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RESPIRATORY FAILURE and ARDS By Laurie Dickson

RESPIRATORY FAILURE and ARDS

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RESPIRATORY FAILURE and ARDS. By Laurie Dickson. Respiration. Exchange of O2 and CO2 gas exchange. Respiratory Failure the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs. Hypoxemic Respiratory Failure- (Affects the pO2). - PowerPoint PPT Presentation

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RESPIRATORY FAILURE

RESPIRATORY FAILUREand ARDSBy Laurie Dickson

#RespirationExchange of O2 and CO2gas exchange

Respiratory Failurethe inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

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#Hypoxemic Respiratory Failure-(Affects the pO2)Causes- 4 Physiologic Mechanisms

1. V/Q Mismatch2. Shunt3. Diffusion Limitation4. Alveolar Hypoventilation- CO2 andPO2#VentilationPerfusion Mismatch (V/Q)Normal V/Q =1 (1ml air/ 1ml of blood)Ventilation=lungsPerfusion or Q=perfusion

#Pulmonary EmbolusPulmonary Embolus- (VQ scan)

#ShuntAnatomic Intrapulmonary blood passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect

blood flows through pulmonary capillaries without participating in gas exchange ex: alveoli filled with fluid* Patients with shunts are more hypoxemic than those with VQ mismatch and they may require mechanical ventilators

#Diffusion LimitationGas exchange is compromised by a process that thickens or destroys the membrane

Pulmonary fibrosis2. ARDS

* A classic sign of diffusion limitation is hypoxemia during exercise but not at rest

#Alveolar HypoventilationMainly due to hypercapnic respiratory failure but can cause hypoxemiaIncreased pCO2 with decreased PO2Restrictive lung diseaseCNS diseasesChest wall dysfunctionNeuromuscular diseases#Hypercapnic Respiratory FailureFailure of VentilationPaCO2>45 mmHg in combination with acidemia (arterial pH< 7.35)

Caused by conditions that keep the air in

#Hypercapnic Respiratory FailureAbnormalities of the:Airways and Alveoli-air flow obstruction and air trappingAsthma, COPD, and cystic fibrosisCNS-suppresses drive to breathedrug OD, narcotics, head injury, spinal cord injuryChest wall-Restrict chest movementFlail chest, morbid obesity, kyphoscoliosis

Neuromuscular Conditions- respiratory muscles are weakened:Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis

#Tissue Oxygen needsTissue O2 delivery is determined by:Amount of O2 in hemoglobinCardiac output

*Respiratory failure places patient at more risk if cardiac problems or anemia

#Signs and Symptoms of Respiratory Failurehypoxemia pO245-50only one cause- hypoventilation

*In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02

#Specific Clinical ManifestationsRespirations- depth and ratePatient position- tripod positionPursed lip breathingOrthopneaInspiratory to expiratory ratio (normal 1:2)Retractions and use of accessory musclesBreath sounds#HypoxemiaTachycardia and Hypertension to comp.Dyspnea and tachypnea to comp.CyanosisRestlessness and apprehensionConfusion and impaired judgmentLater dysrhythmias and metabolic acidosis, decreased B/P and CO.#HypercapniaDyspnea to respiratory depression- if too high CO2 narcosisHeadache-vasodilationPapilledemaTachycardia and inc. B/PDrowsiness and comaRespiratory acidosis**Administering O2 may eliminate drive to breathe especially with COPD patients

#DiagnosisPhysical AssessmentPulse oximetryABGCXRCBCElectrolytesEKGSputum and blood cultures, UAV/Q scan if ?pulmonary embolusPulmonary function tests#TreatmentGoal- to correct Hypoxia

O2 therapyMobilization of secretionsPositive pressure ventilation(PPV) Noninvasively( NIPPV) through maskInvasively through oro or nasotracheal intubation

#O2 TherapyIf secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by maskIf secondary to intrapulmonary shunt- positive pressure ventilation-PPVMay be via ET tubeTight fitting mask

Goal is PaO2 of 55-60 with SaO2 at 90% or more at lowest O2 concentration possible

O2 at high concentrations for longer than 48 hours causes O2 toxicity

#Mobilization of secretionsEffective coughing quad cough, huff cough, staged coughPositioning- HOB 45 degrees or recliner chair or bedGood lung downHydration fluid intake 2-3 L/day Humidification- aerosol treatments- mucolytic agentsChest PT- postural drainage, percussion and vibrationAirway suctioning#Positive Pressure VentilationNoninvasive ( NIPPV) through maskUsed for acute and chronic resp failureBiPAP- different levels of pressure for inspiration and expiration- (IPAP) higher for inspiration,(EPAP) lower for expiration CPAP- for sleep apnea

Used best in chronic resp failure in patients with chest wall and neuromuscular disease, also with HF and COPD.

