Ischemicsyndromes

Acute Coronary Syndromes EMS Professions Temple College

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The History of Paramedics Begins with Cardiac Care ✔The original Paramedic idea was based upon the need for rapid response to, identification of and emergency care for victims of: ➨Sudden Cardiac Death (SCD) ➨Acute Myocardial Infarction (AMI) 2

Ischemic Coronary Syndromes ✔Acute Coronary Syndromes ➨Angina Pectoris ➨Unstable Angina ➨Acute Myocardial Injury ➨Acute Myocardial Infarction ✔ Presentation with suspected ischemia Non-diagnostic ECG ◆ ST segment depression ◆ ST segment elevation/New BBB ◆

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Ischemic Coronary Syndromes ✔Angina Pectoris ➨Acute pain, usually in the chest, resulting from an increased demand for oxygen and a decreased ability to provide it ➨Usually due to a partially occluded coronary artery or vasospasm

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Ischemic Coronary Syndromes ✔Angina Pectoris ➨Typical Presentation ◆

Squeezing, Crushing, Heavy, Tight – Fist to chest = Levine’s sign

Pain/Discomfort may radiate to shoulders, arms, neck, back, jaw or epigastrium ◆ Usually lasts 3-5 min and rarely exceeds 15 min ◆ Not changed by swallowing, coughing, deep breathing or positional changes ◆

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Ischemic Coronary Syndromes ✔Angina Pectoris ➨Typical Presentation Anxiety ◆ Diaphoresis or clammy skin ◆ Nausea, vomiting ◆ Shortness of breath ◆ Weakness ◆ Palpitations ◆ Syncope ◆

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Ischemic Coronary Syndromes ✔Angina Pectoris ➨Usually Provoked by: Exercise ◆ Eating ◆ Emotion/Stress ◆

➨Usually Relieved by: Rest; Removal of provoking factor ◆ Nitroglycerin ◆

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Ischemic Coronary Syndromes ✔Stable Angina Pectoris ➨Reasonably Predictable frequency, onset, duration ➨Relief predictable with rest, nitroglycerin

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Ischemic Coronary Syndromes ✔Stable Angina Pectoris ➨Treatment Goals Reduce myocardial oxygen demand ◆ Improve myocardial oxygen supply ◆

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Ischemic Coronary Syndromes ✔Stable Angina Pectoris ➨Treatment Physical/Psychological rest ◆ Position of comfort, sitting or supine ◆ Oxygen ◆ ECG Monitor ◆

– Assess the underlying rhythm ◆

Nitroglycerin, 0.4 mg SL q 5 min as long as BP > 90 mm Hg – Continue until pain relieved or contraindicated

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Ischemic Coronary Syndromes ✔Stable Angina Pectoris ➨Transport Considerations Many persons stay home and treat themselves ◆ Treat first-time angina, unstable angina or angina requiring more than 3 NTG (>15 min) as AMI ◆ When in doubt, treat as AMI ◆

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Ischemic Coronary Syndromes ✔Stable Angina Pectoris ➨Variant Angina (Prinzmetal’s Angina) Occurs at rest ◆ Episodes at regular times of day ◆ Results from coronary vasospasms ◆ Treated long term with calcium channel blockers ◆ May result in abnormal 12 lead ECG changes that resolve with minimal treatment ◆

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Ischemic Coronary Syndromes ✔Unstable Angina ➨Prolonged chest pain/ischemic symptoms or an atypical presentation of angina without ECG or laboratory evidence of AMI (Injury) ➨Usually associated with significant or progressing occlusion of a coronary artery or severe vasospasm ➨Considered “Pre-infarction Angina” 13

Ischemic Coronary Syndromes ✔Unstable Angina ➨May have Typical or Atypical Signs & Symptoms ◆ Atypical Presentation – Increased frequency or duration of episodes – Onset with less exertion than normal – Increased severity of symptoms – Requires greater number of NTG tablets to relieve symptoms 14

Ischemic Coronary Syndromes ✔Unstable Angina ➨Treatment same as Angina PLUS: ◆

IV, NS (no dextrose), TKO – Some exceptions to restricting fluid

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12 Lead ECG – Assess for RVI

Morphine sulfate, 2 - 4 mg q 5-15 min slow IV titrated to pain relief and BP > 90 ◆ Aspirin, 160-325 mg PO ◆

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– Chewed & swallowed if possible – Determine if hypersensitive to ASA

Ischemic Coronary Syndromes ✔Unstable Angina ➨Treatment Metoprolol, 5 mg slow IV q 5 min to 15 mg total, prn for  HR/BP in absence of contraindications ◆ In longer or interfacility transports, consider: ◆

