Respiratory

The practical nurse's scope is implementation on stable, predictable clients — established procedures, ongoing data collection and reinforcement of teaching. What does not transfer are the bookends of the nursing process: the initial assessment that establishes the baseline, the plan of care built from it, and the evaluation that decides whether the plan is working. Assignment decisions therefore turn on client stability and predictability rather than on the technical difficulty of the task. An unstable client, a first-time procedure or a situation requiring interpretation stays with the registered nurse.

Chronic obstructive pulmonary disease combines airflow limitation with air trapping and, in advanced disease, chronic carbon dioxide retention with a compensated respiratory acidosis. Clients live at saturations lower than most people, and their kidneys have compensated by retaining bicarbonate. Administering oxygen well above their usual level can raise carbon dioxide by several mechanisms, so supplemental oxygen is titrated to a target commonly given as 88 to 92 percent rather than to the highest achievable value. Rising carbon dioxide presents as increasing drowsiness, confusion, headache and eventually a fall in level of consciousness — a client on oxygen who becomes progressively harder to rouse needs an arterial blood gas, not more oxygen. The old teaching that these clients breathe purely on hypoxic drive overstates one mechanism and has been used to justify withholding oxygen, which causes harm. Wider care covers bronchodilators, pursed-lip breathing to prolong exhalation, positioning forward with arms supported, energy conservation, smoking cessation, vaccination, and nutrition, since the work of breathing raises calorie needs while breathlessness reduces intake.

Long-term home oxygen therapy improves survival in clients with chronic hypoxemia, and its safe use depends on teaching. Fire safety dominates: oxygen is not itself flammable but supports combustion vigorously, so smoking is prohibited for the client and everyone in the home, signs are displayed, open flames including gas stoves, candles and fireplaces are kept well away, and petroleum-based lubricants, oils and some aerosols are avoided, with water-based products used for nasal dryness. Equipment is kept away from heat, cylinders stored upright and secured, and adequate ventilation maintained; a functioning smoke detector and fire extinguisher are recommended. Flow rate is prescribed and not adjusted by the client, since in advanced COPD excessive oxygen can worsen carbon dioxide retention — clients are taught to contact the provider rather than self-titrate when breathlessness increases, because increasing breathlessness itself needs assessment. Practical teaching covers humidification where needed, skin care behind the ears and around the nares, cannula and tubing changes, use of portable systems, backup supply and power failure planning, and pursed-lip breathing and energy conservation alongside the oxygen.

Hypoxemia produces a predictable progression. Early compensatory signs include restlessness, anxiety, irritability, tachypnea, tachycardia, mild hypertension, dyspnea and use of accessory muscles; the client is working to maintain oxygenation and largely succeeding. As hypoxemia worsens, confusion, lethargy, dysrhythmia and hypertension progressing to hypotension appear. Late signs indicate decompensation: bradycardia, cyanosis, extreme lethargy or unresponsiveness, and eventually respiratory and cardiac arrest. Cyanosis requires approximately 5 g/dL of deoxygenated hemoglobin to become visible, so it appears late and may never appear in a profoundly anemic client, while a client with polycythemia may appear cyanosed with better oxygenation than expected — which is why it is a poor monitoring parameter. Pulse oximetry is more reliable but is affected by perfusion, motion, nail polish and carbon monoxide, which produces falsely reassuring readings. In chronic carbon dioxide retention, rising drowsiness rather than falling saturation may be the significant change. The clinical implication throughout is that new restlessness in a client at risk is treated as hypoxia and assessed rather than sedated.

Fixed-performance devices deliver a known oxygen concentration independent of the client's respiratory pattern.

Oxygen delivery devices differ in whether the delivered concentration is fixed or varies with the client's breathing pattern.

