Lecture 1 Expanded Notes (Prof Garino) PDF

Exam 1 Cardiac Dysrhythmias CAD ACS Inflammatory & Structural Heart Disorders  Conduction System of the Heart 4 property’s of cardiac cells Allow the conduction system to start an electrical impulse => send it though the cardiac tissue & stimulate the...

Exam 1 Cardiac Dysrhythmias CAD ACS Inflammatory & Structural Heart Disorders  Conduction System of the Heart 4 property’s of cardiac cells Allow the conduction system to start an electrical impulse => send it though the cardiac tissue & stimulate the heart muscle contractions 1) Automaticity - ability to initiate an impulse spontaneously & continuously (pacemaker cells) 2) Excitability - ability to be electrically stimulated 3) Conductivity - ability to conduct impulses to the next cell in an orderly manner 4) Contractility - cell has ability to mechanically contract to an impulse Any deviation/changes from the normal function of these will induce rhythm disturbances/dyrrhythmias Conduction Pathway 1) Normal conduction starts @ SA node (pacemaker cells) in Upper R.Atrium near entrance of vena cava -> 2) conduction spreads over R. & L. Atrium via interatrial & intermodal pathways -> causing atria contractions => 3) conduction travels to AV node -> 4) through bundle of HIs - > 5) down to L. & R. bundle branches -> 6) finally ends @ purkinje fibers -> transmit conduction to ventricles => ventricles contract & produce cardiac output 3 pacemaker cells - property of automaticity Continually generate new action potentials that travel across the heart to initiate depolarization aka contraction All 3 pacemaker cells must work in sequence & synchronously for normal cardiac rhythm to produce adequate CO AV node Purkinje fibers SA node Intrinsic rate: 20-40 bpm Primary pacemaker Acts as triage station (2nd pacemaker to receive impulses from SA node) Final destination of Intrinsic rate of 60-100 bpm conduction that initiates in Setting HR & Rhythm R&L ventricles P wave - When SA node fires => Located in intraatrial septum R. Atrium contracts If AV node fails to fire, then Intrinsic rate of 40-60 bpm Atrial kick - how well left atrium ejects blood purkinje fibers become into left ventricle dominant pacemaker cells w/ Supplied by Right Coronary Artery (Normal transfer of 20-30% blood = leading 20-40 bpm to good CO when L. Ventricle contracts/ AV junction consists of AV node & depolarizes bundle of his If SA node has unorganized chaotic When SA node fails to fire, then AV conduction like Afib, Aflutter, SVT, you can node becomes dominant pacemaker lose atrial kick => & beats 40-60 bpm 1) Less blood going to L ventricle 2) Less CO If AV node acts as triage, stop & delay 3) Less Blood to organs & brain = Supraventricular Disorders (SVT) conductions to generate a ventricular eventually syncope When there’s erratic high speed contraction (the delay is to allow Loss of atrial kick can be identified by conduction between SA node, AV ventricles enough time to fill with abnormal P wave node & AV junction blood before they contract) In Afib, HR increases to compensate for low Sympathetic & Parasympathetic NS W/out AV node delaying conductions CO due to loss of Atrial kick Controls the firing rate of the SA = ventricles become eratic (Vtach or Other factors affecting atrial kick: mitral & node & AV node Vfib ) =>resulting in less ventricular aortic valve disorders filling time & decreased CO Have to work in rhythm PR interval (0.12-0.20 sec) = Speed of conduction from AV node to purkinje fibers (Time from beginning of P wave (atrial depolarization) to beginning of QRS complex (ventricular depolarization)  K+ cat " K+ F- cat µ ,efÑy×iÑ+ Ventricular ÷ Cardiac ⇐ Nat contraction. Cell Plateau. Ñ at µ¥Ñ How the heart contracts 3 ions play a significant role in how ventricles contract (K, Na, Ca) Pacemaker cells generate new action potentials continuous & propagate conduction throughout cell (myocyte) Some K is leaking out b/c cell wants to be negative removing extra K (mostly K inside the cell) Action Potential Process Start Phase 4: At -90mV = resting membrane potential (RP) Inside of the cell is more negative or polarized (no electrical stimulus) Once pacemaker cells fire, Na channels open & influx of Na enters the cell (mostly K+ in the cell) until -70mV = threshold potential (TP) Phase 0 = Depolarization phase (initiation of ventricular contraction) Influx of Na rises the potential to +20mV => cardiac muscle has depolarized Phase 1: Na channel closes (preventing more Na entering) To balance charges in cell => K channels open, more K exit out the cell (diffusion to balance charges) Phase 2: Calcium