Download - Myocardial Infarction
PROF: OFCARDIOLOGY
LUMHS
EVALUATION OF CHEST PAIN
Objectives To be able to rapidly and accurately assess a
patient complaining of acute chest pain To be able to formulate an accurate
differential diagnosis for acute chest pain To understand and be able to initiate basic
initial therapy for a patient in acute chest pain
The background: Chest pain is one of the most common chief
complaints of patients presenting to EDs annually.
8-10% of the 119 million annual ED visits are for chest pain and related symptoms
Accurate diagnosis remains a challenge
there are a lot of importment data of the pain: localisation radiation onset of the pain the type (press, smart,cutting) dinamic of the pain (continouosly, ongoing, undulaiting) answer to the medical therapy
CHEST PAIN
The challenges: Patients presenting with chest pain who have
life threatening underlying disease often look well on initial presentation
It is estimated that 8-10% of patients presenting with ACS are discharged mistakenly from the ED
These patients have 30 day mortality of 2%
Challenges cont: Missed MI is the most common cause for
litigation stemming from ED treatment Higher awards are recovered in medical
malpractice lawsuits for missed MI than for any other condition
Internists are second only to family practitioners as the most likely group to be sued for missed MI
Chest Pain Visceral
Often referred Aching, heaviness, discomfort Difficult to localize pain
Somatic Sharp, easily localized
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
Initial Approach Triage
Chest pain Significant abnormal pulse Abnormal blood pressure Dyspnoea These pts need IV, O2, Monitor, ECG
Initial Approach Evaluation:
Airway Breathing Circulation Vital Signs Focused exam
Cardiac, pulmonary, vascular
Initial Approach History:
Character of pain Presence of associated symptoms Cardiopulmonary history Pain intensity, 0-10 pain
Initial Approach Secondary exam:
History Quality, radiation/migration, severity, onset, duration,
frequency, progression and provoking or relieving factors of pain
Risk factors Physical exam Review old records/ekg’s
Categorizing Chest Pain1. 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
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
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
Categorizing Chest Pain Assessment of Risk Factors CAD:
Cigarette Smoking Diabetes Hypertension Hypercholesterolemia Family History
Differential Diagnosis ofChest Pain Non Cardiac
Cardiac
Non Cardiac Chest Pain Pulmonary
Pneumonia Pleuritis Pneumothorax Pulmonary Embolism Tumor
Gastrointestinal GERD Esophageal spasm Mallory-Weiss Tear Peptic Ulcer disease Biliary/Gallbladder Disease Pancreatitis
Musculoskeletal Costochondritis Cervical Disk Disease Rib Fracture Intercostal Muscle Cramp
Other Herpes Zoster Disorders of the Breast Splenic Infarct Panic Attacks/Anxiety Disorder Fibromyalgia DKA
Cardiac Chest Pain
Aortic Dissection Pulmonary Embolism Pulmonary
Hypertension Pericardial Diseases Aortic Stenosis Heart Failure Cocaine Abuse
Acute Coronary Syndromes Stable Angina Unstable Angina Myocardial Infarction Cardiogenic Shock
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Pulmonary Embolism:
PE: Presentation Presentation variable Suspect in any patient c/o new or worsening
dyspnoea, chest pain or prolonged hypotension without obvious etiology
Symptoms: dyspnoea (sec. to min) > pleuritic chest pain > cough
Signs: tachypnoea > tachycardia > rales > loud P2
PE: Diagnosis
PE: ECG
PE: Management
PE: Clinical guidelines
PE: Anticoagulation Enoxaparin 1mg/kg Q12H UFH: 80IU/kg then 18IU/hr (5000IU max) Fondaparinux
5mg daily if <50kg 7.5mg daily if 50-100kg 10mg daily if >100kg
If clinical suspicion high, initiate anticoagulation prior to confirming diagnosis
Long term management: V-K antagonists LMWH preferred in
patients with malignancy or pregnancy
Duration: 1st provoked: 3mo 1st unprovoked, malignancy
or recurrent, consider indefinite tx
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Pneumothorax: Presentation Primary Spontaneous PTX:
Seen in patinets without underlying lung disease Smoking, FH and Marfans predispose Usually 20s-40s, present with sudden onset dyspnea and
pleuritic CP at rest Physical findings include decreased chest excursion,
