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Anna and louise > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Normal ECG findings in pregnancy

A

Partly related to changes in the position of heart
- Slight left axis deviation due to altered heart position
Sinus tachycardia
Atrial and ventricular ectopics
Q-wave (small) and inverted T wave in lead III
ST segment depression and T wave inversion - inferior and lateral leads
QRS axis leftward shift

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2
Q

Normal cardiovascular examination findings in pregnancy

A 
Bounding / collapsing pulse
Ejection systolic murmur (in >90% of pregnant women)
Loud first heart sound
Third heart sound
Relative sinus tachycardia
Ectopic beats
Peripheral oedema
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3
Q

CXR features in pregnancy

A

Heart is enlarged and pushed up by growing uterus
The aorta unfolds and the heart is rotated upwards and outwards
CXR may show heart displaced into a horizontal position, rotating to the left, with increased transverse diameter
Increased pulmonary vascular markings
Pulmonary venous distension
Elevated right hemidiaphragm

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4
Q

CV changes in pregnancy (physiology)

A

Drop in systemic vascular resistance - from peripheral vasodilation
Increase plasma volume
Increase stroke volume by 10-30%
HR increases from normal 70 to 80-90bpm
Cardiac output rises from 4L/min at week 10 to 6L/min at week 24 (~40% in pregnancy)

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5
Q

BP changes in pregnancy

A

Before the increase in CO can adequately compensate for the fall in SVR, BP begins to decrease in early pregnancy
Continues to decrease in second trimester until the nadir in SBP and DBP is reached by about 22-24 weeks’ gestation
From then on, there is a steady rise to pre-pregnancy levels until term
Post-partum - BP falls immediately after delivery, although tends to rise subsequently reaching a peak 3-6 days postpartum
- This may relate to return of normal vascular tone and a period of vasomotor instability while normal, and non-pregnant vasoregulation is re-established

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6
Q

Describe the New York Heart Association classification

A

Functional system based on symptoms

Class I
No breathlessness / uncompromised
No limitation on physical activity

Class II
Breathlessness on severe exertion / slightly compromised
Ordinary activity –> symptoms

Class III
Breathlessness on mild exertion / moderately compromised
Asymptomatic at rest
Less than ordinary activity –> symptoms

Class IV
Breathlessness at rest / severely compromised

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7
Q

Cardiac lesions that limit the ability to increase CO appropriately:

A
  • Valvular stenosis - especially AS and MS
  • Ventricular systolic impairment
  • Cyanotic heart disease
  • Ischaemic heart disease
  • Dilated aortic root - increased risk of dissection
  • Pulmonary artery HTN - a/w the highest risk of maternal mortality
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8
Q

Class IV of WHO classification

A

Conditions a/w extremely high risk of mortality or severe morbidity
Pregnancy is contraindicated

Severe MS
Symptomatic severe aortic stenosis
Bicuspid aortic valve with ascending aorta diameter >5cm
Marfan’s with aorta >45mm
Severe systemic ventricular systolic dysfunction with LVEF <30%
NYHA III-IV
Native severe coarctation
Fontan circulation with complications
Significant pulmonary arterial HTN
Previous peripartum cardiomyopathy with residual impairment

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9
Q

Antibiotic prophylaxis with heart disease

A

Current UK recommendations (NICE): antibiotic prophylaxis against infective endocarditis is not required for childbirth

Consider cover only for patients deemed to be at high risk of developing IE (e.g. previous IE) and for those who have the poorest outcome (e.g. cyanotic congenital heart disease)
Amoxicillin 2g IV + gentamicin 1.5mg/kg IV at onset of labour / ROM or prior to C/S

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10
Q

Maternal mortality of pulmonary HTN

A

Was 40% but more recent data suggest this may have fallen to 10-25%

Fixed pulmonary vascular resistance (PVR) means that these women cannot increase pulmonary blood flow to match the increased CO and they tolerate pregnancy poorly

High risk scenarios:

  • Right to left shunt in Eisenmenger’s syndrome
  • Right heart failure
  • Escalating pulmonary HTN with pulmonary hypertensive crises
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11
Q

