2015. Why should I listen to this guy?

12/21/2015 Objectives: EKG Patterns Cardiology Section 3 Brent Felton, DO, FACEP Research Director MSU EM Residency Valve Disorders Endocarditis Hy...
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12/21/2015

Objectives: EKG Patterns

Cardiology Section 3 Brent Felton, DO, FACEP Research Director MSU EM Residency

Valve Disorders Endocarditis Hypertensive Emergencies Cardiovascular Meds

Why should I listen to this guy? Cardiology is the largest single area of boards related questions (11%) Lots of Pictures to keep you all awake

EKG Patterns

I will highlight items that examiners love to test on! The boards test on the core knowledge, not the latest and greatest research

Myocardial Infarctions You must know which strain patterns correspond with which type of MI AND which vessel is affected! 2 Types of MI’s: ST Elevation/Q wave/Transmural NSTEMI/Subendocardial/Non-Q wave Worse Prognosis overall If you develop A. fib during MI, BAD PROGNOSIS Q wave defined as 1 box wide, 1/3 height of the “R” wave in 2 contiguous Leads

Myocardial Infarctions: Must Know:

ST Elevation in the leads… II/III/AVF

Inferior MI

I/AVL, V1-V6

Anterior Wall

I/AVL, V5-V6

Lateral Wall MI

RCA (80%) LAD

ST Depression in V1/V2 with upright T waves Posterior Wall MI, usually in conjunction with Inferior Wall MI Circumflex Artery

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Acute Inferior Wall MI

Acute Anterior MI Diffuse ST Elevation V1-V6

Acute Lateral Wall MI

Acute Inferior-Lateral Wall MI

Acute Posterior MI

Acute Anteroseptal MI

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What does this ECG represent?

Subarachnoid Hemorrhage ECG Changes associated with SAH: Large, broad symmetrically inverted T-waves ST Segment elevation or depression Prolonged QT interval Dysrhythmias may occur SVT/A. fib/V Tach

Subarachnoid Hemorrhage

Acute Pericarditis CP that is pleuritic, worse with swallowing Relieved by sitting forward, worse supine 4 phases of Pericarditis: 1. ST elevation with PR depression 2. ST at baseline 3. T-wave inversion 4. Normalization of ECG

Acute Pericarditis

A 48 year-old male presents with pleuritic chest pain, worse with swallowing for the past 3 days. He underwent PTCA placement for an acute inferior MI 21 days ago for an acute proximal RCA occlusion. He is concerned about a re-occurrence of his recent MI. His ECG is demonstrated previously. What is his Diagnosis?

Dressler’s Syndrome

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Dressler’s Syndrome Occurs 2-8 weeks post MI Fever, friction rub, pericardial effusions are common in presentation.

Electrolyte Disorders

Hyperkalemia

Hyperkalemia ECG Progression: Peaked T Waves Increased PR interval Widening of the QRS interval Bundle branch Blocks Sine Wave Asystole

Hypokalemia

Hypokalemia

ECG Findings: Flattened T waves U Waves

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Hypocalcemia Prolonged QT Interval Low PTH, Chvostek’s/Trousseau’s signs

Hypomagnesemia Prolonged QT Interval Think Hypocalcemia Alcoholics/Malnourished Leads to Torsades if untreated

Hypercalcemia Shortened QT interval Stones, bones, moans, groans, psychiatric overtones

Hypothermia Osborn/”J” waves Typically occur < 30⁰ C Can progress to sinus bradycardia OR slow A. fib

Tricyclic Antidepressant OD

Tricyclic Antidepressant OD Amitriptyline, nortriptyline Type 1A, quinidine-like effects QRS duration > 0.10

Corrected QT > 430 ms

Treat!

Treat!

Tx: Sodium Bicarbonate, and lots of it!

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Wolf-Parkinson-White Syndrome

Wolf-Parkinson-White Shortened PR interval Presence of a Delta-wave Occurs in 0.3%-1% of the population

Wolf-Parkinson-White

Wolf-Parkinson-White

Supraventricular Tachycardia

Orthodromic = Narrow Complex Down SA node through the Accessory Pathway Treat with adenosine/calcium channel blocker

Antidromic = Wide Complex Electrical impulses bypass the SA node via the accessory pathway Can allow for ventricular rates greater than 300 beats/min Treat as V-Tach (Defibrillation), amiodarone, or procainamide DO NOT USE ADENOSINE/DILTIAZEM

Wolf-Parkinson White

WPW with A. Fib vs. V. Tachycardia

How can you differentiate WPW with atrial fibrillation from Ventricular Tachycardia? Ventricular Tachycardia is a regular, wide complex rhythm compared to WPW with atrial fibrillation which exhibits irregular rate/rhythm

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Digoxin Toxicity

Digoxin Toxicity Blocks Na+/K+ to increase the refractory period of the AV node; i.e., slows conduction to aid in rate control Toxicity may be chronic or acute Frequently occurs in the presence of hyperkalemia Beware, you cannot use IV calcium to treat hyperkalemia in the presence of Digoxin May result in Stone Heart This may be largely theoretical, but don’t do it on the boards!

