Cardiopulmonary Cerebral Resuscitation: Advanced Cardiac Life Support
Harold Davis, BA, RVT, VTS (ECC)
Cardiopulmonary arrest (CPA) is the sudden, cessation of spontaneous and effective ventilation and systemic perfusion (circulation). CPA may be a result of any disease process carried out to its extreme which disrupts cardiac and / or pulmonary homeostasis. Almost forty years have elapsed since the combined techniques of mechanical ventilation, external precordial compression, and defibrillation were introduced in human medicine. We now know these combined techniques as cardiopulmonary cerebrovascular resuscitation (CPCR). The goal of CPCR is to provide adequate ventilatory and circulatory support until spontaneous functions return. We are fortunate that much of the CPCR research conducted has been carried out in animal subjects. Many of the techniques or procedures utilized in human medicine are also used in veterinary. medicine.
Cardiopulmonary and cerebral resuscitation are the combination of basic and advance cardiac life support. The goal of basic life support ( BLS) is the temporary support of the patient's oxygenation / ventilation and circulation. This is accomplished by administering manual artificial ventilation (one breath every three to five seconds) and external chest compressions (80 - 120 compressions / minute). Advanced cardiac life support (ACLS) is the addition of drugs, electrical defibrillation, and the possibility of internal cardiac compression. ACLS is initiated once effective BLS is achieved and maintained.
MECHANISM OF BLOOD FLOW
There are two theories to explain mechanisms of forward blood flow during CPCR. The classic theory is the cardiac pump theory. The heart is compressed between the two thoracic walls forcing blood out of the heart and into the arterial circulation. This is equivalent to the systolic phase of a normal heart beat. Atrio-ventricular valves prevent retrograde blood flow. Chest relaxation creates sub-atmospheric intrathoracic pressure, allows venous return and heart filling, similar to the normal diastolic phase.
The thoracic pump mechanism of blood flow is a newer theory which was recognized a little over 20 years ago. It is hypothesized that chest compressions cause a rise in intrathoracic pressure which is transmitted to the intrathoracic vasculature; intrathoracic structures are compressed. There is also collapse of venous structures in both cranial and caudal thorax which prevents retrograde venous blood flow. Intrathoracic pressures falls when chest compressions are relaxed allowing return of venous blood from the periphery into the thoracic venous system. It's hard to say which mechanism plays the predominate role in blood flow during CPR, it may depend on several factors. Some of the factors include patient size, chest compliance, the presence or absence of pleural filling defects and / or cardiomegaly.
TECHNIQUES TO AUGMENT CHEST COMPRESSIONS
Simultaneous Ventilation and Chest Compression
Ventilate with every second or third chest compression. This has been shown to increase intrathoracic pressure and to improve cerebral, but not myocardial blood flow.
Intermittent Abdominal Compression
Intermittent abdominal compression, alternating with external chest compression, improves venous return to the chest and has been reported to improve arterial blood pressure and cerebral and myocardial perfusion.
Abdominal counter pressure, a large book or sandbag is placed over the mid abdomen, this prevents the posterior displacement of the diaphragm when the chest is compressed. This technique increases intrathoracic pressure and improves cerebral blood flow.
ROUTE OF DRUG ADMINISTRATION
Several factors may figure into the selection of a drug administration route during CPCR, they include: 1) available venous access sites, 2) speed with which venous access can be obtained, 3) technical abilities of the person attempting venous access, 4) rate of drug delivery to the central circulation and 5) the duration of effective drug levels following injection. Several options (Figure 1) are available for the delivery of drugs during CPA. While drug circulation time is dependant on the cardiac output generated during CPCR. It appears that the central or jugular vein is the most desirable since drugs will be deposited near the heart. Drugs administered at the central venous site has the advantage of providing higher drug concentrations in a shorter period of time. Aside from patient movement during CPCR, it is relatively easy to place a jugular catheter in a patient suffering CPA, the jugular vein is usually palpable.
