resp distress

1. APPROACH TO
RESPIRATORY DISTRESS
Dr.Shreeraj

2. DEFINITIONS
• Dyspnea- Feeling of difficult, laboured or uncomfortable breatheing, SOB
• Tachypnea-Rapid Breathing
• Orthopnea- Dyspnea in recumbent position ( LVF, COPD, Diaphrgm Paralysis)
• PND- Orthopnea which awakens patient to upright posture
• Trepopnea- dyspnea on lying to one side (single lung destroyed/damaged)
• Platypnea-Dyspnea in upright posture ( L-R shunt/ loss of abdominal tone)
• Hyperpnea- Increased minute Ventilation

3. CLINICAL FEATURES
• Asoociated with several condition
• Signs- Use of accessory muscles-SCM, Sternoclavicular, Intercostals, Nasal Flare
• Inability to complete 1 sentence, Lethargy, Agitation, Depressed consciousness.
• S3 Gallop, Elevated Jvp, Pulmonary congestion with cardiomegaly in Xray- Cardiac

4. LAB FINDINGS
• Req- History, Physical examn, Pulse ox, ECG, POCUS Cxray
• ABG- more sensitive than Pulse ox
• POCUS- differentiate b/w- Pl eff,Pneumo, Cardiac Tamponade, Pulmonary
consolidation, Pulmo Edema, IV volume status
• BNP and Ddimer normal D-dimer excludes PE with low probability.

5. TREATMENT
• A- Maintain airway
• B- Oxygenation PaO2<60, SaO2- <90

7. HYPOXIA AND HYPOXEMIA
• Hypoxia-Insufficient arterial O2 content, insufficient delivery to tissues
• O2 delivery dependent on Cardiac out put, Hb, and O2 availibity in alveoli
• Relative Hypoxemia- Low Arterial O2 tension for expected given level of Inhaled O2
• P(A-a)O2- Relative Hypoxemia- Alveolar-arterial O2 Gradient
• P(A-a)O2= 2.5+0.21(age in years)(± 11)
• Normal- <10mmhg in young healthy patient.

8. HYPOXIA
1. Hypoventilation – Increased Pco2 and normal P(A-a)O2
2. R-L shunt- increased A-a O2 gradient. Failure of arterial O2 levels to increase in
response to supplemental O2.
3. V-Q Mismatch- PE,Pneumonia, Asthma, COPD, - Increased A-a O2 gradiet,
Hypoxemia improves with O2.
4. Diffusion Impairment-A-a O2 gradient will be increased.Hypoxia improves with
O2 administration
5. Low atmospheric O2.

9. COMPENSATION
• Increased Minute Ventilation
• Pulmonary artery Vasoconstriction- counter productive in diffuse lung disease
• Incread Cardiac output- increased heart rate
• Chronic- Increased Hb, decreased O2 demand in Tissue
• Acute compensatory mechanism activates usually when PaO2 <60mmhg and Fail
when below PaO2<20mmhg

10. CLINICAL FEATURES
• Agitation , Headache, Somnolence, coma, Seizure.
• Tachypnoea and hyperventilation
• Pulse OX <90
Rx
• Oxygen Supplementation.

11. HYPERCAPNIA
• Alveolar hypoventilation- PaCo2->45mmhg.

12. PATHOPHYSIOLOGY
• Tidal volume reaching alveoli- Ta =Vt(tidal Volume) – Td(Dead Space )
• Alveolar Hypoventilation can increase in decreased RR, Decreased Tidal Volume,
Increased Dead Space
• Medullary Chemoreceptors- Increase rate and Depth.-Highly Sensitive
• CNS lesion, Toxins, Thoracic Cage disorder, Neuromuscular disorders can cause
reduced drive/or low rate/depth
• COPD/ILD caused increased dead space.

13. CLINICAL FEATURES
• Acute increase- Increased Icp- Headache,confusion, Lethargy, Seizure, Coma
• Extreme Increase- cardiovascular collapse
• Chronic Hypercapneia is well tolerated upto even 80mmhg

14. DIAGNOSIS
• Etco2 or ABG
• 10mmhg increase in PCO2- 1 Meq increase in HCO3
• 10mmhg increase in PCO2 c/c – 3.5 meq Increase in Hco3

15. TREATMENT
• Increase Minute Ventilation- RR/ TV or both
• NIV PPV/Mech Ventilation/ Antidote for toxins/respiratory Stimulant
• Admission depends on Clinical Condition, and Persisting respiratory Acidosis even
with Maximum OP therapy.

16. COUGH
• Protective reflex to clear the airway.
• Irritant receptors in larynx and tracheobronchial tree. Travel to medulla via,
phrenic and vagus and forceful expiration against closed glottis then sudden
opening of glottis causing clearing of secretotion.
• Acute cough< 3wk – urti/bronchial infections
• Subacute- 3-8 wk-post infectious with viral bronchitis causing hypersensitive
bronchus/bronchial secretion.

17. • Chronic Cough >8 weeks.
• Chronic bronchitis/asthma/gerd/ACE inhibitor
• Smoking induced c/c bronchitis worse in morning, asthma worse at night and early
morning.
• Gerd- associated with heartburn
• ACE- Brdykinin, Substance P.- 1 week to 1 year after start and upto 4 weeks after
stopping.

18. DIAGNOSIS AND TREATMENT
• CXRAY
• Spirometry and flow volume loops
• Blood culture and other blood inv
RX
• Demulescents, Menthol, Spices antitussive effect
• Naproxen reduces cough in bronchitis
• Neb with 1-2% lidocaine. 4ml
• C/C- opioid antitussive, dextromethorphan, gaba/pregaba

19. HICCUPS
• Involuntary spastic contraction of inspiratory muscles., with no specific purpose
• Afferent- vagus, phrenic, sympathetic plexus of thorax
• If cause is identified- inflammation,stimulation of these nerves.
• >48 hr- intractable.
• Benign are usually due to gastric distention.
• Rarely- hair in External auditory canal pressing on tympanic membrane.
• Drugs- dexa/ Chemo

21. DIAGNOSIS AND TREATMENT
• History- Sleep – Psychogenic
• External Auditory Canal
• Drug- inhibit reflex arc

23. CYANOSIS
• Bluish discoloration of skin and mucus membranes increased reduced hemoglobin or
hb derivatives(>5mg/dl)
• Central- mucous membrane & tounge
• Peripheral tips of finger and toes

24. DIAGNOSIS AND TREATMENT
• Oxygenation after pulse ox (caution with Hb pathy, Carboxyhb)
• ABG is more accurate

25. PLEURAL EFFUSION
• Fluid bw parietal and visceral pleura
• Causes-HF, Pneumonia, Cancer, TB
• C.F- Breathlessness, Pain, dull percussion note, reduced breath sounds
• 150ml- 200ml required for xray to pickup.
• Ultra Sound can detect fluids at much lower levels.

27. • Thoracocentesis usually not done in cardiac failure, but if not resolving in 3-4 days
may be considered.
• Lights criteria is used for pleural fluid analysis

30. TREATMENT
• Thoracocentesis- 1-1.5l if dyspnea is present.
• Optimisation of medical therapy resolves 80% of effusions, due to heart failure
within 2 weeks.