The esophageal-tracheal combitube is an airway device that can be used as an alternative to endotracheal intubation or as a rescue device when endotracheal intubation cannot be accomplished. It has dual lumens, one which passes into the esophagus and one which can pass into the trachea. It can effectively ventilate the lungs in most cases.

1. ADVANCED CARDIAC LIFE
SUPPORT(ACLS) - 2010
Speaker – Dr ; TAREK BELASHHER
Abusetta hospital

2. ACLS Course:
 Arrest scenarios
 VF
 Pulse less VT
 A systole
 PEA
 Pre-arrest scenarios
 Tachyarrhythmia's
 Bradyarrythmias
 Ischemia
 Stable Angina
 Unstable Angina
 MI
 Stroke

3. Key Issues in ACLS
 Airway
 CPR
 Defibrillation
 Drug therapy
 Post-resuscitation management
 Special Situations

4. BLS Key Concepts
 Avoid Hyperventilation (Do not ventilate too fast or too
much volume)
 Push hard and fast, allow complete chest recoil, minimal
interruptions
 Compress chest depth of 1.5 to 2 inches at a rate of 100
compressions per minute
 Resume CPR immediately after shock. Interruption in
CPR for rhythm check should not exceed 10 seconds

5. BLS Key Concepts
Chest compression should not be interrupted except
for:
 Shock delivery
 Rhythm check
 Ventilation (until an advanced airway is inserted)
Do not interrupt CPR:
 To insert cannula or to give drugs
 To listen to the heart or to take BP???
 Waiting for charging the Defibrillator
 To rotate personnel

6. Chances of survival with time

7. ADVANCED CARDIAC LIFE SUPPORT
 ACLS impacts multiple key links in the chain of
survival that include interventions to prevent cardiac
arrest, treat cardiac arrest, and improve outcomes
of patients who achieve return of spontaneous
circulation (ROSC) after cardiac arrest
 Interventions aimed at preventing cardiac arrest
include airway management, ventilation support,
and treatment of bradyarrhythmias and
tachyarrhythmias.

8. AHA ADULT CHAIN OF SURVIVAL
1. Immediate recognition of cardiac arrest and
activation of the emergency response system
2. Early CPR with an emphasis on chest
compressions
3. Rapid defibrillation
4. Effective advanced life support
5. Integrated post–cardiac arrest care

9. CARDIOPULMONARY RESUSCITATION (CPR)
 Cardiopulmonary resuscitation (CPR) is a series of
life saving actions that improve the chance of
survival following cardiac arrest

12. KEY CHANGES FROM THE
2005 BLS GUIDELINES
● Immediate recognition of SCA based on assessing
unresponsiveness and absence of normal breathing
● “Look, Listen, and Feel” removed from the BLS
algorithm
● Encouraging Hands-Only (chest compression only)
CPR
● Sequence change CAB rather than ABC
● Health care providers continue effective chest
compressions/ CPR until return of spontaneous
circulation or termination of resuscitative efforts

13. A CHANGE FROM A-B-C TO C-A-B

14. o 2010 (New): “Look, listen, and feel” was removed
from the CPR sequence. After delivery of 30
compressions, the lone rescuer opens the victim’s
airway and delivers 2 breaths.
 2005 (Old): “Look, listen, and feel” was used to
assess breathing after the airway was opened.
 2010 (New): Initiate chest compressions before
ventilations.
 2005 (Old): The sequence of adult CPR began with
opening of the airway, checking for normal
breathing, and then delivery of 2 rescue breaths
followed by cycles of 30 chest compressions and 2
breaths.

15.  2010 (New): It is reasonable for lay rescuers and
healthcare providers to perform chest
compressions at a rate of at least100/min.
 2005 (Old): Compress at a rate of about 100/mi
 2010 (New): The adult sternum should be
depressed at least 2 inches (5 cm).
 2005 (Old): The adult sternum should be depressed
approximately 1. to 2 inches (approximately 4 to 5
cm).n

16.  2005 (Old): Cricoid pressure should be used only if
the victim is deeply unconscious, and it usually
requires a third rescuer not involved in rescue
breaths or compressions
 2010(new):routine use of cricoid pressure in
cardiac arrest is not recommended.

