ACS - STEMI

Question 1

Occurs when a coronary artery thrombus develops RAPIDLY at a site of vascular injury

Answer 1

STEMI

after an initial platelet monolayer forms at the site of the disrupted plaque, various agonists (collagen, ADP, epinephrine, serotonin) promote platelet activation –> after agonist stimulation of platelets –> thromboxane A2 (a potent local vasoconstrictor) is released –> platelet activation and potential resistance to fibrinolysis develops

Question 2

Hyperactivity
(tachycardia and/or hypertension)

Answer 2

ANTERIOR Infarction

Question 3

PARASYMPATHETIC hyperactivity (bradycardia and/or hypotension)

Answer 3

INFERIOR Infarction

Question 4

STEMI PROGRESSES THROUGH THE FOLLOWING TEMPORAL STAGES:

Answer 4

1. acute (first few hours–7 days)
2. healing (7–28 days)
3. healed (≥29 days)

Question 5

Levels of cTnI and cTnT may remain elevated for how many days after STEMI

Answer 5

7–10 days

Question 6

Rises within 4–8 h and generally returns to normal by 48–72

lack of specificity for STEMI

Answer 6

CK

MB isoenzyme of CK has the advantage over total CK that it is not present in significant concentrations in extracardiac tissue

Question 7

Useful in the detection and quantitation of a VENTRICULAR SEPTAL DEFECT and MITRAL REGURGITATION – 2 serious complications of STEMI

Answer 7

Doppler echocardiography

Question 8

Distributed in proportion to myocardial blood flow and concentrated by viable myocardium a defect (“cold spot”) in most patients during the first few hours after development of a transmural infarct

Answer 8

myocardial perfusion imaging with [201Tl] or [99mTc]- sestamibi

Question 9

Detects MI

Standard imaging agent (gadolinium) is administered and images are obtained after a 10-min delay

Answer 9

high-resolution cardiac MRI

little gadolinium enters normal myocardium, where there are tightly packed myocytes, but does percolate into the intercellular region of the infarct zone, there is a bright signal in areas of infarction that appears in stark contrast to the dark areas of normal myocardium

Question 10

Primary coronary event – PLAQUE RUPTURE, ULCERATION,FISSURING, EROSION or DISSECTION –> intraluminal thrombus in one or more coronary arteries

Answer 10

TYPE 1 MI

Question 11

MISMATCH between oxygen supply and demand secondary to another condition other than CAD

Answer 11

TYPE 2 MI

Question 12

MI resulting in SUDDEN UNEXPECTED cardiac death often with symptoms of myocardial ischemia but death occurs before blood samples can be obtained or at a time before cardiac biomarkers can become available

Answer 12

Type 3 MI

Question 13

MI associated with PCI
cTN > 5 times

Answer 13

TYPE IV MI

Question 14

MI associated with CABG
cTN > 10 times

Answer 14

TYPE 5 MI

Question 15

Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 levels is achieved by buccal absorption of a chewed 160–325-mg tablet in the emergency department

Answer 15

Aspirin

Question 16

May be capable of both decreasing myocardial oxygen demand (by lowering preload) and increasing myocardial oxygen supply (by dilating infarct-related coronary vessels or collateral vessels)

Answer 16

sublingual nitroglycerin

Question 17

Considered in patients whose initially favorable response to sublingual nitroglycerin is followed by the return of chest discomfort, particularly if accompanied by other evidence of ongoing ischemia such as further ST-segment or T-wave shifts

Answer 17

IV nitroglycerin

Question 18

NITRATES SHOULD BE AVOIDED IN PATIENTS

Answer 18

• low systolic arterial pressure (<90 mmHg)
• clinical suspicion of RV infarction (inferior infarction on ECG, elevated jugular venous pressure, clear lungs, and hypotension)
• patients who have taken a phosphodiesterase-5 inhibitor for erectile dysfunction within the preceding 24 h - it may potentiate the hypotensive effects of nitrates