Brugada Syndrome Patients who present with syncopal episode who then go on to have sudden death if unrecognized and treated

Brugada Syndrome Pseudo RBBB V1-V2 ST Elevation in V1-V2

Hereditary, there may be a family history of sudden death in parents/siblings Treatment: AICD placement

Syncope: What to look for on the ECG Look for prolonged QT (usually >500 ms) Rule out the presence of Brugada Syndrome Pseudo RBBB V1-V2 ST elevation in V1-V2

One from the Pit 47 year-old AA male presents with a chief complaint of generalized weakness. He states he thinks he has the flu. Only significant past medical history is cirrhosis with intermittent ascites requiring paracentesis. His ECG is obtained:

Rule out the presence Hypertrophic Cardiomyopathy Deep Q waves in I, AVL

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One from the Pit

One from the Pit What is the most appropriate treatment for this individual? Transvenous Pacing Calcium Chloride C. Glucagon D. Sodium Bicarbonate E. Kayhexylate A. B.

One from the Pit Interpretation: ? Sinus/junctional rhythm 20’s-30’s Low voltage, Peaked T-waves

Further ECG review Carol Rivers EKG Review for the Written Boards https://emeeinc.com/catalog/ECGDownload_R.php

In this case, calcium chloride was given with a subsequent return to NSR in the 50’s within 5 minutes of administration.

Aortic Stenosis Systolic murmur that radiates to the carotids

Valvular Disorders

Harsh crescendo-decrescendo murmur Occurs secondary to congenital bicuspid valve or rheumatic fever EKG demonstrates LVH with strain pattern

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Aortic Stenosis

Aortic Insufficiency

Relatively asymptomatic until valve diameter is 90%)

Symptoms: Exertional Dyspnea, PND, palpitations

EKG findings: Atrial enlargement (P mitrale)

Frequently results in A. fib/CHF Management: Rate control for A. fib, antibiotic prophylaxis, commisurotomy or valve replacement for severe stenosis

Pregnancy + Pulm edema = Mitral Stenosis

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Mitral Regurgitation Acute onset = Rupture of chordae tendinae or papillary muscle

Holosystolic murmur radiating to axilla (differentiate from AS) Causes: Acute MI, endocarditis Symptoms: CHF, sudden dyspnea with MI Management: Afterload reduction (nitroprusside) Antibiotic prophylaxis Balloon pump if severe

Mitral Valve Prolapse Mid-systolic click Most common valvular disorder (5-10%) Associated with connective tissue disorders, scoliosis, pectus excavatum Associated with young females with palpitations and/or anxiety Presentation: Young athlete passes out during training, recovers, but appears anxious and c/o CP with palpitations Management: Beta Blockers, antibiotic prophylaxis

Infective Endocarditis Damage to a valve that results in platelet activation and subsequent bacterial colonization during periods of bacteremia

Infective Endocarditis

Infective Endocarditis Risk Factors: Prosthetic valves Most commonly affected in the first 2 months post-op Staph. epidermidis, Staph. aureus > 2 months, Strep viridans

Congenital heart disease (bicuspid valve) Rheumatic heart disease (most common cause of valve damage) IVDA Indwelling catheters

Left sided vs. Right sided Left Sided

Right Sided

Valvular Disease (congenital/acquired)

IVDA

Subacute + acute Systemic Involvement Mitral valve affected

Usually acute Pulmonary involvement Tricuspid valve affected Staph. aureus (>75%)

Strep viridans > Staph

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Infective Endocarditis Valves affected: Mitral > aortic > Tricuspid > pulmonary

If they give a patient with “flu-like symptoms”, think infectious endocarditis

Infective Endocarditis Symptoms: Fever + murmur (>50%), chest pain, hemoptysis, weight loss, malaise

Signs: Roth Spots: retinal hemorrhages Splinter hemorrhages: under fingernails Osler nodes: tender nodules on finger tips Janeway Lesions: non-tender macular lesions on palms/soles

Infective Endocarditis

Cardiac tumors

Diagnosis Blood cultures x 3: different sites/times Positive >90% of the time

Echo: TEE is best Does not rule out the disease however

CBC/ESR are helpful as well

Treatment: Vancomycin + Gentamycin

Antibiotic prophylaxis for any valvular dysfunction if undergoing dental or GU procedures

Primary benign Secondary usually malignant, result in pericardial effusion/pericarditis Myxomata: Most common (females) 75% occur left atrium

Symptoms: Obstruction (CHF), emboli Treatment: Surgical resection

Hypertensive Emergencies Elevated BP with evidence of end-organ damage End organs:

Hypertensive Emergencies

Brain (Intracranial bleed, CVA, encephalopathy, eclampsia) Heart (MI, angina, CHF, dissection) Kidney (Acute renal failure, proteinuria, RBC casts) Eyes (retinal hemorrhage)

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Hypertensive Emergencies

Hypertensive Emergencies

MAP = DBP + (1/3*(SBP-DBP))

Hypertensive urgency:

Cerebral Perfusion Pressure: CPP = MAP-ICP

Cerebral Autoregulation: MAP 50-150 mmHg

Diastolic > 110 mmHg Asymptomatic, no end organ damage No acute intervention needed, may elect to reduce with oral agents over 24-48 hours

