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Aortic valve area
Mitral valve area
- -narrowed opening due to calcification or fibrosis
- -decreased cross-sectional area
- -valve cusps fuse together limiting opening
Insufficiency / Regurgitation
- -Leaflets don't seal completely
- -Blood goes from a distal to a proximal chamber
What's the cause of concentric hypertrophy?
What causes pressure overload?
MS or AS
What's the cause of eccentric hypertrophy?
What causes volume overload?
AR or MR
Rheumatic heart disease
- -historically was the most common cause of valvular disease
- -caused by group A beta strep (sore thoat, scarlet fever, middle ear infection)
- -inflammatory condition affecting skin, connective tissue, and the heart
- -most common in kids and young adults
How can rheumatic fever cause valvular heart disease?
- -thought to be due to a toxin produced by the strep or autoimmune cross sensitivity between bacterial and cardiac antigens
- -antibodies can persist for 1 year or more following the infection, during this time damage can occur
- -may not see evidence of valvular disease until 20-30 years after the initial infection
What valves are most prone to valvular disease?
- #1- mitral (it receives more trauma just doing its regular job)
- #2- aortic
What percent of pts with rheumatic heart disease will get MS? What additional percent will get aortic valve disease also?
40% and 25%
Most common presenting symptoms of ARF?
fever, chills, fatigue, migratory arthralgias
What are the Jones criteria
S/sx of ARF
Major Jones criteria
- Sydenham chorea
- Erythema marginatum
- Subcutaneous nodules
Minor Jones criteria
- migratory arthralgias
- increased ESR and CRP
- prolonged PR interval
Diagnosis of ARF
- 1) evidence of strep infection
- 2 major criteria or 1 major and 2 minor criteria
caused by vibration of blood flow across the valve
Occurs between S1 and S2
Occurs after S2 and before next S1
Key points to address during pre-op assessment of a pt with valvular heart disease
- -severity of cardiac disease
- -how impaired is contractility?
- -is there other organ involvement?
- -identify compensatory mechanisms
- -current drugs
- -do they have a prosthetic valve?
NY Heart Association Function Classification
- -applies specifically to heart disease
- -when do symptoms occur
- Class 1- asymptomatic
- 2- ok at rest, symptoms with ordinary activity
- 3- ok at rest, symptoms with minimal activity
- 4- symptoms at rest
Most common cause of MS?
- -RF (50% of pts)
- other rare causes (1% of cases):
- -calcification (elderly)
- -thickening and calcification of leaflets
- -fusion of commissures (where they join)
- -thickening and shortening of chordae tendinae
Effects of MS
- -increased LA pressure (and volume)
- -decreased SV (with tachycardia as there's less filling time for the LV), pulmonary venous pressure increases, this can progress to pulmonary edema and elevated right heart pressures
When does MS become significant?
When valve area < 2 cm2
Why does AF frequently develop in pts with MS?
- -there is chronic pressure overload of the LA
- -LA dilates
- -conduction fibers get stretched
- -this throws the conduction system in the atria off
What percent of pts with severe MS get AF?
In what 2 ways does AF reduce CO in a pt with MS?
- 1) loss of atrial kick
- 2) AF frequently has a fast rate and this decreases diastolic filling time
Why does vasoconstriction occur with MS and what effect does this have on the LV?
- -Due to SNS stimulation afterload is increased
- -This decreases preload
- -Contributes to LV dysfunction
Murmur of MS
- -last 2/3 of diastole
- -low rumbling sound
- -may hear an opening "snap"
How does MS affect EDV, ESV, SV?
- All are decreased.
- Significant decrease in EDV (limited filling)
- Slight decrease in ESV
- Overall result is a decreased SV
Where is the murmur of MS heard best?
Apex and axilla
Is the duration or intensity of the MS murmur more indicative of severity?
The duration- speaks to how long it takes for the blood to get from the LA to the LV. More severe MS will have a longer murmur.
How is the valve area and gradient determined?
valve opening of < 1 cm2 and mean valve gradient of > 10 mmHg
valve opening of 1-1.5 cm2 and mean valve gradient of 6- 10 mmHg
valve opening of 1.6-2 cm2 and mean valve gradient of 6 mmHg
Treatment of MS
- -diuretics (pulmonary edema)
- -CCB, BB, digoxin (slow HR to improve ventricular filling)
- -anti-coagulation (pt with AF)
- -mechanical correction
balloon catheter is advanced from femoral artery to RA, across atrial septum, catheter is then passed thru narrow MV, balloon is inflated to "crack" the valve open
What is the estimated event free survival rate 7 years after perc valvuloplasty?
Goal of management of anesthesia in a pt with MS?
- -Prevent or treat events that will decrease CO or produce pulmonary edema.
- -Avoid tachycardia
- -Avoid marked increase in IV volume
- -Avoid drug induced decrease in SVR
- -Avoid SNS stim like hypoxia and hypercarbia
Causes of MR
- rheumatic fever
- hypertrophic obstructive cardiomyopathy
- annulus calcification
- myxomatous degeneration
- -(pan)systolic murmur
- -high frequency blowing / swishing sound
- -due to backflow of blood into LA from LV during systole
Where is the MR murmur best heard?
