Transcript Daily Report 09-14-2016

Daily Report
September 14, 2016
MARIN MCCUTCHEON, PGY-2
OLIVE VIEW MEDICAL CENTER
43 yo F who presents with chest
pain
Discussion: HPI
HPI
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Sharp pinching pain and pressure in left chest
Onset in am while at work (cleaning houses)
Constant
Worse with deep inspiration
Improved with Nitro
Does not radiate
Associated with dyspnea, worse with lying down and better when sitting
up
DOE with pinching sensation in chest
Reports angiography at OSH, adherent to all meds including
clopidogrel
Sxs are similar to MI but not as intense
PMH/PSH
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CKD stage II 2/2 PCKD
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HTN
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No surgeries
Medications
Clopidogrel 75mg daily
Atorvastatin 40mg nightly
MTP 25mg PO BID
ASA 81mg daily
HCTZ 12.5mg daily
Losartan 25mg PO BID
Discussion: Differential
Physical Exam
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VS: 36.7 HR 69 BP 157/94 RR 18 100% on RA
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Gen: NAD
HEENT: NCAT, PERRLA, EOMI, OP clear
CV: RRR, nl S1 S2 no MRG
Lungs: CTAB, no WRR
Abd: soft NTND, +BS, no guarding
Ext: WWP, trace edema BLE, +2 distal pulses
Neuro: A+Ox4, CN 2-12 intact, motor 5/5 throughout, sensation
grossly intact
Discussion: Orders
Labs
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WBC 12.4 / Hgb 12.9 / Plt 195
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Na 138 / K 3.0 / 103 / 28 / BUN 18/ Cr 0.88
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Trop <0.010 x 3
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ESR 16
CXR
EKG
TTE
Summary:
1. Left ventricle: Systolic function is normal. The estimated ejection
fraction is 60-65%. Wall motion is normal; there are no regional wall
motion abnormalities.
2. No significant valvular disease.
3. Pulmonary arteries: Systolic pressure is mildly increased, estimated to
be 37 mm Hg.
Discussion: Post-MI complication
MKSAP Question
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An 82-year-old man was admitted to the coronary care unit (CCU)
48 hours ago after a late presentation with anterior ST-elevation
myocardial infarction. The patient underwent coronary
angiography and was found to have an occluded proximal left
anterior descending coronary artery but did not undergo an
attempt at revascularization at the time of coronary angiography
because of his late presentation and symptomatic improvement.
Today, he felt faint and lost consciousness while visiting with his
family in the CCU.
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On physical examination, blood pressure is 72/54 mm Hg and pulse
rate is 108/min. Cardiac examination shows tachycardia with a
normal S1 and S2, new holosystolic murmur heard best at the left
lower sternal border that radiates to the apex, and a right
ventricular heave
Which of the following is the most appropriate
management?
A) Emergency cardiac surgery
B) Emergency pericardiocentesis
C) Percutaneous coronary intervention to left anterior
descending artery
D) Right heart catheterization and dopamine infusion
Medical Optimization
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Continued ASA, clopidogrel, atorvastatin, losartan
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Discontinued HCTZ
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Increased metoprolol
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Started isosorbide dinitrate
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Started Colchicine
Exercise Treadmill Test
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Clinically positive stress test with no evidence of ischemia
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Good cardiovascular condition for age and gender
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Abnormal clinical response to exercise as patient developed chest
pressure during exertion
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Normal exercise electrocardiogram
Myocardial Infarction
Complications
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Mechanical Complications
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Conduction Abnormalities
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Pericardial Complications
Time Course of Complications
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Hours – days: conduction abnormalities
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1-3 days: Peri-infarction pericarditis
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Days: Pericardial effusion
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Days – 2 weeks: Rupture of LV, IV septum
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Weeks – Months: Postcardiac Injury Syndrome
Mechanical Complications
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Rupture of LV free wall
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Rupture of interventricular septum
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Acute Mitral Regurgitation
Rupture of LV Free Wall
• Within 2 weeks post-MI: within first 5 days in 50% of
cases, within 2 weeks in 90% of cases
• RFs: no history of previous angina/MI, STE or Qs on
presenting EKG, peak CK-MB > 150  large transmural
infarct, absence of collateral blood flow
• Complete rupture  hemopericardium  acute onset
heart failure and shock  PEA  death
• Incomplete/subacute rupture: thrombus and
pericardium seal rupture
• s/s: persistent/recurrent chest pain, nausea,
agitation, transient hypoTN, EKG features of
pericardititis
• Dx: clinical, confirmed by TTE if time, pericardiocentesis
• Tx: hemodynamic support w IVF, inotropes,
vasopressors; pericardiocentesis, surgical repair
Rupture of Interventricular Septum
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Usually 3-5 days after MI (1 day – 2 weeks)
