Cardiology Flashcards

1
Q

Define atrial fibrillation

A

AF is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activity on the surface ECG. AF has an irregularly irregular rhythm.

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2
Q

Describe the aetiology of atrial fibrillation

A

May be no identifiable cause

Systemic:
Advancing age
Infection/sepsis
Diabetes
Hyperthyroidism (thyrotoxicosis)
Hypertension
Alcohol
Electrolyte imbalance
Pneumonia
Heart:
Ischaemic heart disease e.g. MI, Coronary Artery Disease
Congestive heart failure
Hypertensive heart disease
Heart failure
Valvular heart disease
Cardiomyopathies
Pericarditis
Myocarditis
Rheumatic heart disease
Sick sinus syndrome
Atrial myxoma 

Lung:
Bronchial carcinoma
Pulmonary embolism
Pneumonia

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3
Q

Summarise the epidemiology of atrial fibrillation

A

VERY COMMON in the elderly
Present in 5% of those > 65 years
May be paroxysmal
Affects men more than women

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4
Q

What are the presenting symptoms of atrial fibrillation?

A
Asymptomatic
Palpitations
Dizziness
Syncope
SOB
Chest pain
Fatigue
Symptoms of the cause of AF
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5
Q

What are the signs on physical examination of atrial fibrillation?

A

Irregularly irregular pulse
Hypotension
Tachycardia
Difference in apical beat and radial pulse
Check for signs of thyroid disease and valvular disease

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6
Q

What are the appropriate investigations for atrial fibrillation?

A

12 lead ECG - shows irregularly irregular tachycardia (QRS complexes), absent P waves

Echocardiogram - determine if any valvular disease, pericardial disease, cardiomyopathies

Bloods:
Cardiac enzymes
TFT - test for hyperthyroidism as the cause (low TSH)
Lipid profile
U&Es, Mg2+ and Ca2+ (there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia)
Serum transaminases - may be deranged if AF due to alcohol

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7
Q

What is the management of atrial fibrillation?

A

First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection)

If HAEMODYNAMICALLY UNSTABLE - DC CARDIOVERSION

  1. RHYTHM CONTROL
    If > 48 hrs since onset of AF
    Anticoagulate for 3-4 weeks before attempting cardioversion

If < 48 hrs since onset of AF:
DC cardioversion (2 x 100 J, 1 x 200 J)
Chemical cardioversion: flecainide or amiodarone

NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease

Prophylaxis against AF:
Sotalol
Amiodarone
Flecainide
Consider pill-in-the-pocket (single dose of a cardioverting drug for patients with paroxysmal AF) strategy for suitable patients
RATE CONTROL in chronic (Permanent) AF
Control ventricular rate with:
Digoxin
Verapamil (rate-limiting CCB)
Beta-blockers

Aim for ventricular rate ~ 90 bpm

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8
Q

How is stroke risk stratified in atrial fibrillation?

A

CHA2DS2VASc Score

C - congestive heart failure (1)
H - hypertension (1)
A2 - age >75 (2)
D - Diabetes Mellitus (1)
S2 - previous stroke/TIA/thromboembolism (2)
V - vascular disease (1)
A - age 64-75 (1)
Sc - female sex (1)

If low risk (score of 1) - OAC or aspirin
If high risk (score >2) - anticoagulation with warfarin or other oral anticoagulants eg DOACs

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9
Q

Define aortic regurgitation

A

The diastolic leakage of blood from the aorta into the left ventricle due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.

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10
Q

Explain the aetiology of aortic regurgitation

A
  1. Primary disease of the aortic valve leaflets
    - Rheumatic heart disease (developing countries)
    - Congenital bicuspid aortic valve
  2. Aortic root dilation
    - Marfan’s syndrome or related connective tissue disease
    - Aortitis secondary to syphilis, Behcet’s, Takayasu’s, reactive arthritis, or ankylosing spondylitis.
    - Systemic hypertension
    - Aortic dissection
    - Arthritides (e.g. rheumatoid arthritis, seronegative arthritides)
    - Pseudoxanthoma elasticum
    - Osteogenesis imperfecta

Acute aortic regurgitation:
Aortic root dissection
Endocarditis can lead to rupture of leaflets or even paravalvular leaks.
Vegetations on the valvular cusps can also cause inadequate closure of leaflets, resulting in leakage of blood.

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11
Q

Summarise the epidemiology of aortic regurgitation

A

Less common than aortic stenosis and mitral regurgitation
Prevalence increases with age
More common in men than women
Chronic AR often begins in the late 50s
Most frequently seen in patients > 80 years

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12
Q

What are the presenting symptoms of aortic regurgitation?

A
Chronic AR: 
Initially ASYMPTOMATIC 
Later on, the patient may develop symptoms of heart failure: 
- Exertional dyspnoea
- Orthopnoea
- Fatigue
- Paroxysmal nocturnal dyspnoea

Severe Acute AR:
Sudden cardiovascular collapse (LV can’t adapt to the rapid increase in end-diastolic volume). Symptoms related to aetiology (e.g. chest/back pain caused by aortic dissection).

