DOCSLIB.ORG

Obesity and Cardiac Disease OBESITY • Higher Prevalence of Cardiovascular Disease in Obese Individuals • There Are Several W

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Obesity and Cardiac Disease OBESITY • Higher Prevalence of Cardiovascular Disease in Obese Individuals • There Are Several W 05/07/2018 OBESITY Obesity and • Higher prevalence of Cardiac Disease cardiovascular disease in obese individuals MARY N SHEPPARD ST GEORGE’S MEDICAL • There are several ways in which SCHOOL, LONDON obesity directly affects the [email protected] cardiovascular system 7/5/2018 OBESITY 2018 1 7/5/2018 OBESITY 2018 3 7/5/2018 OBESITY 2018 2 7/5/2018 OBESITY 2018 4 1 05/07/2018 7/5/2018 OBESITY 2018 5 7/5/2018 OBESITY 2018 7 7/5/2018 OBESITY 2018 6 7/5/2018 OBESITY 2018 8 2 05/07/2018 OBESITY AND HEART DISEASE • Obesity affects 20% of the population aged under 35 in the UK. • In our cohort of young unexpected SCDs, 20% of individuals were obese. • SADS was the most common post-mortem finding in young obese individuals, • High burden of unexplained LVH and CAD 7/5/2018 OBESITY 2018 9 7/5/2018 OBESITY 2018 11 OBESITY AND SCD ♥ Body weight affects heart weight ♥ Obesity and electrical instability and prolonged QT interval has been described previously, ♥ The QT prolongation is one of the mechanisms underlying fatal arrhythmias in obese individuals with a structurally normal heart ♥ Unexplained LVH was more frequently observed in obese young ♥ CAD is more prevalent in obese young people. ♥ SCD in young obese individuals occurs frequently without antecedent symptoms or a significant past medical history 7/5/2018 OBESITY 2018 10 7/5/2018 OBESITY 2018 12 3 05/07/2018 Sudden Cardiac Death 500,000 deaths in UK 50,000 SCD in the UK CORONARY ARTERY DISEASE 81% Bowker, Sheppard,Wood, Davies et al JRSM 2003 BHF study CRY DEPT. CARDIOVASCULAR 7/5/2018 OBESITY 2018 15 PATHOLOGY, LONDON 2018 Blocked vessel and old damage 7/5/2018 IHD 2016 14 7/5/2018 OBESITY 2018 16 4 05/07/2018 HYPERTROPHY OF THE LEFT VENTRICLE > 15mm 25-30mm Heart weight 500 gms in males 400gms In Females 7/5/2018 OBESITY 2018 17 INCREASED THICKNESS OF VENTRICLE WALL Fibrosis in Left Ventricle >15 mm HYPERTENSIVE HEART DISEASE Post LV wall EVG 5 05/07/2018 CORONARY ARTERY Post Surgery DISEASE ♥ After coronary artery bypass surgery also there are more adverse outcomes in obese patients. ♥ Obesity is an independent predictor of coronary They have increased incidence of artery disease, as observed in the Framingham postoperative thromboembolism, infections of heart study,Manitoba study, and Harvard public the sternum, and saphenous vein harvest sites. health nurses study There is also a higher incidence of atrial ♥ Autopsy among 15 to 34 year olds who died from arrhythmias. accidental causes show plaques and ulceration in Pulmonary complications in the severely obese the coronary arteries and abdominal aorta, which ♥ (BMI >35) and when complicated by diabetes, correlate with the amount of abdominal fat and renal dysfunction or age BMI (PDAY study) 7/5/2018 OBESITY 2018 21 7/5/2018 OBESITY 2018 23 ATHEROMA HYPERTENSION • Men, hypertension is 15% in those with BMI ♥ Obesity accelerates atherosclerosis decades <25 and 42% if BMI is >30; before clinical manifestations appear and this remained significant even after • Women are 15% and 38%, respectively adjustment of other risk factors like high • Factors like low-grade inflammation mediated cholesterol, hypertension, smoking, and through adipokines, hyperinsulinemia, and increased HbA1c. insulin resistance, over-activity of the ♥ The density of macrophages per mm2 of sympathetic nervous system and a disordered plaques also correlate with visceral obesity sleep pattern increase the systemic vascular resistance in obese patients 7/5/2018 OBESITY 2018 22 7/5/2018 OBESITY 2018 24 6 05/07/2018 ADIPOSE TISSUE PULMONARY ♥ Adipose tissue has a resting blood flow of 2 HYPERTENSION to 3 mL/100 g/min, but can increase up