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7. When an adult victim has a pulse but is breathless, what is the recommended
rate of rescue breathing?
Once every 5 to 6 seconds (10 to 12 breaths/min).
8. When a child or infant has a pulse but is breathless, what is the recommended
rate of rescue breathing?
Once every 3 seconds (20 breaths/min). Add compressions if the pulse remains <60 with signs of
poor perfusion.
9. What is the best indicator of effective ventilation?
Seeing the chest rise when delivering breaths.
10. What are the effects of excessive ventilation?
Excessive ventilation (giving breaths too rapidly or with too much force) may decrease cardiac
output and increase the risk of regurgitation and aspiration.
Excessive ventilation increases intrathoracic pressure, decreasing venous return to the heart and
in turn diminishing cardiac output. It increases the risk of regurgitation and aspiration by forcing air into
the stomach, causing gastric inflation once the esophageal opening pressure is exceeded. To reduce
the risk of aspiration, you should deliver air until you make the victim’s chest rise and take 1 second to
deliver the breath. You should also watch the victim’s chest fall as you allow time for the lungs to empty.
11. In a victim with a pulse, how often should the pulse be checked during rescue
breathing?
Once every 2 minutes.
12. What happens if chest compressions are interrupted?
There will be a decreased organ perfusion. During CPR, blood flow is completely dependent on chest
compressions. Any interruption in CPR results in a lack of blood flow during that time.
13. In a pulseless victim, how often should the pulse/rhythm be checked during CPR?
Every 2 minutes. The goal is to minimize interruption during compressions. Do not take longer than
10 seconds to assess the pulse.
14. What are the indicators of effective CPR?
• Seeingthechestrisewhenrescuebreathingisdelivered
• Presenceofapulseduringchestcompressions(Intra-arterialrelaxationpressuresoflessthan
20 mm Hg will not achieve return of spontaneous circulation [ROSC].)
• Capnography(end-tidalCO2) >10 to 15 mm Hg (End-tidal CO2 of less than 10 mm Hg will not
achieve ROSC.)
The team leader should also monitor the quality of the compressions and instruct another
provider to switch if unable to provide high-quality compressions.
15. What are the signs of mild versus severe airway obstruction?
• Mild:goodairexchange,forcefulcough,possiblewheezing
• Severe:poortonoairexchange,weakorabsentcough,high-pitchednoisesduringinhalation,no
noises, respiratory difficulty, unable to speak, cyanosis (turning blue), universal choking sign
16. In the initial assessment, when is breathing assessed?
When assessing the patient for responsiveness, also check for normal breathing. Scan the chest for
movement (for 5 to 10 seconds). If the patient is not breathing or is not breathing normally, begin
chest compressions. After 30 chest compressions, open the airway and deliver two breaths. Abnormal breathing includes gasping for air or agonal breathing. “Look, listen, and feel” was removed
from the 2010 AHA guidelines as a way to assess breathing due to excess delay and confusion
when patients exhibited agonal gasping.
17. What is the most frequent cause of airway obstruction in an unconscious
person?
The tongue.
18. Where is the correct location for applying pressure for external chest compressions in adult and children victims?
The center of the chest, between the nipples (lower half of the sternum). In adults, use the heels
of both hands, with one stacked on the other to perform the compressions. In children ages 1 to 8
years, use the heel of one hand.
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19. Where is the ideal location for applying pressure for external chest compressions in infants?
One finger width below the nipple line, with care being taken to stay off the xiphoid process. Use
two fingers to perform the compressions or use the two thumb encircling hand technique if two
rescuers are available.
20. What is the depth of external chest compressions in adults?
At least 2 inches.
21. What is the depth of external chest compressions in children?
At least one-third the depth of the child’s chest (about 2 inches).
22. What is the depth of external chest compressions in infants?
At least one-third the depth of the infant’s chest (about 1.5 inches).
23. What is the rate of external chest compressions for adults, children, and infants?
>100/min. The number of chest compressions delivered per minute is determined not only by the
rate of compressions, but also by the frequency and duration of interruptions. You must provide an
adequate compression rate and minimize interruptions to provide for adequate compressions.
