Skip to main content

Main menu

  • Home
  • Our journals
    • Clinical Medicine
    • Future Healthcare Journal
  • Subject collections
  • About the RCP
  • Contact us

Clinical Medicine Journal

  • ClinMed Home
  • Content
    • Current
    • Ahead of print
    • Archive
  • Author guidance
    • Instructions for authors
    • Submit online
  • About ClinMed
    • Scope
    • Editorial board
    • Policies
    • Information for reviewers
    • Advertising

User menu

  • Log in

Search

  • Advanced search
RCP Journals
Home
  • Log in
  • Home
  • Our journals
    • Clinical Medicine
    • Future Healthcare Journal
  • Subject collections
  • About the RCP
  • Contact us
Advanced

Clinical Medicine Journal

clinmedicine Logo
  • ClinMed Home
  • Content
    • Current
    • Ahead of print
    • Archive
  • Author guidance
    • Instructions for authors
    • Submit online
  • About ClinMed
    • Scope
    • Editorial board
    • Policies
    • Information for reviewers
    • Advertising

Lessons of the month 2: A forgotten cause of transient T-wave inversion

Hala Alsafadi and William Swain
Download PDF
DOI: https://doi.org/10.7861/clinmedicine.19-4-334
Clin Med July 2019
Hala Alsafadi
ARoyal Hampshire County Hospital, Winchester, UK and Southern Health NHS Foundation Trust, UK
Roles: consultant acute medicine and diabetes
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: hala.alsafadi@hhft.nhs.uk
William Swain
BRoyal Hampshire County Hospital, Winchester, UK
Roles: general practitioner trainee
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
Loading

ABSTRACT

A 19-year-old patient presented with severe chest pain, which is not typical for cardiac angina. However, his smoking history and the strong family history of ischaemic heart disease coupled with evidence of progressive T-wave changes on his electrocardiogram (ECG) caused dilemma in deciding further management. His blood tests were normal apart from hypophosphataemia, and he had two negative troponin results. His arterial blood gases showed respiratory alkalosis. He was given analgesia for a diagnosis of musculoskeletal chest pain and the next morning his ECG, arterial blood gases and phosphate levels all normalised. He had a normal echocardiogram and was reviewed by the cardiologist who diagnosed musculoskeletal chest pain which led to distress and hyperventilation causing hypophosphataemia and transient T-wave inversion. This case is a reminder of an under-recognised physiological phenomenon involving the cardiac conduction during hyperventilation.

KEYWORDS
  • Hyperventilation
  • T-wave inversion
  • hypophosphataemia

Case presentation

A 19-year-old Caucasian male presented to the acute medical unit from the emergency department with severe chest pain which was worse on breathing and moving the arms. He had no previous medical history and was on no medications. He had no risk factors for venous thromboembolism. He smoked 10 cigarettes per day, drank alcohol occasionally and denied any recreational drug use. He works as a farmer and had busy work the previous few weeks in his farm. His father, who was a smoker, died of myocardial infarction at the age of 50.

Examination was unremarkable aside from mild tenderness on palpation of the anterior left chest wall. He was still complaining of chest pain and had tachypnoea (28 breaths per minute) with normal blood pressure, pulse and saturation. Chest X-ray was normal, and initial electrocardiogram (ECG) showed sinus rhythm with T-wave inversion in lead V3 (Fig 1). Serial ECGs were performed which showed further T-wave inversion in lead V4 (Fig 2) and then in lead V5 as well (Fig 3).

Fig 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 1.

Initial electrocardiogram showing sinus rhythm with T-wave inversion in lead V3.

Fig 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 2.

Electrocardiogram showing sinus rhythm with further T-wave inversion in lead V4.

Fig 3.
  • Download figure
  • Open in new tab
  • Download powerpoint
Fig 3.

Electrocardiogram showing sinus rhythm with T-wave inversion in lead V5 as well.

Blood tests including full blood count, renal function, liver function test, two troponin tests, D-dimer and inflammatory markers were all normal. Serum phosphate level was noticed to be significantly low at 0.3 mmol/L (0.8–1.5). His arterial blood gases (ABG) showed marked respiratory alkalosis with pH 7.641, pCO2 2.72 kPa, pO2 16.10 kPa and HCO3 21.5 kPa which was thought to be due to pain-induced tachypnoea and hyperventilation. He had an echocardiogram which was normal. His pain sounded typical of musculoskeletal origin and he required regular strong analgesia during the night. The following morning he was pain-free and his ECG, ABG and PO4 level had all normalised. He was reviewed by the cardiologist who diagnosed musculoskeletal chest pain which led to distress and hyperventilation causing hypophosphataemia and transient T-wave inversion.

Discussion

T-wave inversion on ECG is usually a concerning finding as it is often associated with myocardial ischaemia or ventricular strain. The respiratory variation in the T-wave morphology has been reported in the literature,1 however the frequency of this observation remains unknown as this is not routinely evaluated. Hyperventilation has long been known to cause transient ECG repolarisation abnormalities2 although it is rarely talked about in modern clinical settings. The exact physiological mechanism of these repolarisation changes is not fully understood. It has been posited that they are a direct consequence of respiratory alkalosis or hypocapnia;3 however T-wave changes in some studies occurred after a short period of hyperventilation, which is unlikely to have caused significant pH change.2 T-wave inversion has been demonstrated due to hyperventilation in high CO2 atmosphere where hypocapnia and alkalosis did not occur.2 An interesting study demonstrated that decreasing pCO2 reduced the amplitude of T-waves at a fixed volume ventilation while separately increasing ventilation also decreased T-wave amplitude at a fixed pCO2.3 Extrapolation suggested extreme hyperventilation would decrease the T-wave amplitude enough for it to be inverted.3 T-wave changes due to hyperventilation have also been shown to be unrelated to electrolyte disturbances or changes in heart position.4 Another suggestion of a possible mechanism has been via a vagal reflex similar to the Hering–Breuer reflex that terminates inhalation to prevent overinflation of the lungs, and the reflex responses of coughing, airway constriction and hyperventilation.2

