Jugular Venous Pulse Research Articles

Meaningful Use of Health Information Technology Is Managing Information

PHYSICIANS ENCOUNTERING A NEW TECHNOLOGY SUCH as electronic health records (EHRs) typically use it to solve the same problems they were trying to address with older technologies. It takes time to determine that the new technology creates entirely new possibilities for practice. For instance, when the electrocardiogram was first invented, it was thought to be a better version of an older technology, the Mackenzie polygraph. The Mackenzie instrument, which made a simultaneous visible record of mechanical events (radial pulse, jugular venous pulse) in the cardiac cycle, was a powerful tool in unlocking the problem of cardiac arrhythmia. Initially, the electrocardiogram was considered simply a “better polygraph” and was used only to understand arrhythmias. Because the T wave and ST segment do not have mechanical equivalents, early electrocardiographers ignored them, overlooking tracing changes now considered classic for acute myocardial infarction. Similarly—but perhaps not surprisingly—physicians today often consider the EHR to be simply a better version of the paper chart. The old problem many physicians are trying to solve with an EHR is the efficient generation of a progress note—a document used to justify payment in a fee-for-service system, in which an office visit is the unit of value. This could explain the incomplete adoption of EHRs documented in many studies. For instance, in a 2005 survey, 16% of physicians using an EHR with the capacity to electronically generate prescriptions were still writing prescriptions by hand. In a 2008 survey that defined comprehensive use as using 4 domains of electronic capabilities (recording patient health information and data, order entry, results management, and decision support), only 4% of physicians reported comprehensively using all 4 domains in their practices, and 13% reported only “basic use,” ie, using portions of 3 domains. Perhaps the gap between potential and actual use results from physicians focusing on the word-processing capacity of EHRs, the only capacity needed if the goal is to produce progress notes documenting visits. One study of the financial implications of EHR adoption in small medical practices found that 51% of the financial return came from more aggressive fee-for-service coding and more frequent use of higher-level primary care billing codes, both supported by more comprehensive documentation. If the goal is to justify billing codes to an auditor, word processing is all that is needed. However, primary care practice poses a different problem: managing the massive amount of information received about patients every day and using it quickly, efficiently, and safely to meet patients’ needs. Word processing does not help do that. An analysis of the work in our primary care office revealed that, on average, there were 18.1 office visits per physician per day. In addition to visits, however, 12.1 prescriptions were refilled, 31.5 laboratory panels or imaging reports were reviewed, and 23.7 phone calls were processed. Each of these activities demands ready access to information. When reviewing a cholesterol test result, physicians need to know if the patient has diabetes, when the last cholesterol reading was obtained and what the level was, what medications the patient is currently taking, and perhaps the patient’s most recent blood pressure. If physicians understood their work to be responding safely and efficiently to these requests—none of which generate revenue in a primary care office—they would make very different use of health information technology. Many physicians are pleased to have laboratory results scanned into the EHR; the resulting PDF document is at least never lost and is readily accessible to the physician from any computer. Although these are major advances over a paper filing system, none of the information in that document can be manipulated by the EHR, because these unstructured data are retrievable only in a cumbersome fashion. They cannot be graphed or trended, nor can they be used to generate reports (eg, all patients with hemoglobin A1C levels 9%) unless entered into the EHR as structured data. It is imperative that physicians understand and start to use this capacity of EHRs, even though it is not immediately rewarding to do so in the current environment. Our office has been storing and recording all information relevant to the care of patients in an EHR since July 2004, assuming that all information stored electronically could be easily searched and retrieved electronically. That assumption proved incorrect; the current technology supporting EHRs simply does not work that way. For instance,

Atrial interaction in the form of ‘cross talk’ in patients with ventricular outflow tract obstruction

