abg interpretation - kanonhealth.org

ABG Interpretation

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pH 7.35-7.45

■ pH: acidity or alkalinity of a solution– Acidotic = < 7.35 (H+ ions ↑, pH ↓ acidic state)

– Alkalotic = > 7.45 (H+ ions ↓, pH ↑ basic state)

■ < 6.8 or > 7.8 interferes with cellular functioning death

– H+ ions necessary for membrane integrity and enzymatic reactions

7.35 7.45

7.40

Hypoxemia vs. Impaired ventilation

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Acid-Base Regulation

Response to acid-base changes• Buffering (immediate)

– Bicarbonate-carbonic acid; hemoglobin, protein &

phosphate binding

– K+ and H + exchange

– Acidosis: K+ leaves cell; Alkalosis: K+ into cell

• Lungs (Respiratory) CO₂ (minutes)

– Lungs increase/decrease rate and depth of ventilation

• Renal (Metabolic) HCO₃ˉ (days)

– Kidneys excrete/retain bicarbonate and hydrogen

PaCO2 35-45 mmHg

■ PaCO2: Partial pressure of carbon dioxide in arterial blood– Effectiveness of ventilation related to metabolic rate

■ Acidotic > 45 mmHg■ Alkalotic < 35 mmHg

• Central chemoreceptors sense ↑ or ↓ in pH

• PaCO2 and ventilation work to balance it out

HCO3- 22-26 mEq/L

■ HCO3: Reflection of kidney function

– ↑ or ↓ via renal mechanisms (reabsorption/excretion)

■ Acidotic < 22 mEq/L

■ Alkalotic > 26 mEq/L

■ Respiratory

■ Opposite

■ Metabolic

■ Equal

ROME

CO2

HCO3-


Base Excess/Deficit

-2 to +2

• Non-respiratory contribution to acid-base balance:

– Base Deficit = -2 or below (Metabolic Acidosis)

– Base Excess = +2 or more (Metabolic Alkalosis)

*Follows pH*


Base Deficit

• Amount of additional base that must be added to raise 1L of whole blood to predicted pH, based on PaCO2

• Calculated value based on PaCO2, pH and serum bicarbonate

• Serial measurements commonly used to guide resuscitation and shown to predict:

– Hospital mortality– Length of stay– Severity of sepsis– Organ failure

PaO2 80 – 100 mmHg

■ PaO2: partial pressure of oxygen (O2) dissolved in arterial blood (3% total O2 in blood)

■ Hypoxemia:– Mild Hypoxemia = 60-79– Moderate Hypoxemia = 40-59– Severe Hypoxemia = Less than 40

Age > 60 = normal ↓ by 1 mmHg/year(80-1/year > 60)

SaO2 > 95%

SaO2: Amount of O2 bound to hemoglobin (Hgb) in arterial blood (aka: O2 Saturation)

Normal = >95%

SaO2 is never 100%, why?

Oxyhemoglobin Dissociation Curve

• Right Shift: Hgb has decreased affinity for O2

• Increased PaCO2

• Acidosis

• Left Shift: Hbg has increased affinity for O2

• Decreased PaCO2

• Alkalosis

Relationship between SaO2 & PaO2

ABG Disorders

• Respiratory Acidosis and Respiratory Alkalosis

• Metabolic Acidosis and Metabolic Alkalosis

• Combined/Mixed disorderso Uncompensatedo Partially compensatedo Fully Compensated

Respiratory Acidosis

■ Respiratory disorder: caused by ↓ alveolar ventilation in relation to metabolic production of CO2• CO2 = potent vasoactive substance• CO2 readily crosses blood brain barrier

■ pH < 7.35■ PaCO2 > 45 mmHg

■ Alveolar hypoventilation CO2 retention (hypercapnia) acidosis

Causes of Respiratory Acidosis

• Hypoventilation: (↑CO₂ retention)

o Airway obstructiono Respiratory center depression

− Brainstem trauma, sedation, anesthetics, over dose

o Respiratory muscle paralysis o Chest wall disorderso Lung parenchyma disorderso Exhaustion, paino Hypoventilation with mechanical

ventilation

Clinical Manifestations of Respiratory Acidosis

• Restlessness, apprehension

• Neurologic: o Headache, confusion, lethargy, drowsiness,

decreased responsivenesso Related to ↓ pH in CSF and vasodilation (CO2 x

BBB)

