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3-day certification course in ECG rhythm and 12 lead ECG interpretation

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ICS: Proforma for Brain stem death testing

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ICS: Proforma for Brain stem death testing

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Picture boards to aid communication: available in multiple languages

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Picture boards to aid communication: available in multiple languages

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Communication cue cards available in multiple languages

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Communication cue cards available in multiple languages

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Cue Cards In Community Languages | Eastern Health

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Print off any one of the 11 categories you need, which are divided into: Basic, Instructions, Family, Community, Descriptions, Medical, Objects, People, Religion, Time & Dental and includes charts indicating days of the week, months of the year, level of pain scale.

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Senior 5 - Band 6 shadow in charge shifts

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Senior 5 - Band 6 shadow in charge shifts

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February 2024: Practice Education Coaching rota

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February 2024: Practice Education Coaching rota

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January 2024: Practice Education Coaching rota

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January 2024: Practice Education Coaching rota

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Preparation of Sodium Bicarbonate - Shortage of 1.26%

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Preparation of Sodium Bicarbonate - Shortage of 1.26%

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A really clear concise article regarding specific aspects of cardiac output & monitoring

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Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.

Afterload is the force or load against which the heart has to contract to eject the blood.

Contractility is the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction.

Poor Left Ventricular Function

The waveform below demonstrates the response to a positive inotrope. In the first (left) screenshot, the patient had a 'rounded' flow waveform, with a low Peak velocity (PV) and stroke volume ( SV), possibly indicating left ventricular failure. The patient was not fluid responsive and following administration of a positive inotrope, both PV and SV increase (right screenshot). ​

Systemic Vascular Resistance

Systemic vascular resistance (SVR) is the resistance to blood flow offered by all of the systemic vasculature [2]. An increase in SVR depends on the degree of sympathetic stimulation which itself depends on the degree of sympathetic activation, responsiveness of the vasculature, the number of vascular beds involved and the relative series and parallel arrangement of these beds to each other. Changes in blood viscosity also affect SVR.

SVR is an unreliable indicator of left ventricular afterload [2] since it reflects only peripheral vasomotor tone and not left ventricular systolic wall force. Discordant changes in left ventricular afterload and SVR can occur during pharmacological interventions as shown by Lang et al. They conclude "In the clinical setting, changes in SVR do not necessarily reflect left ventricular loading conditions since the true measure of ventricular afterload must consider the interaction of factors internal and external to the myocardium."

References

1. Klabunde, R.E., Cardiovascular Physiology Concepts. 2005.Philadelphia. Lippincott Williams & Wilkins
2. Lang et al 1986​. Systemic vascular resistance: an unreliable index of left ventricular afterload. Circulation 74:1114-1123

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Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. Afterload is the force or load against which the heart has to contract to eject the blood. Contractility is the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction.

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Charlie Gregory's checklist formulated from the Wessex Neuro guidelines (2016/2017)

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Tracheostomy red flags (National Tracheostomy Safety Project)

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Laryngectomy Emergency Algorithm (National Tracheostomy Safety Project)

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Tracheostomy Emergency Algorithm (National Tracheostomy Safety Project)

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Guidance for principles for caring for Patients in side rooms

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Guidance for principles for caring for Patients in side rooms

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December: Practice Education Coaching rota

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December: Practice Education Coaching rota

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Draeger V800 Paediatric set up guide: Infographic

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Draeger V800 Paediatric set up guide: Infographic

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Draeger V800 NIV set up guide: Infographic

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Draeger V800 NIV set up guide: Infographic

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Flolan guidance for use in Continuous Renal Replacement Therapy: Anticoagulation

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Flolan guidance for use in Continuous Renal Replacement Therapy: Anticoagulation

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Credit to Professor Rob Galloway - Course tools adapted to suit Critical care B6 development programme

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Critical Care SRH & WGH B6 Development programme

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Critical Care SRH & WGH B6 Development programme

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iris learning - university hospitals sussex nhs foundation trust: log in to the site

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iris learning - University Hospitals Sussex NHS Foundation Trust: Log in to the site

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B6 Development day pre:work

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Sepsis introduction: CVS study day Nov 2023

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Sepsis introduction: CVS study day Nov 2023

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University of Brighton updated Skills guidance 2023-2024

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University of Brighton updated Skills guidance 2023-2024

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Trust Staff Update Nov 2023: Covid testing

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Trust Staff Update Nov 2023: Covid testing

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Paediatric transfer checklist: Time Critical

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Paediatric transfer checklist: Time Critical

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Performing suctioning on Paediatrics: Closed circuit

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Performing suctioning on Paediatrics: Closed circuit

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Paediatric Sepsis: Quick reference guide

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Paediatric Sepsis: Quick reference guide

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Sedation guidance: weaning sedation in a Paediatric patient

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Sedation guidance: weaning sedation in a Paediatric patient

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Guidance for secretion clearance in the intubated Paed

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Guidance for secretion clearance in the intubated Paed

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Paediatric Intubation checklist: Including ETT sizes

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Paediatric Intubation checklist: Including ETT sizes

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Guidance for the safe handover of a Paediatric patient: SORT

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Guidance for the safe handover of a Paediatric patient: SORT

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Paediatric Glucose concentrations & calculations

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Paediatric Glucose concentrations & calculations

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SORT guidance

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Paediatric guidelines: Management of severe Asthma

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Paediatric guidelines: Management of severe Asthma

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SORT guidance

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Paediatric anaphylaxis guidelines: Resus council 2021

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Paediatric anaphylaxis guidelines: Resus council 2021

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Cushing Reflex in critically unwell patients

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The Cushing reflex is a physiological nervous system response to acute elevations of intracranial pressure (ICP), resulting in the Cushing triad of widened pulse pressure (increasing systolic, decreasing diastolic) bradycardia, and irregular respirations.

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Cushing Reflex (triad) in critically ill patients

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Improve Article 👀

What is an ECG?

ECG is the abbreviated term for an electrocardiogram. It is used to record the electrical activity of the heart from different angles to both identify and locate pathology. Electrodes are placed on different parts of a patient's limbs and chest to record the electrical activity.

Parts of the ECG explained

P waves

P waves represent atrial depolarisation.

In healthy individuals, there should be a P wave preceding each QRS complex.

PR interval

The PR interval begins at the star t of the P wave and ends at the beginning of the Q wave.

It represents the time for electrical activity to move between the atria and the ventricles.

QRS complex

The QRS complex represents the depolarisation of the ventricles.

It appears as three closely related waves on the ECG (the Q, R and S wave).

ST segment

The ST segment starts at the end of the S wave and ends at the beginning of the T wave.

The ST segment is an isoelectric line representing the time between depolarisation and repolarisation of the ventricles (i.e. ventricular contraction).

T wave

The T wave represents ventricular repolarisation.

It appears as a small wave after the QRS complex.

RR interval

It represents the time between two QRS complexes.

QT interval

It represents the time taken for the ventricles to depolarise and then repolarise.

How to read ECG paper

The paper used to record ECGs is standardised across most hospitals and has the following characteristics:

How the 12-lead ECG works

Understanding the difference between an ECG electrode and an ECG lead is important:

An ECG electrode is a conductive pad attached to the skin to record electrical activity.

An ECG lead is a graphical representation of the heart's electrical activity which is calculated by analysing data from several ECG electrodes.

A 12-lead ECG records 12 leads, producing 12 separate graphs on a piece of ECG paper.

Only 10 physical electrodes are attached to the patient to generate the 12 leads.

Electrodes

An ECG electrode is a conductive pad attached to the skin to record electrical activity.

