Hyper Kale Mia Fair
-
Upload
priyanka-jose -
Category
Documents
-
view
218 -
download
0
Transcript of Hyper Kale Mia Fair
-
8/6/2019 Hyper Kale Mia Fair
1/29
HYPERKALEMIA
Introduction
Hyperkalemia is one of the few potentially lethal electrolyte disturbances
.Hyperkalemia is common in hospitalized patients, and may be associated withadverse clinical outcomes . Its prevalence and clinical impact in critically ill
patients are unknown. Hyperkalaemia is rare in clients with normal kidney
function but affects more than half of people with acute and chronic renal
failure. Extremely high levels of potassium in the blood (severe hyperkalemia)
can lead to cardiac arrest and death. When not recognized and treated properly,
severe hyperkalemia results in mortality rate about 67%. Proper treatment of
hyperkalemia depends on an understanding of the underlying physiology.
What is hyperkalaemia
Hyperkalemia means an abnormally elevated level of potassium in the
blood. The normal potassium level in the blood is 3.5 -5.0 millie quivalents per
liter (mEq/L). Potassium levels between 5.1 mEq/L to 6.0 mEq/L reflect mild
hyperkalemia. Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate
hyperkalemia, and levels above 7 mEq/L are severe hyperkalemia.
Potassium Regulation In The Body
Potassium is the most abundant intracellular cation. It is critically
important for many physiological processes, including maintenance of cellular
membrane potential , homeostasis of cell volume, and transmission of action
potentials in nerve cells. Its main dietary sources are vegetables (tomato and
potato), fruits (orange and banana) and meat. Elimination is through the
gastrointestinal tract and the kidney. At least 98% of the body's potassium is
found inside cells, with the remainder in the blood. This concentration gradient
is maintained principally by the Na+/K+ pump.
-
8/6/2019 Hyper Kale Mia Fair
2/29
The serum 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
The renal elimination of potas sium is passive (through the glomeruli),
and reabsorption is active in the proximal tubule and the ascending limb of the
loop of Henle. There is active excretion of potassium in the distal tubule and the
collecting duct; both are controlled by aldosterone.
The ratio of extracellular to intracellular potassium (K) concentration
largely determines the cell membrane resting electrical potential that, in turn,
regulates the function of excitable tissues(cardiac and skeletal muscle, and
nerve). Small absolute changes in the extracellular K concentration will have
large effects on that ratio, and consequent ly on the function of excitable tissues.
Thus, it is not surprising that the plasma K concentration (PK) normally is
maintained within very narrow limits. This tight regulation is accomplished by
two cooperative systems. One system defends against short -term changes in PK
by regulating internal balance: the equilibrium of K across the cell membrane.
This equilibrium is modulated by insulin, catecholamines and, to a lesser extent,
by acid-base balance, plasma tonicity, and several other factors . The other
system governs K homeostasis over the long-term by regulating external
balance: the parity between K intake and elimination. In individuals with
normal renal function, the kidneys are responsible for elimination of about 95%
of the daily K load with the remainder exiting through the gut. External K
balance is maintained largely by modulating renal K elimination.Almost all the
K excreted by the kidney comes from K secreted in the distal nephron
(connecting tubule and collecting duct) . Virtually all regulatio n of K excretion
takes place at this site in the nephron, under the influence of two principle
factors: the rate of flow and solute (sodium and chloride) delivery through that
part of the nephron; and the effect of aldosterone . K secretion is directly
-
8/6/2019 Hyper Kale Mia Fair
3/29
proportional to flow rate and sodium delivery through the lumen of the distal
nephron, and to circulating aldosterone levels in the setting of an
aldosteronesensitive epithelium. This explains, in part, why the use of diuretic
drugs that work proximal to the K secretory site (loop and thiazide diuretics)
often is accompanied by hypokalemia. K secretion is inversely proportional to
the chloride concentration of the luminal fluid and is stimulated, for example,
by luminal delivery of sodium bicarbonate . Convers ely, hyperkalemia
commonly accompanies acute kidney injury, particularly in the setting of
mineralocorticoid deficiency . Such mineralocorticoid deficiency is often
induced by drugs that interfere with the renin-angiotensinaldosterone axis and
commonly causes hyperkalemia in patients with chronic kidney disease, as well
. Sustained hyperkalemia is always attributable to inadequate renal K
elimination
Causes and risk factors ofhyperkalaemia
Hyperkalemia occurs when the level of potassium in the bloodstream is
higher than normal. This may be related to an increase in total body potassium
or the excess release of potassium from the cells into the bloodstream
1. Ineffectiveelimination
y Renal insufficiencyy Medication that interferes with urinary excretion: ACE inhibitors and angiotensin receptor blockers Potassium-sparing diuretics (e.g. amiloride and spironolactone) NSAIDs such as ibuprofen, naproxen, orcelecoxib The calcineurin inhibitor immunosuppressants ciclosporin and
tacrolimus
The antibiotic trimethoprim The antiparasitic drugpentamidine
-
8/6/2019 Hyper Kale Mia Fair
4/29
y Mineralocorticoid deficiency or resistance, such as: Addison's disease Aldosterone deficiency Some forms ofcongenital adrenal hyperplasia Type IV renal tubular acidosis (resistance of renal tubules to
aldosterone)
y Gordon's syndrome (familial hypertension with hyperkalemia), a raregenetic disorder caused by defective modulators of salt transporters,
including the thiazide-sensitive Na-Cl cotransporter.
