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University of Mosul College of Pharmacy DISORDERS OF ELECTROLYTES AND WATER AND ACID–BASE BALANCES Dr.Saad Kleman Abd 3ed Year Pathophysiology

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University of Mosul College of Pharmacy

DISORDERS OF ELECTROLYTES AND WATER AND ACID–BASE BALANCES

Dr.Saad Kleman Abd

3ed Year

Pathophysiology

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Disorders of electrolytes and water and acid–base balances

http://s528.photobucket.com/user/PikevilleCollegeNursing/media/hypomagnesemia.jpg.html

Hyponatremia; is serum sodium less than 135 mEq/L (Normal SodiumValues 135 to 145 mEq/L). Characterized by:_ Not enough sodium in the ECF (vascular space)._ Possibly, there is too much water diluting the blood which makes serum sodium go down._ Anytime there is a sodium problem there is a fluid problem as well.Sodium;

•Major extracellular fluid cation •Maintains tonicity of extracellular fluid •Regulates acid-base balance by renal reabsorption of sodium ion (base) and excretion of

hydrogen ion (acid) •Facilitates nerve conduction and neuromuscular function •Facilitates glandular secretion •Regulates osmotic forces and therefore regulates water balance. Sodium balance is regulated by aldosterone

What causes it and why:

Signs and symptoms and why:

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Diagnosis:_ The main diagnostic test for hyponatremia is serum electrolytes (blood work); this is the quickest and simplest way to see what the serum sodium actually is.

Serum sodium <135 mEq/L Decreased urine specific gravity Decreased serum osmolality Urine sodium >100 mEq/24 hours

* mEq/L: milliequivalent is one-thousandth of an equivalent—the amount of a substance that will react with a certain number of hydrogen ions. This is measured per liter of fluid.

What can harm the patient?Seizures and brain damage are the major complications associated with hyponatremia. Also, consider what caused the hyponatremia when determining what could harm your patient.

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_ Hypernatremia is serum sodium greater than 145 mEq/L._ Hypernatremia is similar to dehydration: there is too much sodium and not enough water in the body.

What causes it and why: Anything that causes an increased “water” loss or excessive sodium intake can cause hypernatremia.

*NPO= (nothing by mouth)

Alterations in sodium balance are used to maintain the plasma volume and tissue perfusion, not the plasma Na+ concentration. Too much sodium is manifested as edema, and too little sodium results in hypovolemia.

The primary protective mechanism against hypernatremia is the stimulation of thirst, thereby increasing water intake and lowering the plasma Na+ concentration to normal.

• Since aldosterone affects both Na+ and K+ handling, it might be expected that regulation of the excretion of one ion would interfere with that of the other. Aldosterone secretion may be increased by hyponatremia and reduced by hypernatremia.

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Signs and symptoms and why

*(LOC)=level of consciousness *(DTRs)=Decreased deep tendon reflexes Diagnosis:- The quickest way to determine hypernatremia is serum electrolytes (blood work):

Serum sodium >145 mEq/L Urine sodium <40 mEq/24 hours

High serum osmolality

What can harm the patient?As with hyponatremia, seizures and brain damage are the major complications associated with hypernatremia. Don’t forget the complications associated with fluid problems as well.

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When the sodium level in the body increases or decreases rapidly, fatal complications can result. Rapid shifts in the serum sodium are dangerous!In patients with hypo- or hypernatremia, think of BRAIN first.

Potassium imbalances:Potassium:

• Major intracellular fluid cation • Maintains cell electrical neutrality • Facilitates cardiac muscle contraction and electrical conductivity • Facilitates neuromuscular transmission of nerve impulses • Maintains acid-base balance

Hypokalemia; is a serum potassium below 3.5 mEq/L (Normal Potassium Values 3.5 to 5 mEq/L).What causes it and why;

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Signs and symptoms and why;

*(LOC)=level of consciousness

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Paralytic ileus can occur from severe hypokalemia. Abdominal distension will probably be next since there is no peristalsis.

Remember, arrhythmias can lead to decreased cardiac output, resulting in hypotension. When we think about hypokalemia usually we think about muscle cramps first. However,

don’t forget the patients can have muscle weakness too!Diagnosis:_ The quickest way to determine hypokalemia is by looking at the serum electrolytes (blood work/blood chemistries) to determine if the serum K+ is too low._ ECG (shows flattened T wave, depressed ST segment, and a U-wave).The ECG will also be assessed for potentially life threatening arrhythmias such as Premature Ventricular Contractions (PVC’s) and other ventricular arrhythmias such as ventricular tachycardia or ventricular fibrillation.What can harm the patient?

