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Cardiac For NA > Valve Heart Disease > Flashcards

Valve Heart Disease Flashcards

1
Q

What is most common form of valve dz in WESTERN countries

A

Degenerative valve disease

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2
Q

What is most common form of valve dz in DEVELOPING countries

A

Rheumatic Heart disease

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3
Q

What are the 2 most common valve dz in western counties:

A

AS from calcification disease
MR from primary causes like degenerative dz or secondary causes like ischemic heart disease

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4
Q

Stenosis lesions have a _ orifice which _ blood flow.

A

Narrow
Obstructs (fixed vs dynamic)

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5
Q

Which stenotic valves cause issues in systole:
Which cause issues in diastole:

A

Systole: aortic + pulmonic
Diastole: mitral + tricuspid

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6
Q

Stenosis lesions on valves cause flow _ > blood ejects with _ (inc/dec) velocity thru orifice with simultaneous _ (inc/dec) in pressure > with _ (inc/dec) in pressure gradient across valve

A

Convergence
Increased
Decrease
Increase

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7
Q

Stenotic valve obstruction is either fixed or dynamic.
Define + example: Fixed + Dynamic

A

Fixed: constant degree of obstruction (AS)
Dynamic: variable degree of obstruction depending on cardiac cycle phase (hypertrophic obstructive CM)

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8
Q

Regurg valve lesions cause _ overload > chamber _ and _ hypertrophy in originating chamber

A

Volume
Dilation
ECCENTRIC

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9
Q

More than one valve lesion:
-2nd lesion on SAME valve
-2nd lesion on OTHER valve

A

Same valve -> MIXED valve heart dz
Other valve -> MULTIPLE valve heart dz*** most common (AS with AR or MR, AR with MR)

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10
Q

3 basic mechanisms LV responds to hemodynamic changes:

A

-frank starling mechanism
-neurohormonal systems
-chamber remodeling *

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11
Q

3 factors determining LV performance:

A

Preload (venous return + EDV)
Myocardial contractility (force generated at any EDV)
Afterload (aortic impedance + wall stress)

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12
Q

What is the relationship between LV pressure gradient and volume ejection characterized as?

A

Frank starling curve
-positive correlation between increased cardiac filling pressure and increased CO
Up to a point of diminishing return

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13
Q

As cardiac function declines, Frank Starling curve shifts _ and _

A

RIGHT and FLATTENS
-diminished return with added voluem

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14
Q

Frank starling curve shows us how changes in _ _ cause the ventricle to move up or down along a single Frank Starling curve. The slope of the curve is defined by the existing conditions of _ and _.

A

venous return
afterload and inotropy

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15
Q

Initial reductions in LV performance are countered by activation of the _ systems > increased _ _ > increases sarcomere length + _

A

neurohumoral
fluid rtn
contractility

for diastolic function, there is an UPWARD shift in ED pressure-volume relationship bc a higher pressure is needed to achieve the same volume

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16
Q

LV remodeling is defined as _ heart change that occurs to meet the increased demand from increased hemodynamic load or neurohumoral activation

A

structural

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17
Q

Pressure overload is seen in _

A

AS

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18
Q

Volume overload is seen in _ lesions

A

regurg

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19
Q

3 general patterns of LV remodeling:

A

-concentric = PRESSURE overload (AS)
-eccentric = VOLUME overload (regurg)
-mixed hypertrophy = MIXED valve lesions

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20
Q

3 factors affecting degree of remodeling:

A

-decreased contractility from ischemia
-increased vascular resistance
-neurohormonal activation

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21
Q

NYHA Functional Classifications of Heart Disease:
I
II
III
IV

A

I = asymptomatic
II = symptoms with ordinary activity but ok at rest
III = symptoms with minimal activity but ok at rest
IV = symptoms at rest

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22
Q

Angina may not be related to CAD when in presence of valve issues because:

A

may be r/t increased O2 demand from hypertrophied ventricles exceeding supply from patent coronary arteries

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23
Q

Murmurs represent _ flow across a valve

A

turbulent

24
Q

L or R: Pulm edema is a sign of _ heart failure and dependent edema or ascites is a sign of _ heart failure

A

L
R

25
Q

EKG findings of valve dz and what they indicate:
-broad, notched P waves (P mitrale)
-L or RAD and high voltage

A

P mitrale = LAE seen in MV dz
LAD/RAD and high voltage = LV/RV hypertrophy

-other findings: dysrhythmias, conduction issues, evidence of ischemia or previous MI

26
Q

Cornerstone of valve dz dx is _ _

A

doppler echo
-helps monitor progression and show indices of needing surgery

27
Q

Table 6.2 Utility of Echo in eval of valve heart dz

A

-determine significance of heart murmurs
-identify hemodynamic issues
-determine transvalvular pressure gradient
-determine valve area
-determine ventricular EF
-dx valve regurg
-evaluate prosthetic valve function

28
Q

Valve Dx and findings
- 3D Echo

A

assess suitability of repair in valve surg and measurement of LVOT in pts with AS and mitral area in pts with MS

29
Q

Valve dx and findings:
-Stress echo

A

distinguished true severe AS from pseudo-severe
-assess LV flow reserve when pressure gradient is low and LV fraction is reduced

30
Q

Valve dx and findings:
-cath

A

recommended when noninvasive tests are inconclusive or discordant with clinical picture

31
Q

Why is thermodilution more reliable than Fick CO calculations when it comes to valve issues?

