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PHSL232 Cardiovascular and Respiratory > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

What pathologies are we covering in this module?

A

Cardiovascular diseases (CVD): hypertension, atherosclerosis, pulmonary hypertension and obesity

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2
Q

What is arterial blood pressure?

A

Arterial blood pressure is defined as the force that is exerted by the blood on the arterial wall.

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3
Q

What is the equation for arterial blood pressure?

A

MAP = DAP + 1/3(SAP-DAP)

Meaning that diastolic BP defines MAP.

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4
Q

Is SAP or DAP greater?

A

SAP is higher than DAP

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5
Q

What is hypertension?

A

High arterial blood pressure at rest

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6
Q

What is a normal MAP?

A

120:80

(meaning systolic pressure is 120mmHg and diastolic pressire is 80mmHg)

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7
Q

What would be the MAP readings for stage 1 and stage 2 hypertension?

A

Stage 1 hypertension would present with 130-139 SAP OR 80-89 DAP (either can be abnormal)

Stage 2 hypertension would present with greater than 140 SAP OR greater than 90 DAP

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8
Q

What is the ratio of people in NZ currently taking medication for high blood pressure?

A

1 in 5 (21.4% of the population)

*possible an underestimate aswell as this does not include those undiagnosed and also not all people diagnosed will currently take medication.

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9
Q

What is Ohm’s law?

A

Ohm’s law is V = I x R which is the basis of the MAP equation being MAP = CO x TPR or MAP = (HR x SV) x TPR.

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10
Q

What is the most important determinant of resistance?

A

vessel diameter (r^4) e..g, a 10% change in diameter would cause a 50% change in vascular resisatance.

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11
Q

What is happening to arterial blood volume during hypertension?

A

Increase

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12
Q

What is happening to arterial compliance during hypertension?

A

Decrease

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13
Q

How is arterial blood pressure regulated long term?

A

By the kidneys RAS system (Renin-Ang system)

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14
Q

What blood vessel has the greatest amount of elastic tissue?

A

Aorta = gives it the characteristic of high compliance.

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15
Q

What is arteriosclerosis?

A

The structural thickening of the vessell wall (media).

Resulting in less elastin and more collagen = reduced complaince and increased stiffness.

This increases resistance and means the vessel has to work harder to expand as blood flows through - as a result the heart pumps harded which raise blood pressure = hypertension.

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16
Q

What is atherosclerosis?

A

Structural change in the intima of the vessel caused by a bloackage of the lumen.

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17
Q

What effect does age have on arterial compliance?

A

Vessels become less complaint (more stiff) with age

This is because there is a reduction of elastin and increase in collagen –> collagen is stiffer than elastin.

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18
Q

How much stiffer is collagen than elastin?

A

x1000 (because collage cross links).

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19
Q

What effect does a decrease in arterial compliance have on peripheral vascular resistance?

A

Elevation of peripheral vascular resistance

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20
Q

What is the effect of an elevation of peripheral vascular resistance on systolic and diastolic pressure?

A

It increases both but it causes a larger increase to suystolic pressure than to diastolic pressure.

*this is because systole is at a higher pressure than diastole (because greater volume)

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21
Q

Are vessels stiffer in systole or diastole?

A

Systole because higher pressure

*arteries beocme less complaint (more stiff) when arterial pressure rises.

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22
Q

What is the name for disease of the media?

A

Arterisosclerosis

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23
Q

Where is arterial blood flowing during systole and diastole?

A

Arterial blood is flowing through the capillaries throughout systole and continues to throughout diastole.

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24
Q

Where is there a storage of stroke volume?

A

in condit vessels (aorta, carotid, iliac, arteries).

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25
Q

What is meant by distensibility of the aorta?

A

Distensibility refers to how easily the aorta can stretch or expand when blood is pumped through it. A healthy aorta is flexible and can stretch to handle the surge of blood from the heart, helping to maintain smooth blood flow and regulate blood pressure. If the aorta loses its distensibility (becomes stiff), it can’t expand as well, which can lead to higher blood pressure and strain on the heart.

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26
Q

What maintains capillary flow during diastole?

A

Recoil of aorta

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27
Q

Define flow wave and pulse/pressure wave:

A

Flow wave refers to the rhythmic change in blood flow during a heart beat - the ejection of blood from the heart which runs through the vasculature.

Pressure/Pulse wave refers to the change in pressure that runs over the vascularture as a result of contraction of the heart.

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28
Q

What type of flow is occuring when blood hits aorta?

A

Pulsatile

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29
Q

What blood vessel has the greatest compliance?

A

Aorta

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30
Q

Where is there the greatest pulstaility in blood flow?

