Cardiology Flashcards
what is the normal JVP wave form?
A wave - atrial contraction
C WAVE - an invisible flicker in the x decedent due to closure of the tricuspid valve before the start of ventricular systole
X descent - fall in atrial pressure during ventricular systole
V wave - due to passive filling of blood in to the atrium against a closed tricuspid valve
Y resent - opening of the tricuspid valve with passive movement of blood from the right ventriclee
what causes a raised JVP
with a normal waveform
- heart failure
- fluid overload
- severe bradycardia
Raised JVP on inspiration and drops with expiration - Kussmaul’s sign (this implies the right heart chambers cannot increase in size to accommodate increased venous return (e.g. pericardial disease - constriction or tamponade)
Raised JVP with loss of normal pulsation - SVC syndrome is obstruction caused by mediastinal malignancy
when may you get pathological a waves?
absent - AF
Large - tricuspid stenosis stenosis, right heart failure, Pulmonary HTN
Cannon - caused by AV dissociation - Aflutter, AF, complete heart block, VT and ventricular ectopics
what would you see pathological V waves?
giant V waves seen in tricuspid regurgitation
when would you see pathological x and y descent?
x descent - steep - tamponade and cardiac constriction
if steep x descent only then tamponade
Y descent - steep cardiac constriction
slow tricuspid stenosis
When may you have absent radial pulse?
Blalock-Taussig shunt for congenital heart disease e.g. tetralogy of Fallot
Aortic dissection
Trauma
Takayasu’s arteritis
peripheral arterial embolus
what causes collapsing pulse?
aortic regurgitation, arteriovenous fistula, PDA or other large extra cardiac shunt
what causes a slow rising pulse?
aortic stenosis
What is a Bisferiens pulse?
a double shudder due to mixed aortic valve disease with significant regurgitation
what causes a jerky pulse?
HOCM
what is an Alternans pulse?
occurs in severe left ventricular dysfunction - the ejection fraction is reduced meaning the end diastolic volume is elevated. This may sufficiently stretch the myocytes to improve the ejection fraction of the next heart beat - this leads to pulses that alternate from weak to strong
what is paradoxical pulse?
an excessive reduction in the pulse with inspiration (drop in systolic BP>10 mmHg) occurs with left ventricular compression, tamponade, constrictive pericarditis or severe asthma as venous return is compromised.
what may cause absent apex beat?
Obesity/emphysema
right pneumonectomy with displacement
Pericardial effusion or constriction
Dextrocardia (palpable on right side of chest)m
what can cause a pathological apex beat?
Heaving - LVH
Thrusting/hyperdynamic - high left ventricular volume \9eg in mitral regurgitation, aortic regurgitation, PDA, ventricular septal defect)
Tapping - palpable first heart sound in mitral stenosis
Displaced and diffuse/dyskinetic - left ventricular impairment and dilatation
Double impulse - with dyskinesia is due to left ventricular aneurysm; without dyskinesia in hypertrophic cardiomyopathy
Pericardial knock - constrictive pericarditis
Parasternal heave - due to right ventricular hypertrophy (e.g. atrial septal defects (ASD), pulmonary hypertension, COPD, pulmonary stenosis)
Palpable third heart sound - due to heart failure and severe mitral regurgitation
What causes a loud S1?
Mobile mitral stenosis
Hyperdynamic states
tachycardia states
Left to right shunts
short PR interval
what causes a soft first heart sound?
Immobile mitral stenosis
Hypodynamic states
Mitral regurgitation
Poor ventricular function
Long PR interval
what causes a split first heart sound?
LBBB
RBBB
VT
Inspiration
Ebstein’s anomaly
What are the causes of loud/soft second heart sound?
Loud
Systemic hypertension (loud A2)
pulmonary hypertension (loud P2)
Tachycardia states
ASD (loud P2)
Soft/absent
Severe aortic stenosis
What causes splitting heart sounds?
Fixed split - ASD
Widely split
RBBB
Pulmonary stenosis
Deep inspiration
Mitral regurgitation
what causes a opening snap?
In mitral stenosis - an opening snap can be present and occurs after S2 in early diastole. The closer it is to S2 the greater the severity of mitral stenosis. It is absent when mitral cusps become immobile due to calcification, as in very severe mitral stenosis
causes of left axis deviation?
LBBB
left anterior semi-block
LVH
primum ASD
cardiomyopathies
Tricuspid atresia
what causes a low voltage ECG ?
pulmonary emphysema
pericardial effusion
myxoedema
severe obesity
incorrect calibration
cardiomyopathies
global ischaemia
what causes right axis deviation?
infancy
RBBB
Right ventricular hypertrophy
what ECG abnormalities may you see in athletes?
sinus arrhythmia
sinus Brady
1st degree heart block
wenckeback phenomenon
junctional rhythm
What are the causes of LBBB??
