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29 Respiratory Emergencies: Lung and Gas Exchange Disorders.

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1 29 Respiratory Emergencies: Lung and Gas Exchange Disorders

2 Objectives Identify pathophysiologic changes due to diseases that hamper gas diffusion or lung compliance. Discuss the objectives.

3 Introduction This topic deals with disorders that alter lung compliance or the ability of the alveoli to diffuse gas. Compliance refers to the ability of lung tissue to expand when air flows in. Alveolar issues are those that inhibit or prohibit normal gas exchange with the blood stream. Lung compliance refers to the ability of the actual lung tissue to expand when air flows in. If the lungs are “stiff,” then it becomes difficult for the patient to inhale sufficiently to ventilate the alveoli and respiratory distress results. Conversely, if the oxygen in the inhaled gases cannot diffuse across the alveoli because of some disturbance, the body will not be able to adequately oxygenate the tissues—and, again, respiratory distress results. These two pathologies are the focus of this topic.

4 Epidemiology 1.5 million people are diagnosed with emphysema.
Pulmonary edema afflicts 1%-2% of the general population. 250,000 cases of pulmonary emboli a year. Other etiologies like pneumothorax and cystic fibrosis occur also. Discuss the frequency of these disease processes. The intent being that they are a common emergency that will be seen by the Advanced EMT.

5 Pathophysiology Compliance External respiration Internal respiration
Refers to the ability of the lungs to stretch as air enters the passageways. “Stiff” lungs are difficult to ventilate. External respiration Exchange of gases in the alveoli. Internal respiration Exchange of gases at the tissue capillary level. Overview what compliance means. Use a couple of examples of “stiff” lungs (e.g., emphysema) to illustrate. Also, compliance can change if the lung tissues cannot expand due to a force keeping them compressed (e.g., pneumothorax). External and internal respirations relates specifically to the gases going down their partial pressure gradient. Both must occur for adequate oxygenation of the body.

6 Pathophysiology (cont’d)
Emphysema Loss of lung tissue elasticity Destruction of alveolar surfaces Gross disturbances in gas exchange Discuss pathologic changes due to the emphysemic process. Relate risk factors and the resultant drop in the ability of lungs to adequately ventilate and oxygenate. This is primarily a compliance issue. This disease process leads to chronic retention of carbon dioxide, hence the patient eventually converts to hypoxic drive for breathing.

7 Pathophysiologic changes in emphysema include decreased surface area of the alveoli.

8 Pathophysiologic changes in emphysema include decreased surface area of the alveoli.

9 Pathophysiology (cont’d)
Pulmonary edema Fluid collects in alveoli due to increased hydrostatic pressure in perialveolar capillary beds. Hinders normal gas exchange. Primarily a gas exchange problem. Cardiogenic and noncardiogenic causes. The two kinds of pulmonary edema are: Cardiogenic Noncardiogenic Cardiogenic pulmonary edema is typically related to an inadequate pumping function of the heart that drastically increases the pressure in the pulmonary capillaries, which forces fluid to leak into the space between the alveoli and capillaries and, eventually, into the alveoli themselves. Noncardiogenic pulmonary edema, also known as acute respiratory distress syndrome (ARDS), results from direct destruction of the capillary bed that increases capillary permeability and allows fluid to leak out and into the interstitial spaces. Common causes of noncardiogenic pulmonary edema are: Severe pneumonia Aspiration of vomitus Near-drowning Narcotic overdose Inhalation of smoke or other toxic gases Ascent to a high altitude Chest and lung trauma

10 In pulmonary edema, fluid collects between the alveoli and capillaries, preventing normal exchange of oxygen and carbon dioxide. Fluid may also invade the alveolar sacs. Review disease process again, comparing diseased from nondiseased.

11 Pathophysiology (cont’d)
Pulmonary embolism Embolism in blood stream lodges in pulmonary artery. Prohibits blood flow to a region of the lung. Disturbance to normal V/Q ration. Blood passes through lungs without oxygenation. The embolism prevents blood from flowing to the lung. As a result, some areas of the lung have oxygen in the alveoli but are not receiving any blood flow. This leads to a decrease in gas exchange and subsequent hypoxia, the severity of which depends on the size of the embolism or the number of alveoli affected. The hypoxia in this case is the result of the shunting of blood away from the oxygenated alveoli, creating a mismatch between ventilation and perfusion.

12 A blood clot, air bubble, fat particle, foreign body, or amniotic fluid can cause an embolism, blocking blood flow through a pulmonary artery.

