approach to chest pain.ppt

1. Approach to Chest painApproach to Chest pain

2. Presented by
Dr Ashraf-ur-Rahman Tamal
Asst Regitrar, MU VIII
DMCH

3. Chest PainChest Pain
5 Million emergency department visits
2 million hospitalizations annually with cost of
more than $8 billion
Cardiac etiology found <1/3rd
2% of patients with acute MI are unrecognized
and discharged from the ED

4. D/D of Chest painD/D of Chest pain
 Musculoskeletal 36% (costochondritis, strain)
 Gastrointestinal 19% (GERD, E.spasm,cholelithiasis)
 Nonspecific chest pain 16%
 Angina 11% (MI, Angina pectoris, UA)
 Psychosocial 7% (somatization, anxiety)
 Pulmonary causes 5% (PE, Pneumothorax,
pneumonia)
 Other causes of chest pain (AD, AS,
pericarditis) 4%

5. INITIAL APPROACHINITIAL APPROACH
Assume the worst!
100% Oxygen
IV access
Monitoring
ECG quickly
Done in tandem with history taking

6. CHEST PAIN ASSESSMENTCHEST PAIN ASSESSMENT
HISTORY
EXAMINATION
ECG
CARDIAC ENZYMES
CXR
OTHERS

7. Clinical Approach to Chest PainClinical Approach to Chest Pain
History: A- Pain analysis
1- Characteristic:
Sharp 
Squeezing heaviness pressure
Stabbing 
Pluritic 
Tearing 
Burning 
Pericarditis, HZPericarditis, HZ
MI, AnginaMI, Angina
pericarditispericarditis
PEPE,, PneumoniaPneumonia
ADAD
GERDGERD

8. ContCont’’d.. approachd.. approach
2- Site of pain: retrosternal, plural,
epigastric)
3- Radiation:
Neck 
Back (interscapular) 
Neck, jaw, shoulder, Lt arm 
4- Onset:
Sudden
Gradual 
MI,MI,
AnginaAngina
ADAD
E. spasmE. spasm
MI, PE, Pneumothorax, ADMI, PE, Pneumothorax, AD
MSK, GI,MSK, GI,
pneumonia, HZpneumonia, HZ

9. ContCont’’d.. approachd.. approach
5- Duration:
< 15 min ( 2- 10) min  Stable Angina
Upto 30 min  MI, UA
Upto 60 min  E.spasm
Few hours  PE, pnumothorax
Hours to days  pericarditis
Longer  HZ
NOTE: <2/3 min less likely to be cardiac.

10. ContCont’’d.. approachd.. approach
6- Aggravating:
Exertion, cold, stress, meals  ischemia
Swallowing, postprandial, smoking  GI
Deep breathing, movement  MSK,
pericarditis
Deep breathing  PE, Pneumothorax
NOTE: HZ is not aggravated by anything

11. ContCont’’d.. approachd.. approach
7- Relieving factors:
Rest or GTN  angina
Sitting up, leaning forward  pericarditis
Antacid or food  GI causes
GTN  E.spasm
NOTE: Severity doesn’t indicate
seriousness.

12. ContCont’’d.. approachd.. approach
8- Associated symptoms:
Cough, fever, sputum, dyspnea.
Sweating.
Nausea, vomiting .
Heamoptysis.
Heartburn, regurgitation.
Palpitations.
Psychiatric symptoms: Anxiety, depression, panic
attack

13. Physical examinationPhysical examination
A- Vital signs:
- Hypotension can occur in MI,
pericardial temponade, PE, GI bleeding.
- Fever suggests an infectious disease.
B- Inspection and palpation:
- may reveal the rash of shingles,
crepitus associated with rib fracture,
localized pain, signs of trauma.
Hyperesthesia, particularly when
associated with a rash, is often due to
herpes zoster.

