Role Of Tachycardia Research Articles

Normal autonomic neurophysiology of postural orthostatic tachycardia and recommended physiological assessments in postural orthostatic tachycardia syndrome.

The current surge of interest in postural orthostatic tachycardia syndrome commonly known as POTS requires good knowledge of the very complex physiology involved, but this is currently lacking. The often overlooked normal physiology of orthostasis is reviewed including the definition of normal postural orthostatic tachycardia. An illustrated functional anatomy that embeds orthostatic tachycardia within the learned and skilful motor functions in the human population is presented. The four physiological phases of orthostasis and the role of tachycardia are described in a laboratory‐controlled and progressive orthostatic stress in normal human volunteers. Standardized surrogate measures of autonomic control were used to quantify the trigger level for excessive tachycardia and the minimum autonomic control required to sustain viable arterial blood pressure during severe orthostatic stress in normal human volunteers. Tachycardia during orthostasis is part of a “democratic” contribution by four cardiovascular parameters of which the chronotropic function of the heart is just one of the parameters contributing toward cardiovascular compensation. It is adjusted during orthostasis in proportion to contributions from the other three parameters, namely inotropic function of the heart, windkessel vascular resistance and venous vascular capacitance. The physiological effects of the two stressors during orthostasis, gravity and isometric contraction of skeletal muscles are reviewed. A model of how the four cardiovascular parameters are regulated during orthostasis to achieve proportionate contributions is proposed emphasizing the necessity to quantify individual contributions from all these four parameters. Any one or more of these parameters may be compromised due to disease requiring disproportionate contribution of the prevailing magnitude of orthostatic tachycardia in an individual. It therefore requires neurophysiological assessment of the autonomic regulation of all the four cardiovascular parameters to assess the condition fully. We recommend here some current and novel neurophysiological methods that use modern medical technology to quantify laboratory standardized surrogate measures of some of these cardiovascular parameters including central parasympathetic regulation in postural orthostatic tachycardia syndrome.

Knowledge regarding assessment of sepsis among Greek nurses.

The aim of the present survey was to evaluate nurses' knowledge regarding sepsis in Greece. A total of 835 registered nurses (125 males/710 females) from tertiary hospitals in Greece were interviewed from April 2008 to December 2009. All participants completed a self-completed questionnaire about assessment of sepsis (see Figure 1). Basic demographic information was recorded. The protocol and questionnaire were approved by the Ethics Committees of participating hospitals. The majority of the participants answered correctly regarding awareness of systemic inflammation - 83.5% regarding the role of temperature in the definition of systemic inflammation; 81.3% regarding the importance of white blood cell count; and 49.9% and 46.3% regarding the role of tachycardia and tachypnoea, respectively. The same pattern was observed regarding the answers about the assessment of sepsis - 79.4% of the nurses answered correctly about the role of blood pressure; 70.9% about the role of urine volume; and 43.5% about the importance of oxygen saturation. Finally, 57.2% of the participants confirmed that in practice they followed the current guidelines for the diagnosis and treatment of patients with sepsis. The study has established baseline data with which future studies can be compared.

The electrocardiogram during sinus rhythm and tachycardia in patients with Mahaim fibers: The importance of an “rS” pattern in lead III

The purpose of the study was to identify the electrocardiographic (ECG) characteristics of the Mahaim fiber. Mahaim fibers are slowly conducting accessory pathways reaching into the right ventricle. They often play a role in tachycardias. We retrospectively analyzed 40 patients with Mahaim fibers. Five patients had associated Wolff-Parkinson-White syndrome and were excluded from the study. Two patients had a short atrioventricular decremental accessory pathway and were also excluded. The remaining 33 patients had a tachycardia with anterograde conduction over a Mahaim fiber. Twenty were female. Their mean age was 24 +/- 10 years. The most common pattern of minimal preexcitation during sinus rhythm was an rS pattern in lead III. This was found in 20 patients. There was a match between the presence of rS in lead III during sinus rhythm and left axis deviation during tachycardia with anterograde conduction over the Mahaim fiber. After ablation, a different QRS pattern emerged in lead III, indicating the absence of conduction over the Mahaim fiber. To obtain information on the prevalence of an rS pattern in lead III in age-matched controls with palpitations and without structural heart disease, the 12-lead ECG of 200 young individuals were examined. An rS pattern in lead III was found in 6%. A narrow QRS with an rS pattern in lead III during sinus rhythm in a patient with a history of palpitations should alert the physician to the possibility of a Mahaim fiber. During tachycardia, these patients typically show a left bundle branch block-like QRS complex with left axis deviation.

Role of tachycardia and V wave wall stress in the release of ANF during volume loading

Heart rate is believed to be a primary determinant of atrial natriuretic factor (ANF) release; however, we postulated that V wave wall stress is the main signal for ANF release during volume loading. Conscious dogs were volume loaded with 1,000 ml of saline while the heart rate was allowed to vary and on another day while the heart was paced at 240 beats/min. During volume loading, plasma ANF increased from 58 +/- 10 to 221 +/- 31 pg/ml (P < 0.05), and heart rate increased from 97 +/- 3 to 182 +/- 9 beats/min. During pacing, plasma ANF increased from 42 +/- 8 to 85 +/- 10 pg/ml. A wave atrial pressures were increased during pacing and were fixed due to contraction against a closed atrioventricular valve. Volume loading increased plasma ANF to 180 +/- 25 pg/ml. V wave atrial pressure increased markedly, and V wave atrial wall stress increased from 25 +/- 10 to 131 +/- 44 and from 7 +/- 4 to 116 +/- 25 g/cm2, respectively. A wave pressure and wall stress were not increased by volume loading. V wave wall stress and ANF were significantly correlated. V wave atrial wall stress accounts for the majority of change in plasma ANF (60%), while tachycardia and A wave wall stress account for a smaller fraction (40%) of change.

Direct evidence that pancuronium and gallamine enhance the release of norepinephrine from the atrial sympathetic nerve by inhibiting prejunctional muscarinic receptors

The effect of different non-depolarizing muscle relaxants (gallamine, pancuronium, vecuronium, d-tubocuranine) on [ 3H]norepinephrine release in response to electrical stimulation was studied in isolated guinea-pig atrium. High pressure liquid chromatography combined with electrochemical and radiochemical detection revealed that the released radioactivity was mainly in the form of [ 3H]norepinephrine release. Oxotremorine, a pure muscarinic agonist, reduced the release of tritium. Gallamine and pancuronium, like atropine, prevented the inhibitory effect of oxotremorine. d-Tubocurarine and vecuronium had no such effect. These findings indicate that gallamine and pancuronium exert a presynaptic antimuscarinic, atropine-like effect, by inhibiting muscarinic receptors located on the axon terminals of sympathetic neurons thereby enhancing norepinephrine release. It is suggested that this phenomenon might play some role in tachycardia observed during surgical anaesthesia when gallamine or pancuronium have been administered.

Role of Tachycardia as an Inotropic Stimulus in Man

We examined the inotropic effect of tachycardia in nine postsurgical aortocoronary bypass graft patients (with intact cardiac innervation) and nine cardiac allograft recipients (with denervated hearts). The changes in stroke volume (SV) and velocity of circumferential fiber shortening (VCF) which accompany sudden increases and decreases in atrial pacing frequency were determined by computer-aided fluoroscopic analysis of the motion of surgically implanted midwall myocardial markers. Because the first beat after a change in rate retains the frequency characteristics of the preceding rate, we compared the first posttachycardia beat with control beats and late tachycardia beats with the first tachycardia beat; afterload and preload for each pair of beats were similar. For an increase in heart rate of 50 beats/min, SV and VCF rose 79 and 64% from the first tachycardia beat to late tachycardia beats, and SV and VCF rose 8 and 35% from control beats to the first posttachycardia beat in the innervated group. Responses in the denervated group were not significantly different from those in the innervated group. The degree of the inotropic response was positively correlated with the magnitude of the increase in heart rate (r = 0.91). The decay in augmented contractility after decreasing the rate back to control levels fits an exponential relationship with a mean t((1/2)) of 1.7 s. Thus, in conscious man, increases in heart rate represent a positive inotropic stimulus, independent of other factors influencing ventricular performance and unaffected by neural innervation, and should be considered when changes in cardiac function are interpreted during serial studies or after drug administration.

Role of tachycardia in mediating the coronary hemodynamic response to severe exercise

Role of tachycardia in mediating the coronary hemodynamic response to severe exercise

Factors regulating pulmonary “capillary” pressure in mitral stenosis. IV

1. 1. Pulmonary edema occurred at rest in six patients and during exercise in three other patients with severe mitral stenosis during cardiac catheterization. 2. 2. Pulmonary “capillary” pressure was 32 mm. Hg or higher in all nine patients. 3. 3. Pulmonary “capillary” pressure, actually an index of left atrial pressure, was elevated to such high levels in order to maintain blood flow through the mitral valve. 4. 4. Factors which resulted in an increased mitral valve flow rate, thus requiring an elevation in pulmonary “capillary” pressure, were (a) increased cardiac output and (b) decreased diastolic filling period. The latter was decreased by increases in (1) heart rate and (2) duration of ventricular systole. 5. 5. The degree of anatomic mitral stenosis affected the degree of pulmonary “capillary” pressure rise in exponential fashion. 6. 6. The mechanism of elevation of pulmonary “capillary” pressure was believed to be a momentary imbalance in ventricular outputs such that pulmonary blood volume and pressure were increased. 7. 7. It has been demonstrated that in patients with mitral stenosis, a normal cardiac output can be delivered only at the expense of high pulmonary “capillary” pressure. 8. 8. The role of tachycardia, even of a mild degree, in producing or aggravating symptoms of pulmonary edema is emphasized.