Cardiology Board Review Part I

April 2008
Todd C. Villines, MD Cardiology Service Walter Reed Army Medical Center

Outline Part I

CAD

Acute Coronary Syndromes (ACS) Chronic CAD

Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls

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.

Which of the following should be done next ?:

a. clopidogrel 300 mg PO
b. eptifibatide IV c. eptifibatide + dose tPA

d. tPA
e. transfer to facility only 1.5 hrs away for primary angioplasty

Acute Coronary Syndromes

Revascularization

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
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.

.33 million
Admissions per year

ACS - Thrombolytics

ABSOLUTE Contraindications

Greatest benefit of thrombolytics in first 1-2 hours from symptom onset! (Golden Hour)

Thrombolytics
Relative Contraindications

ACS
Things you must know
1.

2.
3.

Rescue Angioplasty If no reperfusion in 60-90 mins. (20-40% will not reperfuse)

4.
(CK washout)

Accelerated Idioventricular Rhythm (AIVR)

If hemodynamically stable: no treatment!

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

Primary PCI

Primary PCI
I IIa IIb III

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.

I IIa IIb III

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.

Facilitated PCI

Meta-analysis: Facilitated PCI vs Primary PCI

Mortality Reinfarction
1.81 (1.19-2.77) 1.40 (0.49-3.98)

Major Bleeding

Lytic alone N=2953 IIb/IIIa alone N=1148 Lytic +IIb/IIIa N=399

1.43 (1.01-2.02) 1.03 (0.49-2.17) 3.07 (0.18-52.0)

1.03 (0.15-7.13)

All (N=4500)

1.38 (1.01-1.87)
0.1
Fac. PCI Better

1.71 (1.16 - 2.51)

1 10 0.1
PPCI Better Fac. PCI Better

1.51 (1.10 - 2.08 )

1 10
PPCI Better

0.1
Fac. PCI Better

10
PPCI Better

Keeley E, et al. Lancet 2006;367:579.

Facilitated PCI
I IIa IIb III

A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI is not recommended and may be harmful.

I IIa IIb III

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, and c. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight).

Rescue and Late PCI

Meta-analysis: Rescue PCI vs Conservative Tx

Outcome Mortality, % (n) HF, % (n) Reinfarction, % (n) Stroke, % (n) Rescue PCI 7.3 (454) 12.7 (424) 6.1 (346) 3.4 (297) Conservative RR (95% CI) Treatment 10.4 (457) 17.8 (427) 10.7 (354) 0.7 (295) 0.69 (0.461.05) 0.73 (0.541.00) 0.58 (0.350.97) 4.98 (1.1022.48) P .09 .05 .04 .04

Minor 16.6 3.6 4.58 <.001 bleeding, (313) (307) (2.468.55) % (n) 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)
Wijeysundera HC, et al. J Am Coll Cardiol. 2007;49:422-430.

Rescue PCI
A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is recommended in patients who have received fibrinolytic therapy and have:
I IIa IIb III

a. Cardiogenic shock in patients < 75 years who are suitable candidates for revascularization
I IIa IIb III

b. Severe congestive heart failure and/or pulmonary edema (Killip class III)
I IIa IIb III

c. Hemodynamically compromising ventricular arrhythmias.

Rescue PCI
I IIa IIb III

A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is reasonable in patients 75 years who have received fibrinolytic therapy, and are in cardiogenic shock, provided they are suitable candidates for revascularization.

Rescue PCI
I IIa IIb III

A strategy of coronary angiography with intent to perform rescue PCI is reasonable for patients in whom fibrinolytic therapy has failed (STsegment 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

Rescue PCI
I IIa IIb III

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.

Rescue PCI
I IIa IIb III

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.

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

Analgesia
I IIa IIb III

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.

Analgesia
I IIa IIb III

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.

Beta-Blockers

COMMIT: Study design

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

Effects of Metoprolol
COMMIT (N = 45,852)
Totality of Evidence (N = 52,411)

Death 13% P=0.0006

Increased early risk of shock

ReMI 22% P=0.0002

VF 15% P=0.002

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

Lancet. 2005;366:1622.

Beta-Blockers
I IIa IIb III

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).

I IIa IIb III 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
I IIa IIb III

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).

Anticoagulants
I IIa IIb III

I IIa IIb III

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)

Anticoagulants
For patients undergoing PCI after having received an anticoagulant regimen, the following dosing 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)
Recommendation continues on the next slide.

I IIa IIb III

Anticoagulants
I IIa IIb III

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.

I IIa IIb III

Anticoagulants
I IIa IIb III

Because of the risk of catheter thrombosis, fondaparinux should not be used as the sole anticoagulant to support PCI. An additional anticoagulant with anti-IIa activity should be administered.

ExTRACT-TIMI 25: Primary End Point (ITT) Death or Nonfatal MI

15

Primary End Point (%)

UFH
12

12.0% 9.9%

17% RRR
9

Enoxaparin
Relative Risk 0.83 (95% CI, 0.77 to 0.90) P<.001

Lost to follow-up = 3
0 0 5 10 15 20 25 30

Days after Randomization

Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354:1477-1488.

CLARITY-TIMI 28 Primary Endpoint:

Occluded Artery (or D/MI thru Angio/HD)
Occluded Artery or Death/MI (%)

25

36%
Odds Reduction

21.7

Odds Ratio 0.64

(95% CI 0.53-0.76)

20

15.0
15

P=0.00000036

10

5 n=1752 n=1739
0.4 0.6 0.8 1.0 1.2 1.6

Clopidogrel
LD 300 mg MD 75 mg

Placebo STEMI, Age 18-75

Clopidogrel better

Placebo better

Sabatine N Eng J Med 2005;352:1179.

COMMIT: Effect of CLOPIDOGREL on Death In Hospital

Placebo + ASA: 1,846 deaths (8.1%)
Clopidogrel + ASA: 1,728 deaths (7.5%) Dead (%)
0.6% ARD 7% RRR P = 0.03

N = 45,852 No Age limit ; 26% > 70 y Lytic Rx 50% No LD given

Chen ZM, et al. Lancet. 2005;366:1607.

Days Since Randomization (up to 28 days)

Thienopyridines
I IIa IIb III

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.

I IIa IIb III

Thienopyridines
I IIa IIb III

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.

I IIa IIb III

Anticoagulants
I IIa IIb III

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.

I IIa IIb III

I IIa IIb III

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.

Invasive Evaluation
I IIa IIb III

I IIa IIb III

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)

Secondary Prevention

Ask, advise, assess, and assist patients to stop smoking I (B) Clopidogrel 75 mg daily:

PCI I (B) no PCI IIa (C) LDL-C < 100 mg/dL I (A) consider LDL-C < 70 mg/dL IIa (A)

Statin goal:

Daily physical activity 30 min 7 d/wk, minimum 5 d/wk I (B) Annual influenza immunization I (B)

Secondary Prevention and Long Term Management

Goals Class I Recommendations
Lipid A fasting lipid profile should be assessed in all patients management: and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized 2007 goal: patients, initiation of lipid-lowering medication is indicated LDL-C << than as recommended below before discharge according to 100 mg/dL (if TG the following schedule: 200 mg/dL, nonHDL-C < 130 LDL-C should be < 100 mg/dL. mg/dL Further reduction to < 70 mg /dL is reasonable. (Class
IIa; LOE: A) NEW 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 LDLlowering 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)
NEW

Secondary Prevention and Long Term Management

Goals
Lipid management: (TG 200 mg/dL or greater) Primary goal: NonHDL-C < 130 mg/dL

Class I Recommendations
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, nonHDL-C target should be less than 130 mg per dL. If TGs are 200 to 499 mg/dL, nonHDL-C target is < 130 mg/dL. (Class I; LOE: B); further reduction of nonHDL-C to < 100 mg dL is reasonable. (Class IIa; LOE: B)

NEW Therapeutic options to reduce nonHDL-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 indicated and useful to prevent pancreatitis are fibrate or niacin before LDL-lowering rx; and treat LDL-C to goal after TGlowering rx. Achieving nonHDL-C < 130 mg/dL is recommended.

Secondary Prevention and Long Term Management

Goals
Physical activity: 2007 Goal: 30 min 7 d per wk; minimum 5 d per wk

Class I Recommendations
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 moderateintensity 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.

NEW

Encouraging resistance training 2 d per week may be reasonable (Class IIb; LOE: C)

Secondary Prevention and Long Term Management

Goals Class I Recommendations

Antiplatelet agents/ For all post-PCI STEMI stented patients anticoagulants: without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162 to 325 mg daily Aspirin
should be given for at least 1 month after baremetal 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.
CHANGED TEXT

Secondary Prevention and Long Term Management

Goals Antiplatelet agents/ anticoagulants: Aspirin Recommendations In patients where the physician is concerned about the risk of bleeding lowerdose 75 to 162 mg of aspirin is reasonable during the initial period after stent implantation. (Class IIa; LOE: C)

NEW REC

Secondary Prevention and Long Term Management

Goals Antiplatelet agents/ anticoagulants: Clopidogrel Class I Recommendations

For all post-PCI patients who receive a drug-eluting stent (DES), clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a bare metal stent (BMS), clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks).

CHANGED TEXT

Secondary Prevention and Long Term Management

Goals Antiplatelet agents/ anticoagulants: Clopidogrel 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)

NEW RECS

Secondary Prevention and Long Term Management

Goals Antiplatelet agents/ anticoagulants: Warfarin
NEW REC

Class I Recommendations
Managing 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). CHANGED
TEXT

Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely. In patients requiring warfarin, clopidogrel, and aspirin 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.

NEW REC

Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal Symptoms with Known Cardiovascular Disease or Risk Factors for Ischemic Heart Disease Acetaminophen, ASA, tramadol, narcotic analgesics (short term) Nonacetylated salicylates Non COX-2 selective NSAIDs NSAIDs with some COX-2 activity
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.

Select patients at low risk of thrombotic events Prescribe lowest dose required to control symptoms Add ASA 81 mg and PPI to patients at increased risk of thrombotic events *

COX-2 Selective NSAIDs

* Addition of ASA may not be sufficient protection against thrombotic events Antman 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.

Secondary Prevention and Long Term Management

Goals
ReninAngiotensinAldosterone System Blockers: ACE Inhibitors
NEW REC

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. CHANGED
TEXT

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)

NEW REC

Secondary Prevention and Long Term Management

Goals
ReninAngiotensinAldosterone System Blockers: ARBs
NEW REC

Class I Recommendations
Use of ARBs is recommended in patients who are intolerant of ACE inhibitors and have HF or have had a STEMI with LVEF 40%. CHANGED
TEXT

It is beneficial to use ARB therapy in other patients who are ACE-inhibitor intolerant and have hypertension.

NEW REC

Considering use in combination with ACE inhibitors in systolic dysfunction HF may be reasonable.

Secondary Prevention and Long Term Management

Goals
ReninAngiotensinAldosterone System Blockers: Aldosterone Blockade
CHANGED TEXT

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.

Secondary Prevention and Long Term Management

Goals BetaBlockers Class I Recommendations It is beneficial to start and continue betablocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without HF symptoms, unless contraindicated.
CHANGED TEXT

A 55 yo male presents to your rural ER with 1-hour of substernal 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 b. Start nitroglycerin drip c. Dopamine drip d. IV fluid bolus e. Place a PA catheter

A 55 yo male presents to your rural ER with 1-hour of substernal 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.

Mobitz I, 2nd-degree AVB (Wenckebach)

a. Place a transvenous pacemaker

d. Observation. Give

b. Atropine 0.5 mg IV
c. Atropine 1.0 mg IV

atropine if develops sxs or

hemodynamic change.

Transvenous Pacing & MI Location

Inferior MI

Anterior MI

Sinus bradycardia (Bezold-Jarish) common Block at AV node

Stable escape rhythm AV block is usually transient & welltolerated

Block usually below AV node

TV Pace:

TV Pace: Mobitz II or higher &:

Symptoms that are unresponsive to atropine

New bifasicular block Mobitz II or worse regardless of symptoms

A 68 yo male presents to your ER after 60 minutes of substernal chest pain, nausea and diaphoresis:

Outline

Hx: HTN, DM, HLD, Distant MI

P 96 BP 146/92 RRR w/+S4. No murmur. Lungs clear.

Arrhythmias & ECGs

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 b. Stress Echo c. Cardiac Catheterization d. Myocardial Perfusion Imaging e. None of the above

Post MI Risk Stratification

What is the overall best predictor of survival post-MI?:

LV Ejection Fraction (EF)

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
*Dont give thrombolytics in NSTEMI!

High Risk
(+) enzymes

GIIb/IIIa Early invasive

- Cath during initial Hospitalization

Dynamic ECG changes

Clinical CHF Depressed LV EF

Non-STEMI / UA
Risk Stratification is key! Intermediate Risk In General:
Diabetics, PVD, Age >65

Prior MI (hx or q-waves on ECG)

Aspirin use Rest angina, < 20 minutes No dynamic ST changes

Best medical therapy In general: Noninvasive risk stratification Cath for:

High-risk noninvasive testing results Pre-existing lifestyle-limiting angina

Baseline pathologic q-waves

Negative enzymes

Low Risk
None of above Minimal risk factors Minimal or atypical symptoms

MI: Initial Medical Therapy

*162-325mg

Heparin: *60 U/kg bolus then 12U/Kg/Hr in patients given lytics or IIb/IIIA

*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

MI: Initial Medical Therapy

*
*Warfarin x 3-6 months: LV thrombus, large anterior MI with akinetic anterior wall. -Dont give warfarin to a patient simply with a depressed EF without Afib or embolism or thrombus (controversial)

Post-MI Complications

Papillary Muscle Rupture

Acute pulmonary edema, hypotension, new decrescendo systolic murmur at apex PA Catheter (wedged):
Afterload reduction
Nitrates IABP

Treatment:

Emergent surgical repair

Post-MI Complications

Papillary Muscle Rupture

Inferior MIs (PDA) Due to single blood supply to postero-medial papillary muscle

Post-MI Complications

LV Free Wall Rupture:

Acute hypotension, JVD, muffled heart sounds Equalization of diastolic pressures on PA catheter Large, STEMI, 1st MI, Anterior MI (LAD) Less common with early reperfusion but may occur earlier (classically ~7d) Treatment: emergent surgery, pericardiocentesis, supportive measures

Post-MI Complications

Ventricular Septal Rupture (Acute VSD):

Hypotension, JVD, holosystolic murmur with a thrill PA catheter: step up in oxygen saturation from RA to RV
Location less important: Anterior = Inferior Treatment
Unstable patient = urgent surgery Afterload reduction, IABP, supportive measures

SCD Prevention Post-MI

Primary Prevention

Referral for AICD if (MADIT I):

MADIT II: Prior MI + EF 30%

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
No EP study

1 SCD Prevention
Non-ischemic Cardiomyopathy
All-cause mortality at 5 years
Amiodarone vs placebo HR 1.06, p=0.529 ICD vs placebo HR 0.77, p=0.007
34.1% 28.9%

40% 35%

35.8%

% Mortality

30% 25% 20% 15% 10% 5% 0%

SCD-HeFT

non-ischemic EF 35% Amio = Placebo

ICD

Amiodarone

Placebo

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) Recent change: 1 spray, if not gone 911 / ER

Nitrates (know dosing, tolerance)

Non-dihydropyridine CCB (e.g,. amlodipine) may use with B-blocker No estrogen for CAD: primary prevention (WHI) or secondary prevention (HERS)

Chronic CAD

Know methods to reduce risk (Board Favorites!):

Smoking cessation Diet Weight loss Exercise Lipid management

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

Lipid Management

LDL goal get there 1st!

HDL and TGs are secondary targets

Once LDL to goal:

Non-HDL chol. goal: 30 higher than LDL goal
(LDL+VLDL+TGs) incorporates all atherogenic particles

Low HDL (<40 men, <50 women)

Exercise, smoking cessation Niacin (most potent), fibrates

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!!

Indications for CABG

Left Main > 50% Left main equivalent:

>70% proximal LAD & proximal Left Circumflex Depressed EF Diabetics Depressed EF <OR> Treated diabetics

3 vessel obstructive CAD, especially if:

2 vessel CAD with proximal LAD disease &

Dont stent the left main

Stress Testing
Exercise ECG

Sens & Spec = ~ 70% Bayesian approach to using for diagnosis:

High pre-test probability: negative test wont change management Low pre-test probability: false + > true + Best: intermediate pre-test probability LBBB, paced rhythm use pharm stress Uninterpretable ECG: ST-dep >1mm (e.g. LVH) Inability to exercise Prior revascularization (to localize)

Go directly to imaging (for diagnosis):

Stress Testing
Exercise 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

Stress Testing
Perfusion Imaging & Stress Echo

More expensive Increased sensitivity & specificity Bayesian approach

Low-pre-test probability + positive stress ECG Patients with prior revascularization Multiple defects, Large defects, increased lung uptake, transient ischemic dilation of LV cavity

Localizes ischemia Poor prognosis: Normal study has good prognosis Adenosine / Persantine: avoid if COPD, asthma

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

Endocarditis Prophylaxis
No prophylaxis:
1. 2. 3. Bicuspid AoV Acquired valvular heart disease Prior surgical valve repair

4.
5. 6.

Isolated SECUNDUM ASD

Surgically repaired ASD, VSD or PDA Pacemakers, defibrillators

7.
8.

History of rheumatic disease without valvular dysfunction

Deliver or C-section

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

Endocarditis Prophylaxis
No Post-treatment
Situation Agent

Regimen: single dose 30 to 60 min before procedure

Adults Children 50 mg/kg 50 mg/kg IM or IV 2g 2 g IM or IV

Oral

Amoxicillin Ampicillin

Unable to take oral medication

OR Cefazolin or ceftriaxone Cephalexin* OR 1 g IM or IV 2g 50 mg/kg IM or IV 50 mg/kg

Allergic to penicillins or ampicillin - oral

Clindamycin OR Azithromycin or clarithromycin Cefazolin or ceftriaxone

600 mg

20 mg/kg

500 mg 1 g IM or IV

15 mg/kg 50 mg/kg IM or IV

Allergic to penicillins or ampicillin and unable to take oral medication

OR Clindamycin 600 mg IM or IV 20 mg/kg IM or IV

Aortic Stenosis

History: angina, syncope, CHF (classic triad) Exam:

Crescendo-decrescendo murmur Best at RUSB; may be heard at apex (Gallavardins) 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

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

Aortic Stenosis

Bleeding tendency:

Increased colonic angiodysplasia Acquired vonWillebrand disease Usually done to eval for obstructive CAD in patients referred for aortic valve replacement No medical treatment Beware of vasodilators or diuretics (decrease preload) Symptoms = surgery! No role for balloon valvuloplasty

Cath: not needed to confirm echo data

Treatment

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

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.

Aortic Insufficiency

Chronic History well-tolerated until severe

CHF symptoms when severe Wide pulse pressure accounts for myriad of peripheral pulsating organs
Water-hammer pulses, etc

Exam:

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

Aortic Insufficiency
Chronic

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 cant take coumadin

Aortic Insufficiency
Acute!

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

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)
Dont tolerate tachycardia well due to transmitral pressure

Exam:

Loud S1 Opening snap in early diastole (after S2) Diastolic rumble Loud P2 if pulmonary hypertension

Mitral Stenosis

ECG:

LAE, RAE RVH (RAD) - No LVH 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

Treatment

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.

Mitral Regurgitation
Chronic

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)

Mitral Regurgitation
Chronic

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

Mitral Regurgitation
Mitral Valve Prolapse

Most common valvular cause of MR & need for MVR Exam:

Mid-systolic click followed by murmur (clickmurmur 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

Mitral Regurgitation
Mitral 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

Mitral Regurgitation
Acute MR

Most common cause: endocarditis Also:

Ischemic Ruptured chord in severe MVP

Large V-waves on PA catheter Decrescendo systolic murmur at apex

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

Noonans syndrome: low-set ears + PS Tx balloon valvuloplasty

Congenital Heart Disease

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.

Atrial Septal Defect (ASD)

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 ?

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

2 4
1. 2. 3. Secundum Primum Sinus venosus

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

4.

Coronary Sinus

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

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

Congenital Heart Disease

Others

Patent Ductus Arteriosus (PDA)

Continuous machine-gun murmur Heard in infraclavicular fossa Preferential clubbing of toes (but not fingers) if R to left shunt Tx: surgical ligation or other form of closure

Congenital Heart Disease

Others

Coarctation of the Aorta

Ejection click & SEM at LLSB Delayed femoral pulses Hypertension in arms CXR
Loss of aortic knob Rib notching due to collateral recruitment

Increased circle-of-Willis berry aneurysms (CVA) Bicuspid AoV 40-60% Turners Syndrome

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 Splits during EXPIRATION Delayed closure of Aortic valve LBBB, Severe AS, RV pacemaker, PVC from RV

Paradoxically Split S2

Fixed Splitting of S2: fixed A2-P2 = ASD Bisferens pulses: significant AI; HCM; AV fistula

Cardiology Board Review Part II 2008

Todd C. Villines, MD Cardiology Service Walter Reed Army Medical Center

Outline Part I

CAD

Acute Coronary Syndromes (ACS) Chronic CAD

Valvular Heart Disease Congenital Heart Disease Physical Exam Pearls

Outline Part II

CHF / Cardiomyopathies Arrhythmias & ECGs Pericardial Disease Peripheral Vascular Disease Preoperative Evaluation Miscellaneous Test Taking Strategies

CHF Systolic Dysfunction

Most common:

Ischemic Hypertensive Dilated CM Cause usually evident in history Extensive workup usually not needed or revealing Echo Ischemic evaluation Thyroid studies for all Consider iron studies

Evaluation

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

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

Systolic Dysfunction
Therapy Overview

xx

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

CRT: CARE HF Trial

NYHA III or IV LVEF 35% In NSR QRS > 120 msec Bi-V vs- Meds alone Symptoms CV Death CV Hospitalization Total Mortality

Improved

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

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

Sudden Death in the Young

Things 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

Hypertrophic Cardiomyopathy

History

Often no symptoms 15-25% prior syncope with exertion 20-30% chest pain Dyspnea, palpitations, fatigue Murmur: crescendo-decrescendo at LLSB Increased murmur with decreased LV cavity size (decreased venous return)
with standing, valsalva or nitro

Physical Exam** (know this)

No radiation to neck and brisk carotid upstroke (unlike AS) Also: MR, S4, prominent PMI

Hypertrophic Cardiomyopathy

ECG

LVH, LAD pseudoinfarct pattern (prominent septal q waves infero-laterally) Concentric form Asymmetric form commonly involving the septum (HOCM)

Echo

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.

Atrial Fibrillation

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)

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

Atrial Fibrillation
Anticoagulation

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 3-4 weeks prior to elective cardioversion 3-4 week after cardioversionat least
In general, need long-term if indicated

Anticoagulation

INR 2-3 for chronic & paroxysmal

Similar risk for stroke!

Atrial Fibrillation
Antiarrhythmic 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

Soeither option is fine if no symptoms but BOTH take warfarin if indicated (see prior slide) Use of Antiarrhythmics:
Dont tolerate a-fib hemodynamically (CHF patient, restrictive cardiomyopathy, etc) Symptoms of afib (palpitations) despite rate control

Atrial Fibrillation
Antiarrhythmic 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

Atrial Flutter

Narrow complex & rate ~150: think 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

Multifocal Atrial Tachycardia

Pulmonary disease Theophylline Use Low K+ & Mg+

Treatment: underlying cause + : Rate control no digoxin No cardioversion if stable

PSVT

Re-entrant tachycardias: AVNRT, AVRT Therapy:

Acute & Stable: 1. Vagal maneuver. 2. Adenosine 6-12 mg IVP 3. AV Nodal agents Chronic BB; most can be ablated if recurrent or frequent

Wolf-Parkinson-White

22 yo with a history of frequent palpitations

Symptoms or A-fib: referral for ablation A-fib that is usually wide-complex and irregular Associated with Ebsteins anomaly

Downward displacement of TV valve

Wolf-Parkinson-White

22 yo with rapid heart beat goes to ER. BP is stable.

Treatment?

A-fib in WPW: Wide complex, irregular Tx: IV ProcainamideNOT dilt, verapamil, b-blocker or digoxin!

Wide-Complex Tachycardia

Wide-complex tachycardia

VT vs - SVT with aberrancy

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

Atrial Fibrillation
Antiarrhythmic Therapy

PVCs

Never treat asymptomatic PVCs Risk of ventricular ectopy is related to underlying structural heart disease
VF or pulseless VT
Shock x 3, epi or vasopressin, then Amio (not lidocaine)

Know ACLS 2000 Guidelines re: WCT

Stable, monomorphic VT
Procainamide If depressed EF Amio

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.
Dx - at least 2: 1. 2. 3. Chest pain ECG changes Rub

Acute Pericarditis: 1. Diffuse ST-elevation & 2. PR-depression *may

evolve to T-wave inversions (later)

Acute Pericarditis

MANY Causes:

Viral / Idiopathic most common

Search for underlying cause - guided by the history

Dont 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

One Approach

Chest Pain suggestive of Pericarditis

Consider: 1. MI 2. Aortic Dissection 3. PE 4. Pneumothorax 5. Esophageal Rupture 6. Pancreatitis Suspect Pericarditis ? YES ECG Diagnostic ? NO

(MKSAP)
Who to Admit ?
Admit: - suspect serious
underlying cause (e.g. - uremic) or on immunosuppressive

Admit / Reconsider
ECHO

Age < 40 & no other suspected systemic illness or traumatic ANY: JVD, Pulsus Paradoxus, +Cardiac Enzymes, Poor Pain Control in ER, No social support NO

If YES to ANY =Admit + Echo

Large or Moderate Effusion

Small Effusion -NSAIDS & F/U

Acute Pericarditis

Refractory symptoms: further diagnostic work-up

Suspect Tb if persistent symptoms after 2 weeks and risk factors NSAIDS Also, may use colchicine up front Steroids ONLY if refractory and an underlying cause has not been found
7-10 day tapering course

Treatment

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 ?

Pericardial Effusion

Pericardiocentesis Indications

Tamponade Hemopericardium Suspected bacterial or tuberculous pericarditis

Pericardial window biopsy best to dx Tb

Rapid reaccumulation post-drainage

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 c. MRI of heart

e. Transesophageal Echo (TEE)

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

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

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) pp 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 b. Repeat u/s in 1 year c. Tell patient to limit physical activity

d. Increase ACE-I e. Refer for surgical repair

Dx: AAA Surgery

Abdominal: >4.5-5.0 cm or expanding (.5cm/6 mos or 1cm/yr) Thoracic AA & no sxs: >6cm or compressing local structures

If no indication for surgery, serial u/s surveillance

Carotid Disease

Know when to refer to surgery! AHA guidelines:

Symptomatic Patients
TIA or CVA past 6 mos + >70% stenosis of ipsilateral carotid Acceptable: Sxs + 50-69% stenosis

Asymptomatic Patients
Stenosis 60% + surgical risk <3% + lifeexpectancy > 5 years

Reminder: PVD = CAD for lipid management, risk-factor reduction

Aortic Dissection

Hx: ripping CP radiating to back

HTN, Marfans**, 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

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

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

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

Pre-Operative Evaluation
A Must Know!
Risk Stratify the Patient

Risk Stratify the Surgery

Miscellaneous

Strep bovis endocarditis

Order a colonoscopy A-V dissociation

Complete heart block, RV Pacing (not a-v sequential)

Cannon a-waves

Reasons for endomyocardial biopsy

Transplant rejection (rarely adriamycin toxicity) Rarely done Low-yield in sarcoid; ETOH CM use hx

Test Taking Strategies

Rest prior to the test they are long days Time is not an issue with this test (unlike the inservice exams) If you dont 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!

Test Taking Strategies

Rely on your knowledge

Dont watch for patterns (last 2 answers were C so this one cant be C)

Steady pace & dont panic if you dont know a question My personal method:

Before reading the question, I quickly scan the answers to see what type of question is it
Dont 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