Management of Respiratory Failure

5th-year medical student seminar presentation under the supervision of Dr. Hasyimah, a registrar at HRPZ II.

1. RESPIRATORY FAILURE PRESENTED BY NURUL HIDAYU BINTI IBRAHIM NIK NOR LIYANA AUDI ADIBAH RAHMAN

2. TERM RESPIRATORY DISTRESS Abnormal (increased or decreased) respiratory rate or effort. It encompasses a spectrum of signs from tachypnea with retractions to agonal gasps. Respiratory distress includes increased work of breathing, inadequate respiratory effort (e.g. hypoventilation or bradypnea ), and irregular breathing . Respiratory distress leads to respiratory failure .

3. TERM That is, there is inadequate blood oxygenation, ventilation, or both to meet the metabolic demands of body tissues. The job of the lungs is to ventilate and oxygenate. When it doesn’t do any of that, it is failing. RESPIRATORY FAILURE Respiratory failure is a clinical state of  inadequate oxygenation, ventilation, or both.   RESPIRATORY ARREST Absence of breathing. The patient isn’t breathing .

4. INTRODUCTION WHAT IS RESPIRATORY FAILURE ? Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions : oxygenation and carbon dioxide elimination . In practice, it may be classified as either type I respiratory failure ( hypoxemic) or type II respiratory failure ( hypercapnic ) , and also acute and chronic respiratory failure . Morbidity and mortality rates increase with age and presence of comorbidities.

5. INTRODUCTION WHAT IS RESPIRATORY FAILURE ? It is also due to dysfunction of one or more essential components of the respiratory apparatus which commonly associated with type II r espiratory failure : CNS or Brain stem Spinal cord Nerves Neuromuscular Junction Muscle of respiration Chest wall movement

6. RISK FACTORS Age Pulmonary infection Cigarette smoking Chronic lung disease Upper or lower airway obstruction Congenital Heart Problem (Right – Left Shunt) History of stroke Opiate and sedative medications (Benzodiazepine) Muscle system abnormalities CNS disorders ( Gullain Barre Syndrome, Myasthenia Gravis) Traumatic spinal injury Pneumothorax Hypercoagulable states (Pulmonary Embolism)

7. CLASSIFICATION TYPE 1 OR HYPOXEMIC ( Pa0 2 <60 mmHg on room air at sea level ), with carbon dioxide level may be low or normal: Failure oxygen exchange due to V/Q mismatch Right to left cardiac shunt TYPE 2 OR HYPERCAPNIC ( PaC0 2 > 50 mmHg on room air at sea level and pH < 7.35 ): Failure to exchange or remove carbon dioxide Indicate a problem with one or more areas of respiratory apparatus causing hypoventilation which result in hypoxemia and markedly increase carbon dioxide. Often accompanied by hypoxemia that corrects with supplemental oxygen. Complications include: damage to vital organs due to hypoxemia, CNS depression due to increased carbon dioxide levels, respiratory acidosis (carbon dioxide retention). This is ultimately fatal unless treated.

8. CLASSIFICATION

9. CLASSIFICATION TYPE 3 OR PERIOPERATIVE FAILURE Increase atelectasis due to low functional residual capacity (FRC) in the setting of abnormal abdominal wall mechanics. Often results in type I or type II respiratory failure Can be ameliorated by anaesthetic or operative technique , posture , incentive spirometry or post-operative analgesia TYPE 4 OR SHOCK Describes patients who are intubated and ventilated in the process of resuscitation for shock Goal of ventilation is to stabilize gas exchange and to unload the respiratory muscles, lowering their oxygen consumption.

10. CLASSIFICATION DISTINGUISH BETWEEN ACUTE AND CHRONIC RESPIRATORY FAILURE Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status , the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. ACUTE RESPIRATORY FAILURE CHRONIC RESPIRATORY FAILURE Develops over minutes to hours Decrease pH rapidly to < 7.2 Example : Pneumonia Develops over days allowing time for renal compensation Increase in HCO3 Decrease pH slightly Polycythemia, Corpulmonale Example : COPD The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases . The clinical markers of chronic hypoxemia , such as polycythemia or cor pulmonale , suggest a long-standing disorder.

11. PHYSIOLOGY CEREBRAL CORTEX PONS MEDULLA OBLONGATA SPINAL CORD APNEUSTIS CENTRE (respiratory centre ) PNEUMOTAXIC CENTRE (respiratory centre ) CHEMORECEPTORS A ortic & carotid bodies (Peripheral) CHEMORECEPTORS M edulla oblongata (central) Motor neurons to respiratory muscles CONTROL OF VENTILATION BY CNS

12. PHYSIOLOGY CONTROL OF VENTILATION BY CNS

13. PHYSIOLOGY WAYS THAT BREATHING CAN FAIL

14. PHYSIOLOGY Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. After diffusing into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen; 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen . The quantity of oxygen combined with hemoglobin depends on the level of blood PaO 2 . This relationship, expressed as the oxygen hemoglobin dissociation curve that has a sigmoid-shaped curve with a steep slope GAS EXCHANGE RESPIRATORY PHYSIOLOGY

