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!Final Year > Cardiovascular (1) > Flashcards

Cardiovascular (1) Flashcards

1
Q

What is an abdominal aortic aneurysm?

A

The permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment

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2
Q

What are the risk factors of an abdominal aortic aneurysm?

A

Smoking
Hypertension
Rarer:
- Syphilis
- Connective tissue disorders e.g. Ehlers Danlos type 1 and Marfan’s syndrome

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3
Q

What is the epidemiology of an abdominal aortic aneurysm?

A

Prevalence among men is 4 to 6 times higher than in women
Increased prevalence with age and smoking status

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4
Q

What are the presenting symptoms of an abdominal aortic aneurysm?

A

Usually asymptomatic
Abdominal and lower back pain may be associated

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5
Q

What is the presentation of a ruptured abdominal aortic aneurysm?

A

Can either be catastrophic (e.g. sudden collapse) or sub-acute (persistent severe central abdominal pain with developing shock

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6
Q

What is the mortality of of a ruptured abdominal aortic aneurysm?

A

Almost 80%

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7
Q

What are the clinical features of a ruptured abdominal aortic aneurysm?

A

Severe, central abdominal pain radiating to the back
Pulsatile, expansile mass in the abdomen
Patients may be shocked (hypotension, tachycardic) or may have collapsed

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8
Q

What are the signs of an abdominal aortic aneurysm on physical examination?

A

Abdominal Aorta on palpation is pulsatile AND expansile

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9
Q

What is the management for a ruptured abdominal aortic aneurysm?

A
  1. Surgical emergency - patients with a suspected ruptured AAA require an immediate vascular review with a view to emergency surgical repair
  2. In haemodynamically unstable patients = diagnosis is clinical
    These patients are not stable enough for a CT scan etc to confirm the diagnosis and should be taken straight to theatre
  3. Patients who are haemodynamically stable may be sent for a CT angiogram where the diagnosis is in doubt - this may also assess the suitability of endovascular repair
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10
Q

What is the screening programme for abdominal aortic aneurysms?

A

Single abdominal ultrasound for males aged 65

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11
Q

What are the screening outcomes of the screening programme for abdominal aortic aneurysms?

A

Aorta width < 3cm = No further action
Aorta width 3- 4.4cm = Small aneurysm, rescan every 12 months
Aorta width 4.5 - 5.4cm = Medium aneurysm, rescan every 3 months
Aorta width > 5.5cm = Large aneurysm, refer within 2 weeks to vascular surgery

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12
Q

What is the management for a low rupture risk AAA?

A

Asymptomatic, aortic diameter < 5.5cm (i.e. small and medium aneurysms)
Abdominal US surveillance (on time-scales) and optimise cardiovascular risk factors (e.g. stop smoking)

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13
Q

What is the management for a high rupture risk AAA?

A

Symptomatic, aortic diameter >=5.5cm or rapidly enlarging (>1cm/year)
Refer within 2 weeks to vascular surgery for probable intervention
Treat with elective endovascular repair (EVAR) or open repair if unsuitable

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14
Q

What is amyloidosis?

A

A (heterogenous) group of diseases characterised by extracellular deposition of insoluble amyloid fibrils

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15
Q

What are the two types of amyloidosis?

A
  1. AL amyloid = primary, immunoglobulin light chain amyloidosis, associated with Myeloma
  2. AA amyloid = secondary, non-familial and familial
    2a. Non- familial AA = Inflammatory polyarthropathies account for 60% of cases, then chronic infections, IBD
    2b. Familial AA = familial periodic Mediterranean fever syndrome
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16
Q

What are the risk factors for amyloidosis?

A

PMH of inflammatory conditions (AA)
Chronic infections (AA)
Positive FH

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17
Q

What are the features of primary amyloidosis (AL)?

A

Dependent on organ involvement:
1. Kidneys: glomerular lesions—proteinuria and nephrotic syndrome
2. Heart: restrictive cardiomyopathy (looks ‘sparkling’ on echo), arrhythmias, angina
3. Nerves: peripheral and autonomic neuropathy; carpal tunnel syndrome
4. GI: macroglossia (big tongue), malabsorption/weight, perforation, haemorrhage, obstruction, and hepatomegaly
5. Vascular: purpura, especially periorbital—a characteristic feature

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18
Q

What are the features of secondary non-familial amyloidosis (AA)?

A

PMH of chronic inflammation (e.g. RA/ IBD) or chronic infection (e.g. TB)
Affects the kidneys, liver, and spleen, and may present with proteinuria, nephrotic syndrome, or hepatosplenomegaly
Macroglossia is not seen; cardiac involvement is rare

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19
Q

What are the appropriate investigations for amyloidosis?

A

Diagnosis made with biopsy of affected tissue: positive Congo Red staining with apple-green birefringence under polarized light microscopy
The rectum or subcutaneous fat are relatively non-invasive sites for biopsy and are positive in 80%
Can also use serum amyloid precursor (SAP) scan

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20
Q

What is the management of amyloidosis?

A

AL: optimize nutrition; PO melphalan + prednisolone extends survival
High-dose IV melphalan with autologous stem cell transplantation may be better
AA: manage the underlying condition optimally

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21
Q

What is the prognosis of patients with amyloidosis?

A

Median survival is 1–2 years
Patients with myeloma and amyloidosis have a shorter survival than those with myeloma alone

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22
Q

What is aortic dissection?

A

A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen

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23
Q

What are the risk factors of aortic dissection?

A

Hypertension (most important RF)
Trauma
Bicuspid aortic valve
Connective tissue disease: Collagen e.g. Marfan’s syndrome, Ehler-Danlos syndrome
Turner’s and Noonan’s syndrome
Pregnancy
Aortitis e.g. from Syphilis, Takayasu’s
Cocaine

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24
Q

What is the classification of 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

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25
Q

What is the epidemiology of aortic dissection?

A

Most common in males between 40 and 60 years

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26
Q

What are the clinical features of aortic dissection?

A
  1. Chest/back pain:
    Typically severe and ‘sharp’, ‘tearing’ in nature
    Pain is typically maximal at onset
    Classically chest pain is more common in type A dissection and upper back pain is more common in type B dissection (but considerable overlap and both chest and back pain are present in many patients)
  2. Pulse deficit:
    Weak or absent carotid, brachial, or femoral pulse
    Variation (>20 mmHg) in systolic blood pressure between the arms
  3. Aortic regurgitation
  4. Hypertension
  5. Other features may result from the involvement of specific arteries, e.g.
    coronary arteries → angina
    spinal arteries → paraplegia
    distal aorta → limb ischaemia
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27
Q

What is pulsus paradoxus (paradoxical pulse)? (Aortic Dissection)

A

An abnormally large decrease (> 10mmHg) in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration

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28
Q

What are the appropriate investigations for aortic dissection?