24. What is the ratio of external chest compressions to breaths for one or two rescuers with an adult victim?
30 compressions for every two breaths (30:2) for both one- and two-rescuer CPR.
25. What is the rate of external chest compressions to breaths for one or two rescuers with a child or infant?
• Onerescuer:30:2(30compressionsforeverytwobreaths).
• Tworescuer:15:2(15compressionsforeverytwobreaths).
26. What is the rate of ventilation in a patient with an advanced airway?
One breath every 6 to 8 seconds (8 to 10 breaths/min). These breaths are not synchronous with
chest compressions.
27. What is the length of time recommended to deliver each breath to an adult
victim?
About 1 second/breath. You should see visible chest rise. Allow for full exhalation between breaths.
28. Why is it important to allow for full chest recoil?
When the chest recoils (re-expands) after each compression, it allows blood to flow into the heart.
This allows for the next chest compression to create blood flow because compressions pump the
blood in the heart into the rest of the body. If the chest does not completely recoil, it decreases the
blood flow created by each chest compression.
29. What is the recommended method of clearing foreign body airway obstructions
in infants?
A combination of back slaps and chest thrusts: five back slaps followed by five chest thrusts,
repeated until the object is dislodged. Do not use the Heimlich maneuver because an infant’s liver
is not well protected by the ribs and is at risk for injury with this technique. If the infant becomes
unresponsive, begin CPR.
30. What is the recommended method of clearing foreign body airway obstructions
in responsive children and adults? What do you do if the victim is unresponsive?
The Heimlich maneuver (abdominal thrusts) is used in responsive victims. If the victim is pregnant
or obese, perform chest thrusts instead of abdominal thrusts. If the victim becomes unresponsive,
activate EMS and begin CPR, starting with compressions.
31. Why should blind finger sweeps not be used in children and infants?
The object may be pushed deeper in the airway. Only attempt to remove the object if you can see it
and it can be easily removed with your fingers.
32. After successful resuscitation (ROSC), what is done with the patient?
If signs of circulation and breathing return, place the patient in the recovery position. Continue
to monitor pulse and blood pressure. Leave the AED in place and turned on while monitoring the
patient. The patient should be transported to the appropriate hospital or critical care unit. Multidisciplinary care is vital.
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33. What are four conditions that require you to change how you use an AED?
1. Victim is in water (remove to dry area and dry off chest)
2. Victim has implanted pacemaker or defibrillator (place electrodes away from device)
3. Victim has transdermal patch (remove and clean area)
4. Victim has a hairy chest (quickly pull pads to remove hair and replace pads)
34. Can you use an AED in children and infants?
Yes. Ideally, in children from 1 to 8 years of age an AED should be used with a dose attenuator if
available. If not available, a standard AED may be used. For infants (<1 year old), a manual defibrillator is preferred. If not available, then an AED with a pediatric dose attenuator would be the next
choice, but if neither is available a standard AED may be used.
35. What does an AED/defibrillator do?
An AED/defibrillator delivers an electric shock to the heart that stops the movement of the heart
muscle fibers and allows the electrical system to reset itself. It does not restart the heart, but it
resets it, hopefully allowing an organized rhythm to take over. If an organized rhythm occurs and the
heart starts contracting effectively, a pulse will be generated, indicating ROSC.
36. What are the major differences between initial resuscitation efforts for pediatric
patients vs. adult patients?
With a child or infant victim, CPR should be started promptly prior to EMS activation if the arrest
is not witnessed. EMS should be called after five cycles (approx. 2 minutes) of CPR have been
performed. In adults, EMS should be activated immediately. Another major difference is, when two
rescuers are available, the compression to breath ratio for children and infants should be 15:2
(compared to adults, for whom the ratio stays at 30:2).
37. Where should you check for a pulse in an infant? In a child?
The brachial pulse in an infant and the carotid or femoral pulse in a child.
38. What age ranges delineate infants and children?
An infant is younger than age 1, and a child is age 1 year old to puberty.
