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A.M. TAKDIR MUSBA EMERGENCY AND TRAUMATOLOGY , 2010
A.M. TAKDIR MUSBA EMERGENCY AND TRAUMATOLOGY , 2010

A.M. TAKDIR MUSBA

EMERGENCY AND TRAUMATOLOGY , 2010

 Cardiorespiratory arrest is the sudden, unexpected cessation of respiration and functional circulation.

Cardiorespiratory arrest is the sudden, unexpected cessation of respiration and functional circulation.

CPCR Principle

4 – 6 minutes
4 – 6 minutes

CPCR

During respiratory and cardiac arrest, CPCR may be

successful

if performed before biological death

of vital tissue develops.

1. Degree of preexisting hypoxia of the cells. 2. The brain depends totally on oxygen and

1. Degree of preexisting hypoxia of the cells.

  • 2. The brain depends totally on

oxygen and is the organ least able to

withstand hypoxia.

  • 3. The whether circulatory or respiratory arrest occurs first.

A. Cardiac asystole . B. Ventricular fibrillation or Pulseless VT Electrical defibrillation is required to reestablish

A. Cardiac asystole. B. Ventricular fibrillation or Pulseless VT

Electrical defibrillation is required to reestablish spontaneous and effective cardiac electrical activity.

C. Electromechanical dissociation

circulatory collapse that occurs despite satisfactory electrical complexes on the ECG

1. Low cardiac output. 2. Hyparcapnia. 3. Hyperkalemia. 4. Hypoxia and vagal stimulation. 5. Stimulation of
  • 1. Low cardiac output.

  • 2. Hyparcapnia.

  • 3. Hyperkalemia.

  • 4. Hypoxia and vagal stimulation.

  • 5. Stimulation of the heart.

  • 6. Coronary occlusion.

  • 7. Overdosage.

  • 8. Hypothermia.

  • 9. Hyperthermia 10. Acidosis

1. Airway obstruction by vomitus, foreign body, blood, secretions, solid material, mucous plugs, laryngeal or bronchial

1. Airway obstruction by vomitus, foreign body, blood, secretions, solid material, mucous plugs, laryngeal or bronchial spasm, or tumor.

2. CNS depression: caused by stroke, head trauma, hypercapnia, barbiturates,narcotics, tranquilizers, or anesthetics.

3. Neuromuscular failure secondary to poliomyelitis, muscular dystrophy, myasthenia, or muscle relaxant drugs.

Flail chest Pneumothorax Massive atelectasis Acute pulmonary embolism Congestive heart failure Overwhelming pneumonia Gram-negative septicemia Lung

Flail chest Pneumothorax Massive atelectasis Acute pulmonary embolism Congestive heart failure Overwhelming pneumonia Gram-negative septicemia Lung burns Carbon monoxide poisoning Massive blood loss.

 In geriatric or pediatric patients.  In patients with a history of arrhythmias, heart block,

In geriatric or pediatric patients.

In patients with a history of arrhythmias, heart block, digitalis toxicity, myocarditis , myocardial infarction, congestive heart failure, electrolyte imbalance , or dehydration.

In massive hemorrhage. During or following heart surgery.

The initial goal of therapy is BRAIN oxygenation The second goal is restoration of circulation. Underlying

The initial goal of therapy is BRAIN oxygenation

The second goal is restoration of circulation.

Underlying condition must be corrected.

CPCR is not indicated for all patients. Natural death in the aged or in the terminal stages of a chronic illness

CPCR should be performed in cases of reversible unexpected death

Basic Life support (BLS):

Airway, Breathing, Circulation, Drug (Defibrillation )

Advanced life support (ALS):

Airway, Breathing, Circulation, Drug (Defibrillation), ECG, Fluid, Gauge, ICU

ABCD steps A, airway. B, breathing. C, circulation. D, drugs and definitive therapy. In a witnessed

ABCD steps

A, airway. B, breathing. C, circulation. D, drugs and definitive therapy.

In a witnessed cardiac arrest (when treatment can be initiated within 1 min of the onset of arrest), the ABCD sequence should include use of a precordial thump.