17. 17
CRICOID PRESSURE
Thyroid
Cartilage
Cricoid

18. 2005 TO 2010 CHANGES
Component of CPR 2005 ECC
recommendations
2010 ECC
Recommendations
DEPTH OF
COMPRESSION
1 ½ - 2 inches Greater than 2
inches
RATE 100 /MINUTE At least 100 /MIN
VENTILATION 8-10 /MINUTE 8-10 /MINUTE
CHEST RECOIL 100% 100%
INTURUPTIONS Minimized Less than 10
seconds goal
PULSE CHECK HCP Only HCP only, Checking
for “DEFNITE pulse”.

19.  2010 (New): The precordial thump should not be
used for un witnessed out-of-hospital cardiac arrest.
The precordial thump may be considered for
patients with witnessed, monitored, unstable VT
(including pulse less VT) if a defibrillator is not
immediately ready for use, but it should not delay
CPR and shock delivery

20. SUMMARY OF KEY ISSUES AND MAJOR CHANGES
 The major changes in advanced cardiovascular life support
(ACLS) for 2010 include the following:
 • Quantitative waveform capnography is recommended for
confirmation and monitoring of endotracheal tube placement
and CPR quality.
 • The traditional cardiac arrest algorithm was simplified and an
alternative conceptual design was created to emphasize the
importance of high-quality CPR.
 • There is an increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC.
 • Atropine is no longer recommended for routine use in the
management of pulse less electrical activity (PEA)/asystole.

21. CAPNOGRAPHY RECOMMENDATION
 2010 (New): Continuous quantitative waveform
capnography is now recommended for intubated
patients throughout the per arrest period. When
quantitative waveform capnography is used for
adults, applications now include recommendations
for confirming tracheal tube placement and for
monitoring CPR quality and detecting ROSC based
on end-tidal carbon dioxide (PETCO2) values .

22. PROGNOSTIC INDICATORS IN THE ADULT POSTARREST
PATIENT TREATED WITH THERAPEUTIC HYPOTHERMIA
 2010 (New): In adult post–cardiac arrest patients
treated with therapeutic hypothermia, it is
recommended that clinical neurologic signs,
electrophysiologic studies, biomarkers, and imaging
be performed where available at 3 days after
cardiac arrest.

23. Hypothermia
 ILCOR Advisory statement (2003):
 Unconscious adult patients with spontaneous
circulation after out-of-hospital cardiac arrest
should be cooled to 32-34°C for 12-24 hrs when the
initial rhythm was ventricular fibrillation (VF).
 Such cooling may also be beneficial for other
rhythms or in-hospital cardiac arrests.

24. Hypothermia
Cooling:
 Retard enzymatic , suppress production of free
radicals
 Reduction of O2 demand in low-flow regions
 Protection of membrane fluidity
 Reduction of intracellular acidosis
 Decrease in cerebral edema and ICP

25.  2010 (New): Advanced life support training
should include training in teamwork.
 Why: Resuscitation skills are often performed
simultaneously, and healthcare providers must be
able to work collaboratively to minimize
interruptions in chest compressions. Teamwork and
leadership skills continue to be important,
particularly for advanced courses that include ACLS
and PALS providers

28. MONITORING DURING CPR
Physiologic parameters
 Monitoring of PETCO2 (35 to 40 mmHg)
 Coronary perfusion pressure (CPP) (15mmHg)
 Central venous oxygen saturation (ScvO2)
 Abrupt increase in any of these parameters is a
sensitive indicator of ROSC that can be monitored
without interrupting chest compressions

29. Quantitative waveform capnography
 If Petco2 <10 mm Hg, attempt to improve CPR
quality
Intra-arterial pressure
 If diastolic pressure <20 mm Hg, attempt to improve
CPR quality
 If ScvO2 is < 30%, consider trying to improve the
quality of CPR

31. HIGH QUALITY CPR
 Chest compressions of adequate rate 100/min
 A compression depth of at least 2 inches (5 cm) in
adults and in children, a compression depth of at
least 1.5 inches [4 cm] in infants
 Complete chest recoil after each compression,
 Minimizing interruptions in chest compressions
 Avoiding excessive ventilation
 If multiple rescuers are available, rotate the task of
compressions every 2 minutes.

32. SOME THINGS REMAIN IMPORTANT
 RATE
 DEPTH
 RELEASE
 UNINTERRUPTED
 DECREASED
VENTILATION
5 KEY
ASPECTS
OF
GOOD
CPR!

33. CHEST COMPRESSIONS

34. CHEST COMPRESSIONS
 Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum.
 Technique ..?

35. DECOMPRESSION PHASE
back
Maintain contact with the skin at your fingertips while
you lift the heel of your hand off the chest. This will
assure that the chest wall recoils completely after
each compression and maximizes the formation of the
vacuum that promotes filling of the heart.

36. COMPRESSION RATE (AT LEAST 100 /
MINUTE)
 Rate per minute is NOT a function of “speed” of
compressions only, but a function of both speed
ands minimizing no-flow periods (discussed later)
for a total compressions/minute.
 Compressions rates as high as 130 resulted in
favorable outcomes
 Compression rates <87/minute saw rapid drop off
in ROSC.
 NEW RECOMMENDATION: At LEAST
100/minute.
 Better too fast than too slow.

37. COMPRESSION DEPTH (AT LEAST 2
INCHES)
 Previous studies show that only about 27% of
compressions were deep enough (Wik, 2005)
 0% (none) were too deep.
 NEW GIUDELINES: The adult sternum should be
depressed at least 2 inches (5 cm) , with chest
compression and chest recoil/relaxation times
approximately equal

38. COMPRESSION RATE…
Percent segments
within 10 cpm
of AHA Guidelines
31 %
36.9%
Abella, et al 2005 Circulation
76 %
75 %
58 %
42%

39. COMPLETE RELEASE/RECOIL (FULL)
 Complete Recoil essential to reduce intrathoracic
pressure between compressions.
 Reducing recoil improves hemodynamic in arrest,
and improves Coronary Perfusion Pressure
(CPP)
 Incomplete chest wall recoil can be reduced
during CPR by using electronic recording devices
that provide real-time feedback.

40. ACTIVE COMPRESSION-DECOMPRESSION
CPR (ACD-CPR)
 Small studies showed
improvement, but a
Cochrane Meta- review of
over 1000 patients did
not.
 ACD-CPR may be
considered for use when
providers are adequately
trained and monitored
(Class IIb, LOE B).

41. MECHANICAL PISTON DEVICES
 L.U.C.A.S., THUMPER, ETC
 In 3 Studies the use of a mechanical piston
device for CPR improved end-tidal CO2 and
mean arterial pressure during adult cardiac
arrest resuscitation.
 No long term benefit over manual CPR
discovered (yet)
 There is insufficient evidence to support or
refute the routine use of mechanical piston
devices in the treatment of cardiac arrest.
 Use of such devices during specific
cercumstances when manual CPR is difficult
may be done (Class IIb, LOE C).

43. INTURRUPTIONS
 Pausing for procedures
 intubation, IV, pulse check, etc.).
 Pausing for rhythm analysis.
 Pausing to charge, clear, and shock.

44. KEY POINT:
“…High-quality CPR is important not only at the onset but
throughout the course of resuscitation. Defibrillation and advanced
care should be interfaced in a way that minimizes any interruption
in CPR.”
AHA 2010 Guidelines

45. Coronary vessel injury
Diaphragm injury
Hemopericardium
Hemothorax
Interference with ventilation

46. Liver injury
Myocardial injury
Pneumothorax
Rib fractures
Spleen injury
Sternal fracture

47. AIRWAY

50. AIRWAY AND VENTILATIONS
 Opening airway – Head tilt, chin lift or jaw thrust
 The untrained rescuer will provide Hands-Only
(compression-only) CPR
 The Health care provider should open the airway
and give rescue breaths with chest compressions

51. AIRWAY
 Assess the airway, ensuring it is
- open
- clear
 Jaw thrust can be used
 Look in mouth for obstruction
 teeth, tongue, vomit,
foreign object
 Ensure airway is clear
 If airway obstructed with fluid
(vomit or blood) roll patient
onto their side & clear airway
or use suction if available

52. AIRWAY

53. RESCUE BREATHS
 By mouth-to-mouth or bag-mask
 Deliver each rescue breath over 1 second
 Give a sufficient tidal volume to produce visible
chest rise
 Use a compression to ventilation ratio of 30 chest
compressions to 2 ventilations
 After advanced airway is placed, rescue breaths
given asynchronus with compression
 1 breath every 6 to 8 seconds (about 8 to 10
breaths per minute)

