Lecture 1- Cardiac cycle Flashcards
Core information from lecture (42 cards)
Describe Aortic pressure during the cardiac cycle
- Low (80mmHg) when aortic valve open
- Peaks during ejection and then lowers
- Aortic valve closes and slowly returns to normal
Describe atrial pressure during CC
- Increases in atrial systole
2. .decreases in ejection
Describe ventricular pressure in CC
- slightly increases in atrial systole
- Rapid increase ub usivolumetric contraction
- Peaks at ejection and decreases rapidly when AV valves close
Describe ventricular volume in CC
- Lowest after ejection
- stays the same in isovolumetric relaxation
- rapid increase in volume in diastole
Describe an ECG trace in the CC
P- atrial contraction
QRS- ventricular contraction
ST- diastole
Where does electrical signal originate from?
SAN
Which tracts does electrical signals branch into from SAN
- Anterior - tract of bachman
- Middle- tract of wenckeback
- Posterior - tract of Thorel
Where do the internodal pathways meet
AVN
What conduction pathways does the Bundle of His consist of?
- RBB
2. LBB –> LAF / LPF
what does the Bundle of His link to
Purkinje system
Describe the function of the SA node
-specialised neurocardiac tissue
-pacemaker
-Connected directly to surrounding artial muscle fibres
SELF-EXCITATION
RHYTHMICITY
Describe the conduction of an electrical impulse in terms of timing
- SAN –> 3 bands (1m/s) and atria (0.3m/s)
- 0.09s delay in AVN
- 4m/s through purkinje fibres –> due to loads of gap junctions
- 0.4-0.05 m/s transmission in ventricular muscle
Why is there a 0.09s delay in the AVN
reduced gap junctions
allows ventricles to fill completely before contraction
Describe Phase 0 of an action potential in a ventricular muscle fibre
Rapid depolarization –> opening of fast Na channels
Phase 1 ventricular action potential
rapid depolarisation –> closure of Na channels
Phase 2 ventricular action potential
plateau –> slow prolonged opening of Ca channels
Phase 3 Ventricular action potential
final repolarization –> Ca channels close
Phase 4
RMP –> -85-90 opening of K channels
Effect of parasympathetic stimulation (microscopic)
releases Ach
- Reduces rhythm of SAN–>RMP becomes more negative
- reduces excitability of A-V junctional fibres
Effect of parasympathetic stimulation (macroscopic)
slowing of HR
if a strong vagal stimulus occurs the ventricles can stop beating for 5-20s the purkinje fibres take over and ventricles contract at 15-40bpm
Effect of sympathetic stimulation (microscopic)
Noradrenaline released
- Increase rate of SAN discharge –> RMP more positive
- increased rate of conduction and overall excitability
- increase force of contraction –> Ca2+permeability increased
Effect of sympathetic stimulation (macroscopic)
Increased HR
Increased strength of contraction
What is excitation-contraction coupling
Mechanism by which AP causes myofibrils to contract
What happens in the first two stages of excitation-contraction ?
- AP reaches T-tubule and depolarises muscle cell membrane
2. Calcium enters muscle cells through DHP receptors in phase 2