Approach to Chest painApproach to Chest pain

Presented by

Dr Ashraf-ur-Rahman TamalAsst Regitrar, MU VIIIDMCH

Chest PainChest Pain5 Million emergency department visits2 million hospitalizations annually with

cost of more than $8 billionCardiac etiology found <1/3rd2% of patients with acute MI are

unrecognized and discharged from the ED

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%

INITIAL APPROACHINITIAL APPROACHAssume the worst!100% OxygenIV accessMonitoringECG quicklyDone in tandem with history taking

CHEST PAIN ASSESSMENTCHEST PAIN ASSESSMENT

HISTORY EXAMINATIONECGCARDIAC ENZYMESCXROTHERS

Clinical Approach to Chest PainClinical Approach to Chest Pain

History: A- Pain analysis1- Characteristic: Sharp Squeezing heaviness

pressure Stabbing Pluritic Tearing Burning

Pericarditis, HZPericarditis, HZ

MI, AnginaMI, Angina

pericarditispericarditis

PEPE, , PneumoniaPneumoniaADAD

GERDGERD

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

ContCont’’d.. approachd.. approach

5- Duration:< 15 min ( 2- 10) min Stable AnginaUpto 30 min MI, UAUpto 60 min E.spasmFew hours PE, pnumothoraxHours to days pericarditisLonger HZ

NOTE: <2/3 min less likely to be cardiac.

ContCont’’d.. approachd.. approach

6- Aggravating:

Exertion, cold, stress, meals ischemiaSwallowing, postprandial, smoking GIDeep breathing, movement MSK,

pericarditisDeep breathing PE, Pneumothorax

NOTE: HZ is not aggravated by anything

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.

ContCont’’d.. approachd.. approach

8- Associated symptoms:Cough, fever, sputum, dyspnea.Sweating.Nausea, vomiting .Heamoptysis.Heartburn, regurgitation.Palpitations.Psychiatric symptoms: Anxiety,

depression, panic attack

Physical examinationPhysical examinationA- 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.

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

DIAGNOSTIC EVALUATION:DIAGNOSTIC EVALUATION:ECGCardiac 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.

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.

LIFE THREATENING CAUSESLIFE THREATENING CAUSES

P is Pericarditis. A is Acute myocardial infarction.P is Pneumothorax P is Pulmonary embolism A is Aneurysm ( AD)

Pulmonary EmbolismPulmonary EmbolismPhysical:Anxious patient, sense of impending

doom.Tachycardia, tachypnea, hypoxia.If severe, can get hypotension,

syncope, and RV failure (↑JVP, RV heave)

Pulmonary EmbolismPulmonary EmbolismHistory:Sudden-onset, sharpExacerbated by inspiratory effortAssociated with hemoptysis, sycope,

dyspnea, calf swelling/pain from DVTRisk 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].

Investigations:↓PaO2 and ↓PaCO2 from increase in

overall minute ventilationD-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 / V\Q

Pulmonary EmbolismPulmonary EmbolismManagement: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.

Aortic dissection: Aortic dissection: PresentationPresentationSharp, “tearing” anterior or

posterior chest and back pain. Typically sudden onset and

severeChest pain more common with

type A dissectionsComplicated by CVA, syncope, MI

(RCA) or HF

Aortic dissection: Aortic dissection: DiagnosisDiagnosisGenerally 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

Aortic Dissection:Aortic Dissection:Predisposing factors:

◦Aortic aneurysm◦HTN◦Vasculitis◦Marfan’s or other collagen diseases◦CABG/cardiac catheterizaion◦Drugs (crack cocaine)◦Trauma

Aortic dissection: Aortic dissection: ClassificationClassification

Aortic dissectionAortic dissection

Aortic dissectionAortic dissection

Aortic Dissection: Aortic Dissection: ManagementManagementType A: SurgicalType B and uncomplicated:

MedicalType 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

Acute ManagementAcute ManagementICU admissionPain control: MorphineReduction 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

PericarditisPericarditisChest 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

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)

Pericarditis: ECG:Pericarditis: ECG:

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

ACSACS

Acute Coronary SyndromeAcute Coronary Syndrome

Ischemic DiscomfortUnstable Symptoms

No ST-segmentelevation

ST-segmentelevation

Unstable Non-QQ-Waveangina AMI AMI

ECG

AcuteReperfusion

HistoryPhysical Exam

ACS: General principlesACS: General principlesUnstable Angina

◦Rest angina: Usually >20 minutes duration

◦New onset severe angina◦Increasing angina( Worsening)-

Crescendo Angina◦Angina not relieved by GTN◦Post MI Angina

NSTEMISTEMI

Symptoms of ACSSymptoms of ACS

Prolonged CHEST PAIN ANXIETYFEAR OF IMPENDING DEATHBREATHLESSNESSVOMITINGCOLLAPSESYNCOPESILENT

SIGNS OF ACSSIGNS OF ACSSIGNS OF SYMPATHETIC

ACTIVATIONPALLORSWEATINGTACHYCARDIA

SIGNS OF VAGAL STIMULATIONVOMITINGBRADYCARDIA

SIGNS of ACSSIGNS of ACS

Signs of impaired myocardial function:Hypotension, Oliguria, Cold

peripheriesNarrow pulse pressureRaised JVPS3Quit S1Diffuse apical impulseBasal creps

ACSACSINVESTIGATIONSINVESTIGATIONSECG HELPFUL DIFFICULT INTERPRETATION IN PREVIOUS MI

PATIENTS AND OLD BBBRARELY NORMAL ECG IN 1/3 OF MI CASES INITIAL CHANGES MAY

NOT BE DIAGNOSTICEARLIEST CHANGE ST ELEVATIONLATER R WAVE SIZE DIMINUTIONQ WAVES IN TRANSMURAL MIT WAVE INVERSIOnCHEK AREA OF INFARCTION

