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Phase 2A extra > Extra Cardio > Flashcards

Extra Cardio Flashcards

1
Q

Where are common places for atherosclerosis to develop?

A
  • circumflex artery
  • Left anterior descending
  • right coronary arteries
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2
Q

Why is older age a risk factor for atherosclerosis?

A

As the body ages the risk for atherosclerosis increases and genetic or lifestyle factors cause plaque to gradually build in the arteries

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3
Q

What is claudication?

A

Claudication is pain caused by too little blood flow to muscles during exercise

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4
Q

Why is tobacco smoking a risk factor for atherosclerosis?

A

Tobacco leads to endothelium erosion of the arteries, which then means that lipids can get in and speed up the process.

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5
Q

Why is high levels of serum Cholesterol and obesity risk factors for atherosclerosis?

A

High levels of LDL’S means more will be deposited in the periphery.
Obesity means there is more pericardial fat and thus increase in inflammation.

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6
Q

Why is diabetes a risk factor for atherosclerosis?

A

Hyperglycaemia damages the endothelium and also magnifies the effect of other risk factors such as raised cholesterol levels, blood pressure, smoking ext.

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7
Q

Why is hypertension risk factor for atherosclerosis?

A

Mechanical stimulus to endothelial layer, weakens it.

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8
Q

Why is family history a risk factor for atherosclerosis?

A

It is a polygenic disease and some of the other risk factors also have a genetic part to them.

  • ANRIL expression is associated with atherosclerosis risk at chromosome 9p21
  • The ACE enzyme gene contains a insertion/deletion polymorphism, the DD genotype of which has been associated with a predisposition to CAD and MI
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9
Q

What are some other risk factors of atherosclerosis?

A

1) Male gender
2) Sedentary lifestyle
3) Psychosocial factors (type A personality)
4) Over consumption of alcohol
5) High levels of coagulation factor VII

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10
Q

Why is the focal distribution of an atherosclerosis along the artery length?

A

Changes in flow/turbulence e.g. at a bifurcation cause the artery to alter endothelial cell pattern. Wall thickness is also changed leading to neointima

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11
Q

What is neointima?

A

A new or thickened layer of arterial intima formed especially on a prosthesis or in atherosclerosis by migration and proliferation of cells from the media.

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12
Q

How can atherosclerosis lead to angina and thrombus formation?

A

Eventually the plaque will either occlude the vessel lumen resulting in restriction of blood flow (ANGINA).
or the plaque may rupture (THROMBUS FORMATION).

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13
Q

What initiates atherosclerosis formation?

A

Injury to the endothelium through smoking, cholesterols, BP, bacterial/viral infection… which leads to endothelial dysfunction(the vessel wall becomes sticky).
Once initiated chemoattractants are released from the endothelium at the site of injury to attract leukocytes which then accumulate and migrate into the vessel wall. When chemoattractants released a concentration gradient is produced.

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14
Q

What are the main cytokines involved in atherosclerosis formation?

A 
IL-1 (MAIN)
IL-6
IL-8
IFN-GAMMA 
C-REACTIVE PROTEIN
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15
Q

What other molecules are involved in leukocyte recruitment to the vessel wall?

A

Selectins, integrins and chemoattractants.

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16
Q

What do the fatty streaks consist of?

A

Aggregations of lipid-laden macrophages and t-lymphocytes within the intimal layer of the vessel wall.

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17
Q

What are foam cells?

A

Macrophages that have taken up lots of lipids

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18
Q

Progression of atherosclerosis: what are constituents of intermediate lesions?

A
  • Foam cells.
  • Vascular smooth muscle cells.
  • T lymphocytes.
  • Platelet adhesion and aggregation.
  • Extracellular lipid pools.
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19
Q

Progression of atherosclerosis: what are the constituents of fibrous plaques?

A

The fibrous cap is made of extracellular matrix proteins including collagen (strength) and elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris. Maybe calcified.

  • Smooth muscle cells.
  • Macrophages.
  • Foam cells.
  • T lymphocytes.
  • Plaque is filled with fibrin

Fibrous plaques can impede blood flow and are prone to rupture.

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20
Q

Progression of atherosclerosis: why might plaque rupture occur?

A

Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions due to increased enzyme activity), the cap becomes weak and the plaque ruptures. Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of the vessel within the plaque. Thrombus formation and vessel occlusion.

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21
Q

Progression of atherosclerosis: why might plaque erosion occur?

A

The fibrous cap may be disrupted by collagen leading to thrombosis. The difference to a plaque rupture is that thrombosis is triggered by collagen and not tissue factors. A platelet-rich clot may overlie the luminal surface and there may be a prominent lipid core.

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22
Q

What is restenosis?

A

Restenosis means that a section of the blocked artery that was opened up with angioplasty or a stent has become narrowed again. This is normally due to the response of the vascular tissue to the injury caused by coronary angioplasty

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23
Q

What are stents made from? why?

A

Made from stainless steel as they are able to withstand the pressure.

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24
Q

What drugs could be put on the stent? why do we do this?

A

Sirolimus. It stops the proliferation of smooth muscle cells from the media layer into the plaque.

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25
Q

What is the normal systolic ejection fraction?

A

60% of what’s in the heart’s chambers

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26
Q

What is cardiac failure? What can it lead to?

A

Failure to transport blood out of the heart. If severe can lead to cardiogenic shock. Cardiogenic shock is a condition in which your heart suddenly can’t pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has a cardiogenic shock.

