Health Outcomes with and Without Use of Inotropic Therapy in Cardiac Surgery Results of a Propensity Score–Matched Analysis

Total Page:16

File Type:pdf, Size:1020Kb

Health Outcomes with and Without Use of Inotropic Therapy in Cardiac Surgery Results of a Propensity Score–Matched Analysis Health Outcomes with and without Use of Inotropic Therapy in Cardiac Surgery Results of a Propensity Score–matched Analysis Dorthe Viemose Nielsen, M.D., Malene Kærslund Hansen, M.B.B.S., Søren Paaske Johnsen, M.D., Ph.D., Mads Hansen, M.D., Karsten Hindsholm, M.D., H.D., Carl-Johan Jakobsen, M.D. This article has been selected for the ANESTHESIOLOGY CME Program. Learning objectives and disclosure and ordering information can be found in the CME section at the front of this issue. Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/120/5/1098/265993/20140500_0-00017.pdf by guest on 29 September 2021 ABSTRACT Background: Inotropes used to obtain short-term hemodynamic benefits in cardiac surgery may carry a risk of increased myocardial ischemia and adverse outcomes. This study investigated the association between intra- and postoperative use of inotropes and mortality and postoperative complications. Methods: A historic cohort study using prospective data from the Western Denmark Heart Registry on 6,005 consecutive car- diac surgery cases from three university hospitals. Propensity matching on pre- and intraoperative variables was used to identify a subgroup of patients receiving inotropic therapy (n = 1,170) versus comparable nonreceivers (n = 1,170) for outcome analysis. Results: Two thousand ninety-seven patients (35%) received inotropic therapy; 3,908 (65%) did not receive any inotropic or vasopressor support perioperatively. Among propensity-matched cohort including 2,340 patients 30-day mortality was 3.2% and 1-yr mortality was 7.6%. In the matched cohort, patients exposed to inotropes had a higher 30-day mortality (adjusted hazards ratio, 3.7; 95% CI, 2.1 to 6.5) as well as a higher 1-yr mortality rate (adjusted hazards ratio, 2.5; 95% CI, 1.8 to 3.5) compared with nonreceivers. Among propensity-matched, the following absolute events rates were observed: myocardial infarction 2.4%, stroke 2.8%, arrhythmia 35%, and renal replacement therapy 23.9%. Inotropic therapy was independently associated with postoperative myocardial infarction (adjusted odds ratio, 2.1; 95% CI, 1.4 to 3.0), stroke (adjusted odds ratio, 2.4; 95% CI, 1.4 to 4.3), and renal replacement therapy (adjusted odds ratio, 7.9; 95% CI, 3.8 to 16.4). Conclusion: Use of intra- and postoperative inotropes was associated with increased mortality and major postoperative mor- bidity. (ANESTHESIOLOGY 2014; 120:1098-108) OW cardiac output syndrome is a common complica- What We Already Know about This Topic Ltion in cardiac surgery patients1 and inotropic support is frequently initiated to improve postbypass ventricular func- • Previous studies have suggested that inotropic therapy after cardiac surgery may be associated with increased morbidity tion. Inotropes may improve hemodynamics, but there is a but the impact of these drugs on overall survival is unknown. potential risk for increased myocardial oxygen consumption resulting in cardiac ischemia and potential damage of hiber- What This Article Tells Us That Is New nating but viable myocardium, particularly in patients with • In an observational study of 6,005 patients using propensity score matching, perioperative use of inotropes was indepen- ischemic heart disease. The clinical efficacy of perioperative dently associated with increased 1-yr mortality (adjusted haz- inotropes has been assessed in randomized clinical trials pri- ard ratio of 2.5). The results indicate that the beneficial effects of current inotropic drugs may be limited to only short-term marily in relation to hemodynamic endpoints. Most previous hemodynamic improvement in patients after cardiac surgery. randomized trials have not been powered to study the effi- cacy in relation to “hard” clinical outcomes, including cardiac morbidity and mortality.2 Use of inotropes has been associ- However, the study sample was too small to investigate mor- ated with adverse clinical outcomes in a few observational tality, and the association between inotrope exposure and studies3–5: In a sentinel study by Fellahi et al.,3 use of dobuta- short- and long-term mortality thus remained unclear. At mine was associated with increased postoperative morbidity. present, there is only limited data to guide practice patterns This article is featured in “This Month in Anesthesiology,” page 1A. Corresponding article on page 1067. Submitted for publication January 10, 2013. Accepted for publication January 22, 2014. From the Department of Anesthesiology and Intensive Care (D.V.N., C.