A

Left ventricle

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31
Q

What allows the aorta to dampen the pulstaile flow from the left ventricle so that there is continuous flow in capillaries?

A

Pulsatile flow is dampened by the aorta due to its high compliance (ability to absorb force).

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32
Q

Why does the aorta have a reduced ability to dampen pulsatile flow as we get older and what is the effect of this?

A

Because compliance decreases with age therefore pulse pressure increases causing an increase in workload on the heart and increased BP (hypertenison).

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33
Q

Why do we not want flow to be pulsatile in capillaries?

A

Would reuslt in less efficient for gas exchange (less O2 nutrients exchange).

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34
Q

Is the flow or pulse/pressure wave faster?

A

Pressure wave is faster

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35
Q

Does systole or diastole cause the pressure wave?

A

Systole - the ejection of blood

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36
Q

Where do reflection waves form

A

Points of resistance or branching in the vasculature system e.g., Aortic Bifurcation (the division into two branches).

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37
Q

What is a reflection wave?

A

A pulse wave travels through arterial system - at points where the pulse wave encounters points of resistance or branching part of the wave is relfected back towards the heart.

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38
Q

Are proximal or distal vessels more compliant?

A

Proximal

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39
Q

Does a pressure wave travel faster in stiffer or complaince vessels?

A

Pressure wave travels faster in stiffer distal vessels than in complant proximal vessels

*this means that pressure wave travels faster in the radial artery than aorta

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40
Q

Do stiffer or complaint vessels have a larger contribution to reflections ?

A

Stiffer (therefore hypertension increases reflections)

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41
Q

Does a reflected wave come back to heart earlier or later with hypertension?

A

Hypertension means the vessels are stiffer - reflected waves return to the heart faster in stifffer vessels.

This increases load and subsequently BP.

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42
Q

How do reflected waves result in afterload being increased in hypertension?

A

Reflected wave reach heart before closure of aortic valves increasing systolic blood pressure = increases afterload = more difficult for heart to eject blood into aorta.

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43
Q

What is hypertension?

A

High blood pressure (caused by high arteriole blood volume = more force exerted on the walls of the arteries).

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44
Q

What is the difference between primary and secondary hypertension?

A

Primary hypertension is 95% of cases and has an unknown/idiopathic cause. It is due to the stiffening of arteries which occurs naturally with age.

Secondary hypertenison is 5% of cases and it has a specific cause.

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45
Q

What are the two physical factors that determine BP?

A

Arterial blood volume
Arterial compliance

*not independant of each other.

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46
Q

What are two underlying reasons for hypertension?

A

A problem in the kidney = arteriole vasoconstriction decreasing arterial compliance and increase TPR therefore less blood flow and more salt retention.

Sympathetic activation = Again arterial vasoconstriction decreasing arterial complaince and increasing TPR meaning less blood flow to the kidney and release of vasoactive substances and salt retention resulting in increased blood volume.

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47
Q

What is the role of the sympathetic system in hypertension?

A

Hypertension is a systemic increase in overall sympathetic activity.

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48
Q

How is the sympathetic system effected by exerise?

A

With exercise there is a balanced increased in symapthetic activity

There is an increase in HR and CO. There is differential flow distribution in vessels: vasodilation in some vascular beds to promot oxygen delviery and constriction in otehr vascualr beds. E.g., regulates blood flow dependant on needs - during exercise we want more oxygen to muscles and less to GI.

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49
Q

Overall does TPR increase or decrease with exercise?

A

Decrease

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50
Q

What is the cause of primary hypertension thought to be due to?

A

A decrease in arterial compliance and/or an increase in arterial blood volume

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51
Q

What are the consequences of hypertension?

A

–> Cardiac Remodelling!!

Kidney disease

Development of atherosclerosis (stroke)

Atrial fibrillation

Coronary artery disease/myocardial infarction

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52
Q

What are the types of pathological cardiac remodelling?

A

Hypertension
Dilated cardiomyopathy
Hypertrophic cardiomyopathy

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53
Q

What is the difference between physiological and pathological cardiac remodelling?

A

Physiological is without fibrosis whereas pathological is with fibrosis

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54
Q

What is afterload and what is it caused by?

A

Afterload is the resistance the heart must overcome in order to ejecct blood during systole (contraction) - the higher the afterload the harder it is for the heart to pump blood.

Afterload is determined by resistance in arteries (because to eject blood requires pushing it into the arteries).

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55
Q

What is the consequence of increased afterload?

A

Remodelling at cellular and organ level

= hypertrophy of the heart muscle (thickening of the ventricular walls), as the heart adapts to pump against higher pressure.

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56
Q

What is hypertrophy?

