PHYSIOLOGY LECTURE PRESENTATIONS BY - DR SHAHAB PhD, MD

Lecture – 9: Applied Aspects - I

Respiratory System

Physiology

ByDr. SHAHAB

SHAIKH••••••••••••••••••••••••••••••••••

PhD MD

Physiology lecture presentations by - DR SHAHAB PhD, MD

Respiratory System Physiology

Applied Aspects - I

Apnea Hypoxia Tachypnea Hypercapnea Hypocapnea Dyspnea Cyanosis O2 Toxicity CO Poisoning Atelectasis Asthma

Asphyxia Periodic

Breathing

Physiology lecture presentations by - DR SHAHAB PhD, MD

Applied Respiratory Physiology Diagnosis and treatment of most respiratory disorders depend

heavily on understanding the basic physiologic principles of

respiration and gas exchange.

Respiratory diseases may result from . . .

Inadequate ventilation

Abnormalities of diffusion through the pulmonary membrane

Abnormal blood transport of gases between the lungs and

tissues.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Apnea• Temporary cessation of breathing • Causes include: - reduced stimulation of resp. centre eg. voluntary hyperventilation - active inhibition of resp.centre or - during deglutition• Apnea time – breath holding time-40-60 sec after

a deep inspiration

Physiology lecture presentations by - DR SHAHAB PhD, MD

Apnea• Conditions when apnea occurs:

Voluntary apnea – arrest of breathing voluntarily; at the end, person forced to breathe

Deglutination Apnea – arrest of breathing during swallowing; occurs reflexly during pharyngeal stage of deglutination

Apnea after hyperventilation – during hyperventilation, PCO2 decreases, apnea ensues to increase PCO2 to normal, then normal breathing starts

Physiology lecture presentations by - DR SHAHAB PhD, MD

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Hypoxia • It is the failure of the tissues to receive adequate

quantity of oxygen.• Haldane : “ not only stoppage of the machine, but

also total ruin of the supposed machinery.”• The essential feature of hypoxia is cessation of

oxidative phosphorylation when mitochondrial PO2 falls below a critical level

• Anaerobic production of energy is insufficient and produces H+ & LACTATE which are not easily excreted and will accumulate

Physiology lecture presentations by - DR SHAHAB PhD, MD

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Hypoxia - Etiological Classification

• Hypoxic hypoxia

– ↓ PO2 of inspired air

– Pulmonary diseases which causes:• increased airway resistance

• decreased pulmonary compliance

• abnormal alveolar ventilation -perfusion ratio

• Diminished respiratory membrane diffusion

• Venous-arterial shunts (right to left cardiac shunt)

• Hypoventilation

Physiology lecture presentations by - DR SHAHAB PhD, MD

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Hypoxia - Etiological Classification• Anemic hypoxia

– Here the O2 delivery is reduced although PAO2 is normal.

– amount of Hb available to carry O2 is reduced.

– E.g. Anemia,

– CO poisoning

– Methemoglobinemia,

– Sulphemoglobinemia

Physiology lecture presentations by - DR SHAHAB PhD, MD

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• Stagnant hypoxia

– Due to reduced tissue perfusion

– General or local

– General eg ↓ cardiac output

– Local eg. Atheroma, embolism, vasoconstriction

• Histotoxic hypoxia

– Failure of the enzyme system in mitochondria to use the

delivered O2 leading to stoppage of aerobic metabolism.

– Eg. Cyanide poisoning

Hypoxia - Etiological Classification

Physiology lecture presentations by - DR SHAHAB PhD, MD

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Effect of Hypoxia

Physiology lecture presentations by - DR SHAHAB PhD, MD

Tachypnoea• this term denotes increased rate of breathing with no

change or even decrease in depth of breathing.It is seen:• In pathological conditions like -PULMONARY

CONGESTION and FEVER.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Hypercapnia• It is excess CO2 in body fluids• Retention of CO2 stimulates respiration• larger amounts of CO2 produces depression of CNS

causing: Confusion diminished sensory acuity eventually coma and death

• Occurs in ventilation-perfusion inequality, when alveolar ventilation is inadequate, also in febrile patients due to increased CO2 production

