P1247176259nHUfd

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NURSING CARE OF THE PATIENT WITH CHEST PAIN IN
THE EMERGENCY DEPARTMENT Hali Saucier,
2008 Pacific Lutheran University School of
Nursing
OPTIONALLOGO HERE
ASSESSMENT
CASE STUDY
EVALUATION
NURSING DIAGNOSES

• A patient in his 50s with known coronary artery
  disease arrives to the ED via ambulance with 4/10
  chest pain that has decreased with 2 sublingual
  nitroglycerin tablets prior to arrival. He still
  experiences mild chest pressure. He is anxious,
  nauseated and diaphoretic.
• Vital signs tachycardic, hypertensive,
  tachypnic, oxygen saturation of 96 on 4L.

• All objectives were met. The patient reported
  complete relief from chest pain and reduced
  anxiety. He was stabilized and admitted to the
  hospital with a diagnosis of acute coronary
  syndrome for further evaluation, diagnostic
  testing, and a consultation with a cardiologist.
  The patient thanked the staff for the care he
  received in the emergency department.
• - Point of care testing is available for
  measuring bedside biomarkers but is generally not
  as sensitive or precise and should always be
  confirmed by conventional qualitative tests.
  However, reperfusion therapy should not be
  delayed in order to wait for the results of a
  qualitative laboratory test (Antman et al, 2004).
  
• There is little research on the efficacy of the
  GI cocktail as a differential diagnostic tool.
  Both cardiac chest pain and dyspepsia can be
  relieved by a GI cocktail (Wrenn et al, 1995).
  Since ischemic chest pain and dyspepsia both
  respond to other co-administered medications such
  as morphine and nitrates, the GI cocktail may be
  inappropriate for ruling out cardiac ischemia and
  should be used with discretion (Berman et al,
  2003).
• Distress and fear during the initial stages of
  an ACS may trigger subsequent depression and
  anxiety, thereby promoting poorer prognosis and
  greater morbidity with time (Whitehead et al,
  2005).
• Diagnosis and treatment of ACS is extremely
  difficult but essential to preserve cardiac
  muscle (Gibler et al, 2005 Lewis, 2007).
• Sudden cardiac death is often the first sign of
  an acute STEMI (Antman et al, 2004). Failure to
  recognize prodromal symptoms of MI may be one
  reason women experience a greater proportion of
  sudden cardiac deaths than men do (McSweeny et
  al, 2003).
• Shorter time to reperfusion therapy decreases
  risk of mortality in patients with STEMI
  (McNamera, et al, 2006). For best outcomes, the
  American Heart Association/American College of
  Cardiology recommend door-to-balloon times (or
  time to reperfusion therapy) of less than 90
  minutes (Antman et al, 2004).
• An objective of Healthy People 2010 is to
  increase the proportion of eligible patients with
  heart attacks who receive artery-opening therapy
  within an hour of symptom onset (Healthy People,
  2010). Current strategies being used to improve
  emergency care include
• Code response teams for all patients with acute
  STEMI (Singer, et al, 2007).
• Care pathways to guide patients presenting with
  chest pain through the system (Repasky, 2005).
• Chest pain observation units for continuing
  care, monitoring, and diagnostic testing of low
  risk patients that are not yet ready for
  discharge. These observation units help reduce
  unnecessary hospital admissions (Finefrock,
  2006).

