ACID BASE BALANCE

DR TINKU JOSEPH

DM ResidentDepartment of Pulmonary Medicine

AIMS, Kochin

Email ID-: tinkujoseph2010@gmail.com

Life is a struggle, not against sin, not against Money Power . . but against hydrogen ions.--H.L. Mencken

OVERVIEW OF DISCUSSION

Basics of acid-base balance.

Role of Renal/Respiratory system in acid-base homeostasis.

Step-wise approach in diagnosis of acid-base disorders.

Some practical examples

Acid Base Balance

The body produces acids daily 15,000 mmol CO2

50-100 mEq Nonvolatile acids

The primary source is from metabolism of sulfur containing amino acids (cystine, methionine) and resultant formation of sulfuric acid.

Other sources are non metabolized organic acids, phosphoric acid, lactic acid, citric acid.

The lungs and kidneys attempt to maintain balance

Respiratory Regulation

• 10-12 mol/day CO2 is accumulated and is transported to the lungs as Hb-generated HCO3 and Hb-bound carbamino compounds where it is freely excreted.

H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-

• Accumulation/loss of Co2 changes pH within minutes

Respiratory Regulation

Balance affected by neurorespiratory control of ventilation.

During Acidosis, chemoreceptors sense ↓pH and trigger ventilation decreasing pCO2.

Response to alkalosis is biphasic. Initial hyperventilation to remove excess pCO2 followed by suppression to increase pCO2 to return pH to normal

Renal Regulation

Kidneys are the ultimate defense against the addition of non-volatile acid/alkali

Kidneys play a role in the maintenance of this HCO3¯ by:– Conservation of filtered HCO3 ¯– Regeneration of HCO3 ¯

Kidneys balance nonvolatile acid generation during metabolism by excreting acid.

Renal Regulation

• Renal Excretion of acid – combining hydrogen ions with either urinary buffers to form titrable acid. eg: Phosphate, urate, ammonia

Acid Base Status• Assessment of status via

bicarbonate-carbon dioxide buffer system in blood.

– CO2 + H2O <--> H2CO3 <--> HCO3

- + H+

– Henderson-Hasselbach equation

– PH = 6.10 + log ([HCO3] / [0.03 x PCO2])

DEFINITIONS AND TERMINOLOGY

3 Component Terminology Acidosis/Alkalosis Respiratory/Metabolic Compensated/Uncompensated

Basic terminology

• pH – signifies free hydrogen ion concentration. pH is inversely related to H+ ion concentration.

• Acid – a substance that can donate H+ ion, i.e. lowers pH.

• Base –a substance that can accept H+ ion, i.e. raises pH.

• Anion – an ion with negative charge.

• Cation – an ion with positive charge.

• Acidemia – blood pH< 7.35 with increased H+ concentration.

• Alkalemia – blood pH>7.45 with decreased H+ concentration.

• Acidosis – Abnormal process or disease which reduces pH due to increase in acid or decrease in alkali.

• Alkalosis – Abnormal process or disease which increases pH due to decrease in acid or increase in alkali.

Assessment of acid base balance

ABG-: pH, PaO2, PaCO2, SaO2, HCO3. Complete and objective overview of respiratory physiology

The pulse-oxymeter or saturation meter

Non invasive measurement Finger probes and ear probes Percutaneous measurements

Pulse Oximeter Sensor

Two LEDs emit red and infrared wavelengths of light through skinHb absorbs red wavelengthsHbO2 absorbs infrared wavelengths

Photodetector on other side picks up intensity of transmitted light

SpO2 is calculated by analyzing received light

Utilizes cardiac pulse to distinguish arterial blood from other mediums

Pulse Oximetry Board

Low powerData outputs: SpO2 and pulse

rate Eight second average (or instantaneous) Serial communication

Pulse Oximetry

FALSE HIGH RESULTS

• Carbon monoxide intoxication (heavy smoker)

• Strong lights

• UV lights (anti bacterial)

• Infra red light (neonatal ICU)

FALSE LOW RESULTS• Vascular disease

(extremities)• Movements of the fingers• Nail polish• High bilirubinemia• Detector obstructions• Wrong placement of the

probe• Blood pressure

fluctuations

Why Order an ABG?

