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The management of pneumothorax depends on:

Type: Primary (no underlying lung disease) vs. Secondary (e.g., COPD)

Size of pneumothorax

Presence and severity of symptoms

Risk of recurrence or complications

Step 1: Determine Type of Pneumothorax

Spontaneous Pneumothorax is the starting point.

First, assess if the patient is bilateral or hemodynamically unstable:

If YES → Immediate chest drain

If NO → Proceed to classify:

Classification:

Primary: No known lung disease, age usually <50, non-smoker.

Secondary: Age >50, history of smoking, clinical or radiological signs of lung disease (e.g., COPD).

Step 2: Measure Size and Symptoms

For Primary Pneumothorax:

If >2 cm rim between lung and chest wall and/or breathless → aspirate

Use a 16–18G cannula

Remove ≤2.5 L of air

If successful (lung re-expands and symptoms improve) → discharge or review

If not → chest drain (8–14 Fr)

If <2 cm and not breathless → observe or discharge with outpatient review in 2–4 weeks

For Secondary Pneumothorax (like AD):

If >2 cm or breathless → chest drain (8–14 Fr) directly

If 1–2 cm → aspirate with cannula

If successful and lung re-expands (<1 cm rim) → admit for observation

If not → insert chest drain

If <1 cm and no severe symptoms → admit and observe with high-flow oxygen for 24 hours

Applying to AD's case:

AD had:

Secondary spontaneous pneumothorax due to COPD

Large pneumothorax on X-ray

Severe symptoms (dyspnea, chest pain, SpO₂ < 90%)

🟢 Therefore, chest tube with underwater seal was the correct management aligned with BTS guidelines.

Other considerations:

1. High-Flow Oxygen Therapy

Administered to promote nitrogen washout → helps resorb air from the pleural space faster.

Especially useful in small pneumothorax or post-drainage.

Relevance to AD:
He was initially desaturated, so oxygen therapy would have supported his SpO₂ while the lung re-expanded.

2. Needle Aspiration (First-line for PSP)

A wide-bore needle is inserted into pleural space to remove air (up to 2.5L).

Not typically done in SSP due to high failure rate.

Not used in AD:
Because AD had SSP and was severely symptomatic, needle aspiration alone is insufficient.

3. Surgical Options (for recurrent or persistent pneumothorax)

VATS (Video-assisted thoracoscopic surgery) for:

Persistent air leak >5 days

Recurrent pneumothorax

Failed tube drainage

Pleurodesis: Chemical (talc) or surgical procedure to adhere the lung to chest wall to prevent recurrence.

Not yet indicated for AD, unless pneumothorax recurs or persists.

Reference(https://thorax.bmj.com/content/78/11/1143)

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Complication of Pneumothorax Treatment Procedure

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Complication of Pneumothorax Treatment Procedure

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Re-expansion Pulmonary Edema:
Rapid lung re-expansion can cause fluid buildup in the lungs.

Iatrogenic Complications:
Procedures like needle decompression or chest tube insertion may cause lung injury, infection, or tissue damage.

Persistent Air Leak:
An ongoing air leak after chest tube placement can prevent full lung expansion.

Empyema:
Infection in the pleural space can lead to pus accumulation.

Hemothorax:
Bleeding into the pleural space can occur during or after treatment.

Pneumomediastinum:
Air may spread to the mediastinum, causing subcutaneous emphysema or pneumopericardium.

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Inappropriateness of combination of diazepam and morphine 

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Inappropriateness of combination of diazepam and morphine 

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1. Share the same metabolism pathway

2. Both opioids and benzodiazepines induce upper airway obstruction by oropharyngeal muscle relaxation.

3. Opioids increase intercostal muscle rigidity and decreasing chest compliance but diazepam causes decrease in diaphragm contraction

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1. Tension Pneumothorax:
Air gets trapped in the pleural space, increasing pressure and shifting the heart and vessels, causing severe distress, low blood pressure, and possible cardiac arrest.

2. Respiratory Failure:
Lung collapse reduces oxygen exchange, leading to shortness of breath, rapid breathing, and low oxygen levels.

3. Hypoxemia:
Low blood oxygen from reduced lung capacity can cause fatigue, cyanosis (bluish skin), and confusion.

4. Death:
If untreated, especially in tension pneumothorax, the condition can be fatal.

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1. Appropriateness of Lignocaine and Tramadol

Lignocaine (1% subcutaneous):

Appropriate for local anesthesia before chest tube insertion.

Provides effective pain relief at the procedure site.

Tramadol (50 mg IV stat):

Potentially inappropriate for AD (COPD patient).

Risks:

Respiratory depression (especially when combined with other CNS depressants).

May worsen hypercapnia (CO₂ retention) in COPD.

Better alternatives:

IV Paracetamol (less respiratory risk).

Low-dose morphine (if strong analgesia needed, but with caution).

2. Appropriateness of Overall Treatment

Chest tube insertion: Correct for large pneumothorax.

Underwater seal drainage: Proper management.

Supplemental oxygen: Initially correct, but must be monitored (risk of CO₂ retention in COPD).

No mechanical ventilation: Appropriate since AD was stable post-chest tube insertion.

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. Clinical Symptoms

Sudden onset of left-sided chest pain (as in AD's case).

Shortness of breath.

Other possible symptoms:

Rapid breathing (tachypnoea)

Rapid heartbeat (tachycardia)

Anxiety or restlessness

Fatigue (due to low oxygen)

Larger pneumothorax = more obvious symptoms.

2. Physical Examination

Decreased air entry on the left side during auscultation (found in AD).

Other possible findings:

Hyperresonance on percussion

Reduced chest expansion (affected side)

Decreased vocal fremitus

Tracheal deviation (if tension pneumothorax)

3. Imaging Tests

Chest X-ray (First-line imaging)

Collapsed left lung (seen in AD).

Air in pleural space without lung markings.

Black (dark) area visible, lung edge may be seen.

CT Scan

Done if X-ray unclear.

More sensitive for small pneumothorax.

Not needed in AD’s case.

Ultrasound (E-FAST)

Rapid bedside detection.

Useful in trauma or emergency settings.

4. Arterial Blood Gas (ABG)

Measures:

Oxygen level (PaO₂)

Carbon dioxide level (PaCO₂)

Blood pH

Used to assess severity of respiratory compromise.

Guides oxygen therapy or ventilation needs.

