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1020: Physiology FM1020 (E) > P: Cardiac cycle > Flashcards

P: Cardiac cycle Flashcards

1
Q

What generates 1st heart sound?

A

Closure of AV valves

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2
Q

What generates 2nd heart sound?

A

Closure of semilunar valves

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3
Q

What is the order of cells generating contraction?

A

Spontaneous depolarizations generated in SA node by autorhythmic cells pass into surrounding myocardial cells and generate contraction as follows:
- atrial myocardial cells
- pause (fibrous layer)
- ventricular myocardial cells

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4
Q

What happens just before atrial systole?

A
  • Both atria and ventricles are in diastole (relaxed)
  • Atrial pressure slightly higher than ventricular –> semilunar valves closed, AV valves open –> blood leaks from atria to ventricle –> fills up 80-100% of ventricle
  • Wave of depolorization spreads through both atria (P wave) generates atrial systole
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5
Q

What happens at atrial systole and at which second does it occur?

A
  • t = 0 sec
  • Pressure in atria increases –> ventricles are full (remaining 0-20%) –> End Dialostic Volume (EDV)
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6
Q

What is the End Dialostic Volume (EDV) at rest?

A

135 mL
(or 120-135 mL)

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7
Q

What happens at isovolumetric contraction phase of ventricular systole and at which second does it occur?

A
  • t = 100 msec
  • Slow rate of conduction at AV node
  • Depolarization wave spreads into ventricles –> QRS wave (onset of ventricular contraction)
  • Ventricle pressure > atrial pressure –> AV valves close (1st heart sound)
  • Ventricular volume is constant
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8
Q

What pressure is required to open semilunar valves into aorta?

A

Minimum 80 mmHg (left ventricle)

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9
Q

What pressure is required to open semilunar valves into pulmonary artery?

A

Minimum 8 mmHg (right ventricle)

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10
Q

How long does isovolumetric contraction phase of ventricular systole last?

A

30 msec

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11
Q

What happens to atrial pressure during isovolumetric contraction phase of ventricular systole and why?

A

Rises slightly: pressure of ventricle causes AV valves to bulge into atria

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12
Q

What happens at ventricular systole and at which second does it occur?

A
  • t = 130 msec
  • Pressure LV > 80 mmHg > pressure aorta
  • Pressure RV > 8 mmHg > pressure pulmonary artery
  • Semilunar valves open
  • Sharp increase in ventricular + aortic pressure to 120 mmHg
  • Abrupt drop in ventricular volume –> rapid ejection
  • Pressure falls as blood leaves ventricle –> reduced ejection
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13
Q

What is the End Systolic Volume (ESV) at rest?

A

60 mL
(or 50-65 mL)

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14
Q

What is stroke volume and how can you calculate it + what is its normal value?

A

Total volume of blood ejected
Stroke volume = EDV - ESV = 75 mL (or 70 mL)

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15
Q

To what pressure do the atria fall to during ventricular systole?

A

0 mmHg

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16
Q

What happens at isovolumetric relaxation phase of ventricular diastole and at what which second does it occur?

A
  • t = 300 msec : repolarization of ventricles begin (T wave)
  • t = 350 msec: LV pressure (100 mmHg) < aortic pressure ; RV pressure (10 mmHg) < pulmonary arterial pressure ; semilunar valves close (2nd heart sound)
  • AV valves remain closed –> ventricular volume constant
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17
Q

What happens to ventricular, atrial and aortic pressures during isovolumetric relaxation phase of ventricular diastole?

A
  • Ventricular pressure falls
  • Atrial pressure increases (filling)
  • Aortic pressure falls back to 80 mmHg
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18
Q

How long does isovolumetric relaxation phase of ventricular diastole last?

A

60 msec

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19
Q

What happens at ventricular diastole, at what which second does it occur and at which second does it end?

A
  • t = 450 msec
  • Atrial pressure > ventricular pressure –> AV valves open
  • Rapid filling phase: blood flows abruptly into ventricles
  • Diastasis (slow ventricular filling): blood entering atria from veins continue into ventricles
  • Ends at 800 msec
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20
Q

How long does systole last in total?

A

0.3 sec

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21
Q

How long does diastole last in total?

A

0.5 sec

22
Q

Does the rise in atrial pressure curve happen before or after P wave?

A

Immediately after

23
Q

Does the ventricular pressure begin to rise before or after QRS complex?

A

After

24
Q

Does the end of ventricular contraction happen before or after T wave?

A

Slightly after (pressure is already falling due to ejection of blood)

25
Q

Explain the importance of atria contraction in slow heart rate vs tachycardia

A
  • Slow heart rate: ventricles are full at diastasis –> atria contraction not so important
  • Tachycardia: diastasis is shortened –> atria contraction is important
26
Q

What can happen if inadequate ventricular filling occurs?

A

Syncope (fainting)

27
Q

Explain A, C and V waves in atrial pressure

A
  • A wave: atrial contraction causes rise in pressure (increase of 7-8 mmHg in LA and 4-6 mmHg in RA)
  • C wave: increase of ventricular pressure causes AV valves to bulge into atria
  • V wave: atrial filling
28
Q

Where is the right atrium pressure change transmitted?

A

Into right jugular vein (jugular venous pulse)

29
Q

Explain atrial fibrillation

A
  • Arrhythmia which causes uncoordinated contractions of atrial fibres –> uncoordinated rippling motion
  • AV node activation is irregular –> ventricular contractions irregular
  • No P wave on ECG
  • Irregular fluctuations: f waves
  • Not usually life threatening, but clots can form in atria
30
Q

What is the normal interval between successive ventricular contractions?

