acid-base

FLUIDS AND ELECTROLYTES

ACID-BASE BALANCE

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

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

Fluid Compartments

Figure 26.1

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

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

CELLS AND TONICITY

FLUID& ELECTROLYTE TRANSPORT

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

Sodium and potassium concentrations in extra- and intracellular fluids are nearly opposites

This reflects the activity of cellular ATP-dependent sodium-potassium pumps

Electrolytes determine the chemical and physical reactions of 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

Electrolyte Composition of Body Fluids

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

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

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

Continuous Mixing of Body Fluids

Figure 26.3

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%)

Normal I and O (insert here)

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)

Water Intake and Output

Figure 26.4

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

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

Regulation of Water Intake: Thirst Mechanism

Figure 26.5

Insert angiotensin-aldosterone system

Insert ADH regulation here

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

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

Figure 26.6

Mechanisms and Consequences of ADH Release

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

Figure 26.7a

Disorders of Water Balance: Dehydration

Excessive loss of H2O from ECF

1 2 3ECF osmotic pressure rises

Cells lose H2O to ECF by osmosis; cells shrink

(a) Mechanism of dehydration

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

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

HYPOVOLEMIA

Etiology (third-space shift):

-acute intestinal obstruction

-acute peritonitis

-burns

-crush injuries

-hip fracture

-hypoalbuminemia

-pleural effusion

HYPERVOLEMIASigns and Symptoms

Tachypnea

Dyspnea

Crackles

Rapid, bounding pulse

Hypertension

Increased CVP, PAP, and PAWP

Distended neck and hand veins

Acute weight gain

S3 gallop

HYPOVOLEMIAInterventions

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

Provide effective skin care

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

Disorders of Water Balance: Hypotonic Hydration

Figure 26.7b

Disorders of Water Balance: Hypotonic Hydration

Excessive H2O enters the ECF

1 2 ECF osmotic pressure falls

3 H2O moves into cells by osmosis; cells swell

(b) Mechanism of hypotonic hydration

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

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

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

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

PITTING EDEMA

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

ELECTROLYTES

Electrolyte

Results Implications Common Causes

Serum Na 135-145 mEq/L

<135 mEq/L

>145 mEq/L

Normal

Hyponatremia

Hypernatremia

Diabetes Insipidus

Serum K 3.5 – 5mEq/L

<3.5 mEq/L

>5 mEq/L

Normal

Hypokalemia

Hyperkalemia

Diarrhea

Burns & renal failure

Total serum calcium

8.9-10.1 mg/dL

<8.9 mg/dL

>10.1 mg/dL

Normal

Hypocalcemia

hypercalcemia

Acute pancreatitis

Hyperparathyrodism

Electrolyte

Results Implications Common Causes

Ionized Ca 4.5-5.1 mg/dL

<4.5 mg/dL

>5.2 mg/dL

Normal

Hypocalcemia

Hypercalcemia

Massive transfusion

Acidosis

Serum Phosphates

2.5–4.5 mg/dL

<2.5 mg/dL

>4.5 mg/dL

Normal

Hypophosphatemia

hyperphosphatemia

Diabetic ketoacidosis

Renal insufficiency

Serum Mg 1.5-2.5 mEq/L

<1.5 mEq/L

>2.5 mEq/L

Normal

Hypomagnesemia

Hypermagnesemia

Malnutrition

Renal Failure

Serum Cl 96-106 mEq/L

<96 mEq/L

>106 mEq/L

Normal

Hypochloremia

Hyperchloremia

Prolonged vomiting

Hypernatremia

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

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

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

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

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

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

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

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

Regulation of Sodium Balance: Aldosterone

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

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”

Maintenance of Blood Pressure Homeostasis

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

Figure 26.10

Mechanisms and Consequences of ANP Release

Estrogens:

Enhance NaCl reabsorption by renal tubules

May cause water retention during menstrual cycles

Are responsible for edema during pregnancy

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

Influence of Other Hormones on Sodium Balance

ELECTROLYTE IMBALANCES

Interventions:

Monitor & record vsCarefully record I and OAssess skin and MM for signs of breakdown and infectionMonitor patient’s serum electrolyte levelsRestrict oral intake, as neededGive oral hydration, as neededGive supplemental feedings, as neededAssist with oral hygienePrevent complicationsAdminister prescribed meds and monitor the pt for their effectiveness

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

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

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

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

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

Regulation of Calcium

Ionic calcium in ECF is important for:

Blood clotting

Cell membrane permeability

Secretory behavior

Hypocalcemia:

Increases excitability

Causes muscle tetany

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

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

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

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

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

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

HYPONATREMIA (<135 mEq/L)

-Maintained by ADH secreted from the posterior pituitary glandDepends on what’s eaten & how it’s absorbed by the intestinesIncreased Na intake: increased ECF fluid volumeDecreased Na intake: decreased ECF fluid volumeIncreased 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

