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Cardiorespiratory > Lecture 13: ACS > Flashcards

Lecture 13: ACS Flashcards

1
Q

what is thr acute coronary syndrome (ACS)?

A

A set of three clinical entities with similar pathophysiology: unstable angina pectoris, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).

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2
Q

ACS is most commonly caused by…

A

atherosclerotic coronary artery disease associated with unstable plaques and -in the case of myocardial infarction- plaque rupture.

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3
Q

what are the 2 conditions classified as non-STE ACS?

A

unstable angina and NSTEMI

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4
Q

what is the pathophysiology of unstable angina?

A

Partial occlusion of coronary vessel → decreased blood supply → ischemic symptoms (also during rest)

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5
Q

what is the pathophysiology of NSTEMI?

A
  • -classically due to partial occlusion of a coronary artery

- -Affects the inner layer of the heart (subendocardial infarction)

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6
Q

what is the pathophysiology of STEMI?

A
  • -Classically due to complete occlusion of a coronary artery
  • -Affects full thickness of the myocardium (transmural infarction)
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7
Q

what is unstable angina?

A
  • -Acute myocardial ischemia that is not severe enough to cause detectable quantities of myocardial injury biomarkers or ST-segment elevations on ECG
  • -Rest angina, which is usually more than 20 minutes in duration
  • -New-onset angina that markedly limits physical activity
  • -Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina
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8
Q

what is the clinical presentation of unstable angina?

A
  • -Angina at rest or with minimal exertion
  • -New-onset angina
  • -Severe, persistent, and/or worsening angina (crescendo angina)
  • -Autonomic symptoms may be present: diaphoresis, syncope, palpitations, nausea, and/or vomiting
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9
Q

what is the acute myocardial infarction (AMI)?

A
  • -detection of a rise and/or fall in cardiac biomarkers, together with evidence of myocardial ischemia with at least one of the following:
  • -Symptoms suggestive of ischemia
  • -ECG changes of ischemia
  • -Development of pathological Q waves
  • -Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality on ECHO
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10
Q

AMI is subdivided into…

A

1) NSTEMI: Acute myocardial ischemia that is severe enough to cause detectable quantities of myocardial injury biomarkers but without ST-segment elevations on ECG
2) STEMI: Acute myocardial ischemia that is severe enough to cause ST-segment elevations on ECG

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11
Q

what are the ECG findings in NSTEMI vs STEMI?

A

1) Normal or nonspecific (e.g., ST depression, loss of R wave, or T-wave inversion). No ST elevations
2) ST elevations (in two contiguous leads) or new left bundle branch block (ST elevations can be masked by a LBBB. Therefore, a LBBB with typical MI symptoms is diagnosed as STEMI.)

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12
Q

what is the treatment of NSTEMI vs STEMI?

A

1)Anticoagulation, aspirin, ADP receptor inhibitor
Invasive management depends on risk stratification (TIMI score).
2)Immediate revascularization. Anticoagulation, aspirin, ADP receptor inhibitor

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13
Q

partial vs complete coronary artery occlusion?

A

1) Decreased myocardial blood flow → supply-demand mismatch → myocardial ischemia
- -Usually affects the inner layer of the myocardium (subendocardial infarction)
- -Typically manifests clinically as unstable angina and/or NSTEMI
2) Impaired myocardial blood flow → sudden death of myocardial cells (if no reperfusion occurs)
- -Usually affects the full thickness of the myocardium (transmural infarction)
- -Typically manifests clinically as STEMI

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14
Q

why subendocardium is most affected?

A

Blood supply of the cardiac muscle extends from the outer to the inner heart. As a result, the inner layer is the least perfused and most affected.

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15
Q

stable vs unstable atherosclerotic plaque?

A
  • -Stable atherosclerotic plaque: manifests as stable angina (symptomatic during exertion)
  • -Unstable plaques are lipid-rich and covered by thin fibrous caps → high risk of rupture
  • -Inflammatory cells in the plaque (e.g., macrophages) secrete matrix metalloproteinases → breakdown of extracellular matrix → weakening of the fibrous cap → minor stress → rupture of the fibrous cap → exposure of highly thrombogenic lipid core → thrombus formation → coronary artery occlusion
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16
Q

how AMS is diagnosed?

