Cardiology - Stanford University



History

Typical angina defined (N Engl J Med 1979;300:1350)

• substernal chest pain

• exertional

• relieved by rest or NTG

Exam (Do Not Edit This Line)

• Assess for hemodynamic stability, check bilateral blood pressures to assess for aortic dissection

• Check for new S4, new MR murmur secondary to ischemic papillary muscle dysfunction, evidence of CHF (elevated JVP, rales, new S3), Kussmaul’s sign for RV MI

EKG (Do Not Edit This Line)

• STE localize better than ST depressions/T wave inversions

• Anterior (V1-V4); apical (V5,V6); lateral (I, aVL)

• Inferior (II, III, aVF), III>II elevation suggests RCA as culprit rather than circumflex

• Posterior (V7-9, “inverse” of V1-V3)

• RV (1 mm STE in V4R most predictive of RV infarct).

• Wellens’s syndrome: pre-anterior wall infarction.

• Two types of Wellens’s T waves (V1-V3) indicative of critical proximal LAD stenosis:

– Deeply inverted T wave

– Biphasic terminal T wave inversion

– Consider catheterization rather than non-invasive investigation

Cardiac biomarkers

• Cardiac troponins more sensitive marker of myocardial damage than CK-MB

• CK-MB more useful for assessing reinfarction and infarct size

• Elevated troponin, negative CK-MB

– Recent MI ~2-10 d prior

– “Microinfarct.” In absence of recent MI, increased long term risk of death, MI, need for urgent revascularization even in pts with renal failure; however, unclear how to use this information; no clear increase in risk for imminent arrhythmia, no clear need for SDU/CCU monitoring

– End stage renal disease; estimated that 29% of patients on dialysis have elevated troponin T without evidence of myocardial injury; portends poor prognosis

Early risk stratification

• Among patients with U A/NSTEMI, there is progressive benefit with increased risk from newer, advanced therapies including LMWH, platelet GP IIb/IIIa inhibition, and early invasive strategy/PCI.

Treatment of ST elevation MI

• Hemodynamic support: if evidence of cardiogenic shock, institute pressors/inotropes, optimize volume status, consider urgent IABP placement

• Electrical stability:

– Sustained VT (more than 30 s), consider lidocaine, amiodarone

– Symptomatic bradycardia, heart block, consider pharmacologic therapy, avoid beta-blockade, institute transcutaneous pacing

• Reperfusion therapy

|a. Thrombolytic therapy |

|Indications |Contraindications |

|1. Angina for at least 30 min and less than 12 hrs |Absolute |

|AND |Prior hemorrhagic CVA at any time, non-hemorrhagic CVA within 1 year|

|2a. ST elevations (1mm in (2 anatomically contiguous leads |Known intracranial neoplasm |

|or |Active internal bleeding (not including menses) |

|2b. LBBB not known to be old |Suspected aortic dissection |

| |Relative |

| |SBP >180 on presentation or chronic HTN |

| |Prior non-hemorrhagic CVA at anytime |

| |INR >2.0 or known bleeding diatheses |

| |Trauma or surgery within 2-4 wks |

| |Prolonged CPR (> 10min) |

| |Noncompressible vascular punctures (e.g. subclavian lines) |

| |Recent internal bleeding (2-4 wks), active PUD |

| |If considering SK, prior SK exposure (esp within 2 yrs) |

| |Pregnancy |

|Complications—“early hazards” |

|Bleeding |

|Intracranial hemorrhage: increased risk in females, African Americans, the elderly, pts with prior CVA, HTN, wt 50% baseline) for 90 minutes after onset of administration of thrombolytics|

|( rescue angioplasty |

|Thrombolytic agent |Dose |

|Alteplase (tPA) “accelerated dosing” |15 mg IV bolus ( 0.75 mg/kg (50 mg) over 30 min ( 0.5 mg/kg (up to |

| |35 mg) over 60 min (100 mg total in average pt) |

|Streptokinase (SK)* |1.5 MU IV over 30-60 min *(only lytic agent not routinely dosed with|

