Acid-base

FLUIDS AND ELECTROLYTES ACID-BASE BALANCE

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Body Water Content  Infants have low body fat, low bone mass, and are 73% or more water  Total water content declines throughout life  Healthy males are about 60% water; healthy females are around 50%  This difference reflects females’:  Higher body fat  Smaller amount of skeletal muscle  In old age, only about 45% of body weight is water Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Fluid Compartments  Water occupies two main fluid compartments  Intracellular fluid (ICF) – about two thirds by volume, contained in cells  Extracellular fluid (ECF) – consists of two major subdivisions  Plasma – the fluid portion of the blood  Interstitial fluid (IF) – fluid in spaces between cells  Other ECF – lymph, cerebrospinal fluid, eye humors, synovial fluid, serous fluid, and gastrointestinal secretions

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Fluid Compartments

Figure 26.1 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

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Composition of Body Fluids  Water is the universal solvent  Solutes are broadly classified into:  Electrolytes – inorganic salts, all acids and bases, and some proteins  Nonelectrolytes – examples include glucose, lipids, creatinine, and urea  Electrolytes have greater osmotic power than nonelectrolytes  Water moves according to osmotic gradients Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Electrolyte Concentration  Expressed in milliequivalents per liter (mEq/L), a measure of the number of electrical charges in one liter of solution  mEq/L = (concentration of ion in [mg/L]/the atomic weight of ion) × number of electrical charges on one ion  For single charged ions, 1 mEq = 1 mOsm  For bivalent ions, 1 mEq = 1/2 mOsm

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CELLS AND TONICITY

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FLUID& ELECTROLYTE TRANSPORT

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FLUID& ELECTROLYTE TRANSPORT

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Extracellular and Intracellular Fluids  Each fluid compartment of the body has a distinctive pattern of electrolytes  Extracellular fluids are similar (except for the high protein content of plasma)  Sodium is the chief cation  Chloride is the major anion  Intracellular fluids have low sodium and chloride  Potassium is the chief cation  Phosphate is the chief anion Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Extracellular and Intracellular Fluids

 Sodium and potassium concentrations in extraand intracellular fluids are nearly opposites  This reflects the activity of cellular ATPdependent sodium-potassium pumps  Electrolytes determine the chemical and physical reactions of fluids

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Extracellular and Intracellular Fluids

 Proteins, phospholipids, cholesterol, and neutral fats account for:  90% of the mass of solutes in plasma  60% of the mass of solutes in interstitial fluid  97% of the mass of solutes in the intracellular compartment

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Electrolyte Composition of Body Fluids

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Figure 26.2

Fluid Movement Among Compartments  Compartmental exchange is regulated by osmotic and hydrostatic pressures  Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream  Exchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranes  Two-way water flow is substantial Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Extracellular and Intracellular Fluids  Ion fluxes are restricted and move selectively by active transport  Nutrients, respiratory gases, and wastes move unidirectionally  Osmolalities of all body fluids are equal; changes in solute concentrations are quickly followed by osmotic changes

PLAY

InterActive Physiology®: Fluid, Electrolyte, and Acid/Base Balance: Introduction to Body Fluids

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Continuous Mixing of Body Fluids

Figure 26.3 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Water Balance and ECF Osmolality

 To remain properly hydrated, water intake must equal water output  Water intake sources  Ingested fluid (60%) and solid food (30%)  Metabolic water or water of oxidation (10%)

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Normal I and O (insert here)

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Water Balance and ECF Osmolality

 Water output  Urine (60%) and feces (4%)  Insensible losses (28%), sweat (8%)  Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH)

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Water Intake and Output

Figure 26.4 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Water Intake

 The hypothalamic thirst center is stimulated:  By a decline in plasma volume of 10%–15%  By increases in plasma osmolality of 1–2%  Via baroreceptor input, angiotensin II, and other stimuli

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Regulation of Water Intake

 Thirst is quenched as soon as we begin to drink water  Feedback signals that inhibit the thirst centers include:  Moistening of the mucosa of the mouth and throat  Activation of stomach and intestinal stretch receptors Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Water Intake: Thirst Mechanism

Figure 26.5 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Insert angiotensin-aldosterone system

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Insert ADH regulation here

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Regulation of Water Output  Obligatory water losses include:  Insensible water losses from lungs and skin  Water that accompanies undigested food residues in feces  Obligatory water loss reflects the fact that:  Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasis  Urine solutes must be flushed out of the body in water Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Influence and Regulation of ADH  Water reabsorption in collecting ducts is proportional to ADH release  Low ADH levels produce dilute urine and reduced volume of body fluids  High ADH levels produce concentrated urine  Hypothalamic osmoreceptors trigger or inhibit ADH release  Factors that specifically trigger ADH release include prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns

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Mechanisms and Consequences of ADH Release

Figure 26.6 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Disorders of Water Balance: Dehydration  Water loss exceeds water intake and the body is in negative fluid balance  Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuse  Signs and symptoms: cottonmouth, thirst, dry flushed skin, and oliguria  Prolonged dehydration may lead to weight loss, fever, and mental confusion  Other consequences include hypovolemic shock and loss of electrolytes Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Disorders of Water Balance: Dehydration