Precordial Thumb

Precordial Thumb

Adult Basic Life Support

If breathing:

recovery position

CHECK

RESPONSIVENESS

Shake and shout

 
OPEN AIRWAY CHECK BREATHING

OPEN AIRWAY

 
OPEN AIRWAY CHECK BREATHING

CHECK BREATHING

 
OPEN AIRWAY CHECK BREATHING

Head tilt / Chin lift

Look, listen and feel

BREATHE

2 effective breaths

Adult Basic Life Support If breathing: recovery position CHECK RESPONSIVENESS Shake and shout OPEN AIRWAY CHECK
ASSESS 10 secs only
ASSESS
10 secs only

Signs of a circulation

ASSESS 10 secs only Signs of a circulation CIRCULATION PRESENT Continue Rescue Breathing NO CIRCULATION Compress

CIRCULATION PRESENT

Continue Rescue Breathing

NO CIRCULATION

Compress Chest

Check circulation Every minute

100 per minute 15:2 ratio

Send or go for help as soon as possible according to guidelines

External Cardiac Compressio

External Cardiac Compressio 1. vertically downward 4-5 cm 2. Push hard push fast 3. 100 x/min.
  • 1. vertically downward 4-5 cm

  • 2. Push hard push fast

  • 3. 100 x/min.

Cardiac Compression

Cardiac Compression

 Defibrillate up to 3 times Ventricular fibrillation  Epinephrine – several dose options  Antiarrhythmic

Defibrillate up to 3 times

Ventricular fibrillation

 Defibrillate up to 3 times Ventricular fibrillation  Epinephrine – several dose options  Antiarrhythmic

Epinephrine – several dose options

Antiarrhythmic agents

Lidocaine Bretylium Magnesium Procainamide

• Search for reversible causes and treat • Epinephrine • Atropine for absolute or relative bradicardia

Search for reversible causes and treat

Epinephrine

Atropine for absolute or relative bradicardia

• Search for reversible causes and treat • Epinephrine • Atropine for absolute or relative bradicardia
 Epinephrine  Atropine  Consider transcutaneous pacing  Search for reversible causes and treat if

Epinephrine Atropine

Consider transcutaneous pacing

Search for reversible causes and treat if possible

 Atropine Atropine  Dopamine Dopamine  Epinephrine Epinephrine  Transcutaneous Transcutaneous pacing pacing  Transvenous
 Atropine Atropine  Dopamine Dopamine  Epinephrine Epinephrine  Transcutaneous Transcutaneous pacing pacing  Transvenous

Atropine Atropine Dopamine Dopamine Epinephrine Epinephrine Transcutaneous Transcutaneous pacing pacing Transvenous Transvenous pacing pacing

 Immediate Immediate cardioversion cardioversion  Premedicate Premedicate when when possible possible  Synchronized Synchronized setting

Immediate

Immediate cardioversion

cardioversion

Premedicate

Premedicate when

when possible

possible

Synchronized

Synchronized setting

setting

 Immediate Immediate cardioversion cardioversion  Premedicate Premedicate when when possible possible  Synchronized Synchronized setting
 Narrow-complex Narrow-complex  Adenosine  Verapamil Verapamil  Diltiazem Diltiazem    -blockers 
 Narrow-complex Narrow-complex  Adenosine  Verapamil Verapamil  Diltiazem Diltiazem    -blockers 

Narrow-complex Narrow-complex

Adenosine

Verapamil Verapamil

Diltiazem Diltiazem

-blockers -blockers

Digoxin Digoxin

Synchronized Synchronized

cardioversion

cardioversion

• Wide-complex – Lidocaine – Procainamide – Bretylium – Consider adenosine • Synchronized cardioversion
• Wide-complex – Lidocaine – Procainamide – Bretylium – Consider adenosine • Synchronized cardioversion

Wide-complex

Lidocaine

Procainamide

Bretylium

Consider adenosine

Synchronized

cardioversion

It is critical to survival from sudden cardiac arrest (SCA) for several reasons: (1) the most

It is critical to survival from sudden

cardiac arrest (SCA) for several reasons:

(1) the most frequent initial rhythm in

witnessed is ventricular fibrillation (VF),

(2) the treatment for VF is electrical

defibrillation,

(3) The probability of successful

defibrillation diminishes rapidly over

time, and

(4) VF tends to deteriorate to asystole

within a few minutes

Defibrillation delivery of current through

the chest and to the heart to depolarize

myocardial cells and eliminate VF.

The energy settings for defibrillators are

designed to provide the lowest effective

energy needed to terminate VF.

Electrophysiologic event that occurs in 300 to

500 milliseconds after shock delivery.

Defibrillation (shock success) is typically

defined as termination of VF for at least 5

seconds following the shock.

 Biphasic defibrillator (initial shock) :  selected energies of 150 J to 200 J (biphasic

Biphasic defibrillator (initial shock) :

selected energies of 150 J to 200 J (biphasic truncated exponential waveform) or 120 J (rectilinear biphasic waveform). For second and subsequent shocks, use the same or higher energy

 Monophasic defibrillator : select a dose of 360 J for all shocks.  If VF

Monophasic defibrillator : select a dose of 360 J for all shocks.

If VF is initially terminated by a shock but then recurs later in the arrest, deliver subsequent shocks at the previously successful energy level.

