Cardio ABC PDF

Cardio A Blood flow and anatomy Blood flow: blood enters right atrium through superior and inferior vena cava -> tricuspid valve -> right ventricle -> pulmonary valve -> pulmonary arteries (only arteries carrying deoxygenated blood) - > left and right lungs (CO2 is exchanged f...

Cardio A Blood flow and anatomy Blood flow: blood enters right atrium through superior and inferior vena cava -> tricuspid valve -> right ventricle -> pulmonary valve -> pulmonary arteries (only arteries carrying deoxygenated blood) - > left and right lungs (CO2 is exchanged for O2) -> pulmonary veins -> left atrium -> mitral valve -> left ventricle -> aortic valve -> aorta (ascending, arch, carotids, left and right subclavian veins, descending, abdominal) -> body Epicardium: external layer Myocardium: muscle layer, pumps/contracts heart Endocardium: internal epithelial layer of tissue and valves Interventricular septum between right and left ventricles Pericardium: external sac of heart, 2 layers, visceral (against epicardium) and parietal (encases visceral and attaches to great vessels, diaphragm, sternal, vertebral column o Pericardial space (20 cc fluid between visceral and parietal) to prevent friction Coronary vasculature Aortic sinus leads to coronary arteries Right side (anterior) o Right coronary artery ▪ Supplies right ventricle, right atrium, SA node, AV node o -> right posterior descending artery ▪ Supplies back/posterior 1/3 of interventricular septum, posterior and inferior walls of left ventricle Left side (posterior) o Left main coronary artery o -> left anterior descending ▪ Supplies anterior left side of heart  o -> left circumflex artery ▪ Supplies left lateral side and posterior Conduction system SA node: pacemaker, 60-100 bpm o SA node fires -> internodal pathway in R and L atria -> depolarization of myocardial cells in atria -> contract -> push blood into R and L ventricles -> AV node (delay) -> bundle of his -> right and left branches -> Purkinje fibers (wrap around lateral aspect of heart) -> depolarize ventricles -> contract o Delay between SA and AV node make sure atria and ventricles contract separately If SA node stops working, AV will take over firing at 40-60 bpm and send impulses straight to bundle of His o Ventricular contraction does most of work to move blood through heart If both SA and AV node stop, Purkinje fibers take over at 30-40 bpm o Bad bp and inadequate oxygenation Which labs are related to CVD? Cardiac Enzymes o CK, CK-MB o Myoglobin o Troponin T and I Lipid profile o LDL, HDL, total cholesterol, triglycerides ▪ Want lower LDL, total cholesterol, triglycerides and higher HDL Brain natriuretic peptide (BNP) o Or NT-proBNP C-reactive protein o Inflammatory marker associated with atherosclerosis in vessel walls o Not cardiac specific Homocysteine o Not common o Amino acid that causes inflammation and damages endothelial layer of blood vessels, interfering with elasticity o Higher levels indicate atherosclerosis is present or developing o Affected by folate and vitamin B12 ▪ Deficiencies in this will cause higher levels of homocysteine (increasing risk of atherosclerosis) Electrolytes o K+ (3.5 – 5.5) o Mg2+ (1.3 – 2.1) ▪ K and Mg abnormalities are commonly associated with abnormal heart rhythms o Ca2+ ▪ Associated with issues of contractility ▪ CCB o Na+ ▪ Higher Na -> fluid retention -> fluid overload Coags  o PT/INR o aPTT CBC o Platelets (150-400) ▪ Clots cause MI **nearly ½ of American adults have one or more types of CVD **CVD is leading cause of death globally CAD risk factors High LDL cholesterol Low HDL cholesterol Hypertension Diabetes Obesity Smoking Family history Aging (↑ risk after 45 for biologic males and after 55 for biologic females) o Estrogen lowers LDL, increases HDL and promotes dilation of blood vessels -> improving blood flow ▪ Post menopause, no more protective effect CVD Atherosclerosis: buildup of plaque within coronary artery that can worsen over time to occlude the vessel and/or rupture to cause a blood clot o This is in coronary artery's -> coronary artery disease (CAD) CAD can cause stable angina or acute coronary syndrome (unstable, NSTEMI, STEMI) o ACS is caused by rupture of atherosclerotic plaque -> blocking blood flow Stable angina o Predictable chest pain that worsens with activity and improves with rest/nitroglycerin Unstable angina o Unpredictable chest pain o Can occur at rest and does not improve with nitroglycerin use NSTEMI and STEMI o Heart attack, MI ▪ ST elevated is generally worse o Cardiac cell death o Elevated cardiac enzymes like troponin o EKG determines NSTEMI, STEMI Chest Pain r/t Myocardial Ischemia Stable Angina Predictable and manageable episodes of chest pain (i.e. Occurs while exercising and disappears with rest, nitroglycerin, or both) Unstable Angina (need PCI or CABG) Unexpected chest pain, occurs while resting. Commonly caused by coronary arteries narrowed by fatty buildup (atherosclerosis) and referred to as acute coronary syndrome Myocardial Infarction (need PCI or Coronary artery blockage leading to cardiac tissue death CABG) The nurse teaches the client with angina prior to discharge. It is most important for the client to report which behavior? A. Pain following sexual activity – stable B. A headache after taking nitroglycerin – expected SE, can take max 3 doses, take bp, check hr, check ST if in hospital C. A change in the character of the pain D. Pain after eating a large meal – stable Nurse instructs outpatient about the purpose of a cardiac stress test. Which is correct? A. “Will assess overall physical function” B. “Determine amount of workload heart can tolerate” C. “Determine adequacy of peripheral circulation” D. “Enable provider to evaluate cardiac output” Cardiac Stress Test Exercise Stress Test o Walking/Running on a treadmill or stationary bike o Intensity ramps up based on the patient’s age and HR goal – stop when pt reaches target HR or if pt experiences signs of ischemia o Monitor ▪ ECG with 2 or more leads for HR, rhythm, and ischemic changes ▪ BP ▪ Skin temp ▪ Physical appearance ▪ Perceived exertion ▪ Active symptoms (ie chest pain, dyspnea, dizziness, leg cramping, fatigue) o Abnormal findings: chest pain, ventricular arrythmias, ST depression, lack of HR or BP elevation with exercise. Pharmacologic stress test o For pts who are unable to achieve their goal HR via exercise ▪ i.e. cognitive impairment, physical limitations o Vasodilating agents (dipyridamole, adenosine, or regadenoson) are given as an IV infusion  ▪ Reversal agent = IV aminophylline ▪ SE of vasodilators: chest pain, HA, flushing, nausea, heart block on EKG, SOB o ECG and VS are monitored before and continuously throughout the test o Can be combined with radionuclide imaging techniques ▪ Pictures to see blockages Cardiac Stress Test – Nursing Interventions Exercise Stress Test o NPO for several hours before o May take meds with sip of water (may be instructed to hold certain meds ahead of time) ▪ May hold beta blockers, CCB, digitalis may skew results o Avoid tobacco and caffeine (may also skew results) o Wear sneakers/exercise clothing o Nurse will explain the procedure, equipment to be used, rationale for IV placement and what symptoms to report o Monitor pt for 10-15 minutes, until the VS return to baseline Pharmacologic stress test o NPO for at least 3 hours before o Avoid chocolate/caffeine (including meds that contain caffeine) for 24 hrs before ▪ If also receiving radioisotope, also should avoid alcohol 24hrs before o Inform the patient they may feel flushed or nauseous after injection (temporary) o Total test time is 1-3 hours o Reassure patients: radiation exposure is at a safe and acceptable level (similar to having an xray) Signs & Symptoms of Acute Coronary Syndrome (ACS) Chest pain/discomfort Pale (in mucus membranes as well) Skin cool and moist Sweating HR, RR high Pain in one or both arms, back, neck, jaw, or stomach o Arm and chest are most common SOB of dyspnea Palpitations (& tachycardia) Unusual fatigue (early warning sign) ***this is an emergency -> heart attack is impending, happening, happened Differences in presentation for biologic females Biologic females are more likely to exhibit “atypical” or non specific symptoms such as chest pain at rest; pain in the jaw, arm, neck, shoulder, middle back, or epigastrium; nausea; vomiting; syncope; sweating (diaphoresis); anxiety; and fatigue Heart and arteries smaller in females -> CC and angioplasty more difficult Aging -> slower HR -> hypertrophy -> reduce blood volume -> reduce CO  o -> valves stiffen -> calcified and stenotic -> murmurs o -> stress (emotional or exercise) -> fatigue, SOB, palpitations (symptomatic) Myocardial Infarction (Heart Attack) Rupture of plaque buildup -> platelets