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Cardiology Board Review Jennifer Carlquist PA-C, CAQ ER Medicine Common arrhythmias and their treatment Demystifying Bundle Branch and AV Blocks Objectives Coronary Artery Disease: Identify patients at risk for CAD, prevention and treatment Heart Failure: Identify, manage and prevent it Arrhythmias Things that go bump in the night Normal conduction Sinus Tachycardia Rate: >100 – 160 BPM Regularity: Regular P wave: Present, PR interval constant __________________ and ________________ can cause sinus tachycardia. Rate: Varies Regularity: Irregular, but PR intervals are the same P wave: Present intermittently Sinus Pause/Arrest Sick sinus syndrome: - Digitalis, CA ++ blockers, Antiarrhythmic drugs, CAD, collagen vascular diseases and or mets - Reversible? Pacer? Palpitations tree Getting to the root of the cause AFIB/Flutter SVT WPW PVC’s Sick sinus VT Atrial Fibrillation Rate: Variable, ventricular response can be fast or slow. Atrial rate is usually over 350 BPM. Regularity: Irregularly irregular P wave: None; chaotic atrial activity Patients lose their ___________ in atrial fibrillation. Things we can fix Atrial Fibrillation Causes •Thyrotoxicosis •Hyperlipidemia •High blood pressure •Heart disease (Valvular) Things the pt can fix •Obesity •Smoking •Caffeine •Alcohol abuse •Sleep apnea Complications Stroke CHF Rate vs Rhythm Assess/address stroke risk CHADS Score Ablation/Cardiovert If elevated risk, need to choose: Xarelto, Apixiban, Pradaxa, ASA Warfarin Assessing stroke risk Warfarin: needs frequent monitoring Pradaxa/Xarelto (Direct thrombin inhibitors) – non valvular $8-12 day AC choices No monitoring No reversal Paroxysmal: Atrial fibrillation that lasts from a few seconds to days, then stops on its own Persistent: Does not stop by itself but will stop if cardioverted Defining AF Permanent (long standing persistent) AFIB begets AFIB wont retain sinus Normal LA with structurally normal hearts are better candidates Afib with RVR Atrial Flutter Rate: Atrial: 250–350 BPM, Vent: 125–175 BPM Regularity: Regular P wave: Saw toothed, “F waves” The mechanism behind atrial flutter is generally reentrant in nature. PE ETOH Ischemic heart disease Atrial Flutter Causes Hypoxia Digitalis toxicity Mitral or tricuspid valve disease AMI SVT These patients will most likely have a ___________ blood pressure. Etiology Rapid atrial depolarization overrides the SA node Stress, pathway, caffeine, drugs Clinical Significance PSVT Decrease in cardiac output = angina, hypotension, or CHF Clinical Features Regular, Rapid, No discernable P wave HR – 160-220 Drugs Pathway SVT Ectopy The Troublemaker Lots of angry cells… What causes ectopic beats? Atrial Ventricular Come in patterns This ectopy pattern is called ______________ . ECTOPY Where’s the PAC? A junctional premature contraction (JPC) is a beat that originates prematurely in the AV node. It can occur sporadically or in a grouped pattern. Junctional Premature Contraction (JPC) If PR interval is present, it does NOT represent atrial stimulation of the ventricles. PVC Bigeminy - every other beat Trigeminy - every third beat Just how mad are you?? Quadrigeminy - every fourth beat Couplets - two in a row Triplets - three in a row V-Tach - 5 or more PVC’s Multifocal – More than one focus PVC Couplet Multifocal Bigeminy Trigeminy Quadrageminy BBB Hemiblock You are driving into the EKG. You need to turn. You signal. Right or left. Bundle Branch BLOCKS J point: the junction between the end of the QRS segment and the beginning of the ST segment Turn signal theory - Courtesy of Mike Taigman “Drive your car” LBBB Causes Aortic stenosis Dilated cardiomyopathy AMI/Extensive CAD Primary disease of the cardiac electrical conduction system Long standing hypertension leading to aortic root dilatation = aortic regurgitation LAFB is NOT benign RBBB Causes •RVH / Cor pulmonale •PE •Ischemic heart disease •Rheumatic heart disease •Myocarditis or cardiomyopathy •Degeneration of conduction system “Drive your car” Sinus Tachycardia Causes Fever Pain Hypovolemia Drugs Sinus tachycardia AV Blocks What is actually blocked? A vessel? Is something really “blocked?” Heart Blocks Defined by PR Interval First-Degree Heart Block Regularity: Regular P wave: Normal PR interval: Prolonged >0.20 sec QRS width: Normal Does this rhythm normally cause symptoms? First degree AV block is a constant and prolonged PR interval 1st Degree AV Block Insult to AV node, hypoxemia, Inferior MI, dig toxicity, ischemia of the conduction system and increased vagal tone Criteria Rhythm: Regular PRI: > .20 2nd Degree AV Block Type I Regularity: Regularly irregular P wave: Present PR interval: Variable QRS width: Normal Dropped beats: Yes, patterned Long, Longer, Longest, DROP! Rinse and repeat. - Wenchebach 2nd Degree AV Block, Type I Wenkebach Wenkebach: Long, longer, longest….drop. Same causes as 1st degree AV block Criteria Rhythm: Irregular PRI: Progressive lengthening of PRI until dropped beat QRS's appear to occur in groups. Mobitz II SecondDegree Heart Block Regularity: Regularly irregular P wave: Normal PR interval: Normal QRS width: Normal Dropped beats: Yes 2nd Degree AV Block Type II Mobitz Can lead to third degree AV block AV conduction normal…then drop. Criteria PRI: Constant on conducted complexes until a sudden block of AV conduction Rate: Separate rates for underlying (sinus) rhythm and escape rhythm Regularity: Regular, but P rate and QRS rates are different P wave: Present P-QRS ratio: Variable Third-Degree Heart Block PR interval: Variable, no pattern QRS width: Normal or wide Grouping/dropped beats: None 3rd Degree AVB Complete Caused by: Acute MI Dig Toxicity Conduction System Disease Something wicked this way comes Ventricular Tachycardia (VTach) Rate: 100–200 BPM Regularity: Regular PR interval: None QRS width: Wide, bizarre Dead? Defib VT Alive? Synch Adenosine Stable? SVT Unstable? Synch Rate: Generally 100 to 220 bpm Width of QRS>0.12 sec Ventricular Tachycardia Rhythm: Regular Stable = treated with lidocaine or Amiodarone Hemodynamically unstable VT (with a pulse) is cardioverted VT without a pulse is defibrillated Three or more beats of ventricular origin (PVCs) in succession at a rate greater than 100 beats per minute . Rate: 200–250 BPM Torsade de Pointes Regularity: Irregular P wave: None P:QRS ratio: None PR interval: None QRS width: Variable Grouping: Variable sinusoidal pattern Dropped beats: None Prolonged __________________ can cause torsades. Changing polarity of the QRS complex from positive to negative and back to positive again Torsades De Pointes Its still VTACH – why do I need to identify it further? Treatment is different! Torsades Magnesium sulfate Felt unwell “like the water ran out of me” Under stress HX: HTN, psyche, chronic neck pain Drank alcohol and did cocaine Case Called 911… “Had an episode of urinary incontinence, pt felt weak” Dizzy, dyspnea, chest discomfort Field EKG: Sinus tachycardia with borderline st elevation in V1, V2 with one PVC EMS says… Then goes into torsades…. Is shocked at 200 j once, brief CPR Post shock in ER K was 2.7 Qt prolonging meds Did cocaine What were her risks? Hx of previous long qt…. Female “I think I need something stronger for pain…” I didn’t take my blood pressure medication as it was too expensive… At clinic visit I did take my nieces medication, it starts with an “L” I did take two methadone that day for pain… Meds: Prozac, Methadone, Trazadone, Pepcid, Rispiridal Clinic EKG Routine EKG in 2012 Coronary Artery Disease Atherosclerosis, Angina, Unstable Angina, NSTEMI, STEMI The menu MI vs. NSTEMI vs.Unstable angina vs Angina