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METABOLIC ACIDOSIS
METABOLIC ACIDOSIS
• A METABOLIC PROBLEM DUE TO THE BUILDUP OF ACID IN THE BODY FLUIDS WHICH
AFFECTS THE BICARBONATE (HCO3 LEVELS) EITHER FROM:
• INCREASED ACID PRODUCTION
• DKA WHERE KETONES (ACIDS) INCREASE IN THE BODY .AS IN DIABETIC
KETOACIDOSIS(DKA) BLOOD GLUCOSE LEVELS ARE CRAZY HIGH ,
PRODUCING A LOT OF KETONES WHICH ARE ACIDS . THUS BUILDING UP
ACIDS IN BODY AS COMPARED TO BICARBONATES SO BICARBONATES
DECREASE AND PH DECREASE.
• DECREASED ACID EXCRETION
• RENAL FAILURE WHERE THERE IS HIGH AMOUNT OF WASTE LEFT IN THE
BODY WHICH CAUSES THE ACIDS TO INCREASE AND BICARB CAN’T
CONTROL IMBALANCE
• LOSS OF TOO MUCH BICARB
• WHEN THIS ACIDIC PHENOMENA IS TAKING PLACE IN THE BODY OTHER SYSTEMS WILL
TRY TO COMPENSATE TO INCREASE THE BICARB BACK TO NORMAL. ONE SYSTEM
THAT TRIES TO COMPENSATE IS THE RESPIRATORY SYSTEM.
• IN ORDER TO COMPENSATE, THE RESPIRATORY SYSTEM WILL CAUSE THE BODY
TO HYPERVENTILATE BY INCREASING BREATHING THROUGH KUSSMAUL’S
RESPIRATIONS. KUSSMAUL RESPIRATIONS ARE DEEP, RAPID BREATHES(INCREASED
RESPIRATORY RATE). THE BODY HOPES THIS WILL HELP EXPEL CO2 (AN ACID) WHICH
WILL “HOPEFULLY” INCREASE THE PH BACK TO NORMAL.
LAB VALUES EXPECTED IN METABOLIC ACIDOSIS:
• HCO3: DECREASED <22
• BLOOD PH: DECREASED <7.35
• CO2: <35 OR NORMAL (MAY BE NORMAL BUT IF IT IS DECREASED THIS IS THE BODY’S
WAY OF TRYING TO COMPENSATE).
• THE RESPIRATORY SYSTEM IS CAUSING HYPERVENTILATION. THE RESPIRATORY
SYSTEM TRIES TO INCREASE THE PH FROM ITS ACIDOTIC STATES THROUGH
TACHYPNEA WITH KUSSMAUL’S BREATHING. THE GOAL IS TO “BLOW OFF” THE CO2
WHICH IS ACIDIC
• MEMORIZE THESE NORMAL VALUES FOR ABGS:
• PH 7.35-7.45
• PACO2 35-45
• HCO3 22-26
CAUSES OF METABOLIC ACIDOSIS
• HIGH ANION GAP & NORMAL ANION GAP PROBLEMS : HIGH + NORMAL ANION GAP:
• MUST KNOW WHETHER IT IS HIGH OR NORMAL ,SO THE CAUSE CAN BE TREATED
CORRECTLY(AS CAN BE LIFE THREATENING)
• WHAT IS ANION GAP?
• SIMPLY THESE ARE VARIOUS LABS VALUES SEEN IN PATIENT BLOOD SAMPLE E.G CHLORIDE
, BICARBONATE , SODIUM AND CALCULATE TO SEE THE DIFFERENCE BETWEEN ANIONS
AND CATIONS , LOOKING FOR A GAP.
