Newborn Resuscitation (PART 2)

TREATMENT :
Prepararation 
Equipment for infant resuscitation should be readily available at all time,suction bulb,oxygen source plus bag and mask oral airway,laryngoscope and endotracheal tube(ET).(3)

Following birth the infant kept head down until the poste
rior pharynx and nose are cleared by suction. 
The airway is maintained by extension of the head but  Not over extension in neonate since it will worse airway obstruction because the neck is flexible.

The depressed infant may respond to clearing of the airway stimulation and oxygen administration helps the vasodilata
tion of the pulmonary vessels.

The respiration may be stimulated by slaping the sole of the feet or rubbing the back for the normal neonate but not for the depressed neonate.

Both depressed and normal newborn infants should be dried off immediately since loss of body heat from evaporation can jepordize the neonate.

Care of infants with Apgar score of 7-10(1)

Dry off  and suction the mouth and pharynx with the suction bulb.

Care of infants with Apgar score of 4-6(1)

a.As above

b.Allow the infant to breath oxygen by mask. If the infant is 
   not breathing spontaneously,positive pressure mask 
   ventilation with the neck moderate extension and towell 
   roll under the shoulders should be instituted at approxi
   mately thirty breaths per min. If respirations appear 
   irregular the infant should be assisted with positive 
   pressure until the respiratory pattern improve.

c.If the infant does not become pink on 100% oxygen after 
   1-2 minutes inspect the pharynx and glottis with direct 
    laryngoscopy and clear the airway.

d If there is gastric distension put in a suction catheter or 
   feeding tube via the mouth and empty the stomach.

Care of infant with Apgar score of 0-3

a Dry off the infant and suction the mouth and pharynx with a suction bulb.

b.Begin positive pressure mask ventilation with 100% oxygen 
   at a rate of 30 breaths per minute. If the heart rate less 
   than 70 times per minute, intubate the infant with a 
   2.5,3.or 3.5 ID.

c.If the infant remain bradycardia give atropine 0,1 mg via 
   the umbilcal vein.    

If there is no heartbeat start external cardiac massage,the neonate's chest should be grasphed in both hands so that the rescuer's middle fingers are joined to support the neonate's back,while compression of midsternum is provided by both thumbs at a rate 30 interpossed with 2 ventilation.

Depth of compression =1/5-1/4 AP diameter of chest. If asystole persist, epinefrine of 1:10.000 solution should be given.(1 cc epinefrine 1:1000 is diluted in 10 cc solution,give 0,1 cc/kg ig iv, intracheal or intraosseus but Not intracardial).

Establish ECG monitoring to differentiate between Asystole,Ventricular fibrilation(VF) or Ventricular tachycardia(VT) etc.

If there is a coarse VF: (5,8)

1. External DC counter shock 

2. May start as low as 30 wattsec in infant

3. Followed by chest compression and ventilation (30:2).Do 
    not reassess the rythm or feel for a pulse.After 2 minutes 
    of CPR, check the rythm and give another shock(if 
    indicated)

4. Persistent VF treated with lidocaine 1mg/kg

If there is fine VF:(5)

1.Epinefrine 1: 10.000 dilution iv.

2.Continue chest compression and ventilation during 2-3 
   minutes.

3.If VF become coarse, DC shock as above.   

Epinefrine increase cardiac contractility and coarsening of VF pattern.

If there is a doubt about wether the rythm is asystole or fine VF do Not attempt defibrilation instead continue chest compression and ventilation. Repeat epinefrine every 3-5 minute thereafter if VF/VT persist until return of spontaneous circulation (ROSC)(8).

If capillary filling is markedly decreased give 10 cc/kg of 5% albumin,ringer lactate or normal saline. Hypertonic solution should not be given via umbilical vein. Insert iv canula,at least 18 Fr even in neonate, blood transfusion will be difficult through 20 Fr.

