*3.4.1.2 Post-cardiac surgery and post-operative pericardial effusions (PPE)*

Patients post-cardiac surgery are another group whose management frequently requires the involvement of the anaesthesiology team [24, 32–38]. Accumulation of blood within the pericardial sac because of ongoing bleeding from either a surgical or medical cause peri-operatively will lead to the development of PPE and tamponade. PPE can be divided into early, presenting within 7 days, and late complications occurring more than 7 days post-procedure. An important cause of persistent PPE is the inflammatory response associated with post-cardiac injury syndrome [13, 14, 33].

The incidence for PPE has a wide range depending on the study quoted and is approximately 20% on the 20th post-operative day [33]. Most effusions are clinically insignificant, defined as less than 10 mm in diastole on TTE, and resolve spontaneously after reaching their maximum volume on day 10 post-operatively [33]. The incidence of significant pre-tamponade and tamponade requiring re-intervention is 1–2.6% [33].

Presenting symptoms are usually non-specific consisting of tachycardia, hypotension, tachypnoea, orthopnoea and decreased heart sounds [24, 32–34]. This low cardiac output state must be differentiated from other common causes of cardiogenic shock in the post-operative period. The differential diagnosis would include hypovolaemia, significant ischaemia, ventricular dysfunction or severe inflammatory response syndrome [32].

The following have been identified as independent risk factors for the development of post-operative effusions [33, 34, 37]: heart transplantation, pulmonary thromboembolism, aortic aneurysm surgery, increased body surface area, valve surgery, immunosuppression, urgent or emergent surgery, renal failure and

#### *Inflammatory Heart Diseases*

prolonged cardiopulmonary bypass (CPB) times. In other studies, female gender, pre-operative use of anticoagulants and early chest drain removal have been associated with increased incidence of PPE [33, 37].

In the setting of post-operative haemodynamic deterioration, critical tamponade may develop quickly with even small amounts of fluid accumulation causing significant haemodynamic effects. The diagnosis should be made immediately in order to facilitate life-saving intervention. TTE remains the diagnostic tool of choice because it is non-invasive and has a high sensitivity and specificity for detecting the signs of cardiac tamponade [6, 24, 32, 35, 38]. It may also be useful in confirming or ruling out other causes for post-operative haemodynamic deterioration. Because tamponade is a dynamic pathological process, especially in the post-operative period, serial or repeat echocardiographic examinations coupled with ongoing clinical evaluation are necessary to ensure appropriate and timeous management.

Although TTE remains the diagnostic tool of choice, detecting effusions and tamponade post-operatively may be challenging [31, 32, 38]. Patients who have altered anatomy are most likely to be on positive pressure ventilation with positive end expiratory pressure (PEEP), may have pneumopericardium (air trapped in the pericardium) and will have drains in situ. Effusions post cardiac surgery are often loculated causing regional compression of only one or some of the cardiac chambers. Blood and clots collect in the posterior sinuses making diagnosis via the traditionally accepted criteria on TTE difficult. Trans-oesophageal echocardiography (TOE) is well tolerated in sedated or anaesthetised patients but is more invasive and may not be readily available. Supplemental modalities such as CT scan and cardiac MRI have been suggested to aid in the diagnosis when TTE is inconclusive [6, 31, 38].

Indications for drainage of effusions are based on clinical and TTE findings of tamponade: left ventricular dysfunction in patients receiving intermittent positive pressure ventilation, loculated effusions or clots causing compression of the left atrium or left ventricle, documented collapse of right-sided chambers and if pericardial separation is >20 mm [3, 32, 35].

Anaesthetic management of post-operative effusions and tamponade remains the same as for an effusion from any other cause. The need for ongoing inotropic support and appropriate mechanical ventilation, massive fluid shifts, ongoing bleeding due to surgical causes, coagulopathy due to anticoagulant use, intrinsic clotting abnormalities, need for massive blood transfusion, renal dysfunction and the significant risks of re-sternotomy are just a few of the unique challenges for the anaesthesiologist to consider when taking a cardiac patient back to theatre for re-intervention. Drainage procedures are most often limited to pericardiocentesis under ultrasound- or video-assisted guidance [25, 32, 35]. A small percentage of patients may require sternotomy for the effective management of post-operative effusions [25, 32].

