Tricuspid valve
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 normally 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.
when the valve does not shut, ventricular systolic pressure is delivered straight back into the atrium and the great veins — which is why tricuspid regurgitation shows itself in the neck, the liver, the legs and the belly rather than in the lungs.
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.
dilating the right ventricle (or, in long-standing atrial fibrillation, the right atrium) stretches the annulus and pulls the papillary muscles apart, so structurally normal leaflets stop meeting — functional regurgitation, where the fault is in the chamber rather than in the valve.
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.
a leaking tricuspid valve converts that small v ripple into a large wave that rises with the carotid pulse instead of before it — the giant v wave — and the same transmitted pressure makes the liver pulsate.
Almost all systemic venous blood crosses this valve before it reaches the lung's filter. The exceptions are small and worth naming: bronchial veins that drain into pulmonary veins, thebesian veins emptying directly into the cardiac chambers, and any right-to-left shunt such as a patent foramen ovale. Anything injected into a peripheral vein — bacteria, particles, injection adulterants — reaches the right heart before it reaches any arterial bed.
the tricuspid valve is the first valve exposed to whatever is injected, and material that breaks off it embolises to the lungs rather than to the brain or limbs — unless a right-to-left shunt lets it cross, which is the one situation where right-sided endocarditis produces systemic emboli.
The leaflets are thin, largely avascular sheets of collagen covered by valvular endothelium. Inflamed valve tissue heals by fibrosis, not by regeneration.
immune valvulitis leaves permanent thickening, fusion at the commissures and leaflet retraction, so a scarred valve neither opens fully nor closes fully — and every recurrence adds more scar.
In a heart without a septal defect the tricuspid orifice is the only route from right atrium to right ventricle, so every transvenous pacing or defibrillator lead must pass between the leaflets and then lie among the chordae.
a lead can pin, tether, entangle or perforate a leaflet, or become encased in fibrous tissue over time, so the valve stops closing cleanly months to years after implantation.
What goes wrong
- Tricuspid regurgitation — the valve leaks backwards← from “It is not a stiff ring. Three thin leaflets ar…”
In most cases the leaflets are normal and the chamber is the problem. Pulmonary pressure rises (left heart failure, chronic lung disease, pulmonary embolism, pulmonary hypertension of any cause), the right ventricle dilates to cope, the annulus stretches and the papillary muscles are displaced, and the leaflets can no longer meet. Long-standing atrial fibrillation can do the same thing from the atrial side. Every systole a jet is then fired back into the right atrium (functional regurgitation), and the extra volume dilates the right heart further — regurgitation begets regurgitation. Primary leaflet disease (endocarditis, rheumatic scarring, a device lead, carcinoid, Ebstein anomaly) is the less common route to the same end point.
Functional, not structural, in most patients — treat the cause of the dilated right ventricle, not the valve. Giant v wave synchronous with the carotid, pulsatile liver, pansystolic murmur at the lower left sternal edge louder on inspiration; a quiet murmur does not mean a mild leak. Echocardiography sizes the leak and estimates pulmonary pressure from the regurgitant jet velocity.
You would find: A giant v wave: the systolic pressure of the ventricle is transmitted to the neck, so a large wave in the JVP rises with the carotid pulse. The liver becomes enlarged and pulsatile, the legs swell, the belly fills with fluid. The murmur is a soft pansystolic sound at the lower left sternal edge that gets LOUDER on inspiration (Carvallo sign) — inspiration draws more blood into the right heart. Loudness tracks turbulence, not leak size: a severe, wide-open leak can be nearly silent.
- Right-sided infective endocarditis in people who inject drugs← from “Almost all systemic venous blood crosses this …”
Bacteria injected into a peripheral vein — most often Staphylococcus aureus carried on skin — reach the tricuspid valve before any lung or arterial filter. S. aureus can adhere to undamaged valve endothelium, which is why right-sided endocarditis often occurs on a previously normal valve. Platelets and fibrin pile on the adherent organisms and a vegetation grows, destroying leaflet and chordal tissue and producing acute severe regurgitation. Fragments break off and follow the flow: to the lungs, as septic pulmonary emboli.
