Cardiology Chapter 1 PDF

TOC Cardiology ACLS: Arrest & Cooling Assess for responsiveness, pulse, and spontaneous respirations (C-A-B) High Quality CPR...

TOC Cardiology ACLS: Arrest & Cooling Assess for responsiveness, pulse, and spontaneous respirations (C-A-B) High Quality CPR No definite pulse within 10 seconds = start chest compressions (CPR)  Minimize interruptions Non–Senior On Tasks:  Fast: 100-120/min  Confirm code status  Compress 2-2.4 in deep  Confirm/stop IV infusions 1. Call Code Blue (x6-3333, blue button on the wall)  Allow complete recoil  Run tele/print strips 2. Call for defibrillator pads, backboard & Ambu bag for mask ventilation  Change compressors  Check labs, med list 3. Establish monitoring: tele, defibrillator, O2 sat probe, place BP cuff every 2mins  Notify attending, family 4. In both witnessed AND unwitnessed arrest, rhythm check ± defib  30:2 CPR:vent (mask) as soon as pads are on (Class IIa recommendation)  PETCO2 >10, DBP>20 2015 AHA Guidelines Update, 2018 AHA Focused Update Reversible Causes (H & Defibrillators: YES NO Pulse/rhythm check Ts) Biphasic (MGH) 120J-200J  Hypovolemia, Monophasic 360J SHOCKABLE hemorrhage − If unknown, use max  Hypoxia VF or VT PEA or Asystole setting  H+ ion (acidosis) − Repeat shocks at  Hypo/hyperkalemia same or higher dose  Hypothermia If return of spontaneous SHOCK!  Thrombosis, coronary circulation (ROSC), AIRWAY go to post-arrest (ACS) & pulmonary (PE) Obtain advanced airway care/cooling evaluation  Tension pneumothorax Avoid excessive ventilation  Tamponade (cardiac) (10 breaths/min with  Toxins (drugs, accidents) continuous CPR) TREAT REVERSIBLE ACCESS HIGH QUALITY CPR 2 MINUTES CAUSES (H&Ts) Establish IV/IO access; Hyperkalemia Treatment: consider femoral central Ca gluc 1-2g IV (or CaCl2), Epinephrine 1mg IV/IO q3-5 mins Bicarb 1-2 amp IV, D50W 1- line if volume resuscitation needed 2 amp (give first) + insulin 10 units IV LABS TO ORDER VT/VF Additional IV/IO Medications Stat ABG with K & Hgb, PROGNOSTICATION CBC, BMP, LFTs, lactate, In intubated pts, failure to Amiodarone (Dose 1= 300mg, Dose 2= 150mg) OR achieve ETCO2 >10 T&S, coags, fibrinogen, cardiac enzymes Lidocaine (Dose 1= 1-1.5mg/kg, Dose 2= 0.5-0.75mg/kg) mmHg by waveform capnography after 20 Magnesium 1-2g over 5-20 mins for torsades min CPR90% sensitive Medication Notes for inability to achieve - Epinephrine: If no IV/IO access, epinephrine can be given via endotracheal tube at 2.5x the IV dose diluted in 10cc water or saline. **For non-shockable rhythms, epinephrine can be administered as ROSC CRITERIA soon as available rather than waiting 3-5 minutes (Class IIb recommendation)** 1. Pulse + blood pressure - VSE protocol: Can consider vasopressin 20U with first 5 doses of epi + hydrocortisone 200mg x1; 2. Sustained increase class IIb evidence for in hospital cardiac arrest; not currently used at MGH ETCO2 >40 - Lidocaine: 1-1.5mg/kg IV/IO (often 100mg); may follow with 0.5-0.75mg/kg (usually 50mg) every 5- 3. Spontaneous arterial 10min x3, maximum dose of 3 mg/kg; consider infusion at 1-4mg/min pressure waves on monitor Thrombolysis for Known or Suspected PE During Code  Alteplase (tPA) Pulseless: 50mg IV/IO bolus over 2 min, may repeat 50mg IV/IO in 15 min Pulse present: 100mg infusion over 2 hours  Reteplase: 10 units IV, may repeat 10 units in 30 min  Contraindications (absolute): prior ICH at any time, ischemic CVA or head trauma within 3mos, known intracranial neoplasm or AVM, suspected aortic dissection or active bleeding  Will need anticoagulation after lysis for compensatory up-regulation of pro-coagulant factors. ASA 325mg + UFH or LMWH. If already on heparin gtt, discontinue infusion and restart without bolus after lysis (if PTT 94%. Do not hyperventilate (can induce cerebral vasoconstriction). Start at 10-12 breaths/minute. Consider advanced airway waveform capnography. Target ETCO2 of 35-40 mm Hg. 2. Hypotension: cycle blood pressure and continuously monitor pulses. Goal MAP > 65mmHg. − IV/IO fluid boluses as needed (LR may be > than NS at larger volumes for treatment of shock) − Start vasopressor infusion (bolus code meds will wear off)  Epinephrine IV infusion 0.1-0.5 mcg/kg/minute  Norepinephrine IV infusion 0.1-0.5 mcg/kg/min  Dopamine IV infusion 2-10 mcg/kg/min 3. Revascularization: obtain 12-lead EKGconsider emergent coronary angiography − Hypothermia does not contraindicate PCI and is not associated with worse outcomes (Resuscitation 2010;81:398) 4. Therapeutic Hypothermia: consider if patient not able to follow commands − If patient does not follow commands, call neurology stroke fellow for full evaluation prior to starting cooling protocol Targeted Temperature Management after Cardiac Arrest (Circulation 2015;132:2448) Rationale: therapeutic hypothermia decreases cerebral oxygen demand and ischemia-related inflammation  Class I recommendation for comatose cardiac arrest patients following ROSC for in- and out-of-hospital arrest (Circulation 2015;132:S465)  Improves neurologic outcomes (NNT 6) and survival to discharge (OR 5.25) following out-of-hospital cardiac arrest from VF, pulseless VT, or PEA/asystole of presumed cardiac cause, although the benefit may be from avoidance of hyperthermia rather than from hypothermia (NEJM 2002;346:549; NEJM 2002;346:557; NEJM 2013;369:2197; Circulation 2015;132;2146) Cooling Criteria  Comatose (GCS70), glucose (140-180)  If water temp 72 hrs post arrest), status myoclonus (72-120 hrs post arrest) o Blood Markers (should not be used alone, no cutoff established): High neuron specific enolase (NSE, 48-72 hrs) o Imaging: Brain MRI (extensive restriction/diffusion, 2-6 days post arrest), head CT (reduced gray-white ratio, 40%) idiopathic VT, baseline QTc: congenital PMVT TdP, long QT syndrome First line medications: − Amiodarone − Treat ischemia − IV magnesium − Amiodarone − Lidocaine (PCI, IABP) − ↑HR: dopamine, − Procainamide − Lidocaine isoproterenol, − Lidocaine − Amiodarone overdrive pacing Causes: − QTc: lidocaine − Adenosine* − Procainamide - Ischemia (scar>active) − Avoid - Electrolytes (low K, Ca, bradycardia: Other medications: Chronic catecholaminergic or Mg) hold nodal agents − Metoprolol PMVT: BB or CCB - Structural heart dz and amiodarone − Sotalol (not first - Drug toxicity (TCA, line; expert digoxin, anti-arrhythmics, consultation inotropes) advised) - Infiltrative dz or scar - Channelopathies (acquired or inherited) *Adenosine should be considered per 2015 ACLS update for stable, regular narrow- and monomorphic wide-complex tachycardia while preparing for DCCV to differentiate SVT w aberrancy from WCT Anti-arrhythmic drug dosing (for stable WCT) - Amiodarone: 150 mg IV over 10 min (may repeat x1); then infusion at 1 mg/min x6hrs followed by 0.5 mg/min x18h (max 2.2 g/24 hours). May complete 10g load with up to 400mg PO TID. - Lidocaine: 1-1.5 mg/kg IV bolus—usually 100 mg (may repeat 0.5-0.75 mg/kg q5-10min, max 3mg/kg); then maintenance infusion at 1-4 mg/min; agent of choice when prolonged QT - Procainamide: 20 mg/min until either VT ceases or hypotension or QRS duration prolongs by 50% from baseline or total 17 mg/kg given (~1.2 g for 70kg person); then maintenance infusion at 1-4 mg/min (adjusted for CrCl); avoid in prolonged QT - Sotalol: 1-1.5 mg/kg IV over 5 min; then maintenance infusion at 10 mg/min; avoid in prolonged QT - (Adenosine: 6mg rapid IV push (followed by NS flush)12 mg if required) Ijeoma Eleazu 4 TOC Cardiology ACLS: Defibrillation, Cardioversion, Pacing External Defibrillation/Cardioversion/Transcutaneous Pacing: About the device: The Zoll R Series is on all code carts and ICUs at MGH. This device allows for external defibrillation, cardioversion, and pacing with additional benefits (e.g. displaying ET-CO2, CPR quality feedback, and saving rhythm strips for upload into Epic). Additional supplies needed at bedside: Ambu bag, intubation equipment, RICU staff, backboard, suction