RESPIRATORY

SYSTEM

Physiology 2

Presented by: Dr. Shaimaa Nasr Amin

Lecturer of Medical Physiology

General Education Program

Part 2

GAS TRANSPORT

PO2= 105 mmHg

PO2= 40 mmHg

PO2= 100 mmHg

Oxygen transport by the blood

• O2 is transported in the blood in two forms:

1. Physically dissolved.

2. Attached in loose chemical combination with hemoglobin

(98%).

O2 in physical solution

• 0.3 ml/100 ml arterial blood and 0.13 ml/100 ml of venous

blood.

• The O2 in physical solution determines the PO2 in the

blood

• 3 ml/L so in blood 15 ml (very low).

O2 carried by hemoglobin

• 19.5 ml of O2 /I00 ml arterial blood.

• loose chemical combination with Hb

• In Hb each one of four ferrous atoms can reversibly

combine with one molecule of O2 (oxygenation).

• Hb ↑O2 carrying capacity 65 time.

Definitions

• The O2 content: volume of O2 carried by blood combined

with Hb / 100 ml blood.

• The O2 capacity of blood: the maximum volume of O2 that

can be carried by hemoglobin, when hemoglobin is fully

saturated with O2.

•Capacity = 8 cubs

•Content = 2 cubs

•Saturation =

25%

• The O2 content depends on:

1- Amount of hemoglobin present.

2- O2 tension.

3- O2 affinity of hemoglobin.

4- Metabolic state of the organ.

• 1 gm Hb combines with 1.34 ml of O2 when it is fully

saturated.

• A healthy adult has 15 gm Hb/ 100 ml.

• O2 capacity = 1.34 x15 = 20.1 ml O2 / 100 of blood.

• The percentage saturation of hemoglobin with O2, (%

HbO2) equals:

100 x capacity O

content

2

2O= 19.5/20.1 = 97%

Saturation is not affected by anemia

The hemoglobin O2 dissociation

curves

High altitude exercise

90

30

venous

70

arterial

O2- Hb dissociation curve

97 Flat part

Steep part

CO2

Fetal Hb

Cause of S shape

• Hb → 4 subunits

• PO2 ↓ from 100 to 60→ little change in saturation → off-

load 1st O2 molecule.

• PO2 ↓ below 60 → off-load the remaining 3 O2 molecule

→ easier

Coefficient of O2 utilization

2 2 2

2

Arterial O content - Venous O content (O utilized by the tissues) X 100

Arterial O content

• 25% at rest 75% in exercise

• Depends on:-

1. Metabolic activity→ direct relation

2. Rate of blood flow → inverse relation

O2- Hb dissociation curve shift

97

CO2

P 50

27

Shift of the curve

Factors that shift the oxyHb

Dissociation curve to the right 1. Increase of temperature and PCO2 (CO2

tension) and decrease of pH. • CO2 and H+ combine with sites on hemoglobin

changing its configuration and facilitating the off loading of O2. However, once partially unsaturated, hemoglobin binds H+ and CO2, this enhances the off loading of O2 (The purpose for this, is to provide more O2 to the tissues when the metabolic rate is increased.

2. Increase of 2,3-diphosphoglycerate (2,3-DPG) • hypoxia (produced by high altitudes) or exercise.

• Binds beta chain in deoxygenated form.

Bohr effect

Factors that shift the curve to the left

• Decrease in temperature and PCO2 and an increase in pH.

• CO (carbon monoxide) (carboxyhemoglobin). • Affinity of CO to Hb more than 200 affinity of O2

• O2 binding site is occupied by CO→ no response to ↓PO2

• Fetal Hb. • 2 alpha +2 gamma.

• Gamma can’t bind 2,3-DPG→ increase affinity.

