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Flashcards in Cardiovascular Deck (334)
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1
Q

What is Atherosclerosis?

A

Plaque rupture leading to thrombus formation, leading to partial/complete arterial blockage by ‘stiff’ ‘paste’.
Principle behind heart attack, stroke and gangrene of the extremities where blood supply to these areas is blocked.
Leading cause of the death in the world.

2
Q

What is the epidemiology of cardiovascular disease in the UK?

A

More prevalent in men than in women.

More prevalent is less affluent areas (Yorkshire and the North).

3
Q

What are the risk factors for Atherosclerosis?

A

Age – over 50s, post-menopausal, chronic disease
Tobacco Smoking – increases systemic inflammation
High Serum Cholesterol
Obesity – metabolic syndrome increases systemic inflammation, high serum cholesterol due to high fat diet
Diabetes
Hypertension
Family History – genetic component, get put on statins early on

4
Q

How are atherosclerotic plaques distributed?

A

Found within peripheral and coronary arteries
Focal distribution along the artery length
Distribution may be governed by haemodynamic factors:
Changes in flow/turbulence (eg at bifurcations) cause the artery to alter endothelial cell function. Wall thickness is also changed leading to neointima.
Altered gene expression in the key cell types is key.

5
Q

What is neointimal hyperplasia?

A

Proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, resulting in the thickening of arterial walls and decreased arterial lumen space.

6
Q

What are the layers of the arterial wall?

A

The wall of an artery consists of three layers.
The tunica intima is simple squamous epithelium surrounded by a connective tissue basement membrane with elastic fibers.
The tunica media, is primarily smooth muscle and is usually the thickest layer. It not only provides support for the vessel but also changes vessel diameter to regulate blood flow and blood pressure.
The outermost layer, which attaches the vessel to the surrounding tissue, is the tunica externa or tunica adventitia. This layer is connective tissue with varying amounts of elastic and collagenous fibers.

7
Q

What is the structure of the atherosclerotic plaque?

A
A complex lesion made up of:
Lipid
Necrotic core
Connective tissue
Fibrous “cap”
The plaque will either occlude the vessel lumen resulting in a restriction of blood flow (angina), or it may “rupture” (thrombus formation – death).
8
Q

What is the ‘Response to Injury’ hypothesis?

A

First suggested in 1856 by Rudolph Virchow and updated by Russell Ross in 1993 and 1999.
Initiated by an injury to the endothelial cells which leads to endothelial dysfunction (inappropriate and abnormal).
Signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.
Inflammation ensues.

9
Q

What is good about inflammation? Why do we need it?

A

Without it we’d be infested with pathogens and parasites, and even if we all lived in sterile conditions, we’d be over-come by tumors and be unable to heal wounds.

10
Q

What can be bad about inflammation?

A

Can be inappropriate and harmful!

11
Q

How can inflammation be harmful in auto-immune diseases?

A

In auto immune diseases such as Rheumatoid arthritis or allergic inflammatory diseases such as asthma the body’s own inflammatory mechanisms are directed against self or respond inappropriately to harmless stimuli such as pollen or house dust mites.

12
Q

How can inflammation be harmful in Ischaemia-reperfusion injury?

A

In Ischaemia-reperfusion injury, tissues that have their blood supply blocked (eg by thrombus in myocardial infarction) are injured. Re-institution of blood flow (by fibrinolysis), necessary to rescue surviving cells, permits inflammatory cells (neutrophils) to enter the injured tissue. Although these neutrophils have an important role in cleaning up dead and injured cells and in wound healing, they can also extend the area of injury beyond that originally cut off from the of blood supply.

13
Q

How can inflammation be harmful in shock?

A

In septic or traumatic shock, large numbers of neutrophils are mobilised from bone marrow and are recruited to tissues to fight potential infection. The availability of antibiotics and advance trauma surgical techniques means that the magnitude of the inflammatory response can actually present more of a threat to the patient than the infection or injuries.

14
Q

How can inflammation be harmful in atherosclerosis?

A

The response to injury hypothesis says that atherosclerosis occurs due to an inappropriate immune response due initiated by endothelial dysfunction.
Necrotic core – when cells die from necrosis, they release pro-inflammatory mediators which encourage other inflammatory cells to migrate.

15
Q

What initiates inflammation in the arterial wall in atherogenesis?

A
LDL - can pass in and out of the arterial wall in excess it accumulates in arterial wall, and undergoes oxidation and glycation.
Endothelial dysfunction (Response to Injury hypothesis)
Not sure what causes this!
16
Q

What is the stimulus for adhesion of leukocytes in atherogenesis?

A

Once inflammation is initiated, chemoattractants (chemicals that attract leukocytes) are released from endothelium and send signals to leukocytes.
Chemoattractants are released from site of injury and a concentration-gradient is produced showing the cells where to go

17
Q

Name some of the inflammatory cytokine found in plaques?

A
IL-1
IL-6
IL-8
IFN-g
TGF-b 
MCP-1 – Monocyte chemoattractant protein 1
(C reactive protein)
18
Q

What is leukocyte adhesion in atherogenesis controlled by?

A

Once the leukocytes receive the chemoattractant signals, they are recruited to the blood vessel wall.
This is the adhesion cascade.
Initial stages are regulated by selectins, later stages regulated by integrins and chemoattractants.
For every adhesion molecule there is a counter receptor – allowing for sticking together.

19
Q

What is the first stage of atherosclerosis progression?

A

Fatty streaks
Earliest lesion of atherosclerosis
Not causative but provide a foundation for the progression
Appear at a very early age (<10 years)
Consist of aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall
No effect on blood flow.

20
Q

What is the second stage of atherosclerosis progression?

A

Intermediate lesions
Composed of layers of :
Lipid laden macrophages (bubbles of lipid - foam cells)
Vascular smooth muscle cells
T lymphocytes
Adhesion and aggregation of platelets to vessel wall
Isolated pools of extracellular lipid

21
Q

What is the third stage of atherosclerosis progression?

A

Fibrous plaques or advanced lesions
Impedes blood flow
Prone to rupture
Covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
Highly pro-inflammatory
May be calcified
Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes

22
Q

What is the fourth stage of atherosclerosis progression?

A

Plaque rupture
Plaques constantly growing and receding.
Fibrous cap has to be resorbed and redeposited in order to be maintained.
If balance shifted eg in favour of inflammatory conditions (increased enzyme activity – matrix metalloproteinases), the cap becomes weak and the plaque ruptures.
Basement membrane, collagen, and necrotic tissue exposure as well as haemorrhage of vessels within the plaque
Thrombus (clot) formation and vessel occlusion

23
Q

What is a TCFA?

A

Thin capped fibroatheroma
A type of vulnerable plaque that is prone to rupture
Can detect plaque rupture by using an ECG

24
Q

What is the fifth stage of atherosclerosis progression?

A

Plaque erosion
Second most prevalent cause of coronary thrombosis (more common in MI in females than plaque rupture).
Lesions tend to be small ‘early lesions’
Don’t understand why this happens
Fibrous cap thick may disrupt by collagen triggering thrombosis rather than tissue factor (as in plaque rupture)
A platelet-rich clot may overlie the luminal surface.
There may be a prominent lipid core.

25
Q

How can plaque erosion be detected?

A

These lesions are very difficult to detect with any kind of imaging so far. OCT is the best and the presence of luminal thrombus over an intact fibrous cap is indicative. OCT is intravascular tomography processing backscattering using infrared light.

26
Q

What is PCI?

A

PCI - Percutaneous Coronary Intervention
Used to treat coronary artery disease
2 million + procedures / year worldwide
More than 90% require stent implantation. Stents made out of stainless steel, cobalt chromium, metals that are cost-effective.
Restenosis was a major limitation, no longer a problem.

27
Q

What is restenosis?

A

The body wants to heal the area where the stent has been put in – smooth muscle cell proliferation.
Used to happen after PCI.
But drug eluting stents (with Taxol and Sirolimus) are so good now that restenosis is not a problem. These drugs work by reducing smooth muscle cell proliferation and in turn, this reduces regrowth after placement of the stent.

28
Q

Name some useful anti-platelet drugs?

A

Patients will be given anti-platelet therapy before a stent.
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel/Ticagrelor – inhibitors of the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis

29
Q

What is canakinumab?

A

New anti-inflammatory biologic (antibody) developed in 2017 to target IL-1 which acts as a major cytokine in atherosclerosis.
Major clinical trial showed beneficial results.

30
Q

What is Colchicine?

A

A generic anti-inflammatory drug that lowers ischaemic events in patients with recent MI.
Already used for gout and pericarditis.
Given within 30 days of a heart attack.

31
Q

Why are the letters PQRST used in an ECG?

A

Original deflections were labelled ABCD
Mathematical convention dating back to Descartes using the second half of the alphabet; N has other meanings in mathematics and O was used for the origin of Cartesian coordinates. Einthoven chose the next letter of the alphabet!

32
Q

What is an ECG?

A

Echo-cardiogram is a representation of the electrical events of the cardiac cycle.
Each event has a distinctive wave form.
The study of the waveform can give insight into the patient’s cardiac pathophysiology.

33
Q

What can you identify using an ECG?

A
Arrhythmia
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances - hyper/hypokalemia
Drug toxicity
34
Q

What is depolarisation of the heart?

A

Contraction of any muscle associated with electrical changes is called depolarisation.
The vast majority of the activity that we see on an ECG is depolarization, rather than repolarization.

35
Q

What are the pacemakers of the heart and their bpm?

A

SA Node - dominant pacemaker with an intrinsic rate of 60-100 bpm
AV Node - back up pacemaker with an intrinsic rate of 40-60 bpm
Ventricular cells - back up pacemaker with a intrinsic rate of 25-40 bpm

36
Q

What is a standard calibration of an ECG?

A

25mm/s
0.1mV/mm
Electrical impulse that travels towards the electrode produces an upward ‘positive’ deflection.

37
Q

What is the pathway of impulse conduction in the heart?

A
Sinoatrial node
AV node
Bundle of His
Bundle branches
Purkinje fibres
38
Q

What do the different waves on the ECG represent?

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

We do have atrial repolarisation but it gets lost behind the QRS complex.

39
Q

What is the PR interval?

A

Atrial depolarisaton
PLUS a delay in AV junction
Delay allows for the atria to contract before the ventricles contract.

40
Q

What does the ECG paper represent?

A
Horizontally
One small box - 0.04 s
One large box - 0.20 s
Vertically
One large box - 0.5 mV
41
Q

What are the ECG leads?

A

They measure the difference in electrical potential between two different points.
Bipolar leads: two different points on the body
Unipolar leads: one point on the body and a virtual reference point with zero electrical potential located in the centre of the heart

42
Q

What are types of leads are the 12 leads of the ECG?

A
VERTICAL PLANE
3 standard leads
3 augmented leads
HORIZONTAL PLANE
6 precordial leads
43
Q

What are the characteristics of the P wave?

A
Always positive in leads I and II
Always negative in lead aVR
Less than 3 small boxes in duration
Less than 2.5 small boxes in amplitude
Best seen in lead II
44
Q

What does the ECG look like for right and left atrial enlargement?

A

Right atrial enlargement: Tall (>2.5mm) and pointed P waves (P pulmonale)
Left atrial enlargement: Notched/bifid M-shaped P wave in limb leads (P ‘mitrale’)

45
Q

What do short and long PR intervals suggest?

A

Short PR interval - Wolff Parkinson’s White syndrome
Accessory pathway allows for early activation of the ventricles
Long PR interval - first degree heart block

46
Q

What are the characteristics of the ST segment?

A

ST segment is flat (isoelectric)
Elevation or depression of the ST segment by 1mm or more
“J” junction is the point between QRS and ST segment.

