Diagnosis of Respiratory disorder process

Diagnosis of Respiratory disorder process

Respiratory acidosis • History and Physical examination • Laboratory evaluation • ABG analysis • Toxicology testing -Pharmacological depressants • Lumbar puncture –CNS infection • Serum electrolyte measurement-Potassium and phosphate levels • Microbiological testing -Pneumonia • Muscle biopsy-Muscular dystrophy, malignant hyperthermia, polymyositis, or dermatomyositis • Imaging studies-CXR and chest CT-lung and chest wall disease • Pulmonary function testing-FVC and maximal inspiratory and expiratory pressures -Guillain-Barre syndrome and myasthenia gravis -Neuromuscular disorders

Cause • Acute - Central nervous lesion(infection or tumour etc) -Drug intake(sedative,narcotics) -Neuromuscular defect(Gullain-Bairre’s syndrome) -Bronchial obstruction(foreign bodies,tumour) -Lung disease(emphysema,asthma) -Mechanical ventilation -In case of hypokalaemia and hypophosphataemia. • Chronic - COPD, obesity ,myasthenia gravis and hypothyroidism

History Consideration Onset of symptoms • Degree of acuity and magnitude of symptoms • COPD -with acute or chronic respiratory acidosis -secondary to lower respiratory tract infection, pulmonary embolism, pneumothorax, corpulmonale. • Pneumonia or empysema -Acute,fever, cough, pleuritic chest pain,and hypoxia • Obesity-hypoventilation syndrome, multiple sclerosis, myasthenia gravis, and kyphoscoliosis. -chronic,few or no symptoms • Guillain-Barre syndrome -Acute,more overt symptoms proggresive,neurological weakening

Preexisting Medical conditions • Chronic disease: COPD, myasthenia gravis, and multiple sclerosis • Atherosclerotic disease or atrial fibrillation-CNS pathology (eg.infarction) • History of Depression-toxic ingestion Medication history • Narcotics and analgesics -Respiratory depression • COPD patient-hypoventilation

Physical examination findings 3 examination findings • Pulmonary examination 1. Egophony, crackles, wheeze, dullness to percussion -pulmonary auscultation,localise chest pathology 2.Shows obstructed breathing patterns -eg. seesaw chest movements, nasal flaring, and supraclavicular and subcostal recession. • Cardiac examination 1.Right ventricular heave and tricuspid regurgitation - chronic right ventricular failure (corpulmonale) with COPD, obesity hypoventilation syndrome 2. Irregular cardiac rhythm, valvular murmurs, or carotid bruits -embolism (in case of CNS ) • Neurologicalexamination 1.Asterixis, myoclonus, seizures, or miosis -ingested substances 2. Symmetrical hyporeflexia/areflexia of the lower extremities- Guillain-Barre syndrome -

Respiratory alkalosis • History and Physical examination • Laboratory evaluation • ABG analysis • CXR-pneumothorax and pulmonary parenchymal • Brain imaging- neurological aetiology,meningitis and encephalitis • Lumbar puncture- CNS infection • Cytology analysis-meningeal metastasis • Pulmonary function tests-chronic(pulmonary fibrosis or asthma) • CT angiography- pulmonary arteries • -when CXR finding normal ,physical examination remains a high probability.

Cause -Central cause(direct action via respiratory centre) • CNS cause(infection,stroke,meningitis) • Anxiety-hyperventilation syndrome (psychogenic) • Other 'supra-tentorial' causes (pain, fear, stress, voluntary) • Various drugs (eg.salicylate intoxication) • Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease) -Hypoxaemia or tissue hypoxia(act via peripheral chemoreceptors) -Pulmonary Causes(act via intrapulmonary receptors) • Pulmonary embolism • Pneumonia • Asthma • Pulmonary oedem -Iatrogenic (act directly on ventilation)

History Consideration • Medical history -Dyspnoea • With pleuritic chest pain- pulmonary embolism (PE), pneumonia, or pneumothorax. • With wheezing- asthma • With exertion- pulmonary oedema or pulmonary hypertension. -Productive cough and fever – pneumonia -Cough- ARDS and interstitial fibrosis -Fever- Systemic inflammatory-response syndrome (SIRS) or sepsis -Fever :with headache, stiff neck, and lethargy- meningitis - Meningeal & focal neurological symptoms- meningoencephalitis -Focal neurological symptoms -CVA or a space-occupying lesion -Anxiety, pain, or psychiatric history- hyperventilation syndrome -Acute tissue hypoxia- hypovolaemic, cardiogenic, or septic shock -Chronic tissue hypoxia- severe anaemia or haemoglobinopathy -Hypoxaemia: due to high altitude, parenchymal lung disease, cyanotic heart disease, or portopulmonary hypertension noted.

