cardiology Flashcards
when does heart start contracting in gestation
day 22
how does heart develop in fetus
develops mainly from mesoderm
formation of primitive heart tube at end of 3rd week
describe fetal cicrulation
vascular shunts bypass non functioning organs e.g. lung and liver
- foramen ovale - connection between 2 atria
- ductus arteriosis - any blood that doesnt pass through foramen ovale, passes through DA
- shunts 30% of umbilical blood to IVC
vessels made up of…
- tunica intima - smooth endothelial cells
- tunia media - elastic fibres and smooth muscle
- tunica adventitia - fibrous layer made of connective tissue
calculate cardiac output
stroke volume (volume ejected by each ventricle) x heart rate
factors that increase sinoatrial node (primary pacemaker site)
- increased sympathetic circulation
- pyrexia
- hyperthyroid
- hypokalaemia
- catecholaemines
- beta adrenoreceptors
factors that decrease sinoatrial node action
- increased parasympathetic action
- beta blockers, digoxin
- hyperkalaemia
- ischaemia
- hypoxia
- Na and Ca channel blockers
- hypothermia
ECG leads and areas of the heart
ANTERIOR = V1-V4
INFERIOR = 2, 3, AVF
LATERAL = 1 , AVL, V5, V6
R atrium = V1 and AVR
ECG changes of L ventricular hypertrophy
inverted T wave in V6
increased R wave voltages in leads 1, 2, aVL and AVF
deep S wave in V1
ECG changes of R ventricular hypertrophy
increased R wave voltage in aVR and 3, dominant S wave in V5-V6
upright T wave in V1
R axis deviation
HIGH AMPLITUDE V1-V3 QRS complex
dominant R wave in lead V1
most common cause of heart failure under 2 y/o
structural heart defects
CXR changes in heart failure
cardiomegaly
pleural effusions
fluid in fissures
pulmonary oedema
management of heart failure
- adequate nutition
- fluid restriction
- diuretics (furosemide 1mg/kg) - reduce preload
- ACE-I - reduce afterload
describe innocent murmurs
short systolic murmur
grade 2/6
loudest at L sternal border
child well
murmur changes with position
ASD cause
failure of endocardial cushion development
describe the murmur in ASD
ejection systolic murmur heard over upper L sternal edge
fixed wide split 2nd heart sound
= due to turbulent flow over pulmonary valve
definition of PDA
persistance of ductus arteriosus beyond one month corrected gestation (usually closes day 7)
causes L to R shunt from aorta to pulmonary circulation and causing over circulation of pulmonary blood
how do PDA present
symptoms of heart failure and from over congestion of lungs
resp distress
recurrent resp tract infections
feeding issues
faltering growth
asymptomatic murmur - machine like murmur at L sternal edge
management of PDA
- fluid restriction
- high calorie milk
- diuretics
- ibuprofen/ paracetamol/ indomethacin - pharmacological closure of ductus in preterm by reducing prostaglandins
- surgical closure with transcatheter when >6kg
may want to keep PDA open if have cyanotic heart disorder e.g. give prostaglandin E1
describe VSD
most common congenital heart defects
causes L -> R shunt
-> cause pulmonary overcirculation and cardiac failure (usually 6-8 weeks old)
magnitude of shunt depends on:
1. size of defect
2. pulmonary vascular resistance
3. pulmonary to aortic flow ratio - est predictor of heart failure
describe eisenmengers syndrome
- L-R shunts (VSD) can cause pulmonary hypertension ( increased pulmonary vascular resistance and R ventricle has increase pressure)
- causes shunt to reverse to R -> L
- become CYANOSED
usually occurs in early childhood
manage with sildenafil
how do VSD present
asymptomatic
pan systolic murmur (louder if smaller) + thrill at L sternal edge
faltering growth
resp distress
recurrent LRTI
reduced exercise tolerance
heart failrue at 6-8 weeks
investigations for VSD
ECG - L ventricular hypertrophy or R ventricular hypertrophy
CXR
ECHO **
describe hypoplastic L heart syndrome
- hypoplasia of L ventricle
- atresia or stenosis of aortic valve +/- mitral valve
- hypoplasia of ascending aorta and aortic arch
= obstructive CHD
presentation of hypoplastic L heart syndrome
collapsed neonate in first few days - 14 days of life (when ductus arteriosus close)
absence of all pulses
unwell looking baby
severe acidosis