Pulmonary embolism most often arises from deep vein thrombosis in the legs or pelvis, and postoperative orthopedic clients carry high risk because all three elements of Virchow's triad are present. Classic presentation is sudden dyspnea, pleuritic chest pain, tachycardia, anxiety and hypoxia, sometimes with cough or hemoptysis; a massive embolism produces hypotension and cardiac arrest. Presentation may be subtle, and unexplained tachycardia or a fall in saturation may be the only sign. Immediate management is oxygen, minimizing exertion, continuous monitoring, and urgent medical assessment, with anticoagulation once diagnosis is established and thrombolysis or embolectomy considered for massive embolism. Prevention is the more important half of the topic and covers early mobilization, mechanical compression devices, pharmacological prophylaxis, and adequate hydration. Deep vein thrombosis itself may present with calf pain, swelling, warmth and erythema, and the affected limb is not massaged.

Oxygen does not burn, but it makes everything else burn faster, hotter and more readily. The entire risk of home oxygen therapy is proximity to ignition, and the great majority of oxygen-related fires involve smoking. Safety teaching therefore covers distance from flames, heaters and gas stoves; an absolute prohibition on smoking in the home; avoidance of petroleum-based lubricants, oils and aerosols near the client; cotton rather than synthetic or wool clothing; and functioning smoke alarms. Cylinders are stored upright, secured, in a cool ventilated place, and the prescribed flow rate is not adjusted by the client.

Arterial blood gas interpretation follows a fixed sequence. Assess the pH against 7.35 to 7.45, identifying acidosis or alkalosis. Then examine PaCO2 against 35 to 45 and bicarbonate against 21 to 28, and determine which moves in the direction that would produce the observed pH: carbon dioxide is acidic, so a raised value causes acidosis; bicarbonate is alkaline, so a raised value causes alkalosis. The value that matches the pH direction identifies the primary disorder as respiratory or metabolic. The other value, if also abnormal, is compensating — and compensation is partial while the pH remains outside the normal range, and full once it has returned to normal even though both other values remain deranged. Compensation is by the opposite system and takes time: respiratory compensation for a metabolic problem occurs within minutes to hours through changes in ventilation, while renal compensation for a respiratory problem takes days, which is why chronically retaining COPD clients show a substantially raised bicarbonate. Oxygenation is assessed separately from acid-base status, using PaO2 and saturation.

Asthma exacerbation involves bronchoconstriction, mucosal edema and mucus plugging, producing expiratory wheeze, cough, chest tightness and dyspnea. Severity is judged by the client rather than by any single finding: ability to speak in sentences, phrases or single words; use of accessory muscles and tripod positioning; respiratory and heart rate; oxygen saturation; and peak expiratory flow against the client's personal best. A silent chest, exhaustion, cyanosis, a falling respiratory rate in a tiring client, altered consciousness, and a normal or rising arterial carbon dioxide all indicate life-threatening asthma — the last because a client with severe asthma should be hyperventilating and blowing carbon dioxide off, so a normal value means they are no longer able to. Treatment is high-flow oxygen, repeated or continuous short-acting beta-agonist with an anticholinergic, systemic corticosteroid early, and consideration of magnesium sulfate, with preparation for ventilatory support. Sedatives are avoided because they depress the drive the client is relying on.

A chest drainage system removes air or fluid from the pleural space and prevents its return, allowing the lung to re-expand. The water seal acts as a one-way valve: air can bubble out through the water, and none can be drawn back in. Gentle tidaling with respiration confirms communication with the pleural space; sudden cessation means either successful re-expansion, confirmed on imaging, or an obstruction. Intermittent bubbling in the water seal chamber during expiration or coughing is expected while air is still being removed, while continuous bubbling indicates a leak somewhere in the system, checked by working from the client toward the unit. The unit stays upright and below chest level at all times, including during transport. Clamping is avoided except very briefly for specific purposes such as changing the unit, because it converts an open pneumothorax into a closed one. Routine stripping or milking generates dangerously high negative pressure and is not done. If the tube is dislodged from the chest, an occlusive dressing taped on three sides allows air to escape without being drawn in; if the system is disconnected, the tube end is placed in sterile water while a new unit is obtained.

A chest drainage system works by gravity, so it is kept below the level of the chest, and pain control is what enables the deep breathing that re-expands the lung.

Expiratory airflow obstruction produces air trapping, prolonged expiration and chest hyperinflation.

