FLUIDS AND ELECTROLYTES

REABSORPTION
FILTRATION OF ELECTROLYTES WITH WATER

Reabsorption of water with ADH Reabsortion of secretion of Na, K, H, NH3

Sodium reabsorption Glucose reabsorption Potassium reabsorption HCO3 Reabsorption PO4 reabsorption Urea reabsorption Water reabsorption Secretion of hydrogen
Water reabsorption Sodium reabsorption

Sodium and water reabsorptio n under influence of ADH HCO3 reabsorpion Secretion of K, urea, H+, NH3 drugs

REABSORPTION AND SECRETION OF ELECTROLYTES ALONG THE KIDNEY TUBULE

A prolonged QT interval is seen on the ECG due to prolongation of the ST segment-- hypocalcemia

CHLORIDE
-

DESCRIPTION: Major anion in ECF Taken through diet, especially from foods rich in salt It is found in combination with sodium in the blood as sodium chloride (NaCl) It is found in combination with hydrogen in the stomach as hydrogen chloride (HCl)

FUNCTIONS: 1. Works with Sodium to maintain serum osmolarity. 2. Maintains the balance of cations in the ICF and ECF 3. Participates in maintaining acid-base balance through a mechanism called chloride shift.

Cl-

RBC

HCO3-

A special CHON bicarbonate-chloride CHON) shifts HCO3 and Cl back and forth into and out of the RBCs

Chloride Imbalances
Normal Function
major anion in ECF mainly exists with sodium

Source and Cause of Imbalance

Clinical Manifestations

HYPOCHLOREMIA or <95 mEq/L GI losses (vomiting, suction, hydrogen follows Na loss and gain diarrhea) has inverse relationship to Burns DKA bicarbonate Diuretics Fever, acute infections HYPERCHLOREMIA >105 mEq/L Cardiac failure Cushing syndrome
(hypercortisolism)
Drugs:

Manifestations of hyponatremia CNS hyperexcitability: tremors

Weakness Lethargy

salicylates

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Treatment: HYPOCHLOREMIA Chloride replacement intravenously --Normal saline or half-strength saline (0.45%) solution Patients receiving the following diureticsloop, osmotic, or thiazide, should be reevaluated. Foods high in chloride are provided. Tomato juice Salty broth Canned vegetables Processed meats and fruits Avoid drinking free water (without electrolyte) which will excrete large amount of chloride.

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Treatment: HYPERCHLOREMIA Increase the bicarbonate level and correct the acidosis Lactated Ringers solution (conversion of lactate to bicarbonate in the liver) Sodium bicarbonate (leads to renal excretion of chloride ions as bicarbonate Diuretics are administered to eliminate chloride. Sodium, fluids, and chloride are restricted.

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III. NORMAL ACID-BASE BALANCE

1. Acids substances that release hydrogen ion when dissolved in water 2. Bases substances that binds free hydrogen ions in solution 3. Buffers can either release a hydrogen ion into a fluid or bind a hydrogen ion from a fluid to assist in regulating pH *Buffers dissolved in water can react in 2 ways: either as an acid (releasing a hydrogen ion) or a base (binding a hydrogen ion). University of San Carlos COLLEGE
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*Two Buffer systems: 1. Kidneys by retaining or excreting NaHCO3 or by excreting acidic urine or alkaline urine. They also help in reabsorbing NaHCO3- and secreting free H+ ions 2. Lungs by retaining carbonic acid in the form of CO2 or by rapid respirations excreting CO2 The body maintains its pH by keeping the ratio of HCO3 (bicarbonate, an alkaline, to H2CO3 (carbonic acid), an acid, at a proportion of 20:1. This relationship constantly changes and is compensated for by the kidneys and lungs. University of San Carlos COLLEGE OF

Acid-Base Assessment: The status of acid-base homeostasis may be monitored clinically through the measurement of arterial blood gases (ABGs).
Normal Arterial Blood Gases
Lab
Ph pO2

Normal Values 7.35-7.45 80-100 mmHg 35-45 mmHg 22-26 mmol/L 95-100%

pCO2 SaO2

HCO3

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Analysis of Arterial Blood Gases

