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Year 1 - BRS > 6.4 - The Cardiac Cycle > Flashcards

6.4 - The Cardiac Cycle Flashcards

1
Q

What are the two main phases of a heart beat?

A
  • diastole - ventricular relaxation (ventricles fill with blood), lasts approx 2/3 of each beat, split into 4 distinct phases
  • systole - ventricular contraction (ventricles generate pressure then eject blood into arteries), lasts approx 1/3 of each beat, split into 3 distinct phases
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2
Q

What are steps of the cardiac cycle?

A
  1. atrial systole (d)
  2. isovolumetric contraction (s)
  3. rapid ejection (s)
  4. slow ejection (s)
  5. isovolumetric relaxation (d)
  6. rapid passive filling (d)
  7. slow passive filling (d)
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3
Q

What is end-diastolic volume?

A

The maximum volume of blood in the heart just before ventricles start to contract (at max relaxation of heart, at isovolumetric contraction) (120 mL)

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4
Q

What is end-systolic volume?

A

The volume of blood that is retained in the heart after contraction has completed - the residual blood left in heart (50 mL)

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5
Q

What is stroke volume?

A
  • volume of blood expelled by heart in any one cardiac cycle/each beat (70 mL)
  • stroke volume = end-diastolic volume - end-systolic volume
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6
Q

What is ejection fraction?

A
  • the fraction of end-diastolic volume that is ejected by the heart
  • ejection fraction (%) = 100 x stroke volume / end-diastolic volume
  • gives indication of heart function - normal range 52-72%
  • failing heart might have ejection fraction of 30%
  • athletes may have a higher e.g. 80-90%
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7
Q

What happens in atrial systole?

A
  • P-wave on ECG signifies start of atrial systole
  • electrical activity of P-wave stimulates atrial muscle contraction
  • atria already almost full from passive filling driven by pressure gradient
  • atria contract to ‘top-up’ the volume of blood in ventricle
  • usually no heart sounds - might hear S4 heart sound (atrial contraction against high ventricular pressure) - abnormal and occurs with congestive heart failure, pulmonary embolism or tricuspid incompetence
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8
Q

What happens in isovolumetric contraction?

A
  • QRS complex marks the start of ventricular depolarisation
  • this is the interval between AV valves closing and semi-lunar valves opening (both are closed)
  • contraction of ventricles with no change in volume (isometric) - as closed valves means nowhere for blood to go
  • ventricular pressure increases to aortic pressure
  • first heart sound (S1 - ‘lub’) due to closure of AV valves and associated vibrations
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9
Q

What happens in rapid ejection?

A
  • opening of aortic and pulmonary valves marks the start of this phase
  • as ventricles contract, pressure within them exceeds pressure in aorta and pulmonary arteries –> SL valves open, blood pumped out due to pressure gradient, and ventricular volume decreases (isotonic contraction)
  • rise in aortic pressure and ventricular pressure
  • no heart sounds due to valves opening, not closing
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10
Q

What happens in reduced/slow ejection?

A
  • this phase marks end of systole
  • reduced pressure gradient means aortic and pulmonary valves begin to close (ventricular Pa < aortic/PA Pa)
  • blood flow from ventricles decreases and ventricular volume decreases more slowly
  • as pressures in ventricles fall below that in arteries, blood begins to flow back = SL valves close to prevent backflow
  • ventricular muscle cells repolarise, producing T wave - repolarisation phase of cardiac cycle
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11
Q

What happens in isovolumetric relaxation?

A
  • SL valves shut, but AV valves remain closed until ventricular pressure drops below atrial pressure
  • rate that ventricular pressure drops due to muscle fibre relaxation is called lusitropy
  • atrial pressure continues to rise
  • dichrotic notch caused by rebound pressure against aortic valve as distended aortic wall relaxes - due to elasticity of aorta
  • 2nd heart sound (S2) - ‘dub’ - due to closure of SL valves and associated vibrations
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12
Q

What happens in rapid passive filling?

A
  • occurs during isoelectric (flat) ECG between cardiac cycles
  • once AV valves open (intraventricular Pa < atrial Pa), blood in the atria flows rapidly into the ventricles
  • 3rd heart sound (S3) - usually abnormal and may signify turbulent ventricular filling, can be due to severe hypertension or mitral incompetence
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13
Q

What happens in reduced passive filling AKA diastasis?

