Acid Base Disorders Peter Seha
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Transcript of Acid Base Disorders Peter Seha
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ACID BASE DISORDERS
Making sense of the basics.
Peter SehaCoffs Harbour Health Campus ED.
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ABG interpretation Not sure?
In a survey conducted at a university teaching hospital,70% of the participating physicians claimed that theywere well versed in the diagnosis of acid-base disordersand that they needed no assistance in the interpretation
of arterial blood gases (ABGs).
These same physicians were then given a series of ABGmeasurements to interpret, and they correctly interpretedonly 40% of the test samples.
Hingston DM. A computerized interpretation of arterial pH and blood gas data: do physicians need it? Respir Care1982;27:809-815.
From: THE ICU BOOK - 2nd Ed. (1998)
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So ! Option 1:
http://www.medcalc.com/acidbase.html
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DIY,Interrupt the ABG with a flow chartassistance till the flow chart becomes yourway of interrupting the ABG , or you have
got your own mental flow chart.
Option 2:
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Definitions.
* Acid:
Substance that is a proton donor (releasesH+ ions).
* Base:
substance that can accept protons H+(protons)
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pH?The negative logarithm (base 10) of the molar concentration of
dissolved Hydronium ions (H3O+)..H+
And that means ?!
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A normal [H+] of 40
nEq/L correspondsto a pH of 7.40.Because the pH is anegative logarithmof the [H+], changesin pH are inverselyrelated to changes
in [H+
] (e.g., adecrease in pH isassociated with anincrease in [H+]).
pH [H+]
7.7 20
7.5 31
7.4 407.3 50
7.1 80
7.0 1006.8 160
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The Buffer ..Hydrogen Ion Regulation
A buffer is a solution which has the ability
to minimize changes in pH when an acidor base is added.
Co2+H20 H2Co3 HCO3- + H+
Proteins
Haemoglobin
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Co2+H20 H2CO3 HCO3- + H+
Sorenson:
Henderson :
[H+] + [HCO3-] = K x ([CO2] + [H2O])
Henderson-Hasselbalch Equation:pH = pK + log ( [HCO3-] / [CO2])
or
pH = 6.1 + log [HCO3-] /(0.03 X PCO2)
http://www.acid-base.com/terminology.phphttp://www.acid-base.com/terminology.phphttp://www.acid-base.com/terminology.phphttp://www.acid-base.com/terminology.php -
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Co2+H20 H2CO3 HCO3- + H+
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HCO3- elimination is controlled bythe kidneys. Decreases(increases) in pH result inincreases (decreases) inHCO3-. It takes hours todays for the renal system tocompensate for changes inpH.
Co2+H20 H2CO3 HCO3- + H+
CO2 elimination (ventilation)is controlled by thelungs (respiratorysystem). Decreases(increases) in pH resultin decreases(increases) in PCO2within minutes.
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Compensation .PCO2/[HCO3-] Ratio
When a primary acid-base disturbance alters one
component of the PCO2/[HCO3- ]ratio, the compensatory
response alters the other component in the samedirection to keep the PCO2/[HCO3- ] ratio constant.
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Compensatory changes:
When the primary disorder is metabolic (i.e., a change in
[HCO3 - ],the compensatory response is respiratory (i.e.,a change in PCO2), and vice-versa.
It is important to emphasize that compensatoryresponses limit changes in pH (i.e., They can not over
do it.)
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Serum Anion Gap
Law of conservation of charge:
Cations+= Anions
The sum of Cations MUST equal the sum of Anion.
Na+ + K+
+
Ca++ + Mg++ + possibleothers+.
Cl- + HCO3-
+
SO42- + PO43- +Ketoacids-+ lactate- +Albumin- + possible
others-.
Cl- + HCO3- + UANa + + K+ + UC
[Na+ + K+] [Cl- + HCO3-] [UA-] [UC+] AG
[Na+ + K+] [Cl- + HCO3-]AG
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Na+ [Cl- + HCO3-]AG [UA-] [UC+]
AG is normally in the range from 8-16.
