PULMONARY CRITICAL CARE
In this section, you will learn about the following topics:
Respiratory Failure
Advanced Airway Training
ARDS
Mechanical Ventilation
Pneumonia
Pleural Effusions/Pleural Fluid
VTE
Respiratory Failure
In the ICU, patients often suffer from severe illnesses or injuries that compromise their ability to breathe effectively. Insufficient oxygen delivery to vital organs can lead to organ dysfunction or failure, making it imperative to address respiratory failure promptly and comprehensively.
Respiratory failure can be classified into two types: hypoxemic respiratory failure and hypercapnic respiratory failure. Hypoxemic respiratory failure is characterized by low levels of oxygen in the blood, while hypercapnic respiratory failure is characterized by high levels of carbon dioxide in the blood.
One of the keys to diagnosing respiratory failure is looking at an arterial blood gas (ABG). This test measures the levels of oxygen, carbon dioxide and pH in the arterial blood. Chest x-rays are commonly performed to assess the condition of the lungs and determine the cause of respiratory failure to guide further diagnostic interventions. In some cases, a computed tomography (CT) of the chest may be necessary to provide more detailed images as well as any structural abnormalities.
Treatment for respiratory failure involves reversing the underlying cause as well as giving supportive care through the use of supplemental oxygen or helping provide ventilation.
Hypoxic Respiratory Failure: oxygen can be delivered through many different devices. The most common you will see is a nasal cannula, face mask, non-rebreather or high flow nasal cannula. All of these devices solely help improve oxygenation, but do not provide ventilation.
Nasal cannula gives the lowest amount of flow and FiO2. The max flow it gives is 6L/minute and it delivers ~4% of oxygen per each liter above room air (21%). If a patient is on 4L NC this implies that the nasal cannula is giving 4L/min flow, therefore the patient is receiving is around 37% FiO2 (16% + 21% off room air); it is hard to calculate this with 100% accuracy due to not ALL of the oxygen being delivered into the patient - some leaks into the air. Typically, when talking about nasal cannula, you only reference the flow - not the estimated FiO2 - since it is so difficult to estimate.
Simple Face Mask provides more flow than a nasal cannula and is most commonly used for respiratory treatments. It is rarely used to treat hypoxia although in some cases where a patient primarily breathes out of their mouth you will see it.
Venturi Mask has more flow than a nasal cannula and simple face mask (up to 15L), but a lower FiO2 than a non-rebreather.
Non-Rebreather delivers 12-15L/min of flow, but can deliver higher amounts of oxygen due to the fact it has a one-way valve that prevents outside air from coming in (hence the name non-rebreather). Sometimes you will hear someone is on “100% NRB” it implies that they are receiving 100% FiO2 from the wall, but due to it being an imperfect device, the patient only receives 80-95%.
High flow nasal cannula is just like a regular nasal cannula, but it provides higher flow rates (and therefore you are able to give higher amounts of FiO2). At Piedmont we have two main types of high flow nasal cannula: salter nasal cannula and optiflow. Both the flow rate and FiO2 can be titrated independently unlike a regular nasal cannula.
Salter HFNC: Looks just like a nasal cannula but a much thicker tube that is colored green entering the wall. Although this is considered a “high flow” nasal cannula by definition (because it has higher flow than a regular nasal cannula) it can only go up to 15 L/min. This is often seen as a transition when stepping DOWN from optiflow to regular NC, but not used when titrating up. In the unit you will hear it called “salter” (the patient is on 10L salter).
Optiflow HFNC: has white tubing like in the picture below. It has a max flow rate of 60L min, so this is often what is referenced as a “high flow nasal cannula” when you are on the unit.
Hypercapnic Respiratory failure: hypercapnia is caused by inadequate ventilation rather than inadequate oxygenation. Ventilation is the process of blowing out carbon dioxide in order to maintain adequate pH. Disease states that affect the patients ability to “blow out” carbon dioxide - either by lack of breathing or by obstruction preventing air from blowing out - cause hypercapnic respiratory failure.
Non-invasive ventilation (NIV) such as BiPAP is a commonly used treatment option for hypercapnic respiratory failure. It involves the delivery of positive pressure ventilation through a mask or nasal prongs, without the need for intubation. NIV helps to improve both oxygenation/ventilation and reduce the work of breathing by providing additional support to the respiratory muscles. It is particularly beneficial for patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) and cardiogenic pulmonary edema. NIV can also be used as a bridge to intubation or as a means of avoiding invasive mechanical ventilation altogether.