47
Q

What are the characteristics of T wave?

A

Normal T wave is asymmetrical, first half having a more gradual slope than the second.
Rarely exceeds 10mm.
Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted.
T waves follow the direction of the QRS deflection.

48
Q

What is the QT interval?

A

Total duration of the depolarisation and repolarisation
QT interval decreases when heart rate increases
Should be between 0.35-0.45 s
Should not be more than half of the interval between adjacent R waves (R-R interval)

49
Q

What is the U wave?

A

Afterdepolarisations that occur after repolarisation
Small, round, symmetrical and positive in lead II with amplitude <2mm.
U wave direction is the same as T wave.
More prominent at slow heart rates.

50
Q

How to calculate the heart rate on an ECG for regular rhythms?

A

Count the number of big boxes between two QRS complexes and divide this by 300 (1500 for smaller boxes).

51
Q

How to calculate the heart rate on an ECG for irregular rhythms?

A

ECGs record 10 seconds of rhythm per page
Count the number of beats present on the ECG
Multiple by 6.

52
Q

What does the QRS axis tell you?

A

Represents overall direction of the heart’s electrical activity.
Abnormalities hint at ventricular enlargement and conduction blocks.
Normal QRS axis is from -30 to +90
-30 to -90 is referred to as left axis deviation (LAD)
+90 to +180 is referred to as right axis deviation (RAD)

53
Q

What are the key features of the heart’s contraction?

A

Involves a two stage electrical generated contraction
Contraction initiated by depolarisation and changes to calcium concentration
Removal of calcium (energy dependent) for relaxation to occur

54
Q

What is myocardial hypertrophy?

A

Enlargement of the heart muscle
Hypertrophic response triggered by angiotensin 2, ET-1 and insulin-like growth factor 1, TGF-β.
Can be an adaptive process in pregnancy/athletes
If you exceed stretch capability of sarcomeres then cardiac contraction force diminishes, there’s only so far the heart can stretch before it goes into heart failure.

55
Q

What effect will different kinds of heart failure have?

A

Left sided cardiac failure – pulmonary congestion and then overload of right side.
Right sided cardiac failure with venous hypertension and congestion.
Diastolic cardiac failure ~ Stiffer heart

56
Q

What is fetal embryogenesis of the heart?

A

The heart comprises a single chamber until the fifth week of gestation, then divided by intra-ventricular and intra-atrial septa from endocardial cushions. The muscular intra-ventricular septum grows upwards from the apex of the heart producing the four chambers and allowing valve development to occur.

57
Q

What is congenital heart disease?

A

Results from faulty embryonic development
May complicate up to 1% of all live births.
Misplaced structures or arrest of the progression of normal structure development.
Ventricular and atrial septal defects are the most common.

58
Q

What can cause congenital heart disease?

A

Single genes associated = trisomy 21 (Downs), Turner Syndrome (XO) and di-George Syndrome.
Homeobox genes particularly associated
Infections – Rubella
Drugs – Thalidomide, alcohol, Phenytoin, amphetamines, lithium, eostrogenic steroids
Diabetes

59
Q

What is the tetralogy of Fallot?

A

Main features:
- Pulmonary stenosis
- Ventricular septal defect
- Dextraposition/over-riding ventricular septal defect
- Right ventricle hypertrophy
Characteristic boot-shape on radiology and macroscopically.
Often associated with other cardiac abnormalities.
As a result of the pulmonary stenosis, right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction usually is performed during the first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases.

60
Q

What are the risk factors for ischaemic heart disease?

A
Systemic hypertension
Cigarette smoking
Diabetes mellitus
Elevated cholesterol
Also: obesity, increasing age, male sex, family history, oral contraceptive pill, sedentary life habit, personality features etc
61
Q

What can cause imperfect blood supply to the heart?

A
Atherosclerosis
Thrombosis
Thromboemboli
Artery spasm
Collateral blood vessels
Blood pressure/cardiac output/heart rate
Arteritis
Anaemia
Altered oxygen dissociation curve
Carbon monoxide
Cyanide
Increased demand from hypertension, valvular heart disease, hyperthyroidism, fever, thiamin (B1) deficiency, catecholamine stress.
62
Q

What are the patterns of infarction?

A

Subendocardial/patchy infarction OR
Transmural infarction
Size and pattern of the infarction varies. Complications of infarcts differ according to which territory has compromised.
Can date the infarct.
The infarct can affect other areas of the heart - the immediate area may be ischaemic and there may be other areas which were already prone to infarction which will now be affected.

63
Q

Why is reperfusion of ischaemic myocardium a problem?

A

Reperfusion of completely infarcted tissue can produce significant haemorrhage - risks of problems downstream. The reperfusion allows oxygen delivery and a further degree of injury as a result of generation of superoxide radicals etc.

64
Q

What is an aneurysm?

A

This is a dilation of part of the myocardial wall, usually associated with fibrosis and atrophy of myocytes.
Variable fatty tissue replacement may also occur.
The dilatation of the thin walled sac allows blood stasis and thrombosis.
Risk of subsequent embolism of such material.

65
Q

What is hypertensive heart disease?

A

Reflects cardiac enlargement due to hypertension, and in the absence of other cause.
Compensatory hypertrophy of the heart initially with increased myocyte size, squaring of the nuclei and slight increase of the interstitial fibrous tissue.
Initially able to handle the increased workload, eventually the hypertrophy no longer compensates.
Falling amount of oxygen delivery to cardiac myocytes produces further fibrosis and progressive contractile dysfunction.

Often associated with coronary atheroma and ischaemic heart disease – aggravating situation.

66
Q

What is Cor pulmonale?

A

Right ventricular hypertrophy and dilatation due to pulmonary hypertension.
May reflect an acute event - causes problems with backstream pressure on the ventricular system.
Classically disproportionate right ventricular hypertrophy as compared with the left.
Progressive features of right side cardiac failure with venous overload, peripheral oedema and progressive hepatic congestion.

67
Q

What is Acute rheumatic fever?

A

Group A β-haemolytic streptococcus infection usually in upper respiratory tract.
Peak age of pathology 9-11 years, but can occur in adults. Seen commonly in those who have migrated to the UK and have not have antibiotics in childhood.
Symptoms and features diminish after 3-6 months.
Some patients die acutely and are shown to have granulomatous foci of inflammation (Aschoff body, Anitchkov cells and some giant cells). There may be pericarditis and endocarditis.

Chronically scarring and deformity produces contracture of the valves (particularly the mitral and aortic valve) and chordae tendinae. These may subsequently calcify and distort blood flow allowing localised thrombosis. They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis.

68
Q

What are the clinical features of acute rheumatic fever?

A

Clinical features include:
carditis (cardiomegaly, murmurs, pericarditis and cardiac failure) polyarthritis, chorea, erythema marginatum and subcutaneous nodules.
Minor criteria for diagnosis include:
previous history of rheumatic fever, arthralgia, raised CRP, ESR and white cell count.
Antibodies against group A streptococcal antigens, anti-streptolysin O, anti-DNAse B and anti-hyaluronidase.

69
Q

What is infective endocarditis?

A

Infection produces rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction.
Apart from the sudden development of cardiac failure and septic problems there are other consequences including generation of infected thromboemboli and damage to the kidneys (focal segmental glomerulonephritis FSGS).
- Protean symptoms
- Fever, anorexia, fatigue
- Progressive splenomegaly, petechiae, clubbing
- Neurological dysfunction due to mitotic emboli and aneurysms
High morbidity and mortality rates.

70
Q

What causes infective endocarditis?

A

In adults causes include rheumatic valvular heart, mitral valve prolapse, intravenous drug abuse, prosthetic valves, diabetes, the elderly and pregnancy.
Characteristic organisms include streptococci and staphylococci although fungi and atypical bacteria are also recognised - will destroy the tissue and cause problems.

71
Q

What is Calcific aortic stenosis?

A

Nodular calcific deposits in cusps with progressive distortion of valves opening/closure.
Obstruction to left ventricle outflow produces pressure overload and cardiac hypertrophy.
Accelerated in bicuspid aortic valves.
Risk of thrombosis and sudden cardiac death, as well as infective endocarditis.

72
Q

What is Mitral valve disease?

A

Degenerative process which makes you prone to regurgitation.
Calcification of the mitral valve annulus is usually asymptomatic and of no significance. It does not usually affect the mobile leaflets.
However, calcification of the valves, following rheumatic valvular disease or previous inflammation/valvitis, is of significance with either mitral stenosis or regurgitant pathology.

73
Q

What is Mitral valve prolapse?

A

Degeneration of the mitral valves such that the inner fibrosa layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material.
The valve cusp bow upwards and may not close adequately producing incompetence/regurgitation.
Risk of sudden cardiac death and infective endocarditis.

74
Q

What is Myocarditis?

A

Inflammation of the myocardium usually associated with muscle cell necrosis and degeneration.
Can be caused by rheumatic fever or other causes.
Viral myocarditis is the commonest.
Direct viral toxicity with associated cell mediated immunity aggravating cell damage. Healing with scarring, but high risk of sudden death.
Symptoms vary, often in association with an upper respiratory tract infection preceding.

75
Q

What causes Myocarditis?

A

Viruses – Coxsackie, Adeno-, Echo, Influenza
Rickettsia – typhus
Bacteria –diphtheria, staphylococcal, streptococcal, borrelia, leptospira
Fungi and Protozoa parasites – toxoplasmosis, cryptococcus
Metazoa - echinococcus

Non-infective:
Hypersensitivity/immune related diseases – rheumatic fever, SLE, scleroderma, drug reaction, rheumatoid arthritis
Radiation
Miscellaneous – sarcoid, uraemia

76
Q

What is Giant cell myocarditis?

A

A very rare highly aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells. Often fatal.
Early treatment is transplantation but disease can often recur.

77
Q

What are the main types of Cardiomyopathy?

A

Various types ~ primary cardiac disease with contractile dysfunction and atypical morphology
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Secondary dilated cardiomyopathy
Rare forms

78
Q

What is dilated cardiomyopathy?

A

1/3 familial: Most autosomal dominant (AD) but some recessive and X-linked.
Poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial fibrosis.
May also follow a viral myocarditis or an inflammatory myocarditis/toxic myocarditis

Enlarged, heavy and dilated heart, possibly cardiac weight up to 900 g.
Histology shows variable atrophy and hypertrophy - increased interstitial tissue, occasional inflammatory cells
Clinical progression slowly deteriorating cardiac failure, dysrrhythmias and ultimately death.

79
Q

What causes secondary dilated cardiomyopathy?

A
Alcohol
Cobalt toxicity
Catecholamines
Micro-infarction
Anthracyclines
Cocaine
Pregnancy.  This may affect up to 1% of females, with an Afro-Caribbean bias.  Many recover spontaneously, but one can be left with permanently damaged and dilated heart.
80
Q

What is Hypertrophic cardiomyopathy?

A

Muscle gene mutation - prone to cause bigger, thicker heart muscle. Bulge into the chambers affecting the valves.
Related to defects in force degeneration/ energy usage allowing progressive sarcomeric dysfunction.
Compensatory hypertrophy often occurs.
Many mutations recognised involving β-myosin, myosin binding protein C, troponin T, titin etc.
Asymmetric hypertrophy with distortion of a papillary architecture.
Increased fibrosis in tissues.
Ventricular outflow distortion.
Myocyte disarray.

81
Q

What is Arrhythmogenic right ventricular cardiomyopathy?

A

A degenerative condition with progressive dilatation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement.
Particularly common in parts of Italy
Familial inheritance pattern with genetic linkage chromosome 14,1 and 2.
Sudden cardiac death.

82
Q

What is Restrictive cardiomyopathy?