O2 dissociation curve of myoglobin Rectangular hyperbola

Myoglobin → 1 Fe++ → 1 O2

Hemoglobin → 4 Fe++ → 4 O2

Co2 transport

CO2 is present in two forms: (arterial 48 ml/100 ml blood)

1. Physically dissolved (3ml)→ 6%

2. In chemical combination:-

• As bicarbonate (42 ml) → 88%

• In combination with the amine group of blood proteins as

carbamino compounds (3 ml) → 6% (4% Hb, 2% plasma Ptn)

Na K

The tidal CO2

• It is CO2 which is given by tissues to 100ml blood.

• The tidal CO2 is 4ml/100ml.

• Transport of tidal CO2:-

1. In physical solution (0.4ml).

2. As bicarbonate (2.6 ml).

3. As carbamino compounds (1 ml).

Arterial PCO2→ 40 mmHg

Venous PCO2→ 46 mmHg

CO2 carried as bicarbonate

Cl- shift phenomena or Hamburger phenomenon

Cl- shift phenomenon

plasma RBCs

↑↑↑↑ HCO3-

↓ (little) PH

↓↓ ↑↑ Cl-

constant Na+, K+

↓↓ ↑↑ Osmotic pressure

↑↑ haematocrite

H2O

Donnans equilibrium

inplasmaHCO

inRBCHCO

inRBCCl

inplasmaCl

3

3

Sites of CA

1. RBCs.

2. Oxyntic cell in stomach→ HCL secretion.

3. Pancreatic acini → HCO3- secretion.

4. Renal tubular cell → HCO3- reabsorption.

5. Eye → HCO3- secretion in aqueous humor.

CO2 Dissociation curve

95% Saturation

0% Saturation 70% Saturation

lung

CO2 content PCO2

48 40 Arterial

52 46 Venous

CONTROL OF

RESPIRATION

Respiratory Center

The medullary respiratory center

two bilateral groups

1- dorsal respiratory group ( DRG)

- Inspiratory neurons

- Inherent rhythmicity of respiration

2- ventral respiratory group ( VRG)

Inspiratory & expiratory neurons ( forced inspiration &

expiration)

The pontine respiratory center

1- Pneumotaxic center…..switch off point of inspiration

2- Apneustic center

Dorsal respiratory group ( DRG)

• Dorsomedial in the medulla

• Inspiratory………normal quite breathing.

• Pacemaker activity ( rhythmicity)

• Send impulses to diaphragm & intercostal muscles

• Receive imulses from lung strech receptors ( X) & apneustic

center

Ventral respiratory group ( VRG )

• Inactive during normal quiet breathing

• Inspiratory & expiratory neurons

• Forced inspiration & expiration

• Receive excitatory impulses from DRG during forced

inspiration

• Send impulses to muscles of expiration & accessory

muscles of inspiration

Pneumotaxic center ( PNC)

• Switch off point of inspiration

• Send inhibitory impulses to APC & DRG

• Limit the duration of inspiration

• Upper Pons

Apneustic center ( APC)

• Lower Pons

• Switch on point of inspiration

• Send impulses to DRG & PNC

• Receive inhibitory impulses from PNS & lung stretch

receptors

Role of the vagus nerve

• Hering Breuer reflex

Inspiration……lung stretch receptors in airway smooth muscle

…….. vagi…….inhibition of DRG & APN

• Together with PNC adjust the Switch Off point of

inspiration…….normal rate & depth of respiration

• Active in animals & newborn

Genesis of respiration

APN

DRG

diaphragm & external intercostal ms

Stretch receptors & X Hering Breuer reflex

Inhibit DRG & APN Switch off inspiration

PNS inhibit APN

Lung deflation Decreased inhibitory impulses

Cycle repeats itself

Regulation of respiration

Chemical regulation -Basic mechanism

-Chemo receptors detect variation of PCO2, H +, & PO2

Non-chemical regulation Impulses from higher centers, lungs, CVS, muscles, viscera &

skin

Chemical regulation of

respiration Increased PCO2 & H+ and decreased PO2 in arterial

blood ……..increases activity of respiratory centers

through stimulation of respiratory chemoreceptors

Types of respiratory chemoreceptors

1- central chemoreceptors

2- peripheral chemoreceptors

Central chemoreceptors

• Beneath Ventral surface of the medulla

• The main direct stimulus is increased H+ in brain interstitial

fluid & CSF

• H+ ions do not cross the BBB, so changes in H+ in blood

have no effect on central chemoreceptors.

