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Cardiology Exam > Valves 1 > Flashcards

Valves 1 Flashcards

1
Q

flow through the normal heart (with normal valves)

A

*when all of the heart valves are working normally, so the blood flow across each valve is the same
*ex: if we have a stroke volume of 50 mL, then 50 mL goes across each valve

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2
Q

valvular stenosis - defined

A

*valve is tight and doesn’t open well
*“constriction or narrowing of a passage or orifice”

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3
Q

valvular regurgitation - defined

A

*valve is “leaky”
*aka valvular insufficiency
*allows blood to flow backward through the valve, into the preceding chamber

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4
Q

flow through a stenotic valve

A

*when the valve doesn’t open well (stenotic), the same amount of blood goes through the valve, but the VELOCITY has to INCREASE to get the same amount of blood through in the same amount of time, due to reduced cross-sectional area [if SV is 50ml, 50mL still goes across each valve, but at a higher velocity across the stenotic valve]

*results in a difference in pressure between the 2 chambers on either side of the stenotic valve → pressure in the chamber PROXIMAL to the stenosis is HIGHER than the distal chamber (pressure gradient)
*pressure gradient is used to indicate how severe the stenosis of a valve is
*the amount of pressure-gradient that indicates disease is different for each valve

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5
Q

pressure gradients in valvular stenosis

A

*pressure in chamber proximal to the stenosis > pressure in distal chamber
*pressure gradient is used to indicate the severity of the stenosis

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6
Q

flow through a regurgitant valve

A

*when the valve is “leaky” (regurgitant or insufficient), both the forward volume and regurgitant volume have to go across the valve
*i.e. if a valve has regurgitation, it has INCREASED VOLUME that goes forward across it
*the other valves (if normal), only have the forward volume crossing them

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7
Q

examples of flow through a regurgitant valve

A

*if we have a forward volume of 50 mL, 50mL goes across each normal valve, but if we have a mitral regurgitant volume of 25 mL, then it means 75 mL has to cross the mitral valve (50 mL forward, and 25 mL backward into L atrium)

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8
Q

flow through a regurgitant AV valve (tricuspid or mitral)

A

*if a tricuspid or mitral valve is regurgitant → they INCREASE THE VOLUME that goes into the VENTRICLE during DIASTOLE → dilation of ventricle

*this increased volume is the blood which goes forward during DIASTOLE and the blood which will go backwards during SYSTOLE

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9
Q

flow through a regurgitant semilunar valve (aortic or pulmonic)

A

*if an aortic or pulmonic valve is regurgitant → they INCREASE THE VOLUME that goes into the AORTA/PULMONARY ARTERY during SYSTOLE

*this increased volume is the blood which goes forward during systole to the body and the blood which will go backwards into the ventricle during DIASTOLE → increased volume in ventricle → dilation of ventricle

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10
Q

which valves are open during systole?

A

*AORTIC & PULMONIC (semilunar) valves are open during systole

*systole: blood is being pumped out of the ventricles and into the aorta/pulmonary artery as the ventricles contract

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11
Q

which valves are closed during systole?

A

*TRICUSPID & MITRAL (atrioventricular) valves are closed during systole

*systole: blood is being pumped out of the ventricles and into the aorta/pulmonary artery as the ventricles contract

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12
Q

which valves are open during diastole?

A

*TRICUSPID & MITRAL (atrioventricular) valves are open during diastole

*diastole: blood is being sucked into the ventricles from the atria; the ventricles are relaxed and they are not sending blood out to the body

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13
Q

which valves are closed during diastole?

A

*AORTIC & PULMONIC (semilunar) valves are closed during diastole

*diastole: blood is being sucked into the ventricles from the atria; the ventricles are relaxed and they are not sending blood out to the body

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14
Q

aortic stenosis - defined

A

*stenosis of blood flow from the left ventricle to the aorta due to aortic valve disease or obstructions just above/below the valve
*because the aortic vale doesn’t open well during systole, it leads to a systolic problem

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15
Q

3 levels of obstructions associated with the aortic valve

A
  1. subvalvular: LVOT [left ventricular outflow tract]
    a. subaortic membrane
    b. HOCM [hypertrophic obstructive cardiomyopathy]
  2. supravalvular (sinotubular junction)
  3. valve level (valvular stenosis)
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16
Q

supravalvular aortic stenosis

A

*almost always associated with Williams Syndrome
*Williams Syndrome is a rare neurodevelopmental disorder caused by a deletion of about 26 genes from the long arm of chromosome 7

*results in:
-“elfin” facial appearance, along with a low nasal bridge
-cheerful demeanor and ease w/ strangers
-developmental delay w/ strong language skills
-supravalvular aortic stenosis [CONSTRICTION AT SINOTUBULAR JUNCTION]
-transient hypercalcemia

