Cardiology

Question 1

Supraventricular tachycardias

Answer 1

Sinus tachycardia
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entrant tachycardia (AVRT)

Question 2

Ventricular tachycardias

Answer 2

Ventricular tachycardia
Polymorphic ventricular tachycardia

Question 3

Accessory pathway

Answer 3

Accessory pathway = abnormal connection between the atria and ventricles away from the AVN that allows electrical activity to pass through
If electrical activity is conducted via accessory pathway, it will take an abnormal slow route -> can lead to a broad QRS

Question 4

Sinus tachycardia

Answer 4

Sinus rhythm with a HR > 100 bpm
Normal physiological response when the body is put under stress
-Exercise
-Intercurrent illness
-Underlying pathology
Management is dependent on the underlying cause

Question 5

Atrial tachycardia

Answer 5

Occurs due a abnormal focus of activity undergoing rapid depolarisation in the atria
Different types depending on the origin: single foci, multiple foci & small re-entrant circuit
Usually a regular tachyarrhythmia but multi-focal atrial tachycardia may present with an irregular rhythm
ECG: tachyarrhythmia, with a narrow QRS and abnormal P waves
-Typically there is an abnormal P wave axis with inverted P waves in the inferior leads (II, III, aVF)
Treatment - medications (beta-blockers, calcium channel blockers), ablation (treats certain areas of your heart to stop them improperly conducting electricity) - very helpful in stopping focal atrial tachycardia

Question 6

Atrial flutter

Answer 6

Specific type of atrial tachycardia - that occurs due to a rapid macro-reentrant circuit within the atria
ECG: typically sawtooth pattern, which is best visualised in the inferior leads
Due to fast atrial rate, the AVN causes a ‘block’ (some atrial activity is not conducted to the ventricles)
-Physiological response to allow time for ventricular filling
-Classically seen as a 2:1 block (two flutter waves to one QRS complex)

Question 7

Atrial fibrillation

Answer 7

Occurs due to multiple waves of spontaneous depolarisation leading to fragmentation of normal electrical activity
Causes muscle fibres to contract independently leading to ‘fibrillation’ of the atrial muscle
Multiple waves of electrical activity (varying in strength) reach the AVN -> intermittently conducts these to the ventricles -> irregular rhythm
-Irregularly irregular rhythm
-Absence of P waves
-Irregular, fibrillating baseline

Question 8

AF rate control

Answer 8

Rate control - first-line to many patients
Beta -blocker first-line: atenolol, bisoprolol
Calcium-channel blocker: diltiazem/verapamil
Digoxin: only in sedentary people with persistent AF, requires monitoring & has a risk of toxicity

Question 9

AF rhythm control

Answer 9

Rhythm control - offered to patients with reversible cause for their AF, new onset AF, heart failure caused by AF, symptoms despite being effectively rate controlled
-Cardioversion - immediate and delayed cardioversion
–Immediate - pharmacological or electrical
—Pharmacological - flecainide or amiodarone
—Electrical - aims to shock the heart back into sinus rhythm, involves using a cardiac defibrillator to deliver controlled shocks
-Long-term rhythm control using medications - beta blockers, dronedarone, amiodarone

Question 10

AF anticoagulation

Answer 10

Anticoagulation to prevent strokes
DOACs are first line

Question 11

Supraventricular tachycardia

Answer 11

Can refer to the origin of a tachyarrhythmia or a subset of abnormally fast heart rhythms that are due to reentrant circuits involving the AVN
Clinical practice -> the term SVT is reserved for these reentrant arrhythmias
1) Atrioventricular nodal reentrant tachycardia
2) Atrioventricular reentrant tachycardia

Question 12

AVNRT

Answer 12

Most common SVT - typically occurs in patients with a structurally normal heart
Due to additional conduction pathways within the AVN, which allows initiation of a reentrant circuit
Usually a rapid, narrow-complex tachycardia with absent P waves

Question 13

AVRT

Answer 13

Second most common SVT, usually presents at a younger age than AVNRT & can occur in children
Due to an accessory pathway away from the the AVN
May enable electrical impulses to pass antegrade (atria to ventricles) or retrograde (ventricles to atria)
Difficult to distinguish AVRT from AVNRT on an ECG

