Echocardiographic assessment and critical care management of peri-partum women with unexpected left ventricular failure

Abstract

Introduction

Cardiac disease remains the largest single cause of maternal death. Whilst uncommon, left ventricular failure during pregnancy and delivery can be devastating to both mother and child. Echocardiography can play a significant role in rapidly establishing a diagnosis, guiding initial therapy and then monitoring response.

Clinical vignettes

The history, presentation and management of three cases of peri-partum left ventricular failure is examined: stress cardiomyopathy in a 34 year old with twins, left ventricular dysfunction secondary to pre-eclampsia in a 22 year old with a singleton pregnancy and a true peri-partum cardiomyopathy in a 42 year old with IVF twins. The defining risk factors, presenting characteristics and echocardiographical findings for each pathology are highlighted.

Conclusion

Echocardiography is playing an increasingly important role in the immediate assessment and management of left ventricular failure. This is especially true in the peri-partum woman, where establishing the correct therapy is both challenging and crucial due to the significant cardiovascular changes that occur around the time of delivery. To this end we believe that echocardiography should be rapidly available to guide the management of these patients by a multidisciplinary team made up of obstetricians, cardiologists, anaesthetists and intensive care physicians.

Keywords

Echocardiography peri-partum heart failure pre-eclampsia cardiomyopathy

Introduction

Whilst uncommon, left ventricular failure during pregnancy and delivery can be devastating to both mother and child. Critical care clinicians may be called on to contribute to the care of these women and their management can be challenging with lack of time a major factor.

The rate of maternal death in the UK from primary cardiac disease has risen over the past 20 years.¹ It has been the leading cause of indirect maternal mortality, and the leading overall cause of maternal mortality in the UK since 2002.²

Clinical diagnosis of cardiovascular collapse in peri-partum women mandates immediate echocardiography. Only bedside transthoracic echocardiography can provide the immediate structural and functional information required to effect immediate therapeutic manoeuvres. This skill also allows rapid reassessment to ensure progress is being made in the right direction.

Transthoracic echocardiography now plays a central role in the assessment of all causes of shock in the critical care arena and is now the modality of first choice in European consensus guidelines.³ Its use as both a diagnostic tool and as a guide to cardiovascular therapies is well documented.⁴ The MBRACE 2019 report will be focusing on both cardiac deaths and deaths after critical care which will place echocardiography at centre stage in managing the sick peri-partum mother.

Rapid recognition of the three most significant causes of de novo left ventricular failure in peri-partum women is the key to their survival. We therefore present three clinical vignettes generated from our own practice designed to signal to the reader the key differentiating clinical and echocardiographic features. We also discuss management options and present an echocardiographic algorithm intended for use at the bedside.

Clinical vignettes

Stress cardiomyopathy (SCM)

