Cardiovascular Flashcards

1
Q

Define abdominal aortic aneurysm

A

• A localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal diameter.
o NOTE: normal diameter of the aorta = 2 cm

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2
Q

Explain the aetiology / risk factors of an abdominal aortic aneurysm

A

• There are NO specific identifiable causes
• Risk Factors
o Severe atherosclerotic damage to aortic wall
o Family history
o Smoking
o Male
o Age
o Hypertension
o Hyperlipidaemia
o Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome
o Inflammatory disorders: Behcet’s disease, Takayasu’s arteritis

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3
Q

Summarise the epidemiology of an abdominal aortic aneurysm

A

Around 4% of men aged between 65 and 74 in England have an AAA (approx. 80,000 men) this results in approximately 6000 deaths per year in England and Wales.

Deaths from AAA account for around 2% of all deaths in men aged 65 and over

Women are much less likely to develop abdominal aortic aneurysms. They are about three times more common in men than in women.

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4
Q

Recognise the presenting symptoms of an abdominal aortic aneurysm

A
•	Unruptured
o	NO SYMPTOMS 
o	Usually an incidental finding 
o	May have pain in the back, abdomen, loin or groin 
•	RUPTURED
o	Pain in the abdomen, back or loin 
o	Pain may be sudden or severe 
o	Syncope
o	Shock 
•	NOTE: degree of shock depends on site of rupture and whether it is contained
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5
Q

Recognise the signs of an abdominal aortic aneurysm on physical examination

A
  • Pulsatile and laterally expansile mass on bimanual palpation of the abdominal aorta
  • Abdominal bruit
  • Retroperitoneal haemorrhage can cause Grey-Turner’s sign
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6
Q

Identify appropriate investigations for an abdominal aortic aneurysm and interpret the results

A

• Bloods
o FBC, clotting screen, renal function and liver function
o Cross-match if surgery is planned
• Scans
o Ultrasound - can detect aneurysm but CANNOT tell whether it is leaking or not

o CT with contrast - can show whether an aneurysm has ruptured

o MRI angiography

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7
Q

Define amyloidosis

A

• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils

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8
Q

Explain the aetiology / risk factors of amyloidosis

A

• Amyloid fibrils are polymers of low-molecular-weight subunit proteins
• These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
• Their deposition progressively disrupts the structure and function of normal tissue
• Amyloidosis is classified according to the fibril subunit proteins
o Type AA - serum amyloid A protein
o Type AL - monoclonal immunoglobulin light chains
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin

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9
Q

Summarise the epidemiology of amyloidosis

A
  • AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
  • AL - 300-600 cases in the UK per year
  • Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
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10
Q

Recognise the presenting symptoms & signs of amyloidosis

A
  • Renal - proteinuria, nephrotic syndrome, renal failure
  • Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
  • GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
  • Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
  • Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
  • Joints - painful asymmetrical large joints, enlargement of anterior shoulder
  • Haematological - bleeding tendency
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11
Q

Identify appropriate investigations for amyloidosis and interpret the results

A
•	Tissue Biopsy
•	Urine - check for proteinuria, free immunoglobulin light chains (in AL)
•	Bloods
o	CRP/ESR 
o	Rheumatoid factor 
o	Immunoglobulin levels 
o	Serum protein electrophoresis 
o	LFTs 
o	U&Es 
•	SAP Scan - radiolabelled SAP will localise the deposits of amyloid
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12
Q

Define 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, creating a false lumen
  • Classification of aortic dissection:

o Type A: ASCENDING aorta (MOST COMMON)
o Type B: DESCENDING aorta (distal to the left subclavian artery)

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13
Q

Explain the aetiology / risk factors of aortic dissection

A

• Aortic dissection is usually preceded by degenerative changes in the smooth muscle of the aortic media
• Common causes and risk factors:
o HYPERTENSION
o Aortic atherosclerosis
o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos, SLE)
o Congenital cardiac abnormalities (e.g. coarctation of the aorta)
o Aortitis
o Iatrogenic (e.g. during angioplasty/angiography)
o Trauma
o Crack cocaine
• NOTE: expansion of the false lumen can lead to obstruction of the subclavian, carotid, coeliac and renal arteries
o Hypoperfusion of the target organs of these major arteries can give rise to other symptoms (e.g. carotid artery –> collapse)

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14
Q

Summarise the epidemiology of aortic dissection

A

• Most common in males aged 40-60 yrs

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15
Q

Recognise the presenting symptoms of aortic dissection

A

• MAIN SYMPTOM: sudden central ‘tearing’ pain, it may radiate to the back in between the shoulder blades (it can mimic MI)
• Other symptoms caused by obstruction of branches of the aorta:
o Carotid artery –> hemiparesis, dysphasia, blackout
o Coronary artery –> chest pain (angina or MI)
o Subclavian artery –> ataxia, loss of consciousness
o Anterior spinal artery –> paraplegia
o Coeliac axis –> severe abdominal pain (due to ischaemic bowel)
o Renal artery –> anuria, renal failure

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16
Q

Recognise the signs of aortic dissection on physical examination

A
•	Murmur on the back (below the left scapula), descending to the abdomen 
•	Hypertension
•	Blood pressure difference between the two arms > 20 mm Hg
•	Wide pulse pressure 
•	Hypotension may suggest tamponade 
o	Check for pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration
o	This may indicate:
•	Tamponade
•	Pericarditis
•	Chronic sleep apnoea
•	Obstructive lung disease 
•	Signs of Aortic Regurgitation
o	High volume collapsing pulse 
o    Early diastolic murmur over aortic area 
•	Unequal arm pulses 
•	There may be a palpable abdominal mass
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17
Q

Identify appropriate investigations for aortic dissection and interpret the results

A
•	Bloods
o	FBC
o	X-match 10 units of blood 
o	U&E - check renal function 
o	Clotting screen
•	CXR
o	Widened mediastinum 
•	ECG
o	Often NORMAL
o	If the ostia of the right coronary artery is compromised you may get signs of:
•	Left ventricular hypertrophy 
•	Inferior MI 

• CT Thorax

o Shows false lumen
• Echocardiography
o Transoesophageal allows visualisation
• Cardiac catheterisation and aortography

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18
Q

Define aortic regurgitation

A

• Reflux of blood from the aorta into the left ventricle during diastole. Also known as aortic insufficiency

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19
Q

Explain the aetiology / risk factors of aortic regurgitation

A

• Aortic valve leaflet abnormalities or damage
o Bicuspid aortic valve
o Infective endocarditis
o Rheumatic fever
o Trauma
• Aortic root/ascending aorta dilatation
o Systemic hypertension
o Aortic dissection
o Aortitis
o Arthritides (e.g. rheumatoid arthritis, seronegative arthritides)
o Connective tissue disease (e.g. Marfan’s, Ehlers-Danlos)
o Pseudoxanthoma elasticum
o Osteogenesis imperfecta
• Pathophysiology
o Reflux of blood into the left ventricle results in left ventricular dilatation
o This means increased end diastolic volume and increased stroke volume
o The combination of increased stroke volume and low end-diastolic AORTIC pressure may explain the high-volume collapsing pulse

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20
Q

Summarise the epidemiology of aortic regurgitation

A
  • Chronic AR often begins in the late 50s

* It is most frequently seen in patients > 80 yrs

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21
Q

Recognise the presenting symptoms of aortic regurgitation

A

• Chronic AR
o Initially ASYMPTOMATIC
o Later on, the patient may develop symptoms of heart failure (e.g. exertional dyspnoea, orthopnoea, fatigue)
• Severe Acute AR
o Sudden cardiovascular collapse (left ventricle cannot adapt to the rapid increase in end-diastolic volume)
• Symptoms related to aetiology (e.g. chest or back pain caused by aortic dissection)

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22
Q

Recognise the signs of aortic regurgitation on physical examination

A

• Collapsing (water-hammer) pulse
• Wide pulse pressure
• Thrusting and heaving displaced apex beat
• Early diastolic murmur over the aortic valve region
o Heard better at the left sternal edge when the patient is sitting forward with the breath held at the top of expiration
• NOTE: an ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume)
• Austin Flint mid-diastolic murmur
o Heard over the apex
o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis
• Rare signs associated with aortic regurgitation:
o Quincke’s Sign - visible pulsation on nail bed
o de Musset’s Sign - head nodding in time with the pulse
o Becker’s Sign - visible pulsation of the pupils and retinal arteries
o Muller’s Sign - visible pulsation of the uvula
o Corrigan’s Sign - visible pulsation in the neck
o Traube’s Sign - pistol shot (loud systolic and diastolic sounds) heard on auscultation of the femoral arteries
o Duroziez’s Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the stethoscope
o Rosenbach’s Sign - systolic pulsations of the liver
o Gerhard’s Sign - systolic pulsations of the spleen
o Hill’s Sign - popliteal cuff systolic pressure exceeding brachial pressure by > 60 mm Hg

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23
Q

Identify appropriate investigations for aortic regurgitation and interpret the results

A

• CXR
o Cardiomegaly
o Dilatation of ascending aorta
o Signs of pulmonary oedema (if accompanied by left heart failure)
• ECG
o May show left ventricular hypertrophy
• Deep S in V1/2
• Tall R in V5/6
• Inverted T waves in lead I, aVL, V5/6
• Left axis deviation
• Echocardiogram
o May show underlying cause (e.g. aortic root dilatation, bicuspid aortic valve)
o May show the effects of aortic regurgitation (e.g. left ventricular dilatation, fluttering of the anterior mitral valve leaflet)
o Doppler echocardiogram can show AR and indicate severity
o Repeat echos allow monitoring of progression (LV size and function)
• Cardiac catheterisation with angiography
o If there is any uncertainty about the functional state of the ventricle or the presence of coronary artery disease

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24
Q

Define aortic stenosis

A

• Narrowing of the left ventricular outflow at the level of the aortic valve

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25
Q

Explain the aetiology / risk factors of aortic stenosis

A
  • Stenosis can be secondary to rheumatic heart disease (MOST COMMON WORLDWIDE)
  • Calcification of a congenital bicuspid aortic valve
  • Calcification/degeneration of a tricuspid aortic valve in the elderly
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26
Q

Summarise the epidemiology of aortic stenosis

A
  • Present in 3% of 75 yr olds
  • More common in males
  • Those with bicuspid aortic valve present earlier
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27
Q

Recognise the presenting symptoms of aortic stenosis

A
  • May be ASYMPTOMATIC initially
  • Angina (due to increased oxygen demand of the hypertrophied left ventricle)
  • Syncope or dizziness on exercise (due to outflow obstruction)
  • Symptoms of heart failure (e.g. dyspnoea, orthopnoea)
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28
Q

Recognise the signs of aortic stenosis on physical examination

A
  • Narrow pulse pressure
  • Slow-rising pulse
  • Thrill in the aortic area (only if severe)
  • Forceful sustained thrusting undisplaced apex beat
  • Ejection systolic murmur at the aortic area, radiating to the carotid artery
  • Second heart sound may be softened or absent (due to calcification)
  • A bicuspid valve may produce an ejection click
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29
Q

Identify appropriate investigations for aortic stenosis and interpret the results

A

• ECG
o Signs of left ventricular hypertrophy
• Deep S in V1/2
• Tall R in V5/6
• Inverted T waves in I, aVL and V5/6
• Left axis deviation
o LBBB
• CXR
o Post-stenotic enlargement of ascending aorta
o Calcification of aortic valve
• Echocardiogram
o Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar)
o Estimation of aortic valve area and pressure gradient across the valve in systole
o Assess left ventricular function
• Cardiac angiography
o Allows differentiation from other causes of angina (e.g. MI)
o Allows assessment of concomitant coronary artery disease
• NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease

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30
Q

Define arterial ulcers

A

• A localised area of damage and breakdown of skin due to inadequate arterial blood supply. Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.

