Successful CPCR is dependent on several factors, the most important factor being the true cause of the arrest.
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.
Capnography should be utilized on the post arrest patient. ETCO2 values generally should be kept between 30-45 mmHg; high CO2 values should first be trouble-shooted for tube occlusion, tube migration, or presence of a pneumothorax. Verify high end-tidal values with an arterial blood gas analysis. Hypercapnia can be corrected by increasing breathes per minute, but ensure mechanical error first by inspecting endotracheal tube length. Often, the endotracheal tube may need to be shortened to decrease dead space. Low ETCO2 values should be monitored for tube occlusion, leaking airway tubing or a non-patent cuff. Verification is also recommended by analyzing an arterial blood gas. Hypocapnia can be corrected by slowing down the ventilatory rate. Hyperventilation can cause cerebral vasoconstriction and may worsen cerebral ischemia.
Pulse-oximetry should also be utilized in the post arrest patient. A non-invasive method of continually measuring hemoglobin oxygen saturation (SpO2), the pulse-oximeter will display an oxygen waveform useful in determining ventilation efficacy. Pulse oximetry can also be a useful tool in assessing respiratory function, but should not take place of blood gas analysis, monitoring lung sounds, and assessing mucus membrane color after the resuscitative process.
Note that pulse oximetry measures oxygen saturation, not content, and keep in mind that the SpO2 is not the arterial oxygenation concentration (PaO2). The PaO2 should be monitored and values maintained at greater than 60mmHg. If hypotension or hypothermia is present, the pulse-oximeter may yield erroneous results. If possible, an arterial blood gas should verify ventilation status, although a venous sample can also be an acceptable way to monitor global tissue perfusion by both the pH and the venous oxygen concentration.
A thoracocentesis may be indicated after resuscitation if excessive pressure is required to achieve adequate chest expansion or if the presumed cause of arrest was acute trauma or pleural space disease is suspected. If possible, thoracocentesis should be performed while the patient is sternal to yield the maximum amount of fluid or air. The chest should be quickly and materials ready for a quick procedure. 20-25 gauge butterfly catheters are recommended for use in felines, a 16-18 gauge in canines, in combination with a three-way stopcock and a syringe. The sixth to eighth intercostals space is the recommended entry site at either a ventral or dorsal approach. Typically, fluid will be collected more ventrally, as opposed to air, which is typically more dorsal. For the small patient, it is recommended to use syringe sizes less than a 20 ml to avoid pain or trauma associated with large syringe evacuation. Frequent monitoring after thoracocentesis is important, as the procedure may actually cause a pneumothorax. If multiple chest taps are performed, placement of a chest tube may be necessary.
Supplemental oxygen via nasal catheter should ALWAYS be provided after extubation of the post arrest patient. Note that if laryngeal paralysis or tracheal collapse is a suspected in the patient's history, nasal-tracheal oxygen should be implemented before the patient regains consciousness. It is important to pre-measure the approximate length of the catheter to the bifurcation of the trachea (just past the thoracic inlet) and the corresponding end marked with permanent marker at the proximal tip attached to the patient's face. Oxygen insufflation is one-fourth rate of nasal oxygen. It is important to clearly mark on both the record and oxygen canister that delivered oxygen is tracheal, to avoid trauma to the lung parenchyma by high delivery rates.
The PaO2 should be above 60 mmHg to assure adequate hemoglobin saturation for effective oxygen delivery to the tissues. Nasal oxygen will provide a fractional inspired oxygen concentration (FiO2) of approximately 40%, which is a safe level to continue for prolonged periods and should not result in oxygen toxicity. Arterial blood gases and pulse oximetry should still be monitoring, particularly after extubation. Note that pulmonary damage can occur if high concentrations of oxygen (>50%) are administered for >12-24 hours. Animals with normal pulmonary function should have a PaO2: FiO2 ratio of 500. A value of < 300 indicates acute lung injury, and values < 200 are seen with patients with Acute Respiratory Distress Syndrome (ARDS), as indicated in phase three.
The post arrest patient will typically be recumbent, and should be turned every four hours from left to right lateral recumbency or intermittently sternal to prevent atelectasis or accumulation of lung secretions. If atelectasis or pneumonia is present, the patient should be propped sternal or positioned with the most normal functioning lung down to improve ventilation.
