Acute Coronary Syndrome (ACS) Flashcards
Acute Coronary Syndrome (ACS) includes … ?
- Unstable angina (UA)
- Non-ST segment elevation (NSTEMI)
- ST segment elevation MI (STEMI)
What is the oxygen demand in patients with UA, and how does this drive management?
The overall oxygen demand is unchanged in unstable angina (UA), but the supply is decreased due to reduced resting coronary blood flow (as opposed to stable angina where the demand is increased). UA is significant because it indicates stenosis via thrombosis, hemorrhage, or plaque rupture. UA may lead to total occlusion of a coronary vessel and has a higher risk of Ml and death than stable angina, therefore patients with this diagnosis should be hospitalized.
The distinction between UA and NSTEMI is based entirely on
cardiac enzymes, unstable angina lacks biomarkers while NSTEMI has elevated biomarkers.
Why is UA is more of a historical term?
With more widespread use of high-sensitivity troponin testing, UA is a rare diagnosis since virtually all cases of ACS will have an elevation in this biomarker.
What is shared between both UA and NSTEMI?
Both UA and NSTEMI lack ST-segment elevations, differentiating them from STEMI
When patients present with suspected ACS, what is the overall priority?
The priority in clinical care is differentiating and managing NSTEMI versus STEMI. This can only be done with an ECG. Therefore, prior to any other diagnostic step, perform an ECG after the initial primary assessment (airway, breathing, circulation, disability and exposure) and establishing IV/IO access.
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Myocardial ischemia occurs in NSTEMI and STEMI, and is defined as an elevation in a cardiac biomarker with evidence of acute myocardial ischemia. However, these tests take hours to come back and an ECG is relatively fast to obtain. Also the treatment varies. For STEMI, patients immediately go to the cath lab for evaluation to determine if PCI or other revascularization is required. For NSTEMI, further stratification is needed. However for both these instances, patients need: 1) Dual antiplatelet therapy with aspirin and platelet P2Y12 receptor blockers (clopidogrel, prasugrel, or ticagrelor), 2) Nitrates, 3) Beta blockers, 4) Statins, 5) Anticoagulant therapy (unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux).
Unexpected death due to cardiac causes within 1 hour of symptom onset, is most commonly due to … ?
The most common cause of sudden cardiac death (SCD), defined as unexpected death due to cardiac causes within 1 hour of symptom onset, is ventricular arrhythmia, most often ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). The most common underlying association is with CAD (up to 70% of cases).
What is the mortality rate for MI?
30% (about 1/2 are in the prehospital setting).
Most cases of MI are due to …. ?
Acute coronary thrombosis.
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MI is due to necrosis of myocardium as a result of an interruption of blood supply. Atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel.
What are the five classes of MI?
- Type 1 MI: Plaque rupture with thrombus
- Type 2 MI: A supply-demand mismatch with oxygen delivery
- Type 3 MI: Typical MI suspected, but death occurs without testing the blood for cardiac biomarkers
- Type 4 Ml: Ml associated with PCI
- Type 5 MI: Ml associated with CABG
What are the most common clinical features of ACS?
- Chest pain (intense substernal pressure sensation)
- Radiation to neck, jaw, arms, or back, commonly to the left side
- Some patients may have epigastric discomfort
- Other symptoms include dyspnea, diaphoresis, weakness, fatigue, nausea and vomiting, sense of impending doom, syncope, and even sudden cardiac death (usually due to ventricular fibrillation).
The chest pain associated with ACS is commonly described as … ?
often described as a “crushing” pain, like “an elephant standing on chest”
What is similar about the chest pain seen in ACS with stable angina? What is different about this pain?
Similar to angina pectoris in character and distribution but much more severe and lasts longer.
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Unlike in angina, pain may not respond to nitroglycerin.
What percentage of patients with acute coronary syndrome (ACS) may present asymptomatically or with atypical symptoms, and which patient populations are at highest risk for this presentation?
ACS can be asymptomatic in up to one-third of patients; painless infarcts or atypical presentations are more likely in postoperative patients, the elderly, diabetic patients, and women.
A 60-year-old man presents to the emergency department with chest pain. The patient describes the pain as a crushing sensation in the middle of his chest that radiates to the jaw. The pain started two hours ago while he was watching television. He has a history of hypertension and diabetes mellitus, but his insurance has lapsed so he does not currently take medication for either condition. The patient has smoked a pack of cigarettes daily for the last 20 years. Temperature is 37.0°C (98.6°F), blood pressure is 90/70 mmHg, pulse is 120 bpm, and respirations are 22/minute. Oxygen saturation is 96%. The patient appears anxious and in distress. Which of the following is the most appropriate next step in the acute management of this patient?
