DOCSLIB.ORG

04. the Cardiac Cycle/Wiggers Diagram

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
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. The cardiac cycle - The “Wiggers diagram” Prof. J Swanevelder The cardiac cycle can be examined in detail by considering the ECG trace, intracardiac pressure and volume curves, and heart valve function. Fig. 1 The “Wiggers Diagram” - Cardiac cycle, showing ventricular volume, ventricular pressure, aortic pressure and atrial pressure Systolic function Systole can be broken down into the following stages: • Isovolumetric ventricular contraction • Ventricular ejection Systole commences with a period of isovolumetric contraction initiated by the QRS complex of the ECG. During this brief period the volume of the ventricle does not change since both the AV and semilunar valves are closed. Isovolumetric contraction ends when the semilunar valve opens and ejection begins. The events during systole are described below and should be considered along with the ventricular pressure, aortic pressure and ventricular volume curves. Left ventricular pressure The QRS complex of the ECG initiates ventricular contraction. As the pressure in the left ventricle increases during isovolumetric contraction, it comes to exceed the pressure in the aorta. At this point the aortic valve opens and ejection begins. The aortic valve opens at about 80 mmHg. Ejection continues as long as ventricular pressure exceeds aortic pressure. The total volume ejected into the aorta is the stroke volume (SV). The ventricular pressure increases initially during ejection, but then starts to decrease as the ventricle relaxes. The gradient between ventricle and aorta starts to reverse at this point, since LV pressure has started to fall but aortic pressure is maintained by the momentum of the last of the ejected blood. When the ventricular to aortic pressure gradient has reversed, the aortic valve closes and isovolumetric relaxation begins. The dicrotic notch on the aortic pressure curve (below) marks this point. The LV pressure normally reaches a systolic maximum of 120 mmHg. At the end of systole the LV pressure is described as the end-systolic pressure and the LV volume is at its smallest (end-systolic volume), about 40–50 ml. Right ventricular pressure This follows a similar course to LV pressure. The tricuspid and pulmonary valves dictate events, with ejection occurring into the pulmonary artery. Right ventricular pressure reaches a maximum of about 20–24 mmHg during systole. Ventricular volume Diastole commences in the left side of the heart with closure of the aortic valve and relaxation of the left ventricle. Since the mitral and aortic valves are both closed at this time the relaxation is described as isovolumetric. The ventricle contains 40–50 ml blood at this stage (end-systolic volume). 4 - 2 The cardiac cycle - The “Wiggers diagram” Prof. J Swanevelder Isovolumetric relaxation ends with opening of the mitral valve, when a period of rapid filling of the ventricle begins, which lasts for the first third of diastole. After the initial period of rapid filling follows a period of passive filling called diastasis and flow continues passively into the ventricle, providing up to 75% (60 ml) of the filling volume. During the last third of diastole the P wave of the ECG initiates atrial contraction, which contributes the remaining 25% of filling to give an end-diastolic volume of about 120 ml. The end-diastolic volume of the ventricle is not always 120 ml, but can vary due to changes in venous return to the heart, contractility and heart rate. A similar sequence of events occurs on the right side of the heart, controlled by the pulmonary and tricuspid valves. Aortic pressure curve Ejection of blood into the aorta begins when the aortic valve opens. During ejection, the aortic pressure follows the ventricular pressure curve with a small pressure gradient of about 1–2 mmHg when the aortic valve is normal. As ejection proceeds aortic pressure increases to a maximum (systolic pressure) and starts to fall as the LV relaxes. When the ventricular pressure has fallen below the aortic pressure, the aortic valve closes and ejection ceases. Following closure of the aortic valve, elastic rebound of the aorta walls