case study respiratory acidosis

Respiratory Acidosis

Respiratory acidosis is a critical acid-base imbalance that demands vigilant monitoring and prompt nursing interventions . As a common occurrence in various clinical conditions, understanding the underlying pathophysiology, recognizing clinical manifestations, and implementing effective nursing care are paramount to improve patient outcomes . This article aims to provide nurses with a comprehensive overview of respiratory acidosis, empowering them to confidently assess, manage, and support patients afflicted by this complex disorder.

Table of Contents

What is respiratory acidosis, complications, signs and symptoms, diagnostic studies, nursing diagnosis, nursing priorities, discharge goals, care setting, nursing care plans, nursing interventions & considerations.

Respiratory Acidosis  is an acid-base imbalance characterized by increased partial pressure of arterial carbon dioxide and decreased blood pH. The prognosis depends on the severity of the underlying disturbance as well as the patient’s general clinical condition.

Compensatory mechanisms include (1) an increased respiratory rate; (2) hemoglobin (Hb) buffering, forming bicarbonate ions and deoxygenated Hb; and (3) increased renal ammonia acid excretions with reabsorption of bicarbonate.

Acute respiratory acidosis:   Associated with acute pulmonary edema , aspiration of foreign body, overdose of sedatives/barbiturate poisoning, smoke inhalation, acute laryngospasm, hemothorax / pneumothorax , atelectasis , adult respiratory distress syndrome (ARDS), anesthesia / surgery , mechanical ventilators, excessive CO 2  intake (e.g., use of rebreathing mask, cerebral vascular accident [CVA] therapy), Pickwickian syndrome.

Chronic respiratory acidosis:  Associated with emphysema , asthma , bronchiectasis; neuromuscular disorders (such as Guillain-Barré syndrome and myasthenia gravis); botulism; spinal cord injuries.

• Chronic obstructive respiratory disorders: emphysema , chronic bronchitis
• Chest wall trauma
• Pulmonary edema
• Atelectasis
• Pneumothorax
• Drug Overdose
• Guillain-Barre syndrome
• Cardiac Arrest

• CNS disturbances: restlessness, confusion , and apprehension to somnolence with fine flapping tremor, or coma.
• Increase in blood pressure
• Mental cloudiness and feeling of fullness in head

Assessment cues are dependent on underlying cause.

ACTIVITY/REST

• May report:  Fatigue , mild to profound
• May exhibit:  Generalized weakness , ataxia/staggering, loss of coordination (chronic), to stupor

CIRCULATION

• 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)
• May report:  Nausea / vomiting

NEUROSENSORY

• 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)

RESPIRATION

• 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

TEACHING/LEARNING

• Refer to specific plans of care reflecting individual predisposing/contributing factors.
• PaCO2 higher than 45 mm Hg
• pH is below normal range of 7.35 to 7.45
• bicarbonate level is normal (acute) or elevate (in chronic stages)
• Chest X-ray , CT scan can help determine the cause
• ABGs :   Pao 2 :  Normal or may be low. Oxygen saturation (Sao 2 ) decreased.
• Paco 2 :  Increased, greater than 45 mm Hg (primary acidosis).
• Bicarbonate (HCO 3 ):  Normal or increased, greater than 26 mEq/L (compensated/chronic stage).
• Arterial pH:  Decreased, less than 7.35.
• Electrolytes :   Serum potassium :  Typically increased.
• Serum chloride:  Decreased.
• Serum calcium :  Increased.
• Lactic acid:  May be elevated.
• Urinalysis:   Urine pH decreased.
• Other screening tests:  As indicated by underlying illness/condition to determine underlying cause.

The following are the possible nursing diagnosis for Respiratory Acidosis:

• Impaired Gas Exchange
• Ineffective Breathing Pattern
• Ineffective Tissue Perfusion
• Acute Confusion
• Risk for Injury
• Achieve homeostasis .
• Prevent/minimize complications.
• Provide information about condition/prognosis and treatment needs as appropriate.
• Physiological balance restored.
• Free of complications.
• Condition, prognosis, and treatment needs understood.
• Plan in place to meet needs after discharge.

This condition does not occur in isolation , but rather is a complication of a broader health problem/disease or condition for which the severely compromised patient requires admission to a medical- surgical or subacute unit.

Main Article: Respiratory Acidosis Nursing Care Plan

• Remain alert for critical changes in patient’s respiratory, CNS and cardiovascular functions. Report such changes as well as any variations in ABG values or electrolyte status immediately.
• Maintain adequate hydration.
• Maintain patent airway and provide humidification if acidosis requires mechanical ventilation . Perform tracheal suctioning frequently and vigorous chest physiotherapy , if ordered.
• Institute safety measures and assist patient with positioning .
• Continuously monitor arterial blood gases.
• Acid-Base Imbalances
• Respiratory Acidosis Nursing Care Plan

4 thoughts on “Respiratory Acidosis”

all these info helping me a lot

Hi JO, That’s great to hear! Respiratory acidosis is a complex topic, so I’m thrilled the study guide is proving helpful for you. If you have any questions or need more insights, just let me know. Keep up the great work!

Thank you so much this helped me with my system disorder sheets.

Hi Sinia, You’re welcome! I’m really glad to hear the information on respiratory acidosis was helpful for your system disorder sheets. If there’s anything else you need or more topics you’re curious about, just let me know. Always here to help out!

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ABG Examples and Case Studies

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Test your arterial blood gas (ABG) interpretation skills with the following ABG case studies . 

For each case, we encourage you to interpret the ABG systematically , commenting on oxygenation, pH, PaCO 2 , HCO 3 – , base excess and compensation.

For each blood gas case study, consider the most likely diagnosis  and formulate a  management plan .

For more information, see our guide to ABG interpretation .

Case study 1

A 21 year old woman presents with a five day history of vomiting and lethargy. She is confused and hypotensive.

An arterial blood gas is performed on room air .

Review the blood gas and document your interpretation below.

Interpretation

Explanation

Oxygenation.

• The PaO 2 is within normal limits and appropriate to the % inspired oxygen concentration (FiO 2 )
• FiO 2 in room air is 21%, and as a rule of thumb, the PaO 2 should be approximately 10 kPa less than the %FiO 2

Acid-base disturbance

Primary acid-base disturbance

• The patient has an acidaemia with a pH of 7.3 (7.35-7.45)
• Acidaemia can either be driven by a respiratory cause (high CO 2 ) or a metabolic cause (low HCO 3 )
• The bicarbonate is low, suggesting a metabolic acidosis

Compensation 

• The PaCO 2 is low, suggesting respiratory compensation . The lungs are blowing off CO 2 to compensate for the acidosis. Blowing off CO 2 moves the carbonic acid equation to the left in order to remove excess H + .

• The anion gap can help differentiate between the different causes of metabolic acidosis
• Anion gap =  Na + – (Cl – + HCO 3 – )
• A normal anion gap is 4 to 12 mmol/L
• In this case the anion gap is high ([135 – [102 +13] = 20 )

Causes of a high anion gap metabolic acidosis include:

• Diabetic ketoacidosis
• Lactic acidosis 
• Aspirin overdose
• Renal failure

Other significant findings

• Raised lactate and significantly raised glucose 

This patient has a high anion gap metabolic acidosis with partial respiratory compensation . The raised glucose makes diabetic ketoacidosis (DKA) the most likely diagnosis.

A blood ketone level is needed to confirm the diagnosis. Respiratory compensation is commonly seen in DKA, and the increased respiratory effort in these cases is known as Kussmaul breathing . 

Management priorities in DKA are: fluid replacement (patients can be significantly dehydrated), starting a fixed rate insulin infusion , identifying and treating underlying causes and close monitoring of glucose and potassium  levels. 

Case study 2

A 24 year old asthmatic patient presents with a wheeze and shortness of breath.

• FiO 2 in room air is 21% , and as a rule of thumb, the PaO 2 should be approximately 10 kPa less than the %FiO 2
• The patient has an alkalaemia with a pH of > 7.45
• Alkalaemia on a blood gas can either be driven by a respiratory cause (low CO 2 ) or a metabolic cause (high HCO 3 )
• The patient has a low CO 2, suggesting a respiratory alkalosis 

Carbon dioxide diffuses rapidly between the capillaries and alveoli, making blood carbon dioxide levels very sensitive to respiratory rate (↑RR = ↓PCO 2 and ↓RR = ↑PCO 2 ).

Compensation

• The bicarbonate is within normal limits ~ there is no evidence of metabolic compensation for the respiratory alkalosis
• No other significant abnormalities

This patient is having an asthma attack , and her ABG demonstrates a respiratory alkalosis caused by a raised respiratory rate .

This is an expected finding during an asthma exacerbation. A normal PaCO 2 in a patient experiencing an asthma exacerbation is a life-threatening feature as it indicates respiratory fatigue.

Case study 3

A 57 year old man suffers an out of hospital cardiac arrest. Return of spontaneous circulation occurs, and he is being ventilated with a Bag-Valve-Mask (BVM).

An arterial blood gas is performed on 15 L/min O 2 .

• Oxygen levels are low , given the expected FiO 2
• As a rule of thumb, the PaO 2 should be approximately 10 kPa less than the percentage of inspired O 2 (%FiO 2 )
• The FiO 2 for a patient receiving 15 L/min O 2 via a BVM with a good seal can approach 100% 
• The hypoxia here may be secondary to a primary hypoxic event leading to the cardiac arrest or secondary to poor ventilation with the BVM
• The PaCO 2 is also significantly elevated, indicating poor ventilation

Primary acid base disturbance

• There is a mixed respiratory and metabolic acidosis
• Acidosis can either be driven by a respiratory cause (high CO 2 ) or a metabolic cause (low HCO 3 )
• In this case, both the CO 2 is high, and the HCO 3 is low, suggesting a mixed acidosis
• There is no evidence of compensation as both the respiratory and metabolic systems are contributing to the acidosis
• Lactate is significantly raised, contributing to the metabolic acidosis
• It is common to see lactic acidosis following organ hypoperfusion during a cardiac arrest 
• Glucose is mildly elevated, which may be a stress response

Potassium  

• Severe hyperkalaemia (K + > 6.5 mmol/L)
• Hyperkalaemia can occur in cardiac arrest secondary to cell death and secondary to acidosis (which pushes K+ extracellularly in exchange for H + )
• Hyperkalaemia is also one of the reversible causes of cardiac arrest

This patient has a mixed respiratory and metabolic acidosis following a cardiac arrest.

It is imperative to identify and treat the potential underlying causes (think 4Hs and 4Ts ).

The patient has severe hyperkalaemia , which requires immediate treatment with IV calcium to stabilise the myocardium, followed by K + lowering measures such as an insulin-dextrose infusion.

