Cardiology Flashcards
State three causes of ‘Blue Baby Syndrome’
Cyanotic Heart Disease
Methaemaglobinaemia
RDS (more transient)
How is Blue Baby Syndrome investigates?
Pulse Oximetry (may be falsely elevated if cause is Methaemaglobinaemia so use Co-Oximeter)
If thinking cause is cardiac then do ECG, Echo, CXR
How is Blue Baby Syndrome secondary to Cyanotic Heart Disease treated?
Prostaglandin E1 to keep Ductus Arteriosus open
Oxygen Therapy
Definitive is corrective surgery
How is Blue Baby Syndrome secondary to Methaemaglobinaemia treated?
Methylene Blue
What is Methaemaglobinaemia?
Congenital or Acquired
Reduced oxygen carrying capacity of haemoglobin due to >1% being Methaemaglobin (iron in ferric instead of ferrous form)
Heart Murmurs can be described as ‘Innocent’ or ‘Flow’, what does this mean?
Caused by fast blood flow through various parts of the heart during systole
Typically soft, short, symptomless, systolic
When would you investigate an innocent murmur?
Murmur louder than 2/6
Diastolic
Louder on standing
Failure to thrive
How do you investigate murmurs?
ECG
CXR
Echo
Give two causes of Pan Systolic Murmurs. Where would these best be heard?
Mitral Regurgitation (Apex in left lateral position) Tricuspid Regurgitation (left lower sternal border)
Give three causes of an Ejection Systolic murmur and where they’d be heard
Aortic Stenosis (Aortic Area) Pulmonary Stenosis (Pulmonary Area) HOCM (4th ICS, Left Sternal Border)
Describe the pathophysiology or ‘Splitting the Second Heart Sound’
Inspiration increases negative intrathoracic pressure
This causes right side of the heart to fill more and faster therefore will take longer to empty
This causes pulmonary valve to close after aortic
How would an Atrial Septal Defect sound on auscultation?
Mid systolic crescendo decrescendo at upper left sternal border
Fixed split of second heart sound (fixed meaning unrelated to inspiration, as left to right shunt causes continuous increased blood on right)
How would a Patent Ductus Arteriosus sound on Auscultation?
If small, may not cause abnormalities
Normal first heart sound and machinery murmur for second
How would Tetralogy of Fallot sound on auscultation?
Ejection Systolic at left sternal edge
State three Acyanotic Heart Defects
ASD
VSD
PDA
What are the two types of ASD and how does it present?
Secundum (defect in central septum, involving foramen ovale)
Primum/Partial (bottom end of septum often involving abnormal leaky AV valves)
Asymptomatic, Arrhythmias, Recurrent chest infections
How would you investigate suspected ASD and what would you see?
CXR - Cardiomegaly, Enlarged Pulmonary Arteries
ECG - Secondum (partial RBBB and RA deviation), Partial AVSD (neg QRS in AVF)
Echo
When and how should ASDs be managed?
If defect is significant enough to cause RV dilation
Secundum - catheterisation and insertion of occlusion
Partial AVSD - Surgical Correction
Normally taken between 3-5 years to prevent RHF and arrhythmias later in life
Describe the types VSD in terms of location
Most common CHD (accounting for 30%)
Perimembranous are the most common (upper by the valves)
Muscular (lower portion of septum)
Describe the types VSD in terms of size - small
Asymptomatic, Loud Murmur, Investigations normal, Closes spontaneously
Describe the types VSD in terms of size - moderate
Increased flow in systole
May have some dilation of left heart
Excess sweating/Tachypnoea
Describe the types VSD in terms of size - large
Heart failure with breathlessness, faltering growth after one week, recurrent chest infections
Tachypnoea, Sweating
Same size or bigger than aortic valve
How would you investigate a suspected (large) VSD, and what would you see?
CXR - Cardiomegaly, Enlarged arteries
ECG - Biventricular Hypertrophy by 2 months
Echo
How would you manage a moderate/large VSD?
Diuretics
ACEI
Increased calories
Surgery at 3-6m (manage heart failure and prevent lung damage from pulmonary hypertension)
Define Patent Ductus Arteriosus
Ductus Arteriosus connects pulmonary artery to descending aorta
In term infants normally closes shortly after birth (therefore it is normal if preterm)
Classed as Patent if remaining open one month past expected delivery date
How does PDA present?
Continuous murmur beneath left clavicle
Normally asymptomatic but if large then heart failure
How should PDA be investigated?
ECG (presents like VSD if large)
CXR (presents like VSD if large)
ECHO
How is PDA managed?
Can try to close the PDA using Indomethacin (PGE1/COX1 inhibitor)
Closure with coil
Introduced by catheter
State three CYANOTIC Heart Defects
Tetralogy of Fallot
Tricuspid Atresia
Transposition of the Great Arteries
What is the Nitrogen Washout Test?