Use procedural sedation (typically fentanyl and midazolam) when possible and call Cardiac Anesthesia early Display/Operation of Zoll R Series: Remove all clothing covering the patient’s chest. Dry chest if necessary. If the patient has excessive chest hair, shave it to ensure proper adhesion of the electrodes Attach hands-free therapy electrodes in anterior-anterior/apical- sternum skin pad placement (pictured) Defibrillation Cardioversion Pacing Indications: pulseless VT or VF Indications: Unstable SVT or VT Indications: Unstable bradycardia 1. Turn the Selector Switch to ON. 1. Turn the Selector Switch to ON. Then press 1. Turn the Selector Switch ON. Then Then press Manual (bottom left Manual (bottom left softkey) to change to ALS. press Manual (bottom left softkey) to softkey) to change to ALS. change to ALS. Then PACER will appear 2. Select the desired energy using the up and as an option on the Selector Switch. Turn 2. The default energy selection is 120 down arrow keys on the front panel. to PACER. J. You can use Energy Select (UP) Narrow, regular: 50-100 J (atrial flutter and (DOWN) arrow keys to often converts with 50 J) 2. Set the PACER RATE to a value 10- increase the energy. Narrow, irregular: 120-200 J (atrial 20 bpm higher than the patient’s intrinsic fibrillation typically requires 150 J) heart rate. If unknown or absent intrinsic 3. If there is a shockable rhythm on Wide, regular: 100 J rate, use 100 bpm. the pulse/rhythm check, press Wide, irregular: 150-200 J Observe the pacing stimulus Charge. Continue CPR while (defibrillation dose) marker on the display and charging. verify that it is well-positioned 3. Press the Sync On/Off button in diastole 4. Once charged, the red shock Confirm that a Sync marker () button illuminates. Shout appears on the monitor above each 3. Increase PACER OUTPUT until the “Clear!” then press and hold the detected R-wave to indicate where paced beats demonstrate capture illuminated Shock button at the top discharge will occur (“threshold”); the output mA value is right of the console. If necessary, use the LEAD and SIZE displayed on the screen. buttons to establish settings that yield Capture = widened QRS 5. Resume CPR for 2 minutes before the best display complex + loss of underlying the next pulse/rhythm check. intrinsic rhythm 4. Press the CHARGE button on the front panel. 4. Set the PACER OUPUT to the lowest setting that maintains consistent capture 5. Press and hold the illuminated SHOCK Usually ~10% above threshold button on the front panel. The defibrillator (typical threshold: ~40 to 80 will discharge with the next detected R mA) wave. Pressing and holding the 4:1 button temporarily withholds 6. If additional shocks are necessary, increase pacing stimuli, thereby allowing the energy level as needed. you to observe pt’s underlying EKG rhythm & morphology Shilpa Sharma 5 TOC Cardiology EKG Interpretation Approach all EKGs systemically. Always note: rate, rhythm, QRS axis, complexes and intervals, chamber enlargement, ischemia/infarction, compare with prior EKG Rate (atrial, ventricular)  If the rhythm is regular, use the counting method (300 / # large boxes). See image at right.  If the rhythm is irregular, count R waves in the rhythm strip and multiply by 6 (EKG printouts record 10 seconds)  Normal 60-100bpm; 100bpm is tachycardia Rhythm (regular or irregular; sinus vs. non-sinus)  Sinus rhythm defined as: P before every QRS, regular w/ rate 60-100, P wave upright I, II, aVF, V5-6  P waves/morphology: Determine (1) If a P wave is present (best leads to visualize P wave are II and V1) (2) The atrial rate (100-180: sinus tachycardia; 140-220: atrial tachycardia, AVNRT, AVRT; 260-320: atrial flutter) and (3) Axis (P wave upright in II and biphasic in V1)  QRS morphology: Narrow (120ms)  aberrant supraventricular conduction or ventricular origin  P wave/QRS complex association: If not 1:1 association, determine if number of P>QRS (AV block) or PS in amplitude at V3 or V4. CCW: transition occurs prior to V3 due to RVH, WPW, LAFB, posterior MI. CW: transition occurs after V4 due to cardiomyopathy, LVH, LBBB, anterior MI. Both CW and CCW rotation are nonspecific and can be normal (Am Heart J 2004;148:80)  Low voltage: Average QRS amplitude < 5 mm in I, II, III and < 10 mm in precordial leads Ddx: obesity, pericardial effusion, pneumothorax, COPD, restrictive or infiltrative CM (particularly amyloidosis), severe hypothyroidism, or anasarca Complexes and Intervals (Circ 2009;119:e241)  P wave: Right and left atrial depolarization; normal duration 120ms represents BBB, ventricular activation (PVC, VT, fusion beats, WPW, paced beats), hyperK, Na channel poisoning, aberrancy, hypothermia LAFB: Left axis deviation (-45 to -90) w/ QRS 120; V1 with rSR'; V6 with LBBB: QRS > 120; V1 with rS in II, III, aVF. Common, nonspecific. wide qRS; I will show a shallow broad S wide negative QS; V6 with LPFB: Right axis deviation (0 to +90) w/ QRS1mm wide and deep, total p wave duration >110ms in II  RAE: p wave >2.5mm in lead II Shawn Li, Nora Abo-Sido 6 TOC Cardiology EKG Interpretation Ischemia/Infarction (JACC 2009;53:1003)  Analyze abnormalities along the vectors of ventricular depolarization and repolarization (QRS-ST-T)  T-wave abnormalities: Hyperacute, symmetric T-waves can be found within minutes; followed by T wave inversions (≥0.1 mV in 2 contiguous leads)  ST depression: Suggests subendocardial injury; ≥0.05 mV below the baseline (PR segment), measured at the J point, in two contiguous leads, downsloping or horizontal = more ominous. ST depressions do not localize to territories (Circ Res 1998;82;957) NB: always look for ST elevations to rule out reciprocal ST depression. Digoxin toxicity: scooping ST depressions.  ST elevation: Suggests transmural ischemia; ≥0.1 mV, except for leads V2 to V3 (≥0.2 mV in men ≥40yo and ≥0.15 mV in women), measured at the J point. PR segment is the isoelectric interval on the ECG and can be used to assess ST segment elevation/depression.  Q-wave: Usually a marker of scar; must be deep (>1 mm) and broad (>0.04 seconds), more likely 2/2 prior MI if inverted T wave in same lead. Pathologic Q wave defined by 40ms duration (1 box wide), 25% height of QRS. “Isolated Q in III is free” (non-pathologic).  Sgarbossa Criteria: Used to diagnose acute MI in presence of LBBB. Score of 3 = 90% Sp Concordant STE > 1mm in any lead = 5 points; Discordant STE > 5 mm in any lead = 2 points; ST depression > 1 mm in V1- V3 = 3 points.  Wellens’ Syndrome: Sign of critical prox LM or prox LAD lesion, 75% MI in 11mm LBBB Concave, ST depressions discordant from QRS Acute pericarditis Diffuse STE (usually < 5mm), PR depression, STE amplitude:Twave amp (in mm) >0.26 specific Stress-Induced (Takotsubo’s) Cardiomyopathy Usually limited to precordial leads w/out reciprocal inferior ST depressions, STE followed by deep TWI Printzmetal’s Angina/Vasospasm ECG mimics MI but STE are transient Ventricular aneurysm Persistent STE in any leads PE Mimics MI, look in inferior and anteroseptal leads Hyperkalemia Look for other ECG findings c/w hyperkalemia Cardioversion Marked (often > 10mm) following DCCV Electrolyte Abnormalities Electrolyte derangement Characteristic ECG Findings Hypokalemia Prolonged QT, ST depression, flattened T wave, prominent U wave Hyperkalemia Peaked, symmetric T wave; prolonged PR; flattened P and widened QRS (severe hyperkalemia) Hypocalcemia Prolonged QT, unchanged T wave Hypercalcemia Shortened QT J-point elevation syndromes Early repolarization: ERP: ST segment elevation in absence of chest pain, terminal QRS slur, or terminal QRS notch Features suspicious for malignant forms of ER: 1) Fh/o sudden cardiac arrest or early unexplained death. 2) evalution and workup suggestive of a channelopathy. 