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31
Q

Explain the aetiology / risk factors of arterial ulcers

A

• The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities
• Risk Factors
o Coronary heart disease
o History of stroke or TIA
o Diabetes mellitus
o Peripheral arterial disease (e.g. intermittent claudication)
o Obesity and immobility

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32
Q

Summarise the epidemiology of arterial ulcers

A
  • 22% of leg ulcers

* Prevalence increases with age and obesity

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33
Q

Recognise the presenting symptoms of arterial ulcers

A

• Often DISTAL - at the dorsum of the foot or between the toes
• Punched-out appearance
• Often elliptical with clearly defined edges
• The ulcer base contains grey, granulation tissue
• NIGHT PAIN - hallmark of arterial ulcers
o Pain is worse when supine (because arterial blood flow is further reduced when supine)
o Pain is relieved by dangling the affected leg off the end of the bed

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34
Q

Recognise the signs of arterial ulcers on physical examination

A
  • Night pain
  • Punched-out appearance
  • Hairlessness
  • Pale skin
  • Absent pulses
  • Nail dystrophy
  • Wasting of calf muscles
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35
Q

Identify appropriate investigations for arterial ulcers and interpret the results

A
  • Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
  • ABPI
  • Percutaneous angiography
  • ECG
  • Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor)
  • FBC - anaemia can worsen the ischaemia
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36
Q

Define atrial fibrillation/flutter

A

• Characterised by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into:
o Permanent
o Persistent
o Paroxysmal

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37
Q

Explain the aetiology / risk factors of atrial fibrillation/flutter

A
•	There may be no identifiable cause
•	Secondary causes lead to an abnormal atrial electrical pathway that results in AF 
•	Systemic Causes
o	Thyrotoxicosis
o	Hypertension
o	Pneumonia
o	Alcohol
•	Heart Causes
o	Mitral valve disease 
o	Ischaemic heart disease 
o	Rheumatic heart disease 
o	Cardiomyopathy
o	Pericarditis
o	Sick sinus syndrome
o	Atrial myxoma
•	Lung Causes
o	Bronchial carcinoma
o	PE
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38
Q

Summarise the epidemiology of atrial fibrillation/flutter

A
  • VERY COMMON in the elderly
  • Present in 5% of those > 65 years
  • May be paroxysmal
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39
Q

Recognise the presenting symptoms of atrial fibrillation/flutter

A
  • Often ASYMPTOMATIC
  • Palpitations
  • Syncope (if low output)
  • Symptoms of the cause of AF
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40
Q

Recognise the signs of atrial fibrillation/flutter on physical examination

A
  • Irregularly irregular pulse
  • Difference in apical beat and radial pulse
  • Check for signs of thyroid disease and valvular disease
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41
Q

Identify appropriate investigations for atrial fibrillation/flutter and interpret the results

A
•	ECG
o	Uneven baseline with absent p waves 
o	Irregular intervals between QRS complexes 
o	Atrial flutter = saw-tooth
•	Bloods
o	Cardiac enzymes 
o	TFT
o	Lipid profile 
o	U&Es, Mg2+ and Ca2+
•	Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia
•	Echocardiogram
o	May show:
•	Mitral valve disease 
•	Left atrial dilatation
•	Left ventricular dysfunction 
•	Structural abnormalities
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42
Q

Generate a management plan for atrial fibrillation/flutter

A

First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection)
There are TWO main components to AF management:
• RHYTHM CONTROL
o If > 48 hrs since onset of AF
• Anticoagulate for 3-4 weeks before attempting cardioversion
o If < 48 hrs since onset of AF
• DC cardioversion (2 x 100 J, 1 x 200 J)
• Chemical cardioversion: flecainide or amiodarone
 NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease
o Prophylaxis against AF
• Sotalol
• Amiodarone
• Flecainide
• Consider pill-in-the-pocket (single dose of a cardioverting drug (e.g. flecainide) for patients with paroxysmal AF) strategy for suitable patients
• RATE CONTROL
o Chronic (Permanent) AF
• Control ventricular rate with:
 Digoxin
 Verapamil
 Beta-blockers
• Aim for ventricular rate ~ 90 bpm
• STROKE RISK STRATIFICATION
o LOW RISK patients can be managed with aspirin
o HIGH RISK patients require anticoagulation with warfarin
o This is based on the CHADS-Vasc Score
o Risk factors include:
• Previous thromboembolic event
• Age > 75 yrs
• Hypertension
• Diabetes
• Vascular disease
• Valvular disease
• Heart failure
• Impaired left ventricular function

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43
Q

Identify the possible complications of atrial fibrillation/flutter and its management

A

• THROMBOEMBOLISM
o Embolic stroke risk of 4% per year
o Risk is increased with left atrial enlargement or left ventricular dysfunction
• Worsening of existing heart failure

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44
Q

Summarise the prognosis for patients with atrial fibrillation/flutter

A

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

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45
Q

Define cardiac arrest

A

• Acute cessation of cardiac function

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46
Q

Explain the aetiology / risk factors of cardiac arrest

A
The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts
•	FOUR Hs
o	Hypothermia
o	Hypoxia
o	Hypovolaemia
o	Hypokalaemia/Hyperkalaemia
•	FOUR Ts
o	Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))
o	Thromboembolic
o	Tamponade
o	Tension pneumothorax
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47
Q

Summarise the epidemiology of cardiac arrest

A

• None available

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48
Q

Recognise the presenting symptoms of cardiac arrest

A
  • Management precedes or is concurrent to history

* Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness

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49
Q

Recognise the signs of cardiac arrest on physical examination

A
  • Unconscious
  • Not breathing
  • Absent carotid pulses
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50
Q

Identify appropriate investigations for cardiac arrest and interpret the results

A
•	Cardiac Monitor
o	Allows classification of the rhythm
•	Bloods
o	ABG
o	U&E
o	FBC
o	X-match
o	Clotting 
o	Toxicology screen
o	Blood glucose
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51
Q

Generate a management plan for cardiac arrest

A

• SAFETY IS IMPORTANT
o Approach any arrest scene with caution
o The cause of the arrest may pose a threat
o Defibrillators and oxygen are hazards
• Basic Life Support
o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist)
o Clear and maintain the airway with head tilt, jaw thrust and chin lift
o Assess breathing by look, listen and feel
• If they are not breathing, give two rescue breaths
o Assess circulation at carotid pulse for 10 seconds
• If absent - give 30 chest compressions at around 100/min
• Continue cycle of 30 chest compressions for every 2 rescue breaths
o Proceed to advanced life support as soon as possible
• Advanced Life Support
o Attach cardiac monitor and defibrillator
o Assess rhythm
• If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)
 Defibrillate once (150-360 J biphasic, 360 J monophasic)
• Make sure no one is touching the patient or the bed
 Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF
 Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins
 If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine)
• If pulseless electrical activity (PEA) or asystole (non-shockable rhythms)
 CPR for 2, and then reassess rhythm
 Administer adrenaline (1 mg IV) every 3-5 mins
 Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm
o During CPR:
• Check electrodes, paddle positions and contacts
• Secure airway
 Once secure, give continuous compressions and breaths
• Consider magnesium, bicarbonate and external pacing
• Stop CPR and check pulse only if change in rhythm or signs of life
• Treatment of REVERSIBLE causes
o Hypothermia - warm slowly
o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels
o Hypovolaemia - IV colloids, crystalloids and blood products
o Tamponade - pericardiocentesis
o Tension Pneumothorax - aspiration or chest drain
o Thromboembolism - treat as PE or MI
o Toxins - use antidote for given toxin

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52
Q

Identify the possible complications of cardiac arrest and its management

A
  • Irreversible hypoxic brain damage

* Death

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53
Q

Summarise the prognosis for patients with cardiac arrest

A
  • Resuscitation is less successful if cardiac arrest happens outside the hospital
  • Increased duration of inadequate effective cardiac output –> poor prognosis
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54
Q

Define cardiac failure (acute and chronic)

A

• Inability of the cardiac output to meet the body’s demands despite normal venous pressures

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55
Q

Explain the aetiology / risk factors of cardiac failure (acute and chronic)

A
•	LOW OUTPUT Cardiac Failure (reduced cardiac output)
o	Left Heart Failure
•	Ischaemic heart disease 
•	Hypertension
•	Cardiomyopathy
•	Aortic valve disease 
•	Mitral regurgitation 
o	Right Heart Failure
•	Secondary to left heart failure (in which case it is called congestive cardiac failure)
•	Infarction 
•	Cardiomyopathy 
•	Pulmonary hypertension/embolus/valve disease 
•	Chronic lung disease 
•	Tricuspid regurgitation 
•	Constrictive pericarditis/pericardial tamponade 
o	Biventricular Failure
•	Arrhythmia
•	Cardiomyopathy (dilated or restrictive)
•	Myocarditis 
•	Drug toxicity 
•	HIGH OUTPUT Cardiac Failure (increased demand)
o	Anaemia 
o	Beri beri
o	Pregnancy 
o	Paget's disease 
o	Hyperthyroidism
o	Arteriovenous malformation
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56
Q

Summarise the epidemiology of cardiac failure (acute and chronic)

A

• 10% > 65 yrs old

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57
Q

Recognise the presenting symptoms of cardiac failure (acute and chronic)

A
•	Left Heart Failure - symptoms caused by pulmonary congestion
o	Dyspnoea - divided based on the New York Heart Association classification:
•	1 - no dyspnoea
•	2 - dyspnoea on ordinary activities
•	3 - dyspnoea on less than ordinary activities 
•	4 - dyspnoea at rest 
o	Orthopnoea
o	Paroxysmal nocturnal dyspnoea
o	Fatigue 
•	Acute Left Ventricular Failure
o	Dyspnoea
o	Wheeze 
o	Cough 
o	Pink frothy sputum
•	Right Heart Failure
o	Swollen ankles 
o	Fatigue 
o	Increased weight (due to oedema) 
o	Reduced exercise tolerance 
o	Anorexia
o	Nausea
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58
Q

Recognise the signs of cardiac failure (acute and chronic) on physical examination

A

• Left Heart Failure
o Tachycardia
o Tachypnoea
o Displaced apex beat
o Bilateral basal crackles
o S3 gallop (caused by rapid ventricular filling)
o Pansystolic murmur (due to functional mitral regurgitation)
• Acute Left Ventricular Failure
o Tachypnoea
o Cyanosis
o Tachycardia
o Peripheral shutdown
o Pulsus alternans
• Arterial pulse waveforms showing alternating strong and weak beats
• Sign of left ventricular systolic impairment
• Explanation:
 In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume
 This causes an increase in end-diastolic volume
 This means that the left ventricle is stretched more for the next contraction
 Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction
 This results in a stronger systolic pulse
o Gallop rhythm
o Wheeze (cardiac asthma)
o Fine crackles throughout lung
• Right Heart Failure
o Raised JVP
o Hepatomegaly
o Ascites
o Ankle/sacral pitting oedema
o Signs of functional tricuspid regurgitation

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59
Q

Identify appropriate investigations for cardiac failure (acute and chronic) and interpret the results

A
•	Bloods
o	FBC
o	U&E
o	LFTs
o	CRP
o	Glucose 
o	Lipids 
o	TFTs
•	In ACUTE Left Ventricular Failure
o	ABG 
o	Troponin
o	BNP
•	Raised plasma BNP suggests diagnosis of cardiac failure 
•	Low plasma BNP rules out cardiac failure (90% sensitivity)
•	CXR
o	Alveolar shadowing 
o	Kerley B lines 
o	Cardiomegaly
o	Upper Lobe Diversion
o	Pleural Effusion
•	ECG
o	May be normal 
o	May show ischaemic changes (pathological q waves, t wave inversion)
o	May show arrhythmia or left ventricular hypertrophy 
•	Echocardiogram
o	Assess ventricular contraction 
o	Systolic dysfunction = LV ejection fraction < 40%  
o	Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect 
•	Swan-Ganz Catheter 
o	Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures
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60
Q

Generate a management plan for cardiac failure (acute and chronic)

