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Year 3 ICSM Sofia > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is an abdominal aortic aneurysm?

A

An unruptured AAA is > 3cm across.

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2
Q

What are aneurysms of the arteries?

A

An artery with a dilatation >50% of it’s original diameter .

True aneurysms are abnormal dilatations that involve all layers of the arterial wall.

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3
Q

What are the causes of an abdominal aortic aneurysm?

A
  • Atheroma
  • Trauma
  • Infection, e.g. mycotic aneurysm in endocarditis, tertiary syphillis
  • Connective tissue disorders (e.g. Marfan’s, Ehler’s-Danlos)
  • Inflammatory e.g. Takayasu’s aortitis
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4
Q

What are the complications of an abdominal aortic aneurysm?

A
  • Rupture
  • Thrombosis
  • Embolism
  • Fistulae
  • Pressure on other structures
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5
Q

What are the symptoms of a ruptured abdominal aortic aneurysm?

A
  • Intermittent or continuous abdominal pain (radiates to the back, iliac fossae or groans)
  • Collapse
  • Expansile abdominal mass (expands and contracts)
  • Shock
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6
Q

What are the symptoms of an unruptured aortic aneurysm?

A

Often none

- Might cause abdominal/back pain, often discovered incidentally on abdominal examination

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7
Q

What tests help identify the size, and rate of growth of an aneurysm?

A
  • Abdominal ultrasound
  • CT
  • Echocardiogram
  • Angiogram
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8
Q

What is an aortic dissection?

A

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

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9
Q

What is the aetiology of aortic dissection?

A

Degenerative changes in the smooth muscle of the aortic media are the predisposing event

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10
Q

What are the risk factors of aortic dissection?

A
  • Hypertension
  • Aortic atherosclerosis
  • Connective tissue disease (e.g. SLE, Marfan’s, Ehlers-Danlos)
  • Congenital cardiac abnormalities (e.g. aortic coarctation)
    Aortisis
  • Iatrogenic
  • Trauma
  • Crack Cocaine
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11
Q

How does the Stanford classification categorise aortic dissection?

A

Type A= ascending aortic tear (most common)

Type B= descending aorta tear distal to the left subclavian artery

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12
Q

What is the epidemiology of aortic dissection?

A

Most common in males between 40 and 60 years

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13
Q

What are the presenting symptoms of aortic dissection?

A

Sudden central ‘tearing’ pain which may radiate to the back (might mimic an MI)
Aortic dissection can lead to occlusion of the aorta and its branches

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14
Q

What are the symptoms of aortic dissection when the carotid is obstructed?

A
  • Hemiparesis
  • Dysphasia
  • Blackout
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15
Q

What are the symptoms of aortic dissection when the coronary artery is obstructed?

A

Chest pain (angina or MI)

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16
Q

What are the symptoms of aortic dissection when the subclavian is obstructed?

A
  • Ataxia

- Loss of consciousness

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17
Q

What are the symptoms of aortic dissection when the anterior spinal artery is obstructed?

A

Paraplegia

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18
Q

What are the symptoms of aortic dissection when the coeliac is obstructed?

A

Severe abdominal pain (ischaemic bowel)

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19
Q

What are the symptoms of aortic dissection when the renal artery is obstructed?

A
  • Anuria

- Renal failure

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20
Q

What are the signs of aortic dissection of physical examination?

A

Murmur on the back below left scapula, descending to abdomen
BP: Hypertension (discrepancy between arms of >20mmHg), wide pulse pressure. If hypotensive, may signify tamponade, check for pulsus paradoxus
Aortic insufficiency: Collapsing pulse, early diastolic murmur over aortic area.
Unequal arm pulses
Might be palpable abdominal mass

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21
Q

What are the investigations for aortic dissection?

A

Bloods: FBC, U&E , clotting
CXR: Widened mediastinum, localised bulge in aortic arch
ECG: Often normal, signs of ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery
CT-Thorac: False lumen of dissection may be visualsed
Echocardiography: transoesopharangeal is highly specific
Cardiac Catheterization and aortography

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22
Q

What is aortic regurgitation?

A

Reflux of blood from aorta into left ventricle during diastole.
Also called aortic insufficiency

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23
Q

What is the aetiology of aortic regurgitation?

A
  • Aortic valve leaflet abnormalities or damage

- Aortic root/ascending aorta dilation

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24
Q

What causes aortic valve leaflet abnormalities or damage leading to aortic regurgitation?

A
  • Bicuspid aortic valve
  • Infective endocarditis
  • Rheumatic fever
  • Trauma
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25
Q

What causes aortic root/ascending aorta dilation leading to aortic regurgitation?

A
  • Systemic hypertension
  • Aortic dissection
  • Aortitis
  • Arthritides
  • Marfan’s syndrome
  • Ehler’s-Danlos syndrome
  • Osteogenesis imperfecta
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26
Q

What is the epidemiology of aortic regurgitation?

A

Chronic AR often begins in the late 50s, documented frequently over 80 years

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27
Q

What are the presenting symptoms of aortic regurgitation?

A

Chronic AR:
Initially asymptomatic. Later, symptoms of heart failure: exertional dyspnoea, orthopnoea, fatigue. Occasionally angina
Severe acute AR:
Sudden cardiovascular collapse
Symptoms related to the aetiology:
E.g. chest or back pain in patients with aortic dissection

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28
Q

What are signs of aortic regurgitation on examination?

A

Collapsing ‘water-hammer’ pulse and wide pulse pressure. Thrusting and heaving (volume-loaded) displaced apex beat.

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29
Q

How is an early diastolic murmur heard in AR?

A

At lower left sternal edge.
Better head with the patient sitting forward with the breath held in expiration
An ejection systolic murmur is often heard because of increase flow across the valve

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30
Q

How is an Austin Flint- mid-diastolic murmur head in AR?

A

Over the apex, from turbulent reflux hitting the anterior cusp of the mitral valve and causing physiological mitral stenosis

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31
Q

What rare signs are associated with a hyperdynamic pulse in AR?

A
  • Quincke’s sign: Visible pulsations on nail-bed
  • de Musset’s sign: Head nodding in time with pulse
  • Becker’s sign: Visible pulsation of the pupils and retinal arteries
  • Muller’s sign: Visible pulsations of the uvula
  • Corrigan’s sign: Visible pulsations in the neck
  • Traube’s sing: ‘Pistol shot’’ heard on auscultation of the femoral arteries
  • Duroziez’s sign: a systolic and diastolic bruit heard on partial compression of femoral artery with a stethoscope
  • Rosenbach’s sign: Systolic pulsations of the liver
    Gerhard’s sign: Systolic pulsations of the spleen
    Hill’s sign: Popliteal cuff systolic pressure exceeding brachial pressure by more than 60mmg
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32
Q

What are the investigations for aortic regurgitation?

A

CXR: Cardimegaly, dilatation of ascending aorta, signs of pulmonary oedema may be seen with left heart failure
ECG: May show signs of left ventricular hypertrophy (Deep S wave is in V1-2, tall R wave in V5-6, Inverted T waves in I, aVL, V5-6 and left axis deviation)
Echo:
Cardiac catheterization with angigraphy

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33
Q

What is aortic stenosis?

A

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

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34
Q

What is the aetiology of aortic stenosis?

A

1) Stenosis secondary to rheumatic heart disease (commonest worldwide)
2) Calcification of a congenital bicuspid aortic valve
3) Calcification/degeneration of a tricuspid aortic valve in the elderly

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35
Q

What is the epidemiology of aortic stenosis?

A
  • Prevalence in 3% of 75 year olds. Affects males more then females.
  • Those with bicuspid aortic valve may present earlier (as young adults)
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36
Q

What are the presenting symptoms of aortic stenosis?

A

May be asymptomatic initially.

  • Angina (because increased oxygen demand of the hypertrophies ventricles)
  • Syncope or dizziness on exercise
  • Symptoms of heart failure (e.g. dyspnoea)
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37
Q

What are the signs of aortic stenosis of physical examination?

A

BP: Narrow pulse pressure
Pulse: Slow-rising
Palpation: Thrill in aortic area (if severe). Forceful sustained thrusting undisplaced apex beat
Auscultation: Harsh ejection systolic murmur at aortic area, radiating to carotid artery and apex. Second heart sound may be softened or absent. Bicuspid valve may produce ejection click.

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38
Q

What are the investigations for aortic stenosis?

A

ECG: signs of left ventricular hypertrophy, LBBB
CXR: Enlargement of ascending aorta, calcification of aortic valve
Echo
Cardiac angiography: allows differentiation from other causes of angina

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39
Q

What are arterial ulcers?

A
  • Caused by poor perfusion to the lower extremities.
    The overlying skin and tissues are deprived oxygen, kill the tissues and causing the area to form an open wound.
    The lack of blood supply can result in minor scrapes or cutes, failing to heal and eventually developing into ulcers
  • Also known as ischaemic ulcers
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40
Q

What is aetiology of arterial ulcers?

A
  • Restrictions to blood vessels due to peripheral vascular disease
  • Chronic vascular insufficiency
  • Vasculitis
  • Diabetes mellitus
  • Renal failure
  • High blood pressure
  • Arteriosclerosis
  • Atherosclerosis
  • Trauma
  • Limited joint mobility
  • Increased age
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41
Q

What are the risk factors for arterial ulcers?

A
  • Diabetes mellitus
  • Foot deformity and callus formation resulting in focal areas of high pressure
  • Poor footwear that inadequately protects against high pressure and shear
  • Obesity
  • Absence of protective sensation due to peripheral neuropathy
  • Limited joint mobility
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42
Q

What are the signs of arterial ulcers on examination?

A
  • Ulcer with punched out appearance
  • Intensely painful
  • Gray or yellow fibrotic base and undermining skin margins
  • Pulses not palpable
  • Most common on distal ends of limbs
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43
Q

What is Curling’s ulcer?

