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IOD - Cell Pathology > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

What is haemostasis?

A

Haemostasis occurs when there is damage to a blood vessel.
- It involves the formation of a solid plug from the constituents of the blood
- It stops loss of blood from the circulation at the site of damage
It is a good thing
- it is physiological.

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2
Q

What is the role of fibrin?

A

stabilises the loose platelet plug to form a stable (secondary) platelet plug.

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3
Q

What can initiate the clotting cascade?

A

exposure of tissue factor initiates the coagulation cascade –> formation of insoluble fibrin.

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4
Q

What does endothelial injury lead to?

A

• Endothelial injury leads to adhesion and aggregation of platelets
–> Formation of a loose (primary) platelet plug

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5
Q

What is fibrinolysis?

A
  • The haemostatic plug is then broken down by activation of the fibrinolytic system.
    • Fibrinolysis is activated by the same injury that initiates homeostasis.
    • Plasminogen is converted to plasmin. Plasmin degrades insoluble fibrin to soluble products.
    • The fibrinolytic system ensure that haemostasis is very tightly regulated and limited to the site of injury.
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6
Q

FIbrinolysis equation?

A

Plasminogen ( + tissue plasminogen activator and urokinase-like plasminogen activator) –> Plasmin.

Plasmin then breaks down fibrin into soluble products.

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7
Q

What is a thrombus made up of?

A
  • A thrombus is made up of the same components as a haemostatic plug i.e. platelets, fibrin and red blood cells.
    • Thrombosis is pathological
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8
Q

What is a thrombus?

A

inappropriate activation of haemostasis:
- Platelets and the coagulation system interact with the vessel wall to form a solid plug (=thrombus) in the blood vessel.

i.e. too much clotting, not enough breakdown.

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9
Q

How does a clot differ from a thrombus?

A

Thrombus:

  • composed of RBCs, fibrin and platelets.
  • Forms within the CVS system
  • Forms in flowing blood i.e. during life.

Clot:

  • Composed of red blood cells and fibrin (no platelets)
  • Forms outside the CVS system (e.g. in a test tube)
  • Forms in stationary blood during or after life.
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10
Q

What is virchows triad?

A
  1. Endothelial injury
    1. Abnormal blood flow
    2. Hypercoagulability
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11
Q

Overall, which is the most important risk factor in arterial thrombosis?

A

Atherosclerosis

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12
Q

Overall, which is the most important risk factor in venous thrombosis?

A

Stasis and hypercoagulability

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13
Q

What are the main complications of thrombi?

A
  1. Partial occlusion
  2. Complete occlusion - stasis proximal to that
  3. Embolism - at a distant site.
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14
Q

What is ischaemia?

A

Tissue dysfunction due to interference with blood flow (supply or damage) to a tissue. It is reversible. - hasn’t completely died, if the body can restore the blood flow that part can restore its function

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15
Q

What is infarction?

A
  • Tissue death (necrosis) due to interference with blood flow (supply or drainage) to a tissue. It is irreversible.
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16
Q

What is atherosclerosis?

A

• Atherosclerosis is a chronic inflammatory process centred on the intima (endothelium) of large and medium sized arteries

Atherosclerotic plaques are composed of a core of lipid debris with foam cells and lymphocytes. The roof is formed by a fibrous cap.

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17
Q

What are the risk factors for atherosclerosis?

A

• It is initiated by endothelial injury which is caused by well known risk factors including:
○ Smoking
○ Hypertension
○ Diabetes
Dyslipidaemia (abnormal lipoprotein levels ie. High ratio of LDL:HDL)

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18
Q

Stable Angina

A

occurs gradually with time.

- Central chest pain, constricting belt, or someone stamping on the chest, radiates down the left arm, neck and jaw, and around the scapula. 
- Exercise/exertions/emotions/ rise in cortisol in the morning makes it worse 
- Resting makes it better
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19
Q

What are the ANS features associated with angina?

A
  • Sweating
  • Palpitations
  • Pale
    Nausea
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20
Q

Cause of stable angina?

A

stenosis due to a stable plaque in a coronary artery .

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21
Q

What does a raise in troponin show?

A

Troponin I - Used as marker - seen in MI. Shows that there has been a heart attack.
Troponin shows myocyte death, when you get the damage you get an inflammatory response therefore the number of neutrophils increases.

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22
Q

What 3 conditions make up ACS?

A

Unstable Angina
STEMI
NSTEMI

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23
Q

What is ACS?

