Week 5 Flashcards
In what situations is ECG first line?
for patients with chest pain, palpitations or blackouts
Which are the unipolar ECG leads?
Limb leads - aVR, aVL, aVF
chest leads V1-V6
Which are the bipolar leads?
Leads I, II and III
What does lead I measure?
RA-LA
What does lead II measure?
RA-LL
What does lead III measure?
LA-LL
Why can atrial depolarisation not be seen in ECG?
lost in QRS complex
What is the P wave?
atrial depolarisation
What does the QRS complex represent?
ventricular depolarisation
What is the ST segment?
plateau phase of repolarisation
What is the T wave?
Final rapid repolarisation
What is the Q wave?
conduction through perkinje fibres
Describe the systemic approach to any ECG
clinical context date, time, patient details assess technical quality Identify P /QRS /T measure heart rate check ECG intervals Determine QRS axis Look at P/QRS /T morphology Do not rely on automatic interpretation
How can you quickly determine heart rate from an ECG?
300 divided by the number of large squares between each QRS complex
or number of QRS complexes across 10 seconds X 6
What is the normal range for a PR interval?
<1 large square
<200ms
What does a prolonged PR interval suggest?
heart block
What us the normal range for QRS?
<3 small squares
<120ms
What does a prolonged QRS complex mean?
bundle branch block
or life threatening hypokalaemia - dehydration, renal impairment
What is the normal QT interval
<11 small squares
<440ms
What does a prolonged QT internal suggest?
Associated with ventricular tachycardia
can go into VF. young patient with syncope
What is meant by the QRS axis?
direction of average depolarisation in the heart - dominated by left ventricular depolarisation
How is the QRS axis determined?
from limb leads
relative to lead I
normal is -30 to +90 degress
axis is approximated by dissing the lead with the most +ve QRS
IN a normal axis, where is the QRS positive?
I and II
Describe left axis deviation
-30 to -90 degrees
positive QRS in I, negative in II and aVF
What does left axis deviation suggest?
left ventricular hypertrophy
Describe right axis deviation
+90 to +180 degrees
(negative QRS in I, positive in aVF
What does right axis deviation suggest?
hypertrophy of the right ventricle - pulmonary hypertension
Describe extreme axis deviation
+180 to -90 degrees
(negative QRS in I and II, positive in aVR
What does extreme axis deviation suggest?
ventricular tachycardia
paced ryhthm, all impulses could be in ventricle if pace maker is there
Describe normal P/QRS/T morphology
P wave is upright in the inferior leads
Normal ST segment is flat
T wave has the same polarity as the QRS
How can P waves be described?
positive, negative or biphasic
How are QRS complexes described if the first deflection is negative?
Q wave
What is the name for a positive deflection in QRS complex?
R wave
Wha t is the name for any negative deflection after R?
S wave
How can the ST segment be described?
isoelectric, elated or depressed
How can any further positive deflection after R be described in the QRS complex?
R’
How can T waves be described?
upright, inverted or flat
- also concordant or discordant vs QRS
Describe left bundle branch block
broadening of QRS complex characteristic negative QRS complex in VI positive in V6 T waves are discordant notching of V6
Describe right bundle branch block
inverted T waves in VI
V6- no discordant T waves
Left ventricular repolarisation
How do you recognise an arryhtmia?
What is the QRS rate are the QRS complexes regular? is the QRS board or narrow? Are there P waves What is the P:QRS relation?
