02/09/2026
ENS, severe hypocapnia, angina-like chest pain and repeated ST–T changes – has anyone else measured this?
I know that many people with Empty Nose Syndrome (ENS) report chest pressure, heart pain, palpitations and exercise intolerance.
What seems much less common is that anyone has actually measured CO₂, blood gases and ECG changes while these symptoms are occurring.
I have now had this investigated repeatedly in several different ways, including blood gases, capnography, resting ECGs and exercise ECG testing.
I want to share the objective findings first, and then explain why I think the existing research on hypocapnia, oxygen delivery, coronary blood flow and cardiac repolarization is highly relevant.
MY CHEST/HEART PAIN
The pain feels like a deep pressure, burning and aching sensation over the heart/chest area.
It is strongly related to physiological workload.
Walking uphill, climbing stairs or anything that increases my heart rate can markedly increase the chest/heart pain. When it becomes severe, I may have to stop and rest until it decreases before continuing.
It can also worsen during cognitive or physiological stress. Prolonged concentration, writing, planning, problem solving, stressful situations and longer conversations can increase both my breathing problems and the heart pain.
During worse episodes I can also experience:
• forceful heartbeats/palpitations
• breathlessness
• dizziness/near-fainting
• severe exercise intolerance
• profound fatigue
The combination of deep chest pressure/burning, worsening with exertion and increasing cardiac workload, and improvement when workload decreases resembles the clinical pattern of angina/ischemia-type chest pain.
This does not mean that obstructive coronary artery disease or myocardial ischemia has been proven in my case.
But this symptom pattern becomes particularly interesting when considered together with the objective CO₂ and ECG findings.
⸻
MY CO₂ AND BLOOD-GAS FINDINGS
During resting physiological testing I have measured:
Blood pCO₂: approximately 25–26.5 mmHg
Normal arterial pCO₂ in healthy adults is approximately:
35–45 mmHg
So this represents substantial hypocapnia.
End-tidal CO₂ (EtCO₂): approximately 20 mmHg
Normal resting EtCO₂ is generally approximately:
35–45 mmHg
So my EtCO₂ has at times been approximately 15–25 mmHg below the normal range.
Blood pH: approximately 7.51
Normal arterial pH is approximately:
7.35–7.45
The combination of very low CO₂ and pH around 7.51 represents marked:
HYPOCAPNIA + RESPIRATORY ALKALOSIS
Ionized calcium: 1.06 mmol/L
Laboratory reference range:
approximately 1.12–1.32 mmol/L
So biologically active ionized calcium was also reduced during this hypocapnic/alkalemic physiological state.
⸻
ELEVATED LACTATE AT REST
Another finding that I think is interesting was:
Resting lactate: approximately 2.9–3.0 mmol/L
Typical adult resting reference ranges are approximately:
0.5–2.0 mmol/L
with some laboratories using an upper limit around 2.2 mmol/L.
So my lactate was already elevated while I was at rest.
During exercise testing, lactate subsequently reached:
Lactate: 16.9 mmol/L
while pCO₂ was still only:
pCO₂: approximately 26.3 mmHg
The post-exercise lactate value should obviously NOT be compared directly with a resting reference range, because lactate can increase substantially during intense exercise.
What interests me more is that lactate was already elevated at rest while severe hypocapnia and respiratory alkalosis were present.
⸻
REPEATED ECG CHANGES at the emergency care
During the same period that the chest/heart symptoms developed, repeated ECG abnormalities were recorded.
They have included:
• Horizontal ST depression in II, III, aVF, V5 and V6
• A small anterior ST elevation/repolarization change in V3
• On another ECG, inferior ST depression in II, III and aVF
• Later resting ECGs showing inferolateral ST depression
• During an exercise ECG, increasing inferolateral ST depression with increasing workload
• At maximal exercise, the ST depression reached approximately 1.8 mm in V6
• The ST depression then became smaller again during recovery
• During another period of significantly worsened chest symptoms, inferior and lateral ST–T/repolarization abnormalities were again recorded
A later ECG could return to normal, suggesting that at least some of these abnormalities are dynamic rather than permanently present.
The exercise test was not considered convincing evidence of classical obstructive exercise-induced ischemia, which is also important to mention.
⸻
THE MOST INTERESTING EPISODE
One emergency-department episode is particularly interesting because several abnormalities were measured almost simultaneously.
I was experiencing significant chest/heart pain.
