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Phase 3b > Cardiovascular 2 > Flashcards

Cardiovascular 2 Flashcards

1
Q

what is a cardiomyopathy?

A

a group of diseases of the myocardium that affect the mechanical or electrical function of the heart

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2
Q

what are the 4 types are cardiomyopathy?

A

hypertrophic
dilated
restricted
arrythmogenic right ventricular

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3
Q

what is dilated cardiomyopathy?

A

Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy, accounting for 90% of cases.

  • dilated heart leading to predominately systolic dysfunction
  • all 4 chambers are dilated, but the left ventricle more so than right ventricle
  • eccentric hypertrophy (sarcomeres added in series) is seen
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4
Q

what causes dilated cardiomyopathy ?

A

idiopathic = the most common cause
myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
ischaemic heart disease
peripartum
hypertension
iatrogenic: e.g. doxorubicin
substance abuse: e.g. alcohol, cocaine
inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy
around a third of patients with DCM are thought to have a genetic predisposition
a large number of heterogeneous defects have been identified
the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
infiltrative e.g. haemochromatosis, sarcoidosis
wet beriberi - thiamine deficiency

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5
Q

what are the features of dilated cardiomyopathy?

A

classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray

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6
Q

what investigations would you perform for cardiomyopathy?

A
  • ECG - often non-specific findings
  • CXR - enlarged heart silhouette
  • Echo - 4 chamber cardiac enlargement, poor systolic function with diminished stroke volume and low ejection fraction
  • FBC - low Hb or haematocrit levels
  • BNP - raised in heart failure
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7
Q

how do you manage dilated cardiomyopathy?

A

manage heart failure and AF in conventional way

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8
Q

what is hypertrophic obstructive cardiomyopathy?

A

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500. HOCM is important as it is the most common cause of sudden cardiac death in the young.

  • the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
  • results in predominantly diastolic dysfunction
    left ventricle hypertrophy → decreased compliance → decreased cardiac output
    -characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy
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9
Q

what are the features of hypertrophic obstructive cardiomyopathy ?

A
  • often asymptomatic
  • exertional dyspnoea
  • angina
  • syncope - typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
  • sudden death (most commonly due to arrhythmias)
  • arrhythmias
  • heart failure
  • jerky pulse, JVP with a large ‘a’ waves, double apex beat
  • ejection systolic murmur
  • S4 gallop

associated with friedreich’s ataxia and wolff-parkinson white

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10
Q

what would an echo show in someone with hypertrophic obstructive cardiomyopathy?

A

Echo findings - mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

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11
Q

what would an ECG show in someone with hypertrophic obstructive cardiomyopathy?

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen

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12
Q

how is hypertrophic obstructive cardiomyopathy managed?

A 
Management - ABCDE
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

Drugs to avoid
nitrates
ACE-inhibitors
inotropes

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13
Q

what are the features of restrictive myocarditis?

A

may be asymptomatic or present with symptoms of cardiac failure

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14
Q

what are some causes of restrictive cardiomyopathy?

A

amyloidosis
post-radiotherapy
Loeffler’s endocarditis

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15
Q

what are examples of genetic cardiomyopathies?

A

Genetic - both conditions listed below are autosomal dominant. An implantable cardioverter-defibrillator is often inserted to reduce the incidence of sudden cardiac death.

they are primary cardiomyopathies which predominantly involve the heart

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16
Q

what are examples of mixed cardiomyopathies?

A

Mixed - rather confusingly most of the causes of dilated and restrictive cardiomyopathy are now listed separately in the ‘secondary’ causes. This category servers as a reminder that many patients will have a genetic predisposition to cardiomyopathy which is then triggered by the secondary process, hence the ‘mixed’ category

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17
Q

what are some causes of secondary cardiomyopathies?

A
  • infective - coaxsackie B virus, Chagas disease
  • infiltrative - amyloidosis
  • storage - haemochromatosis
  • Toxicity - doxorubicin, alcoholic cardiomyopathy
  • inflammatory - granulomatosis - sarcoidosis
  • endocrine - DM, thyrotoxicosis, acromegaly
  • Neuromuscular - Friedreich’s ataxia, Duchenne, myotonic dystrophy
  • nutritional deficiency - berberi - thiamine
  • autoimmune - SLE
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18
Q

what is arrhythmogenic right ventricular cardiomyopathy?