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27
Q

Describe the Frank-Starling mechanism

A

Ventricular contraction becomes more forceful as the cardiac muscle cells are stretched. By increasing the volume of blood in the ventricle at rest, the cardiac muscle is stretched, causing an increase in the force of contraction which ejects more blood and increases the stroke volume.

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28
Q

How does venous return affect stroke volume?

A

If you increase venous return to the heart, you increase the ventricular filling and filling pressure of the ventricle and therefore preload. Because preload is increased by Frank Starling’s mechanism (sarcomere length increased so stronger contraction) the stroke volume also increases.

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29
Q

What is on the X and Y axis of Frank Starling’s graph?

A 
x= ventricular end-diastolic volume
y= ventricular performance
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30
Q

What is preload? 2 definitions

A

1) The amount of sarcomere stretch experienced by cardiomyocytes at the end of ventricular filling during diastole. (heart getting ready for the next big push)
2) Volume of blood in the ventricles at the end of diastole (LVEDP-end-diastolic pressure).

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31
Q

In what conditions does preload increase?

A

1) Hypovolemia
2) Regurgitation of cardiac valves
3) Heart failure

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32
Q

What is after-load?

A

a.k.a systemic vascular resistance
Is the amount of resistance the heart must overcome to open the aortic valve and push blood volume into the systemic circulation.

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33
Q

What is the effect of preload on stroke volume?

A

Increased preload increases stroke volume, whereas decreased preload decreases stroke volume by altering the force of contraction of the cardiac muscle.

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34
Q

What is the effect of afterload on stroke volume?

A

Increasing the afterload decreases the velocity of fibre shortening. Because the period of time available for ejection is finite( around 200msec), a decrease in fibre shortening velocity reduces the rate of volume ejection so more blood is left within the ventricle at the end of systole. This means increased afterload means increased stroke volume and LVEDP.

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35
Q

What is the effect of Inotropy (cardiac contractility) on SV and LVEDP?

A

Decreased inotropy leads to decreased SV and increased LVEDP. When the heart muscle contracts, all muscle fibres are activated so the only way to control the force are inotropy and preload.

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36
Q

Why does the LVEDP fall when SV increase?

A

If the contractility (inotropy) increases there is more blood pumped out so the SV increases, so there is less residual blood after ejection so EDV decreases and therefore the ventricular filling has decreased so the pressure here is also decreased.

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37
Q

In what kind of people would you find physiological hypertrophy?

A

1) Athletes
2) Pregnant women (to cope with the increasing demands for pregnancy)
3) Pathological problem

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38
Q

Embryology of the heart

A

1) Heart derives from the mesodermal germ layer.
2) Heart is initially one tube until week 5, then it divided by the intraventricular and intra-atrial septa from endocardial cushions.
3) The muscular intra-ventricular septum grows upwards from the apex of the heart producing 4 chambers and allowing valve development.

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39
Q

The mesoderm differentiates into these. What does the mesothelium, endothelium and myocardium form?

A

MESOTHELIUM: pericardium
ENDOTHELIUM: endocardium, lymphatics and blood vessels
MYOCARDIUM: myocardium

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40
Q

What has acute rheumatic fever to do with heart disease?

A

It is a Group A B-haemolytic streptococcus infection, which usually affects the upper respiratory tract but has a cross-reaction with heart cells. It is a major cause of heart disease in the developing world as it produces localised inflammation and subsequent scarring fibrosis.

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41
Q

What is myocarditis and give 5 causes for it?

A

The inflammation of the myocardium usually associated with muscle cell necrosis and degeneration.
Causes:
- Viruses(Coxsackie, Adeno, Influenza, COVID)
- Sarcoid
- Cross reaction of antibodies against myocardial tissue.

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42
Q

What is cardiac myxoma?

A

Commonest primary heart tumour

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43
Q

What is Vasculitis? What are the complications?

A

Inflammation of the blood vessels. It may be a primary condition or secondary to other diseases.
Inflammed vessels leads to damaged walls and lumen narrowing this means reduced blood flow = ischemia and distal necrosis.

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44
Q

What are the causes of Vasculitis?

A

1) direct attack on vessels by antibodies
2) deposition of immune complexes that then trigger an immune response
3) cell-mediated immunity
4) viral infection (hep c, b)

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45
Q

Granulomatus arteritis / temporal arteritis

  • what arteries affected?
  • symptoms and signs
  • complications
  • treatment
A
  • Inflammation of mainly temporal arteries.
  • Present with scalp tenderness (hurts when brushing) and headaches, sudden bilateral vision loss.
  • Blindness if arteries of the eye affected.
  • Treatment is prednisolone 60mg (steroid)
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46
Q

What is an aneurysm?

A

An aneurysm is defined if there is a permanent dilatation of the artery to TWICE the normal diameter. The normal diameter of the aorta is around 2cm, however, this increases with age.

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47
Q

What are “true” aneurysms?

What are some arteries that are more frequently involved?

A

Abnormal dilatations that involve ALL LAYERS of the arterial wall.
Arteries most frequently involved are:
- Abdominal aorta (most common)
- Illiac, popliteal and femoral arteries
-Thoracic aorta

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48
Q

What are “false” aneurysms?

What the causes of it?

A

They are also known as pseudoaneurysms. This involves the collection of blood in THE OUTER LAYER ONLY (ADVENTITIA) which then communicates with the lumen.

They can occur:

  • after injury to the artery e.g. trauma from a femoral artery puncture.
  • after cardiac catherisation
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49
Q

What are “false” aneurysms?

What the causes of it?

