বিসমিল্লাহির রহমানির রহিম

MRCP PART 1 & 2

NOTES FROM PASSMEDICINE, PASTEST, Notes & notes
By ABDULLAH TANVIR

ANATOMY & PHYSIOLOGY

Pulsus paradoxus ● > 10 mmHg fall in SBP during inspiration → faint or absent
pulse in inspiration
● Cardiac tamponade
● Severe asthma, COPD
● Constrictive pericarditis (less common)

Slow-rising/plateau ● Aortic stenosis

Collapsing ● Aortic regurgitation

● Patent ductus arteriosus
● Hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Pulsus alternans ● Regular alternation of the force of the arterial pulse

● Severe LVF

Bisferiens pulse ● Double pulse - two systolic peaks

● Mixed aortic valve disease, HOCM

Jerky' pulse ● HOCM

Dicrotic notch >>> Aortic valve closure

HEART SOUNDS

1st heart sound (S1) ● Caused by closure of mitral and tricuspid valve
Causes of a loud S1
● Mitral stenosis
● left-to-right shunts
● Short PR interval (WPW syndrome), atrial premature beats
● Hyperdynamic states
Causes of a quiet S1
● Mitral regurgitation, Heart failure
Variable intensity of S1 : 3° / Complete heart block

2nd heart sound (S2) ● Due to closure of aortic & pulmonary valve
○ Split on inspiration, Single on expiration
○ Causes of a loud S2
■ Hypertension: systemic (loud A2) or pulmonary (loud P2)
■ Hyperdynamic states

NOTES BY ABDULLAH TANVIR

 ○ Soft S2 : Aortic stenosis
○ Quiet or absent of 2nd heart sound : Indicates severe aortic stenosis
○ Wide & Fixed split of S2 : Atrial septal defect
● Wide & Variable split S2 :
○ Deep inspiration, RBBB, pulmonary stenosis, severe MR
● Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)
○ LBBB
○ severe aortic stenosis
○ Right ventricular pacing
○ WPW type B (causes early P2)
○ Patent ductus arteriosus

3rd heart sound (S3) ● Due to abrupt cessation of rapid ventricular filling
○ LVF, MR, DCM
○ 𝗟𝗼𝘂𝗱 𝗲𝗮𝗿𝗹𝘆 𝟯𝗿𝗱 𝗵𝗲𝗮𝗿𝘁 𝘀𝗼𝘂𝗻𝗱 / 𝗣𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗸𝗻𝗼𝗰𝗸 :
𝗖𝗼𝗻𝘀𝘁𝗿𝗶𝗰𝘁𝗶𝘃𝗲 𝗽𝗲𝗿𝗶𝗰𝗮𝗿𝗱𝗶𝘁𝗶𝘀
○ Soft : Cardiac tamponade

4th heart sound (S4) ● Due to atrial contraction against stiff ventricle
Causes
● AS, HOCM, HTN
● Coincides with p wave (After P wave) in ECG
● During late diastole, active left ventricular filling
● Absent in atrial fibrillation

𝗠𝗨𝗥𝗠𝗨𝗥

● Ejection systolic murmur

○ Aortic stenosis, Pulmonary stenosis
○ Hypertrophic obstructive cardiomyopathy (HOCM)
○ Atrial septal defect (ASD), Fallout's
● Pansystolic murmur
○ Mitral regurgitation, Tricuspid regurgitation (high-pitched and 'blowing' in character)
○ Ventricular septal defect ('harsh' in character)
● Late systolic murmur
○ Mitral valve prolapse
○ Coarctation of aorta
● Early diastolic murmur
○ Aortic regurgitation, Pulmonary regurgitation (Graham steel murmur)
● Mid diastolic murmur
○ Mitral stenosis, Tricuspid stenosis
○ Austin flint murmur (Severe AR)
○ Carey coombs murmur (In rheumatic fever)
● 𝗖𝗼𝗻𝘁𝗶𝗻𝘂𝗼𝘂𝘀 𝗺𝗮𝗰𝗵𝗶𝗻𝗮𝗿𝘆 𝗺𝘂𝗿𝗺𝘂𝗿
○ Persistent ductus arteriosus

