Initiation and regulation of the heart L10 + L11 Flashcards

1
Q

Process of a heartbeat

A

Depolarisation -> Contraction -> Relaxation (in a particular sequence, direction, and movement across the heart)

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2
Q

Where does each heart beat start? What is its process?

A

SA node

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3
Q

What are purkinje fibres for?

A

For depolarisation - once it passes the AV node, you want to deliver as much of the depolarisation to the ventricular wall as possible, so that the ventricle wall all contracts at once.

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4
Q

Role of AV node

A

To cause a delay (to ensure that the depolarisation of the atria has time to convert to a contraction)

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5
Q

Process of the cardiac muscle action potential

A
  1. Rapid depolarisation due to opening of voltage-gted fast Na+ channels
  2. Plateau (maintained depolarisation) due to opening of voltage-gated Ca2+ channels and closing of some K+ channels
  3. Repolarisation due to opening of voltage-gated K+ channels and closing of Ca2+ channels
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6
Q

Importance of the plateau phase

A

The point of the heartbeat is to depolarise these myocytes so that they can contract, and for calcium to move into these cells

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7
Q

What is happening electrically during the plateau phase?

A

There is inward and outward currents happening, and ions are moving all directions across the membrane - but all balanced and therefore voltage is zero.

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8
Q

Main location for pacemaker cells

A

SA node (where most our heartbeats start)

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9
Q

What type of nervous system dominates the resting heart rate?

A

The parasympathetic nervous system through the vagus nerve

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10
Q

Steps in cardiac muscle contraction

A

Excitation is initiated by specialised cells in the sinoatrial node which lies close to the point of entry
of the great veins into the right atrium. A wave of depolarisation is then conducted throughout the
myocardium. The cells of the SA node have an unstable resting potential. The membrane potential
between successive action potentials shows a progressive depolarisation. This is the pacemaker.
When threshold is reached, an action potential is triggered to initiate a heartbeat.
The myocytes of the atria, ventricle and conducting system have action potentials with different
characteristics. Although they vary in duration, they all show a fast initial upstroke followed by
a plateau phase of depolarisation prior to repolarisation. The plateau phase is due to the inward
movement of calcium ions.
The calcium influx that occurs during the plateau phase ensures that the action potential lasts almost
as long as the contraction of the cell. Because the muscle is refractory both during and shortly after
the passage of and action potential, the long plateau phase ensures the unidirectional excitation of
the myocardium.
Repolarisation of the myocardial cells occurs when the voltage dependent calcium channels
inactivate.

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11
Q

Are vagus (X) nerves parasympathetic or sympathetic?

A

Parasympathetic

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12
Q

Are cardiac accelerator nerves parasympathetic or sympathetic?

A

Sympathetic

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13
Q

Where do the autonomic nerves - sympathetic and parasympathetic originate from?

A

The cardiovascular centre up in the brainstem - cluster of brain nuclei also known as integration centre

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14
Q

How is heart rate a constant balance?

A

Rest - parasympathetic dominates HR; 50-70bpm

How to increase HR: Down parasympathetic = Up sympathetic

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15
Q

Building of the electrocardiogram

A
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16
Q

What does the P wave stand for?

A

Atrial depolarisation

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17
Q

What does the QRS complex stand for?

A

Onset of ventricular depolarisation

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18
Q

What does the T wave stand for?

A

Ventricular repolarisation

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19
Q

What is a positive chronotrope?

A

A positive chronotrope is a substance or intervention that increases the heart rate by accelerating the rate at which the heart’s pacemaker cells generate electrical impulses.

20
Q

What is cardiac output?

A

Cardiac Output (CO) [mls/min] = Heart rate
(HR) [beats/min] = x stroke volume (SV) [mls/beat]

21
Q

What is the heart rate controlled by?

A

Normal 60-100bpm
SA node
(+) sympathetic activity
(-) parasympathetic activity

22
Q

What is the normal stroke volume?

A

50-100mls

23
Q

What is the equation of SV?

A

SV = End Diastolic volume (EDV = 120-140 mls) - End systolic volume (ESV = 50-70mls)

24
Q

What determines stroke volume?

A
  • Preload
  • Contractility
  • Afterload
25
Q

What is preload?

A

The force that stretches the cardiac muscle prior to contraction.

26
Q

End-Diastolic Volume (EDV)

A

EDV is the total volume of blood in a ventricle at the end of diastole, just before the heart contracts. It represents the preload, or the amount of blood that stretches the ventricular walls before the next contraction.

27
Q

End-Diastolic Pressure (EDP)

A

EDP is the pressure within the ventricles at the end of diastole. It reflects the tension in the ventricular wall as it stretches to accommodate the incoming blood.

28
Q

Pressure-Volume Relationship

A

As EDV increases, the ventricles fill with more blood, causing the walls of the ventricles to stretch. The stretch of the ventricular walls causes an increase in EDP due to the elastic properties of the myocardium.