Physiology lecture presentations by - DR SHAHAB PhD, MD

Hypocapnia• It is decreased CO2 in body fluids• Occurs as a result of hyperventilation• Voluntary hyperventilation arterial PCO2 falls to about

15mm Hg while alveolar PO2 rises to 120-140mm Hg• Chronic hypocapnia seen in neurotic patients who

chronically hyperventilate

Physiology lecture presentations by - DR SHAHAB PhD, MD

Dyspnea• Difficult or labored breathing in which subject is

conscious of shortness of breath; mental anguish associated with inability to ventilate enough to satisfy demand for air1.physiological dyspnea [occurs during exercise

or at high altitudes]2.pathological dyspnea [occurs in patients with

hypoxic cardiopulmonary disorders or metabolic acidosis .

Physiology lecture presentations by - DR SHAHAB PhD, MD

Cyanosis• Bluish discoloration of skin due to excessive amounts of

deoxygenated Hb in skin blood vessels, especially in capillaries

• Deoxygenated Hb dark blue-purple colour• Appears when arterial blood contains > 5gm of

deoxygenated Hb every 100ml of blood

Physiology lecture presentations by - DR SHAHAB PhD, MD

Oxygen toxicity• O2 toxicity occurs due to the production of superoxide

anion (O2– ) which is a free radical and H2O2

• When 80-100% O2 administered for a period of 8hrs or more, respiratory passages are irritated causing: Substernal distress Nasal congestion Sore throat Coughing

Physiology lecture presentations by - DR SHAHAB PhD, MD

• continued inhalation for prolonged period causes damage to the lungs

• another extremely serious complication of O2 therapy is RETROLENTAL FIBROPLASIA seen in some premature infants with RDS who are treated with pure O2 for long periods.

Oxygen toxicity

Physiology lecture presentations by - DR SHAHAB PhD, MD

• Hyperbaric oxygen therapy [high pressure O2 therapy] results in a very high arterial pO2& increased amount of dissolved O2 in the plasma.

• -is used in some special circumstances like:• * cardiac surgeries• * carbon monoxide poisoning or • * treatment of anaerobic bacterial infections• -hyperbaric O2 therapy not only produces symptoms of upper respiratory

irritation but also causes:• muscle twitching• dizziness• convulsions and • coma.

Hyperbaric oxygen therapy

Physiology lecture presentations by - DR SHAHAB PhD, MD

CO poisoning

• Small amounts of carbon monoxide formed in body function as a chemical messenger in the brain

• Larger amounts causes poisoning reacts with Hb to form

carbonmonoxyhemoglobin (carboxyhemoglobin, COHb)

• COHb cannot take up O2 ; total Hb content remains unaffected

• Affinity for CO is 210 times more than that for O2

Physiology lecture presentations by - DR SHAHAB PhD, MD

CO poisoning

• Symptoms of CO poisoning: Headache Nausea Cherry-red colour of COHb visible in

the skin, nail beds, and mucous membranes

• Death results when 70-80% of circulating Hb is converted to COHb

Physiology lecture presentations by - DR SHAHAB PhD, MD

Atelectasis• Collapse of alveoli; atelectatic area

may be a small patch or a whole lung; some blood diverted from collapsed to better ventilated area

• Collapse of large part of lung causes appreciable decrease in lung volume; intrapleural pressure more negative and mediastinum pulled to the affected side

• Causes: Total obstruction of the airway Lack of surfactant in the fluids lining the

alveoli.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Asthma

• Characterized by spastic contraction of smooth muscle in the bronchioles, causing episodic or chronic wheezing, cough and a feeling of tightness of chest.