-J.J.) and Department of Clinical Epidemiology (M.K.H., S.P.J.), Aarhus University Hospital, Aarhus, Denmark; Department of Anesthesia and Intensive Care, Odense University Hospital, Odense, Denmark (M.H.); and Department of Anesthesia and Intensive Care, Aalborg University Hospital, Aalborg, Denmark (K.H.). Copyright © 2014, the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins. Anesthesiology 2014; 120:1098-108 Anesthesiology, V 120 • No 5 1098 May 2014 PERIOPERATIVE MEDICINE and evidence-based use of inotropes in cardiac surgery. This on patient history, type of procedure, intra- and postopera- has resulted in an ongoing debate on the value or harm asso- tive management including inotropic therapy and in-hospital ciated with use of inotropes in cardiac surgery.6 Thus, clinical complications. The registry provides the Danish Heart Regis- practice in inotrope management is highly dependent on the try (DHR) with data on all consecutive patients undergoing individual center and physician preferences.7–10 cardiac surgery in the western part of Denmark. Data quality The aim of the current study was to investigate whether is ensured using automatic validation rules at data entry com- use of inotropes was associated with short- and long-term bined with systematic validation procedures and random spot- mortality and an increased incidence of postoperative checks of data after entry. Coverage of the DHR is routinely complications such as myocardial infarction (MI), stroke, evaluated by comparing with data from the Danish National arrhythmia, and renal failure in patients undergoing cardiac Patient Register including data on all procedures performed in surgery. To obtain a sufficient sample size to investigate the both private and public hospitals in Denmark. These analyses Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/120/5/1098/265993/20140500_0-00017.pdf by guest on 29 September 2021 association between perioperative inotropic therapy and have shown a high coverage of the DHR, with greater than 95% these rare adverse clinical outcomes, a historical cohort study reporting of all CABG procedures.11 Random samples of the was conducted using data from a population-based clinical data reported to the DHR from WDHR have been validated cardiac registry. A propensity score–matched analysis was against the local patient files (both electronic and paper files). used to minimize the risk of selection bias and confounding. The main finding was that the data in the WDHR were correct with κ values between 0.91 to 1 (DHR—Annual Report 2007, Materials and Methods University of Southern Denmark: The Board of Danish Heart Patient Population Registry and National Institute of Public Health, 2008), but This study was a multicenter, historical cohort study involv- there was a high proportion of missing data especially concern- 11 ing 6,005 consecutive adult patients undergoing cardiac sur- ing patient history and late complications. Missing data have gery with or without cardiopulmonary bypass (CPB) at three been retrieved later from local patient files (both electronic and Danish university cardiac centers (Odense University Hospi- paper) and overall missing data constituted less than 0.3 and tal, Aarhus University Hospital, and Aalborg University Hos- 0% for outcome data. The WDHR has proven a valuable data pital) from April 1, 2006 to December 31, 2009. Patients source in research, providing ongoing longitudinal registration 12 met the following inclusion criteria: Coronary artery bypass of detailed data on patients and procedures. grafting (CABG) or CABG with valve surgery or combined with other procedures or surgery involving the thoracic aorta. Perioperative Management Patients were excluded if they had undergone procedures All preoperative cardiac medication was continued until only offered at one of the participating cardiac centers such as the morning of surgery except for angiotensin-converting heart transplantation, pulmonary thrombendarterectomy, or enzyme inhibitors, aspirin, and thrombocyte function percutaneous valve replacement. Patients dying during sur- inhibitors. β-Blocking agents were continued on the day of gery and patients regarded inoperable after sternotomy were surgery in chronically treated patients. All patients received excluded. Patients who underwent more than one cardiac standard premedication in the form of a benzodiazepine 60 surgical procedure during the study period were included to 90 min before surgery. Cardiac centers B: Standard total with only the first surgical procedure to ensure independency. intravenous anesthesia using propofol 40 to 80 μg/kg/min, In case of missing data on procedure type, CPB, or exposure sufentanil 3 to 5 μg/kg, and pancuronium. Cardiac centers A to inotropes patients were excluded (fig. 1). and C: anesthesia induction with midazolam or pentobarbi- Study start was determined as the time when data on ino- tal together with fentanyl 0.01 to 0.025 mg/kg or sufentanil trope treatment were included
Recommended publications
  • Nitric Oxide, the Biological Mediator of the Decade: Fact Or Fiction?
    Eur Respir J 1997; 10: 699–707 Copyright ERS Journals Ltd 1997 DOI: 10.1183/09031936.97.10030699 European Respiratory Journal Printed in UK - all rights reserved ISSN 0903 - 1936 SERIES 'CLINICAL PHYSIOLOGY IN RESPIRATORY INTENSIVE CARE' Edited by A. Rossi and C. Roussos Number 14 in this Series Nitric oxide, the biological mediator of the decade: fact or fiction? S. Singh, T.W. Evans Nitric oxide, the biological mediator of the decade: fact or fiction? S. Singh, T.W. Evans. Unit of Critical Care, National Heart & ERS Journals Ltd 1997. Lung Institute, Royal Brompton Hospital, ABSTRACT: Nitric oxide (NO), an atmospheric gas and free radical, is also an London, UK. important biological mediator in animals and humans. Its enzymatic synthesis by constitutive (c) and inducible (i) isoforms of NO synthase (NOS) and its reactions Correspondence: T.W. Evans with other biological molecules such as reactive oxygen species are well charac- Royal Brompton Hospital Sydney Street terized. NO modulates pulmonary and systemic vascular tone through its vasodila- London SW3 6NP tor property. It has antithrombotic functions and mediates some consequences of UK the innate and acute inflammatory responses; cytokines and bacterial toxins induce widespread expression of iNOS associated with microvascular and haemodynam- Keywords: Acute respiratory distress syn- ic changes in sepsis. drome Within the lungs, a diminution of NO production is implicated in pathological hypoxic pulmonary vasoconstriction states associated with pulmonary hypertension, such as acute respiratory distress nitric oxide syndrome: inhaled NO is a selective pulmonary vasodilator and can improve ven- nitric oxide synthase tilation-perfusion mismatch. However, it may have deleterious effects through mod- pulmonary hypertension ulating hypoxic pulmonary vasoconstriction.
    [Show full text]
  • Medicare National Coverage Determinations Manual, Part 1
    Medicare National Coverage Determinations Manual Chapter 1, Part 1 (Sections 10 – 80.12) Coverage Determinations Table of Contents (Rev. 10838, 06-08-21) Transmittals for Chapter 1, Part 1 Foreword - Purpose for National Coverage Determinations (NCD) Manual 10 - Anesthesia and Pain Management 10.1 - Use of Visual Tests Prior to and General Anesthesia During Cataract Surgery 10.2 - Transcutaneous Electrical Nerve Stimulation (TENS) for Acute Post- Operative Pain 10.3 - Inpatient Hospital Pain Rehabilitation Programs 10.4 - Outpatient Hospital Pain Rehabilitation Programs 10.5 - Autogenous Epidural Blood Graft 10.6 - Anesthesia in Cardiac Pacemaker Surgery 20 - Cardiovascular System 20.1 - Vertebral Artery Surgery 20.2 - Extracranial - Intracranial (EC-IC) Arterial Bypass Surgery 20.3 - Thoracic Duct Drainage (TDD) in Renal Transplants 20.4 – Implantable Cardioverter Defibrillators (ICDs) 20.5 - Extracorporeal Immunoadsorption (ECI) Using Protein A Columns 20.6 - Transmyocardial Revascularization (TMR) 20.7 - Percutaneous Transluminal Angioplasty (PTA) (Various Effective Dates Below) 20.8 - Cardiac Pacemakers (Various Effective Dates Below) 20.8.1 - Cardiac Pacemaker Evaluation Services 20.8.1.1 - Transtelephonic Monitoring of Cardiac Pacemakers 20.8.2 - Self-Contained Pacemaker Monitors 20.8.3 – Single Chamber and Dual Chamber Permanent Cardiac Pacemakers 20.8.4 Leadless Pacemakers 20.9 - Artificial Hearts And Related Devices – (Various Effective Dates Below) 20.9.1 - Ventricular Assist Devices (Various Effective Dates Below) 20.10 - Cardiac
    [Show full text]
  • Caring for Patients Receiving Vasopressors and Inotropes in the ICU
    Caring for patients receiving vasopressors and inotropes in the ICU Vigilant monitoring will maximize outcomes. By Sonya M. Grigsby, DNP, APRN, AGACNP-BC CNE 1.5 contact hours LEARNING O BJECTIVES 1. Identify receptors related to cardiovascular physiology. 2. Differentiate the effects of vasopressors and inotropes. 3. Discuss nursing care of patients receiving vasopressors and inotropes in the ICU. The authors and planners of this CNE activity have disclosed no relevant fi- nancial relationships with any commercial companies pertaining to this ac- tivity. See the last page of the article to learn how to earn CNE credit. Expiration: 2/1/24 SHOCK requires early recognition and quick peutic effect) these medications using the action to prevent organ failure. (See Types of lowest possible dose to avoid adverse effects. shock.) After initial I.V. fluid resuscitation, pharmacologic agents—such as vasopressors Cardiovascular physiology and inotropes—are used in critical care set- Shock disrupts cardiovascular physiology, par- tings as supportive therapies to improve my- ticularly blood pressure, so understanding ocardial contractility, heart rate, and vascular normal function is important. Short-term resistance in patients with low cardiac output. blood pressure (BP) regulation is controlled When critical care nurses understand shock by the autonomic nervous system (ANS) via pathophysiology and hemodynamic monitor- baroreceptors in the aortic arch and carotid si- ing, they can effectively and safely titrate (in- nus. The ANS regulates the heart, secretory crease or decrease an infusion rate for thera- glands, and smooth muscles via activation of MyAmericanNurse.com February 2021 American Nurse Journal 5 Types of shock Shock is a decline in tissue perfusion and oxygen delivery, leading to cellular dysfunction and death.
    [Show full text]
  • 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.
    [Show full text]
  • What Inotrope and Why?
    What Inotrope and Why? a,b, a,b Nilkant Phad, MD, FRACP *, Koert de Waal, PhD KEYWORDS Hypotension Cardiovascular compromise Inotrope Newborn KEY POINTS There are significant gaps in the knowledge about diagnostic thresholds and choices of therapeutic interventions that can improve morbidity and mortality in neonates with car- diovascular compromise. Current use of inotropes in neonates is largely based on the pathophysiology of cardiovas- cular impairment and anticipated actions of inotropes because of limited outcome data from randomized controlled trials. Research studies of alternative study design unraveling the linkage of cardiovascular impairment and use of inotropes with important clinical outcomes are needed for future progress. INTRODUCTION The primary function of the cardiovascular system is to meet oxygen and nutritional demands of organs under various physiologic and pathologic conditions.1 To achieve this, the heart contracts against vascular resistance and drives blood to the lungs for oxygenation and into the systemic circulation for organ perfusion. The force of cardiac contraction, ventricular end-diastolic blood volume, and perfusion pressure are the main determinants of cardiovascular performance through an interplay between car- diac output (CO), vascular resistance, and neuroendocrine mechanisms.2 In neonates, the physiology of blood circulation can get disrupted in many clinical conditions, resulting in impaired organ perfusion and hypoxia. Persistent circulatory compromise can lead to derangement of metabolism,
    [Show full text]
  • Inotropes, Vasopressors, and Chronotropes OH MY! a Review For
    Inotropes, Vasopressors, and Chronotropes OH MY! A Review for the Young and the Seasoned MATT RUBERTUS, PHARMD CLINICAL PHARMACY SPECIALIST – CARDIOTHORACIC SURGERY/CRITICAL CARE EMORY UNIVERSITY HOSPITAL ATLANTA, GA Disclosure I have nothing to disclose pertaining to this presentation http://oz.wikia.com Objectives Review the mechanism of action for vasopressors and inotropes Recognize common side effects of different vasopressors and inotropes Review data for the use of alternative agents to treat vasoplegia Describe where angiotensin II fits into therapy Clinical Scenarios Shock Cardiogenic Vasodilatory Sepsis Cardiac Surgery Valve Disease Decompensated Heart Failure http://thefilmspectrum.com Hypotension Hypotension Baroreceptor Decreased Renal Activation Perfusion Increased RASS Activation Sympathetic Activity Cardiac Stimulation Vasoconstriction Volume Expansion Increased HR and Increased Preload Contractility Increased Cardiac Increased Systemic Increased Cardiac Output Vascular Resistance Output Increased Blood Pressure Hemodynamics The ultimate goal of cardiac function is perfusion Must deliver adequate oxygen to meet metabolic demand of end organs Oxygen delivery is affected by multiple factors Hemoglobin Oxygen saturation Cardiac output Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV) Hemodynamics Stroke Heart Rate CO = X Volume Rate Rhythm Preload Contractility Afterload CVP MAP Vasopressors http://thefilmspectrum.com Alpha Receptors Alpha1 Located in vascular smooth muscle Cause vasoconstriction
