Time,arificial ventilation and cardiac massage,defibrillation and adrenaline (Atkins 1986).
The critical parameter for restoring spontaneous circulation is development of adequate coronary perfusion pressure(CPP).(7)
In human,return of circulation requires that developed CPP exceeds 15-20 mmHg.(7)
Adrenaline with its alpha adrenergic properties ,make peripheral vasoconstriction leads to an increase in aortic pressure during relaxation phase of closed chest compression,causing an increase in coronary perfusion pressure and coronary blood fllow(Michael 1984).
The ability of adrenaline to increase the amplitude of VF (beta adrenergic effects) make defibrillation easier but the beta adrenergic effects of adrenaline are potentially deterious during cardiac arrest,can increases oxygen consumption and decrease the endo/epicardial blood flow does not improve the oxygen supply/demand ratio (Ditchey 1984).
On the otherhand adrenaline has been shown to improve cerebral perfussion during closed chest massage in animals an effect not show with phenylephrine or methoxamine(Holms 80).
In summary the effectiveness of adrenaline during CPR probably due to reduction in myocardial ischaemia because of improved blood flow caused by the raised aortic pressure during closed chest massage,other vasopressor should be useful for augmenting coronary perfusion pressure (CPP) but lack prospective data.(7)
All drugs therapy in cardiac arrest can be devided into three categories : pressors,antidysrhythmics and metabolic drugs.
Adrenaline also to convert fine fibrillation to a coarse fibrillation,to improve the coronary perfusion and to increase myocardial contratility.
In pediatric patients adrenaline is indicated for the treatment of symptomatic bradycardia ascociated with poor systemic perfusion or pulseless arrest,administer adrenaline every 3 to 5 minutes during arrest.In neonates may be administered via umbilical venous catheter if rapidly placed, but adrenaline should not be delayed,and may be administered via the ET as an alternative.(5)
The dose via either route is 0,01 to 0,03/kg of the 1;10.000 dilution or adrenaline 1cc 1:1000 dilute to 10 ml and give 0,1 ml/kg iv(5)
Isoprenaline should never be used in cardiac arrest,as a pure beta adrenergics it increases myodial oxygen consumption while reducing diastolic pressure and coronary blood flow.(1)
Because of its potentially deterious effects,CaCl2 should no longer be used during CPR unless spesific indication exist.If the arrest is precipitated or contibuted by severe hyperkalemia, severe hypocalcemia or calcium channel blockers overdose,calcium may prove useful.(1)
The usual dose is 2-4 mg/kg of the 10%% solution administered slowly intravenously and repeated 10 minutes intervals as deem necessary. Although some animals studies appear promising there is no conclusive evidence that calcium channel blockers will improve the neurological outcome from cardiac arrest.
The known effects of vasodilatation and negative inotropism and dromotropism make the use of these agents in ardiac arrest questionable.Consequently calcium antagonist cannot be recomended for use during CPR in the present state of knowledge.(1)
In recent years,however a better understanding of mechanism of cell damage,high developed with anoxia or ischaemia,cellular phosphate energy stores are rapidly depleted;allowing a large shift of calcium into cells.Because of this increase in intracellular calcium.It has been suggested that additional administration of calcium during CPR is useless or worse than useless.
In the vascular smooth muscle the inflow of calcium results in vasocontriction and this may impede reperfusion of heart and brain.(1)
It has been reported the liberation of CO2 following administration of bicarbonate causes paradoxical CNS acidosis,presumably because CO2 readily diffuses across the blood brain barrier (BBB) while bicarbonate diffuse more slowly(Bereng Wolk and Kellip 1975). It is not appropriate to treat respiratory acidosis with bicarbonat natricus especially since elemination of CO2 during CPR is seldom difficult. Metabolic acidosis as indicated by serum bicarbonate or blood lactate levels,develops very slowly during cardiac arrest and CPR in both animal and humans (Weil et al 1986).
More recent studies suggest that bicarbonate does not improve the success od defibrillation or resuscitation (Minuek and Sharma 1977,Guerci et al 1986).
Hypernatremia and hyperosmolarity cause by bicarbonate natricus administration are frequent during and following CPR and are associated with a poor oputcome (Mattar et al 1974).
