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Cellular pathology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is haemostasis

A

A physiological process which is initiated when there is damage to a blood vessel. It involves the rapid formation of a solid plug at the site of injury.
It is protective and stops loss of blood from the circulation.

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2
Q

What are the constituents of a haemostatic plug

A

Platelets, fibrin and RBCs

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3
Q

Explain the process of haemostasis

A

(1) Endothelial injury leads to adhesion and aggregation of platelets.
(2) Platelets adhere to collagen by vWF and RBCs become enmeshed with the platelets, resulting in the formation of a lose platelet plug
(3) At the same time, exposure of tissue factor initiates the coagulation cascade = formation of fibrin

Fibrin stablises the loose platelet plug

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4
Q

What is the role of the fibrinolytic system

A

It ensures that the haemostatic plug does not become too big- limits it to the site of injury.

Endothelial injury also initiates fibrinolysis (as well as haemostasis) and it results in plasmin formation - which breaks down fibrin to soluble products.

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5
Q

What is thrombosis

A

This occurs when there is an inappropriate (ie. pathological) activation of haemostasis which overwhelms the capacity of the fibrinolytic system, resulting in the formation of a solid plug = thrombus.

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6
Q

What are the constituents of a thrombus

A

The same as a haemostatic plug - platelets, fibrin and RBCs

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7
Q

What is a clot composed of

A

RBCs and fibrin (no platelets)

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8
Q

Explain the difference between clots and thrombi

A 
(1) Composition
Thrombus = RBC, fibrin, platelets
Clot = RBC, fibrin
(2) Location
T = forms within the CVS
C = forms outside the CVS
(3) Blood
T = forms in flowing blood (life)
C = forms in stationary blood (during/after life)
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9
Q

What are the 3 components of Virchow’s triad

A

3 predisposing factors to thrombus formation

(1) Endothelial injury
(2) Abnormal blood flow
(3) Hyper-coagulability

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10
Q

What can cause endothelial injury

A
  • Atherosclerosis
  • Vasculitis
  • Direct Trauma = heat / chemical injury
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11
Q

What can cause abnormal blood flow

A

Turbulence:

  • Atherosclerosis
  • Artificial valves, stents

Stasis:

  • Post-op / trauma
  • Congestive cardiac failure
  • Immobility
  • Pelvic obstruction (mass)
  • Aneurysms
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12
Q

What can cause hypercoagulability

A 
Too many blood cells:
- Erythrocytosis
- Thrombocytosis
Coagulation factor defects:
- Hereditary = factor V Leiden, protein C/S deficiency
- Acquired = OCP, malignancy, pregnancy
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13
Q

What is the most important risk factor for thrombosis in an artery

A

Atherosclerosis (results in endothelial injury and turbulence)

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14
Q

What is the most important risk factor for thrombosis in a vein

A

Stasis and hyper-coagulability

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15
Q

List 3 main ways in which thrombi can cause disease

A
  • Partial occlusion of the vessel at the site of thombosis
  • Complete occlusion at the site of thrombosis
  • Embolism to distant site
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16
Q

What are the complications of thrombosis

A

Partial or complete occlusion results in ischaemia - can progress to infarction.

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17
Q

What is embolism

A

The occlusion of a vessel by undissolved material that is transported in the blood stream.

(In clinical practice most emboli are thromboemboli)

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18
Q

List the types of emboli

A
  • Thrombi
  • Fat/bone marrow
  • Air
  • Amniotic fluid
  • Tumour
  • Septic emboli (eg. infective endocarditis)
  • Atheromatous debris
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19
Q

Where will emboli originating in the venous system occlude

A

A pulmonary artery

Symptoms and signs include swollen calf; PE - results in a pulmonary infarct

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20
Q

Where will emboli originating in the arterial system occlude

A

A systemic artery e.g. mesenteric artery, cerebral artery, renal artery

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21
Q

What is atherosclerotic plaque stability determined by

A

The balance between:
(A) inflammatory cells = destabilise by making MMPs that digest the fibrous cap
Can also cause the SMC in the intima to under go apoptosis
(B) smooth muscle cells = protective as they produce the fibrous cap stabilising the plaque
Also make TIMPs which inhibit MMPs

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22
Q

What are the features of a stable atherosclerotic plaque

A
  • contains few inflammatory cells and large numbers of SMCs
  • thick fibrous cap which is resistant to rupture
  • grow slowly = gradual stenosis
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23
Q

What are the features of an unstable ‘vulnerable’ plaque?

