Specific Laboratory Abnormalities:
9/14/04
ARTERIAL BLOOD GASES:
PH = 7.5 (7.35 - 7.45) elevated
PC02 = 27.2 mmhg (35- 45 mmhg) decline
P02 = 80 mmhg (80-100 mmhg) borderline
SA02 = 81% (pulse oximetry)
Temperature = 97.3 degrees
Carboxyhemoblobin 1% (normal)
COMMON CHEMISTIRES:
BUN = 8.0 (10 -26 mg/dl) decline
HEMOGRAM:
Lymph = 11.2% (21 - 51%) decline
Neut = 84.5% (36 - 72%) elevated
REFERENCE TESTING:
Lead Level = less than 3.0 mcg/dl (normal)
Lyme ELISA and WB - negative
04/27/05
COMMON CHEMISTRIES:
Total Protein = 8.8 (6.3 - 8.5 g/dl) elevated
Albumin = 5.1 (3.3 - 5.0 g/dl) elevated
Liver function OK, AST/ALT/ALK PH OK
HORMONES:
Cortisol PM = 18.6 (2.3 - 12.0 mcg/dl) elevated
HEMOGRAM:
WBC = 3.8 (4.0 - 10.7 thous/cmm) decline
Lymph # = 1.0 (1.0 - 5.4 thou/cmm) borderline
REFERENCE:
ANA 3.3 (Range 0 - 2.9 u) flagged abnormal high positive. Mayo labs
URINALYSIS - negative
07/01/06
COMMON CHEMISTRIES:
Glucose Random - 116 (65 - 110 mg/dl) elevated, UA clear
CARDIAC MARKERS:
CPK-MB = 6.0 (0 - 5.0 ng/ml) elevated
CKMB-INDEX = 5.1 (0 - 5.0) elevated
HEMOGRAM:
Neut = 72.1 (36 - 72 %) elevated
09/10/06 LabCorp
Glucose - 102 (65 - 99) elevated
Total Bilirubin = 1.6 (0.1 - 1.2 mg/dl) elevated
TSH = 0.347 (0.350 - 5.5 uiU/ml) decline
Thyroxine = 13 (4.5 - 12.0 uG/dl) elevated
09/08/06
CPK-MB = 7.0 (0-5 ng/ml) elevated
CKMB-INDEX = 6.6 (0-5.0) elevated
Trop-T = 0.05 (0 - 0.03 ng/ml) elevated
All EKG's taken show non-specific ST-T wave changes, flat or inverted
T's in the inferior leads, complete RBBB (rSr complex with normal P
waves) in leads V1, V2, V6. No evidence of hypertrophy, strain. No ST
segment elevation. Computer mentions "inferior ischemia" and RBBB.
Is the "Chiari Network" in the right atrium of any clinical
consequence? Source of embolic material perhaps?
What can cause a mid to distal inferoapical ischemia finding on a
nuclear stress test?
-Bill
Andrew B. Chung, MD/PhD - 22 Jan 2007 10:57 GMT
> Specific Laboratory Abnormalities:
>
[quoted text clipped - 83 lines]
> Is the "Chiari Network" in the right atrium of any clinical
> consequence? Source of embolic material perhaps?
Associated with PFOs.
> What can cause a mid to distal inferoapical ischemia finding on a
> nuclear stress test?
In your case, without obstructive CAD, the explanation would be
hypoxia:
http://groups.google.com/group/sci.med.cardiology/msg/23d090787a9bc51b?
Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
> -Bill
ryancinman@aol.com - 22 Jan 2007 21:32 GMT
Dear Dr. Chung,
I sincerely appreciate your reply and input. I have printed out your
suggestions, and will take them with me to my next appointment on
2/16/06.
I will note that a standard echo w/bubble study did not reveal any
shunting, but the TEE you recommend seems highly warranted. I will
request the TEE.
What options are available for PFO treatment?
Again, I sincerely appreciate your reply.
Would a D-Dimer and V/Q Scan also be warranted, based on the continual
shortness of breath? Would recurring PE show up on these tests?
Best regards,
Bill
Andrew B. Chung, MD/PhD - 22 Jan 2007 22:36 GMT
> Dear Dr. Chung,
>
> I sincerely appreciate your reply and input.
