ACS Guidelines - CPM Guidelines That Will Be in EPIC

Clinical Practice Guideline:
ACUTE CORONARY SYNDROME (ACS)

Type: Medical Diagnosis/Treatment/Procedure
Target Population: Adult/Geriatric
PROFESSIONAL PROCESS
GOALS/OUTCOMES:
A. Signs and symptoms of listed potential problems will be absent or manageable.

1. Ischemia leading to Infarction
2. Dysrhythmia/Arrhythmia
3. Hemodynamic Instability
4. Pericarditis leading to Pericardial Effusion
5. Cardiovascular Structural Defects
6. Mural Thrombosis leading to Embolism
7. Acute Pain
8. Situational Response
B. Patient/family/significant other (S.O.)/caregiver will verbalize and/or demonstrate an understanding of teaching/learning goals listed below: (Refer to
Education Outcome Record)
1. Acute coronary syndrome overview [e.g., description, anatomy, physiology, cause(s)].
2. Signs/symptoms: Angina [e.g., discomfort (uncomfortable pressure, squeezing, fullness, pain) in chest lasting greater than 2 minutes or
leaves and returns; discomfort in 1 or both arms, upper back, neck, jaw, or stomach; shortness of breath; diaphoresis; lightheadedness;
nausea, vomiting].
3. Signs/symptoms: Myocardial Infarction [e.g., mild or severe discomfort (pressure or pain in middle of chest, may extend into shoulder
and arm, abdomen or jaw); shortness of breath; diaphoresis; nausea/vomiting; weakness or lightheadedness; paleness; burning feeling
in upper abdomen; upset stomach; sudden weakness or unexplained tiredness; more intense than angina and lasts longer than 15
minutes].
4. Treatment plan (e.g., Medications: nitrates, beta-blockers, calcium channel blockers, ACE inhibitors, aspirin, cholesterol-lowering
medicines; Heart Healthy Diet: low saturated fat; Activity: regular exercise, stop activity if experiencing pain, weight-loss program if
overweight).
5. Modifiable risk factors/triggers: Angina (e.g., exercise, heavy physical labor, stress/upset, in cold air, digesting a big meal, high blood
pressure, high cholesterol, high blood sugar).
6. Modifiable risk factors/triggers: Myocardial Infarction (e.g., cigarette smoking, family history of heart attack, diabetes, overweight, high
blood pressure, high blood cholesterol, low HDL cholesterol, stress, lifestyle without physical activity).
7. Self-management (e.g., tobacco cessation; regular blood pressure checks; diet consistent in vitamin K if taking warfarin; regularly
scheduled INR if nonvalvular atrial fibrillation/flutter; pacemaker checks with cardiologist if pacemaker; CPR education for family
/caregiver).
8. Rehabilitation to improve functional independence (e.g., cardiac rehabilitation).
9. When to seek medical attention (e.g., contact EMS or 911 if chest pressure, squeezing or pain that lasts greater than five minutes or
leaves/returns; pain or discomfort in one or both arms, neck, jaw or upper back that lasts more than five minutes or leaves/returns AND
lightheadedness, trouble breathing, nausea or sweating; pain remains after taking three nitroglycerin tablets five minutes apart).
10. General goals (room/unit routine, pain, medication, diagnostic tests/procedures, dietary modifications, hygiene, infection prevention,
rehabilitation, medical equipment/supplies, tobacco cessation, resources for support).
ASSESSMENT/INTERVENTIONS/CLINICAL REASONING/DECISION-MAKING:
A. Assess and document readiness and ability to learn, learning needs and preferences. (Refer to Pre-Teaching Assessment on Education Outcome
Record)
B. Collaborate with interdisciplinary resources related to significant changes in patient status and for the continuum of care (e.g., Physician,
Nursing, Social Work/Services, Dietitian/Nutrition Services, Pastoral Care, Pharmacy, Respiratory Therapy, Occupational Therapy, Physical
Therapy, Child Life, Speech Language Pathology, Home Care Services).
C. Assess, Monitor, and Detect:
 The impact of other preexisting health problems.
 The impact on psychosocial, cultural, sexual, developmental and spiritual well-being.
 The impact of common diagnostic studies/laboratory values: [e.g., electrocardiogram (ECG); laboratory values (electrolytes, blood urea nitrogen
(BUN), creatinine (Cr), magnesium, potassium, glucose, glycosolated hemoglobin (A1C) for diabetics, CBC, Troponins I and T, myoglobulin, C-reactive
protein (CRP), creatine kinase of the cardiac muscle (CK-MB), lactic dehydrogenase (LDH), chest x-ray (CXR), graded exercise test (GXT),
pharmacologic stress echocardiogram, percutaneous coronary intervention (PCI), percutaneous transluminal coronary angioplasty (PTCA);
transesophageal echocardiography (TEE), magnetic resonance imaging (MRI), computed tomography scan (CT scan)].
 Baseline vital signs and trends.
 Risks to safety.
D. Assess, Monitor, Detect, Prevent and/or Modify the listed potential problems and implement interventions as appropriate:
Copyright © 2013, CPM Resource Center, an Elsevier business. All rights reserved.
Acute Coronary Syndrome; Spring release 2013 1
Ischemia leading to Infarction AEB (As Evidenced By): (5; 6; 33; 80; 85)
 Ischemia: substernal chest pain/discomfort/pressure/angina (usually less than 15 minutes duration), may radiate to arm/neck/back/jaw; dysrhythmias;
discomfort of other areas in upper body; shortness of breath (SOB); decreased exercise tolerance; nausea; normal cardiac enzyme/biomarker levels.
Atypical presentation: fatigue, syncope, weakness, SOB (most common in women, diabetic and geriatric patients).
Additional Geriatric considerations: altered mental status. If pre-existing altered mental status or dementia is present the patient may have no
recollection of recent symptoms or have no complaints.
 Acute Myocardial Infarction: change in heart rate (HR) and rhythm/BP/cardiac output; systolic murmur; chest pain/discomfort/pressure (usually
greater than 15 minutes duration), may radiate to arm/neck/back/jaw, unrelieved by nitroglycerine; diminished heart sounds (especially S1), S3 and/or
S4 with left ventricular dysfunction; decreased peripheral pulses, slow capillary refill; tachypnea, SOB; nausea/vomiting (N/V); diaphoresis;
restlessness, anxiety, confusion, agitation, denial, anger, feeling of impending doom; weakness; decrease in urine output
 ST-segment elevation myocardial infarction or presumed new left bundle branch block (LBBB): ST-segment elevation greater than 1mm in two
or more contiguous precordial leads or two or more adjacent limb leads
 High-risk UA/Non-ST-elevation myocardial infarction/new or presumably new left bundle branch block (LBBB): ischemic ST-segment
depression greater than or equal to 0.5 mm or dynamic T-wave inversion with pain or discomfort; nonpersistent or transient ST-segment elevation
greater than or equal to 0.5 mm for less than 20 minutes is also included in this category. Laboratory values: positive cardiac markers (increased CK-
MB/Troponin I or T/myoglobulin)
 Right ventricle (RV) infarction: Jugular venous distension (JVD); decreased BP; clear breath sounds; heart block; right ventricular (RV)
ectopy/bundle branch block (BBB); ST-segment elevation greater than 1mm in right precordial leads (especially V4R); often associated with inferior wall
myocardial infarction
1. Correlate characteristics of chest pain/discomfort/pressure/angina (intensity on pain rating scale) and correlate to type of coronary
artery disease (CAD)/ACS, associated dysrhythmias, oxygenation status, precipitating activity type/level, medications and admitting
baseline chest pain/pressure characteristics and assessment data. (5) {Grade C}
2. Administer oxygen (O2) therapy for first 6 hours of ACS therapy; evaluate for continued need thereafter [e.g., percent peripheral O2
concentration (SpO2) less than 92 percent, overt pulmonary congestion, pain, cyanosis, dysrhythmia]. (5; 85) {Grade B}
3. Establish large bore IV access. (5; 44) {Grade A}
4. Anticipate need for rapid administration of medications [e.g., nonenteric acetylsalicylic acid (ASA) on admission, antianginals
[nitroglycerin (NTG or glyceryl trinitrate), morphine], antidysrhythmics, anxiolytics, anticoagulant/antifibrinolytic therapy, beta blockers,
ACE inhibitors (ACEI)/angiotensin receptor blockers (ARB), HMG CoA reductase inhibitors (statin therapy)]. (5; 6) {Grade B}
5. Avoid nitrates, diuretics and other vasodilators (ACE inhibitors) in patients with RV dysfunction and acute infarction due to dependence
on maintenance of RV “filling” pressure to maintain cardiac output. (5) {Grade C}
6. Avoid nitrates in patients who have received a phosphodiesterase inhibitor (e.g., sildenafil, vardenafil) within the past 24 hours (48
hours for tadalafil). (5; 6) {Grade C}
7. Anticipate need for initial fluid volume challenge in RV infarct patients. (6) {Grade B}
8. Anticipate need for physiologic monitoring [e.g., ECG, central venous pressure (CVP)/pulmonary artery pressure, echocardiography
(especially in geriatric population)], respiratory support (e.g., airway management, noninvasive or invasive mechanical ventilation), fluid
balance and hemodynamic support (e.g. fluids, blood products, inoptropic agents). (5; 49; 65; 81; 85) {Grade A}
9. Prepare for possible intervention [e.g., fibrinolysis (pharmacologic reperfusion), diagnostic cardiac catheterization/PCI/PTCA
(mechanical reperfusion), coronary artery bypass graft (CABG)]. (5; 6; 49; 85) {Grade B}
10. Avoid activities that may predispose to vagal nerve stimulation and/or the valsalva maneuver (e.g., avoid rectal temperatures, use stool
softeners to prevent constipation). (85) {Grade C}
11. Gradually increase and pace activities with rest periods based on patient tolerance and prevent increased O2 demand (e.g., use bedside
commode instead of bedpan). (6; 49; 85) {Grade B}
Dysrhythmia/Arrhythmia AEB:
 labile heart rhythm/rate/pulse amplitude; palpitations; decreased capillary refill; change in BP; dizziness; syncope; N/V; change in mental status;
increased anxiety, increased confusion, increased agitation, change in level of consciousness; cool, clammy skin; change in ECG, increased
ectopy; change in cardiac output; change in cardiac index; change in CVP; change in pulmonary artery wedge pressure (PAWP); change in left
atrial pressure (LAP); change in systemic vascular resistance (SVP); decreased SpO2; decreased percent venous O2 saturation (SvO2); decreased
urinary output
Atrial:
 Symptomatic bradycardia: HR less than 60; syncope or near syncope, transient dizziness or lightheadedness, confusion; fatigue, exercise
intolerance; may lead to heart failure (30)
 Sinus tachycardia: gradual onset and acceleration of rapid beating of sinus node (100 to 180 bpm in adults, up to 200 with extreme exertion, 100
to 140 in older adults) leading to decreased cardiac output (2)
 Supraventricular tachycardia (SVT): rapid beating of sinus node that starts and stops abruptly (2)
 Sinus node dysfunction: symptomatic atrioventricular (AV) pauses greater than or equal to three seconds or sinus bradycardia with rates less than
50 bpm; may lead to syncope (30)
Ventricular:
 Hemodynamically stable: palpitations, complaints of dyspnea, chest pain/pressure, syncope and presyncope (89)
 Hemodynamically unstable: abrupt change in clinical status, hypotension, chest pain/pressure, complaints of dyspnea, lightheadedness, loss of
effective circulation, loss of consciousness, ventricular tachycardia, ventricular fibrillation (62)
 Sudden cardiac death/cardiac arrest: asystole, pulseless electrical activity (PEA) (62)
12. Correlate cardiopulmonary status to medications, treatments/diagnosis/procedure, oxygenation, electrolyte values (e.g., potassium,
sodium, calcium and magnesium); hydration status, age and baseline assessment data. (22; 56; 89) {Grade C}
13. Correlate peripheral pulses to atrial HR for one minute. (56; 58) {Grade A}
14. Correlate dysrhythmias to ischemias; evaluate/anticipate need for respiratory support to maintain O2 saturation above 90 percent [e.g.,
O2 therapy, airway placement, noninvasive/invasive ventilation]. (5; 41) {Grade C}
15. Anticipate need for peripheral vascular access, IV infusion/bolus. (22; 38; 58; 63) {Grade C}
16. Promote hemodynamic stabilization via nonpharmacologic methods [e.g., decrease head of bed (HOB), promote calm environment]. (56)
{Grade C}
17. Anticipate need for baseline diagnostic/laboratory studies [e.g., 12-lead ECG, arterial blood gases (ABGs), electrolytes, cardiac
enzymes, baseline coagulation studies]. (5; 22; 37; 56; 63) {Grade C}
18. Evaluate need for monitored/critical care bed. (56; 89) {Grade A}
19. Screen for anxiety, depressive disorders and/or psychosocial implications related to diagnosis of heart disease. (22) {Grade C}
20. Refer patient to smoking cessation program, if indicated. (22; 37; 56) {Grade C}
Atrial:
21. Mediate underlying cause of dysrhythmia to control sinus rhythm/ventricular rate. (56; 83) {Grade A} ATRIAL: rate versus rhythm
control
22. Anticipate administration of medications (e.g., electrolytes; diuretics, beta-blockers, digoxin, calcium channel blockers,
antidysrhythmics, anticoagulants). (15; 24; 56; 58; 63; 88) {Grade A}
23. Anticipate discontinuation of any medications that would contribute to symptomatic bradycardia (e.g., beta-blockers, digoxin,
verapamil). (22) {Grade C}
24. Anticipate antithrombotic/anticoagulant therapy (in nonvalvular A. fib/flutter) for prophylaxis of VTE [e.g., low molecular weight heparin
(LMWH), heparin, aspirin, vitamin K antagonist (warfarin)]. (32; 38; 56) {Grade A}
25. Monitor for bleeding and correlate laboratory results to dose of antithrombotic medications [e.g., prothrombin time/partial thromboplastin
time (PTT)/international normalized ratio (INR)] and dietary intake of vitamin K. (22; 32; 38; 56) {Grade A}
26. Anticipate need for emergency cardiac intervention (e.g., cardioversion, overdrive pacing). (15; 36; 58) {Grade A}
27. Anticipate need for temporary pacing (transcutaneous or transvenous) in patients with symptomatic bradycardia [e.g., unresponsive to
atropine, presence of anterior myocardial infarction, third degree AV block in inferior myocardial infarction, alternating left/right BBB].
(22) {Grade C}
Junctional/Ventricular:
28. Anticipate need for physiologic monitoring [e.g., continuous ECG, CVP/pulmonary artery pressure, echocardiography (especially in
geriatric population)], respiratory support (e.g., airway management, noninvasive or invasive mechanical ventilation), fluid balance and
hemodynamic support (e.g., fluids, electrolytes, inotropic agents, antidysrhythmics, beta-blockers, anticholinergics, vasopressors). (24;
42; 81; 85; 89) {Grade A}
29. Anticipate need for emergency cardiac intervention (e.g., defibrillation, pacing, cardioversion). (89) {Grade A}
30. Assess for potential of deteriorating cardiac status/impending cardiac arrest with first priority being activation of rapid response team.
(24; 89) {Grade A}
31. Anticipate need for emergent procedure [e.g., coronary angiography, pacemaker/automatic implantable cardiac defibrillator (AICD)]. (5)
{Grade C}
Hemodynamic Instability AEB: (6; 44; 61; 65)