A

• A spectrum of clinical conditions which occur when there is a sudden severe reduction in myocardial perfusion -> ischaemia or infarction
• Pathology: acute change in a coronary artery atherosclerotic plaque
- Typically there is erosion or rupture of the plaque with overlying thrombosis, often accompanied by marked spasm of the vessel.

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24
Q

How ACS confirmed?

A
  • Clinical features
    • ECG changes (presence or absence of ST elevation)
    • Cardiac troponin levels
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25
Q

Which conditions that are part of ACS show non-ST elevation?

A

Unstable Angina
Non-STEMI

Unstable angina and NSTEMI occur when there is partial occlusion of a coronary artery:
• This results in ischaemia or infarction of the myocardium supplied by the affected coronary artery
• Unstable angina and NSTEMI differ mainly in the severity of myocardial ischaemia:
- In NSTEMI the ischaemia is severe enough to result in release of cardiac troponins into blood

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26
Q

Which condition that are part of ACS shows ST elevation?

A

STEMI

STEMI occurs when there is complete occlusion of a coronary artery
• ST elevation and raised troponin (greater than in NSTEMI)
There is transmural infarction of the myocardium supplied by the affected coronary artery

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27
Q

What are the possible outcomes of acute inflammation?

A
  1. Regeneration (resolution)
  2. Repair with scarring
  3. Progression to chronic inflammation
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28
Q

What are the complications of MI?

A

VF - related to the release of potassium.

other arrhythmias seen are bradycardia, ventricular tachycardia, supraventricular tachycardia.

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29
Q

Which parts of the heart does the RCA supply?

A

Right atrium
Right ventricle
Pacemaker
Inferior Left ventricle

Therefore occlusion = Inferior MI
ECG leads II, III AVF

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30
Q

Which parts of the heart does the Left circumflex artery supply?

A

Lateral left ventricle
therefore occlusion = Lateral MI
ECG leads I, aVL, V5-6

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31
Q

Which parts of the heart does the Left anterior descending artery supply?

A

Anterior left ventricle
Therefore occlusion = Anterior MI

ECG leads V1-4

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32
Q

Why does occlusion of the RCA more commonly lead to arrhythmias?

A

The right coronary artery supplies the inferior LV and the pacemaker.
Thus, inferior Mis are more likely to be associated with arrhythmias than other types of Mis

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33
Q

What is a cardiac tamponade?

A

Fluid/blood in the pericardium

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34
Q

What is a ventricular septal defect?

A

An abnormal opening in the wall between the 2 ventricles

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35
Q

What can rupture of the papillary muscles of the mitral valve cause?

A

Mitral regurgitation

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36
Q

What is pericarditis?

A

• A transmural infarct extends to involve the pericardium, inciting an inflammatory response.
Reaction to the underlying myocyte damage

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37
Q

What are the short term complications of an MI?

A

Short term:

  • Sudden death (usually VF)
  • Other arrhythmias (bradycardia, SVT, VT)
  • Muscle rupture (papillary muscle, interventricular septum, free wall)
  • Acute ventricular failure or cardiogenic shock
  • Mural thrombus
  • Acute pericarditis
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38
Q

What are the long term complications of an MI?

A
  • Progression to chronic heart failure
    • Recurrent MI
    • Ventricular aneurysm
    • Dressler’s syndrome (Usually a self-limiting autoimmune pericarditis 2-10months after full-thickness MI)
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39
Q

What is pleuritic chest pain?

A 
Pleuritic chest pain: 
	• Pain worse when they breath in 
	• Worse when they cough 
	• Pulmonary embolism - major cause. 
Always examine the calf of the patient as can see a PE due to a deep vein thrombosis.
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40
Q

Pulmonary embolism

A 
• Pulmonary embolism is almost always due to transportation of thrombus in the bloodstream which then impacts in a pulmonary artery. 
	• The thrombus may originate in the: 
	- Leg (80%) - deep vein thrombosis 
	- Pelvis 
	- Arm 
Right ventricle
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41
Q

What system is used to assess if an individual is likely to have a PE?

A

Wells score

more than 4 points = likely PE
4 or less = PE less likely

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42
Q

What is an ischaemic stroke?

A

The sudden occlusion of the cerebral artery is most often due to atherosclerosis

• Most commonly, an atherosclerotic plaque in an internal carotid artery ruptures and thrombus forms on the surface of the plaque.  Part of the thrombus embolises  and occludes one of the cerebral arteries resulting in a stroke
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43
Q

What is hypertension?