The data gathered from these electrodes allows the 12 leads of the ECG to be calculated (e.g. lead I is calculated using data from the electrodes on both the right and left arm).

The electrodes used to generate a 12-lead ECG are described below.

Chest electrodes

Table 1. The chest electrodes and their placement.

Limb electrodes

There are four limb electrodes.

Table 2. The limb electrodes and their placement

Leads

An ECG lead is a graphical representation of the heart's electrical activity calculated by analysing data from several ECG electrodes.

Chest leads

Table 3. The chest leads.

Other leads

Table 4. Other leads.

The shape of the ECG waveform

Each lead's ECG recording is slightly different in shape. This is because each lead is recording the heart's electrical activity from a different direction (a.k.a viewpoint).

Each deflection (a.k.a. wave) on the ECG represents the average direction of electrical travel (calculated using the ECG machine's mathematical formulae).

The deflection height represents the amount of electrical activity flowing in that direction (i.e. the higher the deflection, the greater the amount of electrical activity flowing towards the lead).

The lead with the most positive deflection is most aligned with the direction the heart's electrical activity is travelling.

If the R wave is greater than the S wave, it suggests depolarisation is moving towards that lead.

If the S wave is greater than the R wave,it suggests depolarisation is moving away from that lead.

Localising pathology on the ECG

It's important to understand which leads represent which anatomical territory of the heart, as this allows you to localise pathology to a particular heart region.

For example, if there is ST elevation in leads V3 and V4, it suggests an anterior myocardial infarction (MI). You can then combine this with some anatomical knowledge of the heart's blood supply to work out which artery is likely to be affected (e.g. left anterior descending artery).

Cardiac axis

In healthy individuals, the electrical activity of the heart begins at the sinoatrial node then spreads to the atrioventricular (AV) node. It then spreads down the bundle of His and Purkinje fibres to cause ventricular contraction.

Whenever the direction of electrical activity moves towards a lead, a positive deflection is produced.

Whenever the direction of electrical activity moves away from a lead, a negative deflection is produced.

The cardiac axis gives us an idea of the overall direction of electrical activity.

Normal cardiac axis

In healthy individuals, you would expect the cardiac axis to lie between -30°and +90º. The overall direction of electrical activity is therefore towards leads I, II and III (the yellow arrow below). As a result, you see a positive deflection in all these leads, with lead II showing the most positive deflection as it is the most closely aligned to the overall direction of electrical spread. You would expect to see the most negative deflection in aVR. This is due to aVR providing a viewpoint of the heart from the opposite direction.

Right axis deviation

Right axis deviation (RAD) involves the direction of depolarisation being distorted to the right (between +90º and +180º).

The most common cause of RAD is right ventricular hypertrophy. Extra right ventricular tissue generates a stronger electrical signal by the right side of the heart. This causes the deflection in lead I to become negative and the deflection in lead aVF/III to be more positive.

RAD is commonly associated with conditions such as pulmonary hypertension, as they cause right ventricular hypertrophy. RAD can, however, be a normal finding in very tall individuals.

Left axis deviation

Left axis deviation (LAD) involves the direction of depolarisation being distorted to the left (between -30° and -90°). This results in the deflection of lead III becoming negative (this is only considered significant if the deflection of lead II also becomes negative). Conduction abnormalities usually cause left axis deviation.

Want to learn more about ECGs?

We have several other articles relevant to ECGs:

Reviewer

Dr Matthew Jackson
Consultant Interventional Cardiologist

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Understanding an ECG | ECG Interpretation | Geeky Medics

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An overview of ECG interpretation, including the different components of a 12-lead ECG, cardiac axis and lots more.

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The Kidneys - An overview to the function of our kidneys

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The Kidneys - An overview to the function of our kidneys

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BJA: Article regarding the guidelines for the management within Critical care of tracheal intubation

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BJA: Article regarding the guidelines for the management within Critical care of tracheal intubation

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We are very excited to welcome our wonderful unit manager back from maternity! Good to have you nack Daisy!

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Farewell and very happy retirement to the wonderful Neil! The unit really will not be the same without you

Goodbye also to Juvi and family as they embark on their new adventure! we wish you all the very best

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November: Practice Education Coaching rota

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November: Practice Education Coaching rota

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Infographic regarding the recording of Inotropes & Vasopressors

Drugs included:

Bolus: Metaraminol, Terlipressin

IVI: Dopamine, Dobutamine, Adrenaline, Noradrenaline, Vasopressin & Phenylephrine

Time critical from time of admission to record administration

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ABG interpretation made easy!

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Interpretation of arterial blood gases (ABGs) is a crucial skill that a lot of student nurses and medical practitioners need to learn. In this guide, we'll help you understand the concepts behind arterial blood gas and teach you the easiest and most fun way to interpret ABGs using the tic-tac-toe method.

Table of Contents

What is arterial blood gas?

An arterial blood gas is a laboratory test to monitor the patient's acid-base balance. It is used to determine the extent of the compensation by the buffer system and includes the measurements of the acidity (pH), levels of oxygen, and carbon dioxide in arterial blood. Unlike other blood samples obtained through a vein, a blood sample from an arterial blood gas (ABG) is taken from an artery (commonly on radial or brachial artery).

What are the components of arterial blood gas?

There are six components of arterial blood gas (ABGs):

pH

The pH is the concentration of hydrogen ions and determines the acidity or alkalinity of body fluids. A pH of 7.35 indicates acidosis and a pH greater than 7.45 indicates alkalosis. The normal ABG level for pH is 7.35 to 7.45.

PaCO₂ (Partial Pressure of Carbon Dioxide)

PaCO₂ or partial pressure of carbon dioxide shows the adequacy of the gas exchange between the alveoli and the external environment (alveolar ventilation). Carbon dioxide (CO2) cannot escape when there is damage in the alveoli, excess CO2 combines with water to form carbonic acid (H2CO3) causing an acidotic state. When there is hypoventilation in the alveolar level (for example, in COPD), the PaCO ₂ is elevated, and respiratory acidosis results. On the other hand, when there is alveolar hyperventilation (e.g., hyperventilation), the PaCO ₂ is decreased causing respiratory alkalosis. For PaCO ₂, the normal range is 35 to 45 mmHg (respiratory determinant).

PaO₂ (Partial Pressure of Oxygen)

PaO₂ or partial pressure of oxygen or PAO2 indicates the amount of oxygen available to bind with hemoglobin. The pH plays a role in the combining power of oxygen with hemoglobin: a low pH means there is less oxygen in the hemoglobin. For PaO ₂, the normal range is 75 to 100 mmHg

SO2 (Oxygen Saturation)

SO₂ or oxygen saturation, measured in percentage, is the amount of oxygen in the blood that combines with hemoglobin. It can be measured indirectly by calculating the PAO2 and pH Or measured directly by co-oximetry. Oxygen saturation, the normal range is 94-100%

HCO₃ (Bicarbonate)

HCO₃ or bicarbonate ion is an alkaline substance that comprises over half of the total buffer base in the blood. A deficit of bicarbonate and other bases indicates metabolic acidosis. Alternatively, when there is an increase in bicarbonates present, then metabolic alkalosis results.

