Acute Coronary Syndrome Flashcards

1
Q

Three coronary vessels supply blood to the heart.

A

Left Anterior Descending artery (LAD)
Left Circumflex artery
Right coronary artery

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2
Q
  • small segment off the aorta and then branches into the Left Anterior Descending artery (LAD) which supplies the anterior and septal part of the left ventricle and the Left Circumflex artery (LCx) which supplies the left lateral aspect of the left ventricle.
A

Left main coronary artery

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3
Q
  • comes off the aorta and runs down the right
    lateral aspect of the heart and to the posterior side of the heart. It
    supplies blood to the right ventricle, SA, and AV node.
A

Right coronary artery

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4
Q

Right and Left Coronary vessels originate off the

A

ascending aorta just above the aortic valve.

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5
Q

Blockages of the LAD and LCx

A

cause the left ventricle to no pump as effectively and leads to CHF.

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6
Q

Blockages of the RCA can lead to

A

either RV infarct with right sided heart failure, or brady arrhythmias due to lack of blood to the SA node.

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7
Q

(1) Oxygenated blood enters either the right or left coronary vessels from the Aorta (sinus of Valsalva).
(2) Will travel down the coronary artery to myocardial tissues where it delivers oxygen and nutrients.
(3) After it passes through the myocardial capillaries it will enter the coronary veins.
(4) The coronary veins will all drain their deoxygenated blood into the coronary sinus.
(5) Coronary sinus then drains its blood into the right atrium.

A

Coronary blood flow

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8
Q

(1) Myocardial Cells are very unique when it comes to oxygen extraction.
(2) Normal tissue will extract only 25% oxygen from a hemoglobin
molecule leaving the hemoglobin returning to the heart 75% saturated.
(3) Under normal conditions, oxygen saturation in the coronary sinus is approximately: 30%. Most tissues extract only about 25% of the oxygen in arterial blood.
**However, the myocardium extracts about 65% of the oxygen resulting in a saturation of only about 30%. Therefore, the myocardium, unlike many other tissues, cannot compensate for a reduction in blood flow by extracting more oxygen from hemoglobin.

A

Coronary oxygen extraction physiology

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9
Q

is chest pain due to myocardial oxygen demand exceeding
delivery (aka ischemia). It is commonly caused by atherosclerotic
disease.

A

Angina

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10
Q

Chest pain with exertion and relieved by rest.

A

Stable Angina

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11
Q

Chest pain while resting. Initially this presents the exact same as NSTEMI until 4-8 hours after the symptoms begin when you will start to get elevated cardiac markers.

A

Unstable Angina

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12
Q

Rare, caused by coronary vasospasm often without
any CAD. drugs, cold weather

A

Prinzmetal’s Angina

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13
Q

________ due to the oxygen demand exceeding supply.

A

Myocardial ischemia:
Myocardial Oxygen Physiology

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14
Q

Because myocardial tissue extracts the maximum amount of oxygen (65%) from hemoglobin increased oxygen requirements must be met by

A

increased coronary blood flow (increased HR or muscle) = chest px

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15
Q

1) Increased HR
2) Increased afterload
3) Increased contractility
4) Increased amount of muscle (from left ventricular or right
ventricular hypertrophy)
5) Increased left ventricular end diastolic volume (how stretched
the LV is just prior to contracting, those hearts in congestive
heart failure will increase volume in the LV in order to assist in
increasing contraction and cardiac output).
6) Increased Preload

A

Factors that increase myocardial oxygen requirements.

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16
Q

1) Increased coronary blood flow either by coronary dilation or by
increased diastolic blood pressure.
Nitro
Morphine
Aspirin

2) Decreasing HR (the most important to control during AMI).
Beta blockers - Metoprolol

3) Increasing hemoglobin if it is < 10 g/dL.
O2 monitor

A

Factors that increase myocardial oxygen content.

17
Q

comprise the spectrum of unstable
cardiac ischemia from unstable angina to acute myocardial infarction.

A

Acute Coronary Syndrome (ACS)

18
Q

ACS is classified based on presenting EKG as either

A

“ST-segment elevation (STEMI) or “non-ST segment elevation (NSTEMI) and the presence of elevated cardiac enzymes.

19
Q

NSTEMI

A

presents with positive cardiac enzymes and non-specific EKG
changes (this represents partial muscle thickness infarct).

20
Q

STEMI

A

or Acute myocardial infarction results from an occlusive
coronary thrombus at the site of a preexisting atherosclerotic plaque. Will present with ST segment elevation and positive cardiac enzymes.
(This represents a transmural or full thickness myocardial infarct).

21
Q

ONAM

A

Oxygen
Nitrogen
Aspirin
Morphine

22
Q

Prinzmetal Angina

A

coronary vasospasm

23
Q

In young individuals with NSTEMI or STEMI without any risk factors

A

you need to think cocaine use, which can cause intense vasoconstriction or coronary dissection leading to myocardial necrosis.