Cutdown immediately to save time wasted in efforts to start percutaneous catheter or scalp vein needles, will avoid accidental Sc injection of irritant drugs such as Ca gluconate, Bicarbonas natricus or glucose 50% etc.(5)

Isoprenaline should never be used in cardiac arrest, as a pure beta adrenergic it increases myocardial oxygen consumption while reducing diastolic pressure and coronary blood flow.(7)     

More recent studies suggest that bicarbonate natricus(bicnat)does not improve the success of defibrilation or resuscitation(Minuek & Sharm).

Hypernatremia and hyperosmolarity cause by bicnat administration are frequent during and following CPR and are ascociated with a poor outcome (Matter et all 1974) (7)

It has been reported the liberation of CO2 following administration of bicnat causes paradoxical CNS acidosis,probably because CO2 readily diffuses across the blood brain barrier (BBB) while bicnat diffuse more slowly.(Kellip 1975) (7)

It is probably bicnat should not be used during CPR unless known preexisting severe metabolic acidosis and blood gases indicates severe metabolic acidosis.                               

Blind repetition of bicnat is not good therapy since alkalosis or under corrected acidosis is undesireable and severe hypo or hypercapnia can lead to increased irritability and decrease cardiac output.(5)

CaCl2 should no longer be used during CPR unless spesific indication exist.If the cardiac arrest is precipitated or contributed by severe hyperkalemia,severe hypocalcemia or Calcium channels blockers overdose calcium may prove useful.

In recent years however a better understanding of mechanism of cell damage, high developed with anoxia or ischemia,cellular phosphate energy stores are rapidly depleted,allowing a large shift of calcium into cell. Because of this increase 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 result in vasoconstriction and this may impede reperfusion of heart and brain.(7)

Dextrose or glucose should not be given during CPR since glucose in condition of hypoxia that glucose is metabolized produces lactic acidosis. Hypotonic solution should be avoided because it will increase brain edema.

The narcotic depressed infant may have central depression of respiration as his only problem. Therefore he may present as a depressed infant who rapidly pink when ventilated but ventilation is stopped breaths very slowly or not at all.If such a sleepy infant's mother has received narcotic medication within 1-3 hours prior to delivery,narcotic antagonist should be considered.The drug of choice is naloxone (in a dose of 0,01mg per kg ) which may be given via the umbilical vein.(5)

The problem of narcotic depressed infant is almost universally caused by analgesics given during labor; it is very rare among infants whose mothers take heroin or mathadone. Infact in these infants naloxone may precipitate an acute withdrawal syndrome.(5).

Transport of infant should be moved to the special care nursery as soon as he is stabilized. Resuscitative efforts should generally proceed in the delivery room until the heart rate is greater than 100 beats per minute,ventilation is established or controlled,the infant is responding and perfusion appears adequate.

The infant with a low Apgar score,who has responded to resuscitation should not be kept in the delivery room if he becomes pink,cries and is in no distress.

All premature infants even if not manifesting depression should be taken to the special care nursery,shortly after delivery (i.e.5-7 minutes after birth) for observation.(5)

If necessary an elevator should be called waiting on the delivery floor to expedite the transport but speed should not excessive to the point pf endangering the infant.

If the infant is being ventilated,the person breathing for the infant should determine the speed of transport.

Grunting, by raising intra alveolar pressure can partially compensate for a lack of surfactant in an infant with RDS.

An endotracheal tube prevents this activity and if left in place with the infant breathing spontaneously,promotes alveolar collapse.Therefore a sick premature infant who requires intubation and ventilation initially but then starts breathing spontaneously should be probably be left and have breathing assisted until he arrives in the newborn care nursery.It is better to extubate the infant after transport than to risk the development of respiratory insuficiency en route.(5)

SUMMARY :

About 35% of all death during the first year of life,occur within the first 24 hours and half of these are related to anoxia and pulmonary pathology.

Diabetic mothers and premature infant prone to have hyaline membrane disease (RDS).and 30% of neonatal fatalities caused by RDS. Infant are primary nose breather and the upper airway predisposed to obstruct due to narrow passage of the nose,glottis and trachea.

