approachto cp

Approach to Chest Pain

Chairperson– Dr.H.S.SandhuSpeaker– Dr. Nagma Bansal

Chest Pain Definitions

• Acute Chest Pain:Acute - Sudden or recent onset (usually

within minutes to hours), presenting typically <24 hrs

Chest - Thorax midaxillary to midaxillary line, xiphoid to suprasternum notch

Pain – Noxious uncomfortable sensation Ache or discomfort

Chest Pain

• Visceral– Often referred – Aching, heaviness, discomfort– Difficult to localize pain

• Somatic– Sharp, easily localized

Categorizing Chest Pain

1. Chest Wall Pain• Sharp, Precisely localized• Reproducible: Palpation, movement

2. Pleuritic or Respiratory CP• Somatic pain, Sharp• Worse with breathing/coughing

3. Visceral CP• Poorly localized, aching, heaviness

Causes

1. Chest wall• Costosternal synd• Costochrondritis• Precordial catch synd• Slipping Rib Synd• Xiphodynia• Radicular Synd• Intercostal Nerve• Fibromyalgia

2. Pleuritic• Pulmonary Embolism• Pneumonia• Spontaneous pneumo• Pericarditis• Pleurisy

Causes cont…..

3. Visceral Pain:• Typical Exertional

Angina• Atypical Angina• Unstable Angina• Acute Myocardial

Infarction (AMI)

• Aortic Dissection• Pericarditis• Esophageal Reflux

or spasm• Esophageal

Rupture• Mitral Valve

Prolapse

Initial Approach

• History:– Character of pain– Presence of associated symptoms– Cardiopulmonary history– Pain intensity, 0-10 pain

Initial Approach

• Triage– Chest pain– Significant abnormal pulse– Abnormal blood pressure– Dyspnea– These pts need IV, O2, Monitor, ECG

Initial Approach

• Evaluation – Airway– Breathing– Circulation– Vital Signs– Focused exam

• Cardiac, pulmonary, vascular

Initial Approach

• Secondary exam:– History– pneumonic OLD CARTS

O- onset L- location D- duration C- character A- associated/ aggravating factors R- relieving factors T- timing or periodicity S- severity

– Risk factors– Physical exam– Review old records/ekg’s

Chest pain incidentals ACS

• AMI Rare under 30 y/o– except with cocaine use

• GI cocktail may cause relief even in AMI

• Nitroglycerin can cause relief of esophagus spasm, biliary colic, and AMI

• NSAIDS can be analgesic for all types of pain

Atypical Chest Pain- AHA guidelines• Sharp or knife like pain brought on by respiratory movements

or cough• Primary or sole location of discomfort in middle or lower abd

region• Pain that may be localized at tip of one finger• Pain reproduced with movement or palpation of chest wall or

arms• Constant pain that persists for many years• Very brief episodes of pain that lasts few sec• Pain that radiates into lower extremities

• Atypicals usually in– DM, females, non-white, elderly, altered MS pts

Acute Coronary Syndrome (ACS)

• ACS = AMI or Unstable Angina• Visceral chest pain pts

– AMI – 15% – UA – 25-30%

Acute Coronary Syndrome (ACS)

• ECG is the most useful test• Incidence

– Significant ST elevation = 80% are AMI– ST depression/T wave inversion = 20%

are AMI– No change <4% are AMI

Differential Dx ACS

• Myocardial Ischemia:– Retrosternal, diffuse, heaviness, or

pressure– Radiation to neck or arm– Usually persistent pain >20 min, severe– Associated Sx or anginal equivalents:

Dyspnea, Diaphoresis, Nausea, fatigue, faintness

– May even be Reproducible

Differential Dx ACS

• Exertional Angina:– Episodic pain, <10 min– Onset with exertion– Resolves with rest, sublingual NTG– Response to exertion and rest follows

same pattern

Differential Dx ACS

• Atypical Angina:– Occurs at rest– Coronary spasm– Pattern of episodes same

Differential Dx ACS

• Unstable Angina (UA):– Change in the pattern of angina

• New Onset• More frequent, severe, easily provoked• More difficult to relieve• Occurs at rest, lasting >20 min• High risk of AMI

Testing for ACS

• EKGs• Serum Markers• Imaging studies

Testing for ACS - EKG

• AHA Guidlines:– Any pt with Ischemic type pain is to have

an EKG done within 10 minutes of arrival.

