Pemeriksaan Laboratorium Pada Kelainan Sistem Respirasi

Dr. Sanarko Lukman Halim, SpPK Bagian Patologi Klinik F.K. UKRIDA

Tujuan Pembelajaran
Setelah mempelajari topik ini, mahasiswa memahami tentang berbagai pemeriksaan laboratorium yang diperlukan pada berbagai kelainan/penyakit saluran pernafasan serta interpretasi hasil pemeriksaan 1. Respiratory Acidosis dan Respiratory Alkalosis akibat penyumbatan saluran pernafasan atau pada kelainan paru,rongga torak. 2. Kelainan paru yang disebabkan infeksi, alergi, trauma, kelainan koagulasi, cystic Fibrosis atau penyakit sistemik

Fungsi Sistem Respiratorik

Oxygen transport Respiration Ventilation Air Pressure Variances Airway Resistance Compliance Lung Volumes and Capacities Diffusion Perfusion Ventilation and Perfusion Balance and Imbalance The act of moving air into and out of the lungs is called breathing.

Respiratory Structures and Organs

Transpor Gas
Oxygen is carried in the blood in two forms: dissolved and attached to hemoglobin PaO2 represents the level of dissolved oxygen in plasma (about 3%) Rest is carried on hemoglobin oxyhemoglobin

Human Respiration
Works together with the circulatory system Exchange of gases between atmosphere, blood, and cells If respiratory system and/or circulatory system fails, death will occur Cells need O2 for work; release CO2 as a waste product Accumulation of excess CO2 is toxic to cells and MUST be removed

Respiratory System Circulatory system Intakes oxygen Transports gases in blood Releases carbon between lungs dioxide waste and cells

Kelainan Paru dan Saluran Pernafasan pCO2 , pO2 Respiratory Acidosis Airway obstruction Asthma Bronchitis, bronchiectasi, pneumonia, Aspiration pneumonia, Hospital acquired pneumonia, Pneumonia in Immuno-supressed pneumonia. TBC Chronic Obstructive Pulmonary Disease (COPD) Pulmonary Embolism

Kelainan Paru dan Saluran Pernafasan pCO2 , pO2 Respiratory Acidosis

Environment Lung Diseases Asbestosis, Building-related Diseases Atelectasis Abcess in the Lungs Lung Cancer Hyalin Membrane Disease

FAKTOR-FAKTOR yang MENGURANGI FUNGSI RESPIRASI

Positioning Environment Air pollution Pollens and allergens Smoking Drugs and alcohol Nutrition Restricted lung movement Airway obstruction

Gagal PernafasanRespiratory Failure

PaO2<60mmHg respiratory failure Notice: sea level, quiet, inspire air rule off other causes ( heart disease) PaCO2: The carbon dioxide partial pressure of arterial blood Normal: 35-45mmHg (4.7-6.0kPa) mean: 40mmHg SaO2: Saturation of arterial blood oxygen Normal: 0.95-0.98 Significance: a parameter to evaluate hypoxia, but not sensitive

Penyebab2 Asidosis Respiratorik

Respiratory pathophysiology respiratory arrest airway obstruction severe pneumonia chest trauma pneumothorax Acute drug intoxication especially narcotics, sedatives Residual neuromuscular blockade Head trauma

Penyebab2 Asidosis Respiratorik menahun

Chronic lung disease Neuromuscular disease Extreme obesity Chest wall deformity

Penyebab2 Alkalosis Respiratorik

Pain Anxiety Hyperventilation Hypoxemia Restrictive lung disease Severe congestive heart failure Pulmonary emboli
Drugs Sepsis Fever Thyrotoxicosis Pregnancy Overaggressive mechanical ventilation Hepatic failure

Four primary conditions are possible

1. Respiratory acidosis + acute blood response + chronic renal response 2. Respiratory alkalosis + acute blood response + chronic renal response 3. Metabolic acidosis + respiratory response 4. Metabolic alkalosis + respiratory response

Blood Gas Alterations 1/2

Respiratory Acidosis
Lower pH due to CO2 accumulation or retention in the blood greater than the high normal value Controlled by the lungs Compensation attempts Kidneys attempt to excrete nonvolatile acids and retain HCO3 -Caused by inefficient respiration and/or hypoventilation -Can be acute or chronic Tachycardia and cardiac arrythmias seen in acute respiratory acidosis

