1 A Cardiac EKG

Basic Electrocardiography and Dysrhythmias Location of the Heart • Hollow muscular organ, Located in the middle of the thoracic cavity, Surrounded by pericardium • Attached to thorax via great vessels • Apex (bottom) – Formed by tip of left ventricle • Base (top) – Approximately 2nd intercostal space • Anterior surface – Consists primarily of right ventricle • Inferior (diaphragmatic) surface – Formed by right and left ventricles, predominantly left Size and Shape of the Heart • Cone-shaped muscular organ • Adult heart is approximately: – 5 inches (12 cm) long,3.5 inches (9 cm) wide,2.5 inches (6 cm) thick, about the size of a man’s fist Heart Chambers • The heart is divided into four cavities or chambers • Functions as a two-sided pump – Two upper chambers = right and left atria – Two lower chambers = right and left ventricles Heart Chambers • Right side of the heart – Low-pressure system – Pumps venous blood to the lungs • Left side of the heart – High-pressure system – Pumps arterial blood into the systemic circulation Atria • Thin-walled, low-pressure chambers that receive blood • Interatrial septum separates right and left atria • “Atrial kick” Ventricles • Pump blood to lungs and systemic circulation • Interventricular septum separates right and left ventricles • Left ventricle – High-pressure chamber Layers of the Heart • The heart wall is made up of three tissue layers: – Endocardium – Myocardium – Epicardium • Epicardium – Also called the visceral layer of the serous pericardium – External layer of the heart – Pericardium – Double-walled sac that encloses the heart – Fibrous parietal pericardium • Rough outer layer of the pericardial sac – Serous pericardium Pericardial space contains about 10 ml of serous fluid Summary – Layers of the Heart Wall Epicardium • External layer of the heart • Coronary arteries, blood capillaries, lymph capillaries, nerve fibers nerves, and fat are found inthis layer Myocardium • Middle and thickest layer of the heart • Responsible for contraction of the heart Endocardium • Innermost layer of the heart • Lines the inside of the myocardium • Covers the heart valves Cardiac Muscle • Walls of the heart are formed by cardiac muscle fibers – Sarcolemma – Myofibrils Cardiac Muscle • Each sarcomere contains two types of protein filaments: actin and myosin Cardiac Muscle • Cardiac muscle fibers fit together tightly at junctions called intercalated disks – Intercalated disks form gap junctions • Function as electrical connections • Allow cells to conduct electrical impulses rapidly Valves of the Heart Heart Valves • Heart contains four valves – Two sets of atrioventricular (AV) valves – Two sets of semilunar valves • Function – Ensure blood flows in one direction through heart chambers – Prevent backflow of blood Atrioventricular (AV) Valves • AV valves separate atria from ventricles • Tricuspid valve – Lies between right atrium and right ventricle – Consists of three separate leaflets – Larger in diameter and thinner than mitral valve Atrioventricular (AV) Valves • Mitral (bicuspid) valve – Has only two cusps – Lies between left atrium and left ventricle Atrioventricular (AV) Valves • Cusps of AV valves are attached to chordae tendineae – “Heart strings” – Originate from papillary muscles – Serve as anchors Semilunar Valves • Prevent backflow of blood from the aorta and pulmonary arteries into the ventricles during diastole – Pulmonic valve – Aortic valve Semilunar Valves • Pulmonic valve – Prevents backflow of blood into right ventricle • Aortic valve – Prevents backflow of blood into left ventricle Heart Sounds • First heart sound (S1 ) – Closure of tricuspid and mitral (AV) valves – Often referred to as “lub” in “lub-dup” • Second heart sound (S2) – Closure of pulmonic and aortic (semilunar) valves – “Dup” in “lub-dup”

Third Heart Sound (S3) • Associated with ventricular filling – Considered normal in healthy persons younger than 40 years of age – S1-S2-S3 sequence is called a ventricular gallop or gallop rhythm • Ken-tuck-y • (S1)-(S2)-(S3) Blood Flow Through the Heart Cardiac Cycle • Systole - Period during which the chamber is contracting and blood is being ejected Cardiac Cycle • Diastole – Period of relaxation during which the chamber is filling Coronary Circulation Coronary Arteries • Supply heart with oxygenated blood • Primary arteries: right and left coronary arteries – Coronary artery filling occurs during ventricular relaxation (diastole) Right Coronary Artery Left Coronary Artery Coronary Veins • Run parallel to coronary arteries • Drain myocardial blood