This presentation addresses respiratory emergencies, and the approach to their management. These include: anaphylaxis, pneumonias, flail chest, pleural effusion, pulmonary embolism,

1. RESPIRATORY
EMERGENCIES
DR KEMI D. DELE
DEPT OF FAMILY MEDICINE | DORA NGINZA HOSPITAL

2. DEFINITIONS
• Apnoea: the cessation of breathing
• Dyspnoea: shortness of breath
• Orthopnoea: a type of dyspnoea that only occurs when a person is lying down
• Tachypnoea: abnormally rapid breathing
• Bradypnea: an abnormally slow breathing rate

3. DEFINITIONS
• Acidosis: overproduction of acid in the blood or an excessive loss of bicarbonate
from the blood
• Alkalosis: build-up of excess base or alkali in the body, decreased CO2 or
increased bicarbonate levels
• Acute respiratory distress syndrome (ARDS) is a type of respiratory failure
characterized by rapid onset of widespread inflammation in the lungs. It is a
rapidly progressive disease occurring in critically ill patients.

4. DEFINITIONS
• Hypercarbia/Hypercapnia: abnormally elevated CO2 levels in the blood
• Hypoxaemia: an abnormally low concentration of oxygen in the blood. arterial
oxygen tension or partial pressure of oxygen (PaO2) is below normal (normal is
between 80 and 100 mmHg)
• Hypoxia: the reduction of oxygen supply at the tissue level, which is not measured
directly by a laboratory value

5. DEFINITIONS
• Respiration: process whereby oxygen is taken into body and distributed to the
cells, and carbon dioxide is returned to the lungs by the circulatory system and
exhaled.
• Ventilation: Movement of air in and out of the lungs
• Diffusion: For oxygen to go from an alveolus to a red blood cell and CO2 vice
versa
• Perfusion: Circulatory component of respiratory system (blood flow in pulmonary
vessels)
• Respiratory failure results from inadequate gas exchange by the respiratory
system, meaning that the arterial oxygen, carbon dioxide or both cannot be kept
at normal level

6. EPIDEMIOLOGY:
RELATIVE FREQUENCY OF MEDICAL EMERGENCIES

7. EPIDEMIOLOGY:
RELATIVE FREQUENCY OF RESPIRATORY EMERGENCIES

8. EPIDEMIOLOGY: PAKISTAN
RELATIVE FREQUENCY OF RESPIRATORY EMERGENCIES

9. ANATOMY AND PHYSIOLOGY

10. STRUCTURES OF THE UPPER AIRWAY

11. STRUCTURES OF THE UPPER AIRWAY
• Nostrils and nose
• Air enters through the nostrils.
• Lined with nasal hairs
• Quiet breathing allows air to flow through the nose.
• Turbinates
• Highly vascular ridges covered with mucus membrane
• Traps particulates
• Warm and humidify air as it passes
• Many blood vessels—swell and bleed easily

12. STRUCTURES OF THE UPPER AIRWAY
• Mouth and oropharynx
• Contain blood vessels and mucous membrane
• Oedema can be extreme.
• Ask patient if their tongue feels thick.
• Monitor speech.
• Larynx and glottis
• Dividing line between upper and lower airway
• Thyroid cartilage: external landmark

13. STRUCTURES OF THE LOWER AIRWAY
• Respiratory system structures look like an inverted tree.

14. STRUCTURES OF THE LOWER AIRWAY
TRACHEOBRONCHIAL TREE
• Trachea — trunk of tree
• Carries air to the lungs
• Extends from the larynx to the mainstem bronchi
• Mainstem bronchi –
• two major branches of the trachea to the lungs. )
• Mainstem bronchi branch into:
• Lobar bronchi
• Segmental bronchi
• Subsegmental bronchi
• Bronchioles

15. STRUCTURES OF THE LOWER AIRWAY
• Bronchioles
• Significant amount of gas exchange
• Goblet cells produce mucus blanketing.
• Smooth muscle surrounds the airway.
• Bronchoconstriction: smooth muscle narrows the airway.
• Alveoli
• Gas exchange interface
• Deoxygenated blood releases carbon dioxide and is resupplied with oxygen.

