Pathological breathing / Abnormal breathing patterns : Kussmaul, Cheyne stokes, Biot's, Cluster

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Pathological breathing patterns : Kussmaul, Cheyne stokes, Biot's, Cluster breathing patterns
The types of clinically relevant normal and abnormal respiration patterns include the following:
Eupnea is normal breathing.
Sighing is an involuntary inspiration that is 1.5 to 2 times greater than normal tidal volume. Sighing breathing is observed in subjects suffering from anxiety with no observed organic pathology.
Dyspnea is the subjective sensation of difficulty breathing.
Paroxysmal nocturnal dyspnea is described as attacks of severe shortness of breath that wake the patient from sleep. They have to sit up to catch their breath. Most commonly, this is a symptom of heart failure.
Orthopnea also is seen in heart failure. Patients are unable to breathe comfortably, lying flat. They must be in a sitting or propped up to breathe without difficulty.
Cheyne-Stokes is a pattern of crescendo-decrescendo respirations followed by a period of apnea. This pattern of breathing was first described by John Cheyne, a British Physician, and William Stokes, an Irish Physician. It is well described in patients with heart failure. Usually observed while asleep and is the result of disordered central control of breathing. Its presence has implications for outcome in that cardiac resynchronization therapy improves outcomes in patients with Cheyne-Stokes respirations.
Bradypnea is a respiratory rate that is lower than normal for age.
Tachypnea is a respiratory rate that is greater than the normal for age.
Hyperpnea in increased volume with or without an increased rate of breathing. Blood gasses are normal.
Agonal breathing is characterized by slow, very shallow irregular respirations that result from anoxic brain injury. This will often progress to apnea depending on the underlying cause.
Apnea is the absence of breathing. This signals a life-threatening situation in which the patient will quickly succumb unless rescue breathing is instituted immediately.
Hyperventilation is over-ventilation above that needed for the body’s CO2 elimination. This results in a decrease in PaCO2 and respiratory alkalosis. Hyperventilation can be driven by chemoreceptor stimulation due to metabolic acidosis.
Hypoventilation is under-ventilation below that needed for the body’s CO2 elimination. It is inadequate to maintain a normal PaCO2.
Kussmaul respirations were originally observed and described by Dr. Adolf Kussmaul in 1874. He made his observation in patients with diabetes mellitus who were comatose and in the late stages of diabetic ketoacidosis. As classically described, Kussmaul respirations are a deep, sighing respiratory pattern. Dr. Kussmaul actually described it as “air hunger.” This is probably the most important of the abnormal respiratory patterns.
Kussmaul respiratory pattern occurs due to increased tidal volume with or without an increased respiratory rate. It is a form of hyperventilation. It results from stimulation of the respiratory center in the brain stem by low serum pH. The effect is the lowering of the partial pressure of carbon dioxide in the alveoli, thereby compensating for metabolic acidosis. Initially, in acidosis, the respiratory pattern is rapid and shallow, but as the acidosis progresses, the inspirations become deeper. It is only in the later stages that true Kussmaul respirations are seen. Kussmaul respirations can be seen with any disorder that causes significant acidosis. Toxic ingestions, particularly alcohols, are another common cause of Kussmaul respirations. Salicylate toxicity is also a cause. Kussmaul was also classically described in patients with uremia. It can also be seen in any disorder that results in lactic or ketoacidosis.
The Biot respiratory pattern was first described by Camille Biot, a French physician, in 1876. He made his observations while studying the pattern of breathing described by John Cheyne and William Stokes. Biot respiratory pattern is characterized by regular deep respirations interspersed with periods of apnea. It is caused by damage to the pons due to stroke, trauma, or uncal herniation. As the insult to the pons progresses, the pattern becomes irregular. At this point, the pattern deteriorates to ataxic breathing. Biot respiratory pattern can also be induced by opiate intoxication.
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[@berrahayr4782]

what is the exact difference between biot's breathing and cluster breathing pattern?

[@JUANSRAINBOW]

Last one in the video spell mistake... Central neurogenic hypoventilation

[@imanhosseini4000]

Thanks alot

[@ritathomas3353]

Awesome explanation 👏 thank you

[@doctorbhanuprakash]

Glad it was helpful!

[@havaskapujari5741]

Thanks doc

[@Rakesha36]

Sir urnombrr

[@jasrajkumawat6944]

Thanks

[@doctorbhanuprakash]

Welcome

[@unknown35514]

Love the new narrator.

[@doctorbhanuprakash]

Yeah he is American medico..

[@keerthik5887]

Best lecture

[@doctorbhanuprakash]

Tysm

[@criticreview8319]

I take a deep breath after ever 15 min? What is name of this pattern?

[@SaraSarita-df9hy]

Esophagitis

[@rosariomurdie6069]

Hello. a question for you, why I can not copy the link? to see it in my power point? do I need some other link to do it?
please help thanks

[@rishiraj2548]

👍👍💯🙏