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!Final Year > Cardiovascular (2) > Flashcards

Cardiovascular (2) Flashcards

1
Q

What is Heart Block?

A
  1. Impairment of the atrioventricular (AV) node impulse conduction
  2. Represented by the interval between P wave and QRS complex
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2
Q

What is first degree Heart Block?

A
  1. Prolonged conduction through the AV node
  2. PR interval > 0.2 seconds
  3. Asymptomatic first-degree heart block is relatively common and does not need treatment
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3
Q

What is second degree Heart Block (Mobitz type 1- Wenchebach)?

A
  1. Progressive prolongation of the PR interval until a dropped beat occurs
  2. The progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node
  3. The cycle then begins again
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4
Q

What is second degree Heart Block (Mobitz type 2)?

A
  1. Intermittent or regular failure of conduction through AV node
  2. PR interval is constant but the P wave is often not followed by a QRS complex
  3. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)
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5
Q

What is third degree Heart Block?

A
  1. Also known as complete heart block
  2. No relationship between atrial and ventricular contraction ( no association between the P waves and QRS complexes)
  3. Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarization within the ventricle (ventricular escape)
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6
Q

What is the aetiology of Heart Block?

A
  1. Most common cause: MI or ischaemic heart disease
  2. Infection e.g. rheumatic fever, infective endocarditis
  3. Drugs e.g. digoxin ,b-blockers, Ca2+ channel blockers
  4. Metabolic e.g. hyperkalaemia, cholestatic jaundice, hypothermia
  5. Infiltration of conducting system e.g. sarcoidosis, cardiac neoplasms, amyloidosis
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7
Q

What is the epidemiology of Heart Block?

A
  1. The majority of pacemakers implanted annually are for heart block
  2. First degree heart block is associated with increased risk of AF
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8
Q

What are the features of Heart Block?

A
  1. First degree and Mobitz 1: Usually asymptomatic
  2. Syncope
  3. Heart failure
  4. Regular bradycardia (30-50 bpm)
  5. Wide pulse pressure
  6. JVP: cannon waves in neck
  7. Variable intensity of S1
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9
Q

What are the signs of Heart Block on physical examination?

A
  1. Often normal
  2. Complete heart block:
    a. Slow large volume pulse
    b. JVP may show ‘cannon waves’
  3. Mobitz type II and third-degree block:
    a. Signs of a reduced cardiac output (e.g. hypotension, heart failure)
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10
Q

What are the ECG findings for First degree Heart Block?

A

Prolonged PR interval (>0.2 s)

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11
Q

What are the ECG findings for Second degree Mobitz 1 (Wenchebach) Heart Block?

A
  1. Progressively prolonged PR interval, culminating in a P wave that is not followed by a QRS
  2. The pattern then begins again
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12
Q

What are the ECG findings for Second degree Mobitz 2 Heart Block?

A
  1. Intermittently a P wave is not followed by a QRS
  2. There may be a regular pattern of P waves not followed by a QRS (e.g. two P waves per QRS, indicating 2:1 block)
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13
Q

What are the ECG findings for Third degree (complete) Heart Block?

A

No relationship between P waves and QRS complexes

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14
Q

What are the investigations for Heart Block?

A
  1. ECG: different findings
  2. CXR: may show hilar lymphadenopathy, cardiac enlargement, pulmonary oedema
  3. Bloods:
    a. TFTs: hypo or hyperthyroidism
    b. Digoxin level: identify cause
    c. Cardiac enzymes, troponin: may be elevated
  4. Echocardiogram:
    Ventricular dysfunction or hypertrophy, valvular disease, wall-motion abnormalities
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15
Q

What is the management for asymptomatic first-degree AV block or type I second-degree Heart Block?

A
  1. No specific treatment is required
  2. Patients are at low risk for progression to higher-degree AV block
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16
Q

What is the management for symptomatic chronic Heart Block?

A
  1. First line: stop all AV-nodal blocking medications: beta-blockers, non-dihydropyridine calcium-channel blockers, and digoxin
  2. While discontinuing these medicines may improve AV conduction, they are not likely to completely reverse a clinically significant AV block
  3. If severe: Permanent pacemakers should be considered (recommended in patients with third-degree heart block, advanced Mobitz type II and symptomatic Mobitz type I)
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17
Q

What is the management for acute Heart Block (e.g. secondary to MI)?