This patient presents with symptoms consistent with acute coronary syndrome. Acute coronary syndrome (ACS) is an emergency that requires immediate care and prompt diagnostic evaluation to determine the cause and appropriate treatment. However, because of the rapidly progressive nature of the disease, any patient with a suspicion for acute coronary syndrome should be managed acutely prior to diagnostic evaluation. Acute management of patients with ACS starts with assessing the stability of the patient (ABCDE criteria). Patients who are unstable (e.g. hypotension) should be immediately stabilized and then assessed for the possible cause. For patients who are unstable (like this patient), acute management begins with obtaining intravenous access, monitoring blood pressure, heart rhythm and oxygen levels, and providing oxygen supplementation if needed (only if SpO2 is less than 90%). After the acute management of ACS is complete, evaluation to obtain an accurate diagnosis should begin immediately, which involves a focused history and physical examination, prompt 12-lead ECG, and cardiac troponin assessment.
What is the initial work-up for patients with suspected ACS?
Initial approach: all patients should, at minimum, include a brief history and physical, lab testing (including cardiac biomarkers, especially high-sensitivity troponin if available), and an ECG. A bedside ultrasound can also be useful to evaluate cardiac function and regional wall motion abnormalities. Obtain a CXR. Establish continuous cardiac monitoring, IV access for electrolyte repletion, and provide oxygen (if SpO2 is < 90%).
What is the initial medical management for patients with ACS entail?
- Sublingual nitroglycerin
- Morphine (only if chest pain is unrelieved by nitrates, this has a minor vasodilator effect)
- Oxygen (for SpO2 <90%)
- High dose ASA (162-325 mg)
- Beta-blocker (cardioselective; metoprolol or atenolol)
- High intensity statin
**Heparin, DAPT, ACEi, etc, are only given after a confirmed ACS.
How are patients with a new ACS episode treated compared to patients with a previous diagnosis of CAD?
Patients with coronary artery disease (CAD) and prior MI should be started on appropriate therapy for secondary prevention of cardiovascular events, including beta blocker, high intensity statin, antiplatelet therapy, and ACE inhibitor or angiotensin-receptor blocker. In patients with a recent MI, beta blockers reduce short-term morbidity (recurrent symptoms, reinfarction, size of infarct) as well as short- and long-term mortality (if continued). They also improve survival in patients with CAD and left ventricular systolic dysfunction. Although there has been concern that beta blockers may mask hypoglycemic symptoms in patients with diabetes, their use after an MI is associated with improved survival rates; therefore, diabetes should not be viewed as a contraindication to their use. In addition to initiation of pharmacologic therapy, this patient should also undergo further evaluation and risk stratification (eg, transthoracic echocardiogram, myocardial perfusion stress test, possibly coronary angiography).
How does the use of cocaine change the initial management of ACS?
Give IV Benzodiazepines. Nitroglycerin is also given to reduce blood pressure and left ventricular wall stress. Because cocaine stimulates platelet activity and encourages thrombus formation, thrombotic occlusion of coronary arteries can occur (even in young patients). Therefore, aspirin should be given early. CCBs can be given to relieve myocardial ischemia. In patients with persistent ST elevation despite initial medical therapy, coronary angiography with percutaneous coronary intervention (PCI) should be performed without delay. Prompt recognition and restoration of myocardial blood flow is critical to minimize myocardial necrosis and to reduce cardiac morbidity and mortality.
Which benzo is preferred in MI secondary to cocaine abuse?
Lorazepam (IV) or Diazepam (IV/PO), but Midazolam (IV).
The setting of ACS, the EKG should be repeated every … ?
15 to 30 minutes to evaluate for dynamic changes
What are the markers for ischemia/infarction on the ECG evaluating for ACS?
- Peaked T-waves
- T-wave inversions
- ST-elvations
- Q-waves
If a patient has symptoms of ACS, but the ECG shows LBBB, what criteria is used to diagnose MI?
Sgarbossa Criteria.
What is the morphology of a LBBB on ECG?
- A “W” shape in V1 (with a deep S-wave and no R-wave)
- A “M” shape in leads I, V5 or V6 (with R-waves)
What lead is most useful for initial recognition of LBBB
Lead V1: Wide QRS complex (≥120 ms), Deep, broad S wave (indicating delayed right ventricular depolarization), Absence of a Q wave
Leads V6 & I: Wide, notched (“M-shaped”) R wave (characteristic of LBBB), Absence of a Q wave, Discordant ST-T changes (opposite direction of QRS complex)
What is the duration of the QRS in LBBB?
120 ms
An R prime wave (second R wave) in V1 accompanied by a widened S wave in V6 describes a … ?
right bundle branch block.
ST-depressions in continuous leads is … ?
NSTEMI
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ST depressions may have STEMI equivalents when there is an ST elevation in aVR and depressions exist in 6 leads.