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17
Q

valvular aortic stenosis - etiologies

A
  1. age-related, degenerative calcified aortic valve disease [most common etiology]
  2. bicuspid aortic valve [congenital]
  3. rheumatic heart valve disease [rare]
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18
Q

histology of valvular aortic stenosis

A
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19
Q

valvular aortic stenosis - relationship to atherosclerosis

A

*aortic valve disease shares many features with atherosclerosis, such as cellular proliferation, inflammation, lipid accumulation, and increased presence of macrophages
*treatments for atherosclerosis are ineffective for valvular aortic stenosis
*60% of those with aortic stenosis have concomitant coronary artery disease

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20
Q

valvular aortic stenosis due to bicuspid aortic valve

A

*1-2% of general population; 2x more common in males > females
*early aortic stenosis due to abnormal, turbulent flow across the aortic valve (patients present in 30s-50s)
*some have regurgitation in addition to stenosis
*25-50% of those with bicuspids will probably never have clinical manifestations
*associated with aortic aneurysms

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21
Q

aortic aneurysms in bicuspid aortic valve stenosis

A

*people with bicuspid valves have a significant chance of developing ascending aortic aneurysms
*treated in a manner similar to those with Marfan’s syndrome

22
Q

valvular aortic stenosis due to rheumatic heart valve disease

A

*result of the autoimmune disease rheumatic fever (caused by Strep pyogenes infection)
*if untreated, the body creates antibodies to a surface protein on the bacteria (M protein) that mimics a protein on the lining of the heart → immune system attacks the lining of the heart → inflammation & scarring of heart valves, esp aortic valve → calcification & stenosis of aortic valve
*causes stiffening/immobilization of leaflet tips, often sparing the valve leaflets

note - mitral stenosis is the most common valve issue associated with RHD

23
Q

compare calcific vs. rheumatic aortic stenosis

A

*with calcific aortic stenosis, the stiffness/rigidity starts at the annulus and moves toward the leaflet tips
*with rheumatic aortic stenosis, the stiffness/rigidity immobilizes the leaflet tips, often sparing the valve leaflets

24
Q

where to auscultate for aortic stenosis

A

*right second intercostal space, along the right sternal border (RUSB)

25
Q

aortic stenosis - auscultation findings

A

*crescendo-decrescendo murmur, loudest at RUSB (systolic murmur that gets louder then softer) (“diamond-shaped murmur”)

*the more severe the stenosis, the later the peak will occur; in very stenotic valve, it may obliterate S2
*may radiate to the carotids:
-carotid upstroke may be delayed in severe aortic stenosis (Pulsus parvus et tardus - weak pulses with delayed peak)

26
Q

ancillary findings of aortic stenosis

A

*in some instances, questions about aortic stenosis may purposefully leave the murmur itself out
*when that’s the case, look for some of the following indications of aortic stenosis:
-weak pulse
-delayed pulse
-paradoxical splitting of S2

27
Q

S1 heart sound represents?

A

*mitral and tricuspid valve closure; the beginning of SYSTOLE
*loudest at mitral area

28
Q

S2 heart sound represents?

A

*aortic and pulmonary valve closure; beginning of DIASTOLE
*loudest at left upper sternal border

29
Q

evaluating the severity of aortic stenosis based on velocity across aortic valve

A

*normal aortic valve: 3-4 cm²
*severe aortic stenosis: < 1cm²
*severe aortic stenosis is mean pressure gradient (between LV and aorta) > 40 mmHg

30
Q

Wigger’s Diagram - aortic stenosis

A

*significant increase in left ventricular pressure relative to aortic pressure in patients with aortic stenosis

note - left image is normal, right image is aortic stenosis

31
Q

afterload & preload in aortic stenosis

A

*aortic stenosis predominantly effect = INCREASED AFTERLOAD (increased ESV, decreased stroke volume)

*initially, no meaningful effect on preload
*as LV compensation fails, may require increased preload in effort to maintain stroke volume

32
Q

LV compensation for aortic stenosis

A

*to reduce wall stress, LV wall thickens → CONCENTRIC left ventricular hypertrophy
*this enables increase force of contraction to overcome the stiff valve

33
Q

preload-dependent aortic stenosis

A

*in normal LV, one can manipulate afterload, contractility, and preload to change stroke volume in order to change cardiac output

*in severe aortic stenosis, apart from aortic valve replacement, there is no way to reduce afterload, and usually no way to meaningfully increase contractility, so the only way to maintain cardiac output is PRELOAD
*need to maintain enough preload so that enough blood is able to flow through aortic valve and out to the body

34
Q

clinical presentation of aortic stenosis

A
  1. angina (chest pain)
  2. syncope
  3. dyspnea
35
Q

pathogenesis of angina in aortic stenosis

A

*increased pressure in the left ventricle → subendocardial ischemia
*it is a global, diffuse process

*note - do NOT give nitroglycerin to someone with angina from aortic stenosis (b/c it reduces preload)

