Pregnancy cardiac

Question 1

+What is a Fontan procedure & what are the requirements for it to work?

Answer 1

Palliative surgical procedure for pts with functional or anatomic single ventricle (eg. if significant hypoplasia of a ventricle with a rudimentary ventricle <30% of expected volume).

High morbidity & mortality after the procedure & require lifelong cardiology follow-up with Specialist experienced in care of complex congenital heart lesions.

The single functional ventricle must pump blood to the high-resistance systemic circulation. Pulmonary circulation is created by a diversion from the venous return from systemic circulation (cavopulmonary) without a pump- therefore driven by CVP & augmented by changes in intra-thoracic pressure, skeletal muscle pump & relaxation of the functional ventricle to move blood forward. Must have low PVR, sufficiently large pulmonary arteries & relatively normal systolic & diastolic function of the functional ventricle.

Question 2

+What are essential things to be aware of in pre-op workup of a pt w Fontan circulation?

Answer 2

Detailed surgical history to understand physiology of their circulation.
Unfenestrated fully separates the pulm & systemic circulations, returning SpO2 to near-normal & aims to return systemic ventricle to near-normal workload
Fenestration may be left or created, functioning as a small ASD allowing some R)–> L) shunt between Fontan connection & LA, used in pts w mildly elevated PVR. Provides a consistent source of systemic ventricular preload but risk paradoxical embolisation & desaturation due to the R) to L) shunt (so pts w fenestration require anticoagulation).

S&S of heart failure: these may exist despite preserved ventricular function, due to the raised CVP.

Question 3

+What are the main physiological difference in a pt w Fontan procedure?

What are the haemodynamic goals with a fontan procedure?

Answer 3

elevated CVP since there’s no ventricle pumping blood from systemic veins to lungs.

reduced CO esp during physical exertion

Mild arterial oxygen desaturation at rest since coronary sinus blood drains into the atrial chamber which drains to systemic ventricle, also V/Q mismatch occurs as PA blood w low kinetic energy gravitates to lower lung segments while apical segments more oxygenated. Pts w fenestrations have lower SpO2 due to R) to L) shunting.

Rhythm: avoid arrhythmias & maintain normal rate (relies on single ventricle systolic & diastolic function)
preload: vital, high CVP to maintain pulmonary forward flow
afterload: maintain normal for diastolic perfusion, excessive afterload detrimental
contractility: maintain
AVOID raised pulmonary pressures/PVR, if ventilating avoid high PEEP, negative Pit better for cardiac output so use minimal ventilator pressures while maintaining cardiac output; short inspiratory time with adequate exp time, get flow to zero to avoid breath stacking. titrate ventilation to ABG.

If come unstuck: adequate preload, reduce PVR, support contractility of the single ventricle.

Question 4

What are considerations for risk stratification & anaesthetic planning in patients with a congenital heart disorder undergoing non cardiac surgery?

Answer 4

Understand the native lesion
Prior palliation & repair
Current cardiopulmonary reserve (exercise tolerance & signs of HF)
Previous cardiopulmonary complications (eg. arrhythmias)
Noncardiac sequelae of CHD
potential adverse effects of planned surgical procedure

Appropriate location: cardiac anaes/cardiologist specialising in congenital heart defects & repairs, adult ICU

Multi-D decisions

Vascular access: knowledge of distortions or interventions to their vascular anatomy

Question 5

What is the most common cardiovascular complication in patients with CHD?

Answer 5

Arrhythmias

Question 6

What are the 5H’s, 4T’s & a V differentials for maternal collapse/cardiac arrest?

