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
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