54. OPEN AIRWAY
Head tilt, chin lift + jaw thrust

55. 55
OPENING THE AIRWAY
Jaw thrust Head tilt–chin lift

56. 56
THE OROPHARYNGEAL AIRWAY

57. 57
MALPOSITION OF
OROPHARYNGEAL AIRWAY
Too short

59. MOUTH TO POCKET MASK

60. 60
POCKET-MASK DEVICES
1-way valve
Port to attach O2
source

61. 61
MOUTH-TO-MASK VENTILATION
Fingers: jaw thrust upward Fingers: head tilt–chin lift

62. 62
BAG-MASK VENTILATION
 Key—ventilation volume: “enough to
produce
obvious chest rise”
1-Person:
difficult, less effective
2-Person:
easier, more effective

63. BAG/VALVE/MASK

64. 64
EQUIPMENT FOR INTUBATION
 Laryngoscope with
several blades
 Tracheal tubes
 Malleable stylet
 10-mL syringe
 Magill forceps
 Water-soluble lubricant
 Suction unit, catheters, and tubing

65. 65
CURVED BLADE ATTACHES TO
LARYNGOSCOPE HANDLE

66. 66
CURVED BLADE ATTACHED TO
LARYNGOSCOPE HANDLE

67. 67
STRAIGHT-BLADE LARYNGOSCOPE
INSERTED PAST EPIGLOTTIS

68. 68
ALIGNING AXES OF UPPER AIRWAY
Extend-the-head-on-neck (“look up”): aligns axis A relative to B
Flex-the-neck-on-shoulders (“look down”): aligns axis B relative
to C
C
A
BA
B
C
Trachea
Pharynx
Mouth

69. SECURING THE AIRWAY
Perform chest compressions with a 30:2
compression to ventilation ratio
back
The head tilt-chin lift with a good
2-handed face mask seal will
provide adequate ventilations in
most cases. Do not delay or
interrupt compressions early in
CPR for a secure airway.

70. CPR AND RESCUE BREATHING
WITH A BAG-VALVE MASK (BVM)
1
When squeezing the bag, use one
hand and only bring the fingertips
together.
DO NOT increase volume!
back

71. RESCUE BREATHING AFTER INTUBATION
DO NOT pause chest compressions to
deliver breaths after tube placement.
back

72. 72
ESOPHAGEAL-TRACHEAL COMBITUBE
A = esophageal obturator; ventilation into trachea through side openings = B
C = tracheal tube; ventilation through open end if proximal end inserted in
trachea
D = pharyngeal cuff; inflated through catheter = E
F = esophageal cuff; inflated through catheter = G
H = teeth marker; blindly insert Combitube until marker is at level of teeth
Distal End
Proximal End
B
C
D
E
F
G
H
A

73. COMBITUBE

74. 74
ESOPHAGEAL-TRACHEAL COMBITUBE INSERTED IN
ESOPHAGUS
A = esophageal obturator; ventilation into
trachea through side openings = B
D = pharyngeal cuff (inflated)
F = inflated esophageal/tracheal cuff
H = teeth markers; insert until marker lines
at level of teeth
D
A
D
B F
H

75. Advanced Airways
Once advanced airway in place, don’t interrupt chest compression for
ventilation and avoid over ventilation 8-10 breaths/m
Endotracheal Tube
Laryngeal Mask Airway
LMA
Combitube

76. LARYNGEAL MASK AIRWAY
LMA

77. 77
LARYNGEAL MASK AIRWAY (LMA)
The LMA is an adjunctive airway that consists
of a tube with a cuffed mask-like projection at
distal end.

78. 78
LMA INTRODUCED THROUGH MOUTH INTO
PHARYNX

79. 79
LMA IN POSITION
Once the LMA is in position, a clear, secure airway is present.

80. 80
ANATOMIC DETAIL

81. CRICOID PRESSURE (REALLY???)
 Cricoid pressure in no arrest patients may offer some
measure of protection to the airway from aspiration and
gastric insufflation during bag-mask ventilation.
 However, it also may impede ventilation and interfere with
placement of a supraglottic airway or intubation.
 If cricoid pressure is used in special circumstances during
cardiac arrest, the pressure should be adjusted, relaxed, or
released if it impedes ventilation or advanced airway
placement.
 The routine use of cricoid pressure in cardiac arrest is not
recommended .

82. FIO2 (DURING ARREST)
 Use of 100% inspired oxygen (FIO21.0) as soon as
it becomes available is reasonable during
resuscitation from cardiac arrest .

83. FIO2 (POST ARREST)
 Increasing Data that hyper-oxia may increase
incidence of poor neurological outcomes and
increased pulmonary injury.
 Exact FiO2 recommendations have not been
determined.
 In the post arrest phase, if equipment is available,
titration of FiO2 to SPO2 04% is recommended .

84. PASSIVE O2 DELIVERY DURING ARREST
 Passive O2 delivery via ETT has been reviewed.
 In theory, because ventilation requirements are lower than
normal during cardiac arrest, oxygen supplied by passive
delivery is likely to be sufficient for several minutes after onset of
cardiac arrest with a patent upper airway.
 The studies involved resulted in improved outcomes., but it is
unsure what role (if any) passive O2 had.
 At this time there is insufficient evidence to support the
removal of ventilations from CPR performed by ACLS
providers.

85. ETT
 There are no studies directly addressing the timing of
advanced airway placement and outcome during
resuscitation from cardiac arrest.
 Although insertion of an endotracheal tube can be
accomplished during ongoing chest compressions,
intubation frequently is associated with interruption of
compressions for many seconds.
 Placement of a supraglottic airway is a reasonable
alternative to endotracheal intubation and can be done
successfully without interrupting chest compressions.

86. ETT (MORAL OF STORY)
 There are two pitfalls of ETT placement:
 1- Interruption of CPR
 2- Poor Placement practices.
 Therefore, Place during CPR if possible, and
optimize first attempt (bougie, etc)
 If you CANT do this, then use a supraglottic
airway.
 If you cant do this, perhaps you should not be a
paramedic? Hmmmmmm……

87. 87
CONFIRMATION:
TRACHEAL TUBE PLACEMENT
End-tidal colorimetric CO2 indicators

88. COMPRESSION-VENTILATION RATIO
 Ventilation rate = 12/min
 Compression rate = 78/min.
 Large amplitude waves = ventilations.
 Small amplitude waves = compressions.
 Each strip records 16 seconds of time

89. REALITY SUCKS…
 Compression: Ventilation Ratio 2:1
 47-48 Breaths a minute
47 Nails in a coffin!

90. PROLONGED VENTILATIONS
 􀂃Ventilation Duration = 4.36 seconds / breath
 􀂃Ventilation Rate = 11 breaths / minute
 􀂃% time under Positive Pressure = 80%

91. DECREASING VENTILATION
 CPR with Advanced Airway: 8 – 10 breaths/minute
 Post-resuscitation: 10 – 12/min

92. CARDIAC ARREST
 Cardiac arrest can be caused by 4 rhythms:
1. Ventricular fibrillation(VF),
2. Pulseless ventricular tachycardia (VT),
3. Pulseless electric activity (PEA), and
4. Asystole.
How to recognise cardiac arrest ..?

95. TREATABLE CAUSES OF CARDIAC ARREST:
THE H’S AND T’S
H’s T’s
 Hypoxia Toxins
 Hypovolemia Tamponade (cardiac)
 Hydrogen ion(acidosis) Tension pneumothorax
 Hypo-/hyperkalemia Thrombosis, pulmonary
 Hypothermia Thrombosis, coronary

96. HYPOKALEMIA: FLAT ST SEGMENTS
See a normal EKG…

97. HYPOKALEMIA: PROMINENT U WAVES

98. HYPERKALEMIA: PEAKED T WAVES
See a normal EKG…

99. TREATMENT OF HYPERKALEMIA
 Antagonize membrane effects of K +
 IV Calcium: onset 1-2 min, duration 30-60 min
 Drive K+ into cells
 Insulin (remember to give with glucose!)
 Beta agonists (high dose) – like albuterol
 Remove K+ from the body
 Kayexalate- binds K+ in gut, onset 1-2 hours
 Diuretics- only work if renal function remains
 Hemodialysis- depends on availability

100. ELECTRICAL ALTERNANS: THE EKG FINDING
OF TAMPONADE

101. TREATMENT OF TAMPONADE: PERICARDIOCENTESIS

102. TENSION PNEUMOTHORAX

103. TREATMENT OF TENSION PTX
 Oxygen
 Insert a large-bore (ie, 14-gauge or 16-gauge)
needle into the second intercostal space (above the
third rib!), at the midclavicular line.

