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DVM Feature Article

Cardiopulmonary Cerebrovascular Resuscitation (CPCR)

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• CPCR - Attempts to provide adequate ventilatory and circulatory support until spontaneous functions return.
• Prior thought- chest compressions moved blood by compression of the heart. 
• Current thought- compressions cause an increase in intrathoracic pressure that helps expel blood from the thorax.
• Success rate is approximately 1 - 10% survival rate for leaving hospital
• Since most C-P arrests are predictable within 24 hrs of occurrence, prevention is best.

• Airway - Check for obstruction
• Breathing- establish an airway via intubation
  • Check for pneumothorax, pleural effusion, pericardial effusion
  • Ambu-bag – controls airway & ventilation
  • Acupuncture- Jen Chung (philtrum point governor vessel [ VG ] 26 – (use 25G needle insert & peck 10 times into point just below midline of nostril)
• Circulation- no palpable pulses, absent heart sounds
  • IV Fluids- OK if dehydrated or shocky (should  be conservative unless hypovolemia is cause, ­ right atrial pressure can decrease coronary perfusion pressure)
  • IV Fluids contra-indicated with heart failure, pulmonary edema or overhydration
• Drugs and Defibrillation based on EKG and clinical findings

• Close patient monitoring during the post- resuscitation period
• Treat damage done during CPCR
• Treat primary cause of CPA

• Cardiac pump mechanism - attendant forward blood flow- better for < 7-10 kg

• Thoracic pump mechanism - done at widest part of chest- better for > 10 kg

  • Chest compressions increase global intrathoracic pressure

  • Pulmonary vascular bed compresses

  • Heart acts as a passive conduction

  • During relaxation, thoracic reservoir refills

• Lower ½ of sternum in dorsal recumbancy
• 5-6^th intercostal space in lateral recumbancy
• Mod depth and force - can monitor with doppler over eye
• Rate - 80 - 120 / min of chest compressions
• Duration - 40 - 50% 0f cycle
• Prefer 100% oxygen, but room air is OK for assisted ventilation
• Ventilate every 3-5 compressions - between compressions is best - 30-40 breathes/min
• Can evaluate with arterial BG - watch PCO2 and PO2

• These do not improve CPCR
  • Compression against occluded airway
  • Simultaneous compression and ventilation - may increase intrathoracic pressure
  • Continuous abdominal binding with an abdominal wrap
• Equivocal Results
  • Circumferential chest compressions
  • Interposed abdominal compressions
  • Active compression and decompression

• Increased cardiac output, blood pressure, cerebral, cardiac, and tissue perfusion, and survival rate
• Decreased acidosis and blood lactate
• The question is not if to use internal massage but when

• Emergency thoracocentesis done under less than ideal conditions to an already compromised patient
• Must be done in a fully equipped 24 hr hospital with trained staff
• Post - op complications

• Open or closed pneumothorax
• Chest trauma, fractured ribs
• Abnormal chest size or shape
• When no success with external massage
  • No evidence of heart beat within 10 minutes
  • No evidence of tissue perfusion within 5 minutes (some say within 2 min)
  • Both of these guidelines may still be too late

• Repeated C-P arrests are common following CPCR
• Re-evaluate management of the case
  • blood transfusion for anemic patients
  • thoracocentesis
  • increase or decrease fluids
• Positive inotropes
• Monitor BP, EKG, urine output (1-2 mls/kg/hr)
• Big concern - loss of strong respiratory drive - not enough to just maintain ventilation, but need good ventilations - a lot of patients require ventilators.
• Serial neuro exams

• a - vasoconstriction redistributes blood from venous capacitance vessels into active arterial circulation.  Arterial constriction decreases loss of arterial blood to periphery.
• Increases pacemaker activity and contractility - once heart starts beating (positive inotrope)
•  Dose (1:1000 = 1mg/ml)
  • Low:  0.01-0.02 mg/kg - less effective at ­ BP (0.1 ml/10 kg)
  • High: 0.1-0.2 mg/kg - more prone to cause arrhythmias, especially V-Fib (1ml/10kg)
  • Recent recommendations – start with low dose and work up
  • Repeat every 3-5 minutes       

• Best used for long cardiac arrest (5-10 minutes or longer in arrest)
• Recovery is better when acidosis is controlled
• Used to be used regularly, but current recommendations call for conservative use
• Keep patient well ventilated during use
• Know HCO3 concentration- meq/ml- different concentrations available.
• Dose: 0.5 mEq/kg per 5 minutes of arrest

• Used to be very commonly used, but now used judiciously
• Currently recommended only with severe hyperkalemia, severe hypocalcemia, or if chest is open and heart is flabby
• Dose- 0.2- 0.6 ml/kg of CaCl 10% - wide range 10-60 mg/kg.

• Indicated for severe bradycardia
• Not proven to be beneficial during asystole
• IV causes central transient vagomimetic effects, whereas IM or SQ, only see the peripheral vagolytic effects. (IV - can see initial bradycardia and first or second degree AV block )
• Dose: 0.02-.04 mg/kg IM(1/2 –1ml/10kg)

• More common to have hypomagnesaemia than we think (intracellularly)
• Recommended for refractory arrhythmias, V Fib and non-responsive CPA
• Dose:  Mg Sulfate 20%-5-15 mls over 1 minute, followed by 500 mls of 2% over 5 hours, or 25-50 mg/kg slowly

• Lidocaine - 1-3 mg/kg post CPCR (1ml/10kg)
• Procainamide 5-15 mg/kg IV

• Best to defibrillate but can use drugs
• KCL, Bretylium 2-10 mg/kg (class 3 antiarrhytmic), MgCl
• Amiodarone - common in people for refractory V-Fib

• Central vein - best choice
•  Intratracheal (via endotracheal tube)- Atropine, Lidocaine, Epinephrine
  • Use double the dose
  • Do not use if significant pulmonary edema is present
  • Do not give NaHCO3 this way
• Intraosseous - may be faster than peripheral vein, and great choice if vascular collapse is present
• Peripheral - can be used, but not all that great.  Drugs should be followed by a saline bolus
• Intracardiac - avoid unless open chest CPR is being performed

• Human textbooks advise to use it very early on, but most human arrests are in V-Fib - not as true in the veterinary patient
• External:  2-20 watt or joules/kg
• Internal:  0.2-2   watt or joules/kg
• Inverse correlation between duration and success
• Thumb rules:
  • Small animal - start 20, go to 100
  •  Large – start 100, go to 360
  • Increase one click each shock
  • Use jelly for contact- do not use alcohol

• Relatively normal EKG with little to no contractile activity
• If caused by heart disease - usually fatal
• If caused by other (ie pulmonary) - better prognosis
• Treatment principles:
  • Fluids if hypovolemic
  • Dex SP – 2-4 mg/kg
  • Epinephrin
  • Atropine
  • Naloxone - may antagonize endogenous opiates, and make myocardium more responsive to catacholamines

• Similar to EMD but these rhythms are usually from end stage disease