A 29-year-old primiparous woman, with no significant medical history, presented to our institution with an antepartum hemorrhage and underwent an uncomplicated cesarean delivery, with minimal blood loss, under spinal anesthesia at 35 weeks’ gestation.
She was hemodynamically stable until 6 hours after delivery when she became hypotensive, tachycardic, and febrile. Despite fluid resuscitation, a hemoglobin level of 122 g/dL, vasopressors, and broad-spectrum IV antibiotics, she remained hypotensive and there was diagnostic uncertainty as to the cause of her hypotension.
The anesthesiologist trained in transthoracic echocardiography (TTE) performed the Rapid Obstetric Screening Echocardiography (or ROSE) scan.1 Qualitative assessment of cardiac function obtained from the parasternal short-axis view at the midpapillary level demonstrated a well-filled left ventricle with significant depression of contractility (estimated ejection fraction of <10%). A diagnosis of hypotension due to systolic cardiac failure was made. M-mode and pulse wave Doppler imaging supported this diagnosis. Parasternal long-axis M-mode at the tips of the mitral valve demonstrated significantly reduced fractional shortening of 7.8% with an end-diastolic diameter of 5.1 cm making concurrent hypovolemia unlikely (Video 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A464; Video 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A465; and Video 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A466). Some areas of vigorous contraction were seen in the basal inferolateral and basal anteroseptal segments; however, overall myocardial contractility was significantly reduced. A reduced cardiac output of 2.6 L·min−1 was calculated using the product of the left ventricular outflow tract velocity time integral, the cross-sectional area of the left ventricular outflow tract, and the heart rate (Fig. 1). Consideration was given to right ventricular outflow tract obstruction with a thrombus causing right ventricular failure; however, no thrombus was identified in the right ventricle or pulmonary arteries, right ventricular size was not larger than the left, and there was no bulging of the interventricular septum into the left ventricle consistent with a large pulmonary embolism. The absence of chest pain, electrocardiographic changes, or gross regional wall motion abnormalities made coronary artery disease or Takotsubo cardiomyopathy unlikely.
The TTE finding of cardiomyopathy, in the absence of cardiac thrombus, hypovolemia, or myocardial ischemia, enabled immediate change of management from fluid resuscitation to inotropic support, diuresis and angiotensin-converting enzyme inhibitor therapy in the intensive care unit. She was systemically anticoagulated despite her recent cesarean delivery because of poor left ventricular function. Severe myocardial depression due to sepsis was considered a possible underlying cause; however, immediate improvement in hemodynamics with inotropic support and negative blood, urine, and respiratory cultures made that diagnosis unlikely. After hospital discharge, she had recovered to New York Heart Association Class II on medical therapy with the diagnosis of peripartum cardiomyopathy. Written consent was obtained from the women described in this Echo Rounds.
Postpartum hypotension is a relatively common clinical event that is caused by a number of serious obstetric diseases and hemodynamic mechanisms (Table 1). The expected cardiovascular changes of pregnancy and the postpartum period (increased heart rate, increased cardiac output, and vasodilation) and the variable ability of a woman to compensate for hemodynamic changes, may lead to diagnostic uncertainty in the postpartum period. In this case, the single image of the parasternal short axis at the level of the midpapillary muscle enabled immediate identification of systolic heart failure. The cause of her heart failure was later found to be peripartum cardiomyopathy, which is a rare complication of pregnancy characterized by the development of new onset heart failure in the last month of pregnancy or the first 5 months postpartum, when no other cause for the heart failure is found.2
Cardiac disease is now the leading cause of maternal mortality in developed countries necessitating early recognition of heart failure.3 Other causes for systolic heart failure in pregnant or recently pregnant women include hereditary cardiomyopathies, congenital heart disease, ischemic heart disease, and Takotsubo cardiomyopathy. In light of the mortality related to cardiac disease in pregnancy, TTE is emerging as a useful technology in the field of obstetric anesthesiology. It provides noninvasive, validated, and precise hemodynamic data1,4–6 and is recommended as a first-line investigation in the diagnosis and management of severe chest pain, breathlessness, and acute pulmonary edema in pregnant women.3 TTE is also recommended for the evaluation of unexplained hypotension, suspected heart failure, or suspected cardiomyopathy.4 Although transesophageal echocardiography is still the major modality used by anesthesiologists in other clinical settings, in pregnant women, anterior and left displacement of the heart and an elevated diaphragm may actually facilitate TTE examination. In emergency situations in conscious females, TTE avoids the risks of sedation and transesophageal echocardiography probe insertion.