• CO2 in blood crosses BBB…….increases H+ in

CSF……..indirect stimulation of central chemoreceptors

CO2 + H2O H2CO3 HCO3 + H +

The blood brain barrier BBB

• Endothelium of blood vessels in the brain that separates

CSF from blood

• it restricts movement of ions .( O2 & CO2 pass easily)

• H + does not cross BBB

• CO2 cross BBB so increases PCO2 in blood will increase

PCO2 in CSF & decreases pH of

CSF…………..stimulation of respiration

• CSF is not highly buffered as blood

Peripheral chemoreceptors

• Aortic bodies over aortic arch . Impulses are carried along

X ( vagus nerve)

• carotid bodies at bifurcation of common carotid artery.

Impulses are carried along Hering nerve (a branch of IX)

• They have high blood flow, O2 needs from dissolved O2 (

not O2 combined with Hb) ……..So they are sensitive to

O2 tension rather than O2 content

• Can be stimulated by marked decrease of blood flow (

hemorrhage & hypotention)

O2 (most potent)

H + ( metabolic acidosis)

CO2 ( to a lesser extent ?)

Stimulus Changes in arterial blood gases

Mechanism of stimulation of peripheral chemoreceptors

Oxygen tension

PO2 100 to 60 mmHg…..increase firing rate but no

effect on ventilation

PO2 60-30 mmHg………most sensitive ,rapid decrease in

HbO2 saturation & rapid increase in ventilation

( 6 times at PO30 mmHg)

PO2 20 mmHg ….direct inhibitory effect

H + concentration

Increase in H + not related to PCO2 ( metabolic acidosis)

CO2 tension

Less sensitive than central chemoreceptors

Important in cases of depression of central chemoreceptors

Non-chemical ( nervous) regulation of

respiration

Regulation of respiratory center by impulses coming from

• Higher centers ( cerebral cortex & hypothalamus)

• Upper respiratory passages

• Lungs

• Chest wall receptors

• Proprioceptors

• Cardiovascular system

• Visceral reflexes

Cerebral cortex

Voluntary control of respiration ( within limits) e.g. talking,

singing

Pathway

Afferents from cerebral cortex to respiratory center or to

spinal motor neuron along corticospinal & bulbospinal

tracts

Experimentally…

voluntary hyperventilation

Voluntary apnea

Voluntary apnea

- Breath holding 45—60 sec then break point caused by

decreased PO2 & increased PCO2

- Duration of breath holding can be prolonged by

1- initial hyperventilation

2- prior inhalation of pure O2 for 1 min

3- holding breath in full inspiratory position

4- some visceral reflexes e.g. swallowing

Upper respiratory passages

Mechanical or chemical irritant …..coughing , sneezing

& or bronchoconstriction

Coughing

Irritation of trachea, larynx, bronchi ….. Vagus ……

deep inspiration followed by forced expiration while

the glottis is closed

Abdominal muscle contraction, increased

intrabdominal P , sudden opening of glottis, air with

foreign matter is expelled out

Sneezing

Irritation of nasal mucosa…..trigeminal nerve…. deep

inspiration followed by forced expiration with opened

glottis & closed posterior nasal opening by soft palate

Chest wall receptors

• Present in chest wall muscles & tendons

• When stimulated by chest wall expansion (

inspiration) ……send inhibitory impulses to DRG via

vagus … determin tidal volume in adult humans

• In case of Increased respiratory effort……..dyspnea

Cardio Vascular System CVS

• O2 supply & CO2 removal from the tissues depend

on ventilation & efficient pulmonary & systemic

circulation

• Respiratory S & CVS are integrated at various

levels of CNS

• Afferents from respiratory chemoreceptors relay on

RC & CVS centers.

