What are these findings in the Holter? If the sinus node fails, the AV node takes over and stimulates the ventricle. In 10% of people there is retrograde conduction, so that beat generated in the AVN stimulates both ventricles and atria, giving a retrograde P as reported in the study. In this sense, no problem. Likewise, there are also no pauses longer than 3 seconds that could cause cardiogenic syncope (which, in fact, he has never suffered). Option 1 is ruled out: it is not a complete AVB. Option 2 cannot be answered either: to exclude, what is said to exclude... It is like never/always. Option 3 does not make much sense: we could suspend those that impair conduction (beta-blockers, calcium antagonists), but drugs that facilitate, as long as we do not give him a perfusion of atropine to take home... In option 4, stating that he has sinoatrial block is a bit of a rap: without an electrophysiological study it cannot be said, he does not necessarily have SA block, and this alone would not indicate the implantation of a pacemaker. So, finally, I would check option 5.

What are these findings in the Holter? If the sinus node fails, the AV node takes over and stimulates the ventricle. In 10% of people there is retrograde conduction, so that beat generated in the AVN stimulates both ventricles and atria, giving a retrograde P as reported in the study. In this sense, no problem. Likewise, there are also no pauses longer than 3 seconds that could cause cardiogenic syncope (which, in fact, he has never suffered). [HIDDEN]. [HIDDEN]. [HIDDEN]. [HIDDEN]. So, finally, I would check [HIDDEN].

An 82-year-old patient presents with sudden and frequent dizziness, without prodromes, of short duration and which subsides spontaneously, without ever presenting syncope. Physical examination and baseline electrocardiogram are normal. In an ambulatory electrocardiogram recording during 24 hours, short phases of absence of P waves prior to QRS with an escape rhythm of the atrioventricular junction with narrow QRS at 40 bpm and a wave at the beginning of the ST segment corresponding to a retrograde P were detected in the vigil period. No asystole periods longer than 3 seconds are detected. Given this you would say:

The patient has a third-degree AVB and requires pacemaker implantation.

The absence of periods of asystole >3 seconds excludes a cardiac cause of dizziness.

Drug treatment to increase conduction in the AV node would be indicated.

The patient presents sinus dysfunction with sinoatrial block and requires pacemaker implantation due to symptoms.

The alterations detected in the ambulatory electrocardiogram are typical of patients of this age and there is no indication for therapeutic intervention.

[Clinical and electrophysiological aspects of median intra-His bundle block with normal electrocardiogram at rest].

The clinical and electrophysiological features and the natural history of median intra-His block with a normal resting electrocardiogram were studied: 11 patients had a fixed split H1-H2 potential with a spontaneous or induced block between H1 and H2. The patients (5 men and 6 women) were aged 17 to 70 years (average 53 years). Associated pathology included 2 cases of aortic stenosis (1 severe), 1 case of ischaemic heart disease (effort angina), 1 case of mitral valve prolapse and 2 cases of hypertension. The presenting symptoms were syncope (4 cases), dizziness (2 cases), effort angina (1 case) and tiredness (3 cases); 1 patient was asymptomatic. Holter monitoring (24 hours) was performed in 8 patients and s-owed paroxysmal conduction defects in 6 cases; 4 Mobitz II 2nd degree AV block, 1 3rd degree AV block with narrow QRS complexes and 1 case of blocked atrial extrasystoles at coupling intervals longer than 480 ms and sinus cycle lengths of over 800 ms. Exercise testing by bicycle ergometry (4 patients) was normal in 1 case and revealed Mobitz II 2nd degree AV block in 3 cases. Baseline electrophysiological studies showed an A-H1 interval ranging from 60 to 100 ms (average 78 ms), a H1-H2 interval of 20 to 40 ms (average 31 ms) and a H2-V interval of 30 to 50 ms (average 32 ms). Block between H1 and H2 was observed: "spontaneously" during electrophysiological investigation in 6 cases, after IV atropine in 1 case, during overdrive atrial pacing at rates slower than 150/min in 7 cases, after atrial extrastimulus with a functional intra-His refractory period of over 420 ms in 7 cases, after ajmaline in 3 of the 4 cases in which this test was performed. A cardiac pacemaker was implanted in 10 patients in whom the initial symptoms have all regressed; the remaining patient considered to be "epileptic" had another syncopal attack under therapy and was finally paced. This series demonstrates that the diagnosis of median intra-His block depends on precise electrophysiological criteria and should be looked for even when the presenting symptoms are atypical; some of our patients complained only of tiredness. The value of Holter monitoring and careful endocavitary investigation is emphasised. Median intra-His block should be distinguished from longitudinal and functional His bundle dissociation.

Usefulness of 24-hour recordings of electrocardiogram for the diagnosis and treatment of arrhythmias with special reference to the determination of indication of artificial cardiac pacing.

Twenty-four-hour recordings of electrocardiogram (ECG) were obtained from 1528 subjects. Sick sinus syndrome (SSS) was observed in 34 and advanced or complete AV block (CAVB) in 13 subjects. During the period studied 21 patients had died, who showed complicated ventricular premature contractions in 9 (multiform 6, short run 2, repetitive 2). Seventy-three patients with artificial cardiac pacing who were admitted at three different institutions were analyzed. The discrepancy of degree of block was observed between His bundle electrocardiographic findings and 24-hour ECG recordings. In 15 patients there was no correlation between sinus node recovery time following overdrive suppression and pauses following the termination of tachycardia (r = 0.0896, N. S.). In 49 normal subjects 24-hour heart rate ranged from a high of 170 to a low of 36 beats/min. Longest R-R interval ranged from 2.08 to 0.86 sec (mean 1.25 +/- 0.22 sec). The critical level of longest R-R interval to differentiate between normal group and groups with SSS or CAVB was about 1.6 sec. Above results suggest that Holter monitoring permits a precise diagnosis of arrhythmias and that both HBE and Holter monitoring should be used for the determination of pacemaker implantation especially in those with syncope or dizziness but without evidence of marked bradycardia.

Third-degree atrioventricular block

Third-degree atrioventricular block (AV block) is a medical condition in which the nerve impulse generated in the sinoatrial node (SA node) in the atrium of the heart can not propagate to the ventricles. Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an escape rhythm. Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG). The P waves with a regular P-to-P interval (in other words, a sinus rhythm) represent the first rhythm. The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is the lack of any apparent relationship between P waves and QRS complexes.

Bradycardia

The third, sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia-tachycardia syndrome (atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia). Atrioventricular junction An AV-junctional rhythm, or atrioventricular nodal bradycardia, is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an electrocardiogram (ECG) with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.

[Syncopes and brief spells of feeling faint: value of Holter monitoring?].

A retrospective study of Holter monitoring of 250 patients referred for syncope and short spells of dizziness suspected of being cardiac in origin was undertaken to assess the diagnostic value of the investigation. The arrhythmias observed were classified in 3 groups, significant, suspect and physiological with respect to their true or potential severity and to previously reported results of Holter monitoring in healthy subjects. The following arrhythmias were classified as significant: supraventricular tachycardia with a ventricular rate greater than or equal to 200 bpm; sustained ventricular tachycardia (greater than 30 s and greater than or equal to 150 bpm), bradycardia (less than bpm), sinus arrest (waking greater than 2 s sleeping greater than or equal to 6 s), complete AV block with wide QRS complexes and pacemaker dysfunction. The following arrhythmias were classified as suspect: paroxysmal supraventricular tachycardia with a ventricular rate less than 200 bpm, salvos of ventricular tachycardia (120 greater than 150 bpm); R/T phenomenon and doublets (greater than or equal to 50/24 hours), sinus arrest of 2 to 6 seconds during sleep, complete AV block with narrow QRS complexes or second degree Mobitz II block. This classification led to a diagnosis of certitude in 20 patients (5.7%) with significant arrhythmias concomitant with syncope or a minor form in only 5 cases, supraventricular tachycardia (4 cases), ventricular tachycardia (4 cases), AV block (5 cases), sinus arrest (3 cases), pacemaker dysfunction (4 cases); a diagnosis of presumption in 74 patients (21.1%) with suspect arrhythmias in the absence of syncope or minor equivalent.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular block

Diagnosis An electrocardiogram, or ECG, is used to differentiate between the different types of AV block. In AV block, there is a disruption between the signal traveling from the atria to the ventricles. This results in abnormalities in the PR interval, as well as the relationship between P waves and QRS complexes on the ECG tracing. If the patient is symptomatic from their suspected AV block, it is important that an ECG is also obtained while having symptoms. Physicians may also order a continuous ECG (i.e. Holter monitor or implanted cardiac monitor) to monitor the patient for symptoms and conduction abnormalities over a longer period of time, as AV blocks can be intermittent. Because some types of AV block can be associated with underlying structural heart disease, patients may also undergo echocardiogram to look at the heart and assess the function.

Bradycardia

Ventricular Idioventricular rhythm, also known as atrioventricular bradycardia or ventricular escape rhythm, is a heart rate of less than 50 BPM. This is a safety mechanism when a lack of electrical impulse or stimuli from the atrium occurs. Impulses originating within or below the bundle of His in the AV node will produce a wide QRS complex with heart rates between 20 and 40 BPM. Those above the bundle of His, also known as junctional, will typically range between 40 and 60 BPM with a narrow QRS complex. In a third-degree heart block, about 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His. AV block may be ruled out with an ECG indicating "a 1:1 relationship between P waves and QRS complexes." Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consists of the administration of atropine and cardiac pacing.

Sinoatrial arrest

Sinoatrial arrest is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. This condition is

Sinus node dysfunction

Diagnosis Electrocardiogram The primary 12-lead electrocardiogram (ECG) finding in sinus node dysfunction is inappropriate sinus bradycardia. Sinus node dysfunction can also present with sudden sinus arrest with or without junctional escape, sinoatrial block, prolonged asystolic period followed by tachycardias, or tachycardia-bradycardia syndrome presenting as various atrial arrhythmias such as atrial fibrillation, flutter, tachycardia, or paroxysmal supraventricular tachycardia.

Second-degree atrioventricular block

Type 2 (Mobitz II/Hay) Type 2 Second-degree AV block, also known as Mobitz II, is almost always a disease of the distal conduction system (His-Purkinje System). Mobitz II heart block is characterized on a surface ECG by intermittently non conducted P waves not preceded by PR prolongation and not followed by PR shortening. There is usually a fixed number of non-conducted P waves for every successfully conducted QRS complex, and this ratio is often specified in describing Mobitz II blocks. For example, Mobitz II block in which there are two P waves for every one QRS complex may be referred to as 2:1 Mobitz II block.:181 The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge. In this case, the person may experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death. The definitive treatment for this form of AV Block is an implanted pacemaker.

Concealed conduction

Concealed conduction is tissue stimulation without direct effect, but leading to a change in conduction characteristics. A common example would be an interpolated PVC (a type of premature ventricular contraction) during normal sinus rhythm; the PVC does not cause an atrial contraction, because the retrograde impulse from the PVC does not completely penetrate the AV node. However, this AV node stimulation can cause a delay in subsequent AV conduction by modifying the AV node's subsequent conduction characteristics. Hence, the P-R interval after the PVC is longer than the baseline P-R interval. Another variation on this concept is seen in atrial flutter. As a result of the rapid atrial rate, some of the atrial activity fails to get through the AV node in an antegrade direction but can alter the rate at which a subsequent atrial impulse is conducted. In this circumstance, an alteration in the F-wave to QRS relationship is seen. See also Atrioventricular node Electrocardiogram

Third-degree atrioventricular block

Complete atrioventricular block in acute myocardial infarction should be treated with temporary pacing and revascularization. Complete atrioventricular block caused by hyperkalemia should be treated to lower serum potassium levels and patients with hypothyroidism should also receive thyroid hormone. If there is no reversible cause, the clear treatment of complete atrioventricular block is mostly permanent pacemaker placement. Prognosis The prognosis of patients with complete heart block is generally poor without therapy. Patients with 1st and 2nd-degree heart block are usually asymptomatic. See also Cardiac pacemaker Electrical conduction system of the heart Electrocardiogram (ECG) Atrioventricular block First-degree AV block Second-degree AV block References External links Cardiac arrhythmia Medical emergencies

Third-degree atrioventricular block

Treatment Early treatment of atrioventricular blockade is based on the presence and severity of symptoms and signs associated with ventricular escape rhythm. Hemodynamically unstable patients require immediate medication and in most cases temporary pacing to increase heart rate and cardiac output. Once the patient is hemodynamically stable, a potentially reversible cause should be evaluated and treated. If no reversible cause is identified, a permanent pacemaker is inserted. Most stable patients have persistent bradycardia-related symptoms and require identification and treatment of any reversible cause or permanent implantable pacemaker. Reversible causes of complete AV block should be ruled out before the insertion of a permanent pacemaker, such as drugs that slow heart rate and which induce hyperkalemia. Complete atrioventricular block in acute myocardial infarction should be treated with temporary pacing and revascularization.

Value of Holter monitoring in assessing cardiac arrhythmias in symptomatic patients.

Holter electrocardiographic monitoring in 55 symptomatic patients with syncope, palpitations or dizziness uncovered significant arrhythmias in 30 patients (55 percent). By providing an observation period of at least 24 hours including a period of sleep, the procedure aided detection and diagnosis in both symptomatic and asymptomatic patients of transient arrhythmias or conduction abnormalities not documented by routine electrocardiograms. Bradyarrhythmias accounted for the majority of arrhythmias recorded in 21 or 30 symptomatic patients (70 percent); 15 had sinus bradycardia (35 to 55 beats/min) alone and 6 also had long episodes of sinus arrest of up to 5 seconds. Two had sinus bradycardia with periods of atrioventricular block with Wenckebach phenomenon. Five patients had a tachycardia-bradycardia syndrome; three had other episodic arrhythmias and one had pacemaker failure. In 15 (60 percent) of the 25 patients without arrhythmias, monitoring did not document the cause of symptoms. Holter monitoring is of considerable value in assessing the efficacy and adequacy of drug treatment, especially in patients with known heart disease, and in detecting pacemaker malfunction. However, very long periods of monitoring may be needed to make a diagnosis in those with only sporadic symptoms.

Arrhythmias -- Clinical Significance -- Tachyarrhythmia

b) Second Degree AV Block: Further classified into Mobitz I block, where there is a progressive prolongation of the PR interval followed by a skipped beat, and Mobitz II block, where there is a randomly dropped QRS complex on an EKG. Sign & Symptoms: Can be asymptomatic, dizziness, palpitations, weakness, syncope. EKG Findings: Mobitz type I shows progressive prolongation of the PR interval followed by a dropped QRS complex or dropped beat. Mobitz type II has randomly dropped QRS complexes. Management: Pacemaker is indicated in symptomatic Mobitz I and all of Mobitz II heart block. c) Third Degree or complete AV Block Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions. Sign & Symptoms: Profound bradycardia, hypotension, and can lead to asystole and cardiac arrest. EKG Findings: Bradycardia, P waves occur independently of QRS and Wide QRS for ventricular rhythm. Management: Pacemaker placement.

Premature atrial contraction

Diagnosis Premature atrial contractions are typically diagnosed with an electrocardiogram, Holter monitor, or cardiac event monitor. Electrocardiogram On an electrocardiogram (ECG), PACs are characterized by an abnormally shaped P wave. Since the premature beat initiates outside the sinoatrial node, the associated P wave appears different from those seen in normal sinus rhythm. Typically, the atrial impulse propagates normally through the atrioventricular node and into the cardiac ventricles, resulting in a normal, narrow QRS complex. However, if the atrial beat is premature enough, it may reach the atrioventricular node during its refractory period, in which case it will not be conducted to the ventricle and there will be no QRS complex following the P wave.

[Values of the effective anterograde refractory period of the bundle of His].

The effective refractory period of the His bundle (ERP.H), the longest H1, H2 interval not followed by a V2 ventricular complex, was measured in 45 cases during the electrophysiological investigation of 500 Patients by premature atrial stimulation techniques. The patients were divided into two groups according to the result: Group I: 22 patients with syncope, a spontaneous HV interval greater than 60 ms, greater than 100 ms after Ajmaline or infrahisian block with atrial pacing at less than 150 bpm. Group II: 23 patients without these abnormalities. The ERP.H was significantly different (p less than 0,001) in the two groups with valves greater than 400 ms in Group I and less than 400 ms in Group II. It is suggested that in the absence of other electrophysiological abnormalities an ERP.H of 400 ms or over may be an indication for permanent pacing in patients with Stokes-Adams attacks. The finding of an ERP.H of over 400 ms is associated with severe infrahisian block. However, the ERP.H depends on the ERP of the AV node which must be shorter to calculate the refractory periods of the His bundle, and, above all, on the basal sinus cycle. The ERP.H decreases with shorter sinus cycles and cannot be calculated when the sinus cycle is less than 600 ms. Conversely, the critical value of 400 ms is not valid for cycles longer than 1000 ms as cycles of that length are associated with lengthening of the ERP.H. The regression of infrahisian block during programmed atrial pacing after Atropine does not seem to be a reliable method of distinguishing between physiological and pathological atrioventricular block.

Permanent atrial standstill with irregular junctional ectopic rhythm mimicking atrial fibrillation.

We present an interesting case of 'pseudo' atrial fibrillation which was further diagnosed as atrial standstill with irregular junctional ectopic rhythm during electrophysiologic study. A 56-year-old woman presented to a health facility with symptoms of palpitation, lightheadedness, and shortness of breath. Upon detection of irregular rhythm with narrow QRS complexes and no visible P waves on the electrocardiogram, newly developed atrial fibrillation was considered and a direct current cardioversion was performed, during which cardiac asystole developed necessitating cardiopulmonary resuscitation. The patient was then transferred to our institution. Echocardiographic examination showed biatrial dilatation, normal left ventricular systolic function, marked left ventricular hypertrophy, severe aortic stenosis, moderate mitral regurgitation, and severe tricuspid regurgitation. The electrocardiogram showed an irregular rhythm with narrow QRS complexes without any fibrillatory f waves and 24-hour Holter monitoring revealed three episodes of ventricular asystole lasting for more than 3.5 seconds. During the electrophysiologic study, no electrical activity was observed at the high and low levels of the right atrial lateral free wall and septal wall. The final diagnosis was established as atrial standstill and irregular junctional ectopic rhythm. The patient refused aortic valve replacement and died due to progression of the underlying disease one year following permanent pacemaker implantation..

