ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS Dr Sajith Damodaran University...

ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS

Dr Sajith Damodaran

University College of Medical Sciences & GTB Hospital, Delhi

Homeostasis

The Interstitial Fluid is the environment of the cells, and life depends on the constancy of this internal sea.

Homeostatic Mechanisms : Maintain within a narrow range.

Tonicity Volume Specific ion concentration

Defence of Tonicity –(280-295mOsm/L) Vasopressin secretion Thirst Mechanism

Increased Osmolality of ECF

Thirst IncreasedVasopressin

SecretionIncreased Water Intake Water Retention

Dilution of ECF

Inhibitory

Homeostasis

Defence of Volume:

ECF Na+ - Most important

Renin-Angiotensin-Aldosterone System

Vasopressin Secretion: Volume stimuli override osmotic regulation

ANP & BNP

Angiotensinogen

Renin

Angiotensin I

ACE

Angiotensin II

Aldosterone Vasopressin

AdrenalCortex Brain

KidneyNa RetentionWater Retention

Blood VesselVasoconstriction

Thirst

Homeostasis

Defence of Specific Ionic Concentration: Glucose Na+ & K+ Ca++ - Mainly by Parathyroid & Calcitonin Mg++ - Incompletely understood mechanisms

Also dependent on H+ ion

pH is maintained within a narrow range.

Acid Base Equilibrium

What is Acid Base Equilibrium About?

?Buffer

s? Fixed Cation

?

Base Excess/ Deficit? Anion

Gap?

Acid Base Equilibrium

Acid Base Equilibrium is all about Maintenance of H+ ion concentration of the ECF.

Source of H+ ion in Body:CO2 from metabolis

m

H+ load from AA

metabolism

Strenuous Exercise Lactic Acid

Diabetic KA

Ingestion of NH4Cl, CaCl2

Failure of Kidneys to Excrete PO4--, SO4--

H+ ion

12500 mEq/d50 - 100 mEq/d

Some Basic Chemistry

Definitions:Arrhenius:

Acid: H+ Donor in Solution Base: OH- donor in Solution

Browsted and Lowry: Acid: Proton Donor Base: Proton Acceptor

H20 can be both


Simple Rule of Thumb:Acid Higher conc. Of H+ ionBase Lower conc. Of H+ ionStrong Acid/Base Dissociates completely and irreversiblyWeak Acid/Base Dissociates partially and reversibly

Strong Electrolyte: Dissociates completely in solution at physiological pH

Eg: NaCl, KCl

Weak Electrolyte: Dissociates incompletely in solution at physiological pH

Eg: CO2 – HCO3- System, Proteins


pH (Puissant of Hydrogen):Negative logarithm of H+ ion concentration to the

base of 10

Why pH? Normal H+ ion conc: 0.00004meq/L or 40nEq/L or

4x10-9 mol/L pH converts to decimal numbers & takes away

negative sign. Normal pH: 7.35-7.45 Normal H+ Conc: 0.00002mEq/L – 0.0001 mEq/L


Pitfalls: Non-linear Negative Logarithmic scale pH Decreases as [H+] increases. Each unit change in pH from 7 represents 10 fold

change in H+ ion conc. Eg: At pH 4, there are 10 times as much H+ than at pH 5,

& 100 times as at pH 6 Same numeric change in different portions of the pH

scale implies vastly different nanomolar change in H+ ions Eg: pH 56 => 100 times greater change in ionic conc

than when pH 7 8 Body H+ ion conc is not as tightly controlled as the

other ion, though the pH scale implies so.


Water (H2O)Water dissociates, but to a very low extent.