17. NEIGHBOURING STRUCTURES
• Chest wall: Forms a bellows system with chest muscles
• The diaphragm: is the primary muscle. Causes pressure changes to move air in and out
• Ribs: maintain pressure.
• Pleural membranes: allow organs to move smoothly.
• Trauma and diseases of the bones and muscles can significantly impair air movement.
• Causes restrictive lung diseases
• Mediastinum: middle of the chest
• Consists of the heart, large blood vessels, the large conducting airways , and other
organs

18. MUSCULAR CONTROL
• Body takes in air by negative pressure
• Air through mouth and nose, over turbinates,
around epiglottis and glottis
• Thorax: airtight box with diaphragm at bottom and
trachea at top
• Diaphragm flattens during quiet breathing.
• Air is sucked in to fill the increasing space.
• Accessory muscles cause dramatic pressure
changes when greater amounts of air must be
moved.

19. NEUROLOGIC CONTROL
• The medulla oblongata is the primary respiratory control centre. Its main function
is to send signals to the muscles that control respiration to cause breathing to
occur.
• At least four parts of brainstem responsible for unconscious breathing
• Stretch receptors cause coughing if taking too deep a breath
• Hering-Breuer reflex – a reflex triggered to prevent the over-inflation of the
lung.
• Other neurologic control mechanisms:
• Phrenic nerve innervates diaphragm.
• Thoracic spinal nerves innervate intercostal muscles.

22. PHYSIOLOGY
• Takes in oxygen
• Disposes of wastes
• Carbon dioxide
• Excess water

23. PHYSIOLOGY
• Inspiration
• Active process
• Chest cavity expands
• Intrathoracic pressure falls
• Air flows in until pressure equalizes
• Expiration
• Passive process
• Chest cavity size decreases
• Intrathoracic pressure rises
• Air flows out until pressure equalizes

24. ADEQUATE RESPIRATIONS
• Inhalation of oxygen and exhalation of CO2
• Rate and depth are adequate
• Adult - Normal range 12-20 breaths/minute
• Child – Normal range 15-30 breaths/minute
• Infant – Normal range 25-50 breaths/minute
• No abnormal breath sounds
• Air moves freely
• Skin color normal, pink, warm

25. ADEQUATE RESPIRATIONS
• Normal rate and depth
• Rhythm – regular breathing pattern
• Quality – Good breath sounds on both sides of lungs
• Chest expansion – adequate/equal chest rise and fall
• Depth (tidal volume) – normal/adequate (500cc/air)

26. INADEQUATE RESPIRATION
• Rate – outside normal ranges <10 or >29
• Rhythm – irregular
• Quality – diminished or absent breath sounds; unequal chest expansion, use of
accessory muscles.
• Children – seesaw breathing, nasal flaring, grunting, retractions, have smaller
airways so easier to obstruct
• Skin – pale or cyanotic, cool and clammy

27. INADEQUATE RESPIRATION
• Signs of breathing but inadequate to support life
• Rate of breathing or depth of breathing or both fall outside normal ranges.
• Shallow ventilations
• Diminished or absent breath sounds
• Decreased minute volume
• END RESULT:
• Respiratory failure
• Reduction of breathing to the point where oxygen intake in insufficient to
support life.
• Respiratory Arrest: Breathing stops completely

28. INADEQUATE RESPIRATION:
GENERAL SIGNS AND SYMPTOMS
• Nasal Flaring
• Grunting
• Retractions between the ribs, above the clavicles and above the sternum
• Increased Pulse Rate
• Decreased Pulse Rate (infants and children)
• Changes in the rate
• Changes in the rhythm

29. INADEQUATE RESPIRATION:
GENERAL SIGNS AND SYMPTOMS
• Skin Color
• Central Cyanosis (Lips and Mouth)
• Peripheral Cyanosis (fingers, toes, tip of nose)
• Gray skin color
• Diaphoresis
• Restlessness, anxiety, irritability, drowsiness
• Coughing up sputum
• Clubbing

