ABG 6 Series

ABG series

ANAS SAHLE , MDDAMASCUSE

HOSPITAL

Acid-Base Disorders and the ABG 6

BREIF PREVIEW

Summary of the Approach to ABGs

1. Check the pH

2. Check the pCO2

3. Select the appropriate compensation formula

4. Determine if compensation is appropriate

5. Check the anion gap AG=NA – (HCO3 + CL):12±4

6. If the anion gap is elevated, check the delta-delta

G:G Ratio =Δ AG (12-AG) \ Δ HCO3 (24-HCO3)

7. If a metabolic acidosis is present, check urine pH

8. Generate a differential diagnosis

EXPECTED CHANGES IN ACID-BASE DISORDERS

From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

Expected Changes Primary Disorder

PCO2 = 1.5 × HCO3 + (8 ± 2) Metabolic acidosis

PCO2 = 0.7 × HCO3 + (21 ± 2) PCO2= 0.9 * HCO3 +16

Metabolic alkalosis

delta pH = 0.008 × (PCO2 - 40)ΔHCO3 = 0.1 × (PCO2-40)

Acute respiratory acidosis

delta pH = 0.003 × (PCO2 - 40)ΔHCO3 = 0.35 × (PCO2-40)

Chronic respiratory acidosis

delta pH = 0.008 × (40 - PCO2)ΔHCO3 = 0.2 × (40 – PCO2 )

Acute respiratory alkalosis

delta pH = 0.003 × (40 - PCO2)ΔHCO3 = 0.4 × (40 – PCO2)

Chronic respiratory alkalosis

PH

PH:7,37-7,43 MIXED VS NORMAL

PH>7,43 ALKALOSIS

PCO2>40

M.AL

PCO2<40

R.AL

PH<7,37 ACIDOSIS

PCO2<40

M.AC

PCO2>40

R.AC

PH(7,37-7,43)PCO2<36,HCO3<21

RES.ALK+ M.AC

PCO2>44,HCO3>27

RES.AC + M.ALK

PCO2(nor),HCO3(nor)

M.AC +M.ALK

AG

Respiratory system includes:

1. CNS (medulla)

2. Peripheral nervous system (phrenic nerve)

3. Respiratory muscles

4. Chest wall

5. Lung

6. Upper airway

7. Bronchial tree

8. Alveoli

9. Pulmonary vasculature

Potential causes of Respiratory Failure

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RESPIRATORYACIDOSIS / ALKALOSIS

CO2 + H2O H2CO3 H+ + HCO3

- Respiratory Acidosis

Respiratory Alkalosis

RESPIRATORY ALKALOSIS

12


©Normal 20:1 ratio is increasedªpH of blood is above 7.4

H2CO3 HCO3-

1 20:= 7.4

H2CO

3 HCO3

-

0.5 20:= 7.4

13


©Cause is HyperventilationªLeads to eliminating excessive

amounts of CO2

ªIncreased loss of CO2 from the lungs at a rate faster than it is produced

ªDecrease in H+

CO2 CO2 CO2CO2

CO2

CO2

CO2

CO2

CO2CO2

CO2CO2

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HYPERVENTILATION

©Hyper = “Over”

Elimination of CO2

H+

pH

15

RESPIRATORY ALKALOSIS©Can be the result of:

ª1) Anxiety, emotional disturbances

ª2) Respiratory center lesions

ª3) Feverª4) Salicylate poisoning

(overdose)ª5) Assisted respirationª6) High altitude (low

PO2)

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RESPIRATORY ALKALOSIS©Anxiety is an emotional disturbance

ªThe most common cause of hyperventilation, and thus respiratory alkalosis, is anxiety

©Respiratory center lesionsªDamage to brain centers

responsible for monitoring breathing rates¨ Tumors¨ Strokes

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RESPIRATORY ALKALOSIS©Fever

ªRapid shallow breathing blows off too much CO2

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RESPIRATORY ALKALOSIS©Salicylate poisoning

(Aspirin overdose)ªVentilation is

stimulated without regard to the status of O2, CO2 or H+ in the body fluids

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RESPIRATORY ALKALOSIS©Assisted Respiration

ªAdministration of CO2 in the exhaled air of the care - giver

Your insurance won’t cover a ventilator any

longer, so Bob here will be giving you mouth to

mouth for the next several days

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RESPIRATORY ALKALOSIS©High Altitude

