please please help!

i'm a 63 year old male from Ireland and suffer from congestive heart failure, i've had several ops in the past including 2 separate by pass ops and the instalation of an internal defib unit under my skin near my heart. I have lost 12 kg in weight in the last 5 months. i have an appitete but constantly vomit after nearly all meals, My doctor cant find a reason why . i've had several full blood works done and an endo scope exam . all negative results.....!  is it possible i can be slowly  posioned by my own meds. i had my first heart attack at 40 years of age. and been on heart meds ever since. my meds include (european brand names) Warfarin, Aldactone,Burinex, Bisiprolol Fumarate, Digoxin, Nexium, Ramipril, Cordarone, Diazepan, Dalmane.     Please can anyone help me !  

[pvcqueen]

The first thought that comes to mind is having your Digoxin levels checked...this is a classic sign of too much dig, but I am sure they did that, right?

[Jack54]

I do hope today is tolerable for you. I have frantically did some research that tells me your doctor should know very well what is causing your weight loss and vomiting, which is due to and leading to increased malnutrition.

I have found 2 conditions that I suspect. The first is Superior Mesenteric Artery (SMA) syndrome, and due to your symptom of vomiting might be effecting you more than the second condition, that your doctor should be aware of and is Cardiac Cachexia.

It is very important that you immediately start getting the proper nutrition, which can only be supplied by special concoctions that replace many important elements your body has lost. There are also medicines that you should be taking and some that you should not be taking with regard to heart failure medicines.

Below is a bunch of gobbly gook and all is from the US government. I have not violated any copyright laws. However, it is difficult to understand maybe, but I thought it best to just post these bits of info now, and not take the time to put it in my own words. I probably couldn't anyway.

What I did want to point out that there is a possibility that your SMA is physically interfering with your duodenum. This can and does cause vomiting and is associated with heart failure and high pulmonary pressures, I believe.

The second condition, Cardiac Cachexia can cause many serious changes within your bodily chemistry and is also associated with chronic heart failure.

I apologize for the unorganized mess of information below, but you might gain more insight and may even relate with some of the symptoms.

If you are fearless, talk a copy of this to your doctor.

Best to you and I hope that this condition/weight loss can be reversed soon. Keep in contact if you will. I am very pushed for time today. My only credentials is that I am a certified Hillbilly :)

Jack

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In severe chronic heart failure, serious weight loss and cachexia (malnutrition) often occur. Cardiac cachexia
(malnutrition) is found in 35-53% of patients with advanced heart failure (Schwengel 1994). The cardiac cachexia
associated with CHF is the result of one or more of the following (Braunwald 1994, Levine 1990, Poehlman 1994):

• Elevated concentrations of tumor necrosis factor
• Elevated basal metabolic rate
• Anorexia, nausea and vomiting due to central causes, digitalis toxicity or congestive  hepatomegaly and
abdominal fullness
• Impaired intestinal absorption due to venous congestion
• A protein-losing enteropathy

Because body weight fluctuations may be marked in heart failure due to dramatic shifts in fluid balance,
parameters useful in the recognition of cardiac cachexia tend to be those which reflect protein status (keeping in
mind that serum albumin, serum prealbumin and muscle volume all contribute to this dilutional variation).
Unrecognized protein depletion could contribute to the progression of heart failure and decreased functional
status. A well-recognized outcome of protein-energy malnutrition is cardiac atrophy (Schwengel 1994). Among
malnourished elderly patients with CHF, the mortality rate was 80% compared to 18% for non-malnourished
patients (Cederholm 1995). These malnourished non-cancer medical patients also had higher infection and
hospitalization rates.

The fatigue, weakness, and reduced exercise capacity of CHF patients may be associated with the anorexia,
nausea and abdominal pain/fullness caused by liver congestion and portal venous symptoms (Braunwald 1994).
Concern has also been expressed regarding the poor thiamin status of patients receiving long-term furosemide
therapy (Shimon 1995, Seligmann 1991). Furosemide therapy (> 80 mg/day for > 3 months) results in increased
urinary thiamin excretion and clinically significant thiamin deficiency. Thiamin deficiency is a cause of high output
cardiac failure (Beriberi) and may contribute to impaired cardiac performance in patients with CHF. Thiamin
supplementation (200 mg/day orally for 6 weeks) improved left ventricular function, diuresis and sodium excretion
in patients with CHF on long term furosemide therapy (Shimon 1995).

In patients with severe, chronic CHF, attention should be paid to the adequacy of the caloric and nutrient content
of the diet. Patients should be routinely asked about appetite and food intake so that interventions can be
instituted and nutritional deficiencies can be avoided. Nutritional supplements (i.e. vitamins/minerals, enteral
products) are indicated when the patient is unable to access or to consume an adequate diet. Vitamin
supplementation may be indicated when there is water-soluble vitamin loss associated with diuresis and/or
problems with gastrointestinal absorption of fat-soluble vitamins (Dracup 1994).

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[Jack54]

Continued

Cardiac Cachexia*
Chronic heart failure (CHF) is a complex syndrome affecting many body systems. Body wasting (ie, cardiac cachexia) is a serious complication of CHF long known but little investigated. Although no specific diagnostic criteria have been established, we have suggested that cardiac cachexia be defined on the basis of the presence of documented nonintentional and nonedematous weight loss > 7.5% of the premorbid normal weight, occurring over a time period of > 6 months. Using this definition, 16% of an unselected CHF outpatient population was found to be cachectic. The cachectic state is predictive of impaired prognosis independently of age, functional disease classification, left ventricular ejection fraction, and peak oxygen consumption.

