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Life Support Systems 1 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Describe the different planes of view with respect to anatomy.

A
  • Coronal/frontal plane
  • Mid-sagittal/median plane
  • Transverse/axial plane
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2
Q

Identify the pairs of words used to describe location in anatomy.

A
  • Anterior and Posterior
  • Superior and Inferior
  • Distal and Proximal (usually for limbs)
  • Lateral and Medial
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3
Q

Where is the heart in the body?

A

Sits in the Pericardium in the mediastinum of the thorax, slightly behind the left lung

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4
Q

What is the mediastinum? What does it contain?

A

The space in the thorax (chest cavity) between the two pleural sacs.
Contains: Heart. aorta, trachea, oesophagus, and thymus gland.

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5
Q

What is the Pericardium?

A
  • Fibroserous sac surrounding the heart and its great vessels
  • Consists of two layers; fibrous and serous
  • Serous has two parts; Parietal (lines the fibrous) and the Visceral (adheres to the heart)
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6
Q

What are the four chambers of the heart?

A
  • Right atrium
  • Left atrium
  • Right ventricle
  • Left ventricle
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7
Q

What are the main vessels that enter and leave the heart?

A 
Enter:
- (inferior and superior) Vena Cava
- Pulmonary veins
Leave:
- Pulmonary trunk/artery
- Aorta
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8
Q

What are the vessels that branch from the aorta?

A
  • Braciocephalic trunk
    - Right subclavian artery
    - Right common carotid artery
  • Left common carotid artery
  • Left subclavian artery
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9
Q

Describe the position and relations of the aortic arch and descending aorta.

A

Aortic arch is above the Pulmonary trunk.

Descending aorta is behind the heart going down to the diaphragm.

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10
Q

How does blood return to the heart from the head and neck?

A

Through the Brachiocephalic veins:

  • Right Brachiocephalic vein
    - Right internal jugular vein
    - Right subclavian vein
  • Left Brachiocephalic vein
    - Left internal jugular vain
    - Left subclavian vein
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11
Q

What do the vessels that branch from the aorta supply?

A
  • Braciocephalic trunk
    - Right subclavian artery - right arm
    - Right common carotid artery - head and neck
  • Left common carotid artery - head and neck
  • Left subclavian artery - left arm
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12
Q

What are the valves of the heart?

A 
Right:
Atrioventricular - Tricuspid valve
Semi-lunar - Pulmonary valve
Left:
Atrioventricular - Mitral valve
Semi-lunar - Aortic valve
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13
Q

What are the structural similarities between the left and right valves?

A

All valves have cusps which close in response to pressure and nodules which allow a tight seal.

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14
Q

What are the structural differences between the left and right valves?

A

Right:
Tricuspid - 3 cusps (anterior, septal and posterior)
Pulmonary - 3 cusps (left, right and anterior)
Left:
Mitral - 2 cusps (anterior and posterior)
Aortic - 3 cusps (right, posterior and left)

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15
Q

What are the main coronary arteries?

A

Right coronary artery; posterior inter-ventricular branch (supplies back of heart) and sinu-atrial nodal branch (supplies SA node)

Left coronary artery; circumflex branch (supplies back of heart), anterior inter-ventricular branch (is between left and right ventricle)

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16
Q

What are the main cardiac veins?

A

Great cardiac vein

The coronary sinus is at the posterior of the heart and is where the coronary veins feed into. The blood is returned to the right atrium of the heart.

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17
Q

Where does the blood from the coronary arteries come from?

A

The arteries join the aorta at the aortic sinus of the cusps in the aortic valves.

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18
Q

What blood vessels go to the head and neck, lungs and thoracic and abdominal cavities?

A

Head and neck - Common carotid arteries
Lungs - Pulmonary arteries
Thoracic and Abdominal cavities - Aorta

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19
Q

What are the four main components of the conduction system of the heart?

A
  • Sinoatrial node
  • Inter-nodal fibre bundles (e.g. Bachmann’s bundle)
  • Atrioventricular node
  • Ventricular bundles (bundle branches and Purkinje fibres)
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20
Q

List the sequence of events from excitation that cause contraction and then relaxation of a ventricular cell.

A
  1. Depolarization of the myocyte (Na+ influx etc.)
  2. Notch as K+ pumped out (voltage gated, efflux)
  3. Action potential maintained due to Ca2+ entry though L-type voltage gated channels and Ca2+ induced Ca2+ release of the sarcoplasmic reticulum stores.
    * Ca2+ causes contraction, so is influx is proportional to the force of contraction*
  4. During relaxation Ca2+ is either taken up into the SR by Ca2+ ATPase or removed from the cell by Na/Ca exchanger. This and K+ efflux causes repolarization.
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21
Q

What are the two forms of contraction?

A

Isometric - Muscle fibres don’t change length but pressure increases

Isotonic - Muscle fibres shorten

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22
Q

What is the preload and afterload with respect to the heart?

A

Preload - Blood filling the ventricles that causes stretching of the ventricular walls

Afterload - The load against which the left ventricle ejects blood after opening of the aortic valve

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23
Q

What is Starling’s Law of the heart?

A

Increased diastolic fibre length increases ventricular contraction.
(and therefore the ventricles pump a greater stroke volume)

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24
Q

Why is Starling’s Law true?

A
  • Increased number of myofilament cross bridges forming

- Increased sensitivity/affinity to Ca2+ of Troponin C

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25
Q

What are the differences between relationship between length and tension for skeletal and cardiac muscle?

A
  • Cardiac muscle is more resistant to stretch
  • There is a larger passive force in cardiac muscle and therefore a greater total force
  • Cardiac muscle is less compliant than skeletal muscle
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26
Q

Why are there differences between the relationship between length and tension for skeletal and cardiac muscle?

A

Due to the properties of the extracellular matrix and cytoskeleton

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27
Q

What does preload depend on?

A

The venous return to the heart (i.e. volume of blood returning)

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28
Q

What are measures of the preload and afterload?

A

Preload - End-diastolic volume, end-diastolic pressure, right atrial pressure

Afterload - Diastolic arterial blood pressure

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29
Q

State the Law of Laplace.

A

When the pressure within a cylinder is held constant the tension on its walls increases with increasing radius.
T=PR/h
Where T= wall tension, P= pressure in ventricle and R= radius

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30
Q

What is the physiological relevance of the law of Laplace?

A
  • The left and right ventricles share a wall (so same wall tension), yet achieve different pressures. How?
  • Right ventricle has a large radius and thinner wall therefore lower pressure
  • Left ventricle has a smaller radius and thicker wall therefore higher pressure
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31
Q

Describe how the law of Laplace can link to the pathophysiology of heart disease.

A

In heart failure, ventricles often become dilated (increased radius) which means greater wall tension is required to pump blood (but this can’t be achieved due to weakened muscle)

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32
Q

What phases make up the Cardiac cycle?

A 
Diastole:
- Isovolumetric ventricular relaxation
- Rapid filling (of the ventricles)
- Late, slow filling (of the ventricles)
- Atrial systole
Systole:
- Isovolumetric ventricular contraction
- Ventricular ejection
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33
Q

What is the Ejection fraction (EF)? What is the average?

A

Stroke volume/End diastolic volume

Average is between 60-70%

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34
Q

What is the stroke volume?

A

End-diastolic volume - End-systolic volume

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35
Q

Describe the mechanical, pressure and electrical changes that occur in Atrial systole.

A

Mechanical - Atria contract ‘topping off’ volume of blood in ventricle

Pressure - Increase in atrial pressure (note - ‘a’ wave seen in jugular venous pressure due to blood being pushed back)

Electrical - P wave is atrial depolarization stimulated by SA node activation

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36
Q

Describe the mechanical, pressure and electrical changes that occur in Isovolumetric contraction.

A

Mechanical - All valves are closed, isometric contraction of ventricles

Pressure - Ventricular pressure exceeds atrial pressure (so AV valves closed). Pressure in ventricles increases without volume change and approaches aortic pressure.

Electrical - QRS complex detected by electrocardiogram is due to ventricular depolarization

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37
Q

Describe the mechanical, pressure and electrical changes that occur in Rapid Ejection.

A

Mechanical - Aortic and pulmonary valves open marking start of phase. Semi-lunar valves open.

Pressure - Ventricular contraction means pressure exceeds that in the aorta and pulmonary arteries.
‘c’ wave in atrial pressure as tricuspid valve is pushed into the atrium.

Electrical - no activity

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38
Q

Describe the mechanical, pressure and electrical changes that occur in reduced ejection.

A

Mechanical - Aortic and pulmonary valves begin to close

Pressure - Pressure in ventricles falls below that in arteries

Electrical - T wave due to ventricular repolarisation

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39
Q

Describe the mechanical, pressure and electrical changes that occur in Isovolumetric relaxation.

A

Mechanical - Semi-lunar valves shut, AV valved shut

Pressure - Atrial pressure rises as it fills with blood. ‘v’ wave caused by blood pushing tricupsid valve. Dichrotic notch due to rebound pressure wave against aortic valve as distended aortic wall relaxes.

Electrical - no activity

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40
Q

During which phases are the heart sounds heart? (normal and abnormal)

A

Normal:
S1 - Isovolumetric contraction
S2 - Isovolumetric relaxation

Abnormal:
S3 - Rapid ventricular filling (sign of turbulent filling due to sever hypertension or mitral incompetence)
S4 - Atrial systole (occurs with congestive heart failure, pulmonary embolism or tricupsid incompetence)

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41
Q

Describe the mechanical, pressure and electrical changes that occur in Rapid ventricular filling.

A

Mechanical - AV valves open, atria rapidly filling

Pressure - Ventricular volume increases and atrial pressures fall

Electrical - no activity

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42
Q

Describe reduced ventricular filling.

A

Can be called Diastasis.

Ventricular volume increases slowly.

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43
Q

Define end diastolic pressure

A

The pressure in the ventricle after diastole (after it has filled up with blood).

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44
Q

What are the normal values for EDV, ESV, SV, and peak systolic pressure?

A

End diastolic volume - 144ml (R) 142ml (L)
End systolic volume - 50ml (R) 47ml (L)
Stroke volume - 94ml (R) 95ml (L)
Peak systolic pressure - 120mmHg (pulmonary artery is 25mmHg)

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45
Q

Define cardiac output. What are its determinants?

A

Heart rate x stroke volume

Stroke volume determines by - Preload, Afterload and contractility

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46
Q

What do the corners/sides of a PV diagram represent?

Going anticlockwise from bottom right

A

(Going anticlockwise from bottom right)

  1. Isovolumetric contraction of ventricles (isometric)
  2. Rapid ejection of ventricles
  3. Isovolumetric relaxation of ventricles
  4. Rapid filling of ventricles
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47
Q

What does an increase in preload lead to?

A

Increase in stroke volume

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48
Q

What does an increase in afterload lead to?

A

Decrease in stroke volume

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49
Q

Define cardiac capability. How can it be measured? What stimulates it?

A
  • The strength of contraction of the heart.
  • Measured by Ejection fraction.
  • Increased by sympathetic stimulation
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50
Q

What changes occur to the heart during exercise?

A
  • Contractility is increased (increased sympathetic activity)
  • End diastolic volume is increased (due to venoconstriction and muscle pump)
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51
Q

What can be used to predict the equilibrium potential of an ion across a semi-permeable membrane? What are its variables?

A 
Nernst equation
Equilibrium potential is dependent on:
- Temperature (kelvin)
- Concentration of ion outside cell
- Concentration of ion inside cell
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52
Q

What does the membrane potential depend on?

A

The relative permeabilities of various ions.

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53
Q

What can be used to predict the membrane potential of a cell?

