2024 Acute Respiratory Failure PDF

ACUTE RESPIRATORY FAILURE Learning Objectives ▪Define acute respiratory failure (ARF) ▪Classification of ARF ▪Causes & clinical features ARF ▪Mechanisms & features of hypoxaemia ▪Identify the causes of tissue hypoxia ▪ABG assessment of hypoxaemia and hypoxia ▪Mechanisms & features of hypercarbia ▪G...

ACUTE RESPIRATORY FAILURE Learning Objectives ▪Define acute respiratory failure (ARF) ▪Classification of ARF ▪Causes & clinical features ARF ▪Mechanisms & features of hypoxaemia ▪Identify the causes of tissue hypoxia ▪ABG assessment of hypoxaemia and hypoxia ▪Mechanisms & features of hypercarbia ▪General treatment of ARF Review of A & P How do we breathe? University of Adelaide 4 University of Adelaide 5 University of Adelaide 6 University of Adelaide 7 University of Adelaide 8 University of Adelaide 9 University of Adelaide 10 University of Adelaide 11 University of Adelaide 12 Recap Definitions ▪Hypoxaemia ▪Deficient oxygenation of arterial blood ▪PaO2 < 80 mmHg ▪Hypoxia ▪Deficient oxygenation of the tissues ABG Analysis PaO2 70 mmHg PH 7.25 PaCO2 51 mmHg HCO3- 24 mEq/L Oxygen delivery- 50% through Invasive ventilation ED presentation- 1st gas PaO2 60 mmHg PH 7.29 PaCO2 32mmHg HCO3- 19mEq/L Lactate 3 Oxygen delivery- Non rebreather Nil urine output since?? ABG’s One more practice- PaO2 200 mmHg PH 7.50 PaCO2 28 mmHg HCO3- 23 mEq/L Oxygen delivery- Nasal Specs 4L Variations VBG Normal Values pH: 7.32-7.43 PvO2: 30-40 PvC02: 41-50 HC03: 19-25 BE: -3-+3 ABG Normal Values pH: 7.35-7.45 PaO2: 80-100 PCO2: 35-45 HCO3: 22-28 BE: -2 to +2 Respiratory Failure - Definition ▪A condition in which the respiratory system fails in one or both of its gas-exchange functions ▪Oxygenation ▪Elimination of Carbon Dioxide (CO2)  Acute Respiratory Failure Conventionally defined as: ▪PaO2 < 60 mmHg and/or ▪PaCO2 > 45 mmHg & pH < 7.35, or both. Respiratory Failure The respiratory system consists of two parts: The lungs (gas exchange) The ventilatory pump Failure of one or the other leads to respiratory failure  Respiratory Failure Lung failure- Type I Pump failure – Type II Failure to oxygenate Failure to ventilate manifest by manifest by hypoxemia hypercarbia Classification of Acute Respiratory Failure Failure To Oxygenate Failure To Ventilate ▪Hypoxemic (type I) ▪Hypercapneic (type II) respiratory failure respiratory failure ▪Characterised by ▪Characterised by hypoxaemia hypercapnia ▪Normocapnia or hypocapnia Causes of Acute Respiratory Failure Intrapulmonary Extra pulmonary Airway Disease Central Nervous System (CNS) Disorders Lung Disease Disorders of the Peripheral Nervous System & Spinal cord Pulmonary Circulation Neuromuscular Disorders Pulmonary Oedema Diseases/Disorders of the Pleura or Chest Wall Clinical Features of Acute Respiratory Failure Variable ▪Dependant on the underlying cause ▪Dependant on the degree of ▪ hypoxaemia, ▪ hypercarbia ▪ acidosis  Clinical Features Dyspnoea, tachypnoea, orthopnoea Inability to speak Use of accessory muscles Intercostal retractions Paradoxical abdominal movement Noisy breathing - crackles, wheezes, stridor Anxiety, restlessness, confusion Lethargy, coma Type 1 Respiratory Failure: Failure to Oxygenate ▪Most common type of respiratory failure ▪Mechanisms of hypoxaemia ▪ Low Fraction of inspired oxygen (FiO2) ▪ V/Q mismatch ▪Diffusion defect Ventilation Perfusion Mismatch (V/Q mismatch) ▪Most common cause of hypoxaemia ▪Normally ventilation equals perfusion ▪As V/Q ratios deviate from normal- gas exchange is impaired Causes of V/Q Mismatch ▪Shunt - Ventilation reduced / perfusion normal ▪Obstructed airways ▪Pneumonia ▪Pulmonary oedema ▪Dead space - Ventilation normal / perfusion reduced ▪Pulmonary embolism ▪Low cardiac output