channel opens & positive calcium enters the cell counteracting the K efflux [(balancing & stabilizing the charges = flattening the wave (phase 2 is the plateau phase)] The influx of Ca ions generates ventricular contraction During contraction phase => phase of absolute refractory -> cells cannot respond to another stimulus & produce another AP Phase 3: Ca channels close, beginning repolarization phase K channel remains open & massive K efflux => cell becoming more negative and negative Ca that came in needs to exit => Ca channel pumps are pumping Ca out the cell (b/c cell wants to be negative/ polarized) Allowing the ventricles to relax Relative refractory = possible to cause another AP during this phase (premature contraction = chambers not filled completely) Back in Phase 4: -90mV Na/K pump is moving Na out and K in Mg regulates the movement of ions through the channels w/in the cardiac tissues. Mg has to be normal for this to work properly. If Mg is off = can cause dysrhythmias Low Mg = torsades de pointes)  Electrocardiogram (ECG/EKG) Monitoring Each large box contains 25 small boxes (5 horizontal, 5 vertical) ECG = graphic tracing of the electrical impulses produced in the 1 small box is 1mm = 0.04 sec = 0.1mV heart Waveforms represent electrical activity produced by the 1 large box = 5mm = 0.2 sec = 0.5mV movement of ions across the membranes of heart cells representing depolarization (contractions) & repolarization 300 large boxes = 60sec = 1 min (ventricular relaxation) (1) P wave (max width 0.11 sec) = atrial depolarization (time of electrical impulse travels through the atrium, causing atrium contraction) Normally: upright in leads 1,2, aVF, V4,V6 Inverted in aVR (2) PR interval (0.12-20 sec) - measures beginning P wave to beginning QRS complex (reflects conductions through AV node) (3) QRS interval (0.6-10 sec) - 3 distinct waves (Q wave is 1st neg. deflection, (septal depolarization) R wave = 1st pos. deflection after Q wave, S wave = 1st neg deflection after R wave) - time taken for depolarization of both ventricules during systole - QRS = ventricular contraction (4) ST segment flat - from S wave to beginning of T wave - measures time of ventricular depolarization to repolarization - should be on isoelectric line=ALWAYS compare ST to isoelectric line = flat line) - isoelectric line = no electrical activity in this area - DO NOT compare ST segment to P wave b/c PR interval always changes (Blue Star) J Point - Point where QRS ends & ST begins - When we measure ST elevation => we measure by J Point Greater than 2mm (2 small boxes) if J point in leads => considered ST elevation - Measure ST segment at the J point (5) T wave - time for ventricle repolarization (ventricles relax) - should be upright (6) QT interval (0.33-0.43) - measured from beginning of QRS complex to end of T wave - represents time taken for entire electrical depolarization & repolarization of the ventricles - shortening QT= hypercalcemia ; elongated QT = hypocalcemia - tall & peaked (tented)= Hyperkalemia ; inverted = hypokalemia  12- Lead ECG/ QRS Morphologies rswa How leads record R R (+) electrode is the recording electrode 5 5 (-) electrode or reference point tells the camera which way to shoot If (+) electrode sees depolarization approaching it, records an upright complex QR If (+) electrode see depolarization heading away from it, negative complex (inverted : deflection) 9 Rs x 10 = 90bpm Assessment of Cardiac Rhythm R R R R R R R R R Have to Know how to calculate HR from strip! When measuring HR, count # of R’s in 6 sec, Then multiply by 10 1. P wave should be preceding QRS, QRS & P waves should be together 9. If QT is prolonged or shortened = check Ca labs 10. Is T wave upright/inverted or tall,peaked most important  Normal Sinus Rhythm P wave: Normal PR interval: Normal QRS Complex: Normal Rhythm: Regular Rate: 60-100 bpm Sinus Bradycardia Same as NSR, but SA node fires at rate less than 60 bpm P wave: Normal PR interval. Normal QRS Complex: Normal shape & duration Rhythm: Regular Rate: 100 bpm P wave: Normal PR interval: Normal QRS Complex: Normal Rhythm: Regular Rate: >100 (SA node fires more) Etiology? Exercise , Fever, pain, Hypotension, hypovolemic (compensate for low BP) Anemia Hypoxia Hypoglycemia Myocardial ischemia HF Hyperthyroidism Anxiety, Fear Epinephrine , NE, Atropine, Caffeine Theophylline (breathing treatment) Hydralazine (Vasodilators) Complications? Beating too fast = doesnt Dizziness, dyspnea, hypotension (heart beating so fast, it doesn’t properly fill ventricle) have time to fill Treatment: Treat underlying cause (fever & pain meds) IVF (might be hypotensive & heart