Pathology of Respiration
24 March 2015
Respiratory failure
Lungs are unable to provide:
an adequate supply of O2
and/or to remove CO2 efficiently
In arterial blood: pO2 - 95 - 100 mm Hg
pCO2 - 43 - 46 mm Hg
Classification:
Acute failure – minutes to hours (bronchial asthma
attack, acute pneumonia).
Subacute –days to weeks (pneumonia, bronchitis).
Chronic – months to years (emphysema of lungs,
disseminated lung fibrosis).
Respiratory failure classification
Type 1 – hypoxia without hypercapnia
low oxygen in the air
ventilation/perfusion mismatch
pnemonia, lung edema
gases diffusion disturbances
Type 2 – hypoxia with hypercapnia
reduced breathing effort;
increased resistance to breathing (asthma);
in the area of the lung that is not available
for gas exchange (COPD,emphysema).
Reasons of respiratory failure
Disturbances of lungs function
ventilation,
perfusion,
alveolar ventilation-perfusion ratio,
gases diffusion through alveolar-
capillary membrane.
Reasons of respiratory failure
Extra-lungs disturbances of:
nervous regulation of respiration (brain
stroke or trauma, tumour, drugs overdose),
respiratory muscles function (myasthenia,
poliomyelitis),
chest respiratory movements (fracture of
ribs or spinal column, chest wall deformities),
blood circulation in the lungs (cardiac
failure, severe anemia).
Disturbances of alveolar
ventilation
MIXED
OBSTRUCTIVE RESTRICTIVE
VIOLATIONS OF RESPIRATION
Alveolar hypoventilation
EXTRA-LUNGS REASONS
depression disorders of thoracic cage
of respiratory center respiratory muscles disorders
Obstructive lung disorders
Obstruction of the upper respiratory ways:
embolism (foreign substance),
compression (tumour),
spasm of larynx (neurogenous, inflammatory).
Decreased permeability of the lower respiratory
ways:
increased bronchial muscles tonus (bronchospasm),
embolism of bronchi:
edema of bronchial mucous membranes
hypersecretion of mucus by bronchial glands
(inflammation, asthma).
Violation of bronchi flexibility
lungs emphysema.
Restrictive lung diseases
Disturbances of lung’s expansion
Pulmonary reasons:
area of lung (resection, tuberculosis)
elasticity of lung tissue
(pneumosclerosis, lung fibrosis,
sarcoidosis)
Alveolar or interstitial lung edema
Acute respiratory distress syndrome
(ARDS).
Deficiency of surfactant (premature
infants)
Restrictive lung diseases
Extrapulmonary reasons:
Changes in pleura and mediastinum
(exudative pleurisy, pneumothorax,
cardiomegaly).
Changes of thorax and respiratory
muscles (deformation of thorax,
paralysis of diaphragm).
Changes of abdominal cavity organs
(hepatomegaly, ascites).
Disorders of perfusion
Hyperperfusion
Local - pneumonia.
Total - stress reaction or asphyxia.
Erythrocytes have less time for normal
gas exchange hypoxemia.
The diffusion of CO2– not altered.
Type 1 respiratory failure
Disorders of perfusion
Hypoperfusion
heart pathology (heart failure, valvular
disorders)
vessels pathology (atherosclerosis,
thromboembolism).
Pathogenetic mechanisms:
low cardiac output
opening of shunts between arteries and
veins of pulmonary circulation
obstruction of lung vessels
Type 1 respiratory failure
Mismatching of ventilation and
perfusion
Ventilation/perfusion ratio differs in lungs
physiologically
Reason of pathological mismatch:
Problems with ventilation
Collapsed airways (emphysema)
Bronchoconstriction (COPD, asthma)
Inflammation (bronchitis, pneumonia)
Lung diseases (fibrosis, pulmonary vascular
congestion)
Low oxygen in alveoli perfusion
Carbon dioxide is increased
Type 2 respiratory failure
Diffusion impairment
distance for diffusion (lung edema,
inflammation, fibrous changes).
permeability of the alveolar
capillary membrane ( ARDS,
pulmonary edema, emphysema).
Type 1 respiratory failure
Manifestations
of respiratory failure
Hypoxemia - pO2 < 50 mm Hg
Hypercapnia - pCO2 >50 mm Hg.
Hypoxemia Manifestations.
resulting from impaired function of
vital centers
resulting from activation of
compensatory mechanisms
Hypoxemia Manifestations
impairment of mental performance
and behavior
peripheral vasoconstriction
diaphoresis (sweating)
central or peripheral cyanosis
blood pressure
heart rate, hyperventilation
Hypercapnia Manifestations
pH and respiratory acidosis
compensated by renal bicarbonate
retention
vasodilating effect of CO2 :
increase in cerebral blood flow and cerebral
spinal fluid pressure (headache);
hyperemic conjunctivae;
warm and flushed skin.
Nervous system effects of CO2
-progressive somnolence, disorientation,
coma.
Acute respiratory distress
syndrome (ARDS)
Causes
aspiration of gastric contents, toxic
gases
trauma (with or without fat emboli),
sepsis
acute pancreatitis
pneumonia, alveolar bleedings
reactions to drugs and toxins.
ARDS pathogenesis and clinics
• Injuryand
permeability of the
alveolar-capillary
membrane lung
edema
•Neutrophils - inactivate
surfactant and damage
of the alveolar cells.