What types of bradyarrythmias are there?
sinus bradycardia
junctional bradicardia
atrioventricular block - first degree, second degree, Mobitz I/II, third degree
Describe sinus bradycardia
rate <60bpm
regular, narrow QRS
P waves present
P:QRS is 1:1
Describe junctional bradycardia
rate <60bpm
regular, narrow QRS
No P waves present
Describe second degree AV block - mobitz type 1
slowest rate <60bpm
irregular narrow QRS
P:QRS not 1:1
regularly irregular
Describe second degree AV block - mobitz type II
slowest rate <60bpm
irregular narrow QRS
P:QRS not !:!
often indication for pace maker
Describe complete AV block
rate <60bpm
regular broad QRS
no relation between P and QRS
What drug may be used to treat bradyrhythmias?
atropine
anticholinergic - decreases vagal tone
What appearance does a pacemaker have on ECG?
looks like left bundle branch block
Give examples of regular narrow complex tachycardias
sinus/junctional
SVT
Give examples of irregular narrow tachycardias
AF
Give examples of broad complex regular tachycardias
monomorphic VT
SVT with BBB
Give examples of broad complex irregular tachycardias
polymorphic VT
AF with BBB
pre-excited AF
Describe sinus tachycarida
rate >100 bpm
regular, narrow QRS
P waves present
P:QRS is I:I
Describe atrial fibrillation
rate variable - fast
irregular, narrow QRS
no P waves
Describe atrial flutter
macro-reentrant atrial tachycardia
regular narrow QRS
sawtooth atrial activity - about 300bpm
may get variable AV block
Describe supraventricular tachycardia
rate - more than 150bpm regular, narrow QRS P waves present P:QRS is 1:1 AVRT, AVNRT or atrial tachycardia
Describe broad complex tachycardia
regular borad QRS P waves may still be seen ventricular tachycardia SVT with BBB SVT over an accessory pathway
How can VT and SVT be differentiated?
fusion beats, capture beats, AV dissociation, extreme rightward or NW axis, or QRS concordance more likely to be VT
if in doubt always treat as VT
What does ST elevation in the anterior leads suggest?
MI in left anterior descending artery
What does ST elevation in lateral leads suggest?
MI is distal, left anterior descending artery or circumflex artery
What does ST elevation in the inferior leads suggest?
MI in right coronary artery or circumflex
What is heart failure?
failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of the tissues - caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure
How is heart failure characterised?
by typical haemodynamic changes (systemic vasoconstriction) and neurohumoral activation
What does heart failure cause clinically?
breathlessness, effort tolerance, fluid retention, and is associated with frequent hospital admission and poor survival
What are common causes of heart failure in the UK?
coronary artery disease hypertension idiopathic toxins genetic
What are the less common causes of heart failure in the UK?
valve disease infections congenital heart disease metabolic pericardial disease (e.g. TB) endocardial disease
Describe HF-REF
systolic HF
younger
more often male
coronary aetiology
Describe HF-PEF
diastolic HF
older
more often female
hypertensive aetiology
Describe chronic (congestive) heart failure
present for a period of time
may have been acute or become acute
Describe acute (decompensated) heart failure
usually admitted to hospital
worsening of chronic
new onset
Describe the pathophysiology of heart failure
myocardial injury
left ventricular systolic dysfucntion
perceived reduction in circulating volume and pressure
neurohumoral activation
systemic vasoconstriction renal sodium and water retention
which leads to further left ventricular systolic dysfuction
What hormones are related in response to heart failure?
SNS
RAAS
ET, AVP etc
natriuretic peptides
What are the symptoms of heart failure?
dyspnoea and cough
ankle swelling
fatigue/ tiredness
What are the signs of heart failure?
peripheral oedema elevated JVP third heart sound displaced apex beat pulmonary oedema pleural effusion
Describe NYHA class I
no symptoms and no limitation in ordinary physical activty
Describe NYHA class II
mild symptoms (shortness of breath or angina) and slight limitation during normal activity
Describe NYHA class III?
marked limitation in activity due to symptoms, even less than ordinary activity - walking short distances
only comfortable at rest
Describe class IV NYHA
severe limitations
experience symptoms even while at rest. mostly bedbound
What investigations will all patients receive for heart failure?
