Heart and Mediastinum

Part 4 · The trunk

Chambers, valves, the conducting system and the coronary supply

Why a physiotherapist needs this

Cardiac rehabilitation is one of the best-evidenced interventions in the whole of physiotherapy — reducing cardiovascular mortality and hospital readmission in a way few of our treatments can claim. But you cannot prescribe exercise safely for a patient after myocardial infarction, valve surgery or heart failure without knowing which artery supplies which wall, why an inferior infarct causes bradycardia, what a sternotomy has actually divided, or why a patient in heart failure cannot lie flat.

Beyond cardiac rehabilitation, every patient you treat has a heart, and a proportion of the “musculoskeletal” chest, shoulder and interscapular pain that arrives in a physiotherapy clinic is not musculoskeletal at all. The anatomy in this chapter is what lets you tell the difference.

Learning outcomes

• Describe the divisions of the mediastinum and the contents of each.
• Describe the pericardium, its layers, sinuses and innervation, and explain tamponade.
• Describe the external features, chambers and valves of the heart.
• Describe the conducting system and relate it to the ECG and to the coronary supply.
• Describe the coronary arteries and venous drainage, and map each vessel to the region it supplies and to the ECG leads.
• Describe the great vessels, the thoracic duct, the oesophagus and the nerves of the mediastinum.
• Explain the cardiac cycle, heart sounds and auscultation areas.
• Explain cardiac autonomic control and the physiological response to exercise.
• Explain angina, myocardial infarction, heart failure, valve disease and their referred pain patterns.
• Apply this anatomy to cardiac rehabilitation, sternal precautions and exercise prescription.

The mediastinum

Figure 1 · The mediastinum, divided

The central compartment of the thorax, between the two pleural sacs, extending from the thoracic inlet to the diaphragm and from the sternum to the vertebral column.

Divided by the transverse thoracic plane — the plane of the sternal angle (T4–T5):

The mediastinum is mobile in the living, which is why a tension pneumothorax can shift it and compress the great veins — an anatomical fact with an immediate clinical consequence.

Mediastinal shift: towards the lesion in collapse, fibrosis or pneumonectomy; away from the lesion in tension pneumothorax, large effusion or a large mass. Checking tracheal position is a two-second bedside test that detects it.

The pericardium

Two sinuses, formed by the reflections of the serous layer:

• Transverse sinus — passes between the arterial outflow (aorta and pulmonary trunk) in front and the venous inflow (SVC and atria) behind. Surgically vital: a clamp or ligature can be passed through it to isolate the arterial outflow during cardiopulmonary bypass.
• Oblique sinus — a blind cul-de-sac behind the left atrium, bounded by the reflections around the pulmonary veins and IVC.

Innervation: the fibrous and parietal serous pericardium are supplied by the phrenic nerve (C3–C5) — so pericarditis pain is referred to the shoulder tip and the neck, and is classically relieved by sitting forward and worsened by lying flat and by inspiration. The visceral layer is insensitive.

Cardiac tamponade — Beck’s triad of hypotension, distended neck veins and muffled heart sounds, with pulsus paradoxus (an inspiratory fall in systolic pressure >10 mmHg). An emergency requiring pericardiocentesis.

The heart: external features and orientation

Figure 2 · The heart in the middle mediastinum

The heart lies obliquely, roughly two-thirds to the left of the midline, in the middle mediastinum. It is about the size of the owner’s closed fist and weighs 250–350 g.

Surface projection (four corners, useful for the chest radiograph and for percussion):

• Superior right: 3rd costal cartilage, ~1 cm from the right sternal edge
• Superior left: 2nd costal cartilage, ~1–2 cm from the left sternal edge
• Inferior right: 6th costal cartilage, ~1 cm from the right sternal edge
• Inferior left (apex): 5th intercostal space, midclavicular line

Grooves: the coronary (atrioventricular) sulcus encircling the heart between atria and ventricles, and the anterior and posterior interventricular sulci — each carrying the corresponding arteries and veins.

The chambers

Figure 3 · The chambers and valves of the heart

Interventricular septum: a large muscular part and a small membranous part superiorly — the commonest site of ventricular septal defect.

Fibrous skeleton of the heart: four fibrous rings (anuli) around the valve orifices, with the right and left fibrous trigones. It anchors the valves, provides attachment for the myocardium, and — crucially — electrically insulates the atria from the ventricles, so the only normal conduction route is the atrioventricular bundle.

The valves

Figure 4 · Where a valve lies, and where it is heard

The auscultation areas are NOT over the valves. They are the points to which the sound is best conducted downstream in the direction of blood flow. The valves themselves lie clustered close together behind the sternum, roughly along a line from the left 3rd costal cartilage to the right 6th. Students who try to listen “over the valve” hear little.

Mnemonic for the sequence Aortic (right 2nd), Pulmonary (left 2nd), Tricuspid (left 5th parasternal), Mitral (apex): All Physiotherapists Take Measurements.

Papillary muscles and chordae tendineae do not open or close the AV valves — pressure does that. They contract during systole to prevent the cusps from everting (prolapsing) into the atrium. Papillary muscle rupture after infarction therefore causes acute, severe mitral regurgitation and abrupt pulmonary oedema.

Semilunar valves have no chordae. Their cusps close passively in diastole as blood attempts to flow back; the coronary ostia lie in the aortic sinuses just above the right and left cusps, and coronary filling therefore occurs during diastole — an essential point (§19.7).

The coronary circulation

Figure 5 · The coronary arteries and the veins of the heart

The arteries

Both arise from the aortic sinuses immediately above the aortic valve.

Dominance is defined by which artery gives the posterior interventricular artery: right dominant in ~85%, left dominant in ~8%, co-dominant in ~7%.

The clinical map — artery to wall to ECG leads

This table is the reason the chapter exists.

Anastomoses between coronary branches exist but are functionally end-arteries in most people — collateral flow is inadequate to protect against acute occlusion, though it develops over time in chronic stenosis, which is one reason gradual disease can be less catastrophic than sudden thrombosis.

Coronary perfusion occurs in diastole

The left ventricular myocardium compresses its own intramural vessels during systole, so left coronary flow occurs almost entirely during diastole. Two consequences follow directly and are directly relevant to exercise prescription:

• Tachycardia shortens diastole disproportionately, reducing coronary perfusion time. This is why angina is rate-dependent and why heart rate limits are the central safety parameter in cardiac rehabilitation.
• Diastolic blood pressure drives coronary perfusion. Coronary perfusion pressure = aortic diastolic pressure − left ventricular end-diastolic pressure. Anything that lowers diastolic pressure or raises LVEDP (heart failure, aortic regurgitation) compromises the myocardium.

The rate–pressure product (heart rate × systolic BP) is the best simple index of myocardial oxygen demand, and the number that determines when a given patient develops angina. It reproduces reliably in the same individual, which is why an angina threshold is a usable prescription tool.

Venous drainage

• Coronary sinus (~60%) — in the posterior coronary sulcus, draining into the right atrium. Tributaries: great cardiac vein (with the LAD), middle cardiac vein (with the posterior interventricular artery), small cardiac vein, and the oblique vein of the left atrium.
• Anterior cardiac veins — draining the right ventricle directly into the right atrium.
• Venae cordis minimae (Thebesian veins) — draining directly into the chambers; a small physiological shunt.

The conducting system

Figure 6 · The conducting system, step by step

The AV node delays conduction by ~0.1 s — the interval that allows atrial systole to complete ventricular filling before ventricular systole begins. It is the PR interval on the ECG.

Because the RCA supplies both nodes in most people, an inferior (RCA) infarct commonly produces bradycardia and AV block — usually transient and usually responsive to atropine, whereas block complicating an anterior (LAD) infarct implies extensive septal necrosis and carries a far worse prognosis. That difference is pure anatomy translated into prognosis.

ECG correlation:

Great vessels and other mediastinal contents

The cardiac cycle, sounds and autonomic control

The cycle (at 75 bpm, ~0.8 s per cycle)

Diastole occupies about two-thirds of the cycle at rest — and this is the fraction that shrinks with tachycardia, compromising both ventricular filling and coronary perfusion.

Heart sounds

Autonomic control and the exercise response

Cardiac pain afferents travel with the sympathetics, entering the cord at T1–T5 — which is exactly why cardiac pain refers to the central chest, the left arm and medial forearm (T1–T2 dermatomes), the neck and the jaw. That referral is a direct consequence of segmental convergence (Chapter 8), and it is the reason a physiotherapist must be able to recognise it.

The response to exercise:

• Heart rate rises — initially by vagal withdrawal (up to ~100 bpm), then by sympathetic drive
• Stroke volume rises through increased preload (Frank–Starling — the muscle pump and respiratory pump returning more blood) and increased contractility
• Cardiac output rises from ~5 L/min at rest to 20–25 L/min in an untrained adult and 35–40 L/min in an endurance athlete
• Systolic BP rises; diastolic BP stays flat or falls slightly in dynamic exercise — a fall in systolic BP during exercise is an absolute indication to stop and is an ominous sign
• Isometric and resistance exercise produce a pressor response with a large rise in both systolic and diastolic pressure, and a smaller rise in cardiac output — which is why breath-holding and Valsalva are discouraged in cardiac rehabilitation, and why resistance training is introduced after aerobic conditioning is established

Clinical conditions and cardiac rehabilitation

Angina and myocardial infarction

• Stable angina: predictable, exertional, relieved by rest and nitrates, and reproducible at a given rate–pressure product.
• Acute coronary syndrome: unstable angina, NSTEMI, STEMI — a spectrum of plaque rupture and thrombosis.
• Referred pain pattern: retrosternal, radiating to the left arm and medial forearm, jaw, neck and interscapular region; associated with sweating, nausea and dyspnoea. Women, older patients and people with diabetes present atypically far more often — with breathlessness, fatigue or epigastric discomfort rather than chest pain.

The screening rule for a physiotherapist

Musculoskeletal pain has a mechanical behaviour: it is provoked and eased by specific positions, movements and palpation. Cardiac pain does not behave that way — it relates to exertion and emotion, not to position, and it is not reproduced by palpation or by movement testing.

Left shoulder, arm, jaw or interscapular pain that is exertional, unrelated to movement, accompanied by breathlessness, sweating or nausea, and not reproducible on examination is a cardiac presentation until proved otherwise. Refer immediately; do not treat, and do not arrange a follow-up.

Heart failure

• Systolic (HFrEF) — impaired contractility. Diastolic (HFpEF) — impaired filling of a stiff ventricle.
• Left-sided failure → pulmonary congestion → dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, crackles. Orthopnoea has an anatomical explanation: lying flat increases venous return and shifts abdominal contents cephalad, raising pulmonary capillary pressure and reducing FRC (Chapter 18).
• Right-sided failure → systemic congestion → raised JVP, hepatomegaly, ascites, peripheral oedema.
• Exercise training is a class I recommendation in stable chronic heart failure, improving exercise capacity, quality of life and hospitalisation rates. Peripheral adaptations (muscle oxidative capacity, endothelial function) account for most of the benefit rather than any change in ejection fraction.

Valve disease

Cardiac rehabilitation — where the anatomy becomes practice

Phase I (inpatient): early mobilisation, positioning, breathing exercises, education, and screening for sternal complications.

Sternal precautions after median sternotomy: the sternum is divided and wired; bony union takes 6–8 weeks, with full strength taking up to 3 months. Traditional advice restricted lifting to 5 kg and prohibited pushing, pulling and shoulder movement beyond 90° for 6–12 weeks. Contemporary practice (“Keep Your Move in the Tube”) has moved away from blanket restriction toward pain-guided, load-graded upper limb movement kept close to the trunk, because prolonged restriction produces stiffness, deconditioning and dependence without demonstrated reduction in sternal complications. Watch for sternal instability — clicking, a palpable rock, or a widening wound.

Phase II (outpatient): the core exercise programme, typically 6–12 weeks, prescribed by heart rate reserve or by rating of perceived exertion (11–14 on the Borg 6–20 scale), with resistance training added once aerobic conditioning is established.

Key prescription principles derived from this chapter:

• Use the rate–pressure product or a heart-rate ceiling 10 bpm below the ischaemic threshold where an angina threshold is known
• Beta-blockers blunt the heart rate response — RPE and the talk test become the primary guides, and target heart rates must be recalculated from a beta-blocked exercise test
• Avoid Valsalva and sustained isometric holds early, because of the pressor response
• Stop immediately for: a fall in systolic BP, chest pain, marked dyspnoea, dizziness, pallor, significant arrhythmia, or ST change if monitored
• Warm-up and cool-down are not optional — abrupt cessation removes the muscle pump, dropping venous return and coronary perfusion pressure at a moment when the heart is still catecholamine-driven, which is when post-exercise arrhythmias occur

The evidence: exercise-based cardiac rehabilitation reduces cardiovascular mortality and hospital admissions after myocardial infarction and in heart failure (Cochrane reviews, repeatedly). It is among the strongest evidence bases in the profession, and it is chronically under-referred.

Where students consistently go wrong

• Placing the auscultation areas over the valves. They are downstream, in the direction of flow.
• Thinking papillary muscles close the valves. They prevent eversion; pressure closes the valves.
• Forgetting that coronary flow occurs in diastole, and therefore why tachycardia causes ischaemia.
• Not knowing the artery-to-lead map. RCA → inferior → II, III, aVF; LAD → anterior → V1–V4; circumflex → lateral → I, aVL, V5–V6.
• Missing why an inferior MI causes bradycardia. The RCA supplies both nodes.
• Forgetting the right main bronchus is more vertical, and where aspiration therefore goes.
• Placing the phrenic nerve behind the lung root. Phrenic in front, vagus behind.
• Treating exertional left arm or jaw pain as musculoskeletal without screening its behaviour.
• Applying target heart rates to a beta-blocked patient without recalculating.
• Continuing to teach rigid six-week sternal precautions as though the evidence had not moved.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 19 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 20 — Abdomen: the abdominal wall, the peritoneum and the viscera.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents