By Dr Lee June Lyng

y Fluid Volume y Electrolyte Imbalance- Sodium, K,Ca y Acid-Base Disturbance

Metabolic Acidosis, Resp Acidosis, Metabolic Alkalosis

y Total body water

y Water constitutes

y % of TBW
Plasma 5% ECF (1/3)

approximately 50 to 60% of total body weight y divided into two functional fluid compartments, the extracellular and intracellular

Interstitial fluid 15%

Intracellular volume 40%

ICF(2/3)

Intake Liquid 1,200 -1,500 ml Water in food 700 - 1,000 ml Metabolism 200 - 400 ml

TOTAL

2,100 2,900 ml

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

y Fluid Movement by Diffusion and Osmosis

y Diffusion- means by which substances such as nutrients and

wastes produces move between blood and interstitial spaces

y Osmolality

refers to the concentration of solutes in 1 liter of solution

y OSMOSIS: diffusion of H2O across a selectively permeable

membrane from an area of lower solute concentration to an area of higher solute concentration.

ECF

Cell membrane

ICF

Na, Cl, and HCO3 Na has osmotic and electrical properties and it is a/w water Any Na containing fluids are distributed throughout the ECF Adds volume at intravascular and interstitial Expand the intravascular volume #Na in ECF high , H2o will be high!!

K, Mg/Phosphate and protein

ATP NaK pump

y ECF volume
y Regulate to help BP by

y ECF osmolarity
y Regulate to prevent

salt balance y 2 mech:

y Short term
y Baroreceptors y Fluid shifts btw plasma

swelling/shrinking of cells by H2O blance

and interstitial fluid

y Long term
y By kidneys and thirst

mechanism

y Short term control measures to maintain BP

y Baroreceptors reflex

y Fluid shifts between plasma and interstitial fluid y Barrier - blood vessels y According to HP and COP y Eg: decreased in plasma volume compensated by shifting fluid from interstitial fluid and vice versa.

y Long term
y By kidney and thirst mechanism.

Decreased Na load in the body Decreased arterial BP Increased aldosterone Increased Na reabsorption Decreased Na excretion

Decreased GFR Decreased Na filteration

Increased Na retention Increased plasma volume Increased ECF volume

y Thirst y Hypothalamus- thirst

center of the brain y Activated by an increase in ECF Osmolality due to:

y Hypotension y Polyuria y Fluid volume depletion

REGULATION OF FLUID VOLUME

HYPERVOLEMIA

HYPOVOLEMIA

inhibits

stimulates

ADH

Aldosterone

Thirst

Thirst

ADH

Aldosterone

INCREASED URINATION of Dilute urine

DECREASED URINATION of Concentrated urine NORMAL FLUID VOLUME RESTORED

Types of Intravenous Fluids:

y

ISOTONIC a solution that has the same osmotic pressure externally as that found across a semi-permeable membrane --0.9% NaCl, D5W, 5% Dextrose in 0.225% Saline and LRS HYPOTONIC a solution that has a lower osmotic press than that of the blood causing the cell to expand and swell.(They contain lower concentration of salt/ solute than other solution) --0.3 % NaCl, D in water, 0.45 % NaCl and distilled water. HYPERTONIC a solution that has a higher osmotic pressure than that of the blood causing the cell to shrink. ( It has higher concentration of solutes.) --D5LRS, Mannitol, 10% D in water, and 5% D in 0.45% NaCl

Electrolyte Solutions for Parenteral Administration Electrolyte Composition (mEq/L) solution Extracellular fluid Lactated Ringer's 0.9% Sodium chloride D5 0.45% Sodium chloride D5 W(isotonic and it becomes hypotonic once dextrose metabolized) 3% Sodium chloride 513 513 Na 142 130 154 77 Cl 103 109 154 77 K 4 4 HCO3 27 28 Ca 5 3 Mg 3 mOs m 280310 273 308 407 253

1026

Alternative Resuscitative Fluids Solution Hypertonic saline (7.5%) Albumin 5% Albumin 25% Dextran 40 Dextran 70 Hetastarch Hextend Gelofusine 70,000 70,000 40000 70,000 450000 670000 30000 Molecular Weight Osmolality (mOsm/L) 2565 300 1500 308 308 310 307 n/a Sodium (mEq/L 1283 130-160 130-160 154 154 154 143 154

y Hypertonic saline (7.5%) -treatment modality in

patients with closed head injuries. It has been shown to increase cerebral perfusion and decrease intracranial pressure, thus decreasing brain edema
y hypertonic saline is an arteriolar vasodilator, thus,it may

cause bleeding

y Colloids are also used in surgical patients and have

long been debated as effective volume expanders compared to isotonic crystalloids

y Due to their molecular weight, they are confined to the

intravascular space and their infusion results in more efficient plasma volume expansion. y However, in severe hemorrhagic shock, capillary membrane permeability increases, permitting colloids to enter the interstitial space, which can worsen edema and impair tissue oxygenation

y four major types of colloids available

albumin,

dextrans, hetastarch, and gelatins y Colloid solutions with smaller size particles and lower molecular weights exert a greater oncotic effect, but are retained within the circulation for a shorter period of time than larger and higher molecular weight colloids

y Disadvantage of colloids
y d/t high molecular weight, kidneys unable to filter and it

may cause plug at the glomerulus filter, thus, may cause kidney failure.

Surgical patients prone to disruption nil orally anaesthesia trauma sepsis

Surgical patients need

yMaintenance volume requirements yOn going losses yVolume excess/deficits yMaintenance electrolyte requirements yElectrolyte excess/deficits

y Body weight

0-10Kg next 10-20Kg subsequent Kg

Fluid required 100ml/kg/d 50 ml/kg/d 20ml/kg/d

y 15ml/Kg/d for elderly

1st 10kg x 100mls = 1000mls 2nd 10kg x 50mls = 500mls Next 50kg x 20mls= 1000mls TOTAL 2500 mls /d

y NG y drains y fistulae y third space losses

Concentration is similar to plasma Replace with isotonic fluids

y Acute
y vital signs changes
y y y

Blood pressure Heart rate CVP

y tissue changes not obvious y urine output low

y Chronic
yDecreased skin turgor ySunken eyes yOliguria yOrthostatic hypotension yHigh BUN/Creatine ratio

y Nil per oral deficit= no.

y Mod surgical trauma 5-

of hours of NPO x maintainence fluid requirement (ml/h) y Bowel prep 1L y Superficial surgical trauma 1-2ml/kg/hr y Minimal surgical trauma 3-4ml/kg/hr ( hernia, head, neck surgery)

6ml/kg/hr (hysterectomy,chest surgery) y Severe surgical trauma 8 -10ml/kg/hr (or more) in AAA repair,nephrectomy

y Eg: 62 yr male, 80kg for hemicolectomy y NPO at 2200 and surgery starts at 8am.he received

bowel prep. y 3 hour procedure y 500cc bl loss y What is the fluid requirement?

y Fluid deficit = 120ml/h (x) 10h = 1200ml (+) 1000ml

(bowel prep) = 2200ml

y Replace 1st hour, at 2nd half, at 3rd hour

y Maintainence

120ml/h (x) 3h= 360ml y 3rd space loss 6ml/kg/hr (X) 3 h=1440ml y Bl loss = 500ml (x) 3= 1500ml y Total fluid replacement= 5500ml

y Na 1-2mEq/Kg/d y K

0.5 - 1 mEq/Kg/d

y y

Usually correct over 24 hours For ill patients calculate over shorter period and reassess e.g. 1, 2 hours or 3 hours for e op cases Deficits - correct half the amount over the period and reassess
y

By fluid challenge
y y

Normally, 10 20ml/kg In elderly or co-morbid, 5ml/kg

y Check i/v regime ordered in op form y Assess for deficits by checking I/O chart and vital

signs
y Maintenance requirements calculated y Usually K not started y Monitor carefully vital signs and urine output y CVP useful in difficult situations (5-15 cm H20)

 Mildly hypertonic Balanced with Chloride

ECF Replacement Fluid contains no protein so the oncotic pressure in the blood is slightly lowered following the saline infusion. This has 2 effects:

Movement of fluid into the ISF is favoured (Starling s

Hypothesis) Glomerulo-tubular imbalance occurs: the lowered oncotic pressure immediately leads to an increase in GFR and less reabsorption of water in the proximal tubule

Urine flow increases. ADH is not affected.

y Problems
y Too much chloride may cause hyperchloraemic

metabolic acidosis due to tendency of H+ reabsorption in kidney tubules y Hypertonicity retention

y Good For
y ECF deficit associated with y Hyponatraemia y Hypochloraemia y Metabolic Alkalosis

y How much?
y Provide normal requirement (1-2 mmol/kg/day) y A 50kg person = 50

100 mmol/kg/day y Means 1 to 2 pints of 0.9% saline is enough

y Isotonic, ECF replacement fluid y lactate as a bicarbonate precursor y metabolism of lactate occurs in the liver y does not contribute to development of an acidosis as

they are administered with Na+ rather than H+ as the cation y Also contains Ca++ and K+

y Problems:
y Gluconeogenic properties y Pro-inflammatory response y Calcium precipitates with citrate (anticoagulant present

in blood causes clotting of blood in the infusion tubing) y Potassium load, especially in hyperkalaemia y Metabolic alkalosis

y Good for:
y ECF deficit associated with y Acidosis y Hypokalaemia (except for existing alkalosis)

y Concentration & Calories

y 5% = 5 gm of dextrose in 100ml of water y 5% = 200 kcal/L y Available in 5%, 10%, 20%, 50%

y Following administration glucose is rapidly taken up

by cells so the net effect is of administering pure water y Distributed to all compartments

y Problems
y Cellular edema y Hyperglycaemia y Vessel irritant (20% concentration and higher)

y Good for
y Pure water loss (i.e. increase in insensible loss) y Hypernatraemia with associated cellular dehydration y Hyperkalemia associated with dehydration y Hypoglycaemia

NOT FOR INTRAVASCULAR VOLUME REPLACEMENT

y Less sodium content y Any solution of < 0.45% sodium will require dextrose

in combination prevents cell lysis y Limited use

y Examples: 3% saline, Mannitol, Sodium Bicarbonate y Good in very few situations. Usage must be specific
y 3% saline: life threatening severe hyponatraemia y Mannitol: Cerebral edema, renal protection y Sodium Bicarbonate: severe metabolic acidosis

y Problems
y Intracellular dehydration

manifested by CNS

symptoms y CVS instability

CATIONS Na- 135-145 m Eq/L K- 3.5 5.0 m Eq/L Ca- 2.1-2.65 mEq/L Mg -1.5 2.5 mEq/L

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

y Derminant of serum osmolality y Chloride is the anion that usually accompanies Na y Sodium balance is regulated by the interaction

among neural, hormonal, and vascular mechanisms y Renal glomerulus filters 1000 mEq of sodium/hr and 99% is reabsorbed in the loop of Henle

y Primary regulator of ECF volume y Establishing electrochemical state necessary for muscle

contraction and nerve impulse transmission WHERE SODIUM GOES WATER FOLLOWS

y Serum Sodium < 135 mEq/L

RF:
y y y y y y y y y

Excessive perspiration Altered thirst mech. w/o access to fluids rapid rehydration after excessive fluid loss altered percentage of total body water decreased intake of sodium: fruits, vegetables, oatmeal, rice, wheat, fresh meat, chicken, fish excessive administration of diuretic and laxatives NGT irrigation with plain water Vomiting, diarrhea

y Types:
y Hypovolemic: Na loss > H2O loss y Euvolemic: TBW is mod. increased & total body Na is

normal y Hypervolemic: Greater increased in TBW than in total Na

Volume status

high

Normal

low

increased intake Post op ADH scretion Drugs eg: ACE-I, tricyclic antidepressants (Dilutional hyponatremia)

Hyperglycemia SIADH Water intoxication diuretics

Decreased sodium intake GI loss(urine Na is low <20mEq/l) Renal loss (primary renal loss)(urine Na is high >20mEq/l) a/w dehydration

Shows < 125

Sign and symptoms of hyponatremia Central nervous system Headache, confusion, hyperor hypoactive deep tendon reflexes, seizures, coma, increased intracranial pressure Weakness, fatigue, muscle cramps/twitching Anorexia, nausea, vomiting, watery diarrhea Hypertension and bradycardia if significant increases in intracranial pressure Lacrimation, salivation Oliguria

Musculoskeletal Gastrointestinal Cardiovascular

Tissue Renal

y Na < 135 mEq/L y Cl < 96 mEq/L y Serum Osmolality <275 mOsm/kg y Urine Osmolality <40 mOsm/kg

y If Na> 120, aggressive treatment not required y If Na < 110,and symptomatic, for rapid correction BUT

can correct 10-12 mmol/l per day. y Rapid correction may cause pontine myelinolysis. y Hypervolemic hyponatremia
y Restrict H2O and Na intake y Diuretics

y Hypovolemic hyponatremia
y Rehydration

usually with normal saline y Amount depleted: mild 5%, mod 5-8%, severe 8-12%
y [% x BW(kg) x 1000] ml

y Isovolemic hyponatremia
y No and mild symptoms y Fluid restriction (eg: 800

1000ml) till serum Na rises

y Severe symptoms: y Seizure and coma require rapid increase of patient s ECF tonicity. Eg: 3 mmol in 3 hr y Severe confusion requires mod increased of ECF tonicity. Eg: 3-6 mmol in 12 hr y 3 % saline(hypertonic) + IV frusemide

y Eg : 60 kg male with level Na is 111 and seizure. y Calculation:

y TBW = 60 x 0.6 = 36L y To correct 3 mmol/l in 1st 3 hours y Change in serum Na= [infusate Na

serum Na]/(TBW +
111)/ (36 +1)=

1)
y So 1 L of 3%NaCl will elevate [Na] by (513

10.9mmol/l

y To aim for 3 mmol/l [Na] elevation, 3/10.9 = 0.275L of

3%NaCl needs to be infused over 3 hour which is 92ml/hr for 3 hr y Frusemide given with itration t ensure that urine output is similar to fluid input y If Na is 114 after 3 hrs, pt has no more seizures but GCS is not full, thus, 3%Nacl infusion can be halved which is 46ml/hr for another 6 hr

y Serum Sodium > 146 mEq/L

Types: y Hypovolemic hypernatremia: TBW is greatly decreased compared to Na

y Euvolemic hypernatremia: TBW is decrease relative to

normal total body Na

y Hypervolemic hypernatremia: TBW is increased but Na

gain is > H2O gain

Volume status

High

Normal

Low

Iatrogenic Na administration Mineralcorticoids excess such as Aldosteronism, Cushing s disease, congenital adrenal hyperplasia Urine Na is typically > 20 mEq/L and urine osmolarity is > 300 mOsm/L

Non-renal water loss thru skin and GI loss Renal water loss such as DI, renal disease , diuretics

Non renal water loss thru skin and GI loss Renal water loss such as renal tubular disease,DI, osmotic diuretics urine Na is less than 20 mEq/L and urine osmolarity is less than 300 to 400 mOsm/L

Shows > 155

Signs and symptoms of hypernatremia Central nervous system Restlessness, lethargy, ataxia, irritability, tonic spasms, delirium, seizures, coma, SAH(d/t shift of fluid fr ICF to ECF, thus causes traction to the cerebral vessels) Weakness Tachycardia, hypotension, syncope Dry sticky mucous membranes, red swollen tongue, decreased saliva and tears, thirst Oliguria

Musculoskeletal Cardiovascular Tissue

Renal

 Hypernatremia
Target fall in serum [Na] is 10 mmol/L/day 1.

Water depletion
1. 2. 3. 4. 5.

Should be given water orally if tolerated If not, set up an IV infusion of D5% or 0.45%NaCL Daily fluid requirement: 40ml/kg/day Change in serum Na = (infusate Na serum Na)/ (total body water + 1) Correction of deficit:
1. 2.

