Acid Base Disorders Peter Seha

8/2/2019 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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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 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



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

Acid Base Disorders Peter Seha

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