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Biomedical subjects

C Kratochwill

Publications and source records attributed to C Kratochwill.

17 recordsLinked to original sources

PR interval adaptation in the denervated transplanted heart.

In the present study, the dynamic PR response upon standardized treadmill exercise was investigated in 21 transplant recipients (recipient age 48 +/- 17 years, donor age 31 +/- 12 years, > 1 year after transplantation). HR and PR interval were measured at rest and at the end of each 25-W increase in workload till peak exercise. In 17 cases norepinephrine (NE) was assessed at rest, and at the end of each workload the HR increased from 99.3 +/- 14 to 143.4 +/- 25 beats/min at individual peak exercise, and NE increased from 1,307 +/- 1,163 to 3,688 +/- 2,036 pg/mL, while the PR interval shortened from 149.2 +/- 13 to 119.3 +/- 20 ms. On average, PR decreased by 3.4 ms for a 10-beat increase in HR, and the HR-PR interval relationship was described by a linear regression (y = 176.8-0.3469x, P = 0.0001). One patient who was unable to increase his NE levels upon exercise showed virtually no decrease in the PR interval and no HR increase. Both recipient age and donor age were moderately and significantly related to the minimum PR interval achieved at peak exercise (r = 0.6, P = 0.008 and r = 0.51. P = 0.049, respectively). These data show the following: (1) adaptation of the PH interval upon exercise does occur in the denervated transplanted heart; (2) the HR-PR relation is similar to that reported in the innervated heart; (3) the overall decline in PR interval is blunted, since denervated patients start at shorter resting PR intervals and achieve relatively longer PR intervals at peak exercise when compared to their innervated counterparts; (4) these exercise induced changes of the PR interval may be explained by circulating NE; and (5) NE levels achieved at peak exercise and the sensitivity of the AV node to NE seem to be age related.

Adaptation, Physiological

Decrease in pacemaker incidence after orthotopic heart transplantation.

A decrease in sinus node dysfunction and pacemaker requirement after orthotopic heart transplantation was observed over a 6.5-year period, probably indicating the effect of a learning curve. Indirect evidence suggests a traumatic genesis of sinus node dysfunction after cardiac transplantation.

Arrhythmia, Sinus

Effects of intraaortic balloon pumping on coronary and carotid flow during percutaneous cardiopulmonary support.

Previous studies have suggested an improved clinical outcome when percutaneous cardiopulmonary support is combined with intraaortic balloon counterpulsation in patients with cardiogenic shock. We evaluated the effect of combined intraaortic balloon counterpulsation and percutaneous cardiopulmonary support therapy on coronary and cerebral blood flow by Doppler measurements in the coronary and the carotid arteries in a patient with cardiac arrest. During pacemaker stimulation, intraaortic balloon counterpulsation in addition to percutaneous cardiopulmonary support markedly improved coronary and carotid blood flow. Possible mechanisms are discussed.

Cardiac Pacing, Artificial

[Monitoring of bone marrow spilling and cardiopulmonary changes in fat embolism syndrome].

After long bone fractures, as well as hip or knee total arthroplasty, the increase in intramedullary pressure induces bone marrow release into the circulation in more than 90% of patients. Three to four percent of the patients reveal fat embolism syndrome with pulmonary and cerebral involvement and a petechial rash. In about 20% of these patients a fulminant and fatal course is possible. Although fat embolism syndrome was described more than a century ago, there is still no sufficient therapeutic strategy. Because of these facts we try to prevent fat embolism syndrome and monitor patients at risk perioperatively. We have evaluated different diagnostic methods and monitoring facilities and recommend pulse oximetry, capnography, ECG, blood pressure controls and, if indicated, blood gas analyses for perioperative monitoring. Patients at risk and patients who are suffering from fat embolism syndrome require more intensive monitoring, such as transesophageal echocardiography and a pulmonary artery catheter to obtain more detailed information about the hemodynamic and oximetric variables. Furthermore, these patients must be admitted to an intensive care unit.

Blood Gas Analysis

[Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis].

Since 1970 the fat embolism syndrome (FES) has been recognised as a severe complication of cemented total hip arthroplasty (THA). Initially and still today the toxicity of bone cement has been though to be responsible for the cardiorespiratory problems. Meanwhile several reports have confirmed the causal relationship between intramedullary pressure (IMP), bone-marrow release into the circulation and subsequent cardiorespiratory deterioration during cemented THA. In recent publications it has been reported that bone-marrow release due to increased IMP also occurs during cementless THA. The clinical implication of these observations is controversial. For this reason in the first part of this paper two autopsy-proven FES deaths and five further clinically manifest FES cases are presented. In the second part of the study, IMP courses during four different surgical techniques (2 conventional, 2 modified) are compared. The aim of the modified surgical technique developed in our department was to minimize IMP peaks and bone-marrow release during cementless THA. Both modified techniques showed significantly lower IMPs during opening of the medullary canal, preparation with rasps, and implantation of the prosthesis than the conventional techniques. The observed FES cases for the first time strongly confirm the clinical relevance of the FES, also during cementless THA. On the basis of the data presented we recommend the modified surgical technique to reduce bone-marrow release during cementless THA.