| |IV heparin) |

|Reteplase (Retavase) |10 MU IV bolus q 30 min x 2 |

|Tenecteplase (TNK-tPA) |0.5 mg/kg IV bolus x 1 (max 50 mg) |

|b. Catheter-based reperfusion |

|Primary angioplasty: Consider if contraindications to lysis, anterior MI, pt is s/p CABG, diabetic, or in cardiogenic shock. |

|PTCA with 20% lower rate of combined cardiac endpoint, 65% lower rate of CVA v. lysis when performed at high volume centers (JAMA |

|1997; 278:2093). |

|Of note: door to balloon time in most trials 1-2h. Opting for angioplasty should not significantly increase time to |

|revascularization. |

|Primary stenting. Lower rate of need for revascularization but equivalent mortality when compared with primary angioplasty alone. |

|Rescue angioplasty. Performed in setting of failed lysis (see above). |

|c. Antiplatelet and antithrombin therapy |

|Drug |Dose |

|Aspirin (ASA) |162-325 mg po x 1 chewed (trans-buccal mucosal absorption) |

|Heparin IV (used in conjunction with |Bolus 60 U/kg IV (max 4000 U); initial infusion 12 U/kg/hr (max 1000 U/h); note lower dosing compared to |

|tPA, rPA, TNK-tPA and PTCA) |previous recommendations |

| |PTT goal 50-70 (lower than DVT/PE goal of 65-80) |

| |Use “cardiac” heparin sliding scale on order entry |

|GP IIb/IIIa inhibitors |The only data in STEMI supports abciximab (ADMIRAL, RAPPORT) |

|Abciximab (Reopro) |0.25 mg/kg IVB ( 0.125 mcg/kg/min x 12-24h |

|Eptifibatide (Integrilin) |180 mcg/kg IVB ( 2 mcg/kg/min x 72h |

|Tirofiban (Aggrastat) |0.4 mcg/kg/min x 30min ( 0.1 mcg/kg/min x 48-96h |

|4. Adjunctive therapy |

|Drug |Dose |Cautions |

|Oxygen |Keep oxygen sat >93% | |

|Morphine |2-4 mg IV boluses |Unusual to see somnolence/ decreased respiratory |

| | |drive in STEMI |

|Beta blockers |5 mg IV q5 min x 3, then 25 mg PO q6h, titrate to HR |HR male; less likely to have STE; EF> in end

• LV function becomes hyperdynamic

• May hear thrill on exam

Right ventricular infarct

• Common sequela of inferior MI

• Typical triad of hypotension, increased JVD, clear lungs

• Kussmaul’s sign from pseudoconstriction

• 1 mm STE in R sided leads, particularly V4R

• RV wall motion abnormal, RV dilatation

• Elevated right atrial pressure

• Increased incidence of high grade AV block

• Volume load and add vasopressors

Infarct expansion

• Thinning and dilatation of infarct segment without pain or CK leak

Infarct extension

• Recurrent pain and CK-MB leak

Left ventricular aneurysm

• Occurs days to weeks post MI

• Begins with infarct expansion, necrosis, removal of debris, replace with scar

• Risk factors include large infarcts, uncontrolled hypertension, receiving steroids or NSAIDs

• Apical dyskinesis/aneurysm predisposes to thrombus

• Can compromise pump function and cause VT

Left ventricular thrombus

• Observed in 10-40% of anterior wall infarcts

• Usually in LV apex

• Increased risk of embolization during first 3-6 months post MI

• Prevent with anticoagulation in patients with:

– Large anterior MI

– CHF

– Large apical aneurysm or dyskinetic segments

Acute management of suspected mechanical complication

• Stat echo

• O2 sat run (oxygen sat step-up between RA and PA >5 indicates VSD)

• Cardiac catheterization ( PCI ( IABP

• Vasodilators (and may require pressors)