The Apgar scoring is numerical index of the aviability of newborn infant at 1 and 5 minutes after completion of childbirth is evaluated for heart rate, respiratory effort,muscle tone,reflex respons to stimulation and color.

Infant with Apgar score less than 4 is considered seriously depressed, begin positive pressure mask ventilation with 100% oxygen,if the heart rate less than 70 beats per minute as soon as intubate,when no heart beat attempt external massage at a rate 30 interpose with two ventilation.

The infant with a low Apgar score who has responded to resuscitation should not be kept in the delivery room even if he becomes pink,cries, and is in no distress and all the premature infants even if not manifesting depression should be taken to the special care nursery for observation.

REFERENCE :

1.Pieter R,Lebowizt P: Newborn Resuscitation in Textbook of Clinical Anesthesia Procedures of The Massachusett General Hospital,1st edit,Little Brown Company, USA 1978,pp.244-52.

2.Thorton L.H,Perkins: Resuscitation of the Newborn in textbook of Emergency Anesthesia 2nd edit,Edward Arnold Publishers,London 1974,pp.214-27.

3.Snow J.C: Resuscitation of the Newborn in Handbook of Manual Anesthesia. 1st edit,The Asian Edition Little Brown and Company,Boston,Igaku shoin Ltd. Tokyo,1977.pp 444.

4.Stewart J.David: Cardiac Pulmonary Resuscitation in Handbook Manual Pediatric, Churchill Livingstone, Newyork Edinburg and London 1979,pp.286-91.

5.Levin M.Richard : Cardio Pulmonary Resuscitation in Handbook of Pediatric Respiratory Intensive Care, Medical Examination Publishing Co Inc.USA 1976 pp.265-73.

6.Smith M.Robert: Unspected Cardiac Asystole in Handbook of Anesthesia for Infant and Children,4th edit,The CV.Mosby Company,St.Louis,Toronto,London,1980,pp.605-8.

7.Otto W,Ch,Nunn F.J.: Cardio Pulmonary Resuscitation in Textbook of General Anesthesia,5thedit,Butterworth,London,Boston,Singapore,Sydney,1989,pp.1333-44.

8.Workshop Module of Cardio Pulmonary Resuscitation 2005,Medical Faculty Airlangga University,2006.

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Newborn Resuscitation (PART 1)

 INTRODUCTION :
Any newborn who does not estabilshment spontaneous respiration should be assisted immediately or hypoxia and acidosis will ensue. About 35% of all death during the first year of life occur within the first 24 hours and half of these are related to anoxia and pulmonary pathology(3). 


Cardiopulmonary resuscitation is concerned with restoration of pulmonary,cardiovascular and neurologic function. Firstly it consist of artificial respiration and circulation by whatever means is immediately available to prevent clinical death from progressing to biological death.(4)
Cardiopulmonary  function can be restored more readily in children than in the adult. If the heart arrest before the moment of delivery cardiac massage probably better avoided since neural damage may well occur in the unknown interval elapsing before the circulation can be restarted.(2)


In addition resuscitation may actually be started before birth for the anesthetist can do much to mitigate or avoid the intrapartum asphyxia which plays a large part in many cases of depression and death of the newborn(Buttler 1963) (e.g.adequate preoperative transfusion,avoidance hypoxia at all time provision with short induction delivery interval).(2)

Diabetic mothers and premature babies prone to have hyaline membrane disease or respiratory distress syndrome (RDS),it responsible for some 30% of neonatal fatalities in certain centers(Brown 1959) (2)


FACTORS CONTRIBUTING TO NEONATAL RESPIRATORY DEPRESSION(2):
These may be broadly devided into two categories (Cook 1958)

1. Failure in function of the central nervous mechanism 
    much often due typoxia or drug depression.
2. Failure in response of the peripheral respiratory 
    structure.