How many people die 1,500,000 M.I.s in the US annually Acute mortality ~ 30% 5-10% of survivors die in the first year CAD Etiology Coronary artery atherosclerosis Coronary artery spasm (Prinzmetals, drug use) Congenital abnormalities (less than 1% of population) Clot Variant Angina (Prinzmetal’s or atypical), Not all chest pain is CAD caused by arterial spasm most often occurs at rest No fixed occlusion CAD Pathophysiology CAD Risk factors High plasma LDL ( > 100 ) Low plasma HDL ( < 40 ) DM Hypertension, Smoker, couch potato Family hx of heart disease <age 55; female <65 THE BIG ONE Provoking: Emotion or exertion Quality: Heaviness, squeezing, pressure, smothering, crushing Radiation: L arm, R arm, jaw, neck, back Relieved: By rest Severity: Quiet patient with a 10/10 pain Time: Variable 3 high risk patients: Diabetics, females and elderly 20 % with proven mi have only upper abd pain 40% pain radiates to right side Atypical Presentations Common Character: 1/3 pressure, but others sharp stab aching or indigestion only 1/3 with exertion JAMA. 2005 Nov 23;294(20):2623-9 You can’t find it if you don’t look for it. High index of suspicion Nausea, vomiting, diaphoresis Fatigue (Levine’s) sign, dyspnea CAD Signs & Symptoms Unstable angina vs stable Gut instinct Quiet, still, diaphoretic patients ¼ of patients with anterior M.I. have ↑HR and/or HTN S4, S3, signs of CHF New murmur (Mitral regurgitation – in systole) Physical EXAM PAD Denial “I feel like I am going to die.” Early morning hours common (circadian BP surge) Similar to CAD - longer duration and more severe More N&V, diaphoresis, anxiety or weakness Worrisome Usually > 30 minutes If lasts > 15 minutes despite 2 nitroglycerin SL separated by 5 minutes, suspect MI 15% of MIs are painless May present as sudden onset SOB due to CHF Previous EKG!! One EKG begets another ~50% of people normal EKG repolarization abnormalities T wave or ST segment changes (depressed, elevated, flipped) NSSTW New BBB ST segment elevation WITH reciprocal ST segment depression OR new LBBB Where is the MI The EKG is a snapshot. 63 y/o male : Chest pain – EMS responds… “ My pain is getting worse…” “I really don’t feel so well…” 50 y/o male with “indigestion” T wave inversion can be seen as the sole ECG change in 10% of AMI. 58 y/o female with chest pain Deep anterior T waves are consistent with LAD (left anterior descending) disease and represent a high-risk group Her cath report Lesion on mid LAD 99% stenosis Post hospital clinic visit Wellens A Can’t Miss EKG Finding 42 y/o male presented with intermittent chest pain. Case HX: HTN, smoking, hyperlipidemia severe, possible ehlers danlos. High stress lifestyle. Worked as a mechanic. Thin framed. 42 year old male C/P clinic EKG PMD note “Has chest tightness after dinner, worse laying down, sometimes when sitting. Connection to activity, but not consistently so. Eases with doing less. No lightheadedness, dizziness, sweats.” What happened? 5 vessel bypass. EF of 40%. AVR Elevation of more than 1mm in aVR in the setting of Acute Coronary syndrome is associated with left main disease Ominous finding! Not a STEMI, but should be treated like one PCI Associated with an increase in mortality TST 2 mm depression of ST segment lasting greater than 0.08 seconds (ST flat or downsloping) Stress TESTING 15% false positives, 15% false negatives Stress echo Radionuclide (Lexiscan scanning) How do you choose which test to order? Cardiac Enzymes Myoglobin: Sensitive/not specific Rises in 2-3 hours/peaks in 3-6 hours Doubling over 90 minutes highly predicative of AMI Labs Troponin: Rises in 3-5 hours/peaks in 12 hours Closest to ideal “MONA” Morphine O2 Nitrates ASA Why guess when you could know? Cardiac catheterization (Angiogram) Invasive Gold Standard Risks: Infection, hematoma, death Indications for CABG CABG is the