management of cardiac arrest

1. CPR

2. Pattern of cardiac arrest
 1-Brady-asystole.
 2-Pulseless electrical activity. (PEA)
 3-Ventricular fibrillation, Pulseless
Ventricular tachycardia.

4. Causes of reversible cardiac arrest
H T
 Hypoxia.  Toxin.
 Hypovolaemia.  Thrombus Pulmonary
 Hypoglycemia. embolism.
 Hypothermia.  Thrombus acute
 H+ions Acidosis. coronary syndrome.
 Hypo- hyperkalemia.
 Tension
pneumothorax.
 Tamponade cardiac.

5. The primary survey
 Airway: Open the airway
 Breathing: Provide positive-pressure
ventilation.
 Circulation: Give chest compressions.
 Defibrillation: Identify and shock
ventricular fibrillation (VF) and ventricular
tachycardia (VT)

6. Airway
Assessment:
 1- look for respiratory activity.
 2-listen for breathing.
 3- feel for air exchange at the patient’s nose and mouth.
If these are present,
assess the patient’s ability to protect the airway by asking
them to speak.
If the patient does not respond to questions, the absence
of a strong gag reflex:
confirms the inadequacy of protective airway mechanisms
 steps must be taken to provide airway support.

7. Steps to support airway
 1- immediately call for assistance.
 2- place the patient in a supine position.
be careful in a patient with neck trauma in-line stabilization
of the cervical spine. This is performed by keeping one
hand behind the head and neck while the other hand
rolls the patient toward you.
 3- open airway: use the head tilt-chin lift
maneuver or the jaw thrust maneuver.
 4- Remove foreign material.

10. Breathing
 1- bag-valve mask.(2 sec) if unsuccessful.
 2-reposition the head and mask and try again.
If unsuccessful, (obstructed airway).
 3- Open the patient’s mouth by grasping both
the tongue and the lower jaw between the
thumb and fingers, and then lift the mandible. If
you see obstructing material.
 4- use a McGill forceps or clamp to remove it. If
this equipment is not available, slide your index
finger down the inside of the cheek to the base
of the tongue and dislodge any foreign bodies
using a hooking action. (if unsuccessful).

11. Breathing-2
 5- Abdominal thrusts.
 6- Reattempt ventilation.
Rate 8-10 breaths min

12. Circulation
 check for a carotid pulse.( the most
central of the peripheral arteries).
 If no pulse is present, chest compressions
should be initiated and the patient should
be placed on a cardiac monitor.
 To adequately perform chest compressions, the
heel of one hand should be placed in the midline
on the lower part of the sternum (just above the
notch where the ribs meet the lower sternum).

13.  The other hand is placed on top of the first hand
and the fingers interlocked and kept off of the
chest.
 Position your shoulders directly over your hands
and lock your elbows.
 Depress the sternum about 1.5–2 inches
approximately 100 times per minute.
 Properly performed compressions can produce a
systolic blood pressure of 60mmHg.

14. Defibrillation
When defibrillation can be successful
performed within the first minute or two,
as many as 90% of patients return to their
pre-arrest neurologic status. The longer
the patient remains in cardiac arrest, the
more likely that defibrillation and
resuscitation will be unsuccessful. Survival
rates are 10% when defibrillation is
delayed 10 minutes or more after a
patient’s collapse.

15.  Deliver an electric shock to convert the
nonperfusing rhythm to a perfusing one.
 one paddle should be placed to the right
of the sternum below the right clavicle and
the other in the midaxillary line at the
level of the nipple.
 Firm pressure of approximately 25 lb
should be applied to each paddle.
 Alternatively, “hands off” defibrillator pads
can be used that are placed on the chest
and the back, sandwiching the heart.

16. Types of defibrillator
 Monophasic
 Biphasic
Less energy needed with
biphasic

17. Prepare patient
 Correct reversible causes
 Check lanoxin level
 12 leads ECG before & after shock
 Iv line present
 Monitoring circulation and respiration
 Fasting 8 hr , sedation if elective
cardioversion.

18. Size of paddle
 Adult debrillation, both handheld paddle
electrodes and self-adhesive pad
electrodes 8—12 cm in diameter are used
and function well.
 Debrillation success may be higher with
electrodes of 12-cm diameter compared
with those of 8-cm.