Special Emergency: Tension Pneumothorax

Signs:

Very low blood pressure (hypotension)

Severe shortness of breath

Distended neck veins

Tracheal deviation (away from affected side)

Immediate treatment required (no delay for imaging)

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Managing Post-Respiratory Failure Recovery

Pharmacists play a role in long-term management:

Ensuring proper oxygen therapy at home

Teaching inhaler and nebulizer use

Ensuring vaccination (e.g., influenza, pneumococcal) to prevent infections

Monitoring for drug side effects or addiction to sedatives/opioids

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1. Cause of Respiratory Failure

Drug-induced (from tramadol + diazepam).

ABG findings:

Respiratory acidosis (↓pH, ↑pCO₂, ↑HCO₃⁻)

Hypoxemia (pO₂ 60 mmHg)

Excessive oxygen worsened CO₂ retention (common in COPD)

2. Antidote & Corrective Management

Naloxone (for tramadol-induced respiratory depression):

Dose: 0.04–0.4 mg IV (titrated to avoid withdrawal)

Flumazenil (for diazepam overdose, but caution in COPD):

Dose: 0.2 mg IV, repeat if needed (risk of seizures)

Oxygen therapy adjustment:

Target SpO₂ 88–92% (to avoid CO₂ narcosis).

Non-invasive ventilation (BiPAP):

Needed if hypercapnia persists.

3. Prevention of Recurrence

Avoid opioids/benzodiazepines in COPD patients.

Use safer analgesics (e.g., paracetamol, NSAIDs).

Smoking cessation counseling (to prevent pneumothorax recurrence)

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(trigger 2) Pathophysiology of drug induced respiratory failure 

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(trigger 2) Pathophysiology of drug induced respiratory failure 

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1. Causative Agents

Tramadol → Opioid analgesic

Diazepam → Benzodiazepine

Both have central nervous system (CNS) depressant effects.

2. Effect of Tramadol

Tramadol causes dose-dependent respiratory depression, especially in vulnerable patients like:

Those with chronic obstructive pulmonary disease (COPD)

Post-pneumothorax patients (like AD)

Dose-dependent respiratory depression means:

Low doses → pain relief

High doses → suppression of the brainstem respiratory centers

Leads to hypoventilation, CO₂ retention, and at very high doses → respiratory arrest

3. Effect of Diazepam

Mechanism:

Enhances GABAergic transmission

Binds to GABA-A receptors at the benzodiazepine binding site

Increases the frequency of Cl⁻ channel opening

↑ Cl⁻ influx → Neuron hyperpolarization → ↓ Neuronal firing

In brainstem respiratory centers, this leads to suppression of respiratory drive

Alone, diazepam usually causes mild sedation

But in patients with:

Pre-existing lung conditions (like COPD)

Or combined with other depressants (like tramadol)

→ It can result in dangerous respiratory depression

4. Combined Effect of Tramadol + Diazepam

The drugs act synergistically to suppress the medullary respiratory centers

Results in:

↓ Respiratory rate (8–9 breaths/min)

Hypoventilation

CO₂ retention → pCO₂ = 58 mmHg → Respiratory acidosis

↓ Oxygen saturation (SpO₂ = 88%, pO₂ = 60 mmHg) despite oxygen therapy

↑ HCO₃⁻ (38 mmol/L) → evidence of metabolic compensation for chronic respiratory acidosis

frm an article ->Benzodiazepines are drugs that reduce anxiety and relax the muscles. People use them to treat anxiety and insomnia.

If someone is already taking a benzodiazepine medication such as lorazepam or alprazolam, also taking tramadol can result in sedation, respiratory depression, coma, and even death. https://www.medicalnewstoday.com/articles/325278#drug-interactions

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-          Normally come on almost immediately

-          Commonly begin with chest pain

-          Shortness of breath

-          Sharp, stabbing chest that worsens when trying to breath in

-          A larger pneumothorax causes more severe symptoms, including:

-          Bluish color of the skin due to lack of oxygen

-          Rapid breathing and heartbeat

-          Dry, hacking cough

Pneumothorax causes a fast respiratory rate because the collapsed lung reduces oxygen intake (hypoxia), and the body tries to compensate by breathing faster.
It also causes a rapid heart rate because the heart pumps faster to deliver the limited oxygen to tissues and maintain blood pressure, especially if major vessels are compressed.
The stress response (sympathetic activation) further speeds up breathing and heart rate.

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Role of oxygen supplementation in patient RF

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Role of oxygen supplementation in patient RF

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Oxygen supplementation plays a crucial role in medical treatment by ensuring adequate oxygen delivery to the body, particularly when individuals experience difficulty breathing or have compromised oxygen levels. It supports essential bodily functions and prevents complications like organ damage and cardiac arrest, which can arise from oxygen deficiency (hypoxia).

Treating Hypoxemia:
Supplemental oxygen raises blood oxygen levels when the lungs can’t provide enough, often due to conditions like COPD or sleep apnea.

Supporting Organ Function:
Oxygen is vital for energy production. Low levels can harm organs like the brain, heart, and kidneys. Oxygen therapy helps keep them functioning properly.

Improving Quality of Life:
It relieves symptoms like breathlessness and fatigue, improving sleep, energy, and overall well-being.

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⁃ Referred to as air in the lungs or collapsed lung

⁃ occurs when air accumulates in the space between the lung and the chest wall (pleural space)

⁃ lead to various symptoms that indicate an imbalance in the chest cavity.

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-       Use for critical intervention to sustain life in acute or emergent settings, particularly in patients with compromised airways, impaired ventilation, or hypoxemic respiratory failure.

-       SpO₂ is also the saturation of Hb,it is read through a pulse oximeter on the finger using light refraction to estimate the binding of hemoglobin. (desaturated 90% below)

-       If SpO₂ is lower than 92%, this usually suggests the patient will require some amount of supplemental oxygen. Supplemental oxygen can be started and increased to attempt to increase the SpO2 to above 92%. Mechanical ventilation would be a subsequent step when high levels of supplementary oxygen is not adequate to support the patient’s oxygen needs, in order to prevent hypoxic failure.

-       Reasons for mechanical ventilation can fall into three main categories:

o   Hypoxic failure (also called hypoxia) is the inability to oxygenate the body adequately.

o   Hypercapnia, or high CO₂ levels. If CO₂ increases to a level the body cannot clear by increasing breathing, mechanical ventilation is indicated.

o   Ineffective drive to breathe can occur if there is an injury to the brain or neurological control to breathing.

