Respiratory system

1. Respiratory system By: Diana Blum MSN MCC NURS 2140

2. Anatomy

3. Pathways (Chapter 33) • Nose to pharynx}behind the mouth to esophagus (approx. 5 inches) • Larynx} voice box: air passes between pharynx and trachea • Trachea} windpipe • Bronchi}this is the main branch that air passes through divides into left and right branch • Bronchioles} subdivides and connects with alveoli for gas exchange

4. More anatomy • Epiglottis} behind the thyroid cartilage • Has a hinged door action to larynx • Glottis} space between the folds of vocal cords • Air from the lungs promote it to open and close • Lungs} 3 lobes on the right and 2 lobes on the left • Pleura}membrane that covers the lungs • Has a lubricant between the layers to allow inhalation and exhalation to occur • Cilia} hair like projections that trap debris

5. Mechanism of breathing • Inspiration : air enters lungs • Active process where Chest muscles and diaphragm contract causing chest cavity to enlarge • Expiration: air leaves lungs • Passive process where muscles relax and the chest returns to normal. • Normal quiet breathing = 500ml of air exchanged with each breath • Pg

7. Apnea • Temporary interruption in the normal breathing pattern in which NO air movement occurs • May occur during sleep and at end of life • http://www.blinkx.com/video/understanding-obstructive-sleep-apnea-osa-1/WDHzxnb1t77AkBsdYIYwdg • http://www.blinkx.com/video/answered-patient-sleep-disorders-living-with-sleep-apnea/FjusOmVoqIX3V0lKzcwlKQ

8. ~pnea • Dyspnea} difficulty breathing or shortness of breath • Orthopnea} difficulty with breathing while in a lying position • Tachypnea} respiratory rate >20 • Bradypnea} respiratory rate <12

9. Lung sounds • Normal Breath Sounds • Normal breath sounds are.  loud pipe-like sounds in the large airways, and softer blowing-like sounds in the small airways.  • Normal breath sounds are loudest during inspiration and softest during expiration. •   The inspiratory phase is shorter with faster airflow.  •   Flow is greatest in the trachea and diminishes in the distal lung fields, until it reaches the alveoli, where there is no flow.  • **If breath sounds are really diminished, listen over the trachea** • Adventitious sounds • Wheezing: musical, whistling sound • Usually more pronounced during expiration • From narrowed airways • Bronchoconstriction • Secretions • Interventions: • Bronchodilation • Hydration • Coughing • http://www.ed4nurses.com/breathsnds.htm

10. Rales: crackling sound • Heard at the end of inspiration • From collapsed or waterlogged alveoli • Fine: beginning of fluid buildup / or atelectasis • Coarse: greater volume of fluid buildup • Interventions: • Manage fluids • Diuretics if needed • Expectorate • Turn & position & Deep breathing • Forced expiration • Vibration & percussion • Rhonchi: bubbling • The sound will be heard throughout inspiration and expiration. • Louder than rales due to larger secretions • Results from air bubbling past secretions in the airways • Interventions: • Deep breathing & Coughing • Hydration (encourage fluids, if no restriction) • Humidify air • Mobilize • Friction rub: creaking, leathery sound • End of inspiration and beginning of expiration • Caused by rubbing of inflamed pleural surfaces against lung tissue. • Interventions: • Chest x-ray • Anti-inflammatory medications

11. Lungs sounds continued Cheyenne Stokes Kussmal’s Regular breathing but breaths are deep Rates are >20 bpm Causes: metabolic acidosis, renal failure, diabetic ketoacidosis • Breaths are deep than become shallow followed by periods of apnea • Cause: severe brain pathology

12. http://rnbob.tripod.com/breath.htm • Lung sounds http://www.med.ucla.edu/wilkes/lungintro.htm • http://www.rnceus.com/resp/respabn.html • case studies http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/pd/step29e.htm

13. Age related changesChart 36-5 • Muscle atrophy in pharynx and larynx and change in vocal cords • Loss of lung elasticity • Decreased number of alveoli • Weaker chest muscles • Diminished chest movement • Less effective cough • Work harder to breath • Enlargement of bronchioles • More suseptible to lung infections r/t decreased defense mechanisms • Rib cage becomes more rigid and diaphragm flattens

14. Nasal Cannula: 1-6 liter flow Simple mask: 6-8 liters/ 40-60% o2 prercentage Partial rebreather: has reservoir bag so patient can rebreath part of inhaled gas: 8-11 liters/ 50-75% Non rebreather mask: non of exhaled gas rebreathed. 12 liters ; 80-100% See figure 35-3

15. What is an acute pulmonary embolism??? • - a thrombus (most originate from lower extremities) that travels thru venous circulation to pulmonary circ. & partially OR completely occludes a pulm. artery - - a massive PE: occlusion of >50% of pulmonary artery bed 150,000 deaths annually in US Pg 973

