ACID BASE DISORDER in critical care

Download
Share  Add to  Flag Embed
Views:
 
Category: Education
     
 
License:   All Rights Reserved

Presentation Description

No description available.

Comments

 

By: araujo80 (7 month(s) ago)

i find this is quaite clear to me , may i have this presentation.. email : flaviobrandao2006@yahoo.com thank you verry much

 

By: utiek (11 month(s) ago)

your presentation help me understand about acid base disorders

Presentation Transcript

Slide 1:

ACID BASE DISORDER Ubaidur Rahaman Senior Resident, CCM, SGPGIMS Lucknow, India

Slide 2:

Life is struggle, not against sin, not against money power…. but against Hydrogen ion. - H .L. MENCKEN

Acid base physiology in body:

Acid base physiology in body Solution- H2O ; 60% of body weight H2O ↔ H + + OH - All H + are derived from water dissociation In pure water, at 25ºC [H + ] and [OH - ] = 1Ë£10 -7 mmol/L and pH= 7 temperature ↑- pH ↓ temperature ↓- pH ↑ pH : ICF= 6.8-7.0, ECF= 7.4 ICF- relatively impermeable to ionic material, pH remains constant despite dramatic change in ECF pH ECF- pH affected due to fluid, electrolytes and CO2

Slide 4:

Effect of changes in these factors H2O↔ H+ + OH- CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- Factors determining [H+] of ECF 1. Strong ions Na, K, Ca, Mg, Cl, SO4, Lactate, Keto ions 2. Weak acids - Albumin, Pi 3. CO2

These factors must obey three distinct laws:

These factors must obey three distinct laws Electrical neutrality sum of all cations = sum of all anions 2. Mass conservation substances remain constant unless added, removed, generated or destroyed 3 . Dissociation equillibrium of all incompletely dissociated substances must be satisfied, according to law of mass action

Therefore :

Therefore [Na + K + Ca+ Mg] – [ Cl+ SO4+ Lactate + Keto ions] – [ HCO3+ Albumin + Pi] = 0 SID = HCO3+ Atot ∆ SID / Atot ∆ [H+] ↑ SID or ↓Atot ↓[H+] – alkalosis ↓ SID or ↑Atot ↑[H+]-- acidosis ↓albumin and ↓Pi may mask the effect of increased acid

Major sources of acids in body:

Major sources of acids in body Volatile acid-CO2 result of oxidative metabolism 12,500 meq of H + / day excreted through lungs buffered by Hb CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- CO2 dHb-histidine residue Cl Haldane effect Chloride shift CO2 also buffered directly by Hb and plasma proteins Also carried in dissolved form

Major sources of acids in body:

Major sources of acids in body Metabolic acids 20-80 meq of H + /day buffered by HCO3 and weak acids( albumin and Pi) excreted through kidney

Slide 9:

ACID BASE ANALYSIS

Historical overview of acid- base analysis:

Historical overview of acid- base analysis Acid base analysis Bicarbonate centered approach Stewart strong ion equation Constable simplified Strong ion equation Hendersen- Hasselbalch equation Singer- Hastings Buffer base Strong ion approach HCO3/ PaCO2 equation Base excess equation Boston approach Copenhegen approach Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches Ira Kurtz, Jeffrey Kraut, Vahram Ornekian and Minhtri K. Nguyen Am J Physiol Renal Physiol 294:F1009-F1031, 2008

Slide 11:

Is it feasible to measure every possible fixed acid? No. BUT indirectly can estimate the total amount of excess fixed acid 1. Fixed acids in ECF- buffered predominantly by bicarbonate One bicarbonate molecule will react with one H+ molecule produced by one molecule of fixed acid HCO3 will decrease by one molecule for every molecule of fixed acid present. Number of fixed acid = ∆ [HCO3] from baseline PCO2/ HCO3 APPROACH ( BOSTON APPROACH) Schwartz and colleague, Tufts University, Boston, USA Normogram was developed using retrospective data from large population of patients

ACID- BASE NORMOGRAM USING BOSTON APPROACH:

ACID- BASE NORMOGRAM USING BOSTON APPROACH

Slide 13:

Metabolic Acidosis- ∆PaCO2= 1.5 Ë£ ∆ HCO3 + 8 ± 2 Alkalosis- ∆PaCO2= 0.7 Ë£ ∆ HCO3 + 21 ± 2 Respiratory acidosis Acute - ∆HCO3= 1 Ë£ (∆ PaCO2/10) Chronic - ∆HCO3= 4 Ë£ (∆ PaCO2/10) Respiratory alkalosis Acute - ∆HCO3= 2 Ë£ (∆ PaCO2/10) Chronic- ∆HCO3= 4 Ë£ (∆ PaCO2/10) ACID- BASE calculation USING BOSTON APPROACH