Hyponatremia

Signs & symptoms:Abdominal cramps Altered LOCHeadache Muscle twitchingNausea Dry MMHypertension Poor skin turgorTachycardia Weight gainRapid, bounding pulse

Hyponatremia

Interventions:Monitor and record vs, esp. BP and pusleMonitor neurologic status frequentlyAccurately measure I and OWeigh the ptAssess skin turgorWatch for & report extreme serum Na levels changesRestrict fluid intake as orderedAdminister oral sodium supplementsMaintain patent IV lineMaintain safety

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

Hypernatremia

Signs & symptoms:

Skin flushedAgitationLow-grade feverThirst

Interventions:Assess…Replenish…Restore…

HYPOKALEMIA (<3.5 mEq/L)

Signs & symptoms:

Skeletal muscle weaknessU waveConstipation, ileusToxic effects of digoxin (from hypokalemia)Irregular, weak pulseOrthostatic hypotensionNumbness (paresthesia)

Hypokalemia

Interventions:Monitor vsCheck heart rate and rhythmMonitor serum K levelsAsess for signs of hypokalemiaMonitor and document I and OObserve proper guidelines in IV K administration

HYPERKALEMIA (>5 mEq/L)

Signs & symptoms:

Abdominal cramping diarrheaEKG changes hypotensionIrregular pulse rate irritabilityMuscle weakness nauseaparesthesia

-Most dangerous of the electrolyte disorders

Hypokalemia

Interventions:Monitor vsMonitor and document I and OPrepare to administer a slow calcium gluconate IV infusionKeep in mind that when giving Kayexalate,, serum Na levels may riseMonitor bowel sounds & the number of BMMonitor serum K levels

HYPOCALCEMIA (<8.9 mg/dL)

Signs & symptoms:

Trousseau’s signChvostek’s signAnxiety ConfusionDecreased CO ArrhythmiasFractures IrritabilityMuscle cramps TetanyTremors twitching

Hypocalcemia

Interventions:Monitor vs, cardiac status; observe for Chvostek’s and Trousseau’s signsMonitor for arrhythmiasInsert and maintain IV line for Ca therapyAdminister oral replacements as orderedMonitor pertinent lab test resultsTake safety and seizure precautionsDocument pertinent info

HYPERCALCEMIA (>10.1 mg/dL)

Signs & symptoms:Abdominal pain, constipationAnorexiaBehavioral changesBone painDecreased DTRsExtreme thirstHypertensionLethargyMuscle weaknessNauseaPolyuriaVomiting

Hypocalcemia

Interventions:Monitor vsMonitor for arrhythmiasInsert and maintain IV lineAdminister a diureticStrain the urine for calculiWatch for signs/symptoms of digitalis toxicityProvide a safe env’t.Provide safety

HYPOPHOSPHATEMIA (<2.5 mg/dL)

Signs & symptoms:

HypotensionDecreased COCardiomyopathyRhabdomyolysisCyanosisRespiratory failure

Hypophosphatemia

Interventions:

Monitor vsAssess the pt’s LOCMonitor the rate and depth of respirationsMonitor the pt for evidence of heart failureMonitor temp frequentlyAssess for evidence of decreasing muscle strength

HYPERPHOSPHATEMIA (>10.1 mg/dL)

Signs & symptoms:AnorexiaChvostek’s/ Trousseau’s signsConjuntivitis, visual impairmentDecreased mental statusHyperreflexiaMuscle weakness, cramps, spasmNausea & vomitingPapular eruptionsParesthesiaTetany

Hyperphosphatemia

Interventions:Monitor vsMonitor for arrhythmiasInsert and maintain IV lineAdminister a diureticStrain the urine for calculiWatch for signs/symptoms of digitalis toxicityProvide a safe env’t.Provide safety

HYPOCHLOREMIA (<96 meQ/L)

Signs & symptoms:

Hyperactive DTRsMuscle hypertonicitys/sx pf acid-base imbalancestetany

Hypochloremia

Interventions:

Monitor vs & LOCMonitor serum electrolyte levelsOffer food high in chlorideInsert and maintain a patent IV lineAccurately measure I and OUse NSS to flush NGTProvide a safe and quiet env’t.

HYPERCHLOREMIA (>106 mEq/L)

Signs & symptoms:

ArrhythmiasDecreased CODecreased LOC that may progress to coma

Hyperchloremia

Interventions:Monitor vs including cardiac rhythmProvide safetyLook for changes in respiratory patternInsert and IV and maintain patencyRestrict fluids, Na, and Cl as neededMonitor serum & electrolyte levels and ABG resultsMonitor I and O

HYPOMAGNESEMIA (<1.5 meQ/L)

Signs & symptoms:

Altered LOC, confusion, hallucinationsMuscular weakness, leg and foot cramps, Hyperactive DTRs, tetany, Chvostek’s & trousseau’s signsTachycardia, hypertensionDysphagia, anorexia, nausea, vomiting

Hypomagnesemia

Interventions:

Monitor vs & LOCMonitor serum electrolyte levelsOffer food high in magnesiumInsert and maintain a patent IV lineAccurately measure I and OProvide a safe and quiet env’t.

