Cardiac Cycle Flashcards

1
Q

What two phases is each heartbeat split into?

How portion of each beat do they respectively cover?
What happens in the ventricles
How many phases is each phase split into

A

Heart beat split into —> diastole & systole

Diastole:
Lasts 2/3 of each beat
Ventricular relaxation - ventricles fill w blood
Split into 4 distinct phases

Systole:
Lasts 1/3 of each beat
Ventricular contraction - ventricles generate pressure then eject blood into the arteries
3 distinct phases

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2
Q

Systole and diastole: what are the stages?

What does end diastolic volume represent?

What does end systolic volume represent?

How do you calculate stroke volume?

How do you calculate ejection fraction?

What is the normal range for ejection fraction?

What purpose does the ejection fraction serve?

A

Atrial systole -> isovolumetric contraction -> rapid ejection -> slow ejection -> isovolumetric relaxation -> rapid passive filling -> slow passive filling

End diastolic vol = max vol of blood in the heart just before the ventricles start to contract

End systolic volume = amount of blood that is in the heart after contraction has been completed. Residual vol in t he heart following contraction.

Stroke volume = vol of blood expelled by the heart in any one cardiac cycle

End diastolic vol (120 mL) - end systolic vol (50 mL) = stroke vol (70 mL)

100 x stroke vol / end diastolic vol = ejection fraction (%)

Normal ejection fraction range: 52-72%

Patient w heart failure may have an ejection fraction of 30-35%
Ejection fraction = clinical indicator of how well the heart is functioning

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3
Q

List the cardiac valves

A

Pulmonary valve
Tricuspid valve
Aortic valve
Mitral (bicuspid) valve

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4
Q

Atrial systole

What on an ECG represents the start of atrial systole?

What happens in the atria during atrial systole? Describe the volume of blood in the atria.

What is the 4th heart sound? Which conditions is it prevalent in?

What % of ventricular filling does atrial contraction account for: At rest and at higher heart rates

A

P-Wave on ECG signifies the start of atrial systole

Atria already almost full from passive filling driven by pressure gradient.
Atria contract to top up the volume of blood in ventricle

4th heart sound - abnormal, occurs w congestive heart failure, pulmonary embolism or tricuspid incompetence

At rest, atrial contraction accounts for ~10% of ventricular filling
At high heart rates when there’s less time for passive ventricular filling, atrial contraction may account for ~40% of ventricular filling

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5
Q

Isovolumetric contraction:

What marks the start of ventricular depolarisation?

What is isovolumetric contraction? What happens in the ventricles. Describe the volume of the ventricles

What produces the 1st heart sound?

A

QRS complex (see graph on notes) marks the start of ventricular depolarisation

Isovolumetric contraction is the interval between AV valves (tricuspid & mitral) closing and semi lunar valves (pulmonary & aortic) opening

Contraction of ventricles with no change in volume

Ventricular pressure increases, increases until it gets near aortic pressure

1st heart sound (lub) due to closure of AV valves and associated vibrations

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6
Q

Rapid ejection:

What marks the start of the rapid ejection phase?

What happens to ventricular pressure and volume during this phase? Where is blood pumped into?

What are the heart sounds for this phase?

A

Opening of the aortic and pulmonary valves (semi lunar valves) mark the start of this phase

As ventricles contract pressure within them exceeds pressure in aorta and pulmonary arteries. 
Semilunar valves (aortic and pulmonary valves) open, blood pumped out and the volume of ventricles decreases

No heart sounds for this phase

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7
Q

Reduced ejection:

What does the reduced ejection phase mark?

Why do the semi lunar valves close?

Describe blood flow and ventricular volume in the rapid ejection phase

What produces the T wave?

A

Reduced ejection marks the end of systole

aortic and pulmonary valves begin to close because of the reduced pressure gradient

Blood flow from ventricles decreases and ventricular volume decreases more slowly

As pressure in ventricles fall below that in the arteries, blood begins to flow back, causing semi lunar valves to close

Ventricular muscle cells repolarise producing T wave (see graph in notes)

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8
Q

Isovolumetric relaxation phase:

Describe the state of the semi lunar valves and AV valves during isovolumetric relaxation

What happens to atrial pressure? What causes the dichrotic notch?

What causes the heart sound is produced and what causes it?

What is the rate of pressure decline determined by?

A

Aortic and pulmonary valves shut, but the AV valves remain closed until ventricular pressure drops below atrial pressure

Atrial pressure continues to rise. Dichrotic notch (green line, see graph) caused by the rebound pressure against aortic valve as distended aortic wall relaxes

Vol of blood in ventricles remains the same and all valves are closed, blood in ventricles at this stage is the end systolic vol (~50 ml)

2nd heart sound (dub) due to closure of semilunar valves and associated vibrations

Rate of pressure decline in the ventricles is determined by the rate of relaxation of the muscle fibres - loosest trophy
Relaxation of muscle fibres is regulated by calcium ATPases and SR membrane

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9
Q

Rapid passive filling phase:

When does rapid passive filling occur between cardiac cycles?