IHD
HTN
LVH
Aortic valve disease
cardiomyopathy
myocarditis
post valve replacement
tachycardia with aberrancy or conceal conduction
ventricular ectopy
what are causes of RBBB?
normal in young people
right ventricular strain - e.g PE
ASD
IHD
myocarditis
idiopathic
tachycardia with aberrancy or concealed conduction
ventricular ectopy
causes of ST elevation?
early depolarisation
acute MI
pericarditis
ventricular aneurysm
coronary artery spasm
what ST-T changes may you see (no elevation in:
Ischaemia
Digoxin therapy
Hypertrophy
Post tachycardia
Hyperventilation
Oesophageal/upper abdominal irritations
Cardiac contusion
Mitral valce prolapse
Acute cerebral event
electrolyte abnormalities
Ischaemia
ST depression, T inversion
Digoxin therapy
Downsloping, ST depression
Hypertrophy
ST depression, T inversion
Post tachycardia
ST depression, T inversion
Hyperventilation
ST depression, T inversion and peaking
Oesophageal/upper abdominal irritations
ST depression, T wave inversion
Cardiac contusion
ST depression, T inversion
Mitral valce prolapse
T-wave inversion
Acute cerebral event
ST depression, T inversion
electrolyte abnormalities
What are Q waves?
Q waves can be permanent (reflecting myocardial necrosis) or transient (suggesting failure of myocardial function, but not necrosis)
What causes permanent Q waves?
Transmural infarction
LBBB
WPW syndrome
HCM
Idiopathic cardiomyopathy
Amyloid heart disease
Neoplastic infiltration
Friedrich’s ataxia
dextrocardia
sarcoidosis
progressive muscular dystrophy
myocarditis (may resolve)
what causes transient Q waves?
coronary spasm
hypoxia
hyperkalaemia
cardiac contusion
hypothermia
what ECG changes would you see in hyperkalaemia?
Tall T waves
Prolonged PR
flattened/absent p waves
Very severe hyperkalameia
wide QRS
sine wave pattern
ventricular tachycardia/ventricular fibrillation/asytole
what are ECG signs of hypokalaemia?
Flat T waves, occasionally inverted
prolonged PR interval
ST depression
Tall U waves
when are contrast echos used?
to identify shunts
e.g.
PFO
ASD
VSD
Agitated saline is injected into the venous system and the patient is asked to undergo valsalva manoeuvre to encourage increase right sided pressure
what patterns would you see in M mode on echo in:
- aortic regurgitation
- HCM
- mitral valve prolapse
- mitral stenosis
aortic regurgitation - fluttering of the anterior mitral valve leaflet is seen
HCM - systolic anterior motion of the mitral valve leaflets and asymetrical septal hypertoprhy
mitral valve prolapse. -one or both leaflets prolapse during systole
mitral stenosis - the opening profile of the cusps are seen when there is calcification of the cusps
what may lead to reduced uptake of perfusion traces in nuclear myocardial perfusion tracing?
ischaemia
infarction
HCM
amyloidosis
What are the complications of cardiac catheterisation ?
coronary dissection, aortic dissection, ventricular perforation
Air or atheroma embolism
ventricle dysrthythmias
when is exercise stress testing contraindicated?
severe aortic stenosis or HCM with marked outflow obstruction
acute myocarditis or pericarditis
pyrexial or coryzal illness
severe left main stem disease
untreated CCF
unstable angina
dissecting aneurysm
achy/Brady arrhythmias
untreated severe hypertension
What are the indicators of a positive exercise test result
development of anginal symptoms
a fall in BP > 155mmHG or failure to increase BP with exercise
arrhythmia development
poor workload capacity
failure to achieve target heart rate
>1mm down-sloping or planar ST segmentt depression, 80ms after the J point
ST segment elevation
Failure to achieve 9 min of the Bruce protocol due to any of the points listed
what effects does posture have on murmurs?
standing significantly increases the murmurs of mital valve prolapse and HCM only
Squatting and passive leg raising increases cardiac after load and therefore decreases the murmur of HCM and mitral valve prolapse, whilst increasing most other murmurs such as VSD, aortic, mitral and pulmonary regurgitation and aortic stenosis
what is the most common cause of mitral stenosis?
Rheumatic hear disease
Other rarer causes include congenital disease, carcinoid, SLE and mucopolysaccharidoses (glycoprotein deposits on cusps)
What is the diagnostic criteria for mitral stenosis?
mitral valve has a valve area of 4-6cm2.
MS is diagnosed when the valve area is <2cm2
It is considered severe <1cm2
what are the symptoms and signs of severe MS?
dyspnoea with minimal activity
Haemoptysis
Dysphagia (due to left atrial enlargement)
Palpitations due to atrial fibrillation
Signs - low pulse pressure
soft first heart sound
long diastolic murmur and apical thrill
very early opening snap i.e. closer to S2
right ventricular heave or loud P2
what would you see on echo, CXR and cardiac catheterisation in severe mitral stenosis?
