Cardiopulmonary resuscitation

An 86-year-old woman with congestive heart failure, coronary artery disease, and syncopal episodes presented for elective permanent pacemaker insertion. A recent 24-hour ambulatory electrocardiogram (ECG) demonstrated multiple episodes of severe sinus bradycardia associated with presyncopal symptoms. Monitored anesthesia care was requested because of the patient’s advanced age and associated medical conditions. Infiltration of local anesthesia and isolation of the cephalic vein in the left deltopectoral groove proceeded uneventfully. During placement of the ventricular pacing lead, ventricular ectopy occurred. As the lead was repositioned, ventricular tachycardia was induced and rapidly deteriorated into ventricular fibrillation.

What is the initial response to a witnessed cardiac arrest?

In 2010, the American Heart Association (AHA) published updated Guidelines for Cardiopulmonary Arrest and Emergency Cardiovascular Care. The guidelines differ for lay rescuers and health care providers. This review focuses only on the recommendations for health care providers. The following major changes were made:

  • Elimination of “look, listen, and feel”

  • Deemphasis on pulse check

  • Sequence of resuscitation is circulation, airway, breathing (C-A-B)

    • Changed from airway, breathing, circulation (A-B-C)

  • Continued focus of ensuring high-quality chest compressions

Basic life support (BLS) protocol ( Figure 84-1 ) is followed during the initial phase of cardiac arrest. Although these steps are described in sequence, they may occur simultaneously in the hospital setting. The initial response to a witnessed cardiac arrest is to confirm that the patient is unresponsive and apneic or has abnormal breathing (i.e., gasping). The health care provider immediately calls for assistance and a defibrillator. The recommendation to call for assistance before initiating chest compressions was established to decrease the time from cardiac arrest to first defibrillation, if appropriate. This recommendation is important because the highest survival rates are in patients who experience a witnessed cardiac arrest and have ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) and who receive early chest compressions and defibrillation.

FIGURE 84-1 ■

Components of basic life support.

The next step is to check for a pulse (carotid artery) for no longer than 10 seconds before initiating cardiopulmonary resuscitation (CPR). One starts with high quality chest compressions. The essential element in treating cardiac arrest is beginning high-quality chest compressions without delay, to provide oxygenated blood to the heart and brain while advanced cardiopulmonary life support (ACLS) protocols are initiated. Components of high-quality chest compressions are as follows:

  • “Push hard and push fast”

    • Adequate rate (at least 100 compressions per minute)

    • Adequate depth (2 inches)

  • Full chest recoil between chest compressions

  • Minimize number (continuous for 2 minutes) and duration (<10 seconds) of interruptions in chest compressions

  • Avoid excessive ventilation

To ensure that rescuer fatigue does not affect the quality of chest compressions, compressors should rotate every 2 minutes when five cycles of chest compressions and ventilations are completed. Additionally, chest compressions should resume immediately after defibrillation without checking for a pulse or rhythm.

If intraarterial blood pressure monitoring is available, a diastolic blood pressure >20 mm Hg indicates adequate chest compressions (i.e., adequate cardiac output). However, diastolic blood pressures <20 mm Hg indicate inadequate cardiac output, and efforts should be focused on improving the quality of chest compressions.

When there is no advanced airway in place, two breaths are given after 30 chest compressions are completed. A breath large enough to see chest wall rise (i.e., 6–7 mL/kg) over a 1-second interval is sufficient to provide adequate oxygenation and ventilation. This compression-to-ventilation ratio of 30:2 applies to single and two-person rescuers and is repeated for five cycles (over 2 minutes) before checking for a pulse or rhythm. The only exception is when the defibrillator first becomes available because early defibrillation (and early chest compressions) is associated with a higher survival rate.

If an advanced airway is in place, chest compressions are no longer synchronized with ventilation. Chest compressions are continuous while one breath is given every 6–8 seconds (8–10 breaths per minute). With or without an advanced airway, care should be taken to avoid excessive ventilation because it results in the following:

  • Increased intrathoracic pressure that impedes venous return and ultimately decreases cardiac output during chest compressions

  • Increased gastric inflation that may result in regurgitation and aspiration

Placement of an advanced airway should interfere minimally with chest compressions because chest compressions are critical to improved outcomes.

When capnography is available, an end-tidal carbon dioxide (ETCO 2 ) of at least 10–20 mm Hg is indicative of adequate chest compressions. ETCO 2 levels <10 mm Hg should prompt efforts to improve the quality of chest compressions.

When a defibrillator is available, a rhythm check should be performed. Further management depends on the rhythm identified.

A precordial thump may be considered for a witnessed cardiac arrest in a monitored patient with unstable or pulseless VT if a defibrillator is not immediately available. Defibrillation and the start of CPR should not be delayed to perform a precordial thump.

The best results (survival of approximately 40%) after cardiac arrest are achieved in patients receiving BLS within 4 minutes and ACLS within 8 minutes of cardiac arrest. Survival rates are <6% when both BLS and ACLS are started after 9 minutes. Patients most likely to be resuscitated include patients outside the hospital with a witnessed cardiac arrest secondary to VF, hospitalized patients with VF secondary to ischemic heart disease, patients with cardiac arrests not associated with coexisting life-threatening conditions, and patients who are hypothermic or intoxicated. Patients with severe multisystem disease, metastatic cancer, or oliguria do not often survive resuscitation efforts.

