Cardiothoracics Flashcards

1
Q

Prevalence of adult congenital heart disease in pregnancy

A

0.8% of all pregnancies

Re babies bornin the UK:

9/1000 babies born in the UK ASD (17% of all CHD, most common)

Tetralogy of Fallot (11%)

Transposition of the great arteries (5%)

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2
Q

Pregnancy induced CVS changes

(to meet the increased metabolic demands of the mother and fetus)

A
  1. Î total blood volume by 45% on average;
  2. Î CO by 30-50%. (peak in 2nd trimester)
  3. hr rises progressively (peak in 3rd TM 25-30% above base)
  4. Fall in Systemic BP (due to hormonal-induced vasodilatation early in gestation)

peak effects at 24-32 weeks of gestation

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3
Q

Adult congenital heart disease and pregnancy

Factors that increase risk of decompensation with the physiological events of labour/early post partum due to:

A
  • Uterine contraction → autotransfusion of blood into systemic circulation
  • Expulsive efforts → î CO ( 50% above baseline)
  • Uterine involution → autotransfusion (peak î 80%)
  • Resorption of dependent oedema → autotransfusion (peak î 80%)
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4
Q

Scoring systems available to evaulate risk of morbidity and mortality of cardiac disease in pregnancy

A
  • (WHO) classification of maternal cardiovascular risk,
  • CARPREG (CARdiac disease and PREGnancy) risk score
  • ZAHARA (Zwangerschap bij Aangeboren HARtAfwijkingen [Dutch; English translation: Pregnancy with Congenital Heart Defects])
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5
Q

Neonatal complications of cardiac disease in pregnancy

A

20-28% of preg w cardiac dis:

  • premature birth
  • small for gestational age,
  • respiratory distress syndrome

1-4%

  • Fetal or neonatal death occurs

Other

  • Children of women with ACHD are at a higher risk of having CHD themselves
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6
Q

Antenatal care in a mother with cardiac disease (around 6 points)

A
  • MDT involvement with cardiologist
  • Delivery to be in a tertiary cardiac centre
  • Serial ECHOs and clinical assessment
  • +/- MRI for aortopathies
  • Plan re delivery: same may need LSCS:
    • aortopathy
    • severe left ventricular outflow tract obstruction
    • severely impaired cardiac function
  • If appropriate for SV, early epidural analgesia
    • reduce pain, sympathetic drive, and associated anxiety
    • facilitate a ‘low CO’ approach
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7
Q

Complete the table for class 1-4:

European Society of Cardiology modified version of the WHO classification of pregnancy risk with cardiac disease, including congenital diseases

A

1 - no incr risk mat mort/morb

2 - mild incr risk “

3 - significat incr risk. “

4 - Extremely high risk of maternal mortality or severe morbidity

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8
Q

Define pulmonary htn

A

mean pulmonary artery pressure of >25 mm Hg and encompasses a range of heterogeneous conditions

(mort 20-30%)

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9
Q

Mx obs patient with pulmonary htn in pregnancy

A
  • Mx in an expert centre
  • vasodilator therapy during pregnancy
  • +/- fluid and salt restriction if right heart failure
  • Planned LSCS best (Pulmonary Vascular Research Institute reccomendation)
    • labour induced pain, hypoxia, hypercarbia, and acidosis can increase pulmonary vascular resistance
    • valsalva can reduce CO
  • Avoid GA
    • all induction and inhalational agents, except eto- midate, reduce RV contractility,
    • PVR is increased in response to laryngoscopy + IPPV
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10
Q

Mx obs patient with severe systemic ventricular impairment

A
  • Mx in expert centre
  • Deliver by LSCS - Avoid labour
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11
Q

Causes of severe systemic ventricular impairment

A
  • Congenital causes
    • residual dysfunction following surgical correction of conditions such as tetralogy of Fallot
    • when the systemic ventricle is a morphological right ventricle e.g. following an atrial switch procedure for transposition of the great arteries
  • Acquired

(all its got in the BJA on cardiac condition in preg)

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12
Q

Causes of LV outflow tract obstruction (most common cause)

A
  • aortic stenosis from a bicuspid aortic valve (most common)
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13
Q

Risks of bicuspid aortic valve and associated aortopathy

A

bicuspid aortic valve and associated aortopathy are at increased risk of

  • aortic dissection
  • aortic rupture

-> They should have imaging of their aorta before and during pregnancy.