1. Classify the pH Normal: 7.35-7.45 Acidemia: <7.35 Alkalemia: >7.45 2. Assess PaCO2 Normal: 35-45 mmHg Respiratory acidosis: >45 mmHg Respiratory alkalosis: <35 mmHg 3. Assess HCO3 Normal: 22-26 mEq/L Metabolic acidosis: <22 mEq/L Metabolic alkalosis: >26 mEq/L 4. Determine presence of Compensation Compensation present: if pH is normal Compensation present: if PaCO2 and HCO3 are abnormal (or nearly so) in opposite directions; i.e. one is acidotic and the other alkalotic Compensation absent: One component (PaCO3 or HCO3) is abnormal, the other normal

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Summary of Compensation: DISORDER Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis INITIAL EVENT COMPENSATION

PaCO2, or normal HCO3 Kidneys eliminate H+ and retain HCO3 pH , PaCO2, or normal HCO3, pH or normal PaCO2, HCO3, pH or normal PaCO2, HCO3, pH Kidneys conserve H+ and excrete HCO3 Lungs eliminate CO2, conserve HCO3 Lungs ventilation to PCO2, kidneys conserve H+ to excrete HCO3

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Analysis of Arterial Blood Gases 5. Identify Primary Disorder, if possible This is done by evaluating the PaCO2 and HCO3 in relation to the pH. Example: pH > 7.4 (alkalosis) a. If the PaCO2 is < 40 mm Hg, the primary disturbance is respiratory alkalosis. b. If the HCO3 is >24 mEq/L, the primary disturbance is metabolic alkalosis Example: pH < 7.4 (acidosis) a. If the PaCO2 is >40 mm Hg, the primary disturbance is respiratory acidosis. (This situation occurs when a patient hypoventilates and thus retains too much CO2, an acidic substance.) b. If the HCO3 is <24 mEq/L, the primary disturbance is metabolic acidosis. (This situation occurs when the bodys bicarbonate Level drops, either because of direct bicarbonate loss or because of gains of acids such as lactic acid or ketones.)

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6. Classify Degree of Compensation, if present

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IV. ALTERED ACID-BASE BALANCE

A. Respiratory acidosis decrease in pulmonary ventilation
Causes
Hypoventilation Neuromuscular

Signs and Symptoms

PR, RR, BP Mental cloudiness Feeling of fullness in the head Ventricular fibrillation ICP Papilledema Dilated conjunctival blood vessel Hyperkalemia Tachypnea Cyanosis

disorders Airway obstruction CNS depression

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Management: Improving ventilation Bronchodilators Antibiotics for infection Thrombolytics and anticoagulants (pulmonary emboli) Mechanical ventilation Semi-Fowlers position
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b. RESPIRATORY ALKALOSISinc.
pulmonary ventilation rate
Causes
Hyperventilation Sepsis Pregnancy Mechanical Fever

Signs and Symptoms

Lightheadedness Inability

to concentrate and tingling

ventilation

Numbness Tinnitus

Loss of consciousness

 MANAGEMENT:

Treatment of the underlying cause Breathe into a paper bag Sedative

c. METABOLIC ACIDOSIS (inc. accumulation of

Causes
Diabetic

metabolic acids (lactic acid and ketoacids) that rise in proportion to bicarbonate, resulting in dec. arterial pH)

Signs and Symptoms

Headache Confusion, RR

ketoacidosis
Renal

Drowsiness

failure

and depth Vomiting output

Methanol/aspirin

overdose
Renal

Nausea,

tubular

Cardiac BP Cold

acidosis
Diarrhea Chronic

and clammy skin

alcoholism

Dysrhythmias Shock Kussmauls Fruity

respiration

breath (if DKA)

MANAGEMENT:
Treatment is correcting the underlying defect. Eliminating source of chloride Bicarbonate Alkalizing agents (sodium bicarbonate, potassium

citrate, calcium carbonate or calcium acetate)

Hemodialysis Peritoneal

for patients with severe chronic kidney disease. The process uses the patient's peritoneum in the abdomen as a membrane across which fluids and dissolved substances (electrolytes, urea, glucose, albumin and other small molecules) are exchanged from the blood

dialysis--Peritoneal dialysis (PD) is a treatment

HEMODIALYSIS-- The objectives of hemodialysis are to extract toxic nitrogenous substances from the blood and to remove excess water. In hemodialysis, the blood laden with toxins and nitrogenous wastes, is diverted from the patient to a machine, a dialyzer, in which the blood is cleansed and then returned to the patient

Peritoneal Dialysis--The goals of peritoneal dialysis are to remove toxic substances and metabolic wastes and to re-establish normal fluid and electrolyte balance

d. Metabolic alkalosis inc. loss of acid (stomach and kidneys)

