P: Cardiac muscle electrical activity Flashcards
What’s the speed of atrial conduction?
1 m/sec
What conducts the impulse from right to left atrium?
Specialized fibres known as Bachmann’s bundle
Where do impulses spread at the end of atrial conduction?
AV node (only route of conduction from atria to ventricles)
What’s the speed of atrioventricular conduction and why?
0.05 m/sec
Delay between atrial and ventricular excitation/contraction allows optimal ventricular filling during atrial conduction
What’s the speed of ventricular conduction in Purkinje fibres and why?
1-4 m/sec due to large cell size of Purkinje fibres compared to myocytes
Explain route of ventricular conduction
Av node conducts to the bundle of His, then to bundle branches –> branches subdivide into the Purkinje fibres –> conduct impulses into ventricles
Locations of autorhythmic cells? When is AP generated + speed in each?
- SA node: APs generated here spread over entire cardiac tissue. 70-80 APs/min
- AV node: only generated if SA node is destroyed. 40-60 APs/min
- Purkinje fibres: APs generated by SA node inhibit their autorhythmic activity. 30-40 APs/min
Types of cardiac APs and cells associated
Fast: myocytes in atria and ventricles
Slow: autorhythmic cells in SA and AV node
Phases of cardiac AP
0: Upstroke
1: Early repolarization (only in fast response)
2: Plateau
3: Repolarization
4: Final repolarization
Steps of AP in myocardial contractile cells
- Arrival of AP at a contractile myocardial cell opens voltage-gated Na+ channels (upstroke/rapid depolarization)
- Voltage-gated Ca2+ open more slowly
- +20 mV: Na+ channels close, K+ channels open –> repolarization begins (early repolarization)
- Slow inward diffusion of Ca2+ balances outward diffusion of K+ (plateau)
- Ca+ channels close and K+ channels complete repolarization (repolarization + final repolarization)
What does inward diffusion of extracellular Ca2+ allow?
It opens Ca2+ channels on SR and is used to initiate contraction in myocardial cells rather than intracellular stores
What happens to Ca2+ during repolarization?
It’s transported out of the cell –> relaxation
What does increase in intracellular Ca2+ trigger?
Triggers contraction in an identical mechanism to skeletal muscle
How is myocardial cell contraction different to skeletal cell contraction?
- Length of AP in myocardial cell (250 msec) is much longer than in skeletal muscle (20 msec) due to plateau phase
- Myocardial: duration of AP is almost as long as associated contraction (skeletal: cell repolarised before contraction begins)
- Myocardial cells are refractory during almost entirety of contraction –> summation and tetany can’t occur in cardiac muscle
Predominant type of Ca2+ channels
L-type (long-lasting)
T/F: quantity of Ca2+ has no effect on strength of contraction
False: greater the influx of Ca2+ = stronger contraction
2 examples of Ca2+ channel antagonists and their function
Diltiazem and Verapamil: Decrease duration of AP and diminish contractility of myocardial cells
(DVD –> Diltiazem Verapamil: Decrease)
How is slow response AP different from fast response AP?
Slow:
- Generated spontaneously in pacemaker cells because resting membrane potential in phase 4 is less negative and unstable
- Depolarization (phase 0) is not as large or as rapid
- Early repolarisation (phase 1) is not apparent
- Plateau (phase 2) less prolonged and less flat
Explain myocardial autorhythmic cells AP with Vm values
- Membrane potential (Vm) is unstable due to slow Na+ and Ca2+ channels (HCN) which open at -60 mV
- Slow drift in Vm from -60 to -50 mV
- At -50 mV (threshold): fast Ca2+ and Na+ channels open –> spontaneous depolarization (AP is generated)
- K+ channels open –> repolarization
What happens during effective refractory period in fast and slow response?
Na+ channels (fast response) and Ca2+ channels (slow response) inactivate when cell is depolarized –> no AP can be generated –> effective refractory period
What happens during relative refractive period?
Na+ channels (fast response) and Ca2+ channels (slow response) go back to a closed/activatable state as the cell is repolarizing (phase 3) and fully closed in phase 4 –> cell is fully excitable
Pacemaker cells have a prolonged … and also have …
relative refractory period
post-repolarization refractoriness
Name and describe the waves on ECG
P: atrial depolarization
QRS: ventricular depolarization
T: ventricular repolarization
(atrial repolarization wave obscured by QRS complex)
Give the time of P-Q (P-R), Q-T and R-R intervals
P-Q (P-R): 0.16 sec (delay in conduction of impulse into ventricles)
Q-T: 0.35 sec (ventricular contraction)
R-R: 0.83 sec (72 bpm)
What does ECG measure?
Overall electricity activity in the heart (NOT individual APs)
When is QRS wave generated?
When ventricles are partially depolarized –> flow of current and QRS wave generated
From where to where does the electricle current flow in the heart?
From depolarized area (base) to polarized area (apex)
What is the mean electrical axis of the heart?
Orientation of cardiac vector during QRS is normally +60° from horizontal plane
Where is the reference electrode placed?
Left leg
What are the bipolar limb leads and where are they located? Give name of the triangle
Einthoven’s triangle:
Lead 1: right arm (-) to left arm (+)
Lead 2: right arm (-) to left leg (+)
Lead 3: left arm (-) to left leg (+)
What happens if direction of cardiac vector is:
- towards positive electrode
- parallel to direction of lead
- upward deflection of ECG
- maximum deflection
What are the 12 leads in 12-lead ECG?
- 3 bipolar limb leads
- 3 unipolar limb leads
- 6 chest leads
Where does the axis shift in heart hypertrophy?
Towards hypertrophied side
Name these cardiac arrhythmias and what causes them?
Sinus tachycardia = increase in heart rate
Sinus bradycardia = reduction in heart rate
Name these and what causes them
