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Semester 2 - alex > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

What is the role of the cardiovascular system?

A

Supplies cells in the body with their metabolic needs.

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2
Q

What factors influence the exchange of substances between teh blood in cappillaries and the surrounding tissues?

A

Area (capillary density)

Diffusion resistance (difficulty of moement through the barrier)

Concentration gradient (drives diffusion)

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3
Q

Why is adequate blood flow important?

A

Ensure metabolic needs for each cell is met

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4
Q

What organs require a constant blood flow and what are they?

A

Brain 0.75

Kidneys 1.2

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5
Q

What is the requireed blood flow to the heart?

A

0.3 - 1.2 l/min

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6
Q

What is the required blood flow to the gut?

A

1.4 - 2.4 l/min

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7
Q

What is the required blood flow to muscle?

A

1 - 16 l/min

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8
Q

what is the required blood flow to skin?

A

0.2 - 2.5 l/min

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9
Q

What is the total flow of blood around the body?

A

5 - 25 l/min

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10
Q

What are the major functional components of the circulation?

A

A pump - heart

Distribution vessels - Arteries

Flow control - resistance vessels, arterioles, pre capillary sphincters

Capacitance (ability to cope with change) - veins

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11
Q

Describe the distribution of blood volume over major parts of the circulation

A

11% arteries/arterioles

5% capillaries

17% heart and lungs

67% veins

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12
Q

How are arteries named?

A

By the amount of elastic and smooth muscle fibres in their walls. They are named Elastic (conducting) and Muscular (distributing) arteries

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13
Q

What type of arteries are usually larger?

A

Elastic - expand with each heart beat

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14
Q

What is the function of arterioles?

A

REgulate the amount of blood reaching an organ or tissue and regultae blood pressure

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15
Q

How is the diameter of arteries and arterioles controlled?

A

Autonomic nervous system

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16
Q

Describe the structure of capillaries

A

one cell thick to allow the exchange of substances.

The wall may be continuous or fenestrated and may be surrounded partially by pericytes

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17
Q

What are the structural differences between arteries and veins?

A

Veins have thinner walls and wider, more irregular lumens, usually with semilunar, paired valves.

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18
Q

What is the purpose of valves?

A

Prevent blood flowing in the wrong direction. Permits blood to flow only one way.

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19
Q

Below what diameter do veins no longer have valves?

A

1mm

Veins in the thoracic and abdominal cavities also do not have valves.

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20
Q

How is blood flow in the veins established?

A

Muscle pump action in the leg and pressure factors in the abdominal and thoracic cavities.

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21
Q

What happens if blood pressure is not maintained in the veins?

A

They collapse

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22
Q

What are the 3 layers in arteries and veins?

A

Tunica intima

Tunica media

Tunica Adventitia

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23
Q

Describe the histological structure of Elastic areteries

A

Tunica intima - Endothelia with long axes orientated parallel to long axis of artery, with a narrow sub-endothelium of connective tissue with discontinuous intrenal elastic lamina

Tunica media - MAIN FEATURE - 40-70 fenestrated elastic membranes with smooth muscle cells and collagen between these lamellae. Thin external elastic lamina

Tunica adventitia - The layer of fibroelastic connective tissue containing vasa vasorum, lymphatic vessels and nerve fibres

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24
Q

Describe the histoogical features of muscular arteries

A

Tunica intima - Endothelium, sub-endothelial layer, thick elastic lamina

Tunica media - MAIN FEATURE - 40 layers of smooth muscle cells (connected by gap junctions), prominent external elastic lamina

Tunica adventita- Thin layer of fibroelastic connective tissue, containing vasa vasorum, lymphatic vessels and nerve fibres

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25
Q

What is the purpose of gap junctions?

A

Enable coordinated conduction

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26
Q

How is depolaristation of smooth muscle in blood vessels acheived?

A

Noradrenaline is released at the nerve endings in the adventitia and diffuses through fenestrations in the external elastic lamina into the external tunica media, where it depolarises some of the superficial smooth muscle cells. Propagated to all cells in the tunica media via gap junctions

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27
Q

What happens to the tunica media as arteries diminish in diameter?

A

Number of smooth muscle layers decreases

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28
Q

How do arteries differ in appearance when they are constricted?

A

Endothelial cells protrude into the lumen, which is narrower

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29
Q

Describe the structure of arterioles.

A

Thin internal elastic lamina is present in larger arterioles.

1-3 layers of smooth muscle in the tunica media - 1 layer in smaller arterioles completely encircles the endothelial cells.

External elastic lamina is absent and teh tunica adventitia is scant.

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30
Q

How do arterioles and metarterioles differ?

A

Metarterioles smooth muscle layer is not continuous. Rather they are spaced apart and each encircles the endothelium of a capillary arising from the metarterioles

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31
Q

What are precapillary sphincters?

A

The discontinuous muscle encircling the endothelium of a capillary arising from the metarteriole which controls blood flow into the capillary bed

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32
Q

How do capillaries serve as a good area for gas exchange?

A

Large surface area

One cell thick

Passing RBCs fill almost the entire lumen minimising the diffusion path to adjacent tissues

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33
Q

What size are capillaries?

A

7-10µm in diameter and usually less than 1mm long

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34
Q

What are preicytes?

A

Cells capable of dividing into muscle cells, or fibroblasts during angiogenesis, tumour growth and wound healing. They form a branching network on the outer surface of the endothelium.

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35
Q

What are sinusoids?

A

Capillaries found in the liver, spleen and bone marrow. They generally have a larger diameter, may contain special lining cells and an incomplete basal lamina.

The larger openings allow RBCs/WBCs to pass using a process aided by discontinuous basal lamina

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36
Q

What are fenestrated capillaries?

A

Capillarries with pericytes and fenestrations in the endothelium

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37
Q

What is the diameter of postcapillary venules?

A

10-30µm

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38
Q

What is the purpose of postcapillary venules and how do they work?