It is probably should not be used during CPR unless a known pre existing severe metabolic acidosis and blood gases indicate a severe metabolic acidosis(very low serum bicarbonate).(1)
Bicarbonate can be used to reverse metabolic acidosis or eithe electrolyte problems when they are recognized,however there are no data to support the rutine use of these drugs for all patients.(7)
Acidosis is managed with ventilation and volume replacement.(5)
Only amiodaron has clinical data supporting its use during VF that persist after rescue shock, Anti dysrhythmic druga are useful for preventing refibrillation in all successfully defibrilated patient not for terminating VF.(5)
Aminophyline is antagonist adenosine released during ischaemia but adenosine hypothesized to suppress cardiac electrical activity.(7)
The high likehood of an acute coronary syndrome in the patient suffering cardiac arrest should prompt consideration of anti platelets therapy,anti coagulation,beta blockade and nitrate during post resuscitation care. Unless clearly non cardiac etiology for cardiac arrest is evident acute coronary angiography may reveal and indication for angioplasty,thrombolysis or other
reperfusion therapy. Early angioplasty or reperfusion therapy is associated with improved survival and outcome.Among out of hospital patients as many as 66% have primary cardiac disturbance. For in hospital patients experiencing cardiac arrest dysrhythmia and cardiac ischaemia account for 59% of events.(7)
If ROSC is successful :(6)
1. Continue oxygenation,ventilate if necessary and establish infus line for rapid giving drugs.
2. Treat hypotension with inotropic and vasoactive
drugs(adrenaline,dopamine,dobutamine)
3. Correction of electrolyte,fluids and blood glucose.
4. Becareful with possibly recurrent of cardiac arrest.
5. Treat the arrhythmia.
6. Monitor in ICU.
When there is intractable cardiac arrest probably caused by:(6)
4 H :Hypoxia,Hypovolemia,Hyperkalemia,Hypothermia.
4 T :Tension pneumothorax,Tamponade of cardiac,thromboembolus of lung,Toxic overdose MA Massive myocard infarct, and Acidosis.
If after ROSC,recurent cardiac arrest :
1.Follow initial algorhytm
2.If necessary ,DC shock 360 J is given and followed with CPR.
TERMINATION OF CPR :(2)
Resuscitation is considered unsuccessful if signs of death of heart and brain are present after one hour of continous CPR effort.
A.Signs of cardiac death
1.Absence of electrical activity of the heart
2.Slurring and widening of the QRS complex
3.Persistyent fibrillation with slowing and loss of amplitude.
B. Signs of CNS death
1.No breathing
2.Unresponsiveness
3.No movement
4.Absence of reflexes
5.Fixed and dilated pupil,not responding to a direct light,
6.Isoelectric EEG
SUMMARY :
It is frequently difficult to determine wether respiratory arrest precedes or follows circulating arrest in any particular patients. Wether the initial event,however,is the cessation of circulation or of respiration,tissue hypoxia occurs rapidly.
The initial goal of therapy is oxygenation of the brain,the second goal is restoration of circulation and in addition the underlying conditions must be corrected.
There are five steps in prevention of biological death from sudden cardiac arrest :
1.Rapidly recognized cardiac and respiratory arrest singly or combination.
2.Immediately institute artificial ventilation.
3.Quickly provide techniques that artificially circulate blood.
4.Promptly administer appropriately drug therapy
5.Apply post resuscitative care procedures designed to minimize the deterious effect of the arrest.
During the first few minutes after non asphyxial cardiac arrest the blood oxygen content remain high and myocardial and cerebral oxygen delivery is limited more by diminished cardiac output than a lack of oxygen in the lung ,therefore chest compression is more important than ventilation. For this reason and to emphasize the priority of chest compression it is recomended that in adult CPR should start with chest compression rather than initial ventilation.
REFERENCES :
1. Otto W.Charles,Nunn F.J,:Cardiopulmonary resuscitation of the adult in Textbook of General Anaesthesia,fifth edit,Butterworth,London,Boston Singapore,Sydney,1989, pp1333-44.
2. Snow J.C. : Cardiac arrest and cardiopulmonary resuscitation,Handbook of Manual Anaesthesia, Asian Edition,Little Brown and Company Boston,Igaku Shoin,Tokyo,1977, pp 61-73.
3. Thornton L.Harry : Cardiac arrest and Resuscitation,in Texbook of Emergency Anesthesia,second edit,Edward Arnold Publishers,Ltd 1974, pp 464-75.
4. Rilex L.Joseph,Ravin BM : Cardiopulmonary Resuscitation in Textbook of Problems in Anesthesia,Little Brown and Company,1981,pp 120-27.
5. Zimmerman,Taylor W.R> : Cardiopulmonary Resuscitation in Textbook of Fundamental Critical Care Support,Course Syllabus Editorial Committee Medicine,USA 1996 pp 16-24.
6. Modul Workshop CPR,Guidlines 2005,Department of Anesthesiology & Reanimation, Sutomo Hospital -Airlangga University,Surabaya,Indonesia December 2006.
7.Pint P.Mitchell,Abraham E. :Cardiopulmonary resuscitation in Textbook of Critical Care 5th edit, Elsevier Saunders, Philadelphia,Pensylvania,2005 pp 311-4.
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