A

They are also known as pseudoaneurysms. This involves the collection of blood in THE OUTER LAYER ONLY (ADVENTITIA) which then communicates with the lumen.

They can occur:

  • after injury to the artery e.g. trauma from a femoral artery puncture.
  • after cardiac catherisation
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50
Q

What causes aneurysms?

A

1) Atherosclerotic disease
2) High blood pressure
3) Connective tissue disorders (Marfans)

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51
Q

What are saccular aneurysms?

A
  • Saccular aneurysms bulge on one side
  • “Berry” aneurysms because they look like berries
  • The most common type of brain aneurysm.
  • Saccular aneurysms have a “neck” that connects the aneurysm to its main (“parent”) artery and a larger, rounded area called the dome.
  • They bulge on only one side of the artery wall.
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52
Q

What are fusiform aneurysms?

A

The more common fusiform-shaped aneurysm bulges or balloons out on all sides of the blood vessel. Most AAAs

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53
Q

What are dissecting aneurysms?

A

An aneurysm in which the wall of an artery rips (dissects) longitudinally. This occurs because bleeding into the weakened wall splits the wall. Dissecting aneurysms tend to affect the thoracic aorta. They are a particular danger in Marfan syndrome.

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54
Q

What is an abdominal aortic aneurysm?

A

An abdominal aortic aneurysm is a bulge in the main blood vessel running from your heart to your tummy.
COVER UP NOTES SHEET AND ANSWER

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55
Q

Pathophysiology of AAA

A
  • Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss.
  • Dilatation affects all three layers of the vascular tunic. if not it is a false aneurysm.
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56
Q

Haemoptysis

A

Coughing up blood

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57
Q

Pathophysiology of TAAs

A
  • Involves inflammation, proteolysis and reduced survival of smooth muscle cells in the aortic wall
  • Once the aorta reaches a crucial diameter (around 6cm in ascending and 7cm in descending) it loses all distensibility so that a rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture.
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58
Q

Valvular diseases

A

see

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59
Q

What is the mitral valve?

A

Mitral valve is on the left side and is also known as the tricuspid valve, it separates the left atrium from the left ventricle. It has two cusps.

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60
Q

What is supra valvular aortic stenosis?

A
  • ABOVE VALVE

- Congenital fibrous diaphragm above the aortic valve

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61
Q

What is sub valvular aortic stenosis?

A
  • BELOW VALVE

- Congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve.

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62
Q

Aortic valve
WHERE?
WHAT?
DESCRIBE

A

The aortic valve is located on the left side of the heart and separates the left ventricle from the aorta.
The aortic valve has 3 cusps.
It is one of the semilunar valves.

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63
Q

Describe 3 main causes of Aortic stenosis

A
  1. Congenital bicuspid valve.
    The valve has 2 instead of 3 cusps. This is the most common congenital heart disease.
  2. Acquired e.g. age-related degenerative calcification 3. Rheumatic heart disease.
    Rare due to eradication.
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64
Q

Describe the pathophysiology of aortic stenosis.

A
  • Aortic orifice is restricted e.g. by calcific deposits.
  • So there is an obstruction to left ventricle emptying.
  • So there is a pressure gradient between the LV and the aorta. Resulting in an increased afterload
  • LV function is initially maintained due to compensatory hypertrophy.
  • Obstruction more severe during exercise (more cardiac output needed), but this cannot happen bc of stenosis so leads to symptoms.
  • Relative ischemia of the LV myocardium since hypotrophy results in increased blood demand.
  • Over time this compensatory mechanism becomes exhausted = LV failure.
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65
Q

Why is there a prominent 4th heart sound in aortic stenosis?

A

Due to LV hypertrophy

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66
Q

Is the apex beat displaced in aortic stenosis?

A

No, as hypertrophy doesn’t produce any noticeable cardiomegaly. A systolic thrill may be felt in the aortic area.

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67
Q

What is TAVI?

A

Transcutaneous aortic valve implantation

  • minimally invasive
  • pass catheter up the aorta then inflate balloon across the narrowed valve which will crack the calcification
  • pass another catheter which leaves a stent with a valve= new valve
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68
Q

How can rheumatic fever lead to mitral valve stenosis?

A
  • Inflammation due to rheumatic fever leads to commissural fusion and a reduction in mitral valve orifice area, causing the characteristic doming pattern seen on echo.
  • over many years, this can progress to vale thickening, cusp fusion, calcium deposition, a severely narrowed valve orifice and progressive immobility of the valve cusps.
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69
Q

Describe the pathophysiology of mitral stenosis.

A
  1. Obstruction of flow from LA to LV so to compensate for CO the LA pressure increases > LA hypertrophy and LA dilation -> pulmonary venous, pulmonary arterial and right heart pressure increase> pulmonary congestion.
  2. Increased trans-mitral pressures -> LA enlargement and AF and pulmonary oedma.
  3. Pulmonary venous hypertension causes RHF symptoms.
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70
Q

Why do you dyspnoea in mitral valve stenosis?

A

Left atrial dilation resulting in pulmonary congestion( reduce emptying), which is worse with exercise, fever, tachycardia and pregnancy.

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71
Q

Why do you get haemoptysis in mitral valve stenosis?

A

Rupture of bronchial vessels due to elevated pulmonary pressure.

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72
Q

Why do you get right heart failure in mitral valve stenosis?

A

Due to the development of pulmonary hypertension. This also is the reason why you get the “a” wave in jugular venous pulsations.