Hypoxemia produces a predictable progression. Early compensatory signs include restlessness, anxiety, irritability, tachypnea, tachycardia, mild hypertension, dyspnea and use of accessory muscles; the client is working to maintain oxygenation and largely succeeding. As hypoxemia worsens, confusion, lethargy, dysrhythmia and hypertension progressing to hypotension appear. Late signs indicate decompensation: bradycardia, cyanosis, extreme lethargy or unresponsiveness, and eventually respiratory and cardiac arrest. Cyanosis requires approximately 5 g/dL of deoxygenated hemoglobin to become visible, so it appears late and may never appear in a profoundly anemic client, while a client with polycythemia may appear cyanosed with better oxygenation than expected — which is why it is a poor monitoring parameter. Pulse oximetry is more reliable but is affected by perfusion, motion, nail polish and carbon monoxide, which produces falsely reassuring readings. In chronic carbon dioxide retention, rising drowsiness rather than falling saturation may be the significant change. The clinical implication throughout is that new restlessness in a client at risk is treated as hypoxia and assessed rather than sedated.

Oxygen delivery devices differ in whether the delivered concentration is fixed or varies with the client's breathing pattern.

Pulmonary embolism most often arises from deep vein thrombosis in the legs or pelvis, and postoperative orthopedic clients carry high risk because all three elements of Virchow's triad are present. Classic presentation is sudden dyspnea, pleuritic chest pain, tachycardia, anxiety and hypoxia, sometimes with cough or hemoptysis; a massive embolism produces hypotension and cardiac arrest. Presentation may be subtle, and unexplained tachycardia or a fall in saturation may be the only sign. Immediate management is oxygen, minimizing exertion, continuous monitoring, and urgent medical assessment, with anticoagulation once diagnosis is established and thrombolysis or embolectomy considered for massive embolism. Prevention is the more important half of the topic and covers early mobilization, mechanical compression devices, pharmacological prophylaxis, and adequate hydration. Deep vein thrombosis itself may present with calf pain, swelling, warmth and erythema, and the affected limb is not massaged.

Thoracentesis removes fluid or air from the pleural space for diagnosis or for relief of dyspnea. The client is positioned sitting upright leaning forward over a bedside table with arms supported, which widens the intercostal spaces and allows fluid to gravitate to the base; where sitting is impossible, the client lies with the affected side uppermost. Informed consent is obtained by the provider performing the procedure, with the nurse verifying it. Coagulation status and platelet count are checked, and the site is confirmed by examination or ultrasound. During insertion the client remains still and avoids coughing or deep breathing, since lung movement against the needle risks laceration and pneumothorax. Volume removed is usually limited at one sitting, since rapid removal of a large volume risks re-expansion pulmonary edema and hypotension. Afterwards the client is positioned on the unaffected side for a period, a chest radiograph is commonly obtained, and observation covers sudden dyspnea, pleuritic chest pain, tachypnea, asymmetrical chest movement, absent or diminished breath sounds, subcutaneous emphysema and hemoptysis. The dressing is checked for drainage and the specimen sent as required.

Arterial blood gas interpretation follows a fixed sequence. Assess the pH against 7.35 to 7.45, identifying acidosis or alkalosis. Then examine PaCO2 against 35 to 45 and bicarbonate against 21 to 28, and determine which moves in the direction that would produce the observed pH: carbon dioxide is acidic, so a raised value causes acidosis; bicarbonate is alkaline, so a raised value causes alkalosis. The value that matches the pH direction identifies the primary disorder as respiratory or metabolic. The other value, if also abnormal, is compensating — and compensation is partial while the pH remains outside the normal range, and full once it has returned to normal even though both other values remain deranged. Compensation is by the opposite system and takes time: respiratory compensation for a metabolic problem occurs within minutes to hours through changes in ventilation, while renal compensation for a respiratory problem takes days, which is why chronically retaining COPD clients show a substantially raised bicarbonate. Oxygenation is assessed separately from acid-base status, using PaO2 and saturation.

