Discussion of common respiratory symptoms, diagnosis and treatment.

1. RESPIRATORY DISTRESS
PGI Karen Cas

2. Common Respiratory Symptoms
 Dyspnea (with assoc hypoxia and hypercapnia)
 Wheezing
 Cough
 Persistent hiccups
 Cyanosis
 Pleural effusions

3. Dyspnea
 Subjective feeling of difficult, labored or uncomfortable
breathing, which patients often describe as “shortness of
breath”, “breathlessness”, or “not getting enough air”

4. Terminologies
 Rapid breathing; it may
or may not be associated
with dyspnea
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

5. Terminologies
 Rapid breathing; it may
or may not be associated
with dyspnea
 a. TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

6.  Essentially
hyperventilation and is
defined as minute
ventilation in excess of
metabolic demand.
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA
Terminologies

7.  Essentially
hyperventilation and is
defined as minute
ventilation in excess of
metabolic demand.
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA
Terminologies

8.  Dyspnea in recumbent
position
Terminologies
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

9.  Dyspnea in recumbent
position
Terminologies
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

10. Terminologies
 Opposite of
orthopnea, dyspnea in
upright position. It
results from abdominal
wall muscular tone
and, in rare cases, from
right-to-left intracardiac
shunting, as occurs from
a patent foramen ovale
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

11. Terminologies
 Opposite of
orthopnea, dyspnea in
upright position. It
results from abdominal
wall muscular tone
and, in rare cases, from
right-to-left intracardiac
shunting, as occurs from
a patent foramen ovale
 a.TACHYPNEA
 b. ORTHOPNEA
 c. PAROXYSMAL
NOCTURNAL DYSPNEA
 d. TREPOPNEA
 e. PLATYPNEA
 f. HYPERPNEA

12. Terminologies
 Orthopnea that awakens
the patient from sleep
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

13. Terminologies
 Orthopnea that awakens
the patient from sleep
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

14. Terminologies
 Dyspnea associated with
only one of several
recumbent positions. It
can occur with unilateral
diaphragmatic
paralysis, with ball-valve
airway obstruction, or
after surgical
pneumonectomy
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

15. Terminologies
 Dyspnea associated with
only one of several
recumbent positions. It
can occur with unilateral
diaphragmatic paralysis,
with ball-valve airway
obstruction, or after
surgical pneumonectomy
 a.TACHYPNEA
 b. ORTHOPNEA
 c.PAROXYSMAL
NOCTURNAL DYSPNEA
 d.TREPOPNEA
 e.PLATYPNEA
 f. HYPERPNEA

16. DYSPNEA: Clinical features
 To identify imminent respiratory failure, evaluate for:
 TACHYPNEA
 TACHYCARDIA
 STRIDOR
 USE OF ACCESSORY REPIRATORY MUSCLE
 INABILITY TO SPEAK
 AGITATION or LETHARGY
 DEPRESSED CONSCIOUSNESS
 HYPERCAPNIA
 PARADOXICAL ABDOMINAL WALL MOVEMENT

17. DYSPNEA: Differentiating cardiac
from pulmonary causes of
dyspnea
 CONGESTIVE HEART FAILURE
 PE: S3 gallop, jugular venous distension
 CXR: pulmonary venous congestion, interstitial edema,
alveolar edema
 B-type Natriuretic Peptide (BNP) <80picograms/ml –
useful in ruling out cardiac causes

18. DYSPNEA:
Laboratoy/Radiographic
Evaluation
 Pulse oximetry – rapid but insensitive screening test for
disorders of gas exchange, and results may be normal in
acute dyspnea
 ABG – more sensitive for detecting impaired gas
exchange , but results may also be normal in acuted
dyspnea
 CXR – may indicate general category of primary disease:
infiltrate, effusion and pneumothorax
 Bedside spirometric analysis before and after
bronchodilator therapy – used to dx and treat dyspnea
resulting from asthma or COPD
 Others: ECG, hemoglobin level

19. DYSPNEA: Treatment
 Primary goal: MAINTENANCE OF AIRWAY and
OXYGENATION WITH PaO2 >60mmHg and/or arterial
oxygen saturation (SaO2) ≥90%
 OPIOIDS / BENZODIAZEPINES

