Arterial Blood Gases: Partially and fully compensated Flashcards
Assessment of oxygenation status of blood
Assessment of ventilation/gas exchange
Assessment of acid/base balance
Evaluation of treatments used to correct acid/base imbalances
Purpose of ABG interpretation
Measurement of oxygenation
Measurement of ventilation (acid-base disorder)
Hypoxemia – inadequate blood O2: mild (PaO2 60-79) moderate (PaO2 40-59) severe (PaO2 less than 40)
ABG Overview
The PaO2 is a measure of the partial pressure (P) of oxygen dissolved in arterial blood plasma.
Normal range: 80-100 mm Hg
Measurement of oxygenation
The pH is the hydrogen ion (H+) concentration of plasma
Normal range: 7.35 to 7.45
PaCO 2 is a measure of the partial pressure of carbon dioxide dissolved in arterial blood plasma
Normal range: 35 to 45 mm Hg
Bicarbonate (HCO3 −) is the acid–base component that reflects kidney function. The HCO3 − level is reduced or increased in the plasma by renal mechanisms.
Normal range: 22 to 26 mEq/L
Measurement of ventilation (acid-base disorder)
pH < 7.35
Respiratory: ↑ PaCo2
Metabolic: ↓ HCO3-
Acidosis
pH > 7.45
Respiratory: ↓ PaCo2
Metabolic: ↑ HCO3-
Alkalsosis
Mild hypoxemia: 60-79
Moderate hypoxemia: 40-59
Severe: <40
PaO2
Base excess and base deficit reflect the nonrespiratory contribution to acid–base balance
Normal range of −2 mEq/L to +2 mEq/L
A high base excess (> +2mEq/L) indicates that there is a higher than normal amount of HCO3- in the blood, which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis.
A low base excess (< -2mEq/L) indicates that there is a lower than normal amount of HCO3- in the blood, suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.”
The base excess is another surrogate marker of metabolic acidosis or alkalosis.
Base excess
The body tries to minimize pH changes and responds to acid-base disturbances with body buffers.
Compensatory responses by the lungs (Co2) and kidney (HCO3-) to metabolic and respiratory disturbances, respectively.
Phosphate system
Hemoglobin and other proteins
Compensatory responses: Involves responses by the respiratory tract and/or kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation is driven by pH changes and opposes the primary disturbance.
Respiratory compensation is rapid
Metabolic compensation is slow
Compensation: compensatory mechanisms
A patient’s acid-base balance can be uncompensated, partially compensated, or fully compensated
Uncompensated or partially compensated acid-base disorder: The pH remains outside the normal range
Fully compensated acid-base disorder: The pH has returned to within normal range, although PaCO2 and HCO3- are generally still abnormal.
The body is unable to ‘overcompensate.’
The lungs act fast but can rarely fully compensate for a metabolic imbalance.
EX:
Compensation
Metabolic acidosis
Compensation: Increased respiratory rate & depth to change PaCo2 to correct pH
Respiratory acidosis
Compensation: More hydrogen excreted by kidneys and more HCO3 − reabsorbed to correct pH
Metabolic alkalosis
Compensation: Less Hydrogen excreted by the Kidneys, O and Less HCO3 − reabsorbed to correct pH
Respiratory alkalosis
Compensation: Less hydrogen excreted by the kidneys and Less HCO3 − reabsorbed to correct pH
EX:
Uncompensated: ↓ pH (acidic), ↑ PaCO2 (acidic), Normal HCO3-
Partially compensated: ↓ pH (acidic), ↑ PaCO2 (acidic), ↑ HCO3- (Basic)
Compensated: Normal pH,↑ PaCO2, ↑ HCO3-
Causes: Airway obstruction, CNS depression (hypoventilation, opioids), brain stem injury, sleep apnea, neuromuscular impairment, ventilatory restriction (asthma, COPD), Increased CO2 production (shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates), Incorrect ventilator settings
Treatment: Treat the underlying cause, oxygen, mechanical ventilation, suction, bronchodilators
Signs and Symptoms: Sx related to the cause.
is usually caused by hypoventilation. When the Pco2 rises in the extracellular fluid compartment, hydrogen and bicarbonate ion concentrations also rise. This occurs as carbonic acid forms and dissociates. When buffer systems cannot keep up, the pH falls rapidly. Just a few minutes of hypoventilation may result in acidosis.
When the body’s chemical and physiological buffers return pH to normal, the acidosis is compensated. This is normally accomplished by chemoreceptors that stimulate an increase in breathing rate.
Injury to the brain stem’s respiratory center, decreasing breathing
Obstruction of air passages and interference with air movement into alveoli
Diseases decreasing gas exchange, such as pneumonia, or reducing respiratory membrane surface area, such as emphysema; also linked to cystic fibrosis
Assessment cues are dependent on underlying cause. (Nurselabs)
ACTIVITY/REST
CIRCULATION
FOOD/FLUID
NEUROSENSORY
RESPIRATION
Respiratory acidosis
In uncompensated acidosis, the pH continues to drop, and the patient can become comatose and eventually die. Acute respiratory acidosis develops when the decline in pH is severe. It is an especially dangerous condition when the patient’s tissues generate large amounts of carbon dioxide or when normal respiratory activity is not possible. Therefore, for victims of cardiac arrest or drowning, reversing acute respiratory acidosis is the major goal.