39. What are the four universal steps of AED operation?
1. Power on AED.
2. Attach AED pads to victim’s chest (use adult pads for victims >8 years old).
3. Clear victim and analyze heart rhythm.
4. Clear victim and deliver shock if indicated.
40. What is the goal for when a shock should be delivered after a victim collapses?
Less than 3 minutes. Early defibrillation results in better outcomes, and the goal is shock delivery
41. What is the predominant determinant of successful CPR?
Time to restoration of spontaneous circulation, which itself is a function of the time to effective chest
42. How do you open an airway? What do you do differently if the victim is an
The two basic maneuvers to open an airway are head tilt with chin lift and jaw thrust. If the
43. What maneuver should the rescuer first use to open the airway in an otherwise
In an uninjured patient, perform the head tilt with chin lift maneuver to open the airway. In an uncon-
Directly after the shock is delivered (or if no shock is needed), immediately resume chest
compressions.
within 3 minutes from the time of collapse.
compression and time to defibrillation in ventricular fibrillation. Early CPR, minimizing interruptions,
and reducing the time from collapse to defibrillation can result in quicker restoration of spontaneous
circulation, which improves survival in hospital and nonhospital settings.
infant?
victim is an infant, do not extend the head beyond the neutral position because it may block the
airway.
uninjured patient? What if the patient has a suspected neck injury?
scious patient with a suspected neck injury, the jaw thrust should be performed. The jaw thrust pulls
the mandible forward, which pulls the tongue and epiglottis anteriorly off the upper airway (with
minimal cervical hyperextension). This is only possible with two rescuers.
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44. How much oxygen does mouth-to-mouth deliver compared to other techniques?
• Mouth-to-mouthventilationdeliversapproximately17%inspiredoxygenand4%carbondioxide.
• Bag-maskventilationdelivers21%oxygen.
• Bag-maskventilationwithanoxygensupplycandelivercloseto100%oxygen.
45. What are some of the complications of external chest compression?
Rib and sternal fractures are the most common iatrogenic injuries. Other complications include
cardiac or pericardial injuries (hematomas, lacerations, ruptures) and damage to other adjacent
structures (e.g., pneumothorax, GI laceration), but these injuries are rare. The number of iatrogenic
injuries increases when the compression depths exceed 6 cm (2.3 inches), but these injuries are
rarely fatal. Do not let fear of complications interfere with effective chest compression.
46. What are the components of high-quality CPR?
According to the advanced cardiac life support (ACLS) guidelines, the following are components of
high-quality CPR:
1. Rate ≥100/min
2. Compression depth of ≥2 inches in adults
3. Complete chest recoil after each compression
4. Minimize interruptions in compressions.
5. Switch providers every 2 minutes to prevent fatigue.
6. Avoid excessive ventilations; one should only provide 500 to 600 ml of tidal volume per breath,
which correlates to half a bag squeeze on the AMBU bag.
47. Why do we need to avoid excessive ventilation during CPR?
Over-ventilation during CPR means too much volume is forcefully delivered into the patient. This
causes multiple problems including gastric distention, which is caused when pressure overcomes
the esophageal sphincters. This may lead to increased risk of aspiration. Over-ventilation also
increases intrathoracic pressure, which decreases venous return and decreases chances of survival.
48. How can one monitor the quality of CPR?
• End-tidalCO2 of less than 10 mm Hg will not achieve ROSC.
• Intra-arterialrelaxationpressuresoflessthan20mmHgwillnotachieveROSC.
• Theteamleadershouldalsomonitorthequalityofthecompressionsandinstructanotherpro-
vider to switch if unable to provide high-quality compressions.
ADVANCED CARDIAC LIFE SUPPORT
49. Why the change from ABC to CAB?
When an adult suffers from cardiac arrest, it is most often caused by ventricular fibrillation or ven-
tricular tachycardia. The heart is quivering but fails to effectively deliver blood to the heart and other
organs. By initiating chest compressions, the responder serves to pump blood and deliver oxygen
to organs. By bypassing the “Airway and Breathing” part of the algorithm, one can deliver oxygen
without additional delays and increase the chance of survival. Chest compressions will generate
negative pressure upon recoil that will allow ambient air to be entrained into the pulmonary system.
