We Need Your Urgent Help To Sustain This Website And All Our Research And Community Initiatives. Please Help By Donating To Our Cause. Go To The Sponsorship Section.
Hypotension or low blood pressure stops organs from getting the necessary blood supply. Acute decrease of blood pressure can result in the shock syndrome, whereas long-term reduction leads to lethargy, fatigue, weakness, dizziness, fainting and other symptoms.
Since arterial pressure is determined by cardiac output, venous pressure and systemic vascular resistance, a reduction in any of these variables can result in hypotension. Thus low blood pressure may be a result of reduced cardiac output, blood volume redistribution, hypovolemia, reduced systemic vascular resistance and vascular obstruction.
Cardiac output (the amount of blood pumped from the heart) can be reduced as a result of three main conditions: arrhythmias, structural disease of the heart or hypovolemia. Older patients are particularly at risk as the aging process further reduces compliance of the heart's ventricles and subsequently lessens its contractility.
Bradycardia or slow heart rhythm caused by a low sinus rate or atrioventricular block reduces cardiac output. On the other hand, tachycardia can also result in reduced cardiac output by decreasing ventricular filling time with a subsequent large reduction in stroke volume. Ventricular fibrillation leads to profound hypotension by plummeting cardiac output down to zero.
Structural disease of the heart such as cardiomyopathies can impede both systolic function (muscle contraction) and diastolic function (ventricular filling), thereby reducing cardiac output and arterial pressure. Pericardial disease, valve disease and congenital defects can compromise ventricular filling or net forward flow with the same consequence.
Ischemic heart disease caused by atherosclerosis or thromboembolism also has a negative effect on ventricular function and often results in exercise-induced hypotension. Primary pulmonary hypertension (abnormally high blood pressure in the arteries of the lungs) can lead to right ventricular failure and in turn impair left ventricular filling and output.
Hypovolemia (most often as a result of hemorrhage) and orthostatic volume changes reduce cardiac output by decreasing central venous pressure and ventricular filling (preload), which impairs the pumping ability of the heart. Excessive water loss (dehydration) caused by profuse sweating, restricted water intake or use of diuretic drugs can also lead to a hypovolemic state.
Hypotension may also be of vascular origin and is generally caused by excessive systemic vasodilation (decreased systemic vascular resistance). This can be a result of anaphylaxis, sepsis, autonomic nerve dysfunction (such as diabetic neuropathy), neurogenic shock (such as spinal cord injury) or different kind of vasodilatative drugs.
A second vascular cause of hypotension is obstruction (e.g. pulmonary embolism) that diminishes venous return to the left ventricle, thereby decreasing its output. Thrombolytic therapy should be used in such patients, but bleeding risk should be adequately assessed.
Vascular endothelial growth factor (VEGF) induces hypotension in normotensive subjects due to endothelium-dependent vasorelaxation, which is considered to be a major side effect for the treatment of ischemic diseases. In addition, hypotension after successful angioplasty with stenting can be a lethal complication.