Pulmonary Artery Catheterization for Evaluation of Pulmonary Hypertension

By Adriano Tonelli MD, MS

Physicians use pulmonary artery catheterization (PAC) to diagnose pulmonary hypertension (PH) and distinguish between the two major hemodynamic types of the disease, pre- and postcapillary PH. While PAC is the current gold standard, awareness among pulmonologists is increasing that traditional hemodynamic determinations may be insufficient to identify early stages of the disease, allocate patients to the pre- or postcapillary groups of the disease and guide treatment decisions. Moreover, a multicenter study showed that a third of patients referred to PH centers were initially misdiagnosed and inappropriately treated. 1 In order to overcome these limitations, our laboratory performs a variety of maneuvers during PAC to better understand the cardiopulmonary hemodynamics and more precisely characterize the type of PH.

Obtaining accurate hemodynamic measures

The recent proceedings of the 6th World Symposium on PH define precapillary PH as a mean pulmonary artery pressure (mPAP) of > 20 mm Hg, a pulmonary artery wedge pressure (PAWP) ≤ 15 mm Hg and a pulmonary vascular resistance ≥ 3 Wood units. Postcapillary PH is present when mPAP is > 20 mm Hg and PAWP is > 15 mm Hg.2

These hemodynamic definitions emphasize the critical importance of obtaining reliable hemodynamic measures, particularly PAWP and cardiac output (CO). At Cleveland Clinic, we pay particular attention to the PAWP determination3 and always confirm unexpected or abnormal CO values with direct Fick determination. Direct Fick CO requires the measurement of arterial and mixed venous oxygen content as well as oxygen uptake (VO2). We determine VO2 at the time of PAC using a metabolic cart.

Established methodologies

Established maneuvers that challenge the pulmonary circulation include vasodilatory testing (commonly performed using inhaled nitric oxide),4 exercise testing and rapid fluid administration. The pulmonary vasodilatory test is used to identify patients with reversible vasoconstriction who could benefit from calcium channel blockers. During exercise, the CO and blood flow through the pulmonary vasculature increase; however, the pulmonary pressures marginally increase given vascular recruitment and vasodilation. A disproportionate increase in mPAP and PAWP could represent exercise PH and/or left ventricular diastolic dysfunction. Rapid fluid infusion increases the left ventricular end-diastolic volume, potentially unmasking heart failure with preserved ejection fraction.

Cardiopulmonary exercise testing can grade the severity of functional limitation and provide prognostic information in patients with PH.5 When combined with invasive hemodynamic determinations, the invasive CPET can better delineate the cardiopulmonary pathophysiology and nature of the exercise limitation, particularly in patients with dyspnea and mild PH.

Other techniques

Other less frequently used methodologies that may provide valuable information include temporary arteriovenous (AV) dialysis access exclusion, dobutamine infusion and estimation of intrathoracic pressure using an esophageal balloon. The temporary AV dialysis access exclusion is important to determine the impact that an AV fistula has on cardiac output (CO) and mPAP, which may be elevated particularly in fistulas with high flow.

A dobutamine infusion increases the CO and thus the mPAP. A disproportionate increase in mPAP for the rise in CO suggests a decrease in the right ventricular contractile and pulmonary vasodilatory reserve.

Pulmonary vascular pressures and PAWP measured during PAC reflect both true intravascular pressure and the effect of surrounding intrathoracic pressure. The intrathoracic pressure can be estimated with an esophageal balloon catheter and may be higher (positive numbers) in subjects with obesity and/or advanced chronic obstructive disease. It is important to recognize cases in which the intrathoracic pressure is elevated, since an oversight of this possibility can lead to the incorrect diagnosis of PH and its attribution to a postcapillary etiology.6 In fact, we previously showed that one-third of patients who are overweight are misdiagnosed with postcapillary PH when PAWP is unadjusted6.

In summary, selected maneuvers during PAC stand to provide critical information to improve the diagnosis, optimize treatment selection and impact prognosis. These maneuvers should be particularly considered in cases of unexplained dyspnea, normal or borderline pulmonary pressures and uncertain PH type.

References

1. 1. Deano RC, Glassner-Kolmin C, Rubenfire M, et al. Referral of patients with pulmonary hypertension diagnoses to tertiary pulmonary hypertension centers: the multicenter RePHerral study. JAMA Intern Med. 2013;173:887-893.
   2. Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. Eur Respir J. 2019;53(1):1801913.
   3. Tonelli AR, Mubarak KK, Li N, Carrie R, Alnuaimat H. Effect of balloon inflation volume on pulmonary artery occlusion pressure in patients with and without pulmonary hypertension. Chest. 2011;139:115-121.
   4. Tonelli AR, Alnuaimat H, Mubarak K. Pulmonary vasodilator testing and use of calcium channel blockers in pulmonary arterial hypertension. Resp Med. 2010;104:481-96.
   5. Frost A, Badesch D, Gibbs JSR, et al. Diagnosis of pulmonary hypertension. Eur Respir J. 2019;53:1801904.
   6. Jawad A, Tonelli AR, Chatburn RL, Wang X, Hatipoglu U. Impact of intrathoracic pressure in the assessment of pulmonary hypertension in overweight patients. Ann Am ThorSoc. 2017;14:1861-1863.