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ACID BASE
DISTURBANCES
DR WAQAR ( MBBS, MRCP)
ASSISTANT PROFESSOR OF MEDICINE
MAAREFA MEDICAL COLLEGE
BASIC DEFINITIONS
ACID : A compound which releases H+ ( HCL)
BASE ( alkali) : A compound which can accept H+
( Na HCO3)
pH : A measure of H+ activity. This number tells us
how “acidic” or “alkaline”( or neutral) is the
solution.
ACIDS ARE PRODUCED DAILY IN THE HUMAN
BODY ( LACTIC, ACETOACETIC, HYDROXYBUTYRIC )
CO2 ALSO PRODUCES ACID ( CO2 + H2O =
H2CO3 ( CARBONIC ACID)
ALKALI IS ALSO PRESENT IN THE BODY
(HCO3)
BUT
 BLOOD IS NEITHER ACIDIC NOR ALKALOTIC
NORMAL pH OF BLOOD : 7.35 TO 7.45
IN THE BLOOD, ACID & ALKALI ARE BALANCED
SO pH IS STABLE
 A NORMAL BLOOD pH IS IMPORTANT FOR
NORMAL CELL FUNCTIONS
Extra acid or alkali in the blood is immediately
“bufferred” ( neutralized) by certain substances in
the blood and then excreted. These substances
are called BUFFERS. ( eg HCO3, organic acids)
eg : H + HCO3 H2CO3 H20 + CO2
BUFFERS : Substances which immediately absorb
excess acid or alkali , so that the pH does not
change
 IF EXCESS ACID REMAINS IN THE BLOOD
ACIDOSIS
 IF EXCESS ALKALI REMAINS ALKALOSIS
pH CHANGES
• ACIDOSIS CAUSES LOW pH ( lower than 7.35)
• ALKALOSIS CAUSES HIGH pH ( higher than 7.45)
WHAT IS ACIDOSIS ?
 ACIDOSIS : * EXCESS ACID or LESS ALKALI
* pH IS LOW ( less than 7.35)
( normal pH is 7.35 to 7.45)
acid alkali acid alkali acid alkali
------------------------------------------------------------------------------------------------------

NORMAL
( ---------- A C I D O S I S ---------------)
WHAT IS ALKALOSIS ?
 EXCESS ALKALI ( BASE) OR LESS ACID
 pH IS HIGH ( MORE THAN 7.45) (normal pH is 7.35 to 7.45)
ACID ALKALI ACID ALKALI ACID ALKALI
------------------------------------------------------------------------------------
NORMAL (------------------ ALKALOSIS---------)
IMPORTANT EQUATION
 H+ HCO3 H2CO3 CO2 + H2O
HCO3 Handled by the kidney
CO2 Handled by the lungs
COMPENSATION
 WHENEVER THE pH CHANGES IN A DISEASE, THE
BODY TRIES TO BRING IT BACK TOWARDS NORMAL.
THIS IS CALLED COMPENSATION.
 COMPENSATION IS NOT 100% COMPLETE, SO pH DOES
NOT RETURN TO COMPLETE NORMAL, IF THE DISEASE
CONTINUES.
3 THINGS WHICH TRY TO COMPENSATE
1) BUFFERS IN THE BLOOD : ACT WITHIN
seconds ( HCO3, Organic acids)
2) LUNGS : WITHIN SECONDS TO MINUTES
( BY KEEPING OR REMOVING CO2)
3) KIDNEYS : WITHIN HRS TO DAYS ( BY
handling HCO3 and H+)
SO
 PH 7.40 ------------------ ( ? )
 PH 7.20 ------------------ ( ? )
 PH 7.50 ------------------ ( ? )
 ( NORMAL IS 7.35 TO 7.45 )
IN DISEASE STATES, ACID – BASE BALANCE
GETS DISTURBED, SO ACIDOSIS OR
ALKALOSIS ( OR MIXED DISTURBANCES )
CAN OCCUR.
