Ignite Creation Date:
2024-05-06 @ 11:10 AM
Last Modification Date:
2024-10-26 @ 12:41 PM
Study NCT ID:
NCT03446326
Status:
RECRUITING
Last Update Posted:
2024-05-17
First Post:
2018-01-31
Brief Title:
Assessment of Stroke Volume and Cardiac Output in Response to Varying Heart Rates
Sponsor:
University of Calgary
Organization:
University of Calgary
Study Overview
Official Title:
Assessment of Stroke Volume and Cardiac Output in Response to Varying Heart Rates and Body Position - a Pacemaker Based Study
Status:
RECRUITING
Status Verified Date:
2024-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
Pacing_SV
Brief Summary:
The investigators will seek to determine the effects of different heart rates on both stroke volume and cardiac output using non-invasive hemodynamic assessments In order to safely manipulate the HR the investigators will study patients with permanent pacemakers in whom heart rate manipulation can be done in a safe and non-invasive manner
Detailed Description:
Permanent pacemakers have sometimes been used to treat patients with recurrent vasovagal syncope This is because patients with vasovagal syncope often experience bradycardia at the time of their syncope Unfortunately pacemakers are often ineffective in preventing syncope
Classical cardiovascular hemodynamics would suggest that increasing the heart rate HR via pacemaker should increase the cardiac output CO This is because
CO HR x Stroke volume SV
The assumption is that the SV is fixed during manipulation of the HR However this might not be the case As the number of beats per minute HR increases the cardiac cycle length R-R interval RRI shortens as a function of simple math This means that the time in cardiac systole shortens and the time in cardiac diastole shortens Since cardiac diastole is when the heart fills up with blood faster HR can be associated with decreased cardiac filling times This in turn could compromise the SV However there is a paucity of data as to what happens to SV and CO at different HR Further it is possible that these effects will be different when a person is lying down supine versus when a patient is upright when stroke volume will be lower
The investigators will seek to determine the effects of different HR on both SV CO In order to safely manipulate the HR they will study patients with permanent pacemakers in whom HR manipulation can be done in a safe and non-invasive manner
Classical cardiovascular hemodynamics would suggest that increasing the heart rate HR via pacemaker should increase the cardiac output CO This is because
CO HR x Stroke volume SV
The assumption is that the SV is fixed during manipulation of the HR However this might not be the case As the number of beats per minute HR increases the cardiac cycle length R-R interval RRI shortens as a function of simple math This means that the time in cardiac systole shortens and the time in cardiac diastole shortens Since cardiac diastole is when the heart fills up with blood faster HR can be associated with decreased cardiac filling times This in turn could compromise the SV However there is a paucity of data as to what happens to SV and CO at different HR Further it is possible that these effects will be different when a person is lying down supine versus when a patient is upright when stroke volume will be lower
The investigators will seek to determine the effects of different HR on both SV CO In order to safely manipulate the HR they will study patients with permanent pacemakers in whom HR manipulation can be done in a safe and non-invasive manner
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
True
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
True
Is an FDA AA801 Violation?:
None