into right atrium – Thebesian veins, Anterior cardiac veins, Coronary sinus Heart Rate • Autonomic nervous system (ANS) influences: – Heart rate – Conductivity – Contractility Baroreceptors • Also called “pressoreceptors” – Specialized nerve tissue – Found in internal carotid arteries / aortic arch – Detect changes in blood pressure Chemoreceptors • Located in internal carotid arteries and aortic arch • Detect and respond to changes in: – Oxygen content of the blood – pH – Carbon dioxide tension Parasympathetic Stimulation • Major parasympathetic nerves are the two vagus nerves – One on each side of the body • Vagus nerve innervates heart at SA and AV nodes – Primary postganglionic neurotransmitter = acetylcholine Parasympathetic Stimulation • Effects of acetylcholine – Slowing of rate of discharge of SA node – Slowing of rate of conduction through AV node Sympathetic Stimulation • Impulses sent from accelerator center in medulla travel along sympathetic fibers • Primary postganglionic neurotransmitter = norepinephrine Receptor Sites • Alpha – Vascular smooth muscle • Beta-1 – Heart • Beta-2 – Bronchial smooth muscle – Skeletal blood vessels • Dopaminergic – Coronary arteries, renal, mesenteric, and visceral blood vessels Effects of Norepinephrine on Receptor Sites • Alpha – No effect on heart – Peripheral vasoconstriction • Beta-1 – Increased heart rate – Increased conductivity – Increased contractility Chronotropic Effect • Refers to a change in heart rate – A positive chronotropic effect refers to an increase in heart rate – A negative chronotropic effect refers to a decrease in heart rate Inotropic Effect • Refers to a change in myocardial contractility – A positive inotropic effect results in an increase in myocardial contractility – A negative inotropic effect results in a decrease in myocardial contractility The Heart as a Pump • Venous return – Most important factor determining amount of blood pumped by heart Cardiac Output • Cardiac output is the volume of blood ejected from the heart over 1 minute – Because the ventricles contract almost simultaneously, their cardiac outputs are normally equal Cardiac Output • Cardiac output (CO) equals stroke volume (SV) multiplied by heart rate (HR) CO = SV x HR • Cardiac output is affected by a change in heart rate OR stroke volume Decreased Cardiac Output • Cold, clammy skin, Color changes in skin/mucous membranes, Dyspnea, Orthopnea, Crackles (rales) • Changes in mental status, Changes in blood pressure, Dysrhythmias, JVD, Fatigue, Restlessness Blood Pressure • Blood pressure – Force exerted by circulating blood volume on walls of arteries • Peripheral resistance • BP = cardiac output (CO) _ peripheral resistance Stroke Volume • Amount of blood ejected during one contraction • Dependent on: – Preload – Afterload – Myocardial contractility Preload • Preload is the force exerted by the walls of the ventricles at the end of diastole • The volume of blood returning to the heart (venous return) influences preload – Hypovolemia = decreases preload – Heart failure = increases preload Frank-Starling Law of the Heart • Up to a limit, the more a myocardial muscle is stretched, the greater the force of contraction (and stroke volume) – Influenced by preload and afterload Afterload • Afterload is the pressure or resistance against which the ventricles must pump to eject blood – Increased afterload usually means an increase in the work of the heart Types of Cardiac Cells • Myocardial cells – Working or mechanical cells – Contain contractile filaments • Pacemaker cells – Specialized cells of the electrical conduction system – Responsible for the spontaneous generation and conduction of electrical impulses Cardiac Action Potential • All living cells maintain a difference in the concentrations of ions across their cell membranes • Electrical impulses are the result of brief but rapid flow of ions (charged particles) back and forth across the cell membrane Cardiac Action Potential • The exchange of electrolytes in myocardial cells creates electrical activity – Appears on the ECG as waveforms • Major electrolytes that affect cardiac function: – Sodium – Potassium – Calcium – Magnesium Cardiac Action Potential • Differences in ion concentrations across the cell (the ionic gradient) determine the cell’s electrical charge • There is normally a slight excess of: – Positive ions outside the membrane – Negative ions inside the membrane • Results in a difference in electrical charge across the membrane called the “membrane potential” Cardiac Action Potential • “Threshold” is the membrane potential