PATHOPHYSIOLOGY II

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RESPIRATORY SYSTEM’S PATHOPHYSIOLOGY I 5
RESPIRATION 5
CLINICAL MANIFESTATIONS IN LUNGS’ DISORDERS 5
DYSPNEA 5
PARTICULAR BREATHING PATTERNS 6
VENTILATORY DYSFUNCTIONS 7
OBSTRUCTIVE VENTILATORY DYSFUNCTIONS 7
RESTRICTIVE RESPIRATORY DYSFUNCTIONS 7
MIXED RESPIRATORY DYSFUNCTIONS 7
RESPIRATORY FAILURE (INSUFFICIENCY ) 8
CLINICAL MANIFESTATIONS OF HYPOXEMIA 11
CLINICAL MANIFESTATIONS OF HYPERCAPNIA 12
ALI - ARDS ALI–ACUTE LUNG INJURY 13
ALI/ARDS–ACUTE RESPIRATORY DISTRESS SYNDROME 13

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 RESPIRATORY SYSTEM’S PATHOPHYSIOLOGY I
RESPIRATION
1) Pulmonary phase - Ventilation
1) Diffusion
2) Perfusion
2) The phase of blood gases’ transport (circulatory phase)
3) Tissue phase – tissue respiration (internal respiration)

CLINICAL MANIFESTATIONS IN LUNGS’ DISORDERS

 Dyspnea  „hyppocratical fingers ”
 Cough  Pathological states caused by lesions or
 Abnormal sputum diseases of the respiratory system-
 Particular breathing patterns hypoxemia and/or hypercapnia
 Hypo or hyperventilation

DYSPNEA
DYSPNEA it is a symptom!!!
Definition:
It is defined as a subjective sensation of breathing discomfort that can vary very much depending on individual
psychological factors, rest or physical effort state, external environment
The patient becomes conscious of breathing
The respiratory reflex pathway can be influenced at any of its levels :
 tissue or nervous receptors,
 sensitive afferent pathways,
 breathing centers found in the brainstem ,
 descending motor pathways and muscular effectors
The most commonly seen pathophysiological mechanisms:
1) Modifications of the breathing pattern:
o Frequency,
o Amplitude,
o Inhale/exhale ratio
2) Abnormalities of the blood gases concentrations:
o Hypoxemia and Hypercapnia
3) Dysfunction of the mechanical ventilator pump- the level of ventilation according to needs it is
overwhelmed :
o Abnormalities of breath regulation or lesions of the respiratory system

TYPES OF DYSPNEA:
1) Sensation of respiratory effort/difficulty
2) Sensation of “thirst for air”
3) Sensation of thoracic constriction
4) Sensation of inutile inspiratory effort
5) Frequent and fast respiration

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PARTICULAR BREATHING PATTERNS
SLEEP APNEA
Pattern
Breathing pause of seconds or minutes during sleep
 Central
 due to a decrease of the central respiratory neurons’ sensibility to the CO2
concentration
 Peripheral
 obstructive by airway collapsing due to bronchial smooth muscle fibers (SMF )
relaxation
It is favoured by
 Constitutional factors,
 Obesity
 Respiratory alkalosis
CHEYNE – STOKES BREATHING PATTERN
Pattern
Irregular breathing pattern
 The amplitude of the respiratory cycles gradually increases than decreases
Late response of the respiratory neurons to the CO2 concentration
The most frequent causes are
 Lesions of the brainstem or
 Congestive heart failure with eccentric left ventricular hypertrophy
KUSSMAUL BREATHING PATTERN
It is a compensatory mechanism for metabolic acidosis.
Pattern
The rhythm is normal, regular but the amplitude of the respirations it is increased
The most frequent causes:
 Diabetic ketoacidosis
 Chronic renal failure (uremia)
BIOT BREATHING PATTERN
Pattern
A series of rapid and shallow respiratory cycles, followed by regular or irregular apnea periods of 5-
10 seconds
The most frequent causes:
 Severe lesions of the respiratory neurons-drugs (opioid
type),
 Head trauma,
 High intracranial pressure,
 stroke, CNS’ infections

VENTILATORY DYSFUNCTIONS
 Obstructive ventilatory dysfunctions – OVD
 Obstructive lung disorders
 Restrictive ventilatory dysfunctions – RVD
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  Restrictive lung disorders
 Mixed ventilatory dysfunctions

OBSTRUCTIVE VENTILATORY DYSFUNCTIONS

CAUSE
 INCREASE OF THE AIRWAY’S RESISTANCE TO AIR FLOW
 At an extra- thoracic level- superior airways
 At an intrathoracic level– reduction or obstruction of the bronchial lumen;
 Intrinsic mechanism
 endoluminal obstruction or
 Extrinsic mechanism
 external compression
SPIROMETRY
 FEV1 (Forced Expiratory Volume per 1 second) < 80%
 FEV1/FVC – Tiffneau Ratio- < 70% (normal values over 80%)
 FVC (Forced Vital Capacity) - Normal
CLASSIFICATION
 Mild OVD FEV1 <80%
 Moderate OVD FEV1 between 55–80%
 Severe OVD FEV1 <55%
 Extremely Severe OVD FEV1 <30% or FEV1< 55 % but which associates chronic respiratory failure

RESTRICTIVE RESPIRATORY DYSFUNCTIONS

DEFINITION
Reduction of the gas exchange due to anatomical destruction or functional impairment of the alveolocapillary
membrane
CAUSES
 Extra-pulmonary causes
 Extraparenchymal  restriction of the respiratory movements
 Pulmonary causes
 Parenchymal  Anatomical destruction of some parts of the lung parenchyma or functional
impairment of the gas exchange surface
SPIROMETRY
 Normal FEV1
 Normal or increased FEV1/FVC ratio – FVC < 80%

MIXED RESPIRATORY DYSFUNCTIONS

SPIROMETRY
FEV1/FVC < 80% (normal value above 80%)
FVC < 80%

RESPIRATORY FAILURE (INSUFFICIENCY )