BE (Base Excess)

BE. Base excess or BE value is routinely checked with HCO ₃ value. A base excess of less than -2 is acidosis and greater than +2 is alkalosis. Base excess, the normal range is -2 to +2 mmol/L

Normal Values in Arterial Blood Gas

To determine acid-base imbalance, you need to know and memorize these values to recognize what deviates from normal. The normal range for ABGs is used as a guide, and the determination of disorders is often based on blood pH. If the blood is basic, the HCO ₃ level is considered because the kidneys regulate bicarbonate ion levels. If the blood is acidic, the PaCO ₂ or partial pressure of carbon dioxide in arterial blood is assessed because the lungs regulate the majority of acid. The normal ABG values are the following:

For pH, the normal range is 7.35 to 7.45

For PaCO₂, the normal range is 35 to 45 mmHg (respiratory determinant)

For PaO₂, the normal range is 75 to 100 mmHg

For HCO₃, the normal range is 22 to 26 mEq/L (metabolic determinant)

Oxygen saturation, the normal range is 94-100%

Base excess, the normal range is -2 to +2 mmol/L

Interpreting Arterial Blood Gas Imbalances

Interpreting arterial blood gases is used to detect respiratory acidosis or alkalosis, or metabolic acidosis or alkalosis during an acute illness. To determine the type of arterial blood gas the key components are checked. The best (and fun) way of interpreting arterial blood gas is by using the tic-tac-toe method below:

Goals of Arterial Blood Gas analysis

For the purpose of this guide, we have set three (3) goals that we need to accomplish when interpreting arterial blood gases. The goals are as follows:

1. Based on the given ABG values, determine if values interpret ACIDOSIS or ALKALOSIS.

2. Second, we need to determine if values define METABOLIC or RESPIRATORY.

3. Lastly, we need to determine the compensation if it is: FULLY COMPENSATED, PARTIALLY COMPENSATED, or UNCOMPENSATED.

We need to keep these goals in mind as they'll come up later in the steps for the ABG interpretation technique.

Steps in ABG analysis using the tic-tac-toe method

There are eight (8) steps simple steps you need to know if you want to interpret arterial blood gases (ABGs) results using the tic-tac-toe technique.

1. Memorize the normal values.

The first step is you need to familiarize yourself with the normal and abnormal ABG values when you review the lab results. They are easy to remember:

For pH, the normal range is 7.35 to 7.45

For PaCO₂, the normal range is 35 to 45

For HCO₃, the normal range is 22 to 26

The recommended way of memorizing it is by drawing the diagram of normal values above. Write it down together with the arrows indicating ACIDOSIS or ALKALOSIS. Note that PaCO ₂ is intentionally inverted for the purpose of the Tic-Tac-Toe method.

2. Create your tic-tac-toe grid.

Once you've memorized the normal values and the diagram, create a blank your tic-tac-toe grid and label the top row as ACIDOSIS, NORMAL, and ALKALOSIS. Based on their values, we need to determine in which column we'll place pH, PaCO ₂, and HCO ₃ in the grid.

3. Determine if pH is under NORMAL, ACIDOSIS, or ALKALOSIS.

The third step of this technique is to determine the acidity or alkalinity of the blood with the given value of the pH as our determining factor. Remember in step #1 that the normal pH range is from 7.35 to 7.45.

If the blood pH is between 7.35 to 7.39, the interpretation is NORMAL but SLIGHTLY ACIDOSIS, place it under the NORMAL column.

If the blood pH is between 7.41 to 7.45, interpretation is NORMAL but SLIGHTLY ALKALOSIS, place it under the NORMAL column.

Any blood pH below 7.35 (7.34, 7.33, 7.32, and so on...) is ACIDOSIS, place it under the ACIDOSIS column.

Any blood pH above 7.45 (7.46, 7.47, 7.48, and so on...) is ALKALOSIS, place it under the ALKALOSIS column.

Please use the diagram below to help you visualize whether the normal value is ACIDOSIS or ALKALOSIS.

Once you've determined whether the pH is under the ACIDOSIS or ALKALOSIS, plot it on your tic-tac-toe grid under the appropriate column.

4. Determine if PaCO₂ is under NORMAL, ACIDOSIS, or ALKALOSIS.

For this step, we need to interpret if the value of PaCO ₂ is within the NORMAL range, ACIDIC, or BASIC and plot it on the grid under the appropriate column. Remember that the normal range for PaCO ₂ is from 35 to 45:

If PaCO₂ is below 35, place it under the ALKALOSIS column.

If PaCO₂ is above 45, place it under the ACIDOSIS column.

If PaCO₂ is within its normal range, place it under the NORMAL column.

5. Determine if HCO₃ is under NORMAL, ACIDOSIS, or ALKALOSIS.

Next, we need to interpret if the value of HCO ₃ is within the NORMAL range, ACIDIC, or BASIC and plot it under the appropriate column in the tic-tac-toe grid. Remember that the normal range for HCO ₃ is from 22 to 26:

If HCO₃ is below 22, place it under the ACIDOSIS column.

If HCO₃ is above 26, place it under the ALKALOSIS column.

If HCO₃ is within its normal range, place it under the NORMAL column.

6. Solve for goal #1: ACIDOSIS or ALKALOSIS.

Now, we will start solving for our goals. Looking at the tic-tac-toe grid, determine whether in what column the pH is placed and interpret the results:

If pH is under the ACIDOSIS column, it is ACIDOSIS.

If pH is under the ALKALOSIS column, it is ALKALOSIS.

If pH is under the NORMAL column, determine whether the value is leaning towards ACIDOSIS or ALKALOSIS and interpret accordingly.

In this step, we can accomplish goal #1 of determining ACIDOSIS or ALKALOSIS.

Looking back again on the tic-tac-toe grid, determine if pH is under the same column as PaCO ₂ or HCO ₃ so we can accomplish our goal #2 of determining if the ABG is RESPIRATORY or METABOLIC. Interpret the results as follows:

If pH is under the same column as PaCO₂, it is RESPIRATORY.

If pH is under the same column as HCO₃, it is METABOLIC.

If pH is under the NORMAL column, determine whether the value is leaning towards ACIDOSIS or ALKALOSIS and interpret accordingly.

8. Solve for goal #3: COMPENSATION.

Lastly, we need to determine the compensation to accomplish our goal #3. Interpret the results as follows:

It is FULLY COMPENSATED if pH is normal.

It is PARTIALLY COMPENSATED if all three (3) values are abnormal.

It is UNCOMPENSATED if PaCO₂ or HCO₃ is normal and the other is abnormal.

Application and Examples

Let's solve for the ABG interpretation with the examples below:

1. Remember the normal values.

2. Make your tic-tac-toe grid.

3. pH of 7.26 ABNORMAL and under ACIDOSIS, so we place pH under ACIDOSIS.

4. PaCO₂ of 32 is ABNORMAL and under ALKALOSIS, so we place PaCO₂ under ALKALOSIS.

5. HCO₃ of 18 is ABNORMAL and under ACIDOSIS, so we place HCO₃ under ACIDOSIS.

6. pH is under ACIDOSIS, therefore solving for goal #1, we have ACIDOSIS.

7. pH is on the same column as HCO₃, therefore solving for goal #2, we have METABOLIC.

8. All three values are ABNORMAL, therefore solving for goal #3, we have a PARTIALLY COMPENSATED ABG.

The answer to Practice Problem #1:
Metabolic Acidosis, Partially Compensated

1. Remember the normal values.

2. Make your tic-tac-toe grid.

3. pH of 7.44 is NORMAL but slightly leaning towards ALKALOSIS, so we place pH under the NORMAL column with an arrow pointing towards the ALKALOSIS column.

4. PaCO₂ of 30 is ABNORMAL and ALKALOSIS, so we place PaCO₂ under the ALKALOSIS column.

5. HCO₃ of 21 is ABNORMAL and ACIDOSIS, so we place HCO₃ under the ACIDOSIS column.

6. pH of 7.44 is NORMAL but leaning towards ALKALOSIS, therefore solving for goal #1, we have ALKALOSIS.

