Hypertension

[Sifu Stier]

The Classical Five Element Style of Oriental Medicine views hyperfunction or overactivity of any internal organ, like high blood pressure or hypertension, for example, to also imply a corresponding hypofunction or underactivity of some other internal organ. Since the Heart is classified as a Fire Element Yin Organ, any overactivity of the Heart could be 'calmed' or dispersed indirectly by supplementing and strengthening any underactivity of the Water Element Yin Organs, which are the Kidneys.

Sometimes, not always, in case specific instances, Water Element Depletion, perhaps aggravated by diuretic beverages, causes the body to be unable to retain sufficient fluid reserves in the kidneys for enough time to be redistributed to other parts of the body to meet moisture and fluid needs there. It was observed that under these circumstances, those parts of the body which normally store some amount of fluid naturally, will begin to store additional fluid to compensate for the kidney depletion. This phenomenon may manifest such symptoms as swollen joints from extra fluid retention in the bursa, cysts, tinnitus from extra fluid in the eardrum, and high blood pressure from the retention of additional fluid in the pericardium.

To eliminate the extra pericardial fluid with diuretics may temporarily reduce the fluid levels there, and thus also reduce the blood pressure temporarily, but may actually aggravate the root cause of the hypertension by overworking and further exhausting the kidneys and urinary bladder. However, once the renal functions have been supplemented, strengthened, and nourished to a normal level of healthy function, the retention of extra fluid in the pericardium, joints, etc. will naturally subside to normal levels since the original need no longer exists.

Certainly, anyone with high blood pressure should not consume any kind of salt until such time as their body is no longer retaining excess fluids. Read the ingredient labels on boxed and canned foods, too, as most of these have salt in them, usually listed as 'sodium' of some kind, and occaisionally as 'natrum muriaticum'. The advice and treatment plan of one's primary health care provider should be followed implicitly, without exception. If your doctor didn't recommend it, or at least ok it, don't do it or don't take it. Period.

[Andrew]

Interesting Sifu Stier. Thanks.

Are there also other views from other schools of Chinese Medicine or is this a common view (Kidneys vs. Heart)?

Andrew

[Sifu Stier]

A Five Element Style Perspective

Dear Andrew:

The information I last posted regarding high blood pressure is a Classical Five Element Style Oriental Medicine perspective. My Master's Degree (MS.OM) and Doctorate Degree (OMD) are specifically in this older method only. Other methods like the newer TCM may diagnose and treat this condition from a much different point of view based on different parameters of practice. I believe that there are others posting here who are trained in TCM, and practice that method, so I would invite them to address the TCM treatment protocols for hypertension.

Please note, however, that I have successfully treated many hundreds of patients with high blood pressure (hypertension) during the past 30+ years of my clinic experience employing the Five Element Style Principles and Point Prescriptions. That being the case, my patient's and I are both pleased with the outstanding results of these treatment protocols. I will certainly continue to treat patients with this method, since I know from personal experience that it works very well. Here in Texas it is said..."If it ain't broke, don't fix it! If it's workin', do it again the same way!"

[Black Hole]

Raw(green) coffee bean is already classified in the Chinese Materia Medica as a herb for regulating Liver Qi due to its cooling effect similar to Chaihu (Bupleurum).Therefore its early use was to regulate menstruation by enhancing the Liver Qi flow, but a roasted coffee bean transforms it to a warming herb.The effect of regulating Liver Qi is probably depending on its dose, in this case a small dose.

Moderate drinking(1-3 cups a day) will probably do no harm to human body because coffee, as well as tea and red wine, contains also polyphenols (antioxydants).Some studies(Harvard and Portugese studies) even suggested that drinking coffee regularly helps to prevent the development of Diabetes Mellitus type 2 and Alzheimer's disease, but a large scale study should be needed to confirm this.

Excessive coffee drinking however is not good for our health because of its diuretic effect and other caffeine related effects such as palpitation, insomnia, restlessness, hypertension etc.This diuretic effect will drain first the Kidney Yin and later the Kidney Yang as well.

The keyword is MODERATION.

P.S.: A few words on Arterial Hypertension; the retention of extra fluid is not in the Pericardium but in the blood vessels, specifically in the arteries that causes arterial hypertension.Diuretics is still used in the treatment of arterial hypertension mainly because of its low price and availability but in the last decennia there are many new anti hypertension drugs which have less long-term side effects than diuretics. Personally I don't use diuretics for arterial hypertension because diuretics tends to overstimulate the kidneys (western medicine term) leading to eventually kidney failure and osteoporosis due to calcium loss.

[Sifu Stier]

Welcome aboard, Doc! I was hoping I might be able to draw Black Hole into this discussion, since you are the resident Wahnam M.D. here.