A

0.8 sec (0.35 - 0.95 sec)

31
Q

What causes the characteristic notch in the aortic pressure curve and what is it called?

A

Incisura or dicrotic notch caused by short period of backward flow of blood into ventricle immediately before closure of aortic valve

32
Q

What values does aortic pressure range from during systole and diastole?

A
  • Pressure increases to 120 mmHg (systolic pressure) –> blood from LV stretches walls of arteries
  • Falls slowly to 80 mmHg (diastolic pressure) –> elastic recoil “pushes” blood continually into peripheral vessels
33
Q

Give a detailed explanation of what causes S1

A
  • Upon systole, AV valves close and bulge into atria until chordae tendineae stop the back bulging
  • Tautness of valves/chordae causes blood to bounce forward again into each ventricle
  • Vibrations of valves and turbulent blood transmitted to ventricle walls and blood vessels
34
Q

Is S1 or S2 louder? Give duration of each

A

S1 is louder and longer
S1 = 0.14 sec
S2 = 0.11 sec

35
Q

Give a detailed explanation of what causes S2

A
  • Upon diastole, semilunar valves close and bulge back into ventricles
  • Elastic stretch recoils blood back into arteries
  • Reverberation of blood between arterial walls and valves, and between valves and ventricular walls
36
Q

When do S1 and S2 happen in relation to ECG waves?

A
  • S1 happens right after QRS complex because contraction of ventricles causes closure of AV valves
  • S2 happens after T wave because ventricular relaxation causes closure of semiliunar valves
37
Q

What is a sign of pulmonary hypertension?

A

Sound of aortic valve < pulmonic valve

38
Q

Describe S3 and S4

A

2 additional sounds that can be detected with a microphone
- S3: inrushing blood from atria during middle third of diastole, low rumbling sound, normal <40 years, abnormal >40 years (hole in septum)
- S4: inflow of blood into ventricles following atrial contraction, very weak sound

39
Q

Describe events at each step of left ventricle pressure-volume loop

A
  • A: opening of mitral valve and beginning of filling
  • A-B: pressure falls as diastole progresses, blood volume increasing (rapid filling)
  • B-C: pressure and volume increase as filling progresses (diastasis), small pressure increase before C = atrial contraction
  • C: mitral valves close, EDV
  • C-D: systole begins, isovolumetric contraction
  • D: aortic valve opens (80 mmHg)
  • D-E: pressure rises (120 mmHg), volume falls, rapid ejection
  • E-F: pressure and volume fall, reduced ejection
  • D-F: stroke volume
  • F: aortic valve closes, ESV
  • F-A: Diastole begins, isovolumetric contraction
40
Q

What’s preload and what point does it represent on the pressure-volume loop?

A
  • Degree of tension on the muscle when it begins to contract
  • Point C: magnitude of EDV and corresponding end diastolic pressure
41
Q

What’s afterload and what point does it represent on the pressure-volume loop?

A
  • Force against which muscle is acting
  • Blood pressure in aorta which ventricle must exceed to open aortic valve
  • Point D: aortic blood pressure
42
Q

What is contractility and what’s another word for it? What is the index of contractility? What can increase/reduce contractility?

A
  • Strength of contraction at a given preload and afterload (inotropy)
  • Index of contractility (A) = maximum dP/dt (slope of ventricular pressure curve)
  • Drugs like adrenaline can increase it (B), cardiac failure reduces it (C)
43
Q

Describe the diastolic pressure curve

A

Pressure generated by progressively larger EDVs right before ventricular contraction (preload)

44
Q

Describe the systolic pressure curve

A
  • During ventricular contraction with increasing EDV
  • It increases linearly with EDV (Frank-Starling law)
45
Q

What happens at large EDVs in systolic pressure curve?

A

Pressures generated fall due to overstretch of actin and myosin filaments in cardiac muscle fibres

46
Q

What does the area of pressure-volume loop represent and what happens to it when heart pumps larger quantities of blood?

A
  • External work (EW) output of the ventricle during contraction cycle
  • EW becomes larger
47
Q

What happens during ventricular fibrilation?

A
  • In normal heart: depolarization waves spread rapidly to myocardial cells, all cells become simultaneously refractory, impulse fades
  • Here, re-entry occurs if cells become excitable again –> generates 2nd wave of depolarization
  • During re-entry, some fibres still refractory, other fully excitable and others can conduct impulses at low rates: abnormal cardiac rhythm/patterns of cardiac contraction ignore pace-setting effects of sinus node
  • Most serious arrhythmia, fatal within 1-3 mins
48
Q

What can cause re-entry?

A
  • Increase in tissue mass causing a “long pathway” for impulses
  • Decreased rate in conduction caused by: blockage of Purkinje system, ischemia of the muscle or high blood K+ levels
  • Shorter refractory period in response to various drugs
49
Q

What is the most serious cardiac arrhythmia?

A

Ventricular fibrilation (fatal within 1-3 min)

50
Q

Explain what a defibrillator does

A
  • Passes high-voltage alternating electrical current through ventricles
  • Stops fibrilation by simultaneously placing myocardium into a refractory state
  • Autorhythmic cells regain pacemaker control

1020: Physiology FM1020 (E) (12 decks)

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