DEFINITION
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 Syndrome which occurs due to the respiratory system’s incapacity of maintaining its main function- to make
adequate gas exchange between the capillary blood and pulmonary alveoli, either in rest or physical effort
state.
Humoral component :
PaO2 below 60 mmHg
With or without increase of the PaCO2 above 46 mmHg
Clinical component :
Can be absent sometimes;
It is represented by signs and symptoms of hypoxemia and/or hypercapnia
RF’s CLASSIFICATION
Classification is done due to he presence or absence of the main humoral signs that define it:
1) Hypoxemia (hO2)
2) Hypercapnia (HCO2) and
3) Respiratory acidosis
It has a tremendous importance from a pathophysiological point of view because treatment it is adjusted
according to these modifications
Classification is done due to the period of time in which hypoxemia and hypercapnia are developing:
 Acute RF
 Chronic RF
 Acute on chronic RF
CLASSIFICATION DUE TO TIME
ACUTE RF
Time
Recent onset (hours, days)  can occur suddenly (recent causes or diseases) or it can complicate
preexisting causes or diseases.
Compensation
The compensatory mechanisms are almost null => dramatic effects on the patient
Humoral
1) Hypoxemia (hO2),
2) hypercapnia (HCO2)
3) respiratory acidosis can settle very quickly
Evolution
It can lead to the patient’s death or it can transform into compensated RF
Chronic RF
Time
Slow onset (months, years)
Compensation
The compensatory mechanisms are effective and lead to hypoxemia and hypercapnia amelioration, and
also they buffer the respiratory acidosis
Acute on chronic RF
Time
Occurs by sudden decompensation of a chronic RF
For a correct management, the most recent and most likely cause of decompensation must be identified
It has a worse prognosis for the patient
PATHOPHYSIOLOGICAL CLASSIFICATION OF RF
 Type I
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  RF without hypercapnia
 Type II
 RF with hypercapnia
 Compensated RF
 with a normal pH (without respiratory acidosis)
 Decompensated RF
 low pH (with respiratory acidosis)

RF occurs when PaO2 drops below 60 mmHg, meaning only in moderate and severe hypoxemia

RF TYPE I - RF without hypercapnia

Characteristics
It is characterized only by hypoxemia
CO2 levels are normal or even decreased
The main mechanisms of generating hypoxemia:
 Mismatch of the ventilation/perfusion ratio (V/Q = 4l air / 5l blood – normal values 0.8)
 Alveolar hypoventilation
 Impairment of the diffusion capacity of the lungs
 Right/left intrapulmonary shunt
Normal values Pathological values -
 PaO2 – 95-96 mmHg Hypoxemia
 SaO2 – 96% I. Mild: 60-
 Blood pH – 7.42 80 mmHg
 MPAP (mean pulmonary arterial pressure) – 15 mmHg II. Moderate: 40-
 PaCO2 – 40-45 mmHg 60 mmHg
III. Severe:
below 40
mmHg

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 Type II - RF with hypercapnia
Characteristics
association between hypoxemia and hypercapnia
Main mechanism of hypercapnia
it is the alveolar hypoventilation
 Pulmonary Disorders That Lead To Hypoventilation
1) Ventilation disorders or abnormalities of the V/Q ratio
2) Lung diseases:
 COPD - emphysema, chronic bronchitis, cystic fibrosis, asthma, acute bronchitis or
bronchiolitis
3) Inhibition of the respiratory center :
 Diseases of the CNS,
 Head trauma,
 CNS’ infections, drugs
4) Spinal cord diseases or diseases affecting the neuromuscular junction, with the involvement
of the respiratory muscles:
 Trauma of the spinal cord,
 Myasthenia gravis,
 Poliomyelitis
5) Thoracic trauma, pleural disease:
 Pneumothorax,
 Hemothorax,
 Pleural effusion,
 Pleural tumors
Normal values Pathological values - Hypercapnia
 PaO2 – 95-96 mmHg I. Mild: 46-50 mmHg
 SaO2 – 96% II. Moderate: 50-70 mmHg
 Blood pH– 7.42 III. Severe: above 70 mmHg
 MPAP (mean pulmonary arterial pressure) – 15 mmHg
 PaCO2 – 40-45 mmHg

RF occurs when PaO2 drops below 60 mmHg, meaning only in moderate and severe hypoxemia
Normal lungs, but extra- pulmonary lesions that lead to hypoventilation.

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 RF’S CLASSIFICATION ACCORDING TO THE BLOOD’S pH
Compensated RF
 Moderate hypoxemia PaO2 50- 60 mmHg
 SaO2 moderately decreased 85-90%
 Blood pH Normal or at the inferior border of normal values
 MPAP (mean pulmonary arterial pressure) 20 mmHg
 PaCO2 40-45 mmHg

Decompensated RF
 Moderate or severe hypoxemia PaO2 50-60 mmHg or below 60 mmHg
 Moderate or severe hypercapnia PaCO2 above 60-70 mmHg
 Blood pH below 7.35 – 7.40
 MPAP more or equal than 25 mmHg

CLINICAL MANIFESTATIONS OF HYPOXEMIA

Acute hypoxemia
Specific signs:
 Cyanosis
Neurological-psychiatric impairment:
 Motor instability,
 troubles with ideation capacity,
 similar with a drunkenness state
Cardiovascular disorders:
 Tachycardia with arterial hypertension or bradycardia with arterial hypotension
 Acute cor pulmonale,
 cardiac arrhythmias
Respiratory problems:
 Tachypnea, dyspnea
Chronic hypoxemia
Specific signs :
1) Hippocratic fingers
2) Polycythemia
Neurological-psychiatric impairment :
 Attention deficit,
 personality disorder
 Sleepiness
Cardiovascular disorders:
 Chronic arteriolo-pulmonary hypertension
 Chronic cor pulmonale
Respiratory problems:
 Chronic dyspnea

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CLINICAL MANIFESTATIONS OF HYPERCAPNIA
Acute Hypercapnia
Neurological-psychiatric impairment:
 Hypercapnic encephalopathy (PaCO2 >70 mmHg)
 Hypercapnic coma or narcosis (PaCO2 >80 mmHg)
Cardiovascular disorders:
 Tachycardia and arrhythmias
 (sympathetic predominance )
 Intracranial hypertension due to cerebral vasodilation - a direct effect of extracellular H+ on
vascular smooth muscle
 Warm and humid extremities (local vasodilation)
Respiratory problems:
 Tachypnea, dyspnea
Chronic Hypercapnia
Neurological-psychiatric impairment:
 Chronic intracranial hypertension
 Funduscopic examination that reveals tortuous vessels and papillary edema
Respiratory problems:
 The patient can tolerate high values of PaCO2 if he receives enough amounts of oxygen

HYPOXEMIA AND HYPERCAPNIA

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 ALI - ARDS
ALI–ACUTE LUNG INJURY
„Acute lesion/impairment of the lungs”

ALI/ARDS–ACUTE RESPIRATORY DISTRESS SYNDROME

SYNONYMS:
 Shock lung,
 Adult’shyaline membrane pneumopathy,
 Posttraumatic respiratory failure,
 Congestive/hemorrhagic atelectasis
Represents a broad spectrum of acute lung injuries, of an inflammatory origin, associated with extensive and
severe lesions of the alveolo- capillary membrane (ACM).
ALI–it is also called acute non-cardiogenic pulmonary edema
It manifests through sudden hypoxemia and diffuse lung infiltrates, in absence of heart failure
ARDS–it is the most severe form of ALI
Both situations are characterized by the combination between:
 An increase of the pulmonary capillaries‘ permeability in an inflammatory context
 Lesions/death of the alveolar and/or endothelial cells
 DAD (diffuse alveolar damage) will result.
Most cases of ALI are associated with sepsis.
If no evident cause of ALI it is identified, the disease it is called AIP - acute interstitial pneumonia.

