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BLOK 3.4


SCENARIO 2: diarrhea and vomiting Mr. Koleri 20 years, was brought to the health center with complaints of diarrhea over 20 times since 2 days ago and accompanied by vomiting. Obtained from the examination, good awareness, blood pressure 80/50 mmHg, pulse 110x/menit, 30 breaths / min rapid and deep, bad turgor. Doctors immediately put on oxygen, calculate the deficit and give intravenous fluids, then after general condition improved Mr. Koleri in reference to the hospital. At the hospital, Mr. Koleri treated at HCU, examined the blood gas analyzer impression of metabolic acidosis. In laboratory tests: Na 130 mEq /L, K2,0 mEq / L and U.Dokter waves on ECG was found immediately corrects acidosis and hypokalemia. How do you explain what happened to Mr.. Koleri?

Identify Terminology
Metabolic acidosis : decrease in blood pH due to accumulation of acid (H ions) or loss of base (HCO3-)

Hypokalemia : Low blood concentrations of K

HCU /Health care unit : care units in hospitals for patients with stable conditions (respiratory, hemodynamic,) who still need treatment and monitoring

Define the Problems

1. Why Mr. Koleri complained of diarrhea over 20 times since 2 days ago with vomiting? 2. How the interpretation of physical examinations, vital sign? 3. What is the purpose of the oxygen, calculate the fluid deficit, and the provision of the infusion? 4. How to calculate the fluid deficit and infuse what is given? 5. How interpretation labor inspection? 6. How EKG interpretation? 7. What does doctor do to correct the acidosis and hypokalemia? 8. How the results of blood gas analysis (metabolic acidosis)?

Analyze Problems
1. Why Mr. Koleri complained of diarrhea over 20 times since 2 days ago with vomiting? diarrhea 2 days (acute) 90% of infectious etiology, 10% treatment, intoxication > 20X: signifies much volume (osmotic diarrhea): increased secretion of water and electrolytes from the gut, but absorption is low)

possible causes: infections such as cholera (Vibrio cholerae produces enterotoxin), E.coli adhesi on mucosa gut secretion of enterotoxin production of cAMP nhibition of NaCl absorption, secretion of Cl -> Na pumped out with Cl ions, followed by water and secretion electrolytes (K out with bicarbonate) -> lost / out of fluid and electrolytes (watery diarrhea) vomiting: discharge the contents of the GI tract through the mouth due to intestinal contractions and wall torakoabdomen regulated by the brain stem, the signal to vomit from the pharynx to duodenum. if there is irritation, then vomiting symptoms (loss of water and Na) depletion volume

2. How the interpretation of physical examinations, vital sign? pulse 110x/menit: tachycardia (n: 60-100x/menit) -> compensation to maintain tissue perfusion TD 80/50 mmHg: Breath 30x/menit: takipnue (n: 14-20x/menit) breathing fast and deep -> Kusmaull Breathing: when the accumulation of acid or increased excretion of bicarbonate ---> will become carbonic acid dissociation into CO2 and H20. CO2 released through the lungs (hyperventilation) bad turgor : skin turgor to assess the adequacy of fluid in the body. skin is assessed usually abdominal skin that does not immediately return to its original position when pinched

3. What is the purpose of the oxygen, calculate the fluid deficit, and the provision of the infusion? - the purpose of the administration of oxygen: maintain tissue oxygenation - the purpose of calculating the fluid deficit: to specify a lot of fluid loss, determine the degree of deficit

the purpose of the infusion: to restore the body's fluid and electrolyte deficiencies
How to calculate the fluid deficit and infuse what is given?
- Score daldiyono (Clinical): fluid deficit (cc) = skor/15x BB (kg) x 100 - possibility given Ringer's lactate (electrolyte content is more complete than NaCl)

4. How interpretation labor test? interpretation of laboratory tests: Na = 130 mEq / L -> hyponatremia (n: 135-145 mEq / l) K = 2 mEq / l -> hypokalemia (n: 3.5 to 5.2 mEq / l) 5. How EKG interpretation? U wave: after the T wave and before the next P wave.

because repolarization slow conduction system (hypokalemia)


What does the doctor do to correct the acidosis and hypokalemia? - correction of acidosis determine the degree of acidosis (pH) determine the anion gap -> possible etiologies count bicarbonate space -> corrected slowly by giving a solution of NaHCO3 - hypokalemia correction: increased intake of K: foods high in K or potassium salts: KCl potassium IV -> not be oral or severe hypokalemia

How the results of blood gas analysis (metabolic acidosis)? pH < 7.35 PCO2 < 40mmHg HCO3- <22mEq/l


Learning objectives
Students are able to explain: Disorders of Fluid & Electrolyte Balance Disorders of Acid-Base Balance




circumstances where the reduced volume of water without electrolytes or water loss exceeds a lack of sodium Etiology vomiting bleeding

use of diuretics kidney disease


clinical manifestations 1. mild dehydration good awareness thirsty and restless

Normal skin turgor normal breath

2. Moderate dehydration Thirsty rapid and weak pulse decreased urine output

3. Severe dehydration decreased consciousness weak and lethargic Tachycardia no urine output Management of dehydration calculate the fluid deficit correction fluid with isotonic dextrose can be given intravenously or orally if the patient is unconscious


Edema is observable swelling from fluid accumulation in body tissues. The swelling is the result of the accumulation of excess fluid under the skin in the spaces within the tissues

Sitting or standing for long periods Certain medications Hormonal changes during menstruation and pregnancy Infection or injury to a blood vessel, blood clots, or varicose veins Blocked lymph channels (lymphedema) Allergies to food or insect bites Kidney, heart, liver, or thyroid disease High or low blood pressure Eating salty foods Brain tumor or head injury Exposure to high altitudes or heat, especially when combined with heavy physical exertion

Signs and Symptoms

These will vary and may include the following: Swollen limbs (possibly accompanied by pain, redness, heat) Facial puffiness Abdominal bloating Shortness of breath, extreme difficulty breathing, coughing up blood Sudden change in mental state or coma Muscle aches and pains

Edema is a sign of an underlying problem, rather than a disease unto itself. A diagnostic explanation should be sought. Patient history and presenting symptoms, along with laboratory blood studies, if indicated, assist the health professional in determining the cause of the edema.

Treatment Options
Drug Therapies diuretics -- for example, loop diuretics or potassium sparing diuretics. These medicines reduce body fluid levels, but they also deplete important vitamins and minerals, which can result in loss of bone mass. Diuretics may have several other possibly serious side effects. Surgical Procedures Nutrition and Supplements







Commonly defined as a serum sodium concentration 135
meq/L Hyponatremia represents a relative excess of water in relation to sodium.

Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia Redistributive hyponatremia Pseudohyponatremia

Clinical Manifestations
most patients with a serum sodium concentration exceeding 125 mEq/L are asymptomatic Patients with acutely developing hyponatremia are typically symptomatic at a level of approximately 120 mEq/L Most abnormal findings on physical examination are characteristically neurologic in origin patients may exhibit signs of hypovolemia or hypervolemia

CT head, EKG, CXR if symptomatic Repeat Na level Correct for hyperglycemia Laboratory tests provide important initial information in the differential diagnosis of hyponatremia
Plasma osmolality Urine osmolality Urine sodium concentration Uric acid level FeNa

four issues must be addressed Asyptomatic vs. symptomatic acute (within 48 hours) chronic (>48 hours) Volume status 1st step is to calculate the total body water total body water (TBW) = 0.6 body weight next decide what our desired correction rate should be Symptomatic immediate increase in serum Na level by 8 to 10 meq/L in 4 to 6 hours with hypertonic saline is recommended acute hyponatremia more rapid correction may be possible 8 to 10 meq/L in 4 to 8 hours chronic hyponatremia slower rates of correction 12 meq/L in 24 hours


Produced by either administration of hypertonic fluids or much more frequently, loss of thirst Because of extremely efficient regulatory mechanisms such as ADH and thirst, hypernatremia generally occurs only in people with prolonged lack of thirst mechanism Patients with loss of ADH (Diabetes Insipidus) usually can compensate with increased fluid intake

Causes of Hypernatremia
Insensible and sweat losses GI losses Diabetes Insipidus (both central and nephrogenic) Osmotic Diuresis DKA Hypothalamic lesions which affect thirst function Causes include tumors, granulomatous diseases or vascular disease Sodium Overload Infusion of Hypertonic sodium bicarbonate for metabolic acidosis

Symptoms of Hypernatremia
Initial symptoms include lethargy, weakness and irritability Can progress to twitching, seizures, obtundation or coma Resulting decrease in brain volume can lead to rupture of cerebral veins leading to hemorrhage Severe symptoms usually occur with rapid increase to sodium concentration of 158 mEq or more Sodium concentration greater than 180 mEq are associated with high mortality

Diagnosis of Hypernatremia
Same labs as workup for hyponatremia: Serum osmolality, urine osmolality and urine sodium Urine sodium should be lower than 25 mEq/L if and water and volume loss are cause. It can be greater than 100 mEq/L when hypertonic solutions are infused or ingested If urine osmolality is lower than serum osmolality then DI is present
Administration of DDAVP will differentiate
Urine osmolality will increase in central DI, no response in nephrogenic DI

Treatment of Hypernatremia
First, calculate water deficit Water deficit = CBW x ((plasma Na/desired Na level)-1) CBW = current body water assumed to be 50% of body weight in men and 40% in women So lets do a sample calculation:
60 kg woman with 168 mEq/L How much water will it take to reduce her sodium to 140 mEq/L

Calculation continued
Water deficit = 0.4 x 60 ([168/140]-1) = 4.8 L But how fast should I correct it? Same as hyponatremia, sodium should not be lowered by more than 12 mEq/L in 24 hours
Overcorrection can lead to cerebral edema which can lead to encephalopathy, seizures or death

So what does that mean for our patient?

The 4.8 L which will lower the sodium level by 28 should be given over 56-60 hours, or at a rate of 75-80 mL/hr Typical fluids given in form of D5 water


Low potassium levels below 3.5 mEq / L Etiology kidneys are not functioning normally or too much potassium is lost through the digestive tract rarely caused by a lack of intake because potassium is found in our food

potassium can be lost due to the use of diuretics that cause the kidneys secrete sodium, water and potassium in excess clinical manifestations muscle weakness feeling tired muscle pain restless legs syndrome is a symptom that arises in muscle potassium less than 3 mEq / L

Indications correction of potassium

absolute indication potassium is given absolute immediately in the patient with severe hypokalemia (K < 2 mEq/L)
strong indication potassium is given in a short time in patients taking the drug, causing the displacement of potassium from the extracellular to the intracellular

Moderate indications potassium does not need to be given for example in patients with mild hypokalemia Management of hypokalemi potassium easier given in oral form if given 40-60 mEq of potassium can raise potassium levels from 1 to 1.5 mEq / L, if given 135-160 mEq can raise potassium levels from 2.5 to 3.5 mEq / L


Hyperkalemia An abnormal physiological state resulting from high extracellular concentrations of potassium. In a homeostatic state, 98% of K+ is located in the intracellular fluid (ICF).

Normal Serum K+ Levels

Infants Children Adults 4.1-5.3mm/L 3.4-4.7mm/L 3.5-5.0mm/L

Critical values: <2.5mm/L or >6.5mm/L

Decreased secretion or excretion as with renal failure, acidosis (K+ excretion is exchanged in the kidney for H+ in order to correct acidotic state), potassium sparing diuretics and adrenal insufficency. Increased intake of K+ as with salt substitutes, vitamins, rapid transfusion of aged blood (lysis of dead blood cells increases extracellular K+).

Cellular shift as seen with acidotic states; sepsis, ketoacidosis and with massive tissue damage; trauma, burns or tumor lysis (causing intracelluar K+ to spill into extracxellular fluid). NOTE: False elevations in serum K+ may occur with vigorous pumping of the hand after application of tourniquet for veinous puncture and in hemolized samples.

Irritability, anxiety, weakness to lower extremities, parethesia, irregular pulse and cardiac standstill if hyperkalemia is sudden or severe. ECG changes include tall, peaked T waves, prolonged PR interval, ST depression, loss of P wave, widened QRS, VF and cardiac standstill.

Potassiums Effect on Cardiac Muscle

STEP 1: Rapid Depolarization Na+ channels open and Na+ floods into the cell. STEP 2: The Plateau Ca++ flows into cell via slow calcium channels, stimulating a contraction. STEP 3: Repolarization K+ escapes the cell through slow potassium channels.

Hyperkalemias Effect on the Heart

The heart is able to function normally in a homeostatic state.

In hyperkalemia cardiac contractions become weak and irregular. In severe cases the heart eventually stops in diastole.

Emergency Treatment
Insulin Glucose Ventolin Calcium Furosemide Sodium Bicarbonate Potassium Binding Resin Hemodialysis







A state of excess acid accumulation and deficient base bicarbonate, metabolic acidosis is produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs, kidneys, and cells.

Metabolic acidosis usually results from excessive burning of fats in the absence of usable carbohydrates. This can be caused by diabetic ketoacidosis, chronic alcoholism, malnutrition, or a low-carbohydrate, high-fat dietall of which produce more keto acids than the metabolic process can handle. Other causes include: anaerobic carbohydrate metabolism renal insufficiency and failure (renal acidosis) diarrhea and intestinal malabsorption

Signs and symptoms

Metabolic acidosis typically begins with headache and lethargy, progressing to drowsiness, central nervous system depression, Kussmauls respirations (as the lungs attempt to compensate by blowing off carbon dioxide), stupor and, if the condition is severe and goes untreated, coma and death. Associated GI distress usually produces anorexia, nausea, vomiting, and diarrhea and may lead to dehydration. Underlying diabetes mellitus may cause fruity breath from catabolism of fats and excretion of accumulated acetone through the lungs.

Arterial pH below 7.35 confirms metabolic acidosis. With severe acidotic states, pH may fall to 7.10 and partial pressure of arterial carbon dioxide may be normal or less than 34 mm Hg as compensatory mechanisms take hold. The bicarbonate level may be less than 22 mEq/L. Supportive findings include: urine pH: < 4.5 in the absence of renal disease serum potassium levels: > 5.5 mEq/L from chemical buffering glucose level: > 150 mg/dl in those with diabetes mellitus serum ketone body level: elevated in those with diabetes mellitus plasma lactic acid level: elevated in those with lactic acidosis anion gap: > 14 mEq/L, indicating metabolic acidosis.

Treatment for metabolic acidosis consists of administration of sodium bicarbonate I.V. for severe cases, evaluation and correction of electrolyte imbalances and, ultimately, correction of the underlying cause. For example, in patients with diabetic ketoacidosis, a low-dose continuous I.V. infusion of insulin is recommended.


a pH imbalance in which the body has accumulated too much of an alkaline substance, such as bicarbonate, and does not have enough acid to effectively neutralize the effects of the alkali.

1) Loss of hydrogen A. Gastrointestinal loss 1. Removal of gastric secretions: Vomiting or nasogastric suction 2. Chloride-losing diarrhea 3. Gastrocolic fistula 4. Villous adenoma 5. Antacid therapy, particularly if combined with cation exchange resin B. Renal loss 1. loop or thiazide diuretics 2. Mineralocorticoid excess (Primary Aldo, Cushings, steroids, licorice) 3. Post chronic hypercapnia 4. Hypercalcemia, including the milk of alkali syndrome C. H+ movement into cells 1. Hypokalemia 2) Exogenous Alkali A. Administration of NaHCO3, sodium citrate, gluconate, acetate, antacids B. Massive blood transfusion C. Antacids - Milk alkali syndrome 3) Contraction alkalosis A. Loop or thiazide-type diuretics B. Sweat losses in cystic fibrosis C. Gastric losses in achlorhydria 4) Miscellaneous A. Bartter's syndrome B. Gitelman's syndrome

When the body has more base than acid in our body system thats the time metabolic alkalosis take place and the levels of both potassium and sodium for this condition decreases dramatically, causing symptoms that may include: Shallow and slow respiration Diarrhea Coma Congenital Chloride Diarrhea ( a unusual warning for this type of condition) Excessive Urination (due to the usage of drugs such as Diuretic) Nausea Headache Cyanosis A discoloration condition of the skin due to inadequate oxygen intake) Muscle Cramps Irregular heart beats Loss of hydrogen ions Lead to the decreasing amount of fluid in the body of the affected person. Drop in Blood Pressure Irritability Convulsions Hyperventilation Loss of consciousness (can progress to coma) Seizures Numbness in the face An individual should seek emergency medical aid when he/she has experienced the following: If you feel confused Problem in breathing A sudden change of the symptoms of this condition

Metabolic alkalosis may be suspected based on symptoms, but often may not be noticeable. The condition is usually confirmed by laboratory tests on blood and urine samples. Blood pH above 7.45 confirms the condition. Levels of other blood components, including salts like potassium, sodium, and chloride, fall below normal ranges. The level of bicarbonate in the blood will be high, usually greater than 29 mEq/L. Urine pH may rise to about 7.0 in metabolic alkalosis.

Treatment focuses first on correcting the imbalance. An intravenous line may be started to administer fluids (generally normal saline, a salt water solution) and allow for the quick injection of other drugs that may be needed. Potassium chloride will be administered. Drugs to regulate blood pressure or heart rate, or to control nausea and vomiting might be given. Vital signs like pulse, respiration, blood pressure, and body temperature will be monitored. The underlying cause of the metabolic alkalosis must also be diagnosed and corrected.

If metabolic alkalosis is recognized and treated promptly, the patient may have no long-term complications; however, the underlying condition that caused the alkalosis needs to be corrected or managed. Severe metabolic alkalosis that is left untreated will lead to convulsions, heart failure, and coma.

Patients receiving tube feedings or intravenous feedings must be monitored to prevent an imbalance of fluids and salts, particularly potassium, sodium, and chloride. Overuse of some drugs, including diuretics, laxatives, and antacids, should be avoided.


Respiratory acidosis is a condition in which a build-up of carbon dioxide in the blood produces a shift in the body's pH balance and causes the body's system to become more acidic. This condition is brought about by a problem either involving the lungs and respiratory system or signals from the brain that control breathing. There is primary increase in Pco2 with compensatory increase in HCO3 -; pH usually low but may be near normal. (Ventilatory failure; Respiratory failure; Acidosis respiratory)

Hypoventilation Diseases of the airways Diseases of the chest Diseases affecting the nerves and muscles that "signal" the lungs to inflate or deflate Drugs that suppress breathing Severe obesity

Signs and symptoms

depend on the rate and degree of Pco2 increase : The most notable symptom will be slowed or difficult breathing. Headache, drowsiness, lethargy, anxiety, sleepiness, easy fatigue, memory loss, restlessness, tremor, and confusion may also occur. Some personality changes like gait disturbance, blunted deep tendon reflexes, myoclonic jerks, asterixis, and papilledema might be seen. A rapid heart rate, changes in blood pressure, and swelling of blood vessels in the eyes may be noted upon examination. Severe cases of respiratory acidosis can lead to coma and death.

Types of Respiratory Acidosis:

Acute: In acute respiratory acidosis, the PaCO2 is
elevated above the upper limit of the reference range (over 6.3 kPa or 47 mm Hg) with an accompanying acidemia (pH <7.35). Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barr syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Chronic : In chronic respiratory acidosis, the PaCO2 is

elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3- >30 mm Hg). Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.

Diagnosis & Treatment

Diagnosis Respiratory acidosis may be suspected based on symptoms. A blood sample to test for pH and arterial blood gases can be used to confirm the diagnosis. In this type of acidosis, the pH will be below 7.35. The pressure of carbon dioxide in the blood will be high, usually over 45 mmHg. Arterial blood gas (measures levels of oxygen and carbon dioxide in the blood; in respiratory acidosis, the level of carbon dioxide is too high), Chest x-ray and Pulmonary function test can be used for the diagnosis. Treatment is aimed at the underlying lung disease, and may include: Bronchodilator drugs to reverse some types of airway obstruction Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or mechanical ventilation if needed Oxygen if the blood oxygen level is low Treatment to stop smoking

Outlook (Prognosis)
Prognosis depends upon the disease causing the respiratory acidosis. If the underlying condition that caused the respiratory acidosis is treated and corrected, there may be no long term effects. Respiratory acidosis may occur chronically along with the development of lung disease or respiratory failure. In these severe conditions, the patient may require the assistance of a respirator or ventilator. In extreme cases, the patient may experience coma and death.

Possible Complications
Poor organ function Respiratory failure Shock

Do not smoke. Smoking leads to the development of many severe lung diseases that can cause respiratory acidosis. Losing weight may help prevent respiratory acidosis due to obesity (obesity-hypoventilation syndrome). Be careful about taking sedating medicines, and never combine these medicines with alcohol. Patients with chronic lung diseases and those who receive sedatives and narcotics need to be monitored closely for development of respiratory acidosis.


Respiratory alkalosis is a condition where the amount of carbon dioxide found in the blood drops to a level below normal range. This condition produces a shift in the body's pH balance and causes the body's system to become more alkaline (basic). This condition is brought on by rapid, deep breathing called hyperventilation. There is a primary decrease in Pco2 with or without compensatory decrease in HCO3 -; pH high or near normal. (Alkalosis respiratory)

Hyperventilation Intracerebral hemorrhage, meningitis, stroke Salicylate and Progesterone drug usage Anxiety, hysteria, stress and pain Cirrhosis of the liver Sepsis Elevated body temperature sexual activity, which may induce excessive breathing due to excitation Hypoxia Any lung disease that leads to shortness of breath can also cause respiratory alkalosis.

Signs and Symptoms:

Symptoms and signs depend on the rate and degree of fall in Pco2. Hyperventilation, the primary cause of respiratory alkalosis, is also the primary symptom. This symptom is accompanied by dizziness, light headedness, agitation, confusions, cramps and tingling or numbing around the mouth and in the fingers and hands. Muscle twitching, trachypnea, hyperpnea, chest pain, blurred vision, spasms, and weakness may be noted. Seizures, irregular heart beats, and tetany (muscle spasms so severe that the muscle locks in a rigid position) can also result. Chronic is usually asymptomatic and has no distinctive signs

Types of Respiratory Alkalosis

Acute: It occurs rapidly. During acute respiratory alkalosis, the person may lose consciousness where the rate of ventilation will resume to normal. Chronic: It is a more long-standing condition. For every 10 mM drop in pCO2 in blood, there is a corresponding 5 mM of bicarbonate ion drop. The drop of 5 mM of bicarbonate ion is a compensation effect which reduces the alkalosis effect of the drop in pCO2 in blood. This is termed metabolic compensation.

Diagnosis & Treatment:

Diagnosis: Respiratory alkalosis may be suspected based on symptoms. A blood sample to test for pH and arterial blood gases can be used to confirm the diagnosis. In this type of alkalosis, the pH will be elevated above 7.44. The pressure of carbon dioxide in the blood will be low, usually under 35 mmHg. Arterial blood gas (measures levels of oxygen and carbon dioxide in the blood; in respiratory alkalosis, the level of carbon dioxide is too low), Chest x-ray, Pulmonary function test may be used.

Treatment focuses on correcting the underlying condition that caused the alkalosis. Hyperventilation syndrome due to anxiety may be relieved by having the patient breath into a paper bag. By rebreathing the air that was exhaled, the patient will inhale a higher amount of carbon dioxide than he or she would normally. Antibiotics may be used to treat pneumonia or other infections. Other medications may be required to treat fever, seizures, or irregular heart beats. If the alkalosis is related to a drug overdose, the patient may require treatment for poisoning. Use of mechanical ventilation like a respirator may be necessary. If the respiratory alkalosis has triggered the body to compensate by developing metabolic acidosis, symptoms of that condition may need to be treated, as well.

Prognose & Complications

Prognose depends on the condition that is causing the respiratory alkalosis. If the underlying condition that caused the respiratory alkalosis is treated and corrected, there may be no longterm effects. In severe cases of respiratory alkalosis, the patient may experience seizures or heart beat irregularities that may be serious and life threatening. Possible Complications: Seizures may occur if the alkalosis is extremely severe. This is very rare.