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YEAR 1 - Physiology and Pharmacology (Anton) > 8.6 Cardiovascular Physiology (HT) > Flashcards

8.6 Cardiovascular Physiology (HT) Flashcards

1
Q

What are some major properties involved in the study of the movement of blood?

A
  • Flow
  • Pressure
  • Tension
  • Compliance
  • Resistance
  • Energy
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2
Q

What is compliance?

A

How easy it is to change volume when pressure is applied.

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3
Q

What is flow and what are the units?

A
  • The volume moving past a given point per unit time
  • Flow = ΔV/Δt
  • Units: L/min
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4
Q

Is flow a rate?

A

Yes

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5
Q

Give the formula for calculating cardiac output.

A

Cardiac output = Stroke volume x Heart rate

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6
Q

Give some typical values for:

  • Stroke volume
  • Heart rate
  • Cardiac output
A
  • Stroke volume = 70ml
  • Heart rate = 70 bpm
  • Cardiac output = 70 x 70 = About 5L/min
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7
Q

What is the normal cardiac output at rest?

A

5L/min

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8
Q

Do larger compartments of the circulatory system have greater flow?

A

No, because of conservation of flow.

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9
Q

What are the two divisions of the circulation?

A
  • Systemic circulation
  • Pulmonary circulation
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10
Q

Is velocity the same as flow?

A

No!

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11
Q

Give the equation relating flow to velocity.

A

Flow (cm3/s) = Velocity (cm/s) x Cross-sectional area (cm2)

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12
Q

Draw graphs to show how cross-sectional area and velocity change throughout the systemic circulation.

A
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13
Q

When the total cross-sectional area of vessels increases, what happens to the velocity?

A
  • It decreases
  • This is because flow is conserved and it is equal to the product of the velocity and cross-sectional area
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14
Q

Is pressure in the aorta constant and is this desirable?

A
  • No, it varies between systole and diastole of the heart
  • Theoretically these pressure waves are not desirable, but we have valves, so it is ok
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15
Q

What happens to pressure waves in the heart and why?

A
  • They decay with distance and become less pulsatile
  • This is due to the elasticity of the vessels
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16
Q

What are ABP and CVP?

A
  • Arterial blood pressure -> The pressure exerted by the blood in the large arteries
  • Central venous pressure -> The blood pressure in the venae cavae, near the right atrium of the heart
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17
Q

Does pulse velocity in vessels measure blood velocity?

A

No, the pulse wave is much faster (400cm/s) than the blood velocity (20cm/s).

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18
Q

What are the standard units for blood pressure?

A

mmHg

(cmH2O is also occasionally used)

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19
Q

Explain why the units of blood pressure are mmHg or cmH2O.

A
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20
Q

How does a failing heart affect CVP?

A
  • Increases the CVP
  • Because blood builds up behind the heart
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21
Q

Name some things that can cause a high or low CVP.

A

High CVP:

  • Heart failure
    • Decreased contractility
    • Valve abnormalities
    • Dysrhythmias
  • Increased pulmonary arterial pressure
  • Increased juxta-cardial pressure (e.g. tension pneumothorax)

Low CVP:

  • Hypovolemia
  • Venodilation
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22
Q

Describe how you can measure CVP.

A
  • CVP is best estimated indirectly by measuring the JVP (jugular venous pressure) -> This is non-invasive
  • The patient is laid down at a 45* angle and their internal jugular vein is located (not to be confused with the carotid artery)
  • The highest level above the sternal angle at which the vein pulsates is measured (the vertical measurement is taken, perpendicular to the ground)
  • 5cm can be added to this to account for the distance between the right atrium and the sternal angle
  • In healthy patients, the value should not exceed 9cmH2O

There are also direct, invasive ways of measuring CVP, such as a central venous catheter placed through either the subclavian or internal jugular veins. An ultrasound may also be used.

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23
Q

What is a normal CVP value?

A

5mmHg (or 7cmH2O)

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24
Q

Describe the principle on which arterial pressure was first measured.

A
  • An animal’s artery could be cut and the blood that spurted out could be made to rise up a tube
  • The higher the pressure, the higher the blood would rise
  • The height to which it rose was the ABP in cmH2O
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25
Q

What are some normal values for the systemic and pulmonary arterial blood pressures (systolic/diastolic)?

A

Systemic: 120/80 mmHg

Pulmonary: 20/10 mmHg

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26
Q

What is MAP?

A
  • Mean arterial pressure
  • It is the average arterial blood pressure in an individual during a single cardiac cycle.
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27
Q

How can MAP be estimated?

A

Where DP is the diastolic pressure and SP is the systolic pressure.

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28
Q

What is pulse pressure and what is its normal value?

A
  • It is the difference between the systolic and diastole arterial blood pressure
  • Normal value: 40mmHg
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29
Q

Describe how ABP may be measured.

A
  • Cuff is placed on the upper arm of a patient, which restricts blood flow to the lower arm, and then it is gradually released so that the cuff pressure eventually drops below the systolic arterial pressure.
  • This point is marked by the presence of K-sounds that are detected by a stethoscope and mark the intermittent opening of the artery when the arterial pressure exceeds the cuff pressure.
  • Thus, the blood pressure when this starts (systolic pressure) can be recorded. When the sounds stop, it is the diastolic pressure.
  • In recent times, digital sphygmomanometers have become commonplace.
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30
Q

What is the name of the device used to measure ABP?

A

Sphygmomanometer

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31
Q

What are Korotkoff sounds?

A
  • These are sounds that can be heard using a stethoscope when measuring ABP using a cuff.
  • The sounds appear when cuff pressures are between systolic and diastolic blood pressure, because the underlying artery is collapsing completely and then reopening with each heartbeat.
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32
Q

What is the tension in vessels needed for?

A
  • A force that keeps the vessels intact in response to internal pressure
  • It can be thought of as a circular force that goes around the wall of the vessel, which means that it exerts a small component to resist internal pressure
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33
Q

What is Laplace’s law?

A

For a cylinder: T = PR / u
For a sphere: T = PR / 2u

Where:

  • T = Tension
  • P = Transmural pressure (difference between internal and external pressure?)
  • u = Wall thickness
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34
Q

Compare and explain the tension in arteries and veins.

A

Arteries experience higher pressure so their walls need to develop greater tension. They have thick walls to reduce the tension in them (?).

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35
Q

Why do capillaries only require thin walls?

A

Their radius is very small, so the tension required to maintain their shape is very low (Laplace’s Law: T = PR / u). This means that they only require thin walls to prevent bursting, since tension in the walls does not get too high.

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36
Q

How are aneurysms related to wall tension?

A

In aneurysms, there is often a thinning of the wall, which means that the tension in the wall increases (Laplace’s Law: T = PR / u).

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37
Q

Compare the compliance of arteries and veins. Explain why this is important.

A
  • Arteries have a lower compliance than veins
  • This is important because arteries would be weakened if they were allowed to stretch too much (Laplace’s Law: T = PR / u)
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38
Q

Give the equation for compliance of a blood vessel.

A

Compliance = ΔV / ΔP

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39
Q

What type of vessels are veins also known as? Why?

A
  • Capacitance vessels
  • They can expand or collapse to compensate for changes in blood volume
  • This is due to their high compliance
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40
Q

Where is most of the blood in the circulation stored?

A

In veins (the capacitance vessels).

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41
Q

How does blood vessel compliance change with age and what affect does this have on the blood pressure?

A
  • Compliance decreases with age
  • This means that there are much greater fluctuations between systolic and diastolic pressure in the elderly
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42
Q

Describe the relationship between resistance, pressure and flow.

A

Flow = Pressure / Resistance

Note: This is analogous to Ohm’s law.

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43
Q

A high resistance requires…

A

A high pressure difference to overcome.

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44
Q

Compare laminar and turbulent flow.

A

Laminar:

  • Normal, parallel flow
  • Occurs in most vessels
  • Ohmic relationship between pressure and slow

Turbulent:

  • Flow in eddies, not all linear
  • Occurs in vessels with wide diameter and fast velocity (e.g. ventricles)
  • Flow is proportional to the root of the pressure
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45
Q

Draw a graph showing laminar flow.

A
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46
Q

Draw a graph showing turbulent flow.

A
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47
Q

What is the effect of turbulent flow?

A

It reduces the flow at a given pressure, so there is an increased chance of blood clot. Atrial fibrillation can lead to this.

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48
Q

What is Poiseuille’s law?