 Heart failure: decreased cardiac index/SpO2; angina; cool, pale, diaphoretic skin; decreased capillary refill/quality of peripheral pulses; S3, S4,
pericardial rub; increased weight; positive intake and output balance; decreased urinary output; fatigue
 Systolic (left heart): decreased BP, increased HR/pulmonary artery pressure (PAP)/pulmonary artery wedge pressure (PAWP)/systemic vascular
resistance (SVR); change in RR, wheezes, crackles, pink frothy sputum, increased work of breathing, orthopnea, cyanosis
 Diastolic (right heart): JVD; increased CVP; pleural effusion; hepatomegaly; ascites; abdominal tenderness; positive hepatojugular reflex; N/V;
dependent peripheral edema
 Cardiogenic shock: signs/symptoms of heart failure plus restlessness, confusion, sense of impending doom; change in level of consciousness;
peripheral vasoconstriction, narrowed pulse pressure; core temperature less than 36 degrees Celsius
32. Correlate cardiovascular/cardiopulmonary status to disease process, precipitating events, fluid status, medications/treatments,
laboratory values, neurologic status, abdominal girth, intra-abdominal pressure, activity tolerance, sleep/rest patterns, visible bleeding,
ECG, echocardiography and baseline assessment data. (44; 49; 61; 65) {Grade A}
33. Promote hemodynamic stability (e.g., lower HOB for hypotension, control of hypertension, blood/fluids, quiet environment). (61; 65)
{Grade A}
34. Anticipate need for electrolyte replacement (e.g., potassium, calcium, magnesium) especially if patient is undergoing diuresis. (61; 65)
{Grade A}
35. Evaluate impact of medication therapy on myocardial workload. (55) {Grade A}
36. Titrate vasodilators to decrease myocardial workload and increase cardiac index. (55) {Grade C}
37. Use vasopressors and inotropes cautiously to avoid increased myocardial O2 demand. (33) {Grade C}
38. Evaluate need for active/passive rewarming techniques (e.g., warm blankets, water/air hyperthermia system, increased ventilator
temperature). (61) {Grade C}.
39. Prepare for possible intervention [e.g., intraaortic balloon pump (IABP)]. (6) {Grade B}
40. Promote rest and minimize O2 consumption (e.g., allow rest periods, coordinate/cluster care, neutral-thermic environment). (61) {Grade A}
Pericarditis leading to Pericardial Effusion AEB:

 Pericarditis: pain described as being different from angina/myocardial infarction pain: sudden or gradual onset, sharp, stabbing, substernal;
movement or deep inspiration aggravates pain; alleviated by sitting up/leaning forward; cough; dysphagia; pain may radiate to left upper back, shoulder
or arm; pericardial friction rub; dysrhythmias; increased HR/respiratory rate (RR)/erythrocyte sedimentation rate (ESR)/white blood cell (WBC); low
grade temperature; diffuse ST-segment elevation; complaints of dyspnea; chills; weakness (86)
 Pericardial effusion: muffled heart tones; paradoxical pulse; increased HR; decreased BP; disappearance of pericardial friction rub; pericardial fluid
seen on echocardiogram; enlarged cardiac silhouette on CXR (84)
41. Coordinate planned activities with pain management plan and position for comfort (e.g., upright). (84; 86) {Grade C}
42. Verify need to continue antiplatelet/anticoagulation therapy. (84) {Grade C}
43. Anticipate need to prepare patient for diagnostic procedures [e.g., CXR, transesophageal TEE, MRI, CT scan] and urgent interventions
(e.g., pericardiocentesis, balloon pericardotomy, pericardial sclerosis). (84) {Grade C}
44. Anticipate need for hemodynamic monitoring (e.g., pulmonary artery catheter) and support (e.g., fluid resuscitation, inotropic agents). (84)
{Grade C}
45. Anticipate need for medications [e.g., steroids, aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) (may be contraindicated due to
possible delayed myocardial scar healing)]. (84) {Grade C}
Cardiovascular Structural Defects AEB: (6; 85)

 Left ventricular aneurysm: paradoxical pulse; bulging of precordium; change in HR; ventricular ectopy
 Septal rupture: acute left ventricular failure; holosystolic murmur with precordial thrill; acute pulmonary edema
 Mitral valve/Papillary muscle rupture: acute left ventricular failure; rapid progression to pulmonary edema and often cardiogenic shock; early or
holosystolic murmur
 Ventricular septal rupture: tamponade; cardiogenic shock with narrow pulse pressure; pulseless electrical activity (PEA) leading to cardiac arrest
46. Flatten head of bed and elevate feet to optimize perfusion to vital organs. (73) {Grade C}
47. Titrate vasopressors, vasodilators and inotropic medications to optimize hemodynamic function. (6) {Grade B}
48. Prepare for emergency intubation and placement of large bore IV devices. (85) {Grade C}
49. Anticipate need for rapid administration of fluid/volume expanders and adjustment of vasoactive medications. (6; 85) {Grade B}
50. Prepare for emergent insertion of intra-aortic balloon pump (IABP) and/or cardiac surgery or pericardiocentesis (in the case of septal
rupture). (6; 85) {Grade B}
Mural Thrombosis leading to Embolism AEB:

 Mural thrombus: asymptomatic unless portion of thrombus dislodges, leads to ischemic CVA, pulmonary/ peripheral embolism
 Cerebral embolus: sudden change in cognitive/sensory/motor function; suddenly changed level of consciousness; failure to regain consciousness
after general anesthetic; seizure
 Pulmonary embolus: sudden cardiovascular instability/respiratory distress; cough; decreased end-tidal carbon dioxide (EtCO2); increased RR;
marked decrease in O2 saturation (hemoglobin) (SaO2); changed arterial blood gases (ABG's); hypoxemia; thoracic/upper abdominal pain;
tachycardia; petechiae; pulmonary infiltrates; positive D-dimer level; positive ventilation perfusion (VQ scan); positive pulmonary angiography or
positive helical computed tomography scan (14; 17; 74)
 Deep vein thrombosis (DVT) leading to venous thromboembolism (VTE): redness, warmth, tenderness, edema of affected area; increased
temperature; impaired neurovascular status; apprehension; restlessness; venous congestion; deep/local muscle pain; size asymmetry; color change;
palpable cord along vein; abnormal D-dimer level; positive venous ultrasonography (17; 74)
51. Initiate strategies to prevent/treat DVT/VTE:

 Prevent venous stasis/pooling of blood in extremities [e.g., compression stockings, prevent pressure/constriction, frequent position
change, avoid compression of vena cava, ankle dorsiplantar exercises, avoid crossing legs, intermittent pneumatic compression,
neutral position, HOB elevated less than 30 degrees]. (4; 7; 16; 50; 66) {Grade A}
 Promote early and frequent ambulation. (17; 50) {Grade B}
 Advocate for VTE prophylactic medication. (7; 50; 51; 53) {Grade B}
 Monitor for bleeding and correlate laboratory results to dose of antithrombotic medications. (16; 50) {Grade B}
 Avoid deep/vigorous massage when suspected signs and symptoms of DVT or receiving antithrombotic therapy. (25; 31) {Grade C}
 Evaluate/anticipate need for measurements of extremities to compare size and symmetry. (13) {Grade C}
 Evaluate/anticipate need for diagnostic studies (e.g., D-dimer level, VQ scan, ultrasound, echocardiography, venography,
arteriography). (14; 40; 50) {Grade B}
 Anticipate need for emergent/urgent procedures (e.g., thrombolysis, embolectomy/thrombectomy, vena cava filter). (40; 50) {Grade B}
 Evaluate/anticipate need for postdischarge anticoagulation. (50) {Grade B}
Acute Pain AEB: (19)

