Cardiac Cycle Flashcards

1
Q

What are the 2 phases of a heartbeat?

A

Diastole lasts approx 2/3 of each beat and comprises ventricular relaxation when the ventricles fill with blood. Can be split into 4 distinct phases.
Systole lasts approx 1/3 of each beat and comprises ventricular contraction when the ventricles generate pressure and then eject blood into the arteries. Can be split into 3 distinct stages.

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2
Q

List the 7 stages of the cardiac cycle and label whether they occur in systole or diastole

A
  1. Atrial systole - diastole
  2. Isovolumetric contraction - systole
  3. Rapid ejection - systole
  4. Slow ejection - systole
  5. Isovolumetric relaxation - diastole
  6. Rapid passive filling - diastole
  7. Slow passive filling - diastole
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3
Q

What are some key measures and when are they taken?

A
  1. End-diastolic volume is the maximum volume of blood in the heart present just before the ventricles start to contract. Maximum relaxation and filling in the heart at end of isovolumetric contraction.
  2. End-systolic volume is the volume of residual blood left in the heart following contraction. Measured at end of systolic period once slow ejection has occured.
  3. Stroke volume = end-diastolic - end-systolic
  4. Ejection fraction = = (stroke volume/end-diastolic volume) x 100
    Normal ejection fraction: 52-72% but may be 30-35% in people with certain heart conditions.
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4
Q

What occurs during atrial systole?

A

P-wave on ECG signifies start of atrial systole as this is when atrial depolarisation occurs. Atria already almost full from passive filling driven by pressure gradient. Atria contract to ‘top-up’ the volume of blood in ventricle. At rest, atrial systole only contributes about 10% to ventricular filling but at high heart rates when there is less time for passive ventricular filling, may contribute up to 40%. Atrial contribution to ventricular filling varies inversely to diastolic period so when diastolic period short during exercise, atrial contribution greater.

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5
Q

What abnormality can occur during atrial systole?

A

4th heart sound could be heard– abnormal, occurs with congestive heart failure, pulmonary embolism or tricuspid incompetence.

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6
Q

How do other parameters change during atrial systole?

A

Increase in atrial pressure, increase in ventricular pressure by a small amount as increase in ventricular volume occurs. Pressure in aorta contrinues to reduce.

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7
Q

What occurs during isovolumetric contraction?

A

QRS complex marks the start of ventricular depolarisation. This is the interval between AV valves (tricuspid & mitral) closing and semi-lunar valves (pulmonary & aortic) opening. Ventricles contract, increasing pressure, without change in volume as all valves closed. 1st heart sound (‘lub’) due to closure of AV valves and associated vibrations.

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8
Q

How do other parameters change during isovolumetric contraction?

A

Atrial volume initially decreases as vena cava and pulmonary artery initially shut during contraction but as they open up again, atrial pressure increases again. Aorta still reducing in pressure.

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9
Q

What occurs during rapid ejection?

A

Ejection begins when the ventricular pressure exceeds the pressure within the pulmonary artery and the aorta – when these exceeded, semi-lunar valves open and opening of the aortic & pulmonary valves mark the start of this phase. Blood is pumped out and the volumes of ventricles decrease. No heart sounds as opening of valves doesn’t create sound.

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10
Q

How do other parameters change during rapid ejection?

A

Ventricular pressure continues to increase as isotonic contraction occurs. Pressure in aorta increases as blood pumped into it. Atrial pressure remains relatively constant. Marks start of T-wave as ventricles finish contracting.

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11
Q

What occurs during reduced ejection?

A

This phase marks the end of systole. Reduced pressure gradient means aortic & pulmonary valves begin to close. 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 causing semilunar valves to close. Ventricular muscle cells repolarize producing T wave.

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12
Q

What occurs during isovolumetric relaxation?

A

The aortic & pulmonary valves are shut, but the AV valves remain closed until ventricular pressure drops below atrial pressure. Atrial pressure continues to rise. Pressure in the aorta experiences a slight increase forming dichrotic notch, caused by rebound pressure against aortic valve as distended aortic wall relaxes. 2nd heart sound (‘dub’) due to closure of semilunar valves and associated vibrations.

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13
Q

How do other parameters change during isovolumetric relaxation?

A

Atrial pressure starts to peak while ventricular pressure rapidly drops. No change in volume of ventricle as all valves closed.

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14
Q

What is inotropy and lusitropy?

A

Myocardial inotropy is the inherent ability of cardiac contractile proteins, actin and myosin, to interact, contract, and develop force. Lusitropy is the rate of myocardial relaxation which determines rate of drop in ventricular pressure depending on how quickly myofibres relax.

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15
Q

What occurs during rapid passive filling?

A

Occurs during isoelectric (flat) ECG between cardiac cycles. Once AV valves open blood in the atria flows rapidly into the ventricles. Sometimes 3rd heart sound heard – usually abnormal and may signify turbulent ventricular filling. Can be due to severe hypertension or mitral incompetence.

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16
Q

How do other parameters change during rapid passive filling?

A

Aortic pressure continues to decrease. Atrial pressure rapidly decreases as atria empty. Ventricular pressure remains constant. Ventricular volume gradually increases.

17
Q

What occurs during reduced passive filling?

A

This phase can be called diastasis. Ventricular volume fills more slowly. The ventricles are able to fill considerably without the contraction of the atria.

18
Q

How does pulmonary circuit pressure differ from systemic circuit pressure?

A

The patterns of pressure changes in the right heart are essentially identical to those of the left. Quantitatively, the 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 volume of blood as left.

19
Q

How is pulmonary capillary wedge pressure measured?

A

Catheter with a balloon attached inserted through a vein, usually femoral vein or jugular vein and this is advanced through the vena cava into the right atrium, right ventricle and pulmonary artery. Pressure measured in each of the chambers and used to indirectly estimate left atrial pressure and ventricular pressure,

20
Q

Why is the pulmonary capillary wedge pressure important clinically?

A

Can point to severity of left ventricular failure or mitral valve stenosis. An increase in left atrial pressure also increases pulmonary oedema which can be life-threatening.

21
Q

How do preload and afterload affect stroke volume?

A

An increase in preload increases stroke volume but an increase in afterload decreases stroke volume. ESPVR is the maximal pressure that can be developed by the ventricle at any given volume.

22
Q

What is the cardiac output equation?

A

Cardiac output = Heart rate x Stroke Volume

23
Q

What factors affect stroke volume? Explain

A

Preload, Afterload and Contractility. Contractility is the contractile capability (or strength of contraction) of the heart. It is increased by sympathetic stimulation and the extrinsic mechanism which drives it is changes in Ca2+ delivery to myofilaments.

24
Q

How does contractility affect pressure volume loop?

A

Cardiac contractility affects steepness of the Frank-Starling relationship and so gradient (elastance) of ESPVR is altered. Hence, end-systolic pressure is also altered.

25
Q

What happens to pressure-volume loops during exercise?

A

End-diastolic volume increases and stroke volume is increased as sympathetic activation of the myocytes increases ventricular contractility and that decreases end-systolic volume. 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). Combination of increased cardiac contractility and increased VR generate increased SV (and EF). However, if HR increases to very high rates, diastolic filling time can be reduced and this decreases EDV.

26
Q

How do parasympathetic and sympathetic stimulaton impact the heart?

A

Parasympathetic stimulation is present at rest, which slows the SA node rate from 110 bpm to 70 bpm.
Sympathetic stimulation increases SA node rate via:
Hormonal: Circulating adrenaline from adrenal gland
Neural: Noradrenaline released from nerves