• Respiratory: dyspnea, respiratory distresso Cyanosis not seen unless with hypoxemia (skin

pink)

• Cardiac: tachycardia, dysrhythmias


• Acute:– Protein buffers = marginal compensation– HCO₃ˉ = not a good buffer for CO₂

– Renal buffering takes time; not effective

*Acute uncompensated: pH < 7.35; PaCO₂ > 45; norm/slightly ↑ HCO₃ˉ*

• Chronic: (COPD, neuromuscular disorders, chest wall deformities)

– Renal compensation effective, established over several days/weeks

– Acidosis stimulates secretion of H+ ions and regeneration of HCO₃ˉ

*Chronic compensated: pH toward normal; PaCO₂ >45; HCO₃ˉ >26*

Compensation: Respiratory Acidosis

Interventions for Respiratory Acidosis

• Evaluation: pH < 7.35; PaCO₂ > 45o Must distinguish acute from chronic

• Increase Ventilation: (treat underlying disorder)

o Raise head of bed (HOB)o Decrease sedationo Increase Tidal Volume (Vt)o Increase respiratory rateo Pulmonary toiletryo Stimulate patient

Slowly!

If hypoxemia and hypercapnia, O2 can 🡪 respiratory

depression

Respiratory Alkalosis

■ Respiratory disorder: caused by ↑ alveolar ventilation in relation to metabolic production of CO2

• Occurs within minutes of hyperventilation• Cerebral vasoconstriction

■ pH > 7.45■ PaCO2 < 35 mmHg

Hyperventilation ↓ CO2 (hypocapnia) alkalosis

Causes of Respiratory Alkalosis

• Hyperventilation:o Hypoxemiao Hypermetabolic states

− Fever, anemia, thyrotoxicosis, pregnancy

o Anxiety, panic disorder, pain, fearo Salicylate toxicity (early)o Iatrogenic or secondary causes

− Mechanical hyperventilation; metabolic acidosis

Clinical Manifestations of Respiratory Alkalosis

• Sweating, dry mouth, blurred vision

• Neurologico Light-headedness, confusion, decreased

concentration, paresthesias, tetanic spasms, CNS lesions

o Irritation of the CNS and PNS

• Cardiac: dysrhythmias


•Acute:– Occurs within minutes of hyperventilation– Cellular buffers 🡪 immediate compensation

• Protein and H+ ions shift from ICF to ECF• Not effective if PaCO₂ levels are significantly

decreased

*pH > 7.45; PaCO₂ < 35; HCO₃ˉ = WNLs*

•Chronic:– Renal compensation restores pH toward normal

• H+ ion excretion, and HCO₃ˉ absorption, are decreased

*pH closer to norm; PaCO₂ < 35; HCO₃ˉ < 22*

Compensation: Respiratory Alkalosis

Interventions for Respiratory Alkalosis

• Evaluation: pH > 7.45; PaCO₂ < 35 mmHgo Distinguish acute from chronic to treat

cause− Acute: HCO3- = normal− Chronic: HCO3- = ↓, pH closer to normal

• Decrease Ventilation:o Reverse hypermetabolic stateo Correct hypoxemia

Metabolic Acidosis

Concentration of non-carbonic acids is increased (or) HCO₃ˉ is lost from ECF or cannot be

regenerated

■ pH < 7.35■ HCO3

- < 22 mmHg

• Occurs quickly with lactic acidosis or slowly with renal failure and diabetic ketoacidosis (DKA)

• Respiratory system rapidly compensates

Causes of Metabolic Acidosis

Increased Acid

• Poor perfusion (lactic

acidosis)

• Renal Failure (uremia)

• DKA (↓ insulin 🡪 ketoacidosis)

• Starvation/Rhabdomyoly

sis

• Drugs/toxins, acid

ingestion

Decreased Base

• Diarrhea

• Intestinal fistula

• Ileostomy

Use ANION GAP to

determine cause

Anion Gap = difference between

measurable EC plasma cations

(Na +, K +) and anions (HCO3-, Cl)

Anion Gap 8-16 mEq/L

■ Anion Gap = [Na+] – ([Cl-] + [HCO3-]) = 8-16 mEq/L

M -- Methanol

U -- Uremia (↓ excretion H+)