Hypotension and cardiac arrhythmias are the most common sequela to the cardiac arrest. Continuous ECG monitoring should be provided to detect arrhythmias such as ventricular premature contractions or ventricular tachycardia. It is important to note that the ECG records electrical changes in heart muscle, not the actual mechanical contractions. The ECG leads, consisting typically of three electrodes, sense and record the electrical changes. The ECG waveform represents different cardiac activity. The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization. Intervals between waveforms are also analyzed to better determine cardiac function. Abnormalities are analyzed in conjunction with other hemodynamic tools in assessing both cardiac output and perfusion. If sustained ventricular tachycardia is present with rates greater than 160 bpm, the most common treatment is lidocaine. Note that refractory ventricular arrhythmias (not responsive to traditional pharmacokinetic agents) may respond to intravenous magnesium as a bolus or a constant rate infusion. Other ECG abnormalities include bradycardia or sinus tachycardia; ensure adequate blood pressures and oxygenation status as both abnormalities can surface as a result of hypovolemia or hypoxia. Atropine administration in the presence of bradycardia should be titrated in small amounts or to effect, in order to avoid ventricular tachycardia and possible atrial fibrillation.
Intravenous fluid therapy is indicated to maintain cardiac output and adequate tissue perfusion. A combination of crystalloid and colloid therapy is typically instituted based upon hemodynamic markers such as blood pressure, pulse quality and capillary refill time, hematocrit and total protein, and serum lactate. Hemoglobin based solutions such as Oxyglobin is also beneficial in improving blood pressure, off-loading oxygen to tissues, and in providing colloid support. Note that oxygen-carrying capability is decreased if the hematocrit is less than 20%.
Blood pressure monitoring is also necessary in the post-resuscitative phase. Blood pressure monitoring can be accomplished by using one of two methods. The most common method, the indirect blood pressure method, uses oscillometric devices such as the Dynamap. Measuring indirect blood pressure, the Dynamap is non invasive and does not require a specialty catheter. In addition, the Dynamap has the advantage of giving systolic, diastolic, and the mean arterial pressure. Requiring only the proper size cuff, measurements can be taken on the dorsal pedal artery or the tail base on feline patients. Disadvantages to the Dynamap include inconsistencies in relation to patient movement, limb edema, hypothermia, or improper positioning or cuff size.
Direct blood pressure monitoring is the most accurate technique in assessing a patient's blood pressure. Designed for continuous assessment of arterial perfusion to the major organ systems of the body, direct measurements are accomplished through an arterial catheter and a transducer. Specialty arterial catheters are available using the Seldinger technique or guide wire system, or regular over the needle peripheral catheters may be utilized.
A mean arterial pressure needs to be greater than 60mm Hg to perfuse vital organs such as the brain and kidneys. Ideal mean pressures range from 75-90 mm Hg. Note that many post-arrest patients need inotropic support to maintain blood pressure and renal perfusion. Commonly used agents include dobutamine or dopamine as a constant rate infusion. Rates of either substance are dependent upon both heart rate and blood pressure.
The mean arterial pressure (MAP) is used in combination with other mechanical parameters such as central venous pressure monitoring to assess hemodynamic stability in the post-arrest patient. In addition, it can become useful in patients at risk for volume overload, including patients with heart disease or renal failure requiring diuresis.
The CVP, like other hemodynamic markers, can be a useful tool only when used in combination with other parameters to assess the critical patient. Note that CVP trends are more important than a single number. Typically, normal CVP values range from 0 to 5cm H2O, with values less than zero indicating hypovolemia, and values over 12cm H2O suggesting volume overload. Again, importance on the physical exam becomes rather critical to supplement findings as opposed to depending solely on machines or equipment.
Measuring CVP values must be obtained through a central venous catheter. Various types of central catheters are available and the choice should reflect the needs of the patient. Central venous catheters are made of different material, varying lengths, and may have single or multiple lumens. The catheter should be flexible, have minimal thrombogenicity, and reach approximately to the patient's right atrium. It is the author's opinion to purchase central catheters using the Seldinger technique, or a guide wire system, to facilitate placement. If a multiple lumen catheter is used, it is important to note that the CVP measurement must be obtained through the distal port.
Protocols in measuring the CVP are important to minimize infection, promote catheter longevity, and most importantly, to yield consistent results. The patient should be placed in right lateral recumbency, neck extended to avoid positional catheter issues, and a zero point identified on the manometer equal to the level of the patient's heart. Ideally, this zero point can also be gauged visually with the most cranial portion of the sternum. After the manometer is filled with saline and allowed to equilibrate, the level of the fluid on the manometer correlates with the CVP. It is recommended by the author to take several readings before recording a measurement.
