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Normal - Abnormal Breathing Pattern

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1 Normal - Abnormal Breathing Pattern
Pulmonary Medicine Department Ain Shams University

2 Introduction Lungs major function
Provide continuous gas exchange between inspired air and blood in the pulmonary circulation

3 Anatomy of Respiratory System
Nasopharynx Larynx Trachea Bronchi Bronchioles Alveoli

4 Anatomy Respiratory tract extends from mouth/nose to alveoli
Upper airway filters airborne particles, humidifies and warms inspired gases Lower airway serves for gas exchange

5 Blood Supply Lungs have a double blood supply
Pulmonary circulation for gas exchange with the alveoli (pulmonary artery with subdivisions) Bronchial arteries arising from descending aorta supplies lung parenchyma

6 Contributors of Respiration
Controlled in the brain stem Mediated by muscles of respiration Diaphragm primary muscle of inspiration Accessory muscles of inspiration SCM Scalenes Intercostals Expiration is a passive process from elastic recoil of lung and chest wall, with passive diaphragm relaxation

7 Mechanism for Breathing
Pressure gradient required to generate air flow Diaphragm contracts, descends and enlarges thoracic cavity Intra-thoracic pressure decreases Air flows through tracheobronchial tree into the alveoli expanding lungs


9 Expiration:-     At a first glance, the mammalian resting breathing pattern appears to be an oscillatory event approximating a sinusoidal function, of which the amplitude is tidal volume (VT) and the period is the total breath duration (Ttot).     In reality, a close look reveals major deviations from the sinusoidal function. For example, Ttot is not equally divided between the inspiratory and expiratory phases of the cycle, the inspiratory time (TI) being most commonly shorter than the expiratory time (TE). Also, the inspiratory phase of the Spiro gram is usually concave toward the time axis, whereas the expiratory phase is convex, occasionally with sudden interruptions of the expiratory flow [Fig.1]. Fig.1. Change in volume as function of time during breathing: Spirogram. On top, the corresponding changes in airflow (pneumotachogram). TI, inspiratory time. TE, expiratory time. TTOT, total cycle duration. VT, tidal volume. V, airflow.

10 Fig.3. The main components
The main components of the neuro-mechanical unit translating the neural output into a mechanical event. At left, some examples of mechanical constraints. Information about the changes in lung volume is fed back to the respiratory pattern generator mostly via activation of muscle proprioceptors and airways receptors ('chest wall' and 'lung' reflexes).     

11 Introduction(cont.) respiration is highly integrated with circulation allowing flexibility between individuals and between species in the best way to optimize gas exchange; control of depth and rate of breathing are essential components of respiratory control Dyspnea :- non-specific symptom of many illnesses the sensation is due to projections from the respiratory controller to higher centers, and projection of sensory information to the brainstem and cortex, and prior experience the relation of dyspnea to the actual physiologic deficits is highly varied across cultures and individuals Þ relief of dyspnea may or may not correspond to adequate relief of the underlying physiologic causes dyspnea can be due to physiologic mechanisms, cortical mechanisms, or a combination of both Þ the whole control system must be examined in the presence of dyspnea (from brain to lungs)

12 Brainstem Control of Respiration – operates breath by breath to control rate and depth
Metabolic Control: concerns O2 and CO2 (acid/base) balance; can briefly be overridden during speech, swallowing, etc., but metabolic control is always re-asserted after a minute or so; control at brainstem level Behavioral Control: coordinates breathing with other complex voluntary functions (eating, talking, etc); control at thalamus and cortex; regulates use of motor systems used by both respiratory control and other activities Reticular Activating System: links the BS and cortex to coordinate respiration with level of alertness (i.e. sleep/wake) Medullary Control: basic regulation occurs even when the cortex and mid-brain are separated from the medulla breathing pattern is controlled by the nucleus tractus solitarius and the nucleus retroambiguus rhythm generation occurs in the pre-Botzinger complex proposed mechanism: tonic inspiratory drive comes from the dorsal motor group via phasic excitatory inputs; expiration is a result of reciprocal inhibition of the tonic drive (influenced by pneumotaxic center in the pons) apneusis: gasping, prolonged inspiration; occurs when pneumotaxic center is destroyed neonates probably have an intrinsic respiratory pacemaker because tonic excitation/reciprocal inhibition systems may not yet be active

