Ch17 Cardiovascular Emergencies.docx

Chapter Cardiovascular Emergencies Unit Summary Upon completion of this chapter and related course assignments students will be able to describe the anatomy and physiology of the cardiovascular system as well as discuss epidemiological and pathophysiological conditions that impact this system Students will be able to apply various patient presentations integrate assessment findings formulate a field impression and implement a comprehensive treatment plan for management of these conditions involving the cardiovascular system They will be able to recognize signs and symptoms of common cardiovascular conditions and disorders demonstrate relevant assessment techniques for cardiac function perform diagnostic testing of cardiac status and manage patients using techniques and skills for cardiovascular emergencies Students will be able to discuss pathophysiology risk factors and common medications that may be seen in the cardiovascular emergency patient They will be able to safely perform interventions and treatments for patients having a cardiovascular emergency National EMS Education Standard Competencies Medicine Integrates assessment findings with principles of epidemiology and pathophysiology to formulate a field impression and implement a comprehensive treatment disposition plan for a patient with a medical complaint Cardiovascular Anatomy signs symptoms and management of Chest pain pp - Cardiac arrest pp - Anatomy physiology epidemiology pathophysiology psychosocial impact presentations prognosis and management of Acute coronary syndrome p - Angina pectoris pp - - Myocardial infarction pp - Heart failure pp - Nontraumatic cardiac tamponade p Hypertensive emergencies pp - Cardiogenic shock pp - Vascular disorders pp - - Abdominal aortic aneurysm p - Arterial occlusion pp - - Venous thrombosis p Aortic aneurysm dissection pp - Thromboembolism p Cardiac rhythm disturbances pp Infectious diseases of the heart p - Endocarditis p - Pericarditis p Congenital abnormalities p Shock and Resuscitation Integrates comprehensive knowledge of causes and pathophysiology into the management of cardiac arrest and pre-arrest states Integrates a comprehensive knowledge of the causes and pathophysiology into the management of shock and respiratory failure or arrest with an emphasis on early intervention to prevent arrest Knowledge Objectives Describe risk factors related to cardiovascular disease p Understand the basic structure and function of the cardiovascular system pp - Identify the major normal and abnormal heart sounds pp - Describe the cardiac cycle including diastole and systole p Identify the various types of blood vessels p Explain how the heart functions as a pump including the concepts of cardiac output stroke volume heart rate and ejection fraction pp - Understand how electrical conduction activity occurs within the heart pp - Understand how the autonomic nervous system controls the functioning of the heart pp - Identify the various classes of drugs that influence the sympathetic nervous system pp - Understand how the sympathetic nervous system regulates blood pressure pp - Explain patient assessment procedures for cardiovascular problems including scene size-up primary assessment history taking secondary assessment and reassessment pp - Recognize the medications commonly prescribed to patients with cardiovascular diseases pp - Describe the placement of leads and electrodes in -lead ECG monitoring pp - Identify the components of an ECG rhythm strip pp - Understand how to determine heart rate pp - Describe the placement of -lead ECG leads pp Describe the placement of - and -lead ECG leads pp - Understand how to interpret -lead ECG findings including atrial junctional and ventricular rhythms pp - - Recognize normal sinus rhythm and list the various types of cardiac dysrhythmias pp - Discuss manual defibrillation cardioversion and transcutaneous pacing as techniques for managing cardiac emergencies pp - Understand the indications and procedure for operating an automated external defibrillator AED pp - Describe emergency medical care for the symptomatic patient with bradycardia pp - Describe emergency medical care for the symptomatic patient with tachycardia pp Describe emergency medical care for the patient with cardiac arrest including the elements of basic life support BLS and advanced cardiac life support ACLS pp - Describe the components of care following resuscitation including how to determine return of spontaneous circulation p Describe the pathophysiology of atherosclerosis peripheral vascular disorders acute coronary syndrome and angina pectoris pp - Discuss the assessment and management of coronary disease and angina pp - List the signs and symptoms of acute myocardial infarction AMI pp - Explain the procedure for managing AMI and suspected AMI in the field including STEMI and non-STEMI presentations pp - Understand the benefits of reperfusion techniques fibrinolysis and percutaneous intervention in patients with AMI or suspected AMI pp - Discuss the pathophysiology of congestive heart failure and its signs symptoms and treatment pp - Discuss the pathophysiology of cardiac tamponade and its signs symptoms and treatment p Discuss the pathophysiology of cardiogenic shock and its signs symptoms and treatment pp - Describe the pathophysiology assessment and management of aortic aneurysms including both acute dissecting aneurysm of the aorta and expanding and ruptured abdominal aortic aneurysms pp - Discuss the pathophysiology of hypertensive emergencies and their signs symptoms and treatment pp - Describe the risks posed by thromboembolism p Identify types of congenital heart disease p Describe the pathophysiology of hypertrophic cardiomyopathy p Describe the pathophysiology of other cardiovascular anomalies coarctation of the aorta truncus arteriosus tricuspid atresia hypoplastic left heart syndrome tetralogy of Fallot transposition of the great arteries and total anomalous pulmonary venous return see chapter Neonatal Emergencies Describe how infections endocarditis pericarditis and rheumatic fever can damage the heart pp - Skills Objectives Demonstrate how to assess and provide emergency medical care for a patient with chest pain or discomfort pp - - Demonstrate how to perform cardiac monitoring p Skill Drill Demonstrate how to acquire a -lead ECG pp - Skill Drill Demonstrate how to perform manual defibrillation pp - Skill Drill Demonstrate how to perform defibrillation with an AED pp - Skill Drill Demonstrate how to perform cardioversion pp - Skill Drill Demonstrate how to perform transcutaneous cardiac pacing pp - Skill Drill Demonstrate how to manage symptomatic bradycardia pp - Demonstrate how to perform ACLS care pp - Demonstrate how to perform postresuscitative care p Readings and Preparation Review all instructional materials including Chapter of Nancy Caroline s Emergency Care in the Streets Seventh Edition and all related presentation support materials Review all local protocols for paramedic treatment of patients with cardiovascular emergencies as well as any protocols for performance and authorization of interventions appropriate for the cardiovascular emergency patient such as defibrillation cardioversion obtaining an ECG and transcutaneous pacing Visit the American Heart Association AHA website for evidence-based research articles relating to cardiovascular topics http www americanheart org Consider reading these articles ahead of time and summarizing for students or using for further discussion of the issues surrounding critical thinking Regional variation in out-of-hospital cardiac arrest incidence and outcome by G Nichol E Thomas C Callaway et al http www ncbi nlm nih gov pmc articles PMC pdf nihms- pdf Survival increases with CPR by emergency medical services before defibrillation of out-of-hospital ventricular fibrillation or ventricular tachycardia Observations from the resuscitations outcome consortium by S Bradley E Gabriel T Aufderheide et al http www ncbi nlm nih gov pmc articles PMC pdf nihms pdf Support Materials Lecture PowerPoint presentation Case Study PowerPoint presentation Skill Drill PowerPoint presentations Skill Drill - Performing Cardiac Monitoring Skill Drill - Acquiring a -Lead ECG Skill Drill - Performing Manual Defibrillation Skill Drill - Performing Defibrillation with an AED Skill Drill - Performing Cardioversion Skill Drill - Performing Transcutaneous Pacing Equipment needed to perform the psychomotor skills presented in this chapter including as many types of monitors and AEDs as needed for demonstration purposes A CD or website providing audio samples of heart sounds Skill Evaluation Sheets Skill Drill - Performing Cardiac Monitoring Skill Drill - Acquiring a -Lead ECG Skill Drill - Performing Manual Defibrillation Skill Drill - Performing Defibrillation with an AED Skill Drill - Performing Cardioversion Skill Drill - Performing Transcutaneous Pacing Enhancements Direct students to visit the companion website to Nancy Caroline s Emergency Care in the Streets Seventh Edition at http www paramedic emszone com for online activities If available consult ECG Cases for EMS available at www jblearning com ISBN Consider contacting the local chapter of the AHA for literature and potential guest speakers on cardiovascular diseases prevention and support groups Encourage students to get involved in a community outreach program such as smoking cessation stress relief and nutritional education Arrange for students to visit a cardiovascular rehabilitation center in your area for patients recovering from myocardial infarctions and cardiac surgery Arrange for students to complete a clinical rotation in the local cardiac catheterization lab and or with a cardiovascular diagnostics technician to observe the importance of these interventions and tests Attend a cadaver lab or dissect an animal heart to allow students to identify cardiac structures follow the flow of blood through the cardiac chambers and visualize the anatomical landmarks of the heart Content connections In this chapter students should begin to see connections between the cardiovascular system and other primary systems in the body such as the respiratory and renal systems Co-morbid factors and the presence of other chronic diseases can affect the cardiovascular system as well as play a contributing role in outcomes of cardiovascular emergencies and the ability of the paramedic to effectively treat these emergencies An area of particular concern is how pharmacological agents used to treat one condition may mask signs and symptoms normally seen in these cardiovascular emergencies or may block or limit the effectiveness of pharmacological therapy used to treat the emergencies Special note should be made of variations in signs and symptoms of common cardiovascular emergencies based on age sex and in the presence of pre-existing conditions Remind students of the significant risk to the pediatric population for unintentional overdose of cardiovascular medications These types of emergencies will be reviewed in greater depth in the pediatric or toxicology section of the text Cultural considerations Cardiovascular risk factors and genetic predisposition for cardiovascular disease may be increased in some cultural segments of the population and students should be aware that this could result in patients presenting with cardiovascular emergencies who are younger than the perceived age range for these types of emergencies Cardiovascular disease is also present in multiple cultures and with the increase in immigrants and travelers to the United States may result in encounters with medications that are foreign and require translation to determine the patients current medications Teaching Tips Students practicing skills in this chapter need to be reminded of the importance of safety when working with cardiac defibrillators and AEDs Instructors should maintain appropriate student-to-instructor ratios to oversee operation during practical exercises Consider posting reminders relevant to specific devices to operate them safely such as use of hands-free pads Incorporate use of emergency medical dispatch pre-arrival instructions into practical scenarios Identify what instructions may be given to the cardiovascular emergency patient in the area students will be completing clinical rotations or practicing in Identify modifications that should be made in treatment protocols if any as a result of pre-arrival instructions Remind students that cardiovascular disease has no limits with regard to age of patients Discuss how symptoms may present atypically among these various populations and the need to be thorough with assessments despite preconceived ideas that the patient may have about whether it could affect them Practice communication techniques with students during practical exercises using role-playing to develop effective strategies for convincing patients who may be in denial about the potential for cardiac emergencies Review pertinent facts about the importance of time to treatment for saving cardiac muscle Emphasize the importance of maintaining cardiovascular health as part of maintaining overall physical and mental health Contact your local American Heart Association to obtain literature for student review and encourage them to practice good health habits to improve cardiovascular health Investigate continuing education activities in your area to determine if any local facilities offer lectures on outcomes from pre-hospital cardiovascular emergencies Plan to encourage students or arrange for students to attend one of these to relate the significance of pre-hospital identification of the STEMI patient and transportation to the appropriate facility in reducing door-to-balloon time as well as event-to-balloon times Unit Activities Writing activities Assign students a cardiovascular condition or emergency to research Have them create realistic scenarios including patient demographics pre-existing conditions that are common risk factors medications and signs or symptoms the paramedic may expect to encounter Use these scenarios to generate practical exercises during group activities to allow students to apply appropriate treatment algorithms and clinical decision making for developing the treatment plan An alternate activity would be to assign students a pharmacological agent commonly prescribed for the cardiovacular disease patient Ask that they investigate the medication identify current conditions for which it is prescribed common dosages encountered side effects and any considerations that are pertinent when treating the patient having a cardiovascular emergency Student presentations Assign students a cardiovascular disease or cardiovascular risk factor Have them research current AHA or medical recommendations for prevention and treatment for this condition or risk factor Encourage students to identify any community-based programs that promote wellness or prevention for this disease or risk factor Allow five to seven minutes for