Cardiovascular revision

Anatomy/Physiology

Clinical

Drugs

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

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

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

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

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

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 valve

Prosthetic 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)