Cardiac emergencies 2

Cardiac emergencies 2 - CARDIOVASCULAR EMERGENCIES...

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Unformatted text preview: CARDIOVASCULAR EMERGENCIES REVIEW-II CORE CONTENT SYNTHESIS-BASED ON ABEM, SAEM, ACEP & ACLS OUTLINES CLINICAL PEARLS David Riley, MD David Director of Ultrasound Training & Resident Didactics Director Department of Emergency Medicine Department St. Luke’s Roosevelt Hospital Center St. Columbia University College of Physicians & Surgeons Columbia DISTURBANCES OF CARDIAC RHYTHM MECHANISMS FOR ARRHYTHMIAS 1. INCREASED AUTOMATICITY: INC. SLOPE OF PHASE 4 (Epi causes this & Lidocaine decreases phase 4 slope) 2. TRIGGERED AUTOMATICITY: OSCILLATIONS OF PHASE 4 AMPLITUDE W/INC. CHANCE OF GETTING TO THRESHOLD 3. CONDUCTION-DISTURBANCES AND RENTRY, IE PROL. QTc MOST STABLE PATIENTS NEED MEDICINE UNSTABLE PATIENTS NEED ELECTRICITY NORMAL ESCAPE RATES SA NODE AV NODE VENTRICLES 80 BEATS/MIN 60 BEATS/MIN 40 BEATS/MIN AHA CLASSIFICATIONS OF INTERVENTIONS IN ACLS Class I: Definitely Helpful Class IIa: Acceptable, Probably Helpful Class IIb: Acceptable, Possible Helpful Class III: Not Indicated, May be Harmful A. ATRIAL FIBRILLATION 1. ATRIAL RATE IS 400-600, RHYTHM IS 600, IRREGULARLY IRREGULAR, can precipitate CHF-espec. w/LVEF < 50%, NO S4, IRREGULARLY w/LVEF CONSIDER THYROTOXICOSIS THYROTOXICOSIS 2. RAPID VENTRICULAR RESPONSE MAY OCCUR: MAX 200:> 200 MAX = WPW: Rx - procanamide 3.RX:HEMODYNAMICALLY UNSTABLE - SYNC 3.RX:HEMODYNAMICALLY CARDIOVERSION WITH 200J: need big CARDI 4. A FIB WITH RVR: USE DILTIAZEM .25MG/KG IV .25MG/KG 4. Joules to cardiovert cardiovert OVER 3-5 MIN TO SLOW THE VENT. RATE 1ST; IN ELDERLY GIVE IN 5MG MIN INCREMENTS TO AVOID HYPOTENSION , LOAD W/DIGOXIN ALSO 0.5mg IV 0.5mg THEN YOU HAVE 48 HRS TO CONVERT THE A FIB TO NSR, WITH A IA-QUINIDINE OR III CLASS DRUG-Ilbutilide OR CARDIOVERSION QUINIDINE OR 5. PTS WITH CHRONIC AFIB HAVE 60% STROKE REDUCTION WITH 5. COUMADIN RX(INR GOAL 2-3;3.5-valves) COUMADIN ATRIAL FIBRILLATION: New Onset 50-70% convert to NSR spontaneously 48 Hour Rule: New onset AF should be converted to normal sinus rhythm w/I 48 hours Clot risk with embolic complications >48 hrs=atrial stunning: lasts 3-6 weeks & need for anticoagulation New Drugs:IV: amiadarone, ilbutilide (torsades 4-8%risk), PO only: propafanone New Onset Atrial Fibrillation ADMIT ALL 50-70% will convert to NSR spontaneously R/O: thyrotoxicosis, pulmonary embolism, pericardial disease, carbon monoxide, lyme disease Refractory AF/Aflutter: can be due to pericardial disease/effusion, or CO poison ELECTRICAL CARDIOVERSION INDICATIONS: UNSTABLE TACHYCARDIA WITH HR >150 AND OR DROPPING BP<90; IE FOR VT, PSVT, ATRIAL FIBRILLATION OR FLUTTER WITH A RAPID VENTRICULAR RESPONSE PREOXYGENATE, CHECK: OXYGEN SATURATION, IV, SUCTION DEVICE, INTUBATION EQUIPMENT at bedside as apnea can result PREMEDICATE WHENEVER POSSIBLE: USE A SEDATIVE(MIDAZOLAM(VERSED) 2-5MG IV, DIAZEPAM, KETAMINE, BARBITUATES) AND AN ANALGESIC( MORPHINE, MEPERIDINE, OR FENTANYL) B. ATRIAL FLUTTER 1. MAY OCCUR WITH AV BLOCK-IE 2:1 HR 150; SAWTOOTH 1. SAWTOOTH AV PATTERN:Especially in INFERIOR LEADS, P-waves=V1-2 upright, V5-6 PATTERN:Especially inverted, Can Can fluctuate from 2:1 to 3:1 to 1:1 NORMAL QRS & PR, MAY HAVE REGULAR OR VARIABLE BLOCK, with 1:1 NORMAL BLOCK CAN GO VERY FAST IE 300 BLOCK 2. RX: UNSTABLE; SYNC. CARDIOVERSION WITH 25-50J, 2. 25 50J, VERY SENSITIVE TO ELECTRICITY SENSITIVE 3. STABLE PATIENTS WITH A RVR USE;AV AV BLOCKER FIRST: DILTIAZEM FIRST: NODAL .25MG/KG IV OVER 3-5 MIN TO CONTROL THE VENTRICULAR RATE, THEN USE IA-QUINIDINE OR III CLASS DRUG , OR CARDIOVERSION, TO OR USE IA CONVERT, IV Amiodarone has been used to slow flutter rate has TO NORMAL SINUS RHYTHM IF ACUTE, MUST ANTICOAGULATE FOR 3 TO WKS PRIOR TO CARDIOVERSION IF CHRONIC WKS C. ATRIAL/JUNCTIONAL ECTOPY 1. IMPULSES THAT ORIGINATE FROM AN ECTOPIC FOCUS 1. WITHIN THE AV NODE OR THE BUNDLE OF HIS BEFORE THE BIFURCATION; NO OR IRREGULAR P WAVES THE 2.CAUSES: DIGTALIS TOXICITY, CAD, CHF, AMI ESPEC INF WALL 2.CAUSES: AMI 3. TREAT THE UNDERLYING CAUSE 4. JUNCTIONAL TACHYCARDIA MUST 4. BE ADMITTED BE 5. Rx: procanamide 5. Rx procanamide MULTIFOCAL ATRIAL TACHYCARDIA IRREGULARLY IRREGULAR 3 DIFFERENT TYPES OF P WAVES CAUSED BY UNDERLYING PULMONARY PATHOLOGY, COPD, THEOPHYLLINE TOXICITY(Big worryhypokalemia), Caffeine: can cause PAT #1, hypokalemia can cause MFAT also TREAT THE PULMONARY PROBLEM TO CORRECT HR CONTROL W/ MG-SULFATE(make sure K is 4) 2gm IV OVER 2min/ DILTIAZEM 0.25mg/kg OVER 2’ Warning: Cardioversion can result in rhythm degeneration Theophylline Toxicity MFAT At therapeutic levels antagonizes the activity of adenosine Rx: in pts w/ COPD, theo & MFAT : small doses of verapamil Activated charcoal is good for OD Intractable emesis: Rx w/ reglan or odansetron Charcoal hemoperfusion is better than hemodialysis due to high protein binding BIG WORRY: HYPOKALEMIA CAN CAUSE TACHYCARDIA-BETA-1 & HYPOTENSION: DUE TO BETA-2 VASODILATATION (CAREFUL PROPRANOLOL MAY BE USEFUL BARRING