*3.5.3 Classification of tamponade*

Not all cases of cardiac tamponade are uniform, and patients can present with different forms [24, 25].

*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 haemorrhage or post-cardiac surgery.

*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 necessitating multimodal diagnostic imaging to make the diagnosis.

*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 hypertension.

*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

make for a mixed clinical picture. Drainage of the effusive fluid provides the best clue as symptoms of constriction persist in spite of appropriate drainage.

#### *3.5.3.1 Clinical signs and diagnosis*

Dyspnoea, orthopnoea, diaphoresis, chest pain and tachycardia are all nonspecific signs of pericardial effusion and tamponade. Muffled heart sounds, raised jugular venous pressure and hypotension are the features classically described as Beck's triad used in the diagnosis.

Pulsus paradoxus is a clinical sign commonly found in tamponade and refers to the exaggeration of the normal physiological variation in systolic blood pressure of more than 10 mmHg during negative pressure ventilation. Under normal physiological conditions, the intra-pericardial pressure mirrors intrathoracic pressures. Negative intrathoracic pressure generated on inspiration is transmitted to the heart, and the intra-pericardial pressure decreases. This in turn increases the transmural pressure gradient. The increase in transmural pressure gradient augments right atrial and ventricular filling during diastole. This is demonstrated on Doppler echocardiography by increased blood flow velocity across the tricuspid valve during inspiration [28].

The augmentation in right ventricular filling causes the intra-ventricular septum to shift to the left which transiently impacts on left ventricular filling. This is known as *interventricular dependence.* With normal pericardial pressures and compliance, compensation for this slight shift is maintained leading to minimal reductions in left ventricular end-diastolic volume. There is a small decrease in left ventricular stroke volume and cardiac output which results in a small decrease in systolic blood pressure during inspiration of not more than 10 mmHg. The augmented right ventricular stroke volume during inspiration translates into increased pulmonary venous return to the left atrium after several cardiac cycles. An increase in left ventricular stroke volume and systolic blood pressure is then seen during expiration.

In cardiac tamponade, this normal systolic pressure variation with respiration is exaggerated. With the decrease in pericardial compliance, the normal pericardial compensation for the left heart shift is lost. As the intra-ventricular septum shifts to the left, the left heart cannot expand because of the increased intra-pericardial pressures. Left ventricular filling and flow through the left ventricular outflow tract are affected to a greater degree resulting in *enhanced ventricular interdependence.* This translates into a decrease of systolic blood pressure of more than 10 mmHg during inspiration.

Pulsus paradoxus is not very sensitive or specific for cardiac tamponade and may be absent even when tamponade is present or be present with conditions other than tamponade [22, 24, 25].

Pulsus may be absent in the presence of tamponade with severe aortic regurgitation where left ventricular filling is maintained due to back flow from the aorta; with localised effusions or clot that compress only certain chambers of the heart; with an atrial septal defect where the pressure effect on the right atrium is balanced by the intra-cardiac shunt; and with severe right ventricular hypertrophy with pulmonary hypertension where the pressure effects from increased intra-pericardial pressure on right heart are less pronounced.

Pulsus paradoxus may exist in the absence of tamponade in severe chronic obstructive pulmonary disease, asthma or severe bronchospasm, hypovolaemia, congestive cardiac failure and obesity.

Pulsus paradoxus will be reversed in patients receiving *positive pressure ventilation* with increased systolic blood pressure noted on inspiration and a fall in systolic

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

as a sign of fluid responsiveness.

tion in patients with tamponade.

the heart within a large effusion [21].

for the diagnosis of tamponade [26].

*3.5.3.2 Special investigations*

blood pressure on expiration [22, 25]. This can be interpreted as systolic pressure variation in patients receiving mechanical ventilation which is often used clinically

Mechanical ventilation with PEEP has three main effects on cardiac physiology. (1) With the increase in intra-thoracic pressure, alveolar pressures increase more than pleural pressures which causes compression of pulmonary capillaries and increased right ventricular afterload. (2) Compression of pulmonary capillaries squeezes blood from the pulmonary bed into the left atrium augmenting left ventricular preload. (3)

The augmentation of left ventricular stroke volume and systolic function during inspiration leads to increased systolic blood pressures. Pulmonary transit time is approximately 2 s, and the drop in right heart cardiac output from positive intrathoracic pressures translates into a drop in left ventricular cardiac output and systolic blood pressure during expiration. A reversed pattern of pulsus paradoxus is seen. As mentioned above, the combination of decreased venous return or preload to the right heart with induction of anaesthesia plus the increased right ventricular afterload effects of mechanical ventilation can severely compromise cardiac func-