    [Show full text]
  • Combination Therapy with Beta Blocker and Inotrope In
    HEART RESEARCH ISSN 2377-164X http://dx.doi.org/10.17140/HROJ-4-136 Open Journal Case Report Combination Therapy With Beta Blocker *Corresponding author and Inotrope in Decompensated Heart Abhishek Jaiswal, MD Tulane University Heart and Vascular Institute Failure: A Clinical Observation Tulane School of Medicine 1430 Tulane Avenue, SL#48 New Orleans * LA 70112, USA Abhishek Jaiswal, MD ; Vinh Q. Nguyen, MD; Brendan Carry, MD; Thierry H. Le Jemtel, Tel. 1-504-988-1612 MD Fax: 1-504-988-4237 E-mail: [email protected] Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL#48, New Orleans, LA 70112, USA Volume 4 : Issue 1 Article Ref. #: 1000HROJ4136 INTRODUCTION Article History Inotropic support is contemplated in the presence of ongoing end-organ hypoperfusion or Received: January 3rd, 2017 refractory symptoms in decompensated heart failure (DHF). However, inotropic agents may Accepted: January 24th, 2017 cause tachycardia leading to increased myocardial oxygen demand and arrhythmogenesis.1 Published: January 24th, 2017 Introduction of beta blocker (BB) therapy in DHF patients requiring inotrope support is discouraged due to the negative hemodynamic impact of acute BB therapy.2-5 On the other hand, reduction in heart rate by BB therapy results in decreased myocardial oxygen demand Citation and increased ventricular diastolic filling.6,7 Additionally, early introduction of BB therapy Jaiswal A, Nguyen VQ, Carry B, Le improves outcome in heart failure.2-5,8 Jemtel TH. Combination therapy with beta blocker and inotrope in decom- pensated heart failure: A clinical ob- We describe our clinical experience in two DHF patients with end-organ hypoperfusion servation.
    [Show full text]
  • Inotropes Are Linked to Increased Mortality in Heart Failure
    The VAD Journal: The journal of mechanical assisted circulation and heart failure Review Inotropes are linked to Increased Mortality in Heart Failure M Chadi Alraies 1, Bill Tran 1 and Sirtaz Adatya 2* 1 Department of Medicine, Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, Minnesota, USA 2 Department of Medicine, Division of Cardiovascular Medicine, University of Chicago, Chicago Illinois. * Corresponding author: [email protected] Keywords Citation: Alrais, M. et al. (2015). Inotropes are linked to Increased Inotropes; Heart failure; ventricular assist device Mortality. VAD Journal , 1. doi:: http://dx.doi.org/10.13023/VAD.2 015.08 Introduction Editor-in-Chief: Maya Guglin, University of Kentucky With the advancement of technology and availability of mechanical Received: June 17, 2015 circulatory support (MCS) devices for the treatment of acute decompensated systolic HF in the 21 st century, the role of inotropes is becoming obsolete. Accepted: June 25, 2015 Medical therapy for acute decompensated heart failure (HF) has not changed Published: June 29, 2015 , 2015 since 1960’s, we still use supplemental oxygen, diuretics, vasodilators and © 2015 The Author(s). This is an inotropes to improve congestion, cardiac output, end organ perfusion and 1 open access article published symptoms related to elevate filling pressures . Despite demonstrated under the terms of the Creative improvements in hemodynamics, the uses of inotropes have not demonstrated Commons Attribution- NonCommercial 4.0 International any improvements in mortality. Mechanical circulatory support (MCS) use is License growing rapidly in the USA, in patients with stage D HF both as destination (https://creativecommons.org/lice nses/by-nc/4.0/ ), which permits therapy and as a bridge to cardiac transplantation.