Clinical process	Clinical learning points
A 34 year-old lady with twins went into premature labour at 34 weeks. She had no relevant previous medical history and was a non-smoker and non-drinker. She had a caesarean section for failure to progress with a significant post-partum haemorrhage that was managed with conservative measures. She remained stable and was discharged home with ibuprofen for post-operative analgesia. Due to issues with wound pain, she increased her dose of ibuprofen. She subsequently presented to a district general hospital with a haemodynamically significant upper gastrointestinal bleed. She received a blood transfusion for hypotension and underwent urgent endoscopy. A duodenal ulcer was seen and injected, but haemodynamic control was not possible. She was transferred to the nearest centre with interventional radiology facilities. Embolisation of a bleeding branch of the gastric artery was unsuccessfully attempted and she proceeded to theatre for a laparotomy where the duodenal ulcer was oversewn. Over the following 12 hours she remained noradrenaline dependent despite fluid resuscitation. In addition there was evidence of tissue hypoperfusion and pulmonary oedema was evident on her chest radiograph.	Patients affected by SCM often have no previous cardiac history. Risk factors for developing stress cardiomyopathy include any factors which exacerbate high cardiac output failure: Inter-current malnutrition Inter-current infection Inter-current illness Anaemia Hyperthyroidism Previous SCM Other cardiovascular disease: current or previous for example arrhythmias, congenital heart diseases High cardiac demands: end of pregnancy, twin or multiple pregnancies. The signs, symptoms and classical chest X-ray changes of congestive cardiac failure are prone to be missed or underestimated in this group of patients if the diagnosis is not carefully considered in this at risk group.
Echocardiography was undertaken urgently which demonstrated biventricular systolic failure, very poor LV relaxation and raised LVEDP. Dilatation of the LV and RV was causing moderate tricuspid regurgitation and mitral regurgitation (Figure 1).	Urgent echocardiography is mandated in these patients and can demonstrate any or all of RV or LV systolic or diastolic failure and acute valve lesions associated with changes in cardiac structure due to chamber dilatation. LV systolic failure is assessed using the biplane Simpsons method and is classed as impaired when the EF is <50% and severe when ≤35%.⁵ RV systolic failure is assessed using fractional area change, with impairment being defined as ≤30% in a male and ≤35% in a female. Pulmonary hypertension may develop acutely due to acute vasoconstriction of the small pulmonary vessels secondary to perfusion/ventilation mismatch caused either by acute cardiogenic pulmonary oedema or other associated pathologies. A takotsubo abnormality can also be seen. Evidence of new pulmonary hypertension should prompt careful thought regarding co-existent pulmonary thromboembolism in this high-risk group. It is important to remember that under stressed conditions the LV should be hyperdynamic. Therefore in this context a ‘normal’ EF may suggest impairment.
Advanced assessment for residual fluid responsiveness demonstrated a >25% variation in LVOT VTi with the respiratory cycle.	Fluid responsiveness assessment can be performed accurately if the patient is invasively ventilated at a tidal volume of 7mls/kg and is receiving mandatory breaths.⁶ Caution needs to be exercised in the interpretation of fluid responsiveness in patients with poor LV and RV function since impaired ventricles tend to demonstrate a degree of FR. However, where a marked effect is seen from ventilation on LVOT VTi variance this should be acted upon, albeit very carefully.⁶