Things we need, to understand
acid- base balance
 ABG ( arterial blood gases)
 SERUM ELECTROLYTES ( NA, K, CL, HCO3)
 ABG report is written as follows:
 ABG : pH/ pCO2/ pO2/ HCO3
eg 7.40/ 45 mmHg / 78 mmHg / 25meq
For our discussion, forget about O2
SOME NORMAL VALUES
1) Blood pH:
* 7.35 to 7.45
2) Blood pCO2 :
* Also 7.35 mmHg to 7.45mmHg
3) Blood HCO3:
* 22 to 28 meq/L ( slightly different in various
labs)
ACIDOSIS
 RESPIRATORY ACIDOSIS METABOLIC ACIDOSIS
 (DUE TO HIGH CO2 ) (DUE TO:
a) Excess acid production
b) Decreased acid excre-
- tion from the kidneys
c) Loss of HCO3
RESPIRATORY ACIDOSIS
* IT IS DUE TO HYPOVENTILATION
* DUE TO HYPOVENT., CO2 CANNOT BE EXCRETED , SO
PCO2 RISES ( think of CO2 as an acid)
 ETIOLOGIES :
* RESP. CENTER DEPRESSION ( MORPHINE)
* NEUROMUSCULAR PATHOLOGIES ( KYPHOSIS, RESP
MUSCLE PARALYSIS )
* LUNG DISEASE ( COPD)
RESPIRATORY ACIDOSIS
 PH IS LOW ----- < 7.35
 PROBLEM IS IN RESP. SYS. OR LUNGS CO2
RETAINED
 HIGH CO2 ACIDOSIS( CO2 + H2O = H2CO3)
 Eg PH / PCO2 / HCO3
 7.30/ 50mmHg/ 30 ( Norm pCO2 35 to 45, HCO3 22 to
28)
COMPENSATION ( in
resp.acidosis)
 KIDNEYS RETAIN MORE HCO3
 SO, THERE IS COMPENSATORY RISE IN HCO3
 END RESULT :
* pH : low
* PCO2 : high
* HCO3 : high ( DUE TO COMPENSATION)
S/S OF RESP. ACIDOSIS
 S/S USUALLY OCCUR IF IT IS ACUTE
 HEADACHE, RESSTLESSNESS, DYSPNEA
 PROGRESSES TO HYPER-REFLEXIA, COMA
RESP. ACIDOSIS MAY BE SEEN IN LATE STAGES OF
ASTHMA EXACERBATION, WHEN THE PATIENT GETS
TIRED
IT IS SEEN IN COPD PATIENTS EVEN AT BASELINE
STATUS (CHRONIC ACIDOSIS)
TREATMENT OF RESP.
ACIDOSIS
1) TREAT THE CAUSE
2) DON’T GIVE HCO3.