ECG CXR echocardiogram blood chemistry haematology natriuertic peptides
What investigations will selected patients get for heart failure?
coronary angiography exercise test adulatory ECG monitoring myocardial biopsy genetic testing
Describe the treatment of heart failure
Beta blocker and ACE inhibitor (or ARB) MRA sacubitril/valsartan ICD or CRTP/CRTD, ivabradine digoxin consider transplant
What affect does angiotensin II have on the blood vessels?
vasoconstriction SMC hypertrophy superoxide generation enodthelin secretion monocyte activation inflammatory cytokines reduced fibrinolysis
What affect does angiotensin II have on the kidneys?
sodium and water retention
efferent arterial vasoconstriction
globular and interstitial fibrosis
What affect does angiotensin II have on the heart?
cellular hypertrophy myocyte apoptosis myocardial fibrosis inflammatory cytokines coronary vasoconstriction positive isotropy proarrythmia
What affect does angiotensin II have on the adrenal gland?
aldosterone secretion
What affect does angiotensin II have on the brain?
vasopressin secretion
sympathetic activation
What do natriuretic peptides do?
vasodilation
natriuresis
diuresis
inhibition of pathologic growth/fibrosis
What does neprilysin do?
breaks down natriuretic peptides
What can be seen in chest X-ray in stage I heart failure?
redistribution pulmonary vessels
cardiomegaly
What can be seen on chest X-ray in stage 2 heart failure?
kerely lines
peribronchial cuffing
hazy contours of vessels
thickened interlobar fissures
What can be seen on chest x-ray in stage 3 heart failure?
consolidation
air bronchogram
cottonwool appearance
pleural effusions
Describe redistribution of pulmonary vessles
in the normal chest x-ray vessels in lower zones are larger than equivalent vessels in upper zones
if vessels in upper zones are enlarged them elevated pulmonary venous pressure should be considered
What are kerley B lines?
spatial lines - fid leakage into interlobular septa
seen at bases perpendicular to the pleural surface
if transient or rapidly developing virtually diagnostic of pulmonary oedema
What are kerly A lines?
caused by distension of the anastomotic channels between the peripheral and central sympathetic
oblique
What are kerly c lines?
reticular opacities at the lung bases
What are the signs of interstitial oedema?
peribronchial cuffing
hazy contour of vessles
Describe peribronchial cuffing
normally walls of bronchi are invisible
when fluid collects in peribronchial interstitial space the bronchial walls become visible
Describe hazy contour of vessels
not only enlarged but lose their defined margin due to surrounding oedema
requires previous examinations
Describe subpleural pulmonary oedema
fluid can accumulate in the loose connective tissue beneath the visceral pleura
seen as a sharply defined band on increased density
Describe alveolar oedema
represents spill of fluid from interstitial into alveolar spaces resulting in airspace opacity
bilateral usually
butterfly distribution
rapid change - infection slower than HF
Describe pleural effusions
fluid within potential space between parietal and visceral layers
divided into transudates and exudates
When are transudates found in pleural effusions?
LVF, cirrhosis, nephrotic syndrom
myxoedema, PE, sarcoidois
When are exudates found in pleural effusions?
PE, bacterial infection, bronchial ca
fungal/viral infection. lymphoma
What is the appearance of pleural effusions on chest X-ray?
homogenous lower zone opacity with a curvilinear upper border
large effusions obscure heart border and displace mediastinum, airways and diaphragm
Describe subpolmonic effusion
fluid can accumulate in a subpulmonic location
can be difficult to detect as upper edge of fluid mimics contour of diaphragm
principle sign is apparent elevation of hemidiaphragm
What is a valve?
a device for controlling the passage of fluid thorough a pipe or duct, especially an automatic device allowing movement in one direction only
What can go wrong with valve leaflets?
calcification thickening degeneration infection prolapse
What can go wrong with the valve apparatus or annulus?
annular dilitation
annular calcification
apparatus tethering/thickeing/ rupture
regional wall motion abnormality
What does stenosis cause?
pressure overload
increased pressure in LV
hypertrophy
What does regurgitation cause?
