Dr.

Ali’s Uworld Notes For Step 2 CK

Electrolytes
In any patient, the pH and PaC02 are the two lab values that provide the best picture of acid-
base status; the HC03- can be calculated from these values using the Henderson-Hasselbalch
equation.

Diuretic abuse, a technique sometimes used by individuals desperate for weight loss, can cause
hypovolemia, orthostatic hypotension and dizziness by increasing the elimination of sodium,
potassium and water by the kidneys. Other causes of orthostatic hypotension include anything
that decreases intravascular volume or vascular tone. Decreased fluid intake, Polyuria, and
diarrhea decrease intravascular volume. Decreased vascular tone can be caused by autonomic
neuropathy or medications. Commonly implicated medications include anti-hypertensive and
psychiatric drugs.

Vs

Self-induced vomiting may lead to low serum sodium and potassium, and the associated loss of
fluid can cause orthostatic hypotension. However, urinary sodium will be low as the kidneys try
to conserve water by maximally resorbing sodium and water.

Vs

Laxative abuse leads to loss of significant amounts of water from the colon, causing
dehydration, orthostatic hypotension, and weight loss. It may also cause electrolyte
imbalances.

Aspirin Poisoning – The patients have tinnitus, fever, tachypnea, nausea and vomiting. This
clinical scenario is highly suggestive of aspirin (salicylate) intoxication. Acute aspirin toxicity
stimulates the central respiratory center and leads to respiratory alkalosis by causing
tachypnea. Aspirin concurrently causes an anion gap metabolic acidosis by a threefold
mechanism. First, salicylate toxicity causes uncoupling of oxidative phosphorylation thereby
increasing the rate of oxygen consumption in the peripheral tissues. Uncoupling of oxidative
phosphorylation is also the cause of the hyperpyrexia seen in aspirin toxicity. Next, salicylate
toxicity inhibits enzymes involved with carbohydrate and lipid metabolism leading to
accumulation of organic acids such as pyruvate, lactic and acetoacetic acid. Finally salicylates
impair renal function causing accumulation of inorganic acids such as sulfuric and phosphoric
acid.

Salicylate toxicity may thus present with a mixed respiratory alkalosis and metabolic acidosis,
which is characterized by a near-normal pH, a primary decrease in PaC02, and a concurrent
primary decrease in HC03-.

Near Normal pH - 7.36 – 7.45 pH.

Respiratory Alkylosis - 22 CO2.
Metabolic Acidosis - 12 HCO3.

Diuretic Overuse - Patients with COPD often have chronic C02 retention, resulting in respiratory
acidosis. Diuretics are often used in the treatment of COPD patients who have developed cor
pulmonale but must be cautiously used because these patients are at risk of having a reduction
in cardiac output, with subsequent development of prerenal renal failure. Look for doubling of
creatinine & BUN after administration of a diuretic. If Prerenal falure occurs, the acidosis will
worsen due to uremia.

Diuretic Use leading to Prerenal Failure = Metabolic Acidosis.

Carbon monoxide (CO) poisoning is the most common systemic toxicity seen in smoke
inhalation. CO binds to hemoglobin with an affinity 260 times that of oxygen. Upon inhalation,
CO displaces oxygen from hemoglobin thereby decreasing the hemoglobin binding sites
available for oxygen and the oxygen content of the blood. Because CO binds so avidly to
hemoglobin, it also is able to change the shape of the oxyhemoglobin dissociation curve.
Specifically, CO causes a left shift of the curve and a shape change from sigmoid to asymptotic.
This change disallows unloading of oxygen from hemoglobin in the tissues. By this twofold
mechanism. CO poisoning causes decreased oxygen delivery to the tissues. This results in
increased anaerobic metabolism by the tissues leading to increased lactic acid production and
development of an anion gap metabolic acidosis.

Acid Base Disorders

Metabolic Alkylosis –
Think on metabolic alkylosis whenever you see Hypokalemia, Hypocholremia & Increased
Bicarbonate.

Metabolic alkalosis is characterized by an alkaline pH and a primary increase in the serum

bicarbonate level (> 24 mEq/L). It can be classified into two broad categories, namely chloride-
sensitive (hypochloremic, saline responsive) and chloride-resistant (normochloremic. saline-
unresponsive) metabolic alkalosis.

