Markovchick Vincent J., Pons Peter T., Bakes Katherine M.(ed.) Emergency medicine secrets. 5th ed
Подождите немного. Документ загружается.
Chapter 1 DECISION MAKING IN EMERGENCY MEDICINE8
8. What is the most inaccurate vital sign taken in the field and ED?
In the field, the most common inaccurate vital sign is the respiratory rate because it is
sometimes estimated rather than counted. In the ED, the temperature may be inaccurate if a
tympanic membrane thermometer was used or if the patient was hyperventilating or mouth
breathing when the oral temperature was taken.
9. Why do I need to compare field vital signs with ED vital signs?
Most prehospital care systems with a level of care beyond basic transport also provide therapy
to patients. Because this therapy usually makes positive changes in the patient’s condition, the
patient may look deceptively well on arrival in the ED. For example, a 20-year-old woman with
acute onset of left lower quadrant abdominal pain, who is found to be cool, clammy, and
diaphoretic, with a pulse of 116 beats per minute, a blood pressure of 78 palpable, and who
receives 1500 mL of intravenous (IV) fluid en route to the ED, may arrive with normal vital
signs and no skin changes. If one does not read and pay attention to the EMT’s description of
the patient and the initial vital signs, the presumption may be made that this is a stable patient.
10. When are normal vital signs abnormal?
This is where the chief complaint comes in and correlating it for consistency with the patient’s
presentation. For example, a 20-year-old man who states he has asthma and has been wheezing
for hours arrives in the ED with a respiratory rate of 14 breaths per minute. An asthmatic who is
dyspneic and wheezing should have a respiratory rate of at least 20 to 30 breaths per minute.
Thus, a normal respiratory rate of 14 breaths per minute in this setting indicates the patient is
fatiguing and is in respiratory failure. This is a classic example of when “normal” is extremely
abnormal.
11. Why do I need to visualize, auscultate, and touch the patient?
In many instances, these measures help to identify the life threat (e.g., is it the upper airway,
lower airway, or circulation?). Touching the skin is important to determine whether shock is
associated with vasoconstriction (i.e., hypovolemic or cardiogenic) or with vasodilatation
(i.e., septic, neurogenic, or anaphylactic). Auscultation will identify life threats associated with
the lower airway (e.g., bronchoconstriction, tension pneumothorax).
12. Once I have identified the life threat, what do I do?
Do not go on. Stop immediately and intervene to reverse the life threat. For example, if the
initial encounter with the patient identifies upper airway obstruction, take whatever measures
are necessary to alleviate upper airway obstruction such as suctioning, positioning, or
intubating the patient. If the problem is hemorrhage, volume restoration and hemorrhage
control (when possible) are indicated.
13. I have identified and stabilized or ruled out an immediate life threat in the
patient. What else is unique about the approach?
The differential diagnosis formulated in the ED must begin with the most serious condition
possible to explain the patient’s presentation and proceed from there. An example is a 60-year-old
man who presents with nausea, vomiting, and epigastric pain. Instead of assuming the condition
is caused by a gastrointestinal disorder, one must consider that the presentation could represent
an acute myocardial infarction (MI) and take the appropriate steps to stabilize the patient (i.e.,
start an IV line, place the patient on O
2
, and a cardiac monitor) and rule out an MI by completing
an adequate history, physical examination, and electrocardiogram ECG).
14. Why does formulating a differential diagnosis sometimes lead to problems?
The natural tendency in formulating a differential diagnosis is to think of the most common
or statistically most probable condition to explain the patient’s initial presentation to the ED.
If one does this, one will be right most of the time but may overlook the most serious, albeit
sometimes a very uncommon, problem. Therefore, the practice of emergency medicine
involves some degree of healthy paranoia in that one must consider the most serious
Chapter 1 DECISION MAKING IN EMERGENCY MEDICINE 9
condition possible and, through a logical process of elimination, rule it out and thereby arrive
at the correct and generally more common diagnosis.
15. Is a diagnosis always possible or necessary with information I can obtain in
the ED?
No. Sometimes it takes days, weeks, or months for the final diagnosis to be made. It is
unreasonable to expect that every patient evaluated in the ED should or must have a diagnosis
made in the ED. If you have an obsessive-compulsive personality with a need to be absolutely
certain about what a patient has before you can act to stabilize or treat the patient, then the ED
is an unhealthy work environment for you.
