Metabolic Acidosis

Acid Base Disorders in Medicine For The Primary Care Provider

Jonathan J. Taliercio, DO, FASN Program Director, Nephrology and Hypertension Fellowship Assistant Professor, CCLCM Cleveland Clinic

JonTaliercio_DO

2 Faculty Disclosure

. No conflicts of interest . The presentation will not include discussion of unapproved or investigational uses of products or devices.

3 Case 1

A hospitalized 62-year-old woman has a 2 day history of SBO manifesting with profuse vomiting requiring NGT suction. Exam BP 80/50, HR 115/min, ↓ skin turgor, and diffuse abdominal pain. The BMP indicates serum Na 135 mEq/L, K 3.5 mEq/L, Cl 85 mEq/l, HCO3 25 mEq/l, BG 90 mg/dl, BUN 110 mg/dl, creatinine 4.5 mg/dl. ABG: pH 7.40, pCO2 40 mm Hg. Which one of the following best applies to this patient?

A.There is no significant disorder because the blood pH and HCO3 are normal B.The patient does not have metabolic acidosis because of the normal blood pH C.The patient has metabolic alkalosis D.The patient has metabolic acidosis and respiratory acidosis E.The patient has a mixed metabolic acidosis and metabolic alkalosis

4 Case 1

5 What We Will Be Talking About

. Relevant, High Yield information for clinical practice . Basic Concepts . Acid Base Nomenclature . Stepwise Approach to Acid Base Problem Solving . Questions and Answers . Conclusions

6 Basic Concepts

. Carbohydrate and fat metabolism generates 15,000 mmol/day of CO2

+ . CO2 is a volatile acid due to its ability to producing a H after hydration with H2O slow fast + CO2 + H20 H2CO3 H + HCO3

. Under normal conditions, the lungs eliminate ALL the CO2 produced from CHO and fat metabolism and thus CO2 has NO impact on acid base balance

7 Basic Concepts

. Dietary protein (amino acids) metabolize into nonvolatile acids – Sulfuric, phosphoric, hydrochloric acid . 1 mmol H+/kg ~ (50-100 mmol/day) . In order to maintain acid-base balance, the kidney’s must – Excrete ALL the metabolized nonvolatile acids with urinary buffers

– Replenish ALL the HCO3 that is consumed via the neutralization of the nonvolatile acids

– Must prevent ALL urinary loss of HCO3

8 Net nonvolatile Net non- acid: Metabolism Diet volatile acid: ECF 40 mmol 30 mmol Lungs pH 7.4 CO2 (volatile acid): 15,000 mmol

Reabsorbed - Filtered HCO3 : - New HCO3 : - HCO3 : 4320 mmol 70 mmol 4320 mmol

Kidneys 30 mmol titratable acids Urine + 40 mmol NH4

Boron & Boulpaep (2009) courtsey of Sarmey 9 Consequences of Acidosis Acute Chronic . Kidney . Cardiovascular – Stone disease – ↓ Cardiac contractility and arterial vasodilatation leading to ↓ BP – CKD – ↑ Risk for dysrhythmias – Bone disease . Respiratory . MSK – Hyperventilation (metabolic) – Growth retardation (children) – Sarcopenia . Cerebral –  albumin synthesis – Obtundation and coma (respiratory) . Endo . Metabolic – Insulin Resistance – Hyperkalemia, ↓ATP synthesis

10 Normal Values for Acid-Base Parameters in Arterial and Venous Blood

+ pH [H ] PCO2 [HCO3] nanoEq/L mmHg mEq/L Arterial 7.35-7.45 37-43 35-45 21-27

Venous .03 to .04 42-48 ↑ 3- 8 ↑ 1-2

Central  .03-.05 42-48 ↑ 4-5 21-27

11 Florence Agnes Henderson David Michael Hasselhoff

12 Henderson Hassalbalch Hasselhoff Equation

13 Henderson-Hasselbalch

What is the expected pH in a patient with HCO3 15 and PCO2 40?

HCO3 (BASE) pH = pK + log (α) PCO2 (ACID)

15 pH = 6.1 + log 0.03 (40)

pH = 7.2

14 Clinical Use

What is the expected pH in a patient with HCO3 15 and PCO2 40?