NOTES BY ABDULLAH TANVIR

*** Right sided murmur increases with inspiration
*** Left sided murmur increases with expiration

Valsalva manoeuvre ● ↓ Preload >>> ↓ / Makes softermurmur

/ Abrupt standing ○ Tricuspid regurgitation, Pulmonary stenosis
○ MR, AS
● ↑ / Makes louder murmur
○ HOCM, Mitral valve prolapse
○ MS, AR

Squatting / Leg raise ● ↑ Most murmurs

● ↓ HOCM & mitral valve prolapse

Sustained Hand grip ● ↓ Aortic stenosis

● ↑ Mitral regurgitation, Mitral valve prolapse, Aortic
regurgitation, VSD,

Pregnancy ● ↓ Aortic regurgitation murmur

● ↑ All stenotic murmur

JVP

● Raised JVP, normal waveform

○ Bradycardia
○ Fluid overload
○ Heart Failure
● Raised JVP, absent pulsation
○ Superior vena cava syndrome
● Kussmaul's sign : Paradoxical rise in JVP during inspiration seen in constrictive pericarditis
● a' wave = atrial contraction
○ large a wave : TS, PS, pulmonary hypertension
○ Absent in AF
● Cannon 'a' waves
○ Caused by atrial contractions against a closed tricuspid valve
○ Irregular : Complete heart block
○ Regular : Ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular
pacing
● c wave : closure of tricuspid valve
○ Not normally visible
● v wave
○ Due to passive filling of blood into the atrium against a closed tricuspid valve
○ Giant v waves in tricuspid regurgitation
● x descent = fall in atrial pressure during ventricular systole

NOTES BY ABDULLAH TANVIR

 ○ Absent 'x' descent : Tricuspid regurgitation
● y descent = opening of tricuspid valve

Stages of the Valsalva manoeuvre

● Increased intrathoracic pressure
● Resultant increase in venous and right atrial pressure reduces venous return
● The reduced preload leads to a fall in cardiac output (Frank-Starling mechanism)
● When the pressure is released there is a further slight fall in cardiac output due to increased
aortic volume
● Return of normal cardiac output

CARDIAC MARKERS

● Myoglobin : Frst to rise

● CK-MB : useful to look for reinfarction as it returns to normal after 2-3 days (troponin T
remains elevated for up to 10 days)
● Glycogen phosphorylase isoenzyme BB (GPBB)
○ Rise significantly by 3 hours post MI
○ An appropriate marker for early cardiac muscle injury

Binding of Troponin : TIC - TAC

● Troponin T : Tropomyosin
● Troponin I : Actin / component of thin filament
● Troponin C : Calcium

BNP
● Produced mainly by left ventricular myocardium in response to strain
● Effects
○ vasodilator
○ diuretic and natriuretic
○ suppresses both sympathetic tone and renin-angiotensin-aldosterone system
● Low BNP
○ Obesity
○ Drugs : ACEi, ARB, Beta blockers, Diuretics

Exercise: physiological changes

● Blood pressure : SBP increases, DBP decreases,Increased pulse pressure, MABP is only
slightly increased in healthy young
● Increase in cardiac output may be 3-5 fold : Increased venous return, vasodilation and
increased myocardial contractility
● Systemic vascular resistance falls in exercise due to vasodilatation in active skeletal
muscles.
● Heart rate up to 3-fold increase
● Stroke volume up to 1.5-fold increase

NOTES BY ABDULLAH TANVIR

 ECG
Anteroseptal V1-V4 Left anterior descending

Anterolateral V1-6, I, aVL Proximal left anterior

descending

Lateral I, aVL +/- V5-6 Left circumflex

High lateral I & aVL

Inferior II, III, aVF Right coronary

Posterior Changes in V1-3 Usually left circumflex, also

right coronary
Reciprocal changes of STEMI are typically seen
● Horizontal ST depression, Upright T waves
● Tall, broad R waves
● Dominant R wave in V2

Posterior infarction is confirmed by ST elevation &

Q waves in posterior leads (V7-9)

Postero-lateral ● Prominent R in V1 & ST depression in V1-V3

● ST elevation in V5 & V6.

