Fluid And Electrolytes

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Physiologic homeostasis depends on normal fluid and electrolyte balance, and is important in both health promotion and treatment of disorders. Fluid and electrolyte imbalances commonly accompany illnesses. Severe imbalances may result to death Some imbalances affect not only the acutely and chronically ill but also clients with faulty diet or those who take selected medication such as diuretics and glucocorticoids preparation. Every nurse must understand the process of fluid and electrolyte balance identify client at risk for imbalances, recognize early signs and symptoms of imbalances, intervene as appropriate and evaluate the outcomes.

*Body Water Principal body fluids ;solvent responsible for the body’s structures and function. Consists of 45-75% of the total body weight.

NORMAL WATER DISTRIBUTION/BALANCE Body Fluids Function  Facilitates transport of nutrients, hormones, CHON and other molecules into the cells.  Aids in the removal of cellular metabolic waste products.  Provides the medium in which cellular metabolism takes place.  Regulates lubrication of musculoskeletal joints.  Acts as a component all body cavities ( pericardial fluid, pleural, CSF)

Fluid Compartments: 1. Intracellular Fluid (ICF) – Includes all water and electrolytes inside the cells. – 2/3 of the body weight is contained within cell membranes 

2. Extra cellular Fluid (ECF) – Includes interstitial fluid, intravascular and Trancellular fluid – Constitutes about 1/3 of body water Functions of ECF: – Transports nutrients and electrolytes to cell and waste products for excretion – Regulates heat – Lubricates and cushions joints – Hydrolyzes food for digestive process

NORMAL WATER BALANCE Intake Liquid 1,200-1,500 ml Water in food 700- 1,000 ml Metabolism 200- 400 ml TOTAL

2,100 – 2,900 ml

Output Urine 1,200 -1,500 ml Feces 100-250 ml Insensible Loses: Skin 350 -400 ml Lungs 350- 400 ml TOTAL 2,100 – 2,900 ml

Fluid Intake & Output

Routes of Gains and Losses

CONTINUAL MOVEMENT OF FLUIDS AND ELECTROLYTES 

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Fluids move between components to maintain homeostasis Fluid Movement from Pressure Changes-body fluid shifts between the interstitial space and the vascular space in the capillary as a result of differences in the hydrostatic pressure and oncotic pressure

 Fluid Movement by Diffusion and Osmosis 

Diffusion- means by which substances such as nutrients and wastes produces move between blood and interstitial spaces.

 Osmolality – refers to the concentration of

solutes in 1 liter of solution 

OSMOSIS: diffusion of H2O across a selectively permeable membrane from an area of lower solute concentration to an area of higher solute concentration.

FACTORS RESPONSIBLE FOR NORMAL REGULATION AND FLUID BALANCE Regulator of fluids Balance: 

Thirst – Hypothalamus- thirst center of the brain – Activated by an increase in ECF Osmolality due to: Hypotension  Polyuria  Fluid volume depletion 

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Hormones/ Hormonal Influence  Antidiuretic Hormone (ADH)stored in the posterior pituitary gland; reduces urinary output; returns fluids to the body rather than excreting them  Aldosterone - secreted by the adrenal cortex and conserves the body’s sodium by promoting potassium excretion from the kidneys.  Lymphatic system – It plays an important role in returning excess fluid and protein from interstitial spaces to the blood.

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RENIN-ANGIOTENSIN MECHANISM ATRIAL NATRIURETIC PEPTIDE

 Nervous

System - when the ECF volume increases, mechanoreceptors in the wall of the atrium respond to atrial distention by increasing cardiac stroke volume and triggering a sympathetic response in the kidney, stimulation of the of the renal sympathetic nerves decreases renal excretion of sodium by both increasing renin release and through a direct effect in the kidneys.

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Kidney – maintain fluid volume and the connection of urine by filtrating the ECF through the glomeruli. Reabsorbtion and excretion of ECF occurs in the renal tubules.

Fxns of the Kidneys  Regulation

of ECF volume and osmolality by selective retention of needes substances and excretion fluids.  Regulation of electrolytes level in the ECF by selective retention of substances and excretion of unneeded substances  Regulation of pH of the ECF by retention of H+ ions

REGULATION OF FLUID VOLUME

HYPERVOLEMIA

HYPOVOLEMIA

inhibits

ADH

stimulates

Aldosterone

INCREASED URINATION of Dilute urine

Thirst

Thirst

ADH

Aldosterone

DECREASED URINATION of Concentrated urine NORMAL FLUID VOLUME RESTORED

FLUID IMBALANCES I. Extra Cellular Fluid Volume Deficit MILD: 1-2 L of H2O (2% body wt.)

Causes: 1. Lack of fluid intake – 1,500 – 2,000 ml

MODERATE: 3-5 L of H2O (5%) SEVERE: 5-10 L of H2O (8%)

RF: – Hospitalized/bed bound – People w/ dysphagia/ risk for aspiration – Tube-fed patients who are not given adequate free water – Pts. w/ decreased access to fluids – Pts. w/ impaired thirst mechanism  

People w/ debilitating illnesses Older adults

2. Excessive Fluid Losses – Vomiting, diarrhea, fever, hyperglycemia, suction, fistula, burns, blood loss, diabetes insipidus, diaphoresis, hyperthyroidism, excessive diuretics, ileostomy, hyperventilation, Diuretic phase of ARF

Types of ECFVD  Hyperosmolar (hypertonic): water loss is > electrolyte loss  Hypotonic: electrolyte loss is > fluid loss  Isotonic (iso-osmolar): water and electrolyte loss are equal

CLINICAL MANIFESTATIONS: 1. Loss of body wt. –

Most accurate indicator of fluid loss – 1 L of sol’n=1 kg of body wt.

2. Changes in I &O –

U. O. of 400-500 ml/day- oliguria – Thirst

3. Changes in V/S – – – – – – –

↓ed BP Weak pulse ↓ed CVP, ↓ed PCWP Postural hypotension ↑ed PR Flat JV and prolonged peripheral venous filling time of more than 5 sec. Elev. Body temp

4. Manifestations of cellular dehydration – – – – –

dry mucus membrane of mouth and eyes cracked lips poor skin turgor muscle weakness cerebral sx (fluid shifting)

FLUID VOLUME DEFICIT

•IS move to IV •ADH & aldosterone is released •Fluids reabsorbed in the ileum & colon •Baroreceptors  SNS: increase HR & Peripheral vasoconstriction •Osmoreceptors: Thirst mechanism

DEHYDRATION

•Impaired temperature regulation •Decrease ability to transport heat •Decrease CSF •Decrease Sodium

II. Intracellular Fluid Volume Deficit (ICFVD) – Due to severe dehydration RF: - older clients; w/ acute water loss s/sx: - Thirst – Oliguria – Fever – Confusion, coma, cerebral hemorrhage

 DIAGNOSTIC TEST FOR ECFVD/ICFVD: Osmolality > 295 mOsm/L BUN > 25 mg/dl Hct > 55%

Na >145 mEq/l Glucose >120 mg/dl Urine sp. Gr. > 1.030

III. Extra Cellular Fluid Volume Excess (ECFVE) Fluid overload 2 types: 1. hypervolemia-↑ed fluids in vascular system 2. third spacing-↑ed fluids in interstitial space

Etiology  Simple overloading of fluids (too many

IVF)  ↑ ADH and aldosterone  ↓ kidney fxn  CHF  Liver Cirrhosis  Venous disorder  Excessive ingestion of fluids/ food with Na

MECHANISM OF EDEMA FORMATION FLUID OVERLOAD Increase hydrostatic pressure in arterial end of capillary Increased peripheral Vascular resistance

Fluid movement into tissues

Increased left Ventricular pressure

Increased left atrial pressure

Pulmonary edema

edema

DECREASE PLASMA & ALBUMIN

ALTERED LYMPHATIC FUNCTION

TISSUE INJURY

Decrease production of plasma CHON

Lymphatic obstruction decreases absorption of interstitial fluid

Increase capillary permeability

Decrease Capillary Oncotic Pressure

Decrease transport of capillary filtered protein

Movement of plasma CHON in tissues

Increase tissue oncotic pressure, which pulls fluid towards it

Increase tissue Oncotic pressure

Decrease Reabsorption At venous end

EDEMA

EDEMA

EDEMA

IMPAIRED RENAL FXN ↓ Na and H20 excretion ↑ Fluid Volume Heart compensates by increasing HR and Hypertrophy If compensatory mechanism fails, heart failure develops

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Clinical Manifestations:

> respiratory > cardiovascular > others Edema Anorexia/bloating Wt. gain Fluid shifting from IV/IS DIAGNOSTICS: Osmolality < 275 mOsm/L BUN < 8 mg/dl Hct < 45%