Diagnosis of pulmonary HTN

A

Non-pregnant elevation of mean (non-systolic) pulmonary artery pressure > 22mmHg at rest or 30mmHg on exercise in the absence of left to right shunt

If there is pulmonary HTN in the presence of a left to right shunt, the diagnosis of pulmonary vascular disease is particularly difficult and further investigation including cardiac catheterisation to calculate PVR is likely to be necessary

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12
Q

Causes of pulmonary HTN

A

Idiopathic pulmonary arterial hypertension (PAH)
Congenital heart disease-associated pulmonary hypertension - E.g. ASD / VSD with PAH - includes Eisenmenger’s syndrome
Chronic thromboembolic pulmonary HTN
Lung disease
- E.g. cystic fibrosis, interstitial lung disease, hypoxia
Connective tissue disease - E.g. scleroderma, SLE

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13
Q

Antenatal management of pulmonary HTN

A

MDT
Review meds re. safety in pregnancy
PAH-targeted therapies should be continued
- Sildenafil (aka VIAGRA) - safe to continue
Thromboprophylaxis
Elective admission for best rest, O2 therapy and escalation of targeted therapies

TOP should be considered
- TOP itself is associated with maternal mortality up to 7% (less than the risk of pregnancy continuing)

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14
Q

Intrapartum management of pulmonary HTN

A

MDT discussion and planning of delivery
No evidence that C/S vs. vaginal delivery, or regional anaesthesia vs. GA reduces mortality
In most case series delivery has been by C/S, often preterm
Telemetry
ICU
Avoid:
- Hypovolaemia (maintain preload)
- Acidosis
- Thromboembolism (heparin bridging)
- Pulmonary artery catheters (carry a risk of thrombus)
Systemic vasodilation (caution with regional anaesthesia, syntocinon - slow bolus)

Aggressive diuresis post-partum

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15
Q

Impacts of ecbolics - pulm HTN

A

Syntocinon - causes vasodilation, therefore give in slow bolus or infusion

Ergometrine - increases SVR (and pulmonary)

Carboprost - increases pulmonary vascular resistance –> pulmonary oedema

Misoprostol - safe

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16
Q

Post-delivery changes in CV physiology

A

Increased CO 60-80% due to relief of IVC obstruction and uterus emptying blood into the systemic circulation
~500-600ml blood from uterine circulation returns ~ autotransfusion (increases pre-load)
Then rapid decline to prelabour values within 1 hour of delivery
Transfer of fluid from extra-vascular space increased VR and SV
CO returns to pre-pregnancy levels 2 weeks after delivery

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17
Q

Impact of patent ductus arteriosus on pregnancy

A

Aorta to pulmonary artery
Left to right shunt, some oxygenated blood into pulmonary circuit
Most cases encountered would have been repaired in childhood (corrected cases) - Pose no problems in pregnancy
Uncorrected cases do well but are at risk of congestive cardiac failure

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18
Q

Impact of ASD on pregnancy

A

Commonest congenital heart defect in women
Usually well tolerated in pregnancy
If unrepaired:
- Potential risk of paradoxical embolism - low risk (Passage of thrombus from a vein to an artery)
- Atrial arrhythmia

If increase in left to right shunt following blood loss at delivery may deteriorate –> hypotension –> drop LVEF

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19
Q

Impact of VSD in pregnancy

A

Small (<1.25cm) or repaired defects - low risk during pregnancy
Increased volume load of left ventricle
Usually well tolerated in pregnancy unless Eisenmenger’s syndrome

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20
Q

Management of coarctation of the aorta

A 
Usually corrected if diagnosed pre-pregnancy
Risks if uncorrected:
- Angina
- HTN
- Congestive heart failure
- Aortic rupture
- Aortic dissection

Ideally have MRI pre-pregnancy to exclude any aneurysm of post-stenotic dilatation around the repair site
Minimise risk of aortic dissection with strict BP control and beta-blockade to decrease cardiac contractility

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21
Q

What is Marfan’s syndrome?