A

Arrhythmogenic right ventricular cardiomyopathy (ARVC, also known as arrhythmogenic right ventricular dysplasia or ARVD) is a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death. It is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.

AD inheritance
the right ventricular myocardium is replaced by fatty and fibrofatty tissue

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19
Q

how does arrhythmogenic right ventricular present?

A

palpitations
syncope
sudden cardiac death after physical exertion
chest pain
dizziness
fatigue
usually in males - first presentation in adolescence
they may have normal cardiac exam, s3, s4 or split s2 may be present

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20
Q

what investigations would you perform for arrhythmogenic right ventricular cardiomyopathy?

A
  • ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
  • echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
  • MRI is useful to show fibrofatty tissue
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21
Q

what management would you perform for arrhythmogenic right ventricular cardiomyopathy?

A

drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator

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22
Q

what is naxos disease?

A

an autosomal recessive variant of ARVC

a triad of ARVC, palmoplantar keratosis, and woolly hair

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23
Q

what are types of acquired cardiomyopathy?

A

peripartum cardiomyopathy

Takotsubo cardiomyopthy

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24
Q

what is peripartum cardiomyopathy?

A

Typical develops between last month of pregnancy and 5 months post-partum
More common in older women, greater parity and multiple gestations

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25
Q

what is Takotsubo cardiomyopathy?

A

‘Stress’-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
they will be ST elevation but normal coronary angiogram
Transient, apical ballooning of the myocardium
Treatment is supportive

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26
Q

what is acute pericarditis?

A
  • inflammation of the pericardium
  • new onset of inflammation lasting less than 4-6 weeks
  • it can be either fibrinous or effusive with a purulent, serous or haemorrhagic exudate
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27
Q

what are the features of pericarditis?

A

it is characterised by a triad of chest pain, pericardial friction rub and serial ECG changes

  • the chest pain is usually pleuritic - and often relieved by sitting forward
  • non productive cough
  • dyspnoea
  • flu like symptoms
  • tachypnoea
  • tachycardia
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28
Q

what are some causes of acute pericarditis?

A 
viral infections (Coxsackie)
tuberculosis
uraemia (causes 'fibrinous' pericarditis)
trauma
post-myocardial infarction, Dressler's syndrome
connective tissue disease
hypothyroidism
malignancy
idiopathic
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29
Q

what investigations would you perform for acute pericarditis?

A

ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis

transthoracic echo

serum troponins, ESR, CRP, FBC, UREA

pericardial fluid/blood culture

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30
Q

how is acute pericarditis managed?

A

treat the underlying cause

a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis

if there is tamponade or symptomatic effusion - pericardiocentesis

if it is purulent - pericardiocentesis and antibiotics - vancomycin and ceftriaxone

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31
Q

what can cause constrictive pericarditis?

A

any cause of pericarditis but particularly TB

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32
Q

what are the features of constrictive pericarditis?

A 
dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul's sign is positive

CXR - will show pericardial calcification

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33
Q

how can you distinguish between constrictive pericarditis and cardiac tamponade?

A

cardiac tamponade
JVP - absent Y descent
Pulsus paradoxus - present
Kaussmaul’s sign - rare

Constrictive pericarditis 
JVP -  X  + Y present 
pulsus paradoxus - absent 
Kussmaul's sign - present 
preicardial calcification on CXR
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34
Q

what is cardiac tamponade?

A

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

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35
Q

what are the features of cardiac tamponade?

A

Classical features - Beck’s triad:
hypotension
raised JVP
muffled heart sounds

Other features:
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans

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36
Q

what investigations would you perform for cardiac tamponade?

A
  • ECG - low voltage, electrical alternans, electromechanical dissociation associated with end stage tamponade
  • Transthoracic echo - large pericardial effusion, chamber collapse and respiratory variation of ventricular filling
  • CXR - enlarged heart
  • FBC, ESR, cardiac enzymes
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37
Q

how is cardiac tamponade managed?

A

pericardiocentesis

or surgical drainage

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38
Q

how do you manage recurrent pericarditis?

