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• TCP
• Fluidchallengeifappropriate
• Dopamineinfusionbeginningwith5μg/kg/min
86. What is pulseless electrical activity (PEA)?
This term is used to describe a group of diverse ECG rhythms that manifest electrical activity but are
similar in that the patient will be without a pulse. Therefore the PEA is a nonperfusing rhythm.
The types of rhythms included in the PEA group are:
• EMD: organized ECG rhythm present, no pulse
• Pseudo-EMD: as above, but with some meaningful cardiac contraction
• Idioventricular, ventricular escape: wide-QRS, no atrial activity, and no pulse
• Bradyasystolic: profound bradycardia with periods of asystole, no pulse
PEA is almost always a secondary disorder resulting from some underlying condition.
87. What are the causes of PEA?
The underlying causes of PEA can be remembered easily using the mnemonic 5 H’s and 5 T’s.
1. Inadequate ventilation:
• Intubation of right main stem bronchus
• Tension pneumothorax
• Bilateral pneumothorax
2. Inadequate circulation:
• Pericardial effusion with tamponade
• Myocardial rupture
• Ruptured aortic aneurysm
• Massive pulmonary embolus
• Hypovolemia
3. Metabolic disorder:
• Electrolyte disturbances (hyperkalemia or hypokalemia, hypomagnesemia)
• Persistent severe acidosis (diabetic ketoacidosis or lactic acidosis)
• Tricyclic overdose
• Hypothermia
88. According to AHA protocol, how is PEA treated?
1. Continue CPR.
2. Intubate/establish IV access.
3. Assess blood flow using Doppler.
4. Consider and treat underlying causes.
5. Epinephrine, 1 mg IV/IO. Repeat every 3 to 5 minutes, or you may give one dose of vasopressin
6. Atropine, 1 mg IV push if pulse is present and absolute bradycardia is <60 beats/min. Repeat
89. What is asystole?
The term asystole indicates the absence of ventricular activity. The patient will be without a pulse.
Five causes that start with H:
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hyperkalemia/hypokalemia
Hypothermia
Five causes that start with T:
Table (ABCDs): antidepressants, beta blockers, calcium channel blocker, and digitalis
Tamponade (cardiac)
Tension pneumothorax
Thrombosis (coronary)
Thrombosis (pulmonary)
Alternatively, the causes of PEA can be divided into three basic categories:
40 U IV/IO to replace the first or second dose of epinephrine.
every 3 to 5 minutes (up to three doses).
ECG will show characteristic flat-line tracing without P-waves and QRS complexes. The underlying
causes of asystole can be remembered using the mnemonic PHD:
Preexisting acidosis
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Hypoxia, hyperkalemia, hypokalemia, hypothermia
Drug overdose
90. How is a flat-line rhythm verified to be asystole?
• Thepatientispulseless.
• Thepatientisunresponsive.
• Themonitoringleadsarecorrectlyhookedup.
• Thereisaat-linerecordinginmorethanonelead.
91. What four conditions other than asystole can lead to a flat-line tracing on ECG?
1. Fine V-fib
2. No power
3. Loose electrode leads
4. Signal gain is turned down.
92. What four conditions are pulseless?
There are four conditions in which the patient will present without a pulse and which are therefore
considered nonperfusing conditions:
1. V-fib
2. Pulseless VT
3. PEA:
• Electromechanical dissociation
• Pseudo-EMD (pulse will be very faint and evident only by Doppler)
• Ventricular escape rhythms
• Postdefibrillation idioventricular rhythms
4. Asystole
93. According to AHA protocol, what is the treatment for asystole?
The treatment sequence for asystole is virtually the same algorithm for PEA:
1. Continue CPR.
2. Intubate/establish IV access.
3. Confirm asystole.
4. Consider and treat underlying causes.
5. TCP only if started early.
6. Epinephrine, 1 mg IV/IO. Repeat every 3 to 5 minutes, or you may give one dose of vasopressin
40 U IV/IO to replace the first or second dose of epinephrine.
7. Atropine,1mgIV/IO.Repeatevery3to5minutes(uptothreedoses).
94. What is shock?
The term shock denotes a clinical syndrome in which there is inadequate cellular perfusion
and inadequate oxygen delivery for the metabolic demands of the tissues. Types of shock
include:
• Cardiogenicshock
• Neurogenicshock
• Hypovolemicshock
• Flowdisruptionshock
• Septicshock
• Anaphylacticshock
• Increasedvascularresistance
• Anxiety
• Coolmottledskin
• Vomiting
• Oliguria
• Diarrhea
• Tachycardia
• Myocardialischemia
• Adrenergicresponse
• Mentalstatuschanges
• Diaphoresis
In general, shock is characterized by:
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95. When is synchronized cardioversion used?
• Tachycardia
• A-fib
• PSVT
• A-utter
96. What are the signs and symptoms of cardiac tamponade?
• Persistenttachycardiawithfallingbloodpressure
• Pulsusparadoxus
• Pulsatileneckveins
• EnlargingheartshadowonchestX-ray
97. What are the signs and symptoms of hypovolemic shock?
• Cardiacoutputwillbelowduetoinadequateleftventricularfilling.
• HypotensionmayleadtochangesintheECG.
98. How is hypovolemic shock treated?
• Volumelosscanbediagnosedthroughhistoryandclinicalevaluation.
• Replacevolumewithcrystalloidorcolloidsolutionwhenthehematocritisnormal.
• Withactivebleeding,hemostasismustbeachievedfirst.Ifthehematocritisdangerouslylow,
transfusion of whole blood or packed red blood cells is indicated.
99. What are the four life-threatening conditions that may mimic acute MI and lead
to cardiovascular collapse?
1. Massive pulmonary embolism
2. Cardiac tamponade
3. Hypovolemic and septic shock
4. Aortic dissection
100. What drugs can be administered through the endotracheal tube?
L-E-A-N (Lidocaine, Atropine, Epinephrine, Narcan). Administer all tracheal medications at 2 to 2.5
times the recommended IV dosage, diluted in 10 mL of normal saline or distilled water. Tracheal
absorption is greater with the distilled water as the diluent than with normal saline, but distilled
water has a greater adverse effect on PaO2.
101. How is sudden cardiac death defined?*
Sudden V-fib or PEA. Acute coronary ischemia and preexisting cardiac disease are the most com-
mon causes. V-fib is becoming less common.
102. Is there an immediate need for an airway?*
No. Defibrillation and chest compression should be initiated first. Waiting for intubation to
be completed before initiation of these interventions is one of the most common mistakes in
advanced life support. Children, in whom primary respiratory arrest is more common, are an
exception. Restoration of ventilation in children often reveals that pulselessness was severe
shock, not cardiac arrest.
103. Is the central line the best access to the circulation?*
Yes. Large volumes of fluid can be delivered to the venous system more quickly, however, via large-bore
peripheral venous catheters. A 14-gauge, 5-cm catheter (peripheral) can deliver twice the flow of a
16-gauge, 20-cm catheter (central). Central line placement may be associated with significant complications, including pneumothorax, air embolus, and arterial puncture. In hypovolemic patients, in whom
central veins are collapsed and peripheral veins are constricted, venous cannulation can be difficult.
104. Does a central line offer therapeutic and diagnostic advantages?*
Yes. A central line permits bolus administration of drugs to the right side of the heart. Identification
of a high central venous pressure may indicate the need to treat reversible causes of PEA, such as
cardiac tamponade or tension pneumothorax.
105. Which is preferred: colloid or crystalloid resuscitation fluid?*
Colloid advocates claim that the big molecules remain in the intravascular space and are more
effective in elevating blood volume. Crystalloid advocates state that capillaries leak albumin, especially in the shock state. Resuscitation with crystalloid is clearly safe. Given its availability, low cost,
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and safety, crystalloid (lactated Ringer’s solution) is the choice for initial fluid resuscitation. When
true cardiac arrest has occurred, however, volume is of little importance.
106. In a patient exhibiting asystole, bradycardia, PEA, or fine fibrillation, what is your
primary goal?*
Adequate vital organ perfusion, especially to the coronary arteries. Done properly, CPR may cause PEA
to progress to stable hemodynamics or V-fib to become coarse enough for successful countershock.
107. When should adenosine be used?
Adenosine is the first line drug of choice for managing stable narrow-complex tachycardia. Adenosine
is effective in terminating arrhythmias due to reentry at the AV or SA node. It is often used as a agent,
to decrease the heart rate for better appreciation of the underlying rhythm. Adenosine will NOT convert
atrial fibrillation, atrial flutter, or ventricular tachycardia. During rapid IV push, adenosine will often
cause short-lived side effects including asystole or significant bradycardia, chest pain, and flushing.
Adenosine is also safe to be used during pregnancy.
