The document outlines the management and diagnosis of acute chest pain in patients, emphasizing the importance of detailed history and physical examination. It details protocols for emergency response, including the use of aspirin, nitroglycerin, and cardiac monitoring, and discusses various electrocardiographic manifestations of ischemia. Furthermore, it addresses risk stratification tools and the management of both ST elevation and non-ST elevation acute coronary syndromes.

1. By
DR.SALAH ELDOKANY
M.D.CARDIOLOGY
CARDILOGY
CONSULTANT
Madinah Munawarah
KSA
Meeqat General
Hospital Medical
Complex

2. EPIDEMIOLOGY IN PRIMARY
CARE POPULATIONS
60 percent not "organic" in origin (
36 percent Musculoskeletal chest pain out of which 13%
reflux eosophigitis
11 percent Stable angina pectoris
1.5 percent unstable angina or myocardial infarction

3. The correct diagnosis is most often derived from a vigilantly obtained, detailed
history:
 pain description;
 associated symptoms;
 and in some cases disease risk factors
supported by specific physical findings, an electrocardiogram, and/or chest x-ray

4. EMERGENCY RESPONSE TO CHEST
PAIN IN THE OFFICE
– potentially unstable based upon
1. history,
2. appearance,
3. or vital signs,
– should be transported immediately to an emergency department in an
ambulance equipped with a defibrillator.

5. Primary approach
– Stabilization of such patients
should begin in the prehospital
setting
1. intravenous access,
2. placement of a cardiac monitor,
3. and supplemental oxygen if
breathlessness, hypoxemia, or
signs of heart failure or shock are
present
– Noninvasive monitoring of oxygen
saturation may be used to decide
on the need for oxygen
administration.
– A 12-lead electrocardiogram and a
blood sample for cardiac enzyme
measurement should be obtained
if possible.

6. Prehospital management
– Patients who are thought to be experiencing an acute coronary syndrome (ACS)
should chew a 325 mg aspirin tablet.
– Sublingual nitroglycerin should be given for chest pain unless the patient has
relatively low blood pressure without intravenous access or has recently taken a
phosphodiesterase inhibitor such as sildenafil (Viagra™).

8. In the emergency department
(ED)
– patients presenting with chest pain should be rapidly evaluated to determine if
their symptoms are suggestive of acute ischemia,
– or some other potentially life-threatening illness.

9. Chest pain suggestive of acute coronary syndrome
Triage for rapid care
Focused history and examination
Asperin 160-325 mg
SL nitroglycerin 0.4 mg every 5 min for 3 doses
Morphine sulphate 2-4 mg iv initially then 2-8 mg
every 5-15 min as needed
GOAL is 10 min
Intravenous access
Initial lab including serum biomarkers
Continuous ECG monitoring (with emergency
defibrillator and airway equipment)
Initial supplementation of O2 > 90 %

10. Initial 12 leads ECG ; if not diagnostic repeat ever 5- 10 min
ST elevation / new LBBB Strong suspicion of ischemia
but no persistent ST elevation
Normal/ non diagnostic ECG
with negative biomarkers
Anticoagulation
Betablockers if no
contraindication
Intravenous nitroglycerin unless
contraindicated
Anticoagulation
Beta-blockers if no
contraindication
Intravenous nitroglycerin unless
contraindicated
Continue evaluation and
monitoring in ED / moitored
bed
ECG /cardiac enzymes every 6-
12 hr
Perimary PCI goal less thann 90
min
OR
Thrombolysis with goal of 30
min
ST depression
Elevated cardiac
biomarkers
Persistent chest pain
HD instability
TIMI Score ≥ 3
Look for high risk
features:
Cathetrization for high risk and medical
therapy for low risk
Evidence of ischemia
or infarction
Treat for
non ST elevation
ACS
Stress test
or
Imaging
study
yesNo

11. HINTS

12. history and focused physical
examination
– presenting symptoms, characteristics of the pain and important associated
symptoms, past history of or risk factors for cardiovascular disease, and
potential contraindications to thrombolytic therapy
– potentially emergent noncardiac causes of chest pain, such as acute aortic
dissection, pulmonary embolism, tension pneumothorax, perforating peptic
ulcer, and esophageal rupture
– Examination should address hemodynamic status and a screening neurologic
examination, especially if thrombolysis is entertained as a potential therapy.

