Management of cardiac arrest
-
Upload
paleenui-jariyakanjana -
Category
Education
-
view
2.067 -
download
4
Transcript of Management of cardiac arrest
Management of Cardiac ArrestPaleerat Jariyakanjana, MD
Chain of Survival
Immediate recognition of cardiac arrest and activation of the emergency response system
Early cardiopulmonary resuscitation (CPR) with an emphasis on chest compressions
Rapid defibrillation Effective advanced life support Integrated post-cardiac arrest care
Chain of Survival
OVERVIEW
Cause ventricular fibrillation (VF) pulseless ventricular tachycardia (VT) pulseless electric activity (PEA) asystole
Ventricular Fibrillation
Ventricular Tachycardia
Asystole
Survival from these cardiac arrest rhythms requires basic life support (BLS) system of advanced cardiovascular life support
(ACLS) integrated post– cardiac arrest care
Periodic pauses in CPR brief as possible assess rhythm, shock VF/VT, perform a pulse check
when an organized rhythm is detected, or place an advanced airway
absence of an advanced airway synchronized compression–ventilation ratio of 30:2 compression rate of at least 100 per minute.
After placement of a supraglottic airway or an endotracheal tube chest compressions should deliver at least 100
compressions per minute continuously without pauses for ventilation
delivering ventilations should give 1 breath every 6-8 seconds (8-10 breaths per minute)
avoid delivering an excessive number of ventilations
Understanding the importance of diagnosing and treating the underlying cause is fundamental to management of all cardiac arrest rhythms.
RHYTHM-BASED MANAGEMENT OF CARDIAC ARREST
Paddles and electrode pads: anterior-lateral position
Iany doubt about the presence of a pulse chest compressions
rhythm can be diagnosed before CPR is initiated
VF/PULSELESS VT
resume CPR while charges the defibrillator chest compressions should switch at every 2-
minute cycle to minimize fatigue
Defibrillation Strategies
Waveform and Energy biphasic defibrillator: manufacturer’s
recommended energy dose (120-200 J) (Class I, LOE B)
unaware of the effective dose range: maximal dose (Class IIb, LOE C)
Defibrillation Strategies
Waveform and Energy Second and subsequent energy levels should
be at least equivalent, and higher energy levels may be considered if available (Class IIb, LOE B).
monophasic defibrillator: 360 J subsequent shocks at the previously successful
energy level
CPR Before Defibrillation
Performing CPR while a defibrillator is readied for use is strongly recommended for all patients in cardiac arrest (Class I, LOE B).
Drug Therapy in VF/Pulseless VT
Amiodarone: first-line antiarrhythmic agent Magnesium sulfate
torsades de pointes associated with a long QT interval
Class IIb, LOE B
Treating Potentially Reversible Causes of VF/Pulseless VT
refractory VF/pulseless VT: AMI
PEA/ASYSTOLE
Drug Therapy for PEA/Asystole
vasopressor can be given as soon as feasible Available evidence suggests that the routine
use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B).
For this reason atropine has been removed from the cardiac arrest algorithm.
Treating Potentially Reversible Causes of PEA/Asystole
PEA reversible conditions treated successfully if those conditions are identified
and corrected
Hypoxemia: advanced airway severe volume loss or sepsis: administration of
empirical IV/IO crystalloid. severe blood loss: blood transfusion pulmonary embolism: empirical fibrinolytic
therapy (Class IIa, LOE B) tension pneumothorax: needle decompression
Treating Potentially Reversible Causes of PEA/Asystole
Asystole end-stage rhythm that follows prolonged VF or PEA,
and for this reason the prognosis is generally much worse
MONITORING DURING CPR
Mechanical Parameters
rate of compression: ≥ 100/min depth of compression: ≥2 inches (5 cm) rate of ventilation: 1 breath every 6-8 s (8-10
breath/min)
Physiologic Parameters
Pulse End-Tidal CO2 Coronary Perfusion Pressure and Arterial
Relaxation Pressure Central Venous Oxygen Saturation Pulse Oximetry Arterial Blood Gases Echocardiography
Pulse
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.
