Hemodynamic Parameters in the Assessment of Fluid Status in A
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Radionuclear Measurement of Peripheral Hemodynamics In
RadionuclearMeasurementof Peripheral Hemodynamics in Selection of Vasodilators for Treatment of Heart Failure Yasuhiro Todo, Mitsumasa Ohyanagi, Ryu Fujisue, and Tadaaki Iwasaki Hyogo College ofMedicine, Nishinomiya, Japan Inorder to select the optimal vasodilator for the treatment of patients with congestive heart failure (CHF), the acute effects of three vasodilators (isosorbide dinitrate (ISDN) 5 mg, nifedipine 10 mg, and prazosin 1 mg) on peripheral capacitance and resistance vessels (CV and RV)were evaluated by a newly devised radionuclear technique (Study 1).Thirty-six @ patients with chronic CHF were dividedinto Group A (ejectionfraction (EF) 35%, n = 20, mean EF: 47.2 ±6.5%) and B (EF < 35%, n = 16, mean EF: 24.8 ±7.1%). ISDNproduced the strongest CVdilatation(25% in both groups). Nifedipinereduced RVtone in Groups A and B (14% and 27%, respectively),and CVtone in Group A (6%). Prazosin had the most prominent effects on both vessels in Group B. From these results, it appeared: (a) ISDN is indicated for the cases with increased CV tone, (b) nifedipine is suitable for those with @ increased RV tone, (C)in cases of increased tone in both vessels, nifedipine (when EF 35%) or prazosin (when EF < 35%) is optimal.To evaluate the validityof this assignment, 49 subjects with CHF were divided into Group 1 (n = 16, increased CV tone), Group 2 (n = 17, increased RV tone), and Group 3 (n = 16, increased CV and RV tone) in Study 2. In Group 1, the changes of all indexes were not significantly different between the subjects treated with optimal drug based on the assignment (subgroup P) and those with a non-optimaldrug (subgroup N)after 2 wk of therapy. -
Relationship Between Vasodilatation and Cerebral Blood Flow Increase in Impaired Hemodynamics: a PET Study with the Acetazolamide Test in Cerebrovascular Disease
CLINICAL INVESTIGATIONS Relationship Between Vasodilatation and Cerebral Blood Flow Increase in Impaired Hemodynamics: A PET Study with the Acetazolamide Test in Cerebrovascular Disease Hidehiko Okazawa, MD, PhD1,2; Hiroshi Yamauchi, MD, PhD1; Hiroshi Toyoda, MD, PhD1,2; Kanji Sugimoto, MS1; Yasuhisa Fujibayashi, PhD2; and Yoshiharu Yonekura, MD, PhD2 1PET Unit, Research Institute, Shiga Medical Center, Moriyama, Japan; and 2Biomedical Imaging Research Center, Fukui Medical University, Fukui, Japan Key Words: acetazolamide; cerebrovascular disease; cerebral The changes in cerebral blood flow (CBF) and arterial-to- blood volume; vasodilatory capacity; cerebral perfusion pressure capillary blood volume (V0) induced by acetazolamide (ACZ) are expected to be parallel each other in the normal circula- J Nucl Med 2003; 44:1875–1883 tion; however, it has not been proven that the same changes in those parameters are observed in patients with cerebro- vascular disease. To investigate the relationship between changes in CBF, vasodilatory capacity, and other hemody- namic parameters, the ACZ test was performed after an The ability of autoregulation to maintain the cerebral 15O-gas PET study. Methods: Twenty-two patients with uni- blood flow (CBF), which resides in the cerebral circulation lateral major cerebral arterial occlusive disease underwent despite transient changes in systemic mean arterial blood 15 PET scans using the H2 O bolus method with the ACZ test pressure, has been shown to occur via the mechanism of 15 after the O-gas steady-state method. CBF and V0 for each arteriolar vasodilatation in the cerebral circulation (1). The subject were calculated using the 3-weighted integral vasodilatory change in the cerebral arteries is assumed for method as well as the nonlinear least-squares fitting method. -
Hemodynamic Effects of Vasodilators and Long-Term Response in Heart Failure
