Restrictive and obstructive respiratory disorders. Pneumonia. Respiratory insuficiency Institute of Pathophysiology Faculty of Medicine Comenius University Respirator insuficiency • Definition: ▪ inability of the respiratory system to ensure adequate gas exchange ▪ result: hypoxemia, hypercapnia or both • Basic criterion: ▪ assessment of blood gases Respiratory inuficiency Hypoxemia +/- hypercapnia • Normal levels of blood gases ▪ PaO2 = 10 – 13,3 kPa (75 – 100 mmHg) ▪ PaCO2 = 4,8 – 6,1 kPa (36 - 46 mmHg) • Definition ▪ PaO2 < 8,0 kPa (hypoxemia) s / bez PaCO2 > 6,5 kPa (hypercapnia) • Classification (according to blood gases levels) ▪ partial (type I, hypoxemic) – hypoxemia ▪ global (type II, hypercapnic) – hypoxemia, hypercapnia + according to ph value: compensated (normal ph value) / decompensated (↓ ph value) • Classification 1. partial / gobal compensated / decompensated 2. acute /chronic / chronic – acutely exacerbated 3. latent / manifest Partial (type I, hypoxemic) Global (type II, hypercapnic) hypoxemia hypoxemia + hypercapnia respiratory alkalosis respiratory acidosis→ compensated / decompensated global RI acute cases chronic cases V-P imbalance, intrapulmonary shunt ↓ minute ventilation / ↑ dead space Acute RI ➢Etiology: dramatic asphyxic conditions, acute CNS poisoning, acute bronchiolitis, pulmonary inflammation, ARDS ➢CP: symptoms of basic disease + symptoms of RI: central cyanosis, convulsions, ph <7,2 = disturbances of consciousness, ph <7 = unconsciousness ➢Therapy: urgent treatment of the underlying disease, airways release, reanimation, artificial respiration, oxygen therapy, ABB treatment Chronic RI • pulmonary causes: ➢chronic obstrction of URT and LRT (tumors, foreign bodies), COPD (80% of cases), pulmonary parenchymal diseases (pulmonary fibroses, pulmonary emphysema), cardiovascular diseases, chronic pleural diseases, pleural effusions ➢direct consequences of RI: pulmonary arterioles muscularization and right ventricular hypertrophy ➢complications: pulmonary hypertension, cor pulmonale ➢CP: hypoxia =fatigue, weakness, restlessness, ↑ irritability, depression, speech and vision disorders; hypercapnia = sleepiness through the day, night restless sleep and dreadful dreams, attenuation of the CNS → coma ➢physical findings: central cyanosis, ↑ neuromuscular irritation (tremor, muscle swelling), signs of hyperkinetic circulation, pulmonary hypertension and cor pulmonale (warm wet skin, raised veins, swelling of the face, passive hyperaemia, increased scleral gloss), increased jugular vein filling, enlarged liver Chronic RI • extrapulmonary causes: ▪ CNS diseases and damage (infection, trauma, vascular disorders), PNS damage ▪ myopathies, chest wall damage, kyphoscoliosis, obesity, surgical procedures • chronic hypoxia → adaptive changes: ➢↑ of increase of 2,3-diphosphoglycerate with the shift of the hemoglobin dissociation curve to the right, polyglobulia (↑ Htc and blood viscosity, ↑ concentration of Hb in erythrocytes) ➢↑ pressure in arteria pulmonalis→ muscularization of pulmonary arterioles, pulmonary hypertension → cor pulmonale ➢severe hypoxemia → lactic acidosis ➢hypercapnia → sequential adjustment of ph value and respiratory acidosis compensation Chronic – acutely exacerbated RI • chronic RI + intercurrent infection / oxygen therapy / sedation / cardiac weakness Latent RI Manifest RI Summary: Etiology: • pulmonary failure – diseases of respiratory tract, alveoli, alveolocapillary membrane or pulmonary vascular system • extrapulmonary failure– disorders of breathing center / prolonged spnal cord / respiratory muscles or their inervation, disorders of chest wall Clinical picture: • tachypnoea, dyspnoea, ortopnoea (involvement of the auxiliary respiratory muscles) • auscultation – weakening / dysappearance of breathing sounds • cyanosis • anxiety, agitation, quantitative disturbance of consciousness Investigation: • ABB and blood gases • history - circumstances of dyspnoea, intoxication, infections, state of consciousness • physical findings - pulmonary sound phenomena, cyanosis • RTG, CT • spirometry, ECG, ECHO Pathophysiology of RI Oxygen-hemoglobin dissociation curve Respiration = 4 processes: ventilation diffusion perfusion breathing control hypoventilation diffusion disorders V-P disproportion R-L pulmonary shunt compensation of hypoventilated alveolus - DLC RI vasoconstriction functional, anatomical and physiological pulmonary shunt Effect of hypercapnia on the organism = acidosis and its effects on the CNS 1. hypercapnia = acidification of internal enviroment → vicious cycle = deepening of hypercapnia 2. hyperkapnia = vasodilatation (hot skin, risk of edema of the brain - headache, ↑ intracranial pressure, optic nerve papillae edema, ↓ mental performance, trauma, purposeless twitch