aggregate -> blood clot forms -> artery is occluded -> myocardium death Blockage in first part of left anterior descending (LAD) -> widow maker o LAD supplies ½ blood to left ventricle (LV pumps blood to entire body) What will the EKG tell us? STEMI vs NSTEMI QRS complex represents ventricular depolarization/contraction o Systole T wave is repolarization  o Diastole 2 ST elevations on EKG indicate STEMI Order: 3 sets of Cardiac Markers How to differentiate STEMI and unstable angina.... Troponin goes high first and stays high after STEMI CK is good supplement to troponin, but drops off sooner o Troponin and CK peak 12-24 hours so most helpful in differentiating Myoglobin peaks very fast, but not specific to cardiac muscle (could be due to exercise) Enzyme Source Timing Myoglobin Heme protein, but NOT specific Increase in 1-3 hrs to cardiac, but negative helps (*fastest), peak in 12 r/o MI Creatine Kinase *specific to cardiac muscle* Detected within a few (CK-MB isoenzyme) hours & peaks @ 24 hrs Troponin (I & T Protein found in myocardial cells Detected within a few isomers) *specific to cardiac muscle* hours of injury, peaks in 12-24h; elevated for 1-3 weeks Medical Management of MIs Major Goals of Treatment o Minimize myocardial damage & preserve myocardial function ▪ Reduce myocardial O2 demand and increase O2 supply ▪ Meds (nitroglycerin, aspirin), bed rest, O2 supplementation 10-20 mins after arrival to ED should get sublingual nitroglycerin, O2, aspirin, anesthesia, 12 lead EKG, continuous cardiac monitoring o Relieve/manage pain and anxiety o Prevent complications Medications: Aspirin (chewable) o Antiplatelet o 160-325 mg o Very important Nitroglycerin o Vasodilator that takes workload off heart and relieves angina o SUBL, IV, tropical Heparin o Break up clots o Do not give if before invasive procedure like Cath lab (increases bleeding risk) Antiplatelets: oTicagrelor (Brilinta) oClopidogrel (Plavix) ▪ More common ▪ Prevents further clotting Beta blocker: Metoprolol o Given for high bp or tachycardia to take workload off heart o Started 24 hours after pt stabilized MONA – perhaps outdated o Morphine, O2, Nitroglycerine, Aspirin o High flow O2 may increase mortality and size of MI ▪ Constrict coronary arteries -> worsen ischemia STEMI Patients should be taken to the cardiac cath lab for immediate Percutaneous Coronary Intervention (PCI)  o Used to open occluded artery and promote reperfusion to myocardium o Preferred intervention o Door to balloon time should be 90 mins or less Percutaneous Transluminal Coronary Angioplasty (PTCA) = Balloon angioplasty o o With or without stent o Drug-eluting stents + ASA + clopidogrel Cardiac Catheterization (aka diagnostic coronary angiography or angiogram) typically left sided (right sided diagnoses pulmonary hypertension) Before: o Check renal labs ▪ Dye is harsh on kidneys and need to be filtered out o Not allergic to shellfish, iodine dye o Empty your bladder ▪ Dye makes pt feel like peeing themself o Cautious movement and monitoring: coding is possible before/during cath lab During: o Conscious sedation ▪ Can hear provider during o Feel the warmth of the dye o Dysrhythmias ▪ May code during After: o Activity restriction: Lie flat for several hours ▪ Sitting up increases pressure in abdomen and femoral artery -> bleeding o Maintain pressure dressing (close femoral artery) o Ok to drink water to help flush out dye o Two main risks: ▪ Bleeding Low bp and high hr Purpura ▪ Circulation  VS ever 15 mins after first hour, VS every 30 mins, then ever hour, etc. Risk for blood clot o Check pedal pulses, cold/pale feet, capillary refill ▪ Dysrhythmias Continuous cardiac monitoring Door-to-balloon time (“Time is muscle”) Time from ED to cath lab Goal: 90 minutes or less o Time is muscle o Irreversible damage can happen within 30 minutes Racial & Ethnic disparities o 11-18 minute difference between white patients and POC Gender disparities What if the patient is at a hospital without PCI capabilities and the transport time to the nearest cath lab is too long? Give a thrombolytic to dissolve clot Does not affect atherosclerosis so still need CABG High risk for bleeding after Need to give drug within 30 mins of symptom onset (door to needle time) Coronary Artery Bypass Graft (CABG) Take large vein from chest/leg and sew it in heart to divert blood around blockage Post-op o Temp o CT output ▪ Chest tube o Hemodynamics ▪ Bp o ECG ▪ Dysrhythmia risk o Incision sites o Q2h turns o Auscultation ▪ Atelectasis and pleural effusion risk o Peripheral pulses ▪ Pedal pulses, DVT risk o Pain o Neuro status ▪ Indicate brain perfusion o Aggressive pulmonary interventions Cardio B Heart Failure Scenario Pt 1: A 67 y/o patient presents to the ED with mild lower extremity edema, orthopnea over 2 weeks, increasing DOE (was after 2 blocks now after 0.5 block). No s/sx of infection. Patient denies nausea, vomiting, diarrhea, and chest pain. Patient has a history of: HTN, HLD, DM, CHF, CAD with one stent. Has been mostly compliant with her medications. 