Echo - doming of valve leaflets, heavily calcified cusps, direct orifice area <1cm2
CXR - left atrial or right ventricular enlargement, splaying of subcarinal angle >90 degrees, pulmonary congestion or hypertension, pulmonary haemosiderosis
Cardiac catheterisation - pulmonary capillary wedge end diastole to left ventricular end-diabolic pressure (LVEDP) gradient > 15mmHg, LA pressures > 25mmHg, elevated right ventricular and pulmonary artery pressures, high pulmonary vascular resistance, cardiac output <2.5L/min per m2 with exercise.
when is mitral balloon valvuloplasty suitable in mitral stenos ?
the mitral leaflet tips and valvular chord are not heavily thickened, distorted or calcified
the mitral cusps are mobile at the base
there in minimal or no mitral regurgitation
there is no left atrial thrombus seen on TOE
what is the full structure of the mitral valve?
annulus
cusps
chordae
papillary musculature
what are indicators for surgery in chronic mitral regurgitation?
the presence of symptoms
left ventricular dilatation
what is functional mitral regurgitation?
a term used to describe MR that is caused by stretching of the annulus secondary to ventricular dilatation
What are the main causes of mitral regurgitation?
Myxomatous degeneration
functional, secondary to ventricular dilation
mitral valve prolapse
ischaemic papillaey muscle rupture
congenital heart disease
collaged disorders
Rheumatic heart disease
Endocarditis
what are the indicators of the severity of mitral regurgitation?
small volume pulse
left ventricular enlargement due to overload
presence of S3
AF
Mid-diastolic flow murmur
Precordial thrill, signs of pulmonary hypertension or congestion
What are the signs of predominant MR in mixed mitral valve disease?
Soft S1; S3 present
Displaced and hyperdynaic apex (LV enlargement)
ECG showing LVH and left axis deviation
what does posture do to mitral valve prolapse murmur?
squatting increases the click and standing increases the murmur
what is the sequelae of mitral valve prolapse?
embolic phenomena
Rupture of mitral valve chordae
Dysrhythmias with QT prolongation
sudden death cardiac neurosis
what conditions are associated with mitral valve prolapse?
coronary artery disease
PKD
DCM,HCM
Secundum ASD
WPW syndrome
PDA
Marfan’s syndrome
Pseudoxanthoma elasticum
Osteogenesis imperfecta
Myocarditis
SLE
Polyarteritis nodosa
muscular dystrophy
left atrial myoxoma
what are acute causes aortic regurgitation?
aortic dissection or valve rupture from endocarditis
what are the causes of aortic regurgitation?
Valve inflammation - chronic rheumatic, IE, RA, SLE, Hurler’s syndrome
Aortitis - syphilis, ankylosing spondylitis, Reiter’s syndrome, psoriatic arthropathy
Aortic dissection/trauma
Hypertension Bicuspid aortic valve
Ruptures sinus of valsalva’s aneurysm
VSD with prolapse of right coronary cusp
Disorders of collaged - Marfan’s syndrome (aortic aneurysm, Hurler’s syndrome, Pseudoxanthoma elasticum)
what are eponymous signs associated with aortic regurgitation?
Quincke’s sign - nail bed fluctuation of capillary flow
Corrigan’s pulse - (Waterhammer); collapsing radial pulse
Corrigan’s sign - visible carotid pulsation
De Musset’s sign - head nodding with each systole
Duroziez’ sign - audible femoral bruits with diastolic flow (indicating moderate severity)
Traube’s sins - pistol shots (systole auscultatory finding of the femoral arteries)
Austin Flint murmur - functional mitral diastolic flow murmur
Argyll Robertson pupils - etiological connection with syphilitic aortitis
Muller’s sign - pulsation of the uvula
What are the features of Aortic regurgitation indicative of the need for surgery?
symptoms of dyspnoea/LV failure (reducing exercise tolerance
rupture of sinus of Valsalva’s aneurysm
IE not responsive to medical management
Enlarging aortic root diameter in Marfan’s syndrome with AR
Enlarging heart
- End-systolic diameter > 55mm at echo
- pulse pressure > 100mmHg
- Diastolic pressure < 40mmHg
- lengthening diastolic murmur
- ECG - lateral lead T -wave inversion
What is normal valve area of aortic valve?
> 2cm2
what is considered severe aortic stenosis?
valve area <1cm2 with a mean pressure gradient of >40mmHg on TTE
what is the aortic pressure gradient dependent on?
severity of aortic stenosis
LV function impairment
MS
Significant AR ]]In these cases the dimensionless index - a ratio of aortic and LVOT velocities can be useful
what are subvalvular causes of aortic gradients?
HCM and subaortic membranous stenosis, whereas supravalvular stenosis is due to aorta coarctation or Williams’ syndrome
why may sudden death occur in aortic stenosis?
due to ventricular tachycardia (this is due to LVH)
what is the mortality of surgical intervention for AS?
surgical mortality is related to LV failure
Absence of LV failure - -8%
Presence of LV failure 10-25%
what are the indicators of severe AS?