A

fluid tends to drain into them because their pressure is lower than that of capillaries or the surrounding tissue. They have a similar wall to capillaries.

If an inflammatory response is operating fluid and leucocytes emigrate from them.

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39
Q

What type of vessels have the largest diameter?

A

Veins (generally)

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40
Q

What is the difference between artery and vein walls?

A

Veins are thinner with more connective tissue and fewer elastic and muscle fibres.

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41
Q

How are superficial veins in the legs different to the rest?

A

They have a well defined muscular wall to reesist distension due to gravity. Valves act together with muscle contraction to return blood to the heart. Most veins have a well developed adventitia

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42
Q

Describe the smooth muscle orientation in the walls of large veins.

A

Well developed longitudinally orientated smooth muscle in the tunica adventitia in addition to the circularly arranged smooth muscle in the tunica media

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43
Q

What properties do cardiac muscle posess that allow the heart to operate as a pump?

A

Striations

Branching

Centrally positioned nuclei

Intercalated discs (for electrical and mechanical coupling with adjacent cells)

Adherens-type junctions (to anchor cells and provide anchorage for actin)

Gap junctions (for electrical coupling)

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44
Q

What are T tubules in line with in cardiac muscle?

A

Z bands

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45
Q

Define systole

A

The period when the myocardium is contracting

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46
Q

Define diastole

A

The relaxation of the myocardium inbetween contractions

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47
Q

Describe the spread of excitation in systole

A
  1. The SAN fires an action potential which spreads over teh atria causing atrial systole. The AP reaches the AVN where it is delayed for about 120ms
  2. From the AVN excitation spreads down the septum between teh ventricles
  3. Excitation spreads from the inner to outer suface
  4. Ventricles contract from the apex up, forcing blood towards the outflow valves
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48
Q

What way is ventricular muscle organised?

A

figure of 8 bands that squeeze the ventricular chamber forcefully in a way most effective for ejection through the outflow valve.

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49
Q

How does the heart contract?

A

The apex contracts first and relaxes last to prevent back flow

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50
Q

Why is the left heart different to the right

A

Left side has thicker myocardium as it has to pump blood to the whole body, whereas the right heart only has to pump it to the lungs.

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51
Q

Where is the pacemaker?

A

Right atrium - Sino Atrial Node

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52
Q

What causes the mitral valves to open?

A

atrial pressure exceeding the interventricular pressure

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53
Q

What is the rapid filling phase?

A

During diastole blood flows rapidly into the ventricles from the atria as the venous return of systole causes an increased pressure in the atria which exceeds that of the ventricles.

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54
Q

What does atrial systole acheive?

A

Increases the pressure in the atria above the ventricles to allow more filling of the ventricles.

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55
Q

What closes valves?

A

Turbulence in blood flow/flowing the wrong way cause valves to shut forcibly.

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56
Q

Define isovolumetric contraction.

A

Contraction of the muscle causing no change in the volume of blood in the heart

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57
Q

What causes the atrial/pulmonary valves to open and when does this occur?

A

When the ventricular pressure exceeds the arterial pressure during ventricular contraction.

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58
Q

What is the rapid ejection period?

A

Blood moves out of the ventricles and into the arteries causing an increase in pressure to their maximums.

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59
Q

What is the first heart sound and what causes it?

A

As the AV valve closes oscillations are induced in other structures. This produces a mixed sound with a crescendo-descendo sound quality - lub

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60
Q

What is the second heart sound and what causes it?

A

The semi-lunar valves close and induce oscillations in other structures. This produces a shorter durateion, higher frequency and lower intensity sound than the first.

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61
Q

What is a murmur?

A

Extra sounds produced by the heart showing the presence of turbulent blood flow through a narrowed valve or back flow

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62
Q

When might a murmur be heard in a healthy individual?

A

During exercise

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63
Q

When might a 3rd heart sound be heard?

A

Early diastole

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64
Q

When might a 4th heart sound be heard?

A

associated with atrial systole

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65
Q

What is a ganglion?

A

A cell body in the PNS

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66
Q

What do neurones act on?

A

Smooth muscle

Viscera

Secretory Glands

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67
Q

What type of neurones are in the parasympathetic nervous system?

A

cholinergic

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68
Q

What is vascular tone and what effect does it have in the CVS?

A

The degree of constriction experienced by a blood vessel. It is a mechanism for controlling the total peripheral resistance

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69
Q

How is sympathetic outflow to bood vessels controlled?

A

From the brainstem, via vasomotor centres in the medulla oblongata which receive information from baroreceptors which are located in the arch of the aorta and carotid sinuses

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70
Q

What type of receptors are expressed in pre ganglionic neurones of the sympathetic nervous system?

A

Nicotinic

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71
Q

What effect does the sympathetic and parasympathetic activity have on the heart rate?

A

Sympatheitc speeds it up

Parasympathetic slows it down

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72
Q

What type of neurones are the post ganglion neurones of the sympathetic nervous system and what type of receptors are expressed?

A

noradrenergic. Two classes of receptors expressed adrenoreceptors alpha (1&2) and beta (1&2)

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73
Q

What is the heart rate if all autonomic inputs are blocked?

A

approx. 100bpm

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74
Q

Does the parasympathetic or sympathetic dominate at rest?

A

parasympathetic - reduces the heart rate to 60bpm

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75
Q

How is an increase in heart rate acheived?

A

Initially by a reduction in parasympathetic outflow and then an increase in sympathetic outflow

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76
Q

Where do sympathetic nerves synapse in the paravertebral chain?

A

At the same level as origin

At different level to the origin

May not synapse in the paravertebral chain

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77
Q

What type of outflow does the sympathetic nervous system have?

A

Thoraco-lumbar

Has cell bodies in all 12 thoracic sections and the first 2 lumbar sections

Short pre, long post

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78
Q

What type of outflow has the parasympathetic nervous system?

A

Cranio-sacral outflow

Long pre, short post

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79
Q

What type of receptors are in the parrasympathetic nervous system?