Hypotension and hypoxemia that occur during a cardiac arrest will result in injury to brain tissue and irreversible neuronal death. Consequently, restoring cerebral blood flow quickly is critical. Assessing cerebral blood flow can be ascertained by use of the Doppler in detecting a retinal pulse both during CPR and after restoration of cardiac activity. Note that monitoring pupillary light response and pupil size/shape after administration of cardiac drugs such as atropine may impair diagnostic testing. However, serial neurologic exams should be performed intermittently to assess presence of palpebral or corneal reflex, response to stimuli, reactivity of pupils to light, and size and symmetry of pupils throughout the post resuscitative period. Blindness and/or dysphoria are common post-arrest, and may be temporary or permanent. Minimizing cerebral damage and supporting cerebral blood flow are the primary goals in supporting the central nervous system. Administration of pharmacologic agents such as Mannitol or Lasix for cerebral ischemia or hypoxia have been reported beneficial in the post-arrest patient. Mannitol is a hypertonic solution, and when administered as an IV bolus, it will immediately expands the intravascular volume. In addition, it will increase cerebral blood flow, reduce intracranial pressure, and increase mean arterial pressure (MAP). Mannitol can also be used synergistically with Lasix as a loop diuretic, possibly lowering the risk of pulmonary edema and promoting rapid mannitol excretion. In addition, both Mannitol and Lasix may promote urinary output. Corticosteroids can also be administered to prevent or treat cerebral edema in post-arrest patients, although its use is still largely controversial. Calcium channel blockers have also been used to prevent neuronal damage and vasoconstriction of cerebral vessels. Note that the brain can also be damaged through depletion of glucose and ATP during a cardiac arrest. Blood glucose levels should be monitored and maintained at normal levels.
Urinary output should be closely monitored in order to assess renal function. Sustained hypotension in the post-arrest phase will only exacerbate renal tubular damage and impair renal blood flow. Blood pressures and central venous pressures should be frequently evaluated to ensure proper renal support. A urinary catheter with a closed urine system should be placed in all post-resuscitation patients for measurement of urine output. Urine sedimentation should be analyzed for the presence of casts or renal epithelial cells, suggestive of acute renal failure. Pharmacokinetic agents such as dopamine, furosemide, and mannitol can be administered to stimulate urine output. Body weight and "ins and outs" should be monitored frequently to ensure proper intravenous fluid administration.
Gastric protectants are often indicated for ulceration and hemorrhage secondary to poor perfusion. Sucralfate is effective in coating ulcerated areas of the bowel and H2 receptor blockers such as Famotidine can reduce gastric acid and pepsid secretion. Enteral nutrition should be instituted as soon as possible to promote healing, prevent bacterial translocation, and maintaining the health of gastrointestinal enterocytes.
Wherein continuous hemodynamic monitoring is required to support the post-arrest patient, other hemodynamic markers in assessing a patient's stability in the post-resuscitative phase include the packed cell volume, total protein, and lactate levels. The packed cell volume should be recorded during the initial arrest, and re-analyzed frequently in response to both fluid therapy and blood pressure analysis in the post-resuscitation phase. Again, trends need to be monitored during course of therapy and in correlation to other physical exam findings. High packed cell volumes can indicate dehydration, hypertension, or primary disease states, whereas low or deteriorating packed cell values can indicate hemorrhage, over- aggressive fluid therapy, or chronic disease states. Note that coagulation abnormalities are common in the post-arrest patient, often seen in phase two (the "leaky capillary" phenomena).
Similarly, the total protein can also provide valuable information pertaining to patient stability. Used as a clinical marker to the choice of colloid therapy, the total protein can enable a clinician to assess hydration status as well as vascular integrity, gastrointestinal function, and chronic disease states.
Lactate levels can also be used as a window into a patient's hemodynamic stability. As lactate is the end product of anaerobic glycolysis, elevated lactate levels can suggest decreased oxygen delivery to the tissues. Used as a monitoring tool, measurement of lactate levels can help assess a patient's perfusion in combination with blood pressure, heart rate and rhythm, packed cell volume, and central venous pressure, etc. Lactate analyzers are relatively inexpensive and require a mere drop of whole blood for testing, as opposed to more expensive blood gas analyzers to determine presence of acidosis.
Macintire, DK: Manual of Small Animal Emergency and Critical Care Medicine; Lippincott, Williams and Wilkins, 2005.