7. pH is NORMAL but is leaning towards ALKALOSIS, therefore under the same column as PaCO₂. Solving for goal #2, we have RESPIRATORY.

8. pH is NORMAL, therefore solving for goal #3, we have a FULLY COMPENSATED ABG.

The answer to Practice Problem #2:
Respiratory Alkalosis, Fully Compensated

1. Remember the normal values.

2. Make your tic-tac-toe grid.

3. pH of 7.1 is ABNORMAL and ACIDOSIS, therefore, we place pH under the ACIDOSIS column in the tic-tac-toe grid.

4. PaCO₂ of 40 is NORMAL, therefore, place it under the NORMAL column.

5. HCO₃ of 18 is ABNORMAL and ACIDOSIS, so we place HCO₃ under the ACIDOSIS column.

6. pH of 7.1 is ACIDOSIS, therefore, solving for goal #1, we have ACIDOSIS.

7. pH is under the same column as HCO₃, therefore, solving for goal #2, we have determined that it is METABOLIC.

8. pH is ABNORMAL so as HCO₃, but PaCO3 is under the NORMAL column. Solving for goal #3, we can interpret it as UNCOMPENSATED.

The answer to Practice Problem #3:
Metabolic Acidosis, Uncompensated

How to draw Arterial Blood Gas?

Arterial blood is usually drawn via the brachial or radial artery.

1. Inform the client about the procedure and that there is no food or fluid restriction imposed.

2. Note if the client is taking anticoagulant therapy or aspirin as this may affect results.

3. Note if the client is receiving oxygen therapy (flow rate, type of administration device), and the client's current temperature.

4. Using a heparinized needle and syringe, collect 1 to 5 mL of arterial blood. Common sites for drawing arterial blood are the radial and brachial artery.

5. Put the syringe with arterial blood in an ice-water bag to minimize the metabolic activity of the sample.

6. Deliver the blood sample immediately to the laboratory.

7. Apply pressure to the puncture site for 5 minutes or longer.

Acid-Base Balance and Imbalances

Acid-base imbalances develop when a person's normal homeostatic mechanisms are dysfunctional or overwhelmed. One type of acid-base imbalance is acidosis wherein the blood is relatively too acidic (low pH). The body produces two types of acid, therefore, there are two types of acidosis: respiratory acidosis and metabolic acidosis. On the contrary, alkalosis is a condition wherein the blood is relatively too basic (high pH), there are also two types of alkalosis: respiratory alkalosis and metabolic alkalosis.

When acid-base imbalances occur, the body activates its compensatory mechanisms (the lungs and kidneys) to help normalize the blood pH. The kidneys compensate for respiratory acid-base imbalances while the respiratory system compensates for metabolic acid-base imbalances. This does not correct the root cause of the problem, if the underlying condition is not corrected, these systems will fail.

Respiratory Acidosis

Respiratory acidosis occurs when breathing is inadequate (alveolar hypoventilation) and the lungs are unable to excrete enough CO2 causing PaCO ₂ or respiratory acid builds up. The extra CO2 combines with water to form carbonic acid, causing a state of acidosis - a common occurrence in emphysema. The kidneys activate its compensatory process (albeit slow, often 24 hours or more) by increasing the excretion of metabolic acids through urination, which increases blood bicarbonate.
Types of Respiratory Acidosis
There are two forms of respiratory acidosis: Acute and Chronic.

Acute respiratory acidosis. This form of respiratory acidosis occurs immediately. Left untreated, symptoms will get progressively worse. It's a medical emergency and can become life-threatening.

Chronic respiratory acidosis. This form of respiratory acidosis develops over time. It doesn't cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis.

Risk Factors
Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure.

Chronic Obstructive Pulmonary Disease (COPD). In chronic respiratory acidosis in COPD patients, the body tries to compensate by retaining more bicarbonate to overcome acidosis.

Drug Intake. Overdose of an opiate or opioid, such as morphine, tramadol, heroin, fentanyl, or magnesium sulfate (MgSO4) can cause respiratory acidosis.

Signs and Symptoms
Signs and symptoms of respiratory acidosis are as follows:

Altered level of consciousness. Respiratory acidosis may be the result of an altered level of consciousness caused by encephalopathy or cerebral edema.

Disorientation. Respiratory acidosis may result in disorientation, headache, or even focal neurologic signs.

Coma. When the lungs can't remove all of the carbon dioxide produced by the body through normal metabolism, the blood becomes acidified, leading to increasingly serious symptoms, from sleepiness to coma.

Tremors. Manifest as shaking or jerking muscle movements.

Asterixis. An inability to maintain the posture of part of the body.

Management of Respiratory Acidosis
Medical and nursing management of an arterial blood gas of respiratory acidosis includes the following:

Treat underlying conditions.

Medications. Bronchodilator medicines and corticosteroids may be used to reverse some types of airway obstruction, like those linked to asthma and COPD.

Weight loss. In the case of obesity hypoventilation syndrome, significant weight loss may be necessary to reduce abnormal compression of the lungs.

Provide mechanical ventilation through oxygen supplementation. Additional oxygen may be provided to alleviate the low oxygen level in the blood.

Manage hyperkalemia through the use of Kayexalate. Acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. Kayexalate increases fecal potassium excretion through the binding of potassium in the lumen of the gastrointestinal tract.

Respiratory Alkalosis

Respiratory alkalosis can result from hyperventilation since the lungs excrete too much carbonic acid which increases pH. Since respiratory alkalosis occurs quickly, the kidneys do not have time to compensate. Neurological symptoms such as confusion, paresthesias, and cell membrane excitability occur when the blood pH, CSF, and ICF increases acutely.
Risk Factors
Causes of hyperventilation include:

Panic. Panic attacks and anxiety are the most common causes of hyperventilation.

Hyperthermia. Fever may manifest as hyperventilation. The exact mechanism is not known but is thought to be due to carotid body or hypothalamic stimulation by the increased temperature.

Brainstem damage. Central neurogenic hyperventilation (CNH) is the human body's response to reduced carbon dioxide levels in the blood. This reduction in carbon dioxide is caused by the contraction of cranial arteries from damage caused by lesions in the brain stem.

Metabolic acidosis. Hyperventilation occurs most often as a response to hypoxia, metabolic acidosis, increased metabolic demands, pain, or anxiety.

Diabetic ketoacidosis (DKA). The only known compensatory response to metabolic acidosis in DKA is hyperventilation with consecutive respiratory alkalosis.

Pregnancy. Progesterone levels are increased during pregnancy. Progesterone causes stimulation of the respiratory center, which can lead to respiratory alkalosis.

Salicylate toxicity. Salicylate toxicity causes respiratory alkalosis and, by an independent mechanism, metabolic acidosis.

Signs and Symptoms
Hyperventilation is a sign that respiratory alkalosis is most likely to occur. However, low carbon dioxide levels in the blood also have a number of physical effects, including:

Numbness. Increased neuromuscular irritability in which a person loses feeling in a particular part of their body.

Tingling sensation. Prickling sensation that is usually felt in the hands, arms, legs, or feet, but can also occur in other parts of the body.

Palpitations. Palpitations are the perceived abnormality of the heartbeat characterized by awareness of cardiac muscle contractions in the chest.

Tetany. Tetany or tetanic seizure is a medical sign consisting of the involuntary contraction of muscles.

Convulsions. A medical condition where body muscles contract and relax rapidly and repeatedly, resulting in uncontrolled actions of the body.