H2O <====>H+ + OH-

But, a glass of water has a billion times more H2O than H+ & OH-

At equilibrium:[H+] [OH-] = Kw[H2O]

{Kw(Dissociation constant of water) changes with temperature}Or, [H+] [OH-] = Kw’

pH of Water:Since at neutral pH, [H+] = [OH-]

[H+] = ROOT (Kw’)Þ Acidic solution, [H+] > ROOT (Kw’), Basic sol, [H+] < ROOT(Kw’)

Þ pH changes with temperature

Acid Base Equilibrium:

Solutions:When substances are added to water, 3

simple rules have to be satisfied at all time:1. Electrical Neutrality2. Mass conservation3. Dissociation Equilibrium

ECF is a complex solution with strong ions, weak ions and CO2 dissolved in water.


CO2 in Water: Can Dissolve in water Can form - Carbonic Acid - Bicarbonate ion - Carbonate ion

CO2(gas) <====> CO2(dissolved)

Rate of Forward Reaction = Kf * PCO2

Rate of Reverse reaction = Kr *[CO2(dissolved) ]

=> [CO2(dissolved)] = Kf /Kr *PCO2

Kf /Kr = SCO2 (Solubility of CO2 ) = 0.03mEq/L/mm Hg at 370 C

}All these reactions have equilibrium Constants and can be solved at equilibrium.


CO2 + H2O <====> H2CO3

=>[CO2][H2O] = K*[H2CO3]

=> [H2CO3] = K’*PCO2

H2CO3 <====> H+ + HCO3

-

Henderson Equation: [H+ ] = K1 [H2CO3]/[HCO3

- ]

Modified Henderson Equation: [H+ ][HCO3

- ] = K2 [CO2][H2O]

[H+ ][HCO3- ] = K3 [CO2]

[H+] = K*PaCO2/[HCO3-]


The Henderson-Hasselbalch Equation:CO2 + H2O <====> H+ + HCO3

-

=> [H+] = K’a * [CO2]/[HCO3-]

Rearranging: =>1/[H+] = 1/K’a*[HCO3

-]/[CO2]

Taking Logarithm on both sides & Rearranging:

=> pH= pK’a + log10[HCO3-]/0.03*PCO2

Significance: Includes components of both Met & Resp Acid base disorders Value of any one variable can be determined if other two

known. Mostly HCO3- is calculated

pH determined by ratio of [HCO3-]/PCO2 . Maintained at 20.

Increase=> alkalosis, Decrease => Acidosis

Clinical Concepts: The Stewart Approach

Dissociation equations can be solved mathematically.

When the equations are solved- Independent Variables: SID, [Atot] &

PaCO2 Constants : Dissociation constants Dependent Variables: [H+], [OH-],

[HCO3-], [CO32-], [A+], [HA], [H2CO3], [CO2

dissolved]


Dissociation equations can be solved mathematically.

When the equations are solved- Independent Variables: SID, [Atot] &

PaCO2 Constants : Dissociation constants Dependent Variables: [H+], [OH-],

[HCO3-], [CO32-], [A+], [HA], [H2CO3], [CO2

dissolved]

Dependent Variables can only be changed by changing the independent variables!!!


SID: Strong Ion Difference – ([Na+] + [K+] + [Ca++] + [Mg++]) – [Cl-]+ [other Strong Anions]

Normal: 40-44mEq/L with normal protein levels Change from normal is equivalent to SBE

Dehydration: Increases SID ==> Alkalosis Dilution, Organic Acids, Hyperchloremia : Decreases SID ==>

Acidosis

[Atot]: Total Amount of Weak Acid in Solution Albumin is the most important weak electrolyte in plasma. Other weak acids are Inorganic Phosphates, Plasma proteins.

Hypoproteinemia: Alkalosis Renal Failure: Accumulation of Phosphate: Acidosis

Clinical Concepts:

Base Excess: Amount of Acid or Alkali required to return plasma in vitro to normal pH under standard conditions.

