2. Acute coronary syndromes
Acute coronary syndrome
Plaque rupture
Partially occlusive
No ST elevation
ST depressions, T-wave inversions
() markers
Unstable
angina
Occlusive
ST elevation
() markers
NSTEMI
() markers
STEMI
Non-Q
wave MI
Q-wave MI
Modified from ACC/AHA Practice Guidelines
History
Typical angina defined (N Engl J Med 1979;300:1350)
 substernal chest pain
 exertional
 relieved by rest or NTG
Exam
 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







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
MGH Medical Housestaff Manual
14
2. Acute coronary syndromes
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
Serum
marker
Time to
initial
increase
Time to
peak
value
Time to
return to
normal
Sens of cardiac
enzymes in detecting
NSTEMI
on
arrival
53%
51%
66%
>6h after
pain onset
91%
94%
100%
 Recent MI ~2-10 d prior
CK-MB
3-12h
24h
48-72h
 “Microinfarct.” In absence of recent MI,
Tn T
3-12h
12-48h
5-14d
increased long term risk of death, MI,
Tn I
3-12h
24h
5-10d
need for urgent revascularization even in
modified from N Engl J Med 1997;337:1648
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.
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.
2.
3.
4.
5.
6.
7.
Age >65
>3 risk factors for CAD
Prior coronary stenosis > 50 percent
ST deviation on admission ECG
>2 anginal episodes within 24 hours
Elevated cardiac biomarkers
ASA use in last 7 days
Treatment of ST elevation MI
 Hemodynamic support: if evidence of cardiogenic shock, institute pressors/inotropes, optimize
volume status, consider urgent IABP placement
 Electrical stability:
MGH Medical Housestaff Manual
15
2. Acute coronary syndromes
 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
1. Angina for at least 30 min and less than
12 hrs
AND
2a. ST elevations 1mm in 2 anatomically
contiguous leads
or
2b. LBBB not known to be old
Contraindications
Absolute
 Prior hemorrhagic CVA at any time, nonhemorrhagic CVA within 1 year
 Known intracranial neoplasm
 Active internal bleeding (not including
menses)
 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 <70 kg, short stature, supratherapeutic lytic dose
 Overall incidence 0.75%: 0 RF 0.26%, 1 RF 0.96%, 2 RF 1.32%, 3 RF 2.17%
 70% bleeding complication at puncture sites
Other
 Myocardial rupture, reperfusion injury, splenic rupture, aortic dissection, cholesterol emboli
Benefit
 Overall 18% decrease in 35d mortality.
 No clear mortality benefit with lysis 12-24h after onset of symptoms (LATE, EMRAS trials).
Failed lysis
 Evolving chest pain and ST elevations that persist (at >50% baseline) for 90 minutes after
onset of administration of thrombolytics  rescue angioplasty
MGH Medical Housestaff Manual
16
2. Acute coronary syndromes
Thrombolytic agent
Dose
Alteplase (tPA) “accelerated dosing”
Streptokinase (SK)*
Reteplase (Retavase)
Tenecteplase (TNK-tPA)
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)
1.5 MU IV over 30-60 min *(only lytic agent not
routinely dosed with IV heparin)
10 MU IV bolus q 30 min x 2
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)
Heparin IV (used in
conjunction with tPA, rPA,
TNK-tPA and PTCA)
162-325 mg po x 1 chewed (trans-buccal mucosal absorption)
Bolus 60 U/kg IV (max 4000 U); initial infusion 12 U/kg/hr (max 1000 U/h); note
lower dosing compared to previous recommendations
PTT goal 50-70 (lower than DVT/PE goal of 65-80)
Use “cardiac” heparin sliding scale on order entry
The only data in STEMI supports abciximab (ADMIRAL, RAPPORT)
0.25 mg/kg IVB  0.125 mcg/kg/min x 12-24h
180 mcg/kg IVB  2 mcg/kg/min x 72h
0.4 mcg/kg/min x 30min  0.1 mcg/kg/min x 48-96h
GP IIb/IIIa inhibitors
Abciximab (Reopro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
4. Adjunctive therapy
Drug
Dose
Oxygen
Morphine
Keep oxygen sat >93%
2-4 mg IV boluses
MGH Medical Housestaff Manual
Cautions
Unusual to see somnolence/
decreased respiratory drive in
STEMI
17
2. Acute coronary syndromes
Beta blockers
Metoprolol (Lopressor)
5 mg IV q5 min x 3, then 25 mg PO
q6h, titrate to HR 55-60
Nitrates
IV nitroglycerin
ACE-inhibitors
Captopril
10-1000 mg/min, titrate to symptom
relief/SBP ~100
6.25 mg PO tid, titrate as tolerated to
SBP ~100
HR <60, SBP <100, severe CHF, 1
(PR>0.24 s), 2, 3 AVB, severe
bronchospastic disease
Idiosyncratic profound
hypotension/bradycardia.
SBP <100, renal failure
Treatment of unstable angina (UA)/Non-ST elevation MI (NSTEMI)
Drug
Dose
Aspirin (ASA)
Clopidogrel (Plavix)
Heparin IV
(unfractionated)
or
LMWH
Enoxaparin (Lovenox)
Dalteparin (Fragmin)
160-325 mg PO x 1 chewed
300 mg PO loading, then 75 mg PO QD
Bolus: 60 U/kg IV (max 4000 U), initial infusion 12 U/kg/hr (max 1000 U/h).
PTT goal 50-70 (lower than DVT/PE goal of 65-80). Use “cardiac” heparin
sliding scale on computer order entry.
Nitrates
IV nitroglycerin
Nitropaste
Beta blockers
Metoprolol (Lopressor)
Propranolol (Inderal)
GP IIb/IIIa inhibitors
Abciximab (Reopro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
1 mg/kg SC bid x 2-8d
120 U/kg SC bid x 5-6d
discuss with cardiology before using LMWH given lack of easy reversibility
Titrate to symptom relief, SBP ~100
10-1000 mcg/min (<300 mcg/min  SDU, >300mcg/min  CCU)
Sliding scale on computer order entry
Titrate as tolerated to HR 55-60, contraindicated in decompensated CHF
5 mg IV q5 min x 3, then 25 mg PO q6h
1 mg IV q5 min x 4, then 20 mg PO q6h
The best data is in favor or eptifibatide and tirofiban (PURSUIT, PRISM-PLUS),
not abciximab.
0.25 mg/kg IVB  0.125 mcg/kg/min x 18-24h (max 10 mcg/min)
180 mcg/kg IVG  2 mcg/kg/min x 72h
0.4 mcg/kg/min x 30 min  0.1mcg/kg/min x 48-108h
Post-catheterization care
Complication
Bleeding groin
Groin hematoma
Retroperitoneal
hematoma
Pseudoaneurysm
AV-fistula
Distal
embolization
Finding
Overt bleeding
Assess for neurovascular
compromise of limb
Decreased Hct ± back, abd,
LE pain; hypotension
Imaging
none
± groin US
Groin: pulsatile mass,
tenderness, bruit
Groin: continuous bruit ±
thrill
Diminished distal pulses,
decreased cap refill, LE
neurologic compromise
Groin US
MGH Medical Housestaff Manual
I abd CT
Groin US
LE arterial
non invasives;
angio
Management
Call cards fellow ASAP, compress
 Stable in size  observation
 Rapidly expanding  cards ASAP
 Stabilize hemodynamically, transfuse
 General surgery consult, to OR if
unstable or LE neurovasc compromise
 Vascular surgery for repair
 IR for graded compression (by US)
 Vascular surgery  observation with
repeat imaging v. OR repair
 Vascular surgery consult
 ? anticoagulation v. urgent
18
2. Acute coronary syndromes
embolectomy
Renal insuff.
 Contrast ATN
 Chol. emboli
Increased Cr ± decreased
urine output
± renal u/s
if concern for
obstruction
 Optimize volume status
 Prophylaxis with N-acetylcysteine 600
mg PO bid x 48h peri-cath if inc Cr
Livedo reticularis, rash,
urine eosinophils
Post-stent care
Antithrombotics
Aspirin 325 mg PO qd
Clopidogrel 300 mg PO x 1 (in cath lab)  75 mg PO qd x 1 year, likely up to 4 yrs
Heparin IV: cont 48h post-sheath pull if poor angiographic result, otherwise discontinue
GP IIb/IIIa: usually continued 12-24h post-procedure
Statins
Folate, B6, B12
Lowers target vessel revascularization rate (LIPS)
Lower restenosis rates independent of homocysteine levels (Swiss Heart Study)
Post-stent
complications
Timing
Abrupt closure
Subacute thrombotic
occlusion
Min-24h
1-30d
In-stent restenosis
Vessel
rupture/perforation
Distal embolization
Incidence
Findings
Pathophys
1%
Severe CP, Dissection,
STE on
thrombosis
4% vs.
<1% with drug- EKG
eluting stent
1-6mo
~15-36% vs.
Increasing
Endothelial
<1% to 8%
angina
proliferation
with DES
Minutes-48h, rare complication, pleuritic chest pain 
cardiac tamponade secondary to hemopericardium.
Do not perform pericardiocentesis
Minutes-48h, common complication, minor ischemic pain
without ECG changes
Management
Contact cards ASAP,
urgent
revascularization
Semi-elective
revascularization
Contact cards ASAP,
stat echo
Follow serial ECGs
Contacting cardiology: 6-9292 (cardiology page operator)

