Clinical Cases in Anesthesia : Cardiopulmonary Resuscitation

Clinical Cases in Anesthesia : Cardiopulmonary Resuscitation

Cardiopulmonary Resuscitation

An 86-year-old woman with congestive heart failure, coronary artery disease, and syncopal episodes presents for elective permanent pacemaker insertion. A recent 24 hour ambulatory electrocardiogram recording demonstrated multiple episodes of severe sinus bradycardia associated with pre-syncopal symptoms. Monitored anesthesia care is requested in light of the patient’s advanced age and associ-ated medical conditions. The infiltration of local anesthesia and isolation of the cephalic vein in the left deltopectoral groove proceeds uneventfully. During placement of the ventricular pacing lead, ventricular ectopy occurs as the lead encounters the right ventricular endocardium. Subsequently, as the lead is repositioned, ventricular tachy-cardia is induced and rapidly deteriorates into ventricular fibrillation.

What is the initial response to a cardiac arrest?

The initial response to a witnessed cardiac arrest is to confirm the diagnosis. Patients in arrest are unresponsive, apneic, and pulseless. Assistance should be called for immediately prior to any intervention. In the past, it was recommended to call for assistance after the initiation of cardiopulmonary resuscitation (CPR), but since 80–90% of patients with sudden cardiac arrest have ventricular fibrillation (VF), which is the most treatable dysrhythmia but which requires urgent defibrillation, the rescuer is advised to call first so that a defibrillator can be brought to the scene. The only exception is in the case of children less than 8 years of age, who usually arrest because of airway problems. In that case, an attempt at securing the airway should first be made.

Monitored patients should be treated according to the Advanced Cardiac Life Support (ACLS) protocol devised for their dysrhythmia. This includes basic life support (BLS), usually in the form of CPR, as well as adjunctive equipment for airway control, dysrhythmia detection and treatment, and post-resuscitation care. Unmonitored, unre-sponsive patients should have their airway assessed first followed by two breaths and a pulse check. In a witnessed cardiac arrest, a precordial thump may be indicated but CPR must be started immediately if the patient remains pulseless. As soon as possible, paddles or electrocardiogram (ECG) leads should be placed on the patient to determine the rhythm. If pulseless ventricular tachycardia (VT) or VF is the initial rhythm, the patient should receive up to three uniphasic countershocks of increasing power: 200 joules (J), 200-300 J, and 360 J, respectively. Biphasic equivalents are approximately half that of uniphasic doses. If VF or pulse-less VT is not the initial rhythm, or if the countershocks are unsuccessful, then chest compressions and ventilation should be continued and the patient treated accordingly.

The essential element in treating cardiac arrest is rapid identification and treatment. The goal of CPR is to provide oxygenated blood to the heart and brain until ACLS proce-dures are initiated. The best results (survival of approxi-mately 40%) are achieved in patients receiving CPR within 4 minutes and ACLS within 8 minutes of arrest, whereas survival is less than 6% when CPR and ACLS are started after 9 minutes.

The groups of patients most likely to be resuscitated include patients outside the hospital with witnessed arrests due to VF, hospitalized patients with VF secondary to ischemic heart disease, arrests not associated with coexisting life-threatening conditions, and patients who are hypother-mic or intoxicated. Patients with severe multisystem disease, metastatic cancer, or oliguria do not often survive CPR.

How do chest compressions produce a cardiac output?

How do chest compressions produce a cardiac output?

It used to be assumed that chest compressions produced a cardiac output by directly compressing the ventricles against the vertebral column. This was thought to produce systole, with forward flow out of the aorta and pulmonary artery, and backward flow prevented by closure of the atrioventricular (AV) values.

This explanation is probably not completely valid. Echocardiographic images during arrest show that the AV valves are not closed during chest compressions. There are reports of patients who, during episodes of monitored VF, have developed systolic pressures capable of maintaining consciousness by coughing. This demonstrates that chest compressions per se are not necessary to maintain a cardiac output. Furthermore, CPR is frequently ineffective in patients with a flail chest until chest stabilization is achieved. If direct compression were the etiology of blood circulation in CPR, then a flail chest would be an advantage by increasing the efficiency of the “direct” compression. These observations have led to the proposal of the “thoracic pump” theory of CPR.

