In this post, I’ll walk you through 10 medications you absolutely must master before your ICU rotation.

These 5 ICU hacks will save you at least two hours a day—and make you look sharp, confident, and in control from day one

Introduction:

Mechanical ventilation doesn’t have to be intimidating. If you are a non-ICU doc who just wants to feel more prepared when your patient gets intubated, this post is for you! I’m pretty sure after this, you won’t shy away from the ventilator again.

So grab a coffee, and let’s finally make sense of mechanical ventilation. Let’s get started.

Concept (1): The respiratory cycle has two phases: expiration and inspiration.

Inspiration is an active process that requires energy. Expiration is typically passive, relying on the lungs’ natural elastic recoil.

The respiratory cycle duration is calculated by dividing 60 seconds by the respiratory rate (RR). This cycle encompasses both inspiratory and expiratory time. The relationship between inspiration and expiration is not equal; physiologically, the ratio of inspiratory time to expiratory time (I:E) is typically 1:2 or 1:3, with expiration being longer than inspiration.

Example:

RR = 20 breaths/minute

The respiratory cycle duration = 60/20 = 3 seconds

Using I:E ratio of 1:3, the inspiratory time would be 0.75 seconds, and the expiratory time would be 2.25 seconds.

Concept (2): The ventilator does the heavy lifting during inspiration, but it doesn’t clock out during expiration!

As we mentioned earlier, inspiration is an active process that requires energy, so the ventilator works mainly during this active, energy-consuming phase. But that doesn’t mean the ventilator just shuts off during expiration—it continues to play a crucial role by maintaining a certain level of pressure that is called PEEP, or Positive End-Expiratory Pressure.

PEEP prevents the alveoli from collapsing at the end of expiration by holding a small amount of pressure in the lungs throughout the entire respiratory cycle, not just during the expiration phase. Think of it like a doorstop that keeps the alveoli slightly open, making the next breath easier and improving oxygenation.

Don’t be fooled by the name—PEEP isn’t just at the end of expiration. It’s present throughout the entire respiratory cycle. During expiration, it’s the only pressure applied, and during inspiration, the ventilator adds pressure on top of the PEEP to deliver the breath.

Concept (3): Air flows from higher-pressure to lower-pressure areas.

During inhalation, air enters the lungs because the pressure at the nose and mouth is higher than in the alveoli. During exhalation, the pressure in the alveoli becomes higher than at the airway opening, so air flows out. This air movement continues as long as a pressure gradient exists. In spontaneous breathing, we actively lower the pressure inside the alveoli below atmospheric pressure, creating suction and pulling air in.

In mechanical ventilation, the ventilator does the opposite: it raises the pressure at the nose and mouth above alveolar pressure to push air in. That’s why we call it a positive pressure breath

Concept (4): To get air in, the ventilator has to fight three battles: the tube, the airways, and the lungs.

During mechanical ventilation, the ventilator delivers air through the endotracheal tube (ETT), down the airways, and into the alveoli. To do this, it must overcome two main types of resistance:

• The airway resistance (from the ETT and conducting airways).
• The elastic resistance (from the alveoli and lung tissue).

The airway resistance

This resistance is primarily due to their narrow lumens and flow dynamics. The pressure required to overcome this kind of resistance is called Resistive pressure, and it is calculated by multiplying the flow by the airway resistance.

The elastic resistance

The alveoli are evaluated based on their compliance—their ability to stretch and accommodate volume. The pressure required to overcome alveolar and lung tissue stiffness is called Elastic pressure, and it’s calculated by dividing volume by compliance.

Therefore, for a full breath to be delivered, the ventilator must generate enough total pressure to overcome both the resistive and elastic or alveolar pressures. In mechanical ventilation, this pressure is called the peak inspiratory pressure (PIP).

Based on this equation:

• PIP is proportionally related to Flow, airway resistance, and TV.
• Inversely related to compliance.

Take a peek at this ventilator screen: The PIP is 20 cmH2O, the flow rate is 44 L/min, and the tidal volume is 500 mL.

• Guess what will happen to the PIP if I increase the flow or the tidal volume? Based on the equation, the peak inspiratory pressure (PIP) will increase.
• What will happen to the PIP if the patient bites the endotracheal tube or develops bronchospasm, both of which increase airway resistance? Again, you’ll also see a rise in PIP.
• Let’s say the patient develops pulmonary edema and bilateral pleural effusion. What would happen to the PIP in such a case? Pulmonary edema and bilateral pleural effusion reduce the alveoli’s ability to accommodate tidal volume (reduce their stretchability and compliance). PIP is inversely related to compliance; now the ventilator has to push harder to get the breath in, which means higher PIP is required!

Concept (5): Plateau Pressure: Your Window into Lung Compliance

Let’s imagine a moment when the flow drops to zero— this occurs briefly at the end of inspiration, just before expiration begins, and again at the end of expiration, just before the next inspiration starts. These are the transition points between phases of the respiratory cycle when there’s no airflow because the pressures between the airway and alveoli are equal.

Guess what happens to the PIP when the flow drops to zero? Let’s go back to our equation:

                                                                                        PIP = (Flow×Resistance) + (Tidal Volume/Compliance)

If the flow drops to zero, the resistive component disappears, and the equation simplifies to:

                                                                                       PIP = TV/Compliance = Alveolar Pressure.

This means when the flow is zero, the PIP is equal to the alveolar pressure, and this makes sense as pressure gradient means flow, and the absence of the gradient means no flow.

In mechanical ventilation, the pressure measured at the end of inspiration when the flow ceases is known as the Plateau pressure. Plateau pressure provides great insight into lung compliance. The lower the plateau pressure, the more compliant, stretchable, and less stiff the lung is, and vice versa!

How do we measure the plateau pressure? Plateau pressure is measured using the inspiratory pause or hold maneuver. In clinical practice, we aim for a PIP < 35 cmH2O and a plateau pressure of < 30 cmH2O.

How about the opposite? I mean the pressure measured at the end of expiration and before the inspiration valve opens? What do you think the alveolar pressure should be in such a case? We mentioned earlier that PEEP is the only pressure the ventilator provides during expiration, which means the expiratory flow will continue until the alveolar pressure drops from the maximum value at the end of inspiration (plateau pressure) down to the PEEP value, when the flow ceases. So normally, the alveolar pressure measured at the end of expiration when there is no flow must equal PEEP.

To confirm that, we perform what we call the expiratory pause maneuver. This maneuver allows us to check for any gas trapping and autoPEEP.

Concept (6): The ventilator can’t think for itself—it needs our guidance

For the ventilator to function properly, we have to give it five instructions:

• When to start the breath.
• How to deliver the breath.
• When to terminate the breath.
• How much oxygen to give?
• How much PEEP to give?

1. When to start the breath or inspiration?

The ventilator listens to the patient to detect the patient’s inspiratory effort. It will pick up any inspiratory effort as a sign that the patient is trying to breathe, and it will assist the patient with that breath! This is known as a patient’s triggered breath or, as we call it in mechanical ventilation, an Assist breath or “A” breath.

But what happens if the ventilator doesn’t detect any patient trigger? Let’s say the patient is paralyzed or brain-dead.

In this case, the ventilator has a built-in safety mechanism: it will deliver a breath if no patient’s trigger is detected for a specific time! This is called a backup breath or, as we call it in mechanical ventilation, a Control breath or “C” breath.

Take a look at these two ventilator screens. The breath on picture A is a controlled or backup breath labeled as C breath, and the breath on picture B is an assist breath triggered by the patient and assisted by the ventilator.

But what decides how long the ventilator should wait before delivering a backup breath? This timing is based on the set respiratory rate (RR), which is known as the backup rate. The backup rate is the minimum number of breaths/minute the patient receives, even if they make no effort to breathe. The ventilator will listen to the patient for a period equal to [60 sec/backup RR] before delivering the backup breath.

Example: If the backup rate is set to 15 breaths per minute, the ventilator waits up to 4 seconds (60 ÷ 15), and if no patient’s trigger is detected, a backup breath will be delivered!

The actual RR is either equal to or higher than the backup rate, but never lower! This is important when trying to adjust the backup RR. Let’s say the backup rate is 14 and the patient is breathing at 20 breaths/min; there is no point here if you increase the backup rate to 16 because the actual RR is already higher!