Saline Responsive metabolic alkalosis is characterized by a urinary chloride level < 20 mEq/day
and signs of volume depletion. The common underlying pathophysiology in all causes of
chloride-sensitive metabolic alkalosis involves ECF volume contraction. Volume contraction
causes increased mineralocorticoid action, which in turn causes bicarbonate retention. H+ loss
and K+ loss. The urinary chloride remains low due to avid renal retention of NaCI and water.
Some causes of this condition are thiazide or loop diuretics and loss of gastric secretions, such
as with surreptitious vomiting (i.e. purging in bulimia nervosa). This condition can be corrected
with saline infusion to restore ECF volume. Replace potassium if low.

Saline Resistant metabolic alkalosis is characterized by a urinary chloride level > 20 mEq/day
and ECF volume expansion. Some disorders associated with chloride-resistant metabolic
alkalosis are primary hyperaldosteronism, Bartter syndrome, Gitelman's syndrome, and
excessive black licorice ingestion. Chloride-resistant metabolic alkalosis is not corrected by
saline infusion.

Congenital Hypertrophic Pyloric Stenosis - This disorder is more common in males and occurs
in slightly less than 1% of births. Classically an affected infant will present in the first few weeks
of life with persistent nonbilious vomiting following feedings. The loss of acidic gastric fluid via
vomiting causes a metabolic alkalosis. Additionally, the loss of large volumes of fluid via
vomiting leads to contraction alkalosis due to the action of aldosterone. The decrease in ECV
volume activates the renin-angiotensin-aldosterone system causing water retention at the
expense of hydrogen ion losses. For eact H+ secreted in urine, a Cl- is cosecreted & a HCO3 is
reabsorbed. This leads to increased HCO3 leading to metabolic acidosis. In order to compensate
for the metabolic alkalosis, the respiratory system responds via hypoventilation to create a
secondary respiratory acidosis.

The patient is expected to have a primary metabolic alkalosis with respiratory compensation.

This is characterized by a plasma pH greater than 7.45, PaC02 greater than 40 mm Hg and
HC03- greater than 24 mEq/L.

Metabolic Acidosis
Winter’s Formula tells if there is any respiratory compensation happening during metabolic
acidosis.

PaC02 = 1 .5[HC03-] + 8 +/- 2.

Winters' formula gives an expected value for the patient's PCO2; the patient's actual (measured)
PCO2is then compared to this.

If the two values correspond, respiratory compensation is considered to be adequate.

If the measured PCO2 is higher than the calculated value, there is also a primary respiratory
acidosis.

If the measured PCO2 is lower than the calculated value, there is also a primary respiratory
alkalosis.

Lactate Acidosis - Suspect this whenever you see hypotension or Seizures. Labs show
decreased bicarbonate. Seizures result in the accelerated production of lactic acid in the muscle
and reduced hepatic lactate uptake. This post-ictal lactic acidosis is transient and typically
resolves within 60 to 90 minutes. In such patients, the most appropriate treatment is
observation and repeating the chemistry panel after 2 hours to see if the acidosis has resolved
on its own. If it has not resolved, it is best to look for other potential causes of metabolic
acidosis.

Bowel ischemia is a common cause of lactic acidosis in patients with atherosclerotic disease and
atrial fibrillation. Lactic acidosis in this scenario results from the production of lactate as an end
product of anaerobic metabolism in the ischemic tissue. The accumulation of lactate in the
serum accounts for the anion gap.

Management - The most important steps in the management of lactic acidosis from septic
shock are IV normal saline with or without vasopressor therapy to maintain the intravascular
pressure and antibiotics to correct the underlying infection.

Addison’s Disease – Think of this whenever you see metabolic acidosis along with Hyperkalemia
& Hyponatremia.
Common extrapulmonary sites for TB include liver, spleen, kidney, bone, and adrenal gland. TB
is a common cause of chronic primary adrenal insufficiency in endemic areas. Patients typically
develop gradual fatigue, weakness, borderline hypotension, and electrolyte abnormalities. This
patient also has hyperkalemia, hypoglycemia, and eosinophilia, findings suggestive of adrenal
insufficiency. Other granulomatous diseases (eg, histoplasmosis, coccidioidomycosis,
cryptococcosis, and sarcoidosis) may also cause adrenal insufficiency.

