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
Unipolar leads
- Single recording electrode placed on body
- 3 augmented unipolar limb leads in same locations as bipolar leads: left arm, right arm and left leg
- Chest leads: 6 electrodes placed on surface of chest (V1-V6)
- 12-lead ECG
- Bipolar + unipolar leads are recorded simultaneously
Normal variations in mean electrical axis
Short/stocky people < 60 degrees
Long/thin people > 60 degrees.
Is an ECG wave generated when the ventricles are fully depolarised
No as all myocardial cells are depolarised and there’s no flow of current
What conduct electrical activity to skin surface in ECG
Tissue fluids