A

Some patients may present acutely and be clinically unstable- take this into account:
1. Chest x-ray = widened mediastinum
2. CT angiography of the chest, abdomen and pelvis = investigation of choice
- suitable for stable patients and for planning surgery
- a false lumen is a key finding in diagnosing aortic dissection
3. Transoesophageal echocardiography (TOE) = more suitable for unstable patients who are too risky to take to CT scanner

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29
Q

What is the management of aortic dissection?

A

Depends on type of dissection:
Type A:
- Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B:
- Conservative management
- Bed rest
- Reduce blood pressure IV labetalol to prevent progression
- Endovascular repair in the future?

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30
Q

What are the complications of aortic dissection?

A

Complications of backward tear:
Aortic incompetence/regurgitation
MI: inferior pattern is often seen due to right coronary involvement

Complications of a forward tear:
Unequal arm pulses and BP
Stroke
Renal failure

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31
Q

What is aortic regurgitation?

A

Reflux of blood from aorta into left ventricle (LV) during diastole

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32
Q

What are the the risk factors of aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic fever
Endocarditis
Connective tissue disorders- e.g. Marfan’s
Aortitis- secondary to systemic diseases such as syphilis

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33
Q

What is the aetiology of aortic regurgitation?

A

Valve disease:
Rheumatic fever: the most common cause in the developing world
Calcific valve disease
Infective endocarditis
Connective tissue diseases e.g. rheumatoid arthritis/SLE
Bicuspid aortic valve (affects both the valves and the aortic root)

Aortic root disease:
Bicuspid aortic valve (affects both the valves and the aortic root)
Aortic dissection
Spondylarthropathies (e.g. ankylosing spondylitis)
Hypertension
Syphilis
Marfan’s, Ehler-Danlos syndrome

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34
Q

What are the features of aortic regurgitation?

A

Early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
Collapsing pulse
Wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing in time with pulse)
Mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
Others: later present with symptoms of HF e.g. exertional dyspnoea, orthopnoea, weakness, fatigue

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35
Q

What is the investigation of choice for aortic regurgitation?

A

Echocardiography = determines aetiology e.g. bicuspid aortic valve
Can also offer ECG, Chest x-ray

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36
Q

What is the management for aortic regurgitation?

A

Medical management of any associated heart failure
Surgery: aortic valve indications include:
- Symptomatic patients with severe AR
- Asymptomatic patients with severe AR who have LV systolic dysfunction

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37
Q

What is aortic stenosis?

A

Obstruction of blood flow across the aortic valve from the left ventricle due to pathological narrowing

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38
Q

What are the causes of aortic stenosis?

A

Degenerative calcification (most common cause in older patients > 65 years)
Bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
Post-rheumatic disease
Subvalvular: HOCM

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39
Q

What is the triad of aortic stenosis?

A
  1. Chest pain
  2. Dyspnoea
  3. Syncope / presyncope (e.g. exertional dizziness)
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40
Q

What is murmur can be heard in aortic stenosis?

A

An ejection systolic murmur (ESM)
Classically radiates to the carotids
This is decreased following the Valsalva manoeuvre

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41
Q

What are some of the features in severe aortic stenosis?

A

Narrow pulse pressure
Slow rising pulse
Delayed ESM
Soft/absent S2
S4
Thrill
Duration of murmur
Left ventricular hypertrophy or failure

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42
Q

What is the investigation of choice for aortic stenosis?

A

Transthoracic echocardiogram:
1. visualises valvular structural changes
2. measure elevated aortic pressure gradient
3. measurement of valve area and left ventricular ejection function
ECG: may demonstrate left ventricular hypertrophy and LBBB (and absent Q waves)
Others:
Cardiac MRI- demonstrates stenotic aortic valve
Angiogram - prior to surgery to identify if CVD is present

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43
Q

What is the management for aortic stenosis?

A

Dependent on symptoms:
Asymptomatic = observe the patient is a general rule
Symptomatic = valve replacement

If asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction = consider surgery

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44
Q

What are the management options for aortic valve replacement in aortic stenosis?

A
  1. Surgical AVR is the treatment of choice for young, low/medium operative risk patients
    Cardiovascular disease may coexist -> an angiogram is often done prior to surgery so that the procedures can be combined
  2. Transcatheter AVR (TAVR) is used for patients with a high operative risk
    Balloon valvuloplasty:
    - may be used in children with no aortic valve calcification
    - in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
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45
Q

What is an arterial ulcer?

A

An ulcer caused by a reduction in arterial blood flow, leading to decreased perfusion of the tissues and subsequent poor healing

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46
Q

What are the risk factors for arterial ulcers?

A

Atherosclerosis
Hypertension
Smoking
DM
Hyperlipidaemia
Increasing age
Positive family history
Obesity and physical inactivity

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47
Q

What are the features of arterial ulcers?

A

Severe pain, particularly at night
Pain is relieved by dependency (hanging leg over side of bed)
Occur on the toes and heel
There may be areas of gangrene
Cold with no palpable pulses
Low ABPI measurements

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48
Q

What are some other features of arterial ulcers?

A

Likely to give a preceding history of intermittent claudication (pain when they walk) or critical limb ischaemia (pain at night)
In pure arterial ulcers, sensation is maintained (unlike neuropathic ulcers)
Characteristics: Irregular edge, poor granulation tissue, dry necrotic base, round or punched-out with sharp demarcation
Trophic changes of chronic ischemia:
Pale, hair loss, atrophic skin, cool feet, thickened nails, necrotic toes
Absence of pulses, prolonged capillary refill (>4–5 s), dependent rubor

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49
Q

What are some appropriate investigations for arterial ulcers?

A

Ankle Brachial Pressure Index (ABPI) measurement:
(>0.9 = normal; 0.9-0.8 = mild; 0.8-0.5 = moderate; <0.5 = severe)
Imaging:
Duplex ultrasound
CT Angiography, and / or Magnetic Resonance Angiogram (MRA)

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50
Q

What is dependent rubor? (Arterial Ulcers)

A

A fiery to dusky-red coloration visible when the leg is in a dependent position

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51
Q

What is acute limb ischemia?

A

A surgical emergency

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52
Q

What are the 6P’s of acute limb ischemia?

A

Pain
Pallor
Pulseless
Perishing cold
Paraesthesia
Paralysis

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53
Q

What is atrial flutter?

A

A form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves

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54
Q

What are the ECG findings in atrial flutter?

A
  1. ‘sawtooth’ appearance
  2. flutter waves may be visible following carotid sinus massage or adenosine
  3. HR is dependent on degree of AV block
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55
Q

What is the management of atrial flutter?

A
  1. Similar to that of atrial fibrillation although medication may be less effective
  2. Atrial flutter is more sensitive to cardioversion so lower energy levels may be used
  3. Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
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56
Q

What is atrial fibrillation?

A

Rapid, chaotic and ineffective atrial electrical conduction resulting in an arrhythmia

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57
Q

What is the epidemiology of atrial fibrillation?