Patient may have nociceptive, neuropathic or a combination of both types of pain:
 Nociceptive (somatic): recent onset; well-localized; sharp, pin-prick, aching, stabbing or throbbing
 Nociceptive (visceral): poorly localized; diffuse with vague complaints such as generalized ache or pressure; may be referred to sites remote
from the primary injury. Autonomic symptoms include N/V, hypotension, bradycardia, sweating
 Neuropathic: radiating or specific burning, electric-like, shooting, tingling or lancinating (stabbing, piercing) pain. Physical exam may reveal
allodynia (pain on light touch), hypoalgesia or hyperalgesia (relatively decreased or increased perception of noxious stimulus) or hyperpathia
(exaggerated pain response). Symptoms usually are experienced distal to the site of injury
 Geriatrics - additional considerations: changes in mental status; changes in appetite; agitation; rigidity-resistance to certain movements during
care; withdrawn affects; paucity of conversation; depression; allodynia; decreased activity levels; loss of function; lack of adaptation skills (9)
 Nonverbal patient (e.g. advanced dementia, mechanically ventilated and/or sedated, unconscious): sympathetic stimulation [e.g. facial expression
(relaxed versus brow lowering, eyelid closing, grimacing), upper limb movements (no movement versus partially bent, fully bent with finger flexion,
permanently retracted), mechanical ventilation compliance (tolerating movement versus coughing but tolerating most of time, fighting ventilator,
unable to control ventilation] (1; 46; 69; 72; 78)
52. For patients able to communicate, evaluate pain using identified tool/self-report description [e.g., onset, location, radiation frequency/
duration, intensity/severity at rest and with activity, aggravating/relieving factors (medications, positioning, treatment devices),
exacerbation]; behavioral indicators [e.g., moaning, rubbing a particular area, guarding; decreased attention span, agitation, inability to
rest/sleep, inability to alleviate distress; facial expression (brow lowering, orbital tightening, levator contraction, eyelid closing), upper
limb movement, mechanical ventilator compliance], patient’s stated perception of pain tolerance, type of procedure/ treatment/disease
process, expected pain progression, cultural factors that may influence pain perception and baseline assessment data. (1; 10; 18; 19; 34;
43; 46; 48; 69; 72; 78) {Grade A}
53. For patients unable to communicate (e.g., advanced dementia, mechanically ventilated and/or sedated, unconscious), evaluate pain
using report of pain/behavior changes from family/caregiver; pain behavior checklist sympathetic stimulation [e.g., facial expression
(relaxed versus brow lowering, eyelid closing, grimacing), upper limb movements (no movement versus partially bent, fully bent with
finger flexion, permanently retracted), mechanical ventilation compliance (tolerating movement versus coughing but tolerating most of
time, fighting ventilator, unable to control ventilation)] and consider analgesic trial. If behaviors do not improve with analgesia, consider
addition of sedatives and/or antipsychotic medications. (1; 46; 69; 70; 72; 78) {Grade C}
54. For patients unable to respond behaviorally to pain (e.g., pharmacologically paralyzed, flaccid) assume pain is present if patient has
chronic painful condition(s), painful activity (e.g., physical therapy) or potentially painful procedures (e.g., suctioning, turning, dressing
changes) and begin to treat appropriately with analgesia trial. (1; 46; 69; 70; 72; 78) {Grade C}
55. Establish with patient what level of discomfort is acceptable that will allow for maximal function with basic/instrumental activities of
daily living (BADL/IADL). (19; 48) {Grade B}
56. Mutually develop plan for pharmacologic/nonpharmacologic comfort measures as appropriate [e.g., medications (appropriate to type of
pain reported), procedures (neuraxial or sympathetic blocks), adjuvants such as complementary and alternative therapies (massage,
touch, hypnosis, acupuncture), physical medicine/rehabilitation techniques (assistive devices, orthotics, transcutaneous electrical
nerve stimulation, ultrasound, massage, therapeutic exercise), psychological interventions (behavioral therapy, biofeedback, cognitive
behavioral therapy, counseling, relaxation)]. (19; 48) {Grade B}
57. Account for the possibility of acute pain in the presence of pre-existing chronic pain syndrome and adjust medications appropriately
(e.g., use patient’s prehospital basal rate plus adjustment for acute pain). Collaborate with patient on what has worked best for him/her
in the past. (19; 26) {Grade B}
58. Initiate pain management plan that includes scheduled around-the-clock pain medication dosing with PRN breakthrough medications as
prescribed if pain is present the majority of a 24-hour time span. (10; 19; 48) {Grade B}
59. Provide individualized pain management measures prior to procedure(s)/planned activities (e.g., turning, suctioning, wound care/drain
removal). (48; 78) {Grade B}
60. Anticipate need for management of drug-induced side effects. For opioids: N/V, constipation, itching, myoclonus and respiratory
depression. For NSAIDs: dyspepsia, prolonged bleeding times, renal dysfunction, urinary retention, hypertension. (10; 11; 19; 48)
{Grade B}
Situational Response AEB:
 expression of anxiety, fear, denial, guilt, frustration, vulnerability, disappointment, anger, shock, blame, sadness, depression, hopelessness,
apprehension, uncertainty, ambiguity, grief/loss (e.g., loss of control, loss of previous family/social role, loss of independence); increase stress
(e.g., financial, relationships, roles, responsibilities) (20; 59; 82)
61. Develop trust relationship/rapport through therapeutic presence, active/empathic listening and sensitivity to nonverbal communication.
(20; 29; 59; 60; 75) {Grade C}
62. Correlate patient/support system response to medical illness/injury with ability and/or readiness to comprehend information, past
experiences/history (including mental health), current situation, developmental stage, medications/substance use and baseline
assessment data. (20; 29; 75) {Grade C}
63. Encourage verbalization of feelings regarding current situation. (20; 29; 59; 75; 82) {Grade C}
64. Support coping by recognizing current strategies and developing new strategies (e.g., journaling, relaxation techniques, guided
imagery, problem solving, prayer). (20; 29; 59; 75; 82) {Grade C}
65. Evaluate the need for anticipatory guidance (e.g., provide information on realistic expectations, education/resources) and encourage
patient/support system to ask questions regarding treatment/procedures. (20; 59; 60) {Grade C}
66. Facilitate the presence of and private time with the patient support system (e.g., partner, family members, children, friend, spiritual
advisor). (20; 29; 60; 75) {Grade C}
67. Address concerns, offer reassurances and provide support for patient/support system. (20; 29) {Grade C}
Clinical Practice Guidelines represent a consistent/standardized approach to the care of patients with specific diagnoses. Care should always be
individualized by adding patient specific information to the Plan of Care.
.
GENERAL INFORMATION: ACUTE CORONARY SYNDROME
A. CLINICAL DESCRIPTION: (33)

