ACID BASE DISORDERS

Making sense of the basics.

Peter Seha Coffs Harbour Health Campus ED.

ABG interpretation Not sure?

In a survey conducted at a university teaching hospital, 70% of the participating physicians claimed that they were well versed in the diagnosis of acid-base disorders and that they needed no assistance in the interpretation of arterial blood gases (ABGs). These same physicians were then given a series of ABG measurements to interpret, and they correctly interpreted only 40% of the test samples.
Hingston DM. A computerized interpretation of arterial pH and blood gas data: do physicians need it? Respir Care 1982;27:809-815.
From: THE ICU BOOK - 2nd Ed. (1998)

So !

Option 1:

http://www.medcalc.com/acidbase.html

Option 2:
DIY,Interrupt the ABG with a flow chart assistance till the flow chart becomes your way of interrupting the ABG , or you have got your own mental flow chart.

Definitions.

* Acid: Substance that is a proton donor (releases H+ ions). * Base: substance that can accept protons H+ (protons)

pH?
The negative logarithm (base 10) of the molar concentration of dissolved Hydronium ions (H3O+)..H+

And that means ?!

A normal [H+] of 40 nEq/L corresponds to a pH of 7.40. Because the pH is a negative logarithm of the [H+], changes in pH are inversely related to changes in [H+] (e.g., a decrease in pH is associated with an increase in [H+]).

pH 7.7 7.5 7.4 7.3 7.1 7.0 6.8

[H+] 20 31 40 50 80 100 160

The Buffer ..Hydrogen Ion Regulation

A buffer is a solution which has the ability to minimize changes in pH when an acid or base is added.
Co2+H20 H2Co3 HCO3- + H+

Proteins

Haemoglobin

Sorenson: Co2+H20 Henderson : H2CO3 HCO3- + H+

[H+] + [HCO3-] = K x ([CO2] + [H2O])

Henderson-Hasselbalch Equation: pH = pK + log ( [HCO3-] / [CO2]) or pH = 6.1 + log [HCO3-] /(0.03 X PCO2)

Co2+H20

H2CO3

HCO3- + H+

Co2+H20

H2CO3

HCO3- + H+

CO2 elimination (ventilation) is controlled by the lungs (respiratory system). Decreases (increases) in pH result in decreases (increases) in PCO2 within minutes.

HCO3- elimination is controlled by the kidneys. Decreases (increases) in pH result in increases (decreases) in HCO3-. It takes hours to days for the renal system to compensate for changes in pH.

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 same direction to keep the PCO2/[HCO3- ] ratio constant.

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 compensatory responses limit changes in pH (i.e., They can not over do it.)

Serum Anion Gap

Law of conservation of charge: Cations+ = Anions The sum of Cations MUST equal the sum of Anion.

Na+ + K+ + Ca++ + Mg++ + possible others+.

Cl- + HCO3+ SO42- + PO43- + Ketoacids-+ lactate- + Albumin- + possible others-. Cl- + HCO3- + UA [UA-] [UC+] [Na+ + K+] [Cl- + HCO3-]

Na + + K+ + UC [Na+ + K+] [Cl- + HCO3-]

AG

AG

AG

Na+ [Cl- + HCO3-]

[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 HCO3concentration falls.

The unmeasured anion- increases ..based on the equation above.

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?

Practically speaking
Clinical condition Acid/Base Disorder

Hypotension/Shocked:

Metabolic acidosis.

Vomiting:

Metabolic alkalosis.

Sever Diarrhea:

Metabolic acidosis.

Renal Failure:

Metabolic acidosis.

Sepsis:

Metabolic acidosis+ Respiratory alkalosis.

COPD:

Respiratory acidosis.

Clinical condition

Acid/Base Disorder

Pregnancy

Respiratory alkalosis.

Pulmonary Embolus

Respiratory alkalosis. I do not know Here the ABG is an important part of the clinical examination till collateral history is available. That is not the only scenario where ABG /VBG of importance. It is still a corner stone of assessment of severity and the follow up of already diagnosed conditions.