Desired TBW =[ TBW(current) x measured Na(mmol/l)]/desired Na Water deficit = Desired TBW(normal) TBW (curent)

y 2. Rate y Rate of 1mmol/L/hr ONLY!!!

y Eg: 60kg female,hypovolomic came in with Na of

165mmol/L
y TBW = 0.5 x 60 = 30L y Identify time period of desirable correction which is 10

mmol/L in 24 hr y 1 L of 0.45% NaCL contains 77mmol/l of Na,will reduce [Na] by (77-165)/(30+1) = 2.8mmol/l

y To aim for 10 mmol/l Na reduction, 10/2.8 = 3.6L of

0.45% Nacl need to be infused over 24 hr at the rate of 150ml/hr for 24 hr. y TBW deficit = [TBW(0.5 x 60) x measured Na (165)/ desired Na(155)] [TBW (0.5x 60)]
y = 1.9L

y Water requirement = 40 x 60= 2.4L y So, total volume required for first day = 1.9 + 2.4 = 4.5L y So, additional 0.9L(4.5

3.6),can be given thru NG

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

Alkalosis
y

can cause hypokalemia can cause hyperkalemia Insulin Glucagon Adrenocortical hormones y cortisol and aldosterone y Stress Catecholamines & beta- adrenergic agonists Alpha-adrenergic agonists Epinephrine has alpha & beta adrenergic properties

Acidosis
y

Substance that can alter K+ levels:

y y y

y y y y

y Serum Potassium < 3.5 mEq/L

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

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

serum K K gradient

resting membrane potential

neuromuscular irritability and excitability

y GI
y Ileus, constipation

y ECG
y U wave

y Neuromuscular
y Decreased reflexes,

fatigue, weakness, paralysis

y CVS
y Cardiac arrest

y Oral therapy
y Oral KCL 1-2 g every 2-4 hrly till K is around 3.5mmol/l y Slow release K(1 tab=8mmol) y Effervescent K( 1tab = 14mmol)

y IV therapy
y Only for symptomatic pt and severe hypok y Around 40 mmol/l(<3g KCl) y Rate of 10 mmol/hr y In emergency, K can be given at rates upto

40mmol/h(eg: KCL 3g/hr) and in[] of 200-400 mmol/l(by mixing 20-40 mmol or 1.5-3 g KCl in 100 ml of saline)

y Serum Potassium > 5.0 mEq/L

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

serum K Altered resting membrane potential

Cell membrane becomes easily excitable

Increased depolarization or action potential

Repeated irritation of cell membrane

Excitation threshold of membrane

Cells become less excitable Weak, flaccid paralysis of muscles

y GI
y Nausea/vomiting, colic,

y ECG
y Peaked T waves (early y y y y y

diarrhea
y Neuromuscular
y Weakness, paralysis,

respiratory failure
y CVS
y Arrhymthia y Cardiac arrest

change) Flattened P wave Prolonged PR interval (first-degree block) Widened QRS complex Sine wave formation Ventricular fibrillation

y COCKTAIL regime y Cation exchange resin

y Kalimate and resonium

A y Orally
y Beta agonist therapy y HD or PD

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

y Serum Calcium < 8.4

y abnormalities in

mg/dl or < 2.1 mmol/l y Etiology

y pancreatitis, y massive soft tissue

infections such as necrotizing fasciitis y renal failure y pancreatic and small bowel fistulas y Hypoparathyroidism

magnesium y tumor lysis syndrome y Hungry bone syndrome y Malignancy

y Prostate Ca- d/t

increased osteoclastic activity

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

y Acute symptomatic
y 10

20 ml of 10% calcium gluconate (90mg of elemental calcium/10 ml) IV over 10 min followed by infusion at 0.5 2mg/kg/hr y Ca mustbe diluted in D5% or saline y Maintain serum Ca between 2-2.25 mmol/l

y Long term Mx:

y Oral calcium supplements y Dosage is 1-2 g elemental calcium daily in divided dose y Calcium lactate 300 mg contains 39 mg of elemental calcium y Calcium carbonate contains 400mg elemental Ca y Vit D y Calcitriol 0.25 mcg od and most maintained on 0.5-2 mcg/day y Alfacalcitriol-0.25-1 mcg od and slower in onset and longer action

y Oral therapy
y Oral KCL 1-2 g every 2-4 hrly till serum K reaches 3.5 y Slow K( 1 tab = 8 mmol)

y IV therapy
y [ ] of less than 40 mmol/l (3 g KCl) y At rate of 10mmol/hr y )

