DOCSLIB.ORG

Transthoracic Echo Report

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Transthoracic Echo Report Transthoracic Echo Report Name:SMITH, IDA Sex: F Exam Loc: OP Referring Physician: Michelle D Miller, MD MRN:1000547354 DOB: 11/18/1942 Age: 73 Reading Physician: Farhat Khairallah, MD FIN:6613303590 Exam Date: 05/25/2016 09:49 Ordering Physician: Miller, Michelle Ht (in):62 Wt (lb): 170 BSA: 1.8 Prior Study Date: Sonographer: Lacy Ward, RCS Ordered: Routine Dr. Notified:No Notify Date/Time: Procedure CPT: 93306 Indications: Cardiac murmur, unspecified ICD Codes: R011 Procedure Performed: E-2D MM Dop. BP:148 / 81 HR: 72 Rhythm: Other Technical Quality: Fair FINDINGS Left Ventricle Left ventricular cavity size normal. Normal left ventricular ejection fraction. Left ventricular ejection fraction is 60-65%. Left ventricular wall thickness mildly increased. Abnormal relaxation filling pattern of the left ventricle for age (stage 1 diastolic dysfunction). Right Ventricle Mild right ventricular dilatation. Normal right ventricular global systolic function. Left Atrium Normal left atrial size. Right Atrium Normal right atrial size. Mitral Valve Mitral valve structurally/functionally normal. No significant MR Aortic Valve Diffuse thickening of the aortic valve cusps with reduced excursion. Mild calcific aortic stenosis. Tricuspid Valve Normally structured tricuspid valve. Mild tricuspid regurgitation (normal variant). Right ventricular systolic pressure estimated to be 34 mm Hg. Pulmonary Valve Structurally normal pulmonic valve. Minimal pulmonic regurgitation (normal variant). Pericardium No pericardial effusion. CONCLUSIONS Normal left ventricular size and systolic function. The estimated ejection fraction of the left ventricle is 60-65%. Dilated right ventricle with preserved function. Mild calcific aortic stenosis. Grade 1 diastolic dysfunction. Page 1 / 2 Transthoracic Echo Report SMITH, IDA 05/25/2016 09:49 MEASUREMENTS (Male / Female) Normal Values 2D ECHO LV Diastolic Diameter PLAX 4.2 cm 4.2 - 5.9 / 3.9 - 5.3 cm LV Systolic Volume 2D Cubed16.2 ml LV Systolic Diameter PLAX 2.5 cm LV Diastolic Volume 2D Cubed 71.5 ml IVS Diastolic Thickness 1.2 cm 0.6 - 1.0 / 0.6 - 0.9 cm LV Ejection Fraction 2D Cubed 77.3 % LVPW Diastolic Thickness 1.2 cm 0.6 - 1.0 / 0.6 - 0.9 cm LV Ejection Fraction 2D Teich69.9 % LV Relative Wall Thickness 0.6 LV Ejection Fraction MOD BP 62.5 % >= 55 % RV Internal Dim ED PLAX 3.3 cm LV Cardiac Index MOD BP 964.8 cm³/min·m² LVOT Diameter 1.9 cm LV Ejection Fraction MOD 4C62.7 % Aortic Root Diameter 2.9 cm LV Cardiac Index MOD 4C 1234.9 cm³/min·m² LA Systolic Diameter LX 3.3 cm 3.0 - 4.0 / 2.7 - 3.8 cm LV Ejection Fraction 4C AL 64.6 % LV Stroke Volume 2D Teich 53.4 ml LV Cardiac Index 4C AL 1282.5 cm³/min·m² LV Stroke Index 2D Teich 30.0 ml/m² LV Ejection Fraction MOD 2C63.0 % LV Stroke Volume 2D Cubed 55.3 ml LV Ejection Fraction 2C AL 66.2 % LV Stroke Index 2D Cubed 31.1 ml/m² LV Cardiac Index 2C AL 746.8 cm³/min·m² LV Systolic Volume 2D Teich 23.0 ml LA Volume Index 14.6 cm³/m² 16 - 28 cm³/m² LV Diastolic Volume 2D Teich 76.4 ml M-MODE Aortic Root Diameter MM 2.5 cm LA Ao Ratio MM 1.4 LA Systolic Diameter MM 3.4 cm AV Cusp Separation MM 1.5 cm DOPPLER AV Peak Velocity 2.3 m/s Isovolumic Relaxation Time 77.0 ms AV Peak Gradient 21.2 mmHg LV E' Lateral Velocity 0.1 m/s AV Mean Gradient 10.0 mmHg Mitral E to LV E' Lateral Ratio13.0 AV Velocity Time Integral 47.8 cm LV E' Septal Velocity 0.1 m/s LVOT Peak Velocity 1.2 m/s Mitral E to LV E' Septal Ratio 9.0 LVOT Peak Gradient 5.6 mmHg TV Peak Velocity 0.5 m/s LVOT Velocity Time Integral 25.3 cm TR Peak Velocity 2.7 m/s LVOT Cardiac Index 2768.2 cm³/min·m² TR Peak Gradient28.5 mmHg AV Area Cont Eq vti 1.5 cm² Right Atrial Pressure 10.0 mmHg AV Area Cont Eq pk 1.5 cm² Pulmonary Artery Systolic Pressure 38.5 mmHg Mitral E Point Velocity 0.8 m/s Right Ventricular Systolic Pressure 38.5 mmHg Mitral A Point Velocity 1.1 m/s PV Peak Velocity 1.1 m/s Mitral E to A Ratio 0.7 PV Peak Gradient 4.4 mmHg Farhat Khairallah MD (Electronically Signed) Final Date: 25 May 2016 11:09 Page 2 / 2.