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

Normal or non-diagnostic Normal or non-diagnostic EKGEKG

ST Depression or Dynamic T ST Depression or Dynamic T wave Inversionswave Inversions

ST-Segment Elevation MIST-Segment Elevation MI

New LBBBNew LBBB

QRS > 0.12 secL Axis deviationProminent R wave V1-V3

Prominent S wave 1, aVL, V5-V6

with t-wave inversion

Wall AffectedWall AffectedLeads Showing ST Leads Showing ST Segment ElevationSegment Elevation

Leads Showing Leads Showing Reciprocal ST Reciprocal ST Segment DepressionSegment Depression

Suspected Culprit Suspected Culprit ArteryArtery

SeptalSeptalV1, V2V1, V2NoneNoneLeft Anterior Left Anterior Descending (LAD)Descending (LAD)

AnteriorAnteriorV3, V4V3, V4NoneNoneLeft Anterior Left Anterior Descending (LAD)Descending (LAD)

AnteroseptalAnteroseptalV1, V2, V3, V4V1, V2, V3, V4NoneNoneLeft Anterior Left Anterior Descending (LAD)Descending (LAD)

AnterolateralAnterolateralV3, V4, V5, V6,I, V3, V4, V5, V6,I, aVLaVL

II, III, aVFII, III, aVFLeft Anterior Left Anterior Descending (LAD), Descending (LAD), Circumflex (LCX), Circumflex (LCX), or or Obtuse MarginalObtuse Marginal

Extensive Anterior Extensive Anterior (Sometimes called (Sometimes called Anteroseptal with Anteroseptal with Lateral extension)Lateral extension)

V1, V2, V3, V4,V5, V1, V2, V3, V4,V5, V6, I, aVLV6, I, aVL

II, III, aVFII, III, aVFLeft main coronary Left main coronary artery (LCA)artery (LCA)

Wall AffectedWall AffectedLeads Showing ST Leads Showing ST Segment ElevationSegment Elevation

Leads Showing Leads Showing Reciprocal ST Reciprocal ST Segment DepressionSegment Depression

Suspected Culprit Suspected Culprit ArteryArtery

InferiorInferiorII, III, aVFII, III, aVFI, aVLI, aVLRight Coronary Right Coronary Artery (RCA) or Artery (RCA) or Circumflex (LCX)Circumflex (LCX)

LateralLateralI, aVL, V5, V6I, aVL, V5, V6II, III, aVFII, III, aVFCircumflex (LCX), Circumflex (LCX), or or Obtuse MarginalObtuse Marginal

Posterior Posterior (Usually (Usually associated with associated with Inferior or Lateral Inferior or Lateral but can be isolated) but can be isolated)

V7, V8, V9V7, V8, V9V1, V2, V3, V4V1, V2, V3, V4Posterior Posterior Descending (PDA)Descending (PDA) (branch of the (branch of the RCA RCA or or Circumflex (LCXCircumflex (LCX))

Right ventricular Right ventricular (Usually associated (Usually associated with Inferior)with Inferior)

II, III, aVF, V1, II, III, aVF, V1, V4RV4R

I, aVLI, aVLRight Coronary Right Coronary Artery (RCA)Artery (RCA)

Myocardial Ischemia or Myocardial Ischemia or Infarction(ACS)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 hypoxicNitro spray/drip for painAspirinLasix if in congestive heart failureInotropes if in cardigenic shockStreptokinase (thrompolytics)Anticoagulation (non Q wave MI : Heparin or

LMWH, Q wave MI :Thrompolytic and

Heparin/LMWH)

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.

Mx of NSTEMIMx of NSTEMIHigh-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.

Mx of NSTEMI/UAMx of NSTEMI/UAA 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.

Mx of STEMIMx of STEMIMeta-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

Prinzemtal’s angina( variant angina or angina inversa,)

a syndrome typically consisting of angina at rest that occurs in cycles.

Cause by vasospasm

FeaturesSymptoms typically occur at rest, rather

than on exertion (attacks usually occur at night).

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.

Treatment

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

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

Risk Scoring – at Risk Scoring – at admissionadmission

Thresholds of RiskThresholds of Risk

MUSCULOSKELETAL CHEST PAINMUSCULOSKELETAL CHEST PAIN

ARTHRITISCOSTOCONDRITI

SINTERCOSTAL

MUSCLE INJURYCOXSACKIE

VIRAL INFECTIONMINOR SOFT

TISSUE INJURIES

VARY WITH VARY WITH POSTUREPOSTURE

VARY WITH VARY WITH POSITIONPOSITION

LOCAL LOCAL TENDERNESSTENDERNESS

TEITZE`S SYNDROMETEITZE`S SYNDROMEIDIOPATHIC COSTOCONDRITISIDIOPATHIC COSTOCONDRITIS

LOCALIZED PAIN/TENDERNESS AT COSTOCONDRAL JUNCTION

ENHANCED BY EMOTION,COUGHING,SNEEZING

2nd.RIB MOST AFFECTED

OESOPHAGEAL PAINOESOPHAGEAL PAINCAN MIMIC ANGINAL PAINMAY GET PRECIPITATED BY

EXERCISEMAY BE RELIEVED BY NITRATESRELATION WITH SUPINE

POSITION,EATING,DRINKING H/O REFLUXCAN RADIATE TO BACK

RUPTURED OESOPHAGUS CLINICAL FEATURES

SEVERE CHEST PAINSHOCKSUB-CUTANEOUS EMPHYSEMAPLEURAL EFFUSIONPNEUMOTHORAXPNEUMOMEDIASTINUM

Questions?Questions?