http://emedicine.medscape.com/article/167981-overview  Diffusion Defect Impaired diffusion of gases ▪Due to conditions that affect the alveolar-capillary (AC) membrane: ▪Loss of alveolar surface area ▪COPD, pneumonectomy, tumour ▪Thickening of the AC membrane ▪Pulmonary fibrosis & pulmonary oedema ▪Response to O2 depends on the severity of the disease Determinates of Gas Exchange The thickness of the membrane e.g., pulmonary fibrosis The surface area of the membrane e.g., atelectasis The diffusion coefficient of the gas (O2 has a lower molecular weight than CO2 and therefore can be expected to diffuse across the respiratory membrane faster) e.g., temperature The pressure difference between the two sides of the membrane (alveoli and capillary) e.g. The partial pressure of oxygen in the alveoli is about 104 mm Hg, whereas its partial pressure in the blood of the capillary is about 40 mm Hg. Hypoxaemia versus hypoxia ▪Hypoxaemia does not necessarily cause tissue hypoxia ▪Depends on the severity of hypoxaemia ▪A precise PaO2 that will cause hypoxia cannot be identified ▪Affected by various factors ▪Cardiac Output, Haemoglobin, shift in Oxy Haemoglobin Dissociation curve ▪Tissue hypoxia is likely with severe hypoxaemia ▪PaO2 < 45  Markers of Tissue Hypoxia ▪ Increased Lactate ▪ Reduced SVO2 < 65% or ScVO2 < 70% ▪ How do you recognise tissue hypoxia ? Other indicators ? Causes of Hypoxia ▪Hypoxaemic hypoxia ▪Inadequate oxygenation of arterial blood ▪Stagnant hypoxia ▪Inadequate blood flow ▪Anaemic hypoxia ▪Insufficient functional haemoglobin ▪Histotoxic hypoxia ▪Inadequate tissue utilisation of oxygen Hypoxaemic hypoxia ▪Inadequate oxygenation of arterial blood ▪V/Q mismatch, right-to-left shunt, diffusion impairment, hypoventilation and low inspired O2. Stagnant hypoxia ▪Inadequate blood flow ▪May affect the entire body ▪Heart failure, cardiogenic shock ▪May be localised ▪Vascular disease Anaemic Hypoxia ▪Insufficient amount of functional Hb ▪Decrease in concentration of Hb ▪Defect in the ability of Hb to carry O2 Histotoxic Hypoxia ▪Impaired tissue utilisation of oxygen ▪Increased metabolic demands ▪Systemic inflammation, sepsis, shivering, burns ▪Impaired tissue utilisation ▪Sepsis, carbon monoxide & cyanide poisoning Clinical Features of Hypoxia ▪Respiratory ▪Early - Dyspnoea, tachypnoea, hyperpnoea ▪Late - Bradypnoea or agonal breathing ▪Cardiovascular ▪Early - Tachycardia, mild hypertension ▪Late - Bradycardia & hypotension, arrhythmias and Angina  Clinical Features of Hypoxia ▪Neurological ▪Headache, restlessness, agitation, confusion, paranoia, combative behaviour ▪Loss of coordination, CNS depression, coma ▪Skin ▪Early - Cool, clammy, diaphoresis ▪Late – Cyanosis Peripheral/Central Other effects of Hypoxia ▪Hypoxic pulmonary vasoconstriction ▪Increased pulmonary vascular resistance ▪Cor pulmonale (right heart failure) ▪Myocardial dyfunction ▪Diaphragmatic fatigue Type 2 Respiratory Failure: Failure to Ventilate ▪Hypercapneic respiratory failure ▪PaO2 > 45 mmHg ▪Usually* hypoxaemia as well ▪Usually caused by hypoventilation Clinical Manifestations of Hypercarbia PaCO2 60 -75mmHg PaCO2 80-100mmHg PaCO2 120-150mmHg Tachypnoea/ Asterixis Anaesthesia Dyspnoea Peripheral Confusion/ DEATH Vasodilation Lethargy Warm peripheries Headache Bounding pulse Coma Other effects of Hypercarbia ▪Displaces alveolar O2 & reduces PaO2 ▪Shifts the Oxy-Haemoglobin Dissociation (OHD) curve to the right ▪Decreases affinity of Hb for O2 ▪Increases unloading O2 to the tissues Who is at risk of CO2 retention? ▪Patients with: ▪ COPD ▪ Severe chronic asthma ▪ Cystic fibrosis ▪ Kyphoscoliosis ▪ Neuromuscular disease ▪ Obesity hypoventilation ▪Most patients with COPD have normal PaCO2 ▪Most admissions with an acute exacerbation of COPD have acute not chronic respiratory failure ▪Distinction has important prognostic & therapeutic implications- consider baseline CO2 levels. Investigations (Type 1 and 2) ▪ABG ▪SaO2, PaO2, PaCO2 ▪A-a gradient, SvO2 ▪pH, bicarbonate, lactate ▪Chest X-Ray Extra investigations (for underlying cause): Electrocardiograph (ECG), haemodynamic monitoring, & echocardiography The Alveolar-arterial gradient (A-a) ▪The difference between the alveolar concentration of oxygen and the arterial concentration of oxygen ▪Normal is approx. 