NUR 265 Exam 2 Study Guide & Exams Q&A

NUR 265 Exam 2 Study Guide & Exams Questions and Answers Lungs Physiology  2 Pleural, 1 attached to outside of lungs and 1 attached to inside of ribs. ● Space between the 2 pleural is negative to atmosphere ● When inhale becomes more positive and atmosphere more negative. Exhaling is passive ● Most of lower lobes are posterior, must listen to lungs posteriorly ● Breath sounds o Bronchial: High pitched & loud, normal in tracheal & larynx o Broncho-vesicular: Moderate pitched & amplitude, normal over major bronchi o Vesicular: Low pitched & soft, like wind through trees, normal in lower lung fields where smaller bronchioles & alveoli are. Pulmonary Emboli (P 603) ● Occlusion of portion of pulmonary artery by a blood clot – from venous circulation – lower extremities or heart. ● Causes ventilation-perfusion mismatch (V/Q) – Ventilated alveoli no longer perfused due to clotted artery. ● Risk Factors o Venous stasis (w/prolonged immobility); Central venous catheters; Surgery (NPO, dehydrated, immobilized pts); Obesity; Advanced age; Hypercoagulability (Platelets >400K and not enough fluids; sticky blood); Hx of thromboembolism. o Greatest r/f in the young is the combo of smoking and hormone based contraceptives. ● Nursing Assessment Findings o Respiratory Classic Manifestations (Hypoxia drives all s/s) ▪ Dyspnea (sudden onset); Chest pain (sharp & stabbing); Apprehension, restlessness; Feeling of impending doom; Cough; Hemoptysis (blood in sputum). o Respiratory Signs ▪ Pleural friction rub (scratching sounds from pleura rubbing together & pain on deep inspiration); Tachypnea; Crackles (or normal); S3 or S4; Diaphoresis; Low grade fever; Petechiae over chest and axillae; Decreased arterial oxygen saturation (SaO2) o Many pts w/ a PE do not have “classic” sx (i.e. hypoxia), but instead have vague sx resembling the flu (n/v & general malaise) o Cardiac Manifestations ▪ Decreased tissue perfusion: tachycardia, JVD, Syncope (loss of consciousness), Cyanosis, & Hypotension. o In patients with r/f for PE, JVD (RSHF), syncope (decreased blood flow to brain), cyanosis (severe hypoxia) and hypotension together, need rapid response team called. have help on way b4 o2 applied o When pt has sudden onset of dyspnea, chest pain, and/or hypotension, immediately notify Rapid Response Team. Reassure pt. and elevate HOB. Prepare for O2 therapy and ABG analysis o Saddle Emboli – Embolism at split of pulmonary artery that blocks both branches to the lungs ● Medical Dx o Chest X-ray – May show PE if large but will help r/o other things o CT scan – Most often used to dx PE o TEE (Transesophageal Echocardiography) – See if there are clots in the atria o Ventilation Perfusion scan (V/Q) ▪ Considered if pt is allergic to contrast dye done w/CT scan ▪ Radioactive substance to see if air is getting into the alveoli; injected into blood to look at clot and can also detect pneumothorax. Done 2x o ABGs ▪ Respiratory Alkalosis FIRST from hyperventilation ▪ THEN Respiratory Acidosis from shunting ● Shunting of blood from the right side of the heart to the left side w/o picking up O2 from lungs – causes PaCO2 level to rise resulting in respiratory acidosis. ▪ LATER Metabolic Acidosis & lactic acid buildup from tissue hypoxia ▪ Even if ABGs & Pulse Ox shows hypoxemia it is not enough to dx PE alone as PE is not the only cause of hypoxemia. ● Medical Management o GIVE O2, IV FLUIDS, INOTROPES (DOBUTAMINE/MILRINONE) ▪ Oxygen therapy to maintain O2 sat at 95% or patient baseline ▪ Hypotension - Tx w/ IV fluids (isotonic) & Inotropes (Dobutamine/Milrinone, make heart contract more forcefully); vasopressors (norepi, epi, dopamine) when hypotension persists after fluids. o Anticoagulation w/ Heparin drip – Goal is PTT 1.5-2.5 x normal (60-70 sec) = 90-175 sec ▪ Minimize growth of existing clots and prevent new ones ▪ Antidote Protamine Sulfate ▪ Do not use w/salicylates (Aspirin) o Convert to Warfarin when stable – On 3rd day of Heparin use, overlap – INR target 2-3 (0.9-1.2 normal) ▪ Antidote – Vit K – phytonadione (Mephyton) ▪ Teach pts to avoid foods high in K (leafy dark green vegis, herbs, spring