Aids in establishing a diagnosis

Helps guide treatment plan Aids in ventilator

management Improvement in acid/base

management allows for optimal function of medications

Acid/base status may alter electrolyte levels critical to patient status/care.

Pre operative fitness.

Logistics

• Where to place -- the options– Radial– Femoral – Brachial– Dorsalis Pedis– Axillary

• When to order an arterial line --– Need for continuous BP

monitoring– Need for multiple ABGs

Technical Errors

• TYPE OF SYRINGE - Glass vs. plastic syringe: pH & PCO2 values unaffected PO2 values drop more rapidly in plastic syringes (ONLY if

PO2 > 400 mm Hg) Other adv of glass syringes:

Min friction of barrel with syringe wallUsually no need to ‘pull back’ barrel – less chance of air bubbles entering syringeSmall air bubbles adhere to sides of plastic syringes – difficult to expel

Though glass syringes preferred, differences usually not of clinical significance plastic syringes can be and continue to be used

Technical Errors

•Excessive HeparinDilutional effect on results HCO3

- & PaCO2 Syringe be emptied of heparin after flushingRisk of alteration of results with:1) size of syringe/needle2) vol of sample 25% lower values if 1ml sample taken in 10 ml syringe (0.25 ml heparin in needle)Syringes must be > 50% full with blood sample

Technical Errors

Hyperventilation or Breathholding May lead to erroneous lab results

Air bubbles PO2 150 mmHg & PCO2 0 mm Hg in air bubble. Mixing with sample lead to PaO2 & PaCO2 Mixing/Agitation diffusion more erroneous results Discard sample if excessive air bubbles Seal with cork/cap after taking sample

Fever or Hypothermia Most ABG analyzers report data at N body temp If severe hyper/hypothermia, values of pH & PCO2 at 37 C can be

significantly diff from pt’s actual values Changes in PO2 values with temp predictable

Technical Errors

Values other than pH & PCO2 do not change with temp

Hansen JE, Clinics in Chest Med 10(2), 1989 227-237 Some analysers calculate values at both 37C and pt’s

temp automatically if entered Pt’s temp should be mentioned while sending

sample & lab should mention whether values being given in report at 37 C/pts actual temp

Technical Errors

WBC COUNT0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLCMarked increase in pts with very high TLC/plt counts – hence chilling/analysis essential

Venous Sample Only the person who has drawn the sample can tell if

he has drawn a pulsating blood’ OR blood under high pressure

PaO2 < 40 Partly mixed sample- Difficult to recognize

ARTERIAL VENOUS

pH 7.38-7.42 7.36-7.39PaO2 80-100 38-42PaCO2 36-44 44-48HCO3 22-26 20-24SaO2 95-100 75

CENTRAL VENOUS

7.37-7.40

50-54

45-49

22-26

78

Acid Base Disorders

The primary disorders:• Respiratory Acidosis

– Acute– Chronic

• Respiratory Alkalosis– Acute– Chronic

• Metabolic Acidosis• Metabolic Alkalosis

Acid Base Disorders

Acidosis/Alkalosis:Any process that tends to

increase/decrease pH• Metabolic: Primarily affects

Bicarbonate• Respiratory: Primarily affects

PaCO2

Acidemia/Alkalemia:Net effect of all primary and

compensatory changes on arterial blood pH.

Normal ABG values

pH 7.35 - 7.45

PaCO2 35 - 45 mm Hg

PaO2 70 - 100 mm Hg

SaO2 93 - 98%

HCO3¯ 22 - 26 mEq/L

Base excess -2.0 to 2.0

mEq/L

----- XXXX Diagnostics ------

Blood Gas Report248 05:36 Jul 22 2000Pt ID 2570 / 00

Measured 37.0o

CpH 7.463pCO2 44.4 mm HgpO2 113.2 mm Hg

Corrected 38.6o

CpH 7.439pCO2 47.6 mm HgpO2 123.5 mm Hg

Calculated DataTPCO2 49HCO3 act 31.1 mmol / LHCO3 std 30.5 mmol / LBE 6.6 mmol / LO2 CT 14.7 mL / dlO2 Sat 98.3 %ct CO2 32.4 mmol / LpO2 (A - a) 32.2 mm HgpO2 (a / A) 0.79

Entered DataTemp 38.6 oCct Hb 10.5 g/dlFiO2 30.0 %

Measured values should be consideredAnd

Corrected values should be discarded

The

Habits ofHighly

SuccessfulBlood Gas

AnalystsABG Interpretation

Step 1Look at the pH

Is the patient acidemic pH < 7.35or alkalemic pH > 7.45

• Step 2• Is it a metabolic or respiratory disturbance ?