students to present their findings An alternate idea would be to have students present their findings from the Writing Activities on common medications taken by a patient with cardiovascular disease Ask that they emphasize any risks associated with overdosage of these medications for both the patient or for unintentional overdose in the pediatric population Group activities Using scenarios developed from the Writing Activities section divide students into groups to role-play and practice skills for each Identify groups large enough to incorporate the roles of a partner the patient family bystander first responder and emergency dispatcher as indicated Assign one student to record actions as the exercise is completed to allow the group to review and discuss the interventions and outcomes as presented Visual thinking Create stations in the classroom with anatomical posters of the body s major organ systems Have students make labels for the pharmacological agents used to treat cardiovascular systems Group pharmacological agents in categories based on mechanisms of action and primary systems affected to label each poster and include notations of how each system is impacted Encourage them to consider how multiple medications may inhibit or enhance overall effectiveness of the agent in the patient having a cardiovascular emergency to develop a global perspective of how these agents affect the physiological response of the body Medical terminology Cardiovascular terminology can be confusing and this is a good opportunity to review suffixes relevant to cardiovascular disease treatment and procedures Identify those with similar spellings that can influence the definition of the term Remind students of appropriate abbreviations for this system as well as those that may have been removed from approved lists Crossword puzzles or word games provide good refresher opportunities Consider creating a cardiovascular terminology Scrabble game for students to work together in teams to review Pre-Lecture You are the Medic You are the Medic is a progressive case study that encourages critical-thinking skills Instructor Directions Direct students to read the You are the Medic scenario found throughout Chapter You may wish to assign students to a partner or a group Direct them to review the discussion questions at the end of the scenario and prepare a response to each question Facilitate a class dialogue centered on the discussion questions and the Patient Care Report You may also use this as an individual activity and ask students to turn in their comments on a separate piece of paper Lecture I Introduction A In the United States heart disease has been the number one killer almost every year since The role of the paramedic was created more than years ago to provide early treatment for patients with acute myocardial infarction AMI Each year more than Americans die of heart disease a Approximately half in the ED or before reaching a hospital b During the first minutes and hours after symptoms begin B A paramedic must be able to integrate pathophysiologic principles and assessment findings to formulate a field impression and implement a treatment plan for patients with cardiovascular disease CVD II Epidemiology A In heart disease attributed to about of all US deaths Risk factor categories a Modifiable b Nonmodifiable More women die of heart disease than men B Prevention strategies include education and early recognition Educating patients may help decrease mortality III Anatomy and Physiology A Structure and function Cardiovascular system a Composed of heart and blood vessels b Primary function Deliver oxygenated blood and nutrients to cells in the body c Transports metabolism waste products from cells to recycling or waste disposal sites B The heart This pump sits in the chest above the diaphragm behind and slightly left of the retrosternal lower sternum a About the size of the person s fist and weighs about oz b Circulates L to L of blood throughout the body daily The apical thrust or point of maximal impulse PMI is located at the fifth intercostals space on the left anterior part of the chest in the midclavicular line a Occurs when heart s apex rotates forward with systole producing pulsation The heart wall has three layers a Epicardium A thin membrane forming the outmost heart layer b Myocardium Muscular middle layer of the heart wall composed of cardiac fibers that can spontaneously contract c Endocardium Thin membrane lining the inside of the hearts cavities forming the valves The pericardium is a tough fibrous sac surrounding the heart a Protects the heart and provides lubrication between the heart and surrounding structures b Parietal pericardium superficial layer Anchors the heart within the mediastinum and surrounding vessels c Visceral pericardium Fused to the epicardium d Potential space between the two layers e Abnormal accumulation of fluid within the pericardial sac can occur from infectious processes cancer and trauma i Pericardial effusion Small accumulation of fluid ii Pericardial tamponade Large accumulation of fluid causing a decrease in cardiac output and eventual cardiovascular collapse Coronary arteries branching off the aorta provide an uninterrupted supply of oxygenated blood to the heart a The left coronary artery LMCA supplies the more muscular left ventricle the interventricular septum and part of the right ventricle by dividing into the i Left anterior descending artery LAD ii Circumflex coronary artery LCx b The right coronary artery RCA travels between the right atrium and ventricle through the atrioventricular groove supplying the right atrium and ventricle and part of the left ventricle c Numerous connections between the arterioles of the different coronary arteries allow for collateral circulation alternative routes of blood flow when plaque deposits begin to narrow the vessel walls Arteries and main coronary veins cross the heart in the coronary sulcus a groove that separates the atria from the ventricles Venous blood empties into the coronary sinus The heart has four chambers a Upper chambers atria separated from lower chambers ventricles by atrioventricular AV valves i Tricuspid valve Separates right atrium from right ventricle ii Mitral valve bicuspid valve Separates left atrium from left ventricle iii Anatomic guide wires chordate tendineae are attached to papillary muscles a Anchor the valve leaflets so they do not prolapse during ventricular contraction iv Semilunar valves Two valves at the junction of the ventricles and the pulmonary and systemic circulation a Pulmonary semilunar valve pulmonic valve Separates right ventricle from the pulmonary artery to prevent backflow into the right ventricle b Aortic semilunar valve aortic valve Prevents blood that has already entered the aorta from flowing back into the left ventricle The cardiac cycle a Represents a complete depolarization and repolarization of the atria and ventricles i Diastole Period of time when the atria or ventricles are resting a Atrial diastole Atrial rest b Ventricular diastole Ventricular rest ii Systole Period of time when atria or ventricles contract a Atrial systole Atrial contraction b Ventricular systole Ventricular contraction b In the relaxation phase the left atrium fills with blood under the influence of venous pressure c In atrial contraction the blood in each atrium is squeezed into the respective ventricle to complete ventricular filling i Atrial kick The contribution to ventricular filling made by contraction the amount of blood kicked in by the atrium a As ventricular contraction begins The two ventricles contract ventricular systole The semilunar valves are forced open Blood from the right ventricle is squeezed forward through the pulmonic valve and into the pulmonary arteries Left ventricle blood is then pushed through the aortic valve and into the aorta Blood flow through the heart a The heart acts as two pumps that work parallel to each other and are separated by the interventricular septum i The right side is a low-pressure pump that pumps against the relatively low-resistance of the pulmonary circulation a Consists of right atrium and right ventricle b The superior vena cava collects deoxygenated blood from the upper part of the body c The inferior vena cava collects deoxygenated blood from the lower part of the body d Deoxygenated blood enters the right atrium and goes into the right ventricle e It is then pumped into the pulmonary artery where it goes to the lungs for oxygenation ii The left side is a high-pressure pump a Pulmonary veins collect oxygen-rich blood from the lungs and send it to the left atrium where it is pumped into the left ventricle b Preload The initial stretching of the cardiac myocytes prior to contraction on the left side of the heart c Afterload When the blood is driven out of the heart against the systemic arteries b The body has two circulations to match the two pumps i Systemic circulation All the blood vessels between the left ventricle and right atrium ii Pulmonary circulation All the blood vessels between the right ventricle and left atrium C The blood vessels Two principle types of blood vessels a Veins b Arteries The two share a common structure a Tunica adventitia A protective outer layer of fibrous tissue with the strength to withstand high pressure b Tunica media A middle layer of elastic fibers and muscles that adds strength and contractility i Thicker and more powerful in arteries than in veins c Tunica intima The innermost layer a one-cell-thick smooth inner lining d Lumen The opening in the blood vessel Arteries carry blood away from the heart a They carry oxygenated blood i The exception is the pulmonary arteries which carry oxygen-depleted blood b Size ranges from the aorta largest in the body to arteriole tiniest arterial branch c Highly sensitive to autonomic nervous system stimulation which helps regulate blood pressure pressure exerted by the blood against the arterial walls d Blood pressure is generated by repeated forceful left ventricle contractions i Influenced by output of the heart and blood volume ii Also influenced by relative constriction or dilation of arteries Veins have thinner walls than arteries and thus less capacity to decrease in diameter a More likely to distend under backpressure b They carry deoxygenated blood back to the heart i The exception is the pulmonary veins which carry oxygenated blood c Venules the smallest veins empty into larger and larger veins terminating into the inferior and superior venae cavae d Contain valves to keep blood flowing forward A network of capillaries separate arteries and veins a One cell thick blood cells pass through them single file D The pump at work The skeletal muscle and thorocoabdominal pumps aid the return of venous blood to the heart Some technical terms are necessary to understand heart function a Cardiac output CO The amount of blood pumped by either ventricle i Left and right ventricle have approximately the same outputs ii Normal CO for an average adult to L min b Stroke volume SV The amount of blood pumped by either ventricle in a single contraction i Normal SV is to mL ii Healthy heart can increase SV by at least c Heart rate HR The number of contractions per minute pulse rate i Normal for adults to beats min d Ejection fraction EF The percentage of blood that leaves the heart on each contraction i Measurement taken from left ventricle ii Normal range of to lower if heart is damaged The CO equation CO SV x HR a The volume of blood that either ventricle pumps out per minute equals the volume of blood it pumps out in a single contraction times the number of contractions per minute b Must be able to increase output to meet changing demands for example exercise c Heart can increase its output by i Increasing SV ii Increasing rate iii Both The heart can increase SV in several ways a When cardiac muscle is stretched it contracts with greater force to a limit the Frank-Starling mechanism i If an increased volume of blood returns to the heart muscles surrounding the cardiac chambers stretch to fit in the larger volume ii The more it stretches the greater the force of contraction and it empties more completely iii The greater the SV b With a constant HR any increase in SV will increase overall CO i If heart walls are stretched slightly a small amount of blood is released ii If walls are stretched more a larger amount of blood is released Preload is influenced by blood volume returned by the veins to the heart a More blood is returned to the heart preload increase when more oxygen is demanded i CO increases through the Frank-Starling mechanism ii The Frank-Starling mechanism is used to achieve a normal resting CO in a diseased heart sometimes causing the heart to enlarge The degree of contraction can vary without changing the stretch on the heart muscle contractility a Change may be induced by medications with a positive or negative inotropic effect b Although the ventricles do not completely empty with a single beat if the heart squeezes harder with contraction more ventricular blood will be ejected c When more CO is needed nervous signals increase myocardial contractility to augment SV Given a constant SV CO can be increased by increasing the number of contractions per minute positive chronotropic effect a Example A heart with a resting SV of mL beat and a resting rate of beats min i CO mL x beats min mL min ii During exercise the oxygen demand increases so nervous mechanisms stimulate an increase in heart rate For example beats min without any change in SV to increase the CO iii CO mL beat x beats min mL min b The Frank-Starling mechanism is not under nervous system control while contractility and heart rate changes are regulated by the nervous system E The electrical conduction system of the heart Cardiac cells that make up heart muscle demonstrate four properties that help the heart to function a Excitability Allows these cells to respond to an electrical impulse b Conductivity Enables cardiac cells the unique ability to pass electrical impulses from one cell to another c Automaticity Heart muscle can generate its own electrical impulses without stimulation from nerves d Contractility The heart s ability to contract The heart has specialized conduction tissue that rapidly propagates electrical impulses to the muscular tissue in the heart a Pacemaker The area of conduction tissue in which the electrical activity arises it sets the rate for cardiac contraction b This system is known as the electrical conduction system The dominant pacemaker is the sinoatrial node a The sinoatrial SA node is located in the right atrium near the inlet of the superior vena cava i Receives blood from the RCA a If RCA is occluded as in an MI the SA node will become ischemic and fire slower than normal or not at all ii Fastest pacemaker in the heart a Electrical impulses generated in the SA spread through intermodal pathways in the atrial wall in about seconds which causes depolarization The Bachmann bundle an interatrial pathway connects the right and