PREGNANCY and VALVULAR HEART

DISEASE

Dr. Chong Tan

Topics

Aortic Stenosis/ Regurgitation Mitral Stenosis/ Regurgitation HOCM/ Primary Pulmonary Hypertension

Pathophysiology

Pressure Volume Loops

Markers of severity

Anaesthetic management with specific regards to the pregnant patient

Mrs HW

30yo multipara mild-mod MS

Symptoms on mod exertion – SOB stairs

Previous LUSCS 2 years ago under spinal – uneventful, BP maintained with few metaraminol boluses

TTE at that time valve area 1.5 cm2 and pressure grad 12mmhg

Repeat echo valve area 1.3cm2 and pressure grad 14mmhg

Mrs HW

Decision made for spinal

Uneventful insertion

BP drop not precipitous

X2 metaraminol boluses given

Total 1L IV fluid

Uneventful progress

OVERVIEW

All lesions produce some compromise of cardiac output

Optimising and avoiding extremes of controllable parameters

Volume state HR Inotropy SVR PVR

Regurgitant Lesions

AR

LV stroke volume falls back into LV during diastole

LV volume overload , hypertrophy and dilation from inc diastolic filling

MR

LV stroke volume falls back into LA during systole

LV volume overload and compensatory inc diastolic filling. Dilation and hypertrophy

Pathophysiology

AR

Pressure grad driving regurg is diastolic aortic root vs. intra-LV pressure

MR

Regurg goes down whichever path has least resistance to LV outflow: aortic root systolic pressure or intra-LA pressure

Pathophysiology

AR MR

Pressure-Volume Loops

AR

EDV (LV Vol o’load) SV comp, EF same LV compliance Eventual contractility

MR

afterload

Contractility line

Afterload line

Factors affecting regurgitation

AR

Diastolic time (HR) causes widening of valve, prolonged time for regurg back into LV

SVR and diastolic aortic root pressure = pressure grad for regurg

MR

Diastolic time (HR) causes widening of valve

SVR favours path of least resistance back into LA during systole

Markers of Severity

Symptoms – rest vs exertion

Signs of cardiac failure at rest indicate falling contractility

Regurgitant fraction Derived from echo velocity readings

Calculating Regurg fraction

Using Doppler

Regurg Volume (mL) = Area of regurg flow ie. Mitral or Aortic orifice (cm2) x velocity-time integral (cm/sec x sec)

Regurg fraction = Regurg volume / total LV stroke volume

Mild <30%, Severe 60%+

Anaesthetic Management

AR

Avoid Bradycardia (diastolic time)

Avoid SVR (SNS activation, vasoconstrictors)

Optimise filling

Avoid neg inotropes esp if decomp contractility

MR

Avoid Bradycardia (LV dilation and valve orifice)

Avoid SVR (SNS activation, vasoconstrictors)

Optimise filling

Avoid neg inotropes esp if decomp contractility

Ephedrine the bolus pressor of choice

Anaesthetic Management

For both AR and MR:

Epidural > Spinal > GA preferred (gradual onset block with benefit of Vdilation)

If GA, volatile OK if contractility preserved/ mild, otherwise opioid-based

Judicious use of intra-op vasodilators

Stenotic Lesions

Narrowing of outflow orifice

Bernoulli principle – distal to stenosis pressure energy converted to potential energy (ie. kinetic = velocity)

To achieve given flow (ml/sec) past stenosis (cm2), blood must flow faster (cm/sec) for narrower stenosis

cm3/seccm/seccm2

FlowSpeed = Area x

Pathophysiology

Bernoulli equation - P = 4v2

Massive P required to generate flows as stenosis gets worse fixed maximum flows past stenosis

AS – fixed max LV stroke volume

MS – fixed max LA stroke volume ie. Fixed max LV preload

Pathophysiology

AS MS

aortic

Pathophysiology

AS

LV Concentric hypertrophy

Fixed max SV means CO demands must be met by HR

But hypertrophy and aortic root venturi effect predispose to coronary ischaemia!