Weakness
Chest pain

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13
Q

What are the signs on physical examination of aortic regurgitation?

A
End-diastolic murmur heard loudest on expiration, when sitting forwards and in the left sternal edge
Collapsing pulse
Pallor
Rapid and faint peripheral pulse
Tachypnoea
Wide pulse pressure 
Thrusting and heaving displaced apex beat 
Basal lung crepitations

Rare signs:
Quincke’s Sign - visible pulsation on nail bed
de Musset’s Sign - head nodding in time with the pulse
Becker’s Sign - visible pulsation of the pupils and retinal arteries
Muller’s Sign - visible pulsation of the uvula
Corrigan’s Sign - visible pulsation in the neck
Traube’s Sign - pistol shot (loud systolic/diastolic sounds) heard at femoral arteries
Duroziez’s Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the 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 60 mm Hg

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14
Q

What are the appropriate investigations for aortic regurgitation?

A
ECG - not diagnostic, may show non-specific ST-T wave changes, left axis deviation, or conduction abnormalities
May show left ventricular hypertrophy: 
· Deep S in V1/2 
· Tall R in V5/6 
· Inverted T waves in lead I, aVL, V5/6 
· Left axis deviation

CXR - may show cardiomegaly, dilatation of ascending aorta, signs of pulmonary oedema if heart failure also present

Echocardiogram - detection and evaluation of severity of AR. Visualisation of the origin of regurgitant jet and its width. May show underlying cause.

Cardiac catheterisation with angiography - If there is any uncertainty about the functional state of the ventricle or the presence of coronary artery disease

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15
Q

Define rheumatic fever

A

An autoimmune disease which can affect many systems including the heart, joints, brain and skin following group A streptococcal throat infection.
The effects on the heart can lead to permanent illness known as chronic rheumatic heart disease. Long-term penicillin secondary prophylaxis, acute rheumatic fever can recur causing cumulative damage to cardiac valvular tissue.

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16
Q

Explain the aetiology of rheumatic fever

A

Acute rheumatic fever is an autoimmune disease.
A group A streptococcal infection triggers an autoimmune response in a susceptible host. The response is targeted against cardiac, synovial, subcutaneous, epidermal and neuronal tissue.

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17
Q

What are the risk factors for rheumatic fever?

A
Poverty
Overcrowded living quarters
Family history of rheumatic fever
D8/17 B cell antigen
Indigenous populations
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18
Q

Summarise the epidemiology of rheumatic fever

A

Mainly in children aged 4-15 years old
Rare in people over 30 years old
94% of cases are in developing countries
No clear sex predilection, however chronic rheumatic heart disease is more common in females
More than 2.4 million children have rheumatic heart disease worldwide

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19
Q

What are the five hallmarks of rheumatic fever?

A
Carditis
Arthritis
Chorea
Erythema marginatum
Subutaneous nodules
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20
Q

What are the four minor manifestations of rheumatic fever?

A

Fever
Arthralgia
Elevated inflammatory markers
Prolonged PR interval on ECG

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21
Q

What are the presenting symptoms of rheumatic fever?

A

Fever
Joint pain (knees, ankles, wrists, elbows, and hips, usually asymmetrical)
Recent sore throat or scarlet fever (2-4 weeks previously)
Chest pain
SOB
Palpitations
Nodules on the skin
Restlessness, clumsiness, emotional lability and personality changes (indicates chorea)

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22
Q

What are the signs on physical examination of rheumatic fever?

A

Heart murmur - mitral regurgitation is the most common valvular problem caused which results in pan-systolic murmur heard loudest at apex and which radiates to the axilla OR aortic regurgitation causing an early diastolic murmur
Pericardial rub
Signs of congestive heart failure
Jerky, uncoordinated choreiform movements
Red, hot or swollen joints
Small, painless nodules beneath the skin
Erythema marginatum

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23
Q

What are the appropriate investigations for rheumatic fever?

A

Bloods:
ESR, CRP, WCC may be raised

Blood cultures - show no growth

ECG - prolonged PR interval

Chest X-Ray - may show congestive cardiac failure or chamber enlargement

Echocardiogram: may reveal morphological changes to the mitral and/or aortic valves. Allows you to see the severity of regurg.

Throat culture: growth of beta-haemolytic group A streptococci

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24
Q

Define abdominal aortic aneurysm

A

A permanent pathologial dilation of the aorta with a diameter >1.5 times the expected anteroposterior diameter of that segment, given the patient’s sex and body size.
Localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal. Usually located BELOW the renal arteries.

(Normal abdominal aorta diameter = 2cm)

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25
Q

What are the risk factors for abdominal aortic aneurysm?

