Transcript [Company Name]

Cardiopulmonary Resuscitation
( CPR )
Houman Teymourian, M.D.
Assistant professor, Department of Anesthesiology and
Critical Care, Shahid Beheshti Medical University
GOAL
 Artificial delivery of oxygenated
blood to systemic circulatory
bed at rates sufficient for
preserving vital organ function
and physiologic substrates until
spontaneous circulation is
reestablished.
History
1) Can be traced to at least Bibilical time
2) Contemporary approaches to CPR
dates back to 1966
3) 2000 Guide line: the first
internationally recognized resuscitation
guideline by AHA and European
resuscitation council
4) 2007 Guide line: different aspects
BLS ( basic life support )
1) Ventilation ( A-B)
2) Perfusion ( C )
3) CPR Assessment
4) Automated External Defibrillation
(D)
But first:
 check responsiveness
 check pulse
 call for help and defibrillator
Assess
circulation
– 10 seconds
– Carotid pulse in
adults
and children
– Brachial in
infants
Airway Control and Ventilation
1. Ventilation is critical for
restoration of spontaneous
circulation
2. Techniques used are dependent on
the clinical situation
In out of hospital setting:
- Mouth to mouth or mask to
mouth
- Head tilt, Chin lift, Jaw thrust
The major cause of upper airway
obstruction in unconscious
human is epiglottis
move
hyoid bone anteriorly
Open the Airway
 Head-tilt/chin lift (no trauma victims)
• The most common cause of obstruction is the
epiglottis
Open the Airway
 Jaw thrust (trauma)
Mouth to mouth
Mouth to Mask Ventilation
Rescue Breathing :
 2 breath slowly ( 1.5 – 2 second ) after
30th compression during 1 or 2 person
CPR until the airway is secured.
 Slowly, to minimize high airway
pressure and not to open esophagus.
( gastric inflation and aspiration )
 Endo tracheal tube is the standard
of airway control
 Alternatives:
- ( LMA ) laryngeal mask airway
- ( C.T. ) Combitube
- ( Ph.T ) Pharyngeal tube
Not protecting from aspiration
Chest compression ( perfusion )
 Delivery of oxygenated blood
during cardiac arrest
 Recommended rate: 100/min
 Depth: 1.5 to 2 inches ( 25 pounds )
 Must generate a palpable carotid or
femoral pulse
 Compression to relaxation: 1:1
 In 1 person CPR 15:2 compression -
ventilation
 In 2 person CPR 15:2 when airway is
not secured
 In 2 person CPR 5:1 when airway is
secured
 Continuous chest compression +
asynchronous ventilation
Physiology
 Direct cardiac compression is the
main mechanism of blood flow
( cardiac pump mechanism )
 Increased intra thoracic pressure is
another
( thoracic pump mechanism )
Other ways of chest
compression
IAC ( Interposed Abdominal
compression )
 Aortic diastolic pressure Coronary blood flow
 Vest CPR ( chest
circumferential bladder )
 Active compression – de
compression
( IRON Lung )
* Classic CPR is recommended.