2. Excessive release from cells
y Rhabdomyolysis, burns,crush inuries,severe infections or any cause ofrapid tissue necrosis, including tumor lysis syndrome
y Massiveblood transfusion or massive hemolysisy Shifts/transport out of cells caused by acidosis, low insulin levels, beta-
blocker therapy, digoxin overdose, or the paralyzing agent
succinylcholine
3. Excessive intake
y Excess intake with salt-substitute, potassium-containing dietarysupplements , (bananas,oranges,tomatoes,high protein diet,salt
substitutes),potassium supplements orpotassium chloride (KCl) infusion.
hyperkalemia by potassium intake would be seen only with large
infusions of KCl or oral doses of several hundred milliequivalents of KCl.
y Alcoholism or excessive consumption of aerated drinksy Stored bank blood transfusion(blood 10 days or older has an elevated
serum potassium due to hemolysis of aging blood
-
8/6/2019 Hyper Kale Mia Fair
5/29
4. Pseudohyperkalemia
Pseudohyperkalemia is a rise in the amount of potassium that occurs due
to excessive leakage of potassium from cells, during or after blood is drawn. It
is a laboratory artifact rather than a biological abnormality and can be
misleading to caregivers. pseudohyperkalemia is typically caused by hemolysis
during venipuncture (by either excessive vacuum of the blood draw ,a collection
needle that is of too fine a gauge,too tight application of tourniquets, multiple
attempts to obtain blood samples from the same site); excessive tourniquet time
or fist clenching during phlebotomy (which presumably leads to efflux of
potassium from the muscle cells into the bloodstream);or by a delay in the
processing of the blood specimen. It can also occur in specimens from patients
with abnormally high numbers ofplatelets (>500,000/mm ), leukocytes (> 70
000/mm ), or erythrocytes (hematocrit > 55%). People with "leakier" cell
membranes have been found, whose blood must be separated immediately to
avoid pseudohyperkalemia.
Kidney dysfunction
The kidneys normally remove excess potassium from the body. Because
the kidneys are responsible for 80% to 90% of potassium excreation,m ost cases
of hyperkalemia are caused by disorders that reduce the kidneys' abili ty to get
rid of potassium.This may result from disorders such as:
acute and chronic renal failure,
glomerulonephritis, lupus nephritis, transplant rejection, and obstructive diseases of the urinary tract, such as urolithiasis (stones
in the urinary tract).
-
8/6/2019 Hyper Kale Mia Fair
6/29
With a decline in the GFR, the patient cannot excrete potassium
normally. Patients with oliguria and anuria are at greater risk for hyperkalemia
than those without oliguria. Protein catabolism results in the release of cellular
potassium into the body fluids, causing severe hyperkalemia . People with as
little as 5% glomular function can maintain normal potassium level if urine
output is atleast 1L/day. In the presence of preserved GFR,the problem may be
a failure of tubular potassium secretory mechanism. In CRF ,adaptation to a
moderately elevated plasma potassium commonly develops, but a further rise
can occure during intercurrent events which desta bilize the new steady state eg
dietary load of potassium, hypovolaemia or drugs.
Patients with kidney dysfunctions are especially sensitive to medications
that can increase blood potassium levels. For example, patients with kidney
dysfunctions can develop worsening hyperkalemia when given salt substitut es
that contain potassium, when given potassium supplements (either orally or
intravenously), or medications that can increase blood potassium levels.
Diseases of theadrenalgland / hypoaldosteronism
Adrenal glands are important in secreting hormones such as cortisol and
aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while
excreting potassium in the urine. Therefore diseases of the adrenal gland, such
as Addison's disease, that lead to decreased aldosterone secretion can decrease
kidney excretion of potassium, resulting in body retention of potassium, and
hence hyperkalemia.