30. INADEQUATE RESPIRATION:
GENERAL SIGNS AND SYMPTOMS
• Shortness of breath
• Inability to speak full sentences
• Use of accessory muscles to breathe
• Gasping for air
• Altered mental status
• Breathing through pursed lips
• Tripod position

31. INADEQUATE RESPIRATION:
GENERAL SIGNS AND SYMPTOMS
• Noisy breathing – crowing, wheezing, gurgling, snoring, stridor
• Restlessness
• Silent chest – found in asthma patients
• Skin color changes
• Unusual anatomy (barrel chest)
• Unusually Slow (bradycardia): less than 8 bpm in adults or less than 10bpm for
children

32. NOISY BREATHING
• Crackles (rales): Fine, wet, crackling sounds – air passing through fluid
• Rhonchi: Coarse, rattling sounds, air passing through mucus
• Wheezes: High-pitched, musical sounds of narrowed airways
• Stridor: Harsh sounding respirations indicating narrowing or obstruction
• Pleural friction rub: Continuous low-pitched, rubbing sound
• Stridor and grunting are generally audible
• The most ominous sound is: “no sound”.

33. RESPIRATORY EMERGENCIES
PATHOPHYSIOLOGY/DIFF DIAGNOSIS

34. OBSTRUCTIVE PATHOPHYSIOLOGY
• Tongue
• Foreign body obstruction
• Anaphylaxis and angioedema
• Facial trauma and inhalation injuries (burns)
• Epiglottitis and Croup
• Aspiration

35. OBSTRUCTIVE PATHOPHYSIOLOGY: LRT
• Asthma
• COPD
• Emphysema
• Chronic Bronchitis

36. DIFFUSION PATHOPHYSIOLOGY
• Pulmonary Edema:
• Left-sided heart failure
• Toxic inhalations
• Near drowning
• Pneumonia
• Pulmonary Embolism:
• Blood clots
• Amniotic fluid
• Fat embolism

37. VENTILATION PATHOPHYSIOLOGY
• Trauma: rib fractures, flail chest, spinal cord injuries
• Pneumothorax, hemothorax
• Diaphragmatic hernia
• Pleural effusion
• Morbid obesity
• Neurological/muscular diseases: polio, MD, myasthenia gravis
• Hyperventilation Syndrome

38. CONTROL SYSTEM PATHOPHYSIOLOGY
• Head trauma
• CVA
• Depressant drug toxicity
• Narcotics
• Sedative-hypnotics
• Ethyl alcohol

39. ASSESSMENT

40. PRIMARY ASSESSMENT: AIRWAY
• Any and all Patient Care Situations You Must
• Evaluate,
• Establish and
• Maintain
• a patent airway

41. PRIMARY ASSESSMENT: BREATHING
• Form a general impression E.g. Body type like barrel chest, wasting,
• Observe condition during typical exertion. E.g. Tachycardia, diaphoresis, and
pallor
• Position and degree of distress e.g. sitting positions, such as tripod position.
• Lying flat or head bobbing may be a sign of sudden deterioration
• Altered rate and depth of respiration
• Abnormal breath sounds
• Abnormal breathing patterns – may indicate neurological insults

42. PRIMARY ASSESSMENT: CIRCULATION
• Assess skin colour – note generalized cyanosis. (Pink in healthy patients)
• Central cyanosis - desaturation
• Chocolate brown skin e.g. in high levels of methaemoglobin
• Pale skin – in vasoconstriction or in shock, blood loss
• Check for dehydration:
• Dry, cracked lips
• Dry, furrowed tongue
• Dry, sunken eyes
• Check for signs of fluid overload

43. PRIMARY ASSESSMENT:
NEUROLOGIC ASSESSMENT
• Note level of consciousness.
• Note that:
• Decline in PaO2: restlessness, confusion, and combative behavior
• Increase in PaCO2: sedative effects

44. HISTORY TAKING
• Investigate chief complaint
• Cough
• Amount or Color of Sputum
• Fever
• Wheezing
• Dyspnea
• Chest pain

45. HISTORY TAKING
• Patient may know exact problem.
• Asthma with fever
• Failure of a metered-dose inhaler
• Travel-related problems
• Dyspnea triggers
• Seasonal issues
• Noncompliance with therapy
• Failure of technology or running out of medicine
• Listen to the patient……they will tell exactly what is wrong!

