Approach to patient with

Chest Pain
By Firyal A. Al-Baloushi
MD3, Oman Medical College, FAMCO Rotation
1st of February 2011
 Introduction
• Chest pain is a common symptom seen in:
– Cardiovascular Diseases
– Respiratory Diseases
– Gastrointestinal
– Musculoskeletal Disease
• The cause/DD of chest pain can be identified by knowing the
history of pain:
– Trauma (car accident, fall, collision)
– site/nature/duration (most painful area, sharp, dull, or burning pain, last
for seconds/minutes/hours)
– provoking/relieving factors (what brings pain/makes worse/better)
– Any medical condition/drug/smoking
– Associated symptoms (dyspnea, nausea, dizziness)
 Types of Chest Pain
Central Chet pain:
Non-Central Chet pain:
• Angina
• Pleuritic pain
• MI
• Fractured rib
• Dissecting thoracic
aneurysm
• Musculoskeletal pin
• Pericarditis
• Tietze’s syndrome
• Shingles
• Oesophageal pain
Differential Diagnose
CVS RS GI MS Other
Ischemia Pulmonary Esophageal Costochondritis Herpes zoster
(Angina) Embolism spasm
Myocardial Pleurisy Esophagitis Muscle trauma Bornholm’s
Infration disease(myalgia)
Pericarditis/myoc Pneumothorax Rib fractures Idiopathic chest
arditis pain
Dissecting Trachitis/pneu osteoarthritis
thoracic monia
aneurysm
Mitral valve malignancy
prolapse
Examination/Investigation
Examination:
- General appearance: sweating, pallor, distress
- BP in both arms ( for aneurysm, will be difference of 15)
- JVP and carotid pulse (bruie in carotid pulse(
- RR/PR
- Apex beat/ heart sounds
- Lung field (crepitating as in HF)
- Localized tenderness/pain over the chest
- Skin rash (HZ)
- Swelling or tenderness of legs (deep vein thrombus)
Investigations:
- ECG and Chest X-Ray
- Others depending on DD
 Common Cause
• Ischemia (Angina)
• Myocardial infraction
 Angina Pectoris
- A strangling sensation in the chest that is a gripping or
crushing discomfort maybe felt around the whole chest or
deep within the chest
- The pain my radiate to the neck, jaw, rarely to the teeth,
back or abdomen
- Types:
Stable Angina Unstable Angina (more serious)
 Stable Angina
Is predictable chest pain
• Any event that increases oxygen demand can cause an angina
attack
Although less serious than unstable angina, it can be extremely
painful.
Relieved by rest and responds well to medical treatment
Some typical triggers include the following:
Exercise.
Cold weather.
Emotional tension.
Large meals.
 Management
No physical signs in examination, but anemia can be seen in sever
attacks
Investigations:
First line investigations:
 CBC
 Fasting lipid profile
 Fasting blood glucose
 ESR
 TFT
 12-lead resting ECG: Provide info on- rhythm, presence of heart block,
previous MI, Myocardial Hypertrophy and Ischemia (if done between the attack,
ECG will be normal. If one during attacks, ECG findings will be S-T depression)
 Further investigations: Exercise ECG and Coronary arteriography
 To know if patient has sever disease or not
 Management
Treatment:
Non-drug treatment: aims to prevent CHD
Stop smoking
Treat/control BP
Diet: decrease salts+ increase fruits/vegetables
Increase exercise
Treat/control diabestus
Drug treatment:
As required medication:
GTN spry: 1-2 puffs
GTN sublingual tablets
Regular treatment:
First line is Beta-Blockers (atenolol 50-100mg/day)
 Management
Treatment:
Second Line treatment:
Dihydropyridine Ca channel blockerAmlodpine
3rd line Long acting nitrate isosorbide mononitrate 20mg bid/tid.
 For patient without left ventricular dysfunction and in whom B-
Blocker are inappropriate:
Diltiazime bid/tid
Verapamil 80-120mgtid as first line and add a long acting
nitrate if symptom are not controlled.
For patient with left ventricular dysfunction long acting nitrate 1st
line and add long acting dihydrpyrimidine calcium channel blocker
if symptom are not controlled.
 Management
Treatment:
For patient with left ventricular dysfunction:
long acting nitrate 1st line and add long acting dihydrpyrimidine
calcium channel blocker if symptom are not controlled.
K channel activator .(Nicorandil).if all above not working
Prevention:
Aspirin
Statins
ACE inhibitors
Aspirin 75mg/ clopidogrel 75mg for secondary prevention
Statins to those with cvd.
 Intro
Stable angina and acute coronary syndrome(ACS)
ACS includes:
ST elevation MI: ECG positive for ST elevation and enzymes also
positive. Do angiography+stant(cathLab)+treat if not available do thrombolytic
trapping
Non ST elevation MI: no ECG finding, but positive enzymes
Unstable angina: normal ECG and normal enzymes
Management differ in each one of these types
 Unstable Angina
 Pain in minimal or no exertion that may occur at night due to
complete blockage to the coronary artery completely
 A patient is usually diagnosed with unstable angina under one or
more of the following conditions:
 Pain awakens a patient or occurs during rest
 A patient who has never experienced angina has severe or
moderate pain during mild exertion (walking two level blocks or
climbing one flight of stairs)
 Stable angina has progressed in severity and frequency within a
two-month period, and medications are less effective in
relieving its pain
 Management
 Management:
Treat as MI
Urgent referral to cardiology
Admit if attacks are sever, occur at rest, or last> 20min event
with GTN spray
Myocardial Infraction
 It is due to the formation of occlusive thrombus at the
site of rupture or erosion of an atheromatous plaque in a
coronary artery
The thrombus undergoes spontaneous lysis over the
course of next few days
By the time irreversible myocardial damage occurred.
Without treatment, the infarct related artery can remain
permanently occluded
 Myocardial Infraction
 Presentation:
Sustained central chest pain not relived by sublingual
GTN
Other features:
Collapsed/ cardiac arrest
Breathlessness
Anxiety/fear of dying
Nausea/vomitting
Sweating
Pain in one or both arms, jaw, back and upper
abdomen
Myocardial Infraction
Investigations:
12-Lead ECG: ECG-ST elevation or R waves and ST depression in
lead V1-V2 ( indicates posterior wall infraction)
CXR
Blood test
Echocardiography
Plasma biochemical markers (CK)
 MI-ECG
To diagnose a myocardial infarction you need to go
beyond looking at a rhythm strip and obtain a 12-Lead
ECG which sees the heart from 12 different views.
helps you see what is happening in different portions
of the heart.
12 ECG Leads:
 3 Limb leads- I,II,III
 3 Augmented leads- aVR, aVL, Avf
6 Precordial leads- V1 – V6
 MI-ECG
Anterior Myocardial Infarction:
If you see changes in leads V1 - V4 that are consistent with a
myocardial infarction, you can conclude that it is an anterior
wall myocardial infarction
 MI-ECG
Lateral Myocardial Infarction:
Leads I, aVL, and V5- V6
Inferior Myocardial Infraction:
Leads II, III and aVF
 MI-ECG
Anterolateral MI
When ECG involves both the anterior wall (V2-V4) and the
lateral wall (V5-V6, I, and aVL)
 MI-ECG
Summary:
1. R waves and ST depression in lead (V1, V2 and sometimes
V3) Posterior wall MI
2. If ST segment elevation in V1-V4 Anterior wall MI
3. If ST segment elevation in lead I,aVL, V5, and V6 Lateral
wall MI
4. If ST segment elevation in lead aVF, lead II,III, V5-V6 Inferior
wall MI
MI-Laboratory evaluation
Biochemical evidence:
blood level of intra cellular macromolecules
that leak out of injured cell is measured:
1. Myoglobin (Not specific for MI)
2. Cardiac Troponin T & I
3. Creatine KinaseMB isoform and LDH(not specific for
MI)
MI-Laboratory evaluation
Troponins (best marker) & CK – MB are highly specific