The patient was managed with careful colloid boluses up to a total of 750mls to reduce the LVOT VTi variability to less than 12% (real-time echocardiography was used to look for a change in VTi during and after each bolus), and low dose Dobutamine with vasodilatation offset using low dose noradrenaline. A target mean blood pressure of 55 mmHg and a target systolic blood pressure of 90 mmHg were used and balanced against maintaining a normal base excess and adequate urine output. Sedation was altered from propofol and fentanyl to low dose midazolam and fentanyl to minimise the directly hypotensive effects of propofol. Electrolytes were carefully optimised and she was treated with pabrinex, vitamin D, trace elements and nasogastric feeding. A random cortisol test was carried out to exclude overt adrenal failure. Low dose ACE inhibition was also carefully introduced at this point. Within 48 hours the patient was extubated and she remained stable with a moderately impaired RV and LV until her discharge to the ward at day four following admission to intensive care. Medications on discharge from intensive care included ACE inhibitor and regular loop diuretic therapy.	Acute management of stress PPCM should include: Exclude adrenal failure: in all cases there should be a low threshold for the administration of rescue doses of hydrocortisone. Assessment of the pituitary adrenal axis can be undertaken when the patient is no longer in extremis. Attention to fluid balance: particularly in the context of fluid shifts occurring during the immediate post-partum period, or on-going bleeding. This can mandate repeated assessments of fluid responsiveness using echocardiography. Haemoglobin level should be kept at a higher trigger of 10 g/dl to ensure adequate cardiac oxygen delivery. Avoidance of increased afterload: although low-level increased afterload may be required to offset vasodilatory drugs such as sedation and inodilators, high afterload increases LVEDP and further reduces impaired longitudinal function. This may mandate the need to tolerate a lower target blood pressure in order to maximise flow and cardiac output. A balance should be reached between pressure and perfusion, which can be judged usefully from urine output and base excess. Optimisation of heart failure medication: Low dose ACE inhibition remains the key cardio-stabilising drug in this situation. Careful titration of loop diuretics should be considered but as in our patient these may not always be required initially depending upon fluid balance and on-going fluid shifts. Beta-blockers may be indicated following a period of cardiovascular stability, but these should not be used in patients with undiagnosed causes of tachycardia and inotrope requirements since they can paralyse a vulnerable circulation to therapeutic life-saving manoeuvres.⁷ Attention to nutrition: Under stress cardiac nutritional requirements must be addressed to prevent the onset of further cardiac hibernation and loss of myocyte mass.⁸ Nutritional screening should include B vitamins, iron levels, thyroid function, calcium, and Vitamin D, which are all at risk in the peri-partum woman.⁹
The patient was discharged from hospital eleven days following her upper gastrointestinal bleeding episode and was re-imaged at three months. Echocardiography at that time demonstrated significant improvement in RV and LV dimensions and function.	Medication should be continued for symptomatic reasons but has no known prognostic benefits.
Echocardiography at six months demonstrated normal cardiac structure and function and she was discharged from follow-up on no cardiac medication. Her final diagnosis was stress peri-partum cardiomyopathy. She was advised on discharge that this could recur in future clinical circumstances causing cardiac stress including but not exclusively, pregnancy.	Stress cardiomyopathy can occur in many settings of acute illness and is well described in intensive care, particularly in the context of sepsis.¹⁰ Stress peri-partum CM refers to the effect of additional cardiac stress on a heart already under the high demands of pregnancy. It is therefore a contextual diagnosis. In keeping with other stress cardiomyopathies such as sepsis related cardiomyopathy there are no known genetic associations therefore family screening is not required for this type of cardiomyopathy.¹¹ Prognosis: There are no long-term follow up studies of women with peri-partum stress CM. Extrapolated data from other stress cardiomyopathies such as Takotsubo’s CM suggest that the prognosis may not be benign.¹² Long-term follow-up studies of a cohort of affected women are needed. Women should be counseled appropriately about future cardiac stress since there is an inherent risk of recurrence if similar cardiac stress is re-encountered.