A

NSAIDs plus PPI plus colchicine

2nd line corticosteroid
3rd line immunosupressant

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39
Q

what is an aneurysm?

A

defined as abnormal dilation of a blood vessel by more than 50% of its normal diameter

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40
Q

what is an abdominal aortic aneurysm?

A

An abdominal aortic aneurysm (AAA) is defined as a dilatation of the abdominal aorta greater than 3cm
they can be true or false aneurysm
true - all 3 layers of the arterial wall are involved
false - only a single layer of fibrous tissue forms the aneurysm wall

*it is important to identify and manage early

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41
Q

what are some causes and risk for AAA?

A

The aetiology of abdominal aortic aneurysm is largely unknown.
Possible causes include:
- atherosclerosis
- trauma
- infection
- connective tissue disease (e.g. Marfan’s disease, Ehler’s Danlos, Loey Dietz)
- inflammatory disease (e.g. Takayasu’s aortitis).

Risk factors for AAA include:

  • smoking, hypertension, hyperlipidaemia, family history, male gender, and increasing age.
  • Diabetes mellitus is a negative risk factor for AAA (the mechanism for this is still poorly understood).
42
Q

what are the clinical features of an AAA?

A

Many abdominal aortic aneurysms are asymptomatic and are simply detected on incidental finding or screening.

Symptomatic patients with an AAA can present with:

  • Abdominal pain
  • Back or loin pain
  • Distal embolisation producing limb ischaemia
  • Aortoenteric fistula

On examination, a pulsatile mass can be felt in the abdomen (above the umbilical level), and rarely, signs of retroperitoneal haemorrhage may be evident.

A patient with a ruptured AAA may present with pain (abdominal, back, or loin) and a degree of shock or syncope

43
Q

what is the screening programme for AAA?

A

In the UK, the national abdominal aortic aneurysm screening programme (NAAASP) offer an abdominal US scan for all men in their 65th year.

44
Q

what are the outcomes of the AAA screening programme?

A

<3 cm - normal - nor further action
3-4.4cm - small aneurysm - rescan every 12 months
4.5 - 5.4cm - medium aneurysm - rescan every 3months
>5.5cm = large aneurysm - refer within 2 weeks to vascular surgery for probable intervention

45
Q

what investigations should be performed for AAA?

A

USS

once USS confirmed diagnosis - CT scan with contrast is warranted when the threshold diameter of 5.5.cm

46
Q

how are AAA managed?

A

Any AAA less than 5.5cm can be monitored via Duplex USS, as surgery prior to this diameter provides no survival benefit either for open repair or endovascular repair

  1. 0 – 4.4cm: yearly ultrasound
  2. 5 – 5.4cm: 3-monthly ultrasound

A patient with a small (3cm-5.5cm) AAA* has a 3% per year risk of cardiovascular mortality, hence cardiovascular risk factors should be reduced as appropriate:
Smoking cessation (reduces rate of expansion and risk of rupture)
Improve blood pressure control
Commence statin and aspirin therapy
Weight loss and increased exercise

surgical intervention - considered when greater than 5.5.cm or if it is increasing >1cm per year or if it is symptomatic in a patient who is otherwise fit
Open repair involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally, before the segment is then removed and replaced with a prosthetic graft
Endovascular repair involves introducing a graft via the femoral arteries and fixing the stent across the aneurysm

47
Q

what is a complication of endovascular aortic repair?

A

endovascular leak, whereby an incomplete seal forms around the aneurysm resulting in blood leaking around the graft.

Endoleaks are often asymptomatic hence regular surveillance (usually ultrasound unless a complication is noted) is needed. If left untreated, the aneurysm can expand and subsequently rupture. As such, any aneurysm expansion following EVAR warrants investigation for endoleak.

48
Q

when does the DVLA have to be informed in a patient with an AAA?

A

In the UK, any AAA >6.5cm requires notification to the DVLA and disqualifies from driving until repaired.

49
Q

what are the complications of AAA?

A
  • rupture
  • retroperitoneal leak
  • embolisation
  • aortoduodenal fistula
50
Q

how does a ruptured AAA present?

