Apex- Valvular Disease Flashcards
What points are you listening to for each valve?
A- Aortic
B- Pulmonic
C- Tricuspid
D- Mitral
“APe To Man”
Heart sounds:
S1=
S2=
S3=
S4 =
S1= Closure of the mitral and tricuspid vlaves
S2 = closure of the aortic and pulmonic valves
S3 = suggests CHF
S4 = suggests poor ventricular compliance
Anatomic locations to listen to each vavle:
Aortic
Pulmonic
Mitral
Tricuspid
Aortic - 2nd ICS, RSB
Pulmonic- 2nd ICS, LSB
Tricuspid - 4th ICS, LSB
Mitral - 5th ICS, Left midclavicular line
Which sounds the onset of diastole vs onset of systole : S1 or S2
S1 = onset of systole (closure of mitral and tricuspid valves)
S2 = onset of diastole (closre of aortic and pulmonaic valves)
What point in the cardiac cycle would you hear an S4 sound
prior to S1
(caused by atrial systole)
At what point in the cardiac cycle would you hear an S3 sound?
during the middle 1/3 of diastole - after S2
When using your sthethoscope, the diaphragm is best for listening to high pitched sounds such as S1 and S2 + but murmurs of what 2 conditions?
AS and MR
The bell of the stethoscope is best used for low pitched sounds such as S3 and S4 and the murmur of which valvular condition?
Mitral Stenosis
Which valvular diseases are associated with eccentric hypertrophy? (2)
Aortic & mitral REGURGITATION
REgurgitant lesions tend to produce volume overload and the heart compensates with eccentric hypertrophy (thin wall + dilated chamber); Stenotic lesions tend to produce pressure overload where the heart compensates with concentric hypertrophy (thick wall + smaller chamber)
Sarcomeres added in parallel vs series : eccentric/concentric hypertrophy
concentric = parallel
eccentric = series
What kind of valves have a Mercedes-Benz sign appearence on the TEE?
Semilunar valves (Aortic and pulmonic)
Aortic Valve replacement (increases/decreases) the transvavular gradient
decreases
*The transvavular gradient from LV to Ao is very high with AS - AVR reduces the gradient
Normal aortic valve orifice
What is severe?
2.5- 3.5cm
Severe < 1 (some say 0.8)
Most common cause of AS
other 2 common eitologies
Bicuspid aortic valve
rheumatic fever and infective endocarditis
Classic presntation triad of AS and 50% survival rate for each
syncope, angina, dysnea (SAD)
3yrs, 5rs, 2yrs
Anesthetic goals for AS
HR:
Rhythm:
Preload:
Afterload:
Contractility:
PVR:
Anesthetic goals for AS
HR → avoid tachycardia
Rhythm → maintain NSR (maintain atrial kick)
Preload → increase
Afterload → maintain or increase
Contractility → maintain
PVR → normal
The arterial waveform of AS may show what 2 things?
pulsus tardus and pulsus parvus
a Mean transvalvular pressure gradient (LV to aorta) > ____mmHg is diagonistic of severe AS
> 40mmHg
What valvular disease results in increased height of the pressure/volume loop + a shift to the right
Aortic Stenosis
increased ventricular pressure → increased height of loop
increased EDV and ESV → shift to the right
What coagulopathy occurs in up to 90% of patients with sever AS?
von Willebrand disease bc the von Willebrand molecule becomes damaged when it passes through the stenotic valve
Why should tachycardia/bradycardia be avoided in AS?
tachycardia → decreased time for ventricular filling → decreased LVEDV → decrased SV + CO → ishemia
bradycardia → decreased CO → LV over-distention with compression of subendocardial vessels → decreased myocardial o2 supply
What leads to the second waveform?
Aortic stenosis
-slower systolic upstroke (pulsus tardus) with delayed peak
-narrow pulse pressure with a small amplitude waveform (pulsus parvus)
-diacrotic notch may not be present
-overall appearence = dampened
Why is spinal anesthesia avoided in patients with severe AS?
sympathectomy rapdily reduces SVR leading to profound hypotension, reduced coronary perfussion pressure, and CV collapse
C.
