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.

What are the new 2016 sepsis criteria?

Usually at some point in a rotation, I’ll end up quizzing a med student about SIRS criteria. I think it’s important to be able to memorize a few numbers that can help you make a quick decision about antibiotics, fluids, or transfer to the ICU.

However, a few investigators working on behalf of the Third International Consensus Definitions Task Force conducted a study of almost 150,000 patients have a new proposal for a “quick-sepsis” or “qSOFA” set of criteria that is more based on SOFA than SIRS.

The new criteria for qSOFA are suspected infection plus ≥2 of the following:

  1. Altered mental status (Glasgow Coma Scale score <15)
  2. Systolic blood pressure ≤100 mm Hg
  3. Respiratory rate ≥22/min

Compare this to the SOFA score, which is now officially considered to be more predictive than SIRS***:

  1. Platelet count
  2. Bilirubin
  3. Glasgow Coma Scale score
  4. Mean arterial pressure (MAP) or administration of vasopressors with type and dose
  5. Creatinine or urine output
  6. PaO2/FiO2 ratio and mechanical ventilation

The team also stated a new definition of septic shock: not just non-responsive to fluids, but having to be on pressors to maintain a MAP >65 mm Hg. A high lactate is also required (>2.0).  They also axed the term “severe sepsis.”

***there is a A LOT of contention about whether SIRS or SOFA are “better.” My co-residents had a lively, very friendly, e-mail debate about this article showing the qSOFA was not actually that helpful for predicting mortality in the ICU. The point is that SIRS is meant to be used for risk stratification, and qSOFA is still too new for us to gauge what it is helpful for, even.

***Update, Feb. 2018: study in Ann Int Med published comparing prognostic accurary of qSOFA and SIRS criteria found that SIRS is more sensitive (=better screening tool), and that qSOFA has moderately better specificity for poor outcome.

 

***

What can I give an opiate user or IV drug user for acute pain?

Imagine this scenario: you get a patient transferred from the surgery service. You glance at her home meds and with a flash of dismay, see 60 mg oxycontin BID with 10 mg oxycodone q4h PRN pain for chronic back pain. She just had hip surgery. What do you prescribe for breakthrough pain?

Or this: you are caring for a patient admitted for aspiration pneumonia. Although his breathing seems fine, he complains about the uncomfortable bed and requests something for pain. His social history notes that he currently buys Percs on the street and has used cocaine in the past. Initial doses of 5 mg oxycodone don’t seem to work, and he demands more and more. The nurses grumble about his neediness. What do you do?

I am, despite my bitterness and tough talk, an idealist and softie. I mean, I want to spend my professional life figuring out chronic abdominal pain and treating patients with malabsorption, dysmotility, and postsurgical anatomy. But in my daily practice, I have several fears when prescribing narcotics for inpatients:

  1. I’m feeding into an addiction. Giving them pain meds will make them worse off in the long run.
  2. They are taking advantage of me. They are lying to me or being nice to my face but laughing behind my back.
  3. When they realize they can get whatever they want, they’ll invent more excuses to stay.

 

Acknowledge these fears. Then let go.

What I’ve come to realize is that despite the patients who burn you, pain is real. Pain may stem from many different sources (deconditioning from being morbidly obese, psychiatric disease, dyspnea, social chaos, nerves that are wired differently and a low pain threshold). We may make us think, c’mon, there is NO way you are actually in that much pain…but they do need SOMETHING treated. Often people just don’t have enough insight to tell you exactly what that is. So your first formulation should be: is this actually pain? Is it anxiety? Is it fear at having to return to an abusive partner? Is it poor coping skills/functional status/dementia? Pain meds are not the only answer.

A final point: in those patients who want to be hooked on pain meds, make up stories, and manipulate the system, isn’t it sad that they would waste their lives trying to get addicted? A patient like this probably needs psychiatric help.

But sometimes you do need pain meds for people with complex pain histories. For instance, like patient #1 above, post-surgical patients have a really real reason to have pain: they just had freaking surgery! Many of your patients may have DEPENDENCE but not be ADDICTED. If you have a patient who is already on oxycodone, like #1 above, it’s a no-brainer they’ll require more than 2.5 mg oxycodone q6h.

NB: You should always make sure the whole team, including nurses, psychiatrists, pain specialists, etc are on the same page about an individual’s regimen. Here are some strategies I’ve seen used successfully:

  • Build trust with your patient and taper down gently. When you acknowledge the validity of your patient’s story and show that you care about them as a person, they are much more willing to listen to your suggestions–like, “how about we not do the extra IV dilaudid because I think you’re ready to try the pills? I really want to see you make progress.” In my experience this really separates the people in real pain from the people who have secondary gain.
  • Make sure you have a good non-narcotic foundation. Put people on standing Tylenol. Use flexeril if they specifically have spasms. Use lidocaine cream over painful joints. You wouldn’t believe how much relief a heat pack can give.
  • Use the appropriate meds for pain-like symptoms: benzodiazepines for anxiety, low-dose antipsychotics for agitation or insomnia, etc.
  • Start the patient on standing pain medications q3-4h instead of PRNs. Relying solely on PRNs is like putting a diabetic only on sliding scale insulin. If they ask for more, increase by 25% at a time until they are satisfied.
  • If one opiate isn’t working, try another. For some reason, different people respond differently to oxycodone or dilaudid or morphine…cross-tolerance is variable, but you can try using an equi-analgesic conversion.
  • I’ve seen methadone work well. It has a 4-8 hr half-life for analgesia (and 24-48 for withdrawal suppression). However it can take several days to titrate and you need to guarantee outpatient followup. If someone comes in already on methadone, you can give them extra narcotics if necessary but you must communicate any changes with their methadone clinic, otherwise, no dice.
  • I would not be so bold as to give known opioid abusers a PCA, but some people have found it works well.
  • Consider a social work consult (especially if you have a patient like #2 above) and offer substance abuse counseling or detox. If you know they’re going to snort or shoot up when they leave, consider writing a suboxone prescription.

References: a concise article from Anaesthesia
Medscape
The school of hard knocks

 

dialysis in the ICU

Up to 70% of patients require renal replacement therapy or dialysis. Dialysis is renal therapy via diffusion of small solutes, whereas filtration is the convection of large solutes. Early treatment is better, obviously…

  1. intermittent hemodialysis: is easier to implement, more practical, better solute clearance and fewer bleeding complications
  2. continuous dialysis: better for hemodynamically unstable patients, if have renal and hepatic failure, or acute brain injury
    1. requires continuous anticoagulation with heparin or UFH
    2. citrate may cause electrolyte issues (chelates ionized Ca)
    3. CVVHDF=continuous venovenous hemodiafiltration=dialysis +filtration. The #1 modality in the ICU. Large volume, requires fluid replacement.
    4. CAVHD or AVHDF requires arterial cannulation, and is unreliable in pts with low BP, PVD. More risky.
  3. peritoneal dialysis
  4. SLEDD (hybrid of intermittent and continuous): more flexible than continuous, less need for anticoagulation, but has the same efficacy as continuous

When to use phenobarbital over lorazepam or chlordiazepoxide for alcohol withdrawal

Phenobarbital is being increasingly used on the wards for alcohol withdrawal because it’s safe, effective, and cheap. Consider using it when the CIWA score is >15, pt is going through rapid withdrawal, or is at a point when you would normally consider IV benzos. Start with a bolus of 65-130 mg phenobarbital. Of note, phenobarbital must be tapered over the course of a week, so patients must be able to be compliant with a week-long regimen.