It is known from past studies such as those done by English physiologist Ernest Starling prior to World War I, that any increase in stroke volume is a common factor of increased arterial pressure, while the condition referred to as cardiac tamonade, which I described in a previous post sometimes reduces the stroke volume. This happens when excessive fluid collects in the pericardial space beyond the normal 5-10 ml., compressing the myocardium, limiting the diastolic filling and, thus, also the stroke volume, which is probably a potential factor in cardiac failure rather than arterial hypertension.

From a Western Medicine perspective, how is the fluid level in the arteries increased? Where is it coming from? How does arterial hypertension, in your opinion, impact the normal fluid movement into the circulation from the interstitial space? And where does the excess fluid of the cardiac tamponade come from in your view?

Since we have touched on this subject, I thought it might be of interest to readers here to know more about the causative factors involved from a Physician's point to view. Thanks, Doc!

[Black Hole]

Sifu Stier,

Your last 3 posts on this thread have nothing to do with the original thread "coffee". In fact, I am getting confused because your posts seem a mixture of different kinds of "Medicines". If you want to discuss hypertension, please start a new thread.

A few comments on those posts though: Tinnitus is unlikely caused by accumulation of extra fluid behind eardrum or in the middle ear.If that is the case, the treatment would be very easy nl. myringotomy or piercing the eardrum to release the extra fluid from the middle ear.As a matter of fact, the leading specialists of Ear, Nose and Throat are still discussing the real cause(s) of tinnitus. A common example of accumulation of fluid (in this case pus) behind eardrum is Otitis Media and the main symptoms are fever,ear pain, hearing loss and NO tinnitus.

The most common cause of heart failure is LEFT VENTRICULAR SYSTOLIC DYSFUNCTION (about 60 % of the cases of heart failure), NOT heart tamponade. Heart tamponade is an acute life threatening situation seen only in emergency room and the common causes of it, as far as I can recall from clinical experience, are infections and trauma.

[Sifu Stier]

A Simple Request!

Dear Doc:

I never said that cardiac tamponade was the leading cause of heart failure, but rather that it was a probable cause thereof, no doubt due to trauma et al
as you said.

I am wondering why it is that you question all the answers, but refuse to answer any of the questions? I am still interested in your answers to the questions I posed to you in my last post. If there are no solid answers to these questions from a Western Medicine point of view, just say so, and that's OK. But if there are, please present them as requested.

Have a great day!

[Black Hole]

Sifu Stier,

I did not question your answers, I simply corrected your statements regarding the causes of tinnitus and heart failure.I did not refuse to answer your questions either, because I thought the questions were irrelevant and secondly, I did not know what you know and what you do not know regarding the water and sodium metabolism and the pathophysiology of fluid accumulation in the interstitial space and connecting tissues surrounding cells.
Your request was not simple!

Therefore, I attach an exerpt from Merck Manual FYI and I highlight the important points to remember.
If you read it, most of your questions would be answered.

I reread your post regarding the accumulation of extra fluid in the interstitial space, including in the pericardium sac and I realized what you described there were probably the symptoms of Kidney Failure with generalized edema and uremia. In the predialysis era, pericarditis (heart tamponade) caused by uremia was common, also in the ancient China. Nowadays it is not common anymore because of the dialysis therapy for patients with end stage kidney failure.

Happy reading!


Exerpt from Merck Manuals:

Water And Sodium Metabolism

Water
Total body water (TBW) content averages 60% of body weight in young men. Fat tissue has a lower water content; thus the fraction of TBW to body weight is slightly lower on average in women (55%) and is substantially lower in obese people and the elderly. About 2/3 of TBW is intracellular and 1/3 extracellular. About 3/4 of the extracellular fluid (ECF) exists in the interstitial space and connective tissues surrounding cells, whereas about 1/4 is intravascular.
Intake: The amount of water ingested can vary greatly from day to day. Ingestion is largely influenced by habit, cultural factors, access, and thirst. The range of water volume that can be ingested is determined by the kidneys' ability to concentrate and dilute the urine. An average adult with normal kidney function requires 400 to 500 mL of water to excrete the daily solute load in maximally concentrated urine. In addition to ingested water, 200 to 300 mL/day of water is formed through tissue catabolism, thus making the minimum water intake needed to prevent renal failure quite low (200 to 300 mL/day). However, a daily intake of 700 to 800 mL is needed to match total water losses and remain in water balance . Chronically ingesting < 700 to 800 mL will result in increased osmolality and stimulation of thirst. The solute load when excreted in maximally diluted urine approaches a volume of 25 L. Chronically ingesting > 25 L of water a day will eventually result in loss of body fluid homeostasis and a lowering of plasma osmolality.