decreased breath sounds, hyperresonance Hypoxeima common, hypercapnea uncommon 2/2
perfusion of PTX but adequate ventilation with contralateral lung
Pneumothorax: Presentation Secondary Spontaneous PTX
Seen in patients with underlying lung disease Any lung disease predisposes however COPD
most common PCP, CF and TB also common causes Similar physical presentation to PSP ABG typically abnormal 2/2 underlying lung
disease
Pneumothorax: Diagnosis CXR: Look for
pleural line Can be difficult in
patients with COPD CT scan can
overestimate size of PTX
Pneumothorax
Pneumothorax
Pneumothorax: Treatment ABCD Assess haemodynamic
stability If < 2cm and stable,
can observe If > 2cm, chest tube If haemodynamically
unstable, chest tube
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Oesophageal rupture: Hospitalized: >50% 2/2 instrumentation of
esophagus Traumatic: MVA, chest wall trauma Spontaneous: (transmural perforation)
Vomiting (Boerhaave’s Syndrome): retching followed by severe chest and epigastric pain, tachypnoea, dyspnoea, fever, cyanosis, shock
Caustic ingestion, pill esophagitis, Barrett’s, oesophageal ulcers in HIV patients
Oesophageal rupture: Diagnosis
CXR: early shows mediastinal or free peritoneal air Hours to days
later: widening of mediastinum, pleural effusion
Oesophageal rupture: CT scan: Oesophageal
oedema, extra oesophageal air, perioesophageal fluid
Oesophagram: Extravasation of contrast
NO role for endoscopy which introduces more air into mediastinum
Oesophageal rupture: Treatment Management variable
and depends on size, location, rapidity of diagnosis and underlying disease
Treatment surgical Complications:
mediastinitis , sepsis, shock, death
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Aortic dissection: Presentation Sharp, “tearing” anterior or posterior chest
and back pain. Typically sudden onset and severe Chest pain more common with type A
dissections Complicated by CVA, syncope, MI (RCA) or
HF
Aortic dissection: Diagnosis Generally 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: Predisposing factors:
Aortic aneurysm HTN Vasculitis Marfan’s or other collagen diseases CABG/cardiac catheterizaion Drugs (crack cocaine) Trauma
Aortic dissection: Classification
Aortic dissection
Aortic dissection
Aortic Dissection: Management Type A: Surgical Type B and uncomplicated: Medical Type 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 Management ICU admission Pain control: Morphine Reduction 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
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Pericarditis Chest 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: 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: 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
Myocarditis Presentation variable Viral most common etiology in developed
countries Presents with HF, chest pain, sudden cardiac
death or arrhythmias Workup with biomarkers, ECG, CXR, TTE,
cardiac MR and endomyocardial biopsy Consider in young male with new onset HF
Chest Pain
Non Cardiac
Cardiac
PE
PTX
Oesophageal disaster
Aortic disease
Myo/pericardium
Coronary disease
Coronary spasm
Obstructive CAD
ACS
Stable angina
Acute coronary syndrome
Pathogenesis of UA/NSTEMI
ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST Elevation Myocardial Infarction
Definition“… any constellation of clinical
symptoms that are compatible with acute myocardial
ischemia..."
Acute Coronary Syndrome
Pathophysiology:Acute coronary perfusion deficit Mechanism:
coronary plaque rupture (95%) lead to partial or total coronary occlusion
coronary spasm Prinzmetal angina (transient ST elevation) myocardial infarction (if the ischemic period is to long)
coronary embolisation
current complaint: pain
there are a lot of importment data of the pain: localisation radiation onset of the pain the type (press, smart,cutting) dinamic of the pain (continouosly, ongoing, undulaiting) answer to the medical therapy
Acute coronary syndrome: diagnosis
ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST Elevation Myocardial Infarction
Unstable Angina / NSTEMI
Definition“… ST-segment depression or
prominent T-wave inversion and/or positive biomarkers of
necrosis… in the absence of ST-segment elevation and in an
appropriate clinical setting..."
ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST Elevation Myocardial Infarction
Unstable Angina / NSTEMI(Unstable Angina)
Unstable Angina / NSTEMI
STEMI
LBBB
Physical ExamT 36oC, P 85, BP 140/80, R 15, Pain 2/10
General – no distress
Neuro - A&O
CVS - normal inspection, PMI normal and nondiplaced, no heave, regular rhythm with normal sounds, no murmers or rubs, JVP 7 cm, radial and pedal pulses normal
Pulmonary - clear
Abdomen – nontender without hepatomegaly
Extremities – no edema
Chest X-RayQuality – exposure and rotation
Bony structures
Mediastinum
Heart
Costophrenic angles
Lung fields
TIMI Risk Score
Antman et al JAMA 2000; 284: 835 - 842www.timi.org
Age 65 3 CAD risk factors(FHx, HTN, chol, DM, active smoker)
ST deviation 0.5 mm cardiac markers
Recent (24H) severe angina
HISTORICAL
PRESENTATION
RISK SCORE = Total Points (0 - 7)
Known CAD (stenosis 50%)
ASA use in past 7 days
1
11
1
1
11
POINTS RISK OF CARDIAC EVENTS (%)BY 14 DAYS IN TIMI 11B*
0/12345
6/7
RISKSCORE
3357
1219
DEATH OR MI
DEATH, MI ORURGENT REVASC
5813202641
*Entry criteria:UA or NSTEMII defined as ischemic pain at rest within past 24H, with evidence of CAD (ST segment deviation or +marker)
A Chest Pain Case
A Chest Pain CaseCAD risk factors
- + Family history- HTN- Dyslipidemia
Home meds- ASA 81 mg po daily- HCTZ 25 mg po daily
Biomarkers- CK 413- MB 7 with index of 2- Troponin I 6.8
TIMI Risk Score- 5
Age 65 3 CAD risk factors(FHx, HTN, chol, DM, active smoker)
ST deviation 0.5 mm cardiac markers
Recent (24H) severe angina
HISTORICAL
PRESENTATION
RISK SCORE = Total Points (0 - 7)
Known CAD (stenosis 50%)
ASA use in past 7 days
1
11
1
1
11
POINTS
A Chest Pain CaseCAD risk factors
- + Family history- HTN- Dyslipidemia
Home meds- ASA 81 mg po daily- HCTZ 25 mg po daily
Biomarkers- CK 413- MB 7 with index of 2- Troponin I 6.8
TIMI Risk Score- 5
RISK OF CARDIAC EVENTS (%)BY 14 DAYS IN TIMI 11B*
0/12345
6/7
RISKSCORE
3357
1219
DEATH OR MI
DEATH, MI ORURGENT REVASC
5813202641
*Entry criteria:UA or NSTEMII defined as ischemic pain at rest within past 24H, with evidence of CAD (ST segment deviation or +marker)
Thygensen, et al JACC 50: 2173, 2007
Other reasons for Troponins
Heart failurePulmonary embolus
Renal failure
ACSACS
STEMISTEMI
high riskhigh risk•early high riskearly high risk•late high risklate high risk
STEMI STEMI >>12 h12 hSTEMI STEMI ≤ 12 h≤ 12 h
cardiogenic cardiogenic shock shock ≤ 36 h≤ 36 h
Ope
n ar
tery
theo
ry
Ope
n ar
tery
theo
ry
Primary PCI Primary PCI ((CABG))((CABG))
ThrombolysisThrombolysis rescue PCI rescue PCI ((CABG))((CABG))
PCI ((CABG))PCI ((CABG))
NSTE-ACSNSTE-ACS
risk stratificationrisk stratification
med. th.med. th.non-inv.im. (echo, stress-test etc.non-inv.im. (echo, stress-test etc.
PCI ((CABG))PCI ((CABG))
First primary PCI program in 1999
24-hour organised primary PCI in Budapest since 01.01.2003.
First primary PCI in 1993
In-hospital mortality (STEMI)
30
1510
70
5
10
15
20
25
30
35
60-s 70-s 80-s 90-s
CCU + defibrillatorCCU + defibrillator
thrombolysisthrombolysis
primary primary PCIPCI
In-hospital mortality dramatically decreased under the last 30 years:In-hospital mortality dramatically decreased under the last 30 years:
STEMI Quick diagnosis (Typical chest pain and ECG ) Time window? Prehospital therapy
aspirin 250 mg morphine nitroglycerin
again the pain, hypertensive state, left ventricular failure Attention! Right ventricular infarction can cause sever hypotension!
