NRS 3015 - Acid-Base Disturbances

solution

solvent+solute

solvent

fluid medium

solute

particles in the solvent

blood

blood cells + plasma

blood cells

◦Erythrocytes (RBC)

◦Leukocytes (WBC)

◦Thrombocytes (platelets)

plasma composition

◦Solvent: 92% water

◦Solutes: proteins (mainly albumin), glucose, lipoproteins, mineral ions (electrolytes)

Osmosis

 - Movement of water across a semipermeable membrane

◦from lower solute concentrate to an area of higher solute concentrate

◦moving water from the extracellular fluid (ECF) to the intracellular fluid (ICF)

diffusion

 solutes move from an area of higher concentration to an area of lower concentration until equilibrium is reached

◦exchange of O₂ and CO₂ between the pulmonary capillaries and alveoli).

filtration

water and solutes move across a membrane - through hydrostatic pressure

kidneys filter approximately 180L of plasma per day

active transport

 - water and solutes move against concentration gradient - requires energy (ATP)

sodium–potassium pump

body fluid is roughly 60% of adult weight

◦Influenced by age, sex, and body fat

◦Younger individuals have higher body fluid percentage

◦Males have more body fluid than females

intracellular fluid (ICF)

two thirds of body fluid

extracellular fluid (ECF)

one third of body fluid

intravascular

blood

interstitial

fluid surrounding cells

transcellular

CSF, pericardial, pleural, intraocular, synovial, sweat, digestive secretions

normal fluid movement through capillary walls

governed by Starlin’s Laws of Capillary Forces

hydrostatic pressure

exerted by fluid on blood vessel walls (water pushing)

osmotic pressure

exerted by solutes within plasma (water pulling)

oncotic pressure

osmotic pressure of albumin within blood. pulls and holds blood

fluid movement direction depends on hydrostatic and osmotic pressures

◦hydrostatic pressure > osmotic pressure = fluid moves from ECF to ICF

fluid and electrolyte gains

drinking and eating, intake and output roughly equal

fluid and electrolyte losses

◦Kidneys: urine

◦Skin: perspiration and insensible water loss

◦Lungs: water vapor

◦GI tract: stool

water of oxidation

water produced inside body through cellular respiration

serum osmolality

 Reflects sodium concentration

◦Influenced by blood urea nitrogen (BUN) and glucose

urine osmolality

 Determined by urea, creatinine, and uric acid

◦Reliable indicator of urine concentration

normal range of serum osmolality

275 to 290 mOsm/kg

urine osmolality

200-800 mOsm/kg

kidneys filter 180L of plasma daily and excrete 1-2L of urine

◦Regulate ECF volume & osmolality

◦Regulate normal electrolyte levels in ECF

◦Regulate pH of ECF

◦Excrete metabolic waste & toxic substances

•Regulation of ECF volume and osmolality by selective retention and excretion of body fluids

•Regulation of normal electrolyte levels in the ECF by selective electrolyte retention and excretion of hydrogen ions

•Regulation of pH of the ECF by retention and excretion of hydrogen ions

•Excretion of metabolic wastes and toxic substances

pumping action of the heart

circulates blood through kidneys and ensures sufficient pressure for urine formation

failure of heart pumping action

interferes with renal perfusion and affects water and electrolyte regulation

lungs maintenance of homeostasis

◦Exhalation removes approximately 300 mL of water daily

◦Hyperventilation or continuous coughing increases water loss

lungs role in acid-base balance

◦Regulate CO₂ levels

◦Influence acid content of the bloodstream

hypothalamus and ADH function

◦Hypothalamus manufactures ADH

◦ADH stored in posterior pituitary gland

hypothalamus makes ADH and stores it in posterior pituitary

•ADH = antidiuretic hormone à HOLDS fluid (anti-diuresis)

ADH release

◦Triggered by dehydration or blood loss

◦Increases water reabsorption at nephron collecting duct

◦Raises water content in bloodstream

aldosterone

◦Secreted by adrenal cortex

◦Causes sodium and water retention, potassium loss

cortisol

◦Less mineralocorticoid action than aldosterone

◦Large quantities cause sodium and fluid retention

parathyroid functions regulation of calcium and phosphate balance

◦Parathyroid hormone (PTH) influences calcium reabsorption

◦PTH affects calcium absorption from bones, intestine, and renal tubules

baroreceptors location

left atrium and carotid and aortic arches

baroreceptors function

◦Respond to changes in circulating blood volume

◦Regulate sympathetic and parasympathetic neural activity

◦Influence endocrine activities

blood pressure drops. Baroreceptors recognize and trigger mechanisms. Blood pressure increases. Hydrostatic pressure restored.

