2 CARDIOPULMONARY RESUSCITATION
Norman A. Paradis M.D., Alden H. Harken M.D.

1. Define sudden cardiac death.

Sudden ventricular fibrillation (VF) or pulseless electrical activity (PEA). Acute coronary ischemia and preexisting cardiac disease are the most common causes. VF is becoming less common.

2. What is the predominant determinant of successful cardiopulmonary resuscitation (CPR)?

Show answer
Time to restoration of spontaneous circulation, which itself is a function of the time to effective chest compression and time to defibrillation of VF. The chance of a good outcome decreases by 10% per minute. Successful outcomes are more likely if CPR is initiated promptly and if preexisting hypothermia is present.

3. What are the ABCs?

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Airway, breathing, and circulation. But things have changed. There are now three recognized phases of CPR: electrical, mechanical, and metabolic.

1. The electrical phase lasts about 5 minutes-during that phase, only immediate electrical cardioversion may be required.
2. The mechanical phase lasts 5 to 10 minutes after onset of arrest-during this phase, a few minutes of chest compression are required before cardioversion.
3. The metabolic phase begins at 10 minutes postarrest. During this phase, pressor and antiarrhythmic drugs are required.

4. How do you electrically cardiovert (shock) a patient?

Show answer
Gel pads now are more common than hand-held paddles. If you are using paddles, place electrolyte (conductive) gel on them. Place one pad or paddle in the right subclavicular area and the other in the midaxillary line at the level of the eighth intercostal space (over the apex of the heart). If you are using a biphasic defibrillator, the fist shock should be only 100 J. With monophasic defibrillators, start at 200 J. If the patient remains in VF, rapidly increase the output to the maximum the machine allows. Take care to confirm that everyone (including you) is clear before delivering a shock.
5. Is there an immediate need for an airway? Show answer
No. Defibrillation and chest compression should be initiated first. Waiting for intubation to be completed before initiation of these interventions is one of the most common mistakes in advanced life support. Children, in whom primary respiratory arrest is more common, are an exception. Restoration of ventilation in children often reveals that pulselessness was severe shock, not cardiac arrest.

6. How do you establish an airway-even in a patient with suspected neck injury?

Show answer
The three basic maneuvers are head tilt, chin tilt, and jaw thrust. In an unconscious patient, the jaw muscles relax. The jaw thrust subluxes the mandible, pulling the tongue and epiglottis anteriorly off the upper airway (with minimal cervical hyperextension).
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7. Is endotracheal intubation mandatory?

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No.

* Mouth-to-mouth ventilation delivers 16% inspired oxygen.
* Bag-mask ventilation delivers 21% oxygen.
* Bag-mask ventilation with an oxygen supply can deliver close to 100% oxygen.

8. Name the advantages of endotracheal intubation. Show answer
A relatively secure airway. Mouth-to-mouth or bag-mask can deliver significant amounts of air to the stomach. Gastric distention impairs diaphragmatic movement and may predispose to aspiration.

9. Does an endotracheal tube (even with the cuff up) prevent aspiration?

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No. If you place a couple of drops of methylene blue on the tongue of an intubated patient, you can suction “blue” from the other end of the tube (beyond the cuff) within 90 seconds.

10. Which size endotracheal tube should you use?

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Select a tube with an internal diameter equal to the width of the patient’s little finger. For a 70-kg adult, a 7.5-mm tube is fine. Do not delay ventilation trying to place a large endotracheal tube. Adequate ventilation can be achieved through smaller tubes.

11. How do you know if the endotracheal tube is in the proper position?

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1. Listen to both lung fields.
2. Observe symmetric chest excursion with each tidal breath.
3. Listen over the epigastrium (you don’t want to hear gurgles from the stomach).

These physical findings are not fully reliable, however. In patients with spontaneous circulation, it is now standard to confirm tube placement with end-tidal CO2 (ET-CO2) measurement. In cardiac arrest, even ET-CO2 may be unreliable. You should confirm tube position as soon as possible by chest x-ray.

12. Which is preferred-oral or nasal intubation?

Show answer
Oral intubation. You can watch the tube pass directly through the vocal cords, ensuring proper placement. Nasal intubation is a blind technique, relatively contraindicated in patients with maxillofacial trauma (because of the risk of intracranial placement of the tube through an anterior fossa fracture) and in patients with known or suspected coagulopathy (because nasal mucosa is well vascularized, intubation may cause major epistaxis). Oral endotracheal intubation with “in-line” neck stabilization is preferred even in patients with suspected neck injury.

13. What is the role of an esophageal obturator airway (EOA)?

Show answer
None. At present, the EOA is not indicated because alternative techniques (mask or endotracheal tube) are safer and more effective.

14. What should be your first consideration if you are unable to ventilate or intubate a patient?

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Foreign body airway obstruction. Attempt to visualize the foreign body directly, and remove it with either suction or Magill forceps.

15. Explain the proper method of external chest compression.

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Place the patient on a firm surface-typically the floor or on a backboard. The rescuer should be positioned beside the patient’s chest. Both hands are placed just above the xiphoid-sternal junction. Keep your arms straight and your shoulders directly over the patient’s sternum. The compression depth should be 4-5 cm. Use the weight of your upper body to achieve adequate depth of compression. Perform 15 compressions followed by 2 ventilations at a rate of 100 compressions/minute.
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16. What are the essentials of external chest compressions?

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Even performed properly, external chest compression produces only a fraction of normal vital organ blood flow. Coronary blood flow occurs only during the release phase. Most providors do not use adequate force-make sure that the chest is compressed at least 2 inches in adults. Interruption in chest compression (to check the ECG rhythm or pulse) significantly reduces the efficacy of CPR.

17. What are the complications of external chest compressions?

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Complications are common but not important. Rib and sternal fractures occur 80% of the time. Major cardiac or pericardial injuries (lacerations) are rare. Bone marrow and fat emboli are common (80% in one series). Do not let fear of complication interfere with effective chest compression.

18. What are the indicators that effective CPR is being performed?

Show answer
Real-time indicators of vital organ perfusion are lacking. Effective CPR and pressor drugs should cause the VF waveform amplitude to increase-so called coarsening. Improved cerebral perfusion may result in gasping. During CPR, ET-CO2 > 15 mmHg predicts return of spontaneous circulation. Switch chest compression providers if the ET-CO2 begins to fall because this may indicate fatigue of the rescuer.

19. Is the central line the best access to the circulation?

Show answer
Yes. Large volumes of fluid can be delivered to the venous system more quickly, however, via large-bore peripheral venous catheters. A 14G, 5-cm catheter (peripheral) can deliver twice the flow of a 16G, 20-cm catheter (central). Central line placement may be associated with significant complications, including pneumothorax, air embolus, and arterial puncture. In hypo-volemic patients, in whom central veins are collapsed and peripheral veins are constricted, venous cannulation can be difficult.

20. Does a central line offer therapeutic and diagnostic advantages?

Show answer
Yes. A central line permits bolus administration of drugs to the right side of the heart. Identification of a high central venous pressure may indicate the need to treat reversible causes of PEA, such as cardiac tamponade or tension pneumothorax.

21. Is it necessary to monitor arterial blood gases during resuscitation?

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No. After you have an adequate airway and presumably are delivering 100% oxygen, you don’t care what the arterial PO2 is because you can do nothing about it. If possible, you may confirm the adequacy of oxygenation on the arterial side through an early arterial blood gas. Then you should focus on the adequacy of chest compression.

22. Which is preferred-colloid or crystalloid resuscitation fluid?

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Colloid advocates claim that the big molecules remain in the intravascular space and are more effective in elevating blood volume. Crystalloid advocates state that capillaries leak albumin, especially in the shock state. Resuscitation with crystalloid is clearly safe. Given its availability, low cost, and safety, crystalloid (lactated Ringer’s solution) is the choice for initial fluid resuscitation. When true cardiac arrest has occurred, however, volume is of little importance.

23. In a patient exhibiting asystole, bradycardia, PEA, or fine fibrillation, what is your primary goal?

Show answer
Adequate vital organ perfusion, especially to the coronary arteries. Done properly, CPR may cause PEA to progress to stable hemodynamics or VF to become “coarse enough” for successful countershock.
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24. Summarize the reversible causes and treatment of PEA.

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PEA is an orderly electrical rhythm in the absence of detectable arterial pulses. The potentially correctable situations that commonly cause electromechanical dissociation (EMD) are:

1. Tension pneumothorax (diagnosis: hyperresonant chest, decreased breath sounds), treated by decompressing the pleural space on the side of the collapsed lung
2. Pericardial tamponade (diagnosis: Beck’s triad-distant heart sounds, distended neck veins/elevated central venous pressure, and hypotension), treated with pericardiocentesis
3. Hypovolemia, treated with volume replacement
4. Pulmonary embolism, treated with fibrinolysis
5. Pump failure secondary to massive myocardial infarction, treated with fibrinolysis or mechanical assistance (intra-aortic balloon pump)
6. Hyperkalemia, treated with calcium and bicarbonate

KEY POINTS: REVERSIBLE CAUSES OF PEA

1. Tension pneumothorax
2. Pericardial tamponade
3. Hypovolemia
4. Pulmonary embolism
5. Pump failure
6. Hyperkalemia

25. Is clinical PEA always full cardiac arrest?

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PEA is a heterogeneous entity with hemodynamics ranging from full cardiac arrest through normal blood pressure. Confirm true cardiac arrest as early as possible through echocardiography or placement of an arterial catheter.

26. Name the most common cause of cardiac arrest in the perioperative period.

Show answer
Although the incidence of VF is increased in the perioperative period, PEA secondary to potentially reversible insults is more common at this time.

27. List the drugs commonly used during resuscitation and the appropriate dosages.

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1. Oxygen: to reverse hypoxia, always provide 100% oxygen initially.
2. Epinephrine: α- and β-adrenergic agonist. IV dose is 5-10 mL of 1:10,000 solution. Because of the short duration of action, a repeat dose may be necessary after 5 minutes. Epinephrine is inactivated by alkali; do not mix with bicarbonate solutions. Although it enhances myocardial performance, epinephrine greatly increases myocardial oxygen demand. Ventilate!
3. Vasopressin: antidiuretic hormone-a new first-line pressor during cardiac arrest. Administer one time as a bolus of 40 U.
4. Amiodarone: first-line, broad-spectrum antidysrhythmic possibly useful in treating VF/ventricular tachycardia (VT) cardiac arrest and atrial arrhythmias. It is active at cardiac sodium, potassium, and calcium channels and has a- and b-adrenergic blocking properties. In cardiac arrest, it is administered as a 300-mg rapid IV infusion. Amiodarone may cause hypotension and bradycardia; a pressor drug, such as epinephrine or dopamine, should be readily available or already administered.
5. Atropine: parasympatholytic (vagolytic) agent that increases the discharge rate of the sinus node. Atropine is useful in treating sinus bradycardia associated with hemodynamic compromise. An IV dose of 0.5 mg is repeated at 5-minute intervals until a desirable rate is achieved (at least 60 beats/min). Increased heart rate increases myocardial oxygen demand; atropine should be used only if the bradycardia causes hemodynamic compromise (heart rate, 60 beats/min).
6. Dopamine: catecholamine precursor of norepinephrine active at dopaminergic receptors. Stimulates the heart and vasoconstricts (high dose) the periphery. Use as a vasopressor to treat hypotension secondary to bradycardia or decreased peripheral vasomotor tone. Dosage should be adjusted based on clinical end points starting at 2-5 μg/kg/min up to 20 μg/kg/min. The principal toxicity, seen with prolonged dosages > 10 μg/kg/min, is splanchnic and systemic vasoconstriction with resultant injury.
7. Dobutamine: synthetic catecholamine that is a cardiac b-receptor agonist used to treat cardiogenic shock. It increases cardiac contractility. Reflex peripheral vasodilation may require combination with a pressor drug, such as dopamine. Dosage should be adjusted based on clinical end points starting at 5 μg/kg/min up to 20 μg/kg/min.
8. Sodium bicarbonate (NaHCO3): no longer commonly used in cardiac arrest; in shock, it is used to reverse acidosis (hypoxia-induced anaerobic metabolism leads to acid accumulation). The initial dose is 1 mEq/kg. One ampule (50 mL) contains 50 mEq of sodium bicarbonate. Bicarbonate combines with hydrogen ions to form CO2 and water; adequate ventilation is required for bicarbonate therapy to be fully effective. Overzealous use of bicarbonate may result in hypernatremia/hyperosmolality (each HCO3- is accompanied by a sodium ion).
9. Magnesium: effective in treating drug-induced torsades de pointes or VT. Administer 1-2 g IV over 3-5 minutes. May cause hypotension.
10. Calcium chloride or gluconate: positive inotropic agent. Calcium ions bind to troponin (the cardiomyocyte-specific calcium regulatory protein used to diagnose an acute myocardial infarction), which enhances the formation of cross-bridges between muscle contractile filaments with resultant fiber shortening. Dose is calcium chloride (or gluconate), 500 mg IV push. Do not mix with bicarbonate because it will precipitate.
11. Lidocaine: local anesthetic that suppresses ventricular arrhythmias (automatic and reentrant; see Chapter 3). An IV bolus of 1 mg/kg is followed by IV infusion at 2-4 mg/min. An additional IV bolus can be given at 10 minutes after initial dose if arrhythmias persist. Amiodarone is accepted as a preferred agent for treatment of arrhythmias.
12. Adenosine: a naturally occurring vasodilating hormone that is synthesized by vascular endothelial cells and dramatically slows artrioventricular (AV) nodal conduction. It is useful in the therapy of supraventricular tachyarrhythmias. Dose is 6 mg or 12 mg injected in a rapid IV bolus (which may be repeated several times). The half-life of IV adenosine is only 12 seconds. Measurable systemic hypotension occurs in < 2% of patients because adenosine is metabolized before it reaches the systemic vessels.
13. Verapamil: slow-channel calcium blocker used to block the AV node and to treat paroxysmal supraventricular tachycardia that causes hemodynamic compromise. Dose is 0.1 mg/kg. Dilute drug with 10 mL of saline, and infuse 1 mL/min until the supraventricular tachycardia either breaks or blocks. Repeat dose after 30 minutes if not effective. The drug reduces systemic vascular resistance and may cause hypotension.

28. What measures should be considered postresuscitation to improve the chances of a good outcome?

Show answer
Laboratory and clinical data support use of mild hypothermia (34°C for 24 hours)in patients who remain comatose after resuscitation from cardiac arrest. Hypotension or causes of increased cerebral oxygen use (e.g., as seizures or fever) should be treated aggressively.

References
WEB SITE
http://www.americanheart.org/presenter.jhtml?identifier=10000056#P
BIBLIOGRAPHY
Harken AH: Cardiac dysrhythmias. In Wilmore DW, Cheung L, Harken AH, et al (eds): Scientific American Surgery. New York, Scientific American, 1999.