Take a look at this ventilator screen, see the set backup rate at 18 while the actual RR on the top is 28. Increasing the backup rate will not have any impact unless it becomes higher than the actual RR.

The values at the bottom of the picture are the set values that we provide, while those at the top are the actual live values! The ventilator tries to fulfill the set values or close to them (See the set TV is 500, but the actual one is 524).

Back to the trigger, how does the ventilator detect the patient’s trigger?

In spontaneous breathing, the patient generates negative pressure in the alveoli, which creates a suction effect that pulls air in. When the patient is intubated and connected to a ventilator, this same effort draws air through the circuit, and that’s how the ventilator knows it’s time to assist.

Take a look at the ventilator circuit picture below: you’ll notice two limbs connected to the endotracheal tube (ETT)—the inspiratory limb, which carries air from the ventilator to the patient (often passing through a humidifier), and the expiratory limb, which returns air from the patient back to the machine.

When the patient is not making any effort, air flows equally through both limbs. When the patient initiates a breath, he pulls some air from the inspiratory limb into his lungs, reducing the flow returning through the expiratory limb. The ventilator senses this imbalance and interprets it as an inspiratory effort and will go ahead and assist the patient with that breath. This is called a flow trigger.

Alternatively, the ventilator can detect a drop in airway pressure (caused by the patient’s inspiratory effort) and use that as a trigger. This is called a pressure trigger.

🔁 To summarize: the ventilator can recognize a patient’s attempt to breathe in two ways:

• Flow Triggering – by sensing a drop in flow through the expiratory limb.
• Pressure Triggering – by sensing a drop in airway pressure.

Take a look at these two screenshots of two ventilators:

• On Picture A, Psens shows the pressure trigger. It’s set at 2 cm H₂O, meaning the patient must reduce his airway pressure by at least 2 cm H₂O to trigger a breath. We usually set this between 2 and 3 cm H₂O.
• On picture B, Vsens represents the flow trigger, set at 3 L/min. This means the patient must draw in at least 3 L/min (approximately 50 mL/sec) for the ventilator to deliver a breath.

Whether using a flow trigger or a pressure trigger makes no clinical difference—neither offers a clear advantage over the other.

2. How should the ventilator deliver this breath?

In mechanical ventilation, we refer to the way of delivering the breath as the “target.” Although the term can be confusing, the concept is straightforward—just give me your full attention!

Let’s bring back our lovely equation again:

PIP = (F x R) + (TV/C).

Which can be rewritten as: PIP = (F x R) + Alveolar pressure. Which can be rearranged into: F = (PIP – Alveolar pressure) / Resistance.

In mechanical ventilation, we can directly set the flow rate and the peak inspiratory pressure (PIP) on the ventilator. However, alveolar pressure and airway resistance are not directly settable—they’re influenced by the patient’s lung mechanics and underlying condition.

Based on the equation, mathematically, for the pressure–flow relationship to hold true, we can only set one variable—either the pressure or the flow, but not both. That’s because one must remain flexible to allow the other to stay fixed. If we fix both, the equation wouldn’t hold under changing patient conditions.

This will leave us with one of two options to deliver the breath:

• You can either set the flow and let the pressure adjust, which is called the flow target.
• Set the pressure and let the flow adjust, which is called the pressure target.

In flow-targeted ventilation, we start by setting the desired flow rate. From there, we have two main subtypes based on how that flow is delivered:

1. We can ask the ventilator to keep the flow rate fixed throughout the inspiratory phase, which results in a square or rectangular flow vs time curve.
2. Or we can ask the ventilator to give the set flow rate only at the beginning of the breath, and let it progressively drop or decelerate throughout the rest of the inspiratory phase! This results in a decelerating ramp flow vs time curve.

Take a look at this flow target on this ventilator screen and notice:

• The green curve shows the decelerating ramp flow pattern.
• On the info panel, the flow target is set at Vmax: 44 L/min with the ramp type set to decelerating.

How about the pressure target ventilation?

Here, we tell the ventilator to apply a fixed amount of pressure on top of the PEEP throughout the inspiratory phase until the breath is delivered.

What do you think the flow pattern will be in the pressure target? To maintain a fixed pressure throughout the inspiratory phase, the flow must progressively decrease to keep this equation valid, “F = (PIP – Alveolar pressure) / Resistance”. Of course, as long as the resistance is constant. That’s why the flow vs time curve is always a decelerating ramp curve in pressure target modes.

Take a look at this ventilator screen, see the fixed pressure here. The ventilator adds 20 cmH2O on top of PEEP of 10 and keeps it there during the whole inspiration. The flow curve is a decelerating ramp curve.

What do you think will happen to the flow rate if we set the inspiratory pressure (Pi) at 30 cmH2O instead of 20?

If we increase the inspiratory pressure from 20 to 30 cmH₂O, the flow rate will increase; so the higher the set pressure, the greater the initial flow the ventilator delivers.

3. When should the ventilator stop delivering the breath (Cycle)?

This is known as the ‘cycle’ in mechanical ventilation. There are three main mechanisms to determine when the ventilator stops inspiration and switches to expiration. These are known as cycling mechanisms:

Volume-Cycled Ventilation:

In volume-cycled breaths, the ventilator ends inspiration once the preset tidal volume (TV) is delivered.

🔍 Look at the ventilator screen below and see the volume vs time curve. Once it reaches the desired TV, it will switch from green color, which represents inspiration, to yellow color, which represents expiration. Also, look at the top panel and see that the actual TV was 315! In reality, the ventilator doesn’t always fulfill the exact set TV, but it will be close to that!

What do you think will happen to the inspiratory time if we increase the TV here? Of course, it will increase; the larger the volume, the longer it takes to deliver it. The opposite is true.

Time-Cycled Ventilation:

In time-cycled breaths, the ventilator switches to expiration after a preset inspiratory time has elapsed, regardless of the volume delivered.

🔍 Check the ventilator screen for the set inspiratory time and see that the green line in all the curves switches to yellow after the set inspiratory time.

What do you think the TV will be if we shorten the insp time? It will be smaller as we spending less time delivering the breath, the opposit is true.

Flow-Cycled Ventilation:

In flow-cycled breaths—used primarily in pressure support mode—the ventilator ends inspiration when inspiratory flow drops to a preset percentage of peak inspiratory flow.

🔍 Look at this screen and see the “Esens” or expiratory sensitivity setting (commonly set at 25%)—the breath ends when flow falls to 25% of its peak during inspiration.

What will happen to the TV if we set ESens at 50% instead of 25%? It will be smaller as we are having a shorter inspiratory time! The opposite is true.

4. How much FiO₂ and how much PEEP? These two are oxygenation parameters, and we’ll discuss them later in this post.

Concept (7): Every Mode Is a Recipe: You Just Change the Ingredients

At the heart of mechanical ventilation are three fundamental modes:
🔹 Volume Control.
🔹 Pressure Control.
🔹 Pressure Support.

Every other mode you’ll encounter is either a hybrid or a modification of these three.

To make sense of any mode, just break it down into the three key ingredients we just explained:

🟢 Trigger – What starts the breath?
🟡 Target – How to deliver the breath?
🔴 Cycle – What ends the breath?

Before I go further!

If you’re finding this helpful, you’re going to love my full mechanical ventilation course. It covers everything we’re walking through in this video—from triggers, targets, and cycling to all the core modes—plus much more, like: Troubleshooting PIP, Rise time, Mean airway pressure, Auto-PEEP and gas trapping, Assessing weaning readiness, and how to do a proper weaning trial.

It’s designed to walk you through mechanical ventilation step-by-step, in a way that’s clear, visual, and practical.

If you’re ready to truly master the vent and feel confident at the bedside, check out the course.

Volume control or VC mode

• Trigger: VC mode typically uses assist/control (A/C) triggering. As we explained earlier, the ventilator delivers a breath either when the patient initiates one or, if the patient doesn’t, the ventilator will trigger a breath based on the set backup respiratory rate.
• Target: VC mode is flow-targeted, commonly using a decelerating ramp flow pattern.
• Cycle: VC is volume-cycled, meaning the breath ends once the preset tidal volume (TV) has been delivered.

So when ordering VC mode, in addition to the FiO2 and PEEP values, we need to provide the respiratory therapist with the following values:

• The backup RR.
• The TV.
• The Flow curve: square or decelerating.
• The Peak flow rate.

