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Respiratory System
Principal Organs
 ANATOMY IN A HEALTHY LUNG

The Right Lung

-Three lobes-the superior, middle and inferior,
which are separated by the horizontal fissure and
the oblique fissure.
-10 bronchopulmonary segments

The Left Lung

-Two lobes which are separated by the oblique fissure.
-10 bronchopulmonary segments
 The main anatomy affected by pleural effusions are the layers in the
Lung

There are two layers-the parietal pleura and the visceral pleura.

• At the Hilum, the parietal pleura folds back on itself to become the visceral
pleura.

The pleural fluid contains –

-contains about 5-15ml of fluid at one time
-about 100-200ml of fluid circulates though the pleural space within a 24-hour
period
-has an alkaline pH of about 7.60 - 7.64
 Protein content less than 2% (1-2 g/dL)
 Glucose content similar to that of plasma
 Mesothelial cells
 Macrophages
 Lymphocytes (few)
 Sodium, potassium and calcium concentrations similar to that of interstitial fluid.
 Lactate Dehydrogenase concentration of less than 50% of that of plasma
ANATOMY
OF A
HEALTHY
LUNG
ANATOMY OF A
LUNG WITH A
PLEURAL
EFFUSION

A pleural effusion is an accumulation of fluid

between the parietal pleura and the visceral
pleura.

Chest X-ray frontal view: 100-200ml pleural fluid

Respiratory System – Lungs
• 3 steps
– Pulmonary ventilation
• Breathing; involves physical movement of air into and
out of lungs
– Gas exchange
• Gas diffusion across respiratory membrane and
capillary and other cells
– Gas transport
• Transport of oxygen and carbon dioxide between
alveolar capillaries and capillary beds in other tissues
 Respiratory System –
Functions
Basic functions of the respiratory system are:
1. provides oxygen to the blood stream and
removes carbon dioxide
2. enables sound production or vocalization as
expired air passes over the vocal chords
3. enables protective and reflexive non-
breathing air movements such as coughing
and sneezing, to keep the air passages clear
4. control of Acid-Base balance
5. control of blood pH
Non-respiratory Air Movements
Respiration Process
A collective term for the following processes:
 Pulmonary Ventilation
Movement of air into the lungs (inspiration)
Movement of air out of the lungs (expiration)
 External Respiration
Movement of oxygen from the lungs to the blood
Movement of carbon dioxide from the blood to the
lungs
 Transport of Respiratory Gases
Transport of oxygen from the lungs to the tissues
Transport of carbon dioxide from the tissues to the
lungs
 Internal Respiration
Movement of oxygen from blood to the tissue cells
Movement of carbon dioxide from tissue cells to blood
 Pulmonary Ventilation

The intercostal muscles and the diaphragm work together

Inspiration, or inhalation – a very active process that requires input of energy
Air flows into the lungs when the thoracic pressure falls below atmospheric
pressure. The diaphragm moves downward and flattens while the intercostal
muscles contract.
Expiration, or exhalation – a passive process that takes advantage of the recoil
properties of elastic fibers Air is forced out of the lungs when the thoracic
pressure rises above atmospheric pressure. The diaphragm and expiratory muscles
relax.
Pulmonary Ventilation -
Volumes
 Measures of Pulmonary
Ventilation
Respiratory volumes – values determined by
using a spirometer
 Tidal Volume (TV) – amount of air inhaled or
exhaled with each breath under resting conditions
 Inspiratory Reserve Volume (IRV) – amount of air
that can be inhaled during forced breathing in
addition to resting tidal volume
 Expiratory Reserve Volume (ERV) – amount of air
that can be exhaled during forced breathing in
addition to tidal volume
 Residual Volume (RV) – Amount of air remaining in
the lungs after a forced exhalation.
 Formulas – Capacities
 Vital Capacity – maximum amount of air that
can be expired after taking the deepest breath
possible (VC = TV + IRV + ERV)
 Inspiratory Capacity – maximum volume of air
that can be inhaled following exhalation of
resting tidal volume (IC = TV + IRV)
 Functional Residual Capacity – volume of air
remaining in the lungs following exhalation of
resting volume (FRC = ERV + RV)
 Total Lung Capacity – total volume of air that
the lungs can hold (TLC = VC + RV)
 Control of Respirato System
 Respiratory control centers – found
in the pons and the medulla
oblongata
 Control breathing
 Adjusts the rate and depth of
breathing according to oxygen and
carbon dioxide levels
 Afferent connections to the
brainstem
 Hypothalmus and limbic system
send signals to respiratory control
centers
Brain Stem Respiratory Centers
• Rhythmicity center in medulla
oblongata – generates
automatic
– Consists of inspiratory neurons
that drive inspiration
– and expiratory neurons that
inhibit inspiratory neurons
– Their activity varies in a
reciprocal way and may be due
to pacemaker neurons
 Respiratory Center
Controls “off
switch of insp.
3 groups of ramp signal =
neurons control freq. control
respiration Brainstem