Na < 135 mEq/l Urine sp. Gr. < 1.010

IV. Intracellular Fluid Vol. excess (ICFVE)- water intoxication; cells are resistant to fluid shifts Etiology: – water excess- number of solutes is normal but there is water excess – solute deficiency=amt. of water is normal but ↓ed solute = most common cause: administration of excessive amts. Of hypoosmolar IVF = adults who consume excessive amts. of tap H2O w/o adequate nutrient intake =SIADH =people w/ psych. d/o → schizophrenia with compulsive water consumption

V. Extracellular Fluid Volume Shifting – third spacing 2 types: 1. vascular fluid shifts to interstitial space (hypovolemia) 2. interstitial fluid shifts to vascular space (hypervolemia) * third space= fluid that shifts into IS and remains there = common sites:pleural cavity, peritoneal cavity, & pericardial sac Etiology:     

↑ ed capillary permeability ↑ ed fluid reabsorption in venous end Decreased serum CHON levels Obstruction of venous end of capillary Non-functional lymphatic drainage system

Clinical Manifestations: 1. Fluid shifting from IV to IS – Pallor, cold limbs, weak &rapid pulse, hypotension, oliguria, ↑ ed skin turgor & ↓ ed level of consciousness – No changes in body wt. because fluid has not been lost but redistributed 2.fluid returns to the IV space from IS – s/sx similar to fluid overload – bounding pulse, crackles, JVD, ↑ ed BP

Types of Intravenous Fluids Types of Intravenous Fluids: 

ISOTONIC – a solution that has the same osmotic pressure externally as that found across a semi-permeable membrane --0.9% NaCl, D5W, 5% Dextrose in 0.225% Saline and LRS

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HYPOTONIC –a solution that has a lower osmotic press than that of the blood causing the cell to expand and swell.(They contain lower concentration of salt/ solute than other solution) --0.3 % NaCl, D in water, 0.45 % NaCl and distilled water.

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HYPERTONIC – a solution that has a higher osmotic pressure than that of the blood causing the cell to shrink. ( It has higher concentration of solutes.) --D5LRS, Mannitol, 10% D in water, and 5% D in 0.45% NaCl

Cell appearance on different solutions

Blood cells in an Hypotonic Fluid

Blood cells in an Hypertonic Fluid

Electrolytes – these are chemical substances which when dissolved dissociates into ions and passes electrical potential. Types:  Cations – ions carrying positive charge – Na – K – Ca – Mg 

Anions – ions carrying negative

CATIONS Na- 135-145 m Eq/L K- 3.5 – 5.0 m Eq/L Ca- 4.5-5.5 mEq/L Mg -1.5 – 2.5 mEq/L

ANIONS HCO3- 22-26 mEq/L Cl- 96-106 mEq/L PO4 – 1.2 -3.0 mEq/L

A. Sodium Imbalances  Derminant of serum osmolality  Chloride is the anion that usually accompanies

Na  Sodium balance is regulated by the interaction among neural, hormonal, and vascular mechanisms  Renal glomerulus filters 1000 mEq of sodium/hr and 99% is reabsorbed in the loop of Henle  Prostaglandin

FUNCTIONS  Primary regulator of ECF volume  Establishing electrochemical state

necessary for muscle contraction and nerve impulse transmission “WHERE SODIUM GOES WATER FOLLOWS”

1. Hyponatremia –one of the most common electrolyte imbalance Hypovolemic: Na loss > H2O loss Euvolemic: TBW is mod. increased & total body Na is normal Hypervolemic: Greater increased in TBW than in total Na Redistributive: no change in TBW or total body Na.

RF:  Excessive perspiration  Altered thirst mech.  w/o access to fluids  rapid rehydration after excessive fluid loss  altered percentage of total body water  decreased intake of sodium: fruits, vegetables, oatmeal, rice, wheat, fresh meat, chicken, fish (1 oz)

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excessive administration of diuretic and laxatives NGT irrigation with plain water Vomiting, drh

Clinical Manifestations: 125 mEq/L  neurological manifestations  Cardiovascular manifestations – Tachycardia– Sympathetic responses – stimulation of chemoreceptors in the aortic and carotid bodies  Respiratory Manifestations – Crackles in the lungs – Tachypnea, dypnea, orthopnea, SOB  GI Manifestations – n/v, drh, abdominal cramping, hyperactive bowel sounds  Others: – Dry skin, tongue & mucus membrane

DX results:  Na < 135 mEq/L  Cl < 96 mEq/L  Serum Osmolality <275 mOsm/kg  Urine Osmolality <40 mOsm/kg