A

Nicotinic pre

Muscarinic GPCR post

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80
Q

What branch of the nervous system inervates the smooth muscle of the vessel walls?

A

sympathetic branch of the autonomic nervous system causing constriction of the arterioles, vasoconstriction, via alpha 1 adrenorecpetors

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81
Q

What is vasomotor tone?

A

Constant level of nervous stimulation in muscle and blood vessels that gives it a resting level of constrction

Also a method of controlling the total peripheral resistance

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82
Q

Where is vasomotor tone high?

A

Skin

Skeletal muscle at rest

Gut unless a meal is consumed

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83
Q

Where is sympathetic outflow to the blood vessels controlled?

A

Vasomotor centres of the medula oblongata in the brainstem

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84
Q

Where are the Baroreceptors and what do they do?

A

In the aortic arch of the carotid sinus. Sends information to the medulla oblongata which controls sympathetic and parasympathetic outflow

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85
Q

Define flow

A

The volume of fluid passing a set point in a given time

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86
Q

Define velocity

A

Rate of movement of fluid particles along the tube

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87
Q

What is laminar flow?

A

There is a gradient of velocity from the middle to the edge of the vessel. Velocity is highest in the centre and fluid is stationary at the edge

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88
Q

Describe turbulent flow.

A

Velocity increases and the velocity gradient breaks down as layers of fluid try to move over each other faster than physics will allow. The fluid tumbles over, greatly increasing flow resistance

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89
Q

Define viscosity

A

The extent to which fluid layers resist flowing over each other.

Higher viscosity, slower central flow, lower av velocity

Lower viscosity, smaller difference between central and edge velocity

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90
Q

How does diameter affect flow rate?

A

Mean velocity is proportional to the cross sectional area of the tube. At a constant gradient, the wider the tube, the faster the middle layers move

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91
Q

Resistance =

A

Pressure/flow

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92
Q

How does resistance change as viscosity changes?

A

Resistance increases as viscocity increases. Thicker the blood, the harder it is to push around blood vessels

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93
Q

How does resistance change as the radius changes?

A

Resistance decreases with the 4th power of the radius. Therefore a small change in the radius makes a big change to resistance. (It is more difficult to puch blood through smaller vessels

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94
Q

If flow is fixed, how does the pressure change as resistance increases?

A

pressure increases from one end of the tube to another

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95
Q

If pressure is fixed, how does flow change as resistance increases?

A

The higher the resistance, the lower the flow

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96
Q

How will putting 2 resistances in series effect total resitance?

A

Add them together

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97
Q

How is the total resistance calculated when 2 resistances are combined in parallel?

A

Re= R1xR2/R1+R2

Effective resistance is lower

The resistance of one of the vessels in series is half of the original, as the blood has 2 paths

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98
Q

What are the high resistance vessels and what happens to pressure in them?

A

Arterioles. Large pressure drop

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99
Q

How does the pressure in the arterioles affect the resistance in the arteries?

A

Increased pressure in the arteries - difficult to push blood through.

Higher resistance in the arterioles, higher pressure in the arteries for set flow

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100
Q

What is transmural pressure?

A

Pressure in a cardiac chamber or blood vessel

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101
Q

How do distensible vessels cause an increase in flow?

A

Vessel stretches, lumen diameter increases, so resistance falls and flow increases

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102
Q

WHy does blood flow cease in distensible vessels before driving pressure reaches 0?

A

Walls collapse as pressure falls

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103
Q

What is capacitance?

A

Ability to store blood

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104
Q

How does distensibilty of a blood vessel increase capacitance?

A

It causes a higher transient flow into the vessel than out

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105
Q

What is systolic pressure?

A

Maximum arterial pressure typically 120 mmHg

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106
Q

What effects systolic pressure?

A

How hard the heart pumps

Total peripheral resistance

Compliance of the arteries

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107
Q

What is diastolic pressure?

A

Minimum arterial pressure. Typically 80mmHg

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108
Q

What affects diastolic pressure?

A

Systolic pressure

Total peripheral resistance

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109
Q

What is pulse pressure?

A

The difference between systolic and diastolic pressure

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110
Q

How is the average pulse pressure determined?

A

Diastolic + 1/3 pulse pressure

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111
Q

Defince total peripheral resistance

A

The sum of the resistance of all peripheral vasculature in the systemic circulation

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112
Q

Why is distensibility of arterial walls important?

A

Allows them to stretch in systole. More blood flows in than out so pressure does not rise too much. The arteries recoil in diastole and flow continues through the arterioles

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113
Q

Describe a pulse wave and where they can be found

A

Contraction of the ventricles generates a pulse wave, which propagates along the arteries faster than blood. This is felt at a variety of locations where arteries can be pushed against a reasonably hard surface

114
Q

How do arterioles effect flow?

A

Variable flow consriction. Smooth muscle contracts to narrow lumen, reducing flow

115
Q

What antagonises vasomotor tone?

A

Vasodilator factors

116
Q

List 3 vasodilator metabolites

A

K+

H+

Adenosine

117
Q

What do vasodilator metabolites do?

A

Cause the relaxation of local smooth muscle, lowering resistance and increasing blood flow

118
Q

Why is blood flow so high when it is restored after it is cut off for a minute or two?

A

Organ or limb continues metabolising and vasodilator is still produced during the period of no circulation but there is no blood flow to remove them. When circulation is restored, the local arterioles dilate maximally and blood flow is very high

119
Q

Describe autoregulation

A

At most levels of metabolic activity, most organs can automatically take the blood flow they need, as long as the pressure in the arteries supplying them is kept within a certain range

120
Q

Define central venous pressure

A

The pressure in the great veins supplying the heart

121
Q

Define venous return

A

The rate of flow of blood back to the heart. Limits cardiac output

122
Q

What happens to arterial and venous pressure if TPR falls?

A

Arterial pressure will fall, venous pressure will rise

123
Q

What happens to arterial and venous pressure if TPR rises?

