False! Employee health workers may say that people who have gotten the BCG vaccination–usually from Asia, Africa, or the Caribbean–do not have reliable PPD readings and therefore need chest x-rays. One magazine article reports: “Current Occupational Safety and Health Administration (OSHA) regulations do not require periodic chest x-rays for a health-care worker who is PPD-positive unless symptoms develop.”
“Prior vaccination with BCG is not a contraindication to TB skin testing, and the CDC guidelines recommend ignoring BCG status when interpreting skin test results and selecting candidates for latent TB treatment. Although BCG vaccination can turn a skin test positive, reactivity due to BCG vaccination wanes over time. If it has been more than 5 years since vaccination, a positive skin test is more likely due to TB infection than vaccination. Furthermore, the larger the size of the PPD reaction, the less likely it is due to BCG. A recent meta-analysis found that reactive skin tests more than 15 years since vaccination or with more than 15 mm of induration were unlikely to be due to prior BCG vaccination.
Interferon-based blood tests such as the QuantiFERON® -TB Gold avoid the possibility of false-positives occurring from BCG vaccination, since cross-reactivity does not occur.”
Be warned that the Quant Gold may come back as “indeterminate” or “borderline” and then you may be in a bit of a pickle and have to get a chest x-ray anyway.
Questions you should make sure to ask someone who has had a past positive PPD:
1. How long ago was it?
2. Have you ever received the BCG vaccine?
3. Did you ever receive treatment for latent TB? (isoniazid)
4. Have you ever had a chest x-ray previously?
If you have a patient with acute O2 desat, one of the things you should consider is: do they have thick secretions? Do they have poor air movement? Could they have a mucus plug?
Abundant thick airway secretions may become impacted in the lower airways, causing obstruction and atelectasis. Mucus plug may cause lung collapse .
If the patient is on a ventilator, you may be able to detect excessive airway secretions on the flow-volume loop, which will show a sawtooth pattern representing intermittent changes in airway resistance.
How can you protect against mucus plugs? Give patients humidified O2. Do pulmonary toilet, with frequent airway suctioning. Give medications like glycopyrrolate, which can thin secretions.
Submassive vs massive PE: this is an old classification that isn’t helpful anymore.
“Submassive” means low to intermediate risk, hemodynamically stable patient with no standard for how big or little the clot is.
“Massive” means high-risk, hemodynamically unstable, and again, no standard for how big or little the clot is.
We freak out about saddle emboli, but a saddle embolus isn’t necessarily high-risk. What is concerning? Elevated troponins or BNP, or signs of RV strain on the ECHO. You may even see RV strain on CT if the ventricle is larger or the septum is bulging inversely; reflux of hepatic contrast indicates that RV filling pressures are higher.
What to do with high-risk patients? Consider giving TPA. This shouldn’t be a knee-jerk reaction due to possible bleeding risk. That being said, there is some evidence such as the PEITHO trial showing that TPA might have a role in intermediate-risk PEs as well.
In this post, I discuss vent management. The overarching principle is that you must constantly adjust different parts of the ventilator depending on the patient’s respiratory/mental/overall status. Think: dynamism.
To read and understand a vent, look at the multiple parts on the screen. Anything on the x-axis is “things we adjust.” Anything on the y-axis is “things we use to measure response.”
First look at the mode—is it pressure control? Pressure support? AC? Volume controlled? These mean different things.
Pressure control—patient’s pressure settings are titrated and number of breaths are controlled by the machine. Breaths are triggered by the machine. Therefore, you can adjust the respiratory rate. If the patient ends up triggering their own breath, the vent acts like PS.
Pressure support/CPAP (“what’s the difference between BiPAP and PS/CPAP?”)—patient’s pressure settings are controlled by the machine, but the patient can trigger their own breaths
Volume controlled—the patient is set to a certain tidal volume, and the machine adjusts pressure accordingly to make sure the TV is maintained. Oftentimes, this is found in low-volume ventilation patients, like ARDS. “Low-volume” is thought to be 4-6 ml/kg of tidal volume, based on IBW (ideal body weight). For reference In a person my size, my low-volume TV is anywhere between 320-420 cc/min, with a minute ventilation up to 12 L. “Normal” volumes would be about 10 ml/kg.
