Respiratory Failure and ARDS - University of Botswana PDF

ARTERIAL BLOOD GASES and RESPIRATORY FAILURE Dr Mamalelala & Prof Dithole  OBJECTIVES Outline the steps of analysis of ABGs Discuss acute respiratory failure Describe the pathophysiology, etiology, clinical manifestations, and direct and indirect causes of acute respirato...

ARTERIAL BLOOD GASES and RESPIRATORY FAILURE Dr Mamalelala & Prof Dithole  OBJECTIVES Outline the steps of analysis of ABGs Discuss acute respiratory failure Describe the pathophysiology, etiology, clinical manifestations, and direct and indirect causes of acute respiratory distress syndrome Identify risk factors and prevention methods associated with ARDS. Discuss the management of ARDS Formulate priority nursing diagnoses appropriate for individual with ARDS.uxpected outcomes for an individual with ARDS.  ARTERIAL BLOOD GASES Arterial blood gases (ABG) are obtained for two basic purposes: 1. To determine oxygenation 2. To determine acid-base status When is an ABG required? 1. To establish a diagnosis 2. To assess illness severity 3. To guide and monitor treatment  PULMONARY GAS EXCHANGE: PARTIAL PRESSURE Pulmonary gas exchange refers to the transfer of O2 from the atmosphere to the bloodstream (oxygenation) and CO2 from the bloodstream to the atmosphere (CO2 elimination)  Arterial blood gases help us to assess the effectiveness of gas exchange by providing measurements of the partial pressure  CARBON DIOXIDE ELIMINATION PaCO2 is determined by alveolar ventilation (ref. range: PaCO2= 35-45 mm Hg). Increased PaCO2 (hypercapnia) implies reduced alveolar ventilation Ventilation is regulated by an area in brainstem called respiratory center. This area contains receptors that sense PaCO2 and connect with the muscles involved in breathing. If PaCO2 is abnormal, the respiratory center adjusts the rate and depth of breathing accordingly.  OXYGENATION The amount of O2 in blood depends on the two factors: 1. Hb concentration - how much O2 blood has the capacity to carry. 2. Saturation of Hb with O2 (SO2 ) - the percentage of available binding sites on Hb occupied by O2 molecules.  THE RESPIRATORY BUFFER RESPONSE Our lungs are responsible for removing CO2. PaCO2 , the partial pressure of carbon dioxide in our blood, is determined by alveolar ventilation. CO2 is carried in the blood to the lungs. In blood CO2 combines with water to form carbonic acid (H2CO3 ). The more CO2 is added to blood, the more H2CO3 is produced, which dissociates to release H+ CO2+H2O⇆H2CO3⇆HCO3−+H+ Activation of the lungs to compensate for an  THE RENAL BUFFER RESPONSE The kidneys secrete H+ ions into urine and reabsorb HCO3 − from urine. HCO3 − is a base (and therefore accepts H+ ions), so it reduces the concentration of H+ ions in blood The system may take hours to days to correct the imbalance.  ABG COMPONENT PH: measures hydrogen ion concentration in the blood, it shows blood’ acidity or alkalinity PCO2 :It is the partial pressure of CO2 that is carried by the blood for excretion by the lungs, known as respiratory parameter PO2: It is the partial pressure of O2 that is dissolved in the blood , it reflects the body ability to pick up oxygen from the lungs HCO3 :known as the metabolic parameter, it reflects theAkidney’s.Y.T ability to retain 9 and  TERMS AND DEFINITIONS Variable Primary Normal Range, Primary Disorder arterial Gas Disorder pH Acidemia 7.35 - 7.45 Alkalemia pCO2 Respiratory 35 - 45 Respiratory alkalosis acidosis HCO3 Metabolic 22 – 26 Metabolic acidosis Alkalosis Respiratory compensation for metabolic disorders is rapid Full metabolic compensation for respiratory disturbances requires renal adjustment and takes 3-5 days SIMPLE ACID-BASE DISORDERS  STEPS TO ABG INTERPRETATION (1)Is the pH normal? (2)Is the CO2 