3) h/o unheralded syncope suggestive of an arrhthmogenic pathogensis (Circ 2016; 133:1520) Brugada Syndrome (Circ Arrhythm Electrophys Osborn Wave Epsilon Wave 2012;5:606) -Hypothermia, -Found in ARVC -Autosomal dominant, SCN5A TF, more common to have height roughly w/ ARVC) nocturnal cardiac arrest proportional to -Low frequency, -p/w VT/VF or sudden cardiac degree of positive terminal death hypothermia (n.b. deflection in V1-V3 neg in V1 & aVR) Shawn Li, Nora Abo-Sido 7 TOC Cardiology Narrow & Wide Complex Tachycardia Narrow Complex Tachycardia (QRS < 120 ms) (NEJM 2012;367:1438)  Diagnostic approach & general principles: o if unstable  synchronized cardioversion o vagal maneuvers/carotid massage/adenosine can resolve diagnostic dilemmas and treat AVNRT and AVRT o acute treatment for all others is BB, CCB or amiodarone (but consider risk of pharmacologic cardioversion if pt is not anticoagulated) Regular Normal P, gradual rise in HR = sinus Abnormal P = AT Retrograde or not visible P = AVNRT, AVRT, junctional tach Flutter waves > 250/min = AFL P-waves? Irregular No P = AFib ≥3 different P’s = MAT Flutter waves > 250/min = ALF with variable block  Sinus Tachycardia o Gradual in onset (if not consider SANRT, which is similar to AVRT and terminates with adenoside or vagal maneuvers) o Consider: hypovolaemia, haemorrhage, withdrawal (EtOH, BZD, opiate, BB), intoxication, fever/infection, pain, hypoxaemia, PE, anaemia, tamponade, dissection, hormonal (hyperthyroidism, adrenal insufficiency, pheochromocytoma)  Atrial Tachycardia (AT)  Atrioventricular Re-entrant Tachycardia (AVRT) o Long RP, single P morphology, non-sinus P wave axis o Usually short RP, uncommon long RP, rarely no RP o Arises from increased automaticity at single atrial focus o Arises from true re-entry via bypass tract o Classic digoxin toxicity is AT w/ variable AV block o Ventricular activation via AV node (orthodromic, NCT) more common than via accessory tract (antidromic, WCT) o Rates usually 150-250  Multifocal Atrial Tachycardia (MAT) o Long RP, 3 or more P wave morphologies o Irregular due to varying PP, PR and RR intervals o COPD, pHTN, CAD, electrolytes, theophylline  Atrial Fibrillation (AF) o No coordinated atrial activity (P wave absent), irregular o Arises from numerous re-entrant tracts in atria or  AVNRT vs AVRT pulmonary veins o Both are regular, paroxysmal, re-entrant NCTs w/ variable RPs that terminate w/ adenosine/vagal/AV block  Atrial Flutter (AFL) o Use baseline ECG, trigger, terminal activity to distinguish o Arises from true (isthmus-dependent, typical) or functional o AVNRT: look for terminal pseudo-r’ in V1-2 during (isthmus-independent, atypical) re-entry w/in R atrium tachycardia that is absent on baseline ECG o PP interval constant but RR may vary (variable AV block) o Counterclockwise: negative flutter waves in II, III and aVF o Clockwise: positive flutter waves in II, III, aVF o Signature: no isoelectric baseline, atrial rate ~300, always > 250, usually with 1:2 conduction  Atrioventricular Nodal Re-entrant Tachycardia (AVNRT) o Usually no RP (slow-fast), uncommon short RP (fast- o AVRT: look for pre-excitation (short PR) on baseline ECG slow), rarely long RP (slow-slow) (delta wave → WPW; no delta wave → Lown-Ganong- o Arises from functional re-entry w/in AV node Levine syndrome) that is absent during tachycardia o Trigger PAC (slow-fast) > PVC (fast-slow) o Young adults, F > M  Junctional Tachycardia o Usually short RP (retrograde P waves), can be no RP o If P waves present, must be negative in aVF o Arises from increased automaticity in AV junction Usama Abbasi and Raymond Parrish 8 TOC Cardiology Narrow & Wide Complex Tachycardia Wide Complex Tachycardia (QRS ≥ 120 ms)  Goal: determine VT or SVT with aberrant conduction  SVT w/ aberrant conduction includes: functional/rate-dependent BBB iso encroachment on bundle refractory period; RBBB > LBBB, SVT w/ pre- existing BBB, antidromic AVRT, antiarrhythmic drugs (digoxin, class IA or IC, amiodarone), hyperkalemia, TCA overdose, pacemaker/endless loop tachycardia (retrograde VA conduction of V-paced beat misidentified as native A-beat leading to additional V-pacing)  As majority of VT is due to re-entry (true about scar vs functional iso heterogeneous conduction), history is crucial. MI, cardiomyopathy, reduced LVEF and infiltrative disease all increase pre-test probability of VT  QRS w/ sharp initial deflection (some His-Purkinje conduction present) followed by broad terminal deflection favours SVT w/ aberrancy  ECG factors that favor VT: o Very broad QRS (ie > 160 ms), superior axis (II, III and aVF completely negative), indeterminate axis (I and aVF negative) o AV dissociation (often V rate > A rate) → diagnostic of VT o Concordance – all QRS across precodium completely positive or completely negative o Partial (fusion beat) or complete (capture beat) depolarisation of ventricle by underlying supraventricular rhythm  Brugada criteria (Circulation 1991;83:1649): o Highly sensitive and specific in initial paper, but subsequent studies have unanimously demonstrated lower sensitivity and specificity o Only applicable if rhythm is regular Management of VT  Monomorphic VT:  Polymorphic VT w/ normal QT: o NSVT: BB if symptomatic, electrolytes (K > 4, Mg > 2) o Ischaemia → BB, revascularisation, mechanical support o Sustained but stable: chemical cardioversion w/ o If unstable → defibrillation amiodarone (150 mg), lidocaine (if c/f ischaemia; 1-1.5  Torsades de Pointes – special case of pmVT iso prolonged QT, often mg/kg) or procainamide (only if no structure heart triggered by R on T disease, preserved LVEF; 20-50 mg/min for 5-10 mins o Mg while monitoring for hypotension, shall slow rate even if o Increase HR (dopa, epi, iso, overdrive pacing) fails to convert), o Avoid bradycardia (amio, CCB, BB) o Unstable: synchronized cardioversion (if pulse) vs o Decrease QTc (lido) defibrillation (pulseless)  Incessasnt VT (VT Storm) – refractory VT (defined differently if ICD vs no ICD) o Amiodarone 150 mg IV plus propranolol 60 mg PO Q6H superior to amiodarone plus metoprolol (JACC 2018;71:1897) o Anti-tachycardia pacing (unsafe to attempt unless prepared for emergent DCCV/defibrillation as can precipitate unstable VT) o Intubation and sedation to suppress adrenergic tone o VANISH trial: in patients with ischaemic cardiomyopathy and ICD w/ persistent VT, ablation superior to escalation of antiarrhythmic drugs (compositive of death, VT storm and ICD shocks) Usama Abbasi and Raymond Parrish 9 TOC Cardiology Atrial Fibrillation & Flutter Atrial Fibrillation Epidemiology and Classification (Heart Rhythm 2012;9:632)  Prevalence increases with age; 7 days Long-standing persistent: continuous afib lasting >12 months Permanent: term used when decision is made to stop further attempts to restore and/or maintain sinus rhythm Clinical Evaluation of New-Onset Atrial Fibrillation  History/Exam: presence and timing of symptoms, HTN, DM, valvular disease, CHF, angina, congenital heart disease, OSA, family hx of AF, acute precipitants (e.g., EtOH, thyrotoxicosis, sympathomimetic drugs, surgery, myocardial ischemia, myocarditis, PE, acute pulmonary disease, infection)  ECG: absence of discernible p waves, irregularly irregular R-R intervals  TTE: LV function, LA/RA size, valve function, pulmonary HTN, LA thrombus (low sensitivity, better with TEE)  CXR: evaluate for pulmonary parenchymal processes and pulmonary vasculature/edema  Labs: TFTs, LFTs, BUN/Cr, CBC, NT-proBNP  Additional testing: Zio patch, Holter monitor, implantable loop recorder, exercise testing (to assess rate control with activity or as part of ischemic evaluation)  Five “domains” of initial assessment: hemodynamic stability, precipitating factors, stroke risk and need for AC, HR and need for rate control, symptom assessment and need for rhythm control Cardioversion (ALWAYS consider high risk of embolic stroke if any breaks in AC for one month prior)  Indications Urgent situations: ischemia, end-organ hypoperfusion, symptomatic hypotension, severe pulmonary edema