A

This is a group of diseases in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body.
This can either be amyloid related to the heart (cardiac amyloid) or part of a systemic disorder (amyloidosis AL, AA).
Firm enlarged and heavy heart with diffuse infiltration of the protein into the myocytes, blood vessels and valves.
Progressive deterioration with right and left side failure.

83
Q

What is Endomyocardial disease?

A

Endomyocardial fibrosis, particularly in African settings and Löeffler endocarditis.
This is a temporate region disorder with high grade eosinophilia , rash and progress endocarditis leading to cardiac failure.
Characteristically grey-white layer of fibrous tissue extending of the endocardial surfaces of the ventricular cavities.
Stiff and poorly compliant ventricle.

84
Q

What is Sarcoidosis?

A

A chronic granulomatous disease with numerous granulomas of non-caseating giant cell type. May involve the heart producing widespread areas of fibrosis and compensatory hypertrophy. It can produce a restrictive disorder. If it involves the conduction system then this may be the prime pathology of the patients with the risk of sudden death.

85
Q

What is Cardiac myxoma?

A

Most common cardiac tumour
At least 75% of cardiac tumours with bias towards atria.
Rather jelly like proliferation of myxoid cells with abundant endothelial vascular channels.
Usually produces obstructive symptoms but risk of embolisation.

86
Q

What is a cardiac sarcoma?

A

These are rare and can show differentiation towards vascular, fibrous and muscle phenotypes. Almost invariably fatal - days or weeks.
Cannot treat.

87
Q

What is Atheroma?

A

A degenerative condition of arteries characterised often by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis.
Associated with ischaemic heart disease, myocardial infarction, stroke, peripheral vascular disease etc.

88
Q

What are the pathological stages of atherosclerosis?

A

Initiation - Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier.
Local cellular proliferation and incorporation of oxidised lipoproteins occurs. Mural thrombi on surface with subsequent healing and repeat of cycle.

Adaptation - As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed. This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix. May progress to unstable plaque.

Clinical stage - The plaque continues to encroach upon the lumen and runs the risk of haemorrhage of exposure of tissue HLA-DR antigens which may stimulate T cell accumulation. This drives an inflammatory reaction against part of the plaque contents.

89
Q

What are the potential complications associated with plaque rupture?

A

Acute occlusion due to thrombus
Chronic narrowing of vessel lumen with healing of the local thrombus
Aneurysm change
Embolism of thrombus +/- plaque lipid content - can break off and travel to other parts of the body

90
Q

What are the risk factors for atherosclerosis?

A
Hypertension
Serum cholesterol level
Tobacco smoking
Diabetes
Increasing age
Male > female
Inactive and stressful life patterns
Homocysteine level
CRP
91
Q

What is essential hypertension?

A

Altered renin-angiotensin system elevates blood pressure by impairing sympathetic output increasing mineralocorticoid secretion and direct vaso-constriction.
In effect the changes to auto-regulation produce an increase in peripheral resistance, that in normality would allow increased blood pressure, diuresis and restoration of normal pressure and volume.

92
Q

What is Raynaud’s phenomenon?

A

Intermittent bilateral ischaemia of digits/extremities precipitated by motional cold temperature. Accelerated in cases of scleroderma and SLE. May produce distal atrophy and ulceration.

93
Q

What is Vasculitis?

A

An inflammatory and variably necrotic process centred on the blood vessels that may involve arteries, veins or capillaries. Inflammation damaging the walls of the vessels.

94
Q

What is Giant cell arteritis?

A

Commonest type of vasculitis.
Focal, chronic and granulomatous inflammation of temporal arteries mostly.
Association with polymyalgia rheumatica.
Can involve large arteries (aortic aneurysm/dissection).
Average age 70+. Female bias.
Feel stiff in the morning, painful head - temporal artery which supplies the scalp.
Can go blind in a couple of hours.

95
Q

What the pathology behind Giant cell arteritis?

A

Thickened blood vessel, often palpable.
Granulomatous inflammation involving the full thickness of the wall with macrophages, lymphocytes, plasma cells, neutrophils and occasionally eosinophils.
Giant cells tend to congregate around IEL. Variable necrosis.
Old areas of inflammation show up as focal scars with fragmentation of elastic laminae. Thrombosis may occur.

96
Q

What is Buerger disease?

A

An inflammatory disease of medium and small arteries affecting the distal limbs.
Strong association with tobacco smoking.
Cell mediated hypersensitivity to collagen II and III with impaired endothelium.
Distal ischaemic symptoms and necrosis.

97
Q

What are aneurysms?

A

These are dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels. The incidence rises with age.
Described as fusiform, saccular, dissecting and arterio-venous.
Prone to bulging off and travelling downstream or bursting.

98
Q

What is an Abdominal aortic aneurysm?

A

> 50% dilatation of aortic diameter
Those greater than 5-6 cm diameter increased risk of aneurysm rupture.
Prevalence rises with age, smoking, high blood pressure
Strong association with atheromatous disease
Familial clustering suggests a genetic component
Local inflammatory changes can be profound and involve ureters and local nerves.
Sudden shocking pain - death within minutes.

99
Q

What is a berry aneurysm?

A

This rounded berry-like vascular dilatation is particularly common in the cerebral circulation.
Consequence of long standing hypertension and/or focal area of weakness within the arterial substructure.

100
Q

What is a Dissecting aneurysm?

A

This is a haematoma within the arterial wall with blood entering under pressure from the lumenal surface and dissecting along the length of the media.

101
Q

What are varicose veins?

A

A varicose vein is an enlarged and torturous vein, principally affecting the superficial leg veins.
Risk factors – age, female (pregnancy related), hereditary, posture, obesity
Progressive incompetence of valves with further back pressure on venous circuit.
Thinning and dilatation of vascular wall in places with patchy calcification.
May produce stasis dermatitis with trophic changes to the skin.

102
Q

What is Haemangioma?

A

This is a benign proliferation of blood vessel tissue, which varies in name and substructure depending on the site and age of the patient.
Capillary haemangioma – birth marks, ruby spots
Juvenile haemangioma – strawberry haemangioma
Cavernous haemangioma – port wine stains
Most are of no consequence.

103
Q

What is a Glomus tumour?

A

A benign neoplasm involving the glomus body.
Small lesion which is intensely painful.
Composed of vascular channels with proliferation of the glomus cells (neuromyoarterial receptors) mainly affect the hands.

104
Q

What is Angiosarcoma?

A

This is a highly aggressive malignant neoplasm of endothelial cells.
Very difficult to control, often fatal.
Commonly skin, soft tissue, breast, bone, live and spleen.
Rapidly enlarging haemorrhagic tumour with rapid dissemination to other organs.
Environmental carcinogens – arsenic and vinyl chloride.

105
Q

What are the risk factors for deep vein thrombosis?

A

Venous flow stasis from any cause (eg. cardiac failure, chronic venous insufficiency, post operative immobilisation, prolonged bed rest)
Injury (trauma, surgery, child birth)
Hypercoaguability (OCP), pregnancy, cancer, inherited thrombophilic disorders)
Advanced age
Sickle cell disease

106
Q

What is an embolism?

A

The passage of material through the venous or arterial circulations.
Commonest process is thrombo-embolus from a deep vein thrombosis.
Post operative deep vein thrombosis occurs often following surgery or immobilisation following illness.
Pulmonary emboli may be asymptomatic and small.
May produce transient dyspnoea for relatively small emboli.
May produce focal pulmonary infarction with chest pain, haemoptysis and secondary effusion (when lung tissue dies it can be painful).
At a certain size, they can produce cardiovascular collapse and sudden death (saddle embolus).

107
Q

What are the sources of an embolus?

A

Atherosclerotic plaques, mural thrombus in heart or vasculature
Infective endocarditis
Sites particularly vulnerable – brain, intestine, distal limbs, kidneys and coronary circulation

108
Q

What is Angina?

A

Mismatch of oxygen supply and demand
Blockage of coronary arteries means that heart muscle cannot receive adequate oxygen
Most common cause is ischemic heart disease

109
Q

What are the risk factors of IHD?

A
Age 
Cigarette smoking
Family history 
Diabetes mellitus
Hyperlipidemia
Hypertension
Kidney disease
Obesity 
Physical inactivity
Stress
110
Q

What are some of the exacerbating factors of IHD that affect the supply of blood to the heart?

A
Anemia
Hypoxemia
Polycythemia
Hypothermia
Hypovolaemia
Hypervolaemia
111
Q

What are some of the exacerbating factors of IHD that affect the demand of blood to the heart?

A
Hypertension
Tachyarrhythmia
Valvular heart disease
Hyperthyroidism
Hypertrophic cardiomyopathy
112
Q

What is the physiology of myocardial ischemia?

A

Myocardial ischemia occurs when there is an imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:

  1. Impairment of blood flow by proximal arterial stenosis
  2. Increased distal resistance eg left ventricular hypertrophy
  3. Reduced oxygen-carrying capacity of blood eg anemia
113
Q

What are some of the other types of angina?

A

Prinzmetal’s angina (coronary spasm)
Microvascular angina – left ventricular hypertrophy, older people, in diabetics
Crescendo angina – no chest pain at rest, but now have an inability to perform physical activity
Unstable angina – critical ischaemia but not quite enough to cause a MI

114
Q

What are the symptoms for IHD?

A

Chest pain
Breathlessness
May have other symptoms like fluid retention, palpitation, syncope or pre-syncope.

115
Q

What aspects should you ask about when a patient complains of pain?

A
Onset
Position  (site)
Quality (nature / character)
Relationship (with exertion, posture, meals, breathing and with other symptoms)
Radiation
Relieving or aggravating factors
Severity
Timing
Treatment
116
Q

What are the differential diagnoses for chest pain?

A
Myocardial ischemia
Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Dissection of the aorta
Gastro-esophageal (reflux, spasm, ulceration)
Musculo-skeletal
Psychological
117
Q

What is the treatment for IHD?

A

Reassure
Lifestyle - stop smoking, lose weight, more exercise, improve diet
Advice for emergency
Medication - Aspirin, B blocker, statin, GTN
Revascularisation

118
Q

What are the diagnostic tests that can be used to investigate angina?

A

Routine bloods, lipids, ECG taken
NICE recommends a CT Coronary Angiography for both typical and atypical presentations of angina (used more as a planning than diagnostic tool).
Exercise testing with an ECG may also be used.
Stress echocardiogram may be used - patient given a stimulant to look at the heart in ischemia (high-skill)
Perfusion MRI

119
Q

What’s the effect of B-blockers on the heart?

A

Negatively chronotropic - reduced heart rate
Negatively inotropic - reduced force of contraction
Reduced cardiac output
Reduced oxygen demand
Side-effects: tiredness, nightmares, erectile dysfunction, bradycardia, cold hands and feet
DO NOT give to asthmatics

120
Q

What’s the effect of nitrates on the heart?

A

Very good at dilating coronary arteries and arterioles, reducing blood pressure and afterload, reducing venous return and preload.
Most common side effect: headache

121
Q

What is preload and afterload?

A

Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.
Afterload is the force or load against which the heart has to contract to eject the blood, the ‘load’ to which the heart must pump against.

122
Q

What’s the effect of calcium channel blockers on the heart?

A

Third-line treatment
Coronary arteries dilate
Negatively inotropic - reduced LV contraction
Negatively chronotropic - reduced heart rate
Reduced blood pressure
Reduced afterload
Side effects are flushing, postural hypotension, swollen ankles.

123
Q

What’s the effect of aspirin?

A

Aspirin is a derivative of salicylic acid - and is also known as acetylsalicylic acid.
Cyclo-oxygenase inhibitor
↓ prostaglandin synthesis, incl. thromboxane
↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic
Most common side effect: gastric irritation

124
Q

What’s the effect of ACE inhibitors?

A

Angiotensin II as part of the renin-angiotensin system causes vasocontriction
ACE inhibitors like ramipril block the angiotensin converting enzymes which convert angiotensin I to angiotensin II.
Given to patients with IHD with high blood pressure or diabetes mellitus.

125
Q

What’s the treatment for angina?

A
Aspirin	
GTN 		
β Blocker – first-line
Long acting nitrate – second-line		 	
Statin					 
ACE inhibitor

If drugs aren’t successful in managing angina
Revascularisation: PCI / CABG: MDT meeting

Third-line
Ca++ channel blocker
Potassium channel opener
Ivabradine

126
Q

What is PCI?

A

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by atherosclerosis.

127
Q

What is CABG?

A

Coronary Artery Bypass Grafting AKA Heart Bypass Surgery
Used when coronary arteries are narrowed or blocked
Blood vessels can be taken from your leg (saphenous vein), inside your chest (internal mammary artery - PREFERRED), or your arm (radial artery) to graft onto the coronary arteries to provide a alternative route around the blockage.

128
Q

What are the pros and cons of PCI?

A
Pros
Less invasive
Convenient
Repeatable
Acceptable
Cons
Risk stent thrombosis
Risk restenosis
Can’t deal with complex disease
Dual antiplatelet therapy
129
Q

What are the pros and cons of CABG?

A

Pros
Better prognosis
Deals with complex disease

Cons
Invasive
Risk of stroke, bleeding
Can’t do if frail, co-morbidities
One time treatment
Length of stay
Time for recovery
130
Q

What are acute coronary syndromes?

A

Covers a spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving myocardial infarction (MI)

131
Q

How is unstable angina clinically classified?

A

Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina

Take history, ECG, troponin levels (no significant rise in unstable angina)

132
Q

How is STEMI and NSTEMI diagnosed?

A

ST-elevation MI can usually be diagnosed on ECG at presentation

Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available.
May also be defined retrospectively as non-Q wave or Q-wave (broader and deeper) MI on the basis of whether new pathological Q waves develop on the ECG.
STEMI and MI with LBBB are more likely to develop pathological Q wave formation.

133
Q

What are the common symptoms of an MI?

A

Cardiac chest pain that is:
unremitting
usually severe but may be mild or absent
occuring at rest
associated with sweating, breathlessness, nausea and/or vomiting
one third occur in bed at night

134
Q

What is the lasting consequences of an MI?

A

Usually causes permanent heart muscle damage although this may not be detectable in small MIs.
Higher risk associated with higher age, diabetes, renal failure, left ventricular systolic dysfunction (elevated NT-proBNP level) and other risk factors.

135
Q

What are the initial management steps for a suspected MI?

A

Get in to hospital quickly – 999 call

Paramedics – if ST elevation, contact primary PCI centre for transfer

Take aspirin 300mg immediately

Pain relief – may be morphine (reduces pain and oxygen demand)

136
Q

What are the hospital management steps for a suspected MI?

A
Make diagnosis – history, ECG, troponin
Bed rest
Oxygen therapy if hypoxic
Pain relief – narcotics/ nitrates
Aspirin +/- P2Y12 inhibitor
Consider beta-blocker
Consider other antianginal therapy
Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy
137
Q

What’s the cause of acute coronary syndromes?

A

Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases

Uncommon causes include coronary vasospasm without plaque rupture, drug abuse (amphetamines, cocaine), dissection of the coronary artery related to defects of the vessel connective tissue, and thoracic aortic dissection

138
Q

What is troponin?

A

Protein complex regulates actin:myosin contraction in muscle
Highly sensitive marker for cardiac muscle injury
Not specific for acute coronary syndrome
May not represent permanent muscle damage
Positive in: gram negative sepsis, pulmonary embolism, myocarditis, heart failures, arrhythmias, cytotoxic drugs

139
Q

What are P2Y12 inhibitors?

A

Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’
Three options: clopidogrel, prasugrel and ticagrelor
Increase risk of bleeding so need to exclude serious bleeding prior to administration
Without inhibition, P2Y12 acts to amplify platelet aggregation

140
Q

What are GPIIb/IIIa antagonists?

A

Only intravenous drugs available
Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS
Increase risk of major bleeding so used selectively
Reducing use globally due to more effective oral antiplatelet therapy
Still useful in STEMI patients undergoing primary PCI to cover delayed absorption of oral P2Y12 inhibitors in these patients (due to opiates delaying gastric emptying).

141
Q

What are anticoagulants used for?

A

Used in addition to antiplatelet drugs
Target formation and/or activity of thrombin
Inhibit both fibrin formation and platelet activation
Fondaparinux (a pentasaccharide) used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used
Full-dose anticoagulation used during PCI: options are heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin) or the direct thrombin inhibitor bivalirudin (expensive, not used in Sheffield)
High dose heparin used during cardiopulmonary bypass for CABG surgery

142
Q

What factors affect a patient’s response to Clopidogrel?

A

Dose
Age
Weight
Disease states including diabetes mellitus and chronic kidney disease
Drug-drug interactions e.g. omeprazole and strong cytochrome P450 (CYP) 3A inhibitors
CYP2C19 loss-of-function (LOF) alleles

143
Q

How does Prasugrel compare to Clopidogrel?

A

Prasugrel is a prodrug like Clopidogrel but it is more effectively converted to its active metabolite.
More effective than Clopidogrel in ACS patients, but does increase bleeding.

144
Q

What are the adverse effects of Ticagrelor?

A

Common to all P2Y12 inhibitors:
Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance

Idiosyncratic
Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel (which are not associated with the same adverse effect but do not have the same evidence for longterm mortality reduction)
Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment

145
Q

How might deep vein thrombosis be diagnosed?

A

Signs: Tenderness, swelling, warmth and discolouration
Symptoms and signs non specific, clinical diagnosis unreliable
Unhelpful as it can have many differential diagnosis

146
Q

What is proximal and distal DVT?

A

Isolated distal DVT has no proximal component, is located below the knee, and is confined to the calf veins (peroneal, posterior, anterior tibial, and muscular veins).

Proximal DVT is one that is located in the popliteal, femoral, or iliac veins. Can break off and travels to the IVC to the heart and then block off the pulmonary artery.

147
Q

How is DVT investigated?

A

Ultrasound compression test for proximal veins - identifies whether there is a clot in the veins. Push with the probe to push the vein flat then it’s empty and if it won’t push flat then it’s full of clot.
D - dimer: Normal excludes diagnosis but a positive doesn’t confirm diagnosis (Can be raised in malignancy, inflammation and infection as well as for DVT)

148
Q

How is DVT treated?

A
LMW Heparin straight away (reliable anticoag for quick therapeutic level, short half life)
Oral warfarin (long half life - several days to build therapeutic dose. Stop LMW heparin at this level)
DOAC - Start from outset, initially twice day, can cut down to once daily after a few weeks. 
Compression stockings
149
Q

What causes DVT?

A

Underlying causes - Malignancy (1/3 of the elderly present with DVT’s) and thrombophilia (Recurrent thrombosis from a young age - genetic predisposition)

  • Spontaneous DVT (No clear factor/out of the blue)
  • Provoked DVT (Injury means chances are higher)
    If spontaneous DVT or PE, then once treatment has stopped there is a higher chance of reoccurance.
150
Q

What are the risk factors for DVT?

A

Surgery, immobility, leg fracture/ daily prophalyxis
Oral contraceptive/HRT/Pregnancy (High oestrogen states)
Long haul flights/travel (Rare) - No increased risk of DVT if flying in Europe
Inheritied thrombophillia (Runs in families)

151
Q

How to prevent DVT?

A

Mechanical - Hydration and early mobilisation, compression stockings, foot pumps.
Chemical - LMW Heparin (Prophylaxis given in hospital - Doesn’t cause bleeding as low dose)

152
Q

How might a pulmonary embolism commonly present?

A

Pleuritic chest pain, shortness of breath, haemoptysis (Pulmonary infarct), non-specific.
Differential diagnosis of chest pain and SOB.
Consider also musculoskeletal, infection ,malignancy, pneumothorax, cardiac and gastro causes.
Symptoms: Could have signs and symptoms of DVT

153
Q

Why is the size of a pulmonary embolism important?

A

Small = Only one of the arteries or at the bifurcations
Massive = Haemodynamically significant
Can block both pulmonary arteries leading to death
Near death experience/medical emergency

154
Q

How would you investigate a possible pulmonary embolism?

A

CXR (Usually normal)
ECG (Sinus tachycardia)
Blood gases (Type 1 resp failure, decreased CO2 and O2)
Mainly to rule out alternatives

D - dimer: Normal excludes diagnosis.
Ventilation/Perfusion scan: Mismatch defects (Used in pregnancy)
CTPA (Spiral CT with contrast, visualise major segmental thrombi, more invasive but quick and efficient, contraindicated in pregnancy)

155
Q

How is a pulmonary embolism treated?

A

Ensure normal Hb, platelets, renal function, baseline clotting.
LMW Heparin
IVC filter - Prevents clot moving and can be used if malignancy is suspected and needs investigations and have a high bleeding risk ie if need or had surgery.

156
Q

What is Warfarin?

A

Orally active tablet
Prevents synthesis of active factors II, VII, IX and X
Indirect anticoagulation
Works in the liver.
Antagonist of vitamin K
Long half life (36 hours)
Difficult to use (Old patients = small dose, Patient with lots of clots = higher dose)
Affected by vit K (Can be affected by diet and lifestyle), constant blood tests)

157
Q

What can reverse the effects of Warfarin?

A

Warfarin interferes with the vitamin K pathway
Means vit K can be given to reverse warfarin (Allows them to start synthesise of active clotting factors but not quickly - Takes around 24 hours to work - Not good for patient who is bleeding so can be used for high INR with no bleeding)

158
Q

How do you give Warfarin?

A
Individual variation in dose
Measure INR (International normalised ratio, derived from prothrombin time (Used with certain reagent and certain machine in each hospital - Different in different hospitals, therefore INR is a correction factor meaning the test can be done anywhere - Patients on warfarin want an increased prothrombin time)
Usual target range 2 - 3. 
Higher range 3 - 4.5 (Artificial Heart Valves)
159
Q

What are DOACs?

A

Direct Oral Anticoagulants
Orally active
Directly acting on factor II or X
No blood tests or monitoring
Shorter half-lives
Dose can be weight adjusted and age adjusted and for renal function (but not constantly changing)
Used for extended thromboprophylasis and treatment of AF and DVT/PE (Equivalent to INR 2-3, not higher so can’t be used for heart valves/ patients with recurrent thrombosis that need high targets)
Not used in pregnancy or breastfeeding (Small molecules so cross the placenta - Patients would usually inject with LMWH Heparin as warfarin is not used either)

160
Q

What is thrombosis?

A

Blood in vessels should be fluid.
Thrombosis is blood coagulation inside a vessel.
Veins = DVT or PE - Low pressure, fibrin rich - Anticoag (Warfarin and DOACs)
Arteries = Heart attack or stroke - High pressure situation, tends to be difficult to clot so it’s platelet rich - Anti platelet medications
Not to be confused with appropriate coagulation when blood escapes a vessel, failure of coagulation in this situation leads to bleeding.

161
Q

What are the consequences of arterial thrombosis?

A

Coronary circulation = Myocardial infarction
Cerebral circulation = cerebrovascular accident/stroke
Peripheral circulation = Peripheral vascular disease, claudication, rest pain or gangrene.

162
Q

How to treat an arterial thrombosis?