A
SMOKING
Family history
Increased age
Male sex (however rupture more likely in females)
Congenital/connective tissue disorders
Dyslipidaemia
COPD
Atherosclerosis
Hypetension
Centripetal obesity

There are NO specific identifiable causes - may be due to atherosclerosis OR altered tissue metalloproteinases diminish the integrity of the arterial wall

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26
Q

Summarise the epidemiology of abdominal aortic aneurysms

A

Epidemiology varies by region, age and sex
Highest prevalence in male smokers
Prevalence increases with age
4-6 times more likely in men

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27
Q

What are the presenting symptoms of abdominal aortic aneurysm?

A

If unruptured: ASYMPTOMATIC and an incidental finding

If ruptured:
Abdominal, back, loin or groin pain which is sudden and severe
Syncope
Shock

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28
Q

What is the triad for the presentation of a ruptured abdominal aortic aneurysm?

A

Abdominal and/or back pain
Pulsatile abdominal mass
Hypotension

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29
Q

What are the signs on physical examination of abdominal aortic aneurysm?

A

Palpable, pulsatile, laterally expansile abdominal mass
Hypotension
Abdominal bruit
Retroperitoneal haemorrhage can cause Grey-Turner’s sign

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30
Q

What are the appropriate investigations for abdominal aortic aneurysm?

A

ABDOMINAL USS - abdominal aorta diameter >3cm. Cannot tell if aneurysm is leaking

Bloods:
ESR/CRP - if elevated, inflammatory AAA
FBC - leukocytosis and anaemia suggest inflectious AAA
Culture - if positive with leukocytosis and anaemia, suggests infectious AAA

CT angiography - shows if ruptured
MRI angiography - anatomical mapping to assist with operative planning

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31
Q

Define aortic dissection

A

A separation occurs in aortic wall intima, usually by a discrete intimal tear, causing blood flow into a new false channel composed of the inner and outer layers of the media.

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32
Q

Explain the aetiology of aortic dissection

A

Results from an intimal tear that expands into the media of the aortic wall which is preceded by degenerative changes in the smooth muscle of the media.

  • HYPERTENSION
  • Bleeding from the vasa vasorum
  • Connective tissue disease: Marfan syndrome and Ehlers-Danlos syndrome (weakening of the media)
  • Bicuspid aortic valve
  • Aortic atherosclerosis
  • Iatrogenic (aortic manipulation with cardiac surgery or interventional procedures.)
  • Congenital cardiac abnormalities (e.g. coarctation of the aorta)
  • Aortitis
  • Trauma
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33
Q

How can aortic dissection give rise to organ hypoperfusion and associated symptoms?

A

Expansion of the false lumen can lead to obstruction of the subclavian, carotid, coeliac and renal arteries. Hypoperfusion of the target organs of these major arteries can give rise to other symptoms (e.g. carotid artery collapse).

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34
Q

What are the risk factors of aortic dissection?

A
Hypertension
Atherosclerotic aneurysmal disease
Marfan’s syndrome
Ehlers-Danlos syndrome
Bicuspid aortic valve
Smoking
Coarctation
Crack cocaine use
Family history of aortic dissection
Increased age
Heavy lifting
Pregnancy
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35
Q

What is aortic coarctation?

A

Congenital abnormality whereby the aorta is narrowed

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36
Q

Summarise the epidemiology of aortic dissection

A

Mostly affects men over 50 years old (40-60 is most common)

0.5-3 cases per 100,000 people annually

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37
Q

What are the presenting symptoms of aortic dissection?

A

Acute severe central TEARING chest pain which radiates to back (interscapular and lower pain)

Other symptoms caused by obstruction of branches of the aorta:
Carotid artery - hemiparesis (weakness of half the body), dysphasia, blackout
Coronary artery - chest pain (angina or MI)
Subclavian artery - ataxia, loss of consciousness
Anterior spinal artery - paraplegia
Coeliac axis - severe abdominal pain (due to ischaemic bowel)
Renal artery - anuria, renal failure

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38
Q

What are the signs on physical examination of aortic dissection?

A

BLOOD PRESSURE DIFFERENCE BETWEEN THE TWO ARMS >20mmHg
Pulse deficit (reduced or absent due to aortic arch involvement)
Diastolic murmur on back below left scapula descending to abdomen (crescendo murmur common in proximal dissections)
Hypertension
Wide pulse pressure
Hypotension associated with tamponade

Signs of Aortic Regurgitation:
High volume collapsing pulse
Early diastolic murmur over aortic area

Pulsus paradoxus - Abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. 
May indicate: 
- Tamponade 
- Pericarditis 
- Chronic sleep apnoea 
- Obstructive lung disease
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39
Q

What are the appropriate investigations for aortic dissection?

