Perioperative implications of pericardial effusions and cardiac tamponade

Learning objectives.

By reading this article you should be able to:

• •Describe the anatomical and physiological features of the pericardium in relation to common causes of pericardial disease.
• •Explain the heart–lung interactions that underpin the haemodynamic manifestations of pericardial effusion and tamponade.
• •Discuss both the clinical and echocardiographic features of pericardial tamponade.
• •Define the aims of anaesthetic management in patients with pericardial effusion and tamponade.

Key points.

• •The rate of fluid accumulation relative to pericardial stretch and the presence or absence of compensatory mechanisms are crucial in the development of cardiac tamponade.
• •The pathophysiology of tamponade entails exaggerated variations in the normal haemodynamic changes that occur during respiration.
• •Echocardiography is key to the diagnosis of pericardial effusions and tamponade.
• •The primary goal in the management of tamponade is to relieve the effect of the fluid or clot on cardiac pressures and restore forward flow.
• •Perioperative goals are to maintain preload and systemic vascular resistance; and to avoid bradycardia and myocardial depression.

Pericardial disease can present clinicians with unique challenges. An understanding of the relevant pathophysiology is essential for optimal management of patients with pericardial disease. This review discusses the pathophysiology and perioperative management of patients with pericardial effusions and cardiac tamponade.

Functional anatomy

The pericardium is a fibroserous sac surrounding the heart with two distinct layers, an outer thick fibrous parietal pericardium and an inner thin serous pericardium. The serous layer or epicardium covers the heart and reflects around the proximal great vessels at the base of the heart forming the pericardial sinuses. Normally, about 20–30 ml of pericardial fluid, which is essentially a plasma ultrafiltrate, fills the potential space between the two layers.¹

The pericardium has several functions. It limits distension of the chambers and prevents torsion and displacement of the heart. The pericardial fluid provides lubrication, which reduces friction during cardiac motion and facilitates interaction and coupling of the ventricles and atria. The pericardium has a fibrinolytic function: any blood that collects between the two layers tends to liquefy, reducing friction. The pericardium also secretes prostaglandins that may have an effect on the epicardial coronary tone.

Aetiology of pericardial disease

Congenital pericardial abnormalities are rare (one in 10,000 autopsies). These comprise partial left (70%), right (17%) or complete absence of pericardium.² Patients are usually asymptomatic but are at risk of traumatic aortic dissection as a consequence of augmented cardiac motion.

Acquired forms of pericardial disease can be classified as infectious and non-infectious; the latter include those of autoimmune origin. They can present as acute or chronic pericarditis, pericardial effusions, pericardial tamponade, constrictive pericarditis and pericardial masses.

Common causes of pericarditis/pericardial effusion include the following. (i) Infectious: viral, bacterial, tuberculosis, fungal and parasitic. (ii) Non-infectious: idiopathic, trauma (penetrating, non-penetrating, after cardiac surgery, type A aortic dissection), uraemia, neoplastic, autoimmune, Dressler's syndrome (after acute myocardial infarction or cardiotomy), metabolic (hypothyroidism) and post-irradiation.

These conditions result in excessive production of fluid in the pericardial space from either inflammatory exudate or bleeding into the confined pericardial space.

Pathophysiology of pericardial effusion and tamponade

Physiology of ventricular filling

Venous return to the right heart is determined by the small pressure gradient that exists between the mean circulatory filling pressure (MCFP) and the right atrial pressure. MCFP is defined as the pressure in the vasculature in the absence of flow and is dictated by the volume distending all vessels and the sum of all their compliances.² The right atrial pressure and in general, the pressure within the cardiac chambers, is influenced by the difference between intrachamber pressure and intrapericardial pressure, also referred to as the transmural pressure. The intrapericardial pressure is normally lower than the mean right atrial and right ventricular (RV) diastolic pressures. Under physiological conditions intrapericardial pressure equals the intrathoracic pressure and varies between +5 and –5 mmHg during spontaneous expiration and inspiration, respectively.³