USA statistics shows a frequency of 64-78 cases/100.000 persons.

Mortality is very high, between 40-60%, despite advanced medical care: orotracheal intubation and mechanical
ventilation.
 Most of the survivors present almost normal respiratory function after 1 year but they present
neurological sequelae: motor deficits, emotional instability, cognitive impairment
ARDS – ETHIOPATHOGENY
The most frequent causes:
 Infections–sepsis
 Physical factors–trauma
 Inhalation of different irritants/toxic substances in the inferior airways
 Chemical factors
 Hematological conditions

Infections
 Sepsis (first cause of ARDS)  bacterial sepsis  septic shock
 Diffuse pulmonary infections:
 viral, Mycoplasma,
 Pneumocystis,
 disseminated TB
Gastric aspiration
Physical factors – trauma
 Mechanic trauma, including head trauma – Hemorrhagic and cardiogenic shock
 Lung contusions
 Burns
 Ionizing radiations
 Fractures with fat emboli

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 Inhalation of irritants/toxic substances in the inferior airways
 Oxygen toxicity
 Smoke
 Irritant gases/toxic fumes
 Chemical substances (gasoline, Diesel oil, diluting substances)
 NH3, NO2
 Phosgene- carbonyl chloride (CO + Cl2 → COCl2)
 In the alveoli it transforms into CO2 and HCl that destroys the alveolar tissue
Chemicalfactors–drugs, illicitor for therapeutic use
 Heroin, methadone overdose
 Aspirin overdose
 Barbiturate overdose
 Colchicine
 Dextran40
 Thiazides
Hematologicalconditions
 Multiple transfusions
 DIC
Other causes
 Metabolic conditions: uremia
 Acute pancreatitis
 Cardiopulmonary bypass
 Post-cardioversion
 Eclampsia, amniotic fluid embolus
ARDS – PATHOGENESIS AND STRUCTURAL MODIFICATIONS
Etiologic factors can affect the ACM by 2 main pathophysiological mechanisms:
1) Either by the respiratory route where, after inhalation, they destroy the alveolar cells
 Gastric content aspiration
 Microorganisms
 Inhalation of toxic gases
 High concentration oxygen
2) Either by vascular route, where the capillary endothelium it is first affected, the alveolar cells being
affected afterwards
 Septic shock
 Pancreatitis
 DIC and micro-emboli Repeated transfusions
ARDS – PATHOPHYSIOLOGY
THE INVOLVED PATHOPHYSIOLOGICAL MECHANISMS
 Massive lung inflammation
 Excessive increase of the lung capillaries’ permeability
 Massive non-cardiogenic pulmonary edema
 Right-left shunt with important hypoxemia
 Impairment of the ventilation-perfusion ratio-V/Q
ARDS has 3 distinct phases, relating to the association between clinical signs and symptoms and
pathophysiological/morphopathological mechanisms and modifications, respectively
I. Phase 1 - Exudative or inflammatory phase
 first 72 hours(1-3 days)
II. Phase 2 - Proliferative phase
 4 – 21 days (after 1-3 weeks since the initial lesion)
III. Phase 3 - Fibrotic phase
 14 – 21 days (after 2-3 weeks since the initial lesion)

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 I. PHASE I– Exudative or inflammatory phase – first 72 hours (1-3 days)
The excessive inflammatory conditions lead to an imbalance between pro- and anti-inflammatory
mechanisms in the pulmonary alveoli.
Primary factors that affect the ACM determine activation of several cells:
 Alveolar macrophages
 Neutrophils and platelets
 Alveolar cells
 Endothelial cells
The pro-inflammatory factors directly involved are:
 The complement system
 Cytokines: IL-1, IL-6, IL-8, TNF-α
 PAF (platelet-activating factor)
 ROS (reactive oxygen species)
 Derivatives of the arachidonic acid:
 prostaglandins (PG),
 thromboxane (Tx)
 leukotrienes (LT) – LTB4
 Chemokins α and β
The activated fractions of the complement and platelets aggregation will lead to formation of vascular
small thrombi with supplementary lesions affecting the pulmonary capillaries.
In sepsis, bacterial toxins will be recognized by the CD14 receptors found on the surface of the alveolar
macrophages and a large number of neutrophils are going to be attracted through chemotaxis.
Neutrophils – they play the key role in ARDS’ apparition and progression.
Inflammatory mediators are going to be released:
 Eicosanoids (PG, Tx, LT)
 Proteolytic enzymes (proteases, catepsins, elastase, collagenase)
 ROS
 PAF
 Extensive damage of the ACM and marked increase of the capillary permeability (Hallmark for ARDS)
 Plasma, plasma proteins and blood cells will reach the interstitium and subsequently inside the
lung alveoli  Hemorrhagic Exudate
 „hyaline membranes” formation – structures formed of fibrin aggregates, modified surfactant,
cellular debris and plasma proteins
 Edema and hemorrhage  reduce lung compliance
 produce an imbalance between ventilation and perfusion

Early occurrence of acute pulmonary hypertension with overloading of the right heart.
Mediators produced by neutrophils and macrophages also determine vasoconstriction in some
pulmonary regions with a supplemental imbalance of the ratio V/Q and hypoxemia
Thrombi formed of neutrophils, macrophages, platelets and fibrin will also affect microcirculation.
The type II alveolar cells are destroyed  surfactant can no longer be produced.
 Alveoli and terminal bronchioles are filled with liquid or they collapse.
The pulmonary compliance decreases,
 Respiratory effort increases,
 Alveolar hypoventilation  Hypercapnia