IT WILL COMBINE WITH H+ IN THE BODY AND PRODUCE
MORE CO2 WHICH CAN NOT BE ELIMINATED. SO,
CONDITION WILL BE WORSE
HCO3 + H = H2CO3 H2O + CO2
3) MAY NEED MECHANICAL VENTILATION ( ventilation
takes out CO2 from the lungs)
RESPIRATORY
ALKALOSIS
 pH IS HIGH
 PROBLEM IS WITH RESPIRATORY RATE
 HYPERVENTILATION EXCESS CO2 IS ELIMINATED
 LOW CO2 ALKALOSIS
 Eg : PH / PCO2/ HCO3
 7.50 / 28 / 18
COMPENSATION
 KIDNEYS LOSE MORE HCO3
 SO, THERE IS COMPENSATORY FALL IN SERUM HCO3
 END RESULT :
* pH : high
* pCO2 : low
* HCO3 : low ( due to compensation)
CAUSES OF RESPIRATORY
ALKALOSIS
 ANXIETY
 RESPIRATORY CENTER STIMULATION all these
 HYPOXIA ( LIVING AT HIGH ALTITUDES ) cause
 PATIENTS ON VENTILATORS MAY DEVELOP hyper-
 ASPIRIN POISONING -ventilation
ABHA IS A HIGH ALTITUDE CITY. LIVING THERE CAN
CAUSE:
a) Resp. Alkalosis
RESP. ALKALOSIS S/S
 ACUTE RESPIR. ALKALOSIS CAUSES LOW Ca, & K
 S/S INCLUDE :
* LIGHTHEADEDNESS
* CONFUSION
* SIEZURES
* HYPERVENTILATION
* TETANY ( DUE TO LOW Ca)
TREAT MENT OF
RESPIRATORY ALKALOSIS
 TREAT THE MAIN CAUSE
 CHANGE THE VENTILATOR SETTINGS
 CAN TRY “REBREATHING EXHALED” AIR IN A PAPER
BAG
SO REMEMBER THAT:
* IN RESP. ACIDOSIS, CO2 WILL BE HIGH
* IN RESP. ALKALOSIS, CO2 WILL BE LOW
METABOLIC ACIDOSIS
 PH IS LOW --------- < 7.35
 MAIN PROBLEM NOT IN RESPIRATION
 PROBLEM : TOO MUCH METABOLIC ACID IS PRODUCED
IN THE BODY, OR IT CANNOT BE EXCRETED
OR
 TOO MUCH ALKALI ( HCO3) IS LOST FROM THE BODY
 LOW HCO3
 Eg: PH/ PCO2/HCO3 7.20 / 30 / 18 ( normal is 22 to
26)
COMPENSATION
 LUNGS EXCRETE MORE CO2
 SO, THERE IS COMPENSATORY FALL IN PCO2
 END RESULT :
* PH : low
* HCO3 : low ( main problem)
* PCO2 : low ( due to compensation)
TYPES OF METABOLIC
ACIDOSIS
 HIGH ANION GAP NORMAL ANION GAP
WHAT IS ANION GAP ?
 CATIONS : Na+, K+ / ANIONS : HCO3-, Cl-
 Normally, the sum of cations should be equal to sum of
anions.
 But Na + K is > HCO3 +Cl
 This difference is called Anion Gap.
 It is actually the unmeasured anions in the blood ( albumin,
phosphates etc)
 NORMAL A.G = 8 TO 16 meq ( Na +K) – (Cl + HCO3)
 IN SOME CONDITIONS, IT GETS HIGH ( SOME TYPES OF
METABOLIC ACIDOSIS) & IN OTHERS, IT IS NORMAL
TYPES OF METABOLIC
ACIDOSIS
HIGH “ ANION GAP” NORMAL “ ANION GAP”
ETIOLOGIES ETIOLOGIES
M methanol * Diarrhea loss of
U uremia * Ileostomy HCO3
D diab.ketoacidosis
P paraldehyde * Renal tubular acidosis (RTA)
I infection/sepsis ( type 1, 2 &4)
L lactic acidosis
E ethanol * Acetazolamide ( a diuretic)
S salicylate poisoning(aspirin)
S/S ( METABOLIC ACIDOSIS)
 HEADACHE, MENTAL STATUS CHANGES,
RESTLESSNESS
 COMA MAY OCCUR
TREATMENT OF
METABOLIC ACIDOSIS
TREAT THE CAUSE
* Drug toxicity (aspirin, methanol)
* ketoacidosis : treat accordingly
* infection/sepsis
* Diarrhea
* Lactic acidosis : iv fluids, treat the cause
* Uremia : NaHCO3 tab / Dialysis ( remember renal failure ?)
I.V. HCO3 CAN BE GIVEN IN METABOLIC ACIDOSIS
IF NEEDED
RENAL TUBULAR ACIDOSIS
 A GROUP OF RENAL DISORDERS ( PROBLEM IN
TUBULES)
 FOUR TYPES.
