Overall Summary

Respiratory Response to High Altitude

• Plus, increased:• No. of RBCs, diffusing capacity of the lungs, vascularity

of the peripheral tissues, ability of tissue cells to use O2 (despite low Po2)

Respiratory Response to High Altitude

• Hypoxemia causes hyperventilation• Hyperventilation causes decrease in Pco2 &

respiratory alkalosis (RA)• These 2 inhibit CNS respiratory centre (‘offsetting’ ++

drive of hypoxemia)

• Body’s solution: • Renal HCO3

- excretion increased – RA resolved (via increased excretion of CSF HCO3

-)• Hyperventilation now will not be ‘offset’ because now,

O2 is the drive* via PCR!

Acute Mountain Sickness

• Symptoms due to hypoxia and RA• Headache, fatigue, dizziness, nausea,

palpitations, and insomnia• Pulmonary & cerebral edema are serious• Prevention: Acclimatization• Treatment: Acetazolamide

Respiratory Response to Exercise

• CNS influences respiratory response• Anticipatory increase in ventilation at exercise onset

– Leads to an initial decrease in Pco2

– Afterwards, the increased Pco2 ‘matches’ the ventilation rate

Summary

Periodic Breathing

• Person breathes deeply (short interval) - then breathes slightly or not at all for an additional interval

• Cycle repeating itself over and over • Cheyne-Stokes breathing

» slowly waxing and waning respiration occurring about every 40 to 60 secs

Hypoxemia

Causes of Hypoxemia

Cause PaO2 A - a Gradient Supplemental O2 Helpful?High altitude (↓ PB; ↓ PIO2) Decreased Normal Yes

Hypoventilation (↓ PAO2) Decreased Normal Yes

Diffusion defect (e.g., fibrosis) Decreased Increased Yes

V/Q defect Decreased Increased Yes

Right-to-left shunt Decreased Increased Limited

Hypoxia & O2 therapy

• Decreased O2 delivery to the tissues• Causes:

• Inadequate oxygenation of blood in lungs (extrinsic reasons)» Oxygen deficiency in atmosphere» Hypoventilation (neuromuscular disorders)

• Disease of the lung itself» Abnormal V/Q » Damaged respiratory membrane» Decreased compliance etc

• Venous-to-arterial shunts (“right-to-left” cardiac shunts)

• Inadequate O2 transport to tissues by blood» Anemia or abnormal hemoglobin» General circulatory deficiency» Localized circulatory deficiency (peripheral, cerebral, coronary vessels)» Tissue edema

• Inadequate tissue capability of using O2» Cyanide poisoning» Vitamin-B deficiency (Beri-beri)

Hypoxia

• Hypoxic hypoxia • PO 2 of the arterial blood is reduced;

• Anemic hypoxia • Arterial PO 2 is normal but amount of Hb reduced

• Stagnant or ischemic hypoxia • Blood flow to a tissue is so low that adequate O2 is not

delivered (despite normal PO2 & Hb)

• Histotoxic hypoxia • Tissue cells cannot make use of the O2 supplied

Hypoxia

• Signs• Cyanosis• Tachypnea (rate) & Hyperpnea (depth)• Tachycardia

Respiratory Control Dysfunction

• Cheyne-stokes breathing• Biot’s breathing• Ondine’s curse• Sleep-Apnea syndromes

• Obstructed apnea• Non-obstructed (central) apnea

CLINICAL CASES

Nitrogen NarcosisRaptures of the Depth!

• At sea-level pressure, nitrogen has no significant effect on bodily function

• But at high pressures (deep sea diving) – varying degrees of narcosis

– Mild narcosis appear is about 120 feet (jovial, no-cares)

– At 150- 200 feet, diver becomes drowsy

– At 200 – 250 feet, strength wanes considerably, & diver often becomes too clumsy to perform the work required

– Beyond 250 feet, the diver usually becomes almost useless

Oxygen Toxicity

• When Po2 in blood rises above 100 mm Hg • Amount of O2 dissolved in blood increases markedly• Delivery of O2 to tissues increases

• Symptoms:• Nausea, muscle twitchings, dizziness, disturbances of

vision, irritability, & disorientation• Brain seizures – coma

• Oxygen free radical accumulation causes toxicity (superoxides hydrogen peroxide)*

Oxygen Toxicity

• Acute – Exposure to very high Po2 for prolonged periods of time– Symptoms develop as mentioned

• Chronic – Exposure to moderately high Po2 doesn’t lead to tissue symptoms– But lung passageway congestion, sore throat, substernal distress,

pulmonary edema, and atelectasis begin to develop*

• In infants with RDS O2 therapy leads to – Chronic condition characterized by lungs cycts & densities

