Respiratory Assessment for Nurses: Lung Sounds, Oxygen Therapy, and Airway Management

A thorough respiratory assessment follows the sequence: inspection, palpation, percussion, auscultation. Most nurses jump straight to auscultation, but the first three steps give you critical information before you even touch the stethoscope. Inspection starts the moment you walk in the room. Count the respiratory rate over a full 60 seconds without telling the patient you are counting — awareness changes breathing patterns. Normal is 12-20 breaths per minute in adults. Look at the breathing pattern: is the chest expanding symmetrically? Is the patient using accessory muscles (sternocleidomastoid, intercostals, abdominals)? Accessory muscle use is one of the earliest visible signs of respiratory distress. Note the position — a patient who spontaneously assumes a tripod position (sitting upright, leaning forward, arms braced on knees) is working hard to breathe. Palpation checks for chest wall symmetry, tenderness, and tactile fremitus (vibrations felt when the patient says ninety-nine). Increased fremitus suggests consolidated lung tissue (pneumonia — the solid tissue transmits vibrations better than air). Decreased fremitus suggests air or fluid between the lung and chest wall (pneumothorax or pleural effusion). Percussion produces resonant sounds over healthy lung tissue and dull sounds over fluid or consolidation. Hyperresonance (an unusually loud, low-pitched sound) suggests trapped air — think COPD or pneumothorax. Auscultation is last. Listen in a systematic pattern: compare right to left at each level, moving from apices to bases. At least six comparison points: upper anterior, lower anterior, lateral, upper posterior, mid posterior, lower posterior. The patient should breathe deeply through an open mouth.

Normal breath sounds have three patterns. Vesicular sounds are soft, low-pitched, and heard over most of the lung fields — the inspiration phase is longer than expiration. Bronchovesicular sounds are moderate pitch, heard near the mainstem bronchi (between the scapulae posteriorly and over the upper sternum anteriorly) — inspiration and expiration are equal. Bronchial sounds are loud, high-pitched, and heard over the trachea — expiration is longer than inspiration. The critical point: bronchial sounds heard in the peripheral lung fields (where vesicular sounds should be) indicate consolidation — sound transmits differently through solid tissue than through air. Adventitious sounds are abnormal additions. Crackles (rales) are short, discontinuous popping or crackling sounds. Fine crackles sound like rubbing hair between your fingers near your ear — they suggest fluid in the alveoli (pulmonary edema, early pneumonia). Coarse crackles are louder and bubblier — they suggest fluid or mucus in the larger airways. Crackles that clear with coughing are usually mucus-related. Crackles that persist after coughing are more concerning for fluid (heart failure, ARDS). Wheezes are continuous, high-pitched, musical sounds caused by narrowed airways. Expiratory wheezes are the hallmark of asthma and COPD. Inspiratory wheezes suggest more severe obstruction. The terrifying scenario: a patient with severe asthma who was wheezing but suddenly becomes silent. Silent chest in the context of respiratory distress means air movement has decreased so severely that there is not enough flow to generate a wheeze. This is a medical emergency. Rhonchi are continuous, low-pitched, rumbling sounds caused by mucus in the larger airways. They often clear or change with coughing. Stridor is a high-pitched, crowing sound heard on inspiration — it indicates upper airway obstruction (croup in children, foreign body, laryngeal edema) and requires immediate attention. NurseIQ generates practice audio scenarios where you listen to lung sounds and identify the type, location, and likely clinical significance.

Oxygen delivery devices are divided into low-flow and high-flow systems. The critical distinction: low-flow devices deliver a variable FiO2 (the actual oxygen percentage the patient inhales depends on their breathing pattern), while high-flow devices deliver a fixed, precise FiO2. Low-flow devices: Nasal cannula delivers 24-44% FiO2 at flow rates of 1-6 L/min. The rough rule: each liter adds about 4% to FiO2 (1 L = 24%, 2 L = 28%, 6 L = 44%). Simple face mask delivers 40-60% FiO2 at 5-10 L/min — never run below 5 L/min because CO2 rebreathing occurs in the mask. Non-rebreather mask delivers 60-95% FiO2 at 10-15 L/min — it has a reservoir bag and one-way valves. The bag must remain inflated during inspiration. If it collapses, the flow rate is insufficient. High-flow devices: Venturi mask delivers a precise, adjustable FiO2 (24-60%) regardless of the patient's breathing pattern. Color-coded adapters set the FiO2 and corresponding flow rate. This is the device of choice for COPD patients who need precise oxygen delivery — too much oxygen can suppress their hypoxic respiratory drive. High-flow nasal cannula (HFNC) delivers heated, humidified oxygen at very high flow rates (up to 60 L/min) at precise FiO2 (21-100%). HFNC also generates a small amount of positive pressure, which helps keep alveoli open. Target SpO2: for most patients, 94-99%. For COPD patients with chronic CO2 retention, 88-92%. Overtreating COPD patients with high-flow oxygen is a common and dangerous mistake — the excess oxygen can suppress their respiratory drive, leading to CO2 narcosis, decreased consciousness, and respiratory arrest.

Respiratory failure does not happen suddenly in most cases — it follows a predictable deterioration pattern that gives you time to intervene if you know what to look for. Early signs: respiratory rate above 24 or below 10, mild accessory muscle use, SpO2 dropping below 94% on room air, increased anxiety or restlessness (the brain senses hypoxia before the numbers change), new-onset cough or change in sputum character. These signs warrant increasing assessment frequency, applying or titrating oxygen, and notifying the provider. Progressive signs: respiratory rate above 30 or below 8, moderate-to-severe accessory muscle use (visible intercostal retractions, nasal flaring), SpO2 below 90% despite oxygen therapy, inability to speak in full sentences, diaphoresis (sweating is an ominous respiratory sign because it indicates the sympathetic nervous system is activated in response to physiological stress). These signs warrant urgent provider notification, preparation for possible escalation to higher-level oxygen delivery or intubation, and continuous monitoring. Late/pre-arrest signs: gasping or agonal breathing, cyanosis (blue lips, nail beds), altered level of consciousness (confusion progressing to obtundation), paradoxical breathing (the chest moves inward during inspiration instead of outward — the diaphragm is fatiguing). These are emergencies requiring immediate activation of the rapid response team or code team. The clinical pearl that saves lives: a suddenly calm, drowsy patient who was previously anxious and tachypneic is getting worse, not better. The anxiety and tachypnea were compensatory responses. The calm drowsiness means the compensation is failing and CO2 is rising. This transition from agitated to quiet is often misread as improvement. It is the opposite. This content is for educational purposes only and does not constitute medical advice.