Pons Pneumotaxic
Center
4th Ventricle
? Apneustic ctr.
Medulla
1. extra drive
Basic DRG VRG 2. SNS stim.
rhythm (NTS)
Dyspnea of
Vagus & CHF, HT, anemia
Glossopharyngeal exercise
Respiratory
Motor Paths

Chemo, baro,
Lung receptors “ramp” signal
 Concept map

cortex

?
 Regulation of Breathing

• Respiratory muscles controlled by 2 major

descending pathways
– One controls voluntary breathing
– Another controls involuntary breathing

• Unconscious rhythmic control of breathing

– influenced by sensory feedback from receptors sensitive to
•PCO2, pH, and PO2 of arterial blood
 Brain Stem Respiratory Centers

• Inspiratory neurons stimulate spinal motor neurons that

innervate respiratory muscles
• Expiration is passive and occurs when inspiratory neurons
are inhibited
• Activities of medullary rhythmicity center are influenced
by centers in pons
– Apneustic center promotes inspiration by stimulating
inspiratory neurons in medulla
– Pneumotaxic center antagonizes apneustic center, inhibiting
inspiration
Chemoreceptors
• Automatic breathing –
influenced by activity of
chemoreceptors
– monitor blood PCO2, PO2,
and pH
• Central chemoreceptors
are in medulla
• Peripheral chemoreceptors
are in large arteries near
heart (aortic bodies) and in
carotids (carotid bodies)
CNS Control
of Breathing
 Effects of Blood PCO2 and pH on Ventilation

• Chemoreceptors modify ventilation to maintain normal

CO2, O2, and pH levels
– PCO2 is most crucial because of its effects on blood pH
•H2O + CO2  H2CO3  H+ + HCO3-
–H2O + CO2  H2CO3
–H2CO3  H+ + HCO3-

• Hyperventilation causes low CO2 (hypocapnia)

• Hypoventilation causes high CO2 (hypercapnia)
 Effects of Blood PCO2
and pH on Ventilation
Effects of Blood PCO2 and pH on Ventilation

• Brain chemoreceptors are responsible for greatest

effects on ventilation
– H+ can't cross BBB but CO2 can, which is why it is monitored
and has greatest effects
– Rate and depth of ventilation adjusted to maintain arterial
PCO2 of ~40 mm Hg

• Peripheral chemoreceptors do not respond to PCO2, only

to H+ levels
Effects of Blood PCO2 and pH on Ventilation

• Rise in blood CO2

increases [H+]
– lowers pH of CSF
– thereby stimulates
chemoreceptor neurons
. in the medulla
oblongata
 Effects of Blood PO2 on Ventilation

• Hypoxemia – low blood PO2 () has little effect on

ventilation
– Does influence chemoreceptor sensitivity to PCO2
– PO2 has to fall to about half normal before ventilation
is significantly affected
– Emphysema blunts chemoreceptor response to PCO2
•Oftentimes ventilation is stimulated by hypoxic drive rather
than PCO2
Comparison of PCO2 and PO2 Effects on Ventilation
Effects of Pulmonary Receptors on Ventilation