A

Special type of ischaemic ulcer developing in duodenum after sever burns

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44
Q

What symptoms do arterial ulcers present with?

A
  • Pain in the extremity at rest and increased pain with elevation of the extremity and activity
  • Relief of symptoms with the extremity in a dependent position
  • Characteristic dependent rubor may be seen
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45
Q

What is the epidemiology of arterial ulcers?

A
  • Difficult to heal by basic would care and require advanced therapy
  • IF not taken care of in time, high chances that these may become infected and may need amputation
  • Individuals with history of previous ulcerations are 36 more likely to develop another ulcer
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46
Q

What investigations are used to diagnose arterial ulcers?

A
  • Arterial doppler
  • Pulse volume recordings
  • Radiographs to rule out osteomyelitis
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47
Q

What is atrial fibrillation?

A

Characterised by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: ‘permanent’, ‘persistent’ and ‘paroxysmal’

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48
Q

What is the aetiology of atrial fibrillation?

A

May be no identifiable cause in ‘lone’ atrial fibrillation. Secondary causes lead to abnormal atrial electrical pathways that results in AF?

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49
Q

What are the systemic causes of atrial fibrillation?

A
  • Thyrotoxicosis
  • Hypertension
  • Pneumonia
  • Alcohol
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50
Q

What are the risk factors in the heart of atrial fibrillation?

A
  • Mitral valve disease
  • Ischaemic heart disease
  • Rheumatic heart disease
  • Cardiomyopathy
  • Pericarditis
  • Sick sinus syndrome
  • Atrial myxoma
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51
Q

What are the risk factors in the heart of atrial fibrillation?

A
  • Bronchial carcinoma

- Pulmonary embolism

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52
Q

What is epidemiology of atrial fibrillation?

A

Very common in the elderly (approx 5% of those more than 65)
May be paroxysmal

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53
Q

What are the presenting symptoms of atrial fibrillation?

A
  • Often asymptomatic
  • Some patients experience palpitations or syncope
  • Symptoms of the cause of the AF
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54
Q

What are the signs of atrial fibrillation on examination?

A
  • Irregularly irregular pulse
  • Difference in apical beat and radial pulse
  • Look for thyroid disease and valvular heart disease
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55
Q

What are investigations for atrial fibrillation?

A

ECG: Uneven baseline with absent P waves, irregular QRS complexes. If saw-tooth baseline, consider if atrial flutter
Blood: Cardiac enzymes, TFT, lipid profile, U&E, Mg2+, Ca2+
Echo: To assess for mitral valve disease, left atrial dilation, left ventricular dysfunction of structural abnormalities

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56
Q

What is the management plan for atrial fibrillation?

A

Treat any reversible cause.

1) Rhythm control
2) Rate control
3) Stroke risk stratification

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57
Q

How is rhythm controlled for atrial fibrillation?

A

If the AF is over 48h from onset, anticoagulate (at least 3-4 weeks) before attempting cardioversion
DC cardioversion: synchronised DC shock
Chemical cardioversion: Flecainide (contraindicated if there is history of ischaemic heart disease) or amiodarone
Prophylaxis against AF: Sotalol, amioadarone or flecainide. Also consider providing ‘pill in the pocket’ strategy for suitable patients

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58
Q

How is rate controlled for atrial fibrillation?

A

Chronic ‘permanent’ AF: Ventricular rate control with digoxin, verapamil and/or beta-blockers. Aim for rate of 90/min

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59
Q

How is stroke risk stratification carried out in atrial fibrillation?

A

Low-risk patients can be managed with aspirin, and high risk-patients require anticoagulation with warfarin. Risk factors indicating high risk are previous thromboembolic event, age >75 years with hyppertension, diabetes or vascular disease, and/or clinical evidence of valve disease, heart failure or impaired left ventricular function

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60
Q

What are the possible complications of atrial fibrillation?

A
  • Thromboembolism (e.g. embolic stroke 4% risk per year, increased risk with left atrial enlargement or left ventricular dysfunction)
  • Worsens any existing heart failure
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61
Q

What is the prognosis of atrial fibrillation?

A

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

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62
Q

What is cardiac arrest?

A

Acute cessation of cardiac function

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63
Q

What is the aetiology of cardiac arrest?

A

4 H’s & 4 T’s
Hypoxia, Hypothermia, Hypovolaemia, Hypo- or hyperkalaemia
Tamponade, Tension pneumothorax, Thromboembolism, Toxins and other metabolic disorders (drugs, therapeutic agents and sepsis)

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64
Q

What are the signs of cardiac arrest on examination?

A
  • Unconscious
  • Patient is not breathing
  • Absent carotid pulses
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65
Q

What are the investigations for cardiac arrest?

A

Cardiac monitor: Classification of rhythm directs management
Bloods: ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose

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66
Q

What is a management plan for cardiac arrest?

A
  • Safety
  • BLS
  • ALS
  • Treatment of reversible causes
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67
Q

How are the reversible causes of cardiac arrest treated?

A

Hypothermia: warm slowly
Hypo-hyperkalaemia: correction of electrolytes
Hypovolaemia: IV colloids, crystalloids or blood products
Tamponade: Pericardiocentesis under xiphisternum up and leftwards
Tension pneumothorac: Needle into second intercostal space, mid-clavicular line
- Thromboembolism
- Toxins

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68
Q

What are the possible complications of cardiac arrest?

A
  • Irreversible hypoxic brain damage

- Death

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69
Q

What is the prognosis of cardiac arrest?

A
  • Resuscitation is less successful in the arrests that occur outside hispital
  • Duration of inadequate effective cardiac output is associate with poor prognosis
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70
Q

What is cardiac failure?

A

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

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71
Q

What is the aetiology of cardiac failure?

A 
Low output 
High output (increased demand)
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72
Q

What are the low output causes of cardiac failure?

A
  • Left heart failure: Ischaemic heart disease, hypertension, cardiomyopathy, aortic valve disease, mitral regurgitation
  • Right heart failure: Secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation constrictive pericarditis/pericardial tamponade
    Biventricular failure: Arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug toxicity
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73
Q

What are the high output causes of cardiac failure?

A
  • Anaemia
  • Berberi
  • Pregnancy
  • Paget’s disease
  • Hyperthyroidism
  • Arteriovenous malformation
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74
Q

What is the epidemiology of cardiac failure?

A

10% of over 65 year olds

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75
Q

What are the signs on examination for left cardiac failure?

A
  • Tachycardia
  • Tachypnoea
  • Displaced apex beat
  • Bilateral basal crackles
  • Third heart sound (‘gallop’ rhythm: rapid ventricular filling), pansystolic murmur (functional mitral regurgitation)
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76
Q

What are the signs on examination for right cardiac failure?

A
  • Raised JVP
  • Hepatomegaly
  • Ascites
  • Ankle/sacral pitting
  • Oedema
  • Signs of functional tricuspid regurgitation
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77
Q

What are the presenting symptoms of left cardiac failure?

A

Symptoms caused by pulmonary congestion

Dyspnoea, Othropnoea, paroxysmal nocturnal dyspnoea, fatigue

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78
Q

What are the presenting symptoms of right cardiac failure?

A
  • Swollen ankes
  • Fatigue
  • Increased weight (resulting from oedema)
  • Reduced exercise tolerance
  • Anorexia
  • Nausea
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79
Q

What are the investigations for cardiac failure?

A

Blood: FBC, U&Es, LFTs, CRP, glucose, lipids, TFTs
CXR: Cardiomegaly, prominent upper lobe vessels, pleural effusion, interstitial oedema (Kerley B lines), perihilar shadowing (bat’s wings), fluid in fissures
ECG: may be normal, may have ischaemic changes, arrhythmia, lvh
Echo: Assess ventricular contraction
Swan-Ganz catheter:

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80
Q

How is acute left ventricular failure managed?

A

Cardiogenic shock: severe cardiac failure with low BP requires the use of inotropes
Pulmonary oedema: sit up patient, 60-100% 02 and consider CPAP.

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81
Q

How is chronic left ventricular failure managed?

A 
Treat the cause e.g. hypertension. Treat exacerbating factors e.g. anaemia.
ACE-inhibitors 
B-blockers 
Loop Diuretics 
Aldosterone antagonists
Angiotensin receptor blockers 
Digoxin
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82
Q

What are the complications of cardiac failure?

A
  • Respiratory failure
  • Cardiogenic shock
  • Death
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83
Q

What is the prognosis of cardiac failure?

A

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

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84
Q

What is cardiomyopathy?

A

Primary disease of the myocardium

- Cardiomyopathy may be dilated, hypertrophic or restrictive

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85
Q

What is the aetiology for dilated cardiomyopathy?

A
  • Post-viral myocarditis
  • Alcohol
  • Drugs (doxorubicin, cocaine)
  • Familial
  • Thyrotoxicosis
  • Haemochromatosis
  • Peripartum
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86
Q

What is the aetiology for hypertrophic cardiomyopathy?

A
  • Up to 50% of cases are genetic with mutations in B-myosin, troponin T or a-tropomyosin (components of the contractile apparatus)
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87
Q

What is the aetiology for restrictive cardiomyopathy?

A
  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
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88
Q

What is the epidemiology of cardiomyopathy?

A

Prevalence of dilated and hypertrophic is 0.05-0.2%.

Restrictive is rare

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89
Q

What are the presenting symptoms of dilated cardiomyopathy?

A
  • Symptoms of heart failure
  • Arrhythmias
  • Thromboembolism
  • Family of sudden death
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90
Q

What are the presenting symptoms of hypertrophic cardiomyopathy?

A
  • Usually none
  • Syncope
  • Angine
  • Arrhythmia
  • Family history of sudden death
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91
Q

What are the presenting symptoms of restrictive cardiomyopathy?

A
  • Dyspnoea
  • Fatigue
  • Arrhythmia
  • Ankle
  • Abdominal swelling
    Enquire about family history of sudden death
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92
Q

What are the signs on examination of dilated cardiomyopathy?

