Hyperventilation is defined as ‘breathing in excess of metabolic requirements’. This is illustrated by an irregular and disorganised breathing pattern with an increased rate and depth of respirations, known as tachypnoea (Gardner, 2003; College of Paramedics (CoP), 2016). Hyperventilation has many causes; however, this review will focus on acute episodes of primary or idiopathic hyperventilation, meaning there is no underlying organic cause (Pfortmueller et al, 2015; Clarke and Townsend, 2016).
Definition
The term hyperventilation syndrome (HVS) was first mentioned in 1938 by Kerr et al who attributed their patients' tetany to hyperventilation associated with anxiety. Since then, the term has been misused to represent a wide variety of medically unexplained symptoms, which has turned HVS into a ‘fashionable disease that is not to be taken seriously’ (Hornsveld and Garssen, 1997). Consequently, Hornsveld and Garssen (1997) suggested abandoning the term HVS despite acknowledging that patients present with HVS symptoms. It is evident from the literature that the term HVS has slowly disappeared in favour of panic or anxiety attack, panic or anxiety disorder, dysfunctional breathing or breathing pattern disorder (Thomas et al, 2001; 2005; Warburton and Jack, 2006; Todd et al, 2018). However, for this review, HVS was preferred as it is used in the UK Joint Royal Colleges Ambulance Liaison Committee (JRCALC) national ambulance service guidelines (Brown et al, 2016).
Pathophysiology
The basic rhythm of respiration is controlled sub-consciously by the medullary respiratory centre (Aehlert, 2011). This automatic activity can be overridden and breathing voluntarily altered or stopped momentarily in order to prevent water or irritating gases entering the lungs (Tortora and Derrickson, 2011). The automatic control can also be overridden by anxiety, which causes central stimulation of the medullary respiratory centre's inspiratory area, leading to an increased rate and depth of respiration (Porth and Litwack, 2009). This results in faster elimination of carbon dioxide (CO2) through exhalation while the body's CO2 production initially stays at the same level; therefore, causing a decrease in alveolar and arterial CO2 known as hypocapnia (Pizzorno et al, 2016).
Hypocapnia reduces the formation of hydrogen ions (H+) and bicarbonate ions (HCO3-) in the blood, causing a rise in pH levels known as respiratory alkalosis (Khurana, 2012). Hypocapnia also reduces blood flow to the brain by 2% per 1 mmHg reduction in arterial partial pressure of carbon dioxide (PaCO2) (Pizzorno et al, 2016). This is because hypocapnia causes the constriction of cerebral arteries, which increases vascular resistance and reduces cerebral blood flow (Pizzorno et al, 2016). This diminished cerebral perfusion may explain some of the neurological symptoms associated with HVS (Evans, 2005).
Signs and symptoms
Signs and symptoms of HVS are wide-ranging, vague and can vary between patients as illustrated in Table 1. The common symptoms of tetany, paraesthesia and carpopedal spasm are believed to be associated with excessive expiration of CO2 during episodes of tachypnoea, leading to hypocapnia and respiratory alkalosis (Porth and Litwack, 2009). Experiencing these frightening symptoms exacerbates anxiety, which promotes further hyperventilation and results in a vicious cycle (Clarke and Townsend, 2016). The physiological mechanisms associated with many symptoms are not entirely clear. However, Chapman et al (2009) emphasise that HVS symptoms are genuine consequences of physiological imbalances and not figments of patients' imagination.