Symptoms of syncope or LV failure
Signs of LV failure
Absent A2
Paradoxically split A2
Presence of pericardial thrill
S4
Slow-rising pulse with narrow pulse pressure
Late peaking of long murmur
valve area >0.5cm2 on echo
what is the tricuspid regurgitation murmur?
Typically an inaudible murmur due to the low pressure in the right heart but may have may have low frequency pan systolic murmur if right ventricular pressures are elevated
What are the clinical signs of tricuspid regurgitation
elevated JVP and giant c-V waves
a pulsatile liner edge may be palpable and peripheral oedema is invariable
causes of tricuspid regurgitation?
- functional - due to right ventricular dilatation (commonly co-exists with significant MR)
- infection: the tricuspid valve is vulnerable to infection introduced by venous cannulation (iatrogenic and through IVDU )
- carcinoid (nodular hepatomegaly and telangiectasia)
Post-rheumatic - Ebstein’s anomaly - tricuspid valve dysplasia with a more apical position to the valve - patients have cyanosis and there is an association with pulmonary atresia or ASD and less commonly congenitally corrected transposition
what are common types of mechanical heart valves?
Ball and cage - ejection systolic murmur in the aortic area and an opening sound in the mitral position are normal
Single tilting disk - a modern variant includes the Medtronic hall valve
Bileaflet valves - now the mos commonly used valve type
what are the types of tissue valves
allografts.- porcine or bovine three cusp valve (3 months anticagulation recommended until tissue endothelialisation if patient is in sinus rhythm
Homografts - usually cadaveric - no need for long term anticoagulation
what is the most common cause of infection in prosthetic valves
staph epidermidids
what would suggest septal access in infected valve?
prolonged PR interval
what are the risks of warfarin in pregnancy?
fetal haemorrhage
teratogenicity risk 5-30% - the risk is dose dependant
abnormalities include chondrodysplasia, mental impairment, optic neuropathy and nasal hypoplasia
clinical presentation of IE?
malaise
tiredness
infective type symptoms
heart failure secondary to valvular regurgitation or heart block may also occur
signs of infective endocarditis?
fever
arthropathy
splinter haemorrhages
Osler’s nodes (painful)
Janeway lesions (painless)
clubbing (late sign)
needle-track signs
Retinopathy - Roth spots
hepatosplenomegaly
signs of atrial embolisation - stoke or digital ischaemia
vasculitic rash
what is the most common cause of IE in native valve?
Streptococcus vitamins
what are causes of non-infective endocarditis?
Marantic (metastatic related)
SLE related (Libman sacks)
How is IE managed ?
usually 4-6 weeks of IV abx
may require surgical replacement
what are the poor prognostic factors in IE?
prosthetic valve
staph aureus
culture negative endocarditis
deflection of complement levels
What are the indications for surgery in infective endicarditis?
cardiac failure or haemodynamic compromise
extensive valve incompetence
large vegetations
septic emboli
septal access
fungal infection
antibiotic resistance
failure to respond to medical therapy
causes of congenital cyanotic heart disease?
with shunts:
Aortic coarctation (with VSD or PDA)
VSD
ASD
PDA
partial anomalous venous drainage (with ASD)
without shunts:
congenital AS
aortic coarctation
what is partial anomalous venous drainage?
Partial anomalous venous drainage (PAPVD) is a rare congenital heart defect that occurs when some pulmonary veins drain into the right atrium of the heart instead of the left atrium
what are causes of cyanotic heart disease?
With shunts:
- tetralogy of ballot (VSD)
- severe Ebsteins anomaly (ASD)
- complete transposition of the great vessels
without shirts:
- tricuspid atresia
- severe pulmonary stenosis
- pulmonary atresia
- hypo plastic left heart
what is the most common congenital heart defect and how does it present?
ASD
they are usually found in adulthood
rarely they may present as a stroke in young people due to paradoxical embolus that originated in the venous system and reached the cerebral circulation via right to left shunting
what is found on clinical examination of a patient with ASD
fixed splitting of the second heart sound
there may also be a left parasternal heave and a pulmonary ESM due to increase blood flow
what are the types of ASD?
Secundum - 70% central fossa ovalis defects often associated with mitral valve prolapse. ECG will show incomplete or complete RBBB with right axis deviation
Primum - 15% sited above the AV valves, often associated with varying degrees of MR and TR and occasional y a VSD - picked up earlier in childhood. ECG shows a RBBB, left axis deviation and first degree heart block. Associate with Down’s Klinefelter’s and Noonan’s syndromes
Sinus venosus - 15% defect in the the upper septum, often associated with anomalous pulmonary venous drainage directly into the right atrium
when is surgical closure of ASD recommended?
surgical close is recommended with pulmonary systolic flow rations >1.5:1
closure of secundum defects may be performed via cardiac catheterisation
What is Holt-Oram syndrome?