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73
Q

Why do you get AF in mitral valve stenosis?

A

Due to atrium dilatation giving rise to palpitations. this can then lead to systemic emboli.

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74
Q

Where is the diastolic murmur in mitral valve stenosis heard prominently?

A

The apex of heart when patient lying on the left side in held expiration.,

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75
Q

Why do you get a loud opening S1 snap-in mitral valve stenosis?

A

Due to abrupt halt in leaflet motion in early diastole after rapid initial opening. The more severe the stenosis, the longer the diastolic murmur and the closer the opening snap is to the second heart sound.

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76
Q

Describe the pathophysiology of aortic regurgitation.

A

1) AR is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole.
2) If the CO is to be maintained then the total volume of blood pumped into the aorta must increase> LV size increase»LV dilatation and hypertrophy
3) Progressive dilatation leads to heart failure
4) The remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole. Regurgitation causes diastolic BP to fall so the coronary perfusion decreases. Due to the larger ventricular size which is mechanically less efficient and needs more oxygen, which is not able to perfuse properly»> ischemia and heart failure.
COMBINED PRESSURE AND VOLUME OVERLOAD = HF

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77
Q

What is a symptom?

A

A symptom is a manifestation of disease apparant to the patient himself.

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78
Q

What is a sign?

A

A sign is a manifestation of the disease that the physician perceives

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79
Q

In Aortic Regurgitation what is the Austin flint murmur a sign of? What is it?

A

Austin Flint murmur is a low-pitched rumbling heart murmur which is best heard at the cardiac apex. It is caused due to the downward eject of the aortic regurgitation murmur pressing on the mitral valve. Severe AR.

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80
Q

AR : diastolic blowing murmur:

  • Where is it heard best?
  • Why is happens?
A
  • Left lower sternal border
  • In expiration when the patient is sat up and forward or in the left lateral decubitus position.
  • Also feel the pulse at the same time to see if the murmur is happening in systole or diastole.
  • FIND OUT WHY
81
Q

AR: systolic ejection murmur:

  • Where is it best heard?
  • Why it happens?
A
  • Right upper sternal border as this is the aortic region
  • In lateral decubitus position
  • Due to increased flow across the aortic valve.
82
Q

What is a collapsing water hammer pulse?

  • Where is it best heard?
  • Why it happens?
A
  • Bounding and forceful rapidly increasing and subsequently collapsing.
  • It is seen in the brachial, ulnar and radial arteries.
  • It is accentuated as you lift the arm up more and you can feel it against your palm.
  • It is due to the increased amount of blood flow going into and out of the heart.
83
Q

What is Quincke’s sign? Why does it happen?

A

Repeated flushing and blanching of the capillaries in the nail beds and lips. It is a result of widened pulse pressure.

84
Q

What is de Musset’s sign? Why does it happen?

A

Bobbing of the head with each heartbeat. FIND OUT WHY?

85
Q

What is pistol shot femoral? Why does it happen?

A

A shotlike systolic sound heard over the femoral artery in high output states, especially aortic insufficiency.
Presumably due to sudden stretching of the elastic wall of the artery.

86
Q

What is the pathophysiology of mitral regurgitation?

A

1) Regurgitation into the LA produces LA dilatation but little increase in LA pressure since regurgitant flow is accommodated by the large LA.
2) Pure volume overload in the LA during systole
3) Compensatory mechanisms happen: LA dilatation, LV hypertrophy
( as the more blood needs to be pumped out to make up for the regurgitant flow so increased contractility to keep the CO the same)
4) Progressive LA dilatation and RV dysfunction due to pulmonary hypertension.
5) Progressive LV volume overload leads to dilatation and progressive heart failure.

87
Q

Why do you get exertional dyspnoea to develop in MV regurgitation?

A

Pulmonary venous hypertension that arises as a direct result of the MR and secondarily as a consequence of left ventricular failure.

88
Q

Why do you experience fatigue and lethargy in MV regurgitation?

A

Reduced CO

89
Q

What is a pan systolic murmur?
Where do you hear it?
Why?

A

High pitched blowing murmur.
Best heard at the apex of the heart but radiates towards the axilla.
The cause is mitral/tricuspid regurgitation or a ventricular septal defect.

90
Q

What is myxomatous degeneration?

A

The weakening of the chordae tendinae resulting in a floppy mitral valve that prolapses.

91
Q

What are the different frequencies that echo is needed for each of these severities of MV regurgitation?

  • MILD
  • MODERATE
  • SEVERE
A

MILD: 2-3 yrs
MODERATE: 1-2 yrs
SEVERE: 6-12 months

92
Q

Indications for surgery for MV regurgitation?

A

1) Symptoms at rest or exercise then initiate repair if feasible
2) Asymptomatic but ejection fraction less than 60%, if new onset of AF, if LV about to dilate.

93
Q

Infective endocarditis infection occurs on what types of valves?

A

1) Valves with congenital or acquired defects (L side usually)
2) Normal valves with virulent organisms such as streptococcus pneumonia or staph aureus
3) Prosthetic valves and pacemakers.

94
Q

Describe the pathogenesis of Infective endocarditis

A

1) Usually the consequence of two factors: the presence of organisms in the bloodstream and abnormal cardiac endothelium that facilitates their adherence and growth.
2) Damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infective vegetation.
3) Aortic and mitra valves are most commonly involved- IV drug user are an exception because they inject into veins so it’s more likely to lodge on the right side.
4) Virulent organisms destroy the valve they are on resulting in reguritation and worsening heart failure.

