NLE Respiratory Nursing — Respiratory Assessment & DiagnosticsDetailed Explanation

Respiratory Physical Assessment: Inspection, Palpation, Percussion, and Auscultation

The respiratory physical assessment follows the classic sequence: Inspection → Palpation → Percussion → Auscultation (IPPA). Always compare both sides of the chest symmetrically — left versus right, anterior versus posterior. This systematic approach ensures no finding is missed and reflects professional nursing practice under NCM 103 and 104 (Medical-Surgical Nursing). **INSPECTION:** Observe the patient's rate, rhythm, depth, and effort of breathing. The normal adult respiratory rate is 12–20 breaths per minute. Any rate below 12 (bradypnea) or above 20 (tachypnea) is abnormal. Look for signs of increased work of breathing: use of accessory muscles (sternocleidomastoid, scalene), nasal flaring, intercostal and subcostal retractions, pursed-lip breathing, and the tripod position (leaning forward with hands on knees). These signs indicate the patient is struggling to breathe and require immediate attention. Check the skin and mucous membranes for cyanosis. Central cyanosis (blue discoloration of the lips and tongue) is a LATE sign of hypoxemia — it only becomes visible when approximately 5 g/dL of deoxygenated hemoglobin is present in the blood. Peripheral cyanosis (fingertips, nail beds) can be caused by poor perfusion, not necessarily low oxygen. Clubbing of the fingers (broadened, rounded fingertips) indicates CHRONIC hypoxemia, as seen in long-standing COPD, cystic fibrosis, or lung cancer. Observe chest shape: a barrel chest (increased anteroposterior diameter, like a barrel) suggests chronic air trapping, commonly seen in emphysema and COPD. Normal AP:lateral ratio is about 1:2; in barrel chest it approaches 1:1. **PALPATION:** Assess for tactile fremitus by placing the palms flat on the chest wall and asking the patient to say 'ninety-nine' (or 'siyamnapu't siyam' in Filipino practice). Vibrations are transmitted through solid or fluid-filled lung tissue. Fremitus INCREASES over consolidated areas (pneumonia — solid tissue transmits vibration well). Fremitus DECREASES over pleural effusion (fluid absorbs vibration), pneumothorax (air doesn't transmit vibration), or emphysema (overinflated, hyperresonant lung). Also palpate for chest expansion (place thumbs at the lower posterior thorax — they should move equally outward on deep inspiration), tracheal position (normally midline — deviation suggests tension pneumothorax, atelectasis, or large effusion), and any tenderness or crepitus. **PERCUSSION:** Tap the chest wall and listen to the sound produced. Normal lung tissue is RESONANT (hollow, drum-like sound). DULLNESS or flatness suggests fluid or consolidation (pleural effusion, pneumonia, hemothorax, tumor). HYPERRESONANCE suggests trapped air (pneumothorax, emphysema, asthma exacerbation). Memorize: Dull = Dense (fluid/solid); Hyper = Air (trapped). **AUSCULTATION:** Use a stethoscope to listen to breath sounds. Always proceed systematically from apex to base, comparing side to side. Normal breath sounds: • Vesicular sounds: soft, low-pitched, heard over most lung fields (like a gentle breeze). Inspiration longer than expiration. • Bronchovesicular sounds: medium pitch, heard over the main bronchi (near the sternum and scapulae). • Bronchial/Tracheal sounds: loud, high-pitched, heard over the trachea only. If heard over lung tissue, it indicates consolidation. Adventitious (abnormal) sounds: • Crackles (rales): discontinuous, popping/crackling sounds, like opening a Velcro strap or walking on dry leaves. They occur when collapsed or fluid-filled alveoli and small airways 'pop' open during inspiration. Found in pneumonia, pulmonary edema, heart failure, and pulmonary fibrosis. Fine crackles: high-pitched, late inspiratory (fibrosis, early pulmonary edema). Coarse crackles: lower-pitched, earlier in inspiration (pneumonia, secretions). • Wheezes: continuous, high-pitched, musical sounds from narrowed airways. Usually expiratory but can be inspiratory. Classic in asthma and COPD exacerbations. A wheeze that disappears (silent chest) in an asthma attack is WORSE — it means no air movement at all. • Rhonchi: low-pitched, rumbling, snoring sounds from secretions in the large airways. Often clear with coughing — unlike crackles which do not clear. • Stridor: a harsh, high-pitched crowing sound audible WITHOUT a stethoscope, heard during inspiration. It indicates UPPER AIRWAY OBSTRUCTION (croup, epiglottitis, foreign body, anaphylaxis, post-extubation laryngeal edema). This is a MEDICAL EMERGENCY requiring immediate intervention. • Pleural friction rub: a grating, leathery sound heard during both inspiration and expiration, caused by inflamed pleural surfaces rubbing together (pleurisy/pleuritis). Differentiate from a pericardial rub (which disappears when the patient holds their breath; pleural rub does not).