Primary adrenal insufficiency (Addison's disease) is characterized by decreased cortisol, adrenal

sex hormone, and aldosterone secretion. Aldosterone normally acts on the distal renal tubules
to increase sodium reabsorption (saves sodium) and secrete potassium and hydrogen ions. If
aldosterone is deficient, the kidney inappropriately loses sodium while retaining excessive
potassium and hydrogen ions. This results in a normal anion gap and hyperkalemic and
hyponatremic metabolic acidosis.
Respiratory Acidosis –

These patients have respiratory acidosis evidenced by arterial blood gas values that show a
decreased pH (<7.35) and a primary increase in PaC02 (>40 mm Hg). High PaC02 and low Pa02
levels are suggestive of alveolar hypoventilation, although an elevated PaC02 alone, in the
range of 50-80 mm Hg, is sufficient to make the diagnosis. Causes of alveolar hypoventilation
and respiratory acidosis include the following:

• Pulmonary/thoracic diseases: Chronic obstructive pulmonary disease, obstructive sleep

apnea, obesity hypoventilation, scoliosis

• Neuromuscular diseases: Myasthenia gravis, Lambert-Eaton syndrome, Guillain-Barre

syndrome

• Drug-induced hypoventilation: Anesthetics, narcotics, sedatives

• Primary central nervous system dysfunction: Brainstem lesion, infection, stroke.

In addition, the A-a gradient (PA02 - Pa02) can help determine the specific cause of hypoxemia.
The A-a gradient is a measure of oxygen transfer from the alveoli to the blood. The alveolar
oxygen tension can be calculated using the following equation:

PA02 = (Fi02 x [Patm- PH2O])- (PaCO2/R).

(0.21 x [760-47]) - (PaCO2/R).

A normal A-a gradient is < 15. Values increase with age, but an A-a gradient > 30 is considered
elevated regardless of age. The A-a gradient is normal in patients with reduced inspired oxygen
tension and hypoventilation.

Pulmonary embolism, atelectasis, pleural effusion, and pulmonary edema cause V/Q mismatch.
In V/Q mismatch, the A-a gradient is elevated. In all these conditions, there is a decrease in
PaC02 (respiratory alkalosis) due to compensatory tachypnea.

Respiratory Alkylosis - Respiratory alkalosis is characterized by an increased pH and a primary

decrease in the PaC02. Typical causes include hyperventilation due to pneumonia, high altitude
or salicylate intoxication.

During pregnancy, there exists a high serum concentration of progesterone, which has a direct
stimulatory effect on the dorsal respiratory group of the medullary respiratory center. By
stimulating this central respiratory center, high progesterone concentrations lead to tachypnea
and consequent chronic mild respiratory alkalosis. The progesterone concentration increases
with increasing gestational age, thereby explaining why chronic respiratory alkalosis with
metabolic compensation is very common in later pregnancy.
Renal Tubular Acidosis –

Type 4 renal tubular acidosis should be suspected in a diabetic patient with a non-anion gap
metabolic acidosis, persistent hyperkalemia and renal insufficiency. Type 4 RTA is caused by
aldosterone deficiency or renal tubular insensitivity to aldosterone. The lack of aldosterone
effect in these patients leads to a failure to secrete acid as NH4+ and retention of potassium.
Type 4 RTA may occur in the setting of diabetic nephropathy due to type I or II OM. and the
condition can be worsened by drugs that inhibit the renin angiotensin- aldosterone system such
as ACE-Is and ARBs.

Vs

Chronic renal failure is a common cause of hypochloremic (anion gap) metabolic acidosis due
to failure to excrete acid as NH4+and accumulation of organic anions.

Electrolyte Abnormalities –

Serum osmolality = [2Na + Glu/18 + BUN/2 .8]

Calcium

Circulating calcium exists in both free and bound states. Only 45% of circulating calcium is free
and physiologically active; this is known as ionized calcium. The remainder is bound to albumin
(40%), other proteins, organic anions, and inorganic anions.

Calcium binds to albumin with a ratio of 0.8 mg/dl of calcium per 1.0 g/dl of albumin. Thus,
every reduction in albumin by 1.0 g/dl reduces the measured serum calcium concentration by
0.8 mg/dl, though the ionized calcium concentration does not change.

For patients with an abnormal serum albumin concentration (as in many with liver disease), a
corrected calcium level can be calculated using the formula below. By convention, normal
albumin is defined as 4.0 g/dl.

Corrected Ca++ = measured Ca++ + 0.8 (Normal albumin – Patient’s measured albumin).