14. PHYSICAL EXAM….CONTPHYSICAL EXAM….CONT
C- Cardiopulmonary examination:
In MI may have audible S4, signs of LVF
such as S3,
pericarditis may cause friction rub and
pulsus paradoxus,
BECK’S TRIAD ( JVP, muffled heart
sounds, low BP) suggests cardiac
temponade.
BP variation in both limbs (AD)
Determine if the breath sounds are
symmetric and if there’s wheezes, crackles
etc

15. DIAGNOSTIC EVALUATION:DIAGNOSTIC EVALUATION:
ECG
Cardiac markers: Troponins are the 1st
enzymes to rise and remain elevated for 5 to 14
days.
Echocardiogram: pericardial effusion, valvular
heart disease.
Chest X-ray: Pneumothorax, pnuomonia
Spiral CT, if PE is suspected.

16. DIAGNOSTIC EVALUATIONDIAGNOSTIC EVALUATION
ANA, BUN, Creatinine, TSH, Tuberculosis
skin test , for pericarditis.
Esophageal pH monitoring, if GERD is
suspected.
Patients with musculoskeletal chest pain
might not require any diagnostic testing.

17. LIFE THREATENING CAUSESLIFE THREATENING CAUSES

P is Pericarditis.
A is Acute myocardial infarction.
P is Pneumothorax
P is Pulmonary embolism
A is Aneurysm ( AD)

18. Pulmonary EmbolismPulmonary Embolism
Physical:
Anxious patient, sense of impending doom.
Tachycardia, tachypnea, hypoxia.
If severe, can get hypotension, syncope, and RV
failure ( JVP, RV heave)↑

19. Pulmonary EmbolismPulmonary Embolism
History:
Sudden-onset, sharp
Exacerbated by inspiratory effort
Associated with hemoptysis, sycope, dyspnea, calf
swelling/pain from DVT
Risk factors: immobilization, fracture of a limb, post-
operative complications, hypercoagulable states
(underlying carcinoma, high-dose exogenous estrogen
administration, pregnancy, inherited deficiencies of
antithrombin III, activated protein C, S, lupus
anticoagulant, prior history of DVT/PE [Virchow’s
triad].

20. Investigations:
↓PaO2 and PaCO2 from increase in overall↓
minute ventilation
D-dimer is sensitive but has a low specificity. Do
NOT order it to rule-in a PE!
CXR:
a. Frequently normal.
b. Often non-specific (atelectasis, pleural
effusion).
c. May see Hampton’s hump (area of
infarction),
ECG: sinus tachycardia most common, S1Q3T3
with large embolus (classic, but rare!), look for
right-axis deviation.
Consider Doppler U/S of legs
Spiral CT / VQ

21. Pulmonary EmbolismPulmonary Embolism
Management:
Anticoagulation to prevent further thrombosis
(heparin initially and then warfarine with
therapeutic INR level of 2-3 for 6 months –
length of therapy still controversial).
Thrombolysis if hemodynamically unstable.
Supportive treatment with oxygen, and fluids.

22. Aortic dissection: PresentationAortic dissection: Presentation
Sharp, “tearing” anterior or posterior
chest and back pain.
Typically sudden onset and severe
Chest pain more common with type A
dissections
Complicated by CVA, syncope, MI (RCA)
or HF

23. Aortic dissection: DiagnosisAortic dissection: Diagnosis
Generally suspected by history/physical
Variations in pulses or blood pressure
(>20 mmHG difference between R and L
arm)
ECG: variable depending on
complications
Imaging when stable
◦ CXR: mediastinal widening
◦ CT chest, TEE, MRI other options and all
superior to TTE

24. Aortic Dissection:Aortic Dissection:
Predisposing factors:
◦ Aortic aneurysm
◦ HTN
◦ Vasculitis
◦ Marfan’s or other collagen diseases
◦ CABG/cardiac catheterizaion
◦ Drugs (crack cocaine)
◦ Trauma