Triphalangeal thumb with ASD
a rare syndrome (AD with incomplete penetration)
associated with absence or reduction anomalies of the upper arm
what is Lutembacher’s syndrome?
a rare combination of an ASD with mitral stenosis (the latter is probably rheumatic in origin)
Investigations for ASD?
right atrial and right ventricular dilation may be seen on any imaging technique
CXR may show pulmonary plethora
Echo - paradoxical spatial motion, septal defect and right to left flow of contrast during the venous injection with valsalva manoeuvre
Catheterisation - pulmonary hypertension - raised right ventricular pressure sand step up in oxygen saturation between various parts of the right circulation
indications for closure in ASD?
symptomatic
systemic embolism (typically stroke)
chamber dilatation
elevated right heart pressures
significant left to right shunt
What is foramen vale?
a channel within the intertribal septum which is typically covered by a flap that opens to allow right to left communication when right sided pressures elevate such as when coughing or sneezing or during valsalva’s manoeuvre
during feral development the foramen oval is open. Upon birth the reduction in resistance in the lungs lowers right sided pressure and the septum premium shuts sealing the foreman ovale
what are the symptoms of PFO
venous embolic material crosses into the arterial circulation ]there may be a history of headache, migraine or paradoxical embolism
stokes can occur in young people
how is PFO diagnosed?
contrast echo -right to left shunt is seen during valsalva’s manoeuvre
what is the ventricular septum made of?
two parts with a superior membranous component which contains the AV node and an inferior muscular component
VSD can occur in either
Indications for closure of VSD?
significant left to right shunt
associated with other defect requiring craniotomy
elevated right heart pressure causing pulmonary HTN
endocarditis
membranous VSD causing AR
what are the signs on examination of VSDS?
parasternal thrill
pan systolic murmur, the murmur mat be ejection systolic in very small or vary large defects
With very large defects the aortic component of the second sound is obscured, or even a single/palpable S2 /palpable S2 is heard
a mitral diastolic murmur may occur
The apex beat is typical hyperdynamic
What would be required if Eisenmenger’s syndrome develops in VSD?
heart lung transplant
what are the cardiac associations of VSD?
PDA
AR
pulmonary stenosis
ASD
tetralogy of fallout
coarctation of the aorta
what is Patent ductus arteriosus?
the connection occurs between the pulmonary trunk and the descending aorta
PDA is common in Prem babies, female infants born at high altitude and also if eternal rubella occurs in first trimester
what are the features of PDA?
a characteristic left subclavicular thrill
enlarged left heart and apical heave
continuous machinery murmur
wide pulse pressure and bounding pulse
Signs if pulmonary HTN and Eisenmenger’s syndrome occurs in 5% of cases
what causes closure of ductus arteriosus ?
Indometacin
what can reverse the close of the ductus arteriosus?
IV prostaglandin E1
(useful when PDA is associated with coarctation of the aorta or hypo plastic left heart syndrome and in complete transposition of the great vessels because it will help maintain the circulation between the systemic and pulmonary circulation)
what is the coarctation of the aorta ?
severe narrowing at the site of the regressed ductus arteriosus
how does coarctation of the aorta present?
severe - can cause heart failure and metabolic acidosis - it is life threatening in early life - IV prostaglandin can be given whilst awaiting surgery
Milder - can present beyond infancy with hypertension, leg cramps, muscle weakness and neurological change. Distal pulses are diminished and delayed. Collateral development can be significant and audible posteriorly and may cause ‘notching’ of the ribs on CXR
Investigations for coarctation of the aorta?
echo
MRI is the definitive investigation
How do you treat coarctation of the aorta ?
surgical or percutaneous
End-to-end anastomosis is the preferred surgical technique but re-stensois can occur
Balloon dilatation of the coarctation is typically focused on recurrent coarctation after surgery
what is associated with coarctation of the aorta?
Berry aneurysms and bicuspid aortic valve are strong associations
cardiac - PDA< VSD, mitral valve disease
Non cardiac - berry aneurysm, turner’s syndrome, renal abnormalities
signs of coarctation of the aorta?
HTN
radio-femoral delay of arterial pulse
absent femoral pulses
mid systolic or continuous murmur (infraclavicular)
sub scapular thrills
Rib notching on CXR
post stenotic aortic dilatation on chest radiograph
What is Esienmenger syndrome ?
when congenital cardiac defect with intracardiac communication leads to severe irreversible pulmonary HTN, reversal of left to right shunts and cyanosis
Signs of Eisenmenger syndrome?
clubbing
central cyanosis
decrease of the original pan systolic murmur
decreasing intensity of the tricuspid/pulmonary flow murmurs
single S2 with louder intensity, palpable S2 and right ventricular heave
appearance of Graham steel murmur due to pulmonary regurgitation
pan systolic murmur and v waves due to TR
What are the causes of Eisenmenger syndrome?
VSD
ASD
PDA
what are the complications of Eisenmenger syndrome?
right ventricular failure
massive haemoptysis
cerebral embolism/abscess
infective endocarditis
What are the features of tetralogy of Fallot?