Assessment precedes planning in discharge coordination exactly as it does at the bedside. A client using a preventer inhaler only when breathless may have poor technique, may believe the device is a rescue inhaler, may be rationing it because of cost, or may be avoiding a side effect — and each cause leads to a different intervention. A return demonstration with the client's own explanation identifies which it is, and inhaler technique errors are extremely common and often unnoticed. Pulmonary rehabilitation, community supervision and corrective teaching are all reasonable options that cannot be chosen until the cause is known.

Wheezing requires airflow, so a chest that falls silent during an active asthma attack has less air moving, not more. Bronchoconstriction, mucus plugging and airway edema progressively narrow the airway; while air still squeezes past, it makes noise. When obstruction becomes severe enough, tidal volume drops below the threshold that generates audible wheeze, and the chest goes quiet. Silence combined with inability to complete a sentence, accessory muscle use, a rising carbon dioxide level or exhaustion signals impending respiratory arrest and needs immediate escalation.

Expiratory airflow obstruction produces air trapping, prolonged expiration and chest hyperinflation.

Chronic obstructive pulmonary disease combines airflow limitation with air trapping and, in advanced disease, chronic carbon dioxide retention with a compensated respiratory acidosis. Clients live at saturations lower than most people, and their kidneys have compensated by retaining bicarbonate. Administering oxygen well above their usual level can raise carbon dioxide by several mechanisms, so supplemental oxygen is titrated to a target commonly given as 88 to 92 percent rather than to the highest achievable value. Rising carbon dioxide presents as increasing drowsiness, confusion, headache and eventually a fall in level of consciousness — a client on oxygen who becomes progressively harder to rouse needs an arterial blood gas, not more oxygen. The old teaching that these clients breathe purely on hypoxic drive overstates one mechanism and has been used to justify withholding oxygen, which causes harm. Wider care covers bronchodilators, pursed-lip breathing to prolong exhalation, positioning forward with arms supported, energy conservation, smoking cessation, vaccination, and nutrition, since the work of breathing raises calorie needs while breathlessness reduces intake.

Long-term home oxygen therapy improves survival in clients with chronic hypoxemia, and its safe use depends on teaching. Fire safety dominates: oxygen is not itself flammable but supports combustion vigorously, so smoking is prohibited for the client and everyone in the home, signs are displayed, open flames including gas stoves, candles and fireplaces are kept well away, and petroleum-based lubricants, oils and some aerosols are avoided, with water-based products used for nasal dryness. Equipment is kept away from heat, cylinders stored upright and secured, and adequate ventilation maintained; a functioning smoke detector and fire extinguisher are recommended. Flow rate is prescribed and not adjusted by the client, since in advanced COPD excessive oxygen can worsen carbon dioxide retention — clients are taught to contact the provider rather than self-titrate when breathlessness increases, because increasing breathlessness itself needs assessment. Practical teaching covers humidification where needed, skin care behind the ears and around the nares, cannula and tubing changes, use of portable systems, backup supply and power failure planning, and pursed-lip breathing and energy conservation alongside the oxygen.

Oxygen delivery devices differ in whether the delivered concentration is fixed or varies with the client's breathing pattern.

Asthma exacerbation involves bronchoconstriction, mucosal edema and mucus plugging, producing expiratory wheeze, cough, chest tightness and dyspnea. Severity is judged by the client rather than by any single finding: ability to speak in sentences, phrases or single words; use of accessory muscles and tripod positioning; respiratory and heart rate; oxygen saturation; and peak expiratory flow against the client's personal best. A silent chest, exhaustion, cyanosis, a falling respiratory rate in a tiring client, altered consciousness, and a normal or rising arterial carbon dioxide all indicate life-threatening asthma — the last because a client with severe asthma should be hyperventilating and blowing carbon dioxide off, so a normal value means they are no longer able to. Treatment is high-flow oxygen, repeated or continuous short-acting beta-agonist with an anticholinergic, systemic corticosteroid early, and consideration of magnesium sulfate, with preparation for ventilatory support. Sedatives are avoided because they depress the drive the client is relying on.