increasing) Beta-blockers & Calcium channel blockers (reduce HR) Synchronized cardioversion (if unstable) ( Above) ( Fast HB) Supraventricular Tachycardia (SVT) Dysrhythmia due to short circuit in upper chamber (Before bifurcation of bundle of his) Sometimes triggered by premature atrial contractions P wave: Abnormal or Hidden PR interval: Shortened/Normal QRS Complex: Normal Rhythm: Regular Rate: 151-220 bpm 0 Etiology? Overexertion Emotional stress BdSghIEDEEEBgg§ Deep inspiration Caffeine Tobacco Rheumatic heart disease Digitalis toxicity CAD Cor pulmonale Complications? Ventricles don’t have time to fill w/ blood b/c HR is beating too fast 1st dose: 6 mg Treatment: Vagal stimulation maneuvers (lease invasive 1st = activate PNS) 2nd dose: 12 mg (carotid massage - stimulate baroreceptors in neck) Doesn’t work: cardioversion (cough, massage neck) IV Adenosine (if least invasive don’t work)(Blocks AV node to restart heart rhythm; half life is < 10 sec., fast IV push w/ stopcock & 30mL NS syringe required at Antecubital -> closer to heart) (After pushing, will create short period of asystole - ~5 sec & then convert to NS rhythm) (Have RT, cardiac monitor, crash cart, doctors present in case rhythm doesn’t return = intubate) (Adenosine only works for stable SVT ; not for unstable SVT & RVT) Cardioversion - HAVE TO SEDATE before shocking (1) if adenosine doesnt work (2) couldn’t use adenosine b/c unstable SVT  Read this! ACLS: Bradycardia and Tachycardia  Premature Atrial Contraction Early electrical impulse in atria causing heart to contract prematurely (extra beat, extra impulse) P wave: Visible or hidden PR interval: Normal or longer QRS Complex: Normal Rhythm: Irregular (have extra beat) Atrial rate: Varies Ventricular rate: Varies Etiology? Emotional stress Fatigue → Oversumption of Caffeine ETOH Hypoxia Electrolyte imbalances Hyperthyroidism COPD CAD Valvular disease Complications? Palpitations, sense heart skipped a beat Treatment: Avoid excessive caffeine intake and alcohol < Stress Give Beta-blockers if HR>100 Atrial Flutter Atrial tachydysrhythmias Occurs when rapid re-entry of electrical circuit in R.Atrium “Saw-tooth shaped flutter” P wave: Flutter (F) wave PR interval: Not measurable QRS Complex: Normal Rhythm: Regular Atrial Rate: 280-320 bpm Ventricular Rate: 150 bpm (2:1) (depends on conduction ratio) Etiology? CAD Hypertension ☆☆ Mitral valve disorders ☆ Pulmonary embolus Chronic lung disease Cor pulmonale Cardio myopathy Hyperthyroidism Digoxin Epinephrine Complications? Less CO = decrease BP, syncope Atria is fluttering so not much blood going in/out => Stagnant blood => blood clot => stroke Treatment: Beta-blockers Calcium channel blockers Amiodarone (anti-arrhythmic) Cardioversion (unstable or hypotension) Ablation (cauterize (kill) some of pacemakers cells causing misfiring) Coumadin (prevent stroke) (anticoagulant)  Atrial Fibrillation Disorganized electrical impulse in atrium Most common cardiac dysrhythmia P wave: Fibrillatory (disorganized) PR interval: Not measurable QRS Complex: Normal Rhythm: Irregularly Irregular Atrial Rate: 350 to 600 bpm Ventricular Rate: >100 bpm (RVR) (rapid ventricular rate) controlled HR = regular HR w/ Afib Etiology? CAD Rheumatic HD Cardiomyopathy Hypertensive HD HF Pericarditis Thyrotoxicosis ETOH intoxication (most precipitating factor of Afib “holiday heart syndrome”) Caffeine Electrolyte disturbances Stress Heart Surgery Complications? Stagnant blood from irregular rhythm Treatment: Beta-blockers (slow down rate) Calcium channel blockers Amiodarone (anti dysrhythmias) Cardioversion (if new onset of Afib= meaning less than 48hrs ) (irregular HR less than 48hrs) (have to wait if after 48 hrs b/c the shock could dislodge blood clot) Coumadin (if after 48 hrs, have to take for 3 wks & want INR between 2-3)  Output measures in Joules Mono phasing Energy delivered in 1 direction : Biphasic deliver energy in two directions ~120 J - 200 J Synchronized vs Unsynchronized Synchronized mode must Use Unsynchronized mode when: be used on those who are Pt has no pulse, no contraction, unstable responsive, talkative We don’t care where shock is delivered b/c unresponsive, pulseless & had cardiac arrest Low energy shock High energy shock Afib, flutter, SVT, Vfib, Vtach Bradycardia, Heart Blocks Use synchronized “sync” button so Low energy shock so a sensor is used to deliver electricity synchronized w/ peaks of QRS Shock will be delayed & synchronizing with peak of R wave in QRS to deliver shock If shock occurs at T wave (where ventricles are relaxing) (DON’T want to shock while ventricles are relaxed) => Vtach or Vfib 1) press