The term acute coronary syndrome (ACS) refers to myocardial ischemia (an imbalance between supply and demand of myocardial O2) and is reflective
of the clinical diseases of acute myocardial infarction and unstable angina. Heart disease is the leading cause of all deaths in people over age 65 in the
U.S. (31.8 percent). (21)
1. Classification and Symptoms of ACS: (5; 33; 85)
a. Angina pectoris (chest pain): classic symptom of ACS. Pain intensity ranges from absent (silent ischemia) to severe. The pain is usually
substernal and may radiate to the epigastric region, jaw, shoulder, elbow or forearm. Chest pain is described as heaviness, tightness/
pressure, constriction, indigestion or burning. Associated symptoms include: SOB, diaphoresis, N/V, weakness, extreme fatigue, anxiety
and/or sense of impending doom.
Variants of angina include:
 Chronic stable: episodic pain lasting 5 to15 minutes. Brought on by predictable increase in physical effort, predictable intensity and
duration of symptoms. Relieved with rest or nitroglycerin.
 Unstable: patient notes a change in severity or duration of symptoms of chronic stable angina. Types include new-onset exertional;
angina of increased frequency or duration or refractory to nitroglycerin and angina at rest.
 Variant (Prinzmetal): occurs at rest or sleep. Related primarily to coronary artery spasm. Triggered by smoking. Frequently seen in
connective tissue disease, arterial inflammation and infection.
b. Unstable angina/non-ST-elevation myocardial infarction: closely related conditions with similar pathogenesis and clinical symptoms. They
differ primarily in whether the ischemia is severe enough to release markers of myocardial injury. If biomarkers are detected in the
bloodstream, the patient is considered to have non-ST elevation myocardial infarction.
 Pathogenesis: decreased myocardial perfusion commonly caused by coronary artery narrowing secondary to nonocclusive thrombus
that developed on a disrupted atherosclerotic plaque.
 Presentations of unstable angina:
 Rest angina (occurs at rest and prolonged greater than 20 minutes)
 New onset severe angina
 Increasing angina (previously diagnosed angina that has become more frequent)
c. ST-segment elevation myocardial infarction or presumed new left bundle branch block (LBBB):
 Pathogenesis: prolonged myocardial ischemia that leads to irreversible injury and necrosis.
 Presentation: chest pain lasting more than 30 minutes. Pain is usually severe, but may be mild or absent.
2. Location of myocardial infarctions: associated findings, management and complications: (39)
a. Inferior myocardial infarction: occlusion of right coronary artery (RCA) and/or left circumflex artery. Right ventricular infarctions should always
be suspected as well. ECG changes: ST-segment increased II, III, AVF; reciprocal changes: aVL, decreased ST, diagnostic Q wave in two
adjacent or contiguous leads.
 common dysrhythmia: bradycardia, primary heart block (HB), accelerated junctional, secondary to heart block (Type I), third degree
heart block (rare) (Note: Do not give lidocaine if ventricular beats are escape beats).
 common findings: N/V; cold, clammy skin; murmur or mitral valve regurgitation (MVR)/papillary muscle dysfunction.
 major complications: A-V nodal blocks; complete heart block.
b. Anterior myocardial infarction: occlusion of the left anterior descending coronary artery (LAD). ECG change, abnormal Q wave and ST
elevation in leads V1-4; ST-segment depression in inferior leads II, III and AVF would be a more ominous feature, T inversion in V4 and 5
 common dysrhythmia: sinus tachycardia, atrial flutter (A flutter), atrial fibrillation (A fib), third degree heart block, ventricular tachycardia
(V-tach), ventricular fibrillation (V-fib), BBB and junctional rhythms
 common findings: decreased BP; decreased urine output; S3, S4; increased PAWP; pulmonary edema
 major complications: septal rupture
c. Lateral myocardial infarction: occlusion of circumflex coronary artery, ECG change, increased ST-segment in I, AVL, V5 and 6. Anterolateral
occlusion of diagonal branch left anterior descending coronary artery (LAD) with reciprocal changes in the inferior leads.
 common dysrhythmia: atrial dysrhythmia. SVT, ST, and junctional rhythms
 common findings: decreased BP, decreased urinary output, S3, S4, increased PAWP
 major complications: watch for extension to anterior inferior or posterior wall
d. Posterior myocardial infarction: occlusion of right coronary artery (RCA), ECG change, increased ST-segment in V1-3, Posteriorlateral: tall R
waves V1-2. Occlusion of circumflex, decreased ST-segment in V1-3, increased ST in 1, AVL, V5 and 6
 common dysrhythmia: bradycardia and heart blocks
 common findings: decreased HR; decreased BP
 major complications: heart failure (HF) and pulmonary edema; monitor for extension to lateral or inferior wall or right ventricle
e. Right Ventricular myocardial infarction: occlusion of proximal RCA, often associated with inferior wall myocardial infarction. ECG change,
increased ST in V3R, V4R.
 common dysrhythmia: AV conduction block
 common findings: hypotension; increased CVP; decreased PAWP/cardiac index; JVD; clear breath sounds; decreased cardiac output
 specific management: consider increasing fluid volume to increase cardiac output/cardiac index that provides adequate left sided filling
pressures. If fluids don’t improve BP, anticipate use of inotropic agents (e.g., Dobutamine). Anticipate reperfusion therapy, fibrinolytics,
pacemaker insertion. Maintain potassium at a level greater than four and magnesium at a level greater than two. DO NOT
ADMINISTER VASODILATORS (e.g., nitrates, diuretics, ACEI) as patients with RV dysfunction and acute infarction are dependent on
maintenance of right ventricular filling pressures to maintain cardiac output.
 major complication: acute hemodynamic instability related to right ventricular failure; A-V Nodal blocks
3. Causes of ACS include: (5; 33; 85)
a. atherosclerotic plaque, ruptured or eroded (most common cause)
b. coronary vasospasm
c. ventricular hypertrophy due to hypertension, valvular disease or cardiomyopathy
d. embolic occlusion of the coronary arteries
e. hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders
f. cocaine and amphetamines, which increase myocardial O2 demand and may cause coronary vasospasm
g. underlying coronary artery disease, which may be unmasked by severe anemia
h. inflammation of epicardial arteries
i. coronary artery dissection; especially in younger women and those who use cocaine
B. PATHOPHYSIOLOGY/ETIOLOGY/RISK FACTORS FOR POTENTIAL PROBLEMS:

1. Ischemia leading to Infarction: occurs when myocardial O2 demand is greater than supply. Area surrounding necrosis is affected by a prolonged
decreased O2 supply to myocardial tissue leading to instability of cell membranes leading to dysrhythmias. Pain is an indicator of decreased O2
supply to tissue. May be indicated by T-wave inversion on ECG. (5; 33; 85)
2. Dysrhythmia:
a. Definition: (27; 28) Arrhythmia: “any cardiac rhythm other than normal sinus rhythm. Such a rhythm may be either sinus or ectopic in origin
and either regular or irregular. An arrhythmia may be due to a disturbance in impulse formation or conduction, or both.” Not all arrhythmias
result in harm, however, they do interact with other organ systems.
b. Pathophysiology/Etiology: (27; 28) Arrhythmias either result from problems of other organ systems (e.g., renal failure) or produce
dysfunction in other organ systems due to hemodynamic compromise or embolic phenomena.
 Iatrogenic: postsurgical; or secondary to multiple etiologies (e.g., postprocedural, mechanical, ischemic, metabolic, infectious and
multifactorial).
 Noniatrogenic: genetic or congenital; may also be secondary to multiple etiologies [e.g., scar-related (stretch or fibrosis), metabolic,
infectious or multifactorial].
Classification: based on the anatomical hierarchy and the type of mechanism of the arrhythmia. (27; 28)
 Atrial
 Junctional
 Ventricular
 Atrioventricular
Subclassification includes:
 Early (also known as perioperative): occur during hospitalization or within 30 days of surgery.
 Sustained: lasting greater than 30 seconds, or requires immediate termination due to hemodynamic compromise.
 Frequency: paroxysmal, recurrent, chronic recurring or permanent
c. Risk factors: anesthesia, hypoxia, hypotension, electrolyte imbalance (e.g., diarrhea, renal failure), invasive lines (e.g., central venous),
coronary artery injury, compression of ventricle by a chest tube, hepatic failure, pain (releases catecholamines that produce tachycardia),
history of smoking.
3. Hemodynamic Instability: an alteration in blood flow through the cardiovascular system circuit in which the circuit can no longer meet the
metabolic demands due to a decrease in cardiac filling pressure. (65)
a. The venous side of the cardiovascular system is conceptually divided into two compartments: the peripheral compartment and the smaller
intrathoracic central venous compartment.
b. Each segment has a different role to play in the overall circulatory operation because of inherent differences in anatomical volume,
compliance and resistance to flow.
c. The ventricular end-diastolic volume (stroke volume and cardiac output) is very sensitive to small changes in the cardiac filling pressure
(blood return to the vena cava preload).
d. Cardiac filling pressure is a crucial factor that determines hemodynamic stability.
e. The intrathoracic venous compartment responds pathologically to pressure and flow changes, hypoxemia, toxins and emboli; causing
endothelial dysfunction, decreased diameter to the lumen of the resistance vessels and the pulmonary arterioles leading to pulmonary
hypertension. (81)
f. Signs and symptoms of pulmonary hypertension include hypoxia, fatigue, shortness of breath, reduced cardiac output, syncope, lower
extremity edema, hepatic congestion, ascites, acidosis, renal failure, malnutrition, hypotension and confusion. (81)
g. Presence of systolic murmur may suggest ventricular septal rupture or acute mitral regurgitation.
h. Intervention considerations for peripheral compartment dysfunction:
 Focus will be on interventions which promote blood return from the peripheral veins (preload) to fill the heart prior to each beat, as a
result will increase stroke volume and cardiac output. (65; 76)
i. Intervention considerations for intrathoracic central venous dysfunction:
 Acute management of dysfunction is focused on the underlying mechanisms.
j. Changes for geriatric population: (61; 80)
 higher BP caused by decreased arterial elasticity
 increasing peripheral vascular resistance and cardiac workload
 baroreceptors in aorta and carotid arches become less sensitive to pressure changes in arterial system and cardiac muscles
 in symptomatic hypotension, chemoreceptors respond less to beta-adrenergic stimulation
 decreased ability of cardiovascular system to vasoconstrict; instead shunting blood from peripheral arteries to major organs
 progressive stiffening of myocardium and heart valves; leading to decreased efficiency
 vascular changes to heart, kidneys and pituitary gland
 increase in vessel wall rigidity and narrowing arterial lumens necessitating greater pump force
 cardiac output and stroke volume decrease as the result of decreased conduction and blood flow
Note: Early placement of pulmonary artery catheter and aggressive management of hemodynamic parameters improve surgical outcomes
in geriatric patients.
k. Heart Failure: cardiac output is insufficient to meet the metabolic needs of the body, possibly related to a large area of the left ventricle being
affected.
 Cardiogenic shock: caused by a decreased cardiac output/cardiac index. O2 and other nutrients become unavailable to the cells of the
body.
 Dysrhythmias: ischemia causes electrical instability of myocardium. Ventricular fibrillation: most common cause of death within first
hour of onset of angina regardless of location of myocardial infarction.
4. Pericarditis leading to Pericardial Effusion:
a. Pericarditis: Inflammation of the pericardial sac (a potential space holding up to 20 mL fluid with electrolyte and protein profiles similar to
plasma). Autoimmune inflammatory response to myocardial infarction may cause an increase in fluid within the sac (2 to 5 percent of
patients). Occurs as early as two days postmyocardial infarction and up to 12 weeks postmyocardial infarction. Up to 80 to120 mL of
additional fluid can accumulate in the pericardium before symptoms of pericardial pressure appear. (86)
b. Pericardial effusion: presence of an abnormal amount and/or character of fluid in the pericardial sac with both infectious and noninfectious
origin (e.g., anterior myocardial infarction). (84)
5. Cardiovascular Structural Defects: related to size and area of infarction. (85)
a. Ventricular aneurysm: noncontractile, thinned left ventricular wall caused by an acute transmural infarction. Most common with acute left
anterior descending (LAD) occlusion with wide area of infarcted myocardium.
b. Ventricular septal rupture: postinfarction rupture of the ventricular septal wall that connects the left and right ventricle. Carries a very high
mortality rate. Afterload reduction is necessary via IABP and vasodilators.
c. Papillary muscle rupture: muscles that support the mitral valve infarct and rupture, causing ineffective valve closure and back-pressure of
blood into the left atrium during ventricular systole.
6. Mural Thrombosis leading to Embolism: A clot in the cardiovascular system formed during life from constituents of blood; it may be occlusive
or attached to the vessel or heart wall without obstructing the lumen (mural thrombus). (67) An embolus (plural “emboli”) is a plug, composed of a
detached thrombus or vegetation, mass of bacteria or other foreign body, occluding a vessel. Thromboembolic complications occur secondary to
increased blood viscosity, increased fibrinogen and bedrest. Mural thrombosis occurs more frequently with large, transmural, anterior myocardial
infarctions. Primary concern is systemic embolism, which can lead to CVA/brain attack, peripheral embolism and pulmonary embolism.
a. DVT/VTE: Immobility leads to venous stasis thereby facilitating coagulation cascade in large veins. DVT causes less inflammation than
thrombophlebitis; lack of inflammation increases risk that portions of clot may break off and travel through the vascular system as VTE. (7; 12)
DVT may develop as late as 7 to 10 days postoperatively in vessels of pelvis and lower extremities. VTE prophylaxis should begin for surgical
cases between 24 hours prior to surgical incision and 24 hours after surgery end time. (53) For nonambulatory stroke patients, DVT
prophylaxis should begin by the end of hospital day two. (51)
b. Cholesterol embolism: rupture of atherosclerotic plaque releases cholesterol crystals into bloodstream; crystals lodge in arterioles producing
inflammation and thrombus formation which leads to fibrosis. (47)
c. Risks of mural thrombosis:
 VTE: more common in Blacks than Caucasians/Asians. Risk factors include: history of past VTE, pregnancy, postpartum or current
estrogen use, recent trauma/surgery, immobilization, presence of cancer, airline flight longer than eight hours, obesity, fractures of
hip/pelvis/lower extremity, central venous catheter; diabetes, hyperlipidemia, hyperuricemia, cardiovascular disease (e.g., hypertension,
varicose veins, atrial fibrillation, angina, myocardial infarction, valvular disease), pulmonary hypertension and history of ischemic stroke.
(3; 8; 14; 17; 68)
 VTE prophylaxis: indicated for vascular, urologic, cardiac, orthopaedic, intracranial, neurologic or multiple trauma surgeries. General
Surgery procedures are graded (low, moderate, high or very high risk) based on patient age/risk factors/duration of surgery.
 Cholesterol embolism: often triggered by vascular radiographic/surgical procedures; incidence 25 to 77 percent in high-risk populations;
common sources of plaque include abdominal aorta, carotid, iliac, femoral arteries. (47)
7. Pain:
a. Acute pain: is a symptom versus a diagnosis. Pain is subjective. Acute pain is usually related to an injury, trauma or surgery, thus is
protective, acting as an early warning sign that tissue damage is about to occur or is occurring. The patient expects to recover after the
injury or surgical wound heals. (19; 26; 43)
b. Chronic or persistent pain: pain that lasts beyond the healing process and has outlived its warning role. It becomes persistent and
debilitating, lasting for more than six months. It can exist when there is no evidence of tissue damage (e.g., phantom pain). It may be
intermittent or continuous, poorly differentiated and may or may not be associated with an injury or chronic disease. Diagnostic tests may
not necessarily reveal a specific source of the pain. Patient may show few or no outward signs of pain as they have learned to tolerate the
pain for so long. (18; 26; 43)
c. Acute-on-chronic pain: person suffering from chronic pain (e.g., cancer or neuropathy) who is admitted to an acute care setting for surgery
or injury. Both types of pain must be treated. (18)
d. Types of Pain (can occur independently or combined):
 Nociceptive (somatic): results from injury of the skin/mucosa, muscle, bone, tendons, ligaments and joints, arteries (e.g., superficial
lacerations/burns, intramuscular injections, IV access, otitis media, stomatitis, extensive abrasions). Responds best to acetaminophen,
cold packs, corticosteroids, localized anesthetic (e.g., topical or infiltrate), NSAIDs, opioids and tactile stimulation. (18; 19; 43)
 Nociceptive (visceral): results from stimulation of nociceptors in internal organs (e.g., stomach, kidney, bladder, gallbladder,
pancreas, intestines). Ischemia/necrosis, inflammation, ligamentous stretching, smooth muscle spasm, and distension of a hollow
organ capsule all contribute to visceral pain (e.g., colic, sickle cell, appendicitis, kidney stone, postoperative abdominal surgery).
Responds best to corticosteroids, intraspinal local anesthetic agents, NSAIDs (IV route Ketorolac for NPO patients) and opioids (via
any route). (18; 19; 43)
 Neuropathic: caused by damage to a nerve, either centrally or peripherally. Pressure on tissues surrounding the neural tissues and
abnormal processing of impulses also causes neuropathic pain [e.g., trigeminal, avulsion neuralgia, post-traumatic neuralgia, peripheral
neuropathy (diabetes, human immunodeficiency virus), limb amputation, herpetic neuralgia]. This type of pain provides no protective
benefit and precipitates ongoing suffering. Responds best to anticonvulsants (e.g., gabapentin), corticosteroids, neural blockade,
NSAIDs, opioids (via any route) and tricyclic antidepressants. (18; 19; 26)
e. Pain assessment for specialty groups:
Geriatric:
 Normal cognitive function: Older patients do not necessarily use the word “pain.” Instead, ask which term they relate best to
[e.g., ache, hurt, discomfort; or just ask the intensity of their pain (none, some, severe)]. Ask which type of scale works best for them
[e.g., visual analogue, Numeric Rating Scale (NRS), Faces Pain Scale-Revised (FPS-R, no smiles or tears), Verbal Descriptor Scale
(VDS) or revised verbal descriptor – includes visual pain thermometer]. Note that decreased hearing/vision may hamper verbal/visual
communication as well as visual tools. (34; 45; 57; 64)
 Mild dementia: If mild dementia is suspected, patient should first receive a cognitive evaluation that includes the Mini Mental State
Examination (MMSE). Appropriate scales include verbal descriptor scale, pain thermometer or FPS-R (patient may have difficulty