A

Hypertension refers to raised blood pressure in the systemic vascular bed. BP >140/90 mmHg (systolic pressure > 140 or diastolic pressure >90)

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44
Q

What are the causes of hypertension?

A

Hypertension may be either essential (primary) or secondary

Essential (95%):
- diagnosed in absence of an identifiable secondary cause.

Secondary:

  • Chronic renal disease (e.f. CKD, polycystic kidney disease, autoimmune like vascilitis)
  • Coarctation of aorta
  • Endocrine disease (e.g. cushing’s conn’s, phaemochromocytoma, acromegaly)
  • Drugs: - steroids, OCP, NSAIDs
  • Preganancy (pre-eclampsia)
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45
Q

Effects of HTN of vessels?

A

Hypertension accelerates atherosclerosis (remember, hypertension is one of the major modifiable risk factors of developing atherosclerosis

46
Q

HTN effects on heart?

A

Hypertension has a number of adverse effects on the heart:
• It accelerates coronary artery atherosclerosis
○ This worsens ischaemic heart disease.
• It causes left ventricular hypertrophy
• The LV has to push harder against the increased pressure in the systemic circulation in order to eject blood into the aorta. Therefore the LV undergoes compensatory left ventricular hypertrophy. The patient may be asymptomatic during this period of compensation.
• As the left ventricular hypertrophy progresses there is increasing metabolic demand of myocardium. However, the heart becomes progressively less able to meet the demands because:
§ The myocardium capillary bed does not expand in tandem with the increased myocardium O2 demand, thus increasing distance across which O2/nutrients must diffuse.
§ Accelerated atherosclerosis (due to hypertension)
• Eventually the hypertrophied LV will decompensate and fall (left heart failure)

47
Q

HTN effect on the kidneys?

A

Progressive hyaline arteriosclerosis in the renal arterioles cause chronic and progressive renal ischaemia. This results in tubular atrophy, interstitial fibrosis and progressive glomerular sclerosis. In turn, this leads to the development of progressive chronic kidney disease (CKD).
A vicious cycle is established: Hypertension causes CKD which in turn worsens the hypertension.
Ultrasound will show small kidneys - they are small because of atrophy and fibrosis.

48
Q

HTN effects on the eyes?

A

Hard exudates
Cotton wool spots
Papilloedema
Flame haemorrhage

49
Q

What is malignant/accelerated HTN?

A

This is a clinicopathological syndrome characterised by a markedly raised diastolic pressure (usually >130-140mmHg) and end organ damage.

50
Q

When does malignant HTN occur?

A

It occurs in less than 1% patients with primary hypertension but more commonly in cases of secondary hypertension (especially when due to renovascular disease)
Malignant hypertension usually affects younger people with hypertension; new cases usually present at 30-40yrs of age.

51
Q

What is the underlying pathology of malignant HTN?

A

The underlying pathogenesis is poorly understood.
The characteristic histological lesion is hyperplastic arteriosclerosis there is also fibrinoid necrosis of small arteries and arterioles.

52
Q

Clinical consequences of malignant HTN?

A

Clinical consequences include:
• Acute left ventricular failure
• Stroke (cerebral haemorrhage)
• Acute renal failure
• Blurred vision (due to retinal haemorrhages/exudates and papilloedema)
• Hypertensive encephalopathy (headache, irritability, alteration in consciousness)
• Microangiopathic haemolytic anaemia and disseminated intravascular coagulation (DIC).

53
Q

Renal damage and encephalopathy in malignant HTN?

A

The renal damage and encephalopathy are due to failure to protect the microcirculation form the increased pressure. i.e. there is a breakdown of the normal autoregulation mechanism
- It is rare in elderly people because the cerebral autoregulatory curve is shifted to the right. Thus, arteriosclerosis protects against the development of the renal damage and encephalopathy. [However, the greatly increased susceptibility to hypotension accounts for the increased mortality of shock in elderly and hypertensive patients].
It is more common in young people whose arteries are unprotective by arteriosclerosis.

54
Q

Malignant HTN and effects on kidney

A

Failure of autoregulation in the kidney transmits increased pressure to the glomeruli, causing fibrinoid necrosis and microaneurysm formation in glomerular capillaries. The pressure also causes fibrinoid necrosis of afferent glomerular arterioles, which may rupture or be associated with luminal thrombosis, resulting in small renal infarcts. Thrombosis causes damage to red blood cells - microangiopathic haemolytic anaemia. Ischaemia of the juxtaglomerular apparatus leads to increased secretion of renin, which further increases blood pressure, leading to a vicious cycle. Together these effects give rise to proteinuria and haematuria. Similar changes occur in the brain in hypertensive encephalopathy.