    [Show full text]
  • Aortic Acceleration As a Noninvasive Index of Left Ventricular Contractility in the Mouse
    www.nature.com/scientificreports OPEN Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse Jorge Enrique Tovar Perez1,3, Jesus Ortiz‑Urbina1, Celia Pena Heredia1,2, Thuy T. Pham1, Sridhar Madala1,4, Craig J. Hartley1, Mark L. Entman1, George E. Tafet1,2 & Anilkumar K. Reddy1,4* The maximum value of the frst derivative of the invasively measured left ventricular (LV) pressure (+ dP/dtmax or P′) is often used to quantify LV contractility, which in mice is limited to a single terminal study. Thus, determination of P′ in mouse longitudinal/serial studies requires a group of mice at each desired time point resulting in “pseudo” serial measurements. Alternatively, a noninvasive surrogate for P′ will allow for repeated measurements on the same group of mice, thereby minimizing physiological variability and requiring fewer animals. In this study we evaluated aortic acceleration and other parameters of aortic fow velocity as noninvasive indices of LV contractility in mice. We simultaneously measured LV pressure invasively with an intravascular pressure catheter and aortic fow velocity noninvasively with a pulsed Doppler probe in mice, at baseline and after the administration of the positive inotrope, dobutamine. Regression analysis of P′ versus peak aortic 2 velocity (vp), peak velocity squared/rise time (vp /T), peak (+ ­dvp/dt or v′p) and mean (+ ­dvm/dt or v′m) 2 2 2 aortic acceleration showed a high degree of association (P′ versus: vp, r = 0.77; vp /T, r = 0.86; v′p, 2 2 r = 0.80; and v′m, r = 0.89). The results suggest that mean or peak aortic acceleration or the other parameters may be used as a noninvasive index of LV contractility.
    [Show full text]
  • Drugs in Cardiology
    Drugs in Cardiology Fozia Ahmed Consultant Cardiologist Manchester Heart Centre What do you need to know about pharmacology for BHRS exam • Cardiac action potential • Vaughn William’s classification • Effects of drugs on pacing thresholds and DFTs • Indications for different drugs • Side effects of drugs – QT interval – Toxicity – contraindications • Drugs for heart failure Phase 4 (Cardiomyocyte AP) • Phase 4= Resting membrane potential – Horizontal line (non-pacemaker cells) – -90mV • In phase 4 membrane most permeable to K+ ions – Fast Na+ channels and slow Ca 2+ channels are closed • Stable vs. unstable phase 4 Phase 0 (depolarisation) • Phase 0=rapid depolarisation – Electrical stimulation of cell by adjacent cell undergoing depolarisation – The K+ channels are closed during phase 0 – Opening of Fast Na+ channels – Influx of Na+ – Increase in membrane potential • Potential inside the cell rises to +10mV Phase 1 (initial repolarisation) • Phase 1 represents initial repolarisation • Closure of fast Na+ channels • Net outflow of K+ – caused by opening of transient + outward K channel (Kto) – hyperpolarising outward K+ current(iKto) Phase 2 (plateau phase) • Phase 2 represents the “plateau phase” • Sustained by: – Inward movement of calcium through Slow (L-type) calcium channels – Slow outward movement of K+ thru the slow delayed rectifier K+ channel • Phase 2 differentiates cardiomyocyte action potentials from those of pacemaker cells, skeletal muscle and nerves Phase 3 (rapid repolarisation phase) • During phase 3, L-type Ca2+ channels
    [Show full text]
  • Inotrope Use in Critically Ill Patients: Prevalence and Effects on Mortality Prasad Sonawane*, Biswajit L Jagtap**, Suprakash Chaudhury***
