Cardiology Dysrhythmias and Basic ECGs PDF

Cardiology: Dysrhythmias and Basic ECG’s BMS200 Week 9 Learning Outcomes Analyze the following characteristics of a normal ECG: Heart rate and determination of rhythm P-R, QRS, Q-T intervals Normal waveforms in the P, QRS, and T waves Describe how triggered activity, abnormal a...

Cardiology: Dysrhythmias and Basic ECG’s BMS200 Week 9 Learning Outcomes Analyze the following characteristics of a normal ECG: Heart rate and determination of rhythm P-R, QRS, Q-T intervals Normal waveforms in the P, QRS, and T waves Describe how triggered activity, abnormal automaticity, and re-entry contribute to the pathophysiology of the most common dysrhythmias Describe the basic epidemiology, pathogenesis, clinical features, ECG findings, and prognosis of the following supraventricular dysrhythmias: Atrial fibrillation, atrial flutter, sinus tachycardia, and paroxysmal supraventricular tachycardia Learning Outcomes Describe the basic epidemiology, pathogenesis, clinical features, ECG findings, and prognosis of the following ventricular dysrhythmias: Premature ventricular contraction, idioventricular rhythm, ventricular tachycardia, ventricular fibrillation, torsades de pointes Describe the basic epidemiology, pathogenesis, clinical features, ECG findings, and prognosis of the following types of conduction block: 1st degree heart block, 2nd degree heart block, 3rd degree heart block Describe the ECG findings that are typical of cardiac ischemia and relate these findings to basic vascular territories Briefly describe the pharmacologic mechanism of action and related adverse effects of common anti-arrhythmic medications Discuss the pathophysiologic contribution of chronic inflammation and myocardial fibrosis to the development of common dysrhythmias What do you think is happening? Did you “catch” a serious dysrhythmia in your colleague? You’ve just purchased a brand-new electronic stethoscope that records heart sounds and can transmit a simple two-lead ECG to your smartphone. The audio is great when you test it on yourself, but the appearance of the ECG seems to change drastically depending on where you place it on your chest. Your classmate asks you to try it out on them – you record the following trace when the device is placed on their chest: Pre-Assessment: What electrical event is occurring during the Q-T interval of an ECG? A. The plateau phase of the atrial myocyte action potential B. The initial depolarization of the atrial myocyte C. The plateau phase of the ventricular myocyte action potential D. Repolarization of the ventricular myocyte Pre-Assessment: Where in the heart would you find the cells that usually perform the role of the cardiac pacemaker? A. The right atrium, close to the entrance of the superior vena cava B. The left atrium, close to the entrance of the right pulmonary veins C. Close to where the tricuspid valve attaches next to the interventricular septum D. Close to where the mitral valve attaches next to the interventricular septum Review: Electrocardiogram (ECG) Recording of Electrical Impulses: An electrocardiogram (ECG or EKG) captures electrical activities produced by the heart by placing electrodes on the skin, which detect the voltage changes resulting from the depolarization and repolarization of the cardiac muscle. Size of the Waves: The amplitude of the waves on an ECG represents the amount of electrical activity occurring in the heart muscle. Larger waves indicate greater amounts of electrical activity, which typically correspond to larger areas of myocardial tissue being activated. This can give insights into the health and functionality of the heart Review: Electrocardiogram (ECG) Direction of Voltage Changes: The upward or downward deflections from the baseline reflect the direction of electrical conduction through the heart. An upward deflection indicates that the electrical impulse is moving toward the electrode a downward deflection suggests that it is moving away. This is crucial for understanding how different parts of the heart are activating Conducting/Automatic Tissues: The conducting tissues (like the SA node, AV node, and bundle branches) are smaller and generate less electrical activity than the myocardial tissues, which makes them difficult to register on an ECG. The ECG primarily reflects the activity of the larger myocardial cells that contract and pump blood. Review: Electrocardiogram (ECG) Duration of the Waves: The duration of the waves (P wave, QRS complex, T wave) provides important information about the timing of electrical events in the heart. For example, a prolonged QRS complex may indicate a delay in ventricular conduction a prolonged QT interval could suggest a risk of arrhythmias. Monitoring the duration of these waves is essential for assessing cardiac health and function. Review: What does