Causes
vomiting diuretics alkali ingestion Gastric suction

Signs and Symptoms

Tingling of fingers and toes Dizziness Hypertonic muscles Symptoms of hypocalcemia RR Atrial tachycardia Hypokalemia Dysrhythmia Paralytic ileus

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Management:

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Treatment of underlying disorder Chloride supply Sodium chloride fluids KCl H2-receptor antagonists (Cimitidine) Carbonic anhydrase inhibitors
OF

Thalassemia
Group of hereditary d/o associated w/ defective Hgb-chain synthesis the rigidity of the RBC and thus the premature destruction of these cells reduction of 1 or more globulin chains within Hgb molecule thus creating imbalance in the configuration of the Hgb

Characterized by:
hypochromia (an abnormal decrease in the hemoglobin content of RBCs), Extreme microcytosis (smaller-thannormal RBCs), destruction of blood elements (hemolysis), variable degrees of anemia

PATHOPHYSIOLOGY
production of one or more globulin chains within the hemoglobin molecule is reduced

imbalance in the configuration of the hemoglobin increases the rigidity of the RBCs Premature destruction of these cells

Thalassemia major (Cooleys anemia)

characterized by severe anemia, marked hemolysis, and ineffective erythropoiesis (production of RBCs). regular transfusion therapy Regular chelation therapy (eg, via subcutaneous deferoxamine) has reduced the complications of iron overload and prolonged the life of these patients Bone marrow transplant

GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY

The abnormality in this disorder is in the G-6-PD gene; this gene produces an enzyme within the RBC that is essential for membrane stability X-linked defects The deficiency is also common in those of Asian ancestry and in certain Jewish populations hemolysis only when the RBCs are stressed by certain situations, such as fever or the use of certain medications

CLINICAL S/S

pallor, jaundice, hemoglobinuria (hemoglobin in the urine). The reticulocyte count rises, and symptoms of hemolysis develop. Special stains of the peripheral blood may then disclose Heinz bodies (degraded hemoglobin) within the RBCs

TREATMENT
The treatment is to stop the offending medication (antimalarial agents, sulfonamides, aspirin in high doses),thiazide diuretics oral hypoglycemic agents, chloramphenicol, vitamin K Transfusion is necessary only in the severe hemolytic state

Nursing Care

Education of the disease process Give a list of meds to avoid - antimalarial - sulfonamides & chloramphenicol - nitrofurantoin - coal tar analgesics - thiazide diuretics - oral hypoglycemia - vitamin k

The Lymphomas
neoplasms of cells of lymphoid origin lymph nodes but can involve lymphoid tissue in the spleen, the gastrointestinal tract (eg, the wall of the stomach), the liver, or the bone marrow Hodgkins disease and non-Hodgkins lymphoma (NHL)

HODGKINS DISEASE

unicentric in origin in that it initiates in a single node The disease spreads by contiguous extension along the lymphatic system

CAUSE: - unknown, - viral etiology is suspected. In fact, fragments of the EpsteinBarr virus have been found in 40% to 50% of patients; this occurs more commonly in the younger patient population

First degree relatives have a higher-thannormal frequency of the disease. There is no increased incidence documented for non-blood relatives (eg, spouses).

S/S

Reed-Sternberg cell, a gigantic tumor cell that is morphologically unique and is thought to be of immature lymphoid origin. It is the pathologic hallmark and essential diagnostic criterion for Hodgkins disease.

S/S
painless enlargement of one or more lymph nodes on one side of the neck. The individual nodes are painless and firm but not hard. The most common sites for lymphadenopathy are the cervical, supraclavicular, and mediastinal nodes

A mediastinal mass may be seen on chest x-ray; occasionally, the mass is large enough to compress the trachea and cause dyspnea Pruritus is common

cough and pulmonary effusion (from pulmonary infiltrates), jaundice (from hepatic involvement or bile duct obstruction), abdominal pain (from splenomegaly or retroperitoneal adenopathy), or bone pain (from skeletal involvement)

B symptoms, they include ever (without chills), drenching sweats (particularly at night), and unintentional weight loss of more than 10%

A mild anemia is the most common hematologic finding. WBC count may be elevated or decreased. The platelet count is typically normal, unless the tumor has invaded the bone marrow,suppressing hematopoiesis. The erythrocyte sedimentation rate (ESR) and the serum copper level are used by some clinicians to assess disease activity

