Lecture 1- Cardiac cycle Flashcards
Core information from lecture
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
What happens during the last two stages of excitation-contraction?
- Presence of calcium causes the release of more calcium goes from 10-7 to 10-5M
- Ca ions catalyse sliding of actin-myosin filaments
What occurs in atrial systole
- Atrial depolarisation
- atrial contraction
- atrial pressure rise
- blood flows across AV valves
What are the features of atrial systole
JVP- a wave
ECG - P wave precedes and PR is depolarisation
S4 can be heard here
What occurs in isovolumetric contraction
- Ventricular rises above atrial pressure which causes AV valves closed
- after 0.02s semilunar valves open
- period between AV close and semilunar opening contraction occurs without emptying
What are the features of isovolumetric contraction
JVP - c wave
ECG - interval between R-S
Heart sounds S1 closure of AV valves
What occurs in ejection
- LV pressure rises above 80 / RV pressure above 8
- semilunar valves open
- rapid ejection –> 70% emptied in first 1/3
- slow ejection –> 30% in last 2/3
What are the features of ejection
JVP- no waves
ECG - T wave
No heart sounds
Aortic pressure–> rapid rise in pressure and slightly maintained due to elastic recoil
What occurs in isovolumetric relaxation
Arterial pressure is greater than ventricular
Semilunar valves close to prevent backflow
0.03-0.06 ventricular relaxation despite no change in volume
-atria fill and pressure increases
-this stage finishes when atrial pressure is greater than ventricular
Features of isovolumetric relaxation
JVP - v wave
ECG - no deflections
Sounds - S2 semilunar valve closure
Aortic pressure curve- incisura–> short period of backflow before valves closes
what occurs in ventricular filling
AV valves open 1. rapid filling first 1/3 2. reduced filling middle 1/3 3.final 1/3 enters heart through atrial contraction as atrial pressure falls
Features of ventricular filling
JVP- y descent
ECG- no deflections
S3 pathological sound
What is the force-velocity relationship
increase in afterload=decrease in shortening velocity
Volume/pressure changes in systolic dysfunction
Impaired ventricular function
EDV increases
inability to contract and pump blood out of ventricles
Volume/pressure changes in diastolic dysfunction
Impaired relaxation ability
reduced EDV
inability for ventricles to relax
What occurs in mitral stenosis
Impaired LV filling
reduced EDV
reduced afterload and ESV
reduced SV + CO
what occurs in mitral regurg
outflow resistance decreases
EDV + EDP increases
stroke volume increases
EF decreases
what occurs in aortic stenosis
high outflow resistance LV emptying impaired peak systolic pressure increases afterload increases SV decreases ESV increases EDV increases
what occurs in aortic regurg
isovolumetric relaxation cannot occur
blood moves from aorta to ventricle throughout diastole
EDV increases
SV increases