Slide 14:

DOES ∆HCO3 truly QUNTIFIES METABOLIC COMPONENT? Is PaCO2 and HCO3 are independent of one another? NO PCO2 also will change the bicarbonate + Buffering in whole blood by HCO3 ≠ buffering In the ECF ( Blood is a better buffer then the whole ECF because of its content of the buffer Hb.) In ECF apart from HCO3, other non volatile buffer- albumin, Pi are also present Boston approach assesses compensation as another primary disorder

Quantification of metabolic component independent of acute change in PCO2:

Quantification of metabolic component independent of acute change in PCO2 BUFFER BASE (BB) 1948 – Singer and Hastings BB = fixed cations – fixed anions = Na + K - Cl BB = [HCO3- ] + [ A- ] [ A- ] = non bicarbonate buffer anions= Hb, Albumin, Pi Fixed ions= strong ions Acute change in PCO2 ↔ equal and opposite change in [HCO3-] and [ A-] BB remains unaffected Buffer solution of two or more chemicals that minimizes changes in pH in response to addition of acid or base. most buffers are weak acids –HCO3- , Hb, Albumin, Pi

Quantification of metabolic component independent of acute change in PCO2:

Quantification of metabolic component independent of acute change in PCO2 Standardized base excess ( SBE) – serum base excess to negate dynamic effect of RBC in acid- base and electrolyte exchange. base deficit/ excess(BDE) 1948 – Sigaard- Anderson amount of strong acid or base that must be added to whole blood in vitro to restore the pH to 7.4 while the PCO2 is kept at 40 mmHg at 38C Blood-gas machines calculate SBE as: SBE = 0.9287 * (HCO3- - 24.4 + (14.83 * (pH – 7.4) based on data derived retrospectively from large population of patients normogram was developed

Acid- base Normogram and calculation based on BDE approach ( Copenhegen approach):

Acid- base Normogram and calculation based on BDE approach ( Copenhegen approach) Metabolic acidosis - ∆PaCO2= ∆ SBE alkalosis- ∆PaCO2= 0.6* ∆ SBE Respiratory Acute acidosis/ alkalosis -∆ SBE= 0 chronic acidosis- ∆ SBE= 0.4* ∆PaCO2

OK, We can detect quantitatively the metabolic acid- base disorder, but can we detect the cause?:

OK, We can detect quantitatively the metabolic acid- base disorder, but can we detect the cause? Metabolic acidosis hyperchloremic vs unmeasured anions( lactic/ ketoacids) Metabolic alkalosis hypochloremic vs hypoalbuminemic Hypoalbuminemic critically ill patient with lactic acidosis may have a normal pH, HCO3 and BE We can miss the presence of acid- base disorder Leading to Inappropriate and inadequate therapy

ANION GAP(AG) Emmett and Narins:

ANION GAP(AG) Emmett and Narins Based on law of electroneutrality AG= [Na + K ] – [Cl+ HCO3] = A + UMA Measured Cations [Na] [K] Measured anions [Cl] [HCO3] A - UMA - A - = weak acids= Albumin, Pi UMA= unmeasured anions = unmeasured strong anions = lactate, keto ions Normal AG= 12 ± 4= A - UMA= 0 } Lactic/ keto acidosis= UMA AG> 16

But if [A-] are reduced (hypoalbuminemia, hypophosphatemia) AG may be normal in lactic/ketoacidosis:

But if [ A - ] are reduced (hypoalbuminemia, hypophosphatemia) AG may be normal in lactic/ketoacidosis CORRECTED ANION GAP FIGGE AND COLLEAGUE Calculated AG+ 2.5 ( 4.5 - s. albumin)

BUT we are still using HCO3 in the equation which may be affected independent to metabolic disturbance :

BUT we are still using HCO3 in the equation which may be affected independent to metabolic disturbance What is the answer? BDE and AG approach may underestimate extent of metabolic disturbance

STRONG ION APPROACH 1878- Stewart:

STRONG ION APPROACH 1878- Stewart Based on law of electroneutrality, mass conservation and dissociation equillibrium SID = [Na + K +Ca + Mg ] – [Cl + UMA] = BB = HCO3 + A TOT Strong cations [Na] [K] [Ca] [Mg] HCO3 Strong anions [Cl] [SO4] [UMA] A TOT A TOT = weak acids= Albumin, Pi UMA= unmeasured anions = unmeasured strong anions = lactate, keto ions Normal SID= 40-44 meq/L= HCO3 + A TOT UMA= 0 }