Cardiology patients covered by either “ward service” or “private attending”




For post-cath complication, call 6-9292 and ask for “interventional fellow on call.”
For urgent overnight assistance, call 4-5110 (Ellison 11) and ask for “access fellow”
For stat or weekend echo, call x 6-9292 and ask for “fellow on call for echo”
Prior to instituting thrombolysis at MGH, call appropriate cardiology coverage; they may wish to
mobilize cath lab instead,
 re: private patients, call 6-9292 and ask for attending coverage
 re: ward patients, call 6-9292 and ask for “ward cardiology fellow on call”
Roderick Tung, M.D.
MGH Medical Housestaff Manual
19
3. Noninvasive testing
General considerations
 Exercise tolerance test with MIBI imaging (ETT-MIBI) is the most commonly used noninvasive risk
stratification for patients who are able to ambulate at MGH
 Adenosine-MIBI, a pharmacologic stress test, is useful for patients who are unable to sufficiently
ambulate for an ETT-MIBI.
 Nuclear imaging (MIBI) is used in nearly all stress tests performed at MGH, though there may be
variation in practice at other institutions.
 In most cases, testing should be performed within 72 hours of presentation for low-risk patients.
Exercise tolerance test (ETT)
 Of choice when patient can ambulate
 Can do without imaging if no baseline ECG abnormalities (digoxin effect, LVH, LBBB, paced,
WPW, ST abnormalities associated with SVT, atrial fibrillation, mitral valve prolapse, severe
anemia). RBBB okay for ECG interpretation
 Advantages: inexpensive, low morbidity, estimates functional capacity, predictor of mortality
 Indications: diagnosis of CAD, risk assessment and prognosis among patients with symptoms or
known CAD, post-MI
 In low risk patients, testing can be performed when patients have been free of active ischemic or
heart failure symptoms for a minimum of 8-12 hours and have ruled out for myocardial infarction
 After MI, can perform submaximal stress test at about 4-76 days post event (but not necessary in
patients who have undergone cardiac catheterization).
 Submaximal test is generally exercise to predetermined end point, i.e. peak heart rate 120 or 70% of
predicted max heart rate, or 5 METs
 Contraindications include acute coronary syndrome, MI within past 2 days, uncontrolled
arrhythmia, acute CHF, severe AS, recent PE/DVT, acute infection, aortic dissection, uncontrolled
hypertension (SBP >200 or DBP >110).
 Sensitivity/specificity: single VD 68/77%, multi VD 81/66%, 3VD or LM 86/53%
 Patient preparation: if to diagnose in CAD, hold beta-blockers if possible unless the test is solely for
functional purposes, NPO within 3 hours of testing and longer if imaging is used (which is generally
the case at MGH)
 Data









