Transcript Acid - Base Disorders: How to obtain a normal pH in the ICU

Acid-Base Disorders
Bradley J. Phillips, MD
Burn-Trauma-ICU
Adults & Pediatrics
Definition
Normal pH = 7.35 - 7.45
 Acidosis

 Primary
respiratory = PCO2 > 44
 Primary metabolic = HCO3 < 22
 Severe acidemia pH < 7.2

Alkalosis
 Primary
respiratory = PCO2 < 36
 Primary metabolic = HCO3 > 26
 Severe alkalosis pH > 7.6
Acid-Base Homeostasis

Acid Metabolism (70 mmol/day)
sulphuric acid 25 mmol (aminoacid catabolism)
 organic acids 40 mmol (non-metabolized)
 phosphoric acid and others


Extracellular space contains 350 mmol HCO3

Renal tubules
 proximal
reabsorbs 3800 mmol/d (85%)
 thick ascending limb reabsorbs 450 mmol (10%)
 collecting duct generates new HCO3 (NH4/PO4)
Metabolic Disorders

Characteristics
 Change
in HCO3
 pH and pCO2 change same direction
Respiratory Disorders

Characteristics
 Change
in PCO2
 pH and PCO2 change in different directions
 Acute and chronic
Compensation
Correct pH to normal
 NO overcompensation

 exception:
exogenous mechanism
 Primary metabolic - respiratory change (PCO2)
 Primary respiratory - metabolic change (HCO3)
Physiologic Effects

Acidosis
 Decreased
myocardial contractility
 Decreased diaphragmatic contractility
 Reduced threshold for ventricular fibrillation
 Complex and variable derangements in vascular smooth
muscle (sympathetic vs. catecholamines)
 Increased cerebral blood flow
 Variable effects upon serum electrolytes
 Alterations in drug mechanisms
 Shifts O2 dissociation curve to right
O2 Disassociation Curve
decrease temperature
2,3-DPG
PCO2
increase in pH
increase temperature
2,3-DPG
PCO2
decrease in pH
Physiologic Effects

Alkalosis
 Arrhythmogenic
 Promotes
coronary artery spasm
 Variable effect upon myocardial contractility
and vascular tone
 Lowers seizure threshold
 Transient reduction in cerebral blood flow
 Lowers ionized calcium ( .03-.09 /0.1 pH)
 Suppresses respiratory function
 Shift O2 dissociation curve to left
Changes in Acid-Base Disorders
Disorder
Primary
Comp.
Expected
Acidosis
Metabolic
 HCO3
 PCO2
 PCO2 =1.5x HCO3(8 +/- 2)
Respiratory
Acute
Chronic
 PCO2
 HCO3
 pH=.008(PCO2 -40)
 pH=.003(PCO2 -40)
Metabolic
 HCO3
 PCO2
 PCO2 =7x HCO3+(20+/-1.5)
Respiratory
Acute
Chronic
 PCO2
 HCO3
 pH=.008(40- PCO2)
 pH=.003(40- PCO2)
Alkalosis
Acid-Base
Disturbances
Metabolic Acidosis
Net retention of H+
 Physiological adaptation

 buffering
(bone/skeletal muscle)
 increased ventilation
 increased reabsorption/generation HCO3
Metabolic Acidosis
Obtain ABG (rule out primary hyperventilation)
 Determine Anion Gap (nl = 12)

 differentiates
between loss of HCO3 and
accumulation of unmeasured acid anions
 AG = serum Na - serum Cl - serum HCO3
 AG affected by hypoalbuminemia
Metabolic Acidosis

Normal AG (Cl-)
(HHARDUP)
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High AG
(MUD-PILES)
 Hypoaldosteronism
 Methanol
 Hyperosmolar
 Uremia
nonketotic coma
 Acetazolamide
 RTA
 Diarrhea
 Utererosigmoidostomy
ileostomy
 Pancreatic fistula
 DKA
 Poisons
 Iron,
INH
 Lactic acidosis
 Ethanol, Ethylene
glycol
 Salicylate, Starvation
Organic Acids

Endogenous
 Ketoacidosis
b-hydroxybutyrate
 acetoacetate

 Lactic
acidosis
 Severe renal
insufficiency
phenolic aromatic acids
 furanoic acid
 dicarboxylic acid

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Ingested
 salicylate
 ethyleneglycol
metabolites
glycolate
 glycoxalate
 oxalate

 methanol

formate
Hyperchloremic Acidosis
Net retention HCl or loss of HCO3 in
proportionate excess of chloride
 normal quotient HCO3/Cl > 0.25
 Loss of HCO3

 renal
vs non-renal
of urine NH4+
 NH4+ excretion < 1 mmol/kg (kidney primary)
 measurement
Evaluation of Hyperchloremic Acidosis
Gluck SL. Lancet 352, Aug, 1998.
RTA
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Distal RTA (type 1) - impaired H+ secretion (urine pH > 5.5)
Gluck SL. Lancet 352, Aug, 1998.
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Proximal RTA (type 2) - impaired proximal HCO3 reabsorption

