Right ventricle
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 normally 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.
Explains why an acute rise in pulmonary pressure (pulmonary embolism) or a chronic one (left heart failure, chronic lung disease) dilates and fails this ventricle, while extra volume alone is usually tolerated.
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.
Explains why the congestive signs of right heart failure — raised JVP, tender pulsatile liver, ascites, dependent oedema — appear together, and why the JVP is the first sign to look for when the right heart is suspected.
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.
Explains why preload-reducing drugs (glyceryl trinitrate, morphine, a diuretic) can cause abrupt hypotension when the right ventricle is the failing chamber, as in right ventricular infarction.
The two ventricles share an interventricular septum and one relatively non-compliant fibrous pericardium. If the right ventricle dilates acutely, the septum bows into the left ventricle and the pericardium limits outward expansion, so left ventricular filling falls (ventricular interdependence).
Explains why an acutely dilated right ventricle can drop systemic blood pressure and cardiac output even though the left ventricle itself is contracting normally.
In most people the right ventricular free wall is supplied by right ventricular (including acute marginal) branches arising from the right coronary artery relatively close to its origin, and the same artery supplies the inferior left ventricular wall in a right-dominant circulation.
Explains why a proximal right coronary occlusion infarcts right ventricular muscle alongside inferior left ventricular muscle, and why right ventricular infarction is looked for in every inferior STEMI.
The tricuspid leaflets hang from an annulus that is part of the right ventricle itself, and are tethered by chordae to right ventricular papillary muscles. Annular dilatation and leaflet tethering therefore track right ventricular size, although the valve can also be damaged in its own right (rheumatic disease, endocarditis, pacing leads, carcinoid).
Explains why a dilated right ventricle commonly develops secondary (functional) tricuspid regurgitation, which then worsens the volume load on the same ventricle.
What goes wrong
- Acute right ventricular failure from pulmonary embolism← from “The right ventricular free wall is thin — roug…”
Clot lodges in the pulmonary arteries and right ventricular afterload rises within seconds. A thin-walled volume pump that has had no time to hypertrophy cannot acutely generate a mean pulmonary artery pressure much above about 40 mmHg (systolic of roughly 50-60 mmHg), so it dilates rather than ejects. Less blood crosses the lungs, the bowing septum further limits left ventricular filling, and cardiac output and systemic blood pressure fall.
Breathless, hypoxaemic, raised JVP, clear chest — a previously normal right ventricle cannot acutely exceed a mean PAP of about 40 mmHg, so it dilates; a much higher pulmonary pressure implies a chronic, not acute, process.
You would find: Sudden breathlessness with a raised JVP and clear lung fields — congestion in the neck but little to hear in the chest. Tachycardia and hypoxaemia, sometimes hypotension. The ECG most often shows sinus tachycardia; right heart strain patterns (T wave inversion in V1-V4, right bundle branch block, S1Q3T3) are specific but insensitive.
- Right ventricular infarction← from “In most people the right ventricular free wall…”
Occlusion of the right coronary artery close to its origin cuts off the right ventricular branches. Right ventricular involvement is found in a substantial minority of inferior myocardial infarctions (commonly quoted as up to about a third to a half), although only around 10-15% are haemodynamically significant. The stunned right ventricle cannot move blood forward and, because its output runs on filling, anything that lowers venous return collapses that output further.
Hypotension + raised JVP + clear lungs after inferior STEMI = right ventricular infarction; get a right-sided ECG (V4R), and expect nitrates and diuretics to drop the pressure.
You would find: Inferior STEMI with hypotension, raised JVP and clear lungs. A right-sided ECG is the investigation to ask for: ST elevation in V4R (≥0.5 mm is the usual diagnostic threshold) supports it, but the change is transient and its absence does not exclude the diagnosis. The giveaway pattern is a blood pressure that falls after a preload-reducing drug such as glyceryl trinitrate or a diuretic. Physiologically this is a ventricle whose output depends on its filling, so management runs towards maintaining preload rather than offloading it — and even that is done cautiously, since over-filling an already dilated right ventricle worsens septal bowing and can reduce output further. Prescribing decisions belong to the treating team and the guidelines.
- Right heart failure caused by the left heart (the common cause)← from “The neck veins sit in a near-continuous column…”
A failing or stiff left ventricle raises left atrial pressure. That pressure is transmitted back through the pulmonary veins and lifts pulmonary artery pressure (post-capillary, group 2 pulmonary hypertension). The right ventricle now faces an afterload it is poorly built for, so it dilates and fails, and pressure rises in the systemic veins behind it.
