Tv General Cardio Boards

Front 1

Sensitivity:

Back 1

Sensitivity: among those w/ disease, the proportion w/ + test (true +)

Front 2

Specificity:

Back 2

Specificity: among those w/out disease, the proportion w/ - test (true -)

Front 3

Predictive Value:

Back 3

Predictive Value: among those w/ + test, the proportion that has the disease

Front 4

Predictive Value:

Back 4

Predictive Value: among those w/ - test, the proportion that does not have the disease

Front 5

Likelihood Ratio:

Back 5

Likelihood Ratio: the ratio of probability of a certain test result in people w/ the disease to the probability in people w/out the disease

Front 6

Differential cyanosis affecting the lower, but not the upper, extremities

Back 6

occurs w/ patent ductus arteriosus and pulm. artery (PA) hypertension w/ R to L shunting at the great vessel

Front 7

Define OslerWeberRendu

Back 7

Hereditary telangiectases on the lips, tongue, and mucous membranes (Osler-Weber-Rendu syndrome) resemble spider nevi and, when present in the lungs, can be a source of R to L shunting and central cyanosis

Front 8

Rubella syndrome:

Back 8

cataracts; deafness; microcephaly; and, either singly or in combination, PDA, pulm. valve and/or arterial stenosis, and ASD

Front 9

Thalidomide

Back 9

major limb deformities ~ w/ cardiac malformations

Front 10

ingestion of lithium during pregnancy.

Back 10

Tricuspid valve anomalies

Front 11

ALCAPA SYNDROME.

Back 11

anomalous LCA arising from PA. aka Bland-White-Garland syndrome

Front 12

Bland-White-Garland syndrome

Back 12

anomalous LCA arising from PA. aka

Front 13

ALAGILLE SYNDROME

Back 13

hereditary syndrome consisting of intrahepatic cholestasis, characteristic facies, butterfly-like vertebral anomalies, and varying degrees of peripheral pulm. artery stenoses or diffuse hypoplasia of pulm. artery and its branches. It is associated w/ deletion in chromosome 20p

Front 14

DIGEORGE SYNDROME.

Back 14

caused by a microdeletion at chromosome 22q11, aka as “CATCH 22” syndrome, ( cardiac defect, abnormal facies, thymic hypoplasia, cL palate, and hypocalcemia). Cardiac defects include conotruncal defects such as interrupted aortic arch, tetralogy of Fallot, truncus arteriosus, and double-outlet RV. Also includes velocardiofacial syndrome.

Front 15

CHARGE ASSOCIATION.

Back 15

coloboma or choanal atresia+ 3 of following defects: CHD, nervous system anomaly or mental retard, genital abns, ear abn, or deafness. Congenital defects seen in CHARGE = tetralogy of Fallot w/ wo other defects, AV septal defect, double-outlet rv, double-inlet lv, TGA, interrupted aortic arch, and others

Front 16

DOWN SYNDROME:

Back 16

trisomy 21 (maybe mosaic forms). (short stature, charact. facial, mental retardation, brachydactyly, atlantoaxial instability, and thyroid + WBC disorders). Congenital defects in 40% w/V septal defect, VSD, and PDA. prone to earlier and more severe pulm. vasc disease Hypothyroidism

Front 17

ELLIS-VAN CREVELD SYNDROME

Back 17

autosomal recessive w/ common atrium, primum ASD, and partial AV septal defects

Front 18

HOLT-ORAM SYNDROME.

Back 18

Autosomal dominant syndrome w/ radial abnormalities of arm associated w/ secundum ASD (most common); VSD; or, others

Front 19

LEOPARD SYNDROME.

Back 19

Autosomal dom w/ lentigines, ECG abnormalities, ocular hypertelorism, pulm. stenosis, abnormal genitalia, retardation of growth, and deafness. Rarely, cardiomyopathy or complex CHD may be present.

Front 20

NOONAN SYNDROME

Back 20

autosomal dominant similar to Turner syndrome but w/ normal chromosomal. Noonan syndrome is associated w/ congenital cardiac anomalies, especially dysplastic pulm. valve stenosis, pulm. artery stenosis, and ASD. Hypertrophic cardiomyopathy is < common.

