NURS 2140

Fluid and Electrolytes Acid Base and IV Therapy

Teresa Champion, RN MSNMetropolitan Community College

Winter 2012

BODY COMPOSITION AND FUNCTION• PRIMARY FLUID = Water

– 60% total body weight (1 L = 2.2 lbs)– 2 – 2.5 L of water per day

• TWO PRIMARY FLUID COMPARTMENTS– Intracellular (ICF)– Extracellular (ECF)

• FUNCTIONS:– Transporting– Removing– Regulation– Lubricating– Food Digestion

Intake = Output

Regulation of Body Fluid

• Osmosis – movement of water from lower particle concentration to higher particle concentration

• Diffusion – movement of molecules from higher to lower concentration (simple or facilitated)

• Filtration – movement of molecules through a semi-permeable membrane from higher concentration to lower concentration as a result of hydrostatic pressure

There are two ways in which substances can enter or leave a cell: 1) Passive

a) Simple Diffusion b) Facilitated Diffusion (carrier)c) Osmosis (water

only) 2) Active

a) Molecules b) Particles

Oncotic vs Hydrostatic Pressure

• Filtration is directly opposed by the oncotic pressure of plasma proteins, especially Albumin in the blood stream.

• Arteriole – high hydrostatic pressure - (~32mmHg)• Venus – low hydrostatic pressure – (~15 mmHg)• Plasma oncotic pressure – (~22mmHg)

• http://www.youtube.com/watch?v=VMvD29-Agtg• http://www.youtube.com/watch?v=mpg7ON2CfFE• http://www.youtube.com/watch?v=dAO8igIysaA

• Homeostasis - thus in a steady state ECF = ICF

OSMOLALITY • Number of molecules of solute per kg of water• NORMAL OSMOLALITY of blood is 275 – 295

milliosmoles per kg (mOsm/kg) of body weight– Isotonic Fluids - same osmolality as blood plasma)– Hypotonic Fluids - less concentration than blood

plasma (< 275 mOsm/kg)– Hypertonic Fluids - greater concentration than blood

plasma (>295 mOsm/kg)

Homeostatic Mechanisms• Fluid Balance - regulated by:

– Osmoreceptors of the hypothalamus - stimulates release of ADH and stimulates thirst.

– Baroreceptors (pressure sensitive cells) in carotids and aorta also stimulate the release of ADH

– Baroreceptors in glomerular arterioles in kidney will secrete Renin and start the Renin-Angiotension (RAA) cascade thus resulting in release of aldosterone from the adrenal glands and cause sodium retention = fluid retention (water follows sodium)

Role of the Heart

• Atrial Natriuretic Peptide: (ANP): secreted from atrial cells of heart (in response to too much volume in the blood) – acts as diuretic– inhibits thirst mechanism– suppresses the RAA cascade

Role of the Kidneys

• Filter approx 180 Liters of blood per day; GFR (glomerular filtration rate)

• Produces urine between 1-2 Liters/day• If loss of 1% to 2% of body water, will conserve

water by reabsorbing more water from filtrate; urine will be more concentrated

• If gain of excess body water, will excrete more water from filtrate; urine will be more diluted

Lab Tests for Evaluating Fluid Balance

SERUM Normal LevelsOsmolality 275-295 mOsm/kg of

water

Hematocrit 40-50%*

BUN 5-20 mg/dl

Sodium 135 – 145 mEq/L

Potassium 3.5 – 5.0 mEq/L

Chloride 95-108 mEq/L

Bicarbonate(CO2)

22-28 mEq/L -Arteriole24-30 mEq/L -Venous

URINE Normal Levels

Specific Gravity 1.005 – 1.030

Osmolality 50-1200 mOsm/kg of water

Sodium 40-220 mEq/day

Potassium 25-100 mEq/day

Evaluation of Fluid Status

• Normal serum hematocrit– 40 – 50%

• Dilute serum– Low hematocrit and electrolyte levels

• Concentrated serum– Elevated hematocrit and electrolyte levels

Clinical Manifestations of Overhydration and Dehydration

OVERHYDRATION DEHYDRATION

Crackles in lungs Dry mouth and tongue, mucous membranes

S3 Heart Sound Tachycardia

Dyspnea Severe thirst (maybe not in elderly)

Reduced blood oxygen levels and increased CO2 levels – respiratory acidosis

Increased temperature (may rise 1 or 2 degrees)

Bounding pulses Weak pulses

Increased blood pressure Orthostatic Hypotension, systemic hypotension

Increased edema, ascites “tenting” skin

Increased neck swelling – jugular vein distension

Flat neck veins

Decreases in HCT, Serum Osmolality, Serum Sodium, Potassium, Chloride, Bicarbonate, BUN; Urine Specific Gravity < 1.005; Urine Osmolality >1,200 mOsm/kg

Increases in HCT, Serum Osmolality, Serum Sodium, Potassium, Chloride, Bicarbonate, BUN, Creatinine; Urine specific Gravity >1.030; Urine Osmolality < 50 mOsm/kg

Nursing Considerations

• Assess for headache, dizziness, syncope• CHF-SOB, dyspnea, activity intolerance• Maintaining accurate I & O• Daily weights• Monitoring Lab values• Frequency and consistency of stools• Meals include adequate fluid intake

Dehydration in the Elderly

Increased risks for dehydration:•Decrease in thirst•Lack of fluid replacement•Use of diuretic medications for high BP•Susceptibility to contagious diseases

Nursing Care Plan

Dehydration• Risk for imbalanced Fluid

Volume Related to excessive fluid loss/inability to take in fluids AEB ….

Overhydration• Risk for Imbalanced Fluid

Volume Related to excessive fluid intake/decreased urination AEB ….

Electrolytes

– Substance that develops an electrical charge when dissolved in water

• Cation - positive charged• Anion - negative charged• Examples of cations: Sodium, Potassium,

Magnesium, Calcium• Examples of anions: Chloride, Bicarbonate,

Phosphorous

SodiumNormal serum values

135-145 mEq/L• Most abundant cation in ECF• Functions

– ECF volume – water balance– Acid-base balance– Nerve impulse control – sodium potassium pump– Levels below 115 mEq/L – brain damage, seizures– Sodium is primarily excreted through the kidneys, but

other avenues are GI Secretions and sweat.

Sodium Deficit - Levels < 135 mEq/LHyponatremia

• Loss through GI tract, skin or kidneys• An increased amount of sodium shift into the

cells when there is a potassium deficit• An excessive ADH release (SIADH) causing

Water retention and sodium deficit• Inadequate sodium intake, increased water

intake• Excessive use of 5% dextrose solution• Levels below 115 mEq/L – brain damage

Pathophysiology of decreased sodium imbalances

• CNS – excess water moves into the cerebral tissues – increased intracranial pressure

• GI – loss causes acid base imbalances• Kidneys – renal dysfunction promotes sodium

and water retention resulting in diluted sodium level (fluid overload)

• Cellular activity - decrease in Na-K pump

Causes of Hyponatremia• Dietary changes – low sodium intake, excessive water

intake, “fad diets”/fasting, anorexia nervosa, prolonged use of IV D5W

• GI Losses – vomiting, diarrhea, GI Suctioning, Tap water enemas, GI surgery, Bulimia.

• Renal Loses – Salt wasting kidney disease, diuretics.• Hormonal Influences - ADH, SIADH.• Decreased adrenocortical hormone: Addison’s disease.• Altered Cellular Function – Hypervolemic state: heart

failure, cirrhosis • Burns• Skin

Sodium Excess - Levels > 145 mEq/LHypernatremia

• Excessive secretion of aldosterone or cortisol• Excessive sodium intake• Decreased water intake• GI disorders• Decreased renal function

Pathophysiology of increased sodium imbalances

• Overproduction of adrenal hormones – excessive secretions of aldosterone and cotrisol promote an increase in the sodium level

• Cellular activity – increases the sodium pump action, causes cellular irritability.

Causes of Hypernatremia• Dietary Changes – Increased sodium intake, decreased

water intake, Administration of 3% saline solutions• GI Disorders – severe vomiting, Diarrhea• Decreased Renal Function – reduced glomerular filtration• Environmental Changes – Increased temperature and

humidity, water loss• Hormonal Influence – Increased adrenocortical hormone

production: oral or IV cortisone or Cushing's syndrome. • Altered Cellular Function – Heart Failure, Renal Diseases• Trauma – Head injury

Clinical Manifestations of Sodium Imbalances

Hyponatremia• Nausea, vomiting, diarrhea,

abdominal cramps• Tachycardia, hypotension• Headaches, apprehension,

lethargy, confusion, depression, seizures

• Muscle weakness• Dry skin, pale dry mucus

membranes• Serum Na <135 mEq/L• Serum osmolality < 275 mOsm/kg• Urine Specific Gravity <1.005• Urine Sodium >220 mEq/day

Hypernatremia• Nausea, vomiting, anorexia• Rough, dry tongue• Tachycardia, possible hypertension• Restlessness, agitation, stupor,

elevated body temperature• Muscular twitching, tremor,

hyperreflexia• Flushed, dry skin and dry sticky

membranes• Serum Na >145 mEq/L• Serum osmolality > 295 mOsm/kg• Urine Specific Gravity >1.030• Urine Sodium < 40 mEq/day

Chloride Normal Levels95-108 mEq/L

• Primary extracellular anion• Creates electrical neutrality when combined with

sodium• Body Water Balance• Hydrochloric acid• Buffers carbonic acid• Anion gap - calculated AG = (Na + K) – (Cl + HC03

(metabolic acidosis)

Hypochloremia <95 mEq/L

• Causes– Loss of gastric fluid– Osmotic diuresis

• Manifestations– Reflects alkalosis– Paresthesias, muscle spasms, slow respirations– Dehydration

Hyperchloremia > 108 mEq/L

• Causes– Hyperparathyroidism, dehydration– Respiratory acidosis

• Manifestations– Lethargy, disorientation– Increased rate and depth of respirations

Chloride

• Primary extracellular anion• Creates electrical neutrality when combined

with sodium• Hydrochloric acid• Buffers carbonic acid• Anion gap - calculated AG = (Na + K) – (Cl +

HC03 (metabolic acidosis)

PotassiumNormal serum values

3.5- 5.0 mEq/L• Most abundant cation in ICF• Functions

– Transmission and conduction of nerve impulses and the contraction of skeletal, cardiac and smooth muscles (na-K pump)

– Assists with regulation intracellular osmolality– Enzyme production for cellular metabolism– Maintains Acid-base Balance– Levels less than 2.5 mEq/L and greater than 7.0 mEq/L can

cause cardiac arrest– Potassium is excreted through the kidneys (80-90%) and feces

(10-20%)

Potassium Deficit - Levels < 3.5 mEq/LHypokalemia causes

• Dietary changes – decrease in dietary intake• Cellular Potassium Loss – Tissue Injury, Muscle contraction• GI losses – vomiting, diarrhea, GI suctioning, intestinal

fistula, laxative abuse, bulimia, enemas• Hormonal Influences – Aldosterone (Cushing syndrome),

licorice, Stress• Drugs – adrenergic, epinephrine, decongestants,

amphotericin B, beta2 –adrenergic agonist, aminoglycosides, large doses of penicillins, potassium wasting diruetics, steroids

• Redistribution - Insulin, alkalotic states• Electrolyte loss - Magnesium

Potassium Excess - Levels > 5.0 mEq/LHyperkalemia causes

• Dietary – excessive intake, supplements, salt substitutes, herbal juices

• IV Potassium replacements – with poor renal function• Decreased renal function – acute and chronic renal

failure• Altered Cellular Function – injury, metabolic acidosis,

stored blood >1-3 weeks old• Hormonal Deficiency – Addison’s disease• Drugs – K-sparing diuretics, ACE inhibitors, beta blockers• Pseudohyperkalemia – poor blood samples

Clinical Manifestations of Potassium Imbalances

Hypokalemia

• GI – anorexia, N/V, diarrhea, abdominal distention, decreased peristalsis or ileus

• Cardiac – dysrhythmias, vertigo (dizziness), cardiac arrest

• ECG – Flat or inverted T waves, depressed ST

• Renal – polyuria• Neuromuscular – malaise,

drowsiness, muscular weakness, confusion, mental depression, diminished deep tendon reflexes, respiratory paralysis

• Lab Values - <3.5 mEq/L• Alkalosis

Hyperkalema

• GI – Nausea, Diarrhea, Abdominal Cramps

• Cardiac – tachycardia, then bradycardia and then cardiac arrest

• ECG - Peaked T waves, shortened QT interval, prolonged PR followed by a disappearance of the P wave, Prolonged QRS.

• Renal - oliguria or anuria• Neuromuscular – weakness,

numbness or tingling sensation, muscle cramps

• Lab Values - > 5.0 mEq/L• Acidosis

Hypokalemia – flattened, inverted T wave with a U wave sometimes present

Hyperkalemia – peaked T Wave

CLINICAL MANAGEMENT OF POTASSIUM IMBALANCES

Hypokalemia• Oral supplements (tablets, capsules,

liquid)– Oral potassium is very irritating to the

gastric mucosa and should be given diluted and not on an empty stomach

• IV Potassium DILUTED in an IV Solution– Never more than 10mEq of KCL per

hour– Never given undiluted as a bolus

injection– For life threatening hypokalemia (<2.6

mEq/L) 30-40 mEq of KCL can be diluted in 100 – 150 ml of IV Fluid and administered in a central line over an hour.

Hyperkalemia• Potassium Restriction• IV Sodium bicarbonate (NaHCO3)

– moves K back into the cells –temporary tx

• 10% Calcium gluconate – decreases irritability of myocardium, does

not promote K loss, use cautiously with patients on digitalis

• Insulin and glucose – (10 units of Insulin and 50% dextrose) – Moves K back into the cells

• Kayexalate (sodium polystyrene) and sorbitol 70%– Cation exchange

• Dialysis

Drugs that effect Potassium Balances

Hypokalemia• Laxatives and enemas• Corticosteroids• Antibiotics• Potassium-wasting diuretics• Beta2 agonists

Hyperkalemia• Oral and intravenous K• Central nervous system

agents• Potassium sparing diuretics• ACE inhibitors• Beta blockers• Heparin/Lovenox• NSAIDS

CalciumNormal serum values 8.5- 10.5 mg/dL Ionized

Calcium 4.0 – 5.0 mg/dL• Cation found in both ECF and ICF, but greater concentration in ECF• Maintains cellular membrane stability • 98% in bones and teeth, 2% in the serum• Of the 2% in serum - 45% is bound to albumin and 50% is ionized

calcium – physiologically active• Serum pH greatly affects calcium levels – metabolic acidosis

increases ionized calcium levels, alkalosis opposite effect• Normal ionized Ca levels are 4.0 to 5.0 mg/dL• Serum Ca levels are regulated by Vitamin D, calcitonin (thyroid glad)

and parathyroid hormone (PTH) from parathyroid gland• There is a direct relationship between Ca and Phosphorous, when Ca

is low Phosphorous is high and vise versa.

Calcium Regulation

When serum Calcium is low: When serum Calcium is High:• PARATHYROID GLAND

releases PTH. PTH mobilizes calcium from the bone, increases renal reabsorption of calcium and promotes calcium absorption in the intestines in the presence of Vitamin D to increase serum Calcium levels

• THYROID GLAND – releases Calcitonin. Calcitonin increases calcium return to the bone and decreases serum Calcium levels

Functions of Calcium• Neuromuscular

– normal nerve and muscle activity, causes transmission of nerve impulses and contraction of skeletal muscles.

• Cardiac– contraction of the myocardium (heart muscle)

• Cellular and Blood– maintenance of normal cellular permeability - decreased calcium

increases cellular permeability– Coagulation of blood. Promotes clotting by converting prothrombin

into thrombin• Bone and teeth construction

– Calcium along with phosphorous forms bones and teeth make them strong and durable

Calcium Deficit - Levels < 8.5 mg/dL and Ionized Ca is <4.0 mg/dL

Hypocalemia causes• Dietary changes – lack of calcium intake (rare), inadequate

Vitamin D, inadequate protein intake, hypoalbuminemia*, chronic diarrhea

• Hormone and electrolyte influence – decreased PTH (thyroid surgeries), increased serum phosphorous, decreased magnesium

• Calcium Binders or Chelators - citrated blood transfusions• Alkalosis• Increased serum albumin* (low ionized Ca)• Renal Failure – decreases phosphorous excretion and results in

excessive Ca Loss• GI Surgery, Pancreatitis and Small Bowel disease

Calcium Excess - Levels >10.5 mg/dL and Ionized Ca is >5.0 mg/dL

Hypercalemia causes• Primary hyperparathyroidism • Bone malignancy, fractures and immobility• Drug toxicity (lithium carbonate, vitamin a and d,

thiazides)• Excessive use of calcium supplements, anti-acids and

calcium salts• Renal Impairment and diuretics (thiazides)• Steroid therapy• Decreased serum phosphorous

Clinical Manifestations of Calcium Imbalances

HYPOCALCEMIA

• CNS and Muscular– Anxiety, irritability– Tetany, muscle twitching (Chvostek’s sign)– Numbness and tingling– Carpopedal spasm (Trousseau’s sign)– Convulsions– Abdominal and muscle cramps

• Cardiac – Weak contractions– ECG/EKG lengthened ST segment and

prolonged QT interval

• Blood – reduction in prothrombin (reduced

clotting)

• Bone– With prolonged deficiency – fractures

occur easily

HYPERCALCEMIA• CNS and Muscular

– Depression/apathy– Weak, flabby muscles

• Cardiac – Signs of heart block– Cardiac arrest in systole– Decreased or diminished ST segment

and shortened QT interval

• Bone– Pathologic fracture– Deep pain over bony areas– Thinning of bones

• Renal– Flank pain– Calcium stones in kidney

Important Clinical tests for Hypocalemia

Chvotsek’s Sign• https://www.youtube.com/

watch?v=ep6IEqnyxJU

Trousseau’s Sign• https://www.youtube.com/

watch?v=H13yn9AwtPY&feature=relmfu

ECG changes with Calcium Imbalances

• Normal ST segment and QT Interval

• Hypocalcemia – ST segment is lengthened, QT interval is prolonged

• Hypercalcemia – ST segment is shortened, QT interval is shortened

Clinical Management of Calcium Imbalances

Hypocalcemia• Oral supplements and IV

calcium diluted in D5W (not normal saline)– IV calcium should be given

slowly at 1-3ml/min

• Vitamin D supplements

Hypercalcemia• Treat underlying cause• IV Normal Saline • Loop Diuretics• Calcitonin SQ• IV phosphates• Others:

– Corticosteroids– Antitumor antibiotics

MAGNESIUMNormal serum values

1.4- 2.1 mg/dL• Intracellular Cation (2nd most)• Only 1% of body magnesium is in the blood serum the rest is stored in

muscle and bone• Of the 1% - 2/3 is ionized (free) and 1/3 is bound to plasma proteins• When calcium absorption goes up magnesium absorption goes down• Alcohol decreases magnesium absorption• Many of the same foods rich in potassium and also rich in magnesium

(green vegetable, whole grains, fish, seafood and nuts). • Mg deficiency is usually asymptomatic until <1.0 mg/dL

Functions of Magnesium

• Neuromuscular activity transmission• Contracts the heart muscle• Cellular

– Activates enzymes for carbohydrate and protein metabolism

– Responsible for proper transportation of sodium and potassium across cell membranes

– Influences utilization of K, Ca, and proteins– Magnesium deficits are FREQUENTLY accompanied by a

Potassium and/or Calcium deficit

Magnesium deficit < 1.4 mg/dLHypomagnesemia Causes

• Dietary – inadequate intake, mal absorption, GI losses, TPN, malnutrition, starvation, chronic alcoholism, GI fistulas, chronic use of laxatives, chronic diarrhea

• Renal Dysfunction – diuresis in diabetic ketoacidosis and in ARF in the diuretic phase

• Cardiac dysfunction – post MI, prolonged diuretic therapy with CHF

• Electrolyte and Acid/Base Influences – hypocalcemia, hypokacemia, metabolic alkalosis

• Drug influence – potassium wasting diuretics, aminoglycosides, cortisone, amphotericin B, digitalis

Magnesium excess > 2.1 mg/dLHypermagnesemia Causes

• Dietary – prolonged use/excessive use of magnesium-containing anta-acids (Maalox), laxatives (MOM) and IV magnesium sulfate

• Renal Dysfunction – Renal insufficiency and failure

• Severe Dehydration – Diabetic ketoacidosis

Clinical Manifestations of Magnesium Imbalances

Hypomagnesemia• Neuromuscular –

hyperirritability, tetany-like symptoms, tremors, twitching of the face, spasticity, increased tendon reflexes

• Cardiac – Hypertension, cardiac dysrhythmias - PVC’s, VT (Torsades), VF, and flat or inverted T wave, ST depression (like low K levels)

Hypermagnesemia• Neuromuscular – CNS

depression, lethargy, drowsiness, weakness, paralysis, loss of deep tendon reflexes

• Hypotension, Complete heart block (3rd degree), bradycardia, Widened QRS complex, prolonged QT interval

• Others: Flushing, respiratory depression

Hypomagnesemia

Clinical Management of Magnesium Imbalances

Hypomagnesemia• Oral or IV replacements• Diet high in magnesium -

green vegetables, whole grains, legumes, nuts

Hypermagnesemia• Correct the underlying

cause• IV saline or calcium• Dialysis

Phosphorous Normal levels

2.5 – 4.5 mg/dL• Major Intracellular anion• Needed for metabolism, nerve and muscle function• Part of energy units• Component of phospholipids (cellular and organelle

membranes)• Regulated by calcitonin, parathyroid hormone AND

Vitamin D• Levels vary with acid-base balance• Glucose, insulin or sugar-containing foods

temporarily shift phosphorous into the cells

Functions of Phosphorous

• Neuromuscular – normal nerve and muscle activity• Bones and teeth – bone and teeth formation,

strength and durability• Cellular

– forms high energy compounds (ATP, ADP, AMP), is the backbone of nucleic acids and stores metabolic energy

– Formation of red blood cell enzyme (2,3-diphosphoglycerate) that delivers oxygen to tissues

– Utilization of B vitamins– Metabolism of fats, carbohydrates and proteins– Maintenance of ACID BASE balance in body fluids

Phosphorous deficit < 2.5 mg/dLHypophosphatemia Causes

• Dietary - Vitamin D deficiency, chronic alcoholism TPN

• GI – malabsorption, vomiting, diarrhea• Hormonal Influence – Hyperparathyroidism

(increased PTH) • Drugs – aluminum containing antacids (binders),

diuretics• Cellular – Diabetic Ketoacidosis• Acid-Base disorders – Respiratory alkalosis,

metabolic alkalosis

Phosphorous excess > 4.5 mg/dLHyperphosphatemia Causes

• Dietary – excessive administration of phosphorous containing substances

• Hormonal – lack of PTH• Renal Insufficiencies – Renal Failure (ARF, CRF)• Drug – frequent use of phosphate laxatives• Cellular destruction – chemo, radiation,

rhabdomyolsis (breakdown of striated muscle)• Acid-Base disorders – Metabolic and Respiratory

Acidosis

Clinical Manifestations of Phosphorous Imbalances

Hypophosphatemia• Neuromuscular – muscle

weakness, tremors, paresthesia, bone pain, hyporeflexia, seizures, delirium, hallucinations, ascending motor paralysis

• Hematologic – tissue hypoxia, possible bleeding, possible infection

• Cardiopulmonary – weak pulse, hyperventilation, respiratory weakness

• GI – Anorexia, dysphagia

Hyperphosphatemia• Neuromuscular – Tetany (with

decreased calcium), hyperreflexia, muscular weakness (more common with hypophosphatemia), flaccid paralysis