A 58-year-old man presents to the emergency department for evaluation of chest pain. The patient was working on his car earlier in the day when he noted substernal chest discomfort radiating down his left arm with associated nausea and vomiting. The patient reports that the pain has been persistent from onset. The patient has a past medical history of hypertension, diabetes, hyperlipidemia, CAD, and a twenty-pack-year smoking history. The patient is anxious and diaphoretic. Temperature is 37°C (98.6°F), blood pressure is 166/71 mmHg, pulse is 100/min, respiratory rate is 16/min, and oxygen saturation is 94% on room air. The rest of the physical examination is otherwise unremarkable. ECG is shown below. Troponin level comes back at 0.154 ng/mL. Which of the following is the best next step in management?
A) Administration of tenectaplase
B) Exercise stress testing
C) Dobutamine stress testing
D) Coronary angiography
E) Dipyridamole stress testing
This patient presents with features concerning acute coronary syndrome (ACS). He is presenting with chest pain consistent with typical angina and although he has a normal ECG, he has a significantly elevated troponin, consistent with a non-ST elevation myocardial infarction (NSTEMI). The next best step in management is administration of aspirin, platelet P2Y12 receptor blocker, heparin, and he should be managed with an invasive strategy with cardiac angiography. Any patients who present to the ED with chest pain that is suspicious for ACS and unstable should initially be managed by immediately assessing airway, breathing, and circulation. History, physical, and ECG should be performed. The patient should be placed on cardiac monitoring and IV access should be obtained. Aspirin should be given and sublingual nitrates if there are no contraindications. Intravenous morphine sulfate may be given for severe, persistent chest pain Supplemental oxygen should be given to maintain oxygen saturation above 90% A statin and a beta blocker should also be given if there are no contraindications.
What is the medical treatment for a patient with angina relieved with nitroglycerin and this ECG?
This patient’s clinical presentation - substernal chest discomfort, relief with nitroglycerine, and electrocardiogram (ECG) findings of ST-segment depression in leads II, aVF, and V3-V6 - is consistent with acute coronary syndrome ([ACS] - unstable angina/non ST-elevation myocardial infarction [NSTEMI]). All such patients should be managed with:
1. Dual antiplatelet therapy with aspirin and platelet P2Y 12 receptor blockers (clopidogrel, prasugrel, or ticagrelor)
2. Nitrates
3. Beta blockers
4. Statins
5. Anticoagulant therapy (unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux)
In multiple randomized trials, treatment with dual antiplatelet therapy and anticoagulant therapy has been shown to significantly reduce the risk of nonfatal MI and cardiovascular death in patients with ACS.
Seeing a pattern on an EKG from an anterior lead is …
an STEMI equivalent (de Winter T wave).
ST-depressions indicate infarction ___% of the time.
25%
ST depressions in V2 and V3 (with concerning posterior ECG), this would be … ?
an STEMI equivalent.
T-wave inversions in continuous leads is … ?
NSTEMI
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These are sensetive but not specifc.
Peaked T waves tend to be an indication of ischemic changes (early or late) in ACS?
Early
What occurs to the T-waves a few hours after in the progression of ACS?
Inversion
After T-wave inversion, what occurs to T-waves?
ST elevation
ST elevations indicate infarction ___% of the time?
75%
ST elevations need to be in ______ contiguous leads.
2
How is an ST-elevation to be defined in terms of the amount of elevation?
1 small box = 1 mm = 0.1 mV
What is the exception for the ST elevations with V2 and V3?
The amount of elevation needs to be at least:
0.15 mV in females (1.5 small boxes = 1.5 mm)
0.2 mV in males older than 40 (2 small boxes = 2 mm)
0.25 mV in males younger than 40 (2.5 small boxes = 2.5 mm)
After the initial MI, what feature tends to occur on the EKG?
Q-waves
For patients with an initial normal troponin, it should be repeated in
3 to 6 hours
Cardiac troponin I usually rises after …. ?
4 hours
What is the maximum time that it might to take for troponin to become detectable?
up to 12 hours!
When does troponin usually peak following an MI?
24 hours
Troponin will remain elevated for … ?
7 to 10 days following infarction
A 52-year-old man comes to the emergency department an hour after the onset of severe substernal chest pressure that lasted 30 minutes. The symptoms started when he was helping his brother move into his new house and were associated with mild dizziness and shortness of breath. His brother has coronary artery disease with stable angina and the patient took 3 of his brother’s nitroglycerin tablets sublingually before his pain eventually subsided. He is currently pain free. Medical history includes hypertension and hyperlipidemia. The patient’s daily medications include losartan, atorvastatin, and low-dose aspirin. Blood pressure is 152/93 mm Hg and pulse is 105/min. BMI is 32 kg/m?. The lungs are clear to auscultation bilaterally. Cardiac examination indicates a prominent point of maximal impulse that is displaced downward and to the left. Auscultation reveals regular, normal heart sounds with an audible S4. There are no murmurs. The rest of the physical examination is within normal limits. ECG shows sinus tachycardia and voltage criteria for left ventricular hypertrophy, similar to the patient’s ECG 6 months ago. His troponin level is normal. He says, “I feel fine! I just want to go home and I will see my primary care doctor.” What is the most appropriate next step in management of this patient?
