Cardiovascular system

The thin-walled collecting chamber where systemic venous blood arrives: the pressure inside it is the back-pressure that venous return has to overcome, so it is readable in the neck veins and felt in every vein that drains into it.

What it 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).

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.

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.

What goes wrong

Right heart failure and systemic venous congestionTricuspid regurgitationThe atrium cannot fill: cardiac tamponade and constrictive pericarditisAtrial flutter and atrial fibrillationRight ventricular infarctionNot enough blood coming back (hypovolaemia and vasodilatory shock)

What we give

Loop diuretics (frusemide, written furosemide in newer references)Nitrates (glyceryl trinitrate)Angiotensin receptor-neprilysin inhibitor (sacubitril with valsartan)AV node blockers: beta blockers (metoprolol) or non-dihydropyridine calcium channel blockers (diltiazem, verapamil)DigoxinAnticoagulants: direct oral anticoagulants (apixaban, rivaroxaban, dabigatran) or warfarinIntravenous fluid (balanced crystalloid, or sodium chloride 0.9%)

The tricuspid valve is the one-way door from the right atrium into the right ventricle: it opens to let venous blood in and shuts when the ventricle squeezes, so blood goes to the lungs and not backwards into the neck veins and liver.

What it does

The valve separates a low-pressure right atrium (normally about 2–6 mmHg) from a right ventricle that generates roughly 25 mmHg in systole. It shuts as the ventricle contracts, so venous blood is driven into the pulmonary artery rather than back up the great veins. The whole right-sided circuit runs at a fraction of left-sided pressures, so the right ventricle is a thin-walled volume pump, tolerant of extra volume but poor at handling a sudden rise in afterload.

It is not a stiff ring. Three thin leaflets are tethered by chordae tendineae to papillary muscles on the right ventricular wall, and they seal only while the annulus they hang from keeps its normal size and shape. That annulus is the largest and least supported of the four valve rings, and it sits in the wall of a chamber that dilates easily.

No valve reliably interrupts the column of blood between the right atrium and the neck veins; most people have a small terminal valve in the internal jugular, but it does not stop right atrial pressure being transmitted back up the vein. So right atrial pressure is visible at the bedside as the JVP, read as vertical height above the sternal angle with the patient at about 45 degrees — normally no more than roughly 3 cm, since the right atrium sits about 5 cm below the sternal angle. The normal waveform is a soft, biphasic, non-palpable ripple: an a wave as the atrium contracts (just before the carotid upstroke), then a v wave as the atrium fills against a shut tricuspid valve.

What goes wrong

Tricuspid regurgitation — the valve leaks backwardsRight-sided infective endocarditis in people who inject drugsRheumatic tricuspid disease — stenosis and regurgitation togetherPacemaker or defibrillator lead across the valve

What we give

Loop diuretic — furosemide (still said as "frusemide" on Australian wards; furosemide is the current approved name)Aldosterone antagonist — spironolactoneAntistaphylococcal penicillin — flucloxacillinGlycopeptide — vancomycinLong-acting intramuscular penicillin — benzathine benzylpenicillin

The right ventricle takes essentially all the venous blood returning from the body and pushes it through the lungs, against roughly a fifth of the pressure the left ventricle has to overcome.

What it does

The right ventricular free wall is thin — roughly 3-5 mm, against about 6-10 mm for the left ventricle (hypertrophy is usually called above about 11 mm in men and above about 10 mm in women). Averaged over time, and in the absence of a shunt, it must eject the same stroke volume as the left ventricle, since the two sit in series. But it ejects into a low-pressure circuit: normal pulmonary artery systolic pressure is about 15-25 mmHg, against about 120 mmHg in the aorta. It is therefore built as a volume pump rather than a pressure pump — it accommodates extra volume well and tolerates extra afterload badly.

The neck veins sit in a near-continuous column of blood with the right atrium. Most people have a small valve at the lower end of the internal jugular vein, but it does not prevent right atrial pressure being transmitted upwards — so the height of that column is a bedside manometer of right atrial, and hence right ventricular filling, pressure. This is the jugular venous pressure (JVP): normally no more than about 3 cm of vertical height above the sternal angle (add roughly 5 cm to estimate right atrial pressure in cmH2O). Volume the right ventricle cannot clear tends to back up into the neck veins, the liver and the dependent tissues.