A

MI - Aspirin, LMWH or Fondraparinuex, thrombolytic therapy (Streoptokinase tissue plasminogen activator)
TPA generates plasmin that degrades fibrin. There is a narrow window to use in. This is narrower when used for strokes as opposed to MI.
Stroke: Aspirin or clopidogrel, prasugrel, tiglacor: anti platelet.

163
Q

What are the potential causes of a venous thrombosis?

A

Circumstantial causes: Surgery, Immobilisation, Oestrogens: Oral contraceptive pill, HRT, Malignancy, Long haul flights

Genetic causes: Factor V Leiden, PT202107A (common)
Antithrombin, Protein C or S deficiency (uncommon)

Acquired causes: Anti phospholipid syndrome, Lupus anticoagulant, Hyperhomocysteinameia

164
Q

What does Heparin do in thromboprophylaxis?

A

Binds to antithrombin and increases it’s activity.
Indirect thrombin inhibitor
Mointer with APTT, aim ratio 1.8 - 2.8
Given by continuous infusion (unfractionated - big so doesn’t move into the vessel)
Only really used in cardiothoracic theatres when patients are on bypass.
Reversible with Protomean

165
Q

What does LMW Heparin do in thromboprophylaxis?

A

Smaller molecules, less variation in dose and renal excretion.
Not reversible with Protomean
Weight adjusted once daily subcutaneous injection.

166
Q

What does Aspirin do in thromboprophylaxis?

A

Inhibits cyclo - oxygenase irreversibly
Act for lifetime of platelet so around 7 - 10 days. Stop aspirin, needs to be stopped a few days before hand.
Inhibits thromboxane formation and hence platelet aggregation
Used in arterial thrombosis form 75 (Daily) to 300 (MI) mg.
Clopidogrel similar, but inhibits ADP induced platelet aggregation.

167
Q

What are the features of the pericardium?

A

2 layers:
- Visceral single cell layer adherent to epicardium
- PERICARDIAL SPACE
- Fibrous parietal layer 2mm thick – has fibrous attachments to fix the heart in the thorax – diapraghm
Acellular collagen and elastin fibres
50ml of serous fluid
Great vessels lie within the pericardium
Left atrium is mainly outside the pericardium

168
Q

What is the function of the pericardium?

A

Mechanical function restrains the filling volume of the heart. Initially stretchy but becomes stiff at higher tension.
Thus pericardial sac has a small reserve volume.
If this volume is exceeded the pressure is translated to the cardiac chambers.
Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount – Tamponade physiology
Prolonged filling and stretch allows the pericardium to adapt.

169
Q

How does chronic pleural effusion occur?

A

Chronic accumulation allows adaptation of the parietal pericardium
This compliance reduces the effect on diastolic filling of the chambers
As a result very slowly accumulating effusions rarely cause tamponade

170
Q

What is acute pericarditis?

A

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion
Clinical diagnosis made with 2 of 4 from:
Chest Pain (85-90%)
Friction rub (33%)
ECG changes (60%)
Pericardial effusion (up to 60% usually mild)

171
Q

What are the infectious causes of acute pericarditis?

A

Viral (common): Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis).

Bacterial: Mycobacterium tuberculosis (other bacteria rare).

172
Q

What are the non-infectious causes of acute pericarditis?

A

Autoimmune (common):
Sjögren syndrome, rheumatoid arthritis, scleroderma,
systemic vasculitides

Neoplastic (secondary to viral causes):
Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).

Metabolic: Uraemia, myxoedema,

Traumatic and Iatrogenic: 
Early onset (rare):
Direct injury (penetrating thoracic injury, oesophageal perforation). 
Indirect injury (non-penetrating thoracic injury, radiation injury). 

Delayed onset: Pericardial injury syndromes (common) iatrogenic trauma (e.g.coronary percutaneous intervention, pacemaker lead insertion and radiofrequency ablation).

Other:
Amyloidosis, aortic dissection, pulmonary arterial hypertension and chronic heart failure.

173
Q

What’s the epidemiology of acute pericarditis?

A

Difficult to quantify
80-90% of all pericarditis idiopathic
Seasonal with viral trends
Higher in young, previously healthy patients

174
Q

How does acute pericarditis present clinically?

A

Chest pain: Severe, Sharp and pleuritic (without constricting crushing character of ischaemic pain)
Rapid onset, Left anterior chest or epigastrium
Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve)
Relieved by sitting forward exacerbated by lying down

Pretty common to have associated symptoms – viral infection that precedes the pericarditis

Dyspnoea
Cough
Hiccups (phrenic)
Skin rash
Joint pain
175
Q

How would you investigate acute pericarditis?

A
Clinical examination
- Pericardial rub – pathognomonic, crunching snow
- Sinus tachycardia
- Fever
- Signs of effusion (pulsus paradoxus, Kussmauls sign)
ECG
Bloods
CXR
Echocardiogram
176
Q

What are the features of an ECG in pericarditis?

A

Diffuse ST segment elevation
Concave ST segment – may resemble acute injury pattern of STEMI
No reciprocal ST depression
Saddle shaped
PR depression
Mechanism is epicardial inflammation as adjacent to pericardium ( parietal is inert)

177
Q

What investigation results would you expect in suspected pericarditis?

A

FBC: Modest increase in WCC, mild lympocytosis
ESR & CRP: High ESR may suggest aetiology
Antinuclear antibody test
Troponin: Pericarditis in itself shouldn’t give a increased Troponin. But if the associate myocytes on the epicardium are damaged then there will be an increase in Troponin.

CXR
Often normal in idiopathic
Pneumonia common with bacterial
Modest enlargement of cardiac silhouette rule out effusion (>300ml to be detectable!)

178
Q

How would you treat acute pericarditis?

A

Sedentary activity until resolution of symptoms and ECG/CRP
NSAID: Ibuprofen or Aspirin
Colchicine limited by nausea and diarrhoea, reduces recurrence

179
Q

What are the complications of acute pericarditis?

A

Major:Fever >38°C, Subacute onset, Large pericardial effusion, Cardiac tamponade, Lack of response to aspirin or NSAIDs after at least 1 week of therapy

Minor: Myopericarditis, Immunosuppression, Trauma, Oral anticoagulant therapy

180
Q

What is the prognosis for a patient with acute pericarditis?

A

Most patients with acute pericarditis have a good long-term prognosis.
Cardiac tamponade rarely occurs in patients with acute idiopathic pericarditis.
Constrictive pericarditis may occur in 1% of patients with acute idiopathic pericarditis.
The risk of developing constriction can be classified as:
- low for idiopathic and presumed viral pericarditis
- intermediate for autoimmune, immune- mediated and neoplastic aetiologies
- high for bacterial aetiologies, especially with TB and purulent pericarditis

15 – 30% of patients with acute pericarditis will develop recurrence. Colchicine reduced recurrence rate by 50%

181
Q

What are some of the more specific causes of pericarditis?

A
  • Viral pericarditis: commonest cause in developed world
  • Purulent bacterial pericarditis and effusion
    Staph, strep and pneumococci (Pneumonia, empyema)
    Rare <1% Very sick, high mortality
  • Tuberculous effusion TB pericarditis
    90% HIV +ve in developed countries. High mortality
  • Dressler’s syndrome (Post cardiac injury syndromes)
    Late post MI 1-2 weeks post MI
182
Q

What is Hypertrophic cardiomyopathy?

A
HCM is a primary heart muscle disease and the most common. The enlargement of the thickened wall encroaches into the left ventricle.This increased thickened wall will make it hugely more powerful than the normal heart. But it is slower and less compliance in relaxation (diastolic dysfunction).
Chaotic arrangement of myofibrils: myofibrillar disarray.
Can be a cause of sudden death in otherwise healthy young people (18-25) – genetically passed through the family.
Protein malfunction (due to genetic abnormality) in sarcomeres, the cytoskeleton and cell adhesion leads to cardiomyopathy.
183
Q

What are the different types of cardiomyopathy?

A

Hypertrophic - muscle is thickened
Dilated
Arrhythmogenic - abnormality of structure which leads to rhythm disturbance

184
Q

What is dilated cardiomyopathy?

A

Wall of the heart is either normal or relatively thin.
Present with heart failure - problems with contraction.
Can have left ventricular dilatation, biventricular or all four chambers dilatation.

185
Q

What is Arrhythmogenic cardiomyopathy?

A

Any of the cardiomyopathies can cause rhythm disturbances but this one particular so.
Death of myocytes and replacement with fibro-fatty tissue, cannot contract properly.
Initially described in the right ventricle but can also occur in the left ventricle.
Often get an abnormal ECG (particular V1-V3). Characteristic epsilon waves that can come and go.
Disease of the desmosome (area between the cells). There are protein structures that cross this intracellular space. If there is an abnormality in any of these proteins, you start to lose the adhesion between the cells.

186
Q

What is Naxos Disease?

A

Patients with woolly hair and palmar plantar keratoderma also have arrhythmogenic cardiomyopathy. Primary problem of cell separation. Physical phenotype.
Recessive disease.

187
Q

Other than cardiomyopathies, what are some other significant inherited cardiac conditions?

A

Marfan’s syndrome - abnormality in fibrillin which is present all over the body, long arm span, long fingers, very tall, prone to aorta aneurysm or vascular aneurysm elsewhere.

Familial Hypercholesterolaemia - 1 in 250/300, genetic mutation affecting the LDL receptor. LDL receptor would usually take up cholesterol from the circulation. Whereas, here there is very high amounts of cholesterol in the circulation.
Very serious - causing 100x risk of a heart attack.
Can get lipid deposition in the hands, tendons, eyes.

188
Q

Why do we treat hypertension?

A

Important preventable cause of premature morbidity and mortality.

Major risk factor for:
	Stroke – ischaemic and haemorrhagic
	Myocardial infarction
	Heart failure
	Chronic renal disease
	Cognitive decline
	Premature death
189
Q

What is the clinical definition of hypertension?

A

Clinic BP 140/90 mmHg or higher

190
Q

What are the different stages of hypertension?

A

Stage 1 hypertension 140/90 and 135/85 (ABPM)
Stage 2 hypertension 160/100 and 150/95 (ABPM)
Severe hypertension SBP 180 or DBP 110

191
Q

How is hypertension treated?

A

Primary (essential) hypertension (no obvious cause)

  • Lifestyle modification – weight, alcohol, smoking, salt intake
  • Antihypertensive drug therapy

Consider secondary hypertension (underlying cause)
eg young patient
resistant BP
symptoms/signs of underlying cause

192
Q

Who should receive antihypertensive drug treatment?

A

People aged under 80 years with stage 1 hypertension who have one or more of the following:

  1. Target organ damage e.g. eyes, heart, kidneys
  2. Established cardiovascular disease
  3. Renal disease
  4. Diabetes
  5. A 10-year cardiovascular risk of 20% or greater.

OR people of any age with stage 2 hypertension.

193
Q

What are the blood pressure targets?

A

Under 80 years < 140/90 < 135/85 (ABPM)

Over 80 years < 150/90 < 145/85 (ABPM)

194
Q

Where does BP therapy target?

A
  • Cardiac output and Peripheral Resistance
  • Interplay between:
    a. Renin-Angiotensin-Aldosterone system
    b. Sympathetic nervous system (noradrenaline)
  • Local vascular vasoconstrictor and vasodilator mediators – also have an impact
195
Q

What are ACE inhibitors?

A

ACE converts angiotensin I to angiotensin II.
Angiotensin II is a powerful vasoconstrictor.
Inhibiting this, reduce vasconstriction.
Clinical indications: Hypertension, Heart failure, Diabetic nephropathy
Ramipril, Enalapril, Perindopril, Trandolapril
Main adverse effects
- Related to reduced angiotensin II formation: Hypotension, Acute renal failure, Hyperkalaemia, Teratogenic effects in pregnancy
- Related to increased kinin production: Cough – dry and persistant, Rash, Anaphylactoid reactions – allergic type reactions

196
Q

What are ARBs?

