cardiac cycle Flashcards

1
Q

how many phases is each heart beat split into

A

2

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2
Q

what is diastole and how long does it last

A

ventricular relaxation
lasts 2/3 of each heart beat
and is split into 4 distinct phases

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3
Q

what is systole and how long does it last

A

ventricular contraction
lasts approx 1/3 of each heart beat
split into 3 distinct phases

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4
Q

what is isovolumetric contraction

A

heart is exerting pressure on the end diastolic volume

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5
Q

what is end diastolic volume

A

volume present at maximum filling of the heart

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6
Q

what is end systolic volume

A

not all blood is ejected from the heart - some blood remains at the end of systole

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7
Q

what is stroke volume

A

the difference between end diastolic and end systolic

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8
Q

equation for stroke volume

A

end diastolic - end systolic

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9
Q

how do you calculate ejection fraction

A

stroke volume / end diastolic x 100

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10
Q

what is the normal range for ejection fraction

A

52-72%

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11
Q

what happens in bad heart failure

A

low ejection fraction > contractility of the ventricle is decreased
heart cannot sustain enough cardiac output for the needs of the body
used clinically to address degrees of failure of the heart

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12
Q

STEPS for what happens in atrial systole

A

contraction of the atria (already blood in the ventricles)
1) the P wave starts the process off
2) atria is stimulated by the pacemaker potential fired off by the SAN (excites atrial muscle cells and depolarisation excites atrial cells)
(P wave on ECG signifies start of atrial systole)
3) atria are already almost full from passive filling driven by pressure gradient
4) atria contract to “top up” volume of blood in ventricle

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13
Q

what is the 4th heart sound

A

abnormal, valve incompetence (leaky blood) - occurs with congestive heart failure, pulmonary embolism or tricuspid incompetence

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14
Q

STEPS for isovolumetric contraction

A

QRS complex - signifies depolarisation of ventricular muscle > activates the muscles (allows Ca influx into cells > calcium release from SR > Ca dumped into cytosol and activates myofilaments and produce contraction)
2) ventricles start to contract against closed valves (2 semi lunar and pulmonary and aortic valves are closed)
3) QRS complex marks the start of ventricular depolarisation (this is the interval between AV valves - tricuspid and bicuspid/mitral - closing and semilunar valves - pulmonary and aortic - opening)
4) ventricular volume doesn’t change - but build up in ventricular pressure
5) contraction of ventricles with no change in volume = isometric
1st heart sound (lub) due to closure of AV valves and associated vibrations

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15
Q

STEPS for rapid ejection

A

signifies ventricular pressure overcomes back pressure/diastolic blood pressure in the aorta and the blood pushes against aortic valve which opens and flows out of the ventricle > decreases volume
2) contraction has moved from isometric to isotonic (shortening of muscle fibres > efflux of blood from both ventricles)
3) opening of the aortic and pulmonary valves marks the start of this phase
4) as ventricles contract, pressure within them exceeds pressure in aorta and pulmonary arteries
5) semi lunar valves open, blood pumped out and the volumes of ventricles decrease (isotonic contraction)
no heart sounds

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16
Q

what are heart sounds associated with

A

closing of a valve

17
Q

STEPS for reduced ejection

A

pressure and volume fall
2) ventricular pressure falls and aortic pressure falls too
3) contraction is subsiding and calcium is being pumped into SR into stores and effluxed outside of cells
4) cells start to relax > repolarisation of the cell
T wave on ECG
5) ventricular repolarisation - marking the end of systole
6) reduced pressure gradient means aortic and pulmonary valves begin to close
7) blood flow from ventricles and ventricular volume decreases more slowly
8) as pressure in ventricles fall below than in arteries, blood begins to flow back causing semi lunar valves to close
9) ventricular muscle cells repolarise producing T wave

18
Q

STEPS for isovolumetric relaxation

A

pressure in ventricle decreases but volume remains unchanged
2) closure of aortic and pulmonary valves give rise to heart sound s2
3) aortic and pulmonary valves shut but the AV valves remain closed until ventricular pressure drops below atrial pressure
4) atrial pressure continues to rise, dichrotic notch (green line) caused by rebound pressure as distended aortic wall relaxes
2nd heart sound “dub” due to closure of semi lunar valves and associated vibrations

19
Q

STEPS for rapid passive filling and _ heart sound?