This patient requires continued monitoring with serial troponin and ECGs. The initial ECG may be nondiagnostic or normal in more than half of patients presenting with myocardial infarction (MI), and serum troponin levels can remain undetectable for 6-12 hours following the onset of MI symptoms. For patients in whom the initial ECG and troponin findings are unremarkable but there is reasonable suspicion for acute coronary syndrome (ACS), the most appropriate approach is further observation with serial ECG and troponin levels (eg, 3 troponin levels 6 hours apart and several ECGs 30 minutes apart). Subsequent elevation in serum troponin levels with or without ECG findings of ischemia (eg, ST segment depression, T-wave inversions with prominent R waves) will confirm non-ST-elevation MI. Alternatively, recurrence of typical anginal pain in the absence of serum troponin elevation may confirm unstable angina.
What are the areas impacted with NSTEMI and STEMI?
NSTEMI: subendocardial (inner 1/3 to 1/2 of myocardium)
STEMI: transmural
ST elevations in V1 to V4 are from an ______ infarction.
anterior wall
ST elevations in V1 to V2 are from an ______ infarction.
septal
ST elevations in V3 to V4 are from an ______ infarction.
apical
ST elevations in V5 to V6 are from an ______ infarction.
lateral (left)
Leads I and aVL are for the _______ portion of the heart.
lateral (left)
The inferior heart is analyzed with leads _____. ______. and ______.
II, III, aVF
What are the dominant features of a posterior wall MI?
A posterior wall ST-segment elevation myocardial infarction manifests with LV posterior wall akinesis and may cause cardiogenic shock if ventricular contractility is severely affected. Evidence of LV failure (eg, acute pulmonary edema) would be present. ECG may show reciprocal changes of horizontal anterior precordial ST-segment depressions.
A posterior wall MI will show ST-__________ in V-__ to V-__, due to occlusion of the _______.
ST-depressions in V1 to V3, due to occlusion of the PDA.
For inferior wall MIs, what medical management is different as compared to other infactions?
IV fluids and atropine due to nodal dysfunction.
In MI, which vessels are most commonly infarcted?
LAD > RCA > circumflex
What are the differences between a left and right sided MI and why is this important?
- Right sided MI will have clear lungs with hypotension and JVD.
- Left sided MI will have pulmonary edema and S3 or S4.
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This is important to distinguish because right-sided MI will involve increased fluids while left sided MI will involve fluid restriction.
Bradyarrhythmias will accompany (right/left) sided MI?
right sided MI.
Which cardiac marker is useful in diagnosing reinfarction following acute MI?
CK-MB
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CK-MB increases after 6–12 hours (peaks at 16–24 hr) and is predominantly found in myocardium but can also be released from skeletal muscle.
Once a STEMI has been diagnosed, what is the cut off in terms of time to have these patients evaluated?
12 hours. Beyond 12 hours with no refractory angina, no hemodynamic instability, no dynamic ECG changes, no ventricular arrhythmia or underlying heart failure is indicative for continuing medical treatment without proceeding to PCI. Otherwise within 12 hours, there is a 90 minute door to balloon time. If the 90 minute constraint can’t be met, then provide fibrinolytics. The 12-hour threshold for reperfusion therapy in STEMI exists because, beyond this period, the risks often outweigh the benefits due to the extent of myocardial necrosis and the potential for reperfusion injury.
What occurs histologically in the initial stages of myocardial infarction?
coagulative necrosis
What cell begins to invade 1 to 3 days following myocardial infarction?
PMNs
What cell begins to invade 3 to 14 days following myocardial infarction?
Macrophages
When does scar tissue develop following myocardial infarction?
2 weeks to several months
What is part of the continued medical therapy for confirmed ACS (STEMI and NSTEMI)?
- Dual antiplatelet agent ( ASA plus clopidogrel, ticagrelor, prasugrel)
- Heparin bolus (UFH, bivalirudin, enoxaparin)
- Beta-blocker (as long as there is no heart failure)
- High-intensity statins
What are the immediate steps for a patient with confirmed ACS?
Emergency cardiac catheterization with revascularization is indicated in patients with evidence of ST-elevation MI on initial ECG or ACS with hemodynamic instability. Cardiac catheterization is also indicated within 24-48 hours in patients with non-ST-elevation MI.
What is performed next if the patient’s diagnosis is still undetermined?
A TIMI risk score assessment to determine if a patient should undergo further evaluation. Patients can have either an exercise ECG, an ECHO stress test, a Pharmacologic stress echocardiogram, or a Pharmacologic radionuclide perfusion to allow for identification of myocardial regions that have inducible ischemia. These tests are appropriate in patients with low-risk non-ST-elevation MI or unstable angina based on thrombolysis in MI.