maternal obesity can prevent detection antenatally
management of hypoplastic L heart syndrome
target sats 75-80%
prostin
avoid pulmonary dilators
surgery
1. norwood procedure - atrial septotomy, first few weeks
2. glenn procedure - few months later
3. fontan procedure - at 2/3 y/o, total cavopulmonary correction
describe coarction of aorta
narrowing of the aorta (commonly at insertion of ductus arteriosus)
10% of cardiac defects
85% have bicuspid aortic valve (murmur= ejection click)
presentation of crtical coarction of aorta
- cardiovascular collapse at day 2-7 of life (when ductus arteriosus closes as depends on R-> L shunt) - tachypnoea, poor feeding, sweating, unwell baby
- weak femoral pulses / not palpable
- hypertension of upper limbs
- high risk fo NEC
- systolic murmur that radiates to the back
investigations for coarction of aorta
- ECHO **
- high lactate
- CXR - normally normal, rib notching
- ECG - L ventricular hypertrophy (deep S wave in V1, tall R wave V6)
management of coarction of aorta
- resuscitate
- intubate and ventilate
- inotropes
- IV prostaglandin
- surgical - ballooon dilatation of aorta / stent
how does total anomalous pulmonary venous drainage present
1st few hours of life
increased work of breathing
high lactate
4 features of tetralogy of fallot
- ventricular septal defect
- overriding aorta
- pulmonary stenosis (causes R ventricular outflow obstruction)
- right ventricular hypertrophy
associated with R sided aortic arch
what type of congenital heart defect in ToF
cyanotic defect : R -> L shunt
right ventricular outflow obstruction due to pulmonary stenosis -> causes R to L shunt across VSD -> deoxygenated blood ejected from aorta -> cyanosis
how does tetralogy of fallot present
collapsed cyanotic neonate in first few days of life (most common cyanotic CHD)
ejection systolic and thrill murmur
finger clubbing
describe a ‘tet’ spell in ToF
begin at 4-6 months of age (< 1 y/o)
increased pulmonary vascular resistance causes worse shunt across VSD -> worsening cyanosis as more deoxygenated blood circulated around body
how to manage tet spell in ToF
- squatting / raising knees to chest - increases pulmonary vascular resistance
- high flow oxygen - pulmonary vasodilator to increase pulmonary flow
- morphine - vasodilator
- fluid bolus - increases RV venous return
- beta blockers
investigations for tetralogy of fallot
- ECG - R ventricular hypertrophy
- CXR - boot shaped heart
- ECHO
management of tetralogy of fallot
- ventilation
- IV prostaglandin
- beta blcokers
- surgical closure at 4-6 months (COMPLICATION = PERICARDIAL EFFUSION)
Describe transposition of great arteries
aorta and pulmonary artery arise from opposite ventricles
incompatible with life if not corrected as no mixing between pulmonary and systemic circulations -> CYANOSIS
presentation of transposition of great arteries
CYANOSIS on day 1-5 life (usually first 24 hours) when ductus arteriosus closes
investigations for transposition of great arteries
CXR - egg on side , congested lung fields
ECHO
management of transposition of great arteries
- IV prostaglandin to keep ductus arteriosus open
- arterial switch procedure (high risk of MI) - if has VSD, Rastelli operation performed
presentation of myocarditis
prior flu like symptoms/ viral gastroenteritis e.g. coxsackie, adenovirus
resting tachycardia ***
fever
—-> heart failure and arrhythmias
presentation of pericarditis
chest pain relieved by sitting forwards
grafting rub
post measles complication
management of pericarditis
- ECG - widespread concave ST elevation and PR depression
- NSAIDs
risk factors for infective endocarditis
- structural / congenital heart disease (turbulent jet of blood)
- prosthetic valve
- immunosuppression
- previous IE
- long term venous catheters
bacterial causes of infective endocarditis
- staph epidermidis - most common in prosthetic valves
- staph aureus
- kingella
- strep
describe mechanism of infective endocarditis
microbes colonize cardiac endothelium -> vegetations on valves -> valve regurgitation or stenosis
infection of endothelial surface of the heart, mainly mitral valves
presentation of infective endocarditis
fever
malaise
new murmur
hepatosplenomegaly
signs of infective endocarditis