• lung becomes harder
ARDS clinical manifestation
rapid onset, 12 to 18 hours after
initial event
in respiratory rate
signs of respiratory failure
diffuse bilateral consolidation of the
lung tissue
marked hypoxemia
multiple organ failure (kidneys, GIT,
CNS, and cardiovascular system)
Pulmonary edema
cardiogenic (left-sided heart failure)
Non-cardiogenic pulmonary edema
alveolar walls damage by toxic compounds
(Phosporus), proteolytic enzymes (a.
pancreatitis)
microbe affection of lungs (local – bacterial
pneumonia, systemic – sepsis)
quick intravenous infusion of big amount of
fluid (physiological solution, blood substitutes)
– due to ”blood dilution”
anaphylactic allergic reaction – due to BAS
influence
catecholamines – generalized
vasoconstriction lung hypertension and
blood congestion.
Pulmonary edema symptoms
Acute Chronic
nocturia (frequent
difficult breathing
urination at night)
coughing up blood orthopnea (inability to
excessive sweating lie down flat due to
anxiety breathlessness)
paroxysmal nocturnal
pale skin
dyspnea (episodes of
coma and death severe sudden
from acute breathlessness at night).
hypoxia
Pulmonary edema
symptoms
Chronic pulmonary edema:
nocturia (frequent
urination at night),
ankle edema
orthopnea (inability to lie
down flat due to
breathlessness)
paroxysmal nocturnal
dyspnea (episodes of
severe sudden
breathlessness at night).
Short breath (dyspnea)
violation of frequency, depth, rhythm
of breath
changes of respiratory movements
“air hunger”
Dyspnea classification
According to pathogenesis
Cerebral dyspnoea (central) - violation of
respiratory center or cortex function.
Lung dyspnoea– diseases of lungs,
bronchi, pleura.
Cardiac dyspnoea - heart diseases with
cardiac failure.
Hematic dyspnoea - in blood oxygen
capacity (anaemia), acidosis.
Dyspnea classification
Due to dyspnea character:
Hyperpnea
Tachypnea
Bradypnea
Apnoea
Due to altered phase of respiration:
Inspiratory dyspnea
Expiratory dyspnea
Mixed dyspnoea
Dyspnoe mechanisms
Humoral – increase of pCO2 and
decrease of pO2, shift of pH to the
acid side.
Neuroregulatory – violated
impulsion from chemoreceptors
and baroreceptors.
Central – dysfunction of respiratory
center, or cortex neurons.
Cerebral dyspnea
Excitation of respiratory centre - frequent
deep respiration.
Inhibition of respiratory center - frequent
superficial respiration.
Periodic breathing appears at brain
affections by:
trauma
stroke
tumour
inflammation
endogenous and exogenous intoxications
Cheyne-Stokes respiration
failure of the respiratory center
bigger concentrations of CO2 are needed
for the excitation of respiratory centre.
causes: strokes, head injuries or brain
tumors, congestive heart failure, morphine
administration.
Bioth's respirations
cluster respiration.
damage to the medulla oblongata
(stroke, trauma, compression).
poor prognosis.
Kussmaul breathing
The cause of Kussmaul breathing is
respiratory compensation for a
metabolic acidosis (ketoacidosis,
uremia).
low pCO2 due to deep breathing.
Agonal respiration
shallow, irregular inspirations followed by
irregular pauses.
gasping, labored breathing, accompanied
by strange vocalizations and myoclonus.
Causes
cerebral ischemia
extreme hypoxia or anoxia
Other dyspnea types
Lungs dyspnea
Embolism or narrowing of upper respiratory
ways (stenotic breath)
bronchial asthma (expiratory dyspnoea)
pneumonia, pleurisy
Cardiac dyspnea
cardiac failure, heart valves pathology
Hematic dyspnea
anemia
metHb formation (CO poisoning).
Asphyxia
a condition of severe deficiency of oxygen
supply with severe disorders of nervous
system, respiration and circulation of the
blood
Causes:
Insufficient environmental oxygen:
Inhalation of non-oxygen gases (helium,
CO2 fire).
Loss of aircraft cabin pressure;
Exposure to a vacuum.
Asphyxia causes
Physical obstruction of air flow
Compressive asphyxia
Drowning (water or other liquids).
Choking due to object in the airways or inhalation
of vomit.
Narrowing of the airways (anaphylaxis, asthma).
Disturbances of respiration
CO inhalation.
Pulmonary agents (phosgene),blood agents
(cyanide).
Drug overdose.
Asphyxia stages
1st stage - frequency of breathing, BP and
heart rate - phase of inspiratory dyspnea –
compensation of acute hypoxia.
2nd stage- more rare respiration with enforced
expiration, slowing-down of heart rate and BP -
phase of expiratory dyspnea.
3rd stage - temporary (from several seconds to
several minutes) stopping of breathing
(preterminal pause); low BP, reflexes, loss of
consciousness.
4th stage - terminal or agonal breathing (rare
deep convulsive «sighs» during several
minutes); respiratory centre paralysis and
death.
Lung volumes
measurement
Forced expiratory volume in one second
(FEV1) is the 1-s-volume exhaled with forceful
pressure from maximal inspiration.
Forced vital capacity (FVC) is the maximum
amount of air forcibly expired after maximum
inspiration.
Total lung capacity (TLC) is the total volume of
air in the lungs, when they are maximally
inflated.
Residual volume (RV) the volume of air left in
the lungs after a maximal expiration.
Difference between obstructive,
restrictive and mixed disorders
Measure Obstructive Restrictive Mixed
Disorders Disorders Disorders
FEV1/FVC Normal or
FEV1 Normal
FVC Normal or
TLC Normal or
RV Normal or Normal
