Valvular Disorders

2.5-3.5 cm²

4-6 cm²

• -narrowed opening due to calcification or fibrosis
• -decreased cross-sectional area
• -valve cusps fuse together limiting opening

• -Leaflets don't seal completely 
• -Blood goes from a distal to a proximal chamber

Pressure overload

MS or AS

Volume overload

AR or MR

• -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

• -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

• #1- mitral (it receives more trauma just doing its regular job)
• #2- aortic

40% and 25%

fever, chills, fatigue, migratory arthralgias

S/sx of ARF

• carditis
• polyarthralgias
• Sydenham chorea
• Erythema marginatum
• Subcutaneous nodules

• migratory arthralgias
• fever
• increased ESR and CRP
• leukocytosis
• prolonged PR interval

• 1) evidence of strep infection
• AND 
• 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

• -severity of cardiac disease
• -how impaired is contractility?
• -is there other organ involvement?
• -identify compensatory mechanisms 
• -current drugs
• -do they have a prosthetic valve?

• -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

• -RF (50% of pts)
• other rare causes (1% of cases):
• -endocarditis
• -congenital
• -calcification (elderly)

• -thickening and calcification of leaflets
• -fusion of commissures (where they join)
• -thickening and shortening of chordae tendinae

• -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 valve area < 2 cm²

• -there is chronic pressure overload of the LA
• -LA dilates
• -conduction fibers get stretched 
• -this throws the conduction system in the atria off

1/3

• 1) loss of atrial kick
• 2) AF frequently has a fast rate and this decreases diastolic filling time

• -Due to SNS stimulation afterload is increased
• -This decreases preload
• -Contributes to LV dysfunction

• -last 2/3 of diastole
• -low rumbling sound
• -may hear an opening "snap"

• All are decreased.
• Significant decrease in EDV (limited filling)
• Slight decrease in ESV
• Overall result is a decreased SV

Apex and axilla

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.

By echo

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

• -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

67-76%

• -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

• endocarditis
• 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

Apex

• Volume
• Blood is regurgitated back into LA from the LV as well as the LA is filling with the normal flow

• -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- 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

• 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)

It will make it worse by increasing the regurgitant fraction

-Large V wave (end of ventricular contraction)

• increased EDV
• decreased ESV
• SV is increased (but net SV into aorta may be decreased)

• -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

• Repair- younger patients
• Replacement- older patients with more extensive disease

• Repair for MR- 2-4%
• Replacement for MR- 5-7%

• Goal is to increase forward flow.
• Vasodilators for acute MR.  
• ACEI
• BB
• CCB
• Digoxin
• Diuretics

• 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

• -Subset of mitral regurg
• -2% of the population
• -AD component
• -associated with connective tissue diseases
• -more common in women, esp. those with lean bodies

• -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

• -usually asymptomatic and benign
• -mid systolic click

• -Is there MR?
• -Management is similar to that of MR
• -avoid hypovolemia, increased sympathetic tone, and decreased afterload

• -congential bicuspid valve
• -degeneration and calcification of the valve ("senile AS")

• -wear and tear of valve motion
• -common patho with atherosclerosis
• -turbulence across the valve disrupting endothelium and collagen matrix 

95%

• -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

In AS, atrial kick accounts for more than the normal 25% of SV, so with it lost, marked deterioration occurs

• -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

Aortic area

• angina
• syncope
• DOE

• Angina- 5 years
• Syncope- 3 years
• DOE- 2 years

• 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

AS

pressure 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

20%

• -Severe AS
• -evidence of progressive LV dysfunction
• -Symptoms develop

• -Yes, but it is less effective than in mitral stenosis
• -Restenosis in up to 50% of pts within 6 months

• -meds that decrease SVR or cause hypotension
• -vasodilators
• -diuretics
• -NTG

• -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

• -It should be avoided if possible
• -If it does occur it needs to be treated aggressively!!

AS

etomidate!!

NO!! It's contraindicated due to the profound sympathectomy that will decrease SVR.  

• abnormal valve leaflets due to
• -bicuspid valve
• -endocarditis
• -rheumatic fever
• dilation of the aortic root due to
• -aortic aneurysm or dissection
• -syphilis
• -annuloaortic ectasia

• -abnormal flow of blood from aorta into LV during diastole
• -LV must pump regurgitant volume and normal volume from LA

Volume overload

Widened pulse pressure

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

• -diastolic
• -blowing / high pitched and swishing

Left sternal border

• -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

It's decreased due to decreased diastolic pressure in the aorta

• -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)

• -There is no true isovolumetric relaxation phase
• -LV fills with blood from aorta before MV opens

As a surgical emergency, the pt needs an AVR

• -afterload reduction when BP>140
• -CCB
• -ACEI
• -only benefits pts with HTN

• -Symptomatic
• -Asymptomatic but evidence of impaired LV function (EF < 50%)

• -widened pulse pressure
• -decreased DBP
• -bounding pulses
• as it progresses to LV failure:
• -orthopnea
• -dyspnea
• -fatigue

• -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

Yes, they increase HR, decrease SVR, and cause minimal myocardial depression

• -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
• -RHD
• -often associated with mitral or aortic disease

-RA volume overload

• -peripheral edema
• -ascites
• -hepatomegaly

• -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

• -occurs in the absence of P or V overload
• -genetic
• -hyperdynamic LV
• -diastolic dysfunction (increased LVEDP)

-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

• -increased LV afterload
• -increased contractility
• -decreased ventricular volume

• evaluate for potential of:
• -significant dynamic obstruction
• -malignant arrhythmias
• -ischemia

• -volatiles provide some myocardial depression
• -neo will increase SVR without increasing contractility

• -Increase preload with IVF
• -Increase afterload with alpha adrenergic agonists

IHSS, MVP, MS