#### *3.4.1.3 Effusions in patients undergoing percutaneous cardiac interventions*

Percutaneous intracardiac intervention is a risk factor for the development of pericardial effusion and tamponade [39–41]. The exact incidence depends on the procedure performed, the extent of the intervention, whether it is diagnostic or therapeutic, and if anticoagulation is used in the peri-procedural period. The exact procedure-specific incidence is difficult to determine, and small to moderate effusions may occur much more frequently than studies suggest [39]. The incidence of tamponade ranges from <1 to 6% depending on the study being quoted. Some of the more commonly performed interventions include atrial fibrillation ablation associated with a 4% risk of tamponade, permanent pacemaker insertion which carries a 1.7% risk of cardiac perforation and life-threatening tamponade and left atrial

**73**

*Anaesthesia for Patients with Pericardial Disease DOI: http://dx.doi.org/10.5772/intechopen.82540*

late hypotension post intervention [40].

*3.4.2 Pathophysiology of pericardial effusions*

of the cardiac chambers and tamponade.

may become fibrotic and confining.

fluid within the space.

low cardiac output state.

sures [3–10, 14–17, 22–24].

**3.5 Tamponade**

tamponade, most commonly due to LAA perforation.

were performed instead of angioplasty and stent placement.

facilitate life-saving treatment drainage procedures as described below.

the intrinsic compliance of the pericardial tissue layers [4, 5, 7, 24].

appendage (LAA) occlusion procedures which are associated with a 1.8–3% risk of

The overall incidence of tamponade following percutaneous coronary intervention (PCI) is 0.12% and is associated with high mortality [40, 41]. Coronary artery perforation following percutaneous coronary intervention is found in 0.3% of patients of which 10% went on to develop tamponade [41]. The risks were increased in patients requiring more complex interventions and if athero-ablative procedures

Pericardial effusion and tamponade following PCI usually present acutely in the catheterisation lab but can have an insidious onset and are an important cause for

The diagnosis of tamponade post PCI remains predominately clinical and should be confirmed with TTE and other imaging techniques as soon as possible in order to

The haemodynamic effects of the effusion and the development of tamponade are dependent on the rate of fluid accumulation within the pericardial space, the total volume of fluid that accumulates, the type of the fluid that accumulates and

Because the pericardium is relatively stiff, it has a limited reserve volume. Small but rapidly accumulating effusions quickly exceed the compliance of the parietal layer. Once the limit of pericardial stretch is exceeded, even small increases in volume cause a steep increase in pericardial pressure causing external compression

Chronic accumulation over a prolonged period allows for pericardial stretch and compensatory mechanisms meaning that the intra-pericardial pressure remains low despite a large amount of fluid within the space. Even with additive amounts of fluid, the pericardial compliance curve remains less steep than in the acute setting resulting in slower increases in intra-pericardial pressures relative to the volume of

The type of fluid that accumulates may influence the haemodynamic presentation. Exudative fluid may become fibrinous and cause constriction, haemorrhagic fluid may contain clots causing isolated chamber compression and chronic effusions

The compliance of the pericardial tissues is also an important determining factor in the overall haemodynamic effects of an effusion. Pericardial compliance is decreased in mesothelioma, scarring from previous cardiac surgery and constrictive states. Once intra-pericardial and intracardiac pressures increase beyond a certain limit, cardiac chamber filling and preload are reduced which causes a drop in stroke volume and cardiac output. This decrease in cardiac output causes a reduction in organ perfusion which triggers compensatory mechanisms including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The resultant tachycardia, peripheral vasoconstriction and fluid retention are an attempt to maintain systemic blood pressure and organ perfusion in the face of a

Tamponade physiology occurs when cardiac chambers exhibit compression due to an increase in intra-pericardial pressures and equalisation of transmural pres-

#### *Anaesthesia for Patients with Pericardial Disease DOI: http://dx.doi.org/10.5772/intechopen.82540*

*Inflammatory Heart Diseases*

ated with increased incidence of PPE [33, 37].

pericardial separation is >20 mm [3, 32, 35].

are necessary to ensure appropriate and timeous management.

prolonged cardiopulmonary bypass (CPB) times. In other studies, female gender, pre-operative use of anticoagulants and early chest drain removal have been associ-