The right ventricle is markedly preload-dependent. Because it generates so little pressure of its own, its output is set largely by how much blood is delivered to it. Drop the filling and output falls steeply — more steeply than for the left ventricle at the same drop in venous return.

What goes wrong

Acute right ventricular failure from pulmonary embolismRight ventricular infarctionRight heart failure caused by the left heart (the common cause)Chronic pulmonary hypertension and cor pulmonaleSecondary (functional) tricuspid regurgitation from a dilated right ventricle

What we give

Loop diuretics — furosemide (frusemide)Mineralocorticoid receptor antagonists — spironolactone (eplerenone where gynaecomastia is a problem)Anticoagulants — apixaban, rivaroxaban, enoxaparin, unfractionated heparinOxygen (long-term oxygen therapy)Pulmonary vasodilators — sildenafil (phosphodiesterase-5 inhibitor), bosentan or macitentan (endothelin receptor antagonists)

Three semilunar cusps at the top of the right ventricle that open to let blood out to the lungs and shut so that none falls back in.

What it does

The right ventricle pumps into a low-pressure circuit — normal pulmonary artery pressure is about 25/10 mmHg (mean around 14 mmHg), roughly a fifth of aortic systolic pressure — so its free wall is thin, about 3 to 5 mm. A thin-walled pump copes with extra volume for years but tolerates extra pressure badly.

Blood leaves the right ventricle through a muscular funnel (the right ventricular outflow tract, or infundibulum) and then through the three cusps. Obstruction can sit below the cusps in that muscle, at the cusps, or above them in the pulmonary artery and its branches. Where it sits decides the fix: balloon valvuloplasty for the typical thin domed valve, surgical resection for fixed muscular subvalvular obstruction, and usually catheter balloon angioplasty with stenting (surgery in selected cases) for supravalvular and branch pulmonary artery stenosis.

The valve opens when right ventricular pressure rises above pulmonary artery pressure and shuts when it falls below; that closure is the pulmonary component of the second heart sound (P2). Flow becomes turbulent, and so audible, when it moves fast enough — which happens either because the orifice is narrowed or because the volume crossing a normal valve is high.

What goes wrong

Congenital valvular pulmonary stenosisOutflow obstruction in tetralogy of FallotPulmonary regurgitation (the valve leaks backwards)A flow murmur that is not valve disease

What we give

Alprostadil (prostaglandin E1)Beta blockers (propranolol orally; esmolol intravenously in the acute setting)Alpha-1 agonists (phenylephrine; metaraminol in older children and adults)Loop diuretics (furosemide, also spelled frusemide)Amoxicillin (endocarditis prophylaxis, per Therapeutic Guidelines)

The pulmonary circulation pushes the whole cardiac output through the lungs at roughly a sixth of systemic arterial pressure and about a tenth of systemic vascular resistance, so blood can pick up oxygen without flooding the alveoli.

What it does

The right ventricle moves the same cardiac output as the left - about 5 L/min at rest - but against a mean pulmonary artery pressure of only about 14 mmHg (normal is roughly 14 plus or minus 3, and 20 mmHg or less is taken as the upper limit of normal). Its free wall is only a few millimetres thick and crescentic in cross-section: it is built to eject volume at low pressure, not to generate pressure. An unprepared right ventricle can acutely raise mean pulmonary artery pressure to only about 40 mmHg (systolic of the order of 50 to 60) before it dilates and fails; a ventricle hypertrophied over months can generate considerably more.

The bed is enormously compliant and much of it is unrecruited at rest, particularly at the lung apices where alveolar pressure can exceed capillary pressure. On exercise, closed capillaries open and open ones widen (recruitment and distension), so pulmonary vascular resistance - normally of the order of 1 Wood unit, against about 15 for the systemic circulation - falls further, and flow can rise threefold or more for only a small rise in pressure.

Pulmonary arterioles do the opposite of systemic ones: a fall in ALVEOLAR oxygen tension (not arterial) makes them constrict. Hypoxic pulmonary vasoconstriction begins as alveolar PO2 falls below roughly 70 mmHg and becomes marked below about 60; the sensor is in the smooth muscle itself, where hypoxia inhibits voltage-gated potassium channels, depolarising the cell and opening L-type calcium channels. Blood is pushed away from poorly ventilated alveoli toward well-ventilated ones.

