Cardiovascular Dysfunction Flashcards

1
Q

Definition - cardiovascular disease

NICE, 2014

British Heart Foundation, 2015

A

No universally agreed definition…

Cardiovascular disease
(CVD) describes disease of
the heart and blood vessels
caused by the process of
atherosclerosis. It is the
leading cause of death in
England and Wales
accounting for almost one third of deaths (NICE, 2014)
Cardiovascular disease
(CVD) includes all the
diseases of the heart and
circulation including
coronary heart disease,
angina, heart attack,
congenital heart disease,
heart failure and stroke.
(British Heart Foundation,
2015)
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2
Q

What disordered are included in CVD?

A

CVD tends to incorporate hypertension, ischaemic heart disease, angina pectoris, myocardial infarction, stroke, rheumatic
heart disease, congenital cardiac defects and
heart failure

Most of the diseases grouped under the
heading CVD are inter-related (e.g. stroke and hypertension = same process)

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3
Q

What causes heart failure?

A
  • CVD is the primary aetiology of heart failure, although a variety of other factors also cause heart failure

(e.g. Heart valve defects caused by diseases such as
rheumatic fever or infection, primary disease of the
heart muscle known as cardiomyopathy, and
congenital heart disease)

  • Much CVD is caused by atheromatous plaque build up
    on the intima or inner layer of the arterial wall
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4
Q

Risk factors for CVD?

A
  • Age
  • Sex (More M)
  • Family history of CVD
  • Ethnic background
  • Smoking
  • Raised Blood Pressure
  • Raised Cholesterol
  • Low income/social deprivation (north/south divide)
     Air pollution
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5
Q

Cholesterol…

What is

Total cholesterol
‘Good’ cholesterol
‘Bad’ cholesterol
Triglycerides

A

 total cholesterol – the overall amount of cholesterol in
your blood, including both “good” and “bad”
cholesterol
 good cholesterol (called HDL) – this makes you less
likely to have heart problems or a stroke
 bad cholesterol (called LDL and non-HDL) – this
contributes to atherosclerosis and makes you more
likely to have heart problems or a stroke
 triglycerides – a fatty substance similar to bad
cholesterol and considered the building blocks of
cholesterol
 High levels of triglycerides and low levels of HDL raise
your risk for heart disease

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6
Q

Normal values for:

Total cholesterol
‘Good’ cholesterol
‘Bad’ cholesterol
Triglycerides

A

Normal

Total cholesterol - 5 or below
‘Good’ cholesterol - 1 or above
‘Bad’ cholesterol- 4 or below
Triglycerides - 2.3 or below

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7
Q

Lifestyle factors ?

A
Stress
Personality - 'type a'
Smoking
Sedentary lifestyle
CVD - brain and heart
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8
Q

Genetic link

A
  • Genetics can influence the risk for heart disease. A
    family history of cardiovascular disease (CVD) modifies
    future risk of CVD depending on the number and age of
    affected first-degree relatives

-Many cardiac disorders can be inherited, including
arrhythmias, congenital heart disease, cardiomyopathy,
and high blood cholesterol

  • CHD leading to heart attack, stroke, and heart failure
    can run in families
  • The gene variant ADAMTS7 is linked to a build up of plaque in the coronary arteries and is one of a number of genes associated with heart disease risk identified within the last few years
  • Variants on chromosomes 9, 6 and 2, as examples, are also associated with heart
    disease
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9
Q

Foetal Origins Hypothesis

David Barker

A

The Barker hypothesis states that adverse influences early in development, and particularly during intrauterine life, can
result in permanent changes in physiology and metabolism, which result in increased disease in adulthood

  • This hypothesis originally evolved from observations by Barker and colleagues that the regions in England that had the highest rates of infant mortality in the early twentieth century also had the highest rates of mortality from coronary heart disease decades later
  • The fetal origins hypothesis states that fetal under-nutrition in middle to late gestation, which leads to disproportionate fetal growth, programmes later coronary heart disease

Like other living creatures in early life,
human beings are “plastic” and able to
adapt to their environment.
The development of the sweat glands in first 3 years of life provides a simple example of this

Plasticity allows a ‘weather forecast’ - if mother is poorly nourished, baby expects environment to be harsh. This leads to reduced size and altered metabolism.
Disparities between predicted environment and actual environment then results in disease

e.g. diabetes, hypertension

Rapid weight gain in early childhood is associated with CVD

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10
Q

Links between cardiovascular factors & babies?

A

A substantial number of published studies suggest
that impaired fetal growth is related to higher risk of
hypertension, diabetes and CVD.

  • Recent studies point to a particularly high risk of
    cardiovascular disease in overweight or obese subjects with a history of impaired fetal growth and in subjects who experienced accelerated growth in childhood
  • Neonatal abdominal circumference has also been
    shown to predict plasma cholesterol and fibrinogen
    levels in men in later life-CVD linked
  • Babies born small in relation to the size of their
    placenta have an increased risk of developing
    hypertension
  • On the other hand babies who were reported to have
    small placentas in relation to their birth weight are
    more at risk of developing type 2 diabetes, sometimes
    in combination with hypertension
  • Babies born small tend to have higher basal plasma
    cortisol levels
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11
Q

Links with birth weight

A

Babies born small in relation to the size of their placenta have an increased risk of developing:

  • Hypertension
  • Coronary heart disease
  • Non-insulin dependent diabetes
  • Stroke
  • Dislipidaemia
  • Elevated clotting factors
  • Impaired neuro-development

less well replicated inc.

depression
schizophrenia
lung disease

High birth weight -
polycystic ovary disease

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12
Q

Heart oxygen journey?

A

deoxygenated blood enters the Right Atrium, travels into the right ventricle, travels into the lungs via the pulmonary artery, oxygenation happens, then via pulmonary VEIN (oxygenated) into Left Atrium,then into left ventricle, via aorta into body, deoxygenated back to RA via vena cava

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13
Q

What illnesses are meant by: Acute Coronary Syndrome?

A
Includes The term 'acute coronary syndromes' encompasses a range of
conditions including unstable angina, non-ST-segment-elevation
myocardial infarction (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI).
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14
Q

Whats the differene between Non-ST elevation MI and Unstable Angina?

A

Non-ST elevation MI is an unstable coronary syndrome which is differentiated from unstable angina by a subsequent rise in cardiac
enzymes.

NICE (2011) clinical guideline 94 – Unstable angina and NSTEMI

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15
Q

What is the disease process of ACS?

A
  • This process is generally initiated by the
    fissuring of an atheromatous plaque in the
    coronary artery.
  • The extent to which the fissuring reduces
    the blood flow to the myocardium determines the nature of the clinical events.
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16
Q

What is artherosclerosis?

A

 From Atheroma which is Greek for porridge
 Atherosclerosis is caused by the build up of fatty
deposits in the lumen of the artery.
 As the fatty deposits build up they cause plaques or
atheroma to develop.
 These plaques cause a narrowing of the artery lumen.
 This narrowing means that there is reduced blood flow to the myocardium.

17
Q

Theories of artherosclerosis?

A

‘Response to injury’ theory - repetitive injury to the inner lining of the artery

  • “Thrombolitic Theory” - arterosclerotic process
18
Q

What are schistocytes?

A

Fragments of RBC, broken off due to atheroma

19
Q

Atheroma formation - describe the process.

A
Damage to Tunica Intima
 LDL enter (cholesterol)
 Oxidation of LDL
Macrophages engulf
 Foam Cells
 Fatty Streak
 Fat moves into the intima = Bulge
Hard white plaque
Ulcerates – platelet aggregation – thrombosis
20
Q

Pathogenesis of ACS - describe…

A

 Haemorrhage into the plaque or atheroma causing internal
swelling and restriction of the lumen.
 Smooth muscle contraction within the artery wall causing further
restriction of the lumen.
 Platelet aggregation & formation of a thrombus on the surface of
the plaque causing partial or complete obstruction of the artery.
 Reduces blood flow through arteries (Ischaemia, peripheral
vascular disease, angina)
 Predisposition to thrombosis - MI
 Weakening of vessel walls - aneurism

21
Q

How many patients are aware that they have CVD prior to heart attack?

A

For 50% of patients their first
indication that they have
cardiovascular disease is the day they have their heart attack

22
Q

Angina Pectoris

A
  • Stable angina is NOT an Acute Coronary Syndrome.
    The pain is usually experienced on exertion is
    predictable, and is relieved with rest.
  • Controlled, preventative therapy, on movement or after
    meals, partial occlusion, relieved with GTN.
  • Glyceryl trinitrate (GTN) is a spray used to relieve
    angina (chest pain). When sprayed under. the tongue, it
    relaxes and widens blood vessels in the heart and in the rest of the body improving oxygen delivery
23
Q

Chest pain could be angina if:

A
Chest pain could be angina if:
 Feels tight, dull or heavy
although some people
(especially women) may
have sharp, stabbing pain
 Spreads to the arm, neck,
jaw or back
 Is triggered by physical
exertion or stress
 Stops within a few minutes
of resting
 Angina can also cause
breathlessness
 Nausea
 Pain similar to indigestion
 Tiredness
 Some people have these
symptoms without pain
 Presents when 70-75% of
artery is occluded
24
Q

How is unstable angina defined?

A

 Unstable angina is defined by one or more of the
following:
1. Angina of effort occurring over a few days with
increased frequency provoked by less exertion
(crescendo angina).
2. Angina that occurs unpredictably and recurrently
without specific provocation. Usually short lived
may settle spontaneous or temporarily relieved by
GTN. But will reoccur within a few hours.
3. An unprovoked and prolonged episode of chest pain raising suspicion of an acute myocardial infarction but without definitive ECG or blood result changes.
4. When myocardial ischaemia is present, but without evidence of actual myocardial necrosis (normal serum troponin level), the clinical syndrome is described as
Unstable Angina.

25
Q

Myocardial Infarction - define?

A

 Occurs when a coronary artery becomes blocked or
significantly narrowed.
 This is due to spasm or atheroma
 Indicates a defined area of myocardial necrosis caused
by local ischaemia.
 Myocardial necrosis begins within approximately 20-30
mins of the time of coronary artery occlusion
 Infarct reaches full size in 3-6 hrs
 Location of the MI is determined by site of the
occlusion within the coronary circulation.

ST elevation OR non ST elevation

26
Q

Assessment of chest pain in MI?

A
 The chest can feel like its
being pressed or
squeezed by a heavy
object
 Pain can radiate across
the chest, jaw, back or
arms
 Accompanied by
shortness of breath
 Weak/light headed
 Overwhelming anxiety
 Only relieved with
opiates
Chest Pain
 P = Precipitating factors
 Q = Quality
 R = Region/Radiation
 S = Symptoms associated
with pain
 T = Timing
27
Q

How can you identify MI?

A

Chest Pain - crushing? heavy? breathlessness?

ECG Changes - ST elevation?

Blood test changes - troponin elevated?

28
Q

Non-ST Elevation Myocardial Infarction vs.

Unstable Angina?

A

No troponin with angina

29
Q

Thombus vs. Embolus

A

both are blood clots

Embolus is a travelling clot

Thrombus is a stationary slot

30
Q

What is troponin?

A

regulatory protein, released with damage to the myocardial cells (as this is where troponin resides)