46. HISTORY TAKING:
SAMPLE HISTORY
• Signs and symptoms
• Allergies
• Medications – Antihistamines / Antitussives / Bronchodilators / Diuretics /
Expectorants
• Pertinent past medical history
• Last oral intake
• Events preceding the onset of the complaint

47. HISTORY TAKING:
OPQRST HISTORY
• O = Onset
• P = Provocation
• Q = Quality
• R = Radiation
• S = Severity
• T = Time

48. VITAL SIGNS
• Patients under respiratory distress can be expected to have tachycardia and
hypertension.
• Ominous signs:
• Bradycardia
• Hypotension
• Falling respiratory rates

49. DETAILED EXAM
• Complete and thorough head, neck-to-toe exam with non critical patients.
• Elicit further information and necessary interventions.
• Key in on critical signs!

50. SECONDARY ASSESSMENT:
NECK
• Jugular venous distention
• Commonly raised with asthma or COPD or CCF
• Rough measure of pressure in right atrium
• Note trachea for deviation.
• E.g. Sign of tension pneumothorax

51. SECONDARY ASSESSMENT:
EXTREMITIES
• Examination of the extremities
• Oedema
• Cyanosis.
• Pulse
• Pulsus paradoxus
• Temperature
• Digital clubbing

52. SECONDARY ASSESSMENT:
SYSTEMIC EXAMINATION
• Cardiovascular
• Respiratory
• Abdominal
• Musculoskeletal

53. SECONDARY ASSESSMENT:
SYSTEMIC EXAMINATION
• Crackles (Rales)
• CHF
• Pneumonia
• Rhonchi
• Pneumonia
• Aspiration
• COPD
• Sometimes Asthma
• Stridor
• FBAO
• Croup
• Anaphylaxis
• Epiglottitis
• Airway burn
• Wheezing
• Asthma / COPD
• CHF

54. INVESTIGATIONS
• Blood –
• FBC,
• U&Es,
• D-dimer
• Trop I
• CRP
• ABGs
• ECG
• CXR

55. PLAN
• ABC’s/Monitor vitals
• Patient in position of comfort.
• Oxygen via ?
• Appropriate medications.
• Maintain body temperature.
• Calm and reassure.
• Minimize patient movement.
• Rapid transport/transfer if referring

56. OXYGEN
• Essential component of respiration
• Inadequate perfusion can have irreversible
effects from organ failure, loss of brain
function to death.
• NEVER DENY OXYGEN TO ANY PATIENT
WHO NEEDS IT!

57. GOLDEN RULES:
• If you are thinking about giving O2, then give it!
• It is not enough to simply make sure the patient is breathing; the patient must be
breathing adequately.
• If you can’t tell whether a patient is breathing adequately, then they aren’t!
• If you’re thinking about assisting a patient’s breathing, you probably should be!
• When a patient quits fighting it does not mean that they are getting better!

58. PULSE OXIMETER
• Non-invasive way to measure the percentage of
haemoglobin with oxygen attached
• Oxygen saturation over 95% = normal
• Oxygen saturation should match patient’s palpated heart
rate.
• If haemoglobin level is low, the pulse oximetry result will
be high.
• Does not differentiate between oxygen or carbon
monoxide molecules

59. END-TIDAL CARBON DIOXIDE DETECTOR
• Capnometry: ETCO2 monitoring
• Wave capnography: ETCO2 monitoring that measures carbon dioxide and plots a
waveform graph
• Colorimetric detector indicates whether carbon dioxide is present in reasonable
amounts
• Special sensor can measure the percentage of carbon dioxide and display a
waveform
• Waveform capnography