A

Very common
Present in around 5% of patients over aged 70-75 years and 10% of patients aged 80-85 years

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58
Q

What are the three classes of atrial fibrillation?

A

Paroxysmal
Persistent
Permanent

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59
Q

What is the aetiology of AF?

A

There may be no identifiable cause (‘lone’ AF)
Secondary causes lead to abnormal atrial electrical pathways that result in AF

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60
Q

What are the secondary systemic causes of AF?

A

Thyrotoxicosis (hyperthyroidism)
Hypertension
Pneumonia
Alcohol

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61
Q

What are the secondary cardiac causes of AF?

A

Mitral valve disease
Ischaemic heart disease
Rheumatic heart disease
Cardiomyopathy
Pericarditis
Atrial myxoma (benign tumour)

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62
Q

What are the secondary respiratory causes of AF?

A

Bronchial carcinoma
Pulmonary embolism

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63
Q

What is the difference in paroxysmal and persistent AF?

A

Paroxysmal = recurrent episodes of AF terminate spontaneously, last less than 7 days (typically < 24 hours)
Persistent = recurrent episodes that are not self-terminating, usually last greater than 7 days

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64
Q

What is permanent AF and why is this a concern for management?

A

There is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate
Longer they have been into AF = less chance of reverting them back into sinus rhythm
Therefore treatment goals are rate control and anticoagulation

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65
Q

What are the features of AF?

A
  1. Palpitations
  2. Dyspnoea
  3. Chest pain

Signs: an irregularly irregular pulse (look for thyroid and valvular disease)

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66
Q

What are the ECG findings for AF?

A

Uneven baseline (fibrillations) with absent P waves, irregular QRS complexes

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67
Q

What are the appropriate investigations for AF?

A
  1. ECG
  2. Bloods: Cardiac enzymes, TFTs, lipid profile, U&Es,
  3. Echocardiogram: To assess for mitral valve disease, left atrial dilation, left ventricular dysfunction or structural abnormalities
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68
Q

What is the management for AF divided into?

A
  1. Rhythm control
  2. Rate control
  3. Stroke risk stratification/ anticoagulation
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69
Q

What is an important consideration of rate vs rhythm control in AF?

A

Not all patients will have rhythm control
1. Rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function
2. Rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose

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70
Q

Which patients are deemed appropriate for rhythm control in AF?

A

NICE guidelines: specific situations such as coexistent heart failure, first onset AF or where there is an obvious reversible cause

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71
Q

What is the rate control management for AF?

A

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF.

If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following:
1. a betablocker
2. diltiazem
3. digoxin

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72
Q

What is the rhythm control management in AF?

A

Not for everyone, if presenting acutely with AF:
1. Haemodynamically unstable: should be electrically cardioverted, as per the peri-arrest tachycardia guidelines
2. haemodynamically stable patients, the management depends on how acute the AF is:
< 48 hours: rate or rhythm control
≥ 48 hours or uncertain (e.g. patient not sure when symptoms started): rate control
(if considered for long‑term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks)

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73
Q

What medications are used to maintain rhythm control in AF?

A
  1. Beta-blockers
  2. Dronedarone: second-line in patients following cardioversion
  3. Amiodarone: particularly if coexisting heart failure
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74
Q

What is catheter ablation therapy in the management of AF?

A

NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication
Aim: to ablate the faulty electrical pathways that are resulting in AF (typically due to aberrant electrical activity between the pulmonary veins and left atrium)
Procedure is performed percutaneously, typically via the groin
both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue

Anticoagulation
- should be used 4 weeks before and during the procedure
- catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm so patients still require anticoagulation as per their CHA2DS2-VASc score

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75
Q

What are the complications of catheter ablation in the management of AF?

A

Cardiac tamponade
Stroke
Pulmonary vein stenosis

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76
Q

What is the prognosis of catheter ablation for AF?

A

Around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
Longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm

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77
Q

What is the CHA2DS2-VASc score?

A

C Congestive heart failure (1)
H Hypertension (or treated hypertension) (1)
A2 Age >= 75 years (2)
Age 65-74 years (1)
D Diabetes (1)
S2 Prior Stroke, TIA or thromboembolism (2)
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) (1)
S Sex (female) (1)

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78
Q

What is the anticoagulation plan in patients with AF?

A

Based on CHA2DS2-VASc score:
0 = No treatment
1 = Males: Consider anticoagulation, Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more = Offer anticoagulation, DOACs e.g. apixaban, dabigatran, ravaroxaban
If 0 do an echo to exclude valvular heart disease (absolute indication for anticoagulantion in AF

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79
Q

What is the scoring assessment for risk of bleeding?

A

ORBIT scoring system:
Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females = 2
Age > 74 years = 1
Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) = 2
Renal impairment (GFR < 60 mL/min/1.73m2) = 1
Treatment with antiplatelet agents = 1

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80
Q

What are the severity scores from the ORBIT risk of bleeding?

A

0-2 = Low
3 = Medium
4-7 = High

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81
Q

What is digoxin?

A

It is a cardiac glycoside that increases the force of myocardial contraction and reduces conductivity within the AVN
Used to treat AF, atrial flutter and heart failure

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82
Q

Which electrolytes need to be measured in AF treated with digoxin, and why?

A

K+, Mg2+, Ca2+
There is a risk of digoxin toxicity if potassium or magnesium are low, or if calcium is high

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83
Q

What is stroke risk stratification management for patients with AF?

A

Based on CHA2DS2-VASc score
Anticoagulation 1st line = DOACs e.g. apixaban, dabigatran, rivaroxaban
2nd line = warfarin (require regular blood tests to monitor the INR)

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84
Q

What is the prognosis for patients with permanent AF?

A

Chronic AF in a diseased heart does not usually return to sinus rhythm

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85
Q

What is cardiac arrest?

A

Acute cessation of cardiac function

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86
Q

What are the reversible causes for a cardiac arrest?

A

4 Hs and 4Ts:
1. Hypo/ hyperkalaemia
2. Hypothermia
3. Hypovolaemia
4. Hypoxia

  1. Tamponade
  2. Tension pneumothorax
  3. Thromboembolism
  4. Toxins
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87
Q

What signs would be seen on physical examination for a patient in cardiac arrest?

A

Unconscious
Patient is not breathing
Absent carotid pulses

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88
Q

What are the ‘shockable’ rhythms in cardiac arrest?

A

Ventricular fibrillation (VF)
(Pulseless) Ventricular tachycardia (VT)

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89
Q

What are the ‘non-shockable’ rhythms in cardiac arrest?

A

Asystole
Pulseless-electrical activity (PEA)

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90
Q

What is the management for a cardiac arrest?

A

Crash call 2222
MEDICAL EMERGENCY
Adult advanced life support:
1. Determine rhythm via cardiac monitor
2. Begin chest compressions to ventilation at a ratio of 30:2
3. Defibrillate if shockable rhythms
4. Adrenaline 1mg
Management depends on cardiac rhythm

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91
Q

What is the management of a shockable rhythm in cardiac arrest?

