Critical Care
=============

þ Best pressor in shock:
 - Norepi, then epi, then dopamine 
 - Norepi had higher mortality and had to be stopped due to arrhythmias
   [De Backer, D., P. Biston, et al. (2010). "Comparison of dopamine and 
   norepinephrine in the treatment of shock." N Engl J Med 362(9): 779- 789. 
   BACKGROUND: Both dopamine and norepinephrine are recommended as first- line 
   vasopressor agents in the treatment of shock. There is a continuing 
   controversy about whether one agent is superior to the other. METHODS: In 
   this multicenter, randomized trial, we assigned patients with shock to 
   receive either dopamine or norepinephrine as first-line vasopressor therapy 
   to restore and maintain blood pressure. When blood pressure could not be 
   maintained with a dose of 20 microg per kilogram of body weight per minute 
   for dopamine or a dose of 0.19 microg per kilogram per minute for 
   norepinephrine, open-label norepinephrine, epinephrine, or vasopressin could 
   be added. The primary outcome was the rate of death at 28 days after 
   randomization; secondary end points included the number of days without need 
   for organ support and the occurrence of adverse events. RESULTS: The trial 
   included 1679 patients, of whom 858 were assigned to dopamine and 821 to 
   norepinephrine. The baseline characteristics of the groups were similar. 
   There was no significant between-group difference in the rate of death at 28 
   days (52.5% in the dopamine group and 48.5% in the norepinephrine group; odds 
   ratio with dopamine, 1.17; 95% confidence interval, 0.97 to 1.42; P=0.10). 
   However, there were more arrhythmic events among the patients treated with 
   dopamine than among those treated with norepinephrine (207 events [24.1%] vs. 
   102 events [12.4%], P<0.001). A subgroup analysis showed that dopamine, as 
   compared with norepinephrine, was associated with an increased rate of death 
   at 28 days among the 280 patients with cardiogenic shock but not among the 
   1044 patients with septic shock or the 263 with hypovolemic shock (P=0.03 for 
   cardiogenic shock, P=0.19 for septic shock, and P=0.84 for hypovolemic shock, 
   in Kaplan-Meier analyses). CONCLUSIONS: Although there was no significant 
   difference in the rate of death between patients with shock who were treated 
   with dopamine as the first-line vasopressor agent and those who were treated 
   with norepinephrine, the use of dopamine was associated with a greater number 
   of adverse events. (ClinicalTrials.gov number, NCT00314704.)]

Amal Mattu, MD
The Crashing Patient
(ACEP 2009)

Amal Mattu's Universal Algorithm (after the ABCs): AABBCCDDEE

A - Aortic Disasters (AAA rupture, dissection > tamponade): check U/S

A - Acidosis: if paralyze and intubate, must overventilate like 
patient's Kussmal respirations; consider Bicarb if paralyzing and 
intubating; can't hyperventilate if in cardiac arrest or 
hypovolemic (e.g., trauma): bag once every five seconds (12/min) 
as hyperventilation causes cerebral vasoconstriction and worse 
outcomes, and intubation or bagging drops BP significantly. 

B - Baggging: see above

B - Baby: ruptured ectopic blood in pelvis causes reflex 
paradoxical bradycardia (also seen with other bleeding): 
Amiodarone is class D for pregnant patients (very bad); 
cardioversion: safe at all stages of pregnancy (remove any fetal 
monitors). If do CPR on pregant patient, move in L lateral 
position and do compressions 2 interspaces higher; ECC only 80% 
effective when tilted; best is do CPR supine and have a second 
person manually deflect uterus to L. Perimortem C-section: do 4 
minutes of CPR/ACLS then extricate baby (best chance for mom, 
too); even if no signs of fetal life and uterus at umbilicus or 
higher, do c-section anyway. 

Compressions: 100/min, 30:2 ratio (maybe 60:2, or ignore airway for first few 
minutes): "push hard, push fast, don't stop"

Cooling

Decline: Trendelenburg position doesn't work.