2. Hypernatremia - associated w/ water loss or sodium gain Types: – Hypovolemic hypernatremia: TBW is greatly decreased compared to Na – Euvolemic hypernatremia: TBW is decrease

relative to normal total body Na – Hypervolemic hypernatremia: TBW is increased

but Na gain is > H2O gain

Etiology/RF:  Inadequate water intake in conjunction w/ decreased thirst (hypodipsia)  Lack of access to drinkable water  Physical or chemical restraint  Mental confusion  NPO  Excessive water loss & insufficient water replacement  Increased Na+ intake: bread, cereals, chips, convenience food, fast foods  IV administration of hypertonic saline or hypertonic tube feedings  Retention of Na+ occurs in heart, renal or liver dse.  Cushing’s Syndrome  Hyperaldosteronism  Uncontrolled DM

Clinical Manifestations: 155 mEq/L         

Polyuria Anorexia, N/V, weakness, restlessness Early neurologic S/Sx Hypervolemic state Hypovolemic state Dysrhythmia Crackles, dysnea, pleural effusion Fever and increased thirst Dry skin and mucous membrane, tongue furrows

Effect of Sodium to cells

B. Potassium Imbalances

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PISO Poorly stored in the body, daily K+ intake is necessary 80 to 90% of K+ is excreted through the kidneys & remainder is excreted in feces

Functions:  Regulates ICF osmolality  Promotes transmission and conduction of nerve impulses  Muscle contraction  Enzyme action for cellular metabolism and glycogen storage in the liver  acid-base balance

Alkalosis – can cause hypokalemia

Acidosis – can cause hyperkalemia

Substance that can alter K+ levels: – Insulin – Glucagon – Adrenocortical hormones

cortisol and aldosterone  Stress 

– Catecholamines & beta- adrenergic agonists – Alpha-adrenergic agonists – Epinephrine – has alpha & beta – adrenergic properties

1. Hypokalemia - common, especially in elderly pop’n Etiology and RF: A. Inadequate K+ intake body does not conserve K+ – Debilitated, confused, restrained, lacking access to K+ sources, malnourished, anorexic, bulimic – Potassium- restricted diets or some wt. reduction diets ( corn, potato, apple, blueberry, cranberry, coffee, cola, gingerale, soda) – Those receiving K+ free IV sol’ns

B. K+ excretion exceeds K+ intake – Vomiting, drh, suctioning, intestinal fistulae, ileostomy – Osmotic diuresis that occurs with DKA – Surgical clients – Alcoholic clients – Certain drugs (loop, osmotic, thiazide diuretics, cathartics, steroids) – Clients who are in the healing phase after a severe tissue injury or burn – Cushing’s syndrome – Diuretic Phase of RF – Hyperaldosteronism

↓ serum K ↓ K gradient ↑ resting membrane potential ↓ neuromuscular irritability and excitability

Clinical Manifestations: 

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GI Manifestations – Slowed smooth muscle contraction – Anorexia, abdominal distention, constipation – Extreme smooth muscle slowing - vomiting ileus, urinary retention Slowed Skeletal Muscle Contraction- muscle weakness, Leg cramps, fatigue, paresthesia, hyporeflexia, paralysis ECG-most reliable tool for identifying abnormalities in intracellular K+ level (peaked P wave, ST depressed & prolonged, Depressed or inverted T wave, prominent U wave). ↓ ed myocardial contractility Pulmonary manifestations Progressive neurologic consequences of altered conduction – dysphasia, confusion, depression, convulsions, areflexia, coma Polyuria, nocturia

2. Hyperkalemia Etiology and RF:  Retention of K+ by the body because of ↓ ed or inadequate urine output  Release of K+ from the cells during the 1st 24 to 72 hours after traumatic injury on burns, or from cell lysis or acidosis  Excessive infusion of IV solution that has K+ or excessive oral intake of K+, especially in a person who has renal dse  Therapy w/ K+ sparing diuretics, use of K+ supplements, ACE inhibitors  Adrenal insufficiency or addison’s disease

↑ serum K Altered resting membrane potential Cell membrane becomes easily excitable Increased depolarization or action potential Repeated irritation of cell membrane ↑ Excitation threshold of membrane Cells become less excitable Weak, flaccid paralysis of muscles

Clinical Manifestations:       

N/V Diarrhea Impaired nerve & muscle function Severe neuromuscular weakness respiratory muscle paralysis ECG changes: (wide flat P wave, Depressed ST segment, Narrow, peaked T wave) Impaired cardiac conduction (tachycardia, hypotension, cardiac arrest, ventricular contractions)