 OVERALL RARE. TYPE 4 IS THE MOST COMMON
 METABOLIC ACIDOSIS WITH NORMAL A.G.
 TYPE 4 RTA SEEN IN DM
METABOLIC ALKALOSIS
 IT IS ALKALOSIS SO, PH IS HIGH ( > 7.45 )
 NO PRIMARY PROBLEM IN RESP.
 ACCUMULATION OF EXCESS ALKALI IN THE BODY OR
LOSS OF ACID
 Eg : PH / PCO2 /HCO3
7.50 / 48 / 35
COMPENSATION
 LUNGS EXCRETE LESS PCO2 SO,
COMPENSATORY RISE IN PC02
 END RESULT :
* pH : high
* HCO3 : high ( main problem)
* pCO2 : high ( due to compensation)
CAUSES OF METABOLIC
ALKALOSIS
 VOMITING, N/G TUBE SUCTION ( loss of acid)
 EXCESS INTAKE OF NaHCO3
 DIURETICS ( thiazides, loop diuretics)
 ALL DIURETICS CAUSE METABOLIC ALKALOSIS
EXCEPT ACETAZOLAMIDE ( DIAMOX) WHICH CAUSES
ACIDOSIS)
S/S
 CEREBRAL DYSFUNCTION
* Restlessness
* confusion, lethargy
* arrhythmias
TREATMENT
 IF VOMITING OR NG SUCTION GIVE i.v. N/S
 If DIURETICS ARE THE CAUSE, GIVE i.v. N/S
 IF HIGH INTAKE OF HCO3, Stop IT.
 If pH > 7.7, give isotonic HCL thru central vein
SO, REMEMBER THAT:
• IN METABOLIC ACIDOSIS, HCO3 IS LOW
• IN METABOLIC ALKALOSIS, HCO3 IS HIGH
THANK YOU
 HOPE YOU FOUND IT EASY

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13040498.ppt

  • 1.
  • 2. ACID BASE DISTURBANCES DR WAQAR ( MBBS, MRCP) ASSISTANT PROFESSOR OF MEDICINE MAAREFA MEDICAL COLLEGE
  • 3. BASIC DEFINITIONS ACID : A compound which releases H+ ( HCL) BASE ( alkali) : A compound which can accept H+ ( Na HCO3) pH : A measure of H+ activity. This number tells us how “acidic” or “alkaline”( or neutral) is the solution.
  • 4. ACIDS ARE PRODUCED DAILY IN THE HUMAN BODY ( LACTIC, ACETOACETIC, HYDROXYBUTYRIC ) CO2 ALSO PRODUCES ACID ( CO2 + H2O = H2CO3 ( CARBONIC ACID) ALKALI IS ALSO PRESENT IN THE BODY (HCO3) BUT  BLOOD IS NEITHER ACIDIC NOR ALKALOTIC
  • 5. NORMAL pH OF BLOOD : 7.35 TO 7.45 IN THE BLOOD, ACID & ALKALI ARE BALANCED SO pH IS STABLE  A NORMAL BLOOD pH IS IMPORTANT FOR NORMAL CELL FUNCTIONS
  • 6. Extra acid or alkali in the blood is immediately “bufferred” ( neutralized) by certain substances in the blood and then excreted. These substances are called BUFFERS. ( eg HCO3, organic acids) eg : H + HCO3 H2CO3 H20 + CO2 BUFFERS : Substances which immediately absorb excess acid or alkali , so that the pH does not change