Answer 6

Hypoxia (high spinal, aspiration, asthma)
Hypotension (APH (eg. abruption, uterine rupture) or PPH (bleeding may be concealed, FAST scan useful), ruptured aneurysm, aortocaval compression, relative with high spinal, septic/neurogenic shock, anaphylaxis)
Hyperkalemia/magnesemia (AKI from PET, Mg++ toxicity from Mg++ infusion, low BSL)
Hypothermia
HYPERTENSION: severe PET/eclampsia,ICH

Thrombus: AFE, PE, air embolus, MI (OR arrhythmias eg with peripartum cardiomyopathy or CHD)
Toxins: LA toxicity from neuraxial, Mg++ toxicity, anaphylaxis, suicide attempt, opioid OD, other anaesthetic drugs
Tension PTs: trauma/DV/suicide attempt
Cardiac tamponade: secondary to aortic dissection, trauma, DV, suicide attempt

Vasovagal

Question 7

When is amiodarone given in the cardiac arrest algorithm? what’s the dose & how is it prepared?

Answer 7

Shockable algorithm, after 3rd shock if unresponsive to CPR, shock delivery & admin of Air. 300mg IV/IO over 1-2 mins (300mg is 2 ampuoules (150mg/3mL) diluted to 20mL in D5W, no other fluids or it precipitates, don’t dilute <600microg/mL)

Question 8

+ What’s the accepted method of cardiovascular risk stratification for a pregnant pt with congenital heart disease?

Answer 8

Modified WHO classification is recommended by both ACC/AHA & ESC (2018), based on a study comparing the ZAHARA & CARPREG & modified WHO classifications & found that the latter had highest AUC for maternal cardiovascular risk in maternal congenital heart disease.

4 classes:
Class 1: no detectable increase in mortality, nil/minor increase morbidity- eg, isolated atrial or ventricular ectopic beats, successfully repaired simple lesions such as ASD or VSD, mild PDA, mild PS, mitral valve prolapse

Class 2: small increase mortality, moderate increase morbidity- eg. un-repaired ASD or VSD, repaired ToF, most arrhythmias

Some lesions fall in class 2-3, depending on the individual: bicuspid AV with asc aortic diameter <4.5cm, marfans with aortic diameter <4cm without dissection, mild LV impairment, hypertrophic cardiomyopathy, valve lesions not in class I or IV, repaired coarctation

Class 3: significant increase in morbidity & mortality, eg. Fontan’s circulation without complications (eg. good ET, min pulm HTN, SpO2 low 90s w fenestration & normal satn fenestration), Marfans with asc aortic diameter 4-4.5cm, bicuspid AV w asc aorta diameter 4.5-5cm, systemic RV, cyanotic congenital heart disease (unrepaired), mechanical valve

Class 4: extremely high risk maternal M&M, pregnancy contraindicated, eg. LVEF <30%, NYHA III or IV, Marfans w aortic diameter >4.5cm, Fontans circulation with complications, bicuspid AV w asc aorta diameter >5cm, severe symptomatic AS, severe MS, significant PAH of any cause

Question 9

What are particular risk factors for sudden cardiac arrest in pregnant pts with a history of congenital heart disease?

Answer 9

history of ventricular failure, arrhythmias or QRS prolongation

Question 10

What proportion of patients with maternal sudden cardiac arrest have no preexisting conditions or physiologic disorders prior to their arrest?

Answer 10

30%

Question 11

What are the top 7 causes of sudden cardiac arrest in pregnancy (in order)?

Answer 11

Pulmonary embolism (30%)
Haemorrhage (17%)
Sepsis (13%)
Peripartum cardiomyopathy (8%)
Stroke (5%)
PET/eclampsia (2.8%)
anaesthesia complications (2%)

Question 12

Does ETCO2 of >10mmHg during cardiac arrest correlate with ROSC?

Answer 12

Yes, but it’s not predictive of survival or LT outcome

Question 13

What measures could be considered if no successful resuscitation after 15 mins in maternal cardiac arrest?

Answer 13

Thoracotomy & direct cardiac massage- particularly effective for pts with chest trauma, tension PTx, massive PE, pericardial tamponade, chest or spine deformities.
Consider cardiopulmonary bypass

Question 14

How many attempts at laryngoscopy & intubation should occur before using SGA in maternal intubation?

Answer 14

2

Question 15

Why should TVs during maternal cardiac arrest be limited to 350-500mL if fundus @ or above umbilicus?