Left ventricular dysfunction secondary to pre-eclampsia

Clinical course	Clinical learning points
A 22-year-old prima gravida lady was admitted at 36 weeks gestation from clinic following the detection of pre-eclampsia. Her mother had also suffered from pre-eclampsia.	Pre-eclampsia is defined as hypertension arising after 20 weeks gestation with one or more organ system involvement.¹³ Generalized vasospasm can result in multi-organ hypo-perfusion. Risk factors include: -Family history -Multi-foetal pregnancy -Diabetes -Pre-existing hypertension -Pre-existing CKD -Previous pre-eclampsia -Lupus or antiphospholipid syndrome -BMI >35 -Age >40 Pre-eclampsia complicates approximately 6% of pregnancies. Acute cardiovascular complications affect 6% of cases of severe pre-eclampsia. Pre-eclampsia complicated by heart failure is significantly more rare affecting 1 in 2000 pregnancies.¹⁴
Over the following 48 hours she developed pulmonary oedema and an urgent echo was requested. This revealed normal left ventricular systolic function, but severe non-valvular mitral regurgitation and high pulmonary artery pressures. This was suggestive of a raised left ventricular end diastolic pressure due to diastolic dysfunction.	Approximately half of patients with severe complicated pre-eclampsia will experience pulmonary oedema: the majority of these occurring post delivery.¹⁵ In the breathless, pregnant patient, early echocardiography can help to distinguish between heart failure due to pre-eclampsia and that due to true PPCM. Increased afterload results in a pattern of left ventricular dysfunction and remodeling similar to that seen in essential hypertension in non-pregnant women. Specifically: -Concentric left ventricular hypertrophy >1 cm¹⁶ -Exaggerated reduction in E/A ratio -Significantly increased E/e’ ratio -Variable effect on systolic function, but often preserved -Other markers of diastolic dysfunction such as abnormal deceleration time, an enlarged left atrium and a pulmonary venous s/d ratio <1 should be sought (Figure 2).¹⁷
Urgent delivery was arranged under neuraxial anaesthesia.	Multi-disciplinary teamwork involving obstetricians, intensivists, anaesthetists and cardiologists is crucial to safe delivery for these women.
A repeat echo the following morning revealed new left ventricular systolic impairment.	Heart failure secondary to pre-eclampsia is commonly mistaken for PPCM. The majority (∼50%) of women with uncomplicated pre-eclampsia present with mild to moderate LV diastolic dysfunction with preserved systolic function. The left ventricle is not dilated. 20% will present with ventricular longitudinal systolic dysfunction and severe LV hypertrophy.¹⁸
She was treated with enalapril and diuretics following which she made a rapid clinical recovery over the subsequent two days.	Acute management includes: 1. Urgent delivery of the foetus is usually required (foetal gestation should be taken into account) 2. Severe hypertension (SBP ≥160 mmHg or DBP ≥110 mmHg for over 15 minutes) should be lowered with IV Labetalol or IV Hydralazine to a SBP of 140–150 mmHg and a DBP of 80–100 mmHg^a 3. IV GTN (5 µg/min) is the antihypertensive of choice if pulmonary oedema is present 4. Furosemide ±morphine should also be considered for pulmonary oedema 5. Fluid restriction and strict fluid balance^19,20 6. Inotropic support should be considered for severe LV systolic dysfunction but afterload increases must be avoided since this worsens longitudinal left ventricular function. 7. Should intubation and mechanical ventilation become necessary, ablation of the response to tracheal intubation is crucial (e.g. with alfentanil or MgSO₄) 8. Magnesium sulphate is the drug of choice for prevention and treatment of eclamptic seizures, but should not be used for lowering blood pressure alone^21,22 9. Ergometrine should be avoided as a uterotonic agent since this can cause sudden surges in blood pressure^1,23 ^aIn most cases anti-hypertensive therapy can be withdrawn 5–7 days after delivery, however some women may require prolonged therapy.
Cardiac MRI eight days after delivery revealed no myocardial oedema. A follow up echo after two weeks revealed full recovery of LV systolic and diastolic function.	Cardiac MRI can be used to exclude peri-partum cardiomyopathy, classically demonstrating left ventricular oedema.
A diagnosis of left ventricular systolic and diastolic dysfunction secondary to pre-eclampsia was therefore made. PPCM was excluded due to the clinical picture, lack of risk factors, cardiac MRI findings and rapid recovery of left ventricular function following treatment. The presence of diastolic dysfunction prior to the development of left ventricular systolic dysfunction was also highly suggestive of pre-eclamptic heart failure.	Pre-eclampsia diagnosis: -New onset hypertension (SBP ≥140 mmHg or DBP ≥90 mmHg) ->20 weeks gestation -≥1 organ system involvement -Complete resolution by 12 weeks post-partum.