A
  • inflammatory cells (foam cells) > smooth muscle cells

- Thinner fibrous cap, which is more prone to rupture = may result in thrombosis/embolism

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24
Q

List 3 main mechanisms by which atherosclerosis causes disease

A

(1) Gradual enlargement of a stable plaque leading to luminal stenosis and reduced blood flow through the artery
(2) Sudden rupture of a vulnerable plaque
(3) Aneurysm formation

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25
Q

What is Poiseuille’s law

A

Flow is proportional to the radius to the power of 4

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26
Q

How does rupture of an atherosclerotic plaque result in formation of a thrombus

A

The rupture results in the exposure of tissue factor and other pro-thrombotic substances. As a consequence a thrombus forms over the site of the rupture - can cause occlusion at the site / embolism to a distant site

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27
Q

What is ischaemic heart disease

A

The term used to describe the spectrum of heart disease which results from coronary artery atherosclerosis. It includes stable angina, ACS and sudden cardiac death.

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28
Q

Why is ischaemic heart disease dangerous

A

The atherosclerosis causes gradual or complete occlusion of one or more coronary arteries = reduction in blood flow to the myocardium = mismatch between supply and demand of oxygen to the myocardium - resulting in ischaemia.

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29
Q

What is angina

A

NB: It is a syndrome not a disease.

It occurs when there is imbalance between supply and demand of oxygen to the myocardium - resulting in myocardial ischaemia, which presents as cardiac-type pain

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30
Q

How does stable angina present clinically

A

Predictable cardiac-type pain.

Precipitated by exertion, lasts for 1-2 minutes and is relived by GTN.

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31
Q

What is the most common cause of stable angina

A

A stable but gradually enlarging atherosclerotic plaque in a coronary artery causing gradually progressive stenosis - which itself gradually reduces blood flow through the artery

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32
Q

What are acute coronary syndromes

A

A spectrum of diseases which occur when there is a sudden and severe reduction in myocardial perfusion - essentially a sudden change in a coronary artery atherosclerotic plaque.

Leads to ischaemia and/or infarction.

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33
Q

List the most common progression of events leading to ACS

A

(1) Sudden rupture of a vulnerable atherosclerotic plaque with superimposed thrombosis
(2) Sudden partial or complete occlusion of the coronary artery
(3) ACS

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34
Q

What does troponin detect

A

Myocardial necrosis.

Levels rise following myocardial injury - peaking at 24 hours

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35
Q

List the different forms of ACS

A
  • Unstable angina (partial occlusion by a thrombus)
  • NSTEMI (partial occlusion by a thrombus leading to a zone of necrosis)
  • STEMI (complete occlusion by a thrombus leading to a zone of necrosis)
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36
Q

How would you differentiate between the forms of ACS

A

Unstable angina = No ST elevation, troponin -ve
NSTEMI = No ST elevation, troponin +ve
STEMI = ST elevation, troponin +ve

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37
Q

How do you determine the management of STEMI and what does the management consist of

A
  • PCI if pt presents <12h of onset AND primary PCI can be delivered within 120 minutes
  • Fibrinolytic treatment/thrombolysis (alteplase) - pts presenting within 12 hours when primary PCI cannot be delivered in 120 minutes
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38
Q

Management of NSTEMI and unstable angina

note these are managed the same as the troponin will not rise until later; often a retrospective diagnosis

A
  • Coronary angiography with follow-on PCI within 96h if GRACE score shows risk of cardiovascular events as imtermediate to high
  • patients who are clinically unstable are offered angiography as soon as possible
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39
Q

Describe the body’s response to MI

A

0-12h = Not visible; Myocyte necrosis
12 - 72h = Pale (<24h) –> Soft and pale (<72); Necrosis induces an acute inflammatory response - the neutrophils infiltrate between dead cardiac muscle
3-10 days = hyperaemic border; repair of the infarct - organisation
weeks - months = White scar; secondly progressive scar tissue deposition