105. CARDIAC ARREST
 Cardiac arrest can be caused by 4 rhythms:
1. Ventricular fibrillation(VF),
2. Pulseless ventricular tachycardia (VT),
3. Pulseless electric activity (PEA), and
4. Asystole.
How to recognise cardiac arrest ..?

106. Arrest Rhythms
Shockable rhythms:
 VF
 Pulseless VT
Non shockable rhythms:
 PEA
 Asystole
Electrical therapies in ACLS
Cardiversion / Defibrillation for
Tachyarrhythmias
 Unsynchronized =
defibrillation (Uses higher
energy levels and delivers
shock immediately)
 Synchronized delivers
shock at peak of QRS
complex (Avoids delivering
shock during repolarization)
Pacing for brady arrhythmias

107. PRE‐CORDIAL THUMP
 • No prospective studies so far
 • Rationale is to convert mechanical energy to
electrical energy
 • In all successful cases, the thump was given
within first 10s
 • More likely to be successful in converting VT to
sinus rhythm
 • Much less likely for VF

108. PRE‐CORDIAL THUMP
 • Consider as an option for witnessed, sudden
collapse and defibrillator NOT immediately
available
 • Thump may cause deterioration:
 – Rate acceleration of VT
 – Conversion of VT to VF
 – Complete Heart Block
 – A systole

109. PRE‐CORDIAL THUMP
 • Only by trained healthcare providers immediately
confirm cardiac arrest
 • Use ulnar edge of tightly clenched fist
 • Deliver a sharp impact to the lower half of the
sternum from a height of 20 cm
 • After that, immediately retract the fist

110. DEFIBRILLATION
 Defibrillation is defined as termination of VF for at
least 5 seconds following the shock.
 Early defibrillation remains the cornerstone therapy
for ventricular fibrillation and pulseless ventricular
tachycardia

111.  Defibrillation Sequence
● Turn the AED on.
● Follow the AED prompts.
● Resume chest compressions immediately after the
shock(minimize interruptions).
Shock Energy
 Biphasic : Manufacturer recommendation (eg,
initial dose of 120-200 J), if unknown, use maximum
available.
 Second and subsequent doses should be equivalent,
and higher doses may be considered.
 Monophasic : 360 J

114. Defibrillation technique
Defibrillation Sequence
Action Announcements
1. Switch on.
2. Place coupling pads/gel in correct position
3. Apply paddles
4. Check ECG rhythm and confirm no pulse
5. Select non-synchronized (VF) setting
6. Charge to required energy level "Charging"
7. Ensure no-one is in contact with anything touching
the patient
"Stand clear"
8. Press paddle buttons simultaneously
"Shocking
now"
9.eturn to ALS algorithm for further steps

115. CAUTION IN USE OF AED
 Don’t apply pads over pacemakers
 Don’t apply pads over skin patches/medications
 Be cautious around water
 NEVER attach to anyone not in cardiac arrest

116. DO I CHECK FOR A PULSE AFTER I
DELIVER A SHOCK ?

117. 1
No stacked shocks
No pulse check after shock
Single shock will be followed by 2
minutes of CPR, then pulse check, and
re-analyze if necessary
DEFIBRILLATION
These measures reduce “no flow time”. Why is it
important to reduce the amount of time when
compressions are not performed?

118. WHAT NEXT ?
 Commence CPR immediately after delivering
the shock
 Use a ratio of 30 compressions to 2 breaths
 Follow the voice prompts & continue CPR until
signs of life return

119. 1-SHOCK PROTOCOL VERSUS 3-SHOCK
SEQUENCE
 Evidence from 2 well-conducted pre/post design
studies suggested significant survival benefit with
the single shock defibrillation protocol compared
with 3-stacked-shock protocols
 If 1 shock fails to eliminate VF, the incremental
benefit of another shock is low, and resumption of
CPR is likely to confer a greater value than another
shock

121. CARDIAC ARREST
 Cardiac arrest can be caused by 4 rhythms:
1. Ventricular fibrillation(VF),
2. Pulseless ventricular tachycardia (VT),
3. Pulseless electric activity (PEA), and
4. Asystole.
How to recognise cardiac arrest ..?