JACC Vol. 3, No.6 1521 June 1984:1521-30 REPORTS ON THERAPY Hemodynamic Effects of Vasodilators and Long-Term Response in Heart Failure JOSEPH A. FRANCIOSA, MD, FACC, W. BRUCE DUNKMAN, MD, FACC,* CHERYL L. LEDDY, MD* Philadelphia, Pennsylvania and Little Rock, Arkansas Hemodynamic responses to vasodilators are commonly ml/min per kg (p < 0.01), and exercise duration also assessed when starting long-term vasodilator treatment increased by 1.8 ± 3.5 minutes (p < 0.01). Changes in in patients with chronic left ventricular failure, although maximal oxygen uptake, however, did not correlate with the relation between short- and long-term responses is short-term changes in pulmonary wedge pressure (cor• not established. Thus, short- and long-term hemody• relation coefficient [r] = - 0.14), cardiac index (r = namic responses to placebo and vasodilators (isosorbide - 0.01) or systemic vascular resistance (r = - 0.20). dinitrate, minoxidil and enalapril or captopril) were Long-term hemodynamic changes also failed to correlate measured and long-term clinical efficacy was assessed with changes in exercise capacity. Baseline hemody• by changes in exercise capacity after 1 to 5 months of namics, cardiac dimensions and left ventricular ejection vasodilator administration (plus digitalis and diuretic fraction before vasodilator administration all failed to agents) in 46 patients with New York Heart Association correlate with baseline exercise capacity or with long• fun~tional class II to IV heart failure caused by cardio• term changes in exercise capacity. myopathy. There were no significant changes in hemo• Thus, hemodynamic measurements at initiation or dynamics or exercise capacity during placebo treatment. -
Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G
& Experim l e ca n i t in a l l C Aliya, J Clinic Experiment Cardiol 2011, 2:11 C f a Journal of Clinical & Experimental o r d l DOI: 10.4172/2155-9880.1000170 i a o n l o r g u y o J Cardiology ISSN: 2155-9880 Review Article Open Access Effects of Vasodilation and Arterial Resistance on Cardiac Output Aliya Siddiqui Department of Biotechnology, Chaitanya P.G. College, Kakatiya University, Warangal, India Abstract Heart is one of the most important organs present in human body which pumps blood throughout the body using blood vessels. With each heartbeat, blood is sent throughout the body, carrying oxygen and nutrients to all the cells in body. The cardiac cycle is the sequence of events that occurs when the heart beats. Blood pressure is maximum during systole, when the heart is pushing and minimum during diastole, when the heart is relaxed. Vasodilation caused by relaxation of smooth muscle cells in arteries causes an increase in blood flow. When blood vessels dilate, the blood flow is increased due to a decrease in vascular resistance. Therefore, dilation of arteries and arterioles leads to an immediate decrease in arterial blood pressure and heart rate. Cardiac output is the amount of blood ejected by the left ventricle in one minute. Cardiac output (CO) is the volume of blood being pumped by the heart, by left ventricle in the time interval of one minute. The effects of vasodilation, how the blood quantity increases and decreases along with the blood flow and the arterial blood flow and resistance on cardiac output is discussed in this reviewArticle. -
Medical Management of Advanced Heart Failure
CLINICAL CARDIOLOGY CLINICIAN’S CORNER Medical Management of Advanced Heart Failure Anju Nohria, MD Context Advanced heart failure, defined as persistence of limiting symptoms de- Eldrin Lewis, MD spite therapy with agents of proven efficacy, accounts for the majority of morbidity and mortality in heart failure. Lynne Warner Stevenson, MD Objective To review current medical therapy for advanced heart failure. EART FAILURE HAS EMERGED AS Data Sources We searched MEDLINE for all articles containing the term advanced a major health challenge, in- heart failure that were published between 1980 and 2001; EMBASE was searched from creasing in prevalence as age- 1987-1999, Best Evidence from 1991-1998, and Evidence-Based Medicine from 1995- adjusted rates of myocardial 1999. The Cochrane Library also was searched for critical reviews and meta-analyses Hinfarction and stroke decline.1 Affect- of congestive heart failure. ing 4 to 5 million people in the United Study Selection Randomized controlled trials of therapy for 150 patients or more States with more than 2 million hospi- were included if advanced heart failure was represented. Other common clinical situ- talizations each year, heart failure alone ations were addressed from smaller trials as available, trials of milder heart failure, con- accounts for 2% to 3% of the national sensus guidelines, and both published and personal clinical experience. health care budget. Developments her- Data Extraction Data quality was determined by publication in peer-reviewed lit- alded in the news media increase pub- erature or inclusion in professional society guidelines. lic expectations but focus on decreas- Data Synthesis A primary focus for care of advanced heart failure is ongoing iden- ing disease progression in mild to tification and treatment of the elevated filling pressures that cause disabling symp- moderate stages2,3 or supporting the cir- toms. -