at which the cell membrane will depolarize and generate an action potential • Action potential – A five-phase cycle that reflects the difference in the concentration of these ions across the cell membrane at any given time Membrane Channels • Cell membranes contain membrane channels (pores) – Specific ions or other small, water-soluble molecules can cross the cell membrane from outside to inside Cardiac Action Potential • A series of events causes the electrical charge inside the cell to change from its resting state (negative) to its depolarized (stimulated) state (positive) and back to its resting state (negative) – The cardiac action potential is an illustration of these events in a single cardiac cell during polarization, depolarization, and repolarization Types of Action Potentials • Two types of action potentials in the heart – Fast – Slow • Classification is based on rate of voltage change during depolarization of cardiac cells Fast-Response Action Potentials • Occur in cells of the atria, ventricles, and Purkinje fibers – Have voltage-sensitive sodium channels • Myocardial fibers with a fast-response action potential can conduct impulses at relatively rapid rates Slow-Response Action Potentials • Normally occur in the SA and AV nodes – Can occur abnormally anywhere in the heart, usually secondary to ischemia, injury, or an electrolyte imbalance • Possess slow calcium and slow sodium channels • Slower rate of conduction compared to cardiac cells with fast sodium channels Polarization, Depolarization, and Repolarization Polarization = Resting • Polarization – Also called the resting membrane potential – Resting state during which no electrical activity occurs – Inside of the cell is more negative than the outside Depolarization and Repolarization • Before the heart can mechanically contract and pump blood, cardiac muscle cell depolarization must take place • Depolarization and repolarization – Changes that occur in the heart when an impulse forms and spreads throughout the myocardium Depolarization = Stimulation • Inside of the cell becomes more positive due to inward diffusion of Na+ • On the ECG: – P wave represents atrial depolarization – QRS complex represents ventricular depolarization Depolarization • Depolarization is not the same as contraction – Depolarization is an electrical event expected to result in contraction (a mechanical event) • It is possible to view electrical activity on the cardiac monitor, yet evaluation of the patient reveals no palpable pulse – Pulseless electrical activity (PEA) Repolarization = Resting (R:R) • Outward diffusion of K+ – Membrane potential returns to its negative resting level • On the ECG: – ST segment represents early ventricular repolarization – T wave presents ventricular repolarization Phases of the Action Potential • Action potential of a cardiac cell consists of five phases • Reflects rapid sequence of voltage changes across cell membrane during electrical cardiac cycle Phase 0 – Depolarization • Begins when the cell receives an impulse – Sodium moves rapidly into cell – Potassium leaves cell – Calcium moves slowly into cell • Cell depolarizes and cardiac contraction begins • Responsible for QRS complex on the ECG • Note: The phases are important because cardiac drugs will work at various phases of the action potential of the heart. These drugs are grouped into classes. Class 1 Drugs Block Sodium: Work in Phase 0 • Phase 0 = Sodium Channel or Fast Channel • Class 1 Drugs = Sodium or Fast Channel Blockers • These drugs block sodium influx into the cell during phase 0 or the action potential • Three other classes of drugs that effect the cardiac cells during different phases of the action potential. • Class 2, Class 3, and Class 4 Class 2 Drugs: Beta Receptor Blockers • B1 Receptors in the SNS increase HR , contractility, and conductivity • B Blockers decrease these actions • Cardioselective BB only block B1 • Noncardioselective BB block both B1 and B2 • B2 Receptors in the SNS relax smooth muscle in bronchi and blood vessels • B Blockers may result in bronchospasms and vasoconstriction • Olol endings • Example: Esmolol ( Brevibloc) Class 3 Drugs : Block Potassium: Work in Phase 3 • Phase 3 = Potassium Channel • Phase 3 Drugs = Potassium Channel Blockers • Potassium movement is blocked during phase 3 of the action potential • Repolarization is prolonged • Refractory period is prolonged • Example: Amiodarone Class 4 Drugs Block Calcium : Work During Phase 2 • Phase 4 = Calcium Channel or Slow Channel • Phase 4 Drugs = Slow or Calcium Channel Blockers • These drugs block the movement of calcium during phase 2 of the action potential • Conductivity is prolonged • AV node refractory period is increased • Example : Diltiazem ( Cardizem ) Drugs Without a Class • Many of the cardiac drugs do not fit into the four classes • Examples: Atropine, Digoxin, Adenosine, and Epinephrine Recap: Phase 0 • Depolarization of the cardiac cells takes place • Sodium rushes inside the cell rapidly Phase 1 – Early Repolarization • Phase 1 is an early, brief period of limited repolarization – Fast Na+ channels partially close – Transient outward movement of K+ through K+ channels – Results in a decrease in positive electrical charges within the cell – ABSOLUTE refractory period Phase 2 – Plateau Phase • Repolarization continues relatively slowly – Caused by slow inward movement of Ca++ and slow outward movement of K+ from the cell: Calcium C Blockers work here • Responsible for ST segment on ECG Phase 3 • Phase of late and rapid repolarization – K+ flows quickly out of the cell – Slow channels close, stopping influx of Ca++ and Na+ – Cell becomes progressively more electrically negative and more sensitive to external stimuli • Corresponds with T wave on the ECG • Early part still in absolute refractory period (no stimulus can excite the cell) • Last half of phase three in Relative refractory period (a very strong stimulus can excite the cell) • Potassium Channel Blockers work here Phase 4 – Return to Resting State • Phase 4 is the resting membrane potential (return to resting state) – Heart is "polarized" during this phase (ready for discharge) • Cell will remain in this state until reactivated by another stimulus Refractory Periods • Refractoriness – The extent to which a cell is able to respond to a stimulus • Absolute refractory period – Onset of QRS complex to approximately peak of T wave – Cardiac cells cannot be stimulated to conduct an electrical impulse, no matter how strong the stimulus Refractory Periods • Relative refractory period – Corresponds with the downslope of the T wave – Cardiac cells can be stimulated to depolarize if the stimulus is strong enough • Supernormal period – Corresponds with the end of the T wave – A weaker than normal stimulus can cause depolarization of cardiac cells Properties of Cardiac Cells • Automaticity – Ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse without being stimulated from another source (such as a nerve) • Excitability – Ability of cardiac muscle cells to respond to an outside stimulus • Conductivity – Ability of a cardiac cell to receive an electrical stimulus and conduct that impulse to an adjacent cardiac cell • Contractility – Ability of cardiac cells to shorten, causing cardiac muscle contraction in response to an electrical stimulus The Conduction System • Conduction system :Specialized electrical (pacemaker) cells in the heart arranged in a system of pathways • Normally, the pacemaker site with the fastest firing rate controls the heart Sinoatrial (SA) Node • Located at the junction of the superior vena cava and the right atrium • Initiates electrical impulses at a rate of 60 to 100 beats/min • Normally the primary pacemaker of the heart Atria • Fibers of SA node connect directly with fibers of atria • Impulse leaves SA node and is spread from cell to cell across the atrial muscle Internodal Pathways • Conduction through the AV node begins before atrial depolarization is completed • Impulse is spread to AV node via internodal pathways – Pathways merge gradually with cells of AV node AV Junction • Area of specialized conduction tissue – Provides electrical links between atrium and ventricle AV Node • Located in the posterior septal wall of the right atrium – Supplied by right coronary artery in most individuals • As the impulse from the atria enters the AV node, there is a delay in conduction of the impulse to the ventricles – Allows time for atria to empty contents into ventricles AV Node • Divided into three functional regions according to their action potentials and responses to electrical and chemical stimulation – Atrionodal (AN) or upper junctional region – Nodal (N) region – Nodal-His (NH) AV Node • The primary delay in the passage of the electrical impulse from the atria to the ventricles occurs in the AN and N areas of the AV node Bundle of His • Also called the “common bundle” or the “AV bundle” • Normally the only electrical connection between the atria and the ventricles – Connects AV node with bundle branches – Has pacemaker cells capable of discharging at an intrinsic rate of 40 to 60 beats/min – Conducts impulse to