Module 5 Section 3 Flashcards
Describe the cardiac conduction system.
IMPORTANT
Autorhythmic cells are localized in very specific regions of the heart.
Sinoatrial (SA) node
- Is a very small area located in the right atrial wall near the opning of the superior venae cavae.
- The autorhythmic cells in the SA node have the fastest rate of depolarization (they reach threshold fastest).
- These cells are considered the pacemaker cells of the heart b/c they control HR and keep it at ~70-80 BPM.
- Once an action potential is generated in these cells, it conducts through the rest of the cardiac conduction system, overriding the pacemaker activity of other autorhythmic cells.
- SA node -> LA and SA node -> AV node -> AV bundle -> down the interventricular septum -> separates on the R and L bundle branches -> purkinje fibres REPEAT
Atrioventricular (AV) node
- Is a small area located in the RA where the RA and RV come together.
- Note: it’s often described as being located in the interatrial septum due to its location in the centre of the heart.
Bundle of His
- Consists of specialized cells that arise from the AV node.
- It divides into 2 buncle branches that travel down each side of the septum to the bottom of the heart where they curve around and travel back towards the atria.
Purkinje fibres
- Are small fibres that branch off the bundle of His and spread along the inner (endocardial) surface of the ventricles.
Describe the cardiac action potential and its underlying currents.
Cardiac action potentials look differently compared to nerve cells and pacemaker cells of the SA node. The differences are caused by the different kinds of voltage-gated ion channels found in ventricular muscle cells.
The resting membrane potential (RMP) for a cardiac myocyte (muscle cell) is ~80 mV. These cells have no pacemaker currents, so the RMP remains steady until the cell is excited.
The 3 stages include:
1) When a cardiac myocyte is excited and reaches threshold, voltage-gated Na channels open and the membrane potential rapidly depolarizes towards +50 mV
2) The rapid depolarization activates a transient outward K channel that rapidly moves K out of the cell to counteract the influx of Na. It also activates L-type Ca channels and what is called delayed rectifying K channel. These currents create a balance of the membrane potential where it is neither depolarizing nor repolarizing. It becomes what’s called the plate potential.
3) Eventually, the transient outward K and L-type Ca currents inactivate the outward K movement through the delayed rectifier allows the cell to hyperpolarize and reach its resting membrane potential once again.
Refractory period: the period during which a cardiac myocyte can’t be re-stimulated. It’s a safety mechanism that prevents twitch summation (can be life-threatening).
Explain excitation-contraction (EC) coupling.
It’s the process by which an action potential triggers a myocyte to contract. Cardiac myocytes also have a well-defined T-tubule system that allows for the spread of excitation and an increase of intracellular Ca necessary for contraction.
Steps on how a myocyte is activated to initiate contraction: action potential in cardiac contractile cell -> release of Ca -> [interaction w/ contractile apparatus OR interact w/ the contractile apparatus] -> contraction
Large release of Ca from SR:
Action potential in cardiac contractile cell:
- During the plateau phase of the action potential, L-type Ca channels, located within the T-tubules, open.
Release of Ca:
- The opening of L-type Ca channels allow Ca to enter the cell.
Interaction w/ contractile apparatus:
- The Ca can directly interact w/ the contractile apparatus.
Large release of Ca from SR:
- The release of Ca can interact w/ the SR membrane which activates them and triggers an additional large release of Ca from internal stores. This process = Ca-induced Ca-release (CICR)
Contraction
- The influx of Ca initiates cardiac muscle contraction. When Ca is removed from the cytosol, either by moving it across the plasma membrane of pumping it back into the SR, contraction ends.
Explain what electrical activity occurs to result in the lead II ECG trace.
Generally, depolarization = upward (positive) deflection and repolarizations are the opposite.
1) Initiation of a heart beat = firing of the SA node. Size and electrical activity of SA node is too small to be detected at the body’s surface. However, the SA node does trigger both of the atria to undergo excitation and their depolarization is observed as the P wave.
2) While the atria are depolarized, there’s no net movement of charge so the ECG remains flat until the AV node delay occurs. After this delay, the wave of excitation -> down the bundle of His and purkinje fibres to depolarize the ventricles. This current = QRS complex.