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 II. PHASE II -Proliferative phase 4–21days (after 1-3 weeks from the original lesion)
Resolution of the pulmonary edema begins
Neutrophils are gradually replaced by lymphocytes
A marked cellular proliferation will take place:
 Type II alveolar cells which will begin surfactant synthesis, fibroblasts and myofibroblasts
 Type II alveolar cells will differentiate into type I alveolar cells and the alveolar barrier will be
in place again
The hemorrhagic exudate
 Transforms into hypercellular granulation tissue
The“hyaline membranes”organize
The alveolar septa are infiltrated with inflammatory cells:
 Leukocytes
 Histiocytes
The surface for gas exchange diminishes even more and progressive hypoxemia unresponsive to
oxygen therapy occurs
III. PHASE III–Fibrotic phase–in 14–21days (after 2-3 weeks since the initial lesion)
Fibrosis and pulmonary remodelling develops
Fibrosis soon involves pulmonary alveoli, respiratory bronchioles and interstitium
 The functional residual capacity decreases, along with the V/Q ratio, while a right-left shunt
appears.
 Finally, acute respiratory failure develops with hypoxemia, hypercapnia and acidosis
Pulmonary fibrosis it is characterized by procollagen type III production
 Presence of this peptide suggests a prolonged ARDS and it has been associated with a high
mortality rate.
The alveolar architecture modifies with the apparition of some “bubbles” very similar to those seen
in emphysema, the patient presenting a high risk for spontaneous pneumothorax
Perivascular pulmonary fibrosis leads to compression of the small vessels found in the septal regions
Neointimal proliferation it is also present
 Both lesions will lead to severe chronic pulmonary hypertension with consequences on the
right heart
Inflammatory mediators that lead to ARDS – ACM and lung capillaries’ lesions-will also lead to
endothelial lesions in other organs and tissues.
 A SIRS – (Systemic Inflammatory Response Syndrome) develops  MODS - Multiple Organ
Dysfunction Syndrom
Severe hypoxemia and hypercapnia will lead to respiratory failure.
 Decrease of the oxygen influx reaching the tissues will lead to metabolic acidosis.
 MODS will develop:
 Renal failure with oliguria/anuria
 Marked impairment of the cognitive function Systemic arterial hypotension
 Low cardiac output heart failure

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 THE NEW BERLIN CLASSIFICATION FOR ARDS
Established three degrees of severity, depending on the hypoxemia severity:
I. Mild: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg
II. Moderate: 100 mmHg < PaO2/FiO2 ≤ 200 mmHg
III. Severe: PaO2/FiO2 ≤ 100 mmHg

ARDS POSITIVE DIAGNOSIS:

 History of pulmonary lesions in an etiologically established context
 Clinical examination of the patient
 Analysis of the blood gases, acid-base and hydroelectrolitic balance – ASTRUP
Astrup parameters (normal values ):
1) Actual pH= NV- 7.38-7.42
2) Standard pH= NV- 7.38-7.42
 (in standard conditions: pCO2 = 40mmHg, temp 37°C, SaO2 = 100%)
3) Actual bicarbonate (HCO3- ) = NV- 24-28mEq/l
4) Standard bicarbonate = NV- 24-28mEg/l
5) pCO2 = 40mmHg or 1.25mEq/l
6) Buffer base = NV 46-52mEq/l
7) Base excess= NB-2to+2

Definition of the ALI/ARDS includes:

Imagistic criteria (thoracic Rx):
 Bilateral pulmonary infiltrates, with a sudden onset
 Bilateral diffuse opacities, initially with an interstitial pattern which then becomes alveolar
Low PaO2 – below 50 mmHg +
 progressive hypoxemia that does not respond to oxygen therapy
Clinical absence of high pressure values in the left atrium
 normal filling pressure of the LA
The initial clinical exam finds diffuse bronchial and crepitant rales
ARDS TREATMENT PRINCIPLES
 Early finding and treatment of the initial cause that lead to the pulmonary lesions.
 Supportive therapy for preventing and stopping the pulmonary lesions.
 Preventing complications, such as pneumonia, stress ulcers, MODS.
Classical therapy:
mechanical ventilation with PEEP with high concentration oxygen therapy

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 RESPIRATORY SYSTEM’S PATHOPHYSIOLOGY II
CHRONIC INTERSTITIAL DISEASES
CHARACTERISTICS
bilateral, often patchy, pulmonary fibrosis mainly affecting the walls of the alveoli.

Many of the entities in this group are of unknown cause and pathogenesis; some have an intraalveolar and an
interstitial component.
Hallmark of these disorders
 Reduced compliance (stiff lungs
 necessitates increased effort to breathe (dyspnea).
 Damage to the alveolar epithelium and interstitial vasculature
 produces abnormalities in the ventilation–perfusion ratio, leading to hypoxia

RESTRICTIVE DISORDERS
CHARACTERISTICS
 Reduced expansion of lung parenchyma
 decreased total lung capacity.
SPIROMETRY
 FVC is reduced
 expiratory flow rate is normal or reduced proportionately.
 Hence, the ratio of FEV to FVC is near normal.

ETIOLOGY
AFFECTIONS OF RESPIRATORY CENTERS
 Brain injury
 Electric shock
 Compression
 Tumors – malignant or benign
 Hematoma
 Abscess
 Cysts
 High intracranial pressure: hypertension, hydrocephaly – Edema:
o Trauma
o Necrosis
o Tumors
o (demyelinating Degenerative thesaurismosis) processes
o Autoimmune diseases disease,
 Intoxications: CO2, CO, opioids, toxic gas, alcohol
AFFECTIONS OF RESPIRATORY TRACTS
 Afection of phrenic nerve
o Trauma – direct lesion
o Mediastinal irritative (e.g. herpes zoster), destructive, compressive processes
 Diaphragm paralysis or high position (pregnancy)
 Intercostal neuralgia – inflammation, infections, degenerative processes
 Poliradiculonevritis (e.g. diabetes mellitus – affection of vasa nervorum)
 Pain – it limits respiratory movements
 Vertebral compressive processes – chronic inflammation, osteophytes

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 AFFECTION OF NEURAL MOTOR PLAQUE
 Intoxications: curare, strychnine
 Tetanus
 Myasthenia gravis
It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block
acetylcholine receptors at the post-synaptic neuromuscular junction, inhibiting the stimulative effect of
the neurotransmitter acetylcholine.
 Myasthenia like syndrome
o peptides that block acetylcholine receptors (in tumors).
AFFECTIONS OF THORACIC CAGE
 Muscles
o Myositis
o Trauma
o Toxic substances
o Infectious diseases
o Autoimmune diseases
o Metabolic diseases (glycogenosis)
 Ribs diseases (fractures, compressions)
 Spine diseases
o Spondylitis, kyphosis, scoliosis, lordosis, Pott disease (tuberculous spondylitis), pathologic
fractures, rachitism, arthrosis, autoimmune diseases (chronic inflammation), inflammatory,
degenerative diseases.
LUNG DISEASES
PNEUMONIAS
 Accompanying pneumonias – reactive:
o trauma, radiations, chemicals (the quality of surfactant is changed)
 Infectious pneumonias
o The most frequent
o They can be produced by bacterias, viruses, funguses, parasites
DISLOCATION DISEASES
 Abscess
 Tuberculosis
 Tumors
 Fibrosis
 Emphysema
 Hydaticcyst (Taeniaechinococcus)
 Pulmonary infarction
o Usually there is as ource of thrombus (varicose vain, hemorrhoids, surgery on the pelvis,
gallbladder, catheterization)
 Pulmonary resection

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 RESPIRATORY DISEASES’ PATHOPHYSIOLOGY
DISORDERS OF THE THORACIC WALL AND PLEURA
Modifications of the thoracic wall
 modifications of the tidal volume => hypercapnia
Pleural anomalies
 ventilation impairment and hypoxemia