Potassium shifts
Potassium can move out of and into cells. Our total body potassium stores
are approximately 50 mEq/kg of body weight. At any given time, about 98% of
the total potassium in the body is located inside of cells (intracellular), with only
-
8/6/2019 Hyper Kale Mia Fair
7/29
2% located outside of cells (in the blood circulation and in the "extracellular"
tissue). The blood tests for measurement of potassium levels measure only the
potassium that is outside of the cells. Therefore, conditions that can cause
potassium to move out of the cells into the blood circulation can increase the
blood potassium levels even though the total amount of potassium in the body
has not changed.
In acidosis compensatory shifting of potassium occurs out of the cell in
exchange for hydrogen which leads to hyperkalaemia. One example of
potassium shift causing hyperkalemia is diabetic ketoacidosis. Insulin is vital to
patients with type 1 diabetes. Without insulin, patients with type 1 diabetes can
develop severely elevated blood glucose levels. Lack of insulin also causes the
breakdown of fat cells, with the release of ketones into the blood, turning the
blood acidic. The acidosis and high glucose levels in the blood work together to
cause fluid and potassium to move out of the cells into the blood circulation. .
Patients with diabetes often also have diminished kidney capacity to excret e
potassium into urine. The combination of potassium shift out of cells and
diminished urine potassium excretion cause hyperkalemia.
People with fast growing cancers such as non Hodgkins Lymphoma,acute
leukemia,small cell carcinomas and some metastatic ca ncer are at risk for tumor
lysis syndrome(TLS).TLS is the consequence of rapid destruction of tumor
cells, chemotherapy or irradiation,which results in hyperkalaemia
Pathophysiology
Hyperkalemia develops when there is excessive production (oral intake,
tissue breakdown) or ineffective elimination of potassium. Ineffective
elimination can be hormonal (in aldosterone deficiency) or due to causes in the
renal parenchyma that impair excretion.
-
8/6/2019 Hyper Kale Mia Fair
8/29
Increased extracellular potassium levels result in depolarization of the
membrane potentials of cells. This depolarization opens some voltage-gated
sodium channels, but not enough to generate an action potential. After a short
while, the open sodium channels inactivate and become refractory, increasing
the threshold needed to generate an action potential. This leads to the
impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of
most concern is the impairment of cardiac conduction which can result in
ventricular fibrillation or asystole
Clinicalmanifestation
Hyperkalaemia can be asymptomatic,sometimes mild hyperkalaemia can
cause vague symptoms like nausea,vomiting,fatigue,muscleweaknessetc. The
most important consequences of hyperkalaemia is its effect on the myocardium.
Cardiac effects of an elevated serum potassium level are usually not significant
below a concentration of 7 mEq/L,but they are almost always present when the
level is 8 mEq/L or greater.
Signs and symptoms associated with mild to moderate hyperkalaemia are the
following:
y Irritability, anxietyy Nausea,diarrhea,abdominal colic and crampsy Muscle weaknessy tachycardiay Paresthesias(numbness.tingling)
As the plasma potassium level reaches 7 mEq/L sodium channels become
progressively inactivated which causes disturbances in muscle and nerve
functions which results in following signs and symptoms
y Impaired cardiac conduction and ventricular contractiony Hypotensiony Cardiac arrest
-
8/6/2019 Hyper Kale Mia Fair
9/29
y Convulsionsy Severe neuro muscular weakness progressing to flaccid paralysis
and respiratory muscle paralysis
Alterations in potassium have a variety of adverse clinical consequences,
the expression of which may be magnified in the critically ill patient. The most
serious of these manifestations are those involving excitab le tissues.
Cardiac effects: More serious symptoms of hyperkalemia include slow
heartbeat and weak pulse. Severe hyperkalemia can result in fatal cardiac
standstill (heart stoppage). Hyperkalemia depolarizesthe cell membrane, slows
ventricular conduction, and decreases the duration of the action potential. These
changes produce the classic electrocardiographic(EKG) manifestations of
hyperkalemia including peaked T waves, wideningof the QRS complex, loss of
the Pwave, sine wave configuration, or ventricular fibrillation and asystole .
Unless the rise in potassium has been very rapid, symptoms of
hyperkalemia are usually not apparent until potassium levels are very high
(typically 7.0 mEq/l or higher).