Is MR related to pressure or volume overload?
- Blood is regurgitated back into LA from the LV as well as the LA is filling with the normal flow
Effects of MR
- -Eccentric LA hypertrophy due to increased LA volume
- -Decreased CO
20-30% regurgitant fraction
30-50% regurgitant fraction
>50% regurgitant fraction
=volume of regurgitation / total LV SV
acute vs chronic MR
acute- non compliant LA, elevated LA pressure, possible pulmonary edema
chronic- dilated LA with less elevated pressure (it's more compliant), eccentric hypertrophy, pulmonary congestion is less common, AF
What 5 factors dictate severity of MR and ratio of forward to backward flow?
- 1) size of mitral orifice
- 2) systolic pressure gradient btw LA and LV
- 3) SVR (opposes forward flow from LV)
- 4) LA compliance
- 5) duration of regurg with systole (systolic ejection time)
How will AS or elevated aortic pressure (BP) affect MR?
It will make it worse by increasing the regurgitant fraction
What abnormality might be seen on a wedge tracing due to MR?
-Large V wave (end of ventricular contraction)
How does MR affect EDV, ESV, and SV?
- increased EDV
- decreased ESV
- SV is increased (but net SV into aorta may be decreased)
Describe how the PV loop for MR differs from the normal loop.
- -There is no true isovolumetric contraction as blood flows back into LA before the aortic valve opens.
- -Also no true isovolumetric relaxation phase, as the ventricle relaxes, the MV is never completely closed so blood flows back into LA.
- -Width (SV) increases
In what pts is repair vs replacement of the mitral valve preferable for MR?
- Repair- younger patients
- Replacement- older patients with more extensive disease
Mortality associated with mitral valve repair for MR? Mitral valve replacement?
- Repair for MR- 2-4%
- Replacement for MR- 5-7%
What's the goal of medical treatment for MR? What meds are used?
- Goal is to increase forward flow.
- Vasodilators for acute MR.
Anesthesia implications of MR
- Prevent and treat events that lead to decreased CO.
- -Prevent bradycardia (goal HR 80-100)
- -Prevent increased SVR
- -Slightly increased preload
- -Minimize drug induced myocardial depression
- -Monitor magnitude of regurg flow with PA line or echo
Who does mitral valve prolapse affect?
- -Subset of mitral regurg
- -2% of the population
- -AD component
- -associated with connective tissue diseases
- -more common in women, esp. those with lean bodies
Patho of mitral valve prolapse
- -Leaflets become enlarged and abnormal collagen replaces the normal collagen.
- -More of a billowing of the leaflets into LA during systole, may or may not be MR
S/sx mitral valve prolapse
- -usually asymptomatic and benign
- -mid systolic click
Anesthetic management of mitral valve prolapse
- -Is there MR?
- -Management is similar to that of MR
- -avoid hypovolemia, increased sympathetic tone, and decreased afterload
Etiology of AS
- -congential bicuspid valve
- -degeneration and calcification of the valve ("senile AS")
Patho of AS
- -wear and tear of valve motion
- -common patho with atherosclerosis
- -turbulence across the valve disrupting endothelium and collagen matrix
What percent of pts with rheumatic heart and AS also have mitral disease?
Consequences of AS
- -LV develops concentric hypertrophy due to pressure overload
- -the hypertrophy decreases wall stress, but also decreases LV compliance
- -later the LA hypertrophies to fill the non compliant LV
- -SV decreases
Why is AF detrimental in AS?
In AS, atrial kick accounts for more than the normal 25% of SV, so with it lost, marked deterioration occurs
How does AS affect ESV, EDV, and SV?
- -Marked increase in ESV (LV emptying is impaired)
- -Slight increase in EDV (ESV is increased and so residual excess volume is added to incoming venous return)
- -SV is decreased
- -harsh systolic-may also feel a thrill in upper chest and lower neck
Where is the murmur of AS best heard
Classic symptoms of critical AS
How does the onset of angina, syncope, and DOE correlate with average time to death, respectively?
- Angina- 5 years
- Syncope- 3 years
- DOE- 2 years
How is the imbalance between O2 supply and demand, manifested as angina, associated with AS?
- 1) due to ventricular hypertrophy there's more mass to perfuse, this increases demand
- 2) increased systolic ventricular pressure increases wall stress but decreases myocardial O2 supply due to decreased diastolic pressure, decreased supply
What valvular disorder has a fixed outflow?
Is AS due to pressure or volume overload?
- mean P gradient > 50 mmHg
- valve area <0.8cm2
- mean P gradient 20-30 mmHg
- valve area 0.8 - 1 cm2
- mean P gradient < 20 mmHg
- valve area 1-1.5 cm2
What percent of pts with AS will progress to severe or symptomatic?
When is AVR indicated?
