FRCA Notes

Cardiac Tamponade

This topic was a CRQ question in March 2022 (77% pass rate) and the examiners commented on a lack of basic science knowledge.

The curriculum asks for knowledge of the 'clinical signs and symptoms of cardiac tamponade, and its management'.

Resources

  • Cardiac tamponade occurs due to an accumulation of fluid in the pericardial space, increasing the pressure within the space and impairing the ability of the heart to fill and pump
  • With impaired cardiac function there is a fall in cardiac output and systemic perfusion i.e. obstructive shock, leading to life-threatening organ dysfunction
  • Cardiac tamponade is a physiological diagnosis, distinct from mere presence of excess fluid within the pericardial space (pericardial effusion)
  • The pericardial sac consists of two layers of tough fibrous tissues, which surround and protect the heart
    • The inner visceral pericardium is continuous with the epicardium
    • The two layers of the pericardium fuse at the points of exit of the great vessels from the heart into the mediastinum

  • The visceral and parietal pericardia are separated by a small amount of lubricating pericardial fluid
    • Normal volume 15-30mls
    • A plasma ultrafiltrate secreted by visceral mesothelial cells
    • Drained by the lymphatic system into the mediastinum and right heart

Functions

  • Buffer the heart from external impact
  • Reduces resistance due to friction during cardiac motion
  • Limits distension of the cardiac chambers
  • Barrier against infection from surrounding structures, particularly the lungs
  • Secretes prostaglandins which affect epicardial coronary tone

Pressure-volume relationship

  • Two distinct phases:
    1. Increase in pericardial fluid volume during which there are only small increases in pericardial pressure
      • I.e. a compensatory phase where there is stretch in pericardial membranes to accommodate the higher volume

    2. Small changes in volume lead to large increases in pericardial pressure as the compliance of the pericardial membranes has been exceeded

  • One factor influencing the rate of pericardial pressure increase is the duration of time over which fluid accumulates
    • Rapid changes e.g. bleeding from penetrating injury will cause rapid increases in pericardial pressure, and 150ml of fluid will cause tamponade
    • Slower changes in volume are less likely to cause rapid rises in pressure as the tissues can adapt; there are reports of nearly 2L of fluid in the pericardial space without tamponade

  • Other factors include:
    • Pericardial membrane compliance, which may be reduced e.g. due to scarring from previous cardiac surgery, pericardial mesothelioma
    • Fluid composition, with blood clots or viscous (chronic) effusions more likely to transmit pressure increases to the underlying heart than transudative effusions

  • Accumulation of fluid in the pericardial space raises the intrapericardial pressure
  • This increases RV and LV filling pressures
    • RV filling pressure eventually equals intrapericardial pressure
    • LV filling pressure typically always remains higher

  • The normal physiological variations in cardiac filling associated with respiration are accentuated
    • Exaggerated shift of the interventricular septum to the left during inspiration, limiting LV filling
    • Consequent variation in MAP during respiration; decrease of >10mmHg during inspiration ('pulsus paradoxus')

  • Eventually all the cardiac chambers are compressed and cardiac output falls

Early tamponade

  • Pericardial pressure begins to rise
  • RV filling pressure equates to pericardial pressure i.e. transmural pressure is 0mmHg, and there is a massive reduction in venous return to the heart
  • There is compression of the RA and RV during diastole, and CVP rises
  • The ventricle is under-loaded, with underfilling and limited contractility, hence low stroke volume

Compensation

  • Increase sympathetic tone leads to tachycardia
  • Sympathetically - mediated vasoconstriction to increase SVR and therefore maintains MAP

  • There is RAAS activation and fluid retention
  • (NB no increase in ANP/BNP levels as there is no atrial stretch)

Late tamponade

  • LA filling pressure is exceeded and dramatic decreases in CO occur
  • There is reduced myocardial blood flow, but also reduced myocardial work hence a lack of ischaemia
  • A cycle of increased fluid retention, decreased CO and decreased venous return ensues
  • Obstructive shock and consequent cardiac arrest eventually occurs


Vascular Infectious/inflammatory Trauma Auto-immune Metabolic Iatrogenic Neoplastic
Retrograde aortic dissection TB Penetrating cardiac trauma SLE Uraemic Post-cardiac surgery e.g. due to coagulopathy Pulmonary or pericardial mesothelioma
Aortic root rupture HIV RA Chyle leak From coronary rupture during PCI Radiation-induced pericarditis
Dressler's syndrome Post - viral pericarditis CREST Hypothyroidism Drugs e.g. isoniazid, cyclosporin, hydralazine
Bacterial/fungal/parasitic Sarcoidosis Idiopathic