  • 7.  IF EXCESS ACID REMAINS IN THE BLOOD ACIDOSIS  IF EXCESS ALKALI REMAINS ALKALOSIS pH CHANGES • ACIDOSIS CAUSES LOW pH ( lower than 7.35) • ALKALOSIS CAUSES HIGH pH ( higher than 7.45)
  • 8. WHAT IS ACIDOSIS ?  ACIDOSIS : * EXCESS ACID or LESS ALKALI * pH IS LOW ( less than 7.35) ( normal pH is 7.35 to 7.45) acid alkali acid alkali acid alkali ------------------------------------------------------------------------------------------------------  NORMAL ( ---------- A C I D O S I S ---------------)
  • 9. WHAT IS ALKALOSIS ?  EXCESS ALKALI ( BASE) OR LESS ACID  pH IS HIGH ( MORE THAN 7.45) (normal pH is 7.35 to 7.45) ACID ALKALI ACID ALKALI ACID ALKALI ------------------------------------------------------------------------------------ NORMAL (------------------ ALKALOSIS---------)
  • 10. IMPORTANT EQUATION  H+ HCO3 H2CO3 CO2 + H2O HCO3 Handled by the kidney CO2 Handled by the lungs
  • 11. COMPENSATION  WHENEVER THE pH CHANGES IN A DISEASE, THE BODY TRIES TO BRING IT BACK TOWARDS NORMAL. THIS IS CALLED COMPENSATION.  COMPENSATION IS NOT 100% COMPLETE, SO pH DOES NOT RETURN TO COMPLETE NORMAL, IF THE DISEASE CONTINUES.
  • 12. 3 THINGS WHICH TRY TO COMPENSATE 1) BUFFERS IN THE BLOOD : ACT WITHIN seconds ( HCO3, Organic acids) 2) LUNGS : WITHIN SECONDS TO MINUTES ( BY KEEPING OR REMOVING CO2) 3) KIDNEYS : WITHIN HRS TO DAYS ( BY handling HCO3 and H+)
  • 13. SO  PH 7.40 ------------------ ( ? )  PH 7.20 ------------------ ( ? )  PH 7.50 ------------------ ( ? )  ( NORMAL IS 7.35 TO 7.45 )
  • 14. IN DISEASE STATES, ACID – BASE BALANCE GETS DISTURBED, SO ACIDOSIS OR ALKALOSIS ( OR MIXED DISTURBANCES ) CAN OCCUR.
  • 15. Things we need, to understand acid- base balance  ABG ( arterial blood gases)  SERUM ELECTROLYTES ( NA, K, CL, HCO3)  ABG report is written as follows:  ABG : pH/ pCO2/ pO2/ HCO3 eg 7.40/ 45 mmHg / 78 mmHg / 25meq For our discussion, forget about O2
  • 16. SOME NORMAL VALUES 1) Blood pH: * 7.35 to 7.45 2) Blood pCO2 : * Also 7.35 mmHg to 7.45mmHg 3) Blood HCO3: * 22 to 28 meq/L ( slightly different in various labs)
  • 17. ACIDOSIS  RESPIRATORY ACIDOSIS METABOLIC ACIDOSIS  (DUE TO HIGH CO2 ) (DUE TO: a) Excess acid production b) Decreased acid excre- - tion from the kidneys c) Loss of HCO3