A

Arterial pressure rises, venous pressure falls

124
Q

What happens to arterial and venous pressure if CO falls at a given TPR?

A

Atrial pressure falls, venous pressure rises.

125
Q

What happens to venous and arterial pressure if CO rises at a given TPR?

A

arterial pressure rises, venous pressure falls

126
Q

The cardiovascular system is demand led and stable. Explain this.

A

TPR changes in response to metabolic demand, altering arterial and venous pressure

127
Q

Define end diastolic volume.

A

Volume of blood in the ventricle at the end of diastole

128
Q

Define end systolic volume.

A

Volume of blood in the ventricle at the end of systole

129
Q

Define stroke volume

A

difference between end systolic and diastolic volume

130
Q

What are the ventricles connected to in diastole?

A

atria

131
Q

What does the filling of the ventricles depend on?

A

Ventricular pressure. They fill until the walls stetch and there is enough blood in the ventricle to equal venous pressure

132
Q

What is the curve showing the relationship between venous pressure and end diastolic volume?

A

The starling curve

133
Q

Define pre load

A

The end diastolic stretch of the myocardium

134
Q

Define after load

A

Force needed to expel blood into the arteries

135
Q

How does end diastolic volume affect the force fo contraction?

A

The more the heart fills, the harder it contracts. The harder it contracts, the larger the stroke volume (starlings law). But there is a limit - when the heart becomes overfilled and the myocardium is overstretched

136
Q

What does the gradient of a curve showing venous pressure against stroke volume show?

A

Contractility - the stroke volume you get for a given venous return

137
Q

What do baroreceptors sense?

A

arterial pressure

138
Q

How does venous return affect cardiac output?

A

Increase venous pressure (return) increase cardiac output

139
Q

How does arterial pressure affect cardiac output?

A

Increase in arterial pressure causes a decrease in cardiac output

140
Q

How does the cardiovascular system respond to eating a meal?

A

Increased gut activity causes metabolites and vasodilator to be released -> TPR falls -> arterial pressure falls, venous pressure rises -> increased cardiac output and heart rate ->Increased output increases atrial pressure and reduces venous pressure - demand met adn system stable

141
Q

What are the risks of increased venous pressure due to exercise?

A

Pulmonary odema.

Venous pressure rises too much and pushes starlings curve into the flat part. The left herat cannot

142
Q

How is the risk of pulmonary oedema reduced during exercise?

A
  • Overfilling of the ventricles is inhibited by the increase in heart rate
  • When venous pressure starts to rise, heart rate is already high
  • Stroke volume kept down but CO increased
    *
143
Q

What happens to blood in the leg on standing?

A
  • Pools in the superficial veins of the legs due to gravity
  • Central venous pressure and arterial pressure fall
  • Cardiac output falls (starlings law)
  • Baroreceptors detect fall in arterial pressure
  • HR raised
  • TPR inreased to defend arterial pressure
144
Q

What is postural hypotension?

A

Reduction in systolic blood pressure on standing of 20mmHg. The barroreceptor reflex does not work efficiently

145
Q

How does the cardiovascular system initially respond to haemorrhage?

A

Reduced volume lowers venous pressure so cardiac output falls.

Arterial pressure falls and baroreceptors detect this

146
Q

How does the CVS initial reaction to haemorrhage cause further probems?

A

Increasing the heart rate will further lower venous pressure

147
Q

How can a haemorrhage problem be soved?

A

Venous pressure needs to be increased to reduce the original problem.

Veno-constriction

Blood transfusion to replace lost blood

148
Q

What organ controls blood volume?

A

kidneys

149
Q

What happens if BP rises for a few days?

A
  • Venous pressure rises
  • CO increases
  • Arterial pressure rises
  • More blood peruses tissues which autoregulate and increase TPR
150
Q

What is the cardiac resting membrane potential and how is it achieved?

A

The potential inside a cardiac cell relative to the outside. Acheived by the selective permeability of the membrane by way of channel proteins. Mostly K+ moves out so resting value approx -90mV

151
Q
A
152
Q

How is initial depolarisation of the ventricular cells acheived?

A

Spread of electrical activity from the pacemaker cells

153
Q

What happens in the ventricular cells once threshold is reached?

A

fast voltage gated sodium channels are opened causing depolarisation towards Na’s equilibrium potential followed by repolarisation - outward flow of K

154
Q

What does the depolarisation by Na cause?

A

Voltage gated Ca channels open (take longer to activate) and cause contraction

250ms later Ca channels close and K efflux returns

155
Q

Why is the maximum -ve voltage of the pacemaker less than that of the ventricular muscle?

A

Fast Na channels remain inactivated

156
Q

How is the spontaneous gradual depolarisation of pacemaker cells carried?

A

Carried by Na ions through slow Na channels that open during the repolarisation of the cell as it reaches it’s most negative value

157
Q

What happens to the pacemaker cells once they have reached their threshold voltage?

A

Ca channels open giving a relatively slow depolarisation

158
Q

What does the size of the interval between beats depend on?

A

How fast the pacemaker potential repolarises.

Shortened by the action of the Sympathetic nervous system on the SAN and shortened by parasympathetic activity.

Noradrenaline speeds up the heart rate by making the pacemaker potential steeper

Acetylcholine slows the heart rate by making the potential shallower

Stretch sensitive baroreceptors

159
Q

How might arrhythmias arise?

A

Ectopic pacemaker activity

After - Depolarisation

Re-entry loop

160
Q

What is ectopic pacemaker activity?

A

Depolarisation and spontaneous activity causes damage to the myocardium

Latent pacemaker regioni activated due to ischaemia

Dominates over SAN

161
Q

What is After-depolarisation?

A

Abnormal depolarisations following the action potential

162
Q

What is a re-entry loop?

A

Conduction delay

Normal spread of excitation disrupted due to damaged area

Incomplete conduction damage (uni-directional block)

163
Q

What are the 4 basic classes of arrhythmia drugs?