Chest X-ray will show an enlarged globular bottle-shaped cardiac shadow if the pericardial fluid volume is >200 ml, a widened mediastinum with a right costophrenic angle <90° and clear lung fluids [7–10, 12, 21–29]. There may be an associ-

ECG may show a sinus tachycardia which is the most common finding. Other findings may include low QRS and T wave voltages, PR segment depression, nonspecific ST-T wave changes and bundle branch block. Electrical alternans is the change in QRS voltage with each beat and reflects excessive swinging movement of

TTE is the investigation of choice to diagnose and evaluate pericardial disease [3–6, 12, 23–28, 30, 31]. It is a class 1 recommendation with a high sensitivity and specificity for the detection of effusions and tamponade. TTE in addition allows for the evaluation of myocardial and endocardial structures and function, aiding to rule out other causes for the clinical picture. A grading system for the size of the effusion is based on echo-free space in diastole with small effusions being <10 mm in size, moderate effusions 10–20 mm and large effusions >20 mm. Right atrial collapse and invagination for >30% of the cardiac cycle on ECHO is 100% sensitive

Other TTE signs of tamponade include distention and loss of respiratory variation in the size of the IVC which reflects increased right atrial pressures, increased respiratory variations in tricuspid and mitral trans-valvular inflow velocities on Doppler studies, intra-ventricular septal shift reflected clinically as pulsus paradoxus [26], localised or loculated effusions showing isolated chamber compression

Cardiac catheterisation is usually not performed in acute tamponade as TTE is less invasive, less time-consuming and diagnostic. If catheterisation is performed, a blunted Y descent may be demonstrated [29]. The Y descent on the CVP tracing after the v wave indicates opening of the tricuspid valve and reflects early diastolic filling of the right ventricle. Attenuation of the y descent reflects rapid equalisation of pressures between the right atrium and ventricle which leads to ineffective

and regional tamponade commonly encountered post-cardiac surgery [32].

ventricular filling during early diastole in tamponade (**Figure 1**).

ated pleural effusion that requires concurrent drainage and management.

Positive inspiratory pressure augments left ventricular systolic function.

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

*Inflammatory Heart Diseases*

*3.5.3.1 Clinical signs and diagnosis*

Beck's triad used in the diagnosis.

inspiration [28].

during inspiration.

tamponade [22, 24, 25].

pressure on right heart are less pronounced.

congestive cardiac failure and obesity.

make for a mixed clinical picture. Drainage of the effusive fluid provides the best

Dyspnoea, orthopnoea, diaphoresis, chest pain and tachycardia are all nonspecific signs of pericardial effusion and tamponade. Muffled heart sounds, raised jugular venous pressure and hypotension are the features classically described as

Pulsus paradoxus is a clinical sign commonly found in tamponade and refers to the exaggeration of the normal physiological variation in systolic blood pressure of more than 10 mmHg during negative pressure ventilation. Under normal physiological conditions, the intra-pericardial pressure mirrors intrathoracic pressures. Negative intrathoracic pressure generated on inspiration is transmitted to the heart, and the intra-pericardial pressure decreases. This in turn increases the transmural pressure gradient. The increase in transmural pressure gradient augments right atrial and ventricular filling during diastole. This is demonstrated on Doppler echocardiography by increased blood flow velocity across the tricuspid valve during

The augmentation in right ventricular filling causes the intra-ventricular septum to shift to the left which transiently impacts on left ventricular filling. This is known as *interventricular dependence.* With normal pericardial pressures and compliance, compensation for this slight shift is maintained leading to minimal reductions in left ventricular end-diastolic volume. There is a small decrease in left ventricular stroke volume and cardiac output which results in a small decrease in systolic blood pressure during inspiration of not more than 10 mmHg. The augmented right ventricular stroke volume during inspiration translates into increased pulmonary venous return to the left atrium after several cardiac cycles. An increase in left ventricular stroke volume and systolic blood pressure is then seen during expiration. In cardiac tamponade, this normal systolic pressure variation with respiration is exaggerated. With the decrease in pericardial compliance, the normal pericardial compensation for the left heart shift is lost. As the intra-ventricular septum shifts to the left, the left heart cannot expand because of the increased intra-pericardial pressures. Left ventricular filling and flow through the left ventricular outflow tract are affected to a greater degree resulting in *enhanced ventricular interdependence.* This translates into a decrease of systolic blood pressure of more than 10 mmHg

Pulsus paradoxus is not very sensitive or specific for cardiac tamponade and may be absent even when tamponade is present or be present with conditions other than

Pulsus may be absent in the presence of tamponade with severe aortic regurgitation where left ventricular filling is maintained due to back flow from the aorta; with localised effusions or clot that compress only certain chambers of the heart; with an atrial septal defect where the pressure effect on the right atrium is balanced by the intra-cardiac shunt; and with severe right ventricular hypertrophy with pulmonary hypertension where the pressure effects from increased intra-pericardial

Pulsus paradoxus may exist in the absence of tamponade in severe chronic obstructive pulmonary disease, asthma or severe bronchospasm, hypovolaemia,

Pulsus paradoxus will be reversed in patients receiving *positive pressure ventilation* with increased systolic blood pressure noted on inspiration and a fall in systolic

clue as symptoms of constriction persist in spite of appropriate drainage.

