cardiology rest Flashcards
cyanotic defects explain
decrease in systemic oxygen saturation as flow of blood bypasses lungs…
tetralogy of fallot
transposition of great arteries, tricuspid atresia
acyanotic explained and types
shunt = VSD, ASD and PDA…abnormal blood flow and volume overload in one or more chambers..can cause pulmonary HTN, congestive HF and right to left shunting…cyanosis
obstructive = coarctation of aorta, pulmonary stenosis and aortic stenosis..narrow or blockage within heart/great vessels..increased pressure load on affected chamber…hypertrophy
HRT 0-11 mths
110-160
HR 1-2 YRS
100-150
HR 2-5 YRS
95-140
5-11 YRS HR
80-120
12+ HR
60-90
rhythm abnormalities in children ECG
sinus arrythmias- irregular rhythm that changes with child’s breathing, every P wave, QRS
ectopic beats - non sinus QRS complexes, can be atrial, junctional, or ventricular
QRS in children
always normal if positive in leads 1 and 11
VT QRS complexes children
VT will show an extreme right (north west) QRS axis, due to ectopic focus located in this ventricle
SVT ECG
a broad complex tachycardia with normal QRS axis may indicate a supraventricular tachycardia
AVSD ECG
newborn with an extreme left QRS axis may have an atrioventricular septal defect (AVSD).
sinus rhythm p wavesq
upright in leads 1 and aVF
Tall p waves
amplitude >3mm
Right atrial hypertrophy
wide and notched p wave
(duration >100ms, or >80ms if younger than 12 months) is a sign of left atrial hypertrophy
normal PR interval
80-200ms
conditions with increased PR interval
(1st degree AV block) include myocarditis, atrial septal defects (ASD) and hyperkalaemia
conditions shortening PR interval
WPW syndrome
normal Q waves
Infants and young children may have very deep Q waves, up to 6mm, and this is normal
QRS complex ECG
abnormally wide if more than 120ms in children or 80ms (2 small squares) in infants
causes - VT, BBB, or WPW
right BBB
M” shape (rsR’) in V1 with a tall and wide second peak of the QRS
left BBB
Left BBB causes a similar pattern but in V6
WPW syndrome
small ‘delta’ wave before the QRS, which can be subtle with only slurring of the R wave
ventricular arrhythmias
can have any shape depending on the ectopic focus, and may look very similar to BBB
RVH ECG
a positive R wave in V1 in an older child indicates right ventricular hypertrophy
LVH ECG
An abnormally tall R wave in V6 usually indicates left ventricular hypertrophy
QRS amplitude
changes in childhood, usually larger than adults
prolonged QTC
more than 450ms is prolonged in all ages, and may increase the risk of arrhythmia and sudden death
T wave inversion
Beyond the first few days of life, T waves are inverted in V1 to V3 and will gradually become upright by adolescence
ST elevation ECG
usually due to early repolarisation or “high take-off”, particularly in adolescent boys, and is a normal finding
pathological T or ST wave
pericarditis
myocarditis
T wave inversion may also result from ventricular strain and severe ventricular hypertrophy
birth-3 days normal ECG
Right axis deviation (+90 degrees to +180 degrees)
Upright T wave in V1 – if persisting beyond day 3 this is a sign of RVH
Positive QRS complexes in V1 and V2, negative QRS in V5 and V6
3 days - 3 years ECG
Right axis deviation (usually normal by 1 month)
Negative T wave in V1
Positive QRS complexes in all chest leads (may become isoelectric in V1)