onions, Brussel sprouts, broccoli, cabbage, asparagus, potatoes, & winter squash). o Enoxaparin or dalteparin o Fibrinolytic (tPA) to tx massive PE or hemodynamic instability ▪ Antidotes – clotting factors, FFP, & aminocaproic acid (Amicar) ▪ Dissolve the clot itself o Embolectomy – surgical removal of the embolus – When tPA can’t be used or for massive PE w/shock o Inferior Vena Cava Filter – to prevent DVTs from moving to the lungs **Bleeding precautions with all blood thinners o Prevent injury to pt on anticoagulation therapy ▪ Use lift sheet; firm pressure on needle stick for 10 minutes; Apply ice to trauma areas; Avoid trauma to rectal tissues; no razor (electric only); soft-bristled toothbrush; NO floss; Not blow nose forcefully; shoes with firm soles; Assess IV sites q4 hrs for bleeding, measure abd girth q8 hrs – internal bleeding ● Nursing Management o Monitor for hypoxemia & respiratory compromise every 1-2 hrs. ▪ VS, lung sounds, cardiac & respiratory status, & urine output (bc hypotensive can cause AKI) o Elevate HOB to high fowlers if BP tolerates. o Obtain venous access and monitor heparin drip/LMWH/Coumadin o Pain and anxiety management w/morphine (vasodilator) – O2 1st then other things b4 morphine. ▪ Communication is critical in allaying anxiety. Acknowledge the anxiety & pt perception of a life- threatening situation. Stay with them, speak calmly, and clearly, providing assurances. o Bleeding precautions, oral care – especially if mouth breather. ● Prevention Measures o Measures that prevent venous stasis and VTE o Passive and active ROM for postop & immobilized pts o Post-op ambulation ASAP o SCDs or Plexipulse compression – for prevention, not for active DVT o Pt repositioning q2 hrs o Low dose anticoagulant & antiplatelet meds o Smoking cessation (especially females on hormone based contraceptives) bc increases risk for DVTs o Traveling – drink plenty of H2O, change positions, avoid crossing legs, get up and move every 1hr for 5 min. ● NANDA Diagnoses o Impaired Gas Exchange; Acute Pain, Anxiety; Risk for Bleeding (when on treatment) Pleural Effusion (P 504-505) ● Collection of fluid (too much) in the pleural space – clear transudative, or exudative (outside the lungs) o Cleat transudative – similar to fluid normally present in pleura space o Exudative – Excess protein, blood, or evidence of inflammation or infection (white, green, cloudy is bad) ● Can cause pleurisy sx o Pleural friction rub, scratching sounds caused by inflamed pleura rubbing together, pain on deep inspiration. ● Caused by – HF (mediastinal fluid leaks into pleural space); Liver or renal failure; Infections; chest trauma (inflammation response; smack lungs on ribs in MVA); Lymphatic destruction by lung tumor; PNA ● Assessment Findings o Dyspnea (lungs can’t expand) o Decreased or absent lung sounds (sounds do not transmit through fluids well) ▪ NO CRACKLES BC OCCURS OUTSIDE THE LUNGS o Dull flat sound on percussion (percuss between ribs) o Decreased tactile fremitus (vibration of chest wall produced when pt speaks) – hands around pt ribs o Chest pain w/respirations if pleurisy develops ● Medical Management o Thoracentesis – Needle aspiration of pleural space to remove fluid for sx relief & dx of causative factor. ▪ Want fluid to be clear, if cloudy or another color, send culture for cell counts. o Recurrent effusions may need chest tube w/closed drainage until source tx o Severe cases caused by lung tumors may need pleural stripping or pleurodesis to cause pleura to adhere together to prevent further effusions. ▪ Causes the 2 pleura to SCAR together to decrease inflammation, pain, decreases dyspnea & pleuritis ▪ Palliative for terminal pts only for pain relief. o Heart monitor needed Acute Respiratory Failure (P 610-612) ● Sudden deterioration of gas exchange function of the lungs ● Ventilatory failure, oxygenation (gas exchange) failure, or combo of both, classified by abnormal ABGs (pa) ● Failure of the pulmonary system to carry out its own major functions o Delivery of adequate amount of O2 to the arterial blood (paO2 <60 hypoxemia) o Removal of corresponding amount of CO2 from blood (paCO2 >45 hypercapnia AND