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Hypotension is a decrease in systemic blood pressure below accepted low values. While there is not an accepted standard hypotensive value, pressures less than 90/60 are recognized as hypotensive. Hypotension is a relatively benign condition that is under-recognized mainly because it is typically asymptomatic. It only becomes a concern once pumping pressure is not sufficient to perfuse key organs with oxygenated blood. This leads to symptoms impacting the quality of life of a patient.  Hypotension is classified based on the biometric parameters of the blood pressure measurement. It may be absolute with changes in systolic blood pressure to less than 90 mm Hg or mean arterial pressure of less than 65 mm Hg. It may be relative to a decrease in diastolic blood pressure to less than 40 mm Hg. It may be orthostatic with a decrease in systolic pressure or 20 mm Hg or greater or a decrease in diastolic pressure of 10 mm Hg or greater on positional change from lying to standing. It may be profound which is defined as being medication-dependent. In acute conditions, the hypotensive shock is a possible and life-threatening condition. Blood pressure is defined as: Blood Pressure = Cardiac output x Total peripheral vascular resistance: The mean arterial pressure is an average blood pressure over the course of one cardiac cycle. It is calculated as: Mean arterial pressure = 2/3 diastolic pressure + 1/3 systolic pressure., (Copyright © 2022, StatPearls Publishing LLC.)

International normalized ratio (INR) is the preferred test of choice for patients taking vitamin K antagonists (VKA). It can also be used to assess the risk of bleeding or the coagulation status of the patients. Patients taking oral anticoagulants are required to monitor INR to adjust the VKA doses because these vary between patients. The INR is derived from prothrombin time (PT) which is calculated as a ratio of the patient’s PT to a control PT standardized for the potency of the thromboplastin reagent developed by the World Health Organization (WHO) using the following formula: INR = Patient PT ÷ Control PT. PT, the time in seconds, is measured in plasma to form a clot in the presence of sufficient concentration of calcium and tissue thromboplastin by activating coagulation via the extrinsic pathway. The reference values for INR take into account in PT measurement in device related variations, type of reagents used, and sensitivity differences in the TF activator. INR value is dimensionless and ranges from a score of 2.0 to 3.0. Optimizing the patient’s INR therapeutic range can be challenging as narrow therapeutic range had been seen in VKAs and can be affected by patient's characteristics, co-morbid conditions, diet, and other drug interactions. Patients are monitored every 3–4 weeks or less at the thrombosis centers (TC), point-of-care (POC) clinics, or in the home setting., (Copyright © 2022, StatPearls Publishing LLC.)

Tricuspid stenosis (TS) is a very rare valvular abnormality occurring due to the narrowing of the tricuspid valve. It results in an elevated gradient between the right atrium and right ventricle, systemic congestion, and failure to augment right ventricle output. The isolated occurrence is rare, and TS usually accompanies other valvular abnormalities. It most often co-exists with mitral valve pathology, especially in patients with rheumatic heart disease. , (Copyright © 2022, StatPearls Publishing LLC.)

Right ventricular hypertrophy (RVH) is an abnormal enlargement or pathologic increase in muscle mass of the right ventricle in response to pressure overload, most commonly due to severe lung disease. The right ventricle is considerably smaller than the left ventricle and produces electrical forces that are largely obscured by those generated by the larger left ventricle. Size and function of the right ventricle are adversely affected by the following: Pulmonary hypertension with or without left ventricular dysfunction. Conditions that affect the tricuspid valve leading to significant tricuspid regurgitation (TR). Anatomy and Physiology The right ventricle is composed of inflow (sinus) and outflow (conus) regions, separated by a muscular ridge, the crista supraventricularis. The inflow region includes the tricuspid valve (TV), the chordae/papillary muscles as well as the body of the RV. The RV body boundaries are formed by the RV free wall, extending from the interventricular septum's anterior and posterior aspects. The standard septal curvature convexes toward the RV cavity and imparts a crescent shape to the right ventricle when cross-sectioned. The RV's interior surface is heavily trabeculated; this feature along with the moderator band and more apical insertion of the TV-annulus impart key morphologic differences that distinguish the RV from the LV by echocardiography. In contrast, the infundibulum is a smooth, funnel-shaped outflow portion of the RV that ends at the pulmonic valve. Thus, the RV has a complex geometry, with traditional RV free-wall thickness of 0.3-0.5 cm, imparting greater distensibility and larger cavity volumes in the RV versus the LV, despite lower end-diastolic filling pressures. This translates to an RVEF that is typically 35% to 45% (versus 55% to 65% in the LV) yet generates the identical SV as the LV. Changes in preload, afterload, and intrinsic contractility of the ventricle influence the systolic function of the RV, like the LV. Differences in RV muscle fiber orientation dictate that the body of the RV shortens symmetrically in the longitudinal and radial planes; thus, longitudinal shortening accounts for a much larger proportion of RV ejection than in the LV. The relatively conspicuous RV shortening along the longitudinal axis can measure RV systolic function using uncomplicated techniques that do not require geometric assumptions or meticulous endocardial definition, both being known limitations to the noninvasive assessment of RV systolic function., (Copyright © 2022, StatPearls Publishing LLC.)