3 years - 16 years normal ECG
Normal QRS axis (0 degrees to +90 degrees)
Negative T waves in V1-4 will gradually become upright during childhood
Negative QRS in V1 and positive (large amplitude) QRS in V5 and V6
foetal circulation before birth
gas exchange occurs in placenta. more oxygenated blood delivered to myocardium and brain by intracardiac and extracardiac shunts. Foetal circulation is defined as ‘duct dependent’ - 1) umbilical arteries and vein, 2) ductus venosus, 3) foramen ovale, 4) ductus arteriosus
at the liver - foetal circulation
oxygenated blood from placenta travels via umbilical vein which branches into left and right umbilical veins at liver
R - oxygenated blood to liver via portal vein
L - branches into ductus venosus - bypasses liver to carry oxygenated blood into IVC
then mix of oxygenated and deoxygenated blood enters RA via IVC and mixing with SVC
at heart and lungs, foetal circulation
as lungs have no role in gas exchange, pulmonary arterioles are in hypoxic state. Hypoxia causes pulmonary vasoconstriction…increases pulmonary vascular resistance and pressure…pressure higher in R side of heart…R ventricular afterload higher..blood shunt via ductus arteriosis (between pulmonary artery and aorta) and foramen ovale (between RA and LA). So bypasses RV and lungs, entering LA or directly into aorta…enters systemic circulation
Aorta bifurcates into R and L common iliac arteries…split into internal and external iliac arteries..each internal give rise to umbilical artery to bring deoxygenated blood back to placenta..cycle continues
foetal circulation after birth
Air into lungs, rise in 02 levels, pulmonary vascular resistance falls due to reduction in hypoxic pulmonary vasoconstriction…lower pulmonary resistance and decreased afterload in R side
Change in pressure gradients between L and R side = closure of foramen ovale
Decreases in pulmonary pressure, means blood flow across ductus arteriosus is reversed…blood initially shunted from aorta to pulmonary artery. as o2 rises, ductus arteriosus constricts and closes (forming ligamentum arteriosum in adults).
After birth - umbilical vessels constrict, form round ligament of liver (umbilical vein), ligamentum venosum of liver (ductus venosus) and superior vesical arteries (umbilical arteries)
foetal HB
higher affinity for o2…transfer of o2 from mother to foetus prenatally
foetal hb oxygen dissociation curve displaced to left - so for a given PP of 02, Hb is more saturated than adult
Infants continue to generate foetal HB for 6mths
epidemiological acute rheumatic fever
4 million cases worldwide
94% in developing countries, most common in tropical
females more
acute rheumatic fever pathophysiology
strep pyogenes - streptolysin O and S
The bacteria contain M proteins in their cell wall. B cells stimulated to produce anti-M protein antibodies against infection which cross react with other tissues…heart, brain, joints and skin
exacerbated by production of activated cross reactive T cells
risk factors acute rheumatic fever
Children and young people
Poverty
Overcrowded and poor hygiene places
Family history of rheumatic fever
D8/17 B cell antigen positivity
diagnostic criteria rheumatic fveer
Positive throat culture for Group A β-haemolytic streptococcus or elevated anti-streptolysin O (ASO) or anti-deoxyribonuclease B (anti-DNASE B) titre.
