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22 Pulmonary Endarterectomy Surgery

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Fig. 22.3 Instruments for pulmonary endarterectomy

Fig. 22.5 Example of

endarterectomy specimen, subsegmental disease

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Fig. 22.4 Small distal web in subsegmental branch

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Fig. 22.6 Example of endarterectomy specimen, ne segmental ‘tails’

D. P. Jenkins

Fig. 22.7 Example of endarterectomy specimen, laminated thrombus on right side

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Concomitant Procedures

If further procedures are required, they are usually performed during this rewarming period. Coronary and valve surgery may be necessary especially in older patients. Although tricuspid regurgitation is often a feature of the presentation, repair is usually unnecessary as once the PVR is reduced and the right heart remodels, it regresses.

Separation fromCPB

Once fully rewarmed, preparation is made to wean from CPB.The lungs are ventilated with a protective reduced tidal volume regimen during the rewarming phase. Our standard practice is to use low dose dopamine and avoid inodilators. I aim to ll to approximately 50% of the pre-CPB right atrial pressure and gradually reduce CPB ow litre by litre aiming to keep the right heart as empty as possible and the PA pressure as low as possible, but achieve adequate cardiac output and perfusion pressure. The latter is critical for optimal right ventricular function and sometimes vasoconstrictors are

required. It is an important time and requires cooperation between anaesthetists, perfusionist, and the surgeon. Many of the specic serious potential complications of PTE surgery will become apparent at this time, airway haemorrhage, reperfusion pulmonary oedema, and residual PH with right heart failure.

Closure

Meticulous haemostasis is required as we try to avoid use of blood products. Otherwise decannulation, reversal of heparin and closure are as for standard cardiac surgery. We leave two pericardial drains and open the right pleura, with a further drain to reduce the risk of pericardial effusion and late tamponade.

Suggested Reading

Delcroix M, Torbicki A, Gopalan D, Sitbon O, Klok FA, Lang I, etal.

ERS statement on chronic thromboembolic pulmonary hyperten-

sion. Eur Respir J. 2021;57:2002828. Jenkins DP, Tsui SS, Taghavi J, Kaul P, Ali J, Ng C. Pulmonary

thromboendarterectomy—the Royal Papworth experience. Ann

Cardiothoracic Surg. 2022;11(2):128.

Part VIII

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Pericardial Disease

Pericardiectomy forConstrictive

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Pericarditis

JasonAli

The heart is found within the pericardial sac. The pericardium is divided into two layers—the brous pericardium and the serous pericardium (Fig.23.1). The brous pericardium is an outer broelastic layer. The inner serous pericardium, formed of a thin layer of mesothelial cells is invested by the heart, thus creating two layers—the visceral serous pericardium which is continuous with the outer layer of the epicardium and the parietal serous pericardium which is continuous with the inner layer of the brous pericardium (Fig.23.2). The potential space between these two layers is the pericardial cavity.

Constrictive pericarditis describes a physiological state whereby the volume of the heart is restricted by the pericardium, which is typically brotic, calcied and thickened (Fig.23.3). The constrictive pericardium limits cardiac lling leading to diastolic heart failure.

Worldwide, the commonest cause of constrictive pericarditis is tuberculosis. This is rarer in developed countries where the commonest causes are idiopathic or related to prior cardiac surgery or irradiation. Other less common causes include mesothelioma, drug-induced, sarcoidosis, carcinoid syndrome, uraemia and following myocardial infarction. A septic pericarditis can also be seen following a range of bacterial or viral infections and may be associated with pleural effusion and pneumonia.

Patients with constrictive pericarditis experience symptoms of both left and right heart failure and display some classic signs including Kussmaul’s sign (paradoxical increase in JVP occurring during inspiration) and pulsus paradoxus (an exaggerated fall in a patient’s systolic pressure during inspiration by greater than 10 mmHg). Imaging usually reveals a markedly thickened and calcied pericardium (Fig.23.4) with evidence of constrictive physiology. There are some physiological similarities with restrictive cardiomyopathy, but the diagnosis can be differentiated with careful imaging.

Constrictive pericarditis is typically a chronic progressive condition, and surgical pericardiectomy is the only denitive treatment available, but leads to a complete symptomatic relief. In the acute/early-stage steroids may ameliorate the condition, but progression will lead to the need for surgical release of the heart.