left atria The anterior intermodal pathway is a branch off the Bachmann bundle that forms a pathway between the SA and AV nodes The middle intermodal tract is formed by the Wenckebach tract The Thorel tract is represented by the posterior intermodal pathway b Electrical impulses move from the SA node to the atrioventricular AV node in the AV junction region including the AVE node surrounding tissue and the bundle of His i The AV node is a gatekeeper to the ventricles ii The impulse conduction is delayed in the AV node for about seconds so the atria will empty into the ventricles iii Approximately to of blood in the atria fills the ventricles by gravity a The rest comes from atrial kick c There are conduction pathways that allow the current to bypass the AV node i James fibers in the internodal pathways bypass the AV node and extend into the ventricles ii Mahaim fibers contained in the bundle branches the bundle of His and the AV node extend into the ventricles to provide a pathway for re-entrant dysrhythmias iii The bundle of Kent typically located between the left atrium and left ventricle enables the depolarization wave to bypass the AV node and trigger early depolarization of ventricular tissue a At the same time depolarization travels through the AV node and bundle of His to the bundle branches These events create a delta wave on the ECG tracing Can trigger tachydysrhythmias d If the atrial rate becomes very rapid not all atrial impulses make it through the AV junction i Normally pass through into the bundle of His and then into the right and left bundle branches on both sides of the interventricular septum ii They then spread into the Purkinje fibers iii An electric impulse spreads across the ventricles in about seconds while the ventricles simultaneous contract iv The effect on conduction velocity is known as the dromotropic effect Depolarization and repolarization a Depolarization Process by which muscle fibers are stimulated to contract i Occurs through changes in the concentration of electrolytes across cell membranes ii Myocardial cells are bathed in an electrolyte solution iii Chemical pumps inside the cell maintain the concentrations of ions which creates an electric gradient across the cell wall iv A polarized cell normally has a net internal charge of - millivolts mV v When the myocardial cell receives a stimulus from conduction the permeability of the cell wall changes to allow sodium ions Na in a Makes the cell more positive vi Calcium ions Ca also enter which helps maintain the depolarized state of the cell membrane vii This depolarization spreads along the cell until it is completely depolarized causing a mechanical contraction b Repolarization begins with the closing of the sodium and calcium channels to stop the inflow of these ions i Potassium channels open to allow the escape of potassium ions K to help restore a negative charge to the inside of the cell ii Sodium ions are pumped out and potassium ions are pumped back into the cell reestablishing the proper electrolyte distribution a Active transport Ions are moved against the natural gradient c A myocardial cell must be fully polarized to respond normally to an electrical stimulus from the conduction system i The refractory period The period when the cell is depolarized or in the process of repolarizing a Absolute refractory period The heart muscle is completed depolarized and cannot respond to any stimulus b Relative refractory period The heart is partially repolarized allowing it to respond to electrical stimuli and be depolarized Secondary pacemakers a The SA node will outpace any slower conduction tissue because it has the most rapid intrinsic firing rate to times min i Any conduction system component can act as a secondary pacemaker if the SA node becomes damaged ii The farther removed from the SA node the slower the intrinsic rate of firing a The AV junction will spontaneously fire to times min b The Purkinje system spontaneously fires at a rate of to time min iii If the SA node is damaged the AV junction might begin firing at its own rate if the SA and AV nodes are not working the Purkinje fibers will initiate an impulse Measuring the heart s electrical conduction activity a The electrical conduction events recorded on an ECG show as a series of waves and complexes i The P wave is produced by the depolarization of the atria ii It is followed by a pause as conductions slow through the AV junction iii The QRS complex representing depolarization of the ventricles occurs next iv A wave occurring during the PR segment is caused by repolarization of the atria a Too small to be seen on the ECG v T waves produced by the ventricles follow the QRS complex b The intervals between waves and complexes are i PR interval Distance from the beginning of the P wave to the beginning of the QRS complex a Represents the amount of time the AV node delays transmission of atrial activity to the ventricles ii ST segment The line from the end of the QRS complex to the beginning of the T wave a J point junction point The beginning of the ST segment Indicates the end of ventricular depolarization and the beginning of ventricular repolarization b The ST segment is normally at the same level as the isoelectric line baseline c An elevated or depressed ST segment may indicate myocardial ischemia or injury iii R-R interval Represents the interval between two ventricular depolarizations a Can be used to calculate heart rate iv QT interval Represents one complete ventricular cycle a Measured from beginning of Q wave to end of T wave F The autonomic nervous system and the heart The autonomic nervous system controls involuntary actions such as the cardiovascular process a These functions are automatically accomplished without any conscious effort The voluntary nervous system and autonomic nervous system work together to allow body functions to proceed smoothly The autonomic nervous system has two conductors a Sympathetic nervous system speeds up the heart constricting blood vessels dilating the bronchi and pupils b Parasympathetic nervous system regulates the body's vegetative functions by slowing the heart rate and encouraging digestion The parasympathetic nervous system a Concerned with vegetative functions and sends messages through the vagus nerve i The vagus nerve can be stimulated in various ways including a Pressure on the carotid sinus b Straining against a closed glottis Valsalva maneuver c Distention of a hollow organ b If the brain senses that the heart should slow its pace i A message in an electrical impulse travels down the vagus nerve to where it abuts the SA node ii The electrical impulse causes the release of the naturally occurring chemical acetylcholine ACh iii ACh crosses over to the SA node and signals the node that the brain wants the heart to slow iv Another ACh molecule travels to the AV node of the heart as a reminder to the SA node v ACh is then broken down by acetycholinesterase AChE c Atropine blocks the actions of the parasympathetic nervous system i Used to increase heart rate The sympathetic nervous system a Prepares the body to respond to stresses fight-or-flight system by adapting to changing demands i Increases the heart rate ii Strengthens the force of cardiac muscle contractions iii Provides other adaptive responses to increase CO b In response to a need for more oxygen i The brain sends a message through the sympathetic nerves that pass through the thoracic and lumbar ganglia to arrive at the heart ii The commands are conveyed through release of norepinephrine which travels to the SA node AV node and ventricles iii The heart speeds up increasing CO to prevent a buildup of lactic acid c If intense stimulation occurs epinephrine adrenaline is used to command the heart to speed up Drugs that act on the sympathetic nervous system a Classified by the receptors with which they interact alpha and beta receptors b The heart has only one receptor for a beta agent i Any beta agent will have the same effect increase the heart's rate force and automaticity c The arteries have receptors for alpha and beta agents i Alpha drugs will turn on the switch that causes vasoconstriction ii Beta agents will activate the switch causing vasodilatation d The lungs have both alpha and beta receptors i Alpha agents do not have much effect on the lungs except for minor bronchoconstriction ii Beta adrenergic agonists trigger significant bronchodilation e Drugs with alpha or beta sympathetic properties sympathomimetic drugs imitate the actions of naturally occurring sympathetic chemicals f If a paramedic knows whether a drug is an alpha or beta agent he or she will be able to predict the responses of the cardiovascular system i Isoproterenol Isuprel a pure beta agent that stimulates the heart dilates the bronchi and dilates the arteries ii Phenylephrine Neo-Synephrine a pure alpha agent that causes slight bronchoconstriction and marked vasoconstriction iii Not always so simple most other sympathomimetic drugs have varying degrees of alpha and beta activity g Several sympathomimetic agents are commonly used in the field i Norepinephrine and epinephrine are also naturally occurring chemicals in the sympathetic nervous system h Beta sympathetic agents are classified into two groups based on differences between the beta receptors in the heart and lungs i Beta- adrenergic agonists work primarily on cardiac beta receptors ii Beta- adrenergic agonists work primarily on pulmonary beta receptors such as albuterol formoterol salbuterol levalbuterol and salmetorol i Sympatholytic or sympathetic blockers act on the sympathetic nervous system by beating sympathetic agents to receptor sites thus blocking the agents i Beta adrenergic blockers occupy beta receptors in the heart lungs arteries and elsewhere in the body j Understanding the actions of the major autonomic stimulating and blocking agents is key i Atropine Parasympathetic blocker opposing the vagus nerve used to speed the heart when excessive vagal firing has caused bradycardia ii Norepinephrine Levophed Sympathetic agent primarily alpha causing vasoconstriction to increase blood pressure iii Isoproterenol Isuprel Medhaler-iso Sympathetic agent almost pure beta causing a strong increase in heart rate and dilation of the bronchi to increase CO and dilate bronchi iv Epinephrine Adrenaline Sympathetic agent predominantly beta with actions similar to those of isoproterenol but having an additional peripheral vasoconstrictor effect v Dopamine Intropine Sympathetic agent used to increase renal perfusion increase rate and force of myocardial contraction and constrict peripheral blood vessels vi Albuterol Proventil Ventolin isoetharine Bronchosol Bronkometer terbutaline Brethine Bricanyl Brethaire Terbulin Sympathetic beta- agents that induce bronchodilation vii Propranolol Inderal Sympathetic beta blocker that opposes the actions of beta-stimulating agents used to slow the heart rate in certain tachydysrhythmias decrease chronic angina pain and to depress irritability in the heart a Contraindicated in cases of asthma G The sympathetic nervous system and blood pressure regulation The body attempts to maintain a constant blood pressure to ensure perfusion The blood pressure is influenced by the CO and resistance of the arterioles a Blood pressure CO x peripheral vascular resistance PVR b Blood pressure can be increased by increasing CO peripheral resistance or both Normally the body balances flow and resistance to maintain stable blood pressure a If one variable is altered they body will compensate by changing the other variable b CO blood pressure peripheral vascular resistance i For any given blood pressure the CO will inversely vary with peripheral vascular resistance ii The higher the peripheral resistance the lower the CO iii The greater the afterload the harder the ventricle must work to pump blood IV Patient Assessment A Cardiovascular problems cause a variety of symptoms The most common complaints are a Chest pain b Dyspnea c Fainting d Palpitations e Fatigue Basic life support BLS measures may be used if a patient has no pulse or breath Advanced life support procedures may be necessary The order of assessment steps may vary according to type of cardiac patient a The normal ABC assessment may be inappropriate if the patient appears to be in cardiac arrest i CAB may be a better choice B Scene size-up Ensure scene safety Anticipate the need for other resources such as extra personnel Look for clues to identify the potential problem medications drug paraphernalia etc C Primary assessment Form a general impression a Observe the patient's general appearance and assess for apparent life threats b Determine the patient's level of consciousness based on his responses to your greeting i Use the AVPU scale by asking Do you know where you are and the day of the week Airway and breathing a Determine the patient's airway patency b Check for open airway and note the rate quality and effort of breathing c Consider initiating oxygen therapy if breathing is in question i Respiratory distress in a cardiac patient suggests congestive heart failure Circulation a Check the patient's pulse i If patient is conscious check the radial pulse ii If unconscious check the carotid pulse b Note the rate regularity and overall quality c Assess the skin color and condition i Pink mucous membranes and warm and dry skin are indicators of good circulation Transport decisions a Determine whether immediate transport is required from your assessment findings i If unsure continue with the history taking and secondary assessment until the determination is more apparent D History taking Inquire into the medical history based on the chief complaint Include the SAMPLE history in this assessment Symptoms a Chest pain is often the presenting symptom of an AMI i The description of pain is important in determining the problem ii The OPQRST format will elaborate on the patient's complaint a What is the Onset or origin of the pain b What Provoked the pain And what makes the pain go away Palliation c What is the Quality of the pain d Does the pain Radiate e What is the Severity of the pain f What was the Timing of the attack b Dyspnea is another chief complaint in ACS i May be the first indicator of heart failure on the left side ii To determine the possibility of left-sided heart failure ask a When did the dyspnea start Did it awaken the patient from sleep Paroxysmal nocturnal dyspnea PND An acute episode of shortness of breath in which the patient suddenly awakens with a feeling of suffocation classic sign of left-sided heart failure b Did the symptoms come on suddenly or gradually c Is it continuous or intermittent d During activity or while at rest e Does any position make it better or worse Example Dyspnea of pulmonary edema worsens when the patient is lying down orthopnea as blood pools in the lungs f Ever had dyspnea before g Is there a cough and is it dry or productive h Are there any associated symptoms c Fainting syncope occurs when CO suddenly declines causing cerebral perfusion