Transcript Metabolic - Shasta Nursing Central

Arterial Blood Gas
Analysis
Joan Bestor,
RN, MSN
Spring 2016
Blood Gas Values
• Arterial blood gas (ABG) values provide
information about
 Acid-base status
 Underlying cause of imbalance
 Body's ability to regulate pH
 Overall oxygen status
ABG Normal Values
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pH 7.35-7.45
PaCO2 35-45 mm Hg
HCO3 22-26 mEq/L
BE/BD + 2 mEq/L
PaO2 80-100 mm Hg
SaO2 95-100%
FiO2 21% (Room Air)
Hgb, Male 14-18 g/dL, Female 12-16 g/dL
pH
• The pH must be maintained within the
normal range for optimal functioning of
the body
 A decreased pH indicated acidosis
 An elevated pH indicates alkalosis
• Two primary systems maintain the body’s
pH within its normal range:
1. Respiratory System
2. Renal (Metabolic) System
pH
• The pH is the partial pressure of hydrogen ions
in the blood
• It reflects the acid base balance of the blood
• An inverse relationship exists between the pH
and the hydrogen ion concentration
• The functioning of most enzymatic systems in
the body are dependent upon a stable
hydrogen ion concentration
Large number of H+ ions, means
acidosis or low pH
Inverse Relationship
The more acid the lower the pH
Acid
pH
Carbon Dioxide
PaCO2
• PaCO2 is considered an acid and it represents
the respiratory component of the ABG test
• An elevated PaCO2 indicates respiratory
acidosis
• A decreased PaCO2 indicates respiratory
alkalosis
 Movement within this equation occurs freely
depending on the body’s needs and can
provide free H+ which is why the PaCO2 is
considered an acid when analyzing ABGs
Carbon Dioxide
PaCO2
• 35-45 mm Hg
• By-product of cellular metabolism
• Carried to the lungs by the blood
stream
• Expelled in exhaling
Bicarbonate Ion
HCO3
22-26 mEq/liter
• HCO3 is a base and it represents the
metabolic component of the ABG test
• An elevated HCO3 indicates
metabolic alkalosis (Too much)
• A decreased HCO3 indicates
metabolic acidosis (Not enough)
Movement within this equation occurs
freely depending on the body’s needs and
can provide free H+ which is why the PaCO2
is considered an acid when analyzing ABGs
CA
CO2 + H2O - H2CO3 - H+ (Hgb buffer) + HCO3
CA equals Carbonic Anhydrase
H2CO3 equals Carbonic Acid
Bicarbonate Ion
HCO3
22-26 mEq/liter
 When the blood becomes acidotic due to
respiratory issues the renal (metabolic)
system increases production and retention of
HCO3 and thus reduces the acid load in the
blood.
 When the blood becomes alkalotic due to
respiratory issues the renal (metabolic)
system decreases production and retention
of HCO3 and thus increases the acid load in
the blood.
BE/BD – 2 +2
• The base excess (BE) / base deficit (BD)
reflects the amount of buffering anions in
the blood. It is calculated using the pH,
PaCO2, and hematocrit values.
 Bicarbonate is the largest of these;
others include hemoglobin, proteins,
and phosphates.
 Base excess is a way to take all of
these anions into account when
determining acid/base treatment
BE/BD - 2 +2
 A positive BE/BD correlates
with metabolic alkalosis >+2
 A negative BE/BD correlates
with metabolic acidosis <-2
Acid-Base Balance
• Increase in H+ = acidosis
• Decrease in H+ = alkalosis
• Acid is a normal end product of
metabolism
• Acid must be neutralized or excreted
1 acid to 20 bicarbonates
Acid Base Balance
Equilibrium
• Equilibrium in extracellular fluid
• Between substances able to give up a hydrogen
ion, acids
• And those capable of accepting hydrogen ions
alkaline or base during chemical exchange
Acid
H+
Base
Alkaline
SaO2
• Oxyhemoglobin - oxygen bound to hemoglobin
molecule is called Oxyhemoglobin
• 97% of the oxygen in the blood, is carried by
hemoglobin molecule.