1 Excessive loss of H2O from ECF

2

ECF osmotic pressure rises

3 Cells lose H2O to ECF by osmosis; cells shrink

(a) Mechanism of dehydration

Figure 26.7a Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Interventions  Monitor s/sx closely  Record I and O  Maintain IV access as ordered. Monitor IV infusions  Monitor serum Na levels, urine osmolality, & urine specific gravity  Insert a urinary catheter as ordered  Initiate safety precautions  Obtain daily weights  Provide skin & mouth care  Assess pt for diaphoresis Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPOVOLEMIA

 -isotonic fluid loss from the extracellular space

Etiology: -abdl. Surgery

DM

Excessive diuretic therapy

excessive laxative use

Excessive sweating

fever

Fistulas

hemorrhage

NG drainage

Vomiting & diarrhea

renal failure w/ increased urination Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPOVOLEMIA Etiology (third-space shift): -acute intestinal obstruction -acute peritonitis -burns -crush injuries -hip fracture -hypoalbuminemia -pleural effusion Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPERVOLEMIA Signs and Symptoms Tachypnea Dyspnea Crackles Rapid, bounding pulse Hypertension Increased CVP, PAP, and PAWP Distended neck and hand veins Acute weight gain Edema S3 gallop

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HYPOVOLEMIA Interventions Ensure patent airway Apply and adjust O2 therapy as ordered Lower the head of the bed to slow a declining BP Stop bleeding, as needed Maintain patent IV access Administer IV fluid, a vasopressor, and blood as prescribed Draw blood for typing and crossmatching, as ordered Closely monitor the pt’s mental status and vs Monitor the quality of peripheral pulses Obtain & record results of lab test results Offer emo support to pt and family Give health teaching Auscultate for breath sounds Prevent complications Weigh pt daily Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Disorders of Water Balance: Hypotonic Hydration  Renal insufficiency or an extraordinary amount of water ingested quickly can lead to cellular overhydration, or water intoxication  ECF is diluted – sodium content is normal but excess water is present  The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling  These events must be quickly reversed to prevent severe metabolic disturbances, particularly in neurons Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Disorders of Water Balance: Hypotonic Hydration

1

Excessive H2O enters the ECF

2

ECF osmotic pressure falls

3 H2O moves into cells by osmosis; cells swell

(b) Mechanism of hypotonic hydration

Figure 26.7b Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPERVOLEMIA

-excess of isotonic fluid in the ECF -mild to moderate fluid gain: 5% to 10% wt increase -severe fluid gain: more than 10% wt increase -prolonged or severe or in pts with poor heart function: can lead to heart failure or pulmonary edema -elderly pts & pts with impaired renal or cardiovascular function: increased susceptibility

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Disorders of Water Balance: Edema  Atypical accumulation of fluid in the interstitial space, leading to tissue swelling  Caused by anything that increases flow of fluids out of the bloodstream or hinders their return  Factors that accelerate fluid loss include:  Increased blood pressure, capillary permeability  Incompetent venous valves, localized blood vessel blockage  Congestive heart failure, hypertension, high blood volume Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Edema  Hindered fluid return usually reflects an imbalance in colloid osmotic pressures  Hypoproteinemia – low levels of plasma proteins  Forces fluids out of capillary beds at the arterial ends  Fluids fail to return at the venous ends  Results from protein malnutrition, liver disease, or glomerulonephritis Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Edema  Blocked (or surgically removed) lymph vessels:  Cause leaked proteins to accumulate in interstitial fluid  Exert increasing colloid osmotic pressure, which draws fluid from the blood  Interstitial fluid accumulation results in low blood pressure and severely impaired circulation

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PITTING EDEMA

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Signs of hypo / hypervolemia:

Volume depletion

Volume overload

Postural hypotension

Hypertension

Tachycardia

Tachycardia

Absence of JVP @ 45o

Raised JVP / gallop rhythm

Decreased skin turgor

Edema

Dry mucosae

Pleural effusions

Supine hypotension

Pulmonary edema

Oliguria

Ascites

Organ failure

Organ failure

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ELECTROLYTES

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Electrolyte Results Serum Na

Serum K

Implications

Common Causes

135-145 mEq/L

Normal

<135 mEq/L

Hyponatremia

SIADH

>145 mEq/L

Hypernatremia

Diabetes Insipidus

3.5 – 5mEq/L

Normal

<3.5 mEq/L

Hypokalemia

Diarrhea

>5 mEq/L

Hyperkalemia

Burns & renal failure

Total serum 8.9-10.1 mg/dL calcium <8.9 mg/dL >10.1 mg/dL

Normal Hypocalcemia

Acute pancreatitis

hypercalcemia

Hyperparathyrodism

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Electrolyte

Results

Implications

Ionized Ca

4.5-5.1 mg/dL

Normal

<4.5 mg/dL

Hypocalcemia

Massive transfusion

>5.2 mg/dL

Hypercalcemia

Acidosis

2.5–4.5 mg/dL

Normal

<2.5 mg/dL

Hypophosphatemia

Diabetic ketoacidosis

>4.5 mg/dL

hyperphosphatemia

Renal insufficiency

1.5-2.5 mEq/L

Normal

<1.5 mEq/L

Hypomagnesemia

Malnutrition

>2.5 mEq/L

Hypermagnesemia

Renal Failure

96-106 mEq/L

Normal

<96 mEq/L

Hypochloremia

Prolonged vomiting

>106 mEq/L

Hyperchloremia

Hypernatremia

Serum Phosphates

Serum Mg

Serum Cl

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Common Causes

Electrolyte Balance  Electrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balance  Salts are important for:  Neuromuscular excitability  Secretory activity  Membrane permeability  Controlling fluid movements  Salts enter the body by ingestion and are lost via perspiration, feces, and urine Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