to 10- • Increased pulmonary vascular resistance is fold; this occurs usually after food intake. combination of intrinsic pulmonary disease, sleep With increasing obesity the perfusion per unit apnea/hypoventilation, recurrent pulmonary ♥ thromboembolism, or left ventricular dysfunction, mass decreases. It falls from 2.36 mL/min to all of which are more common in obese 1.53 mL/min when the percentage of fat individuals increases from 20% to 36% of the body • Nocturnal dysrhythmias, right and left heart weight failure, myocardial infarction, stroke, and ♥ Increase in cardiac output is not directly mortality are more common in those with proportional to the total fat. obstructive7/5/2018 sleep apneaOBESITY 2018 25 7/5/2018 OBESITY 2018 27 Obesity increases adverse cardiac CARDIAC HYPERTROPHY events in many ways ±Indirectly mediated through risk factors • Increased cardiac output in obese patients is associated with metabolic syndrome like to meet the metabolic demand of the dyslipidemia, hypertension, and glucose adipose tissue and is achieved with increase intolerance in stroke volume. ±Pro-inflammatory and prothrombotic state • The left ventricular chamber dilates to causing endothelial damage and vascular accommodate the increased venous return hypertrophy and, in turn, develops an eccentric type of ±Sleep disorders associated with obesity hypertrophy to keep the wall stress normal 7/5/2018 OBESITY 2018 26 7/5/2018 OBESITY 2018 28 7 05/07/2018 7/5/2018 OBESITY 2018 29 7/5/2018 OBESITY 2018 31 Genetic? Autopsy Series of Maternal Cardiopulmonary Deaths from 1994 to 2009 in Two Tertiary Centres in the United Kingdom Keiko Ogo MD Sofia V de Noronha MSc PhD Prof Sebastian Lucas FRCPath (Expert of maternal autopsy) Mary N Sheppard MD FRCPath (Specialist of cardiac pathology) • Department of Histopathology, Royal Brompton and Harefield NHS Foundation Trust Hospital • CRY Centre for Cardiac Pathology, Imperial College London • Department of Histopathology, St Thomas’ Hospital 7/5/2018 OBESITY 2018 30 8 05/07/2018 Result Result Study design - Retrospective s Body mass index (BMI) s Data available in 49/84 cases (58% of the cohort) Retrieval of maternal deaths due to cardiopulmonary causes from combined archives of autopsies and consultation cases (1994 - 2009) Royal Brompton Hospital / CRY St Thomas’ Hospital Underweight (< 18.5) Morbidly obese (≥ 40) (n = 50) (n = 34) Normal (≥ 18.5, < 25) 14% 2% 43% 35% 84 cases 29% 20% Obese (≥ 30, < 40) 61 20 3 Overweight (≥ 25, < 30) Deaths beyond 1 year Maternal deaths Late maternal deaths (Cases of peripartum cardiomyopathy) ! 63% of the cases with known BMI were obese (43%) or overweight (20%) *Septic shock and eclampsia fits were excluded. Result Result Demographics - maternal age at death s Diagnoses s Cardiovascular disease Pulmonary vascular disease Thrombotic disease Mean: 30 ± 7 years 25 Range: 15 - 49 20 15 Median: 31 32% 10 ≥ 5 35 Number of cases 0 MorphologicallyCardiomyopathy normal Coronaryheart arteryCHD pathologyAortic dissectionValvular heartOther disease cardiacPH Pulmonary embolicTTP diseaseOther thrombosis The leading causes 1. Sudden death with a morphologically normal heart 2. Cardiomyopathy 3. PH 4. Pulmonary embolic disease (PTE + AFE) 9 05/07/2018 Emerging entities in maternal death EFFECT ON HEART SD with • Role of channelopathy (e.g. Long QT syndrome) morphologically (genetic inheritable disease) in maternal death normal heart • Importance of family screening* • Cardiomyopathy of obese individuals = SADS (adipositas cordis) is caused by a direct effect of obesity on the heart. • ? Acquired LVH • Obesity, hypertension, diabetes etc • The increase in the fat content of the heart is • ? Genetic – role of family screening because of a metaplastic phenomenon • Known links to ischaemic heart disease and pulmonary • thrombo-embolism in maternal death Obesity • But we also highlight the association of obesity to non- ischaemic heart disease such as normal heart and LVH * Behr ER et al. Sudden arrhythmic death syndrome: familial evaluation identifies 7/5/2018 OBESITY 2018 39 inheritable heart disease in the majority of families. Eur Heart J. 2008 OBESITY CM OBESITY CM • Obesity is becoming a worldwide phenomenon. ♥ The existence of a cardiomyopathy of obesity is Myocardial changes associated with the obese state supported by a range of evidence are increasingly recognized, independent of ♥ Epidemiologic study findings, which have shown hypertension, obstructive sleep apnoea and an association between obesity and heart failure coronary artery disease ♥ Clinical studies that have confirmed the association of adiposity with left ventricular dysfunction, independent of hypertension, coronary artery disease and other heart disease 7/5/2018 OBESITY 2018 38 7/5/2018 OBESITY 2018 40 10 05/07/2018 Important mechanisms in development of obesity cardiomyopathy • Metabolic disturbances (insulin resistance, increased free fatty acid levels • Increased levels of adipokines • Activation of the renin–angiotensin–aldosterone and sympathetic nervous systems • Myocardial remodelLing • Small-vessel disease (both microangiopathy and endothelial dysfunction). 7/5/2018 OBESITY 2018 41 7/5/2018 OBESITY 2018 43 Beware the FATYY heart 7/5/2018 OBESITY 2018 42 7/5/2018 OBESITY 2018 44 7/5/2018 ROLE OF PATHOLOGIST 2008 42 11 05/07/2018 7/5/2018 OBESITY 2018 45 7/5/2018 OBESITY 2018 47 7/5/2018 OBESITY 2018 46 7/5/2018 OBESITY 2018 48 12 05/07/2018 Posterior fat Obese Normal Heart 7/5/2018 OBESITY 2018 49 7/5/2018 OBESITY 2018 51 Immobile fatty heart 7/5/2018 OBESITY 2018 50 7/5/2018 OBESITY 2018 52 13 05/07/2018 Fat on the epicardial surface 7/5/2018 OBESITY 2018 53 7/5/2018 OBESITY 2018 55 7/5/2018 OBESITY 2018 54 7/5/2018 OBESITY 2018 56 14 05/07/2018 Well defined border between Photo 2 Ill-defined border epicardial fat and myocardium 7/5/2018 OBESITY 2018 57 7/5/2018 OBESITY 2018 59 Anterior Photo 1 Adult heart showing the variable amount of epicardial Lateral fat normally seen in different parts of the right ventricle wall. In this case epicardial Posterior fat is thickest in the lateral wall; less fat is present anteriorly; there is no fat on the posterior wall.
Load more

Recommended publications
  • Clinical Significance of Exit Block*
    Clinical Significance of Exit Block* IRANY M. DE AZEVEDO, M.D. YOSHIO WATANABE, M.D. LEONARD S. DREIFUS, M.D. From the Departments of Medicine, Physiology, and Biophysics, Hahnemann Medical College, Philadelphia, Pennsylvania The confinement of an ectopic discharge to its ily reserved for ectopic pacemakers, rather than the focus, and its consequent inability to invade the ad­ sinus node. jacent myocardium when falling outside of the re­ High Grade Atrioventricular Block. In vi rtu­ fractory period of the heart, is a well established ally all instances, exit block occurs in the presence phenomenon called "exit block." This cardiac ar­ of higher degrees of A-V block. Failure of the rhythmia was originally described by Kaufmann impulse to propagate from the subsidiary ectopic and Rothberger ( 8) to explain the failure of a para­ focus to either the ventricles, atria, or both is char­ systolic focus to activate the heart. All pacemakers acteristic of this form of exit block. Several exam­ are subject to exit block (9, 13, 15, 14, 11 , 16, 12, ples are illustrated. In figure 2, there is high grade 3, 10, 7, 1), however, by convention, conduction A-V block causing A-V dissociation. The atria are disturbances involving the sinus node (S-A block) under the control of the sinus node at a rate of 71 are usually excluded from this concept, and the term per minute, and the ventricles are controlled by a is reserved for ectopic pacemakers. Recent electro­ subsidiary ectopic pacemaker, probably originating physiological and clinical studies have shown that in the right bundle branch at a rate of approximately exit block may complicate reentrant arrhythmias and 40 per minute.
    [Show full text]
  • Spontaneous Resolution of Sinoatrial Exit Block and Atrioventricular Dissociation in a Child with Dengue Fever Kaushik J S, Gupta P, Rajpal S, Bhatt S
    Case Report Singapore Med J 2010; 51(9) : e146 Spontaneous resolution of sinoatrial exit block and atrioventricular dissociation in a child with dengue fever Kaushik J S, Gupta P, Rajpal S, Bhatt S ABSTRACT her heart rate was regular at 92/min, respiratory rate at Cardiac rhythm abnormalities, including 22/min and blood pressure (BP) at 110/74 mmHg. There ventricular arrhythmia, atrial fibrillation and was a petechial rash over the patient’s back, trunk and atrioventricular block, have been observed upper extremities. The Hess test (tourniquet test) for during the acute stage of dengue haemorrhagic capillary fragility was positive. Systemic examination fever. Atrioventricular or complete heart did not reveal any abnormality. block can be fatal and may require a temporary Investigations revealed normal haemoglobin (12.1 pacemaker. We report a ten-year-old girl who g/dl), haematocrit (35.2%) and leucocyte (6500/cumm) presented with dengue haemorrhagic fever counts, while the platelet count was observed to be with sinoatrial block and atrioventricular low (38000/cumm). Dengue serology was reactive dissociation that had a spontaneous resolution. for immunoglobulin G (IgG) and immunoglobulin M (IgM), suggesting acute primary infection. The liver Keywords: atrioventricular block, enzymes and renal profile, including serum electrolytes, atrioventricular dissociation, dengue were normal. The patient was managed supportively haemorrhagic fever, rhythm abnormality, according to the World Health Organization (WHO) sinoatrial block recommendations for management of dengue Singapore Med J 2010; 51(8): e146-e148 haemorrhagic fever.(3) The following day, the patient was observed to have INTRODUCTION bradycardia (pulse rate 50/min, regular), with normal Dengue fever is a viral infection that is transmitted BP.
    [Show full text]
  • Cardiac Arrhythmia
    Cardiac Arrhythmia How to approach นพ.พินิจ แกวสุวรรณะ หน่วยโรคหัวใจและหลอดเลือด EKG paper is a grid where time is measured along the horizontal axis. Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds. Voltage is measured along the vertical axis Voltage is measured along the vertical axis. 10 mm is equal to 1mV in voltage. The diagram below illustrates the configuration of EKG graph paper and where to measure the components of the EKG wave form P wave Indicates atrial depolarization, or contraction of the atrium. Normal duration is not longer than 0.11 seconds (less than 3 small squares) Amplitude (height) is no more than 3 mm No notching or peaking QRS complex Indicates ventricular depolarization, or contraction of the ventricles. Normally not longer than .10 seconds in duration Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4 R waves are deflected positively and the Q and S waves are negative T wave Indicates ventricular repolarization Not more that 5 mm in amplitude in standard leads and 10 mm in precordial leads Rounded and asymmetrical ST segment Indicates early ventricular repolarization Normally not depressed more than 0.5 mm May be elevated slightly in some leads (no more than 1 mm) PR interval Indicates AV conduction time Duration time is 0.12 to 0.20 seconds QT interval Indicates repolarization time General rule: duration is less than half the preceding R-R interval Sinus Bradycardia Rate40-59 bpm P wavesinus QRSnormal (.06-.12) ConductionP-R normal or slightly prolonged at slower rates Rhythmregular or slightly irregular This rhythm is often seen as a normal variation in athletes, during sleep, or in response to a vagal maneuver.
    [Show full text]
  • Cardiac Rhythms and Arrhythmias Chapter 12 Sinus Node Dysfunction
    SECTION II Cardiac Rhythms and Arrhythmias Chapter 12 Sinus Node Dysfunction SAROJA BHARATI, NORA GOLDSCHLAGER, FRED KUSUMOTO, RALPH LAZZARA, RABIH AZAR, STEPHEN HAMMILL, and GERALD NACCARELLI Epidemiology: Nora Goldschlager, Fred Kusumoto, and Rabih Azar Anatomy and Pathology: Saroja Bharati Basic Electrophysiology: Ralph Lazzara Etiology: Nora Goldschlager, Fred Kusumoto, and Rabih Azar Diagnostic Evaluation: Gerald Naccarelli Clinical Electrophysiology: Stephen Hammill Evidence-Based Therapy: Nora Goldschlager, Fred Kusumoto, and Rabih Azar In the early 1900s Keith and Flack identified the sinus due to the decrease in vagal tone that occurs with node as the region responsible for activation of the increasing age. heart.1 Laslett first suggested sinus node dysfunction as Sinus node dysfunction should be suspected when a a cause of bradycardia in 1909, and during the 1950s patient describes symptoms of fatigue, syncope or pre- and 1960s Short, Ferrer, Lown, and others described syncope, or exercise intolerance and is noted to have the clinical spectrum of sinus node dysfunction that is sinus bradycardia or pauses on the 12-lead ECG or dur- commonly called the “sick sinus syndrome resting sinus ing Holter monitoring. In general, symptomatic sinus bradycardia.”2-5 Sinus node dysfunction can have multi- node dysfunction increases with age, with the incidence ple electrocardiographic manifestations including sinus doubling between the fifth and sixth decades of life. pauses, the bradycardia-tachycardia syndrome, and inap- In one study of approximately 9000 patients visiting propriate sinus node response to exercise (chronotropic a regional cardiac center in Belgium, Kulbertus et al. incompetence). estimated that the incidence of sinus node dysfunction is less than 5 per 3000 people older than 50 years of age.9 However, sinus node dysfunction is more com- Epidemiology monly identified today because of an increased elderly population and increased physician awareness.
    [Show full text]
  • View Pdf Copy of Original Document
    Phenotype definition for the Vanderbilt Genome-Electronic Records project Identifying genetics determinants of normal QRS duration (QRSd) Patient population: • Patients with DNA whose first electrocardiogram (ECG) is designated as “normal” and lacking an exclusion criteria. • For this study, case and control are drawn from the same population and analyzed via continuous trait analysis. The only difference will be the QRSd. Hypothetical timeline for a single patient: Notes: • The study ECG is the first normal ECG. • The “Mildly abnormal” ECG cannot be abnormal by presence of heart disease. It can have abnormal rate, be recorded in the presence of Na-channel blocking meds, etc. For instance, a HR >100 is OK but not a bundle branch block. • Y duration = from first entry in the electronic medical record (EMR) until one month following normal ECG • Z duration = most recent clinic visit or problem list (if present) to one week following the normal ECG. Labs values, though, must be +/- 48h from the ECG time Criteria to be included in the analysis: Criteria Source/Method “Normal” ECG must be: • QRSd between 65-120ms ECG calculations • ECG designed as “NORMAL” ECG classification • Heart Rate between 50-100 ECG calculations • ECG Impression must not contain Natural Language Processing (NLP) on evidence of heart disease concepts (see ECG impression. Will exclude all but list below) negated terms (e.g., exclude those with possible, probable, or asserted bundle branch blocks). Should also exclude normalization negations like “LBBB no longer present.”