LABS
lymph node biopsy chest x-ray and a CT scan of the chest, abdomen, and pelvis are crucial to identify the extent of lymphadenopathy CBC

MEDICAL MANAGEMENT

CHEMOTHERAPY (doxorubicin (Adriamycin), bleomycin (Blenoxane), vinblastine (Velban), and dacarbazine(DTIC) Radiation therapy is still very useful for patients with extensive adenopathy (often termed bulky disease). use of high doses of chemotherapeutic agents, followed by autologous BMT or stem cell transplantation (PBSCT),

NON-HODGKINS LYMPHOMAS (NHLs)

a heterogeneous group of cancers that originate from the neoplastic growth of lymphoid tissue increased incidence of NHL in people with immunodeficiencies or autoimmune disorders, viral infections (including Epstein-Barr virus and HIV),or exposure to pesticides, solvents, or dyes.

S/S

stages (III or IV), lymphadenopathy is noticeable. One third of patients have B symptoms *(recurrent fever, drenching nightsweats, and unintentional weight loss of 10% or more)*.

DIAGNOSTIC FINDINGS

STAGING through:
CT

scans, bone marrow biopsies, Occasionally cerebrospinal fluid analysis

MANAGEMENT
If not Aggressive: RADIATION THERAPY If Aggressive: CHEMOTHERAPHY 2. Combination 3. If CNS involvement: cranial radiation or intrathecal chemotherapy 4. BMT or PBSCT (peripheral blood stem cell transplant)
1.

Steps in Blood Transfusion

1. 2. 3.

Before transfusing any blood, always check if it has been screened and crossmatched. Check blood for its blood type and if it matches with the blood type of the recipient (patient). Check the IV catheter for its patency and needle gauge, 18 or 19 gauge needle is advisable to avoid clouding

4. Make sure the solution hooked is a normal saline. Other solutions may cause hemolysis to the blood 5. Blood taken from blood banks are cold, this will cause hyperthermia to the patient. Warm blood first before transfusing. Some hospitals have blood warmers

6. Check and record vital signs before transfusion begins, 15 minutes after the start of transfusion, every hour, and 1 hour after transfusion has been discontinued. Together with this, instruct client to report any unusualities. 7. The first 10-15 minutes of transfusion is critical for ABO incompatibility and anaphylactic shock. Therefore, it is recommended to begin transfusion slowly starting at KVO rate. If no evidence is noted within the first 15 minutes, rate can be increased to the prescribed rate.

*** Transfusion of more than 100ml of incompatible blood can result to severe, permanent renal damage, circulatory shock and death. ***Recommended rate of infusion varies with the blood component being transfused. Components such as platelets, plasma and cryoprecipitate may be infused rapidly but care must be taken to avoid circulatory overload

8. If allergic signs and symptoms develop, stop blood transfusion. Maintain an open line, check client vital signs and notify the physician. Allergic reactions to watch for: headache back pain (flank) chest pain similar to angina nausea and vomiting tachycardia, hypotension hematuria / urticaria

pH 7.51, PaCO2 30, HCO3- 31 ANS: Uncompensated metabolic alkalosis

1.

2. pH 7.33, PaCO2 29, HCO3- 16 ANS: Partially compensated metabolic acidosis

3. pH 7.40, PaCO2 40, HCO3- 24: ANS: NORMAL 4. pH 7.12, PaCO2 60, HCO3- 29: ANS: Partially compensated respiratory acidosis 5. pH 7.48, PaCO2 30, HCO3- 23 : ANS: Uncompensated respiratory alkalosis

6. pH 7.62, PaCO2 47, HCO3- 30: ANS: . Partially compensated metabolic alkalosis 7. pH 7.30, PaCO2 59, HCO3- 28: ANS: partially compensated respiratory acidosis 8. pH 7.31 PaCO2 55 mm Hg HCO3- 28 mEq/L: Respiratory acidosis partially compensated

9. pH 7.31 PaCO2 55 mm Hg HCO3- 35 mEq/L PaO2 78: Respiratory acidosis partially compensated 10. pH 7.31 PaCO2 35 mm Hg HCO3- 20 mEq/L PaO2 88 Metabolic acidosis uncompensated 11. pH 7.31 PaCO2 25 mm Hg HCO3- 20 mEq/L PaO2 94 Metabolic acidosis partially compensated