55
Q

What is aortic dissection?

A

Aortic dissection occurs when there is a tear in the intima. A split forms in the media and blood tracks in the newly formed “false lumen”

56
Q

What is the clinical presentation of aortic dissection?

A

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

57
Q

What are the major risk factors for aortic dissection?

A

Major risk factors:
• Hypertension
• Abnormal media e.g. Marfan’s syndrome, Ehlers-Danlos syndrome
* Pregnancy

58
Q

How are aortic dissections classified?

A

Classification of aortic dissection:
Aortic dissections are classified into type A and type B:
• Type A dissection involves the ascending aorta
• Type B dissection does not involve the ascending aorta.

Type A dissections are generally more serious than type B dissections and so the management of type A dissections is more aggressive:
• Type A dissections generally require immediate surgical repair
• Type B dissections generally are managed medically (rigorous BP control) with surgery reserved for if there are complications.

59
Q

How do aortic dissections cause disease?

A

There are two main ways in which dissection causes disease:

  1. The false lumen reduces the blood flow through the true lumen. The dissection may extend into other arteries and cause ischaemia/infarction of the organ supplied by that artery.
  2. The dissection may rupture externally into the pleural cavity, pericardial space or abdominal space.
60
Q

What are the complications of aortic dissection?

A

In a type A dissection, the false lumen may compromise blood flow along branches of the aorta as it spreads along its length: e.g. carotid dissection–> stroke, coronary dissection –> MI.
The dissection may track back to the root of the aorta and rupture into the pericardium, causing cardiac tamponade. Also, a dissection involving the root of the aorta may cause stretching of the aortic valve, leading to the onset of acute aortic regurgitation.

The dissection may rupture externally into the thoracic or abdominal cavity, causing exsanguination. Similar principles can be followed to predict the complications of type B dissections.

61
Q

What are the complications of type A dissections?

A
  • Occlusion of carotid artery leading to stroke.
  • Exsanguination
  • Stretching of the aortic valve leading to aortic regurgitation
  • Rupture into the pericardium leading to cardiac tamponade
  • Occlusion of the coronary artery leading to myocardial infarction.
62
Q

What are the complications of type B dissections?

A
  • Renal artery occlusion leading to renal failure
  • Extension into iliac arteries leading to lower limb ischaemia
  • Coeliac or mesenteric artery occlusion leading to gut ischaemia
63
Q

What is stenosis of a heart valve?

A

• Stenosis:

  • Failure of a valve to open completely –> impede forward flow. [There is also usually failure of full valve closure]
  • Stenosis is virtually caused by a chronic process. The gradual development of stenosis allows time for compensatory changes in heart, blood vessels and other organs.
64
Q

What is regurgitation of a heart valve?

A

• Regurgitation (incompetence)
○ Failure of a valve to close completely –> reverse flow occurs
○ Regurgitation may be caused by an acute or chronic process.

NB: There may be mixed stenosis and regurgitation.

65
Q

What is the most common valve disease?

A

Aortic stenosis

66
Q

What is the prevalence of aortic stenosis?

A

Aortic stenosis is the most common valve disease in developed countries. The prevalence of clinically significant aortic stenosis in patients over 70 years old in Europe is about 1-3%.

67
Q

What are the common causes of aortic stenosis?

A

Common causes:
• Age-related calcification of a normal valve.
○ The normal aortic valve has three leaflets
○ Cumulative “wear and tear” due to valve movement over many years leads to endothelial and fibrous damage, causing gradual calcification and stenosis of an otherwise normal valve.
• Cusp calcification of a bicuspid valve
○ Bicuspid valve is a congenital abnormality in which the valve is made up of two leaflets. It occurs in about 1-2% of the population and has a strong association with aortic coarctation.
○ It is thought that years of turbulent flow across the abnormal valve disrupt the endothelium and collagen matrix of the leaflets, resulting in gradual calcium deposition. The calcification develops by approximately 30yrs, with progressive stenosis.
Post rheumatic valve disease (rare in the UK)

68
Q

What is the pathophysiology of aortic stenosis?

