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Fluid and Electrolytes. F . Mamdouhi M . D Mashhad University of Medical Sciences. اسمولالیته:غلظت ذره یا ماده محلول در یک مایع اسمولالیته طبیعی پلاسما:275-290 اختلالات هموستاز آب: هیپوناترمی یا هیپرناترمی اختلالات هموستاز سدیم :ادم یا هیپوولمی. - PowerPoint PPT Presentation
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Fluid and Electrolytes
F . Mamdouhi M . DMashhad University of Medical
Sciences
در: محلول ماده یا ذره غلظت اسمواللیتهمایع یک
: پالسما طبیعی 290-275اسمواللیته
: یا هیپوناترمی آب هموستاز اختالالتهیپرناترمی
یا : ادم سدیم هموستاز اختالالتهیپوولمی
The major ECF particles are Na+ and its
accompanying anions Cl– and HCO3–.
The predominant ICF osmoles are K+ and
organic phosphate esters (ATP, creatine
phosphate, and phospholipids).
The normal plasma osmolality (Posm ) is 280 to 295 mosmol/kg.
It usually is held within narrow limits as variations of only 1 to 2 percent initiate mechanisms to return the Posm to normal.
These alterations in osmolality are sensed by receptor cells in the hypothalamus which affect water intake (via thirst) and water excretion (via ADH, which increases water reabsorption in the collecting tubules).
REGULATION OF PLASMA OSMOLALITY
The osmolality of human body fluid is
between 280 and 295 mosmol/kg and
regulated by :
–Vasopressin secretion
–water ingestion, and
– renal water transport.
Hypoosmolality and hyperosmolality can produce
serious neurologic symptoms and death, primarily due to
water movement into and out of the brain, respectively.
To prevent this, the plasma osmolality (Posm ), which is
primarily determined by the plasma Na+ concentration, is
normally maintained within narrow limits by appropriate
variations in water intake and water excretion.
This regulatory system is governed by osmoreceptors in
the hypothalamus that influence both thirst and the
secretion of antidiuretic hormone (ADH).
Osmolality
Vasopressin (AVP) is synthesized in the
hypothalamus.
the distal axons of those neurons project
to the posterior pituitary or
neurohypophysis, from which AVP is
released into the circulation.
AVP has a half-life in the circulation of
only 10–20 min.
AVP secretion is stimulated as systemic
osmolality increases above a threshold
level of 285 mosmol/kg,
Thirst sensation and thus water ingestion
also are activated at 285 mosmol/kg.
Changes in blood volume and blood
pressure are also direct stimuli for AVP
release and thirst.
osmoregulation is almost entirely mediated
by changes in
WATER BALANCE
Water intake
Obligatory water output
WATER BALANCE
هیپوولمی
:علل
دادن دست ازطریق از GIاب
کلیوی طریق از اب دادن دست ازپو1ست طریق از اب دادن دست از
سوم فضای به سکستراسیون
ازطریق دادن دست GI:از
استفراغ
NG tube
اسهال
فیستول
Only small amounts of water are normally lost in
the stool, averaging 100 to 200 mL/day.
However, gastrointestinal losses are increased to
a variable degree in patients with vomiting or
diarrhea.
The effect of these losses on the plasma Na+
concentration depends on the sum of the Na+
and K+ concentrations in the fluid that is lost.
Gastrointestinal losses
طریق از دادن دست از:کلیوی
آب کلیوی اتالف) ( نفروژنیک یا مرکزی بیمزه دیابت
سدیم و آب کلیوی اتالف دیورتیک اسموتیک دیورز هیپوآلدوسترونیسم سدیم دهنده دست از نفروپاتی
The obligatory renal water loss is directly related
to solute excretion.
If a subject has to excrete 800 mosmol of solute
per day (mostly Na+ and K+ salts and urea) to
remain in the steady state, and the maximum
Uosm is 1200 mosmol/kg, then the excretion of the
800 mosmol will require a minimum urine volume
of 670 mL/day.
obligatory renal water
طریق از دادن دست از:پوست
نامحسوس اتالف
تعریق
سوختگی
The evaporative losses play an important role in
thermoregulation; the heat required for evaporation,
0.58 kcal/1.0 mL of water, normally accounts for 20
to 25 percent of the heat lost from the body, with the
remainder occurring by radiation and convection.
The net effect is the elimination of the heat produced
by body metabolism, thereby preventing the
development of hyperthermia.
Insensible losses
Sweat is a hypotonic fluid (Na+ concentration equals 30 to 65 meq/L)
It also contributes to thermoregulation, as the secretion and subsequent evaporation of sweat result in the loss of heat from the body.
In the basal state, sweat production is low, but it can increase markedly in the presence of high external temperatures or when endogenous heat production is enhanced, as with exercise, fever, or hyperthyroidism. As an example, a subject exercising in a hot, dry climate can lose as much as 1500 mL/h as sweat
Sensible loss
سوم اسکستر فضای به :سیون
هیپوآلبومینمی سیروز نفروتیک سندرم
مویرگی نشت حاد پانکراتیت ایسکمیک روده رابدومیولیز
هیپوولمی :عالیم- - - - تشنگی کرامپ ضعف پذیری خستگی
گیجی- : اولیگوری انتهایی اعضای ایسکمی
- - خواب- قلبی آنژین شکم درد سیانوزآلودگی
- غشاهای خشکی پوستی تورگور کاهشمخاطی
- هیپوتانسیون ژوگولر ورید فشار کاهشوضعیتی- تاکیکاردی وضعیتی
سدیم تعادل
خارج 85-90% بخش در سدیم. دارد قرار سلولی
منعکس سدیم غلظت تغییراتاب هموستاز خوردن هم بر کننده
است.
به سدیم تام مقدار تغییراتحجم افزایش یا کاهش صورت
ECF . یابد می تظاهر
سدیم : مول 150دریافت میلی
به : بستگی سدیم توبولی GFRدفع بازجذب و
دارد.