• NORMAL ANION GAP IS 10 – 14 MEQ/L
• IF THERE IS A GAP OF 14MEQ/L IT IS A HIGH ANION GAP
• HIGH ANION ACIDOSIS IS CONDITIONS THAT CAUSE THE BODY TO PRODUCE TOO
MUCH ACID OR NOT ENOUGH BICARB (DKA, ASPIRIN TOXICITY, RENAL FAILURE,
HIGH-FAT DIET, LOW CARB DIET, MALNUTRITION)
• NORMAL ANION ACIDOSIS IS LOSS OF THE BICARBONATE FROM THE BODY. EXAMPLES:
DIARRHEA VIA GI FLUIDS, OSTOMIES OR FISTULA DRAINAGE (ILEOSTOMIES OR
PANCREATIC FISTULA)…WHICH ARE RICH IN ALKALOTIC FLUIDS, HOWEVER WHEN
LOST IT CAUSES ACIDOSIS, OR DRUGS INGESTION: DIAMOX (DIURETIC)…. CARBONIC
ANHYDRASE INHIBITOR WHICH REDUCES REABSORPTION OF BICARB.
REMEMBER MNEMONIC “ACIDOTIC”
• A: ASPIRIN TOXICITY: (HIGH ANION GAP)
• WHICH INCREASES THE ACID IN THE BODY AND THIS ALSO CAUSES RESPIRATORY
ALKALOSIS (HYPERVENTILATION)
• C: CARBOHYDRATES NOT METABOLIZED (HIGH ANION GAP):
• WHEN THERE ISN’T ENOUGH OXYGEN TO BREAK DOWN CARBS THE PYRUVIC ACIDS (THAT
SUPPLIES THE CELLS WITH ENERGY) STARTS TO TURN INTO LACTIC ACID AND WHEN YOU
GET ACID BUILDING UP YOU GET ACIDOSIS
• I: INSUFFICIENCY OF KIDNEYS (HIGH ANION GAP):
• KIDNEYS ARE FAILING TO FILTER OUT METABOLIC WASTE PRODUCTS, ACIDS INCREASE,
AND BICARB CANNOT KEEP UP SO IT DEPLETES
• D: DIARRHEA (NORMAL ANION GAP):
• PROFUSE DIARRHEA LEADS TO LOSS BICARBONATE
• O: OSTOMY DRAINAGE (EXCESSIVE) ILEOSTOMIES, URETER ENTEROSTOMIES (NORMAL
ANION GAP)
• OSTOMIES ARE AN OPENING OF AN ORGAN TO ALLOW DRAINAGE
• DEPENDING ON WHERE THE OSTOMY IS THESE FLUIDS ARE RICH IN BICARB AND IF LOSS
DIRECTLY AT THIS SPOT (INSTEAD OF TRAVELLING THROUGH THE BODY TO FORM INTO
STOOL (WHICH DOESN’T LOSE MUCH BICARB)
• IT CAN DEPLETE THE BICARB FAST.
• T: FISTULA (PANCREATIC FISTULA) (NORMAL ANION GAP) FISTULA:
• A FISTULA IS A PASSAGE BETWEEN AN HOLLOW ORGAN AND BODY SURFACE OR BETWEEN
TWO ORGANS….SAME CONCEPT WITH THE OSTOMY…LOSING FLUIDS WHERE YOU
SHOULDN’T BE AND THEY ARE NOT BEING ABSORBED BY THE BODY…WASTING THE BICARB
• I: INTAKE OF HIGH-FAT DIET:
• EATING TOO MUCH FAT LEADS TO THE BUILDING-UP OF WASTE PRODUCT WHICH IN TURN
LEADS TO BUILDUP OF KETONES AND ACIDS
• C: CARBONIC ANHYDRASE INHIBITORS (DIAMOX):
• DIURETIC WHICH REDUCES THE REABSORPTION OF BICARB
SIGNS & SYMPTOMS OF METABOLIC ACIDOSIS
• KUSSMAUL’S RESPIRATION: BODY’S WAY OF TRYING TO
COMPENSATE BY EXHALING THE EXCESSIVE CO2 (IN HOPES
OF INCREASING BICARB AND BLOOD PH), DEEP/RAPID
BREATHING (20 TO 40 BPM)
• CONFUSED, WEAK, LOW BLOOD PRESSURE, CARDIAC
CHANGES IF HYPERKALEMIC ( EXCEPT WITH DIARRHEA OR
WITH DIAMOX USAGE WHICH CAUSES HYPOKALEMIA),
NAUSEA AND VOMITING.