Reduced GCS

ACIDOSIS
effect
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 poor prognosis, the presence of acidosis per se usually has few clinical significant effects, and it is the nature and severity of the underlying illness that determines its outcome.

Metabolic Acidosis
PCO2<35,HCO3 <22, B.E < -2.
Na+ [Cl- + HCO3-] [UA-] [UC+]

AG

ANION GAP ( H+ which consumes HCO3 )

NORMAL ANION GAP Due to loss of HCO3, generally with Cl, hence normal anion gap

Lactic acid: (causes) Ketoacids: (causes) Uric acid/Sulfates/phosphates: (CRF) Exogenous: Acetyl Salicylic acid-late. Formic acid >? Glycolic acid/oxalic acid > ? Mineralocorticoids def. eg: Addison. Addition of CL as the anion of an acid, eg: NH4Cl.

K+
Lower GIT loss. Renal :CA inhibitor. RTA Urinary diversion Vesico-colic.
uretroenterostomy

Mnemonic: USEDCARP

PCO2<35,HCO3 <22, B.E < -2.

Na+ [Cl- + HCO3-] [UA-] [UC+]

AG

ANION GAP ( H+ which consumes HCO3 )

NORMAL ANION GAP Due to loss of HCO3, generally with Cl, hence normal anion gap

Methanol Uremia DKA Paraldahyde, propylene glycol Isoniazide, Iron Lactic acidosis Ethylene glycol, ethanol Salicylates, starvation ketoacidosis & we need to check the Osmolar Gap

U reto-enterostomy.
Small bowel Fistula. Extra Chloride. Diarrhea.

Carbonic Anhydrase Inhibitors.

Addisions disease. RTA Pancreaticfustula.

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 major osmotic particles in plasma are Na+ , Cl- , HCO3-, urea and glucose and as such, plasma osmolarity can be estimated as follows: Plasma osmolarity = 2(Na) + glucose + urea Note that because Cl- and HCO3- are always bound to Na, their contributions to osmolarity are estimated by doubling the Na concentration. Osmolar Gap = Measured Posm Calculated Posm The normal osmolar gap is 10-15 mmol/L .The osmolar gap is increased in the presence of low molecular weight substances that are not included in the formula 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 suggestive of either methanol or ethylene glycol intoxication.

Treating metabolic acidosis

Treat the cause first before the acidosis.
DKA Alcholic Ketoacidosis Ethylene glycol/methanol Salicylates

K+ watch out! NaHCO3:

Usually NO

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.

Occasionally YES :
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.

Respiratory Acidosis
Causes:
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

Hypoventilation

ALKALOSIS effect
The same as those of administration of HCO3 except it does not cause hyperosmolarity :

Ionised Serum Ca++ Hypokalemia, CSF acidosis, Hypercapnia,Tissue hypoxia. Shift to the left of hemoglobin-oxygen dissociation curve (increased Hb affinity to O2).

Metabolic Alakalosis
PCO2>45,HCO3 >28, B.E >+2.

Volume status ( ECFV)

Volume depleted Urinary CL < 10 mmol/L Normal vol. or Volume overload Urinary CL > 15 mml/L 1- Mineralocorticoids excess (Hyper aldosteronism, Cushings.) 2- Oedema states. 3- Rare: Bartters syndrome /Gitelmanss syndrome.

1-Upper GIT losses: Most common in ED. 2-Renal. Eg Diuretics.

Treatment : Treat the cause Watch out for K+. 0.9% NaCl.
Treatment : Treat the cause. Sprionolactone 0.9% NaCl ..detrimental.

Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre) 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 in patients with chronic liver disease) 2. Hypoxaemia (act via peripheral chemoreceptors) 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

Hyperventilation

Resources:

Hingston DM. A computerized interpretation of arterial pH and blood gas data: do physicians need it? Respir Care 1982;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/