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14
Q

Complications of Severe symptomatic left ventricular outflow tract obstruction in pregnancy

A
  • heart failure
  • arrhythmia
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15
Q

Familial conditions that predispose to the risk of aortopathy (and aortic dissection, aneurysm formation and rupture)

A
  • Marfan syndrome
  • LoeyseDietz syndrome
  • Ehlerse Danlos type IV
  • Turner syndrome
  • bicuspid aortic valve with aortic dilatation
  • previous complex coarctation repairs.
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16
Q

If a patient has pre-existing aortopathy, why are the risks of aortic dissection, aneurysm formation and rupture in greater in pregnancy

A

The effects of cardiovascular and hormonal changes to the aortic media

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17
Q

Mx obs patient with aortopathy

A

Once preg

  • Counselled of
    • the risks of acute aortic syndromes and of
    • their children inheriting familial conditions.
  • Interval imaging to assess for progressive dilatation of the aorta.
  • Oft LSCS safest (deps on condition / extent of dilatation)

Pre pregnancy

  • aorta imaged before attempting pregnancy
  • Aortic dilatation of 50 mm, or 45 mm with Marfan syndrome, should be regarded as a contraindication to preg- nancy, and may require surgery prepregnancy.
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18
Q

Optimisation of peripartum anticoagulation management in obs patient w a mechanical valve

A
  • From 36w gestation, replace warfarin with either
    • LMWH
    • /unfractionated heparin (UFH) from 36 weeks gestation;
  • At least 36h before planned delivery, LMWH should be replaced by
    • IV UFH
  • UFH should be continued until 4-6 hours before planned delivery and restarted 4-6 hours after delivery if there are no bleeding complications.
  • MDT Plan made on Mx if unexpected labour presentation.
    • Don’t need full reversal of anti- coagulation for labour or CS but need to consider urgency delivery, degree of MOH and type of valve.
    • Follow AAGBI guidance on RA
    • POCT (TEG/ROTEM) may aid decision on RA if GA is CI/ v high risk

(The European Society of Cardiology)

19
Q

Complications of cyanosis in pregnancy (maternal)

A
  • PE/DVT
  • heart failure
  • supraventricular arrhythmias
  • infective endocarditis
  • PPH
20
Q

Complications of cyanosis in pregnancy (foetal, 1 mark)

A
  • Still birth
    • The degree of hypoxaemia is an important predictor
      • If SpO2 = 85%, the chance of a live birth ≈ 12% (counsel pts)
21
Q

General considerations for delivery in an obs patient with a congential cardiac abnormality

A
  • Monitoring
    • UO - hourly
    • Blood loss - measure swabs etc
    • IABP (if significant vent dysfunction / LSCS)
    • CVP (if severe heart failure)
  • B - Intravascular air
    • Death can occur if even a small amount of air crosses a shunt
  • C - IV access can be difficult (if mutiple prev ops)
  • Drugs/uterotonics
    • Use non-pharm if poss eg bimanual uterine massage or if LSCS: brace sutures / IU balloon tamponade.
    • Oxytocin → systemic vasodilation and pulmonary vasoconstriction.
      • Consider lower dose (titrate usual 10IU/h which is usu ok)
      • Consider IM - lower peak conc.
    • Ergometrine and → pulm + systemic vasoconstriction +/-→ overload impaired ventricles + coronary vasocontruction
    • carboprost (as above, no coronary fx)
    • PR misoprostol: ˚CVS fx, safe
  • Antibiotics* - discuss/consider risk IE vs Abs
  • Fluid balance/haemorrhage
    • :) moderate OH post delivery +/- beneficial to vent decomp due to auto-transfusion)
    • :( significant MOH in pts unable to compensate
    • Fluid resuscitation can be diffic: if aggressive, may ppt ❤︎ failure

*(NICE advises against routinely offering prophylaxis for obstetric procedures or childbirth, but also that this guidance does not override the responsibility to discuss all options with the patient and to use clinical judgement. MBRRACE recommends discussing pro- phylaxis with women prior to childbirth.)

22
Q

Mx of obs pt with congenital cardiac condition for vaginal delivery

A
  • Early initiation of epidural analgesia
    • Low dose regimens should be used, with cautious administration of any boluses.
    • low threshold for replacing a failing epidural.
  • Limit/minimise expulsive efforts (limits vlasalva/risks autotransfusion)
  • Assist delivery by forceps or ventouse if req
  • An epidural also allows conversion to surgical anaesthesia for operative delivery if necessary. This should also be done cautiously and decisions concerning urgency of delivery should be made in this context.
23
Q

Advantages of epidural for obs patient with congenital cardiac abnormality having a SVD

A
  • reduce cardiac after- load + pain-related sympathetic drive.
    • ‘Lower CO’ approach possible with epidural
  • Reduces the urge to push
  • Once the cervix is fully dilated, allows time for the fetal head to passively descend in the pelvis.
  • Allows conversion to surgical anaesthesia for operative delivery if necessary
24
Q

Changes to usual technique if ♀ needed LSCS?

A
  • Regional anaesthesia usu
    • combined spinal-epidural: low-dose spinal, and gradual supplementation via the epidural to minimize haemodynamic instability.
  • If GA:
    • should be tailored towards haemodynamic stability
    • opioids should not be withheld for fear of causing neonatal respiratory depression.
    • If decompensation is a reasonable possibility and poten- tially amenable to cardiac surgery, CS is performed under GA in cardiac theatres, with the facility and personnel for emer- gency cardiopulmonary bypass and surgery.
  • Post partum
    • Close monitoring postpartum (1:1 midwife care)
    • / CCU for 24h w freq obs/anaesthetic r/v

(55% of deaths from heart disease in 2009-2014 occurred in the 6 weeks following delivery)

25
Q

The incidence of cardiac arrest after adult cardiac surgery

A

0.7-2.9%.