Effect of Potassium on ECG

C. Calcium Imbalances: FUNCTIONS:  catalyst (nerve impulses)  stimulates muscle contraction  normal cellular permeability  blood coagulation  absorption of Vitamin B12  Bones and teeth  99% of the body’s Ca# is in the bones & teeth  1 % is in the tses. And IV space

3 types: 1. free/ ionized 2. Ca# bound to CHON 3. Complex Vit. D - is needed to absorb Ca# from GIT PTH – regulates plasma levels of Ca# and PO4 by ↑ ing

resorption from bone and reabsorption from renal tubule or the GIT Calcitonin – thyroid gland – opposes action of PTH – inhibits bone resorption

1. Hypocalcemia Etiology and RF:  common in adult because of inadequate intake of Ca# and Vit. D (GI dses – anorexia, liver dse., lactose intolerance, alcoholism): oatmeal, hamburger, apples, bananas, chicken  decreased intake for several days (NPO), high CHON diet  hypoparathyroidism  people who don’t have exposure to the sun  pancreatitis  Open wounds  Excess Na

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Overcorrection of Acidosis Multiple BT Certain drugs – MgSO4, Colchicine, and neomycin – Aspirin, anticonvulsants, and estrogen – PO4prep’n – Steroids – Loop diuretic – Antacids and laxatives

↓ Calcium Partial depolarization of nerves and muscles because of ↓ threshold potential Smaller stimuli initiates the action potential

Clinical Manifestations:  paresthesia  ↓ ed CO  ↑ ed peristalsis and drh  Prolonged bleeding times and hemorrhage  Bones become brittle and results in pathologic fractures  Facial Twitching (Chvostek’s sign)  Carpopedal spasm (Trousseau’s sign)  ECG changes: prolonged QT interval  Severe: seizure, tetany, hemorrhage, cardiac collapse  True level of free Ca: ionized Ca level

Trousseau’s Sign

2. Hypercalcemia Etiology and RF: Major Causes  Metastatic malignancy (Tumor Lysis Syndrome)  Hyperparathyroidism  Thiazide diuretic therapy     

Other Causes: Excessive intake of Ca supplements w/ vit. D, Ca containing antacids Prolonged immobilization Metabolic acidosis Hypophosphatemia

↑ Calcium ↑ cell membrane potential threshold cell membrane becomes refractory to depolarization cell membrane becomes less excitable and requires greater stimulus to produce response

Clinical Manifestations:  GI- anorexia, N/V, abdominal distention & constipation  Neurologic Depression – weakness, fatigue, depression, difficulty concentrating  Osmotic diuresis  ureteral or kidney stones  ECG Changes: short QT interval, widened T wave (cardiac depression  dysrhythmias & arrest)

D. Phosphate Imbalances  Phosphate promotes strong and durables bones  Phosphate is an integral part of ATP, ADP  Phosphate plasma level is regulated by PTH  Facilitates release of Hgb and maintenance of acid-base balance, nervous system, and intermediary metabolism of CHO, CHON, and fats 1. Hypophosphatemia Etiology and RF:  Major loss/ long term lack of intake  Other RF: periods of ↑ ed growth or tse. Repair and recovery from malnourished states  Prolonged/ excessive intake of antacids  Administration of high levels of glucose via tube feeding/ IV line (glucose cause the P to enter the cell for glucose phosphorylation)  ↑ ed Na+, ↑ ed Ca, ↓ ed PaCO2 in resp. alkalosis  Lead poisoning  Burns

Clinical Manifestations:  ↓ ed cardiac and respiratory fxn  Muscle weakness  Fatigue  Brittle bones  Confusion and Seizures 2. Hyperphosphatemia Etiology and RF:  Excessive intake of high- PO4 foods  Excess vit. D  Impaired colonic motility from ↑ ed absorption  Hypoparathyroidism and Addison’s dse.  Renal failure  TLS  Post menopausal state

Clinical Manifestations:    

↑ ed PR Palpitations Restlessness Anorexia, N/V, tetany, hyperreflexia, dydrhymias

Food rich in PO4:  Milk, ice cream, cheese, large amounts of meat and fish, carbonated beverages

E. Magnesium Imbalances    

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Actions similar to K+ Signs of imbalance similar to K+ 2nd most abundant intracellular cation Fxns: transmission & conduction of nerve impulses – Contraction of Muscle – Responsible for the transportation of Na+ & K+ across cell membrane – Responsible for the synthesis & release of PTH increased Ca and Phosphorus= can ↓ Mg absorption from intestines ↓ ed Mg can lead to hypokalemia and hypocalcemia

 Acts as an activator for many

intracellular enzyme system and plays a role in both carbohydrate and CHON metabolism  1/3 CHON bound  2/3 free Mg  Predominantly found in bones and soft tissues and eliminated by the kidney.

