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MRCP Text book > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what is the normal JVP wave form?

A

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

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2
Q

what causes a raised JVP

A

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

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3
Q

when may you get pathological a waves?

A

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

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4
Q

what would you see pathological V waves?

A

giant V waves seen in tricuspid regurgitation

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5
Q

when would you see pathological x and y descent?

A

x descent - steep - tamponade and cardiac constriction
if steep x descent only then tamponade

Y descent - steep cardiac constriction
slow tricuspid stenosis

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6
Q

When may you have absent radial pulse?

A

Blalock-Taussig shunt for congenital heart disease e.g. tetralogy of Fallot

Aortic dissection

Trauma

Takayasu’s arteritis

peripheral arterial embolus

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7
Q

what causes collapsing pulse?

A

aortic regurgitation, arteriovenous fistula, PDA or other large extra cardiac shunt

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8
Q

what causes a slow rising pulse?

A

aortic stenosis

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9
Q

What is a Bisferiens pulse?

A

a double shudder due to mixed aortic valve disease with significant regurgitation

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10
Q

what causes a jerky pulse?

A

HOCM

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11
Q

what is an Alternans pulse?

A

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

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12
Q

what is paradoxical pulse?

A

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.

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13
Q

what may cause absent apex beat?

A

Obesity/emphysema
right pneumonectomy with displacement
Pericardial effusion or constriction
Dextrocardia (palpable on right side of chest)m

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14
Q

what can cause a pathological apex beat?

A

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

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15
Q

What causes a loud S1?

A

Mobile mitral stenosis
Hyperdynamic states
tachycardia states
Left to right shunts
short PR interval

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16
Q

what causes a soft first heart sound?

A

Immobile mitral stenosis
Hypodynamic states
Mitral regurgitation
Poor ventricular function
Long PR interval

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17
Q

what causes a split first heart sound?

A

LBBB
RBBB
VT
Inspiration
Ebstein’s anomaly

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18
Q

What are the causes of loud/soft second heart sound?

A

Loud
Systemic hypertension (loud A2)
pulmonary hypertension (loud P2)
Tachycardia states
ASD (loud P2)

Soft/absent
Severe aortic stenosis

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19
Q

What causes splitting heart sounds?

A

Fixed split - ASD

Widely split
RBBB
Pulmonary stenosis
Deep inspiration
Mitral regurgitation

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20
Q

what causes a opening snap?

A

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

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21
Q

causes of left axis deviation?

A

LBBB
left anterior semi-block
LVH
primum ASD
cardiomyopathies
Tricuspid atresia

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22
Q

what causes a low voltage ECG ?

A

pulmonary emphysema
pericardial effusion
myxoedema
severe obesity
incorrect calibration
cardiomyopathies
global ischaemia

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23
Q

what causes right axis deviation?

A

infancy
RBBB
Right ventricular hypertrophy

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24
Q

what ECG abnormalities may you see in athletes?

A

sinus arrhythmia
sinus Brady
1st degree heart block
wenckeback phenomenon
junctional rhythm

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25
Q

What are the causes of LBBB??

A

IHD
HTN
LVH
Aortic valve disease
cardiomyopathy
myocarditis
post valve replacement
tachycardia with aberrancy or conceal conduction
ventricular ectopy

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26
Q

what are causes of RBBB?

A

normal in young people
right ventricular strain - e.g PE
ASD
IHD
myocarditis
idiopathic
tachycardia with aberrancy or concealed conduction
ventricular ectopy

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27
Q

causes of ST elevation?

A

early depolarisation
acute MI
pericarditis
ventricular aneurysm
coronary artery spasm

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28
Q

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

A

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

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29
Q

What are Q waves?

A

Q waves can be permanent (reflecting myocardial necrosis) or transient (suggesting failure of myocardial function, but not necrosis)

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30
Q

What causes permanent Q waves?

A

Transmural infarction
LBBB
WPW syndrome
HCM
Idiopathic cardiomyopathy
Amyloid heart disease
Neoplastic infiltration
Friedrich’s ataxia
dextrocardia
sarcoidosis
progressive muscular dystrophy
myocarditis (may resolve)

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31
Q

what causes transient Q waves?