y In emergency, eg in cardiac arrythmias, K can be given

at the rates up to 40mmol/h(KCl 3g/hr) and in [] of 200-400mmol/l (by mixing 20-40 mmol/l or 1.5 3.0 g KCl in 100 cc of saline

y Serum Calcium > 10.5

y Other Causes:
y Excessive intake of Ca

mg/dl or 2.65 mmol/l Etiology and RF: Major Causes y Metastatic malignancy (Tumor Lysis Syndrome) y Hyperparathyroidism y Thiazide diuretic therapy

supplements w/ vit. D, Ca containing antacids y Prolonged immobilization y Metabolic acidosis y Hypophosphatemia

Sign and symptoms of hypercalcemia GI Neuromuscular Renal CVS ECG Anorexia, nausea/vomiting, abdominal pain, constipation Weakness, confusion, coma, bone pain,depression, polyuria and polydipsia as kidneys lose their ability to concentrate hypertension, cardiac arrhythmias Shortened QT interval Prolonged PR and QRS intervals Increased QRS voltage T-wave flattening and widening AV block (can progress to complete heart block, then cardiac arrest with severe hypercalcemia)

y Rehydration and saline diuresis

y Severely hypercalcemia are always dehydrated and ECF

restoration with 0.45 o.9% saline should be the 1st step y Initial infusion rate should be about 300 -500 ml/h and reduced whn ECF volume deficit has been partially corrected.

y Whn ECF volume is restored, infusion of 0.45-0.9% saline 3-4 L

a day for 2-3 day should be given to promoteCa excretion(Na competitively inhibits the renal absortion of Ca)

y Calcitonin
y Inhibits bone resortion and increases renl Ca excretion y 4-8 IU/kg Imor sc every 6-12 hrly up to 3 days

y Biphosphonates
y Treatment of choice in hypercalcemia of malignancy

y Oral phosphate(1-3g/day)
y Reduces Ca absorption as long as phosphate level is <

1.3mmol/l
y Dialysis

y Is a special group of H+ containing substances that

dissociate/separated y When in solution can released free H+ and anions y Strong acid tends to dissociate. Eg: HCl y Weak acid not easy to get dissociate. Eg:H2Co3

y Substance that can combine with a free H+ and thus,

remove it from the solution y Strong base can bindbetter than H+ than weak base.

y pH
y 7.35 - 7.45 y a measurement of acidity or alkalinity, based on the

hydrogen (H+) ions present.

y PaO2
y 80 to 100 mm Hg y The partial pressure of oxygen that is dissolved in

arterial blood y New Born Acceptable range 40-70 mm Hg

y Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg

level for every year over 60 years of age: 80 - (age- 60)

y HCO3
y 22 to 26 mEq/liter y The amount of carbon dioxide dissolved in arterial

blood.

y Base excess

2 to +2 mEq/liter y indicates the amount of excess or insufficient level of bicarbonate in the system. y A negative base excess indicates a base deficit in the blood. A negative base excess is equivalent to an acid excess. y The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35 if the pCO2 were adjusted to normal.
y

y A base excess > +3 = metabolic alkalosis y base excess < -3 = metabolic acidosis

y Changes in [H+] influence in K+ level

y In acidosis, there will decreased K+ secretion, thus,

leading to hyperK+ y In alkalosis, there will be increased in K+ secretion, thus, leading to hypoK+

y Chemical buffer system y Respiratory mechanism y Renal mechanism

y 1st line defense y Is a mixture in a solution of 2 chemical compunds that

minimize pH changes y Consists a pair of substance involved in a reversible reaction

y Eg: H2CO3

H+ (+) HCO3

y Body has 4 buffer system

y Carbonic acid:bicarbonate buffer system y Protein buffer system y Hemoglobin buffer system y Phosphate buffer system

y 2nd line defense y Regulate [H+] by controlling the rate of CO2 removal y Ability to alter pulmonary ventilation y Arterial [H+] increased d/t metabolic causes y Respiratory centre stimulate to increased pul

ventilation
y Thus , decreased CO2

y Can only return pH only 50% to 75%

y During respiratory compensation, y Peripheral chemoreceptor increases ventilation d/t increased [H+] y Central chemoreceptor increases ventilation d/t increased CO2

y In metabolic acidosis,
y PC detect increased [H+] y Stimulate respiratory centre to step up ventilation y Decreased CO2 y In response to decreased CO2, CC inhibits respiratory

centre

y 3rd line defense y Compensation does not begin for at least 6 hours and

continues for several days

y H+ excretion y HCO3 excretion y Increased urinary excretion of NH4+ (H++ NH3+ = NH4+).