A 
Connective tissue disorder
Autosomal dominant disorder
80% have cardiac involvement (usually mitral valve prolapse, mitral regurgitation, aortic root dilatation)
Those with cardiac lesions tend to have offspring with cardiac abnormalities 
Other features of Marfan's
- Increased height
- Arm span > height
- Arachnodactyly
- Joint laxity
- Depressed sternum
- High arched palate
- Dislocation of the lens
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22
Q

Risk of aortic dissection in pregnancy with Marfan’s?

A

1% if <4cm

Predictors for dissection and rupture:

  • Pre-existing or progressive aortic root dilatation (10% if root >4cm)
  • Positive FHx of dissection or aortic rupture
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23
Q

Management of Marfan’s in pregnancy

A

Genetics referral
BP check
Beta blockers shown to reduce the rate of aortic dilatation and the risk of complications in Marfan’s
- Serial growth scans if on beta blocker
Regular ECHO to assess aortic root diameter
Elective C/S - if aortic roots show progressive enlargement or >4.5cm
- Deliver in hospital with cardiothoracic support available

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24
Q

4 features of ToF

A
  1. VSD
  2. Pulmonary artery stenosis
  3. Overriding aorta
  4. RV hypertrophy
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25
Q

Pregnancy impact on ToF

A

Majority of women will have undergone surgical correction
- Main issue is RV dysfunction that can deteriorate in view of pulmonary regurgitation resulting from earlier surgery
If unoperated, those without pulmonary vascular disease may negotiate pregnancy successfully
Two main concerns:
- Paradoxical embolism through right to left shunt –> CVA
- Effects of cyanosis (from increased right to left shunt due to fall in SVR) and maternal hypoxaemia on fetus

FGR, miscarriage, spontaneous and iatrogenic prematurity

26
Q

Important considerations for post-op congenital heart disease

A
  • The risk of ventricular failure (particularly when the RV is acting as the systemic pumping chamber)
  • Any residual pulmonary HTN
27
Q

Fontan circulation

A

Characterised by a single functioning ventricle
Increases in venous pressure may cause hepatic congestion and oedema, but sufficient volume loading is required to ensure adequate perfusion of the pulmonary circulation

Risks of HF, VTE (blood flows slowly through the lungs)
HTN dangerous as quickly cyanotic

Risks with pregnancy:

  • Miscarriage (30%)
  • Premature birth
  • FGR
  • Neonatal death
28
Q

Genetic counselling

A

Risk of fetus having congenital heart disease is higher if the mother rather than the father has congenital heart disease
- Risk is 4% (50% same defect)
Level of risk depends on the specific lesion

In women with ASD, risk in fetus ~5-10%

Refer women for detailed fetal echo

29
Q

Cause of Eisenmengers

A

VSD > ASD > PDA
Syndrome where is a long standing left to right shunt due to a congenital heart defect –> pulmonary HTN and eventual reversal of shunt into a cyanotic right to left shunt

30
Q

Pregnancy implications of Eisenmengers

A

Preload of the RV increases
Afterload of the LV decreases
Shunting, and therefore cyanosis, increases

MATERNAL
Mortality 20-50%
VTE - because of erythrocytosis
Maternal cyanosis

FETAL
Chance of livebirth <50% if sats <90%
PTB
Stillbirth
IUGR
Increased risk of CHD
31
Q

What is rheumatic heart disease?

A

RF - caused by an immunological reaction to a streptococcal infection
Damage to heart valves may remain once the acute episode has resolved
Cardiac inflammation results in fibrosis of the valves and they are either stenotic or insufficient
Mitral stenosis accounts for 90% of RHD in pregnancy
If get another strep bacteraemia, then bacteria land on damaged valve –> endocarditis and more damage to heart
Antibiotic prophylaxis is crucial after acute RF episode (as per local guidelines)

32
Q

Effect of pregnancy on MS

A

Can deteriorate quickly and develop pulmonary oedema, even if asymptomatic at start of pregnancy
40% increase in preload in pregnancy - can’t travel through stenotic valve
Tachycardia –> diastolic filling of the LV is further decreased from fall in SV and a rise in left atrial pressure –> pulmonary oedema
Secondary pulmonary HTN can occur –> RV failure

Most women who develop complications do so in the late second or third trimester, or peripartum period
- Second trimester because preload and CO peak

Poor prognostic features for development of pulmonary oedema:

  • Severe MS - valve area <1cm2
  • Presence of moderate to severe symptoms prior to pregnancy
33
Q

Antenatal management of MS in pregnancy

A

MDT
Beta-blockers
- Slow the heart rate, allows time for left atrial emptying
Treat AF aggressively with digoxin or beta-blockers
VTE prophylaxis if AF, periods rest, or LA dilation
Baseline ECHO
If pulmonary oedema, admit to hospital

Can consider balloon valvotomy and closed mitral valvotomy
Surgical open valvotomy associated with fetal mortality rate 15-35% (compared with 5-15% for closed)

34
Q

Intrapartum management of MS

A

Tertiary centre
Avoid supine and lithotomy positions
- Could decrease preload
Avoid excessive IV fluids - keep women on the dry side
- May need to give frusemide (risk of pulmonary oedema)
- Abrupt increase in preload at delivery may –> increase in RA pressure and pulmonary oedema
Good analgesia
Telemetry
Short second stage +/- instrumental

35
Q

Aortic stenosis in pregnancy

A

Causes:

  • Congenital (usually bicuspid valve)
  • Rheumatic HD

Narrow aortic valve –> LV hypertrophy and LA dilatation
Can restrict blood flow to brain and heart muscle

Preconception functional status provides good estimate of pregnancy risk - if asymptomatic well tolerated

36
Q

Management of AS

A

Maintain adequate preload to maintain SV
- Hypotension and tachycardia are poorly tolerated
Optimise volume status
Avoid hypotension
- Maintenance of left uterine displacement
- Aggressive treatment blood loss
Arterial line monitoring

Third stage:

  • Oxytocin infusion for third stage - bolus can —> severe intractable hypotension
  • Mechanical methods (bimanual) and misoprostol
  • If haemodynamically significant haemorrhage, can use syntometrine
37
Q

Regurgitant valve disease

A

Systemic vasodilation and fall in PVR reduce after load and therefore act to reduce regurgitation
MR and AR are well tolerated in pregnancy, provided there is no significant LV dysfunction
Women with heart failure can be safely treated with diuretics, digoxin and hydralazine and / or nitrates as vasodilators to ‘offload’ the LV

38
Q

Mechanical vs. graft tissue heart valves

A

Mechanical (metal)

  • Life long anticoagulation
  • Last longer - 10-15y
  • High risk of thrombosis on valves
  • Warfarin issues in pregnancy

Graft tissue (bioprosthetic)

  • No anticoagulation
  • Better choice for women of childbearing age?
  • Accelerated deterioration throughout pregnancy
  • Surgery should be one year before pregnancy
39
Q

Management if mechanical heart valve

A

Warfarin

  • Lowest risk of thrombosis (0-4%) and haemorrhagic complications
  • Associated with increased risk of teratogenesis, miscarriage, stillbirth and intracerebral bleeding
  • highest risk time of warfarin is 6-12 weeks, consider clexane for first trimester, then switch depending on how high risk the valve is
  • All women should discontinue warfarin for 10-14 days prior to delivery to allow clearance by the fetus, cover with LMWH or heparin

LMWH

  • Safe for fetus
  • Associated with a higher risk of thrombosis for the pregnant woman
  • Doses should be adjusted according to anti-factor Xa levels - 2 weeks after starting and every trimester
  • Low dose aspirin should be added as adjunctive antithrombotic therapy
40
Q

Hypertrophic cardiomyopathy in pregnancy

A

~70% are familial, autosomal dominant

Mostly well tolerated because of an increase in LV cavity size and the SV is usually able to increase
Beta-blockers should be continued or started for those with symptoms
Caution with regional anaesthesia to avoid hypotension with consequent increased LV outflow tract obstruction
- Hypovolaemia will have the same effect

41
Q

Define PERIPARTUM CARDIOMYOPATHY

A

Rare condition, specific to pregnancy
Defined as the development of heart failure at the end of pregnancy or in the months (up to 5/12) following delivery, where no other cause of heart failure is found

On echocardiography:
- LVEF <45%
Often, echo shows enlarged heart with global dilation of the four chambers and markedly reduced LV function