ST segment is most sensitive for ischemia
ST depression of at least 1 mm that is horizontal or downsloping
ST depression of at least 2 mm that is upsloping
Criteria that further increase probability of ischemia: number of leads, workload at which changes occur,
angle of ST slope, time to ST recovery, ventricular ectopy during recovery
Location of ECG changes does not localize area of ischemia
Age-predicted maximum heart rate (220  age): if 85% is not reached, test is non-diagnostic
SBP monitoring: failure of SBP to rise with exercise indicates CAD and test should be terminated
Functional capacity: in metabolic equivalents (METs), with >6 indicating good prognosis; failure to
achieve 5 METs is associated with a worse prognosis
Symptoms: angina, shortness of breath, etc.
MGH Medical Housestaff Manual
20
3. Noninvasive testing
 Data interpretation: 1. normal, 2. abnormal, 3. normal except for, 4. nondiagnostic (<85% max HR
and no abnormal ECG changes or baseline ECG changes are present)
 Prognosis, can use Duke treadmill score = exercise time (min) – (5  max ST deviation in any lead)
– (4  angina index). Angina index is no angina = 0, non-limiting angina = 1, angina reason for
stopping = 2. See N Engl J Med 1991;325:849.
Risk of death
Low
Moderate
High
Score
+5
10 to +4
<10
Inpatients
% of pts 4 yr surv
34%
98%
57%
92%
9%
71%
Outpatients
% of pts
4 yr surv
62%
99%
34%
95%
4%
79%
Nuclear perfusion imaging
 Improves sensitivity (75-90%) and specificity (65-90%) over standard ETT
 Indications: assessment of physiologic importance of known CAD, pts with abnormal baseline
ECG, major to intermediate clinical predictors, high risk surgeries, unable to exercise
 Advantages: higher sensitivity, localizes ischemic area, can use pharmacologic agents for pts unable
to exercise (see below).
 Limitations: lower specificity for single vessel disease, low PPV for post-op events (~20%),
attenuation from adjoining tissue
 Two major radiopharmaceuticals are used: thallium-201 and technetium-99m-sestamibi (MIBI)
 Thallium
 Produced in cyclotron, 72 hour half life, actively transported into cells, redistributes with time to other
cardiac and non-cardiac cells
 MIBI (most commonly used at MGH)
 Produced on site, 6 hour half life, uptake passive and thus proportional to regional myocardial blood flow,
no redistribution
 Tracer is excreted into the GI tract through biliary system, and appearance of tracer in GI tract can
interfere with imaging of the inferior wall (this is why patients must be NPO)
 Produces sufficient count densities to allow ECG gating and thus allows for calculation of EF
 Defects characterized as fixed (scar), reversible (ischemic), partially reversible (mixture of scar and
ischemia), artifact (breast, diaphragm), high-risk (defect in >1 distribution, increased lung thallium
uptake, LV dilation)
Pharmacologic testing
 Used in concert with nuclear imaging
 Dipyridamole (not commonly used at MGH)
 Indirect vasodilator, flow enhanced in normal vessels and much less so in stenosed vessels (which possess
little flow reserve)
 Side effects: headache, nausea, chest pain, hypotension, dizziness, flushing
 Avoid in severe COPD, theophylline therapy, and critical carotid stenosis
 Adenosine (used at MGH)
 Vasoactive end product of dipyridamole and has much shorter half-life
 Side effects: chest pain, headache, nausea, flushing, dyspnea, AV block
MGH Medical Housestaff Manual
21
3. Noninvasive testing
 Avoid in settings similar to dipyridamole
 Dobutamine (used at MGH)
 Simulates exercise by increasing heart rate
 Side effects: ectopy, headache, flushing, dyspnea, parasthesias, hypotension
Stress echocardiography
 To screen for CAD and localize coronary lesions, with sens and spec similar to nuclear imaging
 Can use exercise or dobutamine. At MGH, exercise imaging is done with nuclear techniques, and
stress echo is limited to dobutamine studies
 Advantages: provides EF, rule out valvulopathy, images not attenuated (useful in women)
 Limitations: severe mitral or aortic regurgitation and dilated cardiomyopathy may make
interpretation difficult
 Dobutamine echo is especially helpful in evaluating pts with LV dysfunction and severe aortic
stenosis to quantify the extent of AS
Myocardial viability
 Key is to differentiate dysfunctional yet viable myocardium from necrosed and scarred myocardium
in order to determine which patients may benefit from revascularization
 Stunned myocardium—viable, occurs after acute episode, can last days to weeks, may recover with
or without revascularization
 Hibernating myocardium—viable, caused by repetitive ischemic injury or chronic reduction in blood
flow, needs revascularization for recovery
 PET is the current standard for assessment, but is not typically used at MGH
 Rest-redistribution thallium imaging—redistribution of tracer can only occur in viable myocardium
 MIBI is less accurate in detecting viability
Daniel Krauser, M.D.
MGH Medical Housestaff Manual
22
4. Complications of myocardial infarction
Pump failure
 Rales, S3, cardiogenic shock (occurs in 7%
patients with MI)
Treatment




