4. Some definitions
Trepopnoea :Breathlessness when lying on one side as a
result of ipsilateral pulmonary disease . Causes are dilated
cardiomyopathy, pleural effusion.
Orthoponea : Breathlessness when lying flat. Ex : Left
Ventricular Failure, diaphramatic weakness, massive
pleural effusion, huge ascitis, any severe lung disease.
Platypnoea : Breathlessness on sitting up. Ex : right to left
shunt, ASD, or large intra pulmonary shunt, pericardial
effusion, liver cirrhosis.
PND : Breathlessness that wakes the patient from sleep. Ex
: Left Ventricular failure. Bronchial Asthma
5. PATIENT FEELING
Chest
tightness
Asthma
CHF
Air hunger
.urge to
breath
CHF
PE,,
asthma,
pulmonary
fibrosis
COPD
In ability to
get a deep
breath
ASTHMA
COPD
FIBROSIS
Heavy .rapid
breath
SEDENTARY
ANY
OTHER
CAUSES
Increase
work or
effort to
breath
COPD
ASTHMA
CHEST WALL
OR
NEUROMUS
CULAR
6. pathophysiology
• MECHANISMS OF DYSPNEA
• Respiratory sensations are the consequence of interactions
between the
• efferent, or outgoing, motor output from the brain to the
ventilatory
• muscles (feed-forward) and the afferent, or incoming,
sensory input
• from receptors throughout the body (feedback) as well as
the integrative
• processing of this information that we infer must be
occurring
• in the brain
7. Sensory Afferents
• Chemoreceptors in the carotid bodies and medulla
• are activated by hypoxemia, acute hypercapnia, and acidemia.
• Stimulation of these receptors and of others that lead to an increase
• in ventilation produce a sensation of “air hunger.” Mechanoreceptors
• in the lungs, when stimulated by bronchospasm, lead to a sensation of
• chest tightness. J-receptors, which are sensitive to interstitial edema,
• and pulmonary vascular receptors, which are activated by acute
• changes in pulmonary artery pressure, appear to contribute to air
• hunger. Hyperinflation is associated with the sensation of increased
• work of breathing, an inability to get a deep breath, or an unsatisfying
• breath. Metaboreceptors, which are located in skeletal muscle, are
• believed to be activated by changes in the local biochemical milieu of
• the tissue active during exercise and, when stimulated, contribute to
• breathing discomfort.
8.
9.
10. Receptors involved in mechanism of
dyspnea
1) J receptors – alveolo-capillary junction
• Stimulated by pulmonary congestion ,oedema,
micro emboli.
• Responsible for rapid shallow breathing
2) Stretch receptors – thoracic cage & lung
3) Chemoreceptors - carotid arteries, aorta &
reticular substance of medulla
Stimulated by hypoxia, excess of CO2, decrease
in PH
4) Receptors in the respiratory muscle – immediate
cause of appreciation of dyspnea
14. • It is a normal symptom of heavy exertion
• Normal pregnancy (around 2/3rd )
• Metabolic acidosis
• Pain
• Trauma
• Neuromuscular disorders
• Functional (anxiety, panic disorders, hyperventilation)
• Chemical exposure
• Obesity
• Psychogenic
15. ACUTE SEVERE DDX
*Acute pulmonary oedema
*Acute severe asthma
*Acute exacerbation of COPD
*Pneumothorax
*Pulmonary embolus
* Cardiac tamponade
• Inhaled foreign body (especially in the child)
• Laryngeal oedema (e.g. anaphylaxis)
• Metabolic acidosis (e.g. diabetic ketoacidosis, lactic
• acidosis, uraemia, overdose of salicylates, ethylene
• glycol poisoning)
16. history
• HISTORY
• Orthopnea is a common indicator
• of congestive heart failure (CHF),
• Nocturnal dyspnea suggests CHF or asthma. Acute, intermittent
• episodes of dyspnea are more likely to reflect episodes of
myocardial
• ischemia, bronchospasm, or pulmonary embolism, while chronic
• persistent dyspnea is typical of COPD, interstitial lung disease, and
• chronic thromboembolic disease. Information on risk factors
25. examination
• PHYSICAL EXAMINATION
• Inability of the patient to speak in full sentences before
• stopping to get a deep breath suggests a condition that leads to
• stimulation of the controller or impairment of the ventilatory pump
• with reduced vital capacity. Evidence of increased work of breathing
• (supraclavicular retractions; use of accessory muscles of ventilation;
• and the tripod position, characterized by sitting with the hands
• braced on the knees) is indicative of increased airway resistance or
• stiffness of the lungs and the chest wall. When measuring the vital
• signs, the physician should accurately assess the respiratory rate and
• measure the pulsus paradoxus); if the systolic pressure
• decreases by >10 mmHg, the presence of COPD, acute asthma, or
• pericardial disease should be considered.
