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26.2 For the patient in Question 26.1, what is the most likely cause of the delayed
postpartum bleeding?
A. Retained tissue with reduced uterine tone
B. Cervical laceration
C. Unrepaired vaginal laceration
D. Coagulopathy
26.3 A 29-year-old first-time mother comes into your office for her routine 6-week
postpartum visit. Her husband, who accompanied her to the visit, reports
that his wife is tearful much of the time. She has not been sleeping well, has
little energy, and has a reduced appetite. She denies any suicidal thoughts,
hallucinations, or feelings that she wants to harm her baby. Which of the following is the most appropriate intervention?
A. Reassurance that these feelings will pass within a week or so
B. Referral to a psychiatrist for outpatient management
C. Institution of SSRI therapy and close follow-up
D. Admission to the hospital and urgent psychiatric consultation
26.4 You see a 30-year-old woman for an acute visit 16 days’ postpartum. She
has been breastfeeding her baby daughter but has developed a very sore left
breast. On examination, the patient has a temperature of 101.3 °F (38.5 °C).
The left breast is diffusely tender, primarily in the upper inner quadrant. The
skin overlying the area of maximal tenderness is erythematous and warm.
There is no nipple discharge, and the remainder of the examination is normal.
Which of the following is the best treatment?
A. This condition is self-limited, but she should stop nursing the baby on
the left breast until this condition resolves.
B. She may nurse from the unaffected breast but should simply pump and
discard the milk from the painful breast.
C. The patient should receive oral dicloxacillin or clindamycin.
D. She should have a fine-needle aspiration.
ANSWERS
26.1 C. This patient is symptomatically hypovolemic, with dizziness, hypotension, and tachycardia. As with any resuscitation, supporting the circulatory
process is extremely important. With hemorrhagic shock, fluid resuscitation with intravenous isotonic solution must be your first intervention.
Once you have started the management of this critical issue, you should
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turn your attention to identifying and correcting the source of the bleeding
and transfuse red blood cells or, if needed, massive transfusion (red cells,
fresh frozen plasma, and possibly platelets). Answer A (oxytocin added to
intravenous fluids of hypotonic saline) will not fill the intravascular space
as effectively since it is hypotonic. Answer B (bimanual massage) may be
needed if the etiology is uterine atony. Certainly, if uterine atony is noted
to be found, then uterotonic agents (answer D) and bimanual massage are
critical to reduce ongoing hemorrhage.
26.2 A. While any of the listed options (answer B, cervical laceration; answer C,
unrepaired vaginal laceration; and answer D, coagulopathy) could result in
this scenario, the most common cause for a delayed postpartum hemorrhage
is retained tissue. This interferes with proper contraction of the uterus and
leads to delayed uterine atony and increased bleeding.
26.3 C. This patient has a classic presentation of postpartum depression, and
the best plan would be to start an antidepressant (an SSRI being the most
common choice). The symptoms are identical to those of a major depressive episode. The maternity blues is a self-limited condition that starts
in the first postpartum week and resolves in the second. Fortunately,
this patient does not have signs of postpartum psychosis (mania, hallucinations, and delusions), which would require admission to the hospital (answer D). Appropriate management includes the use of an SSRI,
counseling, and close follow-up. Answer A (reassurance and follow-up)
is appropriate for postpartum blues or mild symptoms, but this patient
requires therapy. Answer B (referral to a psychiatrist) is not appropriate
since this patient has a straightforward postpartum depressive disorder
without psychosis.
26.4 C. Mastitis is a common complication of breastfeeding. It is caused by gland
obstruction, and sometimes, as in this case, there also are signs of infection.
Treatment is directed at relieving the obstruction, so increased breastfeeding
or pumping is helpful. The antibiotics typically used for this complication
are considered safe to use while nursing. Empiric staphylococcal coverage
is recommended. Dicloxacillin and cephalexin are appropriate for areas
with low rates of methicillin-resistant Staphylococcus aureus (MRSA). Good
choices are clindamycin or sulfamethoxazole-trimethoprim for areas with
high rates of MRSA. Answer A (reassurance, stop breastfeeding, and observation) would be indicated with breast engorgement but not mastitis, where
antibiotic therapy is needed. With mastitis, breastfeeding does not need to
be discontinued (answer B). Answer D (fine-needle aspiration) is indicated
to biopsy a breast mass or cyst and is not indicated in this case.