• Lungs have receptors that influence brain respiratory

control centers via sensory fibers in vagus
– Unmyelinated C fibers are stimulated by noxious substances
such as capsaicin
•Causes apnea followed by rapid, shallow breathing
– Irritant receptors are rapidly adapting; respond to smoke,
smog, and particulates, causes cough

• Hering-Breuer reflex – mediated by stretch receptors

activated during inspiration
– Inhibits respiratory centers to prevent overinflation of lungs
 Hemoglobin (Hb) and O2 Transport

• Methemoglobin – contains oxidized ferric iron (Fe3+)

– Lacks electron to bind with O2
– Blood normally contains a small amount

• Carboxyhemoglobin – heme combined with carbon

monoxide
– Carbon monoxide (CO) bond 210 times stronger than oxygen
bond
– CO poisoning heme cannot bind O2
 Oxyhemoglobin Dissociation Curve
• Affected by changes in Hb-O2 affinity due to pH and temperature
• Affinity decreases when pH decreases (Bohr Effect) or temp increases
– Occurs in tissues where temp, CO2 and acidity are high
– Causes Hb-O2 curve to shift right and more unloading of O2
 CO2 Transport
• CO2 transported in blood in three forms:
– as dissolved CO2 (10%) in the plasma (CO2 ~21 times more
soluble than O2 in water)
– as carbaminohemoglobin (20%) attached to an amino acid in
hemoglobin
– as bicarbonate ion, HCO3-(70%) that accounts for most of the
CO2 carried by blood

• In RBCs carbonic anhydrase catalyzes formation of

H2CO3 from CO2 + H2O
– Favored by the high PCO2 found in capillaries of systemic
circulation
 Acid-Base Balance of the Blood

• Blood pH is maintained within narrow pH range by

lungs and kidneys (normal = 7.4)
• Bicarbonate – most important buffer in blood
– H2O + CO2  H2CO3  H+ + HCO3-
– Excess H+ is buffered by HCO3-

• Kidney – role to excrete H+ into urine

 Acid-Base Balance of the Blood
• Acidosis – when pH < 7.35 and Alkalosis – when pH > 7.45
• Respiratory acidosis – caused by hypoventilation
– Causes rise in blood CO2 and thus carbonic acid

• Respiratory alkalosis – caused by hyperventilation

– Results in too little CO2

• Metabolic acidosis results from excess of nonvolatile acids

– e.g. excess ketone bodies in diabetes or loss of HCO3- (for buffering)
in diarrhea

• Metabolic alkalosis caused by too much HCO3- or too little

nonvolatile acids
– e.g. from vomiting out stomach acid
 Ventilation and Acid-Base Balance

• Ventilation usually adjusted to metabolic rate to

maintain normal CO2 levels
• With hypoventilation not enough CO2 is breathed out in
lungs
– Acidity builds, causing respiratory acidosis

• With hyperventilation too much CO2 is breathed out in

lungs
– Acidity drops, causing respiratory alkalosis
 Effect of Exercise and High
Altitude on Respiratory Function

• Changes in ventilation and oxygen delivery occur

during exercise and acclimatization to a high altitude
• These changes help compensate for:
– The increased metabolic rate during exercise
– The decreased arterial PO2 at high altitudes
Ventilation During Exercise

• Arterial blood gases and pH

do not significantly change
during moderate exercise
– Because ventilation increases
to keep pace with increased
metabolism
– arterial PO2, PCO2, and pH
remain fairly constant
 Ventilation During Exercise

• During exercise, breathing becomes deeper and more

rapid
– delivering much more air to lungs (hyperpnea)