● ST elevation in vR & diffuse ST depression Multivessel ischemia or left

in other leads main coronary artery
obstruction

● Proximal RCA occlusion : V1-3, II, III, Vf

● Distal RCA occlusion : II, III, Vf

● Which ECG changes may be seen earlier in ischaemia : Hyper-acute T-waves, which may
precede ST-segment elevation.

Brugada syndrome ● Convex ST elevation > 2 mm in > 1 of V1-V3 followed by a negative T

● Partial RBBB

Arrhythmogenic ● T inversion in V1-3

Right ventricular ● Epsilon wave (Notch / small positive deflection at the end of QRS)
dysplasia

Wellwn’s ● Biphasic or deep T wave inversion in V2-3

syndrome ● Minimal ST elevation
● No Q waves

NOTES BY ABDULLAH TANVIR

WPW syndrome ● Short PR interval (< 120 ms) with wide QRS complex (> 120 ms)
● Slurred upstroke of QRS complex (delta wave)

Lown – Ganong– ● Short PR interval (<120ms) with normal QRS complex

Levine syndrome ● Absence of a delta wave

Digoxin ● Prolonged PR & short QT

● Down-sloping ST depression ('reverse tick', 'scooped out')
● Flattened / inverted T waves
● Arrhythmias e.g. AV block, bradycardia
● DIGOXIN DOESN'T CAUSE TYPE II 2nd degree HEART BLOCK

Hypokalemia ● Prolonged PR & QT

● ST depression
● Small, Absent or inverted T
● U wave

Hyperkalemia ● Peaked or 'tall-tented' T waves (occurs first)

● QRS prolongation : Consistent with imminent cardiac arrest
● Loss of P waves
● sinusoidal wave pattern

Hypocalcemia ● Short QT interval

Hypercalcemia ● Short QT interval

Dextrocardia ● Right axis deviation

● Inverted P wave in lead I
● Loss of R wave progression

Lead misplacement ● Right axis deviation

● Inverted P wave in lead I
● No loss of R wave progression

Pulmonary ● Sinus tachycardia, RBBB with right axis deviation

embolism ● Classic change : S wave in lead I, a large Q wave in lead III & an
inverted T wave in lead III - 'S1Q3T3'

Subarachnoid ● Long QT interval

haemorrhage ● ST elevation, T inversion

Athlete ● Sinus bradycardia, junctional rhythm

● 1st degree heart block, Wenckebach phenomenon

Hypothermia ● Bradycardia, first degree heart block

● 'J' wave (Osborne waves) - small hump at the end of QRS complex
● Long QT interval
● Atrial and ventricular arrhythmias

NOTES BY ABDULLAH TANVIR

P Wave ● Increased P wave amplitude
○ Cor pulmonale
● Broad, notched (bifid) P waves
○ Often most pronounced in lead II
○ A sign of left atrial enlargement, classically due to mitral stenosis
● In atrial fibrillation, there is an absence of P waves.

T wave ● Peaked T wave

○ hyperkalaemia
○ myocardial ischaemia
● Inverted T waves
○ Myocardial ischaemia
○ Digoxin toxicity, Hypokalemia
○ Brugada syndrome
○ Arrhythmogenic right ventricular cardiomyopathy
○ Pulmonary embolism ('S1Q3T3')
○ Subarachnoid haemorrhage
● Biphasic T waves
○ Ischemia : Wellens’ syndrome (type II)
○ Hypokalaemia

Q wave ● Most specific for a diagnosis of myocardial infarction

● Considered pathological if they are:
○ > 1mm wide
○ > 2mm deep
○ > 25% of the depth of QRS complex, or
○ Seen in leads V1-V3
● Such pathological Q-waves usually indicate prior full thickness myocardial
infarct.