Front 21

SCIMITAR SYNDROME

Back 21

includes total or partial anomalous pulm. venous connection (PAPVC) of R lung to the inferior vena cava, often associated w/ hypoplasia of R lung and R pulm. artery. The lower portion of R lung (sequestered lobe) tends to receive its arterial supply from the abdominal aorta. CXR PA resembles a Turkish sword, or scimitar.

Front 22

SHONE COMPLEX (SYNDROME

Back 22

multiple levels of LV inflow and outflow obs (subvalv and valv LVOT obs, coarct aorta, and mitral sten [parachute mitral valve and supramitral ring]).

Front 23

TURNER SYNDROME.

Back 23

45 XO karyotype in about 50%, others have X abn. postductal coarctation of aorta and other L-sided obstructive lesions, as well as PAPVC w/out ASD. similar to that of Noonan syndrome.

Front 24

WILLIAMS SYNDROME

Back 24

. autosomal dominant, assoc w/ infantile hypercalcemia, characteristic phenotype, and CHD, especially supravalvular aortic stenosis and multiple peripheral pulm. stenoses.

Front 25

WPW isoelectrice or - delta wave in I, aVL or V6 with LBBB in V1

Back 25

R anteroseptal pathway

Front 26

WPW isoelectrice or - delta wave in I, aVL or V6 no LBBB in V1

Back 26

L L ateral pathway

Front 27

WPW Is there an isolectricor - delta wave in II, III, aVF with a large Rs in I, II, III

Back 27

posterior septal pathway

Front 28

WPW Is there an isolectricor - delta wave in II, III, aVF with no large RS in I, II, III

Back 28

R lateral pathway

Front 29

Fontan procedure

Back 29

a generic term to describe a palliative surgical procedure that redirects the systemic venous return directly to the pulm. arteries w/out passing thru a subpulm. ventricle. These include tricuspid atresia, hypoplastic L heart, double inlet ventricle, and isomerism

Front 30

Hypoplastic L heart syndrome

Back 30

a generic term used to describe a group of closely related cardiac anomalies characterized by underdevelopment of L cardiac chambers, in association w/tresia or stenosis of aortic and/or the mitral orifices, and hypoplasia of aorta. The term should be restricted to those w/ normally connected hearts w/ concordant AV and ventriculoarterial connections. Hypoplastic L heart syndrome is characterized by duct-dependent systemic blood flow and so tends to present w/ severe symptoms w/in the 1st week of life, as ductal constriction occurs. Untreated, the disease is almost uniformly fatal in infancy

Front 31

Mustard or a Senning procedure

Back 31

Systemic venous return is diverted thru the mitral valve into the subpulm. LV, and the pulm. venous return is rerouted thru the tricuspid valve into the subaortic RV. By virtue of this repair, the morphological RV is left to support the systemic circulation.

Front 32

cc-TGA is

Back 32

When there is the usual atrial arrangement, systemic venous blood passes from the R atrium thru a mitral valve to a LV and then to the posteriorly located pulm. artery. Pulm. venous blood passes from the L atrium thru a tricuspid valve to a L-sided RV and then to an anterior, L-sided aorta. The circulation is thus “physiologically” corrected, but the morphological RV supports the systemic circulation. Associated anomalies occur in up to 95 % of pts and consist of VSD (75 %), pulm. or subpulm. stenosis (75 %), and L-sided (tricuspid and often “Ebstein-like”) valve anomalies (>75 %

Front 33

Total anomalous pulm. venous return:

Back 33

supracardiac, = pulm. veins drain either via the vertical vein to anomal vein (A) or directly to SVC w/ orifice close to orifice of azygos vein (B). (C), Drainage into R atrium via coronary sinus. (D), Infracardiac drainage via vertical vein into portal vein or IVC.