SODIUM  Sodium holds a central position in fluid and electrolyte balance  Sodium salts:  Account for 90-95% of all solutes in the ECF  Contribute 280 mOsm of the total 300 mOsm ECF solute concentration  Sodium is the single most abundant cation in the ECF  Sodium is the only cation exerting significant osmotic pressure Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Sodium in Fluid and Electrolyte Balance  The role of sodium in controlling ECF volume and water distribution in the body is a result of:  Sodium being the only cation to exert significant osmotic pressure  Sodium ions leaking into cells and being pumped out against their electrochemical gradient  Sodium concentration in the ECF normally remains stable Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Sodium in Fluid and Electrolyte Balance

 Changes in plasma sodium levels affect:  Plasma volume, blood pressure  ICF and interstitial fluid volumes  Renal acid-base control mechanisms are coupled to sodium ion transport

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Regulation of Sodium Balance: Aldosterone  Sodium reabsorption  65% of sodium in filtrate is reabsorbed in the proximal tubules  25% is reclaimed in the loops of Henle  When aldosterone levels are high, all remaining Na+ is actively reabsorbed  Water follows sodium if tubule permeability has been increased with ADH Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Sodium Balance: Aldosterone  The renin-angiotensin mechanism triggers the release of aldosterone  This is mediated by the juxtaglomerular apparatus, which releases renin in response to:  Sympathetic nervous system stimulation  Decreased filtrate osmolality  Decreased stretch (due to decreased blood pressure)  Renin catalyzes the production of angiotensin II, which prompts aldosterone release Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Sodium Balance: Aldosterone

 Adrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECF  Aldosterone brings about its effects (diminished urine output and increased blood volume) slowly

PLAY

InterActive Physiology®: Fluid, Electrolyte and Acid/Base Balance: Water Homeostasis

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Regulation of Sodium Balance: Aldosterone

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Figure 26.8

Cardiovascular System Baroreceptors

 Baroreceptors alert the brain of increases in blood volume (hence increased blood pressure)  Sympathetic nervous system impulses to the kidneys decline  Afferent arterioles dilate  Glomerular filtration rate rises  Sodium and water output increase Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Cardiovascular System Baroreceptors

 This phenomenon, called pressure diuresis, decreases blood pressure  Drops in systemic blood pressure lead to opposite actions and systemic blood pressure increases  Since sodium ion concentration determines fluid volume, baroreceptors can be viewed as “sodium receptors”

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Maintenance of Blood Pressure Homeostasis

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Figure 26.9

Atrial Natriuretic Peptide (ANP)  Reduces blood pressure and blood volume by inhibiting:  Events that promote vasoconstriction  Na+ and water retention  Is released in the heart atria as a response to stretch (elevated blood pressure)  Has potent diuretic and natriuretic effects  Promotes excretion of sodium and water  Inhibits angiotensin II production Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Mechanisms and Consequences of ANP Release

Figure 26.10 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Influence of Other Hormones on Sodium Balance

 Estrogens:  Enhance NaCl reabsorption by renal tubules  May cause water retention during menstrual cycles  Are responsible for edema during pregnancy

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Influence of Other Hormones on Sodium Balance

 Progesterone:  Decreases sodium reabsorption  Acts as a diuretic, promoting sodium and water loss  Glucocorticoids – enhance reabsorption of sodium and promote edema

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ELECTROLYTE IMBALANCES Interventions: Monitor & record vs Carefully record I and O Assess skin and MM for signs of breakdown and infection Monitor patient’s serum electrolyte levels Restrict oral intake, as needed Give oral hydration, as needed Give supplemental feedings, as needed Assist with oral hygiene Prevent complications Administer prescribed meds and monitor the pt for their effectiveness Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Potassium Balance

 Relative ICF-ECF potassium ion concentration affects a cell’s resting membrane potential  Excessive ECF potassium decreases membrane potential  Too little K+ causes hyperpolarization and nonresponsiveness

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Regulation of Potassium Balance  Hyperkalemia and hypokalemia can:  Disrupt electrical conduction in the heart  Lead to sudden death  Hydrogen ions shift in and out of cells  Leads to corresponding shifts in potassium in the opposite direction  Interferes with activity of excitable cells Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulatory Site: Cortical Collecting Ducts  Less than 15% of filtered K+ is lost to urine regardless of need  K+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrate  Excessive K+ is excreted over basal levels by cortical collecting ducts  When K+ levels are low, the amount of secretion and excretion is kept to a minimum  Type A intercalated cells can reabsorb some K+ left in the filtrate Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Influence of Plasma Potassium Concentration

 High K+ content of ECF favors principal cells to secrete K+  Low K+ or accelerated K+ loss depresses its secretion by the collecting ducts

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Influence of Aldosterone  Aldosterone stimulates potassium ion secretion by principal cells  In cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted  Increased K+ in the ECF around the adrenal cortex causes:  Release of aldosterone  Potassium secretion  Potassium controls its own ECF concentration via feedback regulation of aldosterone release Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Calcium  Ionic calcium in ECF is important for:  Blood clotting  Cell membrane permeability  Secretory behavior  Hypocalcemia:  Increases excitability  Causes muscle tetany Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Calcium 

Hypercalcemia:

 Inhibits neurons and muscle cells  May cause heart arrhythmias  Loss of appetite  Weight loss  Nausea  Vomiting  Thirst  Fatigue  Muscle weakness  Restlessness  Confusion  Elevated blood calcium level

Calcium balance is controlled by parathyroid hormone (PTH) and calcitonin Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Calcium and Phosphate  PTH promotes increase in calcium levels by targeting:  Bones – PTH activates osteoclasts to break down bone matrix  Small intestine – PTH enhances intestinal absorption of calcium  Kidneys – PTH enhances calcium reabsorption and decreases phosphate reabsorption  Calcium reabsorption and phosphate excretion go hand in hand Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Calcium and Phosphate  Filtered phosphate is actively reabsorbed in the proximal tubules  In the absence of PTH, phosphate reabsorption is regulated by its transport maximum and excesses are excreted in urine  High or normal ECF calcium levels inhibit PTH secretion  Release of calcium from bone is inhibited  Larger amounts of calcium are lost in feces and urine  More phosphate is retained Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Influence of Calcitonin  Released in response to rising blood calcium levels  Calcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible

PLAY

InterActive Physiology®: Fluid, Electrolyte, and Acid/Base Balance: Electrolyte Homeostasis

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Regulation of Anions  Chloride is the major anion accompanying sodium in the ECF  99% of chloride is reabsorbed under normal pH conditions  When acidosis occurs, fewer chloride ions are reabsorbed  Other anions have transport maximums and excesses are excreted in urine Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPONATREMIA (<135 mEq/L) -Maintained by ADH secreted from the posterior pituitary gland Depends on what’s eaten & how it’s absorbed by the intestines Increased Na intake: increased ECF fluid volume Decreased Na intake: decreased ECF fluid volume Increased Na levels: increased thirst, release of ADH, retention of H2O by the kidneys, dilution of blood -Decreased Na levels: suppression of thirst, suppression of ADH secretion, excretion of H2O by the kidneys

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Hyponatremia Signs & symptoms: Abdominal cramps Headache Nausea Hypertension Tachycardia Rapid, bounding pulse

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Altered LOC Muscle twitching Dry MM Poor skin turgor Weight gain

Hyponatremia Interventions: Monitor and record vs, esp. BP and pusle Monitor neurologic status frequently Accurately measure I and O Weigh the pt Assess skin turgor Watch for & report extreme serum Na levels changes Restrict fluid intake as ordered Administer oral sodium supplements Maintain patent IV line Maintain safety Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPERNATREMIA (>145 mEq/L) -Caused by water loss, inadequate water intake, or Na gain on what’s eaten & how it’s absorbed by the intestines - Increased risk for infants, immobile, and comatose pts - Always results in increased osmolality - Fluid shifts out of cells - Must be corrected slowly to prevent a rapid shift of water back into the cells, which couls cause cerebral edema

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Hypernatremia Signs & symptoms:

Skin flushed Agitation Low-grade fever Thirst Interventions: Assess… Replenish… Restore… Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

HYPOKALEMIA (<3.5 mEq/L) Signs & symptoms:

Skeletal muscle weakness U wave Constipation, ileus Toxic effects of digoxin (from hypokalemia) Irregular, weak pulse Orthostatic hypotension Numbness (paresthesia) Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Hypokalemia Interventions: Monitor vs Check heart rate and rhythm Monitor serum K levels Asess for signs of hypokalemia Monitor and document I and O Observe proper guidelines in IV K administration

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HYPERKALEMIA (>5 mEq/L) -Most dangerous of the electrolyte disorders Signs & symptoms: Abdominal cramping EKG changes Irregular pulse rate Muscle weakness paresthesia

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diarrhea hypotension irritability nausea

Hypokalemia Interventions: Monitor vs Monitor and document I and O Prepare to administer a slow calcium gluconate IV infusion Keep in mind that when giving Kayexalate,, serum Na levels may rise Monitor bowel sounds & the number of BM Monitor serum K levels

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HYPOCALCEMIA (<8.9 mg/dL) Signs & symptoms: Trousseau’s sign Anxiety Decreased CO Fractures Muscle cramps Tremors

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Chvostek’s sign Confusion Arrhythmias Irritability Tetany twitching

Hypocalcemia Interventions: Monitor vs, cardiac status; observe for Chvostek’s and Trousseau’s signs Monitor for arrhythmias Insert and maintain IV line for Ca therapy Administer oral replacements as ordered Monitor pertinent lab test results Take safety and seizure precautions Document pertinent info

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HYPERCALCEMIA (>10.1 mg/dL) Signs & symptoms: Abdominal pain, constipation Anorexia Behavioral changes Bone pain Decreased DTRs Extreme thirst Hypertension Lethargy Muscle weakness Nausea Polyuria Vomiting Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Hypocalcemia Interventions: Monitor vs Monitor for arrhythmias Insert and maintain IV line Administer a diuretic Strain the urine for calculi Watch for signs/symptoms of digitalis toxicity Provide a safe env’t. Provide safety

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HYPOPHOSPHATEMIA (<2.5 mg/dL) Signs & symptoms: Hypotension Decreased CO Cardiomyopathy Rhabdomyolysis Cyanosis Respiratory failure

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Hypophosphatemia Interventions: Monitor vs Assess the pt’s LOC Monitor the rate and depth of respirations Monitor the pt for evidence of heart failure Monitor temp frequently Assess for evidence of decreasing muscle strength