• Measured as SaO2
 SaO2 95-100%
 if < 90% give oxygen
PaO2
Partial Pressure Of Oxygen
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Remaining 3% is dissolved in the blood
Measured at PaO2
Normal - PaO2 80-100 mm Hg
Hypoxemia
 Mild, 60-79mm Hg
 Moderate,40-59mm Hg
 Severe, <40 mm Hg
 Prolonged hypoxemia leads to tissue
hypoxia and anaerobic metabolism
Hypoxia
• Indicates tissue ischemia
• Tachypnea, rate & depth
changes
• Changes in LOC
• Angina
• Tachycardia
• Cyanosis
Acid-Base Balance
1…2…3…4…5...6…7
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8…9…10…11...12…13…14
7.35 - 7.45
Acid
Neutral
Alkaline
Acid-Base Balance
Death
Acidosis Normal
6.8
7.35
Alkalosis
7.45
Death
7.8
Balancing Systems
1. Buffer system-seconds
2. Respiratory system-minutes
3. Renal system-2-3 days
What is Compensation?
• Ability of one system to attempt to
balance the pH when the other system
is causing an imbalance
• If respiratory system C02 is acid the
metabolic system HCO3 will attempt to
bring pH back to normal
Correction
• Correction
 Addressing the primary problem
and correcting it.
 Can be respiratory or metabolic in
nature
 Medical and nursing
interventions.
Acid Base Compensation
• The body will work to keep the pH between
7.35 and 7.45
• When one system fails, leading to an acid
base imbalance the other will work to restore
equilibrium
• The respiratory system compensates quickly
• The metabolic system takes 24 to 48 hours to
fully compensate
• With full compensation the pH will be normal
while all other acid base ABG values will be
abnormal
Acid Base Compensation
• When compensating for an acid base abnormality the
body will never over compensate
 Therefore, the pH is the key to finding the primary
problem with compensated ABGs
 pH > 7.35 but < 7.4 equals acidosis as the primary
problem
 pH > 7.4 but < 7.45 equals alkalosis as the primary
problem
 Partial compensation occurs when the body is still
working to achieve full compensation
 With partial compensation all the acid base ABG
values including the pH will be abnormal
Buffering System
Compensation
• Fastest system
• Primary regulator of acid-base balance
 Chemicals that change strong acids
to weaker acids
 Neutralize acids
• Chemicals inside the body help to keep
balance
• Balance of 20:1 (bicarbonate:acid)
Renal System Regulation
• Conserves bicarbonate and excretes
acid
• Three mechanisms for acid elimination
 Secrete free hydrogen in tubules
 Combine H+ with ammonia (NH3)
 Excrete weak acids
Renal System Regulation
• To compensate for acidosis, the kidneys
can generate additional bicarbonate and
eliminate excess H+, lowering the pH of
the urine.
• If the renal system is the cause of an
acid-base imbalance (renal failure), it
loses its ability to correct a pH
alteration.
Renal System
Compensation
• Main job of kidneys is to filter
metabolites of metabolism
• Reabsorb and conserve bicarbonate
 Excrete H+ in urine
 Reabsorb HC03
 Generate additional bicarbonate
 Eliminate acids
Respiratory System
Compensation
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Lungs help with balance
Excrete PaCO2 and water
By products of cellular metabolism
Respiratory center in Medulla
Increase/decrease breathing
 Rate
 Depth
 Blow-off or hyperventilate
 Retain or hypoventilation
Respiratory System
Compensation
• When the blood becomes acidotic due
to metabolic issues the respiratory
system increases the rate and depth of
ventilation to blow off CO2 and thus
reduce the acid load in the blood
• When the blood becomes alkalotic due
to metabolic issues the respiratory
system decreases the rate and depth of
ventilation to retain C02 and thus
increase the acid load in the blood.
Chemoreceptors
• Chemoreceptors respond to changes in
PaCO2 and pH.
• Central chemoreceptors are located in the
medulla and respond to changes in the
hydrogen ion (H+) concentration.
 An increase in the H+ concentration
(acidosis) causes the medulla to
increase the respiratory rate and tidal
volume (VT).
 A decrease in H+ concentration
(alkalosis) has the opposite effect.
Chemoreceptors
• Peripheral chemoreceptors are located
in the carotid bodies at the bifurcation
of the common carotid arteries and in
the aortic bodies above and below the
aortic arch
• The peripheral chemoreceptors
respond to decreases in PaO2 and pH
and to increases in PaCO2. These
changes also cause stimulation of the
respiratory center.
