One study on endotracheal tube intracuff pressure in 114 patients during helicopter transport showed that with a mean increase in altitude of 2 purchase clomid 100 mg amex breast cancer giveaways,260 ft best clomid 50 mg breast cancer x ray, 72% of patients had an intracuff pressure >50 cm H20 and 20% were >80 cm H2O. This effect can be overcome by carefully monitoring intracuff pres- sures, especially during the ascent/descent phases of a fight . Transport ventilators have different design characteristics resulting in some older or less sophisticated models altering their performance at altitude. For example, the Drager Oxylog 1000 has pneumatic logic controls which require a change in gas pressure to trigger a cycle from inspiration to expiration. As altitude increases a larger volume of gas is required to trigger this switch resulting in the delivery of a larger tidal volume than has been set. More sophisticated ventilators can have a range of pressure sensors and elec- tronic controls to allow for full compensation of any barometric induced change. This is not usually a signifcant issue in most fxed-wing aircraft as there is varying capacity to control the cabin temperature. The greatest fexibility in this regard is when working in a dedicated air ambulance. When transporting a patient on a commercial fight, remember that they have to cater to a wide variety of passengers, with cabin temperature usually set at ~22 +/−2 °C. Most modern commercial aircraft can, however, adjust the temperature across multiple zones allowing for the option to liaise with the crew to try and better optimise the ambient temperature to a patient’s needs. The A380, for example, can set cabin tem- perature between 18 and 30 °C across 15 different temperature control zones . Ramin Temperature control can be harder to achieve in rotary-wing airframes and the capacity to do so is very much dependent on the specifc platform utilised and the environment in which it is operating. Rotary-wing aircraft can expose both patients and crew to signifcant variations in temperature. In cold weather, this can lead to heat loss, especially in children or the critically ill patient. Conversely, in hot cli- mates, rotary-wing aircraft can behave like a greenhouse, increasing cabin tempera- ture signifcantly even at altitude. Whilst it is important to maintain the thermal integrity of patients during aero- medical transportation, it is important to note that thermal stress can also adversely impact the transport team. Excess heat stress, both hot and cold, can lead to fatigue, decreased attention span, impaired judgement, impaired calculation and poor deci- sion-making, all of which in turn can adversely affect patient care . It is unlikely that many aeromedical services are able to maintain their medications at the correct temperature at all times. Whether the typical fuctuations in temperature that might be encountered in the aviation environment alter medication potency is generally not known. However, it is important to consider the thermal environment in which these operations will occur and to develop storage solutions to maintain as optimal thermal integrity of medications as possible. Relative humidity is predominantly a function of temperature and it decreases as the temperature falls. With increasing altitude, there is a progressive fall in temperature and so the relative humidity will also fall. This, however, cannot be maintained in aircraft as it would lead to condensation and corrosion and so relative humidity is typically kept in the range of 10–20%. Generally, the longer the fight time, the lower the average relative humidity will be during that fight. Prolonged exposure over 3 h or more to this level of relative humidity can lead to drying of the skin and mucosal membranes, which can lead to complications such as sore eyes, sore throat, a dry cough, and epistaxis . However, there is no defnitive evidence that this level of humidity results in any signifcant adverse health outcomes in the average passenger. It has also been suggested that breathing dry cabin air leads to an increased number of respiratory tract infections but there is no objective evidence to support this assertion. Despite this, it is appropriate to monitor a patient’s hydration status, humidify supplemental oxygen where possible, and protect the corneas from drying out in the patient with altered consciousness. Gravity is an accelerative force acting on objects to change their velocity over unit time. A negative vertical G force would act in the opposite direction of gravity [3, 4]. Furthermore, Newton’s third law of motion states that for every action, there is an equal and opposite reaction. When an object accelerates or decelerates in one direction, there will therefore be an equal force applied in the opposite direction, referred to as an inertial force. In relation to G forces and Newton’s third law, the most signifcant impact of fight is on the circulatory system. Consider a patient lying on a stretcher with their head to the front of a fxed-wing aircraft. As the air- craft accelerates for take-off, the patient will be exposed to positive G forces. This will result in the inertial force acting in the opposite direction, increasing blood fow away from the brain and towards the feet. The physiological response to these forces will depend on their direction, duration, and intensity. Positive G forces, which increase blood fow away from the brain, are bet- ter tolerated than negative G forces, which increase blood fow into the brain . Healthy individuals can compensate for short-term changes in blood fow, but there may be potentially adverse consequences in the critically ill patient with haemody- namic and/or neurological compromise. For example, venous pooling in the legs may exacerbate hypotension in the haemodynamically-compromised patient with conditions such as sepsis or blood loss, and lead to a decrease in cerebral perfusion. Conversely, increased blood fow to the brain may lead to an increase in intracranial pressure, which may be clinically signifcant in neurologically compromised patients, such as those with head injury. Humans can potentially tolerate very-short-term exposure to positive G forces of up to ~9G, although most will lose consciousness with sustained exposure