The “thoracic pump” theory proposes that forward blood flow is achieved because of phasic changes in intrathoracic pressure produced by chest compressions. During the downward phase of the compression, positive intrathoracic pressure propels blood out of the chest into the extrathoracic vessels that have a lower pressure. Competent valves in the venous system prevent blood from flowing backwards. During the upward phase of the com-pression, blood flows from the periphery into the thorax because of the negative intrathoracic pressure created by release of the compression. With properly performed CPR, systolic arterial blood pressures of 60–80 mmHg can be achieved, but with much lower diastolic pressures. Mean pressures are usually less than 40 mmHg. This only provides cerebral blood flows of approximately 30% and myocardial blood flows of about 10% compared with pre-arrest values.

What are the recommended rates of compression and ventilation?

Animal models of CPR have shown that the optimal blood flows are achieved when chest compressions are performed at 80–100 times per minute and the chest is compressed 1.5 to 2 inches (3–5 cm). The new Guidelines for Cardiopulmonary Resuscitation published by the American Heart Association in 2000 recommend a chest compression rate of 100 times per minute. The proportion of time spent during the compression phase should be 50% of the relaxation phase.

Artificial ventilation is preferentially given by endotra-cheal tube (ETT) at a rate of 10–12 breaths per minute. Nevertheless, the new ACLS guidelines de-emphasize endo-tracheal intubation during CPR due to a high incidence of incorrectly placed ETTs. Mask ventilation or alternative air-ways, such as the laryngeal mask or the esophageal-tracheal Combitube, may be preferable in situations where the rescuer is not properly trained or skilled in ETT placement. It is now mandatory to confirm correct ETT placement by both physical examination and a secondary device, such as capnography, a colorimetric carbon dioxide (CO2) detector, or an esophageal detector device. During two-person CPR, ventilation in the intubated patient should be performed with every fifth compression. With an unprotected airway or during one-rescuer CPR the compression.

Each breath should take about 2 seconds and should make the chest rise clearly. Animal studies demon-strate higher cerebral perfusion pressures when ventilation occurs simultaneously with compressions. However, improved survival has not been demonstrated in humans, and this technique is not recommended.

What are the complications of CPR?

Complications of CPR include skeletal injuries, espe-cially rib fractures, visceral injuries, airway injuries, and skin and integument damage (skin, teeth, lips). Less than 0.5% of the complications are considered life-threatening. These include injuries to the heart and the great vessels. However, a significant number of complications could be expected to require therapy and prolong the hospitalization. These include rib and sternal fractures, myocardial and pul-monary contusions, pneumothorax, blood in the pericar-dial sac, tracheal and laryngeal injuries, liver and spleen ruptures, and gastric perforation and dilatation.

What is the optimal dose of epinephrine?

Pharmacologic therapy has been changed significantly from the previous ACLS protocols. Epinephrine is still the therapy of choice, but vasopressin has emerged as an alter-native in the treatment of VF/VT. The vasoconstriction caused by the α-adrenergic effects of large doses of epi-nephrine that are administered during CPR increases arterial pressure and improves myocardial and cerebral blood flow. Studies have suggested that this is a dose-dependent phe-nomenon. Animal studies have shown better outcomes from cardiac arrest using 0.1–0.2 mg/kg of epinephrine rather than the present recommended dose of 0.01 mg/kg. Two recent large multicenter investigations, however, did not demonstrate survival differences in patients treated with larger doses of epinephrine. This lack of clinical efficacy may arise from the fact that the time elapsed prior to the initial dose of epinephrine was significantly longer than was the case in the animal studies.

The presence of coronary artery disease in many patients hinders coronary artery blood flow even in the pres-ence of higher aortic diastolic pressures. The β-adrenergic effects of epinephrine may actually worsen the outcome by increasing myocardial oxygen requirements. Until further studies clarify this issue, the 2000 ACLS protocol recom-mends a standard dose of 1 mg epinephrine (0.01 mg/kg intravenous (i.v.) push) every 3–5 minutes. Higher doses up to 0.2 mg/kg may be considered, but these doses are not recommended and may be harmful.

What is the indication for vasopressin in CPR?

Vasopressin, also known as antidiuretic hormone, is a potent vasoconstrictor when used at higher doses.Vasopressin’s vasoconstrictive effect increases blood flow to the brain and heart during CPR. The vasoconstrictive effect is mediated via V1 receptors and thus independent of the adrenergic-receptor-mediated effect of epineph-rine. Therefore, vasopressin seems to lack some of the β-adrenergic- mediated adverse effects of epinephrine, such as increased myocardial oxygen demand and tachycardia. Vasopressin currently holds a Class IIb recommendation in the treatment for pulseless VT/VF. It is not yet recom-mended for asystole and pulseless electrical activity, mainly because large studies showing improved outcome are still missing. Thus, vasopressin is currently recommended as a first-line alternative to epinephrine in patients with pulse-less VT/VF, given as a single dose of 40 U i.v. push. Because of the longer half-life of vasopressin (10–20 minutes) compared with epinephrine (3–5 minutes), and lack of supportive evidence in human trials, a second dose is not recommended at this point. Following vasopressin admin-istration and 10–20 minutes of continued CPR without the return of a perfusing rhythm, it is acceptable to return to 1 mg epinephrine every 3–5 minutes.

What are the indications for sodium bicarbonate (NaHCO3) administration?

Before 1986, NaHCO3 was routinely used during CPR, even without knowledge of the patient’s acid–base status. Acidosis inhibits myocardial contractility and also inhibits the effects of catecholamines. However, this inhibitory effect on catecholamines does not appear clinically signifi-cant at the range of pH commonly encountered and the catecholamine doses administered during resuscitation. The myocardial depressant effect of metabolic acidosis is delayed compared with that produced by the intracellular acidosis that follows the administration of NaHCO3. As is apparent from the equilibrium equation,

[HCO3−] + [H+] ⇔ [H2CO3] ⇔ [CO2] + [H2O]

Every 50 mEq of bicarbonate administered produces large amounts of CO2 gas. CO2 gas freely diffuses across cellular membranes, and causes a paradoxical worsening of the intra-cellular acidosis. Intracellular CO2 tensions of greater than 300 mmHg and pH values less than 6.1 have been recorded.

Carbicarb, a buffering agent that does not produce as much CO2, has also been tried without significant improvements in outcome following CPR. Another probable explanation for the ineffectiveness of these buffering agents is that they also cause hypernatremia and hyperosmolality. Hyperosmolar solutions may decrease aortic pressures, and compromise survival. Initially, the leftward shift in the oxy-hemoglobin saturation curve following the administration of NaHCO3 may theoretically decrease oxygen availability.

Thus, NaHCO3 should only be given when the results of arterial blood gas analysis indicate a significant metabolic acidosis in the presence of severe acidemia (e.g., with an arterial pH <7.20). It currently holds a Class III indication in hypercarbic acidosis and thus may be harmful during CPR. NaHCO3 is indicated in known hyperkalemia (Class I), bicarbonate-responsive acidosis (Class IIa), tricyclic anti-depressant overdose (Class IIa), to alkalinize urine in aspirin or other drug overdose (Class IIa), and for intubated and ventilated patients with a long arrest time or return of circulation after prolonged CPR (Class IIb). When NaHCO3 administration is planned, the correct full dose is calculated as follows:

Patient’s weight (kg) × base deficit × 0.3

Many clinicians use half of the calculated dose initially. If blood gas results are unobtainable, an empiric dose of 1 mEq/kg can be administered in prolonged arrest situations.

What are the indications for calcium salt adminis-tration?

Routine calcium chloride or calcium gluconate admin-istration has also been scrutinized. Studies indicate that intracellular calcium accumulation may be a final common mediator of cellular injury and death. Specific indications for calcium therapy during CPR include hyperkalemia, documented hypocalcemia, and calcium-channel blocker overdose. Calcium salts are not recommended in the routine treatment of electromechanical dissociation or asystole.

What is the antidysrhythmic therapy of choice in VF/pulseless VT?

After CPR has been initiated and the underlying rhythm recognized, immediate defibrillation is the mainstay therapy in the treatment of VF/pulseless VT. The choice of antidys-rhythmic therapy has not been shown to influence outcome if repeated countershocks, epinephrine/vasopressin, and appropriately administered CPR are ineffective in a patient with refractory VF or VT. No drug has clearly proven supe-riority in most cases of intractable VT or VF. Despite this, the 2000 ACLS protocol contains many changes in drug administration in VF/pulseless VT compared with older recommendations. Lidocaine is no longer recommended as the antidysrhythmic drug of choice for the treatment of malignant ventricular ectopy, VT, or VF. Lidocaine and procainamide hydrochloride are now classified as drugs with intermediate evidence for this indication. Bretylium is no longer recommended and has been removed from the ACLS algorithm. Instead, amiodarone is now a Class IIb indication for cardiac arrest from VF/pulseless VT that persists after multiple shocks. Amiodarone has been shown to increase the intermediate outcome of admission-to-hospital following out-of-hospital refractory VF arrest in one prospective double-blinded randomized controlled study.

Nonetheless, amiodarone administration is not associated with improvement of long-term outcome. After attempts to defibrillate and epinephrine and/or vasopressin adminis-tration fail to establish a perfusing rhythm, the new ACLS guidelines indicate consideration of antidysrhythmics.

  amiodarone 300 mg i.v. push for persistent or recurrent VF/pulseless VT

  magnesium sulfate 1–2 mg i.v. when an underlying hypo-magnesemic state is suspected or in torsades de pointes

 procainamide 50 mg/min in refractory VF (maximum 17 mg/kg)

What are the management strategies in bradycardias?

Most symptomatic bradycardias (e.g., sinus bradycardia and asystole) should be treated with atropine, transcutaneous pacing (TCP), and dopamine or epinephrine infusions. Patients with third-degree heart block and Mobitz type II second-degree heart block should not receive atropine because it may cause a paradoxical slowing of ventricular escape rates. Isoproterenol should not be used for the treat-ment of bradycardias because it increases myocardial oxygen consumption and may cause hypotension.

In the setting of an acute myocardial infarction, the ACLS protocol recommends that third-degree heart block and Mobitz type II heart block require transvenous pacing. TCP or epinephrine should be used in symptomatic patients until a transvenous pacemaker is inserted.

What is the treatment of supraventricular tachydys-rhythmias?

The most important initial step is to evaluate whether the patient with an underlying tachycardia is stable or unstable. Tachycardias in unstable patients require imme-diate electrical cardioversion, whereas stable tachycardias are usually treated with drugs and/or electric cardioversion until further evaluation and diagnostic measures can be performed. It is extremely important to treat all wide com-plex tachydysrhythmias as VT. Clinical or ECG criteria used to differentiate wide complex supraventricular tachy-cardias from VT are problematic. Administration of verapamil to a patient with VT may cause irreversible hemo-dynamic collapse. However, since adenosine has almost no effect on blood pressure, it can be tried in stable patients who are suspected of having a wide complex supraventric-ular tachycardia. Adenosine is an endogenous purine nucleoside that depresses sinus and AV nodal activity that is extremely short-acting (the serum half-life is less than 5 seconds) and produces few significant side-effects.

In narrow complex supraventricular tachycardias, vagal maneuvers should be performed or adenosine (0.1 mg/kg i.v. push) administered to help identify the exact underlying rhythm. Treatment also depends on the underlying cardiac function (preserved or impaired, ejection fraction (EF) <40%, congestive heart failure). Paroxysmal supraventricular tachy-cardias can be treated with calcium-channel blockers, β-blockers, digoxin, or amiodarone (the latter especially in the patient with impaired cardiac function). In junctional tachycardia or ectopic or multifocal atrial tachycardia, elec-trical cardioversion is not recommended.