The commonest cause of right heart failure is left heart failure — look for the left-sided cause before hunting for lung disease; track the response by daily weight.
You would find: The peripheral signs: raised JVP, pitting oedema of the ankles climbing up the legs (or over the sacrum in someone bed-bound), a tender enlarged liver, ascites, and a rising daily weight. Daily weight is a more reliable bedside measure of fluid on board than the appearance of the ankles.
- Chronic pulmonary hypertension and cor pulmonale← from “The right ventricular free wall is thin — roug…”
Chronic lung and breathing disorders — COPD, interstitial lung disease, obstructive sleep apnoea — leave alveolar oxygen low, either continuously or night after night. Pulmonary arterioles constrict in response (hypoxic pulmonary vasoconstriction), and with time the vessels remodel and part of the vascular bed is destroyed, so pulmonary vascular resistance stays high year after year. The right ventricle hypertrophies to cope with the pressure, then dilates and fails. Pulmonary arterial hypertension (group 1) causes the same right ventricular endpoint by primary disease of the pulmonary arteries themselves.
Hypoxia → sustained hypoxic pulmonary vasoconstriction and remodelling → pressure-loaded right ventricle; correcting the hypoxaemia, not vasodilating the lung, is the treatment in lung-disease (group 3) pulmonary hypertension.
You would find: A parasternal heave felt with the heel of the hand at the left sternal edge, a loud pulmonary component of the second heart sound, raised JVP and peripheral oedema in someone with known lung disease.
- Secondary (functional) tricuspid regurgitation from a dilated right ventricle← from “The tricuspid leaflets hang from an annulus th…”
Because the tricuspid annulus is part of the right ventricle, dilating the ventricle stretches the ring and tethers the leaflets, so they no longer coapt. Blood leaks back into the right atrium with each contraction, so the neck veins and liver take the force of ventricular systole, and the regurgitant volume adds further load to the same ventricle.
Functional tricuspid regurgitation is a marker of right ventricular dilatation, not usually a primary valve disease — giant v waves and a pulsatile liver; treat the ventricle and the cause.
You would find: Giant v waves in the JVP and a liver that pulses under the hand. A pansystolic murmur at the left sternal edge, louder on inspiration (Carvallo's sign). In Australia also consider rheumatic heart disease, which remains far more common in Aboriginal and Torres Strait Islander communities than in the rest of the population, and right-sided endocarditis in people who inject drugs.
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
- NKCC2 cotransporter in the thick ascending limb of the loop of Henle.
- Which does
- Blocking luminal sodium, potassium and chloride reabsorption abolishes the medullary concentration gradient, so water and salt are lost in the urine.
- So you see
- Diuresis with falling circulating volume and venous pressure, relieving the congestion behind the right ventricle — seen as falling weight, receding oedema and a lower JVP.
- And the same mechanism causes
- The same transport block delivers sodium distally and drives potassium and hydrogen loss — hypokalaemia with metabolic alkalosis, hypomagnesaemia and hyponatraemia — while excessive volume loss causes hypotension and prerenal kidney injury; the related NKCC1 in the inner ear explains ototoxicity with rapid high-dose intravenous use.
- Handling
- Gut wall oedema in decompensated right heart failure reduces oral absorption, which is why the intravenous route is used when a patient is congested and not responding — a decision for the treating team.
Catches people out: It empties the veins; it does not fix the pump. In a preload-dependent right ventricle (right ventricular infarction, pulmonary hypertension) over-diuresis drops cardiac output and blood pressure. Response is tracked by daily weight rather than by the look of the ankles.
- Binds
- Cytoplasmic mineralocorticoid receptor in distal nephron principal cells (spironolactone also binds androgen and progesterone receptors).
- Which does
- Prevents aldosterone-driven transcription of epithelial sodium channels and Na/K-ATPase, so sodium reabsorption and the potassium-secreting gradient both fall.
- So you see
- A modest, potassium-sparing natriuresis that adds to the loop diuretic and blunts the neurohormonal salt retention of heart failure.
- And the same mechanism causes
- Because potassium secretion depends on the same aldosterone-driven sodium reabsorption, blocking the receptor causes hyperkalaemia (and can cause a mild metabolic acidosis); spironolactone's off-target binding at androgen and progesterone receptors is what produces gynaecomastia, breast tenderness and menstrual disturbance, which eplerenone largely avoids.