Front 34

Ebstein anomaly

Back 34

apical displacement of septal tricuspid leaflet in conjunction with leaflet dysplasia. Many, but not all, have associated displacement of the posterior mural leaflet, with the anterior leaflet never being displaced. Although the anterior leaflet is never displaced apically, it may be adherent to the free wall of the RV, causing RVOT obstruction. The displacement of the tricuspid results in “atrialization” (functioning as an atrial chamber) of the inflow tract of the RV and consequently produces a variably small, functional RV. Associated anomalies include PFO or ASD in approximately 50% of pts; accessory conduction pathways in 25 percent (usually right sided); and, occasionally, varying degrees of RVOT obs, VSD, aortic coarct, PDA, or mitral valve disease. LV abnorm. resembling noncompaction syndrome have also been

Front 35

The RCA is dominant in 85 % of pts, supplying the

Back 35

the PDA and at least one posterolateral branch (R dominant)

Front 36

The RCA is nondominant in 15 % of pts.

Back 36

One half ofse pts have a L PDA and L posterolateral branches that are provided by the distal LCx artery (L dominant circulation).

Back 37

The remaining pts have an RCA that gives rise to the PDA w/ the LCx artery providing all the posterolateral branches (balanced or codominant circulation).

Front 38

What does slower upstroke on carotid exam in patient with AS signify?

Back 38

higher transvalvular gradient

Front 39

When does parvus and tardus occur even with mild aortic stenosis?

Back 39

LV failure

Front 40

In addition to aortic regurgitaiton, which other processes cause rapid upstroke
and widened pulse pressure?e

Back 40

The most common are the hyperkinetic heart syndromes (high output states). These include
anemia, fever, exercise, thyrotoxicosis, pregnancy, cirrhosis, beriberi, Paget�s disease,
arteriovenous fistulas, patent ductus arteriosus, aortic regurgitation, and anxiety�all typically
associated with rapid ventricular contraction and low peripheral vascular resistance.

Front 41

What is pulsus alternans? and what does it signify?

Back 41

Pulsus alternans is the alternation of strong and weak arterial pulses despite regular rate and
rhythm. First described by Ludwig Traube in 1872, pulsus alternans is often associated with
alternation of strong and feeble heart sounds (auscultatory alternans). Both indicate severe
left ventricular dysfunction (from ischemia, hypertension, or valvular cardiomyopathy), with
worse ejection fraction and higher pulmonary capillary pressure. Hence, they are often
associated with an S3 gallop

Front 42

What is Duroziez’s double murmur

Back 42

Duroziez�s is a to-and-fro double murmur over a large central artery�usually the femoral,
but also the brachial. It is elicited by applying gradual but firm compression with the
stethoscope�s diaphragm. This produces not only a systolic murmur (which is normal) but also
a diastolic one (which is pathologic and typical of AR). Duroziez�s has 58% to 100% sensitivity
and specificity for AR.

Front 43

What is Corrigan's pulse?

Back 43

Corrigan's is one of the various names for the bounding and quickly collapsing pulse of aortic
regurgitation, which is both visible and palpable. Other common terms for this condition
include water hammer, cannonball, collapsing, or pistol-shot pulse. It is best felt for by elevating
the patient�s arm while at the same time feeling the radial artery at the wrist. Raising the
arm higher than the heart reduces the intraradial diastolic pressure, collapses the vessel, and
thus facilitates the palpability of the subsequent systolic thrust.u��ޙ

Front 44

What is the Levine system for grading the intensity of murmurs?

Back 44

1/6: a murmur so soft as to be heard only intermittently and always with concentration and
effort. Never immediately
2/6: a murmur that is soft but nonetheless audible immediately and on every beat
3/6: a murmur that is easily audible and relatively loud
4/6: a murmur that is relatively loud and associated with a palpable thrill (always
pathologic)
5/6: a murmur loud enough that it can be heard even by placing the edge of the
stethoscope's diaphragm over the patient's chest
6/6: a murmur so loud that it can be heard even when the stethoscope is not in contact with the chest, but held slightly above its surface

Front 45

What factors may suggest severe aortic stenosis? (In setting of a murmur?)

Back 45

Murmur intensity and timing (the louder and later peaking the murmur, the worse the
disease)
& A single S2
& Delayed upstroke/reduced amplitude of the carotid pulse (pulsus parvus and tardus)g

Front 46

What is isometric hand grip, and what does it do to AS and mitral regurgitation (MR) murmurs?