A
  • -Cardiac chest pain
  • -Abnormal ECG
  • -Elevated Biomarkers, troponin
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17
Q

what is the epidemiology of ACS?

A
  • -Most common cause of death in Ireland.
  • -Approximately, 5,000 people die in Ireland per year following an acute myocardial infarction
  • -Acute MI is the leading cause of death in North America and Europe
  • -24 people are estimated to have MI in the US over the next hour (duration of this lecture)
  • -Incidence
    1) ∼ 1.5 million cases of myocardial infarction per year in the US
    2) ♂ > ♀ (3:1)
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18
Q

what are the non-modifiable risk factors of ACS?

A
  • -Age
  • -Gender
  • -Family History
  • -Race
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19
Q

what are the modifiable risk factors of ACS?

A
  • -Hypertension
  • -Smoking
  • -Cholesterol
  • -Obesity
  • -Lack of fitness
  • -Diet
  • -Alcohol
  • -Diabetes
  • -Psychosocial factors
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20
Q

what is the role of homocysteine in atherosclerosis?

A
  • -An intermediate molecule that is derived from the amino acid methionine. Can be converted into cystathionine (requires vitamin B6), which is then converted into the amino acid cysteine, or it can be recycled back into methionine (requires folate and vitamin B12). High levels of homocysteine cause.
  • -Hyperhomocysteinemia
    1) Changes in thrombomodulin function are due to increased activation of factor VIIa and V, inhibition of protein C, increased blood viscosity, and decreased endothelial antithrombotic activity.
    2) Homocysteine levels are elevated in patients with vitamin B6 deficiency and mutations in enzymes that metabolize homocysteine (autosomal recessive).
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21
Q

Risk of Coronary Artery Disease Increases with Multiple Risk Factors. Examples…

A

–Systolic blood pressure (>160 mm Hg)
–Total Cholesterol (>6.5 mg/dL)
–HDL cholesterol (<1mmol/L)
–Diabetes
–Smoking
–Left ventricular hypertrophy confirmed by ECG
As reported in the Framingham Heart Study, the likelihood of coronary events is increased by the presence of multiple independent risk factors, such as hypertension, dyslipidemia, diabetes, cigarette smoking, and left ventricular hypertrophy (LVH).

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22
Q

what are the signs and symptoms of ACS?

A

–Classically, severe crushing central chest pain described as squeezing or constricting sensation
–Often described as discomfort rather than pain
In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the centre of the chest - “Levine sign“
–Frequently radiates to the left arm or jaw
–Pain is typically quite severe, usually lasting more than 10 minutes
–Pain may be gradual in onset and fluctuate in intensity
–Exacerbation with exercise and relief with rest or GTN spray

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23
Q

what is the Levine sign?

A

In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the centre of the chest

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24
Q

describe the pain of ACS

A
  • -Typically described as dull, squeezing pressure and/or tightness
  • -Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium
  • -Precipitated by exertion or stress
  • -The peak time of occurrence is usually in the morning (8–11 a.m.).
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25
Q

pain in ACS commonly radiates to right shoulder. T/F

A

F

Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium

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26
Q

at what time is the peak occurrence of pain in ACS?

A

The peak time of occurrence is usually in the morning (8–11 a.m.).

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27
Q

what are other symptoms of ACS except for pain?

A
  • -Dyspnea (especially with exertion)
  • -Pallor
  • -Nausea, vomiting
  • -Diaphoresis, anxiety
  • -Dizziness, lightheadedness, syncope
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28
Q

what are other findings in ACS?

A
  • -Tachycardia, arrhythmias
  • -Symptoms of CHF (e.g., orthopnea, pulmonary edema) or cardiogenic shock (e.g., hypotension, tachycardia, cold extremities)
  • -New heart murmur on auscultation (e.g., new S4)
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29
Q

what are the findings Specific to inferior wall infarction

A
  • -Epigastric pain
  • -Bradycardia
  • -Clear lung fields
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30
Q

why inferior wall MI can cause bradycardia?