13. Deferential diagnosis for ischemic
cardiac pain

15. EKG
who is in need ??
– Any patient over 30 with chest pain
– Any patient over 50 with any of the following: dyspnea, altered mental status,
upper extremity pain, syncope, or weakness
– Any patient over 80 with abdominal pain, nausea, or vomiting
This proposed rule should not replace clinical judgement
Glickman SW, Shofer FS, Wu MC, et al. Development and validation of a prioritization rule for
obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-
elevation myocardial infarction. Am Heart J 2012; 163:372.

16. EKG
– When present, ECG abnormalities are an early sign of myocardial ischemia. Criteria
for the two major categories of electrocardiographic manifestations of acute
myocardial ischemia are listed here:
– Findings consistent with ST elevation myocardial infarction (STEMI): New ST
elevation at the J point in two anatomically contiguous leads using the following
diagnostic thresholds: ≥0.1 mV (1 mm) in all leads other than V2-V3, where the
following diagnostic thresholds apply: ≥0.2 mV (2 mm) in men 40 years; ≥0.25 mV
(2.5 mm) in men <40 years, or ≥0.15 mV (1.5 mm) in women.
– Findings consistent with Non ST elevation myocardial infarction or unstable
angina: New horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two
anatomically contiguous leads and/or T inversion ≥0.1 mV (1 mm) in two
anatomically contiguous leads with prominent R wave or R/S ratio >1.
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial
infarction. Circulation 2012; 126.

17. Localization of the lesion
– Anterior wall ischemia – Two or more of the precordial leads (V1-V6)
– Anteroseptal ischemia – Leads V1 to V3
– Apical or lateral ischemia – Leads aVL and I, and leads V4 to V6
– Inferior wall ischemia – Leads II, III, and aVF
– Right ventricular ischemia – Right-sided precordial leads
– Posterior wall ischemia – Posterior precordial leads
– The right-sided leads V4R, V5R, and V6R should be obtained if there is evidence of inferior
wall ischemia, demonstrated by ST elevation in leads II, III, and aVF.
– The posterior leads V7, V8, and V9 may also be helpful if there is evidence of posterior wall
ischemia, as suggested by prominent R waves and ST depressions in leads V1 and V2.

23. – The initial ECG is often NOT diagnostic in patients with ACS.
– In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20
percent of patients subsequently shown to have an acute MI.
– In the early hours of infarction, peaked, hyperacute T waves may be the only
abnormality. In addition to evolution of the ECG, an uncommon source of error
is pseudonormalization of baseline T wave inversion
Pope JH, Ruthazer R, Beshansky JR, et al. Clinical Features of Emergency Department
Patients Presenting with Symptoms Suggestive of Acute Cardiac Ischemia: A Multicenter
Study. J Thromb Thrombolysis 1998; 6:63.
Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated serial 12-lead ECG
monitoring during the initial emergency department evaluation of patients with chest pain.
Ann Emerg Med 1998; 31:3.

24. CLINICAL PRESENTATION

25. CLINICAL PRESENTATION
– characteristics of the patient's chest discomfort and associated symptoms
increase the likelihood of ACS, while others make the diagnosis unlikely.
– Of note, older patients, diabetics, and women are more likely to present with
symptoms such as dyspnea, weakness, nausea and vomiting, palpitations, and
syncope, and may not manifest chest discomfort.

26. Ischemic chest pain

27. Onset
– Ischemic pain is typically gradual in onset, although the intensity of the
discomfort may wax and wane.

28. Provocation and palliation
– provoked by an activity, such as exercise, which increases cardiac oxygen
demand
– does not change with respiration or position.
– It may or may not respond to nitroglycerin and, if there is improvement, this
may only be temporary.