Several studies have shown that cardiac cachexia is linked to raised plasma levels of tumor necrosis factor. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. The available evidence suggests that cardiac cachexia is a multifactorial neuroendocrine and metabolic disorder with a poor prognosis. A complex imbalance of different body systems may cause the development of body wasting.
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Cachectic CHF patients have raised plasma levels of norepinephrine, epinephrine, and cortisol, and they show high plasma renin activity and increased plasma aldosterone levels. A number of studies have also shown that cardiac cachexia is linked to raised plasma levels of inflammatory cytokines, such as tumor necrosis factor alpha.
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Superior mesenteric artery (SMA) syndrome is an uncommon but well recognized clinical entity characterized by compression of the third, or transverse, portion of the duodenum against the aorta by the SMA, resulting in chronic, intermittent, or acute complete or partial duodenal obstruction.
Medical Care: Reversing or removing the precipitating factor is usually successful in a patient with acute SMA syndrome. Conservative initial treatment is recommended in all patients with SMA syndrome; this includes adequate nutrition, nasogastric decompression, and proper positioning of the patient after eating (ie, left lateral decubitus, prone, or knee-to-chest position). Enteral feeding using a double lumen nasojejunal tube passed distal to the obstruction under fluoroscopic assistance is an effective adjunct in treatment of patients with rapid severe weight loss and also eliminates the need for intravenous fluids and the risks associated with total parenteral nutrition. In some instances, both enteral and parenteral nutritional support may be needed to provide optimal calories.

The patient's weight should be monitored daily. Subsequently, the patient can be started on oral liquids followed by slow and gradual introduction of small and frequent soft meals as tolerated. Finally, regular solid foods are introduced. Metoclopramide treatment may be beneficial. Review of the orthopedic literature reveals that the success rate is 100% with medical management only in cases with an acute presentation of SMA syndrome.

Surgical Care: Surgical intervention is indicated when conservative measures are ineffective, particularly in patients with a long history of progressive weight loss, pronounced duodenal dilatation with stasis, and complicating peptic ulcer disease. Duodenojejunostomy is the most frequently used procedure, and it is successful in about 90% of cases. The use of laparoscopic surgery that involves lysis of the ligament of Treitz and mobilization of the duodenum has been reported.
Imaging Studies:

The diagnosis of SMA syndrome is difficult. Confirmation usually requires radiographic studies, such as an upper GI series, hypotonic duodenography, and CT scanning.

Upper GI study with barium reveals characteristic dilatation of the first and second parts of the duodenum, with an abrupt vertical or linear cutoff in the third part with normal mucosal folds.
Fluoroscopy demonstrates a to-and-fro motion of the barium in the dilated proximal portion of the duodenum. Other findings include delay of 4-6 hours in gastroduodenal transit and relief of the obstruction when the patient is in the left lateral decubitus position.

A Hayes maneuver (ie, pressure applied below the umbilicus in cephalad and dorsal direction), which elevates the root of small-bowel mesentery, may also relieve the obstruction.
In equivocal cases, hypotonic duodenography may depict the site of obstruction and dilation of the proximal duodenum, with antiperistaltic waves within the dilated portion.

CT scanning is useful in the diagnosis of SMA syndrome and can provide diagnostic information, including aorta-SMA distances and duodenal distension. Also, it can be used to assess intra-abdominal and retroperitoneal fat.

Upper GI endoscopy may be necessary to exclude mechanical causes of duodenal obstruction. However, the diagnosis of SMA syndrome may be missed with this study.
Abdominal ultrasonography may be helpful in measuring the angle of the SMA and the aortomesenteric distance.

Manometry may be used to differentiate between the possibility of a myopathic form of chronic intestinal pseudoobstruction syndrome (hollow visceral myopathy) by demonstrating low-amplitude waves throughout the duodenum, and frequently the stomach, versus an irregular or absent phase III and no postprandial motility changes in a neuropathic form of chronic intestinal pseudoobstruction syndrome. The pattern of increased amplitude of propagated contractions and retrograde contractions should hint or suggest the mechanical obstruction in SMA syndrome.
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Increased venous pressure caused by congestive heart failure and vomiting was implicated as the cause of bilateral uveal effusions causing Angle-closure glaucoma in primary pulmonary hypertension.
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Heart failure may cause blood to back up into the liver and intestines, and they may swell. This swelling can lead to nausea and decreased appetite.

absorption of nutrients from the food you eat.
Heart failure may force you to work harder to breathe and cause your body temperature to increase. Both of these conditions burn calories.

In people with severe heart failure, tumor necrosis factor (TNF) and other signaling molecules in the bloodstream called cytokines can increase the metabolic rate of the tissues, thus burning more calories.

[FLBrat]

And then again, Digoxin toxicity is very good theory.  And yes, dehydration along with loss of important electrolytes and minerals will occur from the vomitting.  Dont wait for a visit, call the doctor.  I was told over the phone to stop my Digoxin and felt quite better for it.  Sometimes it is just something simple and easy to handle, hope this is one of those times.

[maggiemag]

My first thought is also to have a Digoxin level drawn.  It would help us to know what bloodwork was done.  They should also draw a BNP to see if your CHF is decompensated.  I would not suspect cardiac cachexia, (sorry, Jack!) as you say you have not lost your appetite.  That condition goes along with end-stage heart failure, they have no appetite, are wasted, nauseated, etc. from excessive fluid in the gut.  I hope you have regular thyroid levels done since you are on Cordorone.  I took Nexium and had severe abdominal pain and nausea, and lost 5 pounds in 4 days.  Have they tried switching you to another drug in its class?  I take Protonix now with no trouble.  When my potassium is low I get severely nauseated, but surely they have checked that level!  If all those have been checked, I would consider another endoscopy by another GI doctor.  Things can be missed.

[carisue]

Are you taking a Potassium supplement with all of these meds.  I'm not familiar (?sp) with some of your meds so I wasn't sure.