25. Aortic dissection: ClassificationAortic dissection: Classification

26. Aortic dissectionAortic dissection

27. Aortic dissectionAortic dissection

28. Aortic Dissection: ManagementAortic Dissection: Management
Type A: Surgical
Type B and uncomplicated: Medical
Type B and complicated (major branch
involved, continued expansion or aortic
rupture
Long term management includes B
blocker, serial imaging at 3, 6 and 12
months and reoperation if indicated

29. Acute ManagementAcute Management
ICU admission
Pain control: Morphine
Reduction of SBP to 100-120 or lowest
tolerated, HR <60, intubate if unstable
◦ IV B blocker 1st
line (labetolol, propranolol, esmolol)
◦ If HR <60 and SBP >100 with good mentation and
renal function nitroprusside
◦ If hypotensive, look for blood loss, tamponade or HF
prior to giving volume

30. PericarditisPericarditis
Chest pain (anterior chest, sharp,
pleuritic, exacerbated by inspiration, can
decrease with leaning forward, radiation
to trapezius)
Often first sign of other systemic disease
Multiple possible etiologies, viral and
autoimmune most common in US
Consider TB outside US

31. Pericarditis: DiagnosisPericarditis: Diagnosis
Typically need 2/4:
◦ Chest pain
◦ Friction rub
◦ ECG changes (wide spread ST elevation with
PR depression)
◦ Pericardial effusion
Consider tamponade (sinus tachycardia,
JVD, pulsus paradoxus, Kussmaul’s sign)

33. Pericarditis: ECG:Pericarditis: ECG:

34. Pericarditis: TreatmentPericarditis: Treatment
NSAIDs are mainstay of therapy (IBU or
high dose ASA
Can also use colchicine or
glucocorticoids
Tamponade: conservative management
with monitoring, serial echo, volume
expansion and treatment of underlying
cause vs. pericardiocentesis

35. ACSACS

36. Acute Coronary SyndromeAcute Coronary Syndrome
Ischemic Discomfort
Unstable Symptoms
No ST-segment
elevation
ST-segment
elevation
UnstableNon-QQ-Wave
anginaAMIAMI
ECG
Acute
Reperfusion
History
Physical Exam

37. ACS: General principlesACS: General principles
Unstable Angina
◦ Rest angina: Usually >20 minutes duration
◦ New onset severe angina
◦ Increasing angina( Worsening)-Crescendo
Angina
◦ Angina not relieved by GTN
◦ Post MI Angina
NSTEMI
STEMI

38. Symptoms of ACSSymptoms of ACS
Prolonged CHEST PAIN
ANXIETY
FEAR OF IMPENDING DEATH
BREATHLESSNESS
VOMITING
COLLAPSE
SYNCOPE
SILENT

39. SIGNS OF ACSSIGNS OF ACS
SIGNS OF SYMPATHETIC
ACTIVATION
PALLOR
SWEATING
TACHYCARDIA
SIGNS OF VAGAL STIMULATION
VOMITING
BRADYCARDIA

40. SIGNS of ACSSIGNS of ACS
Signs of impaired myocardial function:
Hypotension, Oliguria, Cold peripheries
Narrow pulse pressure
Raised JVP
S3
Quit S1
Diffuse apical impulse
Basal creps

41. ACSACS
INVESTIGATIONSINVESTIGATIONS
ECG HELPFUL
 DIFFICULT INTERPRETATION IN PREVIOUS MI
PATIENTS AND OLD BBB
 RARELY NORMAL ECG
 IN 1/3 OF MI CASES INITIAL CHANGES MAY NOT
BE DIAGNOSTIC
 EARLIEST CHANGE ST ELEVATION
 LATER R WAVE SIZE DIMINUTION
 Q WAVES IN TRANSMURAL MI
 T WAVE INVERSIOn
CHEK AREA OF INFARCTION

42. Unstable Angina NSTEMI STEMI
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes
Occluding thrombus
sufficient to cause
tissue damage &
mild
myocardial necrosis
ST depression+/-
T wave inversion on
ECG
Elevated cardiac
enzymes
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms

43. Normal or non-diagnostic EKGNormal or non-diagnostic EKG

44. ST Depression or Dynamic T waveST Depression or Dynamic T wave
InversionsInversions

45. ST-Segment Elevation MIST-Segment Elevation MI

46. New LBBBNew LBBB
QRS > 0.12 sec
L Axis deviation
Prominent R wave V1-V3
Prominent S wave 1, aVL, V5-V6
with t-wave inversion

47. Wall AffectedWall Affected Leads Showing STLeads Showing ST
Segment ElevationSegment Elevation
Leads ShowingLeads Showing
Reciprocal STReciprocal ST
Segment DepressionSegment Depression
Suspected CulpritSuspected Culprit
ArteryArtery
SeptalSeptal V1, V2V1, V2 NoneNone Left AnteriorLeft Anterior
Descending (LAD)Descending (LAD)
AnteriorAnterior V3, V4V3, V4 NoneNone Left AnteriorLeft Anterior
Descending (LAD)Descending (LAD)
AnteroseptalAnteroseptal V1, V2, V3, V4V1, V2, V3, V4 NoneNone Left AnteriorLeft Anterior
Descending (LAD)Descending (LAD)
AnterolateralAnterolateral V3, V4, V5, V6,I,V3, V4, V5, V6,I,
aVLaVL
II, III, aVFII, III, aVF Left AnteriorLeft Anterior
Descending (LAD),Descending (LAD),
Circumflex (LCX),Circumflex (LCX),
oror Obtuse MarginalObtuse Marginal
Extensive AnteriorExtensive Anterior
(Sometimes called(Sometimes called
Anteroseptal withAnteroseptal with
Lateral extension)Lateral extension)
V1, V2, V3, V4,V5,V1, V2, V3, V4,V5,
V6, I, aVLV6, I, aVL
II, III, aVFII, III, aVF Left main coronaryLeft main coronary
artery (LCA)artery (LCA)

48. Wall AffectedWall Affected Leads Showing STLeads Showing ST
Segment ElevationSegment Elevation
Leads ShowingLeads Showing
Reciprocal STReciprocal ST
Segment DepressionSegment Depression
Suspected CulpritSuspected Culprit
ArteryArtery
InferiorInferior II, III, aVFII, III, aVF I, aVLI, aVL Right CoronaryRight Coronary
Artery (RCA) orArtery (RCA) or
Circumflex (LCX)Circumflex (LCX)
LateralLateral I, aVL, V5, V6I, aVL, V5, V6 II, III, aVFII, III, aVF Circumflex (LCX),Circumflex (LCX),
oror Obtuse MarginalObtuse Marginal
PosteriorPosterior (Usually(Usually
associated withassociated with
Inferior or LateralInferior or Lateral
but can be isolated)but can be isolated)
V7, V8, V9V7, V8, V9 V1, V2, V3, V4V1, V2, V3, V4 PosteriorPosterior
Descending (PDA)Descending (PDA)
(branch of the(branch of the
RCARCA oror
Circumflex (LCXCircumflex (LCX))
Right ventricularRight ventricular
(Usually associated(Usually associated
with Inferior)with Inferior)
II, III, aVF, V1,II, III, aVF, V1,
V4RV4R
I, aVLI, aVL Right CoronaryRight Coronary
Artery (RCA)Artery (RCA)

50. Myocardial Ischemia or Infarction(ACS)Myocardial Ischemia or Infarction(ACS)
Management: (MONALISA)
Morphine for pain(5-10 mg) if no morphine Pethidine
(75- 100mg) + anti emetic providing systolic BP is
more than 90
Oxygen if hypoxic
Nitro spray/drip for pain
Aspirin
Lasix if in congestive heart failure
Inotropes if in cardigenic shock
Streptokinase (thrompolytics)
Anticoagulation (non Q wave MI : Heparin or LMWH,
Q wave MI :Thrompolytic and Heparin/LMWH)

52. Presentation within 12 hours of chest pain with :
Pain - needle time : 45 min
1)ST elevation >2mm in 2 or more chest leads or
2)ST elevation >1mm in 2 or more limb leads or
3)Posterior infarction ( dominant R wave and ST depression
in V1-V3 leads)
4)New onset of left bundle branch block.