• Afferents from arterial baroreceptors relay on

centers CVS &RC

• Receptors of CVS are arterial baroreceptors & atrial

receptors

Arterial Baroreceptors ( high pressure receptors)

• Present in aortic & carotid sinus

• Increased arterial blood pressure ABP ….. stimulates

baroreceptors …. IX & X ….decreases ABP & inhibit respiration.

• Decreased ABP………arterial baroreceptors ……. increases

ABP & stimulates respiration

• Experiment – adrenaline apnea

adrenaline injection…… increase ABP ….. Stimulate arterial

baroreceptors………decreases ABP & inhibit respiration ..

adrenaline apnea

Atrial receptors ( low pressure receptors)

• Present in right atrium & big veins

• Increased VR …… stimulate atrial receptors ……… X (

vagus) …….stimulates RC …… increases ventilation during

muscle exercise ( Harrison’ s reflex)

• This help to oxygenate the extra amount of blood

Proprioceptors

• Present in skeletal muscles, tendons, joints & ligaments

• Stimulated by movement of muscles & joints

• When stimulated during exercise……stimulate ventilation

Visceral reflexes

Swallowing

Food stimulates receptors in the pharynx……. IX ....inhibit

RC during deglutition & vomiting

Hiccup

Spasmodic contraction of diaphragm ….. Inspiration with

sudden glottis closure

Improved by increasing arterial PCO2

Yawning

Deep inspiration…..opening of collapsed underventilated

alveoli & Increasing VR

Hypoxia oxygen deficiency at tissue level

It may be due to

• Decreased O2 supply to tissues

• Decreased O2 utilization by the tissues

Types of hypoxia Hypoxic hypoxia

decreased O2 tension in arterial blood

Anemic hypoxia

reduced Hb

Stagnant hypoxia

decreased blood flow

Histotoxic hypoxia

tissues can not utilize O2

Hypoxic Hypoxia ( arterial hypoxia) Definition

decreased oxygenation of arterial blood

( decreased PO2 & O2 content in arterial & venous blood)

Causes

1- Low O2 tension in inspired air e.g. high altitude

2- Pulmonary disorder

- Impaired ventilation ( depression of respiratory centers, obstructive diseases & restrictive diseases, collapse )

- impaired diffusion ( decreased pulmonary membrane e.g. lobectomy or increased thickness e.g. fibrosis & oedema

- ventilation perfusion imbalance ( low V/P ratio)

3- shunting of venous blood into arterial blood

e.g. congenital heart diseases

Impaired ventilation

Depressed respiratory center

Obstructive diseases-asthma

Restrictive diseases- collapse

impaired diffusion

decreased pulmonary membrane

increased thickness

ventilation

perfusion

imbalance

( low V/P ratio

Low O2 tension in

inspired air e.g. high altitude

shunting of venous

blood into arterial

blood Venous blood bypass lung

Pulmonary disorder

Causes of hypoxic hypoxia

Sign: generalized cyanosis

Anemic Hypoxia

Definition

Deficiency of Hb capable of carrying O2

( decreased O2 content of arterial blood & PO2 & O2

content in venous blood)

Causes

1- all types of anemia

2- abnormal form of Hb

- Carboxy - Hb (CO poisoning)

- Met-Hb oxidation of heme ferrous to ferric- grayish

- Sulf-Hb….reducing agent- bluish leaden

-

CO poisoning ( carboxy-Hb)

Causes

• CO –Hb cannot carry O2

• Hb has 210 times more affinity to CO than O2

• CO-Hb breaks very slowly

• CO-Hb shifts O2 dissociation curve to the left

• Death when Co-Hb 70-80 % of Hb

Signs : Cherry red color

Treatment

1- termination of exposure

2- O2 therapy: 95% O2 + 5% CO2 better than pure or hyperbaric O2

3- artificial respiration - Blood transfusion

Stagnant Hypoxia

Definition

Inadequate blood flow through the tissues -slow circulation

( low PO2 & O2 content in venous blood)