A

R = (8 x μ x L) / (π x r4)

Where:

  • R = Resistance
  • μ = Viscosity
  • L = Length of tube
  • r = Radius
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49
Q

What is resistance a property of?

A

The vessel and the fluid it carries.

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50
Q

What is the most powerful regulator of vessel resistance and what is the evidence for this?

A

Radius, which is shown by Pouiseuille’s law: R = (8 x μ x L) / (π x r4)

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51
Q

Describe how haematocrit (the amount of RBCs in blood) affects the viscosity of blood.

A

Viscosity increases linearly as haematocrit increases.

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52
Q

Describe how radius of the blood vessel affects the viscosity of blood.

A
  • This graph is seen because at low radii, there is an outer layer of plasma where another RBC cannot fit.
  • So it is very easy to move blood through capillaries.
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53
Q

Compare and explain the resistance in the systemic circulation and pulmonary circulation.

A
  • It is 6-fold lower in the pulmonary circulation
  • This is mostly due to the length of the systemic circulation -> Affects Poiseuille’s law
  • Therefore, the pressure must be higher in the systemic circulation, even though the flow is the same
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54
Q

Describe the realtionship between total peripheral pressure (a.k.a. systemic vascular resistance), cardiac output, MAP and CVP. Interpret this.

A

TPR = (MAP - CVP) / CO

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55
Q

Describe the pressure gradient across blood vessels of high and low resistance.

A
  • High resistance = High pressure gradient required to overcome resistance
  • Low resistance = Low pressure gradient required to overcome resistance
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56
Q

What type of vessels are arterioles also known as?

A

Resistance vessels

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57
Q

What is the importance of arterioles as resistance vessels?

A

They have the highest resistance, so they can dilate or constrict to change resistance to flow. This is important for directing blood around the body.

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58
Q

Does blood always flow from high to low pressure?

A

No, it doesn’t necessarily. It flows from high energy to low energy, which also depends on gravity and kinetics. This is accounted for in Bernoulli’s principle.

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59
Q

Read up about Bernoulli’s principle if you have time. (Right hand side content)

A

Do it. Pawel’s lecture 2.

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60
Q

Give the equation relating diffusion time to the diffusion distance and diffusion coefficient.

A

Diffusion time = Distance2 / Diffusion coefficient

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61
Q

What are the two types of transport that occur in the human circulatory system?

A
  • Diffusion
  • Bulk flow
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62
Q

Draw the graphs for diffusion and bulk flow.

A
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63
Q

Describe the blood supply to cells from capillaries.

A
  • Often each cell has its own private capillary
  • Most cells are within 100 micrometers of a capillary and can be supplied by diffusion
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64
Q

Draw the branching and merging of blood vessels, including diameters.

A
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65
Q

Draw a graph showing how cross-sectional area changes from arteries to arterioles to capillaries to venules to veins.

A
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66
Q

Draw a graph showing how blood velocity changes from arteries to arterioles to capillaries to venules to veins.

A
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67
Q

Describe the general distribution of blood volume in the herat, pulmonary circuit and systemic circuit.

A
  • Heart = 10%
  • Pulmonary circuit = 10%
  • Systemic circuit = 80%
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68
Q

Draw a pie chart showing the blood volume distribution between the different types of vessel in the body.

A
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69
Q

Aside from a pressure cuff, how can arterial blood pressure be measured?

A
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70
Q

Describe how the pressure in the chambers of the heart can be measured.

A

Catheterisation.

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71
Q

How can peripheral blood flow be measured?

A
  • Venous occlusion plethysmography
    • Cuff is placed downstream of a strain gauge, so that venous return is blocked
    • The rate at which the volume detected by the strain gauge increases is the flow
  • Doppler ultrasound
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72
Q

State the Fick’s principle equation.

A

VO2 = CO x (CA - CV)

Where:

  • VO2 = Oxygen consumption (ml/min)
  • CO = Cardiac output
  • CA = Oxygen conc. in pulmonary vein
  • CV = Oxygen conc. in veins
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73
Q

What can be used to measure cardiac output indirectly?

A

Fick’s principle

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74
Q

Describe how Fick’s principle can be used to calculate cardiac output indirectly.

A
  • CO = VO2 / (CA - CV)
  • Oxygen uptake (VO2) is measured by spirometry
  • Pulmomary venous (CA) and venous (CV) blood oxygen concentrations are determined by taking blood samples
  • From this, cardiac output can be estimated
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75
Q

Name some cardiac imaging techniques.

A
  • Cineangiography - Motion-picture photography of a fluorescent screen recording passage of a contrasting medium through the blood vessels.
  • Echocardiography (ultrasound)
  • Nuclear cardiology
  • Cardiac MRI
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76
Q

How is ejection fraction calculated?

A
  • EF = SV/EDV
  • Where SV = EDV - ESV
EDV = End diastolic volume
ESV = End systolic volume
SV = Stroke volume
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77
Q

Why do we measure ejection fraction?

A

A low ejection fraction is associated with higher mortality.

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78
Q

What is a normal value for left ventricular ejection fraction?

A

More than 55%

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79
Q

Name some techniques used to measure coronary perfusion.

A
  • Echocardiography (ultrasound)
  • Nuclear cardiology
  • Cardiac MRI
  • Cardiac CT
  • Contrast angiography
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80
Q

How is flow in the circulatory system restricted to only one direction?

A

Valves in the heart

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81
Q

How is the heart refilled after contraction?

A
  • The atria act as priming pumps for the ventricles
  • There is some re-filling due to recoil, but this is not as efficient
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82
Q

What is the normal ejection volume for a heart beat?

A

70ml

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83
Q

How are all 4 pumps in the heart co-ordinated and what is the problem with this?

A
  • Syncytium due to gap junctions
  • Problem with this is that an ectopic heartbeat will also be propagated
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84
Q

Compare the volume changes that occur in the 4 chambers of the heart.

A

The volume changes in the ventricles must be the same due to conservation of flow.

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85
Q

Describe the arrangement of myocytes in the heart wall and what the effect of this is.

A

It causes the heatrt to twist upon contraction.

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86
Q

What is the apex beat and where is it heard?

A

The heart twisting and tapping on the 5th intercostal space upon contraction.

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87
Q

Cardiac output is a type of…

A

Flow

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88
Q

Draw the cascade that produces blood flow in the heart.

A
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89
Q

Explain how hypertrophy of the heart can be a vicious loop.

A
  • A larger heart needs greater tension to produce a certain pressure, according to Laplace’s law (P = 2Tu / R).
  • Therefore, hypertrophy can be a vicious loop that results in heart failure
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90
Q

Name the valves in the heart.

A
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91
Q

What are the two types of diseased heart valves?

A
  • Incompetent -> Can’t fully close
  • Stenosed -> Can’t fully open
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92
Q

What happens in the heart in response to valve stenosis?

A

Hypertrophy, in order to try and overcome the stenosis.

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93
Q

What prevents heart valves from flipping?

A
  • Chordae tendinae
  • Papillary muscle
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94
Q

What is the isovolumetric phase of the heart cycle and what is its purpose?

A
  • It is when the ventricular pressure is sufficient to close the inlet valve, but insufficient to open the outlet valve, so both valves are closed
  • The pressure increases at a constant volume
  • This phase “secures stroke volume” -> Ensures that the heart is very efficient
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95
Q

Draw the cardiac cycle.

A

The * indicates the typical start of the cycle.

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96
Q

Describe each stage of the cardiac cycle, including whether each stage is isovolumetric or not. Start with ventricular diastole.

A
  • Ventricular diastole -> Isovolumetric relaxation
  • Ventricular diastole -> Passive filling
  • Atrial systole -> Active filling of ventricle
  • Ventricular systole -> Isovolumetric contraction
  • Ventricular systole -> Ejection
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97
Q

Which of the phases of the ventricular cardiac cycle is longest and why?

A

Ventricular filling is the longest because relaxation is slow.

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98
Q

What is a typical resting heart rate?

A

60-70bpm

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99
Q

How many heart sounds are there?

A

S1 and S2

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100
Q

What is the first heart sound (S1)?

A
  • The “lub” of the “lub-dub”
  • It is the sound of atrioventricular valve closure at the beginning of ventricular systole
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101
Q

What is the first heart sound (S2)?

A
  • The “dub” of the “lub-dub”
  • It is caused by the closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventricular diastole.
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102
Q

Draw the ventricular cardiac cycle, including the points where the inlet and outlet valves open and close, and the heart sounds.