Compensation for AcidBase Abnormalities
• pH is normalized 7.35 - 7.45
• Takes days
• Homeostasis
pH
Acidosis
Acid
pH
pH falls below 7.35 if too much acid is
present
Alkalosis
Acid
pH rises above 7.45 if too little acid or too
much base is present
• Acid Base
 pH
 PaCO2
 HCO3
 BE/BD
• Oxygenation
 PaO2
 SaO2
 FiO2
 Hgb
Analyzing
ABGs
ABG Normal Values
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pH 7.35-7.45
PaCO2 35-45 mm Hg
HCO3 22-26 mEq/L
BE/BD + 2 mEq/L
PaO2 80-100 mm Hg
SaO2 95-100%
FiO2 21% (Room Air)
Hgb, Male 14-18 g/dL, Female 12-16 g/dL
Analyzing ABGs
 Use these identifiers for ABG analysis
 For the pH, PaCO2, HCO3, and BE/BD
use:
• A = acid or acidosis
• B = base or alkalosis
• N = normal
 For the SaO2, PaO2, FiO2, and Hgb. use:
• L = low
• H = high
• N = normal
Analyzing ABGs
 The first step is to analyze the acid base
status
• First assess the pH
• Then assess the PaCO2
• Then assess the HCO3
• Finally assess the BE/BD
 The identifier placed by the pH identifies the
type of acid base imbalance if one is present
• Acidosis (A)
• Alkalosis (B)
Analyzing ABGs
 After placing the identifiers with each
value
• Match the pH identifier with either
the PaCO2 or the HCO3 identifier
• This match determines the etiology
of the acid base disorder
• Respiratory (PaCO2)
• Metabolic (HCO3)
Analyzing ABGs
 The second step is to analyze the
oxygenation status
• First assess the PaO2
• Then assess the SaO2
• Then assess the FiO2
• Finally assess the Hgb
 Determine if the oxygenation status is
impaired (inadequate) or adequate (normal)
 If any of the four oxygenation factors are
abnormal, either high or low, then
oxygenation is impaired (inadequate)
Types of Disturbances
1.
2.
3.
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Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
Respiratory Acidosis
Hypoventilation
• pH less than 7.35
• PaC02 over 45
 Too much C02
• Hypoventilation
• Inadequate ventilation to meet
demands
Hypoventilation Causes
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Pneumonia, asthma
Acute pulmonary edema
Pneumothorax
Emphysema, COPD Depression of
respirator
Drug overdose
center
Head injury
Drowning
Airway obstruction
Trauma to chest wall, ribs
Respiratory arrest, apnea
Respiratory Acidosis
Treatment
• Treatment- underlying cause
 Deep breath & cough
 Respiratory treatment
 Ambulate
 Antibiotics
 Diuretics
 Chest tube
 Intubate
 CPAP Mask
Respiratory Acidosis
Signs & Symptoms
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Restlessness & confusion
Dizziness
Lethargy
Headache
Tachycardia & ventricular dysrhythmias
Warm and flushed skin
Muscular twitching
Convulsions and coma
Respiratory Acidosis
Compensation
 Kidneys conserve HCO3–
 Secrete or eliminate H+ into urine
• Renal compensatory
mechanism within 24 hours.
Case Study 1
• 67-year- old male arrived in the emergency room
via local ambulance. Patient is overweight, and
has history of back pain.
• Patient’s family states he has been taking Norco
15 mg, 2 tabs every 4 hours for back pain.
Evidently he was still in pain, doubles dose.
• Family also states patient had been drinking
whiskey, and took several sleeping pills, and his
antidepressants.
• Family called 9-1-1 when he failed to wake up.