The cardiac cycle can be divided into four distinct stages according to ventricular pressure–volume relationships: isovolumetric contraction, ventricular ejection, isovolumetric relaxation and diastolic ventricular filling. Normal ventricular filling follows a compliant pressure–volume pattern and has four distinct phases: isovolumetric relaxation, rapid filling, slow filling or diastasis, and atrial systole. The first part of diastole is the isovolumetric relaxation phase, an active energy-dependent process that occurs after aortic/pulmonary valve closure and before opening of the atrioventricular valves. Crucially, early ventricular filling starts during the next phase when the intraventricular pressure is negative, referred to as ‘diastolic suction’ by some authors.⁴ As a result of the ‘diastolic suction’ the ventricle fills rapidly during the early more compliant part of the ventricle pressure–volume relationship. Early ventricular filling corresponds to the E wave in Doppler echocardiography of the mitral/tricuspid valve inflow. As the ventricle fills it becomes less compliant and flow decreases, which corresponds to the slow filling phase of diastole. Atrial contraction (mitral/tricuspid inflow Doppler A wave) contributes to the last phase of ventricular diastolic filling. Finally, the closure of the atrioventricular valves marks the end of diastole.

Both spontaneous breathing and positive pressure ventilation (PPV) produce characteristic haemodynamic changes. With spontaneous respiration there is a minor variation in left and right heart stroke volume with each breath. During spontaneous inspiration, intrathoracic pressure decreases resulting in increased inflow to the right heart and increased RV output. The increase in RV filling pushes the interventricular septum to the left and reduces left ventricular (LV) filling. The relationship between ventricular filling, septal motion and respiratory variation is referred to as ventricular interdependence.^5,6 Pooling of blood in the pulmonary venous capacitance vessels during inspiration decreases the gradient between pulmonary veins and the left atrium, reducing flow to the left heart.⁷ These factors together contribute to a decrease in LV output and therefore a slight decrease in blood pressure during inspiration. Reciprocal changes are observed during expiration (Fig. 1a).

Fig 1.

Predominant heart lung interactions and haemodynamic changes during: (a) normal physiology and spontaneous breathing; (b) normal physiology and mechanical ventilation. ↑, increase; ↓, decrease; →, leftward shift; ←, rightward shift; Green solid arrows, inspiratory event; orange dashed arrows, expiratory event. RV, right ventricle; LV, left ventricle; RVI, right ventricle inflow; LVI, left ventricle inflow; Vel, velocity; Syst BP, systolic pressure.

Positive pressure ventilation increases pleural pressure and produces changes opposite to those seen during spontaneous breathing (Fig. 1b). The haemodynamic changes with PPV are: inspiratory reduction in RV preload caused by a reduction in venous return and an increase in afterload. LV preload increases during inspiration as positive pressure enhances blood flow from the pulmonary veins. In addition, there is a reduction in LV afterload during the inspiratory phase of PPV because of a decrease in the transmural pressure of the LV (the difference between pleural and intraventricular pressure).⁵ As a result, LV stroke volume and MAP increase at the end of the inspiratory phase of PPV. Conversely, at the end of the expiratory period both LV stroke volume and MAP decrease because of a reduction in LV preload resulting from the prior decrease of RV stroke volume during inspiration. It takes 2–3 seconds of transpulmonary blood transit time for the decreased venous return and RV preload during expiration to manifest as a reduction of LV preload during end-expiration.

The changes in ventricular filling in relation to the respiratory cycle described above can be observed with Doppler echocardiography signals obtained from the LV or the RV inflow. Doppler findings reflect the changes in ventricular volumes and are the result of the complex heart–lung interactions that occur during the respiratory cycle.⁸ During spontaneous inspiration, early RV diastolic filling increases with a reciprocal reduction in early LV diastolic filling. This is reflected in an increased E-wave velocity across the tricuspid valve and a reduction on the early diastolic peak E-wave velocity across the mitral valve. The reverse findings occur during expiration: increase in E-wave velocity across the mitral valve secondary to increased early LV diastolic filling and reduced in E-wave velocity across the tricuspid valve, reflecting decreased RV early diastolic filling.^8,9

Pathophysiology of cardiac tamponade

Cardiac tamponade is the compression of the heart chambers caused by accumulation of fluid in the pericardial space. Common causes of cardiac tamponade include pericarditis; tuberculosis; trauma; malignancy; and iatrogenic, which includes tamponade after cardiac surgery and invasive procedures.¹⁰

With accumulation of fluid in the pericardial space, the intrapericardial pressure increases, causing an increase in right and LV filling pressures. RV filling pressures may begin to equal intrapericardial pressure, whereas LV filling pressures remain higher. Increased intrapericardial pressure eventually compresses all the cardiac chambers causing a decrease in cardiac output (Fig. 2a).

