ARDS
A case of prolonged CPR - does it make any sense?
Some things just don’t make any sense. It’s like in the “Red fish, blue fish” book be Dr Seuss: “did you ever fly a kite in bed?...did you ever walk with ten cats on your head?... Think about it. Does it make any sense? No, it doesn’t. What about doing CPR on your patient for two hours straight? Does that make any sense? At that time it seemed like it did. Even though, critical care medicine is inherently chaotic, we don’t like any surprises.
You often know who is “supposed” to die and who is not. A thirty one year old previously healthy man just was not supposed to die. You can’t let it happen.
Just a few days ago he was fine. Later he developed some flu-like symptoms and now he is in ICU with severe pneumonia, full-blown Acute Respiratory Distress Syndrome and multiple organ failure. You’ve tried everything there is to try: maximum ventilatory support, Nitric Oxide and even prone positioning (turning the patient on his abdomen) – nothing is working. Transfer to the outside facility for ECMO (extra-corporeal membrane oxygenation) is simply unrealistic – the patient is not going to survive the transport. And now he is coding (developing cardiac arrest). This is one of those what I call a “Rolling Code”. The patient loses his pulse for five to ten minutes. CPR and ACLS (advanced cardiac life support) is initiated. He regains spontaneous circulation just to lose it a few minutes later. Every time you feel his pulse, you “reset the clock” and start all over again. Remember, you just can’t let him die, so you do it again and again and again.
The family was summoned into the room to witness the code. His parents are sitting quietly in the corner staring into space. Twenty, thirty minutes into the code the silence in the room is almost wicked. Nobody talks. All you can hear is the sound of chest compressions and bag-ventilation. If you believe in afterlife, every time the patient “dies” the soul is leaving his body.
You hold the chest compressions after another round of Epinephrine and Atropine – “yeah, we got the pulse”. Every possible medication is running into his vein to keep him alive. The periods between arrests become shorter and shorter. You check his pupils – fixed and dilated. The patient likely sustained a severe brain damage from the lack of oxygen supply. Now, it’s time to talk to the family again and stop. You have done everything you could and beyond, way beyond. Sometimes, it’s not up to us to decide who is not “supposed” to die.
H1N1 - how bad this is going to get?
I guess I was in a bit of denial about it. I was hoping that it would blow right past us until I realized that we are running out of ICU beds and somebody mentioned that we might need to borrow Nitric Oxide equipment. The presentation is quite similar so far. It starts as a flu-like illness with fever (up to 105), myalgias, sore throat etc. Several days later patients develop progressively worsening shortness of breath and cough. Once we see them in ER, they are already quite sick. The chest XR shows bilateral patchy infiltrates consistent with pneumonia. Surprisingly, the rapid swab test was positive in only a few of those patients. It appears that the sensitivity of this test is low. It takes several days to get confirmation on H1N1 from the State lab so the patients are being started on Tami flu empirically. Several patients have already progressed to a full-blown ARDS (click on image above) and multiple organ failure. I had to use high PEEP and FiO2 and yet oxygen saturation was barely in the 80’s. We had to use prone positioning and even Nitric Oxide. Sputum and blood cultures in most cases are coming back negative. The empiric antibiotics are being started to prevent secondary superinfection. Some patients require dialysis for kidney failure.
The H1N1 vaccine is being given to healthcare workers only sporadically so far (I got mine as soon as I could). Apparently, we might have a shortage of respirators and Tami flu. This is only October and I wonder how much worse this is going to get.
Ventilator strategies for ARDS patients.
There is plenty of data on using low tidal volumes (VT) on patients with ARDS. What about the optimum PEEP strategy? Recent Meta-analysis from “Annals of Internal Medicine” did not find any mortality benefit from higher PEEP. I am usually dialing PEEP up as I am decreasing FiO2. It’s not unusual to have somebody with bad ARDS on 17.5 of PEEP or even higher. There is no evidence that higher PEEP hurts patients, though, how high is to high is still unclear.