• Surgery

Pericarditis

• Frequently occurs with transmural MI

• Pericardial rub, pleuritic CP, pericardial effusion

• Dressler’s syndrome: late pericardial inflammation (2 wks-3 months)

• Treat with salicylates, NSAIDs, colchicine

• Try to avoid steroids because of high relapse rate

Conduction disturbances

• Result from ischemic injury to conduction system or surrounding myocardium and abnormal reflexes vagally-mediated

Blood supply

• Sinus node: RCA 60% cases, LCx 40% cases

• A-V node: determines dominance, distal branches RCA 90% cases, distal portions LCx 10% cases

• His bundle: primarily AV nodal artery with LAD septals

• Right bundle branch from LAD septals, some collateral from RCA/circumflex

• Left bundle branch from LAD

• Left anterior fascicle from LAD septals, 50% have AV nodal collaterals

• Left posterior fascicle from proximal AV nodal artery, distally dual supply from LAD/PDA septal perforators

Sinus bradycardia

• Occurs with anterior or inferior MI (up to 40%)

• Atropine if symptomatic

First degree AV block

• More often in inferior than anterior MI due to AV nodal artery ischemia

• May be intranodal, intra, or infra-Hisian

• Usually transient and benign course

Second degree AV block

• Usually develops within first 24 hrs of MI

• Mobitz type I

– Usually with inf/post MI

– Often responds to atropine

– Narrow QRS

– Observe unless symptoms or HR PCWP (e.g. pulmonary hypertension)

– PCWP > LA pressure (e.g. mediastinal fibrosis, veno-occlusive disease)

– LA pressure > LVEDP (e.g. mitral stenosis)

– Alteration of the normal LVEDV/LVEDP relationship (e.g. decreased LV compliance)

– The catheter tip not located in West lung zone 3 such that PCWP approximates alveolar pressure and not LA pressure.

Technical considerations

• The PA catheter used at MGH, the Edwards VIP, has five ports: the distal PA port (yellow bulb), the thermistor (connector on yellow bulb), the balloon (red bulb), the proximal injection used for thermodilution (blue bulb), and the proximal infusion (white bulb)

• Placed preferably in either the right internal jugular vein or the left subclavian vein.

• Rule of 10’s. Hemodynamic changes occur at approximately 10 cm intervals, with RA at 20 cm, RV at 30 cm, PA at 40 cm, and pulmonary capillary wedge pressure (PCWP) at 50 cm.

• The balloon is inflated as the catheter is advanced or when “wedging” the catheter.

• The balloon is deflated when withdrawing the catheter and at all other times.

• Obtain chest radiograph after placement to confirm proper position and daily to assess placement.

Waveforms of normal hemodynamics

• RA waveform

– A wave is due to atrial contraction; the peak follows the peak of the electrical P wave by about 80 ms.

– C wave is due to sudden motion of tricuspid valve ring towards RA at the onset of ventricular contraction; the C wave follows A wave by a time period similar to PR interval.

– V wave is due to atrial filling during ventricular systole when tricuspid valve is closed; peak of V wave occurs near end of T wave.

– X descent reflects atrial relaxation and the sudden downward movement of the atrioventricular junction.

– Y descent corresponds to rapid atrial emptying following opening of the tricuspid valve.

– During inspiration the mean right atrial (and wedge) pressure decreases due to decreased intrathoracic pressure. The A and V waves and X descent typically become more prominent.

• RV waveform. Systolic pressure 15-30 mm Hg. Diastolic pressure 0-4 mm Hg.

• PA waveform. Systolic pressure 15-30 mm Hg. Diastolic pressure 6-12 mm Hg. Mean PA pressure usually 10 cm H2O may artificially raise measurements of intracardiac pressures

Cardiac output

• Thermodilution. A known volume of cold indicator fluid is injected into the proximal (RA) port and the temperature is measured by the thermistor located near the distal tip of the catheter (PA).

– Thermodilution curve is generated by plotting decline in pulmonary artery temperature versus time. Area under the curve is used to calculate cardiac output.

– TR produces significant distortions in this curve

• Fick method.

