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76 yo M with a PMH of aspiraiton PNA s/p CVA and COPD presents with sob.
VSS: 110, 28, 83% on RA ambulance got him to 93% on BiPAP 10/5 100% fio2, 105/60, 38.8 (oral)
Patient is 320 lbs and is a known difficult airway from prior intubations from similar events. He had to be rescued from failed RSI with an LMA and required aintree fiberoptic intubation by anesthesia.
You think the patient is going to fail BiPAP but you have bought yourself some time.
https://vimeo.com/107958796
Severe Sepsis and Septic Shock in 2014
Although sepsis resuscitation has been beaten to death by most ED residencies, with all of the new articles coming to surface and a paradigm shift in management I thought it might be a good time to complete a recap of my biased approach to septic shock in 2014. I welcome comments, suggestions and arguments as I know there will be some controversy in a few of the things we do.
65 y/o M presents to the emergency department with cough and fever for 2 days, and his wife noticed he was more sleepy than usual. His PMH is significant for COPD, HTN, DM II and his wife states she was recently sick with the “flu”.
VSS: 105, 85/55, 88% on 10L facemask, 39.6 (R), 26
My discussion will start with the first hour as I think these are all important things that can be done by the ED:
Obviously this is pounded into emergency physicians of fluids, antibiotics, and source control; here is maybe a few tips you haven’t heard about:
The dose of 1 g of vancomycin load in adult patients is almost always inadequate. Even if you don’t know the renal function you can adjust future doses of vancomycin to help stay within therapeutic range (15-20).
Subsequent dosing for me of these medications has changed to extended infusion at Stanford, and in some rarer circumstances continuous antibiotic infusion. The reason for this is as more MDRO infections arise it is important to have time above the MIC with time-dependent killers (beta-lactams) to help provide clinical and microbiologic cure.
Cephalosporins and penicillins have been shown that the amount of time that free or non-protein bound drug concentration exceed MIC is the best predictor of bacterial killing and microbiologic response for beta-lactams.
Fluid resuscitation:
Traditionally we have given as much fluid as possible until the patient goes into pulmonary edema. I think it is reasonable to give a bolus of IVF in most patients of 1L who are hypotensive, and a second liter if still hypotensive.
Some principles of fluid resuscitation:
1. I like Plasmalyte, or normosol, but understand logistically it isn’t possible or financially acceptable. Also there are basically no studies assessing these particular fluids.
2. Otherwise 99% of the time you can use Lactated ringer, yes it has 4 meq of potassium, most of the time this will not make a huge difference in patients serum K. If need be alternate between LR and NS. Chloride restrictive strategy resulted in less renal failure and RRT in one trial, also in the Process trial higher fluid resus and positive fluid balance was associated with more RRT.
3. Avoid only using NS, More and more evidence is arising that it results in more renal dysfunction (we are seeing this a lot in patients with brain injury on 3% hypertonic saline). It also creates an acidosis that is very annoying to me :)
4. Colloids- the Albios study was a negative NEJM study on pushing the serum albumin up using 20% albumin (not as a resus fluid so not as applicable to ED) but a post-hoc subgroup analysis suggested 90 day mortality benefit in patients with septic shock. In the subgroup analysis of the SAFE trial albumin improved mortality in septic shock.
Therefofre I think albumin is an expensive blood product and is hyperosmolar (Na ~160ish) and it’s use is very controversial. I use it in dialysis patients, patients with cirrhosis and in patients who have already gotten crystalloid boluses and appear to still be volume responsive.
I don’t use starches (6S, CHEST and CRISTAL trial).
4. Try and use fluids that are warmed every liter of room temperature fluid you give will drop the patient’s temperature by 0.25 degrees Celsius.
5. Asses fluid responsiveness after you have loaded the patient with some fluids, using passive leg raising, IVC collapse, echocardiography with VTI, pulse pressure variation or whatever is available to you. Positive fluid balance is a strong predictor of death, results in pulmonary edema and more renal failure. If the nurse calls you and you are busy your response shouldn’t be ordering more fluids without reassessing after your initial load, especially if the patient is not intubated.
Temperature management:
Fevers cause a whole myriad of problems like tachycardia, arrythmias, hypotension, hypoxia etc... but they are also protective in many animal studies by inducing production of protective heat shock proteins necessary for immune-mediated defense. I use tylenol for fever control 1g Q8, I do not use a cooling blanket or ibuprofen unless there is a really good reason ( i.e; the paitent has NMS or Malignant hyperthermia).
Blood Pressure Goals:
The big study SEPSISPAM by Asfar et al published in the NEJM 2014 compared 65-70 and 80-85. Basically no difference in mortality, but if you had baseline hypertension a higher MAP resulted in less renal replacement therapy (RRT). I shoot for 65-70, other people will stand up on their chairs and shout that this study proves what they suspected all along of patients with chronic hypertension needed higher perfusion pressures, go figure.
Vasopressors:
If you find that you have given fluids, and the patient is no longer fluid responsive or you notice that the blood pressure goes up for 10 minutes then back down it may be a problem of capillary leak and lack of vascular tone. Place a CVC above the diaphragm if possible at this point. I do not think the process trial should be interpreted as its now ok to avoid central lines, as that was not studied specifically.
A few things to know about epi:
1. It will make you blood sugar higher and
2. It will make your lactate go up.
At does of 50 nanos/kg/min or 0.05 mcg/kg/min or less epi is considered mostly inotrope dosing. I therefore try and use it to help augment CO early in septic shock since most patients are peripherally vasodilated, later in there course is when they become vasoconstriced and dobutamine may be a better option.
Steroids:
I start them early and do not wait for a day of shock to initiate steroids. If you require two vasopressors (that is vaso @ 0.04 U/min and norepi at 5 mcg/min) you get hydrocortionse 200mg 24-hour infusion.
An infusion is hard to get in the ED but 50mg IVP is pretty easy to find, and so 50 Q 6 is reasonable until they get upstairs. The physiology of a continuous infusion seems to make sense, and there are a few studies showing better glucose control and maintenance of cortisol levels.
Also I don’t usually check random cortisol levels or do a stim test, mostly because it takes time to come back, and because no one really knows the definition of adrenal insufficiency in the ICU. There are a ton of factors that go into a random cortisol level that I won’t get into here.