سدیم : پروگزیمال – 3/2بازجذب لوله -25در
30 - هنله% - 5در در% بقیه دیستال توبول
کننده جمع مجاری
هیپوناترمی
از: کمتر سدیم 135تعریف
علل:
کاذب- 1 هیپوناترمی
هیپواسموالر- 2 هیپوناترمی
HyponatremiaIn almost all cases, hyponatremia results from the
intake and subsequent retention of water.
A water load will be rapidly excreted as the dilutional
fall in plasma osmolality suppresses the release of
antidiuretic hormone (ADH), thereby allowing the
excretion of a dilute urine.
The maximum rate of water excretion on a regular
diet is over 10 liters per day.
: کاذب هیپوناترمی 1: نرمال- اسمواللیته
هیپرلپیدمی هیپرپروتئینمی پروستاتکتومی
2: باال- اسمواللیته هیپرگلیسمی مانیتول
Pseudohyponatremia Is associated with a normal plasma osmolality, refers to those disorders in which marked elevations of substances, such as lipids and proteins, result in a reduction in the fraction of plasma that is water.
In normal subjects, the plasma water is approximately 93 percent of the plasma volume.
A normal plasma sodium concentration of 142 meq/L (measured per liter of plasma) actually represents a concentration in the physiologically important plasma water of 154 meq/L (142 ÷ 0.93 = 154).
Ion-selective electrodes have been used to
directly measure the plasma water sodium
concentration in this setting but have variable
accuracy.
HYPONATREMIA WITH A HIGH PLASMA OSMOLALITY
Hyponatremia with a high plasma osmolality is most often due to hyperglycemia.
A less common cause is the administration and retention of hypertonic mannitol.
The rise in plasma osmolality induced by glucose or mannitol pulls water out of the cells, thereby lowering the plasma sodium concentration by dilution.
Physiologic calculations suggest that the plasma sodium concentration should fall by 1 meq/L for every 62 rmg/dL rise in the plasma concentration of glucose or mannitol (which have the same molecular weight).
The 1:62 ratio applied when the plasma glucose concentration was less than 400 mg/dL.
At higher glucose concentrations, the ratio of 1:42 provided a better estimate of this association than the usual 1:62 ratio
Normal Plasma Osmolality Isosmotic hyponatremia can be produced by the addition of an isosmotic (or near isosmotic) but non-sodium-containing fluid to the extracellular space.
This problem primarily occurs with the use of nonconductive glycine or sorbitol flushing solutions during transurethral resection of the prostate or bladder or irrigation during laparoscopic surgery, since variable quantities of this solution are absorbed.
DISORDERS IN WHICH ADH LEVELS ARE ELEVATED
The two most common causes of
hyponatremia are:
– effective circulating volume depletion and
– the syndrome of inappropriate ADH
secretion, disorders in which ADH secretion
is not suppressed.
Effective Circulating Volume Depletion
Significantly decreased tissue perfusion is a
potent stimulus to ADH release.
This response is mediated by baroreceptors in the
carotid sinus and can overcome the inhibitory
effect of hyponatremia on ADH secretion.
Heart Failure and Cirrhosis
Even though the plasma volume may be markedly
increased in these disorders, the pressure sensed at the
carotid sinus baroreceptors is reduced due to the fall in
cardiac output in heart failure and to peripheral
vasodilatation in cirrhosis.
The rise in ADH levels tend to vary with the severity of
the disease, making the development of hyponatremia an
important prognostic sign.
Syndrome of Inappropriate ADH Secretion
Persistent ADH release and water retention can
also be seen in a variety of disorders that are
not associated with hypovolemia.
These patients have a stable plasma sodium
concentration between 125 and 135 meq/L.
Hormonal Changes Hyponatremia can occur in patients with adrenal
insufficiency (in which it is lack of cortisol that is
responsible for the hyponatremia) and with
hypothyroidism.
The release of HCG during pregnancy may be
responsible for the mild resetting of the osmostat
downward, leading to a fall in the plasma sodium
concentration of about 5 meq/L.
DISORDERS IN WHICH ADH LEVELS MAY BE APPROPRIATELY SUPPRESSED
There are two disorders in which
hyponatremia can occur despite suppression of
ADH release:
– advanced renal failure
– primary polydipsia
Advanced Renal Failure The relative ability to excrete free water (free water
excretion divided by the glomerular filtration rate)
is maintained in patients with mild to moderate
renal failure.
Thus, normonatremia is usually maintained in the
absence of oliguria or advanced renal failure.
Advanced Renal Failure
In the latter setting, the minimum urine
osmolality rises to as high as 200 to 250
mosmol/kg despite the appropriate suppression of
ADH.
The osmotic diuresis induced by increased solute
excretion per functioning nephron is thought to
be responsible for the inability to dilute the urine.
Primary Polydipsia Is a disorder in which there is a primary stimulation of thirst.
It is most often seen in anxious and in patients with psychiatric illnesses, particularly those taking antipsychotic drugs in whom the common side effect of a dry mouth leads to increased water intake.
Polydipsia can also occur with hypothalamic lesions (as with infiltrative diseases such as sarcoidosis) which directly affect the thirst centers
Primary PolydipsiaThe plasma sodium concentration is usually normal or only slightly reduced in primary polydipsia, since the excess water is readily excreted.
These patients may feel asymptomatic or may present with complaints of polydipsia and polyuria.
In rare cases water intake exceeds 10 to 15 L/day and fatal hyponatremia may ensue.
Symptomatic hyponatremia can also be induced with an acute 3 to 4 liter water load (as may rarely be seen in anxious patients preparing for a radiologic examination or for urinary drug testing)
Symptomatic and potentially fatal hyponatremia has also been described after ingestion of the designer amphetamine ecstasy (methylenedioxymethamphetamine or MDMA)
Both a marked increase in water intake and inappropriate secretion of ADH may contribute.