Losses: Insensible water losses due to evaporation occur via expired air and the skin, constituting about 0.4 to 0.5 mL/h/kg body wt or about 650 to 850 mL/24 h in an average 70-kg adult. With fever, an additional 50 to 75 mL/day may be lost for each degree of temperature elevation above normal. Sweat losses are generally negligible but can be significant with fever or in warmer climates. GI water losses are also negligible in health but can be significant in severe diarrhea or protracted vomiting.

Osmolality
There are significant differences in the ionic composition of intracellular fluid (ICF) and ECF. The major intracellular cation is potassium (K), with an average concentration of 140 mEq/L. The extracellular K concentration, though very important and tightly regulated, is much lower, at 3.5 to 5 mEq/L. The major extracellular cation is sodium (Na), with an average concentration of 140 mEq/L. Intracellular Na concentration is much lower at about 12 mEq/L. These differences are maintained by the Na+,K+-ATPase ion pump located in the cell membranes of virtually all cells. This energy-requiring pump couples the movement of Na out of the cell with the movement of K into the cell using energy stored in ATP.

The movement of water between the intracellular and extracellular compartments is largely controlled by each compartment's osmolality, because most cell membranes are highly permeable to water. Normally, the osmolality of the ECF (290 mOsm/kg water) is about equal to that of the ICF. Therefore, the plasma osmolality is a convenient and accurate guide to intracellular osmolality. Body fluid osmolality can be approximated by the following formula:



where serum (Na) is expressed in mEq/L and glucose and BUN are expressed in mg/dL. As indicated by this formula, Na concentration is the major determinant of plasma osmolality. Therefore, hypernatremia usually indicates plasma and cellular hypertonicity (dehydration). Hyponatremia usually indicates plasma and cellular hypotonicity.
Plasma osmolality normally is not greatly affected by glucose or BUN concentrations. However, hyperglycemia or significant azotemia can raise plasma osmolality in some situations. In marked hyperglycemia, ECF osmolality rises and exceeds that of ICF, since glucose penetrates cell membranes slowly in the absence of insulin, resulting in movement of water out of cells into the ECF. Serum Na concentration falls in proportion to the dilution of the ECF, declining 1.6 mEq/ L for every 100 mg/dL (5.55 mmol/L) increment in the plasma glucose level above normal. This condition has been called translational hyponatremia because no net change in total body water (TBW) has occurred. No specific therapy is indicated, because Na concentration will return to normal once the plasma glucose concentration is lowered. Unlike glucose, urea penetrates readily into cells; since the intracellular urea concentration equals the extracellular urea concentration, no significant change in cell volume occurs. Thus, in azotemia, although the plasma osmolality is increased, plasma tonicity, or "effective" plasma osmolality, is not changed.

Finally, apparent changes in plasma osmolality can result from errors in the measurement of serum Na. Pseudohyponatremia with normal plasma osmolality may occur in hyperlipidemia or extreme hyperproteinemia, since the lipid or protein occupies space in the volume of plasma taken for analysis. Newer methods of measuring plasma electrolytes with ion-selective electrodes circumvent this problem.

Plasma osmolality can be directly measured. An osmolar gap exists when the measured plasma osmolality exceeds that calculated by the above formula by > 10 mOsm/L. The presence of an increased osmolar gap may be due to one or more unmeasured osmotically active substances in the plasma. When an increased osmolar gap is found, more specific laboratory tests should be performed promptly to determine the cause and initiate specific therapy.

TBW volume is regulated by thirst, antidiuretic hormone (ADH) secretion, and the kidneys. Osmoreceptors in the anterolateral hypothalamus are stimulated by elevation in plasma osmolality and stimulate the adjacent thirst centers. Stimulation of thirst results in the cognitive perception of thirst and subsequent increased water intake. The osmoreceptors also respond to hyperosmolality by stimulating ADH release by the posterior pituitary. ADH secretion in turn results in increased water reabsorption in the distal nephron by increasing the permeability of this otherwise relatively impermeable segment of the nephron to water. ECF osmolality is normally maintained within narrow limits. A 2% increase leads to thirst and release of ADH. In addition to increased plasma osmolality, nonosmotic stimulation of ADH release can occur. In cases of severe volume depletion, ADH is secreted to defend ECF volume, regardless of the plasma osmolality. In this situation, water is conserved at the expense of plasma osmolality.

Sodium
Since sodium (Na) is the major osmotically active cation in the ECF compartment, changes in total body Na content are paralleled by changes in ECF volume. When total Na content is low, ECF volume is depleted. ECF volume depletion is sensed by pressure receptors located in the cardiac atria and thoracic veins and results in increased renal Na conservation. When total Na content is high, volume overload develops. The high-pressure receptors located in the carotid sinus and renal juxtaglomerular apparatus sense the overload and increase natriuresis so that volume can be adjusted toward normal.