A

Inferior wall infarction is usually caused by obstruction of the right coronary artery (RCA). The RCA also supplies the conduction system of the heart (sinus and atrioventricular nodes, bundle of His), which is why arrhythmia occurs when there is ischemia in the area it supplies.

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31
Q

what are the atypical symptoms of MI?

A
  • -minimal to no chest pain
    1) More likely in elderly, diabetic individuals, and women
    2) Autonomic symptoms (e.g., nausea, diaphoresis) are often the chief complaint.
    3) In patients with diabetes, chest pain may be completely absent (e.g., silent MI) due to polyneuropathy.
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32
Q

which patients are more prone to the atypical presentation of ACS?

A
  • -Diabetics, Elderly, Post-Op patients may have silent infarcts or very atypical symptoms
  • -older patients, diabetics, and women are more likely to present with symptoms such as dyspnoea, weakness, nausea and vomiting, palpitations, and syncope
  • -Inferior wall infarcts may present with gastrointestinal symptoms
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33
Q

what are the other important points in history-taking of ACS

A

1) Establish the patients’ risk factors for coronary artery disease
2) Consider the possibility of cocaine use as a cause of vasospasm in younger patients
3) Ask screening questions which reveal symptoms that suggest vascular disease elsewhere
- -Do you get pain in your calf muscles on walking?
- -Have you ever had an episode of face, arm or leg weakness?
- -Have you ever noticed your speech was slurred or garbled?
- -Have you ever experienced a sudden change in your vision?

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34
Q

what condition should always be considered as a cause of ACS in young patients?

A

Cocaine use

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35
Q

what are the features suggesting non-cardiac chest pain?

A
  • -Pleuritic pain-worse with movement and inspiration
  • -Pain in the mid or lower abdominal region
  • -Any discomfort localized with one finger
  • -Any discomfort reproduced by movement or palpation
  • -Constant pain lasting for days
  • -Fleeting pains lasting for a few seconds or less
  • -Pain radiating into the lower extremities or above the mandible
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36
Q

what are the cardiovascular examination signs in ACS suggesting heart failure?

A

1) Raised JVP
2) Third heart sound
3) Bibasal crepitations
4) Pulsatile tender liver
5) Bilateral lower limb edema

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37
Q

what are the cardiovascular examination signs in ACS suggesting cardiogenic shock??

A
  • -Hypotension
  • -Tachycardia
  • -Impaired cognition
  • -Cool, clammy skin
  • -Pale, ashen skin
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38
Q

what are the cardiovascular examination signs in ACS suggesting mechanical complications???

A

Murmurs: VSD, MR

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39
Q

what are the cardiovascular examination signs in ACS suggesting vascular disease???

A
  • -Listen for carotid bruit
  • -Palpate the abdomen for AAA
  • -Assess peripheral pulses
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40
Q

what are other coronary pathologies that should be differentiated from ACS?

A
  • -Coronary spasm – Prinzmetal angina-rare
  • -Coronary dissection or embolism
  • -Cocaine
  • -Stress broken heart syndrome (Takostubo’s syndrome)
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41
Q

what is the Takotsubo synrome?

A

A condition of acute, stress-induced, reversible dysfunction and apical balloooning of the left ventricle. Symptoms resemble those of acute coronary syndrome but often resolve spontaneously.
–emotional/physical stress → massive catecholamine discharge → cardiotoxicity, multi-vessel spasms and dysfunction → myocardial stunning

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42
Q

what are other pathologies that should be differentiated from ACS?

A
  • -Pulmonary embolism
  • -Aortic dissection
  • -GERD
  • -Pericarditis
  • -Pneumonia
  • -Chest wall pain, costochondritis
  • -Cholecystitis
43
Q

what are the complications in 0–24 hours post-infarction?