20. Differential diagnosis of
consequence: DYSPNEA
Most common causes Most immediately life
threatening
Obstructive airway diseas
(asthma, COPD)
Upper airway obsruction:
foreign body, angioedema,
hemorrhage
Heart failure/cardiogenic
pulmonary edema
Tension pneumothorax
Ischemic heart disease: UA,
MI)
Pulmonary embolism
Pneumonia Neuromuscular weakness:
myasthenia gravis, guillain-
barre syndrome, botulism
Psychogenic Fat embolism

22. HYPOXEMIA
 HYPOXIA - Insufficient delivery of oxygen to the tissues
 HYPOXEMIA – abnormally low arterial oxygen tension;
(PaO2 <60mmHg)
 Relative hypoxemia – arterial oxygen tension is lower
than expected for a given level of inhaled oxygen
 Degree can be assessed by calculating the alveolar
arterial (A-a) oxygen partial pressure gradient, which
measures the efficacy of oxygen transfer from the lungs to
the circulation

23. HYPOXEMIA: PATHOPHYSIOLOGY
 1. HYPOVENTILATION
PaCO2
NORMAL
GRADIENT

24. HYPOXEMIA: PATHOPHYSIOLOGY
 2. RIGHT TO LEFT SHUNT
 Pulmonary consolidation
 Pulmonary atelectasis
 Vascular malformations
A-a O2 gradient
PaCO2
HALLMARK: FAILURE OF ARTERIAL O2
LEVELS TO INCREASE IN RESPONSE TO
SUPPLEMENTAL OXYGEN

25. HYPOXEMIA: PATHOPHYSIOLOGY
 3. VENTILATION/PERFUSION (V/Q) MISMATCH
A-a O2 GRADIENT
Hypoxemia improves
with supplemental
oxygen

26.  4. DIFFUSION IMPAIRMENT
A-a O2 gradient
Hypoxemia improves with
supplemental oxygen

27.  5. LOW INSPIRED OXYGEN
NORMAL A-a O2 gradient
Hypoxemia improves with
supplemental oxygen

28. HYPOXEMIA PATHOPHYSIOLOGY
SUMMARY
Pathophysiology Remarks
Hypoventilation PaCo2, П A-a O2 gradient
R – L shunt A-a O2 gradient
small improvement w/ O2 supp
V/Q mismatch A-a O2 gradient
Improves with O2 supp
Diffusion impairment A-a O2 gradient
Improves with O2 supp
Low inspired oxygen П A-a O2 gradient
Improves with O2 supp

29. HYPOXEMIA: DIAGNOSIS
 ABG analysis
 Pulse oximetry
 Clinically acceptable pulse oximetry saturation readings
(>90%) do not exclude hypoxemia
 If Hb is in a state which it is unable to bind to oxygen (e.g.
Methemoglobin or Carboxyhemoglobin), pulse oximetry
analysis not only overestimates the oxygen saturation but
also reflects a diminshed response to any supplemental
oxygen

30. HYPOXEMIA: TREATMENT
 Ensuring a patent airway
 Providing supplemental oxygenation with a goal of
maintaining a PaO2 >60mmHg

31. Case
 CC: Difficulty of Breathing
 HPI: 74 year old female with 5 days history of
cough, yellowish phlegm, persistent fever and back pain.
Self medicatedwith paracetamol, and noticed no changes
and experienced difficulty of breathing so she sought
medical consultation
 PE: VS: 110/60mmHg, 35.7 C, 78bpm, 26cpm
 Auscultation reveals bilateral diminished vesicular breath
sounds, rhonchi and late inspiratory crackles (are heard)
in the area of the right mid-anterior and right mid-lateral
lung fields.
 IMPRESSION???
 WHAT MECHANISM???

32. HYPERCAPNIA
 Exclusively caused by alveolar hypoventilation and
defined as PaCo2 >45mmHg
 Causes:
 Rapid shallow breathing
 Small tidal volumes
 Underventilation of the lung
 Reduced respiratory drive
HYPERCAPNIA IS NEVER
A RESULT OF INCREASED
CO2 PRODUCTION

33. HYPERCAPNIA:
PATHOPHYSIOLOGY
 ALVEOLAR HYPOVENTILATION can result from:
 1. decrease in respiratory rate
 2. decrease in tidal volume
 3. increase in dead space

34. HYPERCAPNIA: CLINICAL
FEATURES
 Depends on the absolute value of PaCO2 and its rate of
change
 Acute elevations: INCREASED INTRACRANIAL PRESSURE
(headache, confusion, lethargy)
 Severe cases: SEIZURE, COMA, CV COLAPSE
 Chronic hypercapnia may be well tolerated