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40
Q

How would an inferior MI be detected on ECG

A

ECG: leads II, III, aVF

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41
Q

How would a lateral MI be detected on ECG

A

ECG: leads I, aVL, V5-6

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42
Q

How would an anterior MI be detected on ECG

A

ECG: leads V1-4

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43
Q

Which artery is affected in an inferior MI

A

Right coronary artery

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44
Q

Which artery is affected in a lateral MI

A

Left circumflex artery

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45
Q

Which artery is affected in an anterior MI

A

Left anterior descending artery

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46
Q

Why do we worry about inferior MIs

A

Affects the RCA. Supplies the RA, RV, inferior LV and the pacemaker!

Worrying because it can affect the SAN

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47
Q

List short term complications of MIs

A
  • Ventricular fibrillation (causes sudden death)
  • Other arrythmias
  • Acute Cardiac Failure / cardiogenic shock
  • Myocardium Rupture
  • Pericarditis
  • Mural Thrombus (may embolise)
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48
Q

List long term complications of MIs

A
  • Recurrent MI
  • Chronic congestic cardiac failure (loss of contractile myocardium)
  • Dressler’s Syndrome
  • Ventricular aneurysm formation, which predisposes to: congestive cardiac failure, arrythmia, thrombus formation within the aneurysm (due to stasis) which may embolise
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49
Q

How does an MI result in acute cardiac failure

A

The infarcted myocardium no longer contracts and this may cause heart failure - or if a significant proportion of the myocardium is affected may lead to cardiogenic shock

Relates to the size of the infarct - usually >45% of the LV mass

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50
Q

Myocardium rupture is a consequence of MI, but what are the consequences of myocardium rupture

A

(1) Cardiac tamponade - rupture of the free wall
(2) acute LVF - rupture of the papillary muscle, causing acute mitral regurg (heart can’t compensate)
(3) Acute heart failure - rupture of the interventricular septum causing an acute ventricular-septal defect

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51
Q

Why does an MI predispose to the formation of a thrombus

A

A mural thrombus can form because there is:

  • endothelial injury (transmural infarct extends to involve the endothelium causing damage to the endothelium)
  • stasis (the infarcted myocardium does not contract and so there is an akinetic zone)
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52
Q

What is Dressler’s syndrome

A

A self-limiting autoimmune pericarditis 2-10 months after full-thickness MI.

In the era of PCI it is uncommon.

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53
Q

What is a reperfusion injury

A

Following PCI/thrombolysis.
The process of reperfusion may damage some myocytes that were not already dead when reflow occurred.

It is due to toxic oxygen species which are overproduced on restoration of the blood supply

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54
Q

What is chronic ischaemic heart disease

A

There is decreased perfusion to the myocardium as a result of a stable plaque = ischaemia = over a long time the contractile myocardial tissue is replaced by non-contractile scar tissue (progressive fine diffuse myocardial fibrosis)

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55
Q

How does chronic ischaemic heart disease present

A

Often asymptomatic as the remaining myocardium can compensate (LVH)

However they will eventually decompensate and there will be onset of progressive chronic heart failure

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56
Q

Define an ischaemic stroke

A

A sudden occlusion of a cerebral artery leading to a sudden reduction in blood flow to part of the brain = infarction of brain tissue

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57
Q

What is the most common cause of ischaemic stroke

A

Rupture of an atherosclerotic plaque in an internal carotid artery - a thrombus then forms on the surface of the ruptured plaque and part of the thrombus embolises and occludes a cerebral artery

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58
Q

Why are patients with AF at increased risk of ischaemic stroke

A

Stasis within the (left) atrium as a result to fibrillation (virchow’s triad) and this can result in a thrombus which may embolise to occlude a cerebal artery

Pts are anticoagulated to prevent this

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59
Q

Why are patients with infective endocarditis at increased risk of ischaemic stroke

A

Vegetations are present on the mitral or aortic valve - these can embolise and occlude a cerebral artery

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60
Q

Define an aneurysm

A

A localised, permanent, abnormal dilatation of a blood vessel by greater than at least 50% of its normal diameter

