Cardiology 3 Flashcards
1
Q
Define mitral regurgitation
A
Retrograde flow of blood from left ventricle to left atrium during systole
2
Q
Summarise the epidemiology of mitral regurgitation
A
- Affect ~5% of adults
* Mitral valve prolapse is common in young female
3
Q
Explain the aetiology/risk factors 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)
4
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
5
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
6
Q
Identify appropriate investigations for mitral regurgitation
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
7
Q
Define mitral stenosis
A
Mitral valve narrowing causing obstruction to blood flow from the left atrium to the left ventricl
8
Q
Summarise the epidemiology of mitral stenosis
A
Incidence is declining because rheumatic fever is becoming more and more rare
9
Q
Explain the aetiology/risk factors for 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
10
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
11
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
12
Q
Identify appropriate investigations for mitral stenosis
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
13
Q
Define myocarditis
A
Acute inflammation and necrosis of cardiac muscle (myocardium
14
Q
Summarise the epidemiology 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 Americ
15
Q
Explain the aetiology/risk factors 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
16
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)
17
Q
Recognise the signs of myocarditis on examination
A
- Signs of pericarditis
* Signs of complications (e.g. heart failure, arrhythmia)
18
Q
Identify appropriate investigations for myocarditis
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
19
Q
Define pericarditis
A
Inflammation of the pericardium
o It may be acute, subacute or chronic
20
Q
Summarise the epidemiology of pericarditis
A
- UNCOMMON
- < 1/100 hospital admissions
- More common in males
21
Q
Explain the aetiology/risk factors 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)
22
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
23
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
24
Q
Identify appropriate investigations for pericarditis
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
25
Generate a management plan for pericarditis
* 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
26
Identify the possible complications of pericarditis
* Pericardial effusion
* Cardiac tamponade
* Cardiac arrhythmias
27
Summarise the prognosis for patients with pericarditis
* Depends on the underlying cause
* Viral cases have a GOOD prognosis
* Malignant pericarditis has a POOR prognosis
28
Define peripheral vascular disease
Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors
29
Explain the aetiology/risk factors of peripheral vascular disease
* 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
30
Summarise the epidemiology of peripheral vascular disease
* 55-70 yrs = 4-12% affected
* 70+ yrs = 15-20% affected
* More common in MALES
* Incidence increases with AGE
31
Recognise the presenting symptoms of peripheral vascular disease
* 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
32
Recognise the signs of peripheral vascular disease on physical examination
* 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)
33
Identify appropriate investigations for peripheral vascular disease
* 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
34
Define pulmonary hypertension
An increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions.
35
Explain the aetiology/risk factors of pulmonary hypertension
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
36
Summarise the epidemiology of pulmonary hypertension
* Idiopathic pulmonary hypertension is RARE
| * More common in severe respiratory and cardiac disease
37
Recognise the presenting symptoms of pulmonary hypertension
* Progressive breathlessness
* Weakness/tiredness
* Exertional dizziness and syncope
* LATE STAGE - oedema and ascites
* Angina and tachyarrhythmia
38
Recognise the signs of pulmonary hypertension on physical examination
* Right ventricular heave
* Loud pulmonary second heart sound
* Murmur - pulmonary regurgitation
* Tricuspid regurgitation
* Raised JVP
* Peripheral oedema
* Ascites
39
Identify appropriate investigations for pulmonary hypertension
* CXR - exclude other lung diseases
* ECG - right ventricular hypertrophy and strain
* Pulmonar
* 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
40
Define supraventricular tachycardia (SVT)
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)
41
Explain the aetiology/risk factors of supraventricular tachycardia (SVT)
* 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
42
Summarise the epidemiology of supraventricular tachycardia (SVT)
* VERY COMMON
| * 2 x more common in FEMALES
43
Recognise the presenting symptoms of supraventricular tachycardia (SVT)
* May have minimal symptoms or may present with syncope
* Symptoms vary depending on rate and duration of SVT
* Palpitations
* Light-headedness
44
Recognise the signs of supraventricular tachycardia (SVT) on physical examination
* AVNRT - normal except tachycardia
* Wolff-Parkinson-White
o Tachycardia
o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)
45
Identify appropriate investigations for supraventricular tachycardia (SVT)
* 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
46
Generate a management plan for supraventricular tachycardia (SVT)
* 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
47
Identify possible complications of supraventricular tachycardia (SVT)
* Haemodynamic collapse
* DVT
* Systemic embolism
* Cardiac tamponade
48
Summarise the prognosis for patients with supraventricular tachycardia (SVT)
* 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
49
Define tricuspid regurgitation
Backflow of blood from the right ventricle to the right atrium during systole
50
Explain the aetiology/risk factors for tricuspid regurgitation
* 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
51
Summarise the epidemiology of tricuspid regurgitation
* Differs based on cause
| * Infective endocarditis is the MOST COMMON cause
52
Recognise the presenting symptoms of tricuspid regurgitation
* Fatigue
* Breathlessness
* Palpitations
* Headaches
* Nausea
* Anorexia
* Epigastric pain made worse by exercise
* Jaundice
* Lower limb swelling
53
Recognise the signs of tricuspid regurgitation on physical examination
* 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
54
Identify appropriate investigation for tricuspid regurgitation
* 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
55
Define varicose veins
Veins that become prominently elongated, dilated and tortuous, most commonly the superficial veins of the lower limbs.