– [pic]

– In conditions of distributive shock (e.g. sepsis), this method does not correlate well with cardiac output.

• Green dye. Cardiac output estimated by injecting a known amount of indocyanine green dye into a central line and then measuring its concentration in arterial samples taken over time.

– Valvular regurgitation and intracardiac shunts may make this method inaccurate.

– Page the balloon pump techs during regular hours to perform the study.

– Requires arterial line.

Systemic vascular resistance

• Based on Ohm’s equation in electrical circuits (ΔV = IR), vascular resistance can be estimated in hydraulic fluid mechanics (ΔP = QR), multiplied by 80 to convert the units into dynes-sec/cm5:

[pic]

Specific conditions and arrhythmias

|Acute mitral regurgitation |Giant V waves on the wedge tracing (can be mistaken for PA waveform) |

|Tricuspid regurgitation |Accentuation of RA V wave with a steep Y decent and elevation of the mean right atrial pressure. |

|RV infarction |RA pressure > wedge pressure. |

| |RA waveform prominent X and Y descents (Y descent may exceed X descent) |

| |Kussmaul's sign (increase in RA pressure with inspiration) |

| |Narrow PA pulse pressure (from decreased RV stroke volume in severe RV infarction) |

|Pulmonary embolism |Mean PA pressure rarely exceeds 40 mm Hg (mean PA pressures above this suggest chronic component) |

| |PA diastolic pressure > PCWP. |

| |A and V waves frequently disappear from the wedge tracing because transmission of LA pressure disrupted |

|Pericardial tamponade |Elevation and equalization of the RA, PA diastolic and wedge pressures coupled with pulsus paradoxus. |

| |RA waveform, dominant X descent. |

| |Y descent is attenuated or absent. |

| |RA pressure often decreases with inspiration which may help to distinguish tamponade from other conditions |

| |resulting in equalization of pressures, such as RV infarction of constrictive pericarditis |

|VSD |RA, mean PA, and wedge pressures are all elevated. |

| |In acute left-to-right shunt, see increase (7% or more) in O2 saturation from SVC to PA |

|Atrial fibrillation |Atrial systole is lost and the A wave disappears |

|Atrial flutter |Mechanical flutter waves at approximately 300/minute |

|Atrioventricular reentry tachycardia |Regular cannon A waves in RA tracing (atrial contraction when the atrioventicular valves are closed. |

| |Diastole shortened resulting in summation of A and V waves. |

|Ventricular tachycardia |Cannon A waves frequently encountered with ventricular arrhythmias (from AV dissociation). |

Complications

• From central venous cannulation. Pneumothorax or hemothorax (1-3%), arterial puncture, air embolism, or thrombosis.

• From advancement of catheter. Atrial or ventricular arrhythmias, RBBB, complete heart block (about 3% in patients with pre-existing LBBB), catheter knotting, cardiac perforation and tamponade, and pulmonary artery rupture.

• From maintenance of catheter. Infection (especially if left in place for greater than 3 days), thrombus, pulmonary infarction (10 mcg/kg/min), adds |cardiac failure. | | |

| | |(1 agonism, causing | | | |

| | |vasoconstriction. | | | |

|Vasopressin |Pitressin |Renal ADH effects as well as |Refractory septic shock, also |0.04-0.067 U/min (in |Peripheral or visceral |

| | |generalized vasoconstriction. |used in VF/pulseless VT |refractory VF, 40 U |hypoperfusion due to |

| | | |arrests. |bolus) (Circulation |vasoconstriction (though not |

| | | | |2003;107:2313) |observed at lower doses used |

| | | | | |for hypotension) |

|Dobutamine |Dobutrex |(1, (2 agonism increases |Increasing CO in cardiogenic |2-40 mcg/kg/min, titrate |Hypotension due to |

| | |inotropy/chronotropy with |shock, not to be used as a |to desired hemodynamic |vasodilation, arrhythmias. |