A

If associated with clinical deterioration, IV
Atropine (anti-muscarinic) and consider temporary (external) pacemaker

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18
Q

What are the complications of Heart Block?

A
  1. Asystole- cardiac arrest
  2. Heart failure
  3. Complications of any pacemaker inserted
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19
Q

What is the prognosis for Heart Block?

A

Mobitz type II and third-degree block (advanced) usually indicate serious underlying cardiac disease whereas first degree and Mobitz type I have a low risk

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20
Q

What is Hypertension?

A
  1. Defined as systolic BP >140mmHg and/or diastolic BP >90mmHg persistently/ measured on three separate occasions or
  2. A 24 hour blood pressure average reading >= 135/85 mmHg
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21
Q

What is malignant hypertension?

A

Defined as BP 􏰃200/ 130 mmHg

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22
Q

What can hypertension be divided into?

A
  1. Primary (around 90-95%):
    a. Essential hypertension
    b. No single disease causes the rise in BP, associated with ageing
  2. Secondary:
    a. A wide variety of endocrine, renal and other causes
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23
Q

What are the different secondary causes of hypertension?

A
  1. Renal disease:
    a. Glomerulonephritis
    b. Chronic pyelonephritis
    c. Adult polycystic kidney disease
    d. Renal artery stenosis
  2. Endocrine causes:
    a. Primary hyperaldosteronism
    b. Phaeochromocytoma
    c. Cushing’s syndrome
    d. Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
    e. Acromegaly
  3. Other:
    a. Glucocorticoids
    b. NSAIDs
    c. Pregnancy
    d. Coarctation of the aorta
    e. COCP
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24
Q

What are the presenting symptoms of Hypertension?

A
  1. Often asymptomatic
  2. If secondary, symptoms of the cause
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25
Q

What are the symptoms of hypertension if > 200/120 mmHg?

A

Headaches
Visual disturbance
Seizures

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26
Q

What are the signs of Hypertension on physical examination?

A

BP: measure on two to three different occasions before diagnosing hypertension and record lowest reading (>140/90mmHg)
Longstanding hypertension: retinopathy (retinal vascular changes)

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27
Q

What is the Keith–Wagner classification of retinopathy?

A

(I) ‘silver wiring’
(II) as above, plus arteriovenous nipping
(III) as above, plus flame haemorrhages and cotton wool exudates
(IV) as above, plus papilloedema

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28
Q

What are the investigations for Hypertension?

A
  1. 24 h blood pressure
    Ensure no end organ damage:
  2. Fundoscopy: to check for hypertensive retinopathy
  3. Urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
  4. ECG: to check for left ventricular hypertrophy or ischaemic heart disease
    Co-morbidities, Q-RISK:
  5. HbA1c
  6. Lipids
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29
Q

How is hypertension staged?

A
  1. Stage 1:
    Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
  2. Stage 2:
    Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
  3. Severe hypertension:
    Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg
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30
Q

What is the lifestyle management of hypertension?

A
  1. A low salt diet is recommended, aiming for less than 6g/day
  2. Caffeine reduction
  3. Smoking cessation
  4. Less alcohol
  5. Lose weight
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31
Q

What is the management of Stage 1 hypertension (>140/90)?

A
  1. Antihypertensives if:
    < 80 years of age AND any of the following apply;
    a. target organ damage
    b. established cardiovascular disease
    c. renal disease
    d. diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
  2. Consider anti-hypertensives: in addition to lifestyle advice for adults <60 with stage 1 hypertension and an estimated 10-year risk below 10%
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32
Q

What is the management of stage 2 hypertension?

A

Offer drug treatment

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33
Q

What is the management of hypertension in patients < 40 years?

A

Referral to exclude secondary causes

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34
Q

What is the first step of anti-hypertensive treatment?

A
  1. If < 55-years-old or T2DM: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB)
  2. If ≥ 55-years-old or black/ African- Caribbean: Calcium channel blocker
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35
Q

What is the second step of anti-hypertensive treatment?

A
  1. If already on ACE-i or ARB: add a Calcium channel blocker or a thiazide-like Diuretic
  2. If already on Calcium channel blocker: add an ACE-i or ARB (preferred in black/ African-Carribeans) or a thiazide-like Diuretic
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36
Q

What is the third step of anti-hypertensive treatment?

A

Add a third drug:
usually a thiazide diuretic

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37
Q

What is the final step of anti-hypertensive management?