Uncompensated: ↓ pH (acidic), ↑ PaCO2 (acidic), Normal HCO3-
Confusion, lethargy, dyspnea, pale or cyanotic skin, mental cloudiness, restlessness, hypertension, weakness, headache, Increased respiratory effort with nasal flaring/yawning, use of neck and upper body muscles
Decreased respiratory rate/hypoventilation (associated with decreased function of respiratory center as in head trauma, oversedation, general anesthesia, metabolic alkalosis)
Adventitious breath sounds (crackles, wheezes); stridor, crowing
Signs and Symptoms: Sx related to the cause.
May report: Fatigue, mild to profound
May exhibit: Generalized weakness, ataxia/staggering, loss of coordination (chronic), to stupor
ACTIVITY/REST
May exhibit: Low BP/hypotension with bounding pulses, pinkish color, warm skin (reflects vasodilation of severe acidosis)
Tachycardia, irregular pulse (other/various dysrhythmias)
Diaphoresis, pallor, and cyanosis (late stage)
CIRCULATION
May report: Nausea/vomiting
FOOD/FLUID
May report: Feeling of fullness in head (acute—associated with vasodilation)
Headache, dizziness, visual disturbances
May exhibit: Confusion, apprehension, agitation, restlessness, somnolence; coma (acute)
Tremors, decreased reflexes (severe)
NEUROSENSORY
May report: Shortness of breath; dyspnea with exertion
May exhibit: Respiratory rate dependent on underlying cause, i.e., decreased in respiratory center depression/
muscle paralysis; otherwise rate is rapid/shallow
Increased respiratory effort with nasal flaring/yawning, use of neck and upper body muscles
Decreased respiratory rate/hypoventilation (associated with decreased function of respiratory center as in head trauma, oversedation, general anesthesia, metabolic alkalosis)
Adventitious breath sounds (crackles, wheezes); stridor, crowing
RESPIRATION
Uncompensated: ↑ pH (Basic), ↓ PaCO2 (Basic), Normal HCO3-
Partially compensated: ↑ pH (Basic), ↓ PaCO2 (Basic), ↓ HCO3- (acidic)
Compensated: Normal pH, ↓ PaCO2, ↓ HCO3-
Causes: Hypoxemia or hypoxia (lung disease, profound anemia, low FiO2), Incorrect ventilator settings, CNS stimulation (fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection), Pulmonary embolism
Treatment: Treat the underlying cause, mechanical ventilation, buffers, and have the patient rebreathe air that has been exhaled (put a non-rebreather on w/o Oxygen)
Signs and symptoms: Deep Rapid Breathing (40+ bpm)*, CNS and neuromuscular disturbances: lightheadedness, agitation, circumoral and peripheral paresthesias, carpopedal spasms, twitching and muscle weakness. Nausea and vomiting, Muscle twitching
is a less common condition that results from excessive carbon dioxide and carbonic acid loss or hypocapnia, this condition is signified by a Pco2 < 35 mm Hg, with raised blood pH.
Hyperventilation often results from pain or other physical stressors and extreme anxiety or other psychological stressors. It gradually elevates the pH of the cerebrospinal fluid, affecting central nervous system function. There are initial tingling sensations in the lips, hands, and feet. The individual may be light-headed and lose consciousness if the condition continues. Because unconsciousness stops the perception of causative psychological stimuli, the breathing rate declines, and the condition is self-corrected.
Brain stem injuries that cause them to be unable to respond to changes in plasma carbon dioxide concentrations.
Assessment
CIRCULATION
EGO INTEGRITY
FOOD/FLUID
NEUROSENSORY
PAIN/DISCOMFORT
RESPIRATION
SAFETY
TEACHING/LEARNING
Respiratory alkalosis
May report: History/presence of anemia
Palpitations
May exhibit: Hypotension
Tachycardia, irregular pulse/dysrhythmias
CIRCULATION
May exhibit: Extreme anxiety (most common cause of hyperventilation)
EGO INTEGRITY
May report: Dry mouth
Nausea/vomiting
May exhibit: Abdominal distension (elevating diaphragm as with ascites, pregnancy)
Vomiting
FOOD/FLUID
May report: Headache, tinnitus
Numbness/tingling of face, hands, and toes; circumoral and generalized paresthesia
Lightheadedness, syncope, vertigo, blurred vision
May exhibit: Confusion, restlessness, obtunded responses, coma
Hyperactive reflexes, positive Chvostek’s sign, tetany, seizures
Heightened sensitivity to environmental noise and activity
Muscle weakness, unsteady gait
NEUROSENSORY