In most cases, RT will, by default, pick a decelerating ramp flow curve and set the peak flow rate; a reasonable starting peak flow rate is between 40-60 L/min.

Take a look at this VC mode screenshot,

Pressure Control (PC) Mode

• Trigger: Like VC mode, PC mode uses assist/control (A/C) triggering, meaning the breath can be triggered either by the patient’s effort or by the ventilator’s set backup respiratory rate if no spontaneous inspiratory effort is detected.
• Target: As the name suggests, PC mode is pressure-targeted. The ventilator delivers a breath by applying a set inspiratory pressure above the PEEP, and adjusts flow as needed to maintain that pressure throughout inspiration.
• Cycle: PC mode is time-cycled—the breath ends when the set inspiratory time has elapsed, regardless of how much volume was delivered.

When ordering PC mode, in addition to the FiO2 and PEEP values, we need to provide the respiratory therapist with the following values:

• Back up RR.
• Pi or inspiratory pressure, this is the pressure that will be added on top of the PEEP during inspiration.
• Ti or inspiratory time, this is the time the inspiratory pressure will be applied for.

   

Pressure support (PS) mode

• Trigger: This mode is patient-triggered only—there’s no backup respiratory rate. That’s why it’s suitable only for awake, spontaneously breathing patients, typically during the weaning phase of mechanical ventilation.
• Target: PS mode is pressure-targeted, similar to PC mode. The ventilator delivers a breath by applying a set inspiratory pressure above PEEP to assist the patient’s spontaneous effort.
• Cycle: PS mode is flow-cycled. The breath ends when the inspiratory flow decreases to a preset threshold, usually 25% of the peak inspiratory flow.

When ordering PS mode, in addition to FiO2 and PEEP values, we provide the respiratory therapist with the following values:

• Inspiratory pressure. In this mode, it’s called Pressure support.
• The flow cycle percentage is typically 25%.

There’s no backup RR because it only uses the patient’s trigger.

Concept (8): No Mode is perfect!

Each mode has its advantages and limitations.

Key Differences in Volume, Pressure, and Support Modes:

• Volume Control (VC):
  You’re guaranteed a set tidal volume, but there’s no cap on peak inspiratory pressure (PIP)—it can rise significantly if the lungs are stiff or airways are tight.
• Pressure Control (PC):
  The PIP is controlled and capped at the set level, but the tidal volume will vary based on the patient’s lung compliance and airway resistance.
• Pressure Support (PS):
  Similar to PC, PIP is limited by the set pressure support level, but tidal volume is not fixed. This mode is patient-triggered and commonly used for weaning.

How about if I take the good stuff from each mode? If I take the set tidal volume from VC mode and the controlled inspiratory pressure from PC mode? Well—that’s exactly how PRVC (Pressure-Regulated Volume Control) was born!

In PRVC, you set the tidal volume you want delivered along with the maximum pressure limit—this acts as a safety cap, not the actual pressure used in each breath.

Here’s how it works:
The ventilator adjusts the inspiratory pressure breath-to-breath to deliver the set tidal volume, while keeping the pressure as low as possible.

If the patient’s lung compliance worsens (like in ARDS), the ventilator will increase the pressure trying to maintain the tidal volume—but only up to the set pressure limit.
If compliance improves, the ventilator will lower the pressure accordingly.

If the pressure needed to deliver the tidal volume exceeds the set limit, the ventilator won’t go higher—it will under-deliver the volume and often trigger a low tidal volume alarm. That’s why choosing a reasonable pressure limit is important, especially in patients with stiff lungs.

Some ventilators also require or allow you to set an inspiratory time (Ti) in PRVC mode. If used, Ti helps shape how long the inspiratory pressure is applied. A longer Ti can help improve alveolar recruitment and oxygenation in patients with stiff lungs, while a shorter Ti may be needed in patients with obstructive lung disease to prevent air trapping.

So, in addition to FiO₂ and PEEP, the following parameters are typically set in PRVC:

• Backup respiratory rate, since it uses an A/C trigger.
• Tidal volume, because it’s volume-cycled.
• Maximum pressure limit, as a safety guard to prevent barotrauma.
• Inspiratory time (Ti), on some vents, to control the duration of pressure delivery and fine-tune I:E ratio.

Take a look at this ventilator screen (notice this particular ventilator manufacturer calls PRVC mode VC+)

SIMV (Synchronized Intermittent Mandatory Ventilation) is essentially a blend of VC or PC with pressure support. I won’t dive deeper into SIMV here, as I rarely use it in practice today, and there’s no strong clinical justification for choosing it over other modes.

Current evidence does not support the superiority of SIMV, VC, PC, or PRVC over one another in terms of clinical outcomes for patients with acute respiratory failure or other critical care conditions.

The choice of ventilation mode should always be individualized, based on the patient’s clinical status, lung mechanics, and response to therapy! I like PRVC as it may offer advantages in terms of lower peak inspiratory pressures and more stable gas exchange, making it a reasonable first choice among the three modes.

Concept (9): Tuning the Vent (Oxygenation vs. Ventilation)

When managing a ventilated patient, it’s crucial to understand what you’re trying to fix—are you trying to improve oxygenation or ventilation?

These are two distinct goals, and each is managed by adjusting different ventilator settings:

• To improve oxygenation, we focus on increasing FiO₂ and PEEP.
• To improve ventilation ( CO2 removal), we adjust the tidal volume (TV) and respiratory rate (RR).

Knowing which “knob to turn” allows you to make targeted, effective changes based on your patient’s needs—without overcomplicating things.

Hypoxia

I typically start with an FiO₂ of 100% and a PEEP of 10 cmH₂O. From there, I aim to wean the FiO₂ as quickly as possible, targeting ≤60% to minimize the risk of oxygen toxicity.

I avoid reducing PEEP until FiO₂ is down to 60% or less. If I can’t lower FiO₂ safely, I’ll consider increasing PEEP—usually in increments of 2–4 cmH₂O—to improve oxygenation. But keep in mind: raising PEEP will also increase peak inspiratory pressure (PIP).

For refractory hypoxemia, there are additional advanced strategies—such as recruitment maneuvers, paralytics, inhaled pulmonary vasodilators, and ECMO—which are beyond the scope of this video and should be managed by an intensivist.

And don’t forget: in patients with ARDS, early prone positioning is a key intervention that can significantly improve oxygenation.

Ventilation

When it comes to improving ventilation (i.e., CO₂ removal), the two main variables we adjust are the tidal volume (TV) and the respiratory rate (RR).

✅ Key Principles:

• Always use predicted body weight (PBW)—not actual body weight—to calculate tidal volume.
  • In ARDS, we aim for a lung-protective strategy:
    ➤ 6 mL/kg PBW
  • In most other conditions, a range of 6–8 mL/kg PBW is acceptable.
• If more ventilation is needed, it’s generally safer to increase the RR rather than the tidal volume to reduce the risk of volutrauma, but remember that the higher the RR, the shorter the respiratory cycle, which affects the I:E ratio.

🛠 How Tidal Volume Is Set (or Adjusted) in Different Modes:

• In VC and PRVC modes, the tidal volume is set directly and can be easily adjusted.
• In PC and PS modes, tidal volume is not set—instead, it depends on:
  • The pressure gradient between PIP and PEEP.
  • The inspiratory time.

📈 In Pressure Control (PC) Mode:

To increase tidal volume:

• Increase the inspiratory pressure (PIP).
• Decrease the PEEP (carefully, as this may affect oxygenation).
• Or do both to widen the pressure gradient.
• Increase inspiratory time (Ti) to allow more time for lung filling.

📈 In Pressure Support (PS) Mode:

It’s the same concept, just different terminology:

• The “pressure support” setting is analogous to the “inspiratory pressure” in PC mode.
• Inspiratory time is not directly set, but can be adjusted by modifying the flow cycle threshold:
  • Lowering the flow cycle percentage prolongs inspiratory time.
  • Raising it shortens inspiratory time.

Let’s wrap it up here! I hope this post gave you a strong foundation in mechanical ventilation and helped make things clearer and more practical for your clinical work.

If you’re ready to take it to the next level and truly master topics like PIP, mean airway pressure, rise time, gas trapping, and auto-PEEP, inverse ratio ventilation, as well as how to assess weaning readiness and perform a proper weaning trial—then check out my full mechanical ventilation course here. It’s packed with real-world explanations, visuals, and tips I’ve gathered over years of hospitalist practice. You’ll find the link below—I’d love to have you in the course!

