Cardiology Flashcards
cardiothoracic ratio of > 50% can indicate what?
- cardiomegaly
- pericardial effusion
on the LATERAL view, any increase in the mass of the left ventricle extends the cardiac shadow ____
posteriorly and lower – closer to the diaphragm
on the LATERAL view, any increase in the mass of the right ventricle extends the cardiac shadow ____
anteriorly behind the sternum
CXR findings of coarctation of aorta
- absence of normal aortic arch
- “3” sign (prominent left subclavian artery, coarctation, poststenotic dilation of descending aorta)
- “reversed 3” sign on barium swallow
- intercostal rib notching
CXR findings of heart failure
- cardiomegaly
- pulmonary vascular redistribution (visibly thickened upper lobe pulmonary veins)
- Kerley B lines
- pleural effusions (usually right > left)
CXR finding of anomalous pulmonary vein that drains into the IVC
“scimitar sign” (curvilinear opacity in right lower lung field d/t associated lung hypoplasia)
CXR finding of aortic dissection
mediastinal widening on PA view
CXR finding of pericardial effusion
- “WATER BOTTLE” or “water balloon” heart shape
- sometimes significant enlargement of cardiac silhouette
areas of CALCIFICATIONS on CXR:
- aortic
think DISSECTION if separation between calcification and aortic border, especially if mediastinum appears wide
areas of CALCIFICATIONS on CXR:
- myocardial
apical aneurysm
areas of CALCIFICATIONS on CXR:
- valvular
commonly aortic
areas of CALCIFICATIONS on CXR:
- annular (ring-shaped)
mitral annular calcification
if perfect ring, prosthetic valve likely
areas of CALCIFICATIONS on CXR:
- pericardial
- think constrictive pericarditis
- or think TB if clinical history suggests exposure
CXR finding of ventricular pacemaker
single lead in apex of right ventricle
CXR finding of implanted defibrillator
single lead in apex of right ventricle that is LARGER and WIDER than that of the pacemaker
CXR finding of atrioventricular (AV) sequential (dual-chamber) pacemaker
2 leads
CXR finding of biventricular pacemaker
3 leads
- left ventricular structure and systolic function
- right ventricular structure and systolic function
- valvular heart disease
- congenital heart disease
- myocardial infarction (including post-MI complications)
- cardiomyopathy (both loss of EF and hypertrophy of myocardium)
- cardiac masses (tumor, thrombus, and vegetation)
- diseases of aorta and pulmonary artery
- estimation of pulmonary pressure
- diastolic function
- cardiac sources of emboli
BEST use of echocardiogram
echo performed w/ an esophageal probe
TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE)
HIGHER-RESOLUTION images compared to tranTHORACIC echocardiogram
TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE)
- valvular structure and function
- left atrium (including left atrial appendage)
- cardiac masses
- intracardiac shunts
- endocarditis
- aortic dissection
TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE) provides higher-resolution images than TTE
is used to evaluate intracardiac shunts
BUBBLE STUDY
measures the VELOCITY and DIRECTION of blood flow
doppler echocardiography
is useful in determining the severity of valvular stenosis or regurgitation, evaluating LV diastolic function, LV outflow tract gradients, and intracardiac shunts
doppler echocardiography
key factor in use of exercise testing as a diagnostic tool for coronary artery disease (CAD)
INCREASED DEMAND for myocardial oxygen
stress tests have an integral role in what 2 ways?
- detection of CAD (DIAGNOSTIC tool)
- stratification of risk (PROGNOSTIC tool)
diagnostic testing is MOST VALUABLE when?
pretest probability for CAD is INTERMEDIATE
what are the 2 general types of cardiac stress tests?
- exercise tolerance test (w/o imaging)
- stress imaging testing
- “STRESS” is induced w/ exercise or pharmacologic stress
what is the associated IMAGING done w/ stress testing?
- echocardiography (aka stress echo)
- myocardial perfusion imaging (MPI; nuclear stress test)
is the cornerstone of DIAGNOSTIC testing for ISCHEMIA and FUNCTIONAL CAPACITY and for determining PROGNOSIS (including post-MI)
exercise tolerance test (ETT)
level of maximal exercise achieved on the ETT is measured in?
metabolic equivalents (METS)
ETT WITHOUT imaging is NOT recommended in which 2 groups?