D -- Diabetic ketoacidosis

P -- Propylene glycol

I -- Isoniazid / Iron

L -- Lactic acidosis

E -- Ethylene glycol

S -- Salicylates

↑ AG = overproduction or ↓

excretion of acid products = MA

Norm AG = HCO3- loss with

retained CL- = Hyperchloremic

MA

↓ AG = rare

Causes - KUSMAL

■ K Ketoacidosis■ U Uremia■ S Salicylates■ M Methanol■ A Alcohol■ L Lactic Acidosis

Clinical Manifestations of Metabolic Acidosis

• Neurologico HA, confusion, restlessness, lethargy, weakness,

stupor/coma

• Cardiovascularo Dysrhythmias, warm/flushed skin

• Respiratoryo Deep, rapid RR, Kussmaul respirations

• Gastrointestinalo Anorexia, N/V, diarrhea


Compensation:

Metabolic Acidosis

1. Respiratory:

- ↓ pH triggers hyperventilation 🡪 ↓ PaCO₂ and H₂CO₃ in blood

2. Renal:- Excrete H+ via NH4 and H₂PO4

- HCO₃ˉ ↓ serum value of H+ ions and ↑ pH

3. Cellular:- H+ ions move into ICS and K+ moves to ECS- ↑ ionized (free) Ca++ r/t ↓ amount of Ca++ bound to albumin

Severe acidosis depletes buffering systems

Interventions for Metabolic Acidosis

• Evaluation: pH < 7.35; HCO₃ˉ < 22

• Identify underlying causes:– History, lab findings, clinical symptoms– Anion Gap (isolates specific cause)

– Oxyhgb dissociation curve shifted R: ↓ Hgb’s affinity for O2

• Monitor and treat cause and symptoms

Metabolic Alkalosis

HCO3- concentration is increased,

usually related to excessive loss of metabolic acids

■ pH > 7.45■ HCO3

- > 26 mmHg

The respiratory system compensates rapidly, how?


Causes of

Metabolic Alkalosis

• Prolonged vomiting or gastric suctioning– Hypochloremic: depletion of ions: Na+, Cl-, K+

• Excessive HCO₃ˉ intake (i.e., antacids)

• Hyperaldosteronism with hypokalemia:– Aldosterone 🡪 Na+ retention with H+ and K+ loss

(excretion) 🡪 volume expansion 🡪 HCO₃ˉ and Na+

retention 🡪 alkalosis

• Diuretic Therapy:– Na+, Cl-, K+ excretion > HCO₃ˉ excretion

Clinical Manifestations of Metabolic Alkalosis

• Neurologic:o Weakness, muscle twitching and cramps,

tetanyo Lethargy, disorientation, convulsions, coma

• Cardiac: atrial tachycardia, dysrhythmiaso Oxyhgb dissociation curve shifts to L, ↓ dissociation of

oxyhgb dysrhythmias

• Respiratory: depressed respirations

• Gastrointestial: nausea and vomiting

Alkalosis: ↑ Ca++ binding to Albumin ↓ ionized Ca ++

excitable cells and ↑ APs


•Respiratory: (inefficient)

– ↑ pH inhibits respiratory center: ↓ respiratory rate and depth to ↑ CO₂

•Renal: (hypochloremic: depletion Na+, Clˉ, K+) = Ineffective!

– ↓ volume/electrolytes 🡪 ↑ HCO₃ˉ reabsorption (b/c of ↓ ECF Clˉ)

– ↑ Na+ reabsorption to increase fluid volume– When K+ depleted, H+ moves from ECF to ICF and is also

excreted

•Cellular: (alkalemia)

– H+ ions move from ICF to ECF; K+ moves to ICF

Compensation: Metabolic Alkalosis

Interventions for Metabolic Alkalosis

Evaluation: pH > 7.45; HCO₃ˉ > 26

■ Treat cause and symptoms:

• Hypochloremic/volume depletion: Give NaClo ↓ stimulus to retain Na+

o HCO₃ˉ can be excreted (NaHCO₃)

• Hyperaldosteronism/hypokalemia: Give Potassiumo H+ moves back into ECFo H+ loss is ↓ from distal tubule


HypochloremicMetabolic Alkalosis

Recap: Acidosis

Recap: Alkalosis

Compensation

• Uncompensated

• Partially compensated

• Fully compensated


Uncompensated

• pH is not within normal range

• PaCO₂ or HCO₃ˉ is not within normal range (only one value)