Although TTE remains the diagnostic tool of choice, detecting effusions and tamponade post-operatively may be challenging [31, 32, 38]. Patients who have altered anatomy are most likely to be on positive pressure ventilation with positive end expiratory pressure (PEEP), may have pneumopericardium (air trapped in the pericardium) and will have drains in situ. Effusions post cardiac surgery are often loculated causing regional compression of only one or some of the cardiac chambers. Blood and clots collect in the posterior sinuses making diagnosis via the traditionally accepted criteria on TTE difficult. Trans-oesophageal echocardiography (TOE) is well tolerated in sedated or anaesthetised patients but is more invasive and may not be readily available. Supplemental modalities such as CT scan and cardiac MRI have

been suggested to aid in the diagnosis when TTE is inconclusive [6, 31, 38].

*3.4.1.3 Effusions in patients undergoing percutaneous cardiac interventions*

Percutaneous intracardiac intervention is a risk factor for the development of pericardial effusion and tamponade [39–41]. The exact incidence depends on the procedure performed, the extent of the intervention, whether it is diagnostic or therapeutic, and if anticoagulation is used in the peri-procedural period. The exact procedure-specific incidence is difficult to determine, and small to moderate effusions may occur much more frequently than studies suggest [39]. The incidence of tamponade ranges from <1 to 6% depending on the study being quoted. Some of the more commonly performed interventions include atrial fibrillation ablation associated with a 4% risk of tamponade, permanent pacemaker insertion which carries a 1.7% risk of cardiac perforation and life-threatening tamponade and left atrial

Indications for drainage of effusions are based on clinical and TTE findings of tamponade: left ventricular dysfunction in patients receiving intermittent positive pressure ventilation, loculated effusions or clots causing compression of the left atrium or left ventricle, documented collapse of right-sided chambers and if

Anaesthetic management of post-operative effusions and tamponade remains the same as for an effusion from any other cause. The need for ongoing inotropic support and appropriate mechanical ventilation, massive fluid shifts, ongoing bleeding due to surgical causes, coagulopathy due to anticoagulant use, intrinsic clotting abnormalities, need for massive blood transfusion, renal dysfunction and the significant risks of re-sternotomy are just a few of the unique challenges for the anaesthesiologist to consider when taking a cardiac patient back to theatre for re-intervention. Drainage procedures are most often limited to pericardiocentesis under ultrasound- or video-assisted guidance [25, 32, 35]. A small percentage of patients may require sternotomy for the effective management of post-operative

In the setting of post-operative haemodynamic deterioration, critical tamponade may develop quickly with even small amounts of fluid accumulation causing significant haemodynamic effects. The diagnosis should be made immediately in order to facilitate life-saving intervention. TTE remains the diagnostic tool of choice because it is non-invasive and has a high sensitivity and specificity for detecting the signs of cardiac tamponade [6, 24, 32, 35, 38]. It may also be useful in confirming or ruling out other causes for post-operative haemodynamic deterioration. Because tamponade is a dynamic pathological process, especially in the post-operative period, serial or repeat echocardiographic examinations coupled with ongoing clinical evaluation

**72**

effusions [25, 32].

appendage (LAA) occlusion procedures which are associated with a 1.8–3% risk of tamponade, most commonly due to LAA perforation.

The overall incidence of tamponade following percutaneous coronary intervention (PCI) is 0.12% and is associated with high mortality [40, 41]. Coronary artery perforation following percutaneous coronary intervention is found in 0.3% of patients of which 10% went on to develop tamponade [41]. The risks were increased in patients requiring more complex interventions and if athero-ablative procedures were performed instead of angioplasty and stent placement.

Pericardial effusion and tamponade following PCI usually present acutely in the catheterisation lab but can have an insidious onset and are an important cause for late hypotension post intervention [40].

The diagnosis of tamponade post PCI remains predominately clinical and should be confirmed with TTE and other imaging techniques as soon as possible in order to facilitate life-saving treatment drainage procedures as described below.

#### *3.4.2 Pathophysiology of pericardial effusions*

The haemodynamic effects of the effusion and the development of tamponade are dependent on the rate of fluid accumulation within the pericardial space, the total volume of fluid that accumulates, the type of the fluid that accumulates and the intrinsic compliance of the pericardial tissue layers [4, 5, 7, 24].