Defib: if using standard gel pads, may start hands-on defibrillation

E: pericardial Effusion, pulmonary Embolism: bedside Echo: ? 
effusion, ? massive RV May have cardiomegaly on CXR, breathing 
fast, tachycardic, normal pulse ox. If tachycardia + low voltage 
> effusion.

If intubate impending tamponade, will drop pressure.

If give fluid bolus and BP goes down, suspect PE: fluid goes into RV and presses 
on LV. Start pressors early. If intubate, BP improves as get fluid out of 
R ventricle.

New T inversions in V1-3 and inferior: 90% specific for PE

F: forget about drugs like antiarrhythmics, vasopressors don't work. 

Dr. Mattu's Handout:

Aortic Disasters
• Consider TAD and AAA in crashing/arresting patients, regardless of presence or
absence of prior “typical” symptoms…prompt diagnosis can save lives!
• Meron G, et al. (Resuscitation, 2004)
o Evaluated patients from a cardiac arrest registry (Austria) that died of either
TAD or AAA
o Atypical presentations were common
?? Patients with AAA: abdominal pain and/or flank pain in only 52% and
32%
?? Patients with TAD: chest pain in only 48%
o 70% had PEA as the initial cardiac rhythm (most common presenting rhythm)
o Early routine ECHO/ultrasound in all crashing/arresting patients!
?? TAD ?? look for pericardial effusion
?? AAA ?? look for large aorta (> 3 cm diameter)
• Tsai TT, et al. (Am J Cardiol, 2005
o Hypotension was noted in 29% of TAD patients
Acidosis
• Primary metabolic acidosis is associated with compensatory respiratory alkalosis ??
tachypnea, hyperventilation, Kussmaul’s breathing
o Concurrent primary respiratory alkalosis (e.g. sepsis, salicylate toxicity) will
produce even more profound tachypnea
• Beware paralysis and intubation! But if you must, then remember to set respiratory
rate high!
o “Normal RR” (e.g. 12-16) will cause precipitous fall in systemic pH ?? arrest
o If the patient is hypovolemic and you can’t hyperventilate (see below),
consider giving IV sodium bicarbonate before intubation
Bagging/Breathing
• Pitts S, et al. (Lancet, 2004); and Aufderheide TP, et al. (Circulation, 2004)
o Professional rescuers (both pre-hospital and in-hospital) often excessively
ventilate patients during CPR
o Resuscitation guidelines recommend a delivery of only 12 breaths per minute
during CPR…in other words, one breath every 5 seconds
o The elevated intrathoracic pressure from hyperventilation produces
decreases in preload, cardiac output, coronary perfusion, and cerebral
blood flow
o Animal studies confirm that hyperventilation produces decreased coronary
perfusion and decreased survival rates
o New AHA (2005) guidelines also deemphasize importance of bagging/rescue
breathing
?? Often is too fast, compromises circulation and limits chest
compressions
Amal Mattu, MD
The Crashing Patient
3
Baby?
• Consider ruptured ectopic in the crashing/arresting female patient
o Paradoxical relative bradycardia ?? common source of confusion in diagnosis
o Early routine FAST in crashing/arresting patients!
• Dysrhythmias
o Avoid amiodarone in pregnancy
?? Is the only class D antidysrhythmic
?? Risk of fetal hypothyroidism, IUGR, fetal bradycardia, prematurity
?? Only recommended if other drugs fail
?? For ventricular dysrhythmias, use procainamide or lidocaine first
o Cardioversion/defibrillation is considered safe
?? Fetus has high fibrillation threshold
?? Amount of current reaching uterus is small
?? Be certain to remove fetal and uterine monitors before shocks!
o Temporary or permanent pacing and AICDs are considered safe as well
• Positioning during resuscitation
o Current International 2005 Guidelines recommend…
?? Compressions higher on sternum to adjust for diaphragm and
abdominal contents
?? Resuscitation in gravid in partial left lateral tilt position to improve
venous return and improve cardiac output (up to 30%)
?? Kiss G, et al. Resuscitation 2004
• In left lateral tilt position, only 80% of the external
compression forces of CPR are transmitted
• Best compromise for CPR and optimal venous return is in
supine position with manual displacement of the uterus to
the left
• i.e. 3-person CPR is optimal
• Perimortem C-section
o Even if the fetus is not viable emergency C-section is required in order to
improve venous return and consequently the cardiac output during CPR
o Following delivery of fetus cardiac output in mother can increase up to 80%
o Even if EGA 20-23 weeks!
o Maternal brain damage is likely after 4 min of cardiac arrest, irreversible after
6 min ?? perimortem C-section should be considered at the fourth minute
of cardiac arrest!
Compressions
• Background: AHA guidelines recommend chest compression rate of 100/min in
adults
• Valenzuela TD, et al. (Circulation, 2005)
o Reviewed 61 out-of-hospital cardiac arrests
?? Chest compressions were performed during only 43% of the total
time the patients were pulseless!
Amal Mattu, MD
The Crashing Patient
4
• Interruptions were caused by excessive bagging, pulse checks,
drug administrations, intubation attempts
• Abella BS, et al. (Circulation, 2005)
o Evaluated compression rates in 97 cardiac arrests
?? Rate was < 80 in 37%, < 70 in 22%
?? Higher compression rates are significantly correlated with initial
return of spontaneous circulation (ROSC)
?? Compression rate does make a difference (and it’s cheap!)
• Hostler D, et al. (Resuscitation, 2005)
o Using the currently recommended compression:ventilation (C:V) ratio of
15:2, there were only 60 compressions per minute and 26 seconds of “handsoff”
time per minute (patient not getting compressions)
o Best results with 30:2 or greater compression:ventilation ratios (in terms of
approaching the recommended 100/min rate
o New recommendation for 1- or 2-person CPR for adults is 30:2
compression:ventilation ratio
• New AHA motto: “Push hard, push fast!”
o Emphasis on optimizing basic techniques:
?? Proper compression rate (100/min)
?? Minimize interruptions: it is recommended that compressions never
be interrupted by more than 15 seconds at a time when doing
pulse/rhythm checks…unless, of course, a pulse has returned.
Interruptions of compressions should also be minimized or avoided for
airway measures, drug administrations, defibrillations, etc.
?? Avoid hyperventilation (bag rate 12/min)
?? Rapid single defibrillation (see below)
• Cardiocerebral resuscitation: the future is CCR rather than CPR!
o Kellum MJ, et al. (Ann Emerg Med, 2008) and Ewy G. (Resuscitation, 2003;
and J Am Coll Cardiol, 2009)
?? Significant de-emphasis on early ventilations in “typical” cardiac
arrest (doesn’t apply to pulmonary arrest, e.g. drowning, opiate OD,
crashing asthma/COPD, pediatric arrests, etc.)
?? Passive oxygenation, good compressions, early defibrillation when
needed and early EPI
?? No positive pressure ventilation/intubation for the first 8-12 minutes!
?? Increased survival and neurological outcome!
Cooling
• International Liaison Committee on Resuscitation (ILCOR) recommendations:
o Unconscious adults with spontaneous out-of-hospital cardiac arrest and
an initial rhythm of ventricular fibrillation should be cooled to 32-34 C
(~90-93 F) for 12-24 hours
o Based on two studies (Austrian study, 275 patients; Australian study, 77
patients)
Amal Mattu, MD
The Crashing Patient
5
o Cooling may also be beneficial for other rhythms or for in-hospital cardiac
arrest
• Methods of cooling
o Cooling blankets
o Ice packs to groin, neck, and axillae
o Wet towels and fanning
o Cooling “helmet”
o Cool IVF to 4 C
o Internal methods generally considered too invasive for routine use
• Prevent shivering with paralytics and sedatives
o Warnings
?? Increased incidence of dysrhythmias, infection, coagulopathy if < 32 C
?? Uncertain in pediatrics
?? Not intended for cardiogenic shock, pregnancy
“Decline position” (TrenDelenburg)
• Johnson S, et al. (Can J Emerg Med, 2004)
o Maneuver fails to increase BP and/or cardiac output in most patients, does not
improve tissue oxygenation, results in displacement of only 1.8% of total
blood volume, and actually decreases cardiac output in the hypotensive
patients
o Produces right ventricular stress and deterioration of pulmonary function
o Also of limited benefit in placing central venous catheters (subclavian,
internal jugular)
Defibrillation
• Monophasic vs. biphasic defibrillators?? ?? “…no specific waveform (either
monophasic or biphasic) is consistently associated with a greater incidence of
ROSC or survival to hospital discharge rates after cardiac arrest than any other
specific waveform. Research indicates, however, that when doses equivalent to or
lower than monophasic doses are used, biphasic waveform shocks are safe and
effective for termination of VF.” (Circulation, 2005;112(24):page IV-37)
• If unknown down-time or collapse > 4-5 minutes ago in VF arrest, new
recommendation ?? 2 minutes of chest compressions before first shock
• Repeated sequence of initial shocks and escalating dosages of current no longer
recommended
o Modern biphasic defibrillators reportedly have a 90% first-shock efficacy at
terminating (at least temporarily) VF
o Even with monophasic defibrillators, if the first shock is ineffective, it is
unlikely that the subsequent 2 shocks will be effective
o Data does not support the efficacy of escalating dosages of current for either
monophasic or biphasic defibrillators, therefore…
o Therefore, the current recommendation is that only a single shock be given
for VF at a time. Biphasic defibrillators should be set at 120 J – 200 J;
Amal Mattu, MD
The Crashing Patient
6
monophasic defibrillators should be set at 360 J (yes, that means you start
with 360 J).
• Immediately after the shock is delivered, 2 minutes of CPR should be initiated
before the pulse check and before the rhythm check. In other words, shock the
patient, do 2 minutes, of CPR, then check the rhythm and pulse. This applies not just
to the first shock, but to every shock given. This again is meant to minimize delays in
compressions.
Effusion (pericardial)
• Common cause of unexplained dyspnea
o Dyspnea and tachypnea caused by pericardial fluid compression bronchial
structures
o Alveolar oxygen exchange should be unaffected ?? oxygen saturation
usually normal
• Marked cardiomegaly
• ECG triad: low voltage (very common), tachycardia (very common), electrical
alternans (< 30%)
• Patients are preload dependent ?? IVF often helps BP
o Beware intubation, positive pressure ventilation!
?? Decreases venous return ?? decreases cardiac output and BP
?? Think of this when you see sudden deterioration immediately after
intubation; treat with IVF
• Early routine ECHO in crashing/arresting patients!
Embolus (pulmonary)
• Beware overzealous IV hydration…may see BP start falling with IVF!
o Use vasopressors earlier, e.g. dobutamine
• Hypoxia often present with massive PEs, intubation is a better choice
o May actually help BP by decreasing venous return and RV overload
• ECG: new T-wave inversions common in cases of massive PE, especially in
anteroseptal and inferior leads
o Other ECG clues: rightward axis, tall R-wave in lead V1
• Early routine ECHO in crashing/arresting patients!
• Hemodynamically unstable patient with suspected PE (RV distention or dysfunction)
is reasonable indication for empiric thrombolytics