A

Goldman-Hodgkin-Katz equation

takes into account relative permeabilities

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54
Q

Explain how a membrane potential is formed across an excitable cell.

A
  1. At resting potential Na+ channels are closed, and some K+ channels are open. Overall negative charge inside.
  2. Stimulus causes opening of gated Na+ channels which allows Na+ to move in. K+ gated channels are closed.
  3. Movement of ions causes depolarization of the membrane which moves in one direction through the membrane.
  4. After an action potential has been reached Na+ channels begin to close and K+ channels open, repolarizing the membrane.
  5. A small overshoot causes hyperpolarization but the resting membrane potential is restored by the Na+/K+ pump
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55
Q

Explain the changes that occur is ion permeability during an action potential.

A
  • Initially K+ is more permeable than Na+
  • At point of stimulation (and depolarization) Na+ is more permeable
  • During repolarization the membrane is more permeable to K+
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56
Q

What is the difference between a normal action potential and a cardiac potential?

A

Cardiac action potentials are much longer due to Ca2+ influx which maintains depolarization.

This is necessary to produce an effective pump (especially in the ventricles)

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57
Q

What are the refractory periods of cardiac muscle?

A

Absolute refractory period - time at which no action potential can be initiated regardless of stimulus intensity

Relative refractory period - period after ARP where and action potential can be elicited but only with a larger than normal stimulus

Full recovery time - the time at which a normal AP can be elicited with normal stimulus

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58
Q

How does skeletal and cardiac muscle differ with relation to refractory periods and excitation?

A
  • In skeletal muscle the action potential occurs prior to the contraction so it is possible to get re-stimulation and to have summation (therefore can have tetany)
  • In cardiac muscle the action potential and contraction overlaps so that the refractory period includes the majority of the contraction. Therefore it cannot be tetanized.
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59
Q

What is the difference between the action potentials in the SA node cells and the ventricular cells?

A
  • In SA node cells have ‘no true resting membrane potential’ as they constantly reach threshold level
  • Action potentials are achieved by the slow acting Ca2+ channels rather than fast acting Na+ channels
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60
Q

How is an impulse propagated in the heart?

A

The myocytes are closely joined with intercalated discs between them containing many gap junctions to increase movement of ions intercellularly

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61
Q

Explain the role of the SA node in initiating the electrical activity of the heart.

A
  • They have a pacemaker potential which gradually depolarizes until the threshold which generates an action potential
  • The slope of the pacemaker potential gives automacity
  • They have unique channels which when open have increased electrical conductance for that ion
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62
Q

What are the different currents produced by the channels that are in the SA node?

A
  • I(f) or ‘funny’ currents. When membrane potential is very low (-60mV) these open allowing slow, inward (depolarizing) Na+ currents.
  • At about -50mV T-type Ca2+ channels open allowing further depolarization
  • At (-40/-30mV) L-type Ca2+ channels open which are long-lasting and cause more depolarization until the threshold is reached
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63
Q

Describe the pathway of electrical activity through the heart.

A
  1. SA node action potential (AP) generated and spreads through inter-nodal fibre bundles in the atria causing contraction
  2. AP is propagated to the AV node and after a short delay (0.1 sec) the impulse travels to the ventricles through the left and right bundle branches.
  3. AP travels through the Purkinje fibres and ventricular contraction occurs from the apex to the base
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64
Q

Identify the electrical events that take place in the standard PQRST ECG waveform.

A

P - Atrial depolarization
QRS - Ventricular depolarization
T - Ventricular repolarization

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65
Q

In an ECG what would a depolarizing current look like?

A

Towards the electrode - positive

Away from the electrode - negative

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66
Q

In an ECG what would a repolarizing current look like?

A

Towards the electrode - negative

Away from the electrode - positive

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67
Q

What are the positions of the electrodes when doing an ECG?

A

Limb lead:

  • Left arm, left left
  • Right, arm, right leg (ground)

Chest Lead:

  • V1 right 4th intercostal space next to sternum
  • V2 same as V1 but left
  • V4 left 5th intercostal space at mid-clavical line
  • V3 left 5th intercostal space between V2 + V4
  • V6 left 5th intercostal space at mid axillary line
  • V5 left 5th intercostal space anterior to axillary line
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68
Q

Are the waves of PQRST positive or negative?

A

P - Positive
R - Negative
S - Positive
T - Negative

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69
Q

What are the 6 leads and how are they obtained?

A

Limb Leads:
Lead I - Right arm to left arm
Lead II - Right arm to left leg
Lead III - Left arm to left leg
Augmented Leads:
aVR - average of left arm and left leg to right arm
aVL - average of right arm and left leg to left arm
aVF - average of right arm and left arm to left leg

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70
Q

What does an ECG measure?

A

Senses the heart’s electrical activity via electrodes

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71
Q

What is Einthoven’s triangle?

A

The triangle formed by the three electrodes placed on the limbs with the sides representing the limb leads.

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72
Q

Why does the magnitude and direction vary from lead to lead?

A
  • The different leads measure the amount of electrical activity in a particular direction (e.g. from right to left for Lead I).
  • Different directions have different amounts of activity (therefore different magnitude)
  • The direction depends on whether the activity is depolarization/repolarization and whether it’s going away from or towards the electrode
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73
Q

What is the normal physiological range of a mean frontal plane axis?

A

-30 to +90

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74
Q

What is the x axis and y axis for an ECG?

A

x axis - Time (one small box represents 40ms)

y axis - Amplitude (one small box represents 0.1mV)

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75
Q

How do you calculate the Mean frontal plane axis?

A
  • Find the Lead with the flattest peak
  • The MFPA is about 90 degrees from that in either direction
  • Look at a lead which lies within that range
  • If the lead is positive then the activity is going towards that lead, if it’s negative then it’s going away
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76
Q

In what plane are the chest leads?

A

Horizontal plane

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77
Q

What is the positive and negative electrode when measuring chest/precordial leads?

A
  • The chest leads are always the positive electrode
  • The negative pole is Wilson’s central terminal (composite pole of right arm, left arm and left leg - average potential across the body)
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78
Q

What are the 6 chest leads classified as?

A

Septal - V1, V2
Anterior - V3, V4
Lateral - V5, V6

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79
Q

What is the difference between the Limb leads and the Precordial leads?

A

Limb leads - bipolar

Precordial leads - unipolar

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80
Q

What can the ECG be used to detect?

A
  • Tachyarrhythmias
  • Bradyarrhythmias
  • Myocardial infarction
  • Myocardial ischaemia
  • Cardiomyopathy
  • Assessment of pacing
  • Electrolyte disturbances
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81
Q

What are the features of Sinus tachycardia on an ECG?

A
  • Normal P waves
  • Heart rate greater than 100
  • Regular ventricular rhythm
    Often a physiological response e.g. hypovolaemia, stress etc.
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82
Q

What are the features of Atrial Fibrillation on an ECG?

A
  • P waves absent
  • Irregular ventricular rhythm
  • Atrial rate - 350-650bpm Ventricular rate - 100-180bpm
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83
Q

What are the features of Atrial flutter on an ECG?

A
  • Sawtoothed baseline (flutter) waves
  • Atrial rate - 220-430 Ventricular rate - above 300
  • Regular or variable rhythm
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84
Q

What are the features of AV nodal re-entrant tachycardia (AVNRT) on an ECG?

A
  • Regular QRS complexes
  • P waves often buried within QRS or just after
    Due to a re-entrant circuit within the AV node
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85
Q

What are the features of Pre-excitation syndrome on an ECG?

A
  • Short PR interval

Accessory pathway connect atrium to ventricle

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86
Q

What are the different types of Heart block (AV nodal block) and what features are present in an ECG

A
  • 1st degree: Prolonged PR interval
  • 2nd degree: Mobitz Type I (Wenchebach), Mobitz type II
  • 3rd: Complete heart block
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87
Q

What is Mobitz type I (Wenckebach)?

A

Progressive prolongation of the PR interval leading to a non-conducted P wave

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88
Q

What is Mobitz type II?

A

Intermittent non-conducted P waves without progressive prolongation of the PR interval

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89
Q

What is a 3rd degree AV block?

A

P waves and the QRS complex will be independent of each other.

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90
Q

What changes occur in an ECG when the Bundle branch is blocked?

A
  • QRS complex widens (when conduction pathway is blocked it’ll take longer for the signal to pass through)
  • QRS morphology (rabbit ears for right bundle branch block) and (broad, deep waves for left BBB)
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91
Q

What are the features of Ventricular fibrillation on an ECG?

A
  • Irregular rhythm
  • Heart rate 300-600
  • Absent P wave
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92
Q

What is the role of circulation?

A
  • transport blood
  • deliver oxygen, nutrients + signalling molecules
  • remove CO2 + metabolites
  • regulate temperature
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93
Q

What designs of circulation help it to function?

A
  • the action of the muscular pump (heart) generates a pressure gradient which propels blood through vessels
  • double circulation by two pumps (left and right ventricle)
  • capillaries are highly branched to give a shorter diffusion distance
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94
Q

What is the basic cycle that blood goes through in the body?

A 
Starts at pump
Elastic arteries
Resistance (capillaries)
Exchange
Reservoir (veins)
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95
Q

What are the properties of the different blood vessels?

A
  • Arteries: Large, elastic and act as conduits and dampening vessels
  • Arterioles: Extensive smooth muscle in walls to regulate diameters and the resistance to blood flow
  • Veins + venules: Highly compliant and act as a reservoir for blood volume
  • Capillaries: Very thin walls to facilitate transport and diffusion
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96
Q

Which vessels have the largest relative cross-sectional area and which has the largest relative volume of blood contained within them?

A
  • Capillaries have the largest cross-sectional area (exchange function)
  • Vein and venules have the largest volume of blood within them (reservoir function)
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97
Q

Why does blood flow? (simplest answer)

A

Due to the difference in pressure between the aorta and capillaries/veins.

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98
Q

What is Darcy’s law?

A

Darcy’s Law -

Pressure difference = volumetric flow x resistance

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99
Q

What is the equation used to find Mean blood pressure? Is it accurate?

A

Mean blood pressure = cardiac output x resistance (peripheral vascular resistance)

Approximate as it assumes steady flow, rigid vessels and that right atrial pressure is negligible.

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100
Q

By what variables is resistance to blood flow dependent on?

A
  • Fluid viscosity (η)
  • Length of the tube (L)
  • Inner radius of tube (MOST IMPORTANT) (r)
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101
Q

What is Poiseuille’s equation?

A

Resistance = 8Lη / πr^4

where L=length of tube, η=fluid viscosity, r=inner radius

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102
Q

What type of flow can occur in vessels? Which is the normal?

A
  • Laminar flow (normal): when each particle of the fluid follows a smooth path, flowing in layers or streamlines, which never cross each other. Velocity is constant at any point.
  • Turbulent flow: irregular flow characterized by tiny whirlpool regions and associated with pathophysiological changes to the endothelial lining on the vessels. Velocity is not constant at every point.
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103
Q

Why does turbulent flow occur?

A

Pathophysiological changes to endothelial lining of the blood vessels occur because of changes in SHEAR STRESS

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104
Q

What is Shear stress?

A
  • Shear rate (s) is the velocity gradient of the flow at any point ( as velocity increases with distance from wall)
  • Shear stress is (τ) shear rate multiplied by viscosity
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105
Q

What is the relationship between high shear stress and endothelial function?

A

High shear stress (as found in laminar flow), promotes:

  • endothelial cell survival
  • quiescence (stability)
  • cell alignment in direction of flow
  • secretion of substances which promote vasodilation and anti-coagulation
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106
Q

What is the relationship between low shear stress and endothelial function?