A
  • Raised JVP
  • Displaced apex beat
  • Functional mitral and tricuspid regurgitations
  • Third heart sound
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93
Q

What are the signs on examination of hypertrophic cardiomyopathy?

A
  • Jerky carotid pulse
  • Double apex beat
  • Ejection systolic murmur
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94
Q

What are the signs on examination of restrictive cardiomyopathy?

A
  • Raised JVP (Kussmaul’s sign: further increase on inspiration)
  • Palpable apex beat
  • Third heart sound
  • Ascites
  • Ankle oedema
  • Hepatomegaly
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95
Q

What are the investigations for cardiomyopathy?

A 
CXR: may show cardiomegaly, and signs of heart failure 
ECG
Echo
Cardiac catheterization 
Endomyocardial biopsy 
Pedigree or genetic analysis
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96
Q

What is seen on an ECG for cardiomyopathy?

A

All types: Non-specific St changed, conduction defects, arrhythmias
Hypertrophic: Left axis-deviation, signs of left ventricular hypertrophy, Q waves in inferior and lateral leads
Restrictive: Low voltage complexes

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97
Q

What is seen on an Echocardiogram for cardiomyopathy?

A

Dilated: Dilated ventricles with global hypokinesia
Hypertrophic: Ventricular hypertrophy
Restrictive: Non-dilated non-hypoertrophied ventricles. Atrial enlargement.

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98
Q

What is constrictive pericarditis?

A

Medical condition characterised by a thickened, fibrotic pericardium limiting the heart’s ability to function normally.

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99
Q

What are the causes of constrictive pericarditis?

A
  • Tuberculosis
  • Incomplete drainage of purulent pericarditis
  • Fungal and parasitic infections
  • Chronic pericarditis
  • Postviral pericarditis
  • Postsurgical
  • Following MI, post-myocardial infarction
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100
Q

What are the presenting symptoms of constrictive pericarditis?

A
  • Fatigue
  • Swollen abdomen
  • Dyspnoea
  • Swelling of legs
  • General weakness
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101
Q

What are the signs of constrictive pericarditis on examination?

A
  • Raised JVP with inspiration (Kussmaul’s sign)
  • Pulsus paradoxus
  • Hepatomegaly
  • Ascites
  • Oedema
  • Pericardial knock (rapid ventricular filling
  • AF
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102
Q

What investigates are used for constrictive pericarditis?

A
  • CXR: pericardial calcification, pleural effusions
  • Echo
  • ECG
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103
Q

What is percutaneous coronary intervention and coronary angiography?

A

Non-surgical procedure used to treat the stenotic coronary arteries of the heart found in coronary heart disease.
A cardiologists feeds a deflated balloon on a catheter from the inguinal femoral artery or radial artery through blood vessels until the sit of blockage in the heart is reached.
Angioplasty involves inflating a balloon to open the artery and allow blood flow

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104
Q

What are the indications for coronary angiography and PCI?

A
  • Acute ST-elevation myocardial infarction
  • Non-ST elevation acute coronary syndrome
  • Unstable angina
  • Stable angine
  • Anginal equivalent (e.g. dyspnoea, arrhythmia, dizziness or syncope)
  • High risk stress test findings
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105
Q

What are the possible complications of coronary angiography and PCI?

A
  • Intramural haematoma
  • Perforation
  • Distal embolisation
  • Side branch occlusion
  • Access site bleeding
  • Atheroembolism
  • AKI
  • Stroke
  • Infection
  • Arrhythmia
  • Peripheral artery disease
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106
Q

What is a coronary artery bypass graft?

A

A surgical procedure aiming to restore normal blood flow to an obstructed coronary artery
The procedure involves the construction of one or more grafts between the arterial and coronary circulations

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107
Q

What are the indications for a coronary artery bypass graft?

A
  • Disease of the left main coronary artery
  • Disease of all three coronary vessels
  • Diffuse disease not amenable to treatment with a PCI
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108
Q

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

A
  • Postperfusion syndrome
  • Myocardial infarction
  • Acute renal failure
  • Vasoplegic sundrome
  • Pneumothorax
  • Haemothorax
  • Pleural effusion
  • Pericarditis
  • Post-operative atrial fibrillation and atrial flutter
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109
Q

What is DC cardioversion?

A

A medical procedure by which an abnormally fast heart rate (tachycardia) or cardiac arrythmia is converted to a normal rhythm using electricity or drugs

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110
Q

What are the indications for cardioversion?

A
  • Indicated in patients with disabling symptoms. In haemodynamically stable patients with preserved left ventricular function and no evident of hypokalaemia or hypomagnasaemia.
  • Atrial fibrillation, atrial flutter
  • Emergency situations to correct an abnormal rhythm when it is accompanied by faintness, low blood pressure, chest pain, difficulty breathing or loss of consciousness
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111
Q

What are the possible complications of cardioversion?

A
  • Dislodged blood clots: electric cardioversion can cause clots in the heart to move could result in a stroke. May need anticoagulation for several weeks beforehand to reduce risk.
  • Abnormal heart rhythm
  • Low blood pressure
  • Skin burns: from where the electrodes were placed
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112
Q

What is deep vein thrombosis?

A

The development of a blood clot in a major deep vein in the leg, thigh, pelvis or abdomen, which may result in impaired venous blood flow and consequent leg swelling and pain. DVT may also occur in the upper extremities or the brain.

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113
Q

What are the risk factors of deep vein thrombosis?

A
  • Medical hospitalisation within the past 2 months
  • Major surgery within 3 months
  • Active cancer
  • Lower-extremity trauma
  • Increasing age
  • Pregnancy
  • Obesity
  • Factory V Leiden
  • Protein C or S deficiency
  • Antithrombin deficiency
  • Antiphospholipid antibody syndrome
  • Medical comorbidity
  • Recent long-distance air travel
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114
Q

What is the epidemiology of deep vein thrombosis?

A
  • Incidence increased with age
  • Comparable in men and women with a slight female dominance in people under the age of 35 years
  • Incidence 10-15% higher in black people.
  • Hospital acquired DVT (DVT that occurs during hospitalisation or within 90 days of discharge) is common
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115
Q

What are the presenting symptoms of deep vein thrombosis?

A
  • Pain
  • Tenderness
  • Swelling
  • Warmth
  • Redness
  • Discolouration
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116
Q

What are the signs of deep vein thrombosis on examination?

A
  • Asymmetric oedema
  • Collateral superficial veins
  • Calf swelling
  • Localised pain along deep venous system
  • Phlegmasia curulea dolens
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117
Q

How is proximal DVT of the leg in non-pregnant patients managed?

A
  • Anticoagulation
  • Physical activity
  • Gradient stockings
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118
Q

How is distal DVT of the leg in non pregnant patients managed?

A
  • Serial imaging of the deep veins and/or anticoagulation
  • Physical activity
  • Gradient stockings
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119
Q

How are DVTs in pregnant patients managed?

A
  • Low molecular weight heparin or subcutaneous unfractionated heparin
  • Physical activity
  • Gradient stocks
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120
Q

What are the possible complications of deep vein thrombosis?

A
  • Pulmonary embolism
  • Acute bleeding during treatment
  • Heparin induced thrombocytopenia
  • Heparin resistance
  • Post-phlebitic syndrome
  • Delayed bleeding during treatment
  • Osteoporosis due to heparin treatment
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121
Q

What is the prognosis of deep vein thrombosis?

A
  • Whether a DVT is provoked or idiopathic is a significant determinant of recurrence
  • Extent and location of the initial clot influence the risk of post-phlebitic syndrome
  • When a patient dies from DVT, usually it is due to a pulmonary embolus or from a major haemorrhage as a complication of the anticoagulation therapy
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122
Q

What is Gangrene?

A

A complication of necrosis characterised by the decay of body tissues.
2 major categories:
- Infectious gangrene (wet gangrene)
- Ischaemic gangrene (dry gangrene)

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123
Q

What is the aetiology of gangrene?

A

May result from ischaemia, infection or trauma or a combination of these processed. Ischaemia may result from either arterial or venous comprosis, and may be an acute or chronic process.
Critically insufficient blood supply is the most common cause of gangrene and is often associated with diabetes and long term smoking

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124
Q

What are the risk factors of gangrene?

A
  • Diabetes mellitus
  • Atherosclerosis (ischaemic)
  • Smoking (ischaemic)
  • Renal disease
  • Drug and alcohol abuse
  • Malignancy
  • Trauma or abdominal surgery (infectious)
  • Contaminated wounds (infectious)
    Weak factors:
  • Malnutrition (infectious)
  • Hypercoagulable states (ischaemic)
  • Prolonged application of tourniquets (ischaemic)
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125
Q

What is the epidemiology of gangrene?

A
  • Occurs equally in men and women
  • Type I necrotising fasciitis occurs most commonly in patients with diabetes and patients with peripheral vascular disease
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126
Q

What are the presenting symptoms of gangrene?

A
  • Pain: history of chronic claudication-type pain in patients with ischaemic gangrene. A sudden onset of pain is usually the first symptoms of infectious gangrene
  • Oedema (ischaemic)
  • Skin discolouration: ecchymosis, purpura, skin blebs and haemorrhagic bullae
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127
Q

What are the signs of gangrene on examination?

A

Crepitus (gas gangrene): Gentle palpation may demonstrate crepitus

128
Q

How is ischaemic gangrene managed?

A
  • Intravenous heparin
  • Surgical revascularisation and amputation
  • Percutaneous transluminal angioplasty and amputation
  • Thrombolytic therapy
129
Q

How is gas gangrene managed?

A
  • Intensive supportive care, surgical debridement and amputation
  • Intravenous antibiotics
  • Hyperbaric oxygen therapy
130
Q

How is infectious gangrene managed?

A
  • Surgical debridement and intensive supportive care

- Empiric broad-spectrum antibiotics

131
Q

What is heart block?