Elective: new-onset AF or unacceptable symptoms from persistent AF  Electrical Cardioversion (DCCV) Synchronized DCCV at 150J (biphasic); increase energy in stepwise fashion if SR not achieved Use procedural sedation if possible (consult cardiac anesthesia). If elective, should be performed in ICU or EP lab. Consider anti-arrhythmic drugs as adjunct (e.g., amiodarone)  Chemical Cardioversion Success rate significantly higher for acute (90  Usually if HR > 130 or symptomatic prefer IV, otherwise can consider starting PO / increasing current PO dose  Beta-blocker: metoprolol (others: labetalol, propranolol, esmolol) IV: bolus 2.5-10 mg over 2 minutes; repeat as required q10-15 min PO: up to 400mg total daily dose (although doses >200mg usually not effective) Contraindicated: acute decompensated heart failure, history of severe bronchospasm  Calcium channel blocker: diltiazem (others: verapamil) IV: bolus of 0.25 mg/kg (average adult dose 10-25 mg) over 2 minutes; repeat as required q10-15 min PO: up to 360 mg total daily dose David Olshan 10 TOC Cardiology Atrial Fibrillation & Flutter Contraindicated: LV failure with pulmonary congestion, LVEF 140) more likely to cause HoTN alone; lower HRs ( 2mm; define end point using tangent from peak of steepest slope to isoelectric line QTc – Corrected for HR o Bazett’s formula = QT/√RR; overcorrects at high HR and undercorrects at low HR o Fridericia’s formula = QT/3√RR; more accurate at high or low HR (Am J Cardiol 1993 26;72:17B). Assessment of QT with underlying BBB (Heart Rhythm 2014;11:2273) Bundle branch blocks will lengthen QT interval – can use modified QT (QTm) or JT interval (JTI) as surrogate index for repolarization o JTI = JT(HR + 100)/518, with a JTI > 112 identifying repolarization prolongation in all ventricular conduction defects o QTm = QTb - 48.5% * (QRSb) Congenital Long-QT Syndromes (Br J Clin Pharmacol 2010;70:16) LQT1: KCNQ1 – (IKs) Romano Ward, autosomal dom. – triggered by exercise, stress LQT2: hERG – (IKr) Jervell Lange-Nielsen, autosomal rec. – assoc. w/ deafness, triggered by emotional stress (acoustic) LQT3: SCN5A – (INa ) triggered by rest, sleep Sx include pre-syncope/syncope, sudden cardiac death, general population screening not indicated Treatment: beta blockers, ICD if previous cardiac arrest and expected survival > 1 year (Circulation 2006;114:e385) Drug-Induced Prolonged QT Interval (Heart. 2003;89:1363; https://crediblemeds.org/pdftemp/pdf/CombinedList.pdf) Drugs inhibit IKr causing prolonged ventricular repolarization and exaggerate heterogeneity in repolarization times in different layers of myocardium leading to reentry and tachyarrhythmia Torsades de Pointes: Polymorphic VT in setting of prolonged QT; unstable rhythm that can lead to vfib QT-Prolonging Drugs and Risk for TdP Risk factors for TdP in Hospitalized Patients (NEJM 2004;350:1013, Br J Clin Pharmacol 2010;70:16) (Circulation 2010;121:1047) Risk for TdP Medications Elderly, female sex, Demographics Frequent (>1%) – congenital LQTS initiation in hospital Antiarrhythmics: Class IA (quinidine, disopyramide, Renal failure, hepatic with telemetry procainamide), class III (sotalol, dofetilide, ibutilide) dysfunction (or drug-drug Comorbidities recommended interactions impairing Antiarrhythmics: Amiodarone (rarely a/w TdP due to liver metabolism), HF, MI uniform delay in repolarization across myocardium) QTc > 500 ms, Antibiotics: Macrolides (clarithromycin, erythromycin), bradycardia (sinus, AV Rhythm-related fluoroquinolones (moxifloxacin > levofloxacin, block, ectopy causing ciprofloxacin) pauses) Antipsychotics: Haloperidol, thioridazine, Hypomagnesemia, Less frequent chlorpromazine, quetiapine, risperidone increase QTc Electrolytes hypokalemia, 15-30 ms at usual doses and have risk of TdP; hypocalcemia olanzapine, aripiprazole carry ↓ risk of QTc prolongation QT-prolonging drugs and TdP (esp. IV infusions, use of Medication-related Anti-emetics (ondansetron), anti-fungals (fluconazole), >1 concurrently), diuretic anti-malarials (chloroquine), opioids (methadone) use Monitoring for QT/QTc Prolongation Check QTc before and 12 hours after initiation/increased dose of QT-prolonging drug. Continued monitoring if prolongation is seen. Class I indications for QTc monitoring with ECG (Circulation 2004;110:2721) o Initiation of QT-prolonging medication and dose changes Q8-12H o Overdose of proarrhythmic drug o New bradyarrhythmia o Severe hypokalemia or hypomagnesemia Management of Acquired LQTS Offending drug should be stopped if QTc > 500 ms or increase in QTc of > 60 ms; ECG should be checked for bradyarrhythmias and signs of impending TdP (R on T); electrolytes checked and repleted Supratherapeutic repletion of K+ to 4.5 to 5.0 can be used in pts on QT-prolonging drugs who have had TdP Sumeet Khetarpal 13 TOC Cardiology Chest Pain HISTORY PHYSICAL EXAM CVD risk: Use Framingham or ASCVD Risk Likelihood Ratios for ACS New S4, MR (ischemia) Estimator. Women, elderly, and diabetics may (JAMA 2015;314:1955). CHF (rales, +S3, ↑JVP, pedal have atypical presentations of ACS. Age, h/o Low Risk edema) CAD, and male sex most predictive of ACS Pleuritic (0.3) Syncope (0.5) Carotid, subclavian, and abdominal (NEJM 2000;342:1187). Intermediate Risk bruit (indicates vascular disease) Radiation to left Diaphoresis Bilateral femoral and radial pulses Angina (NEJM 1979:300:1350): arm, neck, or (1.4); Exertional Stable (document pre-cath) (1) substernal chest pain jaw (1.3-1.5) (1.5) Angina/ACS Pressure/ Pattern Frank’s sign: bilateral diagonal (2) brought on by stress/exertion earlobe crease (slight ↑ in likelihood typical (1.9) change/24h (2.0) (3) relieved by rest or TNG of CAD) High Risk 3/3 = typical, 2/3 = atypical, 1/3 = noncardiac Similar to prior Pain radiating to Less likely ACS: pleuritic, positional, Antianginals: nitrates – 1st SL, then IV (only ischemia (2.2) both arms (2.6) reproducible by palpation (LR 0.28) on SDU or CCU), avoid if preload sens Abnormal prior (HoTN, AS); BB (avoid in ADHF, long PR, PAD (2.7) stress test (3.1) 2˚/3˚ AV block); CCB. Abrupt onset of tearing/sharp/ripping thoracic or abdominal pain, known aneurysm, (1) classic pain (2) mediastinal widening, Marfan syndrome, HTN. Men 2x > women, age 60s-80s, cocaine use, high-intensity (3) BP>20mmHg difference between Acute Aortic exertion (weight lifting). arms: 0/3 Sx =7% prob, 1/3=31-39%, Syndromes 2/3= 83%; If ∆BP >20, >83% (Arch Int Med 2000;160:2977). √ for AI murmur. Acute Pleuritic, sharp, improves upon leaning forward. May have URI prodrome, though Friction rub (breath hold to distinguish Pericarditis consider bacterial pericarditis if high fevers. from pleural rub); tamponade: pulsus >10. Sudden onset, dyspnea/hypoxemia, pleuritic, hx of cancer/recent surgery/immobility, Tachycardia, tachypnea, hypoxemia PE +/- TnT. Sudden onset, 20-40 yo (spontaneous and more likely if tall), family or personal Ipsilateral absence of breath Pneumothorax history, smoker, known emphysema, men > women, recent chest procedures/lines. sounds/deviation of trachea (if tension, contralateral deviation) Pneumonia/ Sharp, pleuritic CP associated with fever/leukocytosis, productive cough, recent Bronchial breath sounds, rales, dullness pneumonitis radiation, autoimmune (SLE, RA, drug-induced lupus, collagen vascular diseases). Cardiac: HOCM, AS, vasospasm (Prinzmetal’s angina or drug/toxin), Takotsubo CM, cardiac syndrome X; MSK: Costochondritis, Other Zoster; GI: GERD, esophageal spasm (may be relieved by TNG), Boerhaave’s, PUD, biliary colic, pancreatitis; Psych: panic attack ECG: Compare w/prior ECGs & check q10-15m if susp, but Non-diagnostic S in V1-2) or R-sided leads (if STE in II/III/avF) to CXR better evaluate LCx/RCA Signs of PE Normal Widened PNA Pericarditis NSTEMI/UA STEMI RAD, new mediastinum Diffuse 0.5mm STD or TWI New ≥1mm STE in any RBBB, TWI upsloping STE in 2 consec leads 2 consecutive leads V1-4, S1Q3T3 PTX and PR compared to prior ECG suggestive of depression, PR Biomarkers (see ACS chapter) RV strain (Sp, elevation in not Sn) Consider Consider Aortic aVR PE Dissection ACS Pathway Biomarkers Non-Invasive Tests High-Sensitivity Troponin (hs-cTn) Stress Test: used to r/o ACS if MGH ED: Obtain at 0 and 1hr. Rules-in if any cTn ≥52 ng/L or if 1hr ∆ >5; CT-PE pt low-intermideiate risk (neg R/o if 7, AND high/ intermediate/ low w/o CAD. No ∆ in LOS or ED either sx of ischemia, ischemia on ECG, or imaging c/w CAD. risk (PIOPED II). d/c rate vs hs-cTn (JACC High-STEACS Study: ≥5 ng/L at presentation, ∆ ≥3, or >99%ile at 3hr Sn 97-100%, Sp 83- 2016;67:16). CTA reduces 5yr showed improved outcomes vs less-strict criteria. 