STRONG ION GAP:

STRONG ION GAP SIDa = [Na + K +Ca + Mg ] – [Cl ] Strong cations [Na] [K] [Ca] [Mg] HCO3 [UMA] Strong anions [Cl] [SO4] A TOT A TOT = weak acids= Albumin, Pi UMA= unmeasured anions = unmeasured strong anions = lactate, keto ions SID Gap = SIDe – SIDa Normal SID Gap = 0 } SIDe = HCO3 + A TOT } If SID Gap < 0 – UMA SID Gap = UMA

EFFECT OF CHANGE IN STRONG ION:

EFFECT OF CHANGE IN STRONG ION

Slide 25:

Metabolic Acidosis ↓ SID water excess - dilutional ↓ Na ↑ Cl, Lactate, keto ions, ↑A TOT ↑ Pi, Albumin Metabolic Alkalosis ↑ SID water deficit - contraction ↑ Na ↓ Cl, Lactate, keto ions, ↓ A TOT ↓ Pi, Albumin

BASE DEFICIT/ EXCESS (BDE) GAP Gilfix and colleague:

BASE DEFICIT/ EXCESS (BDE) GAP Gilfix and colleague Recalculation of BDE using Strong ion, free water and albumin BDE Gap = BDEmeas – BDE calc Normal BDE gap = 0 If gap + = UMA BDE NaCl = [Na + Cl] – 38 BDE Alb = 2.5 [ 4.2 – s. Alb] BDEcalc = BDE NaCl - BDE Alb

Slide 27:

Na- 117, K-3.9 Ca-3, Mg- 1.4 Cl- 92 Pi- 0.6 mmol/dl Albumin- 0.6 g/dl pH- 7.33 PaCO2-30 HCO3- 15 SBE: -10 AG=10, corrAG=19.5 ∆PaCO2= ∆BE= no respiratory component Impression: high AG metabolic acidosis with respiratory compensation Is this that simple as it appears? Consider following patient :

Slide 28:

ACIDOSIS Excess free water- dilutional Hyperchloremia UMA- lactate/ fixed renal acid/ ketoacids ALKALOSIS: Hypoalbuminemia hypophosphatemia BDENacl= (117-92) – 38 = -13 BDE alb = 2.5 ( 4.2- 0.6) = 9.5 BDEcalc = (-13) - (9.5) = -22.5 BDE gap = (-10) –( -22.5) = 12.5 = UMA corrCl= 110 Let’s re-evaluate it with BDE gap approach : ph and BDE does not mirror this severity of metabolic disturbance. Owing to alkalinizing force – hypoalbuminemia, and hypophosphatemia Knowing this will definitely improve our management strategy Forces at play

Slide 29:

Na-144 K- 4 Cl- 110 pH- 7.28 Pco2- 24 HCO3- 8 BE -16 Lactate- 11 Urea- 10 Creatinine- 2 Albumin- 4 Impression: high AG metabolic acidosis- lactic acidosis with respiratory compensation The patient is aggressively volume resuscitated and brought to the operating room. A blood gas and serum chemistry are taken on the patient, now mechanically ventilated in the intensive care unit A 45-year-old man RTA, is bleeding, pulse is weak, Blood pressure is 90/50 mm Hg, heart rate is 120 beats/min, respiratory rate is 36/min, and temperature is 35°C. Blood chemistry and ABG is following: BDENacl= (144-110) – 38 = -4 BDE alb = 2.5 ( 4.2- 4.0) = 0.5 BDEcalc = (-4) - (0.5) = -4.5 BDE gap = (-16) –( -4.5) = -11.5 = UMA= lactate ∆PaCO2= ∆BE= no respiratory component

After 12 hours, blood chemistry and gas is following::

After 12 hours, blood chemistry and gas is following: Impression- hyperchloremic metabolic acidosis Na-148, K- 3 Cl- 120 lactate 5 pH 7.33 Pco2 35 HCO3- 18 BE -11 urea 10 creatinine 2 albumin 2 Is the patient still under-resuscitated? Let’s re-evaluate ABG using BDE approach Patient is adequately resuscitated but with NS– leading to hyperchloremia BDENacl= (148-120) – 38 = -10 BDE alb = 2.5 ( 4.2- 2.0) = 5.0 BDEcalc = (-10) - (5) = -15 BDE gap = (-11) –( -15) = -5= UMA= latate ∆PaCO2 <∆BE= mild respiratory acidosis

Slide 31:

THANKYOU