Forget About It!
A. High Dose Epinephrine
• HDE may be associated with an increase in ROSC, but is not associated with an
increase in hospital discharge or neurologic recovery; may be associated with a
decrease in neurologic recovery.
o Stiell, et al. (N Engl J Med, 1992)
Amal Mattu, MD
The Crashing Patient
7
o Brown, et al. (N Engl J Med 1992)
o Lipman, et al. (Anaesth Intensive Care, 1993)
o Rivers, et al. (Chest, 1994)
o Sherman, et al. (Pharmacotherapy, 1997)
o Behringer, et al. (Ann Intern Med, 1998)
o Gueugniaud, et al. (N Engl J Med, 1998)
B. Amiodarone
• Pharmacology
o Class III antidysrhythmic (potassium channel blockade)
o Also has some class I (sodium channel blockade), class II (beta blockade), and
class IV (calcium channel blockade) activity
o As effective as procainamide or bretylium in VT
o 60–80% “effective” in refractory VT (outcome??)
o Drawbacks — hypotension (may require vasopressors), bradycardia (may
require pacing), expensive
• Kudenchuk, et al. — ARREST trial (N Engl J Med, 1999)
o Manufacturer-supported study (Wyeth Ayerst)
o Seattle Prehospital study of patients with shock-resistant VT/VF
o Patients received three shocks, intubation, EPI 1 mg
o Then received either 300 mg amiodarone (246 patients) or placebo (258
patients)
o Subsequent treatment at the discretion of medics, physicians (followed general
ACLS guidelines)
o Results
?? Amiodarone patients more likely to survive to hospital admission than
placebo patients (44% vs. 34%; p=0.03)
?? No significant difference between amiodarone and placebo groups for
survival to hospital discharge (13.4% vs. 13.2%) or good neurologic
outcome (7.3% vs. 6.6%)
• Dorian, et al. — ALIVE trial (N Engl J Med, 2002)
o Manufacturer-supported study (Wyeth Ayerst)
o Canadian prehospital study of 348 patients with shock-resistant VT/VF
o IV lidocaine vs. amiodarone
o Patients received three shocks, EPI, repeat shock
o Then received either 1.5 mg/kg lidocaine or 5 mg/kg amiodarone
?? Then repeat shock, EPI, then half-dose of the study drug
o Preliminary results presented March 2001, NASPE Conference
?? Amiodarone patients more likely to survive to hospital admission than
lidocaine patients (22.7% vs. 11%)
?? Survival to discharge…………“data still being analyzed…”
o Final results presented November 2001, AHA Conference
o No significant difference in survival to hospital discharge
Amal Mattu, MD
The Crashing Patient
8
C. Vasopressin
• Pharmacology
o Naturally occurring antidiuretic hormone
o V1 receptors in vascular smooth muscle; V2 receptors in renal collecting duct
o In high doses, acts as a potent non-adrenergic peripheral vasoconstrictor
?? Increases diastolic aortic blood pressure and coronary perfusion
pressure
o Effect is similar to EPI’s alpha effect but without the beta effect
o Beta effect is associated with increased myocardial oxygen consumption
?? Increased incidence of post-resuscitation MI
• Pig studies of cardiac arrest
o Improved coronary perfusion pressure
o Improved vital organ blood flow
o Improved cerebral oxygen delivery
o No increase in myocardial oxygen demand
o Improved ROSC
• Lindner, et al. (Ann Intern Med, 1996)
o Eight cases of hospitalized patients with VF resistant to standard ACLS
treatment
o Vasopressin 40 units given; all patients had ROSC
o Three patients survived to hospital discharge
• Lindner, et al. (Lancet, 1997)
o Vasopressin vs. EPI; randomized, double-blind trial
o Forty out-of-hospital patients with VF resistant to initial CPR and
defibrillation received either EPI 1 mg or vasopressin 40 units, then further
standard ACLS measures
o ROSC: 11/20 EPI, 16/20 vasopressin
o Survival to hospital admission: 7/20 EPI, 14/20 vasopressin
o Survival > 24 hours: 4/20 EPI, 12/20 vasopressin
o Survival to hospital discharge: 3/20 EPI, 8/20 vasopressin
?? Survival to hospital discharge not statistically different (small study)
• Stiell, et al. (Lancet, 2001)
o Vasopressin vs. EPI; randomized triple-blind trial
o 200 in-hospital cardiac arrest (undifferentiated) patients requiring drug
therapy received either EPI 1 mg or vasopressin 40 units, then EPI if “rescue”
medications required
o Survival one hour: 35% EPI vs. 39% vasopressin (not statistically different)
o Survival to hospital discharge: 14% EPI vs. 12% vasopressin (not statistically
different)
o No difference in neurologic outcomes
o Conclusion: “We cannot recommend the routine use of vasopressin for
inhospital cardiac arrest patients, and disagree with American Heart
Amal Mattu, MD
The Crashing Patient
9
Association guidelines, which recommend vasopressin as alternative therapy
for cardiac arrest.”
• Wenzel, et al. (N Engl J Med, 2004)
o Vasopressin vs. EPI; randomized pre-hospital trial
o 1186 patients randomized
?? Either received 40 IU VP (x 2) or 1 mg EPI (x 2)
?? Then received additional EPI as needed
o Ventricular fibrillation: no signif. difference
o PEA: no signif. difference
o Asystole:
?? VP group had higher survival to hospital admission
• 29.0% vs. 20.3%
?? VP group had higher survival to hospital discharge
• 4.7% vs. 1.5%
o 732 patients in whom spontaneous circulation was not restored with the first 2
injections, then received further EPI
?? VP patients: 25.7% survived to admission, 6.2% survived to discharge
?? EPI patients: 16.4% survived to admission, 1.7% survived to discharge
o Conclusions
?? VP and EPI are similar for ventricular fibrillation and PEA
?? VP is better than EPI for asystole
?? VP followed by EPI is better than EPI alone in the treatment of
refractory cardiac arrest
o All patients: identical survival, but VP associated with worse neurologic
outcome
?? Survival to hospital discharge
• 9.9% in both groups
?? Cerebral performance VP vs. EPI
• Good cerebral performance 32.6% vs. 34.8%
• Moderate disability 15.2% vs. 26.1%
• Severe disability 19.6% vs. 15.2%
• Coma/vegetative state 32.6% vs. 23.9%
Summary for drugs in cardiac arrest:
• Antiarrhythmics: “There is no evidence that any antiarrhythmic drug given routinely
during human cardiac arrest increases survival to hospital discharge.”
• Vasopressors: “To date no placebo-controlled trials have shown that administration of
any vasopressor agent at any stage during management of pulseless VT, VT, PEA, or
asystole increases the rate of neurologically intact survival to hospital discharge.”
(Circulation, 2005; Volume 112, Issue 24)
Amal Mattu, MD
The Crashing Patient
10
Final Points
• Post-resuscitation care is now receiving greater emphasis as well.
o Therapeutic hypothermia (goal temperature 86-90 degrees F) has been
shown to improve neurologic outcome among initially comatose survivors
from out-of-hospital adult VFib cardiac arrest. It is uncertain whether this is
also effective for in-hospital cardiac arrest, pediatric arrest, or for non-VFib
arrest rhythms.
o Avoid hyperthermia (e.g. fever), hyperventilation, hyperglycemia, and
further cardiac ischemia post-resuscitation.
o Closely monitor vital organ function (e.g. renal function) post-resuscitation.
End-organ failure will obviously contribute to worse outcomes.
o Early cardiac catheterization for survivors of cardiac arrest (definitely if
STEMI…possibly even if no evidence of STEMI!)
**Recommendation for Further Reading**
If you enjoy reading about and learning from “Pitfalls,” check out the
following text:
Mattu A, Goyal DG (eds). Emergency Medicine: Avoiding the Pitfalls and
Improving the Outcomes. London, Blackwell Publishing, January 2007.
Questions? Contact me:
Amal Mattu, MD
amattu@smail.umaryland.edu