19. Pulmonary Embolus • Obstruction in pulmonary blood vessel causing a ventilation-perfusion mismatch resulting in hypoxemia, followed by < CO, bronchial constriction, collapsed alveoli and may result in sudden death • Cause: blood clot, fat , air, amniotic fluid, clumps of bacteria • Diagnosis: H&P, ABGs, VQ scan, EKG • S/S: sudden severe chest pain increases on inspiration, tachypnea, dyspnea, diaphoresis, hemoptysis, abnormal lung sounds, fever, tachycardia • Tx: Anticoagulation: PTT 2-21/2 normal • Heparin then oral Coumadin using PT and INR to regulate doses • Therapeutic coumadin range varies per doctor but most use goal of 2.0-3.0 • O2, IV ms, support CV system • Surgically may do embolectomy and insert a vena cava filter

20. Acute Pulmonary Emboli • How does PE occur?? • Deep venous thrombus breaks loose (MOST COMMON CAUSE) • ↓ • flows through venous circulation • ↓ • enters right ventricle • ↓ • lodges in small pulmonary arteries • ↓ • embolus may dissolve, grow or fragment • Embolus will most often lodge in Rt LL

21. When obstruction occurs in pulmonary vasculature what happens ??? • - - increases pulmonary artery pressure • - - increases vascular resistance • - - increased dead space ( disruption of blood flow to alveoli = nonfunctioning units)

22. Etiology & Risk factors for thrombus formation: • Virchow’s triad: • 1. damaged vascular endothelium • 2. venous stasis • 3. hypercoagulability • What would cause release of a thrombus? • - direct trauma • - muscle contraction • - changes in perfusion

23. Predisposing factors for PE: • - may have no predisposing factors • - immobilization, obesity, pregnancy, • estrogen use, aging, major trauma • or surgery within 4 weeks, malignancy • DVT, indwelling catheter, electrodes in • right heart (pacer), CHF, acquired • disorder (heparin-induced thrombocytopenia, postspleenectomy)

24. Predisposing risk factors PE (continued): • Hx of DVT • > 40 yrs of age • Extensive abdominal or pelvic surgery • (many PE originate in femoral – iliac- • pelvic veins) • Long-bone or pelvic fractures

25. Massive PE (>50% pulm circ obstructed): • - - occurs suddenly • - - associated with acute Rthrt failure • (  ‘d pulmonary artery systolic • pressure & pulm. vasc resistance) • - - ↓’d CO • - - may have crushing substernal CP • - - Shock: hypotension, dypnea, cyanosis, apprehension, coma • - - resp rapid, shallow, gasping • “impending doom” if pt conscious • Core pulomonale pg 980

26. Complications of PE • Pulmonary hypertension from pulmonary arterial obstruction • Sudden obstruction & total: sudden death • Pulmonary infarction • Stroke, MI, dysrhythmias, liver failure, acute respiratory distress syndrome, shock, death

27. Diagnostic studies for DVT (since 70% of pts with PE are positive DVT) • Ultrasound • D-dimer test: not specific, fibrin product – if positive will do further testing • Pulmonary Venography: gold standard, inject dye noninvasive tests first • MRI with contrast • CT contrast spiral • V/Q scanning (dye give IV AND inhaled )

28. Management Options for PE: • Heparin: Load 80 Units/kg • Drip 18 Units/kg/hr • Measure PTT every 6 hours • Goal: PTT 1.5 to 2.0 X control • Vena Cava Filter: for contraind. anticoag OR clot develops while adeq anticoagulated • Embolectomy: if not anticoag candidate & • acutely unstable • Thrombolytics: tPA

29. Xray image of Vena Cava Filter in place

30. Heparin therapy • Platelet count monitored about every 3 days for heparin-induced thrombocytopenia • Oral Coumadin by day 3 of heparin • Titrate dose heparin so PTT is 1.5-2.5 times normal control. • ADVERSE EFFECTS: • hemorrhage, hypersensitivity, thrombocytopenia

31. Example of dosing heparin drip • measured PTT Heparin adjust • <35 sec (1.2 X ) 80U/kg then  • rate by 4U/kg/hr • 35-45 sec (1.2-1.5X) 40U/kg bolus • then  rate by 2U/ • kg/hr • 46-70 sec (1.5-2.3X) NO CHANGE • 71-90 sec (2.3-3X) ↓rate by 2U/kg/hr >90 sec (3X control) Stop infusionX1hr then ↓ rate by 3U/kg/hr

32. Best physical methods of prevention of DVT: • Leg elevation • Sequential compression devices • EARLY POSTOPERATIVE AMBULATION ( THE • MOST IMPORTANT)