They are also significantly hypoxic relative to the FiO 2 and require a definitive airway with optimised oxygenation and ventilation. 

Case study 4

A 52 year old with severe COPD is reviewed in respiratory clinic.

An arterial blood gas is performed on room air.

• Type 2 respiratory failure ~ hypoxaemia (PaO 2 <8 kPa) with hypercapnia (PaCO 2 >6.0 kPa)
• pH is within normal limits (either suggesting no acid-base disturbance or a compensated acid-base abnormality) 
• The PaCO 2 is high and the bicarbonate is high
• Theoretically, this could either be due to a respiratory acidosis with metabolic compensation or a metabolic alkalosis with a respiratory compensation
• The first clue is the clinical context: this is a patient with chronic COPD who is likely to be a retainer of carbon dioxide
• The second clue is the pH: the pH is tending towards acidosis, indicating the primary abnormality is a respiratory acidosis  

Remember that overcompensation does not occur . Therefore, this could not be a primary metabolic alkalosis, as that would mean the respiratory system has overcompensated and pushed the blood pH back down to borderline acidaemia. 

This is an ABG of a chronic CO 2 retainer showing chronic respiratory acidosis with a compensatory metabolic alkalosis . 

Patients with chronic CO 2 retention can become desensitised to high CO 2 levels and rely instead on oxygen levels to guide the adequacy of ventilation. This is sometimes referred to as the hypoxic drive .

Giving patients too much O 2 in this setting can cause respiratory depression and further increase CO 2 retention. Therefore, it is essential that chronic CO2 retainers and those at risk of hypercapnic respiratory failure have their oxygen saturations titrated to between 88% and 92% .

Case study 5

A 72 year old woman presents to the emergency department with profuse vomiting. Examination reveals global abdominal tenderness and a CT abdomen has been requested.

A venous blood gas is performed on room air .

*Note that reference ranges here are for  arterial  blood samples (ABG), as is standard for blood gas analysers. Key differences between arterial and venous blood gas samples are covered in our  venous blood gas (VBG) analysis  article.

• Venous oxygen tension (PvO 2 ) cannot be used to equate to arterial oxygen tension (PaO 2 ), thus a VBG cannot be used to assess oxygenation
• The patient is alkalaemic with a pH of 7.48
• Alkalaemia can either be driven by a respiratory cause (low CO 2 ) or a metabolic cause (high HCO 3 )
• In this case, there is a high HCO 3 suggesting a metabolic alkalosis
• This is a VBG therefore, we cannot comment accurately on respiratory compensation 
• An elevated PCO 2 on an arterial blood gas would suggest respiratory compensation 
• Hypochloraemia 

This patient has a metabolic alkalosis with associated hypochloraemia . This is in keeping with loss of chloride-rich stomach contents. Remember that gastric juice is rich in hydrochloric acid (HCl), thus marked vomiting leads to a loss of both H + and Cl – ions.

A high degree of suspicion for significant underlying pathology is required in older people with abdominal pain. A CT scan has been ordered in this case to look for surgical causes such as small bowel obstruction . 

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ABG Examples (ABG exam questions for medical students and PACES)

ABG Examples (ABG exam questions for medical students OSCEs and MRCP PACES)

Below are some brief clinical scenarios with ABG results. Try to interpret each ABG and formulate a differential diagnosis before looking at the answer.

Question 1.

You are called to see a 54 year old lady on the ward. She is three days post-cholecystectomy and has been complaining of shortness of breath. Her ABG is as follows:

• pH: 7.49 (7.35-7.45)
• pO2: 7.5 (10–14)
• pCO2: 3.9 (4.5–6.0)
• HCO3:  22 (22-26)
• BE: -1 (-2 to +2)
• Other values within normal range
• This is type 1 respiratory failure. The PO2 is low with a low CO2.
• The accompanying alkalosis is a response, due to the patient blowing off CO2 due to her likely high respiratory rate.

What is the differential diagnosis?

• Pulmonary embolus (PE)
• Pulmonary oedema
• Pneumothorax
• Severe atelectasis

What would you do?

• Acutely unwell: ABCDE and call for help
• All of these conditions can may you tachypnoeic and tachycardic. Wheeze will predominate in asthma. Pyrexia points more towards pneumonia (but PE can give a mild pyrexia). Pulmonary embolus will be the only condition that will likely be normal on auscultation.
• Sudden onset: more likely PE
• Purulent cough: more likely pneumonia
• Raised JVP, ankle swelling, fine basal creps: more likely oedema
• Cultures if pyrexial
• PE : Heparinisation or thrombolysis if unstable. Remember this patient is post-op so it is a complex decision.
• Pneumonia : Antibiotics for hospital acquired pneumonia
• Asthma : Salbutamol, ipatropium and steroid in the first instance
• Pulmonary oedema : Sit patient up, furosemide, consider catheter

Question 2.

A 75 year old gentleman living in the community is being assessed for home oxygen. His ABG is as follows:

• pH: 7.36 (7.35-7.45)
• pO2: 8.0 (10–14)
• pCO2: 7.6 (4.5–6.0)
• HCO3: 31 (22-26)
• BE: +5 (-2 to +2)
• This does not represent acute pathology.
• Rather it reflects a compensation for a chronic respiratory acidosis secondary to chronic pulmonary disease.
• Note this is an acidosis, not an acidaemia (pH normal, but only due to compensatory mechanisms: the high bicarbonate).
• Lifestyle advice and smoking cessation of necessary.
• PaO 2  less than 7.3 kPa when stable.
• Secondary polycythaemia
• Peripheral oedema
• Nocturnal hypoxaemia
• Pulmonary hypertension

Question 3.

A 64 year old gentleman with a history of COPD presents with worsening shortness of breath and increased sputum production .

• pH: 7.21 (7.35-7.45)
• pO2: 7.2 (10–14)
• pCO2: 8.5 (4.5–6.0)
• HCO3: 29 (22-26)
• BE: +4 (-2 to +2)
• Note that the HCO3 is raised in this patient despite the abnormal pH.
• With the above history this is likely to represent an acute on chronic respiratory acidosis.
• This would indicate that the patient normally retains CO2 and has a chronically raised HCO3.
• The drop in pH represents the normal mechanisms of compensation being over whelmed.
• This is one of the cases where having an old ABG from a previous admission can be useful.

How much oxygen would you give this man?

• Oxygen administration in this group is a complicated issue. 100% oxygen makes subsets of COPD patients retain CO2, decreasing respiratory drive and worsening hypoxia and hypercapnia.
• More information can be found on this page: Prescribing oxygen in COPD patients
• The British Thoracic Society have produced guidelines which give a helpful overview and can be found here.

Question 4.

A 21 year-old woman presents feeling acutely lightheaded and short of breath. She has her final university exams next week.

• pH: 7.48 (7.35-7.45)
• pO2: 13.9 (10–14)
• pCO2: 3.5 (4.5–6.0)
• HCO3: 22 (22-26)
• BE: +2 (-2 to +2)
• This is a respiratory alkalaemia
• Pulmonary disease
• Hypermetabolic states (e.g. infection or fever)
• Anxiety hyperventilation

What's the most likely diagnosis?

• Based on the history, anxiety hyperventilation is the most likely cause here. However, it is very important to have considered the other options, in particular and to have ruled out a primary respiratory pathology or infection.
• In the anxious patient who is short of breath and persistently tachycardic have you thought of PE?

Question 5.

A 32 year-old man presents to the emergency department having been found collapsed by his girlfriend.

• pH: 7.25 (7.35-7.45)
• pO2: 11.1 (10–14)
• pCO2: 3.2 (4.5–6.0)
• HCO3: 11 (22-26)
• BE: -15 (-2 to +2)
• Potassium: 4.5
• Sodium: 135
• Chloride: 100
• Anion gap = ([Na + ] + [K + ]) − ([Cl − ] + [HCO 3 − ])
• Reference range usually 7–16 mEq/L (but varies between hospitals, some using 3-11)
• Anion gap = [Na + ] − ([Cl – ] + [HCO 3 − ])

What is the anion gap in this case?

• N.B. Some analysers won’t include potassium in their calculations therefore for them >15 constitutes a raised anion gap.
• Either way, this is a raised anion gap metabolic acidosis.

What is the differential diagnosis for a metabolic acidosis with raised anion gap? The traditional mnemonic for the causes of a metabolic acidosis with raised anion gap is ‘MUDPILES’:

• D iabetic ketoacidosis (and alcoholic/starvation ketoacidosis)
• P ropylene glycol
• E thylene glycol
• S alicylates

However, another way is to think about the mechanism of acidosis:

• DKA, lactic acidosis (produced by poorly perfused tissues)
• Methanol, ethanol, ethylene glycol
• Renal failure

[/toggle title="What is the differential diagnosis for a metabolic acidosis with normal or decreased anion gap?" active="false"]

• From the GI tract (diarrhoea or high-output stoma)
• From the kidneys ( renal tubular acidosis )

Question 6.

A 67 year-old man with a history of peptic ulcer disease presents with persistent vomiting.

• pH: 7.56 (7.35-7.45)
• pO2: 10.7 (10–14)
• pCO2: 5.0 (4.5–6.0)
• HCO3: 31 (22-26)
• BE: +5 (-2 to +2)
• This is metabolic alkalaemia

[/toggle title="What' s the differential diagnosis of this ABG picture?" active="false"]

Differential diagnosis of a metabolic alkalosis or alkalaemia:

• E.g. gastric outlet obstruction (the classic example is pyloric stenosis in a baby)
• Hyperaldosteronaemia
• Diuretic use
• Milk alkali syndrome
• Massive transfusion

Question 7.

A seventeen year-old girl presents to the emergency department after an argument with her boyfriend. He says that she took lots of tablets. She denies this. You persuade her to let you do an ABG:

• pH: 7.46 (7.35-7.45)
• pO2: 12.5 (10–14)
• BE: +1 (-2 to +2)

A few hours later she says she feels increasingly unwell and is complaining of ringing in her ears. A repeat gas shows:

• pH: 7.15 (7.35-7.45)
• pO2: 11.0 (10–14)
• HCO3: 9 (22-26)
• BE: -18 (-2 to +2)
• This is the classic picture of aspirin overdose.
• There is an initial respiratory alkalosis due to central respiratory centre stimulation causing  increased respiratory drive.
• In the later stages a metabolic acidosis develops along side the respiratory alkalosis as a result of direct effect of the metabolite salicylic acid and more complex disruption of normal cellular metabolism.

How would you manage this patient?

How do you manage an aspirin overdose?