60. END-TIDAL CARBON DIOXIDE DETECTOR

61. PEAK EXPIRATORY FLOW
• Maximum rate at which a patient can expel air
• Normal values: 350 to 700 L/min
• Variable by age, sex, and height
• Inadequate level: 150 L/min
• Helpful in Asthma and COPD

62. SUPPORT OR ASSIST VENTILATION
• Breathing may need more aggressive support if the patient becomes fatigued.
• CPAP and BiPAP may prevent the need for intubation.
• Bi-level positive airway pressure (BiPAP)
• Continuous positive airway pressure
• May simply require bag-mask ventilation

63. CPAP
• Continuous Positive Airway Pressure
• A means of providing high flow, low pressure
oxygenation to the patient in pulmonary oedema
• If applied early enough CPAP is an effective way to
treat pulmonary oedema and a means to prevent
the need to intubate the patient, reduces hospital
stay & mortality

64. CPAP
• Pressure that is too high may cause: Tension pneumothorax, Subcutaneous
air/emphysema and may block venous returns
• Newer guidelines emphasize: Lower ventilation rates, Smaller volumes, Lower
pressures
• CPAP also helpful in patients with sleep apnea

65. INTUBATE & VENTILATE THE PATIENT
• Rapid Sequence Intubation (Remembered
as the 9Ps)
• Plan
• Preparation (drugs, equipment,
people, place)
• Protect the cervical spine
• Positioning (some do this after
paralysis and induction)
• Preoxygenation
• Pre-treatment (optional; e.g. atropine,
fentanyl and lignocaine)
• Paralysis and Induction
• Placement with proof
• Postintubation management, such as
ventilation
• Some add a 10th P for (cricoid)
pressure after pre-treatment but this
procedure is optional and has many
drawbacks

67. RESPIRATORY EMERGENCIES

68. UPPER AIRWAY INFECTIONS:
SIGNS & SYMPTOMS
• Dyspnea or respiratory distress
• Seal-bark cough
• Acute angioedema
• Excessive salivation
• Stridor
• Sniff positioning

69. AIRWAY OBSTRUCTION
• Obstruction may result from head position, tongue, aspiration, or foreign body.
• Be prepared to treat quickly and aggressively.
• Head-tilt/chin-lift to open airway

70. UPPER AIRWAY INFECTIONS
• Bronchitis
• Common cold/Influenza
• Diphtheria
• Croup
• Epiglottitis
• Severe Acute Respiratory Syndrome

71. 1. ANAPHYLAXIS
• Characterized by respiratory distress and hypotension
• Usually results from body response to allergen.
• Airway obstruction due to angioedema is major concern

72. ANAPHYLAXIS
• Treatment of angioedema
• This includes
• antihistamine (mainly H1 – promethazine, allergex, cetirizine; sometimes H2
blockers - ranitidine),
• steroids - corticosteroids,
• bronchodilators – e.g. Nebs,
• and, in those with severe symptoms, epinephrine (intramuscular or subcutaneous)
• Epinephrine is the only medication that can reverse the symptoms of anaphylaxis.
Use epinephrine at the first sign of a severe allergic reaction

73. 2. PNEUMONIA
• Infection of the lung parenchyma
• Infection usually caused by bacteria or virus, rare instances fungal
• Patient will present with sick appearance, febrile, shaking, productive cough,
increased sputum.
• Patient with increase respiratory rate/effort, tachycardic,
wheezes/rales/consolidated lung sounds

74. INVESTIGATION
• CXR
• Sputum Gram Stain and culture
• Pulse oximetry
• Routine lab testing – CBC, BMP, LFTs
• ABG
• Thoracentesis if pleural effusion present

75. TREATMENT
• Aminopenicillins + b-lactamase inhibitor:
• Amoxicillin/clavulanate
• Ampicillin/sulbactam
• Second-generation cephalosporin
• Cefuroxime
• Third-generation cephalosporin
• Ceftriaxone
• Cefotaxime

76. TREATMENT OF EARLY ONSET HAP
• Ceftriaxone
• Quinolone (Levofloxacin, Moxifloxacin, Ciprofloxacin)
• Ampicillin/sulbactam
• Ertapenem

77. 3. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
(COPD)
• COPD is characterized by persistent airflow limitation that is usually progressive
and associated with an enhanced chronic inflammatory response in the airways
and the lung to noxious particles or gases.