Electrophysiologic testing in bundle branch block and unexplained syncope.

Thirty-two patients with bundle branch block and unexplained syncope underwent electrophysiologic testing, including programmed ventricular stimulation with up to triple extrastimuli. The infranodal conduction time (HV) was 70 ms or greater in 12 patients. Pathologic infranodal block during atrial pacing occurred in 2 patients. Unimorphic ventricular tachycardia (VT) was induced in 9 patients (28%) and polymorphic VT in 5 (16%). A permanent pacemaker was implanted in patients with infranodal block during atrial pacing and, generally, in patients with an HV of 70 ms or more. Patients with inducible unimorphic or sustained polymorphic VT were treated with an antiarrhythmic drug. The mean follow-up period was 19 +/- 14 months (+/- standard deviation). Three patients died suddenly: a noncompliant patient with inducible sustained VT; a patient with a normal electrophysiologic study treated empirically with quinidine for premature ventricular complexes; and a patient with an HV of 70 ms and no inducible VT treated with a permanent pacemaker. The actuarial incidence of sudden death was 10% at 45 months of follow-up. Only 2 patients had recurrent syncope; both had a normal electrophysiologic study. Approximately 50% of patients with bundle branch block and unexplained syncope who undergo electrophysiologic testing are found to have a clinically significant abnormality (HV of 70 ms or more, infranodal block during atrial pacing and inducible unimorphic VT), and some patients have more than 1 abnormality. Long-term management guided by the results of electrophysiologic testing generally is successful in preventing recurrent syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence and prognostic significance of cardiac arrhythmias detected by ambulatory electrocardiography in subjects 85 years of age.

24 hour ambulatory electrocardiography was performed in a representative group of people born in 1897. Out of 73 people included in the study, 22 were without known heart disease, 15 had definite ischaemic heart disease (IHD) and 36 symptoms of possible cardiac origin. An R-R interval in excess of 2000 ms was seen in only 3 subjects and Wenckebach A-V block in only one. One subject without a history of syncope had a nocturnal episode of complete A-V block with an escape interval of 8000 ms. The most striking difference between healthy subjects and patients with IHD was the higher number of patients with more than 1000 ventricular premature beats (VPBs) per 24 hour and ventricular couplets compared with the number of healthy subjects with such findings. At follow-up two years later 11% had died, with the highest mortality in patients with IHD (33%), and out of 8 patients with IHD who had more than 1000 VPBs per 24 hour, 4 (50%) had died compared with only one (14%) of those with less than 1000 VPBs. Our results seem to indicate that more than 1000 VPBs per 24 hour is a very unusual finding in healthy 85 year old individuals. When it occurs in very old people, it is usually in connection with IHD, and in this setting it signifies a poor prognosis.

Atrioventricular block

Classification There are three types, or degrees, of AV block: (1) first-degree, (2) second-degree, and (3) third-degree, with third-degree being the most severe. An ECG is used to differentiate between the different types of AV blocks. However, one important consideration when diagnosing AV blocks from ECGs is the possibility of pseudo- AV blocks which are due to concealed junctional extrasystoles. It is important to diagnose AV-blocks precisely because unnecessary pacemaker placement in patients with pseudo-AV blocks can worsen symptoms and create complications. First-degree atrioventricular block First-degree AV block occurs when there is a delay, but not disruption, as the electrical signal moves between the atrium and the ventricles through the AV node. On ECG, this is defined by a PR interval greater than 200 msec. Additionally, there are no dropped, or skipped, beats. Second-degree atrioventricular block

Mechanism of syncope without prodromes with normal heart and normal electrocardiogram.

"Unexplained syncope, no prodromes, and normal heart" has been described as a distinct clinical and biological entity. The purpose of this study was to assess the mechanism of syncope. In this prospective multicenter study, 58 patients presenting with unexplained syncope, no prodromes, and a normal heart received an implantable loop recorder (ILR) and were followed up until a diagnosis was established. Their outcomes were compared with those of 389 patients affected by reflex syncope with prodromes who received an ILR. During a mean observation period of 16 ± 13 months, a diagnostic event was documented by the ILR in 29 patients (50%); an asystolic pause of 11 ± 5 seconds (range 3.5-22 seconds) was present at the time of the diagnostic event in 19 patients (66%). Compared with patients affected by reflex syncope with prodromes, patients with unexplained syncope, no prodromes, and a normal heart more frequently had an asystolic syncope (66% vs 47%; P = .001), and this was more frequently due to idiopathic paroxysmal atrioventricular block (47% vs 21%; P = .04). Ten patients with asystolic pauses underwent cardiac pacing, and 8 patients underwent oral theophylline treatment. During the subsequent 17 ± 12 months of follow-up, syncope recurred in 1 patient on theophylline and presyncope occurred in 1 patient with pacemaker. A long asystolic pause, frequently due to idiopathic paroxysmal atrioventricular block, played a role in the mechanism of syncope in two-thirds of patients who had electrocardiographic documentation of a diagnostic event. When a specific therapy was administered in patients with asystolic syncope, the short outcome was favorable.

[Syncope in bradycardic cardiac arrhythmias].

Bradyarrhythmias, depending on the patient population, are the cause of syncope in 3 to 10%. Marked bradycardia or asystole can be due to impaired function of the sinus node (sinus node syndrome) or high-grade AV-conduction block as well as carotid sinus syndrome and pathologic vasodepressor reactions. In particular, in the presence of high-grade AV-block, the diagnosis of bradyarrhythmia-induced syncope can frequently be established on the basis of a standard ECG. One of the most common causes of syncope is functional impairment of the sinus node, in particular, an inadequate permanent sinus bradycardia, sinus node arrest or SA-block and paroxysmal atrial tachycardia alternating with atrial bradycardia. The method of choice for detecting suspected paroxysmal arrthythmias is ambulatory ECG monitoring but interpretation may be encumbered by the absence of concomitant symptoms during the registration. Frequently, the use of non-invasive methods alone, such as detailed history, ambulatory ECG and ECG exercise testing, will not render confirmatory findings to document the cause of syncope, that is, > 3 s pause in sinus rhythm or high-grade AV-block. In this situation, the question arises which patients should undergo electrophysiologic examination. Several studies have shown that in patients with a pathologic resting ECG (first degree AV-block, bundle branch block, inadequate sinus bradycardia) and cardiac disease, electrophysiologic studies will document a cause of syncope in more than 30%.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular escape beat

Diagnosis An electrocardiogram can be used to identify a ventricular escape beat. The QRS portion of the electrocardiogram represents the ventricular depolarisation; in normal circumstances the QRS complex forms a sharp sudden peak. For a patient with a ventricular escape beat, the shape of the QRS complex is broader as the impulse can not travel quickly via the normal electrical conduction system. Ventricular escape beats differ from ventricular extrasystoles (or premature ventricular contractions), which are spontaneous electrical discharges of the ventricles. These are not preceded by a pause; on the contrary they are often followed by a compensatory pause. Management Cilostazol Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate Ouabain Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia. References Cardiac arrhythmia

Cardiac arrhythmias: diagnosis and management. The bradycardias.

To review the diagnosis and management of cardiac arrhythmias in a two-part presentation. Articles and published peer-review abstracts on tachycardias and bradycardias. Bradycardias are caused by a failure of the sinus node to generate normal impulses or due to a defect in cardiac conduction that in turn causes a delay or failure of impulse propagation. During sleep, the heart rate may decrease to 30 beats per minute (bpm) with episodes of sinoatrial block, junctional rhythms and first and second degree atrioventricular block that occur often enough (particularly in trained athletes) to be considered normal variants. However, treatment is required if symptoms of dizziness, confusion, fatigue Stokes-Adams attacks or heart failure occur. Sinus node dysfunction or 'sick sinus syndrome' is usually caused by intrinsic nodal disease and may present with episodes of tachycardia and bradycardia (tachycardia-bradycardia syndrome). Treatment usually requires a permanent pacemaker. Atrioventricular (AV) conduction disturbances are characterised by a delay or failure of the atrial impulse to be conducted through the AV conducting system. If the escape rhythm is unstable the patient also requires a pacemaker. In the critically ill patient tachycardias are more often encountered than bradycardias. However, the intensivist should be familiar and skilled in the management of complete heart block and asystole, correcting the underlying defect (drug toxicity, hyperkalaemia, etc), while using catecholamines, atropine aminophylline and a temporary pacemaker for initial resuscitation. Bradycardias are uncommon in the critically ill patient and often are caused by an underlying disorder (e.g. hyperkalaemia, calcium channel blocker toxicity, beta adrenergic receptor blocker toxicity, etc). However, post cardiac bypass and acute myocardial infarction may cause cardiac conduction defects that may require urgent resuscitation with a temporary pacemaker.

[Dynamic electrophysiological examination of heart in patients with sick sinus syndrome in continuous pacing].

Dynamic electrophysiological examination of the heart with allowances for ECG variants of this syndrome and stimulation regimen was performed to predict the results of continuous pacing in patients operated for sick sinus syndrome (SSS). 32 patients had the diagnosis of bradycardia SSS (group 1), 15 patients--bradytachycardia (group 2). 30 patients were on ventricular VVI stimulation, 17 patients--on atrial AAI stimulation. Electrophysiological examination of the heart was performed by means of transesophageal left atrial pacing under programmed, frequent and ultrafrequent stimulation 1, 2, 3 and 4 years after the start of continuous cardiac pacing. In group 2 depression of the sinus function (corrected time of the sinus function recovery, frequency of spontaneous pacemaker, duration of poststimulation pause) under pacing was more distinct than in group 1. Deterioration of atrioventricular conduction was greater in group 1. Three and four years after pacing the Wenckebach point in group 1 lay significantly lower than in group 2. Within the follow-up period 6 (12.8%) patients developed AB-block of the second degree. 4 patients of them were from group 1. Arrhythmogenic atrial readiness depended on the kind of cardiac affection more than on stimulation regimen. Dynamic electrophysiological cardiac examination in the presence of pacing allows following up of natural course of sick sinus syndrome and early correction of the stimulation regimen.

A proposal of clinical ECG index "vagal score" for determining the mechanism of paroxysmal atrioventricular block.

Paroxysmal atrioventricular block (P-AVB) is a well-known cause of syncope; however, its underlying mechanism is difficult to determine. This study aimed to evaluate a new ECG index, the "vagal score (VS)," to determine the mechanism of P-AVB. We evaluated the VS in 20 patients with P-AVB (13 men, 7 women; aged 25-78 years [mean, 59.3 years]). The VS was developed by assigning 1 point each for the following: (1) no AVB or intraventricular conduction disturbance on the baseline ECG, (2) PR prolongation immediately before P-AVB, (3) sinus slowing immediately before P-AVB, (4) initiation of P-AVB by PP prolongation, (5) sinus slowing during ventricular asystole, and (6) resumption of AV conduction with PP shortening, and by assigning -1 point each for (7) the initiation of P-AVB by a premature beat, and (8) resumption of AV conduction by an escape beat. Based on the clinical situations and electrophysiologic findings, we considered the mechanism of P-AVB as vagally mediated or intrinsic conduction disease (ICD). The VS ranged from 5 to -2 points for each patient. Five patients with a definite vagally mediated P-AVB had high VSs (3-5 points). We observed characteristic ECG findings of ICD consisting of changes in AV conduction by an extrasystole and/or escape beat in only 5 of the 6 patients (83%) with a low VS (1 to -2). The VS is simple and potentially useful for determining the mechanism of P-AVB. P-AVB with a VS ≥3 strongly suggested a vagally mediated mechanism.

First-degree atrioventricular block

Causes The most common causes of first-degree heart block are AV nodal disease, enhanced vagal tone (for example in athletes), myocarditis, acute myocardial infarction (especially acute inferior MI), electrolyte disturbances and medication. The medications that most commonly cause first-degree heart block are those that increase the refractory time of the AV node, thereby slowing AV conduction. These include calcium channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic activity such as cholinesterase inhibitors. Diagnosis In normal individuals, the AV node slows the conduction of electrical impulses through the heart. This is manifest on a surface electrocardiogram (ECG) as the PR interval. The normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the P wave to the beginning of the QRS complex.

[Evaluation of the PR intervals in normal and prolonged maximum limit with short QRS].

Evaluation of the A-V node function by determining the Wenckebach period (WP) and atropine response in cases of normal PR interval, PR interval at maximum normal range and prolonged PR interval, all with short QRS. 129 patients, 79 male and 50 female, aged 17 to 84 years (mean 59), asymptomatic or with complaints of palpitations, dizziness, presyncope or syncope has been studied. ECG showed supra-ventricular tachycardia, first degree A-V block or intermittent Mobitz I type A-V block and sick sinus syndrome. Preexcitation (WPW) syndrome and longitudinal A-V dissociation were excluded. Electrical transoesophageal atrial stimulation was performed in all patients for evaluating the PR interval and WP. Atropine test was performed in a group of 16 patients. Based on the values of the WP, patients were divided into three groups: group I, WP greater than or equal to 125 ppm (N = 88); group II, WP ranging 125-110 ppm (N = 16) and group III, WP less than or equal to 110 ppm (N = 25). There was a good decreasing lineal correlation between the PR interval and the WP only in the group III (r = 0.76, p less than 0.01). PR interval greater than 240 ms had greatest and significant incidence in the group III in relation to the other groups in which the number of WP post-atropine normalization was observed. There is a strong linear decreasing correlation between the PR interval of the ECG and the WP in individuals with WP less than or equal to 110 ppm. PR interval greatest than 0.24 ms corresponds better to WP below 110 ppm (mean 90 ppm) and the majority of these patients do not normalize the WP with the atropine. We suggest the term "first degree A-V block" for those cases with PR interval greater than 240 ms and "A-V depression" for the cases with PR interval shorter than 240 ms when recorded on the surface electrocardiogram and have been normalized with atropine.

Significance of ventricular pauses of three seconds or more detected on twenty-four-hour Holter recordings.

The natural history of patients with asymptomatic prolonged ventricular pauses and the indications for permanent pacing are controversial. To examine this problem, 6,470 consecutive 24-hour Holter recordings were reviewed between 1979 and 1983 for the presence of ventricular pauses of at least 3 seconds. Fifty-two patients (0.8% of total), 22 men and 30 women, were identified with an average longest pause duration of 4.1 seconds. Holter recordings were requested to evaluate syncope in 14 patients (27%), dizziness in 9 (17%) and other reasons in 29 (56%). Causes of the pauses were sinus arrest in 22 patients, atrial fibrillation with slow ventricular response in 18 patients and atrioventricular block in 12. Holter recordings were also evaluated for the presence of tachyarrhythmias. Six patients had nonsustained ventricular tachycardia and 7 had supraventricular tachycardia. Five of the 52 patients (10%) had dizziness or syncope during pauses. Twenty-six patients (50%) received permanent pacemakers. The paced (26 patients) and unpaced (26 patients) groups were similar in the length and etiology of pause, associated tachyarrhythmias, presence of bradycardia-related symptoms, prevalence of organic heart disease, medications and length of follow-up. Four patients in the paced group and 2 in the unpaced group died, yielding 3-year actuarial survival probabilities of 78% and 85%, respectively. It is concluded that ventricular pauses of 3 seconds or longer are uncommon, these pauses usually do not cause symptoms, and the presence of these pauses does not necessarily portend a poor prognosis or the need for pacing in asymptomatic patients.

Second-degree atrioventricular block

2:1 AV block In the case of 2:1 block (2 P waves for every QRS complex) it is impossible to differentiate type I from type II Mobitz block-based solely on the P:QRS ratio or on a pattern of lengthening PR intervals.:182 In this case, a lengthened PR interval with a normal QRS width is most likely indicative of a type I-like pathology, and a normal PR interval with a widened QRS is most likely indicative of a type II-like pathology.:182 See also Electrocardiogram (ECG or EKG) SA node AV node Atrioventricular block First-degree AV block Third-degree AV block References External links Cardiac arrhythmia

Diagnostic and prognostic value of intracardiac electrophysiological studies. Ten years of experience.

Ten years ago a clinical method of recording the electrical activity of the His bundle in man with transvenously inserted electrodes was described. His bundle recording has permitted the breakdown of the P-R interval into three conduction intervals, i.e., intraatrial (P-A), A-V nodal (A-H), and His-Purkinje system (H-V). His bundle studies have demonstrated our inability to accurately predict from the surface electrocardiogram the exact location of most A-V blocks. First- and second-degree A-V block can occur in the atrium, A-V node or His-Purkinje system, and third-degree A-V block in the A-V node or His-Purkinje system. However, Mobitz type II block almost always occurs below the A-V node. Intraventricular conduction defects, especially of the so-called bifascicular block, have a high incidence of H-V time prolongation, indicating additional disease of the third fascicle or the main His bundle. The prognostic value of a prolonged H-V time in patients with and without chronic conduction defects remains controversial, with some agreement that patients with unexplained syncope or dizziness, normal sinus rhythm and 1:1 conduction, who show prolonged H-V times, should probably be paced permanently. No long-term studies exist regarding the value of the H-V time in predicting death or A-V block in patients with conduction defects secondary to acute myocardial infarction, congenital heart disease or after cardiac surgery. Electrophysiological studies have been extremely useful in the diagnosis and management of patients with accessory pathways and in the evaluation of ventricular and supraventricular arrhythmias. The most valuable test in diagnosing sinus node dysfunction is the sinus node recovery time. A clearly abnormal test in a patient with unexplained syncope or dizziness predicts an almost one hundred per cent relief of symptoms with permanent pacing.