A
  • ventricular volume fills more slowly
  • ventricles are able to fill considerably without the contraction of the atria
  • aortic pressure decreases, ventricular and atrial pressure fairly stable
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14
Q

What are the similarities and differences in blood pressure and volume between left and right ventricles?

A
  • patterns of pressure changes are identical in both
  • quantitatively, the pressures in the right heart and pulmonary circulation are much lower (peak of systole - 25mmHg in PA)
  • despite lower pressures, right ventricle ejects same volume of blood as left, just into a lower pressure circuit
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15
Q

What is typical systemic and pulmonary pressure?

A
  • typical systemic pressure is 120/80
  • typical pulmonary pressure is 25/5
  • to calculate from graph, do peak/trough
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16
Q

What does pulmonary capillary wedge pressure indicate and why is it important clinically?

A
  • left atrial pressure
  • gives us idea of severity of left ventricular failure and mitral valve stenosis
  • both caused by increase in left atrial pressure - this increases pulmonary oedema which can be life threatening
17
Q

Explain the pressure volume loop

A
  • X-axis: left ventricular volume (mL), Y-axis: left ventricular pressure (mmHg)
  • width = stroke volume
  • we start with A, end-diastolic volume (RHS bottom)
  • isovolumetric contraction occurs, causing increase in pressure but not volume change since no valves are opened
  • we then encounter aortic pressure, B, causing aortic valve to open when ventricular Pa exceeds aortic Pa
  • blood goes from ventricle to aorta, so ventricular volume will decrease
  • this leads to end-systolic volume, C, after pressure goes up then drops slightly due to rapid then slow ejection
  • then we get isovolumetric relaxation, no change in ventricle volume but drop in ventricle pressure, D
  • then gradually fill heart again with blood to reach end-diastolic volume and cycle repeats
18
Q

What is preload on the pressure volume loop?

A
  • blood filling the ventricles during diastole determines the preload that stretches the resting ventricular muscle
  • larger amount of blood returning to heart –> increased preload –> increased stretch of ventricular muscle –> increased force produced
19
Q

What is afterload on the pressure volume loop?

A
  • the blood pressures in great vessels (aorta and pulmonary artery) represent the afterload
  • if afterload increases, there is less shortening of muscle fibres –> less able to expel blood from ventricles
  • amount of load ventricles need to overcome before they expel blood
20
Q

What is the ESPVR?

A

Maximum pressure that can be developed by ventricle at any given volume

21
Q

How does the pressure volume loop change when we increase preload?

A
  • increases in preload = increased stroke volume
  • this is Frank-Starling relationship
22
Q

How does the pressure volume loop change when we increase afterload?

A
  • increases in afterload = decreased stroke volume, because the amount of shortening of muscle fibres that occurs decreases (as working against increased pressure)
  • greater pressure required to open aortic valve = thinner but taller graph
23
Q

What is the formula for cardiac output?

A

Cardiac output = heart rate x stroke volume

24
Q

What influences stroke volume?

A
  • preload
  • afterload (diastolic blood pressure)
  • contractility
25
Q

What is contractility?

A
  • contractile capability (strength of contraction) of heart
  • increased by sympathetic stimulation
  • increased by phosphorylation of L-type Ca2+ channel, SR Ca2+ release channel and SR Ca2+ ATPase (increases delivery of Ca2+)
  • extrinsic mechanism - changes Ca2+ delivery to myofilaments
26
Q

How does the ESPVR line change with changes in contractility?

A
  • more Ca2+ delivered to myofilaments (more sympathetic activity) = more contractility = steeper ESPVR and vice versa
27
Q

How does exercise affect pressure volume loops?

A
  1. increased venous return aided by muscle and respiratory pump increases end-diastolic volume
  2. main factor: sympathetic activation of the myocytes increases ventricular contractility, that decreases end-systolic volume
  3. the increase in arterial pressure that occurs during exercise increases afterload (and can lessen the reduction in end-systolic volume but offset by large increase in contractility) = increased pressures needed
  4. combination of increased cardiac contractility and increased venous return generate increased stroke volume (and ejection fraction)
  • if heart rate increases to very high rates, diastolic filling time can be reduced and this decreases EDV
  • PV loop = wider and taller

Year 1 - BRS (73 decks)

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