of ~4G. Light-sensitive retinal cells are very sensitive to decreased perfusion and so greying of vision followed by complete loss of vision will often precede loss of consciousness. However, tolerance to negative G forces is much more limited to ~2–3G before losing consciousness as a result of marked intracranial pooling of blood. The forces patients are usually exposed to in aeromedical operations are small and generally within the range of 1G +/−0. There is no good evidence to substantiate the direct clinical impact of these changes in the real-world retrieval environment, but it is prudent to always consider the potential impact of G forces on critically ill patients and take those into account when considering the optimum positioning of the patient in the selected transport platform. Apart from the potential for hearing loss, human performance appears to be adversely infuenced by exposure to both sustained and intermittent noise. This can lead to fatigue, irrita- bility, impaired cognition, and compromised ability to perform tasks. The main impact appears to be with complex tasks where prolonged concentration is required, such as the clinical management of a patient in fight. It should be noted that there is a great degree of inter-individual variation in the tolerance to noise, which is infuenced by an individual’s state of arousal, personality, motivation, and prior experience. It has also been noted that the performance of simple repetitive tasks may in fact be enhanced by noise.
Measurement of sinoatrial conduction time by premature atrial stimulation in the rabbit buy clomid australia menopause 54. Sinus node response to premature atrial stimulation in the rabbit studied with multiple microelectrode impalements safe clomid 100mg womens health 8 week challenge. Effect of an early atrial premature beat on activity of the sinoatrial node and atrial rhythm in the rabbit. The relationship between sinoatrial conduction time and sinus cycle length during spontaneous sinus arrhythmia in adults. The sinus node electrogram in patients with and without sick sinus syndrome: techniques and correlation between directly measured and indirectly estimated sinoatrial conduction time. The estimation of sinoatrial conduction time in rabbit heart by the constant atrial pacing technique. Comparative study of two methods of estimating sinoatrial conduction time in patients with abnormal sinus node function. Premature atrial stimulation during regular atrial pacing: a new approach to the study of the sinus node. Reproducibility of electrophysiological parameters of sinus node following autonomic blockade. Indirectly estimated sinoatrial conduction time by the atrial premature stimulus technique: patterns of error and the degree of associated inaccuracy as assessed by direct sinus node electrography. Characteristics of extracellular potentials recorded from the sinoatrial pacemaker of the rabbit. Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects. The human sinus node electrogram: a transvenous catheter technique and a comparison of directly measured and indirectly estimated sinoatrial conduction time in adults. Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node. Persistent sinus nodal electrograms during abnormally prolonged postpacing atrial pauses in sick sinus syndrome in humans: sinoatrial block vs overdrive suppression. Clinical comparison of indirectly and directly determined sinoatrial conduction time. Indirect measurement of sinoatrial conduction time in patients with sinoatrial disease and in controls. Influence of drugs on the relationship between sinus node recovery time and calculated sinoatrial conduction time in man. Action of driving stimuli from intrinsic and extrinsic sources on in situ cardiac pacemaker tissues. Effects of rapid stimulation on the transmembrane action potentials of rabbit sinus node pacemaker cells. Hemodynamic influences on sinus node recovery time: effects of autonomic blockade. Sinus node recovery times following the spontaneous termination of supraventricular tachycardia and following atrial overdrive pacing: a comparison. Ability of Holter electrocardiographic recording and atrial stimulation to detect sinus nodal dysfunction in symptomatic and asymptomatic patients with sinus bradycardia. Electrophysiologic effects of lidocaine on sinus node and atrium in patients with and without sinoatrial dysfunction. Comparison with simultaneous estimation of sinoatrial conduction using premature atrial stimulation. Sinus nodal function in the intact dog heart evaluated by premature atrial stimulation and atrial pacing. The effects of digitalis on sinoatrial automaticity and atrioventricular conduction. Effects of digoxin on sinus nodal function before and after vagal blockade in patients with sinus nodal dysfunction: a clue to the mechanisms of the action of digitalis on the sinus node. Effects of digitalis on sinus nodal function in patients with sick sinus syndrome. Effects of digitalis on the human sick sinus node after pharmacologic autonomic blockade. Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction. Intracardiac electrophysiologic study of intravenous diltiazem and combined diltiazem-digoxin in patients. Comparative effects of three calcium antagonists, diltiazem, verapamil and nifedipine, on the sinoatrial and atrioventricular nodes. Electrophysiologic effects of procainamide on sinus function in patients with and without sinus node disease. Assessment of oral quinidine effects on sinus node function in sick sinus syndrome patients. Incidence of malignant vasovagal syndrome in 332 syncope patients: results of cardiac pacing. The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. Vagal depressor reflexes elicited by left ventricular C-fibers during myocardial ischemia in cats. Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons. Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope. Prevention of neurally-mediated syncope by selective beta-1 adrenoreceptor blockade. Disopyramide reversal of induced hypotension-bradycardia in neurally-mediated syncope. Electrophysiological studies in screening of the “mixed type” of carotid sinus syncope. Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome. Relevance of diagnostic atrial stimulation for pacemaker treatment in sinoatrial disease. Electrophysiologic testing in patients with sinus pauses and/or sinoatrial exit block. The human sinus nodal electrogram: techniques and clinical results of intra-atrial recordings in patients with and without sick sinus syndrome. Significance of pacemaker recovery time after the Mustard operation for transposition of the great arteries. Chapter 4 Atrioventricular Conduction The usefulness of intracardiac recording and stimulation techniques in humans was first realized during its application to patients with disorders of atrioventricular (A-V) conduction. The A-V block has been traditionally classified by criteria combining implications about anatomic site, mechanism, and prognosis.