• Acidemia: With HCO3 < 20 mmol/L = metabolic

• With PCO2 >45 mm hg = respiratory

• Alkalemia:With HCO3 >28 mmol/L = metabolic

• With PCO2 <35 mm Hg = respiratory

Step 3If there is a primary respiratory disturbance, is it acute?

Expect D pH = 0.08 x D PCO2 / 10

• Step 4• For a respiratory disorder is renal compensation OK?

• Respiratory acidosis: <24 hrs: D [HCO3] = 1/10 D PCO2

• >24 hrs: D [HCO3] = 3/10 D PCO2

• Respiratory alkalosis: 1- 2 hrs: D [HCO3] = 2/10 D PCO2

• >2 days: D [HCO3] = 6/10 D PCO2

Primary disorder Primary defect Compensatory response

Respiratory acidosis ↑ PCO2 ↑ HCO3

Respiratory Alkalosis ↓ PCO2 ↓ HCO3

• Step 5• If the disturbance is metabolic is the respiratory compensation appropriate?

• For metabolic acidosis:Expect PCO2 = (1.5 x [HCO3]) + 8 + 2

• (Winter’s equation)

• For metabolic alkalosis:• Expect PCO2 = (0.7 x [HCO3]) + 21 + 1.5

• If not: • actual PCO2 > expected : hidden respiratory acidosis

• actual PCO2 < expected : hidden respiratory alkalosis

Primary disorder Primary defect Compensatory response

Metabolic Acidosis ↓ HCO3 ↓ PCO2

Metabolic alkalosis ↑ HCO3 ↑ PCO2

During compensation HCO3¯ & PaCO2 move in the same direction

• Remember…….Respiratory

compensation

is always FAST …12-24 hrs

Metabolic compensation

• is always SLOW...5 -7 days

• Step 6• If there is metabolic acidosis, is there an anion gap?

• Na - (Cl-+ HCO3-) = Anion Gap usually <12

• Normal AG -: (loss of HC03, increase in chloride) – Diarrhoea, RTA, carbonic anhydrase inhibitor use.

• High AG-: If >12, Anion Gap Acidosis : Methanol• (Decreased excretion of acids) Uremia • Diabetic Ketoacidosis• Paraldehyde• Infection (lactic acid)• Ethylene Glycol• Salicylate

• Step 7• Does the anion gap explain the change in bicarbonate?• (to rule out co-existence of 2 acid-base disorders)• D anion gap (Anion gap -12) Delta Gap• Delta Gap + [HCO3] = 22-26 mmols/l

• If Delta anion gap is greater(>26); consider additional metabolic alkalosis

• If D anion gap is less(<22); consider additional nonanion gap metabolic acidosis

RESPIRATORY ALKALOSIS

Causes of Respiratory Alkalosis

CENTRAL RESPIRATORY STIMULATION (Direct Stimulation of Resp Center):Structural Causes Non Structural Causes• Head trauma Pain• Brain tumor Anxiety• CVA Fever• Voluntary

PERIPHERAL RESPIRATORY STIMULATION (Hypoxemia Reflex Stimulation of Resp Center via

Peripheral Chemoreceptors)• Pul V/Q imbalance• Pul Diffusion Defects Hypotension• Pul Shunts High Altitude

• INTRATHORACIC STRUCTURAL CAUSES: 1. Reduced movement of chest wall & diaphragm2. Reduced compliance of lungs 3. Irritative lesions of conducting airways

• MIXED/UNKNOWN MECHANISMS:1. Drugs – Salicylates Nicotine Progesterone Thyroid hormone

Catecholamines Xanthines (Aminophylline & related

compounds)2. Cirrhosis3. Gram –ve Sepsis4. Pregnancy5. Heat exposure6. Mechanical Ventilation

