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TAKDIR MUSBA
CPCR Principle
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 is the organ least able to withstand hypoxia.
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 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 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 burns Carbon monoxide poisoning Massive blood loss.
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 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
Precordial Thumb
CHECK RESPONSIVENESS
OPEN AIRWAY
CHECK BREATHING
BREATHE
2 effective breaths
Signs of a circulation
1. 2. 3. 4.
vertically downward 4-5 cm Push hard push fast 100 x/min. Ratio Comp : Vent 30 : 2
Cardiac Compression
Defibrillate up to 3 times
Ventricular fibrillation
Epinephrine several
Epinephrine
Atropine for absolute or relative bradicardia
Epinephrine
Atropine
treat if possible
Immediate cardioversion
Premedicate when possible Synchronized setting
Narrow-complex
Adenosine
Verapamil
Diltiazem -blockers
Digoxin
Synchronized cardioversion
It is critical to survival from sudden cardiac arrest (SCA) for several reasons:
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.
(1)
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 truncated exponential waveform) or 120 J (rectilinear biphasic waveform). For second and subsequent shocks, use the same or higher energy
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.
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 patients rhythm is irregular), use high-energy unsynchronized shocks.
Ventricular tachycardia
Ventricular tachycardia with a pulse responds
well to cardioversion using initial monophasic energies of 200 J. Use biphasic energy levels of 120150 J for the initial shock. Give stepwise increases if the first shock fails to achieve sinus rhythm.
Electrode Position
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, antiarrhythmics and other drugs.
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. .
aetiology: it is included in the ALS algorithm for use every 35 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 23 mg, diluted to 10 ml with sterile water, via the tracheal tube. Absorption via the tracheal route is highly variable.
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 noncompetitive alpha-blocking effects.
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.
refractory VF/VT (when amiodarone is unavailable). Dose. an initial dose of 100 mg (11.5 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.
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.
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.
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