Adenosine Stress Testing In Pulmonary Hypertension
Hemodynamic Study Protocol

Jones AT et al. Quantifying pulmonary perfusion in primary pulmonary hypertension using electron-beam computed tomography. Eur Respir J 2004; 23: 202–207. (National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, Royal Brompton Hospital, London, UK.) [Modified for use in the St. John Cardiac Catheterization Laboratory. JC 040610]

1. Those with overt right heart failure or hemodynamic instability should not undergo acute vasodilator testing. (2009 ACCF/AHA Expert Consensus criterion.)
    
2. Following the placement of arterial and quadruple-lumen pulmonary artery catheters,
    
3. A period of 15-20 min was allowed to reach a hemodynamic steady state.
    
4. An arterial sample for blood gas determination was obtained.
    
5. An intravenous infusion of adenosine commenced (50, 100, 200,300 mcg/kg/min.)
    
6. via the infusion port (the right atrial port) of the pulmonary artery catheter, [Adenosine half-time is approximately 10 seconds, necessitating right atrial infusion.]
    
7. each dose being administered for a period of 3–5 min.
    
8. Pulmonary and systemic hemodynamic data were recorded at baseline and during steady state conditions at the end of each dosing interval.
    
9. Pulmonary artery occlusion pressure was estimated following inflation of the catheter balloon, values being taken at end-expiration and averaged over three respiratory cycles.
    
10. Cardiac output measurements were taken in triplicate, each following an injection of 10 mL of 5% dextrose at room temperature, and averaged. (Comment: Tricuspid regurgitation can produce underestimation of cardiac output by thermodilution. Estimated Fick cardiac output provides confirmation of cardiac output.)
     
11. Optional but recommended: Systemic arterial and PA (from the distal [= yellow] port of the Swan-Ganz catheter) samples were obtained at the end of each dosing period for O2 saturation determination, for estimated Fick cardiac output calculation.
     
12. Vascular resistances were calculated using standard equations.
     
13. The dose of adenosine was increased until a positive response was obtained, the patient suffered side effects (chest discomfort, flushing), there was a clinically relevant fall in systemic arterial pressure or the protocol dose limit was reached.
     
14. The current hemodynamic definition of PAH is a mean pulmonary artery pressure (mPAP) greater than 25 mm Hg; a pulmonary capillary wedge pressure (PCWP), left atrial pressure, or left ventricular end-diastolic pressure (LVEDP) less than or equal to 15 mm Hg; and a pulmonary vascular resistance (PVR) greater than 3 Wood units. (To convert from dyn·s·cm-5 to Wood units you must divide by 80.)  (JACC. 53:1557, 2009)
     
15. The current definition of an acute responder (to identify potential candidates for long-term calcium-channel blocker therapy) is a reduction in mPAP of at least 10 mm Hg to an absolute mPAP of less than 40 mm Hg without a decrease in cardiac output. This definition does not apply to other therapies, such as epoprostenol (Flolan) therapy. (JACC. 53:1557, 2009)
     
16. An older definition of a positive vasodilator response was a 20% decrease in pulmonary vascular resistance.