Presentation of aspirin overdose

• Hyperventilation
• Nausea & vomiting
• Epigastric pain
• ARDS (rare)
• Hypoglycaemia (children in particular)

Investigations in aspirin overdose

• Plasma salicylate concentration (initial and repeats)
• Paracetamol levels (always check in any case of poisoning by anything)
• Renal failure (rare) sometimes other electrolyte imbalances
• If dropping sats or any suspicion of ARDS (non-cardiogenic pulmonary oedema)

Management of aspirin overdose

• ABCDE and supportive care
• Gastric lavage within 1h of ingestion (although no evidence for mortality reduction)
• Activated charcoal
• Correct electrolyte abnormalities
• Give 225ml of 8.4% bicarbonate solution over 1hr
• Bicarbonate will increase any pre-existing hypokalaemia – so don’t let it happen
• N.B. Acidosis increases salicylate transfer across the blood brain barrier
• Monitor U+Es regularly
• Haemodialysis

Prognosis in aspirin overdose

• Generally good with treatment.

Question 8.

A normally fit and well 11 year-old boy presents with diarrhoea and vomiting. He is complaining of non-specific abdominal pain. A venous blood gas shows :

• pH: 7.12 (7.35-7.45)
• pO2: 11.5 (10–14)
• BE: -17 (-2 to +2)
• Lactate: 4.0
• Potassium: 5.5
• Glucose: 22 mmol/L (395 mg/dL)
• This is diabetic ketoacidosis (DKA) .

What are you going to do?

• Priorities for management include fluid resuscitation, insulin administration and careful management of potassium levels. Click here for a page detailing this, and click here for DKA questions 

Question 9.

A 22 year-old lady with a known history of asthma presents to the emergency department with difficulty in breathing. Her initial ABG on 15 litres of oxygen shows:

• pH: 7.54 (7.35-7.45)
• pO2: 10.0 (10–14)
• HCO3: 24 (22-26)
• BE: +0 (-2 to +2)

After initial treatment the nurse in resus calls you to review the patient. The nurse says that although the patient’s respiratory rate has come down slightly she is looking more unwell. Her repeat gas shows:

• pO2: 9.8 (10–14)
• BE: -2 (-2 to +2)
• This patient has asthma, ongoing difficulty in breathing and a rising CO2 (the fact that it is in the normal range is irrelevant) .
• This is an extremely worrying sign as it shows that the patient is tiring.
• This patient should be managed in a high dependency area and closely monitored for further deterioration.

Question 10.

A 62 year-old woman with a history of diabetes and a long smoking history presents to the emergency department with worsening shortness of breath. On auscultation of the chest there are widespread crackles and you notice moderate ankle oedema. ABG shows:

• pH: 7.20 (7.35-7.45)
• pO2: 8.9 (10–14)
• pCO2: 6.3 (4.5–6.0)
• HCO3: 17 (22-26)
• BE: -8 (-2 to +2)
• Note that despite the low pH the pCO2 is also high.
• This is a picture of a mixed respiratory and metabolic acidosis.
• Given the history of diabetes and ankle swelling, renal failure is a unifying diagnosis with pulmonary oedema contributing to a respiratory acidosis whilst the failure to clear acids causes a metabolic acidosis.

Click here for further questions on ABGs

…and click here to learn the best way to interpret abgs.

Perfect revision for MRCP PACES, OSCES and medical student finals

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SEVERE RESPIRATORY ACIDOSIS AND METABOLIC ALKALOSIS IN A PATIENT WITH COVID-19 ARDS

TOPIC: Pulmonary Physiology

TYPE: Medical Student/Resident Case Reports

INTRODUCTION: Patients with SARS-Cov-2 virus (COVID-19) pneumonia and acute respiratory distress syndrome (ARDS) can present with high physiologic dead space due to profound pulmonary vascular micro-thrombosis (1). We present a case of COVID-19 ARDS causing severe respiratory acidosis with a paCO2 >107mmHg (upper detectable level). Arterial pH remained between 7.3-7.4 due to a serum bicarbonate concentration ([HCO3-]) up to 70mEq/L.

CASE PRESENTATION: A 67-year-old male with hypertension and diabetes presented with hypoxia from COVID-19 pneumonia. Arterial blood gas (ABG) on 50L and 100% FiO2 was 7.43/42/164 (arterial pH/paCO2 mmHg/paO2 mmHg) with a [HCO3-] of 23mEq/L. On day 24, he acutely became somnolent; ABG was 7.30/92/76 with a [HCO3-] of 39mEq/L. After an unsuccessful trial of non-invasive ventilation, he was intubated for hypercapnic respiratory failure; paCO2 remained between 100 and >107mmHg for the rest of his hospitalization. On day 34, a bumetanide drip was started for worsening hypoxemia. With diuresis, [HCO3-] increased in parallel with arterial pH and when [HCO3-] reached 70mEq/L on day 46, bumetanide was stopped due to concern for a secondary metabolic alkalosis. Subsequently, there was a drop in [HCO3-] and pH and development of acute renal injury (AKI). Given his multiorgan failure, he was transitioned to comfort care on day 51 and passed away hours after.

DISCUSSION: This case demonstrates the severe hypercapnia that can occur with COVID-19 pneumonia and the acid base disturbances that can consequently develop. After the bumetanide drip was started, the patient's paCO2 remained undetectably high while [HCO3-] continued to increase, peaking at 70mEq/L. It has been suggested that the kidneys cannot compensate beyond a [HCO3-] of 45mEq/L for a chronic respiratory acidosis (2). Therefore, he likely developed a secondary metabolic alkalosis from the bumetanide drip, as supported by the parallel rise in [HCO3-] and persistently normal pH between 7.3-7.4 on days 34 to 47. Shortly after the bumetanide drip was stopped, the patient developed oliguria, azotemia, and a rise in serum creatinine. There was also a drop in pH and [HCO3-] due to loss of metabolic alkalosis and worsening anion gap metabolic acidosis secondary to uremia. The timing of AKI with the discontinuation of the bumetanide drip was coincidental. Prior studies have shown that the use of loop diuretic drips in critically ill patients with AKI did not reduce rate of worsening renal injury or improve renal recovery (3). Most likely, his AKI was due to progression of severe COVID-19 causing acute tubular necrosis and worsening septic shock.

CONCLUSIONS: This is an extreme case of COVID-19 hypercapnic respiratory failure with a near normal pH due to a [HCO3-] up to 70mEq/L. To the best of our knowledge, the highest reported cases of [HCO3-] have been in the 50's in the setting of gastric alkalosis or obstructive pulmonary diseases.

REFERENCE #1: Diehl JL, Peron N, Chocron R, et al. Respiratory mechanics and gas exchanges in the early course of COVID-19 ARDS: a hypothesis-generating study. Ann Intensive Care 2020; 10:95.

REFERENCE #2: Skorecki, Karl, Glenn M. Chertow, Philip A. Marsden, Barry M. Brenner, and Floyd C. Rector. Brenner & Rector's the Kidney. Elsevier 2016.

REFERENCE #3: Bagshaw S, Bigney R, Kruger P, et al. The effect of low-dose furosemide in critically ill patients with early acute kidney injury: A pilot randomized blinded controlled trial (the SPARK study). J Crit Care 2017; 42: 138-146.

DISCLOSURES: No relevant relationships by Esther Chen Etchison, source=Web Response

No relevant relationships by Emily Gilbert, source=Web Response

No relevant relationships by Anila Khan, source=Web Response

No relevant relationships by JULIA SCHNEIDER, source=Web Response

Respiratory Acidosis Clinical Presentation

• Author: Nazir A Lone, MD, MBBS, MPH, FACP, FCCP; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
• Sections Respiratory Acidosis
• Practice Essentials
• Etiology and Pathophysiology
• Physical Examination
• Complications
• Approach Considerations
• Laboratory Tests
• Plain Radiography and Fluoroscopy
• Pulmonary Function Testing
• EMG and Nerve Conduction Velocity
• Measurement of Transdiaphragmatic Pressure
• Other Tests
• Pharmacologic Therapy
• Oxygen Therapy
• Ventilatory Support
• Medication Summary
• Beta2 Agonists
• Anticholinergics, Respiratory
• Xanthine Derivatives
• Corticosteroids
• Benzodiazepine Toxicity Antidotes
• Opioid Antagonists
• Questions & Answers

The clinical manifestations of respiratory acidosis are often those of the underlying disorder. Manifestations vary, depending on the severity of the disorder and on the rate of development of hypercapnia. Mild to moderate hypercapnia that develops slowly typically has minimal symptoms.

Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the partial arterial pressure of carbon dioxide (PaCO 2 ) increases, the anxiety may progress to delirium, and patients become progressively more confused, somnolent, and obtunded. This condition is sometimes referred to as carbon dioxide narcosis.

Physical examination findings in patients with respiratory acidosis are usually nonspecific and are related to the underlying illness or the cause of the respiratory acidosis.

Thoracic examination of patients with obstructive lung disease may demonstrate diffuse wheezing, hyperinflation (ie, barrel chest), decreased breath sounds, hyperresonance on percussion, and prolonged expiration. Rhonchi may also be heard.

Cyanosis may be noted if accompanying hypoxemia is present. Digital clubbing may indicate the presence of a chronic respiratory disease or other organ system disorders.

The patient’s mental status may be depressed if severe elevations of PaCO 2 are present. Patients may have asterixis, myoclonus, and seizures.

Papilledema may be found during the retinal examination. Conjunctival and superficial facial blood vessels may also be dilated.

A study by Zorrilla-Riveiro et al of 212 patients indicated that in persons with dyspnea, nasal flaring is a sign of respiratory acidosis. [ 15 ]

Patients with chronic respiratory acidosis, by definition, have a component of alveolar hypoventilation. Partial arterial pressure of carbon dioxide (PaCO 2 ) and bicarbonate levels are increased, and obligatory decreases in partial pressure of arterial oxygen (PaO 2 ) also occur.

Complications are often related to the chronic hypoxemia, which can result in increased erythropoiesis, leading to secondary polycythemia.

Chronic hypoxia is a cause of pulmonary vasoconstriction. This physiologic response can, in the long term, lead to pulmonary hypertension, right ventricular failure, and cor pulmonale.

Hypopneas and apneas during sleep lead to impaired sleep quality and cerebral vasodilation, causing morning headaches, daytime fatigue, and somnolence.