pH <7.35 acidemia) ● NO MATTER THE PROBLEM, PT IS ALWAYS HYPOXEMIC (low arterial blood O2 levels) ● Pathophysiology o Ventilatory Failure ▪ Blood flow (perfusion) is normal but AIR MOVEMENT (VENTILATION) IS INADEQUATE ▪ To little O2 reaches alveoli and CO2 is retained. ▪ Physical problems of lungs or chest wall, brain defect, poor respiratory muscle function – diaphragm ▪ PaCO2 >45 AND pH <7.35 (acidemia) ▪ Pneumothorax – open or tension, ARDS, pulmonary edema (fluid in lungs) o Oxygenation (gas exchange) failure ▪ Air movement and oxygen intake is normal but LUNG BLOOD FLOW (PERFUSION) IS DECREASED ▪ APPLYING 100% O2 DOESN’T CORRECT THE PROBLEM ▪ Massive PE o Combined Ventilatory & Oxygenation Failure ▪ Involves hypoventilation – poor respiratory movements ▪ BOTH ventilation & perfusion are inadequate – leads to more profound hypoxemia than either alone. ▪ Usually underlying chronic disease – COPD, Asthma, Cystic Fibrosis, Lung disease ● Assessment Findings o Dyspnea (hallmark of respiratory failure) – DOE or when lying down (in slow progression) o Orthopnea – breathe easier in upright position, can’t sleep flat o Change in lung sounds – depends on cause: CHF vs PE o Skin/nail bed color changes (hypoxemia) o Hypoxemia S/S – Pallor, Cyanosis, Increased HR, Restlessness, Confusion ▪ O2 therapy is appropriate for any pt w/acute hypoxemia ▪ If O2 therapy doesn’t maintain acceptable PaO2 levels (>60) (normal 80-100) then mechanical ventilation may be needed. o Decreased O2 sats. on pulse ox – need ABG for most accurate assessment ▪ Pulse ox measures O2 bound to Hgb (increased RBCs = increased O2 sats) ▪ ABGs measure O2 floating free in the blood ▪ Pulse ox measurement can be inaccurate if Hgb is decreased or in CO2 poisoning (smoke inhalation) ● Nursing Management o Assist with O2 therapy up to intubation & ventilation o Monitor ABGs & pulse ox o Monitor VS, urine output, & neuro assessments o Ventilator associated pneumonia prevention ▪ Hand washing, oral care Q2 hrs, HOB 30 degrees, turning Q 2, ulcer prophylaxis o Peptic ulcer prophylaxis (IHI Guidelines) ▪ IV/PO pantaprozole to decrease gastric contents to prevent stress ulcers & aspiration o VTE prophylaxis (IHI guidelines) ▪ SCDs & enoxaparin o HOB elevated 30-45 degrees (IHI guidelines) ▪ Minimizes aspiration & breathing better Acute Respiratory Distress Syndrome (ARDS) (P 612-614) ● Acute respiratory failure with o Hypoxemia that persists even when 100% O2 is given (refractory hypoxemia, a cardinal feature) o Decreased pulmonary compliance o Dyspnea o Nonacardiac-associated bilateral pulmonary edema o Dense pulmonary infiltrates on x-ray (ground-glass appearance) ● Etiology o Direct Injury (lungs or capillaries) – Pulmonary contusion, gastric aspiration (acid in lungs), near drowning, inhalation of toxic gases and vapors, infections, air embolus, fat embolus, amniotic fluid embolus & radiation. o Indirect Injury (damage alveoli wall) – Sepsis, shock or prolonged hypotension, nonthoracic trauma, cardiopulmonary bypass, head injury, pancreatitis, multiple blood transfusions (TRAIL), and diabetic coma. o Trigger is a systemic inflammatory response ● Pathophysiology o Severe diffuse lung injury, especially to the parenchyma (Alveoli) o Sudden, progressive pulmonary edema w/increasing bilateral pulmonary infiltrates on chest x-ray, hypoxemia refractory 100% oxygen supplementation (O2 doesn’t help) & reduced pulmonary compliance. o Crackles or nothing (no air moving) o Acute phase characterized by damage integrity of the alveolar capillary membrane, w/extensive damage to type 1 alveolar cells w/increasing endothelial permeability (they become leaky) o Interstitial edema w/ protein fluid leaking into alveoli (2 way leak now). Lungs become sticky o Tiny emboli form in the pulmonary microcirculation and add to alveolar edema & hemorrhage. ▪ Due to increased clot production & reduction of fibrinolysis (clot breakdown). Small emboli reamin in the lung; DIC plays a role in some pts. o Surfactant decreased from fluid and type 2 alveolar cells secrets less surfactant. ▪ Protein deactivates surfactant = collapsed alveoli ● Signs & Symptoms o Rapid onset of