Hypokalemia can cause life-threatening arrhythmias, such as ventricular tachycardia, ventricular fibrillation, and asystole. Respiratory depression may also occur.

In severe hyperkalemia, ascending flaccid paralysis of the arms and legs may be seen; this paralysis moves distal to proximal.

Regarding potassium imbalances, the severity of the symptoms always depends on how fast the serum potassium is rising or falling.

Hyperkalemia; is serum potassium greater than 5.0 mEq/L.

What causes it and why

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*(ACE)=Angiotensin-converting enzyme

Signs and symptoms and why:

Diagnosis:

_ The quickest way to determine if hyperkalemia is present is to assess the serum electrolytes._ The ECG will also be assessed to determine if any arrhythmias are present so they can be treated at once.

What can harm the patient?Be sure to monitor patients with hyperkalemia for dehydration, neurological changes, and life-threatening arrhythmias.Summary of Disorders of Electrolyte Balance:

ELECTROLYTE IMBALANCE

SIGNS AND SYMPTOMS DIAGNOSTIC TEST RESULTS

Hyponatremia Muscle twitching and weakness Serum sodium <135 mEq/L

ECGchanges.

Ventricular tachycardia or fibrillation,asystole,heart block

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Lethargy, confusion, seizures, and coma

Hypotension and tachycardia

Nausea, vomiting, and abdominal cramps

Oliguria or anuria

Decreased urine specific gravity

Decreased serum osmolality

Urine sodium >100 mEq/24 hours

Increased red blood cell count

Hypernatremia Agitation, restlessness, fever, and decreased level of consciousness

Muscle irritability and convulsions

Hypertension, tachycardia, pitting edema, and excessive weight gain

Thirst, increased viscosity of saliva, and rough tongue

Dyspnea, respiratory arrest, and death

Serum sodium >145 mEq/L

Urine sodium <40 mEq/24 hours

High serum osmolality

ELECTROLYTE IMBALANCE

SIGNS AND SYMPTOMS DIAGNOSTIC TEST RESULTS

Hypokalemia Dizziness, hypotension, arrhythmias, electrocardiogram (ECG) changes, and cardiac and respiratory arrest

Nausea, vomiting, anorexia, diarrhea, decreased peristalsis, abdominal distention, and paralytic ileus

Muscle weakness, fatigue, and leg cramps

Serum potassium <3.5 mEq/L

Coexisting low serum calcium and magnesium levels not responsive to treatment for hypokalemia usually suggest hypomagnesemia

Metabolic alkalosis

ECG changes, including flattened T waves, elevated U waves, and depressed ST segment

Hyperkalemia Tachycardia changing to bradycardia, ECG changes, and cardiac arrest

Nausea, diarrhea, and abdominal cramps

Muscle weakness and flaccid paralysis

Serum potassium >5 mEq/L

Metabolic acidosis

ECG changes, including tented and elevated T waves, widened QRS complex, prolonged PR interval, flattened or absent P waves.

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What is it?Diabetes insipidus occurs when the posterior pituitary does not secrete enough Antidiuretic hormone "ADH" or when kidney tubules are insensitive to ADH. Therefore, the kidneys start excreting more water. The vascular volume decreases to the point of shock and the blood becomes concentrated.

NORMALLY blood and urine like to do the same thing? They like to mirror each other? When someone drinks a lot of water, the blood is dilute and the urine is dilute. In dehydration, the blood is concentrated and the urine is concentrated. In diabetes insipidus Blood and urine DO NOT mirror each other. In DI, there is no ADH to help hold water in. Large amounts of dilute urine are being put out even though the patients is going into shock. In DI, the blood is concentrated and the urine is dilute. The blood and urine are opposite of each other.

There are four types of diabetes insipidus:1. Primary DI (neurogenic): due to disorder in the pituitary or hypothalamus.2. Secondary DI (neurogenic): due to craniotomy, trauma, or surgery (the pituitary/hypothalamus are altered).3. Nephrogenic DI: occurs when kidney tubules are insensitive to ADH (inherited). 4. Drug induced DI: the name says it all!

The only electrolyte that is affected by the amount of water in the vascular space is sodium. If the water level in the blood is too high (making it dilute), the sodium level will go down. If the water level in the blood is too low (making it concentrated), the sodium level will go up.

What causes it and why:

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*(CVA) cerebral vascular accident

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Signs and symptoms and why:

Diagnosis:

Dehydration

Brain changes due to sodium imbalance

Hypernatremia lead to neurological changes

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_ Serum osmolarity increased and urine osmolarity decreased _ Serum sodium up (dehydrated); urine sodium down (dilute urine)._ Specific gravity of blood up; urine specific gravity down._ Urine output must be greater than 4 L in 24 hours._ ↑ Hematocrit , blood is hemoconcentrated due to water loss. _ ↑BUN (blood urea nitrogen) , due to blood is concentration._ ↓ Serum vasopressin.

What can harm the patient?_ Shock due to hypovolemia._ Hypernatremia.

SIADH is when too much antidiuretic hormone (ADH) is produced, the patients goes into fluid volume excess or hypervolemia.The fluid in the vascular space becomes very dilute due to WATER retention. This dilute fluid decreases the serum sodium and the patient becomes hyponatremic. Normally, when someone is hypervolemic, urine output increases in an effort to get rid of the excess fluid. In SIADH Since there is so much ADH being produced, the kidneys hold on to water, so urine output goes down. This makes everything worse!

Anytime you hear SIADH, think water, water, water! _ too much water in the veins!

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What causes it and why:

Signs and symptoms and why

Diagnosis:

_ Serum sodium: decreased, while urine sodium: increased._ Serum osmolarity: decreased, while urine osmolarity increased._ Specific gravity of blood decreased,while of urine increased._ BUN: decreased due to hemodilution._ Urine output, decreased._ Serum ADH, increased.

What can harm the patient?

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_ Seizures._ Cerebral edema._ Confusion._ Coma._ Water intoxication.

Here’s a quick visual aid to help you remember the difference between DI and SIADH.

Meet Si (pronounced sigh) and Di (pronounced die)Notice Si has retained way too much fluid and Di has lost way too much!

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Metabolic acidosis is an acid–base imbalance where the pH is less than 7.35 and the bicarbonate level is less than 22 mEq/L. _Occurs due to acid (H+ ions) builds up in the body, or too much bicarbonate has been lost from the body. _ In metabolic disorders, the problem is not with the lungs but with the kidneys._ The decrease in the alkaline substances (bases) causes a build up of acids in the body, causing acidosis._ Which organ will compensate? The lungs will compensate by increasing respirations in an effort to blow off excess CO2 (acid) and therefore increase pH._ The lungs will start compensating in just few minutes, but it’s not enough to correct the imbalance at this point.What causes it and why:

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Pathophysiology:

As H+ ions begin accumulating in the body, chemical buffers (plasma HCO3–

and proteins) in cells and extracellular fluid bind them. Excess H+ ions decrease blood pH and stimulate chemoreceptors in the

medulla to increase respiration. Consequent fall of partial pressure of CO2 frees H+ ions to bind with HCO3

– ions. Respiratory compensation occurs but isn't sufficient to correct acidosis.

Healthy kidneys compensate by excreting excess H+ ions, buffered by phosphate or ammonia.

For each H+ ion excreted, renal tubules reabsorb and return to blood one Na+

ion and one HCO3– ion.

Excess H+ ions in extracellular fluid passively diffuse into cells. To maintain balance of charge across cell membrane, cells release K+ ions.

Excess H+ ions change the normal balance of K+, Na+, and Ca+ ions, impairing neural excitability.

Signs and symptoms and why:

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Kussmau respiration; is an increase in rate and depth of respiration. CO2 is being blown off in increased amounts.Diagnosis:_ Monitor arterial blood gases (ABGs).In Metabolic acidosis ABGs look as:

What can harm the patient?_ Life-threatening arrhythmias._ Cardiac arrest.

Metabolic alkalosis is an acid–base imbalance where the pH is greater than 7.45 and the bicarbonate level is greater than 26 mEq/L. There is an excess of base in the body and a loss of acid. Basically, pH is increased due to bicarbonate increase._ Metabolic means the “kidneys”, which involve bicarbonate and H+._ The lungs did not cause the problem; that is why it is a metabolic problem and not a respiratory one._ The lungs compensate by retaining CO2 by means of hypoventilation. This compensates for the alkalosis and helps the pH go down into normal range.

What causes it and why: The two most common causes of metabolic alkalosis are ;

loss of stomach acid diuretics.

The kidneys have the ability to make extra bicarbonate when needed and reabsorb it through the kidney tubules.

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Signs and symptoms and why:

Diagnosis:_ Monitoring ABGs

What can harm the patient?Metabolic alkalosis can cause the following life-threatening illnesses:_ Arrhythmias._ Cardiac arrest._ Seizures.SUMMARYThe respiratory and renal systems can be both the ''cause'' and ''cure'' for pH imbalances. Alkalosis inhibits the respiratory center in the medulla

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Remember that the lungs control carbon dioxide levels and the kidneys control bicarbonate levels. By monitoring your patient’s carbon dioxide, bicarbonate, and pH levels you can successfully prevent and treat any acid–base imbalances.

Respiratory acidosis is an acid–base imbalance that occurs when the pH is decreased below 7.35, and the partial pressure of carbon dioxide (PCO2) is increased greater than 45 mm Hg.

Carbon dioxide builds up in the blood due to hypoventilation or others. Since the client retains this acid, this causes the pH to go down. This imbalance can be acute, as in sudden cessation of breathing, or chronic,

such as in lung disease.Hypercapnia; is a buildup of carbon dioxide in the blood to levels greater than 45 mm Hg.What causes it and whyThe first thing to think of when trying to figure out causes of respiratory acidosis is “breathing.” Respiratory acidosis always begins with a breathing problem. Something causes decreased alveolar ventilation, which causes Co2 retention.

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Signs and symptoms and why

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When respiratory acidosis occurs suddenly, hypertension is seen first due to hypercapnia then progressing to hypotension as it worsens.Hypoxia may be the first sign of respiratory acidosis. The early signs of hypoxia are restlessness and tachycardia. Early hypoxia: restlessness, tachycardiaHypoxia causes the heart rate to increase to pump what little oxygen is left to the vital organs. Bradycardia occurs because the heart is not receiving enough oxygen. Late hypoxia: cyanosis,bradycardia.Acute respiratory acidosis causes hyperkalemia. With chronic respiratory acidosis, the K+may be normal as the kidneys have time to readjust and get the K+ back into the normal range.LABORATORY TESTSLaboratory tests that are used in assessing acid-base balance include those for arterial blood gases and pH, CO2 content and HCO3 − levels, base excess or deficit, and the anion gap.

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Therefore, the expected values for a simple respiratory acidosis would be reduced plasma pH, increased PCO2 , and increased plasma HCO3 – concentration after partial renal compensation.

Therefore, in simple metabolic acidosis, one would expect to find a low pH, a low plasma HCO3 - concentration, and a reduction in PCO2 after partial respiratory compensation.

Respiratory alkalosis is an acid–base imbalance where the PCO2 is less than 35 mm Hg and the pH is greater than 7.45. Basically, the pH is increased and the CO2 is decreased. As in respiratory acidosis, the lungs are the cause of the problem in respiratory alkalosis._ The only way the PCO2 can decrease in the blood is through hyperventilation.

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_ When the lungs are impaired, the kidneys compensate with their own chemicals bicarbonate and H+.

_ The kidneys will hold H+ to replace the acid being lost from the hyperventilation._ The kidneys will excrete bicarbonate to raise acid levels and restore the body to

a normal pH._ Respiratory alkalosis means that the client has lost excessive CO2 (acid), thus making

the client alkalotic.

Hypocapnia; occurs when the CO2 is low.Hypercapnia; occurs when the CO2 is high.What causes it and whyRespiratory alkalosis is caused by excess respirations that result in excess loss of CO2 .

Pathophysiology; As pulmonary ventilation increases, excessive CO2 is exhaled. Resulting

hypocapnia leads to reduction of H2CO3, excretion of H+ and HCO3–

ions, and rising serum pH. Against rising pH, the hydrogen-potassium buffer system pulls H+ ions

out of cells and into blood in exchange for K+ ions. H+ ions entering blood combine with HCO3

– ions to form H2CO3, and pH falls.

Hypocapnia causes an increase in heart rate, cerebral vasoconstriction, and decreased cerebral blood flow.

After 6 hours, kidneys secrete more HCO3– and less H+.

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Continued low PaCO2 and vasoconstriction increases cerebral and peripheral hypoxia.

Severe alkalosis inhibits calcium (Ca+) ionization, increasing nerve and muscle excitability.

Signs and symptoms and why

Acute respiratory acidosis causes hyperkalemia. With chronic respiratory acidosis, the K+ may be normal as the kidneys have time to readjust and get the K+ back into the normal range.Diagnosis_ Monitor vital signs, especially respirations._ Monitor electrolytes. _ Monitor ABGs.

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