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Approach to a patient with chest pain
1. Clinical pathways
Dr Saeed Ahmad Chaudhary
Medical Officer ER
Recep Tayyip Erdogan Hospital
(Indus Hospital ) Muzaffargarh
2. Objectives
UNDERSTAND THE CAUSES OF CHEST PAIN
UNDERSTAND THE IMPORTANCE OF HISTORY
TAKING
REALIZE THE LIFE THREATENING CAUSES OF
CHEST PAIN
INVESTIGATIONS
LEARN COMMON ECG CHANGES
3. Chest Pain ( Don’t Panic)
5 Million emergency department visits
2 million hospitalizations annually with cost of more
than $8 billion
Cardiac etiology found in less than one third
2% of patients with acute MI are unrecognized and
discharged from the ED
Accurate Diagnosis Remains A
Challenge
7. Chest Pain? Origin?
• HEART
• LUNGS
• OESOPHAGUS
• MUSCULOSKELETAL STRUCTURES OF
THORAX NECK,OR SHOULDER
• ABDOMEN
• ANXIETY MANIFESTATION
WHAT LIES IN THE CHEST
SKIN
MUSCLES
BONES
JOINTS
HEART AND VESSELS
LUNGS AND AIRWAYS
OESOPHAGUS
NERVES
8. IS THE KEY TO THE
DIAGNOSIS OF ETIOLOGY
OF CHEST PAIN
HISTORY
9.
10. PAIN HOW DESCRIBED?
STABBING
BURNING
TWISTING
TEARING
SQUEEZING
TERRIFYING
NAUSEATING
SICKENING
Penetrating or Tissue
Destructive Process
Bodily Or Emotional
Reaction
11. H/O CHEST PAIN IN THE
EMERGENCY DEPARTMENT
HEART ATTACK
ANSWER IS NO……
RELAX
IS IT ENOUGH TO RULE OUT
HEART ATTACK?
12. Life Threatening Chest Pain in
the Emergency Department
• Myocardial Infarction
• USA
• Aortic Dissection
• Tension Pneumothorax
• Pulmonary Embolus
• Ruptured
Esophagus/Perforated
Life Threatening Chest Pain in
the Emergency Department
17. ISCHEMIC CARDIAC PAIN
Site Of Origin of Chest Pain Central
Character Of
Chest Pain
•TYPICALLY DULL
•CONSTRICTING IN NECK
•CHOKING
•HEAVY
•DESCRIBED BY PATIENTS AS
---SQUEEZING
-------CRUSHING
-----------BURNING
---------------ACHING
•BUT NOT SHARP STABBING
•BUT NOT PRICKING, KNIFE-
LIKE
•SENSATION CAN BE DESCRIBED
AS BREATHLESSNESS
SEVERE
PROLONGED
ASSOCIATED WITH
CLINICAL
EVIDENCE OF
ACUTE SERIOUS
ILLNESS
18. RADIATION
Because of common/overlapping neural pathways, many
conditions, both cardiac and extra-cardiac can result in chest pain.
Cardiac pain is mediated through upper 5 thoracic ganglia and
spinal roots, but ramifications from adjoining spinal roots
always exist.
Therefore pain in the chest may originate from any structure in
thorax and upper abdomen innervated through lower cervical to
D6/D7 spinal roots
•NECK
•JAW
•UPPER OR LOWER ARM
•BACK
22. INVESTIGATIONS
ECG Provides documentary evidence of cardiac
ischemia/infarction when positive.
Normal in ~ 50% initially who are later Dx as having an AMI.
A normal ECG does not exclude an AMI
26. Myoglobin CK-MB
Isoenzyme
Troponin
( T, I)
Specific/Sensitive high sensitivity
but poor
specificity
Less Sensitivity
and specificity
Most Specific &
Most Sensitive
Raises in 1 hour 4-6 Hours 4-8 Hours
Peaks in 4-12 Hours 24 Hours 18-24 Hours
Remains
Elevated
24-36 hours 36-48 Hours 10-14 Days
Remarks 100% within 3 hrs
of AMI
predictive of
mortality
prognostic
information
False Positive Skeletal muscle
injury, Heavy
alcohol, Renal
failure , Shock
states
exercise, trauma,
muscle dz, DM,
PE
renal dz,
poly/dermatomyo
sitis
PLASMA BIOCHEMICAL MARKERS
27. CBC -----------LEUKOCYTOSIS ON 1st DAY—PEAKS 2-4
DAYS
ESR------------RAISED WITHIN 3 DAYS
CRP------------ELEVATED
CXR------------PUMONARY EDEMA,,,CARDIOMEGALY
ECHO--------WMA?
28.
29. Chest Pain
Duration
ECG
a) ST
b) T wave
Cardiac
Enzymes
Troponin
(T,I)
Angina Less than 10 min a) Normal
b) Normal
-ve -ve
Un-stable
Angina
> 10 mins a) Slight
Depression/
Elevation
b) Poor/
Inversion
-ve /slightly
raised
-ve
NSTMI > 20 mins ST Depression +ve +ve
STEMI > 20 mins ST Elevation +ve +ve
30. Aortic Dissection
Clinical Presentation
History:
>90% with abrupt and severe pain in the chest or
between the scapulae
“tearing” or “ripping”
Can be dull or pressure-like
Anterior chest ~ ascending aorta -Type A; Back ~
descending aorta –Type B
Nausea, vomiting, diaphoresis common
Definition:
Intimal tear with entry of blood into the media
“dissects” between the intima and adventitia
#1 site: ascending aorta at the ligamentum arteriosum
Stanford Classification:
A: involves Ascending aorta (w/ or w/o descending)
80% of dissections
B: descending aorta only
31. Associated signs & symptoms based on
progression of dissection:
Carotid arteries: stroke
Spinal arteries: paraplegia
Abdominal aorta/renal arteries/iliacs: Abdominal/flank
pain
Coronary arteries: pericardial effusion/tamponade
Laryngeal nerve compression: hoarseness
Tracheal compression: dyspnea/stridor/wheezing
Esophageal compression: dysphagia
Physical Examination:
•BP differential?
bilateral arm BPs – significant if >20mmHg difference
Most commonly: normal heart and lung
•Aortic insufficiency murmur in 16-20%
•Unequal, decreased, or absent peripheral pulses only found in 50%
32. ECG
– AMI (new Q or STE) – 3.2%
– Ischaemia – 15%
– No abnormalities – 31.3%
– Non specific T wave changes – 41.4%
– LVH – 26.1%
Investigations
Risk Factors – Atherosclerosis, HTN (uncontrolled),
Coarctation of Aorta, Bicuspid Aortic Valve, Aortic
Stenosis, Marfan Syn, Ehlers-Danlos Syn, Pregnancy
34. CXR
a)-Mediastinal widening (61.6%) , b)- Widening of aortic contour (49.9%),
c)-Pleural effusion (L>R) (19.2%), d)-Apical pleural cap, e)-Calcium sign
(14%), f)– Depressed left main bronchus , g)-Tracheal or oesophageal
displacement, h)-No abnormalities noted 12.4%
TEE ( High Sensitivity and Specificity )
Aortic Angiography
CT or MR
35. Pulmonary Embolism
“Classic Triad”:
Sharp Pleuritic CP, Dyspnea, hemoptysis in only 20% of pts.
Pain is often pleural
Reproduciable with breathing, palpation
•Dyspnea (79%)
•Dyspnea at rest (61%)
•Dyspnea exertion (16%)
•Orthopnea (36%)
•Pleuritic chest pain (49%)
•Non pleuritic chest pain (17%)
•Cough (43%)
•Calf or thigh swelling (39%)
•Calf or thigh pain (41%)
SIGNS
•RR > 20/min (57%)
•Tachycardia (26%)
•Increased P2 (15%)
•JVP distension (13%)
•Rales (21%)
•Wheeze (3%)
•Decreased breath sounds (21%)
•Signs of calf or thigh DVT (47%)
36. Hypercoagulability
Pregnancy; malignancy; estrogen
therapy; deficiencies of protein C,
protein S, AT III
Endothelial
damage
Recent surgery, trauma
Venous stasis
Prolonged travel;
bed Ridden
#1 Risk Factor = Prior DVT/PE
Risk Factors;
Virchow’s triad:
10-15% of patients will have no
identifiable risk factor at the time of
presentation
Pre-test Probability
37. Investigations;
ECG
– Tachycardia most common • approx. 1/3 patients
– T wave inversion • V1-3 (inferior leads)
– S1Q3T3 Pattern • 20% patients
38. CXR; Specific signs in massive/submassive PE
Fleisher’s sign – distended central pulmonary artery
41. Biomarkers
– Markers of right heart strain
– Troponin
– BNP
• Takes time for rise
• RV smaller muscle mass therefore threshold lower
• >90
D Dimer
–ve – discharge False –ve <1%
D Dimer +ve
– Many false positives
Malignancy– Recent surgery– Infection– DIC– Trauma– ACS– CVA– AF
Vacuities-Superficial phlebitis
42. ECHO
– RV dilatation
– RV hypokinesis
– Pardoxical septal wall movement
– Tricuspid regurgitation
Imaging
•COLLOR DOPPLER
•VENTILATION–PERFUSION (VQ) SCAN
if normal CXR
•CT PULMONARY ANGIOGRAPHY (CTPA)
if definitive diagnosis urgent
•MRI
43. Tension Pneumothorax
Clinical Presentation;
SUDDEN-ONSET UNILAT. CHEST PAIN,PLEURITIC SHARP
BREATHLESSNESS
ASYMPTOMATIC (NOT TENSION PNEUMOTHORAX)
DEC OR ABSENT BREATH SOUNDS (IF PNEUMOTHORAX MORE THAN15%).