Determines presence of heart disease in a cyanosis neonate
Infant is placed on 100% Oxygen for 10 minutes and then right radial blood gas is taken (<15kPa qualifies as Cyanotic)
What’s the acute management of a Cyanotic heart defect
A to E Assessment Prostaglandin Infusion (can cause apnoea, seizures)
Tetralogy of Fallot is the most common cyanotic heart condition. What is involved in the tetrad?
VSD
Pulmonary Stenosis
RV Hypertrophy
Overriding Aorta (dilated and in severe cases collateral aortopulmonary arteries form)
Give four risk factors for Tetralogy of Fallot
Male
Teratogens (Alcohol, Warfarin)
First degree FH
Genetics (CHARGE, DiGeorge, VACTERL)
Describe the three classifications of Tetralogy of Fallot
Mild - Pink TOF (usually asymptomatic, developing cyanosis in 1-3 years)
Mod to Severe - Presents in first few weeks with Cyanosis and Resp Distress, Recurrent chest infections
Extreme - usually detected in utero, if not presents within four hours. Completely dependent on PDA (pulmonary atresia)
How would a TOF baby present OE?
General cyanosis and clubbing
Loud Single S2 (no pulmonary valve to close)
Pansystolic VSD murmur
Ejection click from dilated aorta
Post PG infusion - machinery murmur
Describe some investigations for TOF and what they would show
ECG - RA Deviation and RV Hypertrophy
CXR - Boot shaped heart and reduced peripheral markings
Echo - Gold Standard
Microarray - ?Genetic Syndromes
Describe the medical management of Tetralogy of Fallot
Encourage squatting
Prostaglandin Infusion (PGE1- Alprostadil, PGE2 - Dinoprostone)
Beta Blockers
Morphine (decrease Tachypnoea by decreasing resp drive)
Why is squatting encouraged in TOF?
Increases venous return and systemic resistance
Describe the surgical management of Tetralogy of Fallot
Palliative - Transcatheter stent in RV outflow tract, Modified Blalock Tausing Shunt (mimics PDA - connects blood flow from aorta to pulmonary artery )
Definitive - under bypass, from 3m to 4y
State three complications of TOF
Polycythaemia
Stroke
CCF
Define Transposition of the Great Arteries
Aorta arises from the right ventricle and pulmonary artery from left, creating a parallel circulation
Describe the classification of Transposition of the Great Arteries
Dextrotransposition - Aorta is anterior and right to PA
Levotransposition - aorta is anterior and left to PA
What is different about Levotransposition?
The ventricles have switched places rather than arteries therefore it is acyanotic
Right ventricle is not used to higher pressure of left side causing Hypertrophy and failure
Give three risk factors for Transposition of Great Arteries
Maternal age >40
Diabetes
Rubella
Describe the clinical features of Transposition of the Great Arteries
Cyanosis in first 24 hours (if no mixing)
CHF features over first 3-6 weeks
RV heave
State four investigations for Transposition of the Great Arteries, and describe what they’d show
Oximetry - Cyanosis with discrepancy between upper and lower
ABG - Metabolic Acidosis
Echo - Definitive diagnosis
CXR - Egg on a string
How is Transposition of the Great Arteries managed?
Emergency PGE1 infusion
Correct Acidosis
Emergency atrial balloon septostomy
Definitive surgical correction after four weeks
State four complications of Transposition of Great Arteries
Neopulmonary Stenosis
Neopulmonary Regurgitation
Coronary Artery Obstruction
Sudden Cardiac Death
Describe the pathophysiology of Infective Endocarditis
Triad of Endothelial Damage, Platelet Adhesion and Microbial Adherence
Organisms : Staph Aureus, Strep Viridans, Strep Pneumoniae
How does Infective Endocarditis present?
Persistent low grade fever (without another clear focus)
New Murmur
Splenomegaly
Oslers Nodes, Janeway Lesions, splinter Haem
How is Infective Endocarditis investigated?
- Blood Cultures (from multiple sites over 24h)
- Microscopic Haematuria
- Echo (aids but doesn’t confirm or deny if vegetation’s are there/not)
Describe the Major Duke’s Criteria
- Positive blood cultures on two separate occasions
- Positive ECHO (oscillating intracardial mass, abscess)
Describe the MINOR Dukes Criteria
Predisposition Fever Vascular Phenomena Immunological Phenomena Echo and Bloods suggestive but not meeting criteria
What is required via the Dukes Criteria to diagnose Infective Endocarditis?
Two Major
One Major and Three Minor
Five Minor
Describe the Surgical Management of Infective Endocarditis
If highly mobile, valvular dysfunction, >1 embolic event in two weeks
Describe the medical management of Infective Endocarditis
IV Amoxicillin (4 weeks) and consider adding Gentamicin (2 weeks)
What is Acute Rheumatic Fever?
Systemic Illness occurring 2-4 weeks after Pharyngitis in some due to cross reactivity of Strep Pyogenes
B Cells produce Anti M Protein AB against S.Pyogenes which interacts with heart/joints/etc (antigenic mimicry)
Give three risk factors for Rheumatic Fever
Children
Poverty
Overcrowding
How does Rheumatic Fever present?