36
Q

pathogenesis of syncope in aortic stenosis

A

*if AS is severe enough, then there can be a maximum limit of cardiac output that can go through the aortic valve
*if patient with such a valve tried to exercise or perform some other activity that required increased cardiac output, then there is a drop in blood pressure → syncope (passing out)

37
Q

pathogenesis of dyspnea in aortic stenosis

A

*dyspnea in people with AS is a sign of congestive heart failure (ventricle is starting to fail)

38
Q

Heyde’s Syndrome

A

*severe aortic stenosis & its higher blood velocity → increased sheer stress on the blood → unraveling of von Willebrand factor in the same way it vWF does on encountering an injury site
*when vWF unravels into its active state, it is degraded by ADAMTS13 enzyme
*as the quantity of vWF in the blood decreases, the rate of bleeding dramatically increases
*in pts with severe AS & intestinal angiodysplasia (AVM), the reduced quantity of vWF increases the risk of GI bleeding

39
Q

treatment of aortic stenosis

A

*no medication can improve a stiff valve or do the job that a normal aortic valve can do
*treatment options:
1. aortic valve replacement (mechanical heart valve, pig valve, or cow valve)
2. catheter-based valves (TAVR - transcatheter aortic valve replacement)

40
Q

aortic regurgitation - defined

A

*an imperfect close of the aortic semilunar valve due to distortion of the valve leaflets or dilation of the aortic annulus, causing blood flow to reverse direction during ventricular diastole
*aortic valve has become “leaky”; aka aortic valve insufficiency
*during DIASTOLE, a jet of blood is able to go from the aorta to the left ventricle

41
Q

acute etiologies of aortic regurgitation

A

*aortic dissection
*endocarditis

42
Q

chronic etiologies of aortic regurgitation

A

*bicuspid aortic valve
*ascending aortic aneurysm
*dilation of aortic annulus (annuloaortic ectasia)
*rheumatic heart disease

43
Q

aortic regurgitation due to dilation of the ascending aorta

A

*dilation of ascending aorta → stretching of the aortic annulus → increased difficulty in closing the aortic valve correctly → aortic regurgitation
*in severe instances, part of the leaflet tips may not even reach each other

44
Q

where to auscultate for aortic stenosis

A
  1. right second intercostal space, along the right sternal border
  2. Erb’s point (left 3rd intercostal space)

best heard at the end of expiration with the patient sitting up and leaning forward

45
Q

aortic regurgitation - auscultation findings

A

*early diastolic decrescendo murmur
*soft, high-pitched, “blowing” murmur; decrescendo (decreasing in intensity as the diastole progresses)

note - aortic regurgitation significantly increases the pulse pressure

46
Q

aortic regurgitation - auscultation findings correlated with severity

A

*the more severe the AR, the shorter the murmur can be
*pressure difference is highest between aorta & LV at the beginning of diastole → loudest part of the murmur
*as diastole continues, aortic pressure decreases and LV pressure increases
*in severe AR, murmur intensity goes down b/c pressure gradient is reduced
*sometimes, b/c the flow has increased across the aortic valve, you can also hear a systolic ejection murmur

47
Q

Wigger’s Diagram - aortic regurgitation

A

*significant decrease in aortic pressure during diastole in patients with aortic regurgitation

note - decreased aortic diastolic pressure leads to a WIDENED PULSE PRESSURE

48
Q

pressure-volume loops in acute aortic regurgitation

A

*increased EDV
*increased stroke volume

note - AR causes widened pulse pressure due to decreased diastolic pressure

49
Q

consequences of acute aortic regurgitation

A

*coronary perfusion pressure (CPP):
-CPP = diastolic blood pressure - LV EDP
-acute severe AR leads to decreased diastolic blood pressure and increased LV EDP → DECREASED CPP
*can lead to global cardiac ischemia, resulting in reduced LV systolic function, which further complicates things

50
Q

LV compensation to aortic regurgitation

A
  1. increased forward flow (systemic flow + regurgitant volume; sending more volume into a higher pressure chamber) → increased afterload → increased LV wall thickness (concentric LV hypertrophy)
  2. increased filling of LV chamber during diastole (b/c of regurgitant flow backwards across aortic valve) → increased preload → increased LV dilation (eccentric LV hypertrophy)
51
Q

clinical presentations of aortic regurgitation

A

*wide pulse pressure
*pistol shot femoral pulse
*pulsation of the capillary bed in the nail (Quincke’s sign)
*head nodding in time with the heart beat

52
Q

treatment for aortic regurgitation

A

*observation if patients are asymptomatic
*we start to treat when…
-when symptoms develop (CHF, cardiogenic shock)
-when LV systolic function starts to decline (LV EF < 50%)
-when LV is significantly dilated, we interpret the severely dilated LV to mean that the severe AR is hemodynamically significant
*tx options: afterload-reducing agents (ACEi, ARBs, etc), aortic valve replacement surgery

Cardiology Exam (52 decks)

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