ECG measure? ECG leads measure the extracellular current that travels from depolarized cells to polarized (resting) cells Differences in charge at the extracellular border of the plasma membrane ECG leads only “notice” changes in membrane potential “plateaus” do not register as waves (i.e. phase 4, phase 2 of a myocyte) Technically, they compare the difference in voltage between different regions of the heart Review: ECG Timing How do the ECG waves and intervals correspond to the excitation along the conduction pathway? Recall Cardiac Physiology lecture and the role of the AV delay: Allowing time for atrial contraction and optimizing ventricular filling  ECG: Amplitude and Vectors Amplitude: The amplitude refers to the height of the waves seen on the ECG. It indicates the magnitude of the electrical potential difference across different parts of the heart. Length of vector: The length of the vector corresponds to the magnitude of the electrical potential difference (size of difference) between two points in the heart during depolarization or repolarization. The direction of the vector indicates the orientation of the electrical activity (which way the electrical impulse is traveling). Placement of ECG Leads - 1 ECG leads are placed to give a “3-D” view of the electrical activity of the heart Coronal view (left and right arms, left leg) Cross-sectional view (precordial leads) The vector of depolarization is displayed relative to the placement of the ECG lead Placement of ECG Leads - 2 Bipolar leads compare voltage changes between leads. i.e., lead I compares voltage changes between the right arm and the left arm “Unipolar” (precordial leads) leads compare voltage changes between a lead (surface of chest wall) and the center of the heart ECG: X and Y axis Electrical potential changes across the heart over time Time – x-axis, in seconds Electrical potential changes – voltage in mV, y-axis “little box” – 0.1 mV high, and 0.04 seconds wide Each “big box” is 0.5 mV by 0.2 seconds Approach to Interpreting ECG Best to approach them in an organized fashion: 1. Determine rate (Step 1) Two methods: Divide 300 by number of large boxes between R-waves (R-R interval) = rate 5 large boxes = 1 second, 50 large boxes = 10 seconds, so # of R waves in 50 large boxes X 6 (60 seconds in 1 minute) (somewhat cumbersome) 2. Determine rhythm (Step 2) Where are the impulses coming from (P-wave before the QRS, or something else going on)? Is it regular? If irregular, is it regularly irregular, or irregularly irregular? Is it a sinus rhythm? (what is a sinus rhythm?) Step 2 – Rhythm Normal Sinus Rhythm? Regular rhythm or Best determined by looking at a rhythm strip regularly irregular Usually lead II, often a 10-second recording (50 rhythm big boxes) Each P-wave is followed Regular or irregular? by a QRS regular – can be a normal finding, artificial FYI - P-wave has a pacemakers can give a regular rhythm as well normal axis and is irregular – irregularly irregular or regularly the same shape irregular? each beat regularly irregular can be normal, as PR interval is constant heart rate varies with respiration – there QRS interval is < 100 ms is a pattern to the irregular rhythm (2.5 small boxes) irregularly irregular is the hallmark of a Each QRS has a P-wave number of tachycardias, most commonly before it atrial fibrillation and is abnormal Normal sinus rhythm = pacemaker is the SA node, no abnormalities of conduction A Normal 12-Lead ECG Rhythm strip Step 3 – Intervals (1) 3. Look at the intervals Are they widened or shortened? Often a change in an interval is a result of a conduction system problem Major intervals of interest: P-R interval – usually prolongation = AV-nodal dysfunction It can be decreased, though in situations where there are abnormal “connections” between the atria and ventricles QRS interval – delay in ventricular excitation QT interval – repolarization abnormalities (as a risk factor for torsades de pointes) We consider S-T intervals in the “waves” portion Step 3 – Intervals (2) The intervals can often tell you much about where the conduction problem lies narrow QRS = usually normal intraventricular conduction pathways normal QT = normal ventricular repolarization normal P-R = no abnormal delays/conduction at the AV node QT varies with Interval Seconds Small boxes heart rate… so how do you figure out a P-R (P-Q) 0.12 – 0.2 3-5 normal QT?? QT corrected = QRS 0.08 – 0.10 2 – 2.5 QT___ QT QTc = QT/√R-R Less than half of R- √R-R R usually good QT interval divided by square root of R-R interval Step 4 – Waves 4. Look at the waves Are they positioned normally (up or down)? Are they “funny-shaped” or do they change morphology from beat to beat? Are the waves larger/smaller than normal? Are there waves present that normally aren’t present in a healthy person? NOTE: when examining the waves, it is