• Abnormalities present:Airway obstructionAirway inflammationAirway hyperresponsiveness

Physiology lecture presentations by - DR SHAHAB PhD, MD

Physiology lecture presentations by - DR SHAHAB PhD, MD

Asthma

• Functional residual capacity [FRC], residual volume [RV] of lung increases during acute attack due to difficulty expiring inspired air

• Over period of years chest cage enlarges forming “barrel chest”, both FRC and RV are permanently increased.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Physiology lecture presentations by - DR SHAHAB PhD, MD

Physiology lecture presentations by - DR SHAHAB PhD, MD

• there is reduction in: 1.tidal volume [TV] 2.vital capacity [VC] 3.FEV1 4.alveolar ventilation and 5.partial pressure of O2 in blood. 6.CO2 accumulates resulting in acidosis, dyspnea and

cyanosis.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Asphyxia• Impairment of ventilatory exchange

of oxygen and carbon dioxide; combined hypercapnia and hypoxia produced by occlusion of the airway.

• Chronic asphyxia- occurs in rt. Ventricular failure due to lung disease.

• Acute asphyxia -occurs in strangulation, acute tracheal obstruction [due to entry of food or due to choking] paralysis of diaphragm as in poliomyelities. It is dangerous need to be treated immediatetly otherwise death occur with in 5 mins.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Contd..

• Pronounced stimulation of respiration with violent respiratory efforts; blood pressure and heart rate rises sharply; blood pH drops.

• Eventually respiratory efforts cease, blood pressure falls and rate slows; cardiac arrest occurs in 4-5 minutes.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Periodic BreathingIt is the repeated sequence of apnoea

followed by respiration

Physiology lecture presentations by - DR SHAHAB PhD, MD

Types

Cheyne-Stokes respiration

Biot’s breathing

Physiology lecture presentations by - DR SHAHAB PhD, MD

Cheyne-stokes Respiration

The repeated sequence of gradual onset of apnoea followed by gradual onset of respiration.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Causes - Physiological

Voluntary hyperventilation

High altitude

During sleep in some normal individuals

Physiology lecture presentations by - DR SHAHAB PhD, MD

Heart failure

Brain damage

Uremia

Causes - Pathological

Physiology lecture presentations by - DR SHAHAB PhD, MD

Physio-clinical SignificanceHyperventilation due to any cause results in hypocapnia. The effects are:-

On Respiration:- Respiratory alkalosis i.e. increased pulmonary ventilation which occurs due to causes other than increase in arterial H+ concentration. This is because with increased pulmonary ventilation, CO2 is washed out, so alveolar and arterial PCO2 fall, as a result respiration slows down, CO2 gets retained restoring H+ concentration of blood towards normal.

Physiology lecture presentations by - DR SHAHAB PhD, MD

On CNS:- decrease in cerebral blood flow by 30% or more because of direct constrictor effect of hypocapnia on the cerebral vessel. The symptoms produced are due to cerebral ischaemia/hypoxia.

On CVS:- constrictor effect on peripheral blood vessels produces:a) Increase in cardiac output

b) Increase in systemic BP ( to slight degree due to simultaneously of VMC which tends to decrease the BP).

Physiology lecture presentations by - DR SHAHAB PhD, MD

Alkalaemic tetany:- hyperventilation, profuse vomiting or the excessive ingestion of sodium bicarbonate may cause Alkalaemic Tetany. This is because alkalosis (decrease in plasma H+) in these states causes more ionization of plasma proteins, providing more protein anions to bind with Ca2+.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Effects of Periodic Breathing1) Fall in arterial PCO2 causes severe

vasoconstriction of cerebral blood vessels, as a result cerebral blood flow decreases producing dizziness.

2) Hyperventilation leads to respiratory alkalosis, therefore, more ionisation of proteins occurs; protein anions bind more Ca2+ and ionised Ca2+ decreases in the body resulting in tetany.

Physiology lecture presentations by - DR SHAHAB PhD, MD

Biot’s BreathingThis is a type of periodic breathing in which

there are 3-4 cycles of normal respiration followed by abrupt onset of apnea and again abrupt onset of normal respiration. This cycle is repetitive.

Physiology lecture presentations by - DR SHAHAB PhD, MD

It is seen in . . .

Meningitis, andDiseases affecting the medullaIncreased intracranial pressure

PHYSIOLOGY LECTURE PRESENTATIONS BY - DR SHAHAB PhD, MD

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