| | |peripheral vasodilation. |pressor due to vasodilation. |profile. | |

|Amrinone |Inocor |Inhibits phosphodiesterase-III, |Similar to dobutamine, but | |Hypotension due to |

| | |increasing CO and peripheral |with less arrhythmogenic | |vasodilation, arrhythmias. |

| | |vasodilation. |potential. | | |

|Milrinone |Primacor |Similar to amrinone. |Similar to amrinone. |0.375-0.75 mcg/kg/min |Similar to amrinone. |

|Epinephrine |Adrenalin | |Generally used in ACLS, |1-10 mcg/min |Variable BP effects limit its |

| | | |anaphylaxis. | |utility |

|Ephedrine | | |Similar to epinephrine, used | | |

| | | |for post-anesthesia-induced | | |

| | | |hypotension. | | |

|Isoproterenol |Isuprel | |Bradycardia. |2-10 mcg/min. |High (2 effect limits pressor |

| | | | | |utility |

|Anti-arrhythmics and anti-hypertensives |

|Amiodarone |Cordarone |Class III anti-arrhythmic, blocks |Treatment and prevention of |1 g iv load is 150 mg |Hypotension, multiple systemic|

| | |K+ channels, delaying |atrial and ventricular |bolus, 1 mg/min for 6 |side effects with long-term |

| | |repolarization. |tachyarrhythmias. |hrs, 0.5 mg/min for 18 |use. |

| | | | |hrs. Use 150 mg boluses | |

| | | | |in ACLS. | |

|Esmolol |Brevibloc |(-blocker, primarily of (1 |Useful as a trial drug, to see| |As with other (-blockers |

| | |receptor. Extremely short |if a patient will tolerate | | |

| | |half-life (9 minutes). |(-blockade (e.g., in RV | | |

| | | |infarct). | | |

|Propranolol |Inderal |Non selective (-blocker. |Useful for heart rate control,|1-40 mg/min. |Similar to other (-blockers, |

| | | |especially in aortic | |but also causes prominent |

| | | |dissection (used with | |change in mental status. |

| | | |nitroprusside). | | |

|Fenoldopam |Corlopam |Selective postsynaptic dopamine |Rapidly lowers BP, as in |1-150 mcg/min. |May decrease SVR, making it |

| | |agonist at D1 receptors. |hypertensive | |difficult to use in some |

| | | |urgency/emergency, but | |patients. |

| | | |theoretically maintains renal | | |

| | | |perfusion (not well studied | | |

| | | |yet). | | |

|Labetalol |Normodyne |Combined ( and (-blocker (( |Rapid lowering of BP, as in |1-6 mg/min. |Bradycardia, bronchospasm, |

| | |blocking effect 7x greater than ( |hypertensive | |hypotension. |

| | |effect when iv). |urgency/emergency. | | |

|Nitroglycerin | |Direct nitric oxide-mediated |Hypertension, angina in acute |1-1000 mcg/min. |Headache, tachycardia, |

| | |vasodilation, venous > arterial. |coronary syndromes. | |hypotension, tachyphylaxis. |

|Nitroprusside |Nipride |Direct nitric oxide-mediated |Rapid lowering of BP, |10-800 mcg/min. |Hypotension, tachyphylaxis, |

| | |arterial and venodilation. |first-line in hypertensive | |rare cyanide toxicity. |

| | | |emergency. | |Caution in renal failure as |

| | | | | |cyanide metabolites are |

| | | | | |renally-cleared. |

|Lidocaine |Xylocaine |Class IB anti-arrhythmic |Used in sustained VT and VF |1-1.5 mg/kg bolus; infuse|Mental status change. |

| | | | |1-4 mg/min | |

|Procainamide |Pronestyl |Class IA anti-arrhythmic |Used in VT, atrial |Load 20 mg/min until 17 |Hypotension with iv infusion. |

