Cardiology Flashcards
What cardiac murmurs present in the first 24hrs of life?
- Semilunar valve stenosis (AV/PV)
- AV valve regurgitation (MR/TR)
NOT: VSD, ASD
What CHD causes cyanosis in the first 24hrs of life?
TGA Single ventricle physiology
What CHD presents as critically ill in the first 24hrs of life?
Valve regurgitation – especially Ebstein’s [large RA], absent PV Obstructed TAPVD “Early” duct dependent presentation
CDH dependent on PDA for pulmonary blood flow
Severe cyanosis when duct closes Critical PS Pulmonary atresia Single ventricle with PS or PA
CDH dependent on PDA for systemic blood flow
Low CO when duct closes Critical AS Critical coarctation HLHS
CDH dependent on PDA for mixing
TGA
CDH that causes massive cardiomegaly in neonate
Ebsteins
CDH that causes the snowman sign
TAPVD
Asymptomatic murmurs
“Functional” commonest ASD VSD PS + AS (ejection click) Coarctation: murmur best heard at the back PDA
What valvular problem is associated with coarctation
Bicuspid aortic valve
Can you eliminate a ‘stills murmur’ with positioning?
Yes, ask the child to sit on the bed with their neck hyperextended + propped up on their arms positioned behind them
Ficks principle
Total uptake (or release) of a substance by an organ is the product of blood flow to that organ and the concentration difference of the substance in the arteries and veins leading into and out of that organ Key rules 1. The lower the CO the more oxygen is extracted 2. High mixed venous sat = shunt (eg. TAPVR) 3. Low mixed venous sat = low CO Normal mixed venous = 75 (high 60’s-75)
Ficks formula
Fick’s method = O2 consumption/ (arterial – venous content difference) → This requires Hb, saturation of O2, O2 binding capacity of Hb and dissolved O2 Qp/Qs = arterial saturation – mixed venous saturation / pulm venous saturation – pulmonary artery saturation QP: QS = 1 no shunt Qp: QS > 2 = large shunt Qp: QS < 1 R to L shunt
What is the formula to calculate pulmonary vascular resistance?
PVR (um2) = mean PA pressure - LA pressure / Qp Qp = pulmonary blood flow LA pressure can be inferred by using PCWP (pulmonary capillary wedge pressure) IF there is no shunt you can use CO as a surrogate for Qp 1-2 = normal 2-4 = mild elevation 4-6 = mod elevation >7.9 = severe, high correlation with irreversible PVR PVR = 1/6th of SVR
Criteria to refer VSD to cardiology
Heart failure FTT Dominant RVH on ECG (suggests tetralogy or variant) Isolated LVH (suggests coarctation or PDA) Aortic regurgitation Qp/Qs > 2: indication to close
Classic triad of symptoms in aortic stenosis
Chest pain Shortness of breath Syncope
Normal pressures in the heart
Right atrium (mean) 2-8 Right ventricle (peak) 17-32 Pulmonary artery (mean) 9-19 >25 = PHTN Left atrium (mean) 2-12 Left ventricle (peak) 90-140 Aorta (mean) 70-105
Pulmonary hypertension
Mean PA pressure > 25mm Hg at rest Mean PA pressure > 30mm Hg with exercise
What is the formula for cardiac output + what are the methods of measurement (direct vs indirect)?
CO = HR x SV Normal CO varies with age (higher in newborns) Children 4-5L/min/m2 In the absence of any shunt, pulmonary flow + CO are the same Direct measurement = thermodilution, indicator dye dilution Indirect measurement = fick method (requires estimation of O2 consumption)
Is clinical cyanosis noted earlier in anaemia or polycythaemia?
Polycythaemia Cyanosis is recognised at a higher level of O2 saturation in polycythaemia (80-85%) and low level of saturation in anaemia (45-50%) Clinical cyanosis is reached when level of reduced HgB reaches 5g/100mL (normal = 2g /100mL)
What factors increase PVR?
