Vascular resistance

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Template:WikiDoc Cardiology News Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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)

## Contents

* 1 Calculation of resistance
* 2 Determinants of vascular resistance
* 3 Regulation of vascular resistance
* 3.1 Role of adenosine
* 4 Coronary vascular resistance
* 5 References
* 6 See also

## Calculation of resistance

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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

<math>\frac {80 \cdot (mean\ pulmonary\ arterial\ pressure - pulmonary\ capillary\ wedge\ pressure)} {cardiac\ output}</math>

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

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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

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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

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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

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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

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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

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* Adenosine
* Cardiac output

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Electrocardiography

Overview|

History of the EKG • EKG interpretation basics • Normal sinus rhythm

EKG Complexes|

P wave • QRS complex • ST Segment • T wave • T wave alternans • Tombstone T wave • U wave

Osborn wave • H wave • K wave • Delta wave

NSSTW changes

EKG Intervals|

PR Interval • QRS Interval • ST Interval • QT Interval

Conduction System & Bradycardia|

Cardiac pacemaker • SA node • AV node• Bundle of His • Purkinje fibers • Sinus bradycardia • First Degree AV Block • Second Degree AV Block • Complete or Third-Degree AV Block • Concealed conduction • AV Junctional Rhythms • LBBB • LAHB • LPHB • RBBB • Trifascicular block

Atrial Arrhythmias|

Sinus tachycardia • Premature Atrial Contractions (PACs) • Ectopic Atrial Rhythm • Paroxysmal Atrial Tachycardia (PAT) • Paroxysmal Atrial Tachycardia (PAT) with Block • Multifocal Atrial Tachycardia (MAT) • Atrial Flutter • Atrial Fibrillation • Wandering atrial pacemaker

Ventricular Arrhythmias|

Differential Diagnosis of Tachycardia with a Wide QRS Complex • Accelerated Idioventricular Rhythm • Ventricular Parasystole • Premature Ventricular Contractions (PVCs) • Ventricular tachycardia • Ventricular Fibrillation • Sudden cardiac death

EKG Abnormalities in Disease States|

Hypertrophy & Dilatation • Right atrial enlargement • Left atrial enlargement • Biatrial enlargement • Left Ventricular Hypertrophy • Right Ventricular Hypertrophy • Biventricular Hypertrophy •

Acute myocardial infarction • NSTEMI • STEMI • Tombstone ST elevation • Right ventricular myocardial infarction • Atrial infarction

Pre-excitation Syndromes • Wolff-Parkinson-White Syndrome • Lown Ganong Levine Syndrome • Mahaim Type Preexcitation

Cardiomyopathies • Arrhythmogenic Right Ventricular Dysplasia • Dilated Cardiomyopathy • Hypertrophic Cardiomyopathy

Drug Effects on the EKG • Adenosine • β-blockers • Digitalis • Quinidine • Procainamide • Disopyramide • Lidocaine • Tocainide and Mexiletine • Phenytoin • Encainide, Flecainide and Propafenone • Amiodarone • Bretylium • Ca Channel Blockers • Phenothiazines • Tricyclic Antidepressants • Lithium

Congenital Heart Disease • Dextrocardia • Atrial Septal Defect • Ventricular Septal Defect • Tetralogy of Fallot • Conjoined Twins or Siamese Twins • Congenital heart block

Electrolyte Disturbances • Hyperkalemia • Hypokalemia • Hypercalcemia • Hypocalcemia • Nonspecific Changes

Other Heart Diseases • Pericarditis • Myocarditis • Tamponade • Heart Transplantation • Sick Sinus Syndrome • Long QT Syndrome

Inherited Disease • Brugada Syndrome

Systemic Diseases • CNS Disease • Cardiac Tumors

Heart Transplantation • EKG Changes in patient with Heart Transplantation

Exogenous Effects • Hypothermia • Chest Trauma • Insect Bites • Electric Injuries

Technical Issues and Potential Errors in Interpretation|

Artifacts • Lead Placement Errors • The EKG in a Patient with a Pacemaker • EKG in athletes

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Physiology of the cardiovascular system

Heart|

| Cardiac output|

* Cardiac cycle
* Cardiac output
* Heart rate
* Stroke volume
* Stroke volume
* End-diastolic volume
* End-systolic volume
* Afterload
* Preload
* Frank–Starling law
* Cardiac function curve
* Venous return curve
* Wiggers diagram
* Pressure volume diagram

|

Ultrasound|

* Fractional shortening = (End-diastolic dimension
* End-systolic dimension) / End-diastolic dimension
* Aortic valve area calculation
* Ejection fraction
* Cardiac index

Heart rate|

* Cardiac pacemaker
* Chronotropic (Heart rate)
* Dromotropic (Conduction velocity)
* Inotropic (Contractility)
* Bathmotropic (Excitability)
* Lusitropic (Relaxation)