- pts unable to exercise sufficiently (MUST ACHIEVE 85% of age-predicted maximum heart rate (PMHR))
- pts w/ BASELINE ECG ABNORMALITIES
what BASELINE ECG ABNORMALITIES can interfere w/ ETT?
- LVH
- LBBB
- WPW
- ventricular pacing
- resting ST depressing
- taking digoxin
definition of a POSITIVE ETT
flat or down-sloping ST-segment depression > 1 mm at 80ms after the J-point in THREE consecutive beats
is an unusual finding suggestive of marked ischemia (can also be seen w/ coronary artery spasm)
ST elevation during an ETT in 3 contiguous leads w/o Q waves of prior MI
- ST elevation > 1 mm in leads w/o Q waves from prior MI and excluding aVR, aVL, and V1
- decrease in SBP > 10 mmHg when accompanied by any other evidence of ischemia or hypoperfusion
- moderate-to-severe angina
- CXS symptoms (ataxia, dizziness, near syncope)
- signs of poor perfusion (cyanosis/pallor)
- sustained 2nd or 3rd degree AV block
- technical difficulties in monitoring ECG/BP
- pt requests to stop
- serious arrhythmia (eg sustained ventricular tachycardia)
absolute indications for termination of an ETT
what correlates w/ a good prognosis independent of degree of CAD?
excellent exercise tolerance (> 10 METS)
absolute CI to ETT
- acute MI w/i 2 days
- unstable angina not previously stabilized by medical therapy
- uncontrolled arrhythmias causing symptoms or hemodynamic compromise
- symptomatic severe aortic stenosis
- uncontrolled symptomatic HF
- acute PE or infarction
- acute myocarditis or pericarditis
- acute aortic dissection
when are stress imaging studies used as the initial diagnostic method?
pt is not a candidate for ETT d/t:
- inability to exercise
- or baseline ECG changes at rest
in which pts are stress imaging studies the preferred diagnostic method?
pts w/ prior revascularization
do stress imaging studies have greater sensitivity and specificity than regular ETT?
YES
when are stress imaging studies used?
to measure EJECTION FRACTION or MYOCARDIAL VIABILITY; in addition to identifying CAD
how is the “stress” portion of stress imaging studies done?
- EXERCISE
- PHARMACOLOGIC agents
when is exercise stress imaging NOT used and why?
- pts w/ PACEMAKERS
- LBBB
- can cause false-positive left ventricular anteroseptal perfusion defects
pharmocologic agent used for stress imaging that is both iontropic and chronotropic
dobutamine
is usually NOT used in stress imaging studies in pts w/ PACEMAKERS
dobutamine
dobutamine is used for pts who are not only unable to exercise, but also have what CI’s to vasodilators?
- BRONCHOSPASM
- SEVERE CAROTID ARTERY STENOSIS
what are the main coronary vasodilators used in pharmacologic MPI stress tests?
- ADENOSINE
- DIPYRIDAMOLE
- REGADENOSEN
vasodilators should be used cautiously in stress imaging studies in pts w/ h/o?
BRONCHOSPASM
which vasodilator for stress imaging studies is a more selective A2A receptor activator, has less bronchospasm effect, and allows for a faster stress test?
REGADENOSEN
pharmacologic agent of choice for stress imaging studies for pts w/ h/o BRONCHOSPASM
DOBUTAMINE
unlike ETT, exercise stress echo and stress MPI can be used in which pts?
- resting ECG changes
- WPW syndrome
- on digoxin therapy
do pts w/ the following:
- resting ECG changes
- WPW syndrome
- on digoxin therapy
require chemical stress?
NO, if they can exercise, CLASS I indication to do stress echo WITH EXERCISE or MPI WITH EXERCISE
(i.e. they need the IMAGING, not the chemical stress)
what is the stress test of choice for pts w/ PACED VENTRICULAR RHYTHM?
MPI w/ vasodilators
how is the target heart rate achieved for stress echo?