A

Note that atrial systole is during the last part of ventricular filling.

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103
Q

What is the importance of the atria in the cardiac cycle?

A
  • Atria assist in ventricular filling
  • By 10-20% in young •By ~50% in elderly
  • More important when filling time is abreviated (e.g. exercise)
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104
Q

Draw a graph showing the pressure, volume and valve changes during the cardiac cycle. How does this relate to the the ECG and heart sounds?

A
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105
Q

How can volume changes in the cardiac cycle be measured experimentally?

A

Measured by MRI.

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106
Q

What is a dicrotic notch?

A

A secondary upstroke in the descending part of a pulse tracing corresponding to the transient increase in aortic pressure upon closure of the aortic valve.

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107
Q

Describe when CVP rises and falls during the cardiac cycle.

A

Rises when:

  • Atrium contracts
  • Atrium collects blood
  • AV valve shuts

Falls when:

  • Atrium relaxes
  • AV valve opens
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108
Q

How many peaks are there in the jugular venous pressure (JVP) per cardiac cycle?

A

2 - the x and y peaks

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109
Q

Draw a labelled graph of the JVP during the cardiac cycle.

A
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110
Q

Draw the pressure-volume graph for active and passive ventricular filling. What is the importance of this?

A

These boundaries are important because the pressure-volume loop for the ventricle cannot go outside of these.

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111
Q

Draw the pressure-volume graph for a ventricle during the cardiac cycle. Include valve opening and closing points.

A
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112
Q

What process triggers contraction in the heart?

A

Excitation-contraction coupling

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113
Q

Describe the process of excitation-contraction coupling.

A
  • Depolarisation of membrane causes L-type Ca2+ channels to open
  • Influx of calcium
  • Calcium triggers calcium release from the SR via ryanodine receptors (CICR)
  • This activates the contractile apparatus
  • After contraction, calcium levels are restored by the NCX and SERCA pump
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114
Q

What is the importance of a long action potential in cardiac myocytes?

A

A long AP means that meaningful amounts of calcium enter the cell.

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115
Q

How is the heart made to synchronise its contraction?

A

There are gap junctions throughout the atria and ventricles, which allow rapid spread of excitation throughout the atria and ventricle.

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116
Q

What is the importance of the number of gap junctions between cardiac myocytes?

A

The number sets the conduction velocity, determining fast and slow-conducting regions of the heart.

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117
Q

For how long is contraction delayed at the AV node?

A

0.1s

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118
Q

What is the name for how the heart generates its own electrical impulses?

A

Myogenic

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119
Q

Describe the path of excitation in the heart.

A
  • SAN initiates heart beat
  • Excitation spreads through atria rapidly
  • Excitation is delayed at AV node for 0.1s + Annulus fibrosus electrically insulates atria from ventricles
  • Excitation spreads rapidly through bundles of His towards the apex
  • Large Purkinje fibres ensure rapid spread across ventricle wall
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120
Q

What does ECG stand for?

A

Electrocardiogram (NOT echocardiogram)

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121
Q

What is an ECG? In 1 sentence, describe how it works.

A
  • A recording of the electrical activity of the heart, which is represented by a voltage-time graph.
  • It functions by detecting the skin surface potential differences that occur as a result of extracellular currents upon propagation of action potentials in the heart.
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122
Q

Where does an ECG detect potential changes?

A

At the skin surface.

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123
Q

What is the approximate size of the potential changes detected at the skin surface?

A

1mV

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124
Q

Why are there potential changes at the skin surface that can be detecting by an ECG?

A

Due to extracellular currents that result from heart activity.

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125
Q

Describe the in depth the principle of how an ECG works.

A
  • Contraction of myocytes in proximity occurs due to gap junctions that allow flow of positive charge from the depolarised myocyte to an adjacent one.
  • The circuit of the flow of charge is completed by an extracellular current in the antiparallel direction, which demonstrates the presence of a potential difference.
  • This potential difference is proportional to the mass of the heart that is activated.
  • The dipole reversed is created and detected when repolarisation occurs, giving a defelection in the opposite direction.
  • Pairs of electrodes can only detect dipoles in a single direction, but the spread of depolarisation in the heart is not in a uniform direction, meaning that a basic clinical ECG requires the use of at least 3 electrodes (allowing 3 potential differences to be measured simultaneously).
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126
Q

In an ECG, a depolarisation towards the positive electrode produces…

A
  • Wave of depolarisation towards a positive electrode results in a positive deflection
  • Wave of depolarisation away from a positive electrode results in a negative deflection
  • Wave of repolarisation towards a positive electrode results in a negative deflection
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127
Q

Draw how the membrane and extracellular potentials vary between these two cells during the passing of an action potential.

A
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128
Q

Is one axis of measurement in an ECG sufficient to map all electrical activity in the heart?

A

No, because dipoles are vector quantities, so they can only be detected when a component of the vector is in the direction of the line between the electrodes.

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129
Q

How many leads are used in a basic ECG? What is the name for this setup?

A

3 leads - This forms Einthoven’s triangle.

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130
Q

Draw the position of Lead I in Einthoven’s triangle, including the positive and negative electrodes, plus the direction of the dipole it measures.

A
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131
Q

Draw the position of Lead II in Einthoven’s triangle, including the positive and negative electrodes, plus the direction of the dipole it measures.

A
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132
Q

Draw the position of Lead III in Einthoven’s triangle, including the positive and negative electrodes, plus the direction of the dipole it measures.

A
133
Q

Draw Einthoven’s triangle, including all of the positive and negative electrodes.

A
134
Q

What factors affect the size of the deflection seen on an ECG?

A
  • Mass of cardiac tissue being excited
  • Speed of transmission through the tissue
135
Q

Draw the shapes of the different action potential types in the heart.

A
136
Q

Does the SAN action potential show up on an ECG trace?

A

No, because the number of SAN cells is too small.

137
Q

Draw a normal ECG trace, labelling each wave.

A
138
Q

What causes each wave of an ECG trace?

A
  • P wave -> Atrial depolarisation
  • QRS complex -> Ventricular depolarisation
  • T wave -> Ventricular repolarisation
139
Q

Which leads are “example” ECG traces typically recorded from?

A

Leads I or II

140
Q

Draw an ECG trace with corresponding mechanical events in the heart.

A
141
Q

Name some of the counter-intuitive observations in the ECG trace.

A
  1. There is no downwards defelction for atrial repolarisation
  2. QRS is a complex and not a simple downwards deflection
  3. The T wave is a positive deflection (like the R wave), even though it is caused by ventricular repolarisation
142
Q

ECG counter-intuitive observation 1: Explain why there is no downwards defelction for atrial repolarisation.

A

Atrial repolarisation is slow and does not produce a sharp electrical dipole.

143
Q

ECG counter-intuitive observation 2: Explain why there is a QRS complex instead of a simple, single deflection.

A

During the cardiac cycle, the ventricle’s electric dipole changes its angle.

144
Q

ECG counter-intuitive observation 3: Explain why if the R wave represents depolarisation, then why is the T wave also a positive deflection, even though it is repolarisation.

A
  • Ventricular APs have different durations depending on what depth they are at.
  • The endocardial AP is longer than the epicardial action potential (since there are fewer K+ in the endocardium)
  • So although the endocardium is the first to be excited, it is last to be repolarised, meaning that the dipole is in the same direction both times
145
Q

Draw a diagram showing the relative conduction velocities in parts of the heart.

A
146
Q

Draw some examples of some pathological ECGs.

A
147
Q

Add some flashcards about different pathological ECGs.

A

Do it - or read through essay about it.

148
Q

What are the two transport processes that occur in capillaries and what is the mechanism of these?

A

Solute exchange:

  • Diffusion
    • Occurs due to concentration gradients across wall
    • Obeys Fick’s Law

Fluid exchange:

  • Bulk flow
    • Occurs due to pressure gradients across wall
    • Obeys Starling’s Principle
149
Q

What are the 3 types of capillary?

A
  • Continuous
  • Fenestrated
  • Sinusoidal (Discontinuous)
150
Q

What is a continuous capillary and where are they found?

A
  • Moderate permeability
  • Found in:
    • Brain and nervous system (blood–brain barrier, v. tight)
    • Muscle, lungs, skin, fat & connective tissue
151
Q

What is a fenestrated capillary and where are they found?