A

CT ANGIOGRAPHY - will show intimal flap
ECG - often normal however if MI, ST segment depression
CXR - may show widened mediastinum

Bloods:
Cardiac enzymes - usually negative
Renal function tests - elevated creatinine and urea if renal perfusion is compromised
LFTs - elevated AST and ALT if liver perfusion is compromised
FBC - may show anaemia if haemorrhage
Type and cross to prepare for surgery

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40
Q

Define aortic stenosis

A

Obstruction of blood flow across the aortic valve due to pathological narrowing.
A progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure.
Narrowing of the left ventricular outflow at the level of the aortic valve

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41
Q

Explain the aetiology of aortic stenosis

A

Calcification of aortic valve - most common cause in adults
Congenital bicuspid valve
Rheumatic heart disease in developing countries

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42
Q

What are the risk factors for aortic stenosis?

A
Smoking
Hypertension
Diabetes
LDL cholesterol
Age >60 years old
Congenitally bicuspid valve
Rheumatic heart disease
Chronic kidney disease
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43
Q

Summarise the epidemiology of aortic stenosis

A

Most common valvular disease in US and Europe - 3% of 75 year olds
2nd most frequent cause for cardiac surgery
More common in males
Patients typically prevent 70s-80s
Patients with bicuspid aortic valves present two decades earlier

44
Q

What are the presenting symptoms of aortic stenosis?

A

May be asymptomatic initially
Dyspnoea on exertion
Exertional chest pain (angina due to increased O2 demand of the hypertrophied left ventricle)
Syncope or dizziness on exercise (due to outflow obstruction)
Symptoms of heart failure (e.g. dyspnoea, orthopnoea)

45
Q

What are the signs on physical examination of aortic stenosis?

A

Ejection systolic murmur (crescendo-decrescendo) which radiates to carotids and is loudest at right upper sternal border
Diminished S2 (softened or absent)
Narrow pulse pressure
Slow-rising pulse
Thrill in the aortic area (only if severe)
Forceful sustained thrusting undisplaced apex beat
A bicuspid valve may produce an ejection click

46
Q

What are the appropriate investigations for aortic stenosis?

A

Transthoracic echocardiogram with Doppler (visualises structural changes and levels of stenosis) - elevated aortic pressure gradient, measurement of valve and LV ejection fraction

Cardiac MRI - shows stenotic aortic valve

Cardiac catheterisation - shows elevated aortic pressure gradient

ECG - may show left bundle branch block and left ventricular hypertrophy:

  • Absent Q waves
  • Deep S in V1/V2
  • Tall R in V5/V6
  • Inverted T waves in I, aVL and V5/6
  • Left axis deviation

CXR - Post-stenotic enlargement of ascending aorta, Calcification of aortic valve
Cardiac angiography - Allows differentiation from other causes of angina (e.g. MI) and assessment of concomitant coronary artery disease

47
Q

Define arterial ulcers

A

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

48
Q

Summarise the aetiology and risk factors of arterial ulcers?

A

The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities

Risk Factors:
Coronary heart disease 
History of stroke or TIA 
Diabetes mellitus 
Peripheral arterial disease (e.g. intermittent claudication)
Obesity and immobility
49
Q

Summarise the epidemiology of arterial ulcers

A

22% of leg ulcers are arterial ulcers

Prevalence increases with age and obesity

50
Q

What are the presenting symptoms of arterial ulcers?

A

Often DISTAL - at the dorsum of the foot or between the toes (over bony prominences)
Punched-out appearance
Often elliptical with clearly defined edges (sharp demarcation)
The ulcer base contains grey, granulation tissue

NIGHT PAIN - hallmark of arterial ulcers

  • Painful, especially at night or when the legs are elevated
  • Pain is worse when supine (arterial blood flow is further reduced when supine)
  • Pain is relieved by dangling the affected leg off the end of the bed
51
Q

What are the signs on physical examination of arterial ulcers?

A
Night pain 
Punched-out appearance 
Hairlessness 
Pale, cold skin 
Absent pulses 
Nail dystrophy 
Wasting of calf muscles
52
Q

What are the appropriate investigations for arterial ulcers?

A

Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
ABPI - < 0.8
Percutaneous angiography
ECG

Bloods:
Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor)
FBC - anaemia can worsen the ischaemia

53
Q

What is ABPI and what do the results mean?

A

Highest ankle pressure DIVIDED by highest brachial pressure
>1.2 - Abnormally hard vessel (e.g. calcified - often false negative)
1.2-1.0 - normal
0.8-0.9 - mild arterial disease and claudication
0.5-0.79 - moderate arterial disease with severe claudication
<0.5 - severe arterial disease with pain at rest, ulceration, gangrene and critical ischaemia

54
Q

What are the 3 types of ulcers and how do you distinguish them?

A

Arterial ulcer - punched out ulcer, night pain, pain when supine, low ABPI, cold skin
Venous ulcer - painful, worse on standing, normal ABPI, warm skin
Neurotrophic ulcer - painless, abnormal sensation, warm skin

55
Q

What is atrial flutter and its pathophysiology?

A

A macro-reentrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm
Wave of muscle contraction through atria
Re-entrant rhythm in atria - overrides sinus node - atria contract repeatedly at fast rate
Between IVC and coronary sinus is CAVOTRICUSPID ISTHMUS which propagates re-entry signal more slowly - allows to get past refractory period

56
Q

What are the two types of atrial flutter?