important to look at them in all leads – they will change from lead to lead Step 4 – Q-Waves Abnormal Q-waves – if these abnormalities are seen, indicates current or prior MI: “significant” Q-waves are: wide (> 1 small box or 0.04 sec) large (> 2 mm deep or > 25% of the total size of the QRS) or > 1/3 height of the R wave in leads V1 – V3 are abnormal, always Since MI is so common, it is key to recognize these Step 4 – ST segments Helps to think about ST segment with waves instead of intervals usually with intervals you’re thinking about times that are shorter or longer than normal with the ST segment you’re concerned about elevation or depression Your biggest concern is ruling out an infarct, but many things can cause ST depression or elevation ST Depression and ST Elevation S-T depression S-T elevation NSTEMI or opposite STEMI or opposite lead from site of lead from site of STEMI NSTEMI digoxin pericarditis hypokalemia LBBB RBBB or LBBB LVH RVH or LVH normal if small implanted implanted pacemaker pacemaker Raised ICP hyperkalemia (intracranial PE pressure) Raised ICP Step 4 – T-Waves T-waves – many abnormalities can The differential for T-wave occur, but they should be upright in changes is large, and depends all of the leads except for V1 on a few things: Some basic abnormalities age – T-wave inversions are normal in kids tall T-waves hyperkalemia ischemia and “metabolic” strain – i.e. the heart is early myocardial infarction working hard with not small T-waves enough to “feed” it hypokalemia electrolyte abnormalities Inverted T-waves what pattern of leads the myocardial infarction T-wave findings appear in ventricular hypertrophy (i.e. does it correspond to a vascular territory)? Step 4 – P-Waves P-wave abnormalities P-wave shapes that change from beat-to-beat (indicates the “pacemaker” is not the same each beat) P-wave absence – think atrial fibrillation FYI - Atria enlarge for the More P-waves than QRS complexes same reason other heart – heart block chambers enlarge FYI: P-waves that indicate atrial Increased atrial “afterload” hypertrophy see diagram for right and left atrial i.e., a stenotic AV valve hypertrophy patterns Atria are “stretched” by many ECGs will also determine an more fluid than usual atrial axis – between 0 and +75 failure of the ventricle degrees General Pathophysiology of Dysrhythmias (1) Re-entry: Normal depolarization wave enters a pathological space in the heart (i.e., area of ischemic injury), contraction cannot occur because the tissue is not functioning properly BUT it may allow a slower conduction of this wave towards healthy tissue IF healthy cardiac tissue have completed their original refractory period, then this wave of depolarization can trigger an action potential called “re-entry” and resulting in tachycardia (1) conditions that slow conduction but not block (2) conditions that shorten refractory period of healthy cells General Pathophysiology of Dysrhythmias (2) Ectopic Foci or Abnormal Automaticity: Scar tissue (i.e., post-MI or other injury) changes local plasma electrolyte concentrations or their movements across channels resulting occurrence of automaticity in previously non- pacemaker cells – ectopic foci Inhibition of Na+/K+ pump results in intracellular accumulation of Na+ and Ca2+ which partially depolarize the membrane Can occur in healthy individuals occasionally Situations that promote abnormal automaticity: (1) Increase of intracellular Ca2+ (2) Decrease of K+ conductance at rest Catecholamines (fatigue, stress), hyperkalemia, hypercalcemia, heart distention General Pathophysiology of Dysrhythmias (2) Ectopic Foci or Abnormal Automaticity: Cardiac Metabolism: IR K+ channels get inactivated by intracellular ATP (when metabolism is ok, no extra K+ is effluxing from the myocyte) and get activated by intracellular ADP (when the cardiac myocyte is metabolically stressed i.e., ischemia) allowing K+ to efflux and thus reducing the refractory period General Pathophysiology of Dysrhythmias (3) Triggered Activity: Ventricular arrhythmia, whereby a normal action potential is followed by an abnormal depolarization of ventricular muscle that occurs before the original action potential has completed its course Example: premature ventricular contractions (PVC) Conditions that favor this: Situations that prolong action potential duration Bradycardia and reduced or prolonged phase 3 (K+ efflux/ repolarization) Tachycardia and increased calcium accumulation within myocyte Chronic Inflammation and Myocardial Fibrosis and Dysrhythmias Chronic inflammation Immune cells (macrophages, mast cells, T-cells) can promote myocardial repair (as in acute inflammation) OR fibrosis by releasing cytokines that direct function of cardiac fibroblasts Cardiac fibroblasts are triggered to transform into myofibroblasts This transformation is supported by fibrosis-promoting