reduction i Cardiac causes include a Dysrhythmias b Increased vagal tone c Heart lesions ii It is important to determine if a patient fainted from cardiac or noncardiac causes a Under what circumstances did the fainting occur b Were there any warning feelings before the episode c What position was the patient in when he or she fainted d Has the patient fainted before e Where there any associated symptoms d Palpitations are a sensation of abnormally fast or irregular heartbeat and are often a symptom in patients with cardiac problems i They are often caused by cardiac dysrhythmia ii Inquire about the onset frequency and duration as well as previous episodes e Patients may also report other related symptoms i Feeling of impending doom ii Feeling nausea or having vomited f Listen for any indication of trauma g Inquire about pertinent aspects of the patient's other medical history i Under treatment for other serious illnesses or conditions a Coronary artery disease b Atherosclerotic heart disease c Valvular disease d Aneurysm e Pulmonary disease f Diabetes g Renal disease h Vascular disease i Inflammatory cardiac disease j Previous cardiac surgery k Congenital anomalies ii Is the patient taking any regular medication a When was it last taken b Is it prescribed to them iii Does the patient have known allergies to foods or medications iv When was the last time the patient ate or drank anything v Get any further information about the history of the current event Medications commonly prescribed to patients with cardiovascular diseases a Patients may be taking a wide variety of medications for a number of reasons i It is not always possible to identify the specific problem based on medications taken ii Example Beta blockers may be taken for angina to lower blood pressure or to prevent recurrence of AMI b Digitalis preparations are prescribed for chronic CHF or certain rapid atrial dysrhythmias i Increases strength of cardiac contractions which improves CO and slowing conduction through the AV junction ii Toxic effects including nausea vomiting headache or various cardiac dysrhythmias develop in at least of people taking the drug a It is important to determine if the patient is taking this drug when cardiac rhythm disturbances are present iii Those taking digitalis will be sensitive to calcium preparations and a decline in the serum potassium level so use caution when giving agents such as diuretics that will reduce the body's potassium stores c Antianginal agents i Three major classes of drugs are available to relieve angina pain and they work by diminishing myocardial oxygen demand a Nitrates for example nitroglycerine come as fast-acting sublingual tablets sustained-release oral tablets topically applied ointment and skin patches Work by decreasing the work of the heart and therefore decreasing the need for oxygen Take to minutes to work Cause significant vasodilatation and are sometimes used in the field as an adjunctive therapy for pulmonary edema secondary to left-sided heart failure If a patient takes nitroglycerin for chest pain find out how many the patient took and if the nitroglycerine relieved the pain Distinctive side effects include a throbbing headache a burning sensation under the tongue and a bitter taste If the side effects do not occur the medication may be outdated or ineffective b Beta blockers block beta sympathetic receptors and work by decreasing the rate and strength of cardiac contractions to decrease the heart's demand for oxygen Can lead to resistance of the action of beta-stimulating agents so administration of such drugs during resuscitation attempts may not work c Calcium channel blockers block the influx of calcium ions into cardiac muscle and relieve angina by preventing coronary artery spasm and by weakening cardiac contractions Hypotension may be a serious side effect d Antidysrhythmic agents are used to control chronic cardiac rhythm disturbances i A patient taking these drugs has had significant dysrhythmias before so monitor carefully ii Some drugs used for other categories are also used for dysrhythmias a Example Digitalis may be used to suppress atrial dysrhythmias b Example Beta blockers are sometimes used to suppress myocardial excitability e Diuretics are used by patients with chronic fluid overload as in chronic CHF and in patients with hypertension i Diuretics trick the kidneys into excreting more sodium and water than usual ii The kidneys also excrete more potassium than normal so the patient may become potassium depleted iii Patients depleted in potassium are prone to cardiac dysrhythmias especially if taking digitalis f Antihypertensive agents are used to treat hypertension i Diuretic agents and beta blockers are often used as antihypertensive agents ii Difficult to regulate the dosage so the patient's blood pressure is lowered but not too much a May cause symptoms of hypotension including weakness dizziness or giddiness with a change in position a phenomenon called orthostatic hypotension b If a patient is taking antihypertensive drugs check blood pressure in both the recumbent and sitting position to find orthostatic hypotension g Anticoagulant and antiplatelet agents i Anticoagulant drugs blood thinners slow the blood's ability to clot and are given to patients with recurrent blood clots or who are prone to develop clots a Patients taking these drugs are likely to bleed excessively from minor trauma or venipuncture b Warfarin Coumadin Panwarfin is a commonly used oral anticoagulant that requires a weekly check on a patient's clotting ability c Dabigatran Pradaxa is a newer drug that does not require testing d The IV anticoagulant heparin is often used in patients undergoing home dialysis ii Clopidogrel Plavix is an antiplatelet drug used in managing myocardial infarctions a Keeps platelets from sticking together h Additional medications may be prescribed for patients with cardiac problems E Secondary assessment The physical exam for a patient with cardiac complaints should emphasize that condition The patient s LOC is an indicator of the adequacy of cerebral perfusion a If alert and oriented the brain is getting enough oxygen b Stupor or confusion indicates poor CO possibly from myocardial damage or dysfunction Skin color and temperature may indicate circulation problems a Example Cold sweaty skin may indicate massive peripheral vasoconstriction Physical exam a Begin with inspection auscultation and palpation of the patient s respirations b Inspect the neck and tracheal position i Trachea should be midline and mobile to manipulation ii Using your finger press down in the suprasternal notch to verify position c Inspect adjacent structures such as neck veins i The external jugular veins are normally collapsed if sitting or standing but if the heart s right side is compromised the veins will distend from blood back-up ii To estimate jugular venous pressure a Place the patient in a semi-Fowler position with the head slightly rotated away from the vein b Observe the height of the distended fluid column in the vein c Note how up the distention extends above the sterna angle d Inspect and palpate the chest i Look for surgical scars indicating previous cardiac surgery ii Check for a nitroglycerin patch on the skin iii There may be a bulge just below the right or left clavicle indicating a pacemaker or automated implanted cardioverter defibrillator ACID iv Check for chest enlargement or a barrel-chest as in COPD v Observe for any sign of crepitus e Listen to the chest with the stethoscope i Crackles or wheezes may indicate left-sided heart failure with pulmonary edema f Examine extremities for pedal edema and the back for sacral edema both signs of right-sided heart failure g Heart sounds i Listen to the heart sounds to identify the lub-dub indicating the cardiac valves are operating properly ii The major heart sounds are S and S normal sounds and S and S abnormal sounds iii S occurs near the beginning of the ventricular contraction when the tricuspid and mitral valves close a These valves should close simultaneously as the pressure increases b The sound should correspond to the pulse at the carotid artery c The sound of the tricuspid valve closing may be louder in cases of hypertension d S may be louder in patients with anemia a fever or hyperthyroidism as well as patients with stenosis of their mitral valve e Decreased S sounds can indicate Mitral valve subject to fibrosis or is calcified Obesity Emphysema Cardiac tamponade f A split sound from any delay in the closing of both valves is considered abnormal iv S occurs near the end of ventricular contraction when the pulmonary and aortic valves close a These valves close because of backward flow into the pulmonary artery and aorta when the ventricles relax b They normally close simultaneously or with a slight delay between them c The sound will be louder in patients with chronic high blood pressure or pulmonary hypertension d The sound will be decreased in patients with hypotension e The sound may be split in the case of a right bundle branch resulting in a delay in the pulmonic valve closing f The aortic valve may close more slowly than the pulmonic valve in situations involving left bundle branch blocks v S is an extra abnormal heart sound in adults caused by ventricular wall vibrations resulting from a rapid filling period of the ventricle during the beginning of diastole a It occurs to ms after S and is generally heard in children and young adults b When heard in older adults it may indicate heart failure vi S is a rare heart sound heard just before S and is caused by turbulent filling of a stiff ventricle in hypertrophy or possible myocardial infarction vii Other abnormal heart sounds include a Opening snap indicative of a noncompliant valve b Ejection click a high-pitched sound just after the S sound that may indicate a dilated pulmonary artery or septal defect c Pericardial friction rub a to-and-fro sound heart in both systole and diastole heard in pericarditis from the visceral and parietal surfaces rubbing together d Murmur an ambiguous sound from turbulent blood flow through the valves caused by Increased blood flow across a normal valve Flow across an irregular or constricted valve Blood flow into an enlarged heart chamber Backwards blood flow through a compromised valve e Thrill Frequently occurring and constant vibration f Pericardial knock High-pitched sound during diastole indicating a thickened pericardium limiting ventricle expansion during the diastole phase h Vital signs i Pulse a Carefully assess the patient s pulse Regular or irregular Slow or abnormally fast Strong or weak b Irregular pulse disturbance in cardiac rhythm c Very rapid pulse anxiety secondary to severe pain or cardiac dysrhythmia d Weak thread pulse reduction in CO e Pulse deficit occurs when the palpated radial pulse rate is less than the apical pulse rate Check the peripheral radial pulse while listening to an apical pulse f Pulsus paradoxus an excessive drop mm Hg in systolic pressure with each inspired breath Sometimes it can be palpated as a decrease in the amplitude of the pulse waveform making the affected pulse beats weaker than the others g Pulsus alternans alternates between strong and weak beats and is indicative of left ventricular systolic damage ii Blood pressure a Systolic blood pressure of more than mm Hg is a more important risk factor for CVD than diastolic pressure in patients over years old b A systolic blood pressure of to mg Hg or a diastolic blood pressure of to mm Hg indicates prehypertension c In emergencies Elevated blood pressure may be from anxiety or pain Systolic blood pressure lower than mm Hg may be hypotension or shock Increased pulse pressure may indicate arteriosclerosis Reduced SV may be a sign of cardiogenic shock or cardiac tamponade d If possible obtain and compare blood pressure in both arms iii Monitoring devices a The ECG monitor-defibrillator enables paramedics to monitor and record -lead ECG tracings and record -lead ECGs to transmit to the receiving facility ECGs enable paramedics to quickly identify suspected AMI transmit the findings and make sound transport decisions The device also gives prehospital providers the ability to defibrillate cardiovert and perform transcutaneous pacing b Attach the cardiac monitor waveform capnography or pulse oximeter when obtaining vital signs if not previously done Use as an assessment tool do not rely only on the monitors If the patient is relatively stable a physical exam can be done while monitoring devices are in use F Reassessment Reassessment should be done on the way to the hospital a Repeat the primary assessment LOC and ABCs b Obtain vital signs every minutes for critical patients and every minutes for stable patients c Repeat the physical exam for changes and for any missed conditions d Assess the effectiveness of the interventions e Create proper documentation f For a patient with STEMI transmit the -lead ECG to the catheterization lab V Electrophysiology A It is imperative to assess the nature of the specific cardiovascular problem Cardiac rhythm disturbances or dysrhythmias may be from various causes not just AMI a Cardiac dysrhythmias are a disturbance in the normal cardiac rhythm and may or may not be significant b A paramedic needs to evaluate dysrhythmia in context with the overall condition which should determine if treatment is necessary A paramedic must be able to anticipate recognize and treat life-threatening dysrhythmias in a patient with an AMI a Dysrhythmias develop after an AMI because i Irritability of the ischemic heart muscle may cause the damaged muscle to generate abnormal electrical currents causing abnormal cardiac contractions a If the dysrhythmia arises from these irritable spots ectopic foci it is usually a tachydysrhythmia Ventricular tachycardia Premature atrial contractions PACs PVCs ii The infarct damages the conduction tissues a This rhythm abnormality will likely be a block or bradydysrhythmia b ECG analysis should be done on any patient with a cardiac condition i A patient with chest pain ii A patient with a history of heart problems iii Often appropriate for elderly patients B Cardiac monitoring and ECG use The ECG monitor can be used to a Continuously monitor cardiac rhythm during transport b Print out a rhythm strip for dysrhythmia interpretation c Print out a -lead ECG for specific diagnosis Three standard limb leads Leads I II and II are used for continuous monitoring a Used during transport to identify changes in heart rhythm b Tracings from lead II are usually most useful when monitoring A paramedic can acquire and document a -lead ECG from the device which provides detailed information about the heart s conduction system by recording activity from separate angles Cardiac monitor leads wires are connected to electrodes placed on the patient a Each lead creates an electrical snapshot of a part of the heart b The monitor records an ECG tracing for each lead which is then reviewed for findings Devices that record -lead ECGs contain interpretation