A

As stenosis progresses, blood flow through the aortic valve becomes more and more impeded during systole. i.e. there is development of the left ventricle (LV) outflow obstruction. In order to maintain cardiac output, the LV must produce more force to drive blood through the aortic valve and into the aorta. Since aortic stenosis develops over a chronic course, the LV is able to do this by undergoing compensatory hypertrophy.
i.e. gradual development of LV outflow obstruction causes gradual pressure overload of LV and results in compensatory LV hypertrophy.

However, the hypertrophy reduces the compliance of the ventricle. The resulting elevation of diastolic LV pressure also causes LA hypertrophy in order to fill the “stiff” LV.

As a consequence of the compensatory changes, there is a long asymptomatic period.

Eventually the heart decompensates and there is deterioration in cardiac function, leading to the development of symptoms.

69
Q

What is the clinical presentation of aortic stenosis (triad)?

A

The classic clinical presentation of aortic stenosis if the triad of:
• Angina
• Syncope on exertion
• Development of congestive cardiac failure.
[AS is also an important cause of unexpected sudden death (due to arrhythmias)]
Once symptoms develop, there is marked reduction in survival. There is no effective medical treatment. The two options for valve intervention ae conventional aortic valve replacement and transcatheter aortic valve implantation

70
Q

What type of murmur is heard in aortic stenosis?

A

AS is an ejection systolic murmur.

71
Q

What is aortic sclerosis?

A

Its is the thickening and calcification of aortic valve leaflets without motion restriction i.e. the valve still opens and closes normally.

72
Q

What is the second most common valve lesion?

A

Mitral regurgitation

73
Q

What are the common causes of mitral regurgitation?

A 
Mitral annulus (valve ring) 
- LV dilatation (e.g. due to any cause of left ventricular failure) causes secondary stretching of the valve ring so that the valve cannot close properly. Often called secondary or functional MR because the papillary muscles, chordae and valve cusps are usually intrinsically normal.

Cusps

  • mitral valve prolapse
  • infective endocarditis
  • post rheumatic fever (scarring and fusion of cusps) [rare in the UK]

Papillary muscles

  • Rupture post MI
  • Ischaemia due to coronary artery atheroma (impaired contraction of the papillary muscle causes failure of complete valve disclosure).
74
Q

Acute mitral regurgitation

A

Mitral regurgitation of sudden onset is usually due to infective endocarditis or rupture of a papillary muscle after a myocardial infarction. When there is sudden onset of mitral regurgitation, the heart does not have time to undergo compensatory changes.

As a consequence, blood flows back into the left atrium, causing the pressure in the LA to rise. The high pressure in the LA is transmitted backwards into the pulmonary circulation and the high pressure in the pulmonary circulation causes transudation of fluid from the circulation into the lung interstitium and alveoli (pulmonary oedema) i.e. acute left heart failure.

75
Q

Pathophysiology of acute mitral regurgitation

A

sudden onset of MR –> blood flows back into the left atrium –> increased pressure in the LA –? increased pressure in the pulmonary circulation –> transduction of fluid from the circulation into the lung interstitium and alveoli (pulmonary oedema)

76
Q

Chronic mitral regurgitation

A

Mitral regurgitation of gradual onset may be due to dilatation of the mitral valve ring, mitral valve prolapse, post-rheumatic fever or papillary muscle ischaemia.
When there is gradual onset of mitral regurgitation, the heart has time to undergo

77
Q

What compensatory changes can be made in chronic mitral regurgitation?

A

compensatory changes:
• The LA dilates so that is can accommodate the back flow of blood without a substantial increase in LA pressure
• The LV undergoes hypertrophy, which mitigates the effects of regurgitation.

These compensatory changes maintain CO at near-normal levels so that the patient may be asymptomatic for many years.

Eventually, the left hypertrophies LV begins to decompensate (i.e. its function deteriorates) and there is development of progressive left ventricular failure.

78
Q

Pathophysiology of chronic mitral regurgitation

A

Gradual onset of mitral regurgitation –> blood flows back into the left atrium –> asymptomatic (maybe for many years) –> progressive left ventricular failure.

79
Q

What is the most common cause of mitral regurgitation?

A

Mitral valve prolapse

80
Q

Mitral valve prolapse

A

It is common with an incidence of approximately 5% mainly women. MVP is usually an isolated finding but it may be found as a complication of genetic disorders of connective tissue synthesis e.g. Marfan’s syndrome, Ehlers-Danlos syndrome.

