Symptoms of Ischemic Heart Disease Chest discomfort with variable characteristics -pain, pressure,...

Symptoms of Ischemic Heart Disease

• Chest discomfort with variable characteristics -pain, pressure, tightness, crushing, squeezing, stabbing, choking sensations -substernal origin with variable radiation to arm, neck, or jaw -especially when associated with exertion -duration in minutes (5-30), not seconds or hours • Associated symptoms or anginal equivalents (dyspnea,

nausea/vomiting, indigestion, diaphoresis, syncope)

Patient history is often diagnostic.

Physical Findings in Ischemic Heart Disease

• Diaphoresis or other sign of hypoperfusion• Congestive signs: JVD, rales, S3• Abnormal heart sounds: S3, new murmur• Hypoxia• Arrhythmias, especially ventricular, although must

rule out MI with new onset afib

Physical exam is most useful to rule out differential diagnoses and often is normal in

ischemic heart disease.

Etiologies of Ischemia

• Atherosclerosis

• Congenital coronary anomalies

• Coronary arteritis

• Radiation therapy

• Cocaine

• Aortic stenosis

• Hypertrophic cardiomyopathy

Differential Diagnosis of Chest PainAcute coronary syndromes

Other cardiovascular causes• Aortic dissection• Aortic stenosis• Pericarditis• Myocarditis• Hypertrophic cardiomyopathy• Aortic regurgitation• Mitral valve prolapse• Severe anemiaPulmonary causes• Pulmonary embolus• Pneumothorax• Pleurisy

Gastrointestinal causes• Esophageal spasm or reflux• Esophageal rupture• Peptic ulcer disease• Biliary or pancreatic diseaseMusculoskeletal causes• Costochondritis• Muscle strain• Thoracic outlet syndrome• Degenerative spine diseasePsychogenic causes• Anxiety/depression/panic attack• Psychosis• Secondary gain

IT IS IMPERATIVE TO ASSESS FOR POSSIBLE LIFE-THREATENING ALTERNATIVE DIAGNOSES, SUCH AS AORTIC DISSECTION, PE,

TENSION PNEUMOTHORAX, OR RUPTURED VISCUS..

Patient Education for Early Recognition and Response to Chest Pain

Healthcare providers should instruct patients previously

prescribed nitroglycerin (NTG) on use for chest

discomfort or pain and to call 9-1-1 if symptoms do not

improve or worsen 5 minutes after ONE sublingual

NTG dose*.

(* Nitroglycerin Dose: 0.4 mg sublingually)

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STEMI: ACC/AHA guidelines at www.acc.org

Prehospital Chest Pain Evaluation and Treatment

Prehospital EMS providers should administer 162 to 325 mg of

aspirin (chewed) to chest pain patients suspected of having

STEMI unless contraindicated or already taken by the patient.

Although some trials have used enteric-coated aspirin for initial

dosing, more rapid buccal absorption occurs with non–enteric-

coated formulations.

It is reasonable for all 9-1-1 dispatchers to advise patients without

a history of aspirin allergy who have symptoms of STEMI to

chew aspirin (162 to 325 mg) while awaiting arrival of

prehospital EMS providers. Although some trials have used

enteric-coated aspirin for initial dosing, more rapid buccal absorption

occurs with non–enteric-coated formulations.




Options for Transport of Patients With STEMI and Initial Reperfusion Treatment

EMS Transport

Onset of symptoms of

STEMI

9-1-1EMS

Dispatch

EMS on-scene• Encourage 12-lead ECGs.• Consider prehospital fibrinolytic if

capable and EMS-to-needle within 30 min.

GOALS

PCIcapable

Not PCIcapable

Hospital fibrinolysis:

Door-to-Needle

within 30 min.

EMS Triage Plan

Inter-HospitalTransfer

Patient EMS Prehospital fibrinolysisEMS-to-needlewithin 30 min.

EMS transportEMS-to-balloon within 90 min.

Patient self-transport Hospital door-to-balloon

within 90 min.Dispatch

1 min.

5 min.

8 min.


Emergent Diagnostic Testing

• 12-lead EKG

• Cardiac enzymes (CPK, CKMB, Troponin)

• CBC

• Basic or comprehensive chemistry panel

• Coagulation studies

• D-Dimer

• PA and lateral CXR

Cardiac Biomarkers in ACSCPK (creatine phosphokinase) – enzyme common in skeletal, smooth, and

cardiac muscle as well as brain and kidney; three isoenzymes:

MB – cardiac and some skeletal muscle

MM – primarily in skeletal muscle

BB – primarily in brain and kidney

Troponin – protein that regulates interaction of actin and myosin

Troponin C – common to skeletal and cardiac muscle

Troponin T and I – diagnostic & prognostic value in myocardial injury

Cardiac biomarkers provide the most accurate diagnosis of acute myocardial injury and are the reference standard for the diagnosis of MI.