A
  1. NICE define step 4 as resistant hypertension and suggest either adding a 4th drug or seeking specialist advice
  2. First confirm elevated clinic BP with ABPM or HBPM
    assess for postural hypotension
  3. Discuss adherence
  4. If potassium < 4.5 mmol/l: add low-dose spironolactone
  5. If potassium > 4.5 mmol/l add an alpha- or beta-blocker
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38
Q

What are the target blood pressures for patients on anti-hypertensives?

A
  1. Age < 80 years:
    Clinic: 140/90 mmHg
    ABPM: 135/85 mmHg
  2. Age > 80 years:
    Clinic: 150/90 mmHg
    ABPM: 145/85 mmHg
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39
Q

What is the most common cause of secondary hypertension?

A

Primary hyperaldosteronism

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40
Q

What is Mitral Regurgitation?

A

The retrograde flow of blood from LV to left atrium during systole (second most common valve disease after aortic stenosis)

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41
Q

What is the aetiology of mitral regurgitation?

A
  1. Regurgitation leads to a less efficient heart as less blood is pumped through the body with each contraction
  2. As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time
  3. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myocardium becomes less efficient, and eventually go into irreversible heart failure
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42
Q

What are the causes of mitral regurgitation?

A
  1. Post- coronary artery disease or post-MI
  2. Mitral valve prolapse: deformity of the mitral valve leaflets: valve does not close properly and allows backflow
  3. Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly
  4. Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves
  5. Congenital
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43
Q

What are the risk factors for mitral regurgitation?

A
  1. Female sex
  2. Lower body mass
  3. Age
  4. Renal dysfunction
  5. Prior MI
  6. Prior mitral stenosis or valve prolapse
  7. Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome
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44
Q

What are the symptoms of mitral regurgitation?

A
  1. Largely asymptomatic
  2. Symptoms develop later due to failure of the left ventricle, arrhythmias or pulmonary hypertension
  3. Presents as fatigue, shortness of breath and oedema
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45
Q

What are the signs of mitral regurgitation on examination?

A
  1. Pansystolic murmur described as “blowing”
  2. It is heard best at the apex and radiating into the axilla
  3. S1 may be quiet as a result of incomplete closure of the valve
  4. Severe MR may cause a widely split S2
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46
Q

What are the investigations for mitral regurgitation?

A
  1. ECG: may show a broad P wave, indicative of atrial enlargement
  2. CXR: Cardiomegaly may be seen with an enlarged left atrium and ventricle
  3. Echocardiography: crucial to diagnosis and to assess severity*
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47
Q

What is the investigation of choice for diagnosis of mitral regurgitation?

A

Transthoracic echocardiogram: visualises presence and severity of MR

48
Q

What is the management of mitral regurgitation?

A
  1. Acute cases: nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
  2. If patients are in heart failure: ACE inhibitors may be considered along with beta-blockers and spironolactone
  3. In acute, severe regurgitation: surgery is indicated (repair > replacement)
49
Q

What is the surgical management of mitral regurgitation?

A
  1. The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates
  2. When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
50
Q

What is a common complication of mitral regurgitation?

A

Heart failure: Echo every 6–12 months for moderate–severe MR to assess the LV ejection fraction and end-systolic dimension

51
Q

What is mitral valve prolapse?

A
  1. Common, occurring in around 5-10 % of the population
  2. It is usually idiopathic but can be caused by cardiovascular conditions (cardiomyopathy) or connective tissue disorders (Marfan’s, Ehlers-Danlos Syndrome)
52
Q

What are the features of a mitral valve prolapse?

A
  1. May have atypical chest pain or palpitations
  2. Mid-systolic click (occurs later if patient squatting)
  3. Late systolic murmur (longer if patient standing)
  4. Complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death
53
Q

What is Mitral Stenosis?

A
  1. The mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle
  2. This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart
54
Q

What is the most common cause of mitral stenosis?

A

Rheumatic fever!

55
Q

What are the rarer causes of mitral stenosis?

A
  1. Congenital mitral stenosis
  2. SLE, rheumatoid arthritis, amyloidosis, carcinoid
  3. Endocarditis
  4. Atrial myxoma (rare cardiac tumour)
56
Q

What is the epidemiology of Mitral Stenosis?

A
  1. Incidence is declining because of declining incidence of rheumatic fever
  2. Women are 3x more likely than men
57
Q

What are the presenting symptoms of mitral stenosis?