Standard BE: BE calculated for Anaemic Blood (Hb = 5Gm%). Since Hb effectively buffers plasma & ECF to a large

extent. Quantity of Acid or Alkali required to return plasma in-vivo

to a normal pH under standard conditions

Anion Gap: AG = [Na+] + [K+] - {[HCO3

-] + [Cl-]}

Normal Value: 8-12mEq/L, Unmeasured Anion: Albumin, Phosphate, sulphate, organic

anions AG decreases by 2.5mEq/L for every 1mEq/L decrease in

Plasma albumin AG>16 ==> Ketones, lactate, salicylate, antifreeze,

methanol

Clinical Concepts:

Acid Base Equilibrium: Elimination of Acid Recovery/Regeneration of Base

Mechanisms that keep pH stable Buffering Compensation Correction

Clinical Concepts:

Buffers:Definition: A substance that can bind or release H+

ions in solution, thus keeping the pH of the solution relatively constant despite addition of large amounts of acid or base.

For Buffer HA,HA <====>H+ + A-

pH = pKa + log [A-]/[HA] When [A-] = [HA], pH= pK, buffering capacity is

maximum. Ideal body buffer has pKa between 6.8 and 7.2

Clinical Concepts:

Most buffers are weak acids (Hbuffer) & their Na Salts (Nabuffer) Strong Acids Buffered by NaBuffer

HCl + NaBuffer <====> H+ + Cl- +Na+ + Buffer <====> Hbuffer + NaCl Strong Bases buffered by Hbuffer

NaOH + H Buffer <====> Na+ + OH- + H+ + Buffer <====> NaBuffer + H2O

Buffer Effectiveness Depends on: Quanitity

H2CO3 /HCO3

- - Most important Extracellular Buffer Protein Buffers – Most improtant Intracellular Buffer

pKa

– Buffering capacity maximum when pH=pKa Function well within 1 pH unit. (Eg: HCO3

- - 5.1-7.1)

Clinical Concepts:

Buffers in ECF: Carbonate-Bicarbonate Buffer 53%

Plasma (35%) Erythrocyte(18%)

Hemoglobin 35% Plasma Proteins 7% Organic & Inorganic Phosphates 5%

Buffers in ICF: Intracellular Proteins H2PO4-HPO4

- system

Intracellular buffers are responsible for ~85% buffering in Met. Acidosis and ~35% in met alk and almost complete buffering in respiratory acidosis and alkalosis

Clinical Concepts:

Bicarbonate Buffer: HCl + NaHCO3

- <==>NaCl + H2CO3<==>NaCl + H2O + CO2

useful only for metabolic acidHb System: Both Respiratory & Metabolic Acid in ECF Forms Carbamino compounds with CO2 Buffers H+ directly

CO2 + H2O <====>H2CO3 + KHb <====> HHb + KHCO3

HCO3- diffuses out & Cl- diffuses into cells – Chloride

shift pKa – 6.8

Clinical Concepts:

Protein Buffer: Predominant Intracellular Buffer – Large total concentration pK = 7.4 AA have Acidic & Basic Free radicles

.COOH + OH- <====> COO- + H2O

.NH3OH + H+ <====> NH3 + H2O

Phosphate Buffer: pK = 6.8 Predominantly Intracellular Also in renal tubular

HCl + Na2HPO4 <====> NaH2PO4 + NaCl

NaOH + NaH2PO4 <====> Na2HPO4 + H2O

Clinical Concepts:

Compensation:Pulmonary Compensation

H+ + HCO3-<====> H2CO3 <====>CO2 + H2O

H+ acts on medullary centres. Increased PaCO2 stimulates ventiallation Metabolic Acidosis – Increased Ventillation Metabolic Alkalosis – Depression of

Ventillation But, limited because Hypoxic stimulus can

override Hypercapnia

Clinical Concepts:

Renal Compensatoin:

Mechanisms:1. Reabsorption of filtered HCO3- (4000-5000

mEq/d)2. Generation of fresh bicarbonate3. Formation of titrable acid – (1mEq/Kg/d)4. Excretion of NH4+ in urine

