Urgent considerations
See Differentials for more details
Pulmonary embolism
Commonly pulmonary embolism (PE) presents with dyspnoea, pleuritic chest pain, cough, and hypocapnia. Symptoms may be mild or severe and present with hypotension or pulseless electrical activity (PEA). The diagnosis is made by CT angiography of the pulmonary arteries or by ventilation-perfusion scan of the lungs.[106][107] Treatment is anticoagulation, which may be started if there is a high clinical suspicion for PE while awaiting the outcome of a diagnostic imaging study. Recommendations for thrombolytic therapy are reserved for patients with haemodynamic compromise and selected high-risk patients with low bleeding risks.[108]
Pneumothorax
Pneumothorax is defined as the presence of air within the pleural space. Tension pneumothorax may develop secondarily. This occurs when intrapleural pressure exceeds atmospheric pressure throughout expiration and, frequently, during inspiration. Tension pneumothorax is associated with haemodynamic instability. It is commonly observed in patients receiving positive pressure mechanical ventilation or CPR. Diagnosis of pneumothorax is confirmed by the presence of a pleural line on chest radiograph. Hypoxaemia is the predominant symptom; therefore, treatment begins with oxygen supplement. If the patient is haemodynamically unstable and there are unilateral decreased breath sounds and hyper-resonance to percussion, immediate and definitive treatment with tube thoracostomy is recommended without waiting for diagnosis by chest radiograph.[109]
Computed tomography is the gold standard for diagnosis and assessing the size of pneumothoraces, yet diagnosis has traditionally been confirmed by chest radiography due to expedience.[110] Pleural ultrasound, with expertise in the procedure, has been increasingly used for diagnosis due to rapidity, availability in urgent situations, and reported higher accuracy. Meta-analyses have demonstrated sensitivities of 78.6-90.9% in pleural ultrasound compared to 39.8-50.2% in chest radiography with near identical specificity in both (~98%).[111][112] Of note, the majority of this data is derived from post-procedure and trauma patients, in which chest radiography is limited to supine or semi-erect positioning. Up to 30% of pneumothoraces can be missed on supine radiograph.[111] Pleural ultrasound is limited in pleural adhesions, bullous emphysema, main-stem intubation of the contralateral side, subcutaneous emphysema, and pleural calcifications.
Pulmonary oedema
Cardiogenic pulmonary oedema is one of several parenchymal lung diseases that may induce hypocapnia. Dyspnoea with exertion may be the presenting sign of pulmonary oedema. Crackling rales are present on auscultation of the lung fields, particularly at the bases. Chest radiograph may confirm the presence of pulmonary effusion and Kerley B lines, as well as cardiomegaly in congestive heart failure. An ominous presentation of respiratory alkalosis with concurrent wide alveolar-arterial PO₂ gradient and anion gap metabolic acidosis occurs in the context of cardiogenic shock. These findings suggest tissue hypoxia. With tissue hypoxia, augmented H+ concentration due to increased lactate production acts as a stimulus to the carotid bodies, leading to hyperventilation.
Central nervous system lesions
A spectrum of disease may cause focal neurological signs or symptoms in tandem with respiratory alkalosis, and includes ischaemic stroke, haemorrhagic stroke, and space-occupying lesions. In most instances, the mechanism for respiratory alkalosis is central neurogenic hyperventilation. Urgent non-contrast CT of the brain should be obtained to diagnose haemorrhage, infarct, mass lesion, or other abnormalities. If ischaemic stroke is present and symptom onset is within 4.5 hours, treatment with tissue plasminogen activator (tPA) should be considered, provided that there are no contraindications to its administration.[113] In ischaemic stroke, patients who do not qualify for tPA should begin with antiplatelet therapy. In haemorrhagic stroke, coagulopathies have to be corrected and neurosurgical consult requested for possible decompression. MRI of the brain is necessary to detect ischaemic stroke or masses not visualised on head CT.
Meningitis and encephalitis
The spectrum between meningitis and encephalitis is often blurred, but both are associated with significant morbidity and mortality. Patients with meningitis present with fever, seizures, headache, and lethargy, but normal sensorium. Patients with encephalitis have abnormal cerebral function, altered mental status, seizures, and motor and sensory deficits. Respiratory alkalosis is a common presence in both groups. It is hypothesised that increased cerebrospinal fluid (CSF) lactate causes decreased CSF pH, leading to stimulation of medullary chemoreceptors and increased minute ventilation.[78]
Lumbar puncture (LP) is necessary for diagnosis unless the risk of complications from the procedure, particularly cerebral herniation, exceeds potential benefit. Raised intracranial pressure is a contraindication to LP. The diagnosis of meningoencephalitis has been advanced greatly with development of MRI of the brain.[114] Empirical antibiotics for acute bacterial meningitis should be administered prior to LP or imaging studies and usually include vancomycin and third-generation cephalosporins (e.g., ceftriaxone, cefotaxime).[115] Administration of corticosteroid (dexamethasone) prior to or simultaneous with antibiotic treatment is considered when Streptococcus pneumoniae is highly suspected as the bacterial agent involved.[116][117] If viral encephalitis is suspected, CSF should be sent for HSV-1, HSV-2, and varicella-zoster virus amplification using the PCR technique. Urgent treatment with aciclovir should be instituted even before PCR results are available, because delays in treatment lead to high mortality.[114]
Systemic inflammatory-response syndrome (SIRS) and sepsis
Tachypnoea is one of the indicators of systemic inflammatory-response syndrome (SIRS) and may be associated with primary respiratory alkalosis, metabolic acidosis, or mixed acid-base disorder. Typically, the diagnosis of SIRS is made when 2 or more of the following are present:[76]
Tachypnoea
Tachycardia
Hyperthermia or hypothermia
Serum leukocyte count of >12,000 cells/mm³, or <4000 cells/mm³, or a differential leukocyte count of 10% bands.
