Lecture 1- Cardiac cycle Flashcards

Core information from lecture

1
Q

Describe Aortic pressure during the cardiac cycle

A
  1. Low (80mmHg) when aortic valve open
  2. Peaks during ejection and then lowers
  3. Aortic valve closes and slowly returns to normal
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2
Q

Describe atrial pressure during CC

A
  1. Increases in atrial systole

2. .decreases in ejection

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3
Q

Describe ventricular pressure in CC

A
  1. slightly increases in atrial systole
  2. Rapid increase ub usivolumetric contraction
  3. Peaks at ejection and decreases rapidly when AV valves close
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4
Q

Describe ventricular volume in CC

A
  1. Lowest after ejection
  2. stays the same in isovolumetric relaxation
  3. rapid increase in volume in diastole
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5
Q

Describe an ECG trace in the CC

A

P- atrial contraction
QRS- ventricular contraction
ST- diastole

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6
Q

Where does electrical signal originate from?

A

SAN

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7
Q

Which tracts does electrical signals branch into from SAN

A
  1. Anterior - tract of bachman
  2. Middle- tract of wenckeback
  3. Posterior - tract of Thorel
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8
Q

Where do the internodal pathways meet

A

AVN

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9
Q

What conduction pathways does the Bundle of His consist of?

A
  1. RBB

2. LBB –> LAF / LPF

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10
Q

what does the Bundle of His link to

A

Purkinje system

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11
Q

Describe the function of the SA node

A

-specialised neurocardiac tissue
-pacemaker
-Connected directly to surrounding artial muscle fibres
SELF-EXCITATION
RHYTHMICITY

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12
Q

Describe the conduction of an electrical impulse in terms of timing

A
  1. SAN –> 3 bands (1m/s) and atria (0.3m/s)
  2. 0.09s delay in AVN
  3. 4m/s through purkinje fibres –> due to loads of gap junctions
  4. 0.4-0.05 m/s transmission in ventricular muscle
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13
Q

Why is there a 0.09s delay in the AVN

A

reduced gap junctions

allows ventricles to fill completely before contraction

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14
Q

Describe Phase 0 of an action potential in a ventricular muscle fibre

A

Rapid depolarization –> opening of fast Na channels

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15
Q

Phase 1 ventricular action potential

A

rapid depolarisation –> closure of Na channels

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16
Q

Phase 2 ventricular action potential

A

plateau –> slow prolonged opening of Ca channels

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17
Q

Phase 3 Ventricular action potential

A

final repolarization –> Ca channels close

18
Q

Phase 4

A

RMP –> -85-90 opening of K channels

19
Q

Effect of parasympathetic stimulation (microscopic)

A

releases Ach

  1. Reduces rhythm of SAN–>RMP becomes more negative
  2. reduces excitability of A-V junctional fibres
20
Q

Effect of parasympathetic stimulation (macroscopic)

A

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

21
Q

Effect of sympathetic stimulation (microscopic)

A

Noradrenaline released

  1. Increase rate of SAN discharge –> RMP more positive
  2. increased rate of conduction and overall excitability
  3. increase force of contraction –> Ca2+permeability increased
22
Q

Effect of sympathetic stimulation (macroscopic)

A

Increased HR

Increased strength of contraction

23
Q

What is excitation-contraction coupling

A

Mechanism by which AP causes myofibrils to contract

24
Q

What happens in the first two stages of excitation-contraction ?

A
  1. AP reaches T-tubule and depolarises muscle cell membrane

2. Calcium enters muscle cells through DHP receptors in phase 2

25
Q

What happens during the last two stages of excitation-contraction?

A
  1. Presence of calcium causes the release of more calcium goes from 10-7 to 10-5M
  2. Ca ions catalyse sliding of actin-myosin filaments
26
Q

What occurs in atrial systole

A
  • Atrial depolarisation
  • atrial contraction
  • atrial pressure rise
  • blood flows across AV valves
27
Q

What are the features of atrial systole

A

JVP- a wave
ECG - P wave precedes and PR is depolarisation
S4 can be heard here

28
Q

What occurs in isovolumetric contraction

A
  • 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
29
Q

What are the features of isovolumetric contraction

A

JVP - c wave
ECG - interval between R-S
Heart sounds S1 closure of AV valves

30
Q

What occurs in ejection

A
  • 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
31
Q

What are the features of ejection

A

JVP- no waves
ECG - T wave
No heart sounds
Aortic pressure–> rapid rise in pressure and slightly maintained due to elastic recoil

32
Q

What occurs in isovolumetric relaxation

A

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

33
Q

Features of isovolumetric relaxation

A

JVP - v wave
ECG - no deflections
Sounds - S2 semilunar valve closure
Aortic pressure curve- incisura–> short period of backflow before valves closes

34
Q

what occurs in ventricular filling

A
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
35
Q

Features of ventricular filling

A

JVP- y descent
ECG- no deflections
S3 pathological sound

36
Q

What is the force-velocity relationship

A

increase in afterload=decrease in shortening velocity

37
Q

Volume/pressure changes in systolic dysfunction

A

Impaired ventricular function
EDV increases
inability to contract and pump blood out of ventricles

38
Q

Volume/pressure changes in diastolic dysfunction

A

Impaired relaxation ability
reduced EDV
inability for ventricles to relax

39
Q

What occurs in mitral stenosis

A

Impaired LV filling
reduced EDV
reduced afterload and ESV
reduced SV + CO

40
Q

what occurs in mitral regurg

A

outflow resistance decreases
EDV + EDP increases
stroke volume increases
EF decreases

41
Q

what occurs in aortic stenosis

A
high outflow resistance
LV emptying impaired
peak systolic pressure increases
afterload increases 
SV decreases
ESV increases 
EDV increases
42
Q

what occurs in aortic regurg

A

isovolumetric relaxation cannot occur
blood moves from aorta to ventricle throughout diastole
EDV increases
SV increases