ANY CONTRAINDICATIONS) D. PRE-EXCITATION: Initial QRS Prolongation w/nl PJ interval delta wave RESULT FROM ABNORMAL CONNECTIONS OR ACCESSORY PATHWAYS BETWEEN THE ATRIA AND VENTRICLES WPW: Kent bundle connects the atria directly to the ventricle; delta wave,SHORT PR, Irreg: wide QRS if ANTIDROMIC CONDUCTION, NL PJ interval, Reg: normal QRS if ORTHODROMIC CONDUCTION Lown-Ganong-Levine: Jame’s fibers connect the atria to the proximal His bundle; no delta wave, normal QRS Treatment: Narrow complex SVT - use Adenosine; wide complex SVT- presume VT and if unstable cardiovert 50-100J; if hemodyamically stable use IV procainamide/amiodarone: DRUGS OF CHOICE VERAPAMIL, BETA BLOCKERS AND DIGOXIN ARE CONTRAINDICATED AS THEY CAN INCREASE CONDUCTION OVER THE ACCESSORY PATHWAY AND FATALLY INCREASE THE VENTRICULAR RATE Procainamide: How to give? Load 100mg IV q10min or 20mg/min until: – – – – QRS widens >50% dysrhythmia suppressed hypotension total of 17mg/kg or 1000mg total = (50minutes to run in) WPW & ESRD: The Procainamide Dilemma? Procainamide is metabolized to Nacetyl-procainamide, an active metabolite that accumulates rapidly in patients with ESRD. This can lead to complications of procainamide toxicity: hypotension, prolonged QTc WPW & ESRD: The Procainamide Dilemma? The solution = cardioversion or amiodarone: renal adjusted dose WHAT IS THE DIFFERENTIAL DIAGNOSIS OF A PATIENT WITH A VENTRICULAR RATE OF 300 ATRIAL FLUTTER 1:1 WPW SYNDROME Pediatric PSVT 220-360 Runaway pacemaker TOTAL QRS PROLONGATION: SINE WAVE PROCAINAMIDE OR QUINIDINE TOXICITY Darvon: propoxyphene: seizures TCA TOXICITY IA, PROLONGED QTc AGENTS SEVERE HYPERKALEMIA KEY IS TO AVOID PROCAINAMIDE Rx: IV Na+ HCO3- E. SUPRAVENTRICULAR TACHYCARDIA P WAVES OFTEN HIDDEN; REGULAR RHYTHM; VENTRICULAR RATE 160-240; QRS USUALLY NARROW BUT MAY BE WIDE DUE TO RBBB CAUSES: preexcitation, mitral disease, digitalis tox., AMI, rheum, hyperthyroidism RX: Unstable; sync. cardioversion - 75-100J(if digoxin tox. is the cause then cardioversion should be avoided); Stable; vagal maneumers, Adenosine(can cause bronchospasm-care w/asthma) (excellent dignostic drug) 6mg IV(antecubital)push then 12mg IV push if no response(use 3mg if carbamezapine or dipyridamole on board); if Adenocard doe not work then second line drugs such as verapamil 5mg over 5min IV; esmolol 500mcg/kg bolus followed by 50mcg/kg/min infusion; digoxin .5mg IVP & .25mg q30’times 2 NEVER GIVE CCB IV AND BETA BLOCKER IV TO SAME PATIENT DIGOXIN INDUCED SVT RX: Mag. Sul. 1-2gm slow IV, or Dilantin 15-18mg/kg IVPB in NS at a rate of 50mg/min or less, DIG TOXICITY, PAT W/BLOCK, AVOID ELECTRICITY AS THIS MAY PRECIPTATE VT OR VF, ALSO FAB’S F. BRADYCARDIA CAUSES: INFERIOR WALL MI, VAGAL RESPONSE, DRUG(IE B-BLOCKER), SINUS NODE DISEASE, Hypothermia, Hypoglycemia RX: IF ASSYMPOMATIC AND NO ESCAPE PVCS or Mobitz II or 3rd deg. HB, then OBSERVE RX: if SX; atropine(I&IIa) .5-1.0mg IV q5min to a total of .04mg/kg(denervated transplanted hearts will not respond to atropine-go directly to pacing); TRANSCUTANEOUS OR TRANSVENOUS PACING (i) if avail; dopamine(2ND LINE) 520ug/kg/min(IIb); epinephrine(THIRD LINE) 2-10 ug/min(IIb); isoproterenol now considered class III PREMATURE VENTRICULAR CONTRACTIONS CAUSES:HYPOXIA, AMI, DRUGS-STIMULANTS, DIGOXIN, HYPERTHYROIDISM, CARDIOMYOPATHY RX: ONLY IF SUSTAINED, IE COUPLETS: LIDOCAINE 1.5MG/KG IV MAY REPAET 0.5MG/KG Q2-5MIN UNTIL NO ECTOPY OR TO TOTAL OF 3MG/KG - 2ND LINE PROCAINAMIDE 20MG/MIN UNTIL NO ECTOPY OR UP TO 1000MG TOTAL 17mg/kg, OR PROLONGED QTc OR QRS ; bretylium; overdrive pacing; once ectopy resolved, start lidocaine drip at 2-4mg/min; or procainamide drip 1-4 mg/min; or bretylium drip 2mg/min ESCAPE PVCS + CP(BRADYCARDIC): RX: ATROPINE, LIDOCAINE MAY WIPE OUT ANY RHYTHM G. VENTRICULAR FIBRILLATION FINE OR COARSE ZIGZAG PATTERN CAUSES:hypothermia, electrolyte imbalance, blunt chest trauma, AMI: if CPR <10min then LYSE, toxins, drugs RX: IMMEDIATE DEBIBRILLATION 200J- 300J- 360J RX: IF RETURN OF CIRCULATION SUPPORTIVE AND IV LIDOCAINE; IF PERSISTENT VF; continue CPR, intubate, obtain IV access, epinephrine 1mg IVP q3-5min,1-3-5MGIVP, HDE:10MG(NO PROVEN BENIFIT IN ADULTS) (sodium bicarbonate 1.0mg/kg is class I if patient has known preexisting hyperkalemia); continued sequenced shocks are class I; then administer medicines of Probable benefit class IIb alternating with drug-shock-drug-shock etc.: lidocaine 1.5mg/kg IVP q35min to a loading dose of 3mg/kg; bretylium 5mg/kg IVP & repeat in 5min at 10mg/kg; magnesium sulfate 1-2gm IV in Torsades de Points(prol QTc) or severe refractory VF; procainamide 30mg/min to a total of 17mg/kg, Amiodarone 300mg IVP, vasopressin 40U IVP PA CATHETER IN POST ARREST PATIENTS WITH PULMONARY EDEMA: Goal is Box I Precordial Thump is Class IIb if witnessed ar. no pulse or defib. How to Mix Drips? Lidocaine, Procainamide & Bretylium: Put 1.0 gram in 250cc of D5W 4mg in 1.0cc 2.0mg/min = 0.5cc/min 60microdrops = 1.0cc 2.0mg/min = 30microdrops/min = 30cc/hr ACLS 2000: New Guidelines Amiodarone & procainamide are now 1st line ahead of lidocaine for stable wide complex tachycardia Bretylium has less recommendation Amiodarone: Class II b:”consider use” for VT/VF Vasopressin (40 U IV): also II b for VF, yet evidence that may be more effective than EPI for promoting the return of spontaneous circulation Airway: lower Tidal-vol. 6-7cc/kg ie 500ccin 70kg person; Skilled intubator: >6 intubations/year Airway: confirm tube placement, and hold tube better VF: AED’s w/I 5 min in public places, no public pulses; aggressive in hospital CPR and early defibrillation ACLS 2000: New Guidelines Amiodarone in VF/pulselessVT: 300mg IVP Amiodarone in Stable VT especially when EF<40% or CHF setting: 150mg IV infusion over 10 minutes, may repeat in 15 minutes Amiodarone: contraindicated in marked bradycardia or heart block; Increases digoxin levels 70%; sig. Increases INR with warfarin ACLS 2000: New Guidelines ACS: Prehospital 12-lead ECG and TPA ( if CP to ED arrival time>60 min (30min in Europe)) Angioplasty: is Class I in patients who are <75 and are not TPA candidates: DUTY TO TRANSFER TO A CENTER with MD in route, ie RH to SL IIB/IIIA inhibitors: Class II a: non-Q wave AMI and high risk Unstable Angina Heparin IV: <70 KG: 60U/kg bolus, 12U/kg/hr drip >70 KG: 4000U max bolus, and 900U/hr drip ACEI’s: large Ant wall AMI, EF <40% w/o low BP Stroke: 3 HR window- TPA; 3-6HRS: ? Prourokinase Post Resuscitation: KEEP PATIENTS COOL Cocaine CP: BB are Class III; TCA’s: ser.pH 7.5-55 Respiratory Failure w/Opiates: TUBE 1st, then Narcan VENTRICULAR FIBRILLATION 200 J DEFIBRILLATION IS FIRST PRIORITY IN V. FIB. H. VENTRICULAR TACHYCARDIA WELLENS CRITERIA:VT vs. SVT w/abberancy: ABSENT P-WAVES, WIDE QRS COMPLEXES>140ms; FUSION-BEATS( CROSS BETWEEN A NORMAL AND WIDE QRS COMPLEX-preceding a run of VT), a-v dissociation, capture beats,+/- all concordant, Brugada criteria: ALL FAVOR VT RATE USUALLY 150-200 BPM; REGULAR RHYTHM. VT: in pts w/mvp, ami-ischemia, cardiomyopathy, TOF. VERAPAMIL + VT=DEATH RX: STABLE - LIDOCAINE 1.5MG/KG IV THEN 2-4 MG/MIN IF CORRECTED. 2nd Line:Procainamide: 20mg/min to 17mg/kg max (watch for hypotension). THIRD LINE DRUG IS AMIADARONE(central only- periph. sclerosis of veins) 150MG iv over 10 min, then 1mg/min inf. over 6 hr. UNSTABLE W/PULSE CARDIOVERSION WITH 100J; PULSELESS VT SAME RX AS V. FIB., WITH 200J ELECTRICAL DEFIBRILLATION WIDE QRS TACHY?: LIDO THEN ADENOSINE(ONLY IF REGULAR RATE(BIG WPW WORRY IF IRREG.), THEN PROCAINAMIDE TORSADES DE POINTS(twisting of the pointes): ATYPICAL VT USUALLY PRECIPITATED BY PROLONGED QTc, ie, IA drugs; TREATMENT: correct underlying problem; MAGNESIUM SULFATE 1overdrive 2GM IV over 2min; isoproterenol, pacing VENTRICULAR TACHYCARDIA ALWAYS RULE OUT HYPERKALEMIA FIRST IN THE SETTING OF STABLE VENTRICULAR TACHYCARDIA BECAUSE: IV LIDOCAINE + SYSTEMIC HYPERKALEMIA = DEATH IMPLANTABLE DEFIBRILLATORS: IN VF Place defib pads Ant/Post INDICATIONS: – SURVIVORS OF CARDIAC ARREST WITH DOCUMENTED VT OR VF – PATIENTS WITH DRUG REFRACTORY, CLINICAL, AND INDUCIBLE SUSTAINED VT – PATIENTS WITHOUT DOCUMENTED SUSTAINED VT AT RISK FOR FUTURE LIFE THREATENING ARRYTHMIAS BECAUSE THEY ARE INDUCED AT ELECTROPHYSIOLOGY STUDY I. IDIOVERTRICULAR RHYTHM VENTRICULAR ESCAPE - RATE 20- 40 CAUSES: TAMPONADE, HYPOXIA, EXSANGUINATION, CAD/AMI RX: THE PRIMARY CAUSE, IF HEMODYNAMICALLY COMPRIMISED: PACEMAKER AVOID LIDOCAINE - NEG INOTROPE MAY OBLITERATE PATIENTS ONLY FUNCTIONING RHYTHM PROLONGED QTc INTERVAL: 440ms men, >450ms women > ACQUIRED: IA,IC & III ANTIDYSRHYTHMICS, PHENOTHIAZINES, TCA’S, ORGANOPHOSPHATES, ANTIHISTAMINES, LOW POTASSIUM-CALCIUMMAGNESIUM, LOW PROTEIN DIET, AV BLOCK&SEVERE BRADYCARDIA, HYPOTHYROIDISM, CVA-INTRAPARENC.bleed, MYOCARDIAL ISCHEMIA, HIGH DOSE 100-200mg IV HALDOL/day CONGENITAL: JERVELL & LANGE-NIELSEN (DEAFNESS, AUT. RECESSIVE), ROMANO-WARD(NL HEARING,AUT. DOM.): Beta Blockers to Rx, MVP RECURRENT SYNCOPE/SUDDEN DEATH Phase 3: K+ delayed rectifier channel is impeded SHORTENED QTc HYPERCALCEMIA: Dx. PAM P SCHMIDT, STONES, ABD. MOANS, PSYCHIC OVERTONES Rx NS first then diuresis-LASIX, third line drug is CALCITONIN PREMATURE INFANTS ECG Digitalis OD CONDUCTION BLOCKS A. SICK SINUS SYNDROME B. ATRIOVENTRICULAR BLOCKS C. BUNDLE BRANCH BLOCKS D. TRIFASCICULAR BLOCKS A. SICK SINUS SYNDROME CHRONIC DISEASE OF THE SA NODE WITH MANY MANIFESTATIONS: PERSISTANT SINUS BRADY( EARLIEST FINDING), SINUS ARREST, SA BLOCK, CHRONIC AF (END-STAGE)OR FLUTTER WITH SLOW VENTRICULAR RATE, HYPERSENSITIVE RESPONSE TO CAROTID S. STIM. OR VALSALVA, FAILURE TO RESTORE TO SINUS RHYTHM AFTER CARDIOVERSION & THE BRADYCARDIATACHYCARDIA SYNDROME----ALL OF THE ABOVE ARE NOT DRUG INDUCED DIAGNOSIS: 12 LEAD OR HOLTER CLINICAL: #1CNS-SYNCOPE, NEAR-SYNCOPE, LIGHTHEADEDNESS; #2 CARDIO-PALPITATIONS, WORSENING CHF IE PULM EDEMA RX: SYMPTOMATIC OR ADVANCE SSS ALL NEED PERMANENT PACEMAKERS, BUT IN THE ED TRANSCUTANEOUS/TRANSVENOUS MAY BE USED; AFTER PACING SOME PTS NEED ANTIARRYTHMICS FOR THE TACHY COMPONENT OF THE BRADY-TACHY SYNDROME PACER CAN STILL HAVE TACHYCARDIA: MEDS TO CONTROL HEART RATE ARGUMENT TO ADMIT ELDERLY PT. W/SYNCOPE OR NEAR SYNCOPE: EPISODE OF BRADYSYNCOPE, NOW IN NSR ON ECG IN ED W/O SX: ADMIT B. ATRIOVENTRICULAR BLOCKS 1. FIRST DEGREE AV BLOCK 2. SECOND DEGREE AV BLOCK – MOBITZ I – MOBITZ II 3. THIRD DEGREE AV BLOCK CAUSES OF AV BLOCKS DRUGS: DIGOXIN, LIDOCAINE, PHENYTOIN, IA(PROCAINAMIDE, QUINIDINE), BETA-BLOCKERS, CALCIUM CHANNEL BLOCKERS INFLAMMATION: MYOCARDITIS HYPERKALEMIA: >7.0 MEQ/L: LBBB w/no Pwaves HYPERMAGNESEMIA >5.0 MEQ/L HYPOTHERMIA < 30 DEG C(86 DEG F) CONGENITAL CONDUCTION DEFECTS ACUTE INFERIOR-MORE COMMON OR ANTERIOR WALLMORE LETHAL MYOCARDIAL INFARCTION Infiltrative diseases: sarcoidosis, amyloidosis, hemachromatosis CONGENITAL HEART BLOCK CTD: RA, SLE, Reiter’s, ankylosing spondylitis HLA-B27 Misc. Addison’s, trauma, tumor-mesothelioma, idiopathic fibrosis=Lenegre’s & Lev’s disease WHAT IS A LBBB-LIKE ECG PATTERN WITH NO or small P WAVES? ANSWER: HYPERKALEMIA Hyperkalemia Treatment #1: Calcium gluconate/chloride(vein sclerosis) Bicarb 1meq/kg if acidotic ( 3amps in 1 litre of D5W=isotonic) D50 1-2 amps & 5-10U iv insulin Kaexylate 30 gm po/pr Dialysis Albuterol nebs( drop K 0.5) Loop diuretics, lasix FIRST DEGREE AV BLOCK P WAVES AND QRS NORMAL 1:1 RELATIONSHIP BET P & QRS *PR INTERVAL >0.20 SECONDS RX: NONE 2ND DEGREE AV BLOCK MOBITZ I WENCKEBACH PR INTERVAL PROGRESSIVELY LENGTHENS UNTIL A BEAT IS DROPPED SEEN IN INFERIOR WALL AMI RX: IF SYMPTOMATIC USE ATROPINE 1ST & PACING IF THIS FAILS 2ND DEGREE AV BLOCK MOBITZ II KEY HERE IS THAT THE PR INTERVALS ARE ALWAYS THE SAME PROLONGED DURATION, ANTERIOR AMI THERE ARE DROPPED BEATS RX: MORE SEVERE, MOST NEED PACING & ATROPINE is Contraindicated as it can lead to paradoxical SLOWING of the ventricles THIRD DEGREE AV BLOCK #1 Cause = Anterior AMI THERE IS NO RELATIONSHIP BETWEEN P WAVES AND QRS COMPLEXES; ATRIAL RATE & SLOWER INDEPENDENT VENTRICULAR ESCAPE RATE NO ATRIAL IMPULSES ARE CONDUCTED RX: ALMOST ALWAYS REQUIRES A PACEMAKER TC or TV PACEMAKER INDICATIONS SYMPTOMATIC BRADYCARDIA UNRESPONSIVE TO DRUGS ACUTE MI+ any 2 bundles out = SHOULD BE PACED IE: AN – – – – MOBITZ II OR COMPLETE H.BLOCK RBBB + LASF BLOCK RBBB + LPIF BLOCK LBBB NEW TRIFASCICULAR BLOCK OVERDRIVE OF TACHYDYSRHYTHMIAS PACEMAKER FAILURE life; SIGNS: SLOWING: If Brady Arrest need Transcutaneus pacer to sustain RUNAWAY PACER - BOTH USUALLY DUE TO BATTERY DEPLETION FAILURE TO PACE: ABSENCE OF PACEMAKER SPIKES; CAUSES: #1 OVERSENSING (suppressing impulse generation); WIRE FRACTURE (usually at sharp bend in the wire), BATTERY OR PULSE GENERATOR FAILURE FAILURE TO SENSE OR CAPTURE: DETECTED BY THE PRESENCE OF PACEMAKER SPIKES OCCURING AT THE WRONG TIME(FAILURE TO SENSE), SPIKES WITHOUT QRS COMPLEXES (FAILURE TO CAPTURE) ; CAUSES: LEAD MALPOSITION, WIRE FRACTURE, DEPLETED BATTERY, ELEVATED MYOCARDIAL THRESHOLD ( DUE TO FIBROSIS, LEAD DISPLACEMENT, ISCHEMIA, AMI), UNDERSENSING (CAN’T DETECT QRS) PACEMAKER MED. TACHY: DUAL CHAMBER PACERS (REENTRY) RX: MAGNET TO TURN OFF SENSING FUNCTION RUNAWAY PACEMAKER: RATE >200, BAT. DEPL., RARE, RX: MAGNET OR MAY NEED TO CUT THE ELECTRODE WIRES PACEMAKER CODES DDD, ADD,VDD,DAD,DVD ETC. 1ST LETTER-PACED: DUAL, ATRIAL OR VENTRICULAR(R) 2ND LETTER-SENSED: DUAL, ATRIAL, OR VENTRICULAR(R) 3RD LETTER: DUAL=INHIBITS & TRIGGERS 4TH LETTER: PROGRAMABLE FEATURES; R:RATE ADAPTIVE – RATE ADAPTIVE FEATURE WILL ALLOW HR TO INCREASE APPROP. W/EXERCISE DDDR=BEST AVAILABLE PACEMAKER effective capture TRANSCUTANEOUS EXTERNAL PACING PLACE ANT. &POST. PADS wide QRS LOOK AT LEAD I ON MONITOR MAKE SURE YOU ARE IN AUTO MODE AND THE PACE SWITCH IS INITIALLY OFF SET INITIAL RATE AT 60 (80-100 FOR ASYSTOLE OR SYMPTOMATIC BRADYCARDIA) SET OUTPUT AT 40mA INITIALLY (IN A CRUNCH START AT 100mA) INITIATE PACING BY TURNING DEMAND PACER SWITCH TO PACE (NON-DEMAND) CONFIRM EFFECTIVE PACING BYCHECKING FOR THE WIDENED QRS WHICH LOOKS LIKE AN ECTOPIC BEAT ( A PACED BEAT IS BY DEFINITION AN ECTOPIC BEAT); AND MOST IMPORTANTLY BY CHECKING PULSES AND BP ONLY PROV. 8 HRS; OPTIMAL CURRENT US. 40-80mA TRANSVENOUS PACING PLACE A RIGHT INTERNAL JUGULAR 8F CORDIS INTRODUCE THE PACING ELECTRODE THROUGH THE CORDIS TO BE POSITIONED IN THE RIGHT VENTRICLE APEX: ULTRASOUND MAY HAVE A ROLE IN ASSISTING PLACEMENT CATHODE:POSITIVE IS AT CATHETER TIP mA 1.5-2 SUFFICIENT TO CAPTURE-IF TOUCHING RV WALL :ECG ST Elevation ECG EFFECTS OF CVA/SAH 60% DEEP T-WAVE INVERSIONS PROMINENT U WAVES MARKED QTc PROLONGATION WATCH ALSO FOR NEUROCARDIOGENIC PULMONARY EDEMA TCA & Terminal 40ms of QRS: Mechanism TCA’s cause a partial RBBB AvR AvL & I C. L&R BUNDLE BRANCH BLOCKS=TERMINAL QRS PROLONGATION 1.RIGHT BBB 2. LEFT BBB LBBB & RBBB WIDE QRS 3. LEFT ANTERIOR SUPERIOR FASCICULAR BLOCK 10 TIMES MORE COMMON THAN LPIFB 4. LEFT POSTERIOR INFERIOR FASCICULAR BLOCK LASFB & LPIFB NORMAL QRS BUNDLE BRANCH BLOCKS R WAVE IS NORMALLY DISCORDANT WITH T WAVE RX: IN AMI 2 OF 3 FAS. BLOCKED NEED PACING LEADS V1 RSR’ DELAY OVER VENT. LOCA. V6 deep S wave RV LBBB no Q wave ANT. & RIGHT LV RBBB POST. & LEFT UNIFASCICULAR BLOCKS LASFB: MAY MASK ANT. & INF. AMI LPIFB: MAY MASK ANT. AMI FRONTAL AXIS RBBB NORMAL LEFT ANT. SUPERIOR HEMIBLOCK LAD (> -45DEG) LAD LEFT POST. INFERIOR HEMIBLOCK RAD (>+120 DEG) RAD (>+120 BIFASCICULAR BLOCKS FRONTAL AXIS RBBB + LASB, RBBB #1 COMBO #1 LAD RBBB + LPIB RAD LBBB NORMAL Prepare to PACE Bifasicular Block: RBBB + LASF Block 40% of the time GOES ON TO THIRD DEGREE HEART BLOCK in the setting of ACS and chest pain TRIFASCICULAR BLOCKS TRIFASCICULAR BLOCKS = 1. (RBBB) + 2. (LASB OR LPIB) + 3. 