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Biomedical subjects

K Dracup

Publications and source records attributed to K Dracup.

At least 19 recordsLinked to original sources
PubMed1997

The physician's role in minimizing prehospital delay in patients at high risk for acute myocardial infarction: recommendations from the National Heart Attack Alert Program. Working Group on Educational Strategies To Prevent Prehospital Delay in Patients at High Risk for Acute Myocardial Infarction.

Physicians and other health care professionals play an important role in reducing the delay to treatment in patients who have an evolving acute myocardial infarction. A multidisciplinary working group has been convened by the National Heart Attack Alert Program (which is coordinated by the National Heart, Lung, and Blood Institute of the National Institutes of Health) to address this concern. The working group's recommendations target specific groups of patients: those who are known to have coronary heart disease, atherosclerotic disease of the aorta or peripheral arteries, or cerebrovascular disease. The risk for acute myocardial infarction or death in such patients is five to seven times greater than that in the general population. The working group recommends that these high-risk patients be clearly informed about symptoms that they might have during a coronary occlusion, steps that they should take, the importance of contacting emergency medical services, the need to report to an appropriate facility quickly, treatment options that are available if they present early, and rewards of early treatment in terms of improved quality of life. These instructions should be reviewed frequently and reinforced with appropriate written material, and patients should be encouraged to have a plan and to rehearse it periodically. Because of the important role of the bystander in increasing or decreasing delay to treatment, family members and significant others should be included in all instruction. Finally, physicians' offices and clinics should devise systems to quickly assess patients who telephone or present with symptoms of a possible acute myocardial infarction.

Algorithms↗
PubMed1997

Australian patients' delay in response to heart attack symptoms.

OBJECTIVES: To examine delay in seeking treatment among patients with an evolving acute myocardial infarction (MI), and to identify factors which contributed to this delay. DESIGN: Patient interview combined with medical record review. PARTICIPANTS AND SETTING: 317 patients with confirmed diagnosis of acute MI interviewed within 72 hours of admission to three hospitals. MAIN OUTCOME MEASURES: Delay from onset of symptoms to arrival at hospital, and cognitive, emotional, sociodemographic and clinical factors which contributed to increased prehospital delay. RESULTS: Median prehospital delay was 6.4 hours; 41% of patients delayed less than four hours, while 28% delayed less than two hours. Prehospital delay was increased in patients with fewer years of education (P = 0.001), lower income (P = 0.003) and transportation to the hospital by private car rather than ambulance (P = 0.02). Delay time was increased by several cognitive and emotional processes (P < 0.001), such as waiting to see if symptoms would go away, being too embarrassed to ask for assistance, and not recognising the importance of symptoms. Delay time was increased with heartburn, breathlessness or intermittent symptoms and decreased with sweating and dizziness (P < 0.05). Independent predictors of increased prehospital time (P < or = 0.01) were fewer than 10 years of education, not wanting to trouble anyone, failing to recognize the symptoms of delay, and the intermittent nature of symptoms. CONCLUSION: Over 50% of acute MI patients delay seeking treatment by six hours or more. Many factors related to cognitive and social processes that contribute to this delay may be remediable with appropriate patient and community education.

Educational Status↗
PubMed1997

Voluntary control of vascular tone by using skin-temperature biofeedback-relaxation in patients with advanced heart failure.

BACKGROUND: Advanced heart failure is characterized by activation of the sympathetic nervous system and intense vasoconstriction. Biofeedback-relaxation techniques have been used successfully to treat conditions with similar pathophysiological features. OBJECTIVES: The purpose of this study was to determine if conscious control of skin temperature via a biofeedback-relaxation technique could produce vasodilation and alter central hemodynamic status and circulating levels of catecholamines in patients with heart failure. METHODS: Forty patients with advanced heart failure were randomly assigned to either an intervention or a control group. The study was done in a special cardiac step-down unit accepting patients for hemodynamic monitoring. The patients in the intervention group had one session of skin-temperature biofeedback augmented by imagery of hand warmth and modified progressive muscle relaxation. Skin temperature, systemic vascular resistance, cardiac output, plasma levels of norepinephrine and epinephrine, oxygen consumption, respiratory rate, and pulmonary wedge pressure were measured before and after the biofeedback session. Control patients had the same measurements made but were not given instruction in biofeedback-relaxation techniques. RESULTS: Patients in the biofeedback-relaxation and control groups had comparable clinical profiles at baseline. Patients undergoing biofeedback-relaxation showed the following changes: (1) increase in skin temperature of 3.1 +/- 2.8 degrees F (1.7 +/- 1.5 degrees C) in the finger and 1.5 +/- 5.2 degrees F (0.4 +/- 1.2 degrees C) in the foot, (2) increase in cardiac output of 0.30 +/- 0.33 L/min, (3) decrease in systemic vascular resistance of 152 +/- 225 dyne.sec.cm-5, and (4) decrease in respiratory rate of 4.5 +/- 3.2 breaths per minute. The biofeedback group exhibited no changes in catecholamine levels or oxygen consumption. No changes in any of these parameters were seen in the control group. DISCUSSION: Despite the presence of marked vasoconstriction in patients with advanced heart failure, a single session of biofeedback-relaxation can increase finger temperature and cardiac output and decrease systemic vascular resistance and respiratory rate, apparently without effect on systemic levels of catecholamines or oxygen consumption.