The total body Na content is regulated by a balance between dietary intake and renal excretion. Significant Na depletion does not occur unless there are abnormal renal or extrarenal Na losses from the skin or GI tract combined with inadequate intake of Na. Defects in renal Na conservation also may be caused by primary renal disease, adrenal insufficiency, or diuretic therapy. Similarly, Na overload results in an imbalance between intake and excretion, but because of the large Na excretory capacity of normal kidneys, Na overload generally implies defective renal Na excretion.

Renal sodium excretion can be adjusted widely to match Na intake. The control of renal Na excretion starts with renal blood flow and GFR. The amount of Na delivered to the nephron for reabsorption varies directly with the GFR. Thus, Na retention may be secondary to chronic renal insufficiency. Also, decreased renal blood flow as in heart failure will decrease GFR and the filtered load of Na, resulting in edema.

The renin-angiotensin-aldosterone axis is perhaps the main regulatory mechanism of renal salt excretion. In volume-depleted states, GFR and Na delivery to the distal nephron decrease, causing release of renin by the afferent arteriolar cells of the juxtaglomerular apparatus. Angiotensinogen (renin substrate) is enzymatically cleaved by renin to form the inactive polypeptide angiotensin I. Angiotensin I is further cleaved by angiotensin converting enzyme (ACE) to the active hormone angiotensin II. Angiotensin II increases Na reabsorption by decreasing the filtered load of Na and enhancing proximal tubular Na reabsorption. Angiotensin II also stimulates cells of the adrenal cortex to secrete the mineralocorticoid aldosterone. Aldosterone increases Na reabsorption through direct effects on the loop of Henle, the distal tubule, and the collecting duct. Disturbances of the regulation of the renin-angiotensin-aldosterone axis result in various fluid volume and electrolyte disturbances. Pharmacologic manipulation of the renin-angiotensin-aldosterone system remains a mainstay of treatment of many such disturbances.
Recently, several natriuretic factors have been identified, including an ouabain-like substance that induces natriuresis by inhibiting Na+,K+-ATPase. A second group of atrial natriuretic peptides (ANP) has also been identified. The active circulating ANP appears to contain 28 amino acids and is derived from the C terminal of a precursor peptide. ANP is found in secretory granules in cardiac atrial tissue and appears to be released in response to pressor-induced acute increases in BP, to salt loading and ECF volume expansion, and to other causes of atrial stretch. Elevated plasma levels of ANP have been reported in patients with ECF volume overload, primary aldosteronism, heart failure, renal failure, cirrhosis with ascites, and in some patients with essential hypertension. Conversely, depressed plasma levels of ANP have occurred in some patients with the nephrotic syndrome and a presumed decrease in effective circulating ECF volume.

In vitro, ANP opposes the vasoconstrictive effects of angiotensin II and inhibits aldosterone release and the Na-retaining action of aldosterone. When ANP is infused into animals or humans, the effects are variable. Infusion of physiologic levels of ANP in humans does induce mild natriuresis but also decreases plasma levels of angiotensin II, aldosterone, and plasma renin activity. Larger doses of ANP augment natriuresis and increase GFR despite falls in renal plasma flow and BP. ANP appears to play an important role in the regulation of ECF volume, Na metabolism, and BP. However, its full physiologic, pathophysiologic, and therapeutic significance remains to be clarified.

DISORDERS OF WATER AND SODIUM METABOLISM
Although disorders of water and Na balance frequently occur together, it is useful to consider them separately.

Water balance: Total body water (TBW) is distributed between the ICF (2/3) and ECF (1/3). Pure deficits or excesses of water are distributed between the ICF and ECF in about the same proportion. Thus, clinical signs of ECF volume alteration usually are not prominent in pure disturbances of TBW; instead, signs are usually related to changes in ECF osmolality. Since serum Na concentration is the major determinant of ECF osmolality, overhydration results in hyponatremia, whereas dehydration results in hypernatremia. The term dehydration is often used to refer to combined Na and TBW deficits but best describes relatively pure TBW depletion. Overhydration best describes a relatively pure TBW increase.

Sodium balance: Because Na is largely restricted to the ECF, deficits or excesses of total body Na content are characterized by signs of ECF volume depletion or overload, respectively. Serum Na concentration does not necessarily change with deficits or excesses of total body Na.

