Grand Rounds Recap: Critical Care Symposium - 2/4/15

Pressor Primer with Dr. Hebbeler-Clark

 Norepinehprine. By Edgar181 at en.wikipedia [Public domain], from Wikimedia Commons

Norepinehprine. By Edgar181 at en.wikipedia [Public domain], from Wikimedia Commons

  • Norepinephrine seems to be on top in terms of vasopressor of choice currently (consider it your "easy button")
  • Per Surviving Sepsis Guidelines, Norepi has level 1B evidence as a first line pressor, while Epi is your second line with level 2B evidence and Vasopressin is currently ungraded in terms of evidence level
  • There have been 4 RCT's confirming that Norepi has no mortality difference from Epi and given it's safer side effect profile, use it regularly
  • Vasopressin should never be utilized alone but may augment other pressors' effects
    • The VASST trial subanalysis demonstrated that vasopressin added to lower doses of norepi may improve mortality in septic shock
  • Dopamine is a pressor of the past and should only be used in those with low risk of tachydysrhythmia (such as bradycardic patients)
    • A meta-analysis has shown that there were no differences in renal outcomes with Dopamine versus placebo
  • Phenylephrine (as a drip) is not currently recommended for septic shock
  • Keep in mind that Epi is associated with an increase in lactate production and thus may cloud your ability to follow this as an end point in resuscitation
  • Alpha-adrenergic effects lead to increased systemic vascular resistance (SVR) and is the primary action of phenylephrine
  • Beta-adrenergic effects lead to ionotropy and chronotropy which is the primary activity of dobutamine (which can then lead to a compensatory vasodilation and lead to a decrease in BP)
    • Norepinephrine is more weighted toward alpha effects, but still has beta activity

Fluid Resuscitation in Sepsis with Dr. Srivastava

1. Which fluids should you use?

NS is harmful due to high chloride load. This can lead to vasoconstriction and diminished perfusion of the kidneys.

  • Use more balanced fluids (LR or normosol)
  • No role for albumin in fluid resuscitation

When to give NS: patients with hypovolemic hyponatremia, TBI or DKA

When to give LR: all other cases

  • It is ok to give LR to patients with hyperkalemia as the K concentration is minimal

2. How much and how fast should I give the fluids?

  • In the acute period, do not be afraid to give fluid (though no reason to be slamming a patient with 15 L in 2 hours)
  • During their hospitalization, patients with negative/even fluid balance have improved mortality

3. When should you add pressors?

  • The truth is, no one knows. It seems reasonable to try a quick 20 ml/kg bolus x2 and then add a pressor if the pt is still hypotensive

4. How do we monitor our patient's fluid status?

  • 50% of all hypotensive patients in the ED are volume responsive
  • PA catheters are a thing of the past and are not accurate as readings are affected by all mechanical abnormalities of the heart
  • Pulse pressure variation in mechanically ventilated patients can predict volume responsiveness however end expiratory occlusion pressure is better
    • Do a 15 second expiratory hold at the end of expiration. This is equivalent to giving a 500 ml bolus. If there is pulse pressure variation > 5%, the pt is fluid responsive
  • IVC diameter is not very accurate as it is affected by multiple comorbidities (COPD, PE, tamponade, R heart disease)
  • NICOM has not been proven to be accurate
  • Perform a limited bedside echo to assess global heart function and chamber size. Also take a look at lung parenchyma for presence of pulmonary edema
  • Follow lactate clearance to evaluate effectiveness of resuscitation

Acid Base Workshop

Be systematic and follow these 5 key steps when evaluating an Acid-Base problem:

  • Step 1: Identify if the patient is acidemic, alkalemic, or neural pH
  • Step 2: Assess the pCO2, if it's high there is a respiratory acidosis, if it's low there is a respiratory alkalosis
  • Step 3: Assess the HCO3, if it is high then there is a metabolic alkalosis, if it is low there is a metabolic acidosis
  • Step 4: Check for an anion gap (Na - Cl - HCO3) and correct for hypoalbuminemia (+2 to the anion gap for every 1 gm drop in albumin)
  • Step 5: Take the anion gap subtract 12 and add the HCO3, if it is greater than 30 you've got an additional metabolic alkalosis, if it is less than 22 you've got a nongap metabolic acidosis

Oral Boards with Dr. Knight

Be systematic in your physical exam. It is best to take a minute to go through the entire exam and note abnormalities that need to be addressed. If you address each abnormality as it is found, you will miss an important exam findings.