• 2 mechanisms have been proposed to underlie this

increase:
– With neurogenic mechanism, sensory activity from exercising
muscles stimulates ventilation; and/or motor activity from
cerebral cortex stimulates CNS respiratory centers
– With humoral mechanism, either PCO2 and pH may be different
at chemoreceptors than in arteries
–Or there may be cyclic variations in their values that cannot be
detected by blood samples
 Acclimatization to High Altitude
• Involves increased ventilation, increased DPG, and increased Hb
levels
• Hypoxic ventilatory response initiates hyperventilation which
decreases PCO2 which slows ventilation
– Chronic hypoxia increases NO production in lungs which dilates
capillaries there
•NO binds to Hb and is unloaded in tissues where may also increase
dilation and blood flow
•NO may also stimulate CNS respiratory centers

• Altitude increases DPG, causing Hb-O2 curve to shift to right

• Hypoxia causes kidneys to secrete EPO which increases RBCs
Acclimatization to High Altitude
 Gas Exchange
and Transport

 Alveolar Gas Exchange – the loading of oxygen and

the unloading of carbon dioxide in the lungs
 Oxygen is carried in the blood bound to hemoglobin
(98.5%) and dissolved in plasma (1.5%)
 Carbon dioxide is transported in three forms
 Carbonic acid – 90% of carbon dioxide reacts with water to form
carbonic acid
 Carboamino compounds – 5% binds to plasma proteins and
hemoglobin
 Dissolved gas – 5% carried in the blood as dissolved gas
 Blood Chemistry &
Respiratory Rhythm

Hydrogen ion concentrations -

strongly influence respiration
Carbon dioxide concentrations -
strongly influence respiration
Oxygen concentrations - have little
effect on respiration
1. Local Manifestations
◦ Cough
 chronic, paroxysmal, dry , productive
◦ Excessive Nasal Secretion
◦ Expectoration of Sputum
 mucoid, purulent, mucopurulent, rusty, hemoptysis
◦ Pain
 pleuritic, intercostal, generalized chest pain
◦ Dyspnea- shortness of breath
2. Systemic Manifestations
 Hypoxemia
 insufficient oxygenation of the blood
 cyanosis- bluish, grayish discoloration of skin & mucous
membranes
 Hypoxia
 inadequate tissue oxygenation
 Hypercapnia
 CO2 in arterial blood above normal limits
 Hypocapnia
 CO2 in arterial blood below normal limits
 Respiratory Failure
Health History
◦ Risk Factors
◦ Major Clinical Manifestations
 Cough
 Sputum production
 Chest pain
 Wheezing
 Clubbing of the fingers
 Cyanosis
Assessment of Respiratory System

 Inspection
◦ posture, shape, movement, dimensions of
chest, flared nostrils, use of accessory
muscles, skin color, and rate, depth, & rhythm
of respiration
 Palpation
◦ respiratory excursion, masses, tenderness
 Percussion
◦ flat, dull, resonant, hyperresonant sounds
 Auscultation
◦ breath sounds, voice sounds, crackles,
wheezes
Common complaint described as
– “shortness of breath”
– “breathlessness”
– “not getting enough air”
2/3 of patients presenting to ED with
dyspnea have either a cardiac or
pulmonary disorder
Definitions:
– Tachypnea: rapid breathing
– Orthopnea: dyspnea in a recumbent position
• Most often a result of LV failure
• May be associated with diaphragmatic paralysis or
COPD
Pathophysiology
– No defined neural pathway, derived from
mechanical, chemical, and vascular receptors
Processes involved in sensation of
dyspnea:

1. Conscious sense of voluntary peripheral skeletal

and respiratory muscular efforts with increased
work of breathing
2. Stimulation of upper airway mechanical and
thermal receptors
3. Decreased stimulation of chest all afferents
4. Stimulation of central hypercapneic
chemoreceptors in the central medulla
5. Stimulation of peripheral hypoxic
chemoreceptors, in carotid body and aortic arch
6. Stimulation of intraparenchymal pulmonary
stretch receptors, airway irritant receptors, and
unmyelinated receptors, responding to
interstitial edema or changes in compliance
7. Stimulation of peripheral vascular receptors
• right and left atrial mechanoreceptors
• pulmonary artery baroreceptor
Input from all of these receptors is
integrated in the CNS at subcortical and
cortical levels
Clinical features that may signify
impending respiratory failure
– Presentation:
• shortness of breath or breathlessness
• tachypnea
• tachycardia
• use of accessory respiratory muscles
• stridor
Clinical features that may signify
impending respiratory failure
– Presentation:
• inability to speak, secondary to breathlessness
• agitation or lethargy
• paradoxical abdominal wall movement with
inspiration (abdominal wall retracts inward)
Most Common Most Immediately
Causes Life Threatening
– Asthma & COPD Foreign body
– CHF/ cardiogenic Angioedema
pulmonary edema Hemorrhage
– Ischemic heart dz Tension pneumo
• Unstable angina &MI
PE
– Pneumonia Myasthenia gravis
– Psychogenic Guillain-Barre
Botulism
 Target
oxygen Saturation
Critical care consensus guidelines Minimum
90%
Surviving sepsis campaign Aim
at 88-95%

But these patients have intensive levels of nursing &

monitoring

This guideline recommends a minimum

of 94% for most patients – combines
what is near normal and what is safe
 Absorption Atelectasis even at FIO2 30-50%
 Intrapulmonary shunting
 Post-operative hypoxaemia
 Risk to COPD patients
 Coronary vasoconstriction
 Increased Systemic Vascular Resistance
 Reduced Cardiac Index
 Possible reperfusion injury post MI
 Worsens systolic myocardial performance
 Oxygen therapy INCREASED mortality in non-hypoxic
patients with mild-moderate stroke
This guideline recommends an upper limit
of 98% for most patients. Combination of
what is normal and safe
Harten JM et al J Cardiothoracic Vasc Anaesth 2005; 19:
173-5
Kaneda T et al. Jpn Circ J 2001; 213-8
Frobert O et al. Cardiovasc Ultrasound 2004; 2: 22
Haque WA et al. J Am Coll Cardiol 1996; 2: 353-7
Thomaon aj ET AL. BMJ 2002; 1406-7
 Severe Pneumonia
 Severe LVF
 Major Trauma
 Sepsis and Shock
 Major atelectasis
 Pulmonary Embolism
 Lung Fibrosis
 Etc etc etc
 Chronic hypoxic lung disease
◦ COPD
◦ Severe Chronic Asthma
◦ Bronchiectasis / CF

 Chest wall disease

◦ Kyphoscoliosis
◦ Thoracoplasty
 Neuromuscular disease
 Obesity hypoventilation
 47% of 982 patients with exacerbation of COPD were
hypercapnic on arrival in hospital

 20% had Respiratory Acidosis (pH < 7.35)

 5% had pH < 7.25 (and were likely to need ICU care)

 Most hypercapnic patients with pO2 > 10 kPa were

acidotic (equivalent to oxygen saturation of above ~
92%) i.e. They had been given too
much oxygen
Plant et al Thorax 2000; 55:550
RECOMMENDED UPPER LIMITS
Keep PaO2 below 10 kPa and
keep SpO2 ≤ 92% in acute COPD
 The target ranges are a consensus agreement by the
guidelines group and the endorsing colleges and
societies

Rationale for the target saturations is combination of

what is normal and what is safe

Most patients 94 - 98%

Risk of hypercapnic respiratory failure 88 – 92%*

*Or patient specific saturation on
Alert Card
 There are 2 type respiration : 1. involuntary, that respiration
usualy rhytmic, influence by peripheral and central
chemoreceptors, 2. voluntary, that respiration regulate by
order, influence by impulse from cortex cerebri.
 Usualy ventilatory drive influence by level of CO2, little
effect level of O2, blood pH, level of ion Hydrogen.
 Ventilatory function regulate to normal blood gas and pH.
 Some condition or disease produce compensate or alteration
in function of the receptors.
 Disorder of chest wall, airway, lung parenchyme, and also
deficiency in chemoreceptor or neural pathway produce
dyspneu sensation.
 Patients with comlaint dyspneu should be investigate what
the causes and the management depend on primary causes