Hydrocortisone is dirt-cheap and the side effects of hyperglycemia are not as significant as you would expect. The superinfection rates are about the same between those getting low dose steroids and placebo (Sligli et al. Safety and Efficacy of Corticosteroids for the Treatment of Septic Shock: A systematic Review and Meta-Analysis). Also we know that steroids will reduce the incidence of vasopressor dependency. In my opinion (as well as many other ICU docs) the CORTICUS study waited WAY too long to enroll someone, there was already a general consensus in Europe that steroids worked (based on the Annane paper published earlier) and the patients were less critically ill than in the original paper. Therefore, in a select subset of patients (2 vasopressors; even if low dose), we start steroids, and RAPDILY taper in ICU as the vasopressors start to come down.
Perfusion parameters:
Lactate-I order two to start, one at time 0, and one at To + 4 hours. This way no matter what that lab gets drawn 4 hours after the original in order to make sure we are making progress at the micro circulatory level.
Also if I have high levels of lactic acidosis not responding to most treatments (and no other apparent cause) I supplement thiamine, in case there is a reason they could be thiamine deficient, since this medication is cheap, and basically inert.
A caveat: lactate is not sensitive or specific for sepsis, it is a marker of poorer prognosis in patients in shock of any cause (post-arrest, septic, cardiogenic etc). If you get an elevated lactate do not assume the patient is septic and call the ICU fellow, do some digging first.
SvO2- probably don’t have to routinely measure this. If the patient is in shock needs vasopressors and has a central line above the diaphragm I will follow SvO2s as I am titrating vasopressors and Inotropes. I don’t transfuse PRBC’s or use dobutamine to push this “number” up.
I check a CVP, so I know what it is, and then look at it in conjunction with 700 other things. I do not bolus fluids to get a certain CVP number. The CVP is based on multiple things and does not predict fluid responsiveness nor does a static CVP give me much information. I would caution that if the CVP is high there is something wrong with the right side of the heart and it should prompt an echocardiogram. It could be LV failure, pulmonary hypertension, PE, RV dysfunction due to ischemia etc, but a CVP > 16 should give you pause, your cvp lying down is probably 0.
Setting up the Vent:
This is a whole article in itself, but I leave you with the basics:
Your hospital needs to develop a lung protective protocol that is RT driven, to take you off the hook. We call this protocol LPV (lung protective ventilation). Basically the RT should start with 8cc/kg IBW for TV and a RR to match their current Minute ventilation. You can then titrate down on TV to 6cc/kg, as tolerated to keep plateau pressures < 30. You should titrate up on PEEP to keep sats up not the FiO2. If your patient is on 70% fiO2 and PEEP of 5, you probably need to rethink that strategy. If your patient is hypoxic do not be afraid of PEEP! An RT driven protocol frees you up and allows them to make adjustments based on ARDSnet, which I know you don't want to be doing.
The FiO2 should be reduced to keep sats >88%, you don’t need an ABG, it should be weaned rapidly.
The pH can be tolerated down to as low as 7.2. Keep in mind MOST patients aren’t this sick to need lower pH’s and patients HATE having an elevated PCO2. It is terribly uncomfortable and often requires high doses of opiates and sedatives. Most patients do fine with AC/VC with low TV and rates between 16-20.
Our sedation/analgesia package right after intubation if they are hemodynamically stable is:
ANALGESIA FIRST:
-1-2mg of dilaudid IVP after securing airway and checking BP, then
1 mg/hr drip of dilaudid for avg adult male (less for granny and more for chronic opiate users), we have abandoned fentanyl drips due to the context sensitive half-life. Others use intermittent pushes of opiates, in the ED that is way too much work, they aren’t getting extubated in an hour or so, but if you are brave please go ahead.
Sedation:
I rarely use benzodiazepines, PERIOD. They increase ICU related delirium, drips result in prolonged wake-up times and if not vigilant about sedation vacations these can hang around for a good deal of time. Once the patient has been on them for a while they can go into benzo withdrawl, another annoying thing to deal with. Basically STOP USING BENZO’s, enough literature is coming out to suggest benzo’s are dangerous. We have gone as far as not using benzo’s in alcohol withdrawl. We use clonidine, dexmedetomidine, gabapentin, and Depakote. (this is a whole different lecture again).
Dexmedetomidine will go generic this winter. Also even though the price tag gives administrators and pharmacists a heart attack, evidence suggests that on the back end dex provides cost savings with shorter ICU LOS, and reduced hospital costs.
It works in about 50-70% of patients to keep them calm on the vent but comfortable enough to interact. The dose is 0.2- 1.2 mcg/kg/hr. I don’t bolus and the major adverse events are bradycardia. Get familiar with this med as it will become a great ED med for obtaining CT’s, conscious sedation for anxiety provoking procedures like LP’s in the near future.
Propofol is excellent for its rapid on and off action but I avoid it in patients with hypotension, for obvious reasons. Avoid doses above 80 mcg/kg/min, as these are associated with propofol infusion syndrome(PRIS) after 24-48 hours. PRIS is devastating and took the life of a pregnant 35 y/o with eclampsia due to high doses at an OSH as we were the recieving hospital of the transfer for ECMO.
Ketamine works but I usually use it as an adjunctive medication to one of the above (ketamine/dex/dilaudid).
I tried to be somewhat breif and still controversial and maybe give a few pointers of thing you had forgotten, let me know what your thoughts are.
-Dave
The use of Sodium Bicarbonate in emergency Situations
The utility of intravenous sodium bicarbonate in severe metabolic acidosis is to say the least controversial. Yet each time we are presented with a patient with severe acidosis it is almost irresistible to give the patient an ampule of sodium bicarbonate to “improve myocardial performance”, after all our endogenous catecholamines work better under more physiologic conditions, right?
I made this review to help delineate the problems of treating acidosis with sodium bicarbonate in the patients with acute metabolic (specifically lactic) acidosis. This is not meant for patients with renal tubular acidosis or patients who have bicarbonate loss, in which bicarbonate therapy is generally accepted (usually oral replacement). Also this is not for toxicologic emergencies, or for use in treating hyponatremia.
When considering bicarbonate replacement we must first consider the following questions:
What are the untoward effects of metabolic acidosis?
Before you read on think out loud what in your mind are the detrimental effects of metabolic acidosis and we are not talking prognostically here.