Pericardiectomy entails mechanical release of the heart by excising as much of the pericardium as possible. The standard procedure is to release the heart from phrenic nerve to phrenic nerve. If there is severe basal and posterior constriction, then diaphragmatic and posterolateral excision of the pericardium is necessary as far as possible to minimise the persistence of restriction to lling of the left side of the heart.

J. Ali (*) Department of Cardiothoracic Surgery, Royal Papworth Hospital, Cambridge, UK e-mail: Jason.ali@nhs.net

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J. Ali

Fig. 23.1 Low-powered section showing the layers

Myocardium

Endocardium

The heart wall

Parietal

pericardium

Visceral

pericardium

Pericardial

cavity

23 Pericardiectomy forConstrictive Pericarditis

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Fig. 23.2 High-powered section showing the cell types

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Fig. 23.3 Constrictive pericarditis

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Fig. 23.4 Axial contrast CT scan demonstrating a calcied and thickened pericardium (grey arrows)

Surgical Correction

Pericardiectomy is typically performed through a median sternotomy incision. The aim is to achieve complete removal of all thickened pericardium and epicardium from the left and right ventricle and diaphragm, whilst preserving both phrenic nerves. Clearance of pericardium from ‘phrenic to phrenic’ alone is likely to fail to release a signicant proportion of the left ventricle leading to a higher incidence of recurrent constrictive pericarditis.

In the majority of cases, cardiopulmonary bypass can be avoided, unless there is marked adherence to the myocardium. In these cases, cardiopulmonary bypass may be used with or without aortic cross-clamping.

The conventional teaching is to consider decorticating the left ventricle rst, to avoid pulmonary oedema developing due to release of the right ventricle whilst the left is still constricted. However, this is rarely performed as the theoretical

J. Ali

risk of pulmonary oedema is not observed in practice, and this approach is not possible via median sternotomy and would require a thoracotomy.

Complete resection of the pericardium overlying the atria is often technically difcult as a result of the weakness of the atrial wall but should be done as leaving it risks residual constrictive haemodynamics. Densely adherent and calcied pericardium overlying the right atrium will need very careful and painstaking work but should be attempted.

Of critical importance is avoidance of injury to the phrenic nerves as this will lead to signicant postoperative morbidity. Particular attention should be made to identify these early. This is achieved by examining the pericardium from the intra-pleural surface upon which the nerves will be found. The left side is more difcult as it frequently lies quite posteriorly. However, the operator will know that it lies anterior to the hilum of the lung. (Fig.23.5) but this can be challenging particularly in constrictive pericarditis following cardiac surgery.

The brous and serous pericardial layers should be dissected off the heart sharply, typically using scissors. It can be difcult to identify the correct plane and there can be bleeding from the raw epicardial surface (hence the aim should be to perform without cardiopulmonary bypass and systemic heparinisation if possible). Great care should be taken to identify and thus avoid injury to the coronary arteries (Fig.23.6).

If it is not possible to dissect areas of constrictive pericardium due to strong adherence to the epicardium, and alternative approach is to score the pericardium sharply with multiple horizontal and vertical lines, creating a grid-like appearance which does allow for some release of constriction and ventricular expansion during diastole (Fig.23.7).

Post-operatively careful medication with diuretics and rhythm control is important as right ventricular overload and pulmonary oedema are easily precipitated as the restricted blood enters the right side more easily causing rapid dilation.

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Fig. 23.5 Anatomy of the phrenic nerves in relation to the hilum of the lung and the mediastinum from both the right and left

Clavicle

Right superior

intercostal vein

Second ganglion

of sympathetic trunk

Intercostal muscles

Sympathetic trunk

Intercostal nerves

Azygos vein

Oesophagus

Parietal pleura

(costal part)

Posterior intercostal

arteries

Posterior intercostal

veins

Greater splanchnic

nerve

Central tendon of

diaphragm

Diaphragm

Right

subclavian artery

Subclavius Right subclavian

vein

Trachea

Vagus nerve (cardiac branches)

Superior vena cava

Pulmonary plexus of vagus nerve

Thymus

Pericardiophrenic artery Pericardiophrenic vein Arch of azygos vein

Right main bronchus Right pulmonary arteries Myocardium

Right phrenic nerve Parietal pleura (costal

part) Right pulmonary

veins

Sympathetic trunk (Communicating branches)

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J. Ali