A

Type 1 - TYPICAL ATRIAL FLUTTER - most common
Single re-entrant cycle which moves around the tricuspid valve of RIGHT atrium in counter-clockwise direction

Type 2 - ATYPICAL ATRIAL FLUTTER
Re-entrant cycle in right or left atrium, exact location less clearly defined

57
Q

What causes atrial flutter?

A

Underlying disease such as ischaemia makes heart cells irritable and changes properties such as refractory period, making re-entrant circuit more likely
Usually initiated by premature atrial contraction due to unknown cause

58
Q

What are the appropriate examinations for atrial flutter?

A

ECG - electrical activity not initiated by SA node so NO P WAVES - F-waves produced instead which have sawtoothed shape most prominent in leads II, III, aVF, and V1.
See 2:1 atrial:ventricular beats, for example as AV node has a much longer refractory period than SA node, therefore not every atrial contraction can cause a ventricular contraction

CXR - may be underlying lung disease
Bloods:
Thyroid function tests - can be underlying thyroid disease
U&Es - may be underlying electrolyte abnormality

59
Q

What are the atrial and ventricular refractory period times?

A
Atrial = 150ms
Ventricular = 330ms
60
Q

What are the presenting symptoms of atrial flutter?

A
If supraventricular tachycardia and underlying condition which means cannot tolerate tachy:
Shortness of breath
Chest pain
Dizziness
Nausea
Palpitations
Fatigue
Syncope

Symptoms of heart failure or pulmonary symptoms

61
Q

What are the possible complications of atrial flutter?

A
  1. Prolonged tachycardia leads to ventricular decompensation which leads to HEART FAILURE
  2. Atria not contracting effectively leads to stasis of blood which can cause clots - embolism to brain causing STROKE
    May degenerate into atrial fibrillation
62
Q

What is the management of atrial flutter?

A
  1. Anticoagulation to prevent clotting of blood to prevent stroke
  2. Rate control to prevent ventricular tachycardia - beta blockers, calcium channel blockers - try this first with anticoagulation
  3. Electrical cardioversion to stop the episode of flutter by depolarising all atrial tissue at once to allow sinus node to take control IF HAEMODYNAMICALLY UNSTABLE
  4. Radiofrequency catheter ablation which destroys cavotricuspid isthmus tissue therefore stopping propagation of signal
    Treat underlying cause
63
Q

What are the risk factors for atrial flutter?

A
Increasing age
Valvular dysfunction
Atrial septal defect
Recent cardiac or thoracic procedures
Surgical or post-ablation scarring of atria
Heart failure
Hyperthyroidism
COPD
Asthma
Pneumonia
Diabetes
Male
Anti-arrhythmic drugs for atrial fibrillation
64
Q

Summarise the epidemiology of atrial flutter

A

Prevalence increases with age
2.5 times more common in men
Often co-exists with atrial fibrillation

65
Q

What are the signs on physical examination of atrial flutter?

A

Hypotension

Jugular venous pulsations with rapid flutter waves

66
Q

What are the possible complications of atrial fibrillation?

A

THROMBOEMBOLISM - Embolic stroke risk of 4% per year
Risk is increased with left atrial enlargement or left ventricular dysfunction

Worsening of existing heart failure

67
Q

What is the prognosis of atrial fibrillation?

A

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

68
Q

Define cardiac arrest

A

Sudden cardiac arrest is a sudden state of circulatory failure due to a loss of cardiac systolic function.
Acute cessation of cardiac function.
It is the result of 4 specific cardiac rhythm disturbances:
1. Ventricular fibrillation
2. Pulseless ventricular tachycardia
3. Pulseless electrical activity
4. Asystole.

Torsades de pointes is a sub-group of polymorphic VT in patients with an underlying prolonged QT interval, sometimes related to hypomagnesaemia.

69
Q

Explain the aetiology of cardiac arrest

A
Main underlying causes:
Ischaemic heart disease
Cardiovascular disease
Dysrhythmias
Cardiomyopathy

Ventricular tachycardia and ventricular fibrillation are the two most common causes

Pulseless electrical activity is caused by myocardial ischaemia/infarction, hypovolaemia, hypoxia, and pulmonary embolism

The REVERSIBLE causes of cardiac arrest are the 4 Hs and 4 Ts: 
Hypothermia
Hypoxia
Hypovolaemia
Hypokalaemia/Hyperkalaemia 

Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis))
Thromboembolic
Tamponade
Tension pneumothorax

70
Q

Summarise the epidemiology of cardiac arrest

A

Survival is estimated at <20% for patients presenting out-of-hospital with Ventricular Fibrillation
Survival is <10% overall for patients presenting with out-of-hospital cardiac arrest

71
Q

What are the presenting symptoms of cardiac arrest?