NURSING INTERVENTIONS FOR
METABOLIC ACIDOSIS
VARY DEPENDING ON THE CAUSES OF ACIDOSIS:
• WATCH RESPIRATORY SYSTEM AND ABGS CLOSELY(RESPIRATORY DISTRESS)
• IF PATIENT DROPS RESPIRATORY LEVELS OF CARBON DIOXIDE LESS THAN 35, THEY MAY
NEED INTUBATION(MECHANICALVENTILATION)
• ASSESS OTHER ELECTROLYTE LEVELS:
• ESPECIALLY ‘POTASSIUM’ BECAUSE DURING ACTIVE ACIDOSIS, IT WILL BE HIGH
• HOWEVER WHEN IT RESOLVES THERE IS AN EXTRACELLULAR TO INTRACELLULAR SHIFT OF
POTASSIUM BACK INTO THE CELL WHICH WILL CAUSES HYPOKALEMIA AS THERE WONT BE
ANY POTASSIUM LEFT IN THE BLOOD
• DIALYSIS MAY BE NEEDED IF THEY PATIENT IS EXPERIENCING ACIDOSIS
• RENAL FAILURE - HIGH ANION GAP ISSUE
• DIABETIC KETOACIDOSIS
• PRESCRIBED INSULIN TO HELP GLUCOSE GO BACK INTO CELL WHICH WILL HELP THE BODY
START REGULATING AS IT METABOLIZES GLUCOSE - HENCE NOT MORE KETONES (ACIDS)
• ABGS: HCO3=11, PH 7.20, PACO2=33
• METABOLIC ACIDOSIS PARTIALLY COMPENSATED
METABOLIC ALKALOSIS
KEY CONCEPTS -PATHOPHYSIOLOGY
• A METABOLIC PROBLEM CAUSED BY THE EXCESSIVE LOSS OF ACIDS (HYDROGEN
IONS) OR INCREASED AMOUNT OF BICARB (HCO3) PRODUCED IN THE BODY THAT
LEADS TO AN ALKALOTIC STATE IN THE BODY. DISEASE PROCESSES AND DRUGS CAN
CAUSE METABOLIC ALKALOSIS.
• WHEN METABOLIC ALKALOSIS HAPPENS IN THE BODY OTHER SYSTEMS TRY TO
COMPENSATE BY HOPEFULLY FIXING THE BLOOD’S PH AND BICARB LEVEL.
• ONE SYSTEM THAT DOES THIS IS THE RESPIRATORY SYSTEM BY STIMULATING THE
RESPIRATORY SYSTEM TO HYPOVENTILATE (DECREASE RESPIRATIONS…<12/MIN)
WHICH WILL RETAIN PCO2 (CARBON DIOXIDE) SO IT WILL DECREASE THE PH BACK TO
NORMAL, HENCE YOU WILL START TO SEE BRADYPNEA IN THE PATIENT.
• IF A PATIENT IS EXPERIENCING METABOLIC ALKALOSIS THEY WILL PRESENT WITH THE
FOLLOWING LABS:
• HCO3: INCREASES >26
• BLOOD PH: INCREASES >7.45
• CO2: >45 OR NORMAL (MAY BE NORMAL BUT IF INCREASED THIS IS THE BODY’S WAY OF
TRYING TO COMPENSATE. THE RESPIRATORY SYSTEM TRIES TO DECREASE THE PH FROM
ITS ALKALOTIC STATE BY CAUSING HYPOVENTILATION ( BRADYPNEA). THE RESPIRATORY
SYSTEM HOPES THAT IF THE CO2 INCREASE ENOUGH IT WILL CAUSE THE PH TO DECREASE
AND THE KIDNEYS WILL START TO EXCRETE THE BICARB WHICH WILL HOPEFULLY DECREASE
THE OVERALL HCO3.