In a digital hypokratitis of recent onset in a smoking patient, the first option to rule out is bronchopulmonary carcinoma. Other pathologies can also occur but not so suddenly.

A former smoker patient, previously diagnosed with COPD comes in for a checkup. The physical examination reveals digital hypokratism of recent onset. What is the most acceptable explanation for this finding in the clinical context described?

Generalized emphysema and chronic obstructive pulmonary disease in a farmer, non-smoker - the more we seek, the more we find.

Although alpha-1 antitrypsin (A1AT) deficiency represents one of the most common genetically conditioned diseases in the population of Caucasian adult individuals, it is rarely diagnosed. Alpha-1 antitrypsin is an important component of the anti-proteolytic protection in the lungs. Individuals affected by the protein deficiency are exposed to a higher risk of developing chronic obstructive pulmonary disease (COPD), emphysema or liver diseases. A 52-year-old farmer, non-smoker, spraying orchards since the age of 15 years, was admitted to the Department with dyspnea at rest and productive cough. He had a medical history of COPD, congestive heart failure, generalized emphysema of ten years' duration On admission the patient's general condition was satisfactory (fair). Physical examination showed symmetric expiratory wheezing over the upper and lower fields of the lungs with loss of vesicular murmur in the lower fields. Spirometry revealed a severe chronic bronchial obstruction, and an arterial blood gas test showed hypoxemia. Laboratory tests demonstrated an increased concentration of inflammatory markers. High resolution computed tomography (HRCT) of the chest showed evidence of generalized emphysema, bronchiectasis and exacerbation of peribronchial inflammatory changes. Intensive anti-inflammatory, bronchodilator treatment and antibiotic therapy were implemented, which resulted in an optimal improvement of the patient's condition. Based on the whole clinical picture A1AT deficiency was suspected. Alpha-1-antitrypsin deficiency, MZ phenotype, with 65 mg/dl concentration was diagnosed. Diagnostic tests for alpha-1 antitrypsin deficiency should always be considered in patients with emphysema or symptomatic COPD identified at an early age. In the described case the period between occurrence of clinical signs and establishing the diagnosis was ten years, which proves that there is a strong need to spread knowledge on A1AT among medical professionals. Otherwise, most of the patients will lose their chance of modifying their lifestyle or receiving proper treatment that could prevent the progression of changes in the lungs.

Chronic obstructive pulmonary disease

A CT scan is not routinely used except for the exclusion of bronchiectasis. An analysis of arterial blood is used to determine the need for oxygen supplementation, and assess for high levels of carbon dioxide in the blood; this is recommended in those with an FEV1 less than 35% predicted, those with a peripheral oxygen saturation less than 92%, and those with symptoms of congestive heart failure. WHO recommends that all those diagnosed with COPD be screened for alpha-1 antitrypsin deficiency. Differential diagnosis COPD may need to be differentiated from other conditions such as congestive heart failure, asthma, bronchiectasis, tuberculosis, obliterative bronchiolitis, and diffuse panbronchiolitis. The distinction between asthma and COPD is made on the basis of the symptoms, smoking history, and whether airflow limitation is reversible with bronchodilators at spirometry. Chronic bronchitis with normal airflow is not classified as COPD.

[Prevalence and difficulties in chronic obstructive pulmonary disease diagnosis in patients suffering from severe peripheral arterial disease].

Cigarette smoking is the most prominent risk factor for chronic obstructive pulmonary disease (COPD) and peripheral arterial disease (PAD). Prevalence of COPD among cigarette smokers is about 23% in Poland. Effort dyspnea which develops in advanced stage of COPD is the leading cause of seeking medical advice. Physical activity among patients with PAD is reduced due to intermittent claudication. It may cause delayed COPD diagnosis in this group of patients. To estimate the prevalence of COPD among patients suffering from severe PAD who were hospitalized in surgery department due to critical limb ischemia and to evaluate difficulties during COPD diagnosis in this group of patients. We examined 64 patients suffering from severe PAD (at least IIb stage according to Fontaine's scale). Patients were asked about the typical symptoms of COPD: chronic cough, regular sputum production and dyspnea. To evaluate the intensity of dyspnea we used British Medical Research Council scale. Spirometry was performed to every patient. Patients with airways obstruction underwent spirometry after the administration of inhaled bronchodilator. Every patient who had the post-bronchodilator value of FEV,/FVC ratio below the lower limit of normal values was diagnosed with COPD. It was not possible to evaluate the dyspnea intensity using MRC scale in 44% of 34 patients who reported dyspnea. During the study we diagnosed 16 patients with COPD (9 pts had 1st stage of COPD according to GOLD classification, 7 pts--2nd). 9 patients had been formerly diagnosed with COPD (2 pts--1st stage, 5 pts--2nd, and 2 pts--3rd). Spirometry-defined COPD was present in 39% of study group. The analysis of data from patients with PAD coexistent COPD revealed that 60% of them were current cigarette smokers and 28% of them declared passive smoking exposure. The other known negative prognostic factors in patients with COPD such as BMI lower than 21 kg/mr2, FEV1% of predicted value below 65% and X-rays photograph visible emphysema were observed in 40%, 32% and 12% of patients with PAD and coexistent COPD respectively. Hypertension was present in 52% of patients with PAD and coexistent COPD, cardiac arterial disease in 52% and chronic heart failure due to cardiac arterial disease in 36%. Further analysis of laboratory tests revealed dyslipidemia and chronic kidney disease in 52% and 60% of these patients respectively. COPD diagnosis among patients suffering from severe PAD involves several difficulties such as uselessness of MRC dyspnea scale and frequent heart diseases which delay the COPD diagnosis being considered as primary dyspnea reason. Many factors which have been proven to be responsible for worse prognosis due to COPD were observed in patients with PAD and coexistent COPD. High prevalence of COPD among patients suffering from PAD suggests the spirometry as a COPD screening would be justified in that group.

[A study of comorbidity in patients with chronic obstructive pulmonary disease].

The impact of the chronic obstructive pulmonary disease (COPD) severity on the number of exacerbations, and the interdependence of COPD and some concomitant diseases were studied in chronic pulmonary patients. In order to determine the actual influence of some risk factors and comorbidity on the course of COPD, we conducted a study in two family medicine consulting offices, one in the city of Split and the other on the island of Brac. This retrospective study included a sample of 64 subjects, mean age 64.43 years, divided into two groups of 32 subjects each (group 1 and group 2). After taking history data and clinical examination, spirometry was performed. The severity of COPD was determined on the basis of lung function tests. There were 15 (46.9%) smokers in group 1, seven of them former smokers, and 20 (65.6%) smokers in group 2, eight of them former smokers. The groups differed significantly according to the mean number of annual exacerbations (1.3 in group 1 and 2.4 in group 2; p < 0.001). The frequency of exacerbations was higher in smokers and depended on the stage of COPD. If COPD was more severe, the exacerbations were more frequent and influenced the progression of irreversible functional changes on the lungs. Productive cough was more frequent in smokers. The correlation of concomitant diseases and degree of COPD was found in group 2 (hypertension, r = 0.305; p = 0.014). In group 1, there was correlation between patient age and concomitant disease (cardiac arrhythmias, r = 0.307; p = 0.013), whereas in group 2 it was significant in case of hypertension (r = 0.474; p < 0.001) and cardiomyopathy (r = 0.301; p = 0.016). Cigarette smoke causes chronic inflammatory changes in the lungs. In our study, the number of patients suffering from persistent cough accompanied by sputum was higher in group 2, which also comprised of more smokers, but differences between smokers and non-smokers according to this characteristic were not statistically significant. Study groups differed significantly according to the number of COPD exacerbations per year (with more exacerbations in the group with more smokers). In group 2, there was a correlation between COPD severity and hypertension. Comorbidity of COPD and cardiovascular diseases was confirmed, along with correlation between age and cardiovascular complications in patients with COPD.

Chronic obstructive pulmonary disease

Use of COPD Diagnostic Questionnaire alone or in combination with hand-held flow meters is appropriate for screening of COPD in primary care. Other tests A chest X-ray is not useful to establish a diagnosis of COPD but it is of use in either excluding other conditions or including comorbidities such as pulmonary fibrosis, and bronchiectasis. Characteristic signs of COPD on X-ray include hyperinflation (shown by a flattened diaphragm and an increased retrosternal air space) and lung hyperlucency. A saber-sheath trachea may also be shown that is indicative of COPD.

Pulmonary fibrosis

Based on these rates, pulmonary fibrosis prevalence in the United States could range from more than 29,000 to almost 132,000, based on the population in 2000 that was 18 years or older. The actual numbers may be significantly higher due to misdiagnosis. Typically, patients are in their forties and fifties when diagnosed while the incidence of idiopathic pulmonary fibrosis increases dramatically after the age of fifty. However, loss of pulmonary function is commonly ascribed to old age, heart disease or to more common lung diseases. References External links Lung disorders Wikipedia medicine articles ready to translate

Lung transplantation

Qualifying conditions Lung transplantation is the therapeutic measure of last resort for patients with end-stage lung disease who have exhausted all other available treatments without improvement. A variety of conditions may make such surgery necessary. As of 2005, the most common reasons for lung transplantation in the United States were: 27% chronic obstructive pulmonary disease (COPD), including emphysema; 16% idiopathic pulmonary fibrosis; 14% cystic fibrosis; 12% idiopathic (formerly known as "primary") pulmonary hypertension; 5% alpha 1-antitrypsin deficiency; 2% replacing previously transplanted lungs that have since failed; 24% other causes, including bronchiectasis and sarcoidosis.

