Professional Documents
Culture Documents
6.21.10
Lisa Rose-Jones, MD
CAD
MKSAP Q 1
60 yo M present to ED w/ chest discomfort for 6
hrs. Tx w/ ASA, IV BB, and NTG. Chest pain
persists. Initial troponin and CK-MB are
elevated.
Pt taken ergently to Cath lab. Occlusion of prox
RCA. PCI is successfully. Following morning
doing well on rounds but progessively more
hypotensive. JVP elevated. Nml S1, S2. +S3,
brief systolic murmur along L sternal border.
ECG is unchanged from previous.
What is the most likely cause for this
patient’s current findings?
1. Heparin
2. Warfarin
3. Eptifbatide
4. Bivalirudin
5. Diltiazem
Early treatment w/ Glycoprotein 2b/3a
receptor blockade improves outcomes of
PCI. *Indicated only if high risk markers
(TIMI Score >3-4, +biomarkers, ST
depression, CHF, h/o of recent PCI, or
hemodynamic instability.
-Abciximab =only if undergoing PCI
-Eptifibitide or Tirofiban (if there is no clear
inidication that PCI will be performed)
1. Valsartan
2. Spironolactone
3. Amlodipine
4. Eplerenone
5. Hydralazine
SHF MEDS:
ACEi (or if intolerant, ARB)
~will usually tolerate a K to 5.5
B-blocker
Hydralazine/Nitrate combo if can’t tolerate an
ACEi or ARB, or adding specifically if african-
american
Spironolactone w/ NYHA class 3 or 4 symptoms
Eplerenone (aldo receptor antag) is useful in
reduced EF after AMI
REMEMBER for HEART FAILURE:
Digoxin alleviates Sx, reduceds
hospitalization 2/2 HF (not mortality)
Diurese HF pt w/ volume overload 1st,
then beta block
Put an AICD in a HF pt that comes in w/
unexplained syncope
Put a Biventricular Device in HF pt on
optimal therapy w/ continued symptoms
and QRS > 120 ms
Arrhythmias
Q 14
23 yo presents w/ palpitations during
exercise. Healthy, no meds. Exam and
resting ECG nml. Stress test shows
sustained monomorphic V tach @ 201
/min. No iscemic changes until arrhythmia
developed. The V tach had a Left bundle
and infoerior axis morphology.
Terminated spontanesouly 7 mins into
rest. ECHO nml, MRI nml.
What is the most likely etiology of V tach in
this patient?
1. Coronary spasm
2. Idiopathic
3. Arrhythmogenic R ventricular
cardiomyopathy
4. Infiltrative heart disease
5. Anomalous origin of the coronary arteries
Idiopathic V Tach (no structural heart
disease) carries a good prognosis. Tx
symptoms, BB first line.
Class IIa
1. Asymptomatic third-degree AV block w/ average awake ventricular rates of >/= 40
2. Asymptomatic type II second-degree AV block
3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found incidentally at
electrophysiological study for other indications
4. First-degree AV block with symptoms suggestive of pacemaker syndrome and documented
alleviation of symptoms with temporary AV pacing
Q 43
68 yo F comes to the ED b/c of racing heart
for past 2 hrs. Reports 2 yr history of
similar episodes. Been told by PMDs in
past to cough/strain, usually works but not
today. No chest pain, no other cardiac
history.
Exam shows BP of 110/60, HR 165, RR 20.
Lungs clear. Carotids w/o murmurs,
attempt massage w/o effect. ECG is
shown.
Which is the drug of choice for terminating
this patient’s arrhythmia?
1. Metoprolol
2. Verapamil
3. Adneosine
4. Digoxin
Q 122
26 yo nurse is evaluated in the ED after
episode of syncope. While working
stressfull day in the ICU, developed
tachycardia and then LOC. +palpitations in
past
Exam wnl. CXR wnl. ECG initially
unremarkable. 10 mins later, developed
brief tachycardia. Repeat ECG shown.
What is the most likely diagnosis in this
patient?
1. Atrioventricular nodal reentrant
tachycardia
2. Accelerated Idioventricular tachycardia
3. Atrioventircular reentrant tachycardia
4. Multifocal atrial tachycardia
AVNRT: >50% of all SVTs. Circuit involves the
AV node, so atria and Ventricle activated
simultaneously. So “p” wave usually buried in
QRS.
AVRT: Circuit involves an accessory pathway.
Most orthodromic: travels anterograde down AV
node, retrograde up accessory path. Some pts
w/ pre-excitation phenomena: during SR, see
short PR interval and delta wave (evidence of
pre-excitation)= *WPW
1. Reassurance
2. Begin a cardiac rehab program
3. HCTZ
4. Start statin therapy
5. Refer for Aortic valve replacement
Aortic Stenosis:
~Reassurance remains appropriate if asymptomatic
and nml exercise tolerance
~w/ severe stenosis the stiff valve doesn’t snap
shut, thus loose aortic component and get only a
single S2 (a physiologic split S2 has specificity of
72% of excluding severe AS)
~controling BP important, but use CAUTION w/ any
peripheral vasodilators b/c compensation in
Stroke Volume across a stenosed valve my be
difficult!!
~ Symptoms: Angina (5), Syncope (3), Heart
Failure (2)
Q 19
36 yo F in the ED w/ fever & dyspnea. 4 wks
of fever to 40C. +heroin use.
Exam: 39.6, 100/52, 70, 91% on RA. JVP
12. Bibasilar crackles. HR reg irregulsr. S1,
muffled s2. 2/6 diastolic murmur @ R 2nd
intercostal space. 1+ pretibial edema.
ECG shows a bifascicular block and Mobitz
II. ECHO shows 2 veges on aortic valve,
w/ leaflet perforation and severe AR.
Echoluceny in paravalvular region. Placed
on broad spectrum Abx.
What is the most appropriate treatment at
this time?
1. Esmolol IV
2. Heparin IV
3. Intraortic ballon pump (IABP)
4. Permanent pacemaker
5. Aortic Valve Replacement
Acute Aortic Regurgitation
Whether from endocarditis or Aortic
dissection, this is a SURGICAL
EMERGENCY!
Esmolol (short acting BB)can slow HR and
prolong diastolic filling to aid in forward
output in some pts w/ AR (this pt has sig
conduction abnml)
IABP is CONTRAINDICATED in AR
Q 44
32 yo M comes in for annual exam. No
personal or fmHx of cardiac disease.
Exam: s1/s2, +s4, 2/6 crescendo-
decrescendo systolic murmur heard best
at LLSB w/o radiation to carotids.
Increased intensity w/ valsalva. Isometric
hand grip, passive leg raising decreases
the intensity. Rapid upstrokes of
peripheral pulses are present.
What is the most likely diagnosis?
1. Mitral Valve Prolapse
2. Hypertrophic cardiomyopathy
3. Atrial septal defect
4. Ventricular Septal Defect
5. Aortic Stenosis
Hypertrophic Cardiomyopathy
If preload is increased (isometric hand grip,
stand-> squat) = increased systolic dimension of
LV and therefore less obstruction & diminished
murmur, Valsalva = decreased preload so
increased murmur
Tx even asymptomatic pts w/ BB, avoid
strenuous exercise
*different from hypertrophied athlete’s LV in
that septum is asymmetrically enlarged
REMEMBER:
ECHO for any Diastolic Murmur,
Continuous murmur, or > grade 3/6
Wide, Fixed split S2 think ASD
Secundum ASD can be prepared
percutaneously