P: Contraction & electrical activity Flashcards
Contraction of cardiac muscle
- Requires external stimulation by somatic motor nerves
- Specialized noncontractile myocardial cells, autorhythmic or pacemaker cells are responsible for triggering contraction of cardiac muscle
- Cell membranes spontaneously depolarize + degenerate Aps which spread into surrounding contractile myocardial cells.
Sinoatrial node
- Autorhythmic cells are concentrated in sinoatrial node located in the right atrium near opening of superior vena cava
- Spontaneous depolarizations generated here pass into surrounding myocardial cells and generate contraction:
1. Atrial myocardial cells
2. Pause (fibrous layer)
3. Ventricular myocardial cells
4. Atrial syncytium + ventricular synsytium
Atrial conduction
- Impulses spread through atrial fibres at rate of 1m/sec
- Bachmann’s bundle conduct impulse from right into left atrium
- Impulses then spread to atrioventricular node
Atrioventricular conduction
- AV node is located on base of right atrium near interatrial septum
- Conduction velocity slows to 0.05m/s
- Results in a delay between atrial and ventricular contraction
- Allows optimal ventricular filling during atrial contraction
Ventricular conduction
- AV node conducts to bundle of His, then to the bundle branches
- These subdivide into Purkinje fibres which conduct impulses into both ventricles.
- Conduction in purkinje fibres is 1-4m/s due to their large cell size.
Auto-rhythmic cells
- SA node in right atrium: APs generated spread over entire cardiac tissue
- 2 AV nodes
- 3 pacemakers in Purkinje fibres. Aps generated by SA node will inhibit autorhythmic activity of these cells.
Types of action potential in cardiac tissue
- Fast response: atrial + ventricular myocytes
- Slow response: autorhythmic cells in SA and AV node.
Action potential in myocardial contractile cells
- Arrival of AP at contractile myocardial cell opens Na+ channels
- Voltage-gated Ca2+ channels open slowly
- At +20mV, Na+ channels close and K+ channels open. Repolarization begins.
- Slow inward diffusion of Ca2+ then balances outward diffusion of K+ plateau phase.
- Ca2+ channels close and K+ channels complete repolarization.
Role of calcium during cardiac AP
Inward diffusion of extracellular Ca2+ during depolarization also opens Ca2+ channels on SR
Extracellular Ca2+ is used to initiate contraction in myocardial cells instead of intracellular stores.
Increase in intracellular [Ca2+] triggers contraction in an identical mechanism to skeletal muscle. During repolarization, Ca2+ is transported out of the cell and relaxation occurs.
Myocardial cell contraction
Length of AP in myocardial cell (250ms) is much longer than an AP in a skeletal muscle cell (20msec) due to a plateau phase.
Myocardial cells are refractory during almost their entire contraction.
Summation cannot occur –> tetany is prevented.
Type of Ca2+ channels in cardiac muscle
Predominantly L-type Ca2+ channels
Ca2+ channel antagonists
Verapamil + diltiazem decrease duration of action potential + contractility of myocardial cells.
Slow response action potential
- Generated spontaneously in pacemaker cells
- Resting memory potential during phase 4 is less negative and is unstable
- Depolarization ( phase 0) is not as large or rapid
- Early repolarization (phase 1) is not apparent and plateau phase (phase 2) is less prolonged and not as flat.
Myocardial autorhythmic cells
- Membrane potential is unstable due to slow Na+ and Ca2+ channels which open at -60mV
- Slow drift In Vm from -60 to -50mV
- At -50mV (threshold) fast Ca2+ and Na+ channels open, spontaneous membrane depolarization occurs
- K+ channels open and membrane repolarization occurs.
Refractory period
- Na+ channels (fast response) and Ca2+ channels (slow response) inactivate when cell is depolarized so no further AP can be generated and there is an effective refractory period
- These channels revert to a closed state as cell is repolarizing (phase 3) and are fully closed in phase 4: cell is now fully excitable
- Pacemaker cells have a prolonged refractory period and also have post-repolarization refractoriness.
P wave
atrial depolarization
QRS wave
ventricular depolarization
T wave
ventricular repolarization
P-Q (P-R) interval
0.16 sec. Indicative of delay in conduction of impulse into ventricles
Q-T interval
0.35 seconds. Duration of ventricular contraction
R-R interval
Duration between 2 consecutive R waves (0.83 sec)
Principles of ECGs
- Depolarization wave enters ventricles via septum + spreads towards apex
- For almost entire ventricular depolarization electrical current flows from depolarized area to polarized area in large circuitous routes
- Heart electrical currents have vector properties
- Normally orientation of cardiac vector during QRS is +60 degrees from horizontal plane.
How to set up ECGs
- Measured using bipolar limb leads
- One positive and one negative recording electrode placed at each side of heart on limbs
- Reference electrode placed on left leg
- Connected via wires to ECG forming a complete circuit.
Einthoven’s triangle
- If direction of cardiac vector is towards +ve electrode: upward deflection on ECG
- If direction of cardiac vector is parallel to direction of lead: maximum deflection
- Magnitude of QRS is largest in lead II if cardiac vector is parallel to lead II