severe dyspnea (as alveoli fill up) o Arterial hypoxemia (refractory to O2 therapy) o Bilateral diffuse infiltrates on CXR – white out or ground glass. o Fibrosing alveolitis – Alveoli inflamed & make scarred tissue ● Assessment: What we will see o Struggling to breath o Assess the work of breathing ▪ Posture if pt seated; Nasal flaring (late sign in adults); Intercostal retractions, use of accessory muscles o Assess rate & depth of respirations – Tachypnea & Hyperpnea (increased depth of breathing) ▪ Can’t expand chest o Palpation – Assess lung expansion – decreased due to compliance o Percussion – Dullness over all lung fields if substernal edema present o Auscultation – Bronchovesicular breath sounds over most lung fields due to the increased density of the lung. ▪ Diffuse crackles and rhonchi over ALL lung fields. EARLY SIGN o BOOK SAYS - Abnormal lung sounds are NOT heard on auscultation bc edema occurs 1st in interstitial spaces & not airways. ● Medical Management o ABGs – Hypoxia is the hallmark & due to intrapulmonary shunting (movement of blood in lungs w/o gas exchange and oxygenation. o Hypoxemia is refractory to O2 therapy – PaO2 <55 on 50% O2 – EARLY SIGN o Respiratory Alkalosis due to hyperventilation o Hypercapnia not seen initially but is ominous sign when it does – LATE SIGN o Chest X-ray – diffuse bilateral alveolar infiltrates o Pulmonary function (Measures air in and out of lungs) – ▪ Reduced compliance ▪ Reduced FRC (functional residual capacity – volume of air present in lungs at end of passive expiration) ▪ Increased dead space ventilation – No O2/CO2 exchange, more space due to fluid ● Treatment o Nursing priority in prevention of ARDS is early recognition of pts at risk for it. o Often needs intubation & mechanical ventilation w/PEEP or CPAP (sedation & paralysis may be needed) o Many pts oxygenate best in PRONE positon (early) – Rotoprone bed o Fluid and electrolytes – as indicated by lab work. Conserve fluid therapy to improved lung function o O2 therapy from NC to 100% to increase O2 w/i space left not filled w/fluid o If vented – Low tidal volumes (6mL/kg) w/ PEEP or CPAP, to prevent lung injury ▪ Monitor lung sounds for pneumothorax; s/e of PEEP is tension pneumothorax. o ABX if pt septic or has PNA o Corticosteroids – Stabilizes alveoli & decreases fluid leaking; reduces inflammation, high dose IV for short time o Pulmonary artery monitoring – especially during acute stages to manage fluids ▪ PCWP is low to normal o Nutritional Support – 35-45 kcal/kg/day o Peptic ulcer prophylaxis – IV/PO pantoprazole, to decrease gastric secretions r/t stress & decrease aspiration o VTE prophylaxis – SCDs, teds & enoxaparin when appropriate o HOB elevated 30 degrees – aspiration precaution, if BP tolerates, if not, 15-20 degrees o Daily sedation vacation if intubated – Wake up each day to assess neuro status, RN must be at bedside. o Oral care Q2 hr & Q12 tooth brushing ● Course of ARDS o Exudative phase – Early changes of dyspnea & tachypnea from alveoli filling w/fluid & pulmonary shunting & atelectasis. ▪ Early intervention focus on supporting pt and O2 o Fibroproliferative phase – Pulmonary hypertension & fibrosis, reduced gas exchange & oxygenation. Multiple Organ Dysfunction Syndrome (MODS) can occur. ▪ Interventions – adequate O2, prevent complications & supporting the lungs o Resolution Phase – After 14 days resolution of injury, death, or chronic disease occurs. Survivors have poor quality of life. Mechanical Ventilation (P614-622) ● Intubation and ventilation indicated when pt CANNOT maintain adequate oxygenation (PaO2 <50) ON O2 device OR adequate CO2 exchange (PaCO2 >55 AND pH <7.30) ● Endotracheal Intubation o ET tube short term, tracheostomy if needed longer than 10-14 days. To reduce tracheal & vocal cord damage. o Tip of ET tube 2cm above carina, Lines for placement at the incisor tooth, XRay determines correct placement o Nasal route for oral surgeries, AVOIDED w/ midface trauma, basilar skull fx, if pt has a blood clotting problem o Tube sizes for adults is 7-9 mm and based on the size of the patient. o Ensure that each intubation attempt no longer than 30 sec, preferably 