EM@3AM: Bradypnea

Authors: Hailey VanRonzelen (MS-3, Kansas City University, RN-BSN); Jessica Pelletier, DO, MHPE (Assistant Professor of EM/Assistant Residency Director, Mizzou – Columbia, MO) // Reviewed by: Sophia Görgens, MD (EM Physician, BIDMC, MA); Cassandra Mackey, MD (Assistant Professor of Emergency Medicine, UMass Chan Medical School); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 53-year-old male with a past medical history of hyperlipidemia and cervical stenosis presents with dyspnea, which has been worsening since his cervical spinal fusion 6 days ago. He states he is very fatigued and feels as though he cannot get a deep breath.

Vital signs revealed a BP of 136/76, HR of 88, RR of 9, SpO2 of 94% on room air, and a temperature of 97.6 F. On physical exam, the patient is lethargic, has nasal flaring, and is using accessory muscles to breathe. Lung sounds are clear. On cardiac exam, there is normal rate and rhythm without murmur, rubs, or gallops. His capillary refill is 2 seconds. His surgical incision looks clean and without any signs of infection. An ABG is drawn and reveals pH of 7.53, pCO2 of 58, and PO2 of 83. Chest X-ray shows some mild atelectasis but no acute infiltrates.

What is the diagnosis?


Answer: Bradypnea

 

Background:

  • Bradypnea is defined as a decreased respiratory rate and varies by age (Table 1)1
  • Hypopnea is shallow breathing that occurs during sleep2

Etiology:

  • Secondary to a number of causes. Most common:
    • Cardiac
      • Cheyne-Stokes respirations 2/2 congestive heart failure (CHF)5
      • Congenital cardiac disease6
      • Bradypnea can be seen after tachypnea as a sign of inevitable cardiopulmonary collapse and is a medical emergency1
        • Agonal breathing: slow and irregular gasping breaths seen in a dying patient as an attempt to oxygenate7
    •  Endocrine/metabolic
      • Hypothyroidism and myxedema coma can be triggered by an inciting stressful event or medication change8
      • Obesity hypoventilation syndrome9
    • Environmental
      • Hypothermia10
    • Gastrointestinal (GI)
      • Liver failure resulting in increased ammonia levels11
    • Neurological
      • Central sleep apnea12,13
      • Cushing’s Reflex/Triad: bradycardia, bradypnea, hypertension seen in patients with increased intracranial pressure (ICP)14
      • Neuromuscular disorders
        • Autonomic dysreflexia begins at T615
        • Phrenic nerve at C3-C516
        • Myasthenic/neuromuscular crisis17
      • Tumor or stroke: Respiratory rate is controlled by the brainstem, nucleus tractus solitarius (NTS), and the nucleus ambiguus, which directly connect to the phrenic nerve18
    • Psych
      • Chronic stress and anxiety19
    • Respiratory
      • Respiratory infections, such as bronchiolitis in children, can lead to apnea lasting up to 20 seconds20,21
      • Sleep apnea12
    • Toxicologic/pharmacologic
      • Alpha-2 agonists, barbiturates, benzodiazepines, ethanol, opioids, etc. (Table 2)22,23
      • Carbon monoxide24
      • Sodium azide, which is found in airbags25

 

Epidemiology:

  • Incidence/prevalence
    • Likely underreported
      • Studies show nurses often are unable to detect and record lower respiratory rates26
      • Respiratory rate is often left blank in EMR27
  •  Increased respiratory rate is more often seen in emergency settings and is an indicator of deterioration28
    • A patient presenting with a decreased respiratory rate is more likely to die during emergency room admission29
  • Opioid overdose is the most common cause of bradypnea in the ED30

 

Clinical Presentation:

  • May present with hypoxia or hypercapnia
    • These patients might have changes in mental status or decreased consciousness
    • Cyanosis may be present
  • Patients should be placed on continuous cardiac and pulse oximetry monitors
    • Slow breathing has been shown to increase cardiac output in heart failure patients due to increased venous return during inspiratory phase
      • This will cause increased heart rate (shorter R-R interval on EKG) during inspiration29

 

Evaluation:

  • Arterial blood gas (ABG) in critically ill patients
    • This will allow determination of oxygenation and ventilation status31
      • PaO2 80-100 mmHg: shows appropriate oxygenation
      • PaCO2 35-45 mmHg: shows adequate alveolar ventilation, removing CO2 from the bloodstream
    • Note that venous blood gas (VBG) may not be as accurate for the assessment of PaO2 but is still useful for PaCO2 and is less painful32,33
    • Metabolic alkalosis could cause the need to retain CO2, slowing the respiratory rate; exclude compensatory bradypnea secondary to GI losses, diuretic use, renal disorders33
  • Urine drug screen or blood alcohol level may reveal illicit substances, causing bradypnea
  • Thyroid-stimulating hormone (TSH)8
    • Evaluate for hypothyroidism
    • T3, T4, and other thyroid hormones could show myxedema coma
  • Chest x-ray
    • Elevated hemidiaphragm (especially on the left, which is less common than the right) may suggest phrenic nerve damage
    • Rule out pulmonology causes, such as COPD, pneumonia, etc.
    • Assess for overt fractures or spinal cord compression
  • MRI of head/cervical/thoracic/lumbar spine if concerns for spinal cord injury are present
  • Electromyography/biopsy in the inpatient setting may be needed to more definitively rule out neuromuscular causes17
  • Pulmonary function testing17
    • Used in patients with suspected neuromuscular causes
    • Negative inspiratory force (NIF) < -20 to -30 cmH2O OR forced vital capacity (FVC) < 10-20 mL/kg: the patient should be admitted to an intensive care unit in anticipation of the need for mechanical ventilation due to neuromuscular respiratory failure

 

Diagnosis:

  • Requires a thorough history and physical exam
    • Bradypnea will always be secondary to another cause

 

Treatment:

  • Place on cardiac and pulse oximetry monitors and obtain IV access
  • Respiratory support: oxygenation, noninvasive ventilation, mechanical ventilation
  • Reversal of the underlying cause

CPAP = continuous positive pressure ventilation, CVA = cerebrovascular accident, BiPAP = bilevel positive pressure ventilation, CHF = congestive heart failure, CPR = cardiopulmonary resuscitation, GHB = gamma-hydroxybutyric acid, GI = gastrointestinal, HOB = head of bed, ICP = intracranial pressure, IVIG = intravenous immune globulin, LES = Lambert-Eaton myasthenic syndrome, LNW = last known well, LVO = large vessel occlusion. *Avoid if the patient uses benzodiazepines chronically, as precipitated withdrawal could cause seizures and death. **IV ethanol is an alternative in limited-resource settings or where fomepizole is not available.

 

Prognosis:

  • Without other abnormal vital signs, respiratory rate alone is not indicative of the need for intensive care stays41

 

Pearls:

  • Bradypnea is always caused by a secondary condition
    • The differential diagnosis is broad
  • Diagnostic workup should be tailored to the suspected underlying cause(s)
  • Treatment involves reversal of the underlying cause

 

 

A 69-year-old man with a history of Alzheimer dementia presents to the ED with dyspnea. The patient’s caregivers noticed that the patient had become more short of breath over the last 12 hours and seemed confused. A chest radiograph is obtained, as seen above. Physical exam is notable for rales on auscultation and bilateral lower extremity pitting edema. Which of the following respiratory patterns would most likely be seen in this patient?

A) Biot respirations

B) Cheyne-Stokes respirations

C) Kussmaul respirations

D) Ondine respirations

 

 

Correct answer: B

This patient is presenting with congestive heart failure, given his pulmonary edema and bilateral lower extremity pitting edema, which are associated with Cheyne-Stokes respirations. Cheyne-Stokes respirations are characterized by episodes of apnea, followed by a gradual increase in respiratory frequency and tidal volume (i.e., hyperpnea), and then a decrease in frequency and tidal volume until the next period of apnea. Cheyne-Stokes respirations are commonly seen in cardiac disease and neurological disorders, including stroke, brain tumors, and brain injury. The pathophysiology is thought to be related to apnea, which causes an increased level of carbon dioxide and leads to excessive compensatory hyperventilation, in turn causing decreased levels of carbon dioxide, which causes apnea again. Often, Cheyne-Stokes respirations are a poor prognostic sign and a potential indicator of severe disease. Treatment involves treating the underlying cause. Patients in hospice with terminal illness presenting with Cheyne-Stokes respirations should receive comfort measures for symptom management.

Biot respirations (A) are associated with severe neuronal damage, in particular, when there is injury to the pons. It presents with quick and shallow breaths followed by episodes of apnea.

Kussmaul respirations (C) are a deep and rapid breathing pattern typically associated with metabolic acidosis, such as diabetes-related ketoacidosis. The increased ventilation decreases carbon dioxide levels, causing a respiratory alkalosis.

Ondine respirations (D) (the pathology is termed the Ondine curse) causes alveolar hypoventilation due to impaired autonomic control of ventilation. These patients will not adequately respire spontaneously. However, their volitional control of respiration is intact. This pattern of breathing can be seen in congenital hypoventilation syndrome, brainstem tumors, and surgical procedures in the cervical spinal cord.

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