A CHEST PAIN MNEUMONIC (Newberry et al., 2005)
Acute Pain related to myocardial tissue damage
from inadequate blood supply as evidenced by
diaphoresis, verbal complaints of crushing chest
pain unrelieved by rest, and patients pain
intensity rating. Decreased cardiac output
related to inability of ischemic myocardial
tissue to pump effectively as evidenced by
decreased blood pressure, delayed capillary
refill, pallor, and extremities cool to the
touch. Anxiety related to actual or perceived
threat of death as evidenced by restlessness,
agitation, and repetitive questioning about
condition.
INTRODUCTION
Cardiovascular disease is the leading cause of
death in the United States and coronary artery
disease (CAD) accounts for the majority of these
deaths (Thom et al., 2005). In the U.S. each
year, over 5.3 million patients present to
emergency departments with chest pain (Gibler et
al., 2005). Due to the time-sensitive nature of
cardiac events and the complexity of diagnosis,
it is essential that emergency department staff
devise efficient methods of identifying and
treating acute coronary syndromes. To promote
preservation of cardiac muscle and the most
favorable patient outcomes, the emergency nurse
must have an advanced understanding of chest pain
management and be skilled in implementing
appropriate interventions. The emergency nurse
can expedite diagnosis and treatment of ACS by
rapidly assessing chest pain, obtaining
appropriate diagnostic tests and results, and
communicating with the physician to advocate for
prompt medical treatment (Quinn, 2005).
PLANNING
Objectives Patient will experience relief from
pain, maintain stable signs of adequate
perfusion, and report decreased anxiety and
increased sense of control. The patients main
desired outcome was pain relief.
INTERVENTIONS

• 1. Decrease chest pain and myocardial oxygen
  demand Nurse will
• Administer oxygen maintain oxygen saturation of
  90 or greater. An oxygen saturation of less than
  90 indicates significant oxygenation problems
  (Grap 2002).
• Enforce bed rest. Limiting activity decreases
  myocardial oxygen demand (Kasper et al, 2005).
• Continuously assess cardiac rhythm and rate.
  Life-threatening dysrhythmias are a potential
  complication of ischemia and MI. Early detection
  and management is critical (Copstead Banasik,
  2005).
• Administer antiplatelet agents as ordered. To
  inhibit platelet aggregation, which prevents
  thrombus formation and inhibits growth of
  existing clots (Deglin Vallerand, 2007).
  Aspirin should be given to all patients with
  possible ACS as soon as possible (Gibler et al,
  2005).
• Administer nitrates as ordered and titrate to
  effect. Causes peripheral vasodilation which
  decreases preload and afterload. Dilation of
  coronary arteries allows increased blood flow to
  the heart (Deglin Vallerand, 2007).
• Administer morphine as ordered. To relieve chest
  pain and reduce anxiety. Also reduces preload and
  myocardial O2 consumption (Lewis, 2007).
• Administer ß-blockers as ordered. To decrease
  myocardial O2 demand by decreasing HR, BP, and
  contractility. Reduces the progression of
  unstable angina to acute MI (Gibler, et al,
  2005). In the case of STEMI, reduces the
  frequency of life-threatening tachyarrhythmias
  (Antman et al., 2004).
• 2. Manage fear and anxiety. Anxiety increases
  oxygen demand (Lewis, 2007) and is associated
  with a hypercoaguable state, which may increase
  risk of clotting (Von Känel et al, 2004 AORN,
  2008). Nurse will
• - Use a calm, reassuring approach so as not to
  increase anxiety level The close presence of a
  nurse is one of the most effective methods for
  anxiety management (Mitchell, 2000).
• Explain interventions and provide factual
  information concerning diagnosis and treatment.
  Decreases fear of the unknown and increases
  coping skills. Match the level of information
  provision to patients preferred coping style
  because too much or too little information can
  both increase anxiety (Mitchell, 2000).
• Instruct patient in using relaxation techniques
  such as breathing or imagery to increase sense of
  control, decrease stress, and reduce oxygen
  demand (Lewis, 2007).
• Encourage patient to express feelings and fears.
  Verbalization of emotions decreases anxiety and
  stress (Lewis, 2007).
• 3. Facilitate efficient and appropriate care To
  facilitate prompt emergency care, nurse will
• - Insert 2 large-bore IV catheters and obtain
  blood samples. Pharmacological management of ACS
  can be complex and many emergency medications are
  not compatible (Deglin Vallerand, 2007). Serum
  cardiac markers are important in the diagnosis of
  MI (Gibler et al., 2005).
• Delegate tasks such as ECG, point of care
  testing, and vital signs to supportive staff.
• Communicate collaboratively with physician and
  other team members.