**76**

blood pressure on expiration [22, 25]. This can be interpreted as systolic pressure variation in patients receiving mechanical ventilation which is often used clinically as a sign of fluid responsiveness.

Mechanical ventilation with PEEP has three main effects on cardiac physiology. (1) With the increase in intra-thoracic pressure, alveolar pressures increase more than pleural pressures which causes compression of pulmonary capillaries and increased right ventricular afterload. (2) Compression of pulmonary capillaries squeezes blood from the pulmonary bed into the left atrium augmenting left ventricular preload. (3) Positive inspiratory pressure augments left ventricular systolic function.

The augmentation of left ventricular stroke volume and systolic function during inspiration leads to increased systolic blood pressures. Pulmonary transit time is approximately 2 s, and the drop in right heart cardiac output from positive intrathoracic pressures translates into a drop in left ventricular cardiac output and systolic blood pressure during expiration. A reversed pattern of pulsus paradoxus is seen.

As mentioned above, the combination of decreased venous return or preload to the right heart with induction of anaesthesia plus the increased right ventricular afterload effects of mechanical ventilation can severely compromise cardiac function in patients with tamponade.

#### *3.5.3.2 Special investigations*

Chest X-ray will show an enlarged globular bottle-shaped cardiac shadow if the pericardial fluid volume is >200 ml, a widened mediastinum with a right costophrenic angle <90° and clear lung fluids [7–10, 12, 21–29]. There may be an associated pleural effusion that requires concurrent drainage and management.

ECG may show a sinus tachycardia which is the most common finding. Other findings may include low QRS and T wave voltages, PR segment depression, nonspecific ST-T wave changes and bundle branch block. Electrical alternans is the change in QRS voltage with each beat and reflects excessive swinging movement of the heart within a large effusion [21].

TTE is the investigation of choice to diagnose and evaluate pericardial disease [3–6, 12, 23–28, 30, 31]. It is a class 1 recommendation with a high sensitivity and specificity for the detection of effusions and tamponade. TTE in addition allows for the evaluation of myocardial and endocardial structures and function, aiding to rule out other causes for the clinical picture. A grading system for the size of the effusion is based on echo-free space in diastole with small effusions being <10 mm in size, moderate effusions 10–20 mm and large effusions >20 mm. Right atrial collapse and invagination for >30% of the cardiac cycle on ECHO is 100% sensitive for the diagnosis of tamponade [26].

Other TTE signs of tamponade include distention and loss of respiratory variation in the size of the IVC which reflects increased right atrial pressures, increased respiratory variations in tricuspid and mitral trans-valvular inflow velocities on Doppler studies, intra-ventricular septal shift reflected clinically as pulsus paradoxus [26], localised or loculated effusions showing isolated chamber compression and regional tamponade commonly encountered post-cardiac surgery [32].

Cardiac catheterisation is usually not performed in acute tamponade as TTE is less invasive, less time-consuming and diagnostic. If catheterisation is performed, a blunted Y descent may be demonstrated [29]. The Y descent on the CVP tracing after the v wave indicates opening of the tricuspid valve and reflects early diastolic filling of the right ventricle. Attenuation of the y descent reflects rapid equalisation of pressures between the right atrium and ventricle which leads to ineffective ventricular filling during early diastole in tamponade (**Figure 1**).

#### **Figure 1.**

*CVP tracing in cardiac tamponade reflecting higher baseline pressures and attenuation of the y descent.*

### *3.5.4 Medical management of pericardial effusions and tamponade*

In about 60% of cases of pericardial effusion, an underlying disease process is known, and medical management would therefore be targeted at the aetiology [6]. In the absence of significant associated inflammation, NSAIDs, colchicine and steroids are generally ineffective, leaving no conservative management options for isolated effusions. In these instances, surgical drainage is indicated.

#### **3.6 Constrictive pericarditis (CP)**

Chronic inflammation of the pericardium causes it to thicken and become non-compliant and rigid [4, 6, 7, 9, 10, 12, 25, 31, 43–49]. This thickening may be concentric or regional depending on the cause. The pericardial space becomes obliterated as the visceral and parietal layers change and stiffen. Restriction of cardiac chamber expansion during diastole causes impedance of cardiac filling and diastolic dysfunction at both the atrial and ventricular levels. The usual form is constriction without effusion but effusive-constrictive forms can occur.