volume overload
ventricles start to dilate due to increased volume
Describe rheumatic valve disease
acute rheumatic fever
mainly strep pyrogens throat infections
antibody cross reactivity affecting connective tissue
cardiac injury generated by recurrent inflammation and fibrinous repair and scarring
less prevalent in antibiotic age
Describe the aortic valve
lies between LV and aorta
3 cusps
right, less, non coronary
What can cause aortic stenosis?
thickening
calcification
rheumatic valve disease
congenital
What are the symptoms of aortic stenosis?
shortness of breath
pre syncope
chest pain
reduced exercise capacity
What can cause aortic regurgitation?
degeneration rheumatic valvular disease aortic root dilatation systemic disease endocarditis
Which systemic diseases can cause aortic regurgitation?
marfan’s syndrome
ehlers danlos syndrome
ankylosing spondyltis
SLE
What are the symptoms of aortic regurgitation?
shortness of breath
reduced exercise capacity
Describe bicuspid aortic valves
prone to premture dysfunction
associated with aortic abnormalities
genetic component
Describe the mitral valve
lies between LA and LV
2 leaflets
anterior and posterior
Describe mitral stenosis
rheumatic valve disease pressure overload dilated LA atrial fibrilation pulomary hypertension secondary right heart dilatation
What are the symptoms of mitral stenosis?
shortness of breath palpitation chest pain haemoptysis right heart failure symptoms
Describe mitral regurgitation?
volume overload - LA/LV LV and LA dilatation pulomary hypertension secondary right heart dilatation atrial fibrillation
What are the symptoms of mitral valve regurgitation?
shortness of breath
palpitation
right heart failure symptoms
Describe the pulmonic valve
3 leaflets
lies between RV and pulmonary artery
Describe the tricuspid valve
3 leaflets
lies between RA and RV
How are valve defects assessed?
history examination blood pressure ECG echo CT MRI exercise tolerance tesr CPET stress echo catheterisation
What is infective endocarditis?
infection of the endocardium and/or intra-cardiac devices
can lead to formation of vegetation and destruction of cardiac tissue
What are the cardiac risk factors for infective endocarditis?
existing valvular heart disease congenital heart disease prosthetic heart valves indwelling cardiac devices `past history of IE
What are the non-cardiac risk factors for infective endocarditis?
immunodeficiency diabetes alchohol dependency indwelling IV lines IV drug use (mostly right sides IE)
How do people get IE?
dental manipulation dental disease extra-cardiac infection invasive procedure cardiac surgery IV drug use no clear cause
Describe staphylococci in endocarditis
aureas - 26.6% - IVDU
coagulase negative staph - epidermis, device/line related or early PVE
Describe streptococci and enterococci in IE
oral stereo - 18.7%
non-oral - associated with colorectal cancer
enterococci - 10.5%
What does HACEK stand or?
haemophilus, aggregatibacter, cardiobacterium, eikenella corrodens, kingella
how does IE develop?
endothelial injury caused by valve sclerosis, rheumatic valvulitis or direct bacterial activty
development of non-infected platelet thrombus
bacterial adherence to thrombus and colonisation
further cycles of endothelial injury and thumbs deposition leads to formation of bacterial vegetation
Describe acute IE
acute and aggressive onset of symptoms
often due to staph areas
progressive valve destruction and metastatic infection
Describe subacute IE
insidious, non specific presentation
strep viridian’s most commonly
metastatic infection uncommon
What are the symptoms of IE?
fever fatigue anorexia weight loss night sweats dyspnoea
What are the symptoms of embolic phenomena in IE?
stroke, meningitis,
lung assess, emboli
abdominal pain
back pain - osteomyelitis
When should IE be considered?
fever in presence of risk factors
sepsis of unknown origin
evidence of embolic phenomena
history,
What are the vascular phenomena in IE?
septic embolism - stroke, digital gangrene spilnter haemorrhages laneway lesions conjunctival haemorrhages pulmonary , renal or splenic infarcts petechial rash
What are the immunological phenomena in IE?
glomerulonephritis
oslers nodes
roth spots
What are some other sign’s of IE?
murmur
splenomegaly
neurological signs
nail clubbing
What are osier’s nodes?