Further breakdown reveals the common predisposing factors in neonatal asphyxia each leading ultimately to one or other of the two main causes of depression.

a.Developmental :
   i.hypoplasia of the lungs,choanal atressia etc.
  ii.other fetal abnormalities
iii.prematurity
iv.post maturity


b. Maternal causes :
i  diabetes                                 v   prolapsed cord
ii  toxaemia                               vi  cord compression
iii hypertension                         vii  placental separation
iv hypotension or hypoxia         viii hypertonic uterus


c. Trauma to fetus at birth :
i   long labor                              iv instrumental delivery
ii  precipitate labor                    v breech delivery
iii disproportion


d. Drugs : Analgesia/anesthesia
e. Maternal hyperventilation during anesthesia
f. i Airway obstruction due to mucus, meconium etc.
  ii Respiratory distress syndrome (hyaline membrane 
    disease)


HAZARDS OF SPECIAL PEDIATRIC SIGNIFICANCE.( 4)
Anesthesiologist should be constantly be aware that factors which may insignificant in the adult may be life threatening in small children.

At anytime the upper airway may become obstructed by :
1.Small amount of mucus
2.Hypertrophie adenoid tissue
3.The relative large tongue,ascociated with:
   a.Flaccidity resultant upon unconciousness.
   b.In advertent displacement of submental soft tissue and 
      tongue by anesthesiologist's fingers.
   c.Inadequate extension or over extension in infant.
   d.Inadequate elevation of jaw.
   e.Premature removal of artificial airway.

4.Regurgitation is a common occurence because of 
   frequency of feedings.

5.The infant stomach is readily inflated by:
      a. Too high inflation pressure 
      b. Partial obstruction of airway.

Remember,infants are primary nose breather,if the nasal airway is inadequate an oral airway should be inserted.(3)
In the infants/neonates the upper airway predispossed to obstruct due to narrow passage of the nose,glottis,trachea and the presence of lymphoid tissue (3)
When there is airway obstruction,substernal,suprasternal and intercostal retraction are more marked both in older children and when dyspnoe is severe.
In the very young child these signs must be looked for very carefully if obstruction is to be recognized early.(3)                                                    
Infant and children require larger amount of oxygen due to an increased metabolic rate.


EVALUATION:(1)
A. Fetal monitoring
    1.Electronic fetal monitoring of both fetal heart rate and 
       intra uterine pressure provides information valuable to 
       predicting which infants will be depressed at birth.

   2.Type II or late deceleration patterns of fetal heart rate 
      are ascociated with fetal hypoxia and may respond to a 
      change of maternal position or to the administration of 
      fluids and oxygen.
      At delivery infants who have had persistent type II 
      decelaration tend to be depressed.

   3.Other ominous fetal heart rate patterns such as 
      fixed,non varrying bradycardia or lost of baselin 
      variability (in tha absence of atropine or diazepam given 
      to the mother) are also ascociated with the births of 
      depressed infants.(1).


B.NEWBORN  ASSESSMENT :
   Assessment depends on the rapid evaluation of a few 
   fundamental sign of normal or depressed tissue oxygen and 
   this should be carried out as soon as possible after 
   delivery.

1. Depression in the newborn is usually due to one of three 
    factors :
             -uteroplacental insufficiency
             -maternal medicales
             -neonatal disease

   The infants should be assessed from the view points of :
   a. Respiratory activity : Ventilation may be depressed 
      centrally from maternal drugs(eg.narcotic),severe 
      acidosis or infections.
      May also be affected by alveolar collapse as in 
      RDS,blockage of air passages with meconium or by 
      aspiration of blood. Finally,mechanical interference with 
      breathing maybe caused by diaphragmatic hernia or 
      pneumothorax.     


  b Cardiac output may be impaired by hemorrhage,hypoxia 
      acidosis or congenital cardiac anomalies.


2 Integrity of the newborn has claissically been assessed 
   using the Apgarscore Apgar scoring methode is numerical 
   index of the aviability of a newborn at 1 and 5 minutes 
   after completion of childbirth, Two points are alloted for 
   each of five clinical signs (a maximum score being 10) and 
   assessment is made at 1 and 5 minutes after birth.