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-       Use: Chest tube insertion also known as a thoracic catheter, is a sterile tube is inserted into the pleural space with a number of drainage holes. (is the space between the parietal and visceral pleura, and is also known as the pleural cavity)

-       If air is in the pleural space, then the chest tube will be inserted above the second intercostal space at the mid-clavicle line.

-       Importance: Restore negative pressure in pleural space, preventing the lung from collapsing and compressing at the end of exhalation.

-       It is disrupted when air, or fluid and air, enters the pleural space and separates the visceral pleura from the parietal pleura. The lung can't stay expanded, so it collapses partially or fully

Normally, a traditional chest tube drainage system  is connected to a closed chest drainage system will have these three chambers:

1.       Collection chamber

2.       Wet or dry suction control chamber

3.       Water-seal chamber

-       This chamber has a one-way valve that allows air to exit the pleural cavity during exhalation but does not allow it to re-enter during inhalation due to the pressure in the chamber.

-       The water-seal chamber must be filled with sterile water and maintained at the 2 cm mark to ensure proper operation, and should be checked regularly.

-       The water in the water-seal chamber should rise with inhalation and fall with exhalation (this is called tidaling), which demonstrates that the chest tube is patent. Continuous bubbling may indicate an air leak, and newer systems have a measurement system for leaks — the higher the number, the greater the air leak. The water-seal chamber can also monitor intrathoracic pressure

Surgical Intervention (thoracostomy) : In rare cases where chest tube insertion does not effectively resolve the pneumothorax, surgical intervention may be necessary. The decision for surgery is made by a specialist, such as a thoracic surgeon, who will evaluate the condition and determine the most appropriate course of action.

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Smoking

Tall thin body habitus in an otherwise healthy person

Pregnancy

Marfan syndrome

Familial pneumothorax

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A pneumothorax is a collection of air outside the lung but within the pleural cavity. It occurs when air accumulates between the parietal and visceral pleurae inside the chest. The air accumulation can apply pressure on the lung and make it collapse (see Image. Upper Lobe Pneumothorax). The degree of collapse determines the clinical presentation of pneumothorax (see Image. Right Tension Pneumothorax Radiograph). Air can enter the pleural space by two mechanisms, either by trauma causing communication through the chest wall or from the lung by rupture of the visceral pleura. There are two types of pneumothorax: traumatic and atraumatic. The two subtypes of atraumatic pneumothorax are primary and secondary. A primary spontaneous pneumothorax (PSP) occurs automatically without a known eliciting event, while a secondary spontaneous pneumothorax (SSP) occurs after an underlying pulmonary disease. A traumatic pneumothorax can be the result of blunt or penetrating trauma. Pneumothoraces can be even further classified as simple, tension, or open. A simple pneumothorax does not shift the mediastinal structures, as does a tension pneumothorax (see Image. Left-Sided Tension Pneumothorax Radiograph). Open pneumothorax is an open wound in the chest wall through which air moves in and out.[1][2][3][4]

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COPD

Asthma

HIV with pneumocystis pneumonia

Necrotizing pneumonia

Tuberculosis

Sarcoidosis

Cystic fibrosis

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A pneumothorax is a collection of air outside the lung but within the pleural cavity. It occurs when air accumulates between the parietal and visceral pleurae inside the chest. The air accumulation can apply pressure on the lung and make it collapse (see Image. Upper Lobe Pneumothorax). The degree of collapse determines the clinical presentation of pneumothorax (see Image. Right Tension Pneumothorax Radiograph). Air can enter the pleural space by two mechanisms, either by trauma causing communication through the chest wall or from the lung by rupture of the visceral pleura. There are two types of pneumothorax: traumatic and atraumatic. The two subtypes of atraumatic pneumothorax are primary and secondary. A primary spontaneous pneumothorax (PSP) occurs automatically without a known eliciting event, while a secondary spontaneous pneumothorax (SSP) occurs after an underlying pulmonary disease. A traumatic pneumothorax can be the result of blunt or penetrating trauma. Pneumothoraces can be even further classified as simple, tension, or open. A simple pneumothorax does not shift the mediastinal structures, as does a tension pneumothorax (see Image. Left-Sided Tension Pneumothorax Radiograph). Open pneumothorax is an open wound in the chest wall through which air moves in and out.[1][2][3][4]

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1. Spontaneous pneumothorax

Primary spontaneous pneumothorax - This happens in people without known underlying lung disease. It is often attributed to the rupture of small air-filled sacs called blebs, typically located at the top of the lungs. PSP is more common in tall, thin individuals, particularly young men.

Secondary spontaneous pneumothorax - This occurs in individuals with pre-existing lung conditions that weaken the lung tissue, making it more susceptible to collapse. Common underlying diseases include chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, tuberculosis, pneumonia, and certain interstitial lung diseases.

2. Traumatic pneumothorax - This type results from an injury to the chest that punctures the lung or chest wall, allowing air to enter the pleural space. Causes can include blunt trauma (e.g. car accidents, falls), penetrating trauma (e.g. stab wounds, gunshot wounds) or rib fractures that lacerate the lung.

3. Iatrogenic Pneumothorax: This is a type of traumatic pneumothorax caused inadvertently by a medical procedure. Examples include lung biopsies, central venous catheter insertion, thoracentesis, and mechanical ventilation (barotrauma).

4. Tension Pneumothorax: This is a particularly dangerous type of pneumothorax where a one-way valve effect occurs. Air enters the pleural space during inhalation but cannot escape during exhalation. This leads to a progressive buildup of pressure, which can collapse the affected lung and shift the mediastinum (the area between the lungs containing the heart, trachea, and major blood vessels) to the opposite side. This shifting can compress the other lung and the heart, leading to severe respiratory distress and cardiovascular collapse. Tension pneumothorax is a medical emergency requiring immediate treatment.

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role of pharmacist - respiratory pharmacist

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role of pharmacist - respiratory pharmacist

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1) Identify potential drug interactions (CNS depression risk) + Recommend safer alternatives (e.g., paracetamol, non-benzodiazepines)

2)Counsel on smoking cessation and provide NRT options if needed

3)Reinforce adherence to COPD medications and follow-up visits

4)Collaborate with other healthcare providers for holistic care (respiratory team, GP, smoking cessation services)

5) Advising on supplemental oxygen to promote pleural air absorption (avoiding high flow in COPD patients)

6) Teach correct inhaler technique

7) Educate on smoking cessation, including offering nicotine replacement therapy (NRT)

8)Explain how to avoid triggers that can worsen COPD or cause pneumothorax recurrence

9) Educate on recognizing signs of respiratory distress or medication side effects

respiratory pharmacists are not just medicine experts but also leaders in sustainability, prevention, and system-wide quality improvement.