PERITUBULAR BLOOD RENAL TUBULAR CELL

GLOMULAR FILTRATE

HCO3- + H+

CO2

HCO3- + H+

HCO3- + H+

HCO3- Na+ HPO4

2- Na+ NH3 Na+

H2CO3

CO2 + H2 O

H2O

H2PO4-

H2PO4-

NH4+

NH4+

1. NaHCO3

2. NaHCO3

3. NaHCO3

MAJOR RENAL MECHANISMS RESPONSIBLE FOR H+ EXCRETION/HCO3- RETENTION

CO2 can be obtained from blood or the tubular fluid

Glutamine

CO2

CA

Clinical concepts: Compensation

Prediction of Compensatory Responses on Simple Acid Base Disorders

Disorder Prediction of Compensation

Metabolic Acidosis PaCO2 = (1.5 x HCO3- ) + 8

OrPaCO2 will 1.25mm Hg per mmol/L in [HCO3

- ]OrPaCO2 = [HCO3

- ] + 15

Metabolic Alkalosis PaCO2 will 0.75 mm Hg per mmol/L in [HCO3- ]

OrPaCO2 will 6mm Hg per 10 mmol/l in [HCO3

- ]OrPaCO2 = [HCO3

- ] + 15

Respiratory Alkalosis

Acute [HCO3- ] will 2mmol/L per 10 mmHg in PaCO2

Chronic [HCO3- ] will 4mmol/L per 10 mmHg in PaCO2

Respiratory Acidosis



Disorder Prediction of Compensation

Metabolic Acidosis PaCO2 = (1.5 x HCO3- ) + 8

OrPaCO2 will 1.25mm Hg (1.0-1.5) per mmol/L in [HCO3

- ]OrPaCO2 = [HCO3

- ] + 15

Metabolic Alkalosis PaCO2 will 0.75 (0.25-1.0) mm Hg per mmol/L in [HCO3

- ]OrPaCO2 will 6mm Hg per 10 mmol/l in [HCO3

- ]OrPaCO2 = [HCO3

- ] + 15, Max – 55mmHg







Acid-Base Nomogram:

Clinical concepts:

Effect of Temp: pH rises 0.015/0C drop in temp

Effect of PaCO2 on pH: pH changes by 0.08/10mm Hg change in

PaCO2

Effect of change of [HCO3-] on pH:

pH changes by 0.1/ 6 mEq change in [HCO3

-]

Clinical Concepts:

Effect of Electrolytes in Buffering: Potassium Ion: Intracellular

Hypokalemia - K+ Moves out H+ moves in - K+ & HCO3

- reabsorption, H+ Excretion

Sodium Ion Hyponatremia -- Na+ & HCO3

- reabsorption & H+ excretion

Clinical Concepts:

Role of Bones: Exchange of Extracellular H+ for Na+ & Ca++

Acid load Demineralise Bones Alkaline load Deposition of CO3

2- in Bones

Time Course of Buffering: Plasma HCO3

- ----> Immediate Interstitial HCO3

- -----> 15-20 Min Intracellular Proteins & Bones ----> 2-4 Hours

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.

Acid Base Disorders

The primary disorders:

Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis

Acute Chronic

Respiratory Alkalosis Acute Chronic

Disorder Primary Change

Compensatory

Change

Metabolic Acidosis

HCO3_ PaCO2

Metabolic Alkalosis

HCO3_ PaCO2


PaCO2 HCO3_


PaCO2 HCO3_

Acidosis:Clinical Effects

CVS:Combination of Effects of Direct depression and Catecholamine

stimulationHeart Rate: Initial Increase then DecreaseRhythm: Increased Atrial & Ventricular Dysrrhythmias

Due to Changes in S K+ Lower threshold for VF

Contractility: Increased contractility. Depression if pH<7.0Cardiac Output: Increased

Increased Catecholamines, Decreased Arterial tone, Increased Venous Tone At <7.0, Decreased d/t direct depressant effects CCF d/t Increased venous tone.