    [Show full text]
  • IHEU-IHES-IHP Front Matter
    IHEU unique 7/13/06 12:03 PM Page i 2007 ICD-9-CM Expert for Hospitals Volumes 1, 2 & 3 International Classification of Diseases 9th Revision Clinical Modification Sixth Edition Edited by: Anita C. Hart, RHIA, CCS, CCS-P Beth Ford, RHIT, CCS Ingenix is committed to providing you with the ICD-9-CM code update information you need to code accurately and to be in compliance with HIPAA regulations. In the case of adoption of additional ICD-9-CM code changes effective April 1, 2007, Ingenix will provide these code changes to you at no additional cost! Just check back at http://www.IngenixOnline.com and look for the ICD-9, CPT® and HCPCS Alerts link under the Quick Access Resources menu to review the latest information concerning any new code changes. Codes Valid October 1, 2006, through September 30, 2007 October 2006 Update 3539/IHEU/U0515 07 ICD9 v1 H 7/11/06 2:24 PM Page 127 Tabular List CIRCULATORY SYSTEM 425.8–426.89 Circulatory System 425.8–426.89 Nerve Conduction of the Heart Normal and Long QT Electrocardiogram QRS Interval ST Interval Normal Long QT R Syndrome R PR Sinoatrial node Segment QT Interval QT Interval (pacemaker) Bachmannʼs bundle PR ST Interval Segment Internodal tracts: Anterior T Middle P T P Posterior Left bundle branch block Left bundle branch: Atrioventricular Q node Anterior fascicle Q Common bundle Posterior fascicle S (of His) S Left bundle branch Atrioventricular block hemiblock 0.2.4.6 0.2.4.6 Accessory bundle MC (of Kent) 426.3 ¥>Other left bundle branch block Right bundle branch Left bundle branch block: Right
    [Show full text]
  • Adams-Stokes Syndrome Caused by Sinoatrial Block
    Br Heart J: first published as 10.1136/hrt.35.10.1002 on 1 October 1973. Downloaded from British Heart Journal, 1973, 35, I002-I008. Adams-Stokes syndrome caused by sinoatrial block Bjarne Sigurd, Gorm Jensen, J0rgen Meibom, and Erik Sand0e From Medical Department B, Rigshospitalet, University of Copenhagen, Denmark Forty-six patients with syncope and/or black-out episodes due to sinoatrial block are presented. Male-to- female ratio was i to i, and mean age at onset of symptoms approximately 63 years in both sexes. Additional heart disease, especially coronary artery disease, was frequently, but not constantly, found. Twenty-five per cent had sinus node dysfunction as the only manifestation of cardiac disease. Ninety per cent had frequent paroxysms of one or several types of a wide spectrum of supraventricular dysrhythmias, which often gave rise to troublesome symptoms in the form of palpitation, fatigue, and/or congestion, but also made it easier to recognize the cardiac origin of the unspecific cerebral symptoms. Cerebral symptoms occurred suddenly and unexpectedly, and often disabled the patients to a severe degree. Drug treatment proved of little value, but pacemaker treatment stopped the cerebral attacks in all the 39 cases in which it was performed. In 3 out of 24 patients pacemaker implantation also abolished the tendency for paroxysms of tachydysrhythmias; in the remaining 2I it allowedfor maximal drug treatment which led to nearly total relieffrom tachydysrhythmias in 17. copyright. Attacks of third-degree sinoatrial block, resulting in Patients cerebral ischaemic symptoms, account for I0 to 20 There were 46 patients with a chronic, intermittent per cent of all cases, in which artificial pacemakers tendency to syncope and/or black-out episodes, assumed are considered necessary (Rasmussen, 197I; Jen- to be caused by paroxysms of third-degree sinoatrial sen et al., I973).