CPR assessment
( monitoring performance of CPR )
 Palpation of carotid or femoral pulse is not
an objective evidence of the effectiveness of
cardiac out put and only shows the
transmission of a pressure wave in to the
arterial tree.
 Pupil size are of prognostic values
constricted, or dilated but contracting to light
are associated with a greater success in CPR
and neurological out comes.
 Direct systemic arterial pressure
monitoring is gold standard
( Central arterial catheter )
 Aortic diastolic pressure = coronary
perfusion pressure
 P Et CO2 : is a precise of lung
perfusion and cardiac out put.
The automated external
defibrillator
 Most frequent cardiac rhythm in
witnessed arrest in adult is VF.
 CPR prolongs the duration of VF
but cannot convert the arrhythmia to
an organized rhythm.
 AED is capable to recognize VF and
VT
 was first introduced in 1979
 AED is a part of BLS now
 Chest compression must be stopped
 3 shocks is given automatically
 150 J Biphasic non escalating
( equivalent to monophasic 200 – 300 J )
 Must take place in less than 5 min in
public places
ACLS
( Advanced Cardiac Life Support )
 ACLS is a body knowledge and skill
with which a physician must be
thoroughly familiar
 In a study using a computer the
simulates cardiac arrest
Only 30% of physician managed a
simulated cardiac arrest in accordance
with AHA ACLS guide line
 Time since the last ACLS training is
an important predictor of proper
management of cardiac arrest.
 Within 6 months 71% successful
management
 6 month to 2 years 30% successful
management
 Longer than 2 years non
Management of cardiac arrest
 Prompt recognition and treatment of
potentially life threatening
arrhythmia are essential components
of ACLS
 Has two compounds: electrical and
pharmacologic
Pulse less ventricular tachycardia
and ventricular fibrillation
 Therapeutically are considered the
same
 The most common form of cardiac
arrest
 The greatest likely hood of short
and long term survival
 Definitive intervention is rapid
defibrillation
 Continue chest compression
 Secure air way( ETT)
 Hyper ventilate
 Obtain IV access

but do not delay defibrillation
Defibrillation
Two practical and important considerations are:
1. Energy out put
Termination of VF is critically dependent on the
amount of energy.
2. Resistance to current flow
Flow is inversely related to resistance to minimize
resistance:
one must use proper electrode position ( sternum
and apex )
Firm pressure ( 11 kg/each paddle )
Optimal chest wall medium
self adhesive paddles
Electrode paste
End expiration defibrillations
Defibrillation
 150 J biphasic or 200 J monophasic
followed by 200 – 300 J and third one of
360 J
 3 shock should be delivered rapidly
 If witness but not monitored arrest is
seen a single pericardial thump can be
applied
 If VF recurs the series of three shocks
must be repeated
 If VF persist
drug therapy
So
1. Airway and ventilation ( ETT and
100% O2 )
2. Defibrillation take precedence
over intubation if defibrillator is
ready
3. Drugs
4. chest compression continues
Routes of Drug
Administration
 Peripheral veins
 Central veins
 Tracheal
 Intraosseous
 Intracardiac
Peripheral Venous Route
 Peak effect 1.5-3 min. after injection
at antecubital fossa
 IV push
– 20 ml NS flush after drug injection
–  circulation time by 40%
– Comparable to drug delivery through a
central vein
Central Venous Route
 Faster, higher peak concentration and
more potent effect compared to
peripheral injection
 Should be used if it is already in situ
 Inserting a central line is associated
with problems of interrupting CPR,
bleeding arterial puncture and air
embolism
Tracheal Route
 Second line route due to impaired
absorption and unpredictable
pharmacodynamics
 Need 2-3 times the IV dose, diluted to at
least 10 ml in 0.9% NS
 Non-ionic drugs only:
– adrenalin, atropine, lidocaine and naloxone
Drugs
1.
-
-
Epinephrine ( through CV line )
Regardless of under lying rhythm has beneficial
effects ( cerebral and coronary flow )
Recommended dose: 1 mg( 10 cc – 1: 10000 )
every 3 to 5 min as long as cardiac arrest persist
Can be injected to tracheal tube
Recommended dose : 2 – 2.5 times the Iv dose
Half life: 3 to 5 min
Large dose: 0.2 mg/kg was thought to be
beneficial but to day is not accepted in CPR
2. Vasopressin
- Clinical data shows endogenous plasma
vasopressin level is significantly higher
in patient successfully resuscitated
versus in those who died
- Acts on V1 smooth muscle receptor
results in longer vasoconstriction and
increase in coronary flow
- Even in sever acidosis
- It is an alternative to adrenaline
- Recommended dose 40 unit/only one
time
- Has longer half life ( 10 – 20 min )
If VF Persists
 Third shock is delivered ( 360 J mono or
200 J Biphasic )
Then if VF persists:
Lidocaine 1.5 mg/kg or amiodarone 300 mg
IV
 Lidocaine enhances ventricular
defibrillation ( lower energy, fewer shock )
but it is controversial
AHA: it is an intermediate intervention
without evidence of benefit or harm
 Amiodarone Prolongs the action
potentials and refractoriness in cardiac
tissue
 Is superior to lidocaine to end VF but
does not increase discharge rate
– Rapid infusion of 300 mg in 20-30 ml NS IV
push (cardiac arrest dose)
– If VF/pulseless VT recurs,
•
•
•
Supplementary doses of 150 mg IV by rapid
infusion
Followed by 1 mg/min for 6 hours and then 0.5
mg/min
Maximum daily dose of 2 g
No response?

