Symptom Finder - Decreased Respirations, Apnea and Cheyne -Stokes Breathing
DECREASED RESPIRATIONS, APNEA, AND CHEYNE–STOKES BREATHING
Nurses frequently become distressed and summon the intern during the night about these signs. Cheyne–Stokes respirations are a frequent source of bewilderment because they may occur at times with no direct evidence of damage to the nervous system. It would be interesting to discuss the physiology of respiration at length in this section, but it will be of little help in the differential diagnosis of apnea and in slow or Cheyne–Stokes respirations except in a few instances. In all cases, these are a result of an insult to the respiratory centers in the brain by some etiologic agent. The causes of these signs can best be remembered by the mnemonic VINDICATE.
V—Vascular includes cerebral thrombosis, embolism, and especially hemorrhage of the brainstem, which may cause depressed respirations or periodic apnea. Diffuse cerebral arteriosclerosis is another cause in this category.
I—Inflammatory disorders signify encephalitis, poliomyelitis, meningitis, and brain abscesses, particularly with increased intracranial pressure.
N—Neoplasms of the brainstem (primary or metastatic) and neoplasms of the cerebrum are associated with increased intracranial pressure and may cause depression of respirations and Cheyne–Stokes breathing.
D—Degenerative diseases of the brain, including senile and presenile dementia and Schilder disease, may cause these signs in the terminal stages.
I—Intoxication is an important category of etiologies of depressed or irregular respirations because the toxic substance may not be obvious at first. Failure of any organ system to function may lead to respiratory depression. When there is respiratory failure from emphysema or other causes, carbon dioxide (CO2) builds up in the blood and CO2 narcosis develops. In this state the important stimulus of high blood CO2 on the respiratory centers is gradually lost and anoxia is the only stimulus left. Periodic or Cheyne–Stokes breathing frequently develops in the following manner: During respiration the blood oxygen builds up to a level at which the respiratory stimulus to anoxia is lost. Respirations cease. During apnea the blood oxygen falls to a point where there is sufficient anoxia to kick the respiratory center over again. The electrolyte disturbances and buildup of toxins in uremia, the high blood ammonia and other toxins that result from hepatic failure, and the anoxia of congestive heart failure (CHF) may all lead to apnea or depressed respirations. Exogenous toxins are more commonly the cause in young people. Alcoholism, morphine, barbiturates, and a host of tranquilizers will cause respiratory depression in sufficient quantities.
C—Congenital disorders that cause these respiratory disturbances include Tay–Sachs disease, cerebral palsy, glycogen storage disease, reticuloendothelioses, epilepsy, and cerebral aneurysms with subarachnoid hemorrhage.
A—Autoimmune disorders such as lupus erythematosus and multiple sclerosis (MS) must be considered in this category.
T—Trauma is another frequent cause of apnea or Cheyne–Stokes respiration. Cerebral concussion, subdural, epidural, and intracerebral hematomas all may cause depressed respirations, especially when associated with increased intracranial pressure.
E—Endocrine disease reminds the reader that whereas diabetic coma may begin with Kussmaul breathing, in the advanced stages bradypnea and Cheyne–Stokes respirations develop from the severe acidosis. Pituitary and suprasellar tumors may grow sufficiently to compress the brainstem and cause apnea.
Approach to the Diagnosis
Obviously, the association of other signs and symptoms will determine the workup in most cases. The most important things to do are to order a blood urea nitrogen (BUN) level, electrolytes, fasting blood sugar (FBS), arterial blood gases, and a drug screen and to check for increased intracranial pressure by examining the eye grounds. If the history or physical findings suggest increased intracranial pressure, and other metabolic studies (e.g., BUN) are normal, a mannitol or urea drip is begun while awaiting the results of other investigations such as computed tomography (CT) scan, electroencephalogram (EEG), and echoencephalogram. A neurosurgeon should be consulted immediately.
Nurses frequently become distressed and summon the intern during the night about these signs. Cheyne–Stokes respirations are a frequent source of bewilderment because they may occur at times with no direct evidence of damage to the nervous system. It would be interesting to discuss the physiology of respiration at length in this section, but it will be of little help in the differential diagnosis of apnea and in slow or Cheyne–Stokes respirations except in a few instances. In all cases, these are a result of an insult to the respiratory centers in the brain by some etiologic agent. The causes of these signs can best be remembered by the mnemonic VINDICATE.
V—Vascular includes cerebral thrombosis, embolism, and especially hemorrhage of the brainstem, which may cause depressed respirations or periodic apnea. Diffuse cerebral arteriosclerosis is another cause in this category.
I—Inflammatory disorders signify encephalitis, poliomyelitis, meningitis, and brain abscesses, particularly with increased intracranial pressure.
N—Neoplasms of the brainstem (primary or metastatic) and neoplasms of the cerebrum are associated with increased intracranial pressure and may cause depression of respirations and Cheyne–Stokes breathing.
D—Degenerative diseases of the brain, including senile and presenile dementia and Schilder disease, may cause these signs in the terminal stages.
I—Intoxication is an important category of etiologies of depressed or irregular respirations because the toxic substance may not be obvious at first. Failure of any organ system to function may lead to respiratory depression. When there is respiratory failure from emphysema or other causes, carbon dioxide (CO2) builds up in the blood and CO2 narcosis develops. In this state the important stimulus of high blood CO2 on the respiratory centers is gradually lost and anoxia is the only stimulus left. Periodic or Cheyne–Stokes breathing frequently develops in the following manner: During respiration the blood oxygen builds up to a level at which the respiratory stimulus to anoxia is lost. Respirations cease. During apnea the blood oxygen falls to a point where there is sufficient anoxia to kick the respiratory center over again. The electrolyte disturbances and buildup of toxins in uremia, the high blood ammonia and other toxins that result from hepatic failure, and the anoxia of congestive heart failure (CHF) may all lead to apnea or depressed respirations. Exogenous toxins are more commonly the cause in young people. Alcoholism, morphine, barbiturates, and a host of tranquilizers will cause respiratory depression in sufficient quantities.
C—Congenital disorders that cause these respiratory disturbances include Tay–Sachs disease, cerebral palsy, glycogen storage disease, reticuloendothelioses, epilepsy, and cerebral aneurysms with subarachnoid hemorrhage.
A—Autoimmune disorders such as lupus erythematosus and multiple sclerosis (MS) must be considered in this category.
T—Trauma is another frequent cause of apnea or Cheyne–Stokes respiration. Cerebral concussion, subdural, epidural, and intracerebral hematomas all may cause depressed respirations, especially when associated with increased intracranial pressure.
E—Endocrine disease reminds the reader that whereas diabetic coma may begin with Kussmaul breathing, in the advanced stages bradypnea and Cheyne–Stokes respirations develop from the severe acidosis. Pituitary and suprasellar tumors may grow sufficiently to compress the brainstem and cause apnea.
Approach to the Diagnosis
Obviously, the association of other signs and symptoms will determine the workup in most cases. The most important things to do are to order a blood urea nitrogen (BUN) level, electrolytes, fasting blood sugar (FBS), arterial blood gases, and a drug screen and to check for increased intracranial pressure by examining the eye grounds. If the history or physical findings suggest increased intracranial pressure, and other metabolic studies (e.g., BUN) are normal, a mannitol or urea drip is begun while awaiting the results of other investigations such as computed tomography (CT) scan, electroencephalogram (EEG), and echoencephalogram. A neurosurgeon should be consulted immediately.