A

A to E assessment/ 2222/ medical emergency
1. Deliver shock
2. Resume chest compressions 30:2
3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus (anti-arrhythmic)

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92
Q

What is the management for a non-shockable rhythm in a cardiac arrest?

A

Medical emergency/ 2222
1. CPR for 2 min at 30:2, and then return to assessing rhythm
2. Administer adrenaline (1 mg IV) every 3–5 min

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93
Q

What is the management of return of spontaneous circulation (ROSC) in a cardiac arrest?

A

A to E approach
Aim for SpO2 sats of 94-98%
2 IV wide bore cannulas
ABG
12 lead ECG
Treat precipitating cause
Targeted temperature management

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94
Q

What is the management for shockable cardiac rhythms?

A
  1. Defibrillate once
  2. Resume CPR immediately for 2 min, and then defibrillate
  3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
  4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus (anti-arrhythmic)
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95
Q

What is the management for non- shockable cardiac rhythms?

A
  1. CPR for 2 min, and then return to assessing rhythm
  2. Administer adrenaline (1 mg IV) every 3–5 min
    No longer give atropine!
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96
Q

What is the treatment for the 4 H reversible causes of cardiac arrest?

A

Hypothermia: Warm slowly
Hypo- or hyperkalaemia: Correction of electrolytes
Hypovolaemia: IV colloids, crystalloids or blood products
Hypoxia: oxygen

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97
Q

What is the treatment for the 4 T reversible causes of cardiac arrest?

A

Tamponade: Pericardiocentesis under xiphisternum up and leftwards
Tension pneumothorax: Aspirate, needle into second intercostal space, mid-clavicular line
Thromboembolism: management for PE, MI
Toxins: antidotes

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98
Q

What are the complications of a cardiac arrest?

A

Irreversible hypoxic brain damage -> death

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99
Q

What is the prognosis for patients with a cardiac arrest?

A

Resuscitation is less successful in the arrests that occur outside hospital
Duration of inadequate effective cardiac output is associated with poor prognosis

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100
Q

What is cardiac failure?

A

Defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body

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101
Q

How can heart failure be classified?

A
  1. By ejection fraction
  2. Acute or chronic
  3. Left or right
  4. High-output
102
Q

What is high-output HF?

A

Refers to a ‘normal’ heart is unable to pump enough blood to meet the metabolic demands of the body

103
Q

What are the causes of a high-output HF?

A
  1. Anaemia
  2. Arteriovenous malformation
  3. Paget’s disease
  4. Pregnancy
  5. Thyrotoxicosis
  6. Thiamine deficiency (Beri-Beri)
104
Q

What are the common causes of left sided HF?

A
  1. Increased left ventricular afterload e.g. arterial hypertension, aortic stenosis
  2. Increased left ventricular preload e.g. aortic regurgitation
105
Q

What is a common feature of left sided HF?

A

Pulmonary oedema:
1. Dyspnoea
2. Orthopnoea
3. Paroxysmal nocturnal dyspnoea
4. Bibasal fine crackles

106
Q

What are the causes of right sided HF?

A
  1. Increased right ventricular afterload e.g. pulmonary hypertension
  2. Increased right ventricular preload e.g. tricuspid regurgitation
107
Q

What are the common features of right sided HF?

A
  1. Peripheral oedema e.g. pedal/sacral oedema
  2. Raised jugular venous pressure
  3. Hepatomegaly
  4. Weight gain due to fluid retention
  5. Anorexia ‘cardiac cachexia’
108
Q

How is ejection fraction in HF measured?

A

By echocardiography

109
Q

What is the terminology for ejection fraction in HF?

A
  1. Reduced ejection fraction (HF-rEF) = < 35-40%
  2. Preserved ejection fraction (HF-pEF)
110
Q

What are the general causes of reduced and preserved ejection fraction HF?

A

Reduced EF:
1. Ischaemic heart disease
2. Dilated cardiomyopathy
3. Myocarditis
4. Arrhythmias
Preserved EF:
1. Hypertrophic obstructive cardiomyopathy
2. Restrictive cardiomyopathy
3. Cardiac tamponade
4. Constrictive pericarditis

111
Q

What is the epidemiology of HF?

A

10% of those over 65 years, usually presents at this age

112
Q

What is acute HF?

A
  1. A life threatening emergency
  2. Used to describe the sudden onset or worsening of symptoms of HF
  3. Usually has a background of pre-existing HF: decompensated
  4. If there is no history of HF: de-novo AHF
113
Q

What are the causes of decompensated HF (background of pre-existing HF)?

A
  1. Acute coronary syndrome
  2. Hypertensive crisis
  3. Acute arrhythmia
  4. Valvular disease e.g. AS
114
Q

What are the causes of de novo acute HF?

A
  1. Usually ischaemia
  2. Other causes e.g. viral myopathy, toxins, valve dysfunction
115
Q

How can patients with acute HF be broadly categorised?

A
  1. With or without hypoperfusion
  2. With or without fluid congestion
116
Q

What are the general symptoms of acute HF?

A
  1. Breathlessness
  2. Reduced exercise tolerance
  3. Oedema
  4. Fatigue
117
Q

What are the general signs of acute HF?

A
  1. Cyanosis
  2. Tachycardia
  3. Elevated jugular venous pressure
  4. Displaced apex beat
  5. Chest signs: bibasal crackles (pulmonary oedema), may have wheeze
  6. S3 heart sound
    *Over 90% of patients with have a normal or increased BP
118
Q

What are the investigations for acute HF?

A

Medical emergency- A to E approach
1. Bloods: look for underlying abnormality e.g. anaemia, infection
2. Chest x-ray: cardiomegaly, pulmonary oedema: venous congestion, interstitial oedema, Kerley B lines
3. Echocardiogram: ejection fraction, pericardial effusion, cardiac tamponade
4. BNP (B-type natriuretic peptide): > 100mg/L is supportive of dx

119
Q

What is the recommended management for all patients with acute HF?

A

IV loop diuretics e.g. furosemide

120
Q

What are some of the other management options for acute HF?

A

(Sit patient up)
1. Oxygen: aim for saturations 94-98%
2. Vasodilators e.g. nitrates (not to all patients)
3. Opiates (again not to all patients)
4. Continue any regular medication for HF e.g. ACE inhibitors

121
Q

When are nitrates used in the management of HF?

A

If patients have concomitant myocardial ischaemia, severe hypertensionor regurgitant aortic or mitral valve disease

122
Q

What is the major side effect/ contraindication to the use of nitrates in the management of acute HF?

A

Hypotension (cardiogenic shock)

123
Q

What is the management of cardiogenic shock (hypotension) in acute HF?

A
  1. < 10% of patients- seek senior support
  2. IV loop diuretics and nitrates may worsen hypotension
  3. Consider inotropic agents e.g. dobutamine
  4. Vasopressors e.g. norepinephrine
  5. Mechanical circulatory assistance e.g. intra-aortic balloon
124
Q

What routine mediations for HF should be continued or stopped in the management of acute HF?