122. VF/ Pulseless VT
Witnessed arrest:
 2 rescue breaths then
 Defibrillate
Unwitnessed arrest:
 5 cycles of CPR (2 min)
then
 Defibrillate
 200 Joules for biphasic
machines
 360 Joules for monophasic
machines
 Single shock (not 3 shocks)
followed by CPR
 No gap between chest
compression and shock
delivery

123. VENTRICULAR FIBRILLATION
Fine VF
Coarse VF

124. VENTRICULAR FIBRILLATION
Rate Cannot be determined, because there are no
discernible waves or complexes to measure
Rhythm Rapid and chaotic, with no pattern or regularity
P waves Not discernible
PR interval Not discernible
QRS duration Not discernible

129. VENTRICULAR TACHYCARDIA
 Treat the following as VF:
 Pulse less monomorphic VT
 Pulse less polymorphic VT

130. POLYMORPHIC VENTRICULAR TACHYCARDIA
Rate 150 to 300 beats/min; typically 200 to 250 beats/min
Rhythm May be regular or irregular
P waves None
PR interval None
QRS 0.12 sec or more; there is a gradual alteration in the
amplitude and direction of the QRS complexes; a
typical cycle consists of 5 to 20 QRS complexes

131. MONOMORPHIC VENTRICULAR TACHYCARDIA
Rate 101 to 250 beats/min
Rhythm Essentially regular
P waves Usually not seen; if present, they have no set
relationship with the QRS complexes that appear
between them at a rate different from that of the VT
PR interval None
QRS 0.12 sec or more; often difficult to differentiate
between the QRS and the T wave

132. MONOMORPHIC VENTRICULAR TACHYCARDIA
 Signs and symptoms associated with VT vary.
 Sustained VT does not always produce signs of
hemodynamic instability.
 VT may occur with or without pulses.
 Treatment is based on signs and symptoms and the
type of VT.

136. WHAT IS THIS RHYTHM?

138. ASYSTOLE PROTOCOL
 Check another lead
 Is it on paddles?
 Power on?
 Check lead and cable connections

139. ASYSTOLE (CARDIAC STANDSTILL)
Rate Ventricular usually not discernible, but atrial activity may
be seen (i.e., “P-wave” asystole)
Rhythm Ventricular not discernible, atrial may be discernible
P waves Usually not discernible
PR interval Not measurable
QRS Absent

140. “P-Wave” Asystole
Asystole

141. PULSELESS ELECTRICAL ACTIVITY
 Pulseless electrical activity exists when organized
electrical activity (other than VT) is present on the
cardiac monitor but the patient is apneic and
pulseless.

143. Copyright © 2012 by Mosby, an imprint of Elsevier Inc. 143
THE RESUSCITATION TEAM

144. GOALS OF THE RESUSCITATION TEAM
 To re-establish spontaneous circulation and
respiration
 To preserve vital organ function during resuscitation
 Your responsibility to the patient continues until
patient care is transferred to a team with equal or
greater expertise.

145. CRITICAL TASKS OF RESUSCITATION
1. Chest compressions
2. Airway management
3. ECG monitoring and defibrillation
4. Vascular access and medication administration

146. TEAM LEADER RESPONSIBILITIES
 Assesses the patient
 Orders emergency care in accordance with protocols
 Considers reasons for cardiac arrest
 Supervises team members
 Evaluates the adequacy of chest compressions
 Ensures that the patient receives appropriate oxygen
therapy
 Evaluates the adequacy of ventilation
 Ensures safe and correct defibrillation, when it is
indicated

147. TEAM LEADER RESPONSIBILITIES
 Ensures the correct choice and placement of
vascular access
 Confirms proper positioning of an advanced airway
 Ensures correct drug, dose, and route of
administration
 Ensures the safety of all team members
 Problem solves
 Decides when to terminate resuscitation efforts