Load more

Recommended publications
  • Blood Vessels: Part A
    Chapter 19 The Cardiovascular System: Blood Vessels: Part A Blood Vessels • Delivery system of dynamic structures that begins and ends at heart – Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus – Capillaries: contact tissue cells; directly serve cellular needs – Veins: carry blood toward heart Structure of Blood Vessel Walls • Lumen – Central blood-containing space • Three wall layers in arteries and veins – Tunica intima, tunica media, and tunica externa • Capillaries – Endothelium with sparse basal lamina Tunics • Tunica intima – Endothelium lines lumen of all vessels • Continuous with endocardium • Slick surface reduces friction – Subendothelial layer in vessels larger than 1 mm; connective tissue basement membrane Tunics • Tunica media – Smooth muscle and sheets of elastin – Sympathetic vasomotor nerve fibers control vasoconstriction and vasodilation of vessels • Influence blood flow and blood pressure Tunics • Tunica externa (tunica adventitia) – Collagen fibers protect and reinforce; anchor to surrounding structures – Contains nerve fibers, lymphatic vessels – Vasa vasorum of larger vessels nourishes external layer Blood Vessels • Vessels vary in length, diameter, wall thickness, tissue makeup • See figure 19.2 for interaction with lymphatic vessels Arterial System: Elastic Arteries • Large thick-walled arteries with elastin in all three tunics • Aorta and its major branches • Large lumen offers low resistance • Inactive in vasoconstriction • Act as pressure reservoirs—expand
    [Show full text]
  • The Icefish (Chionodraco Hamatus)
    The Journal of Experimental Biology 207, 3855-3864 3855 Published by The Company of Biologists 2004 doi:10.1242/jeb.01180 No hemoglobin but NO: the icefish (Chionodraco hamatus) heart as a paradigm D. Pellegrino1,2, C. A. Palmerini3 and B. Tota2,4,* Departments of 1Pharmaco-Biology and 2Cellular Biology, University of Calabria, 87030, Arcavacata di Rende, CS, Italy, 3Department of Cellular and Molecular Biology, University of Perugia, 06126, Perugia, Italy and 4Zoological Station ‘A. Dohrn’, Villa Comunale, 80121, Napoli, Italy *Author for correspondence (e-mail: [email protected]) Accepted 13 July 2004 Summary The role of nitric oxide (NO) in cardio-vascular therefore demonstrate that under basal working homeostasis is now known to include allosteric redox conditions the icefish heart is under the tonic influence modulation of cell respiration. An interesting animal for of a NO-cGMP-mediated positive inotropism. We also the study of this wide-ranging influence of NO is the cold- show that the working heart, which has intracardiac adapted Antarctic icefish Chionodraco hamatus, which is NOS (shown by NADPH-diaphorase activity and characterised by evolutionary loss of hemoglobin and immunolocalization), can produce and release NO, as multiple cardio-circulatory and subcellular compensations measured by nitrite appearance in the cardiac effluent. for efficient oxygen delivery. Using an isolated, perfused These results indicate the presence of a functional NOS working heart preparation of C. hamatus, we show that system in the icefish heart, possibly serving a both endogenous (L-arginine) and exogenous (SIN-1 in paracrine/autocrine regulatory role. presence of SOD) NO-donors as well as the guanylate cyclase (GC) donor 8Br-cGMP elicit positive inotropism, while both nitric oxide synthase (NOS) and sGC Key words: nitric oxide, heart, Antarctic teleost, icefish, Chionodraco inhibitors, i.e.
