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Phase 2A > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What can an ECG identity?

A

Arrhythmia
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbance
Drug toxicity

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2
Q

Risk factors for atherosclerosis?

A

Increasing age
Male
Family history
Obesity
Type 2 diabetes mellitus
Smoking
Hypertension
Hypercholesterolemia

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3
Q

How are atherosclerotic plaques distributed?

A

Peripheral and coronary arteries
Focal distribution along length of artery

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4
Q

What are the components of an atherosclerotic plaque?

A

Lipid
Necrotic core
Connective tissue
Fibrous cap

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5
Q

What is angina?

A

Chest pain caused by reversible myocardial ischaemia

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6
Q

What is the most common cause of angina?

A

Atherosclerotic narrowing

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7
Q

Types of angina?

A

Printzmetal
Stable
Unstable

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8
Q

What are the features of stable angina?

A

Induced by effort
Relieved by rest

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9
Q

What is unstable angina?

A

Angina of recent onset
Symptoms at rest, not relieved by rest or GTN spray
Creshendo pattern of increasing severity of symptoms

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10
Q

What is the cause of prinzmetals angina?

A

Coronary artery spasm

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11
Q

What is the aetiology of angina?

A

Atherosclerosis
Valvular disease
Arrhythmia
Anaemia

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12
Q

What is the pathophysiology of angina?

A

Atherosclerotic narrowing reduces blood flow to myocardium

Vessel undergoes adaptation to maximise blood flow to myocardium

Vessel adaptations are exhausted and myocardium is deprived from oxygen causing symptoms of angina

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13
Q

Risk factors for atherosclerotic cardiovascular disease?

A

Male
Family history
Increasing age
Hyperlipidaemia
Hypertension
Diabetes mellitus
Lack of exercise
Poor diet
Smoking
Obesity
Illicit drug use

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14
Q

Clinical presentation of angina?

A

Central crushing chest pain, relieved by rest/ GTN and exacerbated by exertion
Exertional dyspnoea
Perspiration
Fatigue

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15
Q

Investigations performed to diagnose angina?

A

Resting ECG
Bloods; FBC, lipid profile, troponin, glucose
Exercise ECG

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16
Q

Differentials for angina?

A

Aortic dissection
Pericarditis
PE
Pneumonia
Pneumothorax
Oesophagitis/ oesophageal spasm
GORD
Peptic ulcer disease

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17
Q

Management for angina?

A

Lifestyle modification; healthier diet, stop smoking, exercise and optimise risk factors
GTN spray for symptom relief
Antiplatelet and statin therapy based on Q-RISK score

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18
Q

What are the monitoring requirements for angina?

A

Follow-up every 4-6 months until stable, then convert to annual review
Monitor adherence to lifestyle modification

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19
Q

Complications of angina?

A

Heart failure
Ischaemic cardiomyopathy
Sudden cardiac death
Myocardial infarction
Stroke
Peripheral arterial disease

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20
Q

Prognosis of angina?

A

58% of patients will be angina free within a year of starting treatment
Dynamic process, even with therapy there can be declining symptoms and progression of disease

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21
Q

What is ACS?

A

STEMI
NSTEMI
Unstable angina

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22
Q

What is the difference between MI and unstable angina?

A

In UA there is no myocardial necrosis and hence no rise in cardiac enzymes and loss of cardiac tissue

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23
Q

What is unstable angina?

A

Myocardial ischaemia at rest or on minimal exertion in absence of acute cardiac necrosis

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24
Q

Aetiology of unstable angina?

A

Non occlusive disruption of atherosclerotic plaque
Coronary artery spasm

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25
Q

Pathophysiology of unstable angina?

A

Atherosclerotic lesion narrows blood flow through coronary artery
Acute narrowing, significantly more than normal results in rapid onset anginal symptoms
Resulting in myocardial ischaemia and chest pain with no infarction

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26
Q

Clinical presentation of unstable angina?

A

Prolonged angina lasting longer than 20 minutes
Crescendo pattern; increasing frequency, duration
Epigastric, central chest pain
Sweating
Dyspnoea
Syncope

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27
Q

Investigations performed in unstable angina?