Manifestations of Resp Alkalosis

• NEUROMUSCULAR: Related to cerebral A vasoconstriction & Cerebral BF

1. Lightheadedness2. Confusion3. Decreased intellectual function4. Syncope5. Seizures6. Paraesthesias (circumoral, extremities)7. Muscle twitching, cramps, tetany8. Hyperreflexia9. Strokes in pts with sickle cell disease

• CARDIOVASCULAR: Related to coronary vasoconstriction

1. Tachycardia2. Angina3. ECG changes (ST depression)4. Ventricular arrythmias

• GASTROINTESTINAL: Nausea & Vomitting (cerebral hypoxia)

• BIOCHEMICAL ABNORMALITIES: CO2 PO4

3-

Cl- Ca2+

Homeostatic Response to Resp Alkalosis

In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) release of H+ by blood and tissue buffers react with HCO3- fall in HCO3- (usually not less than 18) and fall in pH

Cellular uptake of HCO3- in exchange for Cl- Steady state in 15 min - persists for 6 hrs After 6 hrs kidneys increase excretion of HCO3-

(usually not less than 12-14) Steady state reached in 11/2 to 3 days. Timing of onset of hypocapnia usually not known

except for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice

Treatment of Respiratory Alkalosis

Resp alkalosis by itself not a cause of resp failure unless work of increased breathing not sustained by resp muscles.

Rx underlying cause Usually extent of alkalemia produced not dangerous. Admn of O2 if hypoxaemia If pH>7.55 pt may be sedated/anesthetised/

paralysed and/or put on MV.

RESPIRATORY ACIDOSIS

Causes of Acute Respiratory Acidosis

• EXCRETORY COMPONENT PROBLEMS:1. Perfusion:

Massive PTECardiac Arrest

2. Ventilation:Severe pul edemaSevere pneumoniaARDSAirway obstruction

3. Restriction of lung/thorax:Flail chestPneumothoraxHemothorax

4. Muscular defects:Severe hypokalemiaMyasthenic crisis

5. Failure of Mechanical Ventilator

CONTROL COMPONENT PROBLEMS:6. CNS:

Drugs (Anesthetics, Sedatives) Trauma Stroke

2. Spinal Cord & Peripheral Nerves:Cervical Cord injury Neurotoxins (Botulism, Tetanus, OPC)Drugs causing Sk. m.paralysis (SCh, Curare,

Pancuronium & allied drugs, aminoglycosides)

Causes of Chronic Respiratory Acidosis

• EXCRETORY COMPONENT PROBLEMS:1. Ventilation:

COPDAdvanced ILD

• Restriction of thorax/chest wall:Kyphoscoliosis, ArthritisFibrothoraxHydrothoraxMuscular dystrophyPolymyositis

Causes of Chronic Respiratory Acidosis

• CONTROL COMPONENT PROBLEMS:1. CNS: Obesity Hypoventilation Syndrome

Tumours Brainstem infarctsMyxedemaCh sedative abuseBulbar Poliomyelitis

2. Spinal Cord & Peripheral Nerves:PoliomyelitisMultiple SclerosisALSDiaphragmatic paralysis

Manifestations of Resp Acidosis

• NEUROMUSCULAR: Related to cerebral A vasodilatation & Cerebral BF

1. Anxiety2. Asterixis3. Lethargy, Stupor, Coma4. Delirium5. Seizures6. Headache7. Papilledema8. Focal Paresis9. Tremors, myoclonus

Manifestations of Resp Acidosis

• CARDIOVASCULAR: Related to coronary vasodilation

1. Tachycardia2. Ventricular arrythmias (related to hypoxemia

and not hypercapnia per se)

• BIOCHEMICAL ABNORMALITIES: CO2 Cl-

PO43-

Homeostatic Response to Respiratory Acidosis

Imm response to rise in CO2 (& H2CO3) blood and tissue buffers take up H+ ions, H2CO3 dissociates and HCO3- increases with rise in pH.

Steady state reached in 10 min & lasts for 8 hours. PCO2 of CSF changes rapidly to match PaCO2. Hypercapnia that persists > few hours induces an

increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH.

