Abstract
Pulmonary vascular surgery comprises emergency procedures such as pulmonary embolectomy and post-traumatic repair, and elective procedures such as palliation of PHT, pulmonary thromboendarterectomy (PTE), tumour resection and the Ross procedure. The focus of this chapter will be PHT and the management of patients undergoing PTE.
Pulmonary vascular surgery comprises emergency procedures such as pulmonary embolectomy and post-traumatic repair, and elective procedures such as palliation of PHT, pulmonary thromboendarterectomy (PTE), tumour resection and the Ross procedure. The focus of this chapter will be PHT and the management of patients undergoing PTE.
Pulmonary Hypertension
PHT is defined as a mean PAP (mPAP) greater than 20 mmHg at rest and can be graded as mild (mPAP 20–30 mmHg), moderate (mPAP 30–40 mmHg) and severe (mPAP > 40 mmHg). It is divided according to PAWP into pre-capillary PHT (PAWP < 15 mmHg) and post-capillary PHT (PAWP > 15 mmHg). The classification of PHT is based on pathophysiology (Box 15.1).
Box 15.1 Classification of PHT
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The PVR (in Wood units) is derived from the CO and mPAP:
A normal PVR is under 3 Wood units (3 mmHg min l–1, i.e. 240 dyne s cm–5).
Management
The treatment of PHT is based on the underlying aetiology.
Class 1 PHT is characterized by medial hypertrophy intimal proliferation of the distal pulmonary arteries. Treatment comprises anticoagulation and pharmacological therapy with pulmonary vasodilators (Table 15.1). Patients whose disease progresses despite maximal medical therapy, with evidence of RV failure, can be considered for lung transplantation.
Table 15.1 Pulmonary vasodilators
| Inhaled | IV | Oral |
|---|---|---|
| NO PGI2 analogues Milrinone | PDE-5 inhibitors PGI2 analogues Milrinone Dobutamine Nitroglycerine | PDE-5 inhibitors PGI2 analogues ET antagonists Riociguat Calcium channel blockers |
ET, Endothelin; PDE, phosphodiesterase; PGI2, prostaglandin I2.
Class 1’ PHT (pulmonary veno-occlusive disease) involves fibrotic occlusion of pulmonary venules. There is no established therapy and early referral for lung transplantation is recommended.
Class 2 PHT is post-capillary in nature and typically presents with pulmonary vein engorgement, capillary dilatation and interstitial oedema. Treatment is aimed at relieving the underlying left-heart pathology. The use of pulmonary vasodilators is not recommended and may be detrimental to outcome.
Class 3 PHT involves intimal obstructive proliferation of distal pulmonary arteries. There is no specific therapy other than oxygen supplementation.
Class 4 PHT is due to CTEPH, with formation of organized thrombi, webs and bands replacing the normal intima, occluding the PAs. In addition, smooth-muscle cell proliferation results in medial thickening and pulmonary vascular remodelling. The mainstay of treatment is surgery, in the form of PTE.
Class 5 PHT is a heterogeneous group of conditions with varying pathology and management is dependent upon aetiology.
Atrial Septostomy
Patients with class 1 PHT have a survival benefit if they have a concurrent PFO. Patients who are refractory to optimal pulmonary vasodilator therapy can be considered for balloon atrial septostomy (BAS) as a palliative or bridging procedure. BAS can decompress the right heart and increase LV preload, enhancing the CO. However, BAS is contraindicated in patients with a baseline SaO2 below 80%, as the right-to-left shunt will worsen the SaO2.
RV Pathophysiology
The normal RV is a thin-walled chamber, vulnerable to acute elevations in the PVR, such as PE. The resultant acute increase in RV afterload can precipitate a lethal RV failure. Chronic increases in the PVR lead initially to compensatory RV hypertrophy and, if left untreated, to dilatation and, ultimately, to RV failure. Right coronary artery (RCA) perfusion pressure is determined by the aortic root pressure and the RV pressure, and in the normal heart occurs throughout the cardiac cycle. As PHT develops, coronary perfusion becomes predominantly diastolic. When suprasystemic PHT occurs, RV perfusion is confined to diastole, which itself is reduced in duration secondary to the compensatory tachycardia of RV dysfunction (Figure 15.1).
The subsequent imbalance between oxygen supply and demand exposes the RV to ischaemia and dysfunction. This in turn results in an elevated RV end-diastolic pressure (RVEDP), a reduced CO and systemic hypotension, which further reduces the coronary perfusion pressure, producing a downward spiral of a worsening RV function and decreased CO, ultimately culminating in RV failure.
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