26. GENERAL EXAM
• During the general examination,
• signs of anemia (pale conjunctivae), cyanosis, and cirrhosis
• (spider angiomata, gynecomastia) should be sought. Examination
• of the chest should focus on symmetry of movement; percussion
• (dullness is indicative of pleural effusion; hyperresonance is a sign
• of emphysema); and auscultation (wheezes, rhonchi, prolonged
• expiratory phase, and diminished breath sounds are clues to disorders
• of the airways; rales suggest interstitial edema or fibrosis).
• paradoxical movement of the abdomen: inward motion during inspiration
is
• a sign of diaphragmatic weakness, and rounding of the abdomen
• during exhalation is suggestive of pulmonary edema. Clubbing of
• the digits may be an indication of interstitial pulmonary fibrosis
27. Cardiovascular examination
Elevated neck veins, extra heart sound (S3 gallop
rhythm), and fluid retention - congestive heart
failure.
Elevated neck veins, pulsus paradoxus, a
pericardial knock, pericardial rub, and the
Kussmaul's sign - Constrictive pericarditis and
effussion
An irregular or fast heart beat - a tachyarrhythmia
or atrial fibrillation.
A loud S2 -PAH
A systolic heart murmur- acute valvular
insufficiency, mechanical valve malfunction.
28. Respiratory examination
Pursed lip breathing - COPD.
Stridor -upper airway obstruction
A barrel chest - emphysema and cystic fibrosis.
Hoarseness - in laryngitis, laryngeal tumours, vocal cord paralysis.
The trachea may deviate
Unilateral dullness to percussion.
Hyper-resonance
Subcutaneous emphysema - pneumomediastinum
B.p
Hypotension, tachycardia, and tachypnea : acute pulmonary edema , ARDS
Hypertension in a dyspnoeic patients:
hypertension-related diastolic heart failure with pulmonary oedema, hyperthyroidism, or
phaeochromocytoma
Pulsus paradoxus - asthma, COPD, cardiac tamponade
29. INVESTIGATION
• CHEST IMAGING
• a chest radiograph should be obtained. The lung volumes should be
• assessed: hyperinflation indicates obstructive lung disease, whereas
• low lung volumes suggest interstitial edema or fibrosis, diaphragmatic
• dysfunction, or impaired chest wall motion. The pulmonary
• parenchyma should be examined for evidence of interstitial disease
• and emphysema. Prominent pulmonary vasculature in the upper
• zones indicates pulmonary venous hypertension, while enlarged
• central pulmonary arteries suggest pulmonary arterial hypertension.
• An enlarged cardiac silhouette suggests dilated cardiomyopathy
• or valvular disease. Bilateral pleural effusions are typical of CHF
• and some forms of collagen-vascular disease. Unilateral effusions
• raise the specter of carcinoma and pulmonary embolism but may
• also occur in heart failure. CT of the chest is generally reserved for
• further evaluation of the lung parenchyma (interstitial lung disease)
• and possible pulmonary embolism.
30.
31. INVESTIGATION
• LABORATORY STUDIES
• electrocardiography to seek evidence of ventricular hypertrophy
and prior myocardial infarction.
• Echocardiography is indicated when systolic dysfunction,
• pulmonary hypertension, or valvular heart disease is suspected.
• Bronchoprovocation testing is useful in patients with intermittent
• symptoms suggestive of asthma but normal physical examination
• and lung function; up to one-third of patients with the clinical
• diagnosis of asthma do not have reactive airways disease when
• formally tested. Measurement of brain natriuretic peptide levels
in
• serum is increasingly used to assess for CHF in patients presenting
• with acute dyspnea but may be elevated in the presence of right
• ventricular strain as well.
32.
33. GRADE 1 –Dyspnoea only with unusual
exertion.
GRADE 2 –Dyspnoea on doing ordinary
activity
GRADE 3 –Dyspnoea on doing less than
ordinary activity.