50. When should a responder alter the CAB and utilize the ABC algorithm for
resuscitation?
Airway and Breathing algorithm components should be emphasized when the clinical scenario
justifies their use, such as a patient in cardiac arrest secondary to drowning or asphyxiation. For
a drowned patient, clearing the airway and providing rescue breaths will allow increased oxygen
delivery. Patients with airway obstruction and the resulting hypoxia benefit from efficient maneuvers
to clear the airway. To put it another way, if the patient’s heart started beating again, but he had a
collapsed airway, no oxygen would be delivered and resuscitation would be futile.
51. What is agonal breathing?
Absent breathing or nonfunctional breathing. This includes gasping, which does not move oxygen.
Agonal gasps are not effective breathing. One should not be fooled into a false sense of security
with agonal breathing; respiratory arrest is occurring and treatment should commence.
†
Written by Robert C. Lampert and Shahid R. Aziz.
†
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52. What are the major updates for ACLS based on the 2010 AHA guidelines?
1. For the cardiac arrest algorithm, emphasis is centered on a 2-minute cycle of chest
compressions.
2. Continued emphasis for vasopressors to be used every 3 to 5 minutes. This may be either epi-
nephrine or vasopressin.
3. Administer amiodarone for refractory ventricular fibrillation or ventricular tachycardia.
4. Atropine is no longer recommended for use in pulseless electrical activity or asystole.
53. When should hypothermia be considered in the ACLS protocol?
The goal of controlled hypothermia is to optimize survival and neurologic function when brain
injury is suspected. Hypothermia is the only intervention shown to improve neurologic recovery.
This intervention should be considered for any patient who is comatose after ROSC and V-fib was
the presenting rhythm. Multiple studies have demonstrated improved outcomes for patients whose
temperature was decreased to 32-34° C for 12 to 24 hours.
54. What is the function and significance of waveform capnography?
Waveform capnography is a measure of CO2 with respiration. The waveform rises with expira-
tion and returns to zero upon inhalation. It serves as the most reliable indicator of endotracheal tube position after intubation. It also serves as a monitor for effectiveness of chest
compressions.
55. What are the current guidelines for cricoid pressure?
Per the 2010 guidelines, the AHA states one should not routinely use cricoid pressure during cardiac
arrest. Cricoid pressure is a maneuver that is difficult to master, may not prevent aspiration as once
thought, and may delay or prevent placement of advanced airway.
56. Where are the sites that intraosseous access can be achieved?
In general, the anatomic sites that are common include sternum, humeral head, anterior superior
iliac spine, medial malleolus, distal radius, distal femur, and proximal tibia. Certain devices are site
specific, so one should be familiar with the specific device at one’s institution. Similar to with all
ACLS medications, one should flush the meds with normal saline to propel the medication into the
central circulation.
57. How is the diagnosis of cardiac arrest established?
By definition, the patient is in full cardiac arrest if he or she:
• Isnotresponsive
• Isnotbreathing
• Hasnopulse
58. What are the three mechanisms of cardiac arrest?
1. V-fib/pulseless VT
2. Pulseless electrical activity
3. Asystole
V-fib is most commonly present during the first minute following the onset of cardiac arrest.
59. Which types of chest pain suggest cardiac ischemia?
• Uncomfortablesqueezingpressure,fullness,orpaininthecenterofthechestlastinglongerthan
15 minutes
• Painthatradiatestotheshoulder,neck,arm,andjaws
• Painbetweentheshoulderblades
• Chestdiscomfortwithlight-headedness,fainting,sweating,andnausea
• Afeelingofdistress,anxiety,orimpendingdoom
60. What is the recommended initial management for a stable adult patient with
chest pain that is suggestive of ischemia?
