NURS3055 Professional Practice 5 Lecture 1 - Week 3 Acute Breathing & Oxygenation Deterioration Notre Dame Australia PDF

NURS3055 – Professional Practice 5 Lecture 1 - Week 3 Acute Breathing & Oxygenation Deterioration School of Nursing and Midwifery ACK NOWLE DGEM ENT OF COUNTR Y The University of Notre Dame Australia is proud to acknowledge the traditional owners and custodians of this land upon which our Universi...

NURS3055 – Professional Practice 5 Lecture 1 - Week 3 Acute Breathing & Oxygenation Deterioration School of Nursing and Midwifery ACK NOWLE DGEM ENT OF COUNTR Y The University of Notre Dame Australia is proud to acknowledge the traditional owners and custodians of this land upon which our University sits. The University acknowledges that the Fremantle Campus is located on Wadjuk Country, the Broome Campus on Yawuru Country and the Sydney Campus on Cadigal Country. Week Three Learning Objectives Explore respiratory anatomy and physiology Recognise and respond to common examples of acute respiratory failure and exacerbations of chronic disease Apply principles of Non-Invasive Ventilation (NIV) to patient care Interpret Arterial Blood Gases (ABGs) in assessing the ongoing care of patients Understand the role and mechanism for common examples of respiratory pharmacology Introduction to Respiration Respiration - act of breathing Inspiration/inhalation - intake of air into the lungs Expiration/exhalation - breathing out Ventilation - movement of air in & out of the lungs; exchange of gases (O2 & CO2) in the alveoli Assessing Breathing Rate Depth Pattern/Rhythm Quality/Sounds Effectiveness Rate Auscultate Trachea Effort Saturations Section 1: Anatomy and Physiology – The Thoracic Cavity 1. Respiratory Organs and Pleurae: Lungs, three lobes on the right and two on the left, separated by fissures. Right lung has a horizontal and oblique fissure Left lung only has an oblique fissure. Lungs surrounded by the parietal pleura, membrane that also lines the chest wall and mediastinum 2. Air Passageways: Trachea, divides into the right and left main bronchus entering each lung. These bronchi further branch into smaller airways within the lungs to carry air to the lung tissues. Section 1: Anatomy and Physiology – The Thoracic Cavity 3. Blood Vessels: Heart sits centrally between the lungs, and from it arises the pulmonary trunk, which divides into the right and left pulmonary arteries. These carry deoxygenated blood to the lungs where gas exchange occurs. Oxygenated blood returns to the heart via the pulmonary veins. 4. Other Thoracic Structures: The aortic arch, main artery coming from the heart, is visible in this illustration. Also the superior vena cava, which is a large vein that brings deoxygenated blood from the upper body back to the heart. Section 1: Anatomy and Physiology - Inspiration 1. Pressure Differences: Inspiration is initiated when the diaphragm and intercostal muscles contract, causing the thoracic cavity to expand. Expansion leads to a decrease in intrapulmonary pressure (inside the lungs), which becomes slightly lower than the atmospheric pressure outside the body. (Boyle’s Law) The image shows atmospheric pressure at 760 mmHg, and intrapulmonary pressure at 758 mmHg. 2. Airflow: Due to this pressure gradient, air flows from an area of higher pressure (the atmosphere) to an area of lower pressure (the lungs). This is the fundamental force behind inhalation, with air moving in to equalise the pressure. Section 1: Anatomy and Physiology - Inspiration 3. Intrapleural Pressure: Intrapleural pressure is the pressure within the pleural cavity, which is between the lung surface and chest wall. This pressure is always slightly negative compared to intrapulmonary pressure, which helps to keep the lungs expanded. Image shows an intrapleural pressure of 754 mmHg. 4. The Role of Pleural Space: The negative pressure in the pleural space acts like a suction to keep the lungs open against the chest wall. Without this negative pressure, the lungs would collapse. During inspiration, the expansion of the chest wall and the outward pull on the lungs create a more negative pressure in the pleural cavity, which further helps in expanding the lungs and drawing in air. Section 1: Anatomy and Physiology - Expiration 1. Pressure Changes: Expiration is generally a passive process during normal, quiet breathing. It begins as the muscles of inspiration relax, leading to a decrease in the size of the thoracic cavity. This reduction causes the intrapulmonary pressure to rise above atmospheric pressure, shown in the image as 763 mmHg compared to the atmospheric pressure of 760 mmHg. 2. Airflow Out of the Lungs: Since air moves from an area of higher pressure to one of lower pressure, the air in the lungs (at a higher pressure) flows out towards the atmosphere (at a lower pressure). This is the core mechanism for expiration. Section 1: Anatomy and Physiology - Expiration 3. Intrapleural Pressure Dynamics: During expiration, the intrapleural pressure becomes less negative than during inspiration, because the lungs are recoiling and the chest cavity is shrinking. This pressure, however, remains negative relative to the intrapulmonary pressure, which is necessary to prevent lung collapse. The image lists an intrapleural pressure of 759 mmHg. 4. Elastic Recoil: The lungs have a natural tendency to recoil due to their elastic properties. After inhalation, the elastic fibers in the lung tissue contract, helping to push air out. During passive expiration, this recoil is largely responsible for pushing air out of the lungs. Section 1: Anatomy and Physiology – Gas Exchange 1. Arrival of Oxygen-Rich Air: When we inhale, air rich in oxygen (20.95%) enters the lungs through the trachea and reaches the alveoli, Each alveolus is surrounded by a network of capillaries, where gas exchange occurs. 2. Diffusion of Gases: Oxygen from the air in the alveoli diffuses into the blood within the capillaries because there is a higher concentration of oxygen in the alveoli than in the blood. At the same time, carbon dioxide, which is more concentrated in the blood, diffuses from the blood into the alveoli. This exchange is Image 4. Hu man ga s e xchan ge. Retrie ved from http s://medi cte sts.com/un its/the-mech ani cs-of- driven by the differences in partial pressures of these gases – resp iratio n a process described by Dalton's law. Section 1: Anatomy and Physiology – Gas Exchange 3. Oxygen Transportation: The oxygen that has diffused into the blood attaches to hemoglobin molecules within red blood cells. This oxygenated blood is then carried from the lungs to the heart, where it is pumped through the arteries to the rest of the body. 4. Release of Carbon Dioxide: As the blood delivers oxygen to the cells, it picks up carbon dioxide produced by cellular metabolism. The blood carrying carbon dioxide returns to the lungs via the veins. Once it reaches the lungs, the carbon dioxide diffuses into the alveoli and is expelled from the body when we exhale. Image 4. Hu man ga s e xchan ge. Retrie ved from http s://medi cte sts.com/un its/the-mech ani cs-of- resp iratio n Section 1: Anatomy and Physiology – Gas Exchange Section 1: Anatomy and Physiology – Gas Exchange 1. Arrival of Oxygen-Rich Air: On inspiration, air rich in oxygen enters the lungs through the trachea and reaches the alveoli. Each alveolus is surrounded by a network of capillaries. This is where gas exchange occurs. 2. Diffusion of Gases: Oxygen from the air in the alveoli diffuses into the blood within the capillaries because there is a higher concentration of oxygen in the alveoli than in the blood. At the same time, carbon dioxide, which is more concentrated in the blood, diffuses from the blood into the alveoli. This exchange is driven by the differences in Image 4. Hu man ga s e xchan ge. Retrie ved from http s://medi cte sts.com/un its/the-mech ani cs-of- resp iratio n partial pressures of these gases – a process described by Dalton's law. Section 1: Anatomy and Physiology – Gas Exchange 3. Oxygen Transportation: The oxygen that has diffused into the blood attaches to hemoglobin molecules within red blood cells. This oxygenated blood is then carried from the lungs to the heart, where it is pumped through the arteries to the rest of the body. 4. Release of Carbon Dioxide: As the blood delivers oxygen to the cells, it picks up carbon dioxide produced by cellular metabolism. The blood carrying carbon dioxide returns to the lungs via the veins. Once it reaches the lungs, the carbon dioxide diffuses into the alveoli and is expelled from the body Image 4. Hu man ga s e xchan ge. Retrie ved from http s://medi cte sts.com/un its/the-mech ani cs-of- resp iratio n when we exhale. Section 1: Anatomy and Physiology – Changes in Airway Even small changes in the diameter of the airways can have a significant impact on resistance to airflow. In the respiratory system, the largest airways do not contribute as much to total resistance due to their larger diameter; however, as air moves through the progressively smaller bronchioles, resistance increases. Conditions that narrow the airways, such as asthma or bronchitis, can significantly increase airway resistance, making breathing more difficult. Section 1: Anatomy and Physiology - Compliance Airway Compliance: The ease at which the lungs can be expanded If we decrease airway compliance this will also result in increased resistance, making breathing more difficult. Section 2: Common Disease and Injury – Asthma Pathophysiology Section 2: Common Disease and Injury – Asthma Management Section 2: Common Disease and Injury – Asthma Management Salbutamol: This is a short-acting beta-2 agonist (SABA) that works by stimulating beta-2 receptors in the smooth muscle of the airways. Activation of these receptors leads to muscle relaxation and bronchodilation, which helps to open the airways and make breathing easier. Salbutamol is typically administered via inhalation to act directly on the airways with rapid onset. Ipratropium Bromide: Ipratropium is an anticholinergic medication that works by blocking the muscarinic cholinergic receptors in the smooth muscles of the airways. This inhibition prevents the muscles from contracting, thereby causing the airways to dilate. Ipratropium is often used in conjunction with beta-2 agonists like salbutamol for a synergistic effect because it provides a different mechanism of bronchodilation Magnesium Sulfate: Magnesium sulfate is thought to work in acute asthma by several mechanisms, including bronchodilation. It can inhibit calcium influx into smooth muscle cells, which prevents contraction, and it may also block certain receptors that lead to bronchoconstriction. Additionally, magnesium has anti-inflammatory properties. It is typically reserved for severe exacerbations and is administered intravenously. Non-Invasive Ventilation (NIV): NIV, such as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), supports the patient's breathing without the need for intubation. It works by providing positive pressure to the airways throughout the respiratory cycle or in synchronisation with the patient's breathing, which helps to keep the airways open, reduce the work of breathing, and improve gas exchange. Section 2: Common Disease and Injury – COPD Pathophysiology Section 2: Common Disease and Injury – COPD Management Section 2: Common Disease and Injury – COPD Management Salbutamol: This is a short-acting beta-2 agonist (SABA) that works by stimulating beta-2 receptors in the smooth muscle of the airways. Activation of these receptors leads to muscle relaxation and bronchodilation, which helps to open the airways and make breathing easier. Salbutamol is typically administered via inhalation to act directly on the airways with rapid onset. Oral Corticosteroids: Anti-inflammatory medications like prednisolone reduce inflammation and swelling in the airways, making it easier for a patient to breathe. During a COPD exacerbation, systemic corticosteroids can speed up recovery, improve lung function (as measured by FEV1), and reduce the risk of early relapse, treatment failure, and length of hospital stay. Intravenous Corticosteroids: It may be common for patients experiencing a COPD exacerbation, and administered NIV, to struggle with oral tablet medications. Intravenous hydrocortisone is also a corticosteroid that ensures anti- inflammatories are included in the patient’s care without the associated risks of pausing NIV or aspiration when swalling oral medications. Non-Invasive Ventilation (NIV): BiLevel Positive Airway Pressure (BiPAP) supports the patient presenting with COPD. It works by providing a higher positive pressure to the airways throughout inspiration, and a lower positive pressure during expiration to ease work of breathing but improve ventilation of carbon dioxide out of the body  Section 2: Common Disease and Injury – COVID-19 Pathophysiology I. Viral Entry & Early Infection - Key events: The SARS-CoV-2 virus enters the body, typically through the respiratory tract, and binds to the ACE2 receptors on the surface of lung cells. It also utilises the TMPRSS2 enzyme for cell entry. - Pathophysiology: Once inside the host cells, the virus begins to replicate. The infected cells eventually undergo pyroptosis, a type of programmed cell death that leads to inflammation and further attracts immune cells. II. Host Immune Response - Immune cell involvement and clearance: In the early phase, immune cells like macrophages and dendritic cells detect the virus and start the immune response. In the late phase, cytotoxic T cells are involved in clearing the virus. - Key events: The body recognises the viral components (DAMPs/PAMPs) and releases pro-inflammatory cytokines and chemokines. This leads to the recruitment of monocytes, macrophages, and virus-specific T cells to eliminate the infected cells. Section 2: Common Disease and Injury – COVID-19 Pathophysiology III. Hyperinflammatory Phase - Transition from mild to severe COVID-19: Some patients experience a severe immune response known as a cytokine storm, marked by a rapid increase in cytokines such as IL-6, IL- 10, IL-2, and others. - Pathophysiology: This excessive immune response leads to the infiltration of too many immune cells into the lungs, causing damage and contributing to respiratory distress. IV. Multiorgan Dysfunction - Key events: The inflammation and immune response can become systemic, affecting other organs beyond the lungs. This may lead to a procoagulant state, causing clots and multiple organ failures. - Pathophysiology: The widespread inflammation and coagulation can compromise the function of various organs such as the heart, kidneys, and liver, leading to their failure. Section 2: Common Disease and Injury – COVID-19 Management COVID-19 presents differently for all individuals. Always ensure you and other practitioners are safe prior to attending to assessment and intervention through adequate Personal Protective Equipment (PPE) Continuously monitor patients suspected for or confirmed COVID-19 and anticipate deterioration Transition all nebulised or aerosolised medications to metred devices to reduce transmission risks Pay particular attention to a comprehensive history taking, strict fluid balance monitoring, and escalation of respiratory support Section 2: Common Disease and Injury – Bronchiolitis Pathophysiology Section 2: Common Disease and Injury – Lung Collapse Pathophysiology Closed pneumothorax: Air enters the pleural space from the lungs themselves Due to rupture of a blister on the lung surface or a tear in the lung tissue, without any external opening. This can happen due to trauma, lung disease, or spontaneously without a clear cause (spontaneous pneumothorax). Since there is no external wound, air can enter the pleural space from the lungs but cannot escape, leading to a buildup of pressure that can collapse the lung. The chest wall remains intact. Unequal Closed Dyspnoea Hypoxia Tachycardia Cough air entry Pneumothorax Section 2: Common Disease and Injury – Lung Collapse Pathophysiology Open pneumothorax: Direct passage between the external environment and the pleural space through a chest wall injury. Due to penetrating trauma, e.g. stab or gunshot wound. Air can pass between the atmosphere and the pleural space with each breath; can lead to the lung collapsing. Condition is sometimes referred to as a "sucking chest wound" because of the sound air makes moving through the wound. Decreased Bruising Penetratin Subcutaneous Open breath and Flail chest emphysema g trauma Pneumothorax sounds abrasions Section 2: Common Disease and Injury – Fluid Surrounding Lung Spaces Haemothorax Accumulation of blood in the pleural cavity, the space between the lungs and the chest wall. Causes: Trauma to the chest (e.g., car accidents, falls, penetrating injuries). Surgical complications. Rupture of blood vessels due to disease. Signs and Symptoms: Chest pain, especially on the injured side. Shortness of breath. Rapid heart rate. Reduced or absent breath sounds on the affected side. Signs of shock in severe cases (e.g., low blood pressure, rapid pulse, clammy skin). Management: Stabilising the patient (ensuring airway, breathing, & circulation deterioration is responded to rapidly). Thoracentesis or chest tube insertion to drain the blood. Surgery, in some cases, to repair the source of bleeding, as seen in vessel rupture. Monitoring for complications like infection or lung collapse. Section 2: Common Disease and Injury – Fluid Surrounding Lung Spaces Empyema Accumulation of pus in the pleural cavity, usually due to infection. Causes: Complication of bacterial pneumonia. Introduction of infection through chest trauma or surgery. Signs and Symptoms: Fever and chills. Chest pain, worsened by coughing or breathing. Cough, possibly with foul-smelling sputum. Shortness of breath. General malaise and weight loss. Management: Antibiotics to treat the underlying infection. Thoracentesis or chest tube insertion to drain the pus. Surgery in severe cases to clean the pleural cavity and remove infected tissue BREAK Section 3: Respiratory Diagnostics – Arterial Blood Gas pH is a measure of acidity and alkalinity Acidosis – systemic pH < 7.35 Alkalosis – systemic pH > 7.45 The body has three buffers that keep the pH within normal levels Remember the H in pH is the measurement of the H+ ions Section 3: Respiratory Diagnostics – Arterial Blood Gas BUFFER 1: H+ in the plasma is buffered by bicarbonate (HCO3-) in the plasma H+ + HCO3- → H2CO3 → CO2 + H2O Some H+ enters the cells and is buffered by: Intracellular bicarbonate Haemoglobin Albumen and globulin Section 3: Respiratory Diagnostics – Arterial Blood Gas BUFFER 2: If the amount of acid exceeds the capability of the first line buffers the increased H+ is detected by the chemoreceptors in the medulla and the rate and depth of breathing is increased Occurs when the pH 75 mmHg breathing air Bedside calculation - the % inspired concentration multiplied by 5 (result should be within 75 mmHg of calculation). 3. Examine the pH (or H+ concentration) Is the patient acidaemic; pH < 7.35 Is the patient alkalaemic; pH > 7.45 4. Compare the CO2 (35 – 45) and the pH to determine the respiratory component If the pH < 7.35, is the PaCO 2 > 45 mmHg – respiratory acidosis if the pH > 7.45, is the PaCO2 < 35 mmHg – respiratory alkalosis 5. Compare the HCO 3- (22-26) and the pH to determine the metabolic component If the pH < 7.35, is the HCO3- < 22 mmol L-1 – metabolic acidosis If the pH > 7.45, is the HCO3- > 26 mmol L-1 – metabolic alkalosis Section 3: Respiratory Diagnostics – Arterial Blood Gas Five-step approach to ABG interpretation In Summary 1. How is the patient? 2. Assess oxygenation (>75mmHg) 3. Examine the pH (7.35-7.45) 4. Compare the CO2 (35 – 45) and the pH 5. Compare the HCO3- (22-26) and the pH Section 3: Respiratory Diagnostics – Arterial Blood Gas Why is this important? How can it help me to become a better Registered Nurse? Acute Respiratory Distress A 65-year-old male with COPD presents to the emergency department with acute shortness of breath, increased respiratory rate, and using accessory muscles to breathe. ABG Results: pH 7.28, PaCO2 60 mmHg, HCO3- 26 mEq/L This ABG result indicates respiratory acidosis (low pH, high PaCO2) due to inadequate ventilation and CO2 retention, a common issue in COPD exacerbations. Understanding these values is crucial for nurses to recognise the need for interventions like oxygen therapy, bronchodilators, or non-invasive ventilation to improve the patient's respiratory function and correct the acidosis. Section 3: Respiratory Diagnostics – Arterial Blood Gas Why is this important? How can it help me to become a better Registered Nurse? Diabetic Ketoacidosis (DKA) A 23-year-old female with type 1 diabetes presents with polyuria, polydipsia, nausea, and a fruity odour on her breath. She admits to missing her insulin doses for the past two days. ABG Results: pH 7.1, PaCO2 25 mmHg, HCO3- 12 mEq/L These ABG results suggest metabolic acidosis with a compensatory respiratory alkalosis (low pH, low HCO3-, low PaCO2). The low bicarbonate indicates a metabolic cause (due to the accumulation of ketoacids in DKA), and the low PaCO2 reflects the body's attempt to compensate by hyperventilating to expel CO2. Nurses must recognise the severity of DKA and the need for urgent treatment, including insulin therapy, fluid resuscitation, strict fluid balance, and electrolyte replacement, to reverse the acidosis and prevent complications. Section 3: Respiratory Diagnostics – Arterial Blood Gas Respiratory imbalance Respiratory acidosis is characterised by a low pH and an increased PaCO2 Respiratory disease Respiratory alkalosis is characterised by a raised pH and a decreased PaCO2 Overventilation due to pain or emotional distress Section 3: Respiratory Diagnostics – Arterial Blood Gas Metabolic imbalance Metabolic acidosis is characterised by low pH and decreased HCO3 occurs when the blood is too acidotic due to a metabolic/kidney disorder Metabolic alkalosis is characterised by a high pH and increased HCO3 Chronic vomiting Sodium bicarbonate overdose Section 3: Respiratory Diagnostics – Arterial Blood Gas Case Study Mr Erikson is a 75 year old Arterial blood gases reveal man admitted to hospital with breathlessness. He has a history of heart pH 7.50 (7.35 – 7.45) failure. PaCO2 30mmHg (35 – 45 mmHg) He is pale and tachypnoeic HCO3 24mmols/L ( 22 – 26mmol/L) and his respiratory rate is 26. Chest auscultation reveals PaO2 75mmHg (80 – 100mmHg) crackles and CXR confirms pulmonary oedema. Section 3: Respiratory Diagnostics – Arterial Blood Gas Case Study Miss Jones has Arterial blood gases been experiencing pH 7.56 (7.35 – 7.45) vomiting for three PaCO2 44mmHg (35 – 45 mmHg) days. HCO3 36mmols/L ( 22 – 26mmol/L) She is extremely PaO2 98mmHg (80 – 100mmHg) dehydrated. Section 3: Respiratory Diagnostics – Arterial Blood Gas with ABG Ninja! https://abg.ninja/abg  Section 4: Respiratory Interventions In Section 4 we will comprehensively explore interventions including Non- Invasive Ventilation and Under-Water Sealed Drainage when responding to respiratory disease and injury Section 4: Respiratory Interventions – Differentiating O2 Therapy and NIV Oxygen Therapy Indicated for patients experiencing: hypoxaemia, as evidenced by SpO2 levels below 94%, dyspneoa, increased work of breathing, Cyanosis altered mental status. The primary goal is to maintain adequate tissue oxygenation while minimising cardiopulmonary work. Target SpO2 levels should generally be between 94% and 98% for most patients but may be adjusted based on individual conditions such as COPD. It's about correcting the oxygen level in the blood. Non-Invasive Ventilation (NIV) NIV supports both oxygenation and ventilation. It is used not just to deliver oxygen but also to assist spontaneous breathing. This is achieved through devices like CPAP or BiPAP, which provide positive pressure to the lungs through a mask. Indicated for patients experiencing respiratory distress but who are still able to breathe spontaneously. It is often used in acute exacerbations of COPD, cardiogenic pulmonary oedema, or conditions leading to acute hypercapnic respiratory failure. NIV can also be used as a preventative measure to avoid intubation. Oxygen Therapy: Indications and Administration Nasal Cannula: Low to moderate O2 needs, delivering 1-6 liters per minute (LPM), achieving 24-44% O2 concentration. Simple Face Mask: 5-10 LPM, providing approximately 35-50% O2 concentration. Venturi Mask: Provides precise O2 concentration by mixing air with O2; commonly used for patients requiring specific oxygen levels, especially those with chronic lung diseases. Non-Rebreather/Reservoir Mask: Offers highest O2 concentration possible without intubation, delivering up to 15 LPM and achieving approximately 60-100% O2. Im age 11. Typ es of o xygen th erapy. Retrieved from htt ps://www.aljazeer a.com/ wp-cont ent/up lo ads/202 1/05/I NT ERACTI VE-COVID-19-Oxyge n-the rapy.p ng?w=77 0&r esize= Oxygen Therapy: Risks and Management Risks  O2 toxicity (particularly with high concentrations over a long period)  dry or irritated nasal passages  decrease in the drive to breathe in patients with chronic CO 2 retention. It requires careful monitoring of O 2 saturation levels to avoid these complications. Adjusting Oxygen Flow Rates: Start with the minimum oxygen flow required to achieve target SpO 2 levels, then adjust based on the patient's response, monitoring for signs of hypoxaemia or oxygen toxicity in patients with chronic CO2 retention. Humidification: For patients receiving high-flow oxygen or those on oxygen therapy for extended periods, humidification helps to prevent mucosal drying, irritation, and potential bleeding. Im age 11. Typ es of o xygen th erapy. Retrieved from htt ps://www.aljazeer a.com/ wp-cont ent/up lo ads/202 1/05/I NT ERACTI VE-COVID-19-Oxyge n-the rapy.p ng?w=77 0&r esize=  What is Non Invasive Ventilation (NIV)? A form of mechanical ventilation without the use of an ETT or tracheostomy Uses CPAP or BiPAP Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Continuous Positive Airway Pressure In CPAP gas is delivered to the patient at a pre-set constant pressure during both inspiration and expiration Ventilation is controlled by the patient’s: Respiratory rate Tidal volume CPAP Indications Asthma Acute cardiogenic pulmonary oedema Hypoxemic respiratory failure Post-op respiratory failure – atelectasis Obstructive sleep apnoea Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Continuous Positive Airway Pressure NIV allows the practitioner to closely regulate the fraction of inspired O2 (FiO2) that is being delivered to patient Anywhere from 21% (room air) to 100% Aim is to maintain PaO2 >80mmHg and/or SpO2 >95% Manipulated in response to SaO 2 and ABG results Must be humidified Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Continuous Positive Airway Pressure Restrictive expiratory valve on mask provides PEEP Valve closes to prevent further exhalation during the patient’s breath out OR Mechanical PEEP provided by flow of gas from ventilator Common ranges of PEEP are between 5-15cm H2O Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Continuous Positive Airway Pressure Positive End Expiratory Pressure (PEEP) Increases the functional residual capacity (FRC) Increases surface area for gas exchange across functioning alveoli Forces open collapsed alveoli so gas exchange can occur Minimises alveolar collapse Improves compliance Improves PaO2 Decreasing work of breathing Improving V/Q mismatch Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) BiPAP and CPAP IPAP = Inspiratory Positive Airway Pressure EPAP = Expiratory Positive Airway Pressure PS = Pressure Support Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) What’s the difference? CPAP BiPAP Provides quantifiable PEEP Provides quantifiable PEEP Increases oxygenation Increases oxygenation Increases Minute Ventilation Reduces PaCO2 Can give timed