108. When should Amiodarone be used?
Amiodarone is a drug that affects sodium, potassium, and calcium channels in addition to having
alpha- and beta-adrenergic blocking components. The AHA recommends that amiodarone be
prescribed by physicians well versed in the treatment of arrhythmias and fully aware of its risks and
benefits. Beyond its warning, amiodarone is indicated for patients with V-fib, pulseless VT unresponsive to defibrillation, CPR and vasopressors, and recurrent, unstable VT. The first dose is 300 mg IV
push, followed by a second dose of 150 mg as necessary. Avoid using amiodarone with other drugs
that increase the QT interval (e.g., procainamide).
109. When should aspirin be used in the ACLS protocol?
Administer to all patients with suspected acute coronary syndrome; this includes patients with
crushing chest pain, chest pressure, or other symptoms consistent with cardiac ischemia. The dose
is 160 to 325 mg non-enteric coated tablet and should be chewed. A rectal suppository may be
substituted in those who cannot take PO medications. The rectal dose is 300 mg. One must weigh
the benefits and risks of giving aspirin (ASA) to someone with a history of active ulcer disease or
asthma. The only true contraindication is someone with a known allergy to ASA.
110. When should atropine be used?
Atropine is the first line drug in symptomatic sinus bradycardia. The 2010 AHA guidelines have
eliminated atropine from the PEA or systole algorithm. The dose for bradycardia is 0.5 mg IV q 3 to
5 min, and not to exceed 3 mg. Doses less than 0.5 mg may cause paradoxical slowing of the heart
rate. Judicious use should be performed in the patient with myocardial ischemia and hypoxia, as
atropine will increase the myocardial oxygen demand. The other indication for atropine use outside
of the ACLS algorithm is for organophosphate poisoning.
111. When should diltiazem be used?
Use to control ventricular rates in the atrial fibrillation and atrial flutter. It is also used to rate control
refractory reentry SVT. For acute rate control one should use 15 to 20 mg IV over 2 minutes. A
second dose of 20 to 25 mg IV may be given 15 minutes later over 2 minutes. Do NOT use calcium
channel blockers in patients with Wolff-Parkinson-White Syndrome. Calcium channel blockers will
cause a drop in blood pressure from peripheral vasodilation. Avoid calcium channel blockers in
patients already receiving IV beta blockers, as this combination may cause severe hypotension.
112. When should epinephrine be used?
There are several indications for epinephrine:
• Cardiacarrest:whichincludesV-fib,pulselessVT,asystole,andPEA.Thedoseis1mgadminis-
tered q 3 to 5 min (10 mL of 1:10k solution). As with all medications in cardiac arrest, they should
be flushed with 20 mL saline and elevation of the limb.
• Symptomaticbradycardia
• Severe hypotension: a dose of 2 to 10 mcg/min is used as a vasopressor.
• Anaphylaxis
* Reprinted from Paradis NA, Harken AH: Cardiopulmonary resuscitation. In Harken AH, Moore EE, editors: Abernathy’s
surgical secrets, ed 5, Philadelphia, 2005, Mosby.
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Epinephrine will raise blood pressure and increase heart rate causing increased myocardial
oxygen consumption. Epinephrine is a medication that may be given through the endotracheal tube.
113. When should magnesium sulfate be used?
There are two major indications for magnesium sulfate: the first is in situations of torsades de pointes
with suspected hypomagnesemia; the second is in ventricular arrhythmias secondary to digitalis toxicity. In the setting of cardiac arrest with torsades de pointes, the dose is 1 to 2 g diluted in 10 ml D5W IV.
114. When should morphine be used?
Morphine is a powerful opiate that provides profound analgesia and euphoria. It is to be used
in cases of chest pain with acute coronary syndrome that does not respond to nitrates. Two
well-known side effects of opiates are respiratory depression and hypotension. For ST-elevation
myocardial infarction (STEMI) patients, the dose is 2 to 4 mg IV, and it may be increased depending on patient tolerance and response. Morphine should be used judiciously in patients with right
ventricular infarction, as these patients are preload dependent and decreases in blood pressure will
worsen coronary perfusion.
115. When should oxygen be delivered to the patient?
Oxygen should be used when there is any suspicion of cardiac or pulmonary emergencies. All
patients with shortness of breath and/or chest pain should receive supplemental oxygen. ACLS
guidelinesrecommendadministeringoxygentopatientsonceoxygensaturationlevelsfallto<94%.
