Current Medications for Stephen Druley - September 29, 2009
Micardis HCT
Finasteride
Ropinerole
Lexapro
Flomax
Warfarin
Simvastatin
PE Medical Chronology
1) In early 2005 had surgery for herniated naval
2) In 2005 had mild shortness of breath at work in December while climbing the steps to work. Went away in Spring
3) In 2006 had shortness of breath at work in December. Went away in Spring
4) In 2007 had worrisome shortness of breath at work in January. Went away in Spring
5) In 2008 had significant shortness of breath at work. Could not walk from office to office. Needed help to get to my car.
6) After CT Scan found several blood clots in my lungs in February 2008. In hospital (CVMC) for 4 days to dissolve clots. Began Warfarin treatment.
7) In February 2009 had negative D-Dimer but was positive after stopping Warfarin for three weeks. Restarted Warfarin in April 2009.
8) In August 2009 was diagnosed with very mild adult onset asthma but inhalers seem not to address the underlying problem. The pulmonologist also noted that the top lobes of the lungs are very slightly enlarged, perhaps demonstrating the onset of some initial malformations.
Medical Symptoms and Issues around PE
1) Continued high blood pressure that began in January of this year but blood pressure medicine took care of this.
2) Low O2 SAT
3) Continued shortness of breath during exertion
Echocardiogram History of Pulmonary Pressure (normal = less than 25 at rest)
12/2007
60
2/2008
40
6/2008
35
8/2009
35
9/2009
30
A Patient's Experiential Perspective on PE
It would appear that HCT has a remarkable impact on increasing the on-demand flow rate of oxygen rich blood from the pulmonary arterial system to the heart. If one were to understand the mechanisms for this success then it might shed some light on both short and long-term post treatments for PE.
Prior to my hospitalization, which included low molecular weight Heparin treatment, it was evident that my pulmonary arterial pressure was elevated. This was verified by an echocardiogram. I can understand this, particularly, since the clots themselves and possibly scarring of the walls of the affected arteries may have created the pressure differential.
Subsequent echocardiograms have shown that the internal pressure has decreased but not to the level that would be considered normal. This leads me to believe that residual scarring may be contributing to the sustained pulmonary pressure.
My O2 levels, since hospitalization, have shown a mean of 93 with a low of 89 and a high of 98. The high reading was when I intentionally tried to over oxygenate prior to the test.
So what does this mean to me and the lifestyle that I am currently experiencing?
1) When I am not under a great deal of exertion I feel fine.
2) When I play tennis, I can only play doubles for a couple of games then have to sit out for two games to bring my O2 level back to above 90.
3) It is as though the rate of oxygenation and transfer reaches a mechanical upper limit and the demand that comes with exertion cannot be meet, although my recovery time is very short.
My Questions for the Medical Community
1) As we look to the future, I am wondering if this residual elevated pressure between the lungs and heart carries with it a favorable prognosis.
2) Should I take some action now to mitigate the extra work that is presumably being carried out by the heart?
3) What long term affects are associated with a borderline residual elevated internal pressure
4) Should I not be proactive?