Answer 15

Tx overinflation decreases Tx compliance, increases intrathoracic pressure & impedes venous return to the heart

Question 16

While pregnancy is associated with mild respiratory alkalosis, why is hyperventilation to non physiologic alkalosis detrimental in pregnancy?

Answer 16

May cause uterine vasoconstriction, foetal hypoxia & acidosis

Question 17

Why should IV access during maternal resus be above the diaphragm?

Answer 17

because drugs delivered via femoral vein may not reach heart until foetus is delivered (uterine compression)

Question 18

Technique for manual uterine displacement?

Answer 18

L) hand to R) upper border of uterus, maximally displace to 1.5inches L) of midline, keep upper torso supine- better during CPR as allows optimal position for chest compressions, airway & defib

Question 19

If use tilt for reducing aortocaval compression, what angle?

Answer 19

No > 30 degrees

Question 20

Does the defibrillator energy change for pregnancy?

Answer 20

No- the increase in blood vol & reduced FRC doesn’t alter trans thoracic impedance or trans myocardial current- use standard biphasic 200J. REMOVE FOETAL MONITORING FIRST

Question 21

Where place defibrillator pads if ICD or pacemaker?

Answer 21

Ant & post chest not over the device

Question 22

What are the most common presenting rhythms in maternal sudden cardiac arrest? What does this suggest?

Answer 22

nonshockable (76%)- PEA in 51% & systole in 25%)
Suggests potentially reversible aetiologies eg. haemorrhage, hypoxemia, thromboembolism, toxin exposure, electrolyte/acid:base disturbance

Question 23

Within what timing should resuscitative hysterotomy (perimortem LSCS) be intimated & complete? How about assisted vaginal delivery?

Answer 23

Initiate within 4 mins of cardiac arrest if pt hasn’t been responsive to resuscitate efforts, newborn delivered by 5 mins.
Assisted vaginal delivery appropriate if cervix is fully dilated, foetus is at a low station & delivery can be accomplished within 5 mins of maternal cardiorespiratory collapse

Question 24

What are 4 reasons for resuscitative hysterotomy within 4-5mins?

Answer 24

Irreversible brain damage can occur in non pregnant pts with 4-6mins anoxia
Pregnant pts become anoxic sooner (lower FRC, higher MRO2)
Improvement in hemodynamics, return of pulse & BP have been noted when uterus (if fundus at or above umbilicus & resus is ineffective) is no longer gravid
Foetal survival diminishes as time between maternal death & delivery lengthens

Question 25

Should broad spectrum antibiotics be given for perimortem CS? How about oxytocin?

Answer 25

yes for the antibiotics
AVOID IV oxytocin bolus due to risk significant hypoT, cardiovascular collapse & death- can do 10U intramyometrial or dilute infusion (20miliunits/minute)

Question 26

What’s the initial dose of lipid rescue at first sign of severe LAST, while airway being secured?
best anti arrhythmic for arrest related to bupivacaine toxicity? Given such arrhythmias may be refractory, what therapy may be lifesaving until the drug dissociates from cardiac tissue?

Answer 26

1.5mL/kg lean body mass of 20% lipid emulsion over 1 minute AND start an infusion of 15mL/kg/hr
amiodarone
Cardiopulmonary bypass

Question 27

How long after achievement of circulatory stability should intralipid infusion be continued following LAST toxicity?

Answer 27

10 mins at least

Question 28

If circulatory stability isn’t achieved within 5 mins of initial lipid emulsion dose, what dose next?

Answer 28

further 1.5mL/kg lean body mass of 20% lipid emulsion over 1 minute, maximum total 3 boluses can be given 5 mins apart, double infusion rate to 30mL/kg/hr any time after 5 mins. Max cumulative dose intralipid 12mL/kg.

Question 29

What condition should pts be monitored for after intralipid administration?

Answer 29

Pancreatitis- with regular clinical review & daily amylase or lipase for 2/7.

Question 30

What are the benefits of CLUE vs TOE during maternal cardiac arrest?

Answer 30

Prior to intubation, don’t need to interrupt ventilation with CLUE. TOE can be useful for placement of venous & arterial ECMO cannula & placement of IABP. TOE can also detect previously unrecognised cardiac conditions. Useful to assess effects of inotropes & intra-aortic balloon counter pulsation.

Question 31

How effective is direct cardiac massage?

Answer 31

Provides near normal systemic perfusion throughout compression cycle & with higher cranial & myocardial flow than w external chest compressions

Question 32

What’s the preferred intervention for STEMI in pregnancy? why?

Answer 32

PCI since fibrinolytic are relatively contraindicated

Question 33

Can aortocaval compression occur postpartum?

Answer 33

Yes, the uterus remains enlarged

Question 34

What are the temperature goals for post-arrest care in pregnant/postnatal pts?

Answer 34

Avoid hyperthermia, evidence for therapeutic hypothermia lacking (pregnant women were excluded from trials)- in pregnancy it may be unsafe for the foetus & postpartum it may impair coagulation. Therapeutic hypothermia (32-34deg C for 24hrs) has been used in comatose pregnant pts or those not following commandos showing purposeful movements after resuscitation- FHR may have low baseline & diminished variability.

Question 35

What are the maternal & neonatal fatality rates for maternal SCA?

Answer 35

30-80% & >=60%

Question 36

Who has higher in-hospital survival after SCA? pregnant or non pregnant reproductive age women?

Answer 36

pregnant

Question 37

What factors associated w better survival after maternal SCA?

Answer 37

in-hospital, etiology of arrest, speed of resuscitative efforts, skills & resource of operators, anaesthetic complications (opportunity for immediate resuscitate, possible better pre-arrest maternal condition)

Question 38

what’s the likely ethology of mitral stenosis in pregnancy?

Answer 38

rheumatic

Question 39

how do stenotic mitral valves & the normal cardiovascular changes of pregnancy & delivery interact? prognosis?

What are the main risks? wy?

Answer 39

unfavourably

there’s increase in maternal & foetal complications with increased severity of MS. There’s 3% maternal mortality with severe MS and a 37% rate of pulmonary oedema or heart failure.

risk pulmonary oedema, right heart failure, atrial arrhythmias & thromboembolism

The stenotic MV restricts diastolic LV filling, increasing transmittal pressure gradient & LA pressure.
This is exacerbated by the physiologic hypervolaemia of pregnancy (incr plasma volume 50% by term), risking pulmonary congestion & pulmonary oedema.
Further exacerbated by cardiac output which increases 50% by end of trimester 2 then during labour increases by 10-25% during 1st stage, by 40% during 2nd stage & by 80-100% immediately after delivery- a stenotic valve and increased heart rate with increased cardiac output greatly increases the transmittal pressure gradient
Autotransfusion with delivery- final uterine contraction= 500mL auto transfusion, further risks pulmonary oedema/right heart failure

increased atrial irritability and hypercoaguable state of pregnancy risk LA thrombus formation

Question 40

Although predominant mitral regurgitation is commonly viewed as being lower risk than MS, what’s the rate of heart failure in mod or severe MR? how is it considered among pregnancy cardiac risk stratification?

Answer 40

15%

mod-severe MR is considered equivalent to mitral stenosis

Question 41

what are the peaks in incidence of heart failure in pregnant pts with heart disease?

Answer 41

late 3rd trimester (28-40/40) & the first postpartum week
correspond to peak haemodynamic load

Question 42

Which pts with mitral stenosis are at highest risk?

Answer 42

mod or severe MS (mitral valve area <=1.5cm2)
baseline NYHA functional class III or IV
Hx cardiac complications (TIA or stroke, pulmonary oedema, arrhythmias requiring Rx) prior to pregnancy
central cyanosis
LV systolic dysfunction
PULMONARY HTN

Question 43

Can warfarin be taken during pregnancy? why?

Answer 43

it’s generally avoided in all but those at exceptionally high risk eg. mechanical valve where it may be considered through careful multi-D discussion, since:
-crosses placenta & is teratogenic, highest risk @ 6-12/40 gestation
-may cause foetal bleeding
-may be ass’d with early miscarriage

Question 44

Can DOACs be used during pregnancy? breastfeeding? why?

Answer 44

no & no- lack of safety & efficacy data.

Question 45

why are heparins the most often used in pregnancy?

Answer 45

don’t cross placenta, don’t result in fatal anticoagulation.

Question 46

anaesthetic considerations for mitral stenosis:

Answer 46

pre (risk identification & stratification/optimisation)
-multi-disciplinary evaluation as early as possible & regular preoperative assessments to optimise patient & plan timing of delivery, incl:
-cardiologist (frequency of follow-up depends on risk level)
-obstetrician with expertise in maternal fetal medicine
-anaesthesia with cardiac anaesthesia consult

elements:
history:
-condition management to date, compliance (including selective B1 blockers with HR to improve LV filling BUT in later pregnancy the goal ventricular rate is 70-90bpm rather than <60bpm in non pregnant since elevated HR is crucial to maintain augmented CO later in pregnancy (digoxin 2nd line, less effective in pregnancy as renal Cl of digoxin incr during pregnancy), diuretics eg. frusemide if signs of HF, anticoagulation w heparins if AF, LA thrombus or prior embolism or may consider if significant MS & heart failure). if needs cardio version for unstable ventricular tacchyarrhtymia, ideally TOE if >48hrs duration, considered safe for foetus. If require PMBV during pregnancy, consider timing weighing maternal & foetal risks- ideally >20wks but before mid-late T3 (venous access & haemostasis issues w femoral approach). This also involves radiation (protect w shielding & limit exposure times, continuous FHR monitoring by trained obstruction provider).
-high risk features: Hx pulmonary oedema, arrhythmias requiring treatment, TIA/CVA prior to pregnancy)
-functional status (NYHA)- III or IV highest risk
examination:
-stability of disease- if pulmonary oedema admit & give O2, IV frusemide, B-blockers
-central cyanosis, blood pressure/heart rate
-auscultation for murmurs
-clinical signs of pulmonary congestion (eg. lung crepitations), right heart failure eg. pedal oedema
investigations:
12-lead ECG to assess for arrhythmias
comprehensive TOE including mitral valve area, extent of MR, LV systolic function, systolic pulmonary artery pressure
stratify by modified WHO class
exercise echo (to assess exercise tolerance & PAP during exercise)

counselling re: increased maternal & neonatal risks & risk modification (eg. smoking cessation, anticoagulation advice, cessations of contraindicated drugs eg. ACE-Is)

Planning for Intraoperative @ tertiary centre daylight hours obs/cardiac anaes/neonatal & adult ICU aware:
controlled induction or caesarean (if obstetric or foetal issues) should be planned if MS with high risk features or if live remotely.
regional anaesthesia to attenuate spikes in CO during labour
assisted 2nd stage
caesarean if abs indication or if anticoagulation can’t be reversed
the only cardiac indication for caesarean= refractory heart failure with need for I&V (rare)
large-bore IV access, group & hold, consider art line if significant haemodynamic compromise eg. pulmonary HTN, consider delivery in OT or ICU with CVC in that case
single-dose diuretics several hrs after delivery if mod or severe MS (redistribution oedema from auto transfusion)

Postop: monitor in ICU or coronary care at least 24hrs due to post-delivery fluid shifts (esp w regional)
resume anticoagulation if no evidence of PPH
post cardiac assessment 4-6wks & repeat echo and cardiac Ax at 6/12 (CV changes of pregnancy don’t fully resolve until 6th postpartum month). avoid any elective invasive cardiac procedures until 6/12 PP to avoid unnecessary thromboembolic risk.

Question 47

what procedure may a patient with mitral stenosis have undertaken prior to pregnancy if moderate severe MS (valve area <=1.5cm2)?