35. HYPERCAPNIA: DIAGNOSIS
 ABG analysis
 Serum bicarbonate – inc in acute setting
 FORMULA:
ACUTE HYPERCAPNIA : (1:10)
HCO3 increases about 1 meq/L for each
increase of 10mmHg in PaCO2
CHRONIC HYPERCAPNIA: (3.5:10)
HCO3 increases 3.5 meq/L for each 10mmHg
increase in PaCO2

36. HYPERCAPNIA: TREATMENT
 Increase minute ventilation, both rate and tidal volume
 Ensuring patent airway
 May require noninvasive ventilation, mechanical
ventilator or a respiratory stimulant (doxapram)
 Hypercapnia with CNS symptoms and with
neuromuscular disease should be HOSPITALIZED

38. WHEEZING
 Adventitious lung sounds best described as
“musical”, produced by airlfow through the central and
distal airways

39. WHEEZING: CLINICAL FEATURES
 Usually associated with ASTHMA and other obstructive
pulmonary diseases characterized by BRONCHIAL
OBSTRUCTION caused by muscular spasm and
inflammation
 Upper airway obstruction causes STRIDOR, loudest at
larynx
PATIENTS WITH SEVERE AIRFLOW
OBSTRUCTION MAY NOT WHEEZE

40. WHEEZING: DIAGNOSIS
 Bedside spirometry
 Obtained maximum value should be compared to
predicted normal values for age, gender and height
 PEF or FEV1 valuesn >80% of the predicted value – N
 50%-80% = mild airflow obstruction
 25% - 50% = moderate
 <25% = severe
 ABG analysis

41. WHEEZING DIFF DX
Upper airway
angioedema Foreign body
Infection: croup, epiglotittis,
tracheitis
Lower airway
Asthma Transient airway
hyperreactivity
broncholitis COPD
Foreign body
Cardiovascular
Cardiogenic pulmonary
edema
Pulmonary embolism (rare)
Noncardiogenic pulmonary
edema
Psychogenic

42. WHEEZING: TREATMENT
 Aerosols of B-agonists and/or anti-cholinergics
 Systemic or inhaled steroids

44. COUGH
 Protective reflex for clearing secretions and foreign
debris from the tracheobronchial tree
 ACUTE COUGH – lasting <3 weeks, self limited
 SUBACUTE COUGH – lasts 3-8 weeks, most commonly
postinfectious
 CHRONIC COUGH – present for >8 weeks

45. COUGH: CLINICAL FEATURES
 Rhinorrhea
 Sinusitis
 Pharyngitis
 Laryngitis
 Productive cough – hallmark of acute bronchitis

46. Chronic cough
 Most common causes:
 SMOKING
 UPPER AIRWAY COUGH SYNDROME (formerly postnasal
discharge)
 ASTHMA
 GERD
 ACE inhibitor or ARB therapy

47. COUGH: DIAGNOSIS
 CXR in patients with purulent sputum and/or fever
 Spirometry in presence of airflow obstruction
 Pertussis – nasopharyngeal swabs or serologic testing
(Bordetella pertussis)

48. COUGH: TREATMENT
 ACUTE:
 Antitussives
 Menthol and pungent spices (pepper, msutard, garlic,
radish, onions)
 For intractable cough paroxysms: nebulize with 4cc of
1% or 2% preservative-free lidocaine (40 or 80 ml)
 Pertussis: macrolide or trimethoprim-sulfamethoxazole x
7days

49. COUGH: TREATMENT
 SUBACUTE & CHRONIC:
 Reduce exposure to lung irritants and discontinue ACEi,
ARB and B blockers
 Treat for postnasal discharge with oral 1st gen
antihistamine/decongestant with or without nasal steroid
 Evaluate and treat for asthma
 Obtain chest and sinus imaging if not already done
 Evaluate and treat GE reflux
 Refer the patient for specialist evaluation, for CT of the
chest and evaluation for pulmonary and nonpulmonary
causes of cough, or bronchoscopy

50. ACUTE or CHRONIC?
 1. Cough due to pertussis?
ACUTE
Pertussis in adults has been
associated with acute cough
lasting 1-6 weeks

