Cardio IX Flashcards

1
Q

What are the 4 stages of the cardiac cycle? Which ones are systole and which ones are diastole?

A
  1. Ventricular filling
  2. Isovolumetric ventricular contraction
  3. Ventricular ejection
  4. Isovolumetric ventricular relaxation
    Steps 1 and 4 are diastole and steps 2 and 3 are systole.
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2
Q

Describe the major events of isovolumetric ventricular contraction, including:
a) The event that marks the start of this phase
b) What valves are open/closed
c) State of contraction/pressure and filling of atria and ventricles
d) Whether it belongs to systole or diastole

A

Isovolumetric contraction begins after the ventricles have just begun to contract. They have gone up in pressure by enough such that their pressure is higher than the pressure in the atrium. The atrioventricular valves that were allowing the ventricles to fill therefore get pushed closed pretty much immediately. This is the start of systole, which is when the ventricles start contracting. Because all the valves are closed, as the ventricle contracts, there is nowhere for the blood to go, so the pressure in the ventricles rises without the volume changing.

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3
Q

Describe the major events of ventricular ejection, including:
a) The event that marks the start of this phase
b) What valves are open/closed
c) State of contraction/pressure and filling of atria and ventricles
d) Whether it belongs to systole or diastole

A

The pressure of the ventricles continues to increase while contracting during the isovolumetric contraction phase until it exceeds the pressure in the pulmonary trunk and the aorta. At this point, the pulmonary valve and the aortic valve will open (the AV valves remain closed), and the phase of ventricular ejection starts. The blood leaves the ventricles to go into the pulmonary trunk and the aorta. This is the second part of systole.

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4
Q

Describe the major events of isovolumetric ventricular relaxation, including:
a) The event that marks the start of this phase
b) What valves are open/closed
c) State of contraction/pressure and filling of atria and ventricles
d) Whether it belongs to systole or diastole

A

After ejection, the pressure in the ventricle will start to fall after the ventricles have relaxed. Eventually, the aortic valve and the pulmonary valve will close once the pressure of the ventricles has fallen below the pressures of the aorta (left ventricle) and the pulmonary trunk (right ventricle). As soon as those valves close, this marks the start of isovolumetric ventricular relaxation and of diastole. The pressure in the ventricles falls to zero.

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5
Q

Describe the major events of ventricular filling, including:
a) The event that marks the start of this phase
b) What valves are open/closed
c) State of contraction/pressure and filling of atria and ventricles
d) Whether it belongs to systole or diastole

A

The pressure in the ventricles eventually falls so low during diastole that now the pressure in the atria is higher than in the ventricle. Then, the atrioventricular valves will open, and the phase of ventricular filling begins. The last event is that on the next beat, you’ll have atrial contraction, which will pump more blood into the ventricles, initiating the buildup towards isovolumetric contraction.

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6
Q

How do the aortic, left ventricular, and left atrial pressure vary throughout the 4 stages of the cardiac cycle?

A

During ventricular filling (1): The left atrial pressure is slightly higher than the left ventricular pressure. Aortic pressure is much higher.

During isovolumetric ventricular contraction (2): The left ventricular pressure surpasses the left atrial pressure and shoots up until it meets the aortic pressure. The left atrial pressure drops.

During ventricular ejection (3): the ventricular pressure is above the aortic pressure, but both follow a similar parabolic shape. The left atrial pressure remains low and slowly rises.

During isovolumetric ventricular relaxation (4), the ventricular pressure drops below the aortic pressure and declines sharply, while the aortic pressure also declines but remains high overall due to the Windkessel effect. The left ventricular pressure at the end of this stage is just above the left atrial pressure.

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7
Q

How does left ventricular volume vary throughout the 4 phases of the cardiac cycle?

A

During ventricular filling (1), the end diastolic volume is rising. It starts to rise faster once the atrium contracts.

During isovolumetric ventricular contraction (2), the volume stays the same (because no valves are open for blood to travel).

During ventricular ejection (3), the ventricular volume drops from the end diastolic volume to the end systolic volume.

During isovolumetric ventricular relaxation (4), the ventricular volume starts rising again.

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8
Q

Describe what is happening on the ECG throughout the 4 stages of the cardiac cycle.

A

During ventricular filling (1), you see the P-wave, which represents the atrial activation, at the same time that the left ventricular volume gets kicked up.

At the same time as isovolumetric ventricular contraction (2) occurs, you see the QRS complex, which shows the activation of the ventricles.

Towards the end of ventricular ejection (3), the T-wave shows up, which represents the reactivation of the ventricles.

During isovolumetric ventricular relaxation (4), nothing is visible on the ECG.

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9
Q

At what points in the cardiac cycle do you hear heart sounds? What events do these sounds coincide with?

A

First heart sound = closing of mitral valve, cusps snapping together (left heart) and tricuspid valve (right heart). This is when systole begins. Occurs at the start of isovolumetric ventricular contraction (2).
Second heart sound = closing of aortic valve and pulmonary valve. This is the end of systole. Occurs at the start of isovolumetric ventricular relaxation (4).