Thus, this patient's corrected calcium is: 7.4 + 0.8 (4.0- 2.5) = 8.6 mg/dl
A serum calcium concentration of 8.6 mg/dl is normal. Thus, this patient does not need
intervention.

Hypocalcemia –

Hypocalcemia can occur during or immediately after surgery in patients requiring multiple
blood transfusions. Usually, hypocalcemia results from volume expansion and
hypoalbuminemia and is therefore asymptomatic because the ionized calcium is typically
normal in that scenario. When the ionized calcium is also decreased (e.g .. due to citrate
binding), symptoms such as hyperactive deep tendon reflexes, muscle cramps and, rarely,
convulsions may occur. Severe hypomagnesemia may mimic hypocalcemia because it causes
decreased PTH secretion and decreased peripheral responsiveness to PTH.

Hypercalcemia –

The signs and symptoms associated with hypercalcemia tend to be vague and non-specific.
Abdominal complaints such as constipation, nausea, vomiting and pain are common.
Symptoms may appear at any elevated calcium level but tend to be seen when plasma
concentrations exceed 12 mEq/L.

One of the common reasons of hypercalcemia in old people is Multiple Myeloma, The
neoplastic cells in multiple myeloma produce osteoclasts activating factors. Activation of
osteoclasts and invasion of bone by tumor cells results in the production of lytic bone lesions
and hypercalcemia. Hypercalcemia may be exacerbated by HCTZ.

Hypercalcemia is best treated in the acute setting by intravenous fluid resuscitation. This
increases renal excretion of calcium by decreasing calcium reabsorption in the proximal tubule.
Loop diuretics are then used to inhibit calcium reabsorption in the loop of Henle. Later,
treatment of the specific cause of hypercalcemia is warranted.

Calcitonin decreases renal and intestinal calcium absorption and decreases bone reabsorption
by inhibiting osteoclast activity. It is not used unless a patient has failed saline and a loop
diuretic.

Bisphosphonates decrease plasma calcium concentrations by decreasing osteoclast activity.

They are more effective than calcitonin and are the second-line agent used for patients with
moderate to severe hypercalcemia.

1st IV Resuscitation
If IV Resuscitation fails, Give Calcitonin or Loop Diuretics.
Long Term – Bisphosphonates
Giving Loop Diuretics before resuscitation will worsen dehydration & Hypercalcemia.

Familial Hypocalciuric Hypercalcemia Vs Primary Hyperparathyroidism - Increased serum

calcium and increased/inappropriately 'normal' PTH levels are suspicious for either primary
hyperparathyroidism or familial hypocalciuric hypercalcemia (FHH). The 24 hour urinary calcium
excretion and creatinine clearance can distinguish between these two diagnoses. FHH presents
with decreased urinary calcium excretion despite the increased serum calcium. Primary
hyperparathyroidism, on the other hand, has an increased 24 hour urinary calcium excretion.
FHH is a benign autosomal dominant condition. Parathyroidectomy is not recommended and
hypocalciuria typically persists following this procedure.

Hyponatremia - Hyponatremia is defined as a serum sodium value less than 130 mEq/L.

Hyponatremia can be classified according to the patient's volume status (hypovolemic,

euvolemic, hypervolemic).

If the patient presents with diarrhea and evidence of volume depletion, it suggests
hypovolemic hyponatremia. Hypovolemia decreases the effective arterial volume to the
kidney, resulting in increased renin and angiotensin levels. This results in increased
aldosterone activity, which works on the distal tubules to increase sodium reabsorption (with
low urinary sodium excretion), increase potassium excretion causing hypokalemia, and increase
hydrogen excretion causing a metabolic alkalosis. The volume depletion also increases the
plasma osmolality and activates ADH release from the pituitary to absorb more water in the
collecting ducts of the kidney.
SIADH - ADH acts on the distal tubule and collecting ducts to increase free water reabsorption
from the urine. Inappropriate secretion of ADH thus causes hyponatremia. Diagnostic criteria
for SIADH include:

1. Sosm <270

2. Uosm >300

3. Uosm > Sosm

4. UNa >20 mEq/L despite hyponatremia

5. Absence of hypovolemia

6. Normal renal, adrenal and thyroid function

7. No obvious surgical, traumatic or painful stimulus known to activate the neuroendocrine

stress response, including ADH release

8. Absence of other known causes of hyponatremia

In SIADH, there is too much water in the blood which leads to decreased RAAS & increased ANP.
Both of these cause natriuresis which contributes to hyponatremia.