Simultaneous pacing captures the local atrial electrogram; its absence helps to determine the onset of the atrial activation during ventricular pacing (arrows) order clomid 50mg without a prescription menstrual extraction abortion. The effect of a paced wavefront from right to left (A) and left to right (B) on local V-A times is shown discount clomid 50mg visa menopause 3 months no period. The ventricular site of insertion should have a constant (V-A) interval regardless of the direction of activation. Using the ventricular approach the catheter is positioned just underneath the mitral annulus as depicted in Figures 13-18 and 13-19, to record a ventricular electrogram and an atrial electrogram. At the appropriate position (near the ventricular insertion site) the atrial deflection is usually one-fourth the size of the ventricular deflection and during ventricular pacing the atrial deflection gets even smaller and sometimes becomes lost in the ventricular electrogram. The maneuvers discussed above can help define the onset of atrial activation during conduction over the bypass tract. During ventricular pacing, retrograde atrial activation is usually earlier than that recorded in the coronary sinus. In rare cases, a left lateral bypass tract with a long A-V conduction time (which may or may not be decremental) is present. In such cases, no overt pre-excitation is obvious in sinus rhythm, but may only be manifest by pacing at the left atrium or via the coronary sinus. When using the ventricular approach, because the contact is usually good, we aim for a temperature of 55° to 65°C with temperature control catheters, or the lowest power, which results in a 10-Ω drop in lead impedance. If one is at the appropriate site, loss of conduction over the bypass tract is accomplished in less than 10 seconds (Figs. If the transseptal approach is used, catheter stability is not as reliable, and a sheath is invariably required to maintain stable contact. The sheath is usually positioned in the lateral left atrium through which the catheter is passed toward the medial aspect of the mitral annulus. The catheter can then be withdrawn slowly to map the mitral annulus until the earliest retrograde atrial activation is recorded during the tachycardia or ventricular pacing. Achievement of appropriate temperatures, or, more importantly, drops in impedance are more difficult from the transseptal approach due to the loss of temperature via convective cooling of the blood. Finally, if the ablation is carried out within the coronary sinus, and a standard 4- to 5-mm tip catheter is used, I recommend keeping temperatures ≤55°C, and use impedance drops to determine how much energy is delivered. I generally use the lowest energy, which results in a 10-Ω drop in impedance, regardless of the temperature. Use of a cool-tip catheter decreases the risk of char and, as stated above, temperature cannot be used and a decrease in impedance demonstrates effective energy delivery. Usually, epicardial pathways are eliminated quickly, but I try to maintain delivery of energy for a minute since I believe many of these bypass tracts insert as multiple twigs or broad bands in the muscular sheath of the coronary vein. The vast majority of bypass tracts around the tricuspid valve can be reached through catheters introduced via the inferior vena cava, although occasionally the catheter must be placed via the superior vena cava when the bypass tract is located inferolaterally (i. As stated earlier in the chapter, although some investigators have suggested using a small catheter placed in the right coronary artery to guide mapping of right-sided bypass tracts, we believe this should not be done routinely and that regionalization of the bypass tract can be readily accomplished using a Halo catheter or a multipolar catheter positioned around the tricuspid annulus. When pre-excitation is present, the earliest onset of ventricular activation recorded on the ablation catheter should precede the delta wave by at least 25 msec using either unipolar or bipolar electrograms. Examples of mapping and ablation of a right anterior manifest, anterogradely conducting and a concealed right lateral bypass tract P. Sheaths are available and helpful for the stabilization of catheters positioned inferolaterally along the tricuspid annulus. Folding over of the atrial myocardium around the annulus is associated with bypass tracts that may insert into the atrium 1 cm from the annulus. Posteroseptal bypass tracts, which are actually the second most common, usually can be readily approached in the inferior septal regions of the tricuspid annulus. This name is actually a misnomer, since they are not truly “septal,” but inferoposterior to the true atrial septum, which ends in the His–A-V node area, at the central fibrous trigone. These are truly septal and may be approached from either the right side or on rare occasions from the left side and are associated with a 5% incidence of heart block if the catheter is positioned in the triangle of Koch. Such bypass tracts should be ablated with the catheter on the tricuspid annulus or on the ventricular side of the tricuspid annulus to decrease the incidence of A-V block. Safety will further be enhanced by using the lowest power required to get an impedance drop of 10 Ω. They often exhibit a bypass tract potential and/or early activation at a site without a His bundle deflection (Fig. The para-Hisian pathways, by definition, are recorded with simultaneous His bundle activity from which it needs to be distinguished. In this particular instance the ablation catheter was positioned so that