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10
Q

What is the formula for stroke volume? What is the typical value?

A

Stroke volume = end diastolic volume - end systolic volume

Typical value: 120 - mL - 50 mL = 70 mL

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11
Q

What is the formula for ejection fraction? What is the typical value?

A

Ejection fraction = stroke volume/end diastolic volume

Typical value: 70 mL/120 mL = 60%

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12
Q

What is the formula for cardiac output? What is the typical value?

A

Cardiac output = heart rate x stroke volume

Typical value: 70 x 70 = 4900 mL/min = 5 L/min

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13
Q

How does the cardiac cycle compare between the left and right heart?

A

The one difference between the cardiac cycle in the right heart vs the left heart is the pressure that the ventricle reaches. In the right heart, pressures in ventricle are a lot lower than for the left heart. Therefore, the pressure of the blood transmitted to the pulmonary trunk is also smaller.
All other events occur at the same time.

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14
Q

What is Starling’s law? Explain what it measures.

A

If you put more blood into the ventricles (making them more full), this will cause an increase in the stroke volume. When you fill the ventricle more, the walls stretch, and cardiac muscle has the intrinsic property of the force of contracting being bigger when it stretches more. However, because stretch (pre-load) can’t be measured, you use either end diastolic volume or the pressure of the right atrium to simulate it.

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15
Q

What is pre-load? How is it measured and why?

A

Pre-load is the stretch of the left ventricle during contraction. This is hard to measure, so we use 2 indices to determine the stretch pre-contraction, or pre-load: the end-diastolic volume and the pressure in the right atrium.

  • If you measure the end-diastolic volume, you can know the amount of stretch right before contraction.
  • If the atrial pressure is higher, we know that more blood will end up in the ventricle, thus leading to a higher stroke volume.
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16
Q

Give 3 examples of organs capable of blood flow autoregulation.

A

Brain, heart, kidneys

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17
Q

What parts of the cardiovascular system are responsible for transporting blood to and from cardiac cells?

A

The left and right coronary arteries.

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18
Q

Coronary autoregulation involves a change in […] to maintain flow in the face of decreased blood pressure. Why?

A

resistance
If perfusion pressure goes down but the flow is maintained, resistance must have decreased.

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19
Q

What is the typical autoregulatory range of an individual?

A

It can work in both directions at a wide range of pressures, but stops working once the blood pressure gets too high (> 200 mm Hg) or too low (< 40 mm Hg)

20
Q

What are the two main mechanisms of autoregulation? What is their timing relative to one another?

A

Metabolic and myogenic. These are separate mechanisms that operate at the same time.

21
Q

Describe how the metabolic mechanism of autoregulation works in a scenario of an increase and a decrease in arterial pressure.

A

If you drop the arteriolar blood pressure to an organ, the blood flow will drop. There will be a fall in the concentration of O2 in the organ. This means that there will be an increase in the concentration of the waste products that would normally be washed away. These products will cause relaxation and dilation of the arteries in the organ, restoring the flow of blood to the organ - this is the metabolic mechanism.

If the blood pressure increases, blood flow will increase as well. These will lead to more O2 and less waste products, therefore less arteriolar dilation and the blood flow will decrease.

22
Q

Describe how the myogenic mechanism of autoregulation works in a scenario of increased and decreased arterial pressure to an organ.

A

When there is a drop in the arteriolar pressure, this will cause a drop in the blood flow to the organ. This will cause a drop in the transmural pressure (pressure from outside to inside), as the amount of stretch will decrease and the muscle will relax. This decrease in stretch will produce dilation, which will lower resistance and restore flow. This is the myogenic component.

23
Q

What autoregulation mechanism is local metabolic control based on? Explain how it works.

A

It is based on the metabolic autoregulation mechanism. It works as follows:

Increased metabolic activity of organ -> decrease in O2, increase in metabolites in organ interstitial fluid -> arterior dilation in organ -> increased blood flow to organ

24
Q

In what situations does local metabolic control occur? What kinds of organs use it?

A

Mechanical work (i.e. exercise) of skeletal muscle, cardiac muscle, etc. or “physio-chemical” work of organs such as the brain and kidney.

25
Q

Another name for local metabolic control in an organ in response to work is […]

A

active hyperemia

26
Q

What is the difference between local metabolic control and metabolic autoregulation?

A

While the stimulus for metabolic autoregulation is a change in blood pressure and the outcome is to restore the blood pressure, for local metabolic control, the stimulus is a change in blood flow as a result of meabolic activity and the outcome is to restore/increase blood flow to the organ. The similarity is that they use the same mechanism to accomplish this.

27
Q

Neural control of the heart and vessels is done by the […]

A

sympathetic and parasympathetic nervous system (ANS)

28
Q

What other variables does changing the heart rate affect? State the relevant formulas.