Is providing oxygen considered controversial in MI?
Yes.
Within what period of time does reperfusion following ACS avoid reperfusion injury?
12 hours.
When is reperfusion (coronary angiography) performed for NSTEMI?
Immediate PCI for shock, severe CHF, ventricular arrhythmias, or structural complications. Otherwise this is done within 24-48 hours depending on TIMI or GRACE stratifications.
Which ionotrope is provided for cardiogenic shock in the setting of ACS?
dobutamine.
When is nitroglycerin avoided?
Inferior wall MI (leads II, III, or aVF).
When are opioids avoided?
Inferior wall MI (leads II, III, or aVF).
Why are nitrates, opioids, and diuretics avoided in right-sided MI?
Right ventricular myocardial infarction (RVMI) behaves differently than left ventricular MI. Acute RV contractile dysfunction causes abruptly increased RV preload with jugular venous distension, and the ventricle is unable to pump adequate blood through the pulmonary circulation to the left side of the heart (decreased left ventricular preload), resulting in reduced cardiac output and hypotension. The failing right ventricle becomes reliant on hydrostatic pressure to force blood through the pulmonary circulation and is highly sensitive to a reduction in preload. Nitrates, diuretics, and opioids are best avoided because they reduce RV preload and can profoundly worsen hypotension. Hypotension in the setting of RVMI is best initially treated with intravenous normal saline to further increase RV preload and provide additional hydrostatic pressure to assist blood flow through the pulmonary circulation. Otherwise, patients with RVMI should undergo standard management of acute ST-segment elevation MI (STEMI), with dual antiplatelet therapy, statins, anticoagulation, and urgent revascularization (percutaneous intervention preferred over thrombolytic therapy). Patients with STEMI involving the right ventricle have particularly high acute mortality, with substantial mortality reduction associated with prompt reperfusion.
Should patients with heart failure get nitrates in the acute setting of ACS?
Nitroglycerin decreases cardiac preload and is indicated for the relief of persistent chest pain in patients with ACS as well as for alleviation of pulmonary edema in those with acute decompensated heart failure and hypertension. It is generally contraindicated in patients with right ventricular myocardial infarction as it may cause severe hypotension in such patients, but not in cases of heart failure. Patients with heart failure and ACS can receive nitrates, but only if they are not hypotensive (SBP <90 mmHg) and do not have contraindications such as right ventricular infarction.
Can patients who take sildenafil be given nitrates for ACS in the acute setting?
No!
This can cause severe hypotension!
What can patients get for chest pain if nitrates are contraindicated?
morphine
What is the purpose of heparin bolus in ACS?
limits thrombus expansion
Do you provide DAPT to patients with NSTEMI?
Patients with NSTEMI or unstable angina, P2Y12 inhibitor therapy is often held until after coronary angiography in case the atherosclerotic coronary anatomy indicates the need for coronary artery bypass grafting.
What are the DAPT doses for ACS?
Clopidogrel 300 mg
Ticagrelor 180 mg
Prasugrel 60 mg
What is the purpose of statin therapy in ACS?
Stabilizes atherosclerotic plaque
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High-intensity statin therapy (eg, atorvastatin, rosuvastatin) is indicated in all patients with ACS (eg, goal of lowering serum LDL to approximately 50 mg/dL) with beneficial effects thought due to plaque stabilization, reduction of inflammation, and atherosclerosis regression. Intolerance of a previous trial of simvastatin is not a contraindication to therapy. Following the acute period, close monitoring and various other strategies (eg, every-other-day dosing, reduction of statin intensity (eg, pravastatin]) should be implemented to try to achieve a tolerable statin regimen if patients were intolerant.
What is the preferred anticoagulation in the acute setting of ACS for patients undergoing cath?
Heparin or bivalirudin
What is the preferred anticoagulation in the acute setting of ACS for patients NOT undergoing cath?
Enoxaparin or fondaparinux
For unstable angina and NSTEMI, which anticoagulant is preferred?
Enoxaparin
In the ESSENCE trail, the risk of death, recurrence, and need for re-vascularization was lower than Heparin treated patients following a sequence of 14 days, 30 days and 1 year.
What is the duration of anticoagulation treatment for ACS?
48 hours.
When are beta-blockers held for ACS?
Contraindicated in cardiogenic shock, bradycardia, or signs of heart failure (JVD or pulmonary crackles).
Which beta blocker has shown a reduction in death in patients with post-MI LV dysfunction?
Carvedilol (CAPRICORN trial)
When fibrinolysis considered in the medical management of ACS?
In STEMI patients after symptoms occur (within 12 hours), and PCI is not able to be performed within 120 mins, provide thrombolytic therapy (alteplase) within 30 mins.