Biofeedback, Psychology↗
PubMed1996

Agency for health care policy and research: Clinical practice guidelines for heart failure.

The Agency for Health Care Policy and Research (AHCPR) and Rand Corporation convened a panel of experts to review published studies on care of the patient with heart failure. The outcome was the Clinical Practice Guideline for the evaluation and care of patients with left ventricular systolic dysfunction, published in June 1994. This article reviews key points in the clinical practice guideline and summarizes important areas for future research to improve patient outcomes.

Health Planning Organizations↗
PubMed1996

Making mistakes.

Explore the source record for details and available documents.

Critical Care↗
PubMed1996

Heart failure secondary to left ventricular systolic dysfunction. Therapeutic advances and treatment recommendations.

Although heart failure secondary to left ventricular systolic dysfunction remains a serious disease with high morbidity and mortality, pharmacologic intervention has been shown to be associated with improved survival and a decreased number of hospitalizations. Primary-care providers must be aware of the potential benefits of recent therapeutic advances and current treatment recommendations for patients with heart failure to receive optimal care. Important aspects of nonpharmacologic care are dietary restrictions, exercise training, and through patient education and counseling. Pharmacologic therapy includes diuretics, angiotensin-converting enzyme inhibitors (ACE) and other vasodilating agents, and digoxin. ACE inhibitors are currently recommended for all patients with left ventricular dysfunction in whom use of these agents is not contraindicated. The mortality and morbidity from heart failure even with ACE inhibitors remain high, however. Promising clinical findings with such investigational agents as vesnarinone and pimobendan and the new-generation beta-blocker carvedilol suggest future new treatments to further improve the prognosis of these patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Causes of delay in seeking treatment for heart attack symptoms.

With the advent of thrombolytic therapy and other coronary reperfusion strategies, rapid identification and treatment of acute myocardial infarction greatly reduces mortality. Unfortunately, many patients delay seeking medical care and miss the benefits afforded by recent advances in treatment. Studies have shown that the median time from onset of symptoms to seeking care ranges from 2 to 61/2 hours, while optimal benefit is derived during the first hour from symptom onset. The phenomenon of delay by AMI patients and those around them needs to be understood prior to the design of education and counseling strategies to reduce delay. In this article the literature is reviewed and variables that increase patient delay are identified. A theoretical model based on the health belief model, a self regulation model of illness cognition, and interactionist role theory is proposed to explain the response of an individual to the signs and symptoms of acute myocardial infarction. Finally, recommendations are made for future research.

Attitude to Health↗
PubMed1995

Predictors of between-method differences in cardiac output measurement using thoracic electrical bioimpedance and thermodilution.

OBJECTIVES: To evaluate the usefulness of transthoracic electrical bioimpedance in trending changes in cardiac output after cardiac surgery, and to identify predictors of differences between cardiac output measured by thermodilution and transthoracic electrical bioimpedance methods. DESIGN: Prospective repeated-measures study. SETTING: University-affiliated tertiary care center. PATIENTS: Thirty-four adult patients undergoing elective cardiac surgery with routine pulmonary artery catheter placement. INTERVENTIONS: Simultaneous paired cardiac output measurements by transthoracic electrical bioimpedance and thermodilution were made at four time points: within 2 hrs of intensive care unit (ICU) admission; when the patient reached a normothermic temperature; after extubation; and 24 hrs after ICU admission. MEASUREMENTS AND MAIN RESULTS: Mean measurements by each method over time did not differ, except at ICU admission, when compared by repeated-measures analysis of variance. For each time point, bias and precision between methods were calculated. Bias calculations ranged from 0.02 to 0.21 L/min/m2. Precision calculations ranged from 1.06 to 1.52 L/min/m2. Predictors of between-method differences identified by a multiple regression model of hemodynamic variables were: increased systemic vascular resistance index, decreased mean arterial pressure (MAP), and the presence of atrial or ventricular pacing. CONCLUSIONS: While mean postoperative cardiac output measurements did not differ by method over time, agreement between transthoracic electrical bioimpedance and thermodilution methods was poor in the immediate postoperative period, with precision calculations indicative of clinically significant differences. Increased systemic vascular resistance index and decreased MAP were predictive of larger between-method differences.

Aged↗