– Not attempting to compensate

– One value is going in direction of pH

– One value is within normal limits

• pH 7.57

• PaCO₂ 41

• PaO₂ 95

• BE 1.0

• HCO₃ˉ 30

• SaO₂ 98%

*Uncompensated Metabolic Alkalosis*


Partially Compensated

• pH is not within normal range

• PaCO₂ and HCO₃ˉ are not within normal range:– Attempting to compensate– One value is going in

direction of pH– One value is going the

opposite direction of pH

7.57• pH

• PaCO₂ 49

• PaO₂ 95

• BE 1.0

• HCO₃ˉ 30

• SaO₂ 98%

*Partially Compensated Metabolic Alkalosis*


Fully Compensated

• pH 7.45

• PaCO₂ 49

• PaO₂ 95

• BE 1.0

• HCO₃ˉ 30

• SaO₂ 98%

• pH is back within normal range

• PaCO₂ and HCO₃ˉ are not within normal range


pH < 7.35

HCO₃ˉ < 22

PaCO₂ > 45

pH > 7.45

HCO₃ˉ > 26

PaCO₂ < 35

Mixed Alkalosis

Combined Acidosis:When pH is acidotic and both PaCO₂ and HCO₃ˉ are acidotic

Combined Alkalosis:When pH is alkalotic and both PaCO₂ and HCO₃ˉ are alkalotic

Mixed Acidosis

Mixed (Combined) Acidosis and Alkalosis

Venous Blood Gas

• Alternative method of estimating systemic CO2 and pH that does not require arterial blood sampling

• Measures venous oxygen tension (PvO2), carbon dioxide tension (PvCO2), acidity (pH), oxyhemoglobin saturation (SvO2) and serum bicarb (HCO3

-)

• PvO2 has no practical value

VBG Values

• Sampling sites: − Peripheral venous (venipuncture)− Central venous (central venous catheter)− Mixed venous (distal port of pulmonary artery catheter)

• Similar to ABG Values:– pH = 0.03-0.05 lower than ABG– PaCO2 = 4-6 mmHg more than ABG– HCO3

- = little or no increase pH: 7.35-7.40

PvCO₂: 41-51

PvO₂: 35-42

HCO₃ˉ: 22-26


Who goes where in ROME?

Steps to ABG Interpretation

1. Is the pH normal? (acid or alkaline side of 7.4)

2. Is the CO₂ normal? (acid or alkaline)

3. Is the HCO₃ˉ normal? (acid or alkaline)

4. Does the CO₂ or HCO₃ˉ match the pH?

5. Does the CO₂ or HCO₃ˉ go the opposite direction of pH?• Compensated, partially compensated,

uncompensated

6. Look at PaO₂ (is hypoxemia present?)

https://www.youtube.com/watch?v=zb51W7C93HM&spfreload=10

Step 1

■ pH 7.54■ PaCO2 26.7■ HCO3 21■ PaO2 65■ BE 2

Is the pH normal? Acid or Alkaline side of 7.4

Step 2

■ pH 7.543■ PaCO2 26.7■ HCO3 21■ PaO2 65■ BE 2

Is the CO2 normal? Acid vs. Alkaline

Step 3

■ pH 7.543■ PaCO2 26.7■ HCO3 21■ PaO2 65■ BE 2

Is the HCO3 normal? Acid vs. Alkaline

Step 4

■ pH 7.543– Alk

■ PaCO2 26.7– Alk

■ HCO3 21– Acid

■ PaO2 65■ BE 2

Does the CO2 or HCO3 match the pH? (Name it)

Respiratory Alkalosis

Step 5

■ pH 7.543– Alk

■ PaCO2 26.7– Alk

■ HCO3 21– Acid

■ PaO2 65■ BE 2

Does the other

component go in

the opposite

direction of pH?

Is it compensated,

partially

compensated, or

uncompensated?

Step 6

■ pH 7.543■ PaCO2 26.7■ HCO3 21■ PaO2 65■ BE 2

Look at PaO2Is hypoxemia present?

Name the ABG

■ pH 7.543■ pCO2 26.7■ HCO3 21■ PaO2 65■ BE 2

Partially Compensated Respiratory Alkalosis

with mild hypoxemia

Questions?

• Buffering systems• ABG components• ABG normal values• ABG disorders• ABG interpretation

Online ABG Tutorial

• Other reference material:

o http://M2hnursing.com/ABG/index.php

http://m2hnursing.com/ABG/index.php

abg interpretation - kanonhealth.org

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