Causes

1- generalized..congestive heart failure – circulatory shock

2- localized…thromosis & embolism

Signs

generalized or localized cyanosis

Histotoxic Hypoxia Definition

Decreased utilization of O2 due to inhibition of cytochrome

system by toxic agents

( increased PO2 & O2 contents in venous blood)

Causes

Cyanide poisoning –inhibits cytochrome oxidase

Alcohol & narcotic – inhibit dehydrogenase enzyme

Characteristics of different types of hypoxia

histotoxic stagnant anemic hypoxic characters

Normal Normal Normal Arterial

PO2

Normal Normal O2 content

Normal Normal Normal % Sat of Hb

Venous

PO2

O2 content

% Sat of Hb

absent

Present absent Present Cyanosis

Oxygen therapy in different types of hypoxia Oxygen is highly beneficial in

1- hypoxic hypoxia due to

decreased atmospheric

hypoventilation

impaired ventilation

2- carbon monoxide poisoning

O2 is less beneficial in

1- hypoxic hypoxia due to AV shunt

2- anemic hypoxia

3- stagnant hypoxia

O2 is not beneficial in

Histotoxic hypoxia

Oxygen toxicity Causes

O2 is converted to active form ( O2 free radicals) …..

Oxidizing cell membrane & enzymes

- oxidative destruction of enzymes

- damage of nervous tissue

Pure O2

100%O2 for 8 hrs-------irritation of upper respiratory tract

For 24-48 hrs-----damage of the lungs

> 48 hrs -------damage to CNS

in pre mature infants ------ retrolental fibroplasia

Hyperbaric O2

More toxicity -----CNS symptoms

Important in treatment of CO poisoning , gas gangrene, &

diabetic foot ulcer

Cyanosis Definition

Bluish coloration of skin & mucous membrane due to

increased deoxygenated Hb in capillaries

( 5 gm reduced Hb / 100 ml capillary blood)

HB content = 15 gm / 100 ml

Arterial blood = 15 x 5/100 = 0.75 / 100 ml

Venous blood = 15 X 30/ 100 = 4.5 gm / 100 ml

Capillary blood = 0.75 + 4.5 ÷ 2 = 2.6 / 100 ml

Causes of cyanosis

Hypoxic hypoxia …… ??

Stagnant hypoxia ….. ??

Asphyxia e.g. airway obstruction, drowning

Cyanosis doesn’ t appear with

Anemic hypoxia ??

Histotoxic hypoxia ??

CO poisoning

Types of cyanosis

Generalized ( central ) cyanosis

Localized ( peripheral ) cyanosis

Relation between hypoxia & cyanosis

Cyanosis & hypoxia don’t run parallel

In hypoxic hypoxia

1- If bleeding occurs

there will be decrease in oxy-Hb …… more hypoxia

there will be decrease in reduced Hb … less

cyanosis

2- with acclimatization ( polycythemia)

increase in oxy-Hb ------------less hypoxia

increase in reduced HB------- more cyanosis

Factors that modify the color of cyanosis

1. Total amount of Hb ( anemia – poycythemia)

2. Amount of reduced Hb ( > 5 gm /100ml)

3. Abnormal composition of the blood

Co Hb- Met-Hb – Sulf-Hb - Lipeamia

4. Skin

Thickness- pigmentation

5. Coetaneous blood flow

Exposure to heat….VD……red skin

Exposure to cold…VC ….blue skin

Extreme cold …….. VD ….red skin

High Altitude Physiology • As we ascend to high altitude , the total barometric

pressure decreases & PO2 decreases.

• Permanent inhabitation is possible up to 20.000 ft

• Aircraft flying at high altitude use pressurized cabins

Symptoms of hypoxic hypoxia

Depend on onset, severity, duration , tissue affected (

the brain) & efficiency of compensatory mechanism.

