Abstract
Pulmonary hypertension is associated with increased morbidity and mortality in patients undergoing surgery. It is important to understand the pathophysiology and causes. Early diagnosis and detection of right ventricular dysfunction allows for prompt intervention. The mainstay of management includes optimization of preload, augmentation of right ventricular contractility, maintenance of right coronary perfusion pressure, and reduction in pulmonary vascular resistance.
Keywords
lung transplantation, pulmonary hypertension, pulmonary vascular resistance, right ventricular failure
Case Synopsis
A 55-year-old man with end-stage lung disease undergoes bilateral lung transplantation for usual interstitial pneumonitis. After reperfusion of the second lung the patient develops ischemia-reperfusion injury with acute graft dysfunction, pulmonary hypertension, and right ventricular failure.
Problem Analysis
Definition
Pulmonary hypertension (PHT) is defined as an increase in mean pulmonary artery pressure (mPAP) greater than or equal to 25 mm Hg at rest. It can be subdivided according to the pulmonary artery wedge pressure (PAWP) into precapillary PHT (PAWP ≤15 mm Hg) and postcapillary PHT (PAWP >15 mm Hg).
PHT can be graded as mild, moderate, or severe:
- •
Mild: mPAP 25 to 40 mm Hg
- •
Moderate: mPAP 40 to 55 mm Hg
- •
Severe: mPAP greater than 55 mm Hg
The relationship of mPAP to cardiac output (CO) and pulmonary vascular resistance (PVR) is described by the following equation:
mPAP = CO × PVR
Therefore an increase in mPAP is due to an increase in either CO or PVR, or both. However, in the normal individual, the pulmonary circulation has high compliance, and an increase in CO is accompanied by pulmonary vessel recruitment and a decrease in PVR. This results in little increase in mPAP.
In postcapillary PHT the transpulmonary gradient (TPG) can be used to identify high-risk patients:
TPG = mPAP − PAWP
Patients with postcapillary PHT initially have a normal TPG (<12 mm Hg) but may progress to develop a mixed precapillary/postcapillary PHT with an elevated TPG. As TPG is influenced by cardiac output, PVR may provide a better indicator of mixed PHT. A normal PVR is less than 3 Wood units (<240 dynes/s/cm 5 ).
PHT can be classified based on pathology and pathophysiology ( Box 74.1 ).
- 1
Pulmonary arterial hypertension
- 1.1
Idiopathic
- 1.2
Inherited
- 1.3
Drug-induced
1 ′ Pulmonary veno-occlusive disease
1 ″ Persistent pulmonary hypertension of the newborn
- 1.1
- 2
Secondary to left-sided heart disease
- 2.1
Systolic dysfunction
- 2.2
Diastolic dysfunction
- 2.3
Valvular disease
- 2.1
- 3
Secondary to lung disease/hypoxia
- 3.1
Chronic obstructive pulmonary disease
- 3.2
Interstitial lung disease
- 3.3
Mixed restrictive/obstructive lung disease
- 3.4
Sleep disorders
- 3.1
- 4
Chronic thromboembolic pulmonary hypertension
- 5
Multifactorial mechanisms
- 5.1
Hematologic disease
- 5.2
Systemic disorders
- 5.3
Metabolic disorders
- 5.1
Recognition
Acute PHT can be readily detected by the presence of a pulmonary artery catheter (PAC).
In the absence of a PAC, transesophageal echocardiography (TEE) can assist in the diagnosis. In the presence of tricuspid regurgitation (TR) and interrogation of the TR jet peak velocity (V TR ) with continuous-wave Doppler, the simplified Bernoulli equation can be applied to estimate the systolic pulmonary artery pressure (sPAP):
sPAP = 4 V 2 TR + CVP
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