Clinical Assessment in Acute Heart Failure
Hellenic J Cardiol 2015; 56: 285-301 Review Article Clinical Assessment in Acute Heart Failure 1 2 NIKOLAOS S. KAKOUROS , STAVROS N. KAKOUROS 1University of Massachusetts, MA, USA; 2Cardiac Department, “Amalia Fleming” General Hospital, Athens, Greece Key words: eart failure (HF) is defined as “a clear precipitant or trigger. It is very im Heart failure, complex clinical syn drome that portant to establish the precipitating diagnosis, physical examination, H can result from any structural or causes, which may have therapeutic and congestion. functional cardiac disorder that impairs the prognostic implications. Approximate ability of the ventricle to fill with, or eject ly 60% of patients with AHF have doc blood.” HF has an estimated overall prev umented CAD. Myocardial ischemia in alence of 2.6%. It is becoming more com the setting of acute coronary syndromes mon in adults older than 65 years, because is a precipitant or cause, particularly in of increased survival after acute myocar patients presenting with de novo AHF.4 dial infarction (AMI) and improved treat AHF is also often precipitated by medica ment of coronary artery disease (CAD), tion and dietary noncompliance, as well val vular heart disease and hypertension.1 as by many other conditions, which are Acute HF (AHF) is an increasingly com summarized in Table 1. Once the diagno mon cause of hospitalizations and mortality sis of AHF is confirmed, initial therapy in worldwide. In the majority of patients, AHF cludes removal of precipitants; if this can Manuscript received: can be attributed to worsening chronic HF, be carried out successfully, the patient’s August 25, 2014; and approximately 4050% of this group have subsequent course may be stable. -
Pulse Pressure Variation Guided Fluid Therapy During Kidney Transplantation
Rev Bras Anestesiol. 2020;70(3):194---201 SCIENTIFIC ARTICLE Pulse pressure variation guided fluid therapy during ଝ kidney transplantation: a randomized controlled trial a,∗ a a a Alessandro De Cassai , Ottavia Bond , Silvia Marini , Giulio Panciera , b b a b a Lucrezia Furian , Flavia Neri , Giulio Andreatta , Paolo Rigotti , Paolo Feltracco a University of Padova, Department of Medicine --- DIMED, Section of Anesthesiology and Intensive Care, Padova, Italy b Padua University Hospital, Department of Surgery, Oncology and Gastroenterology, Kidney and Pancreas Transplant Unit, Padua, Italy Received 12 November 2019; accepted 15 February 2020 Available online 17 May 2020 KEYWORDS Abstract Kidney Purpose: Kidney transplantation is the gold-standard treatment for end stage renal disease. transplantation; Although different hemodynamic variables, like central venous pressure and mean arterial pres- sure, have been used to guide volume replacement during surgery, the best strategy still ought Fluid therapy; Creatinine; to be determined. Respiratory arterial Pulse Pressure Variation (PPV) is recognized to be a good Urea; predictor of fluid responsiveness for perioperative hemodynamic optimization in operating room Urine settings. The aim of this study was to investigate whether a PPV guided fluid management strat- egy is better than a liberal fluid strategy during kidney transplantation surgeries. Identification of differences in urine output in the first postoperative hour was the main objective of this study. Methods: We conducted a prospective, single blind, randomized controlled trial. We enrolled 40 patients who underwent kidney transplantation from deceased donors. Patients random- ized in the ‘‘PPV’’ group received fluids whenever PPV was higher than 12%, patients in the ‘‘free fluid’’ group received fluids following our institutional standard care protocol for kidney -1 -1 transplantations (10 mL.kg . -
JUGULAR VENOUS PRESSURE Maddury Jyotsna
