Respiratory Insufficiencies

By

Dr. Sumaira Iqbal

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Learning Objectives

• By the end of lecture student should be able to

– Elaborate abnormalities of ventilation & perfusion

– Define and explain hypoxia, cyanosis, dyspnea,hypercapnia, hypocapnea and asphyxia

– Summarize the effects of pneumonia, COPD, emphysema and asthma

– Identify and interpret findings of respiratory acidosis and alkalosis

– Differentiate obstructive and restrictive disease and variation of their volumes and capacities

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Respiratory Insufficiency

• Inadequate O2 supply to the tissues due to:

i. Inadequate alveolar ventilation

ii. Abnormalities of O2 & CO2 diffusion through Respiratory membrane.

iii. Decreased O2 transport from lungs to the tissues.– Alveolar Hypoventilation

– Airway resistance

– Tissue resistance

– Compliance of Lungs & chest wall.

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Hypoxia

• Low or reduced O2 conc. or PO2.

• Deficiency of O2 in Insp. air or Gas mixture or Low content or pressure of O2 in transport system i.e. Lungs, Blood, Tissues

Hypoxemia:

• Deficient blood oxygenation i.e. Low Bl. PO2 and low Oxy Hb.

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Hypoxia

Types of Hypoxia:

1. Hypoxic Hypoxia

2. Anemic Hypoxia

3. Stagnant or Ischemic Hypoxia

4. Histotoxic Hypoxia

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Hypoxic Hypoxia

• PO2 of arterial blood is reduced. i.e

– Less O2 content in blood

– Less O2 saturation of blood

• Most common form seen clinically

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Hypoxic Hypoxia

Causes:

i. Pulmonary Diseases in which gas exchange apparatus fails:

a) Decreased Respiratory Membrane Diffusion

• Pulmonary Fibrosis

• Pulmonary Edema

b) Ventilation – perfusion imbalance.

c) Hypoventilation due to Airway Resistance.

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Hypoxic Hypoxia

ii. Inadequate oxygenation of Lungs.

a) Atmospheric Hypoxia (Hypobaric/HA Hypoxia)

b) Hypoventilation in Neuromuscular diseases.

iii. Shunts (Congenital Heart diseases).

Right to Left shunt

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Anemic Hypoxia

• Art. PO2 is normal

• But Hb. Conc. is decreased to carry O2

Causes:

a) Anemia

b) Increased Conc. of Met hemoglobin

Effects:

(compensatory Mechanisms)

• Increase Circulation time

• Shift of O2 dissociation curve to Rt.

• Hyperventilation/breathlessness

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Stagnant Hypoxia

• Slowing of Bl. flow to the tissues.

• But there is normal PO2 & normal Hb conc.

Causes:

i. Generalized circulatory insufficiency

e.g: cardiac failure

ii. Local circulatory insufficiency

e.g: Atherosclerosis

Venous thrombosis

iii. Tissue edema.

iv. Severe polycythemia

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Histotoxic Hypoxia

• Inability of tissues to use O2

• Despite normal PO2 & normal Hb conc.

Causes:

i. Cyanide Poisoning

ii. Beriberi

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Effects of Hypoxia

• Severe Hypoxia– Brain is affected first

– Sudden loss of consciousness.

• Less severe Hypoxia:– Depressed mental activity

– Anorexia, Nausea, Vomiting

– Tachycardia

– Hypertension

– Hyperventilation

– Reduced capacity of muscles for work

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Hypoxia Features Hypoxic

hypoxia Anemic hypoxia

Stagnant hypoxia

Histotoxichypoxia

1. PO2 in arterial blood Reduced Normal Normal Normal

2. Oxygen carrying capacity of blood

Normal Reduced Normal Normal

3. Velocity of blood flow

Normal Normal Reduced Normal

4. Utilization of oxygen by tissues

Normal Normal Normal Reduced

5. Efficacy of oxygen therapy

100% 75% <50% Not Useful13

Dyspnea

• Sensation of ‘shortness of breath’

• Difficult or Labored Breathing.

• Uncomfortable awareness of need for increased breathing.

• Dyspnea occurs when demand of ventilation is out of proportion to the patient’s ability to respond to that demand.

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Dyspnea

• Factors Responsible: (For the sensation)i. Abnormalities of respiratory Gases & pH of body fluids.ii. Amount of work performed ‘to ensure Adequate ventilation’iii. State of mindTypes:• Exertional• Orthopnea• Paroxysmal Nocturnal Dyspnea• Emotional

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Causes of Dyspnea

I. Altered respiratory Mechanics:

– Air flow Resistance

– Lung stiffness

– Kyphoscoliosis

II. Lung reflexes

– Pulmonary Edema

– Pulmonary Embolism

– Low Cardiac output

III. Central Mechanism

– Anxiety

IV. Others

– Anemia

– Uremia

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Hypercapnea

• Excess CO2 in the body fluids.