Introduction

There are three key ingredients to ensure accurate BP measurement at home:

• Choosing the right time.
• Mastering the right technique.
• Using the right device.

Choosing the right time.

The short answer: There’s no single perfect time—but there are best practices.

You can check your blood pressure at different times throughout the day, and I often encourage my patients to do so. However, for the most accurate reading, avoiding certain activities beforehand is crucial.

Tips for Accurate Blood Pressure Readings (Per ACC & AHA Guidelines):

✅ Avoid caffeine, alcohol, exercise, and smoking for at least 30 minutes before measuring.
✅ Sit quietly for 5 minutes before taking your reading—keep your feet flat on the floor and your back supported.
✅ Empty your bladder beforehand, as a full bladder can raise your blood pressure.

These simple steps help eliminate factors that can falsely raise your blood pressure.

What is the technique to check your blood pressure?

When it comes to accuracy, upper-arm monitors are the preferred choice. The American Heart Association (AHA) recommends arm cuff-based devices over wrist monitors because they tend to provide more reliable readings. Research has shown that upper-arm measurements align more closely with ambulatory blood pressure monitoring (ABPM)—the gold standard for assessing blood pressure.

Key Tips for Accurate Blood Pressure Readings:

✔ Use an upper-arm monitor for the most precise measurements.
✔ Keep your arm at heart level while measuring—this applies whether you’re using an upper-arm or wrist monitor.
✔ Choose the right cuff size to ensure accuracy.

Blood Pressure Cuff Sizes:

📏 Small Adult Cuff
📏 Adult Cuff
📏 Large Adult Cuff
📏 Adult Thigh Cuff

Selecting the correct cuff size is crucial—a cuff that’s too small or too large can lead to inaccurate readings. Always check the manufacturer’s sizing guide to find the best fit for your arm.

Choosing the Right Blood Pressure Cuff Size

Selecting the correct cuff size is essential for accurate blood pressure readings. The American Heart Association (AHA) recommends choosing a cuff based on your mid-arm circumference:

📏 Small Adult Cuff → 22-26 cm
📏 Adult Cuff → 27-34 cm
📏 Large Adult Cuff → 35-44 cm
📏 Adult Thigh Cuff → 45-52 cm

Why Cuff Size Matters

Using the wrong cuff size can lead to significant inaccuracies:
❌ Too small? May produce falsely high blood pressure readings.
❌ Too large? Can result in falsely low readings.

How to Ensure Accuracy

For precise measurements, choose a cuff with an inflatable bladder that spans approximately 80% of your arm circumference.

🔎 What is a cuff bladder?
It’s the inflatable chamber inside the blood pressure cuff that, when filled with air, compresses the artery to measure blood pressure accurately.

Using the right cuff improves accuracy and ensures reliable blood pressure monitoring at home.

Which Blood Pressure Monitor Should You Buy?

The American College of Cardiology (ACC) and the American Heart Association (AHA) recommend the following automated, validated blood pressure monitors for home use:

✅ Omron 10 Series BP7450 (HEM-7342T-Z)
✅ Omron Platinum BP5450 (HEM-7343T-Z)
✅ Omron M6 Comfort
✅ Withings BP-800

(I have no financial ties to these manufacturers.)

These models are known for their accuracy and ease of use, making them great choices for home blood pressure monitoring. However, even the best device won’t provide reliable results unless you follow proper measurement techniques.

Prevention

Four important practical steps to reduce the risk of acute kidney injury (AKI) in hospitalized patients:

• Adequate hydration.
• Avoiding hypotension.
• Detecting and treating urine retention early.
• Limiting the use of nephrotoxins.

Let’s break down these points a bit…

Adequate hydration

For most, adequate oral intake provides sufficient hydration. Use IV fluids only when necessary—like in cases of volume depletion or prolonged NPO status.

Precautions:

• Patients with vomiting, diarrhea, fever, or decreased oral intake for any reason have a degree of volume depletion. We must optimize their volume status with IV fluids before introducing nephrotoxic medications, even if their kidney function looks normal.
• Patients on diuretics are at higher risk of dehydration and electrolyte imbalances due to over-diuresis. I always advise my patients to stop taking diuretics if they develop vomiting, diarrhea, fever, or significantly reduced oral intake.
• Patients with rhabdomyolysis and hemolysis are at risk of developing pigment-induced nephropathy particularly when CK > 5000, aggressive IV fluid hydration should be provided to prevent that.
• Patients at risk for contrast-induced nephropathy (CIN) such as those with preexisting renal impairment, should receive IVF hydration with isotonic solutions 1 mL/kg/hour starting 6-12 hours before and continuing for 12-24 hours after the procedures.

Avoiding hypotension.

The kidneys are susceptible to low blood pressure, and even brief episodes of hypotension can cause AKI. We must act quickly to stabilize blood pressure and address hemodynamic instability.

Detecting and treating urine retention early.

Routinely palpate the lower abdomen for bladder distension, especially in elderly males with dementia or encephalopathy. If a Foley catheter is in place, confirm it is patent and draining properly.

Limiting the use of nephrotoxins

• Several medications may cause nephrotoxicity! NSAIDs, IV vancomycin, aminoglycosides, amphotericin B, acyclovir, methotrexate, Cyclosporins, tacrolimus, and IVIG are just some of the medications.
• Among NSAIDs, Ketorolac is the most nephrotoxic and should not be used for more than 5 days.
• IV Vancomycin and aminoglycoside levels should be closely monitored, I typically have our pharmacy handle that. We must switch to less nephrotoxic antibiotics as soon as we can.
• IV Acyclovir can cause crystal-induced nephropathy, particularly at higher doses. Ensure patients are well-hydrated before starting therapy and continue IV fluids during treatment unless contraindicated.

• Always opt for a less nephrotoxic alternative when an equally effective medication is available.
• Kidney function and urine output should be closely monitored whenever nephrotoxic medications are administered.

In patients with CKD, it’s important to avoid nephrotoxins whenever possible. NSAIDs should be avoided entirely, and contrast agents should only be used if necessary. Additionally, ensure all medications are dosed appropriately for renal impairment.

Diagnosis of AKI

AKI is an abrupt decline in kidney function, reflected by a decline in theGFR. Since direct GFR measurement isn’t practical, AKI is diagnosed based on creatinine accumulation or decreased urine output, using the following criteria:

• Increase in serum creatinine by ≥0.3 mg/dL within 48 hours.
• Increase in serum creatinine to ≥1.5 times baseline within 7 days.
• Urine output ≤0.5 mL/kg/hr for 6 hours.

I have three comments on this definition:

1. Trend Over Time Matters – AKI is diagnosed based on serial changes, not a single isolated value. Always compare current kidney function to previous results. If prior values are unavailable and the patient presents with abnormal kidney function, assume AKI until proven otherwise.
2. BUN is Not Included – Serum creatinine is the preferred marker as it more accurately reflects GFR. BUN levels can be influenced by protein intake, catabolism, GI bleeding, or liver dysfunction, making them less specific for AKI.
3. No Creatinine Cutoff – A normal BUN/Cr ratio does not necessarily mean normal kidney function, while an abnormal ratio may indicate chronic kidney disease (CKD) rather than AKI.

The underlying cause

• History and physical exams remain the single most important element in finding out the underlying cause of AKI.
  • Patients who are volume-depleted such as those with vomiting, diarrhea, decreased oral intake, and bleeding are likely to have AKI due to renal hypoperfusion or what we call prerenal AKI.
  • Patients with signs of volume overload such as peripheral edema and ascites are likely to have a prerenal AKI due to decreased effective circulatory volume. When this happens in patients with congestive heart failure with decreased cardiac output we call it cardiorenal syndrome.
  • The development of AKI in patients with decompensated liver cirrhosis suggests possible hepatorenal syndrome.
  • AKI with urine retention suggests obstructive uropathy or what we call post-renal, this is mainly seen in elderly male patients and those with urinary catheters.
  • AKI after hypotension suggests ATN! Remember that even transient episodes of hypotension can cause AKI.
  • Medications can cause AKI via different mechanisms:
    • ATN such as with vancomycin and aminoglycosides.
    • Crystal-induced nephropathy such as methotrexate, acyclovir, amoxicillin, and sulphamethoxazole.
    • AIN (Acute interstitial nephritis) such as with beta-lactam antibiotics, NSAIDs, and PPI.

