Degree Of Hemodynamic Compromise Research Articles

Hemodynamic Support with Intra Aortic Balloon Pump Differs by Etiology of Cardiogenic Shock

Purpose While intra-aortic balloon pump (IABP) counterpulsation has not been shown to be of benefit in patients with acute myocardial infarction (AMI) with cardiogenic shock (CS), emerging data suggest that patients with acute decompensated heart failure (ADHF) might be more likely to stabilize with this device. Methods Patients with hemodynamic evidence of CS related to either AMI or ADHF who received IABP support were studied retrospectively. Cardiac outputs (CO) and indices (CI) were calculated using the Fick method. Hemodynamics were compared before and after IABP insertion and between the AMI and ADHF cohorts. Results During the study period, 77 patients were supported with IABP for AMI related CS while 132 were supported for ADHF related CS. The mean age was 64.7±13.6 years and 75.1% were men. Mean arterial blood pressure was 75.6±10.6mmHg and 78.4±14.6mmHg among ADHF and AMI patients, respectively (p=0.12). Mean pulmonary artery pressure was higher among those with ADHF (37.9±9.3mmHg vs 33.6±8.9mmHg, p=0.002). Left ventricular ejection fraction was 18.0±8.9% among those with ADHF and 28.9±12.0% among those with AMI (p Conclusion While the degree of hemodynamic compromise was similar between those with CS related to AMI and ADHF, the response to IABP counterpulsation differed significantly between these cohorts suggesting that the device's efficacy may differ between etiologies of CS.

Advances in understanding the pathogenesis of chronic thromboembolic pulmonary hypertension

Chronic thromboembolic pulmonary hypertension (CTEPH) comprises organizing thrombotic obstructions in the pulmonary arteries. While roughly 40% of CTEPH cases are not preceded by a venous thromboembolic event, 0.1-5.1% of acute pulmonary thromboemboli evolve into organized obstructions of the pulmonary artery. In patients with predominantly proximal disease, surgical pulmonary endarterectomy provides a potential cure of the disease. For years, the scientific debate of CTEPH was mainly focused around its thromboembolic nature because of striking dissimilarities to classical venous thromboembolism, for example, the lack of risk factors for venous thrombosis, the lack of clinically apparent pulmonary embolism in many patients, the difficulty to reproduce the disease in animal models of thrombosis, and the nature of the pulmonary vascular obstructions that are dissociated from the degree of hemodynamic compromise. Recent studies have confirmed an association between venous thromboembolism and the evolution of CTEPH, and have shed light on disease-modifying conditions.

The Use of Quantitative Magnetic Resonance Perfusion for Assessment of CBF in The Perioperative Management of Carotid Stenosis: Case Illustration

Objective and Importance: Internal Carotid Artery (ICA) stenosis is a common condition with a high preva- lence in the normal population and carries a high risk of stroke. Hemodynamic impairment has been proven to be a power- ful and independent risk factor for stroke. Understanding the hemodynamics beyond a stenosis may play a role in select- ing patients who would benefit from treatment, determining the success of the treatment, and monitoring for disease recur- rence. Our group has developed a unique quantitative approach to MR perfusion. We report on the use of Quantitative Magnetic Resonance Perfusion (MRP) for assessment of Cerebral Blood Flow (CBF) pre- and post- Carotid Angioplasty and Stenting for symptomatic ICA stenosis. Clinical Presentation: A 71-year-old female with significant comorbidities presented with two episodes of left transient ischemic attacks (TIAs) over the course of one month related to high grade left ICA stenosis. Preoperative quantitative MRP showed asymmetry in CBF between the two hemispheres. Carotid angioplasty and stenting was recommended. Intervention: Left ICA angioplasty and stenting was performed and reduced the stenosis to <10%. Quantitative MRP done after the procedure revealed improved CBF to the affected side and normalization in the asymmetry of perfusion between the two hemispheres. Quantitative MRP values showed that affected regions were hypoperfused, but flow was sufficiently maintained so as to avoid infarct. Conclusion: Relative MRP images allowed us to elucidate improvement in perfusion resulting form carotid angioplasty and stenting. This novel quantitative MRP allows quantification of CBF and the potential to provide additional informa- tion on the degree of hemodynamic compromise.