the tip produced pressure perpendicularly to the His bundle region. This led to a rather slowly inscribed ventricular depolarization consistent with the onset of ventricular activity as well as a slowly inscribed “inferior” His bundle deflection, which times identically with the discrete bipolar deflection on the His bundle catheter. With the loss of pre-excitation there is loss of the negative deflection between the A and the broad H and disappearance of the delta wave. These fibers are very superficial and protected by a fibrous sheath, so with use of low power and temperatures not exceeding 52°C the risk of permanent heart block is less than 1%. Rapid ventricular pacing is often necessary to discern the onset of atrial activity (Fig. A left lateral bypass tract is present with a long conduction time, which was associated with a local A-V interval of 90 msec. No overt pre-excitation is present because the area of the ventricle that is “pre-excited” occurs after the onset of normal activation. A and B: Ventricular pre-excitation is recorded from a unipolar rove electrode as an intrinsicoid deflection 25 msec before the delta wave during sinus rhythm. Anteroseptal bypass tracts are characterized by the presence of a bypass tract potential and the absence of a His bundle potential in the apex of the triangle of Koch. The most difficult for me have been the right free wall pathways, particularly if approached from the inferior vena cava. This is due to both poor contact and the fact that these bypass tracts are often off the annulus, crossing through a “folded” right atrium over the ventricle. Initial attempts at ablation from the right side produced transient success but the arrhythmia recurred 6 hours later. On the following day a second ablation was successful using the retrograde aortic approach. The third was right free wall pathway that disappeared in 10 seconds after the onset of ablation, only to recover 2 weeks later; repeat ablation resulted in subsequent durable success. The fourth was in right-sided accessory pathway in a patient with Ebstein anomaly. Bypass tract conduction blocked in less than 10 seconds with ablation, but recurred within 2 weeks; a recurrent ablation attempt resulted in the same sequence of events. This tracing compares the electrograms recorded in the His bundle recording and the ablation catheter before (left) and after (right) catheter pressure caused temporary bypass tract block. This is validated with loss of pre-excitation demonstrating consistent positioning of the His bundle potential associated with the slowly inscribed second potential in the first complex and loss of the pre-excitation in the first negative potential in the first complex. Right bundle branch block is present, which facilitates the observation of a broad slowly inscribed His deflection from the ventricular myocardium.
The investigator can pace at shorter cycle lengths in order to produce A-V nodal conduction delay or block in order to promote conduction over the bypass tract (Fig buy clomid 50 mg with mastercard menstrual ovulation. Therefore clomid 50 mg online menstruation low blood sugar, when using the atrial activation sequence during ventricular pacing to localize the bypass tract, it is necessary to demonstrate that retrograde conduction proceeds solely over the bypass tract during ventricular pacing. When the paced cycle length is reduced to 500 msec (right panel) A-V nodal block is produced allowing manifest retrograde conduction over a left lateral bypass tract. Changes in atrial activation, either spontaneously or in response to ventricular stimulation, can demonstrate the presence of multiple bypass tracts (Fig. If the bypass tract is opposite the site of ventricular stimulation, the V-A interval prolongs during pacing. This can be readily accomplished by observing the response to ventricular pacing during the tachycardia. One must be careful to exclude a “pseudo–V-A-A-V response” produced by a very long V-A, which exceeds the paced cycle P. This can be recognized because the first “A” of the “pseudo”–V- A-A-V response occurs at the paced cycle length. Another reason for a pseudo–V-A-A-V response is A-V nodal tachycardia with a long H-V such that the A occurs before the V (Fig. These responses require intact V-A conduction which is present in perhaps 80% of patients in the absence of bypass tracts. The only difference is the lengthening of V-A intervals, which is characteristic of left-sided bypass tracts during right ventricular pacing. In each panel ventricular overdrive pacing demonstrating retrograde conduction is shown in blue. Recordings should be made using a multipolar catheter and, if possible, one should try to bracket the earliest; that is, demonstrate later activation on either side of the earliest site. In such cases more distal left atrial sites must be mapped through a patent foramen ovale or via a transseptal approach (Fig. Thus, careful mapping of multiple sites around the tricuspid and mitral valves is required for proper diagnosis. This may require a superior vena cava approach and/or the use of catheters with deflectable tips. Specially designed multipolar catheters that can record around the tricuspid ring can be especially useful. This could be a specially designed “halo” catheter or a deflectable 10–20-pole catheter which can be positioned around the tricuspid annulus. While some investigators have employed a fine catheter in the right coronary artery, the potential for endocardial damage and subsequent long-term development of coronary atherosclerosis exists; therefore, I believe this technique should be avoided. As expected, the V-A intervals measured from intracardiac electrograms are more accurate than R-P intervals. The shortest V-A interval we have observed in a septal bypass tract in an adult patient is 70 msec. This is nearly identical to the data of Ross and Uther,124 who found that a V-A interval of 60 msec was the best value to discriminate between the two. Upon cessation of pacing there is a V-A-A- V response prior to resumption of the tachycardia. B: Ventricular pacing is associated with retrograde conduction, but upon cessation of pacing the tachycardia resumes following a V-A-V response. The former response is diagnostic of atrial tachycardia, and the latter excludes it. An