ªLow concentrations of O2 in the arterial blood reflexly stimulates ventilation in an attempt to obtain more O2

ªToo much CO2 is “blown off” in the process

Causes of Respiratory AlkalosisCENTRAL RESPIRATORY STIMULATION

(Direct Stimulation of Resp Center):

Structural Causes Non Structural Causes• Head trauma Pain• Brain tumor Anxiety• CVA Fever• Voluntary

PERIPHERAL RESPIRATORY STIMULATION (Hypoxemia Reflex Stimulation of Resp Center via Peripheral Chemoreceptors)

• Pul V/Q imbalance• Pul Diffusion Defects Hypotension• Pul Shunts High Altitude

INTRATHORACIC STRUCTURAL CAUSES: 1. Reduced movement of chest wall & diaphragm2. Reduced compliance of lungs 3. Irritative lesions of conducting airways

MIXED/UNKNOWN MECHANISMS:4. Drugs – Salicylates Nicotine Progesterone Thyroid hormone

Catecholamines Xanthines (Aminophylline & related

compounds)2. Cirrhosis3. Gram –ve Sepsis4. Pregnancy5. Heat exposure6. Mechanical Ventilation

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RESPIRATORY ALKALOSIS©Kidneys compensate by:

ªRetaining hydrogen ionsªIncreasing bicarbonate

excretion

H+

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

H+

H+

H+

H+

H+

H+

H+

H+

H+

H+

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RESPIRATORY ALKALOSIS©Decreased CO2 in the lungs will

eventually slow the rate of breathingªWill permit a normal amount of

CO2 to be retained in the lung

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RESPIRATORY ALKALOSIS-metabolic balance before onset of

alkalosis-pH = 7.4

-respiratory alkalosis-pH = 7.7

-hyperactive breathing “ blows off ” CO2

-body’s compensation

-kidneys conserve H+ ions and eliminate HCO3

- in alkaline urine

-therapy required to restore metabolic balance

-HCO3- ions replaced by Cl- ions

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-metabolic balance before onset of alkalosis-pH = 7.4

H2CO3 HCO3-

1 20:

H2CO3 : Carbonic Acid

HCO3- : Bicarbonate Ion

(Na+ )HCO3-

(K+ )HCO3-

(Mg++ )HCO3-

(Ca++ )HCO3-

30


-respiratory alkalosis-pH = 7.7-hyperactive breathing “ blows off ” CO2

H2CO

3 HCO3

-

0.5 20:

CO2

CO2 +H2O

31


BODY’S COMPENSATION -kidneys conserve H+ ions and eliminate HCO3

- in alkaline urine

H2CO

3 HCO3

-

0.5 15:

HCO3-

Alkaline Urine

32



-HCO3- ions replaced by Cl- ions

H2CO3 HCO3-

0.5 10:

Cl-

Chloride containing

solution

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RESPIRATORY ALKALOSIS©Usually the only treatment needed is

to slow down the rate of breathing©Breathing into a paper bag or holding

the breath as long as possible may help raise the blood CO2 content as the person breathes carbon dioxideback in after breathing it out

Treatment of Respiratory Alkalosis

Resp alkalosis by itself not a cause of resp failure unless work of increased breathing not sustained by resp muscles

Rx underlying causeUsually extent of alkalemia produced not

dangerous. Admn of O2 if hypoxaemiaIf pH>7.55 pt may be sedated/anesthetised/

paralysed and/or put on MV.

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RESPIRATORY ACIDOSIS

40

RESPIRATORY ACIDOSIS©Caused by hyperkapnia due to

hypoventilationªCharacterized by a pH decrease

and an increase in CO2

CO2 CO2

CO2

CO2

CO2

CO2CO2

CO2CO2

CO2

CO2 CO2

CO2

pH

pH

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HYPOVENTILATION

©Hypo = “Under”

Elimination of CO2

H+

pH

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RESPIRATORY ACIDOSIS©The speed and depth of breathing control

the amount of CO2 in the blood

©Normally when CO2 builds up, the pH of the blood falls and the blood becomes acidic

©High levels of CO2 in the blood stimulate the parts of the brain that regulate breathing, which in turn stimulate faster and deeper breathing