NORMAL VALUES
• REMEMBER WHAT NORMAL VALUES ARE:
• PH = 7.35 TO 7.45
• PACO2 = 35 TO45
• HCO3 = 22 TO 26
CAUSES OF METABOLIC ALKALOSIS
• ALKALI
• A: ALDOSTERONE PRODUCTION EXCESSIVE (HYPERALDOSTERONISM) ACTIVATES RENIN-
ANGIOTENSIN-ALDOSTERONE SYSTEM:
• THE ADRENAL CORTEX IS RELEASING TOO MUCH ALDOSTERONE WHICH CAUSES THE RENAL
TUBULE IN THE KIDNEYS TO KEEP SODIUM WHICH LOSE HYDROGEN IONS AND ALSO POTASSIUM
AND THIS IN TURN CAUSES AN INCREASE IN BICARB (HCO3)
• L: LOOP DIURETICS (LASIX) OR THIAZIDE THERAPY:
• CAUSES THE KIDNEYS TO WASTE HYDROGEN IONS AND CHLORIDE THROUGH THE URINE (ALSO
LOSING K+) WHICH IN TURN INCREASES THE BICARB
• K: ALKALI INGESTION OF FOOD (BAKING SODA, MILK, ANTACIDS) INCREASES BICARB
LEVEL IN THE BLOOD
• A: ANTICOAGULANT “CITRATE” (USED AS A STORAGE AGENT IN BLOOD AND
DURING CONTINUOUS FORMS OF RENAL REPLACEMENT THERAPY)
• CAUSED FROM A MASSIVE TRANSFUSION OF WHOLE BLOOD (PATIENT NEEDS SEVERAL
BAGS OF BLOOD) AND THE BODY METABOLIZES THE CITRATE USED IN THE BLOOD AS
BICARB WHICH INCREASES THE HCO3 LEVEL IN THE BODY. ALSO, PATIENTS WHO
UNDERGO CONTINUOUS FORMS OF RENAL REPLACEMENT THERAPY (CRRT) (AN
ALTERNATIVE THERAPY FOR PATIENTS WHO CAN’T UNDERGO HEMODIALYSIS) ARE
AFFECTED BY THE CITRATE USED IN THE THERAPY.
• L: LOSS OF FLUIDS (VOMITING AND GI SUCTIONING)
• THESE FLUIDS ARE RICH IN K+ AND WHEN YOU LOSE THEM YOU ARE LOSING
HYDROGEN IONS AND THIS CAUSES THE BODY TO INCREASE THE BICARB LEVEL
• LOW POTASSIUM LEVELS CAUSE REABSORPTION OF HCO3.
• I: INCREASED SODIUM BICARB ADMINISTRATION (TRYING TO CORRECT
METABOLIC ACIDOSIS)
SIGNS AND SYMPTOMS OF METABOLIC
ALKALOSIS
• BRADYPNEA (HYPOVENTILATION) <12 BPM
• MANY SYMPTOMS DUE TO LOW POTASSIUM (DYSRHYTHMIA), TETANY, TREMORS, MUSCLE
WEAKNESS/CRAMPING, TIRED, IRRITABLE, VOMITING, DEPRESSION ST, FLAT OR INVERTED T
WAVE AND PROMINENT U-WAVE)
NURSING INTERVENTIONS FOR METABOLIC
ALKALOSIS
• BASED ON THE CAUSE:
• VOMITING (GIVE ANTIEMETIC)
• STOP NG SUCTIONING
• STOP DIURETICS
• DIAMOX (CARBONIC ANHYDRASE INHIBITORS): A DIURETIC WHICH REDUCES THE
REABSORPTION OF BICARB
• WATCH ABGS AND SIGNS OF RESPIRATORY DISTRESS
• MONITOR POTASSIUM AND CHLORIDE LEVELS (WASTED IN THIS CONDITION)
ABGS
• HCO3- 42
• PH 7.46
• PCO2 53
• METABOLIC ALKALOSIS….PARTIALLY COMPENSATED

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METABOLIC ACIDOSIS their medical 2.pptx