Blood Gas Alterations 2/2

Respiratory Alkalosis pH is high due to low CO2 Increased respiratory rate blows off CO2 Blood contains too little carbonic acid (carbonic acid deficits) Compensation Kidneys will excrete bicarbonate

Management of Alterations
Respiratory Acidosis

Determine underlying cause of hypoventilation and treat the cause

Respiratory Alkalosis

Determine underlying cause of hyperventilation and treat the cause

Sampel utk Analisa Gas Darah

clean procedure (gloves, alco wipe) Have gauze for application of pressure post arterial puncture 4 mins of pressure is ideal Especially in patients who are anticoagulated 23G needle easier, but use what you prefer ROTATION and INVERSION of the tube for 20 seconds to dissolve and mix the heparin Ice only necessary if there will be a delay from sampling to testing.

Hasil tes AGD

pH - measures acidity/alkalinity pCO2 (partial pressure of CO2) measures respiratory component [HCO3-] (bicarbonate concentration) measures metabolic component derived value (H-H equation) pO2 (partial pressure of O2) BE (base excess) O2 saturation Sometimes AG (anion gap) Sometimes electrolytes and glucose

Nilai Rujukan Gas Darah

Analisa Gas Darah/Arterial Blood Gases (ABG)
Blood Gas Parameter Parameter Reported and Symbol Used Normal Value

Carbon dioxide tension*

PCO2

35 45 mm Hg (average, 40)

Oxygen tension*
Oxygen percent saturation Hydrogen ion concentration (Log CH+)* Bicarbonate
* Indicates measured parameter

PO2
SO2 pH

80 100 mm Hg
97 7.35 7.45

HCO3-

22 26 mmol/L

Normal values may differ slightly in exams

High pH Alkalosis High PaCO2 Metabolic Low PaCO2

Low pH Acidosis High PaCO2 Low PaCO2 Metabolic

Respiratory Respiratory

Perlu di Tanya
? Is the patient acidotic or alkalotic? If pH < 7.35, the patient is acidotic If pH > 7.45, the patient is alkalotic ? Is the primary cause respiratory or metabolic? ? Is there compensation? ? Is the patient hypoxic? ? (oxygen status, A-a) ? What is going on?

Oxygen status
Hypoxaemia decreased oxygen content of blood pO2 less than 60 mmHg and saturation is less than 90% Hypoxia Levels of pO2 sufficiently low to have an adverse effect on tissue function

Jenis-jenis Hipokia
Hypoxic hypoxia due to low blood pO2 e.g. due to lung disease processes Anaemic hypoxia inadequate O2 delivery to tissues e.g. in anaemia or CO poisoning Circulatory hypoxia inadequate blood flow to tissues e.g. shock Histotoxic hypoxia inability of tissue to use the oxygen classically, in cyanide poisoning

 CO2 and PCO2

Pulmonary function & CO2 homeostasis CO2 elimination

Hyperventilation

Lowering PCO2 Alveolar hyperventilation Causes of alveolar hyperventilation

Hypoventilation

Raising PCO2 Alveolar hypoventilation Causes of alveolar hypoventilation

Equivalences
Disorder acidosis pH
Respiratory

Cause

Mechanism

Respiratory Hypercapnia

Alveolar hypoventilation
CO2 retention Alveolar hyperventilation blow off CO2

PCO2 Hypocapnia PCO2

alkalosis pH

Respiratory Compensation for Preventing Change in pH

Cells/Tissue Acidosis CO2 H+

Blood
Acidaemia pH , PCO2

Lungs

Hypoventilate Slow or CO2 removal

CO2 removal Via respiration Blood Normal or CO2 removal Hyperventilate Normal pH

Acidosis may be accompanied by acidaemia. The change in pH may be prevented by respiratory removal of CO2.

Respiratory Compensation for Preventing Change in pH

Cells/Tissue Alkalosis CO2 HCO3- Blood

Alkalaemia pH , PCO2 , HCO3-

Lungs Hyperventilate Slow or CO2 retention

CO2 retention Via respiration Blood Normal or CO2 retention Hypoventilate Normal pH

Alkalosis will not be accompanied by alkalaemia if enough CO2 has been retained to prevent the change in pH.