A

1) Sudden cardiac death
- -The most common underlying cause in elderly individuals is an acute coronary syndrome (∼ 70% of cases).
- -The most common cause is ventricular arrhythmia.
2) Arrhythmias
- -Ventricular tachyarrhythmias
- -AV block
- -Asystole
- -Atrial fibrillation
3) Acute left heart failure: the death of affected myocardium → absence of myocardial contraction→ pulmonary edema
4) Cardiogenic shock

44
Q

what is the most common cause of sudden cardiac death post-infarction?

A

ventricular fibrillation

45
Q

what are the complications in 1–3 days post-infarction?

A
  • -Early infarct-associated pericarditis
    1) Typically occurs within the first week of a large infarct close to the pericardium
    2) Clinical features of acute pericarditis: pleuritic chest pain , dry cough , friction rub, diffuse ST elevations on ECG
    3) Complications (rare): hemopericardium, pericardial tamponade
46
Q

what are the complications in 3 -14days post-infarction?

A

1)Papillary muscle rupture
–Usually occurs 2–7 days after myocardial infarction
–Can lead to acute mitral regurgitation
–Rupture of the posteromedial papillary muscle due to occlusion of the posterior descending artery is most common.
–Clinical features
–New holosystolic, blowing murmur over the 5th ICS on the midclavicular line
–Signs of acute mitral regurgitation: dyspnea, cough, bilateral crackles, hypotension
2)Ventricular septal rupture
–Usually occurs 3–5 days after myocardial infarction
–Due to structural degradation by macrophages
–Most commonly due to LAD infarction (septal arteries arise from LAD)
–Clinical features
–New holosystolic murmur over the left sternal border
–Acute-onset right heart failure (jugular venous distention, peripheral edema)
–Can progress to cardiogenic shock: tachycardia, hypotension, cool extremities, altered mental status
Treatment: emergency surgery and revascularization (often via CABG)
3)Left ventricular free wall rupture
–Usually occurs 5–14 days after myocardial infarction
Greatest risk during macrophage-mediated removal of necrotic tissue
–Clinical features: chest pain, dyspnea, signs of cardiac tamponade (e.g., Beck triad)
–Complications
–Cardiac tamponade
–LV pseudoaneurysm formation: rupture of LV wall that is contained by the pericardium

47
Q

what papillary muscle is commonly ruptured in the case of AMI?

A
  • -Rupture of the posteromedial papillary muscle due to occlusion of the posterior descending artery is most common.
  • -The anterolateral papillary muscle is less prone to rupture because of dual arterial supply from the LAD and the LCx.
48
Q

New holosystolic, blowing murmur over the 5th ICS on the midclavicular line and radiating to axilla after MI suggests?

A

mitral regurgitation due to rupture of posteromedial papillary muscle

49
Q

what type of MI usually lead to mitral regurgitation?

A

inferior wall MI

50
Q

what artery occlusion is most commonly responsible for ventricular septal rupture?

A

LAD

51
Q

what is the Beck triad?

A

A clinical triad of hypotension, muffled heart sounds, and distended neck veins that is seen in cardiac tamponade.

52
Q

what are the complications 2 weeks to months post-infarction?

A

1) Atrial and ventricular aneurysms
- -Clinical features
- -Persistent (> 3 weeks post-MI) ST elevation and T-wave inversions
- -Systolic murmur, S3 and/or S4
- -Diagnosis: echocardiography
- -Complications
- -Cardiac arrhythmias (risk of ventricular fibrillation)
- -Rupture → cardiac tamponade
- -Mural thrombus formation → thromboembolism (stroke, mesenteric ischemia, renal infarction, acute obstruction of peripheral arteries)
- -Treatment: anticoagulation, possibly surgery
2) Postmyocardial infarction syndrome (Dressler syndrome): pericarditis occurring 2–10 weeks post-MI without an infective cause
- -Thought to be due to circulating antibodies against cardiac muscle cells (autoimmune etiology)
- -Clinical features
- -Signs of acute pericarditis: pleuritic chest pain, dry cough, friction rub
- -Fever
- -Laboratory findings: leukocytosis, ↑ serum troponin levels
- -ECG: diffuse ST elevations
- -Treatment: aspirin, acetaminophen
- -Complications (rare): hemopericardium, pericardial tamponade
3) Arrhythmias (e.g., AV block)
4) Congestive heart failure (e.g., ischemic cardiomyopathy)
- -Can occur at any time after an ischemic event
- -Treatment: for patients with LVEF < 40% or signs of heart failure, ACE inhibitor/ARB and aldosterone antagonists have been shown to confer a mortality benefit.
5) Reinfarction

53
Q

what are the ECG signs fo ventricular aneurysm post-MI?

