Anatomy/Physiology
Clinical
Drugs
1
2
99
Describe how SV, CO, HR, MAP, SVR interact (i.e. what is the formula for MAP, CO, SV etc?)
MAP = CO x SVR. MAP = 1/3(SBP) + 2/3(DBP)
CO = HR x SV
SV = EDV - ESV
99
What does an aortic regurgitation murmur sound like?
What are some clinical features of AR?
Site = aortic area (R 2nd ICS parasternal)
Timing = early diastolic
Radiation = L lower sternal edge
Character = decrescendo
Features = wide pulse pressure
99
What is the Vaughan Williams classification?
Anti-arrhythmic drugs class I to IV
Class I Na channel blockers - Class IA, IB, IC
Class II B blockers
Class III K channel blockers
99
Differentiate type 1 vs type 2 myocardial infarction?
Type 1 - troponin elevation AND ischaemic symptoms, ECG changes, wall motion abnormalities or thrombus
Type 2 - troponin elevation AND supply/demand mismatch
99
What is the most common cause of sudden heart failure in a young, healthy patient?
Hypertrophic cardiomyopathy - autosomal dominant inheritance, concentric hypertrophy
200
Describe the branches of the Left Coronary Artery.
Arises from left aortic sinus of ascending aorta
Left anterior descending artery in the anterior interventricular sulcus towards the apex
L circumflex around heart in coronary sulcus, giving off left marginal artery
200
What is the QRS polarity in leads I, II, III in a right axis deviation?
Negative lead I
Positive in leads II and III
200
Treatment of Rheumatic Fever?
10 days oral Phenoxymethylpenicillin
Or
IM benzathine penicillin
(for GAS)
200
What is the NYHA heart failure classification?
Class I - no symptoms
Class II - mild symptoms, occasional swelling and somewhat limited in ability to exercise, NO symptoms at rest
Class III - noticeable limitations in exercise, comfortable ONLY at rest
Class IV - unable to perform any physical activity without discomfort, symptoms AT rest
200
Compare electrical cardioversion vs defibrillation?
Cardioversion = low-energy shocks timed with cardiac cycle e.g. in VT, AF
Defibrillation = high-energy shocks not timed with any part of cycle (e.g. in ventricular fibrillation)
300
Describe the action potential of a pacemaker cell
1 - spontaneous opening of voltage-gated Na channels, Na influx
2 - T-type Ca channels open, Ca influx raises MP to threshold
3 - L-type Ca channels open, Ca influx, depolarisation
4 - K efflux and repolarisation
300
What is Paroxysmal Nocturnal Dyspnoea? What does it suggest?
Sudden SOB, coughing at night
Suggests LHF
300
Which drugs are used in heart failure not because they reduce mortality but because they help with symptoms? (i.e only used ALONGSIDE other drugs)
Thiazide diuretics
Loop diuretics
Improve symptoms (pulmonary and systemic congestion)
300
What is HFrEF? Describe the causes and the resulting consequences of HFrEF?
Heart failure with reduced ejection fraction <50% (i.e. systolic dysfunction)
Damaged or loss of contractile myocytes (in MI, ischaemic)
Infiltration - amyloid, haemochromatosis, sarcoidosis
> decreased contractility and CO = reduced perfusion
300
What are the shockable and non-shockable rhythms?
Shockable = ventricular fibrillation, pusleless ventricular tachycardia
Non-shockable = pulseless electrical activity, asystole
400
Describe the action potential of a myocardial cell
0 - action potential from adjacent cardiomyocyte raises the membrane potential above -90mV, voltage-gated Na channels open and Na ions influx = depolarisation
1 - slight repolarisation as Na channels close and K channels start to open
2 - prolonged repolarisation, K efflux offsets Ca influx (through slow L-type Ca channels), long refractory period
3 - K efflux in hyperpolarisation
4 - resting membrane potential
400
What are your differential diagnoses for a systolic murmur?
Pansystolic = mitral regurgitation (blowing, apex, radiating to axilla)
Pansystolic = tricuspid regurgitation (rare)
Ejection-systolic = aortic stenosis (crescendo-decrescendo, radiating bilaterally to carotids)
400
What drugs are used for angina? How do they work?
Angina = mismatch between O2 demand/supply
Organic nitrates = reduce preload and afterload, increase coronary artery blood flow
Dihydropyridine Ca blockers (blood vessels) = reduce afterload and dilate coronary blood vessels, do not affect venous supply or preload
B blocker = reduces myocardial demand
400
Describe the ECG changes in an acute MI
Normal
> hyperacute T wave (B)
> marked ST elevation with hyperacute T wave (C)
> pathologic Q waves, less ST elevation, terminal T wave inversion (D)
> pathologic Q wave, T wave inversion (E)
> pathologic Q wave, upright T wave (F)
400
Infective Endocarditis
List some organisms you'd expect to find in a patient with a prosthetic heart valve vs normal valveProsthetic valves - coagulase negative Staphylococci (e.g. S. epidermidis)
Low virulent Streptococcus viridans, Enterococcus, HACEK in abnormal valves
Vs highly virulent S. aureus in normal valves
500
Outline the branches of the Right Coronary Artery.
Arises from the right cusp of the aorta
SA node branch
Right marginal artery (inferior of heart)
Posterior descending artery
AV node branch
500
Describe where you would place the leads on a 12-lead ECG?
L arm, R arm, L foot, R foot
V1 in 4th ICS right parasternal edge
V2 in 4th ICS left parasternal edge
V3 in between V2 and V4
V4 in 5th ICS L MCL
V5 5th ICS L anterior axillary line
V6 5th ICS L mid axillary line
500
Outline the RAAS system.
Discuss why RAAS blockers are useful in heart failure.
Bonus: what is neprilysin?
Renin from kidney converts angiotensinogen from liver into angiotensin I. ACE from lungs convert ang I to ang II which binds to ang II receptor type 1 = vasoconstriction, aldosterone, ADH, thirst...
ACEi - perindopril, inhibit ACE from converting angiotensin I into angiotensin II. No angiotensin II = no aldosterone, vasoconstriction or ADH. Reduced afterload (vasconstriction) and preload (aldosterone).
ARB - blocks angiotensin II from binding to receptor.
ARNI - ARB and neprilysin inhibitor (blocks neprilysin from degrading natriuretic peptides which promote natriuresis and diuresis to reduce preload as well as inhibit RAAS).
500
Draw a table to compare Rheumatic Fever and Infective Endocarditis in terms of the pathophysiology/aetiology and clinical features.
RF - Strep pyogenes infection (GAS), molecular mimicry between streptococcal M protein and cardiac myosin = type 2 HSR (antibody-mediated) = tissue damage to valves
IE - bacteraemia, damaged valves, colonisation of valves, destruction of valve
JONES PEACE in RF
FROM JANE in IE
500
What is 'restrictive cardiomyopathy'? Compare it to dilated cardiomyopathy? Describe the changes on echo?
Restrictive = diastolic dysfunction
Proliferation of connective tissue = reduced elasticity of cardiac tissue
Reduced diastolic filling but normal ejection fraction (EF = SV/EDV x 100), impaired contractility and SV but also impaired EDV
Dilated = systolic dysfunction
Eccentric hypertrophy with dilated ventricles= reduced contractility
= systolic dysfunction (reduced EF)