AG > 16 = High Anion Gap.
A high anion gap acidosis is caused by the addition of a H+ &
Unmeasured anion- .
The H+ is buffered by HCO3- , and therefore the HCO3-
concentration falls.
The unmeasured anion-
increases ..based on the equationabove.
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Base Excess :The quantity of Acid required to return the plasma in-vitro to a normal
pH (7.40) under standard conditions
So, a base excess of 15 means ..,and a base excess of -15 means?
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Clinical condition Acid/Base Disorder
Hypotension/Shocked:
Vomiting:
Sever Diarrhea:
Renal Failure:
Sepsis:
COPD:
Metabolic acidosis.
Metabolic alkalosis.
Metabolic acidosis.
Metabolic acidosis.
Metabolic acidosis+
Respiratory alkalosis.
Respiratory acidosis.
Practically speaking
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Clinical condition Acid/Base Disorder
Pregnancy
Pulmonary Embolus
Reduced GCS
Respiratory alkalosis.
Respiratory alkalosis.
I do not know Here the ABG isan important part of the clinicalexamination till collateral historyis available.
That is not the only scenario
where ABG /VBG of importance.It is still a corner stone ofassessment of severity and thefollow up of already diagnosedconditions.
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ACIDOSISeffect
Affinity of Hb to O2.
Serum K+ ..(not total K+ )
Myocardial contractility (pH< 7.1)
Phospholipase activity and Mitochondrial apoptosis.
Although the presence of acidosis is often associated with a poorprognosis, the presence of acidosis per se usually has few clinical
significant effects, and it is the nature and severity of the underlyingillness that determines its outcome.
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Metabolic AcidosisPCO2 ?
NORMAL ANION GAP
Due to loss of HCO3, generally with Cl, hence
normal anion gap
K+
Mineralocorticoidsdef. eg: Addison.
Addition of CL asthe anion of an acid,eg: NH4Cl.
Lower GIT loss.
Renal :CA inhibitor.
RTA
Urinary diversion
Vesico-colic.
uretroenterostomy
Mnemonic: USEDCARP
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U reto-enterostomy.
Small bowel Fistula.
Extra Chloride.
Diarrhea.
Carbonic Anhydrase Inhibitors.
Addisions disease.
RTA
Pancreaticfustula.
PCO2
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Osmolar Gap:The Osmolar Gap is another important diagnostic tool that can be used in
differentiating the causes of elevated anion gap metabolic acidosis. The majorosmotic particles in plasma are Na+ , Cl- , HCO3-, urea and glucose and assuch, plasma osmolarity can be estimated as follows:
Plasma osmolarity = 2(Na) + glucose + ureaNote that because Cl- and HCO3- are always bound to Na, their contributions toosmolarity are estimated by doubling the Na concentration.
Osmolar Gap = Measured Posm Calculated PosmThe normal osmolar gap is 10-15 mmol/L .The osmolar gap is increased in thepresence of low molecular weight substances that are not included in theformula for calculating plasma osmolarity.Common substances: Ethanol, Ethylene glycol, Methanol, Acetone, Isopropyl
Ethanol and Propylene Glycol.
In a patient suspected of poisoning, a high osmolar gap (particularly if 25)
with an otherwise unexplained high anion gap metabolic acidosis is suggestiveof either methanol or ethylene glycol intoxication.
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Treating metabolic acidosis Treat the cause first before the acidosis.
DKA Alcholic Ketoacidosis Ethylene glycol/methanol Salicylates
K+ watch out! NaHCO3:
UsuallyNO Hypokalemia, Ionised Serum Ca++
Volume overload (High Solute load) CSF acidosis, Hypercapnia,Tissue hypoxia: lt-shift of hemoglobin-oxygen
dissociation curve. Overshoot alkalosis Inactivate Ca++ and Adrenaline if administered through the same IV.