Low ِDietary Solute Intake Beer drinkers or other malnourished patients may have a marked reduction in water excretory capacity.
Normal subjects excrete 600 to 900 mosmol/kg of solute per day (primarily Na, K salts and urea); thus, if the minimum urine osmolality is 60 mosmol/kg, the maximum urine output will be 10 to 15 L/day .Beer contains little or no Na, K , or protein, and the carbohydrate load will suppress endogenous protein breakdown and therefore urea excretion.
Diagnosis of HyponatremiaHyponatremia in virtually all patients reflects
water retention due to an inability to excrete
ingested water.
In most cases, this defect represents the persistent
secretion of ADH, although free water excretion
can also be limited in advanced renal failure
independent of ADH.
In the absence of renal failure, the differential
diagnosis begins with the history and physical
examination, looking for one of the causes of
excess ADH secretion:
effective circulating volume depletion (including
gastrointestinal or renal losses, congestive
heart failure, and cirrhosis);
the syndrome of inappropriate ADH secretion
(SIADH);
adrenal insufficiency or hypothyroidism.
DIAGNOSIS
Three laboratory findings also may provide
important information in the differential
diagnosis of hyponatremia:
the plasma osmolality;
the urine osmolality;
the urine sodium concentration.
Plasma Osmolality
The plasma osmolality is reduced in most
hyponatremic patients, because it is primarily
determined by the plasma sodium
concentration and accompanying anions.
In some cases the plasma osmolality is either
normal or elevated.
Since there is no hypoosmolality and
therefore no risk of cerebral edema due to
water movement into the brain, therapy
directed at the hyponatremia is not indicated
in any of these disorders with the exception
of glycine administration.
In this setting, the plasma osmolality may fall
with time as the glycine is metabolized.
Urine Osmolality The normal response to hyponatremia (which is
maintained in primary polydipsia) is to completely
suppress ADH secretion, resulting in the excretion
of a maximally dilute urine with an osmolality below
100 mosmol/kg and a specific gravity < or =1003.
Values above this level indicate an inability to
normally excrete free water that is generally due to
continued secretion of ADH.
پالسما اسمواللیته
باال طبیعی پایینهیپرگلیسمی هیپرپروتئینمی حجیم بسیار ادرار
مانیتول هیپرلپیدمی رقیق بسیار و
مثانه> 100 تحریک
نه بلهحجم اولیه ECFپرنوشی
افزایش طبیعی کاهش
قلبی SIADHادرار Naغلظت نارساییکبدی سیروز هیپوتیرویئدیکلیوی سندرم آدرنال نارسایی
20 < 10<
کلیوی خارج دفع اتالف Naنفروپاتی Na دیورتیک طوالنی مصرف
کشیده طول استفراغ هیپوآلدوسترونیسمدیورتیک
استفراغ
:SIADHعلل عصبی بیماریهای روانی ریوی بدخیم تومورهای بزرگ جراحی داروها
hyponatremia due to the SIADH is characterized by the
following set of findings:
– • A fall in the plasma osmolality
– • An inappropriately elevated urine osmolality
(above 100 mosmol/kg and usually above 300
mosmol/kg)
– • A urine sodium concentration usually above 40
meq/L.
– • A relatively normal plasma creatinine concentration
– • Normal adrenal and thyroid function.
:SIADHعالئم + هیپواسمواللیتی هیپوناترمی Uosm<100 UNa<40 نرموولمی - نرمال – تیرویید آدرنال کلیه فانکشن – – نرمال پتاسیم باز اسید هیپواوریسمی
Plasma Uric Acid and Urea Concentrations
The initial water retention and volume expansion in the SIADH leads to another frequent finding that is the opposite of that typically seen with volume depletion: hypouricemia (plasma uric acid concentration less than 4 mg/dL ) due to increased uric acid excretion in the urine.
It is presumed that the early volume expansion diminishes proximal sodium reabsorption, leading to a secondary decline in the net reabsorption of uric acid.
Cerebral Salt Wasting All of the changes in electrolyte balance observed in the SIADH have also been described in the putative syndrome of cerebral salt-wasting.
This disorder is characterized by a high urine sodium concentration that is due to defective tubular reabsorption (mediated by the release of a natriuretic hormone, perhaps brain natriuretic peptide) and an elevation in ADH and the subsequent development of hyponatremia due to the associated volume depletion.
Symptoms of Hyponatremia
The symptoms that may be seen with
hyponatremia or hypernatremia are
primarily neurologic and are related both
to the severity and in particular to the
rapidity of onset of the change in the
plasma sodium concentration.
Symptoms of Hyponatremia
The symptoms directly attributable to hyponatremia primarily occur with acute and marked reductions in the plasma sodium concentration and reflect neurologic dysfunction induced by cerebral edema .
In this setting, the associated fall in plasma osmolality creates an osmolal gradient that favors water movement into the cells, leading in particular to brain edema.
The presence of cerebral overhydration generally correlates closely with the severity of the symptoms.
Nausea and malaise are the earliest findings, and may be seen when the plasma sodium concentration falls below 125 to 130 meq/L.
This may be followed by headache, lethargy, and obtundation and eventually seizures, coma and respiratory arrest if the plasma sodium concentration falls below 115 to 120 meq/L.
Hyponatremic encephalopathy may be
reversible, although permanent neurologic
damage or death can occur, particularly in
premenopausal women.
Overly rapid correction also may be
deleterious, especially in patients with
chronic asymptomatic hyponatremia.
بالینی : خصوصیاتعصبی : عالیم
عالمت بی : از کمتر سدیم بیحالی و 125تهوع
: – – سدیم گیجی آلودگی خواب سردرد115-120
: از – – کمتر سدیم کما تشنج ستوپور 115ا
عالمت- + 1 بدون هیپوناترمیکاهشحجم :
سالین نرمالادم- + :2 هیپوناترمی
آب و سدیم محدودیت هیپوکالمی تصحیح + س1دیم کردن جایگزین لوپ دیورتیک
و- – 3 کلیه نارسایی اولیه پرنوشیSIADH:
آب محدودیت
سدیم کمبود محاسبه
ODS:– – دیسفازی دیزآرتری شل فلج مزمن هیپوناترمی در بیشتر باال مورتالیته ساز خطر عوامل :ODSسایر
آنوکسی•هیپوکالمی •سوتغذیه •
Na deficit (mmol) = 0.6 x wt(kg) x (desired [Na] - actual [Na])
60 kg women, serum Na 107, seizure recalcitrant to benzodiazepines.Na defecit = 0.6 x (60) x (120 – 107) = 468 mEqWant to correct at rate 1.5 mEq/L/h: 13/1.5 = 8.7h468 mEq / 8.7h = 54 mEq/h3% NaCl has 513 mEq/L of Na54 mEq/h = x
513 mEq 1Lx = rate of 3% NaCl = 105 cc/h over 8.7h to correct serum Na to 120 mEq/h
Note: Calculations are always at best estimates, and anyone getting
hyponatremia corrected by IV saline (0.9% or 3%) needs frequent
serum electrolyte monitoring (q1h if on 3% NS).
هیپرناترمی
سدیم : < 145تعریف
هیپراسموالریتی = هیپرناترمیهیپرناترمی به مناسب :پاسخ
اب دریافت افزایش ادرار حجم کمترین دفع
Causes of Hypernatremia Hypernatremia is a relatively common problem that can be produced either by the administration of hypertonic sodium solutions or, in almost all cases, by the loss of free water.
It should be emphasized that persistent
hypernatremia does not occur in normal subjects,
because the ensuing rise in plasma tonicity
stimulates both the release of ADH and, more
importantly, thirst.
The net effect is that hypernatremia primarily occurs
in those patients who cannot express thirst normally:
infants and adults with impaired mental status.
The latter most often occurs in the elderly , who also
appear to have diminished osmotic stimulation of
thirst.
Hospitalized persons, whether old or young, can
become hypernatremic iatrogenically as a result of
inadequate fluid prescription or impaired thirst.
Hypernatremia due to water loss is called
dehydration.
This is different from hypovolemia in
which both salt and water are lost.
UNREPLACED WATER LOSS
The loss of solute-free water will, if unreplaced, lead to an elevation in the plasma sodium concentration.
It is important to recognize that the plasma sodium concentration and plasma tonicity are determined by the ratio between total body solutes and the total body water.
Thus, it is the sum of the sodium and potassium concentrations that determines the effect that loss of a given amount of fluid will have.
Patients with secretory diarrheas (cholera, vipoma) have a sodium plus potassium concentration in the diarrheal fluid that is similar to that in the plasma.
Loss of this fluid will lead to volume and potassium depletion, but will not directly affect the plasma sodium concentration.
In contrast, many viral and bacterial enteritides and the osmotic diarrhea induced by lactulose (to treat hepatic encephalopathy) or charcoal-sorbitol (to treat a drug overdose).
Similar considerations apply to urinary
losses during an osmotic diuresis induced by
glucose, mannitol, or urea.
With these considerations in mind, the
sources of free water loss that can lead to
hypernatremia if intake is not increased
include:
Insensible and Sweat Losses
Insensible water loss from the skin and
respiratory tract by evaporation and sweat
are dilute fluids, the loss of which is
increased by fever, exercise, and
exposure to high temperatures.
Gastrointestinal losses
As mentioned above, some
gastrointestinal losses, particularly
osmotic diarrheas, will promote the
development of hypernatremia because
the sodium plus potassium concentration
is less than that in the plasma.
Central or Nephrogenic DiabetesInsipidus Decreased release of ADH or renal resistance to
its effect cause the excretion of a relatively dilute
urine.
Most of these patients have a normal thirst
mechanism . As a result, they typically present
with polyuria and polydipsia.
However, marked and symptomatic
hypernatremia can occur if a central lesion
impairs both ADH release and thirst.
Osmotic Diuresis An osmotic diuresis due to glucose, mannitol, or urea causes an increase in urine output in which the sodium plus potassium concentration is well below that in the plasma because of the presence of the nonreabsorbed organic solute. Patients with diabetic ketoacidosis or nonketotic hyperglycemia typically present with marked hypertonicity, although the plasma Na concentration may not be elevated due to hyperglycemia-induced water movement out of the cells.
Hypothalamic Lesions Affecting Thirst or Osmoreceptor Function
Hypernatremia can also occur in the absence of
increased water losses if there is primary
hypothalamic disease impairing thirst (hypodipsia).
Two different mechanisms have been described,
which in adults, are most often due to tumors,
granulomatous diseases (eg, sarcoidosis), or
vascular disease.
SODIUM OVERLOAD
Acute and often marked hypernatremia (in which the plasma sodium concentration can exceed 175 to 200 meq/L) can also be induced by the administration of hypertonic sodium-containing solutions.
Examples include accidental or nonaccidental salt poisoning in infants and young children, the infusion of hypertonic sodium bicarbonate to treat metabolic acidosis, hypertonic saline irrigation of hydatid cysts.
The hypernatremia in this setting will correct
spontaneously if renal function is normal, since
the excess sodium will be rapidly excreted in the
urine.
Too rapid correction should be avoided if the
patient is asymptomatic; these patients, however,
are less likely to develop cerebral edema during
correction, since the hypernatremia is generally
very acute with little time for cerebral adaptation.