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CLINICAL PEARLS
» Many of the important postpartum issues—mood problems, contracep-
tion, and breastfeeding—are best managed by addressing them in the
prenatal course first and then readdressing or reinforcing them in the
postpartum period.
» Most causes of postpartum hemorrhage can be remembered with the
four Ts: tone, trauma, tissue, and thrombin.
» Uterine atony causes approximately 70% of postpartum hemorrhage.
Initial management includes initiating bimanual uterine compression
and massage and administration of oxytocin, which may be given intravenously or intramuscularly.
» Baby blues develops within the first week after delivery and typically
resolves by the 10th postpartum day.
» Postpartum fever, especially if associated with uterine tenderness and
foul-smelling lochia, is often a sign of endometritis.
» In breastfeeding women, progestin-only pills are preferred because com-
bination OCPs might reduce lactation.
REFERENCES
Blenning CE, Paladine H. An approach to the postpartum office visit. Am Fam Physician. 2005;
72(12):2491-2496.
Conti TD, Patel M, Bhat S., et al. Breastfeeding & infant nutrition. In: South-Paul JE, Matheny SC,
Lewis EL, eds. CURRENT Diagnosis & Treatment: Family Medicine. 4th ed. New York, NY:
McGraw Hill; 2015: Chap. 4. http://accessmedicine.mhmedical.com/content.aspx?bookid=1415&
Sectionid=77054127. Accessed February 10, 2019.
Evensen A, Anderson JM, Fontaine P. Postpartum hemorrhage: prevention and treatment. Am Fam
Physician. 2017;95(7):442-449.
Obstetrical hemorrhage. In: Cunningham F, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM,
Spong CY, eds. Williams Obstetrics. 25th ed. New York, NY: McGraw Hill; 2018: Chap. 41. http://
accessmedicine.mhmedical.com/content.aspx?bookid=1918§ionid=185083809. Accessed May 6,
2019.
Puerperal complications. In: Cunningham F, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM,
Spong CY. eds. Williams Obstetrics 25th ed. New York, NY: McGraw Hill; 2018: Chap. 37. http://
accessmedicine.mhmedical.com/content.aspx?bookid=1918§ionid=141464707. Accessed May 6,
2019.
The puerperium. In: Cunningham F, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM,
Spong CY, eds. Williams Obstetrics. 25th ed. New York, NY: McGraw Hill; 2018: Chap. 36. http://
accessmedicine.mhmedical.com/content.aspx?bookid=1918§ionid=138823398. Accessed May 6,
2019.
CASE 27
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A 66-year-old woman presents to your office complaining of shortness of
breath and bilateral leg edema that have been worsening for 3 months. She
emphatically tells you, “I get out of breath when I do housework, and I can’t even
walk to the corner.” She has also noticed difficulty sleeping secondary to a dry
cough that wakes her up at night and further exacerbation of her shortness of
breath while lying flat. This has forced her to use three pillows for a good night’s
sleep. She denies any chest pain, wheezing, or febrile illness. She has no past
illnesses and takes no medications. She has never smoked and drinks socially. On
examination, her blood pressure (BP) is 187/90 mm Hg, her pulse is 97 beats/min,
her respiratory rate is 16 breaths/min, her temperature is 98 °F (36.6 °C), and her
oxygen saturation is 93% on room air by pulse oximetry. She has a pronounced
jugular vein. Cardiac examination reveals a pansystolic murmur. Examination of
her lung bases reveals dullness bilaterally. You find 2+ pitting edema of both
ankles. An electrocardiogram (ECG) shows a normal sinus rhythm, and a chest
x-ray demonstrates mild cardiomegaly with bilateral pleural effusions. You decide
she needs further workup, so you call the hospital where you have admitting
privileges and arrange for a telemetry bed.
▶ What is the most likely diagnosis?
▶ What is the next diagnostic step?
▶ What is the initial step in therapy?
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ANSWERS TO CASE 27:
Heart Failure
Summary: A 66-year-old woman presents with
Worsening shortness of breath, bilateral leg edema, and three-pillow orthopnea
No known hypertension, but a current BP of 187/90 mm Hg and O
on room air
Jugular venous distension (JVD), a cardiac murmur, and decreased breath sounds at
both lung bases
Bilateral pleural effusions on chest x-ray
Most likely diagnosis: New-onset heart failure (HF).