INDIAN JOURNAL OF CARDIOVASCULAR DISEASES JOURNAL in women (IJCD) 2017 VOL 2 ISSUE 2 CLINICAL ROUNDS 1 WINCARS JVP- JUGULAR VENOUS PRESSURE Maddury Jyotsna DEFINITION OF JUGULAR VENOUS PULSE AND The external jugular vein descends from the angle of the PRESSURE mandible to the middle of the clavicle at the posterior Jugular venous pulse is defined as the oscillating top of border of the sternocleidomastoid muscle. The external vertical column of blood in the right Internal Jugular jugular vein possesses valves that are occasionally Vein (IJV) that reflects the pressure changes in the right visible. Blood flow within the external jugular vein is atrium in cardiac cycle. In other words, Jugular venous nonpulsatile and thus cannot be used to assess the pressure (JVP) is the vertical height of oscillating column contour of the jugular venous pulse. of blood (Fig 1). Reasons for Internal Jugular Vein (IJV) preferred over Fig 1: Schematic diagram of JVP other neck veins are IJV is anatomically closer to and has a direct course to right atrium while EJV does not directly drain into Superior vena cava. It is valve less and pulsations can be seen. Due to presence of valves in External Jugular vein, pulsations cannot be seen. Vasoconstriction secondary to hypotension (as in congestive heart failure) can make EJV small and barely visible. EJV is superficial and prone to kinking. Partial compression of the left in nominate vein is usually relieved during modest inspiration as the diaphragm and the aorta descend and the pressure in the two internal -
Chapter 9 Monitoring of the Heart and Vascular System
Chapter 9 Monitoring of the Heart and Vascular System David L. Reich, MD • Alexander J. Mittnacht, MD • Martin J. London, MD • Joel A. Kaplan, MD Hemodynamic Monitoring Cardiac Output Monitoring Arterial Pressure Monitoring Indicator Dilution Arterial Cannulation Sites Analysis and Interpretation Indications of Hemodynamic Data Insertion Techniques Systemic and Pulmonary Vascular Resistances Central Venous Pressure Monitoring Frank-Starling Relationships Indications Monitoring Coronary Perfusion Complications Electrocardiography Pulmonary Arterial Pressure Monitoring Lead Systems Placement of the Pulmonary Artery Catheter Detection of Myocardial Ischemia Indications Intraoperative Lead Systems Complications Arrhythmia and Pacemaker Detection Pacing Catheters Mixed Venous Oxygen Saturation Catheters Summary References HEMODYNAMIC MONITORING For patients with severe cardiovascular disease and those undergoing surgery associ- ated with rapid hemodynamic changes, adequate hemodynamic monitoring should be available at all times. With the ability to measure and record almost all vital physi- ologic parameters, the development of acute hemodynamic changes may be observed and corrective action may be taken in an attempt to correct adverse hemodynamics and improve outcome. Although outcome changes are difficult to prove, it is a rea- sonable assumption that appropriate hemodynamic monitoring should reduce the incidence of major cardiovascular complications. This is based on the presumption that the data obtained from these monitors are interpreted correctly and that thera- peutic decisions are implemented in a timely fashion. Many devices are available to monitor the cardiovascular system. These devices range from those that are completely noninvasive, such as the blood pressure (BP) cuff and ECG, to those that are extremely invasive, such as the pulmonary artery (PA) catheter. To make the best use of invasive monitors, the potential benefits to be gained from the information must outweigh the potential complications. -
The Utility of Modified Butler-Leggett Criteria for Right Ventricular
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by eCommons@AKU eCommons@AKU Section of Cardiology Department of Medicine March 2010 The utility of modified utleB r-Leggett criteria for right ventricular hypertrophy in detection of clinically significant shunt ratio in ostium secundum-type atrial septal defect in adults Adeel M. Siddiqui Aga Khan University Zainab Samad Nina Hakacova James Kinsella Cary Ward See next page for additional authors Follow this and additional works at: https://ecommons.aku.edu/pakistan_fhs_mc_med_cardiol Part of the Cardiology Commons Recommended Citation Siddiqui, A., Samad, Z., Hakacova, N., Kinsella, J., Ward, C., White, M., Crowley, A., Wagner, G., Harrison, J. (2010). The utility of modified Butler-Leggett criteria for right ventricular hypertrophy in detection of clinically significant shunt ratio in ostium secundum- type atrial septal defect in adults. Journal of Electrocardiology, 43(2), 