right and left bundle branches Right & Left Bundle Branches • Right bundle branch – Innervates the right ventricle • Left bundle branch – Spreads the electrical impulse to the interventricular septum and left ventricle – Divides into three divisions (fascicles) • Anterior fascicle • Posterior fascicle • Septal fascicle Purkinje Fibers • Elaborate web of fibers that penetrate about 1/3 of the way into the ventricular muscle mass – Become continuous with cardiac muscle fibers • Receive impulse from bundle branches and relay it to ventricular myocardium • Intrinsic pacemaker ability of 20 to 40 beats/min Causes of Dysrhythmias Enhanced Automaticity • An abnormal condition in which: – Cardiac cells not normally associated with the property of automaticity begin to depolarize spontaneously or – Escape pacemaker sites increase their firing rate beyond that considered normal Reentry • Propagation of an impulse through tissue already activated by that same impulse Escape Beats or Rhythms • Escape: term used when the SA node slows down or fails to initiate depolarization and a lower site spontaneously produces electrical impulses, assuming responsibility for pacing the heart • “Protective” mechanisms – Maintain cardiac output – Originate in the AV junction or the ventricles Conduction Disturbances • May occur because of: – Trauma – Drug toxicity – Electrolyte disturbances – Myocardial ischemia or infarction • Conduction may be too rapid or too slow The Electrocardiogram (ECG) The ECG • The ECG is a voltmeter – Records electrical voltages (potentials) generated by depolarization of heart muscle • Electrical activity within the heart can be observed by means of electrodes connected by cables to an ECG machine The ECG • Can provide information about: – The orientation of the heart in the chest – Conduction disturbances – The electrical effects of medications and electrolytes – The mass of cardiac muscle – The presence of ischemic damage The ECG • Does not provide information about the mechanical (contractile) condition of the myocardium – Evaluated by assessment of pulse and blood pressure Electrodes • Disposable disk electrodes contain conductive media – Conductive media conducts the skin surface voltage change through color-coded wires to a cardiac monitor • Applied at specific locations on the patient's chest wall and extremities Leads • A lead is a record of electrical activity between two electrodes – Allow viewing of the heart’s electrical activity in two different planes: frontal (coronal) or horizontal (transverse) • Each lead records the average current flow at a specific time in a portion of the heart Types of Leads • There are three types of leads: – Standard limb leads – Augmented leads – Precordial (chest) leads Leads • Think of the positive electrode as an eye – The position of the positive electrode on the body determines the portion of the heart “seen” by each lead Waveform Deflections • If the wave of depolarization moves toward the positive electrode, the waveform recorded on the ECG graph paper will be upright • If the wave of depolarization moves toward the negative electrode, the waveform produced will be inverted Waveform Deflections • A biphasic (partly positive, partly negative) waveform is recorded when the wave of depolarization moves perpendicularly to the positive electrode • When electrical activity is not detected, a straight line is recorded called the “baseline” or “isoelectric” line Frontal Plane Leads • Six leads view the heart in the frontal plane as if the body were flat: three bipolar leads and three unipolar leads • Bipolar lead – A lead that consists of a positive and negative electrode – Leads I, II, and III Frontal Plane Leads • Unipolar lead – A lead that consists of a single positive electrode and a reference point – Augmented limb leads • Leads aVR, aVL, and aVF Horizontal Plane Leads • Six precordial (chest or V) leads view the heart in the horizontal plane • Precordial leads - V1, V2, V3, V4, V5, and V6 Standard Limb Leads • Leads I, II, and III make up the standard limb leads • In the bipolar leads: – Right arm electrode is always negative – Left leg electrode is always positive Lead I • Records the difference in electrical potential between the left arm (+) and right arm (–) electrodes • Views the lateral wall of the left ventricle Lead II • Records the difference in electrical potential between the left leg (+) and right arm (–) electrodes • Views the inferior surface of the left ventricle Lead III • Records the difference in electrical potential between the left leg (+) and left arm (–) electrodes • Views the inferior surface of the left ventricle Limb Leads – Waveform Comparison Modified Chest Leads • The modified chest leads (MCLs) are bipolar precordial (chest) leads that are variations of the unipolar precordial leads – Each MCL consists of a positive and negative electrode applied to a specific location on the thorax Augmented Limb Leads • Leads aVR, aVL, and aVF make up the augmented limb leads – A = augmented – V = voltage – R = right arm – L = left arm – F = foot (usually the left leg) • Unipolar leads – Consist of only one electrode on the body surface Augmented Limb Leads • Lead aVR – Views the heart from the right shoulder – Does not view any wall of the heart • Lead aVL – Views the heart from the left shoulder – Oriented to the lateral wall of the left ventricle • Lead aVF – Views the heart from the left foot (leg) – Views the inferior surface of the left ventricle Summary of Augmented Leads Precordial (Chest) Leads • The six precordial leads are unipolar leads – View the heart in the horizontal plane – Identified as V1, V2, V3, V4, V5, and V6 • Each electrode placed in a V position is a positive electrode – Leads V1 and V2 lie over the right ventricle – Leads V3 and V4 lie over the interventricular septum – Leads V5 and V6 lie over the left ventricle Precordial (Chest) Leads Summary of Precordial Leads ECG Paper ECG Paper • ECG paper is graph paper made up of small and larger, heavy-lined squares – Smallest squares are 1 mm wide and 1 mm high – 5 small squares between the heavier black lines – 25 small squares within each large square Horizontal Axis = Time • Width of each small box = 0.04 second • Width of each large box (5 small boxes) = 0.20 second – 5 large boxes (each consisting of 5 small boxes) = 1 second • 15 large boxes = 3 seconds • 30 large boxes = 6 seconds Vertical Axis = Voltage/Amplitude • Size or amplitude of a waveform is measured in millivolts (voltage) or millimeters (amplitude) Calibration • When the ECG machine is properly calibrated, a 1-millivolt electrical signal will produce a deflection that measures exactly 10 millimeters tall Waveforms Waveforms • A waveform or deflection is movement away from the baseline in either a positive (upward) or negative (downward) direction – A waveform that is partly positive and partly negative is “biphasic” – A waveform or deflection that rests on the baseline is “isoelectric” P Wave • The first wave in the cardiac cycle • Represents atrial depolarization and spread of the electrical impulse throughout the right and left atria The Normal P Wave • Smooth and rounded • Usually no more than 2.5 mm in height and 0.11 second in duration • Positive in leads I, II, aVF, and V2 through V6 • May be positive, negative, or biphasic in leads III, aVL, and V1 Abnormal P waves • May be notched, tall and pointed (peaked), or inverted (negative) • May be seen in conditions such as chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), or valvular disease Terminology • Waveform – Movement away from the baseline in either a positive or negative direction • Segment – A line between waveforms – Named by the waveform that precedes or follows it • Interval – A waveform and a segment • Complex – Several waveforms PR Segment • Part of the PR interval – Horizontal line between the end of the P wave and the beginning of the QRS complex • Normally isoelectric (flat) – Used as a baseline from which to evaluate ST segment elevation or depression PR Interval • The P wave plus the PR segment equals the PR interval • Begins with the onset of the P wave and ends with the onset of the QRS complex • Normally measures 0.12 to 0.20 second PR Interval • Reflects: – Depolarization of the right and left atria (P wave) – Spread of the impulse through the AV node, bundle of His, right and left bundle branches, and Purkinje fibers (PR segment) Abnormal PR Interval • Long PR interval (greater than 0.20 sec) – Indicates the impulse was delayed as it passed through the atria or AV junction • Short PR interval (less than 0.12 sec) – May be seen when the impulse originates in the atria close to the AV node or in the AV junction QRS Complex • A QRS complex normally follows each P wave • Consists of Q wave, R wave, and S wave • Represents the spread of electrical impulse through the ventricles (ventricular depolarization) Q Wave • The first negative, or downward, deflection following the P wave • Always a negative waveform • Represents depolarization of the interventricular septum Q Wave • Physiological Q waves – A normal Q wave is less than 25% of the amplitude of the