The Bernheim 'a' wave in the jugular venous pulse of patients with left ventricular hypertrophy has been shown to reflect accentuated right atrial activity. To study possible atrial interaction in patients with right and left ventricular outflow tract obstruction due to significant pulmonary (PS) and aortic valvular stenosis (AS) respectively. We studied 41 PS patients (age 36 ± 10 year) and 41 AS patients (age 35 ± 12 year) and their results were compared with those of 27 controls (age 30 ± 7 year). RV and LV filling were recorded by conventional PW Doppler. Biventricular segmental function was studied using the PW tissue Doppler imaging (TDI) and M-mode techniques. The 2 patient groups had similar degree of ventricular outflow tract obstruction. Long axis function was impaired while global systolic function was preserved in the pressure-overloaded ventricle. Patients had higher peak late filling (A wave) and TDI late diastolic (Aa) velocities recorded in the disease-free ventricles despite having similar peak early filling velocities (E wave), E wave deceleration time and E/Ea ratios were not different from controls (p > 0.05 for all). Such accentuation of atrial activity (A wave) was moderately correlated with the degree of contralateral ventricular outflow tract obstruction (p < 0.001 for both). Long axis function is more sensitive than global function in revealing myocardial dysfunction in the pressure-overloaded ventricles. The increased contralateral atrial systolic activity suggests an evidence for atrial interaction in the form of 'cross talk'.

Surgical Management of Ischemic Mitral Regurgitation

Case presentation: A 62-year-old man visited his cardiologist describing a 6-month history of increasing fatigue and shortness of breath on exertion. His medical history included an inferoposterior myocardial infarction (MI) 3 years previously that was treated with drug-eluting stents to his left circumflex and right coronary arteries. The result of physical examination was remarkable for crackles audible throughout the lower half of both lung fields, an elevated jugular venous pulse to the angle of the jaw, and a grade 3/6 holosystolic murmur loudest at the apex with radiation to the left axilla. An echocardiogram revealed a left ventricular ejection fraction (LVEF) of 15% to 20%, severe mitral regurgitation (MR), and a left ventricular end systolic dimension of 70 mm. The patient underwent a repeat cardiac angiogram that revealed patent stents in the circumflex and right coronary arteries and no other significant stenoses. The decision was made to surgically correct the patient’s MR with a mitral valve operation. He was brought to the operating room, where he was given general anesthesia, and a transesophageal echocardiogram was performed. Examination of the mitral valve revealed poor leaflet coaptation with a degree of leaflet tethering that resulted in severe MR. Inasmuch as the valve leaflets appeared structurally normal, a mitral valve repair procedure using a complete rigid annuloplasty ring was performed. A postoperative echocardiogram revealed trace MR, and the patient experienced no postoperative complications. This patient is a typical example of a growing problem in our aging population, namely, ischemic mitral regurgitation (IMR). IMR clearly has a negative impact on survival in patients with coronary artery disease, even in patients with mild to moderate MR; greater degrees of MR portend an even worse prognosis.1 With almost a fifth of patients who experience an MI followed by the development of IMR,2,3 and over …

Heart Failure and Cardiac Involvement as Isolated Manifestation of Familial Form of Transthyretin Amyloidosis Resulting From Val30Met Mutation With No Clinical Signs of Polyneuropathy

A 63-year-old white man with a 6-month history of progressive exertional dyspnea was referred for evaluation. In 1997, he presented an episode of unconsciousness as first symptom of a cardiac disease. In 2003, arterial hypertension, as well as atrioventricular block Mobitz type I, was diagnosed. A worsening of the biventricular heart failure over the last 2 years led to his admission at our clinic in 2008, with dyspnea at rest and bilateral pleural effusions. At admission, the patient appeared to be well, with a blood pressure of 142/76 mm Hg and a pulse of 97 bpm. Jugular venous pulse was not elevated, but mild bilateral edema of the lower extremities was noted. The lungs were clear to auscultation, with attenuation on the right side because of pleural effusion. The patient’s symptoms improved slightly through pharmacological therapy, but he remained in New York Heart Association functional class III heart failure. Laboratory studies revealed normal blood cell counts and electrolyte panel, with signs of load on the right side of the heart. The highest B-type natriuretic peptide was 818.6 pg/mL (normal, <100 pg/mL). The 24-hour urine protein collection was outside of normal limits at 0.27 g (normal, <0.15 g), and glomerular filtration rate according to the modified …

An unusual presentation of a tumour of the heart

A 62-year-old woman with a long-standing history of dyspnoea on exertion (NYHA class II) presented with worsening dyspnoea (NYHA class III) since 2 weeks. Clinical examination revealed a right parasternal heave, an elevated jugular venous pulse, bilateral ankle oedema, and a systolic ejection murmur, most pronounced at the upper left sternal edge, consistent with cor pulmonale. Electrocardiogram showed sinus rhythm with left posterior fascicular block, inverted T waves over …