Hypoxemia produces a predictable progression. Early compensatory signs include restlessness, anxiety, irritability, tachypnea, tachycardia, mild hypertension, dyspnea and use of accessory muscles; the client is working to maintain oxygenation and largely succeeding. As hypoxemia worsens, confusion, lethargy, dysrhythmia and hypertension progressing to hypotension appear. Late signs indicate decompensation: bradycardia, cyanosis, extreme lethargy or unresponsiveness, and eventually respiratory and cardiac arrest. Cyanosis requires approximately 5 g/dL of deoxygenated hemoglobin to become visible, so it appears late and may never appear in a profoundly anemic client, while a client with polycythemia may appear cyanosed with better oxygenation than expected — which is why it is a poor monitoring parameter. Pulse oximetry is more reliable but is affected by perfusion, motion, nail polish and carbon monoxide, which produces falsely reassuring readings. In chronic carbon dioxide retention, rising drowsiness rather than falling saturation may be the significant change. The clinical implication throughout is that new restlessness in a client at risk is treated as hypoxia and assessed rather than sedated.

A tracheostomy bypasses the upper airway, which removes its warming, humidifying and filtering functions, so humidification is provided and secretions are managed actively. A newly formed stoma is the highest-risk period, because the tract is immature and accidental decannulation before it matures makes reinsertion difficult; obturator, spare tubes in the same and a smaller size, and suction equipment stay at the bedside, and the first tube change is performed by the team who placed it. Suctioning is performed on the basis of assessment rather than routine, using sterile technique, with preoxygenation, catheter size no more than half the internal diameter of the tube, suction applied only on withdrawal, passes limited to roughly ten to fifteen seconds, and the client allowed to recover between passes. Routine saline instillation is not recommended. Stoma care keeps the site clean and dry to prevent skin breakdown and infection, ties are changed with two people present, and a cuffed tube's pressure is monitored to prevent tracheal mucosal injury. Communication needs are addressed early, since the client cannot vocalize.

Wheezing requires airflow, so a chest that falls silent during an active asthma attack has less air moving, not more. Bronchoconstriction, mucus plugging and airway edema progressively narrow the airway; while air still squeezes past, it makes noise. When obstruction becomes severe enough, tidal volume drops below the threshold that generates audible wheeze, and the chest goes quiet. Silence combined with inability to complete a sentence, accessory muscle use, a rising carbon dioxide level or exhaustion signals impending respiratory arrest and needs immediate escalation.

A chest drainage system removes air or fluid from the pleural space and prevents its return, allowing the lung to re-expand. The water seal acts as a one-way valve: air can bubble out through the water, and none can be drawn back in. Gentle tidaling with respiration confirms communication with the pleural space; sudden cessation means either successful re-expansion, confirmed on imaging, or an obstruction. Intermittent bubbling in the water seal chamber during expiration or coughing is expected while air is still being removed, while continuous bubbling indicates a leak somewhere in the system, checked by working from the client toward the unit. The unit stays upright and below chest level at all times, including during transport. Clamping is avoided except very briefly for specific purposes such as changing the unit, because it converts an open pneumothorax into a closed one. Routine stripping or milking generates dangerously high negative pressure and is not done. If the tube is dislodged from the chest, an occlusive dressing taped on three sides allows air to escape without being drawn in; if the system is disconnected, the tube end is placed in sterile water while a new unit is obtained.

A chest drainage system works by gravity, so it is kept below the level of the chest, and pain control is what enables the deep breathing that re-expands the lung.

Thoracentesis removes fluid or air from the pleural space for diagnosis or for relief of dyspnea. The client is positioned sitting upright leaning forward over a bedside table with arms supported, which widens the intercostal spaces and allows fluid to gravitate to the base; where sitting is impossible, the client lies with the affected side uppermost. Informed consent is obtained by the provider performing the procedure, with the nurse verifying it. Coagulation status and platelet count are checked, and the site is confirmed by examination or ultrasound. During insertion the client remains still and avoids coughing or deep breathing, since lung movement against the needle risks laceration and pneumothorax. Volume removed is usually limited at one sitting, since rapid removal of a large volume risks re-expansion pulmonary edema and hypotension. Afterwards the client is positioned on the unaffected side for a period, a chest radiograph is commonly obtained, and observation covers sudden dyspnea, pleuritic chest pain, tachypnea, asymmetrical chest movement, absent or diminished breath sounds, subcutaneous emphysema and hemoptysis. The dressing is checked for drainage and the specimen sent as required.

Arterial blood gas interpretation follows a fixed sequence. Assess the pH against 7.35 to 7.45, identifying acidosis or alkalosis. Then examine PaCO2 against 35 to 45 and bicarbonate against 21 to 28, and determine which moves in the direction that would produce the observed pH: carbon dioxide is acidic, so a raised value causes acidosis; bicarbonate is alkaline, so a raised value causes alkalosis. The value that matches the pH direction identifies the primary disorder as respiratory or metabolic. The other value, if also abnormal, is compensating — and compensation is partial while the pH remains outside the normal range, and full once it has returned to normal even though both other values remain deranged. Compensation is by the opposite system and takes time: respiratory compensation for a metabolic problem occurs within minutes to hours through changes in ventilation, while renal compensation for a respiratory problem takes days, which is why chronically retaining COPD clients show a substantially raised bicarbonate. Oxygenation is assessed separately from acid-base status, using PaO2 and saturation.

Chronic obstructive pulmonary disease combines airflow limitation with air trapping and, in advanced disease, chronic carbon dioxide retention with a compensated respiratory acidosis. Clients live at saturations lower than most people, and their kidneys have compensated by retaining bicarbonate. Administering oxygen well above their usual level can raise carbon dioxide by several mechanisms, so supplemental oxygen is titrated to a target commonly given as 88 to 92 percent rather than to the highest achievable value. Rising carbon dioxide presents as increasing drowsiness, confusion, headache and eventually a fall in level of consciousness — a client on oxygen who becomes progressively harder to rouse needs an arterial blood gas, not more oxygen. The old teaching that these clients breathe purely on hypoxic drive overstates one mechanism and has been used to justify withholding oxygen, which causes harm. Wider care covers bronchodilators, pursed-lip breathing to prolong exhalation, positioning forward with arms supported, energy conservation, smoking cessation, vaccination, and nutrition, since the work of breathing raises calorie needs while breathlessness reduces intake.

Wheezing requires airflow, so a chest that falls silent during an active asthma attack has less air moving, not more. Bronchoconstriction, mucus plugging and airway edema progressively narrow the airway; while air still squeezes past, it makes noise. When obstruction becomes severe enough, tidal volume drops below the threshold that generates audible wheeze, and the chest goes quiet. Silence combined with inability to complete a sentence, accessory muscle use, a rising carbon dioxide level or exhaustion signals impending respiratory arrest and needs immediate escalation.

Asthma exacerbation involves bronchoconstriction, mucosal edema and mucus plugging, producing expiratory wheeze, cough, chest tightness and dyspnea. Severity is judged by the client rather than by any single finding: ability to speak in sentences, phrases or single words; use of accessory muscles and tripod positioning; respiratory and heart rate; oxygen saturation; and peak expiratory flow against the client's personal best. A silent chest, exhaustion, cyanosis, a falling respiratory rate in a tiring client, altered consciousness, and a normal or rising arterial carbon dioxide all indicate life-threatening asthma — the last because a client with severe asthma should be hyperventilating and blowing carbon dioxide off, so a normal value means they are no longer able to. Treatment is high-flow oxygen, repeated or continuous short-acting beta-agonist with an anticholinergic, systemic corticosteroid early, and consideration of magnesium sulfate, with preparation for ventilatory support. Sedatives are avoided because they depress the drive the client is relying on.

Long-term home oxygen therapy improves survival in clients with chronic hypoxemia, and its safe use depends on teaching. Fire safety dominates: oxygen is not itself flammable but supports combustion vigorously, so smoking is prohibited for the client and everyone in the home, signs are displayed, open flames including gas stoves, candles and fireplaces are kept well away, and petroleum-based lubricants, oils and some aerosols are avoided, with water-based products used for nasal dryness. Equipment is kept away from heat, cylinders stored upright and secured, and adequate ventilation maintained; a functioning smoke detector and fire extinguisher are recommended. Flow rate is prescribed and not adjusted by the client, since in advanced COPD excessive oxygen can worsen carbon dioxide retention — clients are taught to contact the provider rather than self-titrate when breathlessness increases, because increasing breathlessness itself needs assessment. Practical teaching covers humidification where needed, skin care behind the ears and around the nares, cannula and tubing changes, use of portable systems, backup supply and power failure planning, and pursed-lip breathing and energy conservation alongside the oxygen.

Oxygen does not burn, but it makes everything else burn faster, hotter and more readily. The entire risk of home oxygen therapy is proximity to ignition, and the great majority of oxygen-related fires involve smoking. Safety teaching therefore covers distance from flames, heaters and gas stoves; an absolute prohibition on smoking in the home; avoidance of petroleum-based lubricants, oils and aerosols near the client; cotton rather than synthetic or wool clothing; and functioning smoke alarms. Cylinders are stored upright, secured, in a cool ventilated place, and the prescribed flow rate is not adjusted by the client.

Pulmonary embolism causes ventilation-perfusion mismatch, and movement of the source thrombus risks further embolization.

Pulmonary embolism most often arises from deep vein thrombosis in the legs or pelvis, and postoperative orthopedic clients carry high risk because all three elements of Virchow's triad are present. Classic presentation is sudden dyspnea, pleuritic chest pain, tachycardia, anxiety and hypoxia, sometimes with cough or hemoptysis; a massive embolism produces hypotension and cardiac arrest. Presentation may be subtle, and unexplained tachycardia or a fall in saturation may be the only sign. Immediate management is oxygen, minimizing exertion, continuous monitoring, and urgent medical assessment, with anticoagulation once diagnosis is established and thrombolysis or embolectomy considered for massive embolism. Prevention is the more important half of the topic and covers early mobilization, mechanical compression devices, pharmacological prophylaxis, and adequate hydration. Deep vein thrombosis itself may present with calf pain, swelling, warmth and erythema, and the affected limb is not massaged.

The practical nurse's scope is implementation on stable, predictable clients — established procedures, ongoing data collection and reinforcement of teaching. What does not transfer are the bookends of the nursing process: the initial assessment that establishes the baseline, the plan of care built from it, and the evaluation that decides whether the plan is working. Assignment decisions therefore turn on client stability and predictability rather than on the technical difficulty of the task. An unstable client, a first-time procedure or a situation requiring interpretation stays with the registered nurse.

A tracheostomy bypasses the upper airway, which removes its warming, humidifying and filtering functions, so humidification is provided and secretions are managed actively. A newly formed stoma is the highest-risk period, because the tract is immature and accidental decannulation before it matures makes reinsertion difficult; obturator, spare tubes in the same and a smaller size, and suction equipment stay at the bedside, and the first tube change is performed by the team who placed it. Suctioning is performed on the basis of assessment rather than routine, using sterile technique, with preoxygenation, catheter size no more than half the internal diameter of the tube, suction applied only on withdrawal, passes limited to roughly ten to fifteen seconds, and the client allowed to recover between passes. Routine saline instillation is not recommended. Stoma care keeps the site clean and dry to prevent skin breakdown and infection, ties are changed with two people present, and a cuffed tube's pressure is monitored to prevent tracheal mucosal injury. Communication needs are addressed early, since the client cannot vocalize.

Assessment precedes planning in discharge coordination exactly as it does at the bedside. A client using a preventer inhaler only when breathless may have poor technique, may believe the device is a rescue inhaler, may be rationing it because of cost, or may be avoiding a side effect — and each cause leads to a different intervention. A return demonstration with the client's own explanation identifies which it is, and inhaler technique errors are extremely common and often unnoticed. Pulmonary rehabilitation, community supervision and corrective teaching are all reasonable options that cannot be chosen until the cause is known.