Aged

[Modified surgical technique for the reduction of bone marrow spilling in knee endoprosthesis].

In the literature 20 cases of fat embolism syndrome (FES) after total knee replacement (TKR) are reported; 16 cases had cemented hinged TKR and 4 resurfacing TKR. Initially, it was believed that the bone cement was responsible for the FES. Since then, however, Fahmy et al. have published extraordinary data, demonstrating the causal relationship between increased intramedullary pressure (IMP) during the insertion of the intramedullary rod (IR) and cardiorespiratory deterioration. The industry responded by developing a fluted IR, disregarding the overdrilling in the distal femur required by Fahmy. In the first part of this paper clinically manifest FES cases after resurfacing TKR are reported. In the second part of the study the conventional surgical technique is compared with a modified technique, which focuses on a reduction of bone-marrow release into the circulation. In the conventional and the modified group, IRs with and without flutes were compared. It was shown that only the opening of the intramedullary canal and insertion of the IR generated relevant IMP peaks during implantation of resurfacing TKR. When compared with the conventional surgical technique, the modified technique revealed significantly lower IMPs, and in neither group was a difference demonstrated between the IR with or without flutes. In 4 patients (2 conventional, 2 modified) transesophageal echocardiography (TEE) was performed for detection of bone-marrow release into the circulation. In the two patients operated on conventionally, TEE showed a markedly higher bone-marrow release than in the patients with modified operations. In conclusion, we recommend the presented modified surgical technique in order to reduce bone-marrow release into the circulation.

Aged

[Therapeutic approach to the management of fat embolism syndrome].

So far, no clinical or experimental study has demonstrated that any drug has a beneficial effect (heparin, cortisone, dextran, etc.) on the course of fat embolism syndrome (FES). Thus, prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance. Besides surgical measures, such as reduction of intraosseous pressure and bone-marrow release during hip or knee replacement, proper treatment of shock in traumatized patients, recognition of risk factors and maintainance of intraoperative cardiorespiratory stability are cornerstones in the prevention of fat embolism syndrome. It is well documented that bone-marrow release into the circulation and pulmonary embolism occurs during any hip or knee arthroplasty. As a result of improvements in anesthesia management, the clinical appearance of FES has moved into the postoperative period. This calls for mandatory cardiorespiratory monitoring up to 24 h postoperatively. When facing a clinically manifest fat embolism syndrome, monitoring and symptomatic treatment must be adapted to the patient's needs in order to ensure adequate oxygenation and acceptable circulatory conditions to protect organ function.

Catheterization, Swan-Ganz

[Pathophysiology of fat embolisms in orthopedics and traumatology].

It is well known that fat embolisms can occur after long bone fractures, and this has been feared for more than 100 years. Since 1970 fat embolisms have also been recognized in endoprosthetic surgery. The clinical manifestation was described as the fat embolism syndrome (FES) by Gurd in 1974. Based on reports in the literature and our own data, a concise pathophysiological model of the FES is presented in this paper. The increase in intramedullary pressure (IMP) in the long bones is the most decisive pathogenic factor for the development of an FES. Any long bone fracture, stabilization of fractures, or implantation of knee or hip endoprostheses can generate IMP peaks leading to bone marrow release into the circulation. Bone marrow itself is a tremendous stimulus for activation of the clotting system. As a result, hypercoagulation and venous stasis in the draining veins generate mixed macroemboli from the initial bone-marrow microemboli. Bone-marrow embolization of the lung in phase I leads to mechanical obstruction of pulmonary arteries. In phase II, release of local mediators, triggered by a systemic inflammatory response (SIR) of the lungs, causes damage to the pulmonary membranes. Disturbed gas exchange and respiratory insufficiency with possible cardiac and cerebral decompensation are the result. In most cases an FES may not be detected clinically, and any mild cardiorespiratory changes are treated easily with oxygen insufflation and usually disappear within 48 h. Of paramount importance for clinical manifestation of an FES are the quantity and duration of bone-marrow release and co-factors (cardiorespiratory compliance and perioperative stability of the patient). Patients with preexisting cardiorespiratory disease in combination with massive intraoperative bone-marrow release may even face a deadly FES event. Increased IMP causes local obstruction of cortical vessels with bone marrow. In combination with the damaged endosteal blood supply, avascular necrosis of the cortical bone occurs. During endoprosthetic procedures, mechanical-and mediator-triggered damage of the intima of big veins, in combination with venous stasis and hypercoagulation may be responsible for the high incidence of proximal thrombosis of femoral veins. As a delayed result of the disseminated intravascular coagulopathy, petechial bleeding in the trunk and subconjunctiva can be seen. A better understanding and recognition of the FES's pathophysiology may help to use prophylactic, diagnostic and therapeutical measures more effectively.