A

Low/changing shear stress (as found in turbulent flow), promotes:

  • endothelial proliferation
  • apoptosis
  • shape change
  • secretion of substances that promote vasoconstriction, coagulation, and platelet aggregation
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107
Q

What is transmural pressure?

A

The pressure difference between the inside of the vessel and the outside

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108
Q

What determines the distension (expansion) of a vessel?

A

Tension of the wall:

Wall tension force = transmural pressure x resistance

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109
Q

Give 2 examples of where the relationship between pressure and the wall has lead to disease.

A
  • Dilated cardiac myopathy: ventricle radius increased, and to maintain pressure wall tension must increase. (But heart is weak so leads to heart failure)
  • Aneurysms: radius increases, but the wall is weakened so no compensatory increase in wall tension (T=Pxr) radius continues to increase
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110
Q

What is circumferential stress (σ)? What effect does it have?

A

Circumferential stress (σ) = tension force (T) / wall thickness (h)

Maintained high circumferential stress causes vessel distension.

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111
Q

How does standing up affect blood pressure?

A
  • Standing up causes an increase in hydrostatic pressure in the legs (due to gravity)
  • Blood pools in the veins due to their compliance and reduces venous return to the heart
  • This reduces the cardiac output and bp (if there was no compensatory mechanism)
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112
Q

What compensatory mechanisms are in place to deal with postural hypotension?

A

Standing causes:

  • Activation of SNS to:
    • constrict venous smooth muscle and stiffen the veins
    • constrict arteries to increase resistance + maintain blood pressure
    • increase heart rate + force of contraction + maintain cardiac output
  • Myogenic venoconstriction (in response to elevated venous pressure) to stiffen veins
  • Use of muscle and respiratory ‘pumps’ to improve venous return

If the cerebral blood flow still falls too low then the person will faint (syncope).

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113
Q

Give two examples of problems that occur with relation to standing.

A
  • Incompetent valves cause dilated superficial veins in the leg (varicose veins)
  • Prolonged elevation of venous pressure (even with intact compensatory mechanisms) causes oedema in feet
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114
Q

What is the pulse pressure?

A

The difference between the diastolic and systolic blood pressure

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115
Q

Why does the pressure of the aorta differ from the left ventricle?

A
  • Once the aortic valve closes, ventricular pressure falls but the aortic pressure only falls slowly in diastole.
  • This is due to the elasticity of the aorta and large arteries which ‘buffers’ the change in pulse pressure
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116
Q

What is arterial compliance?

A
  • During ejection blood enters the aorta faster than it leaves
  • 40% of the stroke volume is stored by the elastic arteries
  • After the aortic valve closes ejection ceases but due to recoil of the elastic arteries pressure falls slowly and there’s diastolic flow in the downstream circulation
  • This is termed the ‘Windkessel’ effect
  • If arterial compliance decreases (e.g. with age it stiffens) the damping effect of the Windkessel is reduces and pulse pressure increases
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117
Q

What is the vascular endothelium?

A

Single cell layer that acts as the blood-vessel interface.

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118
Q

What functions are performed by the vascular endothelium?

A
  • Vascular tone management: secretes and metabolises vasoactive substances
  • Thrombostasis: prevents clots forming or molecules adhering to wall
  • Absroption and secretion: allows passive/active transport via diffusion/channels
  • Barrier: prevents atheroma development by stopping entry of bad substances
  • Growth: Mediate cell proliferation
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119
Q

What affects vascular function?

A

Circulation:

  • Hormones
  • Drugs
  • Shear stress

Nervous:
- Neurotransmitters

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120
Q

What effect does Nitric oxide (NO) have on smooth muscle, myocytes and platelets?

A

Smooth muscle:

  • relaxation (vasodilation)
  • inhibition of growth

Myocytes:

  • increased blood flow
  • increased contractility

Platelets:
- inhibits aggregation

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121
Q

What effect does Prostacyclin (PG12) have on smooth muscle, myocytes and platelets?

A

Smooth muscle:

  • relaxation (vasodilation)
  • inhibition of growth

Myocytes:
- increased blood flow

Platelets:
- inhibits aggregation

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122
Q

What effect does Thromboxane A2 (TXA2) have on smooth muscle, myocytes and platelets?

A

Smooth muscle:
- contraction (vasoconstriction)

Myocytes:
- reduced blood flow

Platelets:

  • Activation
  • Stimulates aggregation
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123
Q

What effect does Endothelin-1 (ET-1) have on smooth muscle, myocytes ?

A

Smooth muscle:

  • Contraction (vasoconstriction)
  • stimulation of growth

Myocytes:

  • reduced blood flow
  • increased contractility
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124
Q

What effect does Angiotensis II (Ang II) have on smooth muscle, myocytes?

A

Smooth muscle:

  • Contraction (vasoconstriction)
  • stimulation of growth

Myocytes:

  • reduced blood flow
  • remodelling
  • fibrosis (thickening and scarring)
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125
Q

How is the vascular tone controlled?

A

The vascular tone depends on the balance of vasoactive molecules in the blood.

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126
Q

Explain the mechanism of Nitric oxide (NO) production.

A
  • Ligand binds to the G-protein coupled receptor and activates phospholipase C
  • Phopspholipase C cinverts PIP2 to IP3 and DAG
  • IP3 moves to the endoplasmic reticulum and stimulates Ca2+ efflux (SHEAR STRESS also dos this)
  • Rise in intracellular Ca2+ upregulates endothelial Nitric oxide synthase (eNOS)
  • eNOS catalyses the conversion of L-argenine and oxygen to L-citrulline and NO
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127
Q

What are the layers of the blood vessel walls?

A
  • Tunica adventitia: external layer containing blood vessels, fibrous tissue, elastin ancd collagen. Helps keep the shape of the vessel
  • Tunica media: predominantly smooth muscle cells able to contract or dilate depending on the stimulus
  • Tunica intima: predominantly vascular endothelium and has the elastic basal lamina. This is the exchange surface.
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128
Q

How can Endothelin-1 cause both vasoconstriction and vasodilation?

A

It had different receptors on different tissues.

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129
Q

Explain the mechanism of Nitric Oxide (NO) action.

A
  • NO exits the endothelial cell and moves into the smooth muscle cell
  • NO upregulated the activity of Guanylyl cyclase which converts GTP to cGMP
  • cGMP upregulates Protein Kinase G which leads to efflux of Ca2+ and reduction in tension within the myocyte
  • This leads to relaxation
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130
Q

Give an example of a ligand that stimulates the production of NO.

A

Acetylcholine

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131
Q

Explain the mechanism by which Prostacyclin (PGI2) and Thromboxane A2 (TXA2) is synthesised.

A
  • A phospholipid can be converted to arachidonic acid by phospholipase A2 or DAG can be converted by DAG lipase
  • The arachidonic can be converted to Prostaglandin H2 (PGH2) b the COX enzymes (cycooxygenase)
  • Either COX 1 which is found in all cells, or COX 2 which is upregulated during inflammation
  • PGH2 is a precursor which by exposure to different enzymes can either become prostacyclin or thromboxane A2
    - Prostacyclin: prostacyclin synthase
    - Thromboxane A2: thromboxane synthase
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132
Q

What is the other pathway of Arachidonic acid?

A

Leukotrienes:

  • If arachidonic acid follows the LIPOXYGENASE enzyme cascade LTA4, LTB4, LTC4 and LTD4 is produced
  • LTD4 causes broncoconstriction
  • LTD4 is associated with asthma
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133
Q

Explain the mechanism of action of Prostacyclin (PGH2)

A
  • Produced inside endothelial cells then exits and binds to IP receptor on smooth muscle
  • The IP receptor is coupled with adenylate cyclase which converts ATP to cAMP
  • cAMP upregulates Protein Kinase A which results in relaxation of the vascular smooth muscle causing vasodilation
  • Prostacyclin is also secreted into the blood where it has anti-platelet aggregation properties
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134
Q

Explain the mechanism of production of Endothelin-1.

A
  • Endothelin precursor is produced in the nucleus
  • Then it’s cleaved by Endothelin converting enzyme (embedded in membrane) to produce Endothelin-1
  • Endothelin-1 is pushed out if the cell and it can bind alpha or beta receptors
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135
Q

Explain the mechanism of action of thromboxane A2

A
  • Can bind to Alpha receptors on platelets, or Beta receptors on vascular muscle cells
  • Beta receptor: coupled with phospholipase C which converts PIP2 to IP3 which results in constriction of blood vessels
  • Alpha receptor: activates platelets and causes production of more thromboxane which has a domino effect on other platelets stimulating aggregation
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136
Q

Explain the mechanism of action of Endothelin-1.

A
  • Endothelin-1 is pushed out if the cell and it can bind alpha or beta receptors
  • For both receptors, binding causes phospholipase C to convert PIP2 to IP3 which causes contraction
  • Beta receptor: on endothelial cell. Triggers activation of eNOS. NO causes relaxation.
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137
Q

What are some antagonists of Endothelin-1?

A

Antagonists inhibit the production of endothelin-1 precursor:

  • Prostacyclin
  • Nitric oxide
  • ANP (atrial natriuretic peptide)
  • Heparin
  • HGF (hepatocyte growth factor)
  • EGF (epidermal growth factor)
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138
Q

What are some agonists of Endothelin-1?

A

Agonists stimulate the production of endothelin-1:

  • Adrenaline
  • Vasopressin
  • Angiotensis II
  • Interleukin-1
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139
Q

How is Angiotensin II produced?

A
  • Produced in the liver

- Precursor is Angiotensinogen

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140
Q

How is Angiotensin II activated?

A
  • Renin secreted by kidney in response to low blood pressure
  • Renin converts angiotensinogen to Angiotensin I
  • Angiotensin converting enzyme (ACE) converts Angiotensin I to Angiotensin II
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141
Q

What are the actions of Angiotensin II?

A
  • Stimulates ADH secretion
  • Increases aldosterone production
  • Increases sodium reabsorption
  • ALL THE ABOVE INCREASE WATER RETENTION
  • Increased synthetic activity
  • Arteriolar vasoconstriction
  • BOTH THE ABOVE CAUSE INCREASED VASCULAR RESISTANCE

OVERALL - Increased blood pressure

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142
Q

Explain the mechanism of action of Angiotensin.

A
  • Angiotensin II binds to a receptor on vascular smooth muscle cells which leads to the activation of phospholipase C. PIP2 is converted to IP3 leading to contraction.
  • Some angiotensin receptors are bound to SRC which can upregulate the growth of vascular smooth muscle cells. This increases blood pressure.
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143
Q

How does Bradykinin relate to ACE?

A
  • Bradykinin is an inflammatory mediator
  • ACE breaks down bradykinin
  • Prevents bradykinin from causing vasodilation
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144
Q

What is the normal mechanism of action of Bradykinin?

A
  • Binds to bradykinin receptor-1 and activate phospholipase C which converts PIP2 to IP3 which upregulates the production of nitric oxide
  • Nitric oxide then causes relaxation
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145
Q

What are additional effects of Angiotensin II?

A 
Oxidative stress:
- NAD(P)H oxidase activity
- Reactive oygen species
- LDL peroxidation
Inflammation:
- Vascular permeability
- Activation of signalling pathways
- Inflammatory mediators
Remodelling:
- Matrix deposition
- Vascular smooth muscle cell proliferation
- MMP activation (enzymes involved in degradation of ECM)
Endothelial dysfunction:
- Vasoconstriction
- Platelet aggregation
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146
Q

How is Nitric oxide used in pharmacology?

A

Nitric oxide and vasodilation is good, so in order to boost this:

  • Stimulate the production of NO. This is endothelium- dependent and uses acetylcholine.
  • Donate NO. This is endothelium-independent and can be GTN, nocorandil, ISMN
  • Enhance effects. Prevents counterproductive processes. E.g. viagra
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147
Q

How does viagra work?