95
Q

What are the causes of bacteriemia in IE?

A

1) Poor dental hygiene - tooth plaque can cause gum disease»>bleeding and inflammation»>when brushing the bacteria can get into the bloodstream and reach the heart.
2) IV drug use - inject into veins»more likely to lodge up early in the right side of the heart.
3) Soft tissue infections
4) Following dental treatment
5) Intravascular cannulae
6) Cardiac surgery
7) Permanent pacemakers

96
Q

What are some factors that might trigger that it could be IE?

A

1) New valve lesion/regurgitant murmur
2) Embolic events of unknown origin
3) Sepsis of unknown origin
4) Haematuria, glomerulonephritis and suspected renal infarction.

97
Q

Infection of which bacteria would give rise to the quick onset of symptoms?

A

Staphylococcus aureus: high fever and feel ill rapidly

98
Q

When would you exclude endocarditis?

A

In ANY patient with a heart murmur and fever.

99
Q

What is CRP? What is ESR? What do they show?

A

C-reactive protein:
This test is used to help diagnose conditions that cause inflammation. CRP is produced by the liver and if there is a higher concentration of CRP than usual, it’s a sign of inflammation in your body.
Erythrocyte sedimentation rate:
This test works by measuring how long it takes for red blood cells to fall to the bottom of a test tube. The quicker they fall, the more likely it is there are high levels of inflammation.

100
Q

Give 2 advantages and 1 disadvantage of a trans-thoracic echo (TTE).

A
  1. Safe.
  2. Non-invasive, no discomfort.
  3. Poor images and low sensitivity (only identify vegetation if greater than 2mm).
101
Q

If the TTE is negative for vegetations would you exclude the diagnosis for IE?

A

No as it doesn’t pick up small vegetations

102
Q

Give 3 advantages and 2 disadvantages of Transoesophageal echo

A

1) Sensitive
2) Visualise mitral lesions
3) Invasive so discomfort
4) Small risk of perforation/ aspiration
5) BETTER AT DIAGNOSING SO USE THIS
NO PAIN NO GAIN

103
Q

Why does culture-negative endocarditis occur in 5-10% of cases?

A
  • The use of prior antibiotic therapy before the culture is taken.
  • Some varieties of fastidious organisms that fail to grow in normal blood cultures
104
Q

What is an aortic dissection?

A

A tear in the intima layer of the aorta.

105
Q

What is the pathophysiology of aortic dissections?

A

1) Aortic dissections begin with a tear in the intimal lining of the aorta.
2) The tear allows the high-pressure blood to enter the aortic wall into the tunica media, forming a haematoma, separating the intima from the adventitia and creates a false lumen.
3) The false lumen extends for a variable distance in either direction, anterograde and retrograde.

106
Q

What does anterograde and retrograde mean?

A 
Anterograde = towards bifurnication 
Retrograde = towards the aortic root
107
Q

Where are the most common sites for the intimal tears?

A
  • Within 2-3cm of the aortic valve

- Distal to the left subclavian artery in the descending aorta

108
Q

What are the causes of Aortic dissections?

A
  • Inherited
  • Degenerative
  • Atherosclerotic
  • Inflammatory
  • Trauma
  • Chronic hypertension
  • Underlying connective tissue disorders like Marfan’s or Ehlers- Danlos syndrome
109
Q

Clinical presentations of Aortic dissection

A
  • Sudden onset of severe and central chest pain that radiates to the back and down arms
  • Hypertension
  • Shock
  • Peripheral pulses may be absent
110
Q

How would you differentiate aortic dissections to MI?

A
  • Pain is maximal from the time of onset, unlike MI where the pain gains intensity
111
Q

What investigation would you perform for Aortic dissections? What would you see?

A
  • CXR: Widened mediastinum

- CT scan, TOE or MRI to confirm diagnosis

112
Q

What is the treatment for Aortic dissection?

A
  • IV Antihypertensive meds to reduce to less than 120mmHg e.g. IV beta blockers— metoprolo or IV vasodilators ——-IV GTN
  • Analgesia e.g. morphine
  • Surgery to replace aortic arch
  • Endovascuar intervention e.g. stents
  • Long term follow up with CT/MRI
113
Q

What is the treatment for aortic dissection?

A
  • IV Antihypertensive meds to reduce to less than 120mmHg e.g. IV beta blockers— metoprolol or IV vasodilators ——-IV GTN
  • Analgesia e.g. morphine
  • Surgery to replace the aortic arch
  • Endovascular intervention e.g. stents
  • Long term follow up with CT/MRI
114
Q

What is cardiac tamponade? What are the symptoms of cardiac tamponade?

A

Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to impaired cardiac filling and haemodynamic compromise.
Symptoms: BECK’S TRIAD

115
Q

What is Beck’s triad?

A

1) Sinus tachycardia
2) Elevated jugular venous pressure
3) Low blood pressure)

116
Q

What is pulsus paradoxus?

A

Pulsus paradoxus is defined as a fall of systolic blood pressure of >10 mmHg during the inspiratory phase.

117
Q

What is the pericardium? What does it consist of?

A

Is a double-walled sac that encloses the heart, the pericardial fluid and the roots of the great vessels, and is situated in the middle mediastinum.
It has one layer made of fibrous tissue (outer/parietal) and one layer made of serous tissue (visceral).

118
Q

What are 4 functions of the pericardium?