: هیپرناترمی علل سدیم اولیه دریافت: اب دفع
: کلیوی خارج• - – : سوختگی تب تعریق پوستمکانیکی : • تهویه تنفس
: کلیوی اسموتیک • دیورزدارویی • دیورز• DI
Even with optimal therapy, the mortality rate is
extremely high in adults with a plasma sodium
concentration that has acutely risen to above
180 meq/L.
For reasons that are not well understood,
severe hypernatremia is often better tolerated
in young children.
Diagnosis of Hypernatremia Hypernatremia represents a relative deficit of
water in relation to solute.
Although it can be induced by the administration
of Na in excess of water (as with hypertonic
sodium bicarbonate during a cardiac arrest), a
high plasma Na concentration most often results
from free water loss.
DIAGNOSIS The cause of the hypernatremia is usually evident from the history.
If, however, the etiology is unclear, the correct diagnosis can usually be established by evaluation of the integrity of ADH-renal axis via measurement of the urine osmolality.
A rise in the plasma sodium concentration is a potent stimulus to ADH release as well as to thirst; furthermore, a plasma osmolality above 295 mosmol/kg (which represents a plasma sodium concentration above 145 to 147 meq/L) generally leads to sufficient ADH secretion to maximally stimulate urinary concentration.
Thus, if both hypothalamic and renal function are
intact, the urine osmolality in the presence of
hypernatremia will be above 700 to 800 mosmol/kg.
In this setting:
– unreplaced insensible or
– gastrointestinal losses,
– sodium overload, or
– rarely a primary defect in thirst
is likely to be responsible for the
hypernatremia.
Measurement of the urine sodium
concentration may help to distinguish
between these disorders.
it should be less than 25 meq/L when water
loss and volume depletion are the primary
problems, but is typically well above 100
meq/L following the ingestion or infusion or a
hypertonic sodium solution.
The urine osmolality is lower than that of the plasma, then either central (ADH-deficient) or nephrogenic (ADH-resistant) diabetes insipidus is present.
These conditions can be distinguished simply by administering exogenous ADH.
The urine osmolality will rise, usually by 50 percent or more, in central DI but will have little or no effect in nephrogenic DI.
The history is also often helpful in this setting, since severe nephrogenic DI in adults is uncommon in the absence of chronic lithium use or hypercalcemia.
ECFحجم افزایش نیافته افزایش
یافتهتجویز – غلیظ حجم کم ادرار
NACL یاNAHCO3 نه بله
< ادرار اسموالریته کلیوی خارج 750دفع
نه بلهبه پاسخ اسموتیک DDAVPدیورز
افزایش اسموالریته تغییر عدم
اسموالریته NDI CDI
درمان: اب تجویز دسموپرسین نمک کم غذای تیازید کم دوز کلرپروپامید کلوفیبرات کاربامازپین NSAIDs
Treatment of DIAVP, Aqueous vasopressin (Pitressin)
Only parenteral form, 5-10 U SC q2-4hLasts 2-6hCan cause HTN, coronary vasospasm
Chlorpropamide (OHA which stimulates AVP secretion)
100-500 mg po OD-bidOnly useful for partial DI, can cause hypoglycemia
HTCZ (induces volume contraction which diminishes free water excretion)
50-100 mg OD-bidMainstay of Rx for chronic NDI
Amiloride (blunts Lithium uptake in distal tubules & collecting ducts)5-20 mg po OD-bidDrug of choice for Lithium induced DI
Indomethacin 100-150 mg po bid-tid (PGs antagonize AVP action)Clofibrate 500 mg po qid (augments AVP release in partial CDI)
Clinical Manifestations of Hypernatremia
The rise in the plasma sodium concentration and
osmolality causes acute water movement out of
the brain; this decrease in brain volume can
cause rupture of the cerebral veins, leading to
focal intracerebral and subarachnoid
hemorrhages and possible irreversible
neurologic damage.
The clinical manifestations of this disorder
begin with lethargy, weakness, and
irritability, and can progress to twitching,
seizures, and coma.
Values above 180 meq/L are associated
with a high mortality rate, particularly in
adults.
Correction of chronic hypernatremia must occur
slowly to prevent rapid fluid movement into the
brain and cerebral edema, changes that can lead
to seizures and coma.
Although the brain cells can rapidly lose potassium
and sodium in response to this cell swelling, the
loss of accumulated osmolytes occurs more slowly,
a phenomenon that acts to hold water within the
cells.
The delayed clearance of osmolytes from
the cell can predispose to cerebral edema if
the plasma sodium concentration is lowered
too rapidly.
As a result, the rate of correction in
asymptomatic patients should not exceed 12
meq/L per day, which represents an average
of 0.5 meq/L per hour.
free-water deficit=
0.4(0.5) x w x{ (Na p – 140) ÷ 140}
50-kg woman with a plasma Na+ concentration
of 160 mmol/L has an estimated free-water
deficit of 2.9 L {[(160 – 140) ÷ 140] x (0.4 x 50)}
160-140= 20
20 x 0.5 = 40 h
2900 ÷ 40= 73
پتاسیم
پتاسیم :تعادلپالسمایی : 5تا 3/5غلظت
سلولی : داخل 150غلظتNa-K-ATPaseپمپ
: پتاسیم روز 120تا40دریافت در مول میلی: پتاسیم ای روده %60-50تا10دفع
: پتاسیم کلیوی دفعمی 90% بازجذب هنله و پروگزیمال لوله توسط
شود.و دیستال لوله در ترشح در CCDتنظیم
principal cell : و الدسترون کنترل تحت استدیستال جریان میزان و پتاسیم
سدیم : افزایشجذب الدسترون اثراتپمپ Na –K-ATPaseتحریک
لومینال پتاسیم افزایشکانالهای
هیپوکالمی
Causes of Hypokalemia
Hypokalemia is a common clinical problem.
Potassium enters the body largely stored in the
cells, and then excreted in the urine.
