The document discusses acid-base balance and disorders. It notes that blood pH is tightly regulated between 7.35-7.45, and death can occur below 6.8 or above 8.0. The lungs and kidneys work together to maintain homeostasis. The lungs regulate pH by altering respiration rate and depth to eliminate or retain carbon dioxide. The kidneys regulate by selectively excreting or retaining bicarbonate and hydrogen ions. Respiratory and metabolic acidosis and alkalosis can occur due to abnormalities in lung function or kidney function respectively, changing PaCO2 or HCO3 levels. Causes, signs, and treatments of various acid-base imbalances are described.

2. Acid Base Balance
 Homeostasis of pH is tightly controlled
 Blood PH = 7.35 – 7.45
 < 6.8 or > 8.0 death occurs
 Acidosis (acidemia) below 7.35
 Alkalosis (alkalemia) above 7.45
 Balance maintained by buffers (HCO3 – H2CO3)

3. RESPIRATORY CONTROL OF pH

4. Renal control of PH
Acidosis
 Retains bicarbonate ions and eliminates
hydrogen ions
Alkalosis
 Eliminates bicarbonate ions and retains
hydrogen ions

5. Acid-Base Imbalances
 Respiratory acidosis
 Respiratory alkalosis
 Metabolic acidosis
 Metabolic alkalosis

6. Acid Base Disorder
Respiratory-
 primary abnormality in respiratory function
 Change in PaCO2
Metabolic-
 kidney
 Change in HCO3-
Mixed

8. Lungs
 Regulate acid-base balance by eliminating or retaining
carbon dioxide
 Does this by altering rate/depth of respirations
 Faster rate/more depth = get rid of more CO2 and pH
rises
 Slower rate/less depth = retain CO2 and pH lowers

9. HYPOVENTILATION Hypo = “Under”
9
Elimination of CO2
H+
pH

10. RESPIRATORY ACIDOSIS
 Characterized by a pH decrease and an increase
in CO2
 Carbonic acid excess caused by blood levels of CO2 above 45 mm
Hg
10
CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2 CO2
CO2
pH
pH

11. Hypoventilation causes

12. Cont…

13. RESPIRATORY ALKALOSIS
 pCO2 less than 35 mm Hg
(hypocapnea)
Most common acid-base imbalance
Primary cause is hyperventilation
13
CO2 CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2

14. HYPERVENTILATION Hyper = “Over”
14
Elimination of CO2
H+
pH

15. ETHIOLOGY
 Can be the result of:
1) Anxiety, emotional
disturbances
2) Respiratory center
lesions
3) Fever
4) Salicylate poisoning
(overdose)
5) Assisted respiration 15

17. Kidneys
 Regulate by selectively excreting or
conserving bicarbonate and hydrogen ions
 Slower to respond to change

18. Metabolic Acidosis
 Defined as a low arterial pH (<7.35) and a low serum
HCO3- (< 22 meq/L)
 Three major mechanisms
1) Increased acid generation
 Lactic acidosis
 Ketoacidosis (DM, excess alcohol intake, or fasting)
 Ingestions (Methanol or ethylene glycol, Aspirin,
Toluene)

19. Metabolic acidosis…
2) Loss of bicarbonate
Diarrhea or ureteral diversion
Proximal (type 2) renal tubular acidosis
3)Diminished renal acid excretion
Renal failure
Distal (type 1) renal tubular acidosis

21. Metabolic alkolosis
 Defined as an elevations in the serum bicarbonate
concentration and arterial pH.
 HCO3
- concentration in blood is >26mEq/L
 Caused by
 An increase of HCO3
-
 A decrease in H+
 Often accompanied by hypochloremia and
hypokalemia
 Most commonly due to the loss of hydrogen ions from
the gastrointestinal tract or in the urine