78. COPD MEDICATIONS
1. Beta2-agonists
• Short-acting beta2-agonists: e.g. Salbutamol (Asthavent/Ventolin); Fenoterol
(Berotec); Terbutaline (Bricanyl)}
• Long-acting beta2-agonists: e.g. Salmeterol (Serevent); Formoterol (Foradil / Oxis)
2. Anticholinergics, e.g. Ipratropium bromide (Atrovent)
• Short-acting anticholinergics & Long-acting anticholinergics
3. Combination short-acting beta2-agonists + anticholinergic in one inhaler
• e.g. Atrovent beta (Ipratropium bromide 0.5mg + fenoterol hydrobromide
1.25mg/4ml
4. Combination long-acting beta2-agonist + anticholinergic in one inhaler

79. COPD MEDICATIONS
5. Methylxanthines
Sustained release theophylline preparations e.g. Neulin
6. Inhaled corticosteroids
e.g. Beclomethasone; Beclate; Budesonide; Fluticasone propionate; Ciclesonide;
Budeflam/ Inflammide; Flixotide
7. Combination long-acting beta2-agonists + corticosteroids in one inhaler
e.g. budesonide plus formoterol; fluticasone plus salmeterol (Seretide)
8. Systemic corticosteroids
9. Phosphodiesterase-4 inhibitors – roflumilast

80. 4. ASTHMA
• Asthma is a chronic inflammatory disorder of the airways which develops because
of a genetic predisposition and environmental factors e.g. allergens, respiratory
tract infection, pollution
• Asthma is a disease characterized by recurrent attacks of breathlessness and
wheezing, which vary in severity and frequency from person to person.
• intermittent wheeze, tight chest, cough, dspnoea

81. ASTHMA
• Management
• Bronchospasm: aerosol
bronchodilators
• Bronchial oedema: corticosteroids
• Excessive mucus secretion: improve
hydration, mucolytics

82. ASTHMA: TREATMENT
• Corticosteroids : CORNERSTONE of asthma therapy. Useful for control of
inflammation.
• Beta 2 adrenoreceptor agonists: for bronchodilatation.
• Long acting beta 2 – agonists (laba) e.g. budesonide plus formoterol; fluticasone
plus salmeterol= Seretide
• Leukotriene receptor antagonists eg montelukast (singulair), zafirlukast(accolate);
• Sustained release theophyllins: theophylline is a bronchodilator with very modest
anti-inflammatory properties.

83. 5. PULMONARY OEDEMA
• Fluid in/around alveoli, small airways
• Causes
• Left heart failure
• Toxic inhalants
• Aspiration
• Drowning
• Trauma

84. PULMONARY OEDEMA
• Signs/Symptoms
• Laboured breathing
• Coughing
• Rales, rhonchi, crackles
• Wheezes
• Pink, frothy sputum
• Increased swelling in the extremities – pedal oedema
• Hypertension

85. PULMONARY OEDEMA
• Look out for pedal oedema and ascites, RUQ tenderness/hepatomegaly
• By time crackles can be heard, fluid has:
• Leaked out of capillaries
• Increased diffusion space between capillaries and alveoli
• Swollen alveolar walls
• Begun to seep into alveoli
• Listen to lower lobes through the back.
• Crackles heard higher in the lungs as condition worsens
• In severe cases, watery sputum, often with a pink tinged, will be coughed up.