13 Pathophysiology (cont’d)
Pneumothorax Collection of air in the pleural cavity Traumatic and nontraumatic etiologies. Changes lung compliance. Inability to inflate lung for diffusion to occur. Tension versus nontension pneumothorax. If air enters the pleural cavity, either from the outside (open pneumothorax) or from air escaping through a hole in the lung and into the pleural space (closed pneumothorax), the lung may collapse; with larger pneumothoraces, it becomes mechanically impossible for the patient to breathe. The lung collapse decreases lung tissue compliance and causes a disturbance in gas exchange that leads to hypoxia and hypercapnia. Compare and contrast the effects of a simple pneumothorax from a tension pneumothorax.

14 In pneumothorax, the lung collapse decreases lung tissue compliance and causes a disturbance in gas exchange that leads to hypoxia.

15 Pathophysiology (cont’d)
Cystic fibrosis Hereditary disease. Abnormal gene results in overproduction of mucus in the respiratory tree. Repeated respiratory infections and scarring lead to loss of pulmonary function. Due to the disease process, repeated lung infections, in turn: Cause scarring of the lung tissue. Reduce the ability of the lungs to clear the thick mucus. Promote ongoing pulmonary damage. As a result, there is progressive diminution in the efficiency of respiratory function, which leads to eventual pulmonary failure and death. Commonly diagnosed at a young age.

16 Assessment Findings General assessment findings
Common to most patients with dyspnea Changes in respiratory rate and breath sounds Accessory muscle use Tripod positioning and retractions Nasal flaring, mouth breathing Changes in pulse oximetry and vitals Skin change and mental status changes If adequate breathing and gas exchange are not present, the lack of oxygen will cause the body cells to begin to die. Some cells become irritable when they are hypoxic, causing the cells to function abnormally. Oxygen levels decrease, carbon dioxide increases, the blood becomes acidic, and if left unmanaged or improperly managed—there will be a cellular shift from aerobic to anaerobic metabolism. The Advanced EMT must be keenly aware on how to differentiate adequate breathing with inadequate breathing. If the patient is inadequately breathing, there is no way they can oxygenate effectively and the patient will die.

17 Assessment Findings (cont’d)
Additional findings with emphysema On home oxygen Thin, barrel chest appearance Nonproductive cough Diminished breath sounds Dyspnea on exertion Tripod positioning Prescribed MDI or nebulizer With exacerbation, the patient may also start to display wheezing heard upon auscultation.

18 Assessment Findings (cont’d)
Additional findings with pulmonary edema Orthopnea Frothy sputum with cough Tripod positioning Crackles and wheezing on auscultation Distended neck veins Tachycardia and tachypnea Discuss these additional findings that are more specific to pulmonary edema.

19 Assessment Findings (cont’d)
Additional findings with a pulmonary embolism Unexplained dyspnea Sharp, stabbing chest pain Hematemesis Syncope Hypotension and cyanosis (late findings) Discuss these additional findings that are more specific to a patient with a pulmonary embolism.

20 Assessment Findings (cont’d)
Additional findings with a pneumothorax Sudden onset of dyspnea Sharp, localized chest pain Diminished breath sounds on affected side Subcutaneous emphysema Discuss these additional findings that are more specific to a pneumothorax.

21 Assessment Findings (cont’d)
Additional findings with cystic fibrosis Known history of disease Recurrent coughing of thick mucus Rhonchi on auscultation General malaise GI complaints Malnutrition and dehydration Discuss these additional findings that are more specific to a patient with cystic fibrosis.

22 Differential Assessment Findings for Lung and Gas Exchange Disorders.

23 Emergency Medical Care
Ensure airway adequacy. Provide oxygen based on ventilatory need. NRB mask at 15 lpm with adequate breathing. PPV with 15 lpm oxygen with inadequate breathing. Administer inhaled beta-2-specific bronchodilator if warranted. In patients with respiratory distress from pulmonary resistance disorders, the primary management the Advanced EMT should provide should be geared toward ensuring adequate ventilation while maximizing oxygenation. This is accomplished through the use of high-flow oxygen in the adequately breathing patient, or by the application of positive pressure ventilation with oxygen supplementation in the patient who is breathing inadequately. Treatment may also include administration of a beta-2-specific agonist (MDI or small volume nebulizer) if bronchoconstriction is present.

24 Emergency Medical Care (cont’d)
Initiate CPAP at 5-10 cm H2O per protocol for pulmonary edema patients. Keep patient sitting upright if possible. Provide rapid transport to the ED. The use of CPAP in pulmonary edema patients is to help the excessive intra-alveolar fluid diffuse back into the blood stream so the alveoli can oxygenate better.