A

Persistent (> 3 weeks post-MI) ST elevation and T-wave inversions

54
Q

why NSAIDs and glucocorticoids should be avoided in patients with recent AMI?

A

increases risk of the ventricular wall or septal rupture

55
Q

how ACS is diagnosed?

A

Bloods

1) General
- -FBC, renal function, liver function, coagulation profile, fasting risks
2) Cardiac Biomarkers
- -Troponin
- -Myoglobin
- -Creatinine kinase MB fraction

56
Q

what are looked on CBC and CMP in ACS?

A

1) FBC
- -Looking for anemia or infection
2) Renal Function Test
- -Establishing a baseline renal function
- -Dehydration and electrolyte imbalances
3) Liver Function Test
- -Congestion
4) Coagulation Profile
- -Baseline as anticoagulants will be introduced
5) Fasting Risk Factor Profile
- -Fasting Glucose and Lipid profile

57
Q

what is the role of troponin in ACS diagnosis?

A
  • -Very specific and more sensitive than CK
  • -Rises 3-8 hours after injury
  • -May remain elevated for up to two weeks
  • -Can provide prognostic information
58
Q

what other condition can elevated troponin T?

A

Troponin T may be elevated with renal disease, poly/dermatomyositis

59
Q

what is the role of CK-MB in ACS diagnosis?

A
  • -Rises 4-6 hours after injury and peaks at 24 hours
  • -Remains elevated 36-48 hours
  • -Positive if CK/MB > 5% of total CK and 2 times normal
  • -Elevation can be predictive of mortality
60
Q

what other condition can elevated CK-MB?

A

False positives with exercise, trauma, muscle disease, DM, PE

61
Q

The degree of elevation of troponin often correlates with the…

A

size of the infarct.

62
Q

when troponin levels are raised post-infarction?

A

High sensitivity troponin assays (HscTn) may detect an increase in serum troponin level as early as 90 to 180 minutes after myocardial ischemia has occurred

63
Q

what is the main clinical significance of CK-MB?

A

helpful for evaluating reinfarction because of its short half-life but is no longer commonly used. CK-MB has a short half-life, returning to normal within 72 hours of MI, in contrast to troponin.

64
Q

what are the initial investigations in suspected ACS?

A
  • -Serial ECG and biomarkers
  • -CXR
  • -ECHO, stress echo
  • -Exercise stress test
  • -Coronary angiography and/or exercise stress test
  • -MRI
  • -Nuclear Myocardial perfusion imaging
  • -CT coronary angiography
65
Q

what is the pharmacologic treatment in ACS?

A

1) Sublingual or intravenous nitrate (nitroglycerin or ISDN)
- -For symptomatic relief of chest pain
- -Does not improve prognosis
- -Contraindications: inferior wall infarct (due to risk for hypotension), hypotension, and/or PDE 5 inhibitor (e.g., sildenafil) taken within last 24 hours
2) Morphine IV or SC (3–5 mg)
- -Only if the patient has severe, persistent chest pain or severe anxiety related to the myocardial event
- -Administer with caution due to increased risk of complications (e.g., hypotension, respiratory depression) and adverse events
3) Beta blocker
- -Recommended within the first 24 hours of admission
- -Avoid in patients with hypotension, features of heart failure, and/or risk of cardiogenic shock (e.g., large LV infarct, low ejection fraction).
4) Statins: early initiation of high-intensity statin (such as atorvastatin 80 mg) regardless of baseline cholesterol, LDL, and HDL levels
5) Loop diuretic (e.g., furosemide) if the patient has flash pulmonary edema or features of heart failure

66
Q

what is the treatment of STEMI?