Can moderate chronic obstructive pulmonary disease be diagnosed by historical and physical findings alone?

The value of the history and physical examination in diagnosing chronic obstructive pulmonary disease (COPD) is uncertain. This study was undertaken to determine the best clinical predictors of COPD and to define the incremental changes in the ability to diagnose COPD that occur when the physical examination findings and then the peak flowmeter results are added to the pulmonary history. Ninety-two outpatients with a self-reported history of cigarette smoking or COPD completed a pulmonary history questionnaire and received peak flow and spirometric testing. The subjects were independently examined for 12 physical signs by 4 internists blinded to all other results. Multivariate analyses identified independent predictors of clinically significant, moderate COPD, defined as a forced expiratory volume in 1 second (FEV1) less than 60% of the predicted value or a FEV1/FVC (forced vital capacity) less than 60%. Fifteen subjects (16%) had moderate COPD. Two historical variables from the questionnaire--previous diagnosis of COPD and smoking (70 or more pack-years)--significantly entered a logistic regression model that diagnosed COPD with a sensitivity of 40% and a specificity of 100%. Only the physical sign of diminished breath sounds significantly added to the historical model to yield a mean sensitivity of 67% and a mean specificity of 98%. The peak flow result (best cutoff value was less than 200 L/min) significantly added to the models of only one of the four physicians for a mean final sensitivity of 77% and a specificity of 95%. Subjects with none of the three historical and physical variables had a 3% prevalence of COPD; this prevalence was unchanged by adding the peak flow results. Diminished breath sounds were the best predictor of moderate COPD. A sequential increase in sensitivity and a minimal decrease in specificity occurred when the quality of breath sounds was added first to the medical history, followed by the peak flow result. The chance of COPD was very unlikely with a normal history and physical examination.

Northern Westchester Hospital

Cardio-Pulmonary Rehabilitation: Structured rehabilitation designed to manage a wide range of existing conditions for smokers and ex-smokers and those who have chronic obstructive pulmonary disease (COPD), emphysema, asthma, pulmonary fibrosis, interstitial lung disease, bronchiectasis, and cystic fibrosis. Wound Care & Hyperbaric Medicine: Providing wound care for chronic non-healing wounds related to various conditions such as diabetes and obesity, post-surgical non-healing wounds and traumatic wounds. Therapies available to patients include hyperbaric oxygen therapy (HBOT), provided in a multi-seat hyperbaric chamber. HBOT is not only prescribed for patients with wounds, such as diabetic foot ulcers or venous ulcers, but is also an effective treatment for such conditions as delayed radiation injury, compromised grafts and flaps, necrotizing soft tissue infections, intracranial abscess and severe anemia.

[Retrospective studies on 713 cases chronic obstructive pulmonary disease].

To study the diagnostic criteria of severity of chronic obstructive pulmonary diseases (COPD), early intervention, and the effect of health education on the relationship between smoking and health. Data from 713 remissive COPD patients who had results of pulmonary function test in the past 10 years were reviewed. All patients were classified by correlative diagnostic criteria, and the results were compared with the diagnostic criteria of WHO Global Initiative for chronic obstructive lung disease (GOLD). Other indexes such as history of smoking, quantity of smoking and the rate of giving up smoking were also analyzed. According to the diagnostic criteria set by the Chinese Respiratory College in 1997 and traditional pulmonary function criteria, 339 patients were identified as having severe COPD, taking up 56.0% of all COPD patients; 200 patients were moderate (28.0%); 114 patients were mild (16.0%). FEV(1)/FVC in mild COPD patients was 70.5% +/- 1.1%, higher than the criteria of 70% in GOLD. Three hundred and thirty-five patients were smokers, taking up 46.9% of total patients. In these patients, 312 patients were men (93%) and 23 patients were women (7%). The average smoking history was 32.9 years, and the average quantity of daily smoking was 22. Two hundred sixteen patients had given up smoking which took up 64.5% of all the smokers. It was debatable that FEV(1)/FVC was decisive criteria for COPD diagnoses by GOLD and the revised diagnostic criteria of Chinese Respiratory College in 2002. It might miss diagnosing a number of COPD patients who having combined ventilatory disturbance or were in earlier stages. Only 15.9% of mild COPD patients had seen a doctor, that indicated a very low rate of early intervention which was disadvantageous for the prevention and cure of COPD. In contrast to the rate of 28.0% when giving up smoking in ordinary people who had received general intervention, the rate of giving up smoking in COPD patients remained 64.5% much higher and was dissatisfactory. Health education should be improved to include measures to give up smoking.

Acute severe asthma

Differential diagnoses Allergic bronchopulmonary aspergillosis Aspiration Syndromes Bronchiectasis Bronchiolitis Bronchiolitis obliterans Chronic bronchitis Chronic Obstructive Pulmonary Disease (COPD) Eosinophilic Granulomatosis with Polyangiitis (Churg–Strauss Syndrome) Croup Cystic Fibrosis Emphysema Foreign Bodies of the Airway Gastroesophageal Reflux Disease Heart Failure Idiopathic Pulmonary Arterial Hypertension Inhalation injury Pulmonary Artery Sling Vocal Cord Dysfunction

[The differential diagnosis of chronic bronchitis and emphysema from mutually supplemental functional and radiographic criteria].

In a retrospective study in 91 patients an attempt was made to differentiate the primary and/or predominating disorder "emphysema" or/and "chronic bronchitis" by independent evaluation of a number of X-ray signs and lung function criteria in routine diagnosis. Good congruency of the diagnosis from these two different aspects, could be established. Patients with 3 or more X-ray signs of emphysema were found to have larger lung volume and smaller diffusing capacities than those without. Vice versa, patients with functional diagnosis of predominant emphysema more often showed the full X-ray pattern of emphysema, than those with predominant "chronic bronchitis". In either method of diagnostic procedure, the occurence of the "small heart of emphysema" was obviously much more frequent in patients believed to have predominant or primary emphysema. Assessment of X-ray signs of changes of the lesser circulation can be obtained in a stage of the disease, when structural changes have become irreversible. Considering the different pathophysiologic pattern of predominant panacinar emphysema, the destruction of alveolar walls and, consequently of the capillary bed, is more likely to reduce DCO as well as cardiac output before pulmonary hypertension can develop. The X-ray signs resulting from this effect on the lesser circulation, exist in widened right hilar branch and abrupt narrowing of peripheral vessels, with a small heart and lack of prominence of the pulmonary trunk. In chronic bronchitis, however, signs of pulmonary hypertension are expected to occur early in the disease. The relevance of the X-ray changes of the heart size and the pulmonary circulation in both types of lung disease, could be confirmed by lung function data.

Obstructive lung disease

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling, and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms, and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease. Types Asthma

Prevalence of chronic obstructive pulmonary disease in Japanese people on medical check-up.

In Japan, spirometry has not been included as an item in medical check-ups for all persons. The purpose of this study was to show evidence to recommend spirometry routinely on medical check-up for the early detection of chronic obstructive pulmonary disease (COPD). There were 12,760 enrolled persons who underwent medical check-up. COPD was defined as a ratio of forced expiratory volume in one second to slow vital capacity of 70% or less. We investigated the prevalence and its characteristics of COPD in people on medical check-up. The prevalence of COPD was 3.6% in all subjects, 4.5% in males, and 1.8% in females. In the comparison between males and females, the prevalence of COPD in males of most age groups was higher than that of females, and this difference was greater with aging. Males in their 50s and over 60 years old and females over 60 years old showed remarkably high prevalences. Occupations associated with a high smoking rate such as transportation-related occupations showed a higher prevalence of COPD. These results suggest that spirometry for all persons in medical check-ups can identify many COPD patients not aware of this disease. Spirometry should be carried out routinely on medical check-up.

Pulmonary rehabilitation

Background Pulmonary rehabilitation is generally specific to the individual patient, with the objective of meeting the needs of the patient. It is a broad program and may benefit patients with lung diseases such as chronic obstructive pulmonary disease (COPD), sarcoidosis, idiopathic pulmonary fibrosis (IPF) and cystic fibrosis, among others. Although the process is focused primarily on the rehabilitation of the patient, the family is also involved. The process typically does not begin until a medical examination of the patient has been performed by a licensed physician. The setting of pulmonary rehabilitation varies by patient; settings may include inpatient care, outpatient care, the office of a physician, or the patient's home. Although there are no universally accepted procedure codes for pulmonary rehabilitation, providers usually use codes for general therapeutic processes.