Signs and symptoms of hypokalemia and hypocalcemia. Persistent respiratory alkalosis can induce secondary hypocalcemia and hypokalemia that may cause cardiac arrhythmias, conduction abnormalities, and various somatic symptoms such as paresthesia, hyperreflexia, convulsive disorders, muscle spasm, muscle twitching, positive Chvostek's sign, and tetany.

Management of Respiratory Alkalosis
The treatment for respiratory alkalosis depends on the underlying cause. Treating the condition is a matter of rising carbon dioxide levels in the blood. The following strategies and tips are useful for respiratory alkalosis caused by over-breathing due to panic and anxiety.

Breathe into a paper bag. Breathing through a paper bag fills it with carbon dioxide helping in inhaling exhaled air back into the lungs.

Treat underlying condition:

Medications. Administering an opioid pain reliever or anti-anxiety medication to reduce hyperventilation.

Relaxation techniques. Breathing exercises that help relax and breathe from the diaphragm and abdomen, rather than chest wall.

Safety. Stay with the patient.

Lavage. After massive aspirin ingestions, aggressive gut decontamination is advisable, including gastric lavage.

Correction of hypokalemia and hypocalcemia.

Oxygenation as indicated. Providing oxygen to help keep a person from hyperventilating.

Metabolic acidosis is when there is a decrease in bicarbonates and a buildup of lactic acid occurs. This happens in diarrhea, ketosis, and kidney disorders. It has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids.
Risk Factors

Chronic Renal Failure (CRF). This is due to reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the number of acids synthesized by the body and ingested with food.

Chronic Hypoxia. With chronic hypoxia, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8.

Obesity. Obesity, especially in conjunction with insulin resistance, can increase metabolic acidosis and thus result in a reduction of urinary citrate excretion.

Dehydration. Electrolyte disturbances caused by prolonged vomiting or severe dehydration can cause metabolic acidosis.

Aspirin Toxicity. Aspirin overdose causes the body to not produce ATP, leading to anaerobic metabolism with consequent raised lactate and ketone bodies. Acute aspirin or salicylates overdose or poisoning can cause initial respiratory alkalosis through metabolic acidosis ensues thereafter.

Methanol Poisoning. Significant methanol ingestion leads to metabolic acidosis, which is manifested by a low serum bicarbonate level. The anion gap is increased secondary to high lactate and ketone levels. This is probably due to formic acid accumulation.

Signs and Symptoms

Altered level of consciousness

Confusion

Disorientation

Lack of appetite

Coma

Jaundice

Management of Metabolic Acidosis
Patients with arterial blood gas indicating metabolic acidosis are managed and treated by:

Treat the underlying condition.

Hydration for diabetic ketoacidosis. The major treatment of this condition is the initial rehydration.

Dialysis for chronic renal failure. The control of metabolic acidosis in hemodialysis is mainly focused on the supply of bicarbonate during the dialysis sessions.

Use of diuretics.

Initiate safety measures.

Kayexalate. Acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. Kayexalate increases fecal potassium excretion through the binding of potassium in the lumen of the gastrointestinal tract.

Metabolic alkalosis occurs when bicarbonate ion concentration increases, causing an elevation in blood pH. This can occur in excessive vomiting, dehydration, or endocrine disorders.
Risk Factors

Vomiting. Vomiting causes metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Whenever a hydrogen ion is excreted, a bicarbonate ion is gained in the extracellular space.

Sodium bicarbonate overdose. Administration of sodium bicarbonate in amounts that exceed the capacity of the kidneys to excrete this excess bicarbonate may cause metabolic alkalosis.

Hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.

Nasogastric suction. Just like in vomiting, nasogastric (NG) suction also generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl).

Signs and Symptoms
Metabolic alkalosis may not show any symptoms. People with this type of alkalosis more often complain of the underlying conditions that are causing it. These can include:

Numbness

Vomiting

Diarrhea

Swelling in the lower legs (peripheral edema)

Tingling sensation

Agitation

Disorientation

Seizures

Coma

Management of Metabolic Alkalosis

Antiemetic. In the case of vomiting, administer antiemetics, if possible.

Ammonium chloride. Ammonium chloride is a systemic and urinary acidifying agent that is converted to ammonia and hydrochloric acid through oxidation by the liver. Intravenous (IV) ammonium chloride is a treatment option for severe cases of metabolic alkalosis.

Acetazolamide (Diamox). Acetazolamide also appears to be safe and effective in patients with metabolic alkalosis following treatment of respiratory acidosis from exacerbations of chronic obstructive pulmonary disease (COPD).

Arterial Blood Gas Interpretation Quiz

If you need to practice your new skills acquired here, check out our Arterial Blood Gas Interpretation for NCLEX (40 Questions)

References and Sources

The following sources are used as references for this guide. You may find them interesting for your additional reading:

1. Barnette, L., & Kautz, D. D. (2013). Creative ways to teach arterial blood gas interpretation. Dimensions of Critical Care Nursing, 32(2), 84-87.

2. Samuel, R. (2018). A Graphical Tool for Arterial Blood Gas Interpretation using Standard Bicarbonate and Base Excess. Indian J Med Biochem, 22(1), 85-89.

3. Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine, 14(2), 57.

4. Williams, A. J. (1998). Assessing and interpreting arterial blood gases and acid-base balance. Bmj, 317(7167), 1213-1216.

5. Verma, A. K., & Roach, P. (2010). The interpretation of arterial blood gases. Aust Prescr, 33(4), 124-129.

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Indian J Crit Care Med. 2010 Apr-Jun; 14(2): 57-64.

Abstract

Disorders of acid-base balance can lead to severe complications in many disease states, and occasionally the abnormality may be so severe as to become a life-threatening risk factor. The process of analysis and monitoring of arterial blood gas (ABG) is an essential part of diagnosing and managing the oxygenation status and acid-base balance of the high-risk patients, as well as in the care of critically ill patients in the Intensive Care Unit. Since both areas manifest sudden and life-threatening changes in all the systems concerned, a thorough understanding of acid-base balance is mandatory for any physician, and the anesthesiologist is no exception. However, the understanding of ABGs and their interpretation can sometimes be very confusing and also an arduous task. Many methods do exist in literature to guide the interpretation of the ABGs. The discussion in this article does not include all those methods, such as analysis of base excess or Stewart's strong ion difference, but a logical and systematic approach is presented to enable us to make a much easier interpretation through them. The proper application of the concepts of acid-base balance will help the healthcare provider not only to follow the progress of a patient, but also to evaluate the effectiveness of care being provided.

Keywords: Arterial blood gas interpretation, ABG analysis, rules for rapid ABG analysis, Anion gap, Approach to mixed disorders

Introduction

Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient's oxygenation status and acid-base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid-base balance can create complications in many disease states, and occasionally the abnormality may be so severe so as to become a life-threatening risk factor. A thorough understanding of acid-base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception.

The three widely used approaches to acid-base physiology are the HCO ₃⁻ (in the context of pCO ₂), standard base excess (SBE), and strong ion difference (SID). It has been more than 20 years since the Stewart's concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO ₂. The SID is defined in terms of weak acids and CO ₂ subsequently has been re-designated as effective SID (SID e) which is identical to "buffer base." Similarly, Stewart's original term for total weak acid concentration (A TOT) is now defined as the dissociated (A⁻) plus undissociated (AH) weak acid forms. This is familiarly known as anion gap (AG), when normal concentration is actually caused by A⁻. Thus all the three methods yield virtually identical results when they are used to quantify acid-base status of a given blood sample.[ 1]

Why is it Necessary to Order an ABG Analysis?

The utilization of an ABG analysis becomes necessary in view of the following advantages:

Aids in establishing diagnosis.