Answer 47

percutaneous mitral balloon commisurotomy

Question 48

why is atenolol avoided during pregnancy?

Answer 48

ass’d with low birthweight

Question 49

how does the goal HR vary in mitral stenosis in pregnancy?

Answer 49

non pregnant state goal is <60bpm to augment ventricular filling

in late pregnancy rely on higher HR to maintain augmented CO so goal is 70-90bpm

Question 50

can amiodarone be used in pregnancy/breastfeeding

Answer 50

no (cat D)
and no (excreted in breastmilk, affects newborn thyroid)

Question 51

What are some maternal cardiac indications for caesarean?

Answer 51

pulmonary oedema necessitating intubation
aortic dissection
Marfan with asc aortic diameter >45mm

Question 52

Considerations with oxytocin for labour & delivery in high-risk heart disease?

Answer 52

oxytocin decreases MAP & TPR, may slightly increase PAP. Ass’d with tachycardia.
care in pts with HCM, AS, ischaemic heart disease

in these pts, administer oxytocin as dilute solution via continuous infusion, 2.5-7.5IU/hr for elective & 7.5-15IU/hr for intrapartum caeser

DO NOT give oxytocin bolus to pts with cardiovascular disease

Question 53

Considerations for misoprostol in pts with high-risk heart disease?

Answer 53

generally avoid if Hx vasospastic angina or significant coronary artery disease unless consider benefits outweigh risks (eg. uterine atony with haemorrhage).

Question 54

considerations for carboprost in pts with high-risk heart disease?

Answer 54

avoid if intracardiac shunt- may incr shunting due to bronchospasm or alterations in V/Q that may–> incr intrapulm shunt fraction & hypoxaemia

also avoid if single ventricle as it may significantly decrease CO

it may induce HTN at high doses

Question 55

considerations for ergometrine in cardiovascular disease?

Answer 55

it’s contraindicated, esp with systemic, pulmonary or preg-induced HTN as it causes vasoconstriction (may cause systemic HTN, stroke, myocardial ischaemia), coronary vasospasm & increase pulm artery pressure which may cause shunt reversal & cyanosis

Question 56

considerations for B-agonists in pts with heart disease?

Answer 56

avoid if HCM (may cause LVOTO)
avoid in heart failure & use with caution for other cardiac lesions

general side effects incl HTN, tachycardia, arrhythmia, hypotension

Question 57

what is the plan for pts going into labour or CS with ICD?

Answer 57

leave the ICD function on during labour
for emergency causer, leave ICD on, position dispersive electrode on the leg, have a magnet in the room in case need to suspend anti-tacharrhythmia therapy. Have continuous cardiac monitoring.

Question 58

in which patients should single-shot spinal (with risks of rapid-onset sympathectomy) be avoided (careful & well-monitored epidural or low-dose sequential CSE may be appropriate)?

Answer 58

obstructive lesions: severe AS, aortic coarctation, MS
cyanotic congenital heart disease with R)–> L) shunting
severe dilated cardiomyopathies with low EF (<30%)
hypertrophic cardiomyopathy

Question 59

for a pt with high-risk cardiac disease requires an emergency causer, what’s the priority wrt induction speed?

Answer 59

competing interests, generally haemodynamic stability prioritised above aspiration- proceed slowly w induction & use cricoid

ketamine 1-2.5mg/kg in divided doses with phenylephrine boluses or infusion may be appropriate (but avoid ketamine in pre-eclampsia)

use of lignocaine & fentanyl OR remi 1-2microg/kg or alf 20-30microg/kg likely to be useful to blunt SNS responses (notify neonates), 1-1.5mg/kg sux