PCI is ideally performed within _____ mins of presentation of ACS.
90
If PCI is not possible within ____ minutes, give fibrinolytics within ___ minutes.
If PCI is not possible within 120 minutes, give fibrinolytics within 30 minutes.
When are NSTEMI patients revascularized?
New HF, cardiogenic shock, persistent angina despite medical therapy, ventricular arrhythmias, or high risk patients (TIMI or GRACE stratification).
What factors does the TIMI score use to stratify patients?
- Cardiac markers
- ST deviation
- Age older than 65
- Risk factors for CAD (DM, HTN, smoking, dyslipidemia, fam hx)
- Used ASA within 5 days
- 1 or more episodes of angina at rest within 24 hours
- Chest pain with unstable vitals
2 points or more –> stress test
3 points or more –> cath lab
What medications are continued following re-vascularization following ACS?
- DAPT (ASA and P2Y12 inhibitor)
- BBs
- Nitrates
- Statins
- ACE inhibitor
Patients with UA or NSTEMI who are treated conservatively should undergo a … ?
Stress test (prior to discharge).
Which medications are known to decrease mortality following MI?
ACE inhibitor, BBs, and ASA.
Drug eluting or bare metal stents require at least ____ months of DAPT
6 to 12 months
What is the most significant risk factor in restenosis of a stent?
medication noncompliance.
What is used to provoke variant or Prinzmetal angina?
Variant or Prinzmetal angina involves transient coronary spasm that usually is accompanied by a fixed arteriolosclerotic lesions but can also occur in normal coronary arteries. Episodes of angina occur at rest (classically occurs at night) and is associated with ventricular arrhythmias. The Hallmark is transient ST segment elevation, not depression, on EKG during chest pain. Coronary angiography is the definitive test that displays coronary spasms when the patient is given IV ergonovine or acetylcholine to provoke spasms. The treatment is with vasodilators such as calcium channel blockers and nitrates. Risk factor modifications include smoking cessation and lowering of lipid levels.
What is the most common cause of inpatient mortality in the setting of acute MI complications?
Pump failure is the most common cause of in hospital mortality in the setting of acute ACS. If mild, treat medically with an ace inhibitor or a diuretic. If severe this may lead to cardiogenic shock and invasive hemodynamic monitoring or support with tropes or devices may be indicated.
How are premature ventricular contractions (PVCs) treated in the context of complications of acute MI?
PVCs are treated conservatively with observation
Can atrial fibrillation occur as a complication of acute MI?
Yes this is a common arrhythmia that occurs in the setting of ACS
What is the most common cause of death within 24 hours following myocardial infarction?
Ventricular arrhythmias, these can occur at any time following a myocardial infarction (MI).
How is VT in the setting of ACS managed?
Sustained ventricular tachycardia (VT) requires treatment.
If the patient is hemodynamically unstable:
-with a pulse, perform synchronized cardioversion.
-pulseless, perform defibrillation (unsynchronized cardioversion or direct current countershock [DCCS]).
If the patient is hemodynamically stable:
-initiate antiarrhythmic therapy, typically with amiodarone.
How is VF in the setting of ACS managed?
Unsynchronized defibrillation.
How is bradycardia in the setting of ACS managed?
This is a common occurrence in early stages of acute MI especially following a right sided or inferior MI. There is no treatment required other than observation. If bradycardia is severe or symptomatic give atropine. If refractory, transcutaneous pacing, dopamine drip, or epinephrine drip.
Which arrhythmia maybe difficult to differentiate and has a very high mortality in the setting of ACS?
Asystole.
The treatment should begin with electrical defibrillation for V fib which is more common in cardiac arrest and may be difficult to clearly differentiate from Asystole. If Asystole is clearly the cause of arrest perform transcutaneous pacing.
How are AV blocks managed in the setting of ACS?
First and second-degree type one AV blocks do not require treatment, however, second-degree type two and third-degree AV blocks in the setting of an inferior MI the prognosis is better and atropine may be used initially. If conduction is not restored a temporary pacemaker is appropriate. Can use isoproterenol or dopamine while waiting placement of a pacer. AV blocks in the setting of an anterior MI requires first treatment with an emergent placement of a temporary pacemaker, then a permanent pacemaker.
When the RCA is implicated in MI what complication tends to occur?
Right ventricular failure which can occur at any time following the acute event. Presents with hypotension, elevated JVD, and peripheral edema. Avoid nitroglycerin, watch for AV blocks or bradycardia, and give IV fluids and tropes.
Which chamber of the heart is implicated when a patient presents with cardiogenic shock in the setting of ACS?
Left ventricular failure. This is usually treated with furosemide, avoidance of beta blockers, and tropes or mechanical support.
Fibrinous pericarditis usually occurs at what time following an MI?