A

Viagra inhibits the alternate pathway of cGMP (to GMP) by stopping phosphodiesterase. This means more cGMP continues through the nitric oxide pathway.

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148
Q

What is the effect of low-dose aspirin?

A
  • Irreversible inhibition of COX enzymes
  • Therefore decreased thromboxane A2 (and so less vasoconstriction)
  • Associated with less cardiac events
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149
Q

How do calcium-channel blocker work?

A
  • Useful in treatment of variant angina
  • Block Ca2+ influx
  • Vasodilation means reduced afterload in the heart and therefore increased Q
  • Prevents coronary artery vasospasm
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150
Q

How are Calcium-channel blockers specific to heart cells?

A

Their affinity for the channel is related to the membrane potential of their target cells.
In smooth muscle it cause vasodilation, but causes negative inotrope in cardiac myocytes (reduced force/speed of contraction)

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151
Q

How do ACE inhibitors and angiotensin receptor blockers work?

A
  • ACE inhibitors prevent breakdown of bradykinin leading to more vasodilation
  • Angiotensin receptor blockers prevent action of angiotensin which would cause contraction of smooth muscle
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152
Q

What are the issues with some cardovascular drugs?

A
  • Often the same chemical is used for different processes so a drug may interfere with other pathways
  • Some drugs are not tissue specific
  • Receptor expression and distribution varies between tissues
  • People can have different experiences of the same drug
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153
Q

What is the organisation of the Sympathetic nervous system?

A
  • Shorter pre-ganglionic nerves originating from the thoracolumbar (T1-T5 and T12-L3)
  • Longer post-ganglionic nerves start at the sypathetic trunk and end at the organ/gland
  • 3 preverterbral ganglia: Solar plexus, superior mesenteric ganglion and inferior mesenteric ganglion
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154
Q

Describe the Autonomic cardiovascular control.

A

Parasympathetic nervous System:
- Vagus nerve innervates the Sinus node (from the cardioacceleratory centre or cardoinhibitory centre in medulla)
- Carotid sinus, arterial baroreceptors and cardiac baro-receptors send impulses to the hypothalamic autonomic centre
Sympathetic nervous System:
- Cholinergic neurone pre-ganglionic neuron and Adrenergic neurone post-ganglionic neurone innervates the β2 receptor in the heart and α1 receptors on smooth muscle in arterioles

155
Q

What are the receptors in a Sympathetic nerve pathway to the heart?

A
  • At ganglion: Cholinergic receptor for Acetyl choline

- At effector organ: Adrenergic receptor for Noradrenalin

156
Q

How is nor-epinephrine removed from the synapse?

A
  • Uptake 1: Recycled by being taken back up into the neurone and either being re-used or degraded
  • Uptake 2: Taken up by effector (e.g. smooth muscle) and broken down by enzymes e.g. COMT (Catechol-O-methyltransferase), or MAO (Monoamine oxidase)
157
Q

What pre-cursor molecules of Nor-epinephrine?

A
  • Tyrosine
  • Levadopa
  • Dopamine
  • Nor-epinephrine
158
Q

How is neurotransmitter released from the neurone?

A
  • Active process (requires ATP)
  • Stored in granular vesicle
  • Fusion of vesicle with varicosity membrane (Synaptic knob)
  • Exocytic channel opens
  • Vesicle contents expelled by exocytosis (requires ATP)
  • Noradrenaline re-uptake by endocytosis
  • Biosynthesis replenishes granular contents
159
Q

What are the two types of Adrenoreceptors?

A
  • Excitatory on smooth muscle: α-adrenoceptor mediated

- Relaxant on smooth muscle (BUT stimulatiory on heart): β-adrenoceptor mediated

160
Q

What are the subdivisions of β-adrenoreceptors?

A
  • β1-adrenoceptors located on cardiac muscle and smooth muscle of GI tract
  • β2-adrenoceptors located on bronchial, vascular and uterine smooth muscle
  • β3-adrenoceptors found on fat cells and possible smooth muscle of GI tract.
161
Q

What are the subdivisions of α-adrenoreceptors?

A
  • α1-adrenoceptors located post-synaptically (i.e. on effector cells). Important in mediating constriction of resistance vessels in response to sympathomimetic amines
  • α2-adrenoceptors located on presynaptic nerve terminal membrane. Their activation by released transmitter causes negative feedback inhibition of further transmitter release. Some are post-synaptic on vascular smooth muscle
162
Q

How do α1-adrenoceptic work inside the cell?

A
  • Agonist binds to the G protein coupled receptor
  • Activate phospholipase C to break down phospholipids
  • Releases DAG and IP3
  • DAG activates protein kinases
  • IP3 causes release of Ca2+ from intracellular stores
  • Increase in Ca2+ activates cell
163
Q

How β-adrenoreceptors work inside the cell?

A
  • Agonist binds to the G protein coupled receptor
  • GTP is converted to GDP and Adenylyl cyclase is activated
  • ATP is converted to cAMP
  • This increases protein kinase activity
  • Decreases activity of the cell (except in heart)
164
Q

How do α1-adrenoceptic work inside the cell?

A
  • Agonist binds to the G protein coupled receptor
  • GTP is converted to GDP and Adenylyl cyclase is inhibited
  • Less or no production of cAMP
  • cAMP is an antagonist of Ca2+
  • Therefore Ca2+ can have an excitatory effect on the cell
165
Q

What catecholamines have an effect on α1-adrenoceptors?

A
  • Noradrenaline
  • Adrenaline
  • Phenylephrine (synthetic)
    Dopamine has weak effects but has its own receptors.
166
Q

What catecholamines have an effect on α2-adrenoceptors?

A
  • Noradrenaline

- Adrenaline

167
Q

What catecholamines have an effect on β1-adrenoceptors?

A
  • Noradrenaline
  • Adrenaline
  • Isoprenaline (synthetic)
    Dopamine has weak effects but has its own receptors.
168
Q

What catecholamines have an effect on β2-adrenoceptors?

A
  • Adrenaline

- Isoprenaline (synthetic)

169
Q

What are the cardiovascular effects of Noradrenaline?

A
  • Increases systolic BP a lot
  • Increases diastolic BP
  • Increases mean BP
  • Decreases heart rate slightly
170
Q

What are the cardiovascular effects of Adrenaline?

A
  • Increases systolic BP
  • Decreases diastolic BP slightly
  • Increases mean BP slightly
  • Increases heart rate slightly
171
Q

What are the cardiovascular effects of Isoprenaline?

A
  • Increases systolic BP slightly
  • Decreases diastolic BP
  • Decreases slightly/no change in mean BP
  • Increases heart rate
172
Q

What is the reaction of the vascular bed in the skin, visceral and renal vessels to noradrenaline, adrenaline and isoprenaline?

A

Constriction for NA and AD

No effect or dilation for ISO

173
Q

What is the reaction of Coronary vessels to noradrenaline, adrenaline and isoprenaline?

A

Dilation

174
Q

What is the reaction of skeletal muscle vessels to noradrenaline, adrenaline and isoprenaline?

A

Constriction for NA

Dilation for AD and ISO

175
Q

Describe the biosynthetic pathway for Angiotensin II.

A
  • Angiotensinogen produced by the liver
  • Enzyme renin produced by the kidney (juxtaglomerula cells) breaks it down
  • Into Angiotensin I
  • Enzyme Angiotensin converting enzyme (ACE) produced by lungs and kidney converts it
  • Into Angiotensin iI
176
Q

How is the release of Renin regulated?

A

Stimulated by:

  • a decrease in arterial blood pressure
  • a decrease in blood pressure in pre-glomerular vessels
  • a decrease in sodium reabsorption
  • sympathetic nervous activity through β1-receptors in the kidney

Inhibited by:

  • Angiotensin II
  • Adenosine
177
Q

Give examples of pharmalogical manipulation of renin release.

A
  • ACE inhibitor’s prevent Angiotensin II production and so lowers blood pressure
  • β1-receptor blockers and α2 receptor agonist decreases sympathetic activation
  • Loop diuretics inhibit reabsorption of NaCl
    etc
  • AT1 blockers inhibit receptor which normally works to increase BP
178
Q

What are the effects of Angiotensin II on Peripheral resistance?

A

Peripheral resistance

  • Direct vasoconstriction
  • Enhanced action of peripheral norepinephrine
    - increased NE release
    - decreased NE uptake
  • Increased sympathetic discharge
  • Release of catecholamines from adrenal gland

OVERALL rapid increase in BP

179
Q

What are the effects of Angiotensin II on Renal function?

A

Renal function

  • Direct effects to increase Na+ reabsorption in proximal tubule
  • Synthesis and release of aldosterone from adrenal cortex
  • Altered renal haemodynamics
    - renal vasoconstriction
    - enhanced norepinephrine effects in kidney

OVERALL slow increase in BP

180
Q

What are the effects of Angiotensin II on Cardiovascular structure?

A

Haemodynamic effects:
- Increased preload and afterload
- Increased vascular wall tension
Non-haemodynamic effects:
- Increased expression of proto-oncogenes
- Increased production of growth factors
- Increased synthesis of extracellular matrix proteins

181
Q

What are the physiological effects of Aldosterone?

A
  • Increased Na+ retention (and H20 retention)

- Increased K+ excretion (and H+ excretion)

182
Q

Where are the aldosterone receptors in the body?

A
  • Kidneys
  • Brain
  • Vessels
  • Heart
183
Q

Why can stress have such negative results with regards to the cardiovascular system?

A
  • Stimulates the sympathoadrenal system
  • Which stimulates the renin-angiotensin system
  • Both systems lead to
    • Increased blood pressure
    • Increased Heart rate
    • Increased Na+/water retention
    • Increased coagulation and decreased fibrinolysis
    • Increased platelet activation
184
Q

Describe the branching structure of blood vessels, from arteries to veins.

A
  • 1st order arterioles
  • Terminal arterioles
  • Capillary
  • Pericytic (post-capillary) venule
  • Venule
185
Q

List the three types of capillary and order them in terms of their permeability to water and small lipophobic solutes.

A
  • Continuous: Least permeable - H20-filled gap junction between cells
  • Fenestrated: Permeable - Pores in the cells approx. 80nm
  • Discontinuous: Most permeable - Large spaces between cell layers that allows protein and even blood cells through. Only found in the liver.
186
Q

What is blood flow rate?

A

Volume of blood passing through a vessel per unit time.

F= pressure gradient / resistance

187
Q

How does an increased BP affect the blood flow rate?

A

Flow rate = Pressure difference / resistance

  • Pressure difference increases
  • Therefore flow rate increases
188
Q

How does arteriolar vasoconstriction affect the blood flow rate?

A

Flow rate = Pressure difference / resistance

  • Resistance increases
  • Therefore flow rate decreases
189
Q

What is the normal state of Arteriolar smooth muscle? Why is this important?

A
  • Partial constriction (vascular tone)

- Needs to be able to able to relax and contrict

190
Q

What are the independent reasons for a change in the radii of arterioles?

A
  • Match blood flow to metabolic needs of specific tissues: regulated by local (intrinsic) controls, independent of nerves or hormones
  • Help regulate arterial blood pressure: regulated by extrinsic control
191
Q

What is Active hyperemia?

A

Chemical mechanism

  • Increased metabolic activity of tissue
  • Increased oxygen usage
  • Leads to vasodilation
192
Q

What is Myogenic vasoconstriction of arterioles?

A

Physical mechanism

  • Increase in BP (that’s not needed)
  • Stretch detected in arteriole walls
  • Leads to vasoconstriction
193
Q

What effect does temperature have on Arterioles?