PCO2 (ACID) pH [H+] [H+] nEq/L = 24 x HCO3 (BASE) 7.0 100 7.1 80 40 7.2 63 [H+] nEq/L = 24 x 15 7.3 50 7.4 40 [H+] nEq/L = 63 7.5 31 7.6 25

15 Basic Concept

. A simultaneous ABG and a BMP is required for the determination of an acid base disorder

– HCO3 measurement on the ABG is calculated using the henderson-hasselbalch equation

– Total PCO2 on a venous sample is a true measurement of HCO3 fast slow + – H + HCO3 H2CO3 CO2 + H20

16 Acid-base Nomenclature

. Simple (primary) acid-base disturbance – The presence of one primary abnormality coupled with its anticipated secondary response

. Mixed acid-base disturbance – The simultaneous presence of two or more primary abnormalities

17 Acid Base Nomenclature

. Acidemia - pH < 7.35 ↑ [ H+ ] (↓ pH) . Alkalemia- pH > 7.45 ↓ [ H+ ] (↑ pH)

. Acidosis- a pathophysiological process which decreases extracellular fluid pH

– Metabolic acidosis initial disturbance ↓ [HCO3]

– Respiratory acidosis initial disturbance ↑ [PCO2]

. Alkalosis - a pathophysiological process which increases extracellular fluid pH

– Metabolic alkalosis initial disturbance ↑ [HCO3]

– Respiratory alkalosis initial disturbance ↓ [PCO2]

18 Patterns of Simple Acid Base Disorders Compensatory Primary Primary Disorder pH Change Change (PCO2) (HCO3) Metabolic Acidosis ↓ ↓ ↓↓

Metabolic Alkalosis ↑ ↑ ↑↑

Primary Compensatory Primary Disorder pH Change Change (PCO2) (HCO3) Respiratory Acidosis ↓ ↑↑ ↑

Respiratory Alkalosis ↑ ↓↓ ↓

19 Key Concept

In primary acid base disorders, the compensatory response does not fully correct the underlying disorder but rather reduces the magnitude of the change in pH

20 Patterns of Mixed Acid Base Disorders

Change Change Disorder pH (PCO2) (HCO3)

Mixed Respiratory ↑ ↓ ↑ Alkalosis and Metabolic or Alkalosis WNL Mixed Respiratory ↓ ↑ ↓ Acidosis and Metabolic or Acidosis WNL

21 Key Concept

.If the pH is normalized than a mixed disorder is present

.It is impossible to have a simultaneous respiratory acidosis and respiratory alkalosis

22 Respiratory Compensation for Metabolic Acidosis

Primary Compensatory Disorder Change Response

Metabolic ↓ [HCO3] * Expected ↓ PCO2 : 1.2 mmHg ↓ in PCO2 Acidosis for every 1 mmol/L fall in HCO3

(Winters Formula) * Expected ↓ PCO2 : 1.5 X HCO3 + 8 (+/- 2)

* Expected ↓ PCO2 : HCO3 + 15

* Expected ↓ PCO2: Last 2 digits of pH

Time adaptation ~ 30 mins - 24 hours

23 Respiratory Compensation for Metabolic Alkalosis

Primary Compensatory Disorder Change Response

Metabolic ↑ [HCO3] * Expected ↑ PCO2 : 0.7 mmHg ↑ in PCO2 - Alkalosis for every 1 mmol/L rise in HCO3

* Expected ↑ PCO2 : HCO3 + 15 - * Expected ↑ PCO2 : 1.2 [HCO3 ] + 6 (+/-2) - * Expected ↑ PCO2 : 0.9 [HCO3 ] + 9 (+/-3)

HINT: * PCO2 should > 40 and usually is <55 Time adaptation ~ 30 mins - 24 hours

24 Metabolic Compensation for Respiratory Disturbances

Disorder Compensatory Response

- Acute Respiratory Acidosis 1 mEq/L increase in [HCO3 ] for (mins- hours) every 10 mmHg rise in PCO2

- Acute Respiratory Alkalosis 2 mEq/L decrease in [HCO3 ] for (mins- hours) every 10 mmHg fall in PCO2