AND
2 major criteria OR 1 major and 2 minor criteria present for initial ARF. (Same criteria for recurrent ARF plus can also be just 3 minor criteria)
major criteria
SPECS
Sydenham’s chorea
Polyarthritis
Erythema marginatum
Carditis
Subcutaneous nodules
minor criteria
CAPE
CRP or ESR – Raised acute phase reactant
Arthralgia
Pyrexia/Fever
ECG – Prolonged PR interva
rheumatic fever ddx
septic arthritis
reactive arthropathy
infective endocarditis
investigations rheumatic fever
Bloods: ESR, CRP, FBC (WBC),
Blood cultures to exclude sepsis
Rapid Antigen Detection Test
Throat culture: may be negative by the time rheumatic fever symptoms occur
Anti-streptococcal serology: ASO and anti-DNASE B titres
ECG: prolonged PR interval
CXR if carditis is suspected: congestive heart failure may be seen in ARF due to valvular damage
Echocardiography
initial management in confirmed rheumatic fever
abx - benzathine benzylpenicillin, if allergy - cephalosporins
aspirin or NSAIDS
assess for emergency valve replacement
if severe carditis - congestive HF, 3rd degree HB) give steroids and diuretics
definitive and long term management rheumatic fever
secondary prophylaxis with IM benzathine benzylpenicillin every 3-4 weeks, oral phenoxymethylpenicillin x2 daily, oral sulfadiazine daily or oral azithromycin
complications rheumatic fever
2% of the population can get permanent damage to heart valves and chronic rheumatic heart disease
With treatment ARF should resolve within 2 weeks
risk factors infective endocarditis
hx of congenital or acquired cardiac disease - VSD, PDA, aortic valve abnormalities
invasive instrumentation procedures
indwelling prosthetic material
IVDU
pathophysiology infective endocarditis
triad of endothelial damage, platelet adhesion and microbial adherence
bacteriaemia adheres to lesion and invades underlying tissue…attached to lesion, bacteria are protected within vegetation from phagocytic cells and host defence mechanisms so can proliferate
IE organisms
must have specific surface receptors to fibronectin
- Staphylococcus Aureus, Streptococcus Viridans, Streptococcus Pneumoniae, HACEK organisms (Haemophillus, Actinobacillus, Cardiobacterium, Eikenella and Kingella), Group A, C and G Streptococci and Candida albican
dental procedure organisms
s.viridans
GI surgery organisms
enterococci
clinical features IE
persistent low grade fever
heart murmur
splenomegaly
petechiae
osler’s nodes
janeway lesions
splinter haemorrhages
non acute - fatigue, weight loss, myalgia, possibly asx
splinter haemorrhages other causes
embolic phenomena that are seen in IE. Others include pulmonary emboli, haematuria due to glomerular nephritis, cerebral emboli causing seizures or hemiparesis, or roth spots which are retinal haemorrhages with pale centre often seen near optic disc
investigations IE
blood cultures - multiple
echo - identify vegetations and assess damage
blood - anaemia, leukocytosis and raised ESR
urine 0 microscopic haematuria
criteria IE
modified duke’s criteria
two major, one manor and 3 minor or five minor
rejected if no resolution <4 day abx course
major criteria IE
positive blood culture for endocarditis - 2 seperate blood culture
evidence of endocardial involvement - positive echo findings
minor criteria IE
predisposing - heart condition or IVDU
temp >38
vascular phenomena - emboli, infarcts, haemorrhage
immunologic phenomena - glomerulonephritis, osler’s nodes, roth spots
microbiological - positive blood culutres but doesnt meed major crtiera
echo - consistent with IE but not meet major criteria
complications IE
systemic embolization, abscess formation, pseudoaneurysms, valvular perforation or heart failure
management IE
empirical IV abx
surgery - fits criteria
empirical IV abx IE
For highly sensitive streptococci, IV penicillin or IV ceftriaxone for 4 weeks should be sufficient. Alternatively a 2 week course of the above in combination with IV gentamicin may in some instances be sufficient.
For penicillin resistance streptococci, 4 weeks of IV penicillin or ceftriaxone for 4 weeks in combination with gentamicin for the first 2 weeks is required
For methicillin-susceptible staphylococci, a β-lactamase-resistant penicillin may be used for 6 weeks with or without gentamicin for the first 3-5 days
For methicillin-resistant however, vancomycin for 6 weeks with or without gentamicin for the first 3-5 days would be required
Enterococcus causes will need 4-6 weeks of IV penicillin in combination with gentamicin and if penicillin allergic would require 6 weeks of vancomycin and gentamicin
HACEK organisms require ceftriaxone along with gentamicin for 4 weeks
Fungal causes are best treated with amphotericin B
Any case with prosthetic valve in situ should receive a minimum of 6 weeks of appropriate antimicrobial therapy
prophylaxis for IE
not routinely recommended for antibiotic prophylaxis for those interventions previously covered including; dental procedures, upper and lower GI surgery, GU surgery,
