cardiology board review 2008
TRANSCRIPT
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Todd C. Villines, MD
Cardiology ServiceWalter Reed Army Medical Center
Cardiology Board Review Part I
April 2008
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Outline – Part I
CAD Acute Coronary Syndromes (ACS) Chronic CAD
Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls
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A 55 yo male presents to your rural ER with 30 minutes of substernal chest pain, nausea and diaphoresis:
- Hx: HTN, tobacco abuse Rx: HCTZ, diltiazem SR
- P 96 BP 146/92 Apprehensive.
- RRR w/+S4. No murmur. Lungs – clear. Equal pulses.
- He is treated with ASA, heparin, IV beta-blocker.
a. clopidogrel 300 mg PO d. tPA
b. eptifibatide IV e. transfer to facility only 1.5 hrs
c. eptifibatide + ½ dose tPA away for primary angioplasty
Which of the following should be
done next ?:
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Acute Coronary Syndromes
Revascularization
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Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)
Acute Coronary Syndromes*
1.57 Million Hospital Admissions - ACS
UA/NSTEMI† STEMI
1.24 million Admissions per year
.33 million Admissions per year
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary diagnoses. †About 0.57 million
NSTEMI and 0.67 million UA.
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ACS - Thrombolytics
Greatest benefit of thrombolytics in first 1-2 hours from symptom onset! (Golden Hour)
ABSOLUTE Contraindications
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ThrombolyticsRelative Contraindications
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ACS Things you must know…
Accelerated Idioventricular Rhythm (AIVR)
1.
2.
3.
4.
Rescue Angioplasty
If no reperfusion
in 60-90 mins.
(20-40% will not
reperfuse)
If hemodynamically stable: no treatment!
(CK washout)
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Primary PCI Absolute
contraindication to thrombolytics
STEMI Guidelines: Door to balloon: <90
minutes Highest risk
patients benefit the most Treatment of choice
in cardiogenic shock
Late presentation Rescue angioplasty
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Primary PCI
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Primary PCI
STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal.
STEMI patients presenting to a hospital without PCI capability, and who cannot be transferred to a PCI center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Facilitated PCI
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Meta-analysis: Facilitated PCI vs
Primary PCI
1.03(0.15-7.13)
3.07(0.18-52.0)
1.43(1.01-2.02)
1.03
(0.49-2.17)
Mortality Reinfarction Major Bleeding
Fac. PCIBetter
PPCIBetter
Fac. PCIBetter
PPCIBetter
Fac. PCIBetter
PPCIBetter
Keeley E, et al. Lancet 2006;367:579.
0.1 1 10 0.1 1 10 0.1 1 10
1.38 (1.01-1.87)
1.71 (1.16 - 2.51)
1.51 (1.10 - 2.08 )
Lytic alone N=2953
IIb/IIIa alone N=1148
Lytic +IIb/IIIaN=399
All (N=4500)
1.40 (0.49-3.98)
1.81
(1.19-2.77)
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A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI is not recommended and may be harmful.
Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of the following are present:a. Patients are at high risk,b. PCI is not immediately available within 90 minutes, andc. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight).
Facilitated PCI
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Rescue and Late PCI
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Wijeysundera HC, et al. J Am Coll Cardiol. 2007;49:422-430.
Meta-analysis: Rescue PCI vs Conservative Tx
Outcome Rescue PCI Conservative Treatment
RR (95% CI) P
Mortality, %(n)
7.3(454)
10.4(457)
0.69(0.46–1.05)
.09
HF, % (n)
12.7(424)
17.8(427)
0.73(0.54–1.00)
.05
Reinfarction,% (n)
6.1(346)
10.7(354)
0.58(0.35–0.97)
.04
Stroke, % (n)
3.4(297)
0.7(295)
4.98(1.10–22.48)
.04
Minor bleeding,% (n)
16.6(313)
3.6(307)
4.58(2.46–8.55)
<.001
In 3 trials, enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and HF, rescue PCI was associated with a significant RR reduction of 28% (RR 0.72; 95% CI, 0.59-0.88; P=.001)
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A strategy of coronary angiography with intent to
perform PCI (or emergency CABG) isrecommended in patients who have receivedfibrinolytic therapy and have:
a. Cardiogenic shock in patients < 75 years who are suitable candidates for revascularization
b. Severe congestive heart failure and/or pulmonary edema (Killip class III)
c. Hemodynamically compromising ventricular arrhythmias.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Rescue PCI
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Rescue PCI
A strategy of coronary angiography with intent to
perform PCI (or emergency CABG) isreasonable in patients ≥ 75 years who
havereceived fibrinolytic therapy, and are incardiogenic shock, provided they are
suitablecandidates for revascularization.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Rescue PCI
A strategy of coronary angiography with intent to perform rescue PCI is reasonable for patients in whom fibrinolytic therapy has failed (ST-segment elevation < 50% resolved after 90 min following initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and a moderate or large area of myocardium at risk [anterior MI, inferior MI with right ventricular involvement or precordial ST-segment depression].
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Rescue PCI
A strategy of coronary angiography with intent to perform PCI in the absence of any of the above Class I or IIa indications might be reasonable in moderate- or high-risk patients, but its benefits and risks are not well established. The benefits of rescue PCI are greater the earlier it is initiated after the onset of ischemic discomfort.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Rescue PCI
A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is not recommended in patients who have received fibrinolytic therapy if further invasive management is contraindicated or the patient or designee do not wish further invasive care.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Analgesia
Morphine remains Class I for STEMI although may increase adverse events in UA/NSTEMI
NSAID medications increase mortality, reinfarction, and heart failure in proportion to degree of COX-2 selectivity Discontinue on admission for STEMI Do not initiate during acute phase of
management
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Patients routinely taking nonsteroidal anti-
inflammatory drugs (NSAIDs) (except for
aspirin), both non-selective as well as COX-2
selective agents, prior to STEMI should have
those agents discontinued at the time of
presentation with STEMI because of the
increased risks of mortality, reinfarction,
hypertension, heart failure, and myocardial
rupture associated with their use.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Analgesia
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NSAIDs (except for aspirin), both
nonselective as well as COX-2 selective
agents, should not be
administered during hospitalization for
STEMI
because of the increased risks of mortality,
reinfarction, hypertension, heart failure,
and
myocardial rupture associated with their
use.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Analgesia
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Beta-Blockers
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TREATMENT: Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placebo
INCLUSION: Suspected acute MI (ST change or LBBB) within 24 h of symptom onset
EXCLUSION: Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV block
1 OUTCOMES: Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge)
Mean treatment and follow-up: 16 days
COMMIT: Study design
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Effects of Metoprolol
Lancet. 2005;366:1622.
Death13%
P=0.0006
ReMI22%
P=0.0002
VF15%
P=0.002
Totality of Evidence (N = 52,411)COMMIT (N = 45,852)
Increased early risk of
shock
Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
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Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).
It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).
Beta-Blockers
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease).