NPPV#Endotracheal Tube

Fig. 66-17Endotracheal intubation#TracheostomySurgical procedure

Used when need for artificial airway is expected to be long term

Research shows benefit to early trach

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Exhaled C02 (ETC02) normal 35-45Used when trying to wean patient from a ventilator#Drug TherapyRelief of bronchospasm- Bronchodilators metaproterenol (Alupent) and albuterol-(Ventolin, Proventil, Proventil-HFA, AccuNeb, Vospire, ProAir )Watch for what side effect?

Reduction of airway inflammationcorticosteroids by inhalation or IV or po

Reduction of pulmonary congestion-diuretics and nitroglycerine with heart failure#Drug TherapyTreatment of pulmonary infections- IV antibiotics- vancomycin and ceftriaxone (Rocephin)

Reduction of anxiety, pain and agitationpropofol (Diprivan), lorazepam (Ativan), midazolam (Versed), opioids

May need sedation or neuromuscular blocking agent if on ventilatorvecuronium (Norcuron), cisatracurium besylate (Nimbex )assess with peripheral nerve stim.

#Medical Supportive TreatmentTreat underlying causeMaintain adequate cardiac output- monitor B/P and MAP. **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organsMaintain adequate Hemoglobin concentration- need 9g/dl or greater

Nutrition-During acute phase- enteral or parenteral nurtitionIn a hypermetabolic state- need more caloriesIf retain CO2- avoid high carb diet

#Acute Respiratory FailureGerontologic ConsiderationsPhysiologic aging results in Ventilatory capacityAlveolar dilationLarger air spacesLoss of surface area Diminished elastic recoilDecreased respiratory muscle strength Chest wall compliance

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ARDSAlso known as DAD(diffuse alveolar disease)or ALI (acute lung injury)a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias#Memory JoggerAssault to the pulmonary systemRespiratory distressDecreased lung complianceSevere respiratory failure

#150,000 adults develop ARDS

About 50% survive

Patients with gram negative septic shock and ARDS have mortality rate of 70-90%

#Direct CausesInflammatory process is involved

Pneumonia* Aspiration of gastric contents* Pulmonary contusion Near drowning Inhalation injury

#Indirect CausesInflammatory process is involved

Sepsis* (most common) gm -Severe trauma with shock state that requires multiple blood transfusions* Drug overdose Acute pancreatitis

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#*Causes (see notes)DIFFUSE lung injury(SIRS or MODS)Damage to alveolar capillary membranePulmonary capillary leakInterstitial & alveolar edemaInactivation of surfactantAlveolar atalectasisCOMetabolic acidosis

COSevere & refractory hypoxemiaHypoventilationHypercapneaRespiratory AcidosisHyperventilationHypocapneaRespiratory AlkalosisSHUNTINGStiff lungs

#Pathophysiology of ARDSDamage to alveolar-capillary membraneIncreased capillary hydrostatic pressureDecreased colloidal osmotic pressureInterstitial edemaAlveolar edema or pulmonary edemaLoss of surfactant

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#Pathophysiologic Stages in ARDS Injury or Exudative- 1-7 daysInterstitial and alveolar edema and atelectasisRefractory hypoxemia and stiff lungsReparative or Proliferative-1-2 weeks afterDense fibrous tissue, increased PVR and pulmonary hypertension occursFibrotic-2-3 week afterDiffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension

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The essential disturbances of ARDSInterstitial and alveolar edema and atelectasis

Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS

#Clinical Manifestations: EarlyDyspnea-(almost always present), tachypnea, cough, restlessnessLung sounds-may be normal or reveal fine, scattered crackles ABGs -Mild hypoxemia and respiratory alkalosis caused by hyperventilationChest x-ray -may be normal or show minimal scattered interstitial infiltratesEdema -may not show until 30% increase in lung fluid content

#Clinical Manifestations: LateSymptoms worsen with progression of fluid accumulation and decreased lung compliancePFTs show decreased compliance and lung volumeEvident discomfort and increased WOBSuprasternal retractions Tachycardia, Diaphoresis Changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO2/FIO2 ratio 90%Patent airwayClear lungs or auscultation#ARDS DiagnosisProgressive hypoxemia due to shuntingDecreased lung compliance Bilateral diffuse lung infiltrate

