Page 675 - Cardiac Nursing

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C HAPTER 2 7 / Sudden Cardiac Death and Cardiac Arrest 651
is incomplete after a successful cardiac resuscitation. Cessation of cisions regarding timing of angiogram depend on hemodynamic
circulation for 10 to 20 seconds results in loss of consciousness instability, evidence of acute MI, and overall neurological progno-
caused by lack of oxygen. Within 2 to 4 minutes, glucose and sis with an extended cardiac arrest. 52 Studies from Sweden and
glycogen stores are used up, and after 4 to 5 minutes ATP is ex- Norway have shown an increase in survival with early coronary
hausted. Hypoxemia and hypercarbia cause loss of cerebral blood angiography and reperfusion treatment with PCI. 55,56 If the pa-
flow autoregulation; the brain then becomes dependent on cere- tient sustained cardiac arrest as a result of acute MI, evaluation
bral perfusion pressure. 54,57 Cerebral perfusion pressure is equal and treatment are no different from those in any other patient
to mean arterial pressure minus intracranial pressure (CPP with acute MI. The cardiac arrest produces a period of global is-
MAP – ICP). After ROSC, a brief period of hyperemia occurs chemia and stunning to the myocardium; potentially, there is a
along with global hypoperfusion resulting in a “no-reflow phe- need for either inotropic or intra-aortic counterpulsation to
nomenon.” 32,55 Improvement in cerebral recovery after cardiac ar- maintain perfusion. Often, ventricular dysfunction improves af-
rest results when cardiac arrest and CPR times are short, and ter the initial injury, and the initial low ejection fraction may not
7
ROSC is restored quickly. During the Brain Resuscitation Clini- represent a true reading. If the arrest is attributable to proar-
cal Trials, a cardiac arrest duration of 6 minutes or longer and an rhythmic drug effects or electrolyte disturbances, extensive eval-
ROSC time of 28 minutes was associated with poor neurologic uation usually is not indicated. Aggressive evaluation is war-
recovery. 52,58 ranted for most patients whose cardiac arrest was precipitated by
Treatment for the unresponsive patient should include opti- coronary atherosclerosis not associated with acute transmural
mizing cerebral perfusion pressure by maintaining a normal or MI, or with other heart disease that can be managed medically or
slightly elevated mean arterial pressure and reducing intracranial surgically. Diagnostic tests include ECG to rule out ischemia,
pressure. Hyperthermia and seizures increase the oxygen require- long QT interval, and WPW. Other diagnostic tests may include
ments of the brain; therefore, all attempts at maintaining nor- cardiac catheterization (Chapter 20), radionuclide stress testing
mothermia should be made. Research has shown induced hy- (Chapter 14), echocardiography (Chapter 13), electrophysiologic
pothermia of 32 C to 34 C, improves outcomes in comatose studies (Chapter 18), and possibly magnetic resonance imaging
survivors of cardiac arrest; however, optimal duration and tem- (Chapter 14) if arrhythmogenic right ventricular dysplasia is sus-
perature range require further investigation. Future studies and pected. Laboratory tests that focus on possible causes include
clarification of guidelines will help to implement induced hy- electrolytes, magnesium, and toxicology screen if drugs suspected
pothermia as a standard of care during postresuscitation sup- (Chapter 11). 7,32,52
port. 54–57,59 AHA recommends therapeutic hypothermia (class
IIa) when the initial rhythm for SCD is VF and (class IIb) for Hemodynamic Support. After resuscitation and transfer to
non-VF arrest; out-of-hospital or in-hospital arrest. 32 the intensive care unit (ICU), the patient usually will be intubated
Electrolyte imbalances are likely to occur. There is an associa- and will require general support of blood pressure, and heart rate.
tion between hyperglycemia and poor neurologic outcomes. One Patients often require inotropic drugs and fluids to maintain mean
prospective randomized study has shown that maintaining glucose arterial pressure 65 to 70 mm Hg to help support coronary and
55
levels in the normal range reduced hospital mortality rates of crit- cerebral blood flow. There have been no clinical trials to indicate
ically ill patients, but not necessarily post-SCA patients. 60 The the optimal mean arterial pressure postcardiac arrest. Restoration
2005 ECC Guidelines recommend strict glucose control, however of blood pressure and improvement in gas exchange does not nec-
acknowledge that additional studies are required to identify the essarily lead to survival. Most postresuscitation deaths have been
32
appropriate glucose target range for post-SCA patients. 32 noted to occur in the first 24 hours. The patient requires ongo-
Seizures are common after cardiac arrest and can delay recov- ing monitoring and treatment of ventricular arrhythmias. Amio-
ery. They occur in approximately one third of patients. Once darone has been shown to be superior to placebo for shock-
seizures are noted they should be treated with anticonvulsive ther- refractory VT and VF. 4,32
apy to optimize recovery. The patient’s head should be maintained
in a midline position and elevated to 30 degrees to increase cere- Reduction of Ischemia. Depending on the anatomy and
bral venous drainage. Vigilant attention should be made at main- physiology of the disease process, either medical or surgical ther-
taining oxygenation and perfusion to the brain to maximize the apy is indicated. If the patient has had an acute MI, treatment
chance for full neurological recovery. 32,52 guidelines should be consistent with the ACS algorithm (Chapter
22). Treatment options for secondary prevention of SCD include
Ongoing Medical Care statins and aspirin to reduce the incidence of coronary plaque rup-
The medical management for survivors of cardiac arrest depends ture or platelet aggregation and thrombosis. -Blocker therapy
on the patient’s central nervous system function and known pre- stabilizes autonomic balance and helps reduce ischemia; an-
existing factors. Most survivors of cardiac arrest are comatose, and giotensin converting enzyme (ACE) inhibitors improve survival.
recovery is far from certain. Prognosis may not be determined for -Blocker therapy in patients with CAD has been shown to de-
up to 72 hours postarrest. 61 Management of the patient includes crease total mortality by 20%, and decrease SCD by 30%. 62,63
providing effective perfusion of organs and tissues while directing -Blockers are also effective in treating ventricular arrhythmias in
diagnostic evaluation and treatment toward ongoing ischemia, LV the setting of increased sympathetic tone. 63 ACE inhibitor use
dysfunction, structural abnormalities, arrhythmias, and other may reduce SCD, as evidenced by the Trandolapril Cardiac Eval-
concurrent medical conditions. 32 uation Trial (TRACE). The benefit is greatest in patients who
have had a large MI, reduced ejection fraction, or clinical evidence
Diagnostic Evaluation. The most common substrate of of CHF. 64
SCD is CAD, seen in 80% of patients. Therefore patients should Myocardial revascularization has been shown to reduce the in-
undergo coronary angiography after successful resuscitation. De- cidence of SCD in patients with heart disease, both in primary