A

I. Drugs that block voltage gated sodium channels

II. Antagonists of beta adrenoreceptors

III. Drugs that block K channels

IV. Drugs that block Ca channels

164
Q

Give an example of a class I arrythimic drug and explain how they work

A

Local annaesthetic lidocaine

Blocks open or active channels and dissociates rapidly in time for the next AP

Normal firing not blocked but but prevents AP’s too close to one another

165
Q

Give an example of a class II drug and explain how they work

A

Propanolol Atenolol

Block sympathetic action by blocking Beta 1 receptors in the heart, decreasing the slope of the pacemaker potential in the SAN. Inhibits adenyl cyclase decreasing inotropy

166
Q

When are class II anti-arrythmic drugs commonly used?

A

After an MI to combat increases in sympathetic activity and reduce the O2 demand of the myocardium

167
Q

How do class III anti-arrythmic drugs work?

A

Prolongs the action potential by blocking K channels, responsible for repolarisation. ARP is lengthened preventing another AP occuring too soon

Not generally used as they can also be pro-arrhythmic

168
Q

Give an example of a class IV anti-arrythmic drug and explain how they work.

A

Verapamil

Decreases slope of pacemaker action potential at SAN

Also decreases AV nodal conduction and decreases the force of contraction.

Some coronary and vasodilation

169
Q

How is adenosine anti-arrythmic?

A

Produceendogenously and acts on the A1 receptors at teh AV node. Enhances K conductance and hyperpolarises cells of conduction tissue

Resets the heart

170
Q

What is an inotropic drug?

A

A drug which affects the force of contraction of the heart

171
Q

When are negative inotropic drugs used?

A

Circumstances where it is beneficial to reduce workload of the heart eg after MI

172
Q

When are positive inotropic drugs used?

A

When the herat needs to beat more strongly eg cardiogenic shock or acute but reversible heart failure.

Beta adrenoreceptor agonist

173
Q

How are drugs used in heart failure?

A

ACE inhibitors - prevent formation of vasoconstrctor angiotensin II causing vasodilation of arterioles and venous dilation - decrease afterload and preload

Also have diuretic action - angiotensin II ususally promotes aldosterone release from zona glomerulosa which causes Na and water retention, increasing blood volume. Therefore with ACE inhibitors, the opposite occurs

174
Q

Explain angina

A

O2 supply to the heart does not meet its need. Ischameia of the heart leads to chest pain, usually on exertion and relieved by rest. Due to narrowing of the coronary arteries (Atheromatous disease)

175
Q

How is angina treated?

A

Reduce the work load of the heart with Beta blockers, Ca channel blockers* and organic nitrates*

*also improve blood suppy to the heart

176
Q

How do organic nitrates reduce angina?

A

act with thiols in vascular smooth muscle causing NO2 to be released -> reduced to NO which is a powerful vasodilator ->activates Guanylate cyclase, increasing cGMP and lowering intracellular Ca, causing relaxation of vascular smooth muscle

177
Q

What is the primary action to treat angina?

A

Action on the venous system as a venodilator, lowering cenral venous pressure and preload. THe heart fills less thereofre force of contraction is reduced

178
Q

What is the secondary action for treatment angina?

A

Acts on coronary arteries, improving O2 delivery to the ischaemic myocardium

179
Q

Name 2 conditions which increase the risk of thrombus formation

A

Atrial fibrillation

valve disease

180
Q

What is warfarin?

A

anti-thrombotic drug

181
Q

What type of drug is aspirin and when is it used?

A

Anti-platelet drug used following MI or in coronary artery disease when there is an increased risk of MI to reduce the risk of platelet rich arterial clots forming

182
Q

What complications can arise from hypertension?

A

carries the risk of developing cardiovascular disease or stroke

183
Q

What drugs may be used to treat hypertension and how do they work?

A

Act to reduce cardiac output and/or peripheral resistance.

ACE inhibitors

Diuretics

Adrenoreceptor blockers

calcium channel blockers

184
Q

What are the 2 circulations to the lungs?

A

Bronchial circulation - Part of the systemic circulation and meets metabolic needs of the lungs

Pulmonary circulation - Blood supply to alveoli. Required for gas exchange

185
Q

Comment on the pressure and resistance of the pulmonary and systemic circulation

A

Pulmonary - Low pressure and resistance (RA 0-8mmHg, RV 15-30mmHg)

Systemic - Higher (LA 1-10mmHg, LV 100-140mmHg)

186
Q

What are the mean pressures in vasculature of the pulmonary circulation?

A

arteries- 12-15mmHg

capillaries - 9-12mmHg

Veins - 5mmHg

187
Q

How is the low resistance of the pulmonary circulation maintained?

A

Short, wide vessels

Lots of capillareis (many parallel elements)

arterioles have relatively little smooth muscle

188
Q

What adaptations promote efficient gas exchange?

A

High density of capillaries in the alveolar walls

Short diffusion distance

Therefore high O2 and CO2 transport capacity

189
Q

What is the optimum V/Q ratio?

A

0.8

190
Q

What is the Ventilation-Perfusion ratio?

A

For efficient oxidation, need to match ventilation and perfusion of alveoli. Maintaining this means diverting blood from alveoli which are not well ventilated

191
Q

How is optimal V/Q maintained?

A

Hypoxic pulmonary vasoconstriction - regulating vascular tone. Results in vasoconstriction.

Poorly ventilated alveoli are less well perfused

192
Q

How does chronic hypoxia occur?

A

Chronic increase in vascular resistance - chronic pulmonary hypertension

Higher afterload on RV - can lead to right ventricular heart failure

At altitude or as a consequence of lung disease eg. emphysema

193
Q

When is hydrostatic pressure greatest in the lower lung?

A

In upright position (orthostasis)

194
Q

How does exercise influence the pulmonary blood flow?

