Download - ABG 6 Series
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ABG series
ANAS SAHLE , MDDAMASCUSE
HOSPITAL
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Acid-Base Disorders and the ABG 6
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BREIF PREVIEW
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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
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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
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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
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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
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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
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Potential causes of Respiratory Failure
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RESPIRATORYACIDOSIS / ALKALOSIS
CO2 + H2O H2CO3 H+ + HCO3
- Respiratory Acidosis
Respiratory Alkalosis
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RESPIRATORY ALKALOSIS
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RESPIRATORY ALKALOSIS
©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
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RESPIRATORY ALKALOSIS
©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
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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
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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
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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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RESPIRATORY ALKALOSIS
-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-
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RESPIRATORY ALKALOSIS
-respiratory alkalosis-pH = 7.7-hyperactive breathing “ blows off ” CO2
H2CO
3 HCO3
-
0.5 20:
CO2
CO2 +H2O
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RESPIRATORY ALKALOSIS
BODY’S COMPENSATION -kidneys conserve H+ ions and eliminate HCO3
- in alkaline urine
H2CO
3 HCO3
-
0.5 15:
HCO3-
Alkaline Urine
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RESPIRATORY ALKALOSIS
-therapy required to restore metabolic balance
-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
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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
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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
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RESPIRATORY ACIDOSIS
©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
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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
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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)
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Causes of Chronic Respiratory Acidosis
EXCRETORY COMPONENT PROBLEMS:
1. Ventilation:COPDAdvanced ILD
Restriction of thorax/chest wall:Kyphoscoliosis, ArthritisFibrothoraxHydrothoraxMuscular dystrophyPolymyositis
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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
-therapy required to restore metabolic balance
-lactate solution used in therapy is converted to bicarbonate ions in the
liver
40
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RESPIRATORY ACIDOSIS
-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-
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RESPIRATORY ACIDOSIS
-breathing is suppressed holding CO2 in body-pH = 7.1
H2CO3
HCO3-
2 20:
CO2
CO2
CO2
CO2
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RESPIRATORY ACIDOSIS
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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RESPIRATORY ACIDOSIS
-therapy required to restore metabolic balance
-lactate solution used in therapy is converted to bicarbonate ions in the liver
H2CO3 HCO3-
2 40:
Lactate
Lactate
LIVER
HCO3-
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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)
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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
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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)
•???
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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.
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LAB :
Anion gap 24,
Lactate 12 mmol/l.
ABG
6,85 PH
82 PCO2
214 PO2
14 HCO3
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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
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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.
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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.
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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)
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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
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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
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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
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NEXT LECTURE
1. Approche to hypoxiemic patient2. Cases