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61
Q

How can you classify aneurysms

A
  • Saccular = spherical shape, bulges out of side of vessel
  • Fusiform = Spindle shape, involvinf all the circumference of the vessel
  • False = an expanding pulsatile haematoma in continuity with a vessel lumen; it is not lined by endothelium
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62
Q

What is the clinical definition of an aortic aneurysm

A

Aortic diameter of >3cm

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63
Q

What are the main risk factors for atherosclerosis

A
  • Smoking
  • Dyslipidaemia
  • Hypertension
  • DM
  • FHx
  • Male
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64
Q

How does atherosclerosis result in development of an aneurysm

A

The aorta gets its strength from the media (smooth muscle layer)
enlarging atherosclerotic plaque = pressure/ischaemic atrophy of the media and loss of elastic tissue. As a consequence the aortic wall is weakened and it may dilate, forming an aneurysm, which over time will grow in size.

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65
Q

Causes of AAA

A
  • Atherosclerosis
  • Marfan
  • Ehler Danlos
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66
Q

What are complications of AAA

A
  • Rupture (as the radius increases so does the tension in the wall - Laplace’s law)
  • Thrombus + embolism
67
Q

Who gets AAA

A

Men (6:1)

>65

68
Q

What is the NHS AAA screening programme

A

Men aged 65

  • Small (3 - 4.4) / Medium (4.5-5.4) followed up to see if it grows
  • Large (>5.5) referred to a vascular surgeon
69
Q

What is the clinical significance of AAA >5.5cm

A

Classified as large

Risk of repair < risk of rupture

70
Q

What is the management of AAA >5.5cm

A

Open surgery, EVAR or conservative management

71
Q

In the case of pulmonary embolism where do the emboli originate

A

70-80% - vein in the leg

10 - 15% - vein in the pelvis

72
Q

What would be the result of a medium sized PE

A

Occlusion of a segmental pulmonary artery - V/Q perfusion defect

Results in respiratory compromise - usually manifests as pulmonary infarction.

73
Q

List clinical features of PE

A
  • Pleuritic chest pain
  • SOB
  • Haemoptysis (due to infarction of the non-perfused lung tissue)
  • Pleural rub
  • Crackles
  • Effusion
74
Q

Explain logistics of VTE prevention

A

Patients admitted to hospital have a documented VTE assessment.

They should be reassessed within 24hr of admission and whenever the clinical situation changes

75
Q

List examples of VTE prevention offered

A
  • Encourage to mobilise as soon as possible
  • Give information about VTE risk on admission and discharge
  • Mechanical interventions eg. antiembolism stockings
  • Dalteparin
76
Q

What tool assesses clinical likelihood of PE

A

The Wells criteria

Likely if >4 but unlikely if <4

77
Q

What is D-dimer

A

Made from the degradation of fibrin via the action of plasmin.

78
Q

What does a raised D-dimer indicate

A 
PE
MI
Post-operatively
Stroke
Trauma
Pregnancy
79
Q

What is more useful- a normal or a positive D dimer

A

Raised D-dimer can be caused by many things - not specific!

Normal is useful as >90% of these patients will not have a PE

80
Q

When should you test for D-dimer

A

PE is suspected clinically but the Wells score is <4

81
Q

What is the gold standard investigation for suspected PE

A

CTPA (or V:Q scan if allergy to contrast media or renal impairment)

Involves injecting radio-contrast into the circulation and a CT scan is performed. Blood vessels are filled with blood mixed with contrast so appear white, but a thrombus will appear as a darkened area because it formed before the contrast was administered

82
Q

Pt has a suspected PE and a Wells score of 6 - how do you investigate?