A

abdo pain
back pain
syncope
vomiting

on examination they will be haemodynamically compromised with a pulsitle abdominal mass and tendernes

Around 50% patients present with the ‘classic triad’ of ruptured AAA (flank or back pain, hypotension, and a pulsatile abdominal mass).

51
Q

how is a ruptured AAA managed?

A

any suspected AAA warant high flow oxygen, IV access (2 large bore cannulas) and urgent bloods taken with cross match for minimum 6 units
aim to keep BP<100mmHg - termed permissive hypotension to prevet excessive blood loss

send to surgery for repair.

52
Q

what causes a thoracic aortic aneurysm to develop?

A

Thoracic aortic aneurysms develop due to degradation of the tunica media, the layer of the artery which provides tensile strength and elasticity to the wall.

As a result, the artery loses structural integrity and dilates, and as the diameter increases, the wall tension rises and further increases the diameter in a vicious cycle.

The main causes of thoracic aneurysm are:
Connective tissue diseases (e.g. Marfan’s syndrome or Ehlers-Danlos syndrome)
Bicuspid aortic valve
Other causes include trauma, aortic dissection, aortic arteritis (e.g. Takayasu Arteritis), and tertiary syphilis

53
Q

what is a thoracic aortic aneurysm?

A

A thoracic aortic aneurysm can involve the ascending aorta or aortic root (60%), aortic arch (10%), descending aorta (40%), or thoracoabdominal aorta (10%) segments

54
Q

what are risk factors for thoracic aortic aneurysm ?

A 
fam history 
hypertension 
atherosclerosis 
smoking 
high BMI
male gender 
advancing age
55
Q

what are the clinical features of a thoracic aortic aneurysm?

A

typically asymptomatic
In those that are symptomatic, the most common presenting complaint is pain, with the location of the pain potentially localising the aneurysm:
ascending aorta - anterior chest pain
aortic arch - neck pain
descending aorta - pain between the scapula

Other symptoms of thoracic aneurysms include:

  • Back pain – secondary to spinal compression by descending or thoracoabdominal aneurysm
  • Hoarse voice – from damage to the left recurrent laryngeal nerve in arch aneurysms
  • Distended neck veins – from SVC compression
  • Symptoms of heart failure – from involvement of the aortic valve
  • Dyspnoea or cough – secondary to tracheal or bronchial compression
56
Q

what investigations would you perform for a thoracic aortic aneurysm ?

A

Thoracic aneurysms are diagnosed through imaging
They can be seen on plain film CXR however not sensitive enough to make a definitive diagnosis
CT scan with contrast
transoesophageal echo

57
Q

how are thoracic aortic aneurysms managed?

A

they are at increased CV risk so statin and antiplatelet
control BP
stop smoking

Surgical management is dependent on the location of the aneurysm
> Ascending Aorta Treated when the diameter >5.5cm, the affected region of the aorta is excised and replaced with a dacron graft. If the aortic root is involved, a Bentall procedure is often performed, using a graft that also contains a prosthetic aortic valve
> Aortic Arch Once the aneurysm is over 5.5cm surgery should be considered; the affected aorta is replaced with a multi-limbed graft, allowing for the branching of the great vessels (these procedures have a high risk of cerebral ischaemia from embolisation)
> Descending Aorta Intervention is indicated when the diameter exceeds 6.0cm. These can be repaired open or with endovascular techniques, yet endovascular techniques have been shown to produce fewer postoperative complications and to have a lower mortality

58
Q

what is aortic dissection ?

A

The wall of an artery consists of the tunica intima (innermost layer), tunica media (middle layer), and tunica adventitia (outermost layer). An aortic dissection is a tear in the intimal layer of the aortic wall, causing blood to flow between and splitting apart the tunica intima and media.

Aortic dissections from the initial intimal tear can progress distally, proximally, or in both directions from the point of origin. Anterograde dissections propagate towards the iliac arteries and retrograde dissections propagate towards the aortic valve (at the root of the aorta).
Retrograde dissections can result in prolapse of the aortic valve, bleeding into the pericardium, and cardiac tamponade

59
Q

what classification can be used for aortic dissection?

A

Stanford classification
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

60
Q

what are the risk factors for aortic dissection?

