Pressure-Volume Loops in Cardiac Surgery
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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 -
Angiotensin II Protocol
Angiotensin II (Giapreza ™) Protocol Background Sepsis and septic shock are medical emergencies that affect millions of people each year and killing as many as 1 in 4.1 The cornerstones of therapy are fluid resuscitation, early appropriate antibiotics, source control if needed and vasopressors. A small portion of patients fail to respond to these therapies and develop refractory shock. The definition of refractory septic shock varies in the literature but is generally considered to be hypotension, with end-organ dysfunction, requiring high-dose vasopressor support.2 The associated mortality of refractory septic shock is up to 60% and as high as 80-90% in patients requiring more than 1 mcg/kg/min of norepinephrine.2,3 Patients who develop refractory septic shock comprise a very small portion of the population in large randomized controlled trials therefore limited data is available regarding outcomes and management. Indications: Angiotensin II (Ang II) is a vasoconstrictor used to increase blood pressure in adults with septic or other distributive shock. Administration: Starting dose of 5 (nanograms) ng/kg/min intravenously via central line only. Titration: Every 5 minutes by increments of 5 ng/kg/min as needed. Maximum dose should not exceed 80 ng/kg/min (During the first 3 hours of administration); after the first 3 hours the maintenance (maximum) dose is 40 ng/kg/min. Monitoring: Critical care setting only with telemetry, arterial blood pressure, and continuous SpO2 monitoring. DVT Prophylaxis should be started (unless contraindicated) -
Pleth Variability Index: a Dynamic Measurement to Help Assess to Help Measurement a Dynamic Index: Variability Pleth Responsiveness and Fluid Physiology
Pleth Variability Index: A Dynamic Measurement to Help Assess TECHNICAL BULLETIN TECHNICAL Physiology and Fluid Responsiveness SUMMARY PVI®, an index available with Masimo SET® pulse oximetry, is the first and only noninvasive, continuous, easy-to-use method to help clinicians manage fluid responsiveness in sedated patients under positive pressure ventilation. Other clinical uses have also been developed for PVI, including helping clinicians to assess the effects of positive end expiratory pressure on cardiac index and to identify patients at risk for hypotension during anesthesia induction. PVI, along with the other innovative noninvasive monitoring technologies available with the Masimo rainbow SET® platform (SpHb®, SpCO®, SpMet®, RRa™), has helped clinicians to realize improved patient outcomes while lowering the cost of care. INTRODUCTION Many pulse oximetry technologies display a processed and filtered representation of the photoplethysmosgraphic waveform. Each manufacturer uses unique proprietary algorithms to calculate the waveform displayed on the pulse oximeter. Masimo has extracted and processed information from the waveform to create two physiologic indices, perfusion index (PI) and pleth variability index (PVI). PI is calculated by indexing the infrared (IR) pulsatile signal against the nonpulsitile signal and expressing this number as a percentage. Masimo SET® PI has been shown to be useful to gauge the severity of illness in newborns1, 2 to assess the effectiveness of epidural blocks3, 4 to indicate successful interscalene nerve block placement in awake patients5 and to quantify peripheral perfusion for diagnosis of congenital heart disease in newborns.6 PVI is the first and only commercially available measurement that automatically and continuously calculates the respiratory variations in the photoplethysmosgraphic waveform. -
Valve Replacement Alexander Zezulkal, John Mackinnon2 and D.G
Postgrad Med J: first published as 10.1136/pgmj.68.797.180 on 1 March 1992. Downloaded from Postgrad Med J (1992) 68, 180 - 185 i) The Fellowship of Postgraduate Medicine, 1992 Hypertension in aortic valve disease and its response to valve replacement Alexander Zezulkal, John Mackinnon2 and D.G. Beevers' 'University Department ofMedicine and 2Department ofCardiology, Dudley Road Hospital, Birmingham BT18 7QH, UK Summary: We have investigated the prevalence ofhypertension and the response ofblood pressure to operation in 87 patients with lone aortic valve disease who underwent aortic valve replacement. In patients with aortic stenosis alone 26% were hypertensive pre-operatively (age and sex adjusted blood pressure > 160 systolic and or > 95 mmHg diastolic) and 24% were hypertensive post-operatively. In those with aortic regurgitation alone, hypertension was present in 65% before and 57% after valve replacement using the same criterion. For combined stenosis and regurgitation, the prevalence was 54% and 62%, respectively. The post-operative increase in systolic pressure in patients with aortic stenosis occurred mainly in those with a history of left ventricular failure. In those with aortic regurgitation or combined stenosis with regurgitation, diastolic pressure rose after valve replacement resulting in a prevalence of diastolic hypertension of 44% and 35%, respectively. Blood pressure changes were not predicted by the type of valve inserted nor its size. Our data show that despite severe symptomatic aortic valve disease, systolic hypertension was common in aortic stenosis and diastolic hypertension was found in aortic regurgitation. This underlines the by copyright. importance of blood pressure monitoring in patients following aortic valve replacement. -
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. -
04. the Cardiac Cycle/Wiggers Diagram
Part I Anaesthesia Refresher Course – 2018 4 University of Cape Town The Cardiac Cycle The “Wiggers diagram” Prof. Justiaan Swanevelder Dept of Anaesthesia & Perioperative Medicine University of Cape Town Each cardiac cycle consists of a period of relaxation (diastole) followed by ventricular contraction (systole). During diastole the ventricles are relaxed to allow filling. In systole the right and left ventricles contract, ejecting blood into the pulmonary and systemic circulations respectively. Ventricles The left ventricle pumps blood into the systemic circulation via the aorta. The systemic vascular resistance (SVR) is 5–7 times greater than the pulmonary vascular resistance (PVR). This makes it a high-pressure system (compared with the pulmonary vascular system), which requires a greater mechanical power output from the left ventricle (LV). The free wall of the LV and the interventricular septum form the bulk of the muscle mass in the heart. A normal LV can develop intraventricular pressures up to 300 mmHg. Coronary perfusion to the LV occurs mainly in diastole, when the myocardium is relaxed. The right ventricle receives blood from the venae cavae and coronary circulation, and pumps it via the pulmonary vasculature into the LV. Since PVR is a fraction of SVR, pulmonary arterial pressures are relatively low and the wall thickness of the right ventricle (RV) is much less than that of the LV. The RV thus resembles a passive conduit rather than a pump. Coronary perfusion to the RV occurs continuously during systole and diastole because of the low intraventricular and intramural pressures. In spite of the anatomical differences, the mechanical behaviour of the RV and LV is very similar. -
Pulse Wave Analysis to Estimate Cardiac Output
CLINICAL FOCUS REVIEW Jerrold H. Levy, M.D., F.A.H.A., F.C.C.M., Editor Pulse Wave Analysis to Estimate Cardiac Output Karim Kouz, M.D., Thomas W. L. Scheeren, M.D., Daniel de Backer, M.D., Bernd Saugel, M.D. ardiac output (CO)–guided therapy is a promising reference CO value measured using an indicator dilution Capproach to hemodynamic management in high-risk method (transpulmonary thermodilution or lithium dilu- patients having major surgery1 and in critically ill patients tion).5,9 CO measurement using indicator dilution methods with circulatory shock.2 Pulmonary artery thermodilu- requires a (central) venous catheter for indicator injection tion remains the clinical reference method for CO mea- upstream in the circulation and a dedicated arterial catheter Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/134/1/119/513741/20210100.0-00023.pdf by guest on 29 September 2021 surement,3 but the use of the pulmonary artery catheter and measurement system to detect downstream indicator decreased over the past two decades.4 Today, various CO temperature or concentration changes.5,9–11 monitoring methods with different degrees of invasiveness The VolumeView system (Edwards Lifesciences, are available, including pulse wave analysis.5 Pulse wave USA) and the PiCCO system (Pulsion Medical Systems, analysis is the mathematical analysis of the arterial blood Germany) calibrate pulse wave analysis–derived CO to pressure waveform and enables CO to be estimated con- transpulmonary thermodilution–derived CO. To measure tinuously and in real time.6 In this article, we review pulse CO using transpulmonary thermodilution, a bolus of cold wave analysis methods for CO estimation, including their crystalloid solution is injected in the central venous circu- underlying measurement principles and their clinical appli- lation.10 The cold indicator bolus injection causes changes cation in perioperative and intensive care medicine. -
Effects of Neuronal Nitric Oxide Synthase Signaling on Myocyte
Effects of Neuronal Nitric Oxide Synthase Signaling on Myocyte Contraction during β- Adrenergic Stimulation Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Lifei Tang Biophysics Graduate Program The Ohio State University 2013 Dissertation Committee: Dr. Mark T. Ziolo, PhD Advisor Dr. Brandon Biesiedecki, PhD Dr. Jonathan Davis, PhD Dr. Sandor Gyorke, PhD a Copyright by Lifei Tang 2013 i ABSTRACT Nitric oxide (NO) is known to be a key regulator of cardiac contraction. Within ventricular myocytes, NO is produced by two constitutively expressed NO synthase (NOS) isozymes, NOS1 and NOS3. It is well defined that NOS1 signaling results in positive inotropic and lusitropic effects under baseline conditions. This effect is largely due to the phosphorylation of phospholamban (PLB) at Ser16 by the cAMP-dependent protein kinase (PKA) up-regulating sarcoplasmic reticulum (SR) Ca2+ uptake. In addition, our lab also demonstrated that NOS1 increases ryanodine receptor (RyR) activity via S-nitrosylation up- regulating SR Ca2+ release. Physiologically, heart function is largely regulated by the β-adrenergic (β-AR) pathway leading to positive inotropy and lusitropy. Alterations in the β-AR pathway contribute to the contractile dysfunction, adverse remodeling, and arrhythmias in many cardiac diseases (i.e. heart failure (HF)). The purpose of this dissertation is to investigate the role of NOS1 signaling during β-AR stimulation. Previous studies have shown that NOS1 signaling contributes to the positive inotropy, but not lusitropy, during β-AR stimulation. Interestingly, unlike under baseline conditions, PLB phosphorylation is not altered in the condition of NOS1 deficiency (acute NOS1 inhibition or NOS1 knockout) during β-AR stimulation. -