   The signs evaluated are :
   A = Appearance : Is the infant pink or blue ?
         Two points are alloted for a totally pink infants.One 
         point is given to the infant with acro cyanosis and no 
         points are given to the cyanotic infants.

   P =  Pulse             
         Two points are given for a heart rate greater than 100,      
         One point for heart rate less than 100. If there is no 
         spontaneous heart activity,no point are scored.
         This is the most important single sign in assessment and 
         resuscitation (Brown 1954) emphasized this pointing 
         out that although the newborn are tolerant of 
         hypoxia,tolerance of ischemia is no better than in 
         adult.Severe hypoxia may be readily treated,but the 
         presence of circulation failure at once makes the 
         outcome doubtful.

   G= Grimace of reflex irritability :
        Two points are given for a vigorous cry in response to 
        oral suctioning. One point is given for a weak cry or 
        some motion, and no points are scored if response is 
        totally lacking.   
        This often elicited by use of the sucker which may 
        produce grimacing, coughing or sneezing. 
        A widely used reflex stimulus is a slap to soles of the 
        feet which will often causes flexion withdrawal and 
        crying. 
         Failure response in the depressed infant after this 
         manouvres should not call for futher assault.

  A = Activity of muscle tone :
        The well oxygenated infant has good tone at birth. 
         Increasing asphyxia leads to a progressive loss of tone 
        and eventually flaccidity.
        Two points are given for good muscle tone,the infants 
        drawing himself into the flexed position. One point is 
        given when there is some flexion of extrimities but no 
        points are scored when the infant is flaccid.


   R = Respiratory effort 
        Apnoe may occur, perhaps after one or two initial gasp 
        or without any respiratory efforts being made at all.   
        Two points are given for regular respiratory efforts 
        one,one for irregular respiration and none in the 
        absence of spontaneous respiration.

A score 0 to 10 is assigned for each of these five evaluations. The neonates scoring 7 or above is considered in good conditions.                                                                                                                                                                                         
The score of 4 to 6 he is moderately depressed (requires some attention).
If the score less than 4,the neonate is considered seriously depressed, demand major resuscitative intervension (1,3).

Apgar rating at 5 minutes reflects the result of the resuscitative efforts and provides an index of the value of further efforts (3).

The non depressed infant approaches delivery with a mild respiratory and metabolic acidosis,his pH in the range of 7,25 -7.30 with PaCO2 of about 45 mmHg(3).

Following delivery all infants show a transient decrease in pH and increase base deficit, these alteration reaches a maximum at 4 minutes of life.
This mild acidosis in normal term infant does not need to be treated.

An infant with Apgar score of 7 or greater tends to correct its pH by the end of one hour, at which point the pH approaches 7.35.The PaCO2 is likely to be between 35 and 40 mmHg.

The infant with an Apgar score of 6 or less is relatively more acidotic than his counterpart with a score of 7 or more acidosis. The acidosis is both respiratory and metabolic acidosis but metabolic acidosis develops slowly during cardiac arrest and CPR in both animals and humans.

In depressed infants the pH during labor may run from 7.15 to 7,25 and the base deficit may approach 10 meq/L,the PaCO2 ranges from 40 to 55 mmHg.

In the markedly premature infant, surfactant production and even pulmonary blood flow can be reduced by acidosis (1). 
Therefore the acidosis of the depressed all premature infants is treated immediately in the delivery room. But the priority is to treat respiratory acidosis with ventilation and oxygenation and metabolic acidosis is treated when severe because hypernatremia and hyperosmolarity cause by bicarbonat natricus administration during and following CPR and ascociated with a poor outcome (Mattar et al 1974).(7)   


To Be Continued

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Cardiac Respiratory Arrest (PART 3)

ONLY four factors have been shown to be a mayor benefit in successful resuscitation from cardiac arrest:(1)


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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Cardiac Respiratory Arrest (PART 2)

THERAPY


A.The initial goal of therapy is oxygenation of the brain.
The second goal is restoration of circulation. In addition the underlying conditions must be corrected(2).