Determination of ECF volume status relies solely on the physical examination. Central venous pressure (CVP) can be estimated by adding 5 mm Hg to the height of the internal jugular venous pulsation above the second intercostal space with the patient's head and trunk elevated 30° while lying supine. CVP can be directly measured by using a central venous catheter in the right atrium or superior vena cava. The normal CVP is 1 to 8 cm H2O (1 to 6 mm Hg). This measurement reliably indicates intravascular volume status unless the patient has pericardial tamponade, tricuspid valve dysfunction, acute left ventricular failure, or pure right-sided heart failure. If these are present, the pulmonary capillary wedge pressure more accurately assesses the left ventricular filling pressure and effective intravascular volume. The pulmonary capillary wedge pressure typically is 6 to 13 cm H2O (5 to 10 mm Hg). In addition to increased CVP, ECF volume excess also results in edema. An increase in ECF of about 3 L must accumulate in an average 70-kg adult before edema can be detected on physical examination. If local causes of edema, such as venous or lymphatic obstruction, are excluded, the presence of edema is a reliable sign of Na excess. Additional manifestations of Na excess such as pulmonary edema depend largely on cardiac status and the distribution of ECF between the vascular and interstitial spaces.

Extracellular Fluid Volume Contraction
A decrease in the ECF volume caused by a net decrease in total body sodium content.

Pathogenesis
Losses of Na from the body are always combined with water losses. The end result of Na depletion, therefore, is ECF volume depletion. Whether the plasma Na concentration increases, decreases, or stays the same with volume depletion depends largely on the route of volume loss (eg, GI, renal) and the type of replacement fluid ingested by or administered to the person. Other factors may also affect the plasma Na concentration in volume depletion, including ADH secretion or impaired solute delivery to the distal tubule, resulting in water retention. The common causes of ECF volume depletion are listed in

Symptoms, Signs, and Diagnosis
ECF volume depletion should be suspected in patients with a history of inadequate fluid intake (especially in comatose or disoriented patients); vomiting; diarrhea (or iatrogenic GI losses, eg, nasogastric suction, ileostomy, or colostomy); diuretic therapy; symptoms of diabetes mellitus; and renal or adrenal disease. A history of recent weight loss can sometimes be obtained.

In mild ECF volume depletion, the only signs may be diminished skin turgor and intraocular tension. Dry mucous membranes are often unreliable, especially in the elderly or in mouth-breathers. Orthostatic hypotension (decrease of systolic pressure by > 10 mm Hg on standing) and tachycardia and a low CVP are more reliable signs, although orthostatic changes can occur in deconditioned bedridden patients without ECF volume depletion. When ECF volume has diminished by about 5% or greater, orthostatic tachycardia and/or hypotension are generally present. Severe volume depletion can result in disorientation and overt shock.

Normally functioning kidneys respond to volume depletion by conserving Na. When volume depletion is severe enough to result in decreased urine volume, the urine Na concentration is usually < 10 to 15 mEq/L; the fractional excretion of Na (urine Na/serum Na divided by the urine creatinine/serum creatinine) is usually < 1%; and urine osmolality is often elevated. If metabolic alkalosis is present in addition to volume depletion, the urine Na concentration may be high and, therefore, misleading as a measure of volume status; a low urine chloride (Cl) concentration (< 10 mEq/L) more reliably indicates ECF volume depletion in this instance. If the Na losses are due to renal disease, diuretics, or adrenal insufficiency, the urine Na concentration generally is > 20 mEq/L. Laboratory values such as hematocrit are often increased in volume depletion but are difficult to interpret unless the baseline value is known. Significant ECF volume depletion also frequently produces mild-to-moderate rises in the BUN and plasma creatinine levels (prerenal azotemia; BUN/creatinine ratio > 20:1).

Treatment
Mild-to-moderate ECF volume depletion may be corrected by increased oral intake of Na and water if the patient is conscious and does not have GI dysfunction. The underlying cause of volume depletion must be corrected, such as by discontinuing diuretics or treating diarrhea. When volume depletion is severe and accompanied by hypotension or when oral fluid administration is impractical, IV saline is the fluid of first choice (see precautions outlined below). When renal excretion of water is normal, Na and water deficits may be safely replaced with 0.9% saline. When an associated disturbance in water metabolism exists, replacement fluids are modified as discussed in the following sections. When ECF volume depletion is due to or complicated by metabolic disturbances such as diabetic ketoacidosis or Addison's disease, attention should be given to correcting these problems in addition to replacing volume.