A 
hypertension 
Atherosclerotic disease
Male gender
Connective tissue disorders (typically Marfan’s syndrome or Ehler’s-Danlos syndrome)
Biscuspid aortic valve

As a general rule, younger cases often have associated connective tissue disorders, whilst older patients are more likely to have underlying hypertension or atherosclerosis.

61
Q

what are the clinical features of aortic dissection?

A 
tearing chest pain 
radiates through the back 
tachycardia 
hypotension - secondary to hypovolaemia from blood loss into the dissection or cardiogenic from severe aortic regurgitation or pericardial tamponade 
new aortic regurgitation murmur

other features may result from the involvement of specific arteries. For example:
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia
the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

62
Q

what are the DD or aortic dissection?

A

MI
PE
pericarditis
MSK back pain

63
Q

what investigations would you perform for aortic dissection?

A 
baseline bloods (FBC, U&amp;E, LFTs, troponin, coagulation) with a crossmatch of at least 4 units
ABG to aid initial assessment 
ECG to exclude any cardiac pathology 
CT angiogram 
tranoesophageal echo
64
Q

how is aortic dissection managed?

A

Start high flow oxygen and gain IV access (x2 large bore cannulas); fluid resuscitation should be done cautiously. In the setting of a rupture, then the target pressure should be sufficient for cerebral perfusion only. In the setting of an uncomplicated dissection then the target systolic pressure should be kept below 110mmHg systolic

Stanford type A: carry high mortality - surgery is needed (usually removal of ascending aorta with replacement with synthetic graft) BP should be controlled whilst awaiting intervention - target systolic 11-120mmHG)

Stanford type B: best managed medically - management of hypertension with IV BB - labetalol (or CCB as 2nd line). Acutely endovascular repair not recommenced due to risk of retrograde dissection. surgical intervention in Type B dissections is only warranted in the presence of certain complications, such as rupture, renal, visceral or limb ischaemia, refectory pain, or uncontrollable hypertension.

65
Q

what are the complications of aortic dissection?

A 
aortic rupture 
aortic regurgitation 
myocardial ischaemia 
cardiac tamponade 
stroke or paraplegia secondary to cerebral artery or spinal artery involvement
66
Q

what is hypertension defined as?

A

hypertension is defined as a blood pressure above 140/90 in clinic or 135/85 with ambulatory or home readings

67
Q

what are causes of hypertension?

A

essential hypertension = 95% of hypertension

secondary causes of hypertension ROPE:
R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis.
O – Obesity
P – Pregnancy induced hypertension / pre-eclampsia
E – Endocrine. Most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test.

drugs - steroid, MAOIs, COCP, NSAIDs, leflunomide

68
Q

what are the complications of hypertension?

A 
Ischaemic heart disease
Cerebrovascular accident (i.e. stroke or haemorrhage)
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure
69
Q

what are the stages of hypertension?

A

stage 1: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
stage 2: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
stage 3, severe: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

70
Q

why do patients need ABPM or HBPM?

A

Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis. Having your blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

71
Q

what investigations should patients with newly diagnosed hypertension have?

A

> Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities

72
Q

what should you do if BP is >180/20?

A

admit for specialist assessment if:

  • signs of retinal haemorrhage or papilloedema (accelerated hypertension) or
  • life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)

if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)

  • if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM.
  • if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days
73
Q

how is ambulatory blood pressure monitoring done?

A

at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements

74
Q

how is home blood pressure monitoring performed?

A

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
BP should be recorded twice daily, ideally in the morning and evening
BP should be recorded for at least 4 days, ideally for 7 days
discard the measurements taken on the first day and use the average value of all the remaining measurements

75
Q

how is hypertension managed?

A

lifestyle advice: reduce salt intake, reduce caffeine intake, stop smoking, reduce alcohol intake, exercise, weight loss.