A

Impairment of the atrioventricular node impulse conduction, as represented by the interval between P wave and QRS complex

132
Q

What is first degree heart block?

A

Prolonged conduction through the AV node

133
Q

What is second degree AV block?

A

Mobitz type I (Wenckebach): Progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node.
The cycle then begins again

134
Q

What is Mobitz type II heart block?

A

Intermittent or regular failure of conduction through the AV node.
Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)

135
Q

What is third degree (complete) AV block?

A

No relationship between atrial and ventricular contraction.
Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarisation within the ventricle (ventricular escape)

136
Q

What is the aetiology of heart block?

A
  • MI or ischaemic heart disease (most common cause)
  • Infection (e.g. rheumatic fever, infective endocarditis)
  • Drugs (e.g. digoxin, B-blockers, Ca channel antagonists)
  • Metabolic (e.g. hyperkalaemia, cholestatic jaundice, hypothermia)
  • Infiltration of conducting system (e.g. sarcoidosis, cardiac neoplasms, amyloidosis)
  • Degeneration of the conducting system)
137
Q

What is the epidemiology of heart block?

A

Majority of the 250,000 pacemakers implanted are for heart block

138
Q

What are the presenting symptoms of heart block?

A

First degree: Asymptomatic
Wenckebach: Usually asymptomatic
Mobitz type II & third degree: May cause Strokes-Adams attacks (syncope caused by ventricular asystole) Other presentations include dizziness, palpitations, chest pain and heart failure

139
Q

What are the signs of heart block on examination?

A

Often normal. Examine for signs of the cause

  • Complete heart block: Slow large volume pulse: JVP may show ‘cannon waves’
  • Movitz type II and third degree: Signs of reduced cardiac output (e.g. hypotension, heart failure)
140
Q

What are the appropriate investigations for heart block (1st, 2nd, 3rd degree)?

A

ECG (Consider ambulatory Holter or 24h)
Look for other signs of causes.e.g. ischaemia:
CXR: cardiac enlargement, pulmonary oedema
Blood: TFT, digoxin level, cardiac enzymes, troponin
Echocardiogram: Wall motion abnormalities, aortic valve disease, vegetations

141
Q

What are the ECG appearances of first degree heart block?

A

Prolonged PR interval (>0.2s)

142
Q

What are the ECG appearances of Mobitz type 1 (Wenkebach) heart block?

A

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

143
Q

What are the ECG appearances of Mobitz type 2 heart block?

A

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

144
Q

What are the ECG appearances of third degree (complete) heart block?

A

No relationship between P waves and QRS complexes. If QRS initiated by focus in the bundle of His, the QRS is narrow. QRS initiated more distally are wide and slow rate (30 beats/min)

145
Q

How is chronic heart block managed?

A

Permanent pace maker (PPM) insertion is recommended in patients with third degree heart block, advanced Mobitz type II and symptomatic Mobitz type I

146
Q

How is acute heart block (e.g. secondary to anterior MI) managed?

A

If associated with clinical deterioration, IV atropine and consider temporary (external) pacemaker

147
Q

What are the complications of heart block?

A
  • Asystole
  • Cardiac arrest
  • Heart failure
  • Complications of any pacemaker inserted
148
Q

What is the prognosis of heart block?

A

Mobitz type II and third-degree block usually indicate serious underlying cardiac disease

149
Q

What is hypertension?

A

Defined as systolic BP over 140mmHg and/or diastolic BP over 85mmHg, measured on three separate occasions
Malignant hypertension is defined as BP over 200/130 mmHg

150
Q

What is the aetiology of primary hypertension?

A

Essential or idiopathic hypertension (Commonest, over 90% of cases)

151
Q

What is the aetiology of secondary hypertension?

A

Renal: Renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure
Endocrine: Diabetes mellitus, hyperthyroidism, Cushing’s syndrome, Conn’s syndrome, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly
Cardiovascular: Aortic coarctation, increased intravascular volume
Drugs: Sympathomimetics, corticosteroids, oral contraceptive pill
Pregnancy: Pre-eclampsia

152
Q

What is the epidemiology of hypertension?

A

Very common

10-20% of adults in the Western World

153
Q

What are the presenting symptoms of hypertension?

A
  • Often asymptomatic
  • Symptoms of complications
  • Symptoms of cause
    Accelerated or malignant hypertension: Scotomas (visual field loss), blurred vision, headache, seizures, nausea, vomiting, acute heart failure
154
Q

What are the signs of hypertension on examination?

A

Measure on two or three different occasions before diagnosing hypertension and record lowest reading

  • May be loud second heart sound, fourth heart sound
  • Examine for causes e.g. radiofemoral delay (aortic coarctation, renal artery bruit (renal artery stenosis). Examine for end-organ damage e.g. fundoscopy for retinopathy
155
Q

What is the Keith-Wagner classification of retinopathy?

A

1) Siver wiring
2) As above, plus arteriovenous nipping
3) As above, plus flame haemorrhages and cotton wool exudates
4) As above, plus papilloedema

156
Q

What is the pathogenesis of hypertension?

A

Fibrotic intimal thickening of arteries, reduplication of elastic lamina and smooth muscle hypertrophy. Arteriolar wall layers replaced by pick hyaline material with luminal narrowing (hyaline arteriosclerosis)

157
Q

What are the investigations for hypertension?

A

Blood: U&E, glucose, lipids
Urine dipstick: Blood and protein
ECG: May show signs of left ventricular hypertrophy or ischaemia
Ambulatory BP monitoring (BP measured throughout the day): Excludes ‘white coat’ hypertension, allows monitoring of treatment response, assesses preservation of nocturnal dip
Others: Especially in patients <35 years or other suspected secondary cases (see relevant topics)

158
Q

How is hypertension managed?

A

Assessment and modification of other cardiovascular risk factors
Conservative: Stop smoking, lose weight, reduced alcohol, reduce dietary Na+
Investigate for secondary causes: Worthwhile in young patients, malignant hypertension or poor response to treatment
Medical

159
Q

What is the medical management of hypertension?

A
  • Thiazide diuretics: e.g. bendrofluamethiazide). Recommended in first line, especially in over 55 yr olds or black patients
  • ACE inhibitors (e.g. ramipril) or angiotensin-II-antagonist (e.g. losartan): First line in under 55yr olds, diabetic pts, heart failure or left ventricular dysfunction
  • Ca++ channel antagonists (e.g. amlodipine): Recommended first line, especially over 60 yr olds or black patients
  • B-blockers (e.g. atenolol): Not preferred initial therapy, but may be considered in younger patients. Avoid combining with thiazide diuretic to reduce patient risk of developing diabetes. May increase risk of heart failure
  • a-blockers (e.g. doxazosin): Fourth-line agent. May be useful for patients with prostatism
160
Q

Wen is medical management for hypertension recommended?

A

Treatment recommended for systolic BP over160 mmHg and/or diastolic BP over100 mmHg, or if evidence of end-organ damage. Other hypertension patients may still require treatment depending on other cardiac risk factors. Multiple drug therapies often necessary

161
Q

What are target blood pressures?

A
  • Less than 140/85 mmHg (non-diabetic
  • Less than 130/80 mmHg (diabetes without proteinuria)
  • Less than 125/75 mmHg (diabetes with proteinuria)
162
Q

How is severe hypertension treated?

A

Diastolic more than 140 mmHg

Atenolol or nifedipine

163
Q

How is acute malignant hypertension treated?

A
  • IV B-blocker
  • Labetolol or hydralazine sodium nitropruside
    Avoid very rapid lowering which can cause cerebral infarction
164
Q

What are the complications of hypertension?

A
  • Heart failure
  • Coronary artery disease and MI
  • CVA
  • Peripheral vascular disease
  • Emboli
  • Retinopathy
  • Renal failure
  • Hypertensive encephalopathy
  • Posterior reversible encephalopathy syndrome (PRES)
  • Malignant hypertension
165
Q

What is the prognosis of hypertension?

A
  • Good if BP controlled
  • Uncontrolled hypertension linked with increased mortality (6x stroke risk and 3x cardiac death risk)
  • Treatment reduces incidence of renal damage, stroke and heart failure
166
Q

What is an implanted cardiac defibrillator?

A

Small device placed in the abdomen.
Constantly monitor a patient’s heart rhythm and automatically administer shocks for life-threatening arrhythmias, according to the device’s programming
It is able to perform cardioversion and defibrillation

167
Q

What are the indications for an implanted cardiac defibrillator?

A
  • Used to prevent cardiac death indicated under various conditions
  • Primary prevention for patient’s who have not suffered a life threatening arrhythmia episode
  • Secondary prevention for survivors of cardiac arrest secondary to ventricular fibrillation or hemodynamically unstable sustained ventricular tachycardia after reversible causes are excluded.
168
Q

What are the possible complications of an implanted cardiac defibrillator?

A
  • Unnecessary electrical pulses: pulses sent too often or at the wrong time can damage the heart or trigger an irregular or dangerous heart beat
  • Risks related to surgery:
  • Swelling, bruising or infection around the site the ICD was placed
  • Bleeding from the site
  • Blood vessel, heart or nerve damage
  • Collapsed lung
  • Increased risk of heart failure
169
Q

What is infective endocarditis?

A

Infection of the intracardiac endocardial structures (mainly heart valves)

170
Q

What is the aetiology of infective endocarditis?

A

The endocardium can be colonised by virtually any organism, but the most common are:

1) Streptococci (40%) Mainly a-haemolytic Streptococcus viridans or Streptococcus bovis
2) Staphylococcus (35%) Staphylococcus aureus and occasionally Staphylococcus epidermidis (in IV drug users)
3) Enterococci (20%) Usually Enterococcus faecalis
4) Other organisms: HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Coxiella burnetii, histoplasma

171
Q

What is the pathology of infective endocarditis?