- EXERCISE, or
- DOBUTAMINE
what does the stress echo evaluate? (3)
- changes in WALL MOTION
- systolic WALL THICKENING
- systolic EJECTION FRACTION w/ stress
abnormal wall motion of failure of the wall to thicken (contract) appropriately during a stress echo suggests what?
myocardial ischemia to that region
are NOT used for stress echo
vasodilators
MPI uses which radioisotopes with single-photon emission computed tomography (SPECT)
- TECHNETIUM-99m (99mTc)
- THALLIUM-201 (201TI) (less frequently)
in MPI the radioisotope tracers distribute in heart tissue in proportion to _____ which is recorded by a gamma camera and compared visually between resting and stressed states
blood FLOW
in MPI preserved myocardial perfusion at REST, but decreased during STRESS is suggestive of
ischemia (“REVERSIBLE defect”)
in MPI matched reduction in perfusion between rest and stress images is suggestive of a
myocardial infarction (“FIXED defect”)
determining best cardiac stress test:
- resting ECG normal
- able to exercise
ETT
determining best cardiac stress test:
- resting ECG normal
- NOT able to exercise
- dobutamine echo
- dobutamine MPI
- vasodilator MPI
determining best cardiac stress test:
- > 1 mm resting ST depression
- WPW
- LVH
- on digoxin
- able to exercise
- exercise echo (preferred)
- exercise MPI (preferred)
determining best cardiac stress test:
- > 1 mm resting ST depression
- WPW
- LVH
- on digoxin
- NOT able to exercise
- dobutamine echo
- dobutamine MPI
- vasodilator MPI
determining best cardiac stress test:
- LBBB
- able to exercise
N/A
determining best cardiac stress test:
- LBBB
- NOT able to exercise
- vasodilator MPI (preferred)
- dobutamine echo
determining best cardiac stress test:
- pacemaker
- able to exercise
N/A
determining best cardiac stress test:
- pacemaker
- NOT able to exercise
vasodilator MPI
which cardiac stress test is ALWAYS PREFERRED is pt has no limitations and what are the only 2 exceptions?
- EXERCISE STRESS TEST
- LBBB
- pacemaker
which cardiac stress test to choose:
if the pt is simply unable to walk and has no other issues
pharmacologic stress test
which cardiac stress test to choose:
if the pt has bronchospasm or severe carotid artery stenosis
DOBUTAMINE
which cardiac stress test to choose:
if the pt has severe HTN or prior ventricular tachycardia (VT)
use a VASODILATOR (adenosine, dipyridamole, or regadenoson), NOT dobutamine
which cardiac stress test to choose:
if the pt has a paced ventricular rhythm
use a VASODILATOR (adenosine, dipyridamole, or regadenoson), NOT dobutamine
is useful in evaluating pts w/ systolic HF, undergoing a pretransplant assessment, and for pts w/ unexplained exertional dyspnea
cardiopulmonary exercise testing (CPX)
is the GOLD STANDARD for diagnosis of CAD
coronary ANGIOGRAPHY
can also assess EF during coronary angiography
contrast VENTRICULOGRAPHY
- noninvasive modality for imaging the heart
- requires IV CONTRAST
- HR must be < 60 BPM and regular
- pts must be able to HOLD their BREATH
coronary computed tomographic angiography (CTA)
reasonable diagnostic test for symptomatic pts who are at INTERMEDIATE risk for CAD after initial risk stratification, including pts w/ equivocal stress test results
coronary computed tomographic angiography (CTA)
this test’s usefulness is reduced in pts w/ pronounced coronary calcification
coronary computed tomographic angiography (CTA)
is an excellent test for evaluation of pts w/ congenital coronary anomalies
coronary computed tomographic angiography (CTA)
can be used to assess:
- right and left filling pressures
- CO
- RV and PA pressures
- systemic and pulmonary vascular resistance
pulmonary artery catheterization (PAC)
what is pulmonary artery catheterization (PAC) used for?
- determine pt’s volume status
- causes of shock
- existence of pericardial disease
is the dampened LA pressure that reflects left ventricular end-diastolic pressure (LVEDP) in most cases, which reflects LVED volume
pulmonary capillary wedge pressure (PCWP)
normal pressures:
RA
< 8 mmHg
normal pressures:
RV
15-30/1-7 mmHg
normal pressures:
PCWP
4-12 mmHg
jugular venous distention in the upright pt which indicates an elevated RA pressure
> 7 cm H2O (5 mmHg)
what happens to PCWP w/:
- LV systolic failure
- LV diastolic failure
- mitral stenosis
- aortic insufficiency
- mitral insufficiency
- tamponade
- constrictive pericarditis
INCREASES
at what PCWP should LV failure be considered?
> 15-18 mmHg
at what PCWP do you have dyspnea on exertion (DOE)?
15-25 mmHg
at what PCWP do you have dyspnea at rest, orthopnea, and interstitial edema
25-35 mmHg
at what ACUTE PCWP do you have frank pulmonary edema?
> 35 mmHg
pulmonary artery catheterization scenarios:
- RA pressure: 0-5
- PA pressure: (13-28)/(3-13)
- PCWP: 3-11
- BP: 110/70
normal
pulmonary artery catheterization scenarios:
- RA pressure: 18
- PA pressure: 32/18
- PCWP: 19
- BP: 70/50
tamponade or constrictive pericarditis
pulmonary artery catheterization scenarios:
- RA pressure: 15
- PA pressure: 21/11
- PCWP: 10
- BP: 70/50
RV failure to RV infarct
pulmonary artery catheterization scenarios:
- RA pressure: 18
- PA pressure: 30/20
- PCWP: 20
- BP: 70/50
biventricular failure
pulmonary artery catheterization scenarios:
- RA pressure: 18
- PA pressure: 90/32
- PCWP: 30
- BP: 110/70
mitral stenosis
pulmonary artery catheterization scenarios:
- RA pressure: 18
- PA pressure: 90/32
- PCWP: 10
- BP: 110/70
pulmonary HTN
diastolic pressure in all 4 chambers is equalized in both ____ and ____
- pericardial tamponade
- constrictive pericarditis
when is endomyocardial biopsy used?
- to monitor cardiac transplant rejection
- to evaluate the cause of CARDIOMYOPATHY or MYOCARDITIS if cause is unclear or therapy isn’t working
decreased pulse amplitude w/ INSPIRATION seen as absence of Korotkoff sounds during inspiration
pulsus PARADOXUS
can be observed by auscultating BP and listening for an exaggerated decrease in SBP (> 10 mmHg) during inspiration
pulsus PARADOXUS
pulsus PARADOXUS is present w/? (4)
- cardiac tamponade (especially)
- constrictive pericarditis
- asthma
- tension pneumothorax
what is the paradox in pulsus PARADOXUS?
you can hear a heartbeat, but not feel a pulse during inspiration
bifid w/ 2 systolic peaks per cardiac cycle
pulsus BISFERIENS
pulsus BISFERIENS is present w/? (2)
- aortic regurgitation (w/ or w/o stenosis!)
- HCM
varying pulse pressure w/ a regular pulse rate
pulsus ALTERNANS
what is pulsus ALTERNANS seen w/?
severely depressed systolic function of any cause that leads to DECREASED STROKE VOLUME
what is pulsus PARVUS ET TARDUS and when is seen?
- parvus = LOW amplitude
- tardus = slow upswing
- aortic stenosis
what is BRACHIOFEMORAL DELAY and when is seen?
- femoral pulse occurs AFTER brachial pulse
- coarctation of aorta
what is pulse ASYMMETRY and when is seen?