• Cardiopulmonary – tachycardia

• GI- nausea, diarrhea, abdominal cramps

Clinical Management of Phosphorous Imbalances

Hypophosphatemia• Oral phosphorous

replacements• Treat underlying causes • Diet high in phosphorous• Avoid phosphorous binding

antacids• IV phosphorous (only when

levels are below 1 mg/dl) dose 12-15 mmol/L diluted in IV fluid

Hyperphosphatemia• Phosphorous binding antacids• Calcium based antacids are

preferred in renal failure to avoid hypermagnesemia

• If hyperphosphatemia is accompanied by hypocalcemia correcting calcium level will reduce phosphorous levels

• Administer Insulin and glucose

ACID BASE IMBALANCES

NURS 2140Winter 2012

Teresa Champion, RN, MSN

ACID BASE BALANCE

• Hydrogen ions - Low concentrations but highly reactive– Concentration affects physiological functions, for

example: • Alters protein and enzyme functioning• Can cause cardiac, renal, respiratory abnormalities• Alters blood clotting, metabolization of meds

Acid and Bases

• Acids – compounds that form hydrogen ion in a solution– Proton donors– Strong acids give up their hydrogen ion easily– Weak acids hold on to their hydrogen ion more tightly

• Bases – compounds that combine with hydrogen ion in a solution– Proton acceptors– Neutralizes

• 20:1 ratio (20 parts bicarbonate to one part carbonic acid)

The Basics explained:

• 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.– The fewer H+ present, the higher the pH will be.

Plasma pH

• Inversely related to hydrogen ion concentration– ↑ hydrogen ion concentration, ↓ pH– ↓ hydrogen ion concentration, ↑ pH

Body Acids

• Respiratory Acid - CO2 – eliminated by lungs (daily ~288L/day)

• Metabolic acids: (either excreted by kidney or metabolized in liver and Production: 0.1 mol (100 mEq)/day. Eliminated more slowly than respiratory acid – Lactic acids– Pyruvic acid– Ketoacids (DKA)– Acetoatic acids– Beta-hydrobutyric acids

Normal Blood pH

• The normal blood pH range is 7.35 to 7.45. – Slightly alkalotic– Must maintain this range for normal body

functions• < 7.35 Blood pH is acidotic• > 7.45 blood pH is alkalotic• This is the FIRST step in interpretation of

Arterial Blood Gases and plasma pH.

BUFFER SYSTEMS• Extracellular Buffers

– carbonic acid (lungs) and bicarbonate (kidneys)• Intracellular Buffers

– Phosphate Buffer System• Dihydrogen phosphate (H2PO4) – hydrogen donor• Hydrogen phosphate (HPO4) – hydrogen acceptor

• Protein Buffers– Plasma Proteins– Hemoglobin – oxyhemoglobin and deoxygenated Hgb

• Bones– Carbonate and phosphate salts in bone provide a long

term supply of buffer.

Role of the lungs

• Regulate plasma pH minute to minute by regulating the level of Carbon Dioxide (CO2)

• Carbon Dioxide is measured as a partial pressure of carbon dioxide in arterial blood – PaCO2 35-45mmHg

• Lungs alter rate and depth of ventilations in order to retain or excrete CO2

Minute Volume – Tidal Volume• Ventilation is measured by how much air the lungs

move in one minute (minute ventilation)• Minute Ventilation is the product of respiratory rate

and depth and is referred to as the TIDAL VOLUME (Vt)

• NORMAL tidal volume at rest is about 500ml. • Aveolar volume = tidal volume – anatomical dead

space• Aveolar minute ventilation = respiratory rate x

alveolar volume

Terms for Respiration

• Hypercarbic Drive – increased PaCO2 levels raise the level of H+ ions, lowering pH. Central Chemorectptors (in CNS) stimulate the phrenic nerve, increasing respiration

• Hypoxic Drive – peripheral chemoreceptors in carotid arteries and arch of aorta are stimulated by low PaO2 level (<60mmHg) increasing respiratory rate.

• Hypocapnia – Low PaCO2 (<35)• Hypercapnia – High PaCO2 (>45)

The role of the Kidneys• Two main functions to maintain acid/base

– Secrete hydrogen ions– Restore or reclaim bicarbonate

• Secretion – active process of moving substances from blood into the tubular fluid against a concentrated gradient, for example hydrogen ions.

• In high metabolic acidosis, the kidneys can excrete ammonia as a urinary buffer.

• In alkalosis - the kidneys retain hydrogen ion and excrete bicarbonate to correct the pH.

• In acidosis - the kidneys excrete hydrogen ion and conserve bicarbonate to correct the pH.

Assessment of ACID BASE

• Arterial Blood Gases (ABG) most often and the most accurate to assess acid base balances.

• Serum Electrolytes can help fine tune acid base analysis

• NORMAL ABG VALUES:• pH = 7.35 to 7.45• PaCO2 = 35 – 45 mEq/L (7.40 mEq/L – middle range)• HCO3 = 22 – 28 mEq/L

Steps to Interpret ABG’s

1. Assess the pH2. Assess the respiratory component – PaCO23. Assess the metabolic component – HCO3,

base excess4. Evaluate compensation

Respiratory Acidosis

• High PaCo2 (>45 mEq/L) with resultant drop in in pH (<7.35 - acid)

• Respiratory system fails to eliminate the appropriate amount of carbon dioxide to maintain the normal acid-base balance

• Caused by pneumonia, drug overdose, head injury, chest wall injury, obesity, asphyxiation, drowning, or acute respiratory failure

• Medical treatment– Improve ventilation, which restores partial pressure

of carbon dioxide in arterial blood (Paco2) to normal

Respiratory Acidosis

• Nursing care– Assess Paco2 levels in the arterial blood, and pH.– Observe for signs of respiratory distress:

restlessness, anxiety, confusion, tachycardia• Intervention

– Encourage fluid intake – Position patients with head elevated 30 degrees

Respiratory Alkalosis• Low PaCO2 (< 35 mEq/L) with a resultant rise in pH (>7.45 –

alkalotic)– Most common cause of respiratory alkalosis is hyperventilation –

usually caused by pain, anxiety• Medical treatment

• Major goal of therapy: treat underlying cause of condition; sedation may be ordered for the anxious patient