gives rise to a small hump in the aortic pressure curve forming the dicrotic notch. This notch marks the beginning of diastole. During diastole the aortic pressure gradually falls to a minimum (diastolic pressure), due to runoff of blood to the systemic circulation. Atrial pressure Normally blood fills the right atrium (RA) via the superior and inferior venae cavae, continuously throughout the cardiac cycle. This flow is returned from the peripheral circulation and is called the venous return to the heart. On the left side of the heart, the left atrium (LA) receives blood from the pulmonary vascular bed via the pulmonary veins. Passive filling of the atria produces RA pressures of 0–2 mmHg and LA pressures of 2–5 mmHg. During diastole atrial pressures follow ventricular pressures since the AV valves are open and the two chambers are joined. Three waves or peaks are produced in the atrial pressure curve during the cycle. At the end of diastole the atria prime the ventricles by contracting and developing pressures between 0 and 5 mmHg. Atrial contraction is shown on the atrial pressure curve as a smooth peak immediately preceding systole, the ‘a’ wave. As systole begins the AV valves close and a brief period of isovolumetric contraction occurs, producing a second low-pressure peak, the ‘c’ wave. This is due to the AV valve bulging back into the atrium. As blood is ejected during systole the atrium continues to fill with the AV valve closed and atrial pressure increases until early diastole when the AV valve opens. At this point rapid filling of the ventricles commences and a sudden fall in atrial pressure follows. This gives rise to the ‘v’ wave. Diastolic function Diastole can be broken down into the following stages: • Isovolumetric ventricular relaxation • Rapid ventricular filling • Slow ventricular filling (diastasis) • Atrial contraction Although diastole appears to be a passive part of the cardiac cycle, it has some important functions: • Myocardial relaxation – a metabolically active phase. One essential process is the reuptake of calcium by the sarcoplasmic reticulum. Incomplete reuptake leads to diastolic dysfunction due to decreased end-diastolic compliance. The negative slope of the ventricular pressure–time curve during isovolumetric relaxation (termed dP/dt(max)) indicates myocardial relaxation. Increased sympathetic tone or circulating catecholamine levels give rise to an increased dP/dt(max). This is known as positive lusitropy. • Ventricular filling – provides the volume for the cardiac pump. Most of the ventricular filling occurs during early diastole. There is only a small increase in ventricular volume during diastasis. As the heart rate increases diastasis is shortened first. When the heart rate exceeds about 140 bpm, rapid filling in early diastole becomes compromised and the volume of blood ejected during systole (stroke volume, SV) is significantly decreased. • Atrial contraction – contributes up to 25% of total ventricular filling in the normal heart. This atrial contribution can become of greater importance in the presence of myocardial ischaemia or ventricular hypertrophy. • Coronary artery perfusion – the greater part of left coronary blood flow occurs during diastole. 4 - 3 The cardiac cycle - The “Wiggers diagram” Prof. J Swanevelder Cardiac valves The cardiac valves open and close passively in response to the changes in pressure gradient across them. These valves control the sequence of flow between atria and ventricles, and from the ventricles to the pulmonary and systemic circulations. Valve timing in relation to the ventricular pressure curve is shown in Fig 2. The AV valves are the mitral and tricuspid valves. These prevent backflow from the ventricles into the atria during systole. The papillary muscles are attached to the AV valves by chordae tendineae. They contract together with the ventricular muscle during systole, but do not help to close the valves. They prevent excessive bulging of the valves into the atria and pull the base of the heart toward the ventricular apex to shorten the longitudinal axis of the ventricle, thus increasing systolic efficiency. The semilunar (SL) valves are the aortic and pulmonary valves. These prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole.