- good UE pulses, but diminished or absent LE pulses, OR asymmetry between right and left extremities
- aortic dissection
- DECREASED OR ABSENT peripheral pulses
- possible BRUIT over proximal artery (such as femoral artery)
peripheral artery disease (PAD)
maneuvers to differentiate murmurs:
passive straight-leg raise (to 45 degrees, listen after 15 sec)
increases venous return
maneuvers to differentiate murmurs:
Valsalva (hold for 20 sec, listen just before end)
decreases venous return
maneuvers to differentiate murmurs:
standing (squat for > 30 sec then quickly stand; listen during first 15 sec after standing)
decreases venous return
maneuvers to differentiate murmurs:
transient arterial occlusion (BP cuff on both arms, inflated > 20 mm above systolic pressure)
increases systemic vascular resistance
maneuvers to differentiate murmurs:
handgrip (isometric; listen at end of 1 min max grip)
increases systemic vascular resistance
maneuvers to differentiate murmurs:
squatting
increases venous return and increases systemic vascular resistance, but preload effect is stronger than afterload effect
maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use
- standing (from squat)
(95%) INCREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use
- Valsalva (if cannot do squat-to-stand)
(65%) INCREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use
- passive straight-leg raise
(85%) DECREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for HCM use
- handgrip
(85%) DECREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use
- standing and Valsalva
click-murmur moves EARLIER
maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use
- transient arterial occlusion
(80%) click-murmur moves LATER
maneuvers for increasing/decreasing specific systolic murmurs:
- for MVP use
- handgrip
(70%) click-murmur LATER
maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use
- standing and Valsalva
DECREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use
- transient arterial occlusion
(80%) INCREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for VSD use
- handgrip
(70%) DECREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for AS use
- transient arterial occlusion
DECREASED murmur
maneuvers for increasing/decreasing specific systolic murmurs:
- for AS use
- handgrip
DECREASED murmur
what happens to the ALL valve murmurs when blood INCREASES across the valve?
INCREASES murmur
how does STANDING and the strain phase of VALSALVA effect most most valve murmurs, and what are the 2 exceptions?
- DECREASES intensity of murmur
- MVP and HCM
how does STANDING and the strain phase of VALSALVA effect right and left cardiac filling?
decreases filling
sustained handgrip (20-30 seconds) boosts systemic _____ and _____, and therefore decreases the murmurs of _____ and _____
- systemic vascular resistance
- HCM and aortic stenosis (AS)
sustained handgrip (20-30 seconds) boosts systemic _____, which prolongs the murmur of _____ d/t earlier prolapse of the valve
- systemic vascular resistance
- MVP (mitral valve prolapse)
right-sided murmurs and heart sounds are louder during
- INSPIRATION
- anything that increases VR
left-sided murmurs and heart sounds are louder during
EXPIRATION
what is the only semi-exception to right-sided murmurs sounding less loud during inspiration?
right-sided ejection click d/t pulmonic stenosis
what happens to S1 intensity when there is:
- prolonged PR interval
- MR
- acute AR (increased LV pressure cause early valve closure)
- severely calcified mitral valve
DECREASES
what happens to S1 intensity when there is:
- short PR interval
- mitral stenosis
- hyperdynamic ventricular function
INCREASES
what causes S1?
closing of mitral and tricuspid valves
what causes S2?
closing of aortic and pulmonic valves at the end of systole
when does P2 occur?
right after A2
what is PHYSIOLOGIC SPLITTING of S2?
A2 followed by P2
when does PHYSIOLOGIC SPLITTING INCREASE, and why?
- during INSPIRATION
- increased volume of blood in RV, which prolongs systole and delays pulmonic valve closure
causes for PERSISTENTLY (or WIDELY) split S2
- pulmonic stenosis
- acute PE
- ectopic or pacemaker beats originating in the LEFT ventricle
- RBBB
why do pulmonic stenosis, acute PE, actopic or pacemaker beats originating in the LEFT ventricle, and RBBB cause PERSISTENTLY (or WIDELY) split S2?
they cause DELAYED or PROLONGED CONTRACTION of the RIGHT VENTRICLE
cause for FIXED splitting of S2
atrial septal defect (ASD)
other cause for fixed splitting of S2 besides ASD
RV failure when SV is unable to increase w/ inspiration
cause for PARADOXICAL split S2 w/ P2 coming before A2
- LBBB
- ectopic or pacemaker beats originating in the RIGHT ventricle
- advanced HCM
indicates end of rapid ventricular filling; is the first part of diastole
S3
when is the S3 gallop normal?
- children
- high CO, such as pregnant women
when is the S3 gallop abnormal?
pts > 40 yoa
causes for abnormal S3 gallop
- acute ventricular decompensation
- severe aortic regurgitation
- severe mitral regurgitation
(anything that increases early LV filling rate or volume)
S3 in a pt w/ KNOWN left ventricular dysfunction, means what?