What goes wrong

Pulmonary embolism (PE)Cor pulmonale from chronic hypoxic lung diseasePulmonary arterial hypertension (group 1)Pulmonary congestion, pulmonary oedema and post-capillary pulmonary hypertension from left heart disease

What we give

Anticoagulants - direct oral anticoagulants (apixaban, rivaroxaban), low molecular weight heparin (enoxaparin), warfarinThrombolytic - alteplase (recombinant tissue plasminogen activator)OxygenPulmonary vasodilators - phosphodiesterase-5 inhibitors (sildenafil, tadalafil), endothelin receptor antagonists (macitentan, ambrisentan; bosentan, the older agent), prostacyclin pathway agents (inhaled iloprost, intravenous epoprostenol) and the soluble guanylate cyclase stimulator riociguatLoop diuretic - furosemide (still written and spoken as frusemide in Australia)

The thin-walled collecting chamber that takes oxygenated blood from the pulmonary veins (usually four) and hands it through the mitral valve to the left ventricle.

What it 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.

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.

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).

What goes wrong

Mitral stenosis (in Australia, usually rheumatic)Mitral regurgitationAtrial fibrillationAcute decompensation on losing the atrial kickLeft atrial appendage thrombus and cardioembolic strokePulmonary congestion and secondary (post-capillary) pulmonary hypertension

What we give

AV nodal rate control: beta blockers (metoprolol, bisoprolol; atenolol is renally cleared and less favoured) and, as an alternative, the non-dihydropyridine calcium channel blockers verapamil and diltiazemDigoxinDirect oral anticoagulants (apixaban, rivaroxaban, dabigatran)Warfarin (vitamin K antagonist)Rhythm control antiarrhythmics (flecainide, sotalol, amiodarone)Loop diuretics (furosemide, still commonly written and spoken as frusemide in Australia)

The one-way door between the left atrium and the left ventricle: it opens wide in diastole to let the ventricle fill, and seals shut in systole so that the whole stroke volume goes forward to the aorta.

What it does

Two leaflets — a tall anterior leaflet and a broader, scalloped posterior one — coapt to seal the atrioventricular opening throughout systole. The left ventricle generates around 120 mmHg while the left atrium stays near 10 mmHg, so any gap in that seal drives blood backwards down a gradient of roughly 100 mmHg. That gradient exists from the first moment of ventricular contraction to the last, which is why a leaking mitral valve gives a murmur that occupies the whole of systole.

In diastole the orifice opens to roughly 4–6 cm² in an adult, and the ventricle fills largely passively at a mean left atrial pressure of only about 8–12 mmHg, with atrial contraction adding the last fifth or so of filling volume. Forward flow across the valve happens only in diastole — systole is spent with the valve shut.

The leaflets are tethered by chordae tendineae to two papillary muscles that contract with the ventricle and stop the leaflets everting into the atrium. The posteromedial papillary muscle is usually supplied by a single artery (the posterior descending, most often from the right coronary); the anterolateral muscle has a dual supply.

What goes wrong

Acute rheumatic fever and rheumatic heart diseaseMitral stenosisChronic mitral regurgitationAcute mitral regurgitationMitral valve prolapse

What we give

Long-acting intramuscular penicillin — benzathine benzylpenicillinRate-limiting drugs — beta blockers (metoprolol, bisoprolol, atenolol), non-dihydropyridine calcium channel blockers (verapamil, diltiazem), digoxinLoop diuretic — furosemide (the Australian Approved Name since harmonisation, still widely written and spoken as frusemide)Anticoagulant — warfarinAfterload reduction — sodium nitroprusside or a glyceryl trinitrate infusion acutely, ACE inhibitors (perindopril, ramipril) chronically

The thick-walled pressure pump: it fills with oxygenated blood from the left atrium and squeezes hard enough to drive that blood around the entire body.

What it does

Its wall is two to three times thicker than the right ventricle's — roughly 6 to 10 mm at end-diastole, against an RV free wall of 3 to 5 mm — because it ejects into a high-pressure circuit. The aortic valve opens once left ventricular pressure climbs above aortic diastolic pressure, about 80 mmHg, and ventricular pressure then peaks around 120 mmHg in ejection; the right ventricle opens its valve at a pulmonary artery diastolic pressure of about 10 mmHg and peaks at only about 25 mmHg. Built for pressure, the left ventricle answers a pressure load by thickening its wall and a volume load by dilating its cavity.

It holds about 120 mL at end-diastole and ejects about 70 mL of that each beat. The fraction it ejects (ejection fraction, EF) is normally about 55 to 70%, and it is a ratio, not a volume — a big floppy ventricle can eject a near-normal volume with a poor fraction, and a small stiff one can eject a small volume with a high fraction.

Filling is active work, not passive dropping-in: the muscle has to relax and untwist, which consumes ATP, and it can only happen in diastole. Left ventricular myocardium is also perfused almost entirely in diastole, when the muscle is relaxed and not squeezing its own vessels. Anything that stiffens the muscle or shortens diastole (a fast heart rate) therefore cuts both filling and coronary supply, and roughly a fifth to a quarter of end-diastolic volume in a stiff ventricle comes from atrial contraction.

What goes wrong

Thickened wall from pressure overload (concentric hypertrophy)Failure to fill (diastolic heart failure, HFpEF)Failure to empty with a dilated chamber (systolic heart failure, HFrEF)The neurohormonal vicious cycleAngina with a thick ventricle

What we give

ACE inhibitors (perindopril, ramipril) or angiotensin receptor blockers (candesartan, irbesartan) where cough prevents an ACE inhibitor; in Australia the angiotensin receptor-neprilysin inhibitor sacubitril/valsartan is PBS-listed as the alternative to an ACE inhibitor or ARB in symptomatic HFrEFBeta blockers with mortality evidence in heart failure (bisoprolol, carvedilol, metoprolol controlled-release, nebivolol in older patients) — the benefit is not assumed to be shared by every beta blockerMineralocorticoid receptor antagonists (spironolactone, eplerenone)SGLT2 inhibitors (dapagliflozin, empagliflozin)Loop diuretics (furosemide — still labelled frusemide on some older Australian packaging)

The one-way door at the exit of the left ventricle: it opens in systole to let the whole left ventricular output into the aorta, and shuts in diastole so that blood does not fall back into the ventricle.

What it does

Three thin cusps open to roughly 3 to 4 cm² in an adult — a door wide enough that blood crosses it with almost no resistance, so left ventricular and aortic pressure during ejection are within a few mmHg of each other.

It shuts at the start of diastole, when aortic pressure exceeds the falling ventricular pressure. That closure is the first and normally the louder component of the second heart sound (A2), and it is what holds the column of blood up in the aorta through diastole.

The coronary ostia open from the right and left aortic sinuses, above the cusp attachments, and left ventricular myocardium is perfused almost entirely in diastole, when the muscle is relaxed and the shut valve is holding aortic pressure up. Left coronary flow therefore tracks aortic diastolic pressure much more closely than systolic — the thinner-walled right ventricle, at far lower wall tension, keeps some perfusion through systole.

What goes wrong

Aortic stenosisChronic aortic regurgitationAcute severe aortic regurgitationBicuspid aortic valveRheumatic aortic valve disease

What we give

Nitrates (glyceryl trinitrate, isosorbide mononitrate)ACE inhibitors and angiotensin receptor blockers (perindopril, ramipril; candesartan, irbesartan)Loop diuretics (furosemide — the Australian Approved Name since harmonisation, though the older name frusemide is still heard and written)Beta blockers (metoprolol, bisoprolol; atenolol is the agent used in the Marfan trials)Benzathine benzylpenicillin (long-acting intramuscular penicillin)

The aorta is an elastic bag that catches each stroke of blood and pushes it out again between beats; the arteries beyond it are muscular taps that set how hard the heart has to push.

What it does

The aorta stretches in systole and recoils in diastole (the Windkessel effect). That recoil is what drives blood forward between beats, so organs get a fairly steady stream instead of squirts. The difference between systolic and diastolic pressure is the pulse pressure, normally around 40 mmHg. Diastolic pressure matters most to the left coronary bed: the contracting myocardium squeezes its intramural branches shut in systole, so the left ventricular myocardium is perfused mainly in diastole, off that recoil pressure. The right coronary artery, running over a lower-pressure right ventricle, is perfused through both phases.

The small arteries and arterioles are the resistance vessels. Their smooth muscle constricts to noradrenaline (alpha-1 receptors) and to angiotensin II (AT1 receptors), and sustained constriction depends chiefly on calcium entering through L-type calcium channels (with a smaller contribution from calcium released inside the cell and from rho-kinase sensitising the machinery to whatever calcium is present). To a good approximation mean arterial pressure = cardiac output x systemic vascular resistance (strictly, mean arterial minus right atrial pressure), so tone in these vessels is most of what sets blood pressure.

The inner lining (endothelium) is a single cell layer that resists platelet adhesion, releases nitric oxide to relax the muscle underneath, and forms a barrier that limits how much LDL cholesterol enters the wall. Some LDL crosses even a healthy endothelium; injury raises how much gets in and how long it stays.

What goes wrong

Hypertension from raised arteriolar toneStiff aorta and wide pulse pressure (isolated systolic hypertension)AtherosclerosisAbdominal aortic aneurysmAortic dissection

What we give

ACE inhibitors, and angiotensin receptor blockers (sartans) if a cough developsDihydropyridine calcium channel blockersStatinsAntiplatelet drugsIntravenous beta blockade in acute aortic dissection

Veins are the body's blood reservoir and its return road - they store most of the circulating volume at low pressure and, with the help of one-way valves and the calf muscles, push it back uphill to the right side of the heart.

What it does

Veins are thin-walled and distensible, and the systemic venous system holds roughly two thirds of the total blood volume at low pressure (capacitance vessels). Their smooth muscle, under sympathetic alpha-1 control, can tighten and squeeze that reserve back towards the heart, so venous tone, circulating volume and the skeletal muscle pump together set venous return - and over any sustained period the heart can only eject what is returned to it.

Standing turns the veins below the heart into a hydrostatic column. The vertical distance from right atrium to ankle in an adult is a little over a metre, so quiet standing puts an ankle venous pressure of roughly 80 to 90 mmHg on the leg veins. Contracting the calf empties the deep veins upward and the one-way valves stop the blood falling back, so within a few steps ambulatory ankle venous pressure falls to about 20 to 30 mmHg. The calf muscle pump is effectively a second heart.

Venous return runs on a tiny pressure gradient: roughly 12 to 18 mmHg in the venules, about 8 to 10 mmHg in the large peripheral veins, down to a mean right atrial pressure of about 0 to 5 mmHg. Flow is therefore slow and easily stalled, and it depends on external help - the muscle pump, the valves, and the fall in intrathoracic pressure with inspiration.

What goes wrong

Orthostatic (postural) hypotensionDeep vein thrombosisPulmonary embolismVaricose veinsChronic venous insufficiency and venous ulceration

What we give

Low molecular weight heparin (enoxaparin)Direct oral anticoagulants (apixaban, rivaroxaban)WarfarinNitrates (glyceryl trinitrate)

Two arteries leaving the aorta just above the aortic valve, each supplying a fixed patch of heart muscle, and filling the left ventricle mainly while the heart is relaxed.

What it does

The left main and right coronary arteries arise from the aortic sinuses immediately above the aortic valve cusps, and each supplies a territory that is fairly constant between people. The left main divides into the left anterior descending (anterior wall, interventricular septum, apex) and the circumflex (lateral wall); in a minority there is also a ramus intermedius. The right coronary supplies the right ventricle, and in the roughly 85% of people who are right dominant it also gives the posterior descending artery to the inferior wall; in the remaining left dominant or codominant hearts the inferior wall comes from the circumflex. The AV nodal artery arises from the right coronary in about 80 to 90% of people, and the sinus node artery in around 60%. Because territories are fairly fixed, the ECG lead groups map onto vessels: II, III and aVF inferior (usually right coronary), V1 to V4 septal and anterior (left anterior descending), I, aVL, V5 and V6 lateral (usually circumflex, with V5 to V6 sometimes fed by a long left anterior descending).