Back 46

Isometric hand grip is carried out by asking the patient to lock the cupped fingers of both hands
into a grip and then trying to pull them apart. The resulting increase in peripheral vascular
resistance intensifies MR (and ventricular septal defect) while softening instead AS (and aortic
sclerosis). Hence, a positive hand grip argues strongly in favor of MR.

Front 47

What is the Gallavardin phenomenon?

Back 47

One noticed in some patients with AS, who may exhibit a dissociation of their systolic murmur
into two components:
& A typical AS-like murmur (medium to low pitched, harsh, right parasternal, typically
radiated to the neck, and caused by high-velocity jets into the ascending aorta)
& A murmur that instead mimics MR (high pitched, musical, and best heard at the apex)
This phenomenon reflects the different transmission of AS: its medium frequencies to the base
and its higher frequencies to the apex. The latter may become so prominent as to be
misinterpreted as a separate apical ��cooing�� of MR

Front 48

What are the characteristics of the MR murmur?urmur?

Back 48

It is loudest at the apex, radiated to the left axilla or interscapular area, high pitched, plateau,
and extending all the way into S2 (holosystolic). S2 is normal in intensity but often widely split.
If the gradient is high (and the flow is low), the MR murmur is high pitched. Conversely, if
the gradient is low (and the flow is high) the murmur is low pitched. In general, the louder (and
longer) the MR murmur, the worse the regurgitation.�

Front 49

What are the characteristics of the acute MR murmur?

Back 49

The acute MR murmur tends to be very short, and even absent, because the left atrium and
ventricle often behave like a common chamber, with no pressure gradient between them. Hence,
in contrast to that of chronic MR (which is either holosystolic or late systolic), the acute MR
murmur is often early systolic (exclusively so in 40% of cases) and is associated with an S4 in
80% of the patients.ng

Front 50

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Front 52

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Front 53

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Front 54

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Front 55

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Front 56

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Front 57

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Front 58

What is a mammary souffle�

Back 58

Not a fancy French dish but a systolic-diastolic murmur heard over one or both breasts in
late pregnancy and typically disappearing at end of lactation. It is caused by increased flow along
the mammary arteries, which explains why its systolic component starts just a little after S1.
It can be obliterated by pressing (with finger or stethoscope) over the area of maximal intensity��S

Front 59

What are the most commonly used criteria to diagnose left ventricular
hypertrophy (LVH)?

Back 59

R wave in V5-V6 � S wave in V1-V2 > 35 mm
& R wave in lead I � S wave in lead III > 25 mm

Front 60

What are the most commonly used criteria to diagnose right ventricular
hypertrophy (RVH)?

Back 60

R wave in V1  7 mm
& R/S wave ratio in V1 > 1
3.

Front 61

What criteria are used to diagnose left atrial enlargement (LAE)?

Back 61

P wave total width of > 0.12 sec (3 small boxes) in the inferior leads, usually with a
double-peaked P wave
& Terminal portion of the P wave in lead V1  0.04 sec (1 small box) wide and  1 mm
(1 small box) deep�N

Front 62

What electrocardiogram (ECG) finding suggests right atrial enlargement?

Back 62

P-wave height in the inferior leads (II, III, and aVF)  2.5 to 3 mm (2.5�3 small boxes

Front 63

What is the normal rate of a junctional rhythm?

Back 63

The normal rate is 40 to 60 beats/min. Rates of 61 to 99 beats/min are referred to
as accelerated junctional rhythm, and rates of 100 beats/min or higher are referred to as
junctional tachycardia.��

Front 64

How can one distinguish a junctional escape rhythm from a ventricular escape
rhythm in a patient with complete heart block?

Back 64

Junctional escape rhythms usually occur at a rate of 40 to 60 beats/min and will usually be
narrow complex (unless the patient has a baseline bundle branch block), whereas ventricular
escape rhythms will usually occur at a rate of 30 to 40 beats/min and will be wide complex.�

Front 65

What are the ECG findings in pericarditis?ythm?

Back 65

The first findings are believed by some to be PR segment depression caused by repolarization
abnormalities of the atria. This may be fairly transient and is often not present by the time
the patient is seen for evaluation. Either concurrent with PR segment depression or shortly
following PR segment depression, diffuse ST segment elevation occurs (see ECG example in
Chapter 53 on Pericarditis). At a later time, diffuse T-wave inversions may develop

Front 66

What ECG findings may be present in pulmonary embolus?