After 8 hrs, kidneys generate HCO3- Steady state reached in 3-5 d

Treatment of Respiratory Acidosis

• Ensure adequate oxygenation - care to avoid inadequate oxygenation while preventing worsening of hypercapnia due to supression of hypoxemic resp drive

• Correct underlying disorder if possible

Treatment of Respiratory Acidosis

Alkali (HCO3) therapy rarely in ac and never in ch resp acidosis only if acidemia directly inhibiting cardiac functions

Problems with alkali therapy:1)Decreased alv ventilation by decrease in pH

mediated ventilatory drive2)Enhanced carbon dioxide production from

bicarbonate decomposition

METABOLIC ACIDOSIS

Metabolic Acidosis

• pH, HCO3

• 12-24 hours for complete activation of respiratory compensation

• PCO2 by 1.2mmHg for every 1 mEq/L HCO3

• The degree of compensation is assessed via the Winter’s Formula

PCO2 = 1.5(HCO3) +8 2

Causes

• Metabolic Anion Gap Acidosis– M - Methanol– U - Uremia– D - DKA– P - Paraldehyde– L - Lactic

Acidosis– E - Ehylene

Glycol– S - Salicylate

Non Gap Metabolic Acidosis Hyperalimentati

on Acetazolamide RTA (Calculate

urine anion gap) Diarrhea Pancreatic

Fistula

Treatment of Met Acidosis• When to treat?•Severe acidemia Effect on Cardiac function most imp factor for pt survival since rarely lethal in absence of cardiac dysfunction.•Contractile force of LV as pH from 7.4 to 7.2•However when pH < 7.2, profound reduction in cardiac function occurs and LV pressure falls by 15-30%•Most recommendations favour use of base when pH < 7.15-7.2 or HCO3 < 8-10 meq/L.

How to treat?

Rx Undelying CauseHCO3- Therapy• Aim to bring up pH to 7.2 & HCO3- 10

meq/L• Qty of HCO3 admn calculated:

0.5 x LBW (kg) x HCO3 Deficity (meq/L)

Why not to treat?

Considered cornerstone of therapy of severe acidemia for >100 yrs

Based on assumption that HCO3- admn would normalize ECF & ICF pH and reverse deleterious effects of acidemia on organ function

However later studies contradicted above observations and showed little or no benefit from rapid and complete/over correction of acidemia with HCO3.

Adverse Effects of HCO3- Therapy

CO2 production from HCO3 decomposition Hypercarbia (V>A) esp when pul ventilation impaired

Myocardial Hypercarbia Myocardial acidosis Impaired myocardial contractility & C.O.

Cor A perfusion pressure Myocardial Ischemia esp in pts with HF

Hypernatremia & Hyperosmolarity Vol expansion Fluid overload esp in pts with HF

Intracellular (paradoxical) acidosis esp in liver & CNS ( CSF CO2)

• gut lactate production, hepatic lactate extraction and thus S. lactate

CORRECTION OF ACIDEMIA WITH OTHER BUFFERS:•Carbicarb

- not been studied extensively in humans - used in Rx of met acidosis after cardiac arrest

and during surgery - data on efficacy limited

• THAM (Trometamol/Tris-(OH)-CH3-NH2-CH3) - biologically inert amino alcohol of low toxicity.

• Capacity to buffer CO2 & acids in vivo as well as in vitro

• More effective buffer in physiological range of blood pH

• Initial loading dose of THAM acetate (0.3 ml/L sol) calculated:BW (kg) x Base Deficit (meq/L)

Max daily dose ~15 mmol/kg• Use in severe acidemia (pH < 7.2):

METABOLIC ALKALOSIS

Metabolic Alkalosis

Met alkalosis common (upto 50% of all disorders)• pH, HCO3

• PCO2 by 0.7 for every 1mEq/L in HCO3

Severe met alkalosis assoc with significant mortality1)Arterial Blood pH of 7.55 Mortality rate of 45% 2)Arterial Blood pH of 7.65 Mortality rate of 80%

(Anderson et al. South Med J 80: 729–733, 1987)

Metabolic alkalosis has been classified by the response to therapy or underlying pathophysiology

Pathophysiological Classification of Causes of Metabolic Alkalosis

1) H+ loss:

GIT Chloride Losing Diarrhoeal Diseases Removal of Gastric Secretions

(Vomitting, NG suction)

Renal Diuretics (Loop/Thiazide) Mineralocorticoid excess Hypercalcemia High dose i/v penicillin

Black RM. Intensive Care Medicine 2003; 852-864

2) HCO3- Retention:Massive Blood TransfusionIngestion (Milk-Alkali Syndrome)Admn of large amounts of HCO3-

3) H+ movement into cellsHypokalemia

Black RM. Intensive Care Medicine 2003; 852-864

Clinical features

Adrogue et al, NEJM 1998; 338(2): 107-111

Treatment of Metabolic Alkalosis

Rx underlying cause resp for vol/Cl- depletion While replacing Cl- deficit, selection of

accompanying cation (Na/K/H) dependent on:Assessment of ECF vol status

Presence & degree of associated K depletion,

Pts with vol depletion usually require replacement ofboth NaCl & KCl.

Dialysis• In presence of renal failure or severe fluid overload

state in CHF, dialysis +/- UF may be reqd to exchange HCO3 for Cl & correct metabolic alkalosis.

Adjunct Therapy• PPI can be admn to gastric acid production in cases

of Cl-depletion met alkalosis resulting from loss of gastric H+/Cl- (e.g. pernicious vomiting, req for continual removal of gastric secretions.

MILK-ALKALI SYNDROME & OTHER HYPERCALCEMIC STATES • Cessation of alkali ingestion & Ca sources (often milk and calcium carbonate)• Treatment of underlying cause of hypercalcemia• Cl- and Vol repletion for commonly associated vomiting

• ----- XXXX Diagnostics ------

• Blood Gas Report

• Measured 37.0o

C• pH 7.523

• pCO2 30.1 mm Hg

• pO2 105.3 mm Hg

• Calculated Data

• HCO3 act 22 mmol / L

• O2 Sat 98.3 %

• pO2 (A - a) 8 mm Hg D

• pO2 (a / A) 0.93

• Entered Data

• FiO2 21.0 %

Case 1

30 year old female withsudden onset of dyspnea.

No Cough or Chest Pain

Vitals normal but RR 26,anxious.

• ----- XXXX Diagnostics ------

• Blood Gas Report

• Measured 37.0o

C• pH 7.301

• pCO2 76.2 mm Hg

• pO2 45.5 mm Hg

• Calculated Data

• HCO3 act 35.1 mmol / L

• O2 Sat 78%

• pO2 (A - a) 9.5 mm Hg D

• pO2 (a / A) 0.83

• Entered Data

• FiO2 21 %

Case 2

60 year old male smokerwith progressiverespiratory distressand somnolence.

• ----- XXXX Diagnostics ------

• Blood Gas Report

• Measured37.0o C

• pH 7.23• pCO2 23 mm Hg• pO2 110.5 mm Hg

• Calculated Data

• HCO3 act 14 mmol / L

• O2 Sat %• pO2 (A - a) mm Hg D• pO2 (a / A)

• Entered Data• FiO2 21.0%

Case 3

28 year old diabetic withrespiratory distressfatigue andloss of appetite.

8) I shall practice gentle mechanical ventilation and not to try bring ABG to perfect normal.

9) I shall treat the patient, not the ABG report.

10) I shall always correlate ABG report clinically.

References

ICU Book, The, 3rd Edition - Paul L. Marino

Diagnosing Acid-Base Disorders : JAPI • VOL. 54 • SEPTEMBER 2006

Harrison‘s PRINCIPLES OF INTERNAL MEDICINE Eighteenth Edition

Washington Manual of Critical Care - 2nd Ed

Selected Websites – Listed in next slide

References

• Selected Acid-Base Web Sites

http://www.acid-base.com/

http://www.qldanaesthesia.com/AcidBaseBook/

http://www.virtual-anaesthesia-textbook.com /vat/acidbase.html#acidbase

http://ajrccm.atsjournals.org/cgi/content/full/162/6/2246

http://www.osa.suite.dk/OsaTextbook.htm

http://www.postgradmed.com/issues/2000/03_00/fall.htm

http://lungpowerpoints.com http://uptodate.com