A

ECG; normal, non specific changes
Bloods; FBC, U+E, LFT, TFT, CRP, glucose, cardiac enzymes
Chest X-ray

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28
Q

What are cardiac enzyme levels in unstable angina?

A

Normal, not elevated

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29
Q

Differentials for unstable angina?

A

Stable angina
Prinzmetal angina
STEMI/ NSTEMI
Congestive cardiac failure
Pericarditis
Myocarditis
Aortic dissection
PE
Pneumothorax
Pleuritis

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30
Q

Management of unstable angina?

A

Aspirin
Statin
GTN
Consider angiography and revascularisation is symptomatic and high risk of cardiac event

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31
Q

Monitoring requirements in unstable angina?

A

Re-evaluate symptoms 2-6 weeks after discharge and assess need for angiography/ revascularisation

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32
Q

Complications of unstable angina?

A

Bleeding risk
Thrombocytopenia
Congestive heart failure
Ventricular arrythmias

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33
Q

Prognosis of unstable angina?

A

Depends on management and progression of disease

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34
Q

What is a myocardial infarction?

A

Acute compromise of myocardial blood flow resulting in tissue ischaemia, necrosis and death

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35
Q

What is the epidemiology of MI?

A

STEMI incidence is declining and NSTEMI incidence is increasing
More common in males and older people

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36
Q

What is the aetiology of MI?

A

Acute vaso-occlusive event; Atherosclerotic plaque rupture causing complete occlusion of vessel
Dynamic occlusion; Focal coronary artery spasm
Supply demand mismatch; anaemia, blood loss, arterial inflammation

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37
Q

Pathophysiology of MI?

A

Inflammatory mediator mismatch leads to rupture of fibrous cap on atherosclerotic plaque
Thrombus forms after exposure to underlying collagen, which may grow to occlude lumen, equally a fragment may embolise and cause blockage distal to to thrombus

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38
Q

What is the pathophysiology of STEMI?

A

Complete, prolonged occlusion of a major coronary vessel resulting in transmural infarction

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39
Q

What is the pathophysiology of NSTEMI?

A

Severe narrowing or transient occlusion of a major vessel or complete occlusion of a minor vessel resulting in partial thickness infarction

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40
Q

Classification of MI?

A

Type 1; spontaneous MI due to pathological process in wall of coronary artery
Type 2; MI secondary to increased O2 demand or decreased supply
Type 3; sudden unexpected cardiac death before biomarkers can be obtained
Type 4; MI associated with PCI, stent thrombosis, restenosis
Type 5; MI associated with CABG

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41
Q

Clinical presentation of MI?

A

Chest pain; retrosternal srushing, heavy pain, radiating to left arm, neck and jaw, may be intermittent/ constant
Nausea/ vomiting
Dyspnoea
Syncope
Palpitations
Pallor

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42
Q

Investigations to diagnose MI?

A

ECG
Cardiac biomarkers
Baseline bloods; glucose, FBC, U+E, CRP, lipids
Chest X-ray

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43
Q

In which lead would anterior wall changes be seen?

A

V1-V4

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44
Q

In which lead would inferior wall changes be seen?

A

II, III, aVF

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45
Q

In which lead would lateral wall changes be seen?

A

I, aVL, V5-V6

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46
Q

Differentials for MI?

A

Unstable angina
Aortic dissection
Pulmonary embolism
Pneumothorax
Pneumonia
Pericarditis, myocarditis
GORD, Oesophageal spasm
Anxiety, panic attack

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47
Q

Management of STEMI?

A

ABCDE
Initial management; Morphine, Oxygen, Antiplatelet loading dose, Nitrates
Primary PCI if available within 120 minutes of symptom onset
If PPCI is not available then proceed with thrombolysis

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48
Q

What is the loading dose of aspirin?

A

300mg

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49
Q

What is the post STEMI management?

A

DAPT for 12 months
Statin
Beta blocker
ACE-i

Cardiac rehab

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50
Q

What is the management of NSTEMI?

A

Same initial management as STEMI
Invasive coronary angiography is should be offered within 72 hours

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51
Q

Monitoring recommendations post MI?

A

See in clinic 2 weeks post MI and every 6 months until lipids are stable

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52
Q

What is the guidance for driving after MI?

A

No driving for 4 weeks

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53
Q

Complications of MI?

A

Dressler’s syndrome
Cardiac arrhythmias
Acute heart failure
Cardiogenic shock
Ventricular aneurysm/ rupture
Mitral reguargitation
VTE
In-stent thrombosis

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54
Q

Poor prognostic factors in MI?

A

ST depression in NSTEMI
Duration of ischaemia and time to reperfusion
Extent of underlying atherosclerosis
Presence of collateral blood flow
Diameter of affect coronary vessel
Degree of occlusion
Presence of co-morbidities
Elderly with established left ventricular dysfunction

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55
Q

What is Dressler’s syndrome?

A

Pericardial inflammation as a result of of immune response to damaged myocardium in context of infarction, surgery or trauma

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56
Q

Epidemiology of Dressler’s syndrome?

A

0.1% of MI patients will develop dressler’s syndrome

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57
Q

Aetiology of Dressler’s syndrome?

A

Post MI, cardiac surgery or traumatic insult to chest

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58
Q

Risk factors for Dressler’s syndrome?

A

Heart attack
Cardiac surgery
Chest trauma
Previous use of prednisone
Viral infection
Previous case of pericarditis

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59
Q

Clinical presentation of Dressler’s syndrome?

A

Fatigue
Weakness
Fever
Chest pain; worse when lying down, relieved by leaning forward, radiates to shoulder, exacerbated by exertion
Exacerbated by exertion
Dyspnoea
Palpitations
Painful joints
Loss of appetite

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60
Q

Investigations to diagnose Dressler’s syndrome?

A

Bloods; FBC and ESR
ECG
Echocardiogram
Chest X-ray
CMR/ CT

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61
Q

Management of Dressler’s syndrome ?

A

NSAIDs
Colchicine
Prednisolone
Pericardiocentesis in severe effusion

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62
Q

Complications of Dressler’s syndrome?

A

Cardiac tamponade
Constrictive pericarditis
Complications of pericardiocentesis

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63
Q

Complications of Pericardiocentesis?

A

Damage to heart or nearby organs
Collapsed lung
Arrhythmia
Cardiac arrest
Bleeding

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64
Q

Prognosis of Dressler’s syndrome?

A

Majority of patients will make a full recovery
In 10% of patients dressler’s syndrome can reoccur

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65
Q

How can Dressler’s syndrome be avoided?

A

Colchicine dose before planned intervention/ surgery

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66
Q

What is pericarditis?

A

Inflammation of the pericardium
Can be dry (fibrinous) or effusive with purulent/ serous/ haemorrhagic exudate

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67
Q

Epidemiology of pericarditis?

A

Acute pericarditis is common between age 20 and 50
Most common disease of pericardium

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68
Q

Aetiology of pericarditis?

A

Viral infection
Systemic autoimmune disease
Secondary immune response
Post myocardial infarction
Myocarditis
Neoplasm/ Paraneoplastic syndrome
Trauma
Metabolic disorder
Medications

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69
Q

Pathophysiology of pericarditis?

A

Inflammation of pericardial tissue results in pain as pericardium is highly innervated
Effusion is a result of inflammatory cytokine release causing water to enter the pericardium

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70
Q

Classification of pericarditis?

A

Acute pericarditis; new onset, <4-6 weeks
Incessant pericarditis; more than 6 weeks but less than 3 months
Recurrent pericarditis; symptom free intervals
Chronic pericarditis; symptoms more than 3 months

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71
Q

Risk factors for pericarditis?

A

Male sex
Age between 20 and 50 years
Transmural myocardial infarction
Cardiac surgery
Neoplasm
Viral/ bacterial infections
Uraemia/ dialysis
Systemic autoimmune disorders
Pericardial/ mediastinal injury

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72
Q

Clinical presentation of pericarditis?

A

Chest pain; acute onset, sharp, pleuritic pain, relieved by sitting up or leaning forward, may radiate to shoulders
Fever
Malaise
Pericardial rub

73
Q

How can ischaemic pain be differentiated from pericarditis?

A

Pericarditis pain does not respond to nitrates

74
Q

Investigations performed in pericarditis?

A

ECG
Bloods; troponins, CRP, ESR, U+E, FBC, LFT
Chest X-ray
Echocardiogram
Pericardiocentesis

75
Q

Differentials for pericarditis?

A

Pulmonary embolism
Myocardial infarction
Pneumonia
Pneumothorax
Costochondritis

76
Q

Management of pericarditis?

A

Supportive care
Exercise restriction
NSAIDS
Colchicine
Consider steroids in severe cases
Consider pericardiocentesis in severe cases and risk of tamponade

77
Q

Monitoring requirements in pericarditis?

A

Long term surveillance is not necessarily
Repeat imaging maybe required inpatients with associated effusion or suspicion of constrictive pericarditis

78
Q

Complications of pericarditis?

A

Chronic constrictive pericarditis
Cardiac tamponade

79
Q

Prognosis of pericarditis?

A

Generally a self limiting disease
Poor prognostic factors; evidence of large pericardial effusion, high fever, sub-acute course, failure to respond to NSAIDs

80
Q

What is cardiac tamponade?

A

Accumulation of pericardial fluid, blood, pus or air within pericardial space resulting in increased intra-pericardial pressure causing impaired cardiac output and reduced diastolic function

81
Q

Epidemiology of cardiac tamponade?

A

More common in middle and older populations
More common in patients with specific underlying cause rather than idiopathic pericarditis

82
Q

Aetiology of cardiac tamponade?

A

Iatrogenic; cardiac surgery, intervention
Trauma
Malignancy
Idiopathic effusion
Viral, bacterial infection
Radiation
Connective tissue disease

83
Q

Pathophysiology of cardiac tamponade?

A

Accumulation of fluid in pericardial space results in increased pressure
This can rise above chamber pressure impairing cardiac function causing pressures in heart to rise to prevent collapse
Eventually equalisation of pressures can result in collapse of cardiac chambers

84
Q

Risk factors for cardiac tamponade?

A

Malignancy
Aortic dissection
Purulent pericarditis
Large idiopathic pericardial effusion
Iatrogenic- related haemorrhage
Tuberculosis
Autoimmune disease
Hypothyroidism
Uraemia and renal failure
Anticoagulation

85
Q

Clinical presentation of cardiac tamponade?

A

Becks triad
Dyspnoea
Tachycardia
Pulsus paradoxus

86
Q

What is beck’s triad?

A

Elevated JVP
Muffled heart sounds
Hypotension

87
Q

Investigations performed in cardiac tamponade?

A

ECG; low voltage QRS
TTE
Chest X-ray
Bloods; FBC, ESR, cardiac enzymes

88
Q

What is seen on TTE?

A

Large pericardial effusion, >20mm of echo free space in diastole
Chamber collapse

89
Q

Differentials for cardiac tamponade?

A

Constrictive pericarditis
Restrictive cardiomyopathy
Cardiogenic shock

90
Q

Management of cardiac tamponade?

A

Supportive management
NSAIDs
Pericardiocentesis
Surgical drainage

91
Q

Monitoring requirements in cardiac tamponade?

A

Serial follow-up to check for recurrence

92
Q

Complications of cardiac tamponade?

A

Recurrent/ refractory pericarditis and pericardial effusion
Cardiac arrest
Organ hypoperfusion
Effective constrictive pericarditis

93
Q

Prognosis of cardiac tamponade?

A

Patients with underlying malignancy have highest mortality
Penetrating chest wounds/ idiopathic causes have best outcome
Without drainage will progress to cardiovascular collapse

94
Q

What is a congenital heart defect?

A

Abnormality of the heart structure and anatomy which the patient is born with usually due to abnormalities in embryological development

95
Q

Examples of acyanotic heart defects?

A

VSD
ASD
Patent ductus arteriosus
Coarctation of aorta

96
Q

Examples of cyanotic heart defects?

A

Tetralogy of fallot
Transposition of great arteries
Truncus arteriosus

97
Q

What is Eisenmenger’s syndrome?

A

A reversal in a previous left to right shunt due to pressure overload on right side of the heart.

Pressures between two sides equalise and eventually right heart pressure increases above left heart so the shunt now becomes right to left

98
Q

DWhat is a VSD?

A

Congenital or acquired defect in the interventricular septum resulting in communication between right and left ventricle

99
Q

Epidemiology of VSD?

A

Perimembranous is most common type
Associated with down’s syndrome

100
Q

Aetiology of VSD?

A

Congenital; developmental abnormalities, genetics (Down’s syndrome)

Acquired; acute MI, penetrating/ blunt trauma

101
Q

What determines haemodynamic effect of a congenital heart defect?

A

Size of defect
Pulmonary vascular resistance

102
Q

Risk factors for VSD?

A
102
Q

Pathophysiology of VSD?

A

Hole in the interventricular septum creates a channel between ventricles
Creates a left to right shunt and is acyanotic

102
Q

Pathophysiology of VSD?

A

Hole in the interventricular septum creates a channel between ventricles
Creates a left to right shunt and is acyanotic

103
Q

Risk factors for VSD?

A

Family history of congenital heart disease
Downs Syndrome
Maternal consumption of alcohol during pregnancy
Recurrent pulmonary infections
Recent myocardial infarction (usually 2-5 days)
Recent trauma

104
Q

Clinical presentation of VSD?

A

Failure to thrive
Shortness of breath

105
Q

What murmur is heart in VSD?

A

Systolic murmur at left parasternal region
Holosystolic murmur that does not increase with inspiration

106
Q

Investigations performed to diagnose VSD?

A

Echocardiogram
Chest X-ray
ECG

107
Q

Differentials for VSD?

A

Atrial septal defect
Patent ductus arteriosus
Mitral regurgitation
Tricuspid regurgitation
Tetralogy of Fallot
Pulmonic stenosis

108
Q

Management of VSD?

A

Watch and wait if small VSD
Closure of defect
Heart and lung transplantation if Eisenmenger’s syndrome has developed
Prophylactic antibiotics before dental procedures

109
Q

Monitoring requirements in VSD?

A

Asymptomatic patients should be followed annually
After shunt repair monitor for residual shunt, development of heart block and other arrhythmias

110
Q

What should be monitored in routine follow up for VSD?

A

Development of aortic/ tricuspid regurgitation
Assess degree of left to right shunt
Ventricular function
Pulmonary pressures

111
Q

Complications of VSD?

A

Aortic regurgitation
Surgical complications
Infective endocarditis

112
Q

Prognosis of VSD?

A

Restrictive VSD closes spontaneously in ~ 50%
In moderate defects if left untreated can develop congestive heart failure and pulmonary hypertension
Large non restrictive defects require closure and have high risk of Eisenmenger’s syndrome

113
Q

What is an ASD?

A

Congenital cardiac defect as a result of incomplete separation between right and left atrium

114
Q

Types of ASD?

A

Secundum
Ostium primum
Sinus venosus
Coronary sinus
Vestibular

115
Q

Epidemiology of ASD

A

Secundum defects are responsible for 80% of interatrial communications
More common in women
Mostly occur sporadically with no family history

116
Q

Aetiology of ASD?

A

Mutations in NKX2.5 and TBX5
Genetic syndromes; trisomy 21, Holt-Oram syndrome, Noonan syndrome

117
Q

What genetic condition is commonly associated with congenital heart disease?

A

Down’s syndrome `

118
Q

Pathophysiology of ASD?

A

Communication between right and left atrium results in a left to right shunt

In severe defects Eisenmenger’s syndrome can occur

119
Q

Risk factors for ASD?

A

Female sex
Maternal alcohol consumption
Genetic syndromes

120
Q

Clinical presentation of ASD?

A

Can be asymptomatic
Failure to thrive
Dyspnoea
Syncope

121
Q

Differentials for ASD?

A

Partial anomalous pulmonary venous drainage
Ventricular septal defect
Patent ductus arteriosus
Pulmonary stenosis
Right bundle branch block

122
Q

Investigations to diagnose ASD?

A

Chest X-ray
Echocardiogram

123
Q

What murmur is heard in ASD?

A

Systolic ejection murmur radiating to back
Fixed splitting of second heart sound

124
Q

Management of ASD?

A

Corrective closure
Consider pulmonary vasodilator
Prophylactic antibiotics

125
Q

What is echocardiography used to assess in ASD?

A

Size of defect
Location of defect
Shunt size
Shunt pressure
Chamber size and hypertrophy

126
Q

Monitoring requirements for ASD?

A

Serial echo to assess RV function and residual shunting
ECG to assess for arrhythmias

127
Q

Complications of ASD?

A

Device erosion
Pulmonary vascular obstructive disease
Pericardial effusion/ tamponade
Paradoxical embolisation
Congestive heart failure
Infective endocarditis
Atrial fibrillation

128
Q

Prognosis of ASD?

A

Majority of ASD have good prognosis, many remain asymptomatic
In large defects with Eisenmenger’s is associated with poorer prognosis

129
Q

What is patent ductus arteriosus?

A

Persistence of fetal ductus arteriosus resulting in communication between aorta and pulmonary artery

130
Q

Epidemiology of PDA?

A

More common in pre-term infants
Higher incidence in females and babies born at higher altitudes

131
Q

Pathophysiology of PDA?

A

Patency of ductus is maintained by low oxygen environment and circulating prostaglandins
After birth saturations rise causing constriction of the duct through action of potassium channels and reduction in prostaglandins
These mechanisms malfunction and the ductus remains open resulting in a left to right shunt
To compensate there is degree of LV hypertrophy and dysfunction

132
Q

Risk factors for PDA?

A

Prematurity
Maternal rubella
Female sex
Respiratory distress syndrome
High altitude
Family history
Black race

133
Q

Clinical presentation of PDA?

A

Tachypnoea, dyspnoea, apnoea
Low diastolic pressure
Failure to thrive
Diaphoresis
Hyperdynamic precordium
Bounding peripheral pulse

134
Q

What murmur is heard in PDA?

A

Machine like murmur
Third heart sound at apex
Mid diastolic rumble at apex

135
Q

Investigations performed in PDA?

A

Chest X-ray
ECG
Echocardiogram

136
Q

Differentials for PDA?

A

Venous hum
Coronary artery fistula
Left to right shunt
Aortic regurgitation

137
Q

Management for PDA?

A

Ibuprofen or indomethacin
Percutaneous catheter device closure
surgical ligation

138
Q

At what age can ibuprofen be given to an infant?

A

32 weeks and older

139
Q

Monitoring requirements for PDA?

A

Pre-mature infants need closer monitoring
Follow-up between every 3 months - 2 years depending on individual circumstances

140
Q

Complications of PDA?

A

Respiratory distress syndrome
Necrotising enterocolitis in premature infants
Pulmonary haemorrhage in premature infants
Pulmonary hypertension
Congestive heart failure
Aneurysm of the duct

141
Q

Prognosis of PDA?

A

Prematurity is associated with poorer prognosis and associated with chronic lung disease, pulmonary haemorrhage
Spontaneous closure after 3 months of age is rare

142
Q

What is coarctation of aorta?

A

Narrowing of the aorta

143
Q

What is the most common location for aortic coarctation?

A

Site of insertion of ductus, distal to left subclavian artery

144
Q

Epidemiology of coarctation of aorta?

A

6-8% of all congenital heart defects
More common in men
Associated with Turner’s syndrome

145
Q

Aetiology of aortic coarctation?

A

Congenital malformation
Acquired; takayasu arteritis, severe atherosclerotic disease

146
Q

Risk factors for aortic coarctation?

A

Male sex
Turner’s syndrome
DiGeorge syndrome
Hypoplastic left heart syndrome
Shone’s complex
Family history

147
Q

Clinical presentation of coarctation of aorta?

A

Hypertension at young age, resistant to treatment
Diminished lower extremity pulses
Differential upper and lower extremity blood pressure
Radio- femoral delay

148
Q

Investigations performed in coarctation of aorta?

A

ECG
Chest X-ray
Echocardiogram

149
Q

Differentials for coarctation of aorta?

A

Aortic stenosis
Interrupted aortic arch
Left ventricular outflow tract obstruction
Essential hypertension
Renal artery stenosis
Phaeochromocytoma

150
Q

Management for coarctation of aorta?

A

Maintain ductus patency; prostaglandin E1
Surgical repair
Percutaneous balloon angioplasty
Stent placement

151
Q

Monitoring requirements for coarctation of aorta?

A

Lifelong follow up with frequency determined on case basis
Upper and lower extremity blood pressure should be check every visit
Periodic echocardiograms

152
Q

Complications of coarctation of aorta?

A

Coronary artery disease
Systemic hypertension
Re-coarctation after repair
Aortic aneurysm

153
Q

Prognosis of coarctation of aorta?

A

Isolated coarctation has an excellent prognosis
Re-coarctation is seen following repair hence require lifelong follow up

154
Q

What is tetralogy of fallot?

A

Congenital cyanotic heart malformation consisting of 4 abnormalities

155
Q

What abnormalities are found in tetralogy of fallot?

A

Ventricular septal defect
Overriding aorta
Pulmonary stenosis
Right ventricular outflow obstruction resulting in RVH

156
Q

Epidemiology of tetralogy of fallot?

A

Male predominance
Most common cyanotic heart defect
Occurs in 3 out of 10,000 live births

157
Q

Aetiology of tetralogy of fallot?

A

Genetics; trisomy 13, 18, 21
Maternal diabetes

158
Q

What determines degree of cyanosis in tetralogy of fallot?

A

Degree of pulmonary obstruction

159
Q

Classification of tetralogy of fallot?

A

Cyanotic tetralogy of fallot
Acyanotic tetralogy of fallot
Pulmonary atresia/ VSD
Absent pulmonary valve syndrome

160
Q

What is the gold standard investigation in congenital heart defects?

A

Echocardiogram

161
Q

Risk factors for tetralogy of fallot?

A

Trisomy 21, 18, 13
DiGeorge syndrome
MKX2.5 gene
Family history of congenital heart disease
Maternal diabetes, use of retinoids

162
Q

What murmur is heard in tetralogy of fallot?

A

Harsh ejection systolic murmur loudest at left sternal border

163
Q

Clinical presentation of tetralogy of fallot?

A

Tachypnoea
Cyanosis
Hypercyanotic tet spells; crying and deep breathing baby, murmur disappears

164
Q

What is seen on echo in tetralogy of fallot?

A

Infundibular pulmonary stenosis
Overriding aorta
Non restrictive VSD
Concentric right ventricular hypertrophy

165
Q

Investigations performed in tetralogy of fallot?

A

Pulse oximetry
Echocardiogram
Chest X-ray

166
Q

What shaped heart is seen on chest X-ray in tetralogy of fallot?

A

Boot shaped

167
Q

Differentials for tetralogy of fallot?

A

Other cyanotic congenital heart defects
Pulmonary stenosis
Ventricular septal defect
Primary pulmonary disease

168
Q

Management of tetralogy of fallot?

A

Manoeuvres to increase systemic venous return; keep infant calm, in parents arms, beta blockers and phenylephrine
Prostaglandins to maintain duct patency
Surgical repair
ECMO to reverse cyanosis

169
Q

In what scenarios would patency of ductus need to be maintianed?

A

Tetralogy of fallot
Coarctation of aorta
Cyanotic heart defects

170
Q

Monitoring requirements in tetralogy of fallot?

A

Monitored by paediatric cardiologist
Routine echo/ CMR

171
Q

Complications of tetralogy of fallot?

A

Cyanotic spells
Paradoxical emboli
Progressive pulmonary regurgitation and RVF
Ventricular arrhythmias
Sudden cardiac death
Congestive heart failure

172
Q

Prognosis of tetralogy of fallot?

A

After repair prognosis is good
Some patients may require further surgery

173
Q

What are the reasons for reoperation in tetralogy of fallot?

A

Pulmonary obstruction
Pulmonary regurgitations

174
Q

What is mitral stenosis ?

A

Narrowing of the mitral valve orifice resulting in poor flow of blood from left atrium to ventricle

175
Q

What is the epidemiology of Mitral stenosis?

A

Uncommon in western world due to eradication of rheumatic fever
More common in females
Prevalent in developing countries with people living in poverty

176
Q

Most common cause of mitral stenosis?

A

Rheumatic fever

177
Q

Aetiology of mitral stenosis?

A

Rheumatic fever/ rheumatic heart disease
Congenital deformity
Amyloidosis
SLE, rheumatism, arteritis
Mitral annular calcification

Phase 2A (6 decks)

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