Back 66

& Sinus tachycardia (the most common ECG finding)
& Right atrial enlargement (P pulmonale)�tall P waves in the inferior leads
& Right axis deviation
& T wave inversions in leads V1-V2
& Incomplete right bundle branch block (IRBBB)
& S1Q3T3 pattern�an S wave in lead I, a Q wave in lead III, and an inverted T wave in
lead III. Although this is only occasionally seen with pulmonary embolus, it is said to be
quite suggestive that a pulmonary embolus has occurred.�N

Front 67

What are the common radiographic signs of congestive heart failure?ent?

Back 67

Enlarged cardiac silhouette
& Left atrial enlargement
& Hilar fullness
& Vascular redistribution
& Linear interstitial opacities (Kerley�s lines)
& Bilateral alveolar infiltrates
& Pleural effusions (right greater than left���

Front 68

What is vascular redistribution? When does it occur in congestive heart failure

Back 68

Vascular redistribution occurs when the upper-lobe pulmonary arteries and veins become larger
than the vessels in the lower lobes. The sign is most accurate if the upper lobe vessels are
increased in diameter greater than 3 mm in the first intercostal interspace. It usually occurs at a
pulmonary capillary occlusion pressure of 12–19 mm Hg. As the pulmonary capillary occlusion
pressure rises above 19 mm Hg, interstitial edema develops with bronchial cuffing, Kerley’s B
lines, and thickening of the lung fissures. Vascular redistribution to the upper lobes is probably
most consistently seen in patients with chronic pulmonary venous hypertension (mitral valve
disease, left ventricular dysfunction) because of the body’s attempt to maintain more normal
blood flow and oxygenation in this area. Some authors believe that vascular redistribution is a
cardinal feature of congestive heart failure, but it may be a particularly unhelpful sign in the
ICU patient with acute congestive failure. In these patients, all the pulmonary arteries look
enlarged, making it difficult to assess upper and lower vessel size. In addition, the film is often
taken supine, which can enlarge the upper lobe pulmonary vessels because of stasis of blood
flow and not true redistribution.

Front 69

How does LV dysfunction and RV dysfunction lead to pleural effusions?

Back 69

LV dysfunction causes increased hydrostatic pressures, which lead to interstitial edema
and pleural effusions. Right pleural effusions are more common than left pleural
effusions, but the majority are bilateral.
& RV dysfunction leads to system venous hypertension, which inhibits normal reabsorption
of pleural fluid into the parietal pleural lymphatics

Front 70

What is Westermark’s sign?

Back 70

Westermark’s sign is seen in patients with pulmonary embolism and represents an area
of oligemia beyond the occluded pulmonary vessel. If pulmonary infarction results, a wedgeshaped
infiltrate may be visible (

Front 71

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Front 73

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Front 74

Q waves present in V1 and V2 only should an MI be coded?

Back 74

No, to code AS MI, Waves must be present in V1 V2 and V3

Front 75

ECG shows AMI, should other diagnoses be coded?

Back 75

Yes, should code ST/or T abn suggests myocardial injury, Also code ST Segment depressio nin the setting of posterior MI

Front 76

LBBB is present should AMI be coded...

Back 76

probably not. however ST evleve > 1mm Concordant to QRS, or > 1mm depression in V1, V2, or V3, ST elevation > 5mm with opposite direction o the major deflection of the QRS

Front 77

AMI wioth SSTE elev in poart of the tracing and ST seg depression o on aonother part. Is It necessary to code the ST segment Depression?

Back 77

ST depression may be due to reciprocal changes, ischemia adjacent to to r remote from the infarct zone or n-q-wave MI

Front 78

Ischemic looking ST elevation is present without pathological Q wwaves in a patient with chest pain. should a acute MI be coded?

Back 78

No convex upward ST segment elevatio without

Front 79

What is the best criteria of LVH

Back 79

Cornell, which is the R wave in aVl a+ S wave in V3 > 28 mm in male s and >20 in females. Remember to code for St and/or T wave abn 2nd to hypertrophy if a s "strain" pattern is present in association with LVH

Front 80

What are the most important criteris for diagnosis RVH?