 Shock delivery that is timed (synchronized) with the QRS complex.  The energy (shock dose)

Shock delivery that is timed (synchronized) with the QRS complex.

The energy (shock dose) used is lower than that used for unsynchronized shocks (defibrillation).

These low-energy shocks if delivered as unsynchronized are likely to induce VF.

If cardioversion is needed and it is impossible to synchronize a shock (eg, the patient’s rhythm is irregular), use high-energy unsynchronized shocks.

 Ventricular tachycardia  Ventricular tachycardia with a pulse responds well to cardioversion using initial monophasic

Ventricular tachycardia

Ventricular tachycardia with a pulse

responds well to cardioversion using

initial monophasic energies of 200 J.

Use biphasic energy levels of 120—150 J

for the initial shock.

Give stepwise increases if the first shock

fails to achieve sinus rhythm.

Electrode Position

Electrode Position
Electrode Position

Drugs should be considered only after initial shocks have been delivered (if indicated) and chest compressions and ventilation have been started.

Three groups of drugs relevant to the management of cardiac arrest (2005 Consensus Conference): vasopressors, anti-arrhythmics and other drugs.

 Adrenaline - the primary sympathomimetic agent for the management of cardiac arrest for 40 years.

Adrenaline - the primary sympathomimetic

agent for the management of cardiac arrest

for 40 years.

Alpha-adrenergic actions, vasoconstrictive

effects systemic vasoconstriction, which

increases coronary and cerebral perfusion

pressures.

Beta-adrenergic actions, (inotropic,

chronotropic) may increase coronary and

cerebral blood flow.

.

 Indications  Adrenaline is the first drug used in cardiac arrest of any aetiology: it

Indications

Adrenaline is the first drug used in cardiac arrest of any aetiology: it is included in the ALS algorithm for use every 3—5 min of CPR.

Adrenaline is preferred in the treatment of anaphylaxis.

Adrenaline is second-line treatment for cardiogenic shock.

Dose. During cardiac arrest, the initial intravenous dose of adrenaline is 1 mg.

When intravascular (intravenous or intra-osseous) access is delayed or cannot be achieved, give 2—3 mg, diluted to 10 ml with sterile water, via the tracheal tube. Absorption via the tracheal route is highly variable.

 Amiodarone is a membranestabilising anti- arrhythmic drug that increases the duration of the action potential

Amiodarone is a membranestabilising anti- arrhythmic drug that increases the duration of the action potential and refractory period in atrial and ventricular myocardium.

Atrioventricular conduction is slowed, and a similar effect is seen with accessory pathways.

Amiodarone has a mild negative inotropic action and causes peripheral vasodilation through non-competitive alpha-blocking effects.

 Indications .  refractory VF/VT  haemodynamically stable ventricular tachycardia (VT) and other resistant tachyarrhythmias

Indications.

refractory VF/VT

haemodynamically stable ventricular tachycardia (VT) and other resistant tachyarrhythmias

Dose. Consider an initial intravenous dose of 300 mg amiodarone, diluted in 5% dextrose to a volume of 20 ml (or from a pre-filled syringe), if VF/VT persists after the third shock.

Amiodarone can cause thrombophlebitis when injected into a peripheral vein; use a central venous catheter if one is in situ but,if not, use a large peripheral vein and a generous flush.

 Indications . Lidocaine is indicated in refractory VF/VT (when amiodarone is unavailable).  Dose .

Indications. Lidocaine is indicated in refractory VF/VT (when amiodarone is unavailable).

Dose. an initial dose of 100 mg (1— 1.5 mg/kg) for VF/pulseless VT refractory to three shocks.

Give an additional bolus of 50 mg if necessary.

The total dose should not exceed 3 mg/kg during the first hour.

 Atropine . antagonises the action of the parasympathetic neurotransmitter acetylcholine at muscarinic receptors.  Blocks

Atropine. antagonises the action of the parasympathetic neurotransmitter acetylcholine at muscarinic receptors.

Blocks the effect of the vagus nerve on both the sinoatrial (SA) node and the atrioventricular (AV) node, increasing sinus automaticity and facilitating AV node conduction.

 is indicated in:  asystole  pulseless electrical activity (PEA) with a rate <60/min. 

is indicated in:

asystole pulseless electrical activity (PEA) with a rate <60/min. sinus, atrial, or nodal bradycardia when the haemodynamic condition of the patient is unstable. The recommended adult dose of atropine

for asystole or PEA with a rate <60 /min

is

3 mg i.v. in a single bolus.

 CPR must be continued until  Cardiopulmonary system is stabilized  The patient is pronounced

CPR must be continued until Cardiopulmonary system is stabilized The patient is pronounced death Alone rescuer is physically unable to continue