Catches people out: Potassium rises. Combined with an ACE inhibitor or an angiotensin receptor blocker, and with impaired kidneys, that can be dangerous — electrolytes and creatinine are checked after starting and after any dose change.
- Binds
- Factor Xa (direct, for the oral agents) or antithrombin-mediated inhibition of factor Xa and thrombin (for the heparins).
- Which does
- Less thrombin is generated, so fibrin formation and clot propagation stop, leaving endogenous fibrinolysis to clear existing thrombus over weeks.
- So you see
- The pulmonary clot burden falls rather than grows, pulmonary vascular resistance settles and right ventricular afterload comes back down; recurrent embolism is prevented.
- And the same mechanism causes
- The same block on thrombin generation that stops the clot also prevents haemostasis anywhere else, so bleeding (gastrointestinal, intracranial, procedural) is the direct mechanistic adverse effect; heparins additionally carry immune heparin-induced thrombocytopenia.
- Handling
- Unfractionated heparin's short half-life and reversibility make it the choice when thrombolysis or a procedure may be needed; enoxaparin is renally cleared, and the direct oral agents have their own renal thresholds — all guideline-directed choices.
Catches people out: They prevent clot extension and new clot; they do not dissolve the clot already present. For high-risk (massive) pulmonary embolism with shock, Therapeutic Guidelines describes systemic thrombolysis with alteplase as the escalation — a specialist decision. Bleeding is the trade-off every time.
- Binds
- No receptor — it acts on alveolar and mixed venous oxygen tension, the stimulus for hypoxic pulmonary vasoconstriction.
- Which does
- Restoring alveolar PO2 relaxes the hypoxia-sensing pulmonary arteriolar smooth muscle, reducing pulmonary vascular tone.
- So you see
- Pulmonary artery pressure falls, right ventricular afterload eases, and in severe chronic hypoxaemia mortality is reduced with sustained daily use.
- And the same mechanism causes
- Releasing hypoxic pulmonary vasoconstriction also releases it in poorly ventilated lung units, worsening ventilation-perfusion matching; that, with the Haldane effect, raises PaCO2 in COPD — hypercapnia and CO2 narcosis follow directly from the mechanism being exploited.
- Handling
- Assessment for long-term oxygen is made when the patient is stable, not during an exacerbation, since hypoxaemia that resolves with recovery does not qualify.
Catches people out: In people at risk of carbon dioxide retention, COPD above all, Australian practice targets a saturation of 88-92% rather than 94-98% — chasing a normal saturation risks worsening hypercapnia. The survival benefit requires at least 15 hours a day, and home oxygen is a genuine fire risk if the patient is still smoking.
- Binds
- Phosphodiesterase-5 (sildenafil) and endothelin receptors (bosentan, macitentan) on pulmonary vascular smooth muscle, which is relatively rich in both.
- Which does
- Sildenafil prevents breakdown of cyclic GMP so nitric oxide signalling is sustained; the endothelin antagonists remove a potent vasoconstrictor and pro-proliferative signal — both relax the arteriole and reduce vascular remodelling.
- So you see
- Pulmonary vascular resistance falls, so the thin-walled right ventricle can eject again; exercise capacity and, for some agents, time to clinical worsening improve.
- And the same mechanism causes
- The same vasodilatation occurring systemically produces hypotension, headache and flushing with sildenafil; endothelin blockade causes fluid retention and peripheral oedema, which can itself look like worsening right heart failure.
- Handling
- The pulmonary selectivity is relative, not absolute. Sildenafil with any nitrate causes profound hypotension, so the combination is avoided; bosentan requires monitoring of liver function, and endothelin antagonists are teratogenic and need reliable contraception.
Catches people out: Specialist-initiated. Used where the pulmonary hypertension is actually caused by left heart failure, they push more flow into an already congested pulmonary circulation and can precipitate pulmonary oedema; in lung disease they can worsen hypoxaemia by dilating vessels serving poorly ventilated lung. Establish the cause of the pulmonary hypertension first.
Hypotension plus a raised JVP plus clear lungs after an inferior STEMI is right ventricular infarction until proven otherwise — ask for a right-sided ECG and look at V4R. The physiology to carry away: this ventricle runs on preload and tolerates afterload badly, which is why preload-reducing drugs such as glyceryl trinitrate, morphine and furosemide can drop the blood pressure sharply here, and why management runs in the opposite direction, towards preserving filling. Learn the direction; the prescribing belongs to the guidelines and the treating team.
Now test whether it stuck
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