Extracellular Fluid Volume Expansion

An increase in the ECF volume caused by a net increase in total body sodium content associated with edema formation.
Pathogenesis
Since Na is largely restricted to the ECF, increases in total body Na content are reflected by subsequent increases in ECF volume. Increases in intravascular volume usually result in prompt increases in renal Na and water excretion. Hence, the maintenance of volume overload and formation of edema involves the sequestration of fluid within the interstitial space. Movement of fluid between interstitial and intravascular spaces depends on Starling's forces at the level of the capillary. Increased capillary hydrostatic pressure, as occurs in heart failure; decreased plasma oncotic pressure, as occurs in nephrotic syndrome; or a combination, as occurs in severe hepatic cirrhosis, results in net movement of fluid into the interstitial space and edema formation. In these conditions, subsequent intravascular volume depletion results in enhanced Na retention by the kidneys and maintenance of the overload state. The common causes of volume overload are listed in .

Symptoms, Signs, and Diagnosis
Early symptoms of ECF volume overload are fairly nonspecific and can occur before overt edema formation. These include weight gain and weakness. Dyspnea on exertion, decreased exercise tolerance, orthopnea, and paroxysmal nocturnal dyspnea can also occur early when volume overload is caused by left ventricular dysfunction.

Symptoms such as puffy eyes on rising in the morning and tight shoes at the end of the day are frequently present early in edema formation. Edema is often dependent in heart failure and can be accompanied by a myriad of physical findings, including pulmonary rales, elevated CVP, an S3 gallop, and an enlarged heart with pulmonary edema and/or pleural effusions on chest radiograph. Edema is frequently confined to the lower extremities and accompanied by ascites in hepatic cirrhosis. Accompanying signs of cirrhosis are frequently present and include spider angiomas, gynecomastia, palmar erythema, and testicular atrophy. In contrast, edema is often diffuse in nephrotic syndrome and is occasionally accompanied by generalized anasarca with pleural effusions and ascites. Periorbital edema is frequently, but not invariably, seen in nephrotic syndrome.

Treatment
Initial therapy should be directed at correcting the underlying cause of ECF volume expansion. Left ventricular dysfunction, myocardial ischemia, and cardiac arrhythmias must be treated. The use of digitalis, inotropic agents, and afterload reduction to improve cardiac function can decrease or prevent the need for diuretics by improving Na delivery to the kidneys and thus decrease renal Na conservation. Treatment of the underlying causes of nephrotic syndrome is variable and depends on the specific renal histopathology present. Several of the underlying causes of nephrotic syndrome do not respond to therapy; however, the level of proteinuria can often be decreased with the use of an ACE inhibitor. ACE inhibitors must always be used with caution in patients with renal impairment who must be monitored for worsened renal insufficiency and hyperkalemia.

Diuretics are most useful for ECF volume overload. Loop diuretics, such as furosemide, inhibit Na reabsorption in the thick ascending limb of the loop of Henle. Thiazide diuretics inhibit Na reabsorption in the distal tubule. Both loop diuretics and thiazides result in K wasting, which can be problematic in some patients. K-sparing diuretics such as amiloride, triamterene, and spironolactone inhibit Na reabsorption in the distal nephron and collecting duct. When used alone, they have modest natriuretic effects. Both triamterene and amiloride have been used in conjunction with a thiazide to prevent K wasting.

Resistance to diuretics is common; the cause is frequently multifactorial. Inadequate treatment of the underlying cause of volume overload, patient noncompliance (particularly with dietary salt restriction), volume depletion, and renal insufficiency are major contributing causes of resistance in most cases. Escalating doses of loop diuretics are frequently successful in promoting diuresis. Combining a loop diuretic and a thiazide has also been useful in treating patients resistant to diuresis with either alone.

Once volume overload has been corrected by natriuresis, maintenance of euvolemia requires restriction of dietary Na (primarily through adjustment of dietary habits) unless the underlying condition can be completely eliminated. It is often difficult to determine Na intake based on history, but dietary Na intake can be successfully monitored by measuring urinary Na in a 24-h sample once a steady state has been achieved (ie, no recent weight changes or diuretic dose changes). Diets containing 2 to 3 g/day Na are fairly well tolerated and work reasonably well in all but the most severe cases of volume overload. Potassium salts are generally used as salt substitutes to help patients tolerate a low Na diet; however, care should be taken, especially in patients receiving K-sparing diuretics or ACE inhibitors and in those with renal failure, because potentially fatal hyperkalemia can result.

[Sifu Stier]

A Priori Factors

Hello Doc:

Many thanks for the gargantuan effort in posting so much information! Believe it or not, I also own and use a Merck's Manual, PDR, etc. For those readers who do not, let me suggest copying to a saved file the wealth of information provided in Black Holes post. It is information not easily or quickly accessed from other sources.

I would like to take the diagnostic process further back beyond description of physiopathology and symptomology to the inquiry of 'a priori' causative factors, i.e. to an evaluation of the root causes of development. Do you perceive such as due to hereditary predispostions, dietary factors, lifestyle choices, environmental influences, or other causative factors? The identification of symptomology, a diagnostic disease classification of same, and any treatment plan of medical management or surgical management to follow usually only addresses the temporary amelioration of the symptoms rather than the root causes of same.