Aids in ventilator management.

Improvement in acid/base management; allows for optimal function of medications.

Acid/base status may alter electrolyte levels critical to a patient's status.

Accurate results for an ABG depend on the proper manner of collecting, handling, and analyzing the specimen. Clinically important errors may occur at any of the above steps, but ABG measurements are particularly vulnerable to preanalytic errors. The most common problems that are encountered include nonarterial samples, air bubbles in the sample, inadequate or excessive anticoagulant in the sample, and delayed analysis of a noncooled sample.

Potential Preanalytical Errors

Preanalytical errors are caused at the following stages:

During preparation prior to sampling

Missing or wrong patient/sample identification;

Use of the incorrect type or amount of anticoagulant

- dilution due to use of liquid heparin;

- insufficient amount of heparin;

- binding of electrolytes to heparin;

Inadequate stabilization of the respiratory condition of the patient; and

Inadequate removal of flush solution in arterial lines prior to blood collection.

During sampling/handling

Mixture of venous and arterial blood during puncturing;

Air bubbles in the sample. Any air bubble in the sample must be expelled as soon as possible after withdrawing the sample and before mixing with heparin or before any cooling of the sample has been done. An air bubble whose relative volume is up to 1% of the blood in the syringe is a potential source of significant error and may seriusly affect the pO ₂ value.

Insufficient mixing with heparin.

During storage/transport

General Storage Recommendation

Do not cool the sample.[ 2]

Analyze within 30 min. For samples with high paO ₂ e.g., shunt or with high leukocyte or platelet count also analyze within 5 min.

When analysis is expected to be delayed for more than 30 minutes, use of glass syringes and ice slurry is recommended.

During preparation prior to sample transfer

Visually inspect the sample for clots.

Inadequate mixing of sample before analysis.

Insufficient mixing can cause coagulation of the sample. It is recommended to mix the blood sample thoroughly by inverting the syringe 10 times and rolling it between the palms as shown in Figure 1 . This prevents stacking (such as coins or plates) of red blood cells.

During anticoagulation

Modern blood gas syringes and capillary tubes are coated with various types of heparin to prevent coagulation in the sampler and inside the blood gas analyzer:

Liquid nonbalanced heparin

Dry electrolyte-balanced heparin (Na⁺, K⁺, Ca ²⁺)

Dry Ca ²⁺-balanced heparin

Other anticoagulants, e.g., citrate and EDTA are both slightly acidic which increase the risk of pH being falsely lowered.

Liquid heparin

The use of liquid heparin as the anticoagulant causes a dilution of the sample, i.e., dilutes the plasma, but not the contents of the blood cells. As a consequence, parameters such as pCO ₂ and electrolytes are affected. Only 0.05 mL of heparin is required to anticoagulate 1 mL of blood. Dead space volume of a standard 5 mL syringe with 1 inch 22 gauge needle is 0.2 mL; filling the syringe dead space with heparin provides sufficient volume to anticoagulate a 4-mL blood sample. If smaller sample volumes are obtained or more liquid heparin is left in the syringe, then the dilution effect will be even greater. The dilution effect also depends on the hematocrit value. Plasma electrolytes decrease linearly with the dilution of the plasma along with pCO ₂, cGlucose, and ctHb values. pH and pO ₂ values are relatively unaffected by dilution. paO ₂ is only as little as 2% of the O ₂ physically dissolved in the plasma, and so the oximetry parameters given in fractions (or %) will remain unaffected.[ 3]

Syringes for blood gas analysis can have a wide range of heparin amounts.[ 4] The units are typically given as IU/mL (international units of heparin per milliliter) blood drawn into the syringe. In order to obtain a sufficient final concentration of heparin in the sample, blood volume recommended on the syringe must be drawn. Example: a syringe stated to contain 50 IU/mL when filled with 1.5 mL of blood means that the syringe contains a total 75 IU of dry heparin. If the user draws 2 mL of blood, then the resulting heparin concentration will be too low and the sample may coagulate. If the user draws only 1 mL, then the resulting heparin concentration will be higher than that aimed for, which may lead to producing falsely low electrolyte results.

Heparin binds to positive ions such as Ca ²⁺, K⁺, and Na⁺. Electrolytes bound to heparin cannot be measured by ion-selective electrodes, and the final effect will be measurement offalsely low values. The binding effect and the resulting inaccuracy of results are especially significant for corrected Ca ²⁺. The use of electrolyte-balanced heparin significantly reduces the binding effect and the resulting inaccuracy.[ 5]

The following steps for rapid interpretation of ABG are recommended:

Check for the consistency of ABG

While making an interpretation of an ABG always check for the consistency of the report by the modified Henderson equation.

The hydrogen ion is calculated by subtracting the two digits after the decimal point of pH from 80, e.g., if the pH is 7.23 then

[H⁺] = 80 - 23 = 57

or

[H⁺] = 10(9-pH)

The hydrogen can be calculated from Table 1 .

Obtain a relevant clinical history

While making an interpretation of anABG, never comment on the ABG without obtaining a relevant clinical history of the patient, which gives a clue to the etiology of the given acid-base disorder. For example, a patient with a history of hypotension, renal failure, uncontrolled diabetic status, of treatment with drugs such as metformin is likely to have metabolic acidosis; a patient, with a history of diuretic use, bicarbonate administration, high-nasogastric aspirate, and vomiting, is likely to have metabolic alkalosis. Respiratory acidosis would occur in COPD, muscular weakness, postoperative cases, and opioid overdose, and respiratory alkalosis is likely to occur in sepsis, hepatic coma, and pregnancy.

Look at the oxygenation status of the patient

The oxygenation status of the patient is judged by the paO ₂;however, never comment on the oxygenation status without knowing the corresponding FiO ₂. Calculate the expected paO ₂ (generally five times the FiO ₂).[ 6]

Based on the expected paO ₂ classify as mild, moderate, and severe hypoxia.

Ventilatory status

Look at paCO ₂.

Acid-base status

Identify the primary disorder by looking at the pH

pH > 7.40-Alkalemia: - 7.40-Acidemia

Then look at paCO ₂ which is a respiratory acid, whether it is increased, i.e., >40 (acidosis) or decreased <40 (alkalosis) and if this explains the change of pH, then it is respiratory disorder; otherwise, see the trend of change of HCO ₃⁻(whether increased in alkalosis or decreased in acidosis)-if it explains the change of pH, then it is a metabolic disorder.

In a normal ABG

pH and paCO ₂ move in opposite directions.

HCO ₃⁻and paCO ₂ move in same direction.

1. When the pH and paCO ₂ change in the same direction (which normally should not), the primary problem is metabolic; when pH and paCO ₂ move in opposite directions and paCO ₂ is normal, then the primary problem is respiratory.

2. Mixed Disorder-if HCO ₃⁻ and paCO ₂ change in opposite direction (which they normally should not), then it is a mixed disorder: pH may be normal with abnormal paCO ₂ or abnormal pH and normal paCO ₂).[ 7]

If the trend of change in paCO ₂ and HCO ₃⁻ is the same, check the percent difference. The one, with greater % difference, between the two is the one that is the dominant disorder.

e.g.: pH = 7.25 HCO ₃⁻=16 paCO ₂=60

Here, the pH is acidotic and both paCO ₂ and HCO ₃⁻ explain its acidosis: so look at the % difference

HCO ₃⁻% difference = (24 - 16)/24 = 0.33

paCO ₂% difference = (60 - 40)/40 = 0.5

Therefore, respiratory acidosis as the dominant disorder.