Arterial Blood Gas (ABG) Analysis Using the ROME Method

ABG analysis is one of the most critical and consistently tested skills on the NLE. It evaluates three key physiological parameters simultaneously: oxygenation (PaO2, SaO2), ventilation (PaCO2), and acid-base balance (pH, HCO3). The blood sample is drawn from an ARTERY (usually the radial artery) rather than a vein, because arterial blood has just left the lungs and reflects current respiratory function. **NORMAL ABG VALUES (Memorize these — they appear on almost every NLE board exam):** • pH: 7.35–7.45 (measure of acid-base balance) • PaCO2: 35–45 mmHg (carbon dioxide pressure — respiratory component) • HCO3⁻ (bicarbonate): 22–26 mEq/L (metabolic component) • PaO2: 80–100 mmHg (oxygen pressure — reflects oxygenation) • SaO2: 95–100% (oxygen saturation) **THE ROME METHOD (The most reliable systematic approach for the NLE):** Step 1 — DETERMINE THE pH: • pH < 7.35 = ACIDOSIS • pH > 7.45 = ALKALOSIS • pH 7.35–7.45 = Normal (but check if compensation is occurring) Step 2 — CHECK THE PaCO2 (Respiratory component): • PaCO2 > 45 = Too much CO2 = respiratory contribution to ACIDOSIS • PaCO2 < 35 = Too little CO2 = respiratory contribution to ALKALOSIS • ROME Rule: Respiratory OPPOSITE — pH and PaCO2 move in OPPOSITE directions for a primary respiratory disorder. - ↓ pH + ↑ PaCO2 = Respiratory Acidosis - ↑ pH + ↓ PaCO2 = Respiratory Alkalosis Step 3 — CHECK THE HCO3⁻ (Metabolic component): • HCO3 < 22 = Too little bicarbonate = metabolic contribution to ACIDOSIS • HCO3 > 26 = Too much bicarbonate = metabolic contribution to ALKALOSIS • ROME Rule: Metabolic EQUAL — pH and HCO3 move in the SAME direction for a primary metabolic disorder. - ↓ pH + ↓ HCO3 = Metabolic Acidosis - ↑ pH + ↑ HCO3 = Metabolic Alkalosis Step 4 — DETERMINE IF THERE IS COMPENSATION: • Uncompensated: Only one system (respiratory OR metabolic) is abnormal; pH is abnormal. • Partially compensated: Both PaCO2 AND HCO3 are abnormal (body is trying to correct), but pH is still outside normal range. • Fully compensated: Both PaCO2 and HCO3 are abnormal, but pH has returned to normal (7.35–7.45). Identify the PRIMARY disorder by which side of 7.40 the pH falls on (acidotic side = <7.40 means primary acidosis was the problem). **FOUR PRIMARY ABG DISORDERS WITH COMMON CAUSES:** 1. RESPIRATORY ACIDOSIS (↓pH, ↑PaCO2, HCO3 normal or ↑ if compensated) Cause: HYPOVENTILATION — CO2 builds up because the lungs are not expelling it. Clinical causes: COPD exacerbation, drug overdose (opioids, sedatives), respiratory muscle failure (Guillain-Barré, myasthenia gravis), severe pneumonia, CNS depression, obesity hypoventilation. Compensation: Kidneys retain HCO3 to buffer the acidosis (takes 2–3 days). 2. RESPIRATORY ALKALOSIS (↑pH, ↓PaCO2, HCO3 normal or ↓ if compensated) Cause: HYPERVENTILATION — CO2 is 'blown off' faster than it is produced. Clinical causes: Anxiety/panic attacks, pain, fever, early sepsis, pulmonary embolism, pregnancy (normal), mechanical ventilation set too high, salicylate poisoning (early stage), high altitude. Compensation: Kidneys excrete HCO3 (takes days). 3. METABOLIC ACIDOSIS (↓pH, ↓HCO3, PaCO2 normal or ↓ if compensated) Cause: Excess acid production or loss of base (bicarbonate). Clinical causes: Diabetic ketoacidosis (DKA), lactic acidosis (shock, sepsis), renal failure, diarrhea (loses HCO3), salicylate poisoning (late stage), adrenal insufficiency. Compensation: Lungs hyperventilate to blow off CO2 (Kussmaul breathing in DKA — rapid, deep breathing) — this is fast compensation (minutes to hours). 4. METABOLIC ALKALOSIS (↑pH, ↑HCO3, PaCO2 normal or ↑ if compensated) Cause: Excess base (bicarbonate) or loss of acid. Clinical causes: Persistent vomiting, nasogastric suctioning (both lose HCl), excessive antacid use, excessive diuretic use (loop diuretics cause hypokalemia and metabolic alkalosis), massive blood transfusion (citrate metabolizes to bicarbonate). Compensation: Lungs hypoventilate to retain CO2 (limited and slow). **PROCEDURE AND NURSING CARE AFTER ARTERIAL PUNCTURE:** • Perform the ALLEN TEST before radial artery puncture to confirm adequate collateral circulation via the ulnar artery. Occlude both radial and ulnar arteries, have patient clench fist, release ulnar artery — the hand should pink up within 6 seconds (positive Allen test = safe to proceed). • Use a heparinized syringe; collect on ice if transport time >15 minutes. • After puncture: Apply FIRM DIRECT PRESSURE for AT LEAST 5 MINUTES (longer if the patient is anticoagulated — up to 15–20 minutes). This prevents hematoma formation. • Label the sample immediately with the patient's name, time, FiO2 being delivered, and the patient's current temperature. • Monitor the puncture site for hematoma, excessive bleeding, and neurovascular compromise distal to the site.

