Pericardium
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 normally 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.
the speed at which fluid arrives matters more than the amount: about 150 mL of blood within minutes can tamponade the heart, while a litre collecting over a year may cause almost nothing.
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.
once the sac is tight or fluid-filled, restraint becomes the dominant force: interdependence exaggerates that respiratory swing into pulsus paradoxus (fall greater than 10 mmHg), and diastolic pressures equalise across the chambers in both tamponade and constriction.
The two serous surfaces are wet and slippery, so they glide over each other with every beat and make no sound.
inflame them and they grate instead — the friction rub of acute pericarditis — and the movement itself becomes painful.
The parietal pericardium — the fibrous sac and its serous lining — has somatic innervation from the phrenic nerve (C3 to C5) and lies against the diaphragm and mediastinal pleura; the visceral layer on the heart surface carries essentially no somatic pain fibres.
pericardial pain is sharp rather than heavy, felt behind the sternum and referred to the trapezius ridge or shoulder tip, and it changes with posture and breathing — unlike ischaemic pain.
Heart sounds and the heart's electrical signal reach the chest wall across the pericardial space, and the cardiac silhouette on a chest x-ray is the outline of the sac and its contents, not of the myocardium alone.
fluid in the space muffles the heart sounds and shrinks QRS voltage, and once a few hundred millilitres have collected it turns the silhouette into a large globular heart with clear lung fields.
What goes wrong
- Acute pericarditis← from “The two serous surfaces are wet and slippery, …”
Most often viral or idiopathic; also uraemia, recent myocardial infarction (early post-infarction pericarditis, or Dressler syndrome weeks later), cardiac surgery, autoimmune disease such as lupus, tuberculosis and acute rheumatic fever. The serous layers become roughened and swollen so they rub instead of glide, and the somatically innervated parietal layer reports that as sharp pain that posture and breathing change. Inflammation of the epicardium underneath lifts the ST segments (ventricular epicardium) and drags the PR segments down (atrial epicardium) across most leads, because the whole surface is involved rather than one artery's territory.
Widespread concave ST elevation with PR depression and reciprocal change in aVR; pain eased by sitting forward; rub at the left sternal edge; NSAID plus colchicine from the first episode; think acute rheumatic fever in an at-risk young patient.
You would find: Sharp central chest pain, worse lying flat and on deep breaths, better sitting forward, with a scratchy rub at the left sternal edge. ECG shows widespread concave-upward ("saddle-shaped") ST elevation with PR depression, and the mirror image in aVR (PR elevation, ST depression) — not the regional, convex pattern of infarction. Troponin rises if the underlying myocardium is also inflamed (myopericarditis). In Australia most cases are viral or idiopathic, but acute rheumatic fever inflames all three layers of the heart (pancarditis), and rates of rheumatic fever in Aboriginal and Torres Strait Islander communities are among the highest in the world.
- Pericardial effusion← from “Heart sounds and the heart's electrical signal…”
Inflamed, uraemic, infected or malignant pericardium weeps fluid into the space. If it accumulates slowly the fibrous layer stretches, so intrapericardial pressure stays near normal, the heart keeps filling and the patient may feel well. The fluid still separates the heart from the chest wall and from the ECG electrodes.
Size is not severity — echo (chamber collapse, plethoric IVC) decides, not millilitres; low voltage plus electrical alternans means a large effusion, often malignant.
You would find: Muffled heart sounds, low-voltage QRS complexes, and a large globular heart with clear lung fields on chest x-ray once the volume is substantial. When the heart swings inside a big effusion the QRS height alternates beat to beat (electrical alternans). Echocardiography, not the x-ray, tells you how much fluid there is and whether it is compressing the heart.