A

Increase in muscle size

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57
Q

Explain hypertrophy of cardiomyocytes:

A

It is an increase in the number of sarcomeres of the cardiomyocytes wither in series or parallel

NOT an increase in the number of cardiomyocytes themselves or the size of the sarcomeres.

*A sarcomere is a fixed unit.

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58
Q

What is a sarcomere?

A

Once contractile unit in a muscle fibre

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59
Q

How does hypertrophy trigger fibrosis?

A

In short: because there is an increased formation of extracellular matrix.

Explaination: as cardiomyocyte size increase the surrounding ECM adopts to also increase through the increased release of proteins collagen, elastin and fibronectin from fibroblasts. These protein provide structural integrity of a cell. During pathological hypertrophy (continuous stimualtion) there is an imbalnace in the production-degration ratio of ECM leading to too many structural proteins causing fibrosis = stiffness.

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60
Q

What is in the ECM?

A

Collagen (type 1 and 3), elastin, proteoglycans, laminin, fibronectin.

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61
Q

Is there an increase of collagen type 1 or type 3 first in the formation of more ECM?

A

Type 3 followed by type 1

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62
Q

Is pathological remodelling reversible?

A

Generally not - whereas physiologcal remodelling is reversible

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63
Q

Explain LV cardiac remodelling as a result of hypertension:

A

It is a cycle:

An increase in MABP causes the walls of the venticle to thicken (afterload) in order to normalise the increase wall stress. Thicker walls results in an increase in MAP also.

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64
Q

What is compensated hypertrophy?

A

Compensatory cardiac hypertrophy reduces wall stress and oxygen consumption, thereby protecting the heart against acute blood pressure elevation.

But this can lead to cardiac failure

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65
Q

Explain heart failure with perserved ejection fraction:

A

Concentric hypertrophy causes diastolic heart failure. Concentric hypertrophy causes the walls of the heart to thicken making the heart stiffer and reduces its ability to relax and fill during diastole. Although there is less blood filling the hearts ability to contract during systole is not effected and ejection fraction remains normal (EF on basis of volume so not effected).

This leads to diastolic heart failure, also called heart failure with preserved ejection fraction (HFpEF), where the issue is with filling the heart, not contracting/pumping.

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66
Q

Explain heart failure with reduced ejection fraction:

A

Eccentric hypertrophy = causes systolic heart failure.

Eccentric hypertrophy is the enlargement of the heart chambers. The dilation weakens the heart muscle over time, making it harder for the heart to contract and pump blood out effectively during systole. This decreases the ejection fraction leading to systolic heart failure, or heart failure with reduced ejection fraction (HFrEF), where the heart’s contraction (pumping) is the main problem.

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67
Q

Does eccentric or concentric hypertrophy cause an issue with diastole?

A

concentric

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68
Q

What is HFpEF?

A

Heart failure with perserved ejection fraction

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69
Q

What is HFrEF?

A

Heart failure with reserved ejection fraction

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70
Q

Is there RV hypertrophy in early stages of systemic hypertension?

A

No

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71
Q

When is the RV hypertrophied?

A

In the late stage of systemic hypertension

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72
Q

What causes RV remodelling?

A

Pulmonary hypertenion (high pressure in pulmonary system means need stronger conytraction in RV in order to push deoxygenated blood into pulmonary circulation).

PLUS Increase in LV filling pressure translates into pulmonary circulation - so the hypertrophied LV intereacts via septum with the RV = some RV hypertrophy can be caused by LV hypertrophy.

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73
Q

What factors enhance your risk to hypertension?

A

Age, ethnicity, family history.

Smoking, lack of exercise, diet, obesisty, diabetes, stress and medications.

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74
Q

What lifestyle changes can be made to treat hypertension?

A

Weight reduction
Healthy diet
Dietary salt restrictopm
Physcial activity
Moderate alcohol consumption

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75
Q

What is the most effective way to treat hypertension?

A

Lifestyle changes

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76
Q

Why are static (once off) measurements of BP not that effective?

A

Because our BP is variable and to only take a single reading does not give an accurate representation of BP - better to test in dynamuc conditions or repetitively monitor.

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77
Q

What pharmacological treatments are avalible for hypertension?

A

Fluid/diuretics or inotropes that effect SV

Chronotropes that effect HR

Vasoactives that effect TPR

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78
Q

What is an example of a inotrope that can be used to treat hypertenison by effecting on SV?

A

CCB = calcium channel blockers

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79
Q

What is an example of chronotropes that can be used to treat hypertension by acting on HR?

A

BB = b-adrenergic receptor blockers

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80
Q

What do Ang 2 receptor blockers (ARB) and Ang converting enzyme inhibtors (ACE1) do?