24
Q

(1) Substernal chest pain (#1 symptoms).
(2) Chest pain commonly described as pressure on chest (like an elephant is sitting on their chest).
(3) Chest pain can radiate to left shoulder, left arm, neck or jaw.
(4) Occurs at rest, commonly in the morning.
(5) Diaphoresis
(6) Nausea and vomiting
(7) Anxiety
(8) Intense feeling like they are going to die
(9) Weakness or dizziness
10) 1/3 of patients will not have typical chest pain (older, female, diabetics, neuropathy patients) and have worse outcomes due to delay in treatment.
(11) Dyspnea
(12) Patient may appear anxious, diaphoretic, clinching fist over their chest (called the Levine’s sign).
(13) May be bradycardic or tachycardic depending upon what are of the heart is having the infarct (RCA lesions will present with bradycardia more due to it supplying blood to SA node, where LAD and LCx lesion typically will present more with tachycardia and CHF symptoms).
(14) Blood pressure may be elevated or decreased and in shock.
(15) Respiratory distress indicates heart failure.
(16) Can hear a new heart murmur

A

Symptoms/Physical Examination Findings: Acute Coronary Syndrome

25
Q

(a) Can infarct the papillary muscle to the mitral valve cause acute Mitral Regurgitation (Systolic murmur).
(b) Can hear a S3 heart sound indicating large amounts of blood entering the LV quickly into a compliant ventricle indicating volume overload (i.e. CHF).

A

New onset heart murmur: Acute Coronary Syndrome.

26
Q

(1) Troponin I and T: Specific to myocardial cells, they rise 4-8 hours after injury, peak at 12-24 hours and Troponin T will stay elevated for up to 2 weeks and Troponin I will remain elevated for 5-7 days.

(2) CK-MB

(3) Elevated Troponin and/or CK-MB (which are cardiac enzymes) indicate myocardial infarction.

(4) Typically will draw cardiac enzymes every 8 hours to follow trend, the higher the enzymes released the larger the cardiac infarction and injury.

A

Labs/Studies: Acute Coronary Syndrome.

27
Q

(a) NSTEMI may show ST segment depression, T wave inversion, or no changes at all.

(b) STEMI will show a classic evolution of changes from ST segment
elevation, T wave inversion, and finally Q wave development (which represents scar tissue).

(c) You can tell in which area of the heart and which coronary vessel is blocked in an STEMI based on which leads have the ST elevation.

(d) The sum of total ST-segment elevation is a good indicator of the extent of the infarction and risk of subsequent events.

(e) New Left bundle branch block with symptoms of AMI should be treated as a STEMI.

A

EKG: Acute Coronary Syndrome.

28
Q

(a) Check for signs of CHF, but may lag behind other physical exam
findings.
(b) Rule out aortic dissection (widened mediastinum) as an alternate diagnosis

A

Chest Radiograph: Acute Coronary Syndrome

29
Q

Ultrasound of the heart which can evaluate for
regional wall motion abnormalities indicating infarcted tissue.

A

Echocardiogram: Acute Coronary Syndrome

30
Q

Enter either the femoral or radial artery and
place a catheter into each ostia of the coronary vessels and squirt dye to evaluate for blockages. If blockage discovered the cardiologist can perform either a balloon angioplasty or place a stent across the blockage to reopen the vessel.

A

Cardiac Catheterization: Acute Coronary Syndrome

31
Q

(1) #1 goal of treatment is to prevent further cardiac tissue damage.

(2) Monitor and support ABCs, get vitals and Oxygen saturation, assess cardiac rhythm, and obtain IV access.

(3) Administer 4L NC oxygen if saturation < 94%, MONA (Morphine, Oxygen, Nitroglycerine, and Aspirin)

A

Treatment: Acute Coronary Syndrome

32
Q

(a) Aspirin (Acetylsalicylic Acid) 160-325 mg daily chewable.

(b) Nitroglycerine
1) 0.4 mg sublingual every 5 minutes as needed for chest pain,
max dose 3 doses in 15 minutes

(c) Morphine
1) 4-8 mg IV for chest pain unresponsive to Nitroglycerine

(d) Lovenox
1) In the event of a STEMI: 30 mg IV bolus followed by 1 mg/kg
SC q12 hours given 15 minutes after the IV bolus (max 100mg/dose for the first 2 doses).
2) In the event of a NSTEMI: 1 mg/kg SC q 12 hours with ASA

(e) Metoprolol
2) In the event of a STEMI with tachycardia in absence of
hypotension give 5mg IV q 5 minutes to a max dose of 15 mg.
3) In the event of a NSTEMI start with 50mg PO BID.

A

Medications: Acute Coronary Syndrome

33
Q
  • mainstay of treatment is early reperfusion achieved
    with either Fibrinolytic therapy or Percutaneous Coronary
    Intervention (PCI) with stenting.
A

Treatment For STEMI: Acute Coronary Syndrome

34
Q

Unstable angina or NSTEMI progressing to a STEMI.

A

Complications: Acute Coronary Syndrome

35
Q

(a) Cardiac arrhythmias are common post MI.
(b) VF and Pulseless VT are most common in the first few hours.
(c) Sudden cardiac death.
(d) All degrees of AV block.
(e) SVT
(f) Sinus bradycardia
(g) Cardiogenic Shock
(h) Congestive heart failure
(i) Myocardial Rupture: 1% of patients have complete rupture of LV wall post MI day 2-7.
(j) LV aneurysm
(k) Pericarditis
(l) Flail mitral valve leaflet leading to Acute mitral regurgitation.

A

STEMI

36
Q

Need emergent transfer to higher level of care and inpatient treatment and monitoring.

A

Follow up: STEMI