13 Other Control systems higher brain centers (cortex, spinal, cerebellar): cortical outputs descend to the spinal neurons, and to the brainstem; lesions in certain areas of the brainstem can knock out metabolic control, but maintain volitional control (as long as the person is awake); cerebellum helps with coordination spinal cord integration: descending impulses are modified by inter/intra-segmental neurons, and by motor reflexes integration is lost in a hiccup when the diaphragm is able to suck in the rib cage without reflexive activation of the intercostal muscles receptors in the lungs: stretch receptors (smooth muscle layer), irritant receptors (epithelial cells), and un-myelinated C fibers (lung interstitium and alveolar walls) receptors in chest wall: joint, tendon, and muscle spindle receptors; reflex control is the same as other skeletal muscle, gamma motor neurons control the gain of the muscle stretch receptors


15 Abnormal Breathing Patterns
causes of irregular breathing: CHF; CNS disease; sleep apnea; metabolic alkalosis; prematurity causes of persistant hyperventilation: fibrotic lung disease; metabolic acidosis; CNS disorders (midbrain and pons); hepatic coma; ASA intoxication; fever; psychogenic Cheyne-Stokes: alternating episodes of apnea and hyperpnea; instability of ventilatory control causes tidal volume to rhythmically increase and decrease; may occur in circulatory deficits because it takes extra time for the blood to equilibrate and the chemoreceptors may act inappropriately may occur during hypoxia, sleep, high altitude, or after voluntary hyperventilation Apneustic breathing: prolonged inspiration due to interruption of the pneumotaxic center (see above) Biot’s breathing: normal breathing interrupted by sudden apnea; may be a variant of Cheyne-Stokes Ý breathing with hypocapnea: occurs when irritant or C-fiber receptors are activated (asthma, pulmonary embolus) Kussmaul’s breathing: hyperventilation with hypocapnea caused by acidosis (diabetic) hyperpnea of exercise: steady state of ventilation is achieved in 4-6 minutes with moderate exercise ventilation first increases abruptly, then gradually, then reaches a steady state mechanisms: cardiovascular mechanoreceptors; temperature receptors; chemoreceptors; mechanoreceptors in muscle; receptors monitoring metabolic activity

16 Respiratory Failure – ventilation cannot keep up with O2 demand, and CO2 increases
lung disease often blunts the response to CO2 and O2; this can be due to increased effort required to breathe; decreased gas exchange; impaired muscle function; reduced responses to stimuli causes of persistent hypercapnea: sleep apnea; CNS problems; metabolic alkalosis; myxedema; primary alveolar hypoventilation (Ondine’s curse - )spinal cord lesions; chest wall diseases; NM disorders; COPD

17 Abnormal Breathing Patterns
Hypoventilation – an irregular and shallow pattern that may occur at any respiratory rate Biots respirations :- an irregular, but cyclic pattern of an increased and decreased rate and depth, with long periods of apnea; it is associated with brain injury or heat stroke sometimes also called cluster respiration, is an abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea. It is distinguished from ataxic respiration by having more regularity and similar-sized inspirations, whereas ataxic respirations are characterized by completely irregular breaths and pauses.

18 Apnea:- Cessation of respiration from 2 to 60sec. seen in
Primary respiratory disorders : respiratory distress syndrome,brochopulmonary dysplasia Infection/inflammation : pertussis, pneumonia, septicemia, meningitis bronchioloitis Drug related: drug withdrawal CNS: convulsion,intracranial intraventricular or subdural haemorrhage ,cerebral edema GIT disorders: GERD Cardic disorders:conginital heart diseases, conduction disorders(rare) Sleep apnea :enlarged tonsils, adenoids, extreme obesity(rare) , primary alveolar hypoventilation Others: hypoglycemia, hypocalcemia

19 Abnormal Breathing Patterns
Eupnea – normal breathing Tachypnea – rapid shallow breathing and the rate is age related Hyperventilation – a rate greater than that required for normal body function; it is the result of increased respiratory rate, depth or both Bradypnea – slow breathing

20 Abnormal Breathing Patterns
Cheyne-Stokes respirations – a rhythmic pattern of gradually increase&decrease tidal volume interpersed with approximately equal periods of apnea (10-20 sec.) associated with severe CHF, increased ICP, drug OD or induced respiratory depression ,brain damage (strokes, head injuries or brain tumors and meningitis), uremia ,may be normal pattern of children during sleep, or adult sleep in high altitude . In cases of increasing intracranial pressure, it is often the first abnormal breathing pattern to appear. The condition was named after John Cheyne and William Stokes, the physicians who first classified it. This is caused by the failure of the respiratory center in the brain to compensate quickly for changing serum partial pressure of oxygen and carbon dioxide Cheyne-Stokes respirations are not the same as Biot's Respirations ("clusterbreathing"), where groups of breaths tend to be similar in size.   .