Next diagnostic step: ECG; blood work including cardiac enzymes, complete blood
count (CBC), electrolytes, liver function tests, thyroid function test, lipid profile,
B-type natriuretic protein (BNP), and renal function; echocardiogram.
Initial therapy: Telemetry monitoring, intravenous diuretics, and oxygen.
ANALYSIS
Objectives
1. State the common symptoms and clinical signs of HF. (EPA 1, 2, 3)
saturation 93%
2
2. Describe the pathophysiology of common types of HF. (EPA 12)
3. State the mechanism of action and rationale of the drugs used in the treatment
of acute and chronic HF. (EPA 4)
4. Be familiar with the outpatient management of HF and the importance of
patient education and care management. (EPA 4)
Considerations
This 66-year-old woman presented with HF. Her most immediate problem is oxygenation and volume overload on her weakened heart. The first priority is optimiz-
ing oxygen exchange by administering oxygen via nasal cannula, dilating pulmonary
vasculature, and decreasing cardiac preload and afterload. The most common
causes of HF are coronary artery disease (CAD) and hypertension, so it is imperative to evaluate these patients for CAD. The overload of fluid in the lungs is a
common cause of anxiety and distress in patients with acute HF because of the
continuous struggle to oxygenate adequately. This anxiety activates sympathetic
pathways and mounts catecholamine-induced responses, causing tachycardia and
increased peripheral vascular resistance, leading to greater stress on the heart and
worsening of symptoms. These triggers can be reduced by the use of an agent such
as morphine sulfate, which acts as both an anxiolytic and a vasodilator. Furosemide (Lasix) is the diuretic of choice, not only for its diuretic effect but also for its
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immediate vasodilatory action on bronchial vasculature. Admitting these patients
to the hospital allows for closer management of their fluid balances and evaluation
of any underlying condition that may have precipitated the HF. Other medications,
including angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor
blockers (ARBs), and beta-blockers help to control HF symptoms by decreasing
preload, afterload, and cardiac remodeling.
APPROACH TO:
Heart Failure
DEFINITIONS
FRAMINGHAM HEART STUDY: Large, prospective cohort study of the epidemiologic factors associated with cardiovascular diseases.
HEART FAILURE: Impairment of the ventricle’s ability to fill with or eject blood,
which results in inadequate circulation of blood to meet metabolic needs. Some
expert organizations define specific left ventricular ejection fraction thresholds.
CLINICAL APPROACH
Epidemiology
Heart failure is the most common cause of hospitalization and readmission in patients
older than 65 years. Poorer prognosis is seen in patients who are male, older, or have
more severe symptoms, CAD and acute coronary syndrome, hypotension, impaired
renal function, hyponatremia, and elevated plasma BNP. Sudden cardiac death,
often from a ventricular arrhythmia, may account for up to 30% of all deaths.
Pathophysiology
Heart failure can be subdivided into reduced or preserved ejection fraction and
right- or left-sided HF, all of which can coexist. Heart failure with reduced ejection
fraction (HFrEF) exists when there is a dilated ventricle with impaired contractility and, possibly, concomitant valvular disease. Heart failure with preserved ejection
fraction (HFpEF) occurs with normal or intact left ventricular ejection fraction but
impaired ventricular relaxation and filling, frequently with left ventricular hypertrophy and stiffness due to systemic hypertension or valvular disease.
Left HF is a syndrome primarily characterized by pulmonary congestion or
edema. Right HF is characterized by right ventricular (RV) systolic dysfunction
accompanied by RV dilation and tricuspid regurgitation, which cause tissue congestion, including peripheral edema, ascites, and abdominal organ engorgement.
The most common cause of right HF is left HF.
Etiologies. The most common cause of HF in the developed world is CAD. Other
common causes are diabetes, uncontrolled hypertension, and valvular heart disease
(see Table 27–1). In the developed world, senile degeneration of the aortic valve is
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Table 27–1 • ETIOLOGIES OF HEART FAILURE
Heart Failure With Reduced Ejection Fraction (≤ 40%)
Coronary artery disease Nonischