Acid-Base and Electrolyte Pearls

1
Acid-Base and Electrolyte Pearls

• Luis S. Gonzalez III, Pharm.D., BCPS
• Memorial Medical Center

2
In the last year, pick your most frequently
watched television program.

1. Cash Cab
2. Deal or No Deal
3. Dancing With the Stars
4. American Idol
5. Myth Busters
6. Flavor of Love/Rock of Love
7. Hogan Knows Best
8. Wall Street Week
9. 30 Minute Meals
10. Monday Night Football
11. None of the above.

3
What popular computer program turned 21 this year?

1. Access
2. Outlook
3. SPSS
4. Word
5. PowerPoint
6. Excel

4
Electrolyte Disorders

• Luis S. Gonzalez III, Pharm.D., BCPS
• Memorial Medical Center

5
Objectives

• Discuss the pathophysiology of common electrolyte
  disorders.
• Develop an appropriate management plan for common
  electrolyte disorders.

6
Case

• 59 year-old-female with NSC lung CA develops NV
  after chemotherapy. On presentation to the
  clinic, she has flat neck veins, dry mucous
  membranes, and reduced skin turgor.
• Plasma Na 112 meq/L, Plasma OSM 243
  mosmol/kg
• Urine Na 5 meq/L, Urine OSM 498 mosmol/kg

7
Case (Continued)

• What is the appropriate therapy at this time?
• fluid restriction
• 3 NaCl IV at a rate of 50 ml/hr
• 0.9 NaCl IV at a rate of 150 ml/hr
• 0.45 NaCl IV at a rate of 100 ml/hr

8
Assess Volume Status

• Hypovolemia
• History
• Symptoms (related to a decrease in tissue
  perfusion) lassitude easy fatigability thirst
  muscle cramps postural dizziness abdominal
  and/or chest pain lethargy and confusion
• PE Skin, axila, and mucous membranes
  (interstitial volume) BP initially low with
  upright posture to low regardless of posture
  (depends on patients NORMAL BP)

9
Assess Volume Status

• Hypervolemia
• History
• Symptoms pulmonary edema (SOB, orthopnea)
  peripheral edema and ascites (swollen legs,
  difficulty walking, increased abdominal girth)
• PE tachypneic diaphoresis rales pitting edema
  in dependent areas abdominal distension and
  fluid wave on percussion

10
Generation of Hyper(Na gt 145meq/L) or
Hyponatremia(Na lt 135meq/L)

• Plasma (Na)

• Nae____ __Ke
• Total Body Water

11
Pseudohyponatremia

• Low plasma Na concentration with NORMAL Posm
• Severe hyperlipidemia (1 liter of plasma 930ml
  of water 70ml plasma proteins and lipids)
• Severe hyperproteinemia
• Low plasma Na concentration with ELEVATED Posm
• Hyperglycemia (Na Glucose/42)
• Administration of hypertonic mannitol
• IVIG administration with maltose accumulation in
  RF

12
Hypotonic Hyponatremia

• Hypovolemic
• Renal losses hypoaldosteronism, excessive
  diuresis (thiazidesgtgtloop, mannitol, urea,
  glucose), cerebral salt wasting
• Nonrenal losses blood GI and Skin

13
Hypotonic Hyponatremia

• Isovolemic
• Syndrome of Inappropriate Antidiuretic Hormone
  (SIADH)
• Increased hypothalmic production Neuro/psych
  disorders drugs (chemo, psych meds, etc.)
  pulmonary disease post-op patient
• Ectopic ADH production various carcinomas
• Potentiation of ADH effect (carbamazepine)
• Exogenous ADH administration
• Adrenal insufficiency
• Hypothyroidism

14
Hypotonic Hyponatremia

• Hypervolemic
• Conditions associated with effective circulating
  volume depletion congestive heart failure and
  cirrhosis
• Conditions associated with true volume expansion
  renal failure and nephrotic syndrome

