Cardio part 3

Question 1

Effects of bile acid resins on lipid profile

Answer 1

Moderate reduction in LDL
Increase or no change in triglycerides (do not use for people who already have triglyceride issues)
Modest increase in HDL

Question 2

Effects of niacin on lipid profile

Answer 2

Modest reduction in LDL
Significant reduction in TG
Significant increase in HDL

Question 3

Considerations of niacin

Answer 3

Hepatotoxicity
Increased uric acid levels
Caution in pts with renal dysfunction

Question 4

Effects of fibrates on lipid profile

Answer 4

Can increase or decrease LDL
Significant reduction in TG
Significant increase in HDL

Question 5

What is considered part of clinical ASCVD?

Answer 5

Acute coronary syndromes
H/o MI
Stable or unstable angina
Coronary revascularization
Stroke
TIA of atherosclerotic origin
PAD

Question 6

Which statins are considered high-intensity?

Answer 6

Atorvastatin

Rosuvastatin

Question 7

Which statins are considered moderate intensity?

Answer 7

Atorvastatin
Rosuvastatin
Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin

Question 8

What is considered a low-intensity statin?

Answer 8

Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin

Question 9

Pathophys of peripheral vascular dz

Answer 9

Primarily the result of atherosclerosis
The process may gradually progress to complete occlusion of medium-sized and large arteries
May manifest acutely when thrombi, emboli, or acute trauma compromises perfusion

Question 10

What are some factors that can predispose pts to thrombosis?

Answer 10

Sepsis
Hypotension
Low cardiac output
Aneurysms
Aortic dissection
Bypass grafts
Underlying atherosclerotic narrowing of the arterial lumen

Question 11

What are conditions that often coexist with PVD

Answer 11

Primary factor: atherosclerosis
CAD
AFib
Cerebrovascular dz
Renal dz

Question 12

RFs for PVD

Answer 12

Smoking
HLD
DM
Hyperviscosity

Question 13

Hx manifestations of PVD

Answer 13

Intermittent claudication may be the sole manifestation of early symptomatic PVD
Aortoiliac dz- pain the thigh and buttock
Femoropopliteal dz-pain in the calf
Sx are precipitated by walking a predictable distance and are relieved by rest
Claudication may also present as the hip or leg “giving out” after a certain period of exertion and may not demonstrate the typical symptom of pain on exertion
The pain of claudication usually does not occur with sitting or standing
Erectile dysfunction has been linked as a potential early indicator

Question 14

Leriche syndrome

Answer 14

Intermittent claudication
Impotence
Significantly decreased or absent femoral pulses

Question 15

PE of PVD

Answer 15

Pulselessness
Paralysis
Paresthesia
Pain
Pallor
Assess for murmurs or other heart abnormalities
Investigate all peripheral vessels
Skin may have an atrophic, shiny appearance and may demonstrate trophic changes:
Alopecia
Dry, scaly, or erythematous skin
Chronic pigmentation changes 
Brittle nails

Question 16

Presentation of advanced PVD

Answer 16

Mottling in a “fishnet pattern”
Pulselessness
Numbness
Cyanosis

Question 17

Workup of PVD

Answer 17

CBC
BUN
Creatinine
Electrolyte studies
D-dimer
CRP
Interleukin-6
Homocysteine
Arteriography- could have more risks than gains
Doppler u/s
ABI

Question 18

Tx of PVD

Answer 18

Counsel pts regarding the potential effects of various activities and medications on the course of their illness
Counsel on smoking cessation
Avoid cold exposures and medications that can lead to vasoconstriction
Anticoagulants

Question 19

Pathophys of aortic stenosis

Answer 19

When the valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta

Question 20

Etiology of aortic stenosis requiring surgery

Answer 20

Common causes <70 yo in order in order from most common to least common:
Bicuspid AV
Postinflammatory
Degenerative
Unicommisural
Hypoplastic
Indeterminate
Common causes >70 yo in order:
Degenerative
Bicuspid
Postinflammatory
Hypoplastic

Question 21

H/o aortic stenosis

Answer 21

Usually has an asymptomatic latent period of 10-20 years
MC initial complaint is dyspnea
CP
Heart failure
Syncope

Question 22

PE of aortic stenosis

Answer 22

Carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude and gradual downslope (pulsus parvus et tardus)
Jugular venous pulse may show prominent a waves
A2 usually diminished or absent
Paradoxical splitting of the S2
Prominent S4 can be present
Crescendo-decrescendo systolic murmur
Rough low-pitched sound that is best heard at the second intercostal space in right upper sternal border
Radiates to carotid artery