• Paramedics administer oxygen and transport
Case Study 1
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On arrival in the ED ABG’S were done.
pH 7.21
PaCO2 68 mm Hg
HCO3 26 mEq/L
BE/BD + 2 mEq/L
PaO2 75 mm Hg
SaO2 45%
FiO2 50%
Hgb, Male 15 g/dL
Case Study 1
Overdose
Respiratory Acidosis
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Intubate
Consider giving Narcan 4 mg IV push
Oxygen 100%
Ventilator
IV Fluids
Supportive care until awake enough
to support own respirations
Nursing Interventions
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Patient teaching
Medication use, misuse
Psychosocial consult
Discharge planning
Role of diet and exercise
Respiratory Alkalosis
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pH over 7.45
PaC02 under 35
Hyperventilation
Deep rapid respirations
 Anxiety
 CNS disorders
 Pulmonary embolism
 Mechanical over ventilation
Respiratory Alkalosis
• Factors leading to hyperventilation
include:
 Anxiety
 Panic
 Pain
 Hypoxemia
 Gram negative bacteremia
Respiratory Alkalosis
• Treatment is aimed at cause
 Mirror breathing
 Antianxiety medications
 Purse lip breathing
 Oxygen administration
Respiratory Alkalosis
• Carbonic acid deficit caused by
 Hypoxemia from acute pulmonary
disorders that occurs with
hyperventilation
• Compensation
 Rarely occurs when acute
 Can buffer with bicarbonate shift
 Renal compensation if chronic
Hyperventilation
• Ventilation in excess of that required to
eliminate carbon dioxide produced by
cellular metabolism
• Anxiety, infections, drugs, acid-base
imbalance, fever, aspirin poisoning, or
amphetamine use.
 Results in lower CO2, or respiratory
alkalosis
Respiratory Alkalosis
Signs & Symptoms
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Dizziness
Hyperventilation
Light-headedness
Muscle cramps and spasms
Paresthesia
Palpations
Tachypnea
Numbness and tingling of extremities
Convulsions
Coma
Case Study 2
• 36-year-old male patient has history of
anxiety disorder. The patient comes to
the ED with complaints of chest pain.
• Patient has no sign of cardiac
abnormalities EKG, Troponin are
normal. Chest x-ray is normal. Oximeter
show saturation of 100% on room air.
• ABG’s were drawn.
Case Study 2
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pH - 7.46
PaCO2 - 33 mm Hg
HCO3 24 mEq/L
BE/BD + 2 mEq/L
PaO2 100 mm Hg
SaO2 100%
FiO2 21% (Room Air)
Hgb, Male -16 g/dL
Case Study 2
• Patient was instructed to breath in to a
paper bag.
• Nurse does mirror breathing
• Ativan 1 mg was administered.
• Patient was discharged home with
follow-up with family doctor.
Metabolic Acidosis
• pH less than 7.35
• Definition: A decreased pH due to an
elevated H+ ion concentration or a
loss of HCO3
Metabolic Acidosis
• Increase in H+ ions
• Lactic acidosis, poor perfusion,
hypoxemia
• Ketoacidosis
• Late stage of salicylate poisoning
• Methanol ethylene glycol toxicity
• Starvation or extreme dieting
• Excessive exercise without caloric intake
• Renal failure
Metabolic Acidosis
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Loss of HCO3
Diarrhea
Intestinal fistulas
Excessive administration of
chloride
• Bicarbonate poor TPN
Metabolic Acidosis
• Compensatory mechanisms
 Increased CO2 excretion by lungs
• Kussmaul respirations (deep and
rapid)
 Kidneys excrete acid
When acidosis severe the
buffering system is depleted and
cannot compensate
Metabolic Acidosis
Signs & Symptoms
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Hyperventilation
Arrhythmias
Hypotension
Lethargy
Lactic Acidosis
• Lactic acidosis – shock, lactate (< .3)
• Inadequate oxygenation can lead
metabolic acidosis, as in shock-induced
hypoxemia
• Resulting in tissue hypoxia, anaerobic
metabolism and accumulation of lactic
acid.
• Shock
• Death
Metabolic Acidosis
Treatment
• Treat the underlying cause
• Anaerobic metabolism, A-B-C
• Antidiarrheal medications
 Do not give if infectious
• Diabetes care, fluids & Insulin
• Nutrition
• NaHCO3 (Sodium Bicarbonate)
• Supportive care
Metabolic Acidosis
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Early symptoms
Headache
Lethargy
Progress to coma
Anorexia, nausea, vomiting
Diarrhea
Abdominal pain
Case Study 3
• 17 year-old female, flu symptoms, came
into ER. Patient is thin, pale, and looks
dehydrated.
