Professional Documents
Culture Documents
April 2008
Todd C. Villines, MD Cardiology Service Walter Reed Army Medical Center
Outline Part I
CAD
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.
d. tPA
e. transfer to facility only 1.5 hrs away for primary angioplasty
Revascularization
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.
4.
(CK washout)
Primary PCI
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.
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
Major Bleeding
1.03 (0.15-7.13)
All (N=4500)
1.38 (1.01-1.87)
0.1
Fac. PCI Better
0.1
Fac. PCI Better
10
PPCI Better
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.
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).
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
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
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
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
Effects of Metoprolol
COMMIT (N = 45,852)
Totality of Evidence (N = 52,411)
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).
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
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.
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.
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.
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
25
36%
Odds Reduction
21.7
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
Clopidogrel better
Placebo better
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.
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.
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.
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
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)
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.
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)
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
NEW REC
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
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
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 *
* 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.
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
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.
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.
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.
d. Observation. Give
b. Atropine 0.5 mg IV
c. Atropine 1.0 mg IV
Inferior MI
Anterior MI
TV Pace:
A 68 yo male presents to your ER after 60 minutes of substernal chest pain, nausea and diaphoresis:
Outline
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
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
Non-STEMI / UA
Risk Stratification is key! Intermediate Risk In General:
Diabetics, PVD, Age >65
Low Risk
None of above Minimal risk factors Minimal or atypical symptoms
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
*
*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
Acute pulmonary edema, hypotension, new decrescendo systolic murmur at apex PA Catheter (wedged):
Afterload reduction
Nitrates IABP
Treatment:
Post-MI Complications
Inferior MIs (PDA) Due to single blood supply to postero-medial papillary muscle
Post-MI Complications
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
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
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
SCD-HeFT
ICD
Amiodarone
Placebo
Chronic CAD
The Big 4:
Statin Ace-I (HOPE & EUROPA trials vs- PEACE trial) 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)
Chronic CAD
Lipid Management
xx
*CAD Equivalents: - ASPVD Diabetes Multiple risk factors (Framingham > 20%)
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
Notes on Revascularization
2 Goals
PCI: better than medications for relief of angina & ischemia from obstructive CAD Stenting Complications:
>70% proximal LAD & proximal Left Circumflex Depressed EF Diabetics Depressed EF <OR> Treated diabetics
Stress Testing
Exercise ECG
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)
Stress Testing
Exercise ECG
Contraindications:
AS Others (common sense)
>2 mm
Stress Testing
Perfusion Imaging & Stress Echo
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.
7.
8.
Endocarditis 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
Oral
Amoxicillin Ampicillin
600 mg
20 mg/kg
500 mg 1 g IM or IV
15 mg/kg 50 mg/kg IM or IV
Aortic Stenosis
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
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
Treatment
Aortic Stenosis
Aortic Insufficiency
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:
Aortic Insufficiency
Acute!
Etiologies: endocarditis, aortic dissection, trauma, mechanical valve dysfunction Treatment: emergent surgery
Mitral Stenosis
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%
Mitral Regurgitation
Chronic
Dyspnea / CHF
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
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
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
Mitral Regurgitation
Acute MR
TR
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
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 ?
2 4
1. 2. 3. Secundum Primum Sinus venosus
4.
Coronary Sinus
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
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
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
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
Outline Part I
CAD
Outline Part II
CHF / Cardiomyopathies Arrhythmias & ECGs Pericardial Disease Peripheral Vascular Disease Preoperative Evaluation Miscellaneous Test Taking Strategies
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
Chronic Treatment
Systolic CHF
No diltiazem or verapamil
Non-pharmacologic interventions
Systolic Dysfunction
Therapy Overview
xx
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
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
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
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
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
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
Atrial Fibrillation
Consider cardioversion
Anticoagulation (Lovenox, UFH) Chemical: ibutilide best acutely
risk of torsades with severe LV dysfunction
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
Atrial Fibrillation
Antiarrhythmic Therapy
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
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
PSVT
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
Symptoms or A-fib: referral for ablation A-fib that is usually wide-complex and irregular Associated with Ebsteins anomaly
Wolf-Parkinson-White
Treatment?
A-fib in WPW: Wide complex, irregular Tx: IV ProcainamideNOT dilt, verapamil, b-blocker or digoxin!
Wide-Complex Tachycardia
Wide-complex tachycardia
Wide-Complex Tachycardia
Assume VT
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)
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
MANY Causes:
Dont pan-lab! Consider HIV / ppd Usually not 1st presentation of systemic disease
+ in up to 25% of patients
One Approach
(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
Acute Pericarditis
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
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
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:
CXR: pericardial calcification on lateral Best: CT or MRI - pericardial thickening (>4-5mm) Echo in all to assess hemodynamics
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
Abdominal: >4.5-5.0 cm or expanding (.5cm/6 mos or 1cm/yr) Thoracic AA & no sxs: >6cm or compressing local structures
Carotid Disease
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
Aortic Dissection
Exam: HTN, AI murmur, muffled heart sounds if extends to pericardium CXR widened mediastinum Dx: TEE, CT or MRI
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
Best if do before & after exercise Claudication: pain relieved with rest Pseudo-claudication with spinal stenosis: pain relieved with SITTING (not standing still)
Pre-Operative Evaluation
A Must Know!
Risk Stratify the Patient
Miscellaneous
Cannon a-waves
Transplant rejection (rarely adriamycin toxicity) Rarely done Low-yield in sarcoid; ETOH CM use hx
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?
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