Question 23

Workup of aortic stenosis

Answer 23

EKG
CXR
CMP
Cardiac markers
CBC
TTE
Cardiac cath and coronary arteriography
BNP

Question 24

Tx of aortic stenosis

Answer 24

Address ABCs
Perform CPR if in cardiac arrest
With acute sx, hospital admission, telemetry/ICU admission, and cardiology consultation should be considered
Heart failure- oxygen, cardiac and oximetry monitoring, IV access, loop diuretics, nitrates, morphine, and ventilatory support
Percutaneous balloon valvuloplasty is used as a palliative measure
Aortic valve replacement

Question 25

Pathophys of aortic regurgitation

Answer 25

Acute- the LV does not have sufficient time to dilate in response to the sudden increase in volume As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure and altering coronary flow dynamics Chronic- gradual LV volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy There is greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume

Question 26

Etiology of acute aortic regurgitation

Answer 26

``` Infective endocarditis Bulky vegetation Chest trauma Post-TAVR LVAD implantation Aortic dissection (type A) ```

Question 27

Etiology of chronic aortic regurgitation

Answer 27

``` Bicuspid aortic vavle- MCC of isolated AR Certain wt loss medications Rheumatic fever Ankylosing spondylitis Behcet dz Giant cell arteritis RA SLE Takayasu arteritis Whipple disease ```

Question 28

Connective tissue d/os that can cause significant AR

Answer 28

``` Marfan Ehlers-Danlos Floppy aortic valve Aortic valve prolapse Sinus of Valsalva aneurysm Aortic annular fistula ```

Question 29

Hx of acute aortic regurgitation

Answer 29

Sudden, severe SOB Rapidly developing heart failure CP if myocardial perfusion pressure is decreased or an aortic dissection is present

Question 30

Hx of chronic aortic regurgitation

Answer 30

Often have a long-standing asymptomatic period that may last for several years Compensatory tachycardia Severe chronic AR: Palpitations SOB CP Sudden cardiac death: uncommon in asymptomatic pts with preserved LV function

Question 31

PE of acute aortic regurgitation

Answer 31

May be fulminant and lead to cardiogenic shock Pts with CHF or shock associated often appear gravely ill Other sx: Tachycardia Peripheral vasoconstriction Cyanosis Pulmonary edema Alterial pulsus alternans Austin-Flint murmur (Lower piched and short in duration) Decrescendo diastolic murmur that is heard best with the pt leaning forward

Question 32

Chronic aortic regurgitation PE: signs

Answer 32

Widened pulse pressure Becker sign- visible systolic pulsations of the retinal arterioles Corrigan pulse- abrupt distention and quick collapse on palpation of the peripheral arterial pulse de Musset sign- bobbing motion of the pt's head with each heartbeat Hill sign- popliteal cuff SBP 40 mm higher than brachial cuff systolic BP Droziez sign- systolic murmur over the femoral artery with proximal compression of the artery, and diastolic murmur over the femoral artery with distal compression of the artery Muller sign- visible systolic pulsations of the uvula Quincke sign-visible pulsations of the fingernail bed with light compression of the fingernail Traube sign- booming systolic and diastolic sounds auscultated over the femoral artery

Question 33

Chronic AR PE: distention/sx

Answer 33

PMI may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla Peripheral pulses are prominent or bounding S3 gallop if LV dysfunction is present High-pitched sound in diastole that is loudest at the left sternal border

Question 34

Workup of AR

Answer 34

``` Should be guided by clinical scenario Could also include: CBC PT/aPTT Type and screen Electrolytes VDRL LDH TTE CXR Radionuclide imaging Aortic angiography EKG Cardiac cath ```

Question 35

Tx of AR

Answer 35

Severe chronic AR- vasodilator therapy Valve replacement With HTN or hypervolemia, salt restriction Ongoing clinical surveillance with periodic echocardiogarphy for After initial study, clinical eval and a repeat echo are recommended in 3 mos When to subsequently followup is determined based on the stability of the LV end-systolic dimension and LV end-diastolic dimension Consider hydralazine or nifedipine

Question 36

Pathophys of pulmonic stenosis

Answer 36

Can be due to isolated valvular, subvalvular or peripheral obstruction or it may be found in association with more complicated congenital heart disorders Valvular- valve commissures are partially fused and the 3 leaflets are thin and pliant, resulting in a conical or dome-shaped structure with a narrowed central orifice Subvalvular- narrowing of the infundibular or subinfundibular region, often with a normal pulmonic valve Peirpheral- can cause obstruction at the level of the main pulmonary artery, at its bifurcation, or at the more distal branches

Question 37

Hx of pulmonary stenosis

Answer 37

Mos with mild-to-moderately severe PS are asymptomatic Severe: exertional dyspnea and fatigue Right heart failure: peripheral edema and other typical sx Significant right-to-left shunt: cyanosis

Question 38

PE of pulmonary stenosis

Answer 38

Precordial heave or a palpable impulse from the RV along the left parasternal border