A

Patient unresponsive following syncope
Cardiac arrest is usually sudden

May be preceded by:
Fatigue
Fainting
Blackouts
Dizziness
72
Q

What are the signs on physical examination of cardiac arrest?

A

Unconscious and not breathing

Absent carotid pulses (absence of circulation)

73
Q

What are the appropriate investigations for cardiac arrest?

A
Bloods:
FBC - low haematocrit in haemorrhage
U&amp;Es - may show electrolyte abnormalities eg hyper or hypokalaemia as a cause
Cardiac biomarkers - normal or elevated
ABG 

Continuous cardiac monitoring - identify cardiac rhythm
Echo - assesses cardiac activity and left ventricular function. May show valvular abnormalities, myocardial scarring, cardiomyopathy, pericardial effusion, tamponade
ECG: may show QT interval, ST-segment or T-wave changes; conduction abnormalities; ventricular hypertrophy

74
Q

Which rhythms are shockable and which are non-shockable?

A

Shockable:
Ventricular fibrillation
Pulseless Ventricular tachycardia

Non-shockable:
Asystole
Pulseless electrical activity

75
Q

What is the management of cardiac arrest?

A

Attach cardiac monitor and defibrillator

If pulseless VT or VF (shockable rhythms): 
Defibrillate once (150-360 J biphasic, 360 J monophasic)  CPR, reassess rhythm, shock again if still in pulseless VT or VF 
Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins 
If persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine) 

If pulseless electrical activity or asystole (non-shockable rhythms):
CPR for 2, and then reassess rhythm
Administer adrenaline (1 mg IV) every 3-5 mins
Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm

Treatment of REVERSIBLE causes:
Hypothermia - warm slowly
Hypokalaemia/Hyperkalaemia - correction of electrolyte levels
Hypovolaemia - IV colloids, crystalloids and blood products
Tamponade - pericardiocentesis
Tension Pneumothorax - aspiration or chest drain
Thromboembolism - treat as PE or MI
Toxins - use antidote for given toxin

76
Q

What is the rate and ratio of CPR?

A

Rate: 100-120 compressions per minute
30 compressions:2 rescue breaths
Compression at least 5cm

77
Q

What are the possible complications of cardiac arrest?

A

Death
Rib and sternal fractures
Irreversible anoxic brain injury
Recurrent cardiac arrest

78
Q

What is the prognosis of cardiac arrest?

A

Generally poor
Early provision of CPR improves prognosis
Worse outcomes: long time to discovery of arrest, short duration of CPR, pre-existing cerebrovascular accident or renal dysfunction

79
Q

Define cardiac failure

A

Inability of the cardiac output to meet the body’s demands despite normal venous pressures. The impaired ability of the heart to cope with the metabolic needs of the body.

80
Q

What are the types of cardiac failure and their risk factors?

A
LOW OUTPUT Cardiac Failure (reduced cardiac output) 
1. Left Heart Failure: 
IHD
Hypertension
Cardiomyopathy
Aortic valve disease
Mitral regurgitation 
  1. Right Heart Failure:
    Secondary to left heart failure (congestive cardiac failure)
    Infarction
    Cardiomyopathy
    Pulmonary hypertension/embolus/valve disease
    Chronic lung disease
    Tricuspid regurgitation
    Constrictive pericarditis/pericardial tamponade
3. Biventricular Failure: 
Arrhythmia
Cardiomyopathy (dilated or restrictive)
Myocarditis
Drug toxicity 
HIGH OUTPUT Cardiac Failure (increased demand): 
Anaemia 
Beri Beri 
Pregnancy 
Paget's disease 
Hyperthyroidism 
Arteriovenous malformation
81
Q

Summarise the epidemiology of cardiac failure

A

10% of those over 65 years old have heart failure

82
Q

What are the presenting symptoms of the different types of heart failure?

A

Left Heart Failure - symptoms caused by pulmonary congestion causing pulmonary hypertension and oedema

  • Dyspnoea
  • Orthopnoea (more venous blood back to heart and into pulmonary circulation)
  • Paroxysmal nocturnal dyspnoea
  • Fatigue
Acute Left Ventricular Failure: 
Dyspnoea
Wheeze
Cough
Pink frothy sputum 
Right Heart Failure: blood backup in body 
Swollen ankles
Fatigue
Increased weight (due to oedema)
Reduced exercise tolerance
Anorexia
Nausea
83
Q

What are the signs on physical examination of cardiac failure?

A

Left Heart Failure:
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
S3 gallop (caused by rapid ventricular filling)
Pan-systolic murmur (due to functional mitral regurgitation)

Acute Left Ventricular Failure: 
Tachypnoea
Cyanosis
Tachycardia
Peripheral shutdown
Pulsus alternans Gallop rhythm
Wheeze (cardiac asthma)
Fine crackles throughout lung 

Right Heart Failure:
Raised JVP - > 3cm
Hepatomegaly/splenomegaly due to blood back up
Ascites
Ankle/sacral pitting oedema
Signs of functional tricuspid regurgitation

84
Q

What is pulsus alternans and why does it occur with acute left ventricular failure?