1st deg. AV BLOCK WHEN TO PACE?: A NEW OR AGE INDETERMINANT TRIFASCICULAR BLOCK BUNDLE BRANCH BLOCKS 1. RBBB: UNIFASCICULAR,WIDE QRS, RSR’ IN LEAD V1, NORMAL SEPTAL QWAVES IN I & V6 2. LBBB: BIFASCICULAR,WIDE QRS, DEEP S WAVE IN V1, LARGE R AND ABSENCE OF NORMAL SEPTAL Q WAVES IN LEADS I AND V6 3. LASB:UNIFASCICULAR, NORMAL QRS, LAD, SMALL R WAVES IN II,III,& aVF 4. LPIB: UNIFASCICULAR, NORMAL QRS, RAD, SMALL R WAVES IN I & aVL TCA OD & ECG QRS WIDENING – >100 ms ASSOC. W/SEISURES – >160 ms ASSOC. W/DYSRHYTHMIAS TERMINAL 40 ms QRS WIDENING & RIGHT AXIS DEVIATION – aVr: wide QRS & pos. terminal 40 ms – aVl & I: wide QRS & neg. terminal 40 ms Rx. IV HCO3 (7.45-5 plasma goal pH), monitor, admission PULSELESS ELECTRICAL AVENTRICULAR RHYTHMS, CTIVITY INCLUDES: EMD, IDIO VENTRICULAR ESCAPE, BRADYASYSTOLIC RHYTHMS, POSTDEFIBRILLATION IDIOVENTRICULAR RHYTHMS CPR; INTUBATE; IV-NS; ASSESS BLOOD FLOW WITH DOPPLER ULTRASOUND CAUSES TO CONSIDER:HYPOVOLEMIA, TAMPONADE, TENSION PNEUMOTHORAX (BIG THREE THAT CAN BE RAPIDLY CORRECTED-TWO WITH A NEEDLE),HYPOXIA, HYPOTHERMIA, PULMONARY EMBOLISM, DRUG OD; TCA, BB, CCB, DIG, HYPERKALEMIA, ACIDOSIS, AMI RX: EPI 1MG IVP Q3-5MIN & UNDERLYING CAUSE IF ABSOLUTE BRADYCARDIA(<60) OR RELATIVE BRADY GIVE 1MG ATROPINE Q3-5MIN UP TO .04MG/KG MAX PULSELESS ELECTRICAL ACTIVITY & SURVIVAL Cardiac standstill on echocardiogram (bedside US) in ARREST patients, regardless of initial cardiac rhythm resulted in a 100% positive predictive value for DEATH in the ED. Blaivas, Fox. Acad. Emerg. Med., June 2001, Vol 8(6), 616-21. ASYSTOLE CONTINUE CPR, INTUBATE AT ONCE, IV, CONFIRM ASYSTOLE IN MORE THAN ONE LEAD CONSIDER CAUSES: HYPOXIA, HYPERKALEMIA, HYPOKALEMIA, PREEXISTING ACIDOSIS, DRUG OD, HYPOTHERMIA, Lightning strike depolarizes entire myocardium, or brain stem depol. & respiratory arrest CONSIDER IMMEDIATE TRANSCUTANEOUS PACING (If in ED IIB-SHOULD NOT BE TRIED ROUTINELY w/i 10 min of arrest); EPINEPHRINE: 1MG IVP Q3-5MIN; INT-HIGH DOSE EPI .1MG/KG IV ARE IIB INTERVENTIONS ATROPINE 1MG IV Q3-5MIN UP TO .04MG/KG (APPROX 3MG MAX) CONSIDER TERMINATION OF EFFORTS IF ABOVE FAILS HYPOTHERMIA J or Osborne wave or ALL PATIENTS: REMOVE WET CLOTHING, AVOID ROUGH MOVEMENT (cold myocardium is very irritable), monitor core-rectal temp A,B,C’S; NO PULSE OR BREATHING; CPR, INTUBATE, DEFIB VT/VF; VENTILATE WITH WARM HUMIDIFIED O2(42-46C), AND WARM IV NS(43C) CORE TEMP <30C: WITHHOLD IV MEDS; LIMIT SHOCKS FOR VF/VT TO 3 MAX ( WARMING ALONE MAY CONVERT VF) - USE ACTIVE INTERNAL REWARMING (IV, O2, PERITONEAL LAVAGE, EXTRACORPOREAL, ESOPHAGEAL REWARMING TUBES CORE TEMP >30C: CPR; GIVE IV MEDS, BRETYLIUM FOR VF IS IIB, MAY REPEAT DEFIB FOR VF/VT AS CORE TEMP RISES; DEFIB USUALLY NOT SUCESSFUL UNTIL 30C-86F PT IS NOT “DEAD”UNTIL “WARM AND DEAD” : 90F at least; YOUNG PATIENTS CAN SURVIVE PROLONGED (1-2 HR)CIRCULATORY ARREST WITH CARDIAC BYPASS Core temp. afterdrop w/peripheral rewarming & Hunting response HYPOTHERMIA The NON-MOVING Heart in the setting of severe Hypothermia needs BYPASS THERAPY DIGOXIN TOXICITY CLINICAL: GI SX: FLU-LIKE SYNDROME, NAUSEA, BLURRED VISION:yellow halos, CONFUSION & PSYCHOSIS DX: GET DIGOXIN LEVEL; ECG - ANY ARRHYTHMIA CAN OCCUR WITH PVCS #1, PAT W/BLOCK COMMON; CHECK K, Mg, Ca levels:CALCIUM + DIGOXIN =STONE HEART-TETANY RX: STOP THE DRUG (this along may correct many bradyarrhythmias-some may need pacer); treat any underlying problems: low K, Mg, fluids; high Ca; hypoxia RX: TACHYDYSRHYTHMIAS: PHENYTOIN MG-SULFATE & LIDOCAINE, DIGBIND FAB FRAGMENTS:(K>5) FOR LARGE LETHAL INGESTIONS AND HYPERKALEMIA: 10 VIALS: WORKS IN 30 MINUTES (dig. lev. *kg/100=#vials) AVOID DIRECT CURRENT SHOCK & CAROTID S. STIMULATION: MAY CAUSE LETHAL ARRHYTHMIAS Phenytoin & Digoxin Tox. Phenytoin increases AV nodal conduction & supresses atrial ectopy making it the drug of choice for digoxin tachydysrhythmias Dose: 15-17mg/kg @ 50mg/min SYNCOPE:ECG, H&P ARE KEY THREE FACTORS DX: HEAD UP TILT TEST(drop 700-800cc after standing)(45min): FOR VASOVAGAL ETIOL & THE MAJORITY OF UNEXPLAINED - NEUROCARDIOGENIC=VASOVAGAL Bezold-Jarisch reflex (head up tilt - dec LV filling - catecholamines are released(final common pathway of syncope) & inc in contractility excessive response to mechano Rcs in the post wall of the LV - vagal resp, bradycardia & syncope) DX: HOLTER, ARRHYTHMIA EVAL, ECHO, EXCLUSION OF METABOLIC DIS: 30 - 50 % UNEXPLAINED SYNCOPE SITUATIONAL SYNCOPE IN AN OTHERWISE HEALTHY PATIENT CAN BE DISCHARGED FROM THE ED SYNCOPE: DIFFERENTIAL DIAGNOSIS: BIG 3 MECHANISMS 1.