In cases where non-invasive ventilation is ineffective or contraindicated, invasive mechanical ventilation may be necessary. This involves the insertion of an endotracheal tube or tracheostomy tube to deliver positive pressure ventilation directly into the lungs. Invasive mechanical ventilation is commonly used in patients with severe respiratory failure, such as those with acute respiratory distress syndrome (ARDS) or acute exacerbations of other underlying lung diseases. The ventilator settings are carefully adjusted to optimize oxygenation and ventilation while minimizing the risk of ventilator-induced lung injury.
Resources to complete:
FCCS Ch. 4
Marino 3rd ed: Ch. 19,22; 4th ed Ch 20, 23
Pulmcast: Always give 100% (Except when it comes to oxygen)
Advanced Airway training
You will complete advanced airway training at the difficult airway course.
Resources to complete:
Pulmcast - Owning the airway (when you don’t own the airway)
Acute Respiratory distress Syndrome (ARDS)
Acute Respiratory Distress Syndrome (ARDS) is a life-threatening condition characterized by severe respiratory failure. It is a complex disorder that affects the lungs and can occur as a result of various underlying causes. ARDS is a critical condition that requires immediate medical attention and intensive care management.
ARDS is primarily characterized by the rapid onset of severe respiratory distress, which is often accompanied by hypoxemia (low oxygen levels in the blood). The condition can develop in response to direct lung injury, such as pneumonia or aspiration of gastric contents, or indirect lung injury, such as sepsis or trauma. Regardless of the cause, ARDS is characterized by an inflammatory response in the lungs, leading to increased permeability of the alveolar-capillary membrane and subsequent pulmonary edema.
The pathophysiology of ARDS involves a cascade of events that ultimately leads to impaired gas exchange and respiratory failure. The initial insult triggers an inflammatory response, resulting in the release of various pro-inflammatory mediators. These mediators cause damage to the alveolar-capillary membrane, leading to increased permeability and leakage of fluid into the alveoli. This fluid accumulation impairs the exchange of oxygen and carbon dioxide, leading to hypoxemia and respiratory distress.
Mechanical ventilation is a cornerstone of treatment for patients with ARDS who have severe respiratory failure. The primary goal of mechanical ventilation is to provide adequate oxygenation and ventilation while minimizing further lung injury. Different ventilation strategies are employed to optimize lung function and minimize ventilator-induced lung injury (VILI).
Lung-Protective Ventilation: Lung-protective ventilation strategies aim to minimize the risk of VILI by using lower tidal volumes and limiting airway pressures. The use of low tidal volumes (around 6 mL/kg of predicted body weight) and higher positive end-expiratory pressure (PEEP) levels helps to maintain alveolar recruitment and prevent lung collapse.
Prone Positioning: Prone positioning involves placing the patient in a face-down position to improve oxygenation and reduce the risk of ventilator-induced lung injury. Prone positioning helps to redistribute lung perfusion, improve ventilation-perfusion matching, and reduce the pressure on the dependent lung regions. It is one of the only interventions in ARDS shown to improve mortality.
Extracorporeal Membrane Oxygenation (ECMO): In severe cases of ARDS, where conventional mechanical ventilation fails to provide adequate oxygenation, ECMO may be considered. ECMO involves the use of a machine that temporarily takes over the function of the heart and lungs, allowing the lungs to rest and heal.
In addition to the above treatment strategies, several adjunctive therapies may be considered in the management of ARDS. These therapies aim to reduce lung inflammation, improve oxygenation, and promote lung healing. Some of the adjunctive therapies include:
Corticosteroids: The use of corticosteroids in ARDS remains controversial. In certain cases, corticosteroids may be considered to reduce lung inflammation and improve oxygenation. However, their use should be carefully evaluated, considering the potential risks and benefits.
Neuromuscular Blockade: Neuromuscular blockade with medications such as cisatracurium may be used in severe cases of ARDS to improve patient-ventilator synchrony, reduce ventilator-induced lung injury, and optimize oxygenation.
Exhaled Nitric Oxide: Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator that can improve oxygenation in patients with ARDS by reducing pulmonary vascular resistance. However, its use is limited to specific cases and should be carefully monitored. It’s a bit more of hail mary in ARDS treatment.
Resources to complete:
Acute Respiratory Failure: The 5 Types of Hypoxemia
ARDSnet NEJM - Link to Summary / PDF of Article
CESAR - Link to Summary / PDF of Article
FACTT - PDF of Article
Gluzman - ARDS and Rescue Therapies
PROSEVA - Link to Summary / PDF of Article
Post-operative Respiratory Definitions
Pulmcast: To ARDSnet and Beyond Part 1 and 2
Pulmcast: Should They Stay or Should They Go? ECMO, ARDS, and when to Transfer
Mechanical Vent
The primary goal of mechanical ventilation is to ensure adequate gas exchange in patients with respiratory failure. This involves maintaining appropriate levels of oxygenation and carbon dioxide elimination. Additionally, mechanical ventilation aims to reduce the work of breathing and provide respiratory support to patients who are unable to breathe effectively on their own.
Mechanical ventilation can be delivered in various modes, depending on the patient's condition and specific needs. The choice of mode is determined by factors such as the underlying pathology, the patient's respiratory drive, and the desired level of support. Some commonly used modes of mechanical ventilation include:
Assist-Control (AC) Mode: In this mode, the ventilator delivers a set tidal volume at a predetermined rate. The patient can trigger additional breaths, which are then supported by the ventilator. AC mode is often used in patients who require full ventilatory support.
Synchronized Intermittent Mandatory Ventilation (SIMV) Mode: SIMV mode allows the patient to breathe spontaneously between the mandatory breaths delivered by the ventilator. The ventilator provides a set tidal volume and rate for the mandatory breaths, while the patient determines the depth and frequency of their spontaneous breaths.
Pressure Support (PS) Mode: PS mode provides support during the inspiratory phase of each breath. The ventilator delivers a preset pressure, which assists the patient's effort to initiate and maintain inspiration. This mode is commonly used to reduce the work of breathing and facilitate weaning from mechanical ventilation.
To optimize patient outcomes, several ventilator settings must be carefully adjusted based on the patient's condition and response to therapy. These settings include:
Tidal Volume (VT): Tidal volume refers to the volume of air delivered with each breath. It is typically set between 6-8 mL/kg of ideal body weight to avoid lung injury.
Respiratory Rate (RR): The respiratory rate determines the number of breaths delivered by the ventilator per minute. It is adjusted to maintain appropriate levels of carbon dioxide elimination.
Fraction of Inspired Oxygen (FiO2): FiO2 represents the concentration of oxygen delivered by the ventilator. It is adjusted to achieve adequate oxygenation while minimizing the risk of oxygen toxicity.
Positive End-Expiratory Pressure (PEEP): PEEP is the positive pressure maintained in the airways at the end of expiration. It helps prevent alveolar collapse and improves oxygenation by increasing functional residual capacity.
Flow Rate: The flow rate determines the speed at which gas is delivered to the patient. It affects inspiratory time and can be adjusted to optimize patient-ventilator synchrony.
Once the patient is deemed ready for weaning from ventilator support, a spontaneous breathing trial is conducted. During an SBT, the patient is temporarily disconnected from the ventilator and allowed to breathe spontaneously with minimal or no ventilatory support. Common SBT methods include T-piece trials, pressure support trials, or automatic tube compensation. The SBT is typically conducted for 30-120 minutes, and the patient's tolerance and respiratory parameters are closely monitored. Various weaning parameters and indices include rapid shallow breathing index (RSBI), cuff leak and NIF (negative inspiratory force).
RSBI: This is calculated by dividing the tidal volume by the respiratory rate. A RSBI of less than 105 has an approximately 80% chance of being succesfully extubated, whereas an RSBI of greater than 105 virtually guarantees weaning failure.
Cuff leak: the presence of a cuff leak indicates that when the ETT balloon is deflated air goes around the endotracheal tube. A positive (present) cuff leak is NORMAL. If you do not have a cuff leak, this implies that air is not leaking around the tube despite it being inflated; this may be due to swelling in the airway or crust around the tube.
NIF: this is the strength in which a patient is able to take a deep breath. A good NIF is >/= -24 cm H20. This is very patient dependent, as they must be actively participating in order to get the value. If the patient is too encephalopathic or ignores you you will not be able to get an accurate value.
Resources to complete:
FCCS Ch. 5
Marino 3rd ed: Ch’s 24-27; 4th ed: Ch 25,26, 29-30
Pulmcast: Give me Vent Liberty
Pneumonia
Pneumonia is a common and potentially serious respiratory infection that affects the lungs. It can be caused by various pathogens, including bacteria, viruses, fungi, and even certain chemicals. Pneumonia occurs when the air sacs in the lungs, known as alveoli, become inflamed and filled with fluid or pus, making it difficult to breathe.
Pneumonia can be classified into different types based on where and how it is acquired. The two main types are community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP).