Back 80

probably RAD and adominant R wave with 2nd ST and/or T wave changes in leads V1 and V2. RAA is also common. If repol changes are present make sure to code them.

Front 81

2nd or 3rd degree heart block is present, should 1st deg AV block be called?

Back 81

No, not necessary

Front 82

Junctional Rhythm is present, is it necessary to code underlying atrial rhythm.

Back 82

Yes, if presnt (i.e. ventricular escape rhythm is present and sinus rhythm with 3rd degree AVB)

Front 83

Should LAD bed coded when LAFB is present? Similary should RAD be coded when LPFB is present?

Back 83

No, redundant

Front 84

Which cardiac patients should never get
pregnant?

Back 84

1 Those with significant pulmonary hypertension (pulmonary
vascular resistance >2/3 of systemic), especially cyanotic patients
and those with Eisenmenger reaction (maternal mortality ~50%)
and those with residual pulmonary hypertension after e.g. VSD
closure. NB: Even women with modest pulmonary vascular
disease ~1/2 systemic are at risk of death.
2 Those with grade 4 systemic ventricular function (EF <20%).�

Front 85

Which cardiac patients should undergo
elective Caesarean section?

Back 85

1 Those with independent obstetric indications.
2 Caesarean section should be strongly considered for the
following women:
� Those with mechanical valves, especially tilting disc in the
mitral position. The key here is to leave the mother off
warfarin for the minimum time possible. An elective section
is performed at 38 weeks� gestation, replacing the warfarin
with unfractionated heparin for the minimum time possible
� Severe aortic or mitral stenosis

Front 86

Which women should not get pregnant until operated upon?

Back 86

1 Marfan�s syndrome patients with aortic aneurysm/dilated
aortic root.
2 Those with severe left sided obstructive lesions (AS, MS,
coarctation).

Front 87

A patient is on life-long warfarin and wishes to
become pregnant. How should she be managed?�

Back 87

The use of warfarin during pregnancy is associated with a low
risk of maternal complications1 but it readily crosses the placenta
and embryopathy can follow exposure between 6�12 weeks�
gestation, the true incidence of which is unknown. A single study
has reported that a maternal warfarin dose 5mg is without this
embryopathy risk.2 As pregnancy progresses, the immature
vitamin K metabolism of the fetus can result in intracranial haemorrhage
even when the maternal INR is well controlled. In
addition, a direct CNS effect of warfarin has been described,
resulting in structural abnormalities. Conversion to heparin in
the final few weeks of pregnancy is recommended to prevent the
delivery of, what is in effect, an anticoagulated fetus.3

Front 88

What are the (6) indications for surgical
management of endocarditis?

Back 88

1. Congestive heart failure
2. Persistent sepsis (after 3-5 days ABX with blood sterility or lack of clinical improvement after one week)
3. Recognised virulence of the infecting organism (certain SA and most fungal..With prosthetic valve endocarditis, streptococcal tissue valve
infections involving only the leaflets can be cleared in 80%
with antibiotic therapy alone; however, mechanical or tissue valve infections involving the sewing ring generally require
valve replacement. If echocardiography demonstrates a
perivalvular leak, annular extension, or a large vegetation,early operation is necessary)
4. Extravalvular extension
5. Peripheral embolisation
6. Cerebral embolisation

Front 89

Which cardiac abnormalities greatly increase the risk of endocarditis?

Back 89

patent ductus arteriosus, prosthetic valves, hypertrophic
cardiomyopathy, aortic valve disease or previous endocarditis

Front 90

ASD Indications for closure include:

Back 90

symptoms (exercise intolerance,
arrhythmias), right heart volume overload on echocardiography,
the presence of a significant shunt (>2:1) or cryptogenic cerebrovascular
events, especially associated with aneurysm of the oval
foramen and right to left shunting demonstrated on contrast
echocardiography during a Valsalva manoeuvre

Front 91

How do I follow up a patient who has had
correction of aortic coarctation? What should I
look for and how should they be managed?