100% for aortic CHD mortality in pts w/ stable Caveat: intro of hs-cTn, w/ rule-in threshold of cTn ≥99% ULN, may not dissection (NEJM angina (NEJM 2018;379:924). improve 1-yr mortality vs low-sens cTn (Lancet 2018;392:919). 1993;328:35). Angiography Echo Used to r/o ACS in high risk pts (NB: all pts with confirmed ACS Useful for assessing valvular disease, RV strain (in PE), and EF. should undergo angiography). Use GRACE, TIMI, HEART and Mayo TEE first test if evaluating prosthetic MV, suspected proximal aortic Clinic CPC score for risk stratification. dissection (can eval aortic root and valvular function). David Olshan 14 TOC Cardiology Acute Coronary Syndrome Myocardial infarction: 4th universal definition (Type 1-5): myocardial necrosis (trop >99th percentile + ∆) w/ ischemia (EHJ 2019;40:237)  Type 1 MI: spontaneous MI (plaque rupture, ulceration, fissure, erosion, dissectionintraluminal thrombus)  Type 2 MI: supply-demand mismatch – supply may be compromised by dynamic obstruction (e.g., vasospasm), microvascular ischemia (e.g., Takotsubo), non-plaque thromboembolism (e.g., infectious, via PFO), coronary dissection, vasculitis, vascular steal o Must be a clear precipitating factor. If there is no identifiable precipitant, treat as a type 1 MI until further evaluation. o With widespread introduction of hs-troponin assays in the U.S., type 2 MI may now be more prevalent than type 1 MI. o Differs from myocardial injury. T2MI requires evidence of ischemia (EKG changes, symptoms, or new regional wall motion abnormalities on cardiac imaging). o Associated with poor outcomes: 1-year mortality rates are 20% and at 5-year 60%, high readmission rate. o Currently no proven treatment strategies for type 2 MI and no guidelines for management. 50-70% have obstructive CAD; reasonable to initiate ASA, BB, and high-intensity statin. The utility of PCI uncertain (ongoing ACT-2 trial) Evaluation of CP with hsTnT Emergency Department – CP onset ≥ 3h PTA Inpatient or Emergency – CP onset < 3h Check hsTNT immediately and at 1h Check hsTNT immediately and at 3h Rule in: hsTnT ≥52 OR ∆ ≥ 5 from baseline Rule in: hsTnT ≥10(F) or≥15(M) AND ∆ ≥ 7 from baseline AND sx or  consider ACS ECG changes or concerning imaging (CCTA, cath) Rule out: hsTNT II elevation suggests RCA as culprit rather than LCx V7-9 Posterior LCx > RCA ST depressions in V1-V3 or R:S >1 in V1-V2 may represent posterior STE V3-4R RV RCA, LCx Check with inferior STE. 1mm STE in V4R most predictive of RV infarct aVR, V1 L main or 3v disease aVR>V1 STE with diffuse ST depressions = LMCA, 3VD or diffuse ischemia o Posterior leads (V7-V9, “inverse” of V1-V3 on back below scapula); LCx (less commonly RCA) can be electrically silent on conventional ECGcheck posterior leads in setting of cTn elevation and compelling hx with non-diagnostic ECG (Class IIa) o R-sided leads (V3R-V6R mirrors L-chest leads): check with inferior STEs to eval for RVMI; STE in V1 + STD in V2 very specific o Pre-existing LBBB: (NEJM 1996;334:481, Ann Emerg Med 2008;52:329) Sgarbossa criteria: ≥1mm concordant STE in any lead (5 pts); ≥1mm ST depression in V1, V2 or V3 (3 pts); ≥5mm discordant STE in any lead (2 pts). Score ≥3 is 90% Sp for acute MI. Variable Sn of 20-79%. Doesn’t apply to pacers. o Pre-existing RBBB: Interpret ECG as if there were no BBB. If deep discordant ST depressions in V1-V3, check posterior leads o deWinter’s T-waves: 2% of STEMIs p/w tall symmetric T-waves + >1mm STD at J-point in precordial leads +0.5-1mm STE in aVR, may evolve to STEs, consistent w/ acute LAD occlusion (NEJM 2008;359:2071) o Wellen’s pattern: Symmetric, deeply inverted T waves in V2, V3 (75%) > biphasic T waves (25%) Anna O’Kelly, Leslie Chang, Cian McCarthy, Jonathon Salik 15 TOC Cardiology Acute Coronary Syndrome o Wellen’s syndrome: (Am Heart J 1982;103:730) Wellen’s pattern in pts presenting w/ CP w/ resolutionindicates reperfusion of myocardium indicative of LM or proximal LAD stenosis. 75% of pts will have ant MI in days-weeks if not treated. Proceed to cath lab w/o stress testing. DDx: apical HCM, elevated ICP (w/ long QTc & brady), MI, PE, post-tachy/pacing, BBB, WPW, idiopathic Risk Stratification for PCI Timing in NSTEMI/UA:  Multiple risk models: GRACE, TIMI, PURSUIT, AMIS  GRACE score, based on predictors of 6 mo mortality in pts w/ ACS – age, HR, SBP, Cr, cardiac arrest ?, ST deviation, elevated trop (BMJ 2006;333:1091)  4 subgroups for urgency to get to the cath lab (JACC 2014;64:e139)  Very high risk (“immediate invasive,” within 2 hrs): Refractory/recurrent angina, hemodynamic or electrical instability  High risk (“early invasive,” within 24 hrs): temporal change in troponin, EKG changes (STD, TWI), high risk pt (GRACE>140)  Conflicting results between TIMAC (NEJM 2009;360:2165) and VERDICT (Circ 2018;138:2741) trials about outcome benefit of early cath. However both show improved outcomes with early cath in patients with GRACE >140.  Intermediate risk (“delayed invasive,” within 72 hrs): none of above but risk factors at baseline (ie EF 75y (JAMA 2001;285:1711) Updated lipid guidelines recommend in very high risk clinical ASCVD pts w/ LDL>70 mg/dL adding first ezetimibe and then considering PCSK9 inhibitor (JACC 2018;epub, NEJM 2015;372:2387; NEJM 2018;epub) Triple oral anticoagulant therapy (TOAT): grade 2c: For patients with AFib, 1-12mo triple therapy is recommended depending on bleeding risk. If high bleed risk, triple therapy for 1 month, then consider clopidogrel+anticoag w/o ASA x 11 months (Lancet 2013;381:1107). RE-DUAL PCI found that dual therapy with dabigatran + P2Y12 inhibitor led to lower risk of bleeding and was non- inferior to TOAT for risk of thromboembolic events (NEJM 2017; 377:1513). CAD: In pts w stable CAD, Rivaroxaban (2.5mg BID) + ASA v ASA alone has improved cardiovascular outcomes but increased risk of bleeding. Rivaroxaban alone (5mg BID) v ASA alone had no cardiovascular benefit and ↑ bleed. (NEJM 2017; 377:1319-1330). Additional: smoking cessation, BP 140/90), cardiac rehab (1c), depression screening (1b) MGH P2Y12 Switching Guideline Peri-operative P2Y12 Bridging NOTE: This guideline does NOT necessarily apply to triple antithrombotic therapy patients ** PATIENT SHOULD TAKE LAST DOSE ON THIS DAY, THEN STOP 5Initiate at a dose of 0.75 mcg/kg/min (NO bolus) for a minimum of 48 hours and a maximum of 7 days 6 600 mg loading dose of clopidogrel as soon as oral administration is possible and when surgical bleeding risk is acceptable; use of prasugrel or ticagrelor is discouraged. If a patient is at very high-risk for bleeding, consider clopidogrel half load (300 mg) or maintenance dose (75 mg), in lieu of the full 600mg loading dose. 7ONLY resume cangrelor if oral administration is NOT possible (patient NPO, patient not absorbing oral medications) *Consider concomitant PPI therapy if patient is high-risk for GI bleeding Anna O’Kelly, Leslie Chang, Cian McCarthy, Jonathon Salik 17 TOC Cardiology Acute Coronary Syndrome Acute Setting – within 30 days of index event NOTE: This guideline does NOT necessarily apply to triple antithrombotic therapy patients Agent switching TO/STARTING Clopidogrel1 Ticagrelor Prasugrel Cangrelor2,3 Clopidogrel 180 mg