Hypomagnesemia  

Common cause of refractory hypokalemia and hypocalcemia ETIOLOGY AND RF: – Critically ill – Alcoholics – Malabsorption syndromes – GI losses – Diuretic phase of renal failure – Excess Ca and excess Na inhibits Mg – Prolonged IV or TPN therapy w/ Mg replacement – Hyperglycemia, osmotic diuresis – Many medications – Diuretics and antibiotics (aminoglycosides) – Corticosteroids and digitalis – promotes uptake of Mg – Estrogen

Clinical Manifestations:  Myocardial irritability  Anorexia, nausea, abdominal distention  Psychological disorders  Neuromuscular Manifestations- Chvostek’s sign, Trousseau’s sign, tetany, convulsions, vasospasm leading to stroke  ECG changes – prolonged QT, widened QRS, broadened T-waves

2. Hypermagnesemia Etiology and RF:  Renal insufficiency  Excessive use of Mg- containing antacids  Excessive use of Mg- containing laxatives  Administration of K+ sparing diuretics  Severe dhn from DKA  ↓ ed synthesis of aldosterone  Overuse of IV MgSO4 Clinical Manifestations:  Decreased muscle activity  Hypotension  Severe muscle weakness, lethargy, drowsiness, loss of deep tendon reflex, respiratory paralysis and loss of consciousness  ECG – prolonged PR interval, widened QRS

ACID BASE BALANCE Concept : Normal functions of body cells depend or the regulation of Hydrogen ion (H+) concentration – the determinant of serum pH (acidity/ alkalinity) Acid-Base Balance – refers to the Hydrogen (H+) ion concentration in the body. Acid- a substance which when dissolved in H20 can dissociate and increase the H+ ion concentration; hydrogen ion donor. Base – a substance which when dissolved in H20 can dissociate and increase the Hydrogen ion (OH) concentration and the therefore neutralizes the hydrogen ions; hydrogen ion acceptor

pH – used to express the degree of acidity or alkalinity of a solution; normal serum pHs 7.35 -7.45 Normal concentrations of H+ in the body fluids: 0.00004 mEq/L Functions of H+  Necessary for proper cellular function  Efficient functioning of every system  Binding of O2 with hemoglobin  Acts as powerful chemical adjutator with body fluids  Determines the alkalinity and acidity of solution

Regulation of Acid-Base Balance 1. Modulation of serum pH blood buffer system Buffer System – consist of weak acid and salt of base which act together to neutralize either acid or bases; body line of defense against acid-base imbalance. Bicarbonate Buffer System: -Most important buffer system in the body (ECF) -Comprises 1/12 of the buffer system

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NaH CO3(Bicarbonate) – Weak base – Regulated by the kidneys H2CO3 (Carbonic Acid) – A weak acid – Regulated by the lungs through respiration In order to maintain the ph at a normal level (7.35-7.45 or an average of 7.4) the ration of bicarbonate to carbonic acid must be 20:1. The pH of buffered solutions tend to remain fairly stable despite the addition of strong acids or bases because the buffer system converts them to weaker forms.

2.Regulation of volatile acid by the lungs Volatile Acids- acids that can be converted to gases. Carbon dioxide – potential acid; continuously produces by body cells as an end product of complete oxidative metabolism of nutrients for energy. – 99.9 % of carbonic acid dissociates into CO2 to H2o. therefore by

increasing or decreasing respiration, Co2 can be conserved or lost; and carbonic acid concentration is affected. 