factors: angiotensin II, aldosterone, catecholamines, connective tissue growth factor, endothelin, platelet-derived growth factor, reactive oxygen species, TGF-Beta and inflammatory cytokines Myofibroblasts produce more ECM and secrete substances that promote fibrosis Myocardial fibrosis leads to remodeling of myocardial collagen May cause local delay in portion of the heart Promotes reentry Supraventricular Dysrhythmias Atrial fibrillation Most common type of arrhythmia Risk Factors: age, hypertension, chronic lung or heart disease, congenital heart disease, increased alcohol, sleep apnea Pathophysiology: atrial structural (ECM, fibrous tissue deposition) and electrical (tachycardia, shortening of refractory period) remodeling leading to ectopic foci Once fibrillation occurs ! (1) turbulent blood flow (2) reduced effectiveness of heart’s function (3) risk increased thrombus formation Sx: asymptomatic OR chest pain, palpitations, dyspnea, tachycardia, nausea, dizziness, diaphoresis, fatigue ECG: narrow complex “irregular irregular” pattern with no distinguishable p-wave Prognosis: leading cardiac cause of stroke Atrial Fibrillation ECG 1 Narrow complex “irregular irregular” pattern with no distinguishable p-wave Atrial Fibrillation ECG 2 Narrow complex “irregular irregular” pattern with no distinguishable p-wave Supraventricular Dysrhythmias Atrial flutter VERY common Pathophysiology: re-entry mechanism due to fibrosis (1) Different refractory period (2) Fast and slow conductions – together these allow for re- entry ECG: Fast atrial rate (300 bpm) with fixed or variable ventricular rate Flutter waves without an isoelectric line in between QRS complex SX: fatigue, palpitations, syncope Supraventricular Dysrhythmias Sinus tachycardia Normal rhythm, heart beats faster and results in increased cardiac output Often due to exercise or stress; concerning when occurs at rest Physiological (normal): catecholamines due to exercise, stress, pain, or anxiety Pathological (concerning) Cardiac causes include myocarditis, coronary artery syndrome and others Non-cardiac: pulmonary embolism, hypoxia, hypoglycemia, dehydration, infection, electrolyte imbalance, shock and others Supraventricular Dysrhythmias Paroxysmal supraventricular tachycardia (SVT) Intermittent (paroxysmal) episodes of supraventricular tachycardia with sudden onset and termination Originate either in the atria or AV node and can create either regular or irregular rhythms MANY Etiologies: hyperthyroidism, caffeine, cocaine, structural heart disease, rheumatic dz, PE, pneumonia, anxiety, MVP, myocarditis, pericarditis… Pathophysiology: most often re-entry, sometimes due to increased automaticity or trigger Re-entry circuits: SA node, atria, AV node or accessory pathway SX: dizziness, syncope, nausea, dyspnea, palpitations, neck pain, chest discomfort, anxiety, diaphoresis Prognosis: good if no structural problems, otherwise can lead to heart failure, MI or pulmonary edema Paroxysmal supraventricular tachycardia (SVT) – ECG ECG: Regular rhythm Fast heart rate (150-250 bpm) Often narrow QRS complex Ventricular Dysrhythmias Premature ventricular contraction (PVC’s) Heartbeat is initiated by Purkinje fibers Can occur in isolation or as a double (Normal beat (QRS) – PVC – PVC – Normal beat (QRS).) or triplet (Normal beat (QRS) – PVC – PVC – PVC - Normal beat (QRS).) More than three PVC’s are termed ventricular tachycardia Common (FYI 1-4% of population) Etiology: often unknown, caffeine, excess catecholamines, anxiety, electrolyte imbalance, alcohol, sleep deprivation, structural heart disease, anemia, hyperthyroidism Pathophysiology: Ectopic nodal automaticity Re-entry Triggered activity Ventricular Dysrhythmias Premature ventricular contraction (PVC’s) SX: “Skipped heartbeat” followed by fluttering sensation (palpitation), though majority are asymptomatic Lightheadedness, chest pain, chest discomfort, dyspnea, anxiety (syncope very rare) Prognosis: if no heart disease – no problem, if heart disease than increased mortality risk ECG: abnormal and wide QRS complex occurring earlier than expected in cardiac cycle Ventricular Dysrhythmias Idioventricular rhythm Slow regular ventricular rhythm with a rate of less than 50 bpm (typically), absence of P waves, and a prolonged QRS interval – the SA node isn’t working, and the ventricle takes over! Etiology: heart block, electrolyte abnormalities, medications, during reperfusion after MI Pathophysiology: Suppression of SA and AV nodes that allow ventricles to take over and generate rhythm (50 bpm) SX: mostly asymptomatic OR palpitations, lightheadedness, fatigue or syncope ECG: wide QRS complex, rate < 50 (idioventricular) or 50-100 (accelerated idioventricular rhythm) Ventricular Dysrhythmias Ventricular Tachycardia (VT) Most commonly due to ischemic heart disease SX: palpitations, chest