Respiratory disease

Obstructive lung disease Asthma, chronic bronchitis, bronchiectasis and chronic obstructive pulmonary disease (COPD) are all obstructive lung diseases characterised by airway obstruction. This limits the amount of air that is able to enter alveoli because of constriction of the bronchial tree, due to inflammation. Obstructive lung diseases are often identified because of symptoms and diagnosed with pulmonary function tests such as spirometry. Many obstructive lung diseases are managed by avoiding triggers (such as dust mites or smoking), with symptom control such as bronchodilators, and with suppression of inflammation (such as through corticosteroids) in severe cases. One common cause of COPD including emphysema, and chronic bronchitis, is tobacco smoking, and common causes of bronchiectasis include severe infections and cystic fibrosis. The definitive cause of asthma is not yet known. Restrictive lung diseases

Early detection of COPD: a case finding study in general practice.

To estimate the prevalence of undiagnosed chronic obstructive pulmonary disease (COPD) in a population of general practice patients at risk for developing COPD. A further aim was to evaluate the presence of respiratory symptoms as a predictor for the diagnosis of COPD. This study was conducted by eight general practitioners (GP) in six semi-rural general practices. During two consecutive months all patients attending their GP were included if they met the following criteria: current smokers between 40 and 70 yr of age, and a smoking history of at least 15 pack-years. A questionnaire regarding smoking history, respiratory symptoms, exposure to dust or chemical fumes, and history of respiratory diseases was completed for all patients. Subjects without known COPD were invited for spirometric testing. Off the 146 general practice patients included, 17.1% already had an established COPD diagnosis. Screening by spirometry revealed a 46.6% prevalence of COPD. Underdiagnosis of COPD was more frequent in the younger age categories (40-49 Yr; 50-59 Yr). Objective wheezing was the only sign that was significantly more frequent in COPD patients than in non-COPD patients (P<0.001). Patients with previously known COPD were significantly older, and complained more of chronic cough and fatigue than newly detected patients. Almost half of a general practice population of current smokers between 40 and 70 years of age, with a smoking history of at least 15 pack-years, was diagnosed with COPD, and roughly two thirds of these were newly detected as a result of the case finding programme.

Nontuberculous mycobacteria

Rapidly growing NTMs are implicated in catheter infections, post-LASIK, skin and soft tissue (especially post-cosmetic surgery) and pulmonary infections. Pathogenesis The most common clinical manifestation of NTM disease is lung disease, but lymphatic, skin/soft tissue, and disseminated diseases are also important. Pulmonary disease caused by NTM is most often seen in postmenopausal women and patients with underlying lung disease such as cystic fibrosis, bronchiectasis, and prior tuberculosis. It is not uncommon for alpha 1-antitrypsin deficiency, Marfan syndrome, and primary ciliary dyskinesia patients to have pulmonary NTM colonization and/or infection. Pulmonary NTM can also be found in individuals with AIDS and malignant disease. It can be caused by many NTM species, which depends on region, but most frequently MAC and M. kansasii.

Poor sensitivity of symptoms in early detection of COPD.

The prevalence of chronic obstructive pulmonary disease (COPD) has been increasing. However, COPD is often underdiagnosed. The objective of this study was to determine how many outpatients had persistent airflow limitation and could be diagnosed as COPD by post-bronchodilator spirometry. We also evaluated whether the newly diagnosed patients had any symptoms. All outpatients with liver or general diseases over 40 years old who regularly visited to our hospital were tested for pulmonary function by spirometry. Patients with airflow limitation by the first screening spirometry had further examinations including post-bronchodilator spirometry and chest radiograph by pulmonary specialists. A total of 288 patients accepted a first spirometry. The most common chronic diseases of these patients were chronic hepatitis (33.7%), fatty liver (26.4%), liver cirrhosis (8.3%), diabetes (3.5%) and hypertension (3.1%). Approximately half of the patients had a smoking history. 44 of 288 patients (15.3%) showed airflow limitation by pre-bronchodilator spirometry. Of these, 8 patients did not show airflow limitation by a repeat pre-bronchodilator spirometry nor did 5 patients by post-bronchodilator spirometry. The rest were diagnosed as COPD (80.6%), asthma (16.1%) and bronchiectasis (3.2%). The prevalence of COPD was 8.7%. Approximately half of the patients (13/25, 52.0%) diagnosed as COPD had never complained of any respiratory symptoms. Because symptoms such as dyspnea on exertion, cough and sputum are less sensitive for the diagnosis of COPD, the propagation of spirometry in a general practice/setting should be recommended for establishing the diagnosis rate of COPD rather than relying on the presence of respiratory symptoms.

Pulmonary rehabilitation

Medical uses The NICE clinical guideline on chronic obstructive pulmonary disease states that “pulmonary rehabilitation should be offered to all patients who consider themselves functionally disabled by COPD (usually MRC [Medical Research Council] grade 3 and above)”. It is indicated not only in patients with COPD, but also in: Cystic fibrosis Bronchitis Sarcoidosis Idiopathic pulmonary fibrosis Before and after lung surgery It appears not to be harmful and may be helpful for interstitial lung disease. Aim To reduce symptoms To improve knowledge of lung condition and promote self-management To increase muscle strength and endurance (peripheral and respiratory) To increase the exercise tolerance To reduce length of hospital stay To help to function better in day-to-day life To help in managing anxiety and depression

Course of pulmonary hemodynamics in patients with chronic obstructive pulmonary disease.

Eighty-five patients with chronic obstructive pulmonary disease, mainly chronic bronchitis (71 patients), who had arterial hypoxemia and moderate to severe obstruction of the airways underwent at least two right cardiac catheterizations in a clinical steady state, with a delay of three years or more between the first and the last catheterization. The average delay was 60 +/- 19 months (range, 36 to 119 months). Patients were regularly examined (quarterly clinical and functional checkups). The changes in pulmonary hemodynamic data were small. In the group of 53 patients with an initial mean pulmonary arterial pressure of 20 mm Hg or less, this pressure varied from 15.4 +/- 3.1 to 18.3 +/- 6.6 mm Hg (P less than 0.001); in the group of 32 patients with an initial mean pulmonary arterial pressure greater than 20 mm Hg, this pressure varied from 27.7 +/- 6.0 to 31.0 +/- 9.3 mm Hg (P less than 0.05). The mean pulmonary arterial pressure increased by 5 mm Hg or more in only 28 patients. In these patients with hemodynamic "worsening," the final arterial oxygen pressure (PaO2) was lower and the final arterial carbon dioxide tension was higher than in the remaining patients. A significant negative correlation (r = -0.39; P less than 0.001) was observed between changes in PaO2 and mean pulmonary arterial pressure. There was a generally good agreement between the course of pulmonary hemodynamics (mean pulmonary arterial pressure), on the one hand, and the clinical, radiologic (transverse diameter of the heart), and electrocardiographic evolution, on the other hand. In the 33 patients who died, a relatively long survival was observed after the first episode of right-sided heart failure or after ascertaining pulmonary hypertension.

Royal Papworth Hospital

the Respiratory Support and Sleep Centre, providing services for patients with sleep disorders (including common disorders such as obstructive sleep apnea and less common ones such as narcolepsy) and those with ventilatory failure (from conditions such as COPD or neuromuscular disorders including motor neuron disease and poliomyelitis). The service provides non-invasive ventilation and also accepts referrals from other intensive care units to wean patients from invasive ventilation; the pulmonary hypertension (PH) service (Papworth is one of the four UK Pulmonary Hypertension centres and the only one providing pulmonary thromboendarterectomy); the adult cystic fibrosis service; the Lung Defense service, for patients with recurrent lung infection, including those with bronchiectasis and immunodeficiency; the thoracic oncology (lung cancer) service; the ataxia telangiectasia service;

[Clinical aspects and outcome of COPD].

Chronic obstructive pulmonary disease (COPD) is a frequent disease which is too often diagnosed when already severe. Major known risk factors are tobacco smoking, occupational exposure, and severe respiratory infections during childhood. Diagnostic should be evoked on functional non specific symptoms: chronic cough and sputum, progressive dyspnea. Some physical signs, correlated with the degree of airway obstruction, may be more specific but their diagnostic value remains to be assessed. These signs reflect distension of the chest as well as airway obstruction: pursed lips breathing, increased expiration duration, Hoover and Campbell signs, inspiratory contraction of scalen muscles. COPD results over years in chronic respiratory insufficiency and evolution is associated with episodes of bronchial and parenchymal infections as well as pulmonary emboli which are particularly frequent in these patients.

Pneumonia

Differential diagnosis Several diseases can present with similar signs and symptoms to pneumonia, such as: chronic obstructive pulmonary disease, asthma, pulmonary edema, bronchiectasis, lung cancer, and pulmonary emboli. Unlike pneumonia, asthma and COPD typically present with wheezing, pulmonary edema presents with an abnormal electrocardiogram, cancer and bronchiectasis present with a cough of longer duration, and pulmonary emboli present with acute onset sharp chest pain and shortness of breath. Mild pneumonia should be differentiated from upper respiratory tract infection (URTI). Severe pneumonia should be differentiated from acute heart failure. Pulmonary infiltrates that resolved after giving mechanical ventilation should point to heart failure and atelectasis rather than pneumonia. For recurrent pneumonia, underlying lung cancer, metastasis, tuberculosis, a foreign bodies, immunosuppression, and hypersensitivity should be suspected.

