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

ACID BASE BALANCE 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
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 – CO2 + H2O <--> H2CO3 <--> HCO - + H+
Assessment of status via bicarbonate-carbon dioxide buffer system in blood. – CO2 + H2O <--> H2CO3 <--> – Henderson-Hasselbach equation HCO - + H+ 3 – PH = 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
Non invasive measurement Finger probes and ear probes Percutaneous measurements

Pulse Oximeter Sensor Two LEDs emit red and infrared
wavelengths of light through skin Hb absorbs red wavelengths HbO2 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 power Data outputs: SpO2 and pulse rate
Eight second average (or instantaneous) Serial communication

Pulse Oximetry Carbon monoxide intoxication (heavy smoker)
FALSE HIGH RESULTS FALSE LOW RESULTS Carbon monoxide intoxication (heavy smoker) Strong lights UV lights (anti bacterial) Infra red light (neonatal ICU) 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 wall Usually no need to ‘pull back’ barrel – less chance of air bubbles entering syringe Small 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 Heparin
Dilutional effect on results  HCO3- & PaCO2 Syringe be emptied of heparin after flushing Risk of alteration of results  with: 1) size of syringe/needle 2) 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), 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 COUNT
0.1 ml of O2 consumed/dL of blood in 10 min in pts with N TLC Marked 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 PaO2 80-100 38-42 PaCO2 36-44 44-48 HCO3 22-26 20-24 SaO2 95-100 75 CENTRAL VENOUS 50-54 45-49 22-26 78

Acid Base Disorders The primary disorders: Respiratory Acidosis
Acute Chronic Respiratory Alkalosis 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 PaCO2 PaO2 SaO2 7.35 - 7.45 35 - 45 mm Hg
----- XXXX Diagnostics Blood Gas Report 248 05:36 Jul Pt ID 2570 / 00 o Measured 37.0 C pH 7.463 pCO2 44.4 mm Hg pO2 113.2 Corrected 38.6 C 7.439 47.6 123.5 pH PaCO2 PaO2 SaO2 mm Hg mm Hg % mEq/L -2.0 to 2.0 HCO ¯ 3 Calculated Data Base excess mEq/L TPCO2 HCO3 act 49 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 O2 CT 14.7 mL / dl O2 Sat 98.3 % ct CO2 32.4 pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79 Entered Data Temp 38.6 oC Measured values should be considered And Corrected values should be discarded ct Hb 10.5 g/dl FiO2 30.0 %

The Habits of Highly Successful Blood Gas Analysts ABG Interpretation

Step 1 Look at the pH Is the patient acidemic pH < 7.35 or
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 4 Step 3 If there is a primary respiratory disturbance, is
it acute? Expect  pH = 0.08 x  PCO2 / 10 Step 4 For a respiratory disorder is renal compensation OK? Respiratory acidosis: <24 hrs:  [HCO3] = 1/10  PCO2 >24 hrs:  [HCO3] = 3/10  PCO2 Respiratory alkalosis:1- 2 hrs:  [HCO3] = 2/10  PCO2 >2 days:  [HCO3] = 6/10  PCO2

Compensatory response
Primary disorder Primary defect Compensatory response Respiratory acidosis ↑ PCO2 ↑ HCO3 Respiratory Alkalosis ↓ PCO2 ↓ HCO3

Expect PCO2 = (1.5 x [HCO3]) + 8 + 2
Step 5 If the disturbance is metabolic is the respiratory compensation appropriate? For metabolic acidosis: Expect PCO2 = (1.5 x [HCO3]) (Winter’s equation) For metabolic alkalosis: Expect PCO2 = (0.7 x [HCO3]) 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

Respiratory compensation
is always FAST … hrs Metabolic compensation is always SLOW days

Step 6 If there is metabolic acidosis, is there an anion gap?
Na - (Cl-+ HCO -) = Anion Gap usually <12 3 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)  anion gap (Anion gap -12) Delta Gap Delta Gap + [HCO3] = mmols/l If Delta anion gap is greater(>26); consider additional metabolic alkalosis If  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 Head trauma Brain tumor CVA • Non Structural Causes Pain Anxiety Fever Voluntary PERIPHERAL RESPIRATORY STIMULATION (Hypoxemia  Reflex Stimulation of Resp Center via Peripheral Chemoreceptors) Pul V/Q imbalance Pul Diffusion Defects Pul Shunts Hypotension High Altitude

INTRATHORACIC STRUCTURAL CAUSES:
Reduced movement of chest wall & diaphragm Reduced compliance of lungs Irritative lesions of conducting airways MIXED/UNKNOWN MECHANISMS: 1. Drugs – Salicylates Progesterone Catecholamines Nicotine Thyroid hormone Xanthines (Aminophylline & related compounds) Cirrhosis Gram –ve Sepsis Pregnancy Heat exposure Mechanical Ventilation

