24 approach to chest pain
DESCRIPTION
approach to chest pain.pptTRANSCRIPT
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?