19. Position of paddles
 the conventional sternal—apical position.
 The right (sternal) electrode is placed to the
right of the sternum, below the clavicle.
 The apical paddle is placed in the mid axillary
line, approximately level with the V6 ECG
electrode .
 It does not matter which electrode
(apex/sternum) is placed in either
position.

20. Position of paddles-2
 Other acceptable pad positions include:
 each electrode on the lateral chest wall, one
on the right and the other on the left side
(biaxillary);
 one electrode in the standard apical position
and the other on the right or left upper back;
 one electrode anteriorly, over the left
precordium, and the other electrode posterior
to the heart just inferior to the left scapula.

21. Coupling agents
 Do not use medical gels or pastes of poor
electrical conductivity (e.g., ultrasound gel).
Pads versus paddles
 Self-adhesive debrillation pads are safe and
effective and are preferable to standard
debrillation paddles.
 Consideration should be given to use of self-
adhesive pads in peri-arrest situations.

22.  Successful defibrillation depends on the
amount of current transmitted across the
heart. (energy output of defibrillator
transthoracic impedance).
 ↑ paddle size →↑ efficiency of shock
current.
 Conductive gel (contain salt) so less
energy is required, ↓ burn but not ↑
impedence.

23. The secondary survey
 Airway: Definitive airway management
(tube).
 Breathing: Confirmation of adequate
ventilation.
 Circulation: Intravenous access, ACLS
medications, fluids.
 Defibrillation: Continued rhythm analysis
and treatment.

24. Airway
 Endotracheal intubation is the most
effective method of ensuring adequate
ventilation, oxygenation, and airway
protection against aspiration during
cardiac arrest. In addition, it is an
additional route of entry for some
resuscitation medications, such as
atropine, epinephrine, and lidocaine.

25. Breathing
 the adequacy of intubation should be checked
by auscultating the chest for equal bilateral
breath sounds, identifying fog in the
endotracheal tube on exhalation,
 Monitoring end-tidal CO2 (using colorimetry or
capnography). The presence of exhaled CO2 on
a monitor indicates proper tracheal tube
placement and can detect subsequent tube
dislodgement.
 A chest X-ray can help determine the location of
the tip of the endotracheal tube in relation to
the carina.

26. Breathing-2
 The patient should be placed on a
ventilator for positive pressure ventilation.
Continuous high flow oxygen and pulse
oximetry should be maintained.

27. Circulation
 Intravenous (IV) access should be obtained,
preferably with a central venous catheter in the
internal jugular, subclavian, or femoral vein. Two
large bore peripheral lines may be acceptable.
 And IV fluids should be infused. The patient’s
rhythm should be identified and appropriate
interventions instituted based on accepted ACLS
guidelines.

31. Asystole and bradycardia
 Atropine has a vagolytic effect by
antagonizing the parasympathetic system.
 Epinephrine improves myocardial and
cerebral blood flow during CPR.
 Early transcutaneous pacing should be
considered for bradycardia.transcutaneous
pacing for asystole has not been shown to
improve survival. As some

32.  Somme patients with asystole are actually in fine
VF, two or more cardiac leads should be checked
before determining that the patient is truly in
asystole.
 recent large randomized study from Europe
comparing epinephrine with vasopressin for
patients in asystole demonstrated that
vasopressin was superior to epinephrine,
suggesting that vasopressin followed by
epinephrine may be more effective than
epinephrine alone in the treatment of refractory
cardiac arrest.

33. Pulseless electrical activity
electromechanical dissociation
 Focus on determining and reversing the
cause:
The most common causes include severe
hypovolemia (usually related to significant
blood loss), hypoxia, acidosis, pericardial
tamponade, tension pneumothorax, large
pulmonary embolus, myocardial infarction,
hypothermia, or drug overdose.

34.  Patient should be intubated to provide adequate
oxygenation and given a rapid IV infusion of
crystalloid.
 If the patient has a treatable rhythm, appropriate
rhythm-specific ACLS algorithms
 If the situation warrants, pericardiocentesis or
needle thoracostomy should be performed.
 If no reversible cause can be determined, the patient
should be given epinephrine every 3–5 minutes. If
the PEA rate is slow, atropine can also be given.
 Unless a reversible cause is discovered, the
prognosis of PEA is poor, with only 1–4% of patients
surviving to hospital discharge.