Respiratory disorders

After the primary disorder is established as respiratory, then the following points will help us to approach further with regard to the respiratory disorder).[ 8]

Ratio of rate of change in H⁺to change in paCO ₂

Alveolar arterial oxygen gradient

Ratio of rate of change in H⁺to change in paCO₂

The above ratio of rate of change in H⁺to change in paCO ₂ helps in guiding us to conclude whether the respiratory disorder is acute, chronic, or acute on chronic. As we have seen, the hydrogen can be calculated from Table 1 and the change in H⁺ is calculated by subtracting the normal H⁺ from the calculated H⁺ ion.[ 9]

>0.8-acute

0.3-0.8-acute on chronic

Alveolar Arterial Oxygen Gradient

It is calculated as follows:

PAO 2 = FiO 2 (PB-PH 2 O)- PaCO 2 R

where PAO ₂, alveolar partial pressure of oxygen; PiO ₂, partial pressure of inspired oxygen; FiO ₂, fraction of inspired oxygen; PB, barometric pressure (760 mmHg at sea level); PH ₂O, water vapor pressure (47 mm Hg), PaCO ₂, partial pressure of carbon dioxide in blood; R, respiratory quotient assumed to be 0.8.

= FiO 2 (760 - 47) - PaCO 2 0.8

Hypoxemic respiratory failure can be associated with normal (10-15 mmHg) or increasedalveolar arterial oxygen gradient. Figure 2 shows the alogrithim for approach in a patient with hypoxemic respiratory failure. If this gradient is <20, then it indicates an extrapulmonary cause of respiratory failure.

Differentials of extrapulmonary causes of respiratory failure:

1. Central nervous system-Respiratory center depression due to causes such as drug overdose, primary alveolar hypoventilation, and myxedema.

2. Peripheral nervous system-Spinal cord diseases, Guillain-Barré syndrome, Amyotrophic lateral sclerosis.

3. Respiratory muscles-Hypophosphatemia, muscle fatigue, myasthenia gravis, and polymyositis.

4. Chest wall diseases-Ankylosing spondylitis, flail chest, thoracoplasty.

5. Pleural diseases-Restrictive pleuritis

6. Upper air way obstruction-Tracheal Stenosis, vocal cord tumor

Compensation

Rules of compensation

1. The compensatory response depends upon the proper functioning of the organ system involved in the response (lungs or kidneys) and on the severity of acid-base disturbance. For example, the likelihood of complete compensation in chronic respiratory acidosis is <15% when paCO ₂ exceeds 60 mmHg.

2. Acute compensation occurs within 6-24 h and chronic within 1-4 days. Respiratory compensation occurs faster than metabolic compensation.

3. In clinical practice, it is rare to see complete compensation. The maximum compensatory response in most cases is associated with only 50-75% return of pH to normal. However, in chronic respiratory alkalosis, the pH may actually completely return to normalcy in some cases.

Respiratory acidosis

Acute: [HCO ₃⁻] increase by 1 mEq/L for every 10 mmHg increase in paCO ₂ above 40.

Chronic: [HCO ₃⁻] increase by 3.5 mEq/L for every 10 mmHg increase in paCO ₂ above 40.

Respiratory alkalosis

Acute: [HCO ₃⁻] decrease by 2 mEq/L for every 10 mmHg decrease in paCO ₂ below 40.

Chronic: [HCO ₃⁻] decrease by 5 mEq/L for every 10 mmHg decrease in paCO ₂ below 40.

Metabolic disorders

In patients with metabolic acidosis, an excess of acid or loss of base is present. This causes the HCO ₃⁻:H ₂CO ₃ratio and pH to fall while no change occurs in pCO ₂ -uncompensated metabolic acidosis.

As a result of compensatory mechanisms, the lungs in the form of CO ₂ excrete H ₂CO ₃ and the kidneys retain HCO ₃⁻. pCO ₂ falls and HCO ₃⁻: H ₂CO ₃ ratio and pH rise toward normal even though concentrations of HCO ₃⁻and H ₂CO ₃ are less than normal. This is called compensated metabolic acidosis and the expected paCO ₂ is calculated as paCO ₂ = [1.5 × HCO ₃+ 8] ± 2.

Anion gap

For more than 40 years, the AG theory has been used by clinicians to exploit the concept of electroneutrality and has evolved as a major tool for evaluating the acid-base disorder. Anion gap is the difference between the charges of plasma anions and cations, calculated from the difference between the routinely measured concentration of the serum cations (Na⁺ and K⁺) and anions (Cl⁻ and HCO ₃⁻). Because electroneutrality must be maintained, the difference reflects the unmeasured ions. Normally, this difference or the gap is filled by the weak acids (A⁻) principally albumin, and to a lesser extent phosphates, sulfates, and lactates.

When the AG is greater than that produced by the albumin and phosphate, other anions (e.g., lactates and ketones) must be present in higher than normal concentration.

Anion gap = (Na⁺ + K⁺) - [Cl⁻ + HCO ₃⁻]

Because of its low and narrow extracellular concentration, K⁺ is often omitted from the calculation The normal value ranges from 12 ± 4 when K⁺ is considered, and 8 ± 4 when K⁺ is omitted. Figure 3 shows the alogrithm for the approach to patients with normal AG acidosis.

The primary problem with AG is its reliance on the use of the normal range produced by the albumin and to a lesser extent phosphate, the level of which may be grossly abnormal in critically ill patients. Because these anions are not strong anions, their charges will be altered by changes in pH.[ 10, 11]

Serum protein and phosphate

Normal AG = 2{albumin(gm/L)} + 0.5 {phosphate (mg/dL)}

Acid-base status

In Acidemic state - Anion gap decreases by 1-3

In Alkalemic state - Anion gap increases by 2-5

Major clinical uses of the anion gap

For signaling, the presence of a metabolic acidosis and confirm other findings.

Helping to differentiate between causes of metabolic acidosis: High AG versus normal AG metabolic acidosis. In an inorganic metabolic acidosis (e.g., due to HCl infusion), the infused Cl⁻ replaces HCO ₃⁻, and the AG remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not normally measured. This means that the AG is increased.

Providing assistance in assessing the biochemical severity of the acidosis and follow the response to treatment.

Disorders that are associated with a low or negative serum AG are listed in Table 2 .

Table 2

Cause

Comments

Laboratory error

Most frequent cause of low anion gap

Hypoalbuminemia

Second most common cause of low serum anion gap

Multiple myeloma

Level of anion gap correlates with serum concentration of paraprotein

Halide intoxication

Anion gap depends on serum halide concentration

(bromide, lithium, iodide)

(low anion gap with lithium ≥4 mEq/L)

Hypercalcemia

more likely in hypercalcemia associated with 10 hyperparathyroidism

Hypermagnesemia

Theoretical cause but not documented in literature

Polymyxin B

Anion gap depends on serum level; occurs with preparation with chloride

Underestimation of serum sodium

Most frequent with hypernatremia or hypertriglyceridemia

Overestimation of serum chloride

Rare with ion selective electrodes

Overestimation of serum bicarbonate

Spurious ⁭in serum HCO ₃ if cells not separated from sera

Table 3 elaborates the species of the unaccounted anions along with their sources of origin and diagnostic adjunts in case of high AG metabolic acidosis.

Table 3

Cause

High serum anion gap

Comments

Species

Origin

Diagnostic adjuncts

Diabetic

β Hydroxybutyrate

Alcoholic

In the patients with metabolic alkalosis, there is an excess of base or a loss of acid which causes the HCO ₃⁻:H ₂CO ₃ ratio and pH to rise, but with no change occurring in pCO ₂, which is called uncompensated metabolic alkalosis. However, the kidney has a large capacity to excrete excess bicarbonate and so, for sustaining the metabolic alkalosis, the elevated HCO ₃⁻concentration must be maintained through an abnormal renal retention of HCO ₃⁻.