*for patients less than 40 consider specialist referral to exclude secondary causes.

treat stage one hypertension if <80 and any of the following apply; target organ damage, established CV disease, renal disease, diabetes or 10 year CV risk >10%.

stage 2 hypertension - offer drug treatment regardless of age

Step 1 treatment

  • patients < 55-years-old or a background of type 2 diabetes mellitus: (ACE-i or ARB): (A)
  • patients >= 55-years-old or of black African or African–Caribbean origin: CCB (C)

Step 2 treatment
if already taking an ACE-i or ARB add a CCB or a thiazide-like Diuretic
if already taking a CCB add an ACE-i or ARB
(A + C) or (A + D)

Step 3 treatment
add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)

Step 4 treatment
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
- confirm elevated clinic BP with ABPM or HBPM
- assess for postural hypotension.
- discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker

  • ARB can be used instead of ACEi where they are not tolerated because of cough
  • ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line
  • for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
76
Q

what is the target for BP when on treatment?

A

<80 years <140/<90

>80 years <150/<90

77
Q

what can cause hypokalaemia with hypertension?

A

Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency

78
Q

when would you consider cardiac resynchronisation therapy in heart failure?

A

When dealing with heart failure not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, a widened QRS complex favours cardiac resynchronisation therapy

79
Q

what is ivabradine?

A

it is used as a 3rd line management for heart failure

criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%

80
Q

what effects does warfarin have on APTT and PT?

A

Warfarin acts on the extrinsic pathway, whilst heparin acts on the intrinsic pathway. Thus, warfarin efficacy is monitored using the INR – which utilises the prothrombin time.
Heparin is measured using the aPPT

*in a warfarin overdose you would expect the PT and APTT to be prolonged.

81
Q

what is peripheral vascular disease?

A

a chronic condition due to atherosclerosis of arteries in the limbs. The level of arterial occlusion present is proportional to the symptoms. The pathogenesis and risk factors are the same as for coronary artery disease (CAD)

It can present as an emergency as acute limb ischaemia

82
Q

what are some causes/risk factors for peripheral vascular disease?

A 
> Hypertension
> Dyslipidaemia - High LDL and low LDL levels
> Diabetes
> Obesity
> FHx of arterial disease - Significant if a first degree > relative had MI before the age of 55
> Smoking
> Age
> Male gender
83
Q

what are the end results of atherosclerosis?

A 
angina 
ACS
TIA
Stokes
PVD
chronic mesenteric ischaemia
84
Q

what is critical limb ischaemia?

A

Critical Limb Ischaemia is the end stage of peripheral arterial disease, where there is inadequate supply of blood to a limb to allow it to function normally at rest.

85
Q

what is intermittent claudication?

A

Intermittent Chlaudication is the symptom of having ischaemia in a limb during exertion that is relieved by rest. It is typically a crampy, achy pain in the calf muscles associated with muscle fatigue when walking beyond a certain intensity.

86
Q

what is the main differential for peripheral vascular disease?

A

The main differential is “spinal claudication” caused by impingement of the caudal equina by a spinal stenosis. This also classically causes pain in the back of the legs on exertion.

87
Q

how does PVD present?

A

Pain in the calves on walking, relieved by rest
- This pain is also known as claudication
- The pain can occur anywhere along the leg, and down into the foot
- Many patients do NOT present with classic claudication – often because they are not doing enough activity to induce the symptoms – particularly if they have another comorbidity that limits their activity.
Pain may also occur when legs are raised (e.g. in bed), and abate when legs are lowered (e.g. by sitting)

88
Q

what is Leriche’s syndrome?

A 
Associated with occlusion in the distal aorta or proximal common iliac artery
A clinical triad:
- Thigh / buttock claudication
- Absent femoral pulses
- Male impotence
89
Q

what signs on examination may there be in someone with PVD?

A

Elevating the leg may cause it to go pale and cold, as well as causing pain.- Beuger’s angle <20’ – the leg will go pale and cold upon raising it 20’ off the couch.

Increased vascular filling time – Upon lowering, the leg may become hot and red as reperfusion occurs. Perfusion time tends to be reduced (>15s)

Oedema is not usually present

There may be evidence of poor skin health due to poor perfusion, such as ulcers, dry scaly skin, cool peripheries and reduced capillary refill time

Check the pulse in the foot (posterior tibial and dorsals pedis)

Palpable pulses indicate low likelihood of peripheral vascular disease
Absent pulses represent an increased chance of peripheral vascular disease

If you are unable to locate a pulse by hand, you can use a doppler probe to assess if significant blood flow is present in the artery

90
Q

what investigations would you perform for peripheral arterial disease?