Pulmonary stenosis (causes the systolic murmur) /right ventricular outflow obstruction
right ventricular hypertrophy
VSD
overriding of the aorta
right sided aortic knuckle
what are the clinical features of tetralogy of fallot?
cyanotic attacks (pulmonary infundibular spasm)
clubbing
parasternal heave
systolic throes
palpable A2
soft ejection systolic murmur
single s2 (inaudible pulmonary closure
ECG - features of right ventricular hypertrophy
possible complications of Tetralogy of Fallot?
Endocarditis
Polycythaemia
Coagulopathy
paradoxical embolism
cerebral abscess
ventricular arrhythmias
How does tetralogy of fallot present?
typically small for dates, difficulty in feeding, failure to thrive, and episodes of cyanosis when crying or feeding
clubbing is evident from 3 to 6 months
What are cyanotic attacks in infants with tetralogy of fallot caused by?
triggered by exercise, anxiety, dehydration, fever, anaemia, sepsis or spontaneous
The infant becomes inconsolable, cyanotic and tahcypnoea
Cyanotic attacks worsens with catecholamines, hypoxia and acidosis
how is a cyanotic attack in tetralogy of fallot managed?
emergency treatment is necessary to avoid death
parents should hold the infants against their shoulders tucking the infants knees up; this increases systemic vascularr resistance and reduced venous return of acidotic blood from the lower extremities, which reduces right ventricular infundibular spasm and right ventricular pressure so breaking the cycle.
In older children squatting achieves this
when is surgicy done in tetralogy of fallot?
aim is total correction before 12 months
Infants may be stabilised on prostaglandins to maintain patently of the ductus arteriosus
what are some important post-surgical circulations?
systemic right ventricle (after correction of transposition of the great vessels)
Single ventricular circulation - when individuals born with only one functional ventricle are treated by redirecting the vena cave directly into the pulmonary arteries
What are neurocardiogenic symptoms?
An exaggerated vasodepressor (hypotension), cardio-inhibitory (bradycardia) or mixed reflexes which may cause syncope or pre-syncope
The term “neurocardiogenic” is often used to describe symptoms seen in conditions like vasovagal syncope, postural orthostatic tachycardia syndrome (POTS), and neurocardiogenic syncope, which are associated with the malfunctioning of the autonomic nervous system and its effect on cardiovascular function.
What is sinus node disease ?
A condition in which the sinus node—the heart’s natural pacemaker—malfunctions and fails to regulate the heart’s rhythm properly. The sinus node, located in the right atrium of the heart, is responsible for initiating the electrical impulses that control the heart’s beating rate.
Sinus bradycardia and sinus pauses can cause syncope, pre syncope or non-specific symptoms.
Pacing is only indicated in significantly symptomatic cases
What is First-Degree Heart block?
A PR interval > 200ms
what is Mobitz type 1 block?
Second degree heart block
AKA Wenckebach’s
Progressive prolongation and then block of the PR interval in categorised as Mobitz type 1.
It may be normal during sleep in young, physically fit individuals (who have high vagal tone). If it occurs when the patient is awake and is associated with symptoms in older people - pacing may be indicated on symptomatic grounds
when is pacing indicated in first degree block?
The combination of first degree AV block with 1) LBBB, 2) RBBB with axis deviation or 3) alternating LBBB and RBBB is interpreted as trifasicular block. If associated with syncope - trifasicular block represents an indication for pacing
What is Mobitz type 2 block?
A type of High Grade AV block
more than one p wave per QRS
what is 3rd degree heart block
A type of high grade AV block
AV dissociation
what is the treatment for high grave AV block?
If untreated the mortality at 1 year may exceed 50%.
Patient require pacing even if asymptomatic
Which coronary artery occlusion with lead to high grade AV block?
right coronary artery - because the AV nodal branch is usually one of the distal branches of the right coronary arteries.
In patients with anterior infarct - high grade AV block is. a poor prognostic feature, indicating extensive ischaemia .
what are tachyarrhythmias caused by ?
Re-entry - the arrhythmia is anatomically dependant and usually the primary problem as opposed to sequelae of another reversible state
Automaticity - arrhythmia is often secondary to a systemic cause (e.g. electrolyte imbalance, sepsis, adrenergic drive) and is multifactorial
Triggered activity - shares features of both mechanisms and is seen in both primary arrhythmias and drug toxicity
What are supra ventricular tachycardias?
There are two major groups of re-entrant tachycardias often described as SVT
- AV nodal re-entry tachycardia (AVNRT ) - involves a re-entry circuit in and around the AV node
- AV Re-entry tachycardia (AVRT) - this involves an accessory pathway between the atria and ventricles some distance from the AV node
what is an accessory pathway?
a pathway that connects the atrium and ventricle mediates the tachycardia by enabling retrograde conduction from the ventricle to the atrium
More seriously the accessory pathway may predispose to unrestricted conduction of AD from atria to ventricles as a result of anterograde conduction through the pathway. This may lead to ventricular fibrillation.