U wave Causes of prominent U waves

● Hypokalaemia
● Cardiovascular drugs, e.g. digitalis, quinidine, amiodarone
● Psychotropic drugs, e.g. phenothiazines, tricyclic antidepressants

PR ● Prolonged PR (> 200ms)

● IHD, Aortic root pathology
● Digoxin toxicity , Hypokalemia
● Myotonic dystrophy
● Lyme disease, Rheumatic fever ,Sarcoidosis
● Short PR (< 120 Ms)
○ WPW syndrome, Lown–Ganong–Levine syndrome
○ Junctional rhythms.

NOTES BY ABDULLAH TANVIR

 ○ A variable PR interval may indicate other types of heart block.
○ PR segment depression may indicate atrial injury or pericarditis
● PR segment depression : Acute pericarditis

ST ● Causes of ST depression
○ Ischemia
○ LVH, LBBB, RBBB
○ Digoxin, hypokalaemia
○ Syndrome X
● Causes of ST elevation
○ Myocardial infarction
○ Pericarditis / myocarditis
○ Left ventricular aneurysm
○ Prinzmetal's angina (coronary artery spasm)
○ Takotsubo cardiomyopathy
○ Normal variant - 'high take-off'
○ Rare: subarachnoid haemorrhage

QT ● Represents ventricular diastole

● Which ECG interval will show the greatest reduction during ECG stress test : QT
interval

NTK
● Intra aortic balloon inflation : During middle of T Wave
● Synchronised DC shock : During an R wave

LBBB ● New LBBB is always pathological.

● Causes include:
○ Myocardial infarction
■ Diagnosing a myocardial infarction for patients with existing
LBBB is difficult
■ Sgarbossa criteria can help with this
○ Hypertension
○ Aortic stenosis
○ Cardiomyopathy
○ Rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

RBBB ● Right bundle branch block is a common feature seen on ECGs

● Causes of RBBB
○ normal variant - more common with increasing age
○ right ventricular hypertrophy
○ chronically increased right ventricular pressure - e.g. cor pulmonale
○ pulmonary embolism

NOTES BY ABDULLAH TANVIR

 ○ myocardial infarction
○ atrial septal defect (ostium secundum)
○ cardiomyopathy or myocarditis

Bi/tri-fascicular Bifascicular block (RBBB + Axis deviation)

block
● RBBB + left anterior fascicular block (LAFB) / (LAD) or
● RBBB + left posterior fascicular block (LPFB)/ (RAD)

Trifascicular block
● Features of bifascicular block as above + 1st-degree heart block
(Prolonged PR interval) / 3rd degree heart block
● Site of lesion : AV node and Purkinje fibres
● If Symptomatic : Dual chamber pacemaker

Left ventricular hypertrophy

● Sum of S wave in V1 and R wave in V5 or V6 exceeds 40 mm

Left atrial enlargement

● Bifid P wave in lead II with a duration > 120 ms
● In V1 the P wave has a negative terminal portion

Right atrial enlargement

● P waves in both II and V1 which exceed 0.25 mV

Left axis deviation (LAD) ● Left ventricular hypertrophy

● Left bundle branch block
● Left anterior hemiblock
● WPW syndrome* - right-sided accessory pathway
● Congenital: Ostium primum ASD, tricuspid atresia
● Inferior myocardial infarction
● Hyperkalaemia
● Minor LAD in obese people

Right axis deviation (RAD) ● Right ventricular hypertrophy

● Right bundle branch block
● Left posterior hemiblock
● WPW syndrome - left-sided accessory pathway
● Ostium secundum ASD
● Lateral myocardial infarction
● Dextrocardia
● Chronic lung disease → cor pulmonale
● Minor RAD in tall, thin people, athletes

NOTES BY ABDULLAH TANVIR

 ECHOCARDIOGRAM

● Transthoracic : Best for structure, function & evaluation of thrombus in ventricles

● Modern transthoracic : To determine LVEF

EXERCISE TOLERANCE TEST

Contraindications
● Myocardial infarction less than 7 days ago, unstable angina
● Aortic stenosis
● Uncontrolled HTN (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg)
● LBBB : this would make ECG very difficult to interpret