15. PHYSIOLOGY The carbon dioxid e is transported in 3 main forms: In simple solution As bicarbonate Combined with protein of hemoglobin as a carbamino compound. During ideal gas exchange, blood flow and ventilation would perfectly match each other , resulting in no alveolar-arterial oxygen tension (PO 2 ) gradient. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated , while others are overventilated . Similarly, for known alveolar ventilation, some units are underperfused , while others are overperfused . The optimally ventilated alveoli that are not perfused well have a large ventilation-to-perfusion ratio (V/Q) and are called high-V/Q units (which act like dead space ). Alveoli that are optimally perfused but not adequately ventilated are called low-V/Q units (which act like a shunt ). RESPIRATORY PHYSIOLOGY

16. PHYSIOLOGY RESPIRATORY PHYSIOLOGY V – Ventilation (air going in and out of the lung) Q – Perfusion (Blood circulation to that area of lung) V/Q = 1 Both occur simultaneously in the lung. Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, with PAO2 slightly higher than PaO2. V/Q RATIO High V/Q: (>1) High ventilation Low or no perfusion Low V/Q: (<1) Low or no ventilation High perfusion

17. PHYSIOLOGY RESPIRATORY PHYSIOLOGY However , an increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia . V/Q mismatch is basically certain lung unit has high V/Q ratio and certain lung unit has low V/Q ratio which will lead to hypoxemia. V/Q RATIO

18. PATHOPHYSIOLOGY TYPE 1 RESPIRATORY FAILURE Ventilation – Perfusion Mismatch Volume of air flowing in and out of the lungs is not matched with the air flow of blood to the lungs. Shunt Effect TYPE 2 RESPIRATORY FAILURE A problem with one or more areas of respiratory apparatus causing alveolar hypoventilation. Respiratory apparatus: Brainstem Spinal Cord Nerves Neuromuscular junction (NMJ) Muscle of respirations Chest Wall movements

19. AETIOLOGY

20. PATHOPHYSIOLOGY The deoxygenated blood bypass the ventilated alveoli and mixes with oxygenated blood  hypoxemia Persistent of hypoxemia despite 100% oxygen inhalation Hypercapnia occur when shunt is excessive >60% Causes of shunt : TYPE 1 RESPIRATORY FAILURE V/Q MISMATCH Most common cause of hypoxemia Low V/Q ration, may occur either from Decrease of ventilation secondary to airway or interstitial lung disease Overperfusion in the presence of normal ventilation, e.g. PE Administration of 100% oxygen eliminate hypoxemia. SHUNT INTRACARDIAC PULMONARY Right – Left Shunt Tetralogy of Fallot Eisenmenger’s syndrome A/V malformation Pneumonia Pulmonary edema Atelectasis/ collapse Pulmonary contusion

21. PATHOPHYSIOLOGY Occurs when ventilation decrease 4-6 L/min Causes: Depression of CNS from drugs Neuromuscular disease of respiratory muscle Increase PaCO2 and decrease PaO2 Example : Guillan Barre Syndrome, Myasthenia Gravis TYPE 1 RESPIRATORY FAILURE DIFFUSION ABNORMALITY Less common Due to Abnormality of the alveolar membrane Decrease number of alveoli Causes: ARDS Fibrotic Lung Disease HYPOVENTILATION (TYPE 2) TYPE 2 RESPIRATORY FAILURE

22. PATHOPHYSIOLOGY

23. PATHOPHYSIOLOGY

24. AETIOLOGY TYPE I TYPE II Alveolar unit Failure Collapse Flooding: edema, pus, aspiration Fibrosis Nervous System Failure Central hypoventilation Neuropathies Pulmonary Vasculature Failure Pulmonary embolism Pulmonary Hypertension Muscle (pump) failure Muscular dystrophies Myopathies Pneumonia Atelectasis Asthma ARDS Pneumothorax Neuromuscular transmission failure Myasthenia Gravis Airway failure Obstruction Dysfunction Chest wall & pleural space failure Kyphoscoliosis Morbid obesity – Obesity Hypoventilation Syndrome

25. AETIOLOGY TYPE III TYPE IV Inadequate post-operative analgesia, upper abdominal incision Obesity, ascites Preoperative tobacco smoking Excessive airway secretions Cardiogenic shock Septic shock Hypovolemic shock

26. REFERENCES Respiratory failure. ( n.d. ) Retrieved from https://www.thoracic.org/patients/patient-resources/breathing-in-america/resources/chapter-20-respiratory- failure.pdf Acute respiratory failure. ( n.d. ). Retrieved from https://bestpractice.bmj.com/topics/en-us/ 853 Respiratory Failure Guidelines. (2018, September 15). Retrieved from https:// emedicine.medscape.com /article/167981-guidelines Respiratory Failure Guidelines. (2018, September 15). Retrieved from https://emedicine.medscape.com/article/167981- guidelines Respiratory Failure Mechanical Ventilations. ( n.d. ) Retrieved from https :// www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/mechanical-ventilation/respiratory-failure-mechanical-ventilation.pdf Carson SS, Cox CE, Holmes GM, Howard A, Carey TS. The changing epidemiology of mechanical ventilation: a population-based study. J Intensive Care Med 2006;21:173–182 . Nava S, Hill N. Non-invasive ventilation for acute respiratory failure. Lancet 2009; 374:250–259.