#### *3.6.1 Causes of constrictive pericarditis*

Causes are similar to those for acute and chronic pericarditis including infectious disease, radiation to the mediastinum, trauma and autoimmune conditions [4, 13, 14, 48, 49]. In the developing world, tuberculosis remains the most common cause with a prevalence of >90% in places where the HIV infection rates are high [49].

Post-cardiac surgery is the most common cause of CP in the peri-operative period. The usual presentation is constrictive pathophysiology with an increase in pericardial membrane thickness. However, constrictive pathophysiology may present in the absence of pericardial membrane thickening [4, 48].

Post surgery, blood in the pericardial space causes a post-pericardiotomy-type picture with inflammation and adhesions [4, 13, 14]. These adhesions diminish the pericardial space and cause a constrictive pathophysiological picture in spite of normal pericardial thickness. This is termed *normal thickness constrictive pericarditis*. In a Mayo Clinic study from 2003, 18% of patients with proven constriction who underwent pericardiectomy had a normal pericardial thickness of <2 mm on pre-operative imaging [48]. Disease of the pericardium in the normal thickness group consisted of mild focal areas of inflammation, calcification and fibrosis. The majority of patients were post-cardiac surgery and post chest irradiation or had suffered previous infective or idiopathic disease. Pericardiectomy was equally effective in relieving the disease symptoms in these patients compared with those who had a pericardial thickness > 2 mm. It would therefore seem reasonable to consider pericardiectomy in patients with a normal pericardial thickness if the endocardial biopsy is negative for restrictive cardiomyopathy [4, 48].

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disease process.

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

is mostly impeded during mid- to late diastole.

be met by an increase in heart rate.

support in the peri-operative setting.

*3.6.2.1 Clinical signs and diagnosis*

Under normal circumstances, the pericardium can accommodate changes in cardiac volume [4, 6, 9, 12, 25, 43, 46, 47, 49]. With ongoing inflammation, the pericardial compliance decreases. The now thickened, calcified and rigid pericardium encases the heart and limits cardiac chamber expansion during diastole. Initially, early diastolic filling is not affected, and the atrial contribution to ventricular filling

Over time, diastolic filling becomes severely impaired, and the total blood volume within the heart remains relatively constant during diastole, leading to a *fixed stroke volume state*. Any increases in tissue perfusion demands must therefore

One of the most important features of CP is that changes in intrathoracic pressures during the respiratory cycle are *not transmitted to the heart*. This is because the pericardial space has been destroyed by the inflammatory process and intrapericardial pressure no longer mirrors intrathoracic pressures [25]. This means that the normal augmentation of venous return to the right heart during inspiration does not occur. Lack of inspiratory decline in the jugular venous pressure leads rather to

Respiratory variation in systolic blood pressures may still be seen clinically as the pulmonary veins lie outside of the pericardium and the left atrium is only partially within the pericardial sac. Changes in intrathoracic pressures will therefore still cause changes in pulmonary vein flow despite the uncoupling of intra-pericardial and intrathoracic pressures [4]. During negative pressure ventilation, inspiration will cause the pressure gradient between the pulmonary veins and the left ventricle to decrease, resulting in a decrease in LV filling and a small decrease in systolic blood pressure. This effect, however, is not enough to cause pulsus paradoxus.

Another important pathophysiological feature of CP is the dramatic increase in ventricular interdependence [45]. Pressure changes in one ventricle will be transferred to the other which explains the observed equilibration of diastolic ventricular pressures. This increase in ventricular coupling means that there is little, if any, trans-septal pressure gradient during diastole. Abnormal shifting of the intraventricular septum has been observed in some studies but because the ventricles are operating at much higher baseline diastolic pressures, small changes in pressures

Chronic constriction of the myocardium can lead to damage of the underlying muscle tissue. Constriction causes the ventricles to operate at the lower end of the Frank-Starling curve which causes a kind of disuse atrophy within the myocardium. Myocardial atrophy may present with continued diastolic dysfunction coupled with significant systolic dysfunction even after successful pericardiectomy is performed and the myocardium is released. Often these patients will require ongoing inotropic

Signs and symptoms are usually non-specific and mimic right ventricular failure making diagnosis difficult [4, 6, 12, 25]. Tachycardia is the predominant sign because of the fixed stroke volume state. Arrhythmias, especially atrial fibrillation, are not uncommon. Fluid overload ranging from peripheral oedema to anasarca is a usual finding. This is due to venous hypertension which is often worsened by protein-losing enteropathy in decompensated disease. Patients may have associated pleural effusions and cachexia, indicating a chronic and insidious

an increase in CVP with inspiration which is known as Kussmaul's sign.

caused by septal shift have very little effect on overall ventricular filling.

*3.6.2 Pathophysiology of CP*
