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Internal Medicine Review ABIM part 1
10 studiers in 3 days Leave the first rating
Students also studied
Flashcard sets Study guides Practice tests
APHY102 FINAL IM EOR Doppler part 2 SPI review He
128 terms 410 terms 16 terms 1,9
Harding28 Preview kalyn1600 Preview sarahlegg258 Preview
Terms in this set (589)
Flat or Down sloping
What is a positive stress test St-segment depression >1 mm
occurring 80 msec after j point
St segment depression > 2 mm,
ventricular tachycardia,
drop in SBP > 15,
When to stop a stress test
CP,
dyspnea,
lightheadedness
Stress test of choice with a LBBB or Myocardial perfusion imaging with adenosine,
ventricular pacing? NOT exercising!
History of VT,
severe HTN,
When to not use doutamine for stress
Low BP,
poor echo images
Bronchospasm,
severe valvular dysfunction,
When to not use adenosine for stress severe carotid stenosis,
2nd degree heart block, t
heophylline dependent
RA <8
RV 30/8
Normals for PA catheter pressures
PCWP 3-12
PAP 12--12
Diastolic pressures tamponade
elevated & equalized or restrictive pericarditis
in all chambers,
low BP
Elevated RA and PA pressures, RV MI
decreased or nl PCWP,
hypotension
,Elevated PCWP, RA pressure cardiogenic shock
decreased SBP/cardiac output
high RA, mitral stenosis with RV failure
PA very elevated
high PCWP
nl SBP
Elevated PAP, RAP pulmonary HTN
nl PCWP, SBP
decr in SBP>10mmHg with nl inspiration; pulsus paradoxus:
palpated as weakened pulse with Constrictive or restrictive pericarditis,
inspiration & asthma,
more heart contractions to pulse beats tension pneumothorax
What gives you pulsus bisferiens Aortic regurgitation,
(two systolic peaks per cycle) HOCM
What causes pulsus alternans Severe LV dysfunction
What causes pulsus tardus Aortic stenosis
-standing/valsalva:
decreased cardiac filling,
decreases most murmurs
except MVP and HOCM
-squatting/ lying down:
How do positional maneuvers affect
increase cardiac volume,
blood flow and murmurs
increased murmurs
except MVP, HOCM
-sustained handgrip:
increases systemic resistance
decreases murmur in HOCM, AS
Increased blood volume in the RV
What causes a physiologic split S2 prolongs systole and
delays pulmonary valve closure
Pulmonary stenosis,
PE,
LV pacer,
What causes a fixed split S2 RBBB,
MR (early AV closure),
ASD,
RV failue
LBBB,
What causes a paradoxic split S2 RV pacing,
HOCM
Rapid LV filling:
What causes an S3? acute ventricular decompensation,
severe AR or MR
A wave - atrial contraction
X descent - atria relax, RV fills rapidly
Bottom of x descent is TC valve closure
What are the parts of the venous
waveform?
V wave - ventricle contacting against closed TC valve
Y descent - TC valve opens,
passive emptying into ventricle
, Pulmonary HTN,
What gives elevated a and v waves
RV infarction
Large r side v waves Septal rupture
TR (right),
Large v waves
MR (left)
Constrictive pericarditis,
restrictive cardiomyopathy,
Rapid x and y descent
tamponade
(x descent only, loss of y descent)
TS,
Large a waves severe RVH (on right),
MS
AV disassociation -
Cannon a waves complete heart block,
ventricular pacing
Slow Y descent Delayed atrial emptying - TS
Most important prognostic factor with Degree of LV dysfunction
CAD
MI,
pericarditis,
LV aneurysm,
Causes of resting ST elevation LBBB,
ventricular pacing,
LVH,
early repolarization
myocardium near the infarction may be underperfused but not necrotic-
Hibernating myocardium the metabolism of the cells adapts to low energy supplies & are nonfunctional
until perfusion is restored
the re-estab of blood flow after a coronary artery is blocked,
Reperfusion injury which may further damage the heart tissue due to the formation of O2 free
radicals
prolonged post ischemic dysfunction,
Stunned myocardium salvaged by reperfusion,
several days
NSTEMI have _____ initial mortality, Lower,
but have the _____ one year mortality as a Same
STEMI
Persistent angina,
NSTEMI have a higher risk of these vs.
reinfarction, and
STEMI
death within several months
MR due to papillary muscle rupture is Inferior
most common with MI in this region
Junctional escape,
Types of arrythmias with IWMI Mobitz I,
and they are usually temporary
Mobitz II,
Types of arrythmias with AWMI BBB.
