Download Therapeutic Hypothermia Research Paper

Running head: HYPOTHERMIA POST CARDIAC ARREST
Therapeutic Hypothermia Post Cardiac Arrest
Ashley R. Yotkois
Ferris State University
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Abstract
Acute myocardial infarction can lead to out of hospital cardiac arrest. Treatment options that
include reperfusion as well as therapeutic hypothermia are being studied and having favorable
results. In this paper we will discuss AMI and its disease process and complications. Cardiac
arrest and its pathophysiology will also be discussed as well as treatment and brief ACLS
guidelines. Survival of the arrest and treatment after return of spontaneous circulation (ROSC) is
the point when therapeutic hypothermia should be initiated. The end focus will be on
hypothermia and the body’s response, how it preserves organs and tissue after cardiac arrest,
nursing care for the patient receiving therapeutic hypothermia and the statistical evidence
supporting therapeutic hypothermia post arrest.
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Therapeutic Hypothermia Post Cardiac Arrest
Cardiac arrest can be the result of multiple systemic issues in the human body. Acute
myocardial infarction and the complications that can result from it can be life-threatening.
Therapeutic hypothermia is one treatment that can maximize outcomes for these types of
patients. Understanding the complications of AMI, pathophysiology of cardiac arrest, early use
of therapeutic hypothermia and other conjunctive treatments play a large role in the prognosis for
these patients.
AMI
Pathophysiology of AMI
AMI happens when total occlusion of a coronary artery occurs and myocardial tissue is
deprived of blood supply and oxygen (Reed, 2014). According to Reed (2013), approximately
75% of AMI cases are caused by thrombus formation typically due to repeated rupture of
atherosclerotic plaque. This, as well as, platelet aggregation and activation of the clotting
cascade due to glycoprotein release and inflammatory response will cause severe stenosis of
coronary arteries which will impede blood flow to the heart muscle (Reed, 2013).
“Thrombogenesis is perpetuated further by platelet activation, which leads to platelet aggregation
via conformational changes in glycoprotein IIb/ IIIa receptors and cross-linking platelets through
molecules such as fibrinogen” (Reed, 2014). The extent of ischemia correlates with vessels
occluded, duration of occlusion, how much muscle is supplied oxygenated blood by the occluded
vessel, and the effectiveness of reperfusion According to Reed (2013), approximately 75% of
AMI cases are caused by thrombus formation typically due to repeated rupture of atherosclerotic
plaque. This, as well as, platelet aggregation and activation of the clotting cascade due to
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glycoprotein release and inflammatory response will cause severe stenosis of coronary arteries
which will impede blood flow to the heart muscle (Reed, 2013).
Complications of AMI
STEMI has many complications if untreated or late intervention occurs. These
complications include:
 lethal arrhythmias
 cardiogenic shock
 heart failure
 ventricular rupture
 mitral valve regurgitation
Lethal arrhythmias.
Lethal arrhythmias include ventricular tachycardia (VT) and ventricular fibrillation(VF).
VT and VF are often the cause of death in a STEMI (Reed, 2013). Immediate defibrillation, use
of antiarrhythmics, and correction of electrolytes is the treatment for these arrhythmias.
Atrial fibrillation (AF) is another arrhythmia that can result from STEMI. This is treated
much like AF that is not caused by a STEMI. Antiarrhythmics or calcium channel blockers are
recommended treatements. Patients who have chronic AF may also need a permanent
pacemaker or begin Coumadin therapy so as not to form and release a clot.
Bradyarrhythmias and complete heart block are additional rhythms that can be caused by
a STEMI.
This can cause a very slow heart rhythm that can be temporarily treated with
Atropine and eventually will need a permanent pacemaker (Reed, 2013).
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Cardiogenic shock and heart failure.
HF is the leading cause of in-hospital morbidity and mortality following STEMI (Reed,
2013). The extent is dependent on the vessels associated with the STEMI and the area of
myocardium supplied by those vessels (Reed, 2013). Treatment for these patients is fluid
maintenance and insertion of a pulmonary artery catheter, use of inotropes to assist contractility,
reducing afterload, and insertion of intra-aortic balloon pump(IABP) or ventricular assist device
(VAD)(Reed, 2013).
Mitral valve regurgitation and ventricular rupture.