High levels of CO 2 can lead to confusion, often referred to as carbon dioxide narcosis. As a late complication of cerebral vasodilation, patients may have papilledema. [ 16 ]

A study by Lun et al indicated that in patients with acute exacerbation of COPD, those with either compensated or decompensated respiratory acidosis tend to have poorer lung function and a greater risk for future life-threatening events than do normocapnic patients. [ 17 ]

A study by de Miguel-Díez et al indicated that respiratory acidosis is one factor increasing the risk of rehospitalization for patients within 30 days of initial hospitalization for acute exacerbation of COPD and is also a risk factor for inhospital mortality in these readmitted patients. Other factors associated with rehospitalization and inhospital mortality included older age, malnutrition, nonobesity, and treatment with noninvasive ventilation. [ 18 ]

Similarly, a study by Fazekas et al indicated that in patients with COPD who survive a first episode of acute hypercapnic respiratory failure requiring noninvasive ventilation, severe respiratory acidosis predicts decreased long-term survival, as do chronic respiratory failure and lower body mass index. [ 19 ]

In addition, a prospective study by Crisafulli et al indicated that in patients who have been hospitalized for acute exacerbation of COPD, a modified Medical Research Council dyspnea score of 2 or greater and acute respiratory acidosis are independent risk factors, if present at admission, for a hospital stay of more than 7 days (odds ratios of 2.24 and 2.75, respectively). [ 20 ]

A study by Al-Azzam et al indicated that in hospitalized patients with COVID-19, an acid-base imbalance increases the mortality risk. The risk was found to be nearly four-fold in patients with mixed metabolic/respiratory acidosis, and to be two-fold in those with metabolic acidosis with respiratory compensation, respiratory alkalosis with metabolic compensation, or respiratory acidosis with no compensation. [ 21 ]

A study by Bar and Aronson indicated that among acid-base abnormalities found in normotensive patients with acute heart failure, respiratory alkalosis is associated with a greater risk of inhospital mortality than is metabolic acidosis, metabolic alkalosis, respiratory alkalosis, or mixed acidosis or alkalosis. The adjusted odds ratio for in-hospital mortality for respiratory alkalosis was greater than 3. [ 22 ]

A study by Mochizuki et al indicated that in intensive care unit (ICU) patients, mortality rates from acidemia differ by subtype. Of over 640,000 ICU patients, 57.8% were found to have acidemia. Metabolic, combined, and respiratory acidemia had prevalences of 42.9%, 30.3%, and 25.9%, respectively. Combined acidemia had the highest mortality rate (12.7%), followed by metabolic (11%) and respiratory (5.5%) acidemia. Hospital mortality in respiratory acidemia was best predicted by PaCO 2 . [ 23 ]

A retrospective, single-center study by Andreev et al found that in patients with acute spontaneous intracerebral hemorrhage, neither respiratory acidosis nor metabolic acidosis, found in 10% and 23% of the study patients, respectively, was significantly associated with hospital mortality or 90-day functional outcome. [ 24 ]

A study by Hensel et al indicated that in neonates, the likelihood of morbidity from the presence of umbilical artery (UA) respiratory acidosis is less than for UA mixed acidosis and UA metabolic acidosis, the odds ratios for morbidity being 1.48, 6.41, and 7.49, respectively. [ 25 ]

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Karagiannidis C, Merten ML, Heunks L, et al. Respiratory acidosis during bronchoscopy-guided percutaneous dilatational tracheostomy: impact of ventilator settings and endotracheal tube size. BMC Anesthesiol . 2019 Aug 9. 19 (1):147. [QxMD MEDLINE Link] . [Full Text] .

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Alfano G, Fontana F, Mori G, et al. Acid base disorders in patients with COVID-19. Int Urol Nephrol . 2021 Jun 11. [QxMD MEDLINE Link] . [Full Text] .

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Kazmaier S, Weyland A, Buhre W, et al. Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease. Anesthesiology . 1998 Oct. 89(4):831-7. [QxMD MEDLINE Link] .

Wiseman AC, Linas S. Disorders of potassium and acid-base balance. Am J Kidney Dis . 2005 May. 45(5):941-9. [QxMD MEDLINE Link] .

Zorrilla-Riveiro JG, Arnau-Bartes A, Rafat-Sellares R, Garcia-Perez D, Mas-Serra A, Fernandez-Fernandez R. Nasal flaring as a clinical sign of respiratory acidosis in patients with dyspnea. Am J Emerg Med . 2017 Apr. 35 (4):548-53. [QxMD MEDLINE Link] .

Pollock JM, Deibler AR, Whitlow CT, et al. Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity. AJNR Am J Neuroradiol . 2008 Oct 14. [QxMD MEDLINE Link] .

Lun CT, Tsui MS, Cheng SL, et al. Differences in baseline factors and survival between normocapnia, compensated respiratory acidosis and decompensated respiratory acidosis in COPD exacerbation: A pilot study. Respirology . 2016 Jan. 21 (1):128-36. [QxMD MEDLINE Link] .

de Miguel-Diez J, Jimenez-Garcia R, Hernandez-Barrera V, et al. Readmissions following an initial hospitalization by COPD exacerbation in Spain from 2006 to 2012. Respirology . 2016 Apr. 21 (3):489-96. [QxMD MEDLINE Link] .

Fazekas AS, Aboulghaith M, Kriz RC, et al. Long-term outcomes after acute hypercapnic COPD exacerbation : First-ever episode of non-invasive ventilation. Wien Klin Wochenschr . 2018 Jul 31. [QxMD MEDLINE Link] .

Crisafulli E, Ielpo A, Barbeta E, et al. Clinical variables predicting the risk of a hospital stay for longer than 7 days in patients with severe acute exacerbations of chronic obstructive pulmonary disease: a prospective study. Respir Res . 2018 Dec 27. 19 (1):261. [QxMD MEDLINE Link] . [Full Text] .

Al-Azzam N, Khassawneh B, Al-Azzam S, Karasneh RA, Aldeyab MA. Acid-base imbalance as a risk factor for mortality among COVID-19 hospitalized patients. Biosci Rep . 2023 Mar 29. 43 (3): [QxMD MEDLINE Link] . [Full Text] .

Bar O, Aronson D. Hyperlactataemia and acid-base disturbances in normotensive patients with acute heart failure. Eur Heart J Acute Cardiovasc Care . 2022 Mar 16. 11 (3):242-51. [QxMD MEDLINE Link] . [Full Text] .

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Hensel D, Zahedi-Spung L, Carter EB, Cahill AG, Raghuraman N, Rosenbloom JI. The Risk of Neonatal Morbidity in Umbilical Artery Hypercarbia and Respiratory Acidosis. Am J Perinatol . 2022 Dec 21. [QxMD MEDLINE Link] .

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Contributor Information and Disclosures

Nazir A Lone, MD, MBBS, MPH, FACP, FCCP Physician in Pulmonary and Critical Care Medicine, Northwell Health Nazir A Lone, MD, MBBS, MPH, FACP, FCCP is a member of the following medical societies: American Association for Bronchology and Interventional Pulmonology , American College of Chest Physicians , American College of Physicians , International Association for the Study of Lung Cancer , Medical Society of the State of New York , Society of Critical Care Medicine Disclosure: Nothing to disclose.

Nancy W Bethuel, MD Resident Physician, Department of Internal Medicine, Basset Medical Center Nancy W Bethuel, MD is a member of the following medical societies: American College of Physicians , American Medical Association Disclosure: Nothing to disclose.

Laurel Whitney MD Candidate, Columbia University College of Physicians and Surgeons Disclosure: Nothing to disclose.

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians , American College of Physicians , American Federation for Medical Research , American Thoracic Society Disclosure: Nothing to disclose.

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians , American Thoracic Society Disclosure: Nothing to disclose.

Thomas M Roy, MD Chief, Division of Pulmonary Disease and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, Fellowship Program Director, James H Quillen College of Medicine, East Tennessee State University Thomas M Roy, MD is a member of the following medical societies: American College of Chest Physicians , American College of Physicians , American Medical Association , American Thoracic Society , Southern Medical Association , Wilderness Medical Society Disclosure: Nothing to disclose.

Wael El Minaoui, MBBS Fellow in Pulmonary/Critical Care Medicine, East Tennessee State University, James H Quillen College of Medicine

Disclosure: Nothing to disclose.

Jackie A Hayes, MD, FCCP Clinical Assistant Professor of Medicine, University of Texas Health Science Center at San Antonio; Chief, Pulmonary and Critical Care Medicine, Department of Medicine, Brooke Army Medical Center

Jackie A Hayes, MD, FCCP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians , American College of Physicians , and American Thoracic Society

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Interpreting and using the arterial blood gas analysis

Lian, Jin Xiong BSN, RN, CNS

Jin Xiong Lian is a clinical nurse specialist in the intensive care unit at Concord Repatriation General Hospital, a teaching hospital for the University of Sydney in Australia.

Use this 5-step approach to help manage patients on mechanical ventilation.

This article reviews the physiology behind ABGs and describes a 5-step approach to ABG interpretation. The 5-step approach is then applied to case studies that illustrate how to use ABGs to manage patients, particularly those on mechanical ventilation.

An arterial blood gas (ABG) analysis can tell you about a patient's oxygenation, acid-base balance, pulmonary function, and metabolic status. This indispensable tool helps you assess and monitor critically ill patients in the ICU or other critical care settings.

As a critical care nurse, you're often the first healthcare provider who receives ABG results, and you'll monitor changes in the ABG results during the patient's stay in the ICU. In this article, I'll review the indications and physiology of ABGs, and introduce a five-step approach to ABG interpretation, focusing on how it can be used in managing mechanically ventilated patients.

When an ABG analysis is needed

The common indications for ABGs are:

• Respiratory compromise, which leads to hypoxia or diminished ventilation.
• Peri- or postcardiopulmonary arrest or collapse.
• Medical conditions that cause significant metabolic derangement, such as sepsis, diabetic ketoacidosis, renal failure, heart failure, toxic substance ingestion, drug overdose, trauma, or burns.
• Evaluating the effectiveness of therapies, monitoring the patient's clinical status, and determining treatment needs. For instance, clinicians often titrate oxygenation therapy, adjust the level of ventilator support, and make decisions about fluid and electrolyte therapy based on ABG results.
• During the perioperative phase of major surgeries, which includes the preoperative, intraoperative, and postoperative care of the patient. 1-5

Physiology of ABGs

The components of an ABG analysis are PaO 2 , SaO 2 , hydrogen ion concentration (pH), PaCO 2 , HCO 3 - , base excess, and serum levels of hemoglobin, lactate, glucose, and electrolytes (sodium, potassium, calcium, and chloride). Because HCO 3 - and base excess both yield similar information on the status of base (alkali), I'll only discuss HCO 3 - . The parameters most frequently used—PaO 2 , SaO 2 , pH, PaCO 2 , HCO 3 - , and lactate—often are adequate in diagnosing and managing most clinical situations, so I'll focus on them.

See Normal ABG values for more details. Let's look more closely at each parameter.