Pulse Oximetry and Pulmonary Function Tests (PFTs/Spirometry)

**PULSE OXIMETRY (SpO2):** Pulse oximetry is a non-invasive, continuous method of estimating arterial oxygen saturation (SaO2). The probe, usually placed on a finger, toe, or ear lobe, shines red and infrared light through tissue and measures the ratio of oxygenated to deoxygenated hemoglobin based on light absorption. It displays SpO2 (an estimate of SaO2) and heart rate. Normal SpO2: 95–100%. Values of 90–94% indicate mild hypoxemia and require assessment and possible supplemental oxygen. Values <90% indicate significant hypoxemia requiring immediate intervention. CRITICAL LIMITATIONS OF PULSE OXIMETRY: 1. CARBON MONOXIDE POISONING: CO binds to hemoglobin like O2 and is detected by the oximeter as oxyhemoglobin. SpO2 will read FALSELY HIGH (often 99–100%) even though the patient is severely hypoxic. Diagnosis requires CO-oximetry (co-oximeter measures carboxyhemoglobin directly). 2. POOR PERFUSION: Cold hands, hypotension, vasoconstrictors, or peripheral vascular disease reduce perfusion to the probe site and produce inaccurate or absent readings. 3. NAIL POLISH AND ARTIFICIAL NAILS: Dark colors (blue, black, green) and acrylic nails interfere with light transmission. Remove nail polish or use an alternative site (earlobe). 4. MOTION ARTIFACT: Patient movement causes false readings. 5. ANEMIA: SpO2 can be normal even with severe anemia — the available hemoglobin is fully saturated, but there is not enough of it. 6. MOST CRITICAL: SpO2 measures SATURATION, NOT VENTILATION. A patient can have a normal SpO2 while retaining CO2 (as in an obese post-op patient or a COPD patient). You cannot use SpO2 alone to assess CO2 — you need an ABG for that. **PULMONARY FUNCTION TESTS (PFTs) / SPIROMETRY:** PFTs are the gold standard for diagnosing and classifying lung disease. A spirometer measures volumes and flow rates of air. The two most important measurements for the NLE are: • FEV1 (Forced Expiratory Volume in 1 second): The volume of air that can be forcibly exhaled in the first second of a maximal expiration. Reflects airway resistance — reduced in obstructive disease. • FVC (Forced Vital Capacity): The total volume of air that can be forcibly exhaled after a maximal inspiration. Reflects lung and chest wall compliance — reduced in restrictive disease. • FEV1/FVC RATIO: The percentage of FVC exhaled in the first second. This is THE KEY DISCRIMINATOR between obstructive and restrictive disease. **OBSTRUCTIVE LUNG DISEASE (Asthma, COPD, Bronchiectasis, Cystic Fibrosis):** • The airways are narrowed → air cannot get OUT easily → FEV1 is reduced • FVC is relatively preserved (or also reduced, but less so) • FEV1/FVC RATIO is REDUCED (<70%) • Think of blowing through a narrowed straw — you can't exhale quickly • In ASTHMA: FEV1/FVC improves by ≥12% after bronchodilator (REVERSIBLE obstruction) • In COPD: FEV1/FVC does NOT fully reverse with bronchodilator (IRREVERSIBLE obstruction) **RESTRICTIVE LUNG DISEASE (Pulmonary Fibrosis, Pleural Effusion, Kyphoscoliosis, Obesity, Pregnancy, Diaphragm disorders):** • The lungs or chest wall cannot fully EXPAND → total lung volume is reduced • Both FEV1 and FVC are reduced • FEV1/FVC RATIO is NORMAL or INCREASED (because both fall proportionally, or FVC falls more) • Think of breathing with a tight chest binder — you can't take a big breath in **PEAK EXPIRATORY FLOW RATE (PEFR) — for Asthma Monitoring:** PEFR is the maximum flow rate during a forced expiration, measured with a simple peak flow meter. It is used primarily at HOME by asthma patients. The traffic-light zone system: • GREEN ZONE (≥80% of personal best): Good control — continue maintenance medications • YELLOW ZONE (50–79% of personal best): Caution — use rescue bronchodilator (salbutamol/albuterol); increase monitoring; may need step-up therapy • RED ZONE (<50% of personal best): Emergency — use rescue inhaler; seek emergency medical care immediately Patients establish their 'personal best' PEFR when their asthma is well-controlled, and all future readings are compared to this value. Teach patients: measure PEFR at the same time daily (usually morning, before medications); keep a log; know the zones; act on results.

