The Left Coronary Artery

The Left coronary artery begins thicker and is called the left main coronary artery. This branches off into the LAD and the Cx.

The Left Anterior Descending Artery

The LAD lies on the surface of the heart between the right and left ventricles. It often extends to the inferior surface of the left ventricle in most patients. The LAD supplies blood to:

• Anterior surface and part of the lateral surface of the left ventricle
• The anterior 2/3 of the intraventricular septum

The Circumflex Artery

The Cx wraps around the left side of the heart in the groove between the left atrium and left ventricle in the back (the coronary sulcus). The Cx supplies blood to:

• The left atrium
• The other part of the lateral surface of the left ventricle
• Rarely the inferior and/or posterior portions of the LV
• SA node (40%)
• AV bundle (10-15%)

The Posterior Descending Artery

The posterior descending artery usually branches off from the RCA, although less commonly from the Cx. Whichever one does form the posterior descending artery is considered the “dominant coronary artery”.

ACUTE CORONARY SYNDROME

Acute coronary syndrome (ACS) is an umbrella term referring to any condition which causes decreased blood flow to the heart – also known as ischemia. Prolonged ischemia can lead to infarction – which is cell death of the heart tissue.

This cell death causes the release of troponin into the bloodstream, an enzyme that is not usually found in the systemic circulation.

Cardiac ischemia is usually secondary to atherosclerosis which is a buildup of plaque within the coronary arteries. This is usually caused by unhealthy eating habits, obesity, sedentary lifestyle, hyperlipidemia, smoking, and genetics.

This plaque can rupture, releasing contents into the bloodstream which causes a local inflammatory reaction as well as begins a coagulation cascade.

This blood clot can completely occlude an artery – leading to infarction.

A Non-ST segment elevation myocardial infarction (NSTEMI) refers to a complete occlusion of a coronary artery that does not cause ST-segment elevation on the ECG.

While some heart tissue dies, this is usually less extensive than a STEMI. The infarction is usually limited to the inner layer of the myocardial wall.

NSTEMIs will often have nonspecific changes on the EKG. These changes include T wave inversion or ST-segment depression with or without T wave inversion in anatomically contiguous leads. However, NSTEMIs could also present with a completely normal ECG.

Troponin levels will be elevated indicating myocardial cell death. However, the ECG does not have ST-segment elevation.

An ST-segment Elevation Myocardial Infarction (STEMI) refers to a complete occlusion of a coronary artery that causes more significant infarction that extends the entire thickness of the myocardium (termed transmural).

A STEMI will have ST-segment elevation in at least 2 contiguous leads on the ECG.

Where this elevation occurs will indicate which heart wall is infarcting, as well as within which coronary artery.

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ISCHEMIA & INFARCTION (STEMI) ON THE ECG

The ST-segment is the segment on the ECG right after the QRS segment and before the T wave. This represents the initial phase of ventricular repolarization and should be at the isoelectric line.

The TP-segment should be used as the isoelectric baseline, but you can use the PR segment if the TP is difficult to see.

The J-point is the point on the ECG where the QRS complex meets the ST segment. This is important for recognizing ST segment elevation.

ST-SEGMENT DEPRESSION

ST-segment depression most commonly identifies cardiac ischemia, as well as reciprocal changes in an acute MI.

It can also indicate heart strain, digitalis effect, hypokalemia, hypomagnesemia, or even be rate related. However, these changes are usually more diffuse as opposed to localized to at least 2 contiguous leads.

ST-segment depression is defined as ≥0.5 mm depression (1/2 small box) below the isoelectric line 80 ms after the J-point (2 small boxes).

Horizontal and Down-sloping ST-segment depression are more specific to cardiac ischemia, whereas up-sloping tends to be less serious although still could indicate ischemia.

De Winter T waves can be seen in 2% of acute LAD occlusions without significant ST-segment elevation. Instead, there will be ST-segment depression at the J-point with upsloping and tall, symmetric T waves in the precordial leads (V1-V6).

ST-SEGMENT ELEVATION

ST-segment elevation usually indicates myocardial infarction when appearing in at least 2 contiguous leads.

Other possible causes of ST-segment elevation include coronary vasospasm, pericarditis, benign repolarization, left BBB, LV hypertrophy, ventricular aneurysm, Brugada syndrome, ventricular pacemaker, increased ICP, blunt chest trauma, and hypothermia.

ST-segment elevation is defined as ≥1 mm elevation (1 small box) above the isoelectric line at the J-point. However, in leads V2 and V3, it needs to be > 1.5mm in women, > 2mm in men >40, and > 2.5mm in men < 40.

Concave ST elevation is considered less ominous and sometimes can indicate benign variant called early repolarization, especially when diffuse.

Convex upward ST elevation is almost always indicative of a large MI. This is termed “tombstoning”.

Q WAVES

Q waves are the initial positive deflection of the QRS complex indicating septal depolarization. These are normal in all leads except V1-V3.

Pathologic Q waves are abnormal Q waves that indicate underlying pathology – usually a current or previous MI.

Pathologic Q waves are defined as >40ms wide (1 small box) and >2 mm deep (2 small boxes).

Any Q waves seen in V1-V3 are always pathologic.

Q waves can begin hours to days after an infarction begins, and can last for years, even forever.

LBBB OR VENTRICULAR PACED

Recognizing ST-segment elevation or depression can be difficult in the case of a left bundle branch block (LBBB) or ventricular paced rhythm. This is because there is normally some associated ST-elevation and discordant T waves with these conduction abnormalities.