97.6, 95, 150/80, 94% RA improved with NC 2L to 97% o CHF exacerbation o Treat with meds, O2 o Pinpoint why it is occuring o Can lead to Pt 2 Pt 2: A 70 y/o patient presents to the ED with sudden onset SOB. Patient has a history of: HTN, HLD, DM, CHF, CAD with one stent. Cannot answer if they have been complaint with their medications. 97.6, 120, 220/115, 73% RA improved to 90% on BIPAP. o CHF exacerbation o Emergency o Pulmonary edema from fluid overload -> difficulty with gas exchange Hemodynamics: study of how blood flows through vessels Cardiac output: amount of blood the ventricles eject each minute o SV x HR Afterload: pressure heart must work against to pump blood out of the ventricles during systole o Resistance ventricle meets when pushing blood into arterial system (blood pressure) o Affected by bp and constriction of vessels o Assess based on MAP (average blood pressure in persons body during single cardiac cycle) ▪ Normal is 70-100 ▪ We need 60 to perfuse brain so anything lower is dangerous Stroke volume: amount of blood ejected with each beat o End-diastolic volume – end systolic volume  Preload: stretch of myocardium at the end of diastole (fullest) o Blood volume (more blood = more preload) o Measured in central venous pressure End-diastolic volume: amount of blood in ventricles at the end of diastole (fullest) Ejection fraction: % of blood leaving the heart each time it contracts Echocardiogram Ultrasound of the heart Uses sound waves to create live moving image of heart and vessels TTE: non-invasive, most common, ultrasound chest wall TEE: sedated, camera down esophagus Can get end diastolic volme and systolic volume from echo SV/EDV = ejection fraction o 100 is impossible because there will always be an EDV o 55-70 is normal o Less than 40% is HF ▪ If around 20%: fatigue, SOB, fluid buildup Heart failure is a clinical syndrome resulting from structural or functional cardiac disorders that the heart is unable to pump enough blood to meet the body’s metabolic demands or needs 2 kinds: o Systolic heart failure (reduced ejection fraction -> less than 40%) ▪ More common ▪ From reduced contractility or increased afterload leading to ventricular hypertrophy  ▪ This leads to ischemia and a viscous cycle of decreased contractility -> more O2 demand and not enough supply o Diastolic heart failure (preserved ejection fraction -> normal) ▪ Issue of ineffective filling from LVH, cardiomyopathy, fibrosis, pericardial constriction ▪ Less blood is making it into the ventricle and being pumped out (low SV) so the ejection fraction is normal o Systolic can lead to diastolic and vice verse (pts can have both kinds of HF) Differentiation of HF to Right vs Left Sided If one ventricle is affected, it will almost always affect the other after a while The most common cause of right sided heart failure is left sided heart failure Left sided: LV is unable to fill or pump effectively (could be diastolic or systolic HF) o This will back up everything before the left ventricle -> pulmonary congestion and pulmonary edema Right sided: caused by left sided HF from blood backing up into right side and lungs o Cor pulmonale is HF NOT due to left sided HF, but from another lung condition such as pulmonary fibrosis, pulmonary HTN, etc. o Blood backs into venous system and peripheral tissues ▪ Inferior vena cava symptoms: Blood backs up in liver and spleen -> enlarged and tender Blood backs up into peritoneal cavity (ascites), weight gain from water Pressure in GI -> loss of appetite, losing fat ▪ Superior vena cava symptoms: JVD o Elevate bed to check: If you see JVD with the HOB elevated, you know there is increased pressure in the R atrium. o JVD pressure parallels central venous pressure/right