GRADE 4 –Dyspnoea at rest.
NYHA SCALE
34. How to deal with Emergent causes
emergent
p.edema p.emboli c.tamponade
Acute
asthma
Tension
pneumot
horrax
Acute
COPD
35. asthma
• Definition. A disease characterized by inflammatory
hyperreactivity of the respiratory tree to
• various stimuli, resulting in reversible airway
obstruction. A combination of mucosal inflammation,
• bronchial musculature constriction, and an excessive
secretion of viscous mucus-causing
• The mediators are histamine, bradykinin, leukotrienes
(LTs) C, D, and E, and prostaglandins (PGs) E2, Cells are
the mast cells, lymphocytes, and eosinophils. leading
to bronchoconstriction and vascular congestion.
38. 'cough-variant asthma‘
Nocturnal asthma
triggered by medications.
1...aspirin ????? how
2..β- adrenoceptor antagonists (β-blockers), even
when administered topically
3..(NSAIDs
4..oral contraceptive pill,
5..cholinergic agents
6..prostaglandin F2α
39. Signs and Symptoms and investigation.
• In a mild attack, slight tachypnea, tachycardia,
prolonged expirations, wheezing.
• In a severe attack, use of accessory muscles of
respiration, diminished breath sounds, loud wheezing,
hyper-resonance
Poor prognostic factors include fatigue, diaphoresis,
pulsus paradoxus (>20 mm Hg), inaudible breath
sounds, decreased wheezing, cyanosis, and
bradycardia.
Making a diagnosis of asthma
clinical history plus FEV1
40.
41. Acute severe asthma
•PEF 33-50% predicted (< 200 L/min)
•Respiratory rate ≥ 25/min
•Heart rate ≥ 110/min
•Inability to complete sentences in breath
Life threatening
1•PEF < 33% predicted (< 100 L/min
2•SpO2 < 92% or PaO2 < 8 kPa (60 mmHg)Normal or raised PaCO2
Cliniclly Silent chest ,Cyanosis, Feeble respiratory effort,
Bradycardia or arrhythmias Hypotension ,Exhaustion ,Confusion
,Coma
•CPR TO KEEP IT CLINICAL ,,,,RESPIRATORY ARREST ,,,3P
..(PH.PaO2.Paco2)
42.
43.
44. COPD is “airflow limitation that is not fully
reversible. progressive and associated with an
abnormal inflammatory response of the lungs to
noxious particles or gases ”
The 'blue bloaters‘ :
low PaO2 & high PaCO2.
They are cyanosed , but not breathless & may develop
cor pulmonale
Supplemental O2 should be given with caution
The 'pink puffers‘:
increase in the alveolar ventilation , a near normal
PaO2 & normal or low PaCO2 .
breathless but not cyanosed ,,.type 1 respiratory failure
45.
46.
47.
48. The diagnosis requires objective demonstration of
airflow obstruction by spirometry and is
established when the post-bronchodilator FEV1 is
less than 80% of the predicted value and
accompanied by FEV1/FVC < 70%.
Measurement of lung volumes provides an
assessment of hyperinflation
Pulse oximetry may prompt referral for a
domiciliary oxygen assessment if less than 93%.
HRCT is likely to play an increasing role in the
assessment of COPD, as it allows the detection,
characterization and quantification of emphysema
and is more sensitive than a chest X-ray at
detecting bullae.
49.
50.
51. Exacerbation (Acute Setting Treatment). considered acute worsening of the patient’s
respiratory symptoms
(increased dyspnea, increased sputum volume, production of purulent sputum) that
necessitates
a change in medications.
The most common causes of COPD exacerbation are viral lung infections. Other
precipitating
causes that should be sought out are 1..bacterial infections
2..heart failure,
3..myocardial ischemia,
4..pulmonaryembolism,
5..lung cancer,
6..esophageal reflux disease,
7..and medications (e.g., beta-blockers).
52. MANAGEMENT
• Initial Management
• 1. Measure O2 saturation.
• 2. ABG determination
• 3. Chest x-ray pulmonary
• infiltrates = pneumonia
• pulmonary edema = heart failure as the cause of the
exacerbation.
• 4. Spirometry is not helpful in COPD exacerbation not
correlate well with the severity of the exacerbation.
• 5. theophylline level.Drugs like erythromycin, cimetidine, and
ciprofloxacin cause toxicity.