One study involving 474 healthy subjects showed that 15% developed repolarisation changes in response to hyperventilation.3 The majority consisted of T-wave inversion – either from positive to negative, or negative to positive, eg lead III. A minority of the subjects that did show repolarisation abnormalities (13%) demonstrated ST depression. Most of the ST–T changes arose after brief (30–90 seconds) hyperventilation and soon after breathing returned to normal.5

Apart from the ECG changes and respiratory alkalosis our patient had hypophosphataemia on admission which the admitting team initially could not explain. Hypophosphataemia is common in hospitalised patients and the cause of hypophosphataemia is usually multifactorial, but the main mechanism is cellular redistribution, renal loss, malabsorption or gastrointestinal loss.6 Hyperventilation is a common cause of hypophosphataemia in hospitalised patients and may not be obvious.7 Hyperventilation causes a respiratory alkalosis which in turn mediates an increase in intracellular pH. This stimulates phosphofructokinase activity in the glycolytic pathway with a subsequent increase in demand for phosphate, which is driven intracellularly to form glycolytic intermediate metabolites.8

In this case the combinations of respiratory alkalosis, hypophosphataemia and T-wave inversion that all normalised with adequate analgesia have helped to reach the correct diagnosis.

Summary

Our young patient presented with severe chest pain, which is not typical for cardiac angina. However the smoking history and the strong family history of ischaemic heart disease coupled with evidence of progressive T-wave changes on ECG added to the dilemma in deciding further management. This case is a reminder of an under-recognised physiological phenomenon involving the cardiac conduction. In patients with a low risk of coronary artery disease who present with atypical chest pain and an abnormal ECG, arterial blood gas analysis should be considered to exclude hyperventilation and alkalosis.

  • © Royal College of Physicians 2019. All rights reserved.

References

  1. ↵
    1. Goldman MJ.
    Principles of clinical electrocardiography. Los Altos: Lange Medical, 1973:58–73.
  2. ↵
    1. Wasserburge RH
    , Slebesker KL Jr., Lewis WC. The effect of hyperventilation on the normal adult electrocardiogram. Circulation 1956;13.
  3. ↵
    1. Rutherford JJ
    , Clutton-Brock TH, Parkes MJ. Hypocapnia reduces the T-wave of the electrocardiogram in normal human subjects. Am J Physiol Regul Integr Comp Physio 2005;289:R148–55.
    OpenUrl
  4. ↵
    1. Biberman L
    , Sarma RN, Surawicz B. T-wave abnormalities during hyperventilation and isoproterenol infusion. Am Heart J 1971;81:166–74.
    OpenUrlCrossRefPubMed
  5. ↵
    1. Alexopoulos D
    , Christodoulou J, Toulgaridis T, et al. Repolarization abnormalities with prolonged hyperventilation in apparently healthy subjects: incidence, mechanisms and affecting factors. Eur Heart J 1996;17:1432–7.
    OpenUrlPubMed
  6. ↵
    1. Datta BN
    , Stone MD. Hyperventilation and hypophosphataemia. Ann Clin Biochem 2009;46:170–71.
    OpenUrlCrossRefPubMed
  7. ↵
    1. Knochel J
    , Agrawal R. Hypophosphataemia and hyperphosphataemia. In: Brenner B (ed). The kidney, 5th edn. Philadelphia: WB Saunders, 1996:1086–133.
  8. ↵
    1. Brautbar N
    , Lebovici H, Massry SG. On the mechanism of hypophosphataemia during acute hyperventilation: evidence for increased muscle glycolysis. Minor Electro Metab 1983;9:45–50.
    OpenUrl
Back to top
Previous articleNext article

Article Tools

Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Citation Tools
Lessons of the month 2: A forgotten cause of transient T-wave inversion
Hala Alsafadi, William Swain
Clinical Medicine Jul 2019, 19 (4) 334-335; DOI: 10.7861/clinmedicine.19-4-334

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Lessons of the month 2: A forgotten cause of transient T-wave inversion
Hala Alsafadi, William Swain
Clinical Medicine Jul 2019, 19 (4) 334-335; DOI: 10.7861/clinmedicine.19-4-334
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • ABSTRACT
    • Case presentation
    • Discussion
    • Summary
    • References
  • Figures & Data
  • Info & Metrics

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • No citing articles found.
  • Google Scholar

More in this TOC Section

  • Lessons of the month: A challenging presentation of hypopituitarism secondary to an intracerebral aneurysm
  • Lessons of the month: ANCA-associated vasculitis – granulomatosis with polyangiitis: ‘the great mimic’
  • Lessons of the month: Acute liver failure: a case close to the heart
Show more Lessons of the month

Similar Articles

Navigate this Journal

  • Journal Home
  • Current Issue
  • Ahead of Print
  • Archive

Related Links

  • ClinMed - Home
  • FHJ - Home
clinmedicine Footer Logo
  • Home
  • Journals
  • Contact us
  • Advertise
HighWire Press, Inc.

Follow Us:

  • Follow HighWire Origins on Twitter
  • Visit HighWire Origins on Facebook

Copyright © 2021 by the Royal College of Physicians