29
Q

Stroke Volume (SV)

A

The amount of blood ejected by the left ventricle of the heart during each contraction.

30
Q

Frank-Starling Law

A

According to the Frank-Starling mechanism, an increase in EDV (or preload) stretches the ventricular walls, resulting in a more forceful contraction. This happens because stretching the heart muscle fibers increases their optimal overlap of actin and myosin filaments, which enhances the force of contraction.

As a result, when EDV increases, the stroke volume also increases. This relationship is most effective in a healthy heart where the myocardial fibers are not overly stretched beyond their optimal length.

31
Q

How do we change the preload?

A
  • Change in venous return
  • Change in blood volume
  • Change in filling time
  • Change in respiratory pump
  • Change eg MI damage
32
Q

Change in venous return - what it is and how it works?

A

An increase in venous return improves cardiac output (CO) primarily because it enhances the amount of blood available for the heart to pump. The relationship between venous return and cardiac output is crucial because, in a steady state, venous return must equal cardiac output; otherwise, blood would accumulate somewhere in the circulatory system.

Increased Preload (End-Diastolic Volume - EDV):
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction, determined by the volume of blood returning to the heart.
When venous return increases, more blood fills the right atrium and, subsequently, the right ventricle during diastole (ventricular filling phase). This increased volume leads to a higher end-diastolic volume (EDV).

According to the Frank-Starling law of the heart, an increase in EDV stretches the ventricular muscle fibers, resulting in a more forceful contraction. This increased force of contraction increases the stroke volume (SV).

Enhanced Stroke Volume (SV):
With a higher preload (due to increased venous return), the heart muscle fibers are stretched more optimally, enhancing their contractile force. This results in a larger stroke volume, which means more blood is pumped out of the heart with each beat.
An increased stroke volume directly increases cardiac output, provided that the heart rate remains constant or increases appropriately.

33
Q

Where do arteries and veins in the body get innervation from?

A

The sympathetic nervous system which makes your blood vessels constrict or relax.

34
Q

How do we get air into our lungs?

A

When we breathe, our diaphragm pulls down and we expand our chest wall. - Negative thoracic cavity due to bigger space.

35
Q

What is contractility?

A

The performance of the heart at a given preload and afterload. Also known as inotropy.

36
Q

What happens when there is a change in compliance?

A

It is harder for blood to get to the heart, reducing the preload

37
Q

Why does increase in contractility lead to decrease in ESV and increase in SV?

A

When contractility increases, the heart muscle contracts more forcefully. This stronger contraction generates a higher pressure within the ventricles during systole.
The increased force of contraction means the ventricles can eject a greater volume of blood with each beat, which leads to a reduction in the amount of blood remaining in the ventricles at the end of systole (lower ESV).
The more powerful contraction reduces the ESV because less blood is left behind in the ventricle after the heart contracts.

Increase in Stroke Volume (SV):
Since SV is the difference between the volume of blood in the ventricles at the end of diastole (EDV) and the volume remaining after systole (ESV), a decrease in ESV (with EDV remaining the same) directly leads to an increase in SV.
Mathematically, when ESV decreases (due to increased contractility), SV increases:
SV=EDV−ESV
If ESV is lower while EDV remains constant, the stroke volume (SV) will be higher.

38
Q

Afterload

A

The amount of pressure that the heart needs to exert to eject the blood during ventricular contraction.

39
Q

What does the Diastolic Phase represent in the Pressure-Volume (PV) Relationship?

A

Represents the filling phase of the heart, where the ventricle fills with blood.

40
Q

What does the Systolic Phase represent in the Pressure-Volume (PV) Relationship?

A

Represents the ejection phase, where the ventricle contracts and ejects blood into the aorta.

41
Q

Why is the Diastolic Phase Curved?

A

During diastole, the ventricles fill with blood, and the myocardial fibers stretch to accommodate the incoming volume. Initially, when the ventricle is relaxed and not yet stretched, the compliance (or ability to stretch) is high. This means that small increases in volume result in minimal increases in pressure.
As more blood fills the ventricle, the myocardial fibers stretch more, and the ventricle becomes less compliant (stiffer). At this stage, further increases in volume cause a greater increase in pressure. This increasing stiffness as the ventricle fills results in a non-linear, curvilinear relationship during diastole.

42
Q

Why is the Systolic Phase Linear?

A

Active Force Generation:
During systole, the ventricular myocardium actively contracts to eject blood. The linear relationship seen during systole reflects the active force-length relationship of cardiac muscle fibers. When the ventricle contracts, it does so in a relatively linear fashion within a certain range of volumes and pressures, where muscle fibers generate tension proportional to their length.
This means that as the ventricle contracts from a filled state, the pressure increases relatively linearly with decreasing volume due to the synchronous contraction of the myocardial fibers.

43
Q

Ventricular Pressure-Volume Relationship

A
44
Q

Determinants of cardiac output

A
45
Q

Summary

A