Respiratory: Respiratory Failure and ARDS

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Presentation transcript:

Respiratory: Respiratory Failure and ARDS Marnie Quick, RN, MSN, CNRN

Respiratory Failure- outline Resp volume/capacity and definition Resp failure Causes/predisposing factors Classification Hypoxemic (causes/mechanisms/s&s) Hypercapic (causes/s&s) Dx tests Rx RT/artifical airways/mechanical vent/drugs/medical/nutrition Nursing (assessment/Nursing Dx- Plan)

Normal Respirations: Tidal Vol; Inspiratory & Expiratory reserve Vol; Residual Vol; Vital Capacity; Anatomical dead space; Blood

Resp Failure:one or both exchanging systems is inadequate (air to lung or lung to blood)

Blood Supply to Lung

Respiratory Failure Not a disease process, sign of severe dysfunction Predisposing Factors (Lewis 1746 Table 68-2) Airways/alveoli CNS Chest wall Neuromuscular Commonly defined in terms of ABG’s: PO2 of less than 60 mmHg PCO2 greater than 45 mmHg Arterial pH of less than 7.35

Classification of Respiratory Failure

Hypoxemic Respiratory Failure Oxygenation failure- inadequate O2 transfer between alveoli & pulmonary capillary bed PaO2: 60 mm Hg or less on 60 % O2 Inadequate O2 saturation of hemoglobin Causes tissue hypoxia> Metabolic acidosis; cell death; decreased CO; impaired renal function Common causes: disorders that interfere with O2 transfer into the blood- respiratory or cardiac system (Lewis p. 1800 Table 68-1)

V/Q: Volume blood perfusing lungs each minute Hypoxemic Respiratory Failure Mechanisms that may lead to Hypoxemia: 1. Mismatch ventilation & perfusion (V/Q mismatch) V/Q: Volume blood perfusing lungs each minute Each ml of air for each ml of blood 1:1= V/Q ratio of 1 Causes of V/Q mismatch: Ventilation portion blocked (secretions in airway/alveoli, airway/alveolar collapse, decreased movement chest/ventilation) Perfusion portion blocked (pulmonary embolus)

Hypoxemic Respiratory Failure Range of ventilation to perfusion (V/Q relationship) A. Absolute shunt, no ventilation fluid in alveoli B. Ventilation partially compromised- secretions C. Normal lung unit D. Perfusion partially compromised by emboli obstructing blood flow E. Dead space: no perfusion- obstruction of pulmonary capillary

Occurs when blood leaves heart without gas exchange Hypoxemic Respiratory Failure Mechanisms that may lead to Hypoxemia: 2. Shunt- Extreme V/Q mismatch Occurs when blood leaves heart without gas exchange Types: 1. anatomic shunt: O2 blood does not pass through lungs 2. intrapulmonary shunt- alveoli fill with fluid Treatment: Mechanical ventilation to force O2 into lungs; treat cause

Hypoxemic Respiratory Failure Mechanisms may lead to Hypoxemia: 3 Hypoxemic Respiratory Failure Mechanisms may lead to Hypoxemia: 3. Diffusion limitations Alveoli membrane thickened or destroyed Gas exchange across alveolar-capillary membrane can’t occur Classic sign: hypoxemia present during exercise, not at rest Treat the cause such as pulmonary fibrosis; ARDS

Hypoxemic Respiratory Failure Mechanisms may lead to Hypoxemia: Clinical manifestations of hypoxemia Specific: Respiratory: Nonspecific: Cerebral, cardiac, other Treatment: treat cause, O2 and mechanical ventilation

Hypercapic Respiratory Failure Ventatory failure: Inability of the respiratory system to ventilate out sufficient CO2 to maintain normal PaCO2 PaCO2 greater than 45 mm Hg, Arterial pH less than 7.35 PCO2 rises rapidly and respiratory acidosis develops, PO2 drops more slowly Common causes include disorders that compromise lung ventilation and CO2 removal- Lewis Table 68-1 (airways/alveoli, CNS, chest wall, neuromuscular) Clinical manifestations: specific respiratory, nonspecific of cerebral, cardiac, neuromuscular Treatment: adeq O2, airway, meds, treat underlying cause, nutrition

Collaborative Care for Respiratory Failure: Diagnostic tests History/physical assessment Pulse oximetry ABG analysis Chest X-ray CBC, sputum/blood cultures, electrolytes EKG Urinalysis V/Q scan- if pulmonary embolism suspected Hemodynamic monitor/pulmonary function tests

Collaborative care for Respiratory Failure Respiratory Therapy Main treatment- correct underlying cause & restore adequate gas exchange in lung Oxygen Therapy (Maintain PaO2 at least 60 mm Hg, SaO2 90%) Mobilization of secretions Effective coughing & positioning Hydration & humidification Chest physical therapy Airway suctioning Positive pressure ventilation Noninvasive positive pressure ventilation Intubation with mechanical ventilation

Collaborative Care for Respiratory Failure cont Drug Therapy Relief bronchospasm; reduce airway inflam and pulmonary congestion; treat pulmonary infections; reduce anxiety, pain Medical supportive therapy Treat underlying cause Nutritional therapy Enteral; parenteral Protein and energy stores

Collaborative Care: Artifical airways- tracheostomy and endotracheal tubes

Endotracheal tube

Taping and inline suctioning of an endotracheal tube

Exhaled C02 (ETC02) normal 35-45 Used when trying to wean patient from a ventilator