More of the myocardium is involved
, Bradycardia, hypotension,
2nd or 3rd degree AVB,
Contraindications for B-blockers pulmonary edema,
asthma.
NOT DM
Contraindications to B blockers,
When to use non-dihydropyridne CCBs in
continued ischemia,
ACS
but NO LV dysfunction
Not with UA/NSTEMI:
increases mortality
When to use fibrinolytics in ACS
Use in STEMI,
new LBBB if no contraindications
and immediate PCI not available
Plavix
Lipid and BP control
DC NSAIDs except ASA
What to give pt with UA/NSTEMI ASA, O2, B-blocker, nitrate prn
Heparin, enoxaparin, Fondaparanux, or bilavirudin
Gp IIa/IIIb if immediate PCI planned
NO FIBRINOLYTICS!
CHF or hemodynamic instability,
When to do urgent PCI with UA/NSTEMI recurrent or refractory angina,
life threatening arrythmias
elevated troponin,
dynamic ST changes,
DM,
GFR < 60,
When to use invasive therapy within 48
EF < 40%,
hrs with UA/NSTEMI
Early post-MI angina,
PCI in last 6 months,
prior MI / CABG,
intermediate/ high risk score
no indications for invasive therapy,
When to use conservative therapy with good response to initial treatment,
UA/NSTEMI low risk post-ACS stress testing.
Has the same 1 yr mortality
give NTG and CCBs
If no better, do cath
If cath not available, give fibrinolytics
Cocaine/ meth use and UA/NSTEMI
No cath if no ST/T changes,
neg stress, & neg biomarkers
no stent: ASA 75-162mg lifelong + Clopidogrel x 1-12 month
Bare metal: ASA 162-325 x 1 mo,
then 75-162 for life
Anti-platelet therapy after UA/NSTEMI + Clopidogrel x 1 mo-1 yr
Drug eluting stent:ASA 162-325 x 3-6 mo,
then 75-162 for life
+ Clopidogrel x 1 yr minimum
Same as NSTEMI, but
Initial therapy for STEMI/new LBBB MI can use fibrinolytics
if PCI not available within 90min of ER arrival
Internal Medicine Review ABIM part 1
10 studiers in 3 days Leave the first rating
Students also studied
Flashcard sets Study guides Practice tests
APHY102 FINAL IM EOR Doppler part 2 SPI review He
128 terms 410 terms 16 terms 1,9
Harding28 Preview kalyn1600 Preview sarahlegg258 Preview
Terms in this set (589)
Flat or Down sloping
What is a positive stress test St-segment depression >1 mm
occurring 80 msec after j point
St segment depression > 2 mm,
ventricular tachycardia,
drop in SBP > 15,
When to stop a stress test
CP,
dyspnea,
lightheadedness
Stress test of choice with a LBBB or Myocardial perfusion imaging with adenosine,
ventricular pacing? NOT exercising!
History of VT,
severe HTN,
When to not use doutamine for stress
Low BP,
poor echo images
Bronchospasm,
severe valvular dysfunction,
When to not use adenosine for stress severe carotid stenosis,
2nd degree heart block, t
heophylline dependent
RA <8
RV 30/8
Normals for PA catheter pressures
PCWP 3-12
PAP 12--12
Diastolic pressures tamponade
elevated & equalized or restrictive pericarditis
in all chambers,
low BP
Elevated RA and PA pressures, RV MI
decreased or nl PCWP,
hypotension
,Elevated PCWP, RA pressure cardiogenic shock
decreased SBP/cardiac output
high RA, mitral stenosis with RV failure
PA very elevated
high PCWP
nl SBP
Elevated PAP, RAP pulmonary HTN
nl PCWP, SBP
decr in SBP>10mmHg with nl inspiration; pulsus paradoxus:
palpated as weakened pulse with Constrictive or restrictive pericarditis,
inspiration & asthma,
more heart contractions to pulse beats tension pneumothorax
What gives you pulsus bisferiens Aortic regurgitation,
(two systolic peaks per cycle) HOCM
What causes pulsus alternans Severe LV dysfunction
What causes pulsus tardus Aortic stenosis
-standing/valsalva:
decreased cardiac filling,
decreases most murmurs
except MVP and HOCM
-squatting/ lying down:
How do positional maneuvers affect
increase cardiac volume,
blood flow and murmurs
increased murmurs
except MVP, HOCM
-sustained handgrip:
increases systemic resistance
decreases murmur in HOCM, AS
Increased blood volume in the RV
What causes a physiologic split S2 prolongs systole and
delays pulmonary valve closure
Pulmonary stenosis,
PE,
LV pacer,
What causes a fixed split S2 RBBB,
MR (early AV closure),
ASD,
RV failue
LBBB,
What causes a paradoxic split S2 RV pacing,
HOCM
Rapid LV filling:
What causes an S3? acute ventricular decompensation,
severe AR or MR
A wave - atrial contraction
X descent - atria relax, RV fills rapidly
Bottom of x descent is TC valve closure
What are the parts of the venous
waveform?