DISORDERS OF THE THORACIC WALL

Modifications of the thoracic wall  Restrictive ventilatory dysfunctions
 Deformed/traumatized/ immobilized wall
o Kyphoscoliosis
o Pectus excavatum / carinatum
o Musculoskeletal anomalies
o Neuromuscular disorders: muscular dystrophies,
myasthenia gravis, Guillain-Barre syndrome
o Pain in case of thoracic or superior abdomen trauma
 Excessive obesity

FLAIL CHEST
Cause:
 multiple consecutive ribs fractures, or fractures of both sternum and ribs
 Frequently associates lung contusions
Paradoxical movements:
 During inspiration  aspiration of the thoracic wall,
 During expiratio  expansion of the thoracic wall
Clinical manifestations include:
 pain,
 dyspnea,
 unequal and asymmetrical expansion of the chest ,
 hypoventilation with hypercapnia and hypoxemia
Treatment :
Internal fixation of the thoracic wall through mechanical ventilation until the thorax it is stabilized

PLEURAL DISEASES
The pleura is a thin, double-
layered membrane that
encases the lungs.
The two layers of the
pleurae are separated by a
thin layer of serous fluid.

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The pressure in the pleural cavity, which is negative in relation to atmospheric pressure, holds the lungs against
the chest wall and keeps them from collapsing.
Disorders of the pleura include:
 Pleurtis = inflammation of the pleura
 Pleural effusion
 Pneumothorax

PNEUMOTHORAX
Definition:
Air or other gas’ presence in the pleural space caused by a rupture of the visceral or parietal pleura or due to a
rupture of the thoracic wall
Consequences
Loss of the negative pressure existent in the pleural cavity
 The lung parenchyma will then have a tendency to collapse towards the hilum
Etiology
Primary-Spontaneous
Occurs in otherwise healthy patients,especially males, between 20-40 y.o.
Cause
Spontaneous rupture of some emphysema bubbles found near the visceral pleura , especially in the
apical region
 The rupture can produce during sleep, rest state or physical effort
 10% of cases have a positive familial history for this disorder- mutation of the folliculin gene -Birt-
Hogg-Dubé syndrome
Secondary-Traumatic
Cause
 The most common cause- thoracic trauma with costal fractures by stabbing or bullet wounds
 Other causes:
o during surgical procedures,
o rupture of some emphysema bubbles in COPD patients,
o mechanical ventilation with high PEEP (Pozitive End-Expiratory Pressure)
(Iatrogenic) Medically-Induced
Most frequently –needle thoracic aspiration
Open– Communicating
There is an open communication between the lungs and visceral pleura or between parietal pleura and
thoracic wall.
 Pressure from the pleural cavity it is equal with the atmospheric one.
Closed– In Tension– Suffocating
The pleural orifice acts like a valve , air enters during inspiration and can’t be evacuated ;
 after each inspiration the air volume increases and the lung parenchyma rapidly collapses

22
 CLINICAL MANIFESTATIONS
Clinical manifestations depend on the air volume inside the pleural cavity and on the type of the
pneumothorax:
 communicating or suffocating
 Sudden chest pain
 Tachypnea
 Mild dyspnea
 Decrease or absence of breath sounds
 Hypersonority on percussion
 Diagnosis relies on RX, ultrasound or CT
 Asymmetry of chest movement may occur
 Hypoxemia
 usually develops immediately after a large pneumothorax,
 Hypoxemia is followed by vasoconstriction of the blood vessels in the affected lung, causing the
blood flow to shift to the unaffected lung:
 In persons with primary spontaneous pneumothorax, this mechanism usually returns oxygen
saturation to normal within 24 hours.
 Hypoxemia usually is more serious in persons with underlying lung disease in whom
secondary spontaneous pneumothorax develops.
 In these persons, the hypoxemia caused by the partial or total loss of lung function can
be life threatening.

PLEURAL EFFUSION
Pleural effusion refers to an abnormal collection of fluid in the pleural cavity.
 The source of the liquid it can be represented by blood or lymph vessels, abscess or other lesion that
drains in the pleural cavity
 The fluid may be a transudate, exudate, purulent drainage (empyema), chyle, or blood.
– If the vessels are intact, pleural effusion can be either exudate or transudate (hydrothorax)
 Like fluid developing in other transcellular spaces in the body, pleural effusion occurs when the rate of
fluid formation exceeds the rate of its removal.

23
PLEURAL EFFUSION
Five mechanisms have been linked to the abnormal collection of fluid in the pleural cavity:
1) Increased Capillary Pressure
 Congestive heart failure;
2) increased capillary permeability,
 Inflammatory conditions;
3) decreased colloidal osmotic pressure,
 Hypoalbuminemia occurring with liver disease and nephrosis;
4) increased negative intrapleural pressure
 Develops with atelectasis;
5) impaired lymphatic drainage of the pleural space,
 Results from obstructive processes such as mediastinal
carcinoma.
SIGNS OF PLEURAL EFFUSION
The manifestations of pleural effusion vary with the cause.
Fluid in the pleural cavity acts as a space-occupying mass.
 It causes:
 Decrease in lung expansion
 on the affected side that is proportional to the amount of fluid that is present.
 Dyspnea,
 Most common symptom,
 occurs when fluid compresses the lung, resulting in decreased ventilation.
 Dullness or flatness to percussion and diminished breath sounds.
 Pleuritic pain
 usually occurs only when inflammation is present, although constant discomfort may be
felt with large effusions.
 Mild hypoxemia
 may occur and usually is corrected with supplemental oxygen.
PLEURAL TRANSUDATE
Water leaves vascular bed either due to
 increase of the intravascular hydrostatic pressure
 a decrease of the capillary oncotic pressure
Common causes:
 Congestive heart failure
 due to an increase of the venous pressure and an increase of the left atrial pressure
 Liver and kidney chronic disease
 leads to hypoproteinemia

24
 PLEURAL EXUDATE
 Less water,
 High amount of plasmatic proteins and cells: leukocytes
Causes:
Response to inflammation, infection or neoplasia
 The inflammatory response manifests through vascular reaction –the capillary permeability increases

