RESPIRATORY EMERGENCIES ASSESSMENT AND
MANAGEMENT NCLEX LATEST STUDY GUIDE 2026
Pulmonary Embolism (PE)
• Risk Factors: Venous stasis and hypercoagulability (e.g., post-surgical immobility,
recent surgery – components of Virchow’s triad) predispose patients to pulmonary
emboli. Always suspect PE in a post-op patient with sudden respiratory distress and chest
pain.
• Signs & Symptoms: Acute onset of dyspnea and pleuritic chest pain (sharp pain
worsening on inspiration) accompanied by tachycardia (often irregular) and anxiety.
Patients may appear extremely distressed or fearful. Arterial blood gas (ABG) analysis
often reveals low PaCO₂ due to hyperventilation and impaired gas exchange (respiratory
alkalosis).
• Diagnostic Findings: Elevated D-dimer levels indicate possible clot presence, but
definitive diagnosis is via CT pulmonary angiography (CT scan with contrast), which
visualizes clots in pulmonary arteries. Prompt recognition and diagnosis are critical, as
large “saddle” pulmonary emboli can be life-threatening obstructions.
• Interventions: Initiate rapid response and begin oxygen therapy immediately for any
suspected PE (ensure adequate oxygenation). Establish IV access and start
anticoagulation (usually IV heparin) to prevent clot extension. For massive PE causing
hemodynamic instability, anticipate more aggressive treatments such as thrombolytic
therapy or surgical thrombectomy (clot removal) if indicated. Continuous cardiac
monitoring is advised due to risk of arrhythmias or obstructive shock.
Acute Respiratory Failure (ARF)
• Definition (ABG Criteria): Acute respiratory failure is the inability of the lungs to
maintain adequate gas exchange. It is defined by critical ABG values: PaO₂ < 60 mmHg
(hypoxemia) and/or PaCO₂ > 45 mmHg with pH < 7.35 (respiratory acidosis), often
alongside oxygen saturation < 90% on room air. These values are red flags indicating
failure of oxygenation and/or ventilation.
• Types of ARF: Identify whether failure is primarily ventilatory or oxygenation in
origin. Ventilatory failure (hypercapnic) results from inadequate ventilation mechanics
(e.g., neuromuscular disorders, CNS depression, or chest wall injuries) leading to
elevated CO₂. Oxygenation failure (hypoxemic) results from impaired gas exchange in
the lungs (e.g., pneumonia, pulmonary edema) leading to inadequate oxygenation of
blood despite normal ventilation. Determining the type helps target the underlying cause.
• Clinical Presentation: Patients in ARF typically exhibit signs of respiratory distress:
labored breathing, use of accessory muscles, dyspnea at rest, and orthopnea (difficulty
breathing lying flat). Cyanosis (blue-tinged lips or skin) may be present in severe
hypoxemia. Neurologic changes like restlessness, agitation, or confusion indicate
, hypoxia affecting the brain. Vital signs often show tachypnea and potentially
hypertension or arrhythmias as compensatory mechanisms fail.
• Immediate Management: Airway and oxygenation are the priority. Begin
supplemental oxygen (via nasal cannula or non-rebreather mask) at high flow to
improve O₂ saturation. Position the patient upright to maximize ventilation. If
oxygenation remains inadequate or CO₂ climbs despite therapy, prepare for endotracheal
intubation and mechanical ventilation (invasive support). Address underlying causes
concurrently (e.g., bronchodilators for asthma/COPD, antibiotics for pneumonia,
naloxone for opioid overdose). Monitor ABGs frequently to guide therapy.
• Nursing Priorities: Perform continuous assessments – monitor respiratory rate, effort,
and lung sounds; obtain serial ABGs to track gas exchange status. Ensure effective
airway clearance (suction PRN) and prevent exhaustion in a patient working hard to
breathe. Provide calm reassurance to reduce anxiety (which can worsen hypoxia).
Arrange necessary supports (e.g., ventilator setup) early rather than waiting for collapse.
• Tension Pneumothorax (Obstructive Shock) – Emergency Note: In any worsening
respiratory distress, watch for signs of a tension pneumothorax as a possible cause. This
occurs when air becomes trapped in the pleural space with each breath, collapsing the
lung and compressing the heart and great vessels, which can lead to obstructive shock
(drastic drop in blood pressure). Signs include unilateral absent breath sounds, distended
neck veins, hypotension, and tracheal deviation away from the affected side. Immediate
intervention is required: prepare for needle decompression followed by chest tube
insertion to relieve pressure. Rapid recognition and action will prevent cardiovascular
collapse.