A

Increased cardiac output

Small increase in pulmonary arterial pressure

Opens apical capillaries

Increased O2 uptake by lungs

As blood flow increases, capillary transit time is reduced (approx 1 sesc at rest, can fall to 0.3 without compromising gas exchange

195
Q

What forces determine fluid formation?

A

Starling forces

Hydrostatic pressure of blood within the capillary (pushes fluid out of the capillary)

Oncotic pressure - pressure exerted by large molecules such as plasma proteins (draws fluid intot he capillary)

196
Q

How is the formation of lung lymph minimised?

A

Low capillary pressure

197
Q

What does increased capillary pressure cause/

A

More fluid filters out -> oedema

filtration > reabsorption

198
Q

What effects does pulmonary oedema have and how is it treated?

A

impairs gas exchange - affected by posture, mainly at base when upright, throughout lung when lying down

Use diuretics to relieve symptoms and treat underlying cause

199
Q

What % of the cardiac output supplies the brain?

A

15% (although only acounts for 2% of body mass)

20% of total body O2 consumption by brain grey matter

Must be a secure supply

200
Q

How does the cerebral circulation meet the high demand for O2?

A

High capillary density

High bassal flow rate (x10 of av body)

High o2 extraction (35% above av)

201
Q

Why is constant and stable O2 supply to the brain vital?

A

Neurones are very sensitive to hypoxia

Loss of consciousness after a ffew seconds of cerebral ischaemia

Begin to get irreversible damage to neurones in approx 4 mins

Interuption to blood suppy causes neuronal death

202
Q

How is a secure blood supply ensured?

A

Structurally - anastomoses between basilar and internal carotid arteries

Functionally - brainstem regulates other circulations, myogenic autoregulation maintains perfusion during hypotension, metabolic factors control bloodfow

203
Q

How is myogenic autoregulation acheived?

A

Cerebral resistance vessels have well developed myogenic response, responds to changes in transmural pressure

Maintains cerebral blood flow when BP changes

Fails below 50mmHg

204
Q

What does panic hyperventilationi cause?

A

hypocapnia nad cerebral vasoconstriction leading to dizziness or fainting

205
Q

What is cushings reflex?

A

Rigid cranium protects the brain but does not allow for volume expansion

Increase in intracranial pressure impairs cerebral blood flow (tumour/haemorrhage)

Impaired blood flow to vasomotor control regions of the brainstem increases sympathetic vasomotor activity (increase arterial BP and helps maintain cerebral blood flow)

206
Q

What type of molecules readily diffuse across the blood brain barrier?

A

Lipid soluble molecules eg O2 and CO2

Lipid insoluble solutes such as K and catecholamines can’t diffuse freely

207
Q

How is the high required basal rate of O2 facilitated?

A

High capillary density

Diffusion distance <9micro-m

Continuous production of NO by coronary endothelium maintains a high basal flow

208
Q

Describe the realtionship between required O2 and blood flow.

A

Linear until very high O2 demand

Vasodilation due to metabolic hyperaemia

209
Q

What type of arteries are coronary arteries and how does this affect them?

A

Functional end arteries:

Few aterio-arterial anastomoses

Prone to atheroma

Narrowed coronary arteries leads to angina on exercise

Sudden obstruction by thrombus causes myocardial infarction

210
Q

How does exercise effect blood flow to skeletal muscle?

A

Must increase O2 and nutrient delivery and remove metabolites during exercise - increased vasodilation and blood flow to muscle

211
Q

What role does skeletal muscle have in blood pressure?

A

Important in helping regulate arterial blood pressure - 40% of adult body mass is muscle

212
Q

Describe the features of the skeletal muscle circulation

A

Capillary density is dependent on muscle type - postural muscle has higher density

Very high vascular tone - permits lots of dilation, flow can increase >x20 in active muscle

At rest only about half of capillaries are perfused at any one time

213
Q

What effect does the opening of capillaries have on the skeletal system?

A

Increase blood flow and reduces diffusion distance

214
Q

Name some vasodilators

A

Potassium

Increasing osmolarity

Inorganic phosphates

Adenosine

Hydrogen ions

Adrenaline

215
Q

How does Adrenaline act as a vasodilator at arterioles in skeletal muscle?

A

Acts through Beta 2 receptors

Vasoconstriction by noradrenaline acting on Alpha 1 receptors

216
Q

What role does the cutaneous circulation have in the body?

A

Temperature regulation - core temp usually maintained around 37 degrees. Balance between heat production and loss. Skin is the main heat dissipating surface and this is regulated by cutaneous blood flow

Role in blood pressure maintainance

217
Q

What are artereovenous anastomoses (AVAs)?

A

communication between an artery and vein by collaterol channels

218
Q

How do AVAs in the skin affect heat loss from apical skin?

A

Apical skin have a high surface area to volume ratio

AVAs are under neural control not local metabolites

Decrease in core temp increases sympathetic tone in AVAs - decrease blood flow to apical skin

Increased core temp opens AVAs…

219
Q

How do AVAs prevent blood entering capillaries?

A

Low resistance shunt to venous plexus

220
Q
A
221
Q

What is the primary cause of Heart Failure?

A

Ischaemic Heart Disease

222
Q

List a few other causes of Heart Failure.

A

Hypertension

Dilated Cardiomyopathy

Valvular heart disease/congenital

Restrictive cardiomyopathy

Pericardal disease

High-output Heart Failure

Arrythmias

223
Q

What is Class I Heart Failure?

A

No symptomatic limitatino of physical activity

224
Q

What is class II HF?

A

Slight limitation of physical activity

Ordinary physical activity results in symptoms

No symptoms at rest

225
Q

What is class III HF?

A

Marked limitation of physical activity

Less than ordinary physical activity results in symptoms

Mo symptoms at rest

226
Q

What is class IV heart failure?

A

Inabilityto carry out any physical activity without symptoms

May have symptoms at rest

Discomfort increases with any degree of physical activity

227
Q

What is the cardiac output?

A

5l/min

228
Q

What is the average stroke volume?