A

• Acute Left Ventricular Failure
o Treating Cardiogenic Shock:
• This is severe cardiac failure with low blood pressure
• Requires the use of inotropes (e.g. dobutamine)
• Managed in ITU
o Treating Pulmonary Oedema:
• Sit the patient up
• 60-100% Oxygen (and consider CPAP)
• Diamorphine (venodilator + anxiolytic)
• GTN infusion (venodilator –> reduced preload)
• IV furosemide (venodilator and later diuretic effect)
• Monitor:
 BP
 Respiratory rate
 Oxygen saturation
 Urine output
 ECG
• TREAT THE CAUSE! (e.g. MI, arrhythmia)
• Chronic Left Ventricular Failure
o TREAT THE CAUSE (e.g. hypertension)
o TREAT EXACERBATING FACTORS (e.g. anaemia)
o ACE Inhibitors
• Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
• They slow down the progression of heart failure and improve survival
o Beta-Blockers
• Blocks the effects of a chronically activated sympathetic system
• Slows progression of heart failure and improves survival
• The benefits of ACE inhibitors and beta-blockers are additive
o Loop Diuretics
• Alongside dietary salt restriction, can correct fluid overload
o Aldosterone Antagonists
• Improves survival in patients with NYHA class III/IV symptoms on standard therapy
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Angiotensin Receptor Blockers
• May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers
• Monitor K+ (as these drugs may cause hyperkalaemia)
o Hydralazine and a Nitrate
• May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers
o Digoxin
• Positive inotrope
• Reduces hospitalisation but does NOT improve survival
o N-3 Polyunsaturated Fatty Acids
• Provide a small beneficial advantage in terms of survival
o Cardiac Resynchronisation Therapy
• Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms
• These patients are also candidates for implantable cardioverter defibrillator (ICD)
• They may receive a combined device
o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)

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61
Q

Identify the possible complications of cardiac failure (acute and chronic) and its management

A
  • Respiratory failure
  • Cardiogenic shock
  • Death
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62
Q

Summarise the prognosis for patients with cardiac failure (acute and chronic)

A

• 50% with cardiac failure die within 2 years

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63
Q

Define cardiomyopathy

A

• Primary disease of the myocardium. Cardiomyopathy may be:
o Dilated
o Hypertrophic
o Restrictive

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64
Q

Explain the aetiology / risk factors of cardiomyopathy

A
•	The majority are IDIOPATHIC
•	Dilated Cardiomyopathy
o	Post-viral myocarditis 
o	Alcohol
o	Drugs (e.g. doxorubicin, cocaine)
o	Familial
o	Thyrotoxicosis 
o	Haemochromatosis 
o	Peripartum 
•	Hypertrophic Cardiomyopathy

o Up to 50% are genetic
• Restrictive Cardiomyopathy

o Amyloidosis
o Sarcoidosis
o Haemochromatosis

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65
Q

Summarise the epidemiology of cardiomyopathy

A
  • Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20%
  • Restrictive is even rarer
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66
Q

Recognise the presenting symptoms of cardiomyopathy

A
•	Dilated
o	Symptoms of heart failure
o	Arrhythmias 
o	Thromboembolism
o	Family history of sudden death 
•	Hypertrophic
o	Usually NO SYMPTOMS
o	Syncope 
o	Angina 
o	Arrhythmias 
o	Family history of sudden death
•	Restrictive
o	Dyspnoea
o	Fatigue 
o	Arrhythmias 
o	Ankle or abdominal swelling 
o	Family history of sudden death
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67
Q

Recognise the signs of cardiomyopathy on physical examination

A
•	Dilated
o	Raised JVP 
o	Displaced apex beat 
o	Functional mitral and tricuspid regurgitations 
o	Third heart sound 
•	Hypertrophic
o	Jerky carotid pulse 
o	Double apex beat 
o	Ejection systolic murmur 
•	Restrictive
o	Raised JVP 
•	Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles 
o	Palpable apex beat 
o	Third heart sound 
o	Ascites 
o	Ankle oedema 
o	Hepatomegaly
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68
Q

Identify appropriate investigations for cardiomyopathy and interpret the results

A

• CXR

o	May show cardiomegaly 
o	May show signs of heart failure 
•	ECG
o	All Types
•	Non-specific ST changes 
•	Conduction defects 
•	Arrhythmias 
o	Hypertrophic
•	Left-axis deviation
•	Signs of left ventricular hypertrophy
•	Q waves in inferior and lateral leads 
o	Restrictive
•	Low voltage complexes 
•	Echocardiography
o	Dilated
•	Dilated ventricles with global hypokinesia
o	Hypertrophic
•	Ventricular hypertrophy (asymmetrical septal hypertrophy)
o	Restrictive
•	Non-dilated non-hypertrophied ventricles 
•	Atrial enlargement 
•	Preserved systolic function 
•	Diastolic dysfunction 
•	Granular or sparkling appearance of myocardium in amyloidosis 
•	Cardiac Catheterisation
•	Endomyocardial Biopsy
•	Pedigree or Genetic Analysis
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69
Q

Define constrictive pericarditis

A

• Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.

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70
Q

Explain the aetiology / risk factors of constrictive pericarditis

A
•	NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure 
•	Can occur after any pericardial disease process 
•	More common causes of pericarditis:
o	Idiopathic
o	Virus
o	TB
o	Mediastinal irradiation 
o	Post-surgical 
o	Connective tissue disease
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71
Q

Summarise the epidemiology of constrictive pericarditis

A
  • RARE
  • Documented in all ages
  • 9% of patients with acute pericarditis will develop constrictive pericarditis
  • TB has the HIGHEST TOTAL INCIDENCE out of all causes
  • More common in MALES
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72
Q

Recognise the presenting symptoms & signs of constrictive pericarditis

A

• Gradual-onset of symptoms
• EARLY - symptoms and signs may be very subtle
• ADVANCED - jaundice, cachexia, muscle wasting
• Right Heart Failure Signs
o Dyspnoea
o Peripheral oedema
o Raised JVP
o Kussmaul’s sign (paradoxical rise in JVP on inspiration)
o Pulsatile hepatomegaly

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73
Q

Identify appropriate investigations for constrictive pericarditis and interpret the results

A
  • CXR - may show calcification of the pericardium
  • Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy
  • MRI - allows assessment of thickness of pericardium
  • CT - same role as MRI
  • Pericardial biopsy - may be indicated (especially if suspected infective cause)
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74
Q

Define deep vein thrombosis (DVT)

A

• Formation of a thrombus within the deep veins (most commonly in the calf or thigh)

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75
Q

Explain the aetiology / risk factors of deep vein thrombosis (DVT)

A
•	Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (look up Virchow's triad)
•	Risk Factors
o	COCP
o	Post-surgery
o	Prolonged immobility
o	Obesity 
o	Pregnancy 
o	Dehydration 
o	Smoking 
o	Polycythaemia 
o	Thrombophilia (e.g. protein C deficiency) 
o	Malignancy
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76
Q

Summarise the epidemiology of deep vein thrombosis (DVT)

A
  • VERY COMMON

* Especially in hospitalised patients

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77
Q

Recognise the presenting symptoms of deep vein thrombosis (DVT)

A
  • Swollen limb

* May be painless

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78
Q

Recognise the signs of deep vein thrombosis (DVT) on physical examination

A

• Examination of the Leg
o Local erythema, warmth and swelling
o Measure the leg circumference
o Varicosities (swollen/tortuous vessels)
o Skin colour changes
o NOTE: Homan’s Sign - forced passive dorsiflexion of the ankle causes deep calf pain

• Risk is stratified using the WELLS CRITERIA (NOTE: this is different from the PE Wells criteria)
o Score 2 or more = high risk
• Examine for PE
o Check respiratory rate, pulse oximetry and pulse rate

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79
Q

Identify appropriate investigations for deep vein thrombosis (DVT) and interpret the results

A
•	Doppler Ultrasound - GOLD STANDARD 
•	Impedance Plethysmography - changes in blood volume results in changes of electrical resistance
•	Bloods
o	D-dimer: can be used as a negative predictor 
o	Thrombophilia screen if indicated 
•	If PE suspected
o	ECG 
o	CXR 
o	ABG
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80
Q

Generate a management plan for deep vein thrombosis (DVT)

A

• ANTICOAGULATION
o Heparin whilst waiting for warfarin to increase INR to the target range of 2-3
o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months
o DVTs extending beyond the knee require anticoagulation for 6 months
o Recurrent DVTs require long-term warfarin
• IVC Filter
o May be used if anticoagulation is contraindicated and there is a risk of embolisation
• Prevention
o Graduated compression stockings
o Mobilisation
o Prophylactic heparin (if high risk e.g. hospitalised patients)

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81
Q

Identify the possible complications of deep vein thrombosis (DVT) and its management

A
  • PE
  • Venous infarction (phlegmasia cerulea dolens)
  • Thrombophlebitis (results from recurrent DVT)
  • Chronic venous insufficiency
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82
Q

Summarise the prognosis for patients with deep vein thrombosis (DVT)

A
  • Depends on extent of DVT
  • Below-knee DVTs have a GOOD prognosis
  • Proximal DVTs have a greater risk of embolisation
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83
Q

Define dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

Dyslipidemia is an abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood.

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84
Q

Explain the aetiology / risk factors of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

Primary dyslipidemia
Blood sample being tested by lab technician.
Dyslipidemia can be diagnosed with a blood test.
Genetic factors cause primary dyslipidemia, and it is inherited. Common causes of primary dyslipidemia include:

Familial combined hyperlipidemia, which develops in teenagers and young adults and can lead to high cholesterol.
Familial hyperapobetalipoproteinemia, a mutation in a group of LDL lipoproteins called apolipoproteins.
Familial hypertriglyceridemia, which leads to high triglyceride levels.
Homozygous familial or polygenic hypercholesterolemia, a mutation in LDL receptors.
Secondary dyslipidemia
Secondary dyslipidemia is caused by lifestyle factors or medical conditions that interfere with blood lipid levels over time.

Common causes of secondary dyslipidemia include:

obesity, especially excess weight around the waist
diabetes
hypothyroidism
alcohol use disorder, also known as alcoholism
polycystic ovary syndrome
metabolic syndrome
excessive consumption of fats, especially saturated and trans fats
Cushing’s syndrome
inflammatory bowel disease, commonly known as IBS
severe infections, such as HIV
an abdominal aortic aneurysm
Several factors are known to increase the chances of developing dyslipidemia and related conditions. These risk factors include:

obesity
a sedentary lifestyle
a lack of regular physical exercise
alcohol use
tobacco use
use of illegal or illicit drugs
sexually transmitted infections
type 2 diabetes
hypothyroidism
chronic kidney or liver conditions
digestive conditions
older age
a diet rich in saturated and trans fats
a parent or grandparent with dyslipidemia
female sex, as women tend to experience higher LDL levels after menopause
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85
Q

Summarise the epidemiology of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

In high-income countries, over 50% of adults had raised total cholesterol; more than double the level of the low-income countries.

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86
Q

Recognise the presenting symptoms & signs of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

Unless it is severe, most people with dyslipidemia are unaware that they have it. A doctor will usually diagnose dyslipidemia during a routine blood test or a test for another condition.

Severe or untreated dyslipidemia can lead to other conditions, including coronary artery disease (CAD) and peripheral artery disease (PAD).

Both CAD and PAD can cause serious health complications, including heart attacks and strokes. Common symptoms of these conditions include:

leg pain, especially when walking or standing
chest pain
tightness or pressure in the chest and shortness of breath
pain, tightness, and pressure in the neck, jaw, shoulders, and back
indigestion and heartburn
sleep problems and daytime exhaustion
dizziness
heart palpitations
cold sweats
vomiting and nausea
swelling in the legs, ankles, feet, stomach, and veins of the neck
fainting
These symptoms may get worse with activity or stress and get better when a person rests.

Anyone who experiences severe chest pain, dizziness, and fainting, or problems breathing should seek emergency care.

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87
Q

Identify appropriate investigations for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and interpret the results

A

The most common goals are:

Total cholesterol: Below 200 mg/dL
HDL cholesterol: Men - above 40 mg/dL; Women - above 50 mg/dL
LDL cholesterol: Below 100 mg/dL; Below 70 mg/dL for people with diabetes or heart disease.
Triglycerides: Below 150 mg/dL

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88
Q

Generate a management plan for dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

A doctor will usually focus on lowering a person’s levels of triglycerides and LDL. However, treatment can vary, depending on the underlying cause of dyslipidemia and how severe it is.

Doctors may prescribe one or more lipid-modifying medications for people with very high total cholesterol levels of at least 200 milligrams per deciliter of blood.

High cholesterol is usually treated with statins, which interfere with the production of cholesterol in the liver.

If statins fail to lower LDL and triglyceride levels, a doctor may recommend additional medications, including:

ezetimibe
niacin
fibrates
bile acid sequestrants
evolocumab and alirocumab
lomitapide and mipomersen
Some lifestyle changes and supplements can help to encourage healthy blood lipid levels.

