Respiratory Distress and Failure - NREMT: AEMT Level

Inadequate breathing (poor rate, depth, or tidal volume). Assisted ventilation is required when spontaneous breathing fails to achieve adequate minute volume for gas exchange.

Troubleshoot pulse oximeter accuracy before escalating therapy. Poor plethysmograph suggests artifact or poor perfusion, making SpO2 unreliable despite clinical stability.

CPAP, if not contraindicated. Positive end-expiratory pressure recruits alveoli, reduces work of breathing, and decreases cardiac preload.

Systemic corticosteroid (for example, methylprednisolone). Inhibits inflammatory mediators to reduce airway edema and mucus production in exacerbations.

Inhaled beta-2 agonist (for example, albuterol). Stimulates beta-2 receptors to relax bronchial smooth muscle, rapidly relieving acute airway obstruction.

Crackles (rales). Discontinuous sounds produced by air bubbling through alveolar fluid, indicating pulmonary edema or pneumonia.

Naloxone with ventilatory support as needed. Opioid antagonist reverses central respiratory depression by competing for mu-receptors, restoring ventilatory drive.

Severe dyspnea with absent unilateral breath sounds and hypotension. Combination indicates intrathoracic pressure buildup compressing lung and shifting mediastinum, impairing venous return.

Wheezing. High-pitched expiratory sounds result from turbulent airflow through constricted lower airways due to smooth muscle contraction.

Suspected basilar skull fracture or severe midface trauma. Risks inadvertent intracranial placement through cribriform plate defects, potentially causing brain injury or infection.

Increased work of breathing with adequate ventilation and oxygenation. This definition captures the compensatory phase where patients exhibit labored breathing but maintain sufficient gas exchange without immediate decompensation.

Inadequate ventilation or oxygenation, or both, with impending arrest risk. This describes the decompensated state where gas exchange fails, leading to potential cardiopulmonary arrest if not addressed promptly.

Accessory muscle use or retractions. These physical signs reflect the body's effort to recruit additional muscles to overcome increased respiratory resistance or decreased lung compliance.

Decreasing mental status (fatigue with poor respiratory effort). This indicates respiratory muscle exhaustion, signaling progression from distress to failure with imminent risk of arrest.

Low arterial oxygen level. Refers to insufficient oxygen partial pressure in arterial blood, often below 60 mmHg, compromising tissue oxygenation.

Nasopharyngeal airway (NPA), if no contraindication. Tolerated in patients with intact gag reflex as it does not stimulate the oropharynx, maintaining patency in altered mental status.

Nonrebreather mask. Provides high FiO2 up to 100% by using a reservoir bag and one-way valves to minimize room air entrainment.

Venturi mask. Allows delivery of controlled FiO2 percentages to prevent oxygen-induced hypercapnia in patients with chronic hypoxic drive.

Asthma is often reversible bronchospasm; COPD is chronic airflow limitation. Asthma involves episodic, reversible obstruction from inflammation; COPD features persistent structural damage limiting airflow.

Pulmonary edema (often cardiogenic). Increased hydrostatic pressure forces fluid into alveoli, producing characteristic sputum and auscultatory findings.

Wheezing with hypotension and urticaria or angioedema. Systemic allergic response triggers mast cell degranulation, causing bronchoconstriction and vasodilatory shock.

Diminished or absent breath sounds. Reflects profound airflow limitation, such as in pneumothorax or severe asthma, where minimal ventilation reaches lung fields.

Stridor. Inspiratory crowing noise from turbulent flow through narrowed upper airway, often due to edema or obstruction.