86. PULMONARY OEDEMA
• Management
• Place the patient in a full fowlers position
• High concentration O2
• Assist ventilation
• Be prepared to suction
• Diuresis
• Treat underlying condition

87. PULMONARY OEDEMA
• Medications
• Lasix 40 mg IV (80 mg or more as indicated)
• Morphine Sulfate 2 mg IV slowly
• Nitroglycerin 0.4 mg sl - maximum 3 doses
• Albuterol aerosol bronchodilator (nebulize)
• Consider CPAP
• Medications and CPAP are to be administered simultaneously
• CPAP and medications must be discontinued if the blood pressure falls < 100
mmHg

88. 6. PULMONARY EMBOLISM
• Clot from venous circulation
• Passes through right side of the heart
• Lodges in pulmonary circulation
• Shuts off blood flow past part of alveoli

89. PULMONARY EMBOLISM
• Associated with: Inflammation, Hypercoagulable state and Stasis. e.g.
• Prolonged bed rest or immobilization
• Casts or orthopaedic traction
• Pelvic or lower extremity surgery
• Phlebitis – inflammation of a vein
• Sudden Dyspnoea + No Readily Identifiable Cause = consider Pulmonary
Embolism

90. PULMONARY EMBOLISM
• Signs/Symptoms
• Dyspnoea / tachypnoea
• Cyanosis
• Acute pleuritic pain
• Haemoptysis
• Hypoxia

93. PULMONARY EMBOLISM
• Treatment
• LMW heparin
• Oral anticoagulation with warfarin – Aim for INR of 2 –3
• Clot fragmentation by pulmonary artery catheter / interventional radiology
• Embolectomy in massive PE
• Duration of anticoagulation
• Temporary risk factors 4-6/52
• Idiopathic 3-6/12
• May require lifelong anticoagulation

94. 7. PLEURAL EFFUSION
• Collection of fluid outside the lung
• Caused by irritation, infection, or cancer
• Signs & symptoms:
• Dyspnoea
• Decreased breath sounds over effected area
• Positional comfort

95. PLEURAL EFFUSION
Causes include:
• Congestive heart failure
• Kidney failure
• Infection
• Malignancy
• Pulmonary embolism
• Hypoalbuminemia
• Cirrhosis
• Lung cancer
• Trauma

96. PLEURAL EFFUSION
• Transudate is usually composed of ultrafiltrates of plasma due to an imbalance in
vascular hydrostatic and oncotic forces in the chest (heart failure, cirrhosis).
• Exudate is typically produced by inflammatory conditions (lung infection, lung
cancer). Exudative pleural effusions are usually more serious and difficult to treat.

97. TREATMENT OF PLEURAL EFFUSION
• Treatment of pleural effusion is based on the underlying condition and whether
the effusion is causing severe respiratory symptoms
• Diuretics and other heart failure medications are used to treat pleural effusion
caused by congestive heart failure or other medical causes.
• A malignant effusion may also require treatment with chemotherapy, radiation
therapy or a medication infusion within the chest
• Traumatic cause may require intercostal drain
• Infectious causes requires treatment of the infection e.g. antibiotics and anti-TB
drugs

98. 8. PNEUMOTHORAX
• Definition: Air in the pleural space
• Primary – no associated lung disease (subpleural bleb)
• Secondary – associated lung disease
• (typically fibrosis or emphysema)
• Small – visible rim of <2cm
• Large – visible rim of ≥2cm

99. ASPIRATION VS CHEST DRAIN

100. TENSION PNEUMOTHORAX
• Intrapleural pressure exceeds atmospheric due to one-way valve effect –results in
low venous return, low cardiac output, and low BP
• Patient rapidly distressed –sweating, cyanosis, increased HR, increased RR,
EMD/PEA arrest
• Not dependent on the size of the pneumothorax
• Treatment:
• Cannula of at least 4.5cm length in 2ndICS MCL
• Then Chest Drain

101. 9. HAEMOPTYSIS
• Haemoptysis is the coughing up of blood or blood-stained mucus from the
bronchi, larynx, trachea, or lungs.
• This can occur with lung cancer, infections such as tuberculosis, bronchitis, or
pneumonia, and certain cardiovascular conditions.
• Haemoptysis is considered massive at 300 mL
• Haemoptysis greater than 1,000 mL per 24 hours in the presence of malignancy
carries a mortality rate of 80 percent.
• Therefore, massive haemoptysis warrants a more aggressive, expedient approach.