What is WPW?
Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.
What are the ECG features of WPW ?
short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway (type A)
in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
right axis deviation if left-sided accessory pathway - type A
what conditions are associated with WPW?
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
What is atrial flutter?
Atrial flutter involves a macro re-entrant circuit where the electrical activation circles the right atrium.
Generates a saw toothed flutter waves, which typically have a rate between 250 and 350 beats/min, with a ventricular response of 150bom (2:1 block)
How can you uncover flutter waves?
the ventricular response may be slowed by increasing the vagal block of the AVN (e.g. carotid sinus massage) or by adenosine which will uncover the flutter waves.
How may atrial flutter be managed?
It is the most likely arrhythmia to respond to DCCV with low energies
Amioderone and Stall may chemically cardiovert, slow the ventricular response or act as prophylactic agents
Radiofrequency ablation is curative in up to 95% of cases
Adenosine can not terminate atrial flutter but can be useful in revealing it.
where would you typically see the sawtooth appearance in atrial flutter?
inferior leads and positive flutter waves in V1
where does atrial fibrillation arise from?
the source of the arrhythmia may be myocardial tissue in the opening of the four pulmonary veins which enter into the posterior aspect of the left atrium
Other sites include the superior vena cava, coronary sinus, vein of Marshall and atrial appendages. The exact mechanism by which these foci initiate AF is not fully understood but it’s thought to involve automaticity, triggered activity or micro-reentry.
pathophysiology of AF?
Automaticity: This refers to spontaneous depolarisation of myocardial cells in the absence of an external stimulus. In this context, it’s often due to enhanced automaticity where cells outside the sinoatrial node begin firing at a rate faster than the node itself.
Triggered Activity: This involves afterdepolarisations that are caused by influx of calcium ions during phase 4 of the action potential. These can be early (occurring during phase 2 or 3) or delayed (occurring after completion of phase 3).
Micro-reentry: This occurs when there is a small circuit that allows for re-entry within an anatomical or functional obstacle.
what does the substrate in AF refer to?
The substrate refers to structural and electrophysiological changes that facilitate maintenance of AF once it has been initiated. There’s evidence suggesting that atrial fibrosis plays a major role in creating this substrate by causing electrical and structural remodelling.
Electrical Remodelling: This includes shortening of the action potential duration, decrease in wavelength and refractory period heterogeneity leading to multiple wavelet re-entry circuits.
Structural Remodelling: This involves changes in atrial size, shape and fibrosis. Fibrosis disrupts the normal myocardial architecture leading to slow conduction and re-entry circuits.
what are the perpetuators of AF ?
AF itself can lead to further remodelling (termed ‘AF begets AF’) which then perpetuates the arrhythmia. This includes progressive atrial dilatation and fibrosis, as well as alterations in calcium handling proteins and ion channels.
Atrial Dilatation: AF leads to atrial stretch which can increase the dispersion of refractoriness and promote re-entry. It also upregulates angiotensin II, promoting fibroblast proliferation and fibrosis.
Fibrosis: Further fibrosis due to AF creates a more heterogeneous substrate that promotes maintenance of the arrhythmia.
Ionic Remodelling: Changes in ion channel expression (e.g., downregulation of L-type calcium channels) can alter action potential characteristics further promoting AF.
How is AF managed?
Haemodynamic instability - electrically cardioverted
Onset < 48 hours - rate or rhythm control
> 48 hours onset - anticoagulation for at least 3 weeks prior to DCCV
Rate control:
Beta blocker
CCB
Digoxin
Rhythm control
Beta blocker
amioderone
when is rate control not offered first line in AF ?
Rate control should be offered as the first-line treatment strategy for atrial fibrillation except in people:
whose atrial fibrillation has a reversible cause
who have heart failure thought to be primarily caused by atrial fibrillation
with new-onset atrial fibrillation (< 48 hours)
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm-control strategy would be more suitable based on clinical judgement
Risk factors for recurrence of AF after cardioversion?
long duration
rheumatic mitral valve disease
keft atrium size > 5.5cm
older age > 75 years
Left ventricular impairment
Features of VT favouring a broad complex tachycardia?
Capture beats (intermitttent sino-atrial node complexes transmited to the ventricles)
Fusion beats 0 combination of QRS from SA node and VT focus meeting and fusing (causes cannon waves)
RBBB with LA deviation
Very wide QRS > 140ms
Altered QRS compared with sinus rhythm
V lead concordance with all QRS vectors postive or negative
Dissociated P waves marching through theVT
Variable S1
HR < 170 with no effect of carotid sinus massage
Pro-arrhythmic causes of abnormal repolarasitation (ST-T changes)
- Familial - long QT, brugarda’s syndrome, short QT syndrome, arrhyhmogenic right ventricular dysplasia
- Drugs - quinidine, erythromycin, amiodarone, TCAs, phenothiazines, probucol, non sedating antihistamines
- IHD
- Metabolic - hypocalcaemia, hypothyroid, hypothermia, hypokalaemaia
- rheumatic carditis
Long QT syndrome - what chromosome is it commonly on?