3) While the ventricles are depolarized, there is no net current. This, ECG = flat until ventricles repolarize (depicted by the T wave). Once they have repolarized, there is no net current again until the SA node fires again to start the process again.
4) Cardiac abnormalities tend to present themselves as changes in these segments:
• PR segment = AV node delay
• ST segment = time during which ventricles are contracting and emptying
• TP interval = time during which ventricles are relaxing and filling
• QT segment = electrical depolarization and repolarization of the ventricles
5) The muscle mass of the ventricles is much greater than the atria and the atria repolarize while the ventricles are depolarizing, so atrial repolarization is lost in the summation of the electrical activity.
Explained in another way
- Signal spreads across both atria, causing the muscle cells to depolarize contract, which creates atrial systole (P wave).
• PR segment: a flat line following the P wave.
- Signal enters the AV node then bundle of His
- Signal spreads to the bundle branches
- Signal goes to Purkinje fibres along the ventricle walls. The contractole fibres in the ventricles depolarize and contract very rapidly, inducing ventricular systole
~ QRS complex represents this rapid ventricular depolarization. Atrial activity is hidden by this complex
- As signal passes out of the ventricles, the ventricular walls start to relax & recover (ventricular diastole)
• The dome-shaped T-wave makrs this ventricular repolarization
- REPEAT
Nervous system input can modify the electrical activity of the heart in a few ways. Name a few situations when the SNS or PNS could affect heart rate
Physical and emotional stress can cause changes in the heart rate. This stress can be due to exercise, fear, injury and even illness. Exercise increases HR to bring additional blood and O2 to working muscles to rid them of CO2 and other waste.
Fear increases HR due to the “fight or flight” response which releases Epi from the adrenal glands. Epi stimulates the SNS and raises the HR.
Illness and injury cause an increase in blood flow to peripheral tissues, which increases HR via the SNS.
What do you think would happen if the ventricles contracted out of sync?
If the RV and LV contract at different times, such as is the case with a buncle branch block (a block in one of the branches of the bundle of His), the blood pumping to the lungs to be oxygenated, and the blood pumping through the aorta would occur at different times. These blocks can cause unnecessary stress on the ventricular walls and my require a pacemaker to re-coordinate the contraction of the ventricles.
Alone, these blocks are generally not dangerous, however, they can be a symptom of a much greater problem such as heart failure, a valve problem, lung disease, etc.
Even though the electrical signal moves from the SA node to the AV node very quickly, the rate of conduction slows down through the AV node (AV nodal delay). What do you think is the purpose of this delay?
Its purpose is to make sure that the atria has had a chance to contract prior to the ventricles. This maximizes the atrial emptying of blood into the ventricles.
What are autorhythmic cells? How are they activated?
Autorhythmic: specialized cardiac muscle cells that can generate action potentials.
These cells contain ion channels that cause the membrane potential to slowly depolarizes until the threshold potential is reached and an action potential is fired.
Autorhythmic cells contain (If) channels and when these channels are activated, both Na and K enter the cell, resulting in a depolarization of the membrane potential. Activation may be due to the hyperpolarization-activated cyclic nucleotide-gated channel (HCN) family or, possibly, that a type of Ca channel (T-type Ca channel) is involved).
The upstroke of the action potential is due to another type of Ca channel, the L-type Ca channel, instead of Na channels as seen in neurons and cardiac contractile cells.
Match each component of an ECG recording to match its corresponding cardiac event.
- PR segment
- ST segment
- T wave
- P wave
- QRS complex
- TP interval
- QT interval
1) ___: ventricular repolarization
2) ___: atrial depolarization
3) ___: time during which ventricles are relaxing and filling
4) ___: time during which ventricles are contracting and emptying
5) ___: ventricular depolarization (atria repolarizing simultaneously)
6) ___: AV nodal delay
7) ___: electrical depolarization and repolarization of the ventricles
1) T wave: ventricular repolarization
2) P wave: atrial depolarization
3) TP interval: time during which ventricles are relaxing and filling
4) ST segment: time during which ventricles are contracting and emptying
5) QRS complex: ventricular depolarization (atria repolarizing simultaneously)
6) PR segment: AV nodal delay
7) QT interval: electrical depolarization and repolarization of the ventricles