A

Vegetations form as a results of lodging of the organisms on the heart valves during a period of bacteraemia. These vegetations are made platelets, fibrin and infective organisms and are poorly penetrated by the cellular or humoral immune system. Vegetations proceed to destroy the valve leaflets, invade the myocardium or aortic wall leading to abscess cavities. Activation of the immune system also causes formation of immune complexes leading to cutatneous vasculitis, glomerulonephritis or arthritis

172
Q

What are the risk factors infective endocarditis?

A
  • Abnormal valves (e.g. congenital, post-rheumatic, calcification/degeneration)
  • Prosthetic heart valves
  • Turbulent flow (e.g. patent ductus arteriosus or VSD)
  • Recent dental work
  • Bacteraemia
    S bovis may be associated with GI malignancy
173
Q

What is the epidemiology of infective endocarditis?

A

Incidence 16-22 million per year (United Kingdom)

174
Q

What are the presenting symptoms of infective endocarditis?

A
  • Fever with sweats/chills/rigors (may be relapsing and remitting)
  • Malaise, arthralgia, myalgia, confusion (particularly in elderly)
  • Skin lesions
  • Inquire about recent dental surgery or IV drug abuse
175
Q

What are the signs of infective endocarditis on examination?

A
  • Pyrexia, tachycardia or signs of anaemia
  • Clubbing (if long-standing)
  • New regurgitant or muffled heart sounds (right-sided lesions may imply IV drug use)
  • Vasculitic lesiosn
176
Q

What is the frequency of infective endocarditis?

A

Mitral > aortic > tricuspid > pulmonary

Splenomegaly

177
Q

What vasculitic lesions are seen in infective endocarditis?

A
  • Petechiae particularly or retinae (Roth’s spots)
  • Pharyneal and conjunctival mucosa
  • Janeway lesions (painless palmar muscles, which blanch on pressure)
  • Osler’s nodes (tender nodules on finger/toe pads)
  • Splinter haemorrhages (nail-bed haemorrhages)
178
Q

What are the investigations of infective endocarditis?

A

Blood: FBC (increased neutrophils, normocytic anaemia, Increased ESR and CRP, U&E’s, rheumatoid factor positive
Urinalysis: Microscopic haematuria, proteinuria
Blood culture: At least three sets 1h apart (aseptic technique). Culture and sensitivity is vital, but empirical treatment should be started first. Cultures remain negative in 2-5%
Echo: Transthoracic. Transoesophageal echo is more sensitive for detection of endocarditis, especially useful for the detection of vegetations and valve abscess, diagnosis or prosthetic valve endocarditis and assessment of embolic risk
Other: ECG (abscesses can cause conduction changes), CXR (septic pulmonary emboli: focal lung infiltrates and central cavitation, particularly in tricuspid valve endocarditis

179
Q

How is infective endocarditis managed?

A

Antibiotics for 4-6 weeks (at least 6 weeks for prothetic valve endocarditis)
On clinical suspicion: Benzylpenicillin & gentamicin
Streptococci: Continue as above
Staphylococci: Flucoxacillin/vancomycin & gentamycin (for prosthetic valves: vancomycin & gentamicin & rifampin)
Enterococci: Ampicillin & Gentamicin
HACEK: Ampicillin & Gentamicin
Culture negative: Vancomycin & Gentamycin

180
Q

What are the complications of infective endocarditis?

A
  • Valve incompetence
  • Intracardiac fistulae or absecces
  • Aneurysm formation
  • Heart failure
  • Renal failure
  • Glomeulonephritis
  • Artieal emboli from the vegetations (brain, kidneys, lungs, spleen)
181
Q

What is the prognosis of infective endocarditis?

A

Fatal if untreated
Even when treated
15-30% mortality

182
Q

What is ischaemic heart disease?

A

Characterised by decreased blood supply (ischaemia) to the heart muscle resulting in chest pain (angina pectoris). May present as ‘stable angina’ or ‘acute coronary syndrome’ ACS
ABS can further be subdivided into unstable angina (no cardiac injury), non-ST elevation myocardial infarction (NSTEMI) or ST-elevation MI (STEMI, transmural infarction)
MI refers to cardiac muscle necrosis resulting from ischaemia

183
Q

What is the aetiology of ischaemic heart disease?

A

Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply. The most common cause if athersclerosis. Other causes of coronary artery narrowing such as spasm (e.g. from cocaine) arteritis and emboli are rare
MI is caused by sudden occlusion of coronary artery due to rupture of an atheromatous plaque and thrombus formation

184
Q

What are the risk factors of ischaemic heart disease?

A
  • Male
  • Diabetes mellitus
  • Family history
  • Hypertension
  • Hyperlipidaemia
  • Smoking
  • Previous history
185
Q

What is the epidemiology of ischaemic heart disease?

A
  • Common, prevalence is more than 2%
  • More common in males
  • Annual incidence of MI in the United Kingdom is approx 5 in 1000
186
Q

What are the presenting symptoms of ischaemic heart disease that presents as acute coronary syndrome?

A
  • Chest pain or discomfort of acute onset
  • Central heavy tight ‘gripping’ pain that radiates to arms (usually left), neck, jaw, or epigastrum
  • Occurring at rest, increased severity and frequency of previously stable angina
  • May be associated with breathlessness, sweating, nausea, and vomiting
187
Q

What are the signs of stable angina on examination?

A

Look for signs of risk factors

188
Q

What are the signs of ACS on examination?

A
  • May have no clinical signs. Pale, sweating, restless, low-grade pyrexia. Check both radial pulses for aortic dissection
  • Arrhythmias, disturbances of BP. New heart murmurs (e.g. pansystolic murmur of mitral regurgitation from papillary muscle rupture or ventricular septal defect)
  • Signs of complications i.e. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oliguria)
189
Q

What are the investigations for ischaemic heart disease?

A

Blood: FBC, U&Es, CRP, glucose, lipid profile, cardiac enzymes, CK-MB and troponin-T (sensitive marker of cardiac injury) amylase (pancreatitis may mimic MI), TFTs. AST and LDH increase after 24h and 48h.
ECG: Unstable angina or NSTEMI: May show ST depression, T wave inversion (Q waves in these patients may indicate old MIs)
ST-elevation MI: Hyperacute T waves, ST elevation, new onset LBBB
- CXR
- Exercise ECG testing
- Radionuclide myocardial perfusion imaging
- Echocardiogram
- Pharmacological stress testing
- Cardiac catheterisation/angiography
- Coronary calcium scoring

190
Q

How is stable angina managed?

A

Minimise cardiac risk factors
- Control BP, hyperlipidaemia and diabetes
- Provide advice smoking, exercise weight loss and low-fat diet
- All patients should receive aspirin (75mg/day) unless contraindicated
Immediate symptom relief: GTN as a spray or sublingually
Long term treatment: B-blockers
Percutaneous coronary intervention
CABB

191
Q

How is unstable angina/NSTEMI managed?

A
  • Admit to coronary care unit
  • Aspirin
  • Clopidogrel
  • Low molecular weight heparin
  • B-blocker
  • Glucose-insulin infusion if blood glucose over 11mmol/L
192
Q

How is STEMI managed?

A
  • Admit to CCU, oxygen, IV access, monitor vital signs and serial ECG
  • Aspirin
  • Clopidogrel
  • B-blocker
193
Q

What are the possible complications of ischaemic heart disease?

A

At risk of MI and other vascular disease (e.g. stroke, peripheral vascular disease). Cardiac injury can lead secondarily to heart failure and arrhythmias

  • Early complications of MI (24h-72h): Death, cardiogenic shock, heart failure, ventricular arrhythmias, heart block, pericarditis, myocardial rupture, thromboembolism
  • Late complications: Ventricular wall (or septum) rupture, valvular regurgitation, ventricular aneurysms, tamponade, Dressler’s syndrome (pericarditis), thromboembolism
194
Q

What is the prognosis of ACS?

A

TIMI score (range 0-7) can be used for risk stratification (high scores are associated with high risk of cardiac events within 30 days), Consists of:

  • Over 65 years
  • Known coronary artery disease
  • Aspirin in last 7 days
  • Severe angina (more than 2 episodes in 24h)
  • ST deviation more than 1mm
  • Elevated troponin levels
  • More than 3 coronary artery disease risk factors (hypertension, hyperlipidaemia, family history, diabetes, smoking
195
Q

What is the Killip classification of acute MI?

A

Class I: no evidence of heart failure
Class II: mild to moderate heart failure
Class III: overt pulmonary oedema
Class IV: cardiogenic shock

196
Q

What it mitral regurgitation?

A

Retrograde flow of blood from LV to left atrium during systole

197
Q

What is the aetiology of mitral regurgitation?

A

Mitral valve damage of dysfunction

  • Rheumatic heart disease (most common)
  • Infective endocarditis
  • Mitral valve prolapse (prolapse of mitral valve leaflets into the left atrium during systole)
  • Papillary muscle rupture or dysfunction (secondary to ischaemic heart disease or cardiomyopathy)
  • Chordal rupture and floppy mitral valve associated with connective tissue diseases ( Ehlers Danlos, Marfan syndromes, SLE)
198
Q

What is the epidemiology of mitral regurgitation?

A

Affects approx 5% of adults.

Mitral valve prolapse is more common in young females

199
Q

What are the presenting symptoms of acute mitral regurgitation?

A

May present with symptoms of left ventricular failure

200
Q

What are the presenting symptoms of chronic mitral regurgitation?

A

May be asymptomatic or present with exertional dyspnoea, palpitations if in AF and fatigue

201
Q

What are the presenting symptoms of mitral valve prolapse?

A

Asymptomatic or atypical chest pain or palpitations

202
Q

What are the signs of mitral regurgitation on examination?

A
  • Pulse may be normal or irregularly irregular (AF)
  • Apex beat may be laterally displaced and thrusting (left ventricular dilation)
  • Pansystolic murmur loudest at apex, radiating to axilla (palpable as a thrill) S1 is soft, S3 may be heart (rapid ventricular failure in acute mitral regurgitation)
  • Signs of left ventricular failure in acute mitral regurgitation
203
Q

What are the signs of mitral valve prolapse on examination?