42
Q

Risk factors of peripartum cardiomyopathy

A 
Multiple pregnancy
Pregnancy complicated by HTN
Multiparity
Advanced maternal age
Afro-Caribbean race
Obesity
43
Q

Management of peripartum cardiomyopathy

A

Elective delivery if antenatal
Thromboprophylaxis
Conventional heart failure treatment
- Diuretics, vasodilators, beta blockers, digoxin, inotropes
- After delivery - ACE inhibitors
Immunosuppressive therapy may be considered in cases with myocarditis (confirmed with endomyocardial biopsy) that fail to improve within 2 weeks
Bromocriptine has been suggested in view of the link with a pathogenic form of prolactin
Intra-aortic balloon pumps and left ventricular assist devices may provide temporary support
Cardiac transplantation

Follow up in clinic
LARC

44
Q

Prognosis of peripartum cardiomyopathy

A

Mortality much lower than previous suggested, 10%
~50% make a spontaneous and full recovery
Prognosis depends on normalisation of LV size and function within 6 months of delivery
- Mortality increased in those with persistent LV dysfunction

Counsel against further pregnancy if LV size or function does not return to normal - Otherwise significant risk of recurrence, worsening heart failure (50%) and death (25%) in subsequent pregnancies
If cardiomyopathy resolves, recurrence is not known but appears to be lower (? u to 25%)

45
Q

Work up of tachycardia in pregnancy

A

Investigations:
- ECG - look for WPW
- Bloods - TFTs, electrolytes, Hb, iron studies
Consider 24 hour Holter monitor if history suggests frequent and troublesome arrhythmias
If diagnose arrhythmia, should do echo to exclude structural heart disease

46
Q

Prevalence of hypertensive disorders of pregnancy

A

HTN complicates 10-15% of pregnancies
PET 3-5%
Severe PET 1%
Eclampsia 0.03%

47
Q

Placental growth factor (PlGF)-based testing

A

Has a high sensitivity and negative predictive value in diagnosing pre-eclampsia that requires delivery within 14 days

48
Q

Chronic HTN

If first presentation in early first trimester, exam/investigate for clues to a possible secondary cause…

A 
Essential HTN (90%)
Secondary causes (10%)
  • Femoral pulses - radiofemoral delay suggests coarctation of the aorta
  • Renal bruit - possible renal artery stenosis
  • Urinalysis - proteinuria or haematuria suggests renal disease
  • Serum creatinine - to exclude renal impairment
  • Electrolytes - hypokalaemia may suggest hyperaldosteronism / Conn’s syndrome
  • Serum calcium - to exclude hyperparathyroidism
  • Urinary catecholamines - phaeochromocytoma
49
Q

Outcomes with chronic HTN

A

22% will get PET
- 10% <34/40
50% will have a CS
27% will have SGA

if get PET, 50% will have PTB

50
Q

Diagnostic criteria of PET

A

New onset of HTN (SBP >140 or DBP >90) after 20/40 and the coexistence of 1 or more of the following new onset conditions:

  • Proteinuria - PCR >30 mg/mmol, or
  • Renal insufficiency, Cr >90 micromol/L
  • Liver involvement - ALT or AST >40 IU/L with or without RUQ or epigastric pain
  • Neurological complications - Eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, persistent visual scotomata
  • Haematological complications - thrombocytopenia (plt <150,000/microlitre), DIC, haemolysis
  • Uteroplacental dysfunction - FGR, abnormal umbilical artery doppler waveform analysis, stillbirth
  • Pulmonary oedema
51
Q

Aetiology of PET

A

Abnormal trophoblast invasion –> spiral arterioles fail to become high capacitance and low resistance vessels –> inadequate perfusion –> uteroplacental ischaemia

Placenta unable to optimise blood supply from maternal uterine vessels

52
Q

Pathogenic mechanisms of PET and clinical sequalae

A

Impaired trophoblast differentiation and invasion with failure of spiral arteries to remodel –> Uteroplacental unit fails to become a high capacitance, low resistance circulation –> increased placental resistance and ischaemia, and fetal hypoxia, IUGR

Increased pro-inflammatory cytokines –> Widespread microvascular damage / endothelial dysfunction –> HTN, liver and renal impairment. Increased VTE risk

