Vascular resistance
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Vascular resistance is a term used to define the resistance to flow that must be overcome to push blood through the circulatory system. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). The systemic vascular resistance may also be referred to as the total peripheral resistance.
Units for measuring vascular resistance are dyn·s·cm-5 or pascal seconds per cubic metre (Pa·s/m³). Pediatric cardiologists use hybrid reference units (HRU), also known as Wood units, as they were introduced by Dr. Paul Wood. To convert from Wood units to MPa·s/m3 you must multiply by 8, or to dyn·s·cm-5 you must multiply by 80.
| Measurement | Reference Range |
|---|---|
| Systemic vascular resistance | 900–1200 dyn·s/cm5 (90–120 MPa·s/m3) |
| Pulmonary vascular resistance | 100–200 dyn·s/cm5 (10–20 MPa·s/m3) |
Calculation of resistance
The basic tenet of calculating resistance is that flow is equal to driving pressure divided by resistance.
The pulmonary vascular resistance can therefore be calculated in units of dyn·s·cm-5 as
where the pressures are measured in units of millimetres of mercury (mmHg) and the cardiac output is measured in units of litres per minute (L/min).
Determinants of vascular resistance
The major determinant of vascular resistance is small arteriolar (known as resistance arterioles) tone. These vessels are from 450 µm down to 100 µm in diameter. (As a comparison, the diameter of a capillary is about 3 to 4 µm.)
Another determinant of vascular resistance is the pre-capillary arterioles. These arterioles are less than 100 µm in diameter. They are sometimes known as autoregulatory vessels.
Regulation of vascular resistance
There are many factors that alter the vascular resistance. Many of the platelet-derived substances, including serotonin, are vasodilatory when the endothelium is intact and are vasoconstrictive when the endothelium is damaged.
Cholinergic stimulation causes release of endothelium-derived relaxing factor (EDRF) (later it was discovered that EDRF was nitric oxide) from intact endothelium, causing vasodilatation. If the endothelium is damaged, cholinergic stimulation causes vasoconstriction.
Role of adenosine
Adenosine probably doesn't play a role in maintaining the vascular resistance in the resting state. However, it causes vasodilatation and decreased vascular resistance during hypoxia. Adenosine is formed in the myocardial cells during hypoxia, ischemia, or vigorous work, due to the breakdown of high-energy phosphate compounds (e.g., adenosine monophosphate, AMP). Most of the adenosine that is produced leaves the cell and acts as a direct vasodilator on the vascular wall. Because adenosine acts as a direct vasodilator, it is not dependent on an intact endothelium to cause vasodilatation.
Adenosine causes vasodilatation in the small and medium sized resistance arterioles (less than 100 µm in diameter). When adenosine is administered it can cause a coronary steal phenomenon, where the vessels in healthy tissue dilate as much as the ischemic tissue and more blood is shunted away from the ischemic tissue that needs it most. This is the principle behind adenosine stress testing.
Adenosine is quickly broken down by adenosine deaminase, which is present in red cells and the vessel wall.
Coronary vascular resistance
The regulation of tone in the coronary arteries is a complex subject. There are a number of mechanisms for regulating coronary vascular tone, including metabolic demands (ie: hypoxia), neurologic control, and endothelial factors (ie: EDRF, endothelin).
Local metabolic control (based on metabolic demand) is the most important mechanism of control of coronary flow. Decreased tissue oxygen content and increased tissue CO2 content act as vasodilators Acidosis acts as a direct coronary vasodilator and also potentiates the actions of adenosine on the coronary vasculature.