A

valves from atria to ventricle open
2) blood moves passively from the left and right atria into the ventricles
3) increases ventricular volume
4) no excitation
5) ventricles are repolarised
6) passive filling
7) occurs during isoelectric (flat) ECG between cardiac cycles
8) once AV valves open, blood in atria flows rapidly into the ventricles
3rd heart sound - usually abnormal and may signify turbulent ventricular filling
can be due to severe hypertension or mitral incompetence

20
Q

STEPS for reduced passive filling

A

phase can also be called diastasis

2) ventricular volume fills more slowly
3) the ventricles are able to fill considerably without the contraction of the atria

21
Q

describe pulmonary circuit pressures

A
  • the pattern of pressure changes in the right heart are essentially identical to those of the left heart
    quantitatively - pressure in right heart and pulmonary circulation = much lower but even despite this - ejects same volume as the left heart
    IT IS SIMPLY PUMPING THE SAME QUANTITY OF BLOOD INTO A LOWER PRESSURE CIRCUIT
22
Q

describe pressure volume loops

A

a) ventricles are completely full of blood - topped up by atrial contraction - volume is high and pressure is low
b) ventricles contract - generates pressure but no change in volume (ventricular pressure overcomes that back pressure/afterload in the aorta) - aortic valve opens and volume decreases
c) end systolic volume - volume is decreased but high pressure until aortic valve closes again
d) drop in pressure

23
Q

what determines the preload that stretches the resting ventricular muscle

A

blood filling the ventricles during diastole

24
Q

what represents the afterload

A

the blood pressure in great vessels (aorta and pulmonary artery)

25
Q

describe the F-S relationship

A

stretch muscle fibres > change sensitivity to calcium > change crossbridge amount they can form > increases force of contraction

26
Q

what does increasing afterload do to muscle fibres

A

they don’t shorten as much > greater aortic pressure > decreased stroke volume

27
Q

what is end systolic pressure volume relationship

A

the maximal pressure that can be developed by the ventricle at any given volume

28
Q

what is the Frank Starling relationship

A

increases in preload results in increased stroke volume

29
Q

what does increasing afterload do to stroke volume

A

increases in afterload results in decreased stroke volume

amount of shortening decreases as working against increased afterload - greater pressure requires to open aortic valve

30
Q

what is the equation for cardiac output

A

cardiac output = heart rate x stroke volume

31
Q

what is stroke volume affected by

A

preload
afterload
contractility (contractile capability of the heart) increased by sympathetic stimulation of the heart

32
Q

what happens as contractility changes in terms of F-S relationship

A

increase contractility > more Ca delivered to myofilaments = more force produces
decrease contractility > less calcium > more stretch needed to produce the same force

33
Q

what happens to PV loops during exercise

A

1) increased venous return aided by muscle and respiratory pump increases EDV (end diastolic volume)
2) main factor - sympathetic activation of the myocytes increases ventricular contractility - 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 conractility)
4) combination of increased cardiac contractility and increased venous return generates increased stroke volume and (ejection fraction)

34
Q

what can happen if HR increases to a high rate

A

diastolic filling time can be reduced and this decreases EDV

35
Q

what does hardening of the aortic valve do

A

reduces flow and increases afterload

36
Q

what does acute blood loss do

A

loss of blood reduces venous return which decreases preload

37
Q

summary of what exercise does (PV loop)

A

venous return increases due to venoconstriction and skeletal muscle pump, and contractility is increased via sympathetic nervous system

38
Q

does hardening/stenosis of the pulmonary valve change afterload

A

yes but it does not affect preload

39
Q

what is the longest phase of the cardiac cycle

A

reduced passive filling