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Directions: The following exam consists of various types of questions designed to test the critical reasoning skills of the examinee. Answers are found on the following page, with rationales. This is a Twenty question test, with an allotted time of 45 minutes to indulge ones academic and clinical prowess. Questions 1 - 4 are based on the following scenario: A 55 year old male, medium body build of 90 Kg presents complaining of acute shortness of breath. He has a history of CHF and acute respiratory failure, he is agitated and disoriented.
He has been placed on a ventilator two times during the past year. His medications include HCTZ, captopril, digoxin, and lasix. Paramedics have placed him in 100 % O 2 via Non-re breathing mask, established an IV and administered 40 mg of Lasix IV enroute. He is cold, pale, and diaphoretic, with a BP of 200 / 110, HR 120, RR 48, rales are audible throughout. ABGs are drawn, and the results are: pH - 7. 3, PCO 2 55, HCO 3 24, PaO 2 60. 1.
Why is this gentleman's PCO 2 elevated? a. Not enough total ventilation (CNS/Respiratory muscle weakness) b. Too much total ventilation Dead Space (Rapid breathing) (1) d - The only reason for elevated PCO 2 is an inadequate level of alveolar ventilation for the amount of CO 2 produced and delivered to the lungs. Hypercapnea in this case is a combination of both. Since he is tachypneic his respiratory muscles are tiring, he is displaying mental status changes do to hypercarbia effects on the CNS.
Because his RR is 48 he much of his VT ends up as alveolar dead space. 2. Why is this gentleman's PaCO 2 of concern to you clinically? a. Increased PaCO 2 (if no compensatory increase in HCO 3) results in fall in pH b. Increased PaCO 2 results in a decrease in PaO 2 unless FiO 2 can increase enough to compensate c. The higher the PaCO 2, the less well defended this pt is against a further decrease in VA e.
His PaCO 2 in this case is of little concern clinically 2. d - (a) This patients PaCO 2 has resulted in a fall in pH. It is important to remeber that a small change in pH in one direction means a large change in the other direction. a Ph of 7. 30 = a 50 nM/L (25 %) increase in [ H+]. (b and c) Despite the fact that this pt is on 100 % O 2, his PaO 2 is only 60. As his PCO 2 is 55 his VA is further decreased.
Letter E is just bad. 3. How would this patients decrease in inspired O 2 and increase in CO 2 affect the O 2 -Has dissociation curve response as opposed to an increase in CO 2 alone? 3. - The effects are additive, and the response will be amplified (Oxygen will be unloaded from the hemoglobin protein molecule). Increased PCO 2 shifts the curve to the right (Bohr effect). Increased [H+] (even independent of PCO 2 shifts the curve to the right. Should this patient be chronically hypodermic, that would trigger 2, 3 DPG synthesis which would further shift the curve to the right.
These factors are compensatory, since the reduced affinity makes unloading of O 2 in the tissues easier, they facilitating end-organ perfusion. b. Ventilation amount needed to maintain normal CO 2 c. Exertional fatigue (result of cardiovascular, neuromuscular, or non-pulmonary disease) d. Should be treated by placing a paper bag over a patients mouth and having them retreat CO 2 4. b - Hyperventilation is often misdefine d, even among medical professionals.
It is concisely defined as ventilation greater than that amount needed to maintain normal CO 2. A RR 12 - 20 /min is tachypnea, which as we saw in our scenario does not necessarily lead to a ventilation amount needed to maintain normal CO 2. Exertional fatigue may present with tachypnea, but still present with elevated PCO 2. Treating patients with a paper bag a treatment of the past.
Underlying pathology must always be ruled out when a patient presents with respiratory symptoms. 5. During press examination, you patient is SOB at rest with an abnormal ABG. You you grade this patient: 5. - d. Dyspnea (SOB) reflects an uncomfortable awareness of ones own breathing. Significance depends heavily on the stimulus or amount of activity required to participate it. Grade I, pt can walk a distance, but slowly, Grade II, can walk a limited distance before becoming SOB, Grade III, Becomes SOB walking ino a room and may or may not have abnormal ABGs.
Grade IV is SOB @ rest with abnormal ABGs. There is no Grade V based on Dr. Vaccihianos criteria. 6. The proposed mechanisms of dyspnea/SOB share no common link they are: (1) increased WOB due to Increased Raw, "stiff lungs", (2) abnormal ABGs with ether an Increased PCO 2 or decreased PO 2, or (3) altered respiratory drive with normal respiratory system. Having shared the mechanisms What are the proposed sources of breathlessness? a.