Na restriction
Diuretics
Digoxin for symptomatic relief
Afterload reduction (ACE-I or hydralazine and
nitrates)
 Hemodynamic stabilization and look for
reversible causes
 Consider PA catheter, aortic balloon pump or
ventricular assist device
Mechanical complications
 Accounts for 15% mortality after MI
Myocardial free wall rupture
 Accounts for 10% of post MI deaths
 Typically occurs in first 5 days of MI (can occur
day 1-21)
 Occurs in small infarcts and commonly
anterolateral MI
 Single vessel MI with poor collaterals
 Elderly females with first MI or few prior MIs
 Leads to death or PEA
 Associated with less pulmonary edema, more
hypertension
 Not associated with murmur
 Increased risk after thrombolysis
 May lead to false aneurysm
Ventricular septal defect
 Occurs in 1-3% of post MI patients, 1-10 days
post MI
 Causes 5% peri-infarct deaths
 If anterior MI, VSD usually in apical septum
 If inferior MI, defect located on basal inferior
septum (worse outcome/more difficult to repair)
 Associated with new pansystolic murmur and
occasionally thrill
 Can detect shunt with step-up
 Usually seen in elderly females with few prior
MIs and lack of collaterals
 Highest overall mortality, but not acutely fatal
 Class I indication for IABP
MGH Medical Housestaff Manual
Acute disruption of the mitral valve with
severe mitral regurgitation
 Accounts for 5% post MI deaths; occurs 2-7
days post MI; rarest of mechanical
complications
 Associated with inferior MI (due to posteriormedial papillary muscle supplied by PDA)
and/or true posterior MI
 Rarely seen with ALMI
 Females > 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
23
4. Complications of myocardial infarction
 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
MGH Medical Housestaff Manual
 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 <45
 Mobitz type II
 Uncommon in inferior, mostly anterior MI due to
infranodal conduction system injury
 Wide QRS
 1/3 progress to complete heart block
Complete heart block
 3-7% of patients with acute MI
 Inferior MI from intranodal lesion; more benign
with narrow QRS escape
 Anterior MI carries high mortality rate (80%);
wide unstable escape rhythm
 Recovery usually within 3-7 days
 Temporary transvenous pacemaker required
MILIS trial. Prediction of complete heart
block. 1 point assigned for each:
1. New development of PR prolongation
2. Second degree AV block
3. Left anterior or posterior fascicular block
4. LBBB
5. 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%
Bundle branch block of any type
 Identifies patients with extensive infarction
 LAHB 5% pts with benign prognosis
 Complete RBBB or LBBB 10-15%, usually
RBBB
Late post infarction bradyarrhythmias
 If complete heart block, high grade AVB,
persistent second degree type II AVB may need
permanent pacemaker
24
4. Complications of myocardial infarction
 New BBB and transient but resolved CHB
during acute MI may need permanent pacemaker
 If monomorphic implies arrhythmogenic
substrate
Supraventricular arrhythmias
 Sinus tachycardia
 25% of pts with acute MI
 Persistent sinus tachycardia marker of LV
dysfunction, poor prognostic sign
 Goal HR < 70; treat with beta blocker
 Atrial premature beats
 May represent increased left atrial pressure
 If occurs in isolation, observe
Recommendations for Temporary Transvenous
Pacing - ACC/AHA Updated Guidelines (1999)
Class I
1.
2.
 Atrial fibrillation
 10-15% with acute MI
 Presence early signifies atrial ischemia
 Later may represent atrial stretch
3.
4.
 A-V nodal reentry
 Occurs infrequently
 May respond to adenosine or digitalis
Ventricular tachyarrhythmias
 In STEMI, incidence of VT or VF 10%; about
80-85% occurred in first 48 hours
 In NSTEMI, overall incidence of VT or VF
about 2.1%; median time to arrhythmia was 78
hrs, 25-75th percentile 16 hrs-7 days
 Accelerated idioventricular arrhythmia (50-110
bpm)
 Originally seen as reperfusion rhythm
 May occur in up to 40%; generally considered
benign
 If it accelerates to 110-120, consider atropine to
overdrive suppress
 If symptomatic, treat as if VT
 Ventricular tachycardia




15% pts during acute MI
Rate usually 120-140
May degenerate to VF
If non-sustained (<30 s with hemodynamic
stability), does not necessarily need antiarrhythmic treatment
 Ventricular fibrillation




8% pts surviving hospitalization
More frequent in large Q wave MI
May occur without warning
If it occurs late it is usually due to LV
dysfunction and portends poor prognosis
5.
Asystole.
Symptomatic bradycardia (includes sinus
bradycardia with hypotension and type I seconddegree AV block with hypotension not responsive
to atropine).
Bilateral BBB (alternating BBB or RBBB with
alternating LAFB/LPFB) (any age).
New or indeterminate age bifascicular block
(RBBB with LAFB or LPFB, or LBBB) with firstdegree AV block.
Mobitz type II second-degree AV block.
Class IIa
1.
2.
3.
4.
5.
RBBB and LAFB or LPFB (new or
indeterminate).
RBBB with first-degree AV block.
LBBB, new or indeterminate.
Incessant VT, for atrial or ventricular overdrive
pacing.
Recurrent sinus pauses (greater than 3 seconds)
not responsive to atropine.
Class IIb
1.
2.
Bifascicular block of indeterminate age.
New or age-indeterminate isolated RBBB.
Class III
1.
2.
3.
4.