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HYPERPHOSPHATEMIA (>10.1 mg/dL) Signs & symptoms: Anorexia Chvostek’s/ Trousseau’s signs Conjuntivitis, visual impairment Decreased mental status Hyperreflexia Muscle weakness, cramps, spasm Nausea & vomiting Papular eruptions Paresthesia Tetany Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Hyperphosphatemia Interventions: Monitor vs Monitor for arrhythmias Insert and maintain IV line Administer a diuretic Strain the urine for calculi Watch for signs/symptoms of digitalis toxicity Provide a safe env’t. Provide safety

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HYPOCHLOREMIA (<96 meQ/L) Signs & symptoms: Hyperactive DTRs Muscle hypertonicity s/sx pf acid-base imbalances tetany

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Hypochloremia Interventions: Monitor vs & LOC Monitor serum electrolyte levels Offer food high in chloride Insert and maintain a patent IV line Accurately measure I and O Use NSS to flush NGT Provide a safe and quiet env’t.

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HYPERCHLOREMIA (>106 mEq/L) Signs & symptoms: Arrhythmias Decreased CO Decreased LOC that may progress to coma

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Hyperchloremia Interventions: Monitor vs including cardiac rhythm Provide safety Look for changes in respiratory pattern Insert and IV and maintain patency Restrict fluids, Na, and Cl as needed Monitor serum & electrolyte levels and ABG results Monitor I and O

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HYPOMAGNESEMIA (<1.5 meQ/L) Signs & symptoms: Altered LOC, confusion, hallucinations Muscular weakness, leg and foot cramps, Hyperactive DTRs, tetany, Chvostek’s & trousseau’s signs Tachycardia, hypertension Dysphagia, anorexia, nausea, vomiting

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Hypomagnesemia Interventions: Monitor vs & LOC Monitor serum electrolyte levels Offer food high in magnesium Insert and maintain a patent IV line Accurately measure I and O Provide a safe and quiet env’t.

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HYPERMAGNESEMIA (>2.5 mEq/L) Signs & symptoms: Decreased muscle and nerve activity Hypoactive DTRs Generalized weakness, drowsiness, lethargy Nausea, vomiting Slow, shallow, respirations Respiratory arrest ECG changes Vasodilation

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Hyperchloremia Interventions: Monitor vs including cardiac rhythm Provide safety Look for changes in respiratory pattern Insert and IV and maintain patency Restrict fluids, Na, and Cl as needed Monitor serum & electrolyte levels and ABG results Monitor I and O

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ACID-BASE BALANCE

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Acid-Base Balance  Normal pH of body fluids  Arterial blood is 7.4  Venous blood and interstitial fluid is 7.35  Intracellular fluid is 7.0  Alkalosis or alkalemia – arterial blood pH rises above 7.45  Acidosis or acidemia – arterial pH drops below 7.35 (physiological acidosis) Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Sources of Hydrogen Ions  Most hydrogen ions originate from cellular metabolism  Breakdown of phosphorus-containing proteins releases phosphoric acid into the ECF  Anaerobic respiration of glucose produces lactic acid  Fat metabolism yields organic acids and ketone bodies  Transporting carbon dioxide as bicarbonate releases hydrogen ions Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Hydrogen Ion Regulation  Concentration of hydrogen ions is regulated sequentially by:  Chemical buffer systems – act within seconds  The respiratory center in the brain stem – acts within 1-3 minutes  Renal mechanisms – require hours to days to effect pH changes

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Chemical Buffer Systems  Strong acids – all their H+ is dissociated completely in water  Weak acids – dissociate partially in water and are efficient at preventing pH changes  Strong bases – dissociate easily in water and quickly tie up H+  Weak bases – accept H+ more slowly (e.g., HCO3¯ and NH3) Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Chemical Buffer Systems  One or two molecules that act to resist pH changes when strong acid or base is added  Three major chemical buffer systems  Bicarbonate buffer system  Phosphate buffer system  Protein buffer system  Any drifts in pH are resisted by the entire chemical buffering system Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Bicarbonate Buffer System  A mixture of carbonic acid (H2CO3) and its salt, sodium bicarbonate (NaHCO3) (potassium or magnesium bicarbonates work as well)  If strong acid is added:  Hydrogen ions released combine with the bicarbonate ions and form carbonic acid (a weak acid)  The pH of the solution decreases only slightly Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Bicarbonate Buffer System  If strong base is added:  It reacts with the carbonic acid to form sodium bicarbonate (a weak base)  The pH of the solution rises only slightly  This system is the only important ECF buffer

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Phosphate Buffer System  Nearly identical to the bicarbonate system  Its components are:  Sodium salts of dihydrogen phosphate (H2PO4¯), a weak acid  Monohydrogen phosphate (HPO42¯), a weak base  This system is an effective buffer in urine and intracellular fluid Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Protein Buffer System  Plasma and intracellular proteins are the body’s most plentiful and powerful buffers  Some amino acids of proteins have:  Free organic acid groups (weak acids)  Groups that act as weak bases (e.g., amino groups)  Amphoteric molecules are protein molecules that can function as both a weak acid and a weak base Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Physiological Buffer Systems  The respiratory system regulation of acid-base balance is a physiological buffering system  There is a reversible equilibrium between:  Dissolved carbon dioxide and water  Carbonic acid and the hydrogen and bicarbonate ions CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3¯ Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Physiological Buffer Systems  During carbon dioxide unloading, hydrogen ions are incorporated into water  When hypercapnia or rising plasma H+ occurs:  Deeper and more rapid breathing expels more carbon dioxide  Hydrogen ion concentration is reduced  Alkalosis causes slower, more shallow breathing, causing H+ to increase  Respiratory system impairment causes acid-base imbalance (respiratory acidosis or respiratory alkalosis) Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