R wave – Normal Q wave duration does not exceed 0.04 second • Pathological Q waves – More than 0.04 second in duration – More than 25% of the amplitude of the following R wave in that lead R Wave • The first positive, or upward, deflection following the P wave – Always positive S Wave • A negative waveform following the R wave – Always negative • R and S waves represent simultaneous depolarization of the right and left ventricles QRS Terminology • If the QRS complex consists entirely of a positive waveform, it is called an R wave • If the complex consists entirely of a negative waveform, it is called a QS wave QRS Measurement • The width of a QRS complex is most accurately determined when it is viewed and measured in more than one lead – Measure the QRS complex with the longest duration and clearest onset and end • Normal QRS duration in an adult varies between 0.06 and 0.10 second Abnormal QRS Complexes • Duration of an abnormal QRS complex is greater than 0.10 second • A QRS caused by an impulse originating in the Purkinje network or ventricular myocardium is usually greater than 0.12 second (often 0.16 second or greater) • If the electrical impulse originates in a bundle branch, the duration of the QRS may be only slightly greater than 0.10 second ST Segment • The portion of the ECG tracing between the QRS complex and the T wave • Represents the early part of repolarization of the right and left ventricles ST Segment • The point at which the QRS complex and the ST segment meet = “J point” or junction • Normally isoelectric (flat) in the limb leads Normal ST Segment • Begins with the end of the QRS complex and ends with the onset of the T wave • Limb leads – Normal ST segment is isoelectric (flat) – May normally be slightly elevated or depressed (usually less than 1 mm) • Precordial leads – In some precordial leads, ST segment may be normally elevated by as much as 2 to 3 mm – In the left precordial leads, ST segment elevation is not normally greater than 1 mm ST Segment • The PR segment used as the baseline from which to evaluate the degree of displacement of the ST segment from the isoelectric line (elevation or depression) – Measure at a point 0.04 second (one small box) after the end of the QRS complex (J point) ST Segment • The ST segment is considered: – “Elevated” if the segment deviates above the baseline of the PR segment – “Depressed” if the segment deviates below it Abnormal ST Segment • ST segment depression of more than 1 mm is suggestive of myocardial ischemia • ST segment elevation of more than 1 mm is suggestive of myocardial injury – Pericarditis causes ST-segment elevation in virtually all leads Abnormal ST Segment • A horizontal ST segment (forms a sharp angle with the T wave) is suggestive of ischemia • Digitalis causes a depression (scoop) of the ST segment – “Dig dip” T Wave • Represents ventricular repolarization – The beginning of the T wave is identified as the point where the slope of the ST segment appears to become abruptly or gradually steeper – The T wave ends when it returns to the baseline T Wave • It may be difficult to clearly determine the onset and end of the T wave Normal T Waves • Slightly asymmetrical • Not normally more than 5 mm in height in any limb leads or 10 mm in any precordial lead • Not normally less than 0.5 mm in height in leads I and II Abnormal T Waves • The T wave following an abnormal QRS complex is usually opposite in the direction of the QRS • Negative T waves suggest myocardial ischemia Abnormal T Waves • Tall, pointed (peaked) T waves are commonly seen in hyperkalemia • Significant cerebral disease (e.g., subarachnoid hemorrhage) may be associated with deeply inverted T waves – “Cerebral T waves” QT Interval • QT interval represents total ventricular activity—the time from ventricular depolarization (activation) to repolarization (recovery) • Duration of the QT interval varies according to age, gender, and heart rate – As heart rate increases, QT interval decreases – As heart rate decreases, QT interval increases • Measured from the beginning of the QRS complex to end of the T wave – In the absence of a Q wave, measure the QT interval from the beginning of the R wave to the end of the T wave • To rapidly determine the QT interval: – Measure the interval between two consecutive R waves (R-R interval) and divide the number by two – Measure the QT interval • If the measured QT interval is less than half the R-R interval, it is probably normal U Wave • Significance is not definitely known – Thought to represent repolarization of Purkinje fibers • Not easily