5 - 10mmHg (Young adult, non-smoker) ▪One use of the A-a gradient is in patients with hypoxemia & hypercarbia ▪A-a gradient normal : ▪hypoxaemia is caused by hypoventilation alone (e.g., head injury) ▪A-a gradient abnormal (Raised): ▪ hypoxaemia is complicated by an intrapulmonary disorder e.g., pneumonia affecting transfer of oxygen across alveolar membrane. ▪A-a gradient is calculated as PAO2 – PaO2 https://www.nursingcenter.com/ncblog/august- 2020/calculate-a-a-gradient go to calculator and practice For every decade a person has lived, their A–a gradient is expected to increase by 1 mmHg – a conservative estimate of normal A–a gradient is < [age in years/4] + 4 or age x 0.3 Management of Respiratory Failure ▪Failure to oxygenate ▪Oxygen therapy ▪Maintaining lung volumes using alveolar recruitments strategies ▪PEEP / CPAP / *NHF ▪Failure to ventilate ▪NIV / BiPAP / IPPV General Goals of Therapy ▪Maintain airway patency ▪Optimise oxygen delivery ▪Oxygen therapy, NIV, IPPV ▪Patient positioning, C&DB, pain relief ▪Optimise CO & ensure adequate Hb ▪Minimise oxygen demand ▪Identify & treat cause ▪Prevention of complications  Take home messages ▪There are two types of respiratory failure ▪Type 1 - Failure to Oxygenate ▪Type 2 - Failure to Ventilate ▪Hypoxia will kill before hypercarbia ▪Administer oxygen ▪Consider the underlying cause and (if possible) treat/intervene. Type I and Type II RF Type I Type II - Hypoxia – low paO2 -Hypoxaemia AND Hypercapnia -pCO2 is normal or low -Low paO2 and high pCo2 -How is the patient -How is the patient looking? looking? University of Adelaide 52 Case study Maggie is a 25 yo female with no relevant PmHx. She takes no medications besides an oral contraceptive. She presents to ED with mild SOB and chest pain. Her cardiac troponin level is negative. Please see her ECG: University of Adelaide 53 University of Adelaide 54 Please see her CXR University of Adelaide 55 Her SOB worsens. She is now on Nasal Specs 4L (FiO2? ) RR: what do you think? SpO2 94% HR: 110bpm BP: 110/70mmHg (usually low) The team decides to obtain an ABG. University of Adelaide 56  a b c FiO2 36% pH 7.48 paO2 110 pCO2 25 HCO3 24 Interpretation How is the patient? Magic Numbers 35-45! What do we do? pH: 7.35-7.45 PaO2: 80-100 PCO2: 35-45 HCO3: 22-28 University of Adelaide 57  a b c FiO2 35% 50% pH 7.48 7.40 paO2 110 100 pCO2 25 38 HCO3 24 24 Interpretation How is the patient? What do we do? Magic Numbers 35-45! pH: 7.35-7.45 PaO2: 80-100 PCO2: 35-45 HCO3: 22-28 University of Adelaide 58  a b c FiO2 50% 50% 60% pH 7.48 7.40 7.2 paO2 110 100 61 pCO2 25 38 57 HCO3 24 24 24 Interpretation How is the patient? What do we do now? Magic Numbers 35-45! pH: 7.35-7.45 PaO2: 80-100 PCO2: 35-45 HCO3: 22-28 University of Adelaide 59 Maggie does not tolerate NIV as she is very SOB and drowsy. She is quickly intubated. A bedside ECHO is performed where severe RV dysfunction is identified. After stable she is taken to a CTPA where multiple PE are identified. University of Adelaide 60  Treatment - Haemodynamic and respiratory support - Anticoagulation (Heparin, NOACs or warfarin) - Reperfusion treatment - systemic thrombolysis (alteplase/tenecteplase) University of Adelaide 61 Questions?