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1. Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia.

2. Type 2 respiratory failure occurs when the respiratory system cannot sufficiently remove carbon dioxide from the body, leading to hypercapnia.

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Continuing Education Activity

The respiratory system provides oxygen to and removes carbon dioxide from the body; however, the inability to perform either or both of these tasks results in respiratory failure. Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia, and can be caused by alveolar hypoventilation, low atmospheric pressure/fraction of inspired oxygen, diffusion defect, ventilation/perfusion mismatch, and right-to-left shunt. Type 2 respiratory failure occurs when the respiratory system cannot adequately remove carbon dioxide from the body, leading to hypercapnia, and can be caused by respiratory pump failure and increased carbon dioxide production. This activity reviews the evaluation and management of respiratory failure and highlights the role of the healthcare team in evaluating and treating patients with this condition.

Objectives:

Review the etiology of respiratory failure.

Explain the pathophysiology of respiratory failure.

Review the physical exam findings associated with respiratory failure.

Summarize the treatment considerations for patients with respiratory failure.

Access free multiple choice questions on this topic.
Introduction

The respiratory system allows gas exchange between the environment and the body, facilitating the process of aerobic metabolism. Specifically, the respiratory system provides oxygen and removes carbon dioxide from the body. The inability of the respiratory system to perform either or both of these tasks results in respiratory failure. Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia. Type 2 respiratory failure occurs when the respiratory system cannot sufficiently remove carbon dioxide from the body, leading to hypercapnia. Respiratory failure can be classified based on chronicity (i.e., acute, chronic, and acute on chronic). A thorough understanding of respiratory failure is crucial to managing this disorder. If either type of respiratory failure is not identified and addressed early, it will become life-threatening and lead to respiratory arrest, coma, and death. The approach to adult patients with suspected respiratory failure (both hypercapnia and hypoxic), as well as the diagnosis and treatment of acute and chronic respiratory failure, are discussed in this article.

Etiology

Respiratory failure can occur if there is an abnormality with any component of the respiratory system. Components of the respiratory system include the upper and lower respiratory tracts, the central and peripheral nervous systems, in addition to the chest wall and muscles of respiration.[1] The pathophysiology section of this article will review specific etiologies of respiratory failure.

Epidemiology

Respiratory failure (RF) is a syndrome caused by a multitude of pathological states; therefore, the epidemiology of this disease process is difficult to ascertain. In 2017 in the United States of America, however, the incidence of respiratory failure was found to be 1,275 cases per 100,000 adults. The case definition used in this study included all diagnosis codes that included respiratory failure as a component.[2] The epidemiology of respiratory failure is dependent mainly on the cause leading to the failure. Below we list some common causes of respiratory failure and the relevant trends:

Acute myocardial infarction-related (AMI-RF): Between the years 2000 and 2014, 439,436 admissions due to AMI-RF were noted in 57% and required mechanical ventilation in 43% of total cases.[3]

Acute respiratory failure due to acute respiratory distress syndrome (ARDS) ranges in incidence from 10-80/100,000/y based on where it is recorded worldwide. This is partly due t different practices and thresholds for intubation in these cases and the use of different definitions of ARDs. According to one report, it is estimated that 10% of all patients admitted to ICU and 23% of mechanically ventilated patients meet ARDS criteria.[4]

Acute respiratory failure related to Coronavirus (COVID-19): It is estimated early in the COVID-19 pandemic that up to 79% of hospitalized patients developed respiratory failure requiring invasive mechanical ventilation.[5]

Acute exacerbation of COPD (AECOPD) is the third most common etiology in patients hospitalized because of acute respiratory failure.[6]

Pathophysiology

T ype 1 respiratory failure:

The distinguishing characteristic of Type 1 respiratory failure is a partial pressure of oxygen (PaO2) < 60 mmHg with a normal or decreased partial pressure of carbon dioxide (PaCO2); Depending on the cause of hypoxemia, the alveolar-arterial (A-a) gradient may be normal or increased. Formulas of the A-a gradient and alveolar gas equation are provided below, as these concepts are helpful in understanding the pathophysiology of respiratory failure.

A-a gradient:

Alveolar gas equation:[7]

PAO2 = FiO2 (PB - Pwater) - PaCO2/0.8, or PIo2= (PB - 47) × FIo2,

PAO2 = Alveolar partial pressure of oxygen

FiO2 = Fraction of inspired oxygen

PB = Barometric (Atmospheric) pressure

Pwater = Vapor pressure of water at body temperature (37°C)=47 mmHg

PaCO2 = Partial pressure of arterial carbon dioxide

Etiologies of Type 1 respiratory failure with normal A-a gradients include:

Alveolar hypoventilation: Alveolar hypoventilation increases the arterial partial pressure of carbon dioxide (PaCO2). The alveolar gas equation demonstrates that an increase in PaCO2 causes a decrease in the alveolar partial pressure of oxygen (PAO2). In this situation, the A-a gradient is normal, as the PAO2 and PaO2 decrease in equal magnitudes. When severe, alveolar hypoventilation may progress to Type 2 respiratory failure.[8] (as discussed later in this section under Type 2 respiratory failure).

Low atmospheric pressure/fraction of inspired oxygen: The alveolar gas equation demonstrates that the alveolar partial pressure of oxygen (PAO2) decreases with low atmospheric pressures (Patm) and with low levels of inspired oxygen (FiO2). In either situation, the A-a gradient remains normal, and the PaCO2 is decreased, given the response to hypoxia is hyperventilation. Clinically, this cause of respiratory failure occurs at high altitudes.[9]

Diffusion defect: Gas exchange between the environment and the body occurs at the alveolar-capillary interface. Structural changes to the alveolar component of the alveolar-capillary interface, such as decreased surface area or increased thickness, may result in diffusion defects across the membrane. Additionally, reducing pulmonary capillary transit time through the alveolar-capillary interface may result in diffusion defects across the membrane. In either situation, hypercapnia does not occur, as carbon dioxide diffuses more readily across the alveolar-capillary membrane than oxygen.[10] Etiologies of diffusion defects include:

Ventilation/perfusion (V/Q) mismatch: The alveolar gas composition depends on the balance of alveolar ventilation and pulmonary capillary blood flow that occurs at the alveolar-capillary interface. When perfectly matched, the V/Q ratio is equal to one. When ventilation is excessive to perfusion, the V/Q ratio is greater than one; Dead space ventilation occurs when the V/Q ratio reaches infinity. When perfusion is excessive to ventilation, the V/Q ratio is less than one; Shunt occurs when the V/Q ratio reaches zero. In healthy subjects, however, the V/Q ratio is approximately 0.8, as the balance between ventilation and perfusion differs from the apex to the base of the lungs. V/Q mismatch is the most common cause of Type 1 respiratory failure.[11] Etiologies of V/Q mismatch include:

Acute respiratory distress syndrome

Chronic obstructive pulmonary disease

Right-to-left shunt: As discussed above, shunt occurs when the V/Q ratio reaches zero. The absence of gas exchange at the alveolar-capillary interface represents a true shunt and is analogous to intracardiac right-to-left shunting seen in atrial septal defect and patent foramen ovale. Unlike V/Q mismatch, true shunt does not improve with supplemental oxygen therapy.[12] Etiologies of pulmonary right-to-left shunts include:

Etiologies of Type 1 respiratory failure with increased A-a gradients include:

Type 2 Respiratory Failure

Hypercapnic respiratory failure is defined as an increase in arterial carbon dioxide (CO2) (PaCO)> 45 mmHg with a pH < 7.35 due to respiratory pump failure and/or increased COproduction. In general, according to the modified alveolar ventilation equation, the PaCO2 level is proportionally related to the rate of CO2 production (VCO2) and inversely associated with the rate of CO2 elimination (i.e., alveolar ventilation) (PaCO2 =VCO2 /VA). The relationship between minute ventilation and CO2 production in response to exercise can be affected by age and pregnancy.[13]

Alveolar ventilation (VA) is the product of minute ventilation (VE) and the ratio of dead space (VD) to tidal volume (Vt) (VA = VE x [1 - VD/Vt]). While decreased VA is the most common reason for the respiratory failure of hypercapnia, increased CO2 production is a very rare reason. Depending on the cause of respiratory failure, the partial pressure of oxygen (PaO2) may be normal or decreased. The two main paradigms responsible for hypercapnia respiratory failure are either manifested by "won't breathe" due to a central drive issue or "can't breathe" as a result of a peripheral neuromuscular defect, resistive loading (narrow airway) or restrictive defect that lead to hypoventilation and hypercapnia.

Respiratory pump failure: The respiratory pump is comprised of the chest wall, the pulmonary parenchyma, the muscles of respiration, as well as the central and peripheral nervous systems. The inability to ventilate can occur if any of the components mentioned above of the respiratory pump fails.

Decreased central dive: Sedatives (i.e., alcohol, benzodiazepines, and opiates) and diseases of the central nervous system (i.e., encephalitis, stroke, tumor, and SCI) may impair the respiratory drive, resulting in hypoventilation.[14]

Altered neural and neuromuscular transmission: Amyotrophic lateral sclerosis, botulism, Guillain-Barre syndrome, myasthenia graves, organophosphate poisoning, poliomyelitis, spinal cord injury (SCI), tetanus, and transverse myelitis may impair the function of the respiratory pump, resulting in hypoventilation.[14]

Chest wall and pleural disorders: Flail chest, kyphoscoliosis, hyperinflation, large pleural effusions, obesity, and thoracoplasty may impair the function of the respiratory pump, resulting in hypoventilation.

Dead space ventilation: Conditions that increase the V/Q ratio, such as acute respiratory distress syndrome, bronchitis, bronchiectasis, emphysema, and pulmonary embolism, can result in hypoventilation. Hypoventilation typically occurs once dead space ventilation exceeds 50% of total ventilation.

Muscle abnormalities: Diaphragmatic paralysis, diffuse atrophy, muscular dystrophy, and ruptured diaphragm may impair the function of the respiratory pump, resulting in hypoventilation.

Increased dead space: Dead space (VD) refers to areas of the lung that are not anatomically or physiologically able to exchange gas. Tachypnea can contribute to high CO2 by increasing the dead space to tidal volume ratio (VD/Vt). High alveolar VA and the associated ventilation-perfusion mismatch are considered one of the main mechanisms for developing hypercapnia in individuals with COPD.[15]

Increased CO production: CO2 is a by-product of oxidative metabolism, and high CO2 production may occur due to fever, exercise, hyperalimentation, sepsis, and thyrotoxicosis. High C2Oproduction becomes pathologic if the compensatory increase in minute ventilation mechanism fails.[16]

History and Physical

Respiratory failure is a syndrome with a myriad of etiologies; therefore, a thorough history and physical examination are required to narrow the differential diagnosis.

History

Patients typically present with respiratory symptoms (i.e., dyspnea, cough, hemoptysis, sputum production, and wheezing); however, symptoms from other organ systems (i.e., chest pain, decreased appetite, heartburn, fever, and significant weight loss) are important. Loss of smell and/or exposure to sick people or unprotect contact with individuals with coronavirus infection (COVID-19) is essential in suspecting COVID-19 illness and associated respiratory failure, particularly in high-risk patients (older patients, men, and morbidly obese).[17] For a specific population, the presence of immunocompromised conditions or taking immunosuppressants is also essential in risk-stratifying patients at risk for respiratory failure early on.

For patients already diagnosed with airway disease, it is important to assess inhaler compliance and technique, recent steroid use, as well as exposure to environmental triggers. For patients with hypertension and chronic cough, the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers should be investigated.