| Round | Area of expertise |
|---|---|
| Cardiovascular | Palpitations/tachycardia, arrhythmias, chest pain, blotchy flushing |
| Neurological | Paraesthesia to extremities or face, dizziness/unsteadiness, syncope, headache, blurred or tunnel vision, impaired concentration and memory |
| Respiratory | Tachypnoea, shortness of breath, tightness in chest/throat, frequent sighing, yawning, feeling of suffocation/choking |
| Gastrointestinal | Globus, dysphagia, epigastric discomfort, excessive air swallowing, dry mouth, belching, flatulence, nausea |
| Musculoskeletal | Muscle pains, tremors, weakness, tetany of hands or feet (e.g. carpopedal spasm) |
| Psychological | Tension, anxiety, panic, feelings of unreality or disorientation, fear of dying, fear of losing control or going crazy, hallucinations, phobias |
| General | Fatigue, exhaustion, sleep disturbance, sweating, weakness, chills or heat sensations |
Assessment
The JRCALC guidelines advise that paramedics should presume that hyperventilation is secondary to an underlying respiratory or metabolic disorder until proven otherwise (Brown et al, 2016). Consequently, assessment of HVS patients requires comprehensive history-taking and physical examination to exclude physical or bio-chemical causes (Gardner, 2003) (Table 2). Questions during history-taking should include:
| Body system | Differential diagnoses | |
|---|---|---|
| Cardiovascular | Angina |
Myocardial infarction |
| Neurological | Brain stem lesions |
Meningitis |
| Respiratory | Asthma |
Lung tumour |
| Gastrointestinal | Cholecystitis |
Liver cirrhosis |
| Endocrine | Diabetic ketoacidosis |
Thyrotoxicosis |
| Renal | Kidney failure | |
| Environmental | Heat or altitude acclimatisation | Carbon monoxide poisoning |
| Other | Anaemia |
Hypokalaemia |
The National Institute for Health and Care Excellence (NICE) (2017) also suggests enquiring whether breathlessness occurs at rest rather than on exertion as this distinction points towards HVS.
Physical examination should include auscultation of breath sounds to exclude physical causes of breathlessness as may be indicated by a wheeze or crackles (Brown et al, 2016; NICE, 2017). Observation and palpation of the patient's chest should also be included as it may demonstrate paradoxical breathing associated with forced respiration, i.e. abdomen retracts and upper chest expands on inhalation as opposed to normal abdominal protrusion and lower thorax expansion (Pizzorno et al, 2016).
Initial assessment should encompass: measurement of respiratory rate; peripheral oxygen saturations (SpO2); heart rate; blood pressure; and temperature (NICE, 2017). Respiratory rate and heart rate will likely be elevated in patients with acute HVS alongside an abnormally high SpO2 of 99% or 100% (O'Driscoll et al, 2017). Blood pressure and temperature should be within normal limits for the patient's age. In addition to these basic observations, disease-specific measurements such as peak expiratory flow rate and an electrocardiogram (ECG) should be performed. Peak expiratory flow readings should be compared with predicted values according to patients' age, sex and height, in order to exclude significant respiratory restriction (Pizzorno et al, 2016). An ECG should also be performed as temporary changes can occur during acute episodes of HVS and underlying cardiac conditions need to be excluded (Michaelides et al, 2010).
Diagnosis
It is recommended by JRCALC guidelines to compare patients' presentation to signs and symptoms of HVS, which are listed in Table 1 (Brown et al, 2016). Despite Pizzorno et al (2016) emphasising that no symptoms provide absolute diagnostic certainty, the American Psychiatric Association (APA) (2013) suggests that HVS can be diagnosed in a patient who experiences a sudden onset of anxiety, building up over several minutes in the presence of four or more symptoms in Table 1.
To diagnose chronic HVS, the Nijmegen questionnaire is frequently used. This is a 16-item screening tool introduced in the 1980s to identify individuals that could benefit from breathing retraining. However, it is not suitable for diagnosing acute HVS (Pizzorno et al, 2016). In the absence of a standardised method of diagnosis, Pizzorno et al (2016) suggest using end-tidal CO2 measurements obtained via nasal cannula to diagnose HVS, whereby less than 30 mmHg during an acute episode is the cut-off point for HVS diagnosis. An alternative method is the breath holding time test; during an acute episode of HVS, if patients are unable to hold their breath beyond 10–12 seconds, some clinicians use an arbitrary cut-off point of less than 30 seconds to diagnose HVS (Pizzorono et al, 2016).
The lack of agreement in the literature regarding specific HVS diagnostic criteria led Smith (1985) to hypothesise that good patient-clinician relationships are more important than invasive laboratory tests (Jones et al, 2013). To promote a good relationship, Nancy Caroline suggests not contributing to the patient's anxieties and trying to reassure them (CoP, 2016). Communicate to patients that you believe they are suffering with HVS, which may offer sufficient reassurance and relief of anxiety to reduce the severity and frequency of symptoms (Boulding et al, 2016). On the flip side, delaying a diagnosis of HVS by referring patients for extensive testing or insisting they attend the emergency departments following pre-hospital assessment may worsen their condition because of uncertainty and secondary anxiety over symptoms (Sharpe, 2017).
