NUR 265 Exam 2 Study Guide

NUR 265 Exam 2 Study Guide 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

oBronchial: High pitched & loud, normal in tracheal & larynx

oBronchovesicular: Moderate pitched & amplitude, normal over major bronchi

oVesicular: 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 oVenous 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.oGreatest r/f in the young is the combo of smoking and hormone based contraceptives.Nursing Assessment Findings oRespiratory 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).oRespiratory 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) oMany pts w/ a PE do not have “classic” sx (i.e. hypoxia), but instead have vague sx resembling the flu (n/v & general malaise) oCardiac Manifestations Decreased tissue perfusion: tachycardia, JVD, Syncope (loss of consciousness), Cyanosis, & Hypotension.oIn 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 oWhen 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 oSaddle Emboli – Embolism at split of pulmonary artery that blocks both branches to the lungs Medical Dx oChest X-ray – May show PE if large but will help r/o other things oCT scan – Most often used to dx PE oTEE (Transesophageal Echocardiography) – See if there are clots in the atria oVentilation 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 oABGs 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 NUR 265 Exam 2 Study Guide 1 / 3

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 oGIVE 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.oAnticoagulation 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) oConvert to Warfarin when stable – On 3 rd 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).oEnoxaparin or dalteparin oFibrinolytic (tPA) to tx massive PE or hemodynamic instability Antidotes – clotting factors, FFP, & aminocaproic acid (Amicar) Dissolve the clot itself oEmbolectomy – surgical removal of the embolus – When tPA can’t be used or for massive PE w/shock oInferior Vena Cava Filter – to prevent DVTs from moving to the lungs **Bleeding precautions with all blood thinners oPrevent 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 oMonitor for hypoxemia & respiratory compromise every 1-2 hrs.VS, lung sounds, cardiac & respiratory status, & urine output (bc hypotensive can cause AKI) oElevate HOB to high fowlers if BP tolerates.oObtain venous access and monitor heparin drip/LMWH/Coumadin oPain and anxiety management w/morphine (vasodilator) – O2 1 st 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.oBleeding precautions, oral care – especially if mouth breather.Prevention Measures oMeasures that prevent venous stasis and VTE oPassive and active ROM for postop & immobilized pts oPost-op ambulation ASAP oSCDs or Plexipulse compression – for prevention, not for active DVT oPt repositioning q2 hrs oLow dose anticoagulant & antiplatelet meds oSmoking cessation (especially females on hormone based contraceptives) bc increases risk for DVTs oTraveling – drink plenty of H2O, change positions, avoid crossing legs, get up and move every 1hr for 5 min.NANDA Diagnoses oImpaired 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) oCleat transudative – similar to fluid normally present in pleura space oExudative – Excess protein, blood, or evidence of inflammation or infection (white, green, cloudy is bad) Can cause pleurisy sx oPleural friction rub, scratching sounds caused by inflamed pleura rubbing together, pain on deep inspiration.NUR 265 Exam 2 Study Guide 2 / 3

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 oDyspnea (lungs can’t expand) oDecreased or absent lung sounds (sounds do not transmit through fluids well)

NO CRACKLES BC OCCURS OUTSIDE THE LUNGS

oDull flat sound on percussion (percuss between ribs) oDecreased tactile fremitus (vibration of chest wall produced when pt speaks) – hands around pt ribs oChest pain w/respirations if pleurisy develops Medical Management oThoracentesis – 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.oRecurrent effusions may need chest tube w/closed drainage until source tx oSevere 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.oHeart 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 oDelivery of adequate amount of O2 to the arterial blood (paO2 <60 hypoxemia) oRemoval 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 oVentilatory 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) oOxygenation (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 oCombined 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 oDyspnea (hallmark of respiratory failure) – DOE or when lying down (in slow progression) oOrthopnea – breathe easier in upright position, can’t sleep flat

oChange in lung sounds – depends on cause: CHF vs PE

oSkin/nail bed color changes (hypoxemia) oHypoxemia 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.oDecreased 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

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