A

Pulsus alternans = Arterial pulse waveforms showing alternating strong and weak beats.
It is a sign of LV systolic impairment.

In LV dysfunction, ejection fraction significantly decreases.
Causes reduction in stroke volume therefore more blood remains in ventricle.
This causes an increase in end-diastolic volume.
This means that the left ventricle is stretched more for the next contraction.
Due to Starling’s Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume leads to an increase in the strength of the myocardial contraction.
This results in a stronger systolic pulse.

85
Q

What are the appropriate investigations for cardiac failure?

A

Bloods: FBC, U&E, LFTs, CRP, Glucose, Lipids, TFTs

ACUTE Left Ventricular Failure:
ABG
Troponin - rule out MI
BNP - Raised plasma BNP (>400pg/ml) suggests diagnosis of cardiac failure whereas low plasma BNP rules out cardiac failure (<100pg/ml - 90% sensitivity)

CXR:
Alveolar shadowing 
Kerley B lines (interstitial oedema)
Cardiomegaly 
Upper Lobe Diversion 
Pleural Effusion 
Fluid in the fissures
Perihilar shadowing

ECG: May be normal, may show ischaemic changes (pathological q waves, t wave inversion), may show arrhythmia or left ventricular hypertrophy

Echocardiogram - Assess ventricular contraction, systolic dysfunction = LV ejection fraction < 40%, diastolic dysfunction = decreased compliance of myocardium causing restrictive filling

Swan-Ganz Catheter - Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures

86
Q

What is congestive cardiac failure?

A

The inability of the cardiac output to meet the demands of the body without increasing diastolic pressure which results in breathlessness and abnormal sodium and water retention leading to oedema.

87
Q

What is the management of cardiac failure?

A

Acute Left Ventricular Failure:

  1. Treating Cardiogenic Shock (severe cardiac failure with low blood pressure):
    - Use of inotropes (e.g. dobutamine - cardiac stimulant which acts on beta-1 and increases contractility)
    - Managed in ITU
  2. Treating Pulmonary Oedema:
    - Sit the patient up
    - 60-100% Oxygen (and consider CPAP)
    - Diamorphine (venodilator + anxiolytic)
    - GTN infusion to reduce preload
    - IV furosemide if fluid overloaded (venodilator and later diuretic effect)
  3. Monitor: BP, Respiratory rate, Oxygen saturation, Urine output, ECG
  4. TREAT THE CAUSE! (e.g. MI, arrhythmia)

Chronic Left Ventricular Failure:
TREAT THE CAUSE (e.g. hypertension) AND TREAT EXACERBATING FACTORS (e.g. anaemia).

  • ACE Inhibitors: Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling
  • Beta-Blockers: Blocks the effects of a chronically activated sympathetic system!!!
  • Loop Diuretics: Alongside dietary salt restriction, can correct fluid overload
  • Aldosterone Antagonists (must monitor K+ as these drugs may cause hyperkalaemia)
  • Angiotensin Receptor Blockers (must monitor K+ as these drugs may cause hyperkalaemia)
  • Digoxin: Positive inotrope, reduces hospitalisation but does NOT improve survival. Increases strength of heart muscle contraction.

Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and survival in patients with LVEF < 35% - stimulates ventricles to contract at same time

Management of underlying associated conditions eg hypertension, IHD, valvular disease, diabetes, rheumatic fever
Lifestyle modifications - smoking and alcohol cessation, decrease sodium intake to <2g/day, maintain healthy weight, decrease fluid intake to <2L/day

88
Q

What are the possible complications of cardiac failure?

A

Respiratory failure
Cardiogenic shock
Death

89
Q

What is the prognosis of cardiac failure?

A

50% of those with severe cardiac failure die within 2 years

90
Q

What is ejection fraction and what does it mean?

A

The portion of blood pumped out of the left ventricle

Ejection fraction = stroke volume divided by total left ventricular volume

50-70% = normal
40-50% = borderline
<40% = systolic heart failure
91
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic heart failure - ventricles cannot pump enough during systole

Diastolic heart failure - not enough blood fills into the ventricles during diastole. Thick ventricular walls means the chamber doesn’t get an adequate load of blood

  • Low stroke volume
  • Normal ejection fraction
92
Q

Define cardiomyopathy

A

A variety of issues resulting from primary disease of the myocardium (heart muscle)

93
Q

What are the three types of cardiomyopathy and what do they mean?