For example, the medical management of arterial hypertension through pharmaceutical drugs with diuretic and/or vasodilator actions do not eliminate the cause of the problem. If the patient stops taking the medication as directed, the suppressed symptoms of high blood pressure will quickly reappear, oftentimes worse than before. So how can we reverse the factors which lead to the initial development of the disease syndrome in order to free the patient of continuing need for the pharmaceutical drugs, and from the attendant adverse reactions of such medications? This would constitute a true 'healing' of the disease, would it not? What do you think, given your experience in treating patients with both Western and Oriental Medicine? I acknowledge that some of these issues are addressed in part in your lengthy post, but I am mostly interested in your personal, professional point of view based on your own clinical experience rather than in a general textbook case scenario.

I look forward to your perspective on all of this! Have a great day!

[beausimon]

Hi,
Would practicing qigong be able to cure hypertension?

Thanks.

[Luo Lang]

Dear Beausimon,

Would practicing qigong be able to cure hypertension?

Yes, Chi Kung could give a good chance to cure Hypertention.
As you may have noticed, Hypertention is a quite complex disease with a lot of faces. It is meant to be uncurable by most therapists.
Chi Kung is a very suitable way to cure uncurable diseases as it has a holistic approach. You don't have to know where the root of the problem is.

Regards

Roland

[beausimon]

Hi Roland,
Thanks.

[Michael Udel]

curing hypertension

I am getting away from the excellent discussion in terms of Eastern and Western medicine, especially considering the detailed explanation of the why's and wherefore's presented by Sifu Stier and Black Hole. Thanks guys! But since it was asked if qigong could cure hypertension, I must throw in my two cents.

I cured a case of hypertension in a patient with kidney failure who was getting dialysis three times a week. His list of acute and chronic medical problems would likely exceed some limitation in the bulletin board software, and Anthony would track me down for crashing the forum To be brief, the patient was in this early 60's, was diagnosed with kidney failure 9½ years prior, had been on dialysis 1½ years, and had severe hypertension for more than 20 years. A large number of blood pressure medications had been used by medical doctors experimenting with ways to reduce his blood pressure, bringing him close to death many times in his life, and once exceeding the 300 mg/L limit of the machine (according to the patient's account).

He had asthma as a boy and was on steroid medications for many years as a treatment for the asthma. I am not going to bother suggesting what was going on with this patient's health and the underlying cause considering my limited experience and the fact that Sifu Steir has started throwing around a lot of four syllable words in his recent posts

Using the healing method of the qigong I practice, I gave the patient a "qi-healing" for 15 minutes. The next day during his dialysis, his pressure had dropped from the medication controlled 165/170 over 110/120 range down to 140/90. The patient, being very familiar with his various conditions and the efficacy (or lack thereof) of the medications he'd been prescribed since a child, felt that he should immediately discontinue all his blood pressure medication. He informed me of this three weeks later and his pressure had continued to drop another 10-15 points since I taught him this style of qigong. I was dismayed that he stopped his blood pressure meds without telling me, but he had informed his doctors, who were even more dismayed that he was flaunting his new found blood pressure stats without their pills. When they asked how he did it, he apparently just said, "I've got a new Chinese connection," and left it at that. The patient in question has developed an interesting sense of humor since originally being told by an MD some nine plus years ago he would be dying in a few weeks due to kidney failure. You'd sorta have to know this guy to fully appreciate his stories. He's like a death bed stand-up comic. BTW, a Chinese born OMD in Washington, D.C. kept the patient going for 8 years without dialysis after the kidney failure diagnosis using mostly herbs and a few needles.

The second time I gave the patient a "qi-healing" according to the style I teach, I used the technique especially beneficial for the heart. The patient was induced into a deep state of relaxation, but then clutched at his chest and showed some signs of pain. Considering the patient's history, I could have been alarmed at the patient's reaction, but I felt everything was going alright, and continued the qi-healing for a few more minutes. The patient reported the next day his blood pressure had dropped to 110/60, and there it stayed for the next several months while I was treating him.

The style of qigong being used has more than 100,000 students since 1993, and everyone who has practiced has been cured of their heart ailment, or saw significant improvement. I know of a case of a man in his late 30's who had a congenital heart defect where one area of his heart was severely malformed. Six months after starting this qigong, pictures of his heart showed that the abnormality was completely gone. Many, many other such improvements have been reported by qigong practitioners of this style.