A

–Immediate revascularization
–Revascularization is the most important step in the management of acute STEMI and initiation of further therapies (e.g., DAPT, anticoagulation) should not delay this step in management.
1)Emergent coronary angiography: with percutaneous coronary intervention (PCI)
–Preferred method of revascularization
–Balloon dilatation with stent implantation (see cardiac catheterization)
–Ideally, door-to-PCI time should be < 90 minutes. It should not exceed 120 minutes.
2)Thrombolytic therapy: tPA, reteplase, or streptokinase
Indications:
–If PCI cannot be performed < 120 minutes after onset of STEMI
–If PCI was unsuccessful
–No contraindications to thrombolysis

67
Q

what is coronary artery bypass grafting (CABG)?

A

A surgical cardiac revascularization technique used to treat patients with significant, symptomatic stenosis of a coronary artery or its branches. The stenosed segment is bypassed using an arterial (e.g., internal thoracic artery) or venous (e.g., great saphenous vein) autograft, re-establishing blood flow to the ischemic areas of the myocardium.
–Not routinely recommended for acute STEMI
Indications
–If PCI is unsuccessful
–If coronary anatomy is not amenable to PCI
–If STEMI occurs at the time of surgical repair of a mechanical defect

68
Q

what are the contraindications to thrombolytic therapy?

A
  • -Any prior intracranial bleeding
  • -Recent large GI bleeding
  • -Recent major trauma, head injury, and/or surgery
  • -Ischemic stroke within the past 3 months
  • -Hypertension (> 180/110 mm Hg)
  • -Known coagulopathy
69
Q

what antiplatelet and antithrombotic agents are used in ACS?

A

1) Dual antiplatelet therapy: start as soon as possible
- -Aspirin loading dose 162 mg–325 mg
- -PLUS ADP receptor inhibitor: prasugrel, ticagrelor, or clopidogrel
- -Dual antiplatelet therapy should be continued for at least 12 months after PCI with DES.
2) GP IIb/IIIa receptor antagonist (e.g., eptifibatide or tirofiban): should be considered in precatheterization setting
3) Anticoagulation
- -Heparin or bivalirudin recommended
- -Continue until PCI is performed or for 48 hours after a fibrinolytic is given.

70
Q

what is the principles of secondary prevention of ACS?

A

1) Risk factor modification
- -HTN, DM, dyslipidaemia
2) Behavioral
- -smoking, diet, physical activity, weight
3) Cognitive
- -Education, cardiac rehab program

71
Q

what is the prognosis of ACS?

A
  • -Prognosis for an individual varies markedly according to their risk factors
  • -After MI patients face an increased risk of further cardiovascular events, including an increase in mortality rates
  • -However, early post-MI in hospital death rates have fallen with reperfusion strategies
  • -Long-term mortality rates after STEMI have also declined

Limited published data on the long-term outcomes after NSTEMI but increased risk of recurrent events despite OMT

72
Q

do cardiac biomarkers are elevated in NSTEMI?

A

Yes (vs unstable angina)

73
Q

what are the ECG changes in STEMI?

A

1) Acute stage: myocardial damage ongoing
- -Hyperacute T waves (“peaked T wave”)
- -ST elevations in two contiguous leads with reciprocal ST depressions
2) Intermediate stage: myocardial necrosis present
- -Absence of R wave
- -T-wave inversions
- -Pathological Q waves
3) Chronic stage: permanent scarring
- -Persistent, broad, and deep Q waves
- -Often incomplete recovery of R waves
- -Permanent T wave inversion is possible.

74
Q

what is the sequence of ECG changes over several hours to days:

A

hyperacute T wave → ST-elevation → pathological Q wave → T-wave inversion → ST normalization → T-wave normalization

75
Q

what are the ECG changes in NSTEMI?