Fig 2.

Pressure–volume curves of the pericardium illustrating the effect of pericardial effusions on filing pressures and the speed of pericardial fluid accumulation on haemodynamics. (a) As intrapericardial fluid volume increases, right and left filling pressures equalise with intrapericardial pressure. Compensatory mechanisms maintain cardiac output until a precipitous decrease in cardiac output occurs. (b) When pericardial fluid accumulates rapidly in the case of acute or ‘surgical’ tamponade (blue line) the limit of pericardial stretch is reached early causing tamponade. Slow accumulation of fluid as in chronic or ‘medical’ tamponade (red line) allows a longer period of pericardial stretch before reaching a state of tamponade. (Modified with permission from Schairer et al.³).

The intrapericardial volume is relatively fixed. With increasing intrapericardial fluid (and pressure), there is less room for the ventricles to expand during filling. Right and left ventricular filling occur at the expense of each other. The normal physiological variations in cardiac filling associated with respiration are significantly accentuated when tamponade develops. Tamponade leads to an exaggerated shift of the interventricular septum to the left during inspiration resulting in impairment of LV filling (Fig. 3). At this stage there is a clinically significant respiratory variation in systemic arterial pressure with a decrease of >10 mmHg during inspiration. This exaggerated decrease in systolic pressure during inspiration is referred to as pulsus paradoxus. Pulsus paradoxus can also be observed in conditions in which there are exaggerated swings in intrathoracic pressure such as acute severe asthma or exacerbations of chronic obstructive pulmonary disease.

Fig 3.

Predominant heart lung interactions and haemodynamic changes during: (a) pericardial tamponade during spontaneous breathing and (b) pericardial tamponade during mechanical ventilation. ↑, increase; ↓, decrease; →, leftward shift; ←, rightward shift; green solid arrows, inspiratory event; orange dashed arrows, expiratory event; purple dashed arrows, increase in pericardial pressure causing chamber compression. RV, right ventricle; LV, left ventricle; RVI, right ventricle inflow; LVI, left ventricle inflow; Vel, velocity; Syst BP, systolic pressure.

The crucial factors in the development of tamponade are the rate of fluid accumulation relative to pericardial stretch and the presence or absence of compensatory mechanisms.¹¹ An acute increase in intrapericardial fluid, for example haemorrhage after trauma or surgery, will rapidly cause tamponade as there is not enough time for the inelastic fibrous pericardium to stretch and accommodate even small volumes of fluid. However, a gradual increase in pericardial fluid contents over a period of days or weeks can lead to a large effusion, with a volume up to 2 L, without signs of tamponade (Fig. 2b). In the case of slowly developing tamponade, diminished cardiac output results in compensatory mechanisms, which include activation of the sympathetic nervous system producing tachycardia and increased vascular tone. In addition, plasma volume increases from fluid retention secondary to activation of the renin–angiotensin axis.

Diagnosis

Clinical features

Pericardial effusions that develop gradually are largely asymptomatic, whereas rapidly accumulating effusions can present with tamponade.¹² Symptoms of tamponade include dyspnoea (usually the first and most sensitive), orthopnoea and chest discomfort.¹³

Tamponade is a form of obstructive shock with clinical manifestations consistent with a low cardiac output and high central venous pressure. Features of a low cardiac output include low mean arterial pressure, cool peripheries and signs of poor end-organ perfusion (e.g. low urine output). Characteristically, palpating the pulse reveals an apparent variation in pulse volume because of pulsus paradoxus. Jugular venous pressure is typically increased, with distended neck veins apparent. Sympathetic tone is increased in an attempt to compensate for the low cardiac output and manifests as tachycardia, diaphoresis, anxiety and poor distal perfusion.⁹ A pericardial rub might be heard on auscultation in patients with inflammatory pericardial disease.

The classical clinical signs of cardiac tamponade first described by Beck in 1935 and known as the Beck's triad are: hypotension, raised jugular venous pressure and muffled heart sounds. However, a recent retrospective case series review of point-of-care echocardiography procedures performed in an emergency department setting found that none of the patients presenting with tamponade had all the elements of the triad, and the sensitivity of the presence of one element of the triad to diagnose tamponade was only 50%.¹⁴ Accurate and timely diagnosis requires a high index of suspicion with careful evaluation of relevant recent history (e.g. prior cardiac surgery, recent intervention in the cardiac catheter laboratory).