Natural treatments include:

reducing the consumption of unhealthy fats, such as those found in red meats, full-fat dairy products, refined carbohydrates, chocolate, chips, and fried foods
exercising regularly
maintaining a healthy body weight, by losing weight if necessary
reducing or avoiding alcohol consumption
quitting smoking and other use of tobacco products
avoiding sitting for long periods of time
increasing consumption of healthy polyunsaturated fats, such as those found in nuts, seeds, legumes, fish, whole grains, and olive oil
taking omega-3 oil, either as a liquid or in capsules
eating plenty of dietary fiber from whole fruits, vegetables, and whole grains
getting at least 6– 8 hours of sleep a night
drinking plenty of water

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89
Q

Identify the possible complications of dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia) and its management

A

People with minor dyslipidemia usually have no symptoms. They can often manage or resolve the condition by making lifestyle adjustments.

People with dyslipidemia should contact a doctor if they experience symptoms relating to the heart or circulation, including:

chest pains or tightness
dizziness
heart palpitations
exhaustion
swelling of the ankles and feet
trouble breathing
cold sweats
nausea and heartburn
People who have severe dyslipidemia, especially those with other medical conditions, may need to manage their blood lipid levels with medication, in addition to making lifestyle changes.
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90
Q

Summarise the prognosis for patients with dyslipidaema (hypercholesterolaemia & hypertriglyceridaemia)

A

Significantly reduced risk of CHD if managed well.

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91
Q

Define gangrene

A
  • Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
  • Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes
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92
Q

Explain the aetiology / risk factors of gangrene

A
o	Tissue ischaemia and infarction 
o	Physical trauma 
o	Thermal injury 
o	Gas gangrene is caused by Clostridia perfringens
•	Necrotising Fasciitis
o	Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms 
•	Risk Factors
o	Diabetes 
o	Peripheral vascular disease 
o	Leg ulcers 
o	Malignancy 
o	Immunosuppression 
o	Steroid use 
o	Puncture/surgical wounds
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93
Q

Summarise the epidemiology of gangrene

A
  • Gangrene - relatively COMMON

* Necrotising fasciitis and gas gangrene - RARE

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94
Q

Recognise the presenting symptoms of gangrene

A

• Gangrene
o Pain
o Discolouration of affected area
o Often affects extremities or areas subject to high pressure
• Necrotising Fasciitis
o Pain
• Often seems SEVERE and out of proportion to the apparent physical signs
o Predisposing event (e.g. trauma, ulcer, surgery)

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95
Q

Recognise the signs of gangrene on physical examination

A

• Gangrene
o Painful area = erythematous region around gangrenous tissue
o Gangrenous tissue = BLACK because of haemoglobin break down products
o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
• Necrotising Fasciitis
o Area of erythema and oedema
o Haemorrhagic blisters may be present
o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)

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96
Q

Identify appropriate investigations for gangrene and interpret the results

A
  • Bloods - FBC, U&Es, glucose, CRP and blood culture
  • Wound Swab, Pus/Fluid Aspirate - MC&S
  • X-ray of affected area - may show gas produced in gas gangrene
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97
Q

Define heart block (1st, 2nd, 3rd degree)

A

• 1st Degree AV Block: prolonged conduction through the AV node
• 2nd Degree AV Block:
o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle ten begins again.
o Mobitz Type II: intermittent or regular failure of conduction through the AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)
• 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle

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98
Q

Explain the aetiology / risk factors of heart block (1st, 2nd, 3rd degree)

A

• 250,000 pacemakers are implanted every year and they are mostly for heart block

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99
Q

Summarise the epidemiology of heart block (1st, 2nd, 3rd degree)

A
  • MI or ischaemic heart disease (MOST COMMON)
  • Infection (e.g. rheumatic fever, infective endocarditis)
  • Drugs (e.g. digoxin)
  • Metabolic (e.g. hyperkalaemia)
  • Infiltration of conducting system (e.g. sarcoidosis)
  • Degeneration of the conducting system
100
Q

Recognise the presenting symptoms of heart block (1st, 2nd, 3rd degree)

A

• 1st Degree - asymptomatic
• 2nd Degree - usually asymptomatic
• Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole)
o May also cause dizziness, palpitations, chest pain and heart failure

101
Q

Recognise the signs of heart block (1st, 2nd, 3rd degree) on physical examination

A

• Often NORMAL
• Check for signs of a potential cause of heart block
• Complete Heart Block
o Slow large volume pulse
o JVP may show cannon a waves
• Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously
• Mobitz Type II and 3rd Degree Heart Block
o Signs of reduced cardiac output (e.g. hypotension, heart failure)

102
Q

Identify appropriate investigations for heart block (1st, 2nd, 3rd degree) and interpret the results

A

• ECG - GOLD STANDARD
o First Degree - fixed prolonged PR interval (> 0.2 s)

o Mobitz Type I (Wenckebach) - progressively prolonged PR interval, culminating in a P wave that is NOT followed by a QRS complex. The pattern then begins again. ‘Going, going, gone’.

o Mobitz Type II - intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)

o Complete Heart Block - no relationship between P waves and QRS complexes. If QRS is initiated in the:
• Bundle of His - narrow complex
• More distally - wide complex and slow rate (~ 30 bpm)

•	CXR
o	Cardiac enlargement 
o	Pulmonary oedema 
•	Bloods
o	TFTs 
o	Digoxin level 
o	Cardiac enzymes 
o	Troponin 
•	Echocardiogram
o	Wall motion abnormalities 
o	Aortic valve disease 
o	Vegetations
103
Q

Generate a management plan for heart block (1st, 2nd, 3rd degree)

A
•	Chronic Block
o	Permanent pacemaker is recommended in:
•	Complete heart block 
•	Advanced Mobitz Type II 
•	Symptomatic Mobitz Type I
•	Acute Block
o	If associated with clinical deterioration use IV atropine
o	Consider temporary (external) pacemaker
104
Q

Identify the possible complications of heart block (1st, 2nd, 3rd degree) and its management

A
  • Asystole
  • Cardiac arrest
  • Heart failure
  • Complications of any pacemaker inserted
105
Q

Summarise the prognosis for patients with heart block (1st, 2nd, 3rd degree)

A

• Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease

106
Q

Define hypertension

A
  • Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions.
  • Malignant Hypertension: BP > 200/130 mm Hg
107
Q

Explain the aetiology / risk factors of hypertension

A
  • VERY COMMON

* 10-20% of adults in the Western world

108
Q

Summarise the epidemiology of hypertension

A
•	Primary
o	Essential or idiopathic hypertension 
o	Responsible for > 90% of cases
•	Secondary
o	Renal
•	Renal artery stenosis 
•	Chronic glomerulonephritis 
•	Chronic pyelonephritis 
•	Polycystic kidney disease 
•	Chronic renal failure
o	Endocrine
•	Diabetes mellitus 
•	Hyperthyroidism
•	Cushing's syndrome 
•	Conn's syndrome 
•	Hyperparathyroidism
•	Phaeochromocytoma
•	Congenital adrenal hyperplasia 
•	Acromegaly
o	Cardiovascular
•	Coarctation of the aorta 
•	Increased intravascular volume 
o	Drugs
•	Sympathomimetics 
•	Corticosteroids
•	COCP
o	Pregnancy
•	Pre-eclampsia
109
Q

Recognise the presenting symptoms of hypertension

A
•	Often ASYMPTOMATIC
•	Symptoms of complications
•	Symptoms of the cause
•	Accelerated or Malignant Hypertension
o	Scotomas (visual field loss) 
o	Blurred vision 
o	Headache 
o	Seizures 
o	Nausea and vomiting 
o	Acute heart failure
110
Q

Recognise the signs of hypertension on physical examination

A

• Blood pressure should be measured on 2-3 different occasions before diagnosing hypertension
• The lowest reading should be recorded
• Examination may reveal information about causes:
o Radiofemoral delay = coarctation of the aorta distal to the left subclavian artery
o Renal artery bruit = renal artery stenosis
o Fundoscopy to detect hypertensive retinopathy
Keith-Wagner Classification of Hypertensive Retinopathy
i. Silver wiring
ii. As above + arteriovenous nipping
iii. As above + flame haemorrhages + cotton wood exudates
iv. As above + papilloedema

Hypertensive retinopathy
• Silver Wiring
• Arteriovenous nipping
• Flame Haemorrhages, Cotton Wool Exudates and Papilloedema

111
Q

Identify appropriate investigations for hypertension and interpret the results

A

• Bloods:
o U&Es
o Glucose
o Lipids
• Urine Dipstick
o Blood and protein (e.g. if glomerulonephritis)
• ECG
o May show signs of left ventricular hypertrophy or ischaemia
• Ambulatory blood pressure monitoring
o Excludes white coat hypertension
• Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram)

112
Q

Generate a management plan for hypertension (incl. hypertensive emergencies)

A

• Conservative
o Stop smoking
o Lose weight
o Reduce alcohol intake
o Reduce dietary sodium
• Investigate for secondary causes (mainly in young patients)
• Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage. Multiple drug therapies often needed.
o ACE Inhibitors or Angiotensin Receptor Blockers - first line if:
• < 55 yrs
• Diabetic
• Heart failure
• Left ventricular dysfunction
o CCBs - first line if:
• > 55 yrs
• Black
• NOTE: thiazide diuretics can be used if CCBs are not tolerated
o Beta-Blockers
• Not preferred initial therapy
• May be considered in younger patients
• CAUTION: combining with thiazide diuretic may increase risk of developing diabetes
• May increase risk of heart failure
o Alpha-Blockers
• 4th line
• May be used in patients with prostate disease
• Target BP
o Non-Diabetic: < 140/90 mm Hg
o Diabetes without proteinuria: < 130/80 mm Hg
o Diabetes WITH proteinuria: < 125/75 mm Hg
• Severe Hypertension Management (Diastolic > 140 mm Hg)
o Atenolol
o Nifedipine
• Acute Malignant Hypertension Management:
o IV beta-blocker (e.g. esmolol)
o Labetolol
o Hydralazine sodium nitroprusside
o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction
• This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high
• Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted
• A rapid drop in blood pressure with constricted vessels will cause an infarction

113
Q

Identify the possible complications of hypertension and its management

A
  • Heart failure
  • Coronary artery disease
  • Cerebrovascular accidents
  • Peripheral vascular disease
  • Emboli
  • Hypertensive retinopathy
  • Renal failure
  • Hypertensive encephalopathy
  • Posterior reversible encephalopathy syndrome (PRES)
  • Malignant hypertension
114
Q

Summarise the prognosis for patients with hypertension

A
  • Good prognosis if well controlled
  • Uncontrolled hypertension is associated with increased mortality
  • Treatment reduces incidence of renal damage, stroke and heart failure
115
Q

Define infective endocarditis

A

• Infection of intracardiac endocardial structures (mainly heart valves)

116
Q

Explain the aetiology / risk factors of infective endocarditis

A

• Most common organisms causing infective endocarditis:
o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis
o Staphylococci (35%) - S. aureus and S. epidermidis
o Enterococci (20%) - usually E. faecalis
o Other organisms:
• Haemophilus
• Actinobacillus
• Cardiobacterium
• Coxiella burnetii
• Histoplasma (fungal)
• Pathophysiology
o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia
o The vegetations are made up of platelets, fibrin and infective organisms
o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities
o Activation of the immune system can lead to the formation of immune complexes –> vasculitis, glomerulonephritis, arthritis
• Risk Factors
o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)
o Prosthetic heart valves
o Turbulent blood flow (e.g. patent ductus arteriosus)
o Recent dental work/poor dental hygiene (source of S. viridans)

117
Q

Summarise the epidemiology of infective endocarditis

A

• UK Incidence: 16-22/1 million per year

118
Q

Recognise the presenting symptoms of infective endocarditis

A
•	Fever with sweats/chills/rigors 
o	NOTE: this might be relapsing and remitting 
•	Malaise 
•	Arthralgia 
•	Myalgia 
•	Confusion 
•	Skin lesions 
•	Ask about recent dental surgery or IV drug use
119
Q

Recognise the signs of infective endocarditis on physical examination

A
•	Pyrexia 
•	Tachycardia 
•	Signs of anaemia
•	Clubbing 
•	New regurgitant murmur or muffled heart sounds 
•	Frequency of heart murmurs:
o	Mitral > Aortic > Tricuspid > Pulmonary
•	Splenomegaly
•	Vasculitic Lesions
o	Roth spots on retina 

o Petechiae on pharyngeal and conjunctival mucosa
o Janeway lesions (painless macules on the palms which blanch on pressure)
o Osler’s nodes (tender nodules on finger/toe pads)
o Splinter haemorrhages