easy way to do this is to note the response to ventricular stimulation during the tachycardia. An exception to this can occur if there are dual A-V nodal pathways and ventricular pacing shifts antegrade conduction to the slow pathway, yielding a long postpacing cycle. This can be sorted out by comparing the V-A interval during pacing to that during the tachycardia. Finally, para-Hisian pacing can be used to document the presence of an accessory pathway; when a septal pathway is present the St-A will be the same with His capture and pure ventricular capture; while if an accessory pathway is absent, a marked difference between stimulus to A when His capture is lost and pure ventricular pacing ensues. All of the maneuvers discussed above are not useful in the presence of very decremental pathways or left free-wall pathways. In the presence of a septal accessory pathway the difference always is more positive than 30 msec. A limitation of this method is that the H-A interval cannot be measured during ventricular pacing in approximately 15% of cases. Because retrograde activation of the His and the atrium occur in parallel during ventricular pacing, the H-A interval is shorter than that during the tachycardia. Note earliest activation is in the lateral left atrium with spread to the superior and inferior left atrium thereafter. Note the extremely short V-A interval of 70 msec despite the lateral location of the bypass tract. The V-A interval is 60 msec, showing within a range of 5% of patients with A-V nodal reentry. Moreover it is not useful in the presence of decremental pathways and should not be used if a decremental bypass tract is a possibility. This is because retrograde conduction up the normal conducting system is faster than over the decremental bypass tract (Fig. In the presence of a left-sided pathway, it is unnecessary and can be very misleading. A delta H-A interval of +10 msec would accurately identify all patients with A-V nodal reentry and those with septal bypass tracts with no false-positives. When a retrograde His deflection cannot be seen during ventricular pacing, one can use the H-A interval minus V-A interval during ventricular pacing to distinguish A-V nodal reentry from septal bypass tracts. Of note, we have almost as many left free wall slowly conducting bypass tracts as septal. Although the distribution of bypass tracts in patients with and without pre-excitation is similar, we have a much higher incidence of multiple bypass tracts in patients with overt pre- excitation (25% vs. These findings are consistent with data from other investigators15,16,123,124,144 and are particularly true with left bundle branch block aberration. In Figure 8-113, both left and right bundle branch block are induced in the same patient. In both instances, aberration rapidly diminishes, suggesting a normal response of His–Purkinje system refractoriness to shortened cycle length. The ability to achieve short H1-H2 intervals due to enhanced A-V nodal conduction may be responsible for the development of aberration when His–Purkinje refractoriness is normal. Another possible explanation, particularly in the case of left bundle branch block, is that the patient population is selected. The V-A interval is longer during apical pacing than basal pacing because of proximity of the ventricular insertion of the bypass tract to the tricuspid annulus. Aberration is more likely when stimulation is performed during sinus rhythm or during long drive cycle lengths during which His– Purkinje refractoriness is longest and A-V nodal conduction and refractoriness are shortest. In addition, during atrial stimulation, right bundle branch block is twice as common as left bundle branch block, while during right ventricular stimulation, the type of aberration is almost always left bundle branch block. The response to atrial stimulation merely reflects the normal differences of refractoriness of the right and left bundle branch.
Use of procainamide in patients with the Wolff-Parkinson-White syndrome to disclose a short refractory period of the accessory pathway discount clomid american express menstruation quizlet. Value of noninvasive techniques in the Wolff-Parkinson-White syndrome with particular reference to exercise testing buy clomid with mastercard women's health center danvers ma. Evaluation of noninvasive tests for identifying patients with preexcitation syndrome at risk of rapid ventricular response. Importance of initial length of effective refractory period of the accessory pathway. Procainamide infusion test: inability to identify patients with Wolff-Parkinson-White syndrome who are potentially at risk of sudden death. Effect of isoproterenol on the anterograde refractory period of the accessory pathway in patients with the Wolff-Parkinson-White syndrome. Refractory periods of the accessory pathway in the Wolff- Parkinson-White syndrome. Syncope in the Wolff-Parkinson-White syndrome: incidence and electrophysiologic correlates. Transient entrainment and interruption of the atrioventricular bypass pathway type of paroxysmal atrial tachycardia. Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation). Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganong-Levine syndrome. One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of Wolff-Parkinson-White Syndrome. Analysis of anterograde and retrograde fast pathway properties in patients with dual atrioventricular nodal pathways: observations regarding the pathophysiology of the Lown-Ganong-Levine syndrome. Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade. Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the Lown-Ganong-Levine syndrome. Comparison of the ventricular response during atrial fibrillation in patients with enhanced atrioventricular node conduction and Wolff-Parkinson-White syndrome. Nouvelles recherches sur les connections supericures de la branche du faisceau de His-Tawara avec cloison interventriculaire. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Supraventricular tachycardia associated with nodoventricular and concealed atrioventricular bypass tracts. Catheter ablation of Mahaim fibers with preservation of atrioventricular nodal conduction. Electrocardiogram in patients with fasciculoventricular pathways: a comparative study with anteroseptal and midseptal accessory pathways. Radiofrequency catheter ablation of atriofascicular and nodoventricular Mahaim tracts. Paroxysmal tachycardia with atrioventricular dissociation in a patient with a variant of pre-excitation syndrome. His-ventricular dissociation in a patient with reciprocating tachycardia and a nodoventricular bypass tract. These and other observations concerning mechanism are discussed in detail later in this chapter. Over the past four decades, electrophysiologic studies have been responsible for a greater understanding of ventricular arrhythmias. This has led to major advances in their pharmacologic and nonpharmacologic therapy. It is imperative that clinicians and clinical investigators recognize that the study of ventricular arrhythmias is still evolving. The role of electrophysiologic studies in evaluating nonsustained and/or polymorphic arrhythmias associated with metabolic disorders, drug toxicity, cardiomyopathy, and so on is not yet established. A discussion of our current level of understanding of this issue is included and detailed later. Definitions of Ventricular Tachycardias The definitions employed by electrophysiology laboratories are arbitrary but provide a useful framework for both the clinician and the electrophysiologist to distinguish “pathologic” responses from “normal” expected 1 2 3 responses. This is a fairly common mechanism of sudden cardiac 6 7 8 death recorded by Holter monitor. Duration Most laboratories consider a tachycardia sustained if it lasts ≥30 seconds. Repetitive polymorphic responses are also very common (up to 50%), particularly when multiple (≥3) extrastimuli are used with extremely short coupling intervals (<180 msec). The clinical significance of induced nonsustained polymorphic tachycardia is questionable and requires further evaluation to determine its relevance (to be discussed in subsequent paragraphs). They reported good sensitivity and specificity, but I have not found it significantly better than V1–2 criteria. Furthermore, A-V dissociation can be seen with supraventricular rhythms, fusion complexes can result from two ventricular ectopic foci, and morphologic and/or axis characteristics established for patients with normal P. In the absence of pre-excitation a supraventricular impulse must pass through the His bundle and the specialized ventricular conducting system before initiating depolarization of the ventricles. This may result because no engagement of the His–Purkinje system by the ventricular impulse occurs (probably uncommon), or because retrograde His bundle activation occurs during ventricular activation and is obscured by the large ventricular deflection in the His bundle recording. His deflections can usually be observed if attention is given to catheter position. One may identify His bundle activity before ventricular activation (in this instance, the H-V interval is shorter than normal; e. If His bundle deflections are not seen, one must differentiate the absence of retrograde activation of the His– Purkinje P. This can be fortuitously observed if a sinus impulse conducts antegradely to the His bundle producing a clear His deflection. In these instances, linking of the His bundle potential to atrial activation proves that they are due to antegrade depolarization and are unrelated to the tachycardia. Retrograde block in the A-V node is present because atrial activation is dissociated from the tachycardia. It is often difficult to determine whether the recorded His deflection is antegrade or retrograde—or for that matter whether an apparent His bundle deflection is really a right bundle branch potential. Two techniques that may be used to clarify the situation are (a) recording right and left bundle branch potentials to demonstrate that their activation begins before His bundle activation and (b) His bundle pacing producing a longer H-V interval than the one noted during the tachycardia.
One other option is to list “therapeu- jurisdictions—Cuyahoga County generic clomid 50 mg fast delivery pregnancy 1st trimester, Ohio cheap clomid 100 mg line women's health issues canada, and New York tic complication” in parentheses afer “natural,” but this City—include “therapeutic complication” as a choice in probably is not common practice. Terefore, nite future, forensic pathologists will be resigned to use when a death fts the criteria for therapeutic complica- the term as a conceptual tool in the evaluation of these tion as the manner, but the particular jurisdiction does most challenging deaths. Note the hemorrhagic discoloration around each eye (periorbital) and the plastic insert in the opened eye fol- lowing tissue removal. Medical record review and clinician interview revealed that these periorbital hemorrhages were not present at the time of admission. These are artifacts of transport, caused by a strap to secure the child’s head, as they were fown by helicopter from an outside hos- pital to a tertiary pediatric center. He was taken to the hospital in an uncon- scious state and remained so until his death. There was initial speculation that he was struck by another motor vehicle due to the “tire-like” patterns on his legs. Further investigation revealed these injuries were not present at the time of arrival to the Emergency Department. There was a pelvic fracture with blood seeping into the legs, extensive generalized edema, and disseminated intravascular coagulation. This pattern of ecchymosis was caused by the pressure boots in conjunction with the complications of the injuries. It is important for therapy to be left on the body and examined by the pathologist before removal. Also note the early putrefactive change consisting of green coloration of the lower abdomen. It is absolutely essential for the pathologist to examine the eyes before vitreous fuid is obtained. There was no trauma to his trunk except for the attempted resuscitation efforts by family and later by hospital personnel. He had hepatic parenchyma with lacerations and intact capsule and minimal sub Glisson’s capsular hemorrhages. The two lower images show a similar case of hepatic injury due to improperly placed hands while performing chest compres- sions. This is an artifact encountered frequently during resuscitative measures, often referred to in forensic text- books as the “Prinsloo and