Terms used for describing compensation

Compensated

The compensatory mechanisms have come into play in a normal manner; does not necessarily imply that the plasma pH is within the normal range Uncompensated Compensation cannot occur due to some abnormality; patient may show no sign of compensation Partially compensated Intermediate state where compensation is occurring but is not yet as complete as it should be

Metabolic and Respiratory Acid-Base Changes in Blood pH Acidosis 1. Acute metabolic N N N N N pCO2 HCO3-

2. Compensated metabolic
3. Acute respiratory 4. Compensated respiratory Alkalosis

1. Acute metabolic
2. Chronic metabolic 3. Acute respiratory 4. Compensated respiratory
=decreased; =increased; N=normal

Sputum (bukan Ludah) Collection

Proper patient instruction
Food should not have been ingested for 1-2 h prior to expectoration The mouth should be rinsed with saline or water Patient should breathe and cough deeply

Patient should expectorate into a sterile container Transport container immediately to lab Perform Gram stain and plant specimen as soon as possible

Sputum collection
Sputum of less than 2ml should not be processed unless obviously purulent Only 1 sputum per 24hr .submitted Some scoring system should be used to reject specimen that re oral contamination.

Sputum collection
Transportation in <2 hr is recommended with refrigeration if delays anticipated. Handle all samples using universal precautions. Perform Gram stain and plant specimen as soon as possible

Induced sputum
Patients who are unable to produce sputum may be assisted by respiratory therapy technician. Aerosol induced specimen are collected by allowing the patient to breath aerosolized droplets of a solution of 15% sodium chloride and 10% glycerin for approximately 10 minute . Obtaining such specimen may avoid the need for a more invasive procedures ,such as bronchoscopy or needle aspiration, in many cases.

Sputum Gram Stain and Culture

Proponents Demonstration of predominant morphotype on Gram stain guides therapy Accuracy is good when strict criteria are used Cheap, so why not? Antagonists Poor specimen collection Intralaboratory variability (Gram stain interpretation) Low sensitivity and specificity Empiric treatment guidelines Not cost effective

Gastric aspiration
The gastric aspiration is used exclusively for isolation of acid-fast bacilli and may be collected from patients who are unable to produce sputum, particularly young children. The relative resistance of mycobacteria allows them to remain viable for a short period. Gastric lavage must be delivered to the lab immediately so that the acidity can be neutralized. Specimen can be first neutralized and then transported if immediate delivery is not possible.

Definition Pleural Effusions

Increased amount of fluid within the pleural cavity Stedmans Medical Dictionary Accumulation of fluid between the layers of the membrane that lines the lungs and the chest cavity Medline Plus Urgent pleural disorders Pleural emergencies: haemorrhage - haemothorax elevated pleural pressure - tension pneumothorax - massive pleural effusion

Haemothorax pleural fluid with Ht > 50% blood Ht

CAUSES:

chest trauma: penetrating / non penetrating (lung blood vessels, chest wall, diaphragm, pleural adhesions, mediastinum, large vessels, abdomen) iatrogenic (pleural biopsy, subclavian or jugular CVC placement, thoracentesis, transthoracic or transbronchial NA, esophageal variceal TH,...) nonthraumatic (pleural malignancy, anticoagulant TH, spontaneous rupture of vessel (AO aneurism), bleeding disorder, thoracic endometriosis)

Efusi Pleura
Tipe
Hydrothorax Hemothorax Chylothorax Pyothorax / Empyema Klasifikasi
a. Transudate Ultrafiltrate of plasma Small group of etiologies b. Exudate Produced by host of inflammatory conditions Large group of etiologies

DISORDERS
Obstruction of Upper Airway Atelectasis Tracheobronchitis Pneumonia Bacterial Viral Fungal Aspiration Hypostatic Chemical Tuberculosis Abscess

Pleural disorders Pulmonary edema Chest Trauma Pulmonary Emboli (PE) Chronic obstructive pulmonary disease (chronic airflow limitation) Bronchitis Emphysema Asthma Bronchiectasis

Diagnostic Tests
CBC Chest x-ray/ CT MRI/Fluoroscopic studies Sputum culture and sensitivity ABGs Pulse oximetry Bronchoscopy Mantoux Pulmonary angiography Pulmonary Function Test VQ Scan Thoracentesis

The Tuberculosis (TB) Pandemic TB is spread from an infectious person to a vulnerable person through the air TB usually affects the lungs but can affect any part of an infected person

HIV/AIDS and TB: A Deadly Combination

HIV suppresses the human immune system TB suppresses the human immune system Each makes the other worse synergistically

 Chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are associated with widespread but variable airflow obstruction that is reversible either spontaneously, or with treatment.