A

1) Lubricate the moving surfaces of the heart
2) Promotes cardiac efficiency by:
limiting dilatation, maintaining ventricular compliance and distributing hydrostatic forces.
3) Aids atrial filling by:
creating a closed chamber, reduces external friction, a barrier against infection and extension of malignancy.
4) Fixes the heart to:
Sternum, diaphragm and costal cartilages

119
Q

What is the inner serous pericardium made up of?

A

1) Inner visceral pericardium single layer that is adhrent to the epicardium, that lines the heart and the great vessels and it’s reflection.
2) Outer parietal pericardium, an acellular structure made of mainly collagen and elastin fibres that lines the fibrous sac.

120
Q

What would you find in between the two layers of the inner serous pericardium?

A

20-49ml of serous fluid

121
Q

Describe the physiology of the pericardium

A
  • The pericardium is similar to an elastic band- it is initially stretchy but become stiff at a higher tension.
  • At low tension the pericardium has a small reserve volume.
  • If this volume is exceeded the pressure is translated to the cardiac chambers and then puts pressure on the heart
  • Even small amounts of volume e.g. blood added to this space has dramatic effects on filling
  • Pressure in the pericardium is very low
122
Q

What mainly lies outside the pericardium?

A

Left atrium

123
Q

What is the pathophysiology of Acute Pericarditis?

A
  • Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes.
  • A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac and a serous or haemorrhagic effusion may develop.
124
Q

How can you differentiate between MI and acute pericarditis?

A
  • In AP Chest pain is more severe in deep inspiration, relieved when sitting forward and not crushing like in IHD
  • Pain radiates to trapezius ridge than in STEMI where it goes to arm, jaw and teeth
  • in the ECG for AP there is ST elevation in all leads whereas in MI there is only ST Revelation in the infarcted area.
125
Q

What is pericardial effusion?

A

Is a collection of fluid within the potential space of the serous pericardial sac.

126
Q

What are the symptoms of pericardial effusion?

A
  • Commonly reflects the underlying pericarditis
  • Soft and distant heart sounds
  • Apex beat obscured
  • Raised jugular venous pressure
  • Dysponea
127
Q

What is the diagnosis for pericardial effusions?

A

1) Echo ( BEST CHOICE)
2) ECG (low voltage QRS complexes and sinus tachy)
3) CXR (Large globular heart)

128
Q

What is the treatment for pericardial effusions?

A
  • Underlying cause should be sought and treated
  • Most resolve spontaneously
  • Pericardial fenestration (to allow slow release of fluid into surrounding tissues)
129
Q

What is the clinical presentation for cardiac tamponade?

A

1) Beck’s triad
2) Kaussmaul’s Sign
3) Pulsus Paradoxus
4) Reduced Cardiac output

130
Q

What is Kaussmaul’s sign?

A

Rise in jugular venous pressure and increased neck vein distension during inspiration.

131
Q

What is the diagnosis for Cardiac Tamponade?

A 
1) Echo: Diagnostic !!! 
Echo-free zone around heart, Late diastolic collapse of the right atrium, early of the right ventricle 
2) CXR: 
Big globular heart
3) Beck's triad
132
Q

Treatment of cardiac tamponade?

A
  • URGENT DRAINAGE via PERICARDIOCENTESIS (relieve the pressure on the heart)
  • Send fluid for culture, cytology
133
Q

Causes of constrictive pericarditis

A
  • Idiopathic mostly
  • After any pericarditis
  • After open-heart surgery
  • With the use of dopamine agonists
134
Q

How to distinguish constrictive pericarditis from restrictive cardiomyopathy?

A
  • CT/MRI: In pericarditis, you would find pericardium thickened and calcified but looks normal in cardiomyopathy.
  • P waves abnormalities in pericarditis and t wave abnormalities in restrictive cardiomyopathy.
  • Pericarditis is fully treatable whilst most cases of myopathy are not.
135
Q

HYPERTENSION

A

////

136
Q

Describe stage 1 hypertension

  • What value of clinical BP ?
  • Daytime average ambulatory blood pressure monitoring values or home blood pressure monitoring values?
A
  • More than or equal to 140/90mmHg in clinic BP

- Greater than or equal to 135/85mmHg

137
Q

Describe stage 2 hypertension

  • What value of clinical BP ?
  • Daytime average ambulatory blood pressure monitoring values or home blood pressure monitoring values?
A
  • More than or equal to 160/100mmHg in clinic BP

- Greater than or equal to 150/95mmHg

138
Q

Describe severe hypertension

  • What value of systolic and diastolic
  • What should you do?
A

Systolic greater than or equal to 180mmHg
and/or diastolic greater than or equal to 110mmHg.
Start anti-hypertensive drugs immediately

139
Q

What is the difference between essential/ primary hypertension and secondary hypertension?

A

Essential HT= cause is unknown, Multifactorial

Secondary HT= known cause

140
Q

What are some multifactorial causes of essential /primary HT?

A

1) Genetic susceptibility
2) Excessive sympathetic nervous system activity
3) Abnormalities of Na+/K+ membrane transport
4) High salt intake
5) Abnormalities in the renin-angiotensin-aldosterone system.

141
Q

What are some potential causes of secondary hypertension? What is the commonest one?

A

1) Chronic kidney disease (MOST COMMON but can be both cause and result of HT)
2) Endocrine causes
3) Coarctation of the aorta
4) Drug therapy

142
Q

Describe how 3 endocrine diseases can cause secondary hypertension.