16. Suppose I cannot make the diagnosis, what do I do?
It is advisable to be intellectually honest and admit to the patient and document in the medical
record the inability to make a diagnosis. As stated previously, it is the role of the ED physician
to rule out and stabilize serious or life-threatening causes of a patient’s presentation, not to
arrive at the definitive diagnosis. For example, a patient who presents with acute abdominal
pain, who has had an appropriate history taken, who has had a physical examination and
diagnostic studies performed, and who in your best judgment does not have a life-threatening
or acute surgical problem should be so informed. The discharge diagnosis would be abdominal
pain of unknown etiology. This avoids the trap so often encountered of labeling the patient with
a benign diagnosis such as gastroenteritis or gastritis that is not supported by the medical
record. More importantly, it avoids giving the patient the impression that there is a totally
benign process occurring and will help to avoid the medical (and legal) problem of the patient
presenting 2 days later with something more serious, such as a ruptured appendix.
17. What is the most important question to ask a patient who presents to the ED
with a chronic, persistent, or recurrent condition?
“What’s different now?” This question should be asked of all patients who have a chronic
condition that has resulted in their visit to the ED. The classic example is migraine headache.
The patient with a chronic, recurrent migraine headache who is not asked this question may,
on this presentation, have had an acute subarachnoid bleed. Such a patient may not volunteer
that this headache is different from the pattern of chronic migraines unless asked.
18. How do I decide if the patient needs hospitalization?
Obviously, the medical condition is the first factor to consider. The question that must be
answered is: “Is there a medical need that can be fulfilled only by hospitalization?” For
example, does the patient need oxygen therapy or cardiac monitoring? Another factor to
weigh in the decision regarding hospitalization is whether the patient can be safely observed
in the outpatient setting. For example, a patient who has sustained head trauma and needs to
follow head trauma precautions at home, and who is either homeless or lives alone, cannot be
safely discharged. The patient’s ability to pay for services should never enter into ED
disposition decisions. A short-stay ED observation unit can be helpful in avoiding the need for
some inpatient admissions.
19. If the patient does not need admission, how do I arrange a satisfactory
disposition?
Every patient seen in the ED must be referred to a physician or referred back to the ED for
follow-up care. Failure to do so constitutes patient abandonment. Appropriate and specific
follow-up instructions should be given to all patients.
20. What is the most important thing to consider and document in the ED
discharge instructions?
All follow-up instructions must include specific mention of the most serious potential
complication of the patient’s condition. For example, a patient who is being discharged home
with the diagnosis of a probable herniated L4–L5 intervertebral disk should be instructed to
Chapter 1 DECISION MAKING IN EMERGENCY MEDICINE10
return immediately if any bowel or bladder dysfunction develops. This takes into account
the most serious complication of a herniated lumbar disk, which is a central midline disk
herniation (cauda equina syndrome) with bowel or bladder dysfunction and which constitutes
an acute neurosurgical emergency.
21. What two questions should always be asked (and answered) before a patient
is discharged from the ED?
n
Why did the patient come to the ED?
n
Have I made the patient feel better?
Generally, most patients present to the ED because of pain, somatic or psychological, and a
reasonable expectation is that this pain will be acknowledged and appropriately treated. If
such pain cannot be alleviated, a thorough explanation should be given to the patient
regarding the reasons why analgesics cannot be provided. An example of this is a patient with
abdominal pain of unknown etiology, which may evolve into appendicitis, to whom narcotics
are not given because they may delay the recognition of worsening symptoms and localized
abdominal pain. Reassurance is sometimes all that is needed to relieve anxiety about serious
medical conditions such as cancer or heart attack. Other agents such as antiemetics or
antianxiety medications should be administered in the ED to alleviate presenting symptoms.
22. Why is the previous question and answer one of the most important in this
chapter?
Attention to treating and alleviating a patient’s pain will dramatically reduce subsequent
complaints concerning care in the ED and remove one of the significant risk factors for
initiation of a malpractice suit. It is also how you would want to be treated.