POOR prognostic indicator
both S3 and S4 are best auscultated how?
left lateral decubitus position using the bell
when is S3 heard?
just after S2 (lub-dub-huh)
when is S4 heard?
just before S1 (huh-lub-dub)
is caused by ventricular filling during atrial contraction
S4
is heard in pts w/ decreased ventricular compliance
S4
causes for abnormal S4 gallop
- ischemic heart disease
- aortic stenosis
- HCM
- diabetic cardiomyopathy
- hypertensive heart disease w/ concentric hypertrophy
when do you NOT hear an S4 gallop?
- during atrial fibrillation (no atrial contraction!)
- mitral stenosis
which side is the jugular venous pulse assessed?
right
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- pulmonary HTN
- elevated a and v waves
- other physical exam findings of pulmonary HTN
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- tricuspid regurgitation
- large v waves
- TR murmur
- pulsatile liver
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- constrictive pericarditis
- rapid x and y descents
- Kussmaul sign
- pericardial knock
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- tamponade
- rapid x descent
- pulsus paradoxus
- hypotension
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- tricuspid stenosis
- slow y descent
- TS murmur
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- restrictive cardiomyopathy
- rapid x and y descents
- low-voltage ECG
- echo
- myocardial bx
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- tension pneumothorax
- distended neck veins
- dyspnea
- U/L absent breath sounds
- deviated trachea
- CXR
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- superior vena cava syndrome
- U/L distended neck veins
- facial edema and cyanosis
- dx of cancer
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- AV dissociation
- irregular cannon a waves
- ECG
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- RV infarction
- elevated a and v waves
- acute inferior MI
- Kussmaul sign
venous waveforms in clinical setting:
- neck vein appearance
- other diagnostic features
- ASD
- large v waves and rapid y descent
- fixed split S2
- echo
jugular waveform:
- large, RIGHT-SIDED V WAVES
- ventricular septal rupture
- TR
jugular waveform:
- rapid X and Y DESCENTS
constrictive pericarditis
jugular waveform:
- ONLY rapid x descent
tamponade (loss of y descent)
jugular waveform:
- large, RIGHT-SIDED Y WAVES
- TS
- severe pulmonic stenosis
- severe noncompliant RVH
jugular waveform:
- “CANNON” A WAVES
- complete heart block
- ventricular tachycardia
- asynchronous ventricular pacing
- all conditions w/ AV DISSOCIATION (when atrium is contracting against CLOSED tricuspid valve)
tall, LEFT-SIDED V WAVES are d/t
severe MR
large, LEFT-SIDED A WAVES are d/t
mitral stenosis
suspect SECONDARY causes of HTN in which pts?
- onset before 30 yoa or after 55 yoa
- drug-resistant HTN
- development of uncontrolled HTN that was previously well controlled
systolic abdominal bruits (w/o a diastolic bruit) suggests
renal vascular HTN
what are noninvasive tests to diagnose RAS?
- duplex US
- CTA
- MRA
when should you think of primary hyperaldosteronism?