A
  1. Continue ACE inhibitors
  2. Continue B blockers (but if HR is < 50 bpm, second or third degree heart block or shock then stop)
125
Q

What are the features of chronic HF?

A
  1. Dyspnoea
  2. Cough: worse at night, associated with pink/ frothy sputum
  3. Orthopnoea
  4. Paroxysmal nocturnal dyspnoea
  5. ‘Cardiac’ wheeze
  6. Weight loss: ‘cardiac cachexia’/ weight gain secondary to oedema
  7. Bibasal crackles on examination
  8. Signs of right sided HF: raised JVP, ankle oedema, hepatomegaly
126
Q

What is the New York Heart Association (NYHA) for chronic HF?

A

Used to classify the severity of HF:
Class 1: No symptoms/ no limitation
Class 2: Mild symptoms, some limitation of physical activity
Class 3: Moderate symptoms, marked limitation of physical activity (less than normal activity results in symptoms)
Class 4: Severe symptoms, unable to carry out any physical activity without discomfort (symptoms present even at rest)

127
Q

What is the first-line blood test for chronic HF diagnosis?

A

N-terminal pro-B-type natriuretic peptide (NT‑proBNP)

128
Q

How are the N-terminal pro-BNP tests interpreted in chronic HF diagnosis?

A
  1. If ‘high’: arrange specialist assessment (incl echo) within 2 weeks
  2. If ‘raised’: arrange specialist assessment (incl echo) within 6 weeks
129
Q

What is B-type natriuretic peptide (BNP)?

A
  1. Hormone produced mainly by the left ventricular myocardium in response to strain
  2. Very high levels are associated with a poor prognosis:
    a. High = > 400pg/ml
    b. Raised = 100-400ph/ml
    c. Normal = < 100pg/ml
130
Q

What can increase BNP levels?

A
  1. Left ventricular hypertrophy
  2. Ischaemia
  3. Tachycardia
  4. Hypoxaemia (including PE)
  5. GFR < 60ml/min
  6. Sepsis
  7. COPD
  8. DM
  9. Aged > 70 years
  10. Liver cirrhosis
131
Q

What can decrease BNP levels?

A
  1. Obesity
  2. Diuretics
  3. ACE inhibitors
  4. B blockers
  5. ARBs
  6. Aldosterone antagonists e.g. spironolactone
132
Q

What is the first line management for chronic HF?

A

(manage lifestyle and optimise comorbidities)
1. ACE inhibitors (ARB if intolerant)
2. Beta Blockers
(start one at a time)

133
Q

What is the second line management for chronic HF?

A
  1. ACE inhibitors + beta blockers
  2. Add an aldosterone antagonist e.g. spironolactone
134
Q

What should be monitored alongside the management of chronic HF?

A

Potassium levels: both ACE inhibitors and aldosterone antagonists cause hyperkalaemia

135
Q

What other drugs can be given as second line management in chronic HF?

A

SGLT-2 inhibitors:
1. For patients with a reduced EF
2. Reduce glucose reabsorption and increase urinary glucose excretion
3. E.g. dapagliflozin

136
Q

What is the third line management for chronic HF?

A
  1. Only initiated by a specialist
  2. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
137
Q

When is digoxin indicated in the management of chronic HF?

A

If there is coexistent atrial fibrillation

138
Q

When is cardiac resynchronisation therapy indicated in the management of chronic HF?

A

Widened QRS (e.g. left bundle branch block) complex on ECG

139
Q

What are add on treatments for patients with chronic HF?

A
  1. Annual influenza vaccination
  2. One-off pneumococcal vaccine (if the patient has asplenia, splenic dysfunction or chronic kidney disease they need a booster every 5 years)
140
Q

When should ivabradine be added in the management of chronic HF?

A
  1. Third line specialist treatment
  2. If sinus rhythm > 75/min and a left ventricular EF < 35%
141
Q

When should sacubitril-valsartan be added in the management of chronic HF?

A
  1. Third line specialist treatment
  2. When left ventricular EF < 35% and still symptomatic on ACE inhibitors and ARBs
  3. Should be initiated following ACEi/ ARB wash-out period
142
Q

How do beta blockers work in the management of chronic HF?

A
  1. Block the effects of chronically activated sympathetic system, slow progression of the heart failure and improve survival
  2. The benefits of ACE inhibitors and b-blockers are additive*
143
Q

How to ACE inhibitors work in the management of chronic HF?

A

e.g. enalapril, perindopril, ramipril)
1. Inhibit intracardiac renin-angiotensin system which may contribute to myocardial hypertrophy and remodelling
2. ACE inhibitors slow progression of the heart failure and improve survival

144
Q

When should Hydralazine and a nitrate be added in the management of chronic HF?

A

May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker

145
Q

Which drugs should be avoided in chronic HF?

A

Drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil)

146
Q

What are the complications of HF?

A
  1. Respiratory failure
  2. Cardiogenic shock
  3. Death
147
Q

What is the prognosis of heart failure?

A

50% of patients with severe heart failure die within 2 years

148
Q

What is cardiomyopathy?

A

Disease of the myocardium, can be primary or secondary
Used to be hypertrophic, dilated or restrictive

149
Q

What are primary cardiomyopathies?

A

Predominantly involve the heart:
1. Genetic: HOCM
2. Mixed (genetic predisposed to acquired): dilated and restrictive
3. Acquired: peripartum and Takotsubo (‘broken-heart’)

150
Q

What are secondary cardiomyopathies?

A

Pathological myocardial involvement as part of a generalised systemic disorder:
1. Infective: Coxsackie B
2. Infiltrative: Amyloidosis
3. Storage: Haemochromatosis
4. Toxicity: Alcohol
5. Inflammatory: Sarcoidosis
6. Endcrine: DM, Acromegaly, thyrotoxicosis
7. Neuromuscular
8. Nutritional: thiamine deficiency
9. Autoimmune: SLE

151
Q

What is hypertrophic obstructive cardiomyopathies?

A

An autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins

152
Q

Why is HOCM important?

A

The most common cause of sudden cardiac death in the young

153
Q

What is the pathophysiology of HOCM?

A
  1. Most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
  2. Results in predominantly diastolic dysfunction
  3. Left ventricle hypertrophy → decreased compliance → decreased cardiac output
154
Q

What are the features of HOCM?

A
  1. Often asymptomatic
  2. Exertional dyspnoea
  3. Angina
  4. Syncope: typically following exercise, due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
155
Q

What is the most common cause of sudden death in HOCM?

A

Ventricular arrhythmia (can also be due to arrhythmias and HF)

156
Q

What are the signs of HOCM on examination?