renin-angiotensin-aldosterone system

 Kidneys sense ↓ BP or perfusion = Renin released

 Renin travels to liver

◦Angiotensinogen à angiotensin I

 Angiotensin I travels to lungs

◦Angiotensin I à angiotensin II

 Angiotensin II acts to increase BP & perfusion

◦Systemic arterioles constrict (narrow)

◦Stimulates adrenal release of aldosterone (Na & H20 retention)

Stimulates hypothalamus to trigger thirst & release ADH

Kidneys sense low perfusion - renin secreted → RAAS system switched on

types of natriuretic peptides

 Types:

-Atrial natriuretic peptide (ANP)

-Brain natriuretic peptide (BNP)

-N-terminal pro-BNP (NT-pro BNP)

 Functions:

-Affect fluid volume and cardiovascular function

-Promote natriuresis (sodium excretion)

-Oppose renin–angiotensin–aldosterone system

 Clinical Relevance:

-BNP and NT-pro BNP levels used in heart failure diagnosis and
management

NPO

nothing by mouth

parenteral fluid therapy

administering fluids via IV route

goals of IV fluid therapy

◦Provide water, electrolytes, and nutrients to meet daily requirements.

◦Replace water and correct electrolyte deficits.

◦Administer medications and blood products.

IV solutions

 Contain dextrose and/or electrolytes mixed with water

◦Pure, electrolyte-free water cannot be given IV

hypotonic fluids

solute concentration is lower than body’s cells

water moves into cells and out of the blood stream

cells swell and can burst

ex. 0.45% NaCl

used to treat cellular dehydration, hypernatremia, late stage DKA

isotonic fluids

equal to body’s cells

moves fluid in and out equally

cells maintain shape and size

ex. 0.9% NaCl and LR

used for hypovolemia, low BP, minor hyponatremia

hypertonic fluids

higher solutes than body’s cells

water moves out of cells and water moves into bloodstream

cells shrink and shrivel (crenate)

ex. 3% NaCl and 10% D10W

used for cerebral edema, severe hyponatremia, severe organ swelling

D5W

Isotonic in the bag, but hypotonic in the body.

•Only contains 50g of dextrose and 1L water – no electrolytes

•The body immediately metabolizes the dextrose and leaves behind hypotonic solution (free water)

•Treats cellular dehydration and/or hypernatremia

•Treats late stage DKA

0.9% Sodium Chloride (Normal Saline) - Isotonic Solution

 Composition of normal saline:

◦Contains water, sodium, and chloride

◦Remains within ECF, expands intravascular volume

 Uses of normal saline:

◦Correct extracellular volume deficit

◦Used with blood transfusions, replace large sodium losses
(e.g., burns)

 Contraindications:

◦Not used in heart failure, pulmonary edema, kidney impairment, or sodium retention

LR - isotonic

 Contains potassium and calcium in addition to sodium chloride

 Used to correct dehydration, blood loss, sodium depletion, and replace GI losses

 Similarity to ECF:

◦Solutions contain ions similar to ECF composition.

nutritional requirements via IV

◦High concentrations of glucose, protein, or fat

◦Used when patient cannot tolerate food

IV administration of colloids, plasma expanders, and blood products

◦Examples: Whole blood, packed RBCs, fresh-frozen plasma, albumin, cryoprecipitate

IV medication administration

◦Continuous infusion or intermittent bolus

Potentially hazardous due to rapid entry into circulation

nursing management of IV therapy

 Nursing responsibilities:

◦Perform venipuncture, select appropriate site and cannula.

◦Demonstrate competency in IV catheter placement.