normal? (3)Is the HCO3 normal? (4)Match the CO2 or HCO3 with the pH? (Identifying primary cause) (5)Does the CO2 or HCO3 in the opposite direction of the pH? (Compensation) (6)Are the PaO2 and SaO2 normal? P  STEPS TO ABG INTERPRETATION (1) Step 1: PH analysis Normal range of blood pH: 7.35 to 7.45 PH < 7.35 is acidic PH > 7.45 is alkalotic Step 2: CO2 analysis Normal pCO2 level: 35-45mmHg Below 35mmHg is alkalosis Above 45mmHg is acidosis  STEPS TO ABG INTERPRETATION (2) Step 3: HCO3 analysis Normal HCO3 level is 22-26 mEq/L Below 22 mEq/L is acidosis Above 26 mEq/L is alkalosis  STEPS TO ABG INTERPRETATION (3) Step 4: Match CO2 and HCO3 with the pH level Match either PCO2 and HCO3 with pH level to determine the primary cause of acid-base disorder. If primary acid base disorder caused by respiratory, CO2 level is opposite to pH level If Primary acid base disorder caused by metabolic, HCO3 level is equal to Matching Respiratory (Primary cause) pH↓PCO2↑ Respiratory acidosis pH↑PCO2↓ Respiratory Alkalosis Metabolic (Primary cause) pH↓HCO3↓Metabolic acidosis pH↑HCO3↑Metabolic alkalosis  EXAMPLE #1 pH 7.50 Acute Respiratory Alkalosis pCO2 29 HCO3 22 Variable Primary Normal Primary Disorder Range, Disorder arterial Gas pH Acidemia 7.35-7.45 Alkalemia pCO2 Respiratory 35 - 45 Respiratory alkalosis acidosis HCO3 Metabolic 22 – 26 Metabolic acidosis Alkalosis  EXAMPLE #2 pH 7.25 Acute Respiratory Acidosis pCO2 60 HCO3 26 Variable Primary Normal Primary Disorder Range, Disorder arterial Gas pH Acidemia 7.35-7.45 Alkalemia pCO2 Respiratory 35 - 45 Respiratory alkalosis acidosis HCO3 Metabolic 22 – 26 Metabolic acidosis Alkalosis  Example #3 pH 7.50 Metabolic Alkalosis pCO2 48 HCO3 36 Variabl Primary Normal Primary e Disorder Range, Disorder arterial Gas pH Acidemia 7.35-7.45 Alkalemia pCO2 Respiratory 35 - 45 Respiratory alkalosis acidosis HCO3 Metabolic 22 – 26 Metabolic acidosis Alkalosis  COMPENSATION The respiratory and metabolic system works together to keep the body’s acid-base balance within normal limits. The respiratory system responds to metabolic based PH imbalances in the following manner: * metabolic acidosis: ↑ respiratory rate and depth (↓PaCO2) * metabolic alkalosis: ↓ respiratory rate and depth (↑PaCO2) The metabolic system responds to respiratory based PH imbalances in the following manner: *respiratory acidosis: ↑ HCO3 reabsorption 20  COMPENSATION Step 5: Does CO2 or HCO3 go to the opposite direction of pH (determinate the compensation) Either CO2 or HCO3 go to the opposite direction of pH, that means compensation in progress.  COMPENSATION Primary system Compensating system causing imbalance Respiratory (pCO2↑) Metabolic (HCO3 ↑) acidosis Respiratory (pCO2↓) Metabolic (HCO3↓) alkalosis Metabolic (HCO3 ↓) Respiratory (pCO2↓) acidosis Metabolic (HCO3 ↑) Respiratory (pCO2↑) Alkalosis  Respiratory system compensation Respiratory system balances pH by ↑ or ↓ RR to manipulating the CO2 level. Fast and deep breathing “blows off” CO2 in primary metabolic acidosis. Slow and shallow breathing “retains” CO2 in primary metabolic alkalosis. The process is fast.  Renal System Compensation Primary respiratory alkalosis: Kidney▶▶▶Excreting more HCO3- Excreting more HCO3- in in urine and retaining more H+] Primary respiratory acidosis: Kidney▶▶▶Excreting more H+ in urine and retaining more HCO3- and retaining more HCO3- The process is slow but more powerful.  