120
Q

Identify appropriate investigations for infective endocarditis and interpret the results

A

• Bloods
o FBC - high neutrophils, normocytic anaemia
o High ESR/CRP
o U&Es
o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive
• Urinalysis
o Microscopic haematuria
o Proteinuria
• Blood Culture
o Do microscopy and sensitivities as well
• Echocardiography
o Transthoracic or transoesophageal (produces better image)
• Duke’s Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs

121
Q

Generate a management plan for infective endocarditis

A
•	Antibiotics for 4-6 weeks 
•	On clinical suspicion = EMPIRICAL TREATMENT
o	Benzylpenicillin
o	Gentamicin
•	Streptococci - continue the same as above 
•	Staphylococci 
o	Flucloxacillin/vancomycin
o	Gentamicin
•	Enterococci
o	Ampicillin
o	Gentamicin
•	Culture Negative
o	Vancomycin
o	Gentamicin 
•	SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics
122
Q

Identify the possible complications of infective endocarditis and its management

A
  • Valve incompetence
  • Intracardiac fistulae or abscesses
  • Aneurysm
  • Heart failure
  • Renal failure
  • Glomerulonephritis
  • Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
123
Q

Summarise the prognosis for patients with infective endocarditis

A
  • FATAL if untreated

* 15-30% mortality even WITH treatment

124
Q

Define ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A

• Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome.
• ACS can be further subdivided into:
o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
o NSTEMI
o STEMI - ST elevation with transmural infarction
o NOTE: MI = cardiac muscle necrosis resulting from ischaemia

125
Q

Explain the aetiology / risk factors of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A
  • COMMON
  • Prevalence: > 2 %
  • More common in males
  • Annual incidence of MI in the UK ~ 5/1000
126
Q

Summarise the epidemiology of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A

• Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
• This is usually due to atherosclerosis
• Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli
• Atherosclerosis pathophysiology
o Endothelial injury leads to migration of monocytes into the subendothelial space
o These monocytes differentiate into macrophages
o Macrophages accumulate LDL lipids and become foam cells
o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans
o This leads to the formation of an atherosclerotic plaque
• Risk Factors
o Male
o Diabetes mellitus
o Family history
o Hypertension
o Hyperlipidaemia
o Smoking

127
Q

Recognise the presenting symptoms of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A

• ACS
o Acute-onset chest pain
o Central, heavy, tight, crushing pain
o Radiates to the arms, neck, jaw or epigastrium
o Occurs at rest
o More severe and frequent pain that previously occurring stable angina
o Associated symptoms:
• Breathlessness
• Sweating
• Nausea and vomiting
• SILENT INFARCTS occur in the elderly and diabetics
• Stable Angina
o Chest pain brought on by exertion and relieved by rest

128
Q

Recognise the signs of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) on physical examination

A
•	Stable Angina
o	Check for signs of risk factors 
•	ACS
o	There may be NO CLINICAL SIGNS
o	Pale 
o	Sweating 
o	Restless
o	Low-grade pyrexia 
o	Check both radial pulses to rule out aortic dissection
o	Arrhythmias 
o	Disturbances of BP 
o	New heart murmurs 
o	Signs of complications (e.g. acute heart failure, cardiogenic shock)
129
Q

Identify appropriate investigations for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and interpret the results

A

• Bloods
o FBC
o U&Es
o CRP
o Glucose
o Lipid profile
o Cardiac enzymes (troponins and CK-MB)
o Amylase (pancreatitis could mimic MI)
o TFTs
o AST and LDH (raised 24 and 48 hours post-MI, respectively)
• ECG
o Unstable Angina or NSTEMI:
• May show ST depression or T wave inversion
o STEMI:
• Hyperacute T waves
• ST elevation (> 1 mm in limb leads, > 2 mm in chest leads)
• New-onset LBBB
• Later changes:
 T wave inversion
 Pathological Q waves
o Relationship between ECG leads and the side of the heart
• Inferior: II, III, aVF
• Anterior: V1-V5/6
• Lateral: I, aVL, V5/6
• Posterior: Tall R wave and ST depression in V1-3
• CXR
o Check for signs of heart failure
• Exercise ECG
o Indications
• Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
• Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
• NOTE: digoxin is associated with giving a false-positive result
o Results:
• Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
• Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
 NOTE: beta-blockers reduce heart rate and so should be stopped before the test
• Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
• Radionuclide Myocardial Perfusion Imaging (rMPI)
o Uses Technetium-99m sestamibi or tetrofosmin
o Can be performed under stress or at rest
o Stress testing shows low uptake in ischaemic myocardium
• Echocardiogram
o Measures left ventricular ejection fraction
o Exercise or dobutamine stress echo may detect regional wall motion abnormalities
• Pharmacological Stress Testing
o This is used in patients who are unable to exercise
o Pharmacological agents can be used to induce a tachycardia, such as:
• Dipyridamole
• Adenosine
• Dobutamine
o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium
o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease
• Cardiac Catheterisation/Angiography
o Performed if ACS with positive troponin or if high risk on stress testing
• Coronary Calcium Scoring
o Uses specialised CT scan
o May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia

130
Q

Generate a management plan for ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A

• STABLE ANGINA
o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)
• All patients should receive aspirin 75 mg/day unless contraindicated
o Immediate symptom relief (e.g. GTN spray)
o Long-term management
• Beta-blockers
 Contraindicated in:
• Acute heart failure
• Cardiogenic shock
• Bradycardia
• Heart block
• Asthma
• Calcium channel blockers
• Nitrates
o Percutaneous coronary intervention (PCI)
• Performed in patients with stable angina despite maximal tolerable medical therapy
o Coronary artery bypass graft (CABG)
• Occurs in more severe cases (e.g. three-vessel disease)
• UNSTABLE ANGINA/NSTEMI
o Admit to coronary care unit
o Oxygen, IV access, monitor vital signs and serial ECG
o GTN
o Morphine
o Metoclopramide (to counteract the nausea caused by morphine)
o Aspirin (300 mg initially, followed by 75 mg indefinitely)
o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)
o LMWH (e.g. enoxaparin)
o Beta-blocker (e.g. metoprolol)
o Glucose-insulin infusion if blood glucose > 11 mmol/L
o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:
• Undergoing PCI
• At high risk of further cardiac events
o If little improvement, consider urgent angiography with/without revascularisation
o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH
• Morphine
• Oxygen
• Nitrates
• Anticoagulants (aspirin + clopidogrel)
• Beta-blockers
• ACE inhibitors
• Statins
• Heparin
• STEMI
o Same as UAP/NSTEMI management except:
• Clopidogrel
 600 mg if patient is going to PCI
 300 mg if undergoing thrombolysis and < 75 yrs
 75 mg if undergoing thrombolysis and > 75 yrs
 MAINTENANCE: 75 mg daily for at least 1 year
• If undergoing primary PCI:
 IV heparin (plus GlpIIb/IIIa inhibitor)
 Bivalirudin (antithrombin)
o Primary PCI
• Goal < 90 min if available
o Thrombolysis
• Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase)
• Only considered if within 12 hours of chest pain with ECG changes and not contraindicated
• Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis
o Secondary Prevention
• Dual antiplatelet therapy (aspirin + clopidogrel)
• Beta-blockers
• ACE inhibitors
• Statins
• Control risk factors
o Advice
• No driving for 1 month following MI
o CABG
• Considered in patients with left main stem or three-vessel disease

131
Q

Identify the possible complications of ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction) and its management

A
•	Increased risk of MI and other vascular disease (e.g. stroke, PVD)
•	Cardiac injury from an MI can lead to heart failure and arrhythmias 
•	Early Complications (within 24-72 hrs)
o	Death 
o	Cardiogenic shock 
o	Heart failure 
o	Ventricular arrythmias 
o	Heart block
o	Pericarditis 
o	Myocardial rupture 
o	Thromboembolism
•	Late Complications
o	Ventricular wall rupture 
o	Valvular regurgitation 
o	Ventricular aneurysms 
o	Tamponade 
o	Dressler's syndrome 
o	Thromboembolism 
•	MNEMONIC for Complications of MI
o	Death
o	Arrhythmias
o	Rupture
o	Tamponade
o	Heart failure
o	Valve disease 
o	Aneurysm
o	Dressler's syndrome
o	Embolism
132
Q

Summarise the prognosis for patients with ischaemic heart disease (angina pectoris, acute coronary syndrome, myocardial infarction)

A

• TIMI score (0-7) can be used for risk stratification
o NOTE: TIMI = thrombolysis in myocardial infarction
o High scores are associated with high risk of cardiac events within 30 days of MI
• Killip Classification of acute MI can also be used:
o Class I: no evidence of heart failure
o Class II: mild to moderate heart failure
o Class III: over pulmonary oedema
o Class IV: cardiogenic shock

133
Q

Define mitral regurgitation

A

• Retrograde flow of blood from left ventricle to left atrium during systole

134
Q

Explain the aetiology / risk factors of mitral regurgitation

A
  • Affect ~5% of adults

* Mitral valve prolapse is common in young females

135
Q

Summarise the epidemiology of mitral regurgitation

A

• Broadly speaking, it is caused by mitral valve damage or dysfunction, which, in turn could be caused by any of the following:
o Rheumatic heart disease (MOST COMMON)
o Infective endocarditis
o Mitral valve prolapse
o Papillary muscle rupture or dysfunction (secondary to IHD or cardiomyopathy)
o Chordal rupture and floppy mitral valve associated with connective tissue disease (e.g. Ehlers-Danlos syndrome, Marfan’s syndrome)

136
Q

Recognise the presenting symptoms of mitral regurgitation

A

• Acute MR - may present with symptoms of left ventricular failure
• Chronic MR - may be asymptomatic or present with:
o Exertional dyspnoea
o Palpitations if in AF
o Fatigue
• Mitral Valve Prolapse - asymptomatic or atypical chest pain or palpitations

137
Q

Recognise the signs of mitral regurgitation on physical examination

A

• Pulse may be irregularly irregular (if in AF)
• Laterally displaced apex beat with thrusting (due to left ventricular dilation)
• Pansystolic murmur
o Loudest at apex beat
o Radiating to the axilla
o Soft S1
o S3 may be heard due to rapid ventricular filling in early diastole
• Signs of left ventricular failure in acute mitral regurgitation
• Mitral Valve Prolapse
o Mid-systolic click
o Late systolic murmur
o The click moves towards S1 when standing and away when lying down

138
Q

Identify appropriate investigations for mitral regurgitation and interpret the results

A

• ECG
o NORMAL
o May show AF or p mitrale (indicates left atrial hypertrophy)

• CXR
o ACUTE mitral regurgitation may produce signs of left ventricular failure
o CHRONIC mitral regurgitation shows:
• Left atrial enlargement
• Cardiomegaly (due to LV dilation)
• Mitral valve calcification (if rheumatic heart disease is the cause)
• Echocardiography
o Performed every 6-12 months in moderate-severe MR
o Allows assessment of LV ejection fraction and end-systolic dimension

139
Q

Define mitral stenosis

A

• Mitral valve narrowing causing obstruction to blood flow from the left atrium to the left ventricle

140
Q

Explain the aetiology / risk factors of mitral stenosis

A

• Incidence is declining because rheumatic fever is becoming more and more rare

141
Q

Summarise the epidemiology of mitral stenosis

A
•	MAIN CAUSE: Rheumatic Heart Disease (90% of cases) 
•	Rare causes of mitral stenosis:
o	Congenital mitral stenosis 
o	SLE 
o	Rheumatoid arthritis
o	Endocarditis 
o	Atrial myxoma
142
Q

Recognise the presenting symptoms of mitral stenosis

A
•	May be ASYMPTOMATIC
•	Fatigue 
•	Shortness of breath on exertion 
•	Orthopnoea
•	Palpitations (related to AF) 
•	Rare symptoms:
o	Cough
o	Haemoptysis 
o	Hoarseness caused by compression of left recurrent laryngeal nerve by an enlarged left atrium
143
Q