Oxygenation: PaO 2 and SaO 2

Ninety-seven percent of oxygen in the blood is bound to hemoglobin, and this oxyhemoglobin, measured as SaO 2 , is a key means to transport oxygen to tissue cells. 2,6,10 The remaining 3% of oxygen is dissolved in the blood, and exerts pressure on the plasma. The PaO 2 represents the amount of oxygen dissolved in arterial blood. For critically ill patients or patients with chronic obstructive pulmonary disease (COPD), an SaO 2 of 90% or PaO 2 of 60 mm Hg may be acceptable. 2,6,7,10,11

Each hemoglobin molecule can carry a maximum of four oxygen molecules. Hemoglobin's affinity for binding with oxygen is demonstrated by the S-shaped oxyhemoglobin dissociation curve (see Oxyhemoglobin dissociation curve ), which illustrates the relationship between SaO 2 and PaO 2 . 12-15 PaO 2 is the fundamental factor that determines SaO 2 , or hemoglobin's affinity for oxygen. An increase in PaO 2 raises SaO 2 and decreased PaO 2 lowers the SaO 2 level. The oxyhemoglobin dissociation curve shows that a PaO 2 of at least 60 mm Hg is required to maintain an SaO 2 greater than 90%. Tissue hypoxia occurs when the PaO 2 is less than 60 mm Hg. 12,14,15

Hemoglobin's affinity for oxygen is also affected by the patient's pH, PaCO 2 , body temperature, and level of 2,3-bisphosphoglycerate (BPG, also called diphosphoglycerate, a substance in red blood cells). 14 Decreased pH (acidosis), increased PaCO 2 , elevated body temperature, or increased BPG will reduce hemoglobin's affinity for oxygen and cause the oxyhemoglobin dissociation curve to shift to the right. This loose bond means that hemoglobin has more difficulty binding with oxygen in pulmonary alveoli, but oxygen dissociates from hemoglobin more easily for tissue cells to use.

In contrast, increased pH (alkalosis), decreased PaCO 2 , decreased temperature, or reduced BPG will shift the oxyhemoglobin dissociation curve to the left, indicating an increase in hemoglobin's affinity for oxygen. As a result, oxygen is easily bound by hemoglobin in the lungs, but the tighter bond also means that tissue cells have more difficulty taking up oxygen from the blood. 6,12-17 So a patient with alkalosis and a left shift can be hypoxic, even with SaO 2 levels greater than 90%. 16

As you know, oxygen saturation can also be measured by pulse oximetry. But SpO 2 readings are influenced by many factors, including bright ambient light, decreased peripheral perfusion, vasoconstriction, hypothermia, shivering and motion artifact, hyperbilirubinemia, abnormal hemoglobins such as methemoglobinemia, cardiac dysrhythmias, and certain skin or nail conditions. In addition, SpO 2 doesn't provide information about other variables, including pH, PaCO 2 , PaO 2 , and hemoglobin. 4,10,13 Therefore, ABGs are often indicated for critically ill patients to ensure they receive prompt and appropriate care.

Acid-base balance: pH

A patient's pH reflects the concentration of hydrogen ions (H + ) in arterial blood. These two values have an inverse relationship: a low pH means more acid in the blood as the result of increased H + concentration. Conversely, lowered H + concentration leads to a higher pH as the blood becomes more alkaline. 4,6,11,14

The elimination and production of H + (acid) and HCO 3 - (bicarbonate, an alkali) are controlled by the respiratory and metabolic systems. Three mechanisms work together to keep the pH within the normal range.

• Chemical buffer systems . The carbonic acid-bicarbonate buffer system is found in extracellular fluids. Carbonic acid (H 2 CO 3 ) is a weak acid, which can dissociate into either water (H 2 O) and carbon dioxide (CO 2 ) or H + and HCO 3 - . Bicarbonate buffers can bind excess H + or release them into plasma to prevent major changes in H + concentration.

Proteins in plasma and cells, such as albumin and hemoglobin, can also absorb or release H + , and act as a protein buffer system. The phosphate buffer system predominantly stays in intracellular and renal tubular fluids. Apart from regulating the pH in the blood and intracellular fluids, phosphate also influences the acidity of urine in response to acid-base derangement. The phosphate buffer system plays a less-significant role than the other buffer systems in maintaining acid-base balance. 1,4,12,14

All buffer systems respond to changes in H + concentration rapidly, but their actions are temporary.

• Renal regulation . The kidneys are the principal organs in maintaining acid-base balance, adjusting the amount of excretion and reabsorption of H + and HCO 3 - as well as producing new HCO 3 - . When the blood is acidic, the kidneys excrete more H + and retain HCO 3 - . (The reverse is true if the blood is alkaline.) However, because it's a metabolic process, renal regulation occurs slowly, taking several hours to days. But if the patient's renal function is normal, renal regulation of acid-base balance is profound and sustainable.
• Pulmonary regulation . The respiratory system plays a significant role in regulating H + concentrations. CO 2 , a waste product of metabolism, is eliminated via exhalation. The patient's respiratory rate and depth of respirations determine how much CO 2 is exhaled. The respiratory center in the brainstem can respond rapidly to pH changes by adjusting the respiratory rate and depth of breathing.

Respiration: PaCO 2

External respiration is the pulmonary gas exchange that involves the physiological processes of pulmonary ventilation and perfusion and diffusion of oxygen and CO 2 between the pulmonary capillaries and alveoli. Any disturbance in these processes will lead to hypoxemia and/or hypercapnia (CO 2 retention). 14,18

Internal respiration is the exchange of oxygen and CO 2 between tissue cells and capillaries. This process requires adequate tissue perfusion and a normal pH. 14,18

Causes of increased PaCO 2 include increased metabolism (such as from fever), inadequate ventilation, diminished diffusion that often results from pulmonary consolidation or edema, and poor perfusion or an increased ventilation/perfusion (V/Q) mismatch. 6,10,18,19 A V/Q mismatch is an imbalance between alveolar ventilation and perfusion. If ventilated alveoli don't receive adequate perfusion, blood gas exchange doesn't occur. On the other hand, semicollapsed or collapsed alveoli may be adequately perfused, but ventilation is inadequate or doesn't occur. V/Q mismatch and poor diffusion commonly occur in acute respiratory distress syndrome (ARDS), and are the major reasons for hypoxia and hypercapnia. 20-22

You can estimate your patient's respiratory function by reviewing PaCO 2 and PaO 2 values. An increase in PaCO 2 and a decrease in PaO 2 and SaO 2 (hypoxemia) are commonly caused by respiratory failure or cardiovascular collapse.

Respiratory acidosis is defined as a PaCO 2 above 45 mm Hg due to hypoventilation and a pH below 7.35. Causes include respiratory infections, severe airflow obstruction (as in COPD or asthma), neuromuscular disorders such as multiple sclerosis, massive pulmonary edema, pneumothorax, central nervous system depression, spinal cord injury, and chest wall injury.

Respiratory alkalosis is defined as a PaCO 2 below 35 mm Hg and pH more than 7.45 due to hyperventilation. Causes include pain, anxiety, early stages of pneumonia or pulmonary embolism, hypoxia, brainstem injury, severe anemia, and excessive mechanical ventilation. 1,2,6,7,11,23

Metabolic status: HCO 3 -

As mentioned earlier, the kidneys play a vital role in maintaining acid-base balance. The liver also produces HCO 3 - , various proteins (buffers), and enzymes, so a patient's metabolic status is closely related to his kidney and liver function. 2,6,11,13,14

Metabolic acidosis is defined as pH less than 7.35 and HCO 3 - less than 22 mEq/L. Causes include renal failure, diabetic ketoacidosis, lactic acidosis, sepsis, shock, diarrhea, drugs, and toxins such as ethylene glycol and methanol. 20-22

Metabolic alkalosis is defined as a pH greater than 7.45 and an HCO 3 - greater than 26 mEq/L. Causes include diuretics, corticosteroids, excessive vomiting, dehydration, Cushing syndrome, liver failure, and hypokalemia. 1,2,6,7,11,23-25

Compensation

When a patient has an acid-base imbalance, the respiratory and metabolic systems try to correct the imbalances each has produced. For example, when increased metabolism or decreased renal excretion causes an increase in H + ions that lowers pH, the patient's respiratory center is stimulated and the patient hyperventilates to blow off more CO 2 and raise the pH. On the other hand, if the patient had metabolic alkalosis, the respiratory center would be suppressed and the decreased rate and depth of respiration would retain CO 2 to lower the pH. Respiratory compensation occurs within minutes. 6,11,25

On the other hand, respiratory acidosis triggers the kidneys to excrete more H + and elevate HCO 3 - in an effort to maintain a near-normal pH, and respiratory alkalosis will activate the metabolic system to retain H + and to lower serum HCO 3 - . Metabolic regulation takes several hours to days to affect the pH. 6,11,23,25

When these compensatory mechanisms restore a normal pH, we say the patient's acid-base imbalance is fully compensated. This situation is often seen in patients with a chronic disorder—patients with COPD and respiratory acidosis are often compensated by a metabolic alkalosis.

Note that a pH between 7.35 and 7.40 is considered normal acidic; a pH between 7.41 and 7.45 is considered normal alkalotic. So if the pH is below 7.4, the primary imbalance is acidosis. When the pH is greater than 7.4, it indicates primary alkalosis. The compensation involves the opposite direction of respiratory and metabolic processes, and is demonstrated by abnormal PaCO 2 and HCO 3 - parameters.

If the compensation mechanism fails to return the pH to a normal range, it's known as partially compensated, which is shown by three abnormal parameters (pH, PaCO 2 , and HCO 3 - ). One abnormality, either respiratory or metabolic disturbance, that moves the pH in the same direction toward acidosis or alkalosis is the primary cause. The other derangement that moves the pH to the opposite direction is the compensatory change. 2,7,11,12,25,26

When the pH and either PaCO 2 or HCO 3 - are abnormal, but the counterpart is normal, compensation hasn't occurred. This is often associated with an acute problem. Abnormalities of both PaCO 2 and HCO 3 - may indicate mixed respiratory and metabolic disorders, which can move the pH in the same or opposite directions. A combined derangement can lead to acidosis or alkalosis, or produce a normal pH.