- Chronic Respiratory Acidosis 3.5 mEq/L increase in [HCO3 ] for (3-5 days) every 10 mmHg rise in PCO2

- Chronic Respiratory Alkalosis 4 mEq/L decrease in [HCO3 ] for

(3-5 days) every 10 mmHg fall in PCO2

25 Metabolic Compensation for Respiratory Disturbances

Disorder Compensatory Response

- Acute Respiratory Acidosis 1 mEq/L increase in [HCO3 ] for (mins- hours) every 10 mmHg rise in PCO2

- Acute Respiratory Alkalosis 2 mEq/L decrease in [HCO3 ] for (mins- hours) every 10 mmHg fall in PCO2

- Chronic Respiratory Acidosis 3.5 mEq/L increase in [HCO3 ] for (3-5 days) every 10 mmHg rise in PCO2

- Chronic Respiratory Alkalosis 4 mEq/L decrease in [HCO3 ] for

(3-5 days) every 10 mmHg fall in PCO2

26 A Few Words on Metabolic Acidosis

27 Metabolic Acidosis

Primary defect is fall in serum HCO3 Accumulation of metabolic acids caused by: 1. Excess acid production which overwhelms renal capacity for acid excretion (ex. DKA) 2. Renal excretory failure: normal total acid production in face of poor renal function (ex. CKD) 3. Loss of alkali: leaves un-neutralized acid behind (ex. diarrhea)

28 Serum Anion Gap

+ - . Anion Gap = Na - (Cl + HCO3) – Normal range 8-12 meq/L . The gap simply reflects the differences between the unmeasured anions and unmeasured cations . The expected anion gap should be reduced by 2.5 meq/L for every 1 g/dl reduction in albumin below 4 g/dl – Example: Expected AG is 5 in a patient with a albumin of 2 g/dl (10 – (2 x 2.5) = 5)

29 Unmeasured Unmeasured Anions Cations - SO4 = 2 4 - HPO4 = 3

Protein = 16 Mg++= 2

Cl- = 105 Cl- = 105

30 Causes of AGMA . Methanol . Glycols (ethylene, propylene) . Uremia . Oxoproline . Diabetic (ETOH starvation . L-lactate ketosis) . D-lactate . Propylene glycol . Methanol . Isoniazid . Aspirin . Lactic acidosis . Renal failure . Ethylene glycol . Ketosis (ETOH or DKA) . Salicylates

31 Causes of a Low Serum Anion Gap ↓ AG = ↑ UC - ↓ UA - SO4 = 2

4 - HPO4 = 3 Unmeasured Unmeasured Anions Cations Protein = 16 Mg++= 2

Low AG due to ↑ UC Low AG due to ↓ UA Cationic proteins of Myeloma Cl- = 105 Hypoalbuminemia Hypercalcemia Hypermagnesiemia Lithium

32 Case 1

33 Step Wise Approach to Acid Base Problem Solving

1. Is there an acidemia or alkalemia present? 2. Identify the primary disturbance (-oses)

– Examine HCO3 and PCO2 levels in relationship to pH 3. Calculate the expected compensation – If inappropriate, identify the 2nd disorder 4. Is an AGMA present? 5. If an AGMA is present, check the delta-delta

34 Case 1 Answer

Serum: Na 135 mEq/L, K 3.5 mEq/L, Cl 85 mEq/l, HCO3 25 mEq/l, BG 90 mg/dl, BUN 110 mg/dl, creatinine 4.5 mg/dl. ABG: pH 7.40, pCO2 40 mm Hg. Which one of the following best applies to this patient?

1. Is there a acidemia or alkalemia present? No pH=7.4 2. What is the primary disturbance? • pCO2 = 40, HCO3 = 25 (None) 3. Calculate the expected compensation? Not required + - 4. Is an AGMA present? AG = Na - (Cl + HCO3) 135 – (85 + 25) = 25. Yes 5. If an AGMA is present, check the delta-delta AGMA with Metabolic Alkalosis

35 Delta Ratio or Delta Gap

. Used only in AGMA to assess for 2nd metabolic process

. Delta Ratio = AG/ HCO3

. Delta Gap = AG- HCO3 1. Pure AGMA . Delta Ratio = 1-2

. Delta Gap = AG ∼ HCO3 2. AGMA + NAGMA . Delta Ratio < 1

. Delta Gap= AG (more anions) < HCO3 3. AGMA with metabolic alkalosis . Delta Ratio > 2