• Nursing care– Intervention

• In addition to giving sedatives as ordered, reassure the patient to relieve anxiety

• Encourage patient to breathe slowly, which will retain carbon dioxide in the body

Metabolic Acidosis

• Body retains too many hydrogen ions or loses too many bicarbonate ions; with too much acid and too little base, blood pH falls (pH <7.35)

• Causes are starvation, dehydration, diarrhea, shock, renal failure, and diabetic ketoacidosis

• Signs and symptoms: changing levels of consciousness, headache, vomiting and diarrhea, anorexia, muscle weakness, cardiac dysrhythmias

• Medical treatment: treat the underlying disorder

Metabolic Acidosis cont’d

• Nursing care– Assessment of the patient in metabolic acidosis

should focus on vital signs, mental status, and neurologic status

– Emergency measures to restore acid-base balance. Administer drugs and intravenous fluids as prescribed. Reassure and orient confused patients

Metabolic Alkalosis

• Increase in bicarbonate levels or a loss of hydrogen ions and increases pH (>7.45)

• Causes:– Loss of hydrogen ions may be from prolonged nasogastric

suctioning, excessive vomiting, diuretics, and electrolyte disturbances

• Signs and symptoms:– headache; irritability; lethargy; changes in level of

consciousness; confusion; changes in heart rate; slow, shallow respirations with periods of apnea; nausea and vomiting; hyperactive reflexes; and numbness of the extremities

• Medical treatment– Depends on the underlying cause and severity of the

condition

Metabolic Alkalosis

• Nursing care – Assessment

• Take vital signs and daily weight; monitor heart rate, respirations, and fluid gains and losses

• Keep accurate intake and output records, including the amount of fluid removed by suction

• Assess motor function and sensation in the extremities; monitor laboratory values, especially pH and serum bicarbonate levels

• Intervention– To prevent metabolic alkalosis, use isotonic saline solutions

rather than water for irrigating nasogastric tubes because the use of water for irrigation can result in a loss of electrolytes

Infusion Therapy

NURS 2140Winter 2012

Teresa Champion, RN, MSN

Infusion Therapy

• PARENTAL – the Gastrointestinal route (alimentary route) is by-passed. –Medications and solutions are

delivered by Intravenous (IV) routes –Non-vascular routes - (i.e. -

Subcutaneous (SQ), Intramuscular (IM), Intraosseous (IO), Intraspinal, or Intrathecal routes.

Vascular Access Device (VAD)

• Device or catheter introduced through the skin and into the vascular network.– Peripheral Vascular Access Devices (PVAD)

• Inserted in upper extremities and/or lower extremities (per policy) – peripheral vasculature

– Central Vascular Access Devices (CVAD)• Inserted into a Centrally or Peripherally Located Vein with

the tip residing in the vena cava

Vascular Access Devices (VAD)

• Terminology– Bevel – the slant or angle at the end of the needle

• Insertion is Bevel up – facilitates puncture and cannulation of the vascular lumen.

– Flashback chamber – small space in the hub of the stylet that allows confirmation of the presence of blood and indicated access to the vascular lumen

– Self-sheathing stylet - the needle to becomes encased in a protective chamber upon removal (Needle stick Safety and Prevention Act of 2000)

Images of IV Catheters

Needle Stick Prevention

Types of Peripheral Access Devices

• Winged Steel • Over-the-needle Peripheral Short Catheters• Through-the-needle Peripheral Short Catheters• Midline Catheters

Peripheral Vascular Access Devices (PVAD) –Peripheral-Short Catheters

• Most - < 7.5 cm (3.5 inches) in length and Gauge (needle size) 25 (smallest) to 10 gauge (largest).

• Locations of insertion and length of insertion time:– Inserted in upper extremities mostly (lower extremities

- per policy) of adults patients.– Pediatric patients – insertions are upper extremities,

occipital, superficial temporal, posterior auricular(ear) and saphenous veins.

– Dwell times are 72 to 96 hours, in most cases.

Short Catheter Sizes

Common Peripheral IV Stick Sites

Winged Steel Infusion Set

• Winged Steel – flexible plastic attachments “wings” that extend from either side of the steel needle to facilitate insertion. – Length – 3/8 to 1.5 inches– Gauges – 19 to 27 gauge

• Attached to the needle is plastic tubing extending from several inches to 12 inches with an adaptor attachment on the end for infusion administration equipment.

• Now manufactured with safety sheaths.• Complications – infiltration - due to needle rigidity• Temporary / short term infusions < 4hours – supportive

devices – arm boards/splints

Figure 22.2 Winged steel infusion set. Winged safety steel

infusion set.

Over-the-needle and Through-the-needle Peripheral Short Catheters

• OVER-THE-NEEDLE – MOST COMMON– Hollow bore needle (stylet) – inserted through the

lumen of a flexible catheter – needle (stylet) is then withdrawn as the flexible catheter is advanced forward into the vein

• THROUGH-THE-NEEDLE– Allows passage of a catheter through a steel

introducer – introducer needle is then withdrawn from the vessel lumen-and then protected by a cover or sleeve to prevent sheering or patient injury

Through-the-needle short catheterComplication-catheter shearing

Peripheral VAD - Midline• Peripherally inserted but is approximately 7.5 cm to 20 cm (3.1

inches to 8.0 inches)• Longer dwell periods but not to exceed 4 weeks• Insertion sites –

– Adults - antecubital fossa– Pediatrics – antecubital fossa, saphenous, posterior auricular (ear)

superficial temporal• Distal tip – dwells in basilic, cephalic, or brachial veins – level with

the axilla and distal to the shoulder• Inserted using an introducer-once vein is canulated the needle

(stylet) is withdrawn and the midline catheter is threaded though the introducer –then introducer is peeled apart or separated and withdrawn.

• Therapies for midlines-restricted to pH 5-9, osmolarities of <500mOsm/L

Peripheral IV Catheter Insertion/Removal

• RN’s, LPN-C – trained in IV insertion using standard precautions and aseptic technique, RN’s only may be specially trained to insert midlines.

