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This deck focuses on Respiratory Failure And Advanced Respiratory Emergencies, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
Study Respiratory Failure And Advanced Respiratory Emergencies in NREMT Paramedic Level with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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Which option best indicates worsening asthma: decreasing wheeze with increasing work of breathing or loud wheezing?
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Decreasing wheeze with increasing work of breathing. Diminishing wheezes despite heightened effort signal severe airflow limitation and impending fatigue, worse than audible wheezes indicating some air movement.
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This deck focuses on Respiratory Failure And Advanced Respiratory Emergencies, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Decreasing wheeze with increasing work of breathing. Diminishing wheezes despite heightened effort signal severe airflow limitation and impending fatigue, worse than audible wheezes indicating some air movement.
Answer: Right mainstem intubation or unrecognized pneumothorax (evaluate immediately). These conditions impair oxygenation despite apparent ventilation, requiring prompt assessment to correct tube position or decompress the chest.
Answer: Continuous waveform capnography. Waveform capnography provides real-time confirmation of tracheal placement by detecting consistent CO2 exhalation, superior to auscultation or colorimetric methods.
Answer: Nonrebreather mask at high flow (or CPAP if indicated). Nonrebreather delivers high FiO2 for hypoxemia correction, with CPAP adding PEEP for alveolar recruitment if work of breathing is increased.
Answer: Decreasing tidal volume with slowing RR and altered mental status. Fatigue leads to progressive inability to generate sufficient tidal volume and rate, culminating in hypoventilation and CO2 retention with neurological changes.
Answer: Airway edema/bronchospasm, hypotension, and urticaria or mucosal swelling. This triad represents systemic IgE-mediated reaction involving respiratory compromise, circulatory collapse, and cutaneous manifestations from histamine release.
Answer: Adequate ventilation. The primary goal is restoring effective breathing to correct hypoxemia and hypercapnia, even if full alertness is not immediately achieved.
Answer: Inadequate oxygenation and/or ventilation to sustain life. This definition captures the critical failure of gas exchange where oxygen delivery or CO2 removal is insufficient, leading to life-threatening acidosis or hypoxemia.
Answer: Severe respiratory distress with hypotension and unilateral absent breath sounds. These signs indicate mediastinal shift from pleural pressure, compromising ventilation and hemodynamics, though JVD and tracheal deviation are less reliable.
Answer: Ventilate with BVM; administer naloxone as needed to restore adequate breathing. Supportive ventilation ensures gas exchange while naloxone antagonizes mu-receptors to reverse respiratory depression without oversedation reversal.
Answer: BVM ventilation with high-flow oxygen and airway adjuncts. BVM provides immediate positive pressure ventilation to restore oxygenation and CO2 clearance when spontaneous breathing is absent but circulation persists.
Answer: Needle decompression without delay. Needle decompression relieves intrathoracic pressure buildup, restoring venous return and cardiac output in life-threatening tension physiology.
Answer: Elevated PaCO2 with acidemia (low pH). Hypercapnic failure occurs when alveolar hypoventilation causes CO2 retention, resulting in respiratory acidosis as H+ ions increase from carbonic acid dissociation.
Answer: Tube dislodgement/obstruction or apnea (loss of exhaled CO2). Sudden loss of CO2 detection indicates no exhaled gas reaching the sensor, commonly from tube displacement, blockage, or absent ventilation.
Answer: Rising EtCO2 with decreasing RR. Rising EtCO2 indicates CO2 retention from hypoventilation as respiratory rate decreases, signaling decompensation toward arrest unlike compensatory tachypnea.
Answer: COPD often has chronic hypercapnia and prolonged expiratory phase with pursed-lip breathing. COPD features air trapping and baseline CO2 retention with adaptive breathing patterns, distinguishing it from acute reversible bronchospasm in asthma.
Answer: 10 breaths/min (about 1 breath every 6 seconds). This rate maintains adequate minute ventilation while avoiding hyperventilation-induced complications like barotrauma or reduced venous return.
Answer: Hypotension. Hypotension contraindicates CPAP as positive pressure can further reduce preload and cardiac output, unlike wheezing which may benefit from improved airflow.
Answer: Shark-fin waveform with prolonged expiratory upstroke. Bronchospasm prolongs expiratory flow, altering the capnogram to a delayed rise in CO2, resembling a shark fin due to airway obstruction.
Answer: 35–45 mmHg. This range reflects normal alveolar CO2 levels, approximating arterial PaCO2 in healthy lungs due to minimal gradient from efficient gas exchange.
Answer: Decreased venous return and cerebral perfusion from increased intrathoracic pressure. Excessive ventilation elevates mean intrathoracic pressure, impeding venous return to the heart and potentially causing cerebral vasoconstriction from hypocapnia.
Answer: Low PaO2 despite oxygen therapy (often with normal/low PaCO2). Hypoxemic failure reflects impaired oxygen diffusion or V/Q mismatch, where supplemental O2 fails to correct low arterial oxygenation despite adequate ventilation.
Answer: Visible chest rise. Chest rise confirms effective tidal volume delivery to the lungs, whereas high FiO2 alone does not ensure ventilation adequacy without volume confirmation.
Answer: Increases alveolar recruitment and decreases preload/afterload. CPAP applies positive end-expiratory pressure to reopen collapsed alveoli and reduces cardiac workload by decreasing venous return and wall stress.
Answer: Epinephrine (IM preferred if not in extremis). Epinephrine rapidly reverses bronchospasm and hypotension via alpha and beta effects, with IM route preferred for faster absorption in non-critical states.