  • 2. METABOLIC ACIDOSIS • A METABOLIC PROBLEM DUE TO THE BUILDUP OF ACID IN THE BODY FLUIDS WHICH AFFECTS THE BICARBONATE (HCO3 LEVELS) EITHER FROM: • INCREASED ACID PRODUCTION • DKA WHERE KETONES (ACIDS) INCREASE IN THE BODY .AS IN DIABETIC KETOACIDOSIS(DKA) BLOOD GLUCOSE LEVELS ARE CRAZY HIGH , PRODUCING A LOT OF KETONES WHICH ARE ACIDS . THUS BUILDING UP ACIDS IN BODY AS COMPARED TO BICARBONATES SO BICARBONATES DECREASE AND PH DECREASE. • DECREASED ACID EXCRETION • RENAL FAILURE WHERE THERE IS HIGH AMOUNT OF WASTE LEFT IN THE BODY WHICH CAUSES THE ACIDS TO INCREASE AND BICARB CAN’T CONTROL IMBALANCE • LOSS OF TOO MUCH BICARB
  • 3. • WHEN THIS ACIDIC PHENOMENA IS TAKING PLACE IN THE BODY OTHER SYSTEMS WILL TRY TO COMPENSATE TO INCREASE THE BICARB BACK TO NORMAL. ONE SYSTEM THAT TRIES TO COMPENSATE IS THE RESPIRATORY SYSTEM. • IN ORDER TO COMPENSATE, THE RESPIRATORY SYSTEM WILL CAUSE THE BODY TO HYPERVENTILATE BY INCREASING BREATHING THROUGH KUSSMAUL’S RESPIRATIONS. KUSSMAUL RESPIRATIONS ARE DEEP, RAPID BREATHES(INCREASED RESPIRATORY RATE). THE BODY HOPES THIS WILL HELP EXPEL CO2 (AN ACID) WHICH WILL “HOPEFULLY” INCREASE THE PH BACK TO NORMAL.
  • 4. LAB VALUES EXPECTED IN METABOLIC ACIDOSIS: • HCO3: DECREASED <22 • BLOOD PH: DECREASED <7.35 • CO2: <35 OR NORMAL (MAY BE NORMAL BUT IF IT IS DECREASED THIS IS THE BODY’S WAY OF TRYING TO COMPENSATE). • THE RESPIRATORY SYSTEM IS CAUSING HYPERVENTILATION. THE RESPIRATORY SYSTEM TRIES TO INCREASE THE PH FROM ITS ACIDOTIC STATES THROUGH TACHYPNEA WITH KUSSMAUL’S BREATHING. THE GOAL IS TO “BLOW OFF” THE CO2 WHICH IS ACIDIC
  • 5. • MEMORIZE THESE NORMAL VALUES FOR ABGS: • PH 7.35-7.45 • PACO2 35-45 • HCO3 22-26
  • 6. CAUSES OF METABOLIC ACIDOSIS • HIGH ANION GAP & NORMAL ANION GAP PROBLEMS : HIGH + NORMAL ANION GAP: • MUST KNOW WHETHER IT IS HIGH OR NORMAL ,SO THE CAUSE CAN BE TREATED CORRECTLY(AS CAN BE LIFE THREATENING) • WHAT IS ANION GAP? • SIMPLY THESE ARE VARIOUS LABS VALUES SEEN IN PATIENT BLOOD SAMPLE E.G CHLORIDE , BICARBONATE , SODIUM AND CALCULATE TO SEE THE DIFFERENCE BETWEEN ANIONS AND CATIONS , LOOKING FOR A GAP. • NORMAL ANION GAP IS 10 – 14 MEQ/L • IF THERE IS A GAP OF 14MEQ/L IT IS A HIGH ANION GAP
  • 7. • HIGH ANION ACIDOSIS IS CONDITIONS THAT CAUSE THE BODY TO PRODUCE TOO MUCH ACID OR NOT ENOUGH BICARB (DKA, ASPIRIN TOXICITY, RENAL FAILURE, HIGH-FAT DIET, LOW CARB DIET, MALNUTRITION) • NORMAL ANION ACIDOSIS IS LOSS OF THE BICARBONATE FROM THE BODY. EXAMPLES: DIARRHEA VIA GI FLUIDS, OSTOMIES OR FISTULA DRAINAGE (ILEOSTOMIES OR PANCREATIC FISTULA)…WHICH ARE RICH IN ALKALOTIC FLUIDS, HOWEVER WHEN LOST IT CAUSES ACIDOSIS, OR DRUGS INGESTION: DIAMOX (DIURETIC)…. CARBONIC ANHYDRASE INHIBITOR WHICH REDUCES REABSORPTION OF BICARB.