First-degree heart block.
Type I second-degree AV block with normal
hemodynamics.
Accelerated idioventricular rhythm.
Bundle branch block or fascicular block known to
exist before acute MI.
Class I. Conditions for which there is evidence and/or
general agreement that a given procedure or treatment is
useful and effective.
Class IIa. Weight of evidence/opinion is in favor of
usefulness/efficacy.
Class IIb. Usefulness/efficacy is less well established by
evidence/opinion.
Class III. Conditions for which there is evidence and/or
general agreement that the procedure/treatment is not
useful/effective and in some cases may be harmful.
Roderick Tung, M.D.
MGH Medical Housestaff Manual
25
5. Intra-aortic balloon pump
General considerations
 Primary purpose is to decrease afterload/oxygen demand (deflation) and increase coronary blood
flow/oxygen supply (inflation).
Systole
Diastole
Non-augmented
systolic pressure
Augmented
diastolic pressure
Reduced systolic
pressure
Reduced aortic end-diastolic
pressure
Unassisted aortic end-diastolic
pressure
Dicrotic notch
Indications
 Recommendations for IABP in acute MI (ACC/AHA Updated Guidelines (1999)).
 Class I
 Cardiogenic shock not quickly reversed with pharmacological therapy as a stabilizing measure for
angiography and prompt revascularization.
 Acute mitral regurgitation or VSD complicating MI as a stabilizing therapy for angiography and
repair/revascularization.
 Recurrent intractable ventricular arrhythmias with hemodynamic instability.
 Refractory post-MI angina as a bridge to angiography and revascularization.
 Class IIa
 Signs of hemodynamic instability, poor LV function, or persistent ischemia in patients with large areas of
myocardium at risk.
 Class IIb
 In patients with successful PTCA after failed thrombolysis or those with three-vessel coronary disease to
prevent reocclusion.
 In patients known to have large areas of myocardium at risk with or without active ischemia.
Contraindications




Aortic insufficiency.
Aortic dissection or aneurysm.
Peripheral vascular disease, severe aorto-iliac or femoral artery disease, bilateral fem-pop bypass.
Uncontrolled sepsis.
MGH Medical Housestaff Manual
26
5. Intra-aortic balloon pump
 Uncontrolled bleeding diathesis.
Balloon position




Inserted in cardiac cath lab, tip 2 cm from aortic knob.
If balloon is too high (proximal to L subclavian), increased risk of CVA/limb ischemia.
If balloon is too low, decreased renal perfusion, oliguric ARF.
Balloon occludes 70-80% of aorta.
Timing





Key to efficacy  Inflation starts at dicrotic notch (AV closure), deflation starts at end-diastole
Early inflation  Increased afterload
Late inflation  Submaximal augmentation
Early deflation  Submaximal augmentation
Late deflation  Increased afterload
Complications






Bleeding: thrombocytopenia/hemolysis from balloon itself, HIT
Infection: cefazolin or vancomycin prophylaxis while IABP in place
Embolic phenomena leading to visceral and limb ischemia; atheroemboli
Vascular laceration/dissection: check distal pulses qd (can also use pulse volume recorder)
Shift in balloon position: daily CXR to verify position
Balloon rupture: rare
Weaning




Heparin is usually off about 4h prior to balloon pull. Cardiology fellow usually pulls IABP.
IABP must be at 1:1 while off heparin to prevent clot formation
Check EKG and hemodynamics (if PA line in place) with each change
Fast wean (UAP, MI, and/or s/p PTCA and EF > 40%)
 1:2 x 1h  1:4 x 1h  1:8 x 1h  1:1 x 4h  IABP out
 Slow wean (cardiogenic shock)
 1:2 x 4h  1:4 x 4h  1:8 x 4h  1:1 overnight
 In AM 1:2 x 1h  1:4 x 1h  1:8 x 1h  1:1 x 4h  IABP out
Roderick Tung, M.D.
MGH Medical Housestaff Manual
27
6. PA catheterization
Indications
 Diagnostic
 Shock (septic, cardiogenic, etc)
 Pulmonary edema (cardiogenic, increased
permeability)
 Evaluation of ventricular function
 Pericardial tamponade
 Constrictive pericarditis
 Valvular lesions
 Pulmonary hypertension
 Assessment of oxygen transport
 Management




When to send patient to cath lab for
fluoroscopically-guided PA line placement
 Temporary pacemaker or recently
(within 3 months) placed permanent
pacemaker, ICD, or ASD/PFO/VSD
closure device
 Inability to achieve PA or PCW position
on previous attempt without fluoroscopy
 Placement from femoral vein
 Left bundle branch block
 Suspected or known PA systolic
pressure >70 mm Hg
 Severe tricuspid valve disease
ARDS
Shock
Heart failure
Response to therapy (diuretics, vasodilators, pressors, inotropes)
 Perioperative monitoring
Contraindications








Right-sided endocarditis
Prosthetic right heart valve (mechanical incurs more risk than bioprosthetic)
Coagulopathy
Thrombocytopenia
Pacemaker
Ventricular arrhythmias
Severe pulmonary hypertension
Left bundle branch block (there is a 3% incidence of inducing RBBB with PA catheters and thus,
with underlying LBBB, can lead to complete heart block), this should be performed only with
transcutaneous pacemakers applied or in cath lab.
Theoretical considerations






Pulmonary capillary wedge pressure (PCWP) roughly reflects the left ventricular preload:
PCWP approximates left atrial (LA) pressure.
LA pressure approximates left ventricular end diastolic pressure (LVEDP).
LVEDP is proportional to left ventricular end diastolic volume (LVEDV).
Valvular disease and changes in left ventricular compliance alter these underlying assumptions.
Basic assumptions fail under certain circumstances:





PA diastolic pressure > 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.
MGH Medical Housestaff Manual
28
6. PA catheterization
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
 A wave is due to atrial contraction; the peak follows the peak
c
v y
of the electrical P wave by about 80 ms.
x
 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 <20 mm Hg.
 PCWP waveform. This is similar to the RA waveform but dampened and delayed (the peak of the
A wave follows the peak of the electrical P wave by about 240 msec and the peak of the V wave
occurs after the electrical T wave).
Measurements
 The intrathoracic pressure variation during the respiratory
cycle is transmitted to the heart and vasculature. ALL
MEASUREMENTS ARE TAKEN AT ENDEXPIRATION. Intrathoracic pressure closest to
Cardiac index
2.7-4.3
Normal range
2.2-2.7
Subclinical depression
1.8-2.2
Onset of clinical hypoperfusion
<1.8
Cardiogenic shock
Cardiac index = cardiac output/BSA
N Engl J Med 1976;295:1356
atmospheric pressure at end-expiration.
 End-expiration corresponds to the “high point” in the
spontaneously breathing patient and the “low point” in
patients on positive pressure ventilation.
 Note that PEEP >10 cm H2O may artificially raise measurements of intracardiac pressures
MGH Medical Housestaff Manual
29
6. PA catheterization
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.
oxygen consumption
 cardiac output 
arterial oxygen content - mixed venous content
 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 (V = IR), vascular resistance can be estimated in
hydraulic fluid mechanics (P = QR), multiplied by 80 to convert the units into dynes-sec/cm5:
SVR (dynes  sec  cm 5 ) 
MAP (mmHg)  CVP (mmHg )
 80
CO (L/min)
Specific conditions and arrhythmias
Acute mitral regurgitation
Tricuspid regurgitation
RV infarction
Pulmonary embolism
Pericardial tamponade
VSD
Atrial fibrillation
Giant V waves on the wedge tracing (can be mistaken for PA waveform)
Accentuation of RA V wave with a steep Y decent and elevation of the mean right atrial
pressure.
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)
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
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
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 systole is lost and the A wave disappears
MGH Medical Housestaff Manual
30
6. PA catheterization
Atrial flutter
Atrioventricular reentry
tachycardia
Ventricular tachycardia
Mechanical flutter waves at approximately 300/minute
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.
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 (<1.4%), balloon rupture, and pulmonary artery rupture.
Normal PA line tracing
Jonathan Passeri, M.D.
Andrew Yee, M.D.
MGH Medical Housestaff Manual
31
7. ICU drips
Generic
Trade
Mechanism
Usage
Dosing
Side effects
Vasopressors/Inotropes
Norepinephrine
Levophed
Hypotension, especially
1, 1 agonist, causes
vasoconstriction and increases “cold” septic shock.
cardiac output.
0-100 mcg/min.
Peripheral or renal
hypoperfusion, also
potentially
arrhythmogenic.
Phenylephrine
NeoSynephrine
-1 agonist, raises BP by
causing peripheral
vasoconstriction.
Hypotension with high
CO, low SVR (“warm” or
early sepsis, neurogenic
shock).
10-1000 mcg/min.
Peripheral or renal
hypoperfusion due to
vasoconstriction.
Dopamine
Intropin
Low dose (1-3 mcg/kg/min)
acts on D1 receptors, causes
visceral vasodilation (“renal
dose”). Medium dose (3-10
mcg/kg/min), adds 1 agonism,
increasing CO. High dose
(>10 mcg/kg/min), adds 1
agonism, causing
vasoconstriction.
At “renal doses” augments 10-1000 mcg/min.
diuresis but has no clear
renal-protective benefit.
At higher doses, treats
hypotension due to sepsis
or cardiac failure.
Prominent natriuretic
effect, tachycardia and
arrhythmias at higher
doses.
Vasopressin
Pitressin
Renal ADH effects as well as
generalized vasoconstriction.
Refractory septic shock,
also used in VF/pulseless
VT arrests.
Peripheral or visceral
hypoperfusion due to
vasoconstriction (though
not observed at lower
doses used for
hypotension)
Dobutamine
Dobutrex
1, 2 agonism increases
inotropy/chronotropy with
peripheral vasodilation.
Increasing CO in
2-40 mcg/kg/min,
Hypotension due to
vasodilation, arrhythmias.
cardiogenic shock, not to titrate to desired
be used as a pressor due to hemodynamic profile.
vasodilation.
Amrinone
Inocor
Inhibits phosphodiesterase-III, Similar to dobutamine, but
increasing CO and peripheral with less arrhythmogenic
vasodilation.
potential.
Milrinone
Primacor
Similar to amrinone.
Epinephrine
Adrenalin
Hypotension due to
vasodilation, arrhythmias.
Similar to amrinone.
0.375-0.75
mcg/kg/min
Similar to amrinone.
Generally used in ACLS,
anaphylaxis.
1-10 mcg/min
Variable BP effects limit
its utility
Bradycardia.
2-10 mcg/min.
High 2 effect limits
pressor utility
1 g iv load is 150 mg Hypotension, multiple
bolus, 1 mg/min for 6 systemic side effects with
long-term use.
hrs, 0.5 mg/min for
18 hrs. Use 150 mg
boluses in ACLS.
Similar to epinephrine,
used for post-anesthesiainduced hypotension.
Ephedrine
Isoproterenol
0.04-0.067 U/min (in
refractory VF, 40 U
bolus) (Circulation
2003;107:2313)
Isuprel
Anti-arrhythmics and anti-hypertensives
Amiodarone
Cordarone
Class III anti-arrhythmic,
blocks K+ channels, delaying