when decision 60 mg when decision is Start 0.75 is made to switch (no made to switch (no mcg/kg/min 48 hours delay time needed), delay time needed), after discontinuation then 90 mg BID then 10 mg daily Agent switching FROM/STOPPING Ticagrelor 600 mg 24 hours after 60 mg 24 hours after Start 0.75 last dose of ticagrelor, last dose of ticagrelor, mcg/kg/min 48 hours then 75 mg daily then 10 mg daily after discontinuation Prasugrel 600 mg 24 hours after 180 mg 24 hours after Start 0.75 last dose of prasugrel, last dose of prasugrel, mcg/kg/min 96 hours then 75 mg daily then 90 mg BID after discontinuation Cangrelor 600 mg at time of drip 180 mg dose 0 to 120 60 mg dose 0 to 30 discontinuation, then minutes before drip minutes before drip 75 mg daily discontinuation, then discontinuation, then 10 90 mg BID mg daily 1If a patient has active bleeding or is very high-risk for bleeding, consider clopidogrel half load (300 mg) or maintenance dose (75 mg), in lieu of full 600mg loading dose. 2IF there is concern for lack of absorption of initial LOADING DOSE of oral P2y12 at time of cangrelor initiation and patient is not at high bleeding risk, could consider bolusing with 30 mcg/kg before starting infusion 3Please note that the dose of cangrelor recommended for use in the cardiac catheterization lab is different than the recommended bridging dose. The doses listed here are for bridging. The cardiac catheterization PCI dosing is 30 mcg/kg followed by a 4 mcg/kg/min infusion until cardiac catheterization is complete, or 2-4 hours, whichever is longer. Then, the drip rate is dropped to 0.75 mcg/kg/min OR a loading dose of an oral agent is given. *Consider concomitant PPI therapy if patient on triple therapy or high-risk for GI bleeding Chronic/Maintenance Setting – more than 30 days after index event NOTE: This guideline does NOT necessarily apply to triple antithrombotic therapy patients, please discuss switching strategies for these individuals on a case-by-case basis Agent switching TO/STARTING Clopidogrel Ticagrelor Prasugrel Cangrelor Clopidogrel 90 mg BID 24 hours 10 mg daily 24 hours Start 0.75 after last dose of after last dose of mcg/kg/min 48 hours Agent switching FROM/STOPPING clopidogrel clopidogrel after discontinuation Ticagrelor 600 mg 24 hours after 60 mg 24 hours after Start 0.75 last dose of ticagrelor4, last dose of ticagrelor, mcg/kg/min 48 hours then 75 mg daily then 10 mg daily after discontinuation Prasugrel 75 mg daily 24 hours 90 mg BID 24 hours Start 0.75 after last dose of after last dose of mcg/kg/min 96 hours prasugrel4 ticagrelor after discontinuation Cangrelor 600 mg at time of drip 180 mg at the time of 60 mg at time of drip discontinuation, then drip discontinuation, discontinuation, then 10 75 mg daily then 90 mg BID mg daily 4Ifswitch is for high risk of bleeding/active bleeding, could consider starting clopidogrel 75 mg 24 hours after last dose of ticagrelor or prasugrel. *Consider concomitant PPI therapy if patient on triple therapy or high-risk for GI bleeding Anna O’Kelly, Leslie Chang, Cian McCarthy, Jonathon Salik 18 TOC Cardiology MI Complications Mechanical Complications (JACC 2013;61:e78) Complication Prevalence / Risk Factors Timing / Clinical Signs Evaluation Treatment Early Complications (Hours – Days) Cardiogenic  STEMI ~6%  STEMI: 50% develop shock w/in 6  TTE  Inotropes/pressors Shock  NSTEMI ~3% h of MI, 75% w/in 24 h  PA catheter  Emergent PCI, CABG (see CHF chapter)  Anterior MI, LBBB, prior MI,  NSTEMI: 72-96 h after MI (14 h), (PPV 95% w/ 2/3). (JACC scar, more prone to fibrinolysis>>PCI, NSAIDs, 1993;22:720) rupture than female, >70 y  Electromechanical dissociation, aneurysm)  Accounts for 10% post-MI aberrant T wave evolution, abrupt death episodes of ↓HR/BP Interventricular  0.2-3%  Bimodal: 24 h and 3-5 days (can  TTE w/ Doppler  IABP Septal Rupture  1st MI, 1-vessel MI (esp. LAD), occur up to 2 weeks out)  RHC: O2 sat  Vasodilators (use VSD anterior infarct w/ inferior STE  New, harsh holosystolic murmur step-up cautiously) to decrease L 2/2 wrap-around LAD, older (50% w/ thrill), S3, loud P2, between RA to R shunt (nitroprusside age, female hypotension, BiV failure (R>L) and PA >5 preferred)  Accounts for 5% post-MI suggestive death Papillary Muscle  1%  No reperfusion: 2-7 d  TTE  Aggressive afterload Rupture  Posteromedial (supplied by  With reperfusion: median 13 h  CXR: edema reduction (nitroprusside)  acute MR PDA, a/w inf. or post. MI) >>  Abrupt dyspnea, pulmonary (can be  IABP Anterolateral (dual blood edema, hypotension asymmetric to  Emergent surgery supply by LAD and LCx)  Hyperdynamic LV, holosystolic RUL if MR jet  Accounts for 5% post-MI murmur at apex, (radiates to LSB directed at right death w/ posterior pap muscle rupture) pulm veins) possible thrill, murmur may be  Large v wave absent in severe HF Late Complications (Weeks-Months) LV Aneurysm  No reperfusion: 10-30%  Days to weeks  ECG w/  Acute: management of (can be acute or  Apical transmural > posterior-  Acute: diffuse, displaced PMI, S3 persistent STE CHF, ACEi, avoid chronic) basal MIs, steroids, NSAIDs and/or S4, MR murmur, CHF  TTE NSAIDs/steroids, heparin  Chronic: HF, VT/VF, systemic (if EF2  VF >48h post-MI may indicate LV dysfunction MILIS trial: prediction of complete heart block (Am J Cardiol 1986;57:1213) 1 point for each: New PR prolongation; 2nd degree AV block; LAFB or LPFB; LBBB; or RBBB. The risk of progression to CHB was: 0 points 1.2-6.8% 1 point 7.8-10% 2 points 25-30% ≥3 points 36% Maeve Jones-O’Connor 20 TOC Cardiology Cardiac Catherization & Coronary Anatomy Anatomy  LCA and RCA w/ their branches create two rings around the heart: RCA + LCX in AV plane; LAD + PDA in IV plane (see above)  80% of PDA arises from RCA (right dominant), thus inferior MI more likely from RCA lesion Preparation for Catheterization  NPO pMN; INR10mmHg w/ inspiration), STAT TTE, alert cath fellow. Give IVF. o MI/CVA: due to in-stent thrombosis (MI) or distal embolization post-cath (CVA). Discuss all CP/neuro changes with cath fellow Shawn Li, Sumeet Khetarpal 21 TOC Cardiology Non-Invasive Cardiac Testing General Considerations Indications:  Diagnose CAD: Sx of stable angina in patients w/ intermediate or high risk of CAD. Not indicated for low risk or asymp. pts.  Known CAD: Stratify prognosis in new or changing sx c/f ischemia or post-MI prior to discharge (i.e., submaximal stress)  Post-revascularization: Pts w/ angina; asymptomatic pt if incomplete revasc or >2 years post-PCI / >5 years post-CABG  Pre-op risk assessment: Not routinely indicated; no evidence that revasc ↓ mortality or post-op MI for non-cardiac surgery. (NEJM 2004;351:2795)  Other: Newly dx HF/cardiomyopathy likely due to ischemia; functional capacity (for exercise prescription); viability testing Contraindications: untreated ACS, MI within 2d, high-risk or LM CAD, uncontrolled arrhythmia, acute CHF, severe AS or HOCM, recent DVT/PE, acute myo-/peri-/endocarditis, aortic dissection, uncontrolled HTN Patient Preparation: NPO 3h prior, longer if imaging or adenosine. Must reverse DNR/DNI for the test. Stress Modality Imaging Modalities  If the question is “Does this patient have CAD?  