Because the pericardium is relatively stiff, it has a limited reserve volume. Small but rapidly accumulating effusions quickly exceed the compliance of the parietal layer. Once the limit of pericardial stretch is exceeded, even small increases in volume cause a steep increase in pericardial pressure causing external compression of the cardiac chambers and tamponade.

Chronic accumulation over a prolonged period allows for pericardial stretch and compensatory mechanisms meaning that the intra-pericardial pressure remains low despite a large amount of fluid within the space. Even with additive amounts of fluid, the pericardial compliance curve remains less steep than in the acute setting resulting in slower increases in intra-pericardial pressures relative to the volume of fluid within the space.

The type of fluid that accumulates may influence the haemodynamic presentation. Exudative fluid may become fibrinous and cause constriction, haemorrhagic fluid may contain clots causing isolated chamber compression and chronic effusions may become fibrotic and confining.

The compliance of the pericardial tissues is also an important determining factor in the overall haemodynamic effects of an effusion. Pericardial compliance is decreased in mesothelioma, scarring from previous cardiac surgery and constrictive states.

Once intra-pericardial and intracardiac pressures increase beyond a certain limit, cardiac chamber filling and preload are reduced which causes a drop in stroke volume and cardiac output. This decrease in cardiac output causes a reduction in organ perfusion which triggers compensatory mechanisms including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The resultant tachycardia, peripheral vasoconstriction and fluid retention are an attempt to maintain systemic blood pressure and organ perfusion in the face of a low cardiac output state.

#### **3.5 Tamponade**

Tamponade physiology occurs when cardiac chambers exhibit compression due to an increase in intra-pericardial pressures and equalisation of transmural pressures [3–10, 14–17, 22–24].

### *3.5.1 Causes of tamponade*

Patients most at risk for the development of tamponade are those with iatrogenic causes post-cardiac surgery, PCI, insertion of pacemaker or percutaneous valve repair, chest trauma where blunt injuries are five times more commonly associated with tamponade when compared with penetrating injuries [25], malignant disease which is the most common cause of cardiac tamponade accounting for up to 60% of cases [25] and ESRD. Uraemic disease accounts for 10–15% of cases, while the incidence of dialysis pericarditis is 12% in patients on long-term haemodialysis [18–21].

#### *3.5.2 Pathophysiology of cardiac tamponade*

Under normal circumstances, intra-pericardial pressures reflect intrathoracic pressures and are negative [3–10, 12, 21–31]. As fluid accumulates within the pericardial space, the intra-pericardial pressures increase. Pericardial pressures are elevated throughout the cardiac cycle and cause compression of chambers for the duration of diastole when intracardiac chamber pressures are lowest.

Impaired filling of the cardiac chambers leads to diastolic dysfunction and a type of obstructive shock [23]. The venous return pattern to the atria eventually becomes unimodal and is confined to ventricular systole. In severe tamponade, atrial filling only occurs when ventricular contraction forces the atrioventricular valvular apparatus towards the myocardial apex. This caudad motion of the tricuspid and mitral valves causes a decrease in atrial pressures and enhanced systemic and pulmonary venous return.

As tamponade physiology progresses, ventricular filling becomes highly dependent on atrial systole as the intra-pericardial pressures increase. The maintenance of a sinus cardiac rhythm becomes paramount to ensure adequate ventricular filling to maintain end-diastolic ventricular volumes which are equivalent to ventricular stroke volume.

Physiologically speaking, cardiac chamber filling pressures are dependent on the myocardial transmural pressure gradient expressed mathematically by the following:

transmural pressure = intra-pericardial pressure − intracardiac pressure

The intracardiac pressures are different for each chamber with right atrial pressures being the lowest to facilitate systemic venous return.

Based on Ohm's law (V = IR), in order to ensure filling and forward flow in a normal series circulation, there must be a pressure gradient (P1–P2 or V) between the systemic venous return and the aorta. The pressure gradients below are often seen during diagnostic cardiac catheterisation procedures when venous and arterial pressures are obtained and documented:

systemic venous return pressure ➤ right atrial pressure ➤ right ventricular end-diastolic pressure ➤ right ventricular systolic pressure ➤ pulmonary capillary wedge pressure ➤ pulmonary venous return pressure ➤ left atrial pressure ➤ left ventricular end-diastolic pressure ➤ left ventricular systolic pressure ➤ aorta

As the intra-pericardial pressure increases, extrinsic compression of the cardiac chambers occurs. Compression causes the intracardiac chamber pressures to increase, and the transmural pressures begin to equalise. Right-sided filling pressures during diastole are lower than the left and are the first to be equalled and then exceeded by the increasing intra-pericardial pressures.

