Vasovagal syncope after infusion of a vasodilator in a heart-transplant recipient

Article Abstract:

Hypotension, or low blood pressure, is associated with increased nervous system activation and increased heart rate, but one type, hypovolemic hypotension, occurring after hemorrhage or certain drugs, induces a decrease in heart rate. Both effects result from abnormal excitation of the vagus nerve, and hence, the term used to describe the loss of consciousness that may result is vasovagal syncope, or fainting. One theory about the cause of heart rate depression after hemorrhage is that a reflex within the heart itself is activated by nerve endings in the left ventricle, the chamber that pumps blood to the body, signalling that the chamber is full and the heart rate should slow down. This incorrect message results from mechanical pressure put on the nerve endings by an empty ventricle when it is stimulated to contract by another component of the nervous system, the sympathetic system. People who have received heart transplants are ideal for testing this idea since they do not have intact nerve fibers to the ventricles and it is possible to observe local effects within the organ after stimulation by drugs that mimic the sympathetic system's effects. The occurrence of vasovagal syncope in a heart transplant patient who was given a drug that induced hypotension (a vasodilator) is discussed. The patient's atrium, the upper chamber of the heart which still had its nerves intact, began to beat faster, while the ventricle's rate did not change. After about one minute, the patient began to show signs of fainting, while the atrium sped up and the ventricle beat even slower. Intravenous infusion of medication stopped the episode. Evidence from this report shows the induction of vasovagal syncope by hypotension in a person whose heart lacks nerves to the ventricles shows that the reflex can be activated locally by mechanisms as yet unknown. This may explain why an abnormally slow heart rate cannot always be corrected by giving a drug that stimulates the nervous system. (Consumer Summary produced by Reliance Medical Information, Inc.)

Vasodilators, Vasodilator agents

---

The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia

Article Abstract:

Syncope is a brief loss of consciousness due to temporary lack of oxygen to the brain. It may be caused by atrioventricular block, when the pumping of the heart slows, becomes irregular or stops altogether. Syncope may also occur when the sinus node, which controls the pumping of the heart, does not function properly. Pacemakers are usually implanted in individuals with atrioventricular block or dysfunction of the sinus node. When syncope occurs regularly, electrocardiography, a technique that records the electrical activity of the heart, can reveal the origin of the defects in the transmission of the cardiac impulses. However, when syncope is infrequent and the electrocardiogram is normal, the cause of the defect in the heart may be difficult to identify. The sensitivity of intracardiac electrophysiological testing was examined in 21 patients with a slowed heartbeat, a condition known as bradycardia. In 13 of the patients, the irregularity was due to atrioventricular block, while in eight it was due to sinus node dysfunction, as shown by electrocardiogram. Irregular patterns in the electrophysiological testing were seen in only three out of eight (37.5 percent) of the patients with sinus node dysfunction and in two out of the 13 (15.4 percent) patients with atrioventricular block. Thus electrophysiologic testing may fail to identify patients with bradycardia. Other abnormalities were diagnosed with the electrophysiologic testing that may have been mistaken for the cause of the irregular heartbeat. Electrophysiological testing was not an accurate test in the diagnosis of transient bradycardia.

Diagnosis, Testing, Coronary heart disease, Electrocardiography, Bradycardia, Electrophysiology

---

Ventricular syncope: is the heart a sensory organ?

Article Abstract:

Syncope, a loss of consciousness brought on by lack of blood supply to the brain, may have a number of causes. Some research indicates that the condition may, on occasion, be triggered by the excessive activation of sensory nerve endings in the ventricles (the pumping chambers) of the heart. The function of these nerve endings, cardiac mechanoreceptors, seems to be to mediate heart output and arterial pressure in response to changes in pressure inside the ventricles. This cardiac mechanoreflex, similar to the activation of arterial baroreceptors in the carotid sinus, may play a role in a number of clinical conditions, such as the syncope of aortic stenosis (constriction of the aorta, the main arterial trunk of the body), myocardial infarction (heart attack), hypotension (low blood pressure) during exercise and bradycardia (slow heart beat) after using nitroglycerin. If bradycardia and hypotension precede episodes of recurrent syncope in patients who have normal cardiac electrophysiology tests, and especially if tachycardia (heart rate greater than one hundred beats per minutes) occurs before those signs and symptoms, a diagnosis of ventricular syncope may be made and may be attributed to the activation of cardiac mechanoreceptors. Based upon the results of such studies a question arises which demands more research, namely, what is the mechanism of this event?

Heart, Mechanoreceptors, Cardiac nerves, editorial

Similar abstracts:

• Abstracts: Transmission of rabies virus from an organ donor to four transplant recipients. Human infection due to recombinant vaccinia-rabies glycoprotein virus
• Abstracts: Prevalence, detection, and treatment of alcoholism in hospitalized patients. Knowledge, attitudes, and reported practices of medical students and house staff regarding the diagnosis and treatment of alcoholism
• Abstracts: Effect of HLA compatibility on engraftment of bone marrow transplants in patients with leukemia or lymphoma. Transplantation of bone marrow as compared with peripheral-blood cells from HLA-identical relatives in patients with hematologic cancers
• Abstracts: The regulation of investigational drugs. The regulation of discovery and drug development. The federal regulation of food labeling: promoting foods to prevent disease
• Abstracts: Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.