A

coronary spasm
hypoxia
hyperkalaemia
cardiac contusion
hypothermia

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32
Q

what ECG changes would you see in hyperkalaemia?

A

Tall T waves
Prolonged PR
flattened/absent p waves

Very severe hyperkalameia
wide QRS
sine wave pattern
ventricular tachycardia/ventricular fibrillation/asytole

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33
Q

what are ECG signs of hypokalaemia?

A

Flat T waves, occasionally inverted
prolonged PR interval
ST depression
Tall U waves

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34
Q

when are contrast echos used?

A

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

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35
Q

what patterns would you see in M mode on echo in:
- aortic regurgitation
- HCM
- mitral valve prolapse
- mitral stenosis

A

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

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36
Q

what may lead to reduced uptake of perfusion traces in nuclear myocardial perfusion tracing?

A

ischaemia
infarction
HCM
amyloidosis

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37
Q

What are the complications of cardiac catheterisation ?

A

coronary dissection, aortic dissection, ventricular perforation
Air or atheroma embolism
ventricle dysrthythmias

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38
Q

when is exercise stress testing contraindicated?

A

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

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39
Q

What are the indicators of a positive exercise test result

A

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

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40
Q

what effects does posture have on murmurs?

A

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

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41
Q

what is the most common cause of mitral stenosis?

A

Rheumatic hear disease

Other rarer causes include congenital disease, carcinoid, SLE and mucopolysaccharidoses (glycoprotein deposits on cusps)

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42
Q

What is the diagnostic criteria for mitral stenosis?

A

mitral valve has a valve area of 4-6cm2.
MS is diagnosed when the valve area is <2cm2
It is considered severe <1cm2

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43
Q

what are the symptoms and signs of severe MS?

A

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

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44
Q

what would you see on echo, CXR and cardiac catheterisation in severe mitral stenosis?

A

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.

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45
Q

when is mitral balloon valvuloplasty suitable in mitral stenos ?

A

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

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46
Q

what is the full structure of the mitral valve?

A

annulus
cusps
chordae
papillary musculature

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47
Q

what are indicators for surgery in chronic mitral regurgitation?

A

the presence of symptoms
left ventricular dilatation

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48
Q

what is functional mitral regurgitation?

A

a term used to describe MR that is caused by stretching of the annulus secondary to ventricular dilatation

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49
Q

What are the main causes of mitral regurgitation?

A

Myxomatous degeneration
functional, secondary to ventricular dilation
mitral valve prolapse
ischaemic papillaey muscle rupture
congenital heart disease
collaged disorders
Rheumatic heart disease
Endocarditis

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50
Q

what are the indicators of the severity of mitral regurgitation?

A

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

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51
Q

What are the signs of predominant MR in mixed mitral valve disease?

A

Soft S1; S3 present
Displaced and hyperdynaic apex (LV enlargement)
ECG showing LVH and left axis deviation

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52
Q

what does posture do to mitral valve prolapse murmur?

A

squatting increases the click and standing increases the murmur

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53
Q

what is the sequelae of mitral valve prolapse?

A

embolic phenomena
Rupture of mitral valve chordae
Dysrhythmias with QT prolongation
sudden death cardiac neurosis

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54
Q

what conditions are associated with mitral valve prolapse?

A

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

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55
Q

what are acute causes aortic regurgitation?

A

aortic dissection or valve rupture from endocarditis

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56
Q

what are the causes of aortic regurgitation?

A

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)

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57
Q

what are eponymous signs associated with aortic regurgitation?

A

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

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58
Q

What are the features of Aortic regurgitation indicative of the need for surgery?

A

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

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59
Q

What is normal valve area of aortic valve?

A

> 2cm2

60
Q

what is considered severe aortic stenosis?

A

valve area <1cm2 with a mean pressure gradient of >40mmHg on TTE

61
Q

what is the aortic pressure gradient dependent on?

A

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

62
Q

what are subvalvular causes of aortic gradients?

A

HCM and subaortic membranous stenosis, whereas supravalvular stenosis is due to aorta coarctation or Williams’ syndrome

63
Q

why may sudden death occur in aortic stenosis?

A

due to ventricular tachycardia (this is due to LVH)

64
Q

what is the mortality of surgical intervention for AS?