Cardiac surgery-related tamponade can present early in the postoperative period or occur days and even weeks after the operation. Tamponade after cardiac surgery may occur with ongoing bleeding despite the presence of chest drains and an open pericardium as clots may form and produce focal compression of cardiac chambers.¹⁵ Classic signs of tamponade may not be apparent as the collection is often localised, and many patients will have additional signs from underlying cardiac pathology (i.e. RV or LV systolic dysfunction).¹⁶ Tamponade occurring >7 days after surgery is defined as late and carries higher mortality risk than early tamponade.¹⁵ Late tamponade can be associated with events such as removal of temporary pacing wires or initiation of anticoagulation therapy.

Recent developments in the fields of interventional, electrophysiology and structural heart disease cardiology have led to a significant increase in the number and complexity of percutaneous intracardiac procedures. Frequently, these procedures require interatrial transseptal puncture for accessing left-sided heart structures. Examples of common procedures requiring transseptal puncture are radiofrequency pulmonary vein isolation for treatment of atrial fibrillation and insertion of devices for treatment of mitral regurgitation (e.g. Mitraclip). These groups of patients are often receiving anticoagulation or antiplatelet therapy for their underlying condition (e.g. atrial fibrillation). The combination of these factors results in an increased risk of pericardial effusion and tamponade. The use of echocardiography during these procedures allows for early detection of pericardial effusions before haemodynamic compromise develops.¹⁷

Cardiac tamponade after trauma most commonly results from penetrating injuries to the chest. Shock is usually disproportionate to the estimated blood loss. Pulsus paradoxus may be present, but can be missed in the presence of hypovolaemia. The Beck's triad was present in only a minority of patients with tamponade in a case series of patients after trauma.¹⁸ A raised jugular venous pressure may not be present as patients may be hypovolaemic after trauma. It should be noted that the signs associated with a left-sided tension pneumothorax could mimic tamponade.

Investigations

There may be an enlarged globular cardiac silhouette on the plain chest X-ray in chronic large pericardial effusions. The QRS complexes of the ECG may be of lower than normal amplitude as the fluid-filled pericardium attenuates the electrical signal at the skin. Sinus tachycardia is common although atrial dysrhythmias may also be present. In patients with large effusions, there may be ‘electrical alternans’, which refers to the beat-to-beat variation in both amplitude and axis of the QRS complexes. The variation in axis is caused by the swinging motion of the heart when suspended in a large pericardial effusion.

Echocardiography

Echocardiography is crucial in the investigation of pericardial effusions and tamponade. Transthoracic echocardiography (TTE) is usually available and is easily performed at the bedside. Both TTE and transoesophageal echocardiography (TOE) have high sensitivity in determining the various abnormalities seen with tamponade. However, after cardiac surgery the TTE imaging windows may be limited by the presence of drains, surgical dressings and pacing wires; under this circumstance, TOE may be the better modality.

Echocardiography is used to determine the size, location and haemodynamic effects of the pericardial effusion. It is important to evaluate from several imaging windows, as the apparent size of the effusion will vary depending on patient position and fluid location. A circumferential hypoechoic space around the heart represents the fluid layer of a pericardial effusion. Effusions up to 10 mm in thickness during diastole are considered small, between 10 and 20 mm indicate a moderate effusion, and greater than 20 mm signify a large effusion (supplementary online videos 1 and 2). If the effusion is large the heart may be seen to ‘swing’ from side to side in the fluid-filled pericardial cavity. Thin fibrinous strands, loculations or blood clots may also be seen within the fluid collection.

The diagnosis of tamponade is made using findings on clinical examination, with echocardiography providing additional information on the presence of a pericardial effusion and the compression effect of the effusion on the cardiac chambers.⁹ Cardiac tamponade produces characteristic findings on echocardiography. The right side of the heart is usually affected before the left, but a loculated collection around the left heart may cause left-sided effects. Echocardiography findings consistent with pericardial tamponade include collapse of the cardiac chambers, inferior vena cava dilatation, increased respiratory variation in the intracardiac blood flow measured with Doppler and excessive leftward shift of the interventricular septum during spontaneous inspiration. Collapse of cardiac chambers occurs at the time of lowest pressure during the cardiac cycle (right atrial systolic and RV diastolic collapse) (Fig. 4a and b; Figs 3 and 4 online videos). With impaired blood flow into the right atrium the IVC progressively dilates and loses its usual variation in diameter with respiration. Another finding typically seen with tamponade is LV diastolic pseudohypertrophy. With decreasing ventricular volume through reduced filling and external pressure, there is an apparent transient hypertrophy of the left ventricle.⁸

Fig 4.

(a) Apical four-chamber view (TTE) showing a large pericardial effusion with right atrial collapse (arrow) during systole (above); supplementary online video 3. (b) Parasternal long axis view showing right ventricular outflow tract (arrow) diastolic collapse; supplemetary online video 4. Transtricuspid (c) and transmitral (d) pulsed wave Doppler (PWD) traces showing a variation of >30% during respiration suggestive of cardiac tamponade. RA, right atrium; RVOT, right ventricular outflow tract; RV, right ventricle; LA, left atrium; LV, left ventricle; PE, pericardial effusion; TTE, transthoracic echocardiography.

Doppler echocardiography is used to examine transvalvular flow across the mitral and tricuspid valves and evaluate the changes that occur during respiration. A reduction of 30% in inspiratory mitral valve peak E-velocity and an increase in inspiratory tricuspid valve peak E-velocity are consistent with cardiac tamponade^9,19 (Fig. 4c and d). The effect of respiration on the variation of flow across cardiac chambers is modified significantly by mechanical ventilation. Studies in animals have shown a marked reduction in respiratory variation of transvalvular flow during mechanical ventilation with near disappearance of variation when cardiac tamponade is present.²⁰ Therefore, echocardiographic criteria used to diagnose tamponade based on variation of transvalvular velocities may be inaccurate in patients undergoing mechanical ventilation.^9,20

Differential diagnoses of pericardial effusions include epicardial fat and pleural effusions. Epicardial fat, because of its different density to myocardium and pericardium, can appear like pericardial fluid. A pericardial effusion can be differentiated from a pleural effusion by the fact that the former will appear to lie anterior to the descending aorta in the parasternal long axis view, whereas the latter lies posterior.

CT and MRI scans will also detect the presence of pericardial fluid and adverse haemodynamic effects on the heart but they are usually not practical investigations for the patient with tamponade.

In the context of trauma, a FAST (focused assessment with sonography for trauma) scan is a rapid and accurate bedside ultrasound tool used to diagnose pericardial tamponade (89% sensitive and 99% specific).²¹

Management

The primary goal in the management of tamponade is to relieve the pressure effect of the fluid or clot on the heart and restore forward flow. This is achieved by drainage procedures, which can be percutaneous or open surgical techniques.

Percutaneous techniques include needle pericardiocentesis, percutaneous catheter drainage and pericardiotomy (percutaneous balloon dilatation). In the emergency setting pericardiocentesis is usually performed. The European Society of Cardiology has suggested a triage scoring system to aid decision making in the patient presenting with cardiac tamponade.¹⁰ Briefly, items on a checklist related to aetiology, clinical presentation and imaging are given different values that when added up provide a score. A score of ≥6 is indicative of the need for urgent drainage of the effusion.

Pericardiocentesis

Pericardiocentesis is ideally performed with imaging guidance (fluoroscopy or echocardiography). The subxiphoid approach is commonly used. Alternative approaches include the parasternal and the apical approach. In order to improve safety and reduce harm associated with the procedure, local safety standards for invasive procedures (LocSSIPs) should be followed.²² Crucial standards include obtaining informed consent whenever practical and, except in the very urgent situation, checking of clotting status and concurrent use of antiplatelet or anticoagulant medication.²³ A 16 or 18G Teflon-sheathed needle is attached to a syringe. The skin is punctured 1–2 cm inferior to the left of the xiphochondral junction at an angle of 45°. With continuous aspiration on the syringe, the needle is advanced carefully in a cephalad direction aiming towards the left shoulder. Use of real-time US guidance allows direct visualisation of the largest part of the pericardial collection and the needle as it enters the pericardial cavity.²⁴ When the tip of the needle enters the pericardial sac, blood or pericardial fluid is aspirated. The injection of 5 ml agitated saline solution can further enhance visualisation of the pericardial space and increase confidence that the tip of the needle lies within the pericardial space. As little as 50 ml can produce dramatic improvement in the haemodynamics. The incidence of major complications is around 1.5%.¹² These include cardiac arrest, laceration of the ventricle, coronary artery or vein, arrhythmias, injury to surrounding structures (lung, oesophagus), post-pericardiocentesis pulmonary edema (LV dysfunction secondary to increased LV wall stress) and acute ventricular dilatation (rapid removal of large amount of fluid, especially in a chronic effusion).¹⁰