-Reduced myocardial performance and decreased sensitivity of the myocardium to catecholamines, probably due to a reduction in the number of beta-receptors on the myocardial cell surface. In multiple isolated animal studies this has not been confirmed. This is because serum acidosis does not always translate into worsened intracellular acidosis. Also acidosis improves oxygen unloading into metabolically active cells.
-Arrythmogenic especially at a pH < 7.2. This makes resuscitation of individuals in ventricular fibrillation more difficult, and why bicarbonate therapy was adopted during cardiac arrest. Oh the rise and fall of medications during ACLS!
On the other hand we know that most patients tolerate respiratory acidosis fairly well. Everyday we place patients on ventilator settings to optimize their PaO2, and allow the PCO2 to rise without significant untoward hemodynamic effects (permissive hypercapnia). At a pH < 7.0 this is less well characterized, since so few people allow patients to develop such acidemia.
Also MANY patients in DKA are extremely acidemic and do quite well (how many times have you seen a patient with DKA with a pH < 7.2 who walked out of the hospital in 2 days?)
Conclusion: Therefore the assumption that a low pH in it of itself is a precursor to hemodynamic collapse and requires treatment is false. This does not mean you should not recognize the acidemia as a potentially poor prognostic sign, and a marker of severe disease.
Can Bicarbonate raise the pH?
Bicarbonate itself is not the only determinant of blood pH, as everyone knows.
If you follow the physiochemical method of acid base disorders the pH is determined by subtracting strong cations (Na, K, Ca and Mg) from strong anions (Cl- and SO4). The SID increases due to bicarbonate administration because of an increase in sodium (bicarbonate is not a strong ion at all).
However, bicarbonate drives Le Chatelier’s principle of chemical equilibrium: (HCO3 + H+ <==> H20 + CO2)
which will drive CO2 production. Therefore if ventilation is fixed, or MAXED as in a patient with a Minute ventilation of 20L, excess CO2 production cannot be eliminated and a rise in CO2 negates any potentially beneficial effects of the bicarbonate itself.
IF that gave you a migraine let me say it in another way.
Sodium bicarb does increase the serum pH but it also increases CO2 production (think about ETCO2 jumping during a code when giving bicarb if you do this) and if you cannot blow off the CO2 with increased ventilation it has no net effect on the serum pH.
*Another potentially MORE IMPORTANT problem with following the serum pH is that different compartments have different pH’s (i.e; inner mitochondrial membrane, blood brain barrier etc) and CO2 readily crosses many of these membranes whereas bicarbonate itself does not. Therefore are we making the central veins for sampling more alkalemic at the cost of worsening intracellular and cerebral acidemia?
Multiple studies have demonstrated that sodium bicarbonate will worsen acidosis in the brain and CSF (LP sampling and spectroscopy MRI). Several animal studies have shown that intracellular pH drops in RBC’s, muscle, liver and lymphocytes.
Conclusion: Yes bicarbonate can increase the serum pH, but its effects on intracellular pH are unknown, but likely worsen acidosis.
What beneficial effects does sodium bicarb have, if any?
Few studies have addressed specifically if there is any beneficial effect of sodium bicarbonate in vivo. No RCT’s have shown improvements in mortality, there has however been conflicting results on its effect on arterial pH, and several studies have demonstrated untoward hemodynamic effects.
In animals sodium bicarbonate was indistinguishable from saline bolus on hemodynamics (CO, MAP, and CVP)
In two human studies in patients with lactic acidosis, sodium bicarbonate raised serum pH and bicarb, but did not improve hemodynamics or catecholamine responsiveness (ScVO2, MAP, wedge pressure, CO unchanged when compared to saline).
Bicarbonate is an excellent volume expander, since it is like giving hypertonic saline, so potentially it could be use for resuscitation. Also bicarbonate can be given as a bolus for patients with severe hyponatremia with neurologic findings (about the equivalent of 100 cc of 3% saline in one 50 meq ampule.)
Conclusion: Bicarbonate infusion has not definitively shown beneficial effects in patient or surrogate outcomes like hemodynamics or amount of vasoactives being infused . In fact most studies suggest bicarb has no net effects other than volume expansion in the hemodynamically unstable.
The final question remains what are the potentially deleterious effects of administration of sodium bicarbonate?
The first time I brought up the utility of sodium bicarbonate in the cardiac ICU, I was met with
“ DO you know how many times I have regretted giving sodium bicarbonate? That would be 0”.
Essentially clinicians believe it is a benign cheap medication, which has few adverse effects. Oh but so wrong you can be:
Case:
55 y/o M s/p crush injury who had recently come off CVVH and was now making more urine whose bicarbonate had continued to be low (15). He was on the vent, but because of his non-gap metabolic acidosis he was breathing significantly above the vent settings to drive his PCO2 down to compensate for this acidemia. This was making weaning difficult, as the attending did not want to extubate a patient with a RR in the 30’s.
The surgical intern on overnight thought he would order a sodium bicarbonate drip in order to improve his serum bicarbonate and pH to make him “ready” for extubation.
The resident ordered a 50 meq/hr drip at 8pm and at 5am labs were sent. When I arrived for rounds a critical sodium value was 168 (increased from 132). His chloride was also 130 so we thought this was an error, unfortunately a stat ABG had a pH of 7.67 and a HCO3 of 52 from the excessive endogenous bicarbonate that was given. The resident had MEANT to order a bicarb drip (3 amps in a liter of D5W or sterile water) which has a total of 150 mEq in 1L, instead he ordered 50 mEq/hr!
The patient was less arousable after stopping sedation and continuous EEG found the patient to be in non-convulsive status (which alkalemia predisposes you to). It was UGLY.
Detrimental effects of bicarb:
Conclusion: Bicarbonate will raise the serum pH when used in patients with severe acidosis. However, it is more likely that bicarbonate infusion worsens intracellular pH and does not provide any beneficial hemodynamic effects. Therefore in patients with LACTIC acidosis (even at extremes of pH < 7.2) it is difficult to find any reason to recommend sodium bicarbonate therapy.
You are better off attempting to divert more neurons to solving why they are so acidemic. So the next time your nephrologist calls and screams why they aren’t on a bicarb drip you can kindly explain that there literature the use of bicarbonate is at BEST controversial.