This can also occur depending on the area of infarct. Typically the RCA supplies the
mitral valve with blood flow (Reed, 2013).. The RCA also supplies the right ventricle and
papillary muscle. STEMI in these areas can cause papillary muscle rupture, ventricular rupture,
and flail mitral valve. These can all result in pulmonary edema from heart failure, cardiogenic
shock, severe hypotension, and lethal arrhythmias. The treatment for this is fluid management,
decreasing afterload, insertion of assistive devices to decrease workload, inotropes for
contractility, and surgical repair as soon as possible (Reed, 2013).
All of these complications, if not treated especially, can lead to cardiac arrest. These
complications can happen immediately or days after a STEMI.
Cardiac arrest.
“Over 1,000 people suffer sudden cardiac death every day in the United States.11 About
half of these occur in the hospital; the remainder occur in the home, outpatient medical
environments, or public spaces,” (Pozner, 2012). Cardiac arrest can be caused by many things
including electrolyte disturbance, thrombotic event, cardiogenic shock, respiratory failure and
tension pneumothorax to name a few (Pozner, 2012). “Coronary atheroma resulting in ischemic
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heart disease is the most-common cause of cardiac arrest world-wide,” (Nolan, 2012). The goal
is to treat the cause of the event. This must be done quickly in order to revive the patient and
have few deficits due to hypoxia (See Appendix A).
Immediate chest compressions and defibrillation if necessary should be initiated (Pozner,
2012). ACLS protocol should be followed if first responders present or if in an acute care
environment (Appendix B). Advanced airway placement should also be considered if the patient
does not resume spontaneous respirations. Medications such as epinephrine, vasopressin,
vasopressors for blood pressure support and antiarrhythmic medications, such as Amiodarone or
lidocaine, for sustained lethal arrhythmias should be given (see Appendix B).
Patients who suffer an OHCA more often die of neurological injury versus those who
have and in-hospital cardiac arrest who more often die of cardiac or multi-organ injury (Nolan,
2012). Due to the systemic inflammatory response the body goes through post-arrest and the
release of free radicals, therapeutic hypothermia is indicated not only to decrease the myocardial
oxygen consumption but also cerebral oxygen consumption (Nolan, 2012).
Therapeutic hypothermia
Therapeutic hypothermia and its benefits have been studied for over 100 years (Perman,
2014). In the early 1900’s, doctors from Russia had found they had more successful
resuscitative efforts after placing patients in the snow (Perman, 2014). In later years, cooling
tumors was found to shrink them in size and resuscitation efforts of an arresting intraoperative
patient has less neurological deficits due to decreased core temperature (Perman, 2014). More
recently it has been suggested that hypothermia in out-of-hospital cardiac arrest (OHCA), more
specifically occurring from STEMI, have had better outcomes overall than those who did not
receive therapeutic hypothermia treatment (Zimmermann, 2013).
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Pathophysiology of hypothermia.
Hypothermia can be classified as mild, moderate or severe according to temperature
range and there can also be different physiologic effects according to what level of hypothermia
the patient is experiencing (Keresztes, 2006). Moderate hypothermia range, which is the target
for therapeutic hypothermia, physiologic effects can range from confusion and ataxia to changes
in level of consciousness and bradycardia (Keresztes, 2006).
Hypothermia affects all body systems within the patient. “Hypothermia decreases
metabolism 6% to 7% per 1°C decrease in temperature, protecting the brain from further injury
during the early timeframe postanoxic injury,” (Perman, 2014). Thermoregulation is controlled
by the hypothalamus and shivering is the body’s way to regulate the temperature (Keresztes,
2006). Vasoconstriction initiates increased metabolism which initiates shivering (Keresztes,
2006). Uncontrolled hypothermia will cause shivering which will cause tachycardia and
increased respiratory rate (Keresztes, 2006). This increases metabolic rate and oxygen demand.
During therapeutic hypothermia, there will be an increased diuresis, decrease serum potassium,
increased blood viscosity, and decrease in platelets (Keresztes, 2006).
Nursing care during treatment.
There are different approaches for therapeutic hypothermia. Some of these are rapid
infusion of cold saline, icepacks, cooling devices, and wraps (Perman, 2014). Protocols must be
put in place regarding how hypothermic the patient should be, how quickly they should be
cooled, and the process for rewarming. Nursing staff must monitor this patient very closely as
well as manage temperature, shivering, vital signs, and lab work.