21 Kussmaul’s respirations or “air hunger” - a distressing dyspnea occurring in paroxysms (deep regular breathing the rate may be normal ,fast or slow )and is associated with diabetic acidosis, coma and other causes of excess acid in the blood rapid, deep, and labored breathing of people who have acidosis. Kussmaul breathing is named for Adolph Kussmaul, the 19th century German doctor who first noted it. It is also called "air hunger". The cause of Kussmaul breathing is respiratory compensation for a metabolic acidosis, most commonly occurring in diabetics in diabetic ketoacidosis. Blood gases on a patient with Kussmaul breathing will show a low pCO2 because of a forced increased respiratory rate (blowing off the carbon dioxide). The patient feels an urge to breathe deeply, and it appears almost involuntary. The effect can be reproduced, to a degree, by rapidly breathing in the air in a recently-emptied plastic soft-drink bottle, which will normally contain a substantial amount of carbon dioxide.

22 Define Abnormal Breathing: Remember a person in cardiac arrest may have abnormal breathing for a couple of minutes. This abnormal breathing is called "agonal respiration" and is the result of the brain's breathing center sending out signals even though circulation has ceased. The key point is that the abnormal breathing may sound like grunting, gasping or snoring. It disappears in 2-3 minutes. If you see this type of breathing DO NOT delay CPR. The person desperately needs air and only you can provide it. Agonal respiration is an abnormal pattern of breathing characterized by shallow, slow (3-4 per minute), irregular inspirations followed by irregular pauses. They may also be characterized as gasping, labored breathing, accompanied by strange vocalizations and myoclonus. Agonal breathing is an extremely serious medical sign requiring immediate medical attention, as the condition generally progresses to complete apnea and heralds death. The term is sometimes (inaccurately) used to refer to labored, gasping breathing patterns accompanying organ failure (e.g. liver failure and renal failure), SIRS, septic shock, and metabolic acidosis, or in general any labored breathing, including Biot's respirations and ataxic respirations. Correct usage would restrict the term to the last breaths before death.

23 Abnormal Breathing Patterns
Agonal respirations –ataxic breathing “dying breaths”: characterized by continous irregular shifts of hyper/hypoventilation &apnea in no particular succession (unlike biotis &cheyne stoke) As the breathing pattern deteriorates, it merges with ataxic respirations. It is caused by damage to the medulla oblongata due to strokes or trauma or by pressure on the medulla due to uncal or tentorial herniation. It generally indicates a poor prognosis. Our greatest concern during this phase of the evaluation lies in the EMD’s ability to accurately assess the status of a patient’s breathing.

24 Sleep-Disordered Breathing
characterized by breathing abnormalities, intermittent disruptions of gas exchange, sleep interruption Þ excessive daytime sleepiness, cardiac arrhythmias, behavioral abnormalities, Ý auto accidents; snoring (partial obstruction of the upper airway) is associated with HTN and stroke, possibly MI Central Apnea: cessation of all breathing efforts Obstructive Sleep Apnea most common disorder of breathing during sleep (2-4% of the population) breathing efforts persist but the upper airway is obstructed; partial arousal is important in terminating the apnea

25 measuring apnea AHI (apnea-hypopnea index): total apneas and hypopneas divided by hours of sleep RDI (respiratory disturbance index): same as AHI DI (desaturation index): number of times oxygen sat. falls by more than 4% AI (arousal index): number of arousals per hour (may or may not correlate with AHI) Treatment: should be geared towards the degree of disability, not the number of breathing disturbances general: weight loss; relief of mechanical problems; don’t operate heavy machinery CPAP (continuous positive applied pressure): prevents airway collapse and is effective in long-term treatment dental prosthesis and electrical stimulation of the upper airway are currently being evaluated correction of pathologic airways is beneficial remove enlarged tonsils, macroglossia, nasal polyps uvulopalatopharynxgoplasty: 60% effective, but side effects suck (food regurgitation, speech problems) tracheostomy: bypass the problem; most successful, but again, the side effects suck medical: little shown to be effective (weight loss is the most effective medical treatment)

26 Focused History For the patient with respiratory distress obtain the most pertinent information first. When a patient is severely distressed modify questions to yes or no answers. Utilize family/caretakers, etc Obtain OPQRST and SAMPLE information .