 Guidelines and regulations:

◦Follow nurse practice act, organizational policies, and practice guidelines.

infection prevention in IV therapy

 Sources of infection:

◦Needle reuse, IV access port, medication vial contamination

◦Local involvement to systemic dissemination (sepsis)

 Signs and symptoms:

◦Abrupt temperature elevation, backache, headache, increased pulse and respiratory rate

◦Nausea, vomiting, diarrhea, chills, shaking, general malaise

 Preventive measures:

◦Aseptic techniques, hand hygiene, disinfection of vascular access devices

fluid overload in IV therapy

 Causes of fluid overload:

◦Rapid infusion of IV solution, hepatic, cardiac, or kidney disease

◦Increased risk in older patients with cardiac disease

 Signs and symptoms:

◦Moist crackles, cough, restlessness, distended neck veins, edema, weight gain

◦Dyspnea, rapid shallow respirations

 Treatment:

◦Decrease IV rate, monitor vital signs, assess breath sounds, high Fowler position

air embolism in IV therapy

 Causes of air embolism:

◦Cannulation of central veins, size and rate of embolus entry

◦Air travels to right ventricle, blocks pulmonary valve

 Manifestations:

◦Palpitations, dyspnea, coughing, jugular venous distention, wheezing, cyanosis

◦Hypotension, weak rapid pulse, altered mental status, chest, shoulder, low back pain

 Treatment:

◦Clamp cannula, replace infusion system, Trendelenburg position, assess vital signs, administer oxygen

managing local complications

 Types of local complications:

◦Phlebitis, infiltration, extravasation, thrombophlebitis, hematoma, occlusion, catheter dislodgement

 Prevention and treatment:

◦Use aseptic technique, appropriate size cannula, monitor site hourly.

◦Discontinue IV line, apply warm compress, restart IV in another site.

vessicant

medication that is caustic and potential for extravasation (chemo, contrast, many meds)

home infusion therapies

◦Antibiotic, analgesic, antineoplastic medications, blood therapy, parenteral nutrition

role of infusion nurse

◦Implement and monitor IV therapy, assess patient condition, educate patient and family

collaboration and documentation

◦Collaborate with case manager, develop care plan, arrange referrals and follow-up

◦Ensure appropriate documentation for third-party payment.

fluid volume deficit (FVD) aka hypovolemia

◦ECF volume loss > fluid intake

◦Water and electrolytes lost in same proportion as in normal body fluids

◦Serum electrolyte concentrations may vary

dehydration

◦Refers to loss of water alone, with increased serum sodium levels

◦Should not be confused with FVD

hypovolemia

causes: excess loss (vomiting, diarrhea, GI suctioning, sweating), insufficient intake (most rapid cause), third-space fluid shifts (edema in burns, ascites with liver dysfunction), pathologic functions (diabetes insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, coma)

clinical manifestations: weight loss, oliguria and concentrated urine, prolonged cap refill, low BP and high HR, flat neck veins, weakness/dizziness/lightheadedness, thirst and nausea, confusion, muscle cramps, sunken eyes, cool, clammy, pale skin

 Monitor & Measure Intake/Output – AKA I’s and O’s (I/O): Frequency depends on severity (q1h, q4h, q8h), Accuracy is crucial during critical illness

 Physical Monitoring: Skin – turgor, pallor, temp, moisture, Mucous membranes (tongue dryness), Urine concentration, Mental function, Peripheral perfusion – cap refill, Vital signs – late sign!

hypokalemia

can occur with GI and kidney disorders as these organs are major regulators of potassium.

<3.5 mEq/L

contributing factors: diarrhea, vomiting, gastric suction, corticosteroids, hyperaldosteronism, potassium wasting meds, metabolic alkalosis, starvation

manifestations: fatigue, anorexia, N/V, muscle weakness, polyuria, decreased bowel motility, abdominal distention, hypoactive reflexes, EKG CHANGES

management: prevention through K supplements and foods (fresh fruit, veggies, lean meats, salt substitutes) oral potassium supplementation preferred. continuous cardiac monitoring (ECG)

hyperkalemia

can occur with adrenal insufficiency due to aldosterone deficiency, which causes lack of potassium excretion.

>5.0 mEq/L

contributing factors: kidney injury, potassium sparing and increasing meds, metabolic acidosis, addison’s disease, crush injury, burns, excess IV potassium

manifestations: muscle weakness, tachycardia → bradycardia, arrythmias, paralysis, paresthesias, intestinal cramps, abdominal distension, irritability and anxiety

management: potassium restriction, potassium binding meds (excreted through stool) lokelma, kayexelate

emergency management: calcium chloride/gluconate, insulin and dextrose, B2 agonists (albuterol)

nursing: continuous cardiac monitoring

hyponatremia

can occur with increased thirst and ADH release, which increases the water content of the bloodstream

