EKG Big Concepts PDF
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Uploaded by SportyTruth2903
Thomas Jefferson University
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Summary
This document details EKG concepts, focusing on various heart rhythms and related pathologies. It describes normal sinus rhythm, different types of arrhythmias, blocks, and hypertrophy. It is relevant to medical students learning about cardiac analysis.
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SINUS RHYTHMS Normal sinus rhythm Sinus bradycardia HR < 60 bpm Sinus tachycardia HR > 100 bpm Sinus arrest...
SINUS RHYTHMS Normal sinus rhythm Sinus bradycardia HR < 60 bpm Sinus tachycardia HR > 100 bpm Sinus arrest Patho SA node is sick and stops pacing completely → >3sec flatline Sinus arrhythmia tiology E atho P ormal breathing!! N Lung stretch receptors activate SNS → HR speeds up Exhalation causes PNS stimulation → HR slows down ATRIAL & JUNCTIONAL RHYTHMS Atrial fibrillation Etiology Patho ed noncompliance M ultiple signals fromLEFT atriumbombard M Alcohol AV node → only some get transmitted to PE ventricles Heart strain Thyrotoxicosis **Atrial rate 350-450 Infection!! No P waves (replaced by f waves) Irregularly irregular Narrow QRS Atrial flutter atho P Extremely irritable signals coming fromRIGHT atrium *Atrial rate 250-300 Best seen in II, III, aVF, V1 “SAW TOOTH” pattern!! (P waves replaced by F waves) Rhythm still regular Junctional escape beats Patho inus pause → junctional foci take over and make asingularbeat → then back to normal S sinus rhythm Sinus pause →inverted or hidden P wave→ normal sinusrhythm Junctional rhythms Patho Sinus pause/arrest → junctional foci take over and creates a rhythm (consecutive beats) Sinus pause → consecutiveinverted or hidden P wave SLOW rate!!! (40-60) Premature atrial contractions (PACs) Etiology Patho Increased SNS / decreased PNS stimulation Irritable foci in atria → QRS complex comes Adrenergic stimuli (caffeine, cocaine) earlier than expected Hyperthyroidism Digoxin Alcohol Can be bigeminy / trigeminy Early weird P waves Premature junctional contractions Etiology Patho Increased SNS / decreased PNS stimulation Irritable junctional foci → QRS complex Adrenergic stimuli (caffeine, cocaine) comes earlier than expected Hyperthyroidism Digoxin Alcohol Early P wave (inverted or hidden) Atrioventricular reentrant tachycardia (AVRT aka Wolff Parkinson White) Etiology Patho Males ccessory pathway (Bundle of Kent)allows impulsesto A sneak from atria to ventricle → early ventricular depolarization * think Bundle of Kent is EZ pass and normal AV node is cash toll booth Delta wave!!! (slurred QRS onset) Short PR & wide QRS Atrioventricular nodal reentrant tachycardia (AVNRT aka SVT) Etiology Patho Females V node has2 pathways→ impulse will enter a loopcircuit A in AV node → atria and ventricles just there for the ride athways: P Alpha = slow & short refractory Beta = fast & long refractory Never shown one in lecture but for reference: Multifocal atrial tachycardia Etiology Patho OPD!!! C acer site in heart shifts back and forth from P Elderly SA node to 2+ atrial pacer sites →3+ CAD, valvular disease, HTN, cor pulmonale different P wave morphologies Digoxin toxicity Decreased K+ and Mg+ TACHY!!! Triangle P waves in lead II = think COPD VENTRICULAR RHYTHMS Asystole Patho No ventricular depolarization happening at all → “flatline” aka dead Premature ventricular contraction (PVCs) Etiology Patho ow oxygen!!!