23. What about the chart?
The chart must reflect the answers to the preceding questions in this chapter. It need not list
the entire differential diagnosis, but one should be able to ascertain from reading the chart
that the more serious diagnoses were indeed considered. It also must contain appropriate
follow-up instructions.
KEY POINTS: DECISION MAKING IN EMERGENCY MEDICINE
1. Stabilize the patient before performing diagnostic procedures.
2. Always consider the most serious possible cause of every patient’s presentation signs
and symptoms.
3. Always inquire about a patient’s social situation prior to ED discharge.
4. Remember to focus on alleviating the patient’s somatic or psychological pain.
11
CHAPTER 2
MANAGEMENT OF CARDIAC ARREST
AND PRINCIPLES OF RESUSCITATION
Jason S.Haukoos, MD, MSc
1. What are the ABCs of resuscitation?
Airway, breathing, and circulation. The ABCs should be used to guide the resuscitation of all
critically ill patients, including all patients experiencing cardiac arrest.
2. How should cardiopulmonary resuscitation (CPR) be performed as described
by the American Heart Association?
a. If the arrest is in the out-of-hospital setting, activate emergency medical services (EMS) by
calling 911; if it occurs in the hospital, activate the hospital’s cardiac arrest team.
b. Open the airway by performing a head tilt-chin lift or a head tilt-jaw thrust maneuver. These
maneuvers cause anterior displacement of the mandible and lift the tongue and epiglottis
away from the glottic opening. To improve airway patency, suction the mouth and
oropharynx and insert an oropharyngeal or nasopharyngeal airway.
c. Assist breathing by performing mouth-to-mouth, mouth-to-mask, or bag-value-mask
breathing. The recommended technique depends on the clinical setting, the equipment
available, and the rescuer’s skill and training. Although these techniques can sustain
oxygenation and ventilation indefinitely in ideal situations, they can be suboptimal in the
emergency setting. Air leaks around the facemask may result in inadequate ventilation,
insufflation of the stomach, and emesis and aspiration. To reduce the probability of such
problems, deliver slow, even breaths, pausing for full deflation between breaths to avoid
excessive peak inspiratory pressures. Use the Sellick maneuver (using your fingers to
apply continuous posterior pressure to the cricoid cartilage) to compress the esophagus to
reduce the risk of vomiting and aspiration.
d. After opening the airway and initiating rescue breathing, check for spontaneous circulation by
palpating for a carotid or femoral pulse. If the patient is pulseless, begin chest compressions.
Compress the chest smoothly and forcefully 100 times per minute, allowing for complete chest
recoil. Minimize interruptions in chest compressions, providing approximately 30 compressions
followed by two breaths until a defibrillator arrives or the patient begins to move.
3. How important is ventilation during resuscitation efforts in the out-of-hospital
setting?
Active assisted ventilation during cardiac arrest may not always be beneficial and is now
thought to be less important than previously believed. If performing ventilation contributes to
interrupted chest compressions or excessive intrathoracic pressures, it may be deleterious.
4. What is passive oxygen insufflation?
Passive oxygen insufflation is accomplished by placing an oropharyngeal airway and a
nonrebreather facemask with high-flow oxygen on the patient. Preliminary data suggest this
approach may be superior when compared to a traditional active ventilatory approach using a
bag-valve in conjunction with other cardiocerebral resuscitation strategies.
5. What is the squeeze, release, release method of providing mechanical
ventilation?
Squeeze, release, release was first described in 1997 as a bag-valve-mask technique to
provide an appropriate level of ventilation to pediatric patients. Subsequently, this technique
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION12
has been extended to adult patients and consists of performing ventilation at a rate consistent
with someone saying, “squeeze, release, release” to maintain an appropriate ventilation rate.
6. What are the exceptions to the rule of the ABCs?
a. Monitored cardiac arrest. When a patient in a monitored setting experiences sudden
pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), immediate electrical
defibrillation is the priority.
b. Traumatic arrest. In traumatic cardiac arrest, closed-chest CPR is usually ineffective.
In trauma, the cause of the arrest may be a tension pneumothorax, cardiac tamponade, or
exsanguinating hemorrhage from the thorax or abdomen. An immediate thoracotomy, not
CPR, is indicated. When neck injury is suspected, a jaw thrust (never a head tilt) should be
used to open the airway.