Next, look at the pressure settings: usually read “delta/PEEP”
peak=the pressure of the airway at max inspiration. If peak is high, that means there’s airway resistance. Goal peak airway pressure <30. Around 60 mm H2O is when you start worrying that intubation isn’t working.
delta=plateau=peak-PEEP. Tells you how much extra inspiratory pressure the patient requires, or in other words, “the pressure greater than pressure support.” 8 is normal for non-ventilated patients. If plateau is high, this means the patient has stiff lungs (at risk for ARDS), so you should use low volume. Goal O2 sat 88-95%.
PEEP=end expiratory pressure, left at the end of the breath, or how much support the patient requires during expiration. 3-5 cm H2O is normal for non-ventilated patients.
AUTO-PEEPING: is the phenomenon that applies to someone with air hunger, especially in COPD or asthma. The PEEP may be higher than indicated on vent settings, because of mucus plugging, bronchoconstriction, or shortened expiration time. Regardless of cause, auto-PEEP causes more work of breathing—they have to generate a higher inspiratory negative pressure to open up the alveoli during inspiration. Ways to get around auto-PEEP: lengthen the expiration time, shorten the inspiration time, decrease the RR, or use CPAP to create a “waterfall effect”: as long as the positive pressure of the CPAP is higher than the auto-PEEP, you’ve created a “negative” gradient that air can flow down to the alveoli.
Another thing you can adjust is the FiO2. 40% is considered “normal” for a vent; 21% is room air.
To adjust vent pressures, there are several tricks respiratory therapy uses to decide whether to change the settings:
Is it O2 or CO2 status that needs to be improved? Patients with hypoxic respiratory failure benefit more from O2-increasing mechanisms like FiO2. Patients with hypercapnic failure benefit more from CO2-reducing mechanisms like upping the RR or PEEP.
ABG: You should always look at the O2 sat on the monitor, obviously! But ABG is more accurate and tells you pH and CO2 (those are directly measured; the other values are calculated from those). Can get daily or q12h to measure response to the vent. 3.5 bicarcb to 10 PCO2. If there is compensated respiratory acidosis, you don’t need to adjust the vent because we allow “permissive hypercapnia” in ventilated patients in order to maintain them at low lung volumes. It is not infrequent to get hourly ABGs in the intensive care unit.
“recruitment maneuver”=a brief blast of PEEP, like 35-40 cm H2O. This opens alveoli, which theoretically improves oxygenation, but may cause hypotension.
Inspiratory hold=used to determine plateau pressure. Plateau pressure is directly correlated with alveolar pressure, so it’s used to titrate tidal volume.
Expiratory hold=used to see if PEEP should be increased because of impaired elastic recoil or airway resistance (emphysema, bronchospasm, airway collapse). An exp hold sees how much auto-PEEP there is.
Let’s say you’re in the MICU, and you get a report that a 60-year old male found down is rolling up to your floor in the next 30 minutes. “He’s intubated,” the emergency resident reports. Without even asking, for what reasons might this guy be intubated?
Or, you’re on the floor and have a patient admitted for aspiration pneumonia who has become more “sleepy” over the course of the day. The nurse has stopped you multiple times in the hall to ask you how you think the patient is doing, what the plan is, and as she walks away, you hear her sign, “Well, he’s heading towards intubation…”
So how do you know that someone might need to be intubated?
There are three basic reasons to remember:
severely altered mental status or inability to protect airway
hypoxic respiratory failure
hypercapnic respiratory failure
Everything else, ranging from aspiration pneumonitis to anaphylaxis to drug overdose to diffuse alveolar hemorrhage, comes from one of these three reasons.
“Flash” pulmonary edema is pulmonary edema that develops suddenly. It can be defined by:
crackles on exam
may also be associated with a “new O2 requirement”
“Flashing” is a sign of acutely elevated cardiac filling pressures. It must be treated urgently.
The next question you should ask yourself is, “Why is my patient flashing?” Consider acute CHF exacerbation, ischemia (MI), acute mitral or severe aortic regurgitation, or arrhythmia like afib. Hypertension can be an exacerbator of pulmonary edema because it creates diastolic dysfunction. Patients with severe renal disease are in a constantly fluid-overloaded state, so it’s not hard to push them over into pulmonary edema.
How do you treat flash pulmonary edema? The first step is high doses of IV lasix. If the patient is lasix-naive you can start with 20 mg IV lasix, but more often, patients will require 80 to 120 mg IV lasix.