Exercise (treadmill) EKG, TTE, SPECT hold BB and nitrates Vasodilator (adenosine, regadenoson) TTE, SPECT, PET, MRI Pharm  If the question is “How well are meds working in Inotropy (dobutamine) TTE, SPECT, PET, MRI known CAD?”  continue BB and nitrates  Hold caffeine >12h for adenosine. Hold BB >24h for dobutamine (>48h for atenolol). Caveats:  Majority of vulnerable plaques are angiographically insignificant (70% stenosis) 3vD may produce false-negative vasodilator stress test”balanced ischemia” Positive Test Results:  Optimize medical tx. Decision re: angiography/revascularization varies by patient (degree of sx, known stenosis, current meds). Schematic Approach to Noninvasive Cardiac Testing (adapted from UpToDate) Sean Mendez 22 TOC Cardiology Non-Invasive Cardiac Testing Exercise Tolerance Test (ETT)  EKG or imaging (TTE, SPECT) ETT preferred over pharmacologic testing if pt is able to reach goal exertion Additional information obtained during ETT: exercise duration, METs, BP/HR response, HR recovery, double product (HR x SBP), Duke Treadmill Score (estimates risk of CHD in patients w/chest pain undergoing treadmill stress testing) o Duke Treadmill Score = Exercise time (minutes based on the Bruce protocol) - (5 x maximum ST segment deviation in mm) - (4 x exercise angina [0 = none; 1 = nonlimiting; 2 = exercise limiting]) (NEJM 1991;325:849, Circulation 1998;98:1622)  Low risk: score ≥ +5; Moderate risk: score from -10 to +4; High risk: score ≤ -11 Protocols: Bruce (large changes in workload between stages); modified Bruce (for less fit ptsadds stages of lower workload) Data: o Diagnostic if: >85% max-predict HR (220-age); peak double product (HRxBP) >20K; HR recovery (HRpeak – HR1min post-exercise) >12 o Prognosis worse with: failure to achieve 5 METs, increased degree of STD, degree of symptoms, Duke score ≤ -11, LVEF70% graft stenosis. (Circulation 2003;107:1502) cMRI is also preferred for evaluation of suspected or known congenital or acquired coronary anomalies cMRI w/ stress detects significant stenosis (>50%) with Sn/Sp 83%/83% greater than stress echo (Circulation 1999;100:1676) Viability Testing Utility: to determine the viability of ischemic myocardial tissue  “hibernating myocardium” Imaging Modalities: SPECT (thallium or sestamibi), PET, TTE, MRI o NB: SPECT performed using exercise or pharmacologic stress; PET/TTE/MRI performed using pharmacologic stress only Sean Mendez 23 TOC Cardiology Echocardiography View/Description Position View PARASTERNAL LONG AXIS Patient: Lying on left side, with left arm under head. Probe: 2-3 inches left of sternum at 3rd-4th intercostal LV size, function, wall thickness space, probe indicator at 10 o’clock (facing R shoulder). (septum/posterior wall) MV/AoV function/flow (w/ Doppler) LVOT diameter, aortic root size PARASTERNAL SHORT AXIS Patient: Same as above. Probe: From long axis view, turn probe clockwise until Cross-sectional views of the indicator at 2 o’clock (facing L shoulder). heart from base to apex, at level of AoV, MV and mid- ventricle/papillary muscles APICAL 4 CHAMBER Patient: Lying flat on back. Probe: At PMI w/ probe indicator at 3 o’clock (to the RV/LV size, function, thrombus pt’s L side). For 5-chamber view, tilt head of probe TV/MV function/flow (w/ upward. Doppler) Septal size/motion Pericardial effusion In 5-chamber view, can see AoV and proximal ascending aorta SUBCOSTAL VIEW Patient: Lying flat on back, consider slightly elevating head or bending legs. IVC diameter and respiratory Probe: Below xyphoid process variation gives estimate of volume status and RA pressure Pericardial effusion Reviewing the MGH Report: For questions or clarification of findings, call echo lab (x6-8871) or ask for on-call echo fellow (x6-9292)  Valvulopathy: Look for stenosis/regurgitation (valve area, gradients, trace/mild/moderate/severe), leaflet numbers/motion, vegetations  Strucure/chamber dimensions: AOSinus = aortic sinus ASC AO = ascending aorta; → screening for aortic pathology LVIDd = LV internal diameter in diastole LVIDs = LV internal diameter at end-systole → dilated (large) vs. LVH/HOCM (small) PWT = posterior wall thickness → increased thickness seen in LVH, diastolic dysfunction IVS = intraventricular septum → if ↑ along with ↑ PWT, consider diastolic dysfxn; if isolated ↑, consider HOCM  EF and WMA: “Preserved” EF≥50%; “Borderline” EF 40-50%; “Reduced” EF35; not gold standard for dx and requires euvolemia) Clinical Syndromes and Echo Findings  Acute pulmonary embolism: RV WMA/hypokinesis, McConnell’s sign, D sign, RV dilation (RV:LV ratio >1), interventricular septal bowing, IVC collapse  McConnell’s Sign: RV free-wall akinesia w/ normal RV apex motion (77% Sn, 94% Sp for acute PE)  D Sign: septal flattening due to overloaded RV bowing into the LV (ventricular interdependence)  Tamponade: large effusion, swinging heart, R-sided chamber collapse, interventricular septal bowing, dilated IVC (no ↓ w/ inspiration)  ACS/mechanical complications of ACS: regional WMA (can precede symptoms), septal/free wall rupture, acute MR/TV, LV thrombus  Stress (Takotsubo) cardiomyopathy: LV apex ballooning and akinesis/hypokinesis  Heart Failure: depressed EF, RV/LV hypertrophy and/or dilation, regional WMA  E/A Reversal and elevated E/e’ > 14: sign of diastolic dysfunction (i.e. elevated LVEDP and lower LV compliance) E = mitral peak flow velocity during early passive LV filling (v wave on CVP tracing) A = mitral peak flow velocity during active LV filling from atrial systole (a wave on CVP tracing) e’ = longitudinal velocity of mitral annulus during early passive filling Ijeoma Eleazu, Shawn Li 24 TOC Cardiology Inpatient Heart Failure Guidelines: Circulation 2013;128:1810; Circulation 2016:134:e282 Classification and Etiology of Cardiomyopathies  Dilated: ischemic (most common cause, 50-75% pts), HTN/LVH, valvular (e.g., MR), myocarditis, infiltrative (hemochromatosis, sarcoid, amyloid), LVNC, ARVC, peripartum, HIV, CTD, cocaine, EtOH, chemotherapy, nutritional deficiency, stress-induced (Takatsubo’s), tachyarrhythmia, cirrhotic, septic, idiopathic/genetic  Restrictive: infiltrative (amyloid, hemochromotosis, sarcoid), Löffler’s, radiation, metabolic storage disease, carcinoid  Hypertrophic obstructive (HCM): genetic Initial Workup: New Heart Failure Diagnosis  Echocardiogram (TTE): for all new presentations; obtain thereafter only if concern for clinical/functional change (J Am Soc Echo 2011;24:229)  Assess EF/systolic function: HFrEF (EF ≤40%) vs HFpEF (EF >50%) (NB: EF 41-49% is often called HFbEF for ‘borderline EF’)  Other findings: Regional WMA (specificity is low for ischemia), dilated chambers (consistent with dCM if LV dilated and > 6 akinetic segments), pHTN, valvular fxn, pericardial disease, restrictive filling, thickened septum, LVOT gradients, shunts, myocardial texture  Diagnostics: Ischemic: EKG, TnT, stress test, cardiac cath; Non- ischemic: CBC, BMP, LFTs, lipid panel, TSH, urine hCG, iron studies, HIV, SPEP w/ UFLC; also consider ANA, A1c, T. cruzi serologies, viral panel, antimyosin Ab, tox screen, thiamine level, genetic testing, endomyocardial bx if serologic testing neg, new onset 50% familial, 70-80% known genetics  Further imaging: Consider MRI (with gadolinium); TEE for better visualization of MV and AV Clinical Heart Failure Syndromes (JAMA 2002;287:628; JACC 2003;41:1797)  Warm vs. Cold: adequate vs. inadequate tissue perfusion (AKI, decreased UOP, AMS, lactate, cold/clammy)  Dry vs. Wet: presence vs. absence of congestion/edema o CXR signs: cardiomegaly, vascular cephalization, peribronchial cuffing, edema, Kerley B lines, alveolar edema o Chronic pulmonary congestion may lead to fewer signs of pulm edema on exam and CXR given vascular remodeling (Chest 2004;125:669) General Inpatient Considerations – ALL HF Patients:  Admission orders: Tele, Na (2g) and fluid (450 (>900 if age >50) (LR 2.75 for ≥ 900) (NEJM 2002;347:161; Am J Cardiol 2005;95:948; JACC 2009;54:1515) o Studies using BNP to HF management ongoing; TIME-CHF showed NT-proBNP guided tx didn’t improve outcomes, (JAMA 2009;301:383; Am J Cardiol 2006;98:1248; Circulation 2013;127:500) o Increased mortality with elevated discharge BNP/NT-proBNP (JACC 2004;43:635; JACC 2008;51:1874) and variations in NT- proBNP related to readmissions and death w/in 6mths (better prognosis with ≥ 30% decr) (Circulation 2004;110:2168) o NT-proBNP hard to interpret in CKD/dialysis; may be falsely low in obesity, HFpEF; may be higher in women/older individuals (Circulation 2004;109:594; Heart 2003;89:745)  Screen for iron deficiency in all HF pts independent of Hb; replete with IV iron if Tsat < 20% to improve