Decreased intake, increased translocation into
the cells, or, most often, increased losses in the
urine (or gastrointestinal tract or sweat) all can
lead to potassium depletion.
کاهشدریافت :-داری روزهخوری خاک
DECREASED POTASSIUM INTAKE
The normal range of potassium intake is 40 to
120 meq per day, most of which is then excreted
in the urine.
The kidney is able to lower potassium excretion
to a minimum of 5 to 25 meq per day in the
presence of potassium depletion.
INCREASED ENTRY INTO CELLS
The normal distribution of potassium between the cells (which contains approximately 98 percent of exchangeable potassium) and the extra cellular fluid is maintained by the Na-K-ATPase pump in the cell membrane.
In some cases, however, there is increased potassium entry into cells, resulting in transient hypokalemia.
Elevation in Extracellular pHEither metabolic or respiratory alkalosis can promote potassium entry into cells.
Hydrogen ions leave the cells to minimize the change in extracellular pH; the necessity to maintain electro neutrality then requires the entry of some K (and Na) into the cells.
This direct effect is relatively small, as the plasma potassium concentration falls less then 0.4 meq/L for every 0.1-unit rise in pH .
Increased Availability of InsulinInsulin promotes the entry of K into skeletal
muscle and hepatic cells, apparently by
increasing the activity of the Na-K-ATPase
pump.
The plasma potassium concentration can also
be reduced by a carbohydrate load.
Elevated Adrenergic Activity
Catecholamines, acting via the B-adrenergic receptors , can promote potassium entry into the cells, primarily by increasing Na-K-ATPase activity.
As a result, transient hypokalemia can be caused in any setting in which there is stress-induced release of epinephrine, as with acute illness, coronary ischemia, or theophylline intoxication.
lower Gastrointestinal Losses
Hypokalemia is most common when the
losses occur over a prolonged period as
with a villous adenoma or a vasoactive
intestinal peptide secreting tumor
(VIPoma).
INCREASED URINARY LOSSESUrinary potassium excretion is mostly derived from potassium secretion in the distal nephron, particularly by the principal cells in the cortical collecting tubule.
This process is primarily influenced by two factors: aldosterone and the distal delivery of sodium and water.
Thus, urinary potassium wasting generally requires increases in either aldosterone or distal flow, while the other parameter is at least normal or increased.
Diuretics
Any diuretic that acts proximal to the potassium secretory site – acetazolamide, loop diuretics, and thiazide-type diuretics – will both increase distal delivery and, via the induction of volume depletion, activate the renin-angiotensin-aldosterone system.
As a result, urinary potassium excretion will increase, leading to hypokalemia if these losses are greater than intake.
Primary Mineralocorticoid Excess
Urinary potassium wasting is also
characteristic of any condition associated with
primary hypersecretion of a mineralocorticoid,
as with an aldosterone-producing adrenal
adenoma.
These patients are almost always hypertensive.
Loss of Gastric Secretions
This problem is usually suggested from the
history.
If, however, the history is not helpful, the
differential diagnosis of a normotensive
patient with hypokalemia, urinary potassium
wasting, and metabolic alkalosis includes:
surreptitious vomiting or diuretic use and
Bartter's. syndrome.
Hypokalemic Periodic ParalysisIs a rare disorder of uncertain cause characterized
by potentially fatal episodes of muscle weakness
or paralysis which can affect the respiratory
muscles .
Acute attacks, in which the sudden movement of
potassium into the cells can lower the plasma
potassium concentration to as low as 1.5 to 2.5
meq/L.
Hypokalemic Periodic ParalysisThe recurrent attacks with normal plasma
potassium levels between attacks distinguish
periodic paralysis.
Hypokalemic periodic paralysis are often
precipitated by rest after exercise, stress, or a
carbohydrate meal, events that are often
associated with increased release of epinephrine
or insulin.
Hypokalemic Periodic Paralysis
The hypokalemia is often accompanied by
hypophosphatemia and hypomagnesemia.
May be familial with autosomal dominant
inheritance (in which the penetrance may be
only partial) or may be acquired in patients
with thyrotoxicosis.
The oral administration of 60 to 120 meq of potassium chloride usually aborts acute attacks of hypokalemic periodic paralysis within 15 to 20 minutes.
Another 60 meq can be given if no improvement is noted.
However, the presence of hypokalemia must
be confirmed prior to therapy, since potassium
can worsen episodes due to the normokalemic
or hyperkalemic forms of periodic paralysis.
Prevention of hypokalemic episodes consists of the restoration of euthyroidism in thyrotoxic patients and the administration of a B blocker in either familial or thyrotoxic periodic paralysis.
B blockers can minimize the number and severity of attacks.
A nonselective B blocker (such as propranolol)
should be given; B1-selective agents are less
likely to inhibit the B2 receptor-mediated
hypokalemic effect of epinephrine.
Other modalities that may be effective for
prevention include:
K+ supplementation,
K+-sparing diuretics,
a low-carbohydrate diet,
and the carbonic anhydrase inhibitor.
(Acetazolamide)
Marked Increase in Blood Cell Production
An acute increase in hematopoietic cell production
is associated with potassium uptake by the new
cells and possible hypokalemia.
This most often occurs after the administration of
vitamin B12 or folic acid to treat a megaloblastic
anemia or of granulocyte-macrophage colony-
stimulating factor (GM-CSF) to treat neutropenia .
Metabolically active cells can also take up
potassium after blood has been drawn. This has
been described in patients with acute myeloid
leukemia.
In this setting, the measured plasma potassium concentration may be below 1 meq/L (without symptoms) if the blood is allowed to stand at room temperature.
This can be prevented by rapid separation of the plasma from the cells or storage of the blood at 4°C
Hypothermia
Accidental or induced hypothermia can
drive potassium into the cells and lower
the plasma potassium concentration to
below 3.0 to 3.5 meq/L.