A

surgical mortality is related to LV failure
Absence of LV failure - -8%
Presence of LV failure 10-25%

65
Q

what are the indicators of severe AS?

A

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

66
Q

what is the tricuspid regurgitation murmur?

A

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

67
Q

What are the clinical signs of tricuspid regurgitation

A

elevated JVP and giant c-V waves
a pulsatile liner edge may be palpable and peripheral oedema is invariable

68
Q

causes of tricuspid regurgitation?

A
  • 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
69
Q

what are common types of mechanical heart valves?

A

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

70
Q

what are the types of tissue valves

A

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

71
Q

what is the most common cause of infection in prosthetic valves

A

staph epidermidids

72
Q

what would suggest septal access in infected valve?

A

prolonged PR interval

73
Q

what are the risks of warfarin in pregnancy?

A

fetal haemorrhage
teratogenicity risk 5-30% - the risk is dose dependant
abnormalities include chondrodysplasia, mental impairment, optic neuropathy and nasal hypoplasia

74
Q

clinical presentation of IE?

A

malaise
tiredness
infective type symptoms
heart failure secondary to valvular regurgitation or heart block may also occur

75
Q

signs of infective endocarditis?

A

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

76
Q

what is the most common cause of IE in native valve?

A

Streptococcus vitamins

77
Q

what are causes of non-infective endocarditis?

A

Marantic (metastatic related)
SLE related (Libman sacks)

78
Q

How is IE managed ?

A

usually 4-6 weeks of IV abx
may require surgical replacement

79
Q

what are the poor prognostic factors in IE?

A

prosthetic valve
staph aureus
culture negative endocarditis
deflection of complement levels

80
Q

What are the indications for surgery in infective endicarditis?

A

cardiac failure or haemodynamic compromise
extensive valve incompetence
large vegetations
septic emboli
septal access
fungal infection
antibiotic resistance
failure to respond to medical therapy

81
Q

causes of congenital cyanotic heart disease?

A

with shunts:
Aortic coarctation (with VSD or PDA)
VSD
ASD
PDA
partial anomalous venous drainage (with ASD)

without shunts:
congenital AS
aortic coarctation

82
Q

what is partial anomalous venous drainage?

A

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

83
Q

what are causes of cyanotic heart disease?

A

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

84
Q

what is the most common congenital heart defect and how does it present?

A

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

85
Q

what is found on clinical examination of a patient with ASD

A

fixed splitting of the second heart sound
there may also be a left parasternal heave and a pulmonary ESM due to increase blood flow

86
Q

what are the types of ASD?

A

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

87
Q

when is surgical closure of ASD recommended?

A

surgical close is recommended with pulmonary systolic flow rations >1.5:1
closure of secundum defects may be performed via cardiac catheterisation

88
Q

What is Holt-Oram syndrome?

A

Triphalangeal thumb with ASD
a rare syndrome (AD with incomplete penetration)

associated with absence or reduction anomalies of the upper arm

89
Q

what is Lutembacher’s syndrome?

A

a rare combination of an ASD with mitral stenosis (the latter is probably rheumatic in origin)

90
Q

Investigations for ASD?

A

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

91
Q

indications for closure in ASD?

A

symptomatic
systemic embolism (typically stroke)
chamber dilatation
elevated right heart pressures
significant left to right shunt

92
Q

What is foramen vale?

A

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

93
Q

what are the symptoms of PFO

A

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

94
Q

how is PFO diagnosed?

A

contrast echo -right to left shunt is seen during valsalva’s manoeuvre

95
Q

what is the ventricular septum made of?

A

two parts with a superior membranous component which contains the AV node and an inferior muscular component
VSD can occur in either

96
Q

Indications for closure of VSD?

A

significant left to right shunt
associated with other defect requiring craniotomy
elevated right heart pressure causing pulmonary HTN
endocarditis
membranous VSD causing AR

97
Q

what are the signs on examination of VSDS?

A

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

98
Q

What would be required if Eisenmenger’s syndrome develops in VSD?

A

heart lung transplant

99
Q

what are the cardiac associations of VSD?

A

PDA
AR
pulmonary stenosis
ASD
tetralogy of fallout
coarctation of the aorta

100
Q

what is Patent ductus arteriosus?