#Nursing AssessmentLung soundsABGsCXRCapillary refillNeuro assessmentVital signsO2 satsHemodynamic monitoring valuesThe Auscultation Assistant - Breath Sounds

#Diagnostic TestsABGCXRPulmonary Function TestsHemodynamic Monitoring

ABG reviewRealNurseEd (Education for Real Nurses by a Real Nurse)

#ARDSSevere ARDS

#Goal of Treatment for ARDSMaintain adequate ventilation and respirations.Prevent injuryManage anxiety

#TreatmentMechanical Ventilation- goal PO2>60 and O2 sat 90% with FIO2 < 50PEEP-can cause CO + B/P and barotraumaPositioning- prone, continuous lateral rotation therapy and kinetic therapyHemodynamic Monitoring- fluid replacement or diureticsCrystalloids vs ColloidsEnteral or Parenteral Feeding- high calorie, high fat.

#PEEPCannot expire completely. Causes alveoli to remain inflated Peep Complications can include decreased cardiac output, pneumothorax, and increased intracranial pressure

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#Proningtypically reserved for refractory hypoxemia not responding to other therapiesPlan for immediate repositioning for cardiopulmonary resuscitation ***

#ProningMediastinal and heart contents place more pressure on lungs when in supine position than when in proneFluid pools in dependent regions of lungPredisposes to atelectasis

With prone positionnondependent air-filled alveoli become dependent perfusion becomes greater to air-filled alveolithereby improving ventilation-perfusion matching. May be sufficient to reduce inspired O2 or PEEP

#Benefits to Proning

Before proning ABG on 100%O2 7.28/70/70After proning ABG on 100% 7.37/56/227#Other positioning strategies

Kinetic therapy

Continuous lateral rotation therapy

#Oxygen TherapyHigh flow systems used to maximize O2 deliverySaO2 continuously monitoredGive lowest concentration that results in PaO2 60 mm Hg or greater

Risk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hours

Patients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels

#Mechanical ventilationPEEP at 5 cm H2O compensates for loss of glottic function

Opens collapsed alveoli

Higher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater

High levels of PEEP can compromise venous return Preload, CO, and BP

#Medical Supportive TherapyMaintenance of cardiac output and tissue perfusionContinuous hemodynamic monitoringContinuous BP measurement via arterial cathPulmonary artery catheter to monitor pulmonary artery pressure, pulmonary artery wedge pressures, and COAdministration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls #Medical Supportive TherapyUse of inotropic drugs may be necessaryHemoglobin usually kept at levels greater than 9 or 10 with SaO2 90%Packed RBCsMaintenance of fluid balanceMay be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEPMonitor PAWP, daily weights, and I and Os to assess fluid status

#Medical Supportive TherapyPulmonary Artery Wedge PressurePressure in pulmonary arteryIndirect estimate of L Arterial pressureKeep as low as possible without imparing cardiac output (normal 6-12)Prevent pulmonary edema

PAWP increases with Heart FailurePAWP does not increase with ARDS

#Other TreatmentsInhaled Nitric OxideSurfactant therapyNSAIDS and Corticosteroids

#ARDS Prioritization and Critical Thinking Questions #28When assessing a 22 Y/o client admitted 3 days ago with pulmonary contusions after an MVA, the nurse finds shallow respirations at a rate of 38. The client states he feels dizzy and scared. O2 sat is 80% on 6 Ln/c. which action is most appropriate?A.Inc. flow rate of O2 to 10 L/min and reassess in 10 min.B.Assist client to use IS and splint chest using a pillow as he coughs.C.Adminster ordered MSO4 to client to dec. anxiety and reduce hyperventilation.D.Place client on non-rebreather mask at 100% O2 and call the Dr.##15. After change of shift report, you are assigned to care of the following clients.Which should be assessed first?68 y/o on ventilator who needs a sterile sputum specimen sent to the lab.59y/o with COPD and has a pulse ox on previous shift of 90%.72y/o with pneumonia who needs to be started on IV antibiotics.51y/o with asthma c/o shortness of breath after using his bronchodilator inhaler.

#Ventilatora machine that moves air in and out of the lungs#Mechanical VentilationIndicationsApnea or impending inability to breatheAcute respiratory failurepH50Severe hypoxiapO2