Fever plus injecting drug use equals endocarditis until disproven; S. aureus on a normal tricuspid valve. Septic pulmonary emboli, not stroke. Multiple separate sets of blood cultures before antibiotics, then echocardiography — transthoracic imaging visualises tricuspid vegetations reasonably well, transoesophageal if the images are poor or prosthetic material is present. Diagnosis is by the modified Duke criteria; prognosis is better than for left-sided disease.
You would find: Fever, sweats and feeling awful, often with needle marks. The heart may sound normal — a murmur is absent in a large minority, so do not wait for one. Look for pleuritic chest pain, breathlessness and haemoptysis, and a chest X-ray with multiple peripheral nodules, some cavitating. Because the emboli go to the lungs, the strokes and splinter haemorrhages of left-sided disease are usually absent — their absence never excludes endocarditis, and their presence should make you look for a left-sided lesion or a right-to-left shunt as well. Blood cultures first, then echocardiography.
- Rheumatic tricuspid disease — stenosis and regurgitation together← from “The leaflets are thin, largely avascular sheet…”
After acute rheumatic fever, the cross-reactive immune response to group A streptococcus scars valve tissue. Leaflets thicken, fuse at their commissures and shorten. A fused valve will not open fully (stenosis), so the right atrium struggles to empty and its pressure rises; a shortened, retracted valve will not close either, so it leaks as well. Rheumatic tricuspid disease is virtually always accompanied by mitral disease — isolated rheumatic tricuspid involvement is rare.
Mixed stenosis and regurgitation, essentially never without mitral disease. Systemic congestion with clear lungs is the giveaway — tricuspid stenosis protects the lungs and can mask a mitral lesion, so it is easy to miss until the mitral valve is fixed. Prominent a wave in sinus rhythm, gone in AF. Acute rheumatic fever and rheumatic heart disease are notifiable in the Australian jurisdictions running register-based control programs, and the register is what delivers prophylaxis.
You would find: High JVP, big liver, ascites and swollen legs with lungs that stay surprisingly clear — the tricuspid narrowing limits flow into the right ventricle, so it shields the lungs from the pulmonary congestion the accompanying mitral lesion would otherwise cause. In sinus rhythm the a wave is prominent as the atrium strains against a narrowed valve; rheumatic disease often brings atrial fibrillation, and then there is no a wave at all, so its absence does not argue against the diagnosis. Soft diastolic murmur at the lower left sternal edge, louder on inspiration, usually drowned out by the mitral lesion. In Australia this sits overwhelmingly with Aboriginal and Torres Strait Islander people: ask about acute rheumatic fever in childhood and about penicillin injections.
- Pacemaker or defibrillator lead across the valve← from “In a heart without a septal defect the tricusp…”
The lead is threaded through the tricuspid orifice into the right ventricle. It can pin or tether a leaflet, become entangled in chordae, perforate a leaflet, or be encased in fibrous tissue over the years, so the valve no longer closes cleanly. Right ventricular pacing can also dyssynchronise and dilate the ventricle, adding a functional component on top.
Consider lead-related tricuspid regurgitation in anyone with a device and new right-sided congestion. Transthoracic echo can under-call it; the mechanism is best defined on transoesophageal or 3D imaging. Relevant to device choice — it is one of the arguments for leadless or coronary-sinus approaches when tricuspid function is already marginal.
You would find: New or worsening right heart failure — rising JVP, oedema, big tender liver — in the months to years after a device is implanted. Easy to blame on age or lung disease; look at the neck and remember the lead.
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.
- Binds
- The Na⁺/K⁺/2Cl⁻ cotransporter (NKCC2) on the luminal membrane of thick ascending limb cells. The drug is protein-bound in plasma and reaches that luminal surface by being secreted into the proximal tubule by organic anion transporters, not by filtration.