. Delta Gap = AG > HCO3 (more HCO3)

36 Alternative to Delta Ratio or Gap

AG + HCO3 (actual) = ~ 24 (normal HCO3)

~ 24 = No Additional Disturbance > 24 = Metabolic Alkalosis < 24 = Non-Metabolic Acidosis

in other words….. “Reciprocity”

For every ↑ 1 AG : ↓ 1 HCO3

37 Case 1 Answer : Delta Delta

. Serum: Na 135 mEq/L, Cl 85 mEq/l, HCO3 25 mEq/l. ABG: pH 7.40, pCO2 40 mm Hg. Which one of the following best applies to this patient? AG = 25

AG + HCO3 (actual) = 24 (normal HCO3)

. (25-10 (normal AG)) + 25 (actual HCO) = 24 . 15 + 25 = 40 (40 > 24 so metabolic alkalosis)

. For every ↑ 1 AG : ↓ 1 HCO3

. AG goes up by 15, the HCO3 should go down by 15 to have an expected serum HCO3 of 9. However, this patients HCO3 is 25 (excessive HCO3) so therefore “metabolic alkalosis”

38 Treatment of Acute Metabolic Acidosis

1. Treat underlying cause (ex. hypotension, sepsis, DKA) 2. Administration of sodium bicarbonate – ALWAYS if pH < 7.1

– Avoid overzealous administration of HCO3

. Modest increment in plasma HCO3 (e.g., 4-6 mEq/L) . BEWARE of “overshoot alkalemia” . BEWARE of worsening CNS status

HCO3 + H+ H2CO3 CO2 + H2O fast slow

39 Case 2

22 year old man is found unconscious in the street and brought to an OSH ED. He is only responsive to pain. His neurological exam is non focal. Serum: Na 130, K 4, Cl 94, HCO3 11, BUN 56, SC~ 2, Glucose 72, serum osmoles 320. ABG pH 7.27, PCO2 26. Serum lactate, ketones, and ethanol levels are normal. What is the most appropriate first step in the management of this patient?

A. Head CT B. Forced alkaline diuresis C. Fomepizole D. Hemodialysis

40 Case 2

A. Head CT B. Forced alkaline diuresis C. Fomepizole D. Hemodialysis

41 Na 135, K 4, Cl 100, HCO3 11, BUN 56, SC~ 2, Glucose 72, serum osm 320. ABG: pH 7.27, PCO2 26. Serum lactate, ketones, and ethanol are normal

1. Is acidemia or alkalemia present? pH < 7.35 = Acidemia

2. What is the primary disturbance? Metabolic Acidosis (↓ HCO3 11, ↓ PCO2 26)

3. Calculate the expected compensation? • Winters Formula : Expected ↓ PaCO2 : 1.5 X HCO3 + 8 (+/- 2) • Expected ↓ PaCO2 : 1.5 X (11) + 8 (+/- 2) ~ 23-27 appropriate

4. Is an AGMA present? AG = 135 - (100 + 11) = 24. Yes

5. If an AGMA is present, check the delta-delta AG + HCO3 actual= 24; ↑AG (14) : ↓ (14) HCO (24-10) + 11 = 25 ~ 24 so pure AGMA

42 Causes of AGMA

. Methanol . Glycols (ethylene, propylene) . Uremia . Oxoproline . Diabetic (ETOH starvation . L-lactate ketosis) . D-lactate . Propylene glycol . Methanol . Isoniazid . Aspirin . Lactic acidosis . Renal failure . Ethylene glycol . Ketosis (ETOH or DKA) . Salicylates

43 Osmolar Gap

. Na 135, K 4, Cl 100, HCO3 11, BUN 56, SC~ 2, Glucose 72, serum osm 320. ABG pH 7.27, PCO2 26. Serum lactate, ketones, and ethanol levels are normal. . Osmolar gap = measured – calculated osmolality . > 10 suggests the presence of an osmotically active substance . > 20 is almost always due to a toxic alcohol (Methanol, ethylene, propylene glycol)

. Calculated Osmolality = (Na x 2) + (BUN/2.8) + (Glucose/18) = 275-295 mOs/kg

. Calculated osm: (135 x 2) + (56/2.8) + (72/18) = 294 mOs/kg

. Osmolar gap: 320 – 294 = 26 mOs/kg

44 Case 2 Answer

. AGMA with + Osmolar gap

– Ethylene glycol

– Methanol

. What is the most appropriate first step in the management of this patient? A. Head CT B. Forced alkaline diuresis C. Fomepizole D. Hemodialysis

45 Case 3 A patient presents with a Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg. What is the metabolic disturbance?

