Related Experiment Video
Updated: Jun 25, 2026
07:56
A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
Published on: February 17, 2023
Modulation of the sinus rate during ventricular fibrillation.
Stephen L Wasmund1, Rakesh K Pai, Roger A Freedman
1Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah 84112-5000, USA. wasmund@cvrti.utah.edu
Journal of Cardiovascular Electrophysiology
|February 18, 2009
Summary
This study found no link between arterial baroreflex gain and heart rate changes during ventricular fibrillation (VF) or blood pressure recovery after defibrillation. Cardiopulmonary reflexes may play a larger role in some patients during VF.
Area of Science:
- Cardiovascular physiology
- Autonomic nervous system regulation
- Electrophysiology
Background:
- The arterial baroreflex is dominant during supraventricular and ventricular tachycardia.
- The role of arterial baroreflex gain (BRG) during and after ventricular fibrillation (VF) is not well understood.
Purpose of the Study:
- To investigate the correlation between arterial BRG and sinus node cycle length (SNCL) changes during VF.
- To determine if arterial BRG predicts blood pressure (BP) recovery following defibrillation.
Main Methods:
- Arterial BRG was assessed in 18 patients undergoing defibrillator implantation.
- Sinus node cycle length (SNCL) was measured before and during VF.
- Percent SNCL change (%DeltaSNCL) and arterial BP recovery were calculated.
Main Results:
- No correlation was found between arterial BRG and %DeltaSNCL during VF.
- Arterial BRG did not correlate with BP recovery post-defibrillation.
- SNCL surprisingly lengthened in 7 out of 18 patients during VF.
Conclusions:
- Arterial BRG does not appear to correlate with %DeltaSNCL during VF or subsequent BP recovery.
- Findings suggest cardiopulmonary baroreflex may have a greater role in some patients during VF.
- Further research is needed to elucidate baroreflex contributions during VF.
More Related Videos
Related Concept Videos
01:29Disturbances in Heart Rhythm
Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
01:29Dysrhythmias III: Characteristics of Dysrhythmias
Dysrhythmias, also known as arrhythmias, are irregular heart rhythms that result from abnormal electrical activity in the heart, affecting its ability to circulate blood efficiently. Tachyarrhythmias, a subset of dysrhythmias, are characterized by abnormally fast heart rates exceeding 100 beats per minute. Here are some types of tachyarrhythmias with their distinct ECG features:Sinus Tachycardia:Sinus tachycardia presents a regular heart rhythm with an increased rate of 101-180 beats per minute.
01:18Dysrhythmias IV: Characteristics of Bradyarrhythmias
Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
01:25ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias
Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
01:25Dysrhythmias VI: Management of Dysrhythmias
Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...
01:20Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...