-Dave
Treatment of Massive Pulmonary Embolism
CASE:
21-year-old male was admitted to saint elsewhere with severe shortness of breath, epigastric discomfort and vomiting. He had recently been admitted to outside hospital with pancreatitis for 10 days and was discharged home with PMD f/u with improving idiopathic pancreatitis. When the patient arrived in the ED his vital signs were:
HR 140, Sat 92% on RA, BP 140/50
CC: epigastirc pain and vomiting
In the ED the patient was triaged to intermediate care had a chemistry panel sent and a CT A/P ordered. His lipase came back at > 3000. The medicine team was consulted and the patient was to be admitted to the floor pending a CT A/P. Image shown below is the most superior image from the abdominal CT which happened to catch the main pulmonary arteries
The patient requires 4L NC to maintain his sats > 92% but is awake and mentating well and his BP was normal. His EKG is shown:
The ED felt the patient was hemodynamically stable to be admitted to the floor and medicine admitted with IR consults for possible thrombectomy and IA tPA due to large RV seen on CTA. About 5 am the next morning while in the angio-suite the patient codes during thrombectomy. The patient is PEA without an airway in IR.
If you are called to this code, what would you do?
What was done:
A Pulmonary artery catheter was in place because of the attempted thrombectomy and the code team pushed 50mg of IA tPA (after about 10 minutes of me looking in the cath lab for the vial of tPA that was not in 2 mg aliquots). The patient has ROSC about 30 seconds later. Unfortunately his first ABG intubated on the vent was as follows:
6.79/90/85 on AC 30/500/100%/5
What would be your next move, and why do you think the pH and CO2 are so high?
We decided to add inhaled nitric oxide (see below) with only mild improvements in the CO2 to 75, pH still 7.0 on 3 vasopressors. What would you do?
CV surgery was called for immediate ECMO, and the patient was cannulated in the angio suite.
2 days later the patient was decannulated he did suffer from hemorrhagic conversion of his pancreatitis, and large RP hematomas and intra-abdominal hemorrhagic ascites, likely due to heparin and tPA administration.
However the patient was weaned off the ventilator, his pancreatitis improved and he was discharged home with no residual deficits on hospital day 21.
SO what can you do in the ED to set the patient with massive PE up for success?
Disclaimer: I should mention this portion pertains to the specific subset of patients who have right ventricular failure and not simply pulmonary hypertension from a PE and are reasonably well compensated. These people have the findings I mention below.
Some tricks of the trade are as follows:
Although hypotension is almost always treated initially in the ED with IVF's if you suspect massive PE the cause of hypotension is RV failure/dilation and the treatment is RARELY IVF.
1. You will not have hypotension from acute massive PE without RV dilation
This is because the thin highly compliant RV whose afterload is the wimpy pulmonary arterial tree is very pressure sensitive. Rapid increases in pulmonary pressure result in massive increases in RV volume (it does not hypertrophy acutely). Since the right and left ventricles SHARE the septum the right ventricle balloons outward and impairs diastolic filling of the LV when pressure overloaded, hence the D shaped LV seen on parasternal short axis. This impairs the LV filling, reducing the mean arterial blood pressure and cardiac output.
Signs of RV failure are:
1. Distended neck veins/elevated CVP/ Dilated plethroic IVC without resp variation
2. Elevated transaminases (usually more chronic)
3. Hepatomegaly, lower ext edema
4. Kussmal's sign (sudden increase in CVP in spont breathing patients with inspiration)
Echo:
Dilated RV with wide-open tricuspid regurgitation (this is because of the stretch of the annulus of the valve NOT valvular dysfunction per se). Adding additional volume will only overload the RV even more and worsen TR. LV is usually hyperdynamic with small chamber size.
-To complicate matters the RV (which is usually a low pressure ventricle) gets coronary perfusion during both systole and diastole (since it is a low pressure ventricle). However as the RV pressure increases the coronary filling is markedly reduced during diastole, this creates RV ischemia. Ischemia results in stiffness of the ventricle making the RV more dysfunctional and so continues the downward spiral of right heart failure.
2. The treatment of significant RV failure:
-Reduce RV Preload
To reduce preload avoid giving volume in the ED and consider diuresis
Commonly diuretics are given if the CVP is significantly elevated because the normal geometry of the ventricles has been distorted due to an enlarged RV bowing the spetum towards the LV, diuresis will result in improved LV performance even with a decrease in intrasvascular volume.
-Reduce RV afterload:
Inhaled Nitric Oxidie or Inhaled Prostaglandins like Epoprostenol. Usually iNO is given starting at 20ppm, despite the fact that 90% of patients will have maximal response at 5ppm or less.
The problem with giving systemic pulmonary vasodilators in a hypotensive patient should be intuitive, the nice thing about giving inhaled pulmonary vasodilators is they only act where there is ventilation and perfusion. Nitric oxide is rapidly metabolized by local RBC's and thus has no systemic effects like hypotension.
iNO is not standard of care per se, but is a trick up your sleeve for that severely dyspneic patient with massive PE who you want to avoid intubation in. AM I saying you can give iNO non-invasively, absolutely. This is the nice thing about iNO is sometimes it will save you an intubation or at worst in can prevent the precipitous RV failure that will ensue after intubation.
-Maintain MAPS > 65
I know this is an obvious point, but it has to be stressed that even a minute of hypotension can throw a tenuous RV into the spiral of death mentioned. Sedatives will often result in rapid hemodynamic compromise if you are not careful.
Epinephrinebetween 0-50 nanos/kg/min or (0- 0.05mcg/kg/min) at lower doses epinephrine acts as an inotrope, and above that tends to act more as an alpha agonist. At low doses epi will likely not increase the pulmonary vascular resistance but at higher doses (> 50 nanos) it may.
Dobutamine2-5 mcg/kg/min can augment RV function without increasing the PVR seen with epi and levophed, however it can cause systemic hypotension from beta 2 agonism and often will be given with another agent.
Vasopressin can augment the mean arterial pressure, and likely has NO effects on the PVR.
My unevidenced based practice is to start Dobutamine and Vasopressin (2 mcg/kg/min and 0.04 U/min) to keep MAPS > 70 and follow serial bedside echos.
3. If someone with a PE is dyspneic should I intubate sooner rather than later, they are eventually going to tire out right?