Figure 1: Methods of Drug Delivery
Peripheral venous drug administration tends to deliver the drug to the heart in a lower blood concentration and at a slower rate as compared to the central venous route. Experimental studies in animals demonstrate that drug delivery after peripheral injection is enhanced by following the injection with 10 - 30 ml saline flushes and elevation of the extremity. The circulation time was shorter and the peak concentration was higher. In one study, a 0.5 ml/kg flush solution permitted a peripherally administered model drug to reach the central circulation as quickly and in an equivalent concentration as centrally administered drug during CPR in a canine cardiac arrest model.
The intraosseous (IO) route has been used for years in human medicine for treating pediatric CPA. This route requires the placement of a intramedullary cannula. This route is reasonably quick and safe. In addition to drug administration, fluids may be infused although, at a limited rate.
A limited number of drugs (atropine, epinephrine, and lidocaine) can be administered by the intratracheal route.
The intratracheal route has been advocated for drug administration when venous access is not accessible, but peak concentrations will be lower than those obtained by other routes. Some studies have indicated that drug uptake from the tracheal surface during resuscitation is sporadic, undependable, and delayed. If this route is to be utilized, double the IV dose of the drug, dilute with 5 to 10 ml of saline if needed to provide enough volume and inject it via a long catheter placed through the endotracheal tube to the carina. Finally, hyperventilate the patient a few breaths to help disperse the drug.
Several years ago the American Heart Association de-emphasized the use of intracardiac injections. Chest compressions must be stopped while the injection is made. In addition, there are several potential complications associated with this procedure: myocardial trauma, lacerated coronary arteries, pericardial effusion, and refractory ventricular fibrillation if the heart muscle is injected with epinephrine. As a result, use of this route is probably best reserved as a last resort after all other methods have failed, if at all.
Regardless of the drug administration route, effective chest compressions must be maintained throughout the CPCR endeavor so that the drug can circulate.
CPA is a rapidly vasodilating disease process therefore, crystalloid fluids such as Lactated Ringer's are indicated. Dextrose solutions were implicated in increased morbidity and mortality in association with cardiac arrest and shouldn't be used. The initial dose of fluids in the dog is 40 mL/kg, in the cat its 20 mL/kg. The fluids should be given rapidly intravenously, in aliquots sufficient to maintain effective circulating volume. When anemia or hypoproteinemia is present whole blood, plasma, Hetastarch or Dextran 70 may be indicated.
Epinephrine possesses both alpha and beta adrenergic properties. Epinephrine's strong alpha adrenergic properties cause arterial vasoconstriction. Diastolic blood pressure is increased, which results in augmented coronary and cerebral blood flow. Aortic diastolic pressure is the critical determinant of success or failure of resuscitative efforts in animals and humans. The drug also causes constriction of large veins which displace blood out of the venous capacitance vessels. It has been reported that higher doses of epinephrine ( 0.2 mg/kg ) may be more effective than the previously recommended doses ( 0.02 mg/kg ). The higher doses tends to improve cerebral blood flow but also predisposes to ventricular fibrillation. Initial doses of epinephrine should be low and titrated upward until the desired effect is achieved.
Atropine has predominant parasympatholytic effects. Its use in cardiac arrest is based on its vagolytic action. It plays a central role in the prevention and management of CPA associated with intense vagal stimulation. Atropine is indicated in the treatment of ventricular asystole and slow sinus or idioventricular rhythms.
Lidocaine is a class 1 antiarrhythmic agent. Lidocaine is most commonly used to treat ventricular arrhythmias (i.e.,premature ventricular contractions or ventricular tachycardia). Lidocaine may be used to supplement treatment of recurrent ventricular fibrillation. It is used as a background drug to raise the fibrillatory threshold. Studies suggest that lidocaine increases the energy requirements for defibrillation. Lidocaine has no proven short - or long-term efficacy in cardiac arrest.
Magnesium Sulfate or Chloride
Hypomagnesemia has been reported in critically ill dog and can contribute to the development of lethal ventricular arrhythmias such as ventricular tachycardia and fibrillation. Magnesium (Mg) has been used to treat such arrhythmias. The exact mechanism of action is not clear. It is not known whether Mg is effective because it repletes an intracellular or extracelluar deficit or because of some intrinsic antiarrhythmic property irrespective of Mg level. It has been suggested that Mg therapy be considered for patients suffering refractory ventricular fibrillation.