Social history is also crucial when considering respiratory failure. Alcohol use and sexually transmitted diseases may lead to an immunocompromised state, making patients more susceptible to certain infections, while a sedentary lifestyle may increase the risk of pulmonary embolism. Habits such as having birds and hobbies such as diving and flying may have implications when considering etiologies of respiratory failure. Most importantly, a patient's tobacco smoking history should be investigated, including exposure to second-hand smoke, marijuana smoking, smoking e-cigarettes, and vaping.[18]

General inspection: Accessory muscle use, altered mental status, cachectic, conversational dyspnea, diaphoresis, fever, respiratory distress (i.e., at rest or with exertion), obesity, and purse-lipped breathing

Head: Cushingoid appearance, central cyanosis, Horner's syndrome, and pale conjunctiva

Neck: Jugular venous distention, lymphadenopathy, and tracheal deviation

Chest/thorax: Asymmetrical chest expansion, bradypnea, bronchial breath sounds, Cheyne-Stoke breathing, crackles, decreased breath sounds, dullness to percussion, hyper-resonance to percussion, Kussmaul breathing, kyphoscoliosis, loud P2, paradoxical breathing, pectus carinatum, pectus excavatum, pleural rub, reduced chest expansion, rhonchi, stridor, tachypnea, tactile vocal fremitus, vesicular breath sounds, vocal resonance, wheezes, and whispering pectoriloquy

Upper extremities: Asterixis, digital clubbing, peripheral cyanosis, tobacco staining, and tremor

Lower extremities: Edema, peripheral cyanosis, and unilateral swelling.[20]

Finally, an occupational history may be helpful when considering work-related lung disease (i.e., hypersensitivity pneumonitis and pneumoconiosis), while a family history may be beneficial when considering atopic, genetic (i.e., alpha-1-antitrypsin deficiency and cystic fibrosis), and infectious diseases (i.e., tuberculosis).[19]

Physical Examination

Signs of respiratory failure may be present throughout the body. Physical examination findings by region appear below:

Evaluation

As discussed above, respiratory failure is a syndrome caused by a multitude of pathological states. As such, a single algorithm for evaluating respiratory failure does not exist. Appropriate diagnostic studies may include laboratory assays (i.e., complete blood count with differential, comprehensive metabolic panel with magnesium/phosphorous, procalcitonin, troponin, and thyroid-stimulating hormone), infectious workup (i.e., blood cultures, sputum cultures, respiratory pathogen panel test, and urinary antigen test), and 12-lead electrocardiography. Evaluation of respiratory failure with arterial blood gas, capnometry, radiography, pulse oximetry, and ultrasonography are discussed below.

Arterial Blood Gas

Arterial blood gas (ABG) is the gold standard for diagnosing respiratory failure. At a minimum, the information obtained from an ABG includes pH, partial pressure of arterial oxygen (PaO2), partial pressure of arterial carbon dioxide (PaCO2), and serum bicarbonate (HCO3). It should be noted that the HCO3 obtained from an ABG is a calculated value and may therefore be inaccurate. Analysis of an ABG should instead be performed using a measured HCO3 obtained from a basic metabolic panel.

Oxygenation is assessed through the interpretation of the PaO2. Hypoxemia is defined as a PaO2 less than 60 mmHg. Ventilation is assessed through the interpretation of the PaCO2. Hypercapnia is defined as a PaCO2 greater than 45 mmHg.

Information from the ABG can also be used to differentiate acute from chronic respiratory failure by evaluating the renal response to PaCO2. In respiratory acidosis, the kidneys respond by increasing the absorption of HCO3 in the proximal convoluted tube. As this is a slow process, the magnitude of HCO3 absorption in acute respiratory acidosis is less than the magnitude of HCO3 absorption in chronic respiratory acidosis. This difference allows for the distinction between the chronicity in acute and chronic respiratory failure.[21]

Capnometry

Capnometry, the measurement of carbon dioxide in exhaled gas, may be qualitative or quantitative. Colorimetric capnometry is a qualitative measure of carbon dioxide in exhaled gas that relies on the color change of a pH-sensitive indicator. Infrared capnometry is a quantitative measure of carbon dioxide in exhaled gas that relies on measuring the partial pressure of carbon dioxide (pCO2). Quantitative capnometry provides more information than qualitative capnometry.[22]

In the non-pathological state, the partial pressure of carbon dioxide at the end of expiration, or end-tidal pCO2 (PETCO2), approximates the partial pressure of carbon dioxide in the arterial blood (PaCO2). The PaCO2 is typically 2 to 3 mmHg greater than the PETCO2. In the pathological state, where gas exchange is impaired, the difference between the PaCO2 and PETCO2 becomes greater than 3 mmHg due to increased dead space ventilation.[23]

Values obtained from quantitative capnometry can be plotted graphically and displayed as waveform capnography. Analysis of these waveforms allows for detecting pathological states (i.e., apnea, bronchospasm, hyperventilation, and hypoventilation).[24]

Radiography

Various imaging modalities are available for the evaluation of respiratory failure. Such options include plain films, computed tomography, magnetic resonance, nuclear medicine, angiography, and ultrasonography.[25]

Pulse Oximetry

Normal lung surface: Bat sign, lung sliding, and A-lines

Interstitial syndrome: Lung rockets

Lung consolidations: Fractal and tissue-like signs

Pleural effusions: Quad and sinusoid sign

Pneumothorax: Stratosphere sign and the lung point. [27]

Pulse oximetry relies on spectrophotometry, the process of identifying the composition of a substance via measurement of the absorption of specific wavelengths of light transmitted through the substance in question. The composition and structural configuration of hemoglobin are dependent upon molecular oxygen. In the tense state, oxygenated hemoglobin has a lower affinity for oxygen. In the relaxed state, deoxygenated hemoglobin has a higher affinity for oxygen. Pulse oximetry takes advantage of the conformational states of the hemoglobin molecule as deoxygenated hemoglobin absorbs light at wavelengths of 660 nm and oxygenated hemoglobin absorbs light at wavelengths of 940 nm. Measurement of arterial oxygenation is ensured through the analysis of pulsatile blood. Proprietary algorithms allow for the conversion of light absorption to the fraction of hemoglobin saturated with oxygen, known as oxygen saturation (SpO2). This non-invasive modality is greatly useful in diagnosing and managing respiratory failure.[26]

Ultrasonography

The bedside lung ultrasound in emergency (BLUE)-protocol is the bedside gold standard for the immediate diagnosis of acute respiratory failure. The protocol, which allows for reproducible analysis, relies on standardized thoracic locations (BLUE points) and ten ultrasonographic signs or profiles. The BLUE protocol is performed by analyzing the ultrasonographic profiles obtained at each of the three BLUE points on each side of the body. The standardized BLUE points are known as the Upper BLUE point, the Lower BLUE point, and the postero-lateral alveolar and/or pleural syndrome (PLAPS)-point. In total, there are six BLUE points. The theory behind and the application of the BLUE protocol are beyond the scope of this article; however, the ten ultrasonographic profiles are grouped with their corresponding clinical states below:

Bronchoscopy, echocardiography, nocturnal polysomnography, and pulmonary function tests may also be included in evaluating respiratory failure. Pulmonary consultation is warranted if the aforementioned diagnostic studies are required.