**75**

hypertension.

*Anaesthesia for Patients with Pericardial Disease DOI: http://dx.doi.org/10.5772/intechopen.82540*

exceed systemic venous return pressures.

with dramatically reduced cardiac output.

avoided.

patients with tamponade.

*3.5.3 Classification of tamponade*

haemorrhage or post-cardiac surgery.

different forms [24, 25].

The right atrium and ventricle are compressed, right-sided chamber filling is compromised and the right atrial pressure, measured clinically as the central venous pressure (CVP), increases to try and maintain right ventricular filling. This causes a significant decrease in the venous return to the right heart as right atrial pressures

A decrease in right atrial venous return leads to impaired right ventricular filling, an underloaded right ventricle which functions at the lower end of the Frank-Starling curve and a resultant decrease in right ventricular stroke volume. Reductions in right ventricular stroke volume translate into decreased flow through the pulmonary circulation with decreased pulmonary venous return to the left atrium. With continued increases in the intra-pericardial pressures, equalisation of left-sided pressures eventually transpires. This results in massive reductions in and eventual cessation of diastolic filling and forward flow of blood through the heart

A cycle of exhaustive physiological compensation follows with eventual cardiac arrest manifested as pulseless electrical activity. Although reductions in coronary blood flow do occur with the drop in cardiac output and aortic diastolic pressures, this is coupled with limited cardiac work, and ischaemia is usually

It is of utmost importance to note that the equalisation of transmural pressures

found in cardiac tamponade is a dynamic process influenced by extra-cardiac factors. Induction of general anaesthesia causes a decrease in heart rate, vasodilation and direct myocardial depression. Coupled with the institution of positive pressure ventilation, massive decreases in venous return and cardiac output occur. Thus, induction of anaesthesia may precipitate complete cardiovascular collapse in

Patients at risk for the development of tamponade should therefore have echocardiographic studies to confirm their pre-operative haemodynamic state. In the event of potential or imminent tamponade, all elective procedures should be postponed and the pericardium drained via the most appropriate method to relieve

Not all cases of cardiac tamponade are uniform, and patients can present with

*Low-pressure tamponade* occurs at very low diastolic pressures of 6–12 mmHg and is present in patients with severe hypovolaemia. Patients do not present with the full clinical picture of tamponade until they have been adequately fluid resuscitated and are fluid replete. This form is often found in trauma patients with ongoing

*Regional tamponade* occurs when only specific cardiac chambers are compressed from localised amassing of fluid. This is a common finding post-cardiac surgery or myocardial infarction. Typical clinical findings of acute tamponade are often absent

*Hypertensive tamponade* is said to be present when there are classical features of tamponade but with elevated arterial pressures, sometimes over 200 mmHg. It is thought to be due to excessive beta-adrenergic drive in patients with pre-existing

*Effusive-constrictive pericarditis* is present when there is decreased pericardial compliance with a reduced pericardial cavity associated with an effusion. Constrictive physiology is present, and tamponade can occur even with minimal amounts of fluid accumulation. A variety of haemodynamic and imaging signs

transmural pressures before induction of anaesthesia is performed.

necessitating multimodal diagnostic imaging to make the diagnosis.

#### *Anaesthesia for Patients with Pericardial Disease DOI: http://dx.doi.org/10.5772/intechopen.82540*

*Inflammatory Heart Diseases*

*3.5.1 Causes of tamponade*

venous return.

stroke volume.

following:

*3.5.2 Pathophysiology of cardiac tamponade*

Patients most at risk for the development of tamponade are those with iatrogenic

Under normal circumstances, intra-pericardial pressures reflect intrathoracic pressures and are negative [3–10, 12, 21–31]. As fluid accumulates within the pericardial space, the intra-pericardial pressures increase. Pericardial pressures are elevated throughout the cardiac cycle and cause compression of chambers for the

