Respiratory Failure and Advanced Respiratory Emergencies - NREMT: Paramedic Level

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.

$10$ 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.

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.

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.

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.

Rising $EtCO_2$ with decreasing RR. Rising EtCO2 indicates CO2 retention from hypoventilation as respiratory rate decreases, signaling decompensation toward arrest unlike compensatory tachypnea.

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.

Hypotension. Hypotension contraindicates CPAP as positive pressure can further reduce preload and cardiac output, unlike wheezing which may benefit from improved airflow.

$35$–$45$ mmHg. This range reflects normal alveolar CO2 levels, approximating arterial PaCO2 in healthy lungs due to minimal gradient from efficient gas exchange.

Tube dislodgement/obstruction or apnea (loss of exhaled $CO_2$). Sudden loss of CO2 detection indicates no exhaled gas reaching the sensor, commonly from tube displacement, blockage, or absent ventilation.

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.

Elevated $PaCO_2$ 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.

Low $PaO_2$ despite oxygen therapy (often with normal/low $PaCO_2$). Hypoxemic failure reflects impaired oxygen diffusion or V/Q mismatch, where supplemental O2 fails to correct low arterial oxygenation despite adequate ventilation.

Continuous waveform capnography. Waveform capnography provides real-time confirmation of tracheal placement by detecting consistent CO2 exhalation, superior to auscultation or colorimetric methods.

Needle decompression without delay. Needle decompression relieves intrathoracic pressure buildup, restoring venous return and cardiac output in life-threatening tension physiology.

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.

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.

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.

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.

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.

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.

Adequate ventilation. The primary goal is restoring effective breathing to correct hypoxemia and hypercapnia, even if full alertness is not immediately achieved.

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.

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.