    Pravara Medical Review, December 2016, 8(4) 4-11 [ISSN P : 0975- 0533 , ISSN E : 0976- 0164 ] Original article: Inotrope use in critically ill patients: Prevalence and effects on mortality Prasad Sonawane*, Biswajit L Jagtap**, Suprakash Chaudhury*** *Consultant Physician &specialist in Critical Care Medicine, Mumbai ** Asst. Professor *** Professor & Head, Dept of Psychiatry, RMC, PIMS (DU), Loni Corresponding author: Dr. Biswajit L Jagtap, Asst Professor, Dept of Psychiatry, RMC, PIMS (DU), Loni Abstract: Clinical Profile of critically ill patients needing inotropes in medical intensive care unit (MICU) of a tertiary care centre revealed that out of 399 patients admitted during study period, 54 (13.53%) needed inotropes. These 54 patients were suffering from septic shock (n=29), CVT/ GBS/ Infective meningitis (n=8), Acute febrile illness(n=6), fulminant hepatic failure(n=4), malaria(n=4), pulmonary thromboembolism(n=2), and dengue(n=1). The inotropes used included noradrenaline in 45 (83.33%), dopamine in 42 (77.78%) and dobutamine in 5 (9.26%) patients. Of critically ill patients requiring inotropes, 8 (12.96%) needed inotropes for 24 hours, 21(38.89%) needed inotropes for 48 hours and 25(46.30%) needed inotropes for>48 hours duration. There was no association amongst different type of inotropes used and outcome of patients.(p=0.336) Out of 54 needing inotropes, 11( 20.37%) survived and 43 (79.62%) expired while out of 345 patients not needing inotropes, 221 (64.05%) survived and 124 (35.94%) expired. Need of inotropes was associated with significantly increased risk of death. Key Words : inotropes; intensive care unit; adverse effects; mortality INTRODUCTION Sepsis is often a contributory factor for Inotropic drugs enhance myocardial mortality in critically ill patients.
    [Show full text]
  • INDE 221 Spring 2010 Syllabus Part 2
    Human Health & Disease Mondays, Tuesdays, Thursdays and Fridays 9:00 - 11:50 AM Lectures: Room M-112, Labs: Fleischmann IINNDDEE 222211 SSpprriinngg 22001100 Syllabus SSyyllllaabbuuss PPaarrtt 22 (2010) Year's Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Table of Contents CARDIOVASCULAR BLOCK SYLLABUS SCHEDULE 7 SYLLABUS PREFACE 11 CARDIAC MUSCLE AND FHC 15 EXCITATION-CONTRACTION COUPLING Syllabus27 NERNST POTENTIAL AND OSMOSIS 43 EXCITABILITY AND CONDUCTION 51 CIRCULATORY VESSEL HISTOLOGY LAB 63 CARDIAC ACTION POTENTIAL 71 CONTROL OF HEART RHYTHM (2010) 85 AUTONOMIC DRUGS OVERVIEW I 97 ELECTROCARDIOGRAM (ECG) 99 LESIONS OF BLOOD VESSELS 109 THROMBOEMBOLIC DISEASE 117 CARDIAC REFLEXESYear's 123 AUTONOMIC DRUGS OVERVIEW II 141 ECG SMALL GROUPS 143 LastAUTONOMIC DRUGS: CHOLINERGICS 147 CARDIAC MUSCLE MECHANICS 149 AUTONOMIC DRUGS: ANTICHOLINERGICS 175 ARRHYTHMIAS 177 AUTONOMIC DRUGS: SYMPATHOMIMETICS I 203 VENTRICULAR PHYSIOLOGY 205 AUTONOMIC DRUGS: SYMPATHOMIMETICS II 235 STARLING CURVE AND VENOUS RETURN 237 CARDIAC OUTPUT AND CATHETERIZATION 245 AUTONOMIC DRUGS: ADRENOCEPTOR BLOCKERS 267 PHYSICS OF CIRCULATION Syllabus269 CASE DISCUSSIONS: AUTONOMIC DRUGS 289 SMOOTH MUSCLE 291 ISCHEMIC AND VALVULAR HEART DISEASE 303 RENAL CIRCULATION (2010) 323 HYPERTENSION 333 CARDIOMYOPATHY, MYOCARDITIS AND ATRIAL MYXOMA 351 ENDOTHELIUM AND CORONARY CIRCULATION 369 ANGINA PECTORIS 389 DRUGS USEDYear's IN HYPERTENSION 397 SHOCK 399 ADULT CARDIAC LAB 413 CARDIAC ANESTHESIA & BYPASS 421 LastEXERCISE PHYSIOLOGY 431 ISCHEMIC
    [Show full text]