Neuromuscular Effects. Hyperkalemia may result in paraesthesias and
weakness progressing to a flaccid paralysis, which typically spares the
diaphragm. Deep tendon reflexes are depressed or absent. Cranial nerves are
rarely involved and sensory changes are minimal . Severe hyperkalemia causes
skeletal muscle weakness and even paralysis, related to a depolarization block
in muscle. Similarly, ventricular conduction is slowed. Although hyperkalemia
has marked effects on the peripheral nervoussystem,it has little effect on the
central nervous system. Rapidly ascending muscular weakness leading to
flaccid quadriplegia has been reported in patients with very high serum
potassium levels. Paralysis of respiratory and speech muscles can also occur.
-
8/6/2019 Hyper Kale Mia Fair
10/29
Additionally, GI manifestations,such as nausea, intermittent intesti nal colic, and
diarrhea, may occur in hyperkalemic patients.
Diagnostic measures
y Historyy Physical examinationy Blood test : serum electrolytes, RFT, blood sugar.creatin
kinase,cortisol
y Renal ultrasoundy Electrocardiogramy ABG analysis
ECG findings
With mild to moderate hyperkalemia, there is reduction of the size of the
P wave and development of peaked T waves. Severe hyperkalemia results in a
widening of the QRS complex and prolonged PR interval , The faster
repolarization of the cardiac action potential causes the tenting of the T waves,
and the inactivation of sodium channels causes a sluggish conduction of the
electrical wave around the heart, which leads to smaller P waves and widening
of the QRS complex.
The serum K+
concentration at which electrocardiographic changes
develop is somewhat variable.
Serum K5.5 - 6.5 mEq/L: peaked T waves; prolonged PRsegment
Serum K 6.5 - 8.0 mEq/L: loss of P wave, prolonged QRS complex, ST-
segment elevation, ectopic beats and escape rhythms
-
8/6/2019 Hyper Kale Mia Fair
11/29
Serum K > 8.0 mEq/L: progressive widening of QRS complex, sine wave,
ventricular fibrillation, asystole, axis deviations, bundle branch blocks,
fascicular blocks.
.
EKG changes may not accompany changes in PK. The sensitivity of the
electrocardiogram to reveal changes of hyperkalemia is quite low . It does
increase in proportion to the severity of the hyperkalemia , but normal
electrocardiograms have been seen even with extreme hyperkalemia and the
first cardiac manifestation of hyperkalemia may be ventricular fibrillation . The
explanation for a normal electrocardiogram in the setting of extreme
hyperkalemia is not entirely clear, but may relate to a slow rate of rise in thePK
Given this insensitivity of the electrocardiogram, EKG changes should not be
considered necessary for the emergency treatment of severe hyperkalemia.
-
8/6/2019 Hyper Kale Mia Fair
12/29
Treatment of Hyperkalemia
In general, the initial treatment of severe hyperkalemia is independent of
the cause of the disturbance, whereas the rational therapy of chronic
hyperkalemia depends on an understanding of its pathogenesis. In considering
when hyperkalemia constitutes an emergency, several points should be kept in
mind. First, the electrophysiologic effects of hyperkalemia are directly
proportional to both the absolute plasma potassium level and its rate of rise .
Second, concurrent metabolic disturbances may ameliorate (e.g.hypernatremia,
hypercalcemia, alkalemia) or exacerbate (e.g.,hyponatremia, hypocalcemia,
acidemia) the electrophysiologic consequences of hyperkalemia Third, although
the EKG manifestations of hyperkalemia are generally progressive and
proportional to thePK, ventricular fibrillation may be the first EKG disturbance
of hyperkalemia; conversely, a normal EKG may be seen even with extreme
hyperkalemia. With this in mind, it is apparent thatneither the EKG nor the PK
alone is an adequate index of the urgency of hyperkalemia, and that the clinical
context must be considered when assessing a hyperkalemic patient. Thus, any
pronouncement on an absoluteP
K value constituting an emergency must beseen as arbitrary.
Because most patients manifest hyperkalemic EKG changes atPK greater
than 6.7 mmol/L, hyperkalemia should be treated emergently for 1) PK _6.5
mmol/L or 2) EKG manifestations of hyperkalemia regardless of the PK .
Therapy of acute or severe hyperkalemia is directed at preventing or
ameliorating its untoward electrophysiologic effects on the myocardium. The
goals of therapy , are as follows:
1. Antagonize the effect of K on excitable cell membranes.
2. Redistribute extracellular K into cells.
3. Enhance elimination of K from the body.
-
8/6/2019 Hyper Kale Mia Fair
13/29
-
8/6/2019 Hyper Kale Mia Fair
14/29
Redistribution of Potassium into Cells
Insulin. Insulin reliably lowers PK in patients with end-stage renal disease,
confirming its effect to shift K into cells. The effect of insulin on potassium is
dose dependent from the physiolog ic through the pharmacologic range. It is
mediated by activation of Na, K-ATPase, apparently by recruitment of
intracellular pump components into the plasma membrane. An intravenous dose
of ten units of regular insulin given as a bolus along with an intravenous bolus
of dextrose (25 g as a 50% solution) to anephric adult patients lowers the PK by
about 0.6 mmol/L . The onset of action is 15 mins and the effect is maximal
between 30 and 60 mins aftera single bolus . After the initial bolus, a dextrose
infusion should be started, since a single bolus of 25 g of dextrose has been
shown to be inadequate to prevent hypoglycemia at 60 mins. It is interesting to
note that when insulin was given by continuous intravenous infusion for 4 hrs to
normal volunteers, PK fell over the first 90 mins and rose thereafter. Based on
that observation,there seems to be no advantage of a continuous infusion over a
bolus injection.Insulin should be used without dextrose in hyperglycemic
patients; indeed,the cause of the hyperkalemia in those patients may be the
hyperglycemia itself. The administration of hypertonic dextrose alone for
hyperkalemia is not recommended for two reasons: first, endogenous insulin
levels are unlikely to rise to the level necessary for a therapeutic effect; and
second, there is a risk of exacerbating the hyperkalemia by inducing
hypertonicity.
Beta Adrenoceptor Agonists.An appreciation for the effect of catecholamines
on internal potassium balance recently has been applied to the clinic. Patients
with renal failure given the selective beta adrenoceptor agonist, albuterol, by
intravenous infusion (0.5 mg over 15 mins) show a significant decline in PK
(about 1mmol/L) that is maximal between 30 and 60 mins . Nebulized albuterol
in a high dose, administered to patients with ESRD, has a similar effect: PK
-
8/6/2019 Hyper Kale Mia Fair
15/29
declines by 0.6 mmol/L after inhalation of 10 mg of albuterol, and by about 1.0
mmol/L after20mg).The effective dose is at least four times higher than that
typically used for bronchodilation , although a smaller decline in PK (about 0.4
mmol/L after 60 mins) is seen even with a metered-dose inhaler . The effect of
high-dose therapy is apparent at 30 mins and persists for at least 2 hrs . More
recently, subcutaneous terbutaline (7 g/kg body weight) has been shown to
reduce PK in selected dialysis patients by an average of 1.3 mmol/L within 60
mins . Mild tachycardia is the most common reported side effect of high-dose
nebulized albuterol or terbulatine.
Bicarbonate.The putative benefits of a bolus injection of sodium bicarbonate in
the emergency treatment of hyperkalemia pervaded the literature until the past
decade. The administration of NaHCO3 decreases the concentration of H+
in
the extracellular fluid (ECF) compartment. In theory, if the Na+/H
+exchanger
(NHE) were in an active mode, and if the administration of NaHCO3 were to
favour the movement of H+
out of cells via the NHE, more Na+
would enter the
cell in an electroneutral manner. The subsequent electrogenic exit of Na+
via the
Na-K-ATPase would render the cell interior voltage more negative and allow a
shift of K+
into the cell It has now been clearly demonstrated that shortterm
bicarbonate infusion does not reduce PK in patients with dialysis-dependent
kidney failure, implying that it does not cause K shift into cells. Only after a 4-
hr infusion was a small (0.6mmol/L) but significant decrease in PK is
detectable.
Elimination of Potassium from the Body
Enhanced Renal Elimination. Improving urine output by forcing fluids.giving
IV saline,or giving potassium wasting diuretic usually corrects mild
hyperkalaemia.Hyperkalemia occurs most often in patients with renal
insufficiency. However, renal K excretion may be enhanced even in patients
-
8/6/2019 Hyper Kale Mia Fair
16/29
with significant renal impairment by increasing the delivery of solute to the
distal nephron, the site of K secretion.Studies using acetazolamide show that
bicarbonate delivery to this site in the nephron has a particular kaliuretic effect,
even in patients with renal insufficiency (59). It would be unwise to administer
acetazolamide alone to most patients with hyperkalemia, since they tend to
present with a concomitant metabolic acidosis that would be exacerbated by the
drug. But a sodium bicarbonate infusion administered during 46 hrs at a rate
designed to alkalinize the urine may enhance urinary K excretion , and would be
desirable especially in patients with metabolic acidosis. The risk of volume
expansion with the bicarbonate infusion can be mitigated by the use of loop-
acting diuretics, which would be likely to further enhance the kaliuretic effect.
Loop-acting diuretics alone or in combination with a thiazide diuretic will
induce a kaliuresis and will be beneficial in the volume expanded patient.