• The development of AKI in the setting of rhabdomyolysis especially when CK level > 5000 suggests possible pigment-induced nephropathy. Think of rhabdomyolysis in patients with prolonged immobilized state, heat exertion, trauma, and some drugs. Remember that rhabdomyolysis may cause elevated AST/ALT as well.
• AKI that develops within 48 to 72 hours after contrast exposure suggests contrast-induced nephropathy.

W/U

Even when the cause of AKI seems clear based on the history and physical exam, I always perform a urinalysis and renal ultrasound to look for any evidence of obstruction. I reserve additional urine tests—such as FENa, FEUrea, urine creatinine, cast analysis, and sometimes renal biopsy for cases where the etiology of AKI remains unclear after my initial assessment.

Management of AKI

• When my patient develops AKI, I reflexively do these five things:
  • Discontinue any potential nephrotoxin and offending agents.
  • Correct and avoid hypotension.
  • Ask the pharmacy to renally adjust all medication.
  • Switch to a renally safe alternative if possible, for example, switch to LMWH to UFH for DVT prophylaxis or anticoagulation.
  • Palpate the patient’s lower abdomen to check for any bladder distension and place a Foley catheter if detected. This is particularly important in elderly gentlemen.

Obstructive uropathy

• The treatment of obstructive uropathy involves relieving the obstruction and managing volume and electrolytes.
• Urinary catheterization relieves the obstruction in most cases. I always consult urology with these patients.
• If the obstruction is due to BPH, alpha-blockers such as tamsulosin must be initiated.
• Volume management is crucial in these patients given potential post-obstructive diuresis.
  • There is no set rule for a fluid replacement here! Ensuring the patient remains hemodynamic stability is the main goal.
  • Some may opt to track UO and replace it with fluids, a 50–75% strategy can be used which means replacing 50-75% of the previous hour’s urine output with IV fluid.
• Post-decompression hematuria may develop with rapid bladder decompression.

Prerenal AKI

• The management of prerenal AKI depends on the cause of decreased renal perfusion.
• Volume depletion:
  • Aggressive IV fluid resuscitation with isotonic crystalloid solutions, don’t shy away from using LR or plasmalyte because of the concern of hyperkalemia!
  • Bicarb drip should be used instead if metabolic acidosis is present, I use bicarb drip when HCO3 < 22.
• Volume overload:
  • IV loop diuretics. Patients with AKI require higher doses of loop diuretics, the starting dose of furosemide is 80 mg once or twice daily, and 2 mg once or twice daily for bumetanide.

• Patients with congestive heart failure and low CO syndrome may require inotropes as well. Please consult cardiology in addition to nephrology if you decide to use inotropes.
• Albumin along with terlipressin or norepinephrine is the treatment of choice for hepato-renal syndrome.

Acute interstitial nephritis

• Discontinue any potential offending agents as this can lead to partial or complete recovery of renal function.
• If no improvement in kidney function within 5-7 days after stopping the offending drug, corticosteroids are recommended. Prednisone is commonly used, starting at 1 mg/kg/day for 1-2 weeks, followed by a taper over 4-6 weeks. Early initiation of steroids is associated with better outcomes and reduced risk of chronic kidney disease.

Acute tubular necrosis (ATN)

• Acute tubular necrosis (ATN) is probably the most common form of AKI in critically ill patients.
• It frequently results in oliguria, anuria, and the need for renal replacement therapy (RRT).

• Anuric or oligouric AKI always makes me nervous, I consult nephrology right away in these patients as life-threatening hyperkalemia and acidosis can develop quickly requiring RRT.
• Don’t be deceived by the initial normal K! As long as they are oliguric or anuric, potassium likely will rise despite hyperkalemia management, the same applies to metabolic acidosis.

Crystal-induced and pigment-induced nephropathy

The treatment of crystal-induced and pigment-induced nephropathy is similar and involves discontinuing the offending agent and providing supportive care with IV fluid resuscitation. In some cases, urine alkalinization may be necessary. Nephrology consultation is essential to optimize management and minimize the need for renal replacement therapy (RRT).

Initiating Renal replacement therapy (RRT)

• The Nephrology team typically decides when to initiate RRT, whether early or late, and whether to use CRRT or intermittent HD.
• CRRT is typically chosen in patients with hemodynamic instability who can’t handle the fluid shift used in regular HD.
• Critical hyperkalemia and severe metabolic acidosis are the two main reasons for emergent RRT in critically ill patients.

• Volume overload is another indication of RRT in ATN patients! Before starting RRT, if the patient is stable, a high-dose loop diuretic challenge can help assess responsiveness. Typically, we give IV furosemide at 1 mg/kg (or equivalent). If urine output remains ≤600 mL after 6 hours, it suggests poor response and a likely need for dialysis.
• RRT is also indicated for uremic complications such as encephalopathy, pericarditis, and bleeding. RRT is also used for some toxins removal.
• I understand that some of you may consult nephrology for every case of AKI, but that’s not always necessary. Many cases, such as AKI due to volume depletion, are straightforward and typically resolve with IV fluid resuscitation. Let’s reserve nephrology consults for more complex or severe cases, allowing them to focus on the situations that truly require their expertise!

Monitoring

• Patients with AKI should have their Urine output (UO), electrolytes, and kidney function closely monitored.
• While urine output is routinely monitored in critically ill patients, it may not be tracked as closely for those on the regular hospital floor. We must relay the importance of tracking urine output to patients and nurses.

• AKI is a dynamic process with a continuously changing GFR and creatinine clearance and for that reason, serial labs for kidney functions and electrolytes including HCO3 – labeled as CO2 on BMP/CMP- must be obtained!
  • For critically ill patients, particularly those with oliguria or anuria, key labs such as electrolytes, creatinine, and acid-base status should be monitored every 6–8 hours (or up to 12 hours, depending on clinical context). These patients are at high risk for rapid deterioration, including life-threatening hyperkalemia and metabolic acidosis. A single normal potassium (K) level or mildly elevated creatinine on a basic metabolic panel (BMP) should not provide false reassurance, as values can shift abruptly in unstable clinical conditions.
  • For stable inpatients with adequate urine output, daily laboratory monitoring is typically sufficient. However, more frequent testing (e.g., every 12–24 hours) is warranted if significant electrolyte imbalances, worsening renal function, or other clinical concerns arise.

Prognosis

• AKI due to volume depletion and obstructive uropathy resolves quickly if prompt intervention is provided.
• AKI from ATN may take weeks to months to recover, depending on the severity of tubular injury and comorbidities (e.g., diabetes, chronic kidney disease). Some patients may develop residual CKD or progress to ESRD.
• In AIN, Kidney function typically improves within weeks if the offending drug is stopped and steroids are initiated early.
• In crystal-induced nephropathy, recovery within days with early intervention including rapid hydration, urinary alkalinization, and discontinuing the offending drugs.
• In pigment-induced AKI, aggressive IV fluids to flush out nephrotoxic pigments (myoglobin, hemoglobin) can prevent permanent damage. However, severe cases may still progress to ATN or CKD.

Ordering a CT (or CAT) scan and wondering whether contrast is needed? And if you do need contrast, should it be IV or oral? Let’s make this simple for you.

In this post, we’ll break down when to order non-contrast CT, contrast CT, and the different types of contrast to consider (oral, IV, or both). You’ll have a clear framework to guide your decisions by the end.

Types of Contrast

Contrast can be administered in three ways:

• Oral contrast: Helps visualize the gastrointestinal (GI) tract.
• Rectal contrast: Occasionally used for imaging the lower GI tract.
• IV contrast: Highlights blood vessels, organs, and certain tissues.

1. When to Use Oral or Rectal Contrast

The only times you’ll need oral or rectal contrast are:

• GI perforation or anastomosis leak: Use water-soluble iodinated contrast (e.g., Gastrografin) instead of barium-based contrast.
• Distal colonic or rectal perforation/leak: Consider rectal contrast.

Important Note: Oral contrast is unnecessary for diagnosing small bowel obstruction (SBO). Use IV contrast with CT abdomen/pelvis for SBO.