functional status (JACC 2008;15:103) no benefit from PO iron in patients without anemia (JAMA 2017;317:1958)  If persistent hypoNa despite fluid restriction, consider vasopressin antagonism with tolvaptan (class IIB) for short-term sxs benefit EVERST (JAMA 2007;297:1319)  Discharge: o Optimize pre-discharge outpatient regimen focusing on mortality benefit in HFrEF (but not HFpEF!): ACEi/ARB, β-blocker, aldo blockade, ivabradine (for pts with HR ≥70 on maximally tolerated β-blocker) (Lancet 2010; 376:875) isosorbide mononitrate/hydralazine in African-Americans, sacubitril-valsartan (Entresto) (NEJM 2014; 371:993) o Document d/c weight + NT-BNP; consider appt in HF Transitions Clinic (J. Ruckel, NP; 617-724-1400) if pt has MGH cardiologist Acute Decompensated Heart Failure (ADHF) – Floor/SDU:  Etiology: dietary/med non-compliance (~40%), ischemia/infarction, uncontrolled hypertension, arrhythmia, valvulopathy, tamponade, myocarditis, renal dysfunction/volume retention, PE, comorbid illness (GI, pulmonary), toxins (EtOH, cocaine), endocrinopathy, meds (NSAIDs, steroids, Ca-channel blockers, TZDs, anthracyclines), stress-induced cardiomyopathy, nutritional deficiency (i.e. selenium); up to 50% with NO known cause. *high-output HF p/w warm extremities, wide PP, tachycardia and ddx anemia, thyroid, liver failure, Pagets, systemic infection Jeremy Feng, Charlotte Lee 25 TOC Cardiology Inpatient Heart Failure  Management: 1. Continuation of Optimal Guideline-Directed Medical Therapy (GDMT): For most hospitalized HF patients without cardiogenic shock and no obvious contraindication, recommend continuing BB and ACEi/ARBs B-Convinced (Eur Heart J 2009;30:2186). 2. Diuresis: reduce CVP and PCWP optimize Starling curve mechanics  Initial treatment: loop diuretics (furosemide, torsemide, bumetanide); usual initial dose = 2x home dose (IV/PO); No difference between continuous gtt vs bolus dose DOSE (NEJM 2011;364:797)  Diuretic conversions (PO): PO furosemide 80 = IV furosemide 40 = PO torsemide 20 = IV/PO bumetanide 1  Refractory diuresis: Metolazone 2.5-5mg (use chlorothiazide 500mg IV if cannot take PO) administered 30 minutes before loop diuretic. Consider RRT in truly diuretic-refractory pts (CARRESS-HF (NEJM 2012;367:2296); UNLOAD (JACC 2007;49:675); RAPID-CHF (JACC 2005;46:2043))  Low-dose dopamine and/or low-dose nesiritide do not improve diuresis or renal perfusion (ROSE-AHF (JAMA 2013;310:2533), ASCEND-HF (NEJM 2011; 365:32))  Pulm edema: early NIPPV may improve mortality, need for intubation (Ann Intern Med 2010;152:590; JAMA 2005;294:3124)  Limited data to support best end-points; potential targets include daily weights, BNP, hemoconcentration, renal function 3. Vasodilation: arterial/venous dilation results in ↓ afterload and ↑ SV. Early administration of vasodilators controversial (NEJM 2017;376:1956); consider especially in severe HTN, acute MR, acute AR  Floor: captopril, isosorbide dinitrate, hydralazine, nitropaste; SDU/CCU: TNG, nitropaste 4. Neurohormonal Blockade: spironolactone, eplerenone inhibit aldosterone and decrease myocardial remodeling, vascular fibrosis leading to improved mortality in EF < 35% (Class 1A); hold in AKI. (EMPHASIS-HF; RALES) Cardiogenic Shock – CCU:  Definition: MAP18mmHg, evidence of organ hypoperfusion  Etiology: acute MI ± mechanical complications, end-stage cardiomyopathy, acute myocarditis, acute MR/AR, myocardial contusion  Evaluation: TTE for LVEF, mechanical lesions; consider PAC for inotrope/pressor/volume management (see PA Catheter section)  Tailored therapy: uses invasive hemodynamic monitoring (i.e., PAC) to guide therapy o Goal: augment MAP (CO x SVR) and CO (HR x SV); SV is related to preload, afterload, and contractility CO measured via thermodilution or Fick: CO = VO2/(1.34 x Hgb x [SpO2-MvO2]); CI = CO/BSA; MvO2 is proxy for CO/CI o Preload: LVEDV ∝ LVEDP ≈ PCWP; goal PCWP 14-18, PAD 16-20, CVP 8-12 Diuresis, TNG, nitroprusside, RRT o Afterload: wall stress ∝ MAP (Laplace’s law); SVR = (MAP - CVP)/CO; goal MAP>60, SVR4, CI>2.0-2.2, MvO2>65 Milrinone (inodilator): PDE-3 inhibitor (↓ breakdown of cAMP); watch for tachycardia, arrhythmias, ischemia, hypotension; longer half-life, greater pulmonary vasodilatation, slightly less chronotropy, fewer arrhythmic events than dobutamine. Preferred in patients on beta blockade and w/ RV failure; renally cleared. Often choice for home inotrope for palliative therapy Dobutamine (inodilator): β1>β2 agonist (↑ production of cAMP); watch for tachycardia, increased ventricular response to AF, arrhythmias, ischemia, hypotension, tachyphylaxis in infusions >24-48 hrs Dopamine, Epinephrine, Norepinephrine (inopressors): use if severe hypotension, unable to tolerated inodilators; watch for tachycardia, arrhythmias, end-organ hypoperfusion o Limitations: Thermodilution (uses temp gradient between two points on PAC) is less reliable if shunt/valvular insufficiency (e.g., TR); Fick assumes a VO2 (oxygen consumption) that in reality varies depending on physiologic state (e.g., infection)  Mechanical circulatory support: in critical refractory cases as bridge to transplant or other mechanical intervention o Types at MGH: IABP, Impella, VA-ECMO (see MCS & Transplant); if considering, must activate SHOCK team (x6-2241) Heart Failure with Preserved Ejection Fraction (HFpEF): Overview Definition: symptoms of HF, “preserved” LVEF (>50%) and normal LVEDV (M, HTN, CAD, AF, obesity, DM, CKD, OSA  Rarer causes: hypertrophic CM, infiltrative CM (amyloidosis, hemochromatosis), valvular disease, constrictive pericarditis  Prognosis: Possibly lower mortality compared with HFrEF (Eur Heart J 2012;33:1750)  Findings: ↑ NT-proBNP, pulm edema; abnml 6MHW, CPET w/ ↓ MVO2; E/e’ ≥ 15  Treatment goals: No evidence-based treatments; most guidelines extrapolated from HFrEF 1. Prevent volume overload (fluid/salt restriction; judicious use of diuretics/nitrates) 2. Treat risk factors associated with HFpEF development and outcomes Adapted from Braunwald 11ed, Ch 25, p529 3. Selective use of neurohormonal modulators o Consider spironolactone if normal renal function and potassium given improvement in cardiovascular death and HF hospitalizations in US (NEJM 2014;370:1383) o Other therapies including digoxin, beta-blockers, ACEi/ARBs, PDE-5 inhibitors have not been proven to have morbidity/mortality benefit in HFpEF. Nitrates may have a deleterious effect (NEJM 2015;373:2314). Phase III trial of sacubitril/valsartan ongoing (Circ Heart Failure 2018;11) Jeremy Feng, Charlotte Lee 26 TOC Cardiology Inpatient Heart Failure Specific Causes of Cardiomyopathy Hypertrophic Cardiomyopathy (HCM) (Circulation 2011;124:2761) o LV and/or RV hypertrophy of various morphologies: ± LVOT dynamic obstruction (HOCM), diastolic dysfxn, ischemia, MR o Presentation: SOB, arrhythmias/palpitations, CHF, angina, pre-/syncope, SCD (most common in asymptomatic pts 15mm in any pattern, SAM of MV, outflow tract gradient), cMR (late gadolinium enhancement LGE = fibrosis, possibly early detection not seen on TTE, controversial role in decision making since no strong association with outcomes) o Risk Stratification: (1) Ambulatory EKG monitoring 24-48hrs (2) ETT (failure to augment BP to exercise due to dynamic LVOT obstruction, symptoms, arrhythmias, ST depressions) + stress echo (increasing outflow tract gradient, worsening MR) o Genetics: Clinical genetic testing (mutation in ~70% of cases) helpful for family screening; not useful for dx or risk stratification o Treatment: Avoid volume depletion or high dose vasodilators (may worsen obstruction), activity restriction, medical Rx (BB > verapamil). Use phenylephrine to treat hypotension in patients with HOCM who do not repond to fluid boluses (↑ afterload, stents open LVOT), septal ablation or surgical myectomy for medically refractory sx, ICD (for high SCD risk, risk factors below) o Risk factors for SCD/VT in order of decreasing risk: (1