A
  1. Dilated cardiomyopathy - all 4 chambers of the heart dilate, causing thin walls which produce less contraction force
  2. Hypertrophic cardiomyopathy - heart walls become thick, heavy and hypercontractile
  3. Restrictive cardiomyopathy - the heart muscle is stiff and less compliant, meaning the heart cannot fill properly. The muscles and ventricles all stay the same size
94
Q

Summarise the aetiology of cardiomyopathy

A

Usually idiopathic

Dilated:
Post-viral myocarditis infection
Alcohol
Drugs - cocaine, chemotherapy agents
Thyrotoxicosis
Genetic
Peripartum

Hypertrophic:
Genetic - autosomal dominant

Restrictive:
Sarcoidosis
Amyloidosis
Haemochromatosis
Radiation of heart tissue
Endocardial fibroelastosis - children
95
Q

Summarise the epidemiology of cardiomyopathy

A

Dilated cardiomyopathy is the most common type
Hypertrophic cardiomyopathy is the main cause of sudden death in young athletes
Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20%
Restrictive is even rarer

96
Q

What are the presenting symptoms of cardiomyopathy?

A
Dilated:
Heart failure symptoms - fatigue, dyspnoea, ankle oedema
Arrhythmias 
Thromboembolism 
Family history of sudden death
Hypertrophic:
Syncope
Usually NO SYMPTOMS 
Angina 
Arrhythmias 
Family history of sudden death
Restrictive:
Dyspnoea 
Fatigue 
Arrhythmias 
Ankle or abdominal swelling 
Family history of sudden death
97
Q

What are the signs on physical examination of cardiomyopathy?

A

Dilated:
Pan-systolic murmur due to mitral regurgitation
S3 heart sound after S2
S4 heart sounds before S1
Raised JVP
Displaced apex beat
Functional mitral and tricuspid regurgitations

Hypertrophic:
Crescendo-decrescendo (ejection systolic) murmur
Jerky carotid pulse
Double apex beat

Restrictive:
Raised JVP 
Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles
Palpable apex beat
Third heart sound
Ascites
Ankle oedema
Hepatomegaly
98
Q

What are the appropriate investigations for cardiomyopathy?

A

CXR: May show cardiomegaly, may show signs of heart failure

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

Echocardiography: 
Dilated: 
Left ventricular dilation
Normal or decreased wall thickness
Ejection fraction <45%

Hypertrophic:
Ventricular hypertrophy (asymmetrical septal hypertrophy)
Left ventricular volume normal or low

Restrictive:
Non-dilated non-hypertrophied ventricles
Atrial enlargement
Preserved systolic function and diastolic dysfunction (normal ejection fraction)

Cardiac Catheterisation - may be necessary to measure pressures
Endomyocardial Biopsy - find deposits in myocardium in restrictive
Pedigree or Genetic Analysis
Chest MRI/CT - see fat, iron or amyloid deposits in restrictive

99
Q

Define constrictive pericarditis

A

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

100
Q

What is the difference between pericarditis and constrictive pericarditis?

A

Constrictive pericarditis impedes normal diastolic filling and can be a medium to late complication of acute pericarditis.

101
Q

Explain the aetiology of pericarditis

A
Can occur after any pericardial disease process 
Idiopathic
Virus (Coxsackie, mumps, EBV, CMV)
TB
Mediastinal irradiation
Post-surgical
Connective tissue disease
Underlying systemic condition
102
Q

What are the risk factors of pericarditis?

A
Male 
Age 20-50 years
Transmural MI
Cardiac surgery
Neoplasm
Viral and bacterial infections
Systemic autoimmune disorders
Mediastinal radiation
Pericardial injury
103
Q

Summarise the epidemiology of constrictive pericarditis

A

More common in adults (20-50y/o) but documented in all ages
More common in males
Most common disease of the pericardium
RARE
9% of patients with acute pericarditis will develop constrictive pericarditis
TB has the HIGHEST TOTAL INCIDENCE out of all causes

104
Q

What are the presenting symptoms of constrictive pericarditis?

A

Chest pain - sharp, stabbing, pleuritic (worse on inspiration)
Pain is relieved when sitting up or leaning forward.
GTN does not relieve pain and pain is constant, not related to exertion.
Pericardial rub (high-pitched/squeaky)
Fever
Myalgia
Heart failure symptoms - fatigue, dyspnoea, peripheral oedema

105
Q

What are the signs on physical examination of constrictive pericarditis?

A
Signs of right sided heart failure:
Raised JVP
Peripheral oedema
Kussmaul's sign (paradoxical rise in JVP on inspiration)
Pulsatile hepatomegaly

ADVANCED: jaundice, cachexia, muscle wasting

106
Q

What are the appropriate investigations for pericarditis?

A
Bloods:
Serum troponin - mildly elevated
ESR/CRP - may be elevated
Serum urea - elevated if renal failure
FBC - elevated WBC

ECG - upwards concave ST-segment elevation globally with PR depressions (SADDLE SHAPED ST-ELEVATION)

Pericardial fluid/blood culture - positive if infectious cause

CXR - normal or cardiomegaly with water-bottle-shaped enlarged cardiac silhouette if large pericardial effusion. May show calcification of the pericardium.

Echocardiogram - helps distinguish from restrictive cardiomyopathy

MRI/CT - allows assessment of thickness of pericardium

Pericardial biopsy - may be indicated (especially if suspected infective cause)