• RN’s. LPN-C and LPN – trained in IV removal using standard precautions and aseptic technique

• Assess/observe for phlebitis, drainage-apply sterile dressing till hemostasis is observed.

• Inspect cannula, for midline – length of catheter should be measured and be same length as insertion.

CENTRAL VASCULAR ACCESS DEVICE (CVAD)

• Catheter inserted into a centrally located vein with the tip in residing in the vena cava.

• Tip in vena cave must be confirmed with radiologic examination (X-Ray)

• Three major CVAD Categories– Nontunneled and noncuffed– Tunneled and cuffed– Implanted Ports

Nontunneled and Noncuffed CVAD• Inserted percutaneuosly via direct skin puncture with passage

of catheter into the vasculature.• Single or multiple lumens • Indentified by insertion site (i.e. – Subclavian, Jugular, Femoral)• Inserted by physicians or advanced practice clinicians who are

skilled and competent to perform procedure (certified)• Insertion requires – sterile technique and maximum barrier

precautions• Complications – pneumothorax, air embolism, arrhythmias• Once inserted secured – sutures, stat locks• Catheters are not tunneled under the skin – less dwell times

than tunneled • Examples – TRIPLE LUMEN NONCUFFED (ARROW), PICC LINES

Removal of Nontunneled and Noncuffed CVAD’s (including PICC)

• May be done by a nurse skilled and education in the procedure

• Standard precaution and aseptic technique• Recumbent position (preferred) • Removal of occlusive dressing and securing devices• Instruct Patient to perform the valsalva maneuver -

to prevent air from entering – causing air embolism• Pressure is applied 30 minutes to achieve hemostasis

and sterile occlusive dressing applied• Post removal catheter length measured and

compared to insertion length (same)

Nontunneled noncuffed CVP – Triple Lumen (Arrow)

Peripherally Inserted Central Catheter (PICC)

• Nontunneled and non cuffed• Long-term catheter – several weeks to one year.• Therapies with extreme variations in solution pH (>5 and < 9) and

osmolarities >600 mOsm/L with irritant and Vesicant properties• Therapies – Total Parental Nutrition (TPN), Antineoplastic, Anti-

infective and Inotropic• Radiologic confirmation (X-Ray) required for tip location – vena

cava• Complications – device fracture, tip malposition, device

occlusion, thrombus formation• Removal – same as central insertion central venous access

devices

PICC vs. Midline

Tunneled and Cuffed CVAD

• Cuff – piece of the catheter for stabilization and reduces migration of organisms

• Anti-thombogenic catheters• Tunneled under the skin – reduces infection risk• Inserted in surgical or radiologic suite• Inserted by physicians, surgeons, vascular surgeons and

advanced practice clinicians trained in procedure• Long term therapies• Single or multi-lumens• Examples: Broviac, Hickman, Raaf, Groshong

Implanted Ports• Long term – chronic therapies• Chambered device, double or single reservoirs with an attached

single or double lumen catheter• Catheter tip dwells in a designated structure depending on

therapy – could be vascular or non-vascular (CVAD PORTS – Vena Cava)

• Inserted by physicians, surgeons, vascular surgeons and advanced practice clinicians trained in procedure in a surgical or radiological suite

• The septum is the access point-damage to the septum could cause air embolism, infiltration, extravasion, infection

• Access of septum of port requires a noncoring (Huber needle) needle with opening on the side and preventing coring of the septum

• Therapies – antineoplastics, inotropics, TPN, Antibiotics

Additional Info on VAD’s• Tunneled and cuffed and Implanted port removal

only by physicians, advanced clinicians trained in procedure and not included in the scope of practice for nurses

• CVP – Central Venous Pressure Monitoring on CVAD

• CVAD – Lines flushed and patency checked q shift with 10ml of Normal Saline (Heparin per institution) whereas PVAD’s are flushed and checked for patency q shift with 3-5 ml Normal Saline.

SPECIALIZED INFUSION CATHETERS

• Hemodynamic Monitoring – Swan Ganz• Dialysis and Pheresis Catheters• Arterial – Venous Shunts• Arterial Catheters• Hepatic Artery Catheters

Swan-Ganz Catheter• Exclusively for cardiac monitoring and

hemodynamic analysis• Used to measure

– Central Venous Pressure (CVP)– Pulmonary Artery Pressure (PA) – Cardiac Output (CO)– Pulmonary Artery Wedge Pressure (PAWP)– Temporary Pacing– Parental Therapy Administrations

Swan-Ganz Catheter

Hemodialsys and Pheresis Catheters

• RARELY considered for infusions• Used for procedures using large amounts of blood –

Dialysis, Plasmapheresis, Aquapheresis• Dialysis Catheters – temporary till a shunt can be placed• Catheters are large (12 to 16 G) for blood to flow in both

directions on dialysis or pheresis machine, dwell in the vena cava

• Surgical Placement – OR, Radiological suite or at bedside by vascular or general surgeon or advanced practice clinician trained in procedure

• Examples – Quinton, Hohn, Tesio, Perma-Cath, and Trialysis* *(Trialysis-can be used for infusions)

Dialysis and Pheresis Catheters

Arterial-Venous Shunts• Anastomose venous and arterial structures• Arm – radial and cephalic and brachial veins• Dialysis or large blood volume exchanges• Accessed with large bore needle• Can be used for other infusion- rare• Patency assessed by auscultation bruit and palpating

vibration • No IV sticks, phlebotomy or Blood Pressure on Arm

with AV Shunt• If AV shunt is damaged – only surgical repair or

replacement is the option

AV Shunt and AV Graft

Arterial Catheters

• Used for ONLY two reasons:– Invasive Blood Pressure Monitoring– Blood Draws

• Catheters are made of stiff polyurethane material to withstand the high pressure of the artery and blood pressure monitoring attached to pressure transducers and monitor, and to limiting kinking of line.

• Inserted in Radial or Femoral Arteries • Inserted by physician or advanced practice clinician

in OR, or Radiological suite or at bedside.