• Markedly increase PCO2 leads to respiratory acidosis.

• Increase PCO2 in body fluids initially stimulates respiration.

• It is not necessary that conditions leading to hypoxia should also cause hypercapnia except:

– Hypoventilation

– Circulatory deficiency

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Hypercapnea

• Retention of larger amounts of CO2 leads to depression of C.N.S:

– Confusion

– Diminished sensory acuity

– Coma

– respiratory depression

– DEATH

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Hypercapnea

• When alveolar PCO2 rises above 60-75 mmHg

– Dyspnea (Air Hunger)

• When alveolar PCO2 rises above 80-100 mmHg

– Lethargy, semi comatose

• When alveolar PCO2 rises above 100-150 mmHg

– Anesthesia & DEATH

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Hyperventilation

• Hyperventilation blows out CO2 and PCO2 decreases (Hypocapnea).

• If alveolar Vent. rate is doubled----alveolar PCO2 is halved.

• If alveolar PCO2 decreases to 20-25 mmHg:

– Dizziness,

– Numbness and

– Tingling in extremities

– Hypotension

– Cerebral vasoconstriction.

• If alveolar PCO2 decreases to 15-20 mmHg: Tetany

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Hypocapnia & Tetany

• Decreased PCO2 in body fluids

• As a result of hyperventilation leading to cerebral Ischemia causes:

– Light-headedness

– Dizziness

– Parasthesia

• Respiratory alkalosis: pH 7.5-7.6

• Increased HCO3-

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Hypocapnia & Tetany

• Decreased Ionized calcium ---- Tetany

• Tetany is characterized by:

Increased neuromuscular excitability, muscular tension, spontaneous twitching and sustained involuntary muscular contractions “Carpopedal Spasm”.

Mechanism:

• Hyperventilation → respiratory alkalosis →Hypocalcaemia (deciCa) & Increased bound Ca++ leads to Tetany

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Asphyxia

• A condition produced by acute occlusion of the air way

• Causes

– Acute Epiglottitis

– Laryngeal Edema

– Upper airway obstruction: Hanging & Strangulation

– Inhaled foreign body

– Drowning

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Effects of Asphyxia

• Acute Hypercapnea and Hypoxia together

• Pronounced stimulation of Respiration with violent respiratory efforts.

• Increased heart rate & B.P

• Increased Catecholamine secretions --- Myocardial fibrillation

• Decreased Blood pH

• Eventually respiratory efforts cease,

• Heart slows down --- DEATH within 4 – 5 minutes.

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Cyanosis

• Bluish purple discoloration of skin, mucus membranes & nail beds resulting from high conc. of deoxyhemoglobin.

When appears ?• Conc. of DeoxyHb is more than 5 gm/100 ml of blood. i.e Arterial

blood O2 saturation decreases to 83% with normal Hbconcentration

Sites:• Nail Beds, Mucus membranes• Lips, Ear lobes• Fingers (when skin is thin)

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Cyanosis

Factors Affecting:

• Total amount of Hb in blood

• Degree of Hb unsaturation

• State of capillary circulation.

• Types of Cyanosis:

–Central

–Peripheral

• Dusky discoloration of Met-Hb: CYANOSIS (SLAT-BLUE Colour)

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Oxygen Therapy

• Objective:

i. To increase PO2 and relieve hypoxemia

ii. To increase the quantity of O2 carried in solution form.

Uses:

• In premature infants

• CO Poisoning

• Shock

• Myocardial Infarction

• Hypoxic Hypoxia

• Respiratory Insufficiency & severe respiratory failure.

• Cyanide Poisoning 27

Static Lung Volumes

• Lung volumes that are not affected by the rate of air movement in and out of the lungs are termed static lung volumes.

• Examples

• Volumes VT (tidal volume), IRV (inspiratory reserve volume), ERV (expiratory reserve volume), residual volume

• Capacities: Inspiratory capacity, Vital capacity, Total lung capacity, Functional residual capacity

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Dynamic Lung Volumes

• Lung volumes that depend upon the rate at which air flows out of the lungs are termed dynamic lung volumes

• Examples

– Forced vital capacity,

– Forced expiratory volume,

– Maximum ventilation volume,

– Peak expiratory flow

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Obstructive vs. Restrictive

• Obstructive disorders: Obstructive disorders are characterized by a reduction in airflow, particularly the FEV1 and the FEV1/FVC.

• Restrictive disorders: Restrictive disorders are characterized by a reduction in lung volume, specifically a TLC < 80% of the predicted value.