repolarization.
Treatment and prevention
of atrial and ventricular
tachyarrhythmias.
Esmolol
Brevibloc
-blocker, primarily of 1
receptor. Extremely short
Useful as a trial drug, to
see if a patient will
MGH Medical Housestaff Manual
As with other -blockers
32
7. ICU drips
half-life (9 minutes).
tolerate -blockade (e.g.,
in RV infarct).
Propranolol
Inderal
Non selective -blocker.
Useful for heart rate
control, especially in
aortic dissection (used
with nitroprusside).
1-40 mg/min.
Similar to other blockers, but also causes
prominent change in
mental status.
Fenoldopam
Corlopam
Selective postsynaptic
dopamine agonist at D1
receptors.
Rapidly lowers BP, as in
hypertensive
urgency/emergency, but
theoretically maintains
renal perfusion (not well
studied yet).
1-150 mcg/min.
May decrease SVR,
making it difficult to use
in some patients.
Labetalol
Normodyne
Combined  and -blocker ( Rapid lowering of BP, as
blocking effect 7x greater than in hypertensive
urgency/emergency.
 effect when iv).
1-6 mg/min.
Bradycardia,
bronchospasm,
hypotension.
Nitroglycerin
Direct nitric oxide-mediated
vasodilation, venous >
arterial.
Hypertension, angina in
1-1000 mcg/min.
acute coronary syndromes.
Headache, tachycardia,
hypotension,
tachyphylaxis.
Nitroprusside
Nipride
Direct nitric oxide-mediated
arterial and venodilation.
Rapid lowering of BP,
first-line in hypertensive
emergency.
10-800 mcg/min.
Hypotension,
tachyphylaxis, rare
cyanide toxicity. Caution
in renal failure as cyanide
metabolites are renallycleared.
Lidocaine
Xylocaine
Class IB anti-arrhythmic
Used in sustained VT and
VF
1-1.5 mg/kg bolus;
infuse 1-4 mg/min
Mental status change.
Procainamide
Pronestyl
Class IA anti-arrhythmic
Used in VT, atrial
fibrillation
Load 20 mg/min until Hypotension with iv
17 mg/kg reached,
infusion. Drug-induced
lupus, agranulocytosis.
side effects, or
arrhythmia controlled;
infuse 1-4 mg/min.
8-20 mg bolus, 1-10
mg/hr.
Sedatives/Paralytics
Cisatracurium
Nimbex
Neuromuscular blocking
agent, blocks ACh-mediated
transmission at NMJ.
Along with others of its
class, paralysis of patients
to assist in
intubation/ventilation.
Fentanyl
Sublimaze
Binding of opiate receptors.
Sedation and analgesia in 50-300 mcg/hr.
hemodynamically unstable
or morphine sensitive
patients.
Propofol
Diprivan
Phenolic derivative with
IV infusion for ICU
general anaesthetic properties. sedation.
25-300 mg/hr.
Hypotension,
neuroexcitatory effects,
bradycardia.
Midazolam
Versed
Benzodiazepene.
1-7 mg/hr.
Cumulative effects,
respiratory depression,
tolerance.
IV infusion for ICU
sedation, preferred over
other benzos because of
short half life, lack of
active metabolites.
Prolonged paralysis,
myopathy, blockade of
autonomic activity.
Respiratory depression,
dependence, tolerance,
constipation.
Ednan Bajwa, M.D
MGH Medical Housestaff Manual
33
8. Anticoagulation for atrial fibrillation, prosthetic valves
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
Annual stroke rate
Placebo
Warfarin
Risk categories
Age <65
no risk factors
1.0%
1.0%
4.9%
1.7%
1 risk factors
Age 65-75
No risk factors
4.3%
1.1%
5.7%
1.7%
1 risk factors
Age >75
No risk factors
3.5%
1.7%
8.1%
1.2%
1 risk factors
Risk factors in this study are:
hypertension, diabetes, prior stroke or TIA
Arch Intern Med 1994;154:1449
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
Ethan Korngold, M.D.
MGH Medical Housestaff Manual
34
9. Wide complex tachycardia v. SVT
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.
P
P
P
Diagnostic aids
Presenting symptom
History
CAD and previous MI
First arrhythmia after MI
Physical exam
AV dissociation
Blood pressure
Heart rate
EKG
Rate
QRS >0.16 s
QRS <0.16 s
Significant axis shift
Marked left axis
Right or normal axis
QRS morphology
Positive QRS concordance
Negative QRS concordance
AV dissociation
No AV dissociation
Usefulness
Unhelpful
VT
VT
VT
Unhelpful
Unhelpful
Unhelpful
VT
Unhelpful
VT
Suggests VT
Unhelpful
Usually unhelpful
Usually VT (may
be antidromic
AVRT)
Unhelpful
VT
Unhelpful
 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.
Fusion
Dressler
beat
beat
P wave
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).
V1
RBBB-type
R
sens 0.60,
spec 0.84
MGH Medical Housestaff Manual
PQR or RS
sens 0.30,
spec. 0.98
“Rabbit ear,” left > right, triphasic
sens 0.82, spec 0.91
35
9. Wide complex tachycardia v. SVT
 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).
V6
RBBB-type
R:S <1
QS (or QR)
Monophasic R
Triphasic
R:S >1
sens 0.41, spec 0.94
sens 0.29, spec 1.0
sens 0.01, spec 1.0
sens 0.64, spec 0.95
sens 0.30, spec 0.76
 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).
LBBB-type
1. R in V1 or V2 >30 ms
2. Notched or slurred
downstroke S wave
V6
V1 or V2
4. Any Q in V6
Sens 0.17, spec 1.0
3. >60 ms from QRS onset to S nadir
Above V1 or V2 criteria, sens 1.0, spec 0.89
MGH Medical Housestaff Manual
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9. Wide complex tachycardia v. SVT
Brugada algorithm
 See Circulation 1991;83:1649.
 Based on prospective analysis of ventricular tachycardia v. SVT with aberrant conduction by EP
study
 Stepwise approach
Wide complex tachycardia
1. Absence of an RS complex in all precordial leads
Yes
No
VT
sens 0.21, spec 1.0
2. R to S interval >100 ms in one precordial lead