<135 mEq/L

causes: diuretics, loss of GI fluids, kidney disease, adrenal insufficiency, water gain (excess d5w), psychogenic polydipsia, SIADH (cancer, head trauma), pharmacologic causes

treat the cause and correct sodium levels (IV or oral routes), water and fluid restriction (limits), isotonic IV fluids (LR or NS - increase slowly <12 mEq/L in 24 hr)

Emergency: hypertonic IV solutions

Nursing: bed alarm, padded rails, strict I/O monitoring

SEIZURE PRECAUTIONS

hypernatremia

can result from increased insensible water losses and diabetes insipidus

>145 mEq/L

causes: fluid deprivation and loss of thirst, DI, heatstroke, hyperventilation, diarrhea, burns, diaphoresis

Gradual decrease (0.5 to 1 mEq/L per hour), IV fluids hypotonic - 0.45% Na or D5W

if from DI - desmopressin IV

nursing: bed alarm, padded rails, strict i/o monitoring

SEIZURE PRECAUTIONS

management of hypovolemia

 Planning Correction of Fluid Loss & Consider maintenance requirements and other factors (e.g., fever)

 Oral route preferred if deficit is not severe

 IV route required for acute or severe fluid losses

 Isotonic Electrolyte Crystalloid Solutions - First-line choice for hypotensive patients

◦Lactated Ringers (LR)

◦0.9% Sodium Chloride – AKA normal saline

 Hypotonic electrolyte solution used once normotensive (e.g., 0.45% sodium chloride)

 Preventing hypovolemia

◦Identify at-risk patients and minimize losses

◦control diarrhea and provide replacement fluids

hypervolemia

causes: compromised regulatory mechanism (renal injury, heart failure, cirrhosis), excess administration of Na containing fluids, fluid shifts (burns), prolonged steroid therapy, hyperaldosteronism

clinical manifestations: weight gain, peripheral edema/ascites, JVD, lung crackles and cough, SOB, increased RR, BP, urine output and bounding pulse, CXR may show pulmonary congestion

lab changes: lower Hgb and Hct, serum and urine osmolality, urine specific gravity (diluted), Decreased BUN and hematocrit levels due to plasma dilution

Decreased serum osmolality and sodium levels in chronic kidney disease

Increased urine sodium level if kidneys are excreting excess volume

management of hypervolemia

 Management directed at causes

◦Discontinue excessive sodium-containing fluids if applicable

 Symptomatic treatment:

◦ diuretics, fluid and sodium restriction

 Diuretics

◦Reduce sodium and water reabsorption at the nephron

◦Enhance water loss via kidneys à MAKE MORE PEE!

◦AKA “water pill”

symptomatic monitoring of progress

 Monitoring fluid retention

 Measure I&O at regular intervals

◦Assess patient weight daily for rapid weight gain

 Monitor breath sounds and degree of edema

 Edema assessment

◦Evaluate pitting edema using a scale
(1+ to 4+)

Measure extremity circumference with a tape measure

phlebitis

inflammation of the vein

sx. warm skin, red line along vein, pain

tx. replace IV (use new site), apply warm compress, monitor q1 hr

infiltration

leak of fluids or meds into surrounding tissues

sx. cool skin, edema, pallor, pain

tx. discontinue IV, elevate extremity, apply warm or cold compress, monitor q1 hr

extravasation

leak of damaging meds into surrounding tissues

sx. warm skin, edema, redness, pain

tx. discontinue IV, apply cold compress, administer antidote as ordered

electrolyte imbalances

 Super common

◦Trend & compare to previous values

◦May need correction

 Key lytes: sodium, potassium, calcium, magnesium, phosphorus, and chloride.

 Imbalances can lead to significant clinical manifestations and require prompt management.

Na

 Most abundant electrolyte in the ECF.

◦Normal: 135 to 145 mEq/L.

◦Primary determinant of ECF volume and osmolality.

 Regulated by ADH, thirst, and RAAS

 Purpose:

◦water distribution, muscle contraction, and nerve impulse transmission.

 Common imbalances:

◦Hyponatremia

Hypernatremia

severe hyponatremia

 Cellular swelling & cerebral edema – Increased ICP!

◦Altered mental status

◦Status epilepticus (seizure)

◦Coma

◦The faster the drop in Na, the worse the outcome

◦Severe cerebral edema à compression of brain & brain herniation

potassium

 major intracellular electrolyte.

◦98% inside cells, 2% in ECF.

◦Normal serum level: 3.5 to 5 mEq/L.

 Influences neuromuscular and cardiac function.

Alterations affect myocardial irritability and rhythm

calcium

 Major component of bones and teeth.