| | | |fibrillation |mg/kg reached, side |Drug-induced lupus, |

| | | | |effects, or arrhythmia |agranulocytosis. |

| | | | |controlled; infuse 1-4 | |

| | | | |mg/min. | |

|Sedatives/Paralytics |

|Cisatracurium |Nimbex |Neuromuscular blocking agent, |Along with others of its |8-20 mg bolus, 1-10 |Prolonged paralysis, myopathy,|

| | |blocks ACh-mediated transmission |class, paralysis of patients |mg/hr. |blockade of autonomic |

| | |at NMJ. |to assist in | |activity. |

| | | |intubation/ventilation. | | |

|Fentanyl |Sublimaze |Binding of opiate receptors. |Sedation and analgesia in |50-300 mcg/hr. |Respiratory depression, |

| | | |hemodynamically unstable or | |dependence, tolerance, |

| | | |morphine sensitive patients. | |constipation. |

|Propofol |Diprivan |Phenolic derivative with general |IV infusion for ICU sedation. |25-300 mg/hr. |Hypotension, neuroexcitatory |

| | |anaesthetic properties. | | |effects, bradycardia. |

|Midazolam |Versed |Benzodiazepene. |IV infusion for ICU sedation, |1-7 mg/hr. |Cumulative effects, |

| | | |preferred over other benzos | |respiratory depression, |

| | | |because of short half life, | |tolerance. |

| | | |lack of active metabolites. | | |

Atrial fibrillation

• Recommendations are from Sixth American College of Chest Physicians Consensus Conference on Antithrombotic Therapy in Chest 2001;119:1S.

• One or more high risk factors (see below), treat with warfarin (target INR 2.5, range 2.0-3.0)

• Two or more moderate risk factors, treat with warfarin (target INR 2.5, range 2.0-3.0)

• One moderate risk factor, treat with warfarin or aspirin 325 mg qd

• Low risk patients, treat with aspirin 325 mg qd only

High risk factors

• Age >75

• Previous TIA or stroke

• Hypertension

• Poor LV systolic function

• Rheumatic mitral valve disease

• Prosthetic heart valve

Moderate risk factors

• Age 65-75

• Diabetes

• CAD with preserved LV function

Low risk

• Patients less than 65 with no clinical or echocardiographic evidence of cardiovascular disease

Valvular heart disease

• Rheumatic mitral disease with left atrial diameter >5.5 cm or history of systemic embolism, treat with warfarin long-term, target INR 2.5 (2.0-3.0)

• Mitral regurgitation or annular calcification, with systemic embolism, treat with warfarin long-term, target INR 2.5 (2.0-3.0)

Prosthetic heart valves by target INR

• Sinus rhythm, normal left atrium size with an aortic St. Jude Medical bileaflet, Carbomedics bileaflet, or Medtronic-Hall tilting disk ( 2.5 (2.0-3.0)

• Mitral tilting disk and bileaflet valves ( 3.0 (2.5-3.5) or 2.5 (2.0-3.0) and aspirin 81 mg qd

• Bileaflet mechanical aortic valves with AF ( 3.0 (2.5-3.5) or 2.5 (2.0-3.0) and aspirin 81 mg qd

• Caged ball or caged disk in any position ( 3.0 (2.5-3.5) and aspirin 81 mg qd

• Mechanical valve plus other risk factors or systemic embolism( 3.0 (2.5-3.5) and aspirin 81 mg qd

• Bioprosthetic (e.g. Carpentier-Edwards) mitral or aortic valve ( 2.5 (2.0-3.0) for 3 months after insertion, then aspirin 81 mg qd

General considerations

• Wide complex tachycardia is ventricular tachycardia until proven otherwise.

• Patients with prior MI or low EF, pre-test probability that WCT will be VT >98%.

• Consider artifact (patient motion can simulate WCT).

• When in doubt, treat WCT like VT.

• Avoid verapamil.

Differentiation based on atrial activity

• AV dissociation, atrial activity independent of ventricular activity.

[pic]

• Fusion beat, simultaneous activation of the ventricular myocardium and ventricular focus.

• Dressler beat, QRS complex identical to the sinus QRS complex; from normal impulse conduction.

