Cardiac Cycle Flashcards

1
Q

Heart valve review.

A

The valve between atria and ventricle (AV valve) on the right side is called tricuspid (3 leaflets) whereas the left side valve is called mitral (normally 2 leaves).

The valves on the exit from the ventricles are the pulmonic valve on the right side and aortic valve on the left and both are semilunar

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2
Q

When would AV valves be open?

A

when atrial pressure greater than ventricular P

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3
Q

When would the aortic valve be open?

A

when left ventricle P is greater than aortic P

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4
Q

What occurs during the P wave of the cardiac cycle.

A

atrial depolarization. It is not as large as the ventricular depolarization wave (QRS) because the mass of atria is much less than ventricular mass

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5
Q

What part of the cardiac cycle diagram represent atrial depolarization?

A

The atrial repolarization wave is not seen, as it is buried under the QRS complex.

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6
Q

What is the T wave?

A

The T wave represents ventricular repolarization. It is not as intense as the polarization wave because repolarization occurs more slowly than depolarization (recall that K channels operate more slowly than the fast sodium channel), that is, it is spread out over time.

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7
Q

What happens following atrial contraction (after P wave)?

A

-mitral valve closes due to ventricular pressure increase from volume increase

NOTE: atrial systole, there is a slight increase in martial pressure too

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8
Q

What happens as ventricular pressure exceeds atrial pressure and the mitral valve closes?

A
  • Electrical activation of ventricle (QRS complex) leads to isovolumetric contraction during which ventricular pressure increases but there is no flow because both mitral and aortic valves are closed;
  • as ventricular pressure exceed aortic pressure, the aortic valve opens
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9
Q

What happens when the aortic valve opens?

A
  • after aortic valve opens, both ventricular and aortic pressures continue to increase during rapid ejection period (corresponding to approx 40% of ventricular systole)
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10
Q

What happens when ventricular systole ends due to repolarization of the ventricles?

A

Aortic pressure begins to exceed ventricular pressure, the aortic valve closes and the heart enters the period known as isovolumetric relaxation;

mitral valve does not open until atrial pressure exceeds ventricular pressure again.

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11
Q

When is ascending aortic blood flow the highest?

A

peak towards end of rapid ejection phase;

note the retrograde flow for a fraction of a second, associated with aortic valve closure

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12
Q

When is the first heart sound heard?

A

First heart sound occurs after closure of mitral and tricuspid valves; normally these valves close within 10 msec of each other and thus there is no split sound

low in frequency and prolonged

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13
Q

When is the second heart sound heard?

A

the second heart sound originates from closure of aortic and pulmonic valves; it is shorter in duration and higher in frequency; second heart sound can be a split sound under physiological conditions involving deep breathing

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14
Q

What is the S3 sound?

A

The S3 sound results from vibrations set in motion by the filling of ventricles during early diastole (right after S2) and is normally not heard in adults by stethoscope; if heard it may indicate cardiac disease associated with ventricular overload due to heart failure or valve problems; S3 is referred to as ventricular gallop.

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15
Q

What is the S4 sound?

A

S4 is associated with atrial contraction and results from vibrations induced by a stiffened ventricle. It is sometimes referred to as atrial gallop.

associated with ventricle volume overload

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16
Q

What is the eqn for work of the heart?

A

Pressure x Volume

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17
Q

Are the ventricles typically completely empty following contraction?

A

No, the difference between the EDV and end systolic volume (ESV) is the SV. SV is usually around 80 ml. EDV usually around 130 ml and ESV is usually around 50 ml

18
Q

What will examining the cardiac cycle as a pressure/volume loop allow for determination of?

A

the effects of change in preload, after load, and contractility

19
Q

Describe portion A of the PV loop of the cardiac cycle.

A

A represents diastole where it begins with the after load from the previous contraction and pressure builds as ventricular volume increases- this is passive pressure (stiffer ventricles/more volume= greater pressure)

this takes us from the ESV to the EDV

20
Q

Describe portion B of the PV loop of the cardiac cycle.

A

at the end of A, the mitral valve closes and iso-volumetric contraction occurs in the ventricles leading to a large increase in pressure

21
Q

Describe portion C of the PV loop of the cardiac cycle.

A

at the end of B, the aortic valve opens and pressure increases due to contraction and eventually decreases as volume is lost to the aorta.. This brings us to the end of systole

22
Q

Describe portion D of the PV loop of the cardiac cycle.