Bilateral vertebral giant cell arteritis – favourable outcome in two cases

Dear Sirs, giant cell arteritis (GCA) of the vertebral arteries (VA) is a rare, potentially treatable disease with serious prognosis. In a recent literature review [7], eight cases of bilateral VA-occlusion resulting from GCA were identified [1, 2, 7–9]. Six of these patients died. Both surviving patients were left dependent on assisted living [7]. We report on two patients with GCA of both VA with a favourable outcome. Patient 1: A 75-year-old woman suffered from gait disturbance, vertigo, headache and jaw claudication. She lost 10 kilograms in two months. Neurological examination revealed gaze-evoked nystagmus, gait ataxia and pyramidal signs. Erythrocyte sedimentation rate (ESR) was 110 mm/h. The brain MRI showed bilateral cerebellar and left pontine infarction and an enhancement of the intracranial VA after gadolinium (Fig. 1a, b). Sonology detected a halo around both VA (Fig. 1c). Biopsy of the temporal artery confirmed GCA (Fig. 1d). Her symptoms markedly improved after four days of high-dose IVmethylprednisolone treatment (1000 mg/d). The ESR decreased to 38 mm/h. On sonology, the stenoses regressed but the halos persisted. Patient 2: A 81-year-old man had a syncope, headache, vertigo, blurred vision and jaw claudication. He lost 13 kilograms in two months. Bitemporal indurated and painful arteries were clinically prominent. The ESR was 90 mm/h. Sonology showed a halo around the temporal arteries and stenoses of the V4-segment (Fig. 1e). Contrast-enhancement of the VA walls was present on MRI (Fig. 1f). GCA was confirmed upon biopsy of the temporal artery (Fig. 1g, h). The symptoms resolved after five days of high-dose IV-methylprednisolone treatment (500 mg/d). The ESR decreased to 40 mm/h. Sonology showed regression of the vertebral stenoses. Giant cell arteritis of the vertebral arteries is a rare cause of vertebrobasilar stenoses or occlusions. Eight cases of GCA-related bilateral VA-occlusions have been identified between 1966 and 2001, while another 110 cases of VA-occlusions were attributable to atherosclerosis [7]. The majority of GCA-patients with VA-occlusions died [3, 4, 6, 7]. The two patients reported here had a favourable outcome. In contrast to other cases reported with unfavourable courses [1, 2, 7–9], our patients had stenoses rather than occlusions. Although the degree of hemodynamic compromise may be crucial, one recently reported fatal case with VA-stenoses [3] illustrates that patients with stenoses only do not necessarily have a favourable outcome. It remains to be determined why in some patients VA-involvement caused occlusions while in others the involvement was restricted to the level of stenoses. Other variables theoretically predicting an unfavourable outcome are (i) the involvement of the basilar artery, not directly affected by GCA [9], but resulting from bilateral VA occlusion, and (ii) the lack of sufficient collateralisation from the carotideal circulation. It may be postulated that early high-dose immunosuppression is efficacious, as by observation several of the cases with fatal outcome had no immunosuppressive treatment [6, 7]. However in one case reported, even the addition of IV cyclophosphamide to high-dose IV steroids could not prevent the fatal outcome [3]. In another case, conversely, the delay of immunosuppressive treatment resulting from misinterpretation of imaging findings as VAdissection [5] did not prompt an unfavourable course. Systematic observation of GCApatients with symptomatic stenoocclusive disease of both VA is warranted to identify reliable outcome predictors. Taking into account the low frequency of the disease, a multicenter registry compiling clinical, laboratory and imaging data would be of great value. In conclusion, our two cases illustrate favourable courses among patients with GCA-involvement of both vertebral arteries which have not been reported so far. The identification of prognostic features and the role of early immunosuppressive treatment should be addressed in future clinical research.

Hemodynamic Reserve and High-Intensity Transient Signals in Moyamoya Disease

Background: Moyamoya disease (MMD) as a rare obstructive cerebrovascular disease is assumed to present with ischemic symptoms due to hemodynamic compromise. However, alternative mechanisms, such as cerebral embolism in low-flow territories, may also contribute to clinical symptoms. The incidence of high-intensity transient signals (HITS) and the degree of hemodynamic compromise were studied in symptomatic patients with MMD. Methods: Twenty-four patients (17 female, 7 male; mean age 33 ± 13 years) with clinical symptoms attributable to cerebral ischemia and the angiographic features of MMD (21 definite form, 3 probable MMD; 22 patients ‘late stage’ MMD, 2 patients ‘early stage’ MMD) in 45 affected hemispheres were enrolled in the present study. Patients underwent parallel estimation of hemodynamic compromise by means of functional blood flow (rCBF) studies using SPECT, PET or xenon-CT and HITS detection by TCD. Results: Hemodynamic compromise was observed in 37/40 (92%) hemispheres studied. During TCD monitoring, HITS were detected in 3 patients (12.5%), with a total frequency of 3 (6.6%) in the 45 hemispheres investigated. All patients with HITS showed hemodynamic compromise in functional rCBF studies. In these patients, HITS were recorded ipsilateral to the symptomatic hemisphere. HITS occurred in late stage MMD patients only once, while both cases with early stage MMD demonstrated multiple HITS. Conclusions: The incidence of HITS in patients with MMD appears to be lower compared to patients with atherosclerotic or atherothrombotic arterial obstructions. In addition, ischemia-related symptoms in ‘late stage’ MMD seem to be caused by hemodynamic compromise in the majority of these patients.

The role of perforating vein dissection in the treatment concept of venous ulcers--myths and evidence

Crural ulcers represent the most serious form of chronic venous incompetence (CVI). According to duplex studies superficial venous incompetence predominate in this stage of the disease, but combined refluxes of superficial and deep veins are also common. Despite a positive correlation between the number of incompetent perforators and the stage of CVI isolated incompetence of perforating veins in venous ulcers are rarely found. Additionally, only a minority of incompetent perforators depict larger reflux volumes. Therefore, doubts about a causal role of perforators incompetence in ulcer genesis are justified. According to phlebodynamometric studies the risk of crural ulcer development increases with the degree of hemodynamic compromise. Ulcer healing can only be achieved after complete normalization of ambulatory venous hypertension. In case of superficial refluxes and concomitant incompetence of perforating veins exclusion of the superficial component is sufficient to achieve this goal. Incompetent perforators normalize their function consecutively. In contrast, venous hypertension persists after exclusion of superficial refluxes in case of incompetent perforators and irreversible damage of the deep venous system. Surgical therapy studies exactly reflect the results of these hemodynamic examinations. Therefore, the role of endoscopic subfascial perforator dissection (ESPD) in the treatment of venous ulcers remains unclear. Future therapy studies should take into account that the definite role of ESPD in ulcer healing can only be examined without additional treatment of refluxes in the saphena system. Additionally, all study patients should be classified according to the CEAP nomenclature and Hach's classification of chronic compartment syndrome. Methodological differences in technique and extent of ESPD have also to be taken into account.

Oral care for patients with cardiovascular disease and stroke

The authors describe how oral disease, particularly periodontal disease, may place certain patients at increased risk of developing cardiovascular disease and stroke. Although the precise mechanisms of interaction are not clear, two biological mechanisms that may explain the relationship are presented. In addition, the authors describe the dental management issues that need to be understood in treating patients compromised by cardiovascular disease. The patient with cardiovascular disease may present a challenge to the dental health care provider, depending on the degree of hemodynamic compromise and the stability of his or her condition.

The Systemic Inflammatory Response to Cardiopulmonary Bypass

The Systemic Inflammatory Response to Cardiopulmonary Bypass

Sustained Monomorphic Ventricular Tachycardia: Immediate Evaluation and Management, Long-Term Management

Immediate evaluation and management Patients with sustained monomorphic ventricular tachycardia (SMVT) demonstrate a wide range of clinical presentations, from essentially asymptomatic to critically ill. The rate of the tachycardia is the major determinant of the degree of hemodynamic compromise, although the extent of structural heart disease is also important. The acuity of the immediate management is dictated by the severity of the symptoms. Immediate synchronous cardioversion is indicated for the hypotensive, unconscious patient; acute cardioversion is also used after adequate sedation is obtained in conscious but symptomatic patients. Lidocaine infusion has been advocated for patients with well tolerated SMVT, mostly based on analogy to its usefulness in preventing VF in acute myocardial infarction. Several recent studies have that lidocaine is infrequently successful in terminating SMVT. Only 10 of 121 episodes of induced and 0 of 27 spontaneous SMVT terminated with lidocaine infusion in a study by Nasir et al.1 In a small randomized study,2 sotalol (100 mg IV over 5 minutes) converted 69% of SMVT episodes compared to 18% with lidocaine. In unusual cases, recognized by characteristic electrocardiographic manifestations and the absence of structural heart disease (Fig. 1), episodes of SMVT can be treated with medications typically reserved for treating supraventricular arrhythmias, such as adenosine, calcium antagonists and beta-blockers. The need for diagnostic certainty before using agents that could produce hypotension during SMVT cannot be overstated. After termination of the presenting episode, the acute management centers on the prevention of SMVT recurrence. In the majority of cases (digitalis intoxication is one exception) SMVT is the consequence of a permanent electrical substrate. Although it is prudent to investigate and correct contributing factors such as electrolyte abnormalities and acute ischemia, these factors can serve as triggers but not as the proximate cause of the arrhythmia. Lidocaine is often administered continuously after an episode of SMVT, and is may be helpful in selected patients following acute infarction or cardiac surgery. In light of the signi~cant potential for side effects and particularly because most patients with SMVT have infrequent recurrences, antiarrhythmic drugs should not be given re_exively after a single SMVT episode. The unusual patient with multiple acute recurrent episodes of SMVT is often critically ill and very dif~cult to control. Several recent multicenter studies con~rmed previous case reports of the ef~cacy of intravenous amiodarone in the treatment of recurrent, poorly tolerated SMVT.3–5 A dose ranging study by Levine and coworkers3 enrolled 273 patients who had previously failed treatment with lidocaine, procainamide and bretylium. In this extremely high risk group, the initial infusion of intravenous amiodarone (500–2100 mg/24 hours) prevented SMVT recurrence in 40.3%. In the remainder, supplemental doses of amiodarone or addition of another agent often resulted in arrhythmia control. The most frequently encountered acute side effects were hypotension (15%) and bradycardia (5%). Despite this encouraging success, the 24 hour and 90 day allcause mortality in this cohort was 19 and 52%, respectively; the cause of death in just under 50% of patients was refractory VT/VF. In patients with frequently recurring or incessant well tolerated SMVT, particularly if acute attempts at antiarrhythmic drug therapy fails, catheter ablation in the acute setting can be helpful.6 In patients with refractory, poorly tolerated SMVT emergent subendocardial resection has been performed with some degree of success. The second component of the acute management of patients with SMVT involves assessment of the nature and extent of underlying structural heart disease (Table 1). The purpose of this determination is twofold. First, patients with SMVT in the absence of structural heart disease need to be promptly identi~ed as their prognosis, therapeutic options and response to therapy is much different than patients