35.  PEA ASYSTOLE (monitor analysis)
{nonshockable}
 CPR (5 cycles-30:2) 2 min
 Epinephrine 1mg (repeat 3-5 min)
 Vasopressin 40 IU then epinephrine.
 Atropine 1 mg (repeat 3-5 min) {max
3mg} (single dose)
 Then CPR 5 cycles
 Check pulse → CPR →E,A,V →CPR→
check pulse.

36. Ventricular fibrillation )VF( or
pulseless
)ventricular tachycardia )VT
 Attempt debrillation immediately (4 J kg-1 for all
shocks).
 Resume CPR as soon as possible.
 After 2 min, check the cardiac rhythm on the
monitor.
 Give second shock if still in VF/pulseless VT.
 Immediately resume CPR for 2 min and check
monitor; if no change, give adrenaline followed
immediately by a 3rd shock.
 CPR for 2 min.
 Give amiodarone if still in VF/pulseless VT
followed immediately by a 4th shock.

37.  Give adrenaline every 3—5 min during CPR.
 If remains in VF/pulseless VT, continue to
alternate shocks with 2 min of CPR.
 If signs of life become evident, check the
monitor for an organised rhythm; if this is
present, check for a central pulse.
 Identify and treat any reversible causes (4Hs
&4Ts).
 If debrillation was successful but VF/pulseless VT
recurs, resume CPR, give amiodarone and
debrillate again at the dose that was effective
previously. Start a continuous infusion of
amiodarone.

38. Precordial thump
 Consider giving a single precordial thump when
cardiac arrest is confirmed rapidly after a witnessed,
sudden collapse and a defibrillator is not immediately
to hand.
 the technique:
 Using the ulnar edge of a tightly clenched fist, deliver a
sharp impact to the lower half of the sternum from a
height of about 20 cm, then retract the fist immediately to
create an impulse-like stimulus.
 A precordial thump is most likely to be successful in
converting VT to sinus rhythm.

39. Drug administration Routes
IV access: central peripheral
 Drugs typically require 1 to 2 minutes to reach
the central circulation when given via a peripheral
vein but require less time when given via central
venous access.
 If a resuscitation drug is administered by a
peripheral venous route, administer the drug by
bolus injection and follow with a 20-mL bolus of
IV fluid. Elevate the extremity for 10 to 20
seconds to facilitate drug delivery to the central
circulation.

40. Intraosseous (IO) cannulation:
 provides access to a noncollapsible venous
plexus, enabling drug delivery similar to that
achieved by central venous access.
 In the sternum , proximal tibia (2 cm below tt) ,
distal tibia (2 cm above mm)
In endotracheal tube:
 Epinepherine , Atropine , Vasopressin ,
lidocaine , naloxone.
 Give at dose 2.5-3 times usual iv dose.
 Dilute in 5-10 ml saline.

41. Medications for Arrest Rhythms
Vasopressors :
 at any stage during management of pulseless
VT, VF, PEA, or asystole increases the rate of
neurologically intact survival to hospital
discharge.
 Epinepherine: It is appropriate to administer a 1-
mg dose of epinephrine IV/IO every 3 to 5
minutes during adult cardiac arrest. Higher
doses may be indicated to treat specific
problems, such as В-blocker or calcium channel
blocker overdose. may be given by the
endotracheal route at a dose of 2 to 2.5 mg.

42.  Vasopressin: Vasopressin is a
nonadrenergic peripheral vasoconstrictor
that also causes coronary and renal
vasoconstriction.(40 U, with the dose
repetition only once).

43. Atropine
 in asystole or slow PEA arrest.
 The recommended dose of atropine for
cardiac arrest is 1 mg IV, whichcan be
repeated every 3 to 5 minutes (maximum
total of 3 doses or 3 mg) if asystole
persists.
 Endotracheal route also used.

44. Antiarrhythmics
Amiodarone:
 administered for VF or pulseless VT
unresponsive to CPR, shock, and a vasopressor.
 An initial dose of 300 mg IV/IO can be followed
by one dose of 150 mg IV/IO.
Lidocaine:
 considered an alternative treatment to
amiodarone.The initial dose is 1 to 1.5 mg/kg IV.
 If VF/ pulseless VT persists, additional doses of
0.5 to 0.75mg/kg IV push may be administered
at 5- to 10 minute intervals, to a maximum dose
of 3 mg/kg.