A

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

101
Q

what are the features of PDA?

A

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

102
Q

what causes closure of ductus arteriosus ?

A

Indometacin

103
Q

what can reverse the close of the ductus arteriosus?

A

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)

104
Q

what is the coarctation of the aorta ?

A

severe narrowing at the site of the regressed ductus arteriosus

105
Q

how does coarctation of the aorta present?

A

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

106
Q

Investigations for coarctation of the aorta?

A

echo
MRI is the definitive investigation

107
Q

How do you treat coarctation of the aorta ?

A

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

108
Q

what is associated with coarctation of the aorta?

A

Berry aneurysms and bicuspid aortic valve are strong associations

cardiac - PDA< VSD, mitral valve disease

Non cardiac - berry aneurysm, turner’s syndrome, renal abnormalities

109
Q

signs of coarctation of the aorta?

A

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

110
Q

What is Esienmenger syndrome ?

A

when congenital cardiac defect with intracardiac communication leads to severe irreversible pulmonary HTN, reversal of left to right shunts and cyanosis

111
Q

Signs of Eisenmenger syndrome?

A

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

112
Q

What are the causes of Eisenmenger syndrome?

A

VSD
ASD
PDA

113
Q

what are the complications of Eisenmenger syndrome?

A

right ventricular failure
massive haemoptysis
cerebral embolism/abscess
infective endocarditis

114
Q

What are the features of tetralogy of Fallot?

A

Pulmonary stenosis (causes the systolic murmur) /right ventricular outflow obstruction
right ventricular hypertrophy
VSD
overriding of the aorta
right sided aortic knuckle

115
Q

what are the clinical features of tetralogy of fallot?

A

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

116
Q

possible complications of Tetralogy of Fallot?

A

Endocarditis
Polycythaemia
Coagulopathy
paradoxical embolism
cerebral abscess
ventricular arrhythmias

117
Q

How does tetralogy of fallot present?

A

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

118
Q

What are cyanotic attacks in infants with tetralogy of fallot caused by?

A

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

119
Q

how is a cyanotic attack in tetralogy of fallot managed?

A

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

120
Q

when is surgicy done in tetralogy of fallot?

A

aim is total correction before 12 months
Infants may be stabilised on prostaglandins to maintain patently of the ductus arteriosus

121
Q

what are some important post-surgical circulations?

A

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

122
Q

What are neurocardiogenic symptoms?

A

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.

123
Q

What is sinus node disease ?

A

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

124
Q

What is First-Degree Heart block?

A

A PR interval > 200ms

125
Q

what is Mobitz type 1 block?

A

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

126
Q

when is pacing indicated in first degree block?

A

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

127
Q

What is Mobitz type 2 block?

A

A type of High Grade AV block
more than one p wave per QRS

128
Q

what is 3rd degree heart block

A

A type of high grade AV block
AV dissociation

129
Q

what is the treatment for high grave AV block?

A

If untreated the mortality at 1 year may exceed 50%.
Patient require pacing even if asymptomatic

130
Q

Which coronary artery occlusion with lead to high grade AV block?

A

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 .

131
Q

what are tachyarrhythmias caused by ?

A

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

132
Q

What are supra ventricular tachycardias?

A

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
133
Q

what is an accessory pathway?

A

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.

134
Q

What is WPW?

A

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.

135
Q

What are the ECG features of WPW ?

A

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

136
Q

what conditions are associated with WPW?

A

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

137
Q

What is atrial flutter?

A

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)

138
Q

How can you uncover flutter waves?

A

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.

139
Q

How may atrial flutter be managed?

A

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.

140
Q

where would you typically see the sawtooth appearance in atrial flutter?

A

inferior leads and positive flutter waves in V1

141
Q

where does atrial fibrillation arise from?

A

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.

142
Q

pathophysiology of AF?

A

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.

143
Q

what does the substrate in AF refer to?

A

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.

144
Q

what are the perpetuators of AF ?

A

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.

145
Q

How is AF managed?

A

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

146
Q

when is rate control not offered first line in AF ?

A

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

147
Q

Risk factors for recurrence of AF after cardioversion?

A

long duration
rheumatic mitral valve disease
keft atrium size > 5.5cm
older age > 75 years
Left ventricular impairment

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