- janeway lesions -> micro abscess formation from septic emboli, lesions on palms or soles
- oslers node -> immune complex deposition , painful nodes on dorsum of hands
- splinter haemorrhages -> micro embolic necrosis
- roth spots -> retinal haemorrhages
- clubbing
- septic emboli -> osteomyelitis
management of infective endocarditis
- blood cultures x 3 before starting abx
- ECHO
- ECG
- IV antibiotics for 4-6 weeks +/- surgical excision of vegetations
criteria for IE
DUKES CRITERIA
cause of rheumatic fever
group A streptococcus / after strep throat
most common acquired heart disease
criteria / presentation of rheumatic fevers
MAJOR CRITERIA
C- carditis - 50-60%, tachycardia, pansystolic murmur from mitral regurg
A - arthritis - 75% large joints
S - subcutaneous nodules
E - erythema marginatum - macular lesion with pale centre
S - sydenhams chorea - 10-15%, involuntary movement of hands and legs
MINOR CRITERIA
F - fever
R - raised ESR/CRP
A - arthralgia
P - prolonged PR interval
P- previous RF
diagnosis of rheumatic fever
DUCKETT JONES CRITERIA : 2 major or 1 major and 2 minor criteria
throat cultures/ ASOT titres
management of rheumatic fever
penicillin
aspirin for carditis
cardiac defects in DiGeorge syndrome
ToF
interrupted aortic arch
VSD
2 types of SVT
- AV re-entry tachycardia (AVRT) - most common in children <8 y/o, re-enterant loop due to accessory conduction pathway e.g. WPW
- AV nodal re-entry tachycardia (AVNRT) - most common >8 y/o, 15%, re-enterant circuit through the AV node causing rapid conduction and ventricular beats
presentation of SVT
HR 200-300 bpm
palpitations
syncope
chest pain
episodic, resolves spontaneously
ECG of SVT
no p waves
HR 200-300 bpm
QRS normal or narrow
fixed RR interval
regular
sudden onset
describe sinus arrhythmias
normal variation in HR
increases during inspiration and decreases in expiration
diagnosis of SVT
- 24 hour holter monitor
- ECHO
- EP studies
management of SVT with shock
synchronised DC shock 1J/KG - sync to R wave (ventricular depolarisation)
management of SVT if haemodynamically stable
- vagal manouvres e.g. ice dunk, valsava, carotid massage
- IV adenosine 0.1mg/kg (3mg -> 6mg -> 12mg every 1-2 minutes) through large proximal vein, short half life
if haemoodynamically unstable -> synchronised shock 1J/kg
mechanism of adenosine
blocks conduction through AV node and terminates arrhythmia
A1 receptor and inhibits adenyl cyclase and reduces cAMP
management of long term SVT
- beta blockers - prevention
- radiofrequency ablation
describe wolff parkinson white syndrome
accessory pathway (bundle of kent) and gap in myocardial cells to allow conduction through atria and ventricles
ventricles activated before the usual pathway with AVN
AVRT SVT - orthodromic
presentation of wolff parkinson white
AVRT SVT
babies - resp distress, sweaty, pale, poor feeding
children - chest pain, syncope, palpitations
ECG changes in wolff parkinson white
delta wave - slurred QRS upstroke
widened QRS
shortened PR interval
management of wolff parkinson white syndrome
- beta blockers
- amiodarone *** - give amiodarone when present in tachycardia (dont give adenosine)
- calcium channel blockers
- radiofrequency ablation - curatuve
dangerous arrhythmia in WPW
atrial fibrillation in WPW causes broad complex tachycardia irregular
—-> can lead to VF
do not give adenosine or digoxin as can worsen and lead to VF
definition of prolonged QT interval
> 480 ms in lead 2
congenital causes of prolonged qt interval
congenital channelopathy most common cause of prolonged QTc
mutations in myocyte potassium channels **
- LQTS type 1 - defect in KCNQ1 gene, slows potassium channels
- jervell and lange nielsen syndrome (congenital sensorineural deafness, AR)
- romano ward syndrome (AD) - LQTS type 2 - slows cardiac potassium ion channels and causes flatter T waves
- LQT3 - affects sodium channels , causes peaked T wave
acquired causes of prolonged qt interval
hypokalaemia
hypocalcaemia
hypomagnesaemia
medications (azithromycin, olanzapine, quetiapine)
cocaine
HIV
MI
hypothermia
presentation of QT interval
seizures
sudden syncope
cardiac arrest
investigations for QT syndrome
- ECG
- family screening
- holter monitor
- ECHO