A
  • Blood temp. decreases
  • Causes vasoconstriction
  • Reduced blood flow to that area
194
Q

What is Mean arterial pressure?

A

MAP = Cardiac output x Total peripheral resistance

195
Q

From where does nervous control of the heart and blood flow originate?

A

Cardiovascular control system in the medulla (brain stem)

196
Q

What receptors are there in the brain, heart and vessels?

A

Brain - α receptors

Heart and vessels - β receptors

197
Q

What hormones are involved in regulating blood pressure?

A

Vasoconstrictors:
Vasopressin - Neurohypophysis
Angiotensin - Lungs produce ACE which breaks it down

Increased sympathetic activity:
Adrenaline + Noradrenaline - Adrenal medulla

198
Q

How is the design of a capillary suited to its function?

A

Function - Enhance diffusion (Fick’s law)

  • Walls one cell thick to minimise diffusion distance
  • Large surface area to increase diffusion time
199
Q

What is the blood brain barrier?

A
  • Capillaries have tight junctions between them

- Allows control over what enters the tissue

200
Q

Describe fluid movement across a capillary?

A

A volume of protein free plasma filters out of the capillary, mixes with the surrounding interstitial fluid (IF) and is resabsorbed.

201
Q

What are the different pressures that affect fluid movement across a capillary?

A

Hydrostatic pressure - pressure of heart pumping pushes fluid out
Oncotic pressure - diffusion gradient pushes fluid in due to proteins in blood

(Starling’s forces)

202
Q

What is Starling’s Hypothesis?

A
  • There must be a balance between hydrostatic pressure of the blood and osmotic attraction
  • Whereas capillary pressure determines transudation, the osmotic pressure of the proteins of the serum determines absorption
203
Q

What determines if there is ultrafiltration or reabsorption?

A
  • Ultrafiltration: If pressure inside capillary > in the interstitual fluid
  • Reabsorption: If inward driving pressure > outward pressures across the capillary
204
Q

What is the significance that ultrafiltration is more effective than reabsorption in the blood? What are the effects of this?

A
  • A net loss of fluid into the tissue

- Fluid is drained into the lymphatic system and returned to the circulation

205
Q

What is the relationship between activity of tissue and the capillary network that supplies it?

A

The more metabolically active the tissue, the more dense the network of capillaries that supplies it

206
Q

Describe some features of the lymph system.

A
  • No heart to induce flow - must use other pressures, pumps e.g. muscle
  • One way
  • ‘Blind ended’ i.e. not in a loop like circulatory system
  • Has many lymph nodes which is involved in immune response
  • Main ducts where it’s returned to blood is right lymphatic duct and thoracic duct, and drains into the left and right subclavian veins
  • Around 3L per day
207
Q

What causes Oedema?

A

Rate of production of fluid > rate of removal of fluid

208
Q

Give the cause of Elephantiasis.

A

Parasitic blockage of lymph nodes

209
Q

What affects venous volume distribution?

A
  • Peripheral venous tone
  • Gravity
  • Skeletal muscle pump
  • Breathing
210
Q

What does central venous pressure determine?

A

(Mean pressure in the right atrium)

  • Determines the amount of blood flowing back to the heart
  • In turn affects the stroke volume
211
Q

What does constriction determine in veins and arteries?

A

Veins: Determines compliance and venous return

Arteries: Determines

  • blood flow to organs they serve
  • mean arterial blood pressure
  • the pattern of distribution of blood to organs
212
Q

What is the primary method of altering flow?

A

Altering vessel radius by vasoconstriction or vasodilation.

213
Q

What are the methods of altering blood flow?

A

Local mechanisms (INTRINSIC)

Extrinsic:

  • Systemic regulation (e.g. circulating hormones)
  • Autonomic nervous system
214
Q

What is Autoregulation?

A

Autoregulation: the intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance

215
Q

What are the methods in which autoregulation can take place?

A
  • Myogenic theory: smooth muscle fibres responds to tension in vessel wall e.g. increased pressure causes contraction due to stretch-sensitive channels
  • Metabolic theory: as blood flow decreases metabolites accumulate and vessels dilate to increase flow and move them away e.g. CO2
  • Injury: Seratonin release from platelets causes constriction
  • Endothelium: Production of vasoactive hormones e.g. NO, prostacylin, endothelin-1
216
Q

What systemic regulation is there on blood flow?

A
  • Kinins e.g. bradykinin relaxes vascular smooth muscle
  • ANP (atrial natriuretic peptide) secreted from the cardiac atria is a vasodilator
  • Circulation vasoconstricors e.g. ADH (vasopressin), noradrenaline, angiotensin II
217
Q

What is a nicotinic receptor?

A

Cation-permeable ion channels which are activated by acetylcholine.

Very fast

218
Q

What is a muscarinic receptor?

A

Acetylcholine receptors that form G-protein coupled complexes in the cell membranes of neurons and cells.

219
Q

What receptors are there in the parasympathetic pathway?

A

Nicotinic on the post-ganglionic fibre

Muscarinic on the target organ

220
Q

Where are the sympathetic and parasympathetic pathways?

A

Sympathetic - Thoracic and lumbar

Parasympathetic - Cranial and sacral

221
Q

What functions are the two branches of the ANS responsible for with respect to the heart?

A

Sympathetic - controlling circulation

Parasympathetic - regulating heart rate

222
Q

Describe the relationship between the sympathetic nervous system and blood vessels.

A
  • Sympathetic nerve fibres innervate all vessels except capillaries, precapillary sphincters and some metarterioles
  • Heart, large veins and most major organs (except skeletal muscle and brain) are innervated
223
Q

Where is the vasomotor center? What makes up the vasomotor center?

A
  • Located in reticular substance of the medulla oblongata

- Composed of; vasoconstrictor (pressor) area, a vasodilator (depressor) area and a cardioregulatory inhibitory area

224
Q

What do the lateral and medial portions of the vasomotor center control?

A

Lateral - controls heart activity by influencing heart rate and contractility

Medial - transmits via vagus nerve to heard and tends to decrease heart rate

225
Q

What neurotransmitter is released between the post-ganglionic neuron and smooth vessel?

A

Noradrenaline

226
Q

What causes an increase in the heart rate?

A
  • Increased activity of sympathetic nerves to heart
  • Increased plasma adrenaline
  • Decreased activity of parasympathetic nerves to heart
227
Q

How is the force of contraction increased?

A
  • Increased Ca2+ influx

- Increased Ca2+ uptake into intracellular stores

228
Q

How is stroke volume increased?

A

Increased sympathetic activity of heart

Increased plasma adrenaline

Increase end diastolic ventricular volume

  • increased atrial pressure
    - increased venous return
  • decreased intrathoracic pressure
    - increased respiratory movements
229
Q

Where are the baroreceptors?

A

Carotid sinus

Aortic arch

230
Q

How do baroreceptors respond to pressure?

A

As the arterial pressure increases in the carotid sinus, the number of impulses sent by the baroreceptors to the vasomotor centre increases.

231
Q

What is reciprocal innervation of the heart?

A

The afferent input (from vegas nerve):

  • stimulates the parasympathetic nerves to heart
  • inhibits sympathetic innervation to the heart, arterioles and veins
232
Q

What nerves relay impulses from the baroreceptors to the vasomotor centre?

A

Baroreceptors in the carotid sinus - glossopharyngeal nerve

Baroreceptors in the aortic arch - vegas nerve

233
Q

What is the pathway if baroreceptors detect an increase in blood pressure?

A
  • detect increase
  • stretch of baroreceptors
  • impulses through vegas nerve increases
  • increased parasympathetic stimulation, increased sympathetic inhibition
  • decreased heart rate and stroke volume +vasodilation
234
Q

What is the feedback for blood pressure control after haemorrhage?

A
  • decreased blood volume (decreased venous pressure)
  • decreased venous return and so lower atrial pressure
  • lower ventricular end diastolic volume
  • smaller stroke volume
  • lower arterial blood pressure
  • smaller cardiac output
    Baroreceptor feedback and reciprocal innervation
  • increased sympathetic control of veins
  • increased venous constriction
  • increased venous pressure
235
Q

Why is movement from supine to standing position a challenge for the circulatory system?

A
  • Lying down there is a similar mean arterial pressure at all points in the body.
  • When standing the blood is affected by gravity so pressure in the lower limbs is very high, and in the head is very low
236
Q

What causes venous distension in the legs?

A
  • The effect of gravity increases hydrostatic pressure

- More fluid leaves vessel into the tissue

237
Q

Why does standing evoke transient hypotension?

A
  • Reduced venous return
  • Reduced end-diastolic volume
  • Reduced volume ejected (and therefore stroke volume)
    Results in hypotension
238
Q

What are the compensatory mechanisms for postural hypotension?

A
  • Pressure reduction detected by baroreceptors in carotid sinus and aortic arch
  • Decreased impulses to parasympathetic, decreased inhibition of sympathetic
  • Increased heart rate and contractility
  • Splanchnic/renal vasoconstriction
  • Venoconstriction in legs (e.g. muscle pump)
239
Q

Which hormones are useful during a haemorrhage?

A
  • Vasopressin (ADH) for H20 retention
  • Angiotensin II to increase renal blood flow
  • Aldosterone to increase Na+ and H20 retension
240
Q

What amount of blood loss is classified as shock?

A

30-40%

241
Q

What happens to the vessels during exercise?

A
  • Increased metabolic activity
  • Requires increased oxygen
  • Results in vasodilation in local arteries

Only tissue that needs it will have increased blood flow, others will have vasoconstriction.

242
Q

How does cardiac output change during exercise?

A

Stroke volume and heart rate increases
CO = SV x HR
Therefore cardiac output increases

243
Q

How can stroke volume increase during exercise?

A
  • When relaxed blood is ‘stored’ in the veins due to their compliance
  • When exercising muscle pumps cause valves to open in the veins and allows more blood to be circulated
244
Q

Why can cardiac output decrease slightly? (during exercise)

A
  • increased loss of plasma to tissue

- loss of salt and water in sweat

245
Q

What happens to the BP during exercise?

A

BP = CO x TPR

  • Cardiac output increases
  • Total peripheral resistance decreases (due to vasodilation)

Overall increase as the increase in CO is more than the decrease in TPR

246
Q

What is haemostasis?

A

Biochemical process that enables the specific and regulated cessation of bleeding in response to vascular injury

247
Q

What is primary haemostasis?

A

The formation of an unstable platelet plug

 - platelet adhesion
 - platelet aggregation
248
Q

What is secondary haemostasis?

A

Stabilisation of the plug within fibrin

- blood coagulation

249
Q

What is the initial response to injury to the blood vessel?

A

Vessel constriction

250
Q

Describe how platelet adhesion occurs.

A
  • Damage to endothelial lining causes exposure of collagen
  • Collagen binds to Von Willebrand factor (VWF) in blood to bind
  • The force of the blood flow causes VWF to unwind and expose binding site (G1p1b)
  • Platelets bind mainly to G1p1b (but under low shear forces can bind to collagen directly - G1p1a)
  • Binding of platelets recruits more platelets to site of damage
251
Q

How are blood vessels designed to have only regulated heamostasis?

A

The layers of the wall:
- Endothelial cells are an anti-coagulant barrier. Consists of proteins like GAGs, tissue factor pathway inhibitor etc

  • Subendothelium which is procoagulant and consists of elastin, collagen, vascular smooth muscle cells and fibroblasts (both tissue factors)
  • Other vital components circulate in a quiescent state: platelets, clotting factor and plasma proteins
252
Q

Describe how platelet activation occurs.