Surgical drainage

Open surgical drainage procedures usually lead to the creation of a pericardial window. A subxiphoid approach or a direct intrathoracic technique via a thoracotomy or video-assisted thoracoscopy may be used. Posteriorly located effusions, the presence of large blood clots, or tamponade caused by blunt and penetrating trauma may not be amenable to a percutaneous or thoracotomy approach and may necessitate a midline sternotomy.

After pericardiocentesis or surgical drainage, a sample of the pericardial fluid aspirated or the pericardial tissue obtained during open drainage, should be sent for culture analysis, cytology analysis, or both according to the indication.

Management of anaesthesia

The formulation of a perioperative management plan for patients undergoing pericardial drainage procedures should follow general principles common to all causes of pericardial effusion. The plan should be modified specifically according to the aetiology, acuity of presentation, the presence of signs or symptoms of tamponade, and the planned surgical approach.

The general perioperative haemodynamic goals are listed below.

• (i)Preload: Expand intravascular volume in order to augment or at least maintain preload (despite the high central venous pressure observed in tamponade physiology, which essentially is a reflection of chamber compression and not the true filling pressure). This is of particular importance in patients with coexisting depletion of circulating volume.
• (ii)Heart rate and rhythm: Avoid bradycardia, and treat any bradycardias promptly if they occur. Maintain sinus rhythm so that cardiac output remains optimal.
• (iii)Afterload: Maintain systemic vascular resistance (SVR), which is high in patients with tamponade because of high sympathetic nervous activity). It is essential that the compensatory cardiovascular mechanisms (tachycardia and raised SVR) are maintained during induction of anaesthesia.
• (iv)Contractility: Maintain optimal contractility, and avoid myocardial depressants.

The haemodynamic goals can be summarised as ‘fast, full, and squeezed tight’.

In patients who are in a decompensated haemodynamic state, pericardiocentesis or a pericardial window via the subxiphoid incision may be performed under local anaesthesia.

General anaesthesia is usually required for surgical drainage of pericardial collections. Patients with tamponade physiology can decompensate precipitously after induction of general anaesthesia (as a result of a combination of factors including direct myocardial depression, vasodilatation and diminished preload). For this reason, patients requiring general anaesthesia should preferentially be induced in the operating theatre with the surgeon scrubbed, sterile drapes applied and the surgical equipment ready. However, clinical urgency and haemodynamic collapse may dictate opening of the chest outside the operating theatre.

Invasive arterial pressure monitoring is essential and central venous access desirable. However, obtaining central venous access should not delay urgent pericardial drainage. Prompt evacuation of the effusion is the only effective intervention in patients with haemodynamic collapse.

A large bore i.v. cannula with running intravenous fluids is essential to restore preload and ensure vasopressors reach their targets. Emergency drugs should be available before induction of anaesthesia. These include vasopressors (either metaraminol or phenylephrine boluses, and an infusion of noradrenaline [norepinephrine]) and inotropes (adrenaline [epinephrine]). Defibrillator pads should be attached before induction. Most anaesthetic induction drugs are myocardial depressants and vasodilators. An ideal anaesthetic agent for patients with tamponade should have the least effect on heart rate, myocardial contractility and SVR. The authors' induction agent of choice is ketamine at doses of 0.5–1 mg kg⁻¹. Ketamine, because of its advantageous haemodynamic stability profile, closely resembles the ideal agent. Other agents that may be used are etomidate and midazolam. The authors' practice is to ‘chase’ the induction agent with a bolus of metaraminol (0.5–1.0 mg).

Airway and ventilatory management should account for the significant negative effects of PPV on venous return to the right heart. Therefore, it is recommended to avoid high PEEP and large tidal volumes, thus limiting inspiratory pressures until tamponade is resolved.