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. -
Inorganic Nitrate As a Treatment for Acute Heart Failure
Falls et al. J Transl Med (2017) 15:172 DOI 10.1186/s12967-017-1271-z Journal of Translational Medicine PROTOCOL Open Access Inorganic nitrate as a treatment for acute heart failure: a protocol for a single center, randomized, double‑blind, placebo‑controlled pilot and feasibility study Roman Falls1,2, Michael Seman1,2, Sabine Braat2,4, Joshua Sortino1, Jason D. Allen1,3 and Christopher J. Neil1,2,3,5* Abstract Background: Acute heart failure (AHF) is a frequent reason for hospitalization worldwide and efective treatment options are limited. It is known that AHF is a condition characterized by impaired vasorelaxation, together with reduced nitric oxide (NO) bioavailability, an endogenous vasodilatory compound. Supplementation of inorganic sodium nitrate (NaNO3) is an indirect dietary source of NO, through bioconversion. It is proposed that oral sodium nitrate will favorably afect levels of circulating NO precursors (nitrate and nitrite) in AHF patients, resulting in reduced systemic vascular resistance, without signifcant hypotension. Methods and outcomes: We propose a single center, randomized, double-blind, placebo-controlled pilot trial, evaluating the feasibility of sodium nitrate as a treatment for AHF. The primary hypothesis that sodium nitrate treat- ment will result in increased systemic levels of nitric oxide pre-cursors (nitrate and nitrite) in plasma, in parallel with improved vasorelaxation, as assessed by non-invasively derived systemic vascular resistance index. Additional sur- rogate measures relevant to the known pathophysiology of AHF will be obtained in order to assess clinical efect on dyspnea and renal function. Discussion: The results of this study will provide evidence of the feasibility of this novel approach and will be of inter- est to the heart failure community. -
Heartlogic Clinical Compendium Updated As of February 2020 TABLE of CONTENTS
HeartLogic Clinical Compendium Updated as of February 2020 TABLE OF CONTENTS Introduction.............................................................................................. 2 HeartLogic Heart Failure Diagnostic ................................................... 3 Heart Sounds ......................................................................................... 11 Respiration ............................................................................................. 19 Thoracic Impedance ............................................................................ 23 Activity Level.......................................................................................... 25 Night Heart Rate ................................................................................... 26 Sleep Incline .......................................................................................... 27 Weight ..................................................................................................... 29 RV and LV Pacing .................................................................................. 30 Arrhythmia Burden ............................................................................... 33 Heart Failure Assessment ................................................................... 37 THIS DOCUMENT IS A COMPILATION OF RELEVANT CLINICAL PUBLICATION REFERENCES THAT FORM THE CLINICAL FOUNDATION OF THE HEARTLOGIC HEART FAILURE DIAGNOSTIC. PUBLICATIONS ARE LISTED BY SENSOR TREND/TOPIC AREA AND THEN BY RELEVANCE ON FEASIBILITY, -
The Relation Between Cardiac Output and Body Size*
Br Heart J: first published as 10.1136/hrt.25.4.425 on 1 July 1963. Downloaded from Brit. Heart J., 1963, 25, 425. THE RELATION BETWEEN CARDIAC OUTPUT AND BODY SIZE* BY W. JEGIER, PAUL SEKELJ, P. A. M. AULD, R. SIMPSON, AND M. McGREGOR From the Joint Cardio-Respiratory Service of the Montreal Children's Hospital and the Royal Victoria Hospital, The Department of Anesthesia, The Montreal Children's Hospital, and the Department ofPhysiology, McGill University, Montreal, Quebec, Canada Received December 10, 1962 A prerequisite in the study of abnormal body function is the ability to establish the limits of normal. In the case of parameters such as cardiac output that vary with the size of the subject, it has become an accepted practice to standardize values in relation to the body surface area. Thus the cardiac index describes the cardiac output per square metre of body surface area, and the stroke index describes the volume of blood per heart beat per square metre of body surface area. The validity of these expressions depends on the premise that there is a constant or straight line relation between body surface area on the one hand, and cardiac output and stroke volume on the other, over the whole range of body size to be studied, and that the relation can be described by a simple regression equation cutting the intercept at zero. Only where this is so is it meaningful to refer to "the normal" cardiac index or stroke index. Though this premise is backed by observations in the case of adult or adolescent subjects, it was until recently entirely unsupported in the case of children and is still unsupported by any data for infants.