1. Call for help.
2. Perform immediate assessment including:
• Vital signs and SaO2 monitoring
• IV access and electrocardiogram (ECG)
• Targeted history and physical exam
• Initial serum cardiac marker levels, electrolytes, and coagulation studies
• Portable chest X-ray
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3. Immediate general treatment:
• Oxygen at 4 L/min
• Aspirin (160 to 325 mg)
• Nitroglycerin (sublingual or spray)
• Morphine (IV) if pain is not relieved by nitroglycerin
• Memory aid: “MONA greets all patients” (morphine, oxygen, nitroglycerin, and aspirin).
61. What is the initial assessment of a 12-lead ECG in patients with cardiac
ischemia?
• ST-segmentelevationornew-onsetleftbundlebranchblock(LBBB)stronglysuggestsamyocar-
dial injury. New LBBB is caused by occlusion of the left anterior descending (LAD) branch of the
left coronary artery. LAD occlusion causes a loss of a large amount of myocardium.
• ST-segmentdepressionorT-waveinversion(ischemia)
• Non-diagnosticornormalECG
62. What is the relationship between 12-lead EGC findings and coronary artery
disease?
ECG relationship:
• Anteriormyocardiuminjuryorinfarct:leadsV3andV4
• Septalmyocardiuminjuryorinfarct:leadsV1andV2
• Lateralmyocardiuminjuryorinfarct:leadsI,aVL,V5,andV6
• Inferiormyocardiuminjuryorinfarct:leadsII,III,andaVF
Coronary artery branches relationship:
• LADarteryocclusion:leadsV1throughV6
• Circumexarteryocclusion:leadsI,aVL,possiblyV5,andV6
• Rightcoronaryarteryocclusion:leadsII,III,aVF
63. What is the most common arrhythmia following electrical shock?
The most common arrhythmia caused by electrocution is V-fib; hence cardiac arrest is the primary
cause of death from electrical shock. Other rhythms that may occur following electrical shock are VT
progressing to V-fib and asystole.
Electrical shock is the cause of more than 1000 deaths/year in the United States. It results
in injuries ranging from unpleasant sensation to instant cardiac death. Exposure to high-tension
current (>1000 V) is more likely to produce serious injury. However, death can result from exposure
to relatively low voltage (100 V) household currents. Alternating current (AC) is more dangerous than
direct current (DC). AC produces muscle tetany, which may prevent the victim from releasing the
electrical source and thus prolong the contact.
64. What is V-fib?
V-fib is a cardiac dysrhythmia that occurs when multiple areas within the ventricles display unsyn-
chronized depolarization and repolarization. As a result, the ventricles do not contract as a unit.
Instead, the ventricles appear to quiver, or fibrillate, as multiple areas of the ventricle are contracting and relaxing in a disorganized fashion. The net result is no cardiac output and no pulse.
65. How is V-fib/pulseless VT treated initially according to the AHA
recommendations?
1. The initial treatment for V-fib is always defibrillation.
2. Begin with the universal algorithm:
• Assess the airway, breathing, and circulation (ABCs).
• Ascertain that the patient is in cardiac arrest.
• Begin CPR with cycles of 30 compressions and two breaths until defibrillator is attached, and
3. Give one shock:
• Manual biphasic: device specific (120 to 200 J)
• AED: device specific
• Monophasic: 360 J
4. If V-fib persists:
• Resume CPR immediately, intubate, and establish IV access.
• Administer epinephrine 1 mg IV/IO (intraosseous) and repeat every 3 to 5 minutes, or you may
confirm V-fib.
administer one dose of vasopressin 40 U IV/IO to replace the first or second dose of epinephrine.
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5. Give five cycles of CPR.