A

Angiotensin II Receptor Blockers
Blocks the receptor for Angiotensin II, reducing its vasoconstriction effect.
Clinical indications: Hypertension, Diabetic nephropathy, Heart failure (when ACE-I contraindicated)
Candesartan, Losartan, Valsartan, Irbesartan, Telmisartan
Main adverse effects
Symptomatic hypotension (especially volume deplete patients), Hyperkalaemia, Potential for renal dysfunction, Rash, Angio-oedema
Contraindicated in pregnancy
Generally very well tolerated

197
Q

What are calcium channel blockers?

A

Vasodilators
Reducing peripheral pressure
Clinical indications: Hypertension, Ischaemic heart disease (IHD) – angina, Arrhythmia (tachycardia)
Amlodipine, Nifedipine, Diltiazem, Felodipine, Lacidipine, Verapamil

198
Q

What are the different types of calcium channel blockers?

A
  1. Dihydropyridines: nifedipine, amlodipine, felodipine, lacidipine
    Preferentially affect vascular smooth muscle
    Peripheral arterial vasodilators
  2. Phenylalkylamines: verapamil
    Main effects on the heart
    Negatively chronotropic, negatively inotropic
  3. Benzothiazepines: diltiazem
    Intermediate heart/peripheral vascular effects
199
Q

What are the adverse effects of calcium channel blockers?

A
  • Due to peripheral vasodilatation (mainly dihydropyridines): Flushing, Headache, Oedema – ankle swelling due to gravity, Palpitations – if you dilate peripheral vascularisation, your brain thinks that you are losing blood, so causes ventricular tachycardia.
  • Due to negatively chronotropic effects (mainly verapamil/diltiazem): Bradycardia, Atrioventricular block
  • Due to negatively inotropic effects (mainly verapamil): Worsening of cardiac failure
  • Verapamil causes constipation
200
Q

What are Beta-adrenoceptor blockers?

A

Beta-adrenoreceptor antagonists act on the sympathetic nervous system
Clinical indications: Ischaemic heart disease (IHD) – angina, Heart failure, Arrhythmia, Hypertension
Bisoprolol, Carvedilol, Propanolol, Metoprolol, Atenolol, Nadolol

201
Q

Can beta blockers be selective?

A

Selectivity is a spectrum: B1 selective (Metoprolol, Bisoprolol, in the middle (Atenolol), Non-selective (Propanolol, Nadolol, Carvedilol).
The term “cardioselective” is often used to imply β-1 selectivity
This is a misnomer since up to 40% of cardiac β-adrenoceptors are β-2

202
Q

What are the adverse effects of beta blockers?

A
Fatigue
Headache
Sleep disturbance/nightmares – cross the blood brain barrier
Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction

Worsening of: Asthma (may be severe) or COPD, PVD – Claudication or Raynaud’s, Heart failure – if given in standard dose or acutely

203
Q

What are the different types of diuretics?

A

Clinical indications: Hypertension, Heart failure

  • Thiazides and related drugs (distal tubule) - Bendroflumethiazide, Hydrochlorothiazide, Chlorthalidone
  • Loop diuretics (loop of Henle) - Furosemide, Bumetanide
  • Potassium-sparing diuretics - Spironolactone, Eplerernone, Amiloride, Triamterine
  • Aldosterone antagonists
204
Q

What are the adverse effects of diuretics?

A
Hypovolaemia (mainly loop diuretics)
Hypotension (mainly loop diuretics)
Hypokalaemia
Hyponatraemia
Hypomagnesaemia
Hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Erectile dysfunction (mainly thiazides)
Impaired glucose tolerance (mainly thiazides)
205
Q

Other than ACE-I, ARB, CCB, BB and diuretics, what other hypertensives are there?

A

a-1 adrenoreceptor blockers: Doxazosin
Centrally acting anti-hypertensives: Moxonidine, Methyldopa
Direct renin inhibitors: Aliskiren

206
Q

What are the treatment steps for hypertension?

A
1) Under 55s: ACE-I, ARB
Over 55s/Afro-Caribbean: CCB
2) ACE-I/ARB and CCB
3) Addition of thiazide-like diuretic
4) RESISTANT HYPERTENSION: Spironolactone, high dose thiazide-like diuretic, Alpha blocker, beta blocker, (others)
207
Q

What is heart failure?

A

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired.
It is caused by structural or functional abnormalities of the heart.
Can be acute or chronic.
Most common cause is coronary artery disease
Causes morbidity, mortality, hospital admissions and substantial cost
- Heart failure due to left ventricular systolic dysfunction - LVSD
- Heart failure with preserved ejection fraction (diastolic failure) – HFPEF
Main benefit is with vasodilator therapy via neurohumoral blockade (RAAS - SNS) and not from LV stimulants

208
Q

How is heart failure treated pharmacologically?

A

Symptomatic treatment of congestion: Diuretics (usually loop)
Disease influencing therapy – neurohumoral blockade
Inhibition of renin-angiotensin-aldosterone system
Inhibition of the sympathetic nervous system
a. First line: ACE inhibitors and beta blocker therapy (Low dose and slow uptitration)
b. Aldosterone antagonists
c. ACE-I intolerant: Angiotensin receptor blocker
d. ACE-I and ARB intolerant: Hydralazine/nitrate combination
e. Consider digoxin or ivabradine to slow heart rate down

209
Q

What are nitrates?

A

Arterial and venous dilators
Reduction of preload and afterload
Lower BP
Clinical indication: ischaemic heart disease (angina), heart failure
Isosorbide mononitrate, GTN spray, GTN infusion (in ICU)
Aren’t used as anti-hypertensive because they are not as effective and you can become tolerant to them.
GTN syncope – lowers their BP and causes a throbbing headache

210
Q

How does the chest pain vary between the acute coronary syndromes?

A

Chronic stable angina: Anginal chest pain, Predictable, Exertional, Infrequent, Stable
Unstable angina / acute coronary syndrome (NSTEMI): Unpredictable, may be at rest, Frequent, Unstable
ST elevation Myocardial Infarction (STEMI): Unpredictable, Rest pain, Persistent, Unstable

211
Q

What is the treatment plan for chronic stable angina?

A

1) Antiplatelet therapy: Aspirin, Clopidogrel
2) Lipid-lowering therapy: Statins (simvastatin, atorvastatin, rosuvastatin, pravastatin)
3) Short acting nitrate: GTN spray for an attack
4) First-line: Beta-blocker, CCB
5) If intolerant, switch
6) If not controlled, combine
7) If intolerant/not controlled, consider monotherapy or combinations with long acting nitrates, Ivabradine, Nicorandil, Ranolazine

212
Q

What is the treatment plan for NSTEMI and STEMI?

A

1) Pain relief: GTN spray, Opiates
2) Dual anti-platelet therapy: Aspirin plus ticagrelor or prasugrel or clopidogrel
3) Antithrombin therapy: Fondaparinux
4) Consider Glycoprotein IIb IIIa inhibitor (high risk cases): tirofiban, eptifibatide, abciximab
5) Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker
6) Lipid lowering therapy: Statins
7) Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist

213
Q

What are the different types of anti-rhythmic drugs according to the Vaughan Williams classification?

A

Class I: Sodium channel blockers
Ia - disopyramide, quinidine, procainamide
Ib - lidocaine, mexilitene
Ic - flecainide, propafenone

Class II: Beta adrenceptor antagonists

  • propranolol, nadolol, carvedilol (non-selective)
  • bisoprolol, metoprolol (β1-selective)

Class III: Prolong the action potential - amiodarone, sotalol

Class IV: Calcium channel blockers - verapamil, diltiazem

214
Q

What is Digoxin?

A

Cardiac glycoside
Inhibit Na/K pump

Main effects are on the heart:
Bradycardia (increased vagal tone)
Slowing of atrioventricular conduction (increased vagal tone)
Increased ectopic activity
Increased force of contraction (by increased intracellular Ca)

Narrow therapeutic range – can easily become toxic
Nausea, vomiting, diarrhoea, confusion
Difficult to diagnose Digoxin toxicity!

Used in atrial fibrillation (AF) to reduce ventricular rate response
Use in severe heart failure as positively inotropic

215
Q

What is heart failure?

A

An inability of the heart to deliver enough blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.
The syndrome of breathlessness, tiredness and fluid overload caused by a form of cardiac dysfunction

216
Q

What causes heart failure?

A
The commonest cause is myocardial dysfunction.
This usually results from IHD.
Other causes include:
-	Hypertension,
-	alcohol excess,
-	cardiomyopathy,
-	valvular,
-	endocardial,
-	pericardial causes
217
Q

How does the incidence of heart failure change according to age and gender?

A

Higher in men - Men get heart failure earlier because they do not have the protective effects of oestrogen which protect against atherosclerosis.

Incidence rises from the age of 55 and peaks in the over 80 years old

218
Q

What are the symptoms of heart failure?

A
Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight
219
Q

What are the signs of heart failure?

A
Tachycardia
Displaced apex beat
Raised JVP
Added heart sounds/murmurs
Hepatomegaly (eg pulsatile/tender)
Peripheral/sacral oedema
Ascites
220
Q

How is heart failure classified?

A

Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)

221
Q

What does the NTproBNP test tell you?

A

You can check the NTproBNP but if it is positive it doesn’t mean that it is heart failure.
It could be many other conditions too which have nothing to do with heart failure.
400-2000 72% chance of heart failure
Above 2000 96% chance of heart failure

222
Q

How can a transthoracic echocardiogram be useful in heart failure?

A

TTE to assess structural/functional abnormalities
Not needed immediately (or at all) in those with established diagnosis of HF
de Novo AHF require early TTE (within 48 h)
Immediate TTE is only mandatory in patients with haemodynamic instability, and when acute life-threatening and potentially treatable abnormalities are expected.
Repeat TTE is not recommended for its limited use

223
Q

What factors could trigger acute heart failure?

A
Acute coronary syndrome
Tachyarrhythmias
Excessive rise in BP
Infection
Non-adherence with salt/fluid intake or medications
Bradyarrhythmias
Toxic substances
Drugs
Exacerbation of COPD
Pulmonary embolism
Surgery and perioperative complications
Increased sympathetic drive
Metabolic hormonal dearrangements
Cerebrovascular insult
Acute mechanical cause
224
Q

What are the different types of heart failure?

A

LEFT-SIDED
Heart failure with reduced ejection fraction (HFrEF) (aka systolic failure) Left ventricle loses its ability to contract normally. The heart can’t pump with enough force to push enough blood into circulation.
Heart failure with preserved ejection fraction (HFpEF), aka diastolic failure (or diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can’t properly fill with blood during the resting period between each beat.

Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart’s right side.

225
Q

What is used to treat HFPEF?

A
Diuretics
ACEI
ARB
Beta Blockers
Mineralocorticoid receptor antagonists
Ivabradine
Tafamidis - reduces progression of the disease
Sacubitril-Valsartan
226
Q

What is Cardiac re-synchronization therapy?

A

Using multi-site pacemakers (right atrial, right ventricular and coronary sinus pacing leads), to simultaneously pace both sides of the LV, in patients with LBBB and significant dys-synchrony with QRS duration >130 m sec (ideally >150 m sec). These devices reduce morbidity and mortality.

227
Q

Why is palliative care important for patients with heart failure?

A

HF differs from cancer in that the journey towards palliative care is an equilibrium of an excursion between active and palliative therapy, before the eventual event occurs.

228
Q

How is hypertension linked to stroke?