Treatment of Mycoplasma wenyonii Infection in Cows with Imidocarb Dipropionate Injection-acupuncture

Sixteen shorthorn cows from Xiazhuang farm were admitted to the Veterinary Teaching Hospital at the College of Animal Science and Veterinary Medicine, Shandong Agricultural University for evaluation of poor appetite, listlessness, fever, tachycardia, tachypnea, lethargy, positive jugular venous pulse and anemia. Blood smear examination and polymerase chain reaction analysis in these cows revealed an infection with Mycoplasma wenyonii. The subjects were divided into two groups: control group (three cows) treated with intramuscular injection with imidocarb dipropionate (3 mg/kg/day for 2 days) and the experimental group (13 cows), treated with injection-acupuncture (Imidocarb Dipropionate, 1 mg/kg, once every 3 days for 6 days) at BL17, BL18, BL20, BL25, ST36, SP06 and CV04. At day 15, negative results were found using blood smear examination in all control and experimental groups.

A 32‐year‐old woman with arthralgias and severe hypotension

A 32‐year‐old woman with arthralgias and severe hypotension

Acute Hepatitis C in a Post-Lung Transplant Patient

Purpose: Fibrosing cholestatic hepatitis is a rare, aggressive, and usually fatal form of viral hepatitis found in immunosuppressed patients. It has been reported in solid organ and bone marrow transplant recipients. We report a case of acute hepatitis C related FCH in a post-lung transplant patient. Methods: A 72 year old man who underwent a right lung transplantation nine months prior, came to the emergency department with jaundice. He reported 3–4 weeks of fatigue and one week of jaundice and tea-colored urine. He noted pruritis and easy bruising. Past medical history included COPD status post a single-right lung transplantation. His post-transplant course was complicated by CMV treated with valgancyclovir, and one episode of acute cellular rejection treated with solumedrol. His medications included tacrolimus, mycophenolate sodium, prednisone, bactrim, pravastatin, and valganciclovir. Results: His examination revealed a thin, frail man with normal vital signs, scleral icterus, jaundice, and multiple ecchymoses. He had no asterixis or spider angiomata. His jugular venous pulse was not elevated. His mental status was normal. Admission labs showed a bilirubin of 16.1 mg/dL, alkaline phosphatase 442 U/L, AST 175 U/L, and ALT 115 U/L. Serologies including HAV, HBV, HCV, and EBV were normal. CMV PCR showed undetectable virus. Contrasted CT showed ascites without vascular obstruction and no biliary ductal dilation. Liver biopsy showed a mild mixed portal infiltration consisting of lymphocytes, neutrophils, and rare plasma cells. Bile ducts showed mild distortion. There was focal interface hepatitis and mild bile ductular proliferation. Mild lobulitis was present with scattered hepatocyte apoptosis. Multiple foci of bile plugs, intracanalicular and hepatocyte cholestasis, perivenular fibrosis and hepatic venular dilation were noted. These findings were consistent with acute hepatitis C with a suggestion of fibrosing cholestatic hepatitis. All hepatotoxic medications were stopped and immunosuppression was minimized. His condition continued to deteriorate. He developed hepatic encephalopathy and progressive jaundice despite the administration of lactulose and aggressive supportive care. On day 13 of his hospitalization Hepatitis C quantitative PCR revealed over 5,000,000 copies/mL. His clinical status continued to worsen and he died after being transitioned to hospice care. Conclusion: Acute hepatitis C and fibrosing cholestatic hepatitis is a rapidly progressive form of hepatic dysfunction. There is no effective treatment of FCH in immunosuppressed patients. Reduction of immunosuppressive medications is the only feasible option. This case represents a rare presentation of acute Hepatitis C and FCH in a post-lung transplant patient.

Jugular Venous Pulse: Window into the Right Heart

Although physicians began associating conspicuous neck veins with heart disease almost three centuries ago, the jugular venous pulse remains an often ignored component of the physical examination. Many physicians have not invested in the necessary understanding of the technique, and there is a misconception that its examination is difficult and of limited clinical value. When performed properly, evaluation of the jugular venous pulse can be extremely useful in distinguishing the cause of dyspnea and edema. The normal jugular venous pulse is reviewed, and pulse wave abnormalities are described, including ways in which they can provide clues to the diagnosis of certain disease states, ranging from pericardial disease to conduction disturbances. The jugular venous pulse provides a window into the right heart and an occasional glimpse of left heart hemodynamics. By peering through this window, clinicians can gain valuable information in the diagnostic evaluation of the cardiovascular patient.