Gordon” artifact. Because of the rich esophageal venous plexus, this tends to be a very hemor- rhagic area following intubation and therefore may be confused with stigmata of manual strangulation. The epiglottis can be seen slightly behind the endotracheal tube, confrming an esophageal intubation. The close-up of this autopsy photograph depicts an esophageal intubation, with the endotracheal tube clearly within the esophageal lumen and the concentric tracheal rings visible slightly anterior to and (anatomically) to the right of the tube. Esophageal intubations during an elective procedure, on the other hand, would be very important and potentially causal or contributory to the death. Note the mis- placed endotracheal tube that crossed from the right side of her mouth to the left pharyngeal region where it perforated and penetrated the soft tissues of the neck, completely missing the airway. Note the perforations on the posterior surface of the trachea and the anterior aspect of the esophagus. During a bout of crying, the tracheostomy tube became dislodged, and after nurses attempted to reposition it, she rapidly developed subcutaneous emphysema, followed by bilateral tension pneumothoraces. Autopsy demonstrated marked subcutaneous emphysema, including periorbital swelling. The tube had been removed before the autopsy, precluding assessment of its placement. It is important that all tubes remain in the body for objective postmortem (autopsy) evalu- ation of their placement. This may make injury inter- onstrates a catheter placed into an injured blood vessel pretation more challenging. If at all possible, this should never be done because it makes injury interpretation much more difficult. Had it not been for this trauma, the infection that took his life would not have occurred. Notice, however, that along the left margin of this perforation (from the 7 to 11 o’clock positions), there is a distinct abrasion. Further investiga- tion established that the chest tube was inserted through a previously sustained entrance gunshot wound, thus explaining the abraded margin of this perforation. This decedent had also sustained stab and incised wounds in other parts of their body. Autopsy disclosed a large hemoperitoneum with clotted blood extending from a bleeding abdominal wall vein. A large accumulation of clotted blood collapsed his airway while he was sedated at home. Chest tube placement was inserted through the lung parenchyma during resuscitation. Approximately 150 mL of liquid blood was recovered from the left hemithorax, indicating that this injury was perimortem and iatrogenic. The decedent was fed through the nasogastric tube, which is demonstrated by the accumulation of yellow fuid within the thoracic cavity. Similarly appearing exudate can also be seen on the anterior surface of the gastric body and fundus. The picture depicts a large hemoperitoneum, with greater omentum, stomach, and intestines foating on top of a pool of blood. There was advanced end-stage cirrhosis, with confuent scar enveloping and entrapping regenerative parenchy- mal nodules. Liver diseases such as this are associated with an increased risk of hemorrhagic complications due to coagulopathy and portal hypertension. This fatal hemorrhage resulted from laceration of a portal vein branch occur- ring during stent placement. Note the probe demonstrating the perforation through the right internal jugular vein and the hemorrhage within the anterior overlying soft tissues. The procedure was followed by extensive pulmonary hemorrhage, which culminated in respiratory compromise and death. Note at the inferolateral aspect of the left lower lobe is a fragment of gauze that was inadvertently left behind during another operation months earlier. The gauze is adherent to the surface with overlying adhesions and adjacent purulent exudate. It is always important to be careful of sharps that have been inadvertently left behind. She was treated at home by her grandmother with Southeast Asian folklore remedies, including coining. These red to brown contusions, some with abrasions, were produced by another person rubbing her neck with metal dog tags and medicinal oils while praying. For example, one person most people typically have access to various types of may intentionally be abusing a multitude of substances drugs, including legitimately prescribed medications, including illicit drugs, prescribed medications, and and on average, will beneft from their appropriate use. Tis is in contrast to another individual 105 106 Color Atlas of Forensic Medicine and Pathology who may only be taking a single medication, but delib- really a pooled specimen, collected in the bladder over erately using it in a manner that is not consistent with a period of time, and that a quantitative result only rep- normal therapeutic use.
The condition of having already survived to a given time means that the probability of surviving into the future is influenced by having already survived previous time periods purchase 100mg clomid overnight delivery pregnancy ultrasound at 5 weeks. This idea can be very important in some instances generic clomid 50 mg overnight delivery pregnancy in dogs, where surviving the early stages of a disease may dramatically decrease the potential of an event occurring in the near future. As an example, consider cancer where nonrecurrence, or remission, for a period of 5 years generally increases survivorship. Excellent descriptions of the various models used to represent hazard functions are provided by Allison (4) and Kleinbaum and Klein (1). The method we use was introduced by Kaplan and Meier (5) and for that reason is called the Kaplan–Meier procedure. Since the procedure involves the successive multipli- cation of individual estimated probabilities, it is sometimes referred to as the product-limit method of estimating survival probabilities. As we shall see, the calculations include the computations of proportions of subjects in a samplewho survive for various lengths of time. We use these sample proportions as estimates of the probabilities of survival that we would expect to observe in the population represented by our sample. In mathematical terms we refer to the process as the estimation of a survivorship function. Frequency distributions and probability distributions may be