preferred treatment for: 1. Left main coronary artery 2. Disease of all three coronary vessels LAD,LCX and RCA 3. Diffuse disease not amenable to treatment with a PCI. The 2005 ACC/AHA guidelines: Also high-risk patients: severe ventricular dysfunction (i.e. low ejection fraction), or diabetes mellitus Treatment Nitrates BB Ca channel blocker Diuretics Statin ACEI Beta Blockers (Toprol XL, Coreg) ACEI particularly with E.F. <40% If DES, then Plavix plus ASA for one year Special Populations Cardiac rehab MI Complications Dressler's syndrome (Pericarditis) CHF Arrhythmia Left ventricular Aneurysm Prevention Diet, exercise for lipid lowering Stop smoking Treat HTN, DM Reduce inflammation Reduce stress Heart Failure Growing problem one million Americans are admitted for heart failure per year...and up to 20% are readmitted within 30 days. DOE, PND, orthopnea, rales Weight loss/gain, poor appetite S3, MR murmur, displaced PMI, ↑ HR EXAM JVD, HJR, pedal edema, ascites CXR (pulmonary edema) Decreased mentation Oliguria Causes MI Valve disease Anemia Thyroid Toxins NYHA HF Classification Can have both How do we acutely treat CHF? Pressure = BiPap L=Lasix M=Morphine N=Nitrates O=Oxygen… P = Pressure Patients with LVEF 40% or less with symptoms or prior symptoms, unless contraindicated, to reduce morbidity and mortality ACEI Asymptomatic patients with LVEF 35% or less Common ACEI: Lisinopril, Ramipril, Enalapril Check potassium, serum creatinine, and blood pressure within one week of initiation or dosage increase in the elderly, and within one to two weeks of initiation or dose If: Fluid retention Loops preferred, but thiazides can be considered for patients with hypertension and mild fluid retention. Diuretics Furosemide: initial 20 to 40 mg once or twice daily, max total daily dose 600 mg Bumetanide: initial 0.5 to 1 mg once or twice daily, max total daily dose 10 mg Torsemide: initial 10 to 20 mg once daily, max total daily dose 200 mg Beta blockers Stable patients with LVEF 40% or less with sx If hypotension occurs, separate betablocker from other hypotensive agents (e.g., ACEI), or decrease diuretic dose Don’t stop abruptly Use Metoprolol Succinate (Toprol XL, Coreg) Special Populations Use an aldosterone antagonist for patients with class II to IV heart failure...if CrCl is > 30 mL/min and potassium is < 5 mEq/L. Consider adding hydralazine plus isosorbide dinitrate in African Americans with class III or IV symptomatic heart failure. Don’t make it worse NSAIDS Glitazones Diltiazem Verapamil Procardia Sotolol Dronaderone Fight or flight Rubber band theory Heart fails = stress = catecholamine release RAAS activates Retain sodium, heart rate goes up Increased sodium = increased fluids = more failure Things the patient can fix Things we can fix Anemia Arrhythmia Lifestyle, diet HTN Infection Thyroid disease CHF: TREATMENT Less fluid in More fluid out = Loop diuretics Treatment Low salt (2 g max/d) ACEI Cardiac Rehabilitation Patient education Cardiomyopathies Dilated 95% (floppy) Hypertrophic 4% (bulky) Restrictive 1% (squished) Dilated: Floppy Heart Males Idiopathic 30% Drugs (Cocaine/Adriamycin) Thyroid (hypo or hyper) Peripartum Infection Mechanism=Bad Muscle Function CHF = SOB/Rales and JVD/S3 Restrictive Cardiomyopathy “I have CHF symptoms, with a normal size heart.” Heart is normal size, but is too stiff to relax Restrictive Cardiomyopathy Least common cause of cardiomyopathy About 70% of people die within 5 years after symptoms begin Symptomatic treatment usually not helpful Treatment Hemachromatosis, the exception HOCM Syncope Something is in the way. Chest pain DOE MR Dyspnea at rest Palpitations S4 S3 HOCM Clues DOE in a young patient Athlete syncopal during exercise Palpitations, orthopnea ECG Findings Which would you rather have as your “wine glass”? [email protected]