Impaired filling of the cardiac chambers leads to diastolic dysfunction and a type of obstructive shock [23]. The venous return pattern to the atria eventually becomes unimodal and is confined to ventricular systole. In severe tamponade, atrial filling only occurs when ventricular contraction forces the atrioventricular valvular apparatus towards the myocardial apex. This caudad motion of the tricuspid and mitral valves causes a decrease in atrial pressures and enhanced systemic and pulmonary

As tamponade physiology progresses, ventricular filling becomes highly dependent on atrial systole as the intra-pericardial pressures increase. The maintenance of a sinus cardiac rhythm becomes paramount to ensure adequate ventricular filling to maintain end-diastolic ventricular volumes which are equivalent to ventricular

Physiologically speaking, cardiac chamber filling pressures are dependent on the myocardial transmural pressure gradient expressed mathematically by the

transmural pressure = intra-pericardial pressure − intracardiac pressure

sures being the lowest to facilitate systemic venous return.

exceeded by the increasing intra-pericardial pressures.

pressures are obtained and documented:

The intracardiac pressures are different for each chamber with right atrial pres-

Based on Ohm's law (V = IR), in order to ensure filling and forward flow in a normal series circulation, there must be a pressure gradient (P1–P2 or V) between the systemic venous return and the aorta. The pressure gradients below are often seen during diagnostic cardiac catheterisation procedures when venous and arterial

systemic venous return pressure ➤ right atrial pressure ➤ right ventricular end-diastolic pressure ➤ right ventricular systolic pressure ➤ pulmonary capillary wedge pressure ➤ pulmonary venous return pressure ➤ left atrial pressure ➤ left ventricular end-diastolic pressure ➤ left ventricular systolic pressure ➤ aorta

As the intra-pericardial pressure increases, extrinsic compression of the cardiac chambers occurs. Compression causes the intracardiac chamber pressures to increase, and the transmural pressures begin to equalise. Right-sided filling pressures during diastole are lower than the left and are the first to be equalled and then

duration of diastole when intracardiac chamber pressures are lowest.

causes post-cardiac surgery, PCI, insertion of pacemaker or percutaneous valve repair, chest trauma where blunt injuries are five times more commonly associated with tamponade when compared with penetrating injuries [25], malignant disease which is the most common cause of cardiac tamponade accounting for up to 60% of cases [25] and ESRD. Uraemic disease accounts for 10–15% of cases, while the incidence of dialysis pericarditis is 12% in patients on long-term haemodialysis [18–21].

**74**

The right atrium and ventricle are compressed, right-sided chamber filling is compromised and the right atrial pressure, measured clinically as the central venous pressure (CVP), increases to try and maintain right ventricular filling. This causes a significant decrease in the venous return to the right heart as right atrial pressures exceed systemic venous return pressures.

A decrease in right atrial venous return leads to impaired right ventricular filling, an underloaded right ventricle which functions at the lower end of the Frank-Starling curve and a resultant decrease in right ventricular stroke volume. Reductions in right ventricular stroke volume translate into decreased flow through the pulmonary circulation with decreased pulmonary venous return to the left atrium. With continued increases in the intra-pericardial pressures, equalisation of left-sided pressures eventually transpires. This results in massive reductions in and eventual cessation of diastolic filling and forward flow of blood through the heart with dramatically reduced cardiac output.

A cycle of exhaustive physiological compensation follows with eventual cardiac arrest manifested as pulseless electrical activity. Although reductions in coronary blood flow do occur with the drop in cardiac output and aortic diastolic pressures, this is coupled with limited cardiac work, and ischaemia is usually avoided.

It is of utmost importance to note that the equalisation of transmural pressures found in cardiac tamponade is a dynamic process influenced by extra-cardiac factors. Induction of general anaesthesia causes a decrease in heart rate, vasodilation and direct myocardial depression. Coupled with the institution of positive pressure ventilation, massive decreases in venous return and cardiac output occur. Thus, induction of anaesthesia may precipitate complete cardiovascular collapse in patients with tamponade.

Patients at risk for the development of tamponade should therefore have echocardiographic studies to confirm their pre-operative haemodynamic state. In the event of potential or imminent tamponade, all elective procedures should be postponed and the pericardium drained via the most appropriate method to relieve transmural pressures before induction of anaesthesia is performed.