Mechanical Ventilation: Modes, Settings, and Nursing Care
• Indications for Ventilatory Support: Initiate mechanical ventilation when a patient
cannot maintain adequate oxygenation or ventilation on their own. A PaO₂ persistently <
60 mmHg (on supplemental O₂) or rising PaCO₂ with acidosis despite interventions
signals need for intubation. Clinical judgment considering work of breathing and mental
status is used alongside ABGs.
• Ventilator Modes: Two common modes of positive-pressure ventilation are:
o Assist-Control (AC) Ventilation: The ventilator delivers a preset tidal volume
at a fixed rate. The patient may initiate breaths, but each breath (spontaneous or
mandatory) will receive the full set tidal volume from the machine. This mode
provides maximal support – useful for patients who are fully or heavily sedated or
who have minimal spontaneous effort.
o Synchronized Intermittent Mandatory Ventilation (SIMV): The ventilator
delivers breaths at a preset rate and volume, but permits the patient to breathe
spontaneously in between mandatory breaths. Any breaths above the set rate are
unassisted (the patient’s own tidal volume). SIMV helps maintain respiratory
muscle use and is often employed when weaning a patient off the ventilator or
when some spontaneous effort is present.
o Mode Selection: The choice of mode depends on patient condition. AC mode is
preferred for patients who need full respiratory support (e.g., no spontaneous
effort or weak respiratory muscles), ensuring adequate ventilation with each
, breath. SIMV mode is considered for patients who are breathing spontaneously
and can contribute to ventilation, as it encourages muscle conditioning and may
facilitate easier weaning.
• Ventilator Settings: Key settings must be tailored to patient needs:
o Tidal Volume (V<sub>T</sub>): Volume of air delivered per breath. It should
be sufficient to ventilate the lungs but not excessive, to avoid volutrauma. Overly
large volumes can over-distend alveoli (like over-inflating a balloon) and cause
lung injury. Typical initial V<sub>T</sub> is ~6–8 mL/kg of ideal body weight
in adults (to prevent barotrauma).
o Respiratory Rate: The set number of breaths per minute delivered by the
ventilator (often 12-20 bpm initially, adjusted based on PaCO₂ levels).
o FiO₂ (Fraction of Inspired Oxygen): The O₂ concentration provided (21% to
100%). Set to maintain adequate PaO₂/SaO₂; aim for lowest effective FiO₂ to
avoid oxygen toxicity.
o Positive End-Expiratory Pressure (PEEP): The positive pressure maintained in
the lungs at end of exhalation. PEEP keeps alveoli open to improve oxygenation
and prevent alveolar collapse. Low to moderate PEEP (e.g. 5-10 cmH₂O) is
common in ARDS/respiratory failure to enhance gas exchange. High PEEP
improves oxygenation in severe hypoxemia but must be used cautiously –
excessive PEEP can impair venous return and cause barotrauma (pressure-
induced lung injury). Balance is critical to maximize oxygenation while
minimizing intrathoracic pressure effects.
• Nursing Care for Ventilated Patients:
o Monitoring: Vigilant monitoring is required. Continuously assess the patient’s
respiratory status (rate, effort, synchronicity with vent), vital signs, and analyze
ABGs to ensure ventilation goals are met. Auscultate lung sounds regularly
(checking for adequate aeration or evidence of secretions). Observe for any signs
of patient-ventilator asynchrony or distress (e.g., “fighting the vent”). Respond
immediately to ventilator alarms – they may signal high pressure (e.g., from
secretions or biting the tube) or low pressure (disconnection or leak). Ensure the
endotracheal tube is secure and patent (suction as needed).
o Preventing Complications: Ventilator-associated pneumonia (VAP) is a
significant risk. Adhere to the ventilator bundle protocols: keep the head of bed
elevated 30–45° to reduce aspiration risk, perform meticulous oral hygiene
(chlorhexidine mouth care) to limit oropharyngeal bacteria, suction secretions
with sterile technique, and implement daily sedation interruptions and
assessment of readiness to extubate (to minimize sedation duration). Strict hand
hygiene and wearing appropriate protective equipment during airway care are
mandatory to prevent infection.
o Sedation & Comfort: Administer sedatives and analgesics as ordered to maintain
patient comfort and ventilator synchrony (agitation can dangerously increase
oxygen demand and cause ventilator dyssynchrony). Use the lowest effective
sedation level that achieves comfort and synchrony, assessing sedation depth
regularly. Neuromuscular blocking agents may be used in short term for severe
asynchrony or oxygenation issues (with adequate sedation and analgesia).