sync 2) sedate pt BEFORE shock (propofol) 3) shock pt  Junctional Dysrhythmias If SA node fails to fire & AV node becomes primary pacemaker P wave: Inverted or Hidden (if you don’t see P wave) PR interval: 0.12 second (NO Q wave at beginning) QRS Complex: Normal Rhythm: Regular Rate: 40-60 bpm (junctional escape rhythm) 61-100 bpm (junctional accelerated) (body sensed Low CO= SNS activated) 101-180 bpm (junctional tachycardia) ✗ Etiology? CAD HF Cardiomyopathy Electrolyte imbalances Inferior MI Rheumatic HD Digoxin Amphetamtines Caffeine Nicotine Complications? Low CO leading to hypotension Treatment: Atropine (if HR < 60, symptomatic, junctional escape rhythm) Beta-blockers (if above 100 HR) Calcium channel blocker Amiodarone- control HR (high HR) First-Degree AV Block Every impulse is conducted to the ventricles But the time of SA to AV conduction is delayed or prolonged P P P P P P wave: Normal - - - PR interval: Prolonged >0.20 sec (72 squares) __ QRS Complex: Normal Rhythm: Regular Rate: 60-100 bpm Etiology? MI CAD Rheumatic fever Hyperthyroidism Electrolyte imbalance Vagal stimulation Digoxin Beta blockers Ca Channel blockers Flecainide Complications? Sign of other heart block types Treatment: Just Monitor No treatment Monitor pt No Tx Check labs  Second-Degree AV Block TYPE I Mobitz I AV conduction is gradually prolonged until conduction is blocked P wave: Normal PR interval: Progressive Lengthening QRS Complex: Normal until blocked Rhythm: Irregular Atrial Rate: Normal Ventricular Rate: Abnormal *(QRS drop) Etiology? Digoxin Beta blockers CAD Complications? Treatment: Symptomatic- Atropine Transcutaneous Pacemaker (increase HR if symptomatic) If asymptomatic - monitor Second-Degree AV Block TYPE II Mobitz II SA node or P wave is non conductive w/out progressive PR interval Occurs when there’s block in bundle branches More serious b/c SA node is conducted to ventricles P wave: Normal PR interval: Normal or Prolonged (no progressive lengthening) QRS Complex: > 0.12 sec (bundle branch block) Rhythm: Irregular Atrial Rate: Normal * Ventricular Rate: Abnormal (p wave, QRS, p wave then QRS drop) ☆ Etiology? Rheumatic HD CAD Anterior MI Drug toxicity Complications? Decrease CO & potentially lead to 3rd degree heart block Treatment: Transcutaneous Pacing Permanent Pacemaker Don’t use atropine b/c of the block in AV junction; Atropine can only be used if decrease in conduction or SA node fails to fire  Third-Degree AV Heart Block MOST LETHAL! SA node doesn’t communicate w/ AV junction Atria are independently contracting & ventricles are independently contracting (P wave & QRS are doing their own thing) Hallmark: no relationship of P wave to QRS P wave: Normal PR interval: Variable QRS Complex: Normal Rhythm: Regular*** Atrial Rate: 60-100 bpm Ventricular Rate: AV node: 40-60 bpm; His-Purkinje: 20-40 bpm Etiology? CAD MI Myocarditis Cardiomyopathy Digoxin Beta blockers Ca Channel Blockers Complications? No CO or decreased CO => shock Treatment: PACEMAKERS ARE ONLY TX Transcutaneous pacing Transvenous pacing Permanent Pacemaker Help sync at normal rate Across the skin 1 patch releases electricity, other grounds it 1. Place the patches 2. Turn on pacemaker 3. Set the rate (70 HR - will be maintained preventing low HR) 4. Set the output(increase voltage until you capture & every spike has upside down QRS) 5. Once capture is noted, check pulse. 6. Provide patient sedation as needed. Pacemaker spike should be followed by QRS Similar to trancutaneous pacing Directly pace the heart Lead wires are fed through central line to contact myocardium directly Lead wires are attached to external generator Set rate to 70 Then set output & increase until you capture After procedure: look at insertion site, Monitor for signs of bleeding, Pt is placed on cardiac monitor continuously Complications: Infection Pneumothorax Bleeding  Not done in ER or ICU, needs to be performed in OR 3 types of malfunctions The pacemaker spike should be followed by QRS complex A) Failure to sense: B) Failure to Capture C) Failure to Pace When pacemaker doesn’t Electrical charge comes @ the right Caused by battery failure, recognize the atrial & time but the heart won’t respond oversensing, or wires off/ ventricular activity & fires, disconnected ☐ sending electrical impulses Can result if pt has severe randomly or inappropriately bradycardia or asystole Malfunction does not initiate electrical impulses when it Misfiring could result in Vtach Causes: leads damaged , electrode should be fired. or battery failure, Exit Block Malfunction caused by If pt has bradycardia & we pacemaker leads or electrodes, Exit