A
  • -No ST elevations present
  • -Nonspecific changes may be present.
    1) ST depression
    2) Inverted T wave
    3) Loss of R wave
76
Q

ST elevation in V1-V6 indicates…

A
  • -Extensive anterior (Leads aVL and I can also be affected.)
  • -Proximal left anterior descending artery (LAD) : Supplies the anterior wall, anterior part of the lateral wall (left side), apex of the left ventricle, and anterior ⅔ of the ventricular septum (i.e., a large part of the left ventricle)
77
Q

ST elevation in V1-V2 indicates…

A
  • -(Antero)septal

- -LAD

78
Q

ST elevation in V3-V4 indicates…

A
  • -(Antero)apical

- -Distal LAD

79
Q

ST elevation in V5-V6 indicates…

A
  • -Antero)lateral
  • -Diagonal branch of LAD
  • -Distal LAD
  • -Left circumflex artery (LCX)
  • -In rare cases, can also be caused by right coronary artery (RCA) infarct
80
Q

ST elevation in I and aVL indicates…

A
  • -Lateral

- -Proximal LCX: Supplies the posterolateral and posterior walls

81
Q

ST elevation in II, III, aVF indicates…

A
  • -Inferior
  • -RCA (more common): Supplies the posterior wall, especially the right ventricle, the diaphragmatic part of the left ventricle, and the posterior third of the ventricular septum. The sinus and atrioventricular nodes are also usually supplied by the right coronary artery.
  • -Distal LCX (less common)
82
Q

ST elevation in V7-V9 indicates…

A
  • -posterior/posterolateral
  • -Posterior descending artery (from RCA or LCX)
  • -Reciprocal ST depressions in V1–3 may also be seen
83
Q

anterior vs inferior wall MI on ECG?

A

Infarction of the anterior wall is caused by obstruction of the LAD or its branches. Depending on the extent of anterior wall infarction, it results in ECG changes in the anterior wall leads (V1–6) and/or I and aVL. Infarction of the inferior wall is caused by obstruction of the LCX or RCA or their branches, and ECG changes are seen in leads II, III, and aVF.

84
Q

To remember the ECG leads with maximal ST elevation in anterior MI, think “SAL

A

“Septal (V1–2), Apical (V3–4), Lateral (V5–6).

85
Q

what is the most important cardiac biomarker?

A

Serum troponin T is the most important cardiac-specific marker and may be measured 3–4 hours after the onset of myocardial infarction. CK-MB values correlate with the size of the infarct, reach a maximum after approximately 12–24 hours, and normalize after only 2–3 days, making CK-MB a good marker for evaluating reinfarction.

86
Q

what are the other lab markers in AMI?

A
  • -levated inflammatory markers: ↑ WBC, CRP: Both are associated with increased risk of recurrence of ischemia and cardiac death.
  • -Elevated BNP: especially in heart failure
  • -Elevated LDH
  • -Elevated AST (SGOT)
87
Q

what is the coronary angiography?

A
  • -Best test for definitive diagnosis of acute coronary occlusion
  • -Can be used for concurrent intervention (e.g., PCI with stent placement)
  • -Can identify site and degree of vessel occlusion
  • -Indications include
    1) Acute STEMI
    2) Other high-risk ACS
88
Q

what are the most commonly occluded coronary arteries (descending order)?

A

left anterior descending artery, right coronary artery, circumflex artery.

89
Q

what is the role of ECHO in ACS?

A
  • -Identification of any wall motion abnormalities and to assess LV function
  • -Important for risk assessment: In STEMI, the best predictor of survival is LVEF.
  • -Evaluation for complications: aneurysms, mitral valve regurgitation, pericardial effusion, free wall rupture
90
Q

what is the role of CT in AMI?

A
  • -May be considered as an alternative to invasive coronary angiography in patients with an intermediate risk of ACS
  • -Allows for noninvasive visualization of the coronary arteries
  • -Contraindication: arrhythmias, tachycardia
91
Q

what are the microscopic and macroscopic findings in 0–24 hrs post-infarction?

A

1) Early coagulative necrosis (> 4 hours)
- -Release of inflammatory cytokines from necrotic cells → edema, hemorrhage
- -Recruitment of neutrophils (granulocytes)
- -Hypercontraction of myofibrils → wavy fibers
- -Contraction band necrosis (if reperfusion injury has occurred)
2) 0–12 hours: no gross changes
3) 12–24 hours: dark mottling

92
Q

what are the microscopic and macroscopic findings in 1-3 days post-infarction?