56
Explain the aetiology/risk factors of varicose veins
* 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
57
Summarise the epidemiology of varicose veins
* COMMON
* Incidence increases with age
* 10-15% of men
* 20-25% of women
58
Recognise the presenting symptoms of varicose veins
* 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
59
Recognise the signs of varicose veins on physical examination
* 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
60
Identify appropriate investigations for varicose veins
* Duplex Ultrasound
o Locates sites of incompetence or reflux
o Allows exclusion of DVT
61
Generate a management plan for varicose veins
* 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
62
Identify possible complications of varicose veins
* 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
63
Summarise the prognosis for patients with varicose veins
* Slowly progressive
| * High recurrence rates
64
Define vasovagal syncope
Loss of consciousness due to a transient drop in blood flow to the brain caused by excessive vagal discharge.
65
Explain the aetiology/risk factors of vasovagal syncope
* 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)
66
Summarise the epidemiology of vasovagal syncope
* VERY COMMON
| * Syncope (of all causes) affects 40% of people
67
Recognise the presenting symptoms of vasovagal syncope
* 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
68
Recognise the signs of vasovagal syncope on physical examination
Usually NO SIGNS
69
Identify appropriate investigations for vasovagal syncope
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
70
Define venous ulcers
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.
71
Explain the aetiology/risk factors of venous ulcers
* 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
72
Summarise the epidemiology of venous ulcers
* VERY COMMON
| * Increases with age
73
Recognise the presenting symptoms of venous ulcers
* 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
74
Recognise the signs of venous ulcers on physical examination
* Described above
* Other signs of venous ulcers:
o Stasis eczema
o Lipodermatosclerosis (inverted champagne bottle sign if SEVERE)
o Haemosiderin deposition (dark colour)
75
Identify appropriate investigations for venous ulcers
* 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 ulce
76
Generate a management plan for venous ulcers
* 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
77
Identify possible complications of venous ulcers
* Recurrence
| * Infection
78
Summarise the prognosis for patients with venous ulcers
* GOOD
| * Results are better if patients are mobile with few comorbidities
79
Define ventricular fibrillation
An irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death.
80
Explain the aetiology/risk factors of ventricular fibrillation
* 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
81
Summarise the epidemiology of ventricular fibrillation
* The MOST COMMON arrhythmia identified in cardiac arrest patients
* Incidence of VF parallels the incidence of ischaemic heart disease
82
Recognise the presenting symptoms and signs of ventricular fibrillation
* 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-W
o Brugada syndrome
83
Identify appropriate investigations for ventricular fibrillation
* 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
84
Generate a management plan for ventricular fibrillation
* 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)
85
Identify possible complications of ventricular fibrillation
* Ischaemic brain injury due to loss of cardiac output
* Myocardial injury
* Post-defibrillation arrhythmias
* Aspiration pneumonia
* Skin burns
* Death
86
Summarise the prognosis for patients with ventricular fibrillation
* 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
87
Define ventricular tachycardia
A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually > 120 bpm.
(Fuck me this has a weird ECG, look it up - pg 101 Laz)
88
Explain the aetiology/risk factors of ventricular tachycardia
* 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)
89
Summarise the epidemiology of ventricular tachycardia
* 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
90
Recognise the presenting symptoms of ventricular tachycardia
* Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion
* Symptoms:
o Chest pain
o Palpitations
o Dyspnoea
o Syncope
91
Recognise the signs of ventricular tachycardia on physical examination
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
92
Identify appropriate investigations for ventricular tachycardia
* 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
93
Generate a management plan for ventricular tachycardia
* 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
94
Identify possible complications of ventricular tachycardia
* Congestive cardiac failure
* Cardiogenic shock
* VT may deteriorate into VF
95
Summarise the prognosis of ventricular tachycardia
* GOOD if treated RAPIDLY
| * Long-term prognosis depends on the underlying cause
96
Define Wolff-Parkinson-White (WPW) Syndrome
A congenital abnormality which can result in supraventricular tachycardias that use an accessory pathway. It is a pre-excitation syndrome.
97
Explain the aetiology/risk factors of Wolff-Parkinson-White (WPW) Syndrome
* 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)
98
Summarise the epidemiology of Wolff-Parkinson-White (WPW) Syndrome
* Relatively COMMON
* Most common of the ventricular pre-excitation syndromes
* Found in ALL AGES
* More common in the YOUNG
* Prevalence decreases with age
99
Recognise the presenting symptoms and signs of Wolff-Parkinson-White (WPW) Syndrome
* 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)
100
Identify appropriate investigations for Wolff-Parkinson-White (WPW) Syndrome
* 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