A
  1. May be asymptomatic
  2. Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea)
  3. May have palpitations (related to AF)
  4. Malar flush: facial skin changes
  5. Later, rarer symptoms:
    a. Cough
    b. Haemoptysis
    c. Hoarseness caused by compression of the left
    laryngeal nerve by an enlarged left atrium
58
Q

Why do patients experience dyspnoea and haemoptysis in mitral stenosis?

A
  1. Dyspnoea:
    ↑ left atrial pressure → pulmonary venous hypertension
  2. Haemoptysis:
    a. Due to pulmonary pressures and vascular congestion
    b. May range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
59
Q

What are the signs of mitral stenosis on physical examination?

A
  1. May have peripheral or facial cyanosis: Malar flush
  2. Pulse:
    a. May be ‘thready’ or irregularly irregular (AF)
    b. Low volume
  3. Palpation:
    a. Apex beat is undisplaced and tapping
    b. Parasternal heave (right ventricular hypertrophy and pulmonary hypertension)
  4. Auscultation:
    a. Loud first heart sound with opening snap
    b. Mid-diastolic murmur best heard in expiration (LEFT side)
  5. Evidence of pulmonary oedema on lung auscultation (if decompensated)
60
Q

What are the features of severe mitral stenosis on examination?

A
  1. Length of murmur increases
  2. Opening snap becomes closer to S2
61
Q

What are the appropriate investigations for Mitral Stenosis?

A
  1. ECG:
    a. May be normal
    b. Broad bifid p wave (p mitrale) caused by left atrial hypertrophy
    c. AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension
  2. CXR:
    a. Double right heart border: indicating enlarged left atrium b. Cardiomegaly
    c. Pulmonary congestion
    d. Kerley B lines (interstitial oedema)
    e. Mitral valve may be calcified in rheumatic cases
  3. Transthoracic/ Transoesophageal (better visualisation) echo:
    To assess functional and structural impairments: hockey stick-shaped mitral deformity
62
Q

What is the management of mitral stenosis?

A
  1. Asymptomatic patients:
    a. Monitored with regular echocardiograms
    b. Percutaneous/surgical management is generally not recommended
  2. Symptomatic patients:
    a. Percutaneous mitral balloon valvotomy
    b. Mitral valve surgery (commissurotomy, or valve replacement)
63
Q

What is the management of AF in mitral stenosis?

A
  1. Require anticoagulation
  2. Currently warfarin is still recommended for patients with moderate/severe MS
  3. Emerging consensus that direct-acting anticoagulants (DOACs) may be suitable for patients with mild MS who develop atrial fibrillation
64
Q

What is the main complication of mitral stenosis?

A

Due to increased left atrium pressure, the main complication in pulmonary hypertension and left atrial enlargement

65
Q

What is Pulmonary Hypertension?

A

A consistently increased pulmonary arterial pressure (>20mmHg) under resting conditions

66
Q

What is the aetiology of Pulmonary Hypertension?

A
  1. Primary: Idiopathic
  2. Secondary:
    a. Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/thrombosis)
    b. Chronic lung disease (COPD)
    c. Recurrent pulmonary emboli
    d. Increased pulmonary blood flow (atrial/ ventricle septal defect, patent ductus arteriosus)
    e. Connective tissue disease (e.g. SLE, systemic sclerosis)
67
Q

What is the epidemiology of Pulmonary Hypertension?

A
  1. Primary pulmonary hypertension is rare and usually seen in young females
  2. Age 20-50 years
68
Q

What are the presenting symptoms of Pulmonary Hypertension?

A
  1. Main symptom: dyspnoea
  2. Chest pain
  3. Syncope
  4. Tiredness
  5. Symptoms of the underlying cause (e.g. chronic cough)
69
Q

What are the signs of Pulmonary Hypertension on physical examination?

A
  1. Raised JVP (Prominent a wave in the JVP waveform)
  2. Palpation:
    a. Left parasternal heave (right ventricular hypertrophy)
  3. Auscultation:
    a. Loud pulmonary component of S2 (S3/S4 may be heard)
    b. Mitral stenosis/ tricuspid regurgitation
  4. Right sided HF in severe cases
70
Q

What are the appropriate investigations for Pulmonary Hypertension?