Recognise the signs of mitral stenosis on physical examination

A
  • Peripheral cyanosis
  • Malar flush (image)
  • Irregularly irregular pulse (if in AF)
  • Apex beat undisplaced and tapping
  • Parasternal heave (due to right ventricular hypertrophy secondary to pulmonary hypertension)
  • Loud S1 with opening snap
  • Mid-diastolic murmur
  • Evidence of pulmonary oedema on lung auscultation (if decompensated)
144
Q

Identify appropriate investigations for mitral stenosis and interpret the results

A

• ECG
o May be NORMAL
o May see p mitrale (broad bifid p wave caused by left atrial hypertrophy)

o May see AF
o Evidence of right ventricular hypertrophy may be seen if there is severe pulmonary hypertension
• CXR
o Left atrial enlargement
o Cardiac enlargement
o Pulmonary congestion
o Mitral valve calcification (occurs in rheumatic cases)
• Echocardiography
o Assesses functional and structural impairments
o Transoesophageal echocardiogram (TOE) gives a better view
• Cardiac Catheterisation
o Measures severity of heart failure

145
Q

Define myocarditis

A

• Acute inflammation and necrosis of cardiac muscle (myocardium)

146
Q

Explain the aetiology / risk factors of myocarditis

A
  • Incidence is difficult to measure accurately
  • Coxsackie B virus is most common in Europe and USA
  • Chagas disease is most common in South America
147
Q

Summarise the epidemiology of myocarditis

A
•	Usually IDIOPATHIC
•	Viruses
o	Coxsackie B 
o	EBV
o	CMV
o	Adenovirus
o	Influenza
•	Bacteria
o	Post-streptococcal
o	Tuberculosis 
o	Diphtheria
•	Fungal
o	Candidiasis
•	Protozoal
o	Trypanosomiasis (Chagas disease)
•	Helminths
o	Trichinosis
•	Non-infective
o	Systemic: SLE, sarcoidosis, polymyositis 
o	Hypersensitivity myocarditis: sulphonamides 
•	Drugs
o	Chemotherapy agents (e.g. doxorubicin, streptomycin)
•	Others
o	Cocaine, heavy metals, radiation
148
Q

Recognise the presenting symptoms of myocarditis

A
•	Prodromal flu-like illness with:
o	Fever 
o	Malaise
o	Fatigue 
o	Lethargy
•	Breathlessness (due to pericardial effusion/myocardial dysfunction)
•	Palpitations 
•	Sharp chest pain (suggesting there is also pericarditis)
149
Q

Recognise the signs of myocarditis on physical examination

A
  • Signs of pericarditis

* Signs of complications (e.g. heart failure, arrhythmia)

150
Q

Identify appropriate investigations for myocarditis and interpret the results

A
•	Bloods
o	FBC - raised WCC if infective cause 
o	U&E
o	ESR/CRP - raised 
o	Cardiac enzymes - may be raised 
o	Tests to identify cause (e.g. viral/bacterial serology, ANA, TFT)
•	ECG
o	Non-specific T wave and ST changes 
o	PERICARDITIS: widespread saddle-shaped ST elevation
•	CXR
o	May be NORMAL
o	May show cardiomegaly 
•	Pericardial Fluid Drainage
o	Measure glucose, protein, cytology, culture and sensitivity 
o	Helps identify causative organism
•	Echocardiography
o	Assesses systolic/diastolic function 
o	Wall motion abnormalities 
o	Pericardial effusions
•	Myocardial Biopsy
o	Rarely required
151
Q

Define pericarditis

A

• Inflammation of the pericardium

o It may be acute, subacute or chronic

152
Q

Explain the aetiology / risk factors of pericarditis

A
  • UNCOMMON
  • < 1/100 hospital admissions
  • More common in males
153
Q

Summarise the epidemiology of pericarditis

A
•	IDIOPATHIC
•	Infective
Most common causative organisms:
o	Coxsackie B 
o	Echovirus
o	Mumps 
o	Streptococci
o	Fungi
o	Staphylococci
o	TB
•	Connective tissue disease (e.g. sarcoidosis, SLE, scleroderma)
•	Post-MI (within 24-72 hrs of MI - occurs in up to 20% of patients) 
•	Dressler's Syndrome - pericarditis occurring weeks/months after acute MI 
•	Malignancy - lung, breast, lymphoma, leukaemia, melanoma
•	Radiotherapy
•	Thoracic surgery
•	Drugs (e.g. hydralazine, isoniazid)
154
Q

Recognise the presenting symptoms of pericarditis

A
•	CHEST PAIN
o	Sharp and central 
o	May radiate to the neck or shoulders 
o	Worse when coughing and deep inspiration (pleuritic pain)
o	Relieved by sitting forward
•	Dyspnoea
•	Nausea
155
Q

Recognise the signs of pericarditis on physical examination

A
•	Fever 
•	Pericardial friction rub 
o	Heard best at lower left sternal edge, with patient leaning forward during expiration
•	Heart sounds may be faint due to a pericardial effusion
•	Cardiac Tamponade signs
o	Beck's Triad (signs associated with acute cardiac tamponade)
•	Raised JVP
•	Low Blood Pressure 
•	Muffled Heart Sounds 
o	Tachycardia
o	Pulsus paradoxus 
•	Definition: an abnormally large decrease in SBP (> 10 mm Hg drop) and pulse wave amplitude during inspiration
•	Constrictive Pericarditis signs
o	Kussmaul's sign 
o	Pulsus paradoxus 
o	Hepatomegaly 
o	Ascites 
o	Oedema 
o	Pericardial knock (due to rapid ventricular filling) 
o	AF
156
Q

Identify appropriate investigations for pericarditis and interpret the results

A

• ECG - widespread saddle-shaped ST elevation
• Echocardiogram - assesses pericardial effusion and cardiac function
• Bloods
o FBC
o U&Es
o ESR/CRP
o Cardiac Enzymes (usually normal)
o Other investigations for cause: blood cultures, ASO titres, ANA, rheumatoid factor
• CXR
o Usually normal
o May be globular if there is a pericardial effusion

157
Q

Generate a management plan for pericarditis

A
•	Acute - cardiac tamponade is treated with emergency pericardiocentesis
•	Medical 
o	Treat underlying cause 
o	NSAIDs for pain and fever relief 
•	Recurrent
o	Low-dose steroids 
o	Immunosuppressants 
o	Colchicine 
•	Surgical
o	Pericardiectomy is performed in cases of constrictive pericarditis
158
Q

Identify the possible complications of pericarditis and its management

A
  • Pericardial effusion
  • Cardiac tamponade
  • Cardiac arrhythmias
159
Q

Summarise the prognosis for patients with pericarditis

A
  • Depends on the underlying cause
  • Viral cases have a GOOD prognosis
  • Malignant pericarditis has a POOR prognosis
160
Q

Define peripheral vascular disease (acute and chronic limb ischaemia)

A

• Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors

161
Q

Explain the aetiology / risk factors of peripheral vascular disease (acute and chronic limb ischaemia)

A

• Occurs due to ATHEROSCLEROSIS in peripheral arteries
• Types of PVD include:
o Intermittent claudication - calf pain on exercise
o Critical limb ischaemia - pain at rest
• NOTE: this is the MOST SEVERE manifestation of peripheral vascular disease
o Acute limb ischaemia - a sudden decrease in arterial perfusion in a limb, due to thrombotic or embolic causes
o Arterial ulcers
o Gangrene
• Risk Factors (same as the risk factors for any other atherosclerotic disease)
o Smoking
o Diabetes
o Hypertension
o Hyperlipidaemia
o Physical inactivity
o Obesity

162
Q

Summarise the epidemiology of peripheral vascular disease (acute and chronic limb ischaemia)

A
  • 55-70 yrs = 4-12% affected
  • 70+ yrs = 15-20% affected
  • More common in MALES
  • Incidence increases with AGE
163
Q

Recognise the presenting symptoms of peripheral vascular disease (acute and chronic limb ischaemia)

A
•	Intermittent claudication - cramping pain in the calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest 
o	Calf claudication = femoral disease 
o	Buttock claudication = iliac disease
•	Features of Critical Limb Ischaemia
o	Ulcers 
o	Gangrene 
o	Rest pain 
o	Night pain (relieved by dangling leg over the edge of the bed) 
•	Leriche Syndrome (aortoiliac occlusive disease) 
o	Buttock claudication 
o	Impotence 
o	Absent/weak distal pulses 
•	Fontaine Classification of Peripheral Vascular Disease
o	Asymptomatic
o	Intermittent Claudication 
o	Rest pain 
o	Ulceration/gangrene
164
Q

Recognise the signs of peripheral vascular disease (acute and chronic limb ischaemia) on physical examination

A
•	Acute Limb Ischaemia - 6 Ps
o	Pain
o	Pale
o	Pulseless
o	Paralysis
o	Paraesthesia
o	Perishingly Cold 
•	Other symptoms:
o	Atrophic skin 
o	Hairless
o	Punched-out ulcers (often painful) 
o	Colour change when raising leg (to Buerger's angle)
165
Q

Identify appropriate investigations for peripheral vascular disease (acute and chronic limb ischaemia) and interpret the results

A

• Full cardiovascular risk assessment
o Blood pressure
o FBC - anaemia will worsen ischaemia
o Fasting blood glucose
o Lipid levels
o ECG - check for pre-existing coronary artery disease
o Thrombophilia screen - for patients < 50 yrs
• Colour Duplex Ultrasound
o FIRST-line
o Shows site and degree of stenosis
• MRI/CT
o Assesses extent and location of stenoses
• ABPI (Ankle-Brachial Pressure Index)
o Marker of cardiovascular disease
o ABPI < 0.8 = do NOT apply a pressure bandage because this will worsen ischaemia

166
Q

Define pulmonary embolism

A

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site

167
Q

Explain the aetiology / risk factors of pulmonary embolism

A
Thrombus
95% arise from DVT in the lower limbs
Rarely arises in the right atrium (in AF patients)
Other causes of embolus:
Amniotic fluid
Air
Fat
Tumour
Mycotic
Risk Factors
Surgical patients
Immobility
Obesity
OCP
Heart failure
Malignanc
168
Q

Summarise the epidemiology of pulmonary embolism

A
Relatively COMMON (especially in hospitalised patients)
Occur in 10 - 20% of patients with confirmed proximal DVT
169
Q

Recognise the presenting symptoms of pulmonary embolism

A

Depends on the SITE and SIZE of the embolus
Small
may be ASYMPTOMATIC

Moderate
Sudden onset SOB
Cough
Haemoptysis
Pleuritic chest pain
Large (or proximal)
As above and:
Severe central pleuritic chest pain
Shock
Collapse
Acute right heart failure
Sudden death
Multiple Small Recurrent
Symptoms of pulmonary hypertension
170
Q

Recognise the signs of pulmonary embolism on physical examination

A

Severity of PE can be assessed based on associated signs:

Small
often no clinical signs. There may be some tachycardia and tachypnoea

Moderate
Tachypnoea
Tachycardia
Pleural rub
Low O2 saturation (
despite O2 supplementation)
Massive PE
Shock
Cyanosis
Signs of right heart strain
Raised JVP
Left parasternal heave
Accentuated S2 heart sound

Multiple Recurrent PE
Signs of pulmonary hypertension
Signs of right heart failure

171
Q

Identify appropriate investigations for pulmonary embolism and interpret the results

A
The Well's Score is used to determine the best investigation for PE
Low Probability (Wells 4 or less) - use D dimer
High Probability (Wells > 4) required imaging (CTPA)

Additional investigations:

Bloods - ABG, thrombophilia screen

ECG
May be normal
May show tachycardia, right axis deviation or RBBB
May show S1Q3T3 pattern

CXR
often NORMAL
but helps exclude other diagnoses

Spiral CT Pulmonary Angiogram
FIRST LINE INVESTIGATION
Poor sensitivity for
small emboli
VERY sensitive for medium to large emboli

Ventilation - Perfusion (VQ) Scan
Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung

Pulmonary Angiography
Invasive
Rarely necessary

Doppler US of Lower Limb
allows assessment of venous thromboembolism

Echocardiography
may show right heart strain

172
Q

Generate a management plan for pulmonary embolism

A

Primary Prevention
Compression stockings
Heparin prophylaxis for those at risk
Good mobilisation and adequate hydration

If haemodynamically stable
O2
Anticoagulation with heparin or LMWH
Switch over to oral warfarin for at least 3 months
Maintain INR 2 - 3
Analgesia

If haemodynamically UNSTABLE (massive PE)
Resuscitate
O2
IV fluids
Thrombolysis with tPA may be considered if cardiac arrest is imminent

Surgical or radiological
Embolectomy

IVC filters
sometimes used for recurrent PEs despite adequate anticoagulation or
when anticoagulation is contraindicated

173
Q

Identify the possible complications of pulmonary embolism and its management

A

Death
Pulmonary infarction
Pulmonary hypertension
Right heart failure

174
Q

Summarise the prognosis for patients with pulmonary embolism

A

30% mortality in those left untreated
8% mortality with treatment
Increased risk of future thromboembolic disease

175
Q

Define pulmonary hypertension

A

• An increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions.