Yes
No
VT
sens 0.66, spec 0.98
3. Atrio-ventricular dissociation
Yes
No
VT
sens 0.82, spec 0.98
4. Morphology criteria for VT present in both
precordial leads V1, V2, and V6? (see above)
Yes
No
VT
sens 0.987, spec 0.965
SVT
sens 0.965, spec 0.987
Gregory Bashian, M.D.
Jonathan Passeri, M.D.
Andrew Yee, M.D.
MGH Medical Housestaff Manual
37
10. MGH triage guidelines for acute coronary syndromes
Ell 9 - CCU /
Bl 7 - MICU
Floor
Patient/Clinical Characteristics
for Admission
a.
b.
c.
d.
e.
f.
g.
h.
Persistent ST  (>20 minutes)
Refractory HTN
Severe CHF
Cardiogenic shock
IABP
Invasive hemodynamic monitoring
Ventilatory support
VF or sustained VT with hemodynamic
compromise
Interventions/Meds
Supported on
Unit/Floor
Triggers for moving
to more acute unit
a. IABP
b. Sustained high dose
IV pressors and
inotropes
c. Ventilatory support
d. IIb/IIIa inhibitors
NA
Ell 10 - SDU
A positive troponin in a hemodynamically stable patient is not necessarily a direct indication for admission to Ellison 10.
a. Persistent ST  or deep (>3 mm) T wave
inversions (>20 minutes)
b. Uncomplicated MI post-angioplasty
c. Stable acute MI patients post percutaneous
coronary intervention with or without
thrombolysis
d. Unstable angina if hemodynamically stable
e. Typical angina >20 minutes or requiring
morphine
f. SVT
g. Unstable bradyarrhythmias
h. Other malignant arrhythmias (NSVT or VT
without hemodynamic compromise)
i. Syncope
j. Moderate heart failure
k. Comorbidities that compromise cardiac
status, e.g.,
 GI bleed
 Symptomatic bronchospasm (COPD or
asthma)
 Infection
 TIA/CVA
 Renal Failure
k. Transient hypotension
MGH Medical Housestaff Manual
a. IV TNG
b. Temporary and
external
pacemakers
c. IV antiarrhythmics
(e.g. lidocaine,
procainamide,
bretylium, and
amiodarone)
d. Low dose dopamine,
dobutamine (200600 mcg/min), or
milrinone once a
stable dose is
established in the
ICU
e. IIb/IIIa inhibitors
f. Epoprostenol
(Flolan)
a. IV meds requiring
invasive monitoring
e.g., nitroprusside,
high dose dopamine
and dobutamine, and
initial titration of
milrinone
b. Refractory ischemia
despite IV TNG,
heparin, beta blocker,
and ASA
c. Other needs for
invasive monitoring
38
10. MGH triage guidelines for acute coronary syndromes
Ell 8 - Cardiac
Surgery
(criteria for medical
patients)
Ell 11 - Access Unit (cardiac attending)
Floor
Patient/Clinical Characteristics
for Admission
a. Priority for beds goes to referral patients
b. Ischemic or congestive syndromes in need of
a catheterization and/or coronary
intervention.
c. Admit to observe patients (post-cath patients
or RPPR patients)
d. Stable acute MI patients post percutaneous
coronary intervention with or without
thrombolysis
e. Exclusions:
 Life threatening arrhythmia
 Bradycardia or heart block requiring
temporary or external pacemaker
 SVT in need of cardioversion
 Acute renal failure possibly requiring dialysis
 Hemodynamic instability
 Anticipated long lengths of stay due to
comorbidities
a. Post-cath patients from Cardiac Access Unit
(Team 4)
b. Pre-cath referral patients (Team 4)
c. Post-AICD (EP Fellow/Team 4 back-up)
d. Post-cath pre-op cardiac surgery (Team 4)
MGH Medical Housestaff Manual
Interventions/Meds
Supported on
Unit/Floor
Triggers for moving
to more acute unit
a. IV TNG
b. IIb/IIIa inhibitors
a. Life-threatening
arrhythmia
b. Bradycardia or heart
block requiring
temporary or external
pacemaker
c. SVT in need of
cardioversion
d. Hemodynamic
instability
e. Refractory ischemia
despite IV TNG,
heparin, beta blocker,
and ASA
f. Respiratory
compromise requiring
ventilatory support
and/or frequent blood
gas monitoring
a. IV TNG may be
started, but this
generally triggers
move for medical
patients on Ellison 8
b. Temporary or external
pacemaker
39
10. MGH triage guidelines for acute coronary syndromes
Patient/Clinical Characteristics
for Admission
Interventions/Meds
Supported on
Unit/Floor
Triggers for moving
to more acute unit
a. Typical angina with or without ischemic ECG
with resolution in <20 minutes
b. Positive CK-MB/troponin and
hemodynamically and electrically stable after
discussion with attending MD.
a. Defibrillation
a. Continuous IV TNG
b. Recurrent or refractory
ischemia
c. Hemodynamically
unstable
d. Requiring intubation
e. Positive CKMB/troponin in patient
who is hemodynamically unstable
(stable patients may
stay on the unit at the
discretion of the
medical team and
nursing staff.)
f. Life-threatening
arrhythmia
g. Bradycardia or heart
block requiring
temporary or external
pacemaker
g. SVT in need of
cardioversion
a. Short-stay patients at low or moderate risk
for MI
b. Normal ECGs or abnormal ECGs with no
new ischemic changes
c. Chest pain resolved prior to or in ED
d. Hemodynamically and electrically stable
e. History of CAD accepted
f. Exclusions:
 LBBB
 Paced rhythms
 Significant arrhythmia
 Suspected UAP requiring heparin or IV
nitrates
 Comorbidities requiring >24 hours
hospitalization
a. IV TNG
Ell 11 – Four CPOU beds (cardiac
attending)
General Medical Floor
Floor
(Patients will be
supported on Ellison 11
as Cardiac Access
patients if their clinical
course evolves.)
(Same as above for
Ellison 11 Cardiac
Access Unit)
Triage nursing
Cardiology
MGH Medical Housestaff Manual
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