The ECG showed horizontal ST depression in:
II
III
aVF
V5
V6
At the same time, I had brought my own capnograph with me.
While I was experiencing the chest symptoms and the ECG abnormalities, my capnograph was simultaneously showing hypocapnia / abnormally low EtCO₂.
Approximately seven minutes after the abnormal ECG, the hospital performed a venous blood gas.
It showed:
Venous pCO₂: approximately 29 mmHg
A typical healthy venous pCO₂ is usually considerably higher, approximately:
40–50 mmHg
Venous pCO₂ is normally somewhat HIGHER than arterial pCO₂.
So a venous value of approximately 29 mmHg is strikingly low.
Venous pH: 7.46
Typical healthy venous pH is approximately:
7.33–7.43
At approximately the same time:
Respiratory rate: ~24 breaths/minute (way to much)
Blood pressure: ~172/98 mmHg
So during essentially the same symptomatic episode there was:
deep angina-like chest pain
very low EtCO₂ measured by capnography
rapid breathing
very low venous pCO₂
alkalemic blood pH
pathological ST/repolarization changes
Troponin was negative, meaning that there was no biochemical evidence of an acute myocardial infarction at that time.
This does not prove myocardial ischemia.
But it raises an important physiological question:
Could severe hypocapnia itself contribute to reduced myocardial oxygen availability and dynamic cardiac electrical changes?
⸻
WHAT COULD POSSIBLY CONNECT THESE FINDINGS?
There are several mechanisms described in human physiology and cardiovascular research.
Importantly, these mechanisms are not mutually exclusive.
Several could potentially occur simultaneously.
⸻
1. HYPOCAPNIA CAN REDUCE OXYGEN UNLOADING – THE BOHR EFFECT
CO₂ is not simply a waste product.
It plays an important role in determining how easily hemoglobin releases oxygen to tissues.
Normally, metabolically active tissue generates CO₂ and hydrogen ions.
Higher local CO₂ and lower pH reduce hemoglobin’s affinity for oxygen.
Hemoglobin therefore releases oxygen more easily where it is needed.
This is part of the Bohr effect.
But severe hypocapnia pushes this physiology in the opposite direction.
Hyperventilation causes excessive elimination of CO₂:
CO₂ falls
↓
hydrogen ion concentration falls
↓
pH rises
↓
respiratory alkalosis develops
The increased pH produces a left shift of the oxyhemoglobin dissociation curve.
That means:
Hemoglobin develops a higher affinity for oxygen.
In simple terms:
Hemoglobin holds onto oxygen more tightly.
Therefore, even if arterial oxygen saturation or pulse oximetry looks completely normal, oxygen may be released less readily from hemoglobin into metabolically active tissues.
This distinction is important.
Normal SpO₂ does not necessarily mean normal oxygen unloading at tissue level.
The heart has an exceptionally high and continuous oxygen requirement.
Unlike many other tissues, the myocardium already extracts a large proportion of the oxygen delivered to it at rest.
Therefore when cardiac workload increases, the heart depends heavily on increasing coronary blood flow.
If hypocapnia simultaneously reduces coronary flow AND makes hemoglobin hold oxygen more tightly, this could theoretically create an unfavorable situation for myocardial oxygen availability.
⸻
WHERE DOES MY ELEVATED RESTING LACTATE FIT INTO THIS?
This is something I find particularly interesting.
My lactate was approximately:
2.9–3.0 mmol/L AT REST
while marked hypocapnia and respiratory alkalosis had already been documented.
Lactate can increase when glycolytic metabolism increases.
One possible reason for increased lactate production is a situation where oxygen delivery or oxygen utilization does not fully match tissue metabolic requirements.
Therefore, if severe hypocapnia causes:
reduced tissue blood flow
and
less efficient oxygen unloading from hemoglobin
it is physiologically reasonable to ask whether this could contribute to metabolic stress in some tissues.
A possible pathway would be:
reduced tissue oxygen availability
↓
increased reliance on glycolytic metabolism
↓
increased lactate production
However, there is an important qualification:
Elevated lactate does NOT by itself prove tissue hypoxia.
Respiratory alkalosis can itself promote lactate production through metabolic mechanisms.
Intracellular alkalosis can stimulate phosphofructokinase, an important regulatory enzyme in glycolysis.
This can accelerate glycolytic activity and increase lactate production even without classical severe tissue hypoxia.