Arterial Catheter

Hepatic Artery Catheters

• Specialized Catheter Inserted in Hepatic Artery • Only for regional anti-neoplastic therapy for

Liver Cancer Patients

Hepatic Artery Catheter

NONVASCULAR ACCESS DEVICES

• Subcutaneous Infusion Therapy• Intraosseous Therapy• Intraspinal Catheters• Intrathecal Therapy

Subcutaneous Infusion Therapy• Hypodermoclysis – infusing large amounts of isotonic solutions in the

subcutaneous to be absorbed• Continuous Subcutaneous Infusion – infusing small amounts of

medications like pain medications and insulin• Use very small gages of 25-27G and only ½ inch in length• Needle attached to a adhesive disk of may appear as a winged steel

infusion set• May be inserted by a nurse in locations of adequate subcutaneous

tissue• Site is prepared with antiseptic agent, allowed to dry and then

aspirated to confirm absence of blood• Device is then secured with sterile dressing• Complications – localized skin irritation, erythemia, itching, infection

and dislodgement of device

Subcutaneous Infusion Pump

Intraosseous therapy

• Insertion of hollow bore needle into the bone accessing the marrow space

• Screws into long bones of the leg, iliac crest or sternum

• Allows for rapid infusions of large volumes of fluids• Complications – bone fracture, infiltration,

osteomyelitis, cellulitis, occlusions, or needle breakage

• Ideal for patients with difficult venous access• Being used more by EMT, Paramedics

INTRAOSSEOUS

Intraspinal Catheters• Catheters inserted within the spinal spaces – epidural and intrathecal• Delivery of anesthesia and infusions• Diagnostic testing • 22 to 26 Gauge, 10 to 30 inches in length• Catheter inserted percutaneously or tunneled• Infusates, drugs and diluents must be preservative free due to

neurotoxic effects• Epidural space usually cannot accommodate infusion rates greater

15ml/min• Cross the dura mater and have direct effect on the CNS• Complications: malposition and infection• Sterile technique required• Usually inserted by anesthesiology or neurology

Intrathecal Therapy

• Administration of medications directly into the Cerebral Spinal Fluid via an implanted reservoir

• Catheter dwells (terminates) in the ventricular space of the cerebrum

• Ommaya Reservoir – Delivers preservative free opioids– Antineoplastics – Measures CSF pressures– Drains excess CSF– Obtaining CSF samples for Lab– Surgically places via burr hole in the skull and skin secured

over the device– Standard precautions and sterile technique

INFUSION DELIVERYFluid Containers

• Glass– Can be heavy– Requires venting– Accurate to measure

• Plastic– Portable, easy to store, inexpensive– Flexibility may cause volume and dosage

administration to vary

Administration Sets

• The tubing that delivers fluid from the container to the catheter

• Primary set = main tubing • Secondary set = tubing that attaches to the

primary set (piggy backed on the primary set)• Metered-Volume Chambered Set – neonates

and pediatric patients and critical care units for close observation and monitoring with fluid control issues

Primary set with Secondary (Piggy back Set)

Add On Devices

– Flow-control device – controls flow when used with gravity IV set

– Stopcocks – manually directs flow– Extension sets – adds length to tubing, provides

additional stopcocks, access sites– Multi-flow adaptors and Y sets – multiple access

on one catheter– Injection ports, caps or hub – sites for IV catheter

access – Filters – remove particulate, precipitate

ADD ON DEVICESFlow Control Device Stopcock

Add On Devices

Extension Set Multiflow Adaptor

Odd On Devices

Injection Port or Cap Filter

INFUSION DELIVERY DEVICES

• Mechanical infusion devices (MIDs)– Do not require an external power source to operate– Elastomeric Balloons (On Q)– Spring coil containers– Spring Coil Syringes

• Electronic infusion devices (EIDs)– Do require an external power source– Two types: pumps (positive pressure) and controllers

(gravity and drop sensors attached to drip chamber)

Positive Pressure Infusion Pumps• Pressure to overcome vascular resistance• Strict monitoring of medications, fluids• Accurate delivery• PUMP TERMS:

– RATE (R) – amount of ml/hr– Volume to be infused (VTBI) – volume of infusion– Volume Infused (VI) – volume that has already been infused

(Used when calculation I&O)• Alarms:

– AIR IN LINE– OCCLUSION (patient side or pump side)– INFUSION COMPLETE– FREE FLOW– OTHER – LOW BATTERY, DOOR OPEN, PUMP Malfunction

Patient Controlled Analgesia Pumps (PCA)

• Delivers analgesia medications continuously (basal rate)

• Delivers analgesia bolus on patient demand (PCA Mode)

• Time lockout and Maximum Dose settings for safety

IV SKILLS FOR NURSES

• Nursing skills: – Basic competencies – Clinical skill validation – Policies and procedures – regulatory and non-

regulatory agencies• Nurses must be knowledgeable about the

properties of drugs and solutions ordered by the prescriber

• Compatibilities• Rates of Administration

Infusion Practices

• Flow rate determination is used to calculate the amount of fluid to be delivered over a specific time period (Calculation: flow rate x gtt factor / 60 (time in minutes) for gravity sets.

• Safe nursing practices when calculations are consistently applied result in: – Fewer medication errors– Increased patient safety– Positive infusion outcomes

• Smart Pumps – does calculations and keeps a drug library

Infusion Therapy Orders

• Nurses obtain orders from a health care provider to initiate and discontinue infusion therapy. An order includes: – Type of medication or solution– Dose– Volume to be infused– Duration of therapy– Frequency, rate, and route of administration – Five rights

Informed Consent

• An informed consent must be obtained from the patient

• The nurse provides the patient with accurate and complete information: – Description of the procedure– Potential benefits of such a device– Possible risks associated with the procedure – Available alternatives

Infusion Documentation

• Accurate documentation describes the care rendered and the patient’s response

• It facilitates monitoring care and tracking outcomes

Managing Infusion Complications

Complication categories: • Local complications: Bruising, Infiltration,

Extravasation, Phlebitis, Thrombosis, Infection, Occlusion

• Systemic complications: Air embolism, Catheter embolism, Pulmonary edema, Septicemia, Allergic reactions, Needle stick complications