- exercise test
describe hypertrophic cardiomyopathy
25% 1st degree relatives have features of HCM on ECHO
defect in deta cardiac myosin heavy chain
if mild hypertrophy -> mutation in trop T
presentation of hypertrophic cardiomyopathy
dizziness
fatigue
sudden cardiac death
palpitations
angina
syncope
apex beat displaced
murmur - mid to late systolic impulse,heard when squatting to standing, dynamic murmur
management of hypertrophic cardiomyopathy
- avoid heavy exercise
- regular screening
- ACE -i - reduce afterload
- beta blockers - improve LV filling
risk factors for PDA
females
trisomy 21
prematurity - most common CHD in preterm babies
rubella
infants born at high altitude
when does ductus arteriosus close
24-72 hour of age (due to falling prostaglandin level)
most common congenital heart defect
bicuspid aortic valve
cause of cardiomyopathy in chemotherapy
doxorubicin toxicity
inhibits DNA replication and transcription
causes dilated cardiomyopathy + congestive heart failure
describe holt oram syndrome
ASD
hypoplastic thumbs
absent radiii ( radial ray defects)
autosomal dominant
structures passed with umbilical venous catheter
- umbilical vein
- taks blood to liver
- bifurcates and provides blood into portal circulation via portal vein
- blood neters ductus venosus
- enters iVC
- UVC tip sits at junction of R atrium and IVC
murmur in pulmonary stenosis
ejection systolic
upper L sternal edge and radiates to back
thrill
click after 1st heart sound (in valvular PS)
role of umbilical vein
delivers oxygenated blood from placenta to fetus
how does ductus arteriosus stay open in fetus
low oxygen tension
prostaglandin E2 production from placenta
role of umbilical arteries
deoxygentaed blood travels back to placenta via 2 x umbilical arteries (arise from internal iliac artery)
role of foramen ovale
oxygenated blood that arrives in IVC crosses foramen ovale from R atrium to L atrium to then supply the upper body
describe fetal haemoglobin
HbF = 2 x alpha chains + 2 x gamma chains
start to produce adult Hb in 3rd trimester
by birth, 80% HbF and 20% HbA
HbF has higher affinity for oxygen than adult haemoglobin (oxyhaemoglobin dissociation curve shifts to left due to LOW 2,3 DPG in HbF)
describe the 2nd heart sound
caused by closure of aortic and pulmonary valves
splitting increased with ASD - independent of inspiration
louder in pulmonary hypertension
describe murmur in VSD
pansystolic
louder = smaller defect
quieter = larger defect
gallop rhythm/ 3rd heart sound, R ventricular heave, displaced apex beat = heart failure
what is the PR interval
time between onset of p wave (atrial depolarisation) and onset of QRS complex (ventricular depolarisation)
= conduction through the AV node
describe ventricular repolarisation
outward flow of potassium
inward flow of sodium and calcium
= t wave on ECG
presentation of congenital rubella
cardiac defects - PDA (30%), pulmonary artery stenosis, pulmonary arterial hyperplasia
cataract, retinopathy, iris hypoplasia
deafness
microcephaly, IUGR
duct dependent pulmonary blood flow
critical pulmonary stenosis
pulmonary atresia
tricuspid atresia
ductal dependent systemic blood flow
coarction of the aorta
hypoplastic L heart syndrome
interrupted aortic arch
side effect of prostaglandin E1 and E2
HYPOTENSION
flushing
bradycardia (18%)
apnoeas (12%)
causes vasodilation and keeps duct open
ECHO changes in VSD
dilatation of L atrium and L ventricle
types of VSD
- inlet muscular septal defect (8%) -
- outlet or sub pulmonary muscular septal defects (5-7%)
- trabecular muscular septal defect (5-20%)
- perimembranous septal defects (70-80%)
defects likely to resolve spontaneously: small and moderate apical muscular trabecular or perimembranous
inlet and outlet defects less likely to close
cardiac defect in marfans
- aortic regurgitation + aortic dissection due to aortic root dilatation
- mitral regurgitation / mitral valve prolapse
defibrillation in cardiac arrest
unsynchronised 4J/KG
defibrillation in VT with a pulse
synchronised :
1. 1J/KG for first shock
2. 2J/KG for 2nd shock
Murmur in aortic stenosis
ejection systolic murmur - harsh, loud
loudest at R sternal edge
systolic thrill palpable in suprasternal notch