A. AGMA with appropriate respiratory compensation

B. AGMA with inappropriate respiratory compensation

C. NAGMA with appropriate respiratory compensation

D. NAGMA with inappropriate respiratory compensation

46 Case 3 A patient presents with a Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg. What is the metabolic disturbance?

A. AGMA with appropriate respiratory compensation

B. AGMA with inappropriate respiratory compensation

C. NAGMA with appropriate respiratory compensation

D. NAGMA with inappropriate respiratory compensation

47 Serum: Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg

1. Is there a acidemia or alkalemia present? Acidemia (pH < 7.35)

2. What is the primary disturbance? Metabolic acidosis (↓HCO3 5,↓PCO2 17)

3. Calculate the expected compensation? • Winters Formula : Expected ↓ PaCO2 : 1.5 X HCO3 + 8 (+/- 2) • Expected ↓ PaCO2 : 1.5 X (5) + 8 (+/- 2) ~ 13-17 appropriate

+ 4. Is an AGMA present? AG = Na – (Cl + HCO3) • 135 - (120 + 5) = 10. No

NAGMA with appropriate respiratory compensation

48 Causes of Normal Anion Gap Metabolic Acidosis

Hyperalimentation Hyperalimentation Excess NaCl Addisons Disease Acetazolamide Renal Tubular Acidosis RTA, CKD 4 Diarrhea Trotz (diarrhea) Acetazolamide Carbonic anhydrase inhibitors Spirolactone (topiramate) Saline infusion Cholestyramine Uretosigmoidostomy

49 Case 3 continued

Serum: Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg.

Urine: pH 6.5, UNa 28 meq/L, UK 50 meq/L, UCl 57 meq/L

What is the diagnosis? A. Gitelmans B. Classic Distal RTA Type I C. Type IV RTA D. GI bicarbonate loss

50 Case 3 continued

Serum: Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg.

Urine: pH 6.5, UNa 28 meq/L, UK 50 meq/L, UCl 57 meq/L

What is the diagnosis? A. Gitelmans B. Classic Distal RTA Type I C. Type IV RTA D. GI bicarbonate loss

51 Urine Anion Gap in the Evaluation of NAGMA

UAG = (NH+4Cl) = (Na+ + K+) – (Cl-) 4+ . Urinary ammonium (NH ) is a major unmeasured cation in the urine which binds to UCL Na . UAG is a indirect estimate of +4 urinary NH Cl Cl +4 K . A negative UAG = NH is A negative (normal) gap present in the urine Cl (anion) exceeds Na 4+ . & K (cations) NH in the urine suggests +4 -4 effective renal acid secretion NH PO SO-4

52 Urine Anion Gap in the Evaluation of NAGMA UAG = (NH+4Cl) = (Na+ + K+) – (Cl-)

+4 . A positive UAG = NH is +4 absent in the urine =  NH excretion Na +4 . Low NH excretion results A positive Cl in ↑ Na and K in urine (abnormal) gap

Na & K (cations) +4 . Absence of NH in urine is exceeds Cl- K inappropriate in acidemia (anions) PO-4 SO-4 and consistent with RTA NH+4

53 Urine Anion Gap

. Negative UAG means NH4+ (acid) is present in the urine (↓ UpH) during systemic acidemia which is an appropriate renal response

– UAG should be neGUTive in diarrhea

. Positive UAG means NH4+ (acid) is NOT present in the urine (↑ UpH) during systemic acidemia which is an INappropriate renal response

– UAG is positive in RTA

54 Case 3 continued

Serum: Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg.

