The secondary survey - An Introduction to Clinical Emergency Medicine

transthoracic impedance, which depends on chest size, phase of respiration, and other variables.

Current defibrillators are monophasic and do not adjust for the transthoracic impedance. The first biphasic waveform defibrillator was approved in 1996. While not used in all EDs worldwide, the biphasic waveform adjusts for differences in transthoracic impedance, allowing less energy requirements for successful defibrillation. Animal studies showed their superiority over monophasic defibrillation for the termination of VF and pulseless VT. Early clinical experience with 150 J biphasic waveform defibrillation for treatment of VF was very positive. Evidence to date suggests that non-progressive impedance-adjusted low- energy biphasic countershock (150 J three times) is safe, acceptable, and clinically effective.

spontaneous rhythm (Figure 3.4). Primary bradycardia occurs when the heart’s intrinsic electrical system fails to generate an adequate heart rate.

Secondary bradycardia occurs when factors other than the heart’s own electrical system cause a slow rate, such as hypoxia, stroke, or cardiodepres- sant medications (beta blockers, calcium channel blockers, or opiates). Atropine and epinephrine

are two medications that have demonstrated ben- efit in this setting. Atropine has a vagolytic effect by antagonizing the parasympathetic system.

Epinephrine improves myocardial and cerebral blood flow during CPR. Though early transcutaneous pacing should be considered for bradycardia, routine transcutaneous pacing for asystole has not been shown to improve survival. As some

Cardiopulmonary and cerebral resuscitation

Primary ABCD survey Focus: Basic CPR and defibrillation

• Check responsiveness

• Activate emergency response system

• Call for defibrillator A Airway: Open the airway

B Breathing: Provide positive-pressure ventilations C Circulation: Give chest compressions

D Defibrillation: Assess for and shock VF/pulseless VT, up to three times (200 J, 200–300 J, 360 J, or equivalent biphasic) if necessary

Rhythm after first three shocks?

Persistent or recurrent VF/ VT

Secondary ABCD survey Focus: More advanced assessments

and treatments

Resume attempts to defibrillate

1 360 J (or equivalent biphasic) within 30–60 seconds

• Amiodarone (llb for persistent or recurrent VF/pulseless VT)

• Lidocaine (indeterminate for persistent or recurrent VF/pulseless VT)

• Magnesium (IIb if known hypomagnesemic state)

• Procainamide (indeterminate for persistent VF/pulseless VT:

IIb for recurrent VF/pulseless VT) Consider antiarrhythmics

Resume attempts to defibrillate A Airway: Place airway device as

soon as possible

B Breathing: Confirm airway device placement by exam plus confirmation device

B Breathing: Secure airway device;

purpose-made tube holders preferred

B Breathing: Confirm effective oxygenation and ventilation C Circulation: Establish IV access C Circulation: Identify rhythm →

monitor

C Circulation: Administer drugs appropriate for rhythm and condition

D Differential diagnosis: Search for and treat identified reversible causes

• Epinephrine 1 mg IV push, repeat every 3–5 minutes

• Vasopressin 40 U IV, single dose, one time only or

Figure 3.3

Ventricular fibrillation or pulseless ventricular tachycardia algorithm. VF: ventricular fibrillation; VT: ventricular tachycardia; ABCD: Airway, Breathing, Circulation, Defibrillation; CPR: cardiopulmonary resuscitation.

Cardiopulmonary and cerebral resuscitation patients with asystole are actually in fine VF, two

or more cardiac leads should be checked before determining that the patient is truly in asystole. A recent large randomized study from Europe com- paring epinephrine with vasopressin for patients

in asystole demonstrated that vasopressin was superior to epinephrine, suggesting that vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest.

Asystole

Primary ABCD survey Focus: Basic CPR and defibrillation

Secondary ABCD survey

Focus: More advanced assessments and treatments

• Check responsiveness

• Activate emergency response system

• Call for defibrillator A Airway: Open the airway

B Breathing: Provide positive-pressure ventilations C Circulation: Give chest compressions

C Circulation: Confirm true asystole

D Defibrillation: Assess for VF/pulseless VT; shock if indicated

A Airway: Place airway device as soon as possible

B Breathing: Confirm airway device placement by exam plus confirmation device B Breathing: Secure airway device; purpose-made tube holders preferred B Breathing: Confirm effective oxygenation and ventilation

C Circulation: Confirm true asystole C Circulation: Establish IV access C Circulation: Identify rhythm → monitor

C Circulation: Give medications appropriate for rhythm and condition D Differential diagnosis: Search for and treat identified reversible causes

• Consider quality of resuscitation?

• Atypical clinical features present?

• Support for cease-efforts protocols in place?

Rapid scene survey: Is there any evidence that personnel should not attempt resuscitation (e.g., DNAR order, signs of death)?

Atropine 1 mg IV, repeat every 3–5 minutes up to a total of 0.04 mg/kg

Epinephrine 1 mg IV push, repeat every 3–5 minutes Transcutaneous pacing If considered, perform immediately

Asystole persists

Withhold or cease resuscitative efforts?

Figure 3.4

Asystole: The silent heart algorithm. ABCD: Airway, Breathing, Circulation, Defibrillation; CPR:

cardiopulmonary resuscitation; VF: ventricular fibrillation; VT: ventricular tachycardia; DNAR: do-not- attempt resuscitation. Reproduced with permission, ACLS Provider Manual, © 2001, Copyright American Heart Association.