    [Show full text]
  • A Review of the Stroke Volume Response to Upright Exercise in Healthy Subjects
    190 Br J Sports Med: first published as 10.1136/bjsm.2004.013037 on 25 March 2005. Downloaded from REVIEW A review of the stroke volume response to upright exercise in healthy subjects C A Vella, R A Robergs ............................................................................................................................... Br J Sports Med 2005;39:190–195. doi: 10.1136/bjsm.2004.013037 Traditionally, it has been accepted that, during incremental well trained athletes (subject sex was not stated). Unfortunately, these findings were exercise, stroke volume plateaus at 40% of VO2MAX. largely ignored and it became accepted that However, recent research has documented that stroke stroke volume plateaus during exercise of increasing intensity. volume progressively increases to VO2MAX in both trained More recent investigations have reported that and untrained subjects. The stroke volume response to stroke volume progressively increases in certain 7–12 incremental exercise to VO2MAX may be influenced by people. The mechanisms for the continual training status, age, and sex. For endurance trained increase in stroke volume are not completely understood. Gledhill et al7 proposed that subjects, the proposed mechanisms for the progressive enhanced diastolic filling and subsequent increase in stroke volume to VO2MAX are enhanced diastolic enhanced contractility are responsible for the filling, enhanced contractility, larger blood volume, and increased stroke volume in trained subjects. However, an increase in stroke volume with an decreased cardiac afterload. For untrained subjects, it has increase in exercise intensity has also been been proposed that continued increases in stroke volume reported in untrained subjects.89Table 1 presents may result from a naturally occurring high blood volume. a summary of the past research that has quantified stroke volume during exercise.
    [Show full text]
  • 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.
    [Show full text]
  • 60 Arterial Pressure–Based Cardiac Output Monitoring 525
    PROCEDURE Arterial Pressure–Based Cardiac 60 Output Monitoring Susan Scott PURPOSE: Arterial pressure–based cardiac output monitoring is a minimally invasive technology that can be used to obtain hemodynamic data on a continuous basis. PREREQUISITE NURSING • The difference between the systolic and diastolic pressures KNOWLEDGE is called the pulse pressure, with a normal value of 40 mm Hg. • Arterial pressure is determined by the relationship between • Knowledge of the anatomy and physiology of the cardio- blood fl ow through the vessels (cardiac output), the com- vascular system is necessary. pliance of the aorta and larger vessels, and the resistance • Knowledge of the anatomy and physiology of the vascu- of the more peripheral vessel walls (systemic vascular lature and adjacent structures is needed. resistance). The arterial pressure is therefore affected by • Understanding of the pathophysiologic changes that occur any factors that change either cardiac output, compliance, in heart disease and affect fl ow dynamics is necessary. or systemic vascular resistance. • Understanding of aseptic technique is needed. • The average arterial pressure during a cardiac cycle is • Understanding of the hemodynamic effects of vasoactive called the mean arterial pressure (MAP). It is not the medications and fl uid resuscitation is needed. average of the systolic plus the diastolic pressures, because 1 • Understanding of the principles involved in hemodynamic at normal heart rates systole accounts for 3 of the cardiac 2 monitoring is necessary. cycle and diastole accounts for 3 of the cardiac cycle. • Knowledge of invasive cardiac output monitoring is needed. The MAP is calculated automatically by most patient • Knowledge of arterial waveform interpretation is needed.