– – –

Nitroglycerin IV infusion, 10-20 mcg/min Heparin GP IIB/IIIA inhibitors

Thrombolytics Checklist (just in case) ◆ Transport, destination? ◆

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Ischemic Coronary Syndromes ✔Acute Myocardial Injury ➨Presentation of Unstable Angina or Acute Ischemia with potential for myocardium salvage (penumbra) ➨Diagnostic evidence of Injury (ECG or elevated Enzymes) Does not necessarily imply necrosis of the myocardium ◆ Presentation, Signs and Symptoms are the same as Acute MI ◆

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Necrosis of myocardial tissue caused by a lack of oxygenation and blood flow resulting from an occluded coronary artery ➨Often also used to describe acute injury when extent of necrosis is unknown but imminent ➨Diagnostic evidence of injury is present (elevated enzymes and possibly ECG) 18

Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Precipitating Factors Coronary thrombosis (most common) ◆ Coronary vasospasm ◆ Microemboli ◆ Severe Hypotension/Shock ◆ Acute Hypoxia ◆ Acute Volume Overload ◆

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Location, size of infarct and severity depends on site of vessel occlusion majority involve left ventricle ◆ LCA ◆

– anterior, septal, lateral ◆

RCA – inferior, right ventricle

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Often defined further as subendocardial: involves only subendocardial muscle ◆ transmural: full thickness of ventricular wall involved ◆

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Evolution of AMI Anatomy of Plaque Disruption Shoulder region Lipid core Media

Lumen

Lumen Lipid core

Fibrous cap

“Vulnerable” Plaque • Thin, friable fibrous cap separating substantial thrombogenic lipid core from blood

“Stable” Plaque • Thick fibrous cap protecting thrombogenic lipid core from blood • More luminal narrowing

• Lumen could be well preserved Ada pte d from Libby P . Circulat ion. 1995;9 1:2844- 2850, w ith permission.

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Evolution of AMI Plaque Rupture, Stenosis, and Thrombosis Plaque rupture — intraplaque thrombus Mural thrombus Occlusive thrombosis

Total chronic occlusion

Recanalized lumen

Healed plaque — increased stenosis

Healed plaque — decreased stenosis

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Ada pte d from Davies MJ . In: Schla nt RC, Alexander RW, eds. The Heart, Arteries and Ve ins. 8th ed. 1994:1 009-102 0, with permission.

Evolution of AMI Plaque Rupture and Thrombus Progression Complete occlusion

Lysis and residual thrombus

Disease progression

AMI Lipid- Plaque rich disruptio plaque n

Reocclusion

Unstable angina Thrombus

Partial (labile) occ lusion Recurrent pain

Ada pte d from Fus ter V. N Engl J Med. 199 2;326:2 42-250, with perm iss ion.

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Coronary Artery Without Evidence of Plaque

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Source: University of Utah WebPath

Coronary Artery with Significant Plaque Formation In addition to reduced Lumen size, there is also a calcified portion (right side of photo)

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University of Utah WebPath

Coronary Artery with Significant Plaque Formation

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Source: University of Utah WebPath

Rupture of Atheromatous Plaque Results in Thrombus Formation ✔ Rupture of “Vulnerable” plaque’s soft lipid core is the initiating event in most acute ischemic coronary events ✔ Occlusion is dependent on clot formation and and accompanying fibrinolysis ✔ A thrombotic occlusion that is relatively persistent (i.e., 2 to 4 hours or longer) may result in acute myocardial infarction 28

Rupture of Atheromatous Plaque Results in Thrombus Formation ✔ Repeated thrombus formations may further decrease the lumen size ✔ Intermittent non-occlusive thrombus formation results in Unstable Angina ✔ Incomplete occlusion may also result in MI possibly due to coronary artery spasm

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Coronary Artery With Plaque and Thrombus Formation A - Coronary Artery crosssection B - Lumen C - Fissured Plaque w/o Cap D - Acute thrombus 30Source:

Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997

Plaque and Thrombus Formation Resulting in Occlusion

31Source:

University of Utah WebPath

Coronary Artery Thrombus The external anterior view of the heart shows a dark clot formation in this artery

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Source: University of Utah WebPath

Evolution of Infarction/Necrosis Coronary Artery Occlusion: The Evolution of Infarction Progression of myocardial necrosis with time since occlusion 30 min

4h Normal myocardium

Normal myocardium

“At risk” myocardium, ischemic but viable Necrosis starting subendocardially

6 - 12 h Normal myocardium

“At risk” myocardium, ischemic but viable

Necrosis extending towards subepicardium

Completed infarct involving whole area at risk

Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission.

