threshold voltage opens additional Na+ channels triggering a positive feedback cycle, peaking at almost +30mV. In response the Na+ channels close abruptly, causing the rising phase of the action potential to be very short.
PLATEAU – here is where depolarisation is maintained while the myocytes contract. Voltage-gated slow Ca2+ channels open up allowing small amounts of Ca2+ ions from within the ECF to enter the myocytes. With the binding action of Ca2+ ions to the ligand-gated Ca2+ channels on the sarcoplasmic reticulum, more channels open allowing more Ca2+ ions into the cytoplasm, which then bind to troponin, causing the ventricular myocyte to contract by the stimulus. Finally Ca2+ channels close and K+ channels reopen, causing K+ ions to difuse out of the cell and the Ca2+ ions to return to the ECF.
REPOLARIZATION – The negative resting membrane potential is now restored to -90mV.
Baroreceptors in the Cardiovascular Centre
Baroreceptors are found in the aorta and the internal carotid arteries.
Increase in HR = Increase in CO = Increase in BP = Baroreceptors sense changes & signal to the cardiac centre = cardiac centre Decreases HR.
Decrease in HR = Decrease in CO = Decrease in BP = Baroreceptors sense changes & signal to the cardiac centre = cardiac centre Increases HR & re-stabilises CO & BP.
Chemoreceptors in the Cardiovascular Centre
Chemoreceptors are found in the aortic arch, carotid arteries and the medulla oblongata. These are sensitive to blood pH, Carbon Dioxide and Oxygen.
Chemoreceptors can sense Hypercapnia and Acidosis, which then stimulate the cardiac centre, increasing the HR and restores perfusion of the tissues. Accumulated Carbon Dioxide is then removed.
In response to Hypoxaemia, chemoreceptors lead to a slowing down of the HR.
Below you can find a collection of videos that can help provide a more visual approach to the electrical activity of the heart.
Electrical Activity of the Heart
Ventricular Myocyte Action Potential
Regulation of the Heart Activity Through the ans (autonomic nervous system)
Heart Activity Regulation
role of the cardiovascular centre
baroreceptor reflex
baroreceptor reflex animation
baroreceptors and blood pressure
chemoreceptors
Special thanks to the creators of the featured videos on this post, specifically Youtube Channels Registered Nurse RN, Khan Academy Medicine, DrBruce Forciea, PhysioPathoPharmaco, Khan Academy and Alila Medical Media.
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