Other Biomarkers

Nonspecific serum markers – elevated in MI but non-specific

• AST (aspartate aminotransferase)

• LDH (lactate dehyrogenase)

• Myoglobin – rapid release and return to baseline but

elevated with muscle infarct and renal failure

Newer biomarkers – predictive of risk in ACS but not commonly used for this purpose

• BNP (B-type natriuretic peptide)

• CRP (C-reactive protein)

00 11 22 33 44 55 66 7788

Cardiac troponin-no reperfusion Cardiac troponin-no reperfusion

Days After Onset of STEMIDays After Onset of STEMI

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Upper reference limitUpper reference limit11

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Cardiac troponin-Cardiac troponin-reperfusion reperfusion

CKMB-no reperfusion CKMB-no reperfusion

CKMB-CKMB-reperfusion reperfusion

Cardiac Biomarkers in ACS

Alpert et al. J Am Coll Cardiol 2000;36:959.Wu et al. Clin Chem 1999;45:1104. STEMI: ACC/AHA guidelines at www.acc.org

Cardiac Biomarkers in STEMI

Troponins- Now the Gold Standard!

Rise after 3-6 hoursNegative Troponin within 6 hours of onset of S&S rules out the MIPeaks at about 20 hoursMay be raised for 14 days

Cardiac Biomarkers: Troponin T & I

Troponin TLevels may help to stratify risk

Less specific than Troponin I

Increased in angina

Increased in chronic renal failure

Highly sensitive for detecting myocardial ischemia

Troponin I90% sensitivity for MI 8 hours after onset of S&S and 95% specificity

Negative rules out MI

Obtain two negative troponin values 4-6-8 hours apart

Normally exceedingly low

Even a small elevation indicates myocardial damage

Troponin I Levels and Mortality in Patients with

NSTEMI

0

2

4

6

8

0- <0.4

0.4-<1.0

1.0-<2.0

2.0-<5.0

5.0-<9.0

>9.0

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orta

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ays

Adapted with permission from Antman EA, Tanasijevic MJ, Thompson B, et al. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med. 1996;335:1342-1349. Copyright © 1996, Massachusetts Medical Society. All rights reserved.

Troponin I Level

EKG Changes in STEMI

ST elevation of 1mm or more in the limb leads or of 2mm or more in precordial leads is significant.

The pattern of ST elevation indicates the location of infarct and the involved coronary artery.

Dynamic changes in the ST segment or the T wave represent an evolving infarct.

A new left bundle branch block is significant.

EKG Changes: Ischemia

• T-wave inversion (flipped T)

• ST segment depression

• T wave flattening

• Biphasic T-waves

EKG Changes: Injury• ST segment elevation of greater than 1mm in at least 2

contiguous leads

• Heightened or peaked T waves

• Directly related to portions of myocardium rendered electrically inactive

EKG Changes: Infarct

Significant Q-wave where none previously existed

• Impulse traveling away from the positive lead

• Necrotic tissue is electrically dead

Criteria for Q-wave significance

• Depth of Q wave should be 25% the

height of the R wave

• Width of Q wave is 0.04 secs

• Diminished height of the R wave

Dynamic EKG Changes

1 Year

Baseline

Hyperacute T wave

ST elevation

Inverted T wave

Q wave

EKG Changes: Anterior/Septal MI

ST changes: V1,V2, V3, V4 Culprit Vessel: LAD

EKG Changes: Inferior MI

ST Changes: II, III, aVF Culprit Vessel: RCA

EKG Changes: Lateral MI

ST Changes: I, aVL, V5, V6 Culprit Vessel: Circumflex

EKG Changes: Posterior MI

ST Changes: Reciprocal in V1, V2 Culprit Vessels: RCA or Cx

Summary of EKG Changes

Lat: I, aVL, V5, V6 Ant/Septal: V1, V2, V3, V4

Inf: II, III, aVF Post: Rec V1, V2

EKG Changes: Summary

Non-invasive Diagnostic Testing

• Echocardiography• Exercise stress testing• Pharmacologic stress testing -Adenosine -Persantine• Nuclear stress testing• Echocardiography• CTA• Cardiac MRI

May be considered only after acute MI or other emergent process has been ruled out.

Acute Pharmacologic Interventions in STEMI

• Oxygen

• Nitroglycerin

• Analgesia (Morphine)

• Aspirin

• Beta Blockers

MONA MONAB

Supplemental oxygen should be administered to

patients with arterial oxygen desaturation (SaO2

< 90%).

It is reasonable to administer supplemental oxygen to all patients with uncomplicated STEMI during the first 6 hours.