Therefore my elevated resting lactate could potentially reflect:
altered oxygen delivery / metabolic stress
and/or
a direct metabolic effect of respiratory alkalosis
or potentially a combination of both.
What makes the finding interesting to me is not the lactate value in isolation.
It is the combination:
resting lactate ~3.0 mmol/L
pCO₂ ~25–26.5 mmHg
pH ~7.51
EtCO₂ ~20 mmHg
occurring within the same abnormal respiratory physiology.
⸻
2. HYPOCAPNIA CAN REDUCE CORONARY BLOOD FLOW
CO₂ is also an important regulator of vascular tone.
Falling CO₂ can increase vascular resistance in several vascular beds.
Human cardiovascular experiments have demonstrated that hyperventilation-induced hypocapnic alkalosis can impair myocardial oxygen supply.
One classic human study demonstrated two important effects occurring simultaneously:
Coronary blood flow decreased.
AND
Blood developed a higher affinity for oxygen.
This is particularly interesting because these mechanisms potentially act in the same direction.
The heart could theoretically receive:
less coronary blood flow
while at the same time:
hemoglobin releases oxygen less efficiently
This creates a potential double effect on myocardial oxygen supply.
⸻
3. THE SMALL CORONARY VESSELS / MICROCIRCULATION MAY BE IMPORTANT
This does not necessarily require a major coronary artery to be obstructed.
Human researchers have studied patients with:
typical angina-like chest pain
but
normal major coronary arteries on angiography.
During hyperventilation, coronary blood-flow velocity decreased significantly.
Importantly, the diameter of the large coronary artery did NOT decrease.
That suggested that the increased resistance was occurring further downstream:
in the coronary microcirculation / small coronary vessels.
This is important because coronary perfusion is not determined only by the large coronary arteries.
The small resistance vessels play a major role in controlling myocardial blood flow.
A possible pathway is therefore:
Hyperventilation
↓
Hypocapnia
↓
Increased coronary microvascular resistance
↓
Reduced coronary blood flow
↓
Reduced myocardial oxygen supply
Again, this does not mean that this mechanism has been proven in my individual case.
But it provides a biologically plausible mechanism that deserves investigation.
⸻
4. HYPOCAPNIA CAN REDUCE MYOCARDIAL OXYGENATION EVEN IN HEALTHY PEOPLE
Another particularly interesting human experiment used oxygenation-sensitive cardiac MRI.
Healthy subjects deliberately hyperventilated.
After only two minutes of hyperventilation, myocardial oxygenation decreased significantly.
The myocardial oxygenation-sensitive MRI signal fell by approximately:
7.5%
Most importantly, the change in pCO₂ was the variable that correlated with the change in myocardial oxygenation.
These were healthy subjects.
So changing CO₂ through breathing alone was sufficient to produce a measurable change in myocardial oxygenation.
This makes the extremely low CO₂ values I have measured particularly interesting.
⸻
5. RESPIRATORY ALKALOSIS CAN ALTER ELECTROLYTES
There is also another completely different pathway that may influence the ECG.
When blood becomes alkalemic, the change in hydrogen-ion concentration affects several electrolytes.
One particularly important effect concerns calcium.
During alkalosis, more calcium binds to albumin.
This reduces the concentration of biologically active:
IONIZED CALCIUM
even if total calcium remains normal.
My own ionized calcium was:
1.06 mmol/L
compared with the laboratory reference range of approximately:
1.12–1.32 mmol/L
Respiratory alkalosis can also produce shifts involving:
potassium
phosphate
and other ions.
⸻
WHY COULD ELECTROLYTES DIRECTLY AFFECT CARDIAC REPOLARIZATION?
Every heartbeat depends on precisely controlled movement of ions across the membranes of cardiac cells.
The cardiac action potential depends mainly on:
sodium
calcium
and
potassium
Different ion currents create the depolarization, plateau and repolarization phases of every heartbeat.
Repolarization is particularly dependent on potassium currents.
Calcium currents are also extremely important during the plateau phase and influence the duration of the cardiac action potential.
Therefore changes in potassium, calcium or magnesium can directly alter cardiac electrical behavior and the ECG.
For example:
Hypokalemia can produce ST depression, T-wave flattening/inversion and prominent U waves.
Changes in calcium can alter the duration of ventricular repolarization and the QT interval.
