Summary MRCP Study Notes & Pearls for MCQ & SBA

CVS
- Clubbing and cyanosis that is worse in the lower limbs than upper limbs can only be
explained by a patient with Eisemenger’s syndrome secondary to PDA.
- Dual chamber pacemaker – RV, RA (NOT left – for advanced heart failure)
- Interventions to prolong survival after MI
o Non-pharmacological
 Stop smoking – most important
 Weight loss in an obese individual – reduces comorbidity but does not
prolong survival
o Pharmacological – NNT
 ACE-I – 22 (SOLVD)
 Statins – 33 (CARE)
 Aspirin – 42 (ISIS 2)
 B-blockers – 143 (ISIS 1 )
- Ddx severe heart failure (esp right heart failure) in the absence of significant cardiomegaly –
pericardial constriction, restrictive cardiomyopathy
- Arrhythmogenic RV cardiomyopathy
o Fibrofatty replacement of RV  RV dysfunction, arrhythmias of RV origin (LBBB
morphology)
o Due to mutations in genes encoding cell adhesion proteins (desmoplakin,
plakoglobin)
o AD inheritance
o Palpitations, presyncope, syncope, sudden death from VF during physical exercise
o Systolic murmur which resolves on standing; S3
o ECG – T inversion in RV leads, epsilon waves (depolarization abnormalities after QRS
complex)
o Echo – maybe normal/ aneurysms in RV wall
o MRI – reveals fatty infiltration of RV
o Rx – abstinence from strenuous exertion; ICD; amiodarone
- Causes of VT with LBBB morphology
o ARVC
o RV outflow tract VT
o Dilated cardiomyopathy
o Congenital cyanotic heart disease
- Heart failure in Afro-Caribbean patients – addition of isosorbide dinitrate or mononitrate
and hydralazine to the usual combination (ACE-I, beta-blocker, spironolactone) improves
prognosis
- Hypertension in black patients
o Usually occurs at a younger age, is more severe, associated with a higher rate of
stroke, heart failure, renal failure than in white patients
o Salt-sensitive, associated with an expanded vascular volume
o Rx
 Low salt intake
 Thiazide diuretics, CCB – 1st line; combining both are not effective as both
work by increasing urinary Na excretion
 ACE-I, ARB, B-blocker – 2nd line; plasma renin levels are generally low;
effective when added to thiazide diuretic/ CCB as RAAS would have been
offset by diuretic/ CCB
- ACE-I – reduces adverse events in patients with LV dysfunction with no overt heart failure
- Commotio cordis – VF occurring after being struck in precordium by a highly projectile object
- Troponin I measurements in CKD patients are more accurate than troponin T

,- Polymorphic VT
o Torsades de pointes – changing R-R intervals and axis of QRS complexes; prolonged
QT; rx – IV magnesium, correction of electrolyte abnormalities, NOT amiodarone/
flecainide/ sotalol
o Non-torsades – no prolonged QT; occur secondary to scar tissue after MI; rx –
electrical/ chemical cardioversion, overdrive, correction of electrolyte abnormalities
- Ventricular fibrillation
o Window of success for defibrillation – 2 minutes
o Causes
 Cardiomyopathies
 Ventricular aneurysms
 Electrolytes esp hypokalemia
 Certain drug overdose – cocaine, TCA
 Post-MI – ventricular ectopics occuring on preceding T wave (R on T) can
cause monomorphic VT which can degenerate into VF
- Causes of malignant hypertension
o Renal artery stenosis
o HUS
o Scleroderma renal crisis
o Hypertensive nephrosclerosis
o APL syndrome
- Vs Streptokinase, recombinant TPA not usually associated with allergic/ anaphylaxis;
marginally superior in achieving vessel patency
- Dextrocardia
o Can be associated with situs inversus
o M=F
o ECG – inverted P waves in lead I; shift of P axis (usually about +120 degrees;
normally 0 to 75 degrees), reversed R wave progression – corrected by reversed
placement of chest leads
o Normal life expectancy if no cardiac anomalies
o Kartagener syndrome – bronchiectasis, chronic sinusitis, subfertility, situs inversus
with dextrocardia
- Indications for temporary pacing wire insertion
o Widening QRS – indicates more extensive ischemic territory affecting conducting
bundles; pacing allows time for myocardium to recover
- Bradycardia in context of inferior MI no prognostic significance (RCA which is involved, also
gives branch to SA and AV nodes); in anterior MI indicates extensive infarction
- Ticagrelor was evaluated in PLATO trial – reduced rates of CVS mortality, MI, stroke, all-
cause mortality compared to clopidogrel, without associated increase in major bleeding side
effects
- Indications of anticoagulation
o Heart failure with low EF
o Previous VTE
o Intracardiac thrombus
o LV aneurysm
However, warfarin should be discontinued if benefit risk profile not favourable
- Posterior MI
o ECG changes in V1-V3
 Horizontal ST depression
 Tall, broad R waves (>30ms)
 Upright T waves