[Clinical, functional and hemodynamic course in patients with chronic bronchitis at the stage of chronic cor pulmonale].

Twenty seven patients, almost all chronic bronchitic, and with a "chronic cor pulmonale" according to the E. C. G., were followed clinically, radiologically and for E. C. G. and pulmonary functions, and also for the hemodynamics, during a minimum of 3 years, the average length of observation period being about 5 years. Twelve patients died during this observation time. Periods of right heart failure (R. H. F.) were frequent : 3.6 +/- 3.0 in average, slightly more frequent in the deceased patients than in the others. The average delay between the onset R. H. F. and death was of 49.3 +/- 30.8 months ; the survivors on average lived another 54.6 +/- 30.8 months after their first R. H. F. The mean pulmonary arterial pressure (PAP) was quite stable, going from 27.5 +/- 7.0 to 31.2 +/- 9.6 torr (an unsignificicant difference); in only 9 cases did the PAP increase of more than 5 torr during the observation period (acute attacks excepted). The PAP evolution was not significantly different in the deceased and the survivors. PAP worsening by steps after a fit of R. H. F. was observed in only 4 cases. Chronological variations of PAP were well correlated with those of Pao2 during the same period : r = -- 0.68, P less than 0.001. The hemodynamic evolution (PAP), that of the E. C. G. and the volume of the heart were reasonably parallel to the overall clinical evolution ; the E. C. G. evolution had the closest match with the overall clinical evolution (78% of cases). The E. C. G. enables only a late diagnosis of CCP but its evolution is very valuable for prognosis. Hemodynamic tests have a double value initially for diagnosis and later for the evolution.

Lung

Obstructive lung diseases Asthma, bronchiectasis, and chronic obstructive pulmonary disease (COPD) that includes chronic bronchitis, and emphysema, are all obstructive lung diseases characterised by airway obstruction. This limits the amount of air that is able to enter alveoli because of constriction of the bronchial tree, due to inflammation. Obstructive lung diseases are often identified because of symptoms and diagnosed with pulmonary function tests such as spirometry. Many obstructive lung diseases are managed by avoiding triggers (such as dust mites or smoking), with symptom control such as bronchodilators, and with suppression of inflammation (such as through corticosteroids) in severe cases. A common cause of chronic bronchitis, and emphysema, is smoking; and common causes of bronchiectasis include severe infections and cystic fibrosis. The definitive cause of asthma is not yet known.

[Chronic obstructive pulmonary disease as frequent secondary diagnosis at medical department].

Patients with Chronic Obstructive Pulmonary Disease (COPD) often suffer from comorbidities. This study evaluates the need for hospitalization due to comorbidity in COPD patients and the diagnoses these patients have, and it investigates whether COPD comorbidity prolongs the hospital stay. A cross-sectional study performed at a department of internal medicine. A total of 66 of the 101 possible participants were included. They performed a spirometry and filled-in a questionnaire. Furthermore, patients' case records were studied for evaluation of final diagnoses and length of stay. 39% (26/66) suffered from COPD. 54% (14/26) were diagnosed at our examination. 35% had moderate COPD, 26% severe COPD and 19% very severe COPD. 43% (6/14) of the patients with no former knowledge of their COPD had severe or very severe COPD. The COPD patients had accumulated significantly more pack years (p < 0.005) and there were significantly more smokers (p = 0.05) among them compared with patients with no COPD. 38% (10/26) had several concurrent chronic diseases. The admission period was not significantly longer for patients with COPD than for those with no COPD (p = 0.07). The need for hospitalization due to comorbidity in COPD patients significantly exceeded the 20% expected to suffer from COPD in comparative age-groups of the general Danish population (p < 0.05).

Chronic obstructive pulmonary disease

Subtypes The two classic emphysematous and chronic bronchitic phenotypes are fundamentally different conditions with unique underlying mechanisms. It has since been recognized that COPD is more complex, with a diverse group of disorders of differing risk factors and clinical courses that has resulted in a number of other subtypes or phenotypes of COPD being accepted, and proposed. Spirometry measures are inadequate for defining phenotypes, and chest X-ray, CT and MRI scans have been mostly employed. Most cases of COPD are diagnosed at a late stage and the use of imaging methods would allow earlier detection and treatment. The identification and recognition of different phenotypes can guide appropriate treatment approaches. For example the PDE4 inhibitor roflumilast is targeted at the chronic-bronchitic phenotype.

Idiopathic pulmonary fibrosis

Differential diagnosis Recognizing IPF in clinical practice can be challenging as symptoms often appear similar to those of more common diseases, such as asthma, chronic obstructive pulmonary disease (COPD) and congestive heart failure (www.diagnoseipf.com). The key issue facing clinicians is whether the presenting history, symptoms (or signs), radiology, and pulmonary function testing are collectively in keeping with the diagnosis of IPF or whether the findings are due to another process. It has long been recognized that patients with ILD related to asbestos exposure, drugs (such as chemotherapeutic agents or nitrofurantoin), rheumatoid arthritis and scleroderma/systemic sclerosis may be difficult to distinguish from IPF. Other differential diagnostic considerations include interstitial lung disease related to mixed connective tissue disease, advanced sarcoidosis, chronic hypersensitivity pneumonitis, pulmonary Langerhan's cell histiocytosis and radiation-induced lung injury.

Early Detection of Chronic Obstructive Pulmonary Disease in Primary Care.

Objective To evaluate the effectiveness of an early detection program for chronic obstructive pulmonary disease (COPD) in a primary care setting in Japan. Methods Participants of ≥40 years of age who regularly visited a general practitioner's clinic due to chronic disease were asked to complete a COPD screening questionnaire (COPD Population Screener; COPD-PS) and undergo simplified spirometry using a handheld spirometric device. Patients who showed possible COPD were referred to a respiratory specialist and underwent a detailed examination that included spirometry and chest radiography. Results A total of 111 patients with possible COPD were referred for close examination. Among these patients, 27 patients were newly diagnosed with COPD. The patients with COPD were older, had lower BMI values, and had a longer smoking history in comparison to non-COPD patients. COPD patients also had more comorbid conditions. A diagnosis of COPD was significantly associated with a high COPD-PS score (p<0.001) and the detection of possible airflow limitation evaluated by the handheld spirometric device (p<0.01). An ROC curve analysis demonstrated that 5 points was the best COPD-PS cut-off value for the diagnosis of COPD. The combination of both tools showed 40.7% of sensitivity and 96.4% of specificity. Conclusion The use of the COPD-PS plus a handheld spirometric device could facilitate the early detection of undiagnosed COPD in primary care.

Comparison of frequency of undiagnosed chronic obstructive pulmonary disease in current or former tobacco smokers having ischaemic heart disease.

This study compares the frequency of undiagnosed chronic obstructive pulmonary disease (COPD) in tobacco smokers suffering from ischaemic heart disease (IHD) and analyses the association of COPD severity with status, type and duration of smoking. An analytical cross-sectional study conducted in current and former cigarette, hookah and combined cigarette and hookah smokers with IHD to detect previously undiagnosed COPD through spirometry. Among 124 males with IHD, majority [74 (59.7%)] were former smokers and were in the age ranged between 42 to 78 years. All had dyspnoea up to grade 4 and 64 (51.6%) also reported chronic cough and sputum production. According to type of smoking, 64 (51.6%) smoked cigarettes, 30 (24.2%) smoked hookah and 30 (24.2%) smoked both hookah and cigarettes. Forty-seven (37.9%) were found to have COPD, 24 (37.5%) among cigarette smokers, 12 (40%) among hookah smokers, while 11 (36.7%) were from cigarette and hookah smokers. Duration of smoking, its type and magnitude had no association with severity of COPD. The frequency of undiagnosed COPD is high in smokers with IHD. Hookah and combined hookah and cigarette smokers are almost as susceptible to develop COPD as are cigarette smokers.

Nail clubbing

Causes Clubbing is associated with Lung disease: Lung cancer, mainly non-small-cell (54% of all cases), not seen frequently in small-cell lung cancer (< 5% of cases) Interstitial lung disease most commonly idiopathic pulmonary fibrosis Complicated tuberculosis Suppurative lung disease: lung abscess, empyema, bronchiectasis, cystic fibrosis Mesothelioma of the pleura Arteriovenous fistula or malformation Sarcoidosis Heart disease: Any disease featuring chronic hypoxia Congenital cyanotic heart disease (most common cardiac cause) Subacute bacterial endocarditis Atrial myxoma (benign tumor) Tetralogy of Fallot Gastrointestinal and hepatobiliary: Malabsorption Crohn's disease and ulcerative colitis Cirrhosis, especially in primary biliary cholangitis Hepatopulmonary syndrome, a complication of cirrhosis Others: Graves' disease (autoimmune hyperthyroidism) – in this case it is known as thyroid acropachy