Case: 55 year male several hours crushing chest pain. Medic ECG shows inferior STEMI with reciprocal ST depression. Patient is Hypertensive. Sats 90%. CXR with BL edema. Trop 4.5, Lactate 6.7, Cocaine positive. AORTIC DISSECTION WITH STEMI
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3 Major “can’t miss” causes of AFib · Acute myocardial infarction · Congestive heart failure · Pulmonary embolus Other common causes of AFib · Thyrotoxicosis · Hypertensive crisis · Valvular disease · Hypokalemia/Hypomagnesaemia · Drugs e.g. sympathomimetics · Pericardial disease · Cardiomyopathies · Pheochromocytoma · “Holiday heart” - too much ETOH Treatment of AF in the ED Unstable · Emergency Direct Current Cardioversion (DCC) o Biphasic 120J -200J o Pads in the AP position · Reasons DCC may not work o Underlying illness – CHF, thyrotoxicosis, valvular disease o Dilated left atrium o Longer duration of atrial fibrillation o Too low energy · Meds: o Suspicion for accessory pathway, consider one of the following: - Procainamide - Ibutilide - Amiodarone o No suspicion for accessory pathway, consider one of the following: - Ibutilide - Diltiazem - Magnesium - Amiodarone - Procainamide Stable Start with rate control then consider disposition · Rate control o Calcium Channel Blockers – 1st line treatment - Diltiazem - 0.25 mg/kg IV over two minutes then 0.35 mg/kg IV over two minutes, if there is no response at 15 minutes - Veramamil - 2.5-5.0 mg over 2-3 minutes, then 5-10 mg in 15-30 minutes if necessary ± drip 5 mg/h o β-blockers – good in increased adregnergic states - Metoprolol - 5 mg IV every 5 minutes up to 15 mg - Esmolol - 500 mcg/kg IV bolus over 1 minute followed by a 50-200 mcg/kg/min IV infusion. Repeat cycle and increase drip if no effect o Cardiac Glycosides – not used as monotherapy anymore - Digoxin - Load 0.5 mg IV repeat 0.25 mg every 4-6 hours for three doses o Class III Antiarrythmic – beware of unintended rhythm control - Amiodarone - 150 mg IV over 10 minutes followed by infusion of 1 g over six hours. May repeat bolus if needed o Magnesium Sulfate - beware of unintended rhythm control - MgSO4 - 2 g bolus over 10-15 minutes followed by 1 g/h infusion Disposition - “Elective” Cardioversion in the ED “Pro-ED Converters” o Safe if arrhythmia present for <48h and studies show that patients can reliably tell when their symptoms began (i.e within 48h or not) o Cardioversion – electrical, pharmacologic or spontaneous – of patients with recent onset atrial fibrillation carries a less than 1% embolism risk if performed within the first 48h of symptom onset o Early conversion ↓ need for anticoagulation o Many patients discharged means ↓ costs “Anti-ED Converters” o Risk of thromboembolism too great o Patients need heparin prior to cardioversion o New onset AFib patients need a complete diagnostic workup o Use of chemical agents requires prolonged observation in ED after successful cardioversion. o Shouldn’t risk conversion agents or electricity when 40-71% convert spontaneously in the first 24h Rhythm Control (a.k.a. Cardioversion) · Direct Current Cardioversion is the traditional Gold Standard o 90% to 100% acute success rate o IV/O2/Monitor/Sedation o Propofol/Fentanyl or Fentanyl/Versed o Airway Equipment o Defib pads in the AP position · Chemical Cardioversion o Class IA Antiarrythmic - Procainamide - 100 mg IV q 5-10 minutes to maximum of 1000 mg, or 20 mg/kg IV infusion to a maximum of 20 mg/kg o Class IC Antiarrythmic – “Pill in the Pocket Technique” - Flecanaide – 2 mg/kg IV over 10 minutes, or 300 mg PO x1 - Conversion rate 60-70% at 3 hours - 91% at eight hours - Propafenone - 2 mg/kg IV over 10 minutes, or 600 mg PO x1 - Conversion rate up to 76% at 8 hours o Class III Antiarrythmic - Ibutilide - 0.01 mg/kg IV over 10 minutes (max 1 mg), may Repeat times 1 if no response after 10 minutes. - Cardioversion 33-45% in first 70 min - Risk of torsades as high as 8% Ottawa Aggressive Protocol for emergency department patients with recent-onset atrial fibrillation 1. Assessment · Stable without ischemia, hypotension or acute CHF? · Onset clear and less than 48 hours? · Severity of symptoms? · Previous episodes and treatments? · Anticoagulated with warfarin and INR therapeutic? 2. Rate control · If highly symptomatic or not planning to convert · Diltiazem IV (0.25 mg/kg over 10 min; repeat at 0.35 mg/kg) · Metoprolol IV (5 mg doses every 15 min) 3. Pharmacologic cardioversion · Procainamide IV (1 g IV over 60 min; hold if blood pressure < 10 mm Hg) 4. Electrical cardioversion · Consider keeping patient NPO × 6 h · Procedural sedation and analgesia given by emergency physician (propofol IV and fentanyl IV) · Start at 150–200 J biphasic synchronized* · Use anterior–posterior pads, especially if not responding 5. Anticoagulation · Usually no heparin or warfarin for most patients if onset clearly < 48 h or if therapeutic INR for > 3 wk 6. Disposition · Home within 1 h after cardioversion · Usually no antiarrhythmic prophylaxis or anticoagulation given · Arrange outpatient echocardiography if first episode · Cardiology follow-up if first episode or frequent episodes 7. Patients not treated with cardioversion · Achieve rate control with diltiazem IV (target heart rate < 100 beats/min) · Discharge home on diltiazem (or metoprolol) · Discharge home on warfarin and arrange INR monitoring · Arrange outpatient echocardiography · Follow-up with cardiology at 4 wk for elective cardioversion 8. Recommended additions to protocol · Consider transesophageal echocardiography if onset unclear · Alternate rhythm-control drugs: propafenone, vernakalant, amiodarone · If TEE-guided cardioversion > 48 h, start warfarin Thyrotoxicosis and Cardiomyopathy