A

75 ml/beat

229
Q

What factors effects cardiac output?

A

Heart rate

Venous capacity (LV preload)

Aortic and peripheral impedance (after load)

Myocardial contractility

230
Q

What is starlings law?

A

The force developed in a muscle fibre depends on the degree to which the fibre is stretched

231
Q

What happens in systolic dysfunction?

A

Increased LV capacity

REduced LV cardiac output

Thinning of the myocardial wall - fibrosis and necrosis of themyocardium, activity of matrix proteinases

Mitral valve incompetence

Neuro-hormonal activation

Cardiac arrhythmias

232
Q

What are the structural changes of the heart in systolic dysfunction?

A

Loss of muscle

Uncoordinated or abnormal myocardial contraction

Changes to ECM - increased collagen (III>I), slippage of myocardial fibre orientation

Change of cellular structure and function

233
Q

What are the long term deleterious effects of the Sympathetic nervous system?

A

Beta adrenergic receptors are down regulated/uncoupled

Noradrenaline induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha receptors. Induces up regulationi of the RAAS

Reduction in heart rate variability (reduced paraSNS, increased SNS)

234
Q

WHat happens to the RAAS in HF?

A

Commonly activated reducing renal blood flow and SNS induction of renin from macula densa

Elevated Angiotensin II:

  • Potent vasoconstrictor
  • Promotes aldosterone release
  • Promotes NA/H2O retention
  • Stimulates thirst by central action
235
Q

What do Natriuretic Hormones do?

A

Cause Atrial stretch:

  • Predominant renal action - constricts afferent and vasodilates efferent arterioles
  • Decreases Na reabsorption in the collecting duct
  • Inhibits secretion of renin and aldosterone
  • Systemic arterial adn venous vasodilation

Balance the effects of the RAAS on vascular tone and Na/H2O balance

236
Q
A
237
Q

What are common causes of chest pain from the heart and great vessels?

A

Myocardium- Angina, MI

Pericardium- Pericarditis

Aorta- Aortic dissection

238
Q

What are common causes of chest pain from the lungs and Pleura?

A

Pulmonary embolism

Spontaneous Pneumothorax

Pneumonia

239
Q

How do you determine what system chest pain is related to?

A

Circulatory- Central pain

Respiratory- Lateral chest pain, on inspiration, associated respiratory symptoms

GI- Often also epigastric pain

Chest wall- Often localised pain, movements may inc pain, history of trauma/use

240
Q

What are common causes of chest pain due to GI problems?

A

Oesophagus- Gastro oesophageal reflux disease (GORD)

Peptic ulcer disease

GB- Biliary colic, cholecystitis

241
Q

What are common causes of chest pain due to problems in the chest wall?

A

Ribs- fractures, bone metastases

Costo-chondral joints

Muscles

Skin

242
Q

Describe coronary blood flow.

A

in systole small intramuscular vessels are compressedby forces generated in the cardiac muscle; coronary flow through LV muscle decreases to a minimum

Coronary flow occurs during diastole when the heart muscle is relaxed

Shortening of diastole (rapid heart rates) reduces time for this flow

243
Q

What area of the heart is most vulnerable to ischaemia and why?

A

Subendocardial area. Heart muscle is perfused from the epicardial surface to endocardial surface. Myocardial wall pressure is greatest in the sub-endothelial area which is closest to LV cavity

244
Q

Describe the collaterals in the myocardium

A

No collateral vessels between major arteries on the epicardial surface

Collateral vessels present between smaller arteries and arterioles

Expansion of existing collaterals and development of new ones occur whenischaemic but takes time

245
Q

When does ischaemia occur?

A

When supply of oxygen cannot meet demand

Atheromatous Coronary artery disease is the most common cause

246
Q

What are the modifiable risk factors for IHD?

A

Important 4:

Hyperlipidaemia

Cigarette smoking

Hypertension

Diabetes mellitus - doubles risk

Also:

Lack of exercise, obesity, stress, age , gender, family history etc…

247
Q

What is the structure of an atheromatous plaque?

A

Necrotic centre

Fibrous cap

248
Q

How does coronary atheroma occur?

A

Fibrous cap of plaque can undergo erosion or fissuring

Exposes blood to thrombogenic material in the necrotic core

Platelet clot followed by fibrin thrombus

249
Q

What are the clinical syndromes of IHD?

A

Chronic stable angina

Acute coronary syndrome

250
Q

What is chronic stable angina?

A

Stable plaque therefore coronary artery narrowing

Moderate reduction in flow

Blood flow sufficient to meet needs at rest

Ischaemia only whenoxygen demand increases

Relieved when demand ceases

Angina reproducible with the same amount of exertion

251
Q

What is acute coronary syndrome?

A

Plaque fissure with thrombus formation at the site

acute, severe reduction in blood flow

252
Q

What is STEMI?

A

ST elevation MI

90% of cases have total occlusion of coronary artery

extensive ischaemic injury involving full thickness of myocardium

K leak from injured sub epicardial myocytes causes depolarisation. Manifested as ST elevation

Proved benefit from emergency re-opening artery by PCI or Thrombolysis by Fibrinolytic drug

253
Q

What is the difference between partial occlusion and total occlusion STEMI?

A

Only more vulnerable subendocardial areas are affected in partial.

K leak in partial causes depolarisation of subendocardial cells, manifested as ST depression. K leak in total occlusion causes K leak from subepicardial myocytes and the depolarisation is manifested as sST segment elevation

254
Q

What is ischaemic chest pain like?

A

Site - sentral, or left sided diffuse pain

Typical pattern of radiation of the pain - arms and shoulders (one or both), neck, jaw, epigastrium, back. May present with isolated pain at these sites without chest pain

‘Tightening’ ‘heavy’ ‘crushing’ ‘constricting’ ‘pressure’

Occasionally burning epigastric pain particularly in inferior MI

255
Q

What is chest pain in angina like?

