Tuesday, February 15, 2022

Breathing, Neural Control Case File

Posted By: Medical Group - 2/15/2022 Post Author : Medical Group Post Date : Tuesday, February 15, 2022 Post Time : 2/15/2022
Breathing, Neural Control Case File
EUGENE C.TOY, MD, RAHUL JANDIAL, MD, PhD, EVAN YALE SNYDER, MD, PhD, MARTIN T. PAUKERT, MD

CASE 35
A 77-year-old Caucasian man has a history of hypertension, atrial fibrillation, and a remote history of severe alcoholism. He presents to the emergency department after his wife found him unconscious in their yard. Emergency medical services arrived at their home to find a nonresponsive man with an intact papillary reflex and spontaneous respirations. After obtaining this brief history you examine the patient. He is still unresponsive and you notice that his left pupil is significantly larger than his right. His respirations have become noticeably deeper and he is breathing at a rate of 35 respirations per minute. A STAT CT scan of his head without contrast shows an acute 14-mm left-sided subdural hematoma with midline shift. Based on the presentation, the patient is diagnosed with an altered respiratory drive secondary to an uncal herniation.
  • Can other intracranial process have similar effects on respiratory patterns?
  • What is the difference between cortical and brainstem respiratory drives?


ANSWERS TO CASE 35: BREATHING, NEURAL CONTROL

Summary: A 77-year-old man is noted to have an acute intracranial hemorrhage with increased intracranial pressure and uncal herniation.
  • Other intracranial processes: Yes, any intracranial process that increases the intracranial pressure that results in herniation can cause uncal herniation (or any other of the herniation syndromes). Hydrocephalus, intracranial neoplasms, foreign bodies, and hemorrhage are all examples of lesions that can raise the intracranial pressure resulting in herniation.
  • Cortical and brainstem respiratory drives: In general, cortical respiratory drives are involved with voluntary breathing patterns, whereas brainstem drives control involuntary breathing patterns.

CLINICAL CORRELATION

In this case, the patient is a man with a history of alcoholism and atrial fibrillation. The combination of these diagnoses increases the risk of subdural hematomas in the general population. Alcoholism results in cerebral atrophy, which exposes bridging veins to sheering forces during cranial acceleration and deceleration. Atrial fibrillation is usually treated with anticoagulation, such as Coumadin, to prevent intraluminal cardiac thrombus formation. However, in this case, appropriate anticoagulation in the setting of a lacerated bridging vein can result in poor clot formation and further intracranial hemorrhage. The subdural hematoma in this case kept bleeding and resulted in increasing the intracranial pressure until the ipsilateral uncus was forced around and underneath the tentorium, resulting in transtentorial uncal herniation. The herniated uncus exerted unwanted pressure on the brainstem, leading to changes in the respiratory drive. In addition to this clinical picture the physician would expect to find an increased pH, decreased pCO2, and normal or increased pO2 on arterial blood gas measurement. Thus, any insult to the brainstem, notably the pons and medulla, can result in alterations of respiratory function. Other brainstem lesions that could have similar outcomes include tumors, aneurysms, stroke, hemorrhage, and trauma.


APPROACH TO CENTRAL CONTROL OF RESPIRATION

Objectives
  1. Know the three brainstem nuclear centers that are involved in respiration and understand their relative functions.
  2. Realize there is a difference between automatic and voluntary respiration and how these are structurally represented in the spinal cord.
  3. Be able to recognize the different types of pathological respirations.

Definitions

Dorsal medullary respiratory group (DRG): A medullary nucleus containing mostly inspiratory neurons and that is one of the subnuclei of the solitary tract nucleus.
Ventral respiratory group (VRG): A nucleus that is anterolateral to the nucleus ambiguous in the medulla. In its caudal portion, it contains the cell bodies of neurons that fire primarily during expiration and its rostral portion contains cell bodies of neurons that are synchronous with expiration.
Pontine pair of nuclei (PRG): Two nuclei located adjacent to each other in the pons. One fires during the transition from inspiration to expiration and the other fires during the transition from expiration to inspiration.
Pre-Botzinger complex: Located in the rostral portion of the VRG. Although its mechanism of action is not entirely clear, it appears to play some role in setting the automaticity of respiration.


DISCUSSION

Respiration regulation is one of the most fundamental homeostatic drives within the nervous system. There are both chemical and mechanical input pathways that influence respiratory patterns, an automated brainstem drive and the voluntary control mechanisms that begin in the premotor cortices.

Inspiratory neurons are concentrated in the DRG and rostral VRG. The fibers controlling automatic respiration course down the white matter tracts of the spinal cord and descend lateral to anterior horn cells of the first three cervical spinal cord sections to terminate on the anterior horn cells of C3-C5. The premotor cortex in the frontal lobe also gives rise to neurons that terminate onto the same anterior horn cells. These tracts containing the fibers controlling voluntary respiration course more dorsally in the cervical cord. If the ventral tracts are damaged, then automatic respirations are lost while voluntary are preserved. The third, fourth, and fifth cervical (C3-C4) segments project fibers that will ultimately become the phrenic nerve and will innervate the diaphragm. Although normal expiration is a passive process, there are clusters of expiratory neurons that provide upper motor innervation of accessory respiratory muscles as well as creating an inhibitory force on the inspiratory neurons. The caudal portion of the VRG and the rostral portion of the DRG contain these expiratory nerve cell bodies. There is some evidence suggesting the PRG serve as binary switches that control the transition between inspiration and respiration.