Sudden sever hypoxia

PO2 < 20 mmHg ……loss of consciousness & death

Acute hypoxia

PO2 20 -40 mmHg …drowsiness, euphoria, headache,

nausea, vomiting…… unconsciousness

Chronic hypoxia

PO2 40 -60 mmHg ….. compensatory mechanism …mild

symptoms e.g. fatigue, headache, drowsiness , dyspnea

Mountain sickness Symptoms of ascending to high altitude over a short period

and disappear gradually due to acclimatization

Enclude headache, dizziness, poor mental judgment,

anorexia, nausea, dyspnea, palpitation & insomnia

Signs of hypoxic hypoxia

• Hyperventilation

• Tachcardia

• Increased cardiac output

• Generalised cyanosis

Acclimatization to high altitude Activation of compensatory mechanisms to raise arterial PO2 &

increase O2 supply to the tissues

1. hyperventilation

2. Tachycardia & increased cardiac output

3. Polycythemia

4. Increased 2,3 DPG in RBC ( ? P50 - ? O2 unloading)

5. Effect at cells & tissues ( increased mitochondria, oxidative

enzymes & capillary density)

6. Pulmonary hypertension

Acclimatization to high altitude

Hyperventilation

Immediate ( primary) hyperventilation

Hypoxia stimulate peripheral chemoreceptors &

respiratory center …hyperventilation …..increase

PO2 & decrease PCO2 …… alkalosis of CSF &

blood …. Depress respiratory center

After 2-4 days ( secondary hyperventilation)

Correction of alkalosis

- Renal compensatory mechanism…decreases blood

HCO3 by excretion of HCO3 in urine

- In CSF .. Active transport at cerebral capillaries

reducing HCO3 in CSF. So, hypoxia stimulate

respiration

PCO2

H+ α ----------------------------------------------

HCO3

Acclimatization to high altitude

Poycythemia

Hypoxia stimulate erythropoietin ……stmulates bone

marrow …..increase

• RBCs count

• hematocrit ( up to 60%)

• Hb % ( up to 20 gm %)

• Viscosity ( ? ?)

Acclimatization to high altitude

Tachycardia & increased cardiac output

Hypoxia stimulates peripheral chemoreceptors ………

stimulates CVS ….. Increases HR & CO …………

increases O2 delivery to tissues

After 2 weeks …HR & CO return to normal

Acclimatization to high altitude

Pulmonary hypertension

Hypoxia ….. Pulmonary VC …. Even distribution of

pulmonary blood flow …… reduce the rang of V/P values

….. Improve gas exchange

Risk ….. Pulmonary hypertension leads to right side heart

failure

Permanent residents of very high altitude

• Short

• Polycythemic

• Barrel shaped chest

Respiratory adjustment in muscle

exercise

there is increased O2 consumption & CO2

production caused by increased ventilation

Ventilatory changes during exercise

• At the onset: abrupt large increase in ventilation

• During exercise : gradual increase in ventilation

proportionate to increase in tissue metabolism

• At the end : abrupt moderate decrease in ventilation,

doesn’t reach resting level

• Recovery period ( recovery time): gradual decline in

ventilation to resting level ( removal of lactic acid, O2

dept & decrease temperature)

Causes of increased pulmonary ventilation

during muscle exercise

Chemical stimulation of respiratory center

Light to moderate exercise ….no change in PO2, PCO2 or H+

Sever sustained exercise… increased H + ( lactic acid) …. Hyperventilation

Non chemical stimulation of respiratory center by impulses from

1. Prorioceptors

2. Higher centers

3. Cardiac mechanoreceptors

4. Increased metabolism

5. norepinephrine

Non chemical stimulation of respiratory center during muscle exercise

1- Prorioceptors (Muscle, tendon & joint receptors)

Hyperventilation at beginning of exercise

2- Higher centers

Cerebral ( motor) cortex ….. Hyperventilation at beginning of exercise

Conditioned reflexes ….athletes - before exercise

Hypothalamus by increased temperature

3- Cardiac mechanoreceptors in right atrium

Exercise …increase VR ….stimulate RC ( Harrison reflex)

4- norepinephrine stimulate RC

5- Increased metabolism ….increase PCO2 , H + &

temp …stimulate RC

Effects of increased barometric pressure

• Pressure increases one atmosphere every 10 meter

depth

• People working under water tunnel kept in chambers with

increases pressure ( caisson champers)

• Divers use SCUPA (self-contained under water breathing

apparatus) which delivers air at P equal to that upon the

body

• Blood in lungs is exposed to high P in alveoli

Problems associated with increased barometric

pressure During descend ( compression) – P in blood increases ……. Gases dissolved in body tissues

1- nitrogen narcosis … increased N2 in fatty tissues & nervous system ….. Nervous symptoms- helium is better than N2 in gas mixture used by divers.