Definition of Asthma

Bronchial Asthma

Risk Factors for COPD

Environmental factors Tobacco smoke Alpha-1-antitrypsin Occupational deficiency dusts/chemicals Asthma and airway Air pollution hyperresponsiveness Childhood Disordered lung infections development Lower socioeconomic status Host factors

Chronic Bronchitis
Persistent cough with sputum production for at least 3 months in consecutive years Simple / Chronic asthmatic / Obstructive Most frequent in middle-aged men Higher incidence in urban dwellers May coexist with emphysema Presents with exertional dyspnoea and frequent respiratory tract infections

Komplikasi Bronkhitis Menahun

PaO2 PaCO2 .Respiratory failure Respiratory tract infections (H. influenzae, Strep. Pneumoniae) Pulmonary hypertension Cor pulmonale Atypical metaplasia / dysplasia of respiratory epithelium.Bronchogenic carcinoma

Emphysema
Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls Types: (1) centrilobular (2) panlobular (3) paraseptal (4) irregular Associated with heavy cigarette smoking

Patogenesis Emfisema

Bronchiectasis
A chronic necrotising infection of the bronchi and bronchioles associated with abnormal permanent dilation of these airways Presents with cough, productive of large amounts of foul-smelling, purulent sputum, hamoptysis and digital clubbing Pooled secretions in lower lobes respiratory tract infections

Bronchiectasis Aetiology
Bronchial obstruction

Tumour, foreign bodies, mucous impaction Asthma / Chronic bronchitis Infection

Tuberculosis, Staphylococcus aureus, Measles, Pertussis

Congenital

Congenital bronchiectasis, Cystic fibrosis, Intralobar sequestration, Immunodeficiency, Kartageners syndrome, Yellow nail syndrome

Cystic Fibrosis Genetic defect

Lung Abscess
EDA

PM AFC

RB

Figure B16-1. Lung abscess. A, Cross-sectional view of lung abscess. AFC, Air-fluid cavity; RB, ruptured bronchus (and drainage of the liquified contents A of the cavity); EDA, early development of abscess; PM, pyogenic membrane. Consolidation (B) and excessive bronchial secretions (C) are common secondary anatomic alterations of the lungs.

Atelectasis
Assessment and Diagnostic Findings

SpO2 < 90%

PaO2 i < 80

PaCO2 h >

45
HCO3- h to

compensate

Evaluasi Laboratorium
Deteksi berkurangnya fungsi saluran pernafasan dan alveoli Analisa Gas Darah. Deteksi adanya infeksi dengan memperhatikan 1. Petanda hematologi adanya infeksi/inflamasi: * Jumlah Leukosit, Gambaran Darah Tepi, LED, CRP, IgE. 2. Deteksi kuman: pembiakan, preparat,secara imunologis Periksa adanya cystic fibrosis sebagai penyebab sputum kental infeksi, sesak nafas (DD/ Asma)

Retensi CO2 PCO2

Meningkatnya CO2 H+ Asidosis Analisa gas darah Respiratory Acidosis
Retention of CO2 by the lungs CO2, PCO2

Reaction shifts right [H+], pH, acidosis

CO2 + H2O H2CO3 H+

Reaction shifts right

+ HCO3-

Mikrobiologi
The culture of lower respiratory specimens may result in more unnecessary microbiologic effort than any other type of specimen.

Overtreatment has lead to resistance

Multidrug resistant Streptococcus pneumoniae Resistance among hospital acquired pathogens such as Acinetobacter, Pseudomonas aeruginosa E.coli K.pneumonia (ESBLs) MRSA and others

Categories of Lower Respiratory Tract Infections

Acute bronchitis Community acquired pneumonia Hospital acquired pneumonia Pneumonia in the immunocompromised host

Community Acquired Pneumonia Diagnosis Available Test Methodologies

Sputum Gram stain and culture Blood cultures Serologic studies Antigen detection tests Nucleic acid amplification tests

McPherson RA., Pincus MR., Editors Henrys Clinical Diagnosis and Management by Laboratory Methods 21st edition, ISBN-13:978-1-4260-0287-1 Saunders Elsevier 2007 Daftar Kepustakaan 1. Gaw A, Clinical Biochemistry, ISBN 0-443-04481-3 Churchill Living Stone New York, 1995, 92-93 Churchill Living Stone New York ISBN 0-443-04481-3. 1995

2.
3.

Abraham P. editor, Physiology, ISBN-13: 978-1-905704-64-4, Amber Books London , 2007 6

Johnston SL, Holgate ST, Asthma: Critical Debate, ISBN 0-632-05721-1 Oxford, England, Blackwell Science,2002.