A

CTPA

83
Q

Pt has a suspected PE and a Wells score of 2- how do you investigate

A

D-dimer

84
Q

What is hypertension

A

Raised blood pressure in the systemic vascular bed

> 140/90mmHg

85
Q

List causes of hypertension

A

95% Essential

5% Secondary

86
Q

List causes of essential hypertension

A

Genes - those encoding angiotensinogen, renin and atrial natriuretic peptide receptor genes
Environmental - stress, diet, intrauterine environment (eg. low birth weight)

87
Q

List causes of secondary hypertension

A

(1) Chronic renal disease- CKD, renal artery stenosis, PKD, acute glomerulonephritis, autoimmune disease
(2) Coarctation of the aorta
(3) Endocrine diseases- Cushing’s syndrome, Conn’s syndrome, phaeochromocytoma, acromegaly
(4) Drugs- steroids, COCP, NSAIDs
(5) Pregnancy

88
Q

What are the clinical features of hypertension

A

Clinically silent until a complication occurs

89
Q

What are the effects of hypertension of blood vessels

A
  • Accelerates atherosclerosis

- Accelerates arteriosclerosis

90
Q

What is arteriosclerosis

A

Hardening of an artery / arteriole

Two types:

  • Hyaline - SMC replaced by collagen
  • Hyperplastic - characteristic of malignant hypertension. The very high BP causes fibrinoid necrosis in the vessel wall - tries to heal = proliferation of intimal cells
91
Q

What effect does hypertension have on the heart

A
  • Accelerates coronary artery atherosclerosis (worsens IHD)

- Left ventricular hypertrophy

92
Q

Why does hypertension lead to LVH

A

(1) The LV has to push harder against the increased pressure in the systemic circulation in order to eject blood into the aorta.
(2) Therefore the LV undergoes compensatory LVH
(3) As this progresses there is increasing metabolic demands of the myocardium - but the heart is less able to meet these as
(A) hypertrophy renders the myocardium stiff
(B) increasing distance across which O2 has to cross
(C) Accelerated atherosclerosis due to HTN

93
Q

List ways in which hypertensive heart disease may manifest

A
  • Myocardial ischaemia
  • Myocardial infarction
  • Arrhythmias (eg. AF)
  • Progressive left heart failure
94
Q

What is the commonest cause of AF

A

Hypertension

95
Q

Why is AF dangerous

A

(1) Thrombi may form in the atria as a consequence of stasis. These thrombi may embolise.
(2) CO may fall due to loss of normal atrial contraction

96
Q

How does hypertension lead to hypertensive renal disease

A

Progressive hyaline arteriosclerosis in the renal arterioles = chronic, progressive renal ischaemia.

Ischaemia results in development of CKD.

This is a viscous cycle as CKD can in turn worsen the HTN

97
Q

What is the difference between atherosclerosis and arteriosclerosis

A 
Arteriosclerosis = a general term describing a hardening of a medium or large artery.
Atherosclerosis = a hardening of an artery specifically due to an atheromatous plaque.
98
Q

How would you investigate suspected CKD

A

USS - shows small kidneys (due to atrophy and fibrosis)

99
Q

What is the most common cause of an intracerebral haemorrhage (note: presents as a haemorrhage stroke)

A

Hypertension

100
Q

Describe pathophysiology behind a haemorrhagic stroke

A

Haemorrhage is due to the rupture of Charcot-Bouchard aneurysms - weakened by long-standing HTN

101
Q

Describe pathophysiology of a subarachnoid haemorrhage

A

Due to rupture of a Berry aneurysm

102
Q

How do berry aneurysms develop

A

Under the influence of HTN and atherosclerosis in people with a congenital weakness in the media of cerebral vessels.

103
Q

What is malignant hypertension

A

A markedly raised diastolic blood pressure (>130 - 140) and end organ damage

104
Q

Who does malignant hypertension usually affect

A
  • Usually in cases of secondary HTN

- Younger people = new cases 30-40y/o

105
Q

What are clinical consequences of malignant hypertension

A

1) Acute left ventricular failure
2) Stroke (cerebral haemorrhage)
3) Acute renal failure
4) Blurred vision - due to retinal haemorrhage/exudates/papilloedema
5) Hypertensive encephalopathy (headache, irritability, alteration in consciousness)
6) Microangiopathic haemolytic anaemia and DIC

106
Q

What is an aortic dissection

A

There is a tear in the intima. A split forms in the media and blood tracks in the newly formed “false lumen”

107
Q

How does an aortic dissection present

A

Classically a tearing pain between the shoulder blades with HTN and asymmetrical pulses