A
  • Higher water permeability (especially for water)
  • Found in:
    • Exocrine glands, e.g. salivary glands
    • Endocrine glands
    • Other ‘high water turnover’ tissues e.g. kidney, synovial joints, anterior eye, choroid plexus (cerebrospinal fluid), gut mucosa
152
Q

What is a sinusoidal (discontinuous) capillary and where are they found?

A
  • High permeability -> Even allow RBCs through
  • Found in:
    • Liver
    • Spleen
    • Bone marrow
153
Q

What are intercellular clefts in capillaries?

A
  • A channel between two cells through which molecules may travel and gap junctions and tight junctions may be present.
  • They are smallest in continuous capillaries and widest in sinusoidal capillaries.
154
Q

What is glycocalyx?

A
  • Also known as the pericellular matrix, it is a glycoprotein and glycolipid covering that surrounds endothelial cells.
  • It blocks protein access to the intercellular cleft.
155
Q

What allows permeation of proteins THROUGH the capillary wall?

A

A system of vesicles.

156
Q

What are the 3 classes of capillary solutes and how do they permeate across the capillary wall?

A
157
Q

Compare the relative rates of glucose transport by diffusion and bulk flow across the capillary.

A
158
Q

Using Fick’s Law, derives an equation for permeability of a capillary wall and an equation for the flux relative to the permeability.

A
159
Q

Diffusion in the capillaries is a passive process. How can the rate be regulated?

A
  1. Increase blood flow -> This raises the mean concentration in the capillary
  2. Reduce interstitial concentration
  3. Increase capillary permeability (e.g. in response to increased endothelial shear stress)
  4. Recruitment of capillaries
    • Increases total surface area for diffusion
    • Shortens diffusion distance
160
Q

Why does increasing the blood flow through a capillary during exercise increase the rate of diffusion?

A

The concentration of the solute remains high at all points along the capillary.

161
Q

Are all capillaries perfused at rest?

A

No, some are only recruited during, for example, exercise.

162
Q

What is a Krough cylinder?

A

The muscle supplied with oxygen by one capillary.

163
Q

How does capillary recruitment during exercise increase the supply of nutrients to the muscle?

A
  • It reduces the radius of the Krough cylinders (the area supplied with oxygen by one capillary)
  • So the diffusion distance is shortened and diffusion occurs more rapidly
164
Q

What is oedema?

A

A condition characterized by an excess of watery fluid collecting in the cavities or tissues of the body.

165
Q

What are oedema and fluid absorption features of?

A

Oedema is a feature of:

  • Lymphatic disorder
  • Cardiac failure
  • Renal failure
  • Pleural effusions
  • Peritoneal swelling (ascites)
  • Joint effusions

Fluid absorption is a feature of:

  • Haemorrhage & shock
  • Renal & gut mucosa function
166
Q

Explain the Starling principle.

A

The Straling principle states that the bulk flow across a capillary wall is dependent on 4 forces:

  1. Capillary blood pressure (hydraulic force outwards)
  2. Interstitial fluid pressure (hydraulic force inwards)
  3. Colloid osmotic pressure of plasma proteins (osmotic suction force inwards)
  4. Colloid osmotic pressure of interstitial fluid (osmotic suction force outwards)

The rate of flow is proportional to the net flow difference across the wall.

167
Q

In capillary physiology, what is COP?

A
  • Colloid osmotic pressure
  • It is the osmotic suction force that arises from the presence of proteins in the capillaries and interstitial fluid
168
Q

Is all of the osmotic pressure across capillary walls exerted?

A
  • No, only a fraction, σ, is exerted across a semi-permeable membrane.
  • Effective osmotic pressure = σ x Potential osmotic pressure
169
Q

State and explain an equation for the Starling principle of capillary flow.

A

Jv = Lp x A x [(Pc - Pi) - σ(πp - πi)]

Where:

  • Jv = Bulk flow across wall
  • Lp = Hydraulic conductance of endothelium
  • A = Area
  • Pc = Capillary blood pressure
  • Pi = Interstitial fluid pressure
  • σ = Sigma (typically 0.9 in capillaries)
  • πp = Colloid osmotic pressure of plasma proteins
  • πi = cop of interstitial fluid
170
Q

Describe how inflammation relates to the Starling principle (in capillaries).

A
  • σ falls to about 0.4 (40%) in inflammation, due to gap formation
  • So the effective retaining force is greatly reduced
  • So fluid leaks out faster, causing inflammatory effusions & swelling
171
Q

Under normal conditions, the Straling principle dictates that net flow will occur in which direction across the capillary wall.

A
  • The Jv value is usually positive
  • This means there is a net outwards flow of liquid across the capillary wall
  • So lymph is increased and it flows back to the circulation
172
Q

How does lymph return to the circulation?

A

Via the thoracic duct.

173
Q

In terms of Starling principle, describe how oedema occurs.

A
  • Pc is raised or σπp is reduced
  • So there is an increased outwards flow across capillary walls
174
Q

In terms of the Starling principle, describe when increased flow into capillaries across the wall may occur.

A
  • When Pc is reduced
  • This is effectively a drop in pressure, such as after a haemorrhage
  • This results in increased absorption of the interstitial fluid
175
Q

Describe the bulk flow across a capillary wall along the length of the capillary when the capillary is well-perfused.

A
176
Q

Describe the bulk flow across a capillary wall along the length of the capillary when the capillary is under hypovolaemia.

A
177
Q

Classify the different types of oedema by their cause.

A
  • Excessive capillary filtration (see subtypes below)
  • Impaired lymphatic drainage, lymphoedema (high protein oedema)
178
Q

Describe the general ways in which cardiac output can be controlled.

A

Intrinsic:

  • Preload (Frank-Starling law)
  • Afterload (total peripheral resistance)

Extrinsic:

  • Autonomic nerves (these are involved in reflex responses)
  • Circulating agents
179
Q

Compare reflexes and intrinsic mechanisms that affect cardiac output.

A
  • Reflexes (such as the baroreflex) are responses that are actively enabled by the body detecting a change and responding to it, usually via the innervation of the heart
  • Intrinsic mechanisms (such as Frank-Starling and afterload) are effects that occurs simply due to physics and do not involve any active change from the body. For example, Frank-Starling ocurs normally due to the stretching of the heart tissue.

NOTE: Check if this is correct - this is just a good way to think about it.

180
Q

What is the difference between intrinsic and extrinsic control of cardiac output?

A
  • Intrinsic -> The normal firing of the SAN and the internal mechanisms that affect the output
  • Extrinsic -> Hormonal and neuronal control of the heart
181
Q

Describe the general innervation of the heart.

A
  • Sympathetic innervation innervates the entire heart
  • Parasympathetic innervation (vagus nerve) innervates just the SAN
182
Q

What is the equation fo arterial blood pressure (ABP) in relation to flow (cardiac output)?

A

ABP = Q x TPR

Where:

  • ABP = Arterial blood pressure
  • Q = Flow
  • TPR = Total peripheral resistance, related to viscosity and r4
183
Q

Describe how hypertension and heart failure are related to control of cardiac output.

A
  • Disregulation of the heart can lead to hypertension, which can lead to heart failure
  • A pre-disease phenotype is marked by loss of autonomic control, etc.
184
Q

What are preload and afterload? How does each affect cardiac output?

A

Preload:

  • The amount of sarcomere stretch experienced by cardiac muscle cells at the end of ventricular filling during diastole.
  • Related to ventricular filling, so it can be estimated using EDV (end diastolic volume)
  • It increases cardiac output (via Frank-Starling)

Afterload:

  • The pressure the heart must work against to eject blood during systole (ventricular contraction).
  • Proportional to the average arterial pressure.
  • It decreases cardiac output.
185
Q

What are some factors that may increase preload?

A
  • Hypervolemia
  • Regurgitation of heart valves
  • Heart failure
186
Q

What are some factors that may increase afterload?

A
  • Hypertension
  • Vasoconstriction
187
Q

What is the Frank-Starling Law?

A
  • The intrinsic relationship between end-diastolic volume (i.e. heart filling before contraction) and stroke volume.
  • It states that increased EDV results in:
    • Increased force of ventricular contraction
    • Increased stroke volume
    • Increased cardiac output
188
Q

Draw a graph to show Frank-Starling’s Law.

A
189
Q

Give an explanation of why the Frank-Starling Law of the heart is physiologically important.

A
190
Q

How does gravity affect venous return and pulse pressure?

A

This is due to the Frank-Starling mechanism.

191
Q

How does fainting occur?