The problem with intubation in a patient with a PE is positive pressure ventilation increases the afterload via PEEP to the right ventricle. This may tip the RV over into florid RV failure.
There are also the hemodynamic perturbations with giving a sedative during induction, which can cause hypotension, again resulting in rapid hemodynamic compromise.
Initial paralysis will prevent spontaneous ventilation and may make it difficult to match a patient's own intrinsic minute ventilation (young pt breathing RR 40, and large TV of 1L with MiV of 40), try setting the vent to get anything reasonable in these patients afterwards is not ideal. If you have to use something use a shorter acting agent like succinylcholine.
Nothing like someone telling you not to do something every sense in your body is telling you to do. However, if you are forced to intubate them, and you know they have a massive PE, consider thrombolysis up front and:
1. Start iNO, if this process isn't available where you work but iNO is available in house find a way to expedite the process in the ED now before you are really desperate. If you work in a hospital without iNO/CT surgery/IR consider establishing transfer to a facility with higher level of care. Worst thing you can do is admit a patient to an ICU where they won't be seen by an intensivist until the morning and there is minimal backup if the patient decompensates. Without a backup if the patient codes the game has been lost.
2. Have your vasopressors ready to go on a PUMP and push dose pressors in hand epi is the simplest in these situations. I use epinephrine in 10mcg aliquots as a push until I have a MAP > 65 if they drop during intubation. Then I place and titrate a drip as needed.
3. Sometimes flipping into A-fib will result in rapid hemodynamic deterioration and may need cardioversion as the loss of the atrial kick may have significant hemodynamic effects.
4. Call your CV surgeon and IR attending and get them on board early. "I have a young patient with massive PE who is crumping in the ED, is this patient a candidate for surgical thrombectomy and if they crash, would you consider them an ECMO candidate?"
Never be afraid to ask for help and if they are young and salvageable don’t accept NO for an answer.
Intubating the Patient with Hypotension
Before you intubate your next hypotensive patient, think twice and read below.
Positive pressure ventilation has multiple hemodynamic affects on your patient, mostly reduced venous return resulting in reduced preload, and increased right ventricular afterload. The combination of these two along with the systemic affects of your sedation for induction can result in rapid hemodynamic compromise in the already unstable patient.
Case:
58 y/o M with cough fevers and chills with body aches presents to the ED.
VS: 40.1, 135 (ST), sat 90% on NRB and he is breathing a real 30x’s/min, BP 85/55.
You determine the patient would benefit from endotracheal intubation, how do you proceed?
Step 1: Emergent or not?
The first question you always have to ask yourself is this going to be emergent, and do I have time. As ED doctors we are quick to jump to intubation when we know someone needs it, but the reality is most patients can be intubated urgently rather than emergently, while getting everything you need prior to induction. If they are agonal, severely hypoxic and cannot be BVM ventilated then godspeed.
But if you decide this is an urgent intubation, and have 5 minutes proceed
Step 2: What is my access?
The nurses should have 3 minutes to get you two working IV’s before you go to a humerus I/O. If you use the tibia be sure you use a pressure bag to augment the infusion rates, which usually are 65 ml/min vs. 165 ml/min with a pressure bag. In the Obese, sickle cell patient, or patient on hemodialysis this is the rapid IV of choice and results in fewer errors than placing a sterile semi-emergent CVC.
Why 3 minutes?
-Because while that is happening another nurse should be grabbing you two bags of crystalloid and a pressure bag ready to give to this patient.
-If you have a pharmD ask for a vasopressor drip on the pump ready to go, if they can make phenylephrine fastest or epinephrine take what you can get. Otherwise someone should be getting central pharmacy to make you drip, this is preferable to you making the drip yourself.
By now you should have two IV’s and one of the IV’s should be designated for induction medications. Have one bag of crystalloid running wide open on the IV that has been established as the line that will have the meds pushed through. This way we know if the IV is infiltrated (the bag isn’t running, or the skin around the IV has blown up) or if it just so happens that the BP cuff is on the same arm as the designated IV you realize before pushing the meds (cause’ its just embarrassing trying to figure out why your patient isn’t paralyzed).
Now this is where I don’t expect most ED doctors to follow, but I would recommend this. Place an arterial line. You can argue there have been no studies that show that A-lines save lives and that it is a waste of time and not an ED skill, and you may be right. What I will argue is that’s true of chest x-ray’s, MRI’s and most innovative technologies and it is all about what you do with the information that makes the difference.
The A-line gives you beat-to-beat information. There is no recycling of the blood pressure because the cuff couldn’t read and people start feeling for a pulse. CPR? Hit restart, that can’t be right! I know this has happened to all of us.
An US guided A-line doesn’t take much time to put in, once you are familiar with the technique. I believe it allows for a smoother more hemodynamically stable intubation. Are they hypertensive during laryngoscopy, (your unsecured aneurysms that have leaked but not ruptured!?) give him more propofol and take the blade out. Has my patient’s pressure just dropped? bolus him phenylephrine or epinephrine.
This also makes getting an ABG after intubation much easier than asking RT to do radial A-line sticks in hypotensive patients and prevents the dreaded; oh we couldn’t get an ABG so we didn’t do one.
Step 3: Induction Medications:
You can use whatever you want, just know they all cause hypotension. Ketamine seems to be en vogue, and is a good choice, but since we don’t have it in our omnicell in the ICU most of the ICU anesthesiologists here use an opiate like fentanyl first followed by a low dose of propofol; as in 10mg boluses up to 30mg until they are unresponsive to jaw thrust. I personally don’t think 20mg of etomidate is the best answer, but don’t have any science to back this up. Use whatever you like and markedly reduce the dose of the sedative.
Step 4: You were ready for hypotension
It was going to happen, but now atleast you are ready for it. First continue your fluid bolus, which should now be on a pressure bag if the MAP starts to get a little soft.
Then if it is apparent that there is a loss of vasomotor tone, you should replace the lost endogenous catecholamines with temporary vasopressors. I suggest blousing aliquots of phenylephrine 100 mcg Q 1 minute unless the MAP has precipitously dropped, then start with 300mcg. Once you have stabilized their MAP see if you have to keep pushing phenylephrine, if you do they need a drip, if you don’t congratulations you have successfully intubated a sick hypotensive patient without killing them.
If you are slick with the echo probe and see the LV or RV is down consider epinephrine 10mcg boluses instead and an epi infusion if needed.