breaths Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure (BiPAP) A machine that delivers positive pressure in two phases to a spontaneously breathing patient. IPAP (inspiratory positive airway pressure) Inhalation EPAP (expiratory positive airway pressure) (PEEP) Exhalation Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure BiPAP Indications Acute Respiratory Failure Type 2 COPD Pneumonia Acute Pulmonary Oedema Neuromuscular Disease Sleep Apneoa Congestive Heart Failure Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure How does BiPAP work? Patient breathes → triggering a positive pressure gradient is established until the preset inspiratory pressure support is reached. This happens rapidly to support the majority of the inspiratory phase The positive pressure gradient delivers a small amount of assistance to ventilation →  tidal volume & minute ventilation → promotes CO2 removal Expiratory positive airway pressure (EPAP) is maintained as the patient exhales, providing support to FRC as per CPAP EPAP is the same as PEEP Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure Maximise Open Support Improve Reduce removal airways the tidal work of of carbon and breath volume breathing dioxide alveoli Inspiratory Positive Airway pressure (IPAP) Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure Exerts positive Recruits intrapulmonary Increases function underinflated lung pressure on residual capacity tissue expiration (PEEP) Expiratory Positive Airway pressure (EPAP) Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Bi-Level Positive Airway Pressure Improved Improved cardiac compliance Reduced performance Increased because Improved respiratory because of a FRC atelectatic oxygenation muscle work reduction alveoli are preload and opened afterload BiPAP Physiological Effects Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) Contraindications for NIV Unconscious Respiratory arrest Haemodynamic instability Untreated pneumothorax Base of skull fracture Upper airway obstruction Vomiting / copious secretions Facial trauma, burns or recent facial/upper airway surgery Non-compliance Section 4: Respiratory Interventions – Non-Invasive Ventilation (NIV) NIV Patient Care: Patient Assessment NIV Setup Monitoring Skin Integrity (pressure injury risk) Infection Control Communication and Education Emergency Preparedness Potential risks include mask discomfort, nasal congestion, dry mouth, or eye irritation. There is also the risk of aspiration for some patients. Proper fitting of the mask and monitoring by trained professionals are essential to minimize these risks and ensure the effectiveness of the therapy.  From PP1: Case scenario change of shift handover i Hi this is CNM Darren on 5D, I am handing over Marcus Almoro, URN L987654 38yrs old. S Fractured (#) Right Clavicle & Right side pneumo/haemothorax (collapsed lung) following a mountain bike crash early today o Respiratory Rate 22, regular, shallow SpO2 100% on O2 via Nasal Prongs 3 L/min; BP 120/75; Pulse 64, regular Alert; Temp. 37.0 - afebrile; B Pain 2/10 (R) & 5/10 (M) No significant past history & no known allergies A Chest drain inserted, 200 mL blood drained, currently comfortable at rest. Continue to monitor vital signs/obs hourly; R observe chest drain; monitor fluid balance & urinary output; Pressure Injury & falls risk assessment to be completed; for orthopaedic consult & possible surgery; referred to physio. Section 4: Respiratory Interventions – Underwater Sealed Drainage Collection Chamber: The collection chamber is where fluid from the patient's pleural space is collected. This could be blood (in the case of a haemothorax), serous fluid, or pus. The measurements on the side allow practitioners to monitor the amount of drainage over time, which is crucial for assessing patient recovery. Water Seal Chamber: The water seal chamber acts as a one-way valve. It allows air to exit from the pleural space without re-entering. This is the key feature for treating a pneumothorax. The presence of air bubbles in this chamber can indicate an ongoing air leak from the lung. Suction Control Chamber: The suction control chamber is where a controlled amount of suction (negative pressure) is applied. This helps to remove air and fluid from the pleural space more effectively, ensuring the lung can re-expand. The dry suction regulator allows for precise control of this suction level. Air Leak Monitor and Pressure Indicators: The air leak monitor indicates whether there is an ongoing air leak from the chest. The patient pressure indicator, often a float ball, helps in monitoring the intrapleural pressure. A sudden rise in this pressure could indicate a blockage or