Oxygen may be delivered via a variety of devices ranging from a nasal cannula to an endotracheal
tube.Oxygentoxicityisaconcernforintubatedpatients.FiO2higherthan60%maycausefree
radical damage resulting in atelectasis and lung consolidation. In general, one should titrate FiO2
toachieve100%saturationatthelowestpossibleFiO2.Inaddition,anypatientonsupplemental
oxygen should have continuous pulse oximetry.
116. Can you summarize the Acute Coronary Syndrome Algorithm?
The ACS Algorithm should be activated when there is suspicion that a heart attack may be
occurring. Suspicion should be heightened on patients with multiple risk factors (e.g., chest
painradiatingtoleftarm,age>70,malesex,diabetesmellitus,andhistoryofischemic
heart disease). Once initiated, the patient should be connected to cardiac monitors, given
supplemental oxygen, and IV access should be initiated. Aspirin should be given and chewed.
Nitroglycerin and morphine may be given depending on the patient’s blood pressure and symptoms. A 12-lead ECG should be obtained to determine STEMI versus non-STEMI. Labs should
be drawn that include electrolytes, coagulation studies, and cardiac markers. A portable CXR
should be taken. A checklist for reperfusion should be initiated. If the patient is not in a hospital
setting, then EMS should notify a hospital equipped for Percutaneous Cardiac Intervention (PCI).
The ECG result will dictate the next step in treatment. If the patient has STEMI, then a focus on
reperfusion therapy should be priority. The AHA recommends door-to-balloon (PCI) time of 90 minutes, or door-to-needle (fibrinolysis) goal of 30 minutes. Other adjunctive therapy should be initiated
such as nitroglycerin, heparin, antiplatelet agents, and rate control with beta blockers. All patients
with STEMI should be admitted to monitored beds and frequently monitored.
If the patient has ST-segment depression or dynamic T-wave inversion, there is a high
likelihood of ischemia. Adjunctive treatment as listed above should be started. Serial troponin
markers should be measured and the patient should be monitored for signs of heart failure,
persistent ECG changes, or arrhythmias. If these occur, the patient should be considered for
invasive therapy (PCI).
Last, if the patient has a normal ECG, then one should evaluate serial cardiac markers and
perform noninvasive imaging. If these tests are positive for pathology, then the patient should be
treated with adjunctive therapy and be considered for more invasive imaging and intervention. Most
patients with ACS will benefit from an HMG CoA reductase inhibitor, ASA, and blood pressure control.
117. When should nitroglycerin be avoided in the ACLS patient?
Nitrates cause veno-dilation and are used for the treatment of ischemic chest pain. They should be
avoided when the patient cannot tolerate an additional drop in blood pressure caused by the venodilation. The AHA recommends caution with nitrates when SBP <90 mm Hg or >30 mm Hg below
baseline. Avoid nitrates in patients with inferior wall MI and suspected right ventricular involvement,
as these patients are preload dependent. Last, avoid nitrates in someone who has used phosphodiesterase inhibitors in the past 24 to 48 hours.
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118. What are the time limit goals for reperfusion therapy?
Percutaneous coronary intervention within 90 minutes of arrival at the emergency department. Alter-
natively, fibrinolytic therapy within 30 minutes of arrival at the emergency department. To facilitate
this rapid intervention, the chain of response must be tightened. Obtaining a 12-lead ECG in the field
by EMS and forwarding to the emergency department of a PCI-equipped facility, helps to eliminate
unnecessary delay. This will minimize delays and maximize optimum outcomes.
119. Describe the algorithm for managing a patient with cardiac arrest.
Once a cardiac arrest is suspected, the first action is to activate the emergency response by call-
ing for help, or calling for a Code Team. In a hospital setting, cardiac arrest triggers a Code Blue.
Depending on the number of rescuers, clear roles should be assigned; the code leader should be
clear. The next step is immediately starting CPR. With the heart no longer pumping oxygen to the
tissues, the rescuer must preserve the function of these organs by artificially pumping oxygen
via chest compressions. While one person maintains chest compressions at a rate of 30:2 with
respirations, another should be preparing the defibrillator. Emphasis should be placed on activating
the defibrillator as soon as possible, as delay in defibrillation is associated with worse outcomes.
The defibrillator will search for a shockable or nonshockable rhythm. If nonshockable (asystole or
PEA), immediately return to performing CPR. If shockable, rescuers must stand clear until shock is
delivered. The shock is 120 to 200 J on biphasic units, and 360 J on monophasic units. During CPR,
attempts should be made to obtain IV access. Consideration for advanced airways must be made
(either LMA, endotracheal intubation, or an emergency surgical airway). If an advanced airway is
placed, then respirations change to 8 to 10/min and chest compressions continue without interruption for 2 minutes. Waveform capnography should be used to confirm proper placement of advanced
airway. Every 2-minute cycle of CPR triggers a rhythm check by the defibrillator, a drug therapy
check, and reevaluation of the treatment so far. Drug therapy consists of giving a vasopressor
(epinephrine or vasopressin) or antiarrhythmic such as amiodarone. A search for “H’s and T’s” must
be performed to identify and ultimately treat a potential source for cardiac arrest. One should not
deviate from the ACLS algorithm, as deviations are associated with worse outcomes.
120. What are the steps to be taken after return of spontaneous circulation (ROSC)?
The goal after ROSC is to minimize damage from ischemia. Therefore, oxygenation saturation must
be maintained at a level of ≥94%.Considerplacinganadvancedairwayifoxygenationistenuous.
Avoid hyperventilation as this may prevent venous return and cause gastric insufflation. Start at
a rate of 10 to 12 breaths/min and titrate to target end tidal CO2 of 35 to 40 mm Hg. Along with
oxygenation, perfusion must be maintained. Perfusion may be estimated from blood pressure. The
goal is to maintain systolic BP ≥90 mm Hg. To achieve this goal, IVF bolus and vasopressors may
be used. A search for reversible causes must continue (H’s and T’s). Evaluation of mental status will
determine if induced hypothermia is necessary. If the patient cannot follow commands, then induced
hypothermia is recommended. If the initial cardiac arrest was suspected to be STEMI or acute
myocardial infarction, then coronary reperfusion should be initiated as quickly as possible. Induced
hypothermia and coronary reperfusion can be initiated simultaneously when indicated.
121. What is the algorithm for bradycardia?
The first step is identifying the appropriateness of the heart rate for a given clinical scenario (e.g.,
marathon runners may have heart rates in the 40s and be normal). In general, a heart rate <50/min is
considered a bradyarrhythmia. Once determined to be pathologic, a search for the underlying cause
should begin. One should obtain IV access, cardiac monitoring, and supplemental oxygen if hypoxemic. 12-lead ECG should be obtained with all arrhythmias. The next step is determining the severity
of the bradyarrhythmia. If the patient has signs of hypotension, altered mental status, ischemic chest
pain, acute heart failure, or shock, then treatment to raise the heart must begin. Without these signs
of symptoms the patient may be monitored and observed. If symptomatic, atropine is the first line
agent to be used. A dose of 0.5 mg bolus may be repeated q 3 to 5 min until a maximum of 3 mg is
reached. If atropine is ineffective in raising the heart rate, TCP or dopamine infusion or epinephrine
infusion may be started. Transvenous pacing may be required but should be performed by an expert.
122. Can you explain the algorithm for tachycardia?
The first steps are similar to evaluating the patient with bradycardia. First, one must identify the appropri-
ateness of the heart rate for a given clinical scenario (e.g., strenuous activity will raise HR in a physiologic manner). In general, heart rate ≥150/min is considered a tachyarrhythmia. Once determined to be
pathologic, a search for underlying causes should begin. One should obtain IV access, cardiac monitoring,
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and supplemental oxygen if hypoxemic. Monitoring blood pressure frequently is crucial in determining the
severity of tachyarrhythmias. There are two significant checkpoints in the evaluation of tachyarrhythmias:
(1) is the tachyarrhythmia causing hypotension, altered mental status, ischemic chest pain, acute heart
failure, or signs of shock? These are signs of hemodynamic instability. (2) Is the QRS complex wide or
narrow (defined by ≥0.12 s)? The former must be evaluated first. If the patient has signs of hemodynamic
instability, proceed to immediate synchronized cardioversion. The energy for cardioversion is dictated by
the arrhythmia: narrow regular = 50 to 100 J; narrow irregular = 120 to 200; wide regular = 100 J. Sedation
may be considered if the clinical course permits. If the patient has no signs of instability, then evaluate the
QRS complex; if wide, consider adenosine only if regular and monomorphic, consider antiarrhythmic infusion, and obtain expert consultation. Antiarrhythmic infusions for stable wide-QRS tachycardia consist of
procainamide, amiodarone, and sotalol. If the QRS complex is narrow, perform vagal maneuvers, administer adenosine (if regular), beta blockers, or calcium channel blockers, and obtain expert consultation.
123. When is it appropriate to give adenosine for wide-complex tachycardia?
Adenosine may be given in cases of regular, monomorphic wide-complex tachycardia. However, one
should avoid adenosine in cases of irregular, wide-complex tachycardia as it may cause degeneration into ventricular fibrillation.
124. What are the reversible causes of the ACLS protocol?
Commonly known as the H’s and T’s. These are factors that may be causing or may be contributing
to cardiac arrest, bradycardia, or tachycardia. They include:
• H’s:Hypovolemia,Hypoxia,Hydrogenion(acidosis),Hypo/Hyperkalemia,Hypothermia
• T’s:Tensionpneumothorax,Tamponade(cardiac),Toxins,Thrombosis(pulmonaryorcoronary)
125. For maternal cardiac arrest, what are the unique reversible causes specific for
this demographic?
The causes form the acronym BEAU–CHOPS: Bleeding/DIC, Embolism (coronary/pulmonary/amniotic
fluid), Anesthetic complications, Uterine atony, Cardiac disease, Hypertension (preeclampsia/eclampsia),
Other, Placenta aburptio/previa, Sepsis.
126. What is the Cincinnati Prehospital Stroke Scale?
A system developed to predict if a stroke occurred. The test centers around three observations: facial droop,
armdrift,andspeech.Ifanyoneofthesethreeisabnormal,theprobabilityofstrokeis72%.
127. What is the Suspected Stroke Algorithm?
This is a time-sensitive protocol designed to preserve vital brain tissue in a patient suspected of having a
stroke. The first step is identifying the signs and symptoms of a stroke. The EMS team should perform a
prehospital stroke assessment and determine time of symptom onset. The patient should be transported
to a stroke center; the center should be notified that the patient is en route. Once the patient enters the
emergency department (ED), ABC’s, vitals, IV access, glucose levels, neurologic screening, 12-lead ECG,
CT scan, and activation of the stroke team should be performed within 10 minutes. Within 45 minutes the
CT scan should be reviewed and a determination must be made: is there hemorrhage or no hemorrhage? If hemorrhage is found, a neurosurgeon should be notified for possible surgical intervention. If
no hemorrhage is found, acute ischemic stroke is likely and fibrinolytic therapy should be considered.
The checklist for fibrinolytic exclusion criteria must be completed. If no contraindications to fibrinolytic
therapy, it should be administered within 60 minutes of arrival at the ED. If not a candidate for fibrinolytic
therapy, then administer ASA. Regardless of pathway, BP monitoring must be performed frequently.
Serial neurologic exams must be performed. All patients who sustain a stroke must be admitted to a
stroke unit or ICU.
128. What are the time limit goals for acute ischemic stroke?
Three hours from the onset of symptoms to fibrinolytic therapy. For a select group of patients the
fibrinolytic treatment goal limit may be extended to 3 to 4.5 hours. Similar to PCI for ACS patients,
fibrinolytic therapy response for acute ischemic stroke patients should be initiated as soon as
possible to minimize the damage to brain parenchyma. Patients with suspected strokes should be
transported to a comprehensive stroke center for optimal outcomes.
129. According to the AHA, what are the absolute contraindications to fibrinolytic
therapy?
Prior intracranial bleeding, known cerebral vascular lesion, known malignant intracranial mass,
suspected aortic dissection, active bleeding, significant facial/head trauma within 3 months, and
ischemic stroke within 3 months, with the exception of an acute ischemic stroke within 3 hours.
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130. For unstable atrial fibrillation, what is the recommended voltage for synchronized cardioversion?
Initial biphasic energy dose is between 120 and 200 J.
131. For unstable supraventricular tachycardia or unstable atrial flutter, what is the
recommended energy dose for synchronized cardioversion?
50 to 100 J.
132. For monophasic waveforms, what is the recommended energy dose for synchronized cardioversion?
An initial dose of 200 J. One should increase the energy in regular intervals if no response is seen.
133. For unstable monomorphic ventricular tachycardia, what is the recommended
energy dose for synchronized cardioversion?
An initial dose of 100 J. One should increase the energy in regular intervals if no response is seen.
ADVANCED TRAUMA LIFE SUPPORT
†
134. In treating the seriously injured patient, what are the components of the
appropriate systematic approach essential in instituting life preserving
therapy?
Primary and secondary surveys are used for rapid, systematic, and thorough evaluation of the seri-
ously injured patient.
135. What are the components of the primary survey?
The primary survey includes the ABCDE’s: Airway maintenance with cervical spine protection,
Breathing and Ventilation, Circulation with hemorrhage control, Disability (neurological status),
Exposure/Environmental control (undressing patient completely while preventing hypothermia).