1.
2.
3.
4.
5.
Consider:
Procainamide 100 mg every 5 min up to
17 mg/kg (750-1500 mg)
Magnesium sulfate 1 gr IV every 5 min
up to 4 gr
Phenitoin 50 mg/min Iv (250 mg)
Esmolol 0.3 mg/kg/min Iv infusion
Isoproterenol
If VF persists:
Sodium bicarbonate infusion if
1. Pre existing acidosis
2. Acidosis documented with ABG
3. Hyperkalemia
Sodium bicarbonate
 no benefit in survival of VF
 adverse effect are documented:
Plasma hyperosmolality
Paradoxical cerebrospinal fluid acidosis
CO2 generation
vasodilatation
hypotension
In cardiac arrest pulmonary blood flow
Co2 transport and elimination
=Metabolic + respiratory acidosis
* Bicarbonate should not be used
routinely in treatment of cardiac
arrest
1. It is used if prolonged VF arrest
exist ( at least 15 min )
2. Initial does: 1 mEq/kg
3. Followed by: 0.5 mEq/kg every
10 min
4. ABG- treat can be based on
measurement
( PEA )
Pulseless Electrical activity
Refers to heterogeneous group of
cardiac rhythm characterized by
pulseless ness in presence of some type
electrical activities other than VF or VT
2. Included electromechanical dissociation
( Idioventricular rhythm, Bradyasystole)
3. High priority must be given to
identification of a correctible cause.
1.
Possible Underlying
Reversible Causes
T’s
H’s
 Hypovolemia
 Hypoxia
 Hydrogen ion
(acidosis)
 Hyperkalemia/
hypokalemia/
metabolic
disorders
 Hypothermia/
hyperthermia
 Toxins/tablets




(drug overdose)
Tamponade,
cardiac
Tension
pneumothorax
Thrombosis,
coronary
Thrombosis,
pulmonary
1. In any form of PEA
A -B- C
inject Epinephrine
( and atropine if bradycardia is present)
2. Pacing may be indicated
3. Find the cause
Asystole
- Complete and sustained absence of
electrical activity
- Almost irreversible
- Almost after uncorrected derangements
such as hypoxia, severe hyperkalemia
massive drug over dose, MI,
hypothermia
- Epinephrine 1 mg every 3 – 5 min
- Bicarbonate 1 mEq/kg if hyperkalema
or metabolic acidosis is observed
- Pacing is unlikely to be useful
Asystole
Out Comes
 Discharge survival for in hospital CPR range
from 8 to 21% , approximately 14%
( 86% death ).
 Discharge survival rate in ICU arrests is
3.3%
 Most favorable out come is seen in VF – VT
 Almost non of Asystole arrest
would
discharge
 Age is a major determinant, almost non of 70
years or above would discharge
 Presence of sepsis cancer and organ failure
lowers the discharge rate.
CPR
CPR IS A MECHANICAL
PROCEDURE
CPR IS A MECHANICAL PROCEDURE
CPR IS A MECHANICAL
PROCEDURE
CPR IS A MECHANICAL
PROCEDURE
CPR IS A MECHANICAL
PROCEDURE
THANK YOU