◦99% in skeletal system, 1% in serum.

◦Normal total serum calcium: 8.5 to 10.5 mg/dL.

 Functions:

◦Nerve impulse transmission, muscle contraction/relaxation.

◦Enzyme activation, blood coagulation

hypocalcemia

<8.5 mg/dL

causes: hypoparathyroidism, malabsorption, pancreatitis, alkalosis, vitamin D deficiency, massive infections, peritonitis, mass transfusion of blood (citrate binds), chronic diarrhea, acute kidney injury, burns, alcohol use disorder

manifestations: numbness/tingling in fingers and tongue and around the mouth, positive trousseau sign, positive Chvostek sign, carpopedal spasms, hyperactive DTR’s, irritability and anxiety, impaired clotting, bronchospasm, seizures, EKG changes

management: prevention - calcium and vitamin D supplementation. emergency - IV calcium administration (calcium chloride - can cause sloughing and severe skin necrosis if infiltrated, calcium gluconate)

nursing: ECG and seizure precautions - bed alarm/padded rails

hypercalcemia

>10.5 mg/dL

causes: hyperparathyroidism, malignant tumors, prolonged immobilization, excess intake of calcium supp, excess vitamin D, AKI, acidosis, corticosteroid therapy, thiazide diuretics, digoxin toxicity

manifestations: muscle weakness, constipation, anorexia, n/v, hypoactive DTR’s, lethargy, bone pain, pathologic fractures, renal stones and flank pain, hypertension

management: treat the underlying cause - cancer treatment, partial parathyroidectomy, dilute serum calcium and promote excretion (IV fluids), IV phosphate binds to Ca, loop diuretics, calcitonin - reduces bone breakdown, increases excretion

nursing: increases mobility, increase fluids, I/O monitoring, sodium containing fluids will promote calcium excretion, ECG

chvostek sign

contraction of facial muscles elicited in response to a light tap over the facial nerve in front of the ear

trousseau sign

carpopedal spasm induced by inflating a BP cuff above systolic BP

magnesium

 Magnesium: abundant intracellular cation

◦Normal serum level: 1.8 to 3.0 mg/dL

 Functions:

◦Activator for enzyme systems, carbohydrate/protein metabolism

◦Neuromuscular function, cardiovascular system

 Common imbalances: magnesium deficit (hypomagnesemia) and magnesium excess (hypermagnesemia)

hypomagnesium

<1.8 mg/dL

causes: chronic alcohol use disorder, hyperparathyroidism, hyperaldosteronism, AKI, malabsorption, DKA, starvation and refeeding, IV nutrition, chronic laxative use, diarrhea, MI, HF, pharmacologic agents

manifestations: neuromuscular irritability, positive trousseau and chvostek sign, mood changes, anorexia, n/v, seizures, increased DTR’s, BP, and EKG changes

management: prevention, diet and supplementation, IV administration

nursing: continuous cardiac monitoring

hypermagnesium

>3.0 mg/dL

rare - usually from excess IV administration (IV magnesium can cause transient hypotension d/t relaxation of smooth muscle walls, May cause flushing, May cause transient weakness, Monitor vitals closely, Monitor respiratory status closely

Causes: AKI, adrenal insufficiency, excess IV mg admin, DKA, hypothyroidism

manifestations: flushing, hypotension, muscle weakness and decreased DTR’s, drowsiness, shallow breathing, cardiac arrest, coma, diaphoresis, EKG changes

management: prevention and careful administration, loop diuretics, IV fluids (NS/LR). emergency - dialysis

nursing: continuous cardiac monitoring, monitor respiratory status, I/O monitoring

phosphorus

critical constituent of body tissues.

◦Normal serum level: 2.5 to 4.5 mg/dL

 Functions:

◦Muscle and RBC function, ATP formation, acid–base balance

◦Structural support to bones and teeth

 Common imbalances: phosphorus deficit (hypophosphatemia) and phosphorus excess (hyperphosphatemia)

Because phosphorus is such a vital part of energy in the body (Adenosine Triphosphate – ATP), most symptoms of depletion are a result of energy loss