Oxygen Therapy: Delivery Devices, FiO2, and Safety

Oxygen (O2) is considered a DRUG in clinical practice and, under RA 9173 and hospital protocols, requires a physician's order in most Philippine healthcare settings (though nurses can initiate O2 in emergencies). Understanding which oxygen delivery device to use — and at what flow rate — is critical for patient safety and is a consistently tested NLE topic. FiO2 = Fraction of Inspired Oxygen — the percentage of oxygen in the air the patient breathes. Room air FiO2 = 21%. The goal of oxygen therapy is to correct hypoxemia and relieve the work of breathing. **LOW-FLOW SYSTEMS (Variable FiO2 — changes with the patient's breathing pattern):** In low-flow systems, the device delivers less gas than the patient's inspiratory flow rate, so the patient also breathes in some room air. The more the patient breathes, the more room air is entrained, lowering the effective FiO2. 1. NASAL CANNULA: • FiO2: approximately 24–44% at 1–6 L/min • Rule of thumb: Each liter increase adds ~4% FiO2 (1L=24%, 2L=28%, 3L=32%, 4L=36%, 5L=40%, 6L=44%) • Best for: Mild hypoxemia, patients who need to eat, talk, or are ambulatory • Comfort level: HIGHEST — most comfortable and well-tolerated • Important: FLOWS ABOVE 6 L/min do NOT significantly increase FiO2 but DO cause mucosal drying and nosebleeds. Add humidification above 4 L/min. NEVER use more than 6 L/min via nasal cannula. 2. SIMPLE FACE MASK: • FiO2: approximately 40–60% at 5–10 L/min • MINIMUM FLOW: 5 L/min is REQUIRED to flush exhaled CO2 out of the mask. Below 5 L/min, CO2 accumulates in the mask and the patient rebreathes it. • Holes on the sides of the mask allow exhalation and room air entrainment. • Less comfortable than nasal cannula; patient cannot eat with mask on. 3. PARTIAL REBREATHER MASK (Mask + Reservoir Bag): • FiO2: approximately 60–80% at 6–11 L/min • Has a reservoir bag but NO one-way valves on the exhalation ports • Patient rebreathes the FIRST PORTION of exhaled breath (which contains mostly dead-space gas — high O2, low CO2) along with reservoir oxygen • Key: Keep the reservoir bag INFLATED — it should NOT fully collapse on inspiration. If it collapses, increase flow. • Note: The bag does NOT need to be fully rigid — some deflation (1/3 to 1/2) on peak inspiration is acceptable. 4. NON-REBREATHER MASK (NRM): • FiO2: approximately 80–95% at 10–15 L/min (highest FiO2 of any low-flow device) • Has a reservoir bag + ONE-WAY VALVES on exhalation ports • One-way valves prevent exhaled air from entering the reservoir bag → patient only breathes reservoir oxygen • Used for: Severe hypoxemia, emergency situations, CO poisoning, near-drowning, trauma • Key nursing action: KEEP THE RESERVOIR BAG INFLATED — it must never fully collapse; if it does, increase flow immediately. • Note: A 'true' non-rebreather with all ports sealed delivers near 100% O2, but in practice 80–95% is achieved. **HIGH-FLOW / FIXED-PERFORMANCE SYSTEM:** 5. VENTURI MASK (Venti-mask): • FiO2: PRECISE, FIXED percentages — 24%, 28%, 31%, 35%, 40%, 50% • Regardless of the patient's breathing pattern, FiO2 is consistent and accurate • Mechanism: Uses the Bernoulli principle — high-flow oxygen through a narrow jet entrains a fixed amount of room air, diluting O2 to the prescribed FiO2 • Color-coded adapters correspond to FiO2: 24% (blue), 28% (yellow), 31% (white), 35% (green), 40% (pink), 50% (orange) — though colors may vary by manufacturer • DEVICE OF CHOICE FOR COPD: Because these patients need precise, low-concentration O2 (24–28%) to avoid suppressing their hypoxic drive • Also used for patients who need consistent FiO2 for accurate ABG interpretation **HIGH-FLOW NASAL CANNULA (HFNC):** Delivers heated, humidified oxygen at flows up to 60 L/min with adjustable FiO2. Not always available in all Philippine settings but increasingly used in ICUs. Provides positive airway pressure effect and excellent humidification. **OXYGEN THERAPY IN COPD — THE HYPOXIC DRIVE CONCEPT:** In healthy individuals, the primary stimulus to breathe is rising CO2 (hypercapnic drive). However, in some chronic COPD patients with long-term CO2 retention (chronic respiratory acidosis), the CO2 receptors have adapted and become less sensitive. These patients rely on LOW OXYGEN levels (hypoxia) as their primary drive to breathe — this is the HYPOXIC DRIVE. If these patients receive HIGH-FLOW O2 (FiO2 >28–35%), the hypoxic drive is removed → respiratory rate decreases → CO2 accumulates further → CO2 narcosis (drowsiness, confusion, coma). This is called the HALDANE EFFECT. Therefore, for COPD patients: • Target SpO2 = 88–92% (NOT the usual 94–98%) • Use VENTURI MASK at 24–28% or nasal cannula at 1–2 L/min • Monitor closely for signs of CO2 narcosis (drowsiness, confusion, CO2 rising on ABG) • IMPORTANT: Never withhold oxygen from a severely hypoxic COPD patient — the immediate danger of hypoxia exceeds the risk of CO2 retention. Titrate carefully. **OXYGEN SAFETY PRECAUTIONS:** • NO SMOKING within 3 meters (10 feet) of oxygen equipment • No open flames, candles, or combustibles near oxygen • Post 'NO SMOKING / OXYGEN IN USE' signs at the bedside and room entrance • Secure oxygen cylinders upright (chain to wall) to prevent tipping and valve damage • Never grease or oil oxygen equipment (fire risk with compressed oxygen) • Provide humidification for flows >4 L/min via nasal cannula and always with face masks to prevent mucosal drying • Monitor for skin breakdown: check behind the ears (nasal cannula tubing), over the nose (mask), and around the cheeks • Use foam padding or skin protectors at pressure points

Chest Tubes and Water-Seal Drainage Systems

A chest tube (thoracostomy tube) is a flexible plastic tube inserted through the chest wall into the pleural space to drain abnormal accumulations and restore normal negative intrapleural pressure, which is essential for lung expansion. Chest tubes are inserted to drain: • AIR → Pneumothorax • FLUID → Pleural effusion or transudate • BLOOD → Hemothorax (post-trauma, post-thoracic surgery) • PUS → Empyema (infected pleural fluid) Placement site varies based on what is being drained: AIR rises, so tubes for pneumothorax are placed ANTERIORLY at the 2nd intercostal space, midclavicular line. FLUID sinks, so drainage tubes are placed POSTERIORLY at the 4th–5th intercostal space, midaxillary line. However, in practice, many tubes are placed at the 4th–5th ICS midaxillary line for both. **THE THREE-CHAMBER WATER-SEAL DRAINAGE SYSTEM:** The traditional Pleur-evac® or similar commercial systems are based on the classic three-bottle system. Understanding each chamber's function is essential for troubleshooting. CHAMBER 1 — COLLECTION CHAMBER (rightmost, closest to patient): • Collects all drainage from the pleural space • Monitor: AMOUNT (measure in mL), COLOR (serous = clear/yellow; serosanguineous = pink-tinged; sanguineous = bright red blood; purulent = yellow-green/turbid in empyema), and RATE of drainage • Mark the level with tape on the outside of the chamber every 1–4 hours (or per facility protocol), noting the time • Abnormal: >100–200 mL/hour of bright red blood = possible active hemorrhage → notify physician IMMEDIATELY CHAMBER 2 — WATER-SEAL CHAMBER (middle chamber): • Contains water (usually filled to 2 cm mark) that acts as a ONE-WAY VALVE • Mechanism: Air/fluid can exit the pleural space (pushes through the water from below), but air CANNOT re-enter (water prevents backflow) • NORMAL FINDING: TIDALING (also called fluctuation) — the water level rises during inspiration (negative intrathoracic pressure draws water up) and falls during expiration. This is EXPECTED and confirms the system is patent and connected to the pleural space. • ABNORMAL: Sudden CESSATION of tidaling may mean: (a) the lung has FULLY RE-EXPANDED (good — no more air space) OR (b) the tube is KINKED, CLOGGED, or COMPRESSED (bad). Always assess the patient first. • INTERMITTENT BUBBLING in the water-seal during expiration or coughing = NORMAL when a pneumothorax is present and air is being evacuated • CONTINUOUS BUBBLING (non-stop, both inspiration and expiration) = AIR LEAK — this is ABNORMAL and requires investigation CHAMBER 3 — SUCTION-CONTROL CHAMBER (leftmost chamber): • CONTROLS THE AMOUNT OF SUCTION applied to the system • WET SUCTION SYSTEM: Amount of suction is determined by the WATER LEVEL in the chamber (usually 20 cm of water = -20 cm H2O suction), NOT by the wall suction setting. The wall suction is turned up until you see gentle continuous bubbling in this chamber — that confirms active suction is working. • DRY SUCTION SYSTEM: Uses a dial or spring mechanism instead of water; easier to manage • IMPORTANT: DO NOT confuse suction-control chamber bubbling (gentle, normal) with water-seal chamber bubbling (continuous = air leak) **TROUBLESHOOTING — HIGH-YIELD FOR NLE:** FINDING: Continuous bubbling in the WATER-SEAL chamber → AIR LEAK. Locate and fix. → Troubleshooting steps: (1) Check all connections — tighten any loose connections. (2) Inspect the insertion site — is the chest tube dressing intact? (3) If you clamp the tube BRIEFLY just below the insertion site and bubbling STOPS → leak is at the insertion site or within the patient (expected in pneumothorax). If bubbling CONTINUES when clamped → leak is in the drainage system/tubing. → Report to physician if unable to correct. FINDING: No tidaling (fluctuation stopped) → Check if the lung has re-expanded (get chest X-ray to confirm) OR troubleshoot for kinking/clogging. Reposition the patient, check all tubing for kinks. Gently milk the tube if ordered — do NOT routinely strip or milk without an order. FINDING: Drainage system accidentally knocked below AND on the floor → Immediately LIFT back to below chest level. Check connections. Monitor patient. FINDING: Excessive drainage (>200 mL/hour, bright red) → Possible hemothorax or active surgical bleeding. Notify physician immediately. Prepare for possible blood transfusion or return to OR. **CRITICAL NURSING ACTIONS:** 1. ALWAYS KEEP THE DRAINAGE SYSTEM BELOW THE LEVEL OF THE CHEST (at least 45–60 cm below) to prevent drainage from flowing back into the pleural space. 2. DO NOT ROUTINELY CLAMP THE CHEST TUBE. If there is an ongoing air leak (pneumothorax), clamping can cause TENSION PNEUMOTHORAX by trapping air in the pleural space with nowhere to escape. 3. DO NOT ROUTINELY MILK OR STRIP THE TUBING — this creates high negative pressure that can damage pleural tissue. Strip only if specifically ordered by the physician (used only for blood clots in cardiac surgery cases). 4. If the system is DISCONNECTED accidentally: SUBMERGE THE DISTAL END OF THE TUBE into a container of sterile water or saline to re-establish a water seal temporarily, then replace the drainage system. Keep sterile water and extra clamps at the bedside. 5. Encourage DEEP BREATHING AND COUGHING — this creates increased negative intrapleural pressure that helps re-expand the lung and promotes drainage. 6. AMBULATE patients with chest tubes SAFELY — the drainage system must remain upright and BELOW chest level at all times. **IF THE CHEST TUBE IS ACCIDENTALLY PULLED OUT (DISLODGED):** • Immediately cover the insertion site with your GLOVED HAND, then apply a STERILE OCCLUSIVE DRESSING TAPED ON THREE SIDES (leave one side open) • The three-sided dressing creates a FLUTTER VALVE effect: the open side allows air to ESCAPE (preventing tension pneumothorax) but prevents air from ENTERING on inspiration • Taping ALL FOUR SIDES would seal the wound completely and trap air, potentially causing tension pneumothorax • Notify the physician IMMEDIATELY • Monitor for signs of tension pneumothorax: tracheal deviation, absent breath sounds on affected side, severe hypotension, distended neck veins, cyanosis **SIGNS OF TENSION PNEUMOTHORAX (Medical Emergency):** • Tracheal deviation AWAY from the affected side • Absent breath sounds on the affected side • Severe respiratory distress and hypoxemia • Hypotension and tachycardia • Distended neck veins (JVD) • Cyanosis • This is a MEDICAL EMERGENCY — immediate needle decompression (2nd ICS, midclavicular line) is required, followed by chest tube insertion.

Chest X-Ray Interpretation and Nursing Responsibilities

The chest X-ray (CXR) is the most commonly ordered thoracic imaging study and a routine part of respiratory assessment. While diagnosis is the physician's or radiologist's responsibility, nurses must understand basic CXR findings to correlate with clinical assessment, monitor changes, and detect emerging complications. **NURSING RESPONSIBILITIES FOR CXR:** • Remove all metal objects and jewelry from the patient (metal creates artifacts that obscure the image) • Confirm the patient is NOT pregnant before the X-ray (radiation risk to fetus). If pregnant and CXR is unavoidable, shield the abdomen with a lead apron. • PA (Posterior-Anterior) view is standard — patient stands with chest against the film, X-ray beam enters from behind. AP (Anterior-Posterior) is done when patient cannot stand (portable/bedside). AP films appear slightly different (heart looks larger due to magnification). • No special preparation is required (no fasting, no special medications) • For portable bedside X-rays: clear the area, position the patient (sitting or semi-Fowler's for best quality), place the film plate behind the patient's back, and ensure no metal objects are in the field **COMMON CXR FINDINGS BY CONDITION (HIGH-YIELD NLE):** 1. NORMAL CXR: Lungs appear dark (air-filled); costophrenic angles are sharp and clear; heart occupies no more than 50% of the chest width (cardiothoracic ratio ≤0.5); trachea is midline. 2. PNEUMONIA/CONSOLIDATION: Areas of INCREASED density (white/opaque patches) called infiltrates or consolidation — reflect replacement of air with exudate/pus. Lobar consolidation = entire lobe is opaque (classic bacterial pneumonia). Interstitial pattern = diffuse, fine reticular markings (atypical/viral pneumonia, pulmonary fibrosis). 3. PLEURAL EFFUSION: BLUNTED (flattened/obliterated) costophrenic angles. A visible fluid line (meniscus sign) in upright films. Large effusions cause opacification of the lower lung field and may cause mediastinal shift TOWARD the effusion (unlike tension pneumothorax which shifts AWAY). 4. PNEUMOTHORAX: INCREASED lucency (darker than normal) on the affected side with a VISIBLE PLEURAL LINE (edge of the collapsed lung visible as a thin white line). No lung markings are seen beyond this line. In TENSION PNEUMOTHORAX: mediastinal shift AWAY from the affected side (the heart and trachea deviate to the opposite side). Tracheal deviation is one of the most dramatic and recognizable CXR signs. 5. COPD/EMPHYSEMA: HYPERINFLATION — lungs appear larger and darker than normal. FLATTENED DIAPHRAGMS (normally dome-shaped; in COPD they become flat or even inverted). Increased AP diameter on lateral view. Barrel-shaped chest. Bullae (large air pockets) may be visible. 6. PULMONARY EDEMA: Diffuse bilateral infiltrates in a butterfly or bat-wing pattern around the hilum. Kerley B lines (short horizontal lines at the lung periphery = interstitial edema). Cardiomegaly (enlarged heart silhouette) if cardiac cause. Vascular redistribution (more prominent upper lobe vessels). 7. ENDOTRACHEAL TUBE (ETT) PLACEMENT: The tip of the ETT should be 3–5 cm ABOVE the CARINA (where the trachea bifurcates into the two main bronchi). If the ETT is too low, it may preferentially intubate one bronchus (usually the right main bronchus — it is wider and more vertical) causing unilateral lung ventilation and atelectasis of the other lung. 8. CENTRAL VENOUS CATHETER (CVC): The tip should be in the SUPERIOR VENA CAVA (SVC), just above the right atrium. Misplacement can cause arrhythmias (in the heart) or pneumothorax (if lung is perforated during insertion). 9. ATELECTASIS: Increased density (white area) in a linear/band-like or lobar distribution. Volume loss on the affected side (structures shift toward the atelectasis, unlike pleural effusion/pneumothorax which push structures away).

STEP 1 — pH 7.28 = ACIDOSIS. STEP 2 — PaCO2 62 = HIGH (abnormal); pH low + CO2 high = OPPOSITE = Respiratory cause = RESPIRATORY ACIDOSIS. STEP 3 — HCO3 28 = HIGH (above normal 22–26). The kidneys have retained bicarbonate to compensate for the acidosis (Metabolic EQUAL: HCO3 moves up trying to bring pH up). STEP 4 — BOTH PaCO2 and HCO3 are abnormal, but pH is still abnormal = PARTIALLY COMPENSATED respiratory acidosis. For oxygen: This COPD patient has CO2 retention (demonstrated by high PaCO2). He may rely on hypoxic drive. Use a VENTURI MASK at 24% or 28% FiO2. Target SpO2 88–92% (NOT 94–98%). Monitor closely for worsening drowsiness and rising CO2. Prepare for possible NIPPV if the patient does not improve. DO NOT give a non-rebreather mask or high-flow oxygen, as this could further suppress his respiratory drive and worsen hypercapnia.