Symptoms

  • May be asymptomatic if chronic, slowly developing pericardial effusions
  • Primary and most sensitive symptom is dyspnoea
  • Other symptoms:
    • Orthopnoea
    • Chest discomfort
    • Sweating and anxiety from sympathetic activation

Signs

  • The classic description is Beck's triad:
    1. Hypotension
    2. Muffled heart sounds
    3. Raised JVP
  • This has poor sensitivity and patients with tamponade almost never have all elements of the triad

  • Variable pulse volume (pulsus paradoxus)
    • An exaggerated fall in systemic arterial pressure during inspiration
    • Negative intrapleural pressure increases venous return to the right heart
    • This causes the interventricular septum to bulge towards the left heart chambers
      • In health the LV would accommodate the bulging septum by expanding slightly
      • In tamponade the effect is exaggerated owing to the constraining of the left heart by the pericardial sack
    • The impingement on the LV reduces filling volume and therefore SV
    • A pulsus paradoxus >10mmHg in the spontaneously ventilating patient is highly sensitive for tamponade
    • The pattern is reversed in the patient undergoing PPV

  • Raised JVP due to high CVP
    • Sawtooth (M or W) CVP waveform due to raised CVP, tall a and v waves, with steep x-descent and absent y-descent
  • Distended neck veins during inspiration (Kussmaul's sign)
  • Cool peripheries
  • Pericardial rub if inflammatory pericardial disease
  • Pericardial knock
  • Third heart sound
  • Displaced apex beat

  • Features of obstructive shock with sympathetic activation:
    • Tachypnoea
    • Tachycardia
    • Low CO and therefore low MAP
    • Sequelae of poor organ perfusion e.g. cyanosis, oliguria

  • CXR - enlarged, globular cardiac silhouette (typically seen in chronic tamponade)

ECG

  • Tachycardia (sinus or dysrhythmic)
  • Low voltage QRS amplitude owing to attenuation of electrical signal by fluid-filled pericardium
  • Electrical alternans - beat-to-beat variation in amplitude and axis of the QRS
  • Global concave ST-elevation may be present due to global direct pressure on the myocardium
  • Features of pericarditis:
    • PR depression
    • T-wave inversion
    • Global concave ST elevation

Echocardiography

  • Transthoracic echocardiography is the single most important investigation
  • Features in tamponade include:
    • Continuous pericardial effusion ('swinging heart'), although may be absent if the cause is clot rather than liquid
    • Right atrial or right ventricular collapse
    • Septal bounce
    • IVC dilation
    • Reduced mitral flow on inspiration
    • Fluctuating RVOT/LVOT flow velocity >10%

  • TOE provides better imaging of posterior pericardium and is important to exclude retro-atrial haematoma following cardiac surgery

  • Stable patients without tamponade may have time for optimisation prior to drainage; unstable patients require urgent drainage
  1. Avoid I&V unless absolutely necessary as PPV will exacerbate cardiac failure from tamponade
    • If already I&V minimise PEEP (to reduce limitations on venous return)

  2. Adequate oxygenation
    • Avoid high PEEP
    • Avoid large tidal volumes

  3. Instigate invasive haemodynamic monitoring e.g. arterial and central lines
    • Small fluid challenge if hypotension present, to avoid exaggerated effects of hypovolaemia in tamponade
      • Fluid most beneficial if poor preload
      • Avoid repeated boluses

    • Avoid bradycardia and maintain sinus rhythm

    • Increase chronotropy and maintain inotropy, afterload and RA pressures i.e. dobutamine, dopamine or isoprenaline
    • Concern is use of these drugs will increase myocardial metabolic demands whilst the positive chronotropy reduces perfusion time
    • Vasopressors may be better

Drainage

  • Pericardiocentesis
    • Percutaneous placement of catheter into pericardial sac using landmark, ultrasound or fluoroscopic guidance
    • Contraindicated in aortic dissection and severe coagulopathy
    • Can be diagnostic and therapeutic
    • Overall risks low (<5%) but can include:
      • Ventricular puncture
      • Rupture of myocardium/coronary vessels
      • Arrhythmia
      • Damage to other structures e.g. lungs
      • Introduction if infection
      • Cardiac arrest

  • Percutaneous balloon dilatation (pericardiotomy)

  • Surgical drainage
    • Emergency sternotomy and opening of pericardial sac
    • VATS is less invasive but associated with longer duration of surgery and higher perioperative morbidity
    • Typically performed in theatre under GA with surgeon scrubbed and area prepped prior to induction
      • Induction agents of choice include ketamine, etomidate or midazolam ± chasers of metaraminol
      • Anticipate rebound hypertension following drainage