• Diagnosis and differentiation– pulmonary function test via spirometry

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CausesObstructive Lung Disease

• Chronic obstructive pulmonary disease (COPD) includes emphysema and chronic bronchitis

• Asthma

• Bronchiectasis

• Cystic fibrosis

Restrictive Lung Disease

• Interstitial lung disease, such as idiopathic pulmonary fibrosis

• Sarcoidosis, an autoimmune disease

• Obesity

• Scoliosis

• Neuromuscular disease, such as muscular dystrophy or amyotrophic lateral sclerosis (ALS)

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Changes in Lung Volumes and Capacities in Obstructive and Restrictive Lung Diseases

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Pathophysiology

Obstructive Lung Disease

• Alveoli is expanding but it is unable to deflate or slowly.

• Volumes in the lungs increase in obstructive diseases,

• People with obstructive lung disease have shortness of breath due to difficulty exhaling all the air from the lungs. Because of damage to the lungs or narrowing of the airways inside the lungs, exhaled air is less and comes out more slowly than normal.

Restrictive Lung Disease

• Alveoli deflates but is unable to inflate properly due to either lung scarring, fibrosis, or extra-parenchymal problems.

• Volumes in the lungs greatly decreased in restrictive cases.

• Stiffness of the lung (most common), chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion.

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Pneumonia

• Inflammatory condition of lung in which alveoli are filled with fluid and blood cells

• Bacterial pneumonia– pneumococci

• Infection in the alveoli →pulmonary membrane becomes inflamed and porous fluid → fluid, RBCs & WBCs leak in to alveoli

• Infected alveoli filled with fluid and cells

• Infection spreads

• Large areas of the lungs even whole lung, become consolidated

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Pneumonia

Effects

• Reduction in surface area of respiratory membrane

• Decreased ventilation-perfusion ratio

• Cause hypoxemia and hypercapnia

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Emphysema

• Causes:

– Chronic infection--inhaling smoke irritate the bronchi and bronchioles

– Paralysis of cilia--protective mechanisms of the airways—nicotine

• Mucus cannot be removed, excess mucus exacerbates the condition

• Alveolar macrophages are inhibited

• The infection, mucus & inflammatory edema cause obstruction of airways

• Air becomes entrapped in alveoli

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Emphysema

• Effects

1. Increases airway resistance– increase work of breathing

2. Loss of alveolar walls– decrease diffusion capacity

3. Abnormal VA/Q ratio few alveoli are not ventilated others are not perfused

4. Pulmonary hypertension– damage to alveolar wall leads to damage to pulmonary capillaries

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Asthma• Spastic contraction of smooth muscle in bronchioles, which obstructs

the bronchioles and results in difficulty in breathing

• Cause: contractile hypersensitivity of bronchioles in response to foreign substances in the air

• In youngers age group allergic hypersensitivity like plant pollens

• In older always hypersensitivity to non-allergenic types of irritants like smog

• Allergic asthma: allergic person have abnormally high levels of IgEantibodies

• Antibodies are mainly attached to mast cells in lung Interstitium in bronchioles and small bronchi

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Asthma

• Patient breathes in pollen, it reacts with mast cell attached antibodies and release

– Histamine

– Slow-reacting substance of anaphylaxis (mixture of leukotrienes)

– Eosinophilic chemotactic factor

– Bradykinin

• These chemicals cause

– Localized edema in the walls of small bronchioles

– Secretion of thick mucus into bronchiolar lumens

– Spasm of bronchiolar smooth muscle results in airway resistance

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Asthma

• Bronchiolar diameter becomes reduced during expiration than inspiration due to bronchiolar collapse– dyspnea

Effects :

1. Greatly reduced maximum expiratory rate

2. Reduced timed expiratory volume

3. FRC and RV increases during acute asthmatic attack—difficulty in expiring air from lungs

4. Chest cage becomes permanently enlarged– barrel chest

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Respiratory control

• Second line of defense

• 50% control of pH regulation - by lung

• 50% - 75% effective in reversing H+ conc. to normal (not 100%)

• Response in 3-12 minutes

• Role of lungs - alteration in breathing rate

– Minimum ventilation = pH drops to 6.95

– Maximum ventilation = pH rises to 7.63

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Respiratory control

• Continually formed during metabolic processes

• From cells reach lungs to be exhaled

• 1.2mol/L of dissolved CO2 impart PCO2 of 40mmHg

• Metabolism increases CO2 formation increases

• If pulmonary ventilation increases PCO2 decreases

• CO2 H2 CO3 H+ions pH

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Respiratory Regulation

• ↑Hydrogen ions→↑ alveolar ventilation→↓ CO2

• Decreased CO2 will decrease H ions

• Returns pH back to normal

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THANK YOU

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