51. HICCUPS
 hiccups/singultus – involuntary spastic contraction of the
inspiratory muscles; no specific protective purpose

52. HICCUPS: CLINICAL FEATURES
 Benign and self limited or persistent and intractable
 BENIGN HICCUPS – initated by gastric distention from
food, drinking or air
 PERSISTENT HICCUPS – result of injury or irritation to a
branch of the vagus or phrenic nerves

53. HICCUPS: DIAGNOSIS
 Persistence during sleep – ORGANIC CAUSE
 Resolutiong during sleep – PSYCHOGENIC CAUSE
 Although this distinction is not absolute
 External auditory canal should be examined carefully for
foreign body
 CXR to evaluate intrathoracic pathology
 Fluoroscopy to evaluate unilateral versus bilateral
diaphragmatic movement

54. HICCUPS: TREATMENT
 PHYSICAL MANEUVERS
 Remove foreign body from ear
 Swallow a teaspoon of sugar
 Sip ice water
 Drink water quickly
 Concept: stimulating the pharynx will block the vagal
portion of the reflex arc and abolish the hiccups
 For intractable hiccups: CHLORPROMAZINE &
METOCLOPRAMIDE

55. ACUTE or CHRONIC?
 Hiccups caused by alcohol intoxication?
ACUTE
Alcohol ingestion appears to
precipitate hiccups by
relaxing the relationship
between inspiration and
glottic closure, making it
easier for other stimuli to
trigger the reflex.

56. CYANOSIS
 Bluish color of the skin and mucous membranes that
results from an increased amount of reduced Hb or Hb
derivatives.
 CENTRAL CYANOSIS – cyanosis of mucous membranes
and tongue and is due to inadequate pulmonary
oxygenation or an abnormal Hb
 PERIPHERAL CYANOSIS – cyanosis of fingers or
extremities from vasocontriction and diminished
peripheral blood flow.

57. CYANOSIS: DIAGNOSIS
 Pulse oximetry
 ABG analysis with co-oximetry – gold standard

58. CYANOSIS: TREATMENT
 Supplemetal oxygen
 Underlying disorder should be treated
 Failure to improve suggests shock, abnormal Hb, or
pseudocyanosis

59. CENTRAL or PERIPHERAL?
 Reduced cardiac output will lead to what kind of
cyanosis?
PERIPHERAL
When cardiac output is
reduced, cutaneous
vasoconstriction occurs
because blood flow is
preferentially distributed to
more vital areas.

60. PLEURAL EFFUSION
 Result from fluid accumulating in the potential space
between the visceral and parietal pleurae
 Most common causes are:
 CHF
 PNEUMONIA
 CANCER

61. PLEURAL EFFUSION:
PATHOPHYSIOLOGY
 EXUDATIVE EFFUSIONS result from pleural disease,
usually inflammation or neoplasia, that results in active
fluid secretion or leakage with high protein content
 TRANSUDATIVE EFFUSIONS result from imbalance
between hydrostatic and oncotic pressures. This
imbalance results in the production of an ultrafiltrate
with low protein content

62. PLEURAL EFFUSION: CLINICAL
FEATURES
 May be clinically silent or come to a detection from
either:
 Symptoms of an underlying disease
 Increase in volume of the effusion with the production of
dyspnea
 Development of inflammation and associated pain with
respiration
 PE: percussion dullness and decreased breath sounds

63. PLEURAL EFFUSION: DIAGNOSIS
 150-200ml of pleural fluid (adult) – to produce signs on
upright chest radiograph
 Supine CXR – only hazy appearance of pleural fluid in
the posterior pleural space
 CT scan
 Ultrasound
 Diagnostic thoracentesis

64. Pleural fluid diagnostic test
 DETECTION OF EXUDATIVE P.E.
 1 or more of the ff:
 Pleural fluid/serum PROTEIN ratio >0.5
 Pleural f/s LDH ratio >0.6
 Pleural fluid LDH > 2/3 of upper limit for serum LDH

65. P.E.: TREATMENT
 (+) dyspnea at rest -> thoracentesis with drainage of
1.0 to 1.5L of fluid
 Acute drainage of larger volume has been associated
with reexpansion pulmonary edema, thus avoided.
 (+) pleural empyema – drainage with large-bore
thoracostomy tubes
 Diuretic therapy – resolves >75% of effusions due to
CHF within 2-3 days

66. THANK YOU!!!!! 