What happens to the AV valves? Where does blood flow into?

What can the 3rd heart sound signify?

A

Rapid passive filling occurs during isoelectric (flat) ECG between cardiac cycles

Once AV valves open, blood in the 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

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10
Q

Reduced passive filling:

What else can the reduced passive phase be called?

Describe ventricular volume filling

What happens after reduced passive filling?

A

This phase can be called diastasis

Ventricular volume fills more slowly

Ventricles are able to fill considerably without the contraction of the atria

After this point, the cardiac cycle starts again with the contraction of the atria

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11
Q

Pulmonary circuit pressures

How do patterns of pressure change compare in the right and left heart?

Compare pressure in the right and left heart

Compare volume of blood ejected by the right and left ventricle

A

Patterns of pressure changes in the right heart are (nearly) identical to those of the left

Pressures in the right heart and pulmonary circulation are much lower (peak of systole - 25mmHg in pulmonary artery)

Despite lower pressures right ventricle ejects same vol of blood as left (pumps the same quantity of blood into a lower pressure circuit)

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12
Q

Pulmonary circuit pressures:

What is pulmonary capillary wedge pressure used for? And how is it gained?

What does left atrial pressure give us an idea of?

How is pulmonary/left atrial pressure measured?

What are standard values for pressure in systemic and pulmonary circuits?

A

Pulmonary capillary wedge pressure: access to heart chambers is gained from the right side of the heart. Gives an indirect estimate of the left atrial pressure

Left atrial pressure gives an idea of the severity of left ventricular failure and mitral valve stenosis - both caused by an increase in left atrial pressure, tend to get an increase in pulmonary oedema -> can be life threatening

Measuring pulmonary pressures/left atrial pressure: use right side of heart, take ventricular balloon and push it into the right atrium then ventricle and then pulmonary artery to measure pressures

Systemic circuit high pressure - 120/80 mmHg
Pulmonary circuit low pressure - 25/5 mmHg

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13
Q

What connects the right atrium to the right ventricle?

What connects the right ventricle to the pulmonary artery?

A

Right atrium to right ventricle via tricuspid valve

Right ventricle to pulmonary artery via pulmonary valve

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14
Q

Preload and afterload on the pressure volume loop:

What is preload? Effects of having larger preload?

What is afterload? Effects of having larger afterload?

A

Preload: blood filling the ventricles during diastole determines the preload that stretches the resting ventricular muscle
(Amount of blood coming back to the heart and stretching ventricles, so larger amount of blood returning to heart = increased preload -> larger stretch -> increased force -> larger increase of ejection of blood/more forceful increase)

Afterload: the blood pressures in great vessels (aorta and pulmonary artery). Diastolic blood pressure (?). If afterload increases -> less shortening of muscle fibres -> less able to expel blood from the ventricles

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15
Q

Preload and afterload on the pressure volume loop:

What is ESPVR?

What does an increase in preload result in?

What does an increase in afterload result in?

A

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

Increases in preload result in increased stroke volume this = frank starling relationship

Increases in afterload result in decreased stroke volume: less shortening of muscle fibres as working against increased afterload, greater pressure required to open aortic valve

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16
Q

Extrinsic stimulation

What does increased sympathetic stimulation result in?

What activates sympathetic beta receptors?

A

Increased sympathetic stimulation increased cardiac myocyte (cAMP) —> allows delivery of more Ca2+ to myofilaments -> increase in force of contraction

Activation of sympathetic beta receptors by:
Circulating catecholamines from adrenal gland
Noradrenaline released from nerves

17
Q

How do you calculate cardiac output?

What are the three mechanisms affecting stroke volume?

What is contractility? What increases contractility? What is the extrinsic mechanism?

A

Cardiac output = heart rate x stroke volume

3 factors affecting cardiac output:
Preload
Afterload
Contractility

Contractility:
Definition - contractile capability (strength of contraction) of the heart
Contractility increased by - sympathetic stimulation
Extrinsic mechanism - changes Ca2+ delivery to myofilaments

As contractility changes a family of frank starling relations become apparent

18
Q

What happens to PV loops during exercise?

(3 things)

  • what increases EDV (end diastolic volume)?
  • what increases afterload?
  • what generates increased SV (stroke volume) (and EF- ejection fraction)?

What can happen if heart rate increases to very high rates?

A

Increased venous return (VR) aided by muscle and respiratory pump increases EDV (end diastolic vol)

Main factor: sympathetic activation of the myocytes increases ventricular contractility, that decreases end-systolic volume

The increase in arterial pressure that occurs during exercise increases afterload (can lessen reduction in end systolic volume but offset by large increase in contractility)

Combination of increased cardiac contractility and increased VR generate increased SV (and EF- ejection fraction)

If heart rate increases to very high rates, diastolic filling time can be reduced and this decreases EDV