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Resp Failure
Resp Failure + ARDS+ Immune System
| Question | Answer |
|---|---|
| What does Tumor necrosis factor affect to inflammation response? | vasodilation, endothelial cell dysfunction, chemotaxis |
| What does Tissue factor affect to inflammation response in immune system? | clotting activation, platelet activation |
| What does Il-1, Il-6 affect to inflammation response in immune system? | vasodilation platelet activation |
| Leukotrienes affect to inflammation response in immune system? | bronchoconstriction,vasodilation, capillary leak |
| What does Prostaglandins affect to inflammation response in immune system? | smooth muscle constriction; pain |
| Vasodilation cause what to inflammation response in immune system | Redness |
| Increased blood flow cause what to inflammation response in immune system | Redness, heat |
| Vessel permeability cause what to inflammation response in immune system | Edema |
| what are 3 "I" | Ischemia Inflammation Immune alteration |
| Primary role of respiratory system: | Oxygen Delivery CO2 removal |
| System interdependence with respiratory system | CNS Pulmonary system Heart Vascular system |
| what is Acute Respiratory Failure and PaO2? PaCO2 | Inability of the body to meet tissue O2 need &/or CO2 removal PaO2 < 50mm Hg or PaCO2 > 50mm Hg on room air |
| Arterial hypoxemia definition | Can not get O2 into bloodstream Alveolar/capillary membrane issue |
| Ventilatory or hypercapnic (high CO2)definition | Can not get CO2 out of bloodstream Pulmonary structure or CNS issue |
| Examples of Arterial hypoxemia | Pulmonary edema, ARDS, Drowning, Pulmonary Emobolism, lung tumors, bleeding |
| Arterial Hypoxemia | Lower than normal amount of oxygen dissolved in plasma |
| Hypoxemia Moderate what level of PaO2 | 50-60mm Hg |
| what is Alveolar hypoventilation ? when it happen? | Alveoli is receiving little or no oxygen, but has normal perfusion “Shunt Unit” Unoxygenated blood continues goes back to left side of the heart Alveolus = collapsed, blocked or filled with fluid. Low V/Q (ventilation/perfusion ratio) |
| What are some clinical examples for Alveolar hypoventilation | Atelectatis, pneumonia, pulmonary edema |
| How much should your patient pull on the IS? What is a normal tidal volume? | quietly talking about 500-700, big breaths sh/be 1000-1200. |
| What medical interventions help move mucous plugs? | Breathing treatment to encourgage coughing, bronchoscopy: |
| what is Alveolar Dead Space | Alveoli are fully ventilated, but blood is blocked in capillary. Alveolus unable to participate in gas exchange. Severe “wasted” ventilation = dead space. |
| What is a clinical example of alveoli ventilated, but not perfused | PE |
| Hypoxemia: Signs and Symptoms? | Increased RR Increased HR Dyspnea Agitation Increased WOB |
| what cause: Unable to support gas exchange = Hypoventilation | Multiple causes CNS Depression (drugs) Neurological injury COPD or Status Asthmaticus |
| Hypercapnia: Signs and Symptoms? | Lethargy Decreased LOC Decreased RR Low Tidal Volume (shallow breaths) |
| Continuum of Respiratory Deterioration? | normal-> Resp distress-> Resp failure-> Resp arrest |
| what are you looking for when assess for Respiratory Deterioration | Work of breathing HR RR Use of accessory muscles Tripod position Nasal flaring Unable to speak in full sentences |
| what is process when Hypoxemia and Hypercapnia most commonly occur together in Respiratory Distress Failure | PaO2 decreases first Causes drive for more O2 RR increases Initially drops PaCO2 levels Patient tires CO2 levels increase RESULT: Low PaO2 & high PaCO2 |
| what is the result of Acute Resp. Failure ? | Tissue Hypoxia |
| what are Demand Problems cause tissue hypoxia? | Oxygen requirements Fever Infection ADLs Agitation on mechanical ventilation |
| how Tissue Hypoxia effect on Cardiovascular? | Tachycardia, Hypertension, Dysrhythmias, Polycythemia |
| how Tissue Hypoxia effect onRespiratory? | Tachypnea, Hypoxemia (blood gas reading), Cyanosis |
| how Tissue Hypoxia effect on Renal? | Low urinary output |
| how Tissue Hypoxia effect on Neurological? | Anxiety & agitation , Confusion, Headache, Weakness & drowsiness, Double vision, Impaired judgment, Coma |
| How to treat for High CO2 ? | Increase rate and depth of breathing (Get patients out and moving |