- Which does
- Sodium, potassium and chloride reabsorption in the thick ascending limb is blocked, which abolishes both the medullary concentrating gradient and the lumen-positive potential that normally drives paracellular calcium and magnesium reabsorption.
- So you see
- A large diuresis and natriuresis; venous filling pressure falls, so the JVP drops, peripheral oedema and ascites recede and the congested liver decompresses.
- And the same mechanism causes
- Everything follows from blocking NKCC2: hypovolaemia and prerenal kidney injury from over-diuresis, hypokalaemia and metabolic alkalosis from the extra sodium delivered distally being exchanged for potassium and hydrogen ions, and hypomagnesaemia and hypocalcaemia from the loss of the paracellular driving force. The same transporter family (NKCC1) in the stria vascularis of the inner ear explains dose-related tinnitus and hearing loss with rapid high-dose intravenous use.
- Handling
- In right heart failure the gut wall itself is oedematous and oral absorption is erratic, so an intravenous route is often needed to get a response in a patient who appeared resistant to tablets — that is a change in route, not a failure of the drug. Because it is secreted into the tubule, it also works poorly when renal perfusion is very low.
Catches people out: It treats the flood, not the leak. A failing right ventricle is preload-dependent, so diuresing too hard drops cardiac output — blood pressure falls and creatinine rises. Daily weights and a look at the JVP are the practical measures of response.
- Binds
- The intracellular mineralocorticoid receptor of principal cells in the late distal tubule and collecting duct — a nuclear hormone receptor, not a membrane channel. Spironolactone is a competitive antagonist there; it also binds androgen and progesterone receptors, which is off-target.
- Which does
- Aldosterone-driven transcription of epithelial sodium channels and the Na⁺/K⁺-ATPase is prevented, so principal cells reabsorb less sodium; the lumen-negative potential that normally drives potassium and hydrogen ion secretion falls with it.
- So you see
- A modest additional natriuresis with potassium retained rather than lost, so congestion and ascites settle without the potassium wasting the loop diuretic causes; in left ventricular systolic dysfunction, blocking the receptor also reduces myocardial and vascular fibrosis.
- And the same mechanism causes
- Hyperkalaemia follows directly from blocking the receptor that drives potassium secretion, and the same loss of hydrogen ion secretion can produce a mild hyperchloraemic metabolic acidosis. Gynaecomastia, breast tenderness and menstrual disturbance follow from the off-target androgen and progesterone receptor binding of this steroid molecule — eplerenone, a selective blocker, largely avoids that but not the hyperkalaemia.
- Handling
- The antifibrotic benefit takes weeks and is not the reason for the day-to-day dose changes; the diuretic effect is modest on its own, which is why it is added to a loop diuretic and not substituted for it.
Catches people out: Potassium-sparing. Combined with an ACE inhibitor, an angiotensin receptor blocker or impaired kidneys it causes dangerous hyperkalaemia — electrolytes and creatinine are checked after starting and after each dose change.
- Binds
- Bacterial penicillin-binding proteins (the transpeptidases that cross-link peptidoglycan) in the staphylococcal cell wall. There is no human target. Its bulky side chain resists staphylococcal beta-lactamase, which is what makes it antistaphylococcal.
- Which does
- Cell wall cross-linking stops while autolysins keep working, so dividing organisms lyse. It is bactericidal but only against organisms that are actively building wall, which is part of why deep-seated vegetations take weeks.
- So you see
- The vegetation is progressively sterilised, fevers settle and blood cultures clear — though the leaflet damage already done does not reverse.
- And the same mechanism causes
- Because the target is bacterial, direct toxicity is limited; killing off wall-building commensals as well is what produces antibiotic-associated diarrhoea and Clostridioides difficile colitis, and weeks of intravenous access bring their own line infections. Two further effects are immune rather than mechanistic and still matter: beta-lactam hypersensitivity from rash to anaphylaxis, and flucloxacillin's characteristic delayed cholestatic hepatitis, commoner with prolonged courses and in older patients.