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The pH of the blood stimulates the respiration center so that respiration are increased in alkalosis or decrease in acidosis hypoventilation – hypercapnea (increased CO2) hyperventilation –hypocapnea (decrease CO2)

3.Regulation of fixed Acids and Bicarbonate by the Kidneys The Kidneys regulate bicarbonate concentration by:  Excreting excess acid/base  Reabsorbing needed base Urinary Buffer System- the kidney regulate serum pH by secreting H+ into the urine and by regenerating HCO3 for reabsorption into the blood; permits tubular fluid to accept large quantities of H+ while limiting how much the urinary pH decreases. pH is the direct indication of acidity (increased H+ concentration ) or alkalinity (decreased H+ concentration)  pCo2 is inversely proportional with pH – HCO3 and pO2 is directly proportional with pH – pO2 and H2Co3 is directly proportional

Normal Values of ABG ( arterial blood Gas) Analysis pH = 7.35 to 7.45 mmHg pCO2 = 34-45 mmHg HCO3 = 24-26 mEq/L pO2 = 90 -110 mmHg In order to interpret ABG result, remember the following  pCO2 = respiratory parameter where: = acidosis =alkalosis  HCO3 = metabolic parameter where: = acidosis = alkalosis

IV Site Selection for ABG

Interpretation of the Arterial Blood Gas

Overview The pH is a measurement of the acidity or alkalinity of the blood. It is inversely proportional to the number of hydrogen ions (H+) in the blood. The more H+ present, the lower the pH will be. Likewise, the fewer H+ present, the higher the pH will be. The pH of a solution is measured on a scale from 1 (very acidic) to 14 (very alkalotic). A liquid with a pH of 7, such as water, is neutral (neither acidic nor alkalotic).

The normal blood pH range is 7.35 to 7.45. In order for normal metabolism to take place, the body must maintain this narrow range at all times. When the pH is below 7.35, the blood is said to be acidic. Changes in body system functions that occur in an acidic state include a decrease in the force of cardiac contractions, a decrease in the vascular response to catecholamines, and a diminished response to the effects and actions of certain medications. When the pH is above 7.45, the blood is said to be alkalotic. An alkalotic state interferes with tissue oxygenation and normal neurological and muscular functioning. Significant changes in the blood pH above 7.8 or below 6.8 will interfere with cellular functioning, and if uncorrected, will lead to death.

Components of the Arterial Blood Gas pH: Measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The normal range is 7.35 to 7.45 PaO2: The partial pressure of oxygen that is dissolved in arterial blood. The normal range is 80 to 100 mm Hg. SaO2: The arterial oxygen saturation. The normal range is 95% to 100%. PaCO2: The amount of carbon dioxide dissolved in arterial blood. The normal range is 35 to 45 mm Hg. HCO3: The calculated value of the amount of bicarbonate in the bloodstream. The normal range is 22 to 26 mEq/liter

 Step

One Assess the pH to determine if the blood is within normal range, alkalotic or acidotic. If it is above 7.45, the blood is alkalotic. If it is below 7.35, the blood is acidotic.

 Step

Two If the blood is alkalotic or acidotic, we now need to determine if it is caused primarily by a respiratory or metabolic problem. To do this, assess the PaCO2 level. Remember that with a respiratory problem, as the pH decreases below 7.35, the PaCO2 should rise. If the pH rises above 7.45, the PaCO2 should fall. Compare the pH and the PaCO2 values. If pH and PaCO2 are indeed moving in opposite directions, then the problem is primarily respiratory in nature.

 Step

Three Finally, assess the HCO3 value. Recall that with a metabolic problem, normally as the pH increases, the HCO3 should also increase. Likewise, as the pH decreases, so should the HCO3. Compare the two values. If they are moving in the same direction, then the problem is primarily metabolic in nature. The following chart summarizes the relationships between pH, PaCO2 and HCO3.

pH

 Respiratory

Acidosis ↓

 Respiratory

Alkalosis ↑

 Metabolic

Acidosis

 Metabolic

Alkalosis

↓ ↑

PaCO2

HCO3

↑ normal ↓ normal normal ↓ normal ↑

Jane Doe is a 45-year-old female admitted to the nursing unit with a severe asthma attack. She has been experiencing increasing shortness of breath since admission three hours ago. Her arterial blood gas result is as follows:  pH 7.22  PaCO2 55  HCO3 25 Follow the steps: 1. Assess the pH. It is low (normal 7.35-7.45);therefore, we have acidosis. 2. Assess the PaCO2. It is high (normal 35-45) and in the opposite direction of the pH. 3. Assess the HCO3. It has remained within the normal range (22-26). 

Respiratory Acidosis

 Refer

pH PCO2 ↓ ↑

HCO3 Normal

to the chart. Acidosis is present (decreased pH) with the PaCO3 being increased, reflecting a primary respiratory problem. For this patient, we need to improve the ventilation status by providing oxygen therapy, mechanical ventilation, pulmonary toilet or by administering bronchodilators.