constructed from observed survival times, and these observed distributions may show evidence of following some theoretical distribution of known functional form. When the form of the sampled distribution is unknown, it is recommended that the estimation of a survivorship function be accomplished by means of a nonparametric technique, of which the Kaplan–Meier procedure is one. Calculations for the Kaplan–Meier Procedure We let n ¼ the number of subjects whose survival times are available p1 ¼ the proportion of subjects surviving at least the first time period (day, month, year, etc. For any time period, t, where 1 t k, we estimate the probability of surviving the tth time period, pt, as follows: number of subjects surviving at least t À 1 time periods who also survive the tth period p^t ¼ number of subjects alive at end of time period t À 1 (14. They classified patients as having either low-grade (25 patients) or high-grade (14 patients) tumors. The event (status), time to event (months), and tumor grade for each patient are shown in Table 14. We wish to compare the 5-year survival experience of these two groups by means of the Kaplan–Meier procedure. We begin by listing the observed times in order from smallest to largest in Column 1. Column 2 contains an indicator variable that shows vital status ð 1 ¼ died; 0 ¼ alive or censored. In Column 3 we list the number of patients at risk for each time associated with the death of a patient. We need only be concerned about the times at which deaths occur because the survival rate does not change at censored times. Column 4 contains the number of patients remaining alive just after one or more deaths. Column 5 contains the estimated conditional probability of surviving, which is obtained by dividing Column 4 by Column 3. Note that although therewere two deaths at 15 months in the low-grade group and two deaths at 9 months in the high-gradegroup, we calculate only one survival proportion at these points. Each entry after the first in Column 5 is multiplied by the cumulative product of all previous entries. From the table we note the following facts, which allow us to compare the survival experience of the two groups of subjects: those with low-grade tumors and those with high-grade tumors: 1. We can determine the median survival time by locating the time, in months, at which the cumulative survival proportion is equal to. We can determine the 5-year or 60-month survival rate for each group directly from the cumulative survival proportion at 60 months. Since so many of the times in the low-grade group are censored, the true mean survival time for that group is, in reality, higher (perhaps, considerably so) than 88. The true mean survival time for the high-grade group is also likely higher than the computed 18. Thus, we see that we have still another indication that the survival experience of the low-grade tumor group is more favorable than the survival experience of the high-grade tumor group. From the raw data of each group we may also calculate another descriptive statistic that can be used to compare the two survival experiences. A group with a higher average hazard rate will have a lower probability of surviving than a group with a lower average hazard rate. We compute the average hazard rate, designated h by dividing the number of subjects who do not survive by the sum of the observed survival times. For the high-grade tumor group we compute hH ¼ 13=257 ¼ :05084, We see that the average hazard rate for the high- grade group is higher than for the low-grade group, indicating a smaller chance of surviving for the high-grade group. We note that the graph resembles stairsteps with “steps” occurring at the times when deaths occurred. These observations strongly suggest that the survival experience of patients with low-grade tumors is far more favorable than that of patients with high-grade tumors. The following table shows the status of each patient at various periods of time following surgery. Calculate the survival function using the Kaplan–meier procedure and plot the survival curve. Calculate the survival function using the Kaplan–Meier procedure and plot the survival curve. Total Total Total Duration of Duration of Duration of Remission Remission Remission Remission Remission Remission (Months) Statusa (Months) Statusa (Months) Statusa 3 1 8 2 26 1 3 2 9 2 27 1 3 3 3 4 4 4 5 5 5 5 5 5 (Continued) 14. This includes visualizing the temporal trajectory to find time periods in which there were dramatic changes in survival, finding time periods in which relatively little change occurred, or in finding the approximate median of the data distribution. The construction of survival curves, however, finds its greatest use when comparisons among survival distributions are of interest. For example, one may wish to examine differences in treatment in which subjects were randomly assigned, or may wish to know which medication delays the onset of the event of interest for the longest period of time. The results of comparing the survival experiences of different groups will not always be as dramatic as those of our previous example. For an objective comparison of the survival experiences of different groups, it is desirable that we have an objective technique for determining whether they are statistically significantly different. We know also that the observed results apply strictly to the samples on which the analyses are based. Of much greater interest is a method for determining if we may conclude that there is a difference between survival experiences in the populations from which the samples were drawn. In other words, at this point, we desire a method for testing the null hypothesis that there is no difference in survival experience between populations against the alternative that there is a difference. The log-rank test is an application of the Mantel–Haenszel procedure discussed in Section 12. Though we may wish to compare survival curves of many populations, we will limit our discussion to the comparison of two groups: To accomplish this task, we calculate the log-rank statistic and proceed as follows: 1. Order the survival times until death for both groups combined, omitting censored times. For each stratum compute the expected frequency for the upper left-hand cell of its table by Equation 12.