6. Give one shock if the rhythm is shockable.
7. ResumeCPRimmediatelyaftertheshock.
8. Consider antiarrhythmic medications.
66. What is tachycardia?
Tachycardia means that there is a rapid heart rate. The normal adult heart rate is considered by
most to be between 60 and 100 beats/min. Thus a heart rate of >100 beats/min can be classified as
tachycardia. Not all patients with a heart rate of 100 beats/min or more will require treatment. The
following cardiac rhythms are considered tachyarrhythmias:
1. Atrial flutter (A-flutter)/atrial fibrillation (A-fib)
2. Narrow-complex tachycardia:
• Junctional tachycardia
• Paroxysmal supraventricular tachycardia (PSVT)
• Multifocal or ectopic atrial tachycardia
3. Wide-complex tachycardia:
• SVT with aberrant conduction
• Stable monomorphic VT
• Stable polymorphic VT (with and without normal baseline QT interval)
• Torsades de pointes
• Symptoms: shortness of breath, chest pain, dyspnea on exertion, and altered mental status
• Signs: pulmonary edema, rales, rhonchi, hypotension, orthostasis, jugular vein distention,
67. Which tachyarrhythmias are supraventricular?
If the QRS complex is narrow, then the tachyarrhythmia is supraventricular. This means the
• Sinustachycardia
• A-utter
• A-fib
• PSVT
• Wide-complextachycardiaofuncertaintype
• VT
68. What is the pathophysiology of PSVT?
PSVT is a distinct clinical syndrome characterized by repeated episodes of tachycardia with abrupt
69. What are the types of narrow-complex tachycardia?
• PSVT:causedbyareentrycircuitmechanism
• Ectopicormultifocalatrialtachycardia:causedbyanautomaticfocus
• Junctionaltachycardia:causedbyautomaticfocusthatoriginateswithinorneartheAVnode
70. What are the signs and symptoms of A-fib and A-flutter?
A-fib may result from multiple areas of reentry within the atria or from multiple ectopic foci. A-fib
A patient with tachycardia or tachyarrhythmia needs treatment when there are signs and
symptoms associated with the rapid heart rate. The following signs and symptoms indicate that the
patient is already or is becoming hemodynamically unstable:
peripheral edema, ischemic ECG changes, ventricular rate >150 beats/min
arrhythmia is originating at or above the level of the atrioventricular (AV) node:
If the QRS complex is wide, then the tachycardia is of ventricular origin:
onset lasting a few seconds to many hours. PSVT is due to a reentry mechanism involving the AV
node alone or automatic focus.
Reentry tachycardia responds well to antiarrhythmic medications and electrical cardioversion.
Automatic focus tachycardias do not respond to electrical cardioversion and should be treated
with medications that suppress the ectopic foci.
may be associated with sick sinus syndrome, hypoxia, increased atrial pressure, and pericarditis.
Because there is no uniform atrial depolarization, no P-wave will be seen on ECG. Hypotension may
result from A-fib.
A-flutter is the result of a reentry circuit within the atria. A-flutter rarely occurs in the absence
of organic disease. It is seen in association with mitral or tricuspid valvular disease, acute cor
pulmonale, and coronary artery disease. Signs and symptoms include hypotension, ischemic pain,
and severe congestive heart failure.
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71. How are A-fib and A-flutter treated?
According to the AHA, the protocol for treatment of A-fib and A-flutter is:
1. Rule out precipitating causes for A-fib and A-flutter:
• Heart failure
• Pulmonary embolism
• Acute MI/substance abuse
• Hyperthyroidism
• Hypokalemia
• Hypoxia
• Hypomagnesemia
2. Control the rate:
• Preserved heart function: diltiazem (or another calcium channel blocker) or metoprolol (or
• Impaired heart function: diltiazem, digoxin, or amiodarone
• Patients with Wolff-Parkinson-White (WPW) syndrome: Avoid adenosine, calcium channel
• Preserved heart function: DC cardioversion, amiodarone, ibutilide, flecainide, propafenone,
• Impaired heart function: DC cardioversion, amiodarone
3. Convert the rhythm if the duration is >48 hours.
4. Urgent cardioversion: begins with IV heparin, followed by transesophageal echocardiogram to
5. Delayed cardioversion: anticoagulation for 3 weeks; then cardiovert and anticoagulate for 4 more
72. What are the types of wide-complex tachycardias and their AHA treatment
1. Unknown type:
• Attempt to identify and distinguish between VT and SVT with aberrant conduction due to the
• Always assume that any wide-complex tachycardia is VT until proven otherwise, because
• Treatment: DC cardioversion, procainamide, or amiodarone for preserved cardiac function.
2. Monomorphic VT:
• QRS complexes appear identical in shape.