movements, lazy speech, mood swings, somnolencia to coma) 3. alveolar hypoventilation → alveolar hypercapnia + alveolar hypoxia Effects of hypocapnia on the organism • = alkalisation of the inner environment - ↓ degree of ionized calcium = from ↑ neuromuscular irritability to generalized convulsions • = vasoconstriction of the cerebral vessels → symptoms of inadequate oxygen supply of the brain = headache, dizziness The relationship of neuromuscular irritability and concentrations of each ions Na+ K+ Ca2+ Mg2+ H+ Pneumonia Defensive mechanisms of respiratory tract • Anatomical barriers of respiratory tract ▪ mucous membrane traps mucociliary apparatus removes particles / MO cleansing is aided by coughing • Overcoming anatomical barrier ▪ in sleep – aspiration of oropharyngeal secretion ▪ change in viscosity of the secretion / in performance of the ciliary apparatus is involved in the removal of pathogens • Alveoli ▪ do not contain mucociliary apparatus or muciparous cells → cleaning of these spaces by phagocytes and humoral factors in the surfactant Defensive mechanisms of respiratory tract Pneumonia in otherwise healthy people??? → occurs when several mechanisms are broken (anatomical barriers, cellular and humoral mechanisms in alveoli): ▪ changed consciousness ▪ impaired defensive reflexes (cough, disorder of mucociliary apparatus) ▪ bronchial obstruction ▪ impaired function of alveolar macrophages Inflammatory response AM pathogen inflammatory response leukotriene B4, C3a a C5a, components of the kinin system chemotactic factors for PMNL + ↑ vascular permeability = massive supply of PMNL (infiltration) IL-1, cachectin = Proteolytic fever, chills, enzymes malaise, myalgia Pneumonia • inflammation distally from bronchioli terminales (respiratory bronchioli, alveoli, interstitium) • transmission paths: ▪ aspiration from oral cavity / nasopharynx (most often) ▪ inhalation from air ▪ hematogenous ▪ penetration from the neighborhood • especially children and elderly Pathophysiology Immediate functional consequences of inflammation: • ↓ compliance of lung tissue • extension of the diffusion path for the breathing gases • R-L pulmonary shunt → hypoxemia, without accumulation of CO2, cyanosis, dyspnoea, ARDS, abscess, empyema, pleural effusion, organization Classification • according to the course ▪ according to the place of acquisition ▪ acute ▪ community ▪ chronic (˃ 3 months) ▪ nosocomial ▪ recurrent (repeatedly in the same location) • according to X-ray imaging ▪ migrating (infiltrates migrate) ▪ alar, lobar, bronchopneumonia • according to the etiology • according to the clinical picture ▪ infectious ▪ typical ▪ noninfectious = pneumonitis ▪ atypical (aspiration, inhalation, radiation, drugs, allergy) Etiology: the most common are bacterial: ▪ community: 90%, the agents: Str. pneumoniae, Str. pyogenes, St. aureus, Mycoplasma pneumoniae, HI, Klebsiella pneumoniae ▪ nosocomial: acquired from 48 hours to 4 days after hospitalization, the agents: Pseudomonas aeruginosa, Klebsiella pneumoniae, E. coli, Acinetobacter Main symptoms of pneumonia: ▪ cough, fever, sputum production, chest pain and dyspnoea (tachypnoea) Physical examination: ▪ auscultation: tubular breathing ▪ percussion: silenced ▪ bronchophony: strengthened ▪ fremitus pectoralis: enhanced Pneumococcal pneumonia • Str. pneumoniae (pneumococcus) - the most common cause of community-acquired pneumonia • by inhalation / aspiration • usually – infections of the upper RT are prior • 4 stages: 1. hyperaemia / congestion: inflammation begins in alveoli, exsudate formation, hyperaemia, pneumococcal reproduction 2. red hepatization: exudate fills alveoli, accumulation of PMNL, erythrocytes enter alveoli 3. gray hepatization: fibrin formation, accumulation of leucocytes, erythrocyte breakdown 4. resolution: resorption of exudate • fever, painful breathing, cough (dry, later purulent / hemoptysis), expectoration, dyspnea, tachypnoea (20-45 / min), high temperature (38.5-40.5 °C), takychardia (100-140 / min) • bacteraemia, possible extrapulmonary infections • Haemophilus influenzae ▪ 2nd most frequent agent ▪ the most virulent are the Hib strains, pleural exudate occurs in half of the patients • Staphylococcal pneumonia ▪ nosocomial pneumonia; infants, elderly people, addicts (using i.v. drugs) ▪ CP as in pneumococcal, fever • Pneumonia caused by Klebsiella and other G- bacteria ▪ most often in the weakened persons, the elderly and infants, nosocomial • Peudomonas aeruginosa ▪ severe nosocomial pathogen, acute toxic disease, abscesses, pleural effusion / empyema, ARDS and septic shock Atypical pneumonia • Mycoplasma pneumoniae ▪ in children, M. pneumoniae adheres to a ciliated epithelium, which is destroyed → interstitial pneumonia, bronchitis and bronchiolitis ▪ leukocyte