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Renal Mechanisms of Acid-Base Balance  Chemical buffers can tie up excess acids or bases, but they cannot eliminate them from the body  The lungs can eliminate carbonic acid by eliminating carbon dioxide  Only the kidneys can rid the body of metabolic acids (phosphoric, uric, and lactic acids and ketones) and prevent metabolic acidosis  The ultimate acid-base regulatory organs are the kidneys Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Renal Mechanisms of Acid-Base Balance  The most important renal mechanisms for regulating acid-base balance are:  Conserving (reabsorbing) or generating new bicarbonate ions  Excreting bicarbonate ions  Losing a bicarbonate ion is the same as gaining a hydrogen ion; reabsorbing a bicarbonate ion is the same as losing a hydrogen ion Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Renal Mechanisms of Acid-Base Balance

 Hydrogen ion secretion occurs in the PCT and in type A intercalated cells  Hydrogen ions come from the dissociation of carbonic acid

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Reabsorption of Bicarbonate  Carbon dioxide combines with water in tubule cells, forming carbonic acid  Carbonic acid splits into hydrogen ions and bicarbonate ions  For each hydrogen ion secreted, a sodium ion and a bicarbonate ion are reabsorbed by the PCT cells  Secreted hydrogen ions form carbonic acid; thus, bicarbonate disappears from filtrate at the same rate that it enters the peritubular capillary blood

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Kidney Hydrogen Ion Balancing: Proximal Tubule

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Proximal tubule secretion and reabsorption of filtered HCO3-

Generating New Bicarbonate Ions

 Two mechanisms carried out by type A intercalated cells generate new bicarbonate ions  Both involve renal excretion of acid via secretion and excretion of hydrogen ions or ammonium ions (NH4+)

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Hydrogen Ion Excretion  Dietary hydrogen ions must be counteracted by generating new bicarbonate  The excreted hydrogen ions must bind to buffers in the urine (phosphate buffer system)  Intercalated cells actively secrete hydrogen ions into urine, which is buffered and excreted  Bicarbonate generated is:  Moved into the interstitial space via a cotransport system  Passively moved into the peritubular capillary blood Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Hydrogen Ion Excretion  In response to acidosis:  Kidneys generate bicarbonate ions and add them to the blood  An equal amount of hydrogen ions are added to the urine Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 26.13

Ammonium Ion Excretion

 This method uses ammonium ions produced by the metabolism of glutamine in PCT cells  Each glutamine metabolized produces two ammonium ions and two bicarbonate ions  Bicarbonate moves to the blood and ammonium ions are excreted in urine

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Ammonium Ion Excretion

Figure 26.14 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Bicarbonate Ion Secretion  When the body is in alkalosis, type B intercalated cells:  Exhibit bicarbonate ion secretion  Reclaim hydrogen ions and acidify the blood  The mechanism is the opposite of type A intercalated cells and the bicarbonate ion reabsorption process  Even during alkalosis, the nephrons and collecting ducts excrete fewer bicarbonate ions than they conserve Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Acidosis and Alkalosis  Result from failure of the respiratory system to balance pH  PCO2 is the single most important indicator of respiratory inadequacy  PCO2 levels  Normal PCO2 fluctuates between 35 and 45 mm Hg  Values above 45 mm Hg signal respiratory acidosis  Values below 35 mm Hg indicate respiratory alkalosis Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Acidosis and Alkalosis  Respiratory acidosis is the most common cause of acid-base imbalance  Occurs when a person breathes shallowly, or gas exchange is hampered by diseases such as pneumonia, cystic fibrosis, or emphysema  Respiratory alkalosis is a common result of hyperventilation

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Metabolic Acidosis  All pH imbalances except those caused by abnormal blood carbon dioxide levels  Metabolic acid-base imbalance – bicarbonate ion levels above or below normal (22-26 mEq/L)  Metabolic acidosis is the second most common cause of acid-base imbalance  Typical causes are ingestion of too much alcohol and excessive loss of bicarbonate ions  Other causes include accumulation of lactic acid, shock, ketosis in diabetic crisis, starvation, and kidney failure Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Metabolic Alkalosis

 Rising blood pH and bicarbonate levels indicate metabolic alkalosis  Typical causes are:  Vomiting of the acid contents of the stomach  Intake of excess base (e.g., from antacids)  Constipation, in which excessive bicarbonate is reabsorbed Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory and Renal Compensations  Acid-base imbalance due to inadequacy of a physiological buffer system is compensated for by the other system  The respiratory system will attempt to correct metabolic acid-base imbalances  The kidneys will work to correct imbalances caused by respiratory disease