A
  1. Jerky pulse
  2. Large ‘a’ waves
  3. Double apex beat
  4. Systolic murmurs:
    a. ESM: due to left ventricular outflow tract obstruction
    b. Pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
157
Q

What are the features of the ejection systolic murmur auscultated in HOCM?

A

Increases with Valsalva manoeuvre and decreases on squatting

158
Q

What are the ECG findings for HOCM?

A
  1. Left ventricular hypertrophy
  2. Non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
  3. Deep Q waves
  4. Atrial fibrillation may occasionally be seen
159
Q

What are the echo findings for HOCM?

A

Mitral regurgitation (MR)
Systolic anterior motion (SAM) of the anterior mitral valve leaflet
Asymmetric hypertrophy (ASH)

160
Q

What is the management of HOCM?

A
  1. Amiodarone
  2. Beta-blockers or verapamil for symptoms
  3. Cardioverter defibrillator
  4. Dual chamber pacemaker
  5. Endocarditis prophylaxis* (for antibiotic prophylaxis for infective endocarditis)
161
Q

What drugs should be avoided in HOCM?

A
  1. Nitrates
  2. ACE inhibitors
  3. Inotropes
162
Q

What is the aetiology of dilated cardiomyopathy?

A
  1. Post-viral myocarditis
  2. Alcohol, drugs (e.g. doxorubicin, cocaine)
  3. Familial (25% of idiopathic cases, usually autosomal dominant)
  4. Thyrotoxicosis
  5. Haemochromatosis
  6. Peripartum
163
Q

What is the aetiology of restrictive cardiomyopathy?

A

Amyloidosis
Sarcoidosis
Haemochromatosis

164
Q

What is the epidemiology of cardiomyopathy?

A

Prevalence of dilated cardiomyopathy and hypertrophic cardiomyopathy is 0.05–0.2%
*Restrictive cardiomyopathy is rare

165
Q

What are the presenting symptoms of dilated cardiomyopathy?

A
  1. Symptoms of heart failure
  2. Arrhythmias
  3. Thromboembolism
  4. Family history of sudden death
166
Q

What are the presenting symptoms of restrictive cardiomyopathy?

A

Main:
1. Dyspnoea
2. Fatigue
Others:
3. Arrhythmias
4. Ankle or abdominal swelling
5. FH of sudden death

167
Q

What are the signs of dilated cardiomyopathy on physical examination?

A

(similar to heart failure)
1. Raised JVP
2. Displaced apex beat
3. Functional mitral and tricuspid regurgitations
4. Third heart sound
5. On auscultation of the lungs: crackles, indicating pulmonary congestion

168
Q

What are the signs of hypertrophic cardiomyopathy on physical examination?

A
  1. Jerky carotid pulse
  2. Double apex beat
  3. Ejection systolic murmur
  4. On auscultation of the lungs: crackles, indicating pulmonary congestion
169
Q

What are the signs of restrictive cardiomyopathy on physical examination?

A
  1. Raised JVP (Kussmaul’s sign: further increase on inspiration)
  2. Palpable apex beat
  3. Third heart sound
  4. Ascites
  5. Ankle oedema
  6. Hepatomegaly
  7. On auscultation of the lungs: crackles, indicating pulmonary congestion
170
Q

What are the echo findings for the different types of cardiomyopathy?

A
  1. Dilated: Dilated ventricles with ‘global’ hypokinesia
  2. Hypertrophic: Ventricular hypertrophy (disproportionate septal involvement)
  3. Restrictive: Non-dilated non-hypertrophied ventricles
171
Q

What are the echo findings for cardiomyopathy secondary to amyloidosis?

A
  1. Atrial enlargement
  2. Preserved systolic function
  3. Diastolic dysfunction
  4. Granular or ‘sparkling’ appearance of myocardium
172
Q

What are the investigations for cardiomyopathies?

A
  1. Bloods including BNP
  2. ECG
  3. Chest x-ray: cardiomegaly, dilated = ‘balloon’ appearance
173
Q

What is Takotsubo cardiomyopathy?

A

A type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium which may be triggered by stress

174
Q

What is the pathophysiology of Takotsubo cardiomyopathy?

A

Octopus trap:
1. The bottom of the heart (the apex) does not contract and therefore appears to balloon out
2. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap)

175
Q

What are the features of Takotsubo cardiomyopathy?

A
  1. Chest pain
  2. Features of HF
  3. ECG: ST elevation
  4. Normal coronary angiogram
176
Q

What is the management of Takotsubo cardiomyopathy?

A

Supportive, many patients improve with the treatment alone

177
Q

What is a carotid endarterectomy?

A

Removal of a fatty plaque from the carotid artery disease

178
Q

When is a carotid endarterectomy indicated?

A
  1. If patient has suffered stroke or TIA in the carotid territory and are not severely disabled
  2. If the carotid stenosis is > 70% according ECST criteria or > 50% according to NASCET criteria
179
Q

What are the possible complications of a carotid endarterectomy?

A
  1. Stroke/ TIA
  2. MI
  3. Haematoma
  4. Nerve injuries
  5. Infection
  6. Arrhythmia
180
Q

What is pericarditis?

A

Inflammation of the pericardium, may be acute, subacute or chronic

181
Q

What is the criteria for acute pericarditis?

A

New-onset inflammation lasting <4-6 weeks

182
Q

What is the aetiology of pericarditis?

A
  1. Viral infections (Coxsackie) - most common
  2. TB
  3. Uraemia
  4. Post MI:
    a. early (1-3 days): fibrinous pericarditis
    b. late (weeks to months): autoimmune pericarditis = Dressler’s syndrome
  5. Radiotherapy
  6. Connective tissue disease:
    a. SLE
    b. Rheumatoid arthritis
  7. Hypothyroidism
  8. Malignancy
    a. Lung cancer
    b. Breast cancer
  9. Trauma
183
Q

What is the epidemiology of pericarditis?

A
  1. Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men
  2. Pericarditis in general is uncommon- the clinical incidence is <1 in 100 hospital admissions
184
Q

What are the presenting symptoms of pericarditis?

A
  1. Chest pain (85%): may be pleuritic and is often relieved by sitting forwards
  2. Other symptoms:
    a. Non-productive cough
    b. Dyspnoea
    c. Flu-like symptoms
185
Q

What are the signs of pericarditis on examination?

A
  1. Fever
  2. Pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration)
  3. Heart sounds may be faint in the presence of an effusion
186
Q

What are the investigations for pericarditis?

A
  1. ECG
  2. Echocardiogram
  3. Bloods
187
Q

What are the ECG changes in pericarditis?

A
  1. Saddle-shaped ST elevation
  2. PR depression (most specific marker)
    Changes are generally more widespread than in ischaemic events which have ‘territories’
188
Q

What investigation must be performed in all patients with suspected acute pericarditis?

A

A transthoracic echocardiogram

189
Q

What are the blood work findings of acute pericarditis?

A
  1. Inflammatory markers e.g. ESR, CRP
  2. Troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis
190
Q

What is the management of pericarditis?