29. Quality
often characterized more as a discomfort than pain, and it may be difficult for the
patient to describe.
– squeezing,
– tightness,
– pressure,
– constriction,
– crushing,
– strangling,
– burning,
– heartburn,
– fullness in the chest,
– band-like sensation,
– knot in the center of the
chest,
– lump in throat,
– ache,
– heavy weight on chest
(elephant sitting on chest),
like a bra too tight,
– and toothache (when there
is radiation to the lower
jaw).
It is generally not described as sharp, fleeting, knife-like, stabbing, or pins and needles-like
Increased pain severity does not appear to correlate with an increased likelihood of acute MI
In some cases, the patient cannot qualify the nature of the discomfort but places his or her
clenched fist in the center of the chest, known as the "Levine sign."

30. Radiation
– Ischemic pain often radiates to other parts of the body including the upper
abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers,
neck and throat, lower jaw and teeth (but not upper jaw),
– and not infrequently to the back (specifically the interscapular region)
– Pain radiating to the upper extremities is highly suggestive of ischemic pain

31. Site
– Ischemic pain is not felt in one specific spot, but rather it is a diffuse discomfort
that may be difficult to localize.
– The patient often indicates the entire chest, rather than localizing it to a
specific area by pointing a single finger.

32. Time course
– Angina is usually brief (two to five minutes) and is relieved by rest or
with nitroglycerin.
– In comparison, patients with an acute coronary syndrome (ACS) may have chest
pain at rest, and the duration is variable but generally lasts longer than 30
minutes.
– Classic anginal pain lasting more than 20 minutes suggests ACS.

33. Historical features increasing
likelihood of ACS
– prior history of ACS
– other vascular disease
– Risk factors for ACS, particularly age, male sex, diabetes, hypertension,
hyperlipidemia, and cigarette smoking
– Recent cocaine use

34. –Associated symptoms
The most common is shortness of breath,
– which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic
dysfunction.
– Other symptoms may include belching,
– nausea,
– indigestion,
– vomiting,
– diaphoresis,
– dizziness,
– lightheadedness,
– clamminess,
– and fatigue.

35. NONischemic chest discomfort
– Pleuritic pain, sharp or knife-like pain related to respiratory movements or
cough
– Primary or sole location in the mid or lower abdominal region
– Any discomfort localized with one finger
– Any discomfort reproduced by movement or palpation
– Constant pain lasting for days
– Fleeting pains lasting for a few seconds or less
– Pain radiating into the lower extremities or above the mandible
Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is
this patient having a myocardial infarction? JAMA 1998; 280:1256.
Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of
patients with suspected acute coronary syndromes. JAMA 2005; 294:2623.

36. – In a review of over 430,000 patients with confirmed acute myocardial infarction
(MI) from the National Registry of Myocardial Infarction II, one-third had no
chest pain on presentation to the hospital
– These patients often present with symptoms such as dyspnea alone, weakness,
nausea and/or vomiting, palpitations, syncope, or cardiac arrest. They are more
likely to be older, diabetic, and women
Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and
mortality among patients with myocardial infarction presenting without chest pain. JAMA
2000; 283:3223.

38. PHYSICAL EXAMINATION

39. PHYSICAL EXAMINATION
– Responsiveness, airway, breathing and circulation according to guidelines of
ACLS

40. CPR: cardiopulmonary
resuscitation; ET: endotracheal
tube; EtCO2: end tidal carbon
dioxide; IO: intraosseous; IV:
intravenous; PEA: pulseless
electrical activity; VF:
ventricular fibrillation; VT:
ventricular tachycardia.
Reprinted with permission. Adult
Advanced Cardiovascular Life
Support: 2010. American Heart
Association Guidelines for
Cardiopulmonary Resuscitation
and Emergency Cardiovascular
Care. © 2010 American Heart
Association, Inc.

41. Cardiac enzymes
– Troponin as a predictive value for mortality

42. Plasma troponin T
Mortality rates at 30 days related to the plasma level of cardiac troponin T measured
at baseline in 801 patients presenting with symptoms and ECG changes of acute
ischemia. There is a progressive increase in mortality with higher troponin levels.
Data from Ohman EM, Armstrong PW, Christenson RH, et al. N Engl J Med 1996;
335:1333.