pain, dyspnea, syncope, cardiac arrest ECG: Greater than 3 consecutive ventricular beats with rate of 100-250 bpm and wide QRS complex Potentially life threatening (sudden cardiac death due to progression to ventricular fibrillation) Pathophysiology: Diverse group of tachycardia’s Re-entry (most common) – scar related Triggered activity and enhanced automaticity Ventricular Dysrhythmias Ventricular tachycardia (VT) Pathophysiology and Prognosis: Leads to low cardiac output due to significant reduction in preload and thus stroke volume If heart is hypoperfused it may lead to ventricular fibrillation or cardiomyopathy, heart failure or other complications Ventricular Dysrhythmias Ventricular Fibrillation Irregular (uncoordinated) electrical activity, ventricular rate >300 bpm, which compromises cardiac output significantly! Leads to sudden cardiac death (fatal within minutes if not treated – defibrillator and CPR) Etiology: myocardial infarction, electrolyte abnormalities, congenital QT abnormalities, alcohol use, cardiomyopathies, hypothermia and others Pathophysiology: Increased automaticity by Purkinje cells Triggered activity Possible re-entry Ventricular Dysrhythmias Ventricular Fibrillation SX: chest pain, dyspnea, nausea, vomiting prior to sudden collapse (unconscious, unresponsive, no pulse) ECG: (1) fibrillations of various amplitudes and shapes (2) no identifiable P wave, QRS complex or T wave (3) heart rate between 150-500 bpm Ventricular Dysrhythmias Torsades de pointes Form of ventricular tachycardia ECG: polymorphic; “twisting” varying in amplitude QRS complexes Associated with QTc prolongation (>500 ms) Congenital or acquired (LOTS of medications can cause the QTc to be prolonged) Rhythm may terminate spontaneously or progress to ventricular fibrillation Pathophysiology is not fully understood but believed to be due to prolonged repolarization phase due to delay in K+ efflux. If an ectopic beat occurs during this time, it can trigger Torsades de pointes SX: most asymptomatic OR syncope, palpitations, dizziness Cardiac death is the presenting sx in 10% of cases Conduction Block Types of arrhythmias characterized by a delay or complete block in the electrical conduction system of the heart, particularly affecting the atrioventricular (AV) node or the bundle branches. They can lead to inadequate heart rate and may cause symptoms such as dizziness, fatigue, or syncope.  Types of Heart Blocks First-Degree AV Block: Description: Prolonged PR interval (>200 ms) on ECG but every impulse is conducted to the ventricles. Symptoms: Usually asymptomatic and often benign. Second-Degree AV Block: Type I (Wenckebach): Description: Progressive prolongation of the PR interval until a QRS complex is dropped. Symptoms: Often asymptomatic but can cause occasional dizziness. Type II: Description: Consistent PR intervals with sudden drops of QRS complexes (can be more serious). Symptoms: May lead to bradycardia and require monitoring or pacemaker.  Types of Heart Blocks Third-Degree AV Block (Complete Heart Block): Description: No impulses from the atria reach the ventricles, resulting in independent atrial and ventricular rates. Symptoms: Can cause severe bradycardia, syncope, or heart failure; often requires pacemaker insertion. Conduction Block 1st degree AV Heart Block Abnormally slow conduction through the AV node resulting in a prolonged P-R interval (>.20 seconds) without any disruptions of atrial or ventricular conduction Typically, asymptomatic and does not require treatment as typically does not result in complications Possible caused by increased vagal tone (younger patients) or fibrotic changes in cardiac conduction (elderly patients) Conduction Block 2nd degree Heart Block Delay in conduction of the AV node resulting in prolonged PR interval and missing QRS Mobitz Type 1 (aka Wenckebach) No structural problem, high vagal tone but can be due to cardiac problems ECG: progressively prolonged PR interval until finally the action potential wave can’t get through AV node and there is not QRS complex following P wave, then process restarts Mobitz Type 2 Mostly seen in patients with structural heart disease Can progress to complete heart block (3rd degree) ECG: constant PR interval with 1 P wave being dropped every certain number of beats (but only 1!), as in its not followed by a QRS  Conduction Block 2nd degree Heart Block SX: can be asymptomatic OR fatigue, dyspnea, chest pain, presyncope or syncope or even sudden cardiac arrest (Mobitz Type 2) Conduction Block 3rd degree (Complete) Heart Block Complete loss of communications between atria and ventricles via AV node (fairly rare) Cardiac output is significantly reduced – fatal if not treated promptly (FYI most treated with pacemaker) Either the AV node or the Purkinje fibers step in to act as pacemakers for the ventricles Bradycardia