12. pH 7.48 PaCO2 25 mm Hg HCO3- 20 mEq/L PaO2 99 Respiratory alkalosis partially compensated 13. pH 7.48 PaCO2 45 mm Hg HCO3- 33 mEq/L PaO2 74 Metabolic alkalosis uncompensated 14. pH 7.48 PaCO2 55 mm Hg HCO3- 33 mEq/L PaO2 87 Metabolic alkalosis partially compensated 15. pH 7.34 PaCO2 33.9 HCO3 18.2 PaO2 85.2 Metabolic acidosis partially compensated

16. pH 7.34 PaCO2 40.3 HCO3 21.4 PaO2 41.0 Metabolic acidosis uncompensated 17. pH 7.59 PaCO2 49.0 HCO3 48.2 PaO2 58.7 Metabolic alkalosis partially compensated 18. pH 7.07 PaCO2 11.4 HCO3 3.1 PaO2 115.1 Metabolic acidosis partially compensated

19. pH 7.28 PaCO2 79.5 HCO3 37.1 PaO2 30.0 Respiratory acidosis partially compensated 20. pH 7.51 PaCO2 39.4 HCO3 31.3 PaO2 77.3 Metabolic alkalosis uncompensated 21. pH 7.31 PaCO2 58.5 HCO3 26.1 PaO2 74.5 Respiratory acidosis partially compensated 22. pH 7.46 PaCO2 34.0 HCO3 26.0 PaO2 43.8 Respiratory alkalosis uncompensated

24. pH 7.18 PaCO2 42.0 HCO3 15.0 PaO2 69.0 Metabolic acidosis uncompensated 25. pH 7.52 PaCO2 31.0 HCO3 26 PaO2 100 Respiratory alkalosis uncompensated

26. pH 7.44; pCO2 27.8; HCO3 19.2 ANS: COMPENSATED RESPIRATORY ALKALOSIS 27. pH 7.36; pCO2 75.1; HCO3 40.6 ANS: COMPENSATED RESPIRATORY ACIDOSIS 28. pH 7.44; pCO2 48.0; HCO3 32.6 ANS: COMPENSATED METABOLIC ALKALOSIS

Case 1
Little Billy got into some of dads barbiturates. He suffers a significant depression of mental status and respiration. You see him in the ER 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained (after doing the ABCs, of course). It shows pH = 7.16, pCO2 = 70, HCO3 = 22

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ABG Interpretation

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Case 1
Uncompensated respiratory acidosis There has not been time for metabolic compensation to occur. As the barbiturate toxicity took hold, this child slowed his respirations significantly, pCO2 built up in the blood, and an acidosis ensued.

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Case 2
Little Suzie has had vomiting and diarrhea for 3 days. In her moms words, She cant keep anything down and shes runnin out. She has had 1 wet diaper in the last 24 hours. She appears lethargic and cool to touch with a prolonged capillary refill time. After addressing her ABCs, her blood gas reveals: pH=7.36, pCO2=27, HCO3=12
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Case 2
Compensated metabolic acidosis The prolong history of fluid loss through diarrhea has caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool. The body has compensated by blowing off the CO2 with increased respirations.

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Case 3
Mrs. Puffer is a 35-year-old single mother, just getting off the night shift. She reports to the ED in the early morning with shortness of breath. She has cyanosis of the lips. She has had a productive cough for 2 weeks. Her temperature is 102.2, blood pressure 110/76, heart rate 108, respirations 32, rapid and shallow. Breath sounds are diminished in both bases, with coarse rhonchi in the upper lobes. Chest X-ray indicates bilateral pneumonia.
ABG results are: pH= 7.45 PaCO2= 28 HCO3= 24 PaO2= 54

Problems: PaCO2 is low. pH is on the high side of normal, therefore compensated respiratory alkalosis.

Case 5: Mr. Worried is a 52-year-old widow. He is retired and living alone. He enters the ED complaining of shortness of breath and tingling in fingers. His breathing is shallow and rapid. He denies diabetes; blood sugar is normal. There are no EKG changes. He has no significant respiratory or cardiac history. He takes several antianxiety medications. He says he has had anxiety attacks before. While being worked up for chest pain an ABG is done: ABG results are: pH= 7.48 PaCO2= 28 HCO3= 22 PaO2= 85

pH is high, PaCO2 is low respiratory alkalosis