The left ventricle is perfused predominantly in diastole. Contracting muscle compresses the intramural vessels during systole, so wall flow occurs mainly between beats, driven by the coronary perfusion pressure, which is aortic diastolic pressure minus left ventricular end-diastolic pressure. The right ventricle, whose wall tension is far lower, is perfused throughout the cardiac cycle.

Cardiac muscle extracts about 70% of the oxygen delivered to it even at rest, far more than most tissues, so there is very little extraction reserve. Increasing myocardial oxygen supply therefore depends mainly on increasing flow, which can rise roughly four to five-fold from rest in a healthy adult (coronary flow reserve); the other lever is the oxygen content of the blood, so anaemia or hypoxaemia removes supply that flow alone cannot make up.

What goes wrong

Stable anginaAcute coronary syndrome without ST elevation (unstable angina and NSTEMI)ST elevation myocardial infarction (STEMI)Inferior infarction with heart block or right ventricular involvementIschaemia with unobstructed arteries (demand ischaemia, type 2 myocardial infarction)

What we give

Nitrates (glyceryl trinitrate sublingual spray or tablet for attacks; isosorbide mononitrate for prevention)Beta blockers (metoprolol, bisoprolol, carvedilol, atenolol)Antiplatelets (aspirin, plus a P2Y12 inhibitor: ticagrelor, clopidogrel or prasugrel)Statins (atorvastatin, rosuvastatin)Dihydropyridine calcium channel blockers (amlodipine, felodipine)

The heart muscle itself: the layer that converts an electrical signal into a squeeze, and so decides how much blood leaves the heart with every beat.

What it does

Contraction is calcium-driven. Depolarisation opens L-type calcium channels in the T-tubules; that small trickle of calcium opens the ryanodine receptors (RyR2) on the sarcoplasmic reticulum, releasing the much larger internal store (calcium-induced calcium release), and that calcium binds troponin C so actin and myosin can cycle. How hard the heart squeezes comes down to how much calcium reaches troponin C — this is excitation-contraction coupling.

Relaxation is active and costs ATP. SERCA pumps calcium back into the sarcoplasmic reticulum and the sodium-calcium exchanger extrudes the remainder from the cell; only when cytosolic calcium falls do the cross-bridges let go and the ventricle fill. A myocyte short of ATP cannot let go any better than it can pull, so a stiff ventricle and a weak one can share the same energy problem.

The myocardium already extracts roughly 70% of the oxygen from the blood passing through it at rest, close to the practical ceiling, so extra demand is met mainly by increasing coronary flow rather than by extracting more. The left ventricle is perfused almost entirely in diastole, because in systole its own contraction compresses its intramural arteries. Anything that shortens diastole (a fast heart rate) therefore cuts its own supply.

What goes wrong

Stable anginaMyocardial infarctionHeart failure with reduced ejection fractionHeart failure with preserved ejection fraction (the stiff ventricle)Hypertrophic cardiomyopathy

What we give

Beta blockers (bisoprolol, carvedilol, metoprolol, nebivolol)Nitrates (glyceryl trinitrate, isosorbide mononitrate)ACE inhibitors (perindopril, ramipril) — or, in heart failure with reduced ejection fraction, sacubitril with valsartan (an ARNI)Mineralocorticoid receptor antagonists (spironolactone, eplerenone)Digoxin

A tough double-layered bag around the heart with a film of fluid inside it: it lets the heart slide as it beats, and it sets a ceiling on how full the heart can get.

What it does

The heart sits in a stiff outer fibrous sac lined by a serous membrane that folds back over the heart itself, so a film of clear straw-coloured fluid — roughly 15 to 50 mL — lies between the parietal and visceral (epicardial) serous layers. The fibrous layer will not stretch acutely, but it does stretch over weeks to months.

Because the sac barely stretches acutely, it restrains filling of both ventricles at end-diastole, and the two ventricles share one fixed space, so when one fills more the other must fill less (ventricular interdependence). In health this restraint is slack, and the small inspiratory fall in systolic pressure — normally under about 10 mmHg — comes mainly from blood pooling in the expanded pulmonary vessels and from more negative intrathoracic pressure raising left ventricular transmural afterload, rather than from septal shift.

The two serous surfaces are wet and slippery, so they glide over each other with every beat and make no sound.