PARTIAL/COMPLETE COMPENSATION Compensation may not always be complete and time consuming. If pH remains abnormal, it is partial compensation. If pH returns to normal range, the compensation is complete. Note Nothing to do = no compensation  EXAMPLE #4 pH 7.34 Chronic Respiratory Acidosis with pCO2 60 Metabolic HCO3 31 Compensation Variable Primary Normal Primary Disorder Range, Disorder arterial Gas pH Acidemia 7.35-7.45 Alkalemia pCO2 Respiratory 35 - 45 Respiratory alkalosis acidosis HCO3 Metabolic 22 – 26 Metabolic acidosis Alkalosis  EXAMPLE #5 pH=7.18 PaCO2=68 HCO3=29 A: Uncompensated Metabolic Acidosis B: Partly compensated respiratory acidosis C: Combined Acidosis D: Uncompensated respiratory Acidosis  EXAMPLE #6 A patient has the following arterial blood gas results: blood pH 7.43, PaCO2 28 mmHg, and HCO3 18 mEq/L Respiratory alkalosis, fully compensated by the means of metabolic acidosis.  RESPIRATORY FAILURE Respiratory failure is a sudden life- threatening deterioration of the gas exchange of the lung It exists when exchange of oxygen for carbon dioxde in the lungs cannot keep up with the rate of oxygen consumption and carbon dioxide production by the sells of the body. It happen when your blood doesn’t have enough oxygen or it has too much carbon dioxide  TYPES OF ACUTE RESPIRATORY FAILURE Type 1: Hypoxemic respiratory failure Type 2: Hypercapnic respiratory failure Type 3: Perioperative respiratory failure type 4: Shock secondary to  HYPOVENTILATION Alveolar hypoventilation increases the arterial partial pressure of carbon dioxide (PaCO2). The increase in PaCO2 causes a decrease in the alveolar partial pressure of oxygen.  V/P MISMATCH It occurs when air (ventilation) and blood flow (perfusion) to the lungs are not properly matched. The V/Q ratio describes the balance between air reaching the alveoli and blood flow through the lung capillaries. Gas exchange is impaired, leading to low oxygen levels. Administering 100% O2 usually corrects hypoxemia caused by a V/Q mismatch.  SHUNT A shunt is a pathological mechanism in which the alveoli are perfused with blood but not ventilated, leading to impaired gas exchange. The deoxygenated blood bypasses the ventilated areas of the lung and remains unoxygenated even with 100% O2 inhalation.  Type 1: Hypoxemic respiratory failure It is defined by low level of oxygen in the blood (hypoxemia) with normal (normocapnia) or low (hypocapnia) level of carbon dioxide but not increased level of carbon dioxide (hypercapnia) Is caused by ventilation perfusion mismatch; the volume of air in and out of the lungs not matched with the flow of blood to the lungs  Types of Acute Respiratory Failure I PO2 < 60 mmHg on room air. Usually seen in patients with acute pulmonary edema or acute lung injury. These disorders interfere with the lung's ability to oxygenate blood as it flows through the pulmonary vasculature  Types of Acute Respiratory Failure II Type 2 (Hypercapnic/ Ventilatory ) PCO2 > 50 mmHg (if not a chronic CO2 retainer). This is usually seen in patients with an increased work of breathing due to airflow obstruction or decreased respiratory system compliance, with decreased respiratory muscle power due to neuromuscular disease Seen in patients with central respiratory failure and decreased respiratory drive. EG  Types of Acute Respiratory Failure III Type 3 (Peri-operative) This is generally a subset of type 1 failure but is sometimes considered separately because it is so common. Type 4 (Shock) Secondary to cardiovascular instability. CLINICAL PRESENTATION Presentation of respiratory failure is dependent on the underlying cause and associated hypoxemia or hypercapnia.  