A

Standing up causes pooling of blood in the feet, so venous return to the heart is decreased. Therefore, end-diastolic filling is reduced and so stroke volume is reduced (via Frank-Starling). Pulse pressure falls, which triggers fainting.

192
Q

Compare and explain the Frank-Starling curves for the heart:

  • During exercise
  • At rest
  • In heart failure
  • In fatal myocardial depression
A
  • This is due to sympathetic activation during exercise, etc.
  • The dip in the heart failure curve shows that injecting blood into certain patients is bad
193
Q

How is cardiac contraction affected by calcium levels and how can these be changed?

A
  • Raising intracellular calcium increases contraction for a given sarcomere length
  • Sympathetic stimulation drives up calcium levels
194
Q

How does sympathetic stimulation affect the Frank-Starling curve?

A

It shifts it up.

195
Q

In the heart, which beats which: vagus or sympathetic stimulation?

A

Vagus ALWAYS beats the sympathetic stimulation. Therefore, vagus removal is bad and has implications.

196
Q

Compare how stroke volume and heart rate change during dynamic exercise in a healthy state and following heart transplantation.

A

During exercise in a healthy state:

  • Stroke volume increases slightly
  • Heart rate increases a lot

During exercise after heart transplant:

  • Stroke volume increases a lot
  • Heart rate cannot change much since innervation is lost
197
Q

State how ischaemia affects heart contraction.

A

It is negatively ionotropic.

198
Q

Describe how acid affects heart contractility and why.

A
  • Acid decreases contraction
  • This is because the protons in the acid have preferrential binding to troponin C
199
Q

Describe how increased extracellular potassium affects heart contractility and why.

A
  • It decreases contraction
  • Potassium depolarises the cardiomyocytes:
    • Shorter action potential because IK channels are activated, which repolarise membrane
200
Q

What is the effect of a potassium injection on the heart?

A

Injection causes cardiac arrest.

201
Q

Is local blood flow determined by the heart?

A
  • No, it is mostly determined by tissues.
  • In most vascular beds, flow is regulataed to match metabolic demand (and be independent of the blood pressure)
202
Q

Give an example of a tissue that has specialised adaptations superimposed to regulate blood flow to it.

A

Kidneys both filter blood and need blood for oxygen.

203
Q

What is the purpose of reflexes?

A

Reflexes hold arterial blood pressure constant, so that local resistors (diameter of vessels) can regulate blood flow locally to different tissues.

204
Q

In one word, by what process is local blood flow regulated?

A

Autoregulation

205
Q

Write an equation for the local blood flow relative to pressure and resistance.

A
206
Q

What is capillary perfusion pressure?

A

The difference between the arterial and venous blood pressures on either side of the capillary.

207
Q

In this equation, what factors may are used to regulated local tissue blood flow?

A
  • Perfusion pressure (ABP - VBP) is not really used as regulator of local blood flow. Instead, changes in blood pressure are usually associated with pathology.
  • Therefore, resistance is used to regulate local blood flow, mostly via the radius of the vessels.
208
Q

What are some factors that may affect the capillary perfusion pressure (ABP - VBP)?

A
  • Cardiac contraction -> Hormones, Nerves, Frank-Starling
  • Water/Salt balance -> Thirst, Kidneys, Sweating
  • Vessel compliance and tension
209
Q

Across which vessels is there a greatest fall in blood pressure?

A

Arterioles

210
Q

How does halving the radius of a blood vessel change the resistance?

A

Increases it by a factor of 16.

211
Q

How does vasoconstriction of arterioles affect the pressure graph along the length of the circulation?

A
212
Q

How does vasodilation of arterioles affect the pressure graph along the length of the circulation?

A
213
Q

What is capillary recruitment and in which tissues is it especially important?

A
  • In certain capillaries, flow only occurs at higher perfusion pressures. This is capillary recruitment.
  • It is especially important in skeletal muscle.
214
Q

Describe how blood flow in different tissues changes between rest and the maximum.

A
215
Q

Why must a minimum arterial blood pressure be maintained and when must it be maintained?

A
  • Blood flow to tissues may be vulnerable at low ABP
  • It must be maintained when:
    • Standing up & laying down
    • Changes in circulating volume
    • Changes in external pressure
216
Q

For which tissues is low blood flow particularly damaging?

A

Kidney and cerebral vascular beds.

217
Q

What are the two types of auto-regulation involved in local blood flow control?

A
  • Myogenic auto-regulation
  • Metabolic auto-regulation
218
Q

What is myogenic auto-regulation?

A
  • Tissues controlling their perfusion independently of arterial blood pressure.
  • It is essentially an attempt to keep perfusion constant despite change in arterial blood pressure.
219
Q

What is the Bayliss effect and how does it work?

A
  • It is the effect that explains myogenic auto-regulation
  • It is an effect seen in arterioles.
  • When blood pressure is increased in the blood vessels and the blood vessels distend, they react with a constriction; this is the Bayliss effect.
  • Stretch of the muscle membrane opens a stretch-activated ion channel. The cells then become depolarized and this results in a Ca2+ signal and triggers muscle contraction.
  • It is important to understand that no action potential is necessary here; the level of entered calcium affects the level of contraction proportionally and causes tonic contraction.
220
Q

Draw a graph to show how the Bayliss effect allows a response to an increase in blood pressure.

A
221
Q

Draw a real graph of blood flow against ABP (accounting for factors such as the Bayliss effect).

A
222
Q

Explain the mechanism for the Bayliss effect and what the evidence for this is.

A

The evidence is that the ffect can be blocked using verapamil.

223
Q

In which tissues is myogenic auto-regulation (Bayliss effect) of blood flow a major mechanism?

A
  • Major mechanism in: cerebral, renal and coronary tissues
  • Not a major mechanism in: pulmonary and cutaneous tissues (because lungs receive all of the blood from the right ventricle)
224
Q

Is auto-regulation the dominant mechanism controlling local blood flow? What is the evidence for this?

A

No, because autoregulation seeks to keep blood flow almost constant at a wide range of arterial blood pressures, so it could not be used to change perfusion during different metabolic ststes (e.g. exercise).

225
Q

What is metabolic auto-regulation of blood flow?

A
  • Tissues matching local perfusion through them with local metabolism
  • It can be seen as the level that is higher up to myogenic auto-regulation (i.e. the myogenic auto-regulation aims to keep blood flow constant regardless of ABP, while metabolic auto-regulation tweaks the blood flow supplied according to the metabolic needs of the tissue)
226
Q

Perusion of tissues often matches metabolic demand. Which tissues are relatively under-perfused and which are relatively over-perfused?

A

Over-perfused: Kidney and skin

Under-perfused: Brain and heart

227
Q

In general, how is blood rationed fairly according to metabolic demand of individual tissues?

A
  • Arterioles are sensitive to metabolic demand of tissues
  • Vasoconstriction occurs in selected beds
228
Q

What overrides what: myogenic or metabolic auto-regulation?

A

Metabolic overrides myogenic

229
Q

Draw the flow-pressure curve (for perfusion through a tissue) to show the effect of meabolic auto-regulation.

A
230
Q

In what tissues is metabolic auto-regulation especially important?

A

Coronary, Cerebral, Skeletal

231
Q

Arterioles need to be sensitive to different markers of the metabolic state of the tissues they supply so that they can vasoconstrict/vasodilate and provide an appropriate share of the total blood supply. What are some of these markers and in which tissues are they important?

A
  • Adenosine release -> Coronary tissues
  • Acidity -> Cerebral tissues
  • Extracellular K+ -> Skeletal muscle
232
Q

Describe how adenosine release is involved in metabolic auto-regulation and state which tissues this is important in.

A

Important in coronary circulation:

  • Adenosine is a marker of metabolic insufficiency (when the perfusion is insufficient)
  • When perfusion is insufficient, ATP falls and AMP is released from cells (this is the adenosine)
  • The adenosine binds to A2A receptors, which triggers an increase in cAMP
  • The cAMP leads to decreased MLCK activity and therefore vasodilation
233
Q

Describe how acidity is involved in metabolic auto-regulation and state which tissues this is important in.

A

Important in cerebral tissues:

  • Acidity is a marker of a high metabolic demand
  • This is because CO2 from respiration is acidic
  • The acidity causes decreased MLCK activity, which results in vasodilation
234
Q

Describe how extracellular potassium is involved in metabolic auto-regulation and state which tissues this is important in.

