Left atrium

What it normally does

• There is no valve between the left atrium and the lungs, so left atrial pressure - normally a mean of about 4 to 12 mmHg, approximated clinically by the pulmonary capillary wedge pressure - is transmitted straight back into the pulmonary veins and capillaries. Pulmonary lymphatics clear a modest surplus. When the pressure rises acutely, interstitial oedema begins once the mean is somewhere above roughly 18 to 20 mmHg and alveolar flooding follows as it approaches plasma oncotic pressure near 25 mmHg; when the rise is chronic the lymphatics enlarge and considerably higher pressures can be carried with surprisingly few crackles.

  any obstruction or leak at the mitral valve, and any chronic rise in left atrial pressure, is felt by the lungs first - breathlessness and pulmonary oedema before anything else, and later pulmonary hypertension and right heart failure. It also explains why a patient with long-standing mitral stenosis can look deceptively dry at a pressure that would drown someone whose rise was sudden.

• The atrium fills while the mitral valve is shut, then empties: roughly 70 to 80% of ventricular filling occurs passively when the valve opens, and the remaining 20 to 30% is delivered by atrial contraction (the atrial kick). The kick requires organised, coordinated atrial depolarisation - sinus rhythm, or atrial pacing - and its contribution is smallest in a young compliant ventricle at rest and largest when the ventricle is stiff or the heart rate fast and diastole short.

  losing organised atrial contraction removes a filling contribution that matters most in exactly the patients least able to spare it - mitral stenosis, left ventricular hypertrophy, HFpEF - which is why the onset of atrial fibrillation can turn a stable patient acutely breathless within hours.

• The atrial wall is thin and compliant. Faced with extra volume or pressure it dilates far more than it thickens, and stretched atrial muscle - especially the sleeves of myocardium that extend from the atrium a short way into the pulmonary vein openings - generates ectopic beats and sustains re-entry circuits. Enlargement is measurable on echocardiography (a left atrial volume index above about 34 mL/m2 is abnormal).

  sustained mitral valve disease or raised filling pressure ends in atrial fibrillation, the dilated atrium then perpetuates the arrhythmia, and the pulmonary vein sleeves are the structures targeted by catheter ablation.

• The left atrial appendage is a narrow, trabeculated blind pouch off the atrium where flow is slow even in sinus rhythm, and it depends heavily on atrial contraction to empty. It is the site of the great majority - not all - of left atrial thrombi in non-valvular atrial fibrillation.

  when organised atrial contraction is lost, blood stagnates there, thrombus forms, and because the appendage sits in the systemic circulation the embolus goes to the brain rather than the lungs.

What goes wrong

• Mitral stenosis (in Australia, usually rheumatic)← from “There is no valve between the left atrium and …”

  Rheumatic inflammation fuses the commissures and thickens and shortens the leaflets and chordae, narrowing the orifice from a normal 4 to 6 cm2. A pressure gradient now has to exist across the valve throughout diastole for the atrium to empty, so left atrial pressure climbs, and because nothing protects the lungs from that pressure it is driven back into the pulmonary interstitium and alveoli. Anything that shortens diastole or raises flow - tachycardia, exercise, fever, pregnancy, loss of the atrial kick - raises the gradient further and can decompensate a previously stable valve.

  Rheumatic until proven otherwise in a young Aboriginal or Torres Strait Islander adult. Severe when the valve area is about 1.5 cm2 or less. Tachycardia is the enemy - it shortens diastole; slowing the rate is treatment, not just symptom control.

  You would find: Breathless on exertion, sometimes haemoptysis. A loud first heart sound (loud while the leaflets are still pliable; it softens once they calcify), an opening snap, and a low-pitched rumbling mid-diastolic murmur at the apex, heard with the bell and the patient rolled into the left lateral position. A shorter interval between the second heart sound and the opening snap means a higher atrial pressure and a tighter valve. In Australia this is the legacy of acute rheumatic fever, and rates of rheumatic heart disease in Aboriginal and Torres Strait Islander communities are among the highest in the world - so it presents in young adults, and often first declares itself in pregnancy when blood volume and heart rate rise.

• Mitral regurgitation← from “The atrial wall is thin and compliant. Faced w…”

  The valve leaks backwards, so each systole drives part of the ventricular stroke volume back into the atrium. In chronic regurgitation the thin, compliant wall stretches to accommodate it, the atrium dilates, and atrial and pulmonary pressures rise only slowly; in acute regurgitation (chordal rupture, papillary muscle rupture after infarction, endocarditis) the volume lands in a normal-sized, non-compliant atrium and the pressure goes straight to the lungs.

  Chronic: big atrium, late symptoms, murmur to the axilla. Acute: small atrium, immediate pulmonary oedema, unimpressive murmur - the loudness of the murmur does not track severity.

  You would find: A blowing murmur through the whole of systole (pansystolic) at the apex radiating to the axilla, a soft first heart sound, a displaced hyperdynamic apex beat, and a big left atrium on echocardiography. In the chronic form symptoms come late because the compliant atrium absorbs the pressure for years; acute severe regurgitation instead presents as flash pulmonary oedema, and the murmur may be short and quiet because atrial and ventricular pressures equalise early.

• Atrial fibrillation← from “The atrial wall is thin and compliant. Faced w…”

  A stretched, dilated atrium plus ectopic firing from the pulmonary vein muscle sleeves breaks organised activation into chaotic wavelets. The atrium stops contracting effectively, and the AV node is bombarded irregularly, conducting some impulses and blocking others - giving an irregular, often fast ventricular rate.

  The dilated atrium causes AF and AF further dilates the atrium. Pulmonary vein sleeves are the trigger and the ablation target. Rate versus rhythm is a symptom decision; anticoagulation is a separate decision made on stroke risk, not on rhythm.

  You would find: Irregularly irregular pulse, absent P waves with an irregular baseline on ECG, and no a wave in the JVP. Look for the substrate rather than accepting the rhythm at face value - mitral valve disease, hypertension, alcohol, thyrotoxicosis, sepsis, sleep apnoea.

• Acute decompensation on losing the atrial kick← from “The atrium fills while the mitral valve is shu…”

  When atrial fibrillation (or any loss of organised atrial contraction) removes the atrial kick, ventricular filling loses the 20 to 30% contribution that arrives at end-diastole, and any accompanying tachycardia shortens diastole as well. In a ventricle that fills easily this is tolerated; where filling is already limited - tight mitral stenosis, hypertrophy, HFpEF, amyloid - stroke volume falls and left atrial pressure rises sharply.

  Losing the kick can cost of the order of 20 to 30% of cardiac output in a stiff or obstructed heart, and very little in a normal one - the number depends on the ventricle, so the same arrhythmia is trivial in one patient and an emergency in the next.

  You would find: A patient who was stable becomes acutely breathless, hypotensive or oedematous within hours of going into a fast irregular rhythm; restoring rate control or sinus rhythm restores them just as quickly.

• Left atrial appendage thrombus and cardioembolic stroke← from “The left atrial appendage is a narrow, trabecu…”

  Without effective atrial contraction, blood stagnates in the appendage; stasis, endothelial injury and a prothrombotic state combine and thrombus forms. The appendage sits in a systemic chamber, so a fragment that breaks off is carried into the aorta and up the carotid or vertebral arteries to the brain, or to a limb, gut or kidney.

  Stasis in the appendage, not the fibrillation itself, is what embolises - which is why rate or rhythm control does not remove stroke risk and anticoagulation is decided separately. Transthoracic echo cannot see the appendage reliably; transoesophageal echo can.

  You would find: Sudden maximal focal neurological deficit in a patient with an irregular pulse - typically a large-vessel territory infarct rather than a small deep lacunar one, and it may be the first sign that the atrial fibrillation exists at all. Australian practice (Heart Foundation/CSANZ) scores the risk with CHA2DS2-VA, which unlike the older CHA2DS2-VASc does not count female sex; anticoagulation is recommended at a score of 2 or more and considered at 1. Moderate-to-severe rheumatic mitral stenosis and mechanical valves sit outside the score - those patients are anticoagulated on the lesion itself.

• Pulmonary congestion and secondary (post-capillary) pulmonary hypertension← from “There is no valve between the left atrium and …”

  Chronically raised left atrial pressure is transmitted back through the pulmonary veins into the capillaries; with time the pulmonary arterioles remodel, thickening and constricting, so resistance rises on top of the passive back-pressure and the right ventricle has to pump against it.

  Post-capillary pulmonary hypertension: mean pulmonary artery pressure above 20 mmHg with a wedge pressure above 15 mmHg. Fix the left-sided lesion; pulmonary vasodilators used for pulmonary arterial hypertension can make this group worse.

  You would find: Crackles at the lung bases, breathlessness lying flat and waking at night, then later a loud pulmonary component of the second heart sound, a raised JVP, tender hepatomegaly and ankle oedema. Left-sided heart and valve disease is the commonest cause of pulmonary hypertension worldwide.

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