Beta-Blockers
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Anticoagulants
Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). (Level of Evidence: A)
Anticoagulant regimens with established efficacy include:♥ UFH (LOE: C)♥ Enoxaparin (LOE:A)♥ Fondaparinux (LOE:B)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Anticoagulants
For patients undergoing PCI after havingreceived an anticoagulant regimen, the
followingdosing recommendations should be
followed:
a. For prior treatment with UFH: administer additional boluses of UFH as needed to support the procedure taking into account whether GP IIb/IIIa receptor antagonists have been administered. (Level of Evidence: C) Bivalirudin may also be used in patients treated previously with UFH. (Level of Evidence: C)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Recommendation continues on the next slide.
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Anticoagulants
b. For prior treatment with enoxaparin: if the last SC dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg/kg of enoxaparin should be given.
c. For prior treatment with fondaparinux: administer additional intravenous treatment with an anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa receptor antagonists have been administered.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Anticoagulants
Because of the risk of catheter thrombosis,fondaparinux should not be used as the soleanticoagulant to support PCI. An additionalanticoagulant with anti-IIa activity should beadministered.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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ExTRACT-TIMI 25: Primary End Point (ITT) Death or Nonfatal MI
0
3
6
9
12
15
0 5 10 15 20 25 30
Pri
mary
En
d P
oin
t (%
) Enoxaparin
UFH
Relative Risk0.83 (95% CI, 0.77 to
0.90)P<.001
Days after Randomization
9.9%
12.0%
Lost to follow-up = 3
17% RRR
Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354:1477-1488.
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CLARITY-TIMI 28 Primary Endpoint:Occluded Artery (or D/MI thru Angio/HD)
PlaceboClopidogrelLD 300 mgMD 75 mg
P=0.00000036P=0.00000036
Odds Ratio 0.64(95% CI 0.53-0.76)
Odds Ratio 0.64(95% CI 0.53-0.76)
Clopidogrelbetter
Placebobetter
n=1752 n=1739
Sabatine N Eng J Med 2005;352:1179.
STEMI, Age 18-75
15.0
21.7
0
5
10
15
20
25
Occ
lud
ed A
rter
y o
r D
eath
/MI
(%)
1.00.4 0.6 0.8 1.2 1.6
36%Odds
Reduction
36%Odds
Reduction
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De
ad
(%
)
Days Since Randomization (up to 28 days)
Placebo + ASA: 1,846 deaths (8.1%)
Clopidogrel + ASA:1,728 deaths (7.5%)
0.6% ARD7% RRR P = 0.03
N = 45,852 No Age limit ; 26% > 70 y
Lytic Rx 50%
No LD given
COMMIT: Effect of CLOPIDOGREL on Death In Hospital
Chen ZM, et al. Lancet. 2005;366:1607.
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Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy.
Treatment with clopidogrel should continue for at least 14 days.
Thienopyridines
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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In patients < 75 years who receive fibrinolytic therapy or who do not receive reperfusion therapy, it is reasonable to administer an oral clopidogrel loading dose of 300 mg. (No data are available to guide decision making regarding an oral loading dose in patients ≥ 75 years of age.)
Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) can be useful in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Thienopyridines
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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It is reasonable for patients with STEMI who do not undergo reperfusion therapy to be treated with anticoagulant therapy (non-UFH regimen) for the duration of the index hospitalization, up to 8 days.
Convenient strategies that can be used include those with LMWH (Level of Evidence: C) or fondaparinux (Level of Evidence: B) using the same dosing regimens as for patients who receive fibrinolytic therapy.
Anticoagulants
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Coronary arteriography may be considered as part of an invasive strategy for risk assessment after fibrinolytic therapy (Level of Evidence: B) or for patients not undergoing primary reperfusion. (Level of Evidence: C)
Invasive Evaluation
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Secondary Prevention
Ask, advise, assess, and assist patients to stop smoking – I (B)
Clopidogrel 75 mg daily: PCI – I (B) no PCI – IIa (C)
Statin goal: LDL-C < 100 mg/dL – I (A) consider LDL-C < 70 mg/dL – IIa (A)
Daily physical activity 30 min 7 d/wk, minimum 5 d/wk – I (B)
Annual influenza immunization – I (B)
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• A fasting lipid profile should be assessed in all patients and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiation of lipid-lowering medication is indicated as recommended below before discharge according to the following schedule:
• LDL-C should be < 100 mg/dL.• Further reduction to < 70 mg /dL is reasonable.
(Class IIa; LOE: A) • If baseline LDL-C is ≥ 100 mg/dL, LDL-lowering
drug rx should be initiated.• If on-treatment LDL-C is ≥ 100 mg/dL
intensify LDL-lowering drug rx (may require LDL-lowering combination is recommended.
• If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-C < 70 mg/dL. (Class IIa; LOE: B)
Lipid management:2007 goal:LDL-C << than 100 mg/dL (if TG ≥ 200 mg/dL, non–HDL-C < 130 mg/dL
Goals Class I Recommendations
Secondary Prevention and Long Term Management
NEW
NEW
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If TG are ≥ 150 mg per dL or HDL-C < 40 mg per dL, weight management, physical activity, and smoking cessation should be emphasized.
If TGs are 200 to 499 mg per dL, non–HDL-C target should be less than 130 mg per dL.
If TGs are 200 to 499 mg/dL, non–HDL-C target is < 130 mg/dL. (Class I; LOE: B); further reduction of non–HDL-C to < 100 mg dL is reasonable. (Class IIa; LOE: B)
Therapeutic options to reduce non–HDL-C include:•More intense LDL-C-lowering rx is indicated•Niacin (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B)•Fibrate therapy (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B)
If TG are ≥ 500 mg/dL, therapeutic options indicatedand useful to prevent pancreatitis are fibrate or niacinbefore LDL-lowering rx; and treat LDL-C to goal after TG-lowering rx. Achieving non–HDL-C < 130 mg/dL is recommended.
Lipid management:(TG 200 mg/dL or greater)Primary goal:Non–HDL-C < 130 mg/dL
Goals Class I Recommendations
Secondary Prevention and Long Term Management
NEW
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• For all patients, it is recommended that risk be assessed with a physical activity history and/or an exercise test to guide prescription.
• For all patients, encouraging 30 to 60 min of moderate-intensity aerobic activity, such as brisk walking, on most, preferably all, days of the week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work).
• Advising medical supervised programs (cardiac rehabilitation) for high-risk patients (e.g., recent acute coronary syndrome or revascularization, HF) is recommended.
• Encouraging resistance training 2 d per week may be reasonable (Class IIb; LOE: C)
Physical activity:2007 Goal:30 min 7 d per wk; minimum 5 d per wk
Goals Class I Recommendations
Secondary Prevention and Long Term Management
NEW
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Goals Class I Recommendations
For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162 to 325 mg daily should be given for at least 1 month after bare-metal stent implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75 to 162 mg daily.
Antiplatelet agents/ anticoagulants: Aspirin
Secondary Prevention and Long Term Management
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Goals Recommendations
In patients where the physician is concerned about the risk of bleeding lower-dose 75 to 162 mg of aspirin is reasonable during the initial period after stent implantation. (Class IIa; LOE: C)
Antiplatelet agents/ anticoagulants: Aspirin
Secondary Prevention and Long Term Management
NEW REC
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Goals Class I RecommendationsFor all post-PCI patients who receive a drug-elutingstent (DES), clopidogrel 75 mg daily should begiven for at least 12 months if patients are not athigh risk of bleeding.
For post-PCI patients receiving a bare metal stent(BMS), clopidogrel should be given for a minimumof 1 month and ideally up to 12 months (unless thepatient is at increased risk of bleeding; then itshould be given for a minimum of 2 weeks).
Antiplatelet agents/ anticoagulants: Clopidogrel
Secondary Prevention and Long Term Management
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Goals Recommendations
For all STEMI patients not undergoing stenting(medical therapy alone or PTCA without stenting), treatment with clopidogrel should continue for at least 14 d. (Class I; LOE: B)
Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Class IIa; LOE: C)
Antiplatelet agents/ anticoagulants: Clopidogrel
Secondary Prevention and Long Term Management
NEW RECS
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Goals Class I RecommendationsManaging warfarin to INR = 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter is recommended, and in post-STEMI patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus).
Use of warfarin in conjunction with aspirin and/orclopidogrel is associated with increased risk ofbleeding and should be monitored closely.
In patients requiring warfarin, clopidogrel, andaspirin therapy, an INR of 2 to 2.5 is recommended with low dose aspirin (75 to 81 mg) and a 75 mg dose of clopidogrel.
Antiplatelet agents/ anticoagulants: Warfarin
Secondary Prevention and Long Term Management
NEW REC
NEW REC
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• Acetaminophen, ASA, tramadol, narcotic analgesics (short term)
• COX-2 Selective NSAIDs
• Nonacetylated salicylates
• Non COX-2 selective NSAIDs
• NSAIDs with some COX-2 activity
Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal Symptoms with Known Cardiovascular Disease or Risk Factors for
Ischemic Heart Disease
Select patients at low riskof thrombotic events
Prescribe lowest doserequired to control symptoms
Add ASA 81 mg and PPI to patients at increased risk of thrombotic events *
• Regular monitoring for sustained hypertension or worsening of prior blood pressure control), edema, worsening renal function, or gastrointestinal bleeding.
• If these events occur, consider reduction of the dose or discontinuation of the offending drug, a different drug, or alternative therapeutic modalities, as dictated by clinical circumstances.
* Addition of ASA may not be sufficient protection against thrombotic eventsAntman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001.
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Goals Class I Recommendations
ACE inhibitors should be started and continued indefinitely in all patients recovering from STEMI with LVEF ≤ 40% and for those with hypertension, diabetes, or chronic kidney disease, unless contraindicated.
ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI who are not lower risk (lower risk defined as those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed), unless contraindicated.
Among lower risk patients recovering from STEMI (i.e., those with normal LVEF in whom cardiovascular risk factors are well controlled and revascularization has been performed) use of ACE inhibitors is reasonable. (Class IIa; LOE: B)
Renin-Angiotensin-Aldosterone System Blockers: ACE Inhibitors
Secondary Prevention and Long Term Management
NEW REC
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Goals Class I RecommendationsUse of ARBs is recommended in patients who are intolerant of ACE inhibitors and have HF or have had a STEMI with LVEF ≤ 40%.
It is beneficial to use ARB therapy in other patients who are ACE-inhibitor intolerant and have hypertension.
Considering use in combination with ACE inhibitorsin systolic dysfunction HF may be reasonable.
Renin-Angiotensin-Aldosterone System Blockers: ARBs
Secondary Prevention and Long Term Management
NEW REC
NEW REC
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Goals Class I Recommendations
Use of aldosterone blockade in post-STEMI patients without significant renal dysfunction or hyperkalemia is recommended in patients who are already receiving therapeutic doses of an ACE inhibitor and beta blocker, have an LVEF of ≤ 40% and have either diabetes or HF.
Renin-Angiotensin-Aldosterone System Blockers: Aldosterone Blockade
Secondary Prevention and Long Term Management
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Goals Class I Recommendations
It is beneficial to start and continue beta- blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without HF symptoms, unlesscontraindicated.
Beta- Blockers
Secondary Prevention and Long Term Management
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A 55 yo male presents to your rural ER with 1-hour of sub-sternal chest pain, nausea and diaphoresis:
- BP 110/68 Following SL NTG, BP falls to 90/50
A. Suspected Diagnosis?:
As you give tPA + heparin, which of the following are most appropriate next tx?:
a. Additional IV metoprolol d. IV fluid bolus
b. Start nitroglycerin drip e. Place a PA catheter
c. Dopamine drip
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A 55 yo male presents to your rural ER with 1-hour of sub-sternal chest pain, nausea and diaphoresis:
- You give the patient tPA, IV fluids and his blood pressure increases and his symptoms and ECG changes are resolving.
- You notice that his heart rate significantly drops to 40 bpm.
- The BP remains stable and the patient has no symptoms.
a. Place a transvenous pacemaker d. Observation. Give
b. Atropine 0.5 mg IV atropine if develops sx’s or
c. Atropine 1.0 mg IV hemodynamic change.
Mobitz I, 2nd-degree AVB (Wenckebach)
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Transvenous Pacing & MI Location
Inferior MI Sinus bradycardia
(Bezold-Jarish) common
Block at AV node• Stable escape rhythm• AV block is usually
transient & well-tolerated
TV Pace: Mobitz II or higher &: Symptoms that are
unresponsive to atropine
Anterior MI Block usually below
AV node
TV Pace: New bifasicular
block Mobitz II or worse
regardless of symptoms
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Outline
Arrhythmias & ECGs
A 68 yo male presents to your ER after 60 minutes of substernal chest pain, nausea and diaphoresis:
- Hx: HTN, DM, HLD, Distant MI
- P 96 BP 146/92 RRR w/+S4. No murmur. Lungs – clear.
- ECG: 1mm ST-depression infero-laterally that resolves slowly with B-blocker, nitroglycerine & morphine.
- He rules in for MI: peak MB 30, trop-T 2.4.
After stabilization on medical therapy, you recommend which of the following
tests to risk stratify this patient?:a. Exercise stress test d. Myocardial Perfusion Imaging
b. Stress Echo e. None of the above
c. Cardiac Catheterization
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Post MI Risk Stratification
What is the overall best predictor of survival post-MI?:
LV Ejection Fraction (EF)
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Non-STEMI / UA Risk Stratification is key!
Immediate High Risk• Cardiogenic shock / severe CHF /
ischemic MR w/hemodynamic change
• Recurrent angina despite maximal medical therapy
• Unstable ventricular arrhythmias
Urgent Cath
*Don’t give thrombolytics
in NSTEMI!
High Risk• (+) enzymes
• Dynamic ECG changes
• Clinical CHF
• Depressed LV EF
• GIIb/IIIa
• Early invasive
- Cath during initial
Hospitalization
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Intermediate Risk• Diabetics, PVD, Age >65
• Prior MI (hx or q-waves on ECG)
• Aspirin use
• Rest angina, < 20 minutes
• No dynamic ST changes
• Baseline pathologic q-waves
• Negative enzymes
Low Risk• None of above
• Minimal risk factors
• Minimal or atypical symptoms
In General:• Best medical
therapy
• In general: Non-invasive risk stratification
• Cath for:
• High-risk non-invasive testing results
• Pre-existing lifestyle-limiting angina
Non-STEMI / UA Risk Stratification is key!
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MI: Initial Medical Therapy
*Clopidogrel: post-stenting
- Bare-metal stent: at least 4 weeks and no surgery for 6 weeks
- Drug-eluting stent (sirolomus, paclitaxel): plavix for 3 months (sirolomus/Cypher) to 6 months (paclitaxel/Taxus) MINIMUM
- Often given for 1 year (CURE Trial) unless contraindication
*162-325mg
Heparin: *60 U/kg bolus then
12U/Kg/Hr in patients given
lytics or IIb/IIIA
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MI: Initial Medical Therapy
*Warfarin x 3-6 months: LV thrombus, large anterior MI with akinetic anterior wall.
-Don’t give warfarin to a patient simply with a depressed EF without Afib or embolism or thrombus (controversial)
*
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Post-MI Complications
Acute pulmonary edema, hypotension, new decrescendo systolic murmur at apex
PA Catheter (wedged):
Papillary Muscle Rupture
Treatment: Afterload reduction
• Nitrates• IABP
Emergent surgical repair
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Post-MI Complications
Papillary Muscle Rupture
Inferior MI’s (PDA) Due to single blood
supply to postero-medial papillary muscle
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Post-MI Complications
LV Free Wall Rupture:
Large, STEMI, 1st MI, Anterior MI (LAD) Less common with early reperfusion but may
occur earlier (classically ~7d) Treatment: emergent surgery,
pericardiocentesis, supportive measures
Acute hypotension, JVD, muffled heart sounds
Equalization of diastolic pressures on PA catheter
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Post-MI Complications
Ventricular Septal Rupture (Acute VSD):
Location less important: Anterior = Inferior Treatment
• Unstable patient = urgent surgery• Afterload reduction, IABP, supportive measures
Hypotension, JVD, holosystolic murmur with a thrill
PA catheter: “step up” in oxygen saturation from RA to RV
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SCD Prevention Post-MIPrimary Prevention
Referral for AICD if (MADIT I): Non-sustained VT > 48 hours after
MI EF <35% Inducible, non-supressable VT on
EP study Best benefit: lower EF (<26%), wide
QRS, CHF Wait > 1 month post-MI & 3mos.
post CABG MADIT II: Prior MI + EF 30%
No EP study
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1 ° SCD PreventionNon-ischemic Cardiomyopathy
All-cause mortality at 5 yearsAmiodarone vs placebo
HR 1.06, p=0.529ICD vs placebo
HR 0.77, p=0.007
28.9%
34.1%35.8%
0%
5%
10%
15%
20%
25%
30%
35%
40%
ICD Amiodarone Placebo
28.9%
34.1%35.8%
0%
5%
10%
15%
20%
25%
30%
35%
40%
ICD Amiodarone Placebo
% M
ort
alit
y
SCD-HeFT ½ non-ischemic EF ≤ 35% Amio = Placebo
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Chronic CAD The ‘Big 4’:
Aspirin B-blocker (especially post-MI & depressed EF)
• Non-dihyrdropyridine CCB (diltiazem) if B-blocker intolerant
Statin Ace-I (HOPE & EUROPA trials –vs- PEACE trial)
Nitrates (know dosing, tolerance) Recent change: 1 spray, if not gone 911 / ER
Non-dihydropyridine CCB (e.g,. amlodipine) – may use with B-blocker
No estrogen for CAD: primary prevention (WHI) or secondary prevention (HERS)
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Chronic CAD
Know methods to reduce risk (Board Favorites!): Smoking cessation Diet Weight loss Exercise Lipid management
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Lipid Management
xx*CAD Equivalents:
- ASPVD - Diabetes - Multiple risk factors (Framingham > 20%)
• 2004 ATP III Modifications:
• In high risk patients: LDL-C goal < 70 is a therapeutic option based on recent clinical trial data (Heart Protection Study, PROVE-IT)
• High risk: may start statin if LDL-C 100-129 simultaneously with lifestyle changes.
• High risk: If baseline LDL is <100, can start statin
• If high risk & high TGs or low HDL-C: use fibrate or niacin to get non-HDL-C to 30mg/dl higher than LDL goal and to raise HDL
• Moderately high risk (2+ risk factors, 10-20% risk): LDL<100 optional goal
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Lipid Management LDL goal – get there 1st!
HDL and TG’s are secondary targets Once LDL to goal:
“Non-HDL chol.” goal: 30 higher than LDL goal• (LDL+VLDL+TG’s) – incorporates all atherogenic particles
Low HDL (<40 men, <50 women) Exercise, smoking cessation Niacin (most potent), fibrates
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Notes on Revascularization 2 Goals
Symptom relief (angina): PCI or CABG Improved survival: CABG
PCI: better than medications for relief of angina & ischemia from obstructive CAD
Stenting Complications: Early (1st month)
• Acute thrombosis: 24 hours (not subtle - MI)• Sub-acute thrombosis: usually < 4 weeks (not subtle - MI) • With DES (drug-eluting stents), can occur later until fully
endothelialized Late: in-stent restenosis: 1-6 months (angina)
• Reduced by DES• Brachytherapy – FDA approved treatment for symptomatic
restenosis (not for prevention!) – no longer done due to DES!!
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Indications for CABG
Left Main > 50% Left main equivalent:
>70% proximal LAD & proximal Left Circumflex 3 vessel obstructive CAD, especially if:
Depressed EF Diabetics
2 vessel CAD with proximal LAD disease & Depressed EF <OR> Treated diabetics
“Don’t stent the left main”
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Stress TestingExercise ECG
Sens & Spec = ~ 70%… Bayesian approach to using for diagnosis:
High pre-test probability: negative test won’t change management
Low pre-test probability: false + > true + Best: intermediate pre-test probability
Go directly to imaging (for diagnosis): LBBB, paced rhythm – use pharm stress Uninterpretable ECG: ST-dep >1mm (e.g. LVH) Inability to exercise Prior revascularization (to localize)
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Stress TestingExercise ECG
Contraindications: AS Others (common
sense) Reasons to stop High-risk findings
Low-functional capacity
Drop in Systolic BP during exercise
Marked ST-changes Prolonged ST-changes
>2 mm
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Stress TestingPerfusion Imaging & Stress Echo
More expensive Increased sensitivity & specificity Bayesian approach
Low-pre-test probability + positive stress ECG Localizes ischemia
Patients with prior revascularization Poor prognosis:
Multiple defects, Large defects, increased lung uptake, transient ischemic dilation of LV cavity
Normal study – has good prognosis Adenosine / Persantine: avoid if COPD,
asthma
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Endocarditis Prophylaxis Due to limited data re: efficacy of ID
prophylaxis, AHA guidelines revised 2007 Major change: only give IE prophylaxis to
those at HIGHEST RISK: Prosthetic heart valves (mechanical and bio) Prior history of IE 6 months post-repair of congenital defect (whether
by surgery or catheter) Repaired congenital defect with residual defect Complex cyanotic congenital heart disease Valvulopathy in a transplanted heart
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Endocarditis Prophylaxis
No prophylaxis:1. Bicuspid AoV
2. Acquired valvular heart disease
3. Prior surgical valve repair
4. Isolated SECUNDUM ASD
5. Surgically repaired ASD, VSD or PDA
6. Pacemakers, defibrillators
7. History of rheumatic disease without valvular dysfunction
8. Deliver or C-section
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Endocarditis Prophylaxis
Changes: limited procedures need prophylaxis: Dental procedures
GI, GU, Resp and skin:• Only if doing procedure involving active infected tissue
with ‘bugs’ known to cause IE: must be on abx at time of procedures
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Endocarditis ProphylaxisNo Post-treatment
Situation Agent
Regimen: single dose 30 to 60 min before procedure
Adults Children
Oral Amoxicillin 2 g 50 mg/kg
Unable to take oral medication
Ampicillin 2 g IM or IV 50 mg/kg IM or IV
OR
Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV
Allergic to penicillins or ampicillin - oral
Cephalexin* 2 g 50 mg/kg
OR
Clindamycin 600 mg 20 mg/kg
OR
Azithromycin or clarithromycin
500 mg 15 mg/kg
Allergic to penicillins or ampicillin and unable to take oral medication
Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV
OR
Clindamycin 600 mg IM or IV 20 mg/kg IM or IV
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Aortic Stenosis History: angina, syncope, CHF (classic triad) Exam:
Crescendo-decrescendo murmur Best at RUSB; may be heard at apex (Gallavardin’s) Radiates to carotids Increases with squatting Delayed & diminished carotid upstroke +S4 & sustained PMI Soft or delayed A2; loss of physiologic splitting Increased severity if:
• Later peaking murmur• Soft or absent S2• Loss of physiologic splitting (single S2)• Diminished carotid upstroke
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Aortic Stenosis Prevalence increases with age
(“senile, calcific AS”) Young patient with ejection
click = bicuspid Ao valve ~1 in 200 people 30-40% with coarctation have a
bicuspid Ao Valve Increased risk for aortic
dissection or ascending aneurysm
ECG: LVH, LAE; LBBB in some
Echo: accurate Measures velocity Gradient = 4v2
Aortic Valve Area: <1 cm2 severe
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Aortic Stenosis Bleeding tendency:
Increased colonic angiodysplasia Acquired vonWillebrand disease
Cath: not needed to “confirm” echo data Usually done to eval for obstructive CAD in
patients referred for aortic valve replacement Treatment
No medical treatment Beware of vasodilators or diuretics (decrease
preload) Symptoms = surgery! No role for balloon valvuloplasty
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Aortic Stenosis
Surgical Therapy (cont.) Symptoms = surgery! Prostheses:
• Mechanical – more durable; requires anticoagulation
• Bioprosthetic: less durable; short-term coumadin only
• Infective endocarditis risk is the same in both types of valves
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50 yo M c/o progressive DOE and fatigue. BP 160/58. Pulse is bisferens.
- CV exam: systolic thrill at the apex & over the bounding carotid arteries. + systolic ejection sound. +S3, soft S1 and a decrescendo diastolic murmur at the base that is high-pitched, early peaking and last throughout diastole.
- Also: 3rd and 4th interspaces at LLSB you hear a presystolic rumble.
- An echocardiogram confirms your clinical impression
You recommend which of the following?:a. MV replacement and AV replacement with a mechanical
prosthesis
b. MVR and AVR with a bioprosthesis in the aortic position.
c. AVR with a mechanical prosthesis.
d. Vasodilator therapy and observation for six months.
e. Diuretic therapy and observation for six months.
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Aortic InsufficiencyChronic
History – well-tolerated until severe CHF symptoms when severe
Exam: Wide pulse pressure accounts for myriad of
peripheral pulsating organs• Water-hammer pulses, etc…
Auscultation• Early diastolic, decrescendo murmur• Blowing (“cooing dove”, “wind blowing through
leaves”), high-pitched• Pt. sitting up, leaning forward• Afterload sensitive – increases with handgrip• Austin-Flint (diastolic): mimic MS due to AR jet
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Aortic InsufficiencyChronic
Etiologies:
Treatment: Surgery if: symptoms, EF<50% or increasing LV cavity size on serial echocardiograms
Mechanical AVR if <65 yo Bioprosthetic AVR if > 65 yo or can’t take coumadin
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Aortic InsufficiencyAcute!
Medical emergency Hx: severe symptoms
Cardiogenic shock, syncope Exam – classic exam signs not usually
present Softer, shorter diastolic murmur (may not even
be audible) Etiologies: endocarditis, aortic dissection,
trauma, mechanical valve dysfunction Treatment: emergent surgery
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Mitral Stenosis
Etiology: Rheumatic Fever History: disease often latent
Dyspnea – often misdiagnosed as asthma in young pt. Hemoptysis, hoarseness New-onset atrial fibrillation (esp. during pregnancy)
• Don’t tolerate tachycardia well due to transmitral pressure
Exam: Loud S1 Opening snap in early diastole (after S2) Diastolic rumble Loud P2 if pulmonary hypertension
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Mitral Stenosis
ECG: LAE, RAE RVH (RAD) - No LVH
Treatment Medical: lasix, ? B-blockers, limit activity Correct: if mod-severe MS + symptoms or pulmonary
hypertension Balloon valvuloplasty if possible based on valve
characteristics (unlike in AS) Open commissurotomy, surgical repair or
replacement
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55 yo M with a 5 year hx of a “murmur”. No symptoms but he admits to doing little activity. He no longer walks to
the office and does not have to walk stairs to the 3rd floor “because there is an elevator”.
- Exam: Normal carotids. Clear lungs. PMI is diffuse in the 5th intercostal space, midclavicular line.
- Grade III/VI holo-systolic murmur heard best at the apex.
- Echo: floppy mitral valve with severe posterior leaflet prolapse, severe MR. Mildly dilated LV with EF 45-50%
You recommend which of the following?:
a. Close observation and repeat TTE with clinical change.
b. Start ramipril and repeat TTE in 4 months.
c. Refer to surgery for mitral valve replacement.
d. Refer to surgery for mitral valve repair.
e. Start long-actin nifedipine and repeat TTE in 1 year.
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Mitral RegurgitationChronic
History: reflect poor cardiac output & elevated LA pressures Dyspnea / CHF
Multiple Etiologies Exam:
HSM murmur best at apex; may radiate to axilla Increases: afterload (sustained handgrip) or
Increased venous return (leg elevation) Decreases with standing, valsalva, inspiration Hyperdynamic apical impulse Soft S1 Little respiratory variation Wide splitting of S2 (early closure of A2)
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Mitral RegurgitationChronic
Medical Treatment Afterload reduction Diuresis
Surgical: repair (rather than valve replacement) if feasible! Timing – controversial; want to perform
BEFORE LV dysfunction occurs In general – severe MR &:
• Symptoms• EF <55-60%• Dilating LV size on TTE• Afib • Pulmonary HTN
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Mitral RegurgitationMitral Valve Prolapse
Most common valvular cause of MR & need for MVR
Exam: Mid-systolic click followed by murmur (“click-
murmur syndrome”) Maneuvers that decrease Preload (valsalva,
standing) move clicks closer to S1 and murmur starts earlier
Ejection sound of AS or PS – does not move
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Mitral RegurgitationMitral Valve Prolapse
Spectrum of disease Concern – “floppy” redundant MV leaflets
with MR and myxomatous changes Mild increase risk for embolic stroke No anticoagulation prophylaxis
SBE prophylaxis if: MR OR myxomatous leaflets on echo
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Mitral RegurgitationAcute MR
Also: Ischemic Ruptured chord in
severe MVP Large V-waves on PA
catheter Decrescendo systolic
murmur at apex
Most common cause: endocarditis
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R-sided Murmurs in Brief
TR Usually secondary: RV dilation or pulmonary
hypertension • PE, numerous causes of pulmonary HTN, RV disease
Murmur (when heard): HSM LLSB – increases w/inspiration
Prominent V-waves, pulsatile liver Endocarditis in drug users TS + TR, flushing, diarrhea = carcinoid syndrome Tx – underlying cause, ring if fixing mitral valve
PS – congenital; ejection click Noonan’s syndrome: low-set ears + PS Tx – balloon valvuloplasty
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Congenital Heart Disease
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Atrial Septal Defect (ASD)A 30 yo female is found to have cardiomegaly on a CXR obtained as part of routine physical examination. She
is active, can walk indefinitely without symptoms.
- Cardiac exam: grade II/VI SEM at the 2nd intercostal space, LUSB. 2nd heart sound is widely split and does not very with respiration.
- CXR: cardiomegaly with full pulmonary vascular markings.
- Echo: enlarged RV and paradoxical septal motion.
DIAGNOSIS ?
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Atrial Septal Defect (ASD) Exam (cc: “SOB”)
SEM LUSB Fixed splitting of S2 RV volume overload
Secundum: 70% IRBBB or RBBB, right axis NO SBE prophylaxis if isolated
Primum: IRBBB or RBBB, left axis Associated MV or TV disorders
Treatment: closure for Qp/Qs >1.5:1 or symptoms, in general
Surgical or percutaneous Amplatzer device – FDA approved 2001
1. Secundum
2. Primum
3. Sinus venosus
4. Coronary Sinus
4
2
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Patent Foramen Ovale PFO
Common: 20-30% of all patients Usually not patent if LA pressure > RA
pressure & not “stretched” Consider PFO or ASD if cryptogenic stroke in
a young patient• Especially with atrial septal aneurysm
Consider eval for clotting disorder Long-term warfarin (over ASA) for clinical
event Closure if recurrent event on anticoagulation
(FDA guidelines) or large shunt
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Ventricular Septal Defect
Most close in childhood spontaneously or surgically
+ Endocarditis prophylaxis Exam
• Loud murmur w/thrill (gr. 3-6), pan-systolic• Afterload dependent – increases with sustained
handgrip (like MR)• Large – pulmonary HTN (loud P2), RV heave
Treatment – closure if large
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Congenital Heart DiseaseOthers
Patent Ductus Arteriosus (PDA)
Preferential clubbing of toes (but not fingers) if R to left shunt
Tx: surgical ligation or other form of closure
Continuous “machine-gun murmur
Heard in infraclavicular fossa
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Congenital Heart DiseaseOthers
Coarctation of the Aorta
CXR• Loss of aortic knob• Rib notching due to collateral
recruitment Increased circle-of-Willis berry
aneurysms (CVA) Bicuspid AoV – 40-60% Turner’s Syndrome
Ejection click & SEM at LLSB Delayed femoral pulses Hypertension in arms
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Physical Exam Pearls…
Physiologic Splitting S2: splits with inspiration Persistently Split S2
Delayed closure of Pulmonic Valve Normal respiratory variation RBBB, PE, Pulmonic Stenosis, PVC from LV
Paradoxically Split S2 Splits during EXPIRATION Delayed closure of Aortic valve LBBB, Severe AS, RV pacemaker, PVC from RV
Fixed Splitting of S2: fixed A2-P2 = ASD Bisferens pulses: significant AI; HCM; AV
fistula
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Todd C. Villines, MD
Cardiology ServiceWalter Reed Army Medical Center
Cardiology Board Review Part II2008
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Outline – Part I
CAD Acute Coronary Syndromes (ACS) Chronic CAD
Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls
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Outline – Part II
CHF / Cardiomyopathies Arrhythmias & ECGs Pericardial Disease Peripheral Vascular Disease Preoperative Evaluation Miscellaneous Test Taking Strategies
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CHF – Systolic Dysfunction Most common:
Ischemic Hypertensive Dilated CM
Evaluation Cause usually evident
in history Extensive workup
usually not needed or revealing
Echo Ischemic evaluation Thyroid studies for all Consider iron studies
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Chronic Treatment Systolic CHF
ACE-I – all patients B-blockers: metoprolol sustained release,
carvedilol and bisoprolol Benefit in all classes – class I-IV if used
appropriately Start when patient is clinically stable and
euvolemic “Start slow & go slow”
Spironolactone (RALES): class III & IV – on other standard therapies
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Chronic Treatment Systolic CHF
Digoxin – sxs despite Ace-I, BB, diuretic & possibly spironolactone No reduced mortality Reduces symptoms & hospitalizations Careful in renal dysfunction
Warfarin – for afib, mechanical valve, embolic event (not just if depressed EF)
Can use amlodipine for BP – no effect on mortality No diltiazem or verapamil
Non-pharmacologic interventions
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Systolic DysfunctionTherapy Overview
xx
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Cardiac Resynchronization Therapy (CRT)“Biventricular Pacing”
Current Indications NYHA class III or IV heart failure LVEF ≤ 35% In NSR (not studied in afib) Evidence of ventricular dyssynchrony
• Currently: based on QRS width
• QRS > 120 msec– Most evidence in LBBB, but RBBB included
• FUTURE: echo evidence of dysynchrony better than ECG
Most also candidates for ICD
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CRT: CARE HF Trial
NYHA III or IV LVEF ≤ 35% In NSR QRS > 120 msec Bi-V –vs- Meds alone
Improved Symptoms CV Death CV Hospitalization Total Mortality
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Chronic Treatment Primary Diastolic CHF
Clinical syndrome of CHF with LVEF > 50% Causes – many: HTN, ischemia or infarct,
infiltrative diseases Amyloid on echo: “sparkling”, thick myocardium
Treatment – no consensus Treat HTN aggressively Lasix for symptoms Good rate control – esp. with a-fib Ace-I, BB No digoxin Address ischemia – if a factor
• Revascularization, nitrates, b-blockers
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CHF Exacerbation Acute Treatment
You know this stuff! Identify precipitating factors
• Ischemia, diet, arrhythmia, anemia, infection, thyroid, etc…
• Know drugs to avoid & that can exacerbate systolic CHF:
– Metformin, NSAIDS, Thiazoladinediones & ALL antiarrhythmic medications except Amiodarone
Standard therapies – common sense• Diuresis, afterload, nitrates, oxygen• Vasopressors & inotropes - if needed
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Sudden Death in the YoungThings to Think about
Hypertrophic Cardiomyopathy Anomalous coronary artery Inherited Long-QT syndrome
Sudden death with startling Brugada Syndrome RV Dysplasia Premature CAD Coronary Dissection Drug-induced (esp. cocaine) Idiopathic / Familial PE
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Hypertrophic Cardiomyopathy
History Often no symptoms 15-25% prior syncope – with exertion 20-30% chest pain Dyspnea, palpitations, fatigue
Physical Exam** (know this) Murmur: crescendo-decrescendo at LLSB Increased murmur with decreased LV cavity size
(decreased venous return) • with standing, valsalva or nitro
No radiation to neck and brisk carotid upstroke (unlike AS)
Also: MR, S4, prominent PMI
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Hypertrophic Cardiomyopathy ECG
LVH, LAD pseudoinfarct pattern (prominent septal q waves infero-
laterally) Echo
Concentric form Asymmetric form– commonly involving the septum (HOCM)
No competitive sports Tx:
B-blocker or CCB (control rate for filling) Surgical myectomy OR non-surgical ethanol septal ablation
if significant outflow gradient: ~5% of patients currently.
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Atrial Fibrillation
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Atrial Fibrillation Evaluation
ALL: thyroid studies, Echo & CXR Look for underlying cause of new onset or
accelerated rate in chronic afib patient Acute Management
Unstable = urgent cardioversion Stable
• Control Rate: BB, CCB 1st line– Digoxin – slower onset and not good for high adrenergic tone
• Anticoagulation – if able & indicated– Risk factors for CVA: CHF, increasing age, hx of HTN, diabetes,
hx of CVA/TIA, structural heart dz (LAE, significant valvular disease)
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Atrial Fibrillation New onset: known < 48 hours
Consider cardioversion • Anticoagulation (Lovenox, UFH)• Chemical: ibutilide best acutely
– risk of torsades with severe LV dysfunction
• Electrical - synchronized• Coumadin for 3-4 weeks after (“atrial stunning”)
> 48 hours or unknown: 2 choices Warfarin x 3-4 weeks then cardioversion TEE to r/o thrombus & cardioversion Coumadin for 3-4 weeks
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Atrial FibrillationAnticoagulation
Aspirin Lone = <65 yo, no structural heart disease, & no
HTN Contraindication to warfarin (intracranial bleed or
neoplasm, serious falls risk) All others get warfarin… ACTIVE-W: ASA + Plavix inferior to coumadin
Anticoagulation 3-4 weeks prior to elective cardioversion 3-4 week after cardioversion…at least
• In general, need long-term if indicated INR 2-3 for chronic & paroxysmal
• Similar risk for stroke!
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Atrial FibrillationAntiarrhythmic Therapy
Average efficacy of antiarrhythmics: 50-60% Rate control – vs- Rhythm control:
AFFIRM – no difference in QOL, stroke risk Increased strokes in rhythm control arm when
stopped warfarin because of recurrent afib
So…either option is fine if no symptoms but BOTH take warfarin if indicated (see prior slide)
Use of Antiarrhythmics:• Don’t tolerate a-fib hemodynamically (CHF patient,
restrictive cardiomyopathy, etc…)
• Symptoms of afib (palpitations) despite rate control
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Atrial FibrillationAntiarrhythmic Therapy
Amiodarone Best efficacy at maintaining NSR Least pro-arrhythmic Drug of choice if CAD or depressed EF Know: interacts with warfarin & digoxin (increases
potency of both) Know: side-effects
• Thyroid – baseline, at 3 months, then every 6 months• Pulmonary – baseline PFTs and CXR; CXR q 6 months.
PFTs with any symptoms or CXR change.• Liver – baseline LFTs and every 6 months• Corneal – baseline optho exam, then for symptoms
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Atrial Flutter
Treated similarly to atrial fibrillation (anticoagulation, rate control)
More difficult to rate control than fib Often coexists with atrial fibrillation Can be terminated with overdrive pacing Consider curative ablation if difficult to manage
Narrow complex & rate ~150: think flutter ?
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Multifocal Atrial Tachycardia
Pulmonary disease Theophylline Use Low K+ & Mg+
Treatment: underlying cause + :
Rate control – no digoxin No cardioversion if stable
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Re-entrant tachycardias: AVNRT, AVRT Therapy:
Acute & Stable: 1. Vagal maneuver. 2. Adenosine 6-12 mg IVP3. AV Nodal agents
Chronic – BB; most can be ablated if recurrent or frequent
PSVT
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Symptoms or A-fib: referral for ablation A-fib that is usually wide-complex and irregular Associated with Ebstein’s anomaly
Downward displacement of TV valve
Wolf-Parkinson-White 22 yo with a history of frequent palpitations
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A-fib in WPW: “Wide complex, irregular” Tx: IV Procainamide…NOT dilt, verapamil, b-blocker or digoxin!
Wolf-Parkinson-White 22 yo with “rapid heart beat” goes to ER. BP is stable.
Treatment?
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Wide-Complex Tachycardia
Wide-complex tachycardia VT –vs - SVT with aberrancy
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Wide-Complex Tachycardia
Assume VT History - older age, heart disease, CAD
AV-dissociation = VT Capture or Fusion beats = VT QRS duration: wider more likely VT RBBB with LAD – likely VT
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Atrial FibrillationAntiarrhythmic Therapy
PVC’s Never treat asymptomatic PVCs Risk of ventricular ectopy is related to underlying
structural heart disease
Know ACLS 2000 Guidelines re: WCT VF or pulseless VT
• Shock x 3, epi or vasopressin, then Amio (not lidocaine)
Stable, monomorphic VT• Procainamide• If depressed EF Amio
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A 35 yo male presents to the emergency room complaining of chest pain for the past 24 hours.
- Pain is worse when lying flat and worse with deep inspiration.
- No JVD. BP 136/76 Normal heart sounds except for a friction rub.
Acute Pericarditis: 1. Diffuse ST-elevation & 2. PR-depression
*may evolve to T-wave inversions (later)
Dx - at least 2:
1. Chest pain
2. ECG changes
3. Rub
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Acute Pericarditis
MANY Causes: Viral / Idiopathic – most
common Search for underlying
cause - guided by the history Don’t “pan-lab”! Consider HIV / ppd Usually not 1st
presentation of systemic disease
Echo all to rule-out large effusion
MB & Troponin + in up to 25% of
patients
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Chest Pain suggestive of Pericarditis
ECG Diagnostic ?
Age < 40 & no other suspected systemic illness or traumatic
ANY: JVD, Pulsus Paradoxus, +Cardiac Enzymes, Poor Pain
Control in ER, No social support
Admit / Reconsider
If YES to ANY =Admit + Echo
Consider:
1. MI2. Aortic Dissection 3. PE 4. Pneumothorax
5. Esophageal Rupture 6. Pancreatitis
Suspect Pericarditis ?YES
ECHO
NO
Large or Moderate Effusion
Small Effusion
-NSAIDS & F/U
NO
One Approach
(MKSAP)
Who to Admit ?
Admit:
- suspect serious underlying cause
(e.g. - uremic) or on
immunosuppressive
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Acute Pericarditis
Refractory symptoms: further diagnostic work-up Suspect Tb if persistent symptoms after 2
weeks and risk factors Treatment
NSAIDS Also, may use colchicine up front Steroids – ONLY if refractory and an
underlying cause has not been found• 7-10 day tapering course
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Despite treatment, the patient returns complaining of problems “catching his wind”.
- P 105 BP 90/60 PA Cath: RA 18mmHg PA 32/18 PCWP 19
- Physical Exam signs ?
- ECG Findings ?
- Echo Findings ?
- Treatment ?
- Etiologies ?
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Pericardial Effusion
Pericardiocentesis Indications Tamponade Hemopericardium Suspected bacterial or tuberculous
pericarditis• Pericardial window biopsy best to dx Tb
Rapid reaccumulation post-drainage
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55 yo F with hx of Breast CA treated with surgery & XRT 12 years ago complains of DOE x 1 yr.
- CXR: Recurrent R effusion. TTE – no effusion.
- BP 110/60 P 110. JVP 12 & increases with inspiration.
Which of the following is the next most appropriate test??:
a. Liver scan d. Spiral CT of lungs
b. Bilateral mammogram e. Transesophageal Echo (TEE)
c. MRI of heart
Dx: Constrictive Pericarditis Clinically: Suggestive history + signs of RV failure, DOE Exam:
Kussmaul (increased JVD with inspiration) – with prominent x & y descent of venous waves
Diastolic Knock (audible S3) RV overload signs
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Constrictive Pericarditis
Etiologies: XRT, post-surgery, post-pericarditis -
Tb, cocci (long-list) CXR: pericardial calcification on
lateral Best: CT or MRI - pericardial
thickening (>4-5mm) Echo in all to assess hemodynamics
TTE: insensitive to pericardial thickness PA Cath: equalization of pressures Treatment:
Pericardiectomy if severe symptoms & can tolerate the procedure
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pp
68 yo M found to have mid-line pulsatile mass.
Hx: HTN, CABG Rx: ASA, ramipril, atenolol, HCTZ
Careful ROS – no symptoms (no abd pain, back pain, etc)
P 78 BP 132/84 Ultrasound: 5.5 cm AAA below renals
Which is most appropriate at this time?
a. Increase B-blocker to pulse of 60 d. Increase ACE-I
b. Repeat u/s in 1 year e. Refer for surgical repair
c. Tell patient to limit physical activity
Dx: AAA Surgery
Abdominal: >4.5-5.0 cm or expanding (.5cm/6 mos or 1cm/yr) Thoracic AA & no sx’s: >6cm or compressing local structures
If no indication for surgery, serial u/s surveillance
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Carotid Disease
Know when to refer to surgery! AHA guidelines:
Symptomatic Patients• TIA or CVA past 6 mos + >70% stenosis of
ipsilateral carotid• Acceptable: Sx’s + 50-69% stenosis
Asymptomatic Patients• Stenosis 60% + surgical risk <3% + life-
expectancy > 5 years
Reminder: PVD = CAD for lipid management, risk-factor reduction
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Aortic Dissection Hx: “ripping” CP radiating to back
HTN, Marfan’s**, crack cocaine use, bicuspid aortic valve
Exam: HTN, AI murmur, muffled heart sounds if extends to pericardium
CXR – widened mediastinum Dx: TEE, CT or MRI
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Aortic Dissection - Treatment IV B-blocker (labetolol) first! – reduce sheer stress Nitroprusside if needed (SBP>100 after labetolol) &
only with b-blocker first! If ascending aorta involved (type A) = surgery Non-ascending aorta = medical therapy Beware – can involve coronary ostia (MI) Variant – Aortic intramural hematoma – treat the
same as dissection (no heparin / anti-coagulants)Classification
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Peripheral Arterial Disease
Atherosclerosis of arteries to legs ABI < 0.90 – good screening tool
Best if do before & after exercise Claudication: pain relieved with rest Pseudo-claudication with spinal stenosis: pain
relieved with SITTING (not standing still)
Vascular surgeries – high-risk surgeries; account for 70% of operative mortality Preop guidelines – know these!
Buerger disease (thromboangiitis obliterans) – medium/small artery necrosis ONLY if smokes
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77 yo male pre-op aorto-bifemoral bypass for severe PVD.
Hx: DM II, tobacco use. No hx of MI or heart problems.
Able to walk 1 city block slowly – limited by claudication.
ECG – inferior MI – age-undetermined.
What do you recommend to the surgeons?
a. Proceed to surgery – no further preop evaluation
b. Preop Catheterization & Revascularization if needed
c. Preoperative dipyridamole-thallium myocardial scintigraphy
d. Cancellation of surgery - surgical risk too high
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Pre-Operative EvaluationA Must Know!
Risk Stratify the Patient
Risk Stratify the Surgery
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Miscellaneous
Strep bovis endocarditis Order a colonoscopy
Cannon a-waves A-V dissociation
• Complete heart block, RV Pacing (not a-v sequential)
Reasons for endomyocardial biopsy Transplant rejection (rarely adriamycin
toxicity) Rarely done Low-yield in sarcoid; ETOH CM – use hx
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Test Taking Strategies
Rest prior to the test – they are long days Time is not an issue with this test (unlike the in-
service exams) If you don’t know, trust your training experience
& judgment “Is this how we would treat this patient at Walter
Reed?” “Is this how we do things here?”
You know this stuff & come from a premier program!
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Test Taking Strategies
Rely on your knowledge Don’t watch for patterns (“last 2 answers were C so
this one can’t be C”) Steady pace & don’t panic if you don’t know a
question My personal method:
Before reading the question, I quickly scan the answers to see what type of question is it
• Don’t actually read the answers or think about them yet.• e.g. - Are they asking for medicines or treatments ?,
diagnoses ?, best test to order ?, etc… This helps me pick up on what is important as I read
the often long clinical scenarios