What goes wrong

Acute pericarditisPericardial effusionCardiac tamponadeConstrictive pericarditis

What we give

Non-steroidal anti-inflammatory drugs (ibuprofen, or aspirin at anti-inflammatory doses)ColchicineCorticosteroids (prednisolone)Intravenous fluid (sodium chloride 0.9%)Loop diuretics (furosemide, still written frusemide on many Australian charts)

A small patch of self-firing cells at the junction of the superior vena cava and right atrium that depolarises on its own and, under normal conditions, faster than the tissue below it — so it sets the rate for every beat.

What it does

The node sits at the junction of the superior vena cava and the right atrium, at the top of the crista terminalis. Depolarisation spreads from there inferiorly and leftwards across the atria, which is why a sinus P wave is upright in leads II, III and aVF and precedes each QRS at a fixed interval.

Nodal cells have no stable resting potential to sit at. From a maximum diastolic potential of roughly -60 mV a slow inward current (the funny current, I_f, flowing through HCN channels and carried by mixed sodium and potassium movement, net sodium in) drifts them up to threshold, and L-type calcium current then carries the upstroke — so the heart beats with no instruction from the brain. Neither current is exclusive to the node: L-type calcium channels also run the AV node, the working myocardium and vascular smooth muscle, and HCN channels are found in the AV node, conducting tissue, neurons and the retina. Rhythmic calcium release from the sarcoplasmic reticulum contributes to the drift as well.

Under normal conditions the node fires faster than the tissue below it, so it captures the heart and everything downstream follows. Below it sits a hierarchy of slower back-ups: the AV junction around 40 to 60 a minute, the ventricle around 20 to 40. Being driven from above holds those back-ups quiet (overdrive suppression), so they take several seconds to wake once the drive stops. The hierarchy is only a default — a faster ectopic focus or a re-entrant circuit can and does take over.

What goes wrong

Sinus tachycardiaSinus bradycardiaSick sinus syndrome (sinus node dysfunction)Tachy-brady syndromeDrug-induced bradycardiaBradycardia complicating inferior myocardial infarction

What we give

AtropineBeta blockers (metoprolol, bisoprolol, atenolol; carvedilol and nebivolol also used)Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)IvabradineChronotropic infusions (adrenaline, isoprenaline)Digoxin

The electrical gate between atria and ventricles — normally the only route through the insulating fibrous skeleton — which holds each beat up for a fraction of a second and then hands it to a fast wiring system that makes both ventricles squeeze together.

What it does

The atria and ventricles are electrically insulated from each other by the fibrous ring of the cardiac skeleton, and in a normally formed heart the AV node is the only route across it. The node is richly supplied by both limbs of the autonomic nervous system: vagal tone slows conduction through it and lengthens its refractory period, sympathetic tone speeds conduction up. Note what this gate does and does not control — the sinus node sets the heart rate; autonomic tone at the AV node sets how readily impulses get across to the ventricles, which becomes the rate-determining step when the atria are firing very fast. Its blood supply comes from the AV nodal artery, a branch of the right coronary artery in most people (right dominance, roughly 85 to 90 per cent).

Nodal cells depolarise using calcium rather than sodium, so conduction through the node is slow — roughly 0.1 second. That nodal delay is the largest part of the PR interval (normally 120 to 200 ms, which also contains atrial depolarisation and conduction through the His-Purkinje system). The delay lets the atria finish topping up the ventricles (the atrial kick), and it makes the node a decremental filter: bombard it faster and it blocks more impulses instead of passing them on. In many people the node is functionally split into a fast limb and a slow limb with different conduction speeds and different recovery times.

Below the node the wiring is fast: the bundle of His splits into a right and a left bundle branch, and Purkinje fibres spread the impulse through both ventricles in under 120 ms — the narrow QRS. Both ventricles contract as one coordinated squeeze from the apex up.

What goes wrong

Slow conduction through the node (first degree block and Mobitz I second degree block)Block below the node (Mobitz II and complete heart block)Bundle branch blockAV nodal re-entrant tachycardia (AVNRT)Accessory pathway tachycardia (AVRT, Wolff-Parkinson-White)Atrial fibrillation with a rapid ventricular response (the node as filter)

What we give

Beta blockers (metoprolol, bisoprolol, atenolol)Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)AdenosineDigoxinAtropine