The induction phase starts when the patient is being cooled until they reach the desired
temperature (see Appendix D, figure 1). Target core temperature is usually 32-34 degrees
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Celsius (Perman, 2014). . Continuous core temperature monitoring should also be in place
whether it is monitoring from a pulmonary artery catheter, endotracheal probe, rectal probe or
bladder temperature. Axillary or temporal temperatures will not be accurate. During this phase,
as well as rewarming, shivering may be detected (Perman, 2014). Interventions to stop shivering
must be included in the protocol whether it be neuromuscular blockades, opiods, or sedatives
(Perman, 2014). When sedated, the patient should experience bradycardia and lower respiratory
rate which will decrease oxygen demand as well as decrease any cerebral edema and protect the
blood-brain barrier (Keresztes, 2006).
The maintenance phase begins when goal temperature is met until rewarming begins
(Perman, 2014). The maintenance phase usually lasts from 12-24 hours but can last up to 72
hours (Nolan, 2012). Complications during this phase are typically bradycardia, hyperglycemia,
polyuria, hypokalemia and coagulopathy due to a decrease in platelets (Perman, 2014).
The rewarming phase begins when we begin to let the patient’s core temperature rise
until they are normothermic. There are many complications during the rewarming phase
including seizures, ventricular fibrillation due to shift of electrolytes, and hypotension due to
hypovolemia caused by sudden vasodilation (Keresztes, 2006). This process should be done
over 6-8 hours as well as weaning sedation and stopping the potassium replacement (Kertesztes,
2006). Warming may include simply removing the equipment and allowing the patient to warm
passively or by applying a warming device or warm blankets. According to Nolan (2013), to
avoid rebound hyperthermia, rewarming should be controlled at a rate of .25-.5 degrees C per
hour.
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Evidence.
There have been many studies done on therapeutic hypothermia and the benefits for
cardiac arrest patients but also being tested in patients who suffer TBI, sepsis, hepatic
encephalopathy, stroke and multiple other disease processes. Many are still in preliminary
phases.
Cardiac arrest patients who were in a shockable rhythm such as VT/VF, therapeutic
hypothermia is now considered a standard of care in conjunction with reperfusion therapy
(Perman, 2014). In one study, the patients showed the same percentage of mortality at 30 days
after receiving therapeutic hypothermia but a significant percentage less at one year (see
Appendix D, figure 2). In the Zimmermann study (2006), showed a marked difference in those
with CPC score of 1 or 2 after receiving therapeutic hypothermia post arrest as a complication of
a STEMI versus those who did not (see Appendix E, figure 1). The Zimmermann study (2006),
as well as most other studies, showed a more favorable outcome in those who received
therapeutic hypothermia versus those who did not. This data concludes that the was a favorable
neurological recovery of 55% vs. 39% (Zimmermann, 2006). Nolan (2013) also concluded that
after ROSC, a patient who receives not only reperfusion therapy but also therapeutic
hypothermia has better neurologic outcomes.
Patients experiencing a STEMI who also experience an OHCA often have poor
neurological outcomes as well as increased myocardial injury without therapeutic hypothermia
treatment. The studies provided show an increase in neurological outcome at discharge, 30 days
and 1 year post arrest.
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References
Keresztes, P.A. & Brick, K.( 2006). Therapeutic hypothermia after cardiac arrest. Dimensions of
Critical Care Nursing, 25(2), pp.71-76.
Nolan, J. P., Soar, J., Wenzel, V., & Paal, P. (September, 2012). Cardiopulmonary resuscitation
and management of cardiac arrest. Nature Reviews Cardiology, 9, pp. 499-511. Doi:
10.1038/nrcardio.2012.78.
Perman, S. M., Goyal, M., Neumar, R. W., Topjian, A. A., & Gaieski, D. F. (February 2014).
Clinical applications of targeted temperature management. Chest, 145(2), pp. 386-393.
doi:10.1378/chest.12-3025.
Pozner, C. N, Martindale, J. L., & Geyer, B. C. (September 2012). Cardiac resuscitation.
Elizabeth Nabel (Ed). Scientific American Medicine. DOI 10.2310/7900.1155.
Reed, G. M. & Cannon, C. P. (2014). ST-segment elevation myocardial infarction. Elizabeth
Nabel (Ed). Scientific American Medicine. DOI 10.2310/7900.1079
Zimmermann, S., Flachskampf, F. A., Schneider, R., Dechant, K., Alff, A., Klinghammer, L.,
Rittger, H., & Achenbach, S. (2013). Mild therapeutic hypothermia after out-of-hospital
cardiac arrest complicating ST-elevation myocardial infarction: long-term results in
clinical practice. Clinical Cardiology, 36(7), pp. 414-421. DOI:10.1002/clc.22131.
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Appendix A
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Appendix B
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Appendix C
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Appendix D
Figure 1
Figure 2
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Appendix E
Figure 1