Urine: pH 6.5, UNa 28 meq/L, UK 50 meq/L, UCl 57 meq/L UAG = ([Na+] + [K+]) – [Cl-] UAG = 28 + 50 – 57 = +21 What is the diagnosis? A. Gitelmans B. Classic Distal RTA Type I C. Type IV RTA D. GI bicarbonate loss

55 Case 3 continued

Serum: Na 135 meq/L, potassium 2.5 meq/L, chloride 120 meq/L, HCO3 5 meq/L. ABG: pH 7.15, PCO2 17 mmHg. Urine: pH 6.5, UNa 28 meq/L, UK 50 meq/L, UCl 57 meq/L. What is the diagnosis? UAG = ([Na+] + [K+]) – [Cl-] UAG = 28 + 50 – 57 = +21

A. Gitelmans B. Classic Distal RTA Type I C. Type IV RTA D. GI bicarbonate loss

56 Case 4

55 year old male with chronic small bowel obstruction requiring NGT for intermittent drainage comes to the hospital for abdominal pain. Serum: Na 145 meq/L, K 3 meq/L, Cl 95 meq/L, HCO3 40 meq/L. ABG: pH 7.55, PCO2 51 mmHg. Urine: UNa 45 meq/L, UK 23 meq/L, UCl 9 meq/L. What is the metabolic disturbance and the treatment response?

A. Respiratory Acidosis B. Respiratory Alkalosis C. Metabolic Alkalosis, saline resistant D. Metabolic Alkalosis, saline responsive

57 Case 4

A. Respiratory Acidosis B. Respiratory Alkalosis C. Metabolic Alkalosis, saline resistant D. Metabolic Alkalosis, saline responsive

58 Na 145 meq/L, K 3 meq/L, Cl 95 meq/L, HCO3 40 meq/L. ABG: pH 7.55, PCO2 51 mmHg. Urine: UNa 45 meq/L, UK 23 meq/L, UCl 9 meq/L

1. Is there a acidemia or alkalemia present? Alkalemia (pH > 7.45)

2. What is the primary disturbance? Metabolic alkalosis (↑HCO3 40, ↑PCO2 51) 3. Calculate the expected compensation?

• * Expected ↑ PaCO2 : 0.7 mmHg ↑ in PaCO2 for every 1 mmol/L rise in HCO3 • Expected ↑ pCO2 (40-24)= 16 x 0.7 ~ 11 + 40= 51 appropriate

4. Is an AGMA present? AG = Na – (Cl + HCO3) . 145 - ( 95 + 40 ) = 10. No

Metabolic Alkalosis with appropriate respiratory compensation with a low urinary chloride

59 Metabolic Alkalosis

Saline- Responsive (UCl < 20) Saline- Resistant (UCl > 20)

1. GI losses 1. Hypertensive • Vomiting or NGT drainage • Mineralcorticoid excess • 1º hyperaldosteronism 2. Contraction alkalosis • Liddle’s • Massive diuresis • Cushings • Villous adenoma • Licorice ingestion • Factitious diarrhea (laxatives) 2. Normotensive • Bartter’s or Gitelman’s • Severe hypokalemia < 2 *Treatment requires removing the • Current diuretic use offending agent, provide volume, K • Exogenous alkali load supplementation. *Treat the underlying disorder

60 Treatment of Metabolic Alkalosis

.ECF Contraction and Sufficient Kidney Function – Stop diuretics, IVF

.ECF Expansion and Sufficient Kidney Function – Acetazolamide

.Severe Kidney Failure – Dialysis with low HCO bath

Courtesy of Michael Emmett61 Case 5

65 year old female with PMH of CAD s/p CABG in 2010 is admitted to the hospital for SOB. CXR reveals RLL infiltrate. Serum: Na 141 meq/L, Cl 100 meq/L, HCO3 31 meq/L. ABG: pH 7.25, PCO2 60 mmHg. What is the metabolic disturbance?