Block - where the heart no don’t see a pacing spike then or battery issues, or the sensing longer responds to the output from treat the patient like their is set too high the pacemaker & usually caused by experiencing bradycardia w/ Hyperkalemia atropine (Look at lab values to treat the high K) (treat w/ insulin & dextrose)  Premature Ventricular Contractions (PVCs) HB Early conductions initiated by purkinje fibers rather than SA Regular pause eoiw node Purkinje fibers have 20-40 bpm PVC occurs before regular heartbeat & there’s a pause before the next heartbeat Multifocal PVC = Different shapes of PVC in one rhythm strip Couplet = Two consecutive PVCs Ventricular bigeminy = When every other beat is a PVC Ventricular trigeminy = When every 3rd beat is a PVC Ventricular tachycardia = Occurs when there are 3 or more consecutive PVCs (Deadly) R-on-T phenomenon = Occurs when PVC falls on the T wave of a prior beat (Dangerous b/c PVC is firing during relative refractory phase when ventricles are relaxed) Can occur on all T waves on strip P wave: Rarely visible (b/c lost during PVC’s QRS interval) PR interval: Not measurable QRS Complex: Wide, Distorted, >12 sec T wave: Large (& opposite in directions of major QRS complex) Rhythm: Irregular (b/c premature beats) Rate: Varies Etiology? Caffeine ETOH Nicotine Aminophylline Epinephrine Isoproterenol Digoxin Electrolyte imbalances When an impulse is initiated while Hypoxia Fever the ventricles are relaxed, it can Exercise lead to R on T phenomenon and Emotional stress then Vtach & Vfib Complications? Treatment: Treat the cause (if hypoxia give O2, electrolyte imbalance correct electrolytes) Beta- blockers Lidocaine or Amiodarone (prevent Vtach or Vfib) PVCS suppress '  Ventricular Tachycardia When there’s more than 3 PVCs Vtach occurs when conduction fires repeatedly & the ventricles take control as the pacemaker => Purkinje fibers are now the pacemakers mm. P wave: Buried (in QRS complex) PR interval: Not measurable QRS Complex: Wide, Distorted, >12 sec Rhythm: A) Regular or Irregular Ventricular Rate: 150-250 bpm Polymorphic Vtach/ Torsades de pointes: Etiology? Low Mg causes Torsades de pointes MI Correct by giving Mg CAD Significant electrolyte imbalances Cardiomyopathy Long QT syndrome Drug toxicity CNS disorders Complications? Treatment: Treat the cause (Usually low Mg so give Mg) ACLS (epi shock , epi shock until rhythm is corrected) Use Unsynchronized rhythm on defibrillator (they’re Vtach, pulseless, unresponsive) = want high voltage Ventricular Fibrillation Most lethal Vfib is an irregular waveform w/ different shapes & amplitudes & firing irregular conductions in the ventricle Ventricles are quivering, pt is passed out, cardiac arrest => No Cardiac Output P wave: Not visible PR interval: Not measurable QRS Complex: Not measurable Rhythm: Irregular & chaotic Rate: Not measurable Etiology? Acute MI Myocardial ischemia HF Cardiomyopathy Cardiac pacing or cardiac catherization procedures Complications? Pulseless, unresponsive , apneic Treatment: Treat the cause (H & Ts) ACLS Sensing system monitors HR & rhythm Small battery powered device placed on the chest to detect & stop lethal dysrhythmias like Vfib or Vtach (for patients w/ recurrent Vfib or Vtach) ICD leads are placed via subclavian vein into the endocardium so when Vtach or Vfib are detected delivering 25 joules or less to heart (detects lethal dysrhythmia) Also pacemaker capability = detects bradycardia, shocks pt when HR drops below 70 to increase HR ICD malfunctions delivering unnecessary shocks - Apply a magnet onto the device (temporarily disable device)  Pulseless Electrical Activity (PEA) Organized electrical activity (Normal Sinus Rhythm) is seen on the ECG, but there’s no mechanical heart activity & the patient has no pulse. Prognosis is not good, unless cause is treated STAT Normal sinus rhythm but no pulse H & Ts Etiology? Hs & Ts Hypovolemia Hypoxia Complications? Metabolic Acidosis Death Hyper/Hypokalemia Hypoglycemia Treatment: Treat the cause Hypothermia ACLS Toxins (overdose) Cardiac tamponade Thrombosis Tension pneumothorax Trauma Asystole The total absence of ventricular electrical activity. Occasionally, P waves are seen but not usually. No ventricular contraction occurs b/c depolarization does not occur (no QRS) Happened when couldn’t resuscitate pt Unresponsive, not breathing. Lethal b/c pt probably died already. Etiology? Advanced HD severe cardiac system disturbance End-stage HF Complications? Death Treatment: Treat the cause ACLS (compressions, epi, intubation) (Can’t shock pt b/c no electrical movement) When you see asystole on monitor - Assess