- -Severe AS
- -evidence of progressive LV dysfunction
- -Symptoms develop
Is valvuloplasty indicated for treatment of AS?
- -Yes, but it is less effective than in mitral stenosis
- -Restenosis in up to 50% of pts within 6 months
What meds need to be used with caution in AS?
- -meds that decrease SVR or cause hypotension
Anesthesia implications of AS
- -prevent hypotension and any HD change that will decrease CO
- -maintain NSR
- -avoid bradycardia (avoid LV distension)
- -avoid hypotension (will decrease coronary blood flow and cause ischemia)
- -optimize IV volume to maintain preload and LV filling
How should hypotension that occurs with AS be treated?
- -It should be avoided if possible
- -If it does occur it needs to be treated aggressively!!
What valvular disorder is the most severe?
What induction med should be used with AS
Can neuraxial blockade (spinal) be used in a pt with severe AS?
NO!! It's contraindicated due to the profound sympathectomy that will decrease SVR.
Etiology of AR
- abnormal valve leaflets due to
- -bicuspid valve
- -rheumatic fever
- dilation of the aortic root due to
- -aortic aneurysm or dissection
- -annuloaortic ectasia
Patho of AR
- -abnormal flow of blood from aorta into LV during diastole
- -LV must pump regurgitant volume and normal volume from LA
Is AR due to pressure or volume overload?
What's a hallmark sign of AR
Widened pulse pressure
Acute vs chronic AR
acute- LV of normal size, LV has low compliance, so diastolic pressure increases, the increased pressure is reflected back to the LA and the pulmonary vasculature, pulmonary congestion and / or edema occur
chronic- there is adaptive LV and LA enlargement so a greater volume of regurgitant can be accomodated with less of an increase in diastolic LV pressure, pulmonary congestion is less likely
- -blowing / high pitched and swishing
Where is the murmur of AR best heard?
Left sternal border
How does AR lead to a widened pulse pressure?
- -the entire SV is ejected into the aorta so this increases SBP
- -but then regurgitation occurs and some blood goes back into the LV, this reduces aortic diastolic pressure
How does AR affect coronary perfusion?
It's decreased due to decreased diastolic pressure in the aorta
How does AR affect EDV, ESV, and SV?
- -Marked increased in EDV
- -ESV is + or - normal (depends on if LV is in failure or not)
- -marked increase in SV (but amt going to aorta may be decreased)
How does the PV loop for AR differ from the normal loop?
- -There is no true isovolumetric relaxation phase
- -LV fills with blood from aorta before MV opens
How should acute AR be treated?
As a surgical emergency, the pt needs an AVR
How is severe AR with good LV function and HTN treated?
- -afterload reduction when BP>140
- -only benefits pts with HTN
When is AVR indicated for AR?
- -Asymptomatic but evidence of impaired LV function (EF < 50%)
AR clinical presentation
- -widened pulse pressure
- -decreased DBP
- -bounding pulses
- as it progresses to LV failure:
AR anesthesia implications
- -maintain forward LV SV
- -HR > 80 (decrease duration of diastole to decrease amt of regurgitation)
- -avoid abrupt increase in SVR (can precipitate LV failure)
- -minimize myocardial depression
Are the volatiles good to use in a pt with AR?
Yes, they increase HR, decrease SVR, and cause minimal myocardial depression
Tricuspid stenosis etiology
- -rare in adult population
- -common cause is RHD
- -carcinoid syndrome
- -increased RA pressure
- -increased pressure gradient btw RA and RV
- -usually functional, not structural
- -due to RA enlargement (due to P or V overload)
- -can be from PH
- -infective endocarditis
- -carcinoid syndrome
- -often associated with mitral or aortic disease
-RA volume overload
- -peripheral edema
Anesthetic management of TR
- -maintain CVP in high normal range to facilitate RV preload and filling
- -avoid anything that would increase PA pressures
- -usually congenital and corrected in childhood
- -valvulotomy can be used to relieve the obstruction
- -From PH with annular dilation
- -Rarely symptomatic
What is hypertrophic cardiomyopathy
- -occurs in the absence of P or V overload
- -hyperdynamic LV
- -diastolic dysfunction (increased LVEDP)
What effects does hypertrophic cardiomyopathy have?
-dynamic obstruction of the LVOT due to narrowing in the subaortic area due to systolic anteromotion of the anterior mitral leaflet against a hypertrophied septum
What will increase the obstruction associated with hypertrophic cardiomyopathy?
- -increased LV afterload
- -increased contractility
- -decreased ventricular volume
Anesthesia implications of IHSS
- evaluate for potential of:
- -significant dynamic obstruction
- -malignant arrhythmias
Anesthetic management of IHSS
- -volatiles provide some myocardial depression
- -neo will increase SVR without increasing contractility
How is hypotension treated with IHSS?
- -Increase preload with IVF
- -Increase afterload with alpha adrenergic agonists
For what valvular conditions is neo indicated to treat hypotension (over ephedrine)?
IHSS, MVP, MS
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