Pulse
Carotid pulsations during CPR do not indicate the efficacy of myocardial or cerebral perfusion during CPR.
no more than 10 seconds to check for a pulse If it is not felt within that time period chest
compressions should be started
End-Tidal CO2
During untreated cardiac arrest CO2 continues to be produced in the body, but there is no CO2 delivery to the lungs.
Under these conditions PETCO2 will approach zero with continued ventilation. With initiation of CPR, cardiac output is the major determinant of CO2 delivery to the lungs.
If ventilation is relatively constant, PETCO2 correlates well with cardiac output during CPR.
End-Tidal CO2
If PETCO2 is <10 mm Hg, it is reasonable to consider trying to improve CPR quality by optimizing chest compression parameters (Class IIb, LOE C).
If PETCO2 abruptly increases to a normal value (35-40 mm Hg), it is reasonable to consider that this is an indicator of ROSC (Class IIa, LOE B).
Coronary Perfusion Pressure and ArterialRelaxation Pressure
Increased CPP correlates with improved 24-hour survival rates and is associated with improved myocardial blood flow and ROSC
If the arterial relaxation “diastolic” pressure is <20 mm Hg, it is reasonable to consider trying to improve quality of CPR by optimizing chest compression parameters or giving a vasopressor or both (Class IIb, LOE C).
Pulse Oximetry
typically does not provide a reliable signal because pulsatile blood flow is inadequate in peripheral tissue beds
Arterial Blood Gases
Arterial blood gas monitoring during CPR is not a reliable indicator of the severity of tissue hypoxemia, hypercarbia, or tissue acidosis.
Routine measurement of arterial blood gases during CPR has uncertain value (Class IIb, LOE C).
ACCESS FOR PARENTERAL MEDICATIONS DURINGCARDIAC ARREST
worsened survival for every minute that antiarrhythmic drug delivery was delayed
Time to drug administration was also a predictor of ROSC
insufficient evidence to specify exact time parameters or the precise sequence with which drugs
Peripheral IV Drug Delivery
bolus injection and followed with a 20-mL bolus of IV fluid
IO Drug Delivery
all age groups
Central IV Drug Delivery
peak drug concentrations are higher and drug circulation times shorter
interrupt CPR
Endotracheal Drug Delivery
lidocaine, epinephrine, atropine, naloxone, and vasopressin
2-21⁄2 times the recommended IV dose dilute the recommended dose in 5-10 mL of
sterile water or normal saline and inject the drug directly into the endotracheal tube
ADVANCED AIRWAY
delayed endotracheal intubation combined with passive oxygen delivery and minimally interrupted chest compressions was associated with improved neurologically intact survival after out-of-hospital cardiac arrest in patients with witnessed VF/VT
When an advanced airway (eg, endotracheal tube or supraglottic airway) is placed, 2 providers no longer deliver cycles of compressions interrupted with pauses for ventilation.
1 breath every 6-8 seconds (8-10 breaths per minute)
MEDICATIONS FOR ARREST RHYTHMS
Epinephrine
It is reasonable to consider administering a 1 mg dose of IV/IO epinephrine every 3-5 minutes during adult cardiac arrest (Class IIb, LOE A).
If IV/IO access is delayed or cannot be established, epinephrine may be given endotracheally at a dose of 2-2.5 mg.
Vasopressin
nonadrenergic peripheral vasoconstrictor 1 dose of vasopressin 40 units IV/IO may
replace either the first or second dose of epinephrine in the treatment of cardiac arrest (Class IIb, LOE A)
Amiodarone
An initial dose of 300 mg IV/IO can be followed by 1 dose of 150 mg IV/IO.
Lidocaine
considered if amiodarone is not available (Class IIb, LOE B)
The initial dose is 1-1.5 mg/kg IV. If VF/pulseless VT persists, additional doses of
0.5-0.75 mg/kg IV push may be administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg.
Magnesium Sulfate
torsades de pointes IV/IO bolus of magnesium sulfate at a dose of 1-
2 g diluted in 10 mL D5W (Class IIb, LOE C)
ANY QUESTIONS?