software but there are limitations a It is best for paramedics to rely on their own interpretation using the -lead readout as only one part of the assessment b Some devices can transmit ECGs to the receiving hospital so emergency personnel can ready themselves for the patient s specific condition Electrode placement a The electrodes must be placed in the proper predetermined place to get a reliable reading b Electrodes in the prehospital setting are usually adhesive with a gel center for better skin contact although some have a diaphoretic electrode to better stick to a patient that is sweating c Certain basic principles should be followed for best skin contact and to minimize artifacts in the signal i It may be necessary to shave body hair at the electrode site shaving may also be necessary when using hands-free adhesive defibrillation pads ii Rub the electrode site briskly with an alcohol swab before application Wait for it to dry or dry with a gauze pad iii Attach the electrodes to the ECG cable before placement and confirm the appropriate electrode attached to the cable is placed at the correct location on the patient iv Once the electrodes are in place turn on the monitor and print a sample rhythm strip to check for artifact d Artifact on the monitor can give false readings i A straight-line ECG on an alert communicative patient indicates a loose or disconnected lead ii A wavy baseline resembling ventricular fibrillation may be caused by movement or muscle tremor check the patient before using the defibrillator e Refer to Skill Drill - to properly perform cardiac monitoring The leads a The two main groups of leads include i Limb leads ii Precordial leads b Limb leads leads I II III and aVR aVL aVF i For continuous cardiac monitoring place the four electrodes on the torso a White right upper chest near the shoulder b Black left upper chest near the shoulder c Red left lower abdomen d Green right lower abdomen ii For -lead ECG the four electrodes are placed on the limbs a White right wrist b Black left wrist c Red left ankle d Green right ankle c Placing these electrodes enables the ECG device to record all six limb leads using Einthoven s theory every time the heart contracts it emits a tiny amount of electrical energy that travels on the skin i These waves of energy can be recorded by the electrodes and plotted ii Einthoven originally recorded three leads a Lead I between the right and left arms b Lead II between the right arm and left leg c Lead III between the left arm and left leg d The augmented violated aV leads are also created using the four limb electrodes i Leads aVR aVL and aVF are created by combining two of the limb leads and using the other lead as the other pole a Example The lead aVR is created between the right arm and the combination of the left arm and leg electrodes with the green lead serving as a ground e The precordial leads consist of six additional electrodes on the anterior chest i It is critical that these leads are placed correctly a V right of sternum th intercostals space ICS b V left of sternum th ICS c V midclavicular th ICS d V precisely between V and V e V midaxillary th ICS f V precisely between V and V f Right-sided ECGs i In cases where a right-sided ECG is needed to evaluate the electrical activity of the right ventricle the precordial leads are placed on the right anterior thorax a V R left of sternum th ICS b V R right of sternum th ICS c V R right midclavicular th ICS d V R precisely between V and V e V R right midaxillary th ICS f V R precisely between V and V ii Lead V R is the most sensitive and specific for right ventricular AMI g Posterior ECGs i This is used to evaluate left ventricle posterior wall electrical activity ii Three precordial leads are placed on the left posterior thorax a V between V and V th ICS b V midscapular th ICS c V just to the left of the spine th ICS iii This is rarely used in practice h - and -lead ECG i The -lead ECG is the standard -lead ECG plus leads V R V and V a Allows the paramedic to view the right ventricle and posterior wall of the left ventricle b Involves recording a second tracing containing the additional leads ii The -lead ECG is the standard tracing plus leads V R through V R and V through V and is generally not used in the field i Unipolar versus bipolar leads i Leads I II and III are bipolar leads that contain a positive and negative pole ii Leads aVR aVL and AVF are augmented unipolar leads containing one true pole while the other end is referenced against a combination of other leads a Example Lead aVR the white electrode at the right arm referenced against the combination of the left arm and left leg b The precordial leads V to V are unipolar leads and are referenced against a calculated point Wilson s central terminal created by bisecting the limb leads in Eithoven s triangle j Lead polarity i Bipolar leads have a positive and negative end a Lead I is formed between the right and left arm electrodes with the left arm electrode being the positive terminal b Lead II is formed between the right arm and left leg with the left leg being the positive terminal c Lead III is formed between the left arm and left leg with the left leg being the positive terminal ECG concepts a If an electrical wave moves toward a positive electrode it results in a deflection above baseline b If it moves toward a negative electrode it results in a defection below baseline c The baseline isoelectric line TP segment or isomeric line represents the electrically silent period in the cardiac cycle d A wave traveling perpendicular to a lead results in i A perfectly flat line ii A line with a positive and a negative component biphasic waves The ECG paper a ECGs are recorded on graph paper moving past a stylus at a standardized speed mm s i One -mm box equals second of a second or milliseconds while one large box consisting of five small boxes equals second milliseconds ii The vertical axis represents the amplitude gain of deflection in millivolts iii The standard amplitude calibration is millimeters per millivolt iv A calibration box printed at the beginning of all ECGs informs the paramedic about paper speed and amplitude and measures -mm wide and -mm tall Components of the ECG rhythm a The ECG rhythm components correspond to electrical events in the heart i P wave represents atrial depolarization a Characterized by a smooth round upright shape b Normal duration of less than ms c Amplitude less than mm tall ii PR interval PRI includes atrial depolarization and conduction of the impulse through the AV junction a Represents the time it takes for the atria to depolarize and for the impulse to travel through the AV node b Measured from the start of the P wave to the point at which the QRS complex begins with a normal duration of to s iii QRS complex consists of three waveforms and represents depolarization of two simultaneous contracting ventricles a Measured from the beginning of the Q wave to the end of the S wave should follow each P wave consistently b Narrow in healthy people with sharply pointed waves and a duration of less than ms c Indicates that conduction of the impulse has proceeded normally from the AV junction through the bundle of His left and right bundles and the Purkinje system d The first negative deflection is the Q wave which represents conduction through the ventricular septum Should not last more than ms Should be less than one third the height of the QRS complex f The first upward deflection is the R wave with most of both ventricles being depolarized g The S wave is any downward defection after the R wave iv J point the point on the ECG where the QRS complex ends and the ST segment begins a Represents the end of depolarization and the apparent beginning of repolarization b Often depresses or elevates with an ischemic myocardium v ST segment begins at the J point and ends at the T wave and represents early ventricular repolarization vi T wave represents ventricular repolarization should be asymmetric less than half the overall height of the QRS complex and oriented in the same direction as the overall QRS complex a Consists of two halves The first half represents the absolute refractory period ARP a period of time in which the ventricles have not sufficiently repolarized to enable another depolarization The second half represents the relative refractory period RRP which indicates that some cells have repolarized sufficiently to depolarize again vii QT interval represents all the electrical activity of one completed ventricular cycle a Begins with the onset of the Q wave and ends with the T wave b Normally lasts to ms C Approach to dysrhythmia interpretation A paramedic will need to interpret ECG strips and be alert for dysrhythmia using this method a Identify the waves P-QRS-T b Measure the PRI c Measure the QRS duration d Determine rhythm regularity e Measure the heart rate When identifying any P waves note whether they are upright and within normal parameters Rhythm regularity a Determining rhythm regularity can be done by simply measuring the distance between R waves i Regular if the distance between R waves is exactly the same ii Irregularly irregular if no two R waves are equal iii Regularly irregular if the R waves are irregular but appear to follow a pattern Determining heart rate a The -second method the fastest method for measuring heart rate from the ECG i Should be used for rhythms with rates between and beats min ii Can be used on regular and irregular rhythms iii Count the number of QRS complexes in a -second strip then multiply by to obtain the rate per minute b The sequence method reserved for regular rhythms i Memorize the following ii Find an R wave on a heavy line and count off the above sequence for each large box you land on until you reach the next R wave iii If the R-R interval spans fewer than three large boxes the rate is greater than tachycardia If more than five large boxes the rate is less than bradycardia c The method the most accurate typically used for heart rates in excess of beats min and can only be used on regular rhythms i Count the number of small boxes between any two QRS complexes the R-R interval then divide by D Specific cardiac dysrhythmias Cardiac dysrhythmias can be induced by many events a The flow of electricity through damaged or oxygen-deprived tissue is different than healthy tissue which may appear on ECGs as irregularities b Many can be traced to ischemia especially the cardiac conduction system i Ischemia may cause an area of the heart to spontaneously depolarize causing a premature complex that may interfere with normal impulse conduction and cause dysrhythmias c Many dysrhythmias cause no serious effects so it is difficult to estimate the number of people affected d Dysrhythmias are the most common cause of cardiac arrest Dysrhythmias are classified in numerous ways a Disturbances of automaticity or disturbances of conduction b Tachydysrhythmias or bradydysrhythmias c Life threatening or non-life threatening d By the site from which they arise Rhythms originating in the SA node a Normal sinus rhythm intrinsic rate of to beats min with regular rhythm and minimal variations between R-R intervals i Upright P wave that precedes each QRS complex a PR interval to ms b QRS complex to ms b Sinus bradycardia pacemaker is still in the SA node but has a rate of less than beats min i Upright P wave preceding every QRS complex a PR interval to ms b QRS complex to ms ii Very slow heart rates lead to inadequate CO and precede heart electrical instability iii Ectopic pacemakers in the AV node or ventricles may fire and produce escape beats when the sinus rate becomes very slow iv Sinus bradycardia may be asymptomatic in healthy adults and conditioned athletes and may occur during sleep v Serious causes include a SA node disease b AMI which may stimulate vagal tone c Increased intracranial pressure d Use of beta blockers calcium channel blockers morphine quinidine or digitalis vi Treatment focuses on the patient s tolerance and looking for the cause a Atropine may be necessary b If atropine does not work the patient may need a transcutaneous pacemaker c Sinus tachycardia the SA node is still the pacemaker but the rate is more than beats min with regular rhythm i Upright P waves precede every QRS complex a PR interval to ms b QRS complex to ms ii May result for various causes including a Pain b Fever c Hypoxia d Hypovolemia e Exercise f Stimulation of the sympathetic nervous system g AMI h Pump failure i Anemia j Certain drugs caffeine nicotine and alcohol iii Hypoxia metabolic alkalosis hypokalemia and hypocalcemia can lead to electrical instability with cells not normally firing impulses doing so can occur with drugs such as atropine or digitalis a Results in potential for tachycardias flutters and fibrillations in atria or ventricles causing serious rhythms iv Circus reentry may occur v The AV node may have more than one impulse which may cause multiple ectopic beats or ventricular fibrillation vi Prolonged tachycardia increases the work of the heart causing further ischemia and infarction a CO may be significantly reduced if the heart rate exceeds to beats min vii Treatment is related to underlying cause d Sinus dysrhythmia a slight variation in cycling of a sinus rhythm usually exceeding ms between the longest and shortest cycles i The SA node is still the pacemaker with upright P waves preceding every QRS complex a PR interval to ms b QRS complex to ms ii Often more prominent with respiratory cycle fluctuation because the heart rate accelerates during inspiration and slows during expiration iii Increased filling pressures during inspiration stimulate the Bainbridge reflex increasing SV and blood pressure a The increase in blood pressure stimulates the baroreceptor reflex which attempts to block the rate increase iv Often found in children and young adults and may diminish or disappear with age e Sinus arrest the SA node fails to initiate an impulse which eliminates the P wave QRS complex and or T wave for one cardiac cycle then resumes normal functioning i The atrial and ventricular rates are usually within normal limits with regular rhythm except for the missing complexes ii Upright P waves precede every QRS complex a PR interval when present to ms b QRS complex when present to ms iii Common causes include a Ischemia of the SA node b Increased vagal tone c Carotid sinus massage d Use of drugs such as digitalis and quinidine iv Occasional episodes are not significant unless the heart rate drops below to beats min a CO may fall and an ectopic focus from the ventricles takes over v Treatment may include a temporary pacemaker in the field or a permanent pacemaker placed in the hospital f Sick sinus syndrome SSS a variety of rhythms involving a poorly functioning SA node common in elderly patients i It shows on an ECG as a Sinus bradycardia b Sinus arrest c SA block d Alternating patterns of extreme bradycardia and tachycardia ii Patients may exhibit syncope dizziness and palpitations or may have no symptoms Rhythms