Management
Management of HVS focuses on reassuring patients and assisting them in establishing a good respiratory pattern (Kim, 2005). Practical ways to achieve this are to breathe in time with the patient, ask the patient to count to 2 between each breath, or use distraction techniques (CoP, 2016). In clinical practice, a method frequently observed is to verbally coach the patient to breathe in through their nose and out through their mouth in an effort to slow respirations down.
JRCALC guidelines suggest removing the source of the patient's anxiety or moving the patient to a different room if this is practical (Brown et al, 2016). Oxygen therapy is not recommended unless patients are hypoxaemic—with an SpO2 of less than 94%. However, if this is the case, idiopathic HVS should no longer be considered as a working diagnosis as it suggests an underlying organic cause (Brown et al, 2016; O'Driscoll et al, 2017).
Paper bag rebreathing has not been recommended since 1990 because of the risk of hypoxia (Kishikawa, 2015); although, evidence of its implementation can be found anecdotally in current practice and in published literature (Set et al, 2004). In the long term, underlying anxiety can be addressed through psychotherapy or sedative drugs and breathing exercises performed during physiotherapy (Jones et al, 2013).
Relevance for pre-hospital care
Patients with HVS use a significant amount of hospital and emergency service resources because they frequently seek care in the emergency department or from paramedics because they fear they are experiencing life-threatening emergencies (Katerndahl and Realini, 1995; Coley et al, 2009). In the general adult population, HVS has an estimated prevalence of 6–10% rising to 34% in asthmatic patients (Thomas et al, 2001; 2005; Grammatopoulou, 2014). The JRCALC guidelines describe HVS as a common presentation in pre-hospital care but exact data on the prevalence of HVS in the pre-hospital setting has not yet been published (Brown et al, 2016). An unpublished service evaluation presented as a poster by Wilson et al (2017) found a 1% prevalence of HVS in adult patients presenting to a UK ambulance service. This is comparable to published estimates for emergency departments, which range from 0.3–6% (Coley et al, 2009; Pfortmueller et al, 2015; Greenslade et al, 2017).
Attempts have been made to address the high economic cost of patients with HVS presenting to ambulance services and emergency departments by educating doctors and using screening tools; however, these have been largely unsuccessful (Harvison et al, 2004). The literature shows that the use of HVS screening tools is associated with low staff adherence rates and a reluctance of patients to participate, which highlights the need for a more personalised approach to HVS diagnosis and the benefit of GP involvement (Bokma et al, 2015). Nevertheless, a newly developed screening tool known as the Panic Screening Score, which has been designed to detect HVS in the emergency department setting in Canada, is currently being refined and validated in a prospective cohort study (Foldes-Busque et al, 2013).
A successful attempt at reducing pressures on emergency medical staff and improving the symptoms of people with HVS is described by Pinney et al (1987) in the form of an outpatient-based hyperventilation clinic run by staff nurses. However, this pilot study has not resulted in further research projects or been adopted into standard practice judging by the lack of recent literature on this topic. Nevertheless, this study again highlights the benefit of personalised care for patients with HVS in a non-emergency setting.
Conclusion
A diagnosis of HVS is a diagnosis of exclusion of organic causes following detailed history-taking and physical examination. HVS is self-limiting and treatment focuses on establishing a good respiratory pattern in order to normalise patients' observations and reduce their symptoms.
Previous attempts at reducing the high economic cost of patients with HVS to A&E departments have either been unsuccessful or have not been adopted into standard practice. Consequently, Pfortmueller et al (2015) propose that paramedics are ideally placed to diagnose and treat HVS pre-hospitally to avoid unnecessary and costly admissions to A&E departments. This is in line with the JRCALC guidelines, which advise that patients with HVS can be considered for non-conveyance as long as this is not their first HVS episode and symptoms have settled (Brown et al, 2016). Further research is needed to evaluate the pre-hospital prevalence and diagnostic accuracy for HVS, as well as identify clear diagnostic criteria and possible pre-hospital screening tools.