7. Explain the mechanism of blood flow during CPR?
Two basic models explain the mechanism of blood flow during CPR. In the cardiac pump
model, the heart is squeezed between the sternum and the spine. Chest compressions result
in systole, and the atrioventricular valves close normally, ensuring unidirectional, antegrade
flow. During the relaxation phase (diastole), intracardiac pressures fall, the valves open, and
blood is drawn into the heart from the lungs and vena cavae.
In the thoracic pump model, the heart is considered a passive conduit. Chest
compressions result in uniformly increased pressures throughout the thorax. Forward blood
flow is achieved selectively in the arterial system because the stiff-walled arteries resist
collapse and because retrograde flow is prevented in the great veins by one-way valves. In
addition, chest recoil results in increased negative intrathoracic pressures, which improve
ventricular filling and coronary blood flow. These mechanisms have been substantiated in
animal models and both likely contribute to blood flow during CPR.
8. Is blood flow to the brain and heart adequate during CPR?
Even when performed by experts, CPR provides only approximately 30% of normal blood flow
to the brain and 10% to 20% of normal blood flow to the heart. Blood flow to the heart occurs
during the relaxation phase of CPR, whereas blood flow to the brain occurs during the
compression phase of CPR. This is the foundation for the American Heart Association’s
recommended CPR duty cycle of 50% (the ratio of time spent in compression to the time
spent in relaxation).
9. What is coronary perfusion pressure (CPP)?
Coronary perfusion pressure is defined as the aortic pressure minus the right atrial pressure
during diastole.
10. What is the association between CPR, CPP, and return of spontaneous
circulation (ROSC)?
Better CPR produces better CPPs. Higher CPPs translate into higher rates of ROSC. This
emphasizes the importance of performing good CPR and explains how vasopressors
(e.g., epinephrine) impact rates of ROSC by increasing CPPs.
11. Describe hands off CPR?
Hands off CPR refers to lifting the hands off the chest wall during decompression to
maximize chest recoil. Incomplete chest wall recoil during CPR has been shown to result in
hemodynamic deterioration of forward blood flow in animal models. In addition, in an
observational human study, incomplete chest recoil was common during CPR.
12. Discuss the role of pharmacologic therapy during CPR.
The immediate goal of pharmacologic therapy is to improve CPPs, and thus, myocardial
blood flow, which correlates with ROSC. Adrenergic agonists (e.g., epinephrine) augment the
aortic-to-right atrial diastolic gradient by increasing systemic vascular resistance. Reports
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION 13
suggest that nonadrenergic agonists (e.g., vasopressin) may be more effective than adrenergic
agonists in improving myocardial blood flow. Additional clinical studies suggest that
amiodarone improves rates of successful defibrillation and prevents recurrent postarrest
dysrhythmias. These antifibrillatory effects may be independent of myocardial blood flow.
KEY POINTS: STANDARD DOSES OF CARDIAC ARREST
MEDICATIONS
1. Epinephrine: 1 mg IV/IO push
2. Vasopressin: 40 U IV/IO push
3. Atropine: 1 mg IV/IO push
4. Amiodarone: 300 mg IV/IO push
5. Lidocaine: 1.0-1.5 mg/kg IV/IO push
13. Under what circumstances should CPR be used before defibrillation?
A growing body of research suggests that patients with untreated prolonged VF may benefit
from CPR for 2 to 3 minutes prior to defibrillation, and several communities have adopted this
in the prehospital setting.
14. What are the indications for open chest cardiac massage?
The primary indication for open chest cardiac massage is traumatic arrest. However, several
other nontrauma-related indications include: hypothermia, pulmonary embolism, cardiac
tamponade, abdominal hemorrhage, third-trimester pregnancy, and patients with chest wall
deformities that prevent adequate chest compressions.
15. What are the most common causes of cardiopulmonary arrest?
Although the incidence of VF appears to be declining, it still remains a common initial rhythm
encountered in patients suffering from cardiac arrest. Underlying coronary artery disease
accounts for the majority of VF arrests. Other etiologies of VF include: drug toxicity, electrolyte
disturbances (e.g., hyperkalemia), and prolonged hypoxemia.
The second most common initial rhythm encountered is asystole. This commonly results
from prolonged untreated VF and is due to severe hypoxia and acidemia. Other causes of
asystole include: drug toxicity, electrolyte disturbances, and hypothermia.