RESONANT ON PERCUSSION
MEDIASTINAL DISPLACEMENT TO OPPOSITE SIDE
TACHYCARDIA
HYPOTENSION
CYANOSIS
TRACHEAL DISPLACEMENT
ASYMMETRIC LUNG EXPANSION.
Risks Factors:
Sudden Change in barometric pressure
Smokers, COPD, Idiopathic Bleb DZ
Especially tall, thin male smokers
Only 10 – 20% occur with exertion
44. Tension Pneumothorax
when a pneumothorax (primary spontaneous, secondary
spontaneous, or traumatic) leads to significant impairment
of Respiration and/or Blood Circulation
46. Esophageal Rupture: Boerhaave
Syndrome
Substernal, sharp CP
Sudden onset after forceful vomiting
Dyspneic, diaphoretic, and ill-appearing
Shock
Sub-cutaneous Emphysema
Causes?
Most Common Iatrogenic (Endoscopic Perforation)
Malignancy
Corrosive Strictures Perforation
Post Radiotherapy Strictures
47. CXR;
SQ air, Pleural Effusions, Pneumothorax, pneumoperitoneum, pneumomediastinum
Water Soluble Contrast Study
48. Pericarditis
Chest pain , Severe Pleuritic localized
Aggravated by lying supine, coughing swallowing and
deep inspiration.
Relieved by sitting up and leaning forward.
It might be preceded by viral illness.
Inflammation Of Pericardial Sac
Causes;
Idiopathic
Infection
Acute MI
Uremia
Neoplasm
(Hodgkin
Lymphoma,
breast and Ca
lung )
PERICARDIAL FRICTION RUB
FEVER
LEUCOCYTOSIS
52. MITRAL VALVE PROLAPSE
SHARP LEFT SIDED
CHEST PAIN AT APEX
DYSPNEA
FATIGUE
PALPITATION
REDUCE BY LYING
DOWN
FEMALES
THIN
CHEST WALL
DEFORMITIES
MID-SYSTOLIC CLICKS
AT APEX
ECHO
CARDIAC CATH
53. Gastroesophageal Pain
•BURNING
•PROLONGED
•SUBSTERNAL/EPIGASTRIC , CAN RADIATE TO BACK
•REGURGITATION OF LIQUIDS OR FOOD
•INCREASED BY CHOCOLATE,COFFEE
•RELATION WITH SUPINE POSITION, EATING,
DRINKING, & GET PRECIPITATED BY EXERCISE
•AFTER LARGE MEAL
•LYING AFTER MEAL
•OVERWEIGHT
•MAY BE RELIEVED BY NITRATES
CAN MIMIC
ANGINAL PAIN
54. MUSCULOSKELETAL CHEST PAIN
•RAPID ONSET
•CONSTANT
•INCREASES WITH DEEP
BREATHING AND CHANGE IN
POSTURE
•REPRODUCED/TENDER BY
PALPATION
•HISTORY OF RECENT
EXERCISE/EXERTION
•VITALS ARE STABLE
•ANXIETY/ATTENTION
DEMANDING/MOTIVES
•ARTHRITIS
•COSTOCONDRITIS
•INTERCOSTAL MUSCLE
INJURY
•COXSACKIE VIRAL
INFECTION
•MINOR SOFT TISSUE
INJURIES
TEITZE`S SYNDROME
IDIOPATHIC COSTOCONDRITIS
•LOCALIZED PAIN/TENDERNESS AT
COSTOCONDRAL JUNCTION
•ENHANCED BY
EMOTION,COUGHING,SNEEZING
•2nd.RIB MOST AFFECTED
55. Herpes Zoster (Shingles)
Chest pain ,Unilateral
Burning, tickling, tingling,
and/or numbness occurs in the
left parasternal area, following
the dermatomes.
Flu-like symptoms (without a
fever), such as chills
Swelling and tenderness of the
lymph nodes
Chest pain from Shingles can
occur before the onset of vesicles
thus making a reliable diagnosis
difficult.
Hinweis der Redaktion
Positive if CK/MB > 5% of total CK and 2 times normal