Hypoxia Hypercapnia Increased sympathetic tone Polycythaemia Pulmonary emboli Pulmonary oedema Lung compression (effusion)
What factors reduce PVR
Oxygen Adenosine Inhaled NO Prostacyclin Ca channel blockers
% of CHD associated with extra cardiac anomalies
10-15%
Risk of recurrence of CHD in siblings
2-4 % Further increased risk if > 1 sibling affected or if maternal history
Diagnostic criteria for Kawasaki disease
WARM CREAM Fever for > 5 days AND 4 out of 5 of the following Conjunctivitis (bilateral, dry or non-purulent, preferentially in bulbar distribution) Rash (Polymorphous, without vesicles, bullae or crusts, occurs in the first few days. Variable such as urticarial morbilliform, maculopapular or resembling scarlet fever) Extremity changes (hyperaemia and painful oedema of hands and feet that progresses to desquamation in the convalescent stage; perianal desquamation) Adenopathy (cervical, most commonly unilateral, tender, at least one node >1.5cm) Mucosal involvement (intense hyperaemia of lips leading to redness and cracking and/or diffuse erythema or oropharynx; strawberry tongue)
Kawasaki disease fast facts
2nd most common vasculitis in childhood after HSP Most common cause of acquired heart disease in children 85% of cases < 5yrs (peak 18-24 months) Rare in children < 6 months + > 5yrs BUT more likely to develop CAA More common in Asian population 15-25% develop CAA if untreated compared to 4% if treated with IVIG CAA rarely occurs before day 10
Incomplete Kawasaki disease criteria
Children with fever for 5 days + 2 clinical criteria OR fever for 7 days without explanation AND - CRP > 8 + ESR > 20 AND 3 or more: - Anaemia - Plt > 450 after 7th day of fever - Albumin < 30 - Raised ALT - WCC > 15 - Urine > 10 WBC/hpf OR positive echo
Management of rheumatic heart disease
Rest, fluid restriction Diuretics ACEI for afterload reduction if aortic regurgitation Digoxin for SVT No literature evidence for use of corticosteroids and IVIG. However, corticosteroids used commonly if severe
Diagnostic criteria of rheumatic fever
Evidence of strep A infection (elevated or rising ASOT or anti-DNAseB or positive throat culture / rapid antigen / PCR test) AND 2 major OR 1 major + 2 minor MAJOR Joints (polyarthritis or aseptic monoarthritis or polyarthralgia. Usually migratory + asymmetical). Large joints most commonly affected; especially knees + ankles. Should respond to NSAIDs. HEART (carditis, subclinical evidence of rheumatic valvulitis on echo) Nodules (subcutaneous, extensor surfaces). Very rare <2% of cases BUT highly specific. Round, firm, mobile + painless. Strongly associated with carditis. Erythema marginatum. Very rare <2% of cases BUT highly specific. Sydenham chorea (jerky, uncoordinated movements). Predominately affects females in adolescence. Disappears in sleep. MINOR PR prolongation Elevated temperature Arthralgias CRP > 30 ESR > 30
Antibiotic treatment for strep A sore throat / tonsillitis
Benzathine benzylpenicillin IM once OR Phenoxymethylpenicillin 15mg/kg BD for 10 days OR Cefalexin 25mg.kg BD for 10 days OR Azithromycin 12mg/kg daily for 5 days
What are the upper limits of normal for PR interval?
3-11yrs 0.16 12-16yrs 0.18 17+yrs 0.2
Fast facts about sydenham chorea
- May occur after a prolonged latent period following strep A infection (must exclude SLE or chorea gravidarum first) - Diagnosis of ARF can be made without the presence of other manifestations or elevated plasma strep antibody titres if chorea present - ARF manifestation that is most likely to reoccur - May occur in pregnancy or with OCP use - Majority of cases resolve within 6 months - Higher prevalence of ADHD, anxiety, depression + cognitive dysfunction after recovery
Predominantly manifestation of ARF carditis
Myocarditis and pericarditis may occur in ARF however, the predominant manifestation of carditis is the involvement of the endocardium presenting as a valvulitis, especially of the mitral and aortic valves. The incidence of carditis in initial attacks of ARF varies between 30% and 82%
What valve does ARF commonly affect?
Valvulitis most commonly affects the mitral valve, leading to mitral regurgitation (MR), although with prolonged or recurrent disease scarring, may lead to stenotic lesions. MR presents clinically as an apical blowing, holosystolic (pansystolic) murmur. The presence of an associated mid-diastolic flow murmur (Carey Coombs murmur) implies significant mitral valve regurgitation; however, it must be differentiated from the diastolic murmur of mitral stenosis (MS), which is often preceded by an opening snap
Serum ASO + anti-DNAse B titres: time to reach maximum levels
Serum ASO titre rises within 1-2 weeks, and reaches a max at 3-6 weeks Serum anti-DNase B titre up to 6-8weeks to reach a maximum
Strep A (streptococcus pyogenes) susceptibility to antibiotics
Almost universally susceptible to penicillin and related beta lactam antibiotics, e.g. cephalosporins. The organism appears to lack capacity to express beta lactamase that would confer resistance.16 Mutations in penicillin-binding proteins conferring decreased susceptibility to some beta lactam antibiotics but not penicillin have been reported. Strep A can, however, readily become resistant to macrolide antibiotics (azithromycin, roxithromycin, erythromycin etc) with marked geographical variation. Resistance to macrolide antibiotics generally also confers resistance to clindamycin.