- Handling
- It is inactive against MRSA, where an altered binding protein (PBP2a) simply does not bind beta-lactams — so the choice turns on the susceptibility result, and empirical cover is broadened only while that is unknown.
Catches people out: At least two, preferably three, separate sets of blood cultures are taken from separate venepunctures before the first dose — one early dose can blind the diagnosis for days. The exception is the septic, unstable patient: take what cultures you can and give the antibiotic without delay.
- Binds
- Not an enzyme — it binds the D-alanyl-D-alanine terminus of the peptidoglycan precursor itself, the substrate rather than the transpeptidase.
- Which does
- With the precursor capped, the transglycosylation and cross-linking steps of wall assembly cannot proceed, so the cell wall cannot be extended. It is a large, polar molecule that cannot cross the Gram-negative outer membrane, so its spectrum is Gram-positive only.
- So you see
- Staphylococcal killing including MRSA, but slowly — which is why clearance of bacteraemia takes longer than with a beta-lactam.
- And the same mechanism causes
- Accumulation in proximal tubular cells causes dose- and exposure-related nephrotoxicity, which is precisely what the level monitoring exists to prevent, and it compounds any prerenal insult from aggressive diuresis. Infusing the molecule too quickly triggers non-immune mast cell degranulation — the flushing reaction over the upper body, rate-related and not a true allergy.
- Handling
- It is not absorbed orally for a systemic effect, so it must be given intravenously here. Australian practice dose-adjusts against measured levels using AUC-guided monitoring, together with renal function, because clearance is entirely renal.
Catches people out: For methicillin-susceptible S. aureus, vancomycin is inferior to flucloxacillin — it is a holding agent, and treatment is stepped back to the penicillin once susceptibility is confirmed.
- Binds
- Penicillin-binding proteins (transpeptidases) in the group A streptococcal cell wall — no human target.
- Which does
- Peptidoglycan cross-linking is blocked and autolysins are left unopposed, so dividing streptococci lyse. Group A streptococcus has remained reliably penicillin-susceptible, so there is no resistance argument for a broader agent.
- So you see
- Streptococcal pharyngitis and skin infection are treated or prevented, so recurrent acute rheumatic fever — and the further valve scarring each episode leaves — does not happen. It is the only intervention that alters the valve's trajectory; it does not reverse scarring already present.
- And the same mechanism causes
- With a purely bacterial target, systemic toxicity is minimal; the mechanism-linked problem is the depot itself — a viscous suspension that makes the injection genuinely painful, the single biggest driver of missed doses and so of prophylaxis failure. Immune recognition of the beta-lactam gives rash through to anaphylaxis, which is why a reported penicillin allergy is properly evaluated rather than assumed before abandoning the one drug that protects the valve.
- Handling
- The benzathine salt is a depot: it dissolves slowly from the injection site and holds a low sustained penicillin concentration, which is what allows dosing measured in weeks. It is given deep intramuscularly and never intravenously.
Catches people out: The injection hurts and adherence is the whole game — every missed dose is a chance at another attack. Australian practice (RHDAustralia and Therapeutic Guidelines) gives it 4-weekly, with lignocaine as diluent to reduce injection pain, and continues it far longer than older overseas figures: after acute rheumatic fever without resulting rheumatic heart disease, a minimum of 10 years from the most recent episode or until age 21, whichever is longer, extending with the severity of established disease. This is core practice with Aboriginal and Torres Strait Islander communities, where rheumatic heart disease rates are among the highest in the world, and delivery runs through jurisdictional registers.
A big wave in the neck that rises with the carotid pulse, plus a liver that pushes your hand with every beat, is tricuspid regurgitation until proven otherwise — the giant v wave. Add fever and injecting drug use and think right-sided endocarditis: the chest X-ray (multiple peripheral nodules, some cavitating) often shouts louder than the murmur, which is soft or absent in a large minority. And systemic congestion with clear lungs points upstream of the lungs — tricuspid stenosis, rheumatic until proven otherwise, and never alone.
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