A
  1. Majority managed as outpatients
  2. Treat the underlying cause (most common cause is viral so no specific treatment)
  3. Combination of NSAIDs and colchicine is first line for patients with acute idiopathic or viral pericarditis
191
Q

When would a patient with pericarditis be managed as an inpatient?

A

If they had high-risk features e.g. fever > 38°C or elevated troponin

192
Q

How long should a patient with acute idiopathic or viral pericarditis be on NSAIDs and colchicine?

A

Until symptom resolution and normalisation of inflammatory markers = usually 1-2 weeks (then dose will be tapered down)

193
Q

What advice should be given to patients with pericarditis?

A

To avoid strenuous physical activity until symptom resolution and normalisation of inflammatory markers

194
Q

What is constrictive pericarditis?

A
  1. Medium to late complication of pericarditis
  2. When there is impediment (delay) of normal diastolic filling
195
Q

What are the causes of constrictive pericarditis?

A

Any cause of pericarditis, particularly TB

196
Q

What are the features of constrictive pericarditis?

A
  1. Dyspnoea
  2. Right heart failure:
    a. Elevated JVP
    b. Ascites
    c. Oedema
    d. Hepatomegaly
  3. JVP shows prominent x and y descent
  4. Pericardial knock - loud S3
  5. Kussmaul’s sign is positive
197
Q

What is the main investigation for constrictive pericarditis alongside ECG, echo and bloods?

A

Chest x-ray: shows pericardial calcification

198
Q

What is the finding of pericarditis on ECG?

A

Saddle-shaped ST elevation and PR depression (widespread)

199
Q

What is Kussmaul’s sign?

A

A paradoxical rise in JVP during inspiration

200
Q

What is the definitive management of constrictive pericarditis?

A

Pericardiectomy: surgical removal of the pericardium

201
Q

What is cardiac tamponade?

A

Characterized by the accumulation of pericardial fluid under pressure

202
Q

What are the classical features of cardiac tamponade?

A

Beck’s triad:
1. Hypotension
2. Raised JVP
3. Muffled heart sounds

203
Q

What are some of the other features of cardiac tamponade?

A
  1. Beck’s triad: hypotension, raised JVP, muffled heart sounds
  2. Dyspnoea
  3. tachycardia
  4. Pulsus paradoxus: abnormally large drop in BP during inspiration
204
Q

What is the difference in JVP of cardiac tamponade and constrictive pericarditis?

A

Constrictive pericarditis: X +Y present
Cardiac tamponade: Absent Y descent

205
Q

What are the other differences on examination between cardiac tamponade and constrictive pericarditis?

A

Cardiac tamponade: pulsus paradoxus present
Constrictive pericarditis: Kussmaul’s sign positive

206
Q

What is the finding of cardiac tamponade on ECG?

A

Electrical alterans: alternation of QRS complex amplitude between beats

207
Q

What is the management of cardiac tamponade?

A

Urgent pericardiocentesis

208
Q

What can cardiac tamponade lead to?

A

Cardiac arrest (reversible T)

209
Q

What is coronary angiography?

A

An invasive diagnostic procedure to assess the structure and function of the heart, using a contrast medium and x-rays of the heart and coronary arteries

210
Q

What is Percutaneous Coronary Intervention (PCI)?

A

The combination of coronary angioplasty with stenting, widening blocked or narrowed coronary arteries

211
Q

What are the indications for coronary angiography and PCI?

A

Coronary angiography: diagnosis, treatments and procedures:
1. MI: where the heart’s blood supply is blocked
2. Diagnose angina: chest pain is caused by restricted blood supply to the heart
3. Planned interventional or surgical procedures – such PCI
4. Diagnose coronary heart disease

212
Q

What are the possible complications of coronary angiography and PCI?

A
  1. Allergic reaction to contrast dye
  2. Bleeding under the skin where the catheter was inserted
  3. Damage to the artery in the arm or leg where the catheter was inserted
  4. Rare: Heart attack, Stroke, Kidney damage and, very rarely, death
213
Q

What is a coronary artery bypass graft?

A

A surgical procedure used to treat coronary heart disease by diverting blood around narrowed or clogged parts of coronary arteries to improve blood flow and oxygen supply to the heart

214
Q

What are the indications for a Coronary artery bypass graft?

A
  1. Atherosclerosis causing coronary heart disease e.g. stable angina
  2. Ultimately reduce the risk of MI
215
Q

What are the possible complications of a coronary artery bypass graft?

A

Arrhythmias
Infection risk
Rare: stroke or heart attack

216
Q

What is DC cardioversion?

A

A procedure to convert an abnormal heart rhythm to a normal heart rhythm (most commonly AF)

217
Q

What are the indications for DC cardioversion?

A

Arryhthmias

218
Q

What are the possible complications of DC cardioversion?

A

Usually temporary:
1. Headaches and dizziness from a drop in your blood pressure from anaesthetic
2. Discomfort in chest where the shock was given
3. Nausea (from anaesthetic)

219
Q

What is Virchow’s triad?

A
  1. Venous stasis
  2. Vessel wall injury
  3. Blood hypercoagulability
220
Q

What is deep vein thrombosis (DVT)?

A

Formation of a thrombus within the deep veins (most commonly of the calf or thigh) which may result in impaired venous blood flow and consequent leg swelling and pain

221
Q

What are the risk factors for DVT?

A
  1. Oral contraceptive pill
  2. Surgery
  3. Prolonged immobility
  4. Long bone fractures
  5. Obesity
  6. Pregnancy
  7. Dehydration
  8. Smoking
  9. Polycythaemia
  10. Anti-phospholipid syndrome
  11. Thrombophilia disorders (e.g. protein C deficiency)
  12. Active malignancy
222
Q

What is the epidemiology for DVT?

A

Common, especially in hospitalised patients- yearly incidence of approximately 1 in every 1000 adults

223
Q

What are the presenting symptoms of DVT?

A
  1. Asymptomatic or lower limb swelling or tenderness
  2. May present with signs/ symptoms of a pulmonary embolus (sudden onset dyspnoea, chest pain)
224
Q

What are the signs of DVT on physical examination?

A

Examine for swelling, calf tenderness:
1. Severe leg oedema (usually unilateral)
2. Dilated superficial veins over foot and leg
3. Cyanosis (phlegmasia cerulea dolens) is rare
*Respiratory examination for signs of a pulmonary embolus: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain

225
Q

What should be performed in any patient with suspected DVT?

A

A two-level DVT Wells score

226
Q

What is the Two-level DVT Wells score?

A
  1. Active cancer (treatment ongoing, within 6 months, or palliative) = 1
  2. Paralysis, paresis or recent plaster immobilisation of the lower extremities= 1
  3. Recently bedridden for 3 days or more or major surgery within 12 weeks requiring general or regional anaesthesia = 1
  4. Localised tenderness along the distribution of the deep venous system = 1
  5. Entire leg swollen = 1
  6. Calf swelling at least 3 cm larger than asymptomatic side = 1
  7. Pitting oedema confined to the symptomatic leg = 1
  8. Collateral superficial veins (non-varicose) = 1
  9. Previously documented DVT = 1
  10. An alternative diagnosis is at least as likely as DVT = -2
227
Q

How is the Two-level DVT Wells score interpreted for DVT likelihood?

A

DVT likely: 2 points or more
DVT unlikely: 1 point or less

228
Q

What is the next step in management for a patient who scored 1 point or less on the two-level DVT Wells score?

A

DVT ‘unlikely’:
1. Perform a D dimer score within 4 hours
2. If not, interim therapeutic anticoagulation should be given until the result is available, but still performed within 24 hours

229
Q

What should be the next step in management if a D dimer result is negative in a suspected DVT?

A

Then DVT is unlikely and alternative diagnoses should be considered

230
Q

What should be the next step in management if a D dimer result is positive in a suspected DVT?

A

A proximal leg vein ultrasound scan should be carried out within 4 hours (if delayed then give interim therapeutic anticoagulation)

231
Q

What are d-dimer tests in the investigation of DVTs?

A
  1. NICE recommend either a point-of-care (finger prick) or laboratory-based test
  2. Age-adjusted cut-offs should be used for patients > 50 years old
232
Q

What is the next step in management for a patient who scored 2 points or more on the two-level DVT Wells score?

A

DVT is ‘likely’:
1. A proximal leg vein ultrasound scan should be carried out within 4 hours
2. If not, interim therapeutic anticoagulation should be given until the result is available, but still performed within 24 hours

233
Q

What should be the next step in management if a proximal leg vein ultrasound is positive in a suspected DVT?

A

Then a diagnosis of DVT is made and anticoagulant treatment should start

234
Q

What should be the next step in management if a proximal leg vein ultrasound is negative in a suspected DVT?

A

A D-dimer test should be arranged: a negative scan and negative D-dimer makes the diagnosis unlikely and alternative diagnoses should be considered

235
Q

What should be the next step in management if a proximal leg vein ultrasound is negative in a suspected DVT but the D dimer is positive?

A
  1. Stop interim therapeutic anticoagulation
  2. Offer a repeat proximal leg vein ultrasound scan 6 to 8 days later
236
Q

What is meant by interim therapeutic anticoagulation in suspected DVT?

A

Used to be LMWH, now a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban

237
Q

What is the management of a confirmed DVT?

A
  1. NICE now advocate using a DOAC once a diagnosis is suspected, with this continued if the diagnosis is confirmed
  2. All patients should have anticoagulation for at least 3 months
  3. Then if the VTE was provoked, the treatment can be stopped
  4. If the VTE was unprovoked, then treatment is typically continued for up to 3 further months (i.e. 6 months in total)
238
Q

What is the ORBIT score used for?

A

To help assess the risk of bleeding in a patient on anticoagulation

239
Q

In what group of patients are DOACs recommended as first line for the management of DVTs?

A

Essentially all patients including those with active cancer unless contraindicated
Not to be used in patients with:
1. Renal impairment (< 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA
2. Antiphospholipid syndrome then LMWH followed by a VKA should be used

240
Q

How can VTEs be prevented?

A
  1. Use of graduated compression stockings
  2. Mobilisation if possible (physical activity)
  3. At-risk groups (immobilised hospital patients) should have prophylactic heparin, e.g. LMWH if no contraindications
241
Q

What are the complications of DVT?

A

Of the disease:
1. PE
2. Damage to vein valves and chronic venous insufficiency of the lower limb (post-thrombotic syndrome)
3. Rare: Venous infarction (phlegmasia cerulea dolens)
Of the treatment:
1. Heparin-induced thrombocytopaenia
2. Bleeding

242
Q

What is the prognosis of DVT?

A

Depends on the location of DVT:
1. Below-knee DVTs lower risk of embolus
2. More proximal DVTs have higher risk of propagation and embolisation, which, if large, may be fatal

243
Q

What is Dyslipidaemia?

A

Classified as serum Total cholesterol, LDL-C, triglycerides, apolipoprotein B, or lipoprotein(a) concentrations above the 90th percentile for the general population

244
Q

What is the aetiology of Dyslipidaemia?

A
  1. Primary causes: due to single or multiple gene mutations, resulting in a disturbance of LDL and triglyceride production or clearance (most commonly seen in children and young adults)
  2. Secondary causes: caused by lifestyle factors or disorders that interfere with blood lipid levels over time such as obesity, CKD
245
Q

What is the epidemiology of Dyslipidaemia?

A
  1. Common, particularly in developing countries
  2. Strong correlation between body mass index and coronary heart disease
  3. Primary causes are common in children and young adults whereas secondary is seen more in adults
246
Q

What are the presenting symptoms of Dyslipidaemia?

A
  1. Excess body weight
  2. PMH Diabetes Mellitus Type 2 or cardiovascular disease
  3. Consumption of saturated fats
  4. FH of early onset of coronary heart disease or Dyslipidaemia
247
Q

What are the signs of Dyslipidaemia on physical examination?

A
  1. Xanthelasmas: Yellow plaques that occur most commonly near the inner canthus of the eyelid
  2. Tendinous xanthomas: Slowly enlarging subcutaneous nodules (on tendons or ligaments)
248
Q

What are the appropriate investigations for Dyslipidaemia?

A

Lipid profile:
1. Total cholesterol (TC) >5.18 mmol/L (>200 mg/dL)
2. LDL-cholesterol >2.59 mmol/L (>100 mg/dL)
3. triglycerides >1.7 mmol/L (>150 mg/dL)
4. Fasting (12h) triglycerides: ≥2.3 mmol/L (200 mg/dL)
Can also offer TFTs

249
Q

What is the management of dyslipidaemia divided into?

A

Primary prevention: 20mg atorvastatin
1. 10-year cardiovascular risk > 10%
2. Type 1 DM
3. CKD, eGFR < 60ml/min
Secondary prevention: 80mg atorvastatin
1. Known ischaemic heart disease
2. Cerebrovascular disease
3. Peripheral arterial disease

250
Q

What are the management principles of dyslipidaemia?

A

Combination of lifestyle changes to diet and exercise, medications, and dietary supplements
1. Lifestyle changes: dietary reduction in total and saturated fat, weight loss in overweight patients, aerobic exercise
2. Drug therapy: Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, a key enzyme in cholesterol synthesis, which leads to up-regulation of LDL receptors and increased LDL clearance

251
Q

What are the complications of dyslipidaemia?

A

Due to atherosclerosis:
1. Ischaemic heart disease
2. Peripheral vascular disease
3. Acute coronary syndrome
4. Stroke
5. Erectile dysfunction (endothelial dysfunction)

252
Q

What is the prognosis of dyslipidaemia?

A

The rate of adverse outcomes has been significantly reduced with the use of statins

!Final Year (26 decks)

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