(A= mitral stenosis, B= AS, D = chronic MR)
In a patient with aortic regurgitation, before initiated cardiopulmonary bypass, how must cardioplegia be injected?
retrograde (through the coronary sinus)
or
directly into each cornoary ostia
Anesthetic goals for aortic insufficiency (lingo)
HR, rhythm, preload, afterload, contractility, pvr
Full, fast, foward
HR → Faster normal
Rhythm → NSR
Preload → maintain or increase
Afterload → decrease
Contractility → maintain
PVR → maintain
What arterial waveform shows an increased pulse pressure with bisferiens pulse (biphasic peaks)?
aortic regurgitation/insuffiency
Describe this pressure volume loop
First, it’s shifted to the right→ bigger end-systolic volume during isovolumetric relaxation bc regurgitant volume is added to the blood volume entering the left atrium
3 conditions to avoid with someone with AI that would increase regurgitant volume
- Bradycardia → longer diastolic filling time
- Increased SVR → increased aorta-LV pressure gradient
- Large valve orifice → largera area for the blood to return through (no idea how we attribute to this?)
What is acute aortic insufficiency usually caused by and how would it present?
What else may acute AI result from?
endocarditis
leads to rapid cardiovascular instability; LV becomes acutely dilated + increased wall tension + impaired contractility → LV failure & pulmonary edema
Can also result from aortic root dissection (from aneurysm or trauma)
4 conditions associated with chronic AI
- Marfan syndrome
- Ehler-Danlos syndrome
- Ankylosing spondylitis
- Valvular calcification
“MACE” - Marfan, Ankylosing spondylitis, Calcification, Ehler-Danlos,
Anesthetic managment for AI (lingo) + Preload/HR/Cx/SVR/PVR/Regional
Full, fast, foward
Preload → maintain or increase (most SV is lost to the LV, so avoid hypovolemia)
HR → increase ( faster HR reduces regurgitent volume and increases AoDBP and CPP; a slower HR gives more time for the SV to flow back into the LV instead of moving foward, reducing cardiac output; it also reduces pressure at the aortic root and can compromise CPP)
Contractility → maintain → tx LV failure with inotrope and vasodilator
SVR → Decrease → blood flows along the path of least resistance, an elevated afterload increases the regurgitant volume & lower afterload promotes forward flow into the systemic circulation (avoid phenylephrine or vasopressin)
PVR → maintain → acute LV dilation stretches the mitral annulus; LV pressure will reflect to the LA and pulmonary circulation & pulmonary congestion will result
Regional → sympathectomy reduces afterload and will reduce regurgitant fraction (benificial)
What valvular disorder will present as an a-line with a sharp upstroke, low diastolic pressure, and wide pulse pressure?
Aortic regurgitation
Bisferiens pulse (biphasic systolic peaks) from an additional reflective wave from the periphery
Why does aortic regugitation cause biphasic systolic peaks on the aline?
The additional systolic peak is a reflective wave from the periphery
Bisferiens pulse
Why does aortic regugitation cause biphasic systolic peaks on the aline?
The additional systolic peak is a reflective wave from the periphery
Bisferiens pulse
Which drugs are most likely to contribute to hemodynamic instability in the patient who is symptomatic from severe mitral stenosis? (select 2)
-Nitrous oxide
-phenylepherine
-Ephedrine
-fureosemide
Ephedrine & Nitrous oxide
-Any condition that increases CO or HR (ephedrine) will increase LAP and may precipitate pulmonary edema.
-Nitrous oxide increases PVR, increasing the workload of the RV
-Neo supports afterload which is useful in pts with MS
-Lasix minimizes pulmonary congestion by reducing preload and left atrial volume
Normal Mitral valve area & when is it considered severe?
Normal = 4-6cm
Severe = <1cm
What is the most common cause of mitral stenosis in the US vs developing nations
US → endocarditis & mitral calcification
Developing nations → rheumatic fever
4 things to avoid in the pt with pulmonary htn
Hypoxia, hypothermia
Hypercarbia, Acidosis
Two things that should come to mind when doing neuraxial anesthesia for someone with a hx of mitral stenosis
sympathectomy will cause a significant reduction in CO
are they on blood thinners?
blood stasis in the left atrium is prone to thrombus formation and these patients may be on anticoagulants
Other than valve orfice <1cm, what other 2 things can indicate severe mitral stenosis?
transvalvular pressure gradeint (LA to LV) greater than 10mmHg
PASP (pulm artery systolic pressure) greater than 50mmHg
What valve disorder and explain
Mitral stenosis
→ as pressure gradient b/t LA & LV increases, the LV becomes chonrically underfilled and the left atrium becomes chronically overfilled
→this leads to a lower end-diastolic volume, stroke volume, and CO
Which valvular disorder can preciptate afib and why?
Mitral stenosis bc an increased LA pressure and volume alters the anatomy of the atrial conduction system.