Step 5: How do I sedate my hypotensive patient?
Let me start off by saying I think there is enough good evidence to recommend avoidance of benzodiazepines completely in most ICU patients not seizing. BZDs result in increased delirium, prolonged ventilator days, and worse patient outcomes compared with alternatives. This is never truer than in the elderly.
With that said the first thing to address is pain. It’s uncomfortable to sit in a firm bed without moving for hours, while having a toothbrush shoved in the back of your throat and the IV monitor beeping over and over again. If you treat pain first you will have a marked reduction in the requirement for “sedation/amnesia”. I like a dilaudid push of 1mg after hemodynamics have settled out followed by a drip 0.5-2mg/hr.
The sedation choice for me is between low dose propofol (10-30 mcg/kg/min) and dexmedetomidine. I prefer dex, 0.1-0.7mcg/kg/hr and it is going generic this year. If people give you a hard time about choosing this “expensive medication” show them the data on benzodiazepines and hospital LOS, and ventilator days. If you use ketamine, as I know ACMC has, you are ahead of the curve.
When giving these meds you don’t need to SNOW the patient, just make them calm enough that they can be awoken with loud verbal stimuli (we use the RAAS scale, target -1 to -2). Having them be comatose makes repeat exams with fluctuating mental status difficult to monitor.
This isn’t the sexy part of medicine but if you are in the business of saving lives and making your patients comfortable the nuances listed above is worth the extra effort.
The most important part of intubating the hypotensive patient is to be prepared for the rapid hemodynamic consequences that will follow. You shouldn’t sit after an intubation followed by PEA arrest wondering why that happened, it’s usually right in front of your face.
SIDE PEARL HYPOTENSION from obstructive shock:
If by chance you know the patient has a large pulmonary embolism as the cause of their distress you should be aware that intubation is likely to result in rapid hemodynamic deterioration. WHY? The RV is a low-pressure, high compliance chamber and rapid increases in afterload (PE) result in RV dilation. The RV dilation results in bowing of the interventricular septum to the left and causes reduced compliance of the LV, and the LV becomes more underfilled. Since the RV is perfused during diastole and systole, any reduction in MAP (caused by LV dysfunction) will cause a stiffening of the RV again impeding forward flow. The now more dilated RV causes tricuspid annulus dilation and significant tricuspid regurgitation and again impedes forward flow. Intubation will exacerbate the RV failure by decreasing MAP, and increasing RV afterload especially if they become hypoxemic or hypercarbic as both increase pulmonary vascular resistance.
Dave
Left Ventricular Assist Devices:
I'm on call in Cardiothoracic ICU, so if figured I would take a minute to see if I can drop some pearls regarding the management of left ventricular assist devices, since its fresh in my mind.
First what is a left ventricular assist device (LVAD from here on out):
Essentially an LVAD is a device that is used in patients with severe left ventricular dysfunction. If you have pre-operative biventricular dysfunction you are not a candidate for an LVAD, and instead may be a candidate for heart transplant (pending your age usually young like < 65 y/o, good renal and liver function). Because patients with NYHA class IV heart failure become significantly malnourished and develop end organ dysfunction a lot more patients are going to total artificial hearts (we use syncardia) as a bridge to transplant (BTT) and to keep the patients mobile with good end-organ perfusion until a suitable donor is found (which can take a significant amount of time.) These will become more popular over the next few years and are a whole different animal to manage.
There are multiple types of LVADs although most have gone to continuous flow centrifugal pumps, most frequently used is the HEARTMATE II, although some places have started using the Heartware. The older pulsatile pumps have fallen out of favor and were outperformed by the continuous flow pumps with a 58% survival at 2 years vs 24% in the continuous and pulsatile flows respectively.
Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med 2009;361:2241-2251
The LVAD is essentially connected to the left ventricular apex, and to the ascending aorta. See picture:
The patient then has a driveline that is connected to the rotor (located subdiaphragmatic), which exits the patient’s abdomen and connects to their battery pack.
Therefore since the LVAD is a continuous flow device, which unloads the left ventricle continuously, patients may or may not have a pulse.
The pulse is created by opening and closing of the aortic valve as it is directly related to their own intrinsic contractility. If you place an A-line you may see it be mostly flat with a MAP, hopefully, > 65. If a patient starts to regain cardiac function (myocarditis patients) then it is possible to have a strong pulse even with an LVAD. It is important to know that the aortic valve may not open in some patients, and that the patient’s hemodynamics don’t depend on it opening!
OK now that some of the basics are out of the way lets give some of the meat, what are the numbers on the device?
-This is how fast the rotor is moving usually somewhere between 8600-10,000 rpms. This is not picked arbitrarily. The RPMSs essentially is a major determinant of your cardiac output. SO some might say why not just go up higher on the RPMs if the patient is hypotensive? The answer is because the VAD is essentially a vacuum and if the cavity of the LV is too empty it may pull on the free wall or septum of the LV. These are called "suction events" which can precipitate dysrhythmias (have you ever put a guide wire in too deep and irritated the RV with frequent PVCs, try pulling on it with a vacuum).
The normal geometry of the LV should have the inflow cannula (going to rotor) facing the mitral valve without rightward or leftward shift of the septum or free wall.
If the patient becomes hypovolemic the LVAD may start precipitating suction events, because the RPMs are set too high for the relative amount of volume and pull on the septum. The VAD accommodates for these events by temporarily going down on the RPM's to try and reset itself.
PEARL: if the RPM's are changing on its own their it is likely a SUCTION EVENT, think hypovolemia or dysrhythmia.
RECAP: A ramp study (a study where someone “ramps up the RPMs” under echocardiography is required to change the RPMs because the geometry of the LV must be watched real time and therefore the RPMs should rarely be changed in the emergency department without an expereicned VAD provider doing so under echo guiadance.
This is essentially how much power is required for the device to continue running at the set RPM's. There is no one number as it varies between patients and trending this number is usually the most helpful, the patients generally know where they have been running.
Why is the power important? The power and the RPMs are the only numbers on the VAD devices that are NOT GUESSTIMATES. All other numbers are derived from these two values.
If the power is increased it is because more work is required to continue turning the rotor at a fixed rate.
