Managing the post-arrest patient (Proceedings)
Successful CPCR is dependent on several factors, the most important factor being the true cause of the arrest. Patients who were healthy before and whose arrest was initiated by pharmacological or problems easily identified (kinked endotracheal tube, improper anesthetic depth, or allergic reactions) have the best chance of survival. Conversely, patients who experience an arrest as a result of disease or traumatic injury, yet are successfully resuscitated, are still considered extremely critical and unstable. The likelihood of re-arrest is typically 65-68% for dogs and 22-38% for cats, and usually occurs within 4 hours of the initial arrest.
Patients that regain spontaneous heart rhythm need to have continuous care to in order to support normal organ function. Initial efforts should be directed at supporting normal body physiology to protect the cerebral tissue, identifying and correcting any electrolyte and acid-base disturbances, and initiating aggressive pulmonary support. The underlying cause of the arrest should be quickly identified and the primary disease treated accordingly. Managing the post-arrest patient is labor intensive and is inherent upon clinical and technical aptitude.
There are several physiologic events that occur following a cardiac arrest, including hypotension, hypothermia, acid-base disturbances, arrhythmias, renal and neurologic dysfunction. Tissue ischemia secondary to poor perfusion is the cause of such injury to vital organs. Coined the "post resuscitation syndrome", tissue re-oxygenation after successful CPR causes a reperfusion injury by inciting the production of inflammatory cytokines and coagulation disorders such as disseminated intravascular coagulation (DIC). The consequences of tissue hypoxia to certain organs such as the brain may be permanent.There are several reported phases of the post-resuscitation syndrome in both human and veterinary medicine and can be categorized as follows:
Phase One: Myocardial dysfunction surfacing as poor cardiac output, arrhythmias, and hypotension; the end result is poor tissue perfusion. Phase one can last 12-24 hours.
Phase Two: Renal, gastrointestinal, and hepatic damage as a result of tissue ischemia and poor perfusion. Inadequate supportive techniques will result in bacterial translocation and sepsis due to "leaky" capillary beds and endothelial damage. Phase two can occur 1-3 days post arrest.
Phase Three: Septic shock and multiple organ failure. Inappropriate diagnostics and therapeutics in any or all phases will result in Phase Four, death.
Monitoring the patient for clinical signs during the post-resuscitative syndrome is important. Overall, the technician and clinician should institute therapy to provide cardiovascular and respiratory support in order to maintain tissue and organ perfusion immediately post arrest to prevent initiation of phase one. Severity of the post-resuscitation syndrome is dependent upon the degree and duration of tissue ischemia and hypoxia.
Note that excessive crystalloid fluids may have been administered during resuscitation, resulting in increased tissue water. Edematous tissues may have fatal consequences in organs such as the lungs and brain. Colloids do not contribute to tissue water unless the patient suffers a "leaky capillary" syndrome, such as listed in phase two. The critical care staff should provide the clinician with hemodynamic trends and monitor for abnormal parameters in order to prevent decompensation. Immediate monitoring and supportive goals can be divided into four categories or systems, including the respiratory, cardiovascular, neurologic, and renal systems.
Respiratory support is always the first priority in the post arrest patient, as ventilation is typically not voluntary and all other supportive steps will be futile if the animal is not receiving oxygen. Most patients will require positive pressure ventilation (12-24 bpm) with 100% oxygen until they are voluntarily breathing. The patient should remain intubated and breathing 100% oxygen until auscultation, hemoglobin saturation, end tidal CO2, and arterial blood gases are assessed. If auscultation reveals edematous or harsh sounds, thoracic radiographs should be performed to check for rib fractures (either from trauma or CPR), pulmonary edema, pulmonary contusions, or pneumothorax. The patient should not be transported or manipulated for radiographs unless they are breathing voluntarily and cardiac function restored.
Inspiratory pressures during ventilation should rarely exceed 20 cm of water for the dog, and 15cm of water for the cat. However, higher pressures may be indicated (20-30cm water) for patients with pleural fluid, pulmonary edema, or pneumo/hemothorax, in order to obtain adequate lung expansion. Inspiratory time should be less than 1.5 seconds to allow for adequate venous return. In addition, expiratory pressure should be allowed to fall back to zero between inspirations, to allow for adequate venous return and cardiac output. The nursing staff should always monitor the ventilated patient for leaking airway sounds, such as bubbling or fluid sounds on inspiration around the cuff or oral area.