Paraneoplasic Pleural Exudate

EXUDATE VS TRANSUDATE
Transudate
Hydrothorax
The accumulation of a serous transudate (clear fluid, water density, low protein concentration, no cells)
in the pleural cavity.
Causes
 The condition may be unilateral or bilateral
 Caused by increased hydrostatic pressure in venous system that drains pleura.
o The most common cause of hydrothorax is congestive heart failure.
o Other causes are renal failure, nephrosis, liver failure, and malignancy.
Exudate
Definition
An exudate is a pleural fluid that has a specific gravity greater than 1.020, often inflammatory cells and
protein concentration > 2,5 g%.
Causes
 infections,
 pulmonary infarction,
 malignancies,
 autoimmune diseases (e.g. rheumatoid arthritis, lupus erythematosus).
Pleural fluid is classified as an exudate if it meets any one of the following criteria:
 Ratio of pleural fluid protein to serum protein greater than 0.5
 Ratio of pleural fluid lactate dehydrogenase (LDH) to serum LDH greater than 0.6
 Pleural fluid LDH greater than two thirds the upper limit of normal for serum LDH (a cutoff
value of 200 IU/L was used previously)
Although the reason is unclear, cholesterol concentration is higher in exudates than in transudates.
Various studies have looked at the usefulness of cholesterol measurements alone, as a fluid-to-serum
ratio, or in combination with LDH, with cutoffs ranging from 45 to 60 mg/dL, but cannot be used as a
substitute to measurements of protein and LDH.
25
26
 HEMOTHORAX
 Definition
Is the presence of blood in the pleural cavity.
Hemorrhagic pleural fluid is a mixture of blood and pleural fluid.
 Treatment
Hemothorax usually requires drainage, and if the bleeding continues, surgery to control the bleeding
may be required.
 Bleeding may arise from
 Chest injury
 A complication of chest surgery
 Malignancies
 Rupture of a great vessel such as an aortic aneurysm, tuberculosis, pulmonary infarction.
EMPYEMA
 Definition
Pus in the pleural cavity.
 Causative agents
o Staphylococcus aureus,
o Escherichia coli,
o Klebsiella pneumoniae
o and anaerobic species
 Cause
o Direct infection of the pleural space from an adjacent bacterial pneumonia
o Rupture of a lung abscess into the pleural space
o Invasion from a subdiaphragmatic infection
o Infection associated with trauma

CHYLOTHORAX
 Definition
o is the effusion of lymph in the thoracic cavity.
 Causes
o Chylothorax also results from trauma, inflammation, or malignant infiltration obstructing chyle
transport from the thoracic duct into the central circulation.
o It also can occur as a complication of intrathoracic surgical procedures and use of the great veins
for total parenteral nutrition and hemodynamic monitoring.

27
RESTRICTIVE PULMONARY DYSFUNCTIONS
1) Aspiration
2) Atelectasis
3) Bronchiectasis
4) Bronchiolitis
5) Pulmonary fibrosis
6) Pulmonary edema
7) Lung impairment in systemic disorders
ASPIRATION
Represents the entrance of foreign materials- solids or liquids- inside the airways and lungs
The most frequent situations include:
 alterations of the normal deglutition and cough mechanisms
Favoring causes:
 substance abuse,
 sedation, anesthesia,
 epilepsy, cerebrovascular events,
 neuromuscular disorders that lead to dysphagia
The inferior lobe of the right lung has the higher risk to be involved, due to the existent anatomical structure
Gastric content aspiration it is complicated because it also implies a very low (acidic) pH-2.5
 Risk of aspiration pneumonia
 Risk of ARDS

28
ATELECTASIS
Definition
Represents collapse of the lung parenchyma
It has a tendency to occur after surgeries that have been performed using general anesthesia
Clinical manifestations
Similar to those of a pulmonary infection:
 dyspnea, cough, fever, leukocytosis
Classification :
1) Atelectasis Compression atelectasis
External pressure on the lung parenchyma
Causes
 Pleural collections ,
 Tumors,
 Distended abdomen

2) Absorption atelectasis
Gradual absorption of the air from the obstructed or hypoventilated alveoli;
Causes
 Concentrated oxygen or
 Anesthetic agents’ inhalation

3) Surfactant deficit related atelectasis

Decrease of surfactant production or modifying the one that’s already formed
Causes:
 Premature birth,
 ARDS,
 General anesthesia or
 Mechanical ventilation

BRONCHIECTASIS
 Definition
It is a persistent/permanent abnormal dilatation of bronchi caused by destruction of smooth muscle and
the supporting elastic tissue
 Cause
It always occurs secondary to persistent infection or obstruction caused by a variety of conditions
 Associations
o Other respiratory conditions, seen with a chronic bronchial inflammation:
 mucus plug, atelectasis, infections, cystic fibrosis, TB, genetic defects of the bronchial wall
or of the mechanisms of mucociliary clearance
o Systemic disorders:
 Rheumatologic disorders, AIDS, IBD (inflammatory bowel disorders)- Crohn’s disease and
ulcero-hemorrhagic rectocolitis
 Classification according to bronchial dilatation:
o Cylindrical – post pneumonia; can be reversible
o Sacciform
o Varicose
The last 2 can become worse with time and they predispose to cough, abundant expectoration,
hemoptysis and atelectasis
29
 They manifest through signs and symptoms of chronic hypoxemia: dyspnea, Hippocratic fingers

BRONCHIOLITIS
Diffuse inflammation of the small airways.
More frequent in children.
In adults occurs in association with
 chronic bronchitis and
 especially in case of viral respiratory infections or toxic gas inhalation
Atelectasis or emphysema affect the distal region of the airways

By definition, bronchiolitis it is diffuse.

A quick and important reduction of theV/Q ratio occurs so acute hypoxemia, followed by hypercapnia will
develop
 Clinical manifestation:
Tachypnea, usage of the accessory muscles, mild fever, dry cough, overinflated thorax
If it occurs after inhalation of toxic substances, pulmonary edema or even ARDS with severe hypoxemia
can develop.

OBLITERATIVE BRONCHIOLITIS
 Definition
It is a chronic, fibrotic process that permanently damages the small airways
 Cause
Can occur in any type of bronchiolitis but it is more frequent after lung transplant when it is associated
with acute rejection and infections

30
PULMONARY FIBROSIS
 Definition
Fibrosis excess or excessive connective fibrous tissue in the lungs
If a specific cause it cannot be found,the term used it is idiopathic pulmonary fibrosis (IPF)
Secondary pulmonary fibrosis:
Inhealing phases of ARDS (proliferative and fibrotic), autoimmune rheumatologic diseases, toxic gases’
inhalation, inorganic dust inhalation

Idiopathic Pulmonary Fibrosis

it is the most common pathology of the lung interstitium
Usually affects males over 60 yo, with an average survival of 2-4 years since the diagnosis.
The radiologic and histologic pattern of fibrosis is referred to as usual interstitial pneumonia (dg of exclusion)
It is the result of multiple, repeated injury and defective repair of alveolar epithelium, often in a genetically
predisposed individual followed by erroneous, scarring healing
Specifically, approximately 35% of affected individuals have a genetic variant in the MUC5B gene that alters
the production of mucin, while a smaller number of affected patients have germ line mutations in surfactant
genes.
Chronic inflammation and fibrotic proliferation in the interstitium around the alveoli will finally lead to MAC
breaking with hypoxemia, hypoventilation and hypercapnia