This usually occurs within one week. The treatment is with ASA at high dose (650 mg) 3 times a day. NSAIDs and steroids are NOT indicated because they may hinder myocardial scar formation. Patients with post-MI pericarditis typically have pleuritic chest pain that worsens with deep inspiration and improves with sitting up. The pain is usually located retrosternally and often radiates posteriorly to the bilateral trapezius ridges (lower portion of the scapulae). Low-grade fever may be present. Cardiac auscultation should reveal a pericardial friction rub that is classically triphasic (heard in atrial systole, ventricular systole, and early ventricular diastole). ECG characteristically shows diffuse PR depression and ST elevation, but these findings are not always present and may be masked by ECG changes from recent MI.
The patient presents with acute onset of heart failure, low blood pressure, shortness of breath, pulmonary edema, and mitral regurgitation (holosystolic murmur) following an ACS event, what is the underlying cause?
Papillary muscle rupture which are occurs within one week of an MI.
The pulmonary wedge pressure will be increased and patients will likely be hypoxic and cyanotic with signs of right right sided heart failure and low O2 stats. This requires diagnosis with an echo (transthoracic) and treatment with surgical repair. Patient will also need after load reduction with nitro peroxide or intra-aortic balloon pump (IABP).
A patient presents with a holosystolic murmur at the lower left sternal border after experiencing T wave inversions and leads V1 through V4, what is the underlying cause?
This is an interventricular septal rupture which occurs 3 to 10 days following an MI and presents with a hollow systolic murmur and by ventricular CHF. This requires diagnosis with an echo (transthoracic) and treatment with surgical repair. The prognosis and likelihood of survival with this correlates with the size of the defect.
A patient has distant heart sounds, JVD, and hypotension following an MI that occurred two weeks ago, what is the underlying cause?
This is likely a ventricular wall rupture which occurs within one to two weeks following and MI, most commonly 1 to 4 days. Patient’s present with symptoms of cardiac tamponade and chest pain. This often results in PEA arrest. Diagnosis requires an echo (transthoracic) with pericardiocentesis which can be diagnostic and therapeutic. Definitive treatment is with surgical repair although these patients have a very high mortality rate in this is usually fatal (90%).
A 60-year-old man is being treated in the cardiac intensive care unit after he developed an acute ST-elevation myocardial infarction 4 days ago. The patient presented a few hours after symptom onset and was treated with medical therapy and reperfusion using percutaneous intervention to remove a clot in the left anterior descending artery. This morning, the patient developed sudden onset, severe chest pain. Evaluation at the bedside reveals a blood pressure of 60/40 mmHg. Physical examination is significant for distant heart sounds. Which of the following complications is this patient experiencing?
This patient experienced an acute ST-elevation myocardial infarction (STEMI) involving the left anterior descending artery. Four day later, he is experiencing sudden, severe chest pain, hypotension, and distant heart sounds, which are characteristic of cardiac tamponade secondary to left ventricular free wall rupture. Left ventricular free wall rupture is a severe and lethal mechanical complication of STEMI involving the left anterior descending artery. It is most likely to occur within the first 5 days post-MI but can occur up to 2 weeks later. The patient initially develops severe chest pain due to the tearing of the left ventricular wall, followed by very rapid accumulation of blood in the pericardium, resulting in acute cardiac tamponade characterized by hypotension and distant heart sounds. Most patients enter into cardiac arrest, and thus the mortality rate for left ventricular free wall rupture is very high. Mechanical complications of myocardial infarction are summarized in the table below. Other complications that occur after myocardial infarction (MI) include ventricular arrhythmias (the most common cause of the death 24 hours post-MI), postinfarction acute pericarditis (occurs within 1-3 days), Dressler syndrome (weeks to months after Mi), and left ventricular aneurysm (occurs several months after MI). Left ventricular free wall rupture is a deadly compilation of STEMI involving the left anterior descending artery that usually occurs within 5 days post-MI. It is characterized by sudden, severe chest pain, hypotension, and distant heart sounds, and it can progress rapidly to shock and cardiac arrest.
A patient experiences a stroke two weeks after a myocardial infarction, what is the likely cause?
This could be due to a ventricular aneurysm or pseudoaneurysm. This is a free wall rupture contained by scar tissue and pericardium. True aneurysms have dyskinetic left ventricular wall that balloons during systole which increases the risk of thrombus. Patients tend to have Q waves in leads V1 to V4 (or the same leads at the site of infarction). This is diagnosed with an echo (transthoracic) or angiography and requires surgical repair. True aneurysms do not have a propensity for rupture in contrast to pseudo aneurysms. However true aneurysms have a high incidence of ventricular tachyarrhythmias. Medical management maybe protective and involves use of an ace inhibitor with anticoagulation. Surgery to remove the aneurysm may be appropriate in some patients.
A patient has diffuse ST elevations, dry cough, shortness of breath, and chest pain that is relieved by leaning forward. The patient also experienced an MI one month ago, what is the likely underlying ideology for the patient’s pain?