Stop if
● Exhaustion / patient request
● 'severe', 'limiting' chest pain
● Arrhythmia develops
● > 2 mm ST elevation.Stop if rapid ST elevation and pain
● > 3mm ST depression
● Heart rate falling > 20% of starting rate
● Systolic blood pressure falling > 20 mmHg
● Systolic blood pressure > 230 mmHg
● Attainment of maximum predicted heart rate (220 - patient's age)

Not useful if
● Previous conduction block
● Resting ECG abnormalities such as ST depression > 1 mm
● WPW syndrome
● Those taking digitalis
● Those with ventricular paced rhythm

Cardiac catheterisation and oxygen saturation levels

Basics
● Deoxygenated blood returns to right side of heart via superior vena cava (SVC) & inferior
vena cava (IVC)It has an oxygen saturation level of around 70%
● The right atrium (RA), right ventricle (RV) & pulmonary artery (PA) normally have oxygen
saturation levels of around 70%
● Lungs oxygenate the blood to a level of around 98-100%

NOTES BY ABDULLAH TANVIR

 ● The left atrium (LA), left ventricle (LV) and aorta should all, therefore, have oxygen
saturation levels of 98-100%
● Oxygenation in superior vena cava should always be lower than inferior vena cava, due to
the high oxygen demands from brain

The table below shows the oxygen saturations that would be expected in different scenarios:

Diagnosis & notes RA RV PA LA LV Aorta

Normal 70% 70% 70% 100% 100% 100%

Atrial septal defect (ASD) 85% 85% 85% 100% 100% 100%
Oxygenated blood in LA mixes with deoxygenated blood
in RA, resulting in intermediate levels of oxygenation from
RA onwards

Ventricular septal defect (VSD) 70% 85% 85% 100% 100% 100%
Oxygenated blood in LV mixes with deoxygenated blood
in RV, resulting in intermediate levels of oxygenation from
RV onwards.RA blood remains deoxygenated

Patent ductus arteriosus (PDA) 70% 70% 85% 100% 100% 100%
PDA connects higher pressure aorta with lower pressure
PA. This results in only PA having intermediate
oxygenation levels

VSD with Eisenmenger's 70% 70% 70% 100% 85% 85%

PDA with Eisenmenger's 70% 70% 70% 100% 100% 85%

ASD with Eisenmenger's 70% 70% 70% 85% 85% 85%

Pulmonary arterial hypertension

● Pulmonary artery systolic pressure (PASP) > 1/5 Aortic systolic pressure (ASP)*
○ *If suspecting AS, take LVSP instead of ASP
● Pulmonary artery systolic pressure (PASP) > Right ventricular systolic pressure (RVSP)
● Mean PAP > 25 at rest

Pulmonary venous hypertension (PVH) (Seen in MS/ MR)

● Pulmonary capillary wedge pressure (PCWP) / Mean LA pressure - LV end diastolic
pressure (LVEDP) > 5mmHg

Aortic stenosis
● Aortic systolic pressure (ASP) < LV systolic pressure (LVSP)

NOTES BY ABDULLAH TANVIR

 DVLA: cardiovascular disorders

Specific rules
● Hypertension
○ Can drive unless treatment causes unacceptable side effects, no need to notify
DVLA
○ if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180
mmHg systolic or more and/or 100 mm Hg diastolic or more
● Angina - driving must cease if symptoms occur at rest/at the wheel
● Implantable cardioverter-defibrillator (ICD)
○ if implanted for sustained ventricular arrhythmia : Cease driving for 6 months
○ if implanted prophylactically then cease driving for 1 month. Having an ICD results in
a permanent bar for Group 2 drivers
● CABG / ACS - 4 weeks off driving
● Pacemaker insertion / Angioplasty (elective) / ACS successfully treated by angioplasty - 1
week off driving
● Successful catheter ablation for an arrhythmia - 2 days off driving
● Aortic aneurysm of 6 cm or more - Notify DVLA. Licensing will be permitted subject to
annual review.
○ An aortic diameter of 6.5 cm or more disqualifies patients from driving
● Heart transplant : Do not drive for 6 weeks, no need to notify DVLA

..

NOTES BY ABDULLAH TANVIR