When both respiratory (PaCO 2 ) and metabolic (HCO 3 - ) components move the pH in the same direction to cause acid-base disorders, we say mixed respiratory and metabolic acidosis or alkalosis. A mixed respiratory and metabolic acidosis is commonly seen in patients with cardiorespiratory arrest or collapse. 7,11,12,23,25,26

Looking at lactate levels

Some modern blood gas analyzers also provide lactate levels. Hyperlactatemia can be caused by increased lactate production, reduced lactate clearance, or medications such as epinephrine, nitroprusside, or metformin. A mild-to-moderate increase is defined as 2 to 4 mmol/L. Lactic acidosis is characterized by persistently elevated lactate, typically greater than 5 mmol/L, and usually is accompanied by metabolic acidosis. Lactate levels greater than 4 mmol/L are associated with poor patient outcome and higher mortality, so more-intense medical and nursing care is needed for patients with severe hyperlactatemia. 24,27,28

The most common cause of an acute lactate elevation is shock (including septic, cardiogenic, and hemorrhagic). 8,24,27

Anaerobic metabolism from tissue hypoperfusion increases the production of acids, including lactic acid. Multiple trauma, burns, and septic or hemorrhagic shock lead to intravascular volume deficit or cardiovascular collapse. Consequently, patients often develop metabolic acidosis with acute lactate elevation (lactic acidosis). Early and aggressive fluid resuscitation is crucial to patient survival. Restoring tissue perfusion by fluid resuscitation, inotropic support, or other interventions often normalizes lactate levels and pH. 1,9,17,24,27-32

A normal lactate level generally implies that the patient has adequate tissue perfusion, although abnormal levels aren't necessarily the result of tissue hypoxia. Patients with increased lactate levels need a thorough assessment and investigation.

Lactate has been used as one of the markers for systemic hypoperfusion or sepsis severity. 27,33 For patients with septic shock or severe burn, the end point of fluid resuscitation isn't clearly established. Occult tissue hypoperfusion or covert shock may exist, despite normotension and adequate urine output. 27,34

A rapid decrease in lactate during treatment suggested significant improvement in tissue perfusion and oxygenation. Monitoring lactate levels can evaluate the effectiveness and efficiency of resuscitative therapies. Lactate is also used as a marker of quality of care in sepsis management. 27 However, a delay in lactate clearance is often caused by tissue hypoxia or organ dysfunction. Persistent lactate elevations are associated with poor outcomes. 8,27,32-34

When your patient is on mechanical ventilation

Mechanical ventilation aims to improve oxygenation and ventilation. In a mechanically ventilated patient, ABGs can guide clinicians in titrating ventilatory support and weaning. 17,35,36

The patient's oxygenation needs are reflected in the PaO 2 and SaO 2 parameters of the ABG. Increasing the FiO 2 and using positive end-expiratory pressure (PEEP) are the key means to improving oxygenation. However, administering an FiO 2 greater than 0.50 for more than 72 hours may cause oxygen toxicity. High levels of PEEP may cause alveolar overdistention, ventilator-induced lung injury (VILI), and hemodynamic compromise. Once the patient is adequately oxygenated, the FiO 2 and PEEP should be reduced to minimize harm. Reduce the FiO 2 first if the patient is hemodynamically stable. If the patient is hypotensive despite adequate intravascular volume, reduce the PEEP first. 36-38

A person's minute ventilation (respiratory rate multiplied by tidal volume [V T ]) controls the elimination of CO 2 and, consequently, affects the levels of PaCO 2 and pH. With volume control ventilation, the preset respiratory rate and V T determine minute ventilation. For pressure control ventilation, minute ventilation is influenced by the preset inspiratory pressure, respiratory rate, inspiratory time, respiratory resistance, and lung compliance. Pressure support ventilation increases spontaneous V T and, therefore, is commonly prescribed for synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation, and other modes, to lower PaCO 2 for patients who have spontaneous breaths. 17,35-37

During an acute episode of respiratory distress, patients often need mechanical ventilation to improve oxygenation and ventilation. Later, hypoxia may be eliminated but abnormal PaCO 2 levels and respiratory acidosis may persist. The appropriate intervention at this stage is to increase ventilatory support for minute ventilation, but wean down FiO 2 and/or PEEP. Increasing minute ventilation often is achieved by increasing preset V T , respiratory rate, or pressure support. The above adjustment will lower the patient's PaCO 2 and raise the pH. However, high levels of ventilatory support may increase the patient's risk of VILI. At times, some degree of hypercapnia and respiratory acidosis is allowed to manage severe ARDS or status asthmaticus in an effort to minimize VILI. 21,38

To manage hypoxic patients without hypercapnia, the FiO 2 and/or PEEP are often increased to improve oxygenation. But ventilatory support in terms of minute ventilation wouldn't need to be increased. 35-37

Mechanical ventilation can be invasive or noninvasive. The two modes of noninvasive positive pressure ventilation (NPPV) are continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP). With CPAP, continuous positive airway pressure is given to spontaneously breathing patients during inspiration and expiration via a tightly fitting nasal or facial mask. Like PEEP in invasive mechanical ventilation, CPAP increases alveolar recruitment and improves oxygenation. CPAP is indicated for hemodynamically stable patients with hypoxia and/or cardiogenic pulmonary edema, and can alleviate hypercapnia to some degree. 39-42

In BiPAP, inspiratory and expiratory positive airway pressures are set separately. Expiratory pressure produces the same effect as PEEP, and the gap between inspiratory and expiratory pressure creates a pressure support for spontaneous breaths. BiPAP can improve a patient's oxygenation and ventilation quickly, and is indicated for hypercapnic patients with hypoxemia. 39-43

NPPV can cause rhinorrhea, conjunctivitis, skin breakdown, and hypotension. Some clinicians also worry that BiPAP may increase the risk of acute myocardial infarction in patients with cardiogenic pulmonary edema, although other studies have failed to demonstrate such risk. 39,40,42-46 Monitor your patient closely.

Prompt endotracheal intubation and invasive mechanical ventilation is indicated when a patient can't tolerate NPPV or has a contraindication to NPPV, such as decreased level of consciousness, excessive airway secretions, hemodynamic instability, life-threatening cardiac dysrhythmias, severe or worsening acidosis, or rapid clinical deterioration. 39,40,42,43

ABG results should be interpreted in light of the patient's medical history, present health status, and medical therapies. When the patient's PaCO 2 and HCO 3 - are both abnormal, this information will help you determine if another abnormality is the result of compensation or dual pathology. Remember that full compensation or mixed respiratory and metabolic disorders can move pH in opposite directions, resulting in a normal pH. Assess and monitor your patient, and treat the underlying causes of acid-base derangement as well as correcting abnormal parameters. Monitor your patient's response to changes in ventilator settings and inform the healthcare provider as necessary.

For instance, suppose your mechanically ventilated patient's ABGs show hypoxemia, although the patient's FiO 2 is high. A higher level of PEEP is often prescribed for patients in this clinical scenario. But PEEP reduces venous return and cardiac output, so if the patient's BP drops rapidly after PEEP is increased, suspect dehydration—dehydrated patients are more sensitive to increased PEEP. After a fluid challenge or interventions to expand intravascular volume, dehydrated patients often tolerate increased PEEP.

Now let's look at two case scenarios to see how the five-step approach (see Steps to interpreting ABGs ) can help you interpret ABGs and manage your patient's condition.

Putting theory into practice

A 55-year-old man with community-acquired pneumonia was admitted to the ICU for respiratory distress. He was alert, but dyspneic, with an SaO 2 of 87% on supplemental oxygen at 15 L/min via nonrebreather mask. You use the five-step approach to interpret his admission ABGs:

• SaO 2 of 87% and PaO 2 of 56 mm Hg reveal hypoxemia
• pH of 7.26 confirms acidosis
• PaCO 2 of 60 mm Hg indicates that his minute ventilation was inadequate, which lowered the pH
• HCO 3 - of 24 mEq/L indicates no change in metabolic status
• Lactate of 0.7 mmol/L implies that tissue perfusion is adequate.

The patient has an uncompensated respiratory acidosis with hypoxemia. Because the patient was alert and breathing spontaneously, BiPAP is ordered, and the patient's oxygen saturation immediately increases.

However, because of excessive airway secretions, the patient was endotracheally intubated 50 minutes later. Pressure support mode ventilation was used with an FiO 2 of 0.90, pressure support of 6 cm H 2 O, and PEEP of 10 cm H 2 O. Three hours later, you review his ABGs:

• PaO 2 of 84 mm Hg indicates adequate oxygenation
• pH of 7.34 is still acidotic
• PaCO 2 of 53 mm Hg reflects less profound hypercapnia, but ventilatory support in terms of minute ventilation is still inadequate to normalize his PaCO 2 and eliminate respiratory acidosis.
• HCO 3 - has risen to 28 mEq/L, suggesting the metabolic system is attempting to compensate for the respiratory acidosis.

The patient's respiratory compromise moved the pH toward acidosis. This was the primary cause of his acid-base imbalance. However, the metabolic process attempted to normalize the pH. The above abnormal HCO 3 result was the compensatory change.

The patient was diagnosed with a partially compensated respiratory acidosis. Although his hypoxemia had been eliminated, the ventilatory support in terms of ventilation was still inadequate. Elevating pressure support is the key way to enhance minute ventilation for a spontaneously breathing patient, so pressure support was increased to 12 cm H 2 O.

Two days later, his ventilator settings were FiO 2 down to 0.60, pressure support decreased to 8 cm H 2 O, and PEEP continued at 10 cm H 2 O. His ABGs were pH, 7.38; PaCO 2 , 49 mm Hg; PaO 2 , 85 mm Hg; HCO 3 - , 30 mEq/L, and lactate, 0.9 mmol/L, consistent with a fully compensated respiratory acidosis.

His heart rate was between 80 and 90 beats/min with BP of 130/70 mm Hg. The patient had been ventilated with an FiO 2 greater than 0.60 for 2 days. Because he was hemodynamically stable, the priority in weaning him from mechanical ventilation at this stage would be to lower the FiO 2 to minimize oxygen toxicity. On the other hand, if the patient's BP and urine output were low despite adequate fluid replacement, the healthcare provider might consider lowering the level of PEEP.

On the sixth day, the patient was extubated and placed on supplemental oxygen at 3 L/min via nasal cannula. Six hours later, his SaO 2 was 87% with oxygen at 12 L/min via nonrebreather mask. A chest X-ray showed bilateral pulmonary edema. His ABGs at this point were pH, 7.39; PaCO 2 , 44 mm Hg; PaO 2 , 57 mm Hg; HCO 3 - , 25 mEq/L, and lactate, 1.3 mmol/L. The ABGs showed no acid-base imbalance. Both PaCO 2 and HCO 3 - were within normal limits. But hypoxemia was the major problem again, so CPAP was indicated. CPAP can recruit the collapsed alveoli and small airways caused by pulmonary edema as well as improving oxygenation. The patient was discharged from the ICU after 2 more days.

Using lactate values

Let's look at a case scenario that demonstrates the value of lactate levels in the ABG.

