On Tue, 25 Sep 2007 19:59:05 -0400, Wizard of Draws
wrote in
:

But the BP was enough to have him start me on 5 mg Lisinopril
and 25 mg Hydrochlorothiazide daily.

Another point I find lacking in this discussion of the treatment of
high blood pressure with diuretic drugs is the failure to mention the
necessity to supplement dietary potassium to compensate for that
flushed out through increased urination.

Has you doctor mentioned potassium? Are you aware that you may
require supplementing it while on your course of diuretic medication
(Hydrochlorothiazide)?

I took the liberty of doing some fundamental research:


http://en.wikipedia.org/wiki/Lisinopril
Lisinopril (lye-SIN-o-pril) is a drug of the angiotensin
converting enzyme (ACE) inhibitor class that is primarily used in
treatment of hypertension or high blood pressure, congestive heart
failure, heart attacks and also in preventing renal and retinal
complications of diabetes.

Historically, lisinopril was the third ACE inhibitor, after
captopril and enalapril, and was introduced into therapy in the
early 1990s.[1] Lisinopril has a number of properties that
distinguish it from other ACE inhibitors: it is hydrophilic, has
long half life and tissue penetration and is not metabolized by
the liver.

Pharmacology
Lisinopril is the lysine-analog of enalapril. Unlike other ACE
inhibitors, lisinopril is not a prodrug and is excreted unchanged
in the urine. In cases of overdosage, it can be removed from
circulation by dialysis.

Clinical use
Its indications, contraindications and side effects are as those
for all ACE inhibitors. Its long half-life allows for once a day
dosing which aids patient compliance. The usual daily dose in all
indications ranges from 2.5mg in sensitive patients to 40mg. Some
patients have been treated with 80mg daily and have tolerated this
high dose well. Lower dosages must be used in patients with higher
grade renal impairment (glomerular filtration rate (GFR) lower
than 30ml/min). Lisinopril has an iGuard risk rating of Blue[2]
(general risk).
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http://en.wikipedia.org/wiki/Hydrochlorothiazide
Hydrochlorothiazide, sometimes abbreviated HCT, HCTZ, or HZT is a
popular diuretic drug that acts by inhibiting the kidney's ability
to retain water. This reduces the volume of the blood, decreasing
blood return to the heart and thus cardiac output and, by other
mechanisms, is believed to lower peripheral vascular resistance.
Hydrochlorothiazide is sold both as a generic drug and under a
large number of brand names, including: Apo-Hydro, Aquazide H,
Dichlotride, Hydrodiuril, HydroSaluric, Microzide, Oretic.

Activity
Hydrochlorothiazide belongs to the thiazide class of diuretics,
acting on the kidney to reduce sodium (Na) reabsorption in the
distal convoluted tubule. This reduces the osmotic pressure in the
kidney, causing less water to be reabsorbed by the collecting
ducts. This leads to increased urinary output.

Indications
HCT is often used in the treatment of hypertension, congestive
heart failure, symptomatic edema and the prevention of kidney
stones. It is effective for nephrogenic diabetes insipidus
(paradoxical effect, which decreases urine formation) and is also
sometimes used for hypercalciuria.

Hypokalemia, an occasional side-effect, can be usually prevented
by potassium supplements or combining hydrochlorothiazide with a
potassium-sparing diuretic.

Side effects:
Hypokalemia
Hypomagnesemia
Hyperuricemia and gout
High blood sugar
High cholesterol
Headache
Impotence
Nausea/Vomiting
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http://en.wikipedia.org/wiki/Hypokalemia
Hypokalemia is a potentially fatal condition in which the body
fails to retain sufficient potassium to maintain health. The
condition is also known as potassium deficiency. The prefix hypo-
means low (contrast with hyper-, meaning high). The middle kal
refers to kalium, which is Neo-Latin for potassium. The end
portion of the word, -emia, means "in the blood" (note, however,
that hypokalemia is usually indicative of a systemic potassium
deficit).

Signs and symptoms
There may be no symptoms at all, but severe hypokalemia may cause:

Muscle weakness and myalgia
Increased risk of hyponatremia with resultant confusion and
seizures
Disturbed heart rhythm (ranging from ectopy to arrhythmias)
Serious arrhythmias
EKG changes associated with hypokalemia

Flattened (notched) T waves
U waves
ST depression
Prolonged QT interval

Causes
Hypokalemia can result from one or more of the following medical
conditions:

Perhaps the most obvious cause is insufficient consumption of
potassium (that is, a low-potassium diet). However, without
excessive potassium loss from the body, this is a rare cause of
hypokalemia.

A more common cause is excessive loss of potassium, often
associated with excess water loss, which "flushes" potassium out
of the body. Typically, this is a consequence of vomiting,
diarrhea, or excessive perspiration.