References
1. Grossman W, Baim D. Grossman's Cardiac Catheterization, Angiography, and Intervention, Sixth Edition. Page 172, Tabe 8.1 ISBN 0-683-30741-X
See also
Circulatory system pathology (I, 390-459) | |
|---|---|
| Hypertension | Hypertensive heart disease - Hypertensive nephropathy - Secondary hypertension (Renovascular hypertension) |
| Ischaemic heart disease | Angina pectoris (Prinzmetal's angina) - Myocardial infarction (heart attack) - Dressler's syndrome |
| Pulmonary circulation | Pulmonary embolism - Cor pulmonale |
| Pericardium | Pericarditis - Pericardial effusion - Cardiac tamponade |
| Endocardium/heart valves | Endocarditis - mitral valve (regurgitation, prolapse, stenosis) - aortic valve (stenosis, insufficiency) - pulmonary valve (stenosis, insufficiency) - tricuspid valve (stenosis, insufficiency) |
| Myocardium | Myocarditis - Cardiomyopathy (Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Loeffler endocarditis, Restrictive cardiomyopathy) - Arrhythmogenic right ventricular dysplasia |
| Electrical conduction system of the heart | Heart block: AV block (First degree, Second degree, Third degree) - Bundle branch block (Left, Right) - Bifascicular block - Trifascicular block Pre-excitation syndrome (Wolff-Parkinson-White, Lown-Ganong-Levine) - Long QT syndrome - Adams-Stokes syndrome - Cardiac arrest - Sudden cardiac death Arrhythmia: Paroxysmal tachycardia (Supraventricular, AV nodal reentrant, Ventricular) - Atrial flutter - Atrial fibrillation (Familial) - Ventricular fibrillation - Premature contraction (Atrial, Ventricular) - Ectopic pacemaker - Sick sinus syndrome |
| Other heart conditions | Heart failure - Cardiovascular disease - Cardiomegaly - Ventricular hypertrophy (Left, Right) |
| Cerebrovascular diseases | Stroke - Transient ischemic attack - Intracranial hemorrhage/cerebral hemorrhage: Extra-axial hemorrhage (Epidural hemorrhage, Subdural hemorrhage, Subarachnoid hemorrhage) Intra-axial hematoma (Intraventricular hemorrhages, Intraparenchymal hemorrhage) - Anterior spinal artery syndrome - Binswanger's disease - Moyamoya disease |
| Arteries, arterioles and capillaries | Atherosclerosis (Renal artery stenosis) - Aortic dissection/Aortic aneurysm (Abdominal aortic aneurysm) - Aneurysm - Raynaud's phenomenon/Raynaud's disease - Buerger's disease - Vasculitis/Arteritis (Aortitis) - Intermittent claudication - Arteriovenous fistula - Hereditary hemorrhagic telangiectasia - Spider angioma - Dissection (Carotid artery, Vertebral artery) |
| Veins, lymphatic vessels and lymph nodes | Thrombosis/Phlebitis/Thrombophlebitis (Deep vein thrombosis, May-Thurner syndrome, Portal vein thrombosis, Venous thrombosis, Budd-Chiari syndrome, Renal vein thrombosis, Paget-Schroetter disease) - Varicose veins / Portacaval anastomosis (Hemorrhoid, Esophageal varices, Varicocele, Gastric varices, Caput medusae) - Superior vena cava syndrome - Lymph (Lymphadenitis, Lymphedema, Lymphangitis) |
| Other | Hypotension (Orthostatic hypotension) - Rheumatic fever |
| See also congenital (Q20-Q28, 745-747) | |
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| Articles on Vascular resistance | Most recent articles on Vascular resistance • Most cited articles on Vascular resistance • Review articles on Vascular resistance • Articles on Vascular resistance in N Eng J Med, Lancet, BMJ |
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| Evidence Based Medicine Regarding Vascular resistance | Cochrane Collaboration on Vascular resistance • Bandolier on Vascular resistance • TRIP on Vascular resistance |
| Cost Effectiveness of Vascular resistance | Cost Effectiveness of Vascular resistance |
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| Guidelines / Policies / Government Resources (FDA/CDC) Regarding Vascular resistance | US National Guidelines Clearinghouse on Vascular resistance • NICE Guidance on Vascular resistance • NHS PRODIGY Guidance • FDA on Vascular resistance • CDC on Vascular resistance |
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| Genetics, Pharmacogenomics, and Proteinomics of Vascular resistance | Genetics of Vascular resistance • Pharmacogenomics of Vascular resistance • Proteomics of Vascular resistance |
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