differentiating between pain or mood). (45)
 Advanced dementia: assessment traditionally has moved from self-report to clinician observed scale. The “Pain Assessment in
Advanced Dementia” (PAINAD) scale measures the following: breathing independent of vocalization, negative vocalization, facial
expression, body language and consolability. It is rated on a 0 to 2 scale, with a total score range of 10. (35) Use of the Verbal Rating
Scale (VRS) and Faces Pain Scale (FPS) have been used with some success in patients with severe dementia. (71)
 Pharmacology: renal and liver function studies, as well as serum protein levels should be measured in geriatric patients prior to
starting certain medications, especially NSAIDs. (45; 77)
Nonverbal: (e.g. advanced dementia, mechanically ventilated and/or sedated, unconscious): (1; 46; 69; 72; 78)
 More than one measure may be needed to adequately detect the pain and evaluate outcome of interventions. Recommended
hierarchy of assessment steps include:
 Self-report. May be hampered by level of consciousness, artificial airway, medication(s), delirium.
 Search for potential causes of pain/discomfort (e.g., existing medical condition, surgical/medical procedures, traumatic injuries,
blood draws and routine care).
 Observe patient behaviors. Note: behavioral scales are not appropriate for pharmacologically paralyzed patients, or those who
are flaccid and cannot respond behaviorally to pain. In this case, assume pain is present and treat appropriately with analgesics
prior to procedures thought to be painful (including turning).
 Surrogate (family members, caregivers) report of pain and behavior/activity changes.
 Attempt analgesic trial. If behaviors do not improve with analgesia, consider addition of sedatives and/or antipsychotic
medications.
 Sample pain tools for assessment in nonverbal patients include: Assessment of Discomfort in Dementia Protocol by Kovach et al
(ADD), Checklist of Nonverbal Pain Indicators by Feldt, Pain Assessment in Advanced Dementia Scale by Lane et al (PAINAD),
Behavioral Pain Scale by Payen (BPS). (46)
8. Situational Response:
a. Definition: A phase in one’s life during which normal ways of dealing with the world are suddenly interrupted due to a medical
event/illness/injury. (29)
b. Risk factors:
 Adjustments/reactions to a medical event/illness/injury, under any circumstances, are necessary and normal. A history of chronic
mental health issues, substance use/abuse, poor coping abilities/strategies, past experience of trauma/abuse (both personal and
professional), lack of support and low self-esteem contribute to an inability to deal with a medical event/illness/injury successfully. (54)
 Although distress related to the experience of the illness/injury abates over time, the psychological impact of the distress lingers. (59)
 “What happens when my body breaks down happens not just to that body but also to my life, which is lived in that body. When the
body breaks down, so does the life. Even when medicine can fix the body, that doesn’t always put the life back together again.”—
Arthur Frank (59)
 Psychological defenses allow us to cope with our day-to-day life. Increased stress leads to less effective psychological defenses,
therefore, our typically well-managed emotions (e.g., anger, sadness, anxiety, frustration) become less well-managed leading to
emotional instability, interpersonal conflict and diminished social/occupational functioning in many persons. (23)
 The family unit is a system based on interdependency between members and patterns that provides structure and support. Illness
and/or injury in one family member may disrupt these relationships and patterns. (20)
 Individual differences need to be considered regarding response/reaction to medical event/illness/injury and support provided to
patient/support system. Gender and/or cultural differences may influence response/reaction as well as attitudes and beliefs about
support. (60)
 Healthcare practitioners may hesitate to ask questions related to a patient/support system emotional/mental status, for fear of not
feeling prepared to deal with the response. Failure to address this area of patient/support system health can result in suboptimal care.
For this reason, it is essential to refer to someone on the healthcare team that is knowledgeable, competent and comfortable in
assisting the patient/support system in this area. (20; 82)
C. ADDITIONAL INFORMATION:
1. Significant laboratory values/Diagnostic testing: (6; 33; 85)
a. ECG (electrocardiogram): most important diagnostic tool for angina. An ECG shows changes both during symptoms and in response to
treatment. An ECG may also demonstrate pre-existing structural or ischemic heart disease.
b. Laboratory Values:
 Biomarkers (“cardiac enzymes”): released from heart muscle after myocardial injury. Necrosis causes increased permeability of cell
membranes which releases enzymes into blood stream. Enzymes altered due to defibrillation, intramuscular injection, thrombolytic
therapy, PTCA, arthrectomy, stent.
 Troponin I: A protein found in striated muscle and is specific to myocardial muscle necrosis. Preferred biomarker to diagnose
myocardial necrosis. Rises within 3 to 6 hours and peaks within 12 to 16 hours, remains elevated for 14 days.
 Troponin T: release kinetics similar to Troponin I. Remains elevated for 14 days. False-positive results may occur in patients with
renal failure. Minor elevations in Troponin T also identify patients at risk for subsequent cardiac events.
 C-reactive protein (CRP): a marker of acute inflammation. Patients without biochemical evidence of myocardial necrosis but
elevated CRP level are at increased risk of an adverse event.
 Erythrocyte sedimentation rate (ESR): rises above reference range values within three days, may remain elevated for weeks.
 Myoglobin: a nonspecific muscle protein released with any type of muscle damage. Levels rise within 1 to 3 hours and peak at 9 to
12 hours. May be useful for early detection of myocardial infarction when performed with other studies.
 CK-MB: rises within 4 to 6 hours and peaks in 16 to 30 hours. The CK-MB isoenzyme is specific for cardiac injury.
 LDH rises within 24 hours, peaks 3 to 6 days; increased with myocardial infarction, liver disease, lung disease and hematologic
conditions.
c. Basic metabolic panel, including electrolytes, BUN, Cr, magnesium, CBC:
 Hypokalemia: ECG change: increase in PVC's, "U"-wave, depressed ST-segment, flattened T-wave; potentiates digoxin toxicity.
 Hyperkalemia: ECG change: tented T-wave, flattened P-wave, widened QRS leading to asystole
 Hypercalcemia: potentiates digoxin toxicity
 Hypomagnesemia: ventricular dysrhythmias; potentiates digoxin toxicity
 Hypermagnesemia: bradycardia; prolonged P-wave; widened QRS.
 Creatinine levels must be considered prior to initiating ACEI (52)
 CBC to determine if anemia was the precipitant
d. Imaging Studies: (6; 33)
 CXR: provides information on alternative diagnoses (e.g., pneumonia, thoracic aneurysm) or demonstrates complications of ischemia
(e.g. pulmonary edema).
 Echocardiogram: detects wall motion abnormalities due to ischemia or precipitants (e.g. ventricular hypertrophy, valvular disease).
 Radionuclide myocardial perfusion imaging:
 Dual-source 64-slice CT scanners: visualize both the lumen of the coronary artery and plaque within the artery. May also be used
with IV contrast to determine if a stent or graft is open or closed.
 Technetium-99m (99mTc) tetrofosmin single-photon emission computed tomography (SPECT): may be used in the Emergency
Department to exclude high-risk patients among those with chest pain.
 Resting cardiac MRI: detects high fraction of patients with ACS (including enzyme-negative unstable angina), wall thinning, scar,
delayed enhancement (e.g., infarction) and wall motion abnormalities (e.g., ischemia).
 Pharmacologic stress echocardiogram: evaluates effect of increasing myocardial O2 demand by infusing inotropic drug (e.g.
dobutamine) on blood supply to myocardium. Pharmacologic stress echocardiogram takes the place of exercise stress testing for
patients unable to perform vigorous exercise.
e. Graded exercise test (GXT): evaluates the effect of physical activity (increased myocardial O2 demand) on the blood supply to myocardium.
May be combined with Technetium (99mTc) or Cardiolite if resting ECG has nonspecific ST-segment/T wave changes or if patient has
preexisting bundle branch block.
2. Management of ACS: (5; 33; 85) The primary goals of therapy for patients with ACS are to reduce the amount of myocardial necrosis, prevent
major adverse cardiac effect (MACE) and treat acute life-threatening complications [e.g., ventricular fibrillation/pulseless ventricular tachycardia,
symptomatic bradycardia and unstable tachycardia]. The most common interventions include anti-ischemic therapy [e.g., O2 to decrease O2
demand, nitrates (Note: Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction
within the last 24 hours (48 hours for tadalafil)] (6) pain control (morphine), beta blockers, fibrinolytic therapy, anticoagulant therapy, ACEIs,
angiotensin receptor blockers (ARBs), calcium antagonists, HMG CoA reductase inhibitor (statin therapy), antidysrhythmic therapy, early invasive
strategy (catheterization and coronary revascularization), pacemaker, and risk factor modification. See the American Heart Association (AHA)
algorithm for ACS at http://circ.ahajournals.org/cgi/content/short/112/24_suppl/IV-89. Although ARBs and ACEIs are indicated for ACS, they are
contraindicated in the following conditions: chronic cough (a phenomenon caused in some patients by ACE inhibitors possibly related to
increased bradykinin levels), angioedema (a rare but potentially serious side effect), hypotension, hyperkalemia and worsening renal function.
(52)
3. Behavior modification/lifestyle changes: Cardiac rehabilitation program to educate patient/S.O. on low fat/low cholesterol diet, increased
physical activity, stress reduction, smoking cessation, BP and blood sugar control. Specific patient populations will also require counseling for
methamphetamine addiction. (85)
4. Women’s health and cardiovascular disease: Heart disease is the leading cause of death for women both in the United States and in most of
the industrialized world. More than 9,000 US women younger than 45 years sustain a myocardial infarction each year. Among survivors of
myocardial infarction, 25 percent of men versus 38 percent of women die within a year after an initial myocardial infarction. Within six years after
a myocardial infarction, 18 percent of men but 35 percent of women will have a recurrent infarction. Women have a cardioprotective effect of
estrogen, but at 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. (33) Women have more
symptoms of angina than do men following percutaneous coronary intervention, with resultant limitations on their activities and quality of life.
Women have a mortality rate from coronary artery bypass graft (CABG) surgery that is almost double that of their male peers, with women
younger than age 50 years three times more likely to die at CABG surgery than comparably aged men. An excess of bleeding complications
(unexplained pathogenesis) is reported for women who undergo all interventional procedures (e.g., coronary thrombolysis, percutaneous
coronary interventions, CABG surgery), likely contributing to the adverse outcomes for women. (87) Women are more likely to delay seeking
treatment for heart disease. Treatment-seeking delay is defined as the period between onset of symptoms and entry into the healthcare system.
While transport times and therapy times (arrival at the Emergency Department until initiation of medical treatment) have improved, women still
have delayed decision times (interval from onset of acute symptoms to the decision to seek care and act on their decision). (79) Cardiovascular
education targeted specifically for women may be beneficial in improving delay times. Recommendations: The most publicized
recommendations revolve around hormone replacement therapy (HRT). HRT is no longer recommended for cardiac health in women and has
actually been shown to be harmful in some populations. All women should be encouraged to avoid tobacco, exercise regularly, maintain a
healthy weight and eat a heart-healthy diet (including omega-3 fatty acids and folic acid). BP management is key and antihypertensives should
be initiated to maintain BP less than 120/80 mmHg. Blood sugars should be kept at near-normal glycosolated hemoglobin levels. All women
with cardiovascular disease should be evaluated for depression and treated appropriately. For complete risk scoring, refer to the Evidence-
Based Guidelines for cardiovascular health in women at http://circ.ahajournals.org/cgi/content/full/109/5/672.
D. PATIENT/FAMILY RESOURCES:
1. American Heart Association: Heart Attack, Stroke & Cardiac Arrest Warning Signs
http://www.americanheart.org/presenter.jhtml?identifier=3053#Heart_Attack
2. Page 46 of ICSI guideline lists all resources available to families
E. SAFETY CONSIDERATIONS AND INITIATIVES:

1. Acute Myocardial Infarction:
Centers for Medicare & Medicaid Services and the Joint Commission:
 National Hospital Performance Measure: Acute Myocardial Infarction National Hospital Inpatient Quality Measures. Specifications Manual
for National Hospital Inpatient Quality Measures. Last updated 12/17/2012. Retrieved from:
http://www.jointcommission.org/specifications_manual_for_national_hospital_inpatient_quality_measures.aspx
Safer Healthcare Now!:
 Getting Started Kit: Improved Care for Acute Myocardial Infarction, How to Guide. Last updated 7/2011. Retrieved from:
http://www.saferhealthcarenow.ca/EN/Interventions/ami/Documents/AMI%20Getting%20Started%20Kit.pdf
AACN:
 Practice Alert: ST Segment Monitoring. Last updated 5/2009. Retrieved from:
http://www.aacn.org/WD/Practice/Docs/PracticeAlerts/ST_Segment_Monitoring_05-2009.pdf
2. Pain:
The Joint Commission:
2013 Hospital Accreditation Standards:
 Provision of Care:
Standard PC.01.02.07: The hospital assesses and manages the patient’s pain.
Standard PC.02.03.01: The hospital provides patient education and training based on each patient’s needs and abilities.
 Rights and Responsibilities of the Individual: Standard RI.01.01.01: The hospital respects, protects and promotes patient rights.
The Joint Commission International:
2011 Accreditation Standards for Hospitals, 4th ed. (2010):
 Patient and Family Rights: Standard PFR.2.4: The organization supports the patient’s right to appropriate assessment and management
of pain.
 Assessment of Patients: Standard AOP.1.7: All inpatients and outpatients are screened for pain and assessed when pain is present.
 Care of Patients: Standard COP.6: Patients are supported in managing pain effectively.
 Patient and Family Education: Standard PFE.4: Patient and family education includes the following topics, related to the patient’s care:
the safe use of medications, the safe use of medical equipment, potential interactions between medications and food, nutritional guidance,
pain management and rehabilitation techniques.
3. Venous Thromboembolism:
The Joint Commission:
 Performance Measurement. Core Measure Set: Venous Thromboembolism (VTE) Measures. Last updated 12/17/2012. Retrieved from:
http://www.jointcommission.org/specifications_manual_for_national_hospital_inpatient_quality_measures.aspx
2012 Hospital Accreditation Standards:
National Patient Safety Goal:
NPSG 3: Improve the safety of using medications.
NPSG.03.05.01: Reduce the likelihood of patient harm associated with the use of anticoagulant therapy.
National Quality Forum:
 Safe Practices for Better Healthcare – 2010 Update (3/2011): Safe Practice 28 Venous Thromboembolism Prevention: Evaluate each
patient upon admission, and regularly thereafter, for the risk of developing venous thromboembolism. Utilize clinically appropriate,
evidence-based methods of thromboprophylaxis.
 Safe Practice 29 Anticoagulation Therapy. Organizations should implement practices to prevent patient harm due to anticoagulant therapy.
Institute for Healthcare Improvement:
 Improvement Map: Venous Thromboembolism (VTE) Prevention and Treatment Process. Retrieved from:
http://www.ihi.org/imap/tool/#Process=5b9bfd5a-1e17-433b-a9d4-602fafef73c8
Safer Healthcare Now!:
 Getting Started Kit: Venous thromboembolism Prevention, How to Guide. Last updated 5/2012. Retrieved from:
http://www.saferhealthcarenow.ca/EN/Interventions/vte/Documents/VTE%20Getting%20Started%20Kit.pdf
U.S. Department of Health and Human Services:
 The Surgeon General’s Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. Last updated 2008. Retrieved from:
http://www.surgeongeneral.gov/topics/deepvein/calltoaction/call-to-action-on-dvt-2008.pdf
AACN:
 Practice Alert: Venous Thromboembolism Prevention. Last updated 4/2010. Retrieved from:
http://www.aacn.org/WD/Practice/Docs/PracticeAlerts/VTE%20Prevention%2004-2010%20final.pdf
F. Refer to Heart Failure, Cardiac Catheterization with/without Percutaneous Coronary Intervention (PCI), Cardiac Rhythm Management Device
(CRMD) [Includes Pacemaker, Implantable Cardioverter Defibrillator (ICD) and Cardiac Resynchronization Therapy Device (CRT/CRT-D)]
and/or Cardiac Surgery Clinical Practice Guidelines that may apply to the medical diagnosis, treatment, procedure.
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Clinical Practice Guideline:

ACUTE CORONARY SYNDROME (ACS)

A. Signs and symptoms of listed potential problems will be absent or manageable.

Hemodynamic Instability AEB: (6; 44; 61; 65)

Pericarditis leading to Pericardial Effusion AEB:

Cardiovascular Structural Defects AEB: (6; 85)

Mural Thrombosis leading to Embolism AEB:

51. Initiate strategies to prevent/treat DVT/VTE:

Acute Pain AEB: (19)

A. CLINICAL DESCRIPTION: (33)

B. PATHOPHYSIOLOGY/ETIOLOGY/RISK FACTORS FOR POTENTIAL PROBLEMS:

E. SAFETY CONSIDERATIONS AND INITIATIVES:

88Zevitz, M. E. (2006). Ventricular fibrillation. Retrieved from eMedicine [Level VII, +]

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