Community-acquired pneumonia refers to an infection that is acquired outside of a healthcare setting. It is the most common type of pneumonia and can affect individuals of all ages. CAP is typically caused by bacteria, viruses, or, less commonly, fungi.
The pathogens that cause CAP can be transmitted through respiratory droplets when an infected person coughs or sneezes. They can also be present in the environment, such as on surfaces or in the air. Common bacteria that cause CAP include Streptococcus pneumoniae, Haemophilus influenzae, and Mycoplasma pneumoniae. Viruses such as influenza virus, respiratory syncytial virus (RSV), and rhinovirus can also cause CAP.
The symptoms of CAP can vary depending on the age and overall health of the individual. Common symptoms include cough, fever, chest pain, shortness of breath, fatigue, and in some cases, confusion or delirium in older adults. Diagnosis of CAP is usually based on a combination of clinical symptoms, physical examination, and imaging tests such as chest X-rays (although the diagnosis is not dependent on a positive chest x-ray).
Treatment for CAP depends on the severity of the infection and the causative agent. Mild cases of CAP can often be managed with rest, over-the-counter pain relievers, and plenty of fluids. Antibiotics may be prescribed for bacterial pneumonia, while antiviral medications may be used for viral pneumonia.
Hospital-acquired pneumonia, also known as nosocomial pneumonia, is a type of pneumonia that develops during a hospital stay or within 48 hours after discharge. HAP is typically more severe and associated with a higher risk of complications compared to CAP. It is often caused by bacteria that are more resistant to antibiotics.
HAP can occur when bacteria or other pathogens enter the lungs through a breathing tube, ventilator, or other medical devices. The risk of developing HAP is higher for individuals who are on mechanical ventilation, have a weakened immune system, or have underlying health conditions.
The symptoms of HAP are similar to those of CAP and may include cough, fever, chest pain, shortness of breath, and fatigue. However, individuals with HAP may also experience symptoms related to their underlying health conditions or the use of medical devices.
Diagnosing HAP involves a combination of clinical evaluation, physical examination, and laboratory tests. Chest X-rays and other imaging studies may be performed to assess the extent of lung involvement and identify any complications.
Treatment for HAP involves the use of antibiotics that are effective against the specific bacteria causing the infection. In some cases, multiple antibiotics may be prescribed to cover a broad range of pathogens. Supportive care, such as oxygen therapy and respiratory treatments, may also be provided to help manage symptoms and improve lung function.
Preventing both CAP and HAP involves practicing good respiratory hygiene, such as covering the mouth and nose when coughing or sneezing, washing hands regularly, and avoiding close contact with individuals who have respiratory infections. Vaccination against certain pathogens, such as the influenza virus and Streptococcus pneumoniae can also help reduce the risk of developing pneumonia.
Respiratory Cultures at Piedmont
At Piedmont, there are multiple tests available to check for agents that can cause pneumonia. The first is called “Pneumonia Panel by PCR”. This is a multiplex PCR test that detects certain organisms and resistance genes from respiratory samples. Results are typically available after one hour. It is important to note that this test is only capable of detecting the following in the list below, but it won’t detect all gram negative pathogens (e.g. Stenotrophomonas, Morganella, Citrobacter).
The panel will either report that no organisms included in the panel are detected, or it will report an organism + a resistance gene.
Bacteria (on PCR):
Acinetobacter calcoaceticus-baumannii complex
Enterobacter cloacae complex
Escherichia coli
Haemophillus influenzae
Klebsiella aerogenes
Klebsiella oxytoca
Klebsiella pneumoniae group
Moraxela catarrhalsi
Proteus spp.