A

Cardiac output and mean arterial blood pressure.
CO = HR x SV
MAP = CO x TPR = HR x SV = TPR

29
Q

Neural control of the heart rate takes place in the […], because […]

A

sinoatrial node, because the SA node sets the heart rate

30
Q

Describe the path from spinal cord to heart for parasympathetic control of heart rate, including the major receptors and the chemicals released.

A

The primary autonomic neuron is in the medulla oblongata. It sends out the preganglionic axon, which connects to a local ganglion. It then connects to the post-ganglionic axon. This axon travels to the cells on the out side of the heart called ganglion cells. APs will travel in the post-ganglionic axon, which will cause the release of ACh that binds to muscarinic receptors on the SA node.

31
Q

What is the effect of the parasympathetic nervous system on the heart rate? Explain how.

A

If you stimulate the parasympathetic nervous system, you will slow the heart rate. More ACh being released from the cell slows the rate of firing of the SA node.

32
Q

What is the effect of atropine on the heart? Explain how it acts and what system/control it affects.

A

Atropine acts on the parasympathetic nervous system and its control of heart rate. The atropine molecules will bind to the muscarinic receptor on the SA node and block ACh from binding to it. This will prevent the heart rate from slowing, increasing the heart rate. This will increase the cardiac output and the mean arterial pressure.

Atropine increases HR. Therefore, CO and MAP will increase.

33
Q

Describe the path from spinal cord to heart for sympathetic control of heart rate, including the major receptors and the chemicals released.

A

The neurotransmitter going from the sympathetic nervous system to the SA node is norepinephrine, which bind to the beta-adrenergic receptor.

34
Q

What is the effect of the sympathetic nervous system on heart rate?

A

The sympathetic nervous system will cause the heart rate to increase.

35
Q

What is the effect of beta-agonists on the heart? Explain how it acts and what system/control it affects.

A

Beta-agonists affect the sympathetic control of the heart rate. If you give a beta-agonist, it will speed up the heart rate for patients whose heart rate is too low. This will increase cardiac output and low mean arterial blood pressure. It takes action by binding to beta-adrenergic receptors on the SA node and behaving like norepinephrine would.

Increase CO, so MAP will increase.

They also affect sympathetic control of contractility, increasing contractility (increases stroke volume) and thus MAP.

Increase SV, so increase MAP that way too.

36
Q

What is the effect of beta-antagonists on the heart? Explain how it acts and what system/control it affects.

A

Beta-antagonists affect sympathetic control of the heart rate. If you give a beta-antagonist, it will bind to the beta-adrenergic receptor but not activate it, preventing norepinephrine from binding to it. This will bring the heart rate down and the other things down too, including cardiac output and mean arterial pressure.

Decrease HR, so MAP will decrease.

They also act on sympathetic control of contractility. If you give a beta blocker, it will block the normal contractility. There will be a fall in the stroke volume and a fall in the MAP. It acts to reduce blood pressure by both lowering the heart rate and the stroke volume.

Decrease SV, so MAP will decrease that way too.

37
Q

Compare SA node action potentials under sympathetic and parasympathetic stimulation.

A

Sympathetic = faster action potential
Parasympathetic = slower action potential

38
Q

Neural control of contractility is done by the […] system

A

sympathetic nervous

39
Q

Neural control of contractility takes place in the […]

A

ventricular cell

40
Q

Describe the path from spinal cord to heart for sympathetic control of contractility, including the major receptors and the chemicals released.

A

ACh from spinal cord to ganglion, then norepinephrine to beta-adrenergic receptor on ventricular cell.

41
Q

How does increased contractility interact with ventricular end-diastolic volume to affect stroke volume?

A

If you increase contractility by activating the sympathetic nervous system, you will get a stronger contraction and get a higher stroke volume for the same end-diastolic volume.
THIS IS NOT THE FRANK STARLING MECHANISM

42
Q

What is the tone of a vessel?

A

It’s how constricted it is. High tone = very constricted and vice versa.

43
Q

Vessel tone is controlled by the […]

A

sympathetic nervous system

44
Q

Describe the path from spinal cord to heart for sympathetic control of vessel tone, including the major receptors and the chemicals released.

A

Norepinephrine goes to an alpha adrenergic receptor in the blood vessels. The effect of this is to cause the constriction of the smooth muscle.

45
Q

What is the effect of alpha-agonists on the heart? Explain how it acts and what system/control it affects.

A

Alpha agonist: binds to the alpha-adrenergic receptor, contributing to the constriction of the size of the vessel. The total resistance will increase. This is used in the case of a very low blood pressure.

Increase TPR, so MAP will increase.

46
Q

What is the effect of alpha-antagonists on the heart? Explain how it acts and what system/control it affects.

A

Alpha blockers block the alpha-adrenergic receptor. This will prevent norepinephrine from binding, so the smooth muscle will relax. The TPR will fall and the MAP will fall.

Decrease TPR, so MAp will decrease.