PATHOPHYSIOLOGY
Ischemia related to coronary artery disease (CAD)
is the most common cause of angina, or chest pain
(Lewis, 2007). Ischemia occurs when myocardial
demand for oxygen exceeds supply. Many factors
can contribute to an imbalance between oxygen
supply and demand, but the most common cause is
insufficient blood flow to the heart due to
narrowing or blockage of the coronary arteries
(Lewis, 2007). Definitions Acute coronary
syndrome (ACS) refers to a spectrum of clinical
symptoms compatible with acute myocardial
ischemia that is prolonged and not immediately
reversible. ACS includes unstable angina (UA),
non-ST-segment-elevation myocardial infarction
(NSTEMI), and ST-segment-elevation myocardial
infarction (Copstead Banasik, 2005). Unstable
angina (UA) angina that is new in onset, occurs
at rest, or has a worsening pattern. Myocardial
infarction (MI) irreversible cardiac cellular
death caused by sustained myocardial ischemia.
Typically identified by clinical signs of
ischemia, cardiac biomarkers, and ECG changes
(Thygeson et al., 2007). - Non-ST-segment
elevation MI refers to myocardial cell death
without ST-segment elevation on the ECG. NSTEMI
is usually associated with smaller infarct size
and generally better outcomes (Copstead Banasik
2005). - ST-segment elevation MI (STEMI) is
associated with more severe damage to myocardium
and requires immediate reperfusion therapy such
as fibrinolytic drugs or percutaneous
intervention (Lewis, 2007) to restore blood flow
to the heart.

• ALWAYS assess ABCs first!
• Vitals Signs BP and HR may be elevated
  initially. BP could later decrease due to ?
  cardiac output. Respiratory rate will be
  increased, oxygen saturation may be decreased.
  (Lewis, 2007).
• Signs of decreased cardiac output pallor, weak
  or absent peripheral pulses, delayed capillary
  refill, cool, diaphoretic skin, ?HR, ?BP (Kidd,
  Sturt, Fultz, 2000).
• Gender Differences Fewer women present with
  classic signs and symptoms of UA or MI. Fatigue
  is often the first symptom of ACS in women. Women
  are also more likely to experience a silent MI,
  with no profound chest pain (McSweeney et al.,
  2003).
• Right or Left? Signs of a left ventricular MI
  include tachycardia, hypertention, and dyspnea
  due to decreased cardiac output. The classic
  triad of distended neck veins, clear lungs, and
  hypotension may indicate a right-sided MI due to
  the right ventricles inability to handle systemic
  venous return (Litton, 2002).

DIAGNOSTIC TESTING

• The electrocardiogram or ECG, is the single most
  important tool to rule out or confirm UA or MI
  (Lewis, 2007). Changes in the ECG can indicate
  ischemia and/or infarction (Kidd, Sturt, Fultz,
  2000). An ECG should be performed on every
  patient with possible ACS within 10 minutes of
  their arrival to the ED shown to a physician
  (Antman et al., 2004)
• Serum Cardiac Markers Cardiac-specific troponins
  (Troponin I T) are released from necrotic heart
  muscle after MI and increase 3-12 hours after
  onset. Troponin is becoming the standard
  diagnostic biomarker (over creatinine kinase-MB),
  because it is more sensitive and specific to
  myocardial injury (Lewis, 2007 Gibler et al.,
  2005).
• GI cocktail a liquid combination of an
  antacid, antispasmodic, and local anesthetic
  commonly used in the ED to distinguish between
  cardiac-related pain and dyspepsia (Wrenn et al.,
  1995).
• The emergency nurse facilitates the completion of
  diagnostic tests and analyzes the results.

ACKNOWLEDGEMENTS
I would like to thank my clinical instructor Dana
Zaichkin for providing guidance with this poster.
Special thanks to the emergency department staff
at Good Samaritan Hospital and my preceptor,
Caroline Rath for a great experience!