Cardio part 3 Flashcards
Effects of bile acid resins on lipid profile
Moderate reduction in LDL
Increase or no change in triglycerides (do not use for people who already have triglyceride issues)
Modest increase in HDL
Effects of niacin on lipid profile
Modest reduction in LDL
Significant reduction in TG
Significant increase in HDL
Considerations of niacin
Hepatotoxicity
Increased uric acid levels
Caution in pts with renal dysfunction
Effects of fibrates on lipid profile
Can increase or decrease LDL
Significant reduction in TG
Significant increase in HDL
What is considered part of clinical ASCVD?
Acute coronary syndromes H/o MI Stable or unstable angina Coronary revascularization Stroke TIA of atherosclerotic origin PAD
Which statins are considered high-intensity?
Atorvastatin
Rosuvastatin
Which statins are considered moderate intensity?
Atorvastatin Rosuvastatin Simvastatin Pravastatin Lovastatin Fluvastatin Pitavastatin
What is considered a low-intensity statin?
Simvastatin Pravastatin Lovastatin Fluvastatin Pitavastatin
Pathophys of peripheral vascular dz
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
What are some factors that can predispose pts to thrombosis?
Sepsis Hypotension Low cardiac output Aneurysms Aortic dissection Bypass grafts Underlying atherosclerotic narrowing of the arterial lumen
What are conditions that often coexist with PVD
Primary factor: atherosclerosis CAD AFib Cerebrovascular dz Renal dz
RFs for PVD
Smoking
HLD
DM
Hyperviscosity
Hx manifestations of PVD
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
Leriche syndrome
Intermittent claudication
Impotence
Significantly decreased or absent femoral pulses
PE of PVD
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
Presentation of advanced PVD
Mottling in a “fishnet pattern”
Pulselessness
Numbness
Cyanosis
Workup of PVD
CBC BUN Creatinine Electrolyte studies D-dimer CRP Interleukin-6 Homocysteine Arteriography- could have more risks than gains Doppler u/s ABI
Tx of PVD
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
Pathophys of aortic stenosis
When the valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta
Etiology of aortic stenosis requiring surgery
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
H/o aortic stenosis
Usually has an asymptomatic latent period of 10-20 years MC initial complaint is dyspnea CP Heart failure Syncope
PE of aortic stenosis
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
Workup of aortic stenosis
EKG CXR CMP Cardiac markers CBC TTE Cardiac cath and coronary arteriography BNP
Tx of aortic stenosis
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
Pathophys of aortic regurgitation
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
Etiology of acute aortic regurgitation
Infective endocarditis Bulky vegetation Chest trauma Post-TAVR LVAD implantation Aortic dissection (type A)
Etiology of chronic aortic regurgitation
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
Connective tissue d/os that can cause significant AR
Marfan Ehlers-Danlos Floppy aortic valve Aortic valve prolapse Sinus of Valsalva aneurysm Aortic annular fistula
Hx of acute aortic regurgitation
Sudden, severe SOB
Rapidly developing heart failure
CP if myocardial perfusion pressure is decreased or an aortic dissection is present
Hx of chronic aortic regurgitation
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
PE of acute aortic regurgitation
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
Chronic aortic regurgitation PE: signs
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
Chronic AR PE: distention/sx
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
Workup of AR
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
Tx of AR
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
Pathophys of pulmonic stenosis
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
Hx of pulmonary stenosis
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
PE of pulmonary stenosis
Precordial heave or a palpable impulse from the RV along the left parasternal border