originating in the atria a Any area in the atria may originate an impulse b Rhythms originating from the atria will have upright P waves preceding each QRS complex but they are not as well-rounded as those from the SA node c Atrial rhythms usually have heart rates of to beats min d Atrial flutter a rhythm in which the atria contract too fast for the ventricles to match i Atrial complexes are known as flutter or F waves rather than P waves with a distinctive shape resembling a sawtooth or picket fence ii One or more of the F waves gets blocked by the AV node resulting in several F waves before each QRS complex iii The rhythm may be regular with a constant usually conduction or irregular with the QRS complex measuring to ms iv It is usually a sign of a serious heart problem a Often it is a transient rhythm that degenerates into atrial fibrillation v Treatment is usually medication or electrical cardioversion although neither is usually done in the field unless the condition is critical and transport time will be long e Atrial fibrillation a rhythm in which the atria does not contract but fibrillate or quiver without any organized contraction i Many different atria cells depolarized independently rather than in response from the SA node impulse resulting in random depolarization ii There are usually no visible P waves on the ECG strip and no PR interval iii A key identifier is its irregularly irregular appearance iv Impulses are randomly passed on to the ventricles resulting in a highly irregular ventricular rhythm with the QRS complex measuring to ms v Usually a sign of a serious heart problem and is common among elderly patients vi This rhythm has a tendency to cause the formation of small clots which may become emboli and block circulation or cause a stroke a Many elderly patients with this rhythm take an anticoagulant medication and other medications to regulate the ventricular response rate b Direct thrombin inhibitors may be used to prevent blood clots vii Prehospital treatment is rare because of the risks but electrical cardioversion may be necessary if the condition is critical and there will be a long transport time f Supraventricular tachycardia SVT a tachycardic rhythm originating from a pacemaker above the ventricles i Regular rhythm with a rate exceeding beats min ii QRS complexes to ms iii Patients may have cannon A waves created when dissociation between the atria and ventricles exist or if there is a right atrial contraction against a closed tricuspid valve a Larger A waves indicate a decrease in the functionality of the right ventricle or an increase in the right ventricular end diastolic pressure b Depression of the jugular veins forming an A occurs iv Often called a paroxysmal SVT PSVT because of a tendency to begin and end abruptly more up-to-date terminology is reentry SVT v The ventricular filling time is greatly lowered when the ventricular rate exceeds beats min which greatly reduces CO a This should be treated promptly with medication or electrical therapy to slow the heart rate g Premature atrial complex PAC also known as ectopic complexes not technically a dysrhythmia but an existence of a particular complex within another rhythm i Occurs earlier than the next expected sinus complex which causes an abnormally short R-R interval between it and the previous complex causing an irregular rhythm ii Upright P wave precedes each QRS complex but its shape differs from P waves originating from the SA node a PR interval to ms may vary slightly b QRS complex to ms iii PACs are not always conducted to the ventricles a Non-conducted PAC the presence of a P wave that occurs early on the ECG and which is not followed by a QRS complex b Occur infrequently and in no particular pattern iv Can result from a variety of drugs or from organic heart disease v Generally not treated in a prehospital setting but it may be a precursor for future dysrhythmias h Wandering atrial pacemaker pacemaker of the heart moves from the SA node to various areas within the atria i The rate is usually to beats min with a slightly irregular rhythm and variations between R-R intervals based on the pacemaker site for that particular complex ii Upright P wave precedes each QRS although the P wave shapes vary with at least three different shapes of P waves within one ECG strip a PR interval to ms will vary slightly b QRS complex to ms iii Most commonly seen in patients with significant lung disease iv Treatment in the prehospital setting is not usually indicated i Multifocal atrial tachycardia pacemaker of the heart moves within various areas of the atria i Characterized by a rate of more than beats min ii Tachycardic wandering atrial pacemaker with an irregular rhythm and variation between R-R intervals based on the site of the pacemaker iii There is an upright P wave preceding each QRS complex but the P waves vary a PR interval to ms varies slightly b If the MAT increases to more than beats min the P waves may not be visible and the QRS complex will measure to ms iv Most common in patients with significant lung disease v Treatment is not usually at the prehospital level and therapies for SVT are generally ineffective with MAT Rhythms originating in the AV node or AV junction a The AV node will take over if the SA node fails to initiate an impulse i Rhythms of AV node origin are known as junctional rhythms because of the AV node proximity to the junction of atria and ventricles ii Junctional rhythms have inverted or missing P waves but normal QRS complexes iii An impulse generated in the AV node travels down through the conduction system into the ventricles iv At the same time the impulse goes upward through the atria and intermodal pathways toward the SA node v This leads to three possibilities in which the QRS complex appears normal and there is no P wave a If the impulse begins moving upward through the atria before the other part enters the ventricles an upside-down P wave will show followed immediately by the QRS complex b If the impulse moving through the atria occurs at the exact time the impulse travels through the ventricles the smaller P wave will be hidden within the QRS complex giving the appearance of a missing P wave c If the impulse starts late through the atria it will result in an inverted P wave after the QRS complex b The intrinsic rate of the AV node is to so junctional rhythms normally have rates of to beats min c Junctional escape rhythm i Occurs when the SA node does not function and the AV node takes over as the pacemaker a Rate of to beats min usually regular rhythm with little variation between R-R intervals b The P wave is upside down or appears to be absent c PR interval less than ms d QRS complex to ms ii Most common in patients with significant SA node problems iii Treatment is usually a surgically implanted pacemaker a Little can be done in the field besides instituting transcutaneous pacing if the situation is critical d Accelerated junctional rhythm i Present with a rate exceeding its normal upper rate of beats min but remain less than beats min ii The rhythm is regular with little variation between R-R intervals and the P wave if present is inverted or upside down a PR interval less than ms b QRS complex to ms iii Although serious patients seldom need treatment in the prehospital setting e Junctional tachycardia i Junctional rhythm with a ventricular rate higher than beats min ii The rhythm is regular with little variation between R-R intervals iii The P wave if present is inverted or upside down a PR interval less than ms b QRS complex to ms iv Although serious it seldom requires prehospital treatment unless the rate reaches beats min f Premature junctional complex i Existence of a particular complex within another rhythm also known as ectopic complexes ii Occurs earlier in time than the next expected sinus complex iii Irregular rhythm iv The P wave if present will be inverted and upside down and may precede the QRS complex a PR interval Less than ms b QRS complex to ms v Rarely treated in the prehospital setting Heart blocks a The SA node initiates impulses which proceed through the atria and ventricles resulting in heart contractions i When they reach the AV node they are delayed so the atria can contract and fill the ventricle a Occasionally impulses are delayed more than usual causing heart blocks b First-degree heart block i Occurs when each impulse is delayed slightly longer than normal resulting in a PR interval greater than ms ii Considered the least serious type of block but is often the first indication of damage in the AV node iii The intrinsic rate is to beats min typically occurring at the low end of this range iv The rhythm is regular with minimal variations between R-R intervals v Present upright P wave preceding each QRS complex a PR interval greater than ms b QRS complex to ms vi Rarely treated in a prehospital setting unless associated with bradycardia c Second-degree heart block Mobitz type I Wenckebach i Occurs when each successive impulse is delayed a little longer until an impulse cannot continue ii Intrinsic rate of to beats min generally occurring at the low end of the range iii Irregular rhythm with a prolonged R-R interval occurring between the last QRS complex before the blocked P wave and the QRS complex after the first unblocked P wave iv The upright P wave precedes most QRS complexes v PR interval starts out to ms but grows longer with each P wave a Results in a P wave followed by another P wave instead of a QRS complex P wave is then followed by a QRS complex with a normal PR interval Pattern repeats b QRS complex to ms vi Not treated in the prehospital setting unless there is an associated bradycardia d Second-degree heart block Mobitz type II Classical i Occurs when several impulses are not allowed to continue ii Intrinsic rate of to beats min typically on the low end iii Rhythm may be a Regular with every other P wave blocked b Irregular with a prolonged R-R interval between the last QRS complex before the blocked P wave and the QRS complex after the first unblocked P wave iv Upright P wave precedes some QRS complexes with an always constant PR interval v Only treated in the field if associated with bradycardia e Third-degree heart block complete heart block i Occurs when all impulses are prevented from reaching the ventricles and causing a QRS complex a The ventricles will develop their own pacemaker to continue blood circulation but at a greatly reduced rate ii Intrinsic atrial rate of to beats min ventricular rate of less than beats min iii Usually has a regular rhythm with consistent P-P and R-R intervals iv Upright P wave with a nonexistent PR interval v Can be identified by the presence of nonconducted P waves with no relationship between P waves and the QRS complexes vi QRS complexes wider than ms are common vii Treated in the field only if associated with bradycardia Rhythms originating in the ventricles a The ventricles may start originating their own impulses and become the pacemaker if the AV node does not take over after the SA node does not initiate an impulse i Will have wide QRS complexes and missing P waves ii Impulses must travel through the ventricles cell-by-cell because the cell originating the impulse will likely not be located on the conduction system a The impulses will travel more slowly resulting in very wide QRS complexes of more than ms duration iii Ventricular rhythms are normally to beats min b Idioventricular rhythm i Occurs when the SA and VA nodes fail and the ventricles must pace the heart ii Rate of to beats min usually regular with little variation between R-R intervals iii P waves are absent so there is no PR interval iv QRS complex More than ms v May or may not result in a palpable pulse vi Treatment includes improving the CO by increasing the rate and if possible treating the underlying cause c Accelerated idioventricular rhythm i Occurs when an idioventricular rhythm exceeds the normal upper rate of beats min but remains less than beats min ii The rhythm is regular with little variation between R-R intervals iii P waves are absent so there is no PR interval iv QRS complex higher than ms v Although serious they are rarely treated in the prehospital setting d Ventricular tachycardia i Occur when the SA and AV nodes fail as pacemakers and a ventricular rhythm has a rate exceeding beats min ii The rhythm is regular with no variation between R-R intervals iii P waves are absent so the PR interval does not exist iv QRS complex greater than ms v QRS complexes usually have uniform tops and bottoms monomorphic vi Occasionally the QRS complex will vary in height in an alternating pattern polymorphic ventricular tachycardia a The most common is torsades de pointes May be normal for the patient or induced by medications or drugs May require use of magnesium to convert the rhythm b Usually worse than monomorphic ventricular tachycardia vii Requires prehospital treatment to maintain adequate CO a Usually leads to ventricular failure or fibrillation if not treated immediately e Premature ventricular complex ectopic complexes i Existence of a particular complex within another rhythm a Occurs earlier than the next expected sinus complex causing the R-R interval to be less between it and the previous complex ii Irregular rhythm with no P wave or PR interval iii QRS complex higher than ms iv Two different types include a Unifocal premature ventricular complexes Originate from the same spot within the ventricle and will appear the same on the ECG b Multifocal premature ventricular complexes Two premature complexes with different appearances Couplet Two complexes occurring together without any pause between them Salvos Three or more complexes occurring in a row Bigeminy Pattern that occurs when salvos are so frequent they alternate with normal complexes Trigeminy Every third beat is a premature complex v Most commonly originate from ischemia in the ventricular tissue vi More serious than premature atrial or junctional complexes a May occur when the ventricles are not fully repolarized resulting in ventricular fibrillation vii Rarely treated in the prehospital setting unless CO levels are significantly affected f Ventricular fibrillation i Rhythm in which the entire heart is fibrillating without any organized contraction ii Occurs when many different heart cells become depolarized independently rather than from an SA node impulse iii No P waves PR interval or QRS complexes iv In the early stages the cardiac cells have energy reserves allowing electrical energy to be expended causing the chaotic waves height to be large coarse ventricular fibrillation a The energy reserves are gradually used up leading to a reduction in the height of the waves fine ventricular fibrillation v Rhythm most commonly seen in adults going into cardiac arrest vi Responds well to defibrillation within the first to minutes of an arrest a After minutes CPR compressions are necessary b Prehospital treatment is common g Asystole flat line i The only true arrhythmia the entire heart is no longer contracting