,  Dominant R waves in V2
Beware of diagnosing NSTEMI in anterior septal region – prominent R waves and
upright T waves should point towards posterior MI
o Occlusion in RCA
- RV impairment suggestive of respiratory pathology rather than cardiac cause of SOB, eg
pulmonary hypertension from chronic hypoxia/ chronic thromboembolic disease
- RALES trial shows aldosterone antagonists reduce mortality in CCF when given with ACE-I;
but beware of hyperkalemia esp in those with renal impairment
- MAT
o Occurs in patients with obstructive airways disease who may be hypoxic and
hypercapnic
o At least 3 different P wave morphologies with varying PP and PR intervals
o Rx
 IV verapamil 5mg, oral 40-120mg TDS
- High lateral wall MI
o ST elevation in I, aVL (occlusion of first diagonal branch of LAD vs lateral MI due to
occlusion of LCA)
o Due to occlusion of first diagonal branch of LAD/ branch of LCA/ short LAD
- In patients with T2DM, coronary stents (uncoated) are liable to re-stenosis at a rate of 40-
50% by 6 months; drug-eluting stents reduce the RR of restenosis by 80% when antiplatelet
therapy with aspirin and clopidogrel is continued for at least 1 year
- With exercise, SBP progressively increases until maximum exercise; DBP remains the same/
decrease slightly with progressive exercise; in heart disease – a fall in BP, failure to rise or
excessive rise (>250mmHg SBP) is an indication to terminate the exercise test
- When starting amiodarone
o Check TFT, LFT
o Check INR, reduce warfarin dosage if needed (amiodarone potentiates warfarin)
o Monitor HR/ ECG for bradycardia – B-blocker, digoxin, amiodarone
- Diastolic heart-failure
o Normal or near-normal EF
o Mortality rate lower than patients with systolic heart failure
o Rx
 Diuretics – reduce pulmonary venous pressure and congestion
 ARBs – have additional effects independent of ACE inhibition eg anti-
platelet, hypo-uricemic, anti-diabetic, atrial anti-fibrillatory effects
 Candesartan – moderate impact in preventing admissions for CHF
among patients who have heart failure and LVEF >40%
 Digoxin – no effect on natural history end points eg mortality,
hospitalizations
- Target BP
o DM patients, renal patients, those with established cardiovascular disease - <130/80
o Non-diabetic patients with cardiovascular disease - <140/90
- Indications of ICD
o Primary prevention of sudden cardiac death in patients with history of prior MI and
all of the following
 Non-sustained VT
 Refer for EPS – if inducible arrhythmias – ICD insertion
 Inducible arrhythmias on testing
 LVEF <35%, no worse than NYHA class III (if EF >35% - no difference in
outcome from drug treatment)
o Cardiac arrest due to VT/ VF (NOT due to a reversible cause)

, o Spontaneous sustained VT, without syncope
o Unexplained syncope with VT inducible at EPS
o Recorded spontaneous VT with a history of syncope
o High risk of sudden cardiac death
 Long QT syndrome
 Brugada syndrome
 Arrhythmogenic RV dysplasia
 Following repair of ToF
If contraindicated/ inappropriate – antiarrhythmic therapy eg oral amiodarone 200mg TDS
then OD
- In a patient with paroxysmal AF and documented pauses and complete heart block – sick
sinus syndrome due to idiopathic fibrosis of sinus node – rx with dual chamber pacing and
continue B-blocker therapy to prevent tachyarrhythmias; stopping anti-arrhythmics eg
sotalol may improve bradycardic episodes but risk further episodes of AF (dual chamber
preferred for SR; single chamber pacemakers for patients in permanent AF)
- Non-vitamin K oral anticoagulants – contraindicated in mechanical valve/ moderate to
severe MS
- Mobitz type I (Wenckebach phenomenon) – low risk of progression to complete heart block,
can be discharged
- Heart block post
o Inferior MI – indicative of temporary ischemia, may resolve after supportive
management and revascularisation
o Anterior MI – indicative of extensive infarction; rx – temporary pacing wire
- Atropine max 3mg; isoprenaline contraindicated in recent MI
- Malignant hypertension – rx with gradual reduction of BP over 24-48h with oral anti-
hypertensives (aim diastolic 100-110mmHg) (risk of cerebral/ renal/ retinal/ myocardial
infarction if BP reduced too rapidly with parenteral therapy – reserved for hypertensive
encephalopathy or aortic dissection)
- Self-terminating episodes of VT – rx with K and Mg correction with IV fluid replacement;
pharmacological therapies later
- Grade 1 hypertension, with suspicion of white coat hypertension, can be considered for 24h
ambulatory or home BP monitoring
- BER
o ST elevation during early exercise returns to normal as HR increases further
o Common in black males
o Clinical evaluation entirely normal
o ST elevation usually seen in precordial leads
o J point notching
- Normal LA diameter 4cm
- Non-iatrogenic hyponatremia in the context of CCF carries a poor prognosis as it is
secondary to significant fluid overload
- ECG in pericardial effusion – low voltage, sinus tachycardia, electrical alternans
- First DC shocks in witnessed VT/ VF are highly successful at restoring rhythm, but a palpable
pulse may not be felt for some time – hence during this time do CPR without feeling for
pulse
- Stable angina
o Medical management – the first step
 Aspirin, ACE-I, statins, CCBs, B-blockers; long-acting nitrates
o Revascularisation with PCI or CABG – if continued chest pain