A

Important in skeletal muscle:

  • High extracellular potassium is a marker of high metabolic activity, since potassium is released extracellularly when skeletal muscle contracts
  • It could be predicted that this would cause depolarisation of vascular smooth muscle in arterioles, resulting in contraction, but in reality this does not occur
  • Small increases in [K+]o result in hyperpolarisation (as is shown in the graph), which results in vasodilation
235
Q

What is reactive hyperaemia, how does it work and in what tissues is it most important?

A
  • It is the spike in blood flow through a tissue after a period of occlusion
  • It works because ischaemia (caused by the occlusion) causes vasodilation
  • It is important in flushing away metabolites after the period of occlusion
  • Important in: Skeletal muscle
236
Q

According to the spec, what are some factors affecting local vascular control?

A
  • Temperature
  • Metabolic
  • Myogenic
  • Autacoids
  • Nitric oxide
237
Q

What are autacoids?

A
  • Biological factors which act like local hormones, have a brief duration, and act near their site of synthesis.
  • They can be either vasoconstrictors or vasodilators.
  • For example, histamine is a vasodilator.
238
Q

Draw the pathway to show how nitric oxide results in vasodilation (and the involvement of the endothelium in this).

A
239
Q

Describe the role of the endothelium in control of regional blood flow.

A
  • Various blood borne substances that come in contact with vascular endothelial cells cause the production and release of endothelial factors that cause contraction or relaxation of vascular smooth muscle.
  • There are 3 main endothelial-derived factors:
    • Nitric oxide (vasodilator)
    • Prostacyclin (vasodilator)
    • Endothelin (vasoconstrictor)
240
Q

Describe neural control of local blood flow.

A
  • Widespread sympathetic innervation of blood vessels -> Vasoconstriction due to norepinephrine (in response to chemical markers in the blood detected by vasomotor centres)
  • Some parasympathetic innervation of blood vessels -> Vasodilation due to acetylcholine and NO (in response to chemical markers in the blood detected by vasomotor centres)
241
Q

Describe hormonal control of local blood flow.

A
  • Kidneys act via the renin-angiotensin-aldosterone system
  • Adrenal glands act via the release of catecholamines
242
Q

Describe the renin-angiotensin system in the kidneys.

A
243
Q

What is the function of reflexes in the circulatory system and how does it relate to auto-regulatory mechanisms?

A
  • Hold ABP constant, allowing local autoregulatory mechanisms to act independently
  • Help sustain cerebral perfusion during postural changes
244
Q

Describe the effect of temperature on control of regional blood flow and which tissue this is important in.

A

Important in cutaneous tissues:

  • Heat leads to lesser release of NA from sympathetic neurones on arteriovenous anastamoses
  • This leads to increased perfusion of vessels near the skin, so cooling can occur
245
Q

What is the baroreflex?

A
  • One of the body’s homeostatic mechanisms that helps to maintain blood pressure at nearly constant levels.
  • The baroreflex provides a rapid negative feedback loop in which an elevated blood pressure reflexively causes the heart rate to decrease and also causes blood pressure to decrease.
246
Q

What type of feeback is the baroreflex?

A

Negative feedback

247
Q

Where are the baroreceptors involved in the baroreflex found?

A
  • Aortic arch
  • Carotid sinus
248
Q

Describe the mechanism by which the baroreflex works.

A
249
Q

What nerve are the aortic arch baroreceptors and carotid sinus baroreceptors innervated by?

A
  • Aortic arch baroreceptors -> Vagus nerve (X)
  • Carotid sinus baroreceptors -> Glossopharyngeal nerve (IX)
250
Q

What type of receptor are baroreceptors?

A

Stretch-activated mechanoreceptors

251
Q

To what part of the brain do baroreceptors feed information?

A

Brainstem, which influences the vasomotor centre in the medulla.

252
Q

Describe how the baroreflex allows response when standing up (orthostasis).

A

Upon standing, blood pools at the feet, whcih means that arterial pressure falls, but this change is counteracted by the vasoconstriction that occurs as a result of the baroreflex.

253
Q

Aside from arterial baroreceptors (i.e. carotid sinus and aortic baroreceptors), what are the other baroreceptors in the body?

A
  • Cardiopulmonary baroreceptors
  • These may be found in the atria, ventricles and pulmonary vessels
  • Activation of these receptors causes an increase in heart rate
254
Q

Draw a summary of all of the things that can influence systemic and regional blood flow.

A
255
Q

Draw a flowchart to show all of the ways of controlling systemic and local blood flow.

A
256
Q

Compare the effects of sympathetic and parasympathetic stimulation of the heart on:

  • Chronotropy (heart rate)
  • Inotropy (contractility)
  • Dromotropy (conduction velocity)
A

Sympathetic:

  • Chronotropy -> Increases
  • Inotropy -> Increases
  • Dromotropy -> Increases

Parasympathetic:

  • Chronotropy -> Decreases
  • Inotropy -> Little change
  • Dromotropy -> Decreases
257
Q

What is the intrinsic pacemaker pace? Which is the prodominant control over it, sympathetic or parasympathetic?

A
  • Intrinsic = About 00bpm
  • The parasympathetic innervation predominates at rest, which is demonstrated by the fast that the resting heart rate is lower than the rate of firing of the SAN when it is isolated
258
Q

Name all of the channels, carriers and receptors that are found on pacemaker cells in the heart.

A
259
Q

Draw the shape of a pacemaker action potential, showing the resting membrane potential, threshold potential and peak potential.

A
260
Q

Describe the ionic basis of the SAN action potential in the heart.

A
  • The membrane is gradually depolarised by 3 main inwards currents:
  1. Sodium currents are partly background currents and ‘funny’ currents (If) through non-selective channels that open upon hyperpolarisation, allowing sodium and potassium to flow.
  2. The second main current in the pacemaker potential is that created by the electrogenic sodium-calcium exchanger, which moves 3 sodium ions in for every calcium ion moving out.
  3. The third current responsible for the final part of the pacemaker potential is a calcium current that is firstly through transient (T-type) calcium channels, and then also L-type calcium channels at higher membrane potentials.
  • Above the threshold, the rapid depolarisation (phase 0) is caused mostly by the opening of L-type calcium channels.
  • Repolarisation (phase 3) occur due to efflux of K+ through voltage-gated potassium channels.
261
Q

Why is the SAN such an important target for regulation of the heart?

A

The SAN exhibits dominance over the other pacemaker centres electrically downstream, such as the atrioventricular node, since these have a lower frequency of action potentials and are excited before spontaneous firing can occur.

262
Q

Compare and explain the shape of a pacemaker and ventricular action potentials.

A

In non-pacemaker cells, calcium influx prolongs the duration of the action potential and produces a characteristic plateau phase.

263
Q

What is the pacemaker potential?

A

The pacemaker potential (also called the pacemaker current) is the slow, positive increase in voltage across the cell’s membrane (the membrane potential) that occurs between the end of one action potential and the beginning of the next action potential.

264
Q

Why is the resting membrane potential in SAN cells unstable?

A
  • The SA nodal cells have an unstable resting membrane potential that spontaneously depolarizes due to a pacemaker potential.
  • This is caused by the “funny” Na+ current and a decrease in the conductance of the inward rectifier K+ channel.
265
Q

What is the calcium clock mechanism?

A

An alternative mechanism proposed for the generation of the pacemaker rhythm, involving spontaneous Ca2+ release from the sarcoplasmic reticulum (SR).

266
Q

Describe the mechanism by which sympathetic stimulation affects the contraction and relaxation the heart.

A
  • Noradrenaline and adrenaline bind to β1 adrenoceptors (on all parts of the heart), which are Gs-coupled GPCRs that stimulate adenylate cyclase and increase intracellular cAMP, and therefore protein kinase A.
  • cAMP stimulates the funny current (If) -> Increases the heart rate (at SAN)
  • PKA phosphorylates 3 things:
    • L-type calcium channels -> Helps to speed up decay of pacemaker potential (at SAN), so heart rate is increased and contraction is strong due to more calcium entry
    • Delayed rectifier potassium channels -> Enabling faster repolarisation (so max heart rate is increased)
    • Phospholamban -> Stops it inhibiting the Ca2+-ATPase on the sarcoplasmic reticulum, so uptake into the SR is increased (disinhibition) -> Relaxation occurs more quickly and increases amount of calcium stored in SR (for stronger contraction)
  • The higher heart rate is also enabled by faster firing at the atrioventricular node
  • There are also perhaps additional effects (e.g. on kinetics of binding of Ca2+ to myofilaments)
267
Q

How can the duration of action of noradrenaline and adrenaline be extended?

