Lecture 1- Cardiac cycle Flashcards

Core information from lecture (42 cards)

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
What happens during the last two stages of excitation-contraction?
3. Presence of calcium causes the release of more calcium goes from 10-7 to 10-5M 4. Ca ions catalyse sliding of actin-myosin filaments
26
What occurs in atrial systole
- Atrial depolarisation - atrial contraction - atrial pressure rise - blood flows across AV valves
27
What are the features of atrial systole
JVP- a wave ECG - P wave precedes and PR is depolarisation S4 can be heard here
28
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
29
What are the features of isovolumetric contraction
JVP - c wave ECG - interval between R-S Heart sounds S1 closure of AV valves
30
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
31
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
32
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
33
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
34
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 ```
35
Features of ventricular filling
JVP- y descent ECG- no deflections S3 pathological sound
36
What is the force-velocity relationship
increase in afterload=decrease in shortening velocity
37
Volume/pressure changes in systolic dysfunction
Impaired ventricular function EDV increases inability to contract and pump blood out of ventricles
38
Volume/pressure changes in diastolic dysfunction
Impaired relaxation ability reduced EDV inability for ventricles to relax
39
What occurs in mitral stenosis
Impaired LV filling reduced EDV reduced afterload and ESV reduced SV + CO
40
what occurs in mitral regurg
outflow resistance decreases EDV + EDP increases stroke volume increases EF decreases
41
what occurs in aortic stenosis
``` high outflow resistance LV emptying impaired peak systolic pressure increases afterload increases SV decreases ESV increases EDV increases ```
42
what occurs in aortic regurg
isovolumetric relaxation cannot occur blood moves from aorta to ventricle throughout diastole EDV increases SV increases