27 Technique for Respiratory Exam
NEED ORDERLY PROCESS Before beginning, if possible: Quiet environment Proper positioning (patient sitting for posterior thorax exam, supine for anterior thorax exam) Bare skin for auscultation Patient comfort, warm hands and diaphragm of stethoscope, be considerate of women (drape sheet to cover chest) Inspect Palpate Percuss Auscultate

28 Initial Respiratory Survey
Observe the patient’s breathing pattern Rate (normal vs. increased/decreased) Depth (shallow vs. deep) Effort (any sign of accessory muscle use, inspect neck) Assess the patient’s color cyanosis

29 Normal Respiratory Rates
Infant 30-60 Toddler 24-40 Preschooler 22-34 School-age child 18-30 Adolescent 12-16 Adult 10-20

30 Breathing-Interventions Breathing Present: Effective
Administer oxygen via a nonrebreather mask at a flow rate sufficient to keep the reservoir bag inflated: during inspiration, usually requires a flow rate of at least 12 liters/minute and may require 15 liters/minute

31 Breathing-Interventions Breathing Present: Ineffective
When spontaneous breathing is present but ineffective, the following may indicate a life-threatening condition related to breathing: Altered mental status (i.e. restless, agitated) Cyanosis, especially around the mouth Asymmetrical expansion of the chest wall Use of accessory and/or abdominal muscles Sucking chest wounds Paradoxical movement of chest wall during inspiration and expiration Tracheal shift from the midline position.

32 Breathing-Interventions Breathing Absent
Ventilate the. Patient via a bag-valve-mask device with an attached oxygen reservoir system 100% Assist with endotracheal intubation: ventilate with oxygen via a bag-valve device attached to an oxygen reservoir system

33 Breathing-Assessment
Life-threatening compromises in breathing may occur with a history of any of the following: Blunt or penetrating injuries of the thorax Patient striking the steering column or wheel Acceleration, deceleration, or a combination of both types of forces (e.g., motor vehicle crashes, falls. crush injuries)

34 Breathing Assessment Spontaneous breathing
Chest rise and fall (depth and symmetry) Skin color General respiratory rate • Normal • Slow • Fast Pattern of breathing • Regular • Irregular • Cheyne Stokes Integrity of the soft tissue and bony structures of the chest wall Use of accessory and/or abdominal muscles Bilateral breath sounds: Auscultate the lungs bilaterally at the second intercostal space midclavicular line and at the fifth intercostals space at the anterior axillary line. Jugular veins and position of trachea

35 Focused History O – onset P – provocation Q – quality
R – region/referral/radiation S – severity T – time

36 Focused History S – signs/symptoms A – allergies M – medications
P – pertinent past medical history L – last oral intake E – events leading up to

37 Physical Exam Determine patient’s mental status and level of distress.
A patient with moderate to severe distress will have difficulty speaking in full sentences. The inability to speak in full sentences indicates an immediate life threat. A limited number of words spoken between breaths is described as “one, two, or three word dyspnea.”

38 Physical Exam (continued)
Other findings that indicate an immediate life-threat in a patient with respiratory distress include: Altered MS, anxiety or confusion/hypoxia Signs of poor perfusion such as cyanosis, pallor, or diaphoresis Absent or abnormal breath sounds Use of accessory muscles Tachycardia or bradycardia (sustained) Hypotension

39 Abnormal Findings Associated with Respiratory Distress
Nasal flaring – widening of the nostrils indicates partial airway obstruction, most notable in children Carpopedal spasms – spasmotic contractions of the hands, wrists, feet, and ankles from prolonged hyperventilation or any condition that leads to respiratory alkalosis