- Cardiac tamponade← from “The heart sits in a stiff outer fibrous sac li…”
Fluid, blood or pus arrives faster than the stiff sac can stretch — trauma, a cardiac procedure, aortic dissection, malignancy or a rapidly forming inflammatory effusion. Intrapericardial pressure rises to and above right atrial and right ventricular diastolic pressure, so the thin-walled right chambers are squashed in diastole and cannot fill; diastolic pressures equalise across the chambers. Less blood in means less blood out: stroke volume falls, and tachycardia and venoconstriction compensate until they cannot. Because the ventricles share the fixed space, inspiration fills the right ventricle at the expense of the left, so systolic pressure falls further with each breath in.
Rate of accumulation beats volume; absent y descent; pulsus paradoxus over 10 mmHg; pericardiocentesis is the treatment and anything that drops preload is the trap.
You would find: Hypotension, raised JVP and muffled heart sounds (Beck triad — all three together in only a minority), with a fast thready pulse and an inspiratory systolic fall of more than 10 mmHg (pulsus paradoxus). The JVP keeps its x descent but loses the y descent. Echo shows diastolic right atrial and right ventricular collapse with a plethoric inferior vena cava. This is obstructive shock treated by taking the fluid out, not by giving drugs. Pulsus paradoxus can be absent with co-existing severe aortic regurgitation, an atrial septal defect or a stiff hypertrophied right ventricle, and the JVP may look normal in low-pressure tamponade from hypovolaemia or trauma.
- Constrictive pericarditis← from “Because the sac barely stretches acutely, it r…”
After pericarditis heals badly, or after cardiac surgery, chest radiotherapy or tuberculosis, the sac scars into a thickened, sometimes calcified shell. The ventricles fill fast and freely for the first part of diastole, then hit the rigid wall and stop dead. Filling pressures rise behind both ventricles, and because the rigid shell also shields the heart from intrathoracic pressure swings, the extra venous return of inspiration cannot be accommodated. The venous congestion is systemic and chronic rather than sudden.
Right heart failure with clear lungs: prominent y descent, Kussmaul sign, pericardial knock, calcified sac; filling depends on a high venous pressure, so diuretics only palliate and pericardiectomy is the cure.
You would find: Raised JVP with a sharp inward collapse in early diastole (prominent y descent) and a venous pressure that rises rather than falls on inspiration (Kussmaul sign), an early diastolic pericardial knock, ascites and peripheral oedema out of proportion to how well the lungs sound. Echo shows a septal bounce and marked respiratory variation in mitral and tricuspid inflow. Pulsus paradoxus is usually mild or absent, unlike tamponade. Tuberculosis is an uncommon cause in Australia but worth considering in people from high-incidence countries and in communities with higher TB rates, including some Aboriginal and Torres Strait Islander populations.
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 cyclo-oxygenase enzymes COX-1 and COX-2 on the endoplasmic reticulum and nuclear membrane of pericardial inflammatory and mesothelial cells (ibuprofen reversibly and competitively, aspirin by irreversible acetylation)
- Which does
- blocks conversion of arachidonic acid to prostaglandin H2, so downstream prostaglandin E2 and prostacyclin production falls in the inflamed tissue
- So you see
- less vasodilatation, exudation and nociceptor sensitisation in the pericardium: the pain and the rub settle over days
- And the same mechanism causes
- the same loss of prostaglandin removes gastric mucosal protection (COX-1) and the prostaglandin-mediated dilatation of the renal afferent arteriole, so peptic ulceration or bleeding and a fall in glomerular filtration rate are the mechanism-linked harms; sodium and water retention follows for the same renal reason
- Handling
- aspirin is chosen over other NSAIDs when the pericarditis follows a myocardial infarction, because the others are thought to interfere with infarct healing and ibuprofen also blunts aspirin's antiplatelet effect; the whole class is avoided or used cautiously in kidney impairment, heart failure and with anticoagulants
Catches people out: Anti-inflammatories do nothing for tamponade: a shocked patient needs a needle, not a tablet.