If atrial fibrillation/flutter is suspected as the underlying rhythm, it is imperative to evaluate the patient before further management is initiated. If possible, the patient’s cardiac function should be assessed, a Wolff-Parkinson-White (WPW) syndrome ruled out, and the time of onset of atrial fibrillation determined (<48 hours or >48 hours). The goals are to treat unstable patients urgently to control the rate, convert the rhythm, and to provide anticoagulation. Patients with an onset of symptoms > 48 hours should be evaluated for thrombi in the atria using transesophageal echocardiography (TEE) before electric cardioversion is attempted. WPW patients are preferably treated with elec-tric cardioversion or amiodarone. In these patients, adeno-sine, β-blockers, calcium-channel blockers, and digoxin are contraindicated. These drugs can lead to an increased ven-tricular response or may precipitate VF by selectively blocking the AV node in patients with coexisting accessory conduction pathways. Once the diagnosis of atrial fibrilla-tion/flutter is confirmed, treatment usually consists of elec-tric cardioversion, β-blockers, calcium-channel blockers (e.g., diltiazem), or digoxin. Amiodarone is preferred in the unstable patient or the patient with impaired ventricular function.

What are the indications for magnesium therapy?

Magnesium deficiency is associated with ventricular ectopy, sudden cardiac death, and CHF. It can also precipitate refractory VF and impede correction of hypokalemia. Hypomagnesemia should be corrected in cases of refractory VT or VF. Magnesium sulfate is the treatment of choice for torsades de pointes. Magnesium supplementation may also reduce the incidence of post-myocardial infarction ventricular dysrhythmias. Thus, some authorities suggest administering it prophylactically to patients after myocar-dial infarction.

What are the indications for a pacemaker?

The use of transcutaneous or transvenous pacemakers in ACLS is indicated in patients with symptomatic brady dysrhythmias (i.e., myocardial ischemia, hypotension, mental status changes, pulmonary edema), and for over-drive pacing in patients with refractory tachydysrhythmias. They are rarely indicated in asystolic patients who have had prolonged attempts at resuscitation.

Why is it important to monitor serum glucose?

Serum glucose levels may affect post-cardiac arrest neurologic function. Animal studies have shown less functional brain recovery after normothermic cerebral ischemia in hyperglycemic animals. The mechanism prob-ably relates to increased lactic acid production secondary to availability of larger amounts of the precursor, glucose. Unfortunately, it is not clear what levels of glucose should be treated. Severe hypoglycemia as a result of overtreatment of hyperglycemia will cause neuronal injury.

What are the indications for open cardiac massage?

Open cardiac massage is probably indicated only in postoperative cardiac surgical patients (in case of pericar-dial tamponade), in the operating room if the heart is accessible, in patients with severely deformed thoracic cages, and in some cases of penetrating chest trauma. It should be considered in cases of cardiac arrest caused by hypothermia, pulmonary embolism, pericardial tamponade, abdominal hemorrhage, and blunt trauma with cardiac arrest. It has not been found to be of value in patients who have had prolonged closed CPR.

What is the management strategy for pulseless electrical activity (PEA)?

PEA refers to the clinical picture of cardiac electrical activity without a detectable pulse. VF, VT, and asystole are specifically excluded from the wide range of electrical activity that may present. The ACLS guidelines emphasize the search for reversible causes of PEA. This must not exclude basic resuscitation measures, which should be started as soon as possible. After VF/pulseless VT have been ruled out, securing an airway, oxygen administration, and chest compressions must be the primary task. The etiology of PEA must now be sought. Table 1.2 lists the most frequent causes of PEA.

First-line drugs in the continuing resuscitation algorithm include epinephrine 1 mg i.v. push every 3–5 minutes and atropine 1 mg i.v. every 3–5 minutes as needed when the underlying PEA rate is slow. Nevertheless, treatment of PEA is not limited to these drugs and pharmacologic treatment of a patient with PEA must be customized to the suspected underlying cause. PEA is not an indication for defibrillation. “Shockable” rhythms have to be ruled out. Once a patient converts to VF/pulseless VT, however, the appropriate algorithm should be initiated immediately.