Psuedomonas aeurginosa
Serratia marcescens
Staphyloccocus auerus
Streptococcus agalactiae
Streptococcus pneumoniae: “rust colored sputum”
Streptococcus pyogenes
Viruses and Atypical Pathogens: Respiratory Panel
Chlamydia pneumoniae
Legionella pneumophila
Mycoplasma pneumoniae
Adenovirus
Coronavirus
Human metapneumovirus
Human rhinovirus/enterovirus
Influenza A
Influenza B
Parainfluenza Virus
Respiratory Syncytial Virus
Resistance Genes
CRO —> Carbapenemase resistant: IMP, KPC, NDM, OXA-48-like, VIM
ESBL: CTX-M
MRSA —> Methicillin Resistance: mecA/C and MREJ
You can also check a Respiratory 2.1 Panel by PCR. It do this test you must obtain either a nasophrayngeal swab (preferred) or BAL fluid. It typically takes 2-4 hours to process. This checks for the following viruses:
Adenovirus: usually cause febrile illnesses in young children; can also have GI, neurologic manifestations
Common human coronaviruses that usually cause mild to moderate upper respiratory tract illnesses:
Coronavirus 229E
Coronavirus HKU1
Coronavirus NL63
Coronavirus OC43
Human Metapneumovirus
Bordetella pertussis: “whooping cough”
Bordatelle parapertussis: similar to whooping cough, but does not produce pertussis toxin so in general symptoms are less severe and even sometimes asypmtomatic
Chlamydia (Chalmydophila) pneumoinae
Mycoplasma pneumoniae
Human Rhinovirus/Eneterovirus: frequent cause of common cold
Influenza A/Influenza B (the “flu”)
HPIV:
Parainfluenza Virus 1/Parainfluenza Virus 2: causes colds and croup
Parainfluenza Virus 3: more likely to cause bronchiolitis, bronchitis or pneumonia
Parainfluenza Virus 4: we don’t know as much; experts think it causes illness similar to HPIV-3
Respiratory Syncytial Virus: causes mild, cold like symptoms, usually seen in infants or older adults
Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2)
Resources to complete:
Pulmcast: Time To Reconsider Macrolide Monotherapy
Pulmcast: Severe CAP, the ‘Roid Debate Rages on
Pleural Fluid
Pleural fluid accumulation can significantly impact lung function, leading to impaired oxygenation and ventilation, especially in patients with pleural effusions, pneumonia, or other respiratory pathologies. Accurate assessment of pleural fluid volume, composition, and underlying causes is crucial for guiding appropriate interventions to relieve respiratory distress and optimize lung function in critically ill patients.
The visceral pleura and parietal pleura are two layers of membrane that cover the lungs and cover the chest wall. These two layers have a thin layer of fluid between them; this helps the layers slide without creating friction. A pleural effusion is excess fluid that accumulates within this pleural space. The fluid itself is considered either transudative or exudative.
Transudative fluid (or Transudate) is due to an inbalance between hydrostatic pressure and oncotic pressure. The hydrostatic pressure is the pressure in the capillary beds pushing fluid/solute out, and the oncotic pressure is the pressure pulling fluid into the capillaries and preventing fluid from leaving. Some examples of this include fluid from heart failure, hepatic hydrothorax and atelectasis.
Exudative Fluid (or Exudate) is fluid due to inflammation within the pleura that leads to increased capillary permeability. When infections like pneumonia develops, the body sends white blood cells and other immune cells to the affected area to fight off the infection. In response to this immune response, the blood vessels in the lungs become more permeable, allowing fluid to leak into the pleural space. This is commonly from infections, malignancies, ARDS, lung abscesses and sarcoidosis. Chyle (from a ruptured thoracic duct) is also considered exudative.
The best way to see if someone has a pleural effusion is to check an upright chest x-ray, where you will have blunting of the costophrenic angles/loss of silhouette. It’s usually dense but can be cloudy appearing (especially for patients on the ventilator - since they can’t sit upright, the effusion layers more posteriorly)..
Steps To Evaluating Effusions
Get chest x-ray. If you are questioning your x-ray, you can order chest ultrasound to evaluate further
Once determined it’s aminable to thoracentesis, you can:
Do thoracentesis yourself (with an attending)
Order IR or US thoracentesis
Once you have pleural fluid, the following lab studies can help you depending on what you’re looking for:
To determine transudative vs exudative: serum LDH, serum total protein, pleural LDH, pleural protein in order to calculate lights criteria (see below)
If you see cloudiness: check pleural triglycerides (often chylothorax/chyle leak)
If you see blood: pleural Hgb/Hct
Clinical Pearls
Unilateral pleural effusions are mostly exudative, while bilateral effusions are often transudative (e.g. CHF)
Heart failure related effusions are often greater on R than on L
A massively sized unilateral effusion = think malignancy
A loculated effusion = think empyema until proven otherwise
In effusions caused by atelectasis, there is mediastinal shift towards the effusion.
Venous Thromboembolism
Venous thromboembolism (VTE) is a medical condition characterized by the formation of blood clots in the veins, which can lead to serious health complications. It encompasses two main conditions: deep vein thrombosis (DVT) and pulmonary embolism (PE).
There are many risk factors for VTE, listed below:
Prolonged immobility: Sitting or lying down for long periods, such as during long flights or bed rest after surgery, can increase the risk of DVT.