Load more

Recommended publications
  • Chapter 20 *Lecture Powerpoint the Circulatory System: Blood Vessels and Circulation
    Chapter 20 *Lecture PowerPoint The Circulatory System: Blood Vessels and Circulation *See separate FlexArt PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Introduction • The route taken by the blood after it leaves the heart was a point of much confusion for many centuries – Chinese emperor Huang Ti (2697–2597 BC) believed that blood flowed in a complete circuit around the body and back to the heart – Roman physician Galen (129–c. 199) thought blood flowed back and forth like air; the liver created blood out of nutrients and organs consumed it – English physician William Harvey (1578–1657) did experimentation on circulation in snakes; birth of experimental physiology – After microscope was invented, blood and capillaries were discovered by van Leeuwenhoek and Malpighi 20-2 General Anatomy of the Blood Vessels • Expected Learning Outcomes – Describe the structure of a blood vessel. – Describe the different types of arteries, capillaries, and veins. – Trace the general route usually taken by the blood from the heart and back again. – Describe some variations on this route. 20-3 General Anatomy of the Blood Vessels Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Capillaries Artery: Tunica interna Tunica media Tunica externa Nerve Vein Figure 20.1a (a) 1 mm © The McGraw-Hill Companies, Inc./Dennis Strete, photographer • Arteries carry blood away from heart • Veins
    [Show full text]
  • Physiology Lessons for Use with the Biopac Student Lab Lesson 5
    Physiology Lessons Lesson 5 for use with the ELECTROCARDIOGRAPHY I Biopac Student Lab Components of the ECG Richard Pflanzer, Ph.D. Associate Professor Emeritus Indiana University School of Medicine Purdue University School of Science William McMullen Vice President BIOPAC Systems, Inc. BIOPAC® Systems, Inc. 42 Aero Camino, Goleta, CA 93117 (805) 685-0066, Fax (805) 685-0067 Email: [email protected] Web: www.biopac.com Manual Revision PL3.7.5 03162009 BIOPAC Systems, Inc. Page 2 Biopac Student Lab 3.7.5 I. INTRODUCTION The main function of the heart is to pump blood through two circuits: 1. Pulmonary circuit: through the lungs to oxygenate the blood and remove carbon dioxide; and 2. Systemic circuit: to deliver oxygen and nutrients to tissues and remove carbon dioxide. Because the heart moves blood through two separate circuits, it is sometimes described as a dual pump. In order to beat, the heart needs three types of cells: 1. Rhythm generators, which produce an electrical signal (SA node or normal pacemaker); 2. Conductors to spread the pacemaker signal; and 3. Contractile cells (myocardium) to mechanically pump blood. The Electrical and Mechanical Sequence of a Heartbeat The heart has specialized pacemaker cells that start the electrical sequence of depolarization and repolarization. This property of cardiac tissue is called inherent rhythmicity or automaticity. The electrical signal is generated by the sinoatrial node (SA node) and spreads to the ventricular muscle via particular conducting pathways: internodal pathways and atrial fibers, the atrioventricular node (AV node), the bundle of His, the right and left bundle branches, and Purkinje fibers (Fig 5.1).
    [Show full text]
  • 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.
    [Show full text]
  • 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?
    [Show full text]
  • The ECG Made Very Easy Indeed: a Beginner’S Guide
    Part 1 The ECG made very easy indeed: a beginner’s guide The ECG made very easy indeed 1 What is an ECG? 1 The heart is a pump driven by intrinsic electrical When do you need an ECG? 1 impulses which make the heart beat. An ECG is a paper recording of that electrical activity. The ECG records where How to record an ECG 2 electrical impulses start and how they flow through the How to interpret an ECG: the basics 2 heart. It does not measure how well the heart is pumping. The electrical activity of the heart starts in the ‘inter- The ECG waves and what they mean 2 nal pacemaker’, which is called the sinoatrial node. This Interpretation starts here! 4 is in the right atrium. The normal rhythm is called ‘sinus rhythm’ (properly it should be called sinoatrial rhythm, Rhythms you must be able to recognize 8 but it isn’t). The way electrical impulses flow through the Patterns you must be able to recognize 10 heart is called conduction. Abnormalities in the electrical activity of the heart can The normal ECG and its variants 13 result in abnormal conduction or rhythms where the heart ECG red flags 14 may go too quickly, too slowly, or beat irregularly. Changes to the normal flow of electricity through the heart can be shown on an ECG and may indicate damaged This guide has been written for those who are just starting heart muscle. Heart muscle can be damaged by many to use ECGs in their clinical practice.
    [Show full text]
  • Blood Vessels: Part A
    Chapter 19 The Cardiovascular System: Blood Vessels: Part A Blood Vessels • Delivery system of dynamic structures that begins and ends at heart – Arteries: carry blood away from heart; oxygenated except for pulmonary circulation and umbilical vessels of fetus – Capillaries: contact tissue cells; directly serve cellular needs – Veins: carry blood toward heart Structure of Blood Vessel Walls • Lumen – Central blood-containing space • Three wall layers in arteries and veins – Tunica intima, tunica media, and tunica externa • Capillaries – Endothelium with sparse basal lamina Tunics • Tunica intima – Endothelium lines lumen of all vessels • Continuous with endocardium • Slick surface reduces friction – Subendothelial layer in vessels larger than 1 mm; connective tissue basement membrane Tunics • Tunica media – Smooth muscle and sheets of elastin – Sympathetic vasomotor nerve fibers control vasoconstriction and vasodilation of vessels • Influence blood flow and blood pressure Tunics • Tunica externa (tunica adventitia) – Collagen fibers protect and reinforce; anchor to surrounding structures – Contains nerve fibers, lymphatic vessels – Vasa vasorum of larger vessels nourishes external layer Blood Vessels • Vessels vary in length, diameter, wall thickness, tissue makeup • See figure 19.2 for interaction with lymphatic vessels Arterial System: Elastic Arteries • Large thick-walled arteries with elastin in all three tunics • Aorta and its major branches • Large lumen offers low resistance • Inactive in vasoconstriction • Act as pressure reservoirs—expand
    [Show full text]
  • Central Venous Pressure Venous Examination but Underestimates Ultrasound Accurately Reflects the Jugular
    Ultrasound Accurately Reflects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol, Nicole Collett, Andrew Ashby and Gregory A. Schmidt Chest 2011;139;95-100; Prepublished online August 26, 2010; DOI 10.1378/chest.10-1301 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/139/1/95.full.html Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright2011by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692 Downloaded from chestjournal.chestpubs.org at UCSF Library & CKM on January 21, 2011 © 2011 American College of Chest Physicians CHEST Original Research CRITICAL CARE Ultrasound Accurately Refl ects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol , MD ; Nicole Collett , MD ; Andrew Ashby , MD ; and Gregory A. Schmidt , MD , FCCP Background: Bedside ultrasound examination could be used to assess jugular venous pressure (JVP), and thus central venous pressure (CVP), more reliably than clinical examination. Methods: The study was a prospective, blinded evaluation comparing physical examination of external jugular venous pressure (JVPEXT), internal jugular venous pressure (JVPINT), and ultrasound collapse pressure (UCP) with CVP measured using an indwelling catheter. We com- pared the examination of the external and internal JVP with each other and with the UCP and CVP.
    [Show full text]
  • Central Venous Pressure: Uses and Limitations
    Central Venous Pressure: Uses and Limitations T. Smith, R. M. Grounds, and A. Rhodes Introduction A key component of the management of the critically ill patient is the optimization of cardiovascular function, including the provision of an adequate circulating volume and the titration of cardiac preload to improve cardiac output. In spite of the appearance of several newer monitoring technologies, central venous pressure (CVP) monitoring remains in common use [1] as an index of circulatory filling and of cardiac preload. In this chapter we will discuss the uses and limitations of this monitor in the critically ill patient. Defining Central Venous Pressure What is the Central Venous Pressure? Central venous pressure is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure. It is conventionally measured at the junction of the superior vena cava and the right atrium and provides an estimate of the right atrial pressure. The Central Venous Pressure Waveform The normal CVP exhibits a complex waveform as illustrated in Figure 1. The waveform is described in terms of its components, three ascending ‘waves’ and two descents. The a-wave corresponds to atrial contraction and the x descent to atrial relaxation. The c wave, which punctuates the x descent, is caused by the closure of the tricuspid valve at the start of ventricular systole and the bulging of its leaflets back into the atrium. The v wave is due to continued venous return in the presence of a closed tricuspid valve. The y descent occurs at the end of ventricular systole when the tricuspid valve opens and blood once again flows from the atrium into the ventricle.
    [Show full text]
  • 4B. the Heart (Cor) 1
    Henry Gray (1821–1865). Anatomy of the Human Body. 1918. 4b. The Heart (Cor) 1 The heart is a hollow muscular organ of a somewhat conical form; it lies between the lungs in the middle mediastinum and is enclosed in the pericardium (Fig. 490). It is placed obliquely in the chest behind the body of the sternum and adjoining parts of the rib cartilages, and projects farther into the left than into the right half of the thoracic cavity, so that about one-third of it is situated on the right and two-thirds on the left of the median plane. Size.—The heart, in the adult, measures about 12 cm. in length, 8 to 9 cm. in breadth at the 2 broadest part, and 6 cm. in thickness. Its weight, in the male, varies from 280 to 340 grams; in the female, from 230 to 280 grams. The heart continues to increase in weight and size up to an advanced period of life; this increase is more marked in men than in women. Component Parts.—As has already been stated (page 497), the heart is subdivided by 3 septa into right and left halves, and a constriction subdivides each half of the organ into two cavities, the upper cavity being called the atrium, the lower the ventricle. The heart therefore consists of four chambers, viz., right and left atria, and right and left ventricles. The division of the heart into four cavities is indicated on its surface by grooves. The atria 4 are separated from the ventricles by the coronary sulcus (auriculoventricular groove); this contains the trunks of the nutrient vessels of the heart, and is deficient in front, where it is crossed by the root of the pulmonary artery.