-FALL IN CARDIAC OUTPUT; BIG 3 ARRHYTHMIAS: SVT, VT, SSS, BRADY, STOKES-ADAMS, PACEMAK. STRUCTURAL: AS, IHSS, MVP, ARTIAL MYXOMA VASCULAR: AO. DISSECT, CAROTID S.S(TURN NECK)., AMI, PE, P.HTN, AIR.EMB.: Need HBO RX 2.-ORTHOSTATIC HYPOTENSION: VASOVAGAL, POSTURAL SYNCOPE: HYPOVOLEMIA, DRUGS, SITUATIONAL: MICTURIC., DEFECA., COUGH, POSTMEAL;WT-LIFTING; DYSAUTONOMIA, CN9 NEURALGIA 3.-INCREASED CEREBROVASCULAR RESISTANCE: HYPERVENTILATION & BREATH HOLDING, NEUROLOGICAL: SEIZURE, CVA, SAH, Nl Pres. Hydroceph. MISCELLANEOUS: HYPOGLYCEMIA, SUBCLAVIAN STEAL: (OCCURS WITH UPPER EXTRMITY USE), PSYCH Hyperbaric Oxygen Rx: Blast injuries/Air embolism: Box III Decompression sickness/Nitrogen narcosis Rapid Ascent Drank hydrogen peroxide Air intravenous injection Carbon monoxide espec. w/pregnancy Wound infections: necrotizing fascitis, myonecrosis SYNCOPE+? SYNCOPE + HEADACHE=SAH SYNCOPE + CHEST PAIN=AMI, PE, AORTIC DISSECTION, PULMONARY HTN SYNCOPE W/EXERTION= AORTIC STENOSIS, IHSS SYNCOPE + ABD. PAIN= LEAKING AAA, RUPTURED ECTOPIC SYNCOPE +ISCHEMIC ECG+NO CP = CCU/MONITORED ADMISSION ACQUIRED DISEASES OF THE CIRCULATION Peripheral ARTERIAL DISEASE EMBOLISM & THROMBOSIS: IV HEPARIN TO PREVENT CLOT PROPAGATION; RX: VASCULAR SURGERY ASAP HAVE 4-6HOURS RAYNAUD’S: COLD OR EMOTION TRIGGER; BILAT, NO GANGRENE, EXT . WHITE THEN BLUE THEN RED RX: AVOID COLD AND TOBACCO, may need nifedipine Carotid Bruit: = 60- 70% stenosis = endarterectomy Claudication(Claudius-limp): Clinical Dx. pain goes away w/rest. ABI<0.9=abnormal. These patients have atheroscerotic CAD which ultimately kills them AORTIC DISSECTION DISSECTING THORACIC AORTA: NECROSIS OF MEDIAL LAYER OF AORTIC WALL DUE TO: ATHEROSCLEROSIS, CYSTIC MEDIAL NECROSIS(MARFAN’S, PREGNANCY, COARCTATION), HTN – SANFORD CLASSIFICATION: A; ASCENDING, B;DESCENDING – DE BAKEY I:ASCEND+DESCEN, II:ASCEND, III:DESCENDING AORT – DX: A; SUDDENCHEST & MID SCAPULAR EXCRUCIATING TEARING PAIN, OR STROKE LIKE SYNDROME, B; SEVERE BACK PAIN,ABDOMINAL PAIN, MIGRATORY PAIN, MIGRATORY OR SEQUENTIAL DEFICITS, A. RENAL INSUFFIENCY; BLOOD PRESSURE DIFFERENCE OF >15 MM HG BETWEEN EACH ARM – CXR: WIDE MEDIASTINUM, BLURRED AORTIC KNOB, PLEURIAPICAL CAP; R TRACHEAL SHIFT, L PLEURAL EFFUSION – AORTOGRAPHY IS GOLD STANDARD; CT SCAN WITH CONTRAST GOOD IF LOW SUSPICION, TEE VERY GOOD(IE IF RENAL INS) – RX: MEDICINES USED TO DECREASE THE PROPAGATION OF THE DISSECTION: PROPRANOLOL 1mg IVP Q 10’ 1ST TO DEC HR TO 60, THEN NITROPRUSSIDE IS USED TO MAINTAIN BP OF 90-120, THIS BUYS TIME FOR SURGERY, OR IV LABETALOL 2mg/min to 300mg=BEST SINGLE AGENT , Mini-Bolus 20-40-80-80-80 q 10’ AORTIC DISSECTION PHYSICAL EXAM FINDINGS AORTIC REGURGITATION (40%) NEUROLOGIC DEFICITS-L arm emboli (20%) HORNER’S SYNDROME PULSATILE STERNOCLAVICULAR JOINT VOCAL CORD PARALYSIS HEMOPTYSIS, HEMETEMESIS SUPERIOR VENA CAVA SYNDROME CONTINUOUS MURMUR DUE TO RUPTURE INTO RA SIGNS OF MESENTERIC OR RENAL INFARCTION FEVER, Document no carotid bruit VERY DIFFICULT DX: <50% CORRECT ANTEMORTEM DX. Aortic Dissection on CXR Wide mediastinum > 8cm L apical cap Tracheal deviation Depression of L mainstem bronchus Loss of paratracheal stripe Esophageal deviation Ring sign extension of aorta >5mm past calcified intima Blunting of aortic knob Thoracic Aneurysms Thoracic aneurysms usually do not dissect Thoracic aneurysms are associated with Giant cell arteritis & abdominal aortic aneurysms DX. OF AORTIC DISSECTION W/NONINVASIVE IMAGING GOAL: MAKE DX., & get detailed info: extent of dissection, location of entry site, formation of thrombus in false lumen, pericardial effusion, or A. regurgitation? STANDARD: Aortography, or CT w/dye: have procedural or Dx. shortcomings SOLUTION: TRANSESOPHAGEAL ECHO IN UNSTABLE PTS, AND MRI IN HEMODYNAMICALLY STABLE PTS. TEE: SENSITIVITY >97%, rapid, bedside Aneurysm and/or Dissection First Portion of the Ascending Aorta: THE BIG DILEMMA PROCTOR HARVEY- CARDIOLOGY CLINICAL Bedside PEARL: DIASTOLIC HTN + AORTIC DIASTOLIC MURMUR(AI:LEFT STERNAL) + “RIGHT SIDED(3-4 INTERSPACE)>LEFT” AORTIC DIASTOLIC MURMUR = ANEURYSM AND/OR DISSECTION FIRST PORTION OF THE ASCENDING AORTA AORTIC ABDOMINAL ANEURYSM EXPANDING ABDOMOINAL AORTIC ANEURYSM: ELDERLY FLANK PAIN(MANY LOOK LIKE KIDNEY STONE PTS) ,DX: ULTRASOUND: >3CM(IN AP)+ DEC. BP WITH ABDOMINAL, BACK, OR GROIN PAIN, + SYMPTOMS=AAA, CT:CAN DX. LEAKING AAA SURGERY RX:2 LB-IV’S, T&C 10U PRBC’S & GET PATIENT TO ASAP, TO PREVENT THE BOMB FROM GOING OFF! 5%: inflammatory mass w/microscopic hematuria Palpation of abdomen does not lead to rupture Deep Venous Thrombosis RISK FACTORS KEY DVT: :AMI, DIC, UC, BURNS, TRAUMA, ORTHO-SURGERY, HYPERCOAG:SLE, antithrombinIII&protC&S defciency ie due to nephrotic syndrome, Venous Stasis:PV, >6HR trip, CHF, Endothelial Injury:vasculitis, SLE, Oral Contraceptives, obesity, blood type A, cancer, IVDA, pregnancy, sepsis, inflammatory states, folate /B12 deficiency w/ homocysteinuria, lupus anticoagualnt, resistance to activated Protein C: Factor V Leiden gene mutation, Prothrombin gene mutation EDEMA, WARMTH, ERYTHEMA, PAIN, EDEMA, HOMANS