Wide-complex tachycardias. The importance of identifying the mechanism.

Initial assessment of widecomplex tachycardias (WCTs) should begin with patient history and physical examination. If there is a history of remote myocardial infarction, WCT should be considered as ventricular tachycardia until proved otherwise. In most cases, WCT is subsequently shown by electrophysiologic evaluation to be ventricular tachycardia. The presenting symptoms and degree of hemodynamic compromise should not be used to distinguish ventricular tachycardia from supraventricular tachycardia. A 12-lead electrocardiogram (ECG) should be carefully reviewed by looking for signs of ventricular tachycardia (atrioventricular dissociation, captured and fusion beats, certain QRS shapes and concordance). If the surface ECG is inconclusive, changing the position of V1 or use of a transesophageal lead may allow assessment of atrial activity. When more QRS than P waves are documented, the diagnosis is ventricular tachycardia. Cardioversion-defibrillation is required in patients with WCT who are in unstable condition. Atrioventricular node blockers are the agents of choice for arrhythmias that are atrioventricular node-dependent, but they may cause hemodynamic collapse if administered to patients with ventricular tachycardia or with atrial fibrillation and preexcitation. Lidocaine hydrochloride (Xylocaine HCl IV), preferred for ventricular tachycardia, has been reported to cause ventricular fibrillation in patients with atrial fibrillation and preexcitation. When there is doubt about the diagnosis, elective electrical cardioversion may be considered. Medical therapy should consist of intravenous magnesium sulfate and procainamide hydrochloride (Pronestyl). A beta blocker may also be considered if more aggressive blockade of the atrioventricular node becomes necessary.

Hemodynamics during ventricular tachyarrhythmias

The hemodynamic consequences of ventricular tachycardias are caused by cardiac and peripheral reactions. As a result, cardiac output and arterial pressure decrease. Even if the decrease is related to the tachycardia rate and left ventricular function, clinical symptoms do not in each case correlate with the degree of hemodynamic compromise. The explanation for this phenomenon is the different cardiac and peripheral reaction of patients to an immediate rise in heart rate. In this regard, it is questionable if pressure monitoring is superior to heart rate monitoring as a sensor for implantable antitachycardia devices.

Histamine Release by Four Narcotics

Histamine release and hemodynamic changes associated with four narcotics were studied in 60 adults (28 men, 32 women) scheduled for general surgery under balanced anesthesia. Under double-blind conditions, incremental equipotent doses of meperidine, morphine, fentanyl, or sufentanil were administered IV for induction of anesthesia, prior to thiopental, succinylcholine, and intubation. Arterial blood samples were drawn before and 1, 6, and 20 min after narcotic administration. Of the 16 patients given meperidine (mean dose 4.3 +/- 0.2 (SEM) mg/kg), five (31%) had clinical signs (hypotension, tachycardia, erythema) and elevations in plasma histamine levels ranging from 3.2 to 49.7 ng/ml 1 min after narcotic administration. Plasma epinephrine levels at this time were also elevated in these five patients. One of the ten patients given morphine (0.6 +/- 0.02 mg/kg) developed hypotension, tachycardia, and an increase in plasma histamine level to 12.4 ng/ml. None of 34 patients given either fentanyl (7 +/- 0.4 micrograms/kg) or sufentanil (1.3 +/- 0.1 microgram/kg) had clinical signs of histamine release or elevations of plasma histamine levels. In the six patients in whom histamine release occurred, there was a significant correlation between the histamine levels at 1 min and the magnitude of change in heart rate, blood pressure, and plasma epinephrine level. All six histamine releasers were young women, ranging in age from 18 to 35 yr. Histamine release occurred more frequently after meperidine than after the other narcotics, including morphine, and the degree of hemodynamic compromise was related to the increase in plasma histamine concentration.