Complications of endotracheal intubation 1. Extubation Restraints 2. Aspiration Tube at right allows for subglottal suctioning

Independent Lung Ventilation

Collaborative Care: Mechanical Ventilation Provide adeq gas exchange Criteria to put on vent RR > 35-45 pCO2 >45 pO2 <50 Types- Positive, Neg Settings- Table 66-10 Modes- Table 66-12

Types: Negative pressure ventilator

Types: Positive pressure mechanical ventilation with endotracheal tube (PPV) on left and noninvasive mask on right (CPAP)

Ventilator settings of Modes of PPV (Table 66-12 p.1706) Volume Modes AC; SIMV Predetermined tidal volume (TV) is delivered with each inspiration Tidal volume (TV) is consistent, airway pressures will vary Pressure Modes PSV; PC-IRV Predetermined peak inspiratory pressure Tidal volume (TV) will vary, airway pressures will be consistent Other Modes PEEP and CPAP

Ventilator settings: PEEP SIMV

Alarm settings Assess your patient – not the alarm!!!!! Never turn alarms off Alarms sound when you have low pressure or high pressure in the ventilator Note “alarm silence” and “alarm reset” on picture to the right Lewis 1705 Table 66-11

Low Pressure High Pressure Circuit leaks Airway leaks Chest tube leaks Patient disconnect from vent or tube High Pressure Patient coughing  Secretions or mucus in the airway  Patient biting tube  Airway problems  Reduced lung compliance (as a pneumothorax)  Patient fighting the ventilator  Accumulation of water in the tube Kinking of tube 

Complications/Nursing Care of Positive Pressure Mechanical ventilation Cardiovascular: decreased CO; inc intrathoracic pressure Pulmonary: Barotrauma; Volutrauma; alveolar hypoventilation/hyperventilation; ventilator-associated pneumonia Sodium and water imbalance Neurological: impaired cerebral bl flow>IICP Gastrointestional: stress ulcer/GI bleed; gas; constipation Musculoskeletal: dec muscle tone; contractures; footdrop; pressure ulcers from BR Psychosocial: physical & emotional stress; fight vent

Other problems when on mechanical ventilation Machine disconnection or malfunction Nutrition needs Weaning from ventilator/ extubation Spontanenous breathing trial (SBT) Hospital protocol Document progress Table 66-13 p.1712- readiness/assessment

Nursing assessment specific to Respiratory Failure Assess both airway and lungs- note picture to right Refer to hypoxic and hypercapnic respiratory failure symptoms Table 68-4 p. 1751 Subjective data Objective data

Relevant Nursing Problems related to Respiratory Failure Prevention of acute respiratory failure Nursing Care Plans Gerontology considerations Nursing Care Plans Mechanical ventilation Suctioning procedure and oral care (p.1701-8)

ADRS- outline Normal patho/Definition Causes/predisposing factors Phases/patho Injury/exudate Reparative/poliferation Fibrotic Clinical progression/s&s/chest X-ray Complications Rx RT-vent & proning-CLRT Medical support- monitor CO/tissue perfusion & nutrition/fluids Nursing (assessment/Nursing Dx-Plan)

Acute Respiratory Distress Syndrome ARDS Sudden progressive form of acute respiratory failure Follows various pulmonary or systemic conditions Alveolar capillary membrane becomes damaged & more permeable to intravascular fluid Results in noncardiac pulmonary edema and progressive refractory hypoxemia ARDS is NOT primary! Most common cause- Sepsis

Pathophysiology of ARDS

Surfactant keeping alveoli open Fibrotic lung

Clinical progression of ARDS Insidious onset- sym dev 24-48 hrs post initial insult (direct or indirect lung injury) Course determined by nature of initial injury, extent & severity of coexisting disease, and pulmonary complications 50% who develop ARDS die- even with aggressive treatment

Clinical manifestations of ARDS Progressive refractory hypoxemia> Hallmark sign Noncardiac pulmonary edema Early symptoms- labored R- dyspnea, tachypnea, anxiety/restless, dry-nonproductive cough Later symptoms- cyanosis, adventitious breath sounds, use of accessory muscles with retractions and decreased mental status

Diagnosis of ARDS ABG’s> refractory hypoxemia Chest X-ray infiltrates> white out/snow storm. Note progression picture to right Pulmonary artery wedge 18 mm Hg & no evidence of heart failure Identification of a predisposing condition for ARDS within 48 hrs of clinical manifestations

Complications of ARDS Hospital-acquired pneumonia Barotrauma Volu-pressure trauma Physiologic stress ulcer Renal failure

Collaborative Care for ARDS Respiratory therapy & medical support Oxygen Mechanical ventilation- main treatment Positioning strategies Proning CLRT-lateral rotation bed Maintenance of CO & tissue perfusion (fluids) Maintenance of nutrition & fluid balance Treat underlying cause

Rotoprone bed

Benefits to Proning >

Nursing assessment specific to ARDS & Relevant nursing problems R/T ARDS Refer to respiratory failure assessment Assess for clinical progression and clinical manifestations as stated above Nursing care plans- refer to resp failure Goals for recovery from ARDS PaO2 within normal limits on room air SaO2 greater 90% Patent airway Lungs clear on auscultation