A

certain dz states like severe TR and low CO can affect accuracy of results

32
Q

Valve dx and findings:
-CT

A

assess aortic valve Ca++ score when there is evidence of low flow, low gradient AS, and preserved LVEF, also used to correctly size prosthetic for future TAVR
-higher score = increased likelihood of severe AS

33
Q

Valve dx and findings:
-cardiac MRI

A

dx regurg lesions and measures ventricular volumes and systolic function
-accurate identification of serial changes in ventricular volumes, mass, function; changes reflect global burden and worsening pathology, determine optimal time for surg repair

34
Q

Common causes of AS
-western countries
-developing

A

western: age related degen
develop: rheumatic heart disease

35
Q

AS
-histology

A

valves appear thick, inflamed, and calcified
-similar to atherosclerosis: endothelial dysfunction> lipid deposition> oxidative change > inflammation > fibrosis > calcification

36
Q

AS
-risk factors

A

systemic HTN
hypercholesterolemia
DM
smoking
male

37
Q

2nd most common cause of AS in US is _ _ _

A

bicuspid aortic valve

38
Q

Bicuspid aortic valve comes with complications such as:

A

AS
AR
aortic root dilation
aortic coarction

39
Q

Bicuspid aortic valve
-patho

A

leaflets are susceptible to constant low shear stress > thickens + calcifies ~5-6th decade of life

40
Q

Rheumatic heart disease
-patho

A

fusion of commissures of leaflets > fibrosis > calcification > narrowing of valve orifice

41
Q

Rheumatic AS often affects the _ valve often leading to an isolated or combined _ lesion (regurg or stenosis)

A

mitral
mitral

42
Q

AS
-rare causes

A

metabolic dz (Fabry dz), SLE, alkaptonuria

43
Q

AS patho (step 1/3)

Decrease in aortic valve area -> _ to LV forward flow -> compensates by _ LV pressure to maintain _.

A

obstruction
increasing
SV

44
Q

AS Patho (step 2/3)

LV remodeling initially into _ hypertrophy, reducing wall stress for a while. This demonstrates _ ‘s Law of _ _. Eventually chambers _ and _ drops.

A

CONCENTRIC
Laplace’s Law of Wall Tension
dilate
CO

45
Q

AS Patho (step 3/3)

CO may lack reserve to increase with exertion. Leading to:
-Angina
-MI
-Syncope

A

Angina: may be without CAD from mismatch supply + increased O2 demand for concentric hypertrophy AND from increased work offsetting increased afterload from AS

MI: from compression of subendocardial vessels from increased LV pressure

Syncope: exertion-induced vasodilation + obstruction + fixed CO = HoTN and reduced cerebral perfusion

46
Q

AS
-severe dz markers (2)

A

-LV mean pressure gradient > 40mmHg
-valve area < 1cm ^ 3

47
Q

T/F for AS severe dz is present when symptoms of AS appear and require immediate tx

A

True
-symptoms come late bc hypertrophy produces high enough pressures to maintain adequate SV for a while

48
Q

AS
main triad of s/s

A

1 exertional dyspnea
-from diastolic dysfunction from elevated LV filling pressures

2 chest pain

3 syncope

49
Q

AS
physical exam

A
  1. Systolic murmur in aortic area rad to neck similar to carotid bruit
  2. Pulsus Parvus et tardus - palpitation of carotid pulses slowly to a delayed and sustained peak
  3. Splitting of S2 from prolonged LV ejection and audible S4 at apex reflecting hypertrophy
50
Q

Test of choice for dx and monitoring AS and common findings (3):

A

TTE with dopp
-trileaflet or bileaflet
-thickening and calcification with dec mobility
-LVH and LV systolic or diastolic dysfunction

51
Q

AS
CXR findings

A

Prominent ascending aorta from post stenotic dilation

Aortic valve calcification seen in lateral CXR

52
Q

Treatments for AS

A

asymptomatic -> serial echos to monitor
-medical therapy does NOT prevent progression of AS :(

SAVR and TAVR = mainstays

Percutaneous aortic balloon valvotomy (PABV) sometimes for kids and YA with congenital NONcalcified AS
-high rate restenosis and risk for embolism

53
Q

T/F Brisk exercise is recommended as tx plan for AS

A

false, should be avoided!

54
Q

Guidelines recommend TAVR instead of SAVR in low risk pts who meet all 4 criteria:

A

-age > 65
-transfemoral TAVR is feasible
-aortic valve is trileaflet
-absence of high risk anatomical issues like adverse aortic root, LVOT calcification, or low coronary Ostia height

If pt lacks one of these SAVR is indicated

55
Q

Anesthesia mgmt of AS

A
  1. Maintain NSR
  2. Avoid tachy and excessive brady
  3. Maintain preload, optimize venous return and LV filling
  4. Avoid HoTN
  5. Avoid meds that decrease contractility and preserve CO (high dose prop or VA)
  6. GA > regional bc risk for severe HoTN from reduced preload is unpredictable
  7. Induce with drugs that don’t drop SVR or contractility (opioids, benzos, etomidate ok)
  8. Maintain with VA and opioids
  9. Monitor w 5 lead, invasive monitoring, and possible TEE

Cardiac For NA (5 decks)

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