176
Q

Explain the aetiology / risk factors of pulmonary hypertension

A

• Pulmonary hypertension has a variety of causes
o Idiopathic
o Problems with smaller branches of the pulmonary arteries
o Left ventricular failure
o Lung disease (e.g. COPD, interstitial lung disease)
o Thromboses/Emboli in the lungs

177
Q

Summarise the epidemiology of pulmonary hypertension

A
  • Idiopathic pulmonary hypertension is RARE

* More common in severe respiratory and cardiac disease

178
Q

Recognise the presenting symptoms of pulmonary hypertension

A
  • Progressive breathlessness
  • Weakness/tiredness
  • Exertional dizziness and syncope
  • LATE STAGE - oedema and ascites
  • Angina and tachyarrhythmia
179
Q

Recognise the signs of pulmonary hypertension on physical examination

A
  • Right ventricular heave
  • Loud pulmonary second heart sound
  • Murmur - pulmonary regurgitation
  • Tricuspid regurgitation
  • Raised JVP
  • Peripheral oedema
  • Ascites
180
Q

Identify appropriate investigations for pulmonary hypertension and interpret the results

A
  • CXR - exclude other lung diseases
  • ECG - right ventricular hypertrophy and strain
  • Pulmonary function tests
  • LFTs - liver damage –> portal hypertension
  • Lung biopsy - interstitial lung disease
  • Echocardiography - assess right ventricular function
  • Right Heart Catheterisation - directly measure pulmonary pressure and confirm the diagnosis
181
Q

Define rheumatic fever

A

Rheumatic fever is an inflammatory disease that can develop as a complication of inadequately treated strep throat or scarlet fever. Strep throat and scarlet fever are caused by an infection with streptococcus bacteria.

182
Q

Explain the aetiology / risk factors for rheumatic fever

A

Rheumatic fever is most common in 5- to 15-year-old children, though it can develop in younger children and adults.
Family history. Some people carry a gene or genes that might make them more likely to develop rheumatic fever.
Type of strep bacteria. Certain strains of strep bacteria are more likely to contribute to rheumatic fever than are other strains.
Environmental factors. A greater risk of rheumatic fever is associated with overcrowding, poor sanitation and other conditions that can easily result in the rapid transmission or multiple exposures to strep bacteria.

183
Q

Summarise the epidemiology of rheumatic fever

A

Rare in developed countries

184
Q

Recognise the presenting symptoms of rheumatic fever

A

Fever
Painful and tender joints — most often in the knees, ankles, elbows and wrists
Pain in one joint that migrates to another joint
Red, hot or swollen joints
Small, painless bumps (nodules) beneath the skin
Chest pain
Heart murmur
Fatigue
Flat or slightly raised, painless rash with a ragged edge (erythema marginatum)
Jerky, uncontrollable body movements (Sydenham chorea, or St. Vitus’ dance) — most often in the hands, feet and face
Outbursts of unusual behavior, such as crying or inappropriate laughing, that accompanies Sydenham chorea

185
Q

Recognise the signs of rheumatic fever on physical examination

A

Valve stenosis. This narrowing of the valve decreases blood flow.
Valve regurgitation. This leak in the valve allows blood to flow in the wrong direction.
Damage to heart muscle. The inflammation associated with rheumatic fever can weaken the heart muscle, affecting its ability to pump.
An irregular and chaotic beating of the upper chambers of the heart (atrial fibrillation)
An inability of the heart to pump enough blood to the body (heart failure)

186
Q

Identify appropriate investigations for rheumatic fever and interpret the results

A

Major signs and symptoms are strongly associated with ARF and include carditis (swelling of the heart), arthritis (pain, redness and swelling of one or more joints), Sydenham’s chorea (strange movements of the body and face), erythema marginatum (painless skin pigmentation), and subcutaneous nodules (small lumps under the skin). Minor signs and symptoms are used to help support the diagnosis. These include fever, arthralgia (generalised joint aches), blood tests that suggest general illness, and changes seen on heart electrocardiogram.

A combination of these signs and symptoms, plus a positive test for recent group A streptococcus infection is required to confirm ARF diagnosis.

187
Q

Define supraventricular tachycardia

A

• A regular narrow-complex tachycardia (> 100 bpm) with no p waves and a supraventricular origin.
o AF technically counts as a type of SVT
o However, SVT generally refers to:
• Atrioventricular Nodal Re-entry Tachycardia (AVNRT)
• Atrioventricular Re-entry Tachycardia (AVRT)

188
Q

Explain the aetiology / risk factors of supraventricular tachycardia

A
•	AVNRT
o	A localised re-entry circuit forms around the AV node 
•	AVRT
o	A re-entry circuit forms between the atria and ventricles due to the presence of an accessory pathway (Bundle of Kent)
•	Risk Factors
o	Nicotine 
o	Alcohol 
o	Caffeine 
o	Previous MI 
o	Digoxin toxicity
189
Q

Summarise the epidemiology of supraventricular tachycardia

A
  • VERY COMMON

* 2 x more common in FEMALES

190
Q

Recognise the presenting symptoms of supraventricular tachycardia

A
  • May have minimal symptoms or may present with syncope
  • Symptoms vary depending on rate and duration of SVT
  • Palpitations
  • Light-headedness
  • Abrupt onset and termination of symptoms
  • Other symptoms: fatigue, chest discomfort, dyspnoea, syncope
191
Q

Recognise the signs of supraventricular tachycardia on physical examination

A

• AVNRT - normal except tachycardia
• Wolff-Parkinson-White
o Tachycardia
o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)

192
Q

Identify appropriate investigations for supraventricular tachycardia and interpret the results

A

• ECG
o Differentiating between AVNRT and AVRT - once the SVT has been terminated and normal rate and rhythm are re-established:
• AVNRT - appears normal
• AVRT - delta-waves (slurred upstroke of the QRS complex)
o 24 hr ECG monitoring - will be required in patients with paroxysmal palpitations
• Cardiac Enzymes
o Check for features of MI (especially if there is chest pain)
• Electrolytes - can cause arrhythmia
• TFTs - can cause arrhythmia
• Digoxin Level - for patients on digoxin
• Echocardiogram - check for structural heart disease

193
Q

Generate a management plan for supraventricular tachycardia

A

• If Haemodynamically UNSTABLE
o DC cardioversion
• If Haemodynamically STABLE –> vagal monouevres + chemical cardioversion
o Vagal manoeuvres (e.g. Valsalva, carotid massage)
• Carotid massage could dislodge atherosclerotic plaques, so is only performed in young patients
If Vagal manoeuvres fail:
o Adenosine 6 mg bolus (can increase to 12 mg)
• Contraindicated in ASTHMA as it can cause bronchospasm
o Can give verapamil 2.5 - 5 mg if unsuccessful/adenosine contraindicated due to asthma
o Alternatives: atenolol, amiodarone
• If unresponsive to chemical cardioversion or tachycardia > 250 bpm or adverse signs (low BP, heart failure, low consciousness)
o Sedate and synchronised DC cardioversion
o Amiodarone
• Ongoing management of SVT
o AVNRT
• Radiofrequency ablation of slow pathway
• Beta-blockers
• Alternatives: fleicanide, propafenone, verapamil
o AVRT
• Radiofrequency ablation
o Sinus Tachycardia
• Exclude secondary cause (e.g. hyperthyroidism)
• Beta-blocker or rate-limiting CCB

194
Q

Identify the possible complications of supraventricular tachycardia and its management

A
  • Haemodynamic collapse
  • DVT
  • Systemic embolism
  • Cardiac tamponade
195
Q

Summarise the prognosis for patients with supraventricular tachycardia

A
  • Dependent on the presence of underlying structural heart disease
  • If structurally normal heart - GOOD PROGNOSIS
  • People with pre-excitation have a small risk of sudden death
196
Q

Define tricuspid regurgitation

A

• Backflow of blood from the right ventricle to the right atrium during systole

197
Q

Explain the aetiology / risk factors of tricuspid regurgitation

A

• Congenital
o Ebstein’s anomaly (malpositioned tricuspid valve)
o Cleft valve in ostium primum
• Functional
o Consequence of right ventricular dilation (e.g. due to pulmonary hypertension)
o Valve prolapse
• Rheumatic Heart Disease
• Infective Endocarditis
• Other: carcinoid syndrome, trauma, cirrhosis, iatrogenic

198
Q

Summarise the epidemiology of tricuspid regurgitation

A
  • Differs based on cause

* Infective endocarditis is the MOST COMMON cause

199
Q

Recognise the presenting symptoms of tricuspid regurgitation

A
  • Fatigue
  • Breathlessness
  • Palpitations
  • Headaches
  • Nausea
  • Anorexia
  • Epigastric pain made worse by exercise
  • Jaundice
  • Lower limb swelling
200
Q

Recognise the signs of tricuspid regurgitation on physical examination

A

• Pulse - irregularly irregular if AF
• Inspection
o Raised JVP with giant V waves (which may oscillate the earlobes)
o This is caused by transmission of high right ventricular pressures into the great veins
o Giant A waves may also be present
• Palpation - parasternal heave
• Auscultation
o Pansystolic murmur - heard best at lower left sternal edge
o Louder on inspiration (Carvallo sign)
o Loud P2 component of second heart sound
• Chest Examination may show signs of:
o Pleural effusion
o Causes of pulmonary hypertension
• Abdominal Examination may show:
o Palpable liver (tender, smooth and pulsatile)
o Ascites
• Legs - pitting oedema

201
Q

Identify appropriate investigations for tricuspid regurgitation and interpret the results

A

• Bloods
o FBC
o LFT
o Cardiac enzymes
o Blood cultures
• ECG
o P pulmonale - due to right atrial hypertrophy
• CXR
o Right-sided enlargement of cardiac shadow
• Echocardiography
o Extent of regurgitation can be estimated using Doppler ultrasound
o May show valve prolapse and right ventricular dilation
• Right Heart Catheterisation
o Rarely necessary but may be useful for assessing pulmonary artery pressure

202
Q

Define varicose veins

A

• Veins that become prominently elongated, dilated and tortuous, most commonly the superficial veins of the lower limbs.