Back to Basics: Editorial Review of “Jugular Venous Pulse: Window into the Right Heart”

Back to Basics: Editorial Review of “Jugular Venous Pulse: Window into the Right Heart”

Cardiac Herniation and Volvulus with Acquired Dextrocardia: Echocardiographic Diagnosis

We report an extremely rare cause of elevated jugular venous pulse where two esoteric causes for the same-cardiac volvulus and cardiac herniation have occurred together. Echocardiographic evidence for making the diagnosis of cardiac volvulus--subcostal long axis, subcostal short axis, and suprasternal views--have been presented. Awareness of this complication is necessary as immediate intervention is mandatory for a positive outcome.

A Comparison by Medicine Residents of Physical Examination Versus Hand-Carried Ultrasound for Estimation of Right Atrial Pressure

Physicians' ability to accurately estimate right atrial (RA) pressure from bedside evaluation of the jugular venous waveform is poor, particularly when performed by physicians in training. Conventional ultrasound measurement of the inferior vena cava (IVC) accurately predicts RA pressure, but the cost, lack of portability, and specialized training required to acquire and interpret the data render this modality impractical for routine clinical use. The objective of this study was to compare physical examination with hand-carried ultrasound (HCU) in the detection of elevated RA pressure (>10 mm Hg). After limited training (4 hours didactic and 20 studies), 4 internal medicine residents using an HCU device estimated RA pressure from images of the IVC in 40 consecutive patients <1 hour after right-sided cardiac catheterization. RA pressure was also estimated from examination of the jugular venous pulse (JVP) in 40 patients before right-sided cardiac catheterization. RA pressure was successfully estimated from HCU images of the IVC in 90% of patients, compared with 63% from JVP examination. The sensitivity for predicting RA pressure >10 mm Hg was 82% with HCU and 14% from JVP inspection. Specificities were similar between the techniques. Overall accuracies were 71% using HCU and 60% with JVP assessment. In conclusion, internal medicine residents with brief training in echocardiography can more frequently and more accurately predict elevated RA pressure using HCU measurements of the IVC than with physical examination of the JVP.

Chest pain after vomiting

A 66 year old man, previously fit and well, was admitted to the emergency department with sudden pain in his left chest and abdomen after vomiting. He had woken in the early hours of the morning, vomited three times, and started getting progressively worsening pain in the left side of his chest and abdomen, radiating to the shoulder. He was a non-smoker and occasional drinker. He had no history of operations or similar episodes. On arrival he was pale, sweaty, clammy, and had fever. His pulse was 106 beats/min and regular. His blood pressure was 92/52 mm Hg. Jugular venous pulse and heart sounds were normal. Trachea was central, and respiratory rate was 40 breaths/min. Left lung base was dull on percussion, and air entry was diminished. His abdomen was soft, with generalised tenderness and normal bowel sounds. Full blood count, liver function tests, serum electrolytes and serum amylase were normal. His troponin I concentration was below 0.03 (normal range 0-0.1) ng/ml and the concentration of C reactive protein was less than 1 (<10) mg/l. Blood gas analysis showed mild metabolic acidosis, and an electrocardiogram showed sinus tachycardia. Attending doctors took an urgent x ray scan of his chest (fig 1) and a computed tomograph of his chest and abdomen (fig 2). Fig 1 X ray image of the posteroanterior view of the chest, showing left hydropneumoth orax Fig 2 Computed tomography, showing mediastinal air and left hydropneumoth orax Imagine you are managing this patient. 1. What are the possible differential diagnoses, and what is the most likely cause? 2. How would you interpret the radiograph of the chest (fig 1)? 3. What should be the initial management, and how would you reach a definitive diagnosis? 4. How would you interpret the computed tomograph of the chest (fig 2)? 1. Differential diagnoses include …