Question 19

↓ sympathetically mediated arteriolar and venous constriction  venous pooling  ↓ cardiac output and arterial pressure

Answer 19

Morphine

Question 20

Control pain effectively in some patients, presumably by diminishing myocardial O2 demand and hence ischemia

Answer 20

intravenous beta blockers

There is evidence that intravenous beta blockers reduce the risks of reinfarction and ventricular

Question 21

Oral beta blocker therapy should be initiated in the first 24 h EXCEPT in patient with

Answer 21

signs of heart failure

evidence of a low-output state

↑ risk for cardiogenic shock

other relative contraindications to beta blockade
 (PR interval >0.24 s, 2nd or 3rd -degree heart block, active asthma, or reactive airway disease)

Question 22

The primary tool for screening patients and making triage decisions in ACS STEMI

Answer 22

12 L ECG

when ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads is present –> patient should be considered a candidate for reperfusion therapy

Question 23

Can impair infarct healing and ↑ the risk of myocardial rupture, and their use may result in a larger infarct scar

Answer 23

glucocorticoids and nonsteroidal anti-inflammatory agents with the exception of aspirin - should be AVOIDED in patients with STEMI

↑ coronary vascular resistance –> reducing flow to ischemic myocardium

Question 24

Effective in restoring perfusion in STEMI when carried out on an emergency basis in the first few hours of MI

Has the advantage of being applicable to patients who have contraindications to fibrinolytic therapy but otherwise are considered appropriate candidates for reperfusion

Answer 24

Primary PCI - usually angioplasty and/or stenting without preceding fibrinolysis

Question 25

**Should ideally be initiated within 30 min of presentation (i.e., door-to needle time ≤30 min)**

Answer 25

**FIBRINOLYSIS** **prompt restoration of full coronary arterial patency** ## Footnote fibrinolytic agents tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK), and reteplase (rPA) - approved by the U.S. Food and Drug Administration for intravenous use in patients with STEMI promote the conversion of plasminogen to plasmin --> lyses fibrin thrombi

Question 26

**CLEAR CONTRAINDICATIONS TO THE USE OF FIBRINOLYTIC AGENTS**

Answer 26

**history of cerebrovascular hemorrhage at any time** **nonhemorrhagic stroke or other cerebrovascular event within the past year** **marked hypertension (a reliably determined systolic arterial pressure >180 mmHg and/or a diastolic pressure >110 mmHg) at any time during the acute presentation** **suspicion of aortic dissection** **active internal bleeding (EXCLUDING menses)**

Question 27

**Hospital Phase Management Activity**

Answer 27

**patients with STEMI should be kept at bed rest for the first 6–12 h** **in the absence of complications, patients should be encouraged, under supervision, to resume an upright posture by dangling their feet over the side of the bed and sitting in a chair within the first 24 h**

Question 28

**Hospital Phase Management** **Diet**

Answer 28

**patients should receive either nothing or only clear liquids by mouth for the first 4–12 h** **<30% of total calories as fat and cholesterol content <300 mg/d** **complex carbohydrates 50-55% of the total cal** **high in K, Mg, and fiber but low in sodium**

Question 29

**Hospital Phase Management** **Bowel Management**

Answer 29

**BEDSIDE COMMODE rather than a bedpan, a diet rich in bulk, and the routine use of a stool softener such as dioctyl sodium sulfosuccinate (200 mg/d) are recommended**

Question 30

**The primary cause of IN HOSPITAL death from STEMI**

Answer 30

**PUMP FAILURE** ## Footnote **pulmonary rales and S3 and S4 gallop sounds - THE MC CLINICAL SIGNS** **elevated LV filling pressure and elevated pulmonary artery pressure - THE CHARACTERISTIC HEMODYNAMIC FINDINGS**