Oxygen




Patients with ongoing ischemic discomfort should receive sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous NTG.

Intravenous NTG is indicated for relief of ongoing

ischemic discomfort that responds to nitrate therapy,

control of hypertension, or management of pulmonary

congestion.

Nitroglycerin




Nitrates should not be administered to patients with:

Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil/Cialis©).

• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline

• severe bradycardia (< 50 bpm)• tachycardia (> 100 bpm) or• suspected RV infarction.

Nitroglycerin




Analgesia

Morphine sulfate (2 to 4 mg intravenously with

increments of 2 to 8 mg intravenously repeated at

5 to 15 minute intervals) is the analgesic of choice

for management of pain associated with STEMI.



Aspirin


Aspirin should be chewed by patients who have

not taken aspirin before presentation with STEMI.

The initial dose should be 162 mg (Level of

Evidence: A) to 325 mg (Level of Evidence: C)

Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations.



NSAIDs

NSAIDS (except ASA) should not be given during the acute hospitalization due to increased risk of mortality, reinfarction, HTN, heart failure, and myocardial rupture.

This restriction includes both nonselective as well as COX-II forms of NSAIDs.


Oral beta-blocker therapy should be administered

promptly to those patients without a contraindication,

irrespective of concomitant fibrinolytic therapy or

performance of primary PCI.

It is reasonable to administer intravenous beta-

blockers promptly to STEMI patients without

contraindications, especially if a tachyarrhythmia or

hypertension is present.

Beta-Blockers




Primary PCI for STEMI:General Considerations

Patient with STEMI (including posterior MI) or MI with new or presumably new LBBB

PCI of infarct artery within 12 hours of symptom onset

Balloon inflation within 90 minutes of presentation

Skilled personnel available (individual performs > 75 procedures per year)

Appropriate lab environment (lab performs > 200 PCIs/year of which at least 36 are primary PCI for STEMI)

Cardiac surgical backup available



Primary PCI for STEMI:Specific Considerations

Medical contact–to-balloon or door-to-balloon should be within 90 minutes.

PCI preferred if > 3 hours from symptom onset.

Primary PCI should be performed in patients with severe congestive heart failure (CHF) and/or pulmonary edema (Killip class 3) and onset of symptoms within 12 hours.





Times to remember

• 10 minutes time for ED eval• 30 minutes door to needle• 90 minutes door to balloon• 3 hours (symptom onset) Fibrinolytic

vs. PCI therapy• 12 hours (symptom onset) Time limit for

revascularization therapies as supported by data

•Given the current literature, it is not possible to say definitively that a particular reperfusion approach is superior for all pts, in all clinical settings, at all times of day.

•The main point is that some type of reperfusion therapy should be selected for all appropriate pts with suspected STEMI.

• The appropriate & timely use of some reperfusion therapy is likely more important than the choice of therapy.

Caveat on Reperfusion


Caveat on Reperfusion

The medical system goal is rapid recognition and treatment of patients with STEMI such that either:

1. Door-to-needle time for initiation of fibinolytic therapy

can be achieved within 30 miutes

OR

2. Door-to-balloon time for PCI can be kept within 90

minutes.


Maintenance Management of the Patient after MI

• Aspirin

• Plavix

• Beta Blocker

• ACE inhibitor/ARB

• Statin therapy

Aspirin

A daily dose of aspirin (initial dose of 162 to

325 mg orally; maintenance dose of 75 to 162

mg) should be given indefinitely after STEMI to

all patients without a true aspirin allergy.



Thienopyridines (Plavix)

In patients for whom PCI is planned, clopidogrel

(Plavix) should be started and continued:

• ≥ 1 month after bare-metal stent

• ≥ 3 months after sirolimus-eluting stent

• ≥ 6 months after paclitaxel-eluting stent

• Up to 12 months in absence of high risk for bleeding.


STEMI: ACC/AHA guidelines www.acc.org

Duration of Plavix use varies among interventional cardiologists.

Use of generic Plavix was strongly discouraged, but the generic form is no longer available.

Thienopyridines (Plavix)

2007 STEMI guidelines now include long-term use of Plavix regardless of reperfusion therapy (ie-fibrinolysis, PCI, or neither):

• Plavix 75mg po daily (LOE A) for at least 14 days (LOE B) or one year if patients under 75 years of age (LOE C).

• Plavix should be held for 5-7 days prior to to CABG.

STEMI: ACC/AHA guidelines www.acc.org

Maintenance Management

Beta blockers should be continued indefinitely in all patients who have no known contraindications.

ACE inhibitor (or ARB) if necessary should be continued indefinitely in all patients post MI.

Aggressive lipid management with a statin should be initiated promptly and continued.

Symptoms of Ischemic Heart Disease Chest discomfort with variable characteristics -pain, pressure,...

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