    [Show full text]
  • Can We Study the Baroreflex Mechanisms with Other Variables
    Arch Cardiol Mex 2012;82(2):91-92 www.elsevier.com.mx EDITORIAL COMMENT Can we study the baroreflex mechanisms with other variables than blood pressure and heart rate? ¿Podemos estudiar los mecanismos barorreflejo con otras varia- bles de la presión arterial y la frecuencia cardiaca? Received on March 20, 2012; accepted on March 30, 2012. he baroreflex (BR) is a fundamental physiological The high pressure baroreceptors discharge during the mechanism that keeps the blood pressure (BP) sta- stretching of the walls of the arteries (loading of the re- ble by buffering the disturbances that arise in the flex) and decrease or abolish its discharge rate during T 1 system during the activities of the daily life. These dis- the collapse of the walls or decrease of the lumen of the turbances alter the control system and deviate the mean arteries (unloading of the reflex). During the loading of BP either increasing or decreasing it. The BP is maintai- the reflex the cardiovagal system is activated, whereas ned tonically around a “set point” and the disturbances during the unloading of the reflex the cardiosympathetic oscillate around it; they me be profound or relatively and vasoympathetic systems are activated.5,6 minor.2 Sometimes the disturbances occur at predictable The BP system is intrinsically “noisy” and there are times such as those seen during non-Rem sleep or rhyth- external and internal disturbances constantly acting on mic breathing.3 The disturbances could be considered the system requiring dampening or buffering of these “phasic” changes that are randomly added or subtrac- signals.5,7,8 The external disturbances including, changes ted to the tonically maintained set point.
    [Show full text]
  • Time-Varying Elastance and Left Ventricular Aortic Coupling Keith R
    Walley Critical Care (2016) 20:270 DOI 10.1186/s13054-016-1439-6 REVIEW Open Access Left ventricular function: time-varying elastance and left ventricular aortic coupling Keith R. Walley Abstract heart must have special characteristics that allow it to respond appropriately and deliver necessary blood flow Many aspects of left ventricular function are explained and oxygen, even though flow is regulated from outside by considering ventricular pressure–volume characteristics. the heart. Contractility is best measured by the slope, Emax, of the To understand these special cardiac characteristics we end-systolic pressure–volume relationship. Ventricular start with ventricular function curves and show how systole is usefully characterized by a time-varying these curves are generated by underlying ventricular elastance (ΔP/ΔV). An extended area, the pressure– pressure–volume characteristics. Understanding ventricu- volume area, subtended by the ventricular pressure– lar function from a pressure–volume perspective leads to volume loop (useful mechanical work) and the ESPVR consideration of concepts such as time-varying ventricular (energy expended without mechanical work), is linearly elastance and the connection between the work of the related to myocardial oxygen consumption per beat. heart during a cardiac cycle and myocardial oxygen con- For energetically efficient systolic ejection ventricular sumption. Connection of the heart to the arterial circula- elastance should be, and is, matched to aortic elastance. tion is then considered. Diastole and the connection of Without matching, the fraction of energy expended the heart to the venous circulation is considered in an ab- without mechanical work increases and energy is lost breviated form as these relationships, which define how during ejection across the aortic valve.