  • In trauma patients, follow ATLS protocol. Start with ABCs and address abnormalities that are life threatening. Then do an entire secondary survey
  • If there is an orthopedic deformity, you will need to reduce it
  • Always give tetanus and antibiotics if there is an open wound
  • When performing a procedure, you will get points if you use appropriate procedural anesthesia and pain control

Oral Boards with Dr. McDonough

SIRS + Elderly + ?Belly Pain = CT Abdomen/Pelvis

  • These do not always have to be contrasted studies as you are often looking for fairly obvious defects (i.e. pneumoperitoneum or pneumotosis)

Do not be fooled by either a dirty UA or sterile pyuria in sick septic patients and call it a UTI, if a UTI is causing severe sepsis/septic shock, it should be quite evident on UA

  • Sepsis needs a source and especially when dealing with the belly, recognize that it can significantly change the disposition
  • On the oral boards, be sure to collect collateral information if it is available (i.e. family or EMS report)
  • Follow Surviving Sepsis guidelines for septic patients on the Oral Boards: IVF, antibiotics/source control, and pressors with MAP goal >65

Pediatric Critical Care with Dr. Poynter

Sick kids can certainly make us all fairly anxious to care for, but critical care principles general hold true throughout age groups

Kids airways (especially in <2 yo) are different, they've got larger tongues, smaller oropharynx, shorter airway, larger epiglottis and often one of the most narrow areas is the subglottic region

  • Calculate your tube size with ETT = (Age/4) +4
  • Cuffed tubes are safe for kids but you can consider downsizing by a 1/2 size if using regular tubes (though unnecessary if you have a microcuff)
  • Depth measurement in intubation can be easily calculated with 3 x tube size
  • When in doubt about a blade to use in a small child a Miller 2 can be your friend
  • Doing the same thing over and over again unsuccessful in a pediatric airway is bound to go badly, while you're bagging between attempts consider how you will approach it differently on your subsequent attempts
  • Shoulder rolls are necessary the younger the child to align the axis to successfully visualize the airway

When considering RSI meds in kids, be sure to pre-medicate with atropine in kids under 1yo given their strong vagal response to the intubation attempts

  • Induction doses of ketamine for kids is often a bit higher than in adults (2mg/kg)
  • When in doubt about IV access, go to IO quickly

As long as you continue to follow the child's exam, kids usually handle fluid resuscitation fairly well (start with 20cc/kg bolus and reassess and PRN repeat)

End points of resuscitations are similar to adults with SVO2 > 70 and signs of end-organ perfusion

Kids in shock often preserve their BP longer than adults as they have robust responses in SVR changes leading to the traditional "cold shock" kid (cool, pale skin), kids cannot double their heart rate to compensate for decreased CO

Estimate blood volume in kids as 80cc/kg (meaning a newborn has a blood volume of ~1 cup!)

Children do not handle hypoglycemia or hypocalcemia particularly well (and are more apt for both as they have less stores and cannot mobilize them as well as adults)

TBI treatment in kids includes hyperventilation, use of lidocaine for RSI induction (to blunt increase in ICP), C-spine precautions, and hypertonic saline at 8cc/kg


Cardiogenic Shock with Dr. Friedrich

1. Definition (you need both)

  • Hemodynamics
    • Hypotension with SBP 80-90 or pressor requirement
    • Low CI < 1.8
    • LVEDP > 18 or RVEDP > 10-15
  • Evidence of end organ hypoperfusion

2. Classification

  • Preshock: patient is at significant risk of developing cardiogenic shock 
  • Mild: responsive to low dose inotropes
  • Profound: responsive to high dose inotropes or IABP
  • Severe: not responsive to inotropes or IABP
  • Majority of cardiogenic shock is due to acute MI
    • Seen in 5-10% of STEMI and 2-3% of NSTEMI

3. Pathophysiology: myocardial dysfunction due to decreased coronary perfusion pressure, myocardial ischemia and SIRS response

  • Inflammatory markers that circulate in shock lead to increased SVR and myocardial dysfunction
  • Echo findings: large ventricles with poor contractility
    • Get an echo early in your hypotensive patient to evaluate cardiac function
  • Differential diagnosis: MI, CHF, myocarditis, Takotsubo, peripartum cardiomyopathy, tamponade, PE

4. Management

  • Do not give too much volume. It is not necessary to push CVP > 15. The dysfunctional RV cannot handle too much volume
  • Inotropes work by increasing intracellular Ca by increasing cAMP
    • All of them have equal efficacy
  • Keep in mind that all inotropes and pressors lead to increased myocardiac O2 consumption and are arhythmogenic, so use the lowest effective dose

5. Percutaneous Ventricular Assist Devices

  • Rationale for their use is that stunned myocardium takes multiple days to recover
  • IABP have not been shown to improve outcomes
  • Consider IABP use when: 
    • Support for high risk PCI
    • Acute CHF
    • EP procedures
    • Temporary R heart support (PE)
  • Other devices available: Impella, TandemHeart
    • Have not been shown to improve outcomes
  • ECMO: there are no RCTs but cohort studies suggest improvement in survival
  • Over the past decade we have seen an increased number of devices used for cardiogenic shock support and a decrease in mortality, however we have also had better medical management and emphasis on early revascularization