y During alkalosis,
y Decreased secretion and decreased excretion of H+ in

urine y Incomplete reabsorption of filtered HCO3

y During acidosis, increased secretion and subsequent

increased excretion of H+ in the urine

y Reabsorption of all filtered bicarbonate

y d/t abnormal CO2 retention(hypoventilation)

Causes Narcotics Pulmonary Secretions Atelectasis Mucus plug Pneumonia Pleural effusion Pain from abdominal or thoracic injuries or incisions Limited diaphragmatic Ascites excursion from intra-abdominal pathology Abdominal compartment syndrome

y Compensation :
y Chemical buffers

take up additional H+ y Resp mech cant respond y Kidneys MOST IMPORTANT

y Conserved all filtered HCO3 and add new HCO3 to the

plasma and excreting H+

y Treatment :
y Treat underlying cause y may entail patient-initiated volume expansion or

noninvasive (bilevel positive airway pressure; BIPAP) or invasive (endotracheal intubation) ventilation strategies.

y increased intake of acids, an increased generation of

acids, or an increased loss of bicarbonate

y Increased Anion Gap

y Normal Anion Gap

y Gastrointestinal losses

Metabolic Acidosis
y Exogenous acid

ingestion
Salicylate y Methanol
y

y Endogenous acid

production
y Ketoacidosis y Lactic acidosis

(diarrhea, fistulas) y Renal tubular acidosis y Potassium sparing diuretics y Resolving DKA

y Renal insufficiency

y Compensation :
y Chemical buffer: take up H+ y Resp : Increasing ventilation (Kussmaul respirations) y Kidneys: y Increasing renal reabsorption and generation of bicarbonate y increase secretion of hydrogen and thus increase urinary excretion of NH4+ (H++ NH3+ = NH4+)

y administration of bicarbonate is controversial.

1.

The overzealous administration of bicarbonate can lead to metabolic alkalosis, which shifts the oxyhemoglobin dissociation curve to the left, interfering with oxygen unloading at the tissue level, and can be associated with arrhythmias that are difficult to treat.

2.

exacerbate intracellular acidosis

y

bicarbonate can combine with the excess H+ to form carbonic acid, which is then converted to CO2 and water, thus raising the PCO2. CO2 can diffuse into cells, but bicarbonate remains extracellular worsening intracellular acidosis

y increase in bicarbonate generation and impaired renal

excretion of bicarbonate

Causes Increased Bicarbonate Generation 1. Chloride losing (urinary chloride greater than 20 mEq/L) Mineralocorticoid excess Profound potassium depletion 2. Chloride sparing (urinary chloride less than 20 mEq/L) Loss from gastric secretions (emesis or nasogastric suction) Diuretics 3. Excess administration of alkali Acetate in parenteral nutrition Citrate in blood transfusions Antacids Bicarbonate Impaired Bicarbonate Excretion 1. Decreased GFR

y Compensation :
y Chemical buffer: liberates H+ y Resp : increased ventilation y Kidneys:conserve H+ and excrete excess HCO3 in urine y Hydrogen ion reabsorption also ensues with an accompanied potassium ion excretion y resulting hypokalemia

y Treatment
y replacement of the volume deficit with isotonic saline

and potassium once adequate urine output is ensured

y Decreased CO2 y As a result of

y meningitis

hyperventilation y Causes
y Fever y Pain y Drugs such as salicylates y thyrotoxicosis

y Acute hypocapnia can cause an uptake of potassium

and phosphate into cells and increased binding of calcium to albumin, leading to symptomatic hypokalemia, hypophosphatemia, and hypocalcemia, with subsequent arrhythmias, paresthesias, muscle cramps, and seizures. y Treatment treat underlying cause