  • Cushing’s syndrome
  • Conn’s syndrome
  • Phaeochromocytoma
A

Cushing’s Syndrome :
- Too much cortisol which is a corticosteroid which enhances adrenaline resulting in vasoconstriction
Conn’s syndrome:
- Adrenal tumour that secretes aldosterone»>Hyperaldosteronism»>Na+ retention and water retention»increasing blood volume&raquo_space;>increase n blood pressure
Phaemochromocytoma:
- Adrenal tumour that secretes CATECHOLAMINES e.g adrenaline and noradrenaline.
- Stimulation of alpha-adrenergic receptors»vasoconstriction, increased cardiac contractility
- Stimulation of beta-adrenergic receptors» increase HR and contractility&raquo_space;>increase BP

143
Q

How does the coarctation of the aorta cause HT?

How can you test?

A
  • Coarctation= narrowing of the aorta
  • Therefore systemic hypertension is one of the commonest features in coarctation
  • Raised BP in the ARMS but NOT in the LEGS
  • Femoral pulse is often delayed relative to the radial
  • If untreated patients die from cardiac failure, cerebral haemorrhage or dissecting aneursym
144
Q

Name some drugs that are associated with hypertension

A
  • Corticosteroids
  • Cyclosporin
  • Erythropoietin
  • Some types of contraceptive pills
  • Alcohol
  • Amphetamines
  • Cocaine
  • Ecstasy
145
Q

Order of treatment for hypertension if less than 55yrs old

A

1) Ramipril/ Candesartan
+ Nifedipine
+ Bendroflumethizide
+ Furosemide

146
Q

Order of treatment for hypertension if more than 55yrs old/ African-Caribbean origin

A

1) Ramipril/Candesartan + Nifedipine
+ Bendroflumethiazide
+ Furosemide
if higher dose not tolerated then consider beta-blocker.

147
Q

Describe a nd explain some vascular changes in hypertension

A
  • Hypertension accelerates atherosclerosis
  • Also causes the thickening of the media of muscular arteries (hyaline atherosclerosis)
  • Small arteries and arterioles that are especially affected in hypertension
  • This all results in endothelial cell dysfunction which then»> impaired nitric oxide-mediated vasodilation and enhanced secretion of vasoconstrictor e.g. endothelins and prostaglandins.
148
Q

Describe and explain the effects of hypertension on the heart

A
  • Compensatory hypertrophy of the heart as hypertension will lead to peripheral vascular resistance so increase in afterload so to keep the cardiac output the same the heart has to compensate
  • Leads to the myocyte size increase, squaring of nuclei, a slight increase in interstitial fibrous tissue
149
Q

What features would make you think malignant hypertension?

A
  • Raised diastolic pressure (>120mmHg) and progressive renal disease
  • Black males in their 30s-40s
150
Q

ANGINA

A

////

151
Q

What is the difference between Stable IHD and Acute Coronary Syndrome?

A

Stable ischaemic heart disease (SIHD) stands in contrast to acute coronary syndrome (ACS), a term that encompasses unstable angina, ST-elevation myocardial infarction, and non-ST-elevation myocardial infarction.

152
Q

Define Ischaemic Heart Disease

A
  • Ischaemic heart disease, an inability to provide adequate blood supply to the myocardium
  • Ischaemic heart disease is said to be stable when symptoms, if any, are manageable and not rapidly progressive.
153
Q

Define Angina

A

Angina is chest pain or discomfort as a result of reversible myocardial ischaemia.

154
Q

Stable Angina

A

Induced by effort and relieved by rest

155
Q

Unstable angina (crescendo)

A
  • Angina of recent onset (less than 24hrs).
  • Deterioration in previously stable angina with symptoms frequently occurring at rest.
  • Angina of increasing frequency or severity
156
Q

Prinzmetal’s angina

A
  • Caused by coronary artery spasm
157
Q

Microvascular angina

A

Spasms within the walls of these very small arterial blood vessels cause reduced blood flow to the heart muscle leading to a type of chest pain referred to as microvascular angina.

158
Q

Name some supply exacerbating factors for angina

A
  • Anaemia
  • Hypoxemia
  • Hypovolemia
  • Hypervolemia
159
Q

Name some demand exacerbating factors for angina

A
  • Hypertension
  • Valvular heart disease
  • Hyperthyroidism
  • Hypertrophic cardiomyopathy
160
Q

Name some environmental exacerbating factors for angina

A
  • Cold weather
  • Heavy meals
  • Emotional stress
161
Q

ACUTE CORONARY SYNDROMES

A

//////

162
Q

Why do you need antiplatelets in ACS?

A
  • Atheromatous plaque rupture results in platelets being exposed to ADP/Thromboxane A2/ adrenaline/ thrombin/collagen tissue factor.
  • This results in platelet activation/ aggregation via IIb/IIa glycoproteins binding to fibrinogen.
  • Then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin resulting in the formation of a fibrin mesh over a platelet plug and the formation of a thrombotic clot.
  • ANTI-PLATELETS STOP THIS PROCESS.
163
Q

STEMI

A
  1. Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis.
  2. This causes full-thickness damage to heart muscle Usually diagnosed on ECG at presentation:
    - ST-elevation
    - Tall T waves
    - Pathological Q wave
    - May present as a new left bundle branch block.
164
Q

NSTEMI

A

• Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis
• This causes partial thickness damage of heart muscle
• A RETROSPECTIVE diagnosis made after troponin results and
sometimes other investigation results are available
• ST depression/T wave inversion

165
Q

Troponin (T & I)