25 Case Study You are called for a patient complaining of respiratory distress. Upon arrival you find the patient sitting in bed, propped up by three pillows. The patient looks ashen, apprehensive, and is struggling to breathe. The respirations seem fast, but he is still speaking in normal-length sentences. Discuss the case study.

26 Case Study (cont’d) Scene Size-Up
Scene is safe, standard precautions taken. Patient is 61 years old, about 200 lbs. Entry and egress from room is unobstructed. NOI appears to be respiratory distress. No additional resources needed. Discuss the case study.

27 Case Study (cont’d) Primary Assessment Findings
Patient alert and oriented. Airway patent and self-maintained. Breathing adequate as evidenced by speech patterns, productive cough of frothy sputum. Central and peripheral pulses present. Skin is slightly ashen in color. Discuss the case study.

28 Case Study (cont’d) How would you categorize this patient’s stability?
What clue does the sleeping on multiple pillows provide? What are some early differentials you are considering? Patient category is potentially unstable. Sleeping on multiple pillows suggests trouble breathing while lying flat (orthopnea). Differentials at this time include: Pulmonary edema CHF Cystic fibrosis Chronic bronchitis Severe pneumonia

29 Case Study (cont’d) Medical History Medications Allergies
Patient has had two heart attacks previously. Medications Lasix, potassium supplement, nitro PRN. Allergies None per the patient. Discuss the case progression.

30 Case Study (cont’d) Pertinent Secondary Assessment Findings
Objective respiratory distress noted. Inspiratory crackles with expiratory wheeze. JVD and peripheral edema noted. Pulse ox 92% on high-flow oxygen. Discuss the case progression.

31 Case Study (cont’d) Pertinent Secondary Assessment Findings
No chest pain, no abdominal pain. Patient coughs up a frothy white sputum. B/P 168/100, HR 118 and irregular, respirations 26/min. Discuss the case progression.

32 Case Study (cont’d) What pathologic change is causing the abnormal breath sounds? What respiratory condition does this patient likely have? What would be three assessment findings that could confirm your suspicion? The inspiratory crackles is from the fluid accumulation in the alveoli from failure of the left ventricle. The expiratory wheezing is likely from the bronchioles constricting due to the irritation from the fluid accumulation migrating up the bronchioles during exhalation. Given the presentation the patient is likely going into full pulmonary edema. Breath sounds, sleeping upright, JVD and peripheral edema, medications, and past medical history all help complete the clinical picture.

33 Case Study (cont’d) How would you best ascertain if this patient is breathing adequately? Given this patient’s presentation, would it be beneficial to give him nitroglycerin? The best way to find if the patient is breathing adequately is to assess alveolar breath sounds. If the breath sounds are absent in the bases of the lungs, then airflow is not reaching them, hence oxygen and carbon dioxide cannot diffuse. All other findings of inadequate breathing come about from this single change. The second question is somewhat complicated. In a way, the administration of nitro would drop afterload and make it easier for the left ventricle to eject blood—which would then better drain the lungs and improve breathing. A paramedic may do this…however, the Advanced EMT can only administer the medication if the patient is experiencing cardiogenic chest pain.

34 Case Study (cont’d) Care provided: Patient placed on high-flow oxygen.
High-Fowler position on wheeled cot. CPAP initiated at 10 cm H20. Discuss the case provided.

35 Case Study (cont’d) What are the reasons for the following interventions provided to this patient? High-flow oxygen Fowler positioning CPAP administration Increasing the concentration of oxygen in the inspired air will promote better oxygenation of the RBCs and ultimately the tissue cells. The high Fowler position will help keep the fluid accumulation low in the lungs (dependent region) so the mid lobes and upper lobes can oxygenate more effectively. Also, this position will allow for better diaphragmatic excursion to enhance ventilation. CPAP will promote better ventilation of the alveoli by first forcing fluid back into the interstitial spaces of the lungs, and secondly by helping to drive oxygen across the alveolar membrane for diffusion into the RBC’s.

36 Summary Compliance disorders make ventilation difficult, impairing normal oxygenation. Diffusion disorders make O2 and CO2 transfer across the alveolar membrane difficult, impairing normal oxygenation. Review as appropriate.

37 Summary (cont’d) The role of the Advanced EMT is to identify these problems and provide appropriate interventions to improve oxygenation and ventilation. Review as appropriate.

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