Injury or surgery: Trauma to the veins or surgery can damage the blood vessels, making them more prone to clotting.
Pregnancy: Pregnancy increases the risk of DVT due to hormonal changes and increased pressure on the veins.
Obesity: Excess weight puts additional pressure on the veins, increasing the risk of clot formation.
Smoking: Smoking damages the blood vessels and increases the risk of clotting.
Certain medical conditions: Conditions such as cancer, heart failure, and inflammatory bowel disease can increase the risk of DVT.
Genetic factors: Some individuals have an inherited tendency to develop blood clots, which can increase the risk of DVT.
DVT occurs when a blood clot forms in one of the deep veins, usually in the legs or pelvis. This clot can partially or completely block the blood flow, causing swelling, pain, and discomfort in the affected area. If left untreated, the clot can break loose and travel through the bloodstream to the lungs, resulting in a PE. Signs and symptoms of a DVT include swelling, pain, warmth/redness, and vein prominence.
PE is a potentially life-threatening condition that occurs when a blood clot, usually from the legs, travels to the lungs and blocks one of the pulmonary arteries. This occurs when a clot, known as a thrombus, breaks free and enters the bloodstream. The clot then travels through the veins until it reaches the pulmonary arteries, where it becomes lodged and obstructs blood flow. This obstruction can impair blood flow to the lungs, leading to difficulty in breathing, chest pain, and in severe cases, it can cause heart failure or even death.
One of the most common symptoms of pulmonary embolism is sudden shortness of breath, which may occur at rest or during physical activity. Chest pain, often described as sharp or stabbing, may occur with pulmonary embolism. The pain may worsen with deep breaths or coughing. It can cause an increased heart rate, known as tachycardia. Coughing, sometimes with blood-tinged sputum, may occur.
When it comes to the diagnosis of PE, the first step is getting a chest x-ray; not to look for a PE but to look for other conditions that may be causing the patient’s symptoms. The gold standard for diagnosis of a PE is CT chest angiogram with PE protocol. This uses contrast dye to visualize blood flow in the vessels of the lungs. If you are unable to get a CT angiogram, you may also get a Ventilation-Perfusion (V/Q) scan. This is a nuclear medicine test that evaluates the airflow (ventilation) and blood flow (perfusion) in the lungs to detect areas of reduced blood flow; the result will either be low risk, intermediate risk of high risk of PE.
Treatment for VTE include the following:
Anticoagulant Medications: Anticoagulant medications, such as heparin and warfarin, are commonly used to prevent further clot formation and allow the body's natural processes to dissolve existing clots. A lot of the choice of which anticoagulant is based off how stable the patient is, the risk of bleeding, cost and how long you want the medication to work.
Fractionated heparin - works immediately and reverses quickly when stopped, in the form of the drip. Great for inpatient - Unstable ICU patients or floor
Low molecular weight heparin (Lovenox) - works longer than heparin (4.5-7 hour long half life) and is given via subcutaneous shot. Great for inpatient - Stable ICU patients or floor patients
Warfarin - very long half life, titrated based off INR, cheap to buy outpatient
Direct oral anticoagulants - in pill form, very long half life, depending on the medication takes days to reverse when stopped
Thrombolytic Therapy: In severe cases of pulmonary embolism, thrombolytic therapy such as Altepase (tPA) may be used to rapidly dissolve the blood clot. This treatment is typically reserved for individuals with hemodynamic instability (massive pulmonary embolism).
Inferior Vena Cava (IVC) Filter: In some cases, an IVC filter may be inserted to catch blood clots before they reach the lungs. This is often considered for individuals who cannot tolerate anticoagulant medications (e.g. actively bleeding, contraindication to anticoagulation) or have recurrent pulmonary embolism despite treatment.
Catheter Directed Thrombolytics: at certain hospitals, specialists are available to perform CDT placement. This delivers thrombolytic therapy directly to the clot, avoiding the higher risk associated with systemic thrombolytics.
Surgical Embolectomy: In rare cases, surgical embolectomy may be necessary to remove the blood clot from the pulmonary arteries. This procedure is typically reserved for individuals with massive pulmonary embolism who are not candidates for thrombolytic therapy.
Resources to complete:
Marino 3rd ed: Ch. 5; 4th ed: Ch 6
EmCrit: Podcast 128: Pulmonary Embolism Treatment Options and the PEAC Team
Emcrit: Podcast 143: Oren Friedman Massive PE
PERTcast: Catheter-Directed Lysis
PERTcast: PE Risk Stratification