SIGN UNRELIABLE; GROIN MORE RELIABLE OR POPLITEAL TENDERNESS DX: VENOGRAM GOLD STANDARD,comp.US:good RX: IV HEPARIN-STANDARD(80/18), TPA/strepto IF NO CONTRAINDICATIONS:reduce mortality, Compression stockings increase 5X blood flow in DV Deep Venous Thrombosis Difference in calf circumference 1.5 cm from asymptomatic leg is the most specific physical exam finding 80% of patients with proven DVT SUPERFICIAL THROMBOPHLEBITIS –WARMTH, NSAIDS, CORTICOSTEROIDS, VENOGRAM IF GREATER SAPH CLOT HAS MOVED TO FEMORAL VEIN CONGENITAL ANOM. CARDIOVASC. SYSTEM IN ADULTS: MOST COMMON ARE BICUSPID AORTIC VALVE, & ATRIAL SEPTAL DEFECT ASD: FIXED SPLIT S2(ALSO RBBB) HAVE INCREASED RISK FOR ENDOCARDITIS – EISENMENGER’S SYNDROME: INC PULMONARY BLOOD FLOW (DUE TO L-R SHUNTING) LEADS TO PULM HYPERTENSION: POOR PROGNOSIS: Shunt Reversal ARRHYTHMIAS IN 25% ESPECIALLY IF THERE WAS PREVIOUS SURGERY (VENT ARRHYTH-VT #1 AFTER TERALOGY OF FALLOT (VSD,RV-OUTFLOW OBSTRUCTION,OVERRIDING AORTA, RVH) CARDIAC TRANSPLANTATION INDICATIONS:PATIENT’S MAX O2 CONSUMPTION <14CC/KG/MIN & LEFT VENTRICULAR EJECTION FRACTION <25% 40,000 PATIENTS/YR DIE OF HEART FAILURE YET ONLY 2100 HEART TRANSPLANTS DONE/YR INFECTIONS IN CT: IMMUNOSUPPRESSED (CYCLOSPORINE,AZATHIOPRINE,STEROIDS); CMV, TOXOPLASMOSIS, PNEUMOCYSTIS #1 CAUSE OF DEATH AFTER THE FIRST YEAR: CAD-GRAFT ATHEROSCLEROSIS REJECTION: FLU-LIKE SX, DX-BIOPSY, RX: HIGH DOSE STEROIDS BRADYCARDIA DOES NOT RESPOND TO ATROPINE: NEED PACING OR DOPAMINE HYPERTENSION BP > 140/90 OVER 30 Y/O BP > 160/95 OVER 65 Y/O EXTRA SALT BP & CUFF SIZE CUFF TOO SMALL: ARTIFACTUALLY HIGH BLOOD PRESSURE CUFF TOO LARGE: ARTIFACTUALLY TOO LOW BLOOD PRESSURE ESSENTIAL HYPERTENSION INDICATIONS OF POORLY CONTROLLED BP: NEURORETINOPATHY; #2 CAUSE OF KIDNEY FAILURE IN U.S.; LVH & INCREASED LV MASS (IS AN EARLY MARKER OF RISK FOR AMI OR SUDDEN DEATH) GUIDELINES FOR RX: SODIUM RESTRICTION & CALCIUM SUPPLEMENTATION; NO ETOH OR TOBACCO; INC PHYSICAL ACTIVITY & DEC. WEIGHT; DEC. IN SATURATED FATS & CHOLESTEROL 1. HYPERTENSIVE URGENCY DEFINITION: ASYMPTOMATIC PATIENT WITH A DIASTOLIC BP IN THE RANGE OF 115-125 TREATMENT: AS LONG AS THE PATIENT IS ASSYMPTOMATIC, FREQUENT BLOOD PRESSURE CHECKS ARE REQUIRED W/ CLOSE FOLLOW UP DRUGS: AVOID ORAL NIFEDIPINE (PROCARDIA) IN ELDERLY AS THIS CAN RESULT IN A STROKE RX: Add one additional dose of HTN med patient is already taking & re check in 12 hrs F/U vs. one dose of clonidine 0.1mg po 2. HYPERTENSIVE EMERGENCY: HEART, BRAIN & KIDNEY DEF: A PATIENT WITH ELEVATED BP AND SIGNS OF END-ORGAN DYSFUNCTION OR DAMAGE IE: AT BEDSIDE: – ISCHEMIC CHEST PAIN – PREECLAMPSIA/ECLAMPSIA(EDEMA, PROTEINURIA, HTN +/- SEIZURE) – RENAL INSUFFICIENCY: CHECK BUN & CREATININE; AORTIC DISSECTION – ENCEPHALOPATHY/STROKE(MALIGNANT HTN: CHECK FUNDI FOR PAPILLEDEMA-MUST BE PRESENT TO DX, AND – CHF/PULMONARY EDEMA RX: A-LINE-MONITOR BP & IV MEDS TO LOWER THE MAP 20-30% OVER THE FIRST HR; NITROPRUSSIDE(cyanide tox: espec. w/renal insuf) 0.5MG/KG/MIN - THE DRUG OF CHOICE FOR ALL HTN EMERGENCIES EXCEPT ECLAMPSIA:MAGNESIUM SULFATE 3-5GM IV;HYDRALAZINE:5-10mgIV OTHER MEDS: LABETALOL IV 20mg q10’ up to 300mg, or 2mg/min drip; IV NITROGLYCERINE (BEST FOR HTN + ISCHEMIC HEART DISEASE); PROPRANOLOL + NITROPRUSSIDE OR LABETALOL, BEST FOR THORACIC AORTIC DISSECTION HYPERTENSIVE EMERGENCY: HEART, BRAIN & KIDNEY Papilledema: due to MAP > than the autoregulatory zone (50-160 MAP) and resulting cerebral edema Hydralazine is good for preeclampsia / eclampsia because it increases fetal and placental blood flow 3. CATECHOLAMINE CRISIS DEF: ACUTE ELVATION OF CIRCULATING CATECHOLAMINES THAT PRODUCES AN ELEVATED BP WITH HEADACHE, FLUSHING, AND DIARRHEA; SIMILAR TO CLONIDINE WITHDRAWAL CAUSES: PHEOCHROMOCYTOMA; MAO INHIBITORS + SYMPATHOMIMETICS ( TYRAMINE (AGED CHEESE, CHIANTI WINE, BEER, PICKLED HERRING); EPHEDRINE; DIET PILLS) RX: PHENTOLAMINE IV(5mg over 5’-watch for reflex brady) (ALPHA BLOCK-DILATE) + PROPRANOLOL, OR LABETOLOL: 1:7 = alpha:beta PRIMARY TUMORS OF THE HEART MOST COMMON: LEFT ATRIAL MYXOMA: mimics mitral stenosis Consider myxoma in a young person with embolic disease and no obvious heart disease or atrial arrythmias #1 PRIMARY MALIGNANT TUMOR: R ATRIAL SARCOMA #1 BENIGN TUMOR IN CHILDREN: RHABDOMYOMA #1 CARDIAC METASTASES: MALIGNANT MELANOMA; afib presentation DX: ECG, ECHO , RX: SURGERY SYSTEMIC DISEASE & THE HEART 1. INFECTIONS AIDS: METS OR PRIMARY INVOLVEMENT OF KAPOSI’S SARCOMA; MYOCARDITIS(post myocarditis dilated cardiomyopathy) (40-50%), PERICARDIAL EFFUSION, CHF (ESPECIALLY IF CD4 CT <100AND VERY RAPID DETERIORATION) – DX: W/U FOR AIDS PT WITH DYSPNEA: CXR, DOPPLER-ECHO, ECG, – CARDIAC PANEL RHEUMATIC FEVER DUE TO STREPTOCOCCUS #1 CAUSE OF MITRAL STENOSIS ( MAY DEV. AS SOON AS 2YRS AFTER INFECTION) ; ALSO AORTIC REGURGITATION, 95% both mitral & aortic v. DEF: SYSTEMIC INFLAMMATORY DISEASE DX USING JONE’S CRITERIA: GROUP A STREP POSITIVE + 2-MAJOR OR 1-MAJOR + 2-MINOR CRITERIA: MAJOR (carditis,polyarthritis,chorea erythema marginatum, subcutaneous nodules); MINOR ( arthralgia, fever, ESR, CRP, prol PR int. ) BEST RX IS PREVENTION BY DX STREP INF & RX WITH PENICILLIN once MS develops: SURGERY IS ONLY OPTION; IE MITRAL REPAIR, REPLACEMENT, OR BALLOON VALVULOPLASTY Strep. Issues Rheumatic Fever: Prevented w/PCN Pharangitis: Treated w/PCN Scarlet Fever: sandpaper rash Treated w/PCN Post-Strep Hypocomplementemic Glomerulonephritis: triad of edema, hematuria & elevated BP: Rx: Fluid Restrict – NOT PREVENTED W/PCN: Rare, yet must warn patient that this may develop even w/Rx. 2. ENDOCRINE & METABOLIC DISEASES HTN + LOW K + high Na = EXCESS ADRENAL MINERALOCORTICOIDS (met. alkalosis(Ucl>20)) DIABETICS PRONE TO CAD & AUTONOMIC NEUROPATHY, BIG WORRY IS SILENT ISCHEMIA, orthostasis BERIBERI-WET: THIAMINE DEFICIENCY(lactic acidosis: TCA cycle is interupted); ALCOHOLICS; HIGH CO STATE DUE TO DECREASED PERIPH. VASC. RESISTANCE(lactic acidosis) & INCREASED HR; RX: THIAMINE, GLUCOSE, PULM EDEMA RX. Dry Beriberi: peripheral neuropathy related to myelin production 3. RENAL: CAD BIG KILLER LIPID PROBLEMS: NEPHROTIC SYNDROME ( ELEV. LDL CHOLESTEROL, EDEMA, HYPOPROTEINEMIA=LOW VOL & NEED FLUID ); CRF: HTN & HYPERTRIGLYCERIDEMIA-CAD RISK CAUSES OF AZOTEMIA IN CHF: PRE-RENAL (dec perfusion DUE TO CHF), ATN, ischemic nephropathy CHF+NSAIDS=DECREASED GFR UREMIC PERICARDITIS: IMPROVE W/ DIALYSIS; RX: ALL NEED DIALYSIS, SOME NEED PERICARDIOCENTESIS(IF TAMPONADE) CARDIAC RESULTS OF DIALYSIS: HYPOTENSION, ELECTROLYTE IMBALANCES, A/V FISTULA LOW TPR WILL INCREASE CO, WORKLOAD AND CAN CAUSE CHF ESRD + CHF/P. Edema Dialyze or Intubate ACEI’S: CAN BUY TIME; SL CAPTOPRIL OR IV ENALAPRIL: BOTH DECREASE PRELOAD & AFTERLOAD 4. SUBSTANCE ABUSE ETOH SYSTOLIC-DILATED CARDIOMYOPATHY: & BINGE DRINKING (HOLIDAY HEART) ASSOC. WITH SVT COCAINE: BIG PROBLEMS IN ED: HYPERTHERMIA, RHABDO, ENDOCARDITIS(IVDA), & CARDIAC (HTN, ARRHYTHMIAS, AMI(SPASM&THROMBOSIS:1-6/100), AORTIC DISSECTION, STROKE) RX: KEEP PT COOL, IV BENZODIAZEPINES, & RX SPECIFIC PROBLEMS, PTS NEED FULL CARDIAC W/U & MONITORING, & BLOOD CX’S ESPEC IF TEMP & IVDA HX COCAINE + CIGARETTES=MORE SPASM Phentolamine: 1mg IV q 5’ – only if refactory CP/HTN ASA, nitrates, TPA, heparin Cocaine Chest Pain 6% of patients develop biochemical evidence of AMI; 1% have ECG lytic inclusion criteria In Hospital mortality approaches zero Cocaine causes atherscerosis, increased platelet aggregation, & diffuse microvascular injury (with end stage dilated cardiomyopathy) Cocaine has a high false negative ECG rate & high false positive ECG rate due to BER RX: COOL Pt. & Benzos: ASA, heparin, NTG, NO BETA BLOCKERS(labetolol is out), phentolamine ADMIT ALL for 12 hrs, CATH LAB if meds not controlling pain; Consider lytics yet r/o trauma, dissection, CVA, all increased w/cocaine patients Palpitations: H&P, & ECG Flip/Flopping in the chest: heart seems to start & stop: PAC’s & PVC’s Pounding in the neck: Cannon A waves due to dissociation of the atrial & ventricular contractions; PSVT Panic attacks & anxiety Post Exercise: catecholamine excess then withdrawal + surge in vagal tone can cause AF in 20-40 y/o Hx, regular, irregular, FH of sudden death=prol QTc W/U: high risk, Syncope/CHF/CAD/DM/HTN/Prol QTc=admit; others = holter monitoring at home with close cardiology follow up Inapprpriate Sinus Tachycardia Fever: each deg F raises HR 10 points Search for underlying problem: hyperthyroidism, anemia, hypoxia, hypovolemia RARE SVT: right atrial tachycardia & sinus node reentry: Rx: beta blockers or CCB’s Acid Base & the Heart Acidemia: neg. inotrope, sensitization, decrease in TPR,CO, BP,hepatic & renal flow Alkalemia: arteriolar constriction w/reduced coronary flow, sensitizes myocardium Respiratory compensation NEVER full with metabolic acidosis, ie: <7.35 max HCO3 * 1.5 + 8(+/-2) = pCO2=Winter’s formula Metabolic Alkalosis can increase AG to 20max Increase pCO2 10mmHg= dec. pH 0.08 & if acute: HCO3 1.0mmol, if chronic 4.0mmol increases Acid Base & the Heart For each drop in the pH of 0.1 the Potassium level should rise 0.5 For each elevation in the pH of 0.1 the Hb gets Left shifted and Oxygen delivery decreases 10% (hypothermia also causes this) PHARMACOLOGIC AGENTS CLASS DRUGS I membrane-active IA-quinidine,procan IB-lidocaine,phenyt IC-flecainide beta-blockers bretyl,amiodarone sotalol calcium blockers II III IV QTc-rep. QRS-dep. prolonged 0 minimal 0 prolonged minimal 0 prolonged 0 0 0 0 IV CALCIUM GLUCONATE/CHLORIDE INDICATIONS: – HYPERKALEMIA (ALSO IV HCO3(ONLY IF ACDOTIC), INSULIN AND GLUCOSE) – HYPOCALCEMIA – CALCIUM CHANNEL BLOCKER OVERDOSE(not BB): NE, PACERS, IABP, GLUCAGON, GLUCOSE, INSULIN, AMRINONE & MILRINONE – HYDROFLURIC ACID BURNS – Black widow spider: IV CaGluconate – Puss Catepillar bite: IV CaGluconate DOSE: 10 CC OF A 10% SOLUTION Q 10’ CALCIUM CHLORIDE HAS 3 TIMES MORE ELEMENTAL CALCIUM Calcium Gluconate only for intra-arterial RX. of hydrofluric acid hand / foot burns Calcium chloride causes peripheral vein sclerosis; Ca-Gluconate better for peripheral lines ...
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