Diuretic induced volume contraction must be avoided since this will lead to
decreased distal nephron flow and reduced K excretion.
Exchange Resin. Sodium polystyrene sulfonate (SPS, Kayexalate, Kionex) is a
cation-exchange resin that is prepared in the sodium phase but has a higher
affinityfor potassium than sodium . In the lumen of the intestine, it exchanges
sodium for secreted potassium. Most of this exchange takes place in the colon,
the site of most potassium secretion in the gut. Each gram of resin binds
approximately 0.65 mmol of potassium. Kayexalate contains 4 mEq of Na+
per
gram. This Na+
is theoretically exchangeable for 4 mEq of K+. Thus, 30 g of
Kayexalate could possibly remove 120 mEq of K+. However, this degree of
exchange does not occur at the Na+
and K+
concentrations found in thegastrointestinal tract.
The resin causes constipation and, hence, almost always is given with a
cathartic. It may be given orally or by retention enema, although the oral route
-
8/6/2019 Hyper Kale Mia Fair
17/29
is considered to be more effective because of the longer transit time through the
gut lumen .
There are two concerns with the use of SPS for the treatment of urgent
hyperkalemia. The first is its slow effect. When given orally, the onset of action
is at least 2 hrs and the maximum effect may not be seen for 6 hrs or more . The
effect of SPS as a retention enema is more rapid but of lesser magnitude. One
recent study in normokalemic hemodialysis patientsfailed to show any effect on
PK during 12 hrs after an oral dose of 30 g of SPS with cathartic . The second
concern with SPS is its possible toxicity. There are numerous case reports of
patients who have developed intestinal necrosis after exposure to SPS in
sorbitol as an enema and as an oral agent.A retrospective study estimated the
prevalence of colonic necrosis to be 1.8% among postoperative patients
receiving SPS . Thus, the slow onset of action and serious, albeit infrequent,
toxicity make SPS a poor choice for the treatment of urgent hyperkalemia.
Dialysis. Hemodialysis is the method of choice for removal of potassium from
the body. Plasma potassium falls by over 1 mmol/L in the first 60 mins of
hemodialysis and a total of 2 mmol/L by 180 mins, after which it reaches a
plateau .Rebound always occurs after dialysis, with 35% of the reduction
abolished after an hour andnearly 70% after 6 hr; the magnitude of the
postrebound plasma potassium is proportional to the predialysis potassium
level. There is controversy as to whether dialysis for severe hyperkalemia
precipitates serious ventricular arrhythmias. Because of that possibility, patients
dialyzed for severe hyperkalemia should have continuous EKG monitoring .
The rate of potassium removal with peritoneal dialysis is much slower than with
hemodialysis. Indeed, much of the decrement in PK with peritoneal dialysis
seems to be due to translocation of potassium into cells as a result of the glucose
load rather than extracorporeal disposal. This modality may be used forpatients
on maintenance peritoneal dialysis who have modest hyperkalemia .
-
8/6/2019 Hyper Kale Mia Fair
18/29
Treatment ofhyperkalemia
Agent Dose Onset Duration Complication
Calcium
gluconate
10 ml IV
over 10
minutes
Immediate 30-60
minutes
hypercalcaemia
Hypertonic
3% sodium
chloride
50 ml IV Immediate unknown Volume overlod
Insulin regular
with dextrose
10 units IV 20 minutes 4-6 hrs hypoglycaemia
Albuterol 20 mg in 4 ml
NS nebulised
over 10 mts
30 mts 2hrs tachycardia
Loop diuretic-
Furosemide
40-80 mg IV 15 mts 2-3hrs Volume
depletion
Sodium
Bicarbonate
Sodium
polystyrene
sulfonate
(SPS,
Kayexalate,
Kionex)
Hemodialysis
150mmol/L
IV
1530 g in
1530 mL
(70% sorbitol
orally)
2hrs
immediate
4-6hrs
3hrs
Metabolic
alkalosis;volumeoverload
Intestinal
necrosis
Arrythmias
-
8/6/2019 Hyper Kale Mia Fair
19/29
Hyperkalemia Management protocol
Step 1: Start evaluation ofHyperkalemia Confirm Hyperkalemia
Step 2: Determine urgency of treatment Non-Emergent treatment:Go to Step 4
Emergent treatment criteria not met below orSerum Potassium
-
8/6/2019 Hyper Kale Mia Fair
20/29
-
8/6/2019 Hyper Kale Mia Fair
21/29
Monitoring: Follow bedside Serum GlucoseNebulized Albuterol 5 mg/ml (typical neb is 2.5 mg/ml)