•Impaired cellular energy resources

•Impaired oxygen delivery to tissues

•Resultant muscle damage

Most symptoms of hyperphosphatemia come from the reciprocal drop in calcium (see slide)

hypophosphatemia

<2.5 mg/dL - rarely due to insufficient intake - plentiful in food

causes: starvation and refeeding, ETOH withdrawal, DKA, metabolic alkalosis, lower mg, hypoparathyroidism, vomiting and diarrhea, hyperventilation, vit D deficiency, burns, acid-base disorders, IV nutrition, diuretics, antacids

manifestations: paresthesias, muscle weakness, bone pain and tenderness, chest pain, cardiomyopathy, confusion, increased risk of infection, resp failure, seizures, tissue hypoxia, nystagmus

management: monitoring and prevention, treatment of causes, supplementation when needed (oral/IV), vit D (enhance absorption)

nursing: lab monitoring, mental status exams, continuous cardiac monitoring, respiratory monitoring, seizure precautions

hyperphosphatemia

>4.5 mg/dL

causes: AKI, CKD, excess intake of phosphorus and vit D, acidosis (met/resp), hypoparathyroidism, hypovolemia, cancer, cancer treatments, rhabdomyolysis

manifestations: tetany, tachycardia, anorexia, n/v, muscle weakness, symptoms of hypocalcemia

management: monitoring and prevention, reduced intake of phosphorus-rich foods, phosphate binders (sevelamer), monitor I/O, monitor for muscle symptoms

nursing: lab monitoring, mental status exams, continuous cardiac monitoring, respiratory monitoring, seizure precautions

acid-base disturbances

 Commonly - especially in critical care units

 Plasma pH indicates hydrogen ion (H+) concentration

◦Normal pH range: 7.35 to 7.45

 Homeostatic mechanisms maintain pH balance

 Buffer systems, kidneys, and lungs

 Importance of H+ concentration

◦Higher H+ concentration = more acidic, lower pH

◦Lower H+ concentration = more alkaline, higher pH

buffer systems

 Prevent major changes in pH by removing or releasing H+.

 Major extracellular buffer system:

◦Bicarbonate–carbonic acid buffer system

 Normal ratio:

◦20 parts bicarbonate (HCO₃) to 1 part carbonic acid (H₂CO₃)

◦If ratio altered, pH will change

◦Ratio more important than absolute values

 CO₂ as a potential acid (proxy for carbonic acid)

◦Dissolved in water: (CO₂ + H₂O = H₂CO₃)

◦THEREFORE:

◦Increased CO₂ = increased carbonic acid

Decreased CO₂ = decreased carbonic acid

kidney regulation

 Regulate bicarb (HCO₃^-) in extracellular fluid

 Can regenerate bicarb from renal tubular cells

 Correcting acidosis:

◦Excrete hydrogen ions into urine

◦Conserve bicarb in blood

 Correcting alkalosis:

◦Retain hydrogen ions in blood

◦Excrete bicarb into urine

lung regulation

 Adjust ventilation in response to CO₂ in the blood

◦Changes in PaCO₂ stimulates response (particularly a rise)

◦Changes in PaO₂ stimulates response (not as potent)

 Correcting acidosis:

◦↑ RR à elimination of CO₂

 Correcting Alkalosis:

↓ RR à retain CO₂

metabolic acidosis

pH < 7.35 & bicarb < 22 mEq/L

 Due to:

◦Gain of H⁺ ions or Loss of bicarbonate (HCO₃^-)

 Subtypes:

◦High anion gap metabolic acidosis

◦Normal anion gap metabolic acidosis

◦The anion gap helps root out the cause

assessment and diagnostics: abg/vbg for diagnosis pH<7.35, bicarb <22 mEq/L, high K+ in blood d/t cellular shift - monitor closely and may cause arrythmia, ECG monitoring suggested

management: correct metabolic imbalance, if chloride related - reduce intake (change IV fluids), administer bicarb if necessary, continue to monitor K+ as pH corrected, alkalizing agents and dialysis if necessary

normal anion gap metabolic acidosis

◦Direct loss of bicarb

◦GI: diarrhea, lower intestinal fistulas, ureterostomies

◦Renal: renal insufficiency

◦Excess chloride administration (NS excess)

◦IV nutrition low in bicarb

◦Meds: diuretics

high anion gap metabolic acidosis

◦Excess accumulation of acid (H⁺ ions)

◦Lactic acidosis

◦Salicylate poisoning (aspirin)

◦Renal failure

◦Methanol

◦Ethylene/propylene glycol toxicity

◦Diabetic ketoacidosis (DKA)

◦Starvation ketoacidosis

High H⁺ ions neutralized & buffered by bicarb anions – causing bicarb to fall and exhaust à large gap