In MVP the normal dense collagen and elastin matrix of the valve is replaced with loose myxomatous connective tissue containing abundant glycosaminoglycans (so-called “myxomatous degeneration”). The leaflets become enlarged and one of the leaflets “prolapses” back into the LA during systole.

MVP may or may not be associated with regurgitation:
• MVP without MR is generally considered by cardiologists to be asymptomatic (majority of cases)
• MVP with MR: symptomatic. Only a minority of patients have severe enough MR to warrant surgery.

81
Q

What is infective endocarditis?

A

Infective endocarditis refers to infection of part of the endocardium, usually the endocardial surface of a valve (but the atrium can be affected).

82
Q

How common is infective endocarditis?

A

It is rare; the average GP will see one case every 20 years.
However, it is important because it has a high mortality (untreated approx 100%, treated approx 10-30%).

83
Q

What are the causes of infective endocarditis?

A

Causes:
• Usually bacterial:
- Streptococci, usually S. viridans (40-50%) - weakly pathogenic. Usually originating in the mouth
- Staphylococci e.g. s. aureus (20-30%) - highly pathogenic.
S. Aureus is the most common cause in iv drug users; usually affecting the tricuspid valve.
• Other bacteria e.g. gram negative bacteria such as E.coli
• Less commonly fungi e.g. candida, aspergillus
- Typically immunocompromised, iv drug users and patients with indwelling venous lines.

84
Q

What is the pathogenesis of infective endocarditis?

A

Bacteria are delivered to the heart during an episode of bacteraemia. This may be due to an event as trivial as tooth brushing or associated with a more invasive procedure such as surgery. As a consequence of the bacteraemia, the organisms adhere to and invade the valve.

The endocardium is normally resistant to infection, so for infection to occur:
• Either there must be highly pathogenic organisms (e.g. s. aureus) colonising a normal valve
• Or weakly pathogenic organisms (e.g. s. viridans) colonising an abnormal valve e.g. prosthetic valve, mitral or aortic regurgitation, mitral valve prolapse.

As the organisms replicate they become enmeshed with layers of platelets and fibrin on the valve surface, forming vegetations. Inflammatory cells are also present within the vegetations.

85
Q

infective endocarditis causes endothelial injury, T/F?

A

In infective endocarditis the microorganism causes endothelial injury on the heart valve. Also, if the valve is abnormal, there may be turbulent blood flow across the valve.

86
Q

Complications of endocarditis?

A

Complications are due to three distinct processes:
• Disturbance of valve function:
○ Over time the underlying structure of the valve is destroyed by the infection and this results in the development of valve regurgitation
• Embolism
○ Part of the vegetation may break away from the valve and form and embolus (“septic emboli”). The clinical effect will depend on which artery the embolus occluded. The majority of emboli from vegetations enter the cerebral circulation and so present as a stroke.
○ The clinical effects depend on where the immune complexes are deposited. For example, deposition in the glomeruli may result in glomerulonephritis i.e. the immune complex deposition results in damage to cells in the glomerulus with consequent disturbance in normal renal function.

87
Q

What are the methods used to investigate infective endocarditis?

A

Blood cultures:
• At least 3 sets of blood cultures from different sites, taken a minimum of 1 hour apart and before starting antibiotics.
• These confirms the diagnosis and guides appropriate antibiotic therapy.
Endocardiography
• Transoesophageal echocardiography to identify vegetation and any complications.

88
Q

What criteria is used to investigate infective endocarditis?

A

The Duke’s criteria

89
Q

What is needed to diagnose duke’s criteria?

A

Requires:

  • 2 major criteria or
  • 1 major and 3 minor criteria, or
  • 5 minor criteria

Major criteria:

  • Positive blood cultures:
    1. Typical microorganisms consistent with infective endocarditis from 2 separate blood cultures
    2. Persistent positive blood cultures of blood samples taken over 12hrs apart
    3. Three or more positive cultures taken over more than 1hr apart.
  • Evidence of endocarditis involvement noted on endocardiography
    1. New valvular regurgitation
    2. Abscess
    3. Vegetations

Minor criteria

  • predisposing valvular or cardiac abnormality
  • Fever; temperature >38 degrees
  • Vasculitic pnenomena
  • Embolic phenomena
  • Microbiological evidence: positive blood culture but does not meet major criteria
  • Suggestive echocardiographic findings
90
Q

Left heart failure

A

Heart failure is a syndrome which occurs when the pumping action of the heart is inadequate for the needs of the body i.e. the cardiac output is unable to meet the metabolic needs of the tissues.