A

Mid-systolic click and late-systolic murmur. The click moves towards the first heart sound on standing and moves away on lying down

204
Q

What are the investigations for mitral regurgitation?

A
  • ECG: Normal or may show AF or broad bifid p wave (p mitrale) indicating delayed activation of left atrium due to left atrium enlargement
  • CXR: Acute mitral regurgitation may produce signs of left ventricular failure. Chronic mitral regurgitation shows left atrial enlargement, cardiomegaly (caused by LV dilation) or mitral valve calcification in rheumatic cases
  • Echo: Every 6-12 months for moderate-severe MR to assess the LV ejection fraction and end-systolic dimension
205
Q

What is mitral stenosis?

A

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

206
Q

What is the aetiology of mitral stenosis?

A
  • Most common cause is rheumatic heart disease (90%)
  • Rarer causes are congenital mitral stenosis, SLE, rheumatoid arthritis, endocarditis and atrial myxoma (rare cardiac tumour)
207
Q

What is the epidemiology of mitral stenosis?

A

Incidence is declining in industrialised countries because of declining incidence of rheumatic fever

208
Q

What are the presenting symptoms of mitral stenosis?

A
  • May be asymptomatic
  • Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea)
  • Palpitations (related to AF)
    Rare symptoms
  • Cough, haemoptysis, hoarseness caused by compression of the left laryngeal nerve by an enlarged left atrium
209
Q

What are the signs os mitral stenosis on examination?

A

May have peripheral or facial cyanosis (malar flush)
- Pulse: May be ‘thready’ or irregular irregular (AF)
- Palpation: Apex beat is undisplaced and tapping. Parasternal heave (right ventricular hypertrophy and pulmonary hypertension)
- Auscultation: Loud first heart sound with opening snap.
Mid diastolic murmur
Evidence of pulmonary oedema on lung auscultation (if decompensated)

210
Q

What are the investigations for mitral stenosis?

A

ECG: May be normal, broad bifid p wave caused by LA hypertrophy, AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension
CXR: Left atrial enlargement, cardiac enlargement, pulmonary congestion, mitral valve may be calcified in rheumatic cases
Echo
Cardiac catheterisation

211
Q

What is myocarditis?

A

Acute inflammation and necrosis of cardiac muscle (myocardium)
Usually idiopathic but can be caused by cocaine abuse, heavy metals and radiation

212
Q

What is the aetiology of myocarditis with regards to infection?

A
  • Viruses e.g. Coxackie B, echovirus, EBV, CMV, adenovirus, influenza
  • Bacterial e.g. post-streptococcal, tuberculosis, diphtheria, Lyme disease
  • Fungal: e.g. candidiasis
  • Protozoal: e.g. trypanosomiasis (Chagas disease)
  • Helminths: e.g. trichinosis
213
Q

What is the aetiology of myocarditis with regards to non-infective causes?

A
  • Systemic disorders (e.g. SLE, sarcoidosis, polymyositis)

- Hypersensitivity myocarditis (e.g. sulphonamides)

214
Q

What is the aetiology of myocarditis with regards to drugs?

A

Chemotherapy agents

e.g. doxorubicin, streptomycin

215
Q

What is the epidemiology of myocarditis?

A

True incidence is unknown, as many cases are not detected at the time of acute illness. Coxsackie B virus is a common cause in Europe and the USA. Chagas disease is a common cause in South America

216
Q

What are the presenting symptoms of myocarditis?

A
  • Prodromal ‘flu like’ illness, fever, malaise, fatigue, lethargy
  • Breathlessness (pericardial effusion, myocardial dysfunction)
  • Palpitations
  • Sharp chest pain (suggesting associated pericarditis)
217
Q

What are the signs of myocarditis on examination?

A

Signs of concurrent pericarditis or complications: heart failure, arrhythmia

218
Q

What are the investigations for myocarditis?

A
  • Blood: FBC, U&E, Raised ESR or CRP, cardiac enzymes may be raised,
  • ECG: Non-specific T wave ad ST changes, widespread saddle shaped ST elevation in pericarditis
  • CXR: May be normal or show cardiomegaly with or without pulmonary oedema
  • Pericardial fluid drainages: Measure glucose, protein, cytology, culture and sensitivity
  • Echo
  • Myocardial biopsy
219
Q

What is necrotising fasciitis?

A

Life-threatening soft-tissue infection which may extend to deep fascia but not into deep underlying muscle
Type I: polymicrobial infection with an anaerobe such as Bacteroides or Peptostreptococcus
Type II: most commonly a monomicrobial infection with Streptococcus pyogenes (group A streptococci)

220
Q

What are the presenting symptoms of necrotising fasciitis?

A
  • Fever
  • Palpitations, tachycardia, tachypnoea, hypotension, and lightheadedness
  • Nausea and vomiting
  • Delirium
221
Q

What are the signs of necrotising fasciitis on examination?

A
  • Anaesthesia or severe pain over site of cellulitis
  • Crepitus
  • Vesicles or bullae
  • Grey discouloration of skin
  • Oedema or induration
222
Q

What is the epidemiology of necrotising fasciitis?

A
  • Type I is more common than Type II
  • Type II complicates about 5% of invasive group A streptococcal infections at an estimated rate of 2 cases per million population per year
223
Q

What are the investigations for necrotising fasciitis?

A
  • FBC: abnormally high or low WBC count with or without a left shift (elevated percentage of polymorphonuclear leukocytes and/or bands)
  • Serum electrolytes:
    sodium may be decreased
  • Serum urea and creatinine: elevated
  • Gram stain: variables
  • ABG: hypoxaemia, acidosis
  • CT/MRI:
    oedema extending along fascial plane
224
Q

What is pericarditis?

A

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

225
Q

What is the aetiology of pericarditis?

A
  • Idiopathic
  • Infective (commonly, coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB)
  • Connective tissue disease (e.g. sarcoid, SLE, scleroderma)
  • Post-myocardial infarction (24h-72h) in up to 20% of patients
  • Dressler’s syndrome (weeks to months after acute MI)
  • Malignancy (lung, breast, lymphoma, leukaemia, melanoma)
  • Metabolic (myxoedema, uraemia)
  • Radiotherapy
  • Thoracic surgery
  • Drugs e.g. hydralazine, isoniazid
226
Q

What is the epidemiology of pericarditis?

A

Uncommon
The clinical incidence is less than 1 in 100 hospital admissions.
More common in males

227
Q

What are the presenting symptoms of pericarditis?

A
  • Chest pain: Sharp and central, may radiate to neck or shoulders. Aggravated by coughing, deep inspiration and lying flat. Relieved by sitting forward
  • Dyspnoea, nausea
228
Q

What are the signs of pericarditis on examination?

A
  • Fever, pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration, heart sounds may be faint in the presence of an effusion
  • Cardiac tamponade: Increased JVP, Decreased BP and muffled heart sounds (Beck’s triad). Tachycardia, pulsus paradoxus
  • Constructive pericarditis (chronic): Increased JVP with inspiration (Kussmaul’s sign), pulsus paradoxus, hepatomegaly, ascities, oedema, pericardial knock, AF
229
Q

What are the investigations for pericarditis?

A
  • ECG: Widespread ST elevation that is saddle-shaped
  • Echo: For assessment of pericardial effusion and cardiac function
  • Blood: FBC, U&E, CRP, cardiac enzymes (usually normal)
  • CXR: Usually normal (globular heart shadow if more than 250mL effusion). Pericardial calcification can be seen in constrictive pericarditis
230
Q

How is pericarditis managed?

A
  • Acute: Cardiac tamponade treated by emergency pericardiocentesis
  • Medical: Treat the underlying cause, NSAIDs for relief of pain and fever
  • Recurrent: Low dose steroids, immunosuppressants or colchicine
  • Surgical: Surgical exicision of the pericardium (pericardiectomy) in constrictive pericarditis
231
Q

What are the possible complications of pericarditis?

A
  • Pericardial effusion
  • Cardiac tamponade
  • Cardiac arrhythmias
232
Q

What is the prognosis of pericarditis?

A
  • Depends on the underlying cause
  • Good prognosis in viral cases (recover within approx 2 weeks)
  • Poor in malignant pericarditis
  • Pericarditis may be recurrent (particularly in those caused by thoracic surgery)
233
Q

What is peripheral vascular disease?

A

Includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries.

234
Q

What is the aetiology of peripheral vascular disease?

A
  • Most commonly caused by atherosclerosis
  • Rarer causes of claudication are aortic coarctation, arterial fibrodysplasia, arterial tumour, arterial dissection, arterial embolism, thrombosis, vasospasm and trauma
235
Q

What is the epidemiology of peripheral vascular disease?-

A
  • Prevalence increases with age, beginning after 40

- In the UK, one-fifth of people aged 65 to 75 years have evidence of PVD on clinical examination.

236
Q

What are the risk factors of peripheral vascular disease?

A
  • Smoking
  • Diabetes
  • Hyperlipidaemia
  • Being over 40
  • History of coronary artery disease
  • Low levels of exercise
237
Q

What are the presenting symptoms of peripheral vascular disease?

A
  • Asymptomatic
  • Thigh or buttock pain with walking that is relieved with rest
  • Sudden onset of severe leg pain accompanied by numbness, weakness, pale, and cold leg
    Uncommon
  • Erectile dysfunction
  • Pain worse in one leg
  • Non healing wound/ulcer
238
Q

What are the signs of peripheral vascular disease on examination?

A
  • Intermittent claudication
  • Diminished pulse
  • No pulse in lower extremity
239
Q

What are the investigations for peripheral vascular disease?

A
  • Ankle brachial index: Less than 0.9
  • Toe brachial index: Less than 0.6
  • Segmental pressure examination: Gradient of >20 mmHg between adjacent segments
  • Angiography: Stenosis
  • CT angiography: presence of significant stenosis
240
Q

What is pulmonary hypertension?

