Cardiac Learning Objectives Flashcards
Be able to describe the presenting features of cardiac failure
- poor weight gain
- tachypnoea / tachycardia
- heart murmur
- poor feeding
- recurrent chest infections
Be able to consider the differential diagnosis of cardiac failure
neonates: hypoplastic L heart, critical aortic valve stenosis
infants: VSD, ASD, large persistent PDA, severe CoA, interruption of aortic arch
older children: eisenmenger syndrome, rheumatic heart disease, cardiomyopathy
Outline the initial management of a child with cardiac failure
- position at a 45 degree angle
- oxygen (except in L-to-R shunt)
- good diet
- diuretics
- captopril
- B-blocker
- digoxin
- prostaglandin (duct dependent)
List the key features that distinguish innocent from pathologic murmur
(5 Ss) innoSent = aSymptomaptic, Soft blowing, Systolic, L Sternal edge
Describe the features of a venous hum
- above R clavicle + over R jugular vv
- disappears on occlusion
- may disappear if pt is supine / turns head
Following CVS examination, be able to diagnose common murmurs
SYSTOLIC: \+ ejection @ ULSE: sASD @ LSE; ToF PANSYSTOLIC: @ apex: pASD & VSD (louder) CONTINUOUS: PDA
List the epidemiology, features and management of common types of acyanotic heart disease e.g. VSD/ASD/AS/PS
left-to-right shunts inc. ASD, VSD & PDA
ASD:
secundum = centre of atrial septum involving foramen ovale
partial / primum = communication between septum & AV valves – can cause regurgitation
VSD:
small (<3mm) = asymptomatic; panystolic murmur @ LLSE
large (>3mm) = heart failure; soft pansystolic / no murmur (if v large), loud P2
PDA (open after 1 month): continuous murmur, bounding / collapsing pulse
Describe the anatomy and murmur characteristics of Atrioventricular Septal Defect (AVSD)
“blue & breathless^
no murmur but diagnosed antenatally / with echo
often associated w/ Down’s
cyanosis @ birth or heart failure at 2-3/52
Outline the presenting features clinically, on ECG and CXR of AVSD
Echo shows wall and valvular defects
ECG shows superior axis
Outline from fetal circulation to later presenting features and the management of Patent Ductus Arteriosus (PDA).
PDA results in a low diastolic pressure, due to blood flowing back into the pulmonary artery
There may be heart failure presenting as breathlessness
List the key presenting features clinically, on ECG, CXR and echo of VSD/ASD
ASD:
- CXR may show cardiomegaly, enlarged pulmonary arteries and increased pulmonary vascular markings
- ECG
o Secundum ASD partial RBBB with right axis deviation due to RVH
o pAVSD ‘superior’ QRS axis (-ve aVF) occurs because there is a defect close to AVN, so the displaced node conducts to the ventricles superiorly
VSD:
- CXR as in ASD
- ECG = biventricular hypertrophy by 2 months old
Outline the basic medical and surgical management of VSD/ASD.
ASD: Significant ASDs (causes RV dilation) will require treatment undertaken about 3-5yrs old in order to prevent right heart failure and arrhythmias later in life o Secundum ASD = cardiac catherisation with insertion of an occlusion device o pAVSD = surgical correction
VSD:
- Small VSD: these lesions will close spontaneously and is investigated via the disappearance of the murmur = prevention of bacterial endocarditis is also vital using good dental hygiene
- Large VSD
o Manage heart failure = diuretics & captopril
o Additional calorie input
o Surgery 3-6months old
Presenting features and diagnosis of coarctation of the aorta
- common in Turner’s
Clinical features:
o 1st day examination is normal
o Sick baby, with severe heart failure after 48 hours (duct closes)
o Absent femoral pulses
o Severe metabolic acidosis - Cardiomegaly from heart failure and shock may be seen on CXR, but ECG will be normal
Be aware of the association with bicuspid AV and common syndromes
Turner's Marfan's VSD PDA CoA
Be aware of the surgical management for CoA
- Prostaglandins and drugs may be used to manage the heart failure
- Angioplasty +/- stenting may be used to correct the area - sometime open surgery is needed and techniques include resection & anastomoses, a bypass graft or a more tailored reconstructive approach
- Balloon angioplasty only buys time
List the common types of duct dependent lesions
CoA TGA Hypoplastic Left Heart Syndrome Pulmonary Atresia Tricuspid Atresia
- Outline the immediate management when the duct is closing
restore the duct via a prostaglandin (E) infusion
= this is a short term solution and formaldehyde should be infiltrated into the structure for the longer term
Describe the presenting features both clinically and on ECG
- tachycardia (250-300) = poor cardiac output and pulmonary oedema
- present w/ heart failure in the neonate and young infant (causes hydrops fetalis and intrauterine death)
- re-entry tachycardia = a circuit of conduction is set up, with premature activation of the atrium via an accessory pathway
- There is rarely a structural heart problem but an echo should be performed
- Seen on ECG
o Generally show a narrow complex tachycardia
o May be possible to discern P wave after QRS complex due to retrograde activation of the atrium
o If heart failure is severe there may be changes suggestive of myocardial ischaemia = T wave inversion in the lateral leads
o In sinus rhythm short P-R interval may be discernible
o Wolff-Parkinson-White (WPW) = the early antegrade activation of the ventricle via the pathway results in a short P-R interval and a delta wave
Describe both pharmacological and nonpharmacological management options for supraventricular tachycardia
In severely ill children, prompt restoration of sinus rhythm is the key to improvement:
o Circulatory and respiratory support = tissue acidosis is corrected, positive pressure ventilation if required
o Vagal stimulation manoeuvres eg. carotid sinus massage or cold ice pack to face (80% successful)
o IV Adenosine (gold standard) = safe and effective, inducing atrioventricular block after rapid bolus injection terminates the tachycardia by breaking the re-entry circuit that is set up between the AVN and accessory pathway given incrementally in increasing doses
o Electrical cardioversion with a synchronized DC shock if adenosine fails
- Once sinus rhythm is restored, maintenance therapy is required = flecainide or sotalol
- Digoxin can be used on its own when there is no overt pre-excitation wave (delta wave)
- propanolol can be added in the presence of pre-excitation
Resting ECG may remain abnormal, but 90% of children will have no further attacks in infancy treatment is therefore stopped at 1yr old
Those who relapse or are at risk are usually treated with percutaneous radiofrequency ablation or cryoablation of the accessory pathway
List the key features that make tetralogy of fallot (TOF)
large VSD
ovveriding of aorta
subpulmonary stenosis (= RV outflow tract obstruction)
RV hypertrophy
- present w/ severe cyanosis with hypercyanotic spells (which can lead to myocardial infarction, cerebrovascular accidents and even death if left untreated)
o Rapid increase in cyanosis
o Irritability or inconsolable crying
o Severe hypoxia and breathlessness
o Pallor due to tissue acidosis
o Loud harsh ejection systolic murmur on LSE
Early and late managment of TOF
early neonate = prostaglandin E infusion and surgery to fit a shunt (subclavian artery to pulmonary artery) in order to maintain pulmonary blood flow and oxygenation
> 4 months old = Definitive surgery is needed to repair the underlying heart defects carried out - closure of VSD, relieving of right ventricular outflow tract obstruction – sometimes includes an artificial patch which extends across the pulmonary valve
- Hypercyanotic spells: usually self-limiting and followed by a period of sleep but if >15 minutes then require immediate treatment:
o Sedation and pain relief = morphine
o IV propranolol = peripheral vasoconstrictor and relieves subpulmonary muscular obstruction
o IV volume administration
o Bicarbonate = correct acidosis
o Muscle paralysis and artificial ventilation = reduces metabolic demand
management of ToGA
- maintain duct patency w/ prostaglandin E infusion
- balloon atrial septostomy = catheter w/ balloon that reopens the foramen ovale, thus allowing mixing of blood
- arterial switching surgery (in first few days)
Eisenmenger syndrome
persistent high pulmonary blood flow (due to large L-to-R shunt)
- List syndrome associations with cardiac disease
Turner's = CofA Marfan's = increased risk of aortic aneurysm and mitral / tricuspid valve prolapse (MR & TR) Noonan's = pulmonary stenosis, hypertropic cardiomyopathy, ASD / VSD
- Basic understanding of how hypoplastic left heart presents and is managed
a group of disorders associated with underdevelopment of the left side heart structure
- LV is small and non-functional, while RV maintains
- both pulmonary and systemic circulations = the latter is achieved by pulmonary venous blood passing through an ASD or patent foramen ovale, or via retrograde flow through a PDA
physiology:
- Mitral valve = small or atretic
- Left ventricle = diminutive
- Aortic valve = atresia
- Ascending aorta = very small and associated with coarctation of the aorta
presents with early onset (days) of cyanosis and heart failure leading to collapse and death within a few days of life most infants appear sick (blue) with poor peripheral perfusion and weak peripheral pulses central cyanosis and evidence of heart failure will be present
management: - maintaining patency of the duct - followed by a difficult set of neonatal surgical procedures (below) or a heart transplant o Norwood procedure o Glenn or hemi-Fontan at 6 months o Fontan at 3 years
Be aware of the causes and presenting features of myocarditis
inflammation of the myocardium caused by: o Infections (normally viral) – coxsackie B or EBV o Kawasaki disease o Drugs = Adriamycin o Connective tissue disease - SLE, RA, rheumatic fever or sarcoidosis signs: progressive worsening of dyspnea and congestive cardiac failure additionally, sudden onset of ventricular arrhythmias may occur Examination will show o Weak pulses o Tachycardia o Gallop heart rhythm o Distant heart sounds
diagnosis: biopsy from percutaneous endomyocardial biposy
Be aware of the risk factors, causes and management of subacute bacterial endocarditis
children at higher risk if they’ve had repair for:
o PDA or VSD
o Coarctation of the aorta
o Previous rheumatic fever
common pathogens inc:
o haemolytic Streptococcus viridans (50%) - often related to dental procedures
o Staphylococcus aureus = related to central venous catheters
o Group D streptococcus (enterococcus) - often after lower GI surgery
clinical features:
In the early stages symptoms are mild prolonged fever persisting over several months
• Non-specific symptoms myalgia, arthralgia, headache, weight loss, night sweats
• Splinter haemorrhages in nail bed
• Osler’s nodes= tender nodules on fingers or toes
• Janeway lesions = erythematous palms or soles of feet
• Roth’s spots = retinal infarcts
• Anaemia or pallor
• Haematuria (microscopic)
• Clubbing (late)
• Necrotic skin lesions
management:
Antibiotic therapy: immediate high dose IV penicillin/vancomycin for >6 weeks delay may cause progressive endocardial damage and deterioration in cardiac function
surgery to remove infected prosthesis
