Syncope

2010 ◽  
pp. 4838-4841
Author(s):  
A.J. Larner
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Return ◽  
Peripheral Vascular Resistance ◽  
Loss Of Consciousness ◽  
Body Parts ◽  
Peripheral Vascular ◽  
Transient Loss Of Consciousness ◽  
Transient Loss

Syncope is the commonest identified cause of transient loss of consciousness, being ten times more frequent than epilepsy. It is a consequence of cerebral underperfusion due to reduced cardiac output, often related to reduced venous return due to decreased peripheral vascular resistance, with pooling of blood volume in dependent body parts....

Circulatory effects of profound hypothermia during extracorporeal circulation

1962 ◽  
Vol 202 (3) ◽  
pp. 523-526 ◽  
Author(s):  
Richard L. Kahler ◽  
Allan Goldblatt ◽  
Eugene Braunwald
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Extracorporeal Circulation ◽  
Venous Return ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Systemic Blood ◽  
Circulating Blood Volume ◽  
Profound Hypothermia ◽  
Circulatory Effects

The effects of hypothermia on peripheral vascular resistance, venous return, and systemic blood volume were studied in dogs using extracorporeal circulation and a constant systemic perfusion rate. Cooling to 15–20 C produced a significant fall in total systemic peripheral vascular resistance and a large augmentation of systemic blood volume. The latter was superimposed on the gradual increase in systemic blood volume which occurs in many dogs on cardiopulmonary bypass. Both systemic vascular resistance and blood volume returned toward control levels during rewarming. Indicator dilution curves demonstrated a decrease in the "actively" circulating blood volume despite the observed increase in total systemic blood volume. These observations suggest that during hypothermia significant arteriolar dilatation occurred and that substantial volumes of blood were "trapped" in the peripheral vascular bed. This trapping resulted in the striking decrease in venous return and increase in systemic blood volume.

Syncope

2020 ◽  
pp. 5896-5901
Author(s):  
Andrew J. Larner
Keyword(s):  
Cardiac Output ◽  
Heart Disease ◽  
Physical Examination ◽  
Specific Treatment ◽  
Cerebral Hypoperfusion ◽  
Loss Of Consciousness ◽  
Body Parts ◽  
Transient Loss Of Consciousness ◽  
History Of ◽  
Transient Loss

Syncope is the most common identified cause of transient loss of consciousness, being ten times more frequent than epilepsy. It is a consequence of cerebral hypoperfusion due to reduced cardiac output, often related to reduced venous return due to decreased peripheral vascular resistance with pooling of blood volume in dependent body parts. Diagnosis is clinical, based on history of the circumstances of the event obtained from the patient and reliable eyewitness(es). In most patients, particularly under 45 years of age, the condition is benign and self-limiting, with an excellent prognosis, requiring little investigation beyond physical examination and electrocardiogram to exclude heart disease. Cardiac causes of syncope may require specific treatment.

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

1988 ◽  
Vol 66 (1) ◽  
pp. 80-83 ◽  
Author(s):  
M. Levy ◽  
Elizabeth Maher ◽  
Marvin J. Wexler
Keyword(s):  
Cardiac Output ◽  
Liver Function ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Systemic Hemodynamics ◽  
Peripheral Vascular Resistance ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Peripheral Vascular

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i. e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Changes in Cardiac Output and Peripheral Vascular Resistance during Weight Training in Athletes

1988 ◽  
Vol 75 (s19) ◽  
pp. 3P-3P ◽  
Author(s):  
LO Hughes ◽  
Mary E Heber ◽  
H Harries ◽  
A Lahiri ◽  
EB Raftery
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Weight Training ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular

scholarly journals Features of changes in volume-impedance hemodynamic indicators during the tilt test in young males with a history of vasovagal syncopes

Kardiologiia ◽  
2019 ◽  
Vol 59 (11) ◽  
pp. 31-38
Author(s):  
A. V. Barsukov ◽  
O. G. Chepcheruk ◽  
D. V. Glukhovskoi ◽  
V. V. Yakovlev ◽  
A. V. Gordienko
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Negative Response ◽  
Peripheral Vascular Resistance ◽  
Tilt Test ◽  
Peripheral Vascular ◽  
Total Peripheral Vascular Resistance ◽  
History Of ◽  
Group 3 ◽  
Group 1

Background. The direction of changes in hemodynamic parameters during the tilt test (TT) nin individuals with history of vasovagal syncope (VVS) is a subject of discussion. Objective: to study changes of volume-impedance hemodynamic indicators in the process of tilt test in somatically healthy young men with history of VVS. Materials and methods. A total of 102 men aged 18–30 years were divided into 4 groups, taking into account the specific features of fainting history and response to TT. Persons of group 1 (n=14) had history of VVS and positive response to TT (syncope). Subjects of group 2 (n=14) had history of VVS and a pattern of postural tachycardia without fainting during TT. Persons of group 3 (n=42) had history of VVS and negative response to TT. Subjects of group 4 (n=32) had no history of VVS and negative response to TT. During TT, we studied dynamics of some indicators, including cardiac output (CO) and total peripheral vascular resistance (TPVR). Results. In individuals of all groups in the initial horizontal phase of TT values of CO and TPVR corresponded to the norm. Subjects of group 1 had significantly lower CO compared with subjects of groups 2, 3, 4 (p<0.05, p<0.01, p<0.05, respectively). Values of TPVR in subjects of group 1 were significantly higher than in subjects of groups 2, 3, 4 (p<0.05; p<0.05; p<0.05, respectively). In response to orthostasis CO values increased in groups 1, 2, 4 (by 18%, 10%, 5%, respectively) and did not change in group 3; TPVR values decreased in groups 1, 2 (by 8%, 0.5%, respectively), and increased in groups 3, 4 (by 8%, 4% respectively). In the final horizontal phase of TT, CO values in group 1 were significantly lower than in groups 3, 4 (p<0.05), while TPVR values did not significantly differ between all groups (p>0.05). Conclusions. In tilt-positive and tilt-negative subjects with history of VVS, standardized postural stress leads to unidirectional changes in cardiac output, but to multidirectional changes in total peripheral vascular resistance.

Circadian Rhythm of Cardiac Output, Peripheral Vascular Resistance, and Related Variables by a Beat-to-Beat Monitoring

1993 ◽  
Vol 10 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Pietro Cugini ◽  
Loredana Di Palma ◽  
Salvatore Di Simone ◽  
Piernatale Lucia ◽  
Paola Battisti ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Circadian Rhythm ◽  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular
Sign in / Sign up

Export Citation Format

Share Document