Can you run a pressor through a peripheral IV?

We’ve all heard horror stories of patients getting digital necrosis from peripheral pressors:

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However, the data shows that you CAN run pressors safely through peripheral IVs with close monitoring and proper selection of an IV site. How?

The Journal of Critical Care from 2015 reviewed the available literature of the use of peripheral pressors in adults.This review concluded that there are very rare side effects in the first 6 hours of use, and that best practice is to place IVs in veins >4 mm in diameter (use an ultrasound to confirm!) and monitor at least every 2 hours for extravasation. There was poor quality data reporting adverse outcomes from site of administration of pressors–out of 85 studies included, there was only one randomized study. Furthermore, as this study notes, the rate of adverse effects is low when a good-sized vein in the forearm is used, and pressors can be restarted at another peripheral site when extravasation does occur.


What’s the difference between dobutamine and dopamine?

These two medications SOUND similar, but are in different categories.

  Dobutamine Dopamine
Class Inotrope Vasopressor
Receptors affected B1 agonist A1 agonist (dose dependent)
Effect Increased cardiac contractility Vasoconstriction, increased systemic vascular resistance
Common uses “Tailored therapy” for heart failure, ?septic shock Septic shock (>8), cardiogenic shock (4-7), promoting urine flow (0.5-3)
Side effects Tachycardia, may even cause hypotension (mild vasodilation), do not use in patients with HOCM Tachycardia/VT, tachyphylaxis, ischemic limb necrosis (do not give through a peripheral IV)



How to manage chest tubes (5-minute version)

I am no expert in chest tubes, and will add the caveat that for this particular post I really hope everything is correct! If it’s not, let me know! See this post on the different kinds of chest tubes. This is a great but long nursing resource from

You’ve placed a chest tube: great! Now you hook it up to some weird box thing that is called a drainage system…now what? Knowing how chest tubes used to work helps you understand the box thing.

This picture is taken from a truly excellent little video on how chest tube drainage works:

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ThScreen Shot 2017-01-26 at 6.01.21 PM.pngere used to be 3 separate bottles hooked up to the chest tube itself: Bottle #1 is where the patient’s empyema fluid or blood leaked into. Bottle #2 is the waterseal: air is forced to travel through water and can only move in one direction (it cannot move back into the patient). Bottle #3 sets suction power based on how much water is in the bottle–more water=less suction, less water=more suction, and you need to make sure the suction power is just right. You can see how the drainage system has evolved over time on the right.

Should patients be “placed to waterseal” or “placed to -20 suction?” 

“Place to waterseal”= don’t be too crazy with drainage, which is appropriate for most pleural effusions or a mild pneumothorax. If the lung is not fully expanded, you can “turn up the suction.”If you apply suction too aggressively, you put the patient at risk for re-expansion pulmonary edema.

How do I know if there is an “air leak” and what the eff does it mean? 

An air leak is present if there is bubbling in the waterseal chamber when the suction is clamped/on waterseal–this indicates there is positive pressure coming from the pleural space=air getting into the pleural space. Intermittent bubbling with expiration (when pleural pressure is highest in the non-ventilated patient) may be normal, but a continuous air leak is pathological.

Causes include:

  • ruptured bleb (severe emphysema)
  • simple traumatic pneumothorax (from placing the chest tube)
  • a leak in the actual tubing system
  • mechanical ventilation (may see decreased tidal volumes, failure of PEEP increase)
  • bronchopleural fistula (usually more severe or continuous)
  • lung entrapment vs. trapped lung

NB: if your patient has a persistent air leak, think twice about pulling their chest tube because if you do, you may cause a recurrent pneumothorax.

What is “tidaling?” 

You may see movement in the waterseal chamber with respiratory variation. It’s the water being sucked back towards the lung with inspiration due to negative inspiratory pressure. (In mechanically ventilated patients, it’s the opposite.)


How do I know when the tube can be taken out? 

In a 2013 study out of Michigan State, the team found it is reasonable to remove chest tubes when drainage <200 ml/day, on waterseal, with no air leak. In stable patients on the floor, theoretically you don’t need a chest x-ray after removal, but given our litigious society, everyone gets one. In mechanically ventilated patients, you should get a chest x-ray 1-3 hours after removal.

What do I do if the tube falls out? 

Use common sense: cover the area and prepare to re-insert a chest tube. Maintain sterility. The patient is at risk of a tension pneumothorax, so someone should stay with them for close monitoring. More troubleshooting at this nursing website.



What is vent dyssynchrony?

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One of the problems that is not uncommon in patients on ventilators is correcting for “vent dyssynchrony.” Vent dyssynchrony is when the patient’s demand for oxygen is not being met by the ventilator.

Why? Consider three factors:

  • LENGTH OF BREATH (how long is inspiration?)
  • TIMING OF BREATH (when is the switch to expiration/inspiration?)
  • ADEQUATE FLOW (how big are the volumes?)