A

Brief episodes of ischaemic pain brought on by exertion/emotion and relieved by rest or nitrates within about 5 mins

Pain is often predictable ie reproducible

256
Q

How is a diagnosis of stable angina made?

A

Clinical diagnosis based on history

Examination: no specific signs. Look for signs of related risk factors, LV dysfunction, evidence of atheroma elsewhere

Resting ECG usually normal

Exercise ECG stress test - positive if ECG shows ST depressions >=1mm (horizontal/down sloping). Strongly positive test indicates stenosis

257
Q

How is stable angina treated?

A

Nitrates decrease preload by venodilation, Cal CB decreases afterload by peripheral vasodilation, ACEI decreaes afterload. This reduces wall tension

Beta blockers decrease heart rate and contractility

Aspirin decreases platelet aggregation, hence decreasing thrombus formation if plaques disrupted

Statins decrease LDL cholesterol, decreasing progression of atherosclerosis, increasing plaque stability

Revascularisation mechanically restores blood flow

Sub lingual nitrate spray/tablet

258
Q

When is angiography used?

A

To study coronary artery anatomy when revascularisation is planned

259
Q

What are the 2 main types of revascularisation?

A

Percutaneous Coronary intervention (PCI)

Coronary artery bypass (CABG)

260
Q

When is CABG used?

A

Internal mammary artery (internal thoracic artery) grafts

Radial artry grafts

Saphenous vein grafts (using reverse segment of vein

261
Q

How does acute coronary syndrome present?

A

Recurrent chest pain

Occuring frequently and with little or no exertion and with episodes often lasting longer than 15 mins is suggestive.

Priority is to differentiate into STEMI/NSTEMI becasue the treatment is different

262
Q

What are the symptoms of an MI?

A

Ischaemic chest pain

Severe pain, patient distressed

Persistant pain

Pain at rest, often no precipitant (50%)

Not relieved by rest/nitrate spray

Autonomic features - Sweating, pallor

Nausea, vomitting

Breathlessness (due to LV dysfunction)

Faint

263
Q

What are the symptoms of unstable angina?

A

Acute worsening of stable angina - more frequent, severe, longer duration

Angina at rest

Recent onset of new effort limiting angina

Presence of risk factors

264
Q

What is looked for in an examination for MI?

A

Patient anxious, distressed

Sweating, pallor

Cold, clammy skin

Tachycardia/arrhythmias +/-

Low BP +/-

Signs of heart failure

Crackles in lung bases (LVF)

265
Q

What initial investigations are carried out for ACS?

A

ECG

Cardiac Biomarkers

266
Q

What is the difference in ECGs of STEMI and NSTEMI?

A

STEMI: ST elevationin>=2 leads facing same area 1mm limb leads, 2mm chest leads

NSTEMI: ST segment depression, T wave inversion or no ECG change

267
Q

Why is cardiac troponin I (cTnI) and T (cTnT) used as a biochemical marker of myocyte damage?

A

It is a protein important in actin/myosin interaction which is released in myocyte death

Very sensitive and specific marker

Rise 3-4 hours after onset of pain

Peak at 18-36 hrs

Decline slowly upto 10-14 days

268
Q

What is CK and why can it be used as a biochemical marker?

A

Enzyme present in skeletal muscle, heart and brain

3 iso enzymes

CK-MB is the cardiac iso enzyme

rise 3-8 hrs after onset

Peak at 24hrs

Back to normal 48-72 hrs

269
Q

What is the treatment of STEMI?

A

Anti platelet agents

Reperfusion

Anti ischaemic therapy

ACEI esp if LV dysfunction

Statins

Revscularisation

270
Q

What is the treatment of unstable angina?

A

Anti thrombotic therapy - anti platlet agents, antic coagulants

Restore perfusion of partially occluded vessel(s)

Risk stratification

General measures - Pain control, O2

Anti ischaemic therapy - IV nitrates, Beta blockers

Statins, ACEI

271
Q

What is the long term treatment of an MI?

A

Aspirin

Beta Blocker

ACEI

Statin

Manage risk factors

272
Q

What are some complications of MI?

A

Sudden cardiac death

Arrhythmias

Heart block

Ventricular tachycardia/Ventricular fibrillation

Atrial fibrillation

Heart failure

Cardiogenic shock

273
Q

What causes pericarditis?

A

Infections- viral

Post MI/cardiac surgery

Autoimmune

Ureamia

Malignant deposits

274
Q

What are the symptoms of pericarditis?

A

Central/left sided chest pain

Sharp, worse with inspiration

Improved by leaning forward

275
Q

What is looked for on examination for pericarditis?

A

Pericardial rub

Signs of pericardial effusion

276
Q

What investigations would you undergo to diagnose pericarditis?

A

ECG - ST elevation with upward concavity, in all the leads

Echocardiogram - diagnosis of pericardial effusion

277
Q

How do you treat pericarditis?

A

Treat cause

If effusion causing tamponade - pericardiocentesis

278
Q

What can cause tearing of the aorta?

A

Hypertension

Trauma

Iatrogenic - cardiac catheterisation

Inherited defects of collagen

Age

279
Q

What are the symptoms of aortic dissection?

A

Severe tearing type chest pain

Which radiates to the back to between teh shoulder blades

Very abrupt onset

280
Q

What are the signs of an aortic dissection?

A

unequal pulses in the 2 arms

Signs of aortic regurg

Occlusion of aortic branches may cause a variety of complications

281
Q

What are the effects of aortic dissection?

A

Aortic ring dilation - acute aortic regurg = new AR murmur

Obstruction of branches of aorta

Rupture of aorta

Compression - Trachea/oesophagus/SVC

Double-barrelled lumen (if re-enters lumen through another intimal tear)

282
Q

What are the 3 clinical features an acute aortic dissection can generally be identified by?

A

Immediate onset of aortic pain with a tearing and or ripping

Variation inpulse and/or blood pressure between the right and left arm

Mediastinal and/or aortic widening on chest radiograph

Semester 2 - alex (4 decks)

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