What is sydenham chorea and how is it treated?
Sydenham chorea is a neuropsychiatric manifestation of ARF characterised variably by chorea, decreased muscle tone, and psychiatric and behavioural symptoms such as obsessivecompulsive symptoms and hyperactivity. Treatment - Supportive - Carbamazepine or sodium valproate - If very severe can add in risperidone, haloperidol, corticosteroids or IVIG, plasma exchange
Screening tests required prior to immunosuppressive doses of steroids
Tuberculosis: interferon gamma release assay or Tuberculin Skin Test (TST/Mantoux test) Hepatitis B: Hepatitis B serology with HBsAg, HBcAb and HBsAb. In patients with either a positive HBsAg or HBcAb, a hepatitis B DNA PCR should be ordered Hepatitis C: Hepatitis C antibody. If positive, an HCV RNA viral load and genotype should be ordered HIV serology Melioidosis: Strongyloidiasis: Serology and if serology is positive or eosinophilia is present, also perform stool microscopy (single stool as a minimum, but 3 preferable). Treat with ivermectin Scabies Review of immunisation history
What is secondary prophylaxis of ARF
Consistent and regular administration of antibiotics to people who have had ARF or rheumatic heart disease (RHD), to prevent future group A betahaemolytic streptococcus (Strep A) infections and the recurrence of ARF
What is the antibiotic regimen for secondary prophylaxis of ARF?
1st line Benzathine benzylpenicillin G IM every 28 days 2nd line Oral phenoxymethylpenicillin BD Penicillin allergy Oral erythromycin BD
Duration of antibiotic prophylaxis in ARF
Possible ARF 12 months then reassess Probably ARF Min 5yrs then reassess Definite ARF (whichever is later0 Mild: min 10 yrs or until 21 Mod: min 10 yrs or until 35 Severe: min 10 yrs or until 40
Mechanical valve vs bioprosthetic valve
Mechanical valve: proven durability, requires lifelong anticoagulation Bioprosthetic valve: does not require lifelong anticoagulation, limited durability, may enable future valve in valve procedure
Definition of infective endocarditis
Infection of the endocardium +/or heart valves that involved thrombus formation (vegetation)
Common organisms in infective endocarditis - WITH underlying heart disease - WITHOUT underlying heart disease
Among children with underlying heart disease: •Viridans streptococci – 33 percent •Staphylococcus aureus – 28 % •Other streptococci – 17 % •Polymicrobial – 11% •Other Staphylococcus species – 7% •Gram-negative bacilli – 5 % ●Among children without underlying heart disease: •S. aureus – 47% •Viridans streptococci – 18 % •Other streptococci – 10 % •Gram-negative bacilli – 8 % •Other Staphylococcus species – 6% •Polymicrobial – 12% **Blood cultures negative in 5-7% of cases**
Pathogenesis steps in infective endocarditis
- Endothelial damage: turbulent flow or mechanical damage to the endothelium 2. Thrombus formation: deposition of fibrin, plts + RBC forming non-infected thrombus 3. Transient bacteraemia or fungaemia- adherence of microbial pathogens to the injured endocardium + thrombus 4. Infected vegetation- further fibrin + plt deposition result in a protective sheath that isolated the organism from host defences and permits rapid proliferation 5. Other organ involvement- secondary embolisation or immune mediated processes (e.g. glomerulonephritis, brain abscess)
Symptoms dependent on clinical features in infective endocarditis
Bacteraemia- fever, tachycardia, vasodilation Valvulitis- murmur, tachycardia, vasodilation Immunologic- roth spots, janeway lesions, osler nodes Septic emboli- osteomyelitis, pneumonia
Outline Duke’s criteria for endocarditis
2 major OR 1 major 3 minor OR 5 minor MAJOR - Typical microorganism from x 2 blood cultures OR single BC with coxiella burnetii - Persistently positive blood cultures (2 BC drawn >12hrs apart) - Evidence of endocardial involvement: vegetation OR abscess OR new partial dehisence of prosthetic valve OR new valvular regurgitation MINOR - Risk factor - Fever - Vascular phenomena (janeway lesions, conjunctival haemorrhage, emboli, aneurysm, intracranial haemorrhage) - Immunologic phenomena (GN, osler node, roth spots, rheumatoid factor) - Microbiologic evidence
How is TOE superior to TTE in infective endocarditis
TOE is superior to TTE for the detection of aortic root abscess
In pulmonary HTN (PAP >25mmHg), what is the cause IF The PCWP is low / normal (<15mm Hg) OR The PCWP is elevated (>15 mm Hg)
PCWP low / normal = pulmonary vascular disease (aka pulmonary arterial hypertension) PCWP elevated = likely secondary to heart problem (aka pulmonary venous hypertension)
What is the formula for systemic vascular resistance?
