Cardiology 3 Flashcards

1
Q

Define mitral regurgitation

A

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

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2
Q

Summarise the epidemiology of mitral regurgitation

A
  • Affect ~5% of adults

* Mitral valve prolapse is common in young female

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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)

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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
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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

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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

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7
Q

Define mitral stenosis

A

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

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8
Q

Summarise the epidemiology of mitral stenosis

A

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

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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

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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

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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
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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

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13
Q

Define myocarditis

A

Acute inflammation and necrosis of cardiac muscle (myocardium

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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
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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

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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)
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17
Q

Recognise the signs of myocarditis on examination

A
  • Signs of pericarditis

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

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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

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19
Q

Define pericarditis

A

Inflammation of the pericardium

o It may be acute, subacute or chronic

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20
Q

Summarise the epidemiology of pericarditis

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

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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

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25
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

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26
Q

Identify the possible complications of pericarditis

A
  • Pericardial effusion
  • Cardiac tamponade
  • Cardiac arrhythmias
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27
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
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28
Q

Define peripheral vascular disease

A

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

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29
Q

Explain the aetiology/risk factors of peripheral vascular disease

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

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30
Q

Summarise the epidemiology of peripheral vascular disease

A
  • 55-70 yrs = 4-12% affected
  • 70+ yrs = 15-20% affected
  • More common in MALES
  • Incidence increases with AGE
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31
Q

Recognise the presenting symptoms of peripheral vascular disease

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

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32
Q

Recognise the signs of peripheral vascular disease 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)

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33
Q

Identify appropriate investigations for peripheral vascular disease

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

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34
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.

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35
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

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36
Q

Summarise the epidemiology of pulmonary hypertension

A
  • Idiopathic pulmonary hypertension is RARE

* More common in severe respiratory and cardiac disease

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37
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
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38
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
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39
Q

Identify appropriate investigations for pulmonary hypertension

A
  • 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
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40
Q

Define supraventricular tachycardia (SVT)

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)
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41
Q

Explain the aetiology/risk factors of supraventricular tachycardia (SVT)

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

42
Q

Summarise the epidemiology of supraventricular tachycardia (SVT)

A
  • VERY COMMON

* 2 x more common in FEMALES

43
Q

Recognise the presenting symptoms of supraventricular tachycardia (SVT)

A
  • May have minimal symptoms or may present with syncope
  • Symptoms vary depending on rate and duration of SVT
  • Palpitations
  • Light-headedness
44
Q

Recognise the signs of supraventricular tachycardia (SVT) on physical examination

A
  • AVNRT - normal except tachycardia
  • Wolff-Parkinson-White

o Tachycardia

o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)

45
Q

Identify appropriate investigations for supraventricular tachycardia (SVT)

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
46
Q

Generate a management plan for supraventricular tachycardia (SVT)

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
47
Q

Identify possible complications of supraventricular tachycardia (SVT)

A
  • Haemodynamic collapse
  • DVT
  • Systemic embolism
  • Cardiac tamponade
48
Q

Summarise the prognosis for patients with supraventricular tachycardia (SVT)

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
49
Q

Define tricuspid regurgitation

A

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

50
Q

Explain the aetiology/risk factors for 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
51
Q

Summarise the epidemiology of tricuspid regurgitation

A
  • Differs based on cause

* Infective endocarditis is the MOST COMMON cause

52
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
53
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
54
Q

Identify appropriate investigation for tricuspid regurgitation

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

55
Q

Define varicose veins

A

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

56
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

57
Q

Summarise the epidemiology of varicose veins

A
  • COMMON
  • Incidence increases with age
  • 10-15% of men
  • 20-25% of women
58
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
59
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

60
Q

Identify appropriate investigations for varicose veins

A
  • Duplex Ultrasound

o Locates sites of incompetence or reflux

o Allows exclusion of DVT

61
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

62
Q

Identify possible complications of varicose veins

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

63
Q

Summarise the prognosis for patients with varicose veins

A
  • Slowly progressive

* High recurrence rates

64
Q

Define vasovagal syncope

A

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

65
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)

66
Q

Summarise the epidemiology of vasovagal syncope

A
  • VERY COMMON

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

67
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
68
Q

Recognise the signs of vasovagal syncope on physical examination

A

Usually NO SIGNS

69
Q

Identify appropriate investigations for vasovagal syncope

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

70
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.

71
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

72
Q

Summarise the epidemiology of venous ulcers

A
  • VERY COMMON

* Increases with age

73
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
74
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)

75
Q

Identify appropriate investigations for venous ulcers

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 ulce
76
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
77
Q

Identify possible complications of venous ulcers

A
  • Recurrence

* Infection

78
Q

Summarise the prognosis for patients with venous ulcers

A
  • GOOD

* Results are better if patients are mobile with few comorbidities

79
Q

Define ventricular fibrillation

A

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

80
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

81
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
82
Q

Recognise the presenting symptoms and 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-W

o Brugada syndrome

83
Q

Identify appropriate investigations for ventricular fibrillation

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
84
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)
85
Q

Identify possible complications of ventricular fibrillation

A
  • Ischaemic brain injury due to loss of cardiac output
  • Myocardial injury
  • Post-defibrillation arrhythmias
  • Aspiration pneumonia
  • Skin burns
  • Death
86
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
87
Q

Define ventricular tachycardia

A

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
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)

89
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
90
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

91
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

92
Q

Identify appropriate investigations for ventricular tachycardia

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
93
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
94
Q

Identify possible complications of ventricular tachycardia

A
  • Congestive cardiac failure
  • Cardiogenic shock
  • VT may deteriorate into VF
95
Q

Summarise the prognosis of ventricular tachycardia

A
  • GOOD if treated RAPIDLY

* Long-term prognosis depends on the underlying cause

96
Q

Define Wolff-Parkinson-White (WPW) Syndrome

A

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

97
Q

Explain the aetiology/risk factors of Wolff-Parkinson-White (WPW) 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)

98
Q

Summarise the epidemiology of Wolff-Parkinson-White (WPW) 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
99
Q

Recognise the presenting symptoms and signs of Wolff-Parkinson-White (WPW) 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)
100
Q

Identify appropriate investigations for Wolff-Parkinson-White (WPW) Syndrome

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