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NUR265/NUR 265 EXAM 2 STUDY GUIDE LATEST UPDATE WALDEN UNIVERSITY
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NUR265/NUR 265 EXAM 2 STUDY GUIDE LATEST UPDATE WALDEN UNIVERSITY
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NUR 265 Exam 2 Study GuideLungs 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 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.
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
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