    [Show full text]
  • Minnesota 1 Hemodynamics.Pptx
    9/18/17 Applying Your Data to Affect Your Care: Case Studies in Hemodynamics B. McLean, MN, RN, NP-BC, CCNS-BC, CCRN, FCCM 404-626-2843 Barbaramclean.com [email protected] Introduction Critical care is a concept, not a location, which frequently begins with ED intervention and culminates in ICU admission and continued management – Peter Safar Why the microcirculation is important in shock and why we MUST evaluate it! • where oxygen exchange takes place • plays a central role in the immune function • Plays a central role in insulin resistance • Plays a central role in maintaining vascular tone • During shock : first to go and last to recover 1 9/18/17 Cardiac Function • Function – Continuous propulsion of blood through arteries to capillaries to veins • Right heart circulation • Right heart fills from systemic veins (partially deoxygenated) • Right heart ejects to pulmonary artery (partially deoxygenated) • Left heart circulation • Left heart fills from pulmonary veins (maximally oxygenated) • Left heart ejects to aorta (maximally oxygenated) • Capillaries – microscopic vessels that allow for exchange of gases, nutrients and metabolic waste • Pulmonary capillaries perfuse alveoli, delivering CO2 and taking up Oxygen • Systemic capillaries perfuse tissues, delivering oxygen and taking up CO2 Capillaries • Capillaries – Smallest blood vessels connect arterial outflow and venous return – Microcirculation – flow from metarteriole through capillaries and into postcapillary venule – Exchange vessels – primary function is exchange between blood and interstitial fluid – Lack tunica media and tunica externa • Substances pass through just one layer of endothelial cells and basement membrane – Capillary beds – arise from single metarteriole • Vasomotion – intermittent contraction and relaxation • Throughfare channel – bypasses capillary bed Consider this….
    [Show full text]
  • The Jugular Venous Pressure Revisited
    REVIEW CME EDUCATIONAL OBJECTIVE: Readers will measure and interpret the jugular venous pressure in their patients CREDIT with heart failure JOHN MICHAEL S. CHUA CHIACO, MD NISHA I. PARIKH, MD, MPH DAVID J. FERGUSSON, MD Cardiovascular Disease, John A. Burns School Assistant Professor, John A. Burns School Clinical Professor of Medicine, Department of Medicine, University of Hawaii, Honolulu of Medicine, University of Hawaii; of Cardiology, John A. Burns School The Queen’s Medical Center, Honolulu of Medicine, University of Hawaii; The Queen’s Medical Center, Honolulu The jugular venous pressure revisited ■■ ABSTRACT n this age of technological marvels, I it is easy to become so reliant on them as Assessment of the jugular venous pressure is often inad- to neglect the value of bedside physical signs. equately performed and undervalued. Here, we review Yet these signs provide information that adds the physiologic and anatomic basis for the jugular venous no cost, is immediately available, and can be pressure, including the discrepancy between right atrial repeated at will. and central venous pressures. We also describe the cor- Few physical findings are as useful but as rect method of evaluating this clinical finding and review undervalued as is the estimation of the jugular the clinical relevance of the jugular venous pressure, venous pressure. Unfortunately, many practi- especially its value in assessing the severity and response tioners at many levels of seniority and experi- to treatment of congestive heart failure. Waveforms ence do not measure it correctly, leading to a vicious circle of unreliable information, lack reflective of specific conditions are also discussed.
    [Show full text]
  • Flotrac Algorithm Calculating Stroke Volume and Cardiac Output Getting Ml/Beat from Mmhg
    FloTrac Algorithm Calculating stroke volume and cardiac output getting mL/beat from mmHg Summary Traditional: CO = HR * SV The FloTrac algorithm, an arterial pressure-based cardiac FloTrac system: APCO= PR x (sAP * x) output (APCO) method in which cardiac output can be Where x = M (HR, s , C(P), BSA, MAP, µ3 , µ4 ...) AP ap ap continuously calculated using an arterial catheter. This s = standard deviation of arterial pulse pressure technology is based on the basic principles of physics AP in mmHg is proportional to pulse pressure and the application of a sophisticated algorithm. x = scaling multivariate parameter proportional Physics and physiology to the effects of vascular tone on pulse pressure Flow is determined by a pressure gradient along a M = multivariate polynomial equation vessel and the resistance to that flow (F=ΔP/R). The FloTrac algorithm uses a similar principle to calculate BSA =body surface area calculated by Dubois’ pulsatile flow by incorporating the effects of both equation for body surface area vascular resistance and compliance through a MAP = mean arterial pressure calculated by conversion factor known as Khi ( ). x taking sum of sampled pressure point values over 20 seconds and dividing it by the number Cardiac output is an important component of of pressure points global oxygen delivery (DO2) and is the most often manipulated variable when improving oxygen delivery. µ = statistical moments determined by skewness Cardiac output is calculated by multiplying heart rate (symmetry) and kurtosis (distinctness of a peak) by the stroke volume. The FloTrac algorithm uses these calculated along several mathematical derivatives same components but substitutes heart rate with the pulse rate (PR), capturing only truly perfused beats, Arterial pressure-based cardiac output and multiplies PR by a calculated stroke volume.