MANAGEMENT NCLEX LATEST STUDY GUIDE 2026
Pulmonary Embolism (PE)
• Risk Factors: Venous stasis and hypercoagulability (e.g., post-surgical immobility,
recent surgery – components of Virchow’s triad) predispose patients to pulmonary
emboli. Always suspect PE in a post-op patient with sudden respiratory distress and chest
pain.
• Signs & Symptoms: Acute onset of dyspnea and pleuritic chest pain (sharp pain
worsening on inspiration) accompanied by tachycardia (often irregular) and anxiety.
Patients may appear extremely distressed or fearful. Arterial blood gas (ABG) analysis
often reveals low PaCO₂ due to hyperventilation and impaired gas exchange (respiratory
alkalosis).
• Diagnostic Findings: Elevated D-dimer levels indicate possible clot presence, but
definitive diagnosis is via CT pulmonary angiography (CT scan with contrast), which
visualizes clots in pulmonary arteries. Prompt recognition and diagnosis are critical, as
large “saddle” pulmonary emboli can be life-threatening obstructions.
• Interventions: Initiate rapid response and begin oxygen therapy immediately for any
suspected PE (ensure adequate oxygenation). Establish IV access and start
anticoagulation (usually IV heparin) to prevent clot extension. For massive PE causing
hemodynamic instability, anticipate more aggressive treatments such as thrombolytic
therapy or surgical thrombectomy (clot removal) if indicated. Continuous cardiac
monitoring is advised due to risk of arrhythmias or obstructive shock.
Acute Respiratory Failure (ARF)
• Definition (ABG Criteria): Acute respiratory failure is the inability of the lungs to
maintain adequate gas exchange. It is defined by critical ABG values: PaO₂ < 60 mmHg
(hypoxemia) and/or PaCO₂ > 45 mmHg with pH < 7.35 (respiratory acidosis), often
alongside oxygen saturation < 90% on room air. These values are red flags indicating
failure of oxygenation and/or ventilation.
• Types of ARF: Identify whether failure is primarily ventilatory or oxygenation in
origin. Ventilatory failure (hypercapnic) results from inadequate ventilation mechanics
(e.g., neuromuscular disorders, CNS depression, or chest wall injuries) leading to
elevated CO₂. Oxygenation failure (hypoxemic) results from impaired gas exchange in
the lungs (e.g., pneumonia, pulmonary edema) leading to inadequate oxygenation of
blood despite normal ventilation. Determining the type helps target the underlying cause.
• Clinical Presentation: Patients in ARF typically exhibit signs of respiratory distress:
labored breathing, use of accessory muscles, dyspnea at rest, and orthopnea (difficulty
breathing lying flat). Cyanosis (blue-tinged lips or skin) may be present in severe
hypoxemia. Neurologic changes like restlessness, agitation, or confusion indicate
, hypoxia affecting the brain. Vital signs often show tachypnea and potentially
hypertension or arrhythmias as compensatory mechanisms fail.
• Immediate Management: Airway and oxygenation are the priority. Begin
supplemental oxygen (via nasal cannula or non-rebreather mask) at high flow to
improve O₂ saturation. Position the patient upright to maximize ventilation. If
oxygenation remains inadequate or CO₂ climbs despite therapy, prepare for endotracheal
intubation and mechanical ventilation (invasive support). Address underlying causes
concurrently (e.g., bronchodilators for asthma/COPD, antibiotics for pneumonia,
naloxone for opioid overdose). Monitor ABGs frequently to guide therapy.
• Nursing Priorities: Perform continuous assessments – monitor respiratory rate, effort,
and lung sounds; obtain serial ABGs to track gas exchange status. Ensure effective
airway clearance (suction PRN) and prevent exhaustion in a patient working hard to
breathe. Provide calm reassurance to reduce anxiety (which can worsen hypoxia).
Arrange necessary supports (e.g., ventilator setup) early rather than waiting for collapse.
• Tension Pneumothorax (Obstructive Shock) – Emergency Note: In any worsening
respiratory distress, watch for signs of a tension pneumothorax as a possible cause. This
occurs when air becomes trapped in the pleural space with each breath, collapsing the
lung and compressing the heart and great vessels, which can lead to obstructive shock
(drastic drop in blood pressure). Signs include unilateral absent breath sounds, distended
neck veins, hypotension, and tracheal deviation away from the affected side. Immediate
intervention is required: prepare for needle decompression followed by chest tube
insertion to relieve pressure. Rapid recognition and action will prevent cardiovascular
collapse.