A

1) Extensive coagulative necrosis (4–72 hours)
- -Neutrophilic infiltrate
- -Inflammation spreads to the tissue surrounding infarct.
2) Hyperemia
3) Yellow pallor

93
Q

what are the microscopic and macroscopic findings in 3-14 days post-infarction?

A

1) Macrophage infiltration
2) Granulation tissue surrounds infarct margins (3–10 days)
3) The proliferation of blood vessels into granulation tissue (10–14 days)
4) Hyperemic border
5) Center: yellow-brown, soft

94
Q

what are the microscopic and macroscopic findings after 2 weeks post-infarction?

A
  • -Granulation tissue becomes denser → collagenous scar formation
  • -Grayish-white fibrosis
95
Q

what is the reperfusion injury?

A
  • -A condition characterized by endothelial damage caused by a returning blood supply after a period of ischemia (e.g., myocardial infarction, ischemic stroke). Causes increased capillary permeability, tissue swelling, and release of reactive oxygen species
  • -Can occur spontaneously or after revascularization (e.g., fibrinolysis or PCI)
  • -Typically occurs when reperfusion occurs > 3 hours after the acute coronary artery occlusion
  • -Mechanism: blood flow restored → damaged myocytes release reactive oxygen species (ROS) → mitochondrial permeability transition pores are formed → cell swelling → cell death → Ca2+ entry into the cytosol → hypercontraction of myocytes → contraction band necrosis and increase in infarct size
  • -Microscopic findings: neutrophilic infiltration, capillary obstruction, and contraction band necrosis of the myocardium
96
Q

what is the differential diagnosis of increased troponin?

A

1) Cardiac causes
- -Myocarditis
- -Decompensated congestive heart failure
- -Pulmonary embolism (Due to RV overload)
- -Cardiac arrhythmia, tachycardia
- -Cardiac trauma
- -Takotsubo cardiomyopathy
2) Noncardiac causes
- -Renal failure: Troponin elevation in renal failure is due to decreased clearance of serum troponin, not due to an actual elevation in troponin.
- -Stroke
- -Critical illness (e.g., sepsis)

97
Q

Differential diagnosis of ST-elevations on ECG

A
  • -Early repolarization
  • -LBBB
  • -Brugada syndrome
  • -Myocarditis
  • -Pericarditis
  • -Pulmonary embolism
  • -Hyperkalemia
  • -Tricyclic antidepressant use
  • -Poor ECG lead placement
98
Q

what is Brugada syndrome?

A

A genetically inherited disorder that causes a repolarization abnormality in cardiac myocytes that can lead to sudden cardiac death. It is characterized by ECG findings including the presence of a “pseudo-right bundle branch block” and persisting ST elevations in V1–V2.

99
Q

why morphine should be used with caution in MI?

A

Morphine decreases preload by dilating the veins and consequently can worsen cardiac ischemia. Because some studies have shown an increased risk of mortality in association with morphine use, it should be used with caution!

100
Q

what is the role of statins in AMI?

A

Stabilize plaques and lower cholesterol levels; should be part of acute and maintenance therapy

101
Q

Primary interventions of MI treatment include “MONA”

A

Morphine, Oxygen, Nitroglycerin, and Aspirin. But remember: Morphine, oxygen, and nitroglycerine are not necessarily indicated for every patient

102
Q

when oxygen is recommended in AMI?

A

only in case of cyanosis, severe dyspnea, or SpO2 < 90% (< 95% in STEMI)

103
Q

what is the PCI?

A

An endovascular procedure in which an inflatable balloon is passed over a wire into a narrowed or obstructed artery. Upon inflation, the balloon widens the arterial lumen, which improves perfusion.

104
Q

Fibrinolytic treatment is not recommended in patients with unstable angina or NSTEMI. T/F

A

True

Cardiorespiratory (24 decks)

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