53. Mx of NSTEMIMx of NSTEMI
High-risk patients with non-ST elevation
acute coronary syndrome should be
treated with an intravenous glycoprotein
IIb/IIIa receptor antagonist, particularly if
they are undergoing percutaneous
coronary intervention.

54. Mx of NSTEMI/UAMx of NSTEMI/UA
A Cochrane review of seven randomised
controlled trials (RCTs) (n=11,092)
reported that LMWH (principally
enoxaparin) reduced MI and coronary
revascularisation procedure rates
compared to unfractionated heparin.
There was no difference in mortality or
major bleeding episodes.

55. Mx of STEMIMx of STEMI
Meta-analysis confirms that, in patients
treated with thrombolytic therapy
LMWH(enoxaparin) is associated with
better outcomes
but no decrease in mortality when
compared with unfractionated heparin

56. Prinzemtal’s angina( variant angina or angina
inversa,)
a syndrome typically consisting of angina at rest that
occurs in cycles.
Cause by vasospasm
Features
Symptoms typically occur at rest, rather than on
exertion (attacks usually occur at night).

57. Diagnosis of Prinzmetal Angina
CK MB or troponin l or T may show a degree of
positivity, as coronary spasm too can cause
myocardial damage.
The gold standard is coronary angiography.
ECG finding will more often show ST segment
elevation than ST depression.

59. Treatment
Prinzmetal angina typically responds to
nitrates and dihydrophyridine calcium channel
blockers.

60. ACS Risk ScoringACS Risk Scoring
 TIMI
◦ Age - Use of aspirin
◦ Risk Factors - Known CAD
◦ > 1 episode rest pain - ST segment deviation
◦ Cardiac risk markers
 PURSUIT
◦ Age, Sex - CCS class in last 6/52
◦ Signs of CCF - ST depression on ECG
 GRACE
◦ Age - Heart rate and systolic BP
◦ Creatinine - CCF (Killip class)
◦ Cardiac arrest at admission
◦ Elevated cardiac markers - ST segment deviation

61. Risk Scoring – at admissionRisk Scoring – at admission

62. Thresholds of RiskThresholds of Risk

63. MUSCULOSKELETAL CHEST PAINMUSCULOSKELETAL CHEST PAIN
ARTHRITIS
COSTOCONDRITI
S
INTERCOSTAL
MUSCLE INJURY
COXSACKIE VIRAL
INFECTION
MINOR SOFT
TISSUE INJURIES
VARY WITHVARY WITH
POSTUREPOSTURE
VARY WITHVARY WITH
POSITIONPOSITION
LOCALLOCAL
TENDERNESSTENDERNESS

64. TEITZE`S SYNDROMETEITZE`S SYNDROME
IDIOPATHIC COSTOCONDRITISIDIOPATHIC COSTOCONDRITIS
LOCALIZED PAIN/TENDERNESS AT
COSTOCONDRAL JUNCTION
ENHANCED BY
EMOTION,COUGHING,SNEEZING
2nd.RIB MOST AFFECTED

65. OESOPHAGEAL PAINOESOPHAGEAL PAIN
CAN MIMIC ANGINAL PAIN
MAY GET PRECIPITATED BY EXERCISE
MAY BE RELIEVED BY NITRATES
RELATION WITH SUPINE
POSITION,EATING,DRINKING
 H/O REFLUX
CAN RADIATE TO BACK

66. RUPTURED OESOPHAGUS
CLINICAL FEATURES
SEVERE CHEST PAIN
SHOCK
SUB-CUTANEOUS
EMPHYSEMA
PLEURAL EFFUSION
PNEUMOTHORAX
PNEUMOMEDIASTINUM

67. Questions?Questions?