Clevidipine also contains glycerin (22.5 mg/mL), purified egg yolk phospholipids (12 mg/mL), and sodium hydroxide to adjust pH. Clevidipine has a pH of 6.0–8.0
In the perioperative patient population Clevidipine produces a 4–5% reduction in systolic blood pressure within 2–4 minutes after starting a 1–2 mg/hour IV infusion. In studies up to 72 hours of continuous infusion, there was no evidence of tolerance. In most patients, full recovery of blood pressure is achieved in 5–15 minutes after the infusion is stopped. Stereochemistry
Clevidipine contains a stereocenter and consists of two enantiomers. This is a racemate, ie a 1: 1 mixture of ( R ) – and the ( S ) - form:

Dosage and administration
Aseptic technique should be used when handling Cleviprex since it contains phospholipids and can support microbial growth. Cleviprex is administered intravenously and should be titrated to achieve the desired blood pressure reduction. Blood pressure and heart rate should be monitored continually during infusion. Cleviprex is a single use product that should not be diluted and should not be administered in the same line as other medications. Once the stopper is punctured, Cleviprex should be used within 12 hours and any unused portion remaining in the vial should be discarded. Change IV lines in accordance with hospital protocol. An IV infusion at 1–2 mg/hour is recommended for initiation and should be titrated by doubling the dose every 90 seconds. As the blood pressure approaches goal, the infusion rate should be increased in smaller increments and titrated less frequently.
Pathophysiology
The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape. This process is usually associated with a continuous decline in ejection fraction. The concept of cardiac remodeling was initially developed to describe changes that occur in the days and months following myocardial infarction. Compensation effects
As DCM progresses, two compensatory mechanisms are activated in response to impaired myocyte contractility and reduced stroke volume:
Frank-Starling law
Neurohormonal feedback, via activation of the sympathetic nervous system and the renin-angiotensin system.These responses initially compensate for decreased cardiac output and maintain those with DCM as asymptomatic. Eventually, however, these mechanisms become detrimental, intravascular volume becomes too great, and progressive dilatation leads to heart failure symptoms. Computational models
Cardiac dilatation is a transversely isotropic, irreversible process resulting from excess strains on the myocardium. A computation model of volumetric, isotropic, and cardiac wall growth predicts the relationship between cardiac strains (e.g.