Fluid, Electrolyte

& Acid-base
Group B
 Members

Chuleemat Kaewdang 6132101014

Nattacha Chindamai 6132101016
Thanaporn Nisapruksachart 6132101017
Benya Seangvirojanakul 6132101019
Ponpawee Piromboon 6132101020
Pasawat Lertkittiphan 6132101022

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 01
Fluid
Enter a subtitle here if you need it

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Functional body fluid
compartment

60% 50%
TBW TBW 4
Chemical composition of
body fluid compartments

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 Water exchange
(60- to 80-kg man)

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Signs and symptoms of volume disturbances
System Volume deficit Volume excess

● Weight loss ● Weight gain

Generalized
● Decreased skin turgor ● Peripheral edema

● Increased cardiac
● Tachycardia
output
● Orthostasis/hypotensi
● Increased central
Cardiac on
venous pressure
● Collapsed neck veins
● Distended neck veins
● Murmur

Oliguria
Renal -
Azotemia

GI Ileus Bowel edema

Pulmonary — Pulmonary edema 7

 Holliday & Segar’s Traditional Guidelines

For the first 0-10 kg Give 100 mL/kg per day

For the next 10-20 kg Give an additional 50 mL/kg per day

For weight >20 kg Give an additional 20 mL/kg per day

A 60-kg female would receive a total of 2300 mL of fluid daily: 1000 mL for
the first 10 kg of body weight (10 kg x 100 mL/kg per day), 500 ml for the next
20 kg (10kg x 50 mL/kg per day), and 800 mL for the last 40 kg (40 kg x 20
mL/kg per day)

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Composition of GI secretion

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 Isotonic solution
GI losses and correcting extracellular volume deficits

● Lactated Ringer’s solution

○ slightly hypotonic
○ Lactate converted into bicarbonate by liver
○ more stable in IV fluids than bicarbonate during storage

● Plasma-Lyte
○ resembles the electrolyte composition of human plasma.
○ contains small quantities of potassium; risk for renal impairment.

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 Isotonic solution
● 0.9 % sodium chloride ( mildly hypertonic )
■ correcting volume deficits associated with hyponatremia, hypochloremia,
and metabolic alkalosis (gastric outlet obstruction)
■ The high chloride concentration => a hyperchloremic metabolic acidosis.

Hypotonic solution
● 0.45% sodium chloride
○ replacement of ongoing GI losses and fluid therapy in the postoperative period.
○ With 5% dextrose (50 g of dextrose per liter) in Sodium chloride ( [ ] < 0.45%)
■ maintain osmolality
■ prevent the lysis of RBC ( rapid infusion of hypotonic fluids )
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Electrolyte solutions for parenteral administration

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Alternative resuscitative fluids

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 Hypertonic solution

● Hypertonic saline solutions (3.5% and 5%)

○ correction of severe hyponatremia

● Hypertonic saline solutions (7.5%)

○ patients with closed head injuries
■ increase cerebral perfusion and decrease intracranial pressure =>
decreasing brain edema
■ increased bleeding !! (arteriolar vasodilator)

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 Colloids

● Colloids effectiveness as volume expanders > isotonic crystalloids

○ Due to their large molecular weight in intravascular space (more efficient
transient plasma volume expansion)

● Four major types of colloids

○ albumin, dextrans, Hydroxyethyl starch and gelatin

● severe hemorrhagic shock !!

○ capillary membrane permeability increases => permits colloids to enter the
interstitial space => worsen tissue edema and impair tissue oxygenation

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 02
Electrolytes

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 Hyponatremia
Definition : Serum Na < 135 mmol/L

❖ Excess of extracellular water relative to sodium

❖ Extracellular volume can be high, normal or low
❖ Alteration of TBW is the main contributor to hyponatremia

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 Hyponatremia

High serum osmolality Low serum osmolality Normal serum osmolality

Hypertonic True hyponatremia Isotonic hyponatremia
hyponatremia
- Hyperproteinemia
- Hyperglycemia - Hyperlipidemia
- Mannitol
- Alcohol

Hypervolemia Euvolemia Hypovolemia

- Increased intake - SIADH Urine Na < 20 Urine Na > 20

- Postoperative - Secondary AI Non-renal loss Renal loss
ADH secretion - Hypothyroidism -Vomiting -Diuretic
- Drugs -Diarrhea -Primary renal
-Third space disease
loss 18
 SIADH (Syndrome of inappropriate ADH)

Etiologies : ADH secretion independent of

❖ Head injury or surgery to the CNS - Osmotic stimuli
❖ Drugs (morphine, nonsteroidals, - Volume stimuli
oxytocin)
❖ Hypothyroidism, glucocorticoid Fluid restriction
deficiency Isotonic or hypertonic fluid
❖ Malignancies (small cell lung cancer, Diuretic : Furosemide
pancreatic carcinoma, thymoma, Drugs: Vasopressin receptor
Hodgkin’s disease) antagonist

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 Clinical manifestation
Headache, confusion, hyperactive or hypoactive deep tendon
CNS reflexes, seizures, coma, increased intracranial pressure

MSK Weakness, fatigue, muscle cramps/ twitching

GI Anorexia, nausea, vomiting, watery diarrhea

CVS Hypertension and bradycardia

Tissue Lacrimation, salivation

Renal Oliguria
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 Correction of Hyponatremia
★ Neurologic symptoms : 3% NaCl 2 ml/kg (< 1 mEq/L/hr) until serum Na
reaches 130 mEq/L or neurologic symptoms improve
★ Hypovolemic hyponatremia : correct dehydration
If shock : 0.9% NaCl 20 ml/kg
★ Asymptomatic hyponatremia : increase Na level < 0.5 mEq/L/hr to a
maximum increase of 12 mEq/L/day
★ Chronic hyponatremia : increase PNa rate < 1-1.5 mmol/L/hr or < 12
mmol/L in 24 hr or < 18 mmol/L in 48 hr

Rapid correction >> Osmotic demyelination syndrome :

seizure, weakness, paresis, akinetic movements,
unresponsiveness, permanent brain damage and death
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 Hypernatremia
Definition : Serum Na > 145 mmol/L

❖ Loss of free water or gain of sodium in excess of water

❖ Extracellular volume can be high, normal or low

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 Hypernatremia POsm > 295 mOsm/kg

Hypervolemic Normovolemic Hypovolemic

hypernatremia hypernatremia hypernatremia

- Iatrogenic sodium - Nonrenal water loss - Nonrenal water loss

administration from Skin & GI tract from Skin & GI tract
- Mineralocorticoid - Renal water loss - Renal water loss
excess - Renal disease - Renal (tubular)
- Hyperaldosteronism - Diuretics disease
- Cushing’s disease - Diabetes insipidus - Osmotic diuretics
- Congenital adrenal - Diabetes insipidus
hyperplasia - Adrenal failure

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 Correction of Hypernatremia

Estimate the amount of water required to correct hypernatremia :

Water deficit (L) = serum Na - 140 x TBW
140
★ Hypovolemic hypernatremia : administer 0.9% saline solution first,
water deficit is replaced by hypotonic fluid (5% dextrose)
★ Euvolemic hypernatremia : free water replacement
★ Hypervolemic hypernatremia : loop diuretics and free water
replacement, hemodialysis if nothing works

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Correction of Hypernatremia

★ Goal : decreased serum Na by < 12 mEq/L every 24 hr,

a rate of 0.5 mEq/L/hr
★ Chronic hypernatremia : slower correction (0.7 mEq/L)
Overly rapid correction >> cerebral edema and
herniation

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 Hypokalemia
Definition : Serum K < 3.5 mmol/L

Redistribution Inadequate intake Potassium loss

Sweat : extensive exercise,

Systemic alkalosis Dietary heat stroke
● NPO
● Dysphagia GI : diarrhea, vomiting
Insulin intake ● Anorexia nervosa high nasogastric output

Catecholamine excess Renal: renal tubular acidosis

nephritis,
hyperaldosteronism
Periodic paralysis medication(diuretic)
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Hypokalemia
● Potassium decreases by 0.3 mEq/L
for every 0.1 increase in pH above normal
● EKG
○ Prominent U wave
○ T wave flattening
○ ST segment changes

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 Clinical manifestation
GI
Ileus, constipation

Neuromuscular

Decreased reflexes, fatigue, weakness, paralysis

CVS

Arrest

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 Correction of Hypokalemia
● Serum potassium level < 4.0 mEq/L
○ Asymptomatic tolerating enteral nutrition
■ KCl 40 mEq per enteral access * 1 dose
○ Asymptomatic, not tolerating enteral nutrition
■ KCl 20 mEq IV q2h * 2 doses
○ Symptomatic
■ KCl 20 mEq IV q1h * 4 doses
○ Recheck K+ level 2 h after end of infusion
■ If<3.5 mEq/L and asymptomatic replace protocol
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 Hyperkalemia
Definition : Serum K > 5 mmol/L

Factitious Increased intake Increased release Impaired excretion

Collection and Exogenous source Acidosis Renal failure

storage of specimen -Oral/IV K+
-Time,technique -Blood transfusion
Renal tubular disease
-tourniquets
-fist clenching
Endogenous source Hypoaldosteronism
-Intravascularhemolysis
Pseudohyperkalemia -Massive GI bleeding
-RBC hemolysis -Tumor lysis syndrome Addison’s disease
-WBC > 100,000 -Rhabdomyolysis
-Platelet > Diuretics
500,000-1,000,000
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Hyperkalemia
● EKG
○ Peaked T wave(early)
○ Widened QRS complex
○ Flattened P wave
○ Prolonged PR interval
○ Ventricular fibrillation

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 Clinical manifestation
GI
Nausea/vomiting, intestinal colic, diarrhea

CNS

Weakness, paralysis, respiratory failure

CVS

Arrhythmia, arrest

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 Correction of Hyperkalemia

★ Repeat Lap
★ Abnormal EKG
○ Goal stabilized heart
○ 10% calcium gluconate 5-10 ml
★ Shift K+
○ Regular Insulin 5-10 Unit and glucose 1 ampule of D50 IV
○ NaHCO3 1 ampule IV
★ K+ removal
○ Kayexalate
■ Oral administration 15-30 gm in 50-100 ml of 20% sorbitol
■ Rectal administration 50 gm in 200 ml of 20% sorbitol
○ Hemodialysis
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 02
Acid & Base
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 Acid-base balance
Acid-base balance is regulated by 3 systems Chemical buffer
system:
system
Intracellular -> protein ,
phosphate

Extracellular ->
bicarbonate-carbonic acid

Renal
Renal system
system
Respiratory system ( Delayed compensation )

(immediate) : : increase or decrease

HCO3- reabsorption
chemoreceptors activities
(acute or chronic )
H+ -> ventilation

HCO3- -> ventilation

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 Acid-base balance

Normal blood pH 7.35-7.45

Normal PCO2 35-45 mmHg

Normal HCO3- 22-26 mEq/L

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 Metabolic acidosis
pH HCO3- PCO2

Anion Gap = (Na) - ( Cl + HCO3) : normal : = 12 ±2

corrected AG = actual AG - [2.5 x (4.5- Albumin)]

Predicted changes PCO2= (1.5 x HCO3-) +8 37

 Metabolic Acidosis

Etiology
2. Normal anion gap
● Acid administration (HCL)
1. Increased Anion gap of metabolic acidosis ● Loss of bicarbonate
● Exogenous acid ingestion ● GL losses ( ex. diarrhea, enteric
○ Ethylene glycol fistula )
○ Methanol ● Carbonic anhydrase inhibitor
○ Salicylate
● Endogenous acid production
○ Ketoacidosis (ex. DM, alcohol,
starvation )
○ Lactic acidosis (ex. Shock ,metformin)
○ Renal insufficiency

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Clinical manifestation
● Headache
● Decreased blood pressure
● Hyperkalemia
● Muscle twitching
● Warm,flushed skin
(vasodilation)
● Nausea and vomiting
● Confusion , drowsiness
● Kussmaul respirations

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 Metabolic Acidosis
Metabolic acidosis

Compensation : Kussmaul’s respiration ,increase renal HCO3- reabsorption and

regeneration , increase Renal H+ , NH4+ excretion

A common cause of severe metabolic acidosis in surgical patient is lactic acidosis

which is caused by circulatory shock ( inadequate tissue perfusion )