A
  1. CXR:
    a. Cardiomegaly (right ventricular enlargement, left atrial dilation)
    b. Prominent main pulmonary arteries (which taper rapidly)
    c. Signs of the cause (e.g. COPD, calcified mitral valves)
  2. ECG:
    a. Right ventricular hypertrophy (right-axis deviation)
    b. Right atrial enlargement (peaked P wave ‘P pulmonale’)
  3. Echocardiography:
    a. Pulmonary artery systolic pressure (sPAP) is = right ventricular systolic pressure in the absence of pulmonic valve stenosis and outflow tract obstruction
    b. Right ventricular and right atrial dilation
    c. Pericardial effusion
  4. Cardiac catheterization
71
Q

Which investigation is required to confirm the presence of pulmonary hypertension?

A

Cardiac catheterization:
1. Mean pulmonary arterial pressure >25 mmHg at rest or >30 mmHg with exercise
2. Assess severity, right heart pressures and response to vasodilators

72
Q

What is the management of pulmonary hypertension?

A
  1. Treat the underlying cause e.g. mitral valve replacement, COPD
  2. Number of medications:
    a. Epoprostenol (by continuous intravenous infusion)
    b. Iloprost (inhaled)
    c. Sildenafil (oral)
73
Q

What is Supraventricular Tachycardia?

A

An abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart (atria or AVN)

74
Q

What are SVT episodes?

A
  1. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT)
  2. Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias
75
Q

What are the more common types of SVT?

A
  1. Atrial fibrillation
  2. Paroxysmal supraventricular tachycardia (PSVT)
  3. Atrial flutter
  4. Wolff–Parkinson–White syndrome
76
Q

What is the aetiology of Supraventricular Tachycardia?

A
  1. It can occur in healthy people, although often there is underlying cardiac pathology
  2. Associated conditions include cardiomyopathies, ischaemic heart disease, previous cardiac surgery, and hyperthyroidism
  3. Exogenous stimulants can also cause SVT such as amphetamines, cocaine, and acute alcohol intoxication
77
Q

What are the symptoms of Supraventricular Tachycardia?

A
  1. May come and go suddenly, and can last anywhere from a few minutes to a few days
  2. Rapid heartbeat (palpitations)
  3. Dyspnoea
  4. Fatigue
  5. Weakness
  6. Lightheadedness or dizziness, sweating
  7. Pounding sensation in the neck
  8. Syncope or near fainting
    (Some people have no symptoms at all)
78
Q

What are the signs of Supraventricular Tachycardia on physical examination?

A

Heart rate ≥100 bpm
Rales (rattling sound in lungs), oedema

79
Q

What are the investigations for Supraventricular Tachycardia?

A
  1. ECG: regular tachycardia that does not vary in rate, P waves may be unusual (or not present)
  2. CXR: abnormalities suggestive of cardiac disease e.g. cardiomegaly that would predispose to arrhythmias
  3. Bloods:
    a. U&Es: electrolyte imbalance
    b. Toxicology screen: identify cause e.g. amphetamines
    c. Digoxin level
    c. TFTs: hyperthyroidism
  4. Echocardiogram: may show underlying cause such as valvular disease or cardiomyopathy
80
Q

What is the management of acute SVT?

A
  1. Vagal manoeuvres:
    a. Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
    b. Carotid sinus massage
  2. Intravenous adenosine:
    a. Rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
    b. Contraindicated in asthmatics - verapamil is a preferable option
  3. Electrical cardioversion
81
Q

What is the prevention management for SVT?

A
  1. Beta-blockers
  2. Radio-frequency ablation of accessory pathway
82
Q

What is the management of sinus bradycardia?

A

Atropine sulfate: 500mcg IV

83
Q

What is Tricuspid Regurgitation?

A

The backflow of blood from the right ventricle to the right atrium during systole

84
Q

What are the causes of tricuspid regurgitation?

A
  1. Right ventricular infarction
  2. Pulmonary hypertension e.g. COPD
  3. Rheumatic heart disease
  4. Infective endocarditis (especially IVDU)
  5. Ebstein’s anomaly: congenital heart defect from Lithium exposure in utero
  6. Carcinoid syndrome
85
Q

What is the most common cause of Tricuspid Regurgitation?

A

Infective endocarditis

86
Q

What are the presenting symptoms of Tricuspid Regurgitation?

A
  1. Fatigue
  2. Dyspnoea
  3. Palpitations
  4. Headaches
  5. Nausea
  6. Anorexia
  7. Lower limb swelling
87
Q

What are the additional features of tricuspid regurgitation?