Peri-partum cardiomyopathy

Clinical course	Clinical learning points
A 42-year-old lady, pregnant with IVF twins was admitted in premature labour at 34 weeks. The obstetric team gave her nifedipine as a tocolytic. This caused severe hypotension necessitating an emergency caesarean section under general anaesthesia. She was admitted to the intensive care unit post-operatively where she had an echo the same evening. This showed low normal left ventricular systolic function. She remained ventilated overnight and was extubated the following day when a repeat echo showed similar findings. She was discharged from the ICU to a step down ward after 48 hours. The following day she reported feeling unwell and was seen by a cardiologist. She had clinical signs of congestive cardiac failure with hypotension and jugular venous distension.	Peripartum cardiomyopathy is defined as: cardiomyopathy presenting with heart failure secondary to left ventricular dysfunction towards the end of pregnancy (∼last month of pregnancy) or in the months after delivery (∼5 months after), where no other cause of heart failure is found.²⁴ It is rare (between 1:300 and 1:4000 pregnancies). Mortality rates are variable, but can be up to 32%^25,26 The symptoms of severe pre-eclampsia can be very similar, posing diagnostic difficulties. Risk factors for PPCM include: -Family history -Multi-foetal pregnancy -Diabetes -Pre-existing hypertension -Multiparity -Maternal age (advanced or teenage) -Smoking -Malnutrition -Prolonged use of terbutaline for tocolysis -Afro-Caribbean ancestry Most women (71–98%) present in the post-partum period.²⁷
A further echo was performed which showed a non-dilated left ventricle with thickened myocardium and severe systolic dysfunction. Severe mitral regurgitation and very high pulmonary artery pressures suggested a significantly raised LV end-diastolic pressure. A diagnosis of peripartum cardiomyopathy was made from risk factors (age and multiple fetuses) clinical presentation and echo appearances.	There is no single diagnostic test. Other aetiologies of heart failure must be excluded (beware over-diagnosis, most perinatal LV dysfunction is not PPCM). Echo is pivotal to diagnosis: LVEF <45% (chambers often dilated: Figure 3)(cf. pre-eclampsia with preserved systolic function). Left ventricular hypokinesia is often present, making distinction from DCM difficult (temporal relationship to pregnancy is key) Troponin-T is rarely elevated in PPCM.²⁸ Note that the BP can be low, normal or raised.²⁹
The patient was moved to the coronary care unit where she was treated with 1 gram of methylprednisolone and a small dose of enalapril.	Acute management includes: 1. Urgent delivery should be considered if haemodynamically unstable despite treatment. 2. Vasodilators (eg. GTN or Hydralazine) if SBP >100mmHg to reduce afterload. 3. ACE-I post delivery only as they can interfere with kidney development if given in the 2nd trimester (if breast feeding enalapril, captopril or benazepril recommended). 4. Oxygen if hypoxic. 5. IV diuretics such as furosemide if congested. Care should be taken if pre-delivery not to impair placental perfusion (use the minimal dose possible). 6. Inotropic support if signs of hypoperfusion (dobutamine or milrinone). 7. Mechanical cardiac support (IABP/ECMO). 8. Low dose beta-blockade once stable (β₁ selective drug is preferred). 9. Anticoagulation therapy should be considered in those with very low ejection fraction as intracardiac thrombi are common in PPCM.
The following day the patient was symptomatically better with an improved blood pressure. A further echo showed mild-moderate mitral regurgitation, reduced pulmonary artery pressures and severely impaired left ventricular systolic function.	Collaboration between obstetricians, cardiologists, paediatricians and intensivists is essential in the care of women with PPCM.
Cardiac MRI was performed which showed characteristic late sub-epicardial gadolinium enhancement of both the LV and RV. The left ventricle eventually stabilized at 6 months, during which time the patient remained unwell. She has subsequently developed sustained VT for which she has had an implantable defibrillator inserted.	Cardiac MRI can aid diagnosis. Late Gadolinium Enhancement can reveal localized fibrosis and infarction³⁰ It can also help to distinguish between inflammatory and non-inflammatory pathogenesis.³¹ Survivors of PPCM are at risk of recurrence in future pregnancies. Close follow up by a cardiologist is recommended.

Discussion and management

Maternal death is a rare but catastrophic event. Since 2002 cardiac disease has remained the single largest cause of maternal mortality, resulting in 55 deaths per 100, 000 maternities in the triennium from 2014–2016. The mortality rate from cardiac disease has remained largely unchanged despite an overall steady decrease in maternal mortality and is due to be one of the focus areas of the 2019 MBRACE report.

The three most significant causes of de novo left ventricular failure in peripartum women are stress cardiomyopathy, severe pre-eclampsia and autoimmune peri-partum cardiomyopathy in decreasing order of frequency. Autoimmune peri-partum cardiomyopathy accounts for a small number of maternal deaths: 9 out of the 153 deaths attributable to cardiac disease in the six-year period from 2009–2014. It is vital that clinicians understand its rarity, preventing over-diagnosis and potential mismanagement.

When presented with a peripartum women who has the signs and symptoms of acute left ventricular failure the primary focus should be on firstly confirming that the left ventricle has failed, secondly initiating management in a suitable critical care facility and then on locating and confirming the likely cause.

The algorithm shown here in Figure 4 gives a suggested approach based on accurate bedside echocardiography. The majority of hospitals are not equipped with a dedicated obstetric echo service. Some hospitals now have acute echo services bases either in cardiology or intensive care. It is vital that this patient group can access this service within an hour of request, however this is provided at a local level.