Hypomagnesemia
Hypomagnesemia is present in up to 40 percent of patients with hypokalemia.
In many cases, as with diuretic therapy, vomiting, or diarrhea, there are concurrent potassium and magnesium losses.
In addition, hypomagnesemia of any cause can lead to increased urinary potassium losses via an uncertain mechanism.
HypomagnesemiaDocumenting the presence of hypomagnesemia is particularly important because the hypokalemia often cannot be corrected until the magnesium deficit is repaired.
The concurrent presence of hypocalcemia (due both to decreased release of parathyroid hormone and resistance to its calcemic effect) is often a clue to underlying magnesium depletion.
Polyuria Normal subjects can, in the presence of the potassium depletion, lower the urine potassium concentration to a minimum of 5 to 10 meq/L.
If, however, the urine output is over 5 to 10 L/day, then obligatory potassium losses can exceed 50 to 100 meq per day.
This problem is most likely to occur in primary (often psychogenic) polydipsia.
-: بالینی خصوصیاتتحتانی- – – - 1 اندام عضالت ضعف ای ماهیچه درد پذیری خستگی
تنفسی عضالت ضعفکامل- 2 فلجرابدومیولیز-3ایلئوس- 4:EKGتغییرات- 5
موج شدن معکوس یا شدن Tصاف موجU قطعه STافت شدن QUطوالنی فاصله شدن PRطوالنی شدن QRSپهن
بطنی- 6 اریتمی خطر افزایشدیگوکسین- 7 با مسمومیت افزایشمتابولیک- 8 الکالوز9-DI
10-GTTمختل
Diagnosis of Hypokalemia
Hypokalemia is a common clinical problem, the
cause of which can usually be determined from
the history (as with diuretic use, vomiting, or
diarrhea).
Measurement of the blood pressure and urinary
potassium excretion and assessment of acid-base
balance are often helpful.
URINARY RESPONSEA normal subject can, in the presence of potassium depletion, lower urinary potassium excretion below 25 to 30 meq per day.
Random measurement of the urine potassium concentration can also be used, but may be less accurate than a 24-hour collection.
It is likely that extrarenal losses are present if the urine potassium concentration is less than 15 meq/L (unless the patient is markedly polyuric). Higher values, however, do not necessarily indicated potassium wasting if the urine volume is reduced.
DIAGNOSIS
Metabolic acidosis with a low rate of potassium excretion is, in an asymptomatic patient, suggestive of lower gastrointestinal losses due to laxative abuse or a villous adenoma
Metabolic acidosis with potassium wasting is most often due to diabetic ketoacidosis or to type 1 (distal) or type 2 (proximal) renal tubular acidosis.
Metabolic alkalosis with a low rate of
potassium excretion is due to surreptitious
vomiting (often in bulimia in an attempt to
lose weight) or diuretic use (in which the
urinary collection is obtained after the diuretic
effect has worn off).
Metabolic alkalosis with potassium wasting and
a normal blood pressure is most often due to
surreptitious vomiting or diuretic use or to
Bartter's syndrome.
In this setting, measurement of the urine
chloride concentration is often helpful, being
low in vomiting.
Metabolic alkalosis with potassium wasting and
hypertension is suggestive of :
– surreptitious diuretic therapy in a patient with
underlying hypertension,
– renovascular disease,
– or one of the causes of primary
mineralocorticoid excess.
:درمOانپتاسیم کمبود اصالح
پتاسیم کلرید
پتاسیم سیترات
هیپرکالمی
> پتاسیم: 5تعریفپسودوهیپرکالمی
: علل کلیه- 1 نارساییدیستال- 2 جریان کاهشپتاسیم- 3 ترشح کاهش
- سدیم بازجذب در اختالل الف – : کمبود ادرنال نارسایی اولیه هیپوالدوسترونیسم
ادرنال انزیمهای - داروها : هیپورنینمی ثانویه هیپوالدرونیسم – : کاذب هیپوالدرونیسم الدرونیسم به مقاومت
داروها – اینتراستیشیال توبولو بیماریکلر- 4 یون بازجذب افزایش
گوردون سندرم سیکلوسپورین
Causes of Hyperkalemia
The plasma potassium concentration is
determined by the relationship between
potassium intake, the distribution of potassium
between the cells and the extracellular fluid, and
urinary potassium excretion.
In normal subjects, dietary potassium is largely
excreted in the urine.
The degree of potassium secretion is primarily
stimulated by three factors:
– an increase in the plasma potassium
concentration;
– a rise in the plasma aldosterone concentration;
– enhanced delivery of sodium and water to the
distal secretory site.
Ingestion of a K load leads initially to the
uptake of most of the excess K by the cells, a
process that is facilitated by insulin and the B2-
adrenergic receptors, both of which increase the
activity of the Na-K-ATPase pump in the cell
membrane.
This is then followed by the excretion of the
excess K in the urine within six to eight hours .
POTASSIUM ADAPTATION
Hyperkalemia is a rare occurrence in normal
subjects, because the cellular and urinary
adaptations prevent significant potassium
accumulation in the extracellular fluid.
This phenomenon, called potassium adaptation, is mostly due to more rapid potassium excretion in the urine.
INCREASED POTASSIUM RELEASE FROM CELLS
Pseudohyperkalemia
Refers to those conditions in which the
elevation in the measured plasma potassium
concentration is due to potassium movement
out of the cells during of after the blood
specimen has been drawn.
PseudohyperkalemiaThe major cause of this problem is mechanical
trauma during venipuncture, resulting in the
release of potassium from red cells .
It can also occur in hereditary spherocytosis and in
familial pseudohyperkalemia in which there is
increased temperature-dependent leakage of
potassium out of red blood cells after the specimen
is collected.