Molecule Appear Peak Disappear

TnT & TnI 2-4 hrs 48 hrs Remain elevated for
7-10 days

CK-MB 2-4 hrs 24-48 hrs Returns to normal

with in 72 hrs
 Management
Give 300mg aspirin po unless contraindicated
Insert cannula
Give IV analgesia (morphin 2.5-5mg)
Give antiemetics (metoclopramide 10mg)
Give sublingual GTN
Give oxygen if avalible
If bradycardia atropine 3mg IV
Immediate transfer to the hospital
 Management
Summary of Acute management of MI:
Memorize “OMAN”
O: oxygen
M:morphin
A: aspirin
N: nitroglycride (don’t give if there is inferior wall MI because it decreases
the blood pressure right coronary artery involves reducing the blood supply)
Thank you
 Questions
Which one of the following has been shown to decrease mortality
late after a myocardial infarction?
A)Nitrates
B)Beta-Blockers
C)Digoxin
D)Thiazide diuretics
What is the finding of ECG in a patient with Acute Myocardial
infraction?
A. ST elevation
B. R waves
C. ST depression in lead V1-V2
D. Wide QRS
 Question-2
The ECG shows:
• Sinus rhythm
• Normal axis
• Q waves in leads V2-V4
• Raised ST segments in leads V2-V4
• Inverted T waves in leads I, VL, V2-V6
Clinical interpretation
• This is a classic acute anterior myocardial
infarction.