15
Evaluation of Hyponatremia

• History, PE, Plasma Osmo, basic metabolic panel,
  Urine Osmo, Urine Na
• Plasma Osmolality
• Normal or elevated pseudohyponatremia
• Urine Osmolality
• lt100 mosml/kg primary polydipsia
• Urine Sodium
• lt 25 meq/L effective circulating volume
  depletion
• gt 40 meq/L SIADH, renal failure, diuretics,
  adrena insuffciency, hypothyroidism

16
Treatment of Hyponatremia

• 2 basic principles (1) raising plasma Na at a
  safe rate (2) treating cause
• Give Na to patients who are volume-depleted and
  restrict water intake in patients who are
  normovolemic or edematous
• Neurologic symptoms (nausea, malaise, HA,
  lethargy, obtundation, seizures, coma) and/or Na
  lt 110 meq/L 3 NaCl (15-80ml/hr)1-2ml/kg/hour,
  Na Q1-2 hours, stop after rise of 8-12meq in 24
  hours, 18meq in 48 hours

17
Be Careful!

• Overly rapid correction of Na may result in a
  condition known as central pontine myelinolysis
  (CPM) or osmotic demyelination syndrome
• Within 1-4 days development of para/quadriparesis,
  dysarthria, dsyphagia, coma. Confirmed by
  neuroimaging.
• Experimental and clinical observation suggest lt
  10-12meq/L correction over 1st 24 hours and lt
  18meq/L in 48 hours

18
Treatment of Hypotonic Hyponatremia

• Hypovolemic isotonic crystalloid solutions (0.9
  NaCl, Lactated Ringers solution) bolus
  infusion
• Isovolemic correct cause, water restriction,
  NaCl tablets, loop diuretics, demeclocycline, ?
  V2 receptor antagonists
• Hypervolemic water restriction(daily fluid
  intake must be less than urine output), leave it
  alone, anticongestive measures (loop ACEI),
  renal replacement therapy, ? V2 receptor
  antagonists

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Vasopressin Antagonists

• V2 collecting tubule, V1a pressor action, V1B
  secretion of ACTH
• Tolvaptan oral V2 antagonist
• Conivaptan (Vaprisol) parenteral V1/V2 receptor
  antagonist
• NEJM 11/16 two multicenter, randomized,
  placebo-controlled, double-blind trials of oral
  tolvaptan for 30 days
• Chronic HF, cirrhosis, SIADH
• Hypernatremia, hypotension, dizziness, syncope
• Agents may require frequent visits, serum Na and
  daily body weight measurements

20
Conivaptan

• FDA approval of IV form 12/29/05
• Indications eu- and hypervolemic hyponatremia
• Drug Interactions CYP3A4 inhibitor and substrate
  (contraindicated with potent CYP3A4 inhibitors),
• ADEs infusion site reactions
• Dosing 20 mg IV LD, 20-40 mg/day IV CI
• Cost 3632.65/10 vials, 20 mg/vial

21
Case

• 59 year-old-female with NSC lung CA develops NV
  after chemotherapy. On presentation to the
  clinic, she has flat neck veins, dry mucous
  membranes, and reduced skin turgor.
• Plasma Na 112 meq/L, Plasma OSM 243
  mosmol/kg
• Urine Na 5 meq/L, Urine OSM 498 mosmol/kg

22
Case (continued)

• What is the appropriate therapy at this time?
• fluid restriction
• 3 NaCl IV at a rate of 50 ml/hr
• 0.9 NaCl IV at a rate of 150 ml/hr
• 0.45 NaCl IV at a rate of 100 ml/hr

23
Case (Continued)

• After the appropriate therapy, the next day her
  plasma Na is 122meq/L. Her urine Na and
  osmolality are 80 meq/L and 520 mosmol/kg
  respectively.
• A. Both hypovolemia and SIADH contributed to the
  hyponatremia and the patient is euvolemic.
• B. Hypovolemia caused the hyponatremia and the
  patient is euvolemic.
• C. Hypovolemia caused the hyponatemia and the
  patient is still hypovolemic.

24
Case (Continued)

• Distinguish between the possibilities.
• Hypovolemia and SIADH caused the hyponatremia and
  the patient is euvolemic (U Na 80 meq/L, U osm
  520 mosmol/kg)
• Hypovolemia caused the hyponatremia and the
  patient is still volume depleted ( U Na 15
  meq/L, U osm 500 mosmol/kg)
• Hypovolemia caused the hyponatremia and the
  patient is euvolemic (U Na 25 meq/L, U osm 80
  mosmol/kg)

25
Generation of Hyper(Na gt 145meq/L) or
Hyponatremia(Na lt 135meq/L)

• Plasma (Na)

• Nae____ __Ke
• Total Body Water

26
Etiology of Hypernatremia

• hypovolemic
• Hypotonic fluid loss
• Renal causes loop or osmotic diuretics
  postobstructive diuresis polyuric ATN
• GI vomiting NG drainage diarrhea
• Cutaneous causes burns excessive sweating
• Isovolemic
• Pure water loss
• Insensible loss fever hyperthermia
• Central or nephrogenic diabetes insipidus
• hypervolemic
• Administration of hypertonic sodium-containing
  fluids
• Ingestion of sodium

27
Clinical Management Issues

• Outpatients with hypernatremia are either very
  young or very old
• Signs/symptoms thrist, lethargy, muscle
  hyperreflexia, seizures, coma
• 2 basic principles (1) address underlying cause
  (2) correct hypertonicity
• Acute vs chronic
• Acute reduce Na by 1 meq/hr
• Chronic max reduction of 0.5 meq/hr, 10 meq/day

28
Treatment of Hypernatremia

• Hypovolemic
• Isotonic saline unsuitable unless there is
  substantial hemodynamic compromise
• 0.45 sodium chloride
• Isovolemic
• 5 dextrose in water with close monitoring for
  hyperglycemia
• Central diabetes insipidus desmopressin
• Nephrogenic diabetes insipidus address cause if
  possible Li (HCTZ, amilioride)
• Hypervolemia
• No apparent renal failure loop 5 dextrose in
  water
• Renal failure renal replacement therapy

29
Case

• 80-year-old man presents with change in mental
  status, fever, tachypnea, dry mucous membranes,
  and BP of 150/90 mm Hg. His plasma Na
  concentration is 172 meq/L. His other medical
  problems include Alzheimers dementia and HTN.
• Meds donepizil, memantine, lisinopril

30
Case (Continued)

• What is the appropriate therapy at this time?
• 0.9 sodium chloride IV at 100 ml/hr
• 0.45 sodium chloride at IV 100 ml/hr
• 500 ml 6 hetastarch IV bolus
• D 5 in water IV at 150 ml/hr

31
Potassium Disorders

• Total body K stores are roughly 3000-4000 meq
  (50-55 meq/kg body weight) with 90-98
  sequestered within cells
• K homeostasis maintains cellular function and
  neuromuscular transmission
• Net effect of hyper or hypo K depends on
  maintenance of (K)c/(K)e ratio

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Hypokalemia

• Increased entry into cells
• Alkalosis, insulin, elevated b-adrenergic
  activity
• Increased GI losses
• Vomiting, NG suction
• Increased urinary losses
• Diuretics, metabolic acidoses, mineralocorticoid
  excess, penicillin derivatives, ampho B,
  Hypomagnesemia
• Renal replacement therapies

33
Diagnosis

• History vomiting diarrhea diuretic use
• ECG
• Urinary K excretion lt 25meq/day or lt 15 meq/L
  in spot specimen
• Acid-base status
• Metabolic acidosis diarrhea ketoacidosis RTA
• Metabolic alkalosis diuretics, vomiting or NG
  suctioning

34
Hypokalemia
35
Treatment

• Consider assessment of the physiologic effects of
  K depletion
• ECG changes and muscle strength
• K deficits cannot be reliably estimated
• Food sources K phosphate, high-calorie
• Oral crystalline (50-65 meq/level tsp)
  slow-release liquid
• IV nondextrose-containing solution 60meq/L via
  peripheral vein

36
Treatment

• Mild K deficit (3-3.5meq/L)
• Treat with oral KCL 60-80meq/day with correction
  of underlying cause
• Moderate K deficit(2.5-3meq/L)
• Oral KCL 80-120meq/day with correction of cause
• Severe hypokalemia or severe physiologic effects
• Asymptomatic 10-20meq/hour, severe symptoms 40meq
  or ?higher/hr
• Continuous cardiac monitoring administer through
  large vein (e.g. femoral)

37
Case

• 63 yo F with cc of diarrhea for past 4-5 days
  during which her weight has dropped by 4 kg. Her
  PO intake has been limited to fluids and fruits.
  PE postural hypotension, flat neck veins.
• Labs Na 130meq/l, K 6.7meq/l, Cl 98 meq/l, HCO3
  21meq/l, BUN 31mg/dl, Cr. 1.2mg/dl
• ECG compared to old reveals no new findings

38
Case (continued)

• What is the appropriate therapy at this time?
• Ca gluconate 10 10ml IV over 2-3 min, 10 units
  of insulin D50 50ml IV, NaHCO3 50 meq IV, SPS
  30 grams PO
• Above minus Ca gluconate
• SPS 30 grams PO
• 0.9 NaCl 500 ml IV bolus, then 150 ml/hr

39
Hyperkalemia

• Increased intake
• PO and/or IV
• Movement from cells into extracellular fluid
• Pseudohyperkalemia
• Metabolic acidosis
• Insulin deficiency in uncontrolled DM
• B-adrenergic blockade, digoxin overdose
• Decreased urinary excretion
• Renal failure
• Effective circulating volume depletion
• hypoaldosteronism

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Symptoms

• Muscle weakness
• Usually not present until plasma K exceeds 8
  meq/L
• Muscle weakness begins in the lower extremities
  and ascends to the trunk and upper extremities
• Cardiac Arrhythmias
• Causes changes in atrial and ventricular
  repolarization

41
Diagnosis

• History medications, ?DM, dietary sources
• PE muscle weakness, volume status
• Labs ECG, basic metabolic panel, pH
• 3 groups of conditions
• Increased intake
• Release from the cells
• Reduced urinary excretion

42
Hyperkalemia
43
Treatment

• Monitor K, muscle strength, and ECG
• Antagonism of membrane action
• Calcium gluconate 10 10ml IV over 2-3min
• Increase K shift into cells
• Regular insulin 10 units IV plus dextrose 50
  50ml IV
• Sodium bicarbonate 50 meq IV
• B2 adrenergic agonists
• Removal of excess K
• Diuretics
• Sodium polystyrene sulfonate
• Renal replacement therapy

44
Acid-Base Disorders

• Luis S. Gonzalez III, Pharm.D., BCPS
• Memorial Medical Center

45
Case

• A 45-year-old man presents to the DEM with a 3
  day history of vomiting. His past medical history
  is significant for polycystic kidney disease
  causing chronic renal failure.
• PE BP 80/50, decreased skin turgor, flat neck
  veins
• Na 145 meq/L, Cl 100 meq/L, HCO3 24 meq/L, pH
  7.40, PCO2 40 mmHg

46
Case (Continued)

• What is the acid-base abnormality?
• no acid-base abnormality present
• Metabolic acidosis
• Metabolic alkalosis
• Metabolic alkalosis and anion gap metabolic
  acidosis

47
Definitions

• Metabolic acidosis low pH and low bicarbonate
  concentration
• Metabolic alkalosis high pH and high
  bicarbonate concentration
• Respiratory acidosis low pH and high PCO2
• Respiratory alkalosis high pH and low PCO
• pH 7.40 (7.37-7.43), PCO2 40 mmHg (36-44), HCO3
  24 meq/L (22-26)
• H 24 x PCO2/HCO3

48
Renal and Respiratory Compensation
Primary Disorder Compensatory response
Metabolic acidosis 1.2mmHg ?PCO2 for 1meq ? in HCO3
Metabolic alkalosis 0.7mmHg ? PCO2 for 1meq ? HCO3
Acute Resp Acidosis 1 meq ? HCO3 for 10mmHg ? in PCO2
Chronic Resp Acidosis 3.5 meq ? HCO3 for 10mmHg ? in PCO2
Acute Resp Alkalosis 2 meq ? HCO3 for 10mmHg ? PCO2
Chronic Resp Alkalosis 4 meq ? HCO3 for every 10mmHg ?in PCO2
49
Metabolic Acidosis

• Inability of kidney to excrete acid load OR an
  increase in the generation of acid or loss of
  HCO3
• Anion Gap (5-11meq/L) Na - Cl HCO3
• Normal value is reduced by 2.5meq/L for every
  1gm/dl decline in albumin concentration

50
Case

• CC 77 year-old WF with SOB and lethargy
• HPI Decreased PO intake over last several days.
• PMH COPD, diverticulosis, HTN, depression,
  duodenal ulcer resection
• SHx ½-1 PPD X 50 y, 2-4 glasses of wine
• PE abdomen diffusely tender
• LABS/Investigations ABG 2L NC 7.24-19-148-98.2,
  Na 137, K 6.3, Cl 104, C02 8, BUN 69, Cr. 2.1,
  WBC 31.9, CT ABD/Pelvis diffuse diverticulosis,
  enlargement of sigmoid colon

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Case (Cont)

• What acid-base disturbance is present?
• 1. respiratory acidosis
• 2. respiratory alkalosis
• 3. metabolic acidosis
• 4. metabolic alkalosis

52
The Shrinking Anion Gap
53
Case (Cont)

• She was was bolused with fluid and treated with D
  5 150 meq/L NaHCO3 at a rate of 200ml/hour.
  Piperacillin/Tazobactam was started and one dose
  of IV gentamicin was given.
• She looked well the next day and was feeling much
  better.
• LABS Na 146, K 3.7, Cl 100, CO2 24, BUN 42, Cr.
  1.3

54
Case (Cont)

• What acid-base disturbance is present?
• 1. no acid base disturbance
• 2. anion gap metabolic acidosis and metabolic
  alkalosis
• 3. respiratory alkalosis
• 4. pH please
• 5. metabolic acidosis

55
Major Causes of Metabolic Acidosis

• High Anion Gap
• M - methanol
• U uremia
• D Diabetic Ketoacidosis
• P Phenformin/metformin
• I INH/Iron
• L lactic acidosis
• E ethylene glycol
• S salicylates

56
Major Causes of Metabolic Acidosis

• Normal anion gap (hyperchloremic)
• Diarrhea
• Renal Tubular Acidoses
• Iatrogenic (Isotonic crystalloid solutions)

57
Metabolic Alkalosis

• Gastrointestinal H loss (CO2 H2O ?? H HCO3)
• Vomiting or NG suctioning
• Renal H Loss
• Diuretics
• Mineralocorticoid excess
• Hypokalemia
• Contraction alkalosis
• Diuretics

58
Causes of Metabolic Alkalosis
Saline-responsive (urine Cl lt 25 meq/L Saline-resistant (urine Cl gt 40 meq/L)
Vomiting/NG suction Edematous states
diuretics Mineralocorticoid excess
posthypercapnia Severe hypokalemia
59
Treatment

• Saline-responsive
• Oral or IV administration of NaCl and water
  (0.45 or 0.9 NaCl)
• Replete K deficits with KCl
• Can monitor urine pH and Cl
• Saline-resistant
• Edematous states (heart failure, cirrhosis,
  nephrotic syndrome) withhold diuretics if
  possible, acetazolamide, dialysis
• Replete K deficits with KCl

60
Respiratory Acidosis

• The main physiologic stimulus to breathing are an
  elevation in arterial PCO2 and a reduction in
  PO2.
• Hypercapnia indicates advanced pulmonary
  dysfunction (deadspace) and/or and insult to
  ventilatory drive (e.g., opioid use).

61
Pathophysiology of Respiratory Acidosis

• Medullary center inhibition
• Acute medications, O2, cardiac arrest
• Chronic obesity, CNS lesions, Met. Alkalosis
• Respiratory muscles and chest wall
• Acute myasthenia, ?? K/PO4, Guillain-Barre
• Chronic muscle weakness, kyphoscoliosis
• Conditions affecting gas exchange
• Acute COPD, ARDS, Pulm. Edema, pneumonia,
  asthma, pneumo or hemothorax
• Chronic COPD, obesity
• Mechanical ventilation

62
Respiratory Acidoses Most Common Causes

• Acute COPD exacerbation severe asthma or
  pneumonia pulmonary edema drug OD or cardiac
  arrest administration of O2 to chronic CO2
  retainer and MV.
• Symptoms HA blurred vision restlessness and
  anxiety somnolence, arrhythmias, hypotension
• Chronic COPD extreme obesity
• Symptoms peripheral edema (cor pulmonale)
• History complete PM and Med History record 02
  use Baseline HCO3, CO2 and pH, BIPAP

63
Treatment

• Acute Respiratory Acidosis treat underlying
  cause
• Mechanical ventilation (BiPAP or endotracheal
  tube)
• NaHCO3 50 meq IV, if pH lt7.15
• Chronic Respiratory Acidosis
• Avoid excessive oxygen and sedatives, weight
  reduction for obese, carbohydrate restriction
  (200g/d), bronchodilators
• Diuretics for cor pulmonale but avoid
  superimposed metabolic alkalosis
• Acetazolamide 250-375 mg BID, urine pH gt 7, lower
  HCO3 to baseline

64
Respiratory Alkalosis

• Elevated arterial pH and Hypocapnia
• H 24 X PCO2/HCO3
• Causes
• Hypoxemia pulm disease CHF hypotension severe
  anemia
• Pulmonary disease pneumonia PE interstitial
  fibrosis
• Stimulation to Medullary Center psychogenic
  hepatic failure gram sepsis salicylates
  neurologic disease drug withdrawl
• Mechanical ventilation

65
Symptoms, Diagnosis, and Treatment

• Symptoms light-headedness altered
  consciousness paresthesias of extremities,
  cramps, carpopedal spasm arrhythmias
• Phosphate reduction to as low as 0.5-1.5mg/dl
• Diagnosis tachypnea, pH, PCO2, HCO3
• Treatment correct underlying disorder

66
Stepwise Approach

• Detailed history, clinical assessment
• Obtain ABG and Chem 7. Identify all abnormalities
  in pH, PCO2, and HCO3.
• Determine which abnormalities are primary and
  which are compensatory based on pH.
• If the pH is gt 7.40, then a respiratory or
  metabolic alkalosis is primary
• If the pH is lt 7.40, then a respiratory or
  metabolic acidosis is primary
• Calculate the anion gap. If gt 20, metabolic
  acidosis is always present.

67
Stepwise Approach (Continued)

• 5. If anion gap is increased, calculate the
  excess anion gap (Anion gap 10). Add this value
  to the measured HCO3.
• If gt 30, then metabolic alkalosis is present
• If lt 22, then nonanion gap metabolic acidosis is
  present
• 6. Compare the identified disorders to the
  history. Begin patient-specific therapy.

68
Calculation of the Potential Bicarbonate
Concentration
69
(No Transcript)
70
Case Presentations

• Luis S. Gonzalez III, Pharm.D., BCPS
• Memorial Medical Center

71
Case 1

• A 70 year-old woman is started on
  hydrochlorothiazide 25 mg daily and a
  salt-restricted diet for the treatment of
  hypertension (160/100) two weeks ago.
• VS 130/86, HR 90
• PE decreased skin turgor, flat neck veins
• LABS Na 119 meq/L, K 2.1 meq/L, Cl 71 meq/L,
  HCO3 34 meq/L, P osm 252, U Na 4 meq/L.

72
Case 1 (Continued)

• Which of the following contributed to the
  development of hyponatremia?
• Hypokalemia
• retention of water
• Diuretic
• SIADH
• Hypovolemia
• A, B, C, D, E
• A, B, C, E

73
Case 1 (Continued)

• Choose the appropriate therapy.
• 0.9 NaCl with 40 meq KCl at IV 100 ml/hr
• oral potassium chloride
• oral potassium citrate
• Dextrose 5/0.225 sodium chloride IV at 100
  ml/hour

74
Case 2

• An 80 year-old male who resides in a nursing home
  was brought to the clinic with a 4 day history of
  a viral-like illness. He has been having loose
  stools and is confused.
• PMHx hypertension and dementia
• Meds PTA furosemide 20 mg daily, amlodipine 10
  mg daily.
• PE BP 120/80, P 100, decreased skin turgor and
  dry mucous membranes
• Labs Na 177 meq/L, U Na 5 meq/L, U osmo 600
  mosmol/kg

75
Case 2 (Continued)

• What caused the development of hypernatremia?
• Furosemide
• insensible losses
• Hyperglycemia
• All of the above
• A B

76
Case 3

• What is the most appropriate initial therapy for
  the hypernatremia?
• Dextrose 5 in water IV at a rate of 250 ml/hr
• 0.9 sodium chloride IV at a rate of 100 ml/ hr
• Dextrose 5/0.225 sodium chloride IV at a rate
  of 150 ml/hr
• Increase oral water intake

77
Case 4

• 59 year-old white male admitted with crushing
  substernal chest pressure. He ECG is significant
  for ST segment depressions in leads II, III, AVF
  and frequent PVCs.
• PMhx hypertension, hypercholesterolemia
• Meds HCTZ, atorvastatin, ASA
• PE BP 90/50, S3 gallop, crackles on lung
  auscultation
• LABS Na 140 meq/L, K 2.8 meq/L, Cl 102 meq/L,
  HCO3 15, Creat 1 mg/dl

78
Case 4 (Continued)

• What would be the appropriate initial therapy?
• Give oral KCl liquid 40 meq x 2, 4 hours apart
• Dextrose 5/ 0.45 sodium chloride 80 meq
  KCl/liter IV, run at 150 ml/hr
• KCL 20meq/100ml water IV every hour for 4 doses
• 0.9 sodium chloride 80 meq of KCl/liter IV,
  run at 200 ml per hour

79
Case 5

• A 55-year-old woman with CRF (creatinine 2.1
  mg/dl) is started on a low-sodium diet for
  hypertension. 2 weeks later she presents with a
  CC of severe weakness.
• PE slightly decreased skin turgor, new proximal
  muscle weakness
• ECG peaked T waves and widening of the QRS
• LABS Na 130 meq/L, K 9.2 meq/L, Cl 98 meq/L,
  HCO3 17 meq/L, Creatinine 2.7 mg/dl, pH 7.30

80
Case 5 (Continued)

• What would you recommend?
• Sodium polystyrene sulfonate
• Calcium gluconate 10/10ml, IV and repeat after 5
  minutes
• Insulin, dextrose, Sodium bicarbonate
• all of the above

81
Case 6

• An 18-year-old white female is brought to DEM by
  mom because she doesnt look well.
• PMHx none
• Meds PTA none
• VS BP 110/60, Hr 100, RR 30, T 100
• PE normal
• Labs ABG pH 7.50, PCO2 29 mmHg, HCO3 22 meq/L

82
Case 6 (Continued)

• What is the acid-base abnormality?
• Metabolic Acidosis
• Respiratory Acidosis
• Respiratory Alkalosis
• Metabolic Alkalosis