A

pressure drops drastically during isovolumetric relaxation and the cycle resets as the moral valve opens again

23
Q

What is the Frank-Starling relationship?

A

ventricular contractility (end systolic pressure volume relationship=ESPVR) is regulated by left ventricular volume at the end of diastole.

end diastolic pressure volume relationship=EDPVR

24
Q

What is preload?

A

the EDV and pressure before ventricles contract at the end of diastole

25
Q

What is after load?

A

ventricular pressure needed to open the aortic valve (volume is still EDV at this point). it is equivalent to diastolic aortic pressure

26
Q

What does systolic pressure mean?

A

the peak pressure in the AORTA, not the ventricle (the peak ventricle pressure is called the ventricular systolic pressure)

27
Q

What is diastolic pressure?

A

minimum pressure in the AORTA at the end of diastole, not the ventricle

28
Q

What is the effect of preload on pressure/volume relationship?

A

increased preload= increased SV

29
Q

What is contractility?

A

Strength of ventricular contraction independent of preload or afterload. Also known as inotropy.

30
Q

What is ejection fraction?

A

The fraction of end diastolic volume ejected by the ventricle during systole. It can be calculated as stroke volume divided by end diastolic volume. Normal values range from 55% to 75%.

31
Q

What is cardiac output?

A

Volume of blood ejected by ventricle in one minute. Can be calculated as stroke volume multiplied by heart rate.

32
Q

What is stroke volume?

A

Volume of blood ejected by ventricle during systole. Can be calculated as end diastolic volume minus end systolic volume

33
Q

What three factors change pressure/volume curves?

A
  • preload (EDV, EDP)
  • afterload
  • contractility
34
Q

What happens if preload increases (and contractility and after load remain the same)?

A

Thus, based on the Frank-Starling mechanism, we find that stroke volume is increased, peak systolic pressure is increased (greater SV/stiffness= greater systolic pressure) but end systolic volume remains the same. Because arterial pressure equals stroke volume times heart rate times total peripheral resistance, this will increase arterial pressure, assuming that heart rate and resistance are also held constant.

Because arterial pressure equals stroke volume times heart rate times total peripheral resistance, this will increase arterial pressure, assuming that heart rate and resistance are also held constant.

35
Q

How does after load affect shortening velocity?

A

There is a reciprocal relationship between these variables. That is, the greater the force generated, the smaller the shortening velocity. This relationship explains why greater afterload (the pressure against which the ventricle must pump) results in decreased ventricular contraction velocity and therefore in a reduced stroke volume since the heart will therefore pump at a lower contraction velocity.

36
Q

End effect of increasing after load without changing preload or contractility?

A

This causes decreased shortening velocity, and therefore increased ESV and thus decreased stroke volume (because it needs more pressure to get there and maintain the pumping effect).

37
Q

How can increase after load occur?

A

afterload increase can occur if we increase aortic pressure (afterload) by, for example, increasing TPR (recall that aortic pressure equals product of cardiac output and TPR).

38
Q

What is the effect of increasing contractility while keeping preload and after load constant?

A

Increasing cardiac contractility (aka inotropy or end systolic pressure volume relationship) without altering preload or afterload. As can be seen, this event decreases end systolic volume and increases stroke volume and therefore peak systolic pressure.

This represents intrinsic activation of the heart, most frequently under the influence of increased sympathetic activity.

39
Q

What compensatory changes occur after increasing preload?

A

An increase in preload (EDV) causes an increase in stroke volume and therefore an increase in afterload (recall that stroke volume determines cardiac output from the formula: cardiac output equals stroke volume times heart rate and cardiac output determines arterial pressure from the formula: arterial pressure equals cardiac output times TPR). Increased afterload therefore causes a small increase in ESV.

40
Q

What compensatory changes occur after increasing afterload?

A

A primary increase in afterload (by for example an increase of TPR) causes a reduction in stroke volume and an increase in end systolic volume. This in turn causes an increase in end diastolic volume because the increase in end systolic volume gets added to the incoming venous return. The increase in end diastolic volume recovers part of the decreased stroke volume originally resulting from increased afterload (i.e. compensation)

41
Q

What compensatory changes occur after increasing contractility?

A

A primary increase in contractility (caused by increased sympathetic activity) will cause a primary decrease in end systolic volume and thus an increase stroke volume and therefore cause a secondary increase in afterload. Moreover, there will be secondarily decreased end diastolic volume due to the decreased end systolic volume. Afterload will increase due to increased stroke volume.