painful, eryhtmetous nodular lesions, necrotising vasculitis
What are janeway lesions?
non painful, erythematous, blanching macule , embolic microabscesses
What are splinter haemorrhages?
non-blanching, linear, reddish-brown lesions - not full length of nail
Describe roth spots
retinal haemorrhages with pale centres
What can cause nail clubbing?
atrial myxoma, cyanotic congenital heart disease, bronchietactis, interstitial lung disease and lung cancer
What are the major clinical criteria in modified duke diagnosis of IE?
blood cultures positive for infective endocarditis
evidence of endocardial involvement - echo / valvular regurgitation
what are the minor clinical criteria in the diagnosis of IE?
predisposition fever vascular phenomena immunological phenomena microbiological eveidence
When is IE diagnosis definite ?
two major criteria
one major and three minor criteria
5 minor criteria
What antibiotics are used fro NVE?
amoxicillin / flucloxacilin/ gent
What antibiotics are used for PVE?
vancomycin/gentamycin/rifampicin
What are the indications for cardiac surgery in IE?
valve dysfunction leading to heart failure
uncontrolled infection
prevention of embolism
What are the symptoms of MI?
chest pain back pain jaw pain indigestion sweetness/claminess shortness of breath none (diabetes / dementia) death
What are the signs of MI?
tachycardia distressed patient heart failure(crackles, raised JVP) shock arrhythmia none
What is troponin?
part of cardiac myocyte
release in blood stream is a marker of cardiac necrosis
What is the universal definition of MI?
any elevation in troponin in clinical setting consistent with MI
What is type 1 MI?
spontaneous MI due to primary coronary event
What is type 2 MI?
increased oxygen demand /decreased supply - heart failure, sepsis, anaemia, arryhtmias, hypertension or hypotension
What is type 3 MI?
sudden cardiac death
What is type 4a MI?
MI associated with PCI
What is type 4b MI?
Stent thrombosis documented by angiography or PM
What is type 5 MI?
MI associated with CABG
What are cases of type 2 MIs?
congestive heart failure tachyarrythmias PE sepsis apical ballooning syndrome anything that stresses the heart
What can cause chronic troponin elevation (not MI)
renal failure
chronic heart failure
infiltrative cardiomyopathies
What is unstable angina?
an acute coronary event without rise in tropnin
how can a stem in posterior wall be detected in ECG?
anterior ST depression
what is the immediate management of a STEMI?
ABCD ambulance, defib aspirin 300mg PO UF heparin morphine anti-emetics clopidogrel ticagrelor (in hospital) activate PPCI team
How does primary PCI compare to thrombolysis?
improves survival reduced strokes reduces repeated MI reduces further angina speeds up reconvery shortens time in hospital
What is the subsequent management of a STEMI?
coronary care unit
drugs for secondary prevention
echo for LV function and cardiac structure
cardiac rehab
What drugs are used for secondary prevention of MI?
ACE inhibitors
BB
statins
eplerenone (diabetes / clinical heart failure)
When would an ICD be considered following an MI?
if LVSD > 9 months
What are the complications of an MI?
arrthymias heart failure cariogenic shock myocardial rupture psychological
What is the definition of hypertension?
persistant elevevation in retrial blood pressure >140/90
a BP level that increases the vascular risk in patients sufficient to require intervention
the threshold at which benefits of action exceed those of inaction
What is optimal BP?
<120/ <80
What is normal BP?
120-129
80-84
What is high normal BP?
130-139
85-89
What is grade 1 hypertension?
140-159
90-99
What is grade 2 hypertension?
160-179
100-109
What is grade 3 hypertension?
> 180
>110
What is isolated systolic hypertension?
> 140
<90
What are the non-modifiable risk factors for primary hypertension?
age
gender
ethnicity
genetic factors
What are the modifiable risk factors for primary hypertension?
diet physical activity obesity alcohol excess stress
What are the causes of secondary hypertension?
hyperaldosteronism thyroid disorders phaeochromocytoma renal artery stenosis exogenous steroid use NSAIDs herbal remedies cocaine
What are the two out of office BP measurement techniques?