A

Symptoms due to gut congestion related to reduced cardiac output and associated with right-sided heart failure:
a. Epigastric pain made worse by exercise
b. Early satiety
c. Dyspepsia
d. Indigestion
e. Jaundice/ hepatomegaly

88
Q

What are the signs of tricuspid regurgitation?

A
  1. Pan-systolic murmur (louder on inspiration)
  2. Prominent/giant V waves in JVP: caused by transmission of right ventricular pressure to the great veins
  3. Pulsatile hepatomegaly
  4. Left parasternal heave: RVH
89
Q

What are the appropriate investigations for Tricuspid Regurgitation?

A
  1. Bloods:
    a. FBC: thrombocytopenia (e.g., due to liver failure and cirrhosis)
    b. LFTs: patients with chronic severe TR often develop ascites from advanced liver disease, from chronic congestion or fibrosis (cardiac cirrhosis)
    c. Blood cultures: IE
  2. ECG:
    a. Tall P wave (right atrial hypertrophy) if in sinus rhythm
    b. Changes indicative of other cardiac disease (may show atrial flutter/fibrillation; presence of previous MI)
  3. CXR:
    a. Right-sided enlargement of cardiac shadow
    b. Pleural or pericardial effusion
    c. Presence of pacemaker
  4. Echocardiography:
    a. Extent of regurgitation estimated by colour flow Doppler
    b. May be able to detect tricuspid valve abnormality (e.g. prolapse)
90
Q

What are Varicose Veins?

A

They are subcutaneous, permanently dilated veins 3 mm or more in diameter when measured in a standing position; however, they may not be visible

91
Q

What is the aetiology of Varicose Veins?

A

Venous valve incompetence is the most common aetiology
Predisposing factors include:
a. Gender
b. Pregnancy
c. Occupation (with prolonged standing)

92
Q

What is the epidemiology of Varicose Veins?

A
  1. Generally, prevalence rates are higher in industrialised countries and in more developed regions
  2. Prevalence increases with age
  3. Greater prevalence in women than in men
93
Q

What are the presenting symptoms of Varicose Veins?

A
  1. Visible bulges in legs
  2. Leg fatigue or aching with prolonged standing (not present at the beginning fo the day)- improves with elevation
  3. Nocturnal leg cramps
  4. Restless legs
  5. Itching
  6. Ankle swelling
  7. Overlying skin changes: Lipodermatosclerosis: redness, swelling, and a tapering of the legs above the ankles
94
Q

What are the signs of Varicose Veins on physical examination?

A
  1. Dilated tortuous veins: examine the patient standing
  2. Lipodermatosclerosis: indication of high risk for ulceration and is the result of haemosiderin (venous HTN)
    a. Causes inflammation and damaging the soft tissues
    b. This leads to scarred and fibrotic tissues
  3. Ulceration
95
Q

What are the appropriate investigations for Varicose Veins?

A
  1. Tourniquet test (Trendelenburg): when patient stands the veins do not fill
  2. Duplex ultrasond:
    a. Two sound heard, when the blood flows up the vein when the calf is squeezed and then when released the blood that flows back down the incompetent vein
    b. Assesses for reversed flow;
    -valve closure time >0.5 second is indicative of reflux
    -valve closure time >1.0 second is indicative of reflux in the deep system
    This can also be used to exclude DVT
96
Q

What is the management of Varicose Veins?

A

Tnterventional treatment:
a. Endovenous ablation
b. Foam sclerotherapy
c. Phlebectomy- removal of the veins
d. Open surgery (stripping and ligation)
If interventional treatment is unsuitable e.g. pregnant : Compression stockings

97
Q

What is the first line option for varicose veins if the superficial axial system is involved?

A
  1. Superficial axial system: the great saphenous vein, the small saphenous vein, or the anterior accessory saphenous vein
  2. Endovenous thermal ablation (radiofrequency or laser ablation) is first line
98
Q

What are the complications of Varicose Veins?

A
  1. Chronic venous insufficiency: Increased dilation of venous system leading to axial system reflux
  2. Erosion of varices can lead to haemorrhage (low risk)
  3. Venous ulceration
  4. Lipodermatosclerosis: Haemosiderin deposition, capillaries become elongated, fibrotic, and leaky
99
Q

What is the prognosis of Varicose Veins?

A
  1. Generally resolution of symptoms occurs in >95% of patient who are treated
  2. However, patients need to be counselled that new varicosities will very likely occur with time, as varicose veins are a progressive disease
100
Q

Where do most Varicose Veins occur?