1. CPR is not indicated for all patients,natural death in the aged or the terminal stages of chronic illness should not be reversed in this manner.


2. CPR should be performed in cases of reversible unexpected death.       


That occur as a result of myocardial infarction, general and local anesthetic drugs,electric shock,cardiac catheterization or suffocation.


OLD GUIDELINES :


B. Emergency CPR includes the following ABCD steps which should always be started as quickly as possible (2)  
          
1.A ----(Airway)
2.B-----(Breathing)
3.C-----(Circulation)
4.D-----(Drugs and definitive therapy)

5. In a witness cardiac arrest when treatment can be initiated within one minute of the arrest the ABCD sequence should include use precordial pump.


1.AIRWAY : (A)(2)


Time is the critical factor,establishment of an airway as soon as possible. To make the airway clear and clear the airway.      


Artificialventilation and circulation must be initiated within 2-4 minutes.


a.Immediate opening the airway


This can be easily and quickly by tilting the patient brow(head) backward as fare as possible. But in newborn not too excessive that worsen airway obstruction because the neck is flexible.                                                                  


Many times this manuver can resume breathing spontaneously. 


The rescuer places one hand beneath the victim's neck and the other hand on the victim's forehead to carry out head tilt. Then the neck is raised by rescuer with one hand and the head is tilted backward by pressure with the other hand on forehead, this effort raised the tongue away from the back of the throat, this relieved anatomic obstruction of  
the airway created by the tongue dropping against the back of the throat.


b. If head tilt not successful in opening the airway satisfactorily additional forward displacement of the lower jaw, jaw thrust, maybe necessary but not recomended for the lay people.


c.This can be done by triple airway maneuver :   


1.The rescuer places his fingers behind the angles of the patient jaw and forcefully displaces the mandible forward.
2. He tilts the head backward.
3. He uses his thumbs to retract the lower lips to allow the patient to breath through the mouth and nose.


2.BREATHING (B):


If the patient does not promptly resume spontaneous breathing after the airway is opened, artificial ventilation must be started immediately by mouth to mouth or mouth to nose or mouth to mask breathing.


After opening the airway by tilting the head backward and displacing mandible forward, clearing the mouth of secretions, and beginning mouth to mouth ventilation.Keep the head tipped, and close the nose to keep air from escaping by squeezing between the left thumb and index finger.(3)


Take a deep breath and cover the patient's mouth with rescuer's mouth.


Give 2-4 big breaths as rapidly as possible without allowing time for the lungs to collapse between breaths.(4)


But in young children and infant ventilates with exhale volume smaller than an adult.


And in newborn exhale with a mouthful volume is adequate  


There after two breaths are interposed between every 30 chest comppression (3).


In children both mouth and nose are covered by the rescuer's mouth and distension of the stomach is prevented by epigastric pressure with the right hand,the chin being held forward with the left.(3) 


There is enough oxygen (16%) in expired air to secure oxygenation of a patient's circulating blood, by doubling normal tidal volume the rescuer increase the expired oxygen to 18%. During CPR, cardiac output(CO) is (25-30)% of normal so oxygen uptake from the lung and CO2 delivery 
to the lungs are also reduced. As result low minute ventilation (lower than normal tidal volume and respiratory rate) can maintain effective oxygenation and ventilation during CPR.


It is also recognized that rescuers are frequently unwilling to carry out mouth to mouth ventilation for a variety of reasons including for infection and distate for the procedures. For these reasons and to emphasize the periority of chest compression it is recomended that in 
adults, CPR should start with chest compression rather than initial ventilation.(Guidelines 2010) (6)


Alternative methods :


a. A self filling non rebreathing bag and wellfitting anesthesia mask,with oxygen supplied from a cylinder of compressed oxygen may be used as soon as they are available/will add the efficiency and convenience of 
resuscitation.(2,4).


b. Endotracheal intubation must be carried out at the earliest possible moment but not before ventilation is produced for a few minutes by another methode.