In contrast to the examination in the nonpregnant adult, pregnancy necessitates some modifications in positioning and technique. Most important is the requirement to avoid aortocaval compression by providing left lateral tilt throughout the examination. Thus, in the antenatal period, supine positioning for subcostal views is not recommended. Despite larger breasts, the parasternal acoustic window is easy to obtain at the left sternal edge between the breasts. The apical window is obtained by lifting the left breast and placing the probe on the chest wall beneath the breast. The suprasternal window may be associated with discomfort because of compression of the thyroid gland, which may be enlarged in pregnancy. The examination sequence and key findings for the scanning technique are shown in Table 2.
When interpreting TTE findings in pregnant women, small (<0.5 cm) pericardial effusions, mild mitral and tricuspid regurgitation, and moderately increased left ventricular mass are normal findings. Gestational effects on the cardiovascular system should also be considered. Systolic function may decrease at term evidenced by a reduction in cardiac output at times to prepregnancy values (4.4 L·min−1) and diastolic function may be altered with elevation of mitral valve E/septal e′ to >8 in some women.5
TTE can be a useful noninvasive bedside test to determine the cause of hypotension in the antenatal and early postpartum periods. Given the ease of obtaining the parasternal short-axis view in pregnancy, and the ability to rapidly differentiate gross systolic failure from other causes of hypotension, obstetric anesthesiologists should be encouraged to obtain basic entry level education in TTE to identify peripartum cardiac failure.7
Name: Alicia Dennis, PhD, MBBS, PGDipEcho, FANZCA.
Contribution: This author helped acquire the image and prepare the manuscript.
Name: Amber Stenson, MBBS(Hons), FANZCA.
Contribution: This author helped prepare the manuscript.
This manuscript was handled by: Martin J. London, MD.
1. Dennis AT. Transthoracic echocardiography in obstetric anaesthesia and obstetric critical illness. Int J Obstet Anesth. 2011;20:160–8
2. Elkayam U. Clinical characteristics of peripartum cardiomyopathy in the United States: diagnosis, prognosis, and management. J Am Coll Cardiol. 2011;58:659–70
3. Cantwell R, Clutton-Brock T, Cooper G, Dawson A, Drife J, Garrod D, Harper A, Hulbert D, Lucas S, McClure J, Millward-Sadler H, Neilson J, Nelson-Piercy C, Norman J, O’Herlihy C, Oates M, Shakespeare J, de Swiet M, Williamson C, Beale V, Knight M, Lennox C, Miller A, Parmer D, Rogers J, Springett ASaving mothers’ lives: reviewing maternal deaths to make motherhood safer: 2006-2008.. The Eighth Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom. BJOG. 2011;118:1–203
4. Douglas PS, Garcia MJ, Haines DE, Lai W, Manning W, Patel A, Picard M, Polk D, Ragosta M, Parker Ward R, Weiner R. 2011 appropriate use criteria for echocardiography. J Am Soc Echocardiogr. 2011;24:229–67
5. Dennis AT, Castro J, Simmons SW, Carr C, Permezel M, Royse CF. Haemodynamics in women with untreated pre-eclampsia. Anaesthesia. 2012;67:1105–18
6. Faris JG, Veltman MG, Royse CF. Limited transthoracic echocardiography assessment in anaesthesia and critical care. Best Pract Res Clin Anaesthesiol. 2009;23:285–98
7. Price S, Via G, Sloth E, Guarracino F, Breitkreutz R, Catena E, Talmor D. Echocardiography practice, training and accreditation in the intensive care: document for the World Interactive Network Focused on Critical Ultrasound (WINFOCUS). Cardiovasc Ultrasound. 2008;6(49):1–35
Clinician’s Key Teaching Points
By Nikolaos J. Skubas, MD, Kent H. Rehfeldt, MD, and Martin J. London, MD
- Peripartum cardiac disease is a leading cause of maternal mortality. Clinical manifestations may be diagnosed by a properly trained anesthesiologist using transthoracic echocardiography (TTE).
- Imaging is generally performed in the left lateral position. The parasternal view is acquired with the TTE probe to the left of the sternal edge between the breasts and the apical view by placing the probe underneath the left breast. Suprasternal imaging may be associated with discomfort because of compression of an enlarged thyroid gland and subcostal imaging complicated by the need to avoid the supine position.
- In this case, postpartum hypotension unresponsive to fluid and antibiotic therapy prompted bedside TTE imaging. This excluded hypovolemia, tamponade, and pulmonary embolism. Instead, the presence of severely decreased global left ventricular systolic function led to a diagnosis of peripartum cardiomyopathy and prompted a change in medical treatment.
- A focused, bedside TTE examination can be useful in establishing the cause of peripartum cardiovascular emergencies. Normal pregnancy-associated cardiovascular alterations, such as small pericardial effusions, mild tricuspid and mitral regurgitation, and mildly reduced systolic and diastolic function, should be differentiated from acute, more severe cardiovascular disease.