Placental hypo-perfusion –> increased trophoblastic breakdown –> Hyperuricaemia

Increased anti-angiogenic factors with resultant inhibition of angiogenic factors (e.g. VEGF and PlGF) –> Poor placental blood flow

Endothelial cell activation –> Increased capillary permeability - peripheral oedema, cerebral oedema. Increased platelet activation and vascular tone - HTN

Immunological factors -Exposure to paternal and fetal antigens protects against PET. Increased PET in nulliparous women / women who change partners / use barrier contraception

Genetic predisposition - Maternal genes involved - e.g. increased risk in primigravid with FHx or PET in previous pregnancy

53
Q

Doses of MgSO4

A

Loading dose: 4g IV over 5-15 mins

Maintenance dose: 1g / hour for 24 hours
If eclamptic fit, continue for 24h after last fit

Recurrent fit: further dose of 2-4g IV over 5-15 mins

54
Q

Reasons to treat HTN in pregnancy

A

No difference in neonatal outcomes between DBP 85 vs. 100 (CHIPS)
Does not prevent PET or adverse outcome
Decreases incidence of severe HTN

55
Q

Treatment tips for antihypertensives - antenatal

A

LABETALOL - serial growth scans with beta blockers, CI: asthma

METHYLDOPA - CI: depression, switch postnatal (by day 2)
- slow onset of action over 24h

NIFEDIPINE - calcium channel blocker, ADR: headache, flushing. CI: aortic stenosis

56
Q

PET - Counselling for future pregnancies

A

Overall risk of recurrence is ~1 in 5
Advise aiming BMI within health range to lower risk of PET

If PET <34/40, recurrence 25%
- 55% if <28/40

If prev gest HTN, risk of PET 2-7%

57
Q

Monitoring in HTN of pregnancy

A

Chronic HTN

  • Assess for proteinuria each visit
  • PET bloods if new proteinuria or change in BP
  • Early dating
  • Third trimester growth, repeat as indicated

Gest HTN

  • assess for proteinuria 1-2 times per week
  • PET bloods weekly
  • USS 3-4 weekly from time of diagnosis

PET

  • assess for proteinuria at time of Dx, repeat daily if negative
  • PET bloods twice weekly, more frequent if unstable
  • growth USS at time of diagnosis, 2 weekly
  • CTG twice a week
58
Q

Acute BP lowering medications

A

BP 170/110
- Level where cerebral autoregulation is overcome
- Risk of haemorrhage and hypertensive encephalopathy
MDT
ICU / HDU
Aim for gradual and sustained lowering of BP
- Precipitous fall may impair placental perfusion
Given concurrent long-acting and short-acting agent

Labetalol - 20-80mg IV over 2 mins
Max effect 5 mins after dose
Repeat every 10 mins

Nifedipine

Hydralazine - 10mg IV bolus
Onset of action: 20 mins
First dose 5mg if fetal compromise

59
Q

Indicators for high risk of developing eclampsia:

A
  • Persistent headache
  • Hyperreflexia with clonus
  • Liver involvement
  • Severe HTN
60
Q

Principles of management of eclampsia

A

Resuscitation

  • Seizures are self-limiting
  • Ensure patent airway, oxygen, IV access

Prevention of further seizures

  • MgSO4 4g loading dose over 20mins
  • Maintenance: 1g/hr for 24h
  • If second seizure on maintenance, give further 2-4g over 10 mins
  • Don’t monitor Mg levels unless renal function is compromised
  • In AKI same loading dose but half maintenance

Control of HTN

Delivery

61
Q

Aspirin for PET prophylaxis

A

Before 16/40
Corrects imbalance between circulating prostaglandins, inhibits platelet aggregation, dilates blood vessels and anti-inflammatory effect
NNT for high risk women = 19
10-20% reduction in women at moderate to high risk of PET
14% reduction in stillbirth
10% reduction in SGA
No increased bleeding risk

62
Q

Calcium for PET prophylaxis

A

Low Ca stimulates parathyroid hormone and renin release –> increases intracellular Ca in vascular smooth muscle –> vasoconstriction
Reduces risk of PET in high risk women and those with low dietary intake

Anna and louise (28 decks)

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