Right Ventricular Myocardial Infarction: Presentation and Acute Outcomes

Acute inferior wall myocardial infarction can be complicated by right ventricular myocardial infarction (RVMI), and the excess mortality cannot be fully explained by mechanical reasons. The authors try to systematically assess the incidence, clinical presentation and early outcomes of right ventricular infarction in a tertiary-care setup. Their study was a prospective observational series of consecutive patients with RVMI. All patients with acute inferior myocardial infarction (n=135) were enlisted. RVMI was diagnosed by > or = 1 mm ST elevation in lead V(4R) in a right-sided electrocardiogram. Right ventricular (RV) infarction occurred in 37% (n=50) of patients with acute inferior infarctions. Patients with isolated inferior infarction served as controls (n=85). Echocardiography was performed within 24 hours of admission. From both groups, 66% qualified for thrombolysis. The incidence of hypotension-bradycardia and heart blocks requiring pacing support was much higher in right ventricular infarction (n=21) than in inferior infarction (n=13). Clinically manifest RV dysfunction (raised jugular venous pulse [JVP], hypotension, tricuspid regurgitation) and right ventricular dilation detected by echocardiography were seen in only 13 patients. The in-hospital mortality rate was significantly higher (n=8, 16%) in right ventricular infarction group than in inferior infarction group (n=3, 3.5%). Right ventricular infarction was seen in a third of inferior myocardial infarctions (IMIs), but hemodynamically evident right ventricular dysfunction occurred in only a tenth of acute IMIs. Nevertheless, the acute in-hospital mortality rate of patients with right ventricular infarction was much higher than in those with inferior infarction owing to arrhythmic and mechanical complications.

Is it possible to estimate the pressure's change of the right atrium in arrhythmias from jugular venous pulse tracing (JVPT)?

Is it possible to estimate the pressure's change of the right atrium in arrhythmias from jugular venous pulse tracing (JVPT)?

The internal jugular vein valve may have a significant role in the prevention of venous reflux: evidence from live and cadaveric human subjects.

The internal jugular vein valve (IJVV), which is situated just above the termination of the internal jugular vein, is the only valve between the heart and the brain. This means that it plays a role in the prevention of cephalad flow of venous blood. If the IJVV is damaged or becomes incompetent, increase in intrapleural pressure could result in raised intracranial pressure. Additionally, the jugular venous pulse (JVP) is used clinically to estimate right atrial pressure, a functional IJVV may prevent accurate estimation of the JVP. To describe the presence and the competence of the IJVV in post-mortem and live human subjects. DESIGN - setting and methods: The anatomical appearance of the IJVV from 30 cadavers was studied. Competence was checked by measuring maximum hydrostatic pressure before reflux occurred through the valve. The function of the valve was evaluated in 25 live subjects using colour duplex scanning. The IJVV was present in all cadavers just before its termination (60 IJVVs from 30 subjects). The valve was bicuspid in most cases (93%). The competence of 41 IJVVs was checked of which only three (7%) were found to be incompetent. All IJVVs in live subjects were found to be competent. This study confirms that a functional IJVV is present just above the termination of the internal jugular vein. The IJVV may therefore prevent reflux of venous blood from the right atrium into the internal jugular vein.