Treatment / Management

Treatment of respiratory failure should be directed towards the underlying cause while providing support with oxygenation and ventilation, if necessary. The treatment includes supportive measures and treatment of the underlying cause. However, the initial steps in managing patients with acute respiratory failure should start by assessing the airway, breathing, and circulation (ABC). Supportive measures depend on patent airways to maintain adequate oxygenation, ventilation, and correction of blood gas abnormalities.

Correction of Hypoxemia

The goal is to maintain adequate tissue oxygenation, generally achieved with an arterial oxygen tension (PaO2) of 60 mm Hg or arterial oxygen saturation (SaO2), about 90%.

Uncontrolled oxygen supplementation can result in oxygen toxicity and CO2 (carbon dioxide) narcosis. So the inspired oxygen concentration should be adjusted at the lowest level (90-94%), which is sufficient for tissue oxygenation.

Oxygen can be delivered by several routes depending on the clinical situations in which we may use a nasal cannula, simple face mask, nonrebreathing mask, or high-flow nasal cannula.

Extracorporeal membrane oxygenation may be needed in refractory cases.[28]

Correction of Hypercapnia and Respiratory Acidosis

This may be achieved by treating the underlying cause or providing ventilatory support.[29]

Apnea with respiratory arrest

Tachypnea with respiratory rate >30 breaths per minute

Disturbed conscious level or coma

Respiratory muscle fatigue

Failure of supplemental oxygen to increase PaO2 to 55 to 60 mmHg

Hypercapnea with arterial pH less than 7.25[30]

Ventilatory Support

Patients with severe acute respiratory failure are usually intubated.The goals of ventilatory support in respiratory failure are to

Common Indications for Mechanical Ventilation Include the Following

The choice of invasive or noninvasive ventilatory support depends on the clinical situation, whether the condition is acute or chronic, and how severe it is.[31] It also depends on the underlying cause. Noninvasive ventilation (NIV) is preferred, particularly in cases of chronic obstructive pulmonary disease (COPD) exacerbation, cardiogenic pulmonary edema, and obesity hypoventilation syndrome.[32][33][34][33][35][36]

Differential Diagnosis

The differential diagnosis for respiratory failure is broad and includes, but is not limited to, the following:

Prognosis

Respiratory failure is a syndrome caused by a multitude of pathological states; therefore, the prognosis of this disease process is difficult to ascertain. In 2017 in the United States of America, however, the in-hospital respiratory failure mortality rate was 12%. The case definition used in this study included all diagnosis codes, which included respiratory failure.[2] In-hospital mortality rates for patients requiring intubation with mechanical ventilation for asthma exacerbation, acute exacerbation of chronic obstructive pulmonary disease, and pneumonia were found to be 9.8%, 38.3%, and 48.4%, respectively.[37][38][39] Lastly, the in-hospital mortality rate for acute respiratory distress syndrome was found to be 44.3%.[40]

Complications

Respiratory failure is associated with both pulmonary and extrapulmonary complications, especially in the acute setting. Pulmonary complications include bronchopleural fistula, nosocomial pneumonia, pneumothorax, pulmonary embolism, and pulmonary fibrosis, while extrapulmonary complications include acid-base disturbances, decreased cardiac output, gastrointestinal hemorrhage, hepatic failure, ileus, infection, increased intracranial pressure, malnutrition, pneumoperitoneum, renal failure, and thrombocytopenia. Clinicians should be aware of the conditions mentioned earlier and be prepared to offer prophylactic therapy or proper treatment for such complications when applicable.[41][42]

Consultations

Depending on the severity of the respiratory failure, consultation with a Pulmonary specialist may be warranted in the patient's care.

Deterrence and Patient Education

While patients should be educated on the symptoms of respiratory failure, they should also be aware of the importance of device and medication compliance, as well as modifiable risk factors and how they relate to disease prevention. For instance, the following strategies are efficacious in preventing acute exacerbations of chronic obstructive pulmonary disease: Adherence to pharmacological therapy, pulmonary rehabilitation, smoking cessation, and vaccination (i.e., influenza and pneumococcal).[43] Unfortunately, not all causes of respiratory failure are preventable. Patients should seek prompt evaluation and treatment if they become symptomatic.

Enhancing Healthcare Team Outcomes

Diagnosing the underlying cause of respiratory failure and its treatment is challenging as this syndrome can result from numerous pulmonary and extrapulmonary causes. As such, consultation with other specialties (i.e., cardiology and neurology) may be mandatory. Moreover, discussing radiographic findings with a radiologist can sometimes be necessary. Additionally, complications from respiratory failure may be due to improper patient positioning and poor adherence to infection control policies. Fortunately, nurses are vital members of the interprofessional healthcare team, assuring appropriate patient positioning. Nursing is also responsible for feeding, monitoring, and suctioning the patient and can offer patient counseling while serving as a contact point for the various specialties involved in the case. All interprofessional team members are responsible for keeping meticulous records of every interaction and intervention with the patient so that every care team member has access to the same accurate, updated patient information.

Since patients with respiratory failure may require multiple medications, the pharmacist is instrumental in ensuring safe medication administration, performing medication reconciliation, answering drug questions for the care team, and providing medication counseling for the patient. Finally, respiratory therapists also care for a patient with respiratory failure (i.e., administration of oxygen and chest physiotherapy). All interprofessional team members must engage in meticulous documentation and report any changes in patient status to the appropriate team members for possible corrective action. This interprofessional team works to improve patient care and outcomes through collaborative activity and open communication. [Level 5]

References

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The respiratory system allows gas exchange between the environment and the body, facilitating the process of aerobic metabolism. Specifically, the respiratory system provides oxygen and removes carbon dioxide from the body. The inability of the respiratory system to perform either or both of these tasks results in respiratory failure.

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1. Lung and Airway Diseases

COPD (emphysema, chronic bronchitis)

Asthma

Lung cancer

Pneumonia

Cystic fibrosis

Severe pneumonia

2. Conditions Affecting Breathing Muscles and Nerves

Muscular Dystrophy

Guillain-Barre Syndrome

Myasthenia Gravis

ALS

Parkinson’s Disease

3. Chest and Back Injuries

Trauma to chest, spine, or brain

4. . Other Medical Conditions

Heart problems

Severe infections

Severe scoliosis

Obesity Hypoventilation Syndrome

Stroke

5.  Lifestyle Factors

Smoking

Alcohol abuse

Drug overdose

Exposure to smoke/chemicals

Severe allergies

6. Other Factors

Age (older adults = higher risk)

Family history (respiratory diseases)

Medical procedures (lung surgery, ventilation)

Air pollution

# data[].attributes.body
What is ABG?

Arterial Blood Gas (ABG) is a test that measures the levels of oxygen (O₂), carbon dioxide (CO₂), and acidity (pH) in arterial blood. It helps assess how well the lungs and kidneys are maintaining acid–base balance, and how effectively gas exchange is happening in the lungs.