  • 8. REMEMBER MNEMONIC “ACIDOTIC” • A: ASPIRIN TOXICITY: (HIGH ANION GAP) • WHICH INCREASES THE ACID IN THE BODY AND THIS ALSO CAUSES RESPIRATORY ALKALOSIS (HYPERVENTILATION) • C: CARBOHYDRATES NOT METABOLIZED (HIGH ANION GAP): • WHEN THERE ISN’T ENOUGH OXYGEN TO BREAK DOWN CARBS THE PYRUVIC ACIDS (THAT SUPPLIES THE CELLS WITH ENERGY) STARTS TO TURN INTO LACTIC ACID AND WHEN YOU GET ACID BUILDING UP YOU GET ACIDOSIS • I: INSUFFICIENCY OF KIDNEYS (HIGH ANION GAP): • KIDNEYS ARE FAILING TO FILTER OUT METABOLIC WASTE PRODUCTS, ACIDS INCREASE, AND BICARB CANNOT KEEP UP SO IT DEPLETES
  • 9. • D: DIARRHEA (NORMAL ANION GAP): • PROFUSE DIARRHEA LEADS TO LOSS BICARBONATE • O: OSTOMY DRAINAGE (EXCESSIVE) ILEOSTOMIES, URETER ENTEROSTOMIES (NORMAL ANION GAP) • OSTOMIES ARE AN OPENING OF AN ORGAN TO ALLOW DRAINAGE • DEPENDING ON WHERE THE OSTOMY IS THESE FLUIDS ARE RICH IN BICARB AND IF LOSS DIRECTLY AT THIS SPOT (INSTEAD OF TRAVELLING THROUGH THE BODY TO FORM INTO STOOL (WHICH DOESN’T LOSE MUCH BICARB) • IT CAN DEPLETE THE BICARB FAST.
  • 10. • T: FISTULA (PANCREATIC FISTULA) (NORMAL ANION GAP) FISTULA: • A FISTULA IS A PASSAGE BETWEEN AN HOLLOW ORGAN AND BODY SURFACE OR BETWEEN TWO ORGANS….SAME CONCEPT WITH THE OSTOMY…LOSING FLUIDS WHERE YOU SHOULDN’T BE AND THEY ARE NOT BEING ABSORBED BY THE BODY…WASTING THE BICARB • I: INTAKE OF HIGH-FAT DIET: • EATING TOO MUCH FAT LEADS TO THE BUILDING-UP OF WASTE PRODUCT WHICH IN TURN LEADS TO BUILDUP OF KETONES AND ACIDS • C: CARBONIC ANHYDRASE INHIBITORS (DIAMOX): • DIURETIC WHICH REDUCES THE REABSORPTION OF BICARB
  • 11. SIGNS & SYMPTOMS OF METABOLIC ACIDOSIS • KUSSMAUL’S RESPIRATION: BODY’S WAY OF TRYING TO COMPENSATE BY EXHALING THE EXCESSIVE CO2 (IN HOPES OF INCREASING BICARB AND BLOOD PH), DEEP/RAPID BREATHING (20 TO 40 BPM) • CONFUSED, WEAK, LOW BLOOD PRESSURE, CARDIAC CHANGES IF HYPERKALEMIC ( EXCEPT WITH DIARRHEA OR WITH DIAMOX USAGE WHICH CAUSES HYPOKALEMIA), NAUSEA AND VOMITING.