24 hour ambulatory blood pressure monitoring
home blood pressure monitoring
What initial investigations can be carried out in a patient with hypertension?
U&Es electrolytes glucose lipid profile TFTs LFTs urine dipstick 12 lead ECG
What additional tests can be used in the elevation of hypertension?
renin and aldosterone 25 hour urine catecholamines echo renal ultrasound MRA renal
How is the cardiovascular risk assessed in hypertension?
BP category presece of end organ damage presence of diabetes CV renal disease
How can hypertension be managed?
lifestyle measures
pharmacological management
renal denervation
What medications can be used to treat hypertension?
diuretics
ACE inhibitor /ARBs
vasodilators- calcium channel blockers, beta blockers, alpha blockers
IN a patient under the age of 55, what are the steps in the pharmacological management of hypertension?
ACE inhibits or ARB
then add calcium channel blocker
then add thiazide diuretic
consider alpha or beta blocker
What are the stages in the pharmacological management of patients over 55 or black patients with hypertension?
calcium channel blocker
then add ACEI
then add thiazide diuretic
then consider beta/alpha blocker s
How is AF diagnosed?
irregularly irregular rhythm
no discernible P waves
>30 seconds
What are the other key ECG changes in AF?
absence of isoelectric baseline
fibrillary waves may be present
What is atrial flutter?
caused by re-entry circuit within RA
length of re-entry circuit corresponds to size of RA
predictable atrial rate about 300bpm
ventricular rate determined by AV conduction ratio
i.e. if 2:1 then ventricular rate will be about 150bpm
What is meant by a type 1 flutter?
typical
IVC and tricuspid isthmus in circuit
anti-clockwise or clockwise
What is a type 2 flutter?
atypical
does not fit typical criteria
less amenable to ablation
How is AF classified?
paroxysmal (<48 hours)
persistent (>7 days or requires CV)
long standing (>1 year)
permanent (accepted)
Describe the pathophysiology of AF
progressie remodelling of atrial structure and ion channel function
provoked by numerous stressors
structural remodelling usually develops before the onset of AF
What are the hallmarks of AF pathophysiology
activation of fibroblasts, enhanced connective tissue deposition, and fibrosis
What is theory A in the electrophysiological mechanism of AF?
a focal source in pulmonary veins can trigger AF
heirarchic organisation of AF with rapidly activated areas driving the arrhythmia documented in paroxysmal AF, but less obvious in persistent
What is theory B in the electrophysiological mechanism of AF
perpetuated by continuous conduction of several independent wavelets propagating through atrial musculature in seemingly chaotic manner
What are the cardiac causes of AF?
coronary artery disease conduction disease structural heart disease cardiomyopathy heart failure valvular disease hypertension
What are the endogenous causes of AF?
thyroid dysfunction COPD PE sleep apnoea diabetes CKD electrolyte disturbances obesity acid base disturbances
What are the exogenous causes of AF?
infection
alcohol - chronic excess/binges
smoking
caffeine
What investigations are needed in AF?
ECG TFTs echo LFTs electrolytes CRP/blood cultures
What are the symptoms of AF?
palpitations
dyspnoea
chest tightness
pre-syncope
What are the major complications of AF?
thromboembolism
heart failure
What is used to assess whether AF patients need stroke prevention?