ABG is a test that measures:

pH: How acidic or alkaline the blood is.

PaCO₂: Amount of carbon dioxide (reflects lung function).

HCO₃⁻ (bicarbonate): Reflects kidney function and compensation.

PaO₂: Oxygen level in the blood

How It Works (Mechanism):

1. Blood is drawn from an artery (usually radial).

2. A blood gas analyzer measures gas tensions and calculates acid-base balance.

3. Helps differentiate respiratory vs. metabolic disorders and detect respiratory failure.

Using the chart:

1. Identify the Primary Disorder:

pH = 7.30 → Acidosis

PaCO₂ = 58 mmHg → ↑ = Respiratory Acidosis

HCO₃⁻ = 38 mmol/L → ↑ = Renal Compensation

PRIMARY DISORDER: RESPIRATORY ACIDOSIS (↑ CO₂ causes ↓ pH)

+Why Did This Happen to AD?

AD was given IV diazepam (sedative) and IV tramadol.

These drugs suppress breathing → slower RR = less CO₂ removed → CO₂ builds up → respiratory acidosis

2. Is Compensation Present?

Look at the bicarbonate (HCO₃⁻) level:

For chronic respiratory acidosis, every ↑10 mmHg in PaCO₂ → ↑HCO₃⁻ by 4 mmol/L

Normal PaCO₂ = 40 mmHg → AD’s = 58 mmHg → increase = +18 mmHg

Expected increase in HCO₃⁻ = 4 × (18/10) = ~7.2 mmol/L

Normal HCO₃⁻ = 24 → expected ~31.2 mmol/L

AD’s actual HCO₃⁻ = 38 mmol/L → excessive compensation

🔴 Overcompensated → possible combined metabolic alkalosis or prolonged compensation.

3. Final Diagnosis for AD:

✅ Primary Respiratory Acidosis
➕ Metabolic compensation (HCO₃⁻ retention)
➡ Suggestive of chronic respiratory compromise (likely due to COPD)
➕ Aggravated by CNS depressants (IV diazepam + tramadol) causing hypoventilation
➡ Drug-induced Type 2 Respiratory Failure

Referene: https://www.nursingtimes.net/emergency-and-critical-care/essential-critical-care-skills-6-arterial-blood-gas-analysis-28-03-2022/

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1. make sure no complications after removal of chest tube

2. make sure no air leakage during or after chest tube insertion

3. monitor lung function

4. monitor oxygen saturation

5. monitor vital sign

https://moh.gov.my/moh/resources/Penerbitan/Program%20Bebas%20Kesakitan/Garis%20Panduan/Pain_Management_in_ETD_2020_(2nd_Ed.)_.pdf

https://www.moh.gov.my/moh/resources/Penerbitan/Hospital%20Bebas%20Kesakitan/Bahan%20Pendidikan/Pain_Management_in_Emergency_Trauma_Department.pdf

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alternatives for chest tube insertion pain management

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alternatives for chest tube insertion pain management

# data[].attributes.headline
Are underweight people more susceptible to getting pneumothorax?

# data[].attributes.subject
Are underweight people more susceptible to getting pneumothorax?

# data[].attributes.attachment_link.title
Association Between BMI and Recurrence of Primary Spontaneous Pneumothorax

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Whether body mass index (BMI) is a significant risk factor for recurrence of primary spontaneous pneumothorax (PSP) remains controversial. The purpose of this study was to examine whether BMI and other factors are linked to risk of PSP recurrence. A…

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50-100 mg i.v. every 4-6 hrs

https://pmc.ncbi.nlm.nih.gov/articles/PMC4332101/

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Postoperative pain is a very important issue for several patients. Indifferent of the surgery type or method, pain management is very necessary. The relief from suffering leads to early mobilization, less hospital stay, reduced hospital costs, and…

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1. Smoke cessation plan

2. Methadone replacement therapy (chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://pharmacy.moh.gov.my/sites/default/files/document-upload/garis-panduan-pendispensan-rawatan-terapi-gantian-methadone.pdf)

# data[].attributes.body
Smoking

Damages lung tissue and slows recovery.

Increases the risk of another pneumothorax or infection.

Reduces the effectiveness of inhalers and medications.

Alcohol

Can suppress breathing, especially if taken with sedatives like tramadol or diazepam.

Weakens the immune system, increasing infection risk.

May interact with prescribed medications.

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Limit activities involving pressure changes like scuba diving and flying

# data[].attributes.subject
Limit activities involving pressure changes like scuba diving and flying

# data[].attributes.body
Activities like scuba diving, flying, and high-altitude travel can put extra pressure on the lungs and increase the risk of pneumothorax, especially in individuals with a history of the condition.

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A balanced diet rich in fruits, vegetables, and lean proteins, along with adequate hydration, can contribute to overall lung health and recovery.

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Identify and avoid triggers that worsen COPD symptoms, such as allergens, irritants, and secondhand smoke.

Maintain good air quality indoors by using air purifiers and avoiding strong scents.

Be aware of air quality alerts and take precautions during periods of high pollution.

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-       Pain assessment requires taking a detailed pain history.  Use PAIN approach such as where is the pain, aggravating factor, intensity and neutralizing factor.

o   This can provide pharmacist to have better judgement and give appropriate medication.

-       Counsel the SE of the medication and the function of medication use(so able to comply)

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1. 📱 Digital Health Integrator

Problem: AD has COPD, poor medication adherence, and frequent exacerbations.

Pharmacist role: Recommends digital tools like medication reminder apps or smart inhalers with Bluetooth tracking (e.g., Propeller Health, Hailie®).

Impact: Improves inhaler adherence and allows remote monitoring of use patterns by clinicians to pre-empt future exacerbations or pneumothorax risk.

2. 🩺 Transitional Care Coordinator

Post-discharge, AD is at high risk of readmission.

Pharmacist coordinates a "meds-to-beds" program, ensuring all discharge meds are ready and the patient understands how and when to take them.

Conducts a 30-day medication follow-up call to assess adherence, new side effects, and reinforce lifestyle changes.