In practice, sepsis is usually diagnosed by the clinical identification of an infection in a patient who meets the clinical criteria for SIRS.
Sepsis is a spectrum of disease, where there is a systemic and dysregulated host response to an infection.[118] Presentation ranges from subtle, non-specific symptoms (e.g., feeling unwell with a normal temperature) to severe symptoms with evidence of multi-organ dysfunction, and septic shock. Patients may have signs of tachycardia, tachypnoea, hypotension, fever or hypothermia, poor capillary refill, mottled or ashen skin, cyanosis, newly altered mental state, or reduced urine output.[119] Sepsis and septic shock are medical emergencies.
Risk factors for sepsis include: age under 1 year, age over 75 years, frailty, impaired immunity (due to illness or drugs), recent surgery or other invasive procedures, any breach of skin integrity (e.g., cuts, burns), intravenous drug misuse, indwelling lines or catheters, and pregnancy or recent pregnancy.[119]
Early recognition of sepsis is essential because early treatment improves outcomes.[119][120][Evidence C][Evidence C] However, detection can be challenging because the clinical presentation of sepsis can be subtle and non-specific. A low threshold for suspecting sepsis is therefore important. The key to early recognition is the systematic identification of any patient who has signs or symptoms suggestive of infection and is at risk of deterioration due to organ dysfunction. Several risk stratification approaches have been proposed. All rely on a structured clinical assessment and recording of the patient’s vital signs.[119][121][122][123] It is important to check local guidance for information on which approach your institution recommends. The timeline of ensuing investigations and treatment should be guided by this early assessment.[123]
Treatment guidelines have been produced by the Surviving Sepsis Campaign and remain the most widely accepted standards.[120][124]
Recommended treatment of patients with suspected sepsis is:
Measure lactate level, and remeasure lactate if initial lactate is elevated (> 2 mmol/L)
Obtain blood cultures before administering antibiotics
Administer broad-spectrum antibiotics (with methicillin-resistant Staphylococcus aureus [MRSA] coverage if there is high risk of MRSA) for adults with possible septic shock or a high likelihood for sepsis
For adults with sepsis or septic shock at high risk of fungal infection, empiric antifungal therapy should be administered
Begin rapid administration of crystalloid fluids for hypotension or lactate level ≥ 4 mmol/L. Consult local protocols.
Administer vasopressors peripherally if hypotensive during or after fluid resuscitation to maintain MAP ≥ 65 mm Hg, rather than delaying initiation until central venous access is secured. Noradrenaline (norepinephrine) is the vasopressor of choice
For adults with sepsis-induced hypoxaemic respiratory failure, high flow nasal oxygen should be given.
Ideally these interventions should all begin in the first hour after sepsis recognition.[124]
For adults with possible sepsis without shock, if concern for infection persists, antibiotics should be given within three hours from the time when sepsis was first recognised.[120]
For adults with a low likelihood of infection and without shock, antibiotics can be deferred while continuing to closely monitor the patient.[120]
For more information on sepsis, please see our topics Sepsis in adults and Sepsis in children.
Salicylate overdose
Salicylate toxicity manifests initially as respiratory alkalosis, followed by a mixed acid-base disorder and, later in the course, metabolic acidosis.[125] It may present with hyperpnoea, tinnitus, lethargy, agitation, vomiting, or fever. Severe manifestations include:
Coma with seizures secondary to cerebral oedema
Hypoxaemia
Hypoglycaemia
Direct toxicity to the central nervous system
Renal failure
Rhabdomyolysis
Acute lung injury
Myocardial depression.
Serum salicylate level confirms the diagnosis but does not reflect the severity of toxicity. A salicylate nomogram, referred to as the Done nomogram, describes the severity of toxicity according to serum salicylate level at a given time after the ingestion.[126] However, the Done nomogram has limited application in adults.[127] Initial therapy consists of the administration of activated charcoal, restoring intravascular volume, and alkalinisation of the serum and urine. Severe toxicity requires urgent haemodialysis.[125]
Mechanical ventilation
Hyperventilated patients on mechanical ventilation may develop respiratory alkalosis. Treatment is reduction of minute ventilation by decreasing set tidal volume. If patient breathing rate far exceeds the set ventilator rate, sedative or paralytic agents may be necessary.
Use of this content is subject to our disclaimer