HYPERMAGNESEMIA (>2.5 mEq/L)

Signs & symptoms:

Decreased muscle and nerve activityHypoactive DTRsGeneralized weakness, drowsiness, lethargyNausea, vomitingSlow, shallow, respirationsRespiratory arrestECG changesVasodilation

Hyperchloremia

Interventions:Monitor vs including cardiac rhythmProvide safetyLook for changes in respiratory patternInsert and IV and maintain patencyRestrict fluids, Na, and Cl as neededMonitor serum & electrolyte levels and ABG resultsMonitor I and O

ACID-BASE BALANCE

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)

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

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

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)

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

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

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

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

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

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¯

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)

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

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

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

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

Proximal tubule secretion and reabsorption of filtered HCO3-

Kidney Hydrogen Ion Balancing: Proximal TubuleKidney Hydrogen Ion Balancing: Proximal Tubule

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

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

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 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

Ammonium Ion Excretion

Figure 26.14

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

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

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

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

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

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

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

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

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

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

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

Developmental Aspects Water content of the body is greatest at birth

(70-80%) 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

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

Problems with Fluid, Electrolyte, and Acid-Base Balance

ABG Analysis

pH 7.35 - 7. 45

PaCO2 35 - 45 mm Hg

HCO3- 22 - 26 mEq/L

Step 1: Classify the pHNormal: 7.35 - 7.45Acidemia: <7.35Alkalemia: >7.45

Step 2: Assess PaCO2 Normal: 35- 45 mm HgRespiratory acidosis: >45 mm HgRespiratory alkalosis: <35 mm Hg

Step 3: Assess HCO3-

Normal: 22-26 mEq/LMetabolic acidosis: <22 mEq/LMetabolic alkalosis: >26 mEq/L

Step 4: Determine Presence of CompensationCompensation 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 PossibleIf 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

RESPIRATORY ACIDOSIS

UncompensatedCompensated

pH < 7.35 Normal

PaCO2 (mmHg) < 45 > 45

HCO3- (mEq/L) Normal > 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

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

Pathophysiology

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

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 & HCO3- levels, & 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

Signs and Symptoms

apprehensionconfusiondecreased deep-tendon reflexesdiaphoresisdyspnea, with rapid, shallow respirationsnausea or vomitingrestlessnesstachycardiatremorswarm, flushed skin

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 orderedPerform tracheal suctioning, incentive spirometry, postural drainage, & coughing & deep breathing, as indicated

- Make sure the pt takes in enough fluids, both oral & IV, & maintain accurate I & O records

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

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

- need for increased caloric intake, if appropriate

RESPIRATORY ALKALOSIS

Uncompensated Compensated

pH > 7.45 Normal

PaCO2 (mmHg) < 35 < 35

HCO3- (mEq/L) Normal < 22

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 anemia, pulmonary embolus, & hypotension

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

- Stay with pt during periods of extreme stress & anxiety

- Institute safety measures & seizure precautions

Treatment

- focus is on removing the underlying cause

- oxygen therapy

- sedative/anxiolytic

-breathing into a paper bag

Health Teaching

- explanation of the condition & its treatment

- anxiety-reducing techniques, if appropriate

-controlled-breathing exercises, if appropriate

-prescribed medications

METABOLIC ACIDOSIS

UncompensatedCompensated

pH < 7.35 Normal

PaCO2 (mmHg) Normal < 35

HCO3- (mEq/L) < 22 <22

Causes

Loss of HCO3-

Accumulation 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

Poisoning or toxic drug reaction

Signs and Symptoms

confusion dull headache

decreased DT reflexes hyperkalemic s/sx

hypotension Kussmaul’s respirations

lethargy warm, dry skin

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

Treatment

-adjust the K

-Replace the HCO3-

-Ventilatory support

-Dialysis

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

METABOLIC ALKALOSIS

Uncompensated Compensated

pH > 7.45 Normal

PaCO2 (mmHg) Normal > 45

HCO3- (mEq/L) > 22 <26

Causes

Excessive acid loss from the GIT

Diuretic therapy

Cushing’s dse.

HCO3- accumulation in the body

Pathophysiology (diagram here)

Chemical buffers bind w/ ions

Excess HCO3 that don’t bind w/ chemical buffers

Elevated serum pH level

Depressed respiratory system

pH >7.45

HCO3 >26

Slow, shallow resp.

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

Alkaline urine &

Near normal

HCO3 level

Na, H2O, & HCO3- excretion via the kidneys

Ions shifting ( K and H)

Decreased Ca ionization

Nerve cells’ increased permeability to Na ions

polyuria

Hypovolemia s/sx

tetany

belligerence

irritability

Hypokalemia s/sx: anorexia, muscle weakness, etc.

disorientation

seizures

Signs and Symptoms

anorexia apathy

confusion cyanosis

hypotension loss of reflexes

muscle twitching nausea

paresthesia polyuria

vomiting weakness

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

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

acid-base

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