Hyperventilation syndrome pathophysiology: Difference between revisions

Jump to navigation Jump to search
m (Bot: Removing from Primary care)
 
(8 intermediate revisions by one other user not shown)
Line 4: Line 4:


==Pathophysiology==
==Pathophysiology==
The pathophysiology of hyperventilation syndrome can be divided into psycopathology, abnormalities of regulatory system, mechanism of pulmonary and neurologic symptoms.
The pathophysiology of hyperventilation syndrome can be divided into psycopathology, abnormalities of regulatory system, mechanism of pulmonary, and neurologic symptoms.


===Psycopathology===
===Psychopathology===
There is an association between hyperventilation syndrome and psychological conditions such as panic disorder ,but whether the psychological condition is primary or secondary is often unclear.Somatic and respiratory symptoms are common in patients with psychological distress.“Disproportionate breathlessness" is associated with depression, anxiety, bereavement, resentment. <ref name="pmid2278552">{{cite journal |author=Howell JB |title=Behavioural breathlessness |journal=[[Thorax]] |volume=45 |issue=4 |pages=287–92 |year=1990 |month=April |pmid=2278552 |pmc=473775 |doi= |url= |accessdate=2013-05-28}}</ref>
There is an association between hyperventilation syndrome and psychological conditions such as panic disorder, but whether the psychological condition is primary or secondary is often unclear. Somatic and respiratory symptoms are common in patients with psychological distress. “Disproportionate breathlessness" is associated with depression, anxiety, bereavement, and resentment.<ref name="pmid2278552">{{cite journal |author=Howell JB |title=Behavioural breathlessness |journal=[[Thorax]] |volume=45 |issue=4 |pages=287–92 |year=1990 |month=April |pmid=2278552 |pmc=473775 |doi= |url= |accessdate=2013-05-28}}</ref>


===Basis of Pulmonary symptoms===
===Basis of Pulmonary Symptoms===
Imbalance between sensory signals from pulmonary and chest wall stretch receptors and motor signals from the motor cortex  result in feelings of dyspnea.The greater the imbalance, the greater the severity of dyspnea. <ref name="pmid2122135">{{cite journal |author=Schwartzstein RM, Manning HL, Weiss JW, Weinberger SE |title=Dyspnea: a sensory experience |journal=[[Lung]] |volume=168 |issue=4 |pages=185–99 |year=1990 |pmid=2122135 |doi= |url= |accessdate=2013-05-28}}</ref> Patients with hyperventilation syndrome may have an imbalance in these signals leading to a sensation of dyspnea that then precipitates a voluntary increase in minute ventilation.
Imbalance between sensory signals from pulmonary and chest wall stretch receptors and motor signals from the motor cortex  result in feelings of [[dyspnea]]. The greater the imbalance, the greater the severity of dyspnea.<ref name="pmid2122135">{{cite journal |author=Schwartzstein RM, Manning HL, Weiss JW, Weinberger SE |title=Dyspnea: a sensory experience |journal=[[Lung]] |volume=168 |issue=4 |pages=185–99 |year=1990 |pmid=2122135 |doi= |url= |accessdate=2013-05-28}}</ref>