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 compression 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) valves. This explanation is flawed. Echocardiographic images during cardiac 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. Chest compressions per se are unnecessary to maintain a cardiac output. CPR is frequently ineffective in patients with flail chest until chest stabilization is achieved. If direct compression was the etiology of blood circulation in CPR, 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 compression, positive intrathoracic pressure propels blood out of the chest into extrathoracic vessels that have a lower pressure. Competent valves in the venous system prevent blood from flowing backward. During the upward phase of compression, blood flows from the periphery into the thorax because of negative intrathoracic pressure created by release of the compression. With properly performed cardiac compressions, systolic arterial blood pressures of 60–80 mm Hg can be achieved but with much lower diastolic pressures. Mean arterial pressures are usually <40 mm Hg. These pressures provide cerebral blood flows of only approximately 30% and myocardial blood flows of only about 10% compared with values before cardiac arrest.

What is the optimal airway management during cardiopulmonary resuscitation?

Optimal airway management during CPR depends on the experience of the rescuer. When unskilled providers attempted to place endotracheal tubes (ETT), the following complications occurred:

  • Trauma to the oropharynx

  • Unacceptably long periods of interrupted chest compressions and ventilation

  • Hypoxemia

  • Failure to recognize misplacement or dislodgment

Tracheal intubation, particularly by unskilled providers, is no longer considered the optimal way to manage the airway. In these circumstances, bag and mask ventilation or the use of alternative airways is preferable.

Bag and mask ventilation is performed initially in the nonintubated patient but risks gastric inflation, regurgitation, and aspiration. Despite these risks, the routine application of cricoid pressure during CPR is not recommended. In certain circumstances where regurgitation is of particular concern, cricoid pressure may be used. However, if effective ventilation is impeded, the pressure should be relaxed, adjusted, or ultimately released.

There is no specific recommendation regarding the timing of tracheal intubation. Whenever the decision is made to perform tracheal intubation, the following concepts apply:

  • CPR should not be interrupted for >10 seconds.

  • The compressor should be prepared to resume chest compressions as soon as the ETT is passed through the vocal cords.

  • Confirmation of ETT placement should consist of:

    • Visualization of bilateral chest rise

    • Auscultation over the epigastrium and bilateral lung fields

    • Detection of ETCO 2

      • Continuous waveform capnography

      • Colorimetric or nonwaveform

Absence of ETCO 2 does not always indicate misplacement of the ETT ( Box 84-1 ). In situations in which ETCO 2 is absent, a second method of confirmation should include either direct visualization of the ETT passing through the vocal cords or an esophageal detector device.

BOX 84-1

  • Inadequate chest compressions

  • Pulmonary embolus

  • Contamination of detector device by gastric contents or acidic drug (e.g., endotracheal epinephrine)

  • Severe airway obstruction (e.g., status asthmaticus)

  • Pulmonary edema

Conditions Associated with Proper Endotracheal Tube Placement without End-Tidal Carbon Dioxide Detection

Supraglottic devices, such as laryngeal mask airways, are acceptable alternatives to bag and mask ventilation and tracheal intubation. Laryngeal mask airways and other supraglottic devices are not fully protective against aspiration of gastric contents.

What are the complications of cardiopulmonary resuscitation?

Complications of CPR include skeletal (especially rib fractures), visceral, airway, and skin and integument (skin, teeth, lips) injuries. Some of these complications may require therapy and prolong hospitalization. Examples include rib and sternal fractures, myocardial and pulmonary contusions, pneumothorax, pericardial hematoma, tracheal and laryngeal injuries, liver and spleen ruptures, and gastric perforation and dilation. Of these complications, <0.5% are considered life-threatening. Serious harm occurring to patients while performing CPR is uncommon and should not dissuade bystanders from performing CPR.

What is the optimal dose of epinephrine?

Epinephrine is the therapy of choice for VF, pulseless VT, asystole, and pulseless electrical activity (PEA). Vasoconstriction caused by the α-adrenergic effects of epinephrine during CPR increases arterial pressure and improves myocardial and cerebral perfusion pressure. This is most likely a dose-dependent phenomenon.

The presence of coronary artery disease in many patients limits coronary artery blood flow even in the presence of higher aortic diastolic pressures. The β-adrenergic effects of epinephrine may actually worsen the outcome by increasing myocardial oxygen requirements.

Animal models have shown better outcomes from experimental cardiac arrest using 0.1–0.2 mg/kg of epinephrine, compared with the present recommended dose of 0.01 mg/kg. However, two more recent large multicenter investigations did not demonstrate survival differences in patients treated with larger doses of epinephrine. This lack of clinical efficacy may be related to the increased time that elapsed before the initial dose of epinephrine in clinical situations versus the animal studies. Until further studies clarify this issue, the current recommendation is 1 mg administered intravenously or intraosseously of a 1:10,000 epinephrine solution every 3–5 minutes. Higher doses (up to 0.2 mg/kg) are not recommended and may be harmful.

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Jul 14, 2019 | Posted by in ANESTHESIA | Comments Off on Cardiopulmonary resuscitation
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