• Treatment: procainamide, amiodarone, lidocaine, or sotalol with normal cardiac function.
3. Polymorphic VT:
• QRS complexes are subdivided into normal baseline QT and prolonged baseline QT interval.
• Associated with metabolic derangement such as electrolyte abnormalities or drug toxicities.
• Treatment: search for the metabolic derangement. Use DC cardioversion, procainamide,
• Torsades de pointes is an example of this VT with a unique rhythm strip. The drug of choice for
73. What is WPW syndrome? Which drugs can be harmful in the treatment of A-fib
If there is an extra conduction pathway, the electrical signal may arrive at the ventricles too soon.
another beta blocker), flecainide, propafenone, procainamide, amiodarone, or digoxin
blockers, beta blockers, and digoxin to control the rate. Convert the rhythm (electrical cardioversion if drug therapy is unsuccessful) if the duration is 48 hours or less.
procainamide
exclude atrial clot. Then cardiovert within 24 hours and give anticoagulation for 4 weeks.
weeks.
recommendations?
different treatment options for SVT that might compromise a patient with VT.
there is little danger in treating a wide-complex SVT as if it were VT.
Treat with DC cardioversion or amiodarone for impaired cardiac function.
Lidocaine or amiodarone should be given to patients with impaired cardiac function.
amiodarone, or beta blockers.
torsades associated with hypomagnesemia is magnesium sulfate.
or A-flutter associated with WPW syndrome?
This condition is called Wolff-Parkinson-White (WPW) syndrome. It is in a category of electrical
abnormalities called pre-excitation syndromes.
It is recognized by certain changes on the ECG, which is a graphical record of the heart’s
electrical activity. The ECG will show that an extra pathway or shortcut exists from the atria to the
ventricles.
Many people with WPW syndrome who have symptoms or episodes of tachycardia (rapid heart
rhythm) may have dizziness, chest palpitations, fainting, or, rarely, cardiac arrest. Other people with
WPWsyndromeneverhavetachycardiaorothersymptoms.About80%ofpeoplewithsymptoms
first have them between the ages of 11 and 50.
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Drugs that selectively block the AV node without also blocking coexisting accessory conduction
pathways (e.g., adenosine, calcium channel blockers, beta blockers, and digoxin) are contraindicated
when pre-excitation syndromes are present. These medications can increase conduction through the
accessory pathway and paradoxically increase the heart rate. For patients with A-fib or A-flutter, this
poses severe risks and is associated with a very high incidence of clinical deterioration.
74. What is bradycardia?
The term bradycardia simply means that the heart rate is slow. Normal adult heart rate is considered
by most to be 60 to 100 beats/min. According to this definition, every patient with a heart rate <60
beats/min is bradycardic. Not all patients with a heart rate <60 beats/min will need treatment.
Autonomic influence or intrinsic disease affecting the cardiac conduction system most often causes
bradycardia.
A patient may have a relative bradycardia. An example is the patient with severe hypotension
butwithaheartrateof70beats/min;theheartrateof70inahypotensivepatientmaynotsustain
the cardiac output.
75. What are the principal types of bradyarrhythmias?
• Sinusbradycardia
• A-fibwithslowventricularresponse
• AVblock:
• First-degree heart block
• Second-degree heart block, types I and II
• Third-degree heart block
• Relativebradycardia
Other rhythms that may also be considered bradyarrhythmias are:
• Pulselesselectricalactivity
• Asystole
76. When does sinus bradycardia need treatment?
A patient with a slow heart rate needs treatment only if there are serious signs or symptoms associ-
ated with the slow heart rate that indicate the patient is already or is becoming hemodynamically
unstable. These signs and symptoms include:
• Signs: hypotension, congestive heart failure, pulmonary congestion, and acute MI
• Symptoms: chest pain, shortness of breath, and decreased level of consciousness
77. How is a patient with a bradyarrhythmia initially managed according to AHA
protocol?
1. Supportive actions:
• Assess ABCs
• Chest X-ray
• Oxygen, IV, monitors, and pulse oximetry
• Brief history and targeted physical exam
• 12-lead ECG
2. Determine if bradycardia is hemodynamically significant.
• Monitor patient.
