Lecture 18 Nov 17th-cv

1DDX: NOVEMBER 17TH, 2006 Myocardial Infarction 1Page 2: (Additional flow chart): Acute coronary syndromes (ACS) / ST elevation ACS / Q-wave MI (these are positive cardiac markers)

non-Q wave MI

\ Non-st elevation ACS \ \ unstable angina

Acute coronary syndromes (ACS) Cardiac markers will support clinical signs of MI. • cardiac enzymes • troponins Q wave and non-q-wave MI There are both types, discussed below. If ECG shows ST elevation, treatment approach would be revascularization. If within 2 hours patient can have revascularization (balloon+stent, thrombolytic agents): ischemia is reversible. Later, thrombus will be calcified, will be harder to treat. See outline of cardiac cycle (follows pg. 2) Ventricles contract in QRS (depolarization). This will change in patients with MI. Site of infarction will be reflected in leads (we didn’t really talk about this any further…) Page 3 Q-wave infarcts: • First area to suffer is endocardium. In less that 20-40 minutes, there is injury to the area of ischemia. • If pain lasts for 30 minutes or more, ischemia and injury extends, and necrosis begins. Moves outwards towards pericardium. Longer pain (ischemia)? More extensive damage will be seen. In 24 hours, complete necrosis (pt. will not survive 24 hours of ischemia) to a large area of the heart.). • Collateral circulation: develops during physical activity, exercise. If this has developed in a patient, the damage will be less, as the blood can bypass the blocked vessel. See chart that follows Page 8. Q-WAVE MYOCARDIAL INFARCTION: Q wave that will be deep and wide (this is an abnormal Q-wave). They appear after 4-6 hours, amplitude of 25% of associated R wave, will exceed 0.04 seconds. (We just need to know what is “abnormal” for a Q wave, not details!) DDX LECTURE 18, NOVEMBER 17TH – PAGE 1

Representation of large, abnormal Q wave is CAPITAL LETTER Q! Regular (non-pathological) qwave is small q. Final stage (Phase 4): **The large Q wave makes a diagnosis of transmural myocardial infarction. If patient is admitted and treated, there will be the development of a scar. What is positive about scar? The patient survived Negative? This area is non-contractile and the function of the heart is compromised. Amount of damage is based on level of cardiac markers, not on depth of Q wave. Markers used to assess MI damage: • Patient’s post-MI condition • Angiography, number and size of vessel affected. • (Other markers? Not mentioned. Will include enzymes) (Know these!) ECG findings: Negative T: below baseline. ST depression (down-sloping or horizontal): sign of ischemia. See this during stress test. ST elevation: sign of injury Q wave: sign of necrosis (transmural MI) NON-Q-WAVE MYOCARDIAL INFARCTION • May not involve entire thickness of ventricular wall. Sub-endocardial non-q-wave myocardial infarction. • This represents 30-40% of all acute Mis. Can occur as result of transient occlusion of lumina (thrombus), followed by spontaneous lysis before occurrence of MI. • Does not extend through ventricular wall • Rarely results in aneurysm, pericarditis Hallmark of sub-endocardial/non-q-wave are: • Chest pain • T-wave inversion (negative T wave, below the baseline) for more than 3-5 days with/without complaint from patient. • ST depression that lasts • (if it is angina, these changes will go away when the episode ends-when pain is relieved. Will not see change in enzymes.) • More elevation of enzymes in Q-wave MI than in non-Q-wave. Q-wave is transmural, more serious. • 0 hours to 8 weeks: may see T wave depression throughout (see chart). Most important in MI: Maintain cardiac output. Arrhythmia will cause damage. Time is essential. See chart at end of notes: Understanding Chest Pain Most common pathological conditions associated with chest pain. DDX: Pericarditis: Other cases where you might see ST elevation: pericarditis, but in pericarditis, don’t see Q-wave (no necrosis). DDX LECTURE 18, NOVEMBER 17TH – PAGE 2

Will also complain of central chest pain, but it is not associated with physical exertion. Not relieved with rest. Pain will be worsened in supine position: alleviated by sitting and leaning forward. Description of pain is different: Page 4: Laboratory findings for MI: don’t need to know number of hours, but understand which markers present when, for how long. Troponins: remain elevated for up to two weeks (in contrast with other enzymes (CPK, MB)) If there is treatment but the patient still experiences pain, what does this mean? Continuing heart damage: growing MI. Page 5: Leukocytes are not a specific marker. Myocardial imaging: You will see cold spot in area of necrosis To DX MI, need 3 factors: • History: description and patterns of pain. Family history, other risk factors. • ECG changes: evolution of ECG changes • Cardiac markers including: cardiac enzymes and troponins (which are proteins). Management of Myocardial Infarction: Patient has to be admitted to cardiac care unit. Treatment? • Relief of pain (pain causes continued spasm, more damage. • Oxygen therapy: Cells around necrotic area are experiencing damage too. Want to support surrounding cells to prevent extension of MI Page 6: •

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Reperfusion: • Thrombolytic therapy: IV admin of agents that can lyse coronary thrombus. Have to admin in 4-6 hours: reduces mortality by 25%. 50% if administered within 1 hour. • TIME IS CRUCIAL!!!!! Emergency PTCA Coronary bypass surgery.

After treatment, patients should go for stress test in 6 months, then in a year. Stats show that restenosis (stenosis again) may occur in this period. Want to see progression, what coronary tree looks like. See risks and CI for thrombolytic therapy. Prognosis: Depends on ventricle involved, other health concerns (diabetes: less positive outcome), other systemic diseases of vessels. Page 7: DDX LECTURE 18, NOVEMBER 17TH – PAGE 3

Cardiogenic shock Extremely severe condition after transmural MI Very small chance of survival (65% mortality: maybe even more) Unconscious: not enough blood pressure to maintain consciousness Decreased urine production: not enough blood supply to kidney: could cause acute renal failure. Prognosis due to non-cardiac complications: these may also follow MI. 1. Shoulder Hand Syndrome: Pain/tenderness of shoulder, followed by fingers. X-ray for DX. Pain may mimic MI (esp. in pt. with history of MI) 2. Dressler’s syndrome • Autoimmune: from damage to myocardium and pericardium. • Benign disorder. Page 8: Signs of Cardiac Arrest • What do you do? CPR, call 911. • Where do you check for heartbeat? Carotid artery (closest to heart) • Don’t stop CPR: even if you can’t palpate peripheral pulse, you are still circulating blood to the brain. Continue until someone else can take over. See algorithm of chest pain. Help to rule out non-cardiac sources of chest pain. See back page of note package for dietary suggestions. See separate page for Cardiac and non-cardiac causes of chest pain Case #1: A 57-year old auto salesman who is hypertensive and a heavy cigarette smoker, describes a pressure-like sensation that developed for the first tie 3 weeks before The discomfort which begins in the retrosternal area, radiates to the left side of lower jaw, occurs when he walks rapidly in cold air, and more recently develops at rest. Careful history reveals that it lasts for 10-15 minutes, but an especially severe episode awakened him the night before and lasted nearly a half hour before resolving spontaneously. Except for a blood pressure of 150/100mmhg the physical examination findings are normal. An ECG obtained when pain had disappeared reveals deep and symmetrical T wave inversion in leads V1 to V4. After admission and the iv administration of Nitroglycerin and heparin, the patient’s condition stabilizes. An acute myocardial infarction is excluded. DDX: Unstable Angina. Beginning to become worse at rest: he had it already. (Any changes in previous patterns of angina = unstable.) Risk factors: Smoking, hypertension, age, gender. Case #2: (We saw this case on Nov. 15th. This is the complete version) A 66-year old man complains of chest pain and shortness of breath for 2 days. His current problems began abruptly after a “cold” 2 days ago. He noted shaking chills and a cough, productive of rustcoloured sputum. The chest pain is right-sided, sharp, and much worse with deep breathing and coughing. The medical history is significant for chronic alcoholism and smoking. The patient appears acutely ill. His temperature is 104F and his breathing is rapid and shallow. A DDX LECTURE 18, NOVEMBER 17TH – PAGE 4

lung examination reveals that the right lower lobe has decreased breath sounds with some crackles in the periphery, dullness to percussion and increased vocal fremitus. Cardiac examination is normal, and the rest of the physical examination reveals nothing abnormal. DDX: Pneumonia: abrupt onset, association with cold, shaking chills, cough. This doesn’t fit picture of angina. Chest pain worse with breathing and coughing: in angina, pain has nothing to do with breathing and coughing. Fever. No elevation in angina. Crackles: possible consolidation, accumulation of fluid in alveoli. Dullness on percussion (consolidation, fluid): this is nothing to do with angina., increased vocal fremitus increases over consolidated area. Amplifies sound transmission. Decreased or absent over areas of fluid accumulation.

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