Loss of atrial kick reduces ventricular filling and decreases CO
Mitral stenosis anesthetic managment in terms of HR/rhythm:
- goals
- how to tx tachyarrhythmias
- -avoid what drugs
Slower side of NSR
tachycardia → reduced diastolic filling time → decreased time for blood to pass the stenotic MV → increased LAP
-tacchyarrythmia tx with: amio, beta-blockers, CCB, dig, cardioversion
-avoid drugs what will increase HR → anticholinergics, ketamine, atracurium
How to manage preload with someone with mitral stenosis
Maintain
- LV is chronically underfilled → decreased preload → decreased SV and CO
- Hypervolemia increases LAP → pulmonary congestion
-diuretics may be used to decrease LAP
in patients with mitral stenosis, does PAOP overestimate or underestimate LVEDV
PAOP OVERESTIMATES LVEDP
(LA undergoes concentric hypertrophy)
What PAOP waveform may reveal a prominent A-wave and a decreased y-descent
Mitral stenosis
Goals with SVR in someone with mitral stenosis?
Maintain
- in the setting of low SV and CO, systemic vasoconstriction increases SVR and preserves BP
-a rapid decrease in SVR will elicit a baroreceptor mediated rise in HR (no bueno)
- tx hypotension with vasoconstrictor such as neo or vasopressin (no ephedrine)
In pts with an INR < _____; neuraxial anesthesia can be a safe option and should be considered on an individual basis
INR < 1.5
Why is tachycardia a problem with mitral stenosis?
Tachycardia → decreased diastolic filling time → decreased time for blood to pass thru the stenotic MV → increased LAP
3 common causes of MR
- MVP
- Myxomatous of the MV
- Ischemic heart disease
What valve replacement surgery poses a risk of systolic anterior motion (SAM) of the anterior leaflet
-why is this a problem
-how is it treated?
-MVR
-SAM leads to outflow obstruction
- tx: increase intravascular volume and afterload (neo)
What’s the big thing with the pressure volume loop for MR
The ventricular volume gets smaller during isovolumetric contraction (it shouldn’t change at all but some of it is back flowing into the LA)
Which valve disease will show as a PAOP waveform that will have an englarged v wave and what does that represent?
MR
-represents the regurgitant volume passing through the incompetent mitral valve.
What 2 valvular disorders are associated with a systolic murmur?
Aortic stenosis and mitral insufficiency
- try and think that murmurs are caused by turbulent flow
- blood becomes tubulent as it passes through a tight aortic valve during the ejection phase of systole
- -mitral regugitation is an issue during isovolumetic contraction during systole
AR is an issue during isovolumetic relaxation of the LV during diastole;
MS is problematic during atrial systole (atrial kick) which occurs during ventricular diastole.
What 2 valvular disorders are associated with a systolic murmur?
Aortic stenosis and mitral insufficiency
- try and think that murmurs are caused by turbulent flow
- blood becomes tubulent as it passes through a tight aortic valve during the ejection phase of systole
- -mitral regugitation is an issue during isovolumetic contraction during systole
AR is an issue during isovolumetic relaxation of the LV during diastole;
MS is problematic during atrial systole (atrial kick) which occurs during ventricular diastole.
Where to listen for murmurs with:
AS
AR
MS
MR
AS → ASSS → AS = Systolic murmur heard at the right Sternal border
AR → ARDS → AR = Diastolic murmur heard at the right Sternal border
MS → MSDA → MS = Diastolic murmur heard at the apex and left Axilla
MR → MRSA → MR = Systolic murmur heard at the apex and left Axilla
Anesthetic considerations for a transcatheter aortic valve replacement (TAVR) with a SAPIAN valve include : (select 2):
-cardiac standstill
-cardiopulmonary bypass
-rapid ventricular pacing
-ministernotomy
Cardiac standstill & Rapid ventricular pacing
Rapid ventricular pacing (to produce cardiac standstill) is required before valvuloplasty (balloon inflation) and valve deployment.
most common valves for TVARs are SAPIAN and Medtronic CoreValue - Anesthetic considerations vary based on the valve selected
What can happen during at TAVR is the valave doesnt seat properly?
Acute aortic insufficency
(hemodynamic collapse)
When doing a TAVR with a SAPIAN valve, what are some considerations surrounding rapid ventricular pacing
when is it done, why, what rate, what should you ensure before starting
→it’s done during valvuloplasty and valve deployment
→reducing motion caused by ventricular ejection makes it easier to get the valve into the correct positon
→ Rate 160-200
→ Ensure MAP > 75 prior → will help restore blood pressure after valave deployment (consider prophylactic vasopressors before starting pacing)
→ anticpate profound hypotension during this time bc the CO will be near zero during this time
→ apnea is required during deployment to minimize patient movement
With a TAVR using a SAPIAN valve, what should you do if the patient doesn’t resume NSR after rapid ventricular pacing?
defib (radiotransulcent pads should have been placed prior to draping the patient)
T/F- If CoreValve is used for TAVR, there is no need for valvuloplasty (and therefore rapid ventricular pacing/cardiac standstill)
Why?
