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Cardiac > Valvular Lesions > Flashcards

Valvular Lesions Flashcards

1
Q

Mitral Stenosis Etiology

A

Rheumatic Fever, dialysis patients

- usually 20-30 years after insult (CHRONIC)

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2
Q

Pathophysiology of MS

A

Thick calcified valve –> restricted blood flow –> CO becomes dependent on pressure gradient across valve –> LA dilates –> increased LA pressure back into pulmonary circulation

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3
Q

MS arrhythmias?

A

AFib and SVT due to atrium dilation

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4
Q

MS affects on pulmonary circulation

A

Increased PVR due to back congestion from increased LA pressures –> reduction in pulmonary compliance as well
==> can all lead to R heart strain and failure

*can see pulmonary capillary rupture –> hemoptysis

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5
Q

MS affects on LV?

A

LV is chronically underfilled –> acute vasodilation from anesthesia can severely compromise organ perfusion

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6
Q

Calculating valve area and gradient

A

delta P = 4V^2

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7
Q

Anesthetic goals of inducing MS

A 
MAINTAIN SINUS RHYTHM
- avoiding tachycardia or arrhythmias
Euvolemia
- hypovolemic --> further underfilled LV
- hypervolemic --> pulmonary congestion and edema

Adequate preload and careful with the dilation from anesthetics

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8
Q

Treating arrhythmia with MS?

A

Esmolol or cardioversion

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9
Q

Vasoactive of choice with MS

A

Phenylephrine!

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10
Q

Mitral Regurgitation Etiology

A

Acute: MI (posterior-medial papillary), endocarditis, trauma
Chronic: stenosis, HF, calcification

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11
Q

MR Pathophysiology

A

reduction in forward SV –> backward flow into LA –> LA dilation and pulmonary congestion –> LV is volume overloaded and dilates –> Eccentric hypertrophy –> increases wall stress and O2 demand

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12
Q

What does eccentric hypertrophy do to contractility

A

Due to stretching of myocardial fibers and increased wall stress –> contractility is depressed

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13
Q

Drop in SVR does what to MR?

A

blood will follow path of least resistance and lead to more forward flow in MR

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14
Q

When to correct MR?

A

If asymptomatic –> leave alone

If symptomatic or another surgery –> correct!

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15
Q

Hemodynamic treatment of MR

A

Afterload reduction –> promotes forward flow

surgery

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16
Q

Anesthetic Management of MR

A

avoid bradycardia –> Keep high/normal HR
- NSR is best but often have Afib
Limit excessive stimulus/fluid
- euvolemia
Even though they like low afterload, don’t bottom them out with vasodilation from anesthetics

17
Q

Aortic Stenosis Etiology

A

congenital, rheumatic, degenerative

*Most common cause of LVOT obstruction

18
Q

Pathophysiology of AS

A

gradual obstruction –> concentric hypertrophy of LV –> maintains pressure gradient across valve –> decreased LV compliance –> LVEDP elevates and compromises coronary perfusion

19
Q

Triad of symptoms for AS

A

Syncope
Angina
Dyspnea

20
Q

rhythm for AS?

A

Normal Sinus Rhythm!!!!!

- need atrial kick to finish filling ventricle with the high diastolic pressure

21
Q

LV Stiffness in AS?

A

Reduced ventricular compliance from LVH leads to a stiff LV that becomes quiet preload dependent!!!

22
Q

what does high LVEDP mean for coronary perfusion pressure?

A

Patients need a higher afterload to maintain an appropriate diastolic pressure to perfuse the coronaries

23
Q

Severe/Critical AS?

A

Area <1 cm2
Gradient > 40 mmHg
Velocity >4 m/s

24
Q

Anesthetic Management of AS

A

NSR –> a little slow if anything to maintain diastolic filling
- if they lose the atrial kick –> IMMEDIATE Cardioversion
Maintain the diastolic pressure!
- phenylephrine

25
Q

Aortic Regurgitation

A

slow, insidious onset

26
Q

Pathophysiology of AR

A

regurgitant volume into LV –> LV dilation and volume overload –> forward SV reduced

27
Q

Chronic AR

A

slow eccentric hypertrophy leads to large end-diastolic volumes –> increased LV compliance –> SV + CO fall as LV deteriorates

28
Q

Sudden AR

A

LV cannot compensate that acutely –> pressure transmitted back towards LA and pulm circulation
- sudden hypotension and pulmonary edema

29
Q

A-line tracing with AR?

A

Wide pulse pressure

30
Q

what vitals determine regurgitant volume?

A

HR and diastolic pressure

31
Q

Treatment of AR

A

diuretics (volume overloaded)

Afterload reduction –> promotes forward flow

32
Q

Anesthetic Management of AR

A

normal to high HR with NSR (80-100s)
- bradycardia leads to increased time in diastole to allow regurgitation
euvolemia and maintaining normal/low SVR to promote forward flow

Cardiac (3 decks)

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