A 42-year-old male patient had burns over 60% of his body surface area. On admission, his BP was 95/60 mm Hg with a heart rate of 132, respiratory rate of 8, temperature 96° F (35.5° C), and SaO 2 of 90%. He was oliguric. He was receiving I.V. infusions of propofol and morphine. You use the five-step approach to analyze his ABGs:

• PaO 2 of 63 mm Hg and SaO 2 of 90% suggest hypoxia based on his age
• pH of 7.20 is consistent with acidosis
• PaCO 2 of 52 mm Hg indicates inadequate pulmonary ventilation to blow off CO 2
• HCO 3 - of 17 mEq/L suggests a metabolic alteration toward acidosis
• Lactate of 5.2 mmol/L indicates tissue hypoxia due to burn injury.

Both respiratory and metabolic disturbances moved the pH toward acidosis, so the patient is diagnosed with a mixed respiratory and metabolic acidosis with hypoxia. The patient was mechanically ventilated on volume control-SIMV mode with a rate of 14 breaths/min, V T of 550 mL, FiO 2 of 0.50, PEEP of 10 cm H 2 O, and pressure support of 8 cm H 2 O.

Burn injury often causes significant loss of intravascular volume, as evidenced by the patient's low BP and reduced urine output. He was given intensive fluid resuscitation, and 4 hours later, his BP was 140/70 mm Hg and his urine output was greater than 0.8 mL/kg/hour. You again analyze his ABGs:

• PaO 2 of 96 mm Hg indicates no hypoxia
• pH of 7.31 remains acidotic
• PaCO 2 of 32 mm Hg reflects hyperventilation
• HCO 3 - of 20 mEq/L indicates a less profound metabolic disturbance toward acidosis
• lactate of 3.4 mmol/L implies that his tissue perfusion and oxygenation have improved significantly because of the aggressive fluid resuscitation and other interventions.

Because the pH and metabolic process (as shown by the HCO 3 - and lactate values) traveled in the same direction, his acid-base imbalance is primarily caused by the metabolic alteration. The low PaCO 2 indicates that he hyperventilated to compensate for the metabolic derangement.

These ABGs show a partially compensated metabolic acidosis without hypoxemia. However, because of ongoing fluid loss and third-space fluid shift (a fluid shift common after burns), he'll still need intravascular volume expansion to maintain good tissue perfusion and adequate urine output. Twelve hours later, your patient's ABGs are pH, 7.39; PaCO 2 , 33 mm Hg; PaO 2 , 99 mm Hg; HCO 3 - , 21 mEq/L; and lactate, 1.9 mmol/L, indicating a fully compensated metabolic acidosis. The dramatic normalization of pH and lactate level suggests that the patient received prompt and appropriate treatment.

On the third day postadmission, the patient underwent debridement of necrotic tissue and a skin graft surgery. He was readmitted to ICU postoperatively, and you again analyze his ABGs:

• PaO 2 of 93 mm Hg indicated he was well-oxygenated
• pH of 7.30 was acidotic
• Elevated PaCO 2 of 52 mm Hg indicated that his CO 2 elimination was inadequate
• HCO 3 - of 24 mEq/L implied no metabolic disturbance or compensation
• Lactate of 1.3 mmol/L was within the normal range, indicating he had adequate tissue perfusion during surgery.

He had an uncompensated respiratory acidosis. He was ventilated on volume control-SIMV mode with a preset rate of 12, V T of 550 mL, PEEP of 10 cm H 2 O, pressure support of 8 cm H 2 O, and FiO 2 of 0.40.

Three hours later, his temperature was 103.2° F (39.5° C) and ABGs were pH, 7.32; PaCO 2 , 55 mm Hg; PaO 2 , 91 mm Hg; HCO 3 - , 25 mEq/L; and lactate, 1.0 mmol/L. The normal HCO 3 - level suggested his metabolic compensation hadn't started. The patient had respiratory acidosis with worsening CO 2 retention, and his fever increased his CO 2 production.

His ventilatory support was adequate in terms of oxygenation; but it was inadequate for ventilation: Minute ventilation needed to be increased to enhance CO 2 removal. With SIMV volume control ventilation, the set respiratory rate or V T (or both) can be increased to enhance minute ventilation.

The patient's total respiratory rate was 12 breaths/min, which equaled the set SIMV rate. This rate suggested that due to sedation, the patient had not yet gained spontaneous breaths postoperatively. Increasing the level of pressure support wouldn't alter his minute ventilation or improve CO 2 removal at this stage. Once the patient starts to trigger the ventilator, you may need to increase pressure support to help resolve his respiratory acidosis.

Act quickly

In a critical care setting, a patient's condition can change rapidly and dramatically. Using a five-step approach to ABG interpretation can identify an acid-base disorder quickly and accurately so you can intervene appropriately. If your patient is mechanically ventilated, good ABG interpretation skills can guide clinicians in adjusting the ventilator settings to meet the patient's needs.

Normal ABG values

Normal values for these parameters vary among labs, but in general are

• Pao 2 , 80 to 100 mm Hg
• Sao 2 , 95% to 100%
• pH, 7.35 to 7.45
• Paco 2 , 35 to 45 mm Hg
• HCO 3 -, 22 to 26 mEq/L
• lactate, less than 2 mmol/L in critically ill patients. 1,2,6-9

Steps to interpreting ABGs

Follow this five-step approach to interpreting your patient's ABGs.

• Is the patient hypoxic? Look at the Pao 2 and Sao 2 .
• What is acid-base balance? Check the pH.
• How is pulmonary ventilation? Look at the Paco 2 .
• What is the metabolic status? Review the HCO 3 - .
• Is there any compensation or other abnormalities? What is the primary cause of acid-base imbalance and which derangement is the result of secondary (compensatory) change?

Examine serum lactate and electrolyte results; match Paco 2 and HCO 3 - parameters with the pH.

Using the above five-step approach we can interpret ABGs easily in a systemic and logical way without confusion.

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Chapter 4-10:  Respiratory Acidosis

Scott D. C. Stern

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The presentation of respiratory acidosis depends primarily on the underlying cause. The most common causes are severe underlying lung disease (eg, COPD, pneumonia, or pulmonary edema) and such patients are in respiratory distress. Respiratory acidosis may also present as altered mental status in patients with advanced respiratory failure and in those in whom the respiratory failure is due to CNS disorders (ie, intoxication.)

Insufficient ventilation results in increasing levels of PaCO 2 . This in turn lowers arterial pH. Renal compensation occurs over several days, with increased renal HCO 3 − regeneration.

Ventilation is assessed by measuring the arterial PaCO 2 and pH. Significant hypoventilation and acidosis may occur without significant hypoxia.

Etiology: Although most commonly due to lung disease, respiratory acidosis may result from any disease affecting ventilation—from the brain to the alveoli (eg, narcotic overdose is an unfortunately common cause of respiratory failure and death. See differential diagnosis of acid-base disorders in Table 4-1 .)

Manifestations are due to the primary disorder and the effects of hypercarbia on the CNS.

Patients are typically quite dyspneic, in distress, sitting upright, leaning forward, and anxious. The cardiac and pulmonary findings depend on the underlying etiology.

CNS manifestations

Severity depends on acuity. Patients with chronic hypercapnia have markedly fewer CNS effects than patients with acute hypercapnia.

Anxiety, irritability, confusion, and lethargy may be seen.

Headache may be prominent in the morning due to the worsening hypoventilation that occurs with sleep causing vasodilatation and increasing intracranial pressure.

Stupor and coma may occur when the PaCO 2 is > 70–100 mm Hg.

Tremor, asterixis, slurred speech, and papilledema may be seen.

Since respiratory failure can be an indication for emergent mechanical ventilatory support, clinicians should have a low threshold for checking an ABG to obtain the PaCO 2 . This includes patients with respiratory distress, mental status changes, and hypersomnolence.

Respiratory failure is typically characterized by PaCO 2 > 45 mm Hg, causing a respiratory acidosis.

However, occasionally, a normal PaCO 2 also suggests respiratory failure.

For example, during asthma attacks, patients typically hyperventilate and present with a PaCO 2 below normal. A normal PaCO 2 in such a patient may reflect respiratory fatigue and herald the development of frank respiratory failure.

Patients with primary metabolic acidoses typically hyperventilate to compensate, lowering the PaCO 2 below normal.

A PaCO 2 of ≥ 40 mm Hg is inappropriate in such cases and suggests respiratory failure.

Inability to compensate (hyperventilate) during a metabolic acidosis is associated with an increased risk of requiring mechanical ventilation.

Pulsus paradox is an objective marker of severe respiratory distress.

Defined as > 10 mm Hg drop in systolic BP during inspiration

May be seen in patients using unusually strong inspiratory effort due to asthma, COPD, or other respiratory diseases

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  Case Studies

The following are examples of clinical situations and the ABGs that may result, as well as causes and solutions for ABG abnormalities.

Mrs. Puffer is a 35-year-old single mother, just getting off the night shift. She reports to the ED in the early morning with shortness of breath. She has cyanosis of the lips. She has had a productive cough for 2 weeks. Her temperature is 102.2, blood pressure 110/76, heart rate 108, respirations 32, rapid and shallow. Breath sounds are diminished in both bases, with coarse rhonchi in the upper lobes. Chest X-ray indicates bilateral pneumonia.

• PaCO2 is low.
• pH is on the high side of normal, therefore compensated respiratory alkalosis .
• Also, PaO2 is low, probably due to mucous displacing air in the alveoli affected by the pneumonia ( see Shunting ).
• Mrs. Puffer most likely has ARDS along with her pneumonia.
• The alkalosis need not be treated directly. Mrs. Puffer is hyperventilating to increase oxygenation, which is incidentally blowing off CO2. Improve PaO2 and a normal respiratory rate should normalize the pH.
• High FiO2 can help, but if she has interstitial lung fluid, she may need intubation and PEEP, or a BiPAP to raise her PaO2. ( Click here to compare BiPAP to other respiratory treatments.)
• Expect orders for antibiotics, and possibly steroidal anti-inflammatory agents.
• Chest physiotherapy and vigorous coughing or suctioning will help the patient clear her airways of excess mucous and increase the number of functioning alveoli.

Mr. Worried is a 52-year-old widow. He is retired and living alone. He enters the ED complaining of shortness of breath and tingling in fingers. His breathing is shallow and rapid. He denies diabetes; blood sugar is normal. There are no EKG changes. He has no significant respiratory or cardiac history. He takes several antianxiety medications. He says he has had anxiety attacks before. While being worked up for chest pain an ABG is done:

• pH is high,
• PaCO2 is low
• respiratory alkalosis.
• If he is hyperventilating from an anxiety attack, the simplest solution is to have him breathe into a paper bag. He will rebreathe some exhaled CO2.This will increase PaCO2 and trigger his normal respiratory drive to take over breathing control.
• * Please note this will not work on a person with chronic CO2 retention, such as a COPD patient. These people develop a hypoxic drive, and do not respond to CO2 changes.