A 
ankle-brachial index - ABI
arterial doppler 
angiography - CT or RI 
bloods - ESR and CRP to exclude arteritis, platelets and clotting 
ECG - to exclude cardiac involvement
91
Q

how is an ABPI performed and interpreted?

A

ABPI is a measure of the ratio of the blood pressure in the ankle vs the arm.

Using only systolic values, divide the ankle pressure by the brachial pressure
A normal value is >1
A value of <0.9 is pathological for limb ischaemia (PVD). The lower the number, the greater the degree of PVD

> 0.9 is normal
0.6 – 0.9 is mild disease - claudication
0.3 – 0.6 is moderate to severe disease - rest pain
<0.3 is severe disease to critical ischaemic

92
Q

what other signs may patients with severe PVD have?

A
  • ‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event. They are often painful, but diabetic and alcoholic patients may not have pain.
  • Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene).
  • Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse
  • Skin atrophy – in chronic disease
  • Hair loss – in chronic disease
  • Cyanosis
  • Excessive sweating – due to overactivity of the sympathetic nerves
  • Erectile Dysfunction – Leriche syndrome – the result of distal aortic disease. Other features of the syndrome
93
Q

what is a very poor prognostic sign in PVD?

A

Burning pain at night, due to elevation (which reduces limb perfusion), and is relieved by hanging the legs over the side of the bed

94
Q

how is mild PVD managed?

A

anti-platelet therapy - aspirin or clopidogrel
exercise
risk factor modification
statin

if it is lifestyle limiting
add symptomatic relief - cilostazol or naftidrofuryl

if severe it can be treated by:
angioplasty
stenting
bypass surgery

95
Q

what is acute limb ischaemia?

A

sudden decrease in limb perfusion that threatens the viability of the limb

can be caused by:
Embolisation whereby a thrombus from a proximal source travels distally to occlude the artery (most common)
The original thrombus source may be as a result of AF, post-MI mural-thrombus, abdominal aortic aneurysm, or prosthetic heart valves
Thrombosis in situ whereby an atheroma plaque in the artery ruptures and a thrombus forms on the plaque’s cap (presenting as acute or acute-on-chronic)
Trauma (less common), including compartment syndrome

96
Q

what are the clinical features of acute limb ischaemia?

A 
6 P's
Pain 
Pallor 
Pulselessness
Paresthesia 
perishingly cold 
paralysis

usually a sudden onset of the above symptoms

97
Q

what are the differentials for acute limb ischaemia?

A

critical chronic limb ischaemia
acute DVT
spinal cord/peripheral nerve compression

98
Q

what investigations would you perform for acute limb ischaemia?

A

routine bloods - including serum lactate to assess the level of ischaemia
thrombophilia screen if less than 50 without known risk factors
group and save
ECG
doppler USS of both limbs
CT angiography

99
Q

what is the difference between acute limb ischaemia and critical chronic limb ischaemia?

A

acute limb = sudden onset from blockage

critical chronic limb = long term from PVD

100
Q

how do you manage acute limb ischaemia ?

A

Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead to irreversible tissue damage within 6 hours.

High flow oxygen
get adequate IV access
Heparin - bolus then infusion ASAP
also give anti-platelet - aspirin

if the limb is viable
intra-arterial thrombolysis - urokinase
and endovascular revascularisation

if it is an embolic cause

  • embolectomy via a fogarty catheter
  • local intra-arterial thrombolysis
  • bypass surgery

if thrombotic cause

  • local intra-arterial thrombolysis
  • angioplasty
  • bypass surgery

if the limb is not viable - amputation

101
Q

how is chronic severe limb ischaemia managed?

A

assess for revascularisation

aspirin

102
Q

what are the complications of acute limb ischaemia?

A

death

An important complication of acute limb ischaemia is reperfusion injury; sudden increase in capillary permeability can result in:
Compartment syndrome
Release of substances from the damaged muscle cells, such as:
- K+ ions causing hyperkalaemia
- H+ ions causing acidosis
- Myoglobin, resulting in significant AKI

It is imperative that patients at risk of compartment syndrome are closely monitored and rapidly treated. Electrolyte imbalance due to reperfusion injury requires close monitoring and potentially haemofiltration.

Phase 3b (34 decks)

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