pt 1st b/c leads could be off 2:47:30 ACLS: VF/pVT and Asystole/PEA ✗ Vtach or Vfib = we shock it b/c still electrical activity Routine: CPR , shock, CPR , shock epi, CPR, Shock, epi While performing this, find the H & Ts; what’s the cause Asystole or PEA = There’s no heart movement, so perform CPR & Epi every 2 min Routine treatment until ROSC (Return of Spontaneous Circulation) Heart’s a muscle Coronary Arteries Left main coronary artery is divided Every muscle needs O2 into two branches (circumflex & LAD) Heart needs to perfuse body & itself (R & L coronary Circumflex Coronary arteries) Artery supplies blood to: Lateral walls of L. ventricle Coronary arteries are L. Atrium perfused during diastolic phase. L. Anterior Descending During systole, heart (LAD) Coronary Artery contracts & pumps blood to Supplies blood to: the organs Intraventricular septum Right bundle branch Small portion of the left During diastole bundle branch 1) ventricle filling R. Coronary Artery 2) feeding cardiac muscle Supplies blood to: Aortic valve is closed => R. Atrium Blood clot in circumflex coronary driving pressure to perfuse R. Ventricle artery => AV block or L. ventricular HF the coronary artery => SA node providing O2 to cardiac AV node MI or Block in LAD => Left sided HF muscle Bundle of His Part of L. Ventricle Coronary Artery Disease CAD Women higher rate, African Americans earlier onset & more severe, Family Hx higher risk, High lipids= more plaque in arteries Tobacco Obesity HTN Diabetes can all dmg endothelial wall Stress => cortisol secretion => SNS + blood sugar increases Homocysteine = essential amino acid breakdown, found in dietary protein; if elevated = indication of atherosclerosis development in coronary artery Metabolic Syndrome Substance Abuse (cocaine, methamphetamine) reaches 3 Dmg layers ofmh%Fe R L Ischemia Infarction ARMORS off go CAD = type of blood vessel disorder & usually associated w/ atherosclerosis (Primary cause of CAD) Atherosclerosis develops: Diabetic, HTN, toxins, infection => Endothelial damaged -> plaque accumulates & gets bigger => eventually plaque ruptures => Rupture activates thromboxane A2 => leading to PLT aggregation, thrombus forms & occlusion in that area Aspirin prevents thrombus formation (anti-PLT aggregation) Body doesn’t sense difference between dmg to blood vessel & rupture of plaque => activates PLT cascade forming a clot occlusion => MI Size of plaque does not matter; Stability of plaque matters Acute coronary syndrome: (Umbrella for everything related to cardiac ischemia or infarction) Chronic Stable angina: Unstable angina or Non ST-segment elevation MI (partially occluded) Intermittent (on & off) chest pain (discomfort or heaviness) that Thrombus partially occludes vessel that can progress to subendocardial MI worsens w/ strong exertion, but usually relieved w/ Rest & New onset of chest pain, doesn’t go away despite nitrates, pain > 10 min sublingual Nitroglycerin Unpredictable unstable angina Stable = responds to standard tx EKG: ST depression, T wave (Ischemia = decreased perfusion of cardiac muscle) Angina doesn’t develop until lumen occluded 75% ST - segment elevation MI (total occlusion) EKG show: ST segment depression & T wave inversion Thrombus prevents blood flow & oxygenation to cardiac muscle (returned to baseline once treated) Irreversible myocardial necrosis (infarction = ischemia has advanced to myocardial cell death; worse than ischemia) Tx: decrease O2 demand & workload (preload) EKG: ST elevation (always worse then ST depression)  Diagnostic Tests 12-lead EKG & troponin are specific CK-MB & Myoglobin will be elevated w/ muscle injury (Not specific to heart; both are muscle chemicals ) C-RP elevated w/ CAD (pro inflammatory lab) Chest X-ray (CXR) (rule out Pneumonia’s pleuritic chest pain s/s) D-dimer elevated (Pulmonary embolism could cause chest pain) Positive D-dimer, then CT scan Echo to check ejection fraction Stress test (pts walk on treadmill & EKG rhythm is recorded) (Ischemia will show ST depression) How Troponin gets elevated (Red graph) Troponin is a lab specific to heart Takes 4-6 hrs to peak & elevation of Elevated = indication of acute MI Troponin 2 types of Troponin (I & Ts) = all in one lab value Normal: need an ECHO LOOK FOR WHERE DMG is: ST elevations Must be a new ST elevation @ J point in at least 2 consecutive leads greater than 2 mm (2 small boxes) in men & greater than 1 mm (1 small box) in women in leads V2,V3 & greater than 1mm in all other leads ECG evolution with Acute Coronary Syndrome (ACS) Ischemia: Decreased oxygenation to tissues Injury: Current ST elevation at that moment After