    [Show full text]
  • Cardiac Output
    Overview of Human Anatomy and Physiology: Cardiac Output Introduction Welcome to the Overview of Human Anatomy and Physiology course on the Cardiac System. This module, Cardiac Output, discusses measurement of heart activity and factors that affect activity. After completing this module, you should be able to: 1. Define stroke volume and cardiac output. 2. Discuss the relationship between heart rate, stroke volume, and cardiac output. 3. Identify the factors that control cardiac output. Measurement Cardiac Output The activity of the heart can be quantified to provide information on its health and efficiency. One important measurement is cardiac output (CO), which is the volume of blood ejected by the left ventricle each minute. Heart rate and stroke volume determine cardiac output. Heart rate (HR) is the number of heartbeats in one minute. The volume of blood ejected by the left ventricle during a heartbeat is the stroke volume (SV), which is measured in milliliters. Equation Cardiac output is calculated by multiplying the heart rate and the stroke volume. Average Values Cardiac output is the amount of blood pumped by the left ventricle--not the total amount pumped by both ventricles. However, the amount of blood within the left and right ventricles is almost equal, approximately 70 to 75 mL. Given this stroke volume and a normal heart rate of 70 beats per minute, cardiac output is 5.25 L/min. Relationships When heart rate or stroke volume increases, cardiac output is likely to increase also. Conversely, a decrease in heart rate or stroke volume can decrease cardiac output. What factors regulate increases and decreases in cardiac output? Regulation Factors Regulating Cardiac Output Factors affect cardiac output by changing heart rate and stroke volume.
    [Show full text]
  • Anemia on Cardiovascular Hemodynamics, Therapeutic Strategy and Clinical Outcomes in Patients with Heart Failure and Hemodynamic Congestion
    1670 TANIMURA M et al. Circ J 2017; 81: 1670 – 1677 ORIGINAL ARTICLE doi: 10.1253/circj.CJ-17-0171 Heart Failure Effect of Anemia on Cardiovascular Hemodynamics, Therapeutic Strategy and Clinical Outcomes in Patients With Heart Failure and Hemodynamic Congestion Muneyoshi Tanimura, MD; Kaoru Dohi, MD, PhD; Naoki Fujimoto, MD, PhD; Keishi Moriwaki, MD; Taku Omori, MD; Yuichi Sato, MD, PhD; Emiyo Sugiura, MD, PhD; Naoto Kumagai, MD, PhD; Shiro Nakamori, MD, PhD; Tairo Kurita, MD, PhD; Eitaro Fujii, MD, PhD; Norikazu Yamada, MD, PhD; Masaaki Ito, MD, PhD Background: We investigated the effect of anemia on cardiovascular hemodynamics, therapeutic strategies and clinical outcomes in heart failure (HF) patients. Methods and Results: We divided 198 consecutive HF patients who underwent right heart catheterization before in-hospital HF treatment into 2 groups according to the presence or absence of hemodynamic congestion (HC: mean pulmonary capillary wedge pressure ≥15 mmHg and/or mean right atrial pressure ≥10 mmHg). The hemoglobin level correlated with the cardiac index (CI) and systemic vascular resistance index (SVRI) (r=−0.34 and 0.42, P<0.05, respectively), and was the strongest contributor of SVRI only in the HC group. Anemic patients more frequently required intravenous inotropic support despite having higher CI and lower SVRI than non-anemic patients in the HC group. The novel hemodynamic subsets based on mean right atrial pressure and estimated left ventricular stroke work index but not Forrester subsets appropriately predicted the need for intravenous inotropic support. The prob- ability of hospitalization for worsening HF during 2-year follow-up period was significantly higher in anemic patients than in non- anemic patients in the HC group.
    [Show full text]