161-166. Available at: https://ecommons.aku.edu/pakistan_fhs_mc_med_cardiol/36 Authors Adeel M. Siddiqui, Zainab Samad, Nina Hakacova, James Kinsella, Cary Ward, Michael White, Anna Lisa C. Crowley, Galen S. Wagner, and J. Kevin Harrison This article is available at eCommons@AKU: https://ecommons.aku.edu/pakistan_fhs_mc_med_cardiol/36 Available online at www.sciencedirect.com Journal of Electrocardiology 43 (2010) 161–166 www.jecgonline.com The utility of modified Butler-Leggett criteria for right ventricular hypertrophy in detection of clinically significant shunt ratio in ostium secundum–type atrial septal defect in adults ⁎ Adeel M. Siddiqui,a, Zainab Samad, MD,b,c Nina Hakacova, MD,c James Kinsella,d Cary Ward, MD,b Michael White, MD,b Anna Lisa C. -
Acute Vs Chronic Volume Overload on Arterial Stiffness in Haemodialysis Patients
Journal of Human Hypertension (2005) 19, 425–427 & 2005 Nature Publishing Group All rights reserved 0950-9240/05 $30.00 www.nature.com/jhh COMMENTARY Acute vs chronic volume overload on arterial stiffness in haemodialysis patients Y-P Lin1,W-CYu1 and C-H Chen1,2,3 1Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; 2Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; 3Department of Social Medicine, National Yang-Ming University, Taipei, Taiwan Journal of Human Hypertension (2005) 19, 425–427. doi:10.1038/sj.jhh.1001842 Published online 10 March 2005 Volume overload is a cardinal feature of end-stage in the various vascular parameters monitored. renal disease (ESRD) patients. Acute volume over- Each vascular parameter may be affected variably load, as represented by interdialytic weight gain, is by factors such as blood pressure and heart rate. associated with increased aortic pulse wave velocity For instance, augmentation index may be under- (aPWV) and independently related to total mortality estimated for approximately 4% per 10 beats/min in haemodialysis patients.1,2 Based on the Laplace’s increase of heart rate.9 aPWV may increase 41 m/s law, volume expansion increases arterial stiffness (or by an increase in heart rate of 40 beats/min.10 The reduces arterial compliance) by increasing arterial existence of multiple arteriovenous shunts may also distension. Therefore, it would appear intriguing that affect systemic compliance. aPWV is proportional to acute volume reduction by ultrafiltration does not the square root of the product of wall elastance and always acutely improve arterial stiffness.3–7 Dialysis thickness. -
Electrocardiography in Aortic Regurgitation: It's in the Details
THE CLINICAL PICTURE SRIDHAR VENKATACHALAM, MD, MRCP CURTIS M. RIMMERMAN, MD, MBA Department of Hospital Medicine, Cleveland Clinic Gus P. Karos Chair, Clinical Cardiovascular Medicine, Department of Cardiovascular Medicine, Cleveland Clinic The Clinical Picture Electrocardiography in aortic regurgitation: It’s in the details Although not routinely reported, the negative U wave indicates underlying FIGURE 1. The patient’s 12-lead electrocardiogram shows normal sinus rhythm and a rate of 55 beats per minute. The frontal-plane QRS complex vector is deviated leftward. Left atrial abnor- structural or mality is present, given the terminally negative P wave in lead V1 and the bifid P wave in lead II. ischemic heart Left ventricular volume overload is supported by the following findings: increased QRS complex voltage, best seen in the precordial (chest) leads, indicative of increased left ventricular mass; disease prominent septal depolarization, as reflected by Q waves in leads 4V to V6; the absence of an ST- segment or T-wave abnormality; and negative U waves in leads V4 to V6 (arrows). 72-year-old man with a 15-year history taking any cardiac drugs, and his health has A of a heart murmur presents to his cardi- previously been excellent. ologist with shortness of breath on exertion On physical examination, his pulse rate is over the past 12 months. He otherwise feels regular at 55 beats per minute, and his blood well and reports no chest discomfort, palpita- pressure is 178/66 mm Hg. Cardiac ausculta- tions, or swelling of his legs or feet. He is not tion reveals an early- to mid-diastolic murmur heard best with the patient seated and leaning doi:10.3949/ccjm.78a.10141 forward, and located at the left sternal border; CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 78 • NUMBER 8 AUGUST 2011 505 Downloaded from www.ccjm.org on October 2, 2021.