A

Activation is the conversion from a passive cell to an interactive functioning cell

  • Changes shape (spreads and flattens)
  • Change in membrane composition; presents new proteins on surface (Gp2b and Gp3a)
  • Platelets bound to VWF or collagen release ADP and thromboxane which activates the other platelets
253
Q

Describe how platelet aggregation occurs.

A
  • Activated platelets bind more tightly to collagen or VWF via Gp2b/Gp3a
  • Gp2b and Gp3a also binds to fibrinogen to develop the platelet plug
  • Platelet plug helps slow bleeding and provide a surface for coagulation
254
Q

Describe how platelet adhesion occurs?

A

2 methods:
von Willebrand factor;
- von Willebrand factor binds to exposed collagen, and binding sites are exposed due to rheological forces (blood flow).
- Platelets bind to Gp1b sites
directly;
- Platelets can bind directly to collagen by Gp1a in low shear forces

255
Q

What is the result of platelet adhesion?

A

Activated platelets release ADP and thromboxane to lead to platelet aggregation

256
Q

What three things activate platelet aggregation?

A

ADP and thromoxane (from platelets)

Thrombin (from coagulation cascade)

257
Q

What are the sites of synthesis for clotting factors, fibrinolytic factors and inhibitors?

A
  • Liver (most synthesis generally)
  • Endothelial (high vWf)
  • Megakaryocytes (-> platelets) (high factor V)
258
Q

Describe the intrinsic pathway of the coagulation cascade.

A
  • Damaged surface (e.g. exposed collagen) activates factor XII to become XIIa
  • Causes XI -> XIa
  • Causes IX -> IXa (also caused by tissue factor by VIIa)
  • Traces of thrombin cause VIII -> VIIIa (platelet membrane phospholipid)
  • IXa and VIIIa cause X -> Xa
259
Q

Describe the extrinsic pathway of the coagulation cascade.

A
  • Tissue factor, exposed from vessel damage, activates VIIa
  • Causes X -> Xa
  • Also causes IX -> IXa and so X -> Xa
260
Q

Describe the common pathway of the coagulation cascade.

A
  • Traces of thrombin cause V -> Va (platelet membrane phospholipid)
  • Xa and Va causes Prothrombin -> thrombin (IIa)
  • Causes Fibrinogen -> Fibrin
  • Thrombin also causes XIII -> XIIIa
  • Fibrin and XIIIa result in crosslinked fibrin
261
Q

What is the physiological initiator of the coagulation cascade?

A

Tissue factor (vessel damage)

262
Q

What are zymogens?

A

Clotting factors which circulate as inactive pre-cursors, and are activated by specific proteolysis.
(Prothrombin, FVII, F IX, F X, F XI, F XII, F XIII)

263
Q

What are Serine proteinases?

A

Enzymes which cleave peptide bonds is proteins, formed from the zymogens.
(Thrombin, F VIIa, F IXa, F Xa, F XIa, F XIIa)

264
Q

What are Cofactors?

A

Factors which are needed as well as others for activation of a zymogen, they must be activated themselves though.
(F VIII, F V)

265
Q

Which pathway is the primary driver of the coagulation cascade?

A

Extrinsic pathway

266
Q

Name two inhibitory pathways of the coagulation cascade.

A
  • INDIRECT inhibition: Protein C anticoagulant pathway

- DIRECT inhibition: Antithrombin

267
Q

Outline antithrombin inhibition.

A
  • Antithrombin inhibits F XIa, F IXa, F Xa and thrombin preventing continuation of the cascade

Note: Heparin accelerates it’s action and is used as an immediate anticoagulant in venous thrombosis and pulmonary embolism.

268
Q

Outline the protein C pathway in coagulation inhibition.

A
  • Thrombin is produced from factors V (directly) and VIII (indirectly)
  • Thrombin binds to thrombomodulin an endothelial protein receptor, along with protein C
  • Causes release of activated protein C and protein S
  • Both inhibits F Va and F VIIIa by cleaving them (inactivated)
  • Less/no thrombin produced
269
Q

What are ways in which the risk of thrombosis increases?

A
  • Antithrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
  • Factor V Leiden (form of F V which is not easily inactivated)
270
Q

Why doesn’t blood clot fully every time the cascade is initiated?

A

Coagulation inhibitory mechanisms prevent this

271
Q

Outline Fibrinolysis.

A
  • Plasminogen (zymogen) activated by tissue plasminogen activator (tPA) to form Plasmin (proteinase)
  • Plasmin degrades the fibrin clot forming fibrin degradation products (FDP)
272
Q

Explain the balance of haemostasis.

A
  • Normal haemostasis: equilibrium between fibrinolytic factors and coagulation factors
  • Bleeding: increased fibrinolytic factors
  • Thrombosis: increased coagulation factors
273
Q

What are the functions of haemostatic plug function?

A
  • Vessel constriction: Limit blood flow to injured vessel
  • Primary Haemostasis: Limit blood loss + provide surface for coagulation
  • Secondary Haemostasis: Stop blood loss
  • Fibrinolysis and vessel repair: restores vessel integrity
274
Q

What defects can occur in primary haemostasis?

A

Defective/deficiency of:

  • Collagen (vessel wall: e.g. steroid therapy, age, scurvy
  • Von Willebrand factor: Von Willebrand disease (genetic)
  • Platelets: Anticoagulant drugs e.g. Aspirin, thromocytopenia (lack of platelets)
275
Q

What are the symptoms/patterns of bleeding for defects in primary haemostasis?

A
  • Immediate bleeding (smaller vessels)
  • Easy bruising
  • Nosebleeds (prolonged >20 mins)
  • Gum bleeding (prolonged)
  • Menorrhagia (heavy menstruation leading to anaemia)
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
276
Q

What causes defects in secondary haemostasis?

A
  • Haemophilia: Lack of VIII and therefore reduced thrombin
    - Less thrombin means no fibrin cross linking (no stable clot)
  • Liver disease (aquired): most coagulation factors are synthesised in the liver
  • Drugs: e.g. Warfarin
  • Dilution: results from volume replacement
  • Disseminated intravascular coagulation
277
Q

What are the symptoms/patterns of bleeding in defects of secondary haemostasis?

A
  • delayed (after primary haemostasis) and prolonged bleeding
  • deeper: joints and muscles
  • not from small cuts
  • nosebleeds are rare
  • bleeding after trauma/surgery
  • after intramuscular injections
  • Ecchymosis: easy bruiding
  • Haemarthrosis (for haemoohilia)
278
Q

What are the defects affecting clot stability leading to bleeding?

A

Excess fibrinolysis:
- excess fibrinolytic (plasmin, tPA): e.g. therapeutic administration, some tumours
- deficient antifibrinotlytic (antiplasmin): e.g. genetic antiplasmin deficiency
Excess anticoagulant:
- usually from therapeutic administration e.g. heparin, thrombin and Xa inhibitors

279
Q

What are the two possible pathological outcomes of thrombosis?

A
  • Obstructed blood flow

- Embolism

280
Q

What are the possible consequences of obstructed blood flow by thrombosis?

A
  • Artery: Myocardial infarction, stroke, limb ischaemia

- Vein: pain and swelling

281
Q

What are the possible consequences of embolism from thrombosis?

A
  • Arterial emboli: usually from heart and may cause stroke or limb ischaemia
  • Venous emboli: to lungs causing pulmonary embolus
282
Q

What is deep vein thrombosis and pulmonary embolism? How are they linked?

A
  • Deep vein thrombosis: obstruction of venous return. Causes painful, swollen leg
  • Pulmonary embolism: block in artery in the lungs. Causes shortness of breath, chest pain, sudden death.

untreated DVT can embolise and lead to pulmonary embolism

283
Q

What are the risk factors for thrombosis?

A
  • genetic constitution
  • effect of age, previous events/illnesses and medication
  • acute stimulus
284
Q

What is disseminated intravascular coagulation?

A
  • general activation of coagulation by tissue factor
  • associated with sepsis, major tissue damage and inflammation
  • consumes and depletes coagulation factors and platelets
  • activation of fibrinolysis depletes fibrinogen

Consequences:

  • widespread bleeding from IV lines, bruising and internal bleeding
  • deposition of fibrin in vessels causes organ failure
285
Q

What is Virchow’s triad?

A

Three contributory factors to thrombosis:

  • blood (dominant in venous thrombosis)
  • vessel wall (dominant in arterial thrombosis)
  • flow (contributes to both)

These may be inherited or aquired

286
Q

Describe how blood can be a factor for increased thrombosis.

A
  • Deficiency of anticoagulant proteins (antithrombin, protein C, protein S)
  • Increased coagulant proteins/activity (F VIII, F II and others, F V Leiden, thrombocytosis (increased platelets))
287
Q

Describe how vessel wall can be a factor for increased thrombosis.

A
  • Many proteins active in coagulation are expressed in the surface of endothelial cells e.g. thrombomodulin, tissue factor, tissue factor pathway inhibitor
  • Expression is altered in inflammation e.g. malignancy, infection and immune disorders
288
Q

Describe how flow can be a factor for increased thrombosis.

A
  • Reduced flow (stasis) increases risk of venous thrombosis

e. g. surgery, fracture, long haul flight, bed rest

289
Q

What is thrombophilia?

A

Presents with:

  • thrombosis at a young age
  • idiopathic thrombosis or multiple thromboses
  • thrombosis whilst anticoagulated
290
Q

What conditions increase the risk of thrombosis?

A
  • Pregnancy
  • Malignancy
  • Surgery
  • Inflammatory response
291
Q

How are venous thromboses treated?

A

Treatment to lyse clot:
- eg. tissue plasminogen activator
Treatment to limit recurrence/emboli/extension
- increase anticoagulent activity e.g. heparin
- lower procoagulant factors e.g warfarin
- inhibit procoagulant factors e.g. rivaroxaban

292
Q

What is the distribution of BP in the population?

A

Continuous and normal

293
Q

Approximately what is considered normal and what is high blood pressure?

A
  • Normal: (120) up to 140

- High: more than 140

294
Q

What is the relationship between age and blood pressure?

A
  • mean BP increase with age

- Pulse pressure increases

295
Q

What does a high BP increase risk of?

A
  • Stroke (mainly)

- Coronary heart disease and other cardiovascular diseases

296
Q

Outline the classification of hypertension.

A
  • Primary or essential hypertension: 90-95% of cases. No identifiable cause
  • Secondary hypertension:
297
Q

What factors contribute to the risk of primary hypertension?

A 
Genetic: estimated 30-50%
- monogenic (rare)
- complex polygenic (common)
Environmental:
- dietary salt (sodium) MAIN ONE
- obesity/lack of exercise
- alcohol
- pre-natal environment (birth weight)
- pregnancy (pre-eclampsia)
- other dietary factors and exposures
298
Q

What is associated with hypertension?

A
  • Increased total peripheral resistance
  • Reduced arterial compliance (higher pulse pressure)
  • Normal cardiac output
  • Normal blood volume/extracellular volume
  • Central shift in blood volume secondary to reduced venous compliance
299
Q

What explains elevated peripheral vascular resistance in hypertension?

A
  • Active narrowing of arteries (vasoconstriction for short term)
  • Structural narrowing of arteries: adaptive growth and remodelling?
  • Loss of capillaries: rarefaction (loss of density) from adaption/damage?
300
Q

What is isolated systolic hypertension?

A
  • A systolic BP >140 but diatolic
301
Q

What are possible causes of primary hypertension?

A
  • Kidney: relation to salt intake
  • Sypathetic nervous system: evidence that high activity linked to hypertension
  • Endocrine/paracrine factors: inconsistent evidence
302
Q

What diseases are associated with high blood pressure?

