Respiratory patterns

Respiratory Patterns main page
Overview
Classification Eupnea
Tachypnea
Bradypnea
Apnea
Cheyne-Stokes Respiration
Biot's Respiration
Apneustic Respiration
Agonal Respiration
Kussmaul's Respiration
Sighing Respiration

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Synonyms and keywords:

Eupnea

• Normal breathing is consisted of inhalation (sucking the air into the lungs) followed by exhalation (blowing the air out of the lungs).
• Every exhalation is followed by an automatic pause of about 2 second, before the next inhalation.
• Inhalation is an active process using diaphragm muscles, despite exhalation which is a passive process.
• Eupnea is the normal pattern of breathing with a rate of 10-12 per minute, each cycle is composed of:
  • Inhalation of 1.5-2 seconds
  • Exhalation of 1.5-2 seconds
  • Spontaneous stop of 2 seconds
• The main characteristics of eupnea are as following:
  • Slow
  • Regular
  • Nasal inhalation, oral exhalation
  • Diaphragmatic
  • Effortless
  • Clear auscultation:
    • No panting
    • No wheezing
    • No sighing
    • No deep breathing

Normal respiratory rate in every age group is as following:

Age group	Normal respiratory rate (Breath number per minute)
Infants	30 to 60
1 to 3 years	24 to 40
3 to 6 years	22 to 34
6 to 12 years	18 to 30
12 to 18 years	12 to 16

Tachypnea

• Tachypnea is increased rate and decrease depth of breathing.

The main pathophysiology of tachypnea is as following:

Decreased plasma oxygen (hypoxemia)

Increased plasma CO2 (respiratory acidosis)

Decreased pulmonary compliance

Increased airway resistance

Carotid body

Medullary chemoreceptors

Pulmonary or muscle mechanoreceptors

Airway receptors

Tachypnea

The main causes of tachypnea are classified into pulmonary, cardiovascular, hematologic, and metabolic pathophysiologies.

Causes		Other findings
Pulmonary	Asthma	Wheezing Prolonged Expiration Hyperinflated lungs
	Chronic obstructive pulmonary disease (COPD)	Clear lung field in chest X-ray Flattened diaphragm Hyperinflated lungs
	Pneumonia	Rhonchi and scattered wheezing Air-bronchograms Lobar or interstitial infiltrates
	Congestive heart failure (CHF)	Basilar crackles Jugular vein distention (JVD) Pulmonary edema and congestion
	Pneumothorax	Absent breath sounds Loss of pulmonary and vascular marking
Cardiovascular	Pericardial effusion	Low voltage ECG Pericardial fluid accumulation
	Cardiac Tamponade	Electrical alternans Right ventricular collapse during diastole
	Pulmonary embolism	Sinus tachycardia Right ventricular enlargement McConnell sign in echocardiography
	Myocardial infarct	Inverted T-wave or depressed/elevated ST-segment Local or generalized wall motion abnormality
Hematologic	Anemia	Hypoxemia-induced carotid chemoreceptors stimulation Chronic fatigue and numbness
	Sickle cell disease	Severe bone pain Autosplenectomy Hematuria
Metabolic	Metabolic acidosis	Dyspnea and tachypnea May lead to cardiac arrest and death in severe uncompensated cases
	Diabetic ketoacidosis (DKA)	Abdominal pain and ketonemia High blood glucose

Bradypnea

• Bradypnea is decreased count of breath to less than 8-10 per minute in adults and 16 per minute in infants.
• Mostly in bradypnea the exhalation phase is increased.
• The depth of breathes and tidal volume may be increased during bradypnea episodes.
• The main pathophysiology of bradypnea includes:
  • Desensitization of the medullary responses to PCO₂
  • Reduction in respiratory neuronal activity
  • Inhibition of neural transmission within the respiratory center
  • Neuronal damage to the brain stem
• The main causes of bradypnea are as following:

Causes			Other
Drugs	Opioids	Heroin	Can become worse when used along with: Smoking Benzodiazepines Barbiturates Phenobarbital Gabapentinoids Alcohol consuming Obstructive sleep apnea Chronic obstructive pulmonary disease (COPD) Lung cancer
		Codeine
		Hydrocodone
		Morphine
		Oxycodone
	Toxins	Sodium azide	Found in automobile airbags
		Carbon monoxide	Produced from oil or gas furnaces Absorbed by lungs and decrease the blood oxygen level
	Other drugs	Sedatives	Decrease respiratory drive Desensitizing to lowered plasma oxygen level
		Anesthetics
Systemic disease	Lung diseases	Emphysema	-
		Chronic bronchitis
		Severe asthma
		Pneumonia
		Pulmonary edema
	Thyroid	Hypothyroidism	-
	Neuromuscular	Guillain-Barré syndrome	Affect respiratory nerve and muscles Diaphragm Intercostal muscles
		Amyotrophic lateral sclerosis (ALS)

Apnea

• Apnea is the respiratory arrest for couple of seconds.
• The most common form of apnea in generally healthy people is obstructive sleep apnea.
• The pathophysiology of sleep apnea are as following:

Apnea

Sleep disturbances

↓O2, ↑CO2, ↓pH

Excessive motor activity

Loss of deep sleep Sleep fragmentation

Brain malfunction

Severe CO2 retention

Systemic vasoconstriction

Pulmonary vasoconstriction

Vagal bradycardia Ectopic cardiac pulses

Decreased pulmonary pressure Increased cardiac afterload

Restless sleep

Excessive daytime fatigue

Chronic hypoventilation

Systemic hypertension

Pulmonary hypertension

Unexplained nocturnal death

Left heart failure

Intellectual deterioration

Right heart failure

Personality change

Behavioral disorder

• The main causes of apnea include:
  • Obstructive sleep apnea
  • Opioid toxicity
  • Seizure
  • Asthma
  • Neurologic causes
    • Stroke
    • Myotonic dystrophy
    • Neuromuscular respiratory failure
    • Spinal cord injury
    • Bacterial meningitis
  • Pulmonary causes
    • Chronic obstructive pulmonary disease (COPD)
    • Influenza
    • Pulmonary emboli
    • Aspiration pneumonia
    • Atelectasis
    • Chronic bronchitis
    • Foreign body aspiration
    • Pulmonary edema
    • Viral pneumonia
  • Down syndrome
  • Metabolic acidosis
  • Cannabis use

Cheyne-Stokes Respiration

• Cheyne-Stokes respiration is recurrent central apneustic episodes during sleep.
• Tidal volume is in crescendo-decrescendo manner during Cheyne-Stokes respiration.
• Cheyne-Stokes respiration is almost always due to congestive heart failure, contributed with:
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Excessive daytime sleepiness
  • Witnessed apneas
• Patients with congestive heart failure who have already Cheyne-Stokes respiration pattern, would have more mortality rate.

The main pathophysiology of Cheyne-Stokes respiration pattern is as following:

Hypoxemia

Pulmonary vein congestion

Pulmonary C fibers stimulation

Spontaneous arousal

Increased circulating noradrenaline

Decreased cardiac output

Increased cardiac chamber size

Increased blood volume

Hyperventilation during day and night

Restrictive ventilatory defect

Decreased CO2 transfer capacity

Peripheral chemoreceptor stimulation

Increased pulmonary vagal efferent activity

Increased sympathetic activity

Circulatory delay

Decreased total body CO2

Decreased total body O2

Increased pulmonary capillary wedge pressure

Hyperventilation

Length of the apnea-hyperpnea cycle

Crescendo-decrescendo respiratory pattern

Decreased blood gas buffering capacity

Cheyne-Stokes respiration

• Cheyne-Stokes respiration is mostly secondary to heart failure, but can be associated with following conditions:
  • Altitude sickness
  • Brain injury
  • Brain tumors
  • Carbon monoxide poisoning
  • Pulmonary edema
  • Hyponatremia
  • High intracranial pressure
  • Renal failure
  • Toxic encephalopathy

Biot's Respiration

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• Camille Biot, in 1878 distinguished Biot's respiration from Cheyne-Stokes, named it “rhythme meningitique”.
• Biot's respiration is a kind of slow respiration pattern with periodic increasing 10-20 respiration per minute, without crescendo–decrescendo pattern.
• Accelerations are different in a patient with Biot's respiration:
  • Short and incomplete
  • Long and deep
  • Often interrupted by gasps
• The periods are different in length, ended to a sigh just before the pause.
• The main causes of Biot's respiration include:
  • Pontine lesions
  • Damage to the medulla oblongata
    • Stroke
    • Trauma
    • Pressure on the medulla (uncal or tentorial herniation)
  • Prolonged opioid abuse

Apneustic Respiration

• Apneustic respiration is first described in 1888 by Marckwald as prolonged inspiration arrest followed by inadequate expiration.
• The rate of apneustic breathing is about 1.5 breath per minute.
• The main causes of apneustic respiration include
  • Congenital brain-stem abnormalities
  • Upper pons damage secondary to:
    • Stroke
    • Trauma
    • Hypoxia
  • Severe brain injury
  • Ketamine (temporary)
  • Phenobarbital 
• Apneustic respiration almost always carries a poor prognosis

Agonal Respiration

• Agonal breathing is slow, very shallow irregular respirations.
• Agonal breathing is resulted from anoxic brain injury.
• The main causes of agonal breathing include:
  • Cardiac arrest
  • Stroke
    • Cerebral ischemia
    • Hemorrhagic stroke
    • Cerebral hypoxia
• The pathophysiology of agonal respiration in decreased blood flow to the brain, which causes gasps.

Kussmaul's Respiration

• The most important type of disturbed respiratory pattern, Kussmaul's respiration, is first described by Adolf Kussmaul in 1874, as "air hunger".
• Kussmaul's respiration is a deep, sighing respiration with normal or slow rate.
• The main pathophysiology of Kussmaul's respiration is increased tidal volume without increasing respiratory rate.
  1. Compensating metabolic acidosis
  2. Stimulation of the respiratory center which is located in the brain stem by low serum pH
  3. Lowering of the partial pressure of CO2 in the alveoli
  4. Hyperventilation
• Main causes of Kussmaul's respiration include:
  • Diabetic ketoacidosis
  • Renal failure
  • Metabolic (lactic) acidosis
  • Toxic ingestions
  • Alcohols
  • Salicylate toxicity
  • Uremia
• In primary stages of acidosis, breathes are rapid and shallow, while they become deeper and slower in the later stages, which are called Kussmaul's respirations.