• 6..tests of initial evaluation of COPD CBC
• (elevated WBCs and polycythemia); ECG atrial fibrillationthat
mayexacerbate COPD).
• 7. hypercapnia or hypoxemia with severe symptoms, should be
hospitalized.
• 8.. Assisted ventilition
53. Specific Therapy
• 1. Oxygen supplementation.
• 2. Inhaled bronchodilators are the most effective medications (the drugs
of choice, use both beta-agonists (albuterol) and anticholinergics
(ipratropium) simultaneously.
• 3. Systemic corticosteroids ..I.V or orally because the efficacy
• is similar. The equivalent of 60 mg prednisone
• As starting dose and is usually continued for 2 weeks.
• patients who have a severe exacerbation start with IV
• methylprednisolone (then change to oral prednisone as they improve.
• 4. Antibiotics seem to be beneficial in COPD exacerbations despite
“normal” chest Radiograms ..macrolides (clarithromycin, azithromycin
fluoroquinolones (levofloxacin, moxifloxacin), cephalosporins and
amoxicillin clavulanate.
• 5. no benefit to using IV aminophylline. However, if the patient is using
• theophylline on a chronic basis it should be continued during the
exacerbation because abrupt discontinuation may worsen symptoms.
• 6. Always avoid opiates
65. Spontaneous Primary
No evidence of overt lung disease. Air escapes from the lung into the
pleural space through rupture of a small subpleural emphysematous bulla
or pleural bleb, or a pleural adhesion
Secondary
Underlying lung disease, most commonly COPD and TB; also seen in
asthma, lung abscess, pulmonary infarcts, bronchogenic carcinoma, all
forms of fibrotic and cystic lung disease
Traumatic
Iatrogenic (e.g. following thoracic surgery or biopsy) or chest wall injury
66.
67.
68. • If the rim of air is < 2cm and the patient is not short of breath then
discharge should be considered & CXR after 2 weeks.
• Otherwise aspiration should be attempted
• if this fails (defined as > 2 cm or still short of breath) then a chest drain
should be inserted
Primary Pneumothorax
69. Secondary Pneumothorax
All patients should be admitted for at least 24 hours
• if the pneumothorax is less the 1cm then the BTS
guidelines suggest:
giving oxygen (high flow O2) and
admitting for 24 hours
• If the patient is 50 years old and the rim of air is > 2cm
and/or The patient is short of breath then
o A chest drain should be inserted.
70.
71.
72. • Surgical pleurodesis is recommended in all patients
following a second pneumothorax and should be
considered following the first episode of secondary
pneumothorax if low respiratory reserve makes
recurrence hazardous
73. Cardiac Tamponade
Definition Cardiac tamponade occurs when fluid accumulation in the finite
serous pericardial space causes an increase in pressure, with subsequent
cardiac compression and hemodynamic compromise.
74. Treatment : Aspiration of a pericardial effusion is indicated for
diagnostic purposes or for the treatment of cardiac tamponade.
A few millilitres of fluid aspirated through the needle may be
sufficient for diagnostic purposes but pericardial drainage is
needed for symptom relief.
76. Pulmonary embolism
triad of pleuritic chest pain, dyspnea and haemoptysis.
Pulmonary embolism can be difficult to diagnose as it can present with virtually any
cardiorespiratory symptom/sign depending on its location and size.
So, which features make pulmonary embolism more likely?
The relative frequency of common clinical signs is shown below:
Tachypnea (RR>16/min) - 96%
Crackles - 58%
Tachycardia (HR>100/min) - 44%
Fever (>37.8C) - 43%
It is interesting to note that the Well's criteria for diagnosing a PE use
tachycardia rather than tachypnea
77. LMWH or fondaparinux should be given initially after a PE is diagnosed.
An exception to this is for:
Patients with a massive PE where thrombolysis is being considered.
In such a situation unfractionated heparin should be used
• A vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the
diagnosis
the LMWH or fondaparinux should be continued for at least 5 days or
until INR is 2.0 or above for at least 24 hours, whichever is longer, i.e.
LMWH or fondaparinux is given at the same time as warfarin until the INR
is in the therapeutic range
Warfarin should be continued for at least 3 months.
treatment
78. Psychogenic cause of dyspnea
(signs: no cyanosis, no heart or lung signs, carpopedal spasm)
Treatment: anxiolytics, paper bag technique (increases needed
CO2 and reduces symptoms, but may worsen the condition
sometimes)
79. In children, the possibility of inhalation of a foreign body
or acute epiglottitis should always be considered.