ChA2DS2VASc risk scores
What can be used as stroke prevention in AF?
vitamin K antagonists DOACs antiplatelet agents transcatheter therapy surgical therapy
Which treatment strategy should be used in which AF patients?
offer rate control as 1st line strategy, except -
new onset
secondary reversible cause
HF thought primarily due by AF
Give an example of a class 1 antiarrythmic drug
flecainide
sodium channel blocker
Give examples of class II anti arrhythmic drugs
beta blockers
bisprolol
carvedilol
Give examples of class III anti arrhythmic drugs
k+ channel blockers
amioderone
Give examples of class IV anti arrhythmic drugs
Ca2+ Channel blockers
diltiazem
verapamil
Give examples of class V anti arrhythmic drugs
amiodarone
What are the main rhythm control drugs?
flecainide
amioderone
What are the main rate control drugs?
beta blockers
digoxin
calcium channel blockers
What are the risks associated with flecainide?
hypotension
atrial flutter
QT prolongation
avoid in patents with IHD or significant structural heart disease
What are the risks associates with amiodarone?
phlebitis hypotension bradycardia/AV block will slow ventricular rate delated conversion to sinus rhythm
For which patients in catheter ablation used in AF?
with paroxysmal or persistent AF who fail AAD
What are the surgical options in AF treatment?
maze procedure
Describe ablation of AV node
ablation results in iatrogenic 3rd degree heart block
controls ventricular rate in AF when medications fail to do so
patients pacemaker dependent for life
Describe the RA
sinoatrial node
broad appendage
Describe the LA
narrow, long appendage
pulmonary venous confluence
Describe the RV
trabeculated endocardium
insertion of chord to IVS, moderator band
Describe the LV
smooth endocardium, ellipsoid cavity
What are the categories of cyanotic CHD?
no shunt and shunt
Give examples of no shunt CHDs
correction of aorta abstain's anomaly pulmonary stenosis bicuspid aortic valve subaortic membrane ccTGA
Give example of shunt CHDs
atrial septal defect ventricular septal defect AVSD patent ductus arterioles aortopulmonary window partial anomalous pulmonary venous drainage
Give examples of cyanotic CHDs
Eisenmenger syndtome tetralogy of fallot transposition of the great arteries tricuspid atresia pulomary atresia combined lesions - ASD with severe pulmonary stenosis
What is ccTGA?
congenitally correction transposition of the great arteries
usually not in isolation
What are the special considerations in arrhythmia in CHD?
common scar related haemodynamic lesion related emergency if fontan
What are the special considerations in pregnancy in CHD?
higer risk volume shift arrhythmia dissection risk outflow obstruction - CO can't be increased
Describe secundum ASD
shunts left to right in isolation
right heart volume loading
pulmonary flow murmur
fixed, split second heart sound
What can secundum ASD lead to?
RV failure tricuspid regurgitation atrial arrhythmias pulmonary hypetension Eisenmenger syndrome
Describe transposition of the great arteries
oxygenated blood from pulmonary veins is re-ciculated to lungs
deoxygenated blood from the body is recirculated to the body
duct dependent circulation
Describe foetal circulation
in-utero oxygenation is by the maternal placenta
pulmonary circulation is minimal and at high resistaance
oxygenated blood returns to RA bia IVS
it bypasses the RV/PA bia the foramen ovale
of the blood that is pumped to the PA, most passes to the aorta via the ductus arteriosus
What are the consequences on surgery to treat transposition of the great arteries?
atrial switch
systemic RV- dilatation, tricuspid regurgitation, heart failure, atrial arrhythmias
Describe tetralogy of fallot
ventricular septeal defect
overriding arota
RVOT obstruction
right ventricular hypertrophy
How is tetralogy of ballot repaired?
pulmonary artery and right ventricle enlarged using a patch
muscular obstruction removed
VSD closed with patch
What is the repaired history of tetralogy of fallot?
significant pulmonary regurgitation
intrinsic iatrogenic arryhmia risk
residual VSD
pulmonary arterial/branch PA stenoses
Describe fontal/TCPC
single ventricle supports systemic circulation
systemic venous return is directed to pulmonary arteries, bypassing the ventricular mass
pulmonary circulation relies on maintained systemic venous pressure and low pulmonary vascular resistance
dehydration, arrhythmia, bleeding and pulmonary embolus all potentially catastrophic
Describe coarction of the aorta
age at presentation depends on position and severity
pre-ductal may cause lower limb cyanosis
upper body hypertension, berry aneurisms, claudication and renal insufficiency may ensure