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RFs: 1V disease (esp wraparound LAD), large infarction, poor septal
collateral circulation, no previous MI
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Most: inf 1/3 of septum supplied by RCA
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Some: LAD extends past LV apex  wraps around to supply inferior
septum  ant MI 2/2 LAD lesion  decreased collaterals to septum and
larger septal infarction  STE in inf leads
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S/S: hemodynamic compromise
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Dx: PA catheter, TTE with Doppler
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Tx: afterload reduction, inotropes, diuretics, surgery
Acute Mitral Regurgitation
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2/2 ischemic papillary muscle displacement (dysfunction), LV
dilatation/aneurysm, papillary muscle rupture
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S/S: hemodynamic compromise, new systolic murmur
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Dx: TTE  flail segment of MV, TEE
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Tx: afterload reduction (nitrates, nitroprusside, diuretics), surgery
Conduction Abnormalities
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Inferior MI: sinus bradycardia, First degree AV block, Second degree
AV block Mobitz type 1
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Anterior MI: first degree AV block, Second degree Mobitz type II,
Third degree AV block
Pericardial Complications
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Early infarct-associated pericarditis (Peri-infarction pericarditis)
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Pericardial effusion (+/- tamponade)
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Postcardiac Injury Syndrome (Dressler’s syndrome)
Peri-infarction pericarditis
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Early cx  days after MI, self-limited
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S/S: pericardial friction rub, pleuritic chest pain
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Dx: clinical, EKG with ST segments remaining elevated and upright T
waves
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Evaluation: TTE to assess for pericardial effusion  if effusion > 10mm
thick  increased risk of free wall rupture or already with subacute
rupture that is contained
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Importance: a/w larger infarct  risk stratification
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Tx: supportive, ASA+Colchine, avoid NSAIDs/glucocorticoids
Pericardial Effusion
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Usually small, rarely with tamponade physiology
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Occurs within days  can take months for resorption
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S/S: usually asx
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Dx: TTE
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Importance: a/w higher morbidity/mortality  larger infarct
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Tx: supportive
Postcardiac Injury Syndrome (PCIS)
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Can occur after MI, cardiac surgery, PE
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Late cx  weeks – months after MI
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s/s: pleuritic CP, pericardial friction rub, fever, leukocytosis,
pericardial/pleural effusion
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Pathogenesis: immunologic: myocardial injury  release of cardiac
Ags  Ab formation  immune complexes  deposit onto
pericardium, pleura, lungs  inflammatory response
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Dx: clinical, ↑ESR, EKG
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Tx: NSAIDs, Colchine, steroids if refractory
Colchicine in Addition to Conventional Therapy for Acute Pericarditis:
Results of the COlchicine for acute PEricarditis (COPE) Trial 2005
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Inclusion criteria: acute pericarditis of idiopathic, viral, and autoimmune causes,
including postpericardiotomy syndromes and connective tissue diseases
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Acute pericarditis, 2+ of the following: typical chest pain, pericardial friction rub,
and widespread ST-segment elevation on the ECG
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ASA or ASA+Colchine
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ASA 800 mg PO q6-8h x 7 -10 days with taper over 3 - 4 weeks (group I)
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ASA at the same dose + colchicine 1.0 - 2.0 mg x 1 day, then 0.5 - 1.0 mg daily x 3
months (group II)
primary end point: recurrence rate
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recurrent pain + 1 or more: fever, pericardial friction rub, ECG changes, pericardial
effusion on TTE, elevations in the WBC, ESR, or CRP
Results of COPE trial
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2873 patient-months of follow-up
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Higher recurrence rate in patients treated only by aspirin (group I) v.
patients treated with colchicine plus conventional treatment (group
II), (33.3% versus 11.7%; P=0.009)
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Group II with longer symptom-free interval (22.9±10.3 versus
17.2±12.3 months; P=0.007).
References
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Khan, A. H. (1992), The postcardiac injury syndromes. Clin Cardiol,
15: 67–72.
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LeWinter, M et al. Pericardial complications of myocardial infarction.
Up To Date, accessed 9/13/2016.
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Massimo Imazio, et al. Colchicine in Addition to Conventional
Therapy for Acute Pericarditis. Circulation. 2005;112:2012-2016