A
  • Coronary heart diease
  • stroke
  • peripheral vascular disease/atheromatous disease
  • heart failure
  • artrial fibrillation
  • dementia/cognitive impairment
  • retinopathy
303
Q

How does high blood pressure affect the heart?

A

Associated with increased left ventricular wall mass (hypertrophy) and changes in chamber size leading to a change in ventricular volume.

It is strongly associated with heart failure.

304
Q

How does high blood pressure affect blood vessels?

A
  • Associated with changes is larger arteries; thickened walls (hypertrophy) and acceleration of atherosclerosis
  • May cause arterial rupture or dilations (aneurysms) which can lead to thrombosis or haemorrhage e.g. strokes
  • Reduction in capillary density and elevated capillary pressure
305
Q

What effect does hypertension have on the retina?

A
  • Causes micro-vascular damage
  • Thickening of the wall of small arteries, arteriolar narrowing, vasospasm, impaired perfusion and increase leakage of plasma into surrounding tissue
306
Q

What effect does hypertension have of the kidney?

A 
Primary hypertension:
- granular capsular surface
- cortical thinning, renal atrophy
Accelerated hypertension:
- subcapsular haemorrhages

Renal dysfunction is common - increased albumin loss in urine, and renal failure for accelerated hypertension

307
Q

What are the risk factors for atherosclerosis?

A

Not modifiable:

  • Age
  • Sex
  • Genetic background

Modifiable:

  • Smoking
  • Lipids
  • Blood pressure
  • Diabetes
  • Obesity
  • Lack of exercise
308
Q

What do LDLs do?

A

Deposit in sub intimal spaces and bind to matrix proteoglycans.

309
Q

Outline the relationship between age and windows for prevention.

A
  • At around 40 yrs there are intermediate lesions
  • At around 50 yrs there are advanced lesions
    This is the window for primary preventions (lifestyle and risk factor management.
  • At >60 yrs there are complications e.g. stenosis, plaque rupture.
    This is the window of clinical (secondary) intervention .
310
Q

What are the main types of cells involved in atherosclerosis?

A
  • Vascular endothelial cells: barrier function e.g. to lipoproteins, leukocyte recruitment
  • Platelets: thrombus generation, cytokine and growth factor release
  • Monocytes/macrophages: foam cell formation, cytokine and growth factor release, source of free radicals, metalloproteinases
  • Vascular smooth muscle: migration and proliferation, collagen synthesis, remodelling and fibrous cap formation
  • T-lymphocytes: macrophage activation
311
Q

Describe the role of macrophages.

A
  • White blood cells can damage host tissue if activated excessively or inappropriately
  • Derived from monocytes but many different types
  • Two main ones are resident and inflammatory
  • Inflammatory: kill micro-organisms
  • Resident: normally homoeostatic e.g. alveolar macrophages
312
Q

What are the different types of Lipoproteins?

A
  • Low density: ‘bad’ cholesterol, synthesised in liver,carries cholesterol away from liver and to body including arteries
  • High density: ‘good’ cholesterol, carries cholesterol from peripheral tissues including arteries to liver
  • Oxidised, modified: due to action of free radicals of LDL, not one single substance, high inflammatory and toxic forms found in vessel walls
313
Q

Outline sub-endothelial trapping of LDL.

A
  • LDL leak thorugh endothelial barrier
  • Trapped by binding to sticky matrix carbohydrates (proteoglycans) in sub-endothelial layer
  • Trapped LDL is susceptible to modification
314
Q

Outline the modification of subendothelial trapped LDL.

A
  • Best studied is oxidation
  • Chemically represents partial burning
  • LDL becomes oxidatively modified by free radicals
  • Oxidised LDL is phagocytosed by macrophages and if there’s high levels stimulates chronic inflammation
315
Q

What is familial hyperlipidemia?

A
  • autosomal genetic disease
  • massively elevated cholesterol (20mmol/L)
  • failure to clear LDL from blood
  • xanthomas (cholesterol deposit in skin) and early atherosclerosis
  • if untreated could have fatal myocardial infarction before 20
  • No LDL receptor, but they have a second one which has no feedback control so macrophages continuously engulf LDL
316
Q

What is the structure of LDL?

A
  • Phospholipid monolayer
  • Apoproteins of surface act as ‘addresses’
  • Fats held inside mostly triglycerides, and some cholesterolesterase
317
Q

What do macrophages do within plaques?

A
  • Generate free radicals that further oxidise lipoproteins
  • Phagocytose modified lipoproteins and become foam cells
  • Become activated by modified lipoproteins/free intracellular cholesterol to express/secrete:
    • cytokine mediators that recruit more monoytes (e.g. TNFα, IL-1, MCP-1)
    • Chemoattractants and growth factors for VSMC
    • Proteinases that degrade tissue e.g. fibrous cap
    • Tissue factor that stimulates coagulation
  • Die by apoptosis contributing to lipid-rich core of the plaque
318
Q

What oxidative enzymes within macrophages can modify LDL?

A
  • NADPH Oxidase

- Myeloperoxidase

319
Q

How do the molecules released my macrophages recruit monocytes?

A

Cytokines: protein hormones that activate endothelial cell adhesion molecules.

 - Interleukin-1 upregulates vascular cell adhesion VCAM-1
 - VCAM-1 mediates tight monocyte binding

Chemokines: small proteins which chemoattract monocytes

 - Monocyte chemotactic protein-1 (MCP-1)
 - MCP-1 binds to monocyte G-protein coupled receptor CCR2

Positive feedback loop - leads to self-perpetuating inflammation

320
Q

Describe how macrophages recruit vascular smooth muscle cells.

A 
Produces two types of growth factor:
Platelet derive growth factor encourages VSMC:
- chemotaxis
- survival in toxic environment
- cell division

Transforming growth factor beta:

  • Increased collagen synthesis
  • Matrix deposition
321
Q

What is the difference between normal vascular smooth muscle cells and those in plaque?

A
  • Normal VSMC have a lot more contractile filaments

- Normal VSMC have less active matrix deposition genes

322
Q

What is the effect of plaque erosion/rupture?

A

Blood coagulation at site of rupture may lead to occlusive thrombus and cessation of blood flow.

323
Q

What are the characteristics of vulnerable and stable plaques?

A
  • Large, soft eccentric (not central) lipid-rich necrotic core
  • Thin fibrous cap
  • Reduced VSNC and collagen content
  • Increased VSNC apoptosis
  • Infiltrate of activated macrophages expressing matrix metalloproteinases
324
Q

What is the significance of macrophage apoptosis in plaque?

A
  • Once protective systems the maintain survival in toxic lipid loading are overwhelmed the macrophage foam cells die by apoptosis
  • This released tissue factor and toxic lipid into the lipid necrotic core
  • Thromogenic and toxic material accumulates until plaque ruptures and it meets blood triggering coagulation
325
Q

What is nuclear factor κ B?

A
  • transcription factor
  • regulator of inflammation
  • activated by scavenger receptors, toll-like receptors and cytokine receptors
  • switches on MMP genes and inducible nitric oxide synthase
326
Q

Outline the steps in atherosclerosis.

A
  1. Endothelial cell injury: due to toxins, shear stress, smoking etc
  2. Lipoprotein deposition: LDL enter and are modified by oxidation.
  3. Inflammatory reaction: This causes inflammation and attracts macrophages creating ‘foam cells’ and a fatty streak. Further macrophage recruitment by inflammatory mediators. Some die and form a necrotic core.
  4. Smooth muscle cell cap formation: VSMC migrate to surface creating a fibrous cap by synthesising collagen.
  5. Rupture: If unstable e.g. thin fibrous cap it can rupture and thrombosis can occur
327
Q

What are the layers of blood vessels? Which types are the exceptions?

A
  • Tunica intima: endothelium
  • Tunica media: smooth muscle cells
  • Tunica adventitia: vasa vasorum (vessels that supply larger vessels), nerves
328
Q

Give some features of the vascular endothelium.

A
  • acts as a vital barrier separating blood from tissues
  • formed by a mono-layer of endothelial cells
  • cells are flat, 1-2μm thick, 10-20μm in diameter
  • heterogeneity (not all cells the same)
  • have a long life and low proliferation rate unless for angiogenesis
  • they regulate essential functions of blood vessels
329
Q

What processes are endothelial cells involved in?

A
  • Angiogenesis
  • Inflammation
  • Thromosis and haemostasis
  • Vascular tone permeability
330
Q

How do leukocytes get recruited?

A
  • Rolling: When stimulated the endothelium express ICAM-1, VCAM-1 and E-&P-selectin which binds to complementary molecules on leukocytes causing them to roll along the wall.
  • Tight Adhesion: Chemokines released by macrophages cause the bonds to switch to high affinity immobilising the leukocytes.
  • Transmigration: The leukocytes pass through the gaps between endothelial cells and then penetrate the basement membrane.
331
Q

What is the importance of endothelial junction?

A

Proteins on one cell bound to proteins e.g. cadherin on the other which unbind when necessary to let things through without compromising the structure of the endothelium.

332
Q

Why is leukocyte recruitment an issue for arteries but not capilllaries/veins?

A
  • Capillaries/post-capillary venules have a monolayer of endothelial cells, basement mebrane some pericytes (cells that wrap around).
  • Arteries have tunica intima, AND tunica media and adventitia.

Leukocytes that go through endothelium of arteries are stuck.

333
Q

How does vascular permeability relate to atherosclerosis?

A
  • Due to inflammation there is increased permeability in the endothelium
  • Allows LDLs to enter and start process of atherosclerosis
334
Q

Why does atherosclerosis occur at branch points?

A
  • At branch points there tends to be turbulent blood flow

- This promotes: coagulation, leukocyte adhesion, smooth muscle cell proliferation, and epithelial apoptosis

335
Q

What does laminar blood flow promote in the endothelium?

A
  • nitric oxide production
  • factors that inhibit coagulation, leukocyte adhesion, smooth muscle cell proliferation
  • endothelial survival
336
Q

What is angiogenesis?

A

Formation of new blood vessels by sprouting from pre-existing vessels

337
Q

Why does angiogenesis occur?

A
  • Tissue in hypoxia requires oxygen
  • Produces growth factors e.g. vascular endothelial growth factors
  • Stimulate growth of a capillary towards that area via chemotaxis
338
Q

What is the relation of angiogenesis and cardiovascular disease?

A
  • Bad: Could promote plaque growth and other complications e.g. intra-plaque haemorrhage
  • Good: Research suggests that introducing growth factors before an artery is completely occluded could reduce ischemic damage
339
Q

What are the consequences of senescence of cells?

A

Good: prevents transmission of damage to daughter cells

Bad: Senescent cells are pro-inflammatory and contribute to disease
e.g. found in atherosclerotic lesions and may contribute to plaque progression and complication

340
Q

How does coronary artery disease present?

A
  • Sudden cardiac death
  • Acute coronary syndrome: acute myocardial infarction, unstable angina
  • Stable angina pectoris
  • Heart failure
  • Arrhythmia
341
Q

What are the risk factors for coronary artery disease?

A
  • Tobacco use
  • Physical inactivity
  • Harmful alcohol use
  • Unhealthy diet
    Resulting in: Hypertension, obesity, diabetes mellitus, hyperlipidaemia
342
Q

What is it myocardial ischaemia?

A

Mismatch between myocardial oxygen supply and demand because of:

  • Primary reduction in blood flow
  • Inability to increase blood flow to match increased metabolic demand
343
Q

What are the two vessel types of coronary arteries?

A
  • Large epicardial arteries (50% of resistance)

- Smaller arterioles and capillaries (50% of resistance)

344
Q

What is the effect of epicardial stenosis on resting coronary resistance and flow?