    [Show full text]
  • Sinus Bradycardia
    British Heart Journal, I97I, 33, 742-749. Br Heart J: first published as 10.1136/hrt.33.5.742 on 1 September 1971. Downloaded from Sinus bradycardia Dennis Eraut and David B. Shaw From the Cardiac Department, Royal Devon and Exeter Hospital, Exeter, Devon This paper presents thefeatures of 46 patients with unexplained bradycardia. Patients were ad- mitted to the study if their resting atrial rate was below 56 a minute on two consecutive occasions. Previous electrocardiograms and the response to exercise, atropine, and isoprenaline were studied. The ages of thepatients variedfrom I3 to 88years. Only 8 had a past history ofcardiovascular disease other than bradycardia, but 36 hJd syncopal or dizzy attacks. Of the 46 patients, 35 had another arrhythmia in addition to bradycardia; at some stage, i6 had sinus arrest, i.5 hadjunc- tional rhythm, 12 had fast atrial arrhythmia, I6 had frequent extrasystoles, and 6 had atrio- ventricular block. None had the classical features of sinoatrial block. Arrhythmias were often produced by exercise, atropine, or isoprenaline. Drug treatment was rarely satisfactory, but only i patient needed a permanent pacemaker. It is suggested that the majority of the patients were suffering from a pathological form of sinus bradycardia. The aetiology remains unproven, but the most likely explanation is a loss of the inherent rhythmicity of the sinoatrial node due to a primary degenerative disease. The descriptive title of 'the lazy sinus syndrome' is suggested. copyright. Bradycardia with a slow atrial rate is usually attempt to define the clinical syndrome of regarded as an innocent condition common in bradycardia with a pathologically slow atrial certain types of well-trained athlete, but occa- rate and to clarify the nature of the arrhyth- sionally it may occur in patients with symp- mia.
    [Show full text]
  • Dysrhythmias
    CARDIOVASCULAR DISORDERS DYSRHYTHMIAS I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES A. Standard ECG and rhythm strips 1. Recordings are obtained at a paper speed of 25 mm/sec. 2. The vertical axis measures distance; the smallest divisions are 1 mm ×1 mm. 3. The horizontal axis measures time; each small division is 0.04 sec/mm. B. Normal morphology Courtesy of Dr. Michael McCrea 1. P wave = atrial depolarization a. Upright in leads I, II, III, aVL, and aVF; inverted in lead aVR b. Measures <0.10 seconds wide and <3 mm high c. Normal PR interval is 0.12–0.20 seconds. 2. QRS complex = ventricular depolarization a. Measures 0.06-0.10 seconds wide b. Q wave (1) <0.04 seconds wide and <3 mm deep (2) Abnormal if it is >3 mm deep or >1/3 of the QRS complex. c. R wave ≤7.5 mm high 3. QT interval varies with rate and sex but is usually 0.33–0.42 seconds; at normal heart rates, it is normally <1/2 the preceding RR interval. 4. T wave = ventricular repolarization a. Upright in leads I, II, V3–V6; inverted in aVR b. Slightly rounded and asymmetric in configuration c. Measures ≤5 mm high in limb leads and ≤10 mm high in the chest leads 5. U wave = a ventricular afterpotential a. Any deflection after the T wave (usually low voltage) b. Same polarity as the T wave c. Most easily detected in lead V3 d. Can be a normal component of the ECG e. Prominent U waves may indicate one of the following: (1) Hypokalemia (<3 mEq/L) (2) Hypercalcemia (3) Therapy with digitalis, phenothiazines, quinidine, epinephrine, inotropic agents, or amiodarone (4) Thyrotoxicosis f.
    [Show full text]
  • Effects of Selective Site Pacing on Haemodynamic and Functional Recovery in Patients Requiring Permanent Right Ventricular Pacing
    Effects of Selective Site Pacing on Haemodynamic and Functional Recovery in Patients Requiring Permanent Right Ventricular Pacing Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor of Medicine by Klialed Albouaini 2011 Liverpool Heart and Chest Hospital NHS Trust Thomas Drive Liverpool L14 3PE Effects of Selective Site Pacing on Haemodynamic and Functional Recovery in Patients Requiring Permanent Right Ventricular Pacing. (International Standard Randomised Controlled Trial Registration Number: ISRCTN 67629267) The single centre randomised trial aimed to assess whether right ventricular outflow tract (RVOT) compared to right ventricular apical (RVA) pacing is more beneficial at the medium term follow-up. Fifty patients were randomised to either RVA (n—25) or RVOT (n=25) pacing. Baseline and 6 month follow-up investigations included: electrocardiogram, New York heart failure functional (NYHA) class, Minnesota Living with Heart Failure (MLWHF) score. Short Form-36 health survey (SF-36), echocardiogram, and a cardiopulmonary exercise test. The primary endpoint was peak oxygen consumption (PVO2). Secondary endpoints were: NYHA class, MLWHF and SF-36 scores, LVEF, and dyssynchrony criteria. There were no significant differences in changes in PVO2 levels between the study groups. Similarly, QRS duration changes were not significantly different between the study groups. In contrast, MLWHF scores improved significantly in the RVOT group (32 ± 19) compared with the RVA group (21 ± 22), P=0.041. In addition, SF-36 health survey indicated better scores in RVOT patients in the following areas: (1) Physical Function, 36.6 ± 28.0 (RVOT) versus 11.2 ± 26.0 (RVA), P = 0.005; (2) Role Limitation due to Emotional Problem scores, 43.3 ± 9.7 (RVOT) versus 4.5 ±11.6 (RVA arm), P = 0.016; (3) Vitality Energy Fatigue scores 26.3 ± 27.0 (RVOT) versus 7.2 ± 24.0 (RVA), P = 0.024.