SIGNS AND SYMPTOMS OF RF TYPE I (HYPOXEMIA) Dyspnea, irritability Confusion, fits, somnolence Tachycardia, arrhythmia Tachypnea Cyanosis Use of accessory muscles Nasal flarring  SIGNS AND SYMPTOMS OF RF TYPE II Change of(HYPERCAPNIA) behavior Increased cerebral blood flow and CSF pressure Headache Asterixis Papilloedema Warm extremities, with diminishing pulses Acidosis (metabolic and respiratory)  DIAGNOSIS ABGs Renal function tests and liver function tests Pulmonary function test ECG Imaging- CT scans and CXR  MANAGEMENT Mechanical ventilation Extracorporeal membrane oxygenation (ECMO) Oxygen therapy Fluids Manage the underlying condition  RESPIRATOY FAILURE- ARDS - Definition: Is a sudden, progressive form of respiratory failure characterized by severe dyspnea, refractory hypoxemia, and diffuse bilateral infiltrates  Is a life-threatening condition of seriously ill patients, characterized by poor oxygenation, pulmonary infiltrates, and acuity of onset.  An acute disorder that starts within 7 days of the inciting event and is characterized by bilateral lung infiltrates and severe progressive hypoxemia in the absence of any evidence of cardiogenic pulmonary edema.  ARDS is considered a Type 1 respiratory failure because it primarily presents as hypoxemic respiratory failure, meaning the main problem is a lack of oxygen in the blood due to damaged lung tissue, while carbon dioxide levels usually remain normal or lo  Acute respiratory distress syndrome (ARDS) An acute massive lung injury that results from a variety of clinical states. This can be due to bacterial, virial or fungal infection causing lung contusion, fat embolus, aspirates, massive smoke inhalation, inhaled toxins that lead to sepsis and shock. There will be localised inflammation which progresses to generalised inflammation if there is no help. This results in Disseminated Intravascular Coagulation. PATHOPHYSIOLOGY PATHOPHYSIOLOGY  PHASES OF ARDS Exudative phase Proliferative Phase Fibrotic phase  EXUDATIVE STAGE CONT’  this phase begins within 12 to 36 hours after inciting insult and its duration is typically up to 7 days.  It is characterized by alveolar oedema and neutrophil inflammation with subsequent development of hyaline membrane from diffuse alveolar damage.  Alveolar oedema is the most prominent in the dependent portions of the lung and it causes atelectasis and reduction in lung compliance.  Alveolar oedema result in reduction of gas exchange leading to hypoxemia, there would be development of tachypnoea and dyspnoea.  EXUDATIVE PHASE Characterised by:  Accumulation of excessive fluids in the lungs due to exudation (leaking of fluids) and acute injury.  Hypoxemia is usually most severe during this stage, as is injury to the endothelium (lining membrane) and epithelium (surface layer of the cells)  Some individuals quickly recover from this first stage; many others progress after about a week into the second stage.  PROLIFERATIVE PHASE  This phase last from approximately 7 to 21 days after inciting insult  It is characterized by interstitial inflammation and proliferated type 2 pneumocytes persists but hyaline membrane are no longer formed  Alveolar macrophages digest remnants of hyaline membrane and other debris  Dyspnoea and hypoxemia persists  PROLIFERATIVE PHASE cont’  Even though most patient recover some will develop progressive lung injury and pulmonary fibrosis  Connective tissue and other structural elements in the lungs proliferate in response to the initial injury, including development of fibroblasts.  Abnormally enlarged air spaces and fibrotic tissues (scarring) are increasingly apparent  FIBROTIC PHASE it signalise the end of the acute disease process Most patients recover within 3 to 4 weeks of initial pulmonary injury but some experiences ; progressive fibrosis indicating necessity of prolonged ventilator support and supplemental oxygen furthermore there is increased risk of pneumothorax and reduction in lung compliance lung function may continue to improve for as long as 6 – 12 months after onset of respiratory failure, depending on the  EARLY SIGNS AND SYMPTOMS Restlessness Dyspnoea Low Blood pressure Confusion Extreme tiredness Mood swing Disorientation Change in LOC Cough Fever  LATE SIGNS AND