Treatment is to restore perfusion with volume resuscitation With adequate perfusion,

the lactic acid is rapidly metabolized by liver and pH will return to normal

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 Metabolic Acidosis
Alkaline therapy (Sodium bicarbonate therapy )
● The method to treat metabolic acidosis is corrected the etiology.
● Indication
metabolic acidosis pH<7.10 (ex. Cardiac arrest ,severe renal disease , uncontrolled
diabetes , shock or severe hydration )
● Contraindication
Patient who are losing chloride (ex. vomiting or continuous gastrointestinal suction )
● Dosage and administration
7.5% NaHCO3 50 ml (1 vial) = Na 44.6mEq
HCO3 deficit (mEq) = 0.5 x lean body wt (kg) x (8- measured [HCO3-])
● Risk:
Acute pulmonary edema , hypertonicity, Cerebral hemorrhage, edema,
tetany ,hypernatremia,hyperosmolarity,hypocalcemia,hypokalemia

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 Metabolic Alkalosis
➔ Loss of fixed acids or gain of HCO3 - and is worsened by K+ depletion

Hypokalemia: extracellular K+ exchange with intracellular H+ and allow the H+

to buffer excess HCO3 -

Chloride responsive (urine Cl- <10-20 meq/l)

Hypochloremic and hypokalemic metabolic alkalosis can occur from isolated
loss of gastric contents in pyloric obstruction

Chloride resistant (urine Cl- >20 meq/l)

Mineralocorticoid excess

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 Metabolic Alkalosis

Initially, the urinary bicarbonate level is high in compensation for the alkalosis.
In response to the associated volume deficit,
➔ aldosterone-mediated Na reabsorption → increases K+ and H+ excretion
➔ Paradoxical aciduria

Treatment includes replacement of the volume deficit with isotonic saline and
then potassium replacement once adequate urine output is achieved.

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 Respiratory Acidosis
Etiology of respiratory acidosis 4. Pain from abdominal or thoracic
injuries or incision limited
: hypoventilation diaphragmatic excursion from intra
1. Narcotics abdominal
2. Central nervous system injury ● Abdominal dissension
3. Pulmonary :significant ● Abdominal compartment
● Secretions syndrome
● Atelectasis ● Ascites
● Mucus plug
● Pneumonia
● Pleural effusion pH HCO3- PCO2

Predicted change

PCO2 10 mmHg -> HCO3- 1 mEq/L

PCO2 10 mmHg -> HCO3- 4 mEq/L
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Respiratory Acidosis
● Hypoventilation -> Hypoxia
● Rapid,shallow respirations
● BP drop
● Skin/mucosa pale to
cyanosis
● Headache
● Hyperkalemia
● Dysrhythmias
● Drowsiness,
dizziness,disorientation
● Muscle weakness,
hyperreflexia

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 Respiratory acidosis

● Treatment of acute respiratory acidosis is directed at the underlying cause

● Supportive treatment (BIPAP /Ventilator )

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 Respiratory Alkalosis

Most cases of surgical patient are acute and secondary to alveolar

hyperventilation
Acute hypocapnia
➔ uptake K+ into the cells
➔ increased binding of Ca2+ to albumin
➔ Symptomatic hypokalemia, hypocalcemia

Treatment should be directed at underlying cause

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Hypokalemia

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Hypocalcemia

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References

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 Thanks!
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When hyponatremia in presence of hyperglycemia

Corrected serum sodium (mmol/L)

[Na+] by 1.6 mEq/L for every 100 mg/dL in P glucose

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 Acid-base balance
Acid-base balance is regulated by 3 systems

Chemical buffer system : Respiratory system Renal system (acute

(immediate) : or chronic ) : H+
Intracellular -> protein , secretion and HCO3-
phosphate chemoreceptors reabsorption
activities
Extracellular ->
bicarbonate-carbonic acid Acidosis stimulates
increase ventilation

Alkalosis decreases
activity to decrease
ventilation
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Metabolic Alkalosis

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 Hypocalcemia

Acute symptomatic hypocalcemia should be treated with

IV 10% calcium gluconate to achieve a serum concentration of 7 to 9 mg/dL.

Associated deficits in magnesium, potassium, and pH must also be corrected.

Hypocalcemia will be refractory to treatment if coexisting hypomagnesemia is not

corrected first.

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