Blood Coagulation

Sinus node dysfunction after orthotopic heart transplantation: the Vienna experience 1987-1993.

In the present study, the annual incidence of postoperative sinus node dysfunction and the type of sinus node abnormality after cardiac transplantation were followed over a 6 1/2-year period in 185 patients. Each year the sinus node function was systematically characterized by rhythm and corrected sinus node recovery time in a significant number of patients. Over the entire study period, there were 131 patients with normal sinus node function (corrected sinus node recovery time 318 +/- 55 msec) while 54 patients had latent (n = 24, sinus rhythm, corrected sinus node recovery time 8,053 +/- 2,198 msec) or manifest (n = 30, absence of sinus rhythm or pacemaker dependence) sinus node dysfunction. Twenty-nine patients had pacemaker placement. The incidence of sinus node dysfunction declined in absolute terms and when indexed by the actual number of patients transplanted per year (index 1987: 38.5; 1998: 17.6; 1989: 23.2; 1990: 29.1; 1991: 10.4; 1992: 7.5; 1993: 2.2). Among those with sinus node dysfunction, the annual percentage of patients presenting with prolonged recovery time, escape rhythm, and those reverting back to sinus rhythm until discharge did not change significantly over the study period (P = 0.22). On multivariate analysis, only the date of transplantation was significantly associated with the occurrence of postoperative sinus node deficiency (P = 0.0007) while age of recipient (P = 0.85) or donor (P = 0.96), the type of cardioplegia used (P = 0.09) and ischemic time (P = 0.09) were insignificant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

[Thrombolysis of acute myocardial infarct: modifying factors of "door-to-needle time"].

Effect of thrombolytic treatment in acute myocardial infarction depends on several factors, most importantly on time to treatment. The door-to-needle time, the interval between admission and thrombolytic therapy initiation, may be one important factor. In a retrospective study, we analysed 151 patients who were admitted to our emergency department with acute myocardial infarction and who received thrombolytic treatment. We analysed door-to-needle time with respect to the factors age, gender, clinical symptoms, presence of prehospital ECG, presence of prehospital complications, day of admission, hour of admission, duration of pain and infarct site. We observed that the door-to-needle time is significantly shorter in those cases with a prehospital ECG (p < 0.001) or no prehospital complications (p < 0.001) as well as inferior infarction (p < 0.02). There was a trend towards a shorter interval in cases with typical chest pain plus autonomic symptoms (p = 0.05). No statistical significance was seen in respect to age, gender, day and hour of admission, and duration of pain. Door-to-needle time with respect to thrombolytic treatment seems to depend on several factors in the preclinical field. Improvement of prehospital diagnosis and prevention of preclinical complications might result in faster thrombolytic treatment of the patient after arrival at the emergency department.

Adult

Exercise chronotropy in patients with normal and impaired sinus node function after cardiac transplantation.

The chronotropic response during graded, symptom limited exercise was investigated in 32 cardiac transplant recipients a mean of 49 +/- 18 days after transplantation. All patients had systematic evaluation of postoperative donor sinus node (SN) function and the cardioacceleratory response was compared according to the SN function. Twenty-one patients had normal postoperative SN studies (corrected SN recovery time < 520 msec, group I) while the SN function was impaired postoperatively in the remainder (n = 11, group II; corrected SN recovery time 4,149 +/- 6,283 msec in 5 patients, junctional escape rhythm in 6 patients). All patients had regained sinus rhythm at time of the exercise test. Patients in group II had lower basal sinus rates at the beginning of exercise (91.5 +/- 11 vs 101.4 +/- 7 beats/min, P < 0.02). This lower chronotropy was maintained over every incremental step (F rate between groups = 30, P = 0.0001, F rate vs workload = 15, P = 0.0001 by two-way ANOVA) and resulted in a significantly lower heart rate at individual peak exercise (108.3 +/- 20 vs 124.2 +/- 13 beats/min, P < 0.02). A total of 14/16 patients in group I but only 2/16 patients in group II accomplished a peak heart rate > or = 120 beats/min (P = 0.009). The workload achieved did not differ between the groups (107 +/- 29 vs 102 +/- 32 watts, P > 0.5). These data show a lower SN chronotropy during rest and at peak exercise in cardiac transplant recipients with postoperative SN deficiency and apparent normalization of SN function.