- Binds
- beta-tubulin dimers in circulating neutrophils and monocytes, which concentrate the drug
- Which does
- prevents microtubule polymerisation, so the cell cannot remodel its cytoskeleton for chemotaxis, adhesion or degranulation, and NLRP3 inflammasome assembly and interleukin-1 beta release are impaired
- So you see
- fewer neutrophils recruited to the serosa and a shorter, less recurrent attack — it roughly halves the chance of recurrence, which is why it is given from the first episode rather than held in reserve
- And the same mechanism causes
- the rapidly dividing gut epithelium depends on microtubules too, so diarrhoea, nausea and cramping are dose-related and the usual reason people stop it; at toxic concentrations the same antimitotic effect causes myelosuppression and myopathy
- Handling
- cleared partly renally and a substrate of CYP3A4 and P-glycoprotein, so it accumulates in significant kidney impairment and its concentration rises dangerously with clarithromycin, verapamil, diltiazem and ciclosporin
Catches people out: Diarrhoea is the usual reason people stop it, and the interaction and kidney warnings above are what turn a well-tolerated drug into a toxic one.
- Binds
- the cytosolic glucocorticoid receptor in leucocytes and mesothelial cells of the pericardium
- Which does
- the drug-receptor complex moves to the nucleus and represses NF-kappaB-driven transcription while inducing anti-inflammatory proteins, so cytokine, chemokine and COX-2 production all fall
- So you see
- the attack settles quickly, but the underlying inflammatory process is only suppressed, and attacks tend to return as the dose is reduced — steroid use is associated with more recurrences
- And the same mechanism causes
- the same broad transcriptional suppression blunts fever and pain and impairs cell-mediated immunity, so a bacterial or tuberculous cause can be masked or worsened — the specific hazard here, over and above the familiar metabolic effects of prolonged use
- Handling
- not first line; when used, the dose is reduced slowly, because abrupt reduction is what precipitates the rebound attack
Catches people out: Uraemic pericarditis is not a steroid problem at all — it settles when dialysis is intensified.
- Binds
- no receptor — it expands the intravascular compartment
- Which does
- raises mean systemic filling pressure and therefore the pressure gradient driving blood into the compressed right atrium
- So you see
- right ventricular filling and stroke volume improve for a while — most in a patient who is also volume depleted, and very little once filling pressures are already high
- And the same mechanism causes
- in a patient who is not volume depleted the same volume load simply raises intrapericardial and venous pressures further without improving output, and adds pulmonary and systemic congestion
- Handling
- a bridge only; the fix is pericardiocentesis or surgical drainage
Catches people out: The mirror image is the trap: diuretics, nitrates and other preload-reducing drugs can collapse cardiac output in tamponade.
- Binds
- the NKCC2 co-transporter on the luminal membrane of thick ascending limb cells, reached from inside the tubule after secretion into it
- Which does
- blocks sodium, potassium and chloride reabsorption and abolishes the medullary concentration gradient, so a large sodium and water load is delivered distally and excreted
- So you see
- venous pressure, ascites and peripheral oedema fall, and the patient breathes and moves more comfortably
- And the same mechanism causes
- the same distal sodium load drives potassium and hydrogen ion loss (hypokalaemic metabolic alkalosis), and over-diuresis removes the very preload the stiff ventricles need, dropping cardiac output and causing hypotension and prerenal kidney injury; high doses also block NKCC1 in the inner ear, giving reversible ototoxicity
- Handling
- filling in constriction depends on a high venous pressure, so diuresis is deliberately gentle; it does nothing to the shell causing the problem and pericardiectomy is the definitive treatment
Catches people out: Relieves the swelling but does nothing to the scarred sac causing it.
Tamponade is a pressure problem, not a volume problem: how fast the fluid arrived decides whether the patient is shocked, not how much is there. The JVP is high in both tamponade and constriction — the y descent separates them. In tamponade the sac squeezes throughout diastole, so the y descent is absent; in constriction filling is free then stops abruptly, so the y descent is exaggerated. Kussmaul sign points to constriction, pulsus paradoxus over 10 mmHg to tamponade.
Now test whether it stuck
Reading this through is not the same as being able to reconstruct it. Every question in the bank is free, with a full debrief on each option.