45


©Respiratory acidosis develops when the lungs don't expel CO2 adequately

©This can happen in diseases that severely affect the lungs, such as emphysema, chronic bronchitis, severe pneumonia, pulmonary edema, and asthma

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RESPIRATORY ACIDOSIS©Respiratory acidosis can also develop when

diseases of the nerves or muscles of the chest impair the mechanics of breathing

©In addition, a person can develop respiratory acidosis if overly sedated from narcotics and strong sleeping medications that slow respiration

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RESPIRATORY ACIDOSIS©The treatment of respiratory acidosis

aims to improve the function of the lungs

©Drugs to improve breathing may help people who have lung diseases such as asthma and emphysema

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RESPIRATORY ACIDOSIS© Decreased CO2 removal

can be the result of:1)Obstruction of air

passages2)Decreased

respiration (depression of respiratory centers)

3)Decreased gas exchange between pulmonary capillaries and air spacs of lungs

4)Collapse of lung

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RESPIRATORY ACIDOSIS©1) Obstruction of air passages

ªVomit, anaphylaxis, tracheal cancer

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RESPIRATORY ACIDOSIS©2) Decreased Respiration

ªShallow, slow breathing ªDepression of the respiratory centers in

the brain which control breathing rates¨ Drug overdose

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RESPIRATORY ACIDOSIS©3) Decreased

gas exchange between pulmonary capillaries and air sacs of lungsªEmphysemaªBronchitisªPulmonary

edema

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RESPIRATORY ACIDOSIS©4) Collapse of lung

ªCompression injury, open thoracic wound

Left lung collapsed

Causes of Acute Respiratory Acidosis

EXCRETORY COMPONENT PROBLEMS:1. Perfusion:

Massive PTECardiac Arrest

2. Ventilation:Severe pul edemaSevere pneumoniaARDSAirway obstruction

3. Restriction of lung/thorax:Flail chestPneumothoraxHemothorax

4. Muscular defects:Severe hypokalemiaMyasthenic crisis

5. Failure of Mechanical Ventilator

CONTROL COMPONENT PROBLEMS:6. CNS: CSA

Drugs (Anesthetics, Sedatives) Trauma Stroke

2. Spinal Cord & Peripheral Nerves:Cervical Cord injury LGBSNeurotoxins (Botulism, Tetanus, OPC)Drugs causing Sk. m.paralysis (SCh, Curare,

Pancuronium & allied drugs, aminoglycosides)

Causes of Chronic Respiratory Acidosis

EXCRETORY COMPONENT PROBLEMS:

1. Ventilation:COPDAdvanced ILD

Restriction of thorax/chest wall:Kyphoscoliosis, ArthritisFibrothoraxHydrothoraxMuscular dystrophyPolymyositis

CONTROL COMPONENT PROBLEMS:

1. CNS: Obesity Hypoventilation Syndrome Tumours

Brainstem infarctsMyxedemaCh sedative abuseBulbar Poliomyelitis

2. Spinal Cord & Peripheral Nerves:PoliomyelitisMultiple SclerosisALSDiaphragmatic paralysis

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RESPIRATORY ACIDOSIS-metabolic balance before onset of

acidosis-pH = 7.4

-respiratory acidosis-pH = 7.1-breathing is suppressed holding CO2

in body

-body’s compensation-kidneys conserve HCO3

- ions to restore the normal 40:2 ratio

-kidneys eliminate H+ ion in acidic urine


-lactate solution used in therapy is converted to bicarbonate ions in the

liver

40

60


-metabolic balance before onset of acidosis -pH = 7.4

H2CO3 HCO3-

1 20:

H2CO3 : Carbonic Acid

HCO3- : Bicarbonate Ion

(Na+ )HCO3-

(K+ )HCO3-

(Mg++ )HCO3-

(Ca++ )HCO3-

61


-breathing is suppressed holding CO2 in body-pH = 7.1

H2CO3

HCO3-

2 20:

CO2

CO2

CO2

CO2

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BODY’S COMPENSATION-kidneys conserve HCO3

- ions to restore the normal 40:2 ratio (20:1)

-kidneys eliminate H+ ion in acidic urine

H2CO3

HCO3-

2 30:

HCO3-

H2CO3

HCO3-

H+

+

acidic urine

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-lactate solution used in therapy is converted to bicarbonate ions in the liver

H2CO3 HCO3-

2 40:

Lactate

Lactate

LIVER

HCO3-

TREATMENT OF RESPIRATORY ACIDOSIS

The goal is to increase the exhalation of CO2. The treatments are :– Based on the underlying causes – By providing ventilation therapy – Intravenous administration of HCO3

-

– Reversal of sedation or neuromuscular relaxants

– Intubation and artificial ventilation (in severe cases)

CASE -1

A 28 year old woman was admitted electively to a HDU (high dependency unit) following a caesarian section.