So respiratory alkalosis provides another possible route:
Hypocapnia
↓
Respiratory alkalosis
↓
Changes in ionized calcium and intracellular/extracellular electrolyte distribution
↓
Changes in cardiac ion currents
↓
Potential changes in repolarization
↓
ST–T / QT abnormalities
My potassium was normal during the particularly important emergency episode, so I am NOT suggesting that hypokalemia explains my ECG abnormalities.
The point is that severe respiratory alkalosis has several pathways through which cardiac electrophysiology can theoretically be affected.
⸻
6. HYPERVENTILATION ITSELF CAN PRODUCE ST–T/REPOLARIZATION ABNORMALITIES
This has actually been demonstrated experimentally.
In a study of:
474 apparently healthy subjects
prolonged hyperventilation produced transient repolarization abnormalities in:
72 people – 15.2%
The abnormalities included ST and T-wave changes.
So hyperventilation alone can produce dynamic cardiac repolarization abnormalities, even in people without known structural heart disease.
This is highly relevant to my own repeated and partly reversible ST–T changes.
⸻
7. RESPIRATORY ALKALEMIA CAN LOWER THE ANGINA THRESHOLD
Another human study examined patients who had reproducible exercise-induced:
chest pain
and
ST depression.
When hyperventilation produced respiratory alkalemia, angina occurred at a significantly lower cardiac workload.
In other words:
The heart symptoms occurred earlier during exertion when the subjects were alkalemic.
What makes this especially interesting to me is that the average pH during alkalemia in that study was approximately:
pH 7.52
My own resting blood gas showed approximately:
pH 7.51
The similarity in the degree of alkalemia does not prove that the same mechanism is occurring in me, but it makes the physiological comparison particularly interesting.
⸻
PUTTING ALL OF THESE MECHANISMS TOGETHER
What interests me is that severe hypocapnia may potentially affect the heart through several pathways at the same time.
Starting with abnormal breathing regulation:
Abnormal breathing / hyperventilation
↓
Excessive CO₂ elimination
↓
HYPOCAPNIA
↓
RESPIRATORY ALKALOSIS
From there, several pathways can potentially develop.
PATHWAY 1 – CORONARY BLOOD FLOW
Low CO₂
↓
Increased coronary vascular resistance
↓
Possible coronary microvascular constriction
↓
Reduced coronary blood flow
↓
Reduced myocardial oxygen supply
PATHWAY 2 – THE BOHR EFFECT / OXYGEN UNLOADING
Low CO₂ + increased pH
↓
Left shift of the oxyhemoglobin dissociation curve
↓
Hemoglobin binds oxygen more strongly
↓
Less efficient oxygen unloading into tissues
↓
Potentially reduced tissue/myocardial oxygen availability
PATHWAY 3 – METABOLIC EFFECTS / LACTATE
Potentially reduced tissue oxygen availability
and/or
respiratory-alkalosis-induced stimulation of glycolysis
↓
Increased glycolytic activity
↓
Increased lactate production
This could be relevant to my finding of approximately:
2.9–3.0 mmol/L lactate already at rest.
Again, this does NOT prove tissue hypoxia.
It is simply another metabolic abnormality occurring within the same physiological state that deserves investigation.
PATHWAY 4 – ELECTROLYTES
Respiratory alkalosis
↓
Increased calcium binding to albumin
↓
Reduced ionized calcium
possible potassium/phosphate redistribution
↓
Changes in cardiac ion-channel behavior
↓
Potential changes in cardiac repolarization
PATHWAY 5 – DIRECT EFFECTS ON CARDIAC REPOLARIZATION
Hyperventilation / hypocapnia / alkalosis
↓
vascular + autonomic + metabolic + electrolyte effects
↓
transient ST–T/repolarization abnormalities
⸻
THE POSSIBLE OVERALL RESULT
In a susceptible individual, these mechanisms could theoretically combine into:
reduced coronary blood flow
less efficient oxygen unloading
reduced myocardial oxygenation
altered cellular/electrolyte physiology
altered cardiac repolarization
↓
deep pressure/burning chest pain
↓
reduced exercise tolerance
↓
dynamic ST–T changes
This does NOT prove that my repeated ST abnormalities represent myocardial ischemia.
It also does NOT mean that every ENS patient with chest pain has the same mechanism.
But considering the objective findings in my case, I think this question deserves much more investigation.
⸻
WHY I THINK THIS MAY BE PARTICULARLY RELEVANT TO ENS
There is already ENS-specific research showing that abnormal ventilation is common in this patient population.