V wave - ventricle contacting against closed TC valve
Y descent - TC valve opens,
passive emptying into ventricle
, Pulmonary HTN,
What gives elevated a and v waves
RV infarction
Large r side v waves Septal rupture
TR (right),
Large v waves
MR (left)
Constrictive pericarditis,
restrictive cardiomyopathy,
Rapid x and y descent
tamponade
(x descent only, loss of y descent)
TS,
Large a waves severe RVH (on right),
MS
AV disassociation -
Cannon a waves complete heart block,
ventricular pacing
Slow Y descent Delayed atrial emptying - TS
Most important prognostic factor with Degree of LV dysfunction
CAD
MI,
pericarditis,
LV aneurysm,
Causes of resting ST elevation LBBB,
ventricular pacing,
LVH,
early repolarization
myocardium near the infarction may be underperfused but not necrotic-
Hibernating myocardium the metabolism of the cells adapts to low energy supplies & are nonfunctional
until perfusion is restored
the re-estab of blood flow after a coronary artery is blocked,
Reperfusion injury which may further damage the heart tissue due to the formation of O2 free
radicals
prolonged post ischemic dysfunction,
Stunned myocardium salvaged by reperfusion,
several days
NSTEMI have _____ initial mortality, Lower,
but have the _____ one year mortality as a Same
STEMI
Persistent angina,
NSTEMI have a higher risk of these vs.
reinfarction, and
STEMI
death within several months
MR due to papillary muscle rupture is Inferior
most common with MI in this region
Junctional escape,
Types of arrythmias with IWMI Mobitz I,
and they are usually temporary
Mobitz II,
Types of arrythmias with AWMI BBB.
More of the myocardium is involved
, Bradycardia, hypotension,
2nd or 3rd degree AVB,
Contraindications for B-blockers pulmonary edema,
asthma.
NOT DM
Contraindications to B blockers,
When to use non-dihydropyridne CCBs in
continued ischemia,
ACS
but NO LV dysfunction
Not with UA/NSTEMI:
increases mortality
When to use fibrinolytics in ACS
Use in STEMI,
new LBBB if no contraindications
and immediate PCI not available
Plavix
Lipid and BP control
DC NSAIDs except ASA
What to give pt with UA/NSTEMI ASA, O2, B-blocker, nitrate prn
Heparin, enoxaparin, Fondaparanux, or bilavirudin
Gp IIa/IIIb if immediate PCI planned
NO FIBRINOLYTICS!
CHF or hemodynamic instability,
When to do urgent PCI with UA/NSTEMI recurrent or refractory angina,
life threatening arrythmias
elevated troponin,
dynamic ST changes,
DM,
GFR < 60,
When to use invasive therapy within 48
EF < 40%,
hrs with UA/NSTEMI
Early post-MI angina,
PCI in last 6 months,
prior MI / CABG,
intermediate/ high risk score
no indications for invasive therapy,
When to use conservative therapy with good response to initial treatment,
UA/NSTEMI low risk post-ACS stress testing.
Has the same 1 yr mortality
give NTG and CCBs
If no better, do cath
If cath not available, give fibrinolytics
Cocaine/ meth use and UA/NSTEMI
No cath if no ST/T changes,
neg stress, & neg biomarkers
no stent: ASA 75-162mg lifelong + Clopidogrel x 1-12 month
Bare metal: ASA 162-325 x 1 mo,
then 75-162 for life
Anti-platelet therapy after UA/NSTEMI + Clopidogrel x 1 mo-1 yr
Drug eluting stent:ASA 162-325 x 3-6 mo,
then 75-162 for life
+ Clopidogrel x 1 yr minimum
Same as NSTEMI, but
Initial therapy for STEMI/new LBBB MI can use fibrinolytics
if PCI not available within 90min of ER arrival