Intubation should be performed by trained personal,with a cuffed endotracheal.Tube permits easy tracheobronchial toilet, facilitates the connection to a mechanical ventilator, prevent gastric dilatation and regurgitation and decrease dead space.(4)


c. An emergency tracheostomy is indicated when an adequate airway cannot otherwise be effective.


Alternative methodes are :


1.Crycothyrotomy  
2.Transtracheal catheter ventilation or oesophageal obturator airway.


d. In a patient with a laryngectomy,direct mouth to stoma artificial respiration must be carried out.The head tilt and jaw thrust are unnecessary.


During artificial ventilation the following adverse effects may take place :


1.Inflation of the patients stomach with air,followed by regurgitation and/or transmission of infection to the rescuer.


These may occur when there is no tracheal tube in place.


2.Rupture of the patient's lungs.


3.ARTIFICIAL CIRCULATION: (C)


A search for a pulse should always be made following artificial ventilation and before starting sternal compression.


Artificial circulation can be carried out by external cardiac  compresision.    


Which must be started at once because anoxia may cause irreversible damage to the brain after 4 minutes; if resuscitation is successful the patient will probably remain decerebrate.(4)


Proper application of external cardiac compression requires that the patient be in horizontal position and on a firm surface.


Application of pressure must be restricted to the mid of the sternum not half lower of sternum especially not over the xiphoid process to obtain maximum compression of the heart to minimize the dangers of fractured ribs and damage to the liver.


The heel only one hand is placed in the center of the chest over the mid of sternum and the heel of the other hand is placed on top of heel of the first hand. It is very important that fingers be kept elevated at all times and not allowed to touch the chest wall.(4)


Adequate force must be exerted vertically downward to move the lower sternum 4-5 inches toward the vertebral collume, forcing blood into the pulmonary and systemic arteries but for infants and young children, less pressure is required. Following sternal compression the sternum is 
released,and one cycle is repeated.


When the pressure is released,the chest expands and the heart fills with oxygenated blood which is circulated through the tissues with the next compression of the heart. 


Pressure with the finger tips alone on the middle of the sternum is recomended for infants. For children up to 9-10 years of age the use one hand is considered adequate.The compression rate should 100 times perminute with 2 ventilation every 30 compression wether there are one or two rescuers of infant, child or adult is recomended. In the patient trachea has been intubated,the compression rate can be 80 times perminute no pause in compression should be made for ventilation. Synchronizing ventilation between compression is also unnecessary.(2)


Under optimal condition external heart compression produces only 30-40% of the normal amount of blood flow. 


During the first few minutes after non asphyxial cardiac arrest the blood oxygen content remain high and myocardial or cerebral oxygen delivery is limited more by diminished cardiac output than a lack of oxygen in the lungs.Ventilation is therefore, initially less important than chest compression or compression is the first step.( C,A,B )


So initial steps of resuscitation may include for the nonasphyxial cardiac arrest :
Guidlines 2010  : 


1.Cardiac compression 30 times (C)
2.Opening the airway and clear the airway.(A)
3.Giving two breaths using compression ventilation ratio of 
   30:2 (B)D


Main changes in adullt basic life support (BLS)---> guidelines 2005.(6)


- Start CPR when victim is unresponsive and not breathing normally agonal gasp are common in the early stages of cardiac arrest.


- Airway ---> tracheal intubation (A)
- Breathing --- AMBU/Ventilator/O2 (B)
- Circulation --- Cardiac compression (C)
- Defibrillation (D)


Shockable rythm are Venricular tachycardia(VT-pulseless),Ventricular fibrillation (VF). Non shockable are Asystole and Electro mechanical discociation EMD)or Pulseless electro activity (PEA).


Automatic External Defibrillator)(AED) :


Public Access Defibrillation (PAD) Program are recomended for the locations where the expected use of an AED for witnessed cardiac arrest exceeds once in 2 years.