108
Q

What are major risk factors for aortic dissection

A
  • HTN
  • Abnormal media (eg. marfans / ehler-danlos)
  • Pregnancy
109
Q

How are aortic dissections classified

A

Type A: Ascending aorta

Type B: Does not involve the ascending aorta

110
Q

What type of aortic dissection is most dangerous

A

Type A are more serious

111
Q

How are aortic dissections managed

A

Type A: immediate surgical repair

Type B: Medical - rigorous BP control with surgery reserved for if there are complications

112
Q

How do aortic dissections cause disease

A

False lumen reduces blood flow through the true lumen - this may extend into other arteries and cause ischaemia/infarction of the organ supplied by that artery

Dissection may rupture internally into the pleural cavity, pericardial space or abdominal space

113
Q

What are complications of type A aortic dissections

A

Can compromise blood flow along branches of the aorta as it spreads along its length.
It may even track back to the root of the aorta and rupture into the pericardium causing cardiac tamponade.
Involves the root fo aorta = aortic regurg
Rupture into thoracic / abdominal cavity = exsanguination

114
Q

What is cardiac tamponade

A

When fluid in the pericardium builds up and results in compression of the heart.

115
Q

What is the role of the heart valves

A

Ensure one way flow through the heart

116
Q

What are the 2 main types of mechanical defects in the heart valves

A

Stenosis - the failure of a valve to open completely (impairs forward flow). Usually as a result of a chronic process.
Regurgitation - failure of a valve to close completely (reverse flow). May be as a result of an acute or chronic process.

117
Q

What is the most common valve disease

A

Aortic stenosis

Mitral regurg is the 2nd most common

118
Q

List common causes of aortic stenosis

A

1) Cusp calcification of a bicuspid valve (note that the normal aortic valve is tricuspid, but 1-2% of the population have a bicuspid aortic valve)
2) Age related calcification of a tricuspid valve
3) Post rheumatic fever disease

119
Q

Explain pathophysiology behind aortic stenosis

A

Blood flow across the aortic valve is impeded during systole. As a consequence a significantly elevated left ventricular pressure is necessary to drive blood into the aorta. As this is a chronic process, the LV hypertrophies to compensate. The hypertrophy reduces compliance = elevation of diastolic LV pressure.

120
Q

Describe clinical presentation of aortic stenosis

A

A chronic procress with compensatory changes meaning there is a long asymptomatic period.
Eventually, the heart decompensates and presents with the classic triad of:
- Angina
- Syncope on exertion
- Development of congestive cardiac failure

It also is associated with an ejection systolic murmur

121
Q

What is the most likely cause of an ejection systolic murmur

A

Aortic stenosis

122
Q

List common causes of mitral regurgitation

A

MITRAL ANNULUS: LV dilatation (secondary stretching of the valve ring such that it cannot close properly)
CUSPS: Mitral valve prolapse; infective endocarditis; post-rheumatic fever
PAPILLARY MUSCLES: Rupture post-MI; ischaemia due to coronary artery atheroma

123
Q

What is the most common cause of acute mitral regurgitation

A

Sudden onset = infective endocarditis / rupture of papilliary muscle after an MI

124
Q

Explain the pathophysiology of acute mitral regurgitation

A

Sudden onset - the heart does not have time to undergo compensatory changes.
Blood flows back into the left atrium.
Increased pressure in the LA - and therefore also in the pulmonary system.
Transudation of fluid from the circulation into the lung interstitium and alveoli (pulmonary oedema).

125
Q

What is the most common cause of chronic mitral regurgitation

A

Dilatation of mitral valve ring, mitral valve prolapse, post-rheumatic fever or papilliary muscle ischaemia.