To determine possible ischemia or infarction in a patient with these conduction abnormalities, one of the following should be present:

• ST-segment Elevation > 1mm in a lead with a positive QRS complex (concordant ST elevation)
• ST-segment depression >1mm in V1, V2, or V3

These are not always present, but if they are – you should highly suspect ACS in a patient with a pre-existing LBBB morphology.

This is why a new LBBB and acute chest pain or SOB is concerning for acute MI.

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STEMI PROGRESSION

STEMIs typically have a normal progression that will be seen on the ECG.

Hyperacute T waves are first seen, which are tall, peaked, and symmetric in at least 2 contiguous leads. These usually last only minutes to an hour max.

Then, ST-segment elevation occurs in at least 2 contiguous leads at the J-point, initially concave, and then becomes convex or rounded upwards.

The ST-segment eventually merges with the T wave and the ST/T wave becomes indistinguishable. This is a “tombstone” pattern.

Reciprocal ST depression may be seen in opposite leads.

The ST segment then returns to baseline after a week or so.

Q waves eventually develop within hours to days, followed by T wave inversion which could be temporary. Over time, the Q wave deepens.

STEMI LOCATION

STEMIs are classified based on where they are located anatomically – so which leads are they are affecting on the ECG.

Contiguous leads simply means leads that are pertaining to the same anatomical region of the heart.

The following leads pertain to each region of the heart:

• Anteroseptal: V1, V2
• Anteroapical: V3, V4
• Anterolateral: V5, V6
• Lateral: I, aVL
• Inferior: II, III, aVF

The precordial and lateral leads are often affected together as the area of infarction is not always exact. 

As an example, the EKG below is an inferior wall STEMI:

ACUTE MANAGEMENT OF STEMI

STEMIs are true medical emergencies.

The patient is at a high risk of significant conduction disturbances and arrhythmias including cardiac arrest.

The longer you wait – the more heart cells will die, leading to worse cardiac outcomes as well as increasing the possibility of patient death.

A 12-lead ECG should be obtained within 10 minutes of any patient with significant cardiac symptoms including chest pain or SOB.

Women, older adults, and diabetics may have atypical presentations including a “silent” MI, where they don’t even have chest pain.

There are many actions that need to be taken in a short amount of time, and many medications that will need to be administered before the cath team gets there.

A code STEMI should be activated (or whatever your facility’s version of it is), so the interventional cardiologist and the cath team can be alerted ASAP.

The patient should be hooked up to the monitor, vital signs obtained, IV access x 2 should be established (preferably an 18g), labs drawn and sent including troponin and PT/PTT, and the defibrillation pads should be applied.

Any abnormal vital signs should be addressed, and any arrhythmias should be managed via ACLS guidelines.

Oxygen should be administered to maintain O2 >90%.

Aspirin 324mg should be chewed and swallowed. A rectal suppository of 300mg can be given if the patient cannot tolerate PO for some reason.

Antiplatelet therapy with P2y12 receptor blockers such as Plavix or Brilinta should be given in addition to the aspirin.

Nitroglycerin should be administered 0.4mg SL x 3 q5min if the patient has persistent chest discomfort, HTN, or signs of heart failure.

However, do not give if they have used phosphodiesterase inhibitors like Viagra or Cialis within the last 24h.

Don’t give Nitro if they have a low blood pressure, if they have severe aortic stenosis, or if there is a possibility of a right ventricular infarct (sometimes presents with inferior wall MIs). Nitro can cause severe hypotension in these patients.

For persistent symptoms, an IV nitro drip can be used.

Anticoagulants like an unfractionated heparin drip should be given. Other options include Lovenox.

If the patient has signs of left heart failure, treat with nitro as above, loop diuretic like Lasix, +/- Bipap.

Morphine 2-4mg slow IVP q5-15min can be given for persistent severe chest pain or anxiety. However, there is research indicating an increased risk of death when morphine is given in STEMI.

It is possible that morphine may interfere with the antiplatelet effect of P2y 12 receptor blockers. So morphine should be avoided unless absolutely required for pain control.

Atorvastatin 80mg PO should be given ASAP, preferably before PCI in those who are not already on a statin. If the patient on it already, their dose should be increased to 80mg.

Primary percutaneous coronary intervention (PCI) is the preferred reperfusion method and should happen ASAP.

This is when the interventional cardiologist will take the patient to the cardiac cath lab and perform angiography and stent placement to open up the occluded vessel.

Fibrinolytics can alternatively be given, specifically if there is no access to a cath lab within a reasonable time frame (120 min), as long as symptoms < 12 hours and no contraindications (i.e. risk of bleeding).

Beta-blockers are initiated within 24 hours, unless they are contraindicated such as with bradycardia, HF, or severe reactive airway disease. This can be started after PCI.

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Non-ST Segment Elevation Myocardial Infarction (STEMI)

As the name suggests, an NSTEMI does not have ST elevation seen on the ECG, but it is still a heart attack.

An elevated and rising troponin level is associated with an NSTEMI.

The ECG can be completely normal, or it can have nonspecific T wave changes or even ST depression in contiguous leads.

Management of an NSTEMI is similar to a STEMI in terms of medications. However, they are not given fibrinolytic and are not emergently brought to the cath lab. They may or may not get a cardiac cath during their hospital stay.

Instead, medication therapy is maximized like the ones described above. The patient is continued to be monitored, and troponin levels are trended usually every 6-8 hours.

STEMIs and NSTEMIs are critical emergent events that nurses need to know well! You will be running into this at some point in your nursing career, and you want to know exactly what you’re doing when it happens! Being able to recognize a STEMI on the ECG is the first step!

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