Sodium Bicarbonate (NaHCO3) has been one of the primary drugs used in the treatment of cardiac arrest. The premise for its use was that it corrected metabolic acidosis which was generated by anaerobic metabolism in hypoxic tissues. It was felt that the metabolic acidosis was associated with decreased cardiac function and lowered ventricular fibrillation threshold. It is intracellular pH, not blood pH which determines cardiac viability and the likelihood of resuscitation. Ideally NaHCO3 administration should be guided by venous blood gas results but in the absences of blood gases, NaHCO3 may be given empirically at a conservative dose of 0.5 mEq/Kg per 5 minutes of cardiac arrest after the first 5-10 minutes, unless the patient is known to have preexisting metabolic acidosis. Moderate hyperventilation helps to offset a developing respiratory acidosis or is necessary as a result of CO2 development when NaHCO3 is administered.
10 % Calcium
Calcium was used routinely during CPR to augment cardiac contractility. Excessive intracellular calcium concentrations however cause sustained muscular contraction ( "stone heart" ) and myocardial and cerebral vasoconstriction. Calcium has also been implicated in reperfusion injury. Reperfusion injury occurs when ischemic tissue is re-perfused or re-oxygenated leading to cellular damage. It remains to be seen whether calcium is beneficial in patients with prolonged arrest. Calcium is not currently recommended in the routine treatment of cardiac arrest. Calcium may be indicated when the patient is hyperkalemic, hypocalcemic or has calcium channel blocker toxicity.
The purpose of defibrillation is to eliminate the chaotic asynchronous electrical activity of the fibrillating heart. This is accomplished by passing an electrical current through the heart causing the cardiac cells to depolarize and hopefully repolarize in a uniform manner with resumption of organized and coordinated electrical and contractile activity. Defibrillation stands a better chance of being successful if performed early in the CPCR endeavor.
Direct-current defibrillation requires a defibrillator. An energy level is set and the defibrillator is discharged. The energy necessary for external defibrillation is at least 4 - 5 joules/kg. The internal defibrillation energy level is at least .2 - .4 joules/kg. Excessive energy levels and repeated defibrillation can cause myocardial damage therefore, it is best to start at the lower energy levels and increase as needed.
INTERNAL CARDIAC COMPRESSION
Internal cardiac compression should be performed if effective artifical circulation and tissue perfusion are not evident within 5 minutes of cardiac arrest. The thoracotomy is also performed if effective spontaneous rhythm has not commenced after 10 minutes. Immediate internal compression is indicated if the patient has rib fractures, pleural effusion, pneumothorax, or cardiac tamponade. Internal or direct cardiac compression has been shown to be more effective than external chest compression. The advantages over external compressions include greater cardiac output and blood pressure; better cerebral, myocardial, and peripheral tissue perfusion; and higher survival rate with improved neurological recovery. Other advantages include the ability to assess ventricular filling between compressions or the ability to determine what type of cardiac arrest is present in the absence of a ECG monitor. With the chest open the descending aorta may also be compressed to force blood to the brain and coronary circulation. It has been suggested that a pericardectomy be performed to prevent cardiac tamponade.
Vasopressin is an old drug with a potential new use in CPCR. Vasopressin is the naturally occurring antidiuretic hormone. In doses higher than required for the antidiuretic hormone effect, vasopressin acts as a direct peripheral smooth muscle vasoconstrictor. Vasopressin is an effective vasoconstrictor and may be used as an alternative to epinephrine in the treatment of cardiac arrest. Vasopressin has been added to the human ACLS guidelines as an option to treat asystole, refractory ventricular fibrillation, and pulseless electrical activity. It is recommended as a single dose. The half-life of vasopressin in animals with intact circulation is 10 - 20 minutes, which is longer than epinephrine.
The goal of this discussion was to present an overview in the management of CPA patients. Those cases where the resuscitation is successful is due, in part, to a informed, prepared and efficient CPR team.
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