– This is to be handed directly to the physician

Testing for ACS - EKG

• AMI PT EKGs:– 50% = ST elevation > 1mm in 2 contiguous

leads– 20-30% = new ST seg. changes or T wave

inversion– 10-20% = ST depression and T wave

inversions Similar to previous EKGs– 10% nonspecific changes– 1-5% will have NORMAL initial EKG

Testing for ACS - Serum Markers

• AMI on Initial EKG– Markers not required for Dx

• Marker changes may precede EKG Change

• AMI– CK-MB initially elevated in 30-50% – Serial CK-MB elevate in 6 hours in 80-

96%


• CK – elevates 4-8 hours after coronary Art. Occlusion– Peaks = 12 to 24 hours– Nml = 3 to 4 days

• CK-MB– Detectable 4-8 hrs– Peak = before 24 hrs– Nml = in 48hrs

• CK-MB normally can be 5% of total CK (Rapid Index)


• Common Causes of CK-MB Elevation:– UA, ACS– Inflammatory Heart Dz– Cardiomyopathies– Shock– Cardiac

Surgery/Trauma– Trauma– Dermatomyositis– Myopathic Disorders

– Muscular Dystrophy– Extreme Exercise– Malignant Hyperthermia– Reyes Syndrome– Rhabdomyolysis– Delerium Tremens– Ethanol Poisoning,

chronic

Testing for ACS - Troponins

• Main regulatory protein of thin filament of myofibrils that regulate the Ca++ dependent ATP hydrolysis of actinomysin

• 3 Subunits:– Trop I = Inhibitory Subunit

• Myocardial Specific• Elevation indicated worse prognosis

– Trop T = tropomyosin-binding subunit– Trop C = calcium-binding subunit

Testing for ACS - Troponins

• AMI:Cardiac Troponin I (cTnI) and cTnT

• Elevates in 6 hrs• peaks in 12 h• Remain elevated for 7 to 10 days• Higher specificity than CK-MB• Controversy = Troponins are found to be

elevated in Renal Failure pts without proof of ACS/AMI

Other causes of positive trop-T

• Pacing, automated implantable cardioverter-defibrillator• Tachyarrhythmias• Hypertension• Myocarditis• Myocardial contusion• Acute and chronic congestive heart failure• Cardiac surgery• Renal failure• Pulmonary embolism• Subarachnoid hemorrhage• Sepsis• Hypothyroidism• Shock

http://emedicine.medscape.com/article/780825-overview





• Using Myoglobin, CK-MB, and cTnI initially and at 3 hours = 90% of AMI pts diagnosed

• Emerging cardiac markers are– c-BNP– Myeloperoxidase levels– Ischemia modified albumin

Non atherosclerotic causes of angina

• Congenital coronary artery anomalies– Slit like ostia– Presence of major artery b/w wall of pulmonary

trunk and aorta– Origin of major artery from pulmonary trunk– Myocardial bridges– Single coronary artery

• Prinzmetal’s angina• Coronary artery dissection eg kawasaki

disease• Traumatic coronary artery

Vasospastic (prinzmetal’s angina)

• Also called as variant angina/ angina inversus

• Angina at rest usually at night• More in younger women• Negative treadmill test• ECG changes- ST elevation on instead of

depression as in angina• Cardiac markers may be positive• Gold standard is coronary angiogram with

injection of provocative agents

Cardiac syndrome X• Microvascular angina• Post menopausal women• Ass. With insulin resistance syndrome• Typical chest pain usually precipitated after

exercise• Positive exercise test but normal

angiography• Treatment is with nitrates, beta blockers

and CCBs• Prognosis is good

Pulmonary Embolism• History and risk factors– hypercoaguable state,

malignancy, recent immobilization, recent surgery• Clinical features- Atypical, presenting with any

combination of:• Chest Pain, Dyspnea, Syncope, Shock, Hypoxia• Fever, cough, hemoptysis

– Pain is often pleural• Reproducible with breathing, palpation

– Classic presentaion:• Sharp pain, Dyspnea• Tachypnea, tachycardia, hypoxemia

Pulm embolism contd…

• O/E- neck vein distension, signs of RV failure, hypotension, accentuated P2 on auscultation

• ECG- S1Q3T3 sign is characteristic, but most common finding T inversion in V1 to V4.

• Diag- D-dimer more sensitive for PE than DVT• ABG lack diagnostic utility• X-ray chest–westermark’s sign (focal oligemia),

hampton’s pump (wedge shaped density over diaphragm, palla’s sign (enlarged descending pulm artery)

• CT chest with contrast is diagnostic

Aortic syndromes

• Aortic rupture(aortic aneurysms)

• Aortic dissection

• Intramural hematoma

• Penetrating atherosclerotic ulcer

Aortic Dissection• History and Risk Factors – usually a middle

aged male having Atherosclerosis, HTN (uncontrolled), Coarctation of Aorta, Bicuspid Aortic Valve, Aortic Stenosis, Marfan Syn, Ehlers-Danlos Syn

• C/Fs- Pain – sudden onset,midline Substernal CP, tearing, ripping, reaching peak immediately, radiating to interscapular area and also migrates with the propagation of dissection

• Pain Above AND Below Diaphragm• Others are syncope, dyspnoea, diaphoresis,

weakness

Aortic dissection cont…• O/E- • Hypo or hypertension,• loss or irregularity of pulses, • AR, • pulm edema, • findings due to occlusion of major arteries like

stroke, AMI, bowel ischemia, hematuria or compression of adjacent structures

• ECG- no evidence of AMI provided coronary ostia are not involved

• Diagnosis- by trans esophageal echocardiography, CT, MRI

Spontaneous Pneumothorax:

Risks: • Sudden Change in barometric pressure• Smokers, COPD, Idiopathic Blebs

C/Fs: • sudden, sharp, pleuritic chest pain, and dyspnea

O/E: • Absence of breath sounds ipsilaterally• Hyper resonance to percussion

Diagnosis by chest x-ray and CT

Acute PericarditisC/Fs-

• Acute, sharp, severe, constant, substernal CP– Radiation to back, neck, shoulders– Worse with lying down and inspiration– Relief with leaning forward

O/E- FRICTION RUB( best at end of expiration and leaning forwards)

EKG: • ST seg elevation in widespread leads• PR elevation in aVR and depression in other• Q wave not produced• T inversion only after ST becomes isoelectric

Diag- by echocardiography

Pneumomediastinum• 3 main causes

– Alveolar rupture– Perforation or rupture of the esophagus( Boerhaave’s

syndrome)– Dissection of air from neck or abdomen

• Life-threatening• C/Fs- Substernal, sharp CP without radiation into neck and arms

– Dyspneic, diaphoretic, and ill-appearing• O/E-

-subcutaneous emphysema, -Hamman’s sign- crunching or clicking sound synchronous

with heartbeat• CXR: Normal, SQ air, Pleural Effusions, Pneumothorax,

pneumoperitoneum, pneumomediastinum

Musculoskeletal and chest wall disorders

– LOCALIZED, Sharp, positional CP– Reproducible– Pain usually localised at tip of fingerTypes –

• Costochondritis, Tietze Syndrome• Xiphodynia

GI Disorders: GERD/dyspepsia

– Heart burn or pyrosis burning, gnawing low CP– Ass. with Acidic taste and feeling of warm fluid

climbing up the throat– Aggravated by bending forward, straining, or

lying recumbent– Worse after meals– Relief by upright position , swallowing of saliva or

water and per antacids -CAREFUL, can also help in ACS

– Diag by barium swallow, esophagoscopy and mucosal biopsy

Esophageal Spasm:

– Achlasia acardia or diffuse– CP may acute to subacute, dull to sharp,

substernal, radiating to arms, neck,jaw– Aggravated by Hot or cold liquids and large

food bolus– Associated with dysphagia, achlasia

particularily to liquids – Responds to NTG– Diag by manometry and barium swallow (in

achlasia parrot beak, and in DES cork screw shaped)

Peptic Ulcer Disease:

– Gastric:• Postprandial, dull, boring pain• Midepigastric, may awake pt.

– Duodenal Ulcer:• Relieved after eating

– Symptomatic Tx: antacids– DDx: Pancreatitis and Biliary tract Dz

Neuropathic chest pain

• Post herpetic

• Post surgical( post mastectomy, post thoracotomy, phantom limb)

• Complex regional pain syndrome (reflex sympathetic dystrophy and causalgia)

Panic Disorder:

– Recurrent, Unexpected panic – Including at least 4 SX:

• Palpitations, diaphoresis, tremor, dyspnea, choking, CP, nausea, dizziness, derealization, or depersonalization, fear of losing control or dying, paresthesias, chills, hot flashes

– Rule out substance abuse

Testing for ACS Prognosis Categorization Strategy

1. AMI = Immediate Revascularization candidate

2. Probable acute Ischemia: High risk(Any of the following)Clinical InstabilityOngoing painPain at rest with ischemic EKG changesPositive cardiac marker(s)Positive perfusion imaging study


3. Possible acute Ischemia: Intermed. Risk:Hx suggestive of ischemia with…

Rest pain, now resolved New onset of pain

Crescendo pattern of painIschemic pattern on EKG without

CP


4.A. Probably NOT Ischemia: low riskRequires all of followingHx not strong for ischemiaEKG normal, unchanged from

previous,or nonspecific changesNegative markers


4.B. Stable Angina Pectoris: low risk PxRequires all the following> 2wk unchanged Sx pattern, Longstanding Sx with only mild change in exertional pain thresholdEKG normal, unchanged, nonspecific changesNegative initial myocardial markers


5. Definitely not ischemia: very low risk for adverse events

Requires AllClear objective evidence of nonischemic Sx etiologyECG normal, unchanged, nonspecificNegative Initial Markers

Disposition

• Safely Discharge: – Sharp, well localized, reproducible by

position, breathing, palpation and no prior diagnosis of angina or AMI

• Keepers:– Unexplained visceral pain

• Unless ancillary testing excludes ACS

• Close follow up!

TAKE HOME MESSAGE• Out of all admissions in ED with C/O chest pain,

31% are becoz of IHD and 42% due to gastric causes

• Diagnosis of AMI made on initial EKG, markers are only adjunctive

• Door to needle time determines the survival• Missed AMI rate is 2%... Serial ECGs, serial

markers and imaging help in improving this• Other life threatening causes like pulm embolism,

aortic dissection should always be kept in mind

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