Defective ammoniagenesis (type4) - defective NH4+ production
Treatment: Metabolic Acidosis
Correct Underlying Disorder!!!!!
? Sodium Bicarbonate adminstration?
HCO3 required = .4 x wt (kg) x (25 - measured HCO3)
Risk of Sodium Bicarbonate
Hypernatremia/hyperosmolality (1000
mmol/L)
 Extracellular-fluid overload
 “overshoot” alkalosis
 Worsening acidosis

 buffering
protons by bicarbonate = CO2
 raises the partial pressure of CO2 in fluids
 paradoxical worsening intra/extracellular acidosis
 limited
ventilatory reserve, advance circulatory
failure or undergoing CPR
Alternative Alkalinizing Agents
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Carbicarb
 Equal
sodium bicarbonate and sodium carbonate
 Carbonate stronger base, preference for buffering
hydrogen ions
 Generates bicarbonate rather than CO2 and even
consumes CO2 when reacting with carbonic acid
 Results: increases blood and intracellular pH with little
increase in CO2
 Risks: Hypervolemia and hypertonicity
Alternative Alkalinizing Agents

THAM
 0.3
Nitromethamine
 Sodium free, buffers metabolic and respiratory acids
 Limits CO2 generation
 Increases extra- and intracellular pH
 Not documents more efficacious than bicarbonate
 Side effects: hyperkalemia, hypoglycemia, ventilatory
depression, hepatic necrosis in neonates
Metabolic Alkalosis

increase in alkali
addition to ECF
gastric losses
 oral or parenteral
sources
mineralocorticoid

 stimulate

H secretion
increased Na delivery
 increased
Na absorption
 “contraction alkalosis”

impairment in renal
HCO3 excretion
K
deficiency

stimulates HCO3 exit
decreased

Cl delivery
impairs HCO3 exit
raised
CO2
hormonal
angiotensin II
 norepinephrine

Metabolic alkalosis requires both to occur.
Metabolic Alkalosis

Chloride-responsive
Urine (Cl) < 10-20
 Contraction
alkalosis

Chloride-unresponsive
Urine (Cl) > 10-20
 Diuretics
 Diuretics
 Vomiting
 Villous
 Aldosteronism
adenoma
 Gastric losses
 Alkali
intake (antacids)
Treatment of Metabolic Alkalosis
Treat underlying disorder!!
 Correct hypovolemia with NS
 Correct hypokalemia
 Acetazolamide

 inhibit
carbonic anhydrase
 decreased promixal tubular HCO3 by 80%
 IV dose 250 mg x1( pH corrects with 24 hrs)
Treatment of Metabolic Alkalosis

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If chloride deficit
 replace volume
 deficit = .4 x wt (kg) x (100 - measured Cl)
If chloride-unresponsive
 K replacement or mineralcorticoid antagonist
(Aldactone)
If volume overload and unresponsive acetazolamide
 consider CAVH with Cl infusion
Prolonged gastric suctioning
 Use histamine-2 antagonist
Respiratory Acid-Base Disorders

Blood pCO2 tightly regulated
 alternations
alveolar ventilation
 central control (chemoreceptors CO2, pO2, pH)

Acidosis or alkalosis
 primary
increase/decrease in CO2 production
 may coexist with other acid-base disorders
Respiratory Acidosis

Inadequate ventilation
 Acute
 pH
changes .008 for every 1 mmHg change
 Chronic
 pH
changes .003 for every 1 mmHg change
Respiratory Acidosis
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Airway obstruction
Status asthmaticus, severe asthma, COPD
Severe alveolar defects (edema, pneumonia,
ARDS)
CNS depression (drugs, brainstem damage)
Neuromuscular impairment
Ventilatory restriction (PTX, flail chest, burns)
Respiratory Acidosis

Increase in pCO2
increase in HCO3
 intracellular
buffering
 cellular loss of HCO3 to ECF
 adaptive renal HCO3 reabsorption (late)

Clinical manifestations

anxiety

encephalopathy

SOB

myoclonus

delirium

seizures
Respiratory Acidosis

Treatment
 Supplemental
oxygen
 Aggressive pulmonary toilet
 Treatment of pneumonia
 Bronchodilators
 Removal of obstruction
 Mechanical ventilation
Respiratory Alkalosis

Hyperventilation
 Acute
 pH
changes .008 for every 1 mmHg change
 Chronic
 pH
changes .017 for every 1 mmHg change
Respiratory Alkalosis
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Metabolic
encephalopathy
Hepatic failure
Anxiety
Early sepsis
Pulmonary embolism
Hypoxia
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CHF
Severe head injury
CVA
Mechanical
overventilation
Salicylate overdose
Pregnancy
Respiratory Alkalosis