A

Most strokes occur with people with normal blood pressure (just because there are more people with normal BP than high BP). Hypertensive patients have a 30-40% increased risk of a stroke.

229
Q

What lifestyle changes should be made in a hypertensive patient?

A

Increased exercise, reduced salt intake, weight loss smoking, alcohol.
WEIGHT, SALT, ALCOHOL are the main ones.

Smoking itself doesn’t have a huge impact and smokers are often less likely to be obese, but it does increase the likelihood of other cardiovascular events.

230
Q

What are some common drugs that might be contributing to a patient’s hypertension?

A

Venlafaxine (a serotonin-noradrenaline reuptake inhibitor) which can increase blood pressure.
NSAIDs can also increase blood pressure, along with the oral contraceptive pill, corticosteroids, cold cures.

231
Q

Why is the ECG such an invaluable tool?

A
Simple to perform
Can provide information about range of conditions:
Cardiac rhythm - 
Cardiac ischaemia
Myocardial disease
Electrolyte disturbances
232
Q

What are the basic principles of ECGs?

A

Amplitude of deflection is related to mass of myocardium
Width of deflection reflects speed of conduction
Positive deflection is towards the lead/vector

233
Q

What happens when there are abnormalities of axis in the heart?

A

Left axis deviation -30 to -90 degrees

  • Left anterior fascicular block
  • Left bundle branch block
  • Left ventricular hypertrophy

Right axis deviation 90 to 180 degrees

  • Left posterior fascicular block
  • Right heart hypertrophy/strain
234
Q

What is characteristic of a P wave?

A
Positive inferior leads
Positive in lead I
Negative in aVR
Biphasic in V1
Normally <120 ms wide
	        <0.3mV (3 small sq) tall
235
Q

What are the abnormalities of a P wave?

A

Low amplitude: Atrial fibrosis, obesity, hyperkalaemia
High amplitude ‘Tall’: Right atrial enlargement

Broad notched ‘Bifid’: Left atrial enlargement

Alternative pacemaker foci: Focal atrial tacycardias

236
Q

What is the PR interval?

A

Consists of atrial depolarisation and conduction from atria to ventricles.
Normally 120-200 ms
Prolonged in disorders of AV node and specialised conducting tissue
Shorter in younger patients or in pre-excitation (Wolf-Parkinson-White)
P interval may lengthen if the AV node conduction is getting slower with age or due to an ectopic beat.

237
Q

What is characteristic of the QRS complex?

A

Ventricular depolarisation
Normally <120ms
Size of complexes related to myocardial mass
Predominantly negative in V1, transitioning to postive by V6
Normal frontal axis -30 to +90 (positive in leads I, II)

238
Q

What are the abnormalities of a QRS complex?

A

Broad QRS: Ventricular conduction delay/bundle branch block

Small QRS complexes: Obese patient, Pericardial effusion, Infiltrative cardiac disease

Tall QRS complexes: Left ventricular hypertrophy, Thin patient – less tissue present

239
Q

What is the QT interval?

A

From start of QRS to end of T wave
Represents ventricular depolarisation and repolarisation
Corrected for heart rate (380 – 450ms)
Excessively rapid or slow repolarisation can be arrhythmogenic
“Long QT” or “Short QT” syndromes
Congenital, drugs, electrolyte disturbances

240
Q

What is the ST segment?

A

From end of QRS (“J point”) to start of T wave
Normally isoelectric
Can be elevated in early repolarisation, myocardial infarction, pericarditis/myocarditis

241
Q

What are the characteristics of the T wave?

A

Height of T wave normally less than QRS

Direction of deflection usually similar to QRS (in limb leads), but in opposite direction in bundle branch block

242
Q

What are the common tachycardias?

A

Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Focal atrial tachycardia

Ventricular tachycardia
Ventricular fibrillation

243
Q

What might cause bradycardia?

A

Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs

244
Q

What is characteristic of right and left bundle branch block in an ECG?

A

In V1 and V6
Left bundle branch block - William (W shape)
Right bundle branch block - Marrow (M shape)

245
Q

How does electrolyte disturbance affect the ECG?

A

Potassium
Hyperkalaemia: Tall T waves, flattening of P waves, broadening of QRS
Hypokalaemia: Flattening of T wave, QT prolongation

Calcium
Hypercalcaemia: QT shortening
Hypocalcaemia: QT prolongation

246
Q

What is aortic stenosis?

A

Normal Aortic Valve Area: 3-4 cm2
Symptoms occur when valve area is 1/4th of normal.
Types: Supravalvular, Subvalvular, Valvular

247
Q

What is the pathophysiology of aortic stenosis?

A

A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines.

248
Q

What causes aortic stenosis?

A

Congenital: aortic stenosis or bicuspid valve, commonly associated with aortic coarctation, dissection or aneurysm.
Acquired: degenerative calcification, rheumatic heart disease, rare causes. Adhesions and fusion of commissures and cusps. May be a result of infections/radiation.

249
Q

How does aortic stenosis present?

A

Syncope: (exertional) 15%
Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
Sudden death <2%

250
Q

What are the physical signs of aortic stenosis?

A

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)
Heart sounds- soft or absent second heart sound, S4 gallop due to LVH.
Ejection systolic murmur- crescendo-decrescendo character.
“Loudness” does NOT tell you anything about severity

251
Q

What is the prognosis of aortic stenosis?

A

Angina + AS: 50% survive for 5 years.
Syncope + AS: 50% survive for 3 years,
HF + AS mean survival is <2 years.
Risk of sudden cardiac death in asymptomatic or minimally symptomatic patients is rare (<2%).

252
Q

How would you investigate aortic stenosis?

A

Echocardiography
Two measurements obtained are:
Left ventricular size and function: LVH, Dilation, and EF
Doppler derived gradient and valve area (AVA)

253
Q

How is aortic stenosis managed?

A

Fastidious dental hygiene / care
Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS
Surgical Replacement: Definitive treatment
TAVI – Transcatheter Aortic Valve Implantation

254
Q

What occurs in a TAVI – Transcatheter Aortic ValveImplantation procedure?

A

Guided wire through the femoral artery
Blowing up a balloon to open up the narrowing (cracking it open)
Put in a new valve where the old valve was (self-expanding/balloon expanding)
Catheter guide wire removed

255
Q

When should you intervene with a patient with aortic stenosis?

A

Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF
Any patient undergoing CABG with moderate or severe AS

256
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole

Mild (physiological) MR is seen in 80% of normal individuals.

257
Q

What can cause chronic mitral regurgitation?

A

Myxomatous degeneration (MVP)
Ischemic MR – rupture or weakening
Rheumatic heart disease
Infective Endocarditis

258
Q

What is the pathophysiology of chronic mitral regurgitation?

A

Pure Volume Overload – blood going back to where it shouldn’t do
Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
Progressive left ventricular volume overload leads to dilatation and progressive heart failure.

259
Q

How will mitral regurgitation present?

A

Auscultation: pansystolic murmur at the apex radiating to the axilla
In chronic MR, the intensity of the murmur does correlate with the severity.
Displaced hyperdynamic apex beat

Exertion Dyspnoea: ( exercise intolerance)

Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

260
Q

What is the prognosis of mitral regurgitation?

A

Compensatory phase: 10-15 years
Patients with asymptomatic severe MR have a 5%/year mortality rate
Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply
Mortality: From progressive dyspnoea and heart failure

261
Q

How would you investigate mitral regurgitation?

A

ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
(TOE - transoesophageal echocardiography)

262
Q

How would you manage mitral regurgitation?

A

Vasodilator such as ACEI, hydralazine
Rate control for atrial fibrillation with B-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Diuretics for fluid overload
Serial Echocardiography

263
Q

When should the patient have surgery when they have mitral regurgitation?

A

ANY Symptoms at rest or exercise with (repair if feasible)
Asymptomatic:
If EF <60%, LVESD >45mm
If new onset atrial fibrillation/raised PAP

264
Q

What is Aortic Regurgitation?

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

265
Q

What can cause Aortic Regurgitation?

A

Bicuspid aortic valve
Rheumatic
Infective endocarditis

266
Q

What is the pathophysiology of Aortic Regurgitation?

A

Combined pressure AND volume overload

Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

267
Q

What are the physical signs of Aortic Regurgitation?

A

Wide pulse pressure: most sensitive
Hyperdynamic and displaced apical impulse

Auscultation-
Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve

268
Q

What is the prognosis of Aortic Regurgitation?

A

Asymptomatic until 4th or 5th decade
Rate of Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnoea: exertional, orthopnea, and paroxsymal nocturnal dyspnea
- Palpitations: due to increased force of contraction and ectopics

269
Q

What are the investigations of Aortic Regurgitation?

A

CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function

270
Q

How would you manage aortic regurgitation?

A

General: consider infective endocarditis prophylaxis
Medical: Vasodilators (ACEI’s improve stroke volume and reduce regurgitation only if pt symptomatic or hypertensive.
Serial Echocardiograms: to monitor progression.
Surgical Treatment: Definitive Tx

271
Q

When would you consider surgery in aortic regurgitation?

A

ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated

272
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole
Normal MV Area: 4-6 cm2
Transmitral gradients and symptoms begin at areas less than 2 cm2
Rheumatic carditis is the predominant cause
Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.

273
Q

What causes mitral stenosis?

A

Rheumatic heart disease: 77-99% of all cases
Infective endocarditis: 3.3%
Mitral annular calcification: 2.7%

274
Q

What is the pathophysiology of mitral stenosis?

A
  • Progressive Dyspnea (70%): LA dilation leads to pulmonary congestion (reduced emptying)
    worse with exercise, fever, tachycardia, and pregnancy
  • Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation.
  • Right heart failure symptoms: due to Pulmonary venous hypertension
  • Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
275
Q

What is the prognosis of mitral stenosis?

A

Disease of plateaus:
Mild MS: 10 years after initial RHD insult
Moderate: 10 years later
Severe: 10 years later

Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism.

276
Q

What are the physical signs of mitral stenosis?

A

Prominent “a” wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

277
Q

What are the heart sounds in mitral stenosis?

A

Diastolic murmur:
Low-pitched diastolic rumble most prominent at the apex.
Heard best with the patient lying on the left side in held expiration
Intensity of the diastolic murmur does not correlate with the severity of the stenosis

Loud Opening S1 snap: heard at the apex when leaflets are still mobile
Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.
A shorter S2 to opening snap interval indicates more severe disease.

278
Q

How would you investigate mitral stenosis?

A

ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

279
Q

How would you manage mitral stenosis?

A

Serial echocardiography
Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
B-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Diuretics for fluid overload
Identify patient early who might benefit from percutaneous mitral balloon valvotomy.

280
Q

When should mitral valve replacement be recommended?

A

ANY SYMPTOMATIC Patient with heart failure Class III (in activities in daily living)
Asymptomatic moderate or Severe MS with a pliable valve suitable for percutaneous mitral balloon valvotomy

281
Q

What is infective endocarditis?

A

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc).

282
Q

What are the different types of infective endocarditis?

A

Left sided native IE (mitral or aortic)
Left sided prosthetic IE
Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
Device related IE (pacemakers, defibrillators, with or without valve IE)
Prosthetic; can be Early (within year) or Late (after a year) post op

283
Q

How might a patient catch infective endocarditis?

A

Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected.
Introduce infectious material into the blood stream or directly onto the heart during surgery
Have had IE previously

284
Q

What is the epidemiology of infective endocarditis?

A
Used to be a disease of the young affected by rheumatic heart disease.
Now it is a disease of:
the elderly (in an ageing population)
the young i.v. drug abusers
the young with congenital heart disease.
anyone with prosthetic heart valves
285
Q

What is the prognosis for Infective Endocarditis?

A

Incidence and mortality have not fallen over 30 years

10 year survival 60-90%

286
Q

How does infective endocarditis present?