Mechanical receptors in chest wall and lungs c. The sense of respiratory effort (increased with increased WOB) d. Imbalance between respiratory work, and ventilatory output e. all of the above are proposed sources of breathlessness 6.
e - all of the above are proposed sources of breathlessness. It is important to note that despite decades of work to elucidate the underlying mechanisms of dyspnea, no satisfactory explanation yet exists. 7. Respiratory diseases leading to dyspnea as presented in class can be primarily be categorized into which of the following areas? a. Airway disease, Parenchyma l Disease, Pulmonary Vascular Disease, Pleural Disease, and Disease affecting expansion and blood flow b. Hemopneumothorax, pneumothorax, hemothorax, pneumocephalus c.
Diseases which increase in minute ventilation but decrease in alveolar ventilation d. Dyspnea secondary to centrally medullary respiratory depression 7. - a. Diseases that lead to dyspnea most commonly are attributed to airway disease (obstruction, edema, tumor, foreign body); parenchyma l disease (scarring of the lung, which when severe enough may become fibrous and a diffusion barrier. Pulmonary infiltrates may also be considered in this category); pulmonary vascular disease (due to blockage or loss of vessels as in pulmonary emboli, which can cause V/Q mismatch); Pleural disease (air or liquid in the pleural space such as with pneumothorax or pleural effusion; and diseases affecting expansion and blood flow diseases (primary disease of the respiratory muscles, nerve supply, or neuromuscular interaction - examples here may include paralysis @ or below C- 4 which would cause diaphragmatic paralysis, myasthenia gravis, Eaton-Lambert syndrome, or kyphoscoliosis). Answers b, c, and d are incorrect. 8. - PFT abnormalities are categorized into one of two patterns. They are: 8.
c - Patterns of Pulmonary Functional Impairment are categorized into one of two patterns (1) Obstructive, such as asthma, COPD, chronic bronchitis (which increase lung volumes {air is "trapped and stacked" = increased RV, TLC, and RV/TLC and decrease expiratory flow rates (decreased FEV 1, FEV 1 /FVC, and MMFR) (2) Restrictive (decreased expiratory flow rates over time - decreased: TLC, VC, RV, and FRC. FEV 1 /FVC and MMFR are preserved) An FEV 1 80 % is considered decreased. An FEV 1 /FVC ratio 50 % is significant, and these patients are likely going to be more difficult to wean from the ventilator 9. In regard to neural control of the airways, the vagus nerve (PSNS) carries afferent and efferent nerve fibers with neurotransmitters which interact with specific protein macromolecular receptors to mediate airway responses. These responses take place at the goblet cell, blood vessels, sub mucosal glands, smooth muscle, and epithelial cells.
When considering respiratory smooth muscle, it can be said that the neurotransmitter VIP has properties, while the neurotransmitter acetylcholine possesses properties d. Vasoconstrictive, vasoconstriction 9. e - VIP, a short chain amino acid or "small protein" mediates smooth muscle dilation to counter the vasoconstriction properties of the neurotransmitter acetylcholine 10. You are leaving the ED after being paged for an "almost ready to be incubated" young asthmatic patient who subsequently responded well to your treatment of nebulize d beta 2 agonists, and corticosteroids. Youve been up all night writing exam questions, and as you drift off to sleep you are dreaming of hyper responsive airways. Understanding the current hypothesis for pathology includes epithelial injury and airway inflammation you consider the possibilities of airway hyper responsiveness.
You conclude that the possibilities of airway hyper responsiveness include: a. Mediator release from inflammatory cells (luekotrines b. Epithelial disruption which result in increased permeability of inhaled agents c. Injury and inflammation after degradation of certain neuropeptides d. A bronchial smooth muscle relaxant factor produced by the airway perithecium is decreased of absent e. All of the above are possibilities of airway hyper responsiveness. 10.
e - all of the above. Mediator release form inflammatory cells can cause broncho constriction. Mediators such as leukotriene have positive effect on asthma, by modulating the degree of broncho constriction, without modulation, unopposed broncho constriction progresses. Without an epithelial barrier, sub mucosa of the airways are directly exposed to irritants, allergens and infections. Injury and inflammation to exposed submuxcosa may cause a release of tachykinins, which are now unopposed and cause broncho constriction. 11. The two branches of the immune system are: c.
Adaptive (Specific) and Non adaptive (Non-Specific) 11. c - the two branches of the immune system are adaptive (specific), and non-adaptive (non-specific) Adaptive or specific consist of T-Cells, and B-Cells (lymphocytes), while nonadaptive are barriers which involve inflammatory responses, asd the part of the immune system which the body uses to recognize...
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