90% are familial with chromosome 11 defects being common.
Romano-ward syndrome has AD inheritance
Jarvell-Lange-Nielsen syndrome - AR with congenital deafness.
what are causes of electromechanical dissociation?
When faced with cardiac arrest - it is important to appreciate the list of electromechanical dissociation causes
Hypoxia
Hypovolaemia
Hypothermia
Hypo/hyperkalaemia
Tension pneumothorax
Tamponade
Toxic/therapeurtic distrubance
thromboembolic
where is a temporary pacing wire placed and what is seen on ECG?
Temporary pacing wire is placed in the right ventricular apex
ECG will show LBBB morphology
- if the pacing wire has perforated the septum and entered the ventrical it will show RBBB
Complications of temporary pacing?
Crossing the tricuspid valve during insertion, which causes ventricular ectopic as does irritating the outflow tract
atrial or right ventricular perfortion and pericardial effusion
pneumothorax
What is pacemaker syndrome?
a constellation of symptoms related to even subtle impairment of cardiac output or change in periphera resistance caused by suboptimal pacemaker settings.
Typically causes by subtle differences in aatrioventricular synchrony which causes loss of the atrial kick (atrial contribution to cardiac output)
Patients may feel dizzy, hypotensive or develop signs of heat failure.
Pacing in heart failure - indications?
aka - cardiac resynchronisation therapy/biventricular pacing
NYHA III-IV
QRS duration > 130ms
EF less than 35%
there is a lead in both ventricals
one is places in the tributary of the coronary sinus on the lateral aspect of the left ventrical
The aim is to optimise AV delay and reduce interventricular dysnchrony
What is radiofrequency ablation?
It is a resistive, heat mediated protein membrane dysruption causing cell lysis.
It uses cardiac catheterisation with electrodes in the right or left sided chambers it interrupts electrical pathways in cardic structures.
Excellent results are obtained in treatment in accessory pathways and atrial flutter with complete AV nodal ablation or AV node modifcation.
VT is technically for difficult.
Isolatation of the pulmonary veins by ablation therapy is now used for AF.
How does smoking increase the risk of coronary atherosclerosis?
Increased platelet adhesion/aggregation and whole blood viscosity
Increased heart rate, increased catecholamine sensitivity/release
Increased carboxyhaehoglobin level and as a result increased haematocrit
decreased HDL cholesterol and vascular compliance
decreased threshold for VF
What is Decubitus angina?
Angina on lying down - due to increased left ventricular end diastolic pressure or associated with dreaming, cold sheets or coronary spasm during rapid eye movement.
What is variant (prinzmetal’s) angina?
Unpredictable, at rest, with transient ST elevation on ECG. Due to coronary artery spasm, with or without underlying artheroscleotic lesions.
What is syndrome X?
this refers to a heterogeneous group of patients who have ST segment depression on exercise testing but angiographically normal coronary arteries.
They patients may have very small vessel disease and/or abnormal ventricular function.
Causes of non-anginal chest pains?
pericardial pain
Aortic dissection
Mediastinitis
Pleural
MSK
GI
Hyperventilation/anxiety
Mitral valve prolapse
What is considered a STEMI?
> 2mm in two contigous chest leads or > 1mm in two or more limbs
Posterior STEMI casuses dominant R wave in V1 but will reveal ST elevation if posterior ECG is taked
What score can be used to assess mortality risk in NSTEMI?
GRACE score
What other conditions may causes a troponin leak?
Critical illness
Hypotension
Hypertensive crisis
PE
IECOPD
AAA rupture
GI bleed
Chemotherapy
renal impairment
neurological conditions
complications of MI?
Complications of anterior infarcts
Late VT/VF
Laft ventricular aneurysm
LV thrombus and systemic embolism (usually 1-3 weeks post MI)
CHB
MR
CCF
Cardiac rupture
VSD with septal rupture
Pericarditis and pericardial effusion
Dressler’s syndrome
Complications of inferior infarcts
Higher re-infarction rate
Inferior aneurysm wiht MR
PE
CHB
Papillary muscle dysfunction
What coronary arteru supplies the SA and AVN?
the RCA is the dominant vesle in 85% of cases.
Occlusion of the RCA may cause complete heart block.
Contraindications to thrombolysis?
Absolute
- active internal bleeding or uncontrollable external bleeding
- Suspected aortic dissection
- recent head trauma < 2 weeks
- intracranial neoplasms
- history of haemorrhagic stroke or ischaemic stroke < 2 months earlier
- uncontrolled BP
- pregnancy
Relative
- traumatic prolonged cardiopulmonary resuscitation
- bleeding disorders
- recent surgery
- probable intracardiac thrombus
- acitve diabetic haemorrhagic retinopathy
- anticoagulation/INR >1.8