A Heart Defect Found Upon Self-Examination in an Asymptomatic Patient

A 32-year-old echocardiographic technician was honing her skills by self-examination when she noted that her right ventricle was dilated. A cardiologist confirmed her finding and noted a left-to-right shunt across a 1-cm defect in the fossa ovalis region of the atrial septum. The patient was entirely asymptomatic and regularly engaged in an aerobic exercise program. Physical examination revealed mild pectus excavatum. The right ventricle was not palpable. The a wave in the jugular venous pulse was larger than the v wave. The second heart sound was of normal intensity, was persistently split, and moved physiologically with respiration. The only definite auscultatory abnormality was a third heart sound followed by a short diastolic rumble heard at the lower left sternal border. A chest roentgenogram showed mild enlargement of the cardiac silhouette and minimal prominence of the pulmonary trunk and vasculature. A normal electrocardiogram was recorded. The normal electrocardiogram, the inequality of the a and v waves in the jugular pulse, the respiratory movement of the second heart sound, the absence of a systolic ejection murmur, and the size of the defect measured echocardiographically all suggested that the defect was restrictive and the left-to-right shunt smaller than usual. On the other hand, the third heart sound and short diastolic rumble, the minor abnormalities on chest roentgenogram, and the dilated right ventricle on echocardiography indicated that the shunt was hemodynamically important, and operative closure was recommended. After collecting second opinions for over a year, the patient agreed, and the defect was closed by primary suture. This is the second of our patients whose fossa ovalis–type atrial septal defect was discovered in such a serendipitous fashion. The first was a 22-year-old echocardiographic repairman seen 28 years ago. When he finished repairing the echocardiograph, he was asked to volunteer for an echocardiogram to be sure the machine was working properly, and the defect was found. He also underwent primary suture closure despite being asymptomatic. Until the echocardiograph came into daily use in cardiologic practice, atrial septal defects were diagnosed on the basis of symptoms, sometimes subtle but unmistakable physical findings, distinctly abnormal chest roentgenograms, and abnormal electrocardiograms that typically showed incomplete right bundle-branch block, often with right axis deviation. Because symptoms developed in 70% of such patients by age 40 and in virtually all of them by age 60 (1), and because operative closure carried a low risk and improved prognosis when performed early (2–5), closure of fossa ovalis–type atrial septal defects was uniformly recommended in the absence of severe pulmonary arterial disease. Does this conventional wisdom apply to patients, such as ours, whose defects are smaller and probably would not have been discovered except for serendipitous echocardiography? Opinion is divided (6). The patient herself has had second thoughts post-operatively because of several bouts of postpericardiotomy syndrome, a common problem after operative closure of atrial septal defects. She has now been well for more than 3 years, and those doubts are receding. Our own view is that a left-to-right shunt large enough to cause right ventricular enlargement should be closed, even in the absence of symptoms. As catheter-delivered devices to close holes in the atrial septum are perfected (7), perhaps even smaller defects will be closed routinely, regardless of symptoms.

John Hay and the earliest description of type II second-degree atrioventricular block

I t is universally acknowledged that in 1899, Wenckebach first described type I second-degree atrioventricular (AV) block in humans.1 The centennial of this clinical landmark was recently publicized.2 Although Wenckebach called this process “Luciani periods” after the Italian physiologist who observed this phenomenon in the frog heart in 1872, this pattern is now widely known as the Wenckebach phenomenon or periodicity.3 A number of workers have attributed the discovery of both types I and II second-degree AV block solely to Wenckebach.4–6 As a result, types I and II second-degree AV block is sometimes incorrectly designated as Wenckebach type I and type II block.7 Others have claimed that type II block was described independently by Wenckebach and Hay both in 1906.8–13 There are also rare, unfounded claims by compatriots of John Hay that it was he who discovered both types I and II second-degree AV block.14 It was actually John Hay who discovered the form of second-degree AV block currently known as type II block15 (Figure 1). Information about John Hay can be found in the recent article by Upshaw and Silverman.16 Hay’s original contribution was cited by Thomas Lewis in his 1925 book17 and by Schamroth in his 1971 book.18 Yet, Burch in his monograph on the history of electrocardiography merely stated that “incomplete heart block was studied extensively in man by MacKenzie, Wenckebach and Hay, by means of the polygraph.” without citing Hay’s work nor his 1906 article.19 Katz and Pick of the famed Chicago School of Electrocardiography did not mention Hay’s contribution to the understanding of second-degreeAV block in their classic 1956 book.20 In fact, the Chicago electrocardiographers indicated in other publications that Wenckebach and Hay described type II seconddegree AV block independently.12 In 1906 John Hay from Liverpool, England, published a case report in the Lancet describing a new form of second-degree AV block distinct from that previously reported by Wenckebach.15 Hay documented his findings without the benefit of the electrocardiograph, which was introduced clinically years later. Hay analyzed simultaneous tracings from the radial (arterial) and jugular (venous) pulses in a 65year-old patient with lightheadedness. The recordings in Figures 2 and 3 were described as showing a-c intervals (as a measure of AV conduction corresponding to the PR interval of the electrocardiogram) essentially normal and constant in duration regardless of the number of missing ventricular beats. Figure 2 clearly shows what is now considered type II seconddegree AV block with constant a-c intervals before and after a single-blocked atrial impulse (“a” wave not followed by “c” deflection) in a sequence of at least 4:3 AV block. Hay correctly emphasized that no similar case had been recorded in the literature and dismissed the type of AV block described by Wenckebach because the a-c interval failed to vary. The purist will argue that Figure 2 cannot be interpreted as type II second-degree AV block because there are no PR intervals and the behavior of the a-c intervals cannot be determined accurately. However, the diagnosis of type II block can be made with certainty by looking at the heart rate in the arterial recording on top of Figure 2. Note that the duration of the pause between the fourth and fifth arterial beats is exactly double that of the cycle before the block (between the third and fourth arterial beats). This indicates that AV conduction before and after the blocked impulse was constant. This constitutes the hallmark of type II block when there are at least 2 consecutively conducted P waves and only a single nonconducted impulse. A vagal effect on the AV node can be ruled out because the cycle before the block (between the third and From the Broward General Hospital, Fort Lauderdale, Florida; and the University of Bonn, Bonn, Germany. Dr. Barold’s address is: 6237 NW 21st Court, Boca Raton, Florida 33496. E-mail: ssbarold@aol.com. Manuscript received November 24, 2000; revised manuscript received and accepted January17, 2001. FIGURE 1. John Hay 1873 to 1959. (Courtesy of Arthur Hollman MD., London England).