A

Treat hypertension by change TPR

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81
Q

How does targeting the sympathetic overdrive treat hypertension?

A

It involves cutting the nerves from the kidneys that communicate to afferent nerves in the brain to prevent signals that increase BP.

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82
Q

What is the difference between Arteriosclerosis and Atherosclerosis?

A

Arteriosclerosis is disease of the media which alters stiffness whereas Atheriosclerosis is disease of the intima which alters conduit.

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83
Q

Hardening of the arteries, narrowing or blocking of the vessel lumen are characteristics of what disease?

A

Atheroschlerosis

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84
Q

What is “atrophy”?

A

The reduction of muscle mass due to loss of smooth muscle cells.

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85
Q

What can atherosclerosis cause in the cerebral arteries?

A

Transient ischemic attack (TIA) or stroke

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86
Q

What can atherosclerosis cause in cornary arteries?

A

cornoary artery disease

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87
Q

What can atherosclerosis cause in the limb arteries?

A

Peripheral artery disease

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88
Q

What can atherosclerosis cause in the renal arteries?

A

Hypertension (high BP) or kidney failure

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89
Q

What is an aneurysm?

A

A ballooning and weakened area in an artery - life threating if it bursts.

90
Q

What are the phases of atherosclerosis?

A

(1) Hypercholesterolemia (more LDL than HCL)
(2) Formation of fatty streak
(3) Formation of plaque
(4) Activation of plaque

91
Q

What are the types of initial “injury” of endothelium that causes atheroscelerosis?

A

Hypercholesterolemia
Hypertension
High triglycerides (FFA)
Inflammation

92
Q

What is Hypercholesterolemia?

A

High amounts to LDL (the bad cholesterol)

93
Q

What are the two types of cholesterol?

A

Low-density lipoprotein (LDL) = “bad” cholesterol

High-density lipoprotein (HDL) = “good” cholesterol

94
Q

What are the relative concentrations of LDL and HCL that we want?

A

We want to have low levels of LDL and high levels of HCL

95
Q

What makes LDL bad and HDL good in relation to atheroscelerosis?

A

LDL sticks to artery walls leading to plaque formation.

HCL carries LDL away from artery walls (therefore prevents plaque formation).

96
Q

How is a fatty streak formed?

A

High LDL (above it’s eliminating capacity) = LDL migrates from the extracellular matrix into the cell.

Inside the cell LDL is oxidized and expressed as leucocyte adhesion molecules which signals chemokine secretion to attract monocytes (immune response). Monocytes enter the intima and are converted into macrophages.

Macrophages internalise oxLDL to form “foam cells”. Foam cells attract even more monocytes and form a fatty streak in the vessel.

97
Q

Where exactly does LDL migrate to in the cell from extracellular matrix?

A

subendotheliula intima

98
Q

What is LDL oxidised by?

A

Radicals

*radicals are molecules that contain at least one unpaired electron.

99
Q

What do monocytes turn into?

A

Macrophages

100
Q

What do foam cells attract?

A

More monocytes
+ they activate T-cell immune response

101
Q

What is the T-cell immune response?

A

Smooth muscle cells migrate from the media into the intima and turn into fibroblast-like repair cells.

Activates the formation of a plaque.

102
Q

How concerning are fatty streaks?

A

Most are not directly clinically significant or have a life threatening risk - in fact most of us probably have some and they just disappear.

Only few progress to atherosclerotic plaques.

103
Q

How is a plaque formed?

A

Smooth muscle cells migrate from media into the intima and turn into fibre-blast like repaire cells.

They synthesise EXM elastin and collagen and develop calcium crystals.

This initiates an inflammatory repsonse and the formation of fibrous cap in order to isolate the stiffened lipid core to prevent blood clotting.

Essentially the formation of plaque is a repair repsonse - however there are possibly more signficiant problems created.

104
Q

What is a “plaque”?

A

Lipid core and fibrous cap

105
Q

When does a plaque become clinically significant?

A

When activated

106
Q

What activates a plaque?

A

When there is a lesion or fissures (cracks) in the endothelium.

107
Q

What is formed when plaque activated?

A

Thrombus = blood clot on the plaque within the artery or vein

108
Q

What is arterial/venous embolism?

A

Interruption of blood flow due to an embolus (free moving thrombus) potentially causing infraction in almost any organ/part of the body.

109
Q

What is infarction?

A

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area.

110
Q

Why is atherosclerosis regarded as a “vascualr repair response”?

A

Because the formation of a fatty streak and plaque is the vessels way to prevent it from loosing its lumen in the event of an injury - it is the vessel trying to repair and localise the harm. But in some situation it moves onto the later stages and causes complications.

111
Q

What vessels does atherosclerosis occur in?