True - bc the valve is self expanding
What happens is a SAPIAN valve vs CoreValve doesnt seat properly?
→ if SAPIAN, another SAPIAN valve must be placed through the mispositioned one “Valve-in-valve” procedure
→if CoreValve does not seat , it can be retrieved and redeployed
Acute hemodynamic instability after TAVR placement should prompt consideration of what
vascular injury (hemorrhage)
*have plenty of large-bore IV access and blood in the room
What would signs of myocardial ischemia indicate after TAVR placement?
coronary occlusion can occur if the native valve folds to obstruct a coronary artery or the new valve could be malpositioned, obstructing a coronary artery
Valvuloplasty for TAVR can cause annular rupture which would result in what?
treatment?
pericardial tamponae and CV collapse
may require aortic root repair or replacement
What intervention is MOST likely to promote hemodynamic instability in the patient with severe AI?
A. 0.5mcg/kg/min nitroprusside IV
B. 15mL 0.5% BPV via epidural
C. 250ml IV fluid challenge
D. 5mg Metroprolol IV
D.
bradycardia allows more time for blood to flow backwards
Presence of an S1 murmur heard at the midclavicular line 5th intercostal space MOST likely suggets what valvular disorder?
Mitral insufficency
Which vavlular disease is associated with ankylosing spondylitis?
Aortic insufficinecy
Marfans, ehler-danlos as well.
What cardiac changes are consistent with HF with reduced EF
A. Reduced PAOP
B. Increased wall thickness
C. SAM
D. Sacomeres replicate in series
D.
The hallmark of HFrEF is decreased ejection fraction with an increased-end-diastolic volume
Myocardial remodeling attempts to preseve pump function by dilating to accomdate for increased volume, sarcomere replication in series, and eccentric hypertrophy.
HFpEF is associated with sarcomere replication in parallel, increased LV wall thickness, and concentric hyperophy
HF with (reduced/preserved) EF is asssoicated with (concentric/eccentric) hypertrophy
→diastolic vs systolic failure
reduced ef = eccentric → diastolic failure, ventricles cant relax propoerly → volume overload in noncompliant LV → wall dilates in attempt to accomodate more volume
preserved ef = concentric → systolic failure
→ my thought process: chronic HTN, LV wall thickens to generate a higher pressure than aorta to eject blood , it’s still able to eject the blood but ventricular remodeling can lead to failure.
2 complications associated with a malpositioned valve during TAVR
- LV dilation
- pulmonary edema
- decreased aperture
- outflow tract obstruction
LV dilation & pulmonary edema
secondary to acute AI → the increased pressure and volume in the LV causes dilatition & increased LVEDP can lead to pulmonary edema
AI doesnt impede outflow tract or decrease the aortic valve orifice
SVR 1500 & PAOP 12mmHg
-Aortic Stenosis
-maintain slower NSR (bradycardia → LV distension)
- increase preload: keep CVP & PAOP at high/normal
- Afterload is set by the stenotic valve. SVR must be kept high to help perfuse t he cornoary arteries
What segment of the pressure-volume loop is altered by AI?
What segment of the pressure-volume loop is altered by AI?
Following MVR, you observe SAM of the anterior leaflet on the TEE, the patient MOST likely received (select 2):
-nitroprusside
-500ml NaCl bolus
-dobutamine
-neo
Nitroprusside and dobutamine
(bolus and neo make SAM better)
Which drug is MOST likely to increase the degree of prolapse in the patient with mitral valve prolapse?
A. Neo
B. Sevo
C. Edtomidate
D. Ketamine
D. Ketamine
A large ventricle tends to reduce MV prolapse
A small ventricle tends to increase MV prolapse
Primary goal for MVP is to prevent excessive cardiac emptying
Ketamine activates the SNS, increases myocardial contracility and augments LV emptying
Which of the following is LEAST likely to precipitate pulmonary edema with mitral stenosis?
A. Trendelenburg
B. Judicious fluid administration
C. Uterine contraction
D. Afib
B.
in the patient with severe MS, any condition that increases LA volume can precipitate pulmonary edema
uterine contraction and trendlenburg increase preload
afib reduces CO and increases back pressure in the pulmonary circulation