One prospective ENS study found hyperventilation syndrome in:
17 of 22 fully evaluated ENS patients – 77.3%
So abnormal ventilation and CO₂ regulation are not merely theoretical issues in ENS.
If some ENS patients chronically or repeatedly develop significant hypocapnia, I think we need to start asking what this may be doing not only to the brain and breathing sensation, but also to:
coronary circulation
myocardial oxygenation
oxygen unloading
autonomic regulation
electrolytes
cardiac repolarization
and ultimately:
chest pain and exercise tolerance
⸻
HAS ANYONE ELSE WITH ENS ACTUALLY MEASURED THIS?
I would particularly like to hear from ENS patients who experience:
deep pressure/burning heart or chest pain
especially when it becomes worse with:
exercise
increasing heart rate
walking uphill
climbing stairs
stress
or even:
prolonged cognitive activity
Have you ever measured:
EtCO₂ during the actual chest pain?
Blood gas and ECG at approximately the same time?
ST depression or other ST–T/repolarization abnormalities?
An exercise ECG together with capnography or respiratory gas analysis?
Ionized calcium during documented hypocapnia/respiratory alkalosis?
Resting lactate while hypocapnic?
If several ENS patients could perform similar measurements, it would be extremely interesting to see whether the combination:
ENS + HYPOCAPNIA + ANGINA-LIKE CHEST PAIN + DYNAMIC ST–T CHANGES
can be reproduced in other patients.
⸻
RESEARCH RELEVANT TO THIS QUESTION
Neill WA, Hattenhauer M.
Impairment of myocardial O₂ supply due to hyperventilation.
Circulation. 1975;52(5):854–858.
PMID: 1175266
DOI: 10.1161/01.CIR.52.5.854
This study demonstrated decreased coronary blood flow together with increased hemoglobin oxygen affinity during hyperventilation-induced hypocapnic alkalosis.
Neill WA, Pantley GA, Nakornchai V.
Respiratory alkalemia during exercise reduces angina threshold.
Chest. 1981;80(2):149–153.
PMID: 7249758
DOI: 10.1378/chest.80.2.149
This study showed that respiratory alkalemia caused angina to develop at a significantly lower cardiac workload in susceptible patients.
Chauhan A, Mullins PA, Taylor G, Petch MC, Schofield PM.
Effect of hyperventilation and mental stress on coronary blood flow in syndrome X.
British Heart Journal. 1993;69(6):516–524.
PMID: 8343318
DOI: 10.1136/hrt.69.6.516
Hyperventilation reduced coronary blood-flow velocity without reducing the diameter of the large coronary artery, consistent with increased coronary microvascular resistance.
Alexopoulos D, Christodoulou J, Toulgaridis T, et al.
Repolarization abnormalities with prolonged hyperventilation in apparently healthy subjects: incidence, mechanisms and affecting factors.
European Heart Journal. 1996;17(9):1432–1437.
PMID: 8880030
DOI: 10.1093/oxfordjournals.eurheartj.a015079
Transient repolarization abnormalities occurred in 72 of 474 apparently healthy subjects during prolonged hyperventilation.
Guensch DP, Fischer K, Flewitt JA, et al.
Breathing manoeuvre-dependent changes in myocardial oxygenation in healthy humans.
European Heart Journal – Cardiovascular Imaging. 2014;15(4):409–414.
PMID: 24078154
DOI: 10.1093/ehjci/jet171
Using oxygenation-sensitive cardiac MRI, the researchers showed that hyperventilation and falling pCO₂ were associated with decreased myocardial oxygenation even in healthy humans.
Mangin D, Béquignon E, Zerah-Lancner F, et al.
Investigating hyperventilation syndrome in patients suffering from empty nose syndrome.
The Laryngoscope. 2017;127:1983–1988.
DOI: 10.1002/lary.26599
Hyperventilation syndrome was diagnosed in 17 of 22 fully evaluated ENS patients, providing direct ENS-specific evidence that abnormal ventilation and CO₂ regulation may be common in ENS.
Den här versionen är också medicinskt starkare eftersom den skiljer tydligt mellan ”detta är uppmätt hos mig” och ”detta är en möjlig mekanistisk förklaring enligt humanforskningen”. Det minskar risken att någon kan avfärda texten för att den påstår att ischemi redan är bevisad.