22. Metabolic alkalosis: etiologic classification
1. Hypovolemic metabolic alkalosis
 Excess vomiting = loss of stomach acid
 Certain diuretics
→Hydrogen loss in the urine or gastrointestinal tract
2. Normovolemic or hypervolemic metabolic alkalosis
 Excessive use of alkaline drugs(sodium or potassium
bicarbonate )
 Corticosteroid excess

24. ….IN SUMMARY
24

27. Fluid and Electrolyte Abnormalities
 Water constitutes 50-60 % of Total body wt.
 This TBW (total body water) divided into EC fluid
(1/3) and IC fluid(2/3).
 EC fluid comprises principal cation Na
 & anions Cl and HCO3.
 IC fluid is composed primarily of cations K+ and Mg
& anions of Phosphate and proteins.

28. Normal Exchange of fluid and
Electrolytes
Daily water losses for adult:
urine 1L
stool 250 ml
insensible losses (via skin and lungs) 600
ml

29. Hypovolemia
Etiology; loss of GI fluids( NG tube suctioning,
vomiting, diarrhoea)
Third space losses( burn , peritonitis,
prolonged large field surgery)
 S/Sx:
 Mental Status changes, sleepy, apathy, coma
 orthostatic, tachy, decreased pulse pressure
 Poor turgor, hypothermia, dry membranes
 Oliguria, ileus, weakness

30. Hypovolemia, continued
 Treatment:
 Acute: 2L LR via large bore IV then blood
 Subacute:
 Isotonic or hypotonic deficits give isotonic NS or hypotonic
1/2NS or LR (e.g. vomiting = NS, diarrhea = LR)
 Hypertonic deficits (e.g. dehydration with jejunal feedings)
give D5W. Seen in fever, ventilator, or diaphoresis

31. Hypervolemia
 Etiology: Cardiac failure, Renal failure, mobilization of
fluid, iatrogenic, psychologic or Ecstasy
 S/Sx:
 Wt gain over baseline.
 JVP raised, rales or wheezing, pedal/sacral edema
 elevated CentralVenousPressure
 Pulmonary edema on CXR

32. Hypervolemia, continued
 Lab:
 Decreased Hct and albumin
 Na may be low, normal or increased but total body Na is
usually increased
 Treatment:
 Water restrict to 1500 cc/day
 +/- Diuretics
 Sodium restrict to 0.5 gm/day
 (Albumin followed by diuretics)

33. Hyponatremia
 Serum Na < 135 mEq/l.
 Mostly due to abnormal water handling,
 causing defective urinary dilution

34. Hyponatremia, continued
 S/Sx:
 Neurologic: muscle twitching, hyperreflexia, seizures
and HTN
 Salivation, lacrimation, diarrhea
 Often asymptomatic if slow until below 120 mEq/L. (130
mEq/L if acute)
 Treatment: correct underlying disorder
 Fluid restrict, + diuretics
 Hypertonic saline to increase level 2-3 mEq/L/hr and
max rate 100cc of 5% saline/hr

35. • Hyponatremia is a water problem, not a Na+
problem
– water intake > water excretion
• Hyponatremia is defined as plasma serum less
than 135meq/l
• Hyponatremia can occur as a complication of
multiple diseases
• Detection and management results in better
outcome
• Avoid rapid rise of plasma sodium during
treatment

36. Hypernatremia
 >145 mEq/L
 Caused by a relative deficit of free water
 Primary defense- thirst

37. Normal-Volume
 loss of “electrolyte free” fluids (loss of pure
water)
High-Volume
 ingestion or administration of sodium
containing hypertonic solutions
Low-Volume
• loss of hypotonic fluids (fluids containing
more water than sodium)

38. Hypernatremia
 Free water deficit or water loss greater than salt loss.
Always associated with hyper osmolar state.
 Forms:
 Normovoluemic is subclinical hypovolemia seen in
diabetes insipidus , diuretics or renal disease.
 Hypervolemic usually iatrogenic intake of excess Na,
also mineralo corticoid excess as inhyper aldosteronism,
Cushing’s, CAH.
 Hypovolemic: loss of hypotonic fluids with inadequate
replacement with hypertonic fluids