===Basis of Neurologic symptoms===
===Basis of Neurologic Symptoms===
With decreasing PaCO2 Cerebral blood flow decreases in a linear fashion. Raichle Plum has shown that a decrease of 1 mmHg of PaCO2 is associated with a 2 percent decrease in cerebral blood flow.<ref name="pmid4569138">{{cite journal |author=Raichle ME, Plum F |title=Hyperventilation and cerebral blood flow |journal=[[Stroke; a Journal of Cerebral Circulation]] |volume=3 |issue=5 |pages=566–75 |year=1972 |pmid=4569138 |doi= |url= |accessdate=2013-05-28}}</ref> Reduction in cerebral blood flow in the setting of hyperventilation, respiratory alkalosis may explain the neurologic symptoms such as paresthesias, headache, and light-headedness. In Hyperventilation syndrome respiratory alkalosis leads to acute changes in ionized serum calcium levels, which could result in paresthesias and/or tetany.
With decreasing arterial Carbon Dioxide levels (PaCO<sub>2</sub>), cerebral blood flow decreases in a linear fashion. Raichle and Plum has shown that a decrease of 1 mmHg of PaCO<sub>2</sub> is associated with a 2 percent decrease in cerebral blood flow.<ref name="pmid4569138">{{cite journal |author=Raichle ME, Plum F |title=Hyperventilation and cerebral blood flow |journal=[[Stroke; a Journal of Cerebral Circulation]] |volume=3 |issue=5 |pages=566–75 |year=1972 |pmid=4569138 |doi= |url= |accessdate=2013-05-28}}</ref> Reduction in cerebral blood flow in the setting of hyperventilation in combination with [[respiratory alkalosis]] may explain the neurologic symptoms such as [[paresthesia]]s, [[headache]], and light-headedness. In hyperventilation syndrome, [[respiratory alkalosis]] leads to acute changes in ionized serum calcium levels, which could result in paresthesias and/or [[tetany]].
   
   
===Regulating system dysfunction===
===Regulating System Dysfunction===
Abnormalities in control system for ventilation (Reticular activating system) are important in development of symptoms in some patients with hyperventilation syndrome.Under normal conditions, healthy individuals demonstrate regular breathing with no voluntary effort.Hypersensitivity of certain parts of the brain like hippocampus, medial prefrontal cortex, amygdala and its brainstem projections also some times called “Fear Center” have been associated with hyperventilation syndrome<ref name="pmid7045570">{{cite journal |author=Magarian GJ |title=Hyperventilation syndromes: infrequently recognized common expressions of anxiety and stress |journal=[[Medicine]] |volume=61 |issue=4 |pages=219–36 |year=1982 |month=July |pmid=7045570 |doi= |url= |accessdate=2013-05-28}}</ref> .Increased sensitivity to carbon dioxide has also been proposed as mechanisms for the hyperventilation syndrome and its association with psychological symptoms.An activated hypersensitive fear network leads to increased central respiratory drive, causing low PaCO2 levels.
Abnormalities in control system for ventilation, the [[reticular activating system]], are important in the development of symptoms in some patients with hyperventilation syndrome. Under normal conditions, healthy individuals demonstrate regular breathing with no voluntary effort. Hypersensitivity of certain parts of the brain such as the [[hippocampus]], [[medial prefrontal cortex]], [[amygdala]] and its [[brain stem]] projections, also some times called “Fear Center,” have been associated with hyperventilation syndrome.<ref name="pmid7045570">{{cite journal |author=Magarian GJ |title=Hyperventilation syndromes: infrequently recognized common expressions of anxiety and stress |journal=[[Medicine]] |volume=61 |issue=4 |pages=219–36 |year=1982 |month=July |pmid=7045570 |doi= |url= |accessdate=2013-05-28}}</ref> Increased sensitivity to carbon dioxide has also been proposed as a mechanism for hyperventilation syndrome and its association with psychological symptoms. An activated hypersensitive fear network leads to increased central respiratory drive, causing low PaCO<sub>2</sub> levels.
 
   
   
HVS can be part of a [[panic attack]] but, despite all the stigma, most patients are not putting on a show but are in true distress.  
HVS can occur as part of a [[panic attack]]. Despite the stigma, most patients are exaggerating symptoms but are in true distress.  


People with HVS feel like they can't get enough air, but the opposite is actually true:  they have too much oxygen and too little carbon dioxide in their blood. The hyperventilation is self-promulgating as rapid breathing causes [[carbon dioxide]] levels to fall, and [[respiratory alkalosis]] (high blood [[pH]]) develops. This makes the symptoms worse, which causes the patient to try breathing even faster, which further exacerbates the problem.
Patients with HVS feel as though they cannot get enough air, but the opposite is true:  they have too much oxygen and too little carbon dioxide in their blood. Hyperventilation is self-promulgating as rapid breathing causes [[carbon dioxide]] levels to continue to fall, and [[respiratory alkalosis]] (high blood [[pH]]) develops. This makes the symptoms worse, which causes the patient to try breathing even faster, perpetuating the cycle.


