Dealing with Kussmaul Breathing

Kussmaul breathing is simply deep and strenuous breathing. This kind of breathing is associated with severe metabolic acidosis as well as renal failure. Metabolic acidosis makes breathing at first rapid and shallow, however, when the situation worsens, there will be a gradual process of deep slow, labored and grasping of breath. Others have referred to this kind of breathing as abnormally slow deep respiration characteristic of air hunger and occurring especially in acidotic states. It is named kussmaul after a German Doctor Adolph Kussmaul who first noted it among patients with advanced diabetes mellitus. For him he referred to this breathing to be breathing when metabolic acidosis was sufficiently severe for the respiratory rate to be normal.

Patients with Kussmaul breathing will also show a low partial pressure of carbondioxide coupled with low bicarbonate due to the forced increased respiration. The patient feels an involuntary urge to breathe deeply. It a situation of air hunger, the patient feels that the air surrounding them is not enough for them to take in. they are completely in a hopeless state for they cannot reach out to grasp more of the air in the atmosphere. It is a situation an imaginable for a normal person for they cannot figure out how someone can fail to catch the breath with the air just surrounding them.

Metabolic acidosis is a situation when the body produces too much acid or when the kidneys are not doing their job of removing acids in the body, in other words, they are not removing enough acids from the body. There is therefore a big problem for the people under this condition for they are susceptible to facing the problem of Kussmaul breathing. These rapid deep breaths increase the amount of carbon dioxide exhaled, and hence lower the serum carbon dioxide levels which results in some degree of compensation.

Under kussmaul breathing, the metabolic acidosis is detected by both the peripheral as well as the central chemoreceptors, hence the respiratory center is stimulated. This initial stimulation of the central chemoreceptors is caused by small increases in brain ISF (H+), while consequent increase in ventilation leads to a fall in arterial pCO2 which inhibits the ventilatory response. After 12 to 24 hours, the chemoreceptor inhibition limits and delays the full ventilatory response until bicarbonate shifts have stabilized across the blood brain barrier.

In situations where a patient in severe metabolic acidosis, intubation and controlled ventilation in hospital, the acidosis can easily worsen unless hyperventilation is maintained. The ventilation should be set to keep the pCO2 low, otherwise if ventilation is set to a given standard that allows the pCO2 to rise towards 40mmHg, it represents an imposition of an acute respiratory acidosis which can lead to the rapid fall of PH. It is therefore important to study the conditions under which the patient is before administering any medication. Attention and care to such a patient should be by a qualified person or a person trained well to deal with this situation.

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