Earthquake fault types
There are three main types of fault, all of which may cause an interplate earthquake: normal, reverse (thrust), and strike-slip. Normal and reverse faulting are examples of dip-slip, where the displacement along the fault is in the direction of dip and where movement on them involves a vertical component. Many earthquakes are caused by movement on faults that have components of both dip-slip and strike-slip; this is known as oblique slip. The topmost, brittle part of the Earths crust, and the cool slabs of the tectonic plates that are descending into the hot mantle, are the only parts of our planet that can store elastic energy and release it in fault ruptures. Rocks hotter than about 300 °C (572 °F) flow in response to stress; they do not rupture in earthquakes. The maximum observed lengths of ruptures and mapped faults (which may break in a single rupture) are approximately 1,000 km (620 mi). Examples are the earthquakes in Alaska (1957), Chile (1960), and Sumatra (2004), all in subduction zones. The longest earthquake ruptures on strike-slip faults, like the San Andreas Fault (1857, 1906), the North Anatolian Fault in Turkey (1939), and the Denali Fault in Alaska (2002), are about half to one third as long as the lengths along subducting plate margins, and those along normal faults are even shorter. Normal faults
Normal faults occur mainly in areas where the crust is being extended such as a divergent boundary. Earthquakes associated with normal faults are generally less than magnitude 7.
As per Lu and Nightingale, serum magnesium concentrations associated with maternal toxicity (also neonate depression, hypotonia and low Apgar scores) are:

7.0–10.0 mEq/L – Loss of patellar reflex
10.0-13.0 mEq/L – Respiratory depression
15.0-25.0 mEq/L – Altered atrioventricular conduction and (further) complete heart block
>25.0 mEq/L – Cardiac arrest

Complications
Severe hypermagnesemia (levels greater than 12 mg/dL) can lead to cardiovascular complications (hypotension and arrhythmias) and neurological disorder (confusion and lethargy). Higher values of serum magnesium (exceeding 15 mg/dL) can induce cardiac arrest and coma. Causes
Magnesium status depends on three organs: uptake in the intestine, storage in the bone, and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly the intestine or kidney. Predisposing conditions
Hemolysis, magnesium concentration in red blood cells is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis. Chronic kidney disease, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of chronic kidney disease unless magnesium intake is increased. Magnesium toxicity from emergency pre-eclampsia treatment during labor and delivery. Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hypothyroidism, hyperparathyroidism, and lithium intoxication. Metabolism
For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia. Diagnosis
Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.