Question 31

**Signs of SEVERE RV failure**

Answer 31

**jugular venous distention** **Kussmaul’s sign** **hepatomegaly with or without hypotension** ## Footnote **ECG leads particularly lead V4R - frequently present in the first 24 h in patients with RV infarction**

Question 32

**Infrequent, sporadic ventricular premature depolarizations occur in almost all patients with STEMI and do not require therapy**

Answer 32

**Ventricular Premature Beats**

Question 33

**Effective in abolishing ventricular ectopic activity in patients with STEMI and in the prevention of ventricular fibrillation**

Answer 33

**Beta-adrenoceptor blocking agents**

Question 34

**Risk factors for ventricular fibrillation in patients with STEMI**

Answer 34

**hypokalemia and hypomagnesemia**

Question 35

**Can occur within the first 24 hrs of STEMI**

Answer 35

**Ventricular tachycardia and Fibrillation** ## Footnote **sustained ventricular tachycardia - that is well tolerated hemodynamically should be treated with an intravenous regimen of AMIODARONE (bolus of 150 mg over 10 min, followed by infusion of 1.0 mg/min for 6 h and then 0.5 mg/min)**

Question 36

**A ventricular rhythm with a rate of 60–100 beats/min, often occurs TRANSIENTLY during FIBRINOLYTIC therapy at the time of REPERFUSION**

Answer 36

**Accelerated idioventricular rhythm (AIVR, “slow ventricular tachycardia”)** ## Footnote **Most episodes of AIVR do not require treatment if the patient is monitored carefully, as degeneration into a more serious arrhythmia is rare**

Question 37

**Usually the treatment of choice for supraventricular arrhythmias if heart failure is present**

Answer 37

**DIGOXIN**

Question 38

**Frequently encountered in patients with STEMI involving the epicardium** **aspirin (650 mg four times daily)**

Answer 38

**PERICARDITIS**

Question 39

**Important contributing cause of death in 25% of patients with STEMI who die after admission to the hospital**

Answer 39

**Thromboembolism**

Question 40

**FACTORS FOR RISK STRATIFICATION AND MANAGEMENT**

Answer 40

**persistent ischemia (spontaneous or provoked)** **depressed LV ejection fraction (<40%)** **rales above the lung bases on physical examination or congestion on chest radiograph** **symptomatic ventricular arrhythmias**

Question 41

**CONSIDERED AT HIGH RISK FOR RECURRENT MI OR DEATH FROM ARRHYTHMIA**

Answer 41

**patients in whom angina is induced at relatively low workloads** **those who have a large reversible defect on perfusion imaging or a depressed ejection fraction** **those with demonstrable ischemia** **those in whom exercise provokes symptomatic ventricular arrhythmias should be**

Question 42

**Usual duration of hospitalization for an UNCOMPLICATED STEMI**

Answer 42

**3-5 days**

Question 43

**Best non invasive indicator of successful reperfusion**

Answer 43

**>50% resolution of ST segment elevation in the anterior leads or >70% in inferior leads assessed 60-90 minutes after fibrinolytic administration**

Question 44

**Treatment for STEMI + Cardiogenic Shock**

Answer 44

**PCI - regardless of time delay**

Question 44

**Processes that occur during STEMI**

Answer 44

**1. Adherence of circulating platelets to exposed subendothelial matrix components** **2. Platelet activation with thromboxane A2 release and GP IIB/IIIa receptors conformational change** **3. Binding of fibrinogen to GP IIb/IIIa receptors followed by cross linking of adjacent platelets** **4. Conversion of prothrombin to thrombin leading to fibrin formation from fibrinogen** **5. Formation of mural thrombus composed of fibrin strands and aggregated platelets**

Question 45

**3 POSSIBLE PRESENTATIONS OF UNSTABLE ANGINA**

Answer 45

**1. angina occuring at rest or with minimal exertion lasting for prolonged periods >20 minutes** **2. new onset moderate-severe angina which occured in the last 2 months** **3. crescendo angina (more often, more severe occurs at the lower threshold over a short period of time**