OccasionallyYES: Normal anion gap acidosis, pH< 7.2 with shock or myocardial irritability Cardiac arrest if young children , pregnant women or arrest >15 min. Na channel blocking agent. Eg: Tricyclic antidepressants. Salicylates.Ethylene glycol /Methanol toxicity.
Sever Hyper Kalaemia.
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Respiratory Acidosis
CNS Drug depression of resp. center (eg by opiates, sedatives, anaesthetics) CNS trauma, infarct, haemorrhage or tumour Hypoventilation of obesity (eg Pickwickian syndrome) Cervical cord trauma or lesions (at or above C4 level) High central neural blockade Poliomyelitis Tetanus Cardiac arrest with cerebral hypoxia Nerve or Muscle Disorders Guillain-Barre syndrome
Myasthenia gravis Muscle relaxant drugs Toxins eg organophosphates, snake venom
Various myopathies Lung or Chest Wall Defects Acute on COAD Chest trauma -flail chest, contusion, haemothorax Pneumothorax Diaphragmatic paralysis or splinting Pulmonary oedema Adult respiratory distress syndrome Restrictive lung disease
Aspiration Airway Disorders Upper Airway obstruction Laryngospasm Bronchospasm/Asthma External Factors Inadequate mechanical ventilation
Causes:
Hypoventilation
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ALKALOSISeffect
The same as those of administration of HCO3 except it does not causehyperosmolarity :
Ionised Serum Ca++
Hypokalemia, CSF acidosis,
Hypercapnia,Tissue hypoxia.
Shift to the left of hemoglobin-oxygen dissociation
curve (increased Hb affinity to O2).
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Volume status (ECFV)
Metabolic AlakalosisPCO2>45,HCO3 >28, B.E >+2.
1-Upper GIT losses: Most common in ED.
2-Renal. Eg Diuretics.
Treatment :
Treat the cause
Watch out for K+.
0.9% NaCl.
Normal vol. or Volume overload
Urinary CL > 15 mml/L
1- Mineralocorticoids excess (Hyperaldosteronism, Cushings.)
2- Oedema states.
3- Rare:
Bartters syndrome /Gitelmanss syndrome.
Treatment :
Treat the cause.
Sprionolactone
0.9% NaCl ..detrimental.
Volume depletedUrinary CL < 10 mmol/L
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1. Central Causes (direct action via respiratorycentre)
Head Injury Stroke Anxiety-hyperventilation syndrome (psychogenic) Other 'supra-tentorial' causes (pain, fear, stress,
voluntary) Various drugs (eg analeptics, propanidid, salicylate
intoxication) Various endogenous compounds (eg progesterone
during pregnancy, cytokines during sepsis, toxins inpatients with chronic liver disease)
2. Hypoxaemia (act via peripheralchemoreceptors)
Respiratory stimulation via peripheral chemoreceptors 3. Pulmonary Causes (act via intrapulmonary
receptors) Pulmonary Embolism Pneumonia Asthma Pulmonary oedema (all types) 4. Iatrogenic (act directly on ventilation) Excessive controlled ventilation
Respiratory Alkalosis
Hyperventilation
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Resources:
Hingston DM. A computerized interpretation of arterial pH and blood gas data: do physicians need it? Respir Care1982;27:809-815.
THE ICU BOOK - 2nd Ed. (1998)
Text book of Adult Emergency Medicine 3rd efition.
ABG interpretation workshops Coffs Harbour Health Campus ED
Acid-Base , fluids , and electrolytes made rediculously simple. 2nd edition.
http://www.anaesthesiamcq.com/AcidBaseBook
http://www.acid-base.com/
http://www.anaesthesiamcq.com/AcidBaseBookhttp://www.acid-base.com/http://www.acid-base.com/http://www.acid-base.com/http://www.acid-base.com/http://www.anaesthesiamcq.com/AcidBaseBook