Mechanical Ventilation: Modes, Settings, and Nursing Care
• Indications for Ventilatory Support: Initiate mechanical ventilation when a patient
cannot maintain adequate oxygenation or ventilation on their own. A PaO₂ persistently <
60 mmHg (on supplemental O₂) or rising PaCO₂ with acidosis despite interventions
signals need for intubation. Clinical judgment considering work of breathing and mental
status is used alongside ABGs.
• Ventilator Modes: Two common modes of positive-pressure ventilation are:
o Assist-Control (AC) Ventilation: The ventilator delivers a preset tidal volume
at a fixed rate. The patient may initiate breaths, but each breath (spontaneous or
mandatory) will receive the full set tidal volume from the machine. This mode
provides maximal support – useful for patients who are fully or heavily sedated or
who have minimal spontaneous effort.
o Synchronized Intermittent Mandatory Ventilation (SIMV): The ventilator
delivers breaths at a preset rate and volume, but permits the patient to breathe
spontaneously in between mandatory breaths. Any breaths above the set rate are
unassisted (the patient’s own tidal volume). SIMV helps maintain respiratory
muscle use and is often employed when weaning a patient off the ventilator or
when some spontaneous effort is present.
o Mode Selection: The choice of mode depends on patient condition. AC mode is
preferred for patients who need full respiratory support (e.g., no spontaneous
effort or weak respiratory muscles), ensuring adequate ventilation with each
, breath. SIMV mode is considered for patients who are breathing spontaneously
and can contribute to ventilation, as it encourages muscle conditioning and may
facilitate easier weaning.
• Ventilator Settings: Key settings must be tailored to patient needs:
o Tidal Volume (V<sub>T</sub>): Volume of air delivered per breath. It should
be sufficient to ventilate the lungs but not excessive, to avoid volutrauma. Overly
large volumes can over-distend alveoli (like over-inflating a balloon) and cause
lung injury. Typical initial V<sub>T</sub> is ~6–8 mL/kg of ideal body weight
in adults (to prevent barotrauma).
o Respiratory Rate: The set number of breaths per minute delivered by the
ventilator (often 12-20 bpm initially, adjusted based on PaCO₂ levels).
o FiO₂ (Fraction of Inspired Oxygen): The O₂ concentration provided (21% to
100%). Set to maintain adequate PaO₂/SaO₂; aim for lowest effective FiO₂ to
avoid oxygen toxicity.
o Positive End-Expiratory Pressure (PEEP): The positive pressure maintained in
the lungs at end of exhalation. PEEP keeps alveoli open to improve oxygenation
and prevent alveolar collapse. Low to moderate PEEP (e.g. 5-10 cmH₂O) is
common in ARDS/respiratory failure to enhance gas exchange. High PEEP
improves oxygenation in severe hypoxemia but must be used cautiously –
excessive PEEP can impair venous return and cause barotrauma (pressure-
induced lung injury). Balance is critical to maximize oxygenation while
minimizing intrathoracic pressure effects.
• Nursing Care for Ventilated Patients:
o Monitoring: Vigilant monitoring is required. Continuously assess the patient’s
respiratory status (rate, effort, synchronicity with vent), vital signs, and analyze
ABGs to ensure ventilation goals are met. Auscultate lung sounds regularly
(checking for adequate aeration or evidence of secretions). Observe for any signs
of patient-ventilator asynchrony or distress (e.g., “fighting the vent”). Respond
immediately to ventilator alarms – they may signal high pressure (e.g., from
secretions or biting the tube) or low pressure (disconnection or leak). Ensure the
endotracheal tube is secure and patent (suction as needed).
o Preventing Complications: Ventilator-associated pneumonia (VAP) is a
significant risk. Adhere to the ventilator bundle protocols: keep the head of bed
elevated 30–45° to reduce aspiration risk, perform meticulous oral hygiene
(chlorhexidine mouth care) to limit oropharyngeal bacteria, suction secretions
with sterile technique, and implement daily sedation interruptions and
assessment of readiness to extubate (to minimize sedation duration). Strict hand
hygiene and wearing appropriate protective equipment during airway care are
mandatory to prevent infection.
o Sedation & Comfort: Administer sedatives and analgesics as ordered to maintain
patient comfort and ventilator synchrony (agitation can dangerously increase
oxygen demand and cause ventilator dyssynchrony). Use the lowest effective
sedation level that achieves comfort and synchrony, assessing sedation depth
regularly. Neuromuscular blocking agents may be used in short term for severe
asynchrony or oxygenation issues (with adequate sedation and analgesia).