39. Hypernatremia, continued
 S/Sx:
 Neurologic: restless, seizure, coma, delirium and
mania
 Sticky mucus membranes, poor
salivation/lacrimation, hyperpyrexia, Red swollen
tongue
 THIRST, weakness
 Treatment: correct underlying disorder

40. Hypernatraemia
Na + H2O losses
H2O losses Na 
Low total body sodium Normal total body sodium High total body sodium
Renal losses
(diuretics)
Extra Renal
losses
(Diarrhoea)
Renal losses
(DI)
Extra Renal
losses
(insensible)
Hyperaldosteronism
Cushings
Urinary Sodium
>20 mmol/l >20 mmol/l<10 mmol/l Variable
Treatment
Isotonic Saline Water replacement Diuretics and
Water replacement

41. Hypokalemia
 Etiology:
 Intracellular uptake with redistribution seen in acute
alkalosis, insulin therapy, and anabolism
 Depletion due to GI losses, renal/diuretics, steroids, and
renal tubular acidosis
 S/Sx:
 Clinical: muscle weakness/fatigue, decreased DTR’s,
ileus. Insulin resistance in DM
 EKG: low, flat T-waves, ST depression, and U waves

42. Hypokalemia, continued
 Treatment:
 Check renal function
 Treat alkalosis, decrease sodium intake
 PO with 20-40 mEq doses
 IV: peripheral 7.5 mEq/hr, central 20 mEq/hr and
increase K+ in maintenance fluids.

43. Hyperkalemia
 Etiology:
 Psuedohyperkalemia in leukocytosis, hemolysis and
thrombocytosis
 Redistribution in acidosis, hypoinsulinism, tissue
necrosis, digoxin poisoning
 Renal insufficiency, mineralocorticoid deficiency, DM,
spironolactone use

44. Hyperkalemia, continued
 S/Sx:
 Clinical: nausea/vomiting, colic, weakness diarrhea
 EKG: early – peaked T waves then flat P waves,
depressed ST segment, widened QRS progressing to sine
wave and V fib.
 Cardiac arrest occurs in diastole

47. Hyperkalemia, continued
 Treatment:
 Remove iatrogenic causes
 Acute: if > 7.5 mEq/L or EKG changes
 Ca-gluconate – 1 gm over 2 min IV
 Sodium bicarbonate – 1 amp, may repeat in 15min
 D50W (1 ampule = 50 gm) and 10U regular insulin
 Emergent dialysis
 Hydration and diuresis, kayexalate 20-50 g, in 100-200cc
of 20% sorbitol q 4hrs or enema

48. Hypercalcemia
 • Calcium
 > 5.5 mg/dL
 • Risk Factors
hyperparathyroidism, prolonged immobility,
megadoses of vitamin D, bone malignancy, paget’s
disease, thiazide diuretics, overuse of Ca+ containing
antacids and supplements

49.  Defining Characteristics
ECG changes, lethargy, weakness, depressed deep
tendon reflexes, constipation, anorexia, N&V, polyuria,
polydipsia, decreased memory and attention span,
confusion, renal stones, flank pain, neuroses, psychosis
reversible, cardiac arrest

50. Hypocalcemia
Ca <4.5 mEq/L
• Risk Factors:
 – hypoparathyroidism, malabsorption, vitamin D
 deficiency, acute pancreatitis, thyroid CA,
 hypomagnesemia, alkalosis, sepsis, alcohol abuse

51.  Defining Characteristics
 – numbness, tingling, hyperactive deep tendon
reflexes,
 muscle tremors, cramps, progressing to tetany and
 convulsions, cardiac arrhythmias, mental changes,
 Chvostek’s sign, Trousseau’s sign

53. THANKS!