83
Case 7

• A 30-year-old male is brought to the DEM with a
  decreased level of consciousness. His urine drug
  screen is for opioids and his physical exam is
  normal except for pinpoint pupils and a
  respiratory rate of 6 BPM.
• Labs pH 7.25, PCO2 60 mmHg, HCO3 26 meq/L

84
Case 7 (Continued)

• What acid-base disorder is present?
• Metabolic acidosis
• Acute Respiratory acidosis
• Chronic Respiratory Acidosis
• Metabolic alkalosis

85
Case 8

• A 58-year-old white male presents to the fast
  track clinic with a 3 day history of vomiting,
  binge drinking, and a cough productive of
  purulent sputum.
• PMHx chronic alcohol abuse
• PE BP 80/50, Pulse 120, T 102F, RR 32
• Lungs RLL absent breath sounds CV flat neck
  veins, decreased skin turgor ABD tender
• LABS pH 7.50, PCO2 20 mmHg, Na 145 meq/L, Cl
  100 meq/L, HCO3 15 meq/L

86
Case 8 (Continued)

• What acid-base abnormalities are present?
• Respiratory Alkalosis, Metabolic Alkalosis,
  Respiratory Acidosis
• Respiratory Acidosis, Metabolic Alkalosis, anion
  gap Metabolic Alkalosis
• Respiratory Alkalosis, anion gap Metabolic
  Acidosis, Metabolic alkalosis
• Respiratory Acidosis, Metabolic alkalosis

87
Case 9

• A 45-year-old male type I diabetic who has had
  difficulty controlling his sugar recently
  presents to the DEM with a decreased level of
  consciousness.
• PMHx Type I DM on insulin
• PE BP 100/60 mmHg, RR 8, T 100, HR 100, obtunded
• LABS pH 7.10, PCO2 50 mmHg, Na 145 meq/L, Cl
  100 meq/L, HCO3 15, Glucose 425 mg/dl

88
Case 9 (Continued)

• What types of acid-base disturbances are present?
• Respiratory Acidosis, Metabolic Alkalosis,
  Respiratory Alkalosis
• Respiratory Acidosis, Metabolic Acidosis,
  Metabolic Alkalosis
• Respiratory Alkalosis, Metabolic Acidosis,
  Metabolic Alkalosis
• Metabolic Alkalosis, Metabolic Acidosis

89
Case 10

• A 58-year-old man with a PMHx of chronic
  pancreatitis and diabetes adm. with Hx of severe
  vomiting. He had been self medicating with milk
  and NaHCO3 for the ABD pain. On adm, he was
  semi-comatose, dry with BP 100/60, P 120, marked
  orthostasis, no rebound on abd exam. HEME
• Labs Na 140 meq/L, K 3.4 meq/L, Cl 69 meq/L ,
  HCO3 40 meq/L, S. Cr. 4.6 mg/dl, pH 7.86, pCO2
  23 mmHg

90
Case 10 (Continued)

• What types of acid-base abnormalities are
  present?
• A. Respiratory Alkalosis, Metabolic Alkalosis,
  Metabolic Acidosis
• B. Respiratory Acidosis, Metabolic Alkalosis,
  Respiratory Alkalosis
• C. Respiratory Acidosis, Metabolic Acidosis,
  Metabolic Alkalosis
• D. Respiratory Alkalosis, Metabolic Alkalosis

91
CASH CAB

• VIDEO BONUS QUESTION

92
pH 7.27 PCO2 70 PO2 35 HCO3 31

• 1. metabolic acidosis, chronic respiratory
  acidosis
• 2. acute on chronic respiratory acidosis
• 3. acute respiratory acidosis, metabolic alkalosis

• A. Patient with chronic hypercapnia develops
  pneumonia
• B. Patient with COPD develops persistent diarrhea
• C. Patient with Hx of asthma has 5 days of
  vomiting then develops asthma attack