Ao - RA / Qs
Outline pulmonary hypertension management
Diuretics: symptoms of fluid retention Oxygen: mortality benefit for group 3 Anticoagulation: group 4 Exercise training
Where would the intracardiac shunt be in the following examples? Increase in O2 [] in RA Increase in O2 [] in RV Increase in O2 [] in PA
Increase in O2 [] in RA - ASD. DDx PAPVC, cor fistula to RA Increase in O2 [] in RV - VSD. DDx cor fistula to RV Increase in O2 [] in PA - PDA
Types of ASD
Ostrium primum = partial AVSD (15-20%) more common in T21 Ostium secundum 75%. More common in females. Sinus venosus (5-10%) not a true ASD. SVC (most common) + IVC types. Associated with anomalous pulmonary venous return
When to close and when to NOT close an ASD
When to close: Symptomatic RV enlargement Qp:Qs > 1.5 Paradoxical embolism Platypnea- orthodeoxia syndrome When not to close: Eisenmenger
Size of ASD + likelihood of closure
ASD < 5mm = close ASD 5-8 = likely close if no RV dilation ASD >8mm = need surgical closure Usually transcatheter device closure unless large
ASD murmur charachteristics
Splitting of S2 Ejection systolic Mid diastolic murmur due to increased flow across the tricuspid valve
Is heart failure in children most commonly LEFT, RIGHT or biventricular?
Biventricular due to ventricular interdependence
Indications for endocarditis prophylaxis with dental procedures
Prosthetic cardiac valve Previous IE CHD IF it involved unrepaired cyanotic defect (including palliative shunts + conduits) Repaired CHD with prosthetic material for the first 6 months post procedure RHD in indigenous Aus Cardiac transplant recipients
At risk procedures for IE that require prophylaxis
Dental procedures that involve manipulation of gingival tissue Invasive resp procedures (tonsillectomy / adenoidectomy) Invasive GI / GU procedures I + D of abscesses Surgical procedure through infected skin
IE antibiotic prophylaxis
Amoxicillin 50mg/lg oral 1 hr before procedure OR clindamycin 15mg/kg 1 hr before procedure
What cardiac complication is MOST likely to develop in Duchenne muscular dystrophy?
Dilated cardiomyopathy
Murmur in tetralogy of fallot
Harsh ejection systolic LSE Radiates through to the back Loud single S2 due to inaudible P2 closure sound
Tetralogy of fallot associations
T21 22q11
Tetralogy of fallot ECG + CXR findings
ECG RV hypertrophy CXR Boot shaped Up-tilted apex Reduced lung vascularity
Lesions is tetralogy of fallot
Overiding aorta RVH VSD PS (often associated with infundibular muscular obstruction)
Cardiac shape + CHD association - Boot shaped - Egg shaped - Sitting duck - Snowman
- Boot shaped = tetralogy of fallot - Egg shaped = incorrected transposition - Sitting duck = truncus arteriosus - Snowman = supracardiac TAPVD
Ossification of bones
‘CRITOE” Capitellum Radial head Internal epicondyl Trochlear Olecranon External epicondyl 1, 3, 5, 7, 8, 11, ish
What extra feature do you look for on a CXR in a patient with T21?
11th rib
What is the most common CHD in T21?
AV canal defect
- Superior axis
- Usually no murmur
75% of patients with an AV canal defect have T21
Usually complete AV canal defect
What are the features of of pulmonary plethora on CXR and at what point do you see it?
- Enlarged central and peripheral pulmonary arteries
- “DOTS” in the peripheral lung fields
- Lateral film show large pulmonary arteries
CXR findings of pulmonary plethora only present when Qp:Qs > 2:1
What % of patients with Patau have CHD?
80%
What % of patients with Edwards have CHD?
What % of patients with Turner’s Syndrome (XO) have CHD?
What is the most common defect?
35%
What % of patients with Klinefelter 47XXY have CHD?
What is the most common CHD in 22q.11
Tetralogy of Fallot
What is the most common CHD in Williams?
Supravalvular aortic stenosis
What is the most common CHD in Noonan syndrome?
What are the ECG findings in AVSD?
Turner’s syndrome
Tetralogy of Fallot is most likely which is associated with DiGeorge
22q11
They have truncus arteriosus therefore most common with 22q11
Noonan’s syndrome
Pulmonary valve stenosis
Velocardial facial syndrome / 22q11
T21 who is cyanotic most common diagnosis
Tetralogy of fallot
What are the ECG findings in AVSD?
- Left axis deviation
- RA enlargemtn
- Biventricular hypertrophy
- Incomplete RBBB
