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 o Bronchial: High pitched & loud, normal in tracheal & larynx o Bronchovesicular: 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 lifethreatening 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