Administer 10-20 mg over 10 minutes Onset: 15-30 minutes Duration: 2-3 hours Serum Potassium may increase briefly
Bicarbonate (no longer used unless Metabolic Acidosis) Historically used as adjunct to Calcium above Consider in severe Metabolic Acidosis Sodium Bicarbonate 7.5% (44.6 meq)
Give 1 ampule IV over 5 minutesMay repeat every 10-15 min if EKG changes persists
Onset in 30 minutes Duration: 1-2 hours May also add to Glucose infusion below Avoid bicarbonate until Hypocalcemia corrected
Risk ofTetany and SeizuresLowering of totalbodypotassium
Sodium Polystyrene Sulfonate (Kayexalate) Cation-Exchange resin Dose: 50 grams
Oral: Administer in 30 ml ofSorbitolRectal: Enema activity is faster than oral
Onset: Up to 4-6 hours for oral route Precautions
Avoid Sorbitol if bowel necrosis riskUse caution if risk ofCongestive Heart Failure
1. Consider concurrent Furosemide (Lasix)
-
8/6/2019 Hyper Kale Mia Fair
22/29
Furosemide (Lasix) Dose: 20-40 mg IV Coadminister normal saline if dehydrated Onset: 15-60 minutes Duration: 4 hours
Dialysis (last resort) May experience significant Hyperkalemia on rebound
2. Chronic Hyperkalemia Management Eliminate Medication Causes of Elevated Serum PotassiumNon-specific therapy
Loop Diuretics (Lasix) Oral Kayexalate chronically
Specific therapy Hyporeninemic Hypoaldosteronism
Loop Diuretics (Lasix)Fludrocortisone 0.1 mg daily
1. Taper gradually as an outpatient2. Restart ifHyperkalemia recurs
Renal Failure (GFR< 10 ml/min)Restrict Dietary Potassium to 40-60 meq/day
Renal Failure and ACE or ARB induced Hyperkalemia Indications: Metabolic AcidosisSodium Bicarbonate
1. Dose A: 8 meq tabs, 2 tabs twice daily2. Dose B: 0.5 to 1 tsp baking soda daily
-
8/6/2019 Hyper Kale Mia Fair
23/29
Nutrition
y Following these nutritional tips may help reduce symptoms:y Eliminate suspected food allergens, such as dairy (milk, cheese, and ice
cream), wheat (gluten), soy, corn, preservatives, and chemical food
additives. Your health care provider may want to test you for food
allergies.
y Avoid foods that contain high amounts of potassium, including bananas,lentils, nuts, peaches, potatoes, salmon, tomatoes, watermelon.
y Avoid refined foods, such as white breads, pastas, and sugar.y Eat fewer red meats and more lean meats, cold water fish, or beans for
protein. Limit the intake of processed meats, such as fast foods and lunch
meats.
y Use healthy cooking oils, such as olive oil or vegetable oil.y Reduce or eliminate trans-fatty acids, found in commercially baked goods
such as cookies, crackers, cakes, French fries, onion rings, donuts,
processed foods, and margarine.
y Avoid alcohol and tobacco. Talk to your doctor before using products thatcontain caffeine products, such as teas and soft drinks. Caffeine impacts
several conditions and medications.
y Drink more water. Dehydration can make hyperkalemia worse.y Exercise, if possible, 30 minutes daily, 5 days a week.y Avoid noni (Morinda citrifolia) juice, which is high in potassium.
-
8/6/2019 Hyper Kale Mia Fair
24/29
Nursing Management
Nursingassessment
Assessment focuses on identifying risk factors for hyperkalaemia through
history taking and a thorough physical examination.Review laboratory results of
potassium level.Report even borderline plasma potassium level to the phys ician.
Patients at risk for potassium excess, for example those with renal failure,
should be identified so they can be monitored closely for signs of hyperkalemia.
The nurse observes for signs of muscle weakness and dysrhythmias. The
presence of paresthesias is noted,as are GI symptoms such as nausea
andintestinal colic. For patients at risk, serum potassium levels are measured periodically. Potassium supplements are extremely dangerous when patients
have impaired renal function and thus decreased ability to excrete potassium.
Even more dangerous is the IV administration of potassium to such patients, as
serum levels can rise very quickly. Aged (stored) blood should not be
administered to patients with impaired renal function because the serum
potassium concentration of stored blood increases as the storage time increases,
a result of red blood cell deterioration. It is possible to exceed the renal
tolerance of any patient with rapid IV potassium administration, as well as wh en
large amounts of oral potassium supplements are ingested.