136. What are the components of the secondary survey, and when does it begin?
The secondary survey only begins once the primary survey is completed, resuscitative efforts are
underway, and normalization of vital functions has been demonstrated. The secondary survey is
a complete head-to-toe history and physical examination of the trauma patient. This includes a
thorough exam of the skull, head, maxillofacial, neck, chest, abdomen, perineum/rectum/vagina,
musculoskeletal system, and neurological system.
137. What is the useful mnemonic in aiding the complete medical assessment with
the history of the mechanism of the injury?
The AMPLE history can be used for complete medical assessment as well as history of mecha-
nism of the injury: Allergies, Medications currently used, Past illnesses or Pregnancy, Last meal,
Events/Environment related to injury.
138. What assumption should be made regarding patients with maxillofacial or head
trauma?
Patients with maxillofacial or head trauma should be presumed to have an unstable cervical spine
injury. Therefore, these patients should have an immobilized neck until all aspects of the cervical
spine are carefully and adequately studied.
139. When should a definitive airway be placed in the trauma patient?
If there is any doubt in the patient’s ability to maintain airway integrity. Examples include an altered
level of consciousness or a Glasgow Coma Scale (GCS) score of eight or less, severe maxillofacial
trauma, risk for aspiration (bleeding/vomiting), and risk for obstruction (neck hematoma, laryngeal/
tracheal injury, or stridor).
140. What are the initial radiographic studies obtained for the blunt trauma
patient?
Anteroposterior (AP) chest, AP pelvic, and cervical spine films should be obtained and can guide
resuscitation efforts in patients with blunt trauma.
†
Written by John Wessel and Shahid R. Aziz.
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141. What are the signs of laryngeal fracture?
Although fracture of the larynx is a rare injury, it can present with acute airway obstruction. The triad
of clinical signs is hoarseness, subcutaneous emphysema, and palpable fracture.
142. How is proper endotracheal tube placement confirmed?
Proper position of the tube is best confirmed by chest X-ray once the possibility of esophageal
intubation is excluded. A carbon dioxide detector is indicated to help confirm proper intubation of the
airway. Proper placement of the tube is suggested but not confirmed by hearing equal and bilateral
breath sounds.
143. How many intravenous (IV) catheters should be introduced in the trauma
patient?
A minimum of two large caliber IV catheters should be introduced in the trauma patient.
144. What determines the maximum rate of fluid administration through a catheter?
The maximum rate of fluid administration is determined by the internal diameter of the catheter and
inversely by its length. The size of the vessel into which the catheter is placed has no effect on flow
rate.
145. What is the optimal urinary output for adult and pediatric trauma patients?
In an adult patient, urinary output should be at least 0.5 mL per kilogram per hour. In the pediatric
patient older than age 1, it should be 1 mL per kilogram per hour.
146. What is the definition of shock?
Shock is an abnormality of the circulatory system that results in inadequate organ perfusion and
tissue oxygenation.
147. What are the most common forms of shock encountered in trauma patients?
Most patients in shock are hypovolemic, but they may also suffer from neurogenic, obstructive,
cardiogenic, or septic shock.
148. What is the earliest measurable circulatory sign of shock?
Tachycardia is the earliest measurable circulatory sign of shock. The release of endogenous cat-
echolamines increases peripheral vascular resistance. This increases diastolic blood pressure and
reduces pulse pressure but does not increase organ and tissue perfusion.
149. Why do pediatric patients with hemorrhagic injuries deteriorate rapidly?
The ability for a pediatric patient to compensate in the beginning phases of blood loss due to their
abundant physiologic reserve may create an illusion of hemodynamic stability, resulting in inadequate fluid or blood product resuscitation and rapid deterioration.
150. What is cardiogenic shock?
Cardiogenic shock occurs when the blood flow decreases due to an intrinsic defect in cardiac
function in either the heart muscle or the heart valves. A classic example is an acute myocardial
infarction resulting in ischemic damages to the heart muscle impeding cardiac contractility. The
decreased contractility causes a decrease in stroke volume, resulting in decreased cardiac output
and blood pressure; high left ventricular filling pressures (backward failure); increased systemic
vascular resistance (from vasoconstriction, which is a sympathetic compensatory response to the
low blood pressure); and increased heart rate (sympathetic compensatory response to the low blood
pressure). Other features of cardiogenic shock, such as cool extremities, decreased urine output,
and sweating, may also be explained by the sympathetic compensatory response.