ii Occurs when many heart cells have been hypoxic so long there is no energy for any contraction iii Complete absence of electrical activity with no P waves PR intervals QRS complexes or T waves iv Agonal rhythm Flat baseline associated with asystole is interrupted by a small sinusoidal complex a Likely the result of residual electrical discharge from a dead heart v Generally considered a confirmation of death Artificial pacemaker rhythms a Artificial pacemakers cause a unique vertical spike on the ECG tracing b In the past the most common type was the ventricular pacemaker which is only attached to the ventricles i Causes a sharp spike followed by a wide QRS complex c Another type is attached to both the atria and ventricle i Causes a spike followed by a P wave and another spike followed by a wide QRS complex d Many newer pacemakers have sensors that identify the rate of spontaneous depolarization of the heart i Begin generating pacing impulses only when the natural pace of cardiac impulses has slowed below a specific number e If a patient s pacemaker is failing the spikes may be visible but will not be followed by a QRS complex i This loss of capture may be from a Dying battery b Dislodged wire connecting the pacemaker to the heart ii Patients need TCP instituted as quickly as possible iii It may also fail because of a runaway pacemaker which presents as a very tachycardic rhythm that needs to be slowed a A strong magnet placed over the pacemaker will reset a runaway pacemaker Done in the ED by a cardiologist VI -Lead ECGs A The purpose of a -lead ECG is to localize the site of injury to the heart muscle and identify cardiac abnormalities by looking at the heart from several angles Each ECG lead looks at the heart from a different angle a A standard -lead ECG records leads or shows different pictures of the heart s electrical activity b A lead provides an electrical picture taken from a specified vantage point B Precordial leads A -lead ECG adds six precordial leads to the six limb leads a These leads V to V are also called unipolar chest leads anterior leads or V leads b They are placed on the anterior and lateral chest walls and look at the heart in the horizontal plane i V and V septum ii V and V anterior wall of left ventricle iii V and V lateral wall of the left ventricle C Placement of -lead ECG electrodes Correct electrode placement is necessary to ensure the lead is viewing the heart from the correct angle a To identify existing problems b To highlight the appearance of new problems D Acquisition modes ECGs can record tracings using different electromagnetic frequency ranges a For rhythm interpretation ECGs are recorded in monitor mode i Uses electronic filters to remove artifact and unwanted information ii Skews shape and location of the ST segment and T wave iii Captures the range of to or hertz Hz b Diagnostic mode filters out very little electrical information so there is more artifact on the tracing i Used to record a -lead ECG by default and cannot be changed ii Many devices allow users to record -lead ECGs in diagnostic mode a Usually done in early minutes of contact while there is more movement resulting in high levels of artifact and an inability to interpret the rhythm iii Captures electrical information within the range of to Hz iv Pediatric right ventricle and artificial pacemakers emit a higher-frequency electrical signal v Frequency range is always printed near bottom of ECG tracing E Lead placement Make sure the patient does not get chilled as shivering will cause artifact -lead ECGs are more sensitive to artifact than -lead monitoring ECGs To properly acquire a -lead ECG refer to Skill Drill - F -lead ECG concepts When a current moves toward a lead it creates a positive upright deflection on the tracing of that lead a If it is moving away from a lead it creates a negative deflection b Leads II and aVR are nearly opposite each other so will present nearly opposite pictures of the electrical depolarization wave i If a depolarizing wave is coming toward lead II it will be going away from aVR Different colors are associated with each lead each color represents an area of the heart G Approach to interpretation of the -lead ECG The snapshot a Look at the tracings to find anything that stands out i Did all the leads print ii Is artifact present iii Is the rate at one of the extremes Dysrhythmia interpretation a Five-step process to identify the underlying rhythm i P waves morphology shape direction number ii QRS complexes shape duration iii PR intervals duration iv Regularity v Rate atrial ventricular calculation methods parameters Axis a Vector Value of all the electrical charges from all the myocytes at a specific moment in time i Describes the quantity and has magnitude and direction ii Axis of depolarization Vector created by ventricles during depolarization iii Viewed from lead I the QRS wave will be a A positive deflection if heading toward the left arm b A negative deflection if heading toward the right arm iv Viewed from lead aVF the QRS wave will be a A positive deflection if heading toward the patient s feet b A negative deflection if heading toward the patient s head b Fastest method to determine the QRS axis involves using the QRS complexes in leads I and aVF to create a four-quadrant system i The intersection represents the impulse origin with the four quadrants where the impulse can travel a Positive QRS in leads I and aVF Normal QRS axis b Positive QRS in lead I and negative in lead aVF Left axis deviation c Negative QRS in lead I and positive in lead aVR Right axis deviation d Negative QRS in leads I and aVR Extreme right axis deviation ii The QRS axis will always move toward hypertrophy and away from infarction a The direction of the QRS axis axis deviation relates to electrical activity in the ventricles b If a ventricle is enlarged hypertrophy it has more electrical energy c If an area of the ventricle is infarcted dead tissue it has no electrical energy iii Axis deviation may provide important clues about the heart s electrical activity but it is not specific for any particular diagnosis Conduction system disturbances a Bundle branch blocks i QRS complex with a bizarre appearance and a duration of longer than ms ii Most common findings on the -lead ECG iii Right bundle branch blocks RBBB Terminal R wave in lead V a Typically the QRS complex appears as an rSR' complex R-prime wave b Terminal S waves are also seen in leads I aVL and V iv Left bundle branch blocks LBBB Terminal S wave in lead V a Terminal R waves are seen in leads I aVL and V v RBBB or LBBB aberration describes the shape of the QRS complex in aberrantly conducted beats b Fascicular blocks hemiblocks i Occur when the anterior and posterior fascicles become diseased or ischemic and they cannot conduct electrical impulses ii Anterior fascicular block rS complexes in leads II III aVF and qR complexes in leads I and aVL iii Posterior fascicular block qR complexes in leads II III and aVF and rS complexes in lead I iv Bifascicular block A combination of two or more fascicles or conduction pathways are blocked a Combinations vary and produce different effects in different patients RBBB and anterior hemiblock RBBB and posterior hemiblock Anterior hemiblock and posterior hemiblock LBBB v Trifascicular block All three components are blocked or impaired with one component still occasionally providing AV conduction c Pre-excitation i Early depolarization of ventricular tissue due to the presence of an accessory pathway between the atria and ventricles ii Wolff-Parkinson-White syndrome Short PR interval less than ms widened QRS complex and presence of a delta wave a The delta wave indicates an early departure from the PR segment as a result of conduction through the Bundle of Kent b Patients are susceptible to tachydysrhythmias iii Lown-Ganong-Levine syndrome Short PR interval and a normal QRS duration a Patients are susceptible to tachydysrhythmias Chamber size a The -lead ECG gives information about the size of the heart s chambers i If the ventricle is enlarged the R wave may be wide ii If ventricular hypertrophy is present the R wave may be abnormally high iii Hypertrophy of the ventricles will show as an abnormally deep S wave b The right atrium is designed to function in a low-pressure environment i It will dilate if returning venous pressure is elevated or pulmonary pressures are high ii Right atrial enlargement usually results from chronic pulmonary disorders a Characterized by a P wave with an amplitude higher than mm in lead II and or higher than mm in lead V c Left atrial enlargement is characterized by i P wave duration of longer than ms in lead II ii P wave with notched appearance iii Peak-to-peak duration of P wave longer than ms iv P wave in lead V predominantly negative d Left atrial enlargement is caused by i Systemic hypertension ii Mitral or aortic valve stenosis e Right ventricular hypertrophy RVH Right ventricle becomes enlarged i Usually caused by pulmonary hypertension ii Diagnosed by a Large R wave in lead V and or b R wave in lead aVR with an amplitude taller than mm c QRS T discordance in V f Left ventricular hypertrophy LVH Left ventricle becomes enlarged i Commonly due to hypertension but also from some cardiac abnormalities ii The left ventricular wall increases due to increase in workload iii Loses elasticity and fails to pump blood effectively leading to CHF iv Diagnosed by a Deepest S wave in lead V V plus b Tallest R wave in V V taller than mm and or c R wave in lead aVL taller than mm d QRS T discordance v Diagnosis is made by echocardiogram not ECG Ischemia injury infarction a Critical to minimize EMS-to-balloon time door-to-balloon time and door-to-needle time i EMS-to-balloon time the time frame starting at the first moment of patient contact by EMS providers to when definitive therapy occurs ii Door-to-balloon time the time from when the patient reaches the hospital to definitive therapy should be minutes according to the AHA iii Door-to-needle time time from patient presents at the ED to when a fibrinolytic medication is given should be less than minutes according to the AHA b Rapid identification of a myocardial infarction is the most important factor in decreasing EMS-to-balloon time c ECG areas that change dramatically during periods of ischemia i Q wave ii J point iii ST segment iv T wave d Q waves are abnormal if i One small square ms wide on the ECG strip ii Deeper than one third the total height of the QRS complex may indicate an AMI e J point junction point between QRS complex and the ST segment i Signifies the end of ventricular depolarization and beginning of repolarization ii Look for anomalies on the right side of the QRS complex f ST segment Begins at the J point and terminates at the T wave i Represents early repolarization of the ventricles ii If it depresses below the isoelectric line it is a pattern of ischemia iii If it elevates above the isoelectric line it is a pattern of injury iv A lack of change in the presence of acute coronary syndrome symptoms is a nondiagnostic ECG a Does not rule out AMI injury or infarction v Normally isoelectric a If amplitude is significantly taller than mm on one small box above or below the isoelectric line AMI or injury in three contiguous leads is highly suggested g T wave The most dynamic wave i Becomes hyperacute peaked or tented in shape symmetric and broad based during ischemia injury and infarction h The terms TP segment isoelectric line isomeric line and eCG baseline refer to a period of electrical silence in the myocardium i The baseline is neither positive nor negative but there is still electrical activity in the myocardium ii Generally a flat straight horizontal line beginning at the end of the T wave and ending at the start of the P wave iii The baseline is the reference part to compare with the J point a A J point elevated by one or more millimeters from the baseline is diagnostic for AMI b A J point depressed below baseline and or T-wave inversion is indicative of ischemia i Ischemia i Manifests as ST-segment depression and or T-wave inversion ii Can be localized by finding changes in contiguous leads leads that view geographically similar areas of the myocardium j Injury i An AMI diagnosis is made in the presence of ST-segment elevation of mm or more in two or more contiguous leads ii Important concepts in identifying MIs a Right ventricular involvement b Reciprocal changes iii Approximately of patients with an inferior wall MI will also have right ventricular involvement a Indication for performing a right-sided ECG is the presence of an inferior wall STEMI b Steps to acquire a right-sided ECG Place an electrode in the fifth intercostals space at the midclavicular line on right side of chest V R Unsnap the lead V on the left side of the chest and snap it onto a new electrode Press acquire on the -lead ECG monitor A ST-segment elevation greater than mm in the V R lead may indicate a right ventricular MI Be sure to mark an R next to the V and circle it iv Reciprocal changes oppose primary J ST T-wave changes on the ECG a Indicator of AMI although the absence of these changes is not diagnostic b Important reciprocal lead groups are Leads II III aVF and Leads I aVL Leads II III aVF and Leads V to V Leads V to V and Leads V to V v Changes observed during myocardial injury include a ST-segment elevation in leads II III and aVF and reciprocal changes in leads I and aVL b St-segment elevation in leadsV to V and sometimes V and reciprocal changes in leads II III aVF c Diagnosis of posterior wall STEMI QRS duration shorter than ms Large R waves in leads V to V R waves larger than S waves ST-segment depression and T-wave inversion in leads V to V vi The specific area can be localized by noting the areas of the ECG that show changes k Treatment i Prehospital treatment of AMI is the same as for chest pain a Aspirin and nitroglycerin should be administered early b Follow local protocols regarding oxygen and morphine administration ii STEMI treatment involves rapid reperfusion of affected lesions by mechanical methods iii Right ventricular injury in the face of inferior wall injury requires volume replacement prior to administration of nitrates iv For patients presenting with classic atypical or angina-type pain the -lead ECG allows for rapid stratification into categories a STEMI ST elevation in two or more contiguous leads or new or suspected LBBB b NSTEMI new ECG changes non-ST elevation c Normal nondiagnostic v Patients with ST elevation are candidates for emergent primary percutaneous coronary intervention pPCI vi Cardiac catheterization is a minimally invasive procedure used to diagnose and treat blocked coronary arteries a Also called pPCI and percutaneous transluminal coronary angioplasty PTCA b If no local hospital is capable of this procedure most EDs can treat STEMI with fibrinolytic medications to dissolve blood clots fibrinolysis vii Time savings in door-to-perfusion therapy ranges from to minutes when prehospital -lead ECGs are completed and