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 RN.com.

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:

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quizlet.com

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.

Managing an intra-aortic balloon pump (IABP)

The intra-aortic balloon pump (IABP) is one of the devices that you may see in your cardiology/cardiac intensive care unit rotations.

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Taken from the really excellent Liverpool self-directed learning guide by Linda Williams

The physiology of the IABP is intuitive. In heart failure, factors such as increased afterload and decreased contractility are negatives, right? The IABP inflates during diastole and deflates during systole, which generates a suction-cup like negative force that propels blood forward out of the heart. Physiologically, this is like the “suction cup” effect that geckos, treefrogs, and other animals have.

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Don’t let go, Jack! 

Because of the increased forward flow, the IABP can increase myocardial oxygenation (the coronary arteries have more time to perfuse, too), increase cardiac output, and reduce LV workload.  It also decreases pulmonary artery pressure (which is why you’ll see a PAP listed on the monitor).

Which patients get IABP? People who have been through cardiac shock, are post-MI, or have severe cardiomyopathy, valvular disease like MR, or high-risk patients who are awaiting stenting. The important common factor is that IABP is a bridge to something: whether that is cardiac surgery, interventional cath, or transplant. It is not meant to be used indefinitely.

How do you titrate the power of the IABP? The IABP’s power is measured in “augmented beats”: the ratio of how many times the IABP “works” to number of heartbeats. If the IABP is 1:1 for instance, that means that it is being activated with every heart beat. As you wean down a patient, you may see a ratio of 1:2 or 1:3 (which is basically equivalent to not having an IABP).

How can you improve IABP performance? 

  • make sure timing of balloon inflation is optimized: there is an ECG monitor and “trigger” system that can be used to determine how to time a patient correctly.
  • make sure the size of the balloon is correct
  • heart rate >130 reduces efficiency
  • preserve kidney function

Warning signs and complications to watch for: 

  • limb ischemia caused by thrombosis at the insertion site…IABP may also be associated with a compartment syndrome or gut ischemia for the same reason
  • aortic dissection or pseudoaneurysm…ahh!!
  • if augmentation decreases, ask yourself about the possibility of whether this is due to improving cardiac function, or whether there could be new sepsis or balloon rupture
  • thrombocytopenia (there is a well-documented hemolytic and thrombocytopenia that comes from mechanical shearing from the IABP), but sometimes you will be asked to rule out HIT which is just a pain in the rear
  • infection (you may be asked to place the patient on vancomycin…to prevent antibiotic abuse you should make sure there is a plan in place for how long the patient will be on antibiotics for, and if it’s treating anything or just for prophylaxis)
  • acute renal failure (blockage of the renal arteries, catheter migration)
  • peripheral neuropathy
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Table 1 from Baddour (2003) on the rate of incidence of infection in various nonvalvular cardiac devices 

 

When and how can you wean the IABP? A complicated decision that basically is about: is the patient’s cardiac function improving? Will it remain that way even if you take them off the device? As far as weaning goes, it’s a process of reducing the ratio of augmented to non-augmented beats from 1:1 to 1:2 or 1:3 (which is the same as no support) or decreasing balloon volume. It takes 6-12 hours.

 

My ICU patient has metabolic alkalosis…help!

If you’ve identified metabolic alkalosis, congratulations: you’ve already done 50% of the work! Assuming you also have accounted for concomitant acid-base disturbances…

What remains is figuring out the cause of the metabolic alkalosis. Be aware that metabolic alkalosis can be associated with severe electrolyte derangements like hypokalemia, hypomagnesemia, and hypoalbuminemia. Think about processes that would deplete bicarbonate or potassium.

  • Vomiting and diarrhea.This is unlikely to land a patient in the ICU, but villous adenomas can excrete bicarbonate and cause a hyperchloremic alkalosis!
  • Severe potassium depletion
  • Post-hypercapnic alkalosis, seen in COPD patients who have their PaCO2 corrected. This may be associated with a concomitant respiratory acidosis.
  • Iatrogenic: diuretics and steroids are two common players. Think about your patients on a lasix drip. Remember that if you resuscitate someone with ONLY normal saline, they are at risk for a non-gap metabolic ACIDOSIS.
  • Underlying endocrine problems: hyperaldosteronism and Cushing’s syndrome

How is the alkalosis then treated? Correcting the underlying problem is best. There is some data that using acetazolamide, no matter what the cause, is a quick and relatively safe way to correct alkalosis.