The practical nurse's scope is implementation on stable, predictable clients — established procedures, ongoing data collection and reinforcement of teaching. What does not transfer are the bookends of the nursing process: the initial assessment that establishes the baseline, the plan of care built from it, and the evaluation that decides whether the plan is working. Assignment decisions therefore turn on client stability and predictability rather than on the technical difficulty of the task. An unstable client, a first-time procedure or a situation requiring interpretation stays with the registered nurse.

Thoracentesis removes fluid or air from the pleural space for diagnosis or for relief of dyspnea. The client is positioned sitting upright leaning forward over a bedside table with arms supported, which widens the intercostal spaces and allows fluid to gravitate to the base; where sitting is impossible, the client lies with the affected side uppermost. Informed consent is obtained by the provider performing the procedure, with the nurse verifying it. Coagulation status and platelet count are checked, and the site is confirmed by examination or ultrasound. During insertion the client remains still and avoids coughing or deep breathing, since lung movement against the needle risks laceration and pneumothorax. Volume removed is usually limited at one sitting, since rapid removal of a large volume risks re-expansion pulmonary edema and hypotension. Afterwards the client is positioned on the unaffected side for a period, a chest radiograph is commonly obtained, and observation covers sudden dyspnea, pleuritic chest pain, tachypnea, asymmetrical chest movement, absent or diminished breath sounds, subcutaneous emphysema and hemoptysis. The dressing is checked for drainage and the specimen sent as required.

A respirator protects only if air is forced through the filter rather than around the edges. Fit testing establishes which make and size seals on a particular face, and a user seal check is performed on every occasion the respirator is worn, because facial hair, weight change, a shifted strap or a damaged device all break a seal that once fitted. The straps are worn in the position established at fit testing, one above and one below the ears, and a surgical mask worn over a respirator adds no filtration while disturbing the seal. Airborne precautions also require a negative-pressure room.

A chest drainage system works by gravity, so it is kept below the level of the chest, and pain control is what enables the deep breathing that re-expands the lung.

Wheezing requires airflow, so a chest that falls silent during an active asthma attack has less air moving, not more. Bronchoconstriction, mucus plugging and airway edema progressively narrow the airway; while air still squeezes past, it makes noise. When obstruction becomes severe enough, tidal volume drops below the threshold that generates audible wheeze, and the chest goes quiet. Silence combined with inability to complete a sentence, accessory muscle use, a rising carbon dioxide level or exhaustion signals impending respiratory arrest and needs immediate escalation.

The practical nurse's scope is implementation on stable, predictable clients — established procedures, ongoing data collection and reinforcement of teaching. What does not transfer are the bookends of the nursing process: the initial assessment that establishes the baseline, the plan of care built from it, and the evaluation that decides whether the plan is working. Assignment decisions therefore turn on client stability and predictability rather than on the technical difficulty of the task. An unstable client, a first-time procedure or a situation requiring interpretation stays with the registered nurse.

Assessment precedes planning in discharge coordination exactly as it does at the bedside. A client using a preventer inhaler only when breathless may have poor technique, may believe the device is a rescue inhaler, may be rationing it because of cost, or may be avoiding a side effect — and each cause leads to a different intervention. A return demonstration with the client's own explanation identifies which it is, and inhaler technique errors are extremely common and often unnoticed. Pulmonary rehabilitation, community supervision and corrective teaching are all reasonable options that cannot be chosen until the cause is known.

A respirator protects only if air is forced through the filter rather than around the edges. Fit testing establishes which make and size seals on a particular face, and a user seal check is performed on every occasion the respirator is worn, because facial hair, weight change, a shifted strap or a damaged device all break a seal that once fitted. The straps are worn in the position established at fit testing, one above and one below the ears, and a surgical mask worn over a respirator adds no filtration while disturbing the seal. Airborne precautions also require a negative-pressure room.

A respirator protects only if air is forced through the filter rather than around the edges. Fit testing establishes which make and size seals on a particular face, and a user seal check is performed on every occasion the respirator is worn, because facial hair, weight change, a shifted strap or a damaged device all break a seal that once fitted. The straps are worn in the position established at fit testing, one above and one below the ears, and a surgical mask worn over a respirator adds no filtration while disturbing the seal. Airborne precautions also require a negative-pressure room.