A

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

241
Q

What is the aetiology of pulmonary hypertension?

A

Primary: Idiopathic
Secondary: Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/thrombosis), chronic lung disease (COPD), recurrent pulmonary emboli, Increased pulmonary blood flow, connective tissue disease, Drugs e.g. amiodarone

242
Q

What is the epidemiology of pulmonary hypertension?

A

Primary pulmonary hypertension is usually seen in young females

243
Q

What are the presenting symptoms of pulmonary hypertension?

A
  • Dyspnoea (on exertion, chest pain, syncope, tiredness

- Symptoms of the underlying cause (e.g. chronic cough)

244
Q

What are the signs of pulmonary hypertension of examination?

A

Increased JVP (Prominent a wave in the JVP waveform

  • Palpation: Left parasternal heave (right ventricular hypertrophy)
  • Auscultation: Loud pulmonary component of S2, an early diastolic murmur (Graham-Steele murmur) caused by pulmonary regurgitation may be present, if tricuspid regurgitation develops
  • Signs of the underlying condition, or right heart failure in severe cases
245
Q

What are the investigations of pulmonary hypertension?

A
  • CXR: Cardiomegaly (RV enlargement, RA dilation), prominent main pulmonary arteries, signs of cause (COPD, calcified mitral valves)
  • ECG: RV hypertrophy (RA deviation, prominent R wave in V1, T wave inversion in V1), RA enlargements
  • Echo: To visualise RV hypertrophy or dilation and possible underlying cause
  • LFT: To assess for chronic lung disease
  • VQ scan: Assess for pulmonary embolism
  • Cardiac catheterisation: To asses severity, right heart pressures and response to vasodilators
  • High resolution CT-thorax: Images pulmonary arteries and to diagnose lung disease
  • Lung biopsy: Assesses structural changes
246
Q

What is tricuspid regurgitation?

A

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

247
Q

What is the aetiology of tricuspid regurgitation?

A
  • Congenital: Ebstein anomaly (malpositioned tricuspid valve), Cleft valve in ostium primum defect
  • Functional: Consequence of RV dilation (e.g. in pulmonary hypertension), valve prolapse
  • Rheumatic heart disease: Associated with other valvular disease
  • Infective endocarditis: Common in IV drug users, usually staphylococcal
  • Other: Carcinoid syndrome, trauma, cirrhosis (long-standing), iatrogenic (e.g. radiotherapy to the thorax)
248
Q

What is the epidemiology of tricuspid regurgitation?

A

Differs with various causes.

Infective endocarditis is probably the most common cause

249
Q

What are the presenting symptoms of tricuspid regurgitation?

A
  • Fatigue
  • Breathlessness
  • Palpitations
  • Headaches
  • Nausea
  • Anorexia
  • Epigastric pain made worse by exercise
  • Jaundice
  • Lower limb swelling
250
Q

What are the signs of tricuspid regurgitation on examination?

A
  • Pulse: May be irregular due to AF
  • Inspection: Raised JVP with giant v waves which may oscillate the earlobe. Caused by transmission of right ventricular pressure to the great veins. May be giant a wave, if patient is in sinus rhythm
  • Palpation: Parasternal heave
  • Auscultation: Pansystolic murmur heard best at lower left sternal edge, louder on inspiration (Carvallo sign). Loud P2 component of second heart sound
  • Chest: Pleural effusion. Causes of pulmonary hypertension (e.g. emphysema)
  • Abdomen: Palpable liver (tender, smooth, pulsatile), ascites
  • Legs: Pitting oedema
251
Q

What are the investigations for tricuspid regurgitation?

A
  • Blood: FBC, LFT, cardiac enzymes, blood cultures
  • ECG: Tall P wave (right atrial hypertrophy if in sinus rhythm. Changes indicative of other cardiac rhythm
  • CXR: Right-sided enlargement of cardiac shadow
  • Echo: Extent of regurgitation estimated by colour flow Doppler. May be able to detect tricuspid valve abnormality (e.g. prolapse), right ventricular dilation
  • Right heart catheterisation: Rarely necessary but may be considered to assess pulmonary artery pressure
252
Q

What is permanent pacing?

A

A medical device which uses electrical impulses, delivered by electrodes contracting the heart muscles, to regulate the beating of the heart.
Primary purpose is to maintain an adequate heart rate, either because the heart’s natural pacemaker is not fast enough or there is a block in the heart’s conduction system

253
Q

What are the indications for permanent pacing?

A
  • Symptomatic sick sinus syndrome, including, tachycardia, bradycardia syndrome, atrial fibrillation with sinus node dysfunction, and chronotropic incompetence (inability to increase the heart rate to match a level of exercise)
  • Symptomatic sinus bradycary
  • Symptomatic complete AV block (3rd degree heart block)
  • Bradycardia exacerbating prolonged QT syndrome
254
Q

What are the possible complications of a pacemaker?

A
  • Pneumothorax
  • Pericarditis
  • Infection
  • Skin erosion
  • Haematoma
  • Lead dislodgement
  • Venous thrombosis
255
Q

What is supraventricular tachycardia?

A
  • Rate over 300 bpm
  • QRS complex duration less than 120 ms
    Can include atrioventricular nodal re-entry tachycardia and Wolff-Parkinson White syndrome
256
Q

What are the causes of supraventricular tachycardia?

A
  • Nicotine
  • Alcohol
  • Caffeine
  • Common in young people
257
Q

What are the presenting symptoms of atrioventricular nodal re-entry tachycardia?

A
  • Episodic
  • Abrupt onset and termination
  • Chest discomfort
  • Dyspnoea
  • Dizziness
  • Anxiety
  • Regular rapid pounding in neck differentiates from WPW
258
Q

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

A
  • Palpitations
  • AF/Flutter
  • Sudden cardiac death
  • Syncope
  • Presyncope
  • Tachy in pregnancy
259
Q

What are the signs on examination of atrioventricular nodal re-entry tachycardia?

A
  • Normal except tachycardia
260
Q

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

A
  • Tacycardia
  • Secondary cardiomyopathy (S3 gallop, RV heave, Displaced point of maximal impulse laterally, HF: elevated JVP, crackles, lower extremity oedema)
261
Q

What are the investigations for supraventricular tachycardia?

A
  • 12 lead ECG: Narrow complex tachycardia, no p waves, retrograde P wave may be seen in inferior leads
  • TOE: rule out structural heart disease
  • Echo: Sustained flutter, SVT, AF, wide complex tachycardia, structural heart disease
  • Exercise testing: Relate to exercise, rule out CAD
262
Q

How is supraventricular tachycardia managed?

A

If rhythm is regular:

1) Vagal manoeuvres- carotid sinus massage, Valsalva manoeuvre e.g. blowing on to a syringe- increase AV block and unmask rhythm. Massage done in younger people and Valsalva in older people and atherosclerosis as risk of dislodging plaque
2) If unsuccessful- Adenosine 6mg bolus injection, can increase to 12mg, can give verapamil if unsuccessful/asthma. Alt- atenolol/amiodarone
3) Unresponsive to chemical cardioversion or if adverse signs (low BP, HF, low consciousness). Sedate and synchronised DC cardiovert. Give amiodarone
4) If no adverse signs: (B blockers, Digoxin, Amiodarone, Overdrive pacing)

263
Q

What is the prognosis of supraventricular tachycardia?

A

Rarely life threatening

264
Q

What are the possible complications of supraventricular tachycardia?

A
  • Ischaemia and MI in someone with significant CAD
  • Heart failure with diseases of heart valves or cardiomyopathy
  • If persists for long time, normal heart weakens and develops heart failure
265
Q

What are varicose veins?

A

Subcutaneous, permanently dilated veins more than 3mm or more in diameter when measured in a standing position

266
Q

What is the aetiology of varicose veins?

A 
Predisposing factors:
- Gender, pregnancy, occupation, weight, race
Causative factors:
- Previous DVT 
- Genetic factors
267
Q

What causes varicose veins?

A
  • Valve incompetence is the most common aetiology
  • Veins are working against gravity, valves function to compartmentalise the blood, leading to better equalisation of pressures throughout the veins and preventing reflux.
  • Blood pools when valves do not function properly, leading to increased pressure and distension of the veins
268
Q

What is the epidemiology of varicose veins?

A
  • Prevalence rates higher in industrialised countries and more developed regions
  • In Western populations, prevalence is 10-15% in men and 20-25% in women over 15.
  • Prevalence increases with age
269
Q

What are the risk factors of varicose veins?

A
  • Increasing age
  • Family history
  • Female gender
  • Increasing numbers of births
  • DVT
    Weak
  • Occupation with prolonged standing
  • Obesity
270
Q

What are the presenting symptoms of varicose veins?

A
  • Leg fatigue or aching with prolonged standing
  • Leg cramps
  • Restless legs
  • Itching
  • Ankle swelling
  • Ulceration
271
Q

What are the signs of varicose veins on examination?

A
  • Dilates tortuous veins
  • Haemosiderin deposition
  • Corona phlebectatica
272
Q

What are the investigations for varicose veins?

A

Duplex ultrasound

  • Assessed for reversed flow
  • Valve closure time over 0.5 seconds is indicative of reflux
  • Valve closure time over 1 second is indicative of reflux in deep system
273
Q

How are varicose veins managed?

A

If symptomatic superficial vein insufficiency, no evidence of peripheral vascular disease: Graduated compression stockings + phlebectomy + sclerotherapy+ ablative procedures
If deep vein insufficiency without superficial system insufficiency: phlebectomy and compression stockings

274
Q

What are the possible complications of varicose veins?

A
  • Chronic venous insufficiency
  • Haemorrhage
  • Venous ulceration
  • Lipodermatosclerosis
  • Haemosiderin deposition
275
Q

What is the prognosis of varicose veins?