Pulseless electrical activity (PEA) is the third most commonly encountered initial arrest
rhythm. As with asystole, PEA commonly results from prolonged untreated VF or defibrillation
of VF after a prolonged untreated period (usually .5 minutes). Other causes of PEA include:
hypovolemia, hypoxia, cardiac tamponade, tension pneumothorax, hypothermia, massive
pulmonary embolism, drug toxicity, electrolyte disturbances, acidemia, or myocardial
infarction.
16. What are other reversible causes and immediate treatments of
cardiopulmonary arrest?
n
Hyperkalemia. Calcium chloride (preferred over calcium gluconate), sodium bicarbonate,
insulin and glucose, and nebulized albuterol.
n
Anaphylaxis. Intravascular volume expansion (using crystalloid) and epinephrine.
n
Cardiac tamponade. Pericardiocentesis or pericardiotomy.
n
Tension pneumothorax. Thoracic decompression.
n
Hypovolemia. Intravascular volume expansion using crystalloid solutions. In the setting of
trauma, blood products should be given judiciously and concomitantly with crystalloid. Always
consider using a level I infuser when large volumes are required over a short period of time.
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION14
n
Torsades de pointes. Defibrillation, magnesium sulfate, isoproterenol, or overdrive pacing.
n
Toxic cardiopulmonary arrest
Carbon monoxide poisoning occurs after prolonged exposure to smoke and inhalation of
exhaust from incomplete combustion. High-flow and hyperbaric oxygen and
management of acidosis are the cornerstones of treatment.
Cyanide poisoning occurs after intentional ingestion or after exposure to fire involving
synthetic materials. The antidote for this includes intravenous (IV) sodium nitrite and
sodium thiosulfate.
Tricyclic antidepressants act as type Ia antidysrhythmic agents and cause cardiac
conduction slowing, ventricular dysrhythmias, hypotension, and seizures. Vigorous
serum alkalinization and seizure control are required.
n
Primary asphyxia. In addition to anaphylaxis, obstructive asphyxia may occur after foreign
body aspiration, inflammatory conditions of the hypopharynx (e.g., epiglottitis or
retropharyngeal abscess), or neck trauma. The latter results in edema or hematoma
formation, subcutaneous emphysema, or laryngeal or tracheal disruption. Treatment
includes establishment of a patent airway via endotracheal intubation or by cricothyrotomy
and assisted ventilation with 100% oxygen.
17. How should VF be treated?
Rapid treatment is essential as the prognosis worsens with each untreated minute.
Standard treatment consists of immediate defibrillation. Recommended energy levels include
beginning at maximal or near-maximal energy (e.g., 150 J–200 J biphasic). The
antidysrhythmic agent of choice is amiodarone, which enhances the rate of successful
defibrillation and reduces the rate of recurrent VF after successful conversion. Administration
of epinephrine or vasopressin before defibrillation may improve defibrillation success; in
addition, CPR before defibrillation (see question 13) may also improve defibrillation success
in the setting of prolonged VF.
18. What’s the difference between monophasic and biphasic defibrillation?
The terms monophasic and biphasic refer to the energy waveforms produced by the
defibrillation device. Monophasic waveforms vary in speed in which the waveform returns to
the zero voltage point, whereas biphasic waveforms deliver current that first flows in a positive
direction for a specific duration, then reverses direction for a specific duration. Biphasic
defibrillation achieves the same defibrillation success rates as monophasic defibrillation but at
significantly lower energy levels, resulting in less postresuscitation cardiac dysfunction.
19. What if VF persists after initial treatment?
a. Perform endotracheal intubation and ensure adequate oxygenation and ventilation.
b. Continue CPR.
c. Administer epinephrine (1 mg IV push) or vasopressin (40 U IV push) to augment aortic
diastolic blood pressure and to improve myocardial perfusion.
d. Administer amiodarone (300 mg IV push). Amiodarone may be repeated at 150 mg IV
push after 3 to 5 minutes.
e. Consider administering magnesium sulfate (1 g–2 g IV push).
f. Although lidocaine or procainamide have not been shown to improve defibrillation success
rates or restore perfusing rhythms in patients with VF, also consider their administration
(lidocaine 1.0–1.5 mg/kg IV push or procainamide 17 mg/kg at a rate of 30 mg/min
intravenously).