kink in the system that requires immediate attention. Section 4: Respiratory Interventions – Underwater Sealed Drainage Initial Assessment: Verify the Medical Orders: Always check the medical orders before beginning your assessment. This will include the type of suction, the level of suction (if ordered), and the frequency of observations. Observation and Documentation: Drain Site and Dressing: Inspect the insertion site for signs of infection, ensure the dressing is intact, and note any skin changes or reactions. Tubing: Check that the tubing is not kinked, looped, or clamped inadvertently. Verify that all connections are secure and taped if necessary. Chest Drain Unit: Observe the water seal chamber for air leaks (bubbling), and the collection chamber for the amount and type of fluid drainage. Note the suction control chamber to ensure the prescribed level of suction is being applied if applicable. Frequent Monitoring: Immediately Post Insertion: Observations should be half-hourly for the first two hours, then hourly for at least four hours, and then four-hourly when the patient is haemodynamically stable. Routine Monitoring: After the initial phase, observations can be reduced to a minimum of four-hourly, depending on the patient's condition and medical orders. Section 4: Respiratory Interventions – Underwater Sealed Drainage Charting and Reporting: Use the Chart: Fill in the chart accurately and timely. Record the date/time, air leak presence, oscillation of the fluid in the water seal chamber, cumulative drainage, type of drainage (serous, sanguineous, etc.), and any air entry noted. Vital Signs and Pain: Monitor the patient's vital signs, assess for any respiratory distress, and pain score. Document any interventions and the patient's response. Communication: Any variances, such as increased drainage, new air leaks, or pain, should be reported to the medical officer immediately and documented in progress notes. Educational Points: Understand the Mechanics: Explain to the student how the chest drain works and why it is necessary for the patient's condition. Complication Awareness: Teach the student to recognise signs that may indicate complications, such as infection, bleeding, or a dislodged tube. Practical Skills: Ensure the student is competent in the practical skills required, such as changing the drainage unit, dressing the site, and managing the tubes. Section 4: Respiratory Interventions – Underwater Sealed Drainage Monitor for fluid swing (tidalling) and bubbling Fluid swing – A swinging motion in the tubing that occurs with changes in pleural pressure during inspiration and expiration Swing shows that the tube is patient Loss of swing may indicate occlusion (kinks and loops) or blockage of the tube ✓ If not resolved may lead to tension pneumothorax or surgical emphysema Bubbling ✓ Signifies that air is being removed from the pleural space ✓ Seen during expiration or coughing  Section 4: Respiratory Interventions – Underwater Sealed Drainage Indications that require immediate reporting: Respiratory Unexplained Increased Changes in distress or Reduced Development change in drainage, general change in oxygen of surgical patient especially observation respiratory saturation emphysema clinical state blood s or trends rate QUESTIONS  Summary Explored respiratory anatomy and physiology Today we have discussed: Discussed common examples of acute respiratory failure and exacerbations of chronic disease Discussed principles of Non-Invasive Ventilation (NIV) Examined the use of Arterial Blood Gases (ABGs) in assessing the ongoing care of patients Discussed the role and mechanism for common examples of respiratory pharmacology  References Respiratory system. In D. Brown, H. Edwards, T. Buckley & L. Aitken (Eds.)(2024). Lewis’s medical-surgical nursing: Assessment and management of clinical problems (6th ed.) Elsevier. Read pages 568 – 593. Respiratory failure and acute respiratory distress syndrome. In D. Brown, H. Edwards, T. Buckley & L. Aitken (Eds.)(2024). Lewis’s medical-surgical nursing: Assessment and management of clinical problems (6th ed.) Elsevier. Read pages 1873 – 1891. Agency for Clinical Innovation. (2023). Non-invasive ventilation for patients with acute respiratory failure. Retrieved from: https://aci.health.nsw.gov.au/__data/assets/pdf_file/0004/820372/ACI-Non-invasive-ventilation-for-patients-with-acute- respiratory-failure.pdf Obstructive pulmonary diseases. In D. Brown, H. Edwards, T. Buckley & L. Aitken (Eds.)(2024). Lewis’s medical-surgical nursing: Assessment and management of clinical problems (6th ed.) Elsevier. Read pages 659-709. www.resus.org.au With thanks to Fisher & Paykal Healthcare