31
Theunifyingpathogenicfactorisinjurytothe alveoli leading to activation of macrophages and release of fibrogenic
cytokines such as TGF-β.
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary fibrosis Exposuretotoxicgases
 Acute and massive inhalation of toxic gases will lead to lesions of the respiratory epithelium , cilia, mucus
and surfactant production and finally to ARDS: ammonia, gaseous hydrochloric acid, sulfur dioxide,
chloride, phosgene, nitrogen dioxide, smoke that resulted after combustion of household/industrial
substances
 Chronic, small dose inhalation, will lead to pulmonary fibrosis
 Oxygen toxicity in iatrogenic conditions it is due to ROS excess
Pneumoconiosis – any modification in the lungs induced by inorganic dust particles , usually due to work
conditions (professional/work-related diseases)
 Asbestosis – asbestos
 Silicosis – SiO2
 Anthracosis – coal dust
 Talc, glass fibers, cement, cadmium, beryllium, tungsten, cobalt, aluminum, iron
Theycanoccuralsoduetosomeorganic,vegetal particles- byssinosis or “farmer’s lung”
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary fibrosis
Pneumoconiosis–pathophysiologicalmechanism – particles found in the lung parenchyma leads to release of
proinflammatory cytokines (IL-1β), with a chronic inflammatory reaction
 InterstitialfibrosisoccurswithACMdamage
 Clinically:cough,sputum,dyspnea,decreaseofthe lung volumes and hypoxemia
RESTRICTIVE PULMONARY DYSFUNCTIONS Pulmonary fibrosis
 The pulmonary alveolar macrophage is a key cellular element in the initiation and perpetuation of
inflammation, lung injury and fibrosis.
 Following phagocytosis by macrophages, many particles induce production of the pro-inflammatory
cytokine IL-1 as well as the release of other factors, which initiates an inflammatory response that leads
to fibroblast proliferation and collagen deposition

32
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary fibrosis
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary fibrosis
 Hypersensitivepneumonitis–extrinsicallergic alveolitis
 It is an allergic, inflammatory disorder, due to inhalation of organic particles: cereals , silo, resin, maple,
animal skin, coffee beans, fish flour, mushroom derivatives, mold from cereals, fog from still waters,
smoke from paints and resins
 Type III hypersensitivity reaction , induced by alveolar macrophages , with IgG production , followed by a
type IV hypersensitivity reaction , with granuloma formation
RESTRICTIVE PULMONARY DYSFUNCTIONS
Lung impairment in systemic disorders
 Many systemic diseases affect the airways, pleura or lung parenchyma, leading to fibrosis, vasculitis,
pulmonary hemorrhage or granuloma formation
 Clinical manifestations are unspecific and they are superimposed on those of the underlying condition
 Granulomatous diseases: sarcoidosis, Wegener granulomatosis, lymphoid granulomatosis , eosinophilic
granuloma
 Connective tissue disorders: rheumatoid arthritis , systemic lupus erythematosus, scleroderma ,
polymyositis , dermatomyositis , Sjögren syndrome , Polyarteritis nodosa , cystic fibrosis, Goodpasture
syndrome

RESTRICTIVE PULMONARY DYSFUNCTIONS

Lung impairment in systemic disorders
Several immunologic abnormalities in sarcoidosis suggest the development of a cell-mediated response to an
unidentified antigen. The process is driven by CD4+ helper T cells
 IntraalveolarandinterstitialaccumulationofCD4+TH1cells,with peripheral T cell cytopenia
 OligoclonalexpansionofCD4+TH1Tcellswithinthelungas determined by analysis of T cell receptor
rearrangements
 IncreasesinTH1cytokinessuchasIL-2andIFN-γ,resultinginTcell proliferation and macrophage activation,
respectively
 Increasesinseveralcytokinesinthelocalenvironment(IL-8,TNF, macrophage inflammatory protein-1α) that
favor recruitment of additional T cells and monocytes and contribute to the formation of granulomas
 Polyclonalhypergammaglobulinemia
 Familialandracialclusteringofcases,suggestingtheinvolvementof genetic factors
SMOKING-ASSOCIATED INTERSTITIAL LUNG DISEASE
 Desquamative interstitial pneumonia (DIP) and respiratory bronchiolitis are two related examples of
smoking-associated interstitial lung disease.
 The most striking histologic feature of DIP is the accumulation of large numbers of macrophages
containing dusty-brown pigment (smoker’s macrophages) in the air spaces.
 The alveolar septa are thickened by a sparse inflammatory infiltrate (usually lymphocytes); interstitial
fibrosis, when present, is mild.
 Pulmonary function tests usually show a mild restrictive abnormality.
 Overall, patients with DIP have a good prognosis and an excellent response to steroids and smoking
cessation; however, some patients progress despite therapy.
SMOKING-ASSOCIATED INTERSTITIAL LUNG DISEASE
 Respiratory bronchiolitis is a common lesion found in smokers that is characterized by the presence of
pigmented intraluminal macrophages akin to those in DIP, but in a “bronchiolocentric” distribution (first-
and second-order respiratory bronchioles).
 As with DIP, affected patients present with gradual onset of dyspnea and dry cough, and the symptoms
recede with smoking cessation
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema
 It is defined as an excess of fluid in the lungs
 Normally, in the lungs there is a very small amount of fluid

33
  The lung it is maintained dry through an adequate lymphatic drainage and a balance between the
capillary permeability, hydrostatic pressure and oncotic pressure
 The surfactant found in alveoli (lipidic structure) repels water and opposes to fluid entrance into the
alveoli
 The predisposing factors for pulmonary edema include: cardiac diseases, ARDS and toxic gases inhalation

RESTRICTIVE PULMONARY DYSFUNCTIONS

Pulmonary edema
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema
 The most common cause of acute pulmonary edema (APE) it is represented by affections of the left heart
– acute cardiogenic pulmonary edema
 Whenever left ventricular failure exists , the pressure increases in a retrograde manner in the LA,
pulmonary veins and, subsequently, the hydrostatic pressure in the pulmonary capillaries
 When hydrostatic pressure it is greater than oncotic pressure , the fluid from the blood (water from the
plasma) will go initially in the lung interstitium
 The fluid then enters in the lymph vessels and it is drained from the lungs
 When a very large volume of liquid flows from the pulmonary capillaries and it cannot be reabsorbed by
the lymph vessels , the fluid enters in the lung alveoli and APE occurs
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema

34
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema
 Usually,APEdevelopswhenthepressureinthe LA or in the pulmonary capillaries reaches or exceeds 20
mmHg
 Iftheoncoticpressuredrops:hypoproteinemia, anemia etc , APE can occur at a hydrostatic pressure lower
than 20 mmHg
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema

35
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema

36
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema
 Non –cardiogenic APE– ARDS
 APE can occur also in case of a lymph vessel
obstruction.
 Causes that can stop the lymph drainage can be: soft tissue edema, tumors, fibrosis, increase of the
central venous pressure.
RESTRICTIVE PULMONARY DYSFUNCTIONS
Pulmonary edema