A

Methylxanthines (e.g. caffeine) are phosphodiesterase inhibitors, which extend the action by preventing the degradation of cAMP by phosphodiesterase.

268
Q

What can be used to block the binding of catecholamines to β1 receptors in the heart?

A

Propranolol

269
Q

What can be used to block the funny current in SAN cells?

A

Caesium

270
Q

What can be used to block L-type calcium channels in the heart?

A

Verapamil

271
Q

What are the muscarinic ACh receptors on the heart and what type of GPCR are they?

A
  • M2
  • These are Gi-coupled, so they result in inhibition of adenylate cyclase
272
Q

Describe the mechanism by which parasympathetic stimulation affects the contraction and relaxation the heart.

A
  • Acetylcholine binds to M2 muscarinic (only SAN and AVN receive parasympathetic innervation), which are Gi-coupled GPCRs:

α subunit of Gi inhibits adenylate cyclase (therefore has opposing effects to sympathetic stimulation):

  • Reduction in cAMP inhibits the funny current (If) -> Slows the heart rate
  • Reduction in PKA phosphorylating 3 things:
    • L-type calcium channels -> Slows decay of pacemaker potential (at SAN), so heart rate is slower
    • Delayed rectifier potassium channels -> Slowing repolarisation (so max heart rate is decreased)
    • Phospholamban -> Allows it to keep inhibiting the Ca2+-ATPase on the sarcoplasmic reticulum, so uptake into the SR is decreased -> Relaxation occurs more slower and increases amount of calcium stored in SR (for stronger contraction) -> Not really relevant at the SAN and AVN though

βγ subunit directly activates a K+ channel (IKACh) -> This is a hyperpolarisation channel, so it opposes all depolarisation throughout the cardiac cycle.

273
Q

What are inotropes?

A
  • Inotropes are a group of drugs that alter the contractility of the heart.
  • Positive inotropes increase the force of contraction of the heart, whereas negative inotropes weaken it.
274
Q

What are the two main uses of cardiac inotropes?

A
  • Treating heart failure
  • Treating acute hypovolaemic or cardiogenic shock
275
Q

What are the two main classes of positive inotrope?

A
  • Sympathomimetics
  • Non-sympathomimetics
276
Q

What are sympathomimetic inotropes?

A

Drugs that increase the contractility of the heart by mimicking the effects of sympathetic stimulation.

277
Q

What are non-sympathomimetic inotropes?

A

Drugs that increase the contractility of the heart in a way that does not involve mimicking the effects of sympathetic stimulation.

278
Q

When are sympathomimetic inotropes useful?

A

When treating acute shock or hypotension where myocardial ischaemia is not a feature of the disease.

279
Q

What are the different types of sympathomimetic inotropes?

A
  • Phosphodiesterase inhibitors
  • Catecholamines
280
Q

How do phosphodiesterase inhibitors work as positive inotropes? Give an example of one.

A
  • Inhibit phosphodiesterase III, which usually degrades cAMP
  • Normally, beta stimulation of the heart activates production of cAMP (which leads to increased contractility), so PDE3 inhibitors mimick the effects of sympathetic stimulation

Example: Methylxanthines (aminophylline)

281
Q

How do catecholamines work as positive inotropes? Give an example of one.

A
  • Act on cardiac β1 receptors
  • Increase rate and force of contraction
  • Increase myocardial oxygen consumption
  • Adrenaline also increases vascular tone

Examples: Adrenaline, Noradrenaline and Dopamine

282
Q

Describe how elevation of adrenaline levels affects vascular tone. What is the result of this?

A

Moderate elevation of blood adrenaline:

  • Splanchnic vasoconstriction (alpha 1)
  • Skeletal muscle arteriolar dilation (beta 2)
  • Increased cardiac output (beta 1)
  • Result: Little change in blood pressure, so not much use in hypotension

Greater elevation of blood adrenaline:

  • Splanchnic vasoconstriction (alpha 1)
  • Skeletal muscle arteriolar constriction (alpha 1)
  • Increased cardiac output (beta 1)
  • Result: Elevated blood pressure, so can be used in treatment of hypotension
283
Q

What is the best catecholamine to use as a positive inotrope and why?

A
  • Dopamine
  • Other catecholamines cause reduced perfusion of the kidneys and mesenteric beds, leading to potential damage, but there are specific dopamine receptors that mean that dopamine leads to vasodilation of these arterioles, sparing the kidneys
284
Q

What are some of the side effects of use of catecholamines as positive inotropes? [EXTRA]

A
  • Myocardial ischaemia (due to increased workload of the heart)
  • Risk of dysrythmia, which may be fatal
285
Q

When are catecholamines not used as positive inotropes?

A

When there is already a high risk of cardiac ischaemia, since they increase the workload on the heart (increasing the risk of ischaemia occuring).

286
Q

What is dobutamine and when is it used?

A
  • It is a synthetic analogue of dopamine.
  • It can be used as a positive inotrope since it is a sympathomimetic.
  • It is designed to minimise the risk of myocardial ischaemia, which is a risk with standard catecholamine use.
287
Q

When are non-sympathomimetic positive inotropes used?

A

Most useful when there is (or there is a high risk of) ischaemia failure.

288
Q

What are the main types of non-sympathomimetic positive inotropes?

A
  • Calcium sensitizers
  • Glycosides
  • Apelin
289
Q

How do calcium sensitizers work as positive inotropes?

A

They increase the sensitivity of the contractile mechanism to calcium, meaning that the force of contraction is increased without additional ion pumping.

290
Q

How do calcium sensitizers affect cardiac oxygen demand?

A

They only increase it slightly, since contraction increases without an increase in ion pumping.

291
Q

Give two examples of calcium sensitizers (that act as positive inotropes) and their mechanism of action. [EXTRA]

A
  • Levosimendan -> Acts on troponin C
  • Omecamtiv mecarbil -> Prolong thecontractile phase of actin­-myosin cycling, so increasing contractile force
292
Q

What are some examples of cardiac glycosides?

A
  • Digoxin
  • Ouabain
  • Digitalis
293
Q

Describe a proposed mechanism of action for cardiac glycosides.

A

Inhibit Na+/K+-ATPase, leading to:

  • Build-up of sodium within the cell
  • Reduction of sodium gradient to drive sodium-calcium exchanger
  • Hence, less calcium extruded
  • Calcium builds up, so there is increased force of contraction
294
Q

What are the characteristics of how cardiac glycosides work?

A
  • Increase cardiac contractility
  • Little increase in oxygen demand
  • Atrioventricular block (usually partial)
  • Delayed onset of inotropic action: 3‒4h
295
Q

What are some problems with the use of cardiac glycosides as positive inotropes?

A
  • Low therapeutic ratio
  • Risk of dysrhythmia
  • Toxicity enhanced by low plasma potassium level
296
Q

How do indirect inotropes work?

A
  • They work by indirect effects on the cardiovascular system, such as vasodilation, so that afterload is decreased and therefore cardiac output is increased.
  • However, they are not strictly positive inotropes as per the BM definition.
  • They do not have direct effects on the heart, so they may be useful in treating ischaemia.
297
Q

Compare the terms ischaemic and hypoxic.

A
  • Ischaemic -> General reduction of blood flow to a tissue, so many metabolites are afected
  • Hypoxic -> Just refers to a lack of oxygen
298
Q

Is calcium used as an inotrope? Why?

A

No, because the heart cannot fully relax between beats.

299
Q

How does propranolol affect cardiac contractility and why?

A
  • It decreases contractility
  • Because it is an adrenoceptor antagonist
300
Q

How are cardiac dysrhythmias classified?

A
  • Classified by site:
    • Atrial
    • Nodal
    • Ventricular
  • And by type (in order of increasing severity):
    • Ectopics
    • Tachycardia
    • Flutter
    • Fibrillation

These rhythms tend to be progressive, ectopics eventually progressing to flutter and fibrillation.

301
Q

Name some examples of common dysrhythmias.

A
  • Atrial fibrillation
  • Complete heart block
  • Ventricular fibrillation
  • Ventricular tachycardia
302
Q

What are some broad possible causes of cardiac dysrhythmias?