Figure 1.

Moderate mitral and tricuspid regurgitation secondary to biventricular failure and subsequent dilatation.

Figure 2.

Pulsed-wave doppler demonstrating pulmonary vein systolic wave peak velocity less than the diastolic wave peak velocity (s/d ratio <1) suggestive of diastolic dysfunction grade II or III.

Figure 3.

Apical-4-chamber view illustrating dilated left ventricle.

Figure 4.

Algorithm for management of unexpected peri-partum left ventricular failure.

The key echocardiographic information can be obtained from a Level I transthoracic study or a FICE level study.^32,33 The purpose of this initial assessment is to confirm left ventricular failure and rule out other causes of cardiovascular shock. In all cases of peri-partum left ventricular failure we would recommend urgent follow-up with a full Level II study orientated towards ensuring there is no unexpected background cardiac structural disease: for example an unexpected ASD, there is no co-existent valvular pathology not directly causes by the left ventricular failure itself, and that a full assessment of fluid responsiveness is undertaken.

Immediate management

General considerations

In all cases the likely cause of left ventricular failure will be suggested by the risk factor profile, timing of onset of left ventricular failure and balance between left ventricular systolic and diastolic failure found on echocardiography. The key features of each are outlined in Table 1. Distinguishing the precise cause is a secondary consideration to establishing therapy aimed at the major pathological findings on echocardiography: the most important of which is the careful assessment of diastolic and systolic failure since this has the greatest impact on selecting the correct therapy.

Table 1.

comparison of presenting features, risk factors, echocardiographical findings and therapy for PPCM, SPPCM and pre-eclampsia associated cardiac dysfunction.

	SCM	Pre-eclampsia	PPCM
History
Timing of presentation	Sudden onset following another significant clinical event (e.g. bleeding, sepsis)	Variable onset. Always >20 weeks gestation. Commonly post-partum	Often post-partum, signs and symptoms develop insidiously often during pregnancy
Hypertension	Absent	Common (and often fulminant)	Absent: usually hypotensive
Extra-cardiac organ involvement	Common due to sudden hypotension related low-flow organ dysfunction	Common: renal and hepatic involvement should be actively sought	Rarely present as a primary feature but low flow state can result in other organ failures
Improvement with delivery	Some	Marked	Some
Primary cardiac mechanism	Underlying normal myocardium responding to acute severe cardiac stress through metabolic and functional hibernation	Raised LVEDP is the hallmark of this condition with preserved systolic function when uncomplicated, failure to identify and treat could result in systolic LV failure	DCM due to T-cell infiltration and myofibrosis, can progress to restrictive physiology
RV involvement	Often	Very rare	Often
Risk factors
FHx		✔	✔
Multi-foetal pregnancy	✔	✔	✔
Diabetes		✔	✔
Pre-existing HTN		✔	✔
Advanced maternal age		✔	✔
Malnutrition	✔		✔
Multiparity			✔
Smoking			✔
Prolonged terbutaline			✔
Afro-Caribbean			✔
Anaemia	✔
Hyperthyroidism	✔
CKD		✔
Lupus or APL		✔
BMI >35		✔
Echo findings (6: Dennis & Castro)
LV volume	Variable	Normal	Commonly dilated
LVH	Absent	Present	Absent
LV systolic function	Impaired	Preserved (relatively)	Significantly impaired
LV diastolic function	Variable: depends on filling pressures and other management	Always impaired	Normal but can progress to restriction
RV volume/function	Variable: depends on response to stress	Normal	Dilated (less common). Can be impaired
Pericardial effusions	Variable	Common and larger	Uncommon and small
Therapy
Diuretics	±	±	+
Antihypertensives		+
IV GTN		+(If pulmonary oedema present)	+(If SBP > 100 mmHg)
Inotropes	+	±	+
Anticoagulation			+
IV Fluid	Very cautiously	Very cautiously	Very cautiously

Fluid balance

It is vital to remember that intravascular volume may be low in patients with left ventricular failure and as we saw in our stress cardiomyopathy clinical vignette, augmenting intravascular volume by small degrees may be crucial to the management of these patients. This should be done only after echocardiographic assessment of fluid responsiveness and in a critical care setting. Aliquots of 250mls of fluid will provide an immediately assessable response.