You are welcome, Bill :-)
> I have printed out your
> suggestions, and will take them with me to my next appointment on
> 2/16/06.
It is my hope that my suggestions prove helpful toward your receiving
definitive care.
> I will note that a standard echo w/bubble study did not reveal any
> shunting, but the TEE you recommend seems highly warranted. I will
> request the TEE.
The transthoracic echocardiogram simply does not have the sensitivity
to detect a small PFO.
> What options are available for PFO treatment?
(1) Lifetime warfarin anticoagulation preventing both PEs and strokes.
(2) Transcatheter "clamshell" closure of PFO to prevent strokes and
warfarin to prevent PEs.
(2) Surgical closure of PFO to prevent strokes and warfarin to prevent
PEs.
> Again, I sincerely appreciate your reply.
>
> Would a D-Dimer and V/Q Scan also be warranted, based on the continual
> shortness of breath?
Only for sudden changes that suggest an acute PE event.
> Would recurring PE show up on these tests?
Only during the acute phase.
Again, I am sad to learn that you have suffered so long with this
problem.
Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
PetShopQueen007 - 23 Jan 2007 03:59 GMT
Hey Bill.
Going through a very similar thing, myself!!!
In the process of trying to get the same tests done after some rather
strange EKG and Echo results and similar symptoms.
Also, I agree with everything Andrew said.
Most docs seem to overlook Emboli events...
as for the drooping of your face in conjunction with these symptoms, I
most definitely agree some sort of a stroke occured in the fashion
Andrew suspects. not saying it is.. but soemthing to most definitely
look into.
wish ya luck!
> > Dear Dr. Chung,
> >
[quoted text clipped - 44 lines]
> Andrew B. Chung, MD/PhD
> http://EmoryCardiology.com
Kumar - 23 Jan 2007 09:47 GMT
> > Dear Dr. Chung,
Dr Andrew,
I appreciate your helping nature. God Bless you.
Just for curicity; ;
How followings abnormalities are related to this case;)
Elevated Cortisol, Respiratory Alkalosis on ABG
and TSH transiently low (mildly low).
Are these abnormalities as a result of problem or a cause to problem?
Andrew B. Chung, MD/PhD - 23 Jan 2007 10:55 GMT
> Andrew, in the Holy Spirit, boldly wrote:
>
[quoted text clipped - 3 lines]
>
> I appreciate your helping nature. God Bless you.
HE has blessed me more than the world will ever know.
> Just for curicity; ;
>
[quoted text clipped - 4 lines]
>
> Are these abnormalities as a result of problem or a cause to problem?
Presumably the result of recurring hypoxemia.
Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
Kumar - 24 Jan 2007 02:14 GMT
On Jan 23, 3:55 pm, "Andrew B. Chung, MD/PhD" <l...@thetruth.com>
wrote:
> > Andrew, in the Holy Spirit, boldly wrote:
> > > neighbor Bill (ryancin...@aol.com) wrote:
[quoted text clipped - 13 lines]
>
> > Are these abnormalities as a result of problem or a cause to problem?Presumably the result of recurring hypoxemia.
What caused Respiratory Alkalosis or what Respiratory Alkalosis could
cause? Can there be possibility of hypokalemia or electrolyte imbalance
or adrenal problem?
> Andrew <><
> --
> Andrew B. Chung, MD/PhDhttp://EmoryCardiology.com
ryancinman@aol.com - 24 Jan 2007 08:35 GMT
Kumar,
I can describe my findings for you.
The respiratory alkalosis was induced simply by hyperventilation
(overbreathing), trying to compensate for the low oxygen saturation
(hypoxia). Increased respirations are normal for a person who is
severely short of breath. Compensated respiratory alkalosis consists of
a low arterial C02 and elevated arterial pH. If the Bicarb is normal,
it is "compensated". This in itself is not an uncommon finding, and can
be related to many different etiologies (including anxiety).
My potassium was 3.3 measured during the initial event, so there was
Hypokalemia, but it wasn't significant. My potassium generally runs
around 3.5 (on the low side). It has been low all of my life, so I
don't presume that it is significant. It is proportional to the amount
of sodium as well (both are on the low side of normal).
Chloride, Calcium, Magnesium, and Phosphorus are all normal.
The Cortisol measure was 18.6 (with 12.0 being the cutoff value for a
high normal). This is a mild elevation, most likely induced by stress.