Hypertensive Emergency: Diastolic > 140 mmHg with evidence of end organ damage Treatment for Hypertensive Emergency: MAP reduction of 20-25% in 30 minutes

Hypertensive Emergencies Medications: Nitroprusside qttp: Decreases afterload and pre-load by vasodilation, watch for cyanide toxicity

Labatolol qttp: Alpha and Beta receptor antagonists

Nitroglycerine qttp: Decreases pre-load by venous dilation

Esmolol qttp: Beta-1 blocker only, rapid half-life

Nimodipine Oral Dosing:

Hypertensive Emergencies Treatment for Hypertensive Emergency: Intracranial Bleeding: Nitroprusside/Labatolol qttp

Hypertensive Encephalopathy: Nitroprusside qttp

Ischemic CVA: Elevated BP is auto-protective, and BP reduction may increase the penumbra Only treat if DBP > 140 mmHg with Nitroprusside/Labatolol qttps with a goal of lowering 20 mmHg

Calcium channel blocker relaxes vascular smooth muscle

Hydralazine IV/IM: Direct arterial vasodilator

Hypertensive Emergencies Treatments (cont) Subarachnoid hemorrhage: Oral Nimodipine, decreases cerebral vasospasm and is autoprotective Nicardipine qttp

Aortic Dissection: Esmolol/Labatolol + Nitroprusside qttps

Acute MI: Nitroglycerine qttp

Acute Pulmonary Edema: Nitroglycerine qttp, furosemide, morphine, CPAP/BiPAP

Hypertensive Emergencies Treatments (cont) Eclampsia: IV Magnesium (6 grams over 10 minutes) IM Hydralazine/IV Labatolol/Delivery

Acute Hypertensive Renal Insufficiency: IV Nitroprusside

Clonidine Withdrawal: Restart Clonidine

Cocaine Intoxication: IV Benzodiazepine

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Antiarrhythmics: Class I:

Antiarrhythmics

Class Ia: Quinidine, Procainamide Class Ib: Lidocaine Class 1c: Propafenone

Class II: Beta Blockers Class III: Amiodarone, Sotalol Class IV: Calcium Channel Blockers Other: Digoxin, Adenosine

Antiarrhythmics Procainamide: Binds fast sodium channels Prolongs PR, QT intervals Prevent and treat reoccurrence of V-Tach or wide complex tachycardia Convert SVT in presence of WPW

Antiarrhythmics Lidocaine: Binds fast sodium channels Raises ventricular fibrillation threshold Maintain NSR following v-tach/v-fib 2nd line for v-fib/v-tach arrest

Antiarrhythmics Beta Blockers: Block catecholamine effects on β blockers Adverse effects:

Antiarrhythmics Esmolol: Short acting β1 > β2 Indicated for SVT (a. fib/flutter), Hypertensive emergencies, acute myocardial ischemia

Nausea, vomiting Bradycardia Hypotension Bronchospasm, pulmonary edema

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Antiarrhythmics Labatolol: β1/β2 + α1 adrenergic blocker β > α 3:1 Indicated for Hypertensive emergencies, myocardial ischemia

Antiarrhythmics Other β Blockers: Propranolol: MAT, Angina, thyrotoxicosis

Metoprolol: Acute MI

Sotalol: Chronic a. fib rate control Suppress ventricular dysrhythmias

Antiarrhythmics Amiodarone: Inhibits sodium channels Depress AV nodal conduction Indicated for v-fib/v-tach/wide complex tachycardias, a. fib/flutter with CHF Chronic usage can cause Pulmonary fibrosis Hepatotoxicity

Antiarrhythmics Diltiazem: Slows calcium influx into the myocardium Slows AV nodal conduction Indicated for rate control in a. fib, conversion of PSVT to NSR Contraindicated in wide complex tachycardia with WPW

Antiarrhythmics

Antiarrhythmics Digoxin:

Adenosine: Negative chronotropic effects on SA and AV nodal conduction Short acting (< 10 seconds) Indicated in the conversion of PSVT to NSR

Blocks Na+/K+ ATPase Inhibits SA/AV nodal conduction Positive inotrope: Increases cardiac output in CHF Negative chronotrope: Slows ventricular rate in a. fib/flutter

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Antiarrhythmics Digoxin: Don’t use in WPW Watch for toxicity, use Digibind (5 vials) for: K+ > 5.5 mEq/L Digoxin level > 10mg/mL

NEVER GIVE CALCIUM! Most common digoxin toxicity EKG finding? PVC’s

However, the hallmark rhythm of digoxin toxicity: PAT with AV Block

Key points to remember MI Patterns Dressler’s Syndrome Low Ca, Mg, K lead to Prolonged QT WPW: Give Procainamide Brugada Syndrome, recognize it! New systolic murmur in presence of an MI = chordae tendinae/papillary muscle rupture Aortic stenosis triad of symptoms Left vs. Right sided endocarditis Hypertensive Emergency: Drop MAP 20-25%

Good Luck on the Inservice!

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