2. When to Use IV Contrast

Use IV contrast for:

• Cancer: Evaluating suspicious lesions or staging.
  • Exceptions: Low-dose lung cancer screening, colon cancer screening (CT colonography), pulmonary nodule follow-up, and lymphoma assessment.
• Infections: Abscesses, empyema, osteomyelitis, septic arthritis, or infected hardware.
• Trauma with penetrating or vascular injuries. if there are no penetrating or vascular injuries then there is no need to give IV contrast
• Inflammatory conditions: Such as IBD, pancreatitis, diverticulitis, and appendicitis.
  • Exception: Interstitial lung disease (ILD) assessment with high-resolution CT (HRCT)—no IV contrast needed.
• Infarction/Ischemia: This includes kidney infarcts and ischemic bowel.
  • Exception: For brain or lung infarctions, non-contrast CT is preferred.
• Vascular conditions: Thrombosis, dissection, aneurysms, or pseudoaneurysms. Use CT angiography (requires IV contrast).

3. When to Order Non-Contrast CT

Non-contrast CT is sufficient for:

• Initial stroke evaluation.
• Hematomas: Retroperitoneal hematomas (although IV contrast can also be used).
• Kidney stones.
• Musculoskeletal issues: Fractures and spinal diseases (if infection isn’t suspected).
• Non-penetrating trauma.
• Interstitial lung disease (HRCT).
• Screenings:
  • Low-dose lung cancer screening (LDCT).
  • Coronary calcium scoring.
  • CT colonography.

4. Real-Life Clinical Scenarios

Here are practical examples to solidify your understanding:

Scenario 1: Pulmonary Embolism (PE)

A 40-year-old woman on birth control pills presents with sudden shortness of breath. PE is suspected. PE is a vascular condition.

Order: CT chest angiography with IV contrast.

Scenario 2: Diverticulitis

A 65-year-old patient with LLQ abdominal pain. Acute diverticulitis is suspected.
Acute diverticulitis is an inflammatory process.

Order: CT abdomen/pelvis with IV contrast.

Scenario 3: Trauma and Anticoagulation

An 80-year-old man on warfarin falls and sustains a head laceration. CT of head, neck, chest, abdomen, and pelvis ordered. On exam, he only had some head lacerations and no signs of other injuries.

The patient had a trauma without penetrating or vascular injuries, hematoma also needs to be ruled out as he was on anticoagulation.

Order: Non-contrast CT.

Scenario 4: Kidney Stones

A 30-year-old woman with recurrent flank pain and a history of kidney stones, and renal colic was suspected to be the culprit.

Order: Non-contrast CT abdomen/pelvis.

Scenario 5: Severe Abdominal Pain

A 45-year-old patient with severe abdominal pain and vomiting, on physical exam, his abdomen remained soft but with diffuse tenderness, The ED physician ordered CT abd/pelvis.

Order: CT abdomen/pelvis with IV contrast (oral contrast is unnecessary, particularly with vomiting).

Scenario 6: Suspected Stroke

80-year-old man with sudden aphasia. Stroke suspected.
Order: Non-contrast CT head.

Scenario 7: Infection with Hardware

58-year-old woman s/p back surgery involving hardware placement presented with back pain and surgical wound discharge. MRI is unavailable.
Order: CT lumbar spine with IV contrast (infection suspected).

Final Tips

• Always assess for contrast allergies and ensure normal kidney function before ordering contrast studies.
• When in doubt, consider the clinical scenario—contrast should add diagnostic value and improve outcomes.

The coadministration of anticoagulation and thrombolytics

Anticoagulation should be started immediately when administering thrombolytic therapy to a patient with a STEMI, we give both together. The same applies to PE with hemodynamic instability.

This is different from using thrombolytics in ischemic stroke! In ischemic stroke, the American Heart Association/American Stroke Association (AHA/ASA) guidelines recommend delaying the initiation of anticoagulation for 24 hours after thrombolytic therapy with alteplase to minimize the risk of hemorrhagic transformation.

Holding anticoagulation before procedures

Right-sided thoracentesis, paracentesis, central line placement including picc lines, diagnostic endoscopy with or without biopsy, dental procedures, minor dermatological procedures, ophthalmological procedures, and pacemaker and ICD placement are considered minor procedures and considered low risk for bleeding.

The American College of Chest Physicians guidelines support the continuation of anticoagulants for minor procedures due to their low bleeding risk. The same applies to antiplatelets.

In real-world settings, unless the procedure is emergent, I highly recommend checking with the performing physician to see if we should hold oral anticoagulants to avoid unnecessary delays! Unfortunately, not everyone goes with these guidelines for different reasons!

Suppose the performing provider wants to hold oral anticoagulants. In that case, we hold DOAC for 48 and hold warfarin until the INR falls to a level that is deemed safe by the performing physician which is typically ≤ 1.5.

Anticoagulation bridging

Bridging with UFH or LMWH is warranted in patients who are taking warfarin and have a high risk for thromboembolic disease such as mechanical heart valves, AF patients with recent stroke or TIA, recent DVT or PE, and patients with known hypercoagulable status.

Bridging is initiated when the INR falls below the therapeutic range typically less than 2.

LMWH is preferred over UFH in bridging given its more predictable anticoagulation effect and should be stopped 24 hours before the procedure, If UFH is used instead, it should be stopped 4-6 hours before the procedure.

Resuming oral anticoagulants

Oral anticoagulants should be resumed after the procedure and I always ask the performing physicians if it is safe to resume. DOAC can be simply resumed, and the same applies to warfarin if bridging isn’t indicated. If bridging was indicated, it should continue until the INR is therapeutic. Here’s the transitioning strategy we follow:

• From UFH: Start the DOAC at the time of heparin drip discontinuation.
• From LMWH: Start the DOAC when the next LMWH dose is due.
• No loading dose is needed when resuming a DOAC—simply restart the home dose.

Heparin-induced thrombocytopenia

HIT is a serious condition with significant morbidity and mortality if untreated and one should not wait for thrоmbоsis to develop before suspecting НΙТ because thrοmbοϲуtοpeոiа often precedes that.

Calculating the 4T score is the first step when suspecting HIT. this score is a clinical tool used to estimate the probability of heparin-induced thrombocytopenia (HIT). It evaluates four parameters related to HIT and stratifies patients into low, intermediate, or high probability categories. This scoring system helps guide further diagnostic testing and management. You don’t need to memorize it, just use one of the free online calculators.

If the 4 Ts score is a low probability, we generally do not pursue HΙΤ antibody testing or presumptive treatment for НІΤ, we do not discontinue hepariո or start a non-heparin anticoagulant

If the 4 Ts score is an intermediate or high probability, we make a presumptive diagnosis of ΗІТ pending results of НΙT antibody testing.

Нерariո cessation alone is not sufficient since patients with НΙТ remain at risk for subsequent thrоmbοsis. So If you decide to test for HIT, you must act pending test results.

Testing for HIT starts with screening antigen assay tests like ELISA, which detect antibodies against platelet factor 4 (PF4)/heparin complexes. These assays are fast and highly sensitive but have moderate specificity, leading to potential overdiagnosis.

A negative result will rule out HIT, but if positive we send a confirmatory functional assay unless the clinical suspicion is high then there is no need.

Non-heparin anticoagulants include argatroban, bivalirudin, fondaparinux, or a direct oral anticoagulant (DOAC). Remember the use of Fodaparinux and DOAC in HIT is considered off-label.

Argartroban and bivalirudin have short durations of action and are good choices for critically ill patients. Argatroban is safe in renal insufficiency, while bivalirudin is good in liver dysfunction.

Fondaparinux is a good and easier-to-use option but is contraindicated in patients weighing less than 50 kg and those with a creatinine clearance below 30 ml/min. It’s also best avoided when the platelet count is below 50,000/µL.

DOAC agents are best used in stable patients, they are equally effective. Apixaban is the DOAC of choice in renal insufficiency and dialysis patients. A loading dose of DOAC is required similar to treating venous thromboembolic disease.

In cases HIT is confirmed, the duration of anticoagulation therapy should be at least 4 weeks for isolated HIT and 3 months for HIT with thrombosis.

In the case of using Argatroban and Bivalirudin, have your pharmacist help with their protocol and monitoring and transition to oral anticoagulants once the patient is stable preferably DOAC, if you decide to transition into warfarin we must overlap until the INR is therapeutic for at least 24 hours.