[pic]

Morphology

• Determine if RBBB-type or LBBB-type.

• In V1 positive or RBBB-type WCT, morphologies suggestive of VT in lead V1

– See Wellens, Am J Med 1978;64:27, Brugada, Circulation 1991;83:1649 (for sens and spec for VT).

• RBBB-type WCT, morphologies suggestive of VT in lead V6

– See Wellens Am J Med 1978;64:27; see also Brugada, Circulation 1991;83:1649 (for sens and spec for VT).

• Kindwall LBBB-type WCT, morphologies suggestive of VT

– Am J Cardiol 1988;61:1279; see also Brugada, Circulation 1991;83:1649 (for sens and spec for VT).

Brugada algorithm

• See Circulation 1991;83:1649.

• Based on prospective analysis of ventricular tachycardia v. SVT with aberrant conduction by EP study

• Stepwise approach

|Floor |Patient/Clinical Characteristics |Interventions/Meds |Triggers for moving to more acute unit|

| |for Admission |Supported on Unit/Floor | |

|Ell 9 - CCU / |Persistent ST ( (>20 minutes) |IABP |NA |

|Bl 7 - MICU |Refractory HTN |Sustained high dose IV pressors and| |

| |Severe CHF |inotropes | |

| |Cardiogenic shock |Ventilatory support | |

| |IABP |IIb/IIIa inhibitors | |

| |Invasive hemodynamic monitoring | | |

| |Ventilatory support | | |

| |VF or sustained VT with hemodynamic compromise | | |

|A positive troponin in a hemodynamically stable patient is not necessarily a direct indication for admission to Ellison 10. |

|Ell 10 - SDU |Persistent ST ( or deep (>3 mm) T wave inversions (>20 minutes) |IV TNG |IV meds requiring invasive monitoring |

| |Uncomplicated MI post-angioplasty |Temporary and external pacemakers |e.g., nitroprusside, high dose |

| |Stable acute MI patients post percutaneous coronary intervention |IV antiarrhythmics (e.g. lidocaine,|dopamine and dobutamine, and initial |

| |with or without thrombolysis |procainamide, bretylium, and |titration of milrinone |

| |Unstable angina if hemodynamically stable |amiodarone) |Refractory ischemia despite IV TNG, |

| |Typical angina >20 minutes or requiring morphine |Low dose dopamine, dobutamine |heparin, beta blocker, and ASA |

| |SVT |(200-600 mcg/min), or milrinone |Other needs for invasive monitoring |

| |Unstable bradyarrhythmias |once a stable dose is established | |

| |Other malignant arrhythmias (NSVT or VT without hemodynamic |in the ICU | |

| |compromise) |IIb/IIIa inhibitors | |

| |Syncope |Epoprostenol (Flolan) | |

| |Moderate heart failure | | |

| |Comorbidities that compromise cardiac status, e.g., | | |

| |GI bleed | | |

| |Symptomatic bronchospasm (COPD or asthma) | | |

| |Infection | | |

| |TIA/CVA | | |

| |Renal Failure | | |

| |Transient hypotension | | |

|Ell 11 - Access |Priority for beds goes to referral patients |IV TNG |Life-threatening arrhythmia |

|Unit (cardiac |Ischemic or congestive syndromes in need of a catheterization and/or|IIb/IIIa inhibitors |Bradycardia or heart block requiring |

|attending) |coronary intervention. | |temporary or external pacemaker |

| |Admit to observe patients (post-cath patients or RPPR patients) | |SVT in need of cardioversion |

| |Stable acute MI patients post percutaneous coronary intervention | |Hemodynamic instability |

| |with or without thrombolysis | |Refractory ischemia despite IV TNG, |

| |Exclusions: | |heparin, beta blocker, and ASA |

| |Life threatening arrhythmia | |Respiratory compromise requiring |

| |Bradycardia or heart block requiring temporary or external pacemaker| |ventilatory support and/or frequent |