My blood pressure has dropped about 15 points. An example of minimal improvement is my mom, who will not practice every day, but only practices sporadically. My teacher's diagnosis and recommendation to her was to practice twice a day, 15 minutes each, but since she doesn't, she has only seen a marginal decrease in blood pressure, too little to be conclusive.

Qigong is amazing, and can help a lot of problems. Some styles of qigong may be better or quicker for one ailment or another. Based on my experience, qigong can easily cure high blood pressure as long as the patient is willing to practice enough.

Best wishes,
Michael

[Black Hole]

Big dilemma

I apologize for the size of my last post on this thread.The questions were not simple to answer without giving a lengthy explanation; therefore in this post I am not going to describe hypertension in a textbook manner but rather from a practical point of view and from direct experience. I realize that this is not a medical forum and I will also try to avoid using too many medical jargons. For those who are interested in a textbook descriptions of hypertension, they can find them very easily online.

To take or not to take antihypertensive drug(s)?.
Hypertension, known as "silent killer" because the sufferers usually do not have any symptom until the pressure (systolic and diastolic) exceeds a certain level and/or they taken by surprise because they get cardioscular diseases without any prior warning. Actually, hypertension is not a disease such as AIDS or cancer but rather a manifestation of degenerative process or hereditary/genetic predisposition. Many hypertensive patients had no hypertension when they were young. Untreated prolonged hypertension leads to cardiovascular diseases, retinopathy, kidney failure etc.This is a medical fact!
I lost many friends and relatives in Indonesia because they had suffered untreated and uncontrollable hypertension which in my opinion their deaths were avoidable if their hypertension had been treated or controlled. Some of them who survived are still recovering from their strokes.

Many hypertensive patients are easily treated with a non-medically approach, such as quit smoking, reduce body weight etc.etc.I also encourage people taking Chikung, yoga, stress management classes ets. in order to bring their hypertension down. But what if their blood pressures are still high despite these non- medical approach ?? What can be done to help them to avoid the dangerous consequencies of hypertension? "Hypertension leads to more hypertension", is also a fact, because this high pressure will in turn damages the arteries and organs causes more tension in the arteries(chain reaction).
Antihypertensive drug currently available have less side effects comparing with drugs in the time of my graduation day decades ago, but these new drugs still have undesirable side effects, but with the right choice and the right dose, we can reduce these side effects to minimum. By avoiding anti hypertensive drugs at all cost is not only unwise, it is also dangerous. Chikung practitioners who suffer from hypertension should not abandon their drugs until they notice that their blood pressures drop.Then, they can slowly and gradually reduce the dose and hopingly they can at last abandon their drugs. They should also more emphasize on cleansing, clearing blockages and promoting Chi flow first.What about herbs? Most western herbs for hypertension have either diuretic or tranquilizing effects or both and some chinese herbs have also the same diuretics and tranquilizing effects.

Root cause.

What is a root cause?.
90% of hypertensive patients(essential or primary) have no root causes.The so-called secondary hypertension have causes such as renal parenchymal disease or renal vascular disease.This is a western medicine concept.
But what about the Chinese medicine concept?.Do they have root causes of hypertension?.From TCM's point of view, hypertension is only one of many manifestations of certain syndromes.The classical syndromes without going to detail are Kidney Yin deficiency with excess of Yang, Phlegm obstruction in the meridians, Liver Wind, Liver Fire and Deficiency of Chi and Blood. Are these syndromes the root causes?. In my opinion, they are not the root causes, but anyway the chinese treatment goes deeper and more profound than the symptomatic western medicine's approach.The root causes are the situations/conditions that make these syndromes possible.
An illustration from my pratice: A gentleman at his 70's came to my office in 1992 for chronic low back pain. He took 2 antihypertensive drugs for his hypertension.The diagnosis was Kidney Yin deficiency with uprising of Liver Yang. By applying acupuncture on this man, not only his low back pain disappeared but his blood pressure was gradually dropping to normal.I stopped the drugs and continued to treat him regularly and he was free of pain and hypertension until 2 years ago when he got the news about the tragic death of his beloved daughter. He did not recovered from this tragedy and his blood pressure started to rise again and did not drop despite the acupuncture treatment.I had no choice but prescribing an anti hypertensive drug Amlor and his blood pressure was turning to normal again. On his last cardiovascular check up, his cardiologist wrote me that this gentleman of 83 years old has an excellent cardiovascular condition and encouraged me to continue with his acupuncture and medication.What is the root cause of his hypertension? The loss of his daughter? His inability to cope with stress, sorrow or guilty feeling? I do not know.This is open for discussion.

P.S. Michael, did you patient recovered from his kidney failure as well?

[Luo Lang]

Many thanks for your contribution Tai Sihing! Very informing!

Greetings,

Roland