Question 14

Wolff-parkinson-white syndrome

Answer 14

Preexcitation syndrome that is characterised by a congenital accessory pathway & episodic tachyarrhythmias
Accessory pathway = usually referred to as the ‘Bundle of Kent’ & can allow conduction antegrade or retrograde
ECG pattern in WPW is due to preexcitation of the ventricles via the accessory pathway
-Short PR interval
-Early slurred upstroke in the QRS complex = delta wave
-Remaining QRS complex is normal - usual conduction via the AVN
Main concern is development of AF -> can deteriorate into ventricular fibrillation

Question 15

Ventricular tachycardia

Answer 15

Occurs due to a focus of electrical activity in the ventricles undergoing rapid depolarisation
Commonly due to scarring of the ventricles following MI
ECG: rapid, broad-complex tachycardia
Life-threatening arrhythmia -> loss of consciousness, loss of CO and cardiac arrest
VT without a pulse is one of the ‘shockable’ cardiac arrest rhythms

Question 16

Polymorphic VT

Answer 16

Particular types of VT that is due to depolarisation of multiple foci within the ventricles leading to variable QRS complexes
Usually secondary to MI

Torsades de pointes - subtype of polymorphic VT
-Characterised by ventricular tachycardia that ‘twists’ around the isoelectric line
-Subtype occurs secondary to a prolonged QT interval
-Management is aimed at shortening the QT interval with IV magnesium sulphate
-If unstable, they should undergo immediate DC cardioversion as with any unstable tachyarrhythmia

Question 17

Ventricular fibrillation

Answer 17

Ventricular muscle fibres contract independently
ECG: coordinated electrical activity with a chaotic, fibrillating baseline
VF is incompatible with life & patients who develop this rhythm will go into cardiac arrest
One of the ‘shockable’ cardiac arrest rhythms that requires immediate DC cardioversion

Question 18

Escape rhythm

Answer 18

Escape rhythm = SAN fails to undergo spontaneous depolarisation so electrical activity is initiated lower down
Can occur as a single beat or a sustained rhythm

Question 19

Sinus pause/arrest

Answer 19

Failure of the SAN to initiate electrical activity
Sinus pause = transient absence of P waves that lasts from 2 seconds to several minutes
Dysfunction of the SAN may manifest as failed initiation of conduction/failed transmission of electrical activity

Question 20

Sinus node dysfunction (‘sick sinus syndrome’)

Answer 20

Collective term that refers to conduction abnormalities affecting the SAN and surrounding tissue
Manifests as a variety of ECG abnormalities: sinus bradycardia, sinus pause/arrest, sinoatrial exit block, chronotropic incompetence
Also associated with atrial tachyarrhythmias
-Tachy-brady syndrome: presents with alternating bradyarrhythmias and tachyarrhythmias
Occurs due to depression of the normal autorhythmicity of the SAN and surrounding tissue

Question 21

Heart block

Answer 21

Interference of the normal transmission of conduction within the AVN can lead to varying degrees of ‘block’
First-degree heart block - prolongation of PR interval > 200ms
Second-degree heart block - underlying conduction disease
Mobitz type I: progressive prolongation of PR interval, leading to dropped QRS
Mobitz type II: randomly dropped QRS
Third-degree heart block - complete dissociation between P waves and QRS complexes on ECG

Question 22

Bradyarrhythmias clinical features

Answer 22

Asymptomatic
Fatigue, lethargy
Dizziness, pre-syncope
Syncope
Pulmonary oedema
Chest pain
Shock
Impaired consciousness

Question 23

Four cardinal features that suggest an unstable arrhythmia

Answer 23

Syncope
Myocardial ischaemia (chest pain)
Heart failure
Shock

Question 24

Bradyarrhythmias pharmacological management

Answer 24

Pharmacological therapy - used in an attempt to increase the heart rate
Atropine (antimuscarinic): reversible antagonist of muscarinic acetylcholine receptors, blocks the action of the vagus nerve on the SAN & AVN -> leads to increased SAN electrical activity and increased conduction through the AVN
Given as IV bolus, which can be repeated
Isoprenaline (non-selective beta-adrenoreceptor agonist): positive inotropic and chronotropic effects on the heart via beta-receptors, leads to an increase in HR and improved contractility
Given as IV infusion

Question 25

Pacing

Answer 25

Delivers electrical stimuli to the heart via pacing leads May be required in an emergency setting, following MI or a long-term option in patients with bradyarrhythmias Temporary pacing - transcutaneous, epicardial & transvenous Permanent pacing - permanent electronic device that is inserted under the skin (pacemaker box is attached to wires which are inserted into the heart via the transvenous route )

Question 26

Permanent pacemakers

Answer 26

Three main types of pacemaker Single chamber - single lead implanted into the right atrium/ventricle Dual chamber - two leads implanted, one in the right atrium & one in right ventricle Biventricular (cardiac resynchronisation) - left ventricular and right ventricular pacing -Used in heart failure

Question 27

Stable angina

Answer 27

Atherosclerosis affecting the coronary arteries, narrowing the lumen and reducing blood flow to the myocardium Symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN)

Question 28

Angina baseline investigations

Answer 28

Physical examination ECG FBC – anaemia U&Es, LFTs – required before starting medications Lipid profile TFTs HbA1C & fasting glucose (diabetes)

Question 29

Angina specialist investigations

Answer 29

Cardiac stress testing – assessing the patient’s heart function during exertion, can involve having the patient exercise/giving medication (dobutamine) - Options for assessing cardiac function = ECG, echo, MRI or myocardial perfusion scan CT coronary angiography – involves injecting contrast and taking CT imaged timed with heart contractions (gives detailed view of coronary arteries, highlighting any narrowing) Invasive coronary angiography – catheter is inserted into the patient’s brachial/femoral artery -> directed to coronary arteries under x-ray guidance, where contrast is injected to visualise coronary arteries = GOLD STANDARD

Question 30

Angina principles of management

Answer 30

R – refer to cardiology A – advice them about the diagnosis, management & when to call an ambulance M – medical treatment P – procedural or surgical interventions S – secondary prevention Referrals sent to rapid access chest pain clinic

Question 31

Angina medical management

Answer 31

1) Immediate symptomatic relief 2) Long-term symptomatic relief 3) Secondary prevention of CVD

Question 32

Angina immediate symptomatic relief

Answer 32

Sublingual glyceryl trinitrate in the form of spray/tablets GTN causes vasodilation, improving the blood flow to the myocardium Take GTN when symptoms start, take second dose after 5 mins if symptoms remain, take third dose after 5 mins if symptoms remain, call ambulance after a further 5 mins if symptoms remain SE: headaches, dizziness

Question 33

Angina long-term symptomatic relief

Answer 33

Beta blocker Calcium-channel blocker (diltiazem/verapamil – both avoided in HFrEF) Specialist may consider – long-acting nitrates (isosobide mononitrate), ivabradine, nicorandil, ranolazine

Question 34

Angina secondary prevention

Answer 34

Aspirin 75mg once daily Atorvastatin 80mg once daily ACE inhibitor (if diabetes, HTN, CKD, HF present) Already on a beta blocker for symptomatic relief

Question 35

Angina surgical interventions

Answer 35

Percutaneous coronary intervention (PCI) – catheter into patient’s brachial/femoral artery & guided to coronary arteries, contrast injected, areas of stenosis can be treated by dilating a balloon to widen the lumen (angioplasty) & inserting a stent to keep it open Coronary artery bypass graft (CABG) – involves opening the chest along the sternum, with a midline sternotomy incision, graft vessel is attached to the affected coronary artery, bypassing the stenotic area - Saphenous vein - Internal thoracic artery - Radial artery PCI: faster recovery, lower rate of strokes as a complication, higher rate of requiring repeat revascularisation (further procedures)

Question 36

ACS

Answer 36

Result of a thrombus from an atherosclerotic plaque blocking a coronary artery When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets 3 types – unstable angina, STEMI, NSTEMI

Question 37

Coronary arteries

Answer 37

Two coronary arteries branch from the root of the aorta: right coronary artery & left coronary artery Right coronary artery – curves around the right side and under the heart & supplies the right atrium, right ventricle, inferior aspect of the left ventricle, posterior septal area Left coronary artery – circumflex artery, left anterior descending Circumflex artery – curves around the top, left and back of the head & supplies the left atrium and posterior aspect of the left ventricle Left anterior descending – travels down the middle of the heart & supplies the anterior aspect of the left ventricle, anterior aspect of the septum

Question 38

ACS presentation

Answer 38

Central, constricting chest pain Pain radiating to the jaw/arms N&V Sweating and clamminess Feeling of impending doom SoB, palpitations Symptoms should continue at rest for more than 15 mins

Question 39

Artery, heart area, ECG leads

Answer 39

Left coronary artery – anterolateral, I, aVL, V3-6 Left anterior descending – anterior, V1-4 Circumflex – lateral, I, aVL, V5-6 Right coronary artery – inferior, II, III, aVF

Question 40

ACS investigations

Answer 40

ECG Troponin Baseline bloods – FBC, U&E, LFT, lipids, glucose CXR Echo

Question 41

ACS initial management

Answer 41

CPAIN C – call an ambulance P – perform an ECG A – aspirin 300mg I – intravenous morphine for pain is required with anti-emetic N – nitrate (GTN)

Question 42

STEMI management

Answer 42

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either: 1) Percutaneous coronary intervention (PCI) if available within 2 hours of presenting 2) Thrombolysis (if PCI not available) – involves injecting a fibrinolytic agent, significant risk of bleeding, examples are streptokinase, alteplase & tenecteplase

Question 43

NSTEMI management

Answer 43

BATMAN B – base the decision about angiography and PCI on GRACE score A – aspirin 300mg stat dose T – ticagrelor 180mg stat dose (clopidogrel if high bleeding risk or prasugrel if having angiography) M – morphine titrated to control pain A – antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography) N – nitrate (GTN) Give O2 only if sats < 95%

Question 44

NSTEMI angiography

Answer 44

Unstable patients are considered for immediate angiography GRACE score – 6-month probability of death after having an NSTEMI (above 3% is considered medium to high risk) Patients at medium to high risk are considered for early angiography with PCI (within 72 hours)

Question 45

ACS ongoing management

Answer 45

Echo Cardiac rehabilitation Secondary prevention

Question 46

ACS secondary prevention

Answer 46

6 As A – aspirin 75mg once daily indefinitely A – another antiplatelet (ticagrelor or clopidogrel) for 12 months A – atorvastatin 80mg once daily A – ACEi titrated as high as tolerated A – atenolol (or another beta-blocker, usually bisoprolol) titrated as high as tolerated A – aldosterone antagonist for those with clinical HF

Question 47

MI complications

Answer 47

DREAD Death Rupture of the heart septum or papillary muscles oEdema Arrhythmia and aneurysm Dressler’s syndrome

Question 48

Dressler’s syndrome

Answer 48

Post-myocardial infarction syndrome Caused by a localised immune response that results in inflammation of the pericardium -> pericarditis Presents with pleuritic chest pain, low-grade fever, pericardial rub on auscultation Can cause a pericardial effusion & rarely a pericardial tamponade Diagnosis can be made with ECG (global ST elevation & T wave inversion), echocardiogram (pericardial effusion) and raised inflammation markers Management – NSAIDs and in more severe cases, steroids. Pericardiocentesis may be required to remove fluid from around the heart if there is significant pericardial effusion

Question 49

Pericarditis

Answer 49

Inflammation of the pericardium Most common causes are idiopathic and viral

Question 50

Pericardial effusion

Answer 50

Potential space of the pericardial cavity fills with fluid Creates an inward pressure on the heart, making it more difficult to expand during diastole

Question 51

Pericardial tamponade

Answer 51

Pericardial effusion is large enough to raise the intra-pericardial pressure Increased pressure squeezes the heart -> reduces heart filling in diastole, decreasing CO during systole Emergency and requires prompt drainage to relieve pressure

Question 52

Pericarditis presentation

Answer 52

Chest pain – sharp, central, worse with inspiration, worse on lying down, better on sitting forward Low-grade fever Pericardial friction rub on auscultation – rubbing, scratching sound that occurs alongside the heart sounds

Question 53

Pericarditis investigations

Answer 53

Blood tests – raised inflammation markers (WCCs, CRP & ESR) ECG changes – saddle-shaped ST elevation, PR depression Echo – diagnose a pericardial effusion

Question 54

Pericarditis management

Answer 54

NSAIDs – mainstay of treatment Colchicine – taken longer-term to reduce the risk of recurrence Steroids are taken second line Underlying causes should be treated appropriately Pericardiocentesis may be required to remove fluid from around the heart

Question 55

Acute left ventricular failure

Answer 55

Occurs when an acute event results in the left ventricle being unable to move blood efficiently through the left side of the heat & into systemic circulation Backlog leading to pulmonary oedema

Question 56

Acute LVF triggers

Answer 56

Iatrogenic – aggressive IV fluids MI Arrhythmias Sepsis HTN emergency

Question 57

Acute LVF symptoms and signs

Answer 57

Symptoms – SoB, feeling unwell, cough with frothy white/pink sputum Signs on examination – raised RR, reduced oxygen sats, tachycardia, 3rd heart sound, bilateral basal crackles, hypotension

Question 58

Acute LVF investigations

Answer 58

Clinical assessment – history and examination ECG Bloods – anaemia, infection, kidney function, BNP ABG CXR Echo

Question 59

B-type natriuretic peptide

Answer 59

Hormone released from the heart ventricles when the cardiac muscle is stretched beyond normal range – raised BNP indicates the heart is overloaded beyond its normal capacity to pump effectively BNP – acts to relax the smooth muscle in blood vessels (reduces systemic vascular resistance) & also acts on kidneys as a diuretic to promote water excretion in the urine Sensitive but not specific, helps rule out HF when negative

Question 60

Acute LVF management

Answer 60

SODIUM S – sit up O – oxygen D – diuretics I – IV fluids should be stopped U – underlying causes need to be identified and treated M – monitor fluid balance Inotropes & vasopressors

Question 61

Chronic heart failure

Answer 61

Refers to the clinical features of impaired heart function, specifically the function of the LV to pump blood out of the heart and around the body HFrEF = ejection fraction < 50% HFpEF = ejection fraction > 50%, result of diastolic dysfunction where there is an issue with the left ventricle filling with blood during diastole

Question 62

Chronic HF causes

Answer 62

Ischaemic heart disease Valvular heart disease (aortic stenosis) HTN Arrhythmias Cardiomyopathy

Question 63

Chronic HF presentation

Answer 63

Breathlessness, worsened by exertion Cough Orthopnoea – breathlessness when lying flat Paroxysmal nocturnal dyspnoea Peripheral oedema Fatigue Signs – tachycardia, tachypnoea, murmurs, 3rd heart sound, bilateral basal crackles, raised JVP, peripheral oedema

Question 64

Chronic HF investigations

Answer 64

Clinical assessment NT-proBNP ECG Echo Bloods – anaemia, renal function, thyroid function, liver function, lipids, diabetes CXR and lung function tests to exclude lung pathology

Question 65

New York heart association classification

Answer 65

Used to grade the severity of symptoms related to heart failure Class I – no limitation on activity Class II – comfortable at rest but symptomatic with ordinary activities Class III – comfortable at rest but symptomatic with any activity Class IV – symptomatic at rest

Question 66

Chronic HF management principles

Answer 66

RAMPS R – refer to cardiology A – advise them about the condition M – medical treatment P – procedural or surgical interventions S – specialist heart failure MDT input eg. heart failure nurses Flu, covid and pneumococcal vaccines, stop smoking, optimise treatment of co-morbidities, written care plan, cardiac rehabilitation

Question 67

Nt-proBNP referral criteria

Answer 67

400-2000 ng/litre = should be seen and have an echo within 6 weeks >2000 ng/litre should be seen and have an echo within 2 weeks

Question 68

Chronic HF medical management

Answer 68

ABAL ACE inhibitor Beta blocker Aldosterone antagonist Loop diuretics U&Es closely monitored – particularly ACEi and aldosterone antagonists (both can cause hyperkalaemia) Additional specialist treatments – SGLT2 inhibitor, sacubitril with valsartan, ivabradine, hydralazine with a nitrate, digoxin

Question 69

Chronic HF procedural and surgical interventions

Answer 69

Implantable cardioverter defibrillators – continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus if they identify a shockable arrhythmia (used if patients who previously has VT/VF) Cardiac resynchronisation therapy – involves biventricular (triple chamber) pacemakers, the objective is to synchronise the contractions in these chambers to optimise heart function Heart transplant may be suitable in patients with severe disease

Question 70

Hypertensive emergency

Answer 70

Accelerated hypertension (malignant HTN) refers to BP > 180/120, with retinal haemorrhages/papilloedema Recommended a same-day referral Require a fundoscopy examination & assessed for secondary causes and end-organ damage IV options include: sodium nitroprusside, labetalol, GTN, nicardipine

Question 71

Aortic stenosis murmur

Answer 71

Narrowing of the aortic valve, restricting blood flow from the left ventricle to the aorta Causes an ejection-systolic, high-pitched murmur due to high blood flow velocity through the valve Has a crescendo-decrescendo character Murmur radiates to the carotids

Question 72

Aortic stenosis signs

Answer 72

Thrill in the aortic area on palpation Slow rising pulse Narrow pulse pressure (different between systolic and diastolic BP) Exertional syncope

Question 73

Aortic stenosis causes

Answer 73

Idiopathic age-related calcification Bicuspid aortic valve Rheumatic heart disease

Question 74

Aortic regurgitation murmur

Answer 74

Incompetent aortic valve, allowing blood to flow back from the aorta into the left ventricle Typically causes an early diastolic, soft murmur Austin-flint murmur: heard at the apex as a diastolic ‘rumbling’ murmur – caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate

Question 75

Aortic regurgitation signs

Answer 75

Thrill in the aortic area on palpation Collapsing pulse – forcefully appearing and rapidly disappearing Wide pulse pressure HF and pulmonary oedema

Question 76

Aortic regurgitation causes

Answer 76

Idiopathic age-related weakness Bicuspid aortic valve Connective tissue disorders – EDS, Marfan syndrome

Question 77

Mitral stenosis murmur

Answer 77

Narrowed mitral valve restricting blood flow from the left atrium into the left ventricle Mid-diastolic, low-pitched rumbling murmur, loud S1, opening snap after S2

Question 78

Mitral stenosis signs

Answer 78

Tapping apex beat Malar flush – due to back pressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation AF

Question 79

Mitral stenosis causes

Answer 79

Rheumatic heart disease Infective endocarditis

Question 80

Mitral regurgitation murmur

Answer 80

Incompetent mitral valve allowing blood to flow back from the left ventricle to the left atrium Pan-systolic, high pitched whistling murmur, radiates to the left axilla, may heart a third heart sound

Question 81

Mitral regurgitation signs

Answer 81

Thrill in the mitral area on palpation Signs of HF and pulmonary oedema AF

Question 82

Mitral regurgitation causes

Answer 82

Idiopathic weakening of the valve with age Ischaemic heart disease Infective endocarditis Rheumatic heart disease Connective tissue disorders – EDS, Marfan

Question 83

Tricuspid regurgitation murmur

Answer 83

Incompetent tricuspid valve, allowing blood to flow back from the right ventricle to the right atrium during systolic contraction Pan-systolic murmur, split second heart sound due to pulmonary valve closing earlier than the aortic valve

Question 84

Tricuspid regurgitation signs

Answer 84

Thrill in tricuspid area on palpation Raised JVP with giant C-V waves (Lancisi’s sign) Pulsatile liver Peripheral oedema Ascites

Question 85

Tricuspid regurgitation causes

Answer 85

Pressure due to left sided HF or pulmonary HTN Infective endocarditis Rheumatic heart disease Carcinoid syndrome Ebstein’s anomaly Connective tissue disorders

Question 86

Pulmonary stenosis murmur

Answer 86

Narrowed pulmonary valve, restricting blood flow from the RV into the pulmonary arteries Ejection systolic murmur loudest in the pulmonary area with deep inspiration, widely split secondary heart sound

Question 87

Pulmonary stenosis signs

Answer 87

Thrill in pulmonary area on palpation Raised JVP with giant A waves Peripheral oedema Ascites

Question 88

Pulmonary stenosis causes

Answer 88

Usually congenital & may be associated with Noonan syndrome or tetralogy of Fallot