(bronchopulmonary dysplasia) + retinopathy of prematurity (retrolental fibroplasia)

Hyperbaric O2 therapy

• Intense oxidizing properties of high-pressure oxygen (hyperbaric oxygen) can have valuable therapeutic effects

• Especially use in infectious conditions caused by organisms that thrive in anaerobic conditions

• Gas gangrene (clostridial organisms)• Also useful in decompression sickness, arterial gas

embolism, CO poisoning, osteomyelitis, and MI

CO2 toxicity

• At very high Pco2 – CO2 depresses respiratory centres

Decompression Sickness

• Nitrogen dissolves in body fluids• Nitrogen is not metabolized in body• Hence to remove it – one needs to exhale it!• In high pressure scenarios:

• Alveolar PN2 is high – so is tissue PN2

• High P in blood gases AND outside body maintains the dissolved state of N2 in tissues• Sudden drop in P may cause bubbles to form – escape

of N2 from tissues* (decompression)

Decompression Sickness• Symptoms are mostly due to bubble embolism

• Pain in joints (‘bends’)• CNS symptoms:

– Dizziness (5% cases)– Paralysis* or collapse and unconsciousness in 3% cases

• Respiratory symptoms (‘chokes’)– caused by massive numbers of microbubbles plugging lungs

capillaries ; » Leading to serious shortness of breath, severe pulmonary

edema & may be death

• Prevention– Divers to ascend slowly– Tank Decompression

Asthma• Disease of airway inflammation and airflow

obstruction • Characterized presence of intermittent symptoms:

– wheezing, – chest tightness, – shortness of breath (dyspnea), and – cough together with demonstrable bronchial hyperresponsiveness

• Pathophysiology – Airway resistance increases due to

» airway inflammation, » smooth muscle hyperresponsiveness, and » airway narrowing, » small-caliber peripheral airways are the site of increased

resistance » This is worsened by the superimposed mucus hypersecretion

and by any additional bronchoconstrictor stimuli

Asthma Contd..

• Pathophysiology– Airway obstruction occurs diffusely but not homogeneously– As a result, variability in V/Q mismatch occurs – Areas of low & high V/Q ratios exist – Low V/Q ratio regions - contributes to hypoxemia– Pure shunt is unusual in asthma – Arterial CO2 tension is usually normal to low (due to increased

ventilation seen with asthma exacerbations)– Hypercapnia - late and ominous sign!

Asthma – Symptoms & Signs– Cough– wheezing– Dyspnea & Chest tightness– Tachypnea and tachycardia – Pulsus paradoxus

• Hypoxemia • Hypercapnia and respiratory acidosis (severe asthma)• Obstructive defects by pulmonary function testing:

» Normal between attacks (mild asthma)» During attacks: Decreased FEV1, FEV1/FVC, peak expiratory flow

rates• Bronchial hyperresponsiveness

» 20% decrease in FEV1 in response to a provoking factor OR» 20% increase in the FEV1 in response to an inhaled

bronchodilating

COPD• Chronic bronchitis

– Productive cough for 3 months of the year for 2 consecutive years

– Productive cough– Wheezing– Inspiratory and expiratory coarse crackles – Tachycardia– Imaging: increased lung volumes with relatively depressed

diaphragms consistent with hyperinflation

• Pulmonary function tests: FEV1, FVC, and the FEV1/FVC – all reduced • Blood gases: hypoxemia is common (abnormal V/Q)

– Polycythemia present

COPD

• Emphysema – Abnormal permanent enlargement of the

airspaces distal to the terminal bronchioles, accompanied by destruction of their walls• Decreased breath sounds• Tachycardia• Imaging: hyperinflation• Pulmonary function tests: all reduced• Blood gases: may be normal (but exercise induces decreased Po2)• Polycythemia present

Clinical Scenarios

• Restrictive Lung Disease (Interstitial Lung Disease)– A category of extrapulmonary, pleural, or

parenchymal respiratory diseases that:• Restrict lung expansion • Decreased lung volume• Increased work of breathing• Inadequate ventilation and/or oxygenation • Pulmonary function test demonstrates a decrease in

the forced vital capacity

Non-Respiratory Functions of Lungs

• Immune• Acid base balance• Blood reservoir• Conversion of precursor molecules

Respiratory Function Tests

• Max. voluntary ventilation• Respiratory responses to CO2• Forced vital capacity• Diffusion capacity• FRC & VC• Blood gases