Right ventricular infarction--diagnosis and treatment.

Right ventricular infarction (RVI) as assessed by various diagnostic methods accompanies inferior-posterior wall myocardial infarction (MI) in 30 to 50% of patients. Recognition of the syndrome of RVI is important as it defines a significant clinical entity, which is associated with considerable immediate morbidity and mortality and has a well-delineated set of priorities for its management. Patients may clinically present with hypotension, elevated jugular venous pulse (JVP), and occasionally shock, all in the presence of clear lung fields. The ST-segment elevation of > or = 0.1 mV in the right precordial leads V4R is a readily available electrocardiographic sign used for diagnosis of RVI. Other diagnostic approaches for assessing RVI include echocardiography, radionuclide ventriculography, technetium pyrophosphate scanning, and hemodynamic measurements. The proper management of RVI includes volume loading to maintain adequate right ventricular preload, ionotropic support, and maintenance of atrioventricular synchrony. Reperfusion therapy should be initiated at the earliest signs of right ventricular dysfunction. Finally, complete recovery over a period of weeks to months is a rule in a majority of patients, suggesting right ventricular "stunning" rather than irreversible necrosis has occurred.

Thrombosis of bileaflet tricuspid valve prosthesis: Clinical spectrum and the role of nonsurgical treatment

Background Thrombosis of a mechanical tricuspid valve prosthesis is a potentially hazardous event. This study aimed to explore the incidence and the clinical presentation of tricuspid valve thrombosis occurring in bileaflet valves and to evaluate the diagnostic and the therapeutic approach. Methods and Results Tricuspid valve thrombosis was sought in 22 late survivors with the CarboMedics valve in a follow-up period of 36.0 ± 20.8 months. Limited leaflet motion and/or a visible thrombus were considered diagnostic of valve thrombosis. Eight episodes of tricuspid valve thrombosis were diagnosed among 5 patients (12.1 episodes per 100 patient-years). Anticoagulation was inadequate in 3 patients and fair in 2. Florid right heart failure occurred in 3 episodes. Common physical findings included increased jugular venous pulse (5 patients), diastolic tricuspid murmur (4 patients), and peripheral edema (4 patients). The diagnosis was suspected in all clinically and by transthoracic echocardiography and confirmed by fluoroscopy and/or transesophageal echocardiography. In 4 patients, both leaflets were involved. No thrombi were visualized. Three patients received thrombolytic therapy in 4 episodes (complete success in 3, partial success in 1) without hemorrhagic or embolic complications. One patient responded to aggressive anticoagulant therapy. One patient required an emergent repeat surgery. In 1 patient, valve thrombosis recurred thrice. Conclusions In patients with fair or poor anticoagulation, a bileaflet valve in the tricuspid position is associated with a high incidence of valve thrombosis. Hinge entrapment requires only a small amount of thrombotic material. Valve thrombosis may be asymptomatic. Involvement of both leaflets is usually required to produce symptoms. A nonsurgical approach (thrombolysis or intensified anticoagulation) is usually successful. Patients should be instructed about heralding signs of valve thrombosis. (Am Heart J 1999;137:721-5.)