15 sec. After 30 sec provide O2 by mask & manual resuscitation bag to prevent hypoxia & cardiac arrest (also critical until help arrives out of hospital) o Bring crash cart to bedside if pt requiring emergency intubation & ventilation. Maintain pt airway with chin lift & insertion of oral or nasal airway until intubated, delivering manual breaths w/bag-valve-mask. o Check bilateral breath sounds & symmetric chest movement. If breath sounds and chest movement are absent on left side, tube may be in right mainstem bronchus and just needs to be repositioned w/o redoing procedure o PATIENT CANNOT TALK WHEN CUFF IS INFLATED PROPERLY o If tube is in stomach, the abd may be distended and must be decompressed w/NG tube after ET tube is placed o Stabilize with 2 people using a head halter technique to secure the tube, one holds in position and other applies holding device. Use bite block or oral airway to prevent pt from biting on the ET tube. o Document bilateral & equal breath sounds & the level of the tube o If pt shows manifestations of decreased oxygenation, check for DOPE: Displaced tube, Obstructed tube (most often from secretions), Pneumothorax, and Equipment problems. o Restraints are used as last resort to prevent accidental extubation. o Sedation (chemical restraint) may be needed to decrease agitation or prevent extubation ● Ventilator Settings o Tidal Volume (VT) – Volume of air pt receives w/each breath, ranges between 7-10 mL/kg of body weight. Adding a “0” to pt’s weight in Kg gives estimate of VT o Rate or breaths/min – Number of ventilator breaths delivered per min. Rate set between 10-14 o Flow Rate – How fast each breath is delivered. Usually 40 L/min. If pt is agitated or restless, has a widely fluctuating inspiratory pressure reading, or has other signs of air hunger, the flow rate may be set to low. Increase flow b4 using chemical restraints o Fraction of Inspired Oxygen (FiO2) – Oxygen level delivered to the pt. ▪ Based on ABG values and pt condition. 21% (room air) to 100% oxygen ▪ O2 is warmed to body temp (98.6) & humidified to 100% to prevent mucosal damage o Peak Airway (Inspiratory) Pressure (PIP) – pressure used by vent to deliver set VT at lung compliance ▪ Highest pressure reached during inspiration ▪ Increased means airway resistance in pt or in the ventilator tubing (bronchospasm or pinched tubing), increased secretions, pulmonary edema, or decreased pulmonary compliance (lungs or chest wall is “stiffer” and harder to inflate) ▪ Upper pressure limit is set to prevent barotrauma, alarm sounds when full volume not given ● Modes of Ventilation o CMV – Controlled Mechanical Ventilation ▪ Pt must be fully anesthetized, sedated & paralyzed; vent does all the work. (OR or ICU) ▪ Vent delivers positive pressure breaths at fixed timed intervals. o AC – Assist-control Ventilation ▪ “Resting mode”, pt triggers own breaths at own rate w/ back up rate set if pt doesn’t breathe. ▪ Each respiratory attempt is assisted by the ventilator (works w/pt) ▪ When pt attempts to inhale the ventilator takes over the work of breathing for the pt w/ set VT ▪ Disadvantage is that vent continues to deliver preset TV even when pt’s spontaneous breathing rate increases. **Can cause hyperventilation & respiratory alkalosis. Correct the cause o SIMV – Synchronized Intermittent Mandatory Ventilation ▪ Delivery of a pre-set number of ventilator breaths to a spontaneously breathing pt. ▪ Allows spontaneous breathing at pt’s own rate AND VT between vent breaths. ▪ Weaning mode – used to wean pts off the vent.# of vent breaths gradually decreased from 12 to 2 ● Ventilator Adjuncts o PEEP – Positive End Expiratory Pressure ▪ Positive pressure to the airways at the end of expiration ▪ Forces alveoli open @ end of expiration to prevent atelectasis. Keeps lungs partially inflated ▪ Lower FiO2 whenever possible bc prolonged use of high FiO2 damages lungs from toxic effects of O2 ▪ 5-15 cm H20, when PEEP added dial doesn’t return to 0 but to baseline by the amount of PEEP applied o CPAP – Continuous Positive Airway Pressure ▪ Positive airway pressure throughout the entire respiratory cycle for spontaneous breathing