A
  • Abnormal initiation
    • Spontaneous depolarisation of the resting membrane
  • Abnormal propagation
    • Abnormal circuits
    • Shortened action potential
303
Q

What are some different examples of anti-dysrhythmic drugs? [IMPORTANT]

A
  • Lidocaine
  • Propranolol (beta-blocker)
  • Amiodarone
  • Verapamil
  • Adenosine
304
Q

How can lidocaine work as an anti-dysrhythmic drug? [IMPORTANT]

A

Bind to voltage-gated sodium channels, so:

  • Extend effective refractory period (until the drug dissociates from the channel) -> Reduces risk of propagation of abnormal impulses
  • Reduces excitability -> Decreased availability of sodium channels reduces risk of spontaneous depolarization

Ideally, should dissociate from the channel just before the next sinus beat (so as not to depress normal rhythm), but in practice kinetics vary widely between drugs.

305
Q

Explain the concept of frequency dependence of lidocaine when treating cardiac dysrhythmias.

A
  • An impulse arriving soon after the lidocaine begins to dissociate will be suppressed more than an impulse arriving later (when more dissociation has occurred and so more sodium channels are available)
  • Therefore, high-frequency dysrythmias (such as tachycardia, flutter and fibrillation) should be suppressed more than low-frequency impulses (such as in normal sinus rhythm).
306
Q

What are some side effects of lidocaine (when treating cardiac dysrythmias)?

A
  • Reduced cardiac contractility (i.e. cardiac failure)
  • Reduced contractility may lead to reduced coronary perfusion, so ischaemia, so more dysrhythmia.
307
Q

What are two examples of beta blockers that are used as anti-dysrhythmic drugs?

A
  • Propranolol -> Non-specific
  • Atenolol -> Beta-1 specific
308
Q

How can beta blockers (e.g. propranolol) be used to treat cardiac dysrhythmias?

A

Two modes of action:

  • Acutely, reduce sympathetic drive:
    • Reduce myocardial oxygen debt (both sympathetic drive and ischaemia contribute to dysrhythmias)
    • Reduce disparity and shortening of action potentials stimulated by sympathetic drive
    • Reduce pacemaker currents induced by sympathetic stimulation.
  • Chronically:
    • Increase action potential length (and so increase effective refractory period), said by some to be an anti-dysrhythmic effect
    • Reduce cardiac workload and hence reduce oxygen debt

Useful in “secondary prophylaxis”, preventing further ischaemic episodes and associated dysrhythmia.

309
Q

What are some side effects of use of beta blockers as anti-dysrhythmic drugs?

A

Fall in contractility (block positive inotropic effect of sympathetic drive).

310
Q

How can amiodarone work as an anti-dysrhythmic drug?

A

Mechanism:

  • Primary mechanism of action: Blockage of voltage-gated potassium channels → Prolonged repolarization of the cardiac action potential
  • Secondary mechanism of action: Inhibits β-receptors and sodium and calcium channels → Decreases conduction through the AV and sinus node

Effects:

  • Lengthened action potential (takes about three weeks to develop)
  • Reduced cardiac workload, hence reduced myocardial ischaemia.
311
Q

What are some side effects of amiodarone (when treating cardiac dysrythmias)?

A
  • Fall in cardiac contractility
  • Many low-level side effects that limit its use in practice
312
Q

How can verapamil work as an anti-dysrhythmic drug?

A
  • Calcium antagonist
  • Not commonly used, but occasionally useful in nodal and ischaemic dysrhythmia.
  • In ischaemic cells, depolarizing current may be carried by calcium: verapamil may act as an antagonist, and so reduce excitability.
  • Reduced intracellular calcium might also discourage cellular uncoupling, so improving conduction and decreasing the risk of spontaneous depolarization of individual cells.
313
Q

What are some side effects of verapamil (when treating cardiac dysrythmias)?

A

Fall in cardiac contractility.

314
Q

How can adenosine act as an anti-dysrhythmic drug?

A

The mechanism is not fully understood. It slows transmission at the AV node.

315
Q

How is aspirin used in treatment of cardiac dysryhthmias?

A

It has a long-term antithrombotic effect, so it is involved in secondary prophylaxis since they prevent myocardial ischaemia (which contributes to cardiac dysrythmias).

316
Q

How are cardiac glycosides related to cardiac dysryhthmias?

A
  • Ouabain is used to treat congestive heart failure and supraventricular arrhythmias due to re-entry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation
  • This is because its action (inhibition of Na+/K+-ATPase, which stimulates NCX and accumulates calcium in the cell) causes a decrease in heart rate since the length of the action is reduced
  • However, cardiac glycosides can also induce a range of dysrhythmias, including bradycardia

[CHECK THIS]

317
Q

What is a secondary pacemaker? [IMPORTANT]

A
  • A “secondary pacemaker” is any focal collection of heart muscle cells that has the ability to take over in case the primary pacemaker goes down.
  • Generally, it is the AVN.
  • It’s like a backup system. Whenever the primary pacemaker is working, the secondary pacemakers are “overdriven” by the primary pacemaker and so they never fire on their own.
318
Q

Give an example of an anti-muscarinic drug used as anti-dysrhythmic. How does it work? [IMPORTANT]

A
  • Atropine
  • Inhibits M2 muscarinic receptor stimulation
  • Increases heart rate so can be used to treat bradycardia
319
Q

What are some common examples of cardiac dysrhythmias? [IMPORTANT]

A

Mentioned in spec:

  • Atrial fibrillation
  • Heart block -> All 3 types
  • Ventricular fibrillation
  • Ventricular tachycardia

Other types:

  • Wolf-Parkinson-White syndrome
  • Torsade de Pointes
  • Atrial flutter
320
Q

What are atrial flutter and atrial fibrillation? How do they appear on an ECG?

A
  • Atrial flutter
    • A type of atrial tachycardia where the atria of the heart beat too quickly in a fast, usually regular, rhythm
    • Multiple “sawtooth” P waves for each ventricular wave, but ventricular waves are
  • Atrial fibrillation
    • Closely related to atrial flutter. However, the arrhythmia that occurs in AFib is much more chaotic and results in a fast and usually very irregular heart rhythm or an atypical and irregular ventricular rate that can effect heart health.
    • No P waves. Irregular ventricular waves.

Atrial flutter can develop into atrial fibrillation. They lack a P-wave.

321
Q

What is ventricular fibrillation? How does it appear on an ECG?

A
  • Where the ventricles of the heart quiver instead of pumping normally. It is due to disorganized electrical activity
  • ECG: No discernable P wave, QRS complex or T wave. Complete mess.
322
Q

What is ventricular tachycardia? How does it appear on an ECG?

A
  • A regular, fast heart rate that arises from improper electrical activity in the ventricles of the heart. Ventricular tachycardia may result in ventricular fibrillation and turn into sudden death.
  • ECG: More than 3 ventricular beats in a row. Wide QRS complex.
323
Q

What is Torsade de Pointes? How does it appear on an ECG?

A
  • “Twisting of peaks”
  • A specific type of abnormal heart rhythm that can lead to sudden cardiac death.
  • It is a polymorphic ventricular tachycardia.
  • ECG: QRS complexes “twist” around the isoelectric lines
324
Q

What is Wolff-Parkinson-White syndrome? How does the ECG appear?

A
  • A dysrhythmia with an underlying mechanism that involves an accessory electrical conduction pathway between the atria and the ventricles.
  • ECG: Shows pre-excitation.
325
Q

What is heart block and what are the different types? [IMPORTANT]

A
  • Disturbance of conduction at the AVN/bundle branches
  • 1st degree = slowed conduction
  • 2nd degree = partial conduction
  • 3rd degree = complete block (ventricular rate = 30-40 bpm)
326
Q

How does a first-degree heart block appear on an ECG?

A
  • Long PR interval
  • P wave may blend into previous wave
327
Q

What are the different types of secondary heart block and how do they appear on an ECG?

A

Mobitz I:

  • Usually an AVN problem.
  • ECG: Progressively longer and longer PR intervals until eventually an entire wave is missed. Then returns to normal.

Mobitz II:

  • Usually a distal conduction system (His-Purkinje System) problem.
  • ECG: An entire wave is missed every few waves. This is not preceded by progressive PR lengthening like Mobitz I.

2: 1 AV block:
* ECG: 2 P waves for each QRS complex.

328
Q

How does a third-degree heart block appear on an ECG?

A
  • Since there is no communication between the SAN and AVN, the two function independently and the AVN fires independently to trigger contraction at a much lower rate (about 40bpm)
  • This means that the P waves are at constant intervals and the QRS complexes are at constant intervals, but these are totally indendent and don’t line up

YEAR 1 - Physiology and Pharmacology (Anton) (13 decks)

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