avoid nitrous

Question 60

Anaesthetic considerations for labour & delivery in high-risk heart disease

Answer 60

PREOP: Risk identification/stratification and optimisation:
-summarise cardiovascular (eg. Previous surgery), obstetric & anaesthesia history & risk factors
-cardiac history focussed on:
-previous or current HF or arrhythmias
-L) heart obstructive lesions
-R) and left heart function
-intracardiac shunting or cyanosis
-examination for signs of heart failure or reduced cardiac output
-investigations including previous echos, ecgs, holter monitors, stress tests, pacemaker reports, heart catheterisation etc
-risk stratify as per modified WHO criteria
An individualised management plan developed antepartum through multidisciplinary consultation & collaboration with the patients’ pregnancy heart team:
-cardiologists
-obstetricians
-maternal-foetal medicine specialists/neonatologists
-anaesthetists
-delivery location & timing & personnel (eg. In HDU or OT)
*in high-risk pts scheduling vs waiting for spont labour helps ensure appropriate specialists readily available
Vaginal delivery generally preferred unless obstetric indication
-determine anticoagulation plan to facilitate neuraxial
-clarify plan for postdelivery monitoring

Risk discussion & explanation of plan, answer questions

INTRAOPERATIVE: risk mitigation
Monitoring/access:
-large bore IVC x2
-art line prior to induction
-consider CVC if considering vasoactive drug infusions
-continuous 5-lead ECG
-may be necessary to labour in an area with nursing qualified at monitoring telemetry eg. CCU or ICU or bring qualified nurse to birthsuite

-have vasopressors immediately available Assistance: Delivery plan: -likely epidural before contractions begin, epidural generally considered essential & if not an option, reconsider VD (epidural benefit= limits CO peaks during labour as blunts catecholamine release due to pain & anxiety)
-avoid epinephrine in test doses -load with 3mL epidural solution at a time up to 15mL, ensuring adequate block @ least T10 before start infusion 6-12mL/hr titrate to adequate analgesia sans hypotension. Could add PCEA 4-6mL every 15mins If pt needs a CSE, could just use 15microg intrathecal fentanyl to decr likelihood of hypoT. Or could use 1.5-2.5mg intrathecal isobaric bupivacaine. -pts with significant CV disease should be in semi-recumbent position with lateral tilt intrapartum -maternal “cardiac delivery” with an epidural= foetal descent during majority of the 2nd stage achieved by uterine contractions sans maternal expulsive efforts, aiming to avoid the increases Pit & decr venous return/preload/CO with Valsalva. When foetal head reaches pelvic floor, forceps or vacuum extraction performed
-Consider this vs instructing the pt to push with open glottis.
-monitor the pt continuously eg. Pulse oximetry or art line- to Ax haemodynamic tolerance
-in pts with Hx of poorly-tolerated tachyarrhythmias, consider external defib pads -encourage clear fluids- if doesn’t want to drink, IVT at 1mL/kg/hr, titrate according to haemodynamic response, any boluses watch for signs pulm congestion & limit fluid in pre-eclampsia

If caesarean, low-dose CSE or slowly titrated epidural, with an art line in place. Vasopressors running for pts @ risk of CV collapse with vasodilation. Crystalloid co-loading with avoidance of overhydration or rapid preloading in pts with HF or PET. For HF, small increments & monitor response to each increment.
-CSE with 2.5-5mg isobaric bupivacaine & 15microg fent & 0.10mg preservative-free morphine then slowly load epidural catheter (3-5mL every 5 mins) with 0.75% ropivacaine to T6 level over 20mins
-could put 100microg fent after baby born or before delivery if no foetal compromise. Or preservative free morphine 3mg after baby delivered, monitoring maternal RR & sedation score for 24hrs post administration.

POSTOPERATIVE: complication surveillance
Likely HDU at least 24hrs as CO returns to pre-labour levels by 24hrs but pre-preg by 3/12
After caeser, CO increases by 25% immediately after birth, partial recovery to pre-ceaser values by fascial closure

Question 61

Car-preg categories & points

Answer 61

NYHA III-IV or cyanosis (SpO2 <90%)
LVEF <40%
prior cardiac event (TIA/CVA, symptommatic arrhythmia, HF or pulm oedema)
LVOTO (eg. AVA <1.5cm2, MVA <2cm2)

5% risk 0 points, 27% 1 point, 75% 2 points (maternal CV complications)