33. Nursing Interventions PE • High-fowler’s • Oxygen (prepare for intubation) • Auscultate breath sounds • Admin thrombolytics/anticoag (monitor • bleeding) • ***HEPARIN/THROMBOLYTICS IV • INCOMPATIBLE IN SAME IV LINE • Analgesics to ↓pain, ↓ anxiety • Maintain calm environment

34. Nursing Diagnosis PE: • Impaired gas exchange • Ineffective breathing pattern • Anxiety • Decreased CO • Risk for inability to sustain spontaneous • ventilation

35. Goals & Desired Pt Outcomes for PE • Adequate oxygenation • Reversal of thrombus • Reduction in risk for additional thrombus formation • Prevention of pulmonary infarction • Improved V/Q ratio

36. V/Q Ratio • V = ventilation • Q = perfusion • The amt of air reaching lung must be equal to blood reaching lung for the ideal exchange of O2 and CO2, ratio is 0.8 • If airway is blocked, then ventilation zero • If blood flow blocked, (PE) VQ is infinite “dead space” • Pg 974

37. V/Q ratio > 0.8 dead space producing • - PE, pneumothorax • - increased vent with decrease perfusion • V/Q ratio < 0.8 Shunt producing • - hypoventilation, obstructive • - decreased vent with increase perfusion • Pg 1005

38. Critical Thinking: Nursing management of the pt with a pulmonary embolism: • Situation: 55 yr old woman returned to her room at 2 pm yesterday following abdominal hysterectomy. Her vitals have been stable & dressing dry, intact. She was up to the side of the bed & ambulated a few feet before returning to bed. A few minutes later, she turns on her call light stating she is having difficulty breathing. The nurse hurries to her room & finds the pt tachycardic, diaphoretic, gasping for air, & C/O Chest pain.

39. 1. How can the nurse determine if the pt is experiencing a PE or a MI? • 2. Why is it essential to establish the cause of the pt’s symptoms as rapidly as possible? • 3. What risk factors does the woman have for development of PE? • 4. What can nurses do to help identify those pts at  ‘d risk for PE?

40. Acute Respiratory Failure • - the result of abnormalities in ventilation, perfusion, or compliance which leads to hypercapnia &/or hypoxemia • - respiratory acidosis • - must identify underlying condition before treatment • Pg 1006

41. Acute resp. failure (continued): • - an alteration in oxygenation is most common form of resp. failure • - perfusion (Q)exceeds ventilation (V) • which is a low V/Q ratio causes decreased oxygenation of venous blood & a mixing of less oxygenated blood with arterial blood • - so have reduced arterial oxygen value

42. Causes of Acute Resp. Failure PE Pneumonia CVA COPD Pneumothorax Lung trauma atlectasis Pulm. Edema

43. S/S Acute Resp. Failure: • Tachycardia, atrial dysrhythmias tachypnea, dyspnea on exertion or rest, labored breathing, use of accessory muscles, rales

44. Management of acute resp. failure: • - correct hypoxia & acidosis with CPAP or may need intubation, ventilator, PEEP • - if medication induced: discontinue med • - if due to trauma or ICP must focus on relieving the ICP • - if due to high V/Q ratio (dead-space) must reestablish perfusion (if from PE, thromolytic therapy)

45. Goals/pt outcomes for Acute Resp Failure: • Ability to sustain spontaneous ventilation • Adeq. Ventilation: pH 7.35-7.45 • PCO2 35-45 • SaO2: >92%

46. Pt Interventions for Acute Resp. Failure • Correction of hypoxia & acidosis: • - CPAP, ET, mechanical vent, PEEP • Resp. muscle rest • Control of shock • nutrition

47. Complications Acute Resp. Failure: • Severe resp & met acidosis • Infection • Failure to wean from ventilator • Lack of adeq. Nutitional support

49. ARDS • Progressive pulmonary disorder after chest trauma 1-96 hrs after • Also seen with aspiration, prolonged mechanical ventilation, severe infection and open heart surgery • Involves: pulmonary capillary damage with loss of fluid and interstitial fluid, Impaired alveolar gas exchange and tissue hypoxia due to pulmonary edema, Altered surfactant production, Collapse of alveoli, Atelectasis resulting in labored breathing and ineffective respirations • Pg 1014

50. ARDS Continued • The damaged tissue of the lungs has increased capillary permeability and fluid accumulates in the tissues of the lungs. The production of pulmonary surfactant < and atelectasis occurs. Lung compliance < meaning the lungs are losing the ability to carry out the process of breathing. • As a result, hypoxia develops. Some clients recover but the scar tissue becomes fibrous and lung fibrosis may progress. • Systemic effects: cardiac dysrhythmia, renal failure, stress ulcers