    [Show full text]
  • Bio 104 Cardiovascular System
    29 Bio 104 Cardiovascular System Lecture Outline: Cardiovascular System Hole’s HAP [Chapters 14, 15, 16] Blood: Introduction (Chapter 14) - - - - A. Characteristics of Blood 1. Blood Volume - - - 2. Blood Composition a. Blood Cells Red blood cells White blood cells Platelets b. Plasma 3. Origin of Blood Cells - - 30 Bio 104 Cardiovascular System B. Red Blood Cells 1. Characteristics - - - oxyhemoglobin - deoxyhemoglobin - 2. Red Blood Cell Counts 4.6 – 6.2 4.2. – 5.4 reflects blood’s ___________________________ 3. Red Blood Cell Production low blood oxygen ________________________ RBC production vitamin B12, folic acid, Fe are necessary Dietary Factors Affecting RBC Production 31 Bio 104 Cardiovascular System 4. Life Cycle of RBC lifespan worn out RBCs destroyed by Hb heme and globin 5. Anemia Def. = C. White Blood Cells 1. Functions & Types diapedesis positive chemotaxis granulocytes - - - agranulocytes - - 32 Bio 104 Cardiovascular System 2. White Blood Cell Counts 5, 000 - 10,000 leukopenia leukocytosis differential WBC count Granulocytes Agranulocytes Neutrophils (segs, PMNs, bands) Monocytes Eosinophils Lymphocytes Basophils D. Platelets - cell fragments -130,000 - 360,000 - helps control _______________ Plasma A. Characteristics 33 Bio 104 Cardiovascular System B. Plasma Proteins C. Gases and Nutrients Gases Nutrients - - - - - - D. Nonprotein Nitrogenous Substances Urea - Uric acid - Amino acids – Creatine – Creatinine – BUN – E. Plasma Electrolytes Absorbed from the _____________ or released as by-products
    [Show full text]
  • Basic Rhythm Recognition
    Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat.
    [Show full text]
  • Abnormally Enlarged Singular Thebesian Vein in Right Atrium
    Open Access Case Report DOI: 10.7759/cureus.16300 Abnormally Enlarged Singular Thebesian Vein in Right Atrium Dilip Kumar 1 , Amit Malviya 2 , Bishwajeet Saikia 3 , Bhupen Barman 4 , Anunay Gupta 5 1. Cardiology, Medica Institute of Cardiac Sciences, Kolkata, IND 2. Cardiology, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 3. Anatomy, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 4. Internal Medicine, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, IND 5. Cardiology, Vardhman Mahavir Medical College (VMMC) and Safdarjung Hospital, New Delhi, IND Corresponding author: Amit Malviya, [email protected] Abstract Thebesian veins in the heart are subendocardial venoluminal channels and are usually less than 0.5 mm in diameter. The system of TV either opens a venous (venoluminal) or an arterial (arterioluminal) channel directly into the lumen of the cardiac chambers or via some intervening spaces (venosinusoidal/ arteriosinusoidal) termed as sinusoids. Enlarged thebesian veins are reported in patients with congenital heart disease and usually, multiple veins are enlarged. Very few reports of such abnormal enlargement are there in the absence of congenital heart disease, but in all such cases, they are multiple and in association with coronary artery microfistule. We report a very rare case of a singular thebesian vein in the right atrium, which was abnormally enlarged. It is important to recognize because it can be confused with other cardiac structures like coronary sinus during diagnostic or therapeutic catheterization and can lead to cardiac injury and complications if it is attempted to cannulate it or pass the guidewires.
    [Show full text]