37
Pneumonias

LUNG DISEASES
 Accompanying pneumonias – reactive: trauma, radiations, chemicals (the quality of surfactant is changed)
 Infectious pneumonias
 The most frequent
 They can be produced by bacterias, viruses, funguses, parasites
Dislocation diseases
 Abscess
 Tuberculosis
 Tumors

38
  Fibrosis
 Emphysema
 Hydatic cyst (Taenia echinococcus)
 Pulmonary infarction – usually there is a source of thrombus (varicose vain, hemorrhoids, surgery on the
pelvis, gallbladder, catheterization)
 Pulmonary resection

PNEUMONIAS
The term pneumonia describes inflammation of parenchymal structures of the lung, such as the alveoli and the
bronchioles.
 It is the most common cause of death from infectious disease, particularly among the elderly and persons
with debilitating diseases.
 Etiologic agents include infectious and non infectious agents.
 Pneumonias can be classified as:
– Typical (i.e. bacterial)
Typical pneumonia results from infection by bacteria that multiply extracellularly in the alveoli and cause
inflammation and exudation of fluid into the air-filled spaces of the alveoli.
– Atypical (i.e. viral or mycoplasmal)
Atypical pneumonias produce inflammatory changes that are confined to the alveolar septum and the interstitium
of the lung. They usually produce less striking symptoms and physical findings than bacterial pneumonia.
PNEUMONIAS
Community-acquired pneumonia results from organisms found in the community, rather than in the hospital or
nursing home.
– Common causes of community - acquired pneumonia include Streptococcus pneumoniae (single most common
cause), Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae and other gram-negative bacilli,
Legionella pneumophila and the influenza and respiratory syncytial viruses.
Hospital-acquired, or nosocomial, pneumonia is defined as a lower respiratory tract infection that was not present
or incubating on admission to the hospital.
 Usually, infections occurring 48 hours or more after admission are considered hospital acquired.
 Mosthospital-acquiredpneumoniasarebacterial.
 The organisms are those present in the hospital environment and include Pseudomonas aeruginosa, S.
aureus, Enterobacter species, Klebsiella species, Escherichia coli, and Serratia.
 The organisms that are responsible for hospital - acquired pneumonias are different from those
responsible for community-acquired pneumonia, and many of them have acquired antibiotic resistance
and are more difficult to treat.
 Persons requiring mechanical ventilation are particularly at risk, as are those with compromised immune
function, chronic lung disease, or airway instrumentation, such as endotracheal intubation or
tracheotomy.
TYPICAL BACTERIAL PNEUMONIA
 Most of the bacteria that cause typical bacterial pneumonia are normal inhabitants of the nasopharynx or
oropharynx and are aspirated into the lung.
 Acute bacterial pneumonias are also classified according to two anatomic and radiologic patterns:
– Lobarpneumonia
Affectingapartorallofalunglobe Colonizationbyair
– Multifocalpneumonia
 Multiplefociintheupperandmiddlelobes
 Colonizationbyair
 Usually when there is a higher amount of bacteria or immune system suppression
– Bronchopneumonia
Apatchydistributioninvolvingmorethanonelobe
Bloodorlymphcolonization
Itissupposedtheexistenceofadistancesourceofbacteria,sepsis
ATYPICAL PNEUMONIAS
 The pathologic process affects the alveolus - capillary membrane.

39
  They are usually preceded by pharyngitis and systemic flulike symptoms that evolve into laryngitis and
finally tracheobronchitis and pneumonia.
 The most common pathogens are Mycoplasma pneumoniae, viruses, and Chlamydia pneumoniae.
 The symptoms may remain confined to fever, headache, and muscle aches and pains.
 Cough, when present, is characteristically dry, hacking, and nonproductive.
 Viruses impair the respiratory tract defenses and predispose to bronchopneumonia.
 Some viruses such as herpes simplex, varicella and adenovirus may be associated with acute inflammation
and necrosis of the alveolar epithelium.
PNEUMONIA
 Worldwide, approximately 7-13% of cases of pneumonia in children require hospitalization, while in
developed countries, 22 to 42% of adults with community-acquired disease are hospitalized.
 CURB-65 score is useful to determine whether adults require hospitalization.
 Patients with score 0 or 1 can be treated, usually at home, patients with score 2 requires a brief
hospitalization and careful monitoring, and patients with score 3-5 must be hospitalized.
CURB-65
Symptom Points
Confusion 1
Urea >7 mmol/l 1
Respiratory rate > 30/min 1
SBP < 90mmHg, DBP < 60mmHg 1
Age ≥ 65 1
PNEUMONIA
The children with respiratory distress or oxygen saturation below 90% should be hospitalized.
Pneumonia severity index is a score useful for decision to the emergency room.
 A patient with pneumonia risk class I may be sent home with oral antibiotics.
 A patient with pneumonia risk class II-III can be sent home with antibiotics or treated and monitored for
24 hours in the hospital.
 Patients with pneumonia risk class IV-V should be hospitalized for treatment.
Step 1: Stratify to Risk Class I vs. Risk Classes II-V
Presence of:
Over 50 years of age Yes/No
Altered mental status Yes/No
Pulse ≥125/minute Yes/No
Respiratory rate >30/minute Yes/No
Systolic blood pressure <90 mm Hg Yes/No
Temperature <35°C or ≥40°C Yes/No
History of:
Neoplastic disease Yes/No
Congestive heart failure Yes/No
Cerebrovascular disease Yes/No
Renal disease Yes/No
Liver disease Yes/No
If any "Yes", then proceed to Step 2
If all "No" then assign to Risk Class
I
Step 2: Stratify to Risk Class II vs III vs IV vs V
Demographics Points Assigned
If Male +Age (yr)
If Female +Age (yr) - 10

40
Nursing home resident +10
Comorbidity
Neoplastic disease +30
Liver disease +20
Congestive heart failure +10
Cerebrovascular disease +10
Renal disease +10
Physical Exam Findings
Altered mental status +20
Pulse ≥125/minute +10
Respiratory rate >30/minute +20
Systolic blood pressure <90 mm Hg +20
Temperature <35°C or ≥40°C +15

Lab and Radiographic Findings

+30
+20
+20
+10
+10
41
+10
+10
Arterial pH <7.35
Blood urea nitrogen ≥30 mg/dl (9 mmol/liter)
Sodium <130 mmol/liter
Glucose ≥250 mg/dl (14 mmol/liter)
Hematocrit <30%
Partial pressure of arterial O2 <60mmHg
Pleural effusion
∑ <70 = Risk Class II
∑ 71-90 = Risk Class III
∑ 91-130 = Risk Class IV
∑ >130 = Risk Class V

42