A

Only done when ACS unsuspected
Troponin is highly sensitive for cardiac muscle injury, though not specific to MI ( could be pulmonary embolism, myocarditis, heart failure)
Serum levels increase within 3-12 hrs from the onset of the chest pain and peak at 24-48 hours. Then they fall back to normal over 5-14 days.
Troponin elevation = worse prognosis

166
Q

CK-MB

A
  • CK-MB can be used as a marker for myocyte death - but has low accuracy since it can be present in the serum of normal individuals and in patients with significant skeletal muscle damage
  • However it can be used to determine re-infarction as levels drop back to normal after 36-72 hours
167
Q

Type 1 MI

A

Spontaneous Ml with ischaemia due to primary coronary event:

  • plaque erosion / rupture
  • fissuring
  • dissection
168
Q

Type2 MI

A

MI secondary to ischaemiadueto increased 02 demand or decreased supply in suchas in:

  • coronary spasm
  • coronary embolism
  • Anaemia
  • Arrhythmias
  • hypertension
169
Q

Type 3,4,5 MI

A

Mi due to sudden cardiac death , related to PCI and related to CABG

170
Q

Evolution of STEMI on ECG

A
  • After the first few minutes, the T waves become tall, pointed and upright, and there is ST segment elevation
  • After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
  • After a few days, the ST segment returns to normal
  • After weeks or months, the T wave may return to upright but the Q WAVE REMAINS
171
Q

Infarct site: anterior

What leads will show the change?

A

ST ELEVATION

V1-V3

172
Q

Infarct site: Inferior

What leads will show change?

A

ST ELEVATION

II, III, AVF

173
Q

Infarct site: lateral

What leads will show changes?

A

I, AVK, V5-V6

174
Q

Infarct site: Posterior

What leads will show change?

A

ST depression V1-V3
ST elevation V5-V6
Dominant R wave

175
Q

Infarct site : subendocardial

What leads will show a change?

A

Any

176
Q

Pathophysiology of Aortic dissection

A

Tear in the intimate layer&raquo_space; Blood then passes through the media propagating dismally or proximally»> false lumen
As the dissection propagates, flow through the false lumen can occlude flow through branches of the aorta, including the coronary, brachiocephalic, intercostal,visceral and renal or iliac vessels&raquo_space;» ischaemia of the supplied organs

177
Q

GRACE Score to assess for PCI in NSTEMI

A

This scoring system gives a 6-month risk of death or a repeat MI after having an NSTEMI:
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

178
Q

Dressler’s syndrome what is it?

A

This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced.

179
Q

Presentations of Dressler’s syndrome

A
  1. Pleuritic chest pain
  2. Low grade fever
  3. Pericardial rub on auscultation
  4. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function).
180
Q

Diagnosis of Dressler’s syndrome

A

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

181
Q

Treatment and management for Dressler’s syndrome

A
  1. Management is with NSAIDs (aspirin/ibuprofen) and in more severe cases steroids (prednisolone).
  2. They may need pericardiocentesis to remove fluid from around the heart.
182
Q

If a patient presents with constricting chest pain what are your differential diagnoses?

A

constricting – angina, oesophageal spasm, anxiety

183
Q

If a patient presents with central crushing chest pain for over 20 minutes what are your differential diagnoses?

A

over half an hour central crushing – MI

184
Q

If a patient presents with central crushing chest pain for over 20 minutes what are your differential diagnoses?

A

over half an hour central crushing – MI

185
Q

What is epistaxis?

A

Nosebleed

186
Q

What is Brain natriuretic peptide?

A

Secreted by ventricles in response to increase myocardial wall stress
- Increased in patients with heart failure
- Levels correlate with ventricular wall stress and the severity of
heart failure

187
Q

What are Kerley’s B lines?

A

Septal lines aka kerleys lines are seen when the interlobular septa in the pulmonary interstitium become prominent. B lines are 1-2cm in length in the periphery of the lungs. They represent the thickened sub-pleural interlobular septa.

188
Q

CARDIOMYOPATHY

A

//////

189
Q

In hypertrophic cardiomyopathy why does fibrosis lead to arrhythmias?

A

Fibrosis is an electrical insulator so when the impulse meets the fibrosis it has to stop and find a different pathway, in this way it can meet myocytes that were already repolarised and depolarise them»»circuit arrhythmias and tachycardia

190
Q

Cardiomyopathy

A

A group of diseases of the myocardium that affect mechanical or electrical function.
They all carry an arrhythmic risk, can occur at younger ages, however restrictive CM is rare in childhood.

191
Q

Four types of cardiomyopathy:

A
  1. Hypertrophic
  2. Dilated
  3. Restrictive
  4. Arrhythmic right ventricular
192
Q

Incomplete penetrance

A

When some individuals who carry the pathogenic variant express the associated trait while others do not.

193
Q

What is the classification used for anti arrhythmiatic drugs?

A

Vaughan Williams classification

Classes 1 & 3 = Rhythm control e.g. sodium channel blockers and beta blockers
• Classes 2 & 4 = Rate control
E.g. amiodarone, ccbs

194
Q

Orthopnea

A

Orthopnea - it is the sensation of dyspnoea in the recumbent position, relieved by sitting or standing.

195
Q

Paroxysmal nocturnal dyspnoea

A

It is a sensation of dyspnoea that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.

196
Q

Trepopnea

A

it is a sensation of dyspnoea that occurs in one lateral decubitus position as opposed to the other.

197
Q

Platypnea -

A

it is a sensation of dyspnoea that occurs in the upright position and is relieved with recumbency.

198
Q

lateral decubitus position

A

laying on on side

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