126
Q

Explain the pathophysiology of chronic mitral regurgitation

A

Gradual onset = heart has time to undergo compensatory changes.
LA dilates such that it can accomodate the back flow of blood without a substansial increase in LA pressure.
The LV undergoes hypertrophy - mitigates the effects of regurgitation
Asymptomatic for years - eventually LV decompensates and pts progress to left ventricular failure

127
Q

What is the most common cause of mitral valve regurgitation

A

Mitral valve prolapse

128
Q

Who gets mitral valve prolapse

A

Women > men
Usually an isolated finding
May be a complication of marfans/ehlers-danlos (genetic disorders of tissue synthesis)

129
Q

What is the pathophysiology behind mitral valve prolapse

A

The normal dense collagen and elastic matrix of the valve is replaced with loose myxomatous connective tissue containing abundant glycosaminoglycans (‘myxomatous degeneration’). The leaflets become enlarged and one of the leaflets ‘prolapses’ back into the La during systole

130
Q

What is the mortality of infective endocarditis

A

High
Untreated = 100%
Treated = 10-30%

131
Q

List causes of infective endocarditis

A

Bacterial (usually)
- streptococcus = S. viridans (weakly pathogenic)
- Staph = staph A (highly pathogenic), most common in IVDUs - usually affects the tricuspid valve.
Other bacteria eg. g-ve = E. Coli
Less commonly, fungi = candida / asperillis. This is more likely in immunocompromised, IVDU, pts with indwelling venous line

132
Q

Describe pathogenesis of infective endocarditis

A

Episode of bacteriaemia = bacteria delivered to the heart.
(could be due to tooth brushing / surgery)
Organisms adhere to and invade the valve

133
Q

What conditions must be fulfilled in order for an infection of the endocardium to occur

A

1) Highly pathogenic organism (staph) colonising a normal valve
OR
2) Weakly pathogenic (strep) colonising an abnormal valve - eg. prosthetic / mitral or aortic regurg / mitral valve prolapse

134
Q

What is a vegetation and how do they form in infective endocarditis

A

A thrombus containing microorganisms.

As the organisms on the valves replicate, they become enmeshed within layers of platelets and fibrin on the valve surface forming vegetations.

135
Q

What components of Virchows triad occur in infective endocarditis

A

Endothelial injury. if the valve is abnormal, there may be turbulent blood flow across the valve.

136
Q

What are 3 complications of infective endocarditis

A

1) Disturbance of valve function (valve is destroyed by infection = regurg)
2) Embolism (vegetations can break off and embolise - mostly present as a stroke)
3) Formation of antigen-antibody immune complexes (antibodies made againts the antigen of the infection causing microorganism - can be deposited in the glomeruli = activates complement)

137
Q

How would you confirm a diagnosis of infective endocarditis

A
  • Blood cultures = at least 3 sets of blood cultures from different sites taken a minimum of 1h apart and before starting antibiotics (confirms diagnosis and guides appropriate ABx therapy)
  • Transoesophageal echo to identify vegetations and complications
138
Q

What criteria are used to help diagnose infective endocarditis

A

Duke’s (this criteria places heavy emphasis on blood culturs and echo)

139
Q

What is heart failure

A

A syndrome which occurs when the pumping action of the heart is inadequate for the needs of the body. Ie. the cardiac output is unable to meet the metabolic needs of the tissue

140
Q

What is the mortality of heart failure

A

30% in first year

10% after

141
Q

How can you classify heart failure

A

Acute / Chronic (depends on speed of onset)

Left / Right (depends on dominant site of injury)

142
Q

Describe pathophysiology of acute left heart failure

A

Sudden major insult to the left side of the heart
no time for compensation, CO falls catastrophically
Sudden failure of LV leads to severe congestion in the pulmonary venous system and rapid accumulation of fluid in the alveolar spaces and interstitium. This causes pulmonary oedema and presents as severe SOB. In bad cases there is underperfusion of organs = cardiogenic shock

143
Q

What is acute left heart failure most often caused by

A

A complication of an MI affecting the LV

  • extensive MI renders a large volume of the LV non-functional
  • rupture of a mitral valve papilliary muscle
  • development of an arrythmia
144
Q

What is the most common form of heart failure

A

Chronic left heart (ventricular) failure

145
Q

What are the common causes of chronic left heart failure

A

Damage to the LV slowly:

  • chronic ischaemic heart disease (due to coronary artery atherosclerosis)
  • systemic HTN
  • valvular (mitral/aortic) heart disease
146
Q

What is the relevance of heart disease occurring acute vs chronic

A

Can help you to determine cause.
Chronic disease means that compensation (hypertrophy) can occur and therefore there will be a period where the patient is asymptomatic, before they decompensate