What could possibly cause the rotor to require more power to maintain the same set RPMs? Well the VAD is a synthetic device that is prone to clotting (about 1% incidence). If the INR is low, and you don't hear that nice hum of the VAD on auscultation, and instead hear a trapped weasel (I swear this is the closest thing I can imagine this as) maybe its a clot on the rotor. The machine is still trying to turn at constant RPMs but is pushing against a clot so more power is required.
Other causes of increased power are an increase in speed (RPMs) increase in volume status or an increased afterload.
What if the power is low, well you can imagine this means that the rotor is seeing less volume, this could be caused by hypovolemia or a CLOT either pre or post- cannula. A clot in the rotor will cause an increase in power, where as an LV thrombus or a thrombus on the outflow cannula will cause a drop in power.
The flow is a guesstimate of CO. Let me repeat that the FLOW is a guesstimate of the cardiac output. The flow depends upon volume status, LV contractility, the speed, RV function and afterload.
The heartmate II will alarm at low flow states < 2.5L/min and will show --- and flows that are above physiologic limits for a set RPMs just present as +++ on the LVAD.
Why is this important, well if there is a clot on the rotor, the machine has increased power, the same RPMs and the CALCULATED flow will be high even though the real flow will be far less. The machine knows this and gives you a clue to this by presenting +++ as a flow estimate since it is outside the physiologic range.
As mentioned before this is a flow estimate and is not analgous to cardiac output.
Now things get really hairy. The flow is a calculated flow based on power and RPMs. And the PI is calculated from flow (max flow- min flow/avg flow over 15 seconds). So its calculated from a calculated number!
What it’s supposed to represent is the intrinsic contractilty of the LV. As the LV increases its contractility the flow will theoretically increase as more blood goes through the LVAD.
Joe Hsu my mentor puts it this way:
As the LV contracts, the flow through the pump increases due to an increased pressure at the pump inlet approximating the pressure at the outlet cannula (aortic pressure). During cardiac diastole, this inlet pressure drops, while the outlet pressure remains high (increased pressure difference) and, consequently, flow decreases. Therefore, pulse index is directly proportional to amount of LV contractility (increased due to preload, inotropic support, and myocardial recovery) and inversely proportional to the assistance provided by the pump.
So what you need to take from this is the PI estimates the amount of LV function, and as the patient becomes hypovolemic often times the PI will drop with their MAPs.
1. Acute Anemia/Bleeding:
You have all seen this and is the most common reason patients with LVADs present to the ED, especially with GI bleeding. The question always comes up can you reverse the INR, and the answer is of course yes. If the patient has a significant bleed you should consider reversing it. They can bridge to heparin or integrilin in the ICU if need be when the patient is more stable. We do not start heparin for 5 days in fresh post-ops and a lot of times mid-ICU course they go unanticoagulated for days, and people don't clot off.
Hemolysis is another cause, which can cause significant anemia especially with a pump thrombus. LDH, haptoglobin, bilirubin as well as cell-free plasma hemoglobin can aid if you are very suspicious.
Can I give too much blood too quickly if they are end stage HF? Yes and NO the LV, sucks but that’s why they got the LVAD and as long as the RV is working please give the blood rapidly. If you notice RV failure (significant JVD, hepatomegaly, lower ext edema, assuming you don’t have a CVC for a CVP, which the CVP is not completely dead in this circumstance) then I would urge caution. Which brings us to
2. RV dysfunction:
This is a complication in about 20% of post-op patients and sometimes they have to crash onto an RVAD. This is badness. If the patient is not hypovolemic, and they are hypotensive and have signs of RV dysfunction you need a stat echo or do a bedside. Get an EKG are they ischemic, are they sub therapeutic in INR, did they throw a PE, is the LV so big its causing the septum to bow into the RV? do your best to figure out why is the RV failing.
Remember these were sick hearts to begin with, the LV gets fixed with an LVAD and then the RV sees all this additional flow it wasn't seeing before, and now a sluggish but getting by RV can become sick. If you have RV dysfunction you have got problems, and need a surgeons help quick. Thankfully this won't be common as most of these occur quickly after surgery.
How can you manage RV dysfunction, well a lot of times milrinone will aid in reducing pulmonary vascular resistance (PVR), and increases RV contractility. If you need to intubate do so cautiously as the PEEP from mechanical ventilation will worsen RV dysfunction and you should minimize hypoxia and hypercapnia as these two entities will worsen PVR.
If you suspect RV dysfunction get a VAD specialist in the ED immediately.
3. Infections:
These can be ugly, depending on where they are. These patients get blood cultures if they are febrile because they have a device, and will need long-term abx if infected. Replacing an LVAD is a morbid procedure and not one people are likely to do if they can avoid it.
Be a good doc and examine the abdomen and the site where the driveline comes out since it can be your source if its related to the LVAD (not a viral syndrome). These should get a CT scan to evaluate for an abscess if you don't find another otherwise obvious source (skin/ua/chest), and plain CT C/A/P usually will suffice. We usually start BROAD spectrum abx vanco and zosyn, and because of the device if the patient is in septic shock consider up front adding anti-fungal coverage with an echinocandin (micafungin, caspofungin or anadilafungin).
4. Tachydysrrthmias:
Ventricular arrhythmias
Why did they get the LVAD in the first place, ischemic cardiomyopathy is more likely to have irritable myocardium, but NICM is certainly entitled. These don't go away because they have an LVAD, and VTACH or VFIB can precipitate suction events as the RV may not be able to coordinate an adequate contraction which reduces LV preload. These dysrhythmias can be managed with cardioversion, which is not problematic, but can cause myocardial stunning afterwards. If they are stable VTACH consider amiodarone/procainimide or lidocaine and most of the patients have their own ICD's from their prior CM so make them comfortable if possible. If one of the first two doesn't work we usually add lidocaine as a bolus.
AFIB with RVR
Afib will also be problematic reducing RV function and therefore LV preload most surgeons here opt for rhythm control with amiodarone bolus and drip since they are anti-coagulated already with INRs 2-2.5.
5.Cardiac Arrest
Can I do chest compressions? Sure you can, but remember the LVAD is taking care of perfusion to the body so solving why its not doing that should be a priority. PE, hemorrhagic shock, RV failure, tamponade, hypovolemia etc…
The risks of doing chest compressions are dislodging the inflow and outflow cannula which if that occurs will likely result in massive exsanguination. So if you have to do it, you have to do it but take a second and try and figure out why the patient has coded. Otherwise continue with ACLS as per usual.