Alternatively, some authors have suggested that spontaneous breathing techniques are advantageous for induction of anaesthesia in patients with cardiac tamponade.²⁴

Anaesthesia can be maintained with a balanced technique using volatile inhalation agents, intravenous opioids, ketamine and short- or intermediate-acting neuromuscular blocking agents. Intraoperative TOE, if available, can be particularly useful to monitor and guide haemodynamic management, especially after cardiac surgery. TOE also helps to ensure the effusion is adequately drained. After chest opening and surgical evacuation there may be a rebound hypertension, and during this period anaesthesia is deepened and doses of vasopressor agents reduced. Optimal management of coagulation can be guided by the use of point-of-care coagulation monitors (e.g. thromboelastography) if ongoing bleeding is an issue. Dramatic improvements in the haemodynamic state typically occur after drainage of fluid in patients with tamponade.

Postoperative pain relief can be achieved with longer-acting opioids (e.g. morphine, oxycodone). Depending on the surgical approach, regional anaesthetic blocks such as intercostal nerve block may be appropriate.

Postoperative care is dictated by need for ongoing organ support and continuous monitoring. Usually a period of observation in a critical care environment is required after drainage of an acute effusion.

Patients with chronic pericardial effusion may require a general anaesthetic for a drainage procedure or creation of a pericardial window. The key objective in the preoperative assessment is to identify the presence or absence of tamponade. It is also important to evaluate the patient for pleural effusions that may coexist. The most common group of patients presenting with chronic effusions are those with metastatic disease. These patients may have multisystem involvement and may have had received chemo- or radiotherapy affecting their ability to tolerate anaesthesia and surgery. Anaesthetic management goals are similar to that in the acute setting. It is important to avoid preoperative hypovolaemia. The vasodilatation that occurs with induction of anaesthesia may lead to severe deterioration in cardiovascular function and the previously compensating patient may develop acute tamponade.²⁴

Patients with chronic or recurrent pericardial effusions may present for elective non-cardiac surgery. Stable patients with pericardial effusions without haemodynamic compromise do not require drainage before elective surgical procedures. However, perioperative volume depletion may lower the central venous pressure below the intrapericardial pressure and cause haemodynamic decompensation. Therefore, the intravascular volume status of the patient should be carefully monitored and volume loss replaced promptly.

Conclusions

Pericardial disease frequently presents with pericardial effusions. The volume and speed of fluid accumulation are major determining factors for the development of tamponade. Safe perioperative management of patients with pericardial effusions with or without tamponade, requires sound knowledge of the causes of pericardial disease and the pathophysiological principles responsible for different clinical presentations.

Biographies

Pradeep Madhivathanan FRCA MRCP (UK) EDIC FFICM is a consultant in cardiothoracic intensive care medicine, extracorporeal membrane oxygenation (ECMO) and anaesthesia, at the Royal Papworth Hospital NHS Foundation Trust. His interests include medical education; critical care and perioperative echocardiography and ultrasound; acute respiratory failure; and ECMO.

Carlos Corredor MRCP (UK) FRCA FFICM is a consultant in cardiothoracic anaesthesia and intensive care medicine at Barts Heart Centre, Barts Health NHS Trust. His interests include anaesthesia for major aortovascular surgery, mechanical circulatory support and perioperative echocardiography.

Andrew Smith FRCA FFICM is a consultant in cardiothoracic anaesthesia and intensive care medicine at Barts Heart Centre, Barts Health NHS Trust. His interests include perioperative echocardiography

Matrix codes: 1A01, 2A07, 3G00

Acknowledgements

We thank Professor Mark Monaghan and the Department of echocardiography at King's College Hospital, London, for support with some of the images included in this article.

Declaration of interests

The authors declare that they have no conflicts of interest.

MCQs

The associated MCQs (to support CME/CPD activity) are accessible at www.bjaed.org/cme/home for subscribers to BJA Education.

Appendix A. Supplementary data

The following are the supplementary data to this article:

Multimedia component 1

Parasternal long axis window demonstrating a large pericardial effusion with no features of tamponade.

Multimedia component 2

Parasternal long axis window demonstrating a pericardial effusion associated with diastolic collapse of the right ventricular outflow tract suggestive of tamponade.

Multimedia component 3

Apical four chamber window demonstrating a large effusion with right atrial systolic and right ventricular diastolic collapse suggestive of tamponade.

Multimedia component 4

Subcostal window demonstrating a large circumferential pericardial effusion with no features of tamponade.