20. Describe the three-phase model of cardiac arrest?
n
The first phase, called the electrical phase, suggests that immediate defibrillation is the
most efficacious treatment within the first 4 minutes of VF.
n
The second phase, called the circulatory phase, follows the first phase and suggests
that successful ROSC and overall survival are maximized with a period of CPR before
defibrillation.
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION 15
n
The third phase, called the metabolic phase, is reached after about 10 minutes, is
associated with a profound systemic inflammatory response syndrome, and no current
therapies offer survival benefit in this setting.
21. How should asystole be treated?
a. Confirm the absence of cardiac activity in more than one electrocardiogram (ECG) lead.
Check for loose or disconnected cables and monitor leads. Finally, increase the amplitude
to detect occult, fine VF.
b. Administer epinephrine (1 mg IV push) or vasopressin (40 U IV push).
c. Administer atropine (1 mg IV push) to counteract high vagal tone.
KEY POINTS: MANAGEMENT OF CARDIAC ARREST
CPR and defibrillation are the most important components to the initial management of the
cardiac arrest patient.
1. Treat VF with immediate defibrillation (if the arrest is witnessed), CPR, then defibrillation
(if the arrest is unwitnessed), or amiodarone.
2. If the arrest is due to PEA, remember its common reversible causes (i.e., hypovolemia,
hypoxia, cardiac tamponade, tension pneumothorax, hypothermia, massive pulmonary
embolism, drug toxicity, electrolyte disturbances, acidemia, or myocardial infarction)
and treat them appropriately.
3. If the arrest is due to asystole, remember to exclude fine VF.
22. Is defibrillation or electrical pacing useful for asystole?
Defibrillation is reserved for cases in which differentiation between asystole and fine VF is
difficult. In these ambiguous situations, defibrillation should be employed after administration
of epinephrine. Electrical pacing is occasionally attempted for asystole but is rarely effective in
restoring pulses.
23. What are the appropriate routes of drug administration?
IV administration is the preferred route of drug therapy during CPR. A central venous
catheter is ideal, although placement should not supersede optimal resuscitation, including
performance of chest compressions. Use of a peripheral venous catheter results in a slightly
delayed medication onset of action, although the peak drug effect is similar to that for the
central route. An intraosseous (IO) line may also be used and should take precedence over
other approaches, including intramuscular or endotracheal routes. All drugs used for
resuscitation can be given in conventional doses using IO access. Intracardiac administration
should be reserved for cases of open cardiac massage. Endotracheal drug administration
should be used as a last resort.
24. I thought IO cannulation was only used as a last resort and for pediatric
patients. What’s the deal?
IO cannulation provides a quick, effective, and safe means to access a noncollapsible venous
plexus, either in the proximal tibia, proximal humerus, or sternum. (The sternum should be
avoided as an IO site in cardiac arrest because it would interfere with chest compressions.)
It can be used in all age groups and allows for effective fluid resuscitation, drug delivery, and
blood sampling for laboratory evaluation. In fact, the IO functions similar to that of a central line.
25. When may prehospital resuscitation efforts be terminated?
According to the most recent American Heart Association’s Advanced Cardiac Life Support
(ACLS) guidelines, prehospital resuscitation can be discontinued by EMS authorities when a
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION16
valid no-CPR order is presented to the rescuers or when a patient is deemed nonresuscitable
after an adequate trial of ACLS, including successful endotracheal intubation, achievement of
IV access and administration of appropriate medications, determination of a persistent
asystolic or agonal rhythm, and when no reversible cause for the arrest is identified.
26. Which vasopressor should I administer in the setting of cardiac arrest,
epinephrine or vasopressin?
This remains controversial. Epinephrine has been evaluated in human trials in approximately
9,000 patients. The recommended 1-mg dose was extrapolated from animal research, and
trials comparing this dose with high-dose regimens (i.e., 0.1 to 0.2 mg/kg) demonstrated
increased rates of ROSC in patients who received high-dose epinephrine; however, these
studies have not shown improvements in survival or survival with good neurologic outcomes.