147
Q

Explain pathophysiology of chronic left ventricular failure

A

It is a progressive disorder in which a viscious cycle becomes established which escalates cardiac workload and worsens the degree of LVF.
Because poor cardiac output reduces tissue perfusion, the body responds by increasing the SNS - activates RAAS
Sodium and water retention - which leads to more myocardial stress and declining cardiac function

148
Q

Explain what decompensation means in the context of chronic heart failure

A

Patients may decompensate if the heart is stressed.
Patients with chronic heart failure frequently experience episodes of acute worsening in their symptoms = relapsing-remiting course (acute decompensation) - commonly seen when a concurrent illness (usually trivial) places additional burden on a critically failing heart

149
Q

Chronic left ventricular failure can be split into systolic and diastolic. What is the difference

A

Systolic: the underlying problem is a failure of the pumping action of the ventricle during systole. The ventricle is usually dilated and fails to contract normally such that the ejection fraction is reduced.
Diastolic: failure of the ventricle to fill due to increased stiffness of the wall

150
Q

How do you investigate chronic left ventricular failure

A

1) History and Examination
2) ECG (usually abnormal)
3) CXR (cardiomegaly)
4) Echo (to confirm systolic or diastolic dysfunction and see if underlying cause eg. valvular disease)
5) BNP level

151
Q

What is BNP

A

A hormone secreted by ventricular myocytes in response to volume and pressure overload of the LV. Its normal function is to promote a salt and water diuresis by the kidney.

152
Q

What is the most common cause of right sided heart failure

A

Left sided heart failure. As the definition for right heart failure is when it develops in the absence of left heart failure, this is not actually right heart failure and is called congestive (biventricular) heart failure

153
Q

What is the most common cause of acute right sided heart failure

A

A massive pulmonary embolism causing sudden blockage of a major pulmonary bifurcation (saddle embolus)

An MI involving the right ventricle, but sparing the left is another important cause

154
Q

How can a massive PE result in acute right heart failure

A

Blocks a major pulmonary bifurcation. This causes the pressure in the pulmonary artery system to rise dramatically = development of pulmonary HTN. The heart does not have time to undergo compensation and can’t generate enough force to maintain an output

155
Q

How does acute right heart failure present clinically

A

Circulatory collapse, shock and/or instantaneous death

156
Q

What is pulmonary hypertension

A

An increase in blood pressure in the pulmonary vasculature. It is defined as a resting mean pulmonary artery pressure at or above 25mmHg

157
Q

What are the clinical features of chronic right heart failure

A

Raised JVP, hepatomegaly, ascites, peripheral oedema

158
Q

What are the most common causes of chronic right heart failure

A 
Lung diseases:
- COPD
- Pulmonary fibrosis
- Recurrent small PEs
The damage to the lungs results in pulmonary HTN, but there is time for compensation to occur.
159
Q

What is cor pulmonale

A

Right heart failure due to lung disease:

  • massive PE = acute cor pulmonale
  • COPD, pulmonary fibrosis, recurrent small PEs = chronic cor pulmonale
160
Q

What is the most common cause of cor pulmonale

A

COPD

161
Q

What is a non-massive PE and how does it present

A

A medium-sized embolus occludes a segmental pulmonary artery. This results in a segment of lung being ventilated but not perfused ie. V/Q defect = Respiratory compromise, manifests as pulmonary infarction (haemopytsis) +/- pleuritis/effusions

162
Q

What is a massive PE and how does it present

A

A massive embolus occludes a proximal pulmonary artery. Result = blood unable to enter lungs = sudden pulmonary HTN - acute right heart failure. Blood is also unable to pass through the lungs = decreased filling of left side of the heart and therefore decreased left ventricular output. This presents as haemodynamic compromise in the form of shock, collapse and sudden death.

163
Q 
A patient presents to A+E. They have recently collapsed.
O/E:
- Tachycardia
- Hypotension
- Raised JVP
- RV heave
- Normal chest examination
- Low O2 sats

What is wrong with them

A

Haemodynamic compromise due to massive PE

164
Q

What are recurrent small PEs and how do they present

A

Usually subclinical. But will gradually result in pulmonary HTN and can result in chronic right heart failure

Cellular pathology (8 decks)

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