    [Show full text]
  • The Evaluation of Sinoatrial Node Function 1N Man*
    The Evaluation of Sinoatrial Node Function 1n Man* J. THOMAS BIGGER, JR, M.D.t Associate Professor of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York HAROLD C. STRAUSS, M.D., C.M.t Associate in Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York The function of the sinoatrial node is com­ ence with the extracellular fluid and often shows plex. In nearly all hearts, this small bit of tissue is some overshoot, that is, the inside of the cell may responsible for spontaneously generating the impulse become slightly positive relative to the extracellular which will be distributed to the remainder of the potential. After reaching this peak inside-positive heart, maintaining coordinated electrical and me­ value of transmembrane voltage (V111 ), the sinus chanical function. In recent years, it has become node cell slowly repolarizes to a maximum inside­ clear that S-A node dysfunction is not rare, can negative value-so-called maximum diastolic volt­ cause disabling symptoms, and often presents diffi­ age. Then, the transmembrane voltage spontaneously cult management problems. The challenges pre­ begins to decrease ( phase 4 depolarization) until sented by the "Sick Sinus Syndromes" have in­ a critical value of V 111 , threshold voltage, is reached creased our desire to know more about normal and self-excitation recurs. The rate of recurring S-A node function and about function in disease self-excitation could theoretically be altered by states. changes in: 1) maximum diastolic voltage, 2) The intimate mechanisms of sinus node func­ threshold voltage, and 3) rate of phase 4 depolari­ tion remain a mystery despite the "prying eye" of the zation.
    [Show full text]
  • The Heart in Portuguese Amyloidosis
    Postgraduate Medical Journal (1986) 62, 601-605 Postgrad Med J: first published as 10.1136/pgmj.62.728.601 on 1 June 1986. Downloaded from The heart in Portuguese amyloidosis A. Falcao de Freitas School ofMedicine, Oporto University, 4200 Porto, Portugal. Summary: A systematic investigation was performed in patients with familial amyloidotic poly- neuropathy, Portuguese type (AFp) to assess the pattern and incidence of cardiac involvement. Of 327 patients investigated, ECG abnormalities were present in 285 (87.2%). Low voltage and QS pattern in V1, V2, V3 were found in 51.3% and 35.7% patients respectively. Conduction disturbances were present in 211 (64.5%). Sinus node disease, 1st degree and Wenckebach interventricular blocks were frequent. Complete atrioventricular block was observed in only 2 patients (0.6%). Left anterior hemi-block was present in 30.8%, left bundle branch block in 3.9%, left posterior hemi-block in 2.4% and right bundle branch block in 2.1%. Holter monitoring showed a much higher incidence of conduction disturbances, most of these occurring at night. The mean values of septum and posterior wall thickness and mass evaluated by echocardiography in 72 patients were normal. The systolic and diastolic global and regional functions, determined in 12 patients, analysing the echo by a digitization computer technique, were normal. In 7% a trivial pericardial effusion was observed. In 16 patients with ECG changes and normal echocardiograms the technetium 99m pyrophosphate scanning was negative. We conclude that the ECG is the most precise, sensitive and clinically useful method for detecting cardiac amyloidosis in patients with AFp.
    [Show full text]