PseudohyperkalemiaPotassium also moves out of white cells and platelets after clotting has occurred. Thus, the serum potassium concentration normally exceeds the true value in the plasma by 0.1 to as much as 0.5 meq/L.
Although this difference in normals is not clinically important, the measured serum potassium concentration may be as high as 9 meq/L in patients with marked leukocytosis or thrombocytosis.
Metabolic Acidosis
The buffering of excess hydrogen ions in the
cells can lead to potassium movement into the
extracellular fluid; this transcellular shift is
obligated in part by the need to maintain
electroneutrality.
Insulin deficiency, Hyperglycemia, and Hyperosmolality
The combination of insulin deficiency and the hyperosmolality induced by hyperglycemia frequently leads to hyperkalemia in uncontrolled diabetes mellitus, even though the patient may be markedly potassium depleted due primarily to potassium losses in the urine.
An elevation in plasma osmolality results in osmotic water movement from the cells into the extracellular fluid. This is accompanied by potassium movement out of the cells.
Increased Tissue CatabolismAny cause of increase tissue breakdown result
in the release of potassium into the extracellular
fluid.
Clinical examples include trauma, the
administration of cytotoxic or radiation therapy
to patients with lymphoma or leukemia.
Beta-adrenergic Blockade Nonselective B-adrenergic blockers interfere with
the B2-adrenergic facilitation of K uptake by the
cells.
This effect is associated with only a minor
elevation in the plasma potassium concentration
in normal subjects (less than 0.5 meq/L), since the
excess potassium can be easily excreted in the
urine.
ExerciseK is normally released from muscle cells during exercise. This response may be mediated by two factors:A delay between potassium exit during
depolarization and subsequent reuptake by the Na-K-ATPase pump.
With severe exercise, an increased number of open K channels in the cell membrane. These channels are inhibited by ATP, an effect that is removed by the exercise-induced decline in ATP levels which.
The release of potassium during exercise may
have a physiologically important role.
The local increase in the plasma potassium
concentration has a vasodilator effect, thereby
increasing blood flow and energy delivery to the
exercising muscle.
The degree of elevation in the systemic plasma potassium concentration is less pronounced and is related to the degree of exercise:
0.3 to 0.4 meq/L with slow walking; 0.7 to 1.2 meq/L with moderate exertion (including prolonged aerobic exercise with marathon running); and as much as 2 meq/L following exercise to exhaustion.
The rise in the plasma K concentration is reversed
after several minutes of rest, and is typically
associated with a mild rebound hypokalemia
(averaging 0.4 to 0.5 meq/L below the baseline
level) that may be arrhythmogenic in susceptible
subjects.
The degree of K release is attenuated by prior physical conditioning , but may be exacerbated by the administration of nonselective B-blockers and, for uncertain reasons, in patients with CHF.
REDUCED URINARY POTASSIUM EXCRETION
Impaired urinary potassium excretion
generally requires an abnormality in one or
both of the two major factors required for
adequate renal potassium handling:
aldosterone and
distal sodium and water delivery.
Hypoaldosteronism Any cause of decreased aldosterone release or effect, such as that induced by hyporeninemic hypoaldosteronism or certain drugs, can diminish the efficiency of K secretion.
Rise in the plasma K concentration directly stimulates K secretion, partially overcoming the relative absence of aldosterone.
The net effect is that the rise in the plasma K concentration is generally small in patients with normal renal function.
Renal Failure The ability to maintain K excretion at near normal levels is generally maintained in patients with renal disease as long as both aldosterone secretion and distal flow are maintained.
Hyperkalemia generally develops in the patient who is oliguric or who has an additional problem such as a high K diet, increased tissue breakdown, hypoaldosteronism, or fasting in dialysis patients (which may both lower insulin levels and cause resistance to B-adrenergic ).
Effective Circulating Volume Depletion
Decreased distal flow due to marked effective
volume depletion (as in heart failure, cirrhosis,
or a salt-wasting nephropathy) can also lead to
hyperkalemia.
Transtubular Potassium Concentration Gradient
The differential diagnosis of persistent hyperkalemia consists of those disorders in which urinary potassium excretion is impaired.
The three most common causes of this problem are advanced renal failure, marked effective volume depletion (as with severe heart failure), and one of the causes of hypoaldosteronism.
TTKG is dependent upon two assumptions:
1: that the urine osmolality at the end of the cortical collecting tubule is similar to that of the plasma, since equilibration with the isosmotic interstitium will occur in the presence of antidiuretic hormone;
2: little or no potassium secretion or reabsorption takes place in the medullary collecting tubule.
Thus, the TTKG between the tubular fluid
at the end of the cortical collecting tubule
and the plasma can be estimated from:
TTKG = [Urine K ÷ (Urine osmolality
/ Plasma osmolality)] ÷ Plasma K
The TTKG in normal subjects on a regular
diet is 8 to 9, and rises to above 11 with a
potassium load, indicating increased
potassium secretion .
Thus, a value below 7 and particularly
below 5 in a hyperkalemic patient is highly
suggestive of hypoaldosteronism .
for example, the urine potassium
concentration is 30 meq/L, the plasma
potassium concentration is 6.5 meq/L, and
the urine and plasma osmolality are 560
mosmol/kg and 280 mosmol/kg,
respectively, then:
TTKG = [30 ÷ (560/280)] ÷ 6.5
= 2.3
بالینی :خصوصیاتتهویه – – – کاهش شل فلج عضالنی ضعف
متابولیک اسیدوزEKGتغییرات
T Tall فاصله مدت PRافزایش QRSو – رفتن بین از بطنی دهلیزی هدایت تاخیر
Pموج موج شدن موج QRSپهن با Tوادغام
سینوسی) ( موج طرح بطنی اسیستول یا فیبریالسیون
:درمانکلسیم گلوکونات
دکستروز + انسولینسدیم بیکربنات
B اگونیستسدیم استیرن پلی سولفونات
همودیالیز