A diagnosis of 'fatty liver of pregnancy' had been made preoperatively.

She was commenced on a continuous morphine infusion at 5 mg/hr and received oxygen by mask.

This was continued overnight and she was noted to be quite drowsy the next day.

Arterial blood gases were

ABG7,16 PH

61,9 PCO2

115 PO2

21,2 HCO3

PH<7,37 •ACIDOSIS

PCO2>40 •RESPIRATORY

ACUTE.R.AC COMP

•∆HCO3=0,1(62- 40)=2,2(+24)•26,2≠ 21

• concomitant M.AC

AG?=Normal AG (12±4)

•???

CASE-2

A 69 year old patient had a cardiac arrest soon after return to the ward following an operation.

Resuscitation was commenced and included intubation and ventilation.

Femoral arterial blood gases were collected about five minutes after the arrest.

LAB :

Anion gap 24,

Lactate 12 mmol/l.

ABG

6,85 PH

82 PCO2

214 PO2

14 HCO3

PH<7,37 •ACIDOSIS

PCO2>40 •RESPIRATORY

ACUTE.R.AC COMP

•∆HCO3=0,1(82- 40)=4,2 (+24)•28,2≠ 14

• concomitant M.AC

AG=24Normal AG (12±4)

•High AG M.ACGAP:ga

p=1,2•NO other metabolic disorders

Discussion Cardiac arrest with low cardiac output and tissue hypo-perfusion causing a: – severe lactic acidosis.

Ventilation is depressed causing a: – respiratory acidosis.

Inadequate ventilation in this pre-arrest phase may have been related to several factors, in particular :– inadequate reversal of neuromuscular paralysis, – airway obstruction in a supine sedated patient or– acute pulmonary oedema.

CASE-3

A 70 year old man was admitted with severe congestive cardiac failure.

He has been unwell for about a week and has been vomiting for the previous 5 days.

He was on no medication.

He was hyperventilating and was very distressed.

Admission biochemistry is listed below.

He was on high concentration oxygen by mask.

LAB:BIOCHEMISTRY

127 NA

5,2 K

79 CL

20 HCO3

50,5 mmol\l UREA

0,38 mmol\l CREAT

9,5 mmol\l GLUCO

33 AG

ABG

7,58 PH

21 PCO2

154 PO2

19 HCO3

Creat = 5 mg\dl (\0,075) Urea =141,4 (\0,357)

Glucose =171 (*18)cNA=128

Corrected Sodium = Measured sodium + 0.016 * (Serum glucose - 100)

PH>7,43 •ALKALOSIS

PCO2<40 •RESPIRATORY

C,R .ALK COMP

•∆HCO3=0,4(40 -21)=24 – 7,6•16,4 ≠19• concomitant M.ALK

AG=28Normal AG (12±4)

•HIGH AG M.AC

GAP:gap=(4> 2) • concomitant M.ALK

Discussion

The history suggests the following possibilities:

Respiratory alkalosis in response to the dyspnoea associate with the congestive heart failure

A lactic acidosis is possible if cardiac output is low and tissue perfusion is poor

Vomiting suggests metabolic alkalosis

The renal failure could be associated with a high anion gap acidosis

Discussion

This patient has a triple acid-base disorder:Acute metabolic acidosis probably due to renal failure (?prerenal failure) and possibly to lactic acidosis (hypoperfusion due heart failure and hypovolaemia)

Metabolic alkalosis due to severe vomiting

Respiratory alkalosis due to dyspnoea from congestive heart failure.

The pO2 is elevated due to administration of a high inspired oxygen concentration

NEXT LECTURE

1. Approche to hypoxiemic patient2. Cases

ABG 6 Series

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