45. Magnesium:
 When VF/pulseless VT cardiac arrest is
associated with torsades de pointes,
magnesium sulfate at a dose of 1 to 2 g
diluted in 10 mL D5WIV/IO push, typically
over 5 to 20 minutes.
 When torsades is present in the patient
with pulses, the same 1 to 2 g is mixed in
50 to 100 mL of D5Wand given as a
loading dose. It can be given more slowly
(eg, over 5 to 60 minutes IV)

46. Pacing in Arrest
 Several randomized controlled trials failed
to show benefit from attempted pacing for
asystole.
 At this time use of pacing for patients
with asystolic cardiac arrest is not
recommended.

47. Routine Administration of IV Fluids
During
Cardiac Arrest
 There were no published human studies
evaluating the effect of routine fluid
administration during normovolemic cardiac
arrest
 There is insufficient evidence to recommend
routine administration of fluids to treat cardiac
arrest.
 Fluids should be infused if hypovolemia is
suspected.

48. Monitoring
Assessment During CPR:
 At present there are no reliable clinical
criteria that clinicians can use to assess
the efficacy of CPR. Although end-tidal
CO2 serves as an indicator of cardiac
output produced by chest compressions
and may indicate return of spontaneous
circulation

49. Assessment of Hemodynamics
1-Coronary Perfusion Pressure
 (CPP= aortic relaxation [diastolic] pressure
minus right atrial relaxation phase blood
pressure)
 during CPR correlates with both myocardial
blood flow and ROSC.
 A CPP of 15 mm Hg is predictive of ROSC.
Increased CPP correlate with improved 24-hour
survival rates in animal studies.
 Rarely available

50. Pulses-2
 Clinicians frequently try to palpate arterial pulses
during chest compressions to assess the
effectiveness of compressions.
 No studies have shown the validity or clinical
utility of checking pulses during ongoing CPR.
Because there are no valves in the inferior vena
cava, retrograde blood flow into the venous
system may produce femoral vein pulsations.
Thus palpation of a pulse in the femoral triangle
may indicate venous rather than arterial blood
flow.
 Carotid pulsations during CPR do not indicate the
efficacy of coronary blood flow or myocardial or
cerebral perfusion during CPR.

51. Assessment of Respiratory
Gases
1-Arterial Blood Gases
 not a reliable indicator of the severity of
tissue hypoxemia, hypercarbia, or tissue
acidosis.
2-Oximetry
 During cardiac arrest, pulse oximetry will
not function because pulsatile blood flow
is inadequate in peripheral tissue beds.

52. End-Tidal CO2 Monitoring
 useful as a noninvasive indicator of cardiac
output generated during CPR.
 major determinant of CO2 excretion is its rate of
delivery from the peripheral production sites to
the lungs.
 In the low-flow state during CPR, ventilation is
relatively high compared with blood flow, so that
the end-tidal CO2 concentration is low.
 If ventilation is reasonably constant, then
changes in end-tidal CO2 concentration reflect
changes in cardiac output.

53. Duration of CPR
 Arrest time< 6 min→30 min CPR
 Arrest time> 6 min→15 min CPR

54. Post-CPR Management
 Induced hypothermia(32-34o)(12-24 hr)
 Glucose control
 Organ-Specific Evaluation and Support

55. Prognosis
1-strongly predict death or poor neurologic
outcome, with 4 of the 5 predictors
detectable at 24 hours after resuscitation:
 Absent corneal reflex at 24 hours
 Absent pupillary response at 24 hours
 Absent withdrawal response to pain at 24
hours
 No motor response at 24 hours
 No motor response at 72 hours

56.  2-An electroencephalogram performed 24
2-
to 48 hours after resuscitation has also
been shown to provide useful predictive
value.
 3-GCS: <5 ON 3rd day =no chance for
neurological recovery.
 4- Duration of coma:
 >4-6 hr =poor prognosis
 >24 hr =10% recovery
 >72 hr = 5% recovery
 > 2 wk = no recovery at all.