Echocardiography can be used to identify frank hypovolaemia by looking at the left ventricle and the IVC. Papillary muscle apposition, a left ventricular internal dimension in diastole (LVIDd) <2.2 cm/BSA and a left ventricular end diastolic area (LVEDA) <5.5 cm²/BSA are all indicative of hypovolaemia as is an IVC diameter <1.5 cm with collapse during respiration.³⁴ Echocardiography can also be used to predict the response to a fluid bolus by looking at the variation of both left ventricular outflow tract (LVOT) velocity time integral (VTi) and IVC diameter with the ventilatory cycle. Alternatively in a spontaneously breathing patient, LVOT VTi increment with a passive leg raise can also be used to assess fluid responsiveness.

In some cases where there is no evidence of fluid responsiveness intravenous loop diuretics may be appropriate, especially in the presence of pulmonary oedema. Their vasodilatory effect will reduce preload and their diuretic effect will reduce total body water. Judicious dosing is required to take into account the large fluid shifts around the time of delivery.

Using data generated from echocardiography, the Nagueh equation (1.24 × (E/e*) + 1.9)³⁵ can be used to generate an estimate of mean pulmonary capillary wedge pressure. This becomes particularly useful when considering the effect that fluid administration or removal might have on extravascular lung water in the context of predominantly diastolic heart failure, such as that seen in pre-eclampsia associated cardiomyopathy.

Vasoactive drugs

The guiding principle for the use of vasoactive drugs in the setting of a failing ventricle is that they will universally increase the workload of the ventricle and this should be the primary consideration in their use.

There will also be circumstances when a vasopressor such as Noradrenaline has to be used, for example when SCM is precipitated by sepsis or to offset the effect of sedative infusions. In these situations, repeated assessment of left ventricular function using echocardiography can be utilised to ensure that adequate cardiac output is being maintained. Maintenance of cardiac output and therefore flow as measured by the trans aortic velocity time integral is a more important but co-existent consideration to absolute measured systolic pressure.

As a general rule, reducing the afterload on the LV using vasodilatory drugs is beneficial in an effort to reduce its workload. To this end, both enteral and intravenous vasodilators such as ACE inhibitors and GTN can be used to good effect. However, this should always be done cautiously as dropping systemic blood pressure precipitously can result in a reduction in coronary perfusion pressure and thus impaired myocardial oxygen delivery.

Inotropic therapy

On occasion left ventricular function may be so severely impaired that reduction in afterload alone is not enough to compensate. When there are systemic signs of hypo-perfusion: for example, poor peripheral capillary refill, oligo-anuria, rising lactate and an echo has confirmed adequate filling with a significantly reduced cardiac output, it may be appropriate to utilize an inotrope such as Dobutamine or Enoximone. Again caution should be used and hypotension secondary to systemic vasodilation anticipated and managed cautiously. Repeated echo assessment of cardiac output and contractility can again be used to titrate the infusion rate, which should be maintained at the minimum required dose to achieve adequate cardiac output appreciating that this will come at the expense of increased demand on the failing ventricle.

Global consideration for optimum cardiac working conditions should also be given including haemoglobin level, vitamin deficiencies in particular the B complex and vitamin D, micronutrients such as selenium and electrolyte provision.

Follow on therapy and management

Once the immediate situation has been stabilized through repeated diagnostic echocardiography and provision of adequate cardiovascular support including invasive ventilation where required, longer-term therapy should be initiated. This may include ACE inhibition, rate control and other drugs aimed at managing left ventricular impairment in the medium to long term. If PPCM is thought to be the likely cause consideration can be given to steroid therapy at 24 hours from presentation.³⁶ This should be guided by a consultant cardiologist who can also monitor and counsel the patient following further appropriate tests in the out patient setting. Differentiation between the causes of left ventricular failure is vital at this juncture to prevent further episodes of left ventricular failure for example due to PPCM which can recur with subsequent pregnancies.

Conclusions

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Ben Greatorex

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