 John

Doe is a 55-year-old male admitted to your nursing unit with a recurring bowel obstruction. He has been experiencing intractable vomiting for the last several hours despite the use of antiemetics. Here is his arterial blood gas result:  pH 7.50  PaCO2 42  HCO3 33  Follow

the three steps again: 7. Assess the pH. It is high (normal 7.35-7.45) 2. Assess the PaCO2. 3. Assess the HCO3.

Metabolic Alkalosis  Again,

pH

PCO2

HCO3

↑

normal

↑

look at the chart. Alkalosis is present (increased pH) with the HCO3 increased, reflecting a primary metabolic problem. Treatment of this patient might include the administration of I.V. fluids and measures to reduce the excess base.

Compensation  When a patient develops an acid-base imbalance, the body attempts to compensate. Remember that the lungs and the kidneys are the primary buffer response systems in the body. The body tries to overcome either a respiratory or metabolic dysfunction in an attempt to return the Ph into the normal range. A

patient can be uncompensated, partially compensated, or fully compensated. When an acidbase disorder is either uncompensated or partially compensated, the pH remains outside the normal range. In fully compensated states, the pH has returned to within the normal range, although the other values may still be abnormal. Be aware that neither system has the ability to overcompensate.

Partial compensation: 

1. Assess the pH.



2. Assess the PaCO2. In an uncompensated state, we have already seen that the pH and PaCO2 move in opposite directions when indicating that the primary problem is respiratory. But what if the pH and PaCO2 are moving in the same direction? We would then conclude that the primary problem was metabolic. In this case, the decreasing PaCO2 indicates that the lungs, acting as a buffer response, are attempting to correct the pH back into its normal range by decreasing the PaCO2. If evidence of compensation is present, but the pH has not yet been corrected to within its normal range, this would be described as a metabolic disorder with a partial respiratory compensation.



3. Assess the HCO3. In our original uncompensated examples, the pH and HCO3 move in the same direction, indicating that the primary problem was metabolic. But what if our results show the pH and HCO3 moving in opposite directions? That is not what we would expect to see. We would conclude that the primary acid-base disorder is respiratory, and that the kidneys, again acting as a buffer response system, are compensating by retaining HCO3, ultimately attempting to return the pH back towards the normal range.

Partially Compensated States

Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

pH ↓ ↑ ↓ ↑

PaCO2 ↑ ↓ ↓ ↑

HCO3 ↑ ↓ ↓ ↑

Fully Compensated States

Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis

pH

PaCO2

HCO3

normal but <7.40 normal but >7.40 normal but <7.40 normal but >7.40

↑

↑

↓

↓

↓

↓

↑

↑

 John Doe is admitted to the hospital. He is a

kidney dialysis patient who has missed his last two appointments at the dialysis center. His arterial blood gas values are reported as follows:  pH 7.32  PaCO2 32  HCO3 - 18

Metabolic Acidosis

pH

PaCO2

↓

↓

HCO3

↓

1. Assess the pH. It is low (normal 7.35-7.45); therefore we have acidosis. 2. Assess the PaCO2. It is low. Normally we would expect the pH and PaCO2 to move in opposite directions, but this is not the case. Because the pH and PaCO2 are moving in the same direction, it indicates that the acid-base disorder is primarily metabolic. In this case, the lungs, acting as the primary acid-base buffer, are now attempting to compensate by “blowing off excessive C02”, and therefore increasing the pH. 3. Assess the HCO3. It is low (normal 22-26). We would expect the pH and the HCO3 to move in the same direction, confirming that the primary problem is metabolic. Because there is evidence of compensation (pH and PaCO2 moving in the same direction) and because the pH remains below the normal range, we would interpret this ABG result as a partially compensated metabolic acidosis.

Jane Doe is a patient with chronic COPD being admitted for surgery. Her admission lab work reveals an arterial blood gas with the following values: pH = 7.35 PaCO2 = 48 HCO3 = 28

pH

Respiratory Acidosis 1.

normal but <7.40

PaCO2

HCO3

↑

↑

Assess the pH. It is within the normal range, but on the low side of neutral (<7.40).

2. Assess the PaCO2. It is high (normal 35-45). We would expect the pH and PaCO2 to move in opposite directions if the primary problem is respiratory. 3. Assess the HCO3. It is also high (22-26). Normally, the pH and HCO3 should move in the same direction. Because they are moving in opposite directions, it confirms that the primary acidbase disorder is respiratory and that the kidneys are attempting to compensate by retaining HCO3. Because the pH has returned into the low normal range, we would interpret this ABG as a fully compensated respiratory acidosis.