Acidosis:Clinical Effects

Vascular Effects: Direct Vasodilatation Vasoconstriction d/t Catecholamines

Respiratory: Vasodilatation predominates Metabolic: Vasoconstriction

Splanchnic & Renal Vasoconstriction Variable effects on Coronary, Cutaneous, Uterine

BP doesn’t change till extremes imbalance Hypotension occurs when pH falls below 7.0

Clinical Effects of Acidosis:

Respiratory System: Minute Ventilation: TV RR

Twice more for RA than MA Airway Resistance:

Direct: Decrease by Smooth muscle relaxation Indirect: Increased by Vagal Tone

Vagal Effect predominates: Increased WoB Pulmonary Vasculature:

Vasoconstriction Enhanced HPV

Right shift of ODC: But tissue hypoxia can occur due to hypotension


GI System: Variable effects in splanchnic BF

Renal System Vasoconstriction

Uteroplacental: CO2 freely diffuses HCO3

- slowly over hours

Similar effects in Fetal systemsElectrolytes:

Calcium: Increased Free Ca++ Potassium: Increased S K+


NeuroEndocrine: CBF (by PaCO2) Mental Changes: CNS Depression

More with RA Decreased Body Temp

Impaired central regulation Cutaneous vasodilatation Decreased Cellular Metabolism

Increased secretion of catecholamines


Effect Direct Indirect Clinical

Cerebral blood flow + + +

Heart rate - + +

Cardiac inotropy - + 0

Systemic arterial tone - + -

Systemic venous tone + + +

Pulmonary artery tone + + +

Airway tone - + +

Uterine blood flow + - 0

Renal blood flow + - -

Ionised calcium + 0 +

Serum potassium + 0 +

Respiratory Acidosis:

Primary Increase in PaCO2

Cause: Production/ Elimination

Produced by: Carbohydrate and fat metabolism, muscle activity, body temp thyroid hormone activity

Elimination by Lungs. Immense capacity CO2 - ventilation compromised

Respiratory Acidosis:Causes:

Alveolar Hypoventilation

CNS Depression Drugs Cerebral Ischemia/trauma Sleep Disorders Pickwickian Syndrome

Neuromuscular Disorders

Neuropathy Myopathy

Chest Wall Abnormality Kyphoscoliosis Flail Chest

Pleural Abnormality Pneumothorax Pleural Effusion

Airway Obstruction FB/Tumor COPD/Sever Asthma

Parenchymal Lung Disease Pul edema/embolus Pneumonia ILD

Ventilator Dysfunction

Respiratory Acidosis:Causes Contd…

Increased CO2 Production: Large Carbohydrate meal Malignant Hyperthermia Intensive shivering Prolonged seizures Thyroid Storm Extensive Burns

Respiratory Acidosis:

pH – 7.36

PaCO2 – 64

HCO3- - 33

pH is acidic, but normal

PaCO2 > 40 => Resp Acidosis

Compensation expected:

HCO3- = 24 + (64-40) x 0.1 = 24+2.4 = 26.4 or

24 + (64-40) x 0.4 = 24 + 9.6 = 33.6

Diagnosis: Chronic Respiratory Acidosis

Metabolic Acidosis: Causes:

Increased Anion Gap

Increased Production of Endogenous Acid Ketoacidosis- DM,

Starvation Lactic Acidosis Mixed- NKHC, Alcoholic Abnormal AA Met. CRF

Ingestion of Toxins Salicylate Methanol Ethylene Glycol Paraldehyde, Toluene,

Sulphur Rhabdomyolysis

Metabolic Acidosis: Causes Contd…

Normal AG(Hyperchloremic)

GI Loss of HCO3-

Diarrhea Fistula- Pancreatic,

Biliary, Small Intestinal Ureterosigmoidostomy Obstructed Bowel Loop Cholestrylamine,