If there are problems with any of those things, dyssynchrony can result. Dyssynchrony results in those annoying beeps you hear from the vent. This is called “triggering the vent.” This can happen if:

  • ineffective triggering: PEEP is too high, musculoskeletal weakness
  • inappropriate triggering: tidal volume is too low, inspiratory time is too short or flow is too low, coughing or hiccups
  • autotriggering: coughing, hiccups, shivering, seizures

What should you do about it? The best thing would be to correct the underlying problem. You may have to change the vent setting, the flow rate or tidal volume, or the insp/exp times. Sometimes, all you need to do is change the trigger sensitivity threshold!

As with many of my posts, I turn to Life in the Fast Lane as a reference.


When should the cooling protocol be used as part of ACLS?

“Cooling” is based on the theory that hypothermia can help stabilize patients in cardiopulmonary arrest and improve neurological outcomes.

Cooling should be started as soon as possible when applied (within 6 hours). It should be used in non-traumatic cases of cardiac arrest when ROSC is obtained within 30 minutes. There should be a low GCS and NO purposeful movement. Female patients should not be pregnant.

Parameters to use when titrating temperatures:

  • MAP >65 or 90 when concerned about ICP
  • PCO2 35-45
  • FiO2 > 94%
  • RASS -5
  • EEG monitoring

You should be able to see a J-point on EKG:


Potential complications:

  • Shivering and seizures (can use paralytics if there is concern this is causing respiratory complications. I’ve heard of surgeons using meperidine but haven’t done this myself)
  • Hypo/hyperglycemia
  • Skin injury from the pads
  • Sepsis
  • Rhabdomyolysis
  • Bradycardia refractory to atropine

NB: if there is any question about brain death, you need to wait 72 hours until after someone comes off the cooling protocol to make any determination of prognosis.


When to initiate paralytics in a ventilated patient?

Although it is a big deal to start paralytics in a patient, the decision is a relatively simple one. If your patient gets RSI (rapid sequence intubation) then they will have already gotten a dose of a paralytic anyway! The table below highlights the major indications for using a paralytic in the ICU:

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The decision to start a paralytic (neuromuscular blockade agent) is yes if the patient is intubated and flailing about, overbreathing the vent, in tetany, or has increased intracranial pressure.

There is also some evidence that paralytics may be helpful in ARDS (due to decreased chest wall muscle use), and decrease lung inflammation.

The most important thing to remember is that the patient MUST be adequately sedated!! Here is a good overview of analgesia and sedation from Open Anesthesia. Being awake on a paralytic, aware of what’s going on but not being able to move your body, probably counts as a form of torture. Make sure that they are on something like propofol or midazolam. My favorite combination is fentanyl (analgesic) and propofol (sedation).

One thing to remember is that there are depolarizing agents–namely, succinylcholine–and non-depolarizing agents, such as rocuronium. Life in the Fast Lane makes a good case for why non-depolarizing agents are usually better.

What is a NICOM (or a Vigileo?) 

First, let’s understand the point of non-invasive cardiac output monitoring. Patients who are entering septic, cardiac, or what-have-you shock have inadequate tissue perfusion. Tissue perfusion is dependent on cardiac output, which in turn depends on stroke volume.

You can get an idea of how well tissues were being perfused by looking at the lactate. You could try to see if a person was fluid-responsive by bolusing them a small amount and reassessing. But if you wanted more precise methods? Just a decade ago, the only way to monitor cardiac output was with a pulmonary artery catheter (PAC) using thermodilution. While thermodilution is still the gold standard, we have a couple of other options now.

Here are some terms that are useful to know:

  • SVI (stroke volume index): amount of blood being pumped with each beat, indexed to body surface area (normal is 35-40 ml//M2 )
  • CI (cardiac index): normal is 2.5- 4.0 L/min/M2
  • SVV (stroke volume variation): percentage of variability in the stroke volume between inspiration and expiration. Heart rate variability will make the SVV less reliable

The NICOM has been clinically validated as a tool for non-invasive cardiac monitoring. It sounds like something out of a sci-fi novel: using the amount of time it takes for an electric current to pass through the chest as a reference point, the NICOM translates this time into flow into SVI. Increased time=increased stroke volume.

The Vigileo monitor can be use to monitor continuous cardiac output (with the Flotrac) or continuous central venous oxygen saturation (using the PreSep triple lumen oximetry catheter). It can provide data on SVI, SVV, and CI. The advantage of the Flotrac is that you can quickly see if the SVI is rising with volume. ˆUnlike the NICOM, the Vigileo probably shouldn’t be used if the patient has an arrhythmia or vasospasm or vasoplegia (as sometimes post-operative patients who have gotten anesthesia are).

  • most accurate when patient has normal lung compliance and regular heart rate
  • an SVV of >13% suggests the patient is dry and you can try giving fluids
  • if the SVV is <13% but the patient has non-compliant lungs, you can still try giving fluids
  • SVV may not be reliable in cases of: arrhythmias, low ejection fraction, noncompliant lungs, other modes of ventilation besides assist control.

Does it matter which one you choose? The ICU nurses I’ve worked with pledge allegiance to one or the other, but there is evidence that NICOM and the Vigileo have similar monitoring capabilities.