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Presentation ◆

Similar to Angina but – – – –

Some present atypically with complaints of only weakness or shortness of breath ◆ Dysrhythmias ◆ Sudden Cardiac Death ◆

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Last longer Not easily relieved with rest or NTG Sx/Sx may be more severe (feeling of impending doom) Pain often radiates to arms, neck, jaw, back, epigastrium

Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Presentation ◆

10-20% have “silent” MI (no chest pain) – common in elderly, older women, diabetics

If adding chest pain to the patient’s list of Sx/Sx completes a clear picture of AMI, then the patient is having an AMI!! ◆ Vital Signs and monitoring ECG leads DO NOT provide DIAGNOSTIC evidence of AMI!! ◆ Clinical diagnosis in absence of 12 Lead ECG or Enzyme changes ◆

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Therapies Goals for AMI Therapy Shorten time to reperfusion

Preserve LV function

Avoid heart failure or cardiac shock

Limit Infarct Size

REDUCE MORTALITY IMPROVE OUTCOME

Yusuf, et al. Circulation. 199 0;82(suppl II):II-11 7-134.

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Schroder R. e t al. J Am Coll Cardiol. 1995;2 6:1657- 1664

Resolve ST-segment elevation

Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Treatment Goals ◆

Decrease myocardial oxygen demand – Remove physical/psychological stressors – Relieve pain – Reduce workload of the heart (BP, HR)

Inhibit further clot formation ◆ Rapid identification/diagnosis ◆ Transport for reperfusion therapy ◆

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Treatment same as Angina PLUS: ◆

IV, NS, large bore – – – – –

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TKO with some exceptions No dextrose containing solutions Fluid boluses appropriate in some cases 2nd line if time permits Minimize number of attempts

12 Lead ECG – Diagnostic evidence of AMI present – Assess for RVI

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Treatment ◆

Morphine sulfate, 2 - 4 mg q 5-15 min slow IV – Maintain BP > ~ 90 mm Hg – Titrated to Pain relief – Reduce PVR and workload on the heart

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Aspirin, 160-325 mg PO – Chewed & swallowed if possible – Determine if hypersensitive to ASA

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“MONA greets all patients”

Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Treatment Metoprolol, 5 mg slow IV q 5 min to 15 mg total, prn for  HR/BP in absence of contraindications ◆ In longer or interfacility transports, consider: ◆

– Nitroglycerin IV infusion – Heparin ◆

Thrombolytics Checklist – Exclusions for thrombolysis

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Ischemic Coronary Syndromes ✔Acute Myocardial Infarction (AMI) ➨Treatment ◆

Transport for reperfusion therapy; Destination? – Thrombolysis vs Coronary Artery Catheterization – For patients with associated pulmonary edema, hypotension or cardiogenic shock, consider transport to facility with capability of angiography & revascularization

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Considerations for Fibrinolytics Acute Ischemic Syndromes: Diagnostic Considerations Thrombolytics are not appropriate in all acute ischemic syndromes • Not all acute ischemic syndromes are AMIs • ST-segment elevation suggests thrombic occlusion and need for immediate reperfusion • No proven benefit of thrombolytic therapy in patients without ST-segment elevation • Patients with ST-segment depression and/or T-wave inversion are currently not candidates for thrombolytic therapy

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Contraindications for Fibrinolytics

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✔ Lack of diagnostic 12 Lead ECG changes ✔ Chest pain < 20 min or > 12 hours ✔ Not oriented, can not cooperate ✔ History of stroke or TIA ✔ Known bleeding disorder ✔ Active internal bleeding in past 2-4 weeks

✔ Surgery or trauma in past 3 weeks ✔ Terminal illness ✔ Jaundice, hepatitis, kidney failure ✔ Use of anticoagulants ✔ Systolic BP < 180 mm Hg ✔ Diastolic BP < 110 mm Hg

Ischemic Coronary Syndromes

“Ischemic and injured tissue have reduced blood flow but may be salvaged. The area of the Penumbra may be viable for several hours after onset of occlusion.” 44

Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997

Ischemic Coronary Syndromes ✔Sudden Cardiac Death (SCD or SCA) ➨Sudden, unexpected biologic death presumably resulting from cardiovascular disease ➨Most common rhythm of SCA is Ventricular Fibrillation ➨May be primary or secondary VF ➨Chain of Survival is the greatest determinant of outcome ➨Treatment based on ECG rhythm & arrest events 45

Time is Muscle!!!

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References and Resources

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✔ Advanced Cardiac Life Support, Edited by R O Cummins, MD, American Heart Association, Dallas, 1997 ✔ “Emergency Cardiovascular Care Library” (CD-ROM), American Heart Association and ProEducation International, Dallas, 1997 ✔ Eisenberg, M S, Life in the Balance: Emergency Medicine and the Quest to Reverse Sudden Death, Oxford University Press, New York, 1997 ✔ “A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis”, A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association, 1995 ✔ “Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Methods, and Clinical Implications”, A Statement for Health Professionals From the American Heart Association, 1995 ✔ Cardiovascular Disease Statistics, American Heart Association, Dallas, 1997 ✔ “Diagnosis and Therapy of Acute Myocardial Infarction: Today’s Look at Tomorrow’s Therapies and Outcomes”, DuPont Pharma, 1997 ✔ University of Utah WebPath, http://medstat.med.utah.edu/webpath/