Dressler syndrome. This is post MI autoimmune pericardial inflammation and is treated with NSAIDs.
(this also can be treated with ASA plus colchicine)
A patient experiences dermatologic changes (Levido reticularis), petechiae, and a blue toe, what is the underlying cause?
This is blue toe syndrome caused by a crystalized embolus made of cholesterol intends to occur following revascularization following ACS. Patients might encounter renal failure, colonic ischemia, muscle ischemia, and CVA.
What is a pseudoaneurysm and how does it occur?
A pseudoaneurysm occurs when arterial bleeding from an inadequately sealed puncture site remains confined within the periarterial connective tissue, forming a contained hematoma that communicates with the arterial lumen. Pseudoaneurysms are a potential complication of arterial access for cardiac catheterization. They occur due to inadequate post-procedural compression, forming a contained hematoma that communicates with the arterial lumen. Diagnosis is confirmed by ultrasonography.
What is the characteristic physical exam finding of an arterial pseudoaneurysm?
A tender, pulsatile mass with a systolic bruit at the puncture site.
What is the most common cause of post-procedural pseudoaneurysm formation?
Inadequate post-procedural manual compression to achieve arterial hemostasis after catheterization.
How is a pseudoaneurysm diagnosed?
Diagnosis is confirmed with ultrasonography, which shows blood flow in and out of the pseudoaneurysm cavity.
How are small pseudoaneurysms managed?
Ultrasound-guided compression or thrombin injection into the pseudoaneurysm cavity.
How are large or rapidly expanding pseudoaneurysms managed?
Surgical repair due to the risk of rupture and catastrophic bleeding.
How does a femoral arteriovenous fistula differ from a pseudoaneurysm?
A femoral AV fistula presents with localized pain, no mass, and a continuous bruit, whereas a pseudoaneurysm presents with a pulsatile mass and a systolic bruit.
Why is reassurance and symptomatic management not appropriate for a pseudoaneurysm?
Because pseudoaneurysms carry a risk of expansion, rupture, and catastrophic bleeding and require definitive management.
Why is discontinuation of dual antiplatelet therapy (DAPT) not recommended in patients with a pseudoaneurysm and a recently placed drug-eluting stent?
Stopping DAPT in such patients carries a high risk of stent thrombosis, which can be fatal.
What cardiovascular conditions require a detailed assessment before resuming sexual activity?
Severe heart failure (NYHA class IV), uncontrolled arrhythmias, severe aortic stenosis, or recent unstable angina.
A patient presents with rapidly developing hemodynamic instability and ipsilateral flank or back pain after cardiac catheterization, what is the best step for diagnosing this condition?
This is suspected retroperitoneal hematoma, which can result as a complication of arterial access for cardiac catheterization. A noncontrast CT scan of the abdomen and pelvis is indicated for hemodynamically stable patients. Noncontrast CT scan of the abdomen and pelvis is the gold standard for diagnosis.
How much cardiovascular exertion is associated with sexual activity?
Sexual activity is estimated to require 3-4 metabolic equivalents (METs), similar to moderate physical exertion (e.g., brisk walking).
How are cardiovascular disease (CVD) patients classified for sexual activity safety?
Patients are classified as low-risk, high-risk, or intermediate-risk based on their cardiovascular disease status.
What defines a low-risk cardiac patient who can safely resume sexual activity?
Patients with controlled hypertension, few CVD risk factors, asymptomatic left ventricular dysfunction, or successful revascularization (>50%-60% stenosis corrected).
Which cardiac patients are considered high-risk for sexual activity?
Patients with refractory angina, NYHA class IV heart failure, significant arrhythmias, or severe valvular disease.
What is the recommendation for intermediate-risk patients before resuming sexual activity?
They should undergo stress testing to determine if they can be reclassified as low- or high-risk.
When can a low-risk patient safely resume sexual activity after an MI?
According to Princeton guidelines, 3-4 weeks after MI; AHA suggests as early as 1 week in successfully revascularized patients.
Is dual antiplatelet therapy (DAPT) a contraindication to physical activity or sexual activity?
No, DAPT is not a contraindication. Patients may have minor bleeding risk (e.g., when brushing teeth or shaving) and should use a soft toothbrush or an electric razor.
Why is sexual activity deferred immediately after an acute MI?
The myocardium is vulnerable to increased oxygen demand and ischemia risk during early post-MI recovery.
What factors support classifying a post-MI patient as low-risk for sexual activity?
Successful revascularization, uncomplicated hospital course, normal/mildly abnormal left ventricular function, and ability to perform moderate physical activity (e.g., walking).
What is the role of cardiac rehabilitation in post-MI sexual activity?
Cardiac rehab is recommended but does not limit a patient’s ability to engage in sexual activity if they remain asymptomatic.