Conduction|

* Conduction system
* Cardiac electrophysiology
* Action potential
* cardiac
* atrial
* ventricular
* Effective refractory period
* Pacemaker potential
* Electrocardiography
* P wave
* PR interval
* QRS complex
* QT interval
* ST segment
* T wave
* U wave
* Hexaxial reference system

Chamber pressure|

* Central venous
* Right
* atrial
* ventricular
* pulmonary artery
* wedge
* Left
* atrial
* ventricular
* Aortic

Other|

* Ventricular remodeling

Vascular system/
Hemodynamics|

| Blood flow|

* Compliance
* Vascular resistance
* Pulse
* Perfusion

|

Blood pressure|

* Pulse pressure
* Systolic
* Diastolic
* Mean arterial pressure
* Jugular venous pressure
* Portal venous pressure

Regulation of BP|

* Baroreflex
* Kinin–kallikrein system
* Renin–angiotensin system
* Vasoconstrictors
* Vasodilators
* Autoregulation
* Myogenic mechanism
* Tubuloglomerular feedback
* Cerebral autoregulation
* Paraganglia
* Aortic body
* Carotid body
* Glomus cell

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Cardiovascular disease (heart)

Ischaemic|

| Coronary disease|

* Coronary artery disease (CAD)
* Coronary artery aneurysm
* Spontaneous coronary artery dissection (SCAD)
* Coronary thrombosis
* Coronary vasospasm
* Myocardial bridge

|

Active ischemia|

* Angina pectoris
* Prinzmetal's angina
* Stable angina
* Acute coronary syndrome
* Myocardial infarction
* Unstable angina

Sequelae|

* hours
* Hibernating myocardium
* Myocardial stunning
* days
* Myocardial rupture
* weeks
* Aneurysm of heart / Ventricular aneurysm
* Dressler syndrome

Layers|

| Pericardium|

* Pericarditis
* Acute
* Chronic / Constrictive
* Pericardial effusion
* Cardiac tamponade
* Hemopericardium

|

Myocardium|

* Myocarditis
* Chagas disease
* Cardiomyopathy
* Dilated
* Alcoholic
* Hypertrophic
* Tachycardia-induced
* Restrictive
* Loeffler endocarditis
* Cardiac amyloidosis
* Endocardial fibroelastosis
* Arrhythmogenic right ventricular dysplasia

Endocardium /
valves|

| Endocarditis|

* infective endocarditis
* Subacute bacterial endocarditis
* non-infective endocarditis
* Libman–Sacks endocarditis
* Nonbacterial thrombotic endocarditis

|

Valves|

* mitral
* regurgitation
* prolapse
* stenosis
* aortic
* stenosis
* insufficiency
* tricuspid
* stenosis
* insufficiency
* pulmonary
* stenosis
* insufficiency

Conduction /
arrhythmia|

| Bradycardia|

* Sinus bradycardia
* Sick sinus syndrome
* Heart block: Sinoatrial
* AV
* 1°
* 2°
* 3°
* Intraventricular
* Bundle branch block
* Right
* Left
* Left anterior fascicle
* Left posterior fascicle
* Bifascicular
* Trifascicular
* Adams–Stokes syndrome

|

Tachycardia
(paroxysmal and sinus)|

| Supraventricular|

* Atrial
* Multifocal
* Junctional
* AV nodal reentrant
* Junctional ectopic

|

Ventricular|

* Accelerated idioventricular rhythm
* Catecholaminergic polymorphic
* Torsades de pointes

Premature contraction|

* Atrial
* Junctional
* Ventricular

Pre-excitation syndrome|

* Lown–Ganong–Levine
* Wolff–Parkinson–White

Flutter / fibrillation|

* Atrial flutter
* Ventricular flutter
* Atrial fibrillation
* Familial
* Ventricular fibrillation

Pacemaker|

* Ectopic pacemaker / Ectopic beat
* Multifocal atrial tachycardia
* Pacemaker syndrome
* Parasystole
* Wandering atrial pacemaker

Long QT syndrome|

* Andersen–Tawil
* Jervell and Lange-Nielsen
* Romano–Ward

Cardiac arrest|

* Sudden cardiac death
* Asystole
* Pulseless electrical activity
* Sinoatrial arrest

Other / ungrouped|

* hexaxial reference system
* Right axis deviation
* Left axis deviation
* QT
* Short QT syndrome
* T
* T wave alternans
* ST
* Osborn wave
* ST elevation
* ST depression
* Strain pattern

Cardiomegaly|

* Ventricular hypertrophy
* Left
* Right / Cor pulmonale
* Atrial enlargement
* Left
* Right
* Athletic heart syndrome

Other|

* Cardiac fibrosis
* Heart failure
* Diastolic heart failure
* Cardiac asthma
* Rheumatic fever

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