• Be prepared to begin transcutaneous pacing (TCP) on standby.
If the patient is hemodynamically unstable:
• Atropine, 0.5 to 1.0 mg IV
• Epinephrine infusion, 2 to 10 mg/min
• TCP
• Isoproterenol infusion, 2 to 10 mg/min
• Dopamine infusion, 5 to 20 mg/kg/min
78. What is meant by the term heart block?
Heart block is used interchangeably with the correct term, atrioventricular (AV) block. AV block
describes a delay or interruption in conduction between the atria and the ventricles, which may be
caused by one or more of the following:
• Lesionintheconductionpathway
• Prolongedrefractoryperiodalongtheconductionpathway
• SupraventricularheartratesthatsurpasstherefractoryperiodoftheAVnode
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79. What is first-degree heart block?
First-degree heart block is the prolonged delay in conduction at the AV node or the bundle of His.
The diagnosis of first-degree heart block is based on the PR interval. First-degree heart block exists
when the PR interval is longer than 0.2 seconds.
80. According to AHA protocol, how is first-degree heart block treated?
First-degree heart block requires no treatment unless there are associated symptoms.
81. What is second-degree heart block?
In second-degree heart block, not every atrial impulse is able to pass through the AV node into the
ventricles. The atrial impulses that are conducted to the ventricle will stimulate ventricular contraction. Therefore the ratio of P to QRS will be >1:1.
• OccursattheleveloftheAVnode
• Isusuallyduetoincreasedparasympathetictoneordrugeffects
• IscharacterizedbyprogressiveelongationofthePRinterval
• ConductionvelocitythroughtheAVnodegraduallydecreasesuntiltheimpulseisblocked,resulting
• OccursbelowtheleveloftheAVnode,uncommonlyatthebundleofHis
• Isusuallyduetoalesionalongthepathway
• HasaPRintervalthatdoesnotlengthenbeforeaskippedventricularbeat
• Mayhavemorethanoneskippedventricularbeatinarow
• HasapoorerprognosisthantypeIsecond-degreeheartblock
• IsmorelikelytoprogresstocompleteheartblockthantypeI
82. According to AHA protocol, how is type I second-degree heart block treated?
Type I second-degree heart block rarely requires treatment unless symptoms associated with brady-
• Decreasedparasympathetictone
• Propranololtoxicity/overdose
• Digitalistoxicity
• Verapamiltoxicity/overdose
• Atropine,0.5to1.0mg
• Epinephrineinfusion,1to2μg/min
• TCP
• Fluidchallengeifappropriate
• Dopamineinfusion,beginningwith5μg/kg/min
83. According to AHA protocol, how is type II second-degree heart block treated?
Type II second-degree heart block requires no treatment unless symptoms associated with brady-
• Atropine,0.5to1.0mg
• Epinephrineinfusion,1to2μg/min
• TCP
• Fluidchallengeifappropriate
• Dopaminebeginningwith5μg/kg/min
84. What is third-degree heart block?
Third-degree heart block occurs when no atrial impulses are transmitted to the ventricles. The atrial rate
85. According to AHA protocol, how is third-degree heart block treated?
Third-degree heart block is treated only if there are signs and symptoms that the patient is or is
• Atropine,0.5to1.0mg
• Epinephrineinfusion,1to2mg/min
Type I second-degree heart block (Wenckebach):
in a skipped ventricular beat.
Type II second-degree heart block:
cardia develop. Treatment should be directed at addressing the underlying cause of the block, such as:
If serious symptoms occur, then the following treatment is recommended:
cardia develop.
If serious symptoms develop, then the following treatment is recommended:
will be equal to or greater than the ventricular rate. If block occurs at the AV node, a junctional pacemaker
may initiate ventricular depolarizations at a regular rate of 40 to 60 beats/min. If the block is infranodal,
usually both bundle branches are blocked and there is significant disease of the conduction pathway.
becoming hemodynamically unstable. Recommended treatment for third-degree heart block is:
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