It may also be an immune response. I think Dr. Chung's suggestion of
antiphospholipid antibodies is the culprit for the elevation in plasma
Cortisol. I do not believe that the Cortisol itself is the problem, but
a response to an underlying problem. Cortisol is an immunosupressant.
Note the low white counts that I posted. The synthetic form of Cortisol
(Prednisone), is used to treat autoimmune diseases, as it supresses the
immune system.
The transient low TSH hasn't been explained. It varies from a low 0.347
to a normal range of 0.500. Again, it is probably a stress response to
an underlying condition. The figures of TSH and Cortisol are not
grossly abnormal, making them non-specific markers. The other data
gathered (cardiac data), is much more specific.
I've been evaluated for adrenal disease (no adenoma found), and for
extra-adrenal tumors (ACTH secreting tumors) of both the pituitary
gland and lungs. Nothing was found, because no endocrine problem
exsists.
The positive ANA finding that was non-specific is most certainly
related to the antiphospholipid antibodies that Dr. Chung has
described. My doctor has since ordered the tests recommended by Dr.
Chung, and I will post their results once I have them. I'm willing to
bet they will be positive.
In addition to the labwork Dr. Chung has recommended, I will be
undergoing a TEE w/bubble study, MRI of the brain and neck with
contrast, and a V/Q Scan of the lungs (all looking specifically for
embolic damage). These will take place mid February, and I'll post the
results in a new thread.
I would like to thank all of those who contributed to this thread, and
I am confident that my illness of two years duration will be resolved
by the data obtained from Dr. Chung.
For the two other posters, I hope that you find the answers you seek.
Best of regards,
Bill
Kumar - 24 Jan 2007 10:25 GMT
> Kumar,
>
> I can describe my findings for you.
Thanks. I am not the authority to advice. I just wanted to know as
alkalosis is also related to hypokalemia. Aldosterone level was another
thought. Dr.Andrew can explain better about potassium level.
"Metabolic acidosis (for example, caused by uncontrolled diabetes) or
alkalosis (for example, caused by excess vomiting) can affect blood
potassium.
Small changes in the potassium concentration outside cells can have
substantial effects on the activity of nerves and muscles. This is
particularly true of heart muscle. Low levels of potassium cause
increased activity (which can lead to an irregular heartbeat), whereas
high levels cause decreased activity. Either situation can lead to
cardiac arrest in some circumstances.
http://www.nlm.nih.gov/medlineplus/ency/article/003484.htm
Best wishes for better health.
Andrew B. Chung, MD/PhD - 26 Jan 2007 14:22 GMT
> Andrew, in the Holy Spirit, boldly wrote:
> > > Andrew, in the Holy Spirit, boldly wrote:
[quoted text clipped - 21 lines]
> What caused Respiratory Alkalosis or what Respiratory Alkalosis could
> cause?
Hyperventilation.
> Can there be possibility of hypokalemia or electrolyte imbalance
> or adrenal problem?
If there is, it would be secondary to the PEs.
Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com
> Hello all,
>
> My name is Bill, and for the past two years I've had an illness of
> unknown etiology. Prior to two years ago, I was in a normal state of
> health, and rarely, if ever became ill.
Sad to read that you still continue to suffer. I remember when you
posted a couple of years ago when I suggested that you request a
transesophageal echocardiogram (TEE) for a possible cardiac source of
peripheral emboli.
> The symptoms started on September 8 of 2004, with the abrupt onset of
> shortness of breath, tachycardia, left sided facial droop, tingling of
> the extremities, and cyanosis of the fingernails. At that time, not
> much testing was performed, but pulse oximetry revealed an SA02 of 86%
> which was self-resolving on oxygen.
Still sounds as though you suffered a pulmonary embolus (PE) with
paradoxical embolus to the brain.
> The hospital advised follow-up with my family doctor on 9/13/04. While
> in his office, another event transpired, similar to the original, but
> slightly worse. The SA02 reading was 81% at this time, again,
> self-resolving with supplemental oxygen. Blood gases revealed
> respiratory alkalosis with low P02 (80%).
Suspect a recurrent PE event.
> Spiral CT scan was used to rule out pulmonary embolus, and I have been
> evaluated by pulmonary, rheumatology, cardiology, neurology, and
> infectious disease doctors with no known etiology for the constellation
> of symptoms.