148. Copyright © 2012 by Mosby, an imprint of Elsevier Inc. 148
TEAM MEMBER RESPONSIBILITIES

149. AIRWAY TEAM MEMBER
 Manual airway maneuvers
 Oral airway
 Nasal airway
 Oxygen-delivery devices
 Bag-mask ventilation
 Suctioning
 Advanced airway placement
 If within scope of practice
 Waveform capnography, exhaled
carbon dioxide detector, and
esophageal detector device

150. CARDIOPULMONARY RESUSCITATION TEAM
MEMBER
 The ACLS or BLS team member who is responsible
for CPR must be able to do the following:
 Properly perform CPR
 Provide chest compressions of adequate rate, force,
and depth in the correct location

151. ELECTROCARDIOGRAPHY/DEFIBRILLATION
TEAM MEMBER
 Synchronized versus unsynchronized shocks
 Pad or paddle placement
 Safety precautions
 Indications for and complications of transcutaneous
pacing
 Problem solving with regard to equipment failure

152. KEY CONCEPTS REVISITED…
 Avoid Hyperventilation
 Push hard and fast, allow complete chest recoil, minimal
interruptions
 Compress chest depth of 1.5 to 2 inches at a rate of 100
compressions per minute
 Compression to ventilation ratio 30:2, after advanced
airway no need to interrupt compression
 Turing defibrillator on…
 5 Hs and 5 Ts…

153. EPINEPHRINE
 Indications
 Cardiac arrest
 VF; VT; a systole; PEA
 Symptomatic bradycardia
 After atropine; alternative to dopamine
 Severe hypotension
 When atropine and pacing fail; hypotension accompanying
bradycardia; phosphodiesterase enzyme inhibitors
 Anaphylaxis; severe allergic reactions
 Combine with large fluid volume; corticosteroids;
antihistamines

154. EPINEPHRINE
 Precautions
 May increase myocardial ischemia, angina, and oxygen
demand
 High doses do not improve survival; may be detrimental
 Higher doses may be needed for poison/drug induced
shock
 Dosing
 Cardiac arrest 1 mg (1:10,000) IV/IO every 3-5 min.
 High dose up to 0.2 mg/kg for specific drug OD’s
 Infusion of 2-10 mcg/min.
 Endotracheal of 2-2.5 times normal dose
 SQ/IM 0.3-0.5 mg

155. VASOPRESSORS
Drug Therapy
 Epinephrine IV/IO Dose: 1 mg every 3-5 minutes
 Vasopressin IV/IO Dose: 40 units can replace first
or second dose of epinephrine
 Amiodarone IV/IO Dose: First dose: 300 mg bolus.
Second dose: 150 mg.

156. KEY CHANGES FROM THE 2005 ACLS
GUIDELINES
 Continuous quantitative waveform capnography is
recommended
 Cardiac arrest algorithms are simplified and
redesigned to emphasize the importance of high
quality CPR
 Atropine is no longer recommended for routine use
in the management of pulseless electrical activity
(PEA)/asystole

157.  Increased emphasis on physiologic monitoring to
optimize CPR quality and detect ROSC
 Chronotropic drug infusions are recommended as
an alternative to pacing in symptomatic and
unstable bradycardia.
 Adenosine is recommended as a safe and
potentially effective therapy in the initial
management of stable undifferentiated regular
monomorphic wide-complex tachycardia

160.  Synchronised cardioversion - shock delivery that is
timed (synchronized) with the QRS complex
 Narrow regular : 50 – 100 J
 Narrow irregular : Biphasic – 120 – 200 J and
Monophasic – 200 J
 Wide regular – 100 J
 Wide irregular – defibrillation dose
 Adenosine : 6 mg rapid iv push, follow with NS
flush.. Second dose 12 mg

161. INITIAL OBJECTIVES OF POST– CARDIAC
ARREST CARE
 Optimize cardiopulmonary function and vital organ
perfusion.
 After out-of-hospital cardiac arrest, transport patient
to an appropriate hospital with a comprehensive
post–cardiac arrest treatment
 Transport the in-hospital post– cardiac arrest patient
to an appropriate critical-care unit
 Try to identify and treat the precipitating causes of the
arrest and prevent recurrent arrest

163. THANK YOU