(think poor ventilation/MI) L Irritable ventricular foci → asymmetric Low K+ depolarization of ventricle →wide QRS >6/min = pathological (low oxygen warning!!) Ventricular bigeminy Ventricular trigeminy Ventricular tachycardia Etiology Patho More hypoxic 3+ PVCsin a row!! ustained VT > 30 sec S Non-sustained VT < 30 sec Rate 150-250 Ventricular fibrillation Patho ultiple ventricular focifiring → ventricles arejust quivering and not actually producing any M beats (no pulse) → cardiac arrest!! Kid scribbling (no pattern at all!) Ventricular flutter atho P ingle ventricular focifires → ventricular rate 250-350 S Sinusoidal curve (looks like VT butfaster!!) Torsades de Pointe Etiology Patho ecreased K+ D competing ventricular irritable foci → poor 2 Congenitallong QT cardiac output Drug-induced long QT (quinine / procainamide / methadone / lithium / TCA) ATRIOVENTRICULAR BLOCKS First-degree block Patho Delay between atria and ventricle depolarization →PR > 0.2 sec *not technically a block Mobitz type-I (Wenckebach) atho P rogressively lengthening PR intervals→ QRS is eliminated P Mobitz type-II atho P Block below AV node (Purkinje, His, bundle branches) → normal PR interval butsuddenly eliminated QRS Third degree block Patho Complete dissociationbetween atria and ventricle→ PR & QRS not communicating at all waves come from normal sinus origin P QRS come from automaticity foci Brady!! HYPERTROPHY Atrial hypertrophy Etiology Patho eft atrial enlargement: mitral valve stenosis, HTN L Atrium is thick →P > 2.5 mm Stressor Infarction Heart failure Look at V1:Diphasic P wave!!(bigger upward hump= R atrial enlargement / bigger downward hump = L atrial enlargement) Right ventricular hypertrophy Etiology Patho tressor S ventriclewall is super thick → R Infarction depolarization toward leadV1(huge R wave) Heart failure Inverted Tscan also be seen (usually in LVH) Strain pattern = ST depression + odd hump pattern Left ventricular hypertrophy Etiology Patho tressor S ventriclewall is super thick → big QRS L Infarction deflections in chest leads (R peaks atV4/V5) Heart failure (S in V1) + (R in V5) > 35 mm Touching QRS!! Inverted Tscan also be seen (usually in LVH) Strain pattern = ST depression + odd hump pattern MYOCARDIAL ISCHEMIA & INFARCTION Right bundle branch block Patho lock in right bundle branch → delays ipsilateral ventricular depolarization →wide bunny ear B looking QRS in V1/V2 QRS > 0.12 sec Left bundle branch block Patho lock in left bundle branch → delays ipsilateral ventricular depolarization →wide curved B bunny ear looking QRS in V5/V6 QRS > 0.12 sec Angina pectoris (stable angina) Patho Decreased coronary blood flow (but no infarction) → chest pain on exertion ST segment depression / T wave inversion when sx present Unstable angina atho P ecreased coronary blood supply from partial thickness blockage in endocardium → ischemia D Inverted T waves & ST segment depression!! T waves must be inverted inaVR & V1(and sometimesIII) ST depression = more ischemia Myocardial Infarction: ≥ 2 mm elevation in men / ≥ 1.5 mm in women in V2-V3 ≥ 1 mm elevations in other contiguous limb or chest leads Anterior wall MI Etiology Patho Lack of blood flow to LAD artery Infarction → ST elevations inV3-V4 Anteroseptal region MI Etiology Patho Lack of blood flow to LAD artery Infarction → ST elevations inV1-V4 Inferior wall MI Etiology Patho ack of blood flow to right coronary artery L Infarction → ST elevations inII, III, aVF (which supplies SA, AV, & Bundle of His) If elevations in III > II → right sided infarction! III > II → so right-sided MI Lateral wall MI Etiology Patho Lack of blood flow to left circumflex artery Infarction → ST elevations inI, aVL, V5, V6 Posterior wall MI atho P IfST depressions in V1/V2→ get posterior EKG tosee if there is infarction on posterior side of the heart (ST elevations) Speed of tachy-arrhythmias Paroxysmal 150-250 Flutter 250-350 Fibrillation 350-450 Foci speeds Atrial 60-80 Junctional 40-60 Ventricular 20-40