A

Elastic arteries: Aorta, caarotid arteries, iliac arteries
Large-medium sized muscular arteries (coronary + femoral)

*Seldom in small arteries

112
Q

Are the risk factors of artherosclerosis local?

A

No

Artherosclerosis is lcoal but the risk factors are systemic

113
Q

What three things cause artherosclerosis to occur?

A

(1) Abnormalities of blood vessel wall

(2) Abnormalities of blood constituents (coagulation/platelet activation)

(3) Abnormalties of blood flow (shear stress)

114
Q

What is shear stress?

A

The force that results from the friction of flowing blood on the luminal surface.

115
Q

What makes “normal shear stress” good?

A

Normal shear stress is good because it triggers NO production

116
Q

What does shear stress cause the release of?

A

Nitric oxide (NO)

117
Q

Why is the release of NO good?

A

Decreases the expression of inflammatory repsonse mediators, adhesion molecules, vasoconstrictors and oxidants.

*Therefore causes dilation which decreased TPR and BP.

118
Q

Why is low or turbulent shear stress not good?

A

It reduces the NO production

119
Q

What happens as a result of reduced NO production?

A

Enhance monocyte adhesion, platelet actiavtion, SMC proliferation, oxidant activity and vasoconstriction.

120
Q

What areas have higher risk of atherosclerosis?

A

Places with low shear stress and altered flow directions during cardiac cycles e.g., branches, bifurcations.

Therfore places with pulsatile flow such as the elastic arteries (aorta, carotid arteries and iliac arteries) and large-medium sized muscular arteries (coronary and femoral).

121
Q

Is atherosclerosis more like to occur in places with lamianr or turbulent flow?

A

Turbulent flow

122
Q

What makes carotid arteries susceptible to plaque formation?

A

Carotid arteries are particularly susceptible to plaque formation because they have lower BP due to being located above the heart and flow is turbulent due to the forking of the two carotid arteries.

123
Q

What makes coronary arteries susceptible to plaque formation?

A

More turbulent and pulsatile flow due to altered flow directions (branches, bifurcations, stenosis)

124
Q

What vessels have the highest blood pressure from the aorta?

A

Coronary arteries

125
Q

What are the pharmacological treatments for atherosclerosis?

A

Statins
Cholesterol absorption inhibitors
Inclisiran
Bempedoic acid

126
Q

Where do cholesterol absorption inhibitors block absorption of cholesterol?

A

Intestine

127
Q

What is an angiography?

A

Xray taken of blood vessels - vessel injected with contrast dye to be able to view the plaque and reduced lumen size.

128
Q

What is restenosis?

A

Word for where remedy is unsuccessful therefore it is the recurrence of abnormal narrowing of an artery or valve after corrective surgery.

(e.g., unsuccessful angioplasty and stenting).

129
Q

What are the two types of stents that can be used to treat artherosclesis?

A

Ballooning (physically opens up vessel) or drug-eluting (stent directly releases synthetic drugs to dilate the vessel).

130
Q

What is a endarterectomy?

A

Surgery to remove the atheromatous plaque material

131
Q

What is a bypass in relation to artherosclosis?

A

Artificial artery or vein

132
Q

What is aortic aneuyrsm?

A

Aorta dialtion

Aneuyrsm in aorta is almsot certain to burst and cause death but can be repaired with a stent.

133
Q

What is pulmonary hypertension?

A

Pulmonary hypertension is an alteration in the structure and function of the pulomary arteries (arteries between RV and lungs) as a result of high blood pressure.

134
Q

What is the normal BP in pulmonary arteries?

A

10-15mmHg

135
Q

What does BP exceed in pulmonary hypertension?

A

> 25 mmHg

136
Q

What are the symptoms of pulmonary hypertension?

A

Symptoms for pulmonary hypertension are non-specific but can include breathlessness, fatigue and chest pain

137
Q

How do symptoms to PH develop?

A

Gradually - when the disease is very advanced.

138
Q

What is the cause of primary PH?

A

Unknown exact cause

139
Q

What percentages of PH is primary and secondary?

A

primary = 40%
secondary = 60%

140
Q

What are the possible causes of secondary PH?

A

COPD (chronic obstructive pulmonary disease)
Lung condiitons
Mitral valve disease
Sleep apnea
Sickle cell anemia
HIV

141
Q

What causes pulmonary artery remodelling?

A

Increase in pressures - causes an alteration in shear stresses - endothelial dysfunction and proliferation - disturbed vasodilator to vasoconstrictor balance

142
Q

What is meant by a disturbed vasodilator to vasoconstrictor balance?

A

Decrease in nitrix oxide and prostacyclin (vasodilators) and an increase in endothelin and thromboxane (vasoconstrictors).