| |SVT in need of cardioversion | |blood gas monitoring |

| |Acute renal failure possibly requiring dialysis | | |

| |Hemodynamic instability | | |

| |Anticipated long lengths of stay due to comorbidities | | |

| |Post-cath patients from Cardiac Access Unit (Team 4) | |IV TNG may be started, but this |

|Ell 8 - Cardiac|Pre-cath referral patients (Team 4) | |generally triggers move for medical |

|Surgery |Post-AICD (EP Fellow/Team 4 back-up) | |patients on Ellison 8 |

|(criteria for |Post-cath pre-op cardiac surgery (Team 4) | |Temporary or external pacemaker |

|medical | | | |

|patients) | | | |

|General Medical |Typical angina with or without ischemic ECG with resolution in 24 hours hospitalization | | |

-----------------------

Acute coronary syndrome

Plaque rupture

Partially occlusive

No ST elevation

ST depressions, T-wave inversions

Occlusive

ST elevation

(() markers

(() markers

NSTEMI

Unstable angina

Modified from ACC/AHA Practice Guidelines

Non-Q wave MI

Q-wave MI

(() markers

STEMI

Serum marker |Time to initial increase |Time to peak value |Time to return to normal |Sens of cardiac enzymes in detecting NSTEMI | | | | | |on arrival |>6h after pain onset | |CK-MB |3-12h |24h |48-72h |53% |91% | |Tn T |3-12h |12-48h |5-14d |51% |94% | |Tn I |3-12h |24h |5-10d |66% |100% | |modified from N Engl J Med 1997;337:1648 | |

Rates of all-cause mortality, MI, need for urgent revascularization through 14 days

TIMI risk score. 7 independent predictors of outcome (JAMA 2000;284:835)

1. Age >65

2. >3 risk factors for CAD

3. Prior coronary stenosis > 50 percent

4. ST deviation on admission ECG

5. >2 anginal episodes within 24 hours

6. Elevated cardiac biomarkers

7. ASA use in last 7 days

Roderick Tung, M.D.

| |Inpatients |Outpatients | |Risk of death |Score |% of pts |4 yr surv |% of pts |4 yr surv | |Low |(+5 |34% |98% |62% |99% | |Moderate |(10 to +4 |57% |92% |34% |95% | |High |100 ms in one precordial lead

3. Atrio-ventricular dissociation

4. Morphology criteria for VT present in both precordial leads V1, V2, and V6? (see above)

SVT

sens 0.965, spec 0.987

VT

sens 0.987, spec 0.965

VT

sens 0.82, spec 0.98

VT

sens 0.66, spec 0.98

VT

sens 0.21, spec 1.0

No

No

No

No

Yes

Yes

Yes

Yes

Gregory Bashian, M.D.

Jonathan Passeri, M.D.

Andrew Yee, M.D.

Wide complex tachycardia

3. >60 ms from QRS onset to S nadir

Above V1 or V2 criteria, sens 1.0, spec 0.89

4. Any Q in V6

Sens 0.17, spec 1.0

V6

V1 or V2

2. Notched or slurred downstroke S wave

1. R in V1 or V2 >30 ms

LBBB-type

R:S 1

sens 0.30, spec 0.76

QS (or QR)

sens 0.29, spec 1.0

Monophasic R

sens 0.01, spec 1.0

V6

RBBB-type

Triphasic

sens 0.64, spec 0.95

“Rabbit ear,” left > right, triphasic

sens 0.82, spec 0.91

QR or RS

sens 0.30,

spec. 0.98

R

sens 0.60, spec 0.84

V1

RBBB-type

P

Fusion beat

Dressler beat

P wave

P

P

P

Diagnostic aids |Usefulness | |Presenting symptom |Unhelpful | |History | | | CAD and previous MI |VT | | First arrhythmia after MI |VT | |Physical exam | | | AV dissociation |VT | | Blood pressure |Unhelpful | | Heart rate |Unhelpful | | EKG | | | Rate |Unhelpful | | QRS >0.16 s |VT | | QRS ................
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