• Patient has no history of diabetes
• Vital Signs: Temp 102, BP, 96/54, RR 30,
saturation 100%
• Blood glucose level 553
• Fruity sweet smelling breath
• Patient has difficulty focusing and
answering questions
Case Study 3
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pH 7.21
PaCO2 25 mm Hg
HCO3 11 mEq/L
BE/BD - 5 mEq/L
PaO2 100 mm Hg
SaO2 100%
FiO2 21% (Room Air)
Hgb, Female 12-16 g/dL
Case Study 3
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Metabolic Acidosis
IV fluids, normal saline
Insulin drip
Electrolyte replacement
Food when able to eat
Patient teaching on new onset
Type 1 diabetes
Metabolic Alkalosis
• pH over 7.45
• Definition: An increased pH due
to a decreased H+ ion
concentration or retention of
HCO3
Metabolic Alkalosis
• Decrease in H+ ions=acid lost
 Vomiting
 Gastric suctioning
• Stimulates excessive retention of HCO3
 Diuretic use long term
 Cushing’s syndrome
 Ingestion of baking soda
 IV Bicarbonate
Metabolic Alkalosis
• Treatment-underlying cause
 Antiemetic
 Replace NG tube output with
NaCL 0.9%
 Do not use sodium bicarbonate
as an antacid
Metabolic Alkalosis
Signs & Symptoms
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Hypertonic muscles and cramping
Hypotension
Warm, flushed skin
Arrhythmias
Confusion
Apathy
Stupor
Muscle weakness
Hypoventilation secondary to compensation
Tetany
Metabolic Alkalosis
Compensation
• Compensatory mechanisms
• Response is limited
 Renal excretion of HCO3–
 Decreased respiratory rate to
increase plasma CO2 (limited)
Case Study 4
• 56 year-old female, post op day 2
from open Cholecystectomy, with
N/G tube to continuous suction.
• Patient complains of pain and
nausea
• Family is bringing in bicarbonate of
soda
Case Study 4
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pH 7.51
• Compensation will
PaCO2 40 mm Hg
be to decrease
HCO3 32 mEq/L
respiratory rate to
try and keep pH
BE/BD + 8 mEq/L
normal
PaO2 97 mm Hg
• Hold on to acids
SaO2 100%
FiO2 21% (Room Air)
Hgb, Female 15 g/dL
Metabolic Alkalosis Case
Study 4
• Treatment
 Address pain
 Give antiemetic's
 Consider clamping N/G tube
 Electrolyte replacement
Case Study 5
• 55 year-old male admitted for
shortness of breath and a 1-week
history of coughing up tan sputum.
• Chest x-ray reveals bilateral
pneumonia
• Patient has a history of smoking.
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ABG Values
Case Study 5
pH 7.28
PaCO2 56 mm Hg
HCO3 25 mEq/L
BE/BD + 2 mEq/L
PaO2 70 mm Hg
SaO2 88%
FiO2 21% (Room Air)
Hgb, Male 15 g/dL
Treatment Pneumonia
Respiratory Acidosis
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Oxygen
Antibiotics
Fluids
Breathing treatment with albuterol
Case Study 6
• 75-year-old male, 40-pack-year
history of smoking, worked in
cement plant for 40 years. He has a
history of COPD.
• The patient was admitted to sleep
clinic for evaluation of bi-pap.
• Work up includes labs, chest x-ray.
ABG Case Study 6
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pH - 7.37
PaCO2 - 53 mm Hg
HCO3 - 32 mEq/L
BE/BD + 3 mEq/L
PaO2 - 58mm Hg
SaO2 - 85%
FiO2 - 21% (Room Air)
Hgb, Male 19 g/dL,
Compensated
Respiratory Acidosis
Metabolic Alkalosis
Do Nothing
Nursing & Collaborative
Care
• Assessment
 Oximetry
 Vital signs
 Diagnostic Test
• Oxygen therapy
• Medications
• Pain medication
• Respiratory Care
• Physical Therapy
Nursing Diagnosis
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Impaired gas exchange
Impaired spontaneous ventilation
Ineffective breathing pattern
Activity intolerance
Ineffective airway clearance
Decreased cardiac output
Fatigue
Risk for aspiration
Risk for infection
Risk for suffocation