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Respiratory Compensation  In metabolic acidosis:  The rate and depth of breathing are elevated  Blood pH is below 7.35 and bicarbonate level is low  As carbon dioxide is eliminated by the respiratory system, PCO2 falls below normal  In respiratory acidosis, the respiratory rate is often depressed and is the immediate cause of the acidosis Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Respiratory Compensation  In metabolic alkalosis:  Compensation exhibits slow, shallow breathing, allowing carbon dioxide to accumulate in the blood  Correction is revealed by:  High pH (over 7.45) and elevated bicarbonate ion levels  Rising PCO2 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Renal Compensation  To correct respiratory acid-base imbalance, renal mechanisms are stepped up  Acidosis has high PCO2 and high bicarbonate levels  The high PCO2 is the cause of acidosis  The high bicarbonate levels indicate the kidneys are retaining bicarbonate to offset the acidosis Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Renal Compensation  Alkalosis has Low PCO2 and high pH  The kidneys eliminate bicarbonate from the body by failing to reclaim it or by actively secreting it

PLAY

InterActive Physiology®: Fluid, Electrolyte, and Acid/Base Balance: Acid/Base Homeostasis

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Developmental Aspects  Water content of the body is greatest at birth (7080%) and declines until adulthood, when it is about 58%  At puberty, sexual differences in body water content arise as males develop greater muscle mass  Homeostatic mechanisms slow down with age  Elders may be unresponsive to thirst clues and are at risk of dehydration  The very young and the very old are the most frequent victims of fluid, acid-base, and electrolyte imbalances Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Problems with Fluid, Electrolyte, and Acid-Base Balance  Occur in the young, reflecting:  Low residual lung volume  High rate of fluid intake and output  High metabolic rate yielding more metabolic wastes  High rate of insensible water loss  Inefficiency of kidneys in infants Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

ABG Analysis pH

7.35 - 7. 45

PaCO2 35 - 45 mm Hg HCO3- 22 - 26 mEq/L

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Step 1: Classify the pH Normal: 7.35 - 7.45 Acidemia: <7.35 Alkalemia: >7.45 Step 2: Assess PaCO2 Normal: 35- 45 mm Hg Respiratory acidosis: >45 mm Hg Respiratory alkalosis: <35 mm Hg Step 3: Assess HCO3Normal: 22-26 mEq/L Metabolic acidosis: <22 mEq/L Metabolic alkalosis: >26 mEq/L Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Step 4: Determine Presence of Compensation Compensation present PaCO2 and HCO3- are abnormal (or

nearly so) in opposite directions; that is, one is acidotic and the other alkalotic

Step 5: Identify Primary Disorder, If Possible

If pH is clearly abnormal: The acid-base component most consistent with the pH disturbance is the primary disorder. If pH is normal or near-normal: The more deviant component is probably primary. Also note whether pH is on acidotic or alkalotic side of 7.4. The more deviant component should be consistent with this pH

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RESPIRATORY ACIDOSIS Uncompensated

Compensated

pH

< 7.35

Normal

PaCO2 (mmHg)

< 45

HCO3- (mEq/L)

Normal

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> 45 > 26

Causes Hypoventilation from CNS trauma or tumor that depresses respiratory center Neuromuscular diseases that affect respiratory drive Lung diseases that decrease amount of surface area available for gas exchange Airway obstruction Chest-wall trauma Certain drugs that depress repiratory center primary hypoventilation

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Pathophysiology When pulmonary ventilation decreases, retained CO2 combines with H2O to form H2CO3. The carbonic acid dissociates to release free H ions and HCO3 ions. The excessive carbonic acid causes a drop in pH. Look for PaCO2 level above 45 mm H g and a pH level below 7.35 As the pH level falls, 2,3-diphosphoglycerate (2,3-DPG) increases in the RBC and causes a change in Hb that makes the Hb release O2. The altered Hb now strongly alkaline picks up H ions and CO2, thus eliminating some of the free H ions and excess CO2. Look for decreased arterial oxygen saturation Whenever PaCO2 increases, CO2 builds up in all tissues and fluids, including CSF & the respiratory ctr. in the medulla. The CO2 reacts with H20 to form H2CO3, which then breaks into free H ions & HCO3- ions. The increased amount of CO2 & free H ions stimulate the respiratory center to increase the respiratory rate. An increased respiratory rate expels more CO2 & helps to reduce the CO2 level in the blood & other tissues. Look for rapid, shallow respirations & a decreasing PaCO2 Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Eventually, CO2 and H ions cause cerebral blood vessels to dilate, which increases blood flow to the brain. That increased flow can cause cerebral edema and depress CNS activity Look for headache, confusion, lethargy, nausea, or vomiting As respiratory mechanisms fail, the increasing PsCO2 stimulates the kidneys to conserve HCO3- and Na ions & to excrete H ions, some in the form of NH4. The additional HCO3- & Na combine to form extra NaHCO3, which is then able to buffer more free H ions. Look for increased acid content in the urine, increasing serum pH & HCO3levels, & shallow, depressed respirations As the concentration of H ions overwhelms the body’s compensatory mechanisms, the H ions move into the cells, and K ions move out. A comncurrent lack of oxygen causes an increase in the anaerobic production of lactic acid, which further skews the acid-base balance & critically depresses neurologic & cardiac functions. Look for hyperkalemia, arrhythmias, increased PaCO2, decreased PaO2, decreased pH, & decreased LOC Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Signs and Symptoms apprehension confusion decreased deep-tendon reflexes diaphoresis dyspnea, with rapid, shallow respirations nausea or vomiting restlessness tachycardia tremors warm, flushed skin

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Nursing Management - Monitor vs & assess cardiac rhythm - Continue to assess respiratory patterns & report changes quickly - Monitor the pt’s neurologic status, & report significant changes - Report any variations in ABG, pulse oximetry, or serum electrolyte levels - Give meds (antibiotic & bronchodilators) as ordered - Administer O2 as ordered Perform tracheal suctioning, incentive spirometry, postural drainage, & coughing & deep breathing, as indicated - Make sure the pt takes in enough fluids, both oral & IV, & maintain