151. How is hemorrhage classified?
There are four classes of hemorrhage: Class Ihemorrhageiswherethepatienthasupto15%
bloodvolumeloss(upto750mL).Theclinicalsymptomsareminimalandcrystalloidistheinitial
fluid replacement. Class IIhemorrhageiswherethepatienthasbetween15%and30%blood
volumeloss(750to1500mL).Clinically,thepatienthasaslightlyincreasedpulserate(100to120)
and respiratory rate (20 to 30 beats/min). Crystalloid is the initial fluid replacement therapy. Class
IIIhemorrhageisacomplicatedhemorrhagicstatewherethepatienthasbetween30%and40%
(1500 to 2000 mL). Clinically, the patient has an even increased pulse rate (between 120 and 140),
as well as an increased respiratory rate (30 to 40 bpm). This patient will require both crystalloid
infusion and blood product replacement. In Class IV hemorrhage where the patient lost
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greaterthan40%totalbloodvolume(greaterthan2000mL),thepatientwilldeteriorateveryquickly
unless aggressive measures are taken. This patient is considered preterminal and may die within
minutes. Clinically, the pulse rate is >140 and respirations are >35 beats/min.
152. What are the urinary outputs expected in each stage of hemorrhagic shock in
mL/hr?
Class I is 30 mL; Class II is 20 to 30 mL; Class III is 5 to 15 mL; Class IV is negligible.
153. What are the steps in a Rapid Sequence Intubation?
1. Prepare for the need for a possible surgical airway.
2. Prepare section and the ability to deliver positive pressure ventilation.
3. Preoxygenatethepatientwith100%oxygen.
4. Apply cricoid pressure.
5. Administer an induction agent or sedation, according to local practice.
6. Administer IV succinylcholine (1 to 2 mg per kilogram).
7. Directlaryngoscopyandintubationofthepatient.
8. The endotracheal tube cuff is inflated and tube placement is confirmed by equal and bilateral
9. Cricoid pressure is released.
10. The patient is ventilated.
154. Why is etomidate (Amidate) the drug of choice for sedation for intubation of the
Etomidate is more cardio-stable, not having a significant effect on blood pressure or intracranial
155. In which patient is a surgical cricothyroidotomy contraindicated?
Children (under age 11), crush injury to larynx, and known preexisting laryngeal or tracheal pathol-
156. What is a tension pneumothorax?
A tension pneumothorax is a true surgical emergency that requires immediate diagnosis and
157. How is a tension pneumothorax diagnosed?
Diagnosis of a tension pneumothorax should be made based on clinical evaluation.
158. What are some signs or symptoms of a tension pneumothorax?
Acute respiratory distress, subcutaneous emphysema, absent breath sounds, hyperresonance to
159. What is the treatment of a tension pneumothorax?
A tension pneumothorax requires immediate thoracic decompression and is managed initially by
160. What are epidural and subdural hematomas and how do they differ?
These hematomas are focal brain lesions. Epidural hematomas are neurosurgical emergencies
breath sounds on auscultation. An end-tidal CO2 detector is used at this point if available.
trauma patient?
pressure. Etomidate inhibits adrenal steroidogenesis; repeated doses should not be used because of
the risk of adrenal suppression.
ogy are generally contraindications to surgical cricothyroidotomy.
treatment. A tension pneumothorax develops when there is a violation of the visceral space and
the visceral pleura acts as a one-way valve, allowing air to escape into the pleural space. As the
pneumothorax expands, the diaphragm is pushed downward and the mediastinum is shifted to the
contralateral hemithorax. This causes impaired venous return and a decline in cardiac output.
percussion, and tracheal deviation support the diagnosis of a tension pneumothorax.
rapidly inserting a needle into the second intercostal space along the mid-clavicular line of the
affected hemithorax.
andoccurin0.5%ofallbrain-injuredpatients.Theyarelocatedoutsidethedurabutwithinthe
skull and are typically biconvex or lenticular in shape. They are typically caused by laceration of
an anterior or posterior division of the middle meningeal artery and are most often located in the
temporal or temporoparietal region; less commonly they can be caused by laceration over a large
intracranial venous sinus with resultant accumulation of blood in the epidural space. Subdural
hematomasoccurinapproximately30%ofseverebraininjuries.Thesebraininjuriesresultfrom
hemorrhage into the subdural space from laceration of the bridging veins, laceration of a cortical
vessel, or laceration of the cortex itself and commonly cover the entire surface of the hemisphere.
An acute subdural hematoma usually results in much more severe brain damage than an epidural
hematoma.
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