injury will lead to infarction Infarction: Ischemia that has progressed to tissue necrosis Pathologic Q wave (Deep wide Q wave): Presence of MI in the past Q wave will go 25% deeper than R wave & be wide  12-Lead EKG: NSTEMI Inverted g- waves Unstable angina No ST elevation Just ST depression 12-Lead EKG: STEMI ode is Anterior wall MI V2 J-Point is >2 small boxes = ST elevation V3 = ST elevation V4, V5 = ST elevations Have to have 2 consecutive leads to classify so can’t call it anterolateral b/c no ST elevation in V6  V1 anything ST Elevation ST elevation -71mm is ST 5T Depression elevation Septal anterior o g wall STEMI steleuation ST Elevation ST Depression Jpoint. Me A song ST elevations: J point V2 /V3 Jpoint > zinnias → ST elevation ST Depression V1,V2, V3, V4, ST Elevation ST Depression.. Jpoint V5 Anterolateral STEMI ST Elevations: I, aVL, V2, V3, V4, V5, V6 Be & @ ☆ Inferolateral STEMI ST Elevations: I, II, III, aVF, V5, V6 q ar p & * M , ☆ Inferior STEMI (Isolated Inferior Wall MI) ST Elevation: II, III, aVF R Ventricle HF (Cor pulmonale) M @ & Lungs will be clear Hypoperfusion = decrease CO y is A h S/S: Hypotension, JVD, peripheral edema R. Ventricle is preload sensitive: TX is lots of IVF fluids (will push blood forward to L.Ventricle) Avoid meds that decrease preload (no morphine, nitrates, beta blockers ) = worsens R.Ventricular Failure Inferior STEMI ST elevation II,III, aVF a Posterior STEMI ST depression V1, V2, V3 (If depression in these 3 suspect g. ☆ posterior wall MI)  Nursing Management for ACS Have now verified pt is having chest pain & positve for STEMI 12 Lead EKG In cardiac unit VS (02 supplement) (need O2 due to injury from Heparin (if no ST elevation right away) infarction) ACE Inhibitors & ARBS Cardiac Monitor Calcium Channel Blockers Peripheral IV Statin (decrease lipids) Labs- Troponin, PT/INR, Chem7, CBC Stool softeners (prevent constipation) Give Nitro (3x) (Left sided HF) or Morphine (if taking viagra @ home) (These meds decrease workload of heart) (contraindicated for Isolated R. Sided Infarction) (R Sided: give fluids) (L.sided avoid giving fluids) Aspirin 325mg (have to chew it & crush it in mouth) Plavix or Brilinta (anti-PLT, prevents further thrombus) Beta-blockers (as long as BP is normal) Cath Lab Thrombolytic Therapy ( If NO Cath lab)  Cardiac Catheterization (Cath Lab) (+) STEMI have to report to Cath lab right away! Visualize & locate blockages (diagnostic) Open blockages (interventional) -Percutaneous coronary intervention (PCI)-Balloon angioplasty & Stent, Placed in obstructive coronary artery & restore Reperfusion is critical! bloodflow Goal is to open blocked artery restoring perfusion -Goal: open blocked artery w/in 90 mins of arrival to cath lab Do a 12 lead EKG after PCI: Want T wave inverted after PCI Nursing Management: Monitor for recurrent angina B/c if it’s upright then there’s Frequent VS, including HR & cardiac rhythm reocclusion of the artery Monitor catheter insertion site for bleeding (psuedonormalization of T wave) (Prone to bleeding b/c plavix, aspirin…) Neurovascular assessment Acute renal failure (kidney fxn test b/c contrasts can cause renal artery vasoconstriction) Bed rest per institutional policy Ensure pts not allergic to dyes or contrast! If Cath lab find multiple vessels occluded & severe left main stenosis & significant blockage => gonna do CABG  Coronary Artery Bypass Graft (CABG) We are going to bypass the occlusion to restore perfusion in cardiac muscle Requires sternotomy (open chest) & bypass (blood is circulated & pumped back by a machine) Coronary artery bypass graft (CABG) Requires sternotomy and cardiopulmonary bypass (CPB) Uses arteries (internal mammary artery) and veins for grafts to do an anastomosis to the heart Complications related to CPB: Inflammation Hypoxia Atelectasis Decreased alveolar recruitment (lungs are down during this CPB procedure) Nursing Management: ICU for first 24-36 hours Assess patient for bleeding (due to open chest & CPB) Monitor hemodynamic status Pleural/mediastinal chest tubes (chest drainage) Continuous ECG (Afib complication after CPB) ET tube with mechanical ventilation Epicardial pacing wires (transvenous wires if heart stops pumping) Urinary catheter NG tube Replace blood and electrolytes PRN Assess fluid status Restore temperature, DVT prevention (compression devices) Summary of Everything Discussed  Pericarditis Inflammation of the visceral and parietal pericardium. One possible complication after MI Occur 2-3 days after MI Think of 2 things when this occurs: 1) it activates your inflammatory response + inflammatory mediators 2) increase in capillary