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Treatment - bronchodilators -supplemental oxygen, prn -drug therapy for hyperkalemia -antibiotic for infection -chest physiotherapy -removal of a foreign body from the pt’s airway, if needed

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Health Teaching - description of the condition & how to prevent it - reasons for repeated ABG analyses - deep-breathing exercises - prescribed meds - home oxygentaion therapy, if indicated - warning signs & symptoms & when to report them - proper techniques for using bronchodilators, if appropriate - need for frequent rest

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RESPIRATORY ALKALOSIS Uncompensated

Compensated

pH

> 7.45

PaCO2 (mmHg)

< 35

< 35

HCO3- (mEq/L)

Normal

< 22

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Normal

Causes Any condition that increases respiratory rate & depth Hyperventilation Hypercapnia Hypermetabolic states Liver failure Certain drugs Conditions that affect brain’s respiratory control center Acute hypoxia 2o to high altitude, pulmonary disease, severe

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Nursing Management - Monitor pts at risk for developing respiratory alkalosis - Allay anxiety whenever possible - Monitor vs. Report changes in neurologic, neuromuscular, or cardiovascular functioning - Monitor ABG & serum electrolyte levels, & immediately report any variations - Pts with MV: check settings frequently - Provide undisturbed rest periods after the pt’s respiratory rate returns to normal Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Treatment - focus is on removing the underlying cause - oxygen therapy - sedative/anxiolytic -breathing into a paper bag

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Health Teaching - explanation of the condition & its treatment - warning signs & symptoms & when to report them - anxiety-reducing techniques, if appropriate -controlled-breathing exercises, if appropriate -prescribed medications

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METABOLIC ACIDOSIS Uncompensated

Compensated

pH

< 7.35

Normal

PaCO2 (mmHg)

Normal

< 35

HCO3- (mEq/L) < 22

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<22

Causes Loss of HCO3Accumulation of metabolic acids Overproduction of ketone bodies Decreased ability of kidneys to excrete acids Excessive GI losses from diarrhea, intestinal malabsorption, or urinary diversion to the ileum Hyperaldosteronism Use of K-sparing diuretics Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Signs and Symptoms confusion

dull headache

decreased DT reflexes

hyperkalemic s/sx

hypotension

Kussmaul’s respirations

lethargy

warm, dry skin

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Nursing Management -Monitor vs and assess cardiac rhythm -Prepare for mechanical ventilation or dialysis, as required -Monitor the pt’s neurologic status closely -Insert an IV line, as ordered, and maintain patent IV access -Administer NaHCO3 as ordered -Position the pt to promote chest expansion & facilitate breathing -Take steps to help eliminate the underlying cause -Watch for any 2o changes, such as declining BP -Monitor pt’s renal function through I & O -Watch for changes in the serum electrolyte levels; continuously monitor ABG results -Orient the pt as needed -Investigate reasons for pt’s ingestion of toxic substances

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Treatment -adjust the K -Replace the HCO3-Ventilatory support -Dialysis

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Health Teaching - basics of the condition & its treatment - testing of blood glucose levels, if indicated - need for strict adherence to antidiabetic therapy, if appropriate - avoidance of alcohol - warning s/sx & when to report them -prescribed meds -avoidance of ingestion of toxic substances

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METABOLIC ALKALOSIS

Uncompensated

Compensated

pH

> 7.45

PaCO2 (mmHg)

Normal

> 45

HCO3- (mEq/L)

> 22

<26

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Normal

Causes Excessive acid loss from the GIT Diuretic therapy Cushing’s dse.

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Pathophysiology (diagram here) HCO3- accumulation in the body

Chemical buffers bind w/ ions

Excess HCO3 that don’t bind w/ chemical buffers

pH >7.45

Elevated serum pH level

HCO3 >26 mEq/L

Depressed respiratory system

Excess HCO3- excreted via the kidneys (>28 mEq/L)

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Alkaline urine & pH Near normal HCO3 level

Slow, shallow resp.

polyuria Na, H2O, & HCO3- excretion via the kidneys

Hypovolemia s/sx

Ions shifting ( K and H) Hypokalemia s/sx: anorexia, muscle weakness, etc. Decreased Ca ionization tetany Nerve cells’ increased permeability to Na ions

belligerence irritability disorientation

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seizures

Signs and Symptoms anorexia

apathy

confusion

cyanosis

hypotension

loss of reflexes

muscle twitching

nausea

paresthesia

polyuria

vomiting

weakness

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Nursing Management -Monitor vs & assess cardiac rhythm & monitor resp. pattern -Assess LOC -Administer O2, as ordered -Institute seizure precautions; explain to pt and family -Maintain patent IV access as ordered -Administer diluted K solutions w/ an infusion device -Monitor I & O - Infuse 0.9% ammonium chloride no faster than 1 L over 4 hrs. -Irrigate NG tube w/ NSS -Assess lab test results; inform doctor of any changes -Watch closely for signs of muscle weakness, tetany, or decreased activity Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Health Teaching - basics of the condition & its treatment - need to avoid overuse of alkaline agents & diuretics - prescribed meds, esp. adverse rxns of K-wasting diuretics or KCl supplements - warning signs & symptoms & when to report them

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