143
Q

How does PH effect oxygen consumption?

A

Increase in pulmonary artery pressure (PAP) and Increase in pulmonary resistance.

Therefore it is more difficult to pump the blood from the heart to the lungs in the pulomary artery.

Can result in severe bronchial obstruction due to the production of fibrosis or increased mucus production. This thickens the diffusion distances = decreased diffusion capacity for oxygen = hypoexmia (decrease PO2).

144
Q

Is pressure higher in the pulmonary or systemic system?

A

Systemic

145
Q

What percentage of circulating blood does the pulmonary system recieve?

A

100%

146
Q

What is the difference between the pulmonary arterial tree and the systemic arterial tree?

A

In the pulmonary arterial tree compliance and resistance are distributed over the entire system - whereas in the systemic arterial tree 80% of total compliance is located in the aorta but reisstance is distributed over all reistance arteries in all vascular beds.

147
Q

What percentage of total systemic compliance is located in the aorta?

A

80%

148
Q

Does small changes in resistance have larger effects in the systemic or pulmonary system?

A

Pulmonary

149
Q

What is the consequence of PH on cardiac function?

A

Increase in pressure of the pulmonary arteries affects the RV.

Increases RV afterload which decreases SV.

150
Q

What is occuring during compensated RV hypertrophy?

A

Compensated RV hypertrophy is concentric hypertrophy = RV wall thickens to pump blood more effectively, in response to an increase in pulmonary pressure and resistance (PH). During this stage, the heart can still manage to work properly and maintain normal blood flow.

Compensated = heart still coping.

151
Q

What are the two stages of cardiac remodelling that occurs as a result of PH?

A

(1) Compensated RV hypertrophy
(2) Decompensated RV hypertrophy

152
Q

What is occuring during decompensated RV hypertrophy?

A

Decompensated RV hypertrophy occurs when the thickened heart muscle can no longer keep up with the demand (meaning that the limit of RV hypertrophy is reached and therefore can no longer increase strength of muscles to compensate for the continued increase in pulmonary pressure and resistance). The heart starts to struggle and can’t pump blood efficiently anymore.

Decompensated = heart failing to keep up.

153
Q

What results in there being a limit on RV hypertropy?

A

Due to the increase in wall thickness it gets to a point where the difussion distance to center of the cardiomyocytes is too big that it is not receiving oxygen therefore not going to be able to increase anymore.

154
Q

What happens to CO during decompensated RV-hypertrophy?

A

Decreases (resistance and pressure increase cannot be counteracted)

155
Q

In a healthy heart what ventricle is biggest?

A

Left

156
Q

In a heart at the end stage of PH what venticle is the biggest?

A

Right

157
Q

How has the survival rates of PH changed since 1994?

A

In 1994 there was a 100% death rate in 5 years - latest study in 2018 the death rate was 20-50% in 5 years shwoing that treatments have significantly advanced

158
Q

Is loss of alveoli reversible?

A

No - there is no way to regain alveoli’s (smoking kills alveoli’s)

159
Q

Explain why it was partically damaging for Amy Winehouse to smoke?

A

Because she had lung emphysema and COPD causing vasocontriction and reduction in capillary capacity. This increased totoal peripheral pulomary reistance and pulomary artery pressure leading to her developing pulomnary hypertension.

Smoking irrevsibly kills alveoli and therefore futher reduced her CO2 sensitive of regualtion to ventilation.

160
Q

What is PDE5-inhibitor and how does it work?

A

It is a treatment to PH.

PDE5-inhibotrs increase cGMP levels by inhibiting the PDE5 which normally breaks it down.

cGMP relaxes smooth muscle causing vasodilation - therefore enhacned with more cGMP.

161
Q

What is the drug form of PDE5-inhibitor?

A

Sidenafil

*Acts selectively in the lung and reproductive organs (viagra)
*Can oppose high altitude induced pulmonary hypertension

162
Q

What is the most effective treatment for PH?

A

Combination therapy of PDE5i and ERA (endothelin recptor antagonist)

163
Q

What is obesity?

A

An excess accumulation of body fat

164
Q

What is BMI?

A

BMI = Body Mass Index

It is a measure of body fat based on height and weight.

BMI = body weight / body length squared

165
Q

What are the units for BMI?

A

kg/m2

166
Q

What does a BMI less than 18.5 indicate?

A

Underweight

167
Q

What is a normal BMI?

A

18.5 - 24.9

168
Q

A BMI value of what indicates that you are overweight?

A

25.0-29.9

169
Q

What is the BMI value that indicates obesisty and the subsequent subcatergories?

A

A BMI of more than 30.0 indicates obesity.