Myocardial Infarction in TTP
Penetrating Scrotal Trauma:
Diagnotic Error in Medical Decision Making
Mechanical Issues Acute mitral regurg - 7 to 10 days post MI - can result from papillary muscle rupture - often complication of inferior MI - can cause abrupt cardiogenic shock - best tx = afterload reduction with diuretics, nitroprusside, Surgery. Ventricular septal rupture - first 24 hrs and at 2-5 days - findings: holosystolic murmur, CP, painless hypotension - tx: O2, surgery, vasodilators, nitroprusside Ventricular aneurysm - findings: CHF +/- shock - dx: CXR w/ enlarged silhouette - At risk for thromboembolism. Ventricular free wall rupture - cause hemopericardium/tamponade - signs: CP, hypotension, tamponade Post MI Arrhythmias
Dressler's Syndrome
Pathophysiology Based on 2 concepts - Increased hydrostatic pressure - Decreased oncotic pressure CXR - Upright films will detect effusions >400mL - Lateral decubitus films will detect as little as 50mL of fluid Fluid analysis - Order: cell count, gram stain, culture, pH, protein, LDH Exudate vs transudate - use Light's Criteria Transudates: CHF Nephritis Nephrotic syndrome Exudates: Infection Traumatic HTX Malignancy CT disorders Management: - Treat the underlying pathology! - Avoid large volume taps (>1L) if CHF, renal or hepatic pathology - Unstable - septic shock, tension hydropneumothorax - If tapping: - Avoid NV bundle - Have patient lean over table - Use ultrasound - When to tap: - Typically, these patients will not need a tap or tube in the ED. - If patients have persistent hypoxia in spite of other interventions, consider tap. - Severe respiratory failure. Complications: PTX Infection Hemorrhage Rare - air embolism, sheared catheter loss Wide Complex Tachycardia... and Overthinking If it is a Wide Complex Tachycardia... DON'T OVERTHINK IT!! Treat it as VTACH! > Wide complex tachycardia - vtach 80% of the time; but also consider SVT with aberrancy or preexcitation, toxic metabolic (hypomag, hyperk, TCAs IC antiarrythmics) or pacemaker related > Regular wide complex tachycardia - Unstable - synchronized cardioversion > Cardioversion may be resistant if tox/metabolic > Consider bicarb if resistant > If recurrent start amio, procainimaide or lidocaine - If stable - procainamide; amio/lido Pericarditis vs. MI Your goal is not to diagnose pericarditis... it is to not miss MI. Pericarditis = fever, position dependent pain, diffuse elevation, no reciprocal changes, no Q wave MI = focal ST changes, reciprocal changes, Q waves, +/- pulmonary edema {From Dr. Mattu's ECG Lessons} Factors strongly favoring Acute MI: -- ST Depression in any lead other than V1 or aVR -- ST elevation that is Convex upwards (tombstone) or Slant-like/Horizontal. -- ST elevation in III > II If you have none of those, then consider the Factors that favor pericarditis: -- Pronounced PR depression in multiple leads (often only seen early in viral pericarditis) -- Friction rub Spodick's Sign: downsloping of QRS-TP segment in 80% of acute pericarditis When in doubt, check SERIAL ECGs!! What to order? - Consider troponin, CRP, WBC, ESR, CXR - CRP can be used for diagnosis and disease monitoring Treatment: - NSAIDS = mainstay - Colchicine + conventional therapy => decrease in recurrence rate in patients with a first eposide of acute pericarditis - dose is 0.5mg daily (<70kg) or 0.5mg BID (>70kg) x 3months (none of our cardiologists treat for that long) Recurrent pericarditis = symptom-free for 6 weeks and then symptoms recur Caution with Colchicine - elderly, hepatic/renal failure, pregnant patients In refractory cases, consider steroids, chemotherapeutic agents Acute Mitral Regurgitation - acute vs chronic Most common cause of acute: 1. Rupture chordae tendinae due to myxomatous disease, infectious endocarditis, rhemuatic heart disease 2. Rupture papillary muscle due to MI (2-7 days prior) Can get pulmonary edema, cardiogenic shock, mimics ARDS, PNA, difficult exam findings Echo enables you to quantify degree of MR; use color flow doppler echo to evalute for acute MR Persistent Tachycardia
Buergers disease
Case 1 - Lower extremity weakness
> Stanford classification - A involves the aortic root, B is limited to the descending aorta > Prsenting sx of type B dissections- chest or back pain, abrupt onset of pain > Imaging - CXR - 56,5% are nl, TTE - usef for aortic root, CT best sensitivity and specificity Therapy
Case 2 - Fatigue - dyspnea
b. Admitted to hospital - heparin drip stopped and echo gotten - shows right heart strain c. CTA showed massive Bilateral PEs Predictors of Complications from PE
Submassive PE - Rigth ventricle with dilitation and systolic dysfunction, CT - RV dysfunction, elevated BNP or troponin |
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