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}


[[Category:Pulmonology]]
[[Category:Pulmonology]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Primary care]]
[[Category:Psychiatry]]
[[Category:Disease]]
[[Category:Needs overview]]
[[Category:Needs overview]]
{{WH}}
{{WS}}

Latest revision as of 22:18, 29 July 2020

Hyperventilation syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Hyperventilation syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hyperventilation syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hyperventilation syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hyperventilation syndrome pathophysiology

CDC on Hyperventilation syndrome pathophysiology

Hyperventilation syndrome pathophysiology in the news

Blogs on Hyperventilation syndrome pathophysiology

Directions to Hospitals Treating Hyperventilation syndrome

Risk calculators and risk factors for Hyperventilation syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Farman Khan, MD, MRCP [2]

Pathophysiology

The pathophysiology of hyperventilation syndrome can be divided into psycopathology, abnormalities of regulatory system, mechanism of pulmonary, and neurologic symptoms.

Psychopathology

There is an association between hyperventilation syndrome and psychological conditions such as panic disorder, but whether the psychological condition is primary or secondary is often unclear. Somatic and respiratory symptoms are common in patients with psychological distress. “Disproportionate breathlessness" is associated with depression, anxiety, bereavement, and resentment.[1]

Basis of Pulmonary Symptoms

Imbalance between sensory signals from pulmonary and chest wall stretch receptors and motor signals from the motor cortex result in feelings of dyspnea. The greater the imbalance, the greater the severity of dyspnea.[2]

Basis of Neurologic Symptoms

With decreasing arterial Carbon Dioxide levels (PaCO2), cerebral blood flow decreases in a linear fashion. Raichle and Plum has shown that a decrease of 1 mmHg of PaCO2 is associated with a 2 percent decrease in cerebral blood flow.[3] Reduction in cerebral blood flow in the setting of hyperventilation in combination with respiratory alkalosis may explain the neurologic symptoms such as paresthesias, headache, and light-headedness. In hyperventilation syndrome, respiratory alkalosis leads to acute changes in ionized serum calcium levels, which could result in paresthesias and/or tetany.

Regulating System Dysfunction

Abnormalities in control system for ventilation, the reticular activating system, are important in the development of symptoms in some patients with hyperventilation syndrome. Under normal conditions, healthy individuals demonstrate regular breathing with no voluntary effort. Hypersensitivity of certain parts of the brain such as the hippocampus, medial prefrontal cortex, amygdala and its brain stem projections, also some times called “Fear Center,” have been associated with hyperventilation syndrome.[4] Increased sensitivity to carbon dioxide has also been proposed as a mechanism for hyperventilation syndrome and its association with psychological symptoms. An activated hypersensitive fear network leads to increased central respiratory drive, causing low PaCO2 levels.

HVS can occur as part of a panic attack. Despite the stigma, most patients are exaggerating symptoms but are in true distress.

Patients with HVS feel as though they cannot get enough air, but the opposite is true: they have too much oxygen and too little carbon dioxide in their blood. Hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to continue to fall, and respiratory alkalosis (high blood pH) develops. This makes the symptoms worse, which causes the patient to try breathing even faster, perpetuating the cycle.

References

  1. Howell JB (1990). "Behavioural breathlessness". Thorax. 45 (4): 287–92. PMC 473775. PMID 2278552. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  2. Schwartzstein RM, Manning HL, Weiss JW, Weinberger SE (1990). "Dyspnea: a sensory experience". Lung. 168 (4): 185–99. PMID 2122135. |access-date= requires |url= (help)
  3. Raichle ME, Plum F (1972). "Hyperventilation and cerebral blood flow". Stroke; a Journal of Cerebral Circulation. 3 (5): 566–75. PMID 4569138. |access-date= requires |url= (help)
  4. Magarian GJ (1982). "Hyperventilation syndromes: infrequently recognized common expressions of anxiety and stress". Medicine. 61 (4): 219–36. PMID 7045570. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)

Template:WH Template:WS