| what are S/S of Pulmonary Embolism? | Dyspnea • Tachypnea • Apprehension • Diaphoresis • Syncope • Chest pain • Hemoptysis • Cough |
| PE Diagnosis? | Physical exam with history: Does patient have risk factors?; ABG analysis; Low O2; Initial low PaCO2increasing PaCO2; Doppler ultrasound: Presence of DVT; Spiral CT ; V/Q scan (older test, not as valid); Pulmonary angiogram |
| what do you do if PE Suspected? | Thorough respiratory assessment; Report onset of symptoms immediately; Administer increasing O2 immediately Goal O2 stat > 94% |
| how to treat PE? | Pain control: Narcotics & NSAIDS; Heparin therapy (continuous IV infusion); Adjust dose according to PTT results; Goal: 2-2.5 x normal; Thrombolytic therapy to break clot up; Surgically placed filters; Surgical embolectomy; |
| what is Acute Respiratory Distress Syndrome (ARDS) | Sudden progressive respiratory failure.; Severe dyspnea; Hypoxemia despite increasing FiO2; Diffuse infiltrates |
| what are some of direct cause for ARDS? | Pneumonias ; Shock; Aspiration ; Chest trauma |
| what is ARDS Etiology | injury to lungs that causes ischemia or inflammation that traumatizes the alveolar capillary membrane |
| what are some of in direct cause for ARDS? | Pancreatitis ; Sepsis ; Trauma |
| ARDS Pathophysiology? | Massive inflammatory response by the lungs Changes permeability of pulmonary capillary membrane; Alveoli fill with fluid Loss of surfactant ; Loss of pulmonary compliance Impaired oxygenation |
| what are 3 phase of ARDS Pathophysiology | Phase 1: Exudative phase; Phase 2: Proliferative ; Phase 3: Fibrotic |
| Phase 1: Exudative phase | Starts ~24 hours post initial insult; Damage to capillary membrane and fluid leaking ; Microemboli; Inflammatory mediators released |
| Phase 2: Proliferative | Day 7-10 surfactant changes ; Type II Alveoli surfactant cells that secrete surfactant are damaged; Remember back to Phyiology: What is surfactant? Lipoprotien substance that decreased the surface tension of the alveloi, increase lung compliance and |
| Phase 3: Fibrotic | 2-3 weeks fibrin develops in lung ; the inflammatory changes cause the development of fibin deposits in the lung….fibrin does not allow gas exchange. Long term damage that can not be reversed. |
| Early Signs of ARDS ? | Restlessness, change in LOC ; increase HR ; increae RR with normal lung sounds ; Dyspnea ; Resp Alkalosis, increase PaCO2 |
| Late Signs of ARDS ? | decrease PaO2 (despite incsrease levels of O2 ); Chest X-ray: Bilateral infiltrates “White Out” ; Severe dyspnea and WOB ; PIP, functional residual capacity Cyanosis, pallor (grunting, retractions); Lungs with crackles, rhonchi; Hypercapnia a |
| What are we doing to maximize oxygenation? | FiO2 ; PEEP; PS |
| How do we maximize ventilation? | Rate ; Volume |
| ARDS: What do we do? | Identify those patients at risk. ; Treat cause. ; Prevent further alveolar capillary membrane damage… ; Change the mode to pressure control to keep PIP under 25cm/H2O; Support tissue oxygenation |
| What are the value to set the vent for Oxygenation and ventilation support? Tidal volume? PS? PEEP? FiO2? | Small tidal volumes (6mL/kg); Keep inspiratory pressure < 25 by changing to pressure control ventilation ; Goal: FiO2 < 70% with PaO2 60-70% ; Position HOB 30 degrees ; Exquisite oral care (q 2-4 hrs) ; |
| How to prevent complications of ARDS? | Handwashing ; Prevent stress ulcers ; Prevent DVT ; Prevent VAP ; Prevent skin breakdown ; ROM ; Monitor for symptoms of infection: Trend WBCs, Chest Xray ; Provide psychosocial support to patient and family |
| what are criteria to Wean Mechanical Ventilation? | Mode to Spontaneous: Volumes > 500 ; FiO2 to 40% ; PEEP 5 ; PS 10 ; Minimal secretions ; Clear chest X-ray ; CPAP trials |
| What will be the nursing responsibilities post extubation? | remain with patient assess o2 sat, work of breathing, stridor. |
| what is the bigest concern of Fractured Ribs ? | Atelectasis |
| what is Pulmonary Contusion? | Damaged lung parenchyma with impaired gas exchange ; Interstitial hemorrhage, alveolar collapse, and alveolar flooding ; Continued perfusion of unventilated lung portions shunting and hypoxia |
| treatment for flail chest? | Position good lung down Provide adequate ; oxygenation and ventilation… May require intubation. ; Closed chest drainage ; Frequent respiratory assessments ; Pain control |
Created by:
tp667
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