2- O2 toxicity > 12 hrs - helium is better than N2

3- CO2 toxicity – rare

During ascend ( decompression)

Gradual slow ascend ………no bad effects

Rapid ascend ……

1- decompression sickness

2- air embolism

Decompression sickness ( Caisson’s disease)

Rapid ascend ….gas bubles in body fluids

O2 ……. Binds to Hb & utilized by tissues

CO2 …. Buffered in tissues & blood

N2 bubbles …. Block capillaries

in CNS – paralysis

in bones – pain

in coronary – myocardial damage

Treatment ….recompression & slow decompression

Air embolism

Rapid ascend ….. Gas P in lung is high ( tank) & P outside is low …..lung expansion & rupture pulmonary vessels ….air embolism ( also in breached cabins of airplane)

Abnormal Patterns of Breathing Eupnea : normal resting breathing

Tachypnea: rapid breathing

Hyperpnea: deep breathing

Hyperventilation: increased rate & depth of breathing

Dyspnea: difficult breathing

Apnea: temporary stoppage of breathing

Asphyxia: prevention of ventilation in alveoli

Periodic breathing: alternate periods of apnea & breathing

Orthopnea: dyspnea on lying down relieved by sitting up

Dyspnea

• Awarness of shortness of breath

• Hyperventilation changes into dyspnea when ventilation is

doubled

• Dyspnic endex = BR / MBC

Normally > 90% …..

If < 70 % dyspnea appears

(BR = MBC – PV)

Types & causes of dyspnea

1- Respiratory dyspnea

Ventilation dysfunction ( obstruction, restriction, obesity)

diffusion dysfunction (pneumonia, pulmonary edema)

perfusion dysfunction (pulmonary embolism & AV shunt)

2- Cardiac dyspnea

left side heart failure … lung congestion – J receptors

Orthopnea: dyspnea on lying down relieved by sitting up??

3- Neurogenic ( psychic ) dyspnea

4- Acidosis – DM , ureamia

5- Increased metabolism

hyperthyroidism- fever

Apnea

Definition : temporary stoppage of respiration

Types

1- apnea following voluntary hyperventilation

2- apnea with periodic breathing

3- adrenaline alnea

4- voluntary apnea

5- swallowing apnea

6- sleep apnea- decreased sensitivity to P CO during sleep

Asphyxia

Prevention of ventilation of alveoli

Causes

1- airway obstruction

2- drowning

3- paralysis of respiratory muscles

4- bilateral pneumothorax

5- rebreathing in a closed system with limited volume of air

Changes in asphyxia

1- stimulation of respiration- cyanosis

2 increased catecholamine , blood pressure & heart rate

3- then decreased respiration, BP, HR …cardiac arrest

Periodic Breathing

Alternate periods of apnea & breathing

Physiological

After voluntary hyperventilation, high altitude - premature infants during sleep

Pathological (chyne-Stokes breathing)

1- respiratory failure

2- circulatory failure

Mecahanism

Hyperventilation …….increased PO2 & decreased PCO2

increased PO2 …. Apnea ….. Shallow breaths …. Increase PO2…… apnea …..cycle repeats until PCO2 gradually returns to normal value

Artificial respiration

1- Mouth to mouth breathing

Emergency & temporary respiratory failure

2- Pressure breathing machines ( ventilators)

Acute respiratory failure

The equipment is connected to endotracheal tube

& forces air into the lungs

3- Tank respirator

Chronic respiratory failure

The pateint is put inside the tank except head &

alternate positive & negative pressures are

applied to chest