102. HAEMOPTYSIS

103. HAEMOPTYSIS
• Evaluation of the “ABCs” (i.e., airway, breathing, and circulation) is the initial step.
• The goals of management are threefold:
• bleeding cessation,
• aspiration prevention, and
• treatment of the underlying cause.

104. 10. CARBON MONOXIDE INHALATION
• Odourless, colourless, tasteless
• Binds 200 times faster to haemoglobin than O2
• Signs and Symptoms
• Headache
• Seizures
• Vomiting
• Chest pain
• Confusion
• Initially cyanosis / near death cherry red lips and nail beds

105. CARBON MONOXIDE INHALATION
• Treatment
• High flow oxygen
• Hyperbaric oxygen therapy

106. OTHER TOXIC INHALANTS
• Pathophysiology
• Damage depends on water solubility of toxic gas.
• Highly water-soluble gases react with moist mucous membranes.
• Causes upper airway swelling and irritation
• Less water-soluble gases get deep in lower airway.
• More damage over time
• Management
• Immediate removal from contact with gas
• Provide 100% oxygen or assisted ventilation.
• If exposure is to slightly water-soluble gases, patients may have acute dyspnea hours
later

107. 11. RESPIRATORY FAILURE
• Respiratory failure is a clinical condition that happens when
the respiratory system fails to maintain its main function which is gas exchange,
in which PaO2 lower than 60 mmHg and/or PaCO2 higher than 50 mmHg
• Type 1(hypoxemic) respiratory failure: in which PaO2 < 60 mmHg with normal or
subnormal PaCO2
• Type 2 (hypercapnic) respiratory failure: in which PaCO2 > 50 mmHg.

108. RESPIRATORY FAILURE

109. RESPIRATORY FAILURE
TREATMENT / MANAGEMENT
• This includes supportive measures and treatment of the underlying cause.
• Supportive measures which depend on depending on airways management to
maintain adequate ventilation and correction of the blood gases abnormalities
• Correction of Hypoxemia
• The goal is to maintain adequate tissues oxygenation, generally achieved with an
arterial oxygen tension (PaO2) of 60 mm Hg or arterial oxygen saturation (SaO2)
about 90%.
• Correction of hypercapnia and respiratory acidosis
• This may be achieved by treating the underlying cause or providing ventilatory
support.

110. RESPIRATORY FAILURE : COMMON INDICATIONS
FOR MECHANICAL VENTILATION
• Apnoea with respiratory arrest
• Tachypnoea with respiratory rate >30 breaths per minute
• Disturbed conscious level or coma
• Respiratory muscle fatigue
• Hemodynamic instability
• Failure of supplemental oxygen to increase PaO2 to 55-60 mm Hg
• Hypercapnea with arterial pH less than 7.25

111. 12. HYPERVENTILATION SYNDROME
• Occurs when people breathe in excess by increasing rate and/or depth of
respiration
• Releases more carbon dioxide than normal
• Results in alkalosis
• Triggered by emotional distress or panic: hysterical hyperventilation or
hyperventilation syndrome
• Causes numbness in hands, feet, and mouth
• Ultimately leads to carpopedal spasm
• Symptoms often cause more hyperventilation.

112. HYPERVENTILATION SYNDROME
• Tachypnoea
• Dyspnoea
• Chest pain
• Numbness or tingling in the fingers, toes and around lips.
• Carpal/Pedal spasms
• Dry mouth
• Light-headedness

113. HYPERVENTILATION SYNDROME
• Emotional stress, some medications and trauma can cause hyperventilation
syndrome
• Treatment
• Calm patient
• Oxygen
• Discharge
• May need referral to psychologist

114. HYPERVENTILATION SYNDROME
• Treatment may include:
• Sedation
• Psychological support:
• Breathing exercises, breathing with the patient
• Distraction techniques e.g.
• Having the patient count to two between breaths, Having the patient sing
a song

115. THANK YOU FOR LISTENING