EKG Interpretations
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Cardiac Symptoms and Physical Signs 11
CHAPTER 1 1 Cardiac Symptoms and Physical Signs 1.1 Common Cardiac Symptoms Angina Typical angina presents as a chest tightness or heaviness brought on by effort and relieved by rest. The sensation starts in the retrosternal region and radi- ates across the chest. Frequently it is associated with a leaden feeling in the arms. Occasionally it may present in more unusual sites, e.g. pain in the jaw or teeth on effort, without pain in the chest. It may be confused with oesopha- geal pain, or may present as epigastric or even hypochondrial pain. The most important feature is its relationship to effort. Unilateral chest pain (sub- mammary) is not usually cardiac pain, which is generally symmetrical in distribution. Angina is typically exacerbated by heavy meals, cold weather (just breath- ing in cold air is enough) and emotional disturbances. Arguments with col- leagues or family and watching exciting television are typical precipitating factors. Stable Angina This is angina induced by effort and relieved by rest. It does not increase in frequency or severity, and is predictable in nature. It is associated with ST- segment depression on ECG. Decubitus Angina This is angina induced by lying down at night or during sleep. It may be caused by an increase in LVEDV (and hence wall stress) on lying fl at, associ- ated with dreaming or getting between cold sheets. Coronary spasm may occur in REM sleep. It may respond to a diuretic, calcium antagonist or nitrate taken in the evening. Swanton’s Cardiology, sixth edition. By R. H. Swanton and S. -
Cardiology-EKG Michael Bradley
Cardiology/EKG Board Review Michael J. Bradley D.O. DME/Program Director Family Medicine Residency Objectives • Review general method for EKG interpretation • Review specific points of “data gathering” and “diagnoses” on EKG • Review treatment considerations • Review clinical cases/EKG’s • Board exam considerations EKG EKG – 12 Leads • Anterior Leads - V1, V2, V3, V4 • Inferior Leads – II, III, aVF • Left Lateral Leads – I, aVL, V5, V6 • Right Leads – aVR, V1 11 Step Method for Reading EKG’s • “Data Gathering” – steps 1-4 – 1. Standardization – make sure paper and paper speed is standardized – 2. Heart Rate – 3. Intervals – PR, QT, QRS width – 4. Axis – normal vs. deviation 11 Step Method for Reading EKG’s • “Diagnoses” – 5. Rhythm – 6. Atrioventricular (AV) Block Disturbances – 7. Bundle Branch Block or Hemiblock of – 8. Preexcitation Conduction – 9. Enlargement and Hypertrophy – 10. Coronary Artery Disease – 11. Utter Confusion • The Only EKG Book You’ll Ever Need Malcolm S. Thaler, MD Heart Rate • Regular Rhythms Heart Rate • Irregular Rhythms Intervals • Measure length of PR interval, QT interval, width of P wave, QRS complex QTc • QTc = QT interval corrected for heart rate – Uses Bazett’s Formula or Fridericia’s Formula • Long QT syndrome – inherited or acquired (>75 meds); torsades de ponites/VF; syncope, seizures, sudden death Axis Rhythm • 4 Questions – 1. Are normal P waves present? – 2. Are QRS complexes narrow or wide (≤ or ≥ 0.12)? – 3. What is relationship between P waves and QRS complexes? – 4. Is rhythm regular or irregular? -
Evidence of Atrial Functional Mitral Regurgitation Due to Atrial Fibrillation Reversal with Arrhythmia Control
Journal of the American College of Cardiology Vol. 58, No. 14, 2011 © 2011 by the American College of Cardiology Foundation ISSN 0735-1097/$36.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2011.06.032 Heart Rhythm Disorders Evidence of Atrial Functional Mitral Regurgitation Due to Atrial Fibrillation Reversal With Arrhythmia Control Zachary M. Gertz, MD,* Amresh Raina, MD,* Laszlo Saghy, MD,† Erica S. Zado, PA-C,* David J. Callans, MD,* Francis E. Marchlinski, MD,* Martin G. Keane, MD,* Frank E. Silvestry, MD* Philadelphia, Pennsylvania; and Szeged, Hungary Objectives The purpose of this study was to determine whether atrial fibrillation (AF) might cause significant mitral regurgi- tation (MR), and to see whether this MR improves with restoration of sinus rhythm. Background MR can be classified by leaflet pathology (organic/primary and functional/secondary) and by leaflet motion (nor- mal, excessive, restrictive). The existence of secondary, normal leaflet motion MR remains controversial. Methods We performed a retrospective cohort study. Patients undergoing first AF ablation at our institution (n ϭ 828) were screened. Included patients had echocardiograms at the time of ablation and at 1-year clinical follow-up. The MR cohort (n ϭ 53) had at least moderate MR. A reference cohort (n ϭ 53) was randomly selected from those patients (n ϭ 660) with mild or less MR. Baseline echocardiographic and clinical characteristics were compared, and the effect of restoration of sinus rhythm was assessed by follow-up echocardiograms. Results MR patients were older than controls and more often had persistent AF (62% vs. 23%, p Ͻ 0.0001). -
Giant Right Atrium Or Ebstein Anomaly? Hacer Kamalı1, Abdullah Erdem1*, Cengiz Erol2 and Atıf Akçevin3
ISSN: 2378-2951 Kamalı et al. Int J Clin Cardiol 2017, 4:104 DOI: 10.23937/2378-2951/1410104 Volume 4 | Issue 4 International Journal of Open Access Clinical Cardiology CASE REPORT Giant Right Atrium or Ebstein Anomaly? Hacer Kamalı1, Abdullah Erdem1*, Cengiz Erol2 and Atıf Akçevin3 1Department of Pediatric Cardiology, Istanbul Medipol University, Turkey 2Department of Radiology, Istanbul Medipol University, Turkey 3Department of Cardiovascular Surgery, Istanbul Medipol University, Turkey *Corresponding author: Abdullah Erdem, Associate Professor of Pediatric Cardiology, Department of Pediatric Cardiology, Istanbul Medipol University, Istanbul, Turkey, Tel: +905-0577-05805, Fax: +90212467064, E-mail: drabdullaherdem@ hotmail.com partment for exercise intolerance. She had been diag- Abstract nosed and followed up as Ebstein anomaly for ten years. Many acquired and congenital pathologies could cause en- Her heart rate was 75/min with normal jugular venous largement of Right Atrium (RA). In rare pathologies we couldn’t find an obvious reason for enlargement of RA. Sometimes it pressure. Findings of lung examination were normal. leads to misdiagnosis if we try to explain an unknown pa- Auscultation of heart revealed a 2/6 systolic murmur on thology with well known pathology. In this article we de- the lower left edge of the sternum. On abdominal ex- scribe a woman who presented with giant enlargement of amination, there was no organomegaly. Arterial Oxygen the RA misdiagnosed as Ebstein anomaly. Cardiac MRI is highly helpful for differential diagnosis of these kinds of atrial Saturation (SpO2) was 98%. Electrocardiography (ECG) pathologies. Although it is rare, giant RA should be consid- revealed absence of atrial fibrillation, the rhythm was ered in differential diagnosis of huge RA without an obvious sinus but there was right axis deviation and right bundle cause. -
Nitric Oxide-Mediated Flow-Dependent Dilation Is Impaired in Coronary Arteries in Patients with Coronary Spastic Angina
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector 920 JACC Vol. 30, No. 4 October 1997:920–6 Nitric Oxide-Mediated Flow-Dependent Dilation Is Impaired in Coronary Arteries in Patients With Coronary Spastic Angina KIYOTAKA KUGIYAMA, MD, MASAMICHI OHGUSHI, MD, TAKESHI MOTOYAMA, MD, SEIGO SUGIYAMA, MD, HISAO OGAWA, MD, MICHIHIRO YOSHIMURA, MD, YOSHITO INOBE, MD, OSAMU HIRASHIMA, MD, HIROAKI KAWANO, MD, HIROFUMI SOEJIMA, MD, HIROFUMI YASUE, MD Kumamoto City, Japan Objectives. This study sought to examine whether flow- Results. Flow-dependent dilation of the proximal LAD was dependent dilation is impaired at the site of coronary artery found to be less in spasm arteries than in control arteries. G spasm in patients with coronary spastic angina. Infusion of N -monomethyl-L-arginine (L-NMMA) in the proxi- Background. Physiologic stimuli such as exercise and exposure mal LAD suppressed flow-dependent dilation in control arteries to cold have been shown to cause an increase in coronary blood but had no significant effect on spasm arteries. The dilator flow, leading to flow-dependent dilation of coronary arteries in response to nitroglycerin was not impaired in spasm coronary normal subjects, but cause coronary constriction in patients with arteries. coronary spastic angina. Conclusions. Our results indicate that flow-dependent coronary Methods. A maximal increase in blood flow was induced dilation is impaired in spasm arteries, partly due to a deficiency in selectively in the left anterior descending coronary artery (LAD) endothelial nitric oxide bioactivity, which in turn may contribute by infusion of adenosine through a Doppler flow catheter tip in the to the increase in coronary tone during physiologic stimuli in midportion of the LAD in 10 patients with coronary spastic patients with coronary spastic angina. -
Clinical Manifestation and Survival of Patients with I Diopathic Bilateral
ORIGINAL ARTICLE Clinical Manifestation and Survival of Patients with Mizuhiro Arima, TatsujiI diopathicKanoh, Shinya BilateralOkazaki, YoshitakaAtrialIwama,DilatationAkira Yamasaki and Sigeru Matsuda Westudied the histories of eight patients who lacked clear evidence of cardiac abnormalities other than marked bilateral atrial dilatation and atrial fibrillation, which have rarely been dis- cussed in the literature. From the time of their first visit to our hospital, the patients' chest radio- graphs and electrocardiograms showed markedly enlarged cardiac silhouettes and atrial fibrilla- tion, respectively. Each patient's echocardiogram showed a marked bilateral atrial dilatation with almost normal wall motion of both ventricles. In one patient, inflammatory change was demonstrated by cardiac catheterization and endomyocardial biopsy from the right ventricle. Seven of our eight cases were elderly women.Over a long period after the diagnosis of cardiome- galy or arrhythmia, diuretics or digitalis offered good results in the treatment of edema and congestion in these patients. In view of the clinical courses included in the present study, we conclude that this disorder has a good prognosis. (Internal Medicine 38: 112-118, 1999) Key words: cardiomegaly, atrial fibrillation, elder women,good prognosis Introduction echocardiography. The severity of mitral and tricuspid regur- gitation was globally assessed by dividing into three equal parts Idiopathic enlargement of the right atrium was discussed by the distance from the valve orifice. The regurgitant jet was de- Bailey in 1955(1). This disorder may be an unusual congenital tected on color Doppler recording in the four-chamber view malformation. A review of the international literature disclosed and classified into one of the three regions (-: none, +: mild, that although several cases have been discussed since Bailey's ++:moderate, +++: severe). -
Young Adults. Look for ST Elevation, Tall QRS Voltage, "Fishhook" Deformity at the J Point, and Prominent T Waves
EKG Abnormalities I. Early repolarization abnormality: A. A normal variant. Early repolarization is most often seen in healthy young adults. Look for ST elevation, tall QRS voltage, "fishhook" deformity at the J point, and prominent T waves. ST segment elevation is maximal in leads with tallest R waves. Note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2- 6 is concave upwards, another characteristic of this normal variant. Characteristics’ of early repolarization • notching or slurring of the terminal portion of the QRS wave • symmetric concordant T waves of large amplitude • relative temporal stability • most commonly presents in the precordial leads but often associated with it is less pronounced ST segment elevation in the limb leads To differentiate from anterior MI • the initial part of the ST segment is usually flat or convex upward in AMI • reciprocal ST depression may be present in AMI but not in early repolarization • ST segments in early repolarization are usually <2 mm (but have been reported up to 4 mm) To differentiate from pericarditis • the ST changes are more widespread in pericarditis • the T wave is normal in pericarditis • the ratio of the degree of ST elevation (measured using the PR segment as the baseline) to the height of the T wave is greater than 0.25 in V6 in pericarditis. 1 II. Acute Pericarditis: Stage 1 Pericarditis Changes A. Timing 1. Onset: Day 2-3 2. Duration: Up to 2 weeks B. Findings 1. -