43. Kaplan-Meier estimates of survival show that a positive serum troponin, obtained any time during the
first 24 hours after admission for an acute coronary syndrome, predicts a higher mortality at 30 days
and one year.
Data from Newby LK, Christenson RH, Ohman M, et al. for the GUSTO IIa Investigators, Circulation

44. Trponin I
Mortality rate at 42 days according to the level of cardiac troponin I measured at baseline in 1404 patients with
unstable angina or non-Q wave myocardial infarction. There was a progressive increase in risk with higher
troponin levels.
Data from Antman EM, Tanasijevic MJ, Thompson B, et al. N Engl J Med 1996; 335:1342.

46. EARLY RISK STRATIFICATION
– TIMI risk score
– TIMI risk index
– ACCF/AHA classification
– GRACE risk models
– CHADS2 score
– Patients at low risk
– Individual risk factors

47. LATE RISK STRATIFICATION
– Left ventricular function
– Right ventricular function
– Stress testing
– Candidates for testing
– Timing
– Stress protocol
– Stress testing in women
– Continuous electrocardiography

48. LATE RISK STRATIFICATION
– Left ventricular function
– Right ventricular function
– Stress testing
– Candidates for testing
– Timing
– Stress protocol
– Stress testing in women
– Continuous electrocardiography

49. TIMI score
– To calculate the score, a value of one is assigned when each variable was
present and 0 when it was absent
1. Age ≥65 years
2. Presence of at least three risk factors for CHD
3. Prior coronary stenosis of ≥50 percent
4. Presence of ST segment deviation on admission ECG
5. At least two anginal episodes in prior 24 hours
6. Elevated serum cardiac biomarkers
7. Use of aspirin in prior seven days

50. A higher TIMI risk score correlated significantly with increased numbers of
events (all-cause mortality, new or recurrent MI, or severe recurrent
ischemia requiring revascularization) at 14 days
– Score of 0/1 — 4.7 percent
– Score of 2 — 8.3 percent
– Score of 3 — 13.2 percent
– Score of 4 — 19.9 percent
– Score of 5 — 26.2 percent
– Score of 6/7 — 40.9 percent
A similar predictive value has been noted for postdischarge events at six weeks and for major cardiac events
at 30 days in patients who have undergone PCI, which is now performed in most patients with a non-ST ACS

51. ACCF/AHA classification

53. LATE RISK STRATIFICATION
– Left ventricular function
– Right ventricular function
– Stress testing
– Candidates for testing
– Timing
– Stress protocol
– Stress testing in women
– Continuous electrocardiography

55. MANAGEMENT

57. MANAGEMENT
ST elevation
– Selection and implementation of the optimal reperfusion strategy is the most
important step in the management of STEMI
– Reperfusion therapy, whether percutaneous coronary intervention (PCI) or
thrombolytics, should NOT await the result of cardiac biomarker measurement.
– Rapid implementation of primary PCI is more likely to be achieved if the
hospital protocol involves immediate activation of the PCI team by the
emergency clinician and immediate transfer of the patient to the
catheterization laboratory

59. MANAGEMENT
Non-ST elevation

61. ACS with no evidence of ischemia or
infarction

63. Stress testing
– Stress testing, usually with exercise, can be used to detect residual ischemia and
to assess the exercise capacity needed for the cardiac rehabilitation exercise
prescription

64. Candidates for testing
– Predischarge stress testing to detect residual ischemia is generally not
performed in patients who have undergone PCI or CABG and have
been fully revascularized
– Such patients often undergo exercise testing a few weeks or more after
discharge as part of a cardiac rehabilitation program or for activity counseling.

65. Candidates for testing
– In contrast, patients who have undergone partial revascularization or no
revascularization are candidates for predischarge testing, but should be
properly screened.

66. Exercise testing appears to be
safe if
– he patient has undergone in-hospital cardiac rehabilitation
– There have not been symptoms of heart failure or recurrent angina for 12 to 24
hours
– The electrocardiogram has been stable for 12 to 24 hours

67. Timing
– before or after soon after discharge.
– While the high-risk patient will often undergo an invasive study, lower-risk
patients may undergo stress testing after being symptom free and stable for 12
to 24 hours.