A
  • Up to 70% stenosis has no effect on flow due to auto-regulation of vessels
  • Above that flow decreases rapidly
  • Resistance decreases because micro-circulation is maximally dilated
345
Q

What is the effect coronary stenosis has on flow response to vasodilators?

A

As % of stenosis increases

  • resting flow rate decreases
  • coronary vasodilator reserve decreases
346
Q

What is Angina Pectoris?

A
  • Clinical diagnosis
  • Discomfort in chest, jaw, shoulders, arms or back
  • Provoked by exertion or emotional stress
  • Relieved by rest or glyceryl trinitrate (GTN - vessel relaxant) in less than 5mins
347
Q

Name Non-invasive investigative methods for CHD.

A

Functional:

  • Exercise ECG
  • Stress echo
  • Stress cardiac MRI
  • PET/PT
  • Stress nuclear medical perfusion scan
  • Fractional flow reserve (CT) FFR CT

Anatomical:

  • CT coronary calcium score
  • CT coronary angiogram
348
Q

Name Invasic investigative methods for CHD.

A

Functional:

  • Coronary flow reserve (CFR)
  • Pressure wire (fractional flow reserve)
  • iFR
  • IVUS
  • OCT

Anatomical:
- Coronary angiogram

349
Q

What are the treatment strategies for CHD?

A

Prevent atherosclerosis progression and risk of death/MI

  • Education
  • Lifestyle modification
  • Drugs: aspirin, statins, ACE inhibitors

Reduce myocardial oxygen demand

  • Heart rate: β blockers, Ca antagonists, If blockers
  • Wall stress: ACE inhibitors, Ca antagonists
  • Metabolic modifiers

Improve blood supply

  • Vasodilators: nitrates, nicorandil, Ca antagonists
  • Revascularisation: PCI (stent), CABG (bypass)
350
Q

What are the mechanisms of myocardial cell death?

A
  • Oncosis: Accidental/passive cell death where cells swell abnormally
  • Apoptosis: Programmed cell death
351
Q

What are the possible events after atherosclerosis?

A
  • 20-30% plaque erosion
  • 70%-80% plaque rupture

Both lead to thrombosis and therefore acute coronary syndrome (e.g. MI)

352
Q

What are features of a white thrombus?

A
  • Platelet rich
  • Common in arterial thrombosis (high pressure/turbulent circulation)
  • Benefit from antiplatelet therapy
353
Q

What are features of a ref thrombus?

A
  • Fibrin rich, with trapped erythrocytes
  • Common in venous or low pressure situations (stasis)
  • Benefit from anticoagulant or anti-fibrinolytic therapy
354
Q

What are the effects of coronary stenosis on haemodynamics?

A
  • Low shear stress before stenosis due to deceleration
  • High shear stress in stenosis due to acceleration
  • Low shear stress and energy dissipation after stenosis
355
Q

What is the universal definition of Acute myocardial infarction?

A

Detection of a rise or fall in biomarker troponin with one value >99th centile of upper reference limit AND atleast one of:

  • symptoms suggestive of ischaemia
  • new or presumes new ST-T changes or LBBB on ECG
  • imaging evidence of new loss of viable myocardium or wall motion abnormality
  • identification of intra-coronary thrombus on angiography or at autopsy
356
Q

List the symptoms of Acute Myocardial infarction.

A
  • Chest or left arm pain or discomfort or jaw, shoulder and back
  • Hypotension
  • Nausea, indigestion, heartburn or abdominal pain
  • Shortness of breath
  • Fatigue
  • Dizziness or light-headedness
357
Q

What molecule is used to indicate cardiomyocyte death?

A

Cardiac troponin

  • peak release around 20 hours after admission
  • can be detected after 1 hour after MI
358
Q

What are the two categories acute coronary syndromes can be divided into? What are the indications on an ECG? What is the treatment?

A

ST segment elevation acute coronary syndromes - Complete occlusion of coronary artery

  • ST elevation
  • Immediate catheterisation

Non-ST segment elevation acute coronary syndromes - incomplete occlusion of coronary artery

  • ST depression
  • T wave inversion
  • Medication and catheterisation within 24hrs
359
Q

What are the complications of a Non-ST segment elevation acute coronary syndrome?

A

Due to enzyme release and necrosis, the thrombus can embolise and travel to the micro-circulation where it can cause persistent angina and necrosis.

360
Q

In an untreated MI how is the tissue affected?

A
  • In a complete infarct the area the vessel should be supplying is at risk of ischaemia
  • Necrosis starts in the tissue furthest from the vessel (as they have increased demand and furthest from O2 supply)
  • If there is necrosis through the whole wall - transmural infarction
361
Q

What is a re-perfusion injury?

A

When a myocardial infarction is treated the re-perfusion of blood to the area causes injury as the make up of the blood has changed.

Due to oxidative free radicals and the change in mitochondria in the cardiac myocytes which induces apoptosis.

Cardioprotection during re-perfusion results in less ischaemia.

362
Q

What are the consequences of the damage done in an MI?

A

Part of the cardiac muscle is not working, so the rest must compensate for it:
REMODELLING: Immune response to clear dead tissue, and replacement with a collagen scar which thins and expands increasing loading (ventricular dilatation). Increased risk of heart failure.

363
Q

What are the consequences of left ventricle remodelling?

A
  • Increased systolic wall tension/stress
  • Increased mixed venous oxygen saturation (MVO2)
  • Reduced myocyte shortening
  • Increased diastolic wall tension/stress
  • Reduced subendocardial perfusion
  • Dysynchronous depolarization/contraction
  • Mitral regulation
  • Ventricular arrythmias
  • Ventricular fibrillation
364
Q

What are the methods of stabilising plaque?

A

Mechanical: Stent

Drugs: Statins (high dose), ACE inhibitors

365
Q

What are the methods of managing left ventricle remodelling?

A

Non-drug:

  • Pacemaker (CRT-P) or Defibrillator (CRT-D)
  • Progenitor cells (stem cells)

Drug:

  • β blockers
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Aldosterone receptor antagonists
366
Q

What is an embolism?

A

Obstruction in blood vessel due to thrombus or other foreign matter that gets stuck while travelling through the bloodstream.

Arterial: thrombus (ACS, transient ischaemic attack ,stroke), air, fat, amniotic, foreign body
Venous: thrombus (DVT, PE)

367
Q

Outline the possible causes and treatment for an embolic TIA/Stroke.

A

Causes:

  • Internal carotid artery plaque rupture
  • Intracardiac e.g. AF, old MI, valve disease

Treatment:

  • Fibrinolysis
  • Clot extraction
  • Antiplatelet drugs
  • Modify atherosclerotic risk factors
  • Endarterectomy (removal of deposits), stent
  • Hole closure
368
Q

Outline the possible causes and treatment for an haemorrhagic TIA/Stroke.

A

Cause:

  • Vascular malformation
  • Hyptertension
  • Tumor
  • Iatrogenic (due to medical examination or treatment)

Treatment:

  • Coil/clip aneurysm
  • Withdraw pro-haemorrhagic medication
  • Control hypertension
369
Q

Define heart failure.

A

Clinical Syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses.

370
Q

List the general causes of heart failure.

A
  • Arrhythmias
  • Valve disease
  • Pericardial disease
  • Congenitial heart disease
  • Myocardial disease: most common
371
Q

What is the main cause of heart failure with regard to myocardial disease?

A

Coronary artery disease
Cardiomyopathy: chronic disease of heart muscle
- Dilated ventricles: specific or idiopathic
- Hypertrophic: thickened wall
- Restrictive: rigid walls
- Arrhythmic right ventricular cardiomyopathy
Hypertension
Drugs
Other/unknown

372
Q

What is the epidemiology of heart failure?

A
  • Incidence and prevalence is increasing
  • Poor prognosis (50% 5 year mortality rate)
  • Age is the biggest risk factor
373
Q

What are the causes of dilated cardiomyopathy?

A
  • Idiopathic
  • Genetic/Familial
  • Infectious e.g. virus and HIV, mycobacteria, fungus etc
  • Toxins and poisons e.g. ethanol, metals, cocaine, CO2 or hypoxia
  • Drugs: chemotherapeutic agents, antiviral agents
  • Others; Collagen disorders, autoimmune, peri-partum (just before delivery), neuromuscular disorders
374
Q

What are the causes of restrictive cardiomyopathy?

A
  • Associated with fibrosis; diastolic dysfunction
  • Infiltrative disorders e.g. amyloidosis, neoplasia
  • Storage disorders e.g. haemochromatosis, haemosiderosis Fabry disease
  • Endomyocardial disorders e.g. endomyocardial fibrosis, metastases etc
375
Q

What are the causes of death in heart failure?

A
  • Progression of heart failure: increased wall stress and retention of sodium and water
  • Sudden death: opportunistic arrhythmia, acute coronary event
  • Cardiac event e.g. MI
  • Other cardiovascular event e.g. stroke, peripheral vascular disease
  • Non cardiovascular cause
376
Q

What are the three types of hormonal mediators in heart failure?

A
  • Constrictors e.g. noradrenalin, renin/angiotensin II, endothelin, vasopressin
  • Dilators e.g. Prostaglandins E2, dopamine
  • Growth factors e.g. insulin, TNFα, growth hormone, angiotensin II, catecholamines, NO, cytokines, oxygen radicals
377
Q

What are the symptoms of heart failure?

A
  • Ankle swelling
  • Exertional breathlessness
  • Fatigue
  • Othopnoea
  • Paroxymal nocturnal dyspnoea (PND)
  • Nocturia (frequent unrination at night)
  • Anorexia
  • Weight loss
378
Q

What are the signs of heart failure?

A
  • Tachycardia
  • Decreased pulse volume
  • Pulsus alternans (alternating strong and weak pulse)
  • Increased jugular venous pressure (JVP)
  • Oedema e.g. pitting oedema
  • Rales (abnormal rattling sound in unhealthy lungs)
  • Hepatomegaly (abnormal enlargement of liver)
  • Ascites (fluid accumulation in peritoneal cavity causing abdominal swelling)
379
Q

What investigations are done for heart failure?

A
  • X-ray
  • Echocardiogram
  • Radionuclide ventriculography
  • Ambulatory ECG monitoring
  • Exercise test (VO2)
  • Cardiac catheter
380
Q

Outline the classification of functional capacity for patients with cardiac disease.

A
  • Class 1: With disease but no limitation on physical activity
  • Class 2: With disease and slight limitation of physical activity though comfortable at rest
  • Class 3: With disease and marked limitations in physical activity and symptoms of less that ordinary activities. Comfortable at rest.
  • Class 4: With disease, inability to carry out physical activity without discomfort, symptoms present at rest.
381
Q

What are the types of heart failure?

A

Chronic: develops over time

  • Systolic heart failure: reduced ejection fraction
  • Diastolic heart failure: preserved ejection fraction

Acute:

  • De novo: no previous signs/symptoms e.g. shock (sepsis)
  • Acute decompensation: life threatening heart failure e.g. pulmonary oedema
382
Q

Describe the management of heart failure after diagnosis.

A
  • Identify cause
  • Assess severity
  • Anticipate complications
  • Treat and tailor to patient
383
Q

What are the main aims of treating chronic heart failure?

A
  • Prevention of myocardial damage and re-occurrence
  • Relief of symptoms and signs
  • Improve prognosis
384
Q

What lifestyle and medical measures are taken in treating heart failure?

A

Lifestyle:
- Weight reduction, stop smoking, avoid excess alcohol, exercise

Medical:

  • Treat hypertension/diabetes/arrhythmias, anticoagulation
  • Immunization, sodium/fluid restriction
  • Diuretics, ACE inhibitors, β blockers, aldosterone antagonists, digoxin, devices (e.g. cardiac resynchronization)

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