Adult

Normal AV node function in patients with sinus node dysfunction after cardiac transplantation.

Postoperative atrioventricular nodal (AVN) function was compared in 55 patients with normal and 50 patients with impaired sinus node (SN) function after cardiac transplantation (corrected SN recovery time > 520 msec or sinus arrest +/- escape rhythm). Fifty-two patients had fixed atrial pacing at cycle lengths between 600 and 430 msec, and 53 patients at cycle lengths from 600 to 300 msec between postoperative weeks 1 to 3. Relative (stimulus-R interval; AVNRRP) and effective AVN refractory period (AVNERP) were determined in 53 patients at a cycle length of 500 msec. Only one of 105 recipients had high degree AVN conduction disturbance characterized by a Wenckebach phenomenon at cycle length < 630 msec in the first postoperative week. Three patients with normal and two patients with impaired SN function had Wenckebach cycle lengths > 430 msec while the Wenckebach cycle lengths were < or = 430 msec in the remainder (p = NS). Resting PQ interval (146 +/- 18 vs 162 +/- 32; p = 0.09), Wenckebach cycle length (350 +/- 53 vs 362 +/- 50 msec), AVNRRP (356 +/- 38 vs 367 +/- 37 msec), and AVNERP (217 +/- 48 vs 244 +/- 49 msec) did not differ significantly between patients with normal and impaired SN function. AVN conduction did not deteriorate during 318 +/- 130 days of follow-up (PQ at follow-up 154 +/- 17 and 158 +/- 22 msec, patients with normal and impaired SN function, respectively). One DDD pacemaker was placed for AVN conduction disturbance while 22 pacemakers were implanted for SN deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Long-term intrinsic pacemaker function in patients paced for sinus node deficiency after cardiac transplantation.

Fifteen cardiac transplant recipients requiring permanent pacing (AAI, n = 9; VVI, n = 6; rate responsive devices, n = 11) for postoperative sinus node (SN) insufficiency underwent evaluation of long-term SN function 240 to 1,461 days after transplantation. The intrinsic rhythm at the time of discharge was sinus in 7 patients; junctional escape in 6 patients; and pacemaker dependent in 2 patients. At follow-up, 5 patients had regained regular sinus rhythm, accounting for a total of 11 patients in sinus rhythm while 4 patients were in junctional bradycardia. The SN recovery time as determined by the permanent pacemaker was normal (< 1,500 msec) in only 1/8 patients in whom it was determined, although 4 of these 8 patients were temporarily overriding the pacemaker during ambulatory monitoring. Patients with pathological SN recovery times included 3 patients with late return of sinus rhythm and 4 patients who had recovered normal sinus rhythm before their discharge from the hospital. Three patients developed late symptoms despite apparent early normalization and underwent delayed pacemaker implantations on postoperative days 35, 52, and 225, respectively. We conclude that, in patients requiring pacemaker implantation after cardiac transplantation, normalization of SN function cannot be inferred from just return of sinus rhythm, regardless of whether it occurs early or late. These findings may have implications when a pacemaker exchange or explantation is being considered.

Electrocardiography

Inducible atrial flutter and fibrillation after orthotopic heart transplantation.

Inducible atrial flutter (two patients) and fibrillation (two patients) were observed in a series of 35 heart transplant patients who underwent evaluation of sinus node function including premature atrial stimulation. The sinus node function was entirely normal in both patients with inducible atrial flutter. In contrast it was profoundly abnormal in the patients with inducible atrial fibrillation. Atrial fibrillation was no longer inducible as the sinus node function became borderline normal. These observations suggest extensive electrical atrial abnormality, including the sinus node, in patients with atrial fibrillation, and temporary pacing should be available when considering cardioversion in patients with atrial fibrillation early after heart transplantation. Atrial flutter, in contrast, may be inducible in the absence of any sinus node abnormality and without any evidence of rejection.

Adult

Thromboembolism associated with junctional escape rhythm and atrial standstill after orthotopic heart transplantation.

We report on thromboembolism in a heart transplant recipient with mechanical atrial standstill and spontaneous echocardiographic contrast during intermittent periods of sinus arrest and junctional escape rhythm. The temporal relationship between the conversion of atrial flutter to junctional bradycardia and two episodes of thromboembolism strongly suggest a role of the lack of atrial contraction during junctional rhythm for the development of spontaneous echocardiographic contrast and thromboembolism.

Arrhythmias, Cardiac