Physical examination • Respiratory rate, temperature, blood pressure, heart rate, and pulse oximetry. • Tachycardia- SIRS, PE, or salicylate toxicity, or with pain • Lethargy or somnolence- meningitis or encephalitis • Scleralicterus and jaundice- hepatic failure • Crackles- pulmonary oedema, pneumonia, ARDS, and interstitial fibrosis • Haemoptysis- infarction • Ascites, hepatomegaly, and caput medusae- failure or cirrhosis • Altered mental status- CVA, meningoencephalitis, sepsis, or hepatic failure • Focal neurological signs- CVA, encephalitis, and space-occupying brain lesions • Headache, neck stiffness, and meningeal signs- meningitis

ABG analysis(pH,PCO2, HCO3-) 1. Look at the pH. Is there an acid base disorder present? - If pH < 7.35, then acidemia - if pH > 7.45, then alkalemia - If pH within normal range, then acid base disorder not likely present. - pH may normal ,other ABG parameters abnormal,then (mixed acid base disorder) 2. Look at PCO2, HCO3-. What is the acid base process (alkalosis vs acidosis) leading to the abnormal pH? Are both values normal or abnormal? - both values: abnormal ,same direction of the abnormal change.(simple base-acid disorder) - One abnormal value- primary change, the other -compensatory response.

2a. Distinguish the primary change from the compensatory response. - The initial change -abnormal value correlates with the abnormal pH. - If Alkalosis, then PCO2 low or HCO3- high - If Acidosis, then PCO2 high or HCO3- low. The primary change identified, other abnormal parameter-compensatory response (same direction of the changes).If not,mixed disorder. • 2b.After distinguish Primary chemical change and the compensatory response, identify specific disorder. - If PCO2 -primary chemical change-respiratory. - if HCO3- primary chemical change -metabolic. Eg. pH < 7.35 and pCO2 < 40  metabolic acidosis pH < 7.35 and pCO2 > 40  respiratory acidosis pH > 7.45 and pCO2 < 40  respiratory alkalosis pH > 7.45 and pCO2 > 40  metabolic acidosis

3. If respiratory process, is it acute or chronic?- An acute respiratory process -compensatory response- rapid intracellular buffering. - A chronic respiratory -more significant compensatory response -renal adaptation-longer time - extent of compensation- assess acute or chronic

ABG analysis of acute and chronic respiratory process • Respiratory acidosis(acute) -abnormally low pH (<7.35) ,elevation in the PaCO2 (>45 mmHg) -pH decrease by 0.08 for every 10 mmHg increase in PaCO2,serum bicarbonate and base excess (normal) -HCO3− Compensation - 4 to 12 hours, no increase or only 1 to 2 mEq/L. • Respiratory acidosis (chronic ) - pH decrease 0.03 units for every 10 mmHg increase in PaCO2. - renal compensation- within 24 hours -eg.compensated COPD(normal PH in spite of elevated PaCO2);if abnormal PH-metabolic abnormality -hypoxaemia-determine alveolar hypoventilation( sedative overdose ,CNS infarction); regional ventilation-perfusion mismatch

Respiratory alkalosis(acute) - change in HCO3- (mmol/L) equal to 0.1 x change in PaCO2 (mmHg) • Respiratory alkalosis(chronic) -change in HCO3- (mmol/L) equal to 0.4 x change in PaCO2 (mmHg) Result with history, physical examination, and clinical data- determine cause. -Acute: sign&symptoms(eg. hypocapniaimmediate prior 6 hours ) -Chronic: -compensation begins 6 hours after the onset of hypocapnia ,complete within 2 to 4 days. -hormonal aetiologies (eg.prenancy), chronic causes of hypoxia,liver disease. -Hyperventilation syndrome is excluded

Diagnosis of Respiratory disorder process