Decrease in pCO2
HCO3
 cellular
decrease in
uptake HCO3
Induces cellular uptake of K and phosphate
 Increases binding of ionized Ca to albumin
 Manifestations

 arrhythmias
 facial/peripherial
 muscle
cramps
 syncope
 seizures
paraesthesias
Respiratory Alkalosis

Treatment
 Calm
patient
 Carbon dioxide rebreathing
 Treat underlying disorder
 Administer sedative
 Mechanical ventilation
Case Study #1
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87 m found unresponsive in hospital bed
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Hospital History
 POD
1 bladder cystoscopy-TURP
 Overnight hydrated D5 1/2 NS at 75 cc/hr
 PMH: HTN, kidney stones, prostate CA, CAD
Case Study #1
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Transferred to ICU
Vitals
 Temp
37.2
 BP 80/42
 P 116, RR 24,
 O2 sat 84%
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PE
 Lungs
crackles
 Responsive to pain only, otherwise non-focal
Case Study #1
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WBC
Hct
PLT
NA
K
Cl
CO2
BUN
Cr
Glucose
Alb
Ca
Mg
Osm
Case Study #1
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WBC
Hct
PLT
NA
K
Cl
CO2
BUN
Cr
Glucose
Alb
Ca
Mg
Osm
Admission
POD1
9.95
28.5
183
137
3.3
105
28
23
1.4
250
3.65
17.7
81
117
3.7
86
16
24
2.1
105
2.2
6.4
0.7
288
Case Study #1
Admission POD1
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WBC
Hct
PLT
NA
K
Cl
CO2
BUN
Cr
Glucose
Alb
Ca
Mg
Osm
9.95
28.5
183
137
3.3
105
28
23
1.4
250
3.65
17.7
81
117
3.7
86
16
24
2.1
105
2.2
6.4
0.7
288
PT/PTT
ABG
CXR
EKG
CPK
Anything else ?
Case Study #1
Admission POD1
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WBC
Hct
PLT
NA
K
Cl
CO2
BUN
Cr
Glucose
Alb
Ca
Mg
Osm
9.95
28.5
183
137
3.3
105
28
23
1.4
250
3.65
17.7
81
117
3.7
86
16
24
2.1
105
2.2
6.4
0.7
288
PT 1.3 / PTT 44
ABG 7.26/83/29
CXR: pulm edema
EKG: NS ST-T changes
CPK: wnl
Anything else… ?
Case Study #1
Admission POD1
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WBC
Hct
PLT
NA
K
Cl
CO2
BUN
Cr
Glucose
Alb
Ca
Mg
Osm
9.95
28.5
183
137
3.3
105
28
23
1.4
250
3.65
17.7
81
117
3.7
86
16
24
2.1
105
2.2
6.4
0.7
288
PT 1.3/PTT 44
ABG 7.26/83/29
CXR: pulm edema
EKG: NS ST-T changes
CPK: wnl
Anion gap…
S Osmolarity…
NA - CO2 - Cl = 15
2 Na + Glu/18 + BUN/2.8 = 248
Case Study #1
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ICU Day 1
 Intubated
 Vasopressors
 PA catheter
CI 2.1 L/min/m2
 Wedge 18 mmHg
 CVP 16
 SVR 2100

 CT
brain negative
 EEG metabolic encephalopathy
Diagnosis: Glycine Toxicity
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TURP/continuous bladder irrigation
Solution 1.5% glycine
 hypotonic (200 mOsm/L)
Usually continuous aspirated during procedure
 absorption through venules in bladder wall
 absorption through ruptured prostate capsule
Remains extracellular
 osmotically active
 dilutional hyponatremia/elevated osmolal gap
Diagnosis: Glycine Toxicity
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Metabolic fate
 transported
intracellular
 breakdown

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
creatinine, CO2, H2O, NH4, glucose
hippurate, glyoxylate, formate, oxalate
Constellation of labs
 hyponatremia
and elevated osmolal gap
 increased serum NH4 (metabolism to ammonia)
 hypocalcemia (binding oxalates)
 anemia and thrombocytopenia (hemolysis/dilution)
Diagnosis: Glycine Toxicity

Clinical presentation
 nausea
and emesis
 hypotension
 mental status changes
 thrombocytopenia
 SOB (edema, worse with CHF)

Therapy
 Fluid
and electrolyte management
Diagnosis: Glycine Toxicity

Outcome
 sepsis
could not be ruled out
 started on antibiotics
 dialysis could not be performed due to pt’s
wishes
 cystogram negative for perforation
 blood cx: e coli
 developed ARDS, ATN, SB ischemia
 POD 13 death