Vasopressin acts directly on V
1
-receptors and, unlike epinephrine, is more effective in an
acidemic environment. Vasopressin has been compared to epinephrine in three human trials,
totaling approximately 1,500 patients without a significant difference in survival.
27. Should I use amiodarone in the setting of cardiac arrest?
Amiodarone is a class III antidysrhythmic agent used, in part, to treat VT or VF. Two
randomized clinical trials have demonstrated a survival to hospital admission (but not to
hospital discharge) benefit for amiodarone over placebo and lidocaine, respectively. In most
settings amiodarone has become the first-line agent for treating VT or VF.
28. Should I routinely administer sodium bicarbonate during resuscitation?
Sodium bicarbonate is not recommended as routine therapy in the setting of cardiac arrest.
A no- or low-flow state causes progressive respiratory and metabolic acidosis as a result of
accumulation of CO
2
and lactate. Neither state can be corrected without adequate oxygenation,
ventilation, and tissue perfusion. At present, no clinical data support its routine use except in
cases of hyperkalemia, tricyclic antidepressant overdose, or preexisting metabolic acidosis.
29. Should I routinely administer calcium during resuscitation?
Calcium is not recommended as routine therapy in the setting of cardiac arrest. Although no data
exist to support its routine use, it may be beneficial in the setting of hyperkalemia (most often
seen in chronic renal failure/dialysis patients), hypocalcemia, or calcium channel blocker toxicity.
30. What should I do after ROSC?
Once ROSC is achieved, the vulnerable postresuscitation period begins. This period is marked
by a profound systemic inflammatory response syndrome resulting from whole-body ischemia
and reperfusion. Patients commonly develop hemodynamic instability, resulting in multiple
organ dysfunction and subsequent death (hours to days later). Prompt recognition and
treatment of the inciting event and meticulous intensive care unit support are required to
provide patients with the best probability for survival. Use of hemodynamic and inotropic
agents is important for supporting patients during this period, and recent description of a
hemodynamic optimization protocol has been reported. In addition, mild therapeutic
hypothermia should be performed to improve neurologic recovery.
31. What percentage of all cardiac arrest patients survive to hospital discharge?
5%.
WEBSITES
www.americanheart.org/
http://circ.ahajournals.org/content/vol112/24_suppl/
Chapter 2 MANAGEMENT OF CARDIAC ARREST AND PRINCIPLES OF RESUSCITATION 17
BIBLIOGRAPHY
1. Aufderheide TP, Pirallo RG, Yannopoulos D, et al: Incomplete chest wall decompression: a clinical evaluation of
CPR performance by EMS personnel and assessment of alternative manual chest compression-decompression
techniques. Resuscitation 64:353–362, 2005.
2. Bobrow BJ, Ewy GA: Ventilation during resuscitation efforts for out-of-hospital primary cardiac arrest. Curr
Opin Crit Care 15:228–233, 2009.
3. Dorian P, Cass D, Schwartz B, et al: Amiodarone as compared with lidocaine for shock-resistant ventricular
fibrillation. N Engl J Med 346:884–890, 2002.
4. Gaieski DF, Band RA, Abella BS, et al: Early goal-directed hemodynamic optimization combined with therapeutic
hypothermia in comatose survivors of out-of-hospital cardiac arrest. Resuscitation 80:418–424, 2009.
5. Gausche M, Lewis RJ, Stratton SJ, et al: Effect of out-of-hospital pediatric endotracheal intubation on survival
and neurologic outcome: a controlled clinical trial. JAMA 283:783–790, 2000.
6. Hypothermia after Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neurologic
outcome after cardiac arrest. N Engl J Med 346:549–556, 2002.
7. Paradis NA, Martin GB, Rivers EP, et al: Coronary perfusion pressure and the return of spontaneous circulation
in human cardiopulmonary resuscitation. JAMA 263:1106–1113, 1990.
8. Wenzel V, Krismer AC, Arntz, HR, et al: A comparison of vasopressin and epinephrine for out-of-hospital
cardiopulmonary resuscitation. N Engl J Med 350:105–113, 2004.
9. Wik L, Hansen TB, Fylling F, et al: Delaying defibrillation to give basic cardiopulmonary resuscitation to patients
with out-of-hospital ventricular fibrillation: a randomized trial. JAMA 289:1389–1395, 2003.