SYMPTOMS Severe difficulty in breathing i.e., labored, rapid breathing Shortness of breath Tachycardia Thick frothy sputum Metabolic acidosis Cyanosis Abnormal breath sounds, like crackles Decreased PaCO2 with respiratory alkalosis Decreased PaO2  ASSESSMENT Complete history On Physical Examination Auscultation reveals abnormal breath sounds (wheezing, crackles)  DIAGNOSIS ABGs Blood tests Chest x-ray Bronchoscopy Sputum culture and analysis Chest CT scan Echocardigram  DIAGNOSIS WITH ARTERIAL BLOOD GASES The diagnosis of ARDS is made based on the following criteria:  Acute onset  Moderate to severe impairment of oxygenation  The gold standard for the diagnosis of acute respiratory failure is an arterial partial pressure of oxygen (PaO2) on room air less than 60 mmHg measured by arterial blood gases (ABG).  In the absence of an ABG, saturation of oxygen (SpO2) less than 91% measured by pulse oximetry on room air can serve as a substitute for the PaO2 because SpO2 of 91% equals PaO2 of 60 mmHg (Parhar et al., 2019).  MEDICAL MANAGEMENT Persons with ARDS are hospitalized and require treatment in ICU Fluid therapy No specific therapy for ARDS exists Supportive measures – Supplemental oxygen – Mechanical ventilation Prone strategies – Turn the patient from supine to prone – Lateral rotation therapy  PRONE POSITIONING About 2/3 of patients with ARDS improve their oxygenation after being placed in prone position Mechanisms that may explain the improvement include – Increased functional residual capacity – Change in regional diaphragmatic motion – Perfusion redistribution – Improved clearance of secretions (PaO2 level in prone is more than supine  LATERAL ROTATION THERAPY To stimulate postural drainage and help mobilise the secretion The  MANAGEMENT The management of ARDS typically involves a multidisciplinary approach, including medical, surgical, and nursing interventions. The goal of treatment is to support the patient's respiratory function, address the underlying cause, and prevent complications, (Cruz et al,2019). They include; 1. MEDICAL MANAGEMENT Oxygen therapy: Supplemental oxygen is usually the first-line treatment for acute respiratory distress syndrome with the aim of maintaining adequate oxygen levels in the blood. High-flow nasal cannula oxygen therapy and non-invasive positive pressure ventilation (NIPPV) may be used in some cases. Monitoring: Continuous monitoring of vital signs, oxygen saturation, and fluid balance is essential in patients with ARDS.  MANAGEMENT cont’ Mechanical ventilation: In severe cases, patients may require mechanical ventilation to help support their breathing. Sedation and analgesia: Patients with ARDS who require mechanical ventilation may require sedation and analgesia to manage pain and anxiety. Pharmacotherapy: Medications such as bronchodilators, corticosteroids, and diuretics may be used to manage symptoms and address underlying causes.  MANAGEMENT cont’ Nutrition support: Adequate nutrition is essential for the recovery of patients with ARDS, and enteral nutrition (feeding through a tube) may be initiated early in the course of treatment. Infection control: Infection control measures, such as hand hygiene and appropriate use of personal protective equipment (PPE), are essential in preventing the spread of infections that can cause or exacerbate ARDS.  MANAGEMENT cont’ Fluid management: Fluid management is important in patients with ARDS, as excessive fluid administration can worsen lung function. Careful monitoring of fluid balance and adjustment of intravenous fluids may be necessary.  