Compensatory respiratory acidosis may be so marked that pCO ₂ may rise higher than 55 mmHg. Expected paCO ₂is calculated as paCO ₂ = [0.7 × HCO ₃⁻+ 21] ± 2 or 40 + [0.7 ΔHCO ₃]. This is called compensated metabolic alkalosis.

Most of the patients with metabolic alkalosis can be treated with chloride ions in the form of NaCl (saline responsive) rather than KCl (which is preferable). When NaCl is given, Cl⁻ions are supplied, and so the blood volume increases and the secretion of aldosterone in excess decreases. Thus, excessive urinary loss of K⁺and excessive reabsorption of HCO ₃⁻ stops. When metabolic alkalosis is due to the effects of excessive aldosterone or other mineralocorticoids, the patient does not respond to NaCl (saline resistant) and requires KCl.

Based on the urinary chloride, metabolic alkalosis is divided into:

Chloride responsive or extracellular volume depletion (urinary chloride < 20)

Chloride resistant (urinary chloride > 20)

Severe potassium depletion

Mineralocorticoid excess-Primary hypealdosteronism, Cushing's Syndrome, Ectopic ACTH

Secondary hypereldosteronism-Renovascular disease, malignant hypertension, CHF, cirrhosis

Aproach to mixed disorder

Mixed metabolic disturbances (e.g., high AG from diabetic ketoacidosis plus normal AG from diarrhea) can be identified using the relationship between AG and HCO ₃⁻, which is called the gap-gap ratio. It is the ratio of change in anion gap (ΔAG) to change in HCO ₃⁻ (ΔHCO ₃⁻). When hydrogen ions accumulate in blood, the decrease in serum HCO ₃⁻ is equivalent to the increase in AG and the increase in AG excess/HCO ₃⁻ deficit ratio is unity, i.e., pure increase in AG metabolic acidosis. When a normal AG acidosis is present, the ratio approaches zero. When a mixed acidosis is present (high AG + normal AG), the gap-gap ratio indicates the relative contribution of each type to the acidosis. If it is <1, then it suggests that there is a normal AG metabolic acidosis associated with it and if >2 it suggests that there is associated metabolic acidosis.

Rules for rapid clinical interpretation of ABG

When required to make a proper approach towards the evaluation of blood gas and acid-base disturbances in the body, the following scheme is suggested:

1. Look at pH - < 7.40 - Acidosis; > 7.40 - Alkalosis

2. If pH indicates acidosis, then look at paCO ₂and HCO ₃⁻

3. If paCO ₂ is ↑, then it is primary respiratory acidosis

1. To determine whether it is acute or chronic

ΔH⁺ / ΔpaCO ₂ <0.3-chronic

>0.8-acute

0.3-0.8-acute on chronic

2. Calculate compensation by the respective methods

Acute: [HCO ₃⁻] ↑ by 1 mEq/L for every 10 mmHg ↑ in paCO2 above 40.

Chronic: [HCO ₃⁻] ↑ by 3.5 mEq/L for every 10 mmHg ↑ in paCO2 above 4

4. If paCO ₂↓ and HCO ₃⁻ is also ↓→ primary metabolic acidosis

Calculate expected paCO ₂ as follows:

paCO ₂ = [1.5 × HCO ₃+ 8] ± 2 metabolic acidosis only

paCO ₂ < expected paCO ₂ → concomitant respiratory alkalosis.

paCO ₂ > expected paCO ₂ → concomitant respiratory acidosis

5. If HCO ₃⁻ is ↓, then AG should be examined.

6. If AG is unchanged → then it is hyperchloremic metabolic acidosis.

7. If AG is ↑ → then it is wide AG acidosis.

8. ΔAG/Δ HCO3⁻ = 1, pure increased AG metabolic acidosis

<1 normal anion gap metabolic acidosis

>2 associated metabolic acidosis.

9. If pH indicates alkalosis, then look at HCO ₃⁻ and paCO ₂.

10. If paCO ₂ is ↓ → then it is primary respiratory alkalosis.

1. Whether it is acute or chronic (with the same formula as above)

2. Calculate compensation by the respective methods:

Acute: [HCO ₃⁻]↓ by 2 mEq/L for every 10 mmHg

↓ in paCO ₂ below 40.

Chronic: [HCO ₃⁻] ↓ by 5 mEq/L for every

10mmHg ↓ in paCO ₂ below 40.

11. If paCO ₂ ↑ and HCO ₃⁻ also ↑ → then it is primary metabolic alkalosis.

Calculate the expected paCO ₂

paCO ₂ = [0.7 × HCO3⁻+ 21] ± 2 Or 40 + [0.7 ΔHCO3] → metabolic alkalosis only

paCO ₂ < expected paCO2 → concomitant respiratory alkalosis.

paCO ₂ > expected paCO2 → concomitant respiratory acidosis

12. if urinary chloride < 20 → chloride responsive or ECV depletion

if urinary chloride > 20→ chloride resistant

13. If pH is normal ABG may be normal or mixed disorder

1. ↑paCO ₂ and ↓HCO ₃⁻ → respiratory and metabolic acidosis

2. (b) ↓paCO ₂ and↑ HCO ₃⁻ → respiratory and metabolic alkalosis.

Calculate % difference (ΔHCO ₃⁻/HCO ₃⁻and ΔpaCO ₂/paCO ₂) to see which is dominant disorder.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

References

1. Kellum JA. Making Strong Ion Difference the "Euro" for Bedside Acid-Base Analysis. Yearbook of Intensive Care and Emergency Medicine. Spr Ber Heid Publ. 2005;5:675. [ Google Scholar]

2. Phillips B, Peretz DI. In: National Committee for Clinical Laboratory Standards. villanova PA: NCCLS publication; 1985. Blood Gas Pre-analytical considerations. Specimen collection, Calibration, and Controls (proposed guidelines) NCCLS. [ Google Scholar]

4. Hutchison AS, Ralston SH, Dryburgh FJ, Small M, Fogelman I. Too much heparin: possible source of error in blood gas analysis. Br Med J. 1983;287:1131-2. [[ PMC free article] [ PubMed] Google Scholar]

8. Marino PL. Arterial Blood Gas Interpretation. 2nd edi. Lippincott: Williams and Wilkins Publishers; 1998. pp. 582-605. [ Google Scholar]

9. Bartter TC, Abouzgheib WB, Pratter MR, Irwin RS. In: Irwin and Rippe's Intensive Care Medicine. 6th edi. Lippincott: Williams and Wilkins Publishers; 2008. Respiratory Failure-Part 1; pp. 485-9. [ Google Scholar]

10. Rao SM, Nagendranath V. Arterial Blood Gas Monitoring: Indian J Anaesth. 2002;46:289-97. [ Google Scholar]

11. Chawla LS, Shih S, Davison D, Junker C, Seneff MG. Anion gap, anion gap corrected for albumin, base deficit and unmeasured anions in critically ill patients: implications on the assessment of metabolic acidosis and the diagnosis of hyperlactatemia. BMC Emerg Med. 2008;8:18. [[ PMC free article] [ PubMed] Google Scholar]

Articles from Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine are provided here courtesy of Indian Society of Critical Care Medicine

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Disorders of acid-base balance can lead to severe complications in many disease states, and occasionally the abnormality may be so severe as to become a life-threatening risk factor. The process of analysis and monitoring of arterial blood gas ...

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