26
Q

survival rates of cardiac arrest post cardiac surgery

A

79% (vs 18% for tradition post arrests as higher incidence reversible causes)

27
Q

key differences in Mx of cardiac arrest post cardiac surgery (vs traditional in hosp cardiac arrest)

A
  • Avoidance of external chest compressions (ECC) for up to 1min
    • following identification of either VF or pulseless ventricular tachycardia (pVT) to allow for expe- ditious defibrillation
  • Avoidance of full dose adrenaline in favour of three-stacked shocks (@150J) and
  • Resternotomy within 5 minutes of arrest.
28
Q

Common causes for the deterioration of the postoperative cardiac surgical patient

A
  • Hypovolaemia and bleeding
  • Low cardiac output state
  • Graft and valve failure
  • Tamponade
  • Arrhythmias (usu AF)
  • Vasodilation
29
Q

Risk factors for hypovolaemia and bleeding post cardiac surgery

A
  • Preoperative anti- coagulation/antiplatelet treatments
  • Inherited or acquired bleeding diathesis
  • Emergency surgery
  • Prolonged bypass times
  • Re-do surgery.
30
Q

Causes of intra vascular volume depletion (→hypovolaemia and bleeding) post cardiac surgery

A
  • capillary leakage
  • haemodilution
  • re-distribution
  • polyuria
31
Q

2 Ix in a hypovolvaemic/Bleeding patient post cardiac surgery

A
  • POCT and haematological analysis
    • ? residual heparin/clotting factor de- ficiencies, and extensive fibrinolysis
  • CXR + urgent TOE
    • hidden surgical bleeding from sternal wire sites and anas- tomotic or side branch leaks from graft sites (not seen in drains)
  • Also T (vasodilation), Ix for sepsis, anaphylaxis, adrenal insufficiency, the vasoplegic syndrome
32
Q

Ix in ventricular impairment/Low CO state post Cardiac surgery

A
  • ECG
    • Shows myocardial ischaemia post coronary revascularisation
  • TOE excludes:
    • myocardial oedema
    • reperfusion injury
    • RH failure: increased pulmonary vascular resistance and volume overload.
    • tamponade
  • Bichemical tests
    • Ca for hypocalcaemia
    • lactate/base deficit (+ low UO, cool peripheries can show vent fail)
      • peripherally cool with dysrhythmias + low UO

Not sure if this question is worded at its best.

33
Q

Define cardiac tamponade

A
  • Surgical emergency involving
    • rapid compression of the heart
    • by an accumulation of fluid (of blood) within pericardial sac that
    • reduces
      • ventricular filling and
      • CO
34
Q

Classical signs of cardiac tamponade

A
  • a falling blood pressure,
  • reduced CO
  • rising filling pressures
  • tachycardia
  • Becks triad:
      • hypotension
      • elevated jugular venous pressure
      • muffled heart sounds
35
Q

Why might it be difficult to diagnose tamponade post cardiac surgery?

A
  • ‘classical’ signs may be masked
    • e.g. a hypovolaemic, beta blocked patient with poor LV
  • Small volumes of blood can easily be missed on either transthoracic echocardiogram (TTE) or TOE + can cause significant compression and haemodynamic instability.
36
Q

First step in CALS algorithm (Cardiac Advanced Life Support)

Complete blanks 0, 1, 2, 3

A
37
Q

Second steps in CALS algorithm

Complete 0, 1, 2, 3 in this CALS protocol

A
38
Q

Third steps in CALS algorithm

Complete 0, 1, 2, 3 in this CALS protocol

A
39
Q

Name the 6 key roles during resusitation in arrest post cardiac surgery

A
40
Q

What are the two triggers for an intra-arterial baloon pump

A

IABPs are triggered by either

  • ECG
  • arterial line pressure
41
Q

Mx of an IA baloon pump in cardiac arrest post cardiac surgery

A
  • Set the IABP to pressure trigger in a 1:1 ratio
    • with maximal augmentation
    • ⇒enables IABP to augment diastolic perfusion in line with ECC
    • ⇒thereby î coronary/cerebral perfusion
42
Q

Mx of a pacemaker in cardiac arrest post cardiac surgery

Rhythm: severe bradycardia, asystole, or PEA

A
  • Wires should be attached (if not already)
  • The pacemaker set to DDD
  • Pace at 80-100 beats/min1
  • With stimulation thresholds at maximum to ensure pacing.
  • +/-activate asynchronous pacing during resusitation
43
Q

In cardiac arrest post cardiac surg, if ROSC is not achieved after resternotomy, further consideration:

A

ECMO