A single shock is delivered immediately followed by two minutes of uninterrupted CPR without a check for signs of life or a pulse.


If VF appears give the first  shock recomendation for higher energy (360 Joule) when using monophasic waveform, immediately begin chest compression.


Don't interrupt chest compression to check rhythm or pulse until 5 cycles or 2 minutes of CPR are given.


Biphasic : Monophasic  ( 96% vs 54% )


When biphasic is given before 5 minutes > ( 50- 70)% probably recovery of spontaneous circulation (ROSC).


Main changes in AED :


PAD programmes are --> A single defibrillatory shock (at least 150 Joule)(biphasic) or 360 Joule(monophasic) is delivered immediately followed by two minutes of uninterrupted CPR without a check for termination of VF or check for signs of live or a pulse.


                   CARDIAC ARREST
                                  I
               ------------------------------
              I                                           I
         unwitness                               witness
              I                                           I
         CPR 2 min                          single shock
              I                                    contnued with
          evaluate                             CPR 2 min -----> evaluate
              I                                           I
   -------------------->            <---- ------------ unshockable        unshockable             shockable
          I                             I                                               I                                                                                                                 CPR 2 min                single shock                         CPR 2 min c            
adrenaline                continued with                     adrenaline                                          
                                  CPR 2 min                                      I?                               
          I ?                          I?                                                                                                                                 
                               


Main changes in Adult Advance Life Support (6)
-----------------------------------------------------------
1. CPR before decfibrillation
2. Defibrillation strategies
3. Fine VF
4. Adrenaline
5. Anti arrhythmia drugs
6. Thrombolytic theraphy for cardiac arrest
7. Post resuscitation care.--therapeutic hypothermia.


CPR before defibrillation :


Unwitness : Give CPR 2 minutes about 5 cycles at 30:2 before defibrillation dont delay defibrillation if an out of hospital arrest is witnessed by a healthcare professional. Dont delay defibrillation for in hospital arrest.


Defibrillation strategy :


Treat VF/pulseless VT with a single shock followed by immediate resumption of CPR ( 30 compression to 2 ventilation). Do not reasses the rhythm or feel for a pulse. 


After 2 minutes of CPR check the rhythm and give another shock (if indicated).


The recomended initial energy for biphasic defibrillators is 150-200 J. Give second and subsequent shocks at 150-360 J. The recomended energy when using monophasic defibrillators is 360 J for both the initial and subsequent shocks. The children 2 joule/kg.


Fine Fibrillation :


If there is doubt about another the rhythm is asystole or fine VF do not attempt defibrillation,instead,continue chest compression and ventilation.


For VF/VT give adrenaline 1 mg iv if VF/VT persist after a second shock. Repeat the adrenaline every 3-5 minutes thereafter if VF/VT persist. For Pulseless electrical activity(PEA)/asystole,give adrenaline 1 mg iv as soon as intravenous access is obtained and repeat every 3-5 min thereafter up to return of ROSC is achieved.


If VT with palpable carotid pulse give lidocaine 1 mg /kg iv or amiodaron 300mg. Pulseless VT give a single shock 360 J immediately CPR 30:2 in 2 minutes. Lidocaine 1-1,5 mg/kg every 3-5 minutes maximal 3 mg/kg in 1 hour.


INTERNATIONAL LIAISON  COMMITEE ON RESUSCITATION (ILCOR) guidelines 2005 (6)


1. Adrenaline 1 mg iv repeated every 3-5 minutes.


2. Amiodaron 300 mg iv bolus,if VT/VF persist after 3 shocks. Doses of 150mg may be given for recurrent or refractory VF/VT followed by an infusion of 900 mg over 24 hours.


3. Lidocaine 1 mg/kg, iv if amiodaron is not available,do not exceed a total dose of 3 mg/kg during the first hour. Do Not give lidocaine if amiodaron has already been given. Atropine,adrenaline and lidocaine may be given intravenously,intratracheal or transtracheal the dosis 3-10 times intraveneously or intraosseus but Not intra cardiac.

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