- HTN
- HYPOkalemia
- LOW renin
common cardiac medications:
- digoxin
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. +
c. +
d. no
e. no
f. no
g. no
h. systolic HF, arrhythmias
common cardiac medications:
- BB
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. +++
b. +++
c. +++
d. no
e. yes
f. yes
g. yes
h. HTN, angina, HF, arrhythmias
common cardiac medications:
- carvedilol
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. ++
b. +++
c. +++
d. yes
e. yes
f. yes
g. yes
h. HTN, angina, HF, arrhythmias
common cardiac medications:
- nifedipine
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. ++
b. no
c. no
d. yes
e. yes
f. no
g. no
h. HTN, angina
common cardiac medications:
- amlodipine
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. +
b. no
c. no
d. yes
e. yes
f. no
g. yes (in DCM)
h. HTN, angina, DCM
common cardiac medications:
- diltiazem
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. ++
b. ++
c. ++
d. yes
e. yes
f. no
g. no
h. HTN, angina, arrhythmias
common cardiac medications:
- verapamil
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. +++
b. +++
c. +++
d. yes
e. yes
f. no
g. no
h. HTN, angina, arrhythmias
common cardiac medications:
- nitrates
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. yes
e. yes
f. no
g. yes (w/ hydralazine)
h. angina, HF
common cardiac medications:
- ACEIs
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. yes
e. no
f. yes
g. yes
h. HTN, HF
common cardiac medications:
- ARBs
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. yes
e. no
f. yes
g. yes
h. HTN, HF
common cardiac medications:
- hydralazine
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. yes
e. no
f. no
g. yes (w/ nitrates)
h. HTN, HF
common cardiac medications:
- spironolactone
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. no
e. no
f. no
g. yes
h. HTN, HF
common cardiac medications:
- eplerenone
a. negative inotrope
b. negative chronotrope
c. negative dromotrope
d. vasodilator
e. antianginal
f. prolong survival post-MI
g. prolong survival in HF
h. indications
a. no
b. no
c. no
d. no
e. no
f. yes (w/ HF)
g. yes (post-MI)
h. HF post-MI
chest pain d/t “supply-demand” mismatch between coronary perfusion and cardiac workload
angina
angina is either classified as
STABLE or UNSTABLE
3 characteristics of UNSTABLE angina
- pain at rest
- new onset
- increased frequency
most common underlying process triggering ACUTE coronary syndrome
plaque rupture or erosion w/ superimposed thrombus
what are causes of INCREASED DEMAND in angina?
- tachycardia
- fever
- thyrotoxicosis
what are causes of DECREASED SUPPLY in angina?
- hypotension
- coronary vasospasm
- anemia
- hypoxia
in what conditions can coronary blood flow be impaired, even in the ABSENCE of epicardial CAD?
- severe aortic valve disease w/ LVH
- HTN
- idiopathic dilated CM
- hypertrophic CM
what percentage of pts actually have classic angina at the moment of ischemic ST changes?
20%
silent ischemia is seen in what pts?
- DIABETICS
- pts w/ prior ischemic events
silent ischemia, MIs, and thrombotic strokes occur at what time during day w/ the highest incidence?
early morning hours
what is the MOST IMPORTANT, easily determinable PROGNOSTIC factor in pts w/ CAD?
DEGREE of LV DYSFUNCTION
severe LV dysfunction can be a reflection of what?
multi-vessel, or left main/left main-equivalent disease
is an excellent, objective way to determine SEVERITY of angina and to determine prognosis
exercise tolerance test
what is the 5-year survival rate for pts able to go to stage 4 of Bruce protocol?
nearly 100%
what is the 5-year survival rate for pts NOT able to go to stage 1 of Bruce protocol?
only 50%
coronary ANGIOGRAPHY is NOT REQUIRED to determine what?
prognostic factor for pt w/ ACS
transient ST-elevation that occurs during stress testing
coronary artery SPASM
what are causes of RESTING ST-segment elevation?
- acute MI
- coronary artery spasm
- pericarditis
- LV aneurysm
- LBBB
- ventricular pacing
- LVH
- benign early repolarization
chronically underperfused myocardium WITHOUT irreversible myocyte injury
hibernating myocardium
occurs when severely ischemic myocardium is reperfused after about 1 hour, causing further irreversible microvascular damage to myocytes
reperfusion injury
d/t acute ischemia and takes 7-10 days for ventricle to return to normal
stunned myocardium
treatment of all angina
modify risk factors and correct aggravating factors (anemia, HTN, smoking, drug abuse, noncompliance)
what are the main drugs used to treat angina?
- BB’s and nitrates; CCB’s can also help
- ASA +/- clopidogrel (if allergic to aspirin, or if indicated)
which pts might benefit from ranolazine (Ranexa)?
pts w/ persistent angina on maximal standard therapy, or as a substitute for BB’s
these meds ALL decrease myocardial O2 demand, and ALL decrease afterload
BB’s, nitrates, and CCB’s
which meds decrease preload > afterload and can cause severe DECOMPENSATION in acute RIGHT ventricular MI?
nitrates
- cause sympathetic reflex tachycardia
- degraded in LIVER
- tachyphylaxis
nitrates
how do BB’s decrease myocardial O2 demand?
- decrease HR
- decrease BP
- decrease contractility
which medication can actually prolong vasospasm in pts w/ variant angina?
nonselective BBs