NursingDiagnoses:
y Decreased cardiac output related to dysrhythmiasy Ineffective breathing pattern related to muscle hyperactivity
progresses to respiratory muscle flaccidity and paralysis
y Pain related to muscle crampy Diarrhea related to increased smooth muscle irritability
-
8/6/2019 Hyper Kale Mia Fair
25/29
Nursing interventions
Preventinghyperkalemia
Measures are taken to prevent hyperkalemia in patients at risk, when
possible, by encouraging the patient to adhere to the prescribed potassium
restriction. Potassium-rich foods to be avoided include coffee, cocoa, tea, dried
fruits, dried beans, and wholegrain breads. Milk and eggs also contain
substantial amounts of potassium. Conversely, foods with minimal potassium
content include butter, margarine, cranberry juice or sauce, ginger ale,
gumdrops or jellybeans, hard candy, root beer, sugar, and honey.
Correctinghyperkalemia
High potassium level have the potential to induce life threatening
arrhythmia.So treat according to protocols.,and report ECG changes that
indicates worsening hyperkalaemia or over correction resulting in
hypokalaemia.Set cardiac monitor alarms with narrow limits to ensure e arly
detection of lethal dysrhythmias
It is possible to exceed the tolerance for potassium in any person if it is
administered rapidly by the IV route. Therefore, great care should be taken to
monitor potassium solutions closely, paying close attention to the solutions
concentration and rate of administration. When potassium is added to parenteral
solutions, the potassium is mixed with the fluid by inverting the bottle several
times. Potassium chloride should never be added to a hanging bottle because the
potassium might be administered as a bolus (potassium chloride is heavy and
settles to the bottom of the container). It is important to caution patients to use
salt substitutes sparingly if they are taking other supplementary forms of
potassium or potassium-conserving diuretics. Also, potassium-conserving
diuretics, such as spironolactone (Aldactone), triamterene (Dyrenium), and
amiloride (Midamor); potassium supplements; and salt substitutes should not
-
8/6/2019 Hyper Kale Mia Fair
26/29
be administered to patients with renal dysfunction. Most salt substitutes contain
approximately 5060 mEq of potassium per spoon
Elevated serum potassium levels may be erroneous; thus, highly
abnormal levels should always be verified. To avoid false reports of
hyperkalemia, prolonged use of a tourniquet while drawing the blood sample is
avoided, and the patient is cautioned not to exercise the extremity immediately
before the blood sample is obtained. The blood sample is delivered to the
laboratory as soon as possible, because hemolysis of the sample res ults in a
falsely elevated serum potassium level.
CONCLUSION
Hyperkalemia is one of the few potentially lethal electrolyte disorders. Its
rational treatment has evolved as a result of our more complete understanding of
the physiology of potassium homeostasis. Fortunately, most patients have mild
hyperkalemia (which is usually well tolerated). However, any condition causing
even mild hyperkalemia should be treated to prevent progression into more
severe hyperkalemia. Evaluate the clients response to therapy every hour if
severe hyperkalaemia is present or every 8 hrs if mild hyperkalaemia exist.
-
8/6/2019 Hyper Kale Mia Fair
27/29
BIBLIOGRAPHY
y Dona D Ignatavicius, Linda workman: Medical surgical nursing,Anursing process approach 2
ndedition, Saunders publications,page
no:1139-1143.
y Brunner and Suddarths; Text book of medical surgical nursing, 11 thedition
y Hawks and Black: medical surgical nursing, clinical management forpositive outcome,7
thedition, Mosby publications,2004
y Lewis etal medical surgical nursing 7 th edition(2005) mosbypublication
y Harrisons principles of internal medicine 17 th edition (2008)Mc GrowHill publication pp-237-239
y Davidsons principles and practice of Medicine 20 th edition.ChurchillLivingstone,Elsevier
y www.wikipedia.comy www.nursing planet.comy www.medscape.com
-
8/6/2019 Hyper Kale Mia Fair
28/29
Seminar on
HYPERKALAEMIA
Submitted to : Submitted by:
Mrs. SUMANGALA T.J Priyanka Jose
Associate professor 1st
year msc nursing
Govt: college of nursing Govt: college of nursing
Calicut Calicut
Date of seminar: -4-2011
Remarks :
-
8/6/2019 Hyper Kale Mia Fair
29/29
Masterplan on hyperkalaemia
Objectives:
Define hyperkalaemia Explain the types, causes and risk factors of hyperkalaemia Explain the pathophysiology of meningitis explain the signs and symptoms of hyperkalaemia List the diagnostic measures Explain the management
y Introductiony Definitiony Typesy Etiology and risk factorsy Pathophysiologyy Signs and symptomsy Collaborative managementy Nursing managementy Conclusiony Bibliography