  • 18. RESPIRATORY ACIDOSIS * IT IS DUE TO HYPOVENTILATION * DUE TO HYPOVENT., CO2 CANNOT BE EXCRETED , SO PCO2 RISES ( think of CO2 as an acid)  ETIOLOGIES : * RESP. CENTER DEPRESSION ( MORPHINE) * NEUROMUSCULAR PATHOLOGIES ( KYPHOSIS, RESP MUSCLE PARALYSIS ) * LUNG DISEASE ( COPD)
  • 19. RESPIRATORY ACIDOSIS  PH IS LOW ----- < 7.35  PROBLEM IS IN RESP. SYS. OR LUNGS CO2 RETAINED  HIGH CO2 ACIDOSIS( CO2 + H2O = H2CO3)  Eg PH / PCO2 / HCO3  7.30/ 50mmHg/ 30 ( Norm pCO2 35 to 45, HCO3 22 to 28)
  • 20. COMPENSATION ( in resp.acidosis)  KIDNEYS RETAIN MORE HCO3  SO, THERE IS COMPENSATORY RISE IN HCO3  END RESULT : * pH : low * PCO2 : high * HCO3 : high ( DUE TO COMPENSATION)
  • 21. S/S OF RESP. ACIDOSIS  S/S USUALLY OCCUR IF IT IS ACUTE  HEADACHE, RESSTLESSNESS, DYSPNEA  PROGRESSES TO HYPER-REFLEXIA, COMA RESP. ACIDOSIS MAY BE SEEN IN LATE STAGES OF ASTHMA EXACERBATION, WHEN THE PATIENT GETS TIRED IT IS SEEN IN COPD PATIENTS EVEN AT BASELINE STATUS (CHRONIC ACIDOSIS)
  • 22. TREATMENT OF RESP. ACIDOSIS 1) TREAT THE CAUSE 2) DON’T GIVE HCO3. IT WILL COMBINE WITH H+ IN THE BODY AND PRODUCE MORE CO2 WHICH CAN NOT BE ELIMINATED. SO, CONDITION WILL BE WORSE HCO3 + H = H2CO3 H2O + CO2 3) MAY NEED MECHANICAL VENTILATION ( ventilation takes out CO2 from the lungs)
  • 23. RESPIRATORY ALKALOSIS  pH IS HIGH  PROBLEM IS WITH RESPIRATORY RATE  HYPERVENTILATION EXCESS CO2 IS ELIMINATED  LOW CO2 ALKALOSIS  Eg : PH / PCO2/ HCO3  7.50 / 28 / 18
  • 24. COMPENSATION  KIDNEYS LOSE MORE HCO3  SO, THERE IS COMPENSATORY FALL IN SERUM HCO3  END RESULT : * pH : high * pCO2 : low * HCO3 : low ( due to compensation)
  • 25. CAUSES OF RESPIRATORY ALKALOSIS  ANXIETY  RESPIRATORY CENTER STIMULATION all these  HYPOXIA ( LIVING AT HIGH ALTITUDES ) cause  PATIENTS ON VENTILATORS MAY DEVELOP hyper-  ASPIRIN POISONING -ventilation ABHA IS A HIGH ALTITUDE CITY. LIVING THERE CAN CAUSE: a) Resp. Alkalosis
  • 26. RESP. ALKALOSIS S/S  ACUTE RESPIR. ALKALOSIS CAUSES LOW Ca, & K  S/S INCLUDE : * LIGHTHEADEDNESS * CONFUSION * SIEZURES * HYPERVENTILATION * TETANY ( DUE TO LOW Ca)
  • 27. TREAT MENT OF RESPIRATORY ALKALOSIS  TREAT THE MAIN CAUSE  CHANGE THE VENTILATOR SETTINGS  CAN TRY “REBREATHING EXHALED” AIR IN A PAPER BAG
  • 28.
