Dyspnea, hyperpnea, tachypnea, hyperventilation and their "Goals"

[E.S.Prakash]

Lam Hui Yuan, 

Minute Ventilation is respiratory rate times tidal volume. 

Tachypnea refers to an increase in respiratory rate but it may not necessarily result in an increase in minute ventilation if for some reason the depth of each breath (tidal volume) is reduced. 

Hyperpnea is an increase in minute ventilation well above the resting value (which is around 6 liters per minute) in an adult weighing about 70 kg. 

Hyperpnea and hyperventilation are synonymous. 

Dyspnea is a sensation of being short of breath and can occur in apparently normal individuals such as when minute ventilation is quadrupled during exercise. Philosophically speaking, its value may be to indicate to the individual to lessen the intensity of exercise or to stop it so the body can restore oxygen debts and pH shifts in body fluids. That is dyspnea is closely associated with the sensation of fatigue during intense exercise. 

Apart from this, dyspnea could occur even when minute ventilation is apparently within "normal limits" such as in individuals with asthma, heart failure, interstitial lung disease, pneumothorax. The common denominator that drives dyspnea under these conditions again is likely the chemistry (pO2, H ion concentration) of blood and body fluids. Thus, dyspnea is associated with hypoxia and acidosis. 

In terms of afferent mechanisms driving breathing (ventilation) the candidates are: systemic arterial chemoreceptors; but there are others as well including afferents from muscle that signal to the brain the chemical milieu that prevails in muscle (the muscle metaboreflex); signals from pulmonary interstitium (from J receptors); stretch receptors in lung parenchyma and irritant receptors in airways; and finally "central" commands from motor areas in the brain to the respiratory center such as during exercise. 

To answer Question 2 of yours, it appears that the drivers of breathing are the composition of arterial plasma, interstitial fluid and intracellular fluid in metabolically active tissue, and in that sense it would be reasonable I think to conceptualize that the "goal" of hyperventilation is to protect pO2 (from falling to low levels) and maintaining H ion concentration in ECF and ICF within normal limits. 

I and some of my students earlier did reflect upon "goals" of these mechanisms and have published our views here. You may like to read this: http://advan.physiology.org/cgi/content/full/31/1/51

All the best

ESP

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On Tue, Dec 7, 2010 at 9:26 AM, Lam hui yuan lam hui yuan <viye...@yahoo.com> wrote:

Dear Dr. Prakash, 'Hyperventilation, hypernea and tachypnea.''  1. Would you mind to explain about the pathophysiology & conditions behind these three terms? Can these conditions co-exist at the same time? 2. Are these terms considered defensive mechanisms in pulmonary ventilation? If yes, is the ultimate result goal the same for these three mechanisms? 3. Would these conditions give rise to dyspnea (as associated symptoms) ? Thank you. Lam Hui Yuan MBBS Batch 14