Primary polydipsia is relatively common among patients with schizophrenia. Because patients
with primary polydipsia have normally functioning kidneys, they excrete dilute urine (low
specific gravity, <1.003) as their bodies attempt to regain osmotic balance. Primary polydipsia
causes both hyponatremia and maximally dilute urine. Simultaneous administration of
phenothiazines to schizophrenic patients with primary polydipsia can worsen the hyponatremia
because dry mouth is a side effect that further stimulates thirst.

Polydipsia = Hyponatremia + Urine Osmolarity <300.

Adrenal Insufficiency - Hyponatremia is the most common electrolyte abnormality in adrenal

insufficiency, affecting up to 90% of patients. It is the result of volume contraction (due to
mineralocorticoid deficiency) and increased vasopressin secretion (due to lack of cortisol
suppression). Hyperkalemia is also a common electrolyte abnormality, occurring in up to 65%
of affected individuals due to decreased activation of aldosterone receptors. In most cases the
hyperkalemia is accompanied by a mild hyperchloremic acidosis. Anorexia and fatigue occur in
close to 1 00% of patients. Gastrointestinal symptoms like nausea, vomiting, abdominal pain,
and diarrhea or constipation occur in up to 90% of patients. Other signs include weight loss,
hyperpigmentation, decreased blood pressure, and vitiligo.

Hyponatremia causes brain swelling. When hyponatremia develops slowly, cells in the brain
compensate by extruding osmolytes (e.g. Na+, K+) and intracellular water, thus reducing the
cerebral edema. However, in rapidly developing hyponatremia, as in patients receiving
hypoosmolar IV fluids like 0.45 Saline, there is not time for cells to adjust to the lower serum
osmolality, and symptoms develop quickly.

In patients with chronic hyponatremia, the sodium deficit must be corrected slowly. Increases
in the serum sodium concentration by more than 0.5 mEq/Uh in these patients raise the risk of
central pontine myelinolysis.

In patients with acute hyponatremia, however, the brain has not yet lost volume to
accommodate the new serum concentration and, therefore, the correction can happen much
more rapidly. So treat immediately with 3% Saline.

Hypernatremia –

Hypovolemic hypernatremia develops secondary to renal losses ( eg, diuretic use, glycosuria)
or extrarenal losses ( eg, gastrointestinal upset, excessive sweating).

Hypervolemic hypernatremia occurs due to exogenous sodium intake or mineralocorticoid

excess ( eg, hyperaldosteronism).

Hypernatremia reflects a water deficit in relation to sodium, and occurs when there is increased
hypotonic fluid loss and decreased access to free water. It most often occurs in people who are
debilitated (severe muscular or neurological diseases where they cannot move and drink water)
or have altered levels of consciousness and cannot access free water.

The initial treatment for severe hypovolemic hypernatremia is isotonic 0.9% saline, which acts
to gradually correct the hyperosmolality while normalizing the patient's volume status. Isotonic
saline is usually hypoosmolar in comparison to the hypernatremic plasma. Once the volume
deficit has been restored, such patients are then switched to half-normal (0 .45%) saline in
order to better replace the free water deficit. The goal rate of plasma sodium correction is no
more than 1 mEq/Uh. A greater rate of correction may result in cerebral edema.

Patients with mild hypovolemic hypernatremia are initially treated with 5% dextrose in 0.45%
saline.

5% dextrose in water (D5W) is the treatment of choice for patients with euvolemic and
hypervolemic hypernatremia.

Diabetes insipidus (DI) is a leading cause of euvolemic hypernatremia. It typically presents with
severe polyuria and mild hypernatremia. It can be divided into two types based on urine
osmolality, as well as etiology. Based on urine osmolality, Dl may be complete or partial.

1. Complete Dl - the urine osmolality is less than 300 mOsm/kg (often less than 1 DO mOsm/kg)

2. Partial Dl - urine osmolality ranges from 300-600 mOsm/kg.

The serum osmolality is elevated in both types. Based on etiology, DI may be central or
nephrogenic.

1. Central DI is due to decreased production of antidiuretic hormone (ADH). Common causes

include trauma, hemorrhage, infection, and tumors.