The precise mechanism accounting for the brainstem’s ability to generate adequate respiration is unknown. There is a region in the VRG, the pre- Botzinger complex, which appears to be involved with autonomous rhythmicity.

The carotid sinus is sensitive to changes in pH and hypoxia. Afferent fibers merge into the glossopharyngeal nerve and terminate in the solitary tract nucleus. There are also medullary chemoreceptors that detect pH changes in the extracellular fluid. J-type receptors detect material in the interstitial fluid of the lungs and can stimulate increased respiration.

When structural or metabolic factors divorce the brainstem respiratory centers from the cerebrum Cheyne-Stokes respirations may result. This pattern of breathing is alternating hyperpnea with hypopnea that ends in apnea and then repeats itself. Bilateral hemispheric lesions, large unilateral hemispheric lesions, or metabolic encephalopathies can cause Cheyne- Stokes. Because of the separation of communication between the brainstem centers and cerebral function, carbon dioxide accumulates until it triggers chemoreceptors to stimulate inspiration. This results in hyperpnea. As carbon dioxide is gradually removed from the body, the chemoreceptors fire less frequently until apnea occurs.

Central neurogenic breathing usually occurs with midbrain-pontine lesions. In this case, the minute ventilation is increased because both tidal volume and respiratory rate are increased. Thus, the pCO2 drops and hyperventilation persists. This type of breathing is usually seen in transtentorial uncal herniation, per the example in Case 2.

Pontine lesions often result in apneustic breathing, which consists of a pause between inspiration and expiration.

Medullary lesions result in completely disordered, or ataxic, breathing. It is thought that these pathological forms of respiration are interrelated and most patients will progress through various stages before complete respiratory failure ensues.


COMPREHENSION QUESTIONS

Refer to the following case scenario to answer questions 35.1-35.3:

A 43-year-old woman with known insulin-dependent diabetes presents to the emergency department complaining of nausea, vomiting, generalized weakness, and increased urinary frequency and amount. She states that she has not taken any insulin for 4 or 5 days because she does not have the money to pay for it. On examination she has a fruity odor to her breath and has a respiratory rate of 35 breaths/min. A fingerstick blood glucose level comes back 573 and an ABG shows her pH to be 7.12. The physician correctly diagnoses her with diabetic ketoacidosis and begins appropriate therapy.

[35.1] Her increased respiratory rate is at least in part because of afferent signals coming from which peripheral receptor that measure blood pH?
A. Carotid body
B. J-type receptors in the lung
C. Medullary chemoreceptors
D. Carotid sinus

[35.2] The increased signal from the peripheral chemoreceptors stimulates which CNS site to increase respiratory rate?
A. DRG
B. PRG
C. Premotor cortex
D. Pre-Botzinger complex

[35.3] Efferent signals from the central respiratory centers travel by what path to the diaphragm in this patient?
A. Via ventral respiratory spinal tracts to C3-C5
B. Via dorsal respiratory spinal tracts to C3-C5
C. Via ventral respiratory spinal tracts to C2-C4
D. Via dorsal respiratory spinal tracts to C2-C4


Answers

[35.1] D. The carotid sinus, located at the bifurcation of the internal and external carotid arteries, and innervated by the glossopharyngeal nerve, measures arterial blood pH. It responds to increased concentration of hydrogen ions (decreased pH) by increasing its rate of firing, which stimulates central respiratory centers to increase respiratory rate. This increased respiratory rate will “blow off” excess carbon dioxide, thereby partially compensating for the acidemia. Medullary receptors also respond to decreased pH, but they are centrally located and do not directly measure blood pH, but rather the pH of the extracellular fluid. J-type receptors respond to changes in the interstitial fluid of the lungs.

[35.2] D. Pre-Botzinger complex is involved in automaticity. The dorsal and rostral ventral medullary respiratory groups are the primary sites responsible for inspiratory drive. They receive afferent connections from the carotid sinus, the medullary chemoreceptors, and other sites in the body converge in the nucleus of the solitary tract and from there project to the breathing centers, primarily the dorsal respiratory group. The PRG is involved in cycling from inspiration to expiration, the premotor complex is involved in voluntary breathing, and the pre- Botzinger complex is involved in automaticity.

[35.3] A. Because the ventral respiratory tracts carry signals related to involuntary respiration, and the diaphragm is innervated by the phrenic nerve, which carries fibers from spinal levels C3-C5, the correct answer is ventral respiratory spinal tracts to C3-C5. The anterior horn cells projecting fibers C3-C5 receive signals from both dorsal and ventral respiratory tracts in the spinal cord, but the ventral tracts, located lateral to the anterior horn, carry signals related to involuntary respiration, while the more dorsally located respiratory tract carries signals related to voluntary respiration.


NEUROSCIENCE PEARLS

Inspiratory neurons are concentrated in the DRG and rostral VRG.
The C3-C4 segments become the phrenic nerve which innervates the diaphragm.
The carotid sinus is sensitive to changes in pH and hypoxia.
When the connection between the respiratory centers and cerebrum is completely destroyed, Cheyne-Stokes respiration may result.
Pontine lesions result in apneustic breathing while medullary lesions result in ataxic breathing.


REFERENCES

Bear MF, Connors B, Paradiso M, eds. Neuroscience: Exploring the Brain. 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2006. 

Kandel E, Schwartz J, Jessell T, eds. Principles of Neural Science. 5th ed. New York, NY: McGraw-Hill; 2000. 

Purves D, Augustine GJ, Fitzpatrick D, et al, eds. Neuroscience. 3rd ed. Sunderland, MA: Sinauer Associates, Inc.; 2004.

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