MS

LA Dilation

Fixed max LV preload means:

7.CO demands must be met by HR

9. LV SV dependant on atrial kick, volume state, LA venous return and diastolic time for LV filling

Pathophysiology

AS

Higher L heart “forward-failure” risk ie shock/ hypotension

MS

Higher L heart “backward-failure” risk ie APO

Pressure-Volume Loops

MS AS

LVEDV

EF

Afterload, LVEDP, contractility

EDV, SV same at rest

Markers of Severity

Symptoms – rest vs exertion

Signs of cardiac failure at rest indicate falling contractility

Valve area (echo, cardiac catheterisation)

Pressure gradient (echo)

Markers of Severity

Echo

Estimation of area from velocity measurements before and after stenosis

Area (valve) x Velocity (valve) = Area (proximal) x Velocity (proximal)

Calc pressure grad from measured velocity

P = 4V2

Markers of Severity

AS

Valve area = moderate: 0.7-0.9 cm2, severe 0.5-0.7 cm2

Valve gradient = critical at 50mmhg

MS

Valve area = Mild: 1.5 - 2 cm2,

moderate: 1 - 1.5 cm2, severe <1 cm2

Valve gradient = critical at 20 mmhg

Anaesthetic Management

AS

Avoid SVR (fixed max CO)

Avoid HR (LV filling time, ischaemia) and HR (fixed SV will CO)

Ideal HR 80-90

MS

Avoid SVR (fixed max CO)

Avoid HR (LV filling time)

Not too full or dry (APO vs. LV filling)

Treat AF!

Anaesthetic Management

GA (volatile)>Epidural>Spinal

Vasoconstrictors the pressor of choice

Opioid–based if severe or poor contractility

Decompensation with AF needs cardioversion!

MS: Avoid N20 (PVR)

Hypertrophic Obstructive CardioMyopathy

Diastolic dysfunction, LVH

25% subaortic stenosis to LV outflow

Dynamic – may vary from beat to beat

Arrhythmias Sudden death in age <30

Hypertrophic Obstructive CardioMyopathy

Systolic Anterior Motion Systole squashes together septum and

anterior mitral valve leaflet Worse under any conditions that LV

chamber size at End Diastole

2. LV filling

3. afterload

4. contractility

“Venturi Effect” draws open mitral valve MR

Anaesthetic Management

Avoid + inotropes Avoid Veno- and arterio- dilators Optimise filling

GA>Epidural>Spinal

Vasoconstrictors the pressor of choice

Primary Pulmonary Hypertension

Chronic PVR unknown cause

Young females, amphetamine use

RV output to L heart, hence LV preload

RVF

Primary Pulmonary Hypertension

Avoid PVR Hypercarbia Hypoxia Acidosis Hyperinflation vasoconstrictors

Optimise filling

LV preload so avoid sudden SVR

Anaesthetic Management

GA>Epidural>Spinal

Volatile for GA - PVR

Physiology of Pregnancy

Generalised vasodilation, Uterine circ is low pressure

shunt

By 30%, blood

volume 40% and VR

10%

TPRCO xMAP =

Gravid Uterus vena caval obstruction

Physiology of Pregnancy

Labour Pain, SNS stim further in O2 demand

so CO/ SV 45%

Uterine contraction, rpt valsalvas autotransfusion, blood volume, VR and CO 10-25%

Physiology of Pregnancy

Post delivery

Further autotransfusion from placenta and relief of IVC obst blood volume, VR and CO (80% of prelabour figures)

Haemorrhage, oxytocin, etc..

Anaesthetic considerations

NVD vs. LUSCS decision usu. Made by Obstetrician

If critical severity of valve compromise - ?LUSCS primarily to avoid any SNS stim of labour

Epidural>spinal>GA, avoid N20

LUSCSEpidural>spinal>GA, avoid N20

LUSCS

Epidural>CSELabourEpidural>CSELabour

MRAR

GA>regional esp. if critical, opioid based if contractility, avoid N20

LUSCSGA>regional esp. if critical, opioid based if contractility

LUSCS

No regional >epi >CSE

LabourNo regional >epi >CSE

Labour

MSAS

HOCM

Labour Systemic analgesia > local blocks >

neuraxial (avoid VR / TPR)

LUSCS GA – neg inotropy of benefit, avoiding

neuraxial for same reasons

Primary Pulmonary Hypertension

Labour

Attain maximal analgesia – pain/ SNS stim PVR

Systemic analgesia > local blocks > neuraxial (avoid VR / TPR)

LUSCS GA – avoid PVR triggers