A

Depends on site, organism, etc
Signs of systemic infection (fever, sweats, etc)
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction
Valve dysfunction; heart failure, arrythmia
New regurgitant heart murmur
Embolic events of unknown origin
Sepsis of unknown origin

287
Q

What is the criteria for infective endocarditis?

A

Definite IE
2 major, 1 major+3 minor, 5 minor
Possible IE
1 major, 1 major+3 minor, 5 minor

Major Criteria
Bugs grown from blood cultures
evidence of endocarditis on echo, or new valve leak
Minor Criteria
Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures
288
Q

What are the different types of Echocardiography that can be used in infective endocarditis?

A

Transthoracic echo (TTE). Safe, non-invasive, no discomfort, often poor images so lower sensitivity

Transoesophageal (TOE/TEE). Excellent pictures as long as you don’t mind having a big tube pushed down your throat. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration. Easiest if ventilated (but never ventilate just for TOE)

289
Q

What are some of the peripheral signs of infective endocarditis?

A

Petechiae rash 10 to 15%,
Splinter hemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
Roth spots on fundoscopy, soft exudates are also seen (retinal infarcts)

290
Q

How would you diagnose infective endocarditis?

A

Cultures may remain negative in 2% to 5% of patients with IE. Certain organisms: cell media; special media or microbiological methods, or may require long incubtion 7-21/7.
The most common cause for negative blood cultures in patients with IE is prior antimicrobial therapy.

ECG (ischemia or infarction, new appearance of heart block)
Transthoracic echocardiography is of crucial importance in detecting a vegetation.
Transoesophageal echo (TOE) has improved the rate of detection of vegetations on native valves to 90–95%
A negative TTE/TOE does not eliminate the possibility that IE is present.
291
Q

How would you treat infective endocarditis?

A

Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities
Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc
Surgery

292
Q

When would you operate in a patient with infective endocarditits?

A

The infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall)
Complications (aortic root abscess, severe valve damage
to remove infected devices (always needed)
To replace valve after infection cured (may be weeks/months/years later
To remove large vegetations before they embolise

293
Q

How can we prevent infective endocarditis?

A

For years, patients with valve disease were given antibiotic prophylaxis during interventions (esp dental)
NICE guidance in 2008 recommended not to give prophylaxis to anyone (and remains current)
ESC guidance is to consider prophylaxis in high risk patients (prosthetic valves, previous IE, cyanotic heart disease)

294
Q

How has the prognosis of congenital heart disease changed?

A

Vary from minor problems to issues that incompatible with life ex-utero
Many lesions used to have a very poor prognosis before cardiac childhood surgery
The advent of surgery and interventional cardiology mean that >85% will survive to be > 18 years

295
Q

What are some of the potential issues in congenital heart patients?

A

Intellectual disability in 10% (Down’s syndrome)
Psychosocial issues
Transition – mother’s care to independence can be difficult
Explaining the lesion and the prognosis
Building independence/ self reliance

296
Q

Are congenital heart defects genetic?

A

Incidental, rather than genetic in most cases. However there are increased risks if you have a family history.

297
Q

What conditions would indicate a severe risk of maternal mortality in pregnancy?

A

Pulmonary hypertension
Severe left heart obstruction
Systemic ventricular impairment (Ejection fraction < 30%)
Marfans syndrome with aortic root diameter > 47 mm

298
Q

What is tetralogy of fallot?

A

4 DEFECTS: Ventricular septal defect, pulmonary stenosis, hypertrophy of right ventricle (boot sign), overriding aorta
10% of all congenital heart defects
The stenosis of the right ventricle outflow leads to the right ventricle being at higher pressure than the left.
Therefore de-oxygenated blood passes from the right ventricle to the left ventricle, sent round the body.
The patients are BLUE (Fallot spells)

299
Q

How can surgical repair aid tetralogy of fallot patients?

A

1986 first repair in infancy
Now mostly repaired before the age of two years
Mostly do very well
Often get pulmonary valve regurgitation in adult life and require redo surgery

300
Q

What are ventricular septal defects?

A

Abnormal connection between the two ventricles
Common – 20% of all congenital heart defects
Many close spontaneously during childhood
High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber - increased blood flow through the lungs

301
Q

What are the clinical signs and symptoms of a large ventricular septal defect?

A

Very high pulmonary blood flow in infancy
Breathless, poor feeding, failure to thrive
Require fixing in infancy (PA band, complete repair)
May lead to Eisenmengers syndrome
Small breathless skinny baby
Increased respiratory rate
Tachycardia
Big heart on chest X ray
Murmur varies in intensity

302
Q

What are the clinical signs and symptoms of a small ventricular septal defect?

A
Small increase in pulmonary blood flow only
Asymptomatic
Endocarditis risk
Need no intervention
Loud systolic murmur
Thrill (buzzing sensation)
Well grown
Normal heart rate
Normal heart size
303
Q

What is Eisenmengers syndrome?

A

High pressure pulmonary blood flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
The patient becomes BLUE

304
Q

What are atrial septal defects?

A

Abnormal connection between the two atria (primum, secundum, sinus venosus)
Common
Often present in adulthood
Slightly higher pressure in the LA than the RA
Shunt is left to right
Therefore NOT blue
Increased flow into right heart and lungs

305
Q

What is the physiology of a large atrial septal defect?

A

Significant increased flow through the right heart and lungs in childhood
Right heart dilatation
Increased chest infections
If any stretch on the right heart should be closed

306
Q

What is the physiology of a small atrial septal defect?

A
Small increase in flow
No right heart dilatation
No symptoms
Leave alone
The shunt on small to moderate sized defects increases with age
307
Q

What are the clinical signs of an atrial septal defect?

A

Pulmonary flow murmur
Fixed split second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X ray

308
Q

What is a Atrio-Ventricular Septal Defect?

A

Often Downs syndrome
A hole in the very centre of the heart
Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
Can be complete or partial
Instead of two separate AV valves there is one big malformed one
It usually leaks to a greater or lesser degree

309
Q

What are the physiological signs of a complete Atrio-Ventricular Septal Defect?

A
Breathless as neonate
Poor weight gain
Poor feeding
Torrential pulmonary blood flow
Needs repair or PA band in infancy
Repair is surgically challenging
310
Q

What are the phyiological signs of a partial Atrio-Ventricular Septal Defect?

A

Can present in late adulthood
Presents like a small VSD / ASD
May be left alone if there is no right heart dilatation

311
Q

What is Patent Ductus Arteriosus?

A

A persistent opening between the pulmonary arteries and the aorta. The opening, called the ductus arteriosus, is a normal part of a baby’s circulatory system before birth that usually closes shortly after birth.

312
Q

What are the clinical signs of Patent Ductus Arteriosus?

A

Continuous ‘machinery’ murmur
If large, big heart, breathless
Eisenmenger’s syndrome
Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)

313
Q

What are the physiological signs of a large Patent Ductus Arteriosus?

A

Torrential flow from the aorta to the pulmonary arteries in infancy
Breathless, poor feeding, failure to thrive
More common in prem babies
Need to be closed (surgically)

314
Q

What are the physiological signs of a small Patent Ductus Arteriosus?

A

Little flow from the aorta to pulmonary arteries
Usually asymptomatic
Murmur found incidentally
Endocarditis risk

315
Q

How can a Patent Ductus Arteriosus be closed?

A

Surgical or percutaneous
Local anaesthetic
Venous approach (sometimes requires an AV loop)
Low risk of complications

316
Q

What is Coarctation of the aorta?

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

317
Q

What are the physiological signs of a severe coarctation of the aorta?

A

Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair

318
Q

What are the physiological signs of a mild coarctation of the aorta?

A

Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term

319
Q

What are the clinical signs of a coarctation of the aorta?

A

Right arm hypertension
Bruits (buzzes) over the scapulae and back from collateral vessels
Murmur

320
Q

What are the long term problems of a coarctation of the aorta?

A
Hypertension
- Early coronary artery disease
- Early strokes
- Sub arachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair
321
Q

What is a Bicuspid aortic valve?

A

Normal AV has three cusps
Bicuspid AVs are common
1-2% of the population (M>F)
Can be severely stenotic in infancy or childhood
Degenerate quicker than normal valves
Become regurgitant earlier than normal valves
Are associated with coarctation and dilatation of the ascending aorta

322
Q

What is pulmonary stenosis?

A

Narrowing of the outflow of the right ventricle
Can be: valvar, sub valvar, supra valvar, branch
8-12 % of all congenital heart defects

323
Q

What effects do pulmonary stenosis have depening on their severity?

A

Severe: Right ventricular failure as neonate, Collapse, Poor pulmonary blood flow, RV hypertrophy, Tricuspid regurgitation
Mild: Well tolerated for many years, right ventricular hypertrophy

324
Q

What’s the treatment for pulmonary stenosis?

A

Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)

325
Q

Where can Peripheral vascular disease occur?

A

Legs - aorto-iliac, femoro-popliteal, tibial
Brain - carotids, vertebrals
Organs - coeliac , mesenterics, renals
Arms - subclavian, axillary

326
Q

What are the complications of plaques?

A
Progression (increase in size)
Haemorrhage
Plaque rupture/fissure
Overlying thrombosis
Dissection
Aneurysm
327
Q

What are the organ-specific symptoms of atherosclerosis?

A

Stress-induced physiological malfunction - exercise induced angina, intermittent claudication
Structural and functional breakdown - ischaemic cardiac failure, critical limb ischemia, vascular dementia
Infarction - gangrene

328
Q

What are the common clinical presentations of peripheral vascular disease?

A

Intermittent claudication - muscle cramps on walking (calf, thigh, buttock)
Critical leg ischaemia - rest pain (particularly at night in bed), ulceration, gangrene
Acute limb ischaemia (embolism or thrombosis) - 6Ps: pain, pale, paralysis, paraesthesia, perishing cold, pulseless
4-6 hours, may need to amputate rather than revascularize
Carotid artery disease - stroke, transient ischaemic attack (resolves within 24 hours), amaurosis fugax
Abdominal aortic aneurysm (AAA) - usually asymptomatic until rupture occurs

329
Q

What are the different types of claudication?

A

Intermittent claudication
Moderate ischemia
Anaerobic metabolism when O2 demand

Critical ischaemia
Blood supply barely adequate to allow basal metabolism
No reserve available for increased demand

330
Q

What are the causes of aneurysms?

A

Most often atherosclerotic - medial thinning beneath the plaque
Arteriomegaly - sometimes familial
Collagen diseases - Marfan, vascular Ehlers Danlos

Most common site: Infrarenal abdominal (6cm) - rupture risk 20% over 3 years

331
Q

How would you investigate an aneurysm?

A

Investigate the pathophysiology - Blood glucose, Lipids, Vasculitic Screen, BP
Image the vessels - Duplex (not very good quality if there is calcification), CT/MRA (gives good anatomical detail)

332
Q

How would you treat an aneurysm?

A

Risk factor modification
Revascularization for ‘critical ischaemia’ - acute/chronic: open it up or bypass it
Alternative is amputation

If you have multiple risk factors - consider statins
Antiplatelet agents
Controlled blood pressure and diabetes

333
Q

How to treat peripheral vascular disease?

A

Prescribe walking exercise programme to treat PAD
If that fails, bypass (femoral). Can use another vein or a prosthetic material. Carries risk.
PCI preferred (balloon angioplasty/stents).
If that fails, amputation.

334
Q

How to modify the risk factors in a patient with peripheral vascular disease?

A

Aim is to reduce risk of death from MI or stroke and relieve symptoms
Exercise and weight reduction
Control of hypertension, hyperlipidaemia, diabetes
Antiplatelet therapy
Smoking cessation