CaCl2, MgSO4

Renal Loss of Bicarb RTA CA Inhibitors Hypoaldosteronism

Dilutional- Bicarb free fluid

TPN Increased Intake of Cl

containing Acids – NH4Cl, Lysine

hydrochloride, Arginine Hydrochloride

Metabolic Acidosis:

pH – 7.36 PaCO2 – 26

HCO3- - 13

BE - -11

pH – Acidic but normal

PaCO2 – Decreased => Not Respiratory

HCO3- - Decreased => Metabolic Acidosis

Compensation expected: 40 - (24-13)x1.25 =40-13.75 = 26.25

Diagnosis: compensated Metabolic Acidosis

Treatment:

Alkali Therapy: Indications

Normal AG (Hyperchloremic Acidosis) Slightly elevated AG (Mixed Hyperchloremic & AG Acidosis) AG due to Non Metabolisable Anion (Renal Failure)

Goal: To slowly increase plasma HCO3- to 20-22 mmol/L

AG Acidosis due to Accumulation of Organic metabolizable anion, if pH< 7.2 Goal: pH to 7.15, Plasma HCO3

- ~10mmol/L

Either orally (NaHCO3 / Shohl’s solution) or IV (NaHCO3) Carbicarb, THAM

Acute Respiratory Acidosis

Chronic Respiratory Acidosis

•Correction of the cause•Restoration of Adequate vent – Mechanical ventillation

•Difficult to Correct•Measure to Improve lung function

Treatment:

Problems with Bicarbonate Therapy Cardiac Arrest: Both MA & RA

50mL NaHCO3 Releases 200 mL CO2 Bicarb corrects MA but worsens RA Intracellular Acidosis

COP increase maybe due to increased intravascular vol CSF Acidosis Increased Plasma Osmolarity (3 mmol/50mL) Extracellular alkalosis - ODC to Left - Decreased Tissue

Oxygenation Rebound Alkalosis Decreased Ca++ ---> Myocardial depression

Acidosis: Anaesthetic Considerations:

Potentiation of depressant effects of sedatives and anaesthetic agents

Exaggerated circulatory depressant effects more pronounced with agents that rapidly decrease

symp tone Increased opioid penetration into brain

basic drugs increased non ionised form Increased arrhytmogenicity of halothane Respiratory Acidosis augments NDMR delayed

reversal Succinyl Choline increases Serum K+ further

Alkalosis:

Physiologic Effects:1. Left shift of ODC2. Hypokalemia3. Low ionised Ca++4. Decreased CBF5. Depressed

Ventilatoin6. Respiratory Alkalosis

Bronchoconstriction Decreased PVR

Effect Direct

Indirect

Clinical

Cerebral BF - 0 -

Heart rate 0 0 0

Cardiac inotropy

0 0 0

Systemic Art tone

+ 0 +

Syst venous tone

0 0 0

PA tone 0 - -

Airway tone + - +

Uterine BF - 0 -

Renal BF 0 0 0

Ionised Ca++ - 0 -

Serum Potassium

- 0 -

Respiratory Alkalosis: Primary Decrease in PaCO2

Causes: Central Stimulation

Pain Anxiety Ischemia Tumor Infection Fever Drugs: Salicylates,

Progesterone, Doxapram

Peripheral Stimulation Hypoxemia High Altitude Pulmonary Disease:

CHF, NCPE, PE, Asthma Severe Anemia

Unknown Sepsis, Metabolic

Enceph Iatrogenic:

Ventilator Induced

Respiratory Alkalosis:

pH – 7.5 PaCO2 – 35 HCO3

- - 22

pH – AlkalemiaPaCO2 – Decrease => Respiratory Alkalosis

Expected Compensation: 24-(40-35)x0.2 = 23 or24-(40-35)x0.4 = 22

Diagnosis: Chronic Respiratory Alakalosis

Respiratory Alkalosis:Treatment:

Treatment of Underlying cause Ventilator adjustments Reassurance, Rebreathing from paper

bag

Metabolic alkalosis: Causes:

ECF Contraction, Normotension,

K+ Deficiency & 20 Hyperreninemic

Hyperaldosteronism Gastrointestinal

Vomiting NG suction Villous Adenoma

Renal Diuretics Mg++ Deficiency Chronic Hypokalemia Hypercalcemia/

Hyperpara. Post Hypercapnic State Barter’s syndrome

Sweat Cystic Fibrosis

Metabolic alkalosis:Causes:

ECF Expansion, Hypertension, K+ Deficiency & Mineralocorticoid Excess

High Renin Renal Artery Stenosis Accelerated HTN

Low Renin Primary Aldosteronism Adrenal Enzyme defects Cushing’s Syndrome

Other Liquorice

Exogenous HCO- Loads:

Massive Blood Transfusion

Acetate containing colloids

Alkali therapy + Renal Failure

Milk-Alkali Syndrome

Metabolic Alaklosis:

pH – 7.58 PaCO2 – 48 HCO3

- - 44 BE - +19pH – AlkalemiaPaCO2 – Increased => Not Respiratory

HCO3- - Increased => Metabolic Acidosis

Expected Compensatoin: 40+(44-24)x0.8 = 56Diagnosis: Partially compensated Metabolic

Alkalosis

Metabolic Alkalosis:Treatment:

Correction of underlying stimulus for HCO3- generation:

Correction of cause of 10 Hyperaldosteronism Reduction of Gastric secretions: H2 Blockers, PPI Reduction of Renal loss of H+ : Discontinue Diuretics

Remove factors that sustain HCO3- Reabsorption

ECF contraction – NaCl administration K+ deficiency – KCl administration

Acetazolamide But can cause K+ loss

Dilute HCl (0.1N HCl) Oral NH4Cl

Alkalosis:Anaesthetic considerations:

Increased protein binding of opioids prolonged respiratory depression

Decreased cerebral blood flow Cerebral Ischemia

Atrial and Ventricular dysrhythmias with hypokalemia

Potentiation of NDMR due to hypokalemia

Acid Base Disorders:

PO2 – 90.6

PCO2 – 53.8 pH – 7.484 K+ - 3.7 Na+ - 151 HCO3

- (A) – 37.7

HCO3- (S) – 34.3

BE – 13.9 SBE – 14.1 SO2 – 97.3

pH – Alkalemia

PCO2 – Increased => Metabolic Alkalosis

Expected Compensation: PaCO2 = 40+(13.7x0.75) = 50.2

Body never overcompensates

Diagnosis:

Metabolic Alkalosis + Respiratory Acidosis

Summary: Acid Base Homeostasis is all about maintenance of normal H+

concentration. Changes in acid base status of ECF have profound and often

unpredicatble clinical and laboratory effects, more so during anaesthesia.

pH scale is a negative logarithmic scale with it’s inherent counterintutive results.

The three independent variables which affect acid base status are SID, [Atot] & PaCO2.

SBE as a measure for Metabolic acid base disturbance is most accurate and clinically validated.

Anion gap must always be calculated, and effect of Plasma Albumin considered to decipher more accurately the complex acid-base disorders in critically ill patients.

Bicarbonate therapy must be used with caution in view of it’s various deleterious effects.

References:

Miller’s Anesthesia, 7th Edition Wylie And Churchill Davidson’s A Practice of

Anaesthsia, 7th Edition Morgan Michael & Clinical Application of Blood Gases, Shapiro, 5th Edition Harrison’s Principles of Internal Medicine, 16th Edition Ganong’s Review of Medical Physiology, 20th Edition ‘Acid-Base tutorial. Prof. Alan W Grogono, MD, FRCA

www.acid-base.com A Basic Approach to body pH

www.anaesthetist.com/icu/elec/ionz/Findex.htm#Stewart.htm

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

http://www.anaesthetist.com/icu/elec/ionz/Findex.htm

http://www.anaesthetist.com/icu/elec/ionz/Findex.htm

Thank You

ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS Dr Sajith Damodaran University...

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