atrium o  Left and right sided heart failure at the same time = congestive heart failure (can be systolic or diastolic) Diagnose & Treat Heart Failure ECHO to determine ejection fraction Draw labs, especially to check BNP and NT proBNP  o Released from heart in response to RAAS activation o When ventricles stretch, release BNP (more stretch = more BNP released) o BNP signals Na release and water release to decrease blood volume o In HF, ongoing stretch in ventricles causes increase in BNP levels -> diagnostic tool o NT proBNP is pro hormone (inactive form of BNP) Treat: o Angiotensin receptor-neprilysin inhibitor (ARNI) ▪ Combines a neprilysin inhibitor and an ARB: sacubitril – valsartan (Entresto) ▪ First line for symptomatic hefref (HF with reduced ejection fraction or systolic HF) ▪ Increases BNP levels, but does not impact NT proBNP ▪ Do not give with ACE-I ▪ Expensive o ACE-I or ARBs ▪ Act on RAAS system o Beta blocker (BB) o No use of Ca channel blockers ▪ Ineffective in morbidity and mortality even though they relieve symptoms *do not memorize, but notice trends A: at risk, no dx; lifestyle changes B: early changes in heart, but no symptoms; start medications C: structural changes and symptoms; add diuretics (Lasix, loop is more common) D: end stage, highly symptomatic; palliative care, inotropes (digoxin) o Dig increases contractility and CO; symptom relief; narrow TI Digoxin Toxicity *impact of digoxin is enhanced if low K+ levels / hypokalemia *filtered out kidneys, careful with kidney pts GI symptoms o Anorexia o Nausea Blurry vision Yellowing or green tint to vision Confusion Color changes Bradycardia or pre-ventricular contractions (PVCs) ANTIDOTE: digoxin immune fab (DIGFab) ICU Additions… Unstable HF pts go to ICU Place A-line in radial artery (after performing Allen test ofc) to measure MAP o Red line = arterial BP o Green = cardiac leads o MAP indicates afterload ▪ Normal is 70-100 ▪ NEED 60, titrate meds to MAP of 65 o Central venous pressure is related to preload (blood volume) = blue lines ▪ Central venous catheter is placed in superior vena cava in internal jugular vein ▪ Can vary with position changes (up when lying down and low when head elevated) Should be 2-8 mmHg If too low, may be dehydrated If too high, may have fluid overload o Pause if pt needs fluid bolus o Most reasons for hospitalization are due to fluid volume overload  Normal age-related changes: decline in cardiac output, fatigue, activity intolerance, slow heart rate, ventricular hypertrophy Cardio C Arrythmias Electrocardiogram – electrode placement Lead Portion of Heart Associated CA II, III, avF Inferior Right CA I, avL, V5 & V6 Lateral (left) L circumflex  V1 & V2 IV Septum L Anterior Descending V3 & V4 Anterior L Anterior Descending P wave = atrial depolarization (contraction, SA node fires) QRS complex = ventricular depolarization T wave = ventricular repolarization (resting, regaining negative charge, no wave should be here) PR interval = how long it takes for atrial depolarization to occur before ventricular depolarization ST segment = neutral period between ventricular depolarization and repolarization (between beginning of QRS to end of T wave) QT interval = length of time from start of ventricular depolarization through repolarization; varies with hr, sex, age o QTC interval is adjusted for hr/sex/age factors o Ventricles fill with blood here o QT prolongation is dangerous *know the seconds ECG paper (lead # = views of the heart) NORMAL SINUS RHYTHM (NSR) Reading the strip: Rate: count QRS x 10 to make full minute o 7 x 10 = 70 bpm Rhythm: even spaces between tip of QRS o Is it irregular, irregularly or regularly? o 4 boxes between each R wave P wave: is there s P wave for each QRS and is PR interval consistent o About 0.16 secs This is normal sinus rhythm Sinus Node Arrythmias Sinus tachycardia (over 100 bpm) o Sinus bradycardia (under 60 bpm) o Premature atrial contraction (PAC) o Feels like heart skips a beat o Over 6 in minute, need medical management o Extra P wave that comes sooner than should o NSR with isolated PVC o Ventricle contraction above and on top of normal rythm o Pattern is concerning (ever other beat or every third beat) o Aka ectopic beats  o Atrial Arrhythmias Afib Common Visible changes in P waves Risk of blood clotting because blood is stagnant on heart o Patients usually on anticoagulants CO may be