  • 29. SO REMEMBER THAT: * IN RESP. ACIDOSIS, CO2 WILL BE HIGH * IN RESP. ALKALOSIS, CO2 WILL BE LOW
  • 30. METABOLIC ACIDOSIS  PH IS LOW --------- < 7.35  MAIN PROBLEM NOT IN RESPIRATION  PROBLEM : TOO MUCH METABOLIC ACID IS PRODUCED IN THE BODY, OR IT CANNOT BE EXCRETED OR  TOO MUCH ALKALI ( HCO3) IS LOST FROM THE BODY  LOW HCO3  Eg: PH/ PCO2/HCO3 7.20 / 30 / 18 ( normal is 22 to 26)
  • 31. COMPENSATION  LUNGS EXCRETE MORE CO2  SO, THERE IS COMPENSATORY FALL IN PCO2  END RESULT : * PH : low * HCO3 : low ( main problem) * PCO2 : low ( due to compensation)
  • 32. TYPES OF METABOLIC ACIDOSIS  HIGH ANION GAP NORMAL ANION GAP
  • 33. WHAT IS ANION GAP ?  CATIONS : Na+, K+ / ANIONS : HCO3-, Cl-  Normally, the sum of cations should be equal to sum of anions.  But Na + K is > HCO3 +Cl  This difference is called Anion Gap.  It is actually the unmeasured anions in the blood ( albumin, phosphates etc)  NORMAL A.G = 8 TO 16 meq ( Na +K) – (Cl + HCO3)  IN SOME CONDITIONS, IT GETS HIGH ( SOME TYPES OF METABOLIC ACIDOSIS) & IN OTHERS, IT IS NORMAL
  • 34. TYPES OF METABOLIC ACIDOSIS HIGH “ ANION GAP” NORMAL “ ANION GAP” ETIOLOGIES ETIOLOGIES M methanol * Diarrhea loss of U uremia * Ileostomy HCO3 D diab.ketoacidosis P paraldehyde * Renal tubular acidosis (RTA) I infection/sepsis ( type 1, 2 &4) L lactic acidosis E ethanol * Acetazolamide ( a diuretic) S salicylate poisoning(aspirin)
  • 35. S/S ( METABOLIC ACIDOSIS)  HEADACHE, MENTAL STATUS CHANGES, RESTLESSNESS  COMA MAY OCCUR
  • 36. TREATMENT OF METABOLIC ACIDOSIS TREAT THE CAUSE * Drug toxicity (aspirin, methanol) * ketoacidosis : treat accordingly * infection/sepsis * Diarrhea * Lactic acidosis : iv fluids, treat the cause * Uremia : NaHCO3 tab / Dialysis ( remember renal failure ?) I.V. HCO3 CAN BE GIVEN IN METABOLIC ACIDOSIS IF NEEDED
  • 37. RENAL TUBULAR ACIDOSIS  A GROUP OF RENAL DISORDERS ( PROBLEM IN TUBULES)  FOUR TYPES.  OVERALL RARE. TYPE 4 IS THE MOST COMMON  METABOLIC ACIDOSIS WITH NORMAL A.G.  TYPE 4 RTA SEEN IN DM
  • 38. METABOLIC ALKALOSIS  IT IS ALKALOSIS SO, PH IS HIGH ( > 7.45 )  NO PRIMARY PROBLEM IN RESP.  ACCUMULATION OF EXCESS ALKALI IN THE BODY OR LOSS OF ACID  Eg : PH / PCO2 /HCO3 7.50 / 48 / 35
  • 39. COMPENSATION  LUNGS EXCRETE LESS PCO2 SO, COMPENSATORY RISE IN PC02  END RESULT : * pH : high * HCO3 : high ( main problem) * pCO2 : high ( due to compensation)
  • 40. CAUSES OF METABOLIC ALKALOSIS  VOMITING, N/G TUBE SUCTION ( loss of acid)  EXCESS INTAKE OF NaHCO3  DIURETICS ( thiazides, loop diuretics)  ALL DIURETICS CAUSE METABOLIC ALKALOSIS EXCEPT ACETAZOLAMIDE ( DIAMOX) WHICH CAUSES ACIDOSIS)
  • 41. S/S  CEREBRAL DYSFUNCTION * Restlessness * confusion, lethargy * arrhythmias
  • 42. TREATMENT  IF VOMITING OR NG SUCTION GIVE i.v. N/S  If DIURETICS ARE THE CAUSE, GIVE i.v. N/S  IF HIGH INTAKE OF HCO3, Stop IT.  If pH > 7.7, give isotonic HCL thru central vein
  • 43. SO, REMEMBER THAT: • IN METABOLIC ACIDOSIS, HCO3 IS LOW • IN METABOLIC ALKALOSIS, HCO3 IS HIGH
  • 44. THANK YOU  HOPE YOU FOUND IT EASY