STEP 1 — pH 7.52 = ALKALOSIS. STEP 2 — PaCO2 26 = LOW (abnormal); pH high + CO2 low = OPPOSITE = Respiratory cause = RESPIRATORY ALKALOSIS. STEP 3 — HCO3 22 = NORMAL. STEP 4 — Only respiratory component abnormal = UNCOMPENSATED. Cause: Anxiety-driven hyperventilation blows off excessive CO2, raising pH. Symptoms: Dizziness (cerebral vasoconstriction from low CO2) and perioral/digital tingling (carpopedal spasm from low ionized calcium in alkalosis). Nursing interventions: (1) Ensure patient safety — prevent falls from dizziness. (2) Speak calmly and reassure. (3) Guide slow, controlled breathing (breathe in for 4 counts, out for 4 counts). (4) In a controlled clinical setting, rebreathing into a paper bag may be used briefly to raise CO2. (5) Address the anxiety trigger. (6) Re-check ABG after intervention. (7) Document findings and interventions.

CONCERN 1 — DRAINAGE RATE: 175 mL/hour of dark red blood is above the threshold of 100–200 mL/hour that warrants immediate physician notification. This suggests possible post-operative bleeding (hemothorax). Priority actions: Notify the surgeon IMMEDIATELY. Monitor vital signs (BP, HR, RR, SpO2) for signs of hemodynamic instability. Prepare for potential blood transfusion or return to operating room. Continue marking drainage levels every 30–60 minutes. CONCERN 2 — ABSENT TIDALING: This may indicate the lung has re-expanded (expected post-lung resection) OR the tube is kinked or compressed. Actions: Visually inspect the entire length of tubing for kinks, compression under the patient, or dependent loops. Reposition the patient. Do NOT clamp or strip the tube without a physician order. Notify physician. Request a portable chest X-ray to confirm lung re-expansion status. INTERMITTENT BUBBLING: This is NORMAL — post-operatively, some air may still be present in the pleural space and is being evacuated. This is not an air leak (which would be CONTINUOUS).

This is a RESPIRATORY EMERGENCY. The open chest wound is acting as a 'sucking chest wound' — air enters the pleural space with each breath, collapsing the left lung (open pneumothorax). STEP 1: Immediately cover with your gloved hand to stop air entry while preparing the dressing. STEP 2: Apply a STERILE OCCLUSIVE DRESSING TAPED ON THREE SIDES only. The three-sided seal creates a flutter valve: the open (fourth) side allows air to escape on expiration (preventing tension pneumothorax) while the sealed sides prevent air from rushing in on inspiration. DO NOT tape all four sides — this would seal air in and can cause life-threatening tension pneumothorax. STEP 3: Apply supplemental oxygen (non-rebreather mask if available, targeting SpO2 94–98%) to treat hypoxemia. STEP 4: Notify the physician IMMEDIATELY for chest tube reinsertion. STEP 5: Monitor closely for developing tension pneumothorax (tracheal deviation to the RIGHT, absent breath sounds on the left, worsening hypotension, distended neck veins, worsening cyanosis). Position the patient: elevate head of bed 30–45 degrees. Document all events, actions, and patient response.

ABG A (pH 7.48, CO2 32, HCO3 23): pH=ALKALOSIS. CO2=LOW (abnormal); pH high + CO2 low = OPPOSITE = Respiratory Alkalosis. HCO3=NORMAL = no compensation. → UNCOMPENSATED Respiratory Alkalosis. Cause: Hyperventilation (anxiety, pain, early sepsis, PE, mechanical ventilator set too high). ABG B (pH 7.33, CO2 40, HCO3 17): pH=ACIDOSIS. CO2=NORMAL (not the primary problem). HCO3=LOW (abnormal); pH low + HCO3 low = EQUAL = Metabolic Acidosis. CO2 normal = no respiratory compensation yet (or early). → UNCOMPENSATED Metabolic Acidosis. Cause: DKA, diarrhea, renal failure, lactic acidosis (shock). ABG C (pH 7.38, CO2 50, HCO3 29): pH=NORMAL (but on the acidotic side of 7.40). CO2=HIGH (abnormal) — respiratory acidosis present. HCO3=HIGH (abnormal) — kidneys have retained HCO3 to compensate. pH returned to normal. → FULLY COMPENSATED Respiratory Acidosis. Cause: Chronic COPD with chronic CO2 retention (CO2 chronically elevated, kidneys have fully compensated). ABG D (pH 7.46, CO2 42, HCO3 30): pH=ALKALOSIS. CO2=NORMAL. HCO3=HIGH (abnormal); pH high + HCO3 high = EQUAL = Metabolic Alkalosis. CO2 normal = no respiratory compensation. → UNCOMPENSATED Metabolic Alkalosis. Cause: Persistent vomiting, NGT suction, excessive diuretics.