6.Aortic Insufficiency:
This adversely affects the pumps function by causing rapid LV filling and high pump flow as the outflow cannula is valveless and merely follows the path of least resistance (low pressure LV vs. higher pressure systemic vasculature).
Patients can present with left heart failure, pulmonary edema and hypoxemia. Treatment for mild AI is usually afterload reducing agents and diuretics, but for mod-severe AI may require a new valve or over-sewing completely of the original aortic valve in an effort to reduce the regurgitant jet.
BELOW is a TABLE of common complications and treatment options, its good reference in-case you need to look it up on a shift its courtesy of Joe Hsu, Critical Care at Stanford.
OK that’s a lot of information but it will get you started. Please e-mail me with questions and I’ll post-em on the site. If you have had a particularly challenging LVAD case let me know and if I don’t know the answer I have the mentors who will.
Talk soon!
-Dave
Table 1: Diagnosis and Management of Adverse Events and Complications
Complication
Clinical features
LVAD Parameters
Diagnosis
Management strategies
Diagnostic Studies
CT scan findings (7)
Inflow Cannula Complications
Kinking of inflow cannula
é Cardiac pulse pressure, Hypotension
ê Flow, power,
Variable flow
Coagulation parameters (INR 1.5-2.5), CT scan
--Kinking of inflow cannula
--Cannula malposition (Figure 6)
--Surgical consultation
--Anticoagulation
--Maintain adequate volume status
Thrombus in cannula
é Cardiac pulse pressure
Acute anemia (due to hemolysis), Hypotension
ê Flow, power
Evaluate for hemolysis: é cell-free plasma Hgb, indirect bilirubin, LDH; ê Haptoglobin
CT scan
--Low attenuation lesion in inflow/outflow cannula
--Surgical consultation
--Anticoagulation
Outflow Cannula Complications
Tearing of aortic anastomosis
Hypotension, Hemorrhage
No specific change
Serial Hgb, TEE, CT scan
--Extravasation of contrast material at anastomosis
-- Emergent surgical consultation
--Can occur over time
Kinking of outflow
Cannula
é Cardiac pulse pressure, Hypotension
ê Flow, power
Variable flow (positional)
Coagulation parameters (INR 1.5-2.5), CT scan
--Kinking of outflow cannula
--Disruption of cannula patency
--Surgical consultation
--Anticoagulation
Hemodynamic Complications
Arrhythmia
± Hemodynamic instability, Symptoms of ê perfusion
ê Flow, power
ECG, Electrolyte panel, TTE/TEE (to assess LV geometry, fluid status and cannula position)
None
--Control arrhythmia, defibrillation
--Evaluate for suction events-VT
--Watch for RVF
--External chest compression-onlyif in extremis
Right
Ventricular Failure
Hypotension, é CVP, PVR
ê Flow, power
Suction events
TTE, TEE, CT scan
CVC ± PAC
--Intraventricular septum bowed leftward,
--RV dilated,
--Dilation of IVC
--RV contractility: inotropes (Milrinone)
--Decrease PVR: avoid hypercapnia, hypoxemia, pulmonary vasodilators (iNO)
--Avoid overfilling
--Control arrhythmias
Pericardial tamponade
é CVP
Hypotension,
Preload dependent
ê Flow, power
Suction events
TTE, TEE (pericardial effusion may not be visualized on TTE), CT scan
--Dilation of IVC,
--Compression of right ventricle or atrium, flattening of heart border
--Pericardial effusion
--Pericardiocentesis
Aortic valve insufficiency
Decompensated heart failure, êSystemic perfusion, Cardiogenic shock
é High flow
TTE ramp study to evaluate speed, ECG-gated CT scan
--Presence of valvular thickening,
--Aortic valve visualized on ECG-gated CT scan
--May develop over time
--Consult cardiology and cardiac surgery
--Diuretics, afterload reduction
-- AI may improve with decreased pump speed
Coagulation-related complications
Thrombus on Rotor
Acute anemia (due to hemolysis)
é Cardiac pulse pressure
“+++” Flow,
éPower (>10-12 W)—hrs to days
Evaluate for hemolysis: é cell-free plasma Hgb, indirect bilirubin, LDH; ê Haptoglobin
CT scan
--Low attenuation lesion near inflow
--Surgical consultation
--Anticoagulation
Hemorrhage
Primarily GI also: Epistaxis, Hematuria, Mediastinal, Thoracic
ICH
ê Flow, power
Suction events
TTE, TEE, EGD, serial CBC, coagulation parameters, CT scan
Evaluate for acquired vWD: vWF antigen, vWF activity, factor VIII activity
Evaluate for hemolysis: é cell-free plasma Hgb, indirect bilirubin, LDH; ê Haptoglobin
--Evidence of bleed (e.g., ICH on CT head)
--PRBC and pro-coagulant factors as indicated
--Avoid excessive transfusions in:
-Bridge to transplant
-History of RVF
--?vWF replacement
Infectious Complications
LVAD-specific (41)
LVAD-related (41)
Fever, Chills, Hypotension 2/2 sepsis,
Sequelae of embolic events
Variable effect on LVAD
CBC with differential, lactate
Exit site Wound Cx (+ Fungal Cx): if risk factors
TEE, if TTE negative
Blood Cx, if + CVC obtain “Time to positivity”Cx
Imaging: Ultrasound, CT (c/a/p)
--Gas or fluid collection around pump components, percutaneous lead
--Figure 4, pocket infection
--Figure 5, percutaneous lead infection
--Broad spectrum antimicrobials for nosocomial pathogens
± Fungal coverage based on risk factors
--EGDT
--Surgical consultation for incision and drainage, debridement, device exchange
Abbreviations: CVC: Central venous catheter, CVP: Central venous pressure, Cx: Culture, EGDT: Early goal directed therapy, GI: Gastrointestinal, Hgb: Hemoglobin, ICH: Intracranial hemorrhage, LDH: Lactate dehydrogenase, PAC: Pulmonary artery catheter, PVR: Pulmonary vascular resistance, RV: Right ventricle, RVF: Right ventricular failure, TEE: Transesophageal echocardiogram, TTE: Transthoracic echocardiogram, vWD: von Willebrand disease vWF: von Willebrand factor, W: Watts
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