A

Although there are small variations in overall efficacy depending on the type of intervention, generally resolution of symptoms occurs in >95% of patients. Patients need to be counselled, however, that new varicosities may occur with time.

276
Q

What is vasovagal syncope?

A

Malaise mediated by vagus nerve.
Most common type of fainting
Is a type of neurally mediated reflex syncope (NMRS)

277
Q

What is the aetiology of vasovagal syncope?

A
  • May be triggered by prolonged periods of upright posture
  • Relative dehydration
  • Excessively warm, closed-in environments
  • Extreme emotions
    Common places for these events are churches, restaurants and long queues
278
Q

What are presenting symptoms of vasovagal syncope?

A
  • Nausea
  • Lightheadedness
  • Pallor
  • Diaphoresis
  • Physical injury
  • Fatigue after episode
  • Palpitations
279
Q

What are the signs of vasovagal syncope on examination?

A
  • Bradycardia
  • Absence of family history of sudden death
  • Neuralgia (uncommon)
280
Q

What is the epidemiology of vasovagal syncope?

A
  • 1% of A&E visits in Europe

- Tends to peak in young adults and then again in older people

281
Q

What are the investigations of vasovagal syncope?

A
  • 12-Lead ECG: rules out AV block, bradycardia, asystole, long QT, bundle branch block
  • Serum haemoglobin: Normal, low in anaemia
  • Plasma blood glucose: Normal: low in hypoglycaemia
  • Serum beta-human chorionic gonadotrophin: Normal, positive in pregnancy
  • Cardiac enzymes: Normal, elevated in MI
  • D-dimer level: Normal, elevated in PE
  • Serum cortisol: Normal or decreased
  • Urea and serum creatinine: Normal or elevated
282
Q

What are venous ulcers?

A

Chronic venous insufficiency refers to functional changes that may occur in the lower extremity due to persistent elevation of venous pressures
The wounds are thought to be due to improper functioning of venous valves, usually of the legs

283
Q

What is the aetiology of venous ulcers?

A
  • Abnormality is usually reflux but can also be chronic obstruction or combination of the two
  • Congenital absence of the venous valves is a less common cause, and isolated primary varicose veins (pure superficial incompetence) uncommonly causes severe CVI.
284
Q

What is the epidemiology of venous ulcers?

A

Occurs in an as many as 50% of people within 5 to 10 years of an episode of DVT

285
Q

What are the presenting symptoms of venous ulcers?

A
  • Corona phlebectatica (malleolar flare or ankle flare)
  • Ankle swelling
  • Hyperpigmentation brawny oedema)
  • Leg ulcers
286
Q

What are the signs of venous ulcers on examination?

A
  • Atrophic blanche
  • Lymphedema
  • Lipodermatosclerosis
287
Q

What are the investigations for venous ulcers?

A
  • Duplex ultrasound: Retrograde or reversed flow, valve closure time over 0.5 seconds
288
Q

How are venous ulcers managed?

A
  • Graded compression stockings
  • Moisturiser
  • Diosmin/ Pentoxifylline
  • Skin graft
289
Q

What are the possible investigations of venous ulcers?

A
  • Infected
  • Leading to cellulitis or gangrene
  • May need amputation of part of limb in future
290
Q

What is the prognosis of venous ulcers?

A

Significant chance they will recur after healing

291
Q

What is ventricular fibrillation?

A

Irregular rapid ventricular fibrillation with no cardiac output

292
Q

What is the aetiology of ventricular fibrillation?

A
  • Ischaemic heart disease and ongoing ischaemia
  • Rapid haemodynamic collapse and syncope
    History of:
  • Progressive angina
  • Cardiac arrest
  • Valvular disease
  • Depressed LV systolic function
293
Q

What are the presenting symptoms of ventricular fibrillation?

A
  • Chest pain
  • Dizziness
  • Nausea
  • Rapid, fluttering heart beat
  • SOB
294
Q

What are the signs of ventricular fibrillation on examination?

A
  • Absent pulse
  • Loss of consciousness
  • Depressed LV systolic function
295
Q

What are the investigations for ventricular fibrillation?

A
  • Serum K/Mg: predispose to VT
  • Cardiac markers: new ischaemia
  • Tox screen: anti-arrhythmics
  • TTE: systolic function
  • Coronary angiogram: CAD
  • EPS
296
Q

How is ventricular fibrillation managed?

A

1) High flow 02
2) Rx reversible cause: electrolyte abnormalities of Low Mg, K a) Mg sulphate b) K chloride
3) Cardioversion may be repeated as needed until rhythm is controlled
4) Amiodarone 300mg IV 20 min- 1 hr
5) And lidocaine
6) IV Mg sulphate if Torsades de Pointes
7) ICD- to prevent recurrence
8) Get expert help, sedate, shock

297
Q

What is the epidemiology of ventricular fibrillation?

A

Higher in men than women 3:1

298
Q

What are the possible complications of ventricular fibrillation?

A
  • Central nervous system ischaemic injury
  • Myocardial injury
  • Post-defibrillation arrhythmias
  • Aspiration pneumonias
  • Anoxic encephalopathy
  • Death
299
Q

What is the prognosis of ventricular fibrillation?

A
  • Depends on time elapsed between onset and myocardial intervention
  • VF that occurs within the first 48 hours of the onset of acute MI has no bearing on prognosis, but VF that occurs more than 48 hours after acute MI is associated with a high rate of recurrence and a poorer prognosis.
  • After resuscitation, the prognosis is largely dependent on haemodynamic stability, early neurological recovery and duration of the resuscitation
300
Q

What is a non-sustained ventricular tachycardia?

A

Ectopic ventricular rhythm with a wide QRS complex (120 ms or greater), rate faster than 120 bpm, lasting for at least 3 beats that spontaneously resolves in less than 30 seconds

301
Q

What is the aetiology of non-sustained ventricular tachycardia?

A
  • Commonly observed in patients with underlying ischaemic or non-ischaemic cardiac disease although can be observed in healthy people
  • Infectious diseases such as Chagas disease in Central America
  • Structural heart diseases such as hypertrophic cardiomyopathy, idiopathic dilated cardiomyopathy, congenital heart disease, and valvular heart disease are also associated with NSVT
  • Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia can contribute
302
Q

What is the epidemiology of non-sustained ventricular tachycardia?

A
  • Not sex specific

- Men more likely to be affected due to higher incidence of CAD

303
Q

What are the presenting symptoms of ventricular tachycardia?

A
  • Asymptomatic
  • Tachycardia
  • Palpitations
  • Dizziness
  • Light-headedness
  • Pre-syncope
  • Syncope
  • Hypotension
304
Q

What are the signs of ventricular tachycardia on examination?

A
  • Weak pulse in carotids
  • Sustained ventricular tachycardia: canon ‘a’ waves in JVP
  • Broad complexes on ECG
305
Q

What are the investigations for ventricular tachycardia?

A
  • 12-lead ECG: +ve QRS concordance in chest leads, L axis deviation, AV disassociation, Fusion beats
  • 24h ambulatory ECG monitoring:
  • Electrolytes: Low Mg or K associated with Torsades de Pointes
  • Troponin- checks for ischaemia
306
Q

What is sustained ventricular tachycardia?

A

Ventricular tachycardia faster than 100 bpm lasting at least 30 seconds or requiring termination earlier due to haemodynamic instability
- VT is defined as a wide complex tachycardia (QRS 120 milliseconds or greater) that originates from one of the ventricles, and is not due to aberrant conduction (e.g., from bundle branch block), at a rate of 100 bpm or greater.

307
Q

How is sustained ventricular tachycardia managed?

A
  • Synchronised cardioversion according to ACLS protocol & treatment of reversible cause
  • Anti-arrhythmic medication
  • Amiodarone/lidocaine
308
Q

How is non-sustained ventricular tachycardia managed?

A
  • No cardiac comorbidity/asymptomatic: correct electrolytes/ reassure and self monitor
  • Post MI: reperfusion, optimise meds, lifestyle
  • With HF: reperfuse, anti-failure therapy, lifestyle modifications
309
Q

What are the possible complications of ventricular tachycardia?

A
  • Ventricular fibrillation
  • Sudden cardiac death
  • ICD
  • Cardiomyopathy
  • Amiodarone induced thyroid function
310
Q

What is the prognosis of ventricular tachycardia?

A

Worse prognosis if non-idiopathic ventricular tachycardia

311
Q

What is Wolff-Parkinson White syndrome?

A
  • Short PR interval and ‘Delta’ wave on ECG predisposing to supraventricular tachycardias (SVT)
  • WPW Syndrome is restricted to symptomatic patients with a typical ECG abnormality
  • WPW pattern signifies asymptomatic patients with typical ECG abnormalities
312
Q

What are the risk factors or Wolff-Parkinson White syndrome?

A
  • Ebstein abnormality
  • HOCM
  • Transposition of great vessels
  • Dextrocardia
  • Marfan’s
  • Family history
  • Right and left atrial aneurysms
313
Q

What is the aetiology of Wolff-Parkinson White syndrome?

A
  • Conduction from the atrium reaches the adjacent ventricle earlier via the AP, and a part of the ventricle is pre-excited.
  • Accessory pathway (bundle of Kent) bypasses the atrioventricular node causing ventricular pre-excitation
314
Q

What is the epidemiology of Wolff-Parkinson White syndrome?

A
  • Encountered at any age

- Higher incidences in third and fourth decades of life

315
Q

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

A
  • Shortness of breath
  • Palpitations
  • Dizziness
  • Chest pain
  • Sudden cardiac death
  • Syncope and presyncope
316
Q

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

A
  • Antrioventricular re-entrant tachycardia (AVRT)
  • Atrial flutter
  • Tachy on pregancy
317
Q

What are the investigations for Wolff-Parkinson White syndrome?

A
  • ECG
  • Cardiac electrophysiology
  • Echocardiogram (to detect any associated cardiac abnormalities)

Year 3 ICSM Sofia (16 decks)

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