EKG Workshop Texas Academy of Physician Assistants 2018 TAPA 43Rd Annual CME Conference
EKG Workshop Texas Academy of Physician Assistants 2018 TAPA 43rd Annual CME Conference David J. Klocko, MPAS, PA-C Associate Professor and Academic Coordinator UT Southwestern Department of PA Studies Disclosures Content in this presentation is licensed under a Creative Commons Attribution 4.0 International license. David J. Klocko is receiving a stipend from TAPA to do this workshop. Objectives Review basic electrophysiology. Recognize common cardiac dysrhythmias. Recognize common conductive disorders. Review axis, bundle branch block, chamber enlargement and hypertrophy. Recognize common ECG changes associated with myocardial ischemia and infarction. Systematic Evaluation of the 12- lead EKG –Our ultimate goal ! Step Check for: LOOK AT: 1. Rhythm Rhythm Strip 2. Axis I, AvF ** 3. BBB V1, V6 4. Ischemia, Injury or I-AvL, V5-V6 Infarct V1-V4 II, III, AvF 5. Chamber II, V1 Enlargement Intervals & Segments PR interval (PRI): start of atrial depolarization to start of ventricular depolarization Normal: 0.12 – 0.20 sec QRS complex: depolarization of ventricles Normal: 0.04 – 0.11 sec When QRS >0.12 sec, think about an interventricular conduction delay Intervals & Segments ST segment: end ventricular depolarization to start of repolarization QT interval (QTI): both ventricular depolarization & repolarization Normal: 0.3 – 0.4 sec; varies with heartrate Faster heartrates….shorter QTIs; slower heartrates ….longer QTIs Heart Rate For regular rhythms, measure the interval between complexes in large boxes 300-150-100-75-60-50-43-37-33 -
Changes in Cardiac Geometry Due to Hypertrophy
Changes in Cardiac Geometry Due to Hypertrophy By Marta Ellen Pedersen A Master’s Paper Submitted in Partial Fulfillment of The Requirements for the Degree of Master of Science in Clinical Exercise Physiology Dr. Joseph O’ Kroy Date University of Wisconsin-River Falls 2014 Introduction For any given body size, men have larger hearts than women, athletes have larger hearts than nonathletes, and often times, an enlarged heart is a symptom of an underlying disorder that is causing the heart to work harder than normal. This review will emphasize the differences between a pathologically enlarged heart and an athletically enlarged heart. Pathologically induced hypertrophy (myopathy) When heart cells get bigger, (often is the case when heart disease is present) the total heart works less efficiently. Some people suffer from conditions like hypertrophic cardiomyopathy, which includes significant heart muscle enlargement, and can be genetic or caused by high blood pressure. Cardiomyopathy decreases the size of the heart's chambers, reducing blood flow. Hypertrophy, or thickening, of the heart muscle can occur in response to increased stress on the heart. The most common causes of Cardiomyopathy are related to increased blood pressure. The extra work of pumping blood against the increased pressure causes the ventricle to thicken over time, the same way a body muscle increases in mass in response to weightlifting. Cardiomyopathy can occur in both the right and left atrium and the right and left ventricles. Blood travels through the right ventricle to the lungs. If conditions occur that decrease pulmonary circulation, extra stress can be placed on the right ventricle, and can lead to right ventricular myopathy. -
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. -
Veno-Occlusive Unloading of the Heart Reduces Infarct Size in Experimental
www.nature.com/scientificreports OPEN Veno‑occlusive unloading of the heart reduces infarct size in experimental ischemia–reperfusion Esben Søvsø Szocska Hansen2, Tobias Lynge Madsen1, Gregory Wood1, Asger Granfeldt3, Nikolaj Bøgh2, Bawer Jalal Tofg1, Peter Agger4, Jakob Lykke Lindhardt1, Christian Bo Poulsen1, Hans Erik Bøtker1 & Won Yong Kim1,2* Mechanical unloading of the left ventricle reduces infarct size after acute myocardial infarction by reducing cardiac work. Left ventricular veno‑occlusive unloading reduces cardiac work and may reduce ischemia and reperfusion injury. In a porcine model of myocardial ischemia–reperfusion injury we randomized 18 pigs to either control or veno‑occlusive unloading using a balloon engaged from the femoral vein into the inferior caval vein and infated at onset of ischemia. Evans blue and 2,3,5‑triphenyltetrazolium chloride were used to determine the myocardial area at risk and infarct size, respectively. Pressure–volume loops were recorded to calculate cardiac work, left ventricular (LV) volumes and ejection fraction. Veno‑occlusive unloading reduced infarct size compared with controls (Unloading 13.9 ± 8.2% versus Control 22.4 ± 6.6%; p = 0.04). Unloading increased myocardial salvage (54.8 ± 23.4% vs 28.5 ± 14.0%; p = 0.02), while the area at risk was similar (28.4 ± 6.7% vs 27.4 ± 5.8%; p = 0.74). LV ejection fraction was preserved in the unloaded group, while the control group showed a reduced LV ejection fraction. Veno‑occlusive unloading reduced myocardial infarct size and preserved LV ejection fraction in an experimental acute ischemia–reperfusion model. This proof‑of‑concept study demonstrated the potential of veno‑occlusive unloading as an adjunctive cardioprotective therapy in patients undergoing revascularization for acute myocardial infarction. -
Abnormal ECG Findings in Athletes Normal ECG
SEATTLE CRITERIA Abnormal ECG findings in athletes These ECG findings are unrelated to regular training or expected physiologic adaptation to exercise, may suggest the presence of pathologic cardiovascular disease, and require further diagnostic evaluation. Abnormal ECG finding Definition T wave inversion > 1 mm in depth in two or more leads V2-V6, II and aVF, or I and aVL (excludes III, aVR, and V1) ST segment depression ≥ 0.5 mm in depth in two or more leads Pathologic Q waves > 3 mm in depth or > 40 ms in duration in two or more leads (except III and aVR) Complete left bundle branch block QRS ≥ 120 ms, predominantly negative QRS complex in lead V1 (QS or rS), and upright monophasic R wave in leads I and V6 Intra-ventricular conduction delay Any QRS duration ≥ 140 ms Left axis deviation -30° to -90° Left atrial enlargement Prolonged P wave duration of > 120 ms in leads I or II with negative portion of the P wave ≥ 1 mm in depth and ≥ 40 ms in duration in lead V1 Right ventricular hypertrophy R-V1 + S-V5 > 10.5 mm and right axis deviation > 120° pattern Ventricular pre-excitation PR interval < 120 ms with a delta wave (slurred upstroke in the QRS complex) and wide QRS (> 120 ms) Long QT interval* QTc ≥ 470 ms (male) QTc ≥ 480 ms (female) QTc ≥ 500 ms (marked QT prolongation) Short QT interval* QTc ≤ 320 ms Brugada-like ECG pattern High take-off and downsloping ST segment elevation followed by a negative T wave in ≥ 2 leads in V1-V3 Profound sinus bradycardia < 30 BPM or sinus pauses ≥ 3 sec Mobitz type II 2° AV block Intermittently non-conducted P waves not preceded by PR prolongation and not followed by PR shortening 3° AV block Complete heart block Atrial tachyarrhythmias Supraventricular tachycardia, atrial fibrillation, atrial flutter Premature ventricular contractions ≥ 2 PVCs per 10 second tracing Ventricular arrhythmias Couplets, triplets, and non-sustained ventricular tachycardia *The QT interval corrected for heart rate is ideally measured with heart rates of 60-90 bpm.