  • 12. NURSING INTERVENTIONS FOR METABOLIC ACIDOSIS VARY DEPENDING ON THE CAUSES OF ACIDOSIS: • WATCH RESPIRATORY SYSTEM AND ABGS CLOSELY(RESPIRATORY DISTRESS) • IF PATIENT DROPS RESPIRATORY LEVELS OF CARBON DIOXIDE LESS THAN 35, THEY MAY NEED INTUBATION(MECHANICALVENTILATION) • ASSESS OTHER ELECTROLYTE LEVELS: • ESPECIALLY ‘POTASSIUM’ BECAUSE DURING ACTIVE ACIDOSIS, IT WILL BE HIGH • HOWEVER WHEN IT RESOLVES THERE IS AN EXTRACELLULAR TO INTRACELLULAR SHIFT OF POTASSIUM BACK INTO THE CELL WHICH WILL CAUSES HYPOKALEMIA AS THERE WONT BE ANY POTASSIUM LEFT IN THE BLOOD • DIALYSIS MAY BE NEEDED IF THEY PATIENT IS EXPERIENCING ACIDOSIS • RENAL FAILURE - HIGH ANION GAP ISSUE • DIABETIC KETOACIDOSIS • PRESCRIBED INSULIN TO HELP GLUCOSE GO BACK INTO CELL WHICH WILL HELP THE BODY START REGULATING AS IT METABOLIZES GLUCOSE - HENCE NOT MORE KETONES (ACIDS)
  • 13. • ABGS: HCO3=11, PH 7.20, PACO2=33
  • 14. • METABOLIC ACIDOSIS PARTIALLY COMPENSATED
  • 16. KEY CONCEPTS -PATHOPHYSIOLOGY • A METABOLIC PROBLEM CAUSED BY THE EXCESSIVE LOSS OF ACIDS (HYDROGEN IONS) OR INCREASED AMOUNT OF BICARB (HCO3) PRODUCED IN THE BODY THAT LEADS TO AN ALKALOTIC STATE IN THE BODY. DISEASE PROCESSES AND DRUGS CAN CAUSE METABOLIC ALKALOSIS. • WHEN METABOLIC ALKALOSIS HAPPENS IN THE BODY OTHER SYSTEMS TRY TO COMPENSATE BY HOPEFULLY FIXING THE BLOOD’S PH AND BICARB LEVEL. • ONE SYSTEM THAT DOES THIS IS THE RESPIRATORY SYSTEM BY STIMULATING THE RESPIRATORY SYSTEM TO HYPOVENTILATE (DECREASE RESPIRATIONS…<12/MIN) WHICH WILL RETAIN PCO2 (CARBON DIOXIDE) SO IT WILL DECREASE THE PH BACK TO NORMAL, HENCE YOU WILL START TO SEE BRADYPNEA IN THE PATIENT.
  • 17. • IF A PATIENT IS EXPERIENCING METABOLIC ALKALOSIS THEY WILL PRESENT WITH THE FOLLOWING LABS: • HCO3: INCREASES >26 • BLOOD PH: INCREASES >7.45 • CO2: >45 OR NORMAL (MAY BE NORMAL BUT IF INCREASED THIS IS THE BODY’S WAY OF TRYING TO COMPENSATE. THE RESPIRATORY SYSTEM TRIES TO DECREASE THE PH FROM ITS ALKALOTIC STATE BY CAUSING HYPOVENTILATION ( BRADYPNEA). THE RESPIRATORY SYSTEM HOPES THAT IF THE CO2 INCREASE ENOUGH IT WILL CAUSE THE PH TO DECREASE AND THE KIDNEYS WILL START TO EXCRETE THE BICARB WHICH WILL HOPEFULLY DECREASE THE OVERALL HCO3.