Obesity 1: 30-34.9
Obesity 2: 35-39.9
Extreme Obesity 3: greater than 40.0

170
Q

Why is BMI a problematic measure of obesity?

A

Because it does not take into account muscle which is heavier than fat.

171
Q

What percentage of NZ adults are overweight or obese?

A

67%

(34% overweight and 33% obese)

Therefore only 32% (one in three) NZ adults are of a “healthy” body weight.

172
Q

How has the obesity statistics in NZ changed in the kast 5-7 years?

A

They haven’t - stats have been stable meaning no increase nor decrease.

173
Q

What is the “metabolic syndrome”?

A

A group of conditions that increase risk of developing cardiovascular disease.

The presense of 3 or more of the conditions means you are in the catergory of metabolci syndrome - includes adiposity, lipid profile, blood pressure and blood glucose levels.

174
Q

What is adiposity?

A

Body fat

175
Q

What are the four key mechanisms that contribute to cardiac dysfunction as a result of obesity?

A

(1) hemodynamic load (cardiac remodelling)

(2) heart fat - conduction system

(3) Adipocytes - adipokines - myocardial fibrosis

(4) microangiopathy - endotherlial dysfunction

176
Q

What are the extrinsic changes that occur to the heart as a result of obesity?

A

Remodelling
Heart fat
Microangiopathy

177
Q

What is the intrinsic change we are focuing on that occurs as a result of obesity?

A

Lipotoxicity

Lipotoxicity is defined as the process where excess accumulation of lipids and over-activation of lipid signaling pathways trigger cellular distress and dysfunction, which may manifest as insulin resistance,

178
Q

What is “hemodynamic load”?

A

Refers to the load of blood that the body demands - in relation to the heart this is deteremined by size.

E.g., if you are. taller you will hvae a bigger heart because there is more tissue to diffuse blood to (greater load than someone smaller).

179
Q

Do obese people have bigger hearts?

A

Yes - because increase mass results in oncrease in overall blood blood in order to perfuse the extra tissue with blood.

Obesity increases CO.

180
Q

How much extra blood flow is required per 100g of body mass?

A

2-3mL/min/100g

181
Q

How does hemodynamic load change as a result of obesity?

A

Increased mass results in increase in preload (more filling of heart) therefore CO is increase. As is HR and SV.

TPR is decreased (as result of volume increase).

182
Q

Does the volume overload as a result of obesity cause eccentric or concentric remodeling of the heart?

A

Eccentric (outward)

183
Q

How is the heart remodelled as a result of obesity (primary and secondary remodelling)?

A

Primary response is LA and LV eccentric hypertrophy (increase in lumen size therefore volume) in order to meet the increase CO demand as a result of larger body mass = volume overload.

Secondary response is LV concentric hypertrophy (increase thickness of the wall) this is because with the increase lumen size in order to maintain blood pressure need stronger contraction = pressure overload.

= tells us that hypertension (increase in BP) goes hand in hand with obesity.

184
Q

What is epicardial fat?

A

The layer of fat surrounding the heart

185
Q

Where is epicardial fat located?

A

Within the pericardium therefore it is actually part of the heart

because it is part of the heart it is supplued with blood and innervated by cardiac nerves.

186
Q

Explain epicardial fat infiltartion:

A

The fat can infiltrate into the myocardiocytes - this lipid accumulation causes toxicity.

187
Q

What does an increases in epicardial fat deposition and infiltration cause/effect?

A

Mechanical impairment
Thermoregulation (higher body core temperature)
Interference with cardiac conduction
Endocrine effects (adipokines, cytokines)

188
Q

What are adipokines/cytokines?

A

Protein produced in and released from adipose tissue

189
Q

How does heart fat effect the conduction system?

A

Adipose produces and releases adipokines/cytokines which cause fatty infiltration in the conduction system - which prolongs the QT interval (V depolarisation to repolarisation)

190
Q

What are examples of adipocytes?

A

Leptin
NEFA
TNF-a
IL-6
C-reactive protein
Angiotensinogen
Adiponectin
ROS

191
Q

What are adipocytes?

A

Primary cells composing adipose tissue - cells contain large fat/lipid droplets which force the nucleus to the cell membrane - adipocytes have an endocrine function by the proudtcion of adipokines.

192
Q

What is different about adiponectin than other adipokines?

A

As adipocyte size increases adiponectin concentration decreases (whereas other adipokines increase in concentration as adipose size increases).

193
Q

Why do adipocytes increase in size with obesity?

A

Because they are storing more lipids (fat)

194
Q

What causes inflammation in obesity?

A

As size of adipocytes increase macrophage immune response is triggered and this causes inflammation of adipocytes

195
Q

What cells do adipokines have effects on?