Cardiopulmonary and cerebral resuscitation

Pulseless electrical activity

Pulseless electrical activity (PEA), formerly known as electromechanical dissociation (EMD), is defined as cardiac electrical activity without associated mechanical pumping. These patients will have a rhythm but no pulse. Successful resuscitation of patients with PEA should focus

on determining and reversing the cause (Figure 3.5). The most common causes include severe hypovolemia (usually related to significant blood loss), hypoxia, acidosis, pericardial tamponade, tension pneumothorax, large pulmonary embolus, myocardial infarction, hypothermia, or drug overdose. A patient identified as having

• Hypovolemia

• Hypoxia

• Hydrogen ion – acidosis

• Hyper/hypokalemia

• Hypothermia

• “Tablets” (drug OD, accidents)

• Tamponade, cardiac

• Tension pneumothorax

• Thrombosis, coronary (ACS)

• Thrombosis, pulmonary (embolism) Review for most frequent causes

Atropine 1 mg IV (if PEA rate is slow), repeat every 3–5 minutes as needed, to a total dose of 0.04 mg/kg Epinephrine 1 mg IV push,

repeat every 3–5 minutes

Pulseless electrical activity (Rhythm on monitor, without detectable pulse)

Primary ABCD survey Focus: Basic CPR and defibrillation

• Check responsiveness

• Activate emergency response system

• Call for defibrillator A Airway: Open the airway

B Breathing: Provide positive-pressure ventilations C Circulation: Give chest compressions

D Defibrillation: Assess for and shock VF/pulseless VT

Secondary ABCD survey

Focus: More advanced assessments and treatments A Airway: Place airway device as soon as possible

C Circulation: Establish IV access C Circulation: Identify rhythm → monitor

C Circulation: Administer drugs appropriate for rhythm and condition C Circulation: Assess for occult blood flow (“pseudo-EMD”)

D Differential diagnosis: Search for and treat identified reversible causes

Figure 3.5

Pulseless electrical activity algorithm. ABCD: Airway, Breathing, Circulation, Defibrillation; CPR:

cardiopulmonary resuscitation; VF: ventricular fibrillation; VT: ventricular tachycardia; EMD: electromechanical dissociation; ACS: acute coronary syndrome; OD: overdose; PEA: pulseless electrical activity. Reproduced with permission, ACLS Provider Manual, © 2001, Copyright American Heart Association.

Cardiopulmonary and cerebral resuscitation PEA should be intubated to provide adequate

oxygenation and given a rapid IV infusion of crys- talloid. If the patient has a treatable rhythm, appropriate rhythm-specific ACLS algorithms should be utilized. If the situation warrants, peri- cardiocentesis or needle thoracostomy should be performed. If no reversible cause can be deter- mined, the patient should be given epinephrine every 3–5 minutes. If the PEA rate is slow, atropine can also be given. Unless a reversible cause is dis- covered, the prognosis of PEA is poor, with only 1–4% of patients surviving to hospital discharge.

Tachycardias

Tachycardias may be common in patients prior to hemodynamic collapse. There are numerous reasons for patients to have tachycardia, not all of which cause hemodynamic compromise. The key issue in patients with tachycardia is whether or not the patient tolerates their heart rate. In other words, is the patient stable and able to support a reasonable blood pressure that provides perfusion to the brain at that heart rate. Using the heart rate alone to determine hemodynamic sta- bility is inappropriate. Other issues to investigate include whether or not the tachycardia is causing the patient’s symptoms, whether it is regular or irregular, has narrow or wide complexes, and what might be the underlying cause (or causes). The diagnosis and management of brady- arrhythmias and tachyarrhythmias is discussed in greater detail in Chapter 4.

History

Obtaining historical information about a patient in cardiac arrest can be difficult. Utilizing other resources becomes paramount. Information must be gathered from pre-hospital providers, family, previous medical records, medication lists, or primary care physicians. Clues on the patient’s body (wallet, ID bracelet, traumatic injuries, needle marks, scars, dialysis shunts) may be identified. An attempt to learn the following information should be made:

What were the events surrounding the arrest?

Determine whether the patient had a witnessed arrest or was found unconscious. What was the approximate duration of time prior to initiation of CPR (downtime)? Patients with shorter down- times have a better chance of recovery. Ask whether the patient was having any concerning

symptoms prior to the arrest like chest pain, pal- pitations, or shortness of breath.

What has been the extent of the resuscitation thus far?

Determine the patient’s initial cardiac rhythm and any subsequent changes in rhythm through- out the resuscitation. Find out which interventions have been made including defibrillation, airway intervention, and medications, and the patient’s response to these interventions.

What is the patient’s past medical history?

Concentrate on the patient’s cardiac history and risk factors for coronary artery disease. Heart disease is the most common cause of dysrhythmias and sudden cardiac death. Knowing the patient’s prior medical problems or medications can point to other possible causes of the cardiac arrest.

This information is likely to be obtained while the patient is being resuscitated or stabilized.

Another member of the health care team may search for it if the physician cannot leave the bed- side. Much of this information may be obtained from family members. It is important to ask questions in a concise but sensitive manner.

Communicate the critical nature of the situation while providing reassurance that care is being pro- vided and that the patient is not suffering. If appropriate, it is also important to reassure the family that they did not cause or contribute to the situation.

Physical examination

Following the secondary survey, the physical examination should focus on vital systems and additional clues that might point to the cause of the arrest. The physician should begin with the baseline rhythm and vital signs (if they are present). A quick cardiopulmonary examination will determine cardiac activity, pulses, and the pres- ence or absence of breath sounds. If the patient is already intubated, the adequacy of the airway should be rechecked. A quick head to toe survey, including the skin and neurologic examination may provide further clues. Subsequent examina- tions should focus on assessing the response to interventions. After every intervention, vital signs and rhythm should be reassessed for any change.

A focused examination should be repeated after each procedure to assess for possible complica- tions (Table 3.1).

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