  • 18. NORMAL VALUES • REMEMBER WHAT NORMAL VALUES ARE: • PH = 7.35 TO 7.45 • PACO2 = 35 TO45 • HCO3 = 22 TO 26
  • 19. CAUSES OF METABOLIC ALKALOSIS • ALKALI • A: ALDOSTERONE PRODUCTION EXCESSIVE (HYPERALDOSTERONISM) ACTIVATES RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM: • THE ADRENAL CORTEX IS RELEASING TOO MUCH ALDOSTERONE WHICH CAUSES THE RENAL TUBULE IN THE KIDNEYS TO KEEP SODIUM WHICH LOSE HYDROGEN IONS AND ALSO POTASSIUM AND THIS IN TURN CAUSES AN INCREASE IN BICARB (HCO3) • L: LOOP DIURETICS (LASIX) OR THIAZIDE THERAPY: • CAUSES THE KIDNEYS TO WASTE HYDROGEN IONS AND CHLORIDE THROUGH THE URINE (ALSO LOSING K+) WHICH IN TURN INCREASES THE BICARB • K: ALKALI INGESTION OF FOOD (BAKING SODA, MILK, ANTACIDS) INCREASES BICARB LEVEL IN THE BLOOD
  • 20. • A: ANTICOAGULANT “CITRATE” (USED AS A STORAGE AGENT IN BLOOD AND DURING CONTINUOUS FORMS OF RENAL REPLACEMENT THERAPY) • CAUSED FROM A MASSIVE TRANSFUSION OF WHOLE BLOOD (PATIENT NEEDS SEVERAL BAGS OF BLOOD) AND THE BODY METABOLIZES THE CITRATE USED IN THE BLOOD AS BICARB WHICH INCREASES THE HCO3 LEVEL IN THE BODY. ALSO, PATIENTS WHO UNDERGO CONTINUOUS FORMS OF RENAL REPLACEMENT THERAPY (CRRT) (AN ALTERNATIVE THERAPY FOR PATIENTS WHO CAN’T UNDERGO HEMODIALYSIS) ARE AFFECTED BY THE CITRATE USED IN THE THERAPY. • L: LOSS OF FLUIDS (VOMITING AND GI SUCTIONING) • THESE FLUIDS ARE RICH IN K+ AND WHEN YOU LOSE THEM YOU ARE LOSING HYDROGEN IONS AND THIS CAUSES THE BODY TO INCREASE THE BICARB LEVEL • LOW POTASSIUM LEVELS CAUSE REABSORPTION OF HCO3. • I: INCREASED SODIUM BICARB ADMINISTRATION (TRYING TO CORRECT METABOLIC ACIDOSIS)
  • 21. SIGNS AND SYMPTOMS OF METABOLIC ALKALOSIS • BRADYPNEA (HYPOVENTILATION) <12 BPM • MANY SYMPTOMS DUE TO LOW POTASSIUM (DYSRHYTHMIA), TETANY, TREMORS, MUSCLE WEAKNESS/CRAMPING, TIRED, IRRITABLE, VOMITING, DEPRESSION ST, FLAT OR INVERTED T WAVE AND PROMINENT U-WAVE)
  • 22. NURSING INTERVENTIONS FOR METABOLIC ALKALOSIS • BASED ON THE CAUSE: • VOMITING (GIVE ANTIEMETIC) • STOP NG SUCTIONING • STOP DIURETICS • DIAMOX (CARBONIC ANHYDRASE INHIBITORS): A DIURETIC WHICH REDUCES THE REABSORPTION OF BICARB • WATCH ABGS AND SIGNS OF RESPIRATORY DISTRESS • MONITOR POTASSIUM AND CHLORIDE LEVELS (WASTED IN THIS CONDITION)
  • 23. ABGS • HCO3- 42 • PH 7.46 • PCO2 53