80.
81. Foreign body---- Heimlich maneuver, supportive measures(oxygen,
pulse oximetry), racemic epinephrine as temporary measure until
bronchoscopy can be done, bronchoscopy
Acute epiglottitis---- intubation (difficult if laryngeal edema present) ,
antibiotics.
treatment
82. A.Immediate ABC Management :
Emergency Airway Management
Emergency Breathing Management
Emergency Circulation Management
B. Obtain initial vital signs :
Temperature, Blood Pressure, and Pulse
Respiratory Rate and Oxygen Saturation
83.
84. Immediately triage unstable patients :if
1. Hypotension
2. Altered Level of Consciousness
3. Hypoxia (decreased Oxygen Saturation)
4. Arrhythmia
5. Stridor or other signs of upper airway
obstruction
6. Unilateral breath sounds or other
Pneumothorax signs
7. Respiratory Rate >40 breaths per minute
8. Accessory muscle use with retractions
9. Cyanosis
85. D. Initial management of acute distress
1. Obtain Intravenous Access (when appropriate)
2. Administer High Flow Oxygen
3. Evaluate and treat Hypoxia if present
4. Consider Pulmonary Embolism Diagnosis
E. Initiate disease specific management
1. Emergency Management of Acute severe Asthma
2. COPD Exacerbation Management
3. Acute Pulmonary Edema Management
4. Tension Pneumothorax -Needle Thoracentesis
86.
87. A 24-year-old man presents to the Emergency department
with a two hour history
of pleuritic chest pain. He denies feeling breathless, with
oxygen saturations of 96%
on air.
A chest x ray is performed and an observant CT1
recognises a small apical
pneumothorax, which when measured is 1.8 cm.
Accordingly to current guidelines, what intervention should
be undertaken?
What`s your action ??
88. This patient has a small pneumothorax with no
known underlying lung disease and
as such can be classed as a spontaneous
pneumothorax. According to current BTS
guidelines, if the patient is not breathless and
the rim of air is less than 2 cm they can
be considered for early discharge and repeat
chest x ray in two weeks.
89. A 19-year-old man with recurrent admissions to hospital for exacerbations of his
asthma attends the Emergency department with a short history of increasing
breathlessness and cough.
On examination he is obviously dyspnoeic and wheezy and becoming exhausted.
His
respiratory rate is 16 breaths per minute, his HR is 125 bpm (sinus tachycardia)
and
his PEF is 30% predicted.
An arterial blood gas is taken and the results are as follows:
pH 7.43 (7.36 - 7.44)
pO2 7.3 kPa (11.3 - 12.6)
pCO2 5.2 kPa (4.7 - 6.0)
What`s the severity of asthma in this case ?
90. A life threatening exacerbation of asthma can be
diagnosed based on one of the
following:
• PEF <33% best or predicted
• SpO2 <92%
• PaO2 <8 kPa
• Normal PaCO2 (4.6-6.0 kPa)
• Silent chest
• Cyanosis
• Poor respiratory effort
• Arrhythmia
• Exhaustion, altered conscious level.
91. An 87-year-old man was admitted to the Emergency department with a
two hour
history of sharp central chest pain and breathlessness.
One week ago he noticed his left leg had become swollen, but had
decided not to
consult medical advice. Apart from essential hypertension, for which he
was taking
bendroflumethiazide, he had no other medical conditions. He was a
lifelong nonsmoker.
On clinical examination he was dyspnoeic at rest with a respiratory rate
of 28 breaths
per minute. His blood pressure was 90/60 mmHg, pulse 110 beats per
minute and
regular with oxygen saturations of 86% on room air. Auscultation of his
chest
revealed a loud second heart sound over the right second intercostal
space.
What`s the diagnostic test you shoud send the patient for?
What`s your treatment ?
92. A 14-year-old boy with a known nut allergy was admitted to the
Emergency
department following the accidental ingestion of a pistachio nut biscuit.
On examination he had audible stridor and looked peripherally shut
down. His blood
pressure was 70/50 mmHg, oxygen saturations 86% on room air and
respiratory rate of 26 breaths per minute. His pulse was feeble
What is the most appropriate immediate management?
93. Anaphylactic shock requires urgent
treatment with adrenaline, which is absorbed
at a
faster rate intramuscularly than
subcutaneously.