Anticoagulation reversal

For warfarin-associated life-threatening bleeding, 4-factor Prothrombin Complex Concentrate (4-factor PCC) which contains factors II, VII, IX, and X is the first-line reversal solution, if not available, we can use the combination of 3-factor PCC and factor 7 as factor-3 PCC lacks factor 7. FFP is used when PCC solutions are not available.

In most cases, the goal is to bring INR to ≤ 1.5. Check the INR level 15-30 minutes after completion of the infusion and repeat the infusion until INR is ≤ 1.5, repeat the infusion if INR is still elevated.

In general, it is reasonable to consider restarting anticoagulation therapy 7 to 14 days after an episode of major bleeding.

Final approval should always be secured from the subspecialists overseeing the bleeding management.

For DOAC reversal, we follow the following strategy:

• Dabigatran: Idarucizumab is the first line, or PCC/aPCC, if Idarucizumab is unavailable. If PCC is not available then HD may be considered to remove the drug as the next step.

• Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban): Andexanet alfa (preferred), or PCC/aPCC if andexanet alfa is unavailable.

Protamine sulfate is the primary agent to reverse the anticoagulation effect of UFH and LMWH in life-threatening bleeding.

Anticoagulation and bleeding

In cases of significant bleeding, the immediate priority is to discontinue all anticoagulation. The next step is to reverse the coagulopathy when clinically appropriate.

In cases of minor bleeding, such as gum bleeding, epistaxis, bloody stools from inflammatory bowel disease (IBD), microscopic hematuria, or hemoptysis caused by a lung abscess, anticoagulation can often be continued with caution. However, addressing the underlying cause of the bleeding is essential. Importantly, if hemoptysis is due to pulmonary embolism (PE), anticoagulation should not be withheld, as treating the PE is the priority.

n thrombocytopenia is drug-induced, plt transfusion is indicated in active bleeding to keep the plt count above 50k.

Anticoagulation can be resumed 7-14 days after a major bleeding episode.

For anticoagulation in critically ill patients and those at high rebleeding risk, UFH infusion is preferred given its short duration of action. LMWH or DOAC can be considered when the patient becomes more stable and low bleeding risk.

A platelet count of ≥ 50k is considered safe to start anticoagulation, a lower threshold of ≥ 30k can be considered if the benefit outweighs the risk of starting anticoagulation.

The IVC filter debate

The use of inferior vena cava (IVC) filters is a topic of considerable debate in the medical community. IVC filters are indicated primarily for patients with venous thromboembolism (VTE) who have an absolute contraindication to anticoagulation or in those who have recurrent VTE despite adequate anticoagulation. This recommendation is supported by the American Society of Hematology (ASH) and the Society of Interventional Radiology, among others.

However, there are significant concerns regarding the routine use of IVC filters due to the associated risks and limited evidence of long-term benefits. Studies have shown that while IVC filters can reduce the incidence of pulmonary embolism (PE) in the short term, they are associated with an increased risk of deep vein thrombosis (DVT) and other complications such as filter migration, perforation, and thrombosis.

The American Society of Hematology guidelines conditionally recommend against the use of IVC filters in patients who can be safely treated with anticoagulant therapy, citing low certainty in the evidence of their effects. Similarly, the Society of Interventional Radiology advises that IVC filters should be used selectively and recommends the use of retrievable filters, with removal once the patient can be safely anticoagulated.

In summary, while IVC filters have a role in specific clinical scenarios, their use should be carefully considered, weighing the potential benefits against the risks. The current consensus advises against their routine use in favor of anticoagulation whenever possible.

Recognizing hypoxic patients

Most critically hypoxic patients exhibit early warning signs of mild hypoxia before deteriorating. Recognizing and addressing these early signs can save lives and prevent the severe complications associated with untreated hypoxia.

“O2 sat reading is an essential part of vital signs and must always be mentioned along with whether on RA or O2 supplement and how much supplement the patient is on”

Take a look at patients A and B, can you tell who is more hypoxic?

You can see that patient A is worse than B despite the O2 sat of patient A being better than B because patient A requires 10 L compared to none in patient B.

The moment I observe any of the following conditions, I need to determine the cause and address the underlying issue promptly:

• RA O2 sat < 95%.
• A patient who does not normally use home oxygen but now requires supplemental oxygen to maintain an O2 saturation of 95% or higher.
• A patient who normally uses home oxygen but now requires a higher oxygen flow than their usual baseline.

By doing this, you can prevent most patients from deteriorating due to untreated progressive hypoxia, effectively saving their lives!

We also need to pay close attention when nurses call about an oxygen-related issue. They may not explicitly mention a problem with oxygenation because, like physicians, nurses may vary in experience and may not always convey a sense of urgency. Let me provide some examples of what they might say during such calls:

• Hey doc, I am having a hard time keeping the patient’s O2 saturation up, I have to increase his O2 to 8 L/m but he’s doing better now.
• Hey doc, nothing urgent! I forgot to tell you that I have to crank the patient’s O2 a bit up but he’s doing okay now and his O2 sat is in the 90s
• Hey doc, my patient’s O2 sat dropped to low 80% a while ago, I put him on 2 L/min and it quickly improved to 92%, just wanted to let you know
• And of course, they may tell you straight to come and see the patient immediately because of very low O2 saturation

In all these scenarios, I always ask the nurse for the exact current pulse oximetry reading, the amount of oxygen the patient is receiving, a full set of vital signs, and how the patient is feeling. Then, I immediately go to evaluate the patient in person.

Stabilizing hypoxic patients

The moment I suspect, smell, or know my patient is hypoxic, I have to correct this hypoxia ASAP!

We categorize patients into:

• Stable patients: These are the patients whose nurses have already increased their oxygen supplementation and now have an O2 saturation above 92%, are asymptomatic, and have stable vital signs. They still need to be evaluated promptly to determine the cause of their increased oxygen requirement and to address it appropriately, preventing future deterioration.
• Unstable patients: O2 sat is low, they are symptomatic, and the rest of the vital signs are unstable, this is a medical emergency, leave everything and go see your patient, Over the phone, I instruct the nurse to increase the patient’s oxygen supplementation to the maximum capacity of the available oxygen delivery device. At a minimum, the patient should be placed on a 100% non-rebreather mask. If the patient is already on BiPAP, CPAP, or HFNC, I direct them to increase the FiO2 to 100%.

 

“Remember to activate the RRT if you have it at your hospital to speed up the response to your patient”

Upon entering the room, I ensure the patient is receiving the maximum oxygen supplementation available at the bedside, is connected to a monitor, the crash cart is nearby, and defibrillator pads are applied. If the Rapid Response Team (RRT) is activated, these steps should already be in place.

Proceed with endotracheal intubation immediately if hypoxic respiratory failure is associated with:

• Encephalopathy, whether the patient is agitated, lethargic, or obtunded. Begin bag-valve-mask ventilation immediately if the patient is extremely lethargic or obtunded.
• Recurrent aspiration due to persistent vomiting.

In these situations, don’t hesitate—proceed with intubation immediately.

If the patient is not encephalopathic, rapid action is still crucial to prevent further deterioration and, if possible, avoid the need for mechanical ventilation.

Quickly assess the patient by listening to their lungs (if possible), checking for any fluids or blood products being administered, and gathering a brief history from the nurse. Then, position yourself at the foot of the bed to take control of the situation. All of this should be accomplished within 30 seconds.

If the patient’s O2 saturation remains below 90-92%, escalate to the highest level of oxygen delivery available. Here’s what I mean:

At my facility, we have a high-flow nasal cannula (HFNC), CPAP, and BiPAP, all capable of delivering 100% FiO2. The choice between them depends on the underlying condition:

• Choose BiPAP over CPAP or HFNC if there is confirmed or suspected hypercapnia (e.g., COPD or obesity hypoventilation syndrome) based on ABG results or clinical suspicion. Use BiPAP until ABG results are available.
• Choose CPAP or HFNC for pure hypoxia without hypercapnia:
  • CPAP is preferred if the patient has significant respiratory distress or increased work of breathing.
  • HFNC is ideal if the patient cannot tolerate a mask, has facial injuries, or is at high risk of aspiration.

In the heat of the moment, choosing any of these devices is acceptable. If you’re feeling stressed or overwhelmed and can’t decide, default to any device—it will suffice until the patient stabilizes.