You are the critical care nurse about to receive Mr. Sweet, a 24-year-old DKA (diabetic ketoacidosis) patient from the ED. The medical diagnosis tells you to expect acidosis. In report you learn that his blood glucose on arrival was 780. He has been started on an insulin drip and has received one amp of bicarb. You will be doing finger stick blood sugars every hour.

• The pH is acidotic,
• PaCO2 is 25 (low) which should create alkalosis.
• This is a respiratory compensation for the metabolic acidosis .
• The underlying problem is, of course, a metabolic acidosis .
• Insulin, so the body can use the sugar in the blood and stop making ketones, which are an acidic by-product of protein metabolism.
• In the mean time, pH should be maintained near normal so that oxygenation is not compromised (see Oxyhemoglobin Dissociation Curve ).

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COPD Case Study: Patient Diagnosis and Treatment (2024)

by John Landry, BS, RRT | Updated: May 16, 2024

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that affects millions of people around the world. It is primarily caused by smoking and is characterized by a persistent obstruction of airflow that worsens over time.

COPD can lead to a range of symptoms, including coughing, wheezing, shortness of breath, and chest tightness, which can significantly impact a person’s quality of life.

This case study will review the diagnosis and treatment of an adult patient who presented with signs and symptoms of this condition.

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COPD Clinical Scenario

A 56-year-old male patient is in the ER with increased work of breathing. He felt mildly short of breath after waking this morning but became extremely dyspneic after climbing a few flights of stairs. He is even too short of breath to finish full sentences. His wife is present in the room and revealed that the patient has a history of liver failure, is allergic to penicillin, and has a 15-pack-year smoking history. She also stated that he builds cabinets for a living and is constantly required to work around a lot of fine dust and debris.

Physical Findings

On physical examination, the patient showed the following signs and symptoms:

• His pupils are equal and reactive to light.
• He is alert and oriented.
• He is breathing through pursed lips.
• His trachea is positioned in the midline, and no jugular venous distention is present.

Vital Signs

• Heart rate: 92 beats/min
• Respiratory rate: 22 breaths/min

Chest Assessment

• He has a larger-than-normal anterior-posterior chest diameter.
• He demonstrates bilateral chest expansion.
• He demonstrates a prolonged expiratory phase and diminished breath sounds during auscultation.
• He is showing signs of subcostal retractions.
• Chest palpation reveals no tactile fremitus.
• Chest percussion reveals increased resonance.
• His abdomen is soft and tender.
• No distention is present.

Extremities

• His capillary refill time is two seconds.
• Digital clubbing is present in his fingertips.
• There are no signs of pedal edema.
• His skin appears to have a yellow tint.

Lab and Radiology Results

• ABG results: pH 7.35 mmHg, PaCO2 59 mmHg, HCO3 30 mEq/L, and PaO2 64 mmHg.
• Chest x-ray: Flat diaphragm, increased retrosternal space, dark lung fields, slight hypertrophy of the right ventricle, and a narrow heart.
• Blood work: RBC 6.5 mill/m3, Hb 19 g/100 mL, and Hct 57%.

Based on the information given, the patient likely has chronic obstructive pulmonary disease (COPD) .

The key findings that point to this diagnosis include:

• Barrel chest
• A long expiratory time
• Diminished breath sounds
• Use of accessory muscles while breathing
• Digital clubbing
• Pursed lip breathing
• History of smoking
• Exposure to dust from work

What Findings are Relevant to the Patient’s COPD Diagnosis?

The patient’s chest x-ray showed classic signs of chronic COPD, which include hyperexpansion, dark lung fields, and a narrow heart.

This patient does not have a history of cor pulmonale ; however, the findings revealed hypertrophy of the right ventricle. This is something that should be further investigated as right-sided heart failure is common in patients with COPD.

The lab values that suggest the patient has COPD include increased RBC, Hct, and Hb levels, which are signs of chronic hypoxemia.

Furthermore, the patient’s ABG results indicate COPD is present because the interpretation reveals compensated respiratory acidosis with mild hypoxemia. Compensated blood gases indicate an issue that has been present for an extended period of time.

What Tests Could Further Support This Diagnosis?

A series of pulmonary function tests (PFT) would be useful for assessing the patient’s lung volumes and capacities. This would help confirm the diagnosis of COPD and inform you of the severity.

Note: COPD patients typically have an FEV1/FVC ratio of < 70%, with an FEV1 that is < 80%.

The initial treatment for this patient should involve the administration of low-flow oxygen to treat or prevent hypoxemia .

It’s acceptable to start with a nasal cannula at 1-2 L/min. However, it’s often recommended to use an air-entrainment mask on COPD patients in order to provide an exact FiO2.

Either way, you should start with the lowest possible FiO2 that can maintain adequate oxygenation and titrate based on the patient’s response.

Example: Let’s say you start the patient with an FiO2 of 28% via air-entrainment mask but increase it to 32% due to no improvement. The SpO2 originally was 84% but now has decreased to 80%, and his retractions are worsening. This patient is sitting in the tripod position and continues to demonstrate pursed-lip breathing. Another blood gas was collected, and the results show a PaCO2 of 65 mmHg and a PaO2 of 59 mmHg.

What Do You Recommend?

The patient has an increased work of breathing, and their condition is clearly getting worse. The latest ABG results confirmed this with an increased PaCO2 and a PaO2 that is decreasing.

This indicates that the patient needs further assistance with both ventilation and oxygenation .

Note: In general, mechanical ventilation should be avoided in patients with COPD (if possible) because they are often difficult to wean from the machine.

Therefore, at this time, the most appropriate treatment method is noninvasive ventilation (e.g., BiPAP).

Initial BiPAP Settings

In general, the most commonly recommended initial BiPAP settings for an adult patient include this following:

• IPAP: 8–12 cmH2O
• EPAP: 5–8 cmH2O
• Rate: 10–12 breaths/min
• FiO2: Whatever they were previously on

For example, let’s say you initiate BiPAP with an IPAP of 10 cmH20, an EPAP of 5 cmH2O, a rate of 12, and an FiO2 of 32% (since that is what he was previously getting).

After 30 minutes on the machine, the physician requested another ABG to be drawn, which revealed acute respiratory acidosis with mild hypoxemia.

What Adjustments to BiPAP Settings Would You Recommend?

The latest ABG results indicate that two parameters must be corrected:

• Increased PaCO2
• Decreased PaO2

You can address the PaO2 by increasing either the FiO2 or EPAP setting. EPAP functions as PEEP, which is effective in increasing oxygenation.

The PaCO2 can be lowered by increasing the IPAP setting. By doing so, it helps to increase the patient’s tidal volume, which increased their expired CO2.

Note: In general, when making adjustments to a patient’s BiPAP settings, it’s acceptable to increase the pressure in increments of 2 cmH2O and the FiO2 setting in 5% increments.

Oxygenation

To improve the patient’s oxygenation , you can increase the EPAP setting to 7 cmH2O. This would decrease the pressure support by 2 cmH2O because it’s essentially the difference between the IPAP and EPAP.

Therefore, if you increase the EPAP, you must also increase the IPAP by the same amount to maintain the same pressure support level.

Ventilation

However, this patient also has an increased PaCO2 , which means that you must increase the IPAP setting to blow off more CO2. Therefore, you can adjust the pressure settings on the machine as follows:

• IPAP: 14 cmH2O
• EPAP: 7 cmH2O

After making these changes and performing an assessment , you can see that the patient’s condition is improving.

Two days later, the patient has been successfully weaned off the BiPAP machine and no longer needs oxygen support. He is now ready to be discharged.

The doctor wants you to recommend home therapy and treatment modalities that could benefit this patient.

What Home Therapy Would You Recommend?

You can recommend home oxygen therapy if the patient’s PaO2 drops below 55 mmHg or their SpO2 drops below 88% more than twice in a three-week period.

Remember: You must use a conservative approach when administering oxygen to a patient with COPD.

Pharmacology

You may also consider the following pharmacological agents:

• Short-acting bronchodilators (e.g., Albuterol)
• Long-acting bronchodilators (e.g., Formoterol)
• Anticholinergic agents (e.g., Ipratropium bromide)
• Inhaled corticosteroids (e.g., Budesonide)
• Methylxanthine agents (e.g., Theophylline)

In addition, education on smoking cessation is also important for patients who smoke. Nicotine replacement therapy may also be indicated.

In some cases, bronchial hygiene therapy should be recommended to help with secretion clearance (e.g., positive expiratory pressure (PEP) therapy).

It’s also important to instruct the patient to stay active, maintain a healthy diet, avoid infections, and get an annual flu vaccine. Lastly, some COPD patients may benefit from cardiopulmonary rehabilitation .

By taking all of these factors into consideration, you can better manage this patient’s COPD and improve their quality of life.

Final Thoughts

There are two key points to remember when treating a patient with COPD. First, you must always be mindful of the amount of oxygen being delivered to keep the FiO2 as low as possible.

Second, you should use noninvasive ventilation, if possible, before performing intubation and conventional mechanical ventilation . Too much oxygen can knock out the patient’s drive to breathe, and once intubated, these patients can be difficult to wean from the ventilator .

Furthermore, once the patient is ready to be discharged, you must ensure that you are sending them home with the proper medications and home treatments to avoid readmission.

Written by:

John Landry is a registered respiratory therapist from Memphis, TN, and has a bachelor's degree in kinesiology. He enjoys using evidence-based research to help others breathe easier and live a healthier life.

• Faarc, Kacmarek Robert PhD Rrt, et al. Egan’s Fundamentals of Respiratory Care. 12th ed., Mosby, 2020.
• Chang, David. Clinical Application of Mechanical Ventilation . 4th ed., Cengage Learning, 2013.
• Rrt, Cairo J. PhD. Pilbeam’s Mechanical Ventilation: Physiological and Clinical Applications. 7th ed., Mosby, 2019.
• Faarc, Gardenhire Douglas EdD Rrt-Nps. Rau’s Respiratory Care Pharmacology. 10th ed., Mosby, 2019.
• Faarc, Heuer Al PhD Mba Rrt Rpft. Wilkins’ Clinical Assessment in Respiratory Care. 8th ed., Mosby, 2017.
• Rrt, Des Terry Jardins MEd, and Burton George Md Facp Fccp Faarc. Clinical Manifestations and Assessment of Respiratory Disease. 8th ed., Mosby, 2019.

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