Back 91

Recoarctation, hypertension, insetting of bicuspid AV, you may have endocarditis, berry aneurysms, AI,

Front 92

What are risk factors for SCD in patients with HCM?

Back 92

family history of sudden deaths, recurrent syncope, non-sustained ventricular tachycardia and an abnormal blood pressure drop during exericise, LV thickness > 3 cm,

Front 93

What is the medical therapy for HCM?

Back 93

In those without
obstruction, the choice is between either a beta blocker or a calcium
antagonist, such as high dose verapamil (up to 480mg/day). In those with obstruction a beta blocker with or without disopyramide
is usually the first choice for those patients with outflow obstruction (~25% of patients). refractory symptoms may be candidates for
invasive treatment modalities such as dual chamber pacing with a
short AV delay, alcohol septal ablation or surgical myectomy.

Front 94

What does CHADS stand for?

Back 94

Congestive HF
HTN
Age > 65
Diabetes
Stroke

Front 95

What does CHA2DS2-VAS stand for?

Back 95

Congestive HF
HTN
Age > 65 >75
Diabetes
Stroke
Vascular disease (PVD)

Front 96

What does HAS-BLED stand for?

Back 96

Risk factors that make a patient likely to bleed on anticogaulation..
Hypertension
Abd (renal or liver disease)
Stroke
Bleeding HIstory
Labile INR
Elderly (>65)
Drugs/Alcohol

Front 97

Investigation of a patient with collapse
The history

Back 97

• ECG
• 24 hour ECG
• 24 hour BP
• Carotid sinus massage – supine and erect (only if negative
supine)
• External loop recorder
• Electrophysiological studies
• Head up tilt test
• CT head and EEG if appropriate
• Implantable loop recorder

Front 98

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Front 101

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Front 103

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Front 108

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Front 109

What is the clinical signs of severe acute aortic insuff?

Back 109

Short diastolic murmur, soft S1 (from premature mitral closure), low output state, pulm edema

Front 110

What do you expect after mitral valvuloplasty (short time)?

Back 110

with acute changes in atrial and ventricular compliance, the PHT is unreliiable, usuallyi needs 72 hours or more before it becomes reliable, planimetry is more reliable, clinically listen for a longer S2-OS interval and a shorter murmur...

Front 111

How would you reconcile the findings of a loud sys murmur with 4-5 m/s doppler gradient across the LVOT that is not dagger shaped, but has crisp S1 and S2 sounds, normal appearing aortic valve in short axis?

Back 111

TEE to look for subaortic membrane...

Front 112

What is high risk MVP and what is the role of ASA in this patient?

Back 112

leaflet thickening, elongated chordae, LAE, LV dilation..... aspirin is IIb recommend. and clearly indicated in prior stroke or TIA

Front 113

what is the physical exam in HOCM

Back 113

brisk bisiferiens carotids, normal S2, murmur that increases with Valsalva and decrease with hand grip. Echo with amyl nitrate may eval this better

Front 114

What are the expected physical findings in a patient with a mitral valve replacement with a bileaflet tilting disk mechanical valve?

Back 114

prominent closing click and soft and brief diastolic rumble

Front 115

What are the expected physical findings in a patient with a mitral valve replacement with a ball and cage valve

Back 115

prominent opening and clsoing clicks with soft and brief diastolic rumble

Front 116

Over a 3 year period, what is the likelihood that someone with severe asymptomatic AS will become symptomatic or come to surgery??

Back 116

>50%, from obs studies

Front 117

The presence of soft S1, normal carotid upstrokes, holosyst murmur that increases with handgrip and an S3 indicates what?

Back 117

mitral regurg and not Aortic stenosis

Front 118

What are the physical signs that indicate severe AS?

Back 118

no A2, late peaking murmur, diminshed carotid upstrokes.

Front 119

What are the signs of prosthetic mitral stenosis

Back 119

long diastolic rumble, muffled closures click, clinical heart failure

Front 120

In the setting of aortic stenosis with moderate AI, which of the following methods is most reliable for assessing AVA? A. invasive hemo with Gorlin. B. Dopple using continuity eq. C. pressure half time, D. Bernoulli

Back 120

B. Doppler using continuity EQ