Remember, during this acute phase, I’m less concerned about inappropriately reducing CO2 (hypocapnia) because it isn’t immediately life-threatening. Hypoxia, however, can be fatal

What settings should we use?

Regardless of the device chosen, all patients should initially be placed on 100% FiO2. Here’s how to set up each device:

• HFNC (High-Flow Nasal Cannula):
  Specify the flow rate in addition to FiO2. The maximum flow rate depends on the machine’s brand. For example, at our hospital, we use Vapotherm, which allows a maximum flow rate of 40 L/min. Start with the maximum flow rate.
• CPAP (Continuous Positive Airway Pressure):
  Set the CPAP value. A good starting point is 10 cmH2O.
• BiPAP (Bilevel Positive Airway Pressure):
  Set both the EPAP (equivalent to CPAP) and IPAP values:
  • Start with an EPAP of 10 cmH2O.
  • For the IPAP, add 5 cmH2O to the EPAP to achieve a PIP (peak inspiratory pressure) that is 5 cmH2O higher than the EPAP. For instance, begin with 10/15 (EPAP of 10 cmH2O and IPAP of 15 cmH2O).

These initial settings provide effective oxygenation and ventilation while allowing for quick adjustments based on the patient’s response.

There are two ways to improve oxygenation:

1. The quick way: Increase the FiO2.
2. The gradual way: Increase the flow rate on HFNC, the CPAP value on the CPAP machine, or the EPAP on the BiPAP machine.

It’s important to note that only BiPAP can assist with ventilation due to the pressure difference between IPAP and EPAP.

Remember, oxygen saturation may not improve immediately. Stay calm—it can take several minutes for O2 saturation or pO2 levels to increase. As long as there is steady improvement, you can be reassured.

If the O2 saturation isn’t improving or is declining despite being on maximum HFNC, switch to CPAP or BiPAP using the previously recommended settings. If the patient is already on CPAP or BiPAP, consider increasing the CPAP or EPAP value in increments of 2-3 cmH2O. For BiPAP, ensure that the IPAP is adjusted to maintain a PIP at least 5 cmH2O above the EPAP.

When to consider intubation and mechanical ventilation in patients who are not encephalopathic?

The decision to proceed with mechanical ventilation isn’t always clear-cut, multiple factors need to be considered including code status, mental status, and hemodynamic stability.

In general, mechanical ventilation should be strongly considered if a patient’s oxygen saturation remains below 80% despite maximum oxygen support and there are no signs of clinical improvement. However, during the COVID era, we encountered patients with oxygen saturations in the 70s who were managed without intubation. Always use your clinical judgment to guide the decision.

Let’s compare two examples:

• Patient A initially had an oxygen saturation in the 40s. After being placed on CPAP at 10 cmH2O with 100% FiO2, their O2 saturation began to progressively improve, reaching the high 60s and continuing to rise. For this patient, I would give more time, as their oxygen levels are steadily improving with oxygen therapy and treatment of the underlying cause.
• Patient B started with oxygen saturation in the low 80s, but despite CPAP at 10 cmH2O with 100% FiO2, their O2 levels continued to decline, dropping to the 60s and then the 50s. This patient will require intubation and mechanical ventilation to stabilize their condition.

Don’t hesitate to ask the people around you if we should proceed with intubation including your colleagues or nurses.

Workup and Management of the underlying cause

When stabilizing a patient’s oxygenation, it’s equally important to investigate the underlying cause. Here’s a step-by-step framework:

Initial Steps to Stabilize and Investigate

1. Gather a brief history from the patient’s nurse.
2. Listen to the patient’s lungs for clues.
3. Inspect the room for IV fluids or blood products being administered.
4. Order essential diagnostics:
   • Stat chest X-ray (CXR)
   • Electrocardiogram (EKG)
   • Arterial blood gas (ABG)

Understanding the Causes of Acute Hypoxemia

While hypoxemia can result from five mechanisms—hypoventilation, V/Q mismatch, right-to-left shunt, diffusion limitations, and low-inspired FiO2—clinical practice often reveals a more focused list of causes.

Suspect one of the following Conditions in patients who develop sudden shortness of breath and severe acute hypoxic RF:

• Pulmonary edema (cardiogenic or non-cardiogenic)
• Pulmonary embolism (PE)
• Aspiration pneumonia
• Pneumothorax (PTX)
• Lung collapse or atelectasis
• Large pleural fluid collection (e.g., pleural effusion, empyema, or hemothorax)

Breaking Down the Conditions

1. Pulmonary Edema

• Clues to Diagnosis:
  • Orthopnea, crackles on lung exam, jugular venous distension (JVD), peripheral edema.
  • Presence of IV fluid or blood product infusions.
• Management:
  • Stop IV fluid or blood product infusions immediately.
  • Administer 80 mg IV furosemide.
  • Use CPAP if no CO2 retention is suspected.
  • Start a nitroglycerin drip if blood pressure is elevated.
  • Perform diagnostics: EKG, chest X-ray, cardiac enzymes, and echocardiogram.

2. Aspiration Pneumonia

• Clues to Diagnosis:
  • Reports of choking or visible vomiting around the mouth or bed.
• Management:
  • Proceed with intubation if the patient is actively vomiting or aspirating.
  • If intubation isn’t required immediately, initiate HFNC at maximum settings.
  • Avoid CPAP/BiPAP if the patient cannot clear secretions unless a nasogastric tube (NGT) is placed for suction.
  • Start antibiotics to address potential infection.

3. Pneumothorax, Atelectasis, or Large Pleural Fluid Collection

• Pneumothorax (PTX):
  • Clues: Absent breath sounds on one side.
  • Management:
    • Confirm diagnosis with CXR and place a chest tube immediately.
    • For tension PTX, perform needle decompression if chest tube placement is delayed.
    • Use maximum HFNC to manage hypoxia until a chest tube is in place.
• Atelectasis:
  • Clues: Weak cough, difficulty clearing secretions, tracheal shift toward the affected side.
  • Management:
    • Initiate chest physiotherapy (CPT), suctioning, mucolytics, and breathing treatments.
    • If no improvement, consult pulmonary for bronchoscopy.
• Large Pleural Space Collection:
  • Clues: Tracheal shift toward the unaffected side.
  • Management:
    • Perform therapeutic thoracentesis, ideally with chest tube placement.
  • Key Considerations:
    • Pleural effusion: Common with malignancy, cirrhosis, or heart failure.
    • Empyema: Severe leukocytosis, pleuritic chest pain, systemic illness.
    • Hemothorax: Often linked to trauma or thoracic procedures.

4. Pulmonary Embolism (PE)

• When to Suspect:
  • Hypoxia unexplained by lung exam or CXR findings.
• Management:
  • If suspicion is high and there are no contraindications, start full anticoagulation immediately.
  • Obtain a chest CTA, but ensure the patient is stable enough for the scan.
  • Use bedside POCUS to assist in diagnosis if trained.

For all these patients, keep them NPO (nothing by mouth) until they are more stable. If aspiration was the underlying issue, request a speech therapy evaluation. Transfer the patient to a higher level of care, typically the ICU; however, an IMC (Intermediate Care Unit) or step-down unit may be appropriate for select patients. A comprehensive panel of blood tests is usually ordered, including:

• CBC (Complete Blood Count)
• CMP (Comprehensive Metabolic Panel)
• Cardiac enzymes
• Lactic acid

This ensures thorough assessment and monitoring of their clinical status.

Ensure continued treatment and monitoring as needed based on the patient’s condition. For example:

• Administer additional diuretics for persistent pulmonary edema.
• Perform more frequent chest physiotherapy (CPT) or consider bronchoscopy if indicated.
• Confirm that a chest CTA is completed and promptly follow up on the results if PE is suspected.

Adjust care dynamically to address the evolving clinical situation.

Further workup and treatment may be necessary based on the findings. For instance, if the EKG indicates evidence of an acute MI, follow the appropriate treatment guidelines.

Ensure to order a follow-up ABG and adjust treatment as needed. As the patient stabilizes:

• Gradually wean FiO2 down as tolerated.
• Avoid reducing the flow rate on HFNC or the CPAP/EPAP values until FiO2 is decreased to 60%. Once FiO2 is at this level, begin weaning both the FiO2 and flow/pressure settings together.

This approach helps optimize oxygen delivery while ensuring patient safety during recovery.

The end