40 Abnormal Findings Associated with Respiratory Distress
One or two word dyspnea = severe distress Purses-lip breathing – creates airway pressure to help keep the alveoli from collapsing Retractions – accessory muscle use, most notable during inspection (ribs, clavicles, sternum)

41 Abnormal Findings Abnormal or adventitious breath sounds using numerous terms and definitions with few agreeing on the same words When assessing breath sounds: Listen to skin not the shirt! Apex to base comparing side-to-side Use simple terms to describe your findings

42 Abnormal Findings Abnormal lung sounds include:
Wheezing – continuous whistling sound caused by narrowing of the lower airways Stridor – is a disturbing high-pitched sound associated with upper airway obstruction Grunting – is a sound that occurs primarily in infants/small children when the child breathes out against a partially closed epiglottis (usually a sign of distress)

43 Abnormal Findings Abnormal lung sounds include:
Wheezing – continuous whistling sound caused by narrowing of the lower airways Stridor – is a disturbing high-pitched sound associated with upper airway obstruction Grunting – is a sound that occurs primarily in infants/small children when the child breathes out against a partially closed epiglottis (usually a sign of distress)

44 Abnormal Findings Absent sounds – no sounds heard in the lungs may be due to consolidation of edema or pneumonia, complete FBAO, and severe asthma Absent unilateral sounds may be due to pneumothorax, pneumoectomy, increased consolidation (pneumonia) decompensated COPD or partial FBAO Pleural friction rub – is not a lung sound but is heard in the chest as a grating sound over the area that is painful

45 Breathing Patterns Apnea:  absence or cessation of breathing in the resting expiratory position. Apneusis: respiration ceases in inspiratory position, because of sustained contraction of the inspiratory muscles. Biot's Respiration:  sequences of uniformly deep gasps, apnea, then deep gasps. Breath-holding: voluntary apnea, either by continuous contraction of the inspiratory muscles, or by  relaxation against glottis closure. Cheyne-Stokes Respiration:  cycles of gradually increasing tidal volume followed by gradually decreasing  tidal volume, usually separated by brief periods of apnea. Dyspnea:  difficult or laboured breathing; an uncomfortable awareness of the act of breathing, "air hunger".  Eupnea:  normal spontaneous breathing.  Hyperpnea:  increased pulmonary ventilation (above the normal resting value) 

46 Hyperventilation:  increase in pulmonary ventilation (VE, ml/min) (strictly, alveolar ventilation VA, ml/min)  relative to metabolic rate, irrespective of the absolute value of ventilation.   Hypopnea: ventilation below the normal level.  Hypoventilation:  ventilation less than required by metabolic demands, irrespective of the absolute value of ventilation.   Orthopnea:  dyspnea experienced only in the recumbent position, usually supine, and relieved by sitting or standing. It often occurs in patients with left ventricular insufficiency.  Panting: breathing pattern both very rapid and shallow. In some conditions, this pattern is adopted to   dissipate heat (thermal panting).   Periodic breathing, abnormal breathing pattern, with a series of cycles separated by pauses.  Tachypnea: increased rate of breathing. 

47 Dyspnea Features Causes of dyspnea with exertion are either pulmonary or cardiac Dyspnea from pulmonary causes tend to resolve quicker with cessation of exertion than cardiac causes Causes of dyspnea without exertion include: anemia, chest trauma, acute MI, pulmonary embolism, spontaneous pneumothorax

48 Dyspnea Features Acute dyspnea in children most often occurs due to asthma, bronchiolitis, croup, or upper airway FBAO Acute dyspnea in the elderly is often caused by exacerbation of COPD or heart failure

49 Dyspnea Features Common factors that can trigger respiratory conditions include: Exercise or stress Infection Allergies Tobacco smoke Chemicals or other irritants Medications may worsen COPD (ie: beta-blockers)

50 Conclusion The management of a patient with a respiratory problem includes a prompt and accurate assessment with recognition of immediate life-threatening conditions, followed by prompt intervention and resuscitation as appropriate. When the patient’s condition is unstable or critical these steps take priority over a detailed assessment.

51 Conclusion The FH & PE are always a high priority, as the information obtained guides the course of treatment. Ask the most pertinent questions first. Be alert for signs of rapid deterioration and quickly formulate a plan to intervene. Many patients with dyspnea are having a cardiac problem. The assessment process is dynamic and the EMS provider must modify the FH & PE to include more than one body system.


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