identified due to its low amplitude U Wave - Normal Characteristics • Rounded and symmetrical • Usually less than 2 mm in amplitude • In general, a U wave of more than 1.5 mm in height in any lead is considered abnormal Abnormal U Waves • Abnormally tall U waves may be the result of: – Electrolyte imbalance – Medications – Hyperthyroidism – Central nervous system disease – Long QT syndrome • Negative U waves – Strongly suggestive of organic heart disease – May be seen in patients with ischemic heart disease Waveforms – Review Segments & Intervals – Review Artifact • Distortion of an ECG tracing by electrical activity that is noncardiac in origin • Can mimic various cardiac dysrhythmias, including ventricular fibrillation • Patient evaluation essential before initiating any medical intervention Causes of Artifact • Loose electrodes • Broken ECG cables or broken wires • Muscle tremor • Patient movement • External chest compressions • 60-cycle interference Artifact – Loose Electrodes – Muscle Tremor – 60-cycle Interference Rate Measurement Six-Second Method • Ventricular rate – Count the number of complete QRS complexes within a period of 6 seconds – Multiply that number by 10 to determine the number of QRS complexes in 1 minute • May be used for regular and irregular rhythms Large Box Method • Count the number of large boxes between two consecutive waveforms (R-R interval or P-P interval) and divide into 300 • Best used if the rhythm is regular Large Box Method Small Box Method • Count the number of small boxes between two consecutive waveforms (R-R interval or P-P interval) and divide into 1500 • Time consuming, but accurate Sequence Method • Select an R wave that falls on a dark vertical line – Number the next 6 consecutive dark vertical lines as follows: • 300, 150, 100, 75, 60, and 50 – Note where the next R wave falls in relation to the 6 dark vertical lines already marked—this is the heart rate Rhythm/Regularity • When analyzing a rhythm strip, determine: – Atrial (P-P intervals) rhythm – Ventricular (R-R intervals) rhythm • If the rhythm is regular, the R-R intervals (or P-P intervals if assessing atrial rhythm) are the same – Generally, a variation of plus or minus 10% is acceptable Terminology • Essentially regular rhythm • Irregular rhythm • Regularly irregular rhythm • Irregularly irregular rhythm Analyzing a Rhythm Strip Assess the Rate • What is the rate? – Determine ventricular rate (R-R intervals) – Determine atrial rate (P-P intervals) • A “tachycardia” exists if the rate is greater than 100 bpm • A “bradycardia” exists if the rate is less than 60 bpm Assess Rhythm/Regularity • Ventricular rhythm – Measure the distance between two consecutive R-R intervals – Compare with other R-R intervals • Atrial rhythm – Measure the distance between two consecutive P-P intervals – Compare with other P-P intervals • Variation of plus or minus 10% is acceptable Identify & Examine P Waves • Look to the left of each QRS complex • Normally: – One P wave precedes each QRS complex – P waves occur regularly and appear similar in size, shape, and position PR Interval (PRI) • Measured from the point where the P wave leaves the baseline to the beginning of the QRS complex • Normal PR interval is 0.12 to 0.20 second • If the PR intervals are the same, they are said to be constant • If the PR intervals are different, is there a pattern? – Lengthening – Variable (no pattern) QRS Complex • Identify the QRS complexes and measure their duration – Narrow (normal) if it measures 0.10 second or less – Wide if it measures more than 0.10 second QT Interval • Measure in the leads that show the largest amplitude T waves – Measured from the beginning of the QRS complex to end of the T wave – If the measured QT interval is less than half the R-R interval, it is probably normal ST Segment • Usually isoelectric in the limb leads • To determine ST segment elevation or depression, measure at a point 0.04 second (one small box) after the end of the QRS complex – Use the PR segment as the baseline T Waves • Are the T waves upright and of normal height? • The T wave following an abnormal QRS complex is usually opposite in direction of the QRS • Negative T waves suggest myocardial ischemia • Tall, pointed (peaked) T waves are commonly seen in hyperkalemia Interpret Rhythm & Evaluate Clinical Significance • Interpret the rhythm – Specify the site of origin (pacemaker site) of the rhythm (sinus) – Specify the mechanism (bradycardia) and ventricular rate • For example: “sinus bradycardia at 38/min” • Evaluate the patient’s clinical presentation to determin