O2
Send the patient to the hospital
ACSACS
STEMISTEMI
high riskhigh risk•early high riskearly high risk•late high risklate high risk
STEMI STEMI >>12 h12 hSTEMI STEMI ≤ 12 h≤ 12 h
cardiogenic cardiogenic shock shock ≤ 36 h≤ 36 h
Ope
n ar
tery
theo
ry
Ope
n ar
tery
theo
ry
Primary PCI Primary PCI ((CABG))((CABG))
ThrombolysisThrombolysis rescue PCI rescue PCI ((CABG))((CABG))
PCI ((CABG))PCI ((CABG))
UA/NSTEMIUA/NSTEMI
risk stratificationrisk stratification
med. th.med. th.non-inv.im. (echo, stress-test etc.non-inv.im. (echo, stress-test etc.
PCI ((CABG))PCI ((CABG))
Inferior STEMI
RCA PCI
RCA occlusion
After stenting ►
In the CCU a lot of technical devices (IABP,respirator, dialysator) are necessary
IAB Inflation
IAB Deflation
Complication of myocardial infarction Arrhythmias
Life-threating: Ventricular tachycardia / ventricular fibrillation – sudden death (I.
symptom?) II-III degree AV block – asystolie
Ventricular failure (LV mass loss >40%) pulmonal oedem cardiogenic shock right ventricular failure – impared filling pressure (CAVE: NITRO!)
Mechanical complication mitral papillar rupture – acute mitral regurgitation ventricular septal rupture free wall rupture – pericardial Tamponade
Acute mitral flail, chordal rupture
Cardiac rupture syndromes complicating STEMI
Anterior myocardial rupture
Rupture of the ventricular septum
Complete rupture of a necrotic papillary muscle
Pericardial Tamponade
Pericardial Tamponade
Pericardial Tamponade
Pericardial Tamponade
Conclusion The acute coronary syncrome is an acute, life-threating
coronary event Need an urgent hospitalisation Short anamnesis (mostly the pain!!), physical examination rapidly perfom an ECG according to the ECG: NSTE-ACS or STEMI In case of NSTE-ACS: risk stratification In case of STEMI:
If the patient has typical chest pain + typical ECG with acut STEMI – If the patient has typical chest pain + typical ECG with acut STEMI – it is enough to diagnose!it is enough to diagnose!
If the time-window is <12 hours: reperfusion therapy (primary PCI or if pPCI is not feasible thrombolytic therapy)
ACS: General principles Unstable Angina
Rest angina: Usually >20 minutes duration New onset severe angina Increasing angina
NSTEMI STEMI
ACS: Management Initial therapy: Oxygen, nitro, ASA, ECG HR control Antiplatelets: Clopidogrel, Prasugrel Anticoagulation: Pain control: Conservative vs. Invasive management
ACS: Cautions B blockers Morphine Inferior MI (RV infarct) Compare ECGs UH vs. LMWH Repeat ECGs Always consider chief complaint
ACS: A word about troponin Just because there is no troponin, doesn’t
mean it’s not ACS Just because there is troponin, doesn’t mean
it’s ACS Troponin is prognostic more than diagnostic
Practical application: Called by nursing to evaluate patient with
chest pain Ask for vitals over phone, stability of the
patient and brief details ECG Go see the patient
Practical application Focused history and physical exam
Focused history and chart review Vitals: BP in both arms, pulsus paradoxus GEN: Distress Neck: JVD, carotid bruits Lungs: Crackles, wheezing, effusions Precordium: Heaves, reproducible pain CVS: Regular/irregular, new murmurs, rubs or gallops, muffled
heart sounds Abd: Pulsatile masses, renal bruits Ext: LE edema, peripheral pulses
Practical application ECG: compare to old, repeat frequently Other imaging studies as indicated by
presentation: CXR, stat TTE, CT scan Biomarkers if applicable KEY: Commit to a diagnosis Begin initial therapy Call for help at any point you are not
comfortable
Conclusions: Chest pain is one of the most frequently encountered
complaints in both the inpatient and outpatient settings and is a significant financial burden on our health care system
Clinicians must be able to rapidly and accurately assess a patient with chest pain to maximize patient outcomes and minimize unnecessary workup
The evaluation of chest pain requires good history and physical exam skills, ECG, CXR and few other diagnostic tests
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