68. Stress protocol
– varies with physician preferences,
– patient characteristics,
– and local laboratory expertise.

69. – Exercise ECG testing, which is most often performed, relies on both symptoms
and objective changes on the ECG.
– In selected low risk patients (ie, without heart failure, arrhythmias, or angina),
an early full Bruce (symptom limited) protocol has been safely completed as
early as 24 hours or before discharge

70. Other consideration
– Cocaine-related ACS: Give benzodiazepines (eg, Lorazepam 2 to 4 mg IV every
15 minutes or so) as needed to alleviate symptoms; do NOT give beta blockers
– Stop NSAID therapy if possible
– Correct any electrolyte abnormalities, especially hypokalemia and
hypomagnesemia

71. Cardiac arrhythmias during
ACS
– Sustained ventricular tachyarrhythmias in the peri-infarction period must be
treated immediately as previously noted in ACLS guidelines
– supraventricular tachyarrhythmias in the peri-infarction period may pose less
immediate risk of cardiac arrest

74. Cardiac arrhythmias during
ACS
– Sustained ventricular tachyarrhythmias in the peri-infarction period must be
treated immediately as previously noted in ACLS guidelines
– supraventricular tachyarrhythmias in the peri-infarction period may pose less
immediate risk of cardiac arrest
– Bradyarrhythmias occurring early in the setting of an inferior wall MI (within the
first 24 hours) may respond to treatment with atropine
– Later bradyarrhythmias, wide QRS-complex bradyarrhythmias, and those
occurring in the setting of an anterior wall MI may require temporary
pacemaker placement

75. Disposition of patient without
STEMI
– For patients without STEMI, the ECG remains a critical component in
determining risk for adverse outcomes in ACS. The patient's hemodynamic
status, serum biomarkers, and historical risk factors, as well as available hospital
resources, should also be used to determine appropriate disposition.

76. High-risk patient
– The patient has a high-risk ACS if ST segment depression (≥0.05 mV [0.5 mm]) is
present in two or more contiguous leads,
– elevated serum biomarkers,
– and/or the TIMI risk score is ≥5.

77. High-risk patient
1. This patient is typically admitted to an intensive care unit, coronary care unit,
or monitored cardiac unit depending upon the persistence of symptoms and
evidence of hemodynamic compromise.
2. Those with persistent pain or hemodynamic compromise generally undergo
urgent angiography and revascularization.
3. Others with resolution of symptoms and stable hemodynamics are typically
referred for early elective angiography and revascularization if appropriate.

78. High-risk patient
– If there is no ST segment elevation or depression or new LBBB, regardless of the
presence or absence of Q waves, the patient with definite or probable ACS
should still be admitted to a monitored care unit for further evaluation.
– Those patients manifesting high-risk features either on presentation or during
their emergency department course should be admitted and considered for
early PCI.

79. Low and moderate risk patient
– Make an initial determination of the likelihood of ACS after the history, physical
examination and serial (two or three) electrocardiograms have been performed
– As shown in next table

80. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Writing Committee to revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation).

81. Low and moderate risk patient
– Make an initial determination of the likelihood of ACS after the history, physical
examination and serial (two or three) electrocardiograms have been performed
– Consider alternative life-threatening diagnoses.
– Reassess the likelihood of ACS and assess the short-term risk of an adverse
event after return of the first and second biomarkers.
– If after reassessment, the patient is felt to be at low or intermediate risk of an
adverse event, noninvasive diagnostic testing is generally performed.
– If after reassessment, the patient is felt to be at low or intermediate risk of an
adverse event, noninvasive diagnostic testing is generally performed.

82. FINAL DISPOSITION —
– The final disposition decision in most patients will occur after clinical observation,
serial cardiac markers, serial ECGs, and cardiac stress testing or imaging:
1. Patients with indeterminate stress testing or imaging results may benefit from
cardiology consultation if not already obtained. Many such patients will be
admitted.
2. Patients with positive stress testing or imaging results should be evaluated by a
cardiologist and admitted to the hospital.
3. If the results of this testing are negative for a cardiac cause, and other life
threatening components of the differential diagnosis have been ruled out,
discharge home is appropriate for stable patients. These patients are labeled as
having noncardiac chest pain.