permeability -> increase fluids in pericardial sac µ Leading to complication of pericardial effusion Etiology: Coxsackievirus B Acute MI Dressler syndrome (pt develops fever after acute MI) Cancers Clinical Sx: Chest pain (sharp,burning chest pain that worsens taking deep breath;may radiate to trapezius) Pericardial friction rub (when auscultating) Fever (Dressler Syndrome) Dressler syndrome Diffuse ST elevations (across 12 lead ECG) & PR depressions (hallmark diagnosis) Dx test: ECG CRP & ESR (pro-inflammation) Troponin WBC CT (visualize pericardium & pericardial space) Nursing Management: Abx (if infection) NSAIDs (decrease inflammation) Corticosteroids (decrease inflammation) Colchicine (decrease inflammation) Pericardiocentesis (Pericardial effusion/Cardiac Tamponade) (to remove fluids) Developing Pericardial effusion => worry about Cardiac Tamponade Cardiac tamponade:Occurs when pericardial effusion volume increases rapidly & compresses the heart Compressing the heart can lead to decrease CO Papillary Muscle Rupture Papillary muscles are located in ventricles of heart attached to cusp of AV valves (mitral & tricuspid) via chordae tendinae Chordae tendinae = Fibrous Connective Tissue attached to mitral & tricuspid valves to prevent valve prolapse into atria Papillary muscle rupturing is another complication from an MI Valves fxn= continue unidirectional blood flow & prevent blow flow from going back & forth Murmurs (Extra Heart sounds) = related to heart valve disorders/changes in heart structures Stenosis = stiff valve that doesn’t open well or is very narrow => blood is having hard time moving forward=> decrease CO & increase workload of other heart chambers Regurgitation = puffy valve that doesn’t close well => losing unidirectional of blood flow (have blood backflow) => decrease CO & increasing heart workload  Mitral Valve Mitral Regurgitation Mitral Stenosis Incomplete valve closure Valve orifice is smaller (Stiff or narrowing of mitral Backward flow of blood valves) (Floppy valve that doesn’t close well, allowing Results in decreased blood flow from left atrium to blood to flow back across the valve) left ventricle => Afib (Blood is backing up => putting pressure on L. Etiology: Atrium => risk of Afib) MI Chronic rheumatic Etiology: Heart disease Rheumatic heart disease Clinical Sx: Clinical Sx: Pulmonary edema (blood backing up to lungs) Exertional dyspnea Peripheral edema Loud S1 Thready peripheral pulses Murmur Cool and clammy extremities Fatigue Weakness, fatigue Palpitations Progressive dyspnea Hoarseness Palpitations Hemoptysis S3 Chest pain Murmur Seizures/stroke (decreased CO) RN Management: (decrease workload) RN Management: Vasodilators Restrict Na intake (s/s of HF) Diuretics Diuretics (decrease pulmonary fluid overload) Nitrates (decrease afterload) Nitrates (decrease afterload, preload, workload) Anticoagulants (Lovenox or aspirin) Beta-blockers (decrease workload) IABP (Intraaortic Balloon Pump) (increase coronary Digitalis (decrease workload) perfusion, decrease afterload = reduce workload) Calcium antagonist (decrease workload) Anticoagulants Surgery (for severe stenosis)  Aortic Valve Aortic Regurgitation Aortic Stenosis Backward blood flow from ascending aorta into left Obstruction of flow from left ventricle to aorta ventricle (Stiff Aortic Valve & doesn’t open fully => leading (Floppy aortic valve that doesn’t close well => to Ventricular hypertrophy b/c of L.ventricle trying allowing blood to move backward from aorta into to push blood harder) L.ventricle Etiology: Chronic aortic regurgitation = L. ventricle becomes Rheumatic fever dilated & hypertrophy => eventually pulmonary HTN => R.Sided HF (Cor Pulmonale) Clinical Sx: (heart failure s/s) Angina (chest pain) Etiology: Syncope IE (inflammation of endocardium) (endocarditis) Exertional dyspnea (SOB) Trauma, or aortic dissection Rheumatic heart disease RN Management: (increase Oxygen demand & decrease workload Clinical Sx: Use nitroglycerin cautiously Water hammer pulse (pulse amplitude is very Low Na diet strong trying to pump. So, if Antihypertensives you feel the pulse- normally it decreases when Antiarrhythmics raising the hand, but w/ this disorder the pulse Digitalis (if showing HF s/s) remains strong) Diuretics (decrease preload) Severe dyspnea ACE inhibitors (reduce workload) Chest pain Surgery Hypotension Cardiogenic shock RN Management: Inotropic agents (positive inotropes) Ace inhibitors (decrease workload & increase oxygen demand) Diuretics (decrease preload) Nitrates Avoid Beta blockers (we don’t want pts heart to slow down, we want them tachycardiac to stimulate blood flow)