affected if ventricular rate is above or over 100 AFib can be controlled or uncontrolled based on ventricular rate o Hr WNL = controlled o Hr tachycardic = uncontrolled o Associated with aging Atrial flutter Conduction defect in atria causing atria to contract at 250-400 bpm Ventricular Arrythmias Vfib Common in pts with cardiac arrest Characterized by rapid, disorganized ventricular quivering Low CO and no pulse No QRS complex, T or P waves Most common cause is MI from CAD Vtach  Wide QRS complex, no P or T wave Fires at rate over 100 bpm May have 3 or 4 then back to normal If continues, incompatible with life Monomorphic = same pattern o Polymorphic = shape changes o Tussauds du point o Heart Blocks! 4 to know 1: delay in conduction through AV node -> PR intervals are long (over 0.2 secs) o More common in those with increased vagal tone (those who need ongoing suctioning); those on beta blockers, CCB, digoxin o Asymptomatic 2: o Mobitz 1: PR gets longer until dropped QRS complex ▪ Increasing PR interval before dropped QRS ▪ From high vagal tone, MI, hyperkalemia o Mobitz 2: long PR interval, P wave with no QRS complex ▪ Fix PR interval ▪ Due to MI, fibrosis ▪ Symptomatic, fatigue, dizziness ▪ More serious Need pacing 3: complete o No association between atrial and ventricular contractions o Random P waves, random QRS complexes o May have more P waves with bradycardic QRS o End stage 2nd degree (from AV nodal blocking) o Fainting, fatigue, chest pain, cardiac arrest ▪ Need immediate intervention; pacer Dysrhythmias: Initial Assessment 1. Is the patient symptomatic? dizziness, syncope, palpitations, CP, N/V, dyspnea 2. Is the patient hemodynamically stable? HR > 100? BP dropping? ↓CO o Systolic less than 100 o Map less than 65 Bradycardia -> decreased CO too 3. What could be causing the arrythmia? Point of Care testing for electrolytes, hypoxia, glucose o K, Mg Think through the patient’s history for causes If we discover the cause – can we correct the underlying cause or do we need some other intervention? Your s/p CABG patient displays this rhythm: 1. Name rhythm Afib – no discernable P wave 2. Before you call provider, what do you want to know? Rate! o 11 x 10 = 110 (uncontrolled) BP o 105/64 o Call provider Is patient on any anti-arrhythmic already? Which labs should we look at? o Careful, there are standing orders for correcting electrolyte imbalances 3. What are the main concerns with this rhythm? (Note chronic v acute) New issues or post procedure, need to make sure provider is aware 4. How would you treat? (Tx rate, tx rhythm, med v procedure) Beta blockers, CCBs for rate Amiodarone for rhythm o Can go home on this orally Cardioversion: awake defibrillation, current is set at QRS complex/ventricular depolarization Cardiac ablation: cardiac cath where cells causing excessive firing are ablated (for chronic conditions) Supraventricular Tachycardia (SVT) Rate is 150-200 bpm Report fatigue Low CO Stimulate vagal reflux to slow hr: blow through straw, cough, bear down, carotid massage Treat with adenosine/cardioversion o Push adenosine heard and fast with immediate flush after o Pt will momentarily flatline before feeling better https://youtu.be/8fpJXPSC7w8 Cardioversion vs defibrillation Pacemaker/ICD insertion https://clinicalgate.com/implantable-cardiac-devices/ If pacemaker set for 70 bpm, device will not allow hr to drop below 70 (at 70 or above, pacemaker will do nothing ICD will shock pt if they go into lethal rhythm o Vtac, Vfib pts Keep incision clean and dry for 48 hours but leave steri strips on for week, will fall off by self  Avoid vigorous arm movements or lifting first 4-6 weeks (on side with device) because can pull wires out of place Don’t drive for 1 week o Seatbelt trauma Avoid large electromagnetic field: microwave & cell ok, but generally airport security is not Check incision for signs of infection No MRI, (but there are new MRIs that are ok) “Failure to capture” vs “Failure to sense” vs “Failure to pace” o Issues with pacemaker Failure to capture Ventricles are not responding to pacer stimulation Spikes should follow contractions Failure to pace Pacer is not stimulating contraction (no spikes) Failure to sense Pacemaker does not detect patients myocardial depolarization Body triggers beat and pacemaker does not sense it Spikes will follow QRS too closely Dangerous -> can cause arrythmia like vfib