Certain medications can accelerate the removal of potassium from
the body; including thiazide diuretics, such as
hydrochlorothiazide; loop diuretics, such as furosemide; as well
as various laxatives. The antifungal amphotericin B has also been
associated with hypokalemia.

A special case of potassium loss occurs with diabetic
ketoacidosis. In addition to urinary losses from polyuria and
volume contraction, there is also obligate loss of potassium from
kidney tubules as a cationic partner to the negatively charged
ketone, ß-hydroxybutyrate.

Hypomagnesemia can cause hypokalemia. Magnesium is required for
adequate processing of potassium. This may become evident when
hypokalemia persists despite potassium supplementation. Other
electrolyte abnormalities may also be present.

Disease states that lead to abnormally high aldosterone levels can
cause hypertension and excessive urinary losses of potassium.
These include renal artery stenosis and tumors (generally
non-malignant) of the adrenal glands. Hypertension and hypokalemia
can also be seen with a deficiency of the 11ß-hydroxylase enzyme
which allows cortisols to stimulate aldosterone receptors. This
deficiency can either be congenital or caused by consumption of
glycyrrhizin, which is contained in extract of licorice, sometimes
found in Herbal supplements, candies and chewing tobacco.

Rare hereditary defects of renal salt transporters, such as
Bartter syndrome or Gitelman syndrome can cause hypokalemia, in a
manner similar to that of diuretics.

Rare hereditary defects of muscular ion channels and transporters
that cause hypokalemic periodic paralysis can precipitate
occasional attacks of severe hypokalemia and muscle weakness.
These defects cause a heightened sensitivity to catechols and/or
insulin and/or thyroid hormone that lead to sudden influx of
potassium from the extracellular fluid into the muscle cells.

Pathophysiology
Potassium is essential for many body functions, including muscle
and nerve activity. Potassium is the principal intracellular
cation, with a concentration of about 145 mEq/L, as compared with
a normal value of 3.5 - 5.0 mEq/L in extracellular fluid,
including blood. More than 98% of the body's potassium is
intracellular; measuring it from a blood sample is relatively
insensitive, with small fluctuations in the blood corresponding to
very large changes in the total bodily reservoir of potassium.

The electrochemical gradient of potassium between intracellular
and extracellular space is essential for nerve function; in
particular, potassium is needed to repolarize the cell membrane to
a resting state after an action potential has passed. Decreased
potassium levels in the extracellular space will cause
hyperpolarization of the resting membrane potential. This
hyperpolarization is caused by the effect of the altered potassium
gradient on resting membrane potential as defined by the Goldman
equation. As a result, a greater than normal stimulus is required
for depolarization of the membrane in order to initiate an action
potential.

Pathophysiology of Hypokalemic Heart Arrythmias
Potassium is essential to the normal muscular function, in both
voluntary (i.e skeletal muscle, e.g. the arms and hands) and
involuntary muscle (i.e. smooth muscle in the intestines or
cardiac muscle in the heart). Severe abnormalities in potassium
levels can seriously disrupt cardiac function, even to the point
of causing cardiac arrest and death. As explained above,
hypokalemia makes the resting potential of potassium [E(K)] more
negative. In certain conditions, this will make cells less
excitable. However, in the heart, it causes myocytes to become
hyperexcitable. This is due to two independent effects that may
lead to aberrant cardiac conduction and subsequent arrhythmia: 1)
there are more inactivated sodium (Na) channels available to fire,
and 2) the overall potassium permeability of the ventricle is
reduced (perhaps by the loss of a direct effect of extracellular
potassium on some of the potassium channels), which can delay
ventricular repolarization.

Treatment
The most important step in severe hypokalemia is removing the
cause, such as treating diarrhea or stopping offending medication.

Mild hypokalemia (3.0 mEq/L) may be treated with oral potassium
chloride supplements (Sando-K®, Slow-K®). As this is often part of
a poor nutritional intake, potassium-containing foods may be
recommended, such as tomatoes, oranges or bananas. Both dietary
and pharmaceutical supplements are used for people taking diuretic
medications (see Causes, above).

Severe hypokalemia (3.0 mEq/L) may require intravenous
supplementation. Typically, saline is used, with 20-40 mEq KCl per
liter over 3-4 hours. Giving intravenous potassium at faster rates
may predispose to ventricular tachycardias and requires intensive
monitoring.

Difficult or resistant cases of hypokalemia may be amenable to
amiloride, a potassium-sparing diuretic, or spironolactone.

When replacing potassium intravenously, infusion via central line
is encouraged to avoid the frequent occurrence of a burning
sensation at the site of a peripheral iv, or the rare occurrence
of damage to the vein. When peripheral infusions are necessary,
the burning can be reduced by diluting the potassium in larger
amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq
of kcl per 50 ml of IV fluid. The practice of adding lidocaine,
however, raises the likelihood of serious medical errors [1].
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