A. Acute Respiratory Acidosis B. Chronic Respiratory Acidosis C. NAGMA D. AGMA with Metabolic Alkalosis

62 Case 5

A. Acute Respiratory Acidosis B. Chronic Respiratory Acidosis C. NAGMA D. AGMA with Metabolic Alkalosis

63 Na 141 meq/L , Cl 100 meq/L, HCO3 31 meq/L. ABG: pH 7.25, PCO2 60 mmHg

1. Is there a acidemia or alkalemia present? pH < 7.35 = Acidemia

2. What is the primary disturbance? Respiratory Acidosis ↑HCO3 31, ↑PCO2 60 3. Calculate the expected compensation? - • Acute Resp. Acidosis: 1 mEq/L increase in [HCO3 ]for every 10 mmHg rise in PCO2

• Expected ↑ in HCO3 (60-40 = 20) 20/10 = 2 x 1 = 2 so expected HCO3= 26 - • Chronic Resp. Acidosis: 3.5 mEq/L increase in [HCO3 ] for every 10 mmHg rise in PCO2

• Expected ↑ in HCO3 (60-40 = 20). 20 /10 = 2 x 3.5 = 7 so expected HCO3= 31. Appropriate

4. Is an AGMA present? AG = Na – (Cl + HCO3) 141 - (100 + 31 ) = 10. No

Chronic Respiratory Acidosis

64 Clinical Causes of Respiratory Acidosis

. Disorders Affecting Gas Exchange – COPD, asthma, PNA, pulmonary edema, pneumothorax . Airway Obstruction – Aspiration of foreign body, OSA, broncho/laryngospasm . CNS depression – Sedation/opioids, CNS lesion, oxygen in patient with chronic hypercapnia . Chest Wall Abnormalities – Obesity-Hypoventilation syndrome, kyphoscoliosis, flail chest, scleroderma, rib fracture, myxedema . Neuromuscular Disorders – Myasthenia gravis, Guillain-Barre, ALS, Poliomyelitis, MS, phrenic nerve palsy

65 Clinical Causes of Respiratory Alkalosis

Hyperthyroidsim Anxiety Hypoxia Pain Ventilator-induced CNS disorders Pregnancy  CVA  Tumor Cirrhosis  Infection Pulmonary edema Hormones - Drugs Lung disease  Salicylates  ARDS  Catecholamine's  Pulmonary emboli  Progesterone  Pneumonia Sepsis, gram (+) or (-)  Pneumothorax Fever

66 Clues to Diagnosis a Simple Acid-Base Disorders

History Acid-Base Disorder COPD Respiratory Acidosis

Renal failure NAGM or AGMA Diarrhea NAGMA Shock AGMA (lactic acid)

67 Clues to Diagnosis a Simple Acid-Base Disorders

History Acid-Base Disorder Cirrhosis Respiratory Alkalosis Sepsis Respiratory Alkalosis

Diuretics Metabolic Alkalosis Vomiting Metabolic Alkalosis NG suction Metabolic Alkalosis

68 Clues to Diagnosis a Mixed Acid-Base Disorders

History Acid-Base Disorder

COPD + diuretics Respiratory Acidosis and Metabolic Alkalosis Sepsis Respiratory Alkalosis and Metabolic Acidosis Salicylate intoxication Respiratory Alkalosis and Metabolic Acidosis

69 Conclusions

. Use Clinical Clues to help identify disorders . Step Wise Approach to Acid Base Problem Solving . Anion Gap Metabolic Acidosis – Osmolar Gap . Non Anion Gap Metabolic Acidosis – Urine Anion Gap . Metabolic Alkalosis – Saline-Responsive vs. Saline-Resistant . Respiratory Acidosis or Alkalosis – Acute versus Chronic Process

70 Thank You JonTaliercio_DO /L mEq Bicarbonate Bicarbonate

pCO2 mm Hg

. Overshoot alkalemia occurs when "potential" bicarbonate (ie, lactate or ketoacids) have been retained and can be converted back to bicarbonate when the underlying metabolic derangement has been reversed as the patient is getting bicarbonate infusion.

. CO2 must be removed from the tissue bed via an intact circulation and respiration. Adequate perfusion and ventilation is a prerequisite to the effective use of a bicarbonate drip. CO2 readily penetrates cell membranes, leading to intracellular acidosis. And bicarbonate infusion decreases the drive to hyperventilate

. Oxalaic acid (oxalate), Glycolic Acid

. Alpha is the solubility factor for PCO at 37 degrees C

. Cholestyramine: The cationic resin binds with bicarb in the lumen of the intestine and is eliminated in the stool.