Current Concepts in Cardiopulmonary Resuscitation

1
Current Concepts in Cardiopulmonary Resuscitation

• 
  
  
• R3 ? ? ?

2
Current Concepts in Cardiopulmonary Resuscitation

• Elam, Safar late 1950's. mouth-to-mouth
  ventilation
• Internal defibrillation in 1933
• ? external cross-chest defibrillation in 1956 and
  1957
• ? Kouwenhoven
• Redding, Pearson in 1963. epinephrine or other
  vasopressor drug

3
The factors most related to poor outcome

• long arrest time before CPR
• prolonged ventricular fibrillation without
  definitive therapy
• inadequate coronary and cerebral perfusion during
  cardiac massage

4
The useful method

• rapid application of effective ventilation
• closed chest compression
• early defibrillation
• epinephrine treatment

5

• The cardiac pump theory
• compressed between the sternum and spine
• ejection of blood from the heart into the aorta,
  with the atrioventricular valves preventing
  backward blood flow
• The thoracic pump theory(heart as a passive
  conduit)
• chest compression raises intrathoracic pressure,
  forcing blood out of the chest, with venous
  valves and dynamic venous compression preventing
  backward blood flow
• fluctuation in intrathoracic pressure play a
  significant role in blood flow during CPR

6
Distribution of Blood Flow during Cardiopulmonary
Resuscitation
7
Physiologic Measurements Associated with
Successful Resuscitation
8
Alternative Techniques of Circulatory Support

• Raised intrathoracic pressure
• Simultaneous ventilation/compression
• Abdominal binding with compression
• Pneumatic antishock garment
• Frequent right atrial and intracranial pressure
• No improvement in cerebral or myocardial blood
  flow
• Pneumatic CPR
• Interposed abdominal compression
• Active compression-decompression CPR

9
Epinephrine

• used in resuscitation since the 1890s
• Preferred vasopressor since 1960s(Redding and
  Pearson)
• Alpha adrenergic property
• Peripheral vasoconstriction
• Aortic diastolic pressure
• Coronary perfusion pressure, myocardial blood
  flow
• Beta adrenergic property
• Potentially deleterious during cardiac arrest
• Increase oxygen consumption and decrease the
  endocardial-epicardial blood flow ratio
• Increase the amplitude of ventricular
  fibrillation
• All strong alpha adrenergic drugs are equally
  successful in resuscitation(epinephrine,
  phenylephrine, methoxamine, dopamine)
• Beta adrenergic agonists without alpha activity
  are no better than placebo(isoproterenol,
  dobutamine)

10
Epinephrine Dose(1)

• Higher doses of epinephrine in human CPR might
  improve myocardial and cerebral perfusion
• Standard dose in humans 0.5 1.0
  mg(0.015mg/kg)
• Studies in swine
• Standard dose(0.02 mg/kg) - insufficient to
  improve coronary
• perfusion pressure and blood flow
• High dose(0.2 mg/kg) improve hemodynamics to
  levels
• compatible with successful resuscitation
• Children case reports(0.1 0.2 mg/kg)

11
Epinephrine Dose(2)

• Outcome studies have not shown conclusively that
  higher doses of epinephrine will improve survival
• Swine cardiac arrest model
• No difference in 24-hour survival or neurologic
  status
• More of the animals in the high dose group died
  in the early postresuscitation period as a result
  of a hyperdynamic state
• Five published studies standard doses(1-2 mg)
  to high doses(5-18mg)
• Improvement in immediate resuscitation may be
  possible in high-dose group

12
Epinephrine Dose during CPR

• Adults
• 1mg intravenously repeated every 3-5 min
• If this dose fails, consider giving 5mg or
  0.1mg/kg intravenously
• Children Asystolic, pulseless arrest
• 0.01mg/kg intravenously, first dose
• 0.1mg/kg intravenously, subsequent doses repeated
  every 3-5 min

13
Physiology of Gas Transport during CPR

• Arterial resp. alkalosis / venous resp. acidosis
• The cause is not respiratory in origin but rather
  reduced cardiac output
• Decreased carbon dioxide excretion
• Milliliters of carbon dioxide / min in exhaled
  gas
• Exhaled carbon dioxide
• Reflect only the metabolism of the part of the
  perfused body
• Shunting of blood flow away from the lower half
  of the body
• Increased mixed venous partial pressure of CO2
• Buffering acid cause a reduction in serum
  bicarbonate

14
Clinical Application of Gas Transport Physiology
during CPR(1)

• End-tidal carbon dioxide during CPR
• Useful to monitor the effectiveness of CPR
  efforts
• Flow dependent rather than ventilation dependent
• During CPR alveolar dead space is large during
  low-flow (lt10mmHg) states, end-tidal carbon
  dioxide is very low
• During successful CPR If cardiac output
  increases, more
• (gt20mmHg) alveoli are perfused and
  end-tidal carbon
• dioxide increases
• Spontaneous circulation the earliest sign is a
  sudden (gt40mmHg) increase in end-tidal carbon
  dioxide

15
Clinical Application of Gas Transport Physiology
during CPR(2)

• Sodium bicarbonate administration during CPR
  could be harmful
• Sodium bicarbonate
• combine with hydrogen ion, liberation of carbon
  dioxide
• An effective buffer only with the elimination of
  the volatile acid
• Tissue acidosis is primarily caused by the low
  blood flow and accumulation of carbon dioxide in
  the tissues
• Paradoxical worsening of intracellular and
  cerebral acidosis
• Can be reduced by giving slowly rather than by
  rapid intravenous bolus
• Acidosis decreases the fibrillation threshold and
  impairs the physiologic response to catecholamines

16
Physiology of ventilation during CPR

• The distribution of gas between the lungs and
  stomach during mouth-to-mouth or mask ventilation
  will be determined by the relative impedance to
  flow into each
• Esophageal opening pressure lt 20 cm water
• Reduced lung thorax compliance
• Three recent reports(swine model)
• 5 minutes of untreated fibrillar cardiac arrest
  and 10 minutes of chest compressions without
  airway control
• Myocardial infarction model
• Asphyxial arrest model
• If the arrest is cardiac cause, closed chest
  compression alone may be as efficacious as
  compressions and mouth-to-mouth ventilation