Manifestations of Resp Alkalosis
NEUROMUSCULAR: Related to cerebral A vasoconstriction &  Cerebral BF Lightheadedness Confusion Decreased intellectual function Syncope Seizures Paraesthesias (circumoral, extremities) Muscle twitching, cramps, tetany Hyperreflexia Strokes in pts with sickle cell disease

CARDIOVASCULAR: Related to coronary vasoconstriction Tachycardia
Angina ECG changes (ST depression) Ventricular arrythmias GASTROINTESTINAL: Nausea & Vomitting (cerebral hypoxia) BIOCHEMICAL ABNORMALITIES:  CO2 PO 3- 4 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: Perfusion: Massive PTE Cardiac Arrest Ventilation: Severe pul edema Severe pneumonia ARDS Airway obstruction Restriction of lung/thorax: Flail chest Pneumothorax Hemothorax

4. Muscular defects: Severe hypokalemia Myasthenic crisis
5. Failure of Mechanical Ventilator CONTROL COMPONENT PROBLEMS: CNS: Drugs (Anesthetics, Sedatives) Trauma Stroke 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: COPD Advanced ILD Restriction of thorax/chest wall: Kyphoscoliosis, Arthritis Fibrothorax Hydrothorax Muscular dystrophy Polymyositis

Causes of Chronic Respiratory Acidosis
CONTROL COMPONENT PROBLEMS: 1. CNS: Obesity Hypoventilation Syndrome Tumours Brainstem infarcts Myxedema Ch sedative abuse Bulbar Poliomyelitis 2. Spinal Cord & Peripheral Nerves: Poliomyelitis Multiple Sclerosis ALS Diaphragmatic paralysis

Manifestations of Resp Acidosis
NEUROMUSCULAR: Related to cerebral A vasodilatation &  Cerebral BF Anxiety Asterixis Lethargy, Stupor, Coma Delirium Seizures Headache Papilledema Focal Paresis Tremors, myoclonus

Manifestations of Resp Acidosis
CARDIOVASCULAR: Related to coronary vasodilation Tachycardia Ventricular arrythmias (related to hypoxemia and not hypercapnia per se) BIOCHEMICAL ABNORMALITIES:  CO2  Cl-  PO43-

to Respiratory Acidosis
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: Decreased alv ventilation by decrease in pH mediated ventilatory drive 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 Non Gap Metabolic M - Methanol
U - Uremia D - DKA P - Paraldehyde L - Lactic Acidosis E - Ehylene Glycol S - Salicylate Non Gap Metabolic Acidosis Hyperalimentation 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 % Most recommendations favour use of base when pH < or HCO3 < 8-10 meq/L.

How to treat? Rx Undelying Cause HCO3- 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 mortality 1)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
H+ loss: 1) 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;

H+ movement into cells Hypokalemia
2) HCO3- Retention: Massive Blood Transfusion Ingestion (Milk-Alkali Syndrome) Admn of large amounts of HCO3- 3) H+ movement into cells Hypokalemia Black RM. Intensive Care Medicine 2003;

Clinical features Adrogue et al, NEJM 1998; 338(2):

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 of both NaCl & KCl.

Dialysis Adjunct Therapy
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

Case 1 30 year old female with sudden onset of dyspnea.
----- XXXX Diagnostics Gas Report Blood Case 1 o Measured 37.0 C pH 7.523 pCO2 30.1 mm Hg pO2 105.3 Calculated Data HCO3 act 22 mmol / L O2 Sat 98.3 % pO2 (A - a) 8 mm Hg  pO2 (a / A) 0.93 Entered FiO2 21.0 30 year old female with sudden onset of dyspnea. No Cough or Chest Pain Vitals normal but RR 26, anxious.

Case 2 60 year old male smoker with progressive respiratory distress
----- XXXX Diagnostics Blood Gas Report Measured o 37.0 C pH 7.301 pCO2 76.2 mm Hg pO2 45.5 Calculated Data HCO3 act O2 Sat 35.1 mmol / L 78% pO2 (A - a) 9.5 mm Hg  pO2 (a / A) 0.83 Entered FiO2 21 % Case 2 60 year old male smoker with progressive respiratory distress and somnolence.

Case 3 28 year old diabetic with respiratory distress fatigue and
----- XXXX Diagnostics Blood Measured pH pCO2 pO2 Calculated HCO3 act O2 Sat pO2 (A - a) pO2 (a / A) Entered FiO2 Gas Report Case 3 o 37.0 C 23 mm Hg 110.5 mm Hg Data 14 mmol / L % mm Hg  28 year old diabetic with respiratory distress fatigue and loss of appetite. Data %

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
/vat/acidbase.html#acidbase

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

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

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Presentation on theme: "ACID BASE BALANCE Life is a struggle, not against sin, not against Money Power . . but against hydrogen ions. --H.L. Mencken."— Presentation transcript:

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