SURGICAL MANAGEMENT Extracorporeal membrane oxygenation (ECMO): In some cases, ECMO may be used to provide temporary respiratory support to patients with severe acute respiratory distress syndrome who are unresponsive to other treatments. ECMO involves circulating the patient's blood through a machine that provides oxygen and removes carbon dioxide, allowing the lungs to rest and heal. Thoracentesis: In patients with ARDS who develop pleural effusions (fluid accumulation in the lungs), a thoracentesis may be performed to drain the fluid and relieve pressure on the lungs.  SURGICAL MANAGEMENT cont; Lung transplantation: In severe cases of ARDS, a lung transplant may be necessary to improve lung function and oxygenation. Tracheostomy: A tracheostomy is a surgical procedure that involves making an incision in the neck and inserting a tube directly into the trachea to help with breathing. This can be useful in patients who require long-term ventilation support  NURSING ASSESSMENT FOR (ARDS) Respiratory Status: Monitor respiratory rate, depth, and pattern continuously to assess for signs of increased work of breathing, use of accessory muscles, and adequacy of ventilation. Oxygen Saturation: Continuously measure oxygen saturation using pulse oximetry to assess the patient’s oxygenation status. Document any fluctuations and response to interventions. Hemodynamic Parameters: Monitor blood pressure, heart rate, and other hemodynamic parameters regularly to identify signs of hemodynamic instability, such as hypotension or tachycardia.  NURSING ASSESSMENT FOR (ARDS) cont’ Lung Sounds: Auscultate lung sounds to identify abnormal breath sounds, such as crackles or diminished breath sounds, which may indicate fluid accumulation in the lungs. Ventilator Settings: Assess and document ventilator settings, including mode, tidal volume, positive end-expiratory pressure (PEEP), and FiO2, to ensure appropriate mechanical ventilation and identify the need for adjustments. Fluid Balance: Monitor fluid intake and output, as well as daily weights, to assess fluid balance.  NURSING ASSESSMENT FOR (ARDS) Laboratory Values: cont’ Review laboratory results, including arterial blood gases, complete blood count, and electrolyte levels, to evaluate respiratory and metabolic status, as well as the impact on other organ systems. Mental Status: Assess the patient’s mental status and level of consciousness regularly, as changes may indicate hypoxia or impaired  OUTCOMES Improved Oxygenation: Achieve and maintain improved oxygenation, as evidenced by increased oxygen saturation levels and improved arterial blood gas values, indicating effective management of hypoxemia. Resolution of Pulmonary Edema: Facilitate the resolution of pulmonary edema, leading to improved lung compliance and effective gas exchange. Stabilized Hemodynamic Parameters: Attain stability in hemodynamic parameters, including blood pressure and heart rate, to ensure adequate tissue perfusion and support vital organ function. Successful Ventilator Weaning: Work towards successful weaning from mechanical ventilation,  NURSING INTERVENTIONS AND RATIONALES Provide supplemental oxygen as appropriate Supplemental oxygen will ideally increase their oxygen levels. The earlier we can intervene, the better for the patient. If you notice you are requiring more oxygen and not seeing results, notify the provider. Monitor hemodynamics Because of the damage and decreased compliance in the lungs, the pressure in the lungs builds up. This can cause pressure on the major vessels leading to decreased cardiac output  EVALUATION Oxygenation Status: Evaluate the effectiveness of interventions by assessing sustained improvements in oxygenation, as evidenced by stable or improved oxygen saturation levels and arterial blood gas values Hemodynamic Stability: Assess the stability of hemodynamic parameters, including blood pressure and heart rate, to ensure adequate tissue perfusion and identify any signs of