A
  1. Long saphenous vein: groin to the medial aspect of the lower leg
  2. Short saphenous vein: popliteal fossa along the calf to the lateral malleolus
101
Q

What are the indications for surgical treatment of Varicose Veins?

A
  1. Oedema
  2. Skin changes: Lipodermatosclerosis
  3. Venous eczema and ulceration
102
Q

What is Vasovagal syncope?

A
  1. A particular type of reflex syncope also known as the common faint
  2. Generally considered to encompass faints triggered by emotional upset, fear, and pain, as well as those occurring in less well-defined circumstance
103
Q

What is the aetiology of syncope?

A

Syncope has many possible causes commonly grouped in 3 main groups:
1. Neurally-mediated reflex syncopal syndromes (vasovagal): most common
2. Orthostatic
3. Cardiovascular

104
Q

What are the causes of Reflex syncope (neurally mediated)?

A
  1. Vasovagal: triggered by emotion, pain or stress (often referred to as ‘fainting’)
  2. Situational: cough, micturition, gastrointestinal
  3. Carotid sinus syncope
105
Q

What are the causes of Orthostatic syncope?

A
  1. Primary autonomic failure: Parkinson’s disease, Lewy body dementia
  2. Secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  3. Urug-induced: diuretics, alcohol, vasodilators
  4. Volume depletion: haemorrhage, diarrhoea
106
Q

What are the causes of Cardiac syncope?

A
  1. Arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
  2. Structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
  3. Others: pulmonary embolism
107
Q

What is the epidemiology of Syncope?

A
  1. Reflex syncope is the most common cause in all age groups
  2. Orthostatic and cardiac causes become progressively more common in older patients
108
Q

What are the features of Vasovagal syncope?

A
  1. Pallor
  2. Diaphoresis: sensation of feeling sweaty and experiencing a coldness and/or clammy sensation
  3. Fatigue after episode
  4. Bradycardia
109
Q

What are the investigations for syncope?

A
  1. Cardiovascular examination
  2. Postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
  3. ECG
  4. Vagal manoeuvres for SVT: e.g. carotid sinus massage
  5. Tilt table test: is it posture related?
  6. 24 hour ECG
  7. Others: hypoglycaemia, d-dimer for PE, cardiac enzymes
110
Q

What is Wolff-Parkinson-White syndrome?

A
  1. Caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)
  2. As the accessory pathway does not slow conduction: AF can degenerate rapidly to VF (most serious cardiac rhythm)
111
Q

What are the associated conditions with Wolff-Parkinson-White syndrome?

A

Congenital conditions:
1. Ebstein’s anomaly: strong RF
2. Hypertrophic cardiomyopathy
3. Mitral valve prolapse
4. Atrial/ ventricular septal defect
5. Marfan’s
Thyrotoxicosis

112
Q

What are the presenting symptoms of Wolff-Parkinson-White syndrome?

A
  1. Palpitations (form of SVT)
  2. Dizziness
  3. Dyspnoea
  4. Chest pain
  5. Syncope (uncommon)
113
Q

What are the signs of Wolff-Parkinson-White syndrome on physical examination?

A

Arrhythmia:
1. Most common: atrioventricular re-entrant tachycardia (AVRT)- 70-80%
2. Atrial fibrillation (irregularly irregular)
3. Atrial flutter

114
Q

What is the investigation of choice for Wolff-Parkinson-White syndrome?

A

ECG:
1. Short PR interval
2. Wide QRS complexes with a slurred upstroke - ‘delta wave’
3. Left axis deviation if right-sided accessory pathway (majority)
4. Right axis deviation if left-sided accessory pathway
Can offer cardiac electrophysiology to determine pathway

115
Q

How can right and left sided pathways in Wolff-Parkinson-White syndrome be differentiated?

A
  1. Type A (left-sided pathway): dominant R wave in V1
  2. Type B (right-sided pathway): no dominant R wave in V1 (more common)
116
Q

What is the definitive management of Wolff-Parkinson-White syndrome?

A

Radiofrequency ablation of the accessory pathway

117
Q

What is the medical management of Wolff-Parkinson-White syndrome?

A
  1. Sotalol: avoid if coexistent AF: can deteriorate to VF
  2. Amiodarone
  3. Flecainide

!Final Year (26 decks)

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