A spiral CT would not detect small peripheral emboli.
> An Echo and EKG taken November of 2004 were completely normal, as was a
> Technetium stress test. No abnormalities were noted, other than for
> non-specific ST-T wave changes on the EKG.
A TEE with bubble study probably should have been done.
> The symptoms and return of "events" that persisted over a two year
> period prompted me to seek a second opinion from another cardiologist.
[quoted text clipped - 3 lines]
>
> (1) Complete RBBB
Abnormal.
> (2) Tall R wave in lead V1 (normal P wave)
This would suggest an enlarged RV.
> (3) Flat and inverted T waves in all inferior leads
> (4) Prominent Q waves in leads AVL and V6
>
> Echocardiogram (present)
>
> (1) LVEDD measure of 61 mm
A bit enlarged.
> (2) LVESD measure of 44 mm
near normal fractional shortening.
> (3) IVSD thickness 11 mm
> (4) PWD thickness 9 mm
> (5) LVEF = 52%
near normal
> (6) Aortic Root 30 mm
> (7) Left Atrium 38 mm
borderline enlarged.
> Left Atrium - Normal
>
> Left Ventricle - Mildly dilated with preserved systolic function and EF
> of 50 - 55%
> Aortic Root - The aortic root is normal
>
> Right Atrium - normal
>
> Right Ventricle - normal
no measurement of size given however.
> Pulmonary Artery - normal
>
[quoted text clipped - 9 lines]
> Tricuspid Valve - Trace regurgitation with estimated peak pressure of
> 22 mmhg. CHIARI NETWORK seen in right atrial chamber
Folks with Chiari's network are more likely to have a patent foramen
ovale which would be permissive for the paradoxical emboli suspected by
your history of sudden left-sided weakness. (J Am Coll Cardiol 1995
Jul;26(1):203-10)
> Pulmonic Valve - normal
>
[quoted text clipped - 9 lines]
> (6) Aortic Root 28 mm
> (7) Left Atrium 33 mm
The progressive enlargement of left atrium and left ventricle suggests
that shunting from right to left (through a patent foramen ovale or
PFO) with PE events may indeed have been occurring.
> Stress Test (present)
>
[quoted text clipped - 31 lines]
> left ventricular function. No indication is needed here, and his stress
> test was a false positive.
Not surprising.
> After receiving the news of having a normal cardiac cath, I was still
> experiencing symptoms. The cardiologist diagnosed my condition as
[quoted text clipped - 3 lines]
> blood pressure, and Klonopin for anxiety. The Klonopin is not having
> any effect on my symptoms, and seemingly makes SOB worse.
Not surprising.
> What I would like is an opinion on the comments above. Can someone
> steer me in the right direction as to what the possible etiology may
> be?
GOD has made me able.
> Below is a list of symptoms:
>
[quoted text clipped - 15 lines]
>
> (1) Positive ANA (no pattern given)
Suspect you have anti-phospolipid antibodies making you
hypercoagulable.
> (2) Mildly elevated bilirubin (AST.ALT normal)
> (3) Elevated CPK-MB (Trop-T under 0.01)
> (4) Abnormal white counts (elevated neutrophils, low lymph)
> (5) Elevated Cortisol PM (18.6, with 12.0 being high normal)
> (6) Respiratory Alkalosis on ABG
Not surprising for chronic recurrent PEs
> (7) TSH transiently low (mildly low)
> (8) Low BUN (Creat normal)
>
> Cushings, Pheochromocytoma, Renal Artery Stenosis ruled out with
> testing.
Hypercoagulable state with chronic recurrent PEs with right-to-left
shunting via a PFO causing paradoxical embolic strokes has not been
ruled out by the testing you have undergone.
Would suggest you request the following be done:
(1) Hypercoagulable state workup which entails several different blood
tests, especially checking for antiphospholipid antibody which is
associated with a positive ANA as in your case.
(2) Transesophageal echocardiography with bubble study to evaluate for
a patent foramen ovale (PFO)
> Any comments would be greatly appreciated, as these symptoms have been
> ruling my life for the past two years.
Would suggest you print this out and take this to your doctor(s).
Andrew <><
--
Andrew B. Chung, MD/PhD
http://EmoryCardiology.com