91
Q

Prevelance of left heart failure

A

It is common: prevalence of 2-3% of population; approximately 20% in 70-80 year olds.
It is serious: mortality is 30% in the first year and 10% each year after.

92
Q

How can you classify heart failure?

A

There are a variety of ways of classifying heart failure:
• Acute or chronic (depending on speed of onset)
Left or right (depending on where the dominant site of injury is)

93
Q

What are the causes of heart failure?

A

Heart failure has many different causes and, when managing a patient with heart failure, it is important to attempt to elucidate the underlying cause.

94
Q

Acute left heart failure

A

In acute left heart failure there is a sudden major insult to the left side of the heart (usually the left ventricle). There is no time for compensatory mechanisms to kick in and so contractile force of the LV is greatly reduced, resulting in a catastrophic fall in cardiac output. The sudden failure of the 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 breathlessness. In the worst cases, there is under perfusion of organs and development of cardiogenic shock

Acute left heart is almost always a complication of MI affecting the left ventricle:
• An extensive MI renders a large volume of the LV non-functional
• Rupture of a mitral valve papillary muscle
• Development of an arrhythmia

95
Q

Chronic left heart failure

A

Chronic left heart failure is by far the most common form of heart failure; it is almost always due to chronic left ventricular failure.
The left ventricle is damaged slowly over a period of time. The commonest causes of slow damage to the left ventricle are:
• Chronic ischaemic heart disease (due to coronary artery atherosclerosis)
• Systemic hypertension
• Valvular (mitral/aortic) heart disease

Because the damage occurs slowly, there is enough time for compensatory myocardial hypertrophy to occur. This maintains cardiac output and prevent symptoms of heart failure.
Eventually the myocardium becomes irreversibly damaged and the left ventricle decompensates leading to chamber dilatation and falling cardiac output.

Chronic LVF is a progressive disorder in which a vicious 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 sympathetic drive and activating the renin-angiotensin-aldosterone system (see endocrine pathology for more notes of the RAAS system.

The end result is retention of sodium and water by the kidneys, which leads to increase myocardial stress and declining cardiac function.

96
Q

Decompensation of chronic left heart failure

A

Patients with chronic heart failure may decompensate if their heart is stressed.
Patients with chronic heart failure frequently experience episodes of acute worsening in their symptoms. This is often described as “acute decompensation” and is very common seen in routine practice when a concurrent illness (often only a trivial infection) places additional burden on a critically failing heart and pushes the patient into acute failure.

Most patients with chronic heart failure experience a relapsing and remitting course, with periods of stability interspersed with episodes of decompensation.

97
Q

What can chronic heart failure be divided into?

A

systolic and diastolic

98
Q

Systolic chronic failure

A

Systolic failure
• The underlying problem is failure of the pumping action of the ventricle during systole.
• Usually a consequence of ischaemic heart disease or hyperventilation
The ventricle is usually dilated and fails to contract normally such that the proportion of blood ejected in each beat (normally 50-70%), the ejection fraction, is reduced.

99
Q

Diastolic chronic failure

A

Diastolic failure (= heart failure normal ejection fraction (HFNEF)
• Systolic function is not impaired
• There is failure of the ventricle to fill adequately due to increased stiffness of the wall.
• It may be a consequence of massive LV hypertrophy, myocardial fibrosis or other conditions e.g. amyloidosis.
• Diastolic LVF is increasingly recognised in older patients
Diastolic HF accounts for 50% of cases of HF. The prognosis in diastolic HF is the same as for systolic HF.

100
Q

Diagnosing LVF

A

Diagnosing LVF
• History and Examination
• ECG (usually abnormal)
• CXR (cardiomegaly)
• Echocardiography
○ Can confirm systolic or diastolic dysfunction
○ It may identify the underlying cause e.g. aortic or mitral valve disease
• B type natriuretic peptide (BNP) plasma levels
○ BNP is 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.
○ BNP plasma levels are useful because low levels effectively rule out the diagnosis of LVF.
○ In contrast, in the correct clinical context, high BNP plasma levels make the diagnosis of LVF very likely.

Investigations to identify the underlying cause of the heart failure are also important.

101
Q

Right ventricular heart failure

A

Right heart failure is much less common than left heart failure.
By convention, the term ‘right heart failure’ is usually reserved for cases developing in the absence of left sided heart failure.
ie. we don’t use the term ‘right heart failure’ when the right heart failure is secondary to left heart failure.

