41 HEART

# Heart

👩‍⚕️ Examiners hammer the same themes: which chambers form which surface, the coronary arteries and their territories, conduction anatomy, valve auscultation areas, the four classic murmurs, and the haemodynamic patterns of tamponade and pump failure. If you remember one thing: aortic stenosis is the most dangerous valvular lesion intraoperatively because stroke volume is fixed and cardiac output cannot compensate for the SVR drop on induction. Second: Beck's triad (hypotension, raised JVP, muffled heart sounds) plus pulsus paradoxus = tamponade until proven otherwise.

Detailed notes

Position and surface anatomy

The heart sits in the middle mediastinum, two-thirds to the left of midline. Long axis: right 2nd costal cartilage (base) → left 5th ICS, MCL (apex). Right border = RA; inferior border = mostly RV; left border = LV and left auricle.

The four surfaces

Surface	Chambers	Relations
Anterior (sternocostal)	RA + RV, small LV strip	Sternum, costal cartilages
Inferior (diaphragmatic)	LV + part RV	Central tendon of diaphragm
Left pulmonary	LV + left auricle	Left lung (cardiac notch)
Posterior (base)	LA + small RA	Oesophagus, descending aorta, T5–T8

Trauma to the anterior chest preferentially injures the RV. An enlarging LA (e.g. MS) compresses the oesophagus → dysphagia.

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Chambers — surgical highlights

- RA — receives SVC, IVC, coronary sinus. Crista terminalis, pectinate muscles, fossa ovalis on the IAS.

- RV — trabeculae carneae, chordae tendineae to papillary muscles, moderator band carrying the right bundle branch. Smooth infundibulum → pulmonary trunk.

- LA — four pulmonary veins; AF thrombi form in the auricle.

- LV — wall ~3× RV, two papillary muscles, outflow via aortic vestibule.

Valves and auscultation (APTM)

Four valves — two AV (tricuspid, mitral) and two semilunar (pulmonary, aortic). All built from dense fibrous connective tissue — no cartilage or muscle in the leaflets.

Valve	Auscultation area
Aortic	R 2nd ICS, parasternal
Pulmonary	L 2nd ICS, parasternal
Tricuspid	L 4th–5th ICS, parasternal
Mitral	L 5th ICS, MCL (apex)

Mnemonic APTM ("All Patients Take Medications"). Anatomical position differs from auscultation site because turbulent flow projects downstream.

Coronary arteries

Both coronaries arise from the sinuses of Valsalva above the aortic cusps. Coronary flow happens in diastole — in systole the cusps cover the ostia.

Left main → LAD + LCx.

- LAD — anterior IV groove → anterior LV, anterior 2/3 septum, apex.

- LCx — left AV groove → lateral LV. Runs millimetres from the mitral annulus, at risk in MV surgery.

RCA — right AV groove → RA, RV, inferior LV, posterior 1/3 septum (via PDA in right dominance).

Conduction supply (memorise):

- SA node — RCA in ~60%, LCx in ~40%.

- AV node — RCA in ~90%.

- Bundle of His — LAD septal branches.

Inferior MI (RCA) → bradyarrhythmias and AV block — both nodes are ischaemic.

Dominance = who gives off the PDA. RCA in ~80–90%.

Groove	Contents
Right AV	RCA + small cardiac vein
Left AV	LCx + great cardiac vein
Anterior IV	LAD + great cardiac vein
Posterior IV	PDA + middle cardiac vein

Coronary veins drain via the coronary sinus (posterior AV groove) into the RA.

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Conduction system

SAN (RA, near SVC; 60–100/min) → atrial myocardium → AVN (IAS, near coronary sinus; ~0.1 s delay = atrial kick) → bundle of His → bundle branches → Purkinje → ventricles. Loss of AV synchrony (AF, CHB) costs ~20% of CO.

Sympathetic β1 ↑ rate/contractility/conduction. Vagal M2 ↓ rate, ↓ AV conduction. Vagal tone dominates at rest.

ECG basics

➡ P atrial depolarisation. PR 120–200 ms (>200 = first-degree block). QRS <120 ms (wide = BBB / ventricular / hyperK).

➡ ST: elevation = transmural MI/pericarditis; depression = subendocardial ischaemia.

➡ T inverted in ischaemia, RV strain (PE), post-MI.

➡ QTc <440 M, <460 F. Long QT → torsades.

➡ Axis normal −30° to +90°. RAD in PE/RVH; LAD in LVH/LBBB/inferior MI.

STEMI localisation:

Leads	Territory	Artery
II, III, aVF	Inferior	RCA
V1–V4	Anteroseptal	LAD
I, aVL, V5–V6	Lateral	LCx
V1–V2 reciprocal	Posterior	RCA / LCx

BBB (QRS >120 ms): RBBB = rSR' (M) in V1, slurred S in V6 (MarroW). LBBB = notched R in V6 (WilliaM), QS in V1. New LBBB + chest pain = treat as STEMI.

Rhythms: AF = irregularly irregular, no P. Flutter = sawtooth, often 2:1 at 150. VT = broad complex. CHB = independent P and QRS, cannon a waves.

ECG fingerprints: hyperK = wide QRS + flat P + peaked T; hypoK = U waves; short QT = hyperCa; long QT = hypoCa or drugs; J wave = hypothermia; delta + short PR = WPW; S1Q3T3 or T inv V1–V3 = PE.

Heart sounds

- S1 — MV + TV close at start of systole. Loud in MS.

- S2 — AV + PV close at end of systole. Physiological inspiratory split; fixed split = ASD.

- S3 — early diastolic, rapid passive filling. Physiological in young/athletes/pregnancy; pathological in CCF, MR.

- S4 — late diastolic, atrial kick into a stiff ventricle (LVH, AS, HOCM). Always pathological. Absent in AF.

Valvular disease (the four to know cold)

Lesion	Murmur	Site	Cause	Exam clue
AS	Ejection systolic, radiates to carotids	R 2nd ICS	Senile calcification, bicuspid valve (young)	Triad: syncope, angina, dyspnoea. Slow rising pulse. Tx AVR/TAVI
AR	Early diastolic decrescendo	LSE leaning forward	Marfan, dissection, IE, rheumatic	Collapsing pulse, wide pulse pressure, Corrigan's
MS	Mid-diastolic rumble + opening snap	Apex, L lateral	Rheumatic fever	AF, malar flush, haemoptysis, loud S1
MR	Pansystolic to axilla	Apex	MVP, IE, post-MI papillary rupture, LV dilatation	Soft S1, S3, displaced apex

👩‍⚕️ AS is the most dangerous valve lesion under anaesthesia — fixed CO can't compensate for the SVR drop. AR is often helped by anaesthesia-induced afterload reduction.

Cardiac cycle and haemodynamics

Phases: atrial systole → isovolumetric contraction → ejection → isovolumetric relaxation → filling. Isovolumetric = all valves shut, volume constant, pressure changes rapidly.

Normals: SV 70 mL, HR 60–100, CO ≈ 5 L/min (HR × SV), EF 55–70%. MAP = CO × SVR.

Regional CO at rest: brain 15%, heart 5%, kidneys 20–25%, splanchnic 25%, muscle 20%, skin 5%.

Tachycardia → angina: diastole shortens, coronary perfusion time falls (flow is diastolic), and O₂ demand rises — supply-demand gap.

Frank-Starling: ↑ preload → ↑ stretch → ↑ SV. The only way a denervated transplanted heart augments CO is via preload.

Heart failure

- HFrEF (EF <40%) — systolic failure (IHD, DCM, valve regurgitation). Eccentric hypertrophy.

- HFpEF (EF >50%) — diastolic failure, stiff ventricle (hypertension, AS, HOCM, amyloid). Concentric hypertrophy.

NYHA: I none; II ordinary activity; III minimal activity; IV at rest.

HFrEF management: ACEi/ARB + β-blocker + MRA + loop diuretic + SGLT2 inhibitor. ICD/CRT if EF ≤35% with broad QRS.

Pericardial disease

Tamponade — pericardial fluid blocks diastolic filling.

- Beck's triad — hypotension, raised JVP, muffled heart sounds.

- Pulsus paradoxus — inspiratory SBP fall >10 mmHg.

- Electrical alternans — heart swinging in fluid.

- Treatment: urgent pericardiocentesis.

Constrictive pericarditis — thickened fibrotic pericardium restricts filling. Prominent y descent, pericardial knock, calcified pericardium on CXR. Cause: TB worldwide, post-surgery/radiation in UK.

👩‍⚕️ Tamponade = blunted y descent. Constriction = prominent y descent.

JVP waveform

➡ a ➡ atrial contraction. Absent in AF; giant in TS/pulmonary HTN; cannon in CHB/VT.

➡ c ➡ tricuspid bulge in early systole.

➡ x descent ➡ atrial relaxation. Blunted in TR.

➡ v ➡ atrial filling. Giant in TR.

➡ y descent ➡ tricuspid opens. Prominent in constriction; blunted in tamponade.

[Image: MCQs banner]

Test yourself

Which chambers form most of the anterior (sternocostal) surface?

• ((Right atrium and right ventricle::☑️ Right-sided chambers dominate the anterior surface.))
• ((Left atrium and left ventricle::LA forms the posterior surface (base).))
• ((Right ventricle and left ventricle::LV makes only a thin anterior contribution.))
• ((Left atrium and right atrium::Both atria sit predominantly posteriorly.))

Which structure rests on the central tendon of the diaphragm?

• ((Lungs::Lateral to the heart — no cardiac surface.))
• ((Left ventricle alone::LV plus part of RV form the inferior surface.))
• ((Left ventricle plus part of the right ventricle::☑️ Inferior (diaphragmatic) surface.))
• ((Ascending aorta::Superior — exits the LV at the base.))
• ((Pericardium::Encloses the heart; doesn't define chamber surfaces.))

Which statement about the SA node is correct?

• ((It lies in the wall of the left atrium::SAN sits in the RA at the SVC junction.))
• ((It lies in the right ventricle::It's atrial, never ventricular.))
• ((It receives parasympathetic fibres from the vagus nerve::☑️ Vagal M2 slows; sympathetic β1 speeds up.))
• ((It is supplied by the LCA in most people::SA nodal artery is from the RCA in ~60%.))
• ((It is part of the somatic nervous system::Intrinsic conduction; ANS only modulates.))

Where does the LAD run?

• ((Anterior interventricular groove::☑️ Supplies anterior LV, anterior 2/3 septum, apex.))
• ((Left AV groove::That's the LCx with the great cardiac vein.))
• ((Posterior IV groove::That's the PDA.))
• ((Right AV groove::That's the RCA.))

The RCA arises from which site?

• ((Left aortic sinus::Origin of the LMCA.))
• ((Right aortic sinus, anterior aortic root::☑️ Both coronaries arise above the cusps at the sinuses of Valsalva.))
• ((Posterior aortic sinus::Non-coronary sinus — no coronary here.))
• ((Below the aortic valve cusps::Ostia sit above the cusps so diastolic flow opens them.))

👩‍⚕️ The non-coronary (posterior) sinus is a useful negative — examiners use it as a distractor.

Which artery supplies the AV node in ~90% of people?

• ((LAD::LAD supplies the bundle of His and anterior septum, not the AV node.))
• ((Left circumflex::Supplies the AV node only in left-dominant circulations (~10%).))
• ((Right coronary artery::☑️ AV nodal artery is a branch of the RCA at the crux in ~90%.))
• ((Posterior descending artery::PDA supplies posterior septum but not the AV node directly.))

👩‍⚕️ Inferior MI (RCA) commonly causes bradyarrhythmias and AV block — both SA and AV nodes are ischaemic.

MV repair is complicated by inferolateral ischaemia. Which artery is injured?

• ((Left circumflex::☑️ LCx runs in the left AV groove millimetres from the mitral annulus.))
• ((LAD::Anterior IV groove, distant from the mitral annulus.))
• ((PDA::Posterior IV groove, not adjacent to MV.))
• ((RCA::Right AV groove, away from MV.))
• ((Aortic root::Relevant to AVR, not MV surgery.))

During which phase does the tricuspid valve close?

• ((Atrial systole::AV valves open for ventricular filling.))
• ((Ventricular ejection::AV valves already shut.))
• ((Isovolumetric contraction::☑️ AV valve closure starts isovolumetric contraction — all valves shut, volume constant.))
• ((Isovolumetric relaxation::Semilunar valves just closed; AV valves still shut, about to open.))
• ((Late diastolic filling::AV valves wide open.))

Elderly patient, syncope, ejection systolic murmur radiating to carotids — diagnosis?

• ((Mitral stenosis::Mid-diastolic rumble at the apex.))
• ((HOCM::Louder with Valsalva; not typical in the elderly.))
• ((Pulmonary stenosis::L 2nd ICS, radiates to the back.))
• ((Calcific aortic stenosis::☑️ Triad of syncope, angina, dyspnoea — commonest valve lesion in the elderly.))
• ((Tricuspid regurgitation::Pansystolic, louder on inspiration, JVP v wave.))

Which valvular lesion is most dangerous intraoperatively?

• ((Aortic stenosis::☑️ Fixed SV; SVR drop on induction causes catastrophic hypotension and coronary hypoperfusion.))
• ((Aortic regurgitation::Afterload reduction often helps.))
• ((Mitral stenosis::Sensitive to tachycardia but less acutely dangerous.))
• ((Mitral regurgitation::Afterload drop reduces regurgitant fraction.))
• ((Tricuspid regurgitation::Rarely critical perioperatively.))

24 h post-AVR: HR 40, BP falling, RA pressure 7 → 15 mmHg. Diagnosis?

• ((Cardiac tamponade::☑️ Rising CVP with falling BP after cardiac surgery = pericardial blood compressing filling.))
• ((Tension pneumothorax::Tracheal deviation, unilateral absent breath sounds.))
• ((Massive PE::Typically tachycardia.))
• ((Hypovolaemic shock::CVP would be low.))
• ((Cardiogenic shock::Possible, but the rising CVP after cardiac surgery points to tamponade.))

👩‍⚕️ Beck's triad + pulsus paradoxus + electrical alternans = tamponade.

Postop patient: HR 65, BP 80/50, CVP 20. Diagnosis?

• ((Hypovolaemia::CVP would be low.))
• ((Sepsis::Distributive — low CVP, tachycardia.))
• ((Cardiac (pump) failure::☑️ Low BP with high CVP = adequate filling but failing pump.))
• ((Heart block::Would not raise CVP alone.))
• ((Pulmonary embolism::Typically tachycardic.))

👩‍⚕️ Low BP + high CVP = pump failure or obstruction. Low BP + low CVP = bleeding or distributive.

In tamponade, arrest occurs because of:

• ((Reduced LV contractility::Contractility is preserved.))
• ((Reduced LV diastolic filling::☑️ Pericardial pressure prevents filling, collapsing stroke volume.))
• ((Reduced RV contractility::Not the mechanism.))
• ((Coronary artery compression::Not the primary mechanism.))
• ((Acute valvular incompetence::Not caused by tamponade.))

Double mechanical valve replacement, Hb 72 g/L. Most likely cause?

• ((Mechanical haemolysis::☑️ Shear on prosthetic valves fragments RBCs — schistocytes, raised LDH, low haptoglobin.))
• ((Acute haemorrhage::Would show instability and active bleeding.))
• ((Autoimmune haemolysis::Unlikely de novo here.))
• ((Iron deficiency::Doesn't develop acutely post-op.))
• ((Drug reaction::Possible but mechanical haemolysis is classic.))

Which ECG sign indicates hypothermia?

• ((Delta wave::WPW.))
• ((U wave::Hypokalaemia.))
• ((Short PR::WPW or junctional rhythm.))
• ((J (Osborn) wave::☑️ Positive deflection at the J point — pathognomonic for hypothermia.))
• ((Peaked T waves::Hyperkalaemia.))

Wide QRS with flattened P waves suggests:

• ((Hypercalcaemia::Shortens QT.))
• ((Hyperkalaemia::☑️ Slows conduction → flat P, wide QRS, peaked T, eventually sine wave.))
• ((Hypokalaemia::U waves and flat T waves.))
• ((Hyponatraemia::No characteristic ECG change.))
• ((Hypocalcaemia::Prolongs QT.))

Why does tachycardia precipitate angina?

• ((Increased preload::Filling time is reduced, not increased.))
• ((Decreased oxygen extraction::Myocardial extraction is already near-maximal at rest.))
• ((Shortened diastole reduces coronary perfusion::☑️ Coronaries fill in diastole; demand rises too.))
• ((Increased coronary resistance::Not the primary mechanism.))
• ((Decreased oxygen demand::Demand rises with tachycardia.))

Normal resting stroke volume in a healthy adult?

• ((30 mL::Severe dysfunction.))
• ((50 mL::Below normal.))
• ((70 mL::☑️ Normal SV ~70 mL (60–100 mL range).))
• ((120 mL::Above normal at rest.))
• ((200 mL::Non-physiological.))

Normal resting cardiac output (L/min)?

• ((2–3::Cardiogenic shock territory.))
• ((3–4::Below normal.))
• ((5–6::☑️ CO = HR × SV ≈ 70 × 70 mL = ~5 L/min.))
• ((8–10::Moderate exercise.))
• ((12–15::Vigorous exercise.))

What percentage of cardiac output goes to cerebral blood flow at rest?

• ((5%::Approximately the myocardial share.))
• ((15%::☑️ Cerebral blood flow ≈ 15% of CO (~750 mL/min).))
• ((20–25%::Renal share.))
• ((25%::Splanchnic share.))
• ((40%::No single organ takes this much at rest.))

Sudden left forearm pain; echo shows systolic mitral leaflet prolapse. Most likely event?

• ((Radial artery thrombosis::Local thrombosis isn't caused by MVP.))
• ((Brachial artery embolism::☑️ Valvular thrombi embolise to peripheral arteries.))
• ((Axillary artery dissection::Not caused by MVP.))
• ((Subclavian stenosis::Chronic atheromatous process.))
• ((Deep vein thrombosis::Venous and unrelated.))

How does a denervated transplanted heart raise CO on exercise?

• ((Sympathetic nerve stimulation::Heart is denervated.))
• ((Decreased ventricular compliance::Would impair filling.))
• ((Decreased venous tone::Would reduce preload.))
• ((Increased preload (Frank-Starling)::☑️ Greater venous return stretches the myocardium and raises SV.))
• ((Decreased intrathoracic pressure::Not the primary mechanism.))

Immediate cardiovascular effect of IPPV?

• ((Increased stroke volume::IPPV reduces SV.))
• ((Reduced venous return::☑️ Raised intrathoracic pressure compresses great veins → lower preload.))
• ((Increased afterload::Not the dominant effect.))
• ((Increased contractility::Unaffected directly.))
• ((Increased heart rate::A reflex, not the immediate effect.))

Hypothyroid patient — greatest perioperative risk?

• ((High cholesterol::True but not acute.))
• ((Reduced cardiac contractility and output::☑️ Hypothyroidism slows the heart; anaesthesia can collapse haemodynamics.))
• ((Cold intolerance::Symptom, not surgical risk.))
• ((Menstrual irregularity::Not surgically relevant.))
• ((Bleeding diathesis::Not characteristic.))

What tissue forms the framework of cardiac valves?

• ((Dense fibrous connective tissue::☑️ Collagenous leaflets — no cartilage or muscle.))
• ((Hyaline cartilage::Not present in valves.))
• ((Smooth muscle::Vessel walls, not leaflets.))
• ((Elastic tissue::Minor component only.))
• ((Cardiac muscle::Doesn't extend into leaflets.))

Which of the following is the primary pacemaker of the heart?

• ((Musculi pectinati::Atrial muscle ridges — contractile, not conducting.))
• ((Chordae tendineae::Tether AV valve leaflets — mechanical, not electrical.))
• ((SA node::☑️ Pacemaker in the right atrium; sets the intrinsic ~70 bpm rhythm.))
• ((AV node::Part of the conducting system, but delays conduction — not the primary pacemaker.))
• ((Trabeculae carneae::Ventricular muscle ridges — contractile.))

👩‍⚕️ The moderator band carries the right bundle branch — also part of the conduction system.

Most specific ECG finding for PE?

• ((ST depression::Non-specific.))
• ((T wave inversion V1–V3::☑️ Reflects right ventricular strain.))
• ((LBBB::Not associated with PE.))
• ((Left axis deviation::PE causes right axis deviation.))
• ((Tall R in V1::Suggests RVH or posterior MI.))

👩‍⚕️ Commonest ECG in PE = sinus tachycardia. Classic = S1Q3T3.

Which JVP wave is prominent in tricuspid stenosis?

• ((Giant a wave::☑️ Atrium contracts against a narrowed tricuspid valve.))
• ((Giant v wave::Tricuspid regurgitation.))
• ((Prominent y descent::Constrictive pericarditis.))
• ((Cannon a wave::CHB, VT, junctional rhythm.))
• ((Absent a wave::Atrial fibrillation.))

Revision summary

Surfaces: Anterior = RA + RV. Inferior = LV + part RV on diaphragm. Left = LV. Base = LA.

Coronaries: LAD → anterior LV + ant 2/3 septum + apex. LCx → lateral LV (at risk in MV surgery). RCA → RA, RV, inferior LV, posterior 1/3 septum. SAN = RCA 60%. AVN = RCA 90%. His = LAD.

Conduction: SA → AV (delay) → His → bundles → Purkinje.

APTM: Aortic R2, Pulmonary L2, Tricuspid L4–5, Mitral apex.

Sounds: S1 MV+TV; S2 AV+PV; S3 rapid filling (CCF if pathological); S4 stiff ventricle (AS/LVH/HOCM, absent in AF).

Valves: AS — ejection systolic, syncope/angina/dyspnoea, most dangerous intraop. AR — early diastolic, collapsing pulse. MS — mid-diastolic rumble, rheumatic. MR — pansystolic to axilla.

Haemodynamics: SV 70 mL, CO 5 L/min, EF 55–70%. Coronary flow in diastole.

Tamponade: Beck's triad + pulsus paradoxus + electrical alternans. Low BP + high CVP = pump failure/obstruction.

ECG fingerprints: hyperK = wide QRS + flat P + peaked T; hypoK = U waves; long QT = hypoCa; J wave = hypothermia; delta = WPW; T inv V1–V3 = PE.

STEMI: II/III/aVF inferior (RCA); V1–V4 anterior (LAD); I/aVL/V5–V6 lateral (LCx). New LBBB + chest pain = STEMI.

Transplanted heart: CO rises via preload (Frank-Starling) only.