2. Nephrogenic DI results from renal ADH resistance. Common causes include hypercalcemia,
severe hypokalemia, tubulointerstitial renal disease, and medications. The most commonly
implicated mediations are lithium, demeclocycline, foscarnet, cidofovir, and amphotericin.

Potassium

Hypokalemia –

Cushing’s Syndrome - Iatrogenic steroid administration is the most common cause, but
Cushing's syndrome can also result from a patient's own overproduction of cortisol. The signs
and symptoms of Cushing's syndrome include fatigue, weight gain, easy bruising, central
adiposity, proximal muscle weakness, hyperglycemia, osteopenia and osteoporosis,
hypertension, acne, cataracts, and susceptibility to infections.

Hypokalemia is a common electrolyte abnormality in patients with excessive cortisol. It occurs

because most corticosteroids have some mineralocorticoid activity and will bind to aldosterone
receptors in the kidney, causing renal potassium wasting. If severe, the hypokalemia of
Cushing's syndrome can be treated with an aldosterone antagonist like spironolactone.

Chronic alcoholism eventually results in multiple electrolyte abnormalities such as

hypomagnesemia, hypokalemia and hypophosphatemia.
Hypomagnesemia is notorious for causing refractory hypokalemia. Mg is an important cofactor
for potassium uptake and maintenance of intracellular potassium levels. For these reasons,
magnesium levels in alcoholics must also be checked and corrected to successfully correct the
coexisting hypokalemia. Another cause of hypomagnesemia is intake of diuretics.

Hyperkalemia –

Hyperkalemia is usually asymptomatic, but can cause muscle weakness. Flaccid paralysis can
develop in severe cases. Severe hyperkalemia can cause life-threatening arrhythmias, and
therefore requires urgent treatment.

The earliest symptom of hyperkalemia is weakness. One of the most common causes of
hyperkalemia is medications. After addressing the hyperkalemia with a K + binding resin such
as sodium polystyrene sulfonate, it is best to obtain a complete medical history and review all
of the patient's medications. Commonly used drugs that may precipitate hyperkalemia include
ACE inhibitors, angiotensin receptor blockers and spironolactone, all of which may cause
hyperkalemia by blocking aldosterone synthesis or action. Other medications that may cause
hyperkalemia include trimethoprim and pentamidine.
Trimethoprim (TMP) and sulfamethoxazole (SMX) work sequentially to block the bacterial
synthesis of tetrahydrofolic acid. TMP-SMX is commonly used for treating uncomplicated
urinary tract infections (Gram-negative rods), Pneumocysfis jirovecii pneumonia, community-
acquired MRSA skin infections, and nocardiosis.

Trimethoprim can cause hyperkalemia by blocking the epithelial sodium channel in the
collecting tubule, similar to the action of the potassium-sparing diuretic amiloride. This occurs
more commonly in HIV-infected patients who are treated with high doses of trimethoprim, but
even normal doses can produce a modest elevation in the plasma potassium concentration.
Thus, patients treated with high-dose trimethoprim require serial monitoring of potassium to
avoid serious complications. Trimethoprim also competitively inhibits renal tubular creatinine
secretion and may cause an artificial increase in serum creatinine; however, glomerular
filtration rate is unchanged.

Succinylcholine is a depolarizing neuromuscular blocker often used during rapid-sequence

intubation because it has a rapid onset (45-60 seconds) and offset (6-1 0 minutes) of action.
However, it can cause significant potassium release and life-threatening arrhythmias, and so
should not be used in patients with or at high risk for hyperkalemia. This includes patients with
crush or burn injuries more than 8 hours old (high risk of rhabdomyolysis), patients with
demyelinating syndromes like Guillain-Barre, and patients with tumor lysis syndrome. Non-
depolarizing agents such as vecuronium or rocuronium are a better choice in these patients.

Therapy for Hyperkalemia includes emergent administration of IV calcium gluconate to

stabilize the cardiac membrane. The next step is to lower serum potassium by driving
potassium intracellularly. Finally, the excess potassium should be eliminated it from the body.
Agents used to shift potassium intracellularly include insulin and glucose, sodium bicarbonate,
and beta-2 agonists. Albuterol, a selective beta-2 agonist, is widely used for this purpose.

1st – IV Calcium Gluconate

2nd – Drive potassium intracellularly
3rd – Eliminate from body whatever that is excess.