203
Q

Explain the aetiology / risk factors of varicose veins

A
•	Primary
o	Due to genetic or developmental weakness in the vein wall 
o	Results in increased elasticity, dilatation and valvular incompetence 
•	Secondary
o	Due to venous outflow obstruction
•	Pregnancy 
•	Pelvic malignancy
•	Ovarian cysts 
•	Ascites 
•	Lymphadenopathy
•	Retroperitoneal fibrosis 
o	Due to valve damage (e.g. after DVT)
o	Due to high flow (e.g. arteriovenous fistula) 
•	RISK FACTORS
o	Age 
o	Female 
o	Family history 
o	Caucasian
o	Obesity
204
Q

Summarise the epidemiology of varicose veins

A
  • COMMON
  • Incidence increases with age
  • 10-15% of men
  • 20-25% of women
205
Q

Recognise the presenting symptoms of varicose veins

A
  • Patients may complain about the cosmetic appearance
  • Aching in the legs
  • Aching is worse towards the end of the day of after standing for long periods of time
  • Swelling
  • Itching
  • Bleeding
  • Infection
  • Ulceration
206
Q

Recognise the signs of varicose veins on physical examination

A

• Inspection
o Inspect when the patient is standing
• Palpation
o May feel fascial defects along the veins
o Cough impulse may be felt over the saphenofemoral junction
o Tap Test - tapping over the saphenofemoral junction will lead to an impulse felt distally (this would not happen if the valves were competent)
o Palpation of a thrill or auscultation of a bruit would suggest an AV fistula
• Trendelenburg Test
o Allows localisation of the sites of valvular incompetence
o Leg is elevated and the veins are emptied
o A hand is placed over the saphenofemoral junction
o The leg is put back down and filling of the veins is observed before and after the hand is released from the saphenofemoral junction
o A Doppler ultrasound can be used to show saphenofemoral incompetence
• Rectal or Pelvic Examination
o If secondary causes are suspected
• Signs of Venous Insufficiency
o Varicose eczema
o Haemosiderin staining
o Atrophie blanche
o Lipodermatosclerosis
o Oedema
o Ulceration

207
Q

Identify appropriate investigations for varicose veins and interpret the results

A

• Duplex Ultrasound
o Locates sites of incompetence or reflux
o Allows exclusion of DVT

208
Q

Generate a management plan for varicose veins

A
•	Conservative
o	Exercise - improves skeletal muscle pump
o	Elevation of legs at rest 
o	Support stockings 
•	Venous Telangiectasia and Reticular Veins
o	Laser sclerotherapy 
o	Microinjection sclerotherapy
•	Surgical
o	Saphenofemoral ligation 
o	Stripping of the long saphenous vein 

o Avulsion of varicosities

o NOTE: short saphenous vein isn’t stripped because of the risk of damaging the sural nerve

209
Q

Identify the possible complications of varicose veins and its management

A
•	Venous pigmentation 
•	Eczema
•	Lipodermatosclerosis 
•	Superficial thrombophlebitis 
•	Venous ulceration 
•	Complications of Treatment
o	Sclerotherapy - skin staining, local scarring 
o	Surgery - haemorrhage, infection, recurrence, paraesthesia, peroneal nerve injury
210
Q

Summarise the prognosis for patients with varicose veins

A
  • Slowly progressive

* High recurrence rates

211
Q

Define vasovagal syncope

A

• Loss of consciousness due to a transient drop in blood flow to the brain caused by excessive vagal discharge.

212
Q

Explain the aetiology / risk factors of vasovagal syncope

A
•	Vasovagal syncope is a very common cause of fainting 
•	Can be precipitated by:
o	Emotions (e.g. fear, severe pain, blood phobia) 
o	Orthostatic stress (e.g. prolonged standing, hot weather)
213
Q

Summarise the epidemiology of vasovagal syncope

A
  • VERY COMMON

* Syncope (of all causes) affects 40% of people

214
Q

Recognise the presenting symptoms of vasovagal syncope

A
  • Loss of consciousness lasting a short time
  • Patients may experience vagal symptoms (sweating, dizziness, light-headedness) before passing out
  • There may be some twitching of limbs during the blackout
  • Recovery is normally very quick
215
Q

Recognise the signs of vasovagal syncope on physical examination

A

• Usually NO SIGNS

216
Q

Identify appropriate investigations for vasovagal syncope and interpret the results

A

• Investigations are involved with checking for other causes of syncope
o ECG - check for arrhythmia
o Echocardiogram - check for outflow obstruction
o Lying/standing blood pressure - check for orthostatic hypotension
o Fasting blood glucose - check for DM/hypoglycaemia

217
Q

Define venous ulcers

A

• Large, shallow, sometimes painful ulcers usually found superior to the medial malleoli. They are caused by incompetent valves in the lower limbs leading to venous stasis and ulceration.

218
Q

Explain the aetiology / risk factors of venous ulcers

A
•	They are caused by incompetent valves in the lower limbs 
•	Valve incompetence leads to venous stasis and increased venous pressure 
•	This results in ulceration 
•	Risk Factors
o	Obesity 
o	Immobility
o	Recurrent DVT 
o	Varicose veins 
o	Previous injury/surgery to the leg 
o	Age
219
Q

Summarise the epidemiology of venous ulcers

A
  • VERY COMMON

* Increases with age

220
Q

Recognise the presenting symptoms of venous ulcers

A
•	Large, shallow, relatively painless ulcer with an irregular margin situated above the medial malleoli (most of the time) 
•	Features of the history:
o	Varicose veins 
o	DVT 
o	Phlebitis 
o	Fracture, trauma or surgery 
o	Family history 
o	Other symptoms of venous insufficiency:
•	Swelling
•	Itching 
•	Aching
221
Q

Recognise the signs of venous ulcers on physical examination

A
•	Described above 
•	Other signs of venous ulcers:
o	Stasis eczema 
o	Lipodermatosclerosis (inverted champagne bottle sign if SEVERE)
o	Haemosiderin deposition (dark colour)
222
Q

Identify appropriate investigations for venous ulcers and interpret the results

A

• ABPI
o Exclude arterial ulcer
o If ABPI < 0.8 - do NOT apply a pressure bandage as this could worsen the ulcer
• Measure surface area of ulcer - allows monitoring of progression
• Swabs for microbiology - if signs of infection
• Biopsy - if possibility of Marjolin’s ulcer

223
Q

Generate a management plan for venous ulcers

A

• Graduated compression (reduced venous stasis)
o NOTE: must exclude diabetes, neuropathy and PVD before this is attempted
• Debridement and cleaning
• Antibiotics - if infected
• Topical steroids - may help with surrounding dermatitis

224
Q

Identify the possible complications of venous ulcers and its management

A
  • Recurrence

* Infection

225
Q

Summarise the prognosis for patients with venous ulcers

A
  • GOOD

* Results are better if patients are mobile with few comorbidities

226
Q

Define ventricular fibrillation

A

• An irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death

227
Q

Explain the aetiology / risk factors of ventricular fibrillation

A
•	The ventricular fibres contract randomly causing complete failure of ventricular function
•	Most cases occur in patients with underlying heart disease
•	Risk Factors
o	Coronary artery disease 
o	AF 
o	Hypoxia
o	Ischaemia 
o	Pre-excitation syndrome
228
Q

Summarise the epidemiology of ventricular fibrillation

A
  • The MOST COMMON arrhythmia identified in cardiac arrest patients
  • Incidence of VF parallels the incidence of ischaemic heart disease
229
Q

Recognise the presenting symptoms & signs of ventricular fibrillation

A
•	History of:
o	Chest pain
o	Fatigue 
o	Palpitations 
•	There may be known pre-existing conditions:
o	Coronary artery disease 
o	Cardiomyopathy 
o	Valvular heart disease 
o	Long QT syndrome 
o	Wolff-Parkinson-White syndrome
o	Brugada syndrome
230
Q

Identify appropriate investigations for ventricular fibrillation and interpret the results

A
  • ECG
  • Cardiac enzymes (e.g. troponins) - check for recent ischaemic event
  • Electrolytes - derangement can cause arrhythmias, including VF
  • Drug levels and toxicology screen - anti-arrhythmics can (ironically) cause arrhythmia, as can various recreational drugs (e.g. cocaine)
  • TFTs - hyperthyroidism can cause tachyarrhythmias
  • Coronary angiography - if patient survives VF, to check the integrity of coronary arteries
231
Q

Generate a management plan for ventricular fibrillation

A
  • VF requires urgent defibrillation and cardioversion
  • Patients who survive need full assessment of left ventricular function, myocardial perfusion and electrophysiological stability
  • Most survivors will need an implantable cardioverter defibrillator (ICD)
  • Empirical beta-blockers
  • Some patients may be treated with radiofrequency ablation (RFA)
232
Q

Identify the possible complications of ventricular fibrillation and its management

A
  • Ischaemic brain injury due to loss of cardiac output
  • Myocardial injury
  • Post-defibrillation arrhythmias
  • Aspiration pneumonia
  • Skin burns
  • Death
233
Q

Summarise the prognosis for patients with ventricular fibrillation

A
  • Depends on the time between onset of VF and medical intervention
  • Early defibrillation is essential (ideally within 4-6 mins)
  • Anoxic encephalopathy is a major outcome of VF
234
Q

Define ventricular tachycardia

A

• A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually > 120 bpm.

235
Q

Explain the aetiology / risk factors of ventricular tachycardia

A

• Electrical impulses arise from a ventricular ectopic focus
• Risk Factors
o Coronary heart disease
o Structural heart disease
o Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia)
o Use of stimulant drugs (e.g. caffeine, cocaine)

236
Q

Summarise the epidemiology of ventricular tachycardia

A
  • Fairly common
  • It is one of the shockable rhythms that is seen in cardiac arrest patients
  • VT incidence peaks in the middle decades of life
237
Q

Recognise the presenting symptoms of ventricular tachycardia

A
•	Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion 
•	Symptoms:
o	Chest pain 
o	Palpitations 
o	Dyspnoea 
o	Syncope
238
Q

Recognise the signs of ventricular tachycardia on physical examination

A
•	Signs are dependent on the degree of haemodynamic instability
o	Respiratory distress
o	Bibasal crackles 
o	Raised JVP 
o	Hypotension
o	Anxiety 
o	Agitation
o	Lethargy
o	Coma
239
Q

Identify appropriate investigations for ventricular tachycardia and interpret the results

A

• ECG
o It can sometimes be difficult to distinguish between VT and SVT with aberrant conduction
o If in doubt, treat as a VT
o ECG Features:
• Rate > 100 bpm
• Broad QRS complexes
• AV dissociation
• Electrolytes - derangement can cause arrhythmias
• Drug levels - e.g. check for digoxin toxicity
• Cardiac enzymes - e.g. troponins to check for recent ischaemic event

240
Q

Generate a management plan for ventricular tachycardia

A

• ABC approach
• CHECK WHETHER THE PATIENT HAS A PULSE OR NOT
• Pulseless VT - follow advanced life support algorithm
• Unstable VT - reduced cardiac output
o NOTE: VF and pulseless VT require defibrillation (unsynchronised), but other VTs can be treated with synchronised cardioversion
o Correct electrolyte abnormalities
o Amiodarone
• Stable VT
o These patients DO NOT experience symptoms of haemodynamic compromise
o Correct electrolyte abnormalities
o Amiodarone
o Synchronised DC shock (if steps above are unsuccessful)
• Implantable Cardioverter Defibrillator (ICD)
o ICD is considered if:
• Sustained VT causing syncope
• Sustained VT with ejection fraction < 35%
• Previous cardiac arrest due to VT or VF
• MI complicated by non-sustained VT

241
Q

Identify the possible complications of ventricular tachycardia and its management

A
  • Congestive cardiac failure
  • Cardiogenic shock
  • VT may deteriorate into VF
242
Q

Summarise the prognosis for patients with ventricular tachycardia

A
  • GOOD if treated RAPIDLY

* Long-term prognosis depends on the underlying cause

243
Q

Define Wolff–Parkinson–White syndrome

A

• A congenital abnormality which can result in supraventricular tachycardias that use an accessory pathway. It is a pre-excitation syndrome.

244
Q

Explain the aetiology / risk factors of Wolff–Parkinson–White syndrome

A

• The accessory pathway (bundle of Kent) is likely to be congenital
• Associations:
o Congenital cardiac defects
o Ebstein’s anomaly (congenital malformation of the heart characterised by displacement of septal and posterior tricuspid leaflets)
o Mitral valve prolapse
o Cardiomyopathies (e.g. HOCM)

245
Q

Summarise the epidemiology of Wolff–Parkinson–White syndrome

A
  • Relatively COMMON
  • Most common of the ventricular pre-excitation syndromes
  • Found in ALL AGES
  • More common in the YOUNG
  • Prevalence decreases with age
246
Q

Recognise the presenting symptoms & signs of Wolff–Parkinson–White syndrome

A

• SVT may occur in early childhood
• Often ASYMPTOMATIC - may be an incidental finding of an ECG
• Symptoms:
o Palpitations
o Light-headedness
o Syncope
• Paroxysmal SVT may be followed by a period of polyuria, due to atrial dilatation and release of ANP
• Sudden death - if SVT deteriorates into VF
• Clinical features of associated cardiac defects (e.g. mitral valve prolapse, cardiomyopathy)

247
Q

Identify appropriate investigations for Wolff–Parkinson–White syndrome and interpret the results

A

• ECG may be normal if the conduction speed of the impulse along the accessory pathway matches the conduction speed down the bundle of His
• Classic ECG findings:
o Short PR interval
o Broad QRS complex
o Slurred upstroke producing a delta wave
• Patient may be in SVT (AVRT)
• Bloods - check for other causes of arrhythmia
• Echocardiogram - check for structural heart defects