Remember, overall, the most common cause of RHF is as a consequence of LHF, when it is called congestive heart failure (or biventricular heart failure).

102
Q

Acute right ventricular heart failure

A

Acute right heart failure is much less common than acute left heart failure.
The most common cause of acute right heart failure is a massive pulmonary embolism causing sudden blockage of a major pulmonary artery or the pulmonary bifurcation (saddle embolus):
• the pressure in the pulmonary arterial system rises dramatically ie. development of pulmonary hypertension. The right heart does not have time to undergo compensatory changes and so cannot generate enough force to maintain an output. This results in acute right heart failure, which presents clinically as circulatory collapse, shock and/or instantaneous death.

103
Q

What is pulmonary hypertension?

A

Refers to an increase in blood pressure in the pulmonary vasculature (pulmonary arteries, veins and capillaries). It is defines as a resting mean pulmonary artery pressure at or above 25 mmHg (normal is in the range of 18-25mmHg)

104
Q

Chronic right heart failure

A

Chronic right heart failure is much less common than chronic left heart failure.
The clinical features of chronic right heart failure are shown in the diagram opposite.

Preceding the development of chronic right failure, the right ventricle is damaged slowly over a period of time.

105
Q

Signs of right sided heart failure

A

Elevated JVP
Hepatomegaly
Ascites
Peripheral oedema

106
Q

Commonest causes of slow damage to the right ventricle

A

The commonest causes of slow damage to the right ventricle are lung diseases:
• Chronic Obstructive Pulmonary Disease
• Pulmonary Fibrosis (diffuse parenchymal lung diseases)
• recurrent small pulmonary emboli

These lung diseases damage the right ventricle by causing pulmonary hypertension. [See the Respiratory Pathology notes for discussion of how COPD and pulmonary fibrosis causes pulmonary hypertension].

In the early stages, there is enough time for compensatory right ventricular hypertrophy to occur. The RV undergoes hypertrophy so that it can effectively ‘push harder’ against the increased pressure in the pulmonary circulation. The RV hypertrophy maintains cardiac output in the face of the increased pressure in the pulmonary circulation.

107
Q

What is cor pulmonale?

A

Cor pulmonale is the term used to indicate right heart failure due to lung disease (including diseases of the pulmonary vessels):
• massive PE → acute cor pulmonale.
• COPD, pulmonary fibrosis or recurrent small PEs → chronic cor pulmonale.
The link between lung disease and the development of right heart failure is that the lung disease causes pulmonary hypertension (ie. increased pressure in the pulmonary circulation).

108
Q

What is the commonest cause of cor pulmonale?

A

COPD

109
Q

Non massive PE

A

Non-massive PE is due to a medium-sized embolus occluding a segmental pulmonary artery. This results in a segment of lung being ventilated but not perfused ie. there is a ventilation/perfusion defect.
As a consequence there is respiratory compromise which usually manifests as pulmonary infarction with or without pleuritis and an effusion.
Clinically, typically there is pleuritic chest pain and shortness of breath. There may be haemoptysis due to infarction of the non-perfused lung tissue. There may also be a pleural rub, crackles, effusion.

110
Q

Massive PE

A

Massive PE is due to a massive embolus occluding a proximal pulmonary artery or the pulmonary artery bifurcation (‘saddle embolus’).
As a consequence, blood cannot enter the lungs, which causes a sudden
increase in resistance to pulmonary blood flow and results in sudden
pulmonary hypertension.
The right side of the heart does not have time to compensate for this sudden increase in pressure in the pulmonary circulation, and so there is onset of acute right heart failure (cor pulmonale).
In addition, blood cannot pass through the lungs, which results in decreased filling of left side of heart and therefore decreased left ventricular output. This presents as haemodynamic compromise in the form of shock, collapse and sudden death. On examination there is tachycardia, hypotension, raised JVP, RV heave, normal chest examination, low 02 sats.

111
Q

Recurrent small PEs

A

A third presentation of pulmonary embolism is in the form of recurrent small PEs.
Each individual episode is usually subclinical (ie. does not result in symptoms) but over time the multiple small emboli occlude arterioles resulting in gradual occlusion of the pulmonary arterial bed, leading to the gradual development of pulmonary hypertension.
Because the onset is gradual, the heart has time to undergo compensatory right ventricular hypertrophy.
Eventually the right ventricle will decompensate and right heart failure (cor pulmonale) ensues.

IOD - Cell Pathology (18 decks)

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