results transmitted to the receiving facility a Standard of care for paramedics to acquire and transmit ECGs or communicate findings to the ED l The many faces of ischemia Summary i Ischemic patients do not necessarily benefit from emergent PCI but do benefit from myocardial ischemia treatment that may prevent a myocardial infarction m Other cardiovascular conditions i The -lead ECG can provide information about noncardiovascular problems such as a Pulmonary embolism b Acute intracranial hemorrhage c Electrolyte abnormalities ii Benign early repolarization Normal variant affecting about of the population a Almost always a coincidental finding on ECG b Characterized by ST-segment elevation or J-point elevation a J or fishhook appearance at the J point and concave ST-segment morphology c Changes are often seen exclusively in the left precordial leads V to V and or inferior leads d Reciprocal changes are never seen iii Pericarditis Inflammation of the pericardial sac from an infection or trauma a Patients present with Positional chest pain often alleviated by sitting forward Shortness of breath History of recent infection or fever b Characterized by diffuse ST-segment elevation not exceeding mm and a depressed or down-sloping PR segment c PR segment is elevated or up-sloping in lead aVR d ST segment is concave and reciprocal ST-segment depression is never seen Noncardiac causes of ECG abnormalities a Pulmonary embolism i Can be identified on a -lead ECG by the presence of a An S Q T pattern Deep S wave in lead I Deep narrow Q wave in lead III T-wave inversion in lead III b New RBBB c ST-segment depression in leads V to V ii Critical to collect other pertinent information and perform a thorough physical exam b Severe hypothermia i Patients may develop J waves Osborne which is often large and upright occurring on the terminal wave of the QRS complex ii Typically appears as a bradycardic rhythm and baseline containing artifact from shivering and poor electrode adhesion iii J wave may be accompanied by ST-segment depression and T-wave inversion iv The more serious the condition the larger the J wave c Electrolyte imbalances i Hyperkalemia shows on an ECG with a Tall peaked asymmetric T waves develop and P waves can become flattened b T waves may be tall and sharply peaked c In severe cases wide QRS complexes appear ii Hypokalemia shows on an ECG with a Flat or seemingly absent T waves b Developed U wave a small wave occurring after a T wave but before the next P wave iii Hypercalcemia may cause a shortened QT interval iv Hypocalcemia may slightly lengthen the QT interval a Both lengthening and shortening are due to length change in the ST segment b The T wave is unaffected by calcium concentration changes d Hypertrophic cardiomyopathy i Condition in which the myocardial walls become very thick ii Patients will experience often associated with physical exercise a Shortness of breath b Chest pain c Syncope iii Often diagnosed in the s and s iv Characterized by deep narrow Q waves in the inferior and high lateral leads and very tall precordial leads e Brugada syndrome i Genetic disorder involving sodium channels in the heart ii Believed to be responsible for about of all sudden cardiac arrest iii Most common in men of Southeast Asian origin iv Often diagnosed in the s or s patients are unaware of the condition until sudden onset with syncope or cardiac arrest v Characterized by a Incomplete RBBB b ST-segment elevation that aggressively returns to baseline f Long QT syndrome LQTS i Characterized by a QT interval exceeding approximately ms a Indicates that the heart is experiencing an extended refractory period that may create a ventricular dysrhythmia vulnerability ii A result of a Genetic mutation of several genes b Administration of certain drugs such as amiodarone c Certain conditions such as hypocalcemia AMI and pericarditis iii The QT interval is age-specific and gender-specific iv Predisposes patients to ventricular dysrhythmias g Intracranial hemorrhage i May cause deeply inverted symmetric T waves in the precordial leads and a prolonged QT interval ii Patient will almost always have neurologic symptoms including unresponsiveness VII Emergency Medical Care A The AHA guidelines suggest that a checklist be used for triage of patients with ACS B Treating dysrhythmias Defibrillation a Process by which a surge of electric energy is delivered to the heart i Delivers a current that is powerful enough to depolarize all of the heart s component muscle cells ii When the cells repolarize after the shock they should respond to an impulse from the SA node and begin organized depolarization b Need to be carried out as soon as possible for i Ventricular fibrillation ii Pulseless ventricular tachycardia c If arrest was not witnessed and CPR is not in progress immediately begin CPR continuing for minutes before delivering the first shock d If the rhythm converts to ventricular fibrillation or pulseless ventricular tachycardia perform CPR only long enough to charge up the defibrillator e Defibrillation is not useful in asystole i May be harmful because of unnecessary interruption of compressions ii If unsure of asystole resume CPR and follow the asystole pathway in the pulseless arrest algorithm until the next pulse and check again f Manual defibrillation i Some defibrillators can perform either manual or automated defibrillation ii An automated external defibrillator AED interprets the cardiac rhythm to determine if defibrillation is needed iii In manual defibrillation the paramedic interprets the cardiac rhythm to determine if defibrillation is needed iv Switch an AED to manual mode when a All electrical therapy functions are needed b Patient is in cardiac arrest Saves time waiting for the AED mode to analyze the rhythm and make a recommendation v Follow the same safety measures for manual defibrillation and AED a Make sure no one is touching the patient b Do not defibrillate a patient in pooled water You can defibrillate a soaking patient but try to dry the chest first c Do not defibrillate a patient who is touching metal that others are touching d If the patient has an implanted pacemaker or internal defibrillator place the pad below the pacemaker or defibrillator or in anterior and posterior positions vi To perform manual defibrillation a Attach the adhesive defibrillation pads to the patient s chest b Dry the chest if necessary c Check the instructions on whether to place the pads or turn on the device first d Set the energy level to J for biphasic devices J for monophasic devices or follow the manufacturer s recommendations e Charge the defibrillator f If device requires hand-held paddles apply a conductive gel on the paddle surface and apply about lb of pressure to hold the paddles to the chest g Follow the manufacturer s recommended placement h Make sure the devices are not placed over metal objects or medication patches i Position the negative pad to just right of the upper part of the sternum below the right clavicle and the positive pad just below and to the left of the left nipple j Clear the area and make sure no one is touching the patient k Announce All clear then discharge the defibrillator l Contraction of the chest and other muscles will be evident if the current reaches the patient m If no contraction check the defibrillator n Resume CPR immediately and continue for minutes or cycles before pausing to check for a pulse If you see an organized rhythm on the monitor check for a pulse If the rhythm requires another shock deliver one shock followed immediately by CPR If the rhythm does not require a shock but there is no pulse perform five cycles of CPR then reanalyze the cardiac rhythm If still not shockable continue CPR transport the patient and contact medical control o If the rhythm does not require a shock and there is a pulse check the breathing If the patient is breathing but with an SpO of less than administer oxygen and transport vii An implanted artificial pacemaker is not a contraindication to defibrillation but make certain the pads are not placed directly over the pacemaker battery viii Inspect the defibrillator at the beginning of each shift checking a Defibrillation pads b Cables and connectors c Power supply d Monitor e ECG f Recorder g Ancillary supplies electrode gel pads spare battery ix To properly perform manual defibrillation refer to Skill Drill - x Patients who do not regain a pulse on the scene usually do not survive a Transport decisions should be dictated by the local medical control protocols b CPR administration during transport is usually not effective c Following local protocols transport when one of the following occurs The patient regains a pulse Six to nine shocks have been delivered or as by local protocol The defibrillator gives three consecutive messages that no shock is advised or as by local protocol d If you must perform CPR during transport it is helpful to have two EMS providers in the patient compartment e Defibrillation during transport is not safe so come to a complete stop if needed g Automated external defibrillator i Analyze the ECG rhythm for ventricular fibrillation or ventricular tachycardia to determine if a shock is needed a Charge the pads and deliver countershocks without intervention by the rescuer b A semiautomated AED prompts the rescuer to press the shock button ii Remember to observe safety measures same as for manual defibrillator iii If you witness cardiac arrest begin CPR and attach the AED as soon as available iv If the cardiac arrest was not witnessed perform five cycles of CPR before applying the AED v To properly perform defibrillation with an AED refer to Skill Drill - vi Patient care after shock depends on the EMS system and location of call vii After the AED protocol is completed a Pulse is regained b No pulse is regained and the AED indicates no shock is advised c No pulse is regained and the AED indicates a shock is advised viii For each of these the sequence of compressions and defibrillations is the same as for manual defibrillation h Cardiac arrest during transport i If transporting an unresponsive patient closely monitor and watch for an ECG rhythm change and a pulse change ii If pulse is not present a Stop the vehicle b If the defibrillator is not immediately ready perform CPR until it is available c Analyze the rhythm d Deliver one shock if indicated and immediately resume CPR e Continue resuscitation according to your local protocol iii If en route and an adult patient with chest pains loses consciousness a Check for a pulse b Stop the vehicle c If the defibrillator is not immediately ready perform CPR until it is available d Analyze the rhythm e Deliver one shock if indicated and immediately resume CPR f Continue resuscitation according to your local protocol Cardioversion a Synchronized cardioversion Use of the defibrillator to terminate hemodynamically unstable tachydysrhythmias i Involves a timed energy delivery at the peak of the R wave a R wave indicates ventricular depolarization b Delivering energy at this point increases the probability of depolarizing any polarized myocytes Allows the SA to resume primary pacemaker function ii Performed just as defibrillation except the user selects the synchronize setting first iii Emergency cardioversion is indicated for rapid ventricular and supraventricular rhythms associated with severely compromised CO iv In the field cardioversion is done only on patients with severely impaired CO a When done on a conscious patient he or she must be sedated Commonly used sedatives include diazepam Valium or midazolam Versed v To properly perform cardioversion refer to Skill Drill - Transcutaneous cardiac pacing TCP a Artificial pacemakers deliver repetitive electric currents to the heart i Can substitute for a blocked or nonfunctional natural pacemaker b The first artificial pacemakers consisted of a small battery pack and wire that was threaded through a vein into the right ventricle c Effective transcutaneous pacemakers pacemakers that deliver their current through the skin of the chest are now widespread d A small electrical charge passes through the skin across the heart between one externally placed pacing pad and another i Pacer is set for a specific rate ii Energy is increased until the heart just begins to respond known as capture iii Generally appears as a wide QRS complex resulting in a corresponding pulse e TCP has several useful applications in prehospital care i Interhospital patient transfer needing pacemaker implantation ii Symptomatic patients with artificial pacemaker failure iii Patients with bradydysrhythmias or blocks associated with severely reduced CO and unresponsive to atropine f To properly perform transcutaneous pacing refer to Skill Drill - g TCP also depolarizes chest wall muscles beneath the pacing electrode i Conscious patients usually have chest discomfort or sometimes severe pain from the procedure ii If patient is conscious use sedation C Management of symptomatic bradycardia Patient needs treatment that will increase heart rate and improve CO Symptoms such as altered mental status and hypotension indicate treatment Support airway and breathing then a Establish an IV line with normal saline b Administer atropine at mg IV bolus i Repeat every to minutes until the heart reaches the desired rate or the maximum total dose of mg kg is reached c If the patient does not respond or is severely compromised begin TCP immediately i If second-degree type II or third-degree heart block TCP is the first-line treatment d If unsuccessful consider a sympathomimetic drug dopamine or epinephrine as a drip i Dopamine dose to g kg min ii Epinephrine dose to g min a To mix put mg into a -mL bag of normal saline and start at drops min titrating until desired heart rate is reached e Transport patient to a hospital with transvenous pacing and pacemaker implantation capabilities Symptomatic patients and those requiring TCP in the field often require pacemaker implantation in the hospital a Early identification and notification can often expedite this D Management of tachycardia Tachycardia is a more complicated situation than bradycardia Many possible variations of signs requires judgment before treatment is begun a Decide on the seriousness of signs and symptoms i Unstable tachycardia needs immediate treatment with serious signs and symptoms such as a Chest pain b Dyspnea c Hypotension d Altered mental status ii Must decide if signs and symptoms indicate tachycardia or another condition a Rates of beats min rarely cause serious signs and symptoms of tachycardia b Slowing the heart rate of a patient whose heart is compensating for a medical condition may be fatal b If unstable signs and symptoms are determined to result from tachycardia cardioversion is needed i Similar to defibrillation ii Limited to patients who are likely to arrest if treatment is not administered quickly a Most will be unconscious but sedation is necessary if conscious c If signs and symptoms are limited or mild slower but safer treatment is recommended i