A

cardiomyocytes
fibroblasts (= increase in ECM and fibrosis)
endothelial cells
smooth muscle cells

196
Q

What is microangiopathy?

A

Changes in microvasculature = changes in small vessels

197
Q

What are perivascular spaces?

A

Fluid-filled spaces that surround small arterioles, capillaries and venules in the brain.

198
Q

What is the effect of adipocytes on perivascular structure?

A

Decreases structural integritiy of vessel (less structured)

Increase in the amount of adipocyte surrounding vessel

199
Q

What is the effect of adipose on vascular regulation?

A

Changes the balance between vasoconstrucion and vasodilation

–> caused by the high insulin levels which means increase in ET-1 release (more vasocontriction) and decrease in NO release (less vasodilation) = increase BP

200
Q

Explain why obesisty leads to hyperinsulinemia:

A

In obesity, tissues such as muscle, liver, and adipose become less sensitive to insulin due to adipose inflammation. This means that the body requires more insulin to help glucose enter cells. The pancreas compensates by producing and secreting higher amounts of insulin to overcome this resistance, leading to hyperinsulinemia (high insulin levels in the blood).

201
Q

What is NEFA?

A

Non-esterified fatty acid

202
Q

What other things are effected from microangiopathy?

A

Retinopathy (eye condition)
Nephropathy (kidney)
Neuropathy (effect on nerve cells = changes in SNS)

203
Q

What is the number one most efficient therapeutic method for obesity?

A

Bariatric surgery

Works by modfiying your digestive system (stomach and small intestines) by gastric bands, bypass, sleeve gastectomy and duodenal switch. It reduces the amount of calories you can consume and reduces hunger siganls.

*can have ambivalent effects on BP.

204
Q

What is the most effective lifestyle change to reduce obesity?

A

Reduction in consumption of energy-dense food

205
Q

What is the obesity paradox?

A

Obesity (BMI) associated with increase survival among patients with CVD

206
Q

What is the nature (genetics) VS nurture (environment) influences on obesity?

A

Body length and body weight are both influenced by genetics and environment.

Height is 50-80% genetic (max height is genetically determined but whether you reach it is based on environmental factors).

Weight is 40-70% genetic.

207
Q

What are some pharmocolgical (drugs) remedies for obesity in NZ?

A

Duromine or phentermine
Contrave
Xenical or orlistat
Semiglutide or liraglutide

Don’t Count X Sleepovers

208
Q

What is the negative of weight management drugs?

A

Many side effects: nausea, vomiting, diarrhoea, panreatitis, low BG, kideny problems, thyroid tumours, dangerous for pregnancy.

That you regain body weight when you stop taking them and often regain more than pre-medication.

209
Q

What are alternative methods to BMI to measure obesity?

A

Waist circumference (WC) = measure the waist

Waist to hip ratio (WHR) = measure hip and waist and calculate ratio

Bioelectrical impedance (BIA) = electrical current through the body that measures the resistance to the current which is different for water and fat so gives fat %

Denstiometry (underwater weighing)

Dual energy X-ray absorptiometry (DEXA)

Computerised Tomography and Magentic resonsce imaging

210
Q

Is visceral obesity or subcutaneous obesity worse?

A

Viseral obesity = dysfunctional adipose tissue

Subcutaneous obesity = healthy adipose tissue

211
Q

Why is viseral adiposity worse than subcutaneous adiposity?

A

Subcutaneous fat alters FFA metabolism and release of adipokines = ectopic fat

Whereas, there is no ectopic fat with subcutaneous obesity therefore normal metabolic profile.

212
Q

What is increased in viseral obesity as a result of ectopic fat?

A

Increase in liver fat and altered function

Increase in epicardial fat

Increase in msucle fat and intracellular lipids.

213
Q

What does fatty infiltration in the conduction system prolong?

A

the QT interval

214
Q

What is released as a result of fatty infiltartion of the conduction system?

A

Adipokines and cytokines

215
Q

What is “EAT”?

A

Epicardial Adipose Tissue

216
Q

Is there a relationship between EAT and arrhythmias?

A

Yes - direct functional relation between EAT and arrhythmias in humans.

(When EAT is added to myocardium it induces sponatneous contractions which is what causes arrhythmias).

217
Q

What is a proxy for arrhythmia?

A

Spontaneous contractions (induced by EAT).

218
Q

How do duromine or phentermine drugs treat obesity?

A

They suppress central appetite

219
Q

How does Xenical or orlistat treat obesity?

A

Suppresses fat absorption from food

220
Q

What obesity pharmacological drug is a GLP1 stimulator?

A

Semiglutude and Liraglutide

PHSL232 Cardiovascular and Respiratory (12 decks)

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