Right atrium

What it normally does

• The right atrium collects systemic venous blood only: the superior vena cava, the inferior vena cava, the coronary sinus (most of the heart's own venous drainage) and the small thebesian veins of the atrial wall. The pulmonary veins are the exception to the usual rule that veins end in the right heart - they carry oxygenated blood to the LEFT atrium. The interatrial septum has a thin depression, the fossa ovalis, which fails to seal in roughly a quarter of adults (patent foramen ovale).

  congestion behind a failing right heart shows up in the systemic veins - neck, liver, legs - with clear lungs, while congestion behind the left heart shows in the lungs; venous clot from the legs lodges in the pulmonary arteries, and only if a patent foramen ovale lets it cross does it reach the systemic circulation as a paradoxical embolus.

• Venous return runs down a very small pressure gradient: roughly 8 to 10 mmHg in the peripheral veins falling to a mean right atrial pressure of about 0 to 6 mmHg. Right atrial pressure IS central venous pressure. It is the gradient that drives return, so a rising right atrial pressure narrows the gradient and slows venous return rather than speeding it, and a falling venous volume narrows it from the other end.

  anything that stops the atrium emptying (right ventricular failure, pulmonary hypertension, tamponade, right ventricular infarct) raises CVP and backs pressure into the veins, while anything that empties the venous side (bleeding, dehydration, vasodilatory sepsis) drops the gradient and the stroke volume with it - opposite problems that look different at the neck.

• There are no competent valves between the right atrium and the great veins of the neck (the internal jugular does carry a valve near its lower end, but it does not stop atrial pressure being transmitted upward), so the vein behaves as an open fluid column reporting right atrial pressure. Measured vertically above the sternal angle, the top of the internal jugular pulsation is normally 3 cm or less (some texts allow 4 cm); add about 5 cm as the rough sternal-angle-to-atrium distance. The a wave is atrial contraction, the x descent atrial relaxation, the v wave the atrium filling against a shut tricuspid valve and the y descent its emptying once the valve opens. The column normally falls on inspiration as intrathoracic pressure drops.

  the JVP works as a bedside manometer: it is raised in congestion, it loses its a wave in atrial fibrillation, it gains giant v waves in tricuspid regurgitation, and it rises rather than falls on inspiration (Kussmaul sign) when the right heart cannot accept the extra inspiratory return.

• The atrium is a thin (a few millimetres), distensible, low-pressure chamber - the thinnest-walled and lowest-pressure of the four - whose contraction tops the ventricle up with roughly the last 20 percent of its filling (range about 10 to 30 percent, and more like 30 to 40 percent when the ventricle is stiff). Because the wall is thin it dilates readily when volume or pressure rises, and it is compressed readily by anything pressing from outside.

  it is the first chamber squashed when the pericardial sac fills or stiffens, it dilates rather than hypertrophies under chronic load, and losing the atrial kick matters most in exactly the stiff, hypertrophied or ischaemic ventricle that depends on it.

• The right atrium carries the heart's electrical starting point and its only normal gate. The sinoatrial node sits at the junction of the superior vena cava and the atrium in the crista terminalis; the impulse spreads across both atria to the atrioventricular node in the triangle of Koch, which in a normal heart is the sole electrical connection to the ventricles - the fibrous annuli insulate the rest, unless an accessory pathway is present. The strip of atrial muscle between the tricuspid annulus and the inferior vena caval orifice (the cavotricuspid isthmus) is a slow-conducting corridor, and stretched atrial muscle conducts more unevenly still.

  the isthmus completes a ready-made macro-re-entry circuit for typical atrial flutter (and is the target of ablation), and drugs that slow the AV node control the ventricular rate in flutter and fibrillation - a strategy that fails, and becomes dangerous, when an accessory pathway bypasses the node.

• Stretch is a signal, not just a change in shape. Stretched atrial myocytes release atrial natriuretic peptide (ANP); the stressed ventricle releases the related BNP, cleaved from proBNP into active BNP and the inactive fragment NT-proBNP. These peptides make the kidney excrete salt and water, dilate vessels and oppose the renin-angiotensin-aldosterone and vasopressin systems, and they are broken down largely by the enzyme neprilysin.

  a blood BNP or NT-proBNP reports that a heart chamber is being stretched (a low NT-proBNP, under about 300 ng/L, makes acute heart failure very unlikely, while age, kidney impairment and atrial fibrillation raise it and obesity lowers it), and blocking neprilysin is a way of amplifying the heart's own volume brake.

What goes wrong

• Right heart failure and systemic venous congestion← from “Venous return runs down a very small pressure …”

  The right ventricle fails, or the load it pumps against rises (chronic lung disease and hypoxic pulmonary vasoconstriction, pulmonary hypertension, large pulmonary embolism, or - most commonly of all - left heart failure raising pulmonary pressures). The atrium cannot empty, CVP rises, and because the systemic veins are one continuous column that pressure backs into the neck, the liver and the dependent tissues. The stretched atrium releases ANP and the loaded ventricle BNP, but the salt-retaining hormones overwhelm this brake, so the patient keeps holding fluid despite high peptide levels.

  Raised JVP plus oedema plus a raised natriuretic peptide equals congestion, and that is the setting where a loop diuretic helps; the commonest cause of right heart failure is left heart failure, so look at the left side before blaming the lungs.

  You would find: JVP visible more than 3 cm above the sternal angle, pitting oedema of the ankles (or the sacrum if bed-bound), a tender enlarged and sometimes pulsatile liver, ascites, and a raised BNP or NT-proBNP. Lungs are clear if the right heart is failing alone. Chronic lung disease driving cor pulmonale is a common Australian cause, and in northern Australia and in Aboriginal and Torres Strait Islander communities rheumatic heart disease is a further important cause of right-sided load.

• Tricuspid regurgitation← from “There are no competent valves between the righ…”

  In systole the tricuspid valve should be shut, which is why the atrium fills quietly and produces only a gentle v wave. If the valve leaks, right ventricular systolic pressure is transmitted straight back into the atrium and up the open jugular column with every beat. Most cases are functional - the annulus is pulled open by a dilated right ventricle, usually from pulmonary hypertension or left heart disease. Primary causes include rheumatic heart disease, right-sided infective endocarditis (classically in people who inject drugs), carcinoid, pacemaker or defibrillator leads and Ebstein anomaly.

  Systolic waves in the neck plus a pulsatile liver plus a murmur that increases on inspiration; most tricuspid regurgitation is functional, so the question to answer is what dilated the right ventricle.

  You would find: Giant v waves flicking up the neck with each systole, a liver that pulsates under the hand, and a soft pansystolic murmur at the left lower sternal edge that gets louder on inspiration (Carvallo sign).

• The atrium cannot fill: cardiac tamponade and constrictive pericarditis← from “The atrium is a thin (a few millimetres), dist…”

  The right atrium has the thinnest wall and the lowest pressure of the four chambers, so it is compressed first when fluid collects under pressure in the pericardial sac or the sac scars into a rigid shell. Filling is limited, so CVP climbs while the volume actually reaching the ventricle falls, diastolic pressures equalise across the chambers, and cardiac output drops. In constriction (and in tamponade with a rigid or overloaded right heart) the inspiratory fall in intrathoracic pressure can no longer be transmitted or accommodated, so the neck veins rise on inspiration instead of falling.

  High JVP with a low blood pressure is a filling problem until proved otherwise; pulsus paradoxus with an absent y descent means tamponade and needs drainage, Kussmaul sign with a brisk y descent means constriction - and preload-lowering drugs are harmful in both.

  You would find: A high JVP with a low blood pressure, tachycardia and muffled heart sounds; an inspiratory fall in systolic pressure of more than 10 mmHg (pulsus paradoxus) points to tamponade, where the y descent is lost. A JVP that rises on inspiration (Kussmaul sign) points instead to constriction, restrictive disease or right ventricular infarction, and constriction gives a sharp prominent y descent and a pericardial knock. Echocardiography, not the chest x-ray, decides whether fluid is compressing the heart.

• Atrial flutter and atrial fibrillation← from “The right atrium carries the heart's electrica…”

  A stretched, dilated, fibrosed atrium conducts unevenly. In typical flutter the impulse circles the tricuspid annulus through the cavotricuspid isthmus at about 250 to 350 per minute (commonly near 300), and the AV node typically lets every second impulse through, giving a ventricular rate near 150. In fibrillation there is no coordinated atrial contraction at all, and the AV node passes impulses irregularly. Either way the atrial kick is lost, which matters most in a stiff ventricle. Both atria are involved and blood stagnates where contraction is lost: thrombus forming in the left atrial appendage (the source of the great majority of thrombi in non-valvular atrial fibrillation) embolises to the brain and systemic circulation, while right atrial thrombus embolises to the lungs.

  Regular 150 means flutter with 2:1 conduction until proved otherwise; rate control and rhythm control both leave the stroke risk untouched, so anticoagulation is decided separately on the risk score, and flutter is scored exactly like fibrillation.

  You would find: An irregularly irregular pulse, or a suspiciously regular rate near 150; sawtooth flutter waves negative in leads II, III and aVF in typical flutter; loss of the a wave from the venous pulse in fibrillation; sometimes stroke as the first presentation. Look for the driver - thyrotoxicosis, alcohol, sepsis, hypertension, sleep apnoea, mitral valve disease.

• Right ventricular infarction← from “Venous return runs down a very small pressure …”

  Occlusion of the right coronary artery proximal to its right ventricular branches (usually with an inferior infarct) stuns the right ventricle. It cannot move blood forward into the lungs, so right atrial pressure rises while left ventricular filling falls: the patient is hypotensive with a high JVP and clear lungs. Output becomes critically dependent on preload and on atrial contraction, and heart block from the same territory is common.

  High JVP, clear lungs, low blood pressure after an inferior infarct: this ventricle runs on filling, so nitrates, diuretics and morphine can cause collapse and the immediate treatment is fluid plus reperfusion.

  You would find: Inferior ST elevation (II, III, aVF) with hypotension, raised JVP, clear lung fields, often bradycardia; ST elevation in V4R on right-sided chest leads confirms it. Kussmaul sign may be present.

• Not enough blood coming back (hypovolaemia and vasodilatory shock)← from “Venous return runs down a very small pressure …”

  The whole system runs on the small gradient from vein to atrium. Bleeding, vomiting, diarrhoea or burns remove volume; sepsis and anaphylaxis dilate the venous capacitance beds so the volume is there but not returning. Either way mean systemic filling pressure falls, the gradient into the right atrium narrows, and stroke volume falls with it.

  Flat JVP with tachycardia and hypotension equals underfilling; the same low blood pressure with a HIGH JVP means the opposite problem and the opposite treatment.

  You would find: A JVP you cannot see even with the patient lying flat, collapsed peripheral veins, tachycardia, narrow pulse pressure, cool peripheries and poor urine output. This is a volume problem, not a pump problem, and a diuretic makes it worse.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.