Recent Sore Throat/Scarlet Fever
New Murmur
Arthritis
Describe the Jones Diagnostic Criteria
Positive throat culture and positive anti streptolysin titre
AND
2 major or 1 major 2 minor
Describe the major criteria for Rheumatic Fever
SPECS Syndenhams Chorea Polyarthritis Erythema Marginatum Carditis Subcut Nodules
Describe the minor criteria for Rheumatic Fever
CAPP CRP raised Arthralgia Pyrexia Prolonged PR interval
How is Rheumatic Fever investigated?
Cultures Rapid Antigen Test Anti Strep Serology ECG Echo
How is Rheumatic Fever managed initially?
1) Benzathine Benzylpenicillin
2) NOT Asparin - simple analgesia
3) Assess valves/any carditis
What is the long term management for Rheumatic Fever?
Antibiotic therapy for at least 5 years/ or until child is 21
IM Benzylpenicillin every 3-4 weeks
What is Sinus Arrhythmia?
Normal in children
Cyclical change with respiration by up to 30 bpm
What is the most common arrhythmia in children, and the underlying problem
SVT (rapid between 250-300bpm)
Rarely a structural problem, normally a re-entrant tachy
What will be seen on ECG of Sinus Tachycardia in children?
Narrow complex tachycardia between 250-300 bpm
Potentially delta wave if WPW is underlying cause
How is SVT managed in Children?
Circulatory and Respiratory support
Vagal Stimulating Manouvres IV Adenosine (terminating re-entrant)
Maintenance with Flecainide/Sotalol if required
What is Kawasaki Disease?
Systemic vasculitis mainly affecting children 6m-5y
Diagnosis of Kawasaki is based on clinical findings, such as …?
- Fever >5 days
- Conjunctivitis
- Mucous Membranes Changes (red or dry lips etc)
- Cervical Lymphadenopathy
- Polymorphous Rash
- Red and Oedematous Palms and Soles
Why do congenital arrhythmias occur?
Anti Ro/ Anti La bodies from mother prevent normal conduction of developing heart
How is Kawasaki disease managed?
IVIG and Aspirin
If persistent then corticosteroids and infliximab
Name two complications of Kawasaki
Myocardial Disease
Coronary Aneurysms
What is Eisenmenger’s?
When blood flows from the right side of the heart to the left across a structural lesion
Associated with ASD,VSD,PDA
When does Eisenmenger’s develop?
After 1-2y of large shunts, or in adulthood with small shunts
Describe the pathophysiology of Eisenmenger’s
Overtime, increased blood flow from left to right leads to pulmonary hypertension
When pulmonary pressure>systolic, blood flows right to left
The cyanosis can lead to Polycythaemia (plethora, increased VTE risk)
How does Eisenmenger’s appear OE
As pulmonary hypertension
Right Ventricular Heave
Loud S2
Raised JVP
Peripheral Oedema
How is Eisenmenger’s managed?
Ideally the defect would be corrected before Eisenmenger’s has occurred
Only definitive management is heart lung transplant
Symptom management: Sildenafil, Anticoagulation, Prophylactic Abx, Venesection
What is Coarctation of the Aorta?
Narrowing of the aortic arch, normally around the Ductus Arteriosus
Reduces pressure in distal vessels and increases pressure in the heart
How does Coarctation of the Aorta present in the neonate?
Weak femoral pulses
Lower limb blood pressure < upper limb blood pressure
How does Coarctation of the Aorta present in infancy?
Tachypnoea and increased work
Poor feeding
Grey and floppy
Describe the murmur of Coarctation of the Aorta
Systolic murmur below left clavicle/scapula
Describe the longer term effects of Coarctation of the Aorta
LV heave
Underdeveloped Left Arm
Underdeveloped Legs
How is Coarctation of the Aorta managed?
Surgical correction
PGE keeps DA open until surgical correction and DA ligation
What is Ebsteins Anomaly?
Tricuspid valve appears lower in the heart causing a large RA and small RV
Results in reduced blood flow from RA-RV and subsequently from RV to pulmonary vasculature
Often associated with a R-L shunt via ASD
What condition can Ebstein’s Anomaly go on to cause?
Wolf Parkinson White
How does Ebstein’s Anomaly present?
Evidence of Heart Failure
Gallop rhythm (addition of 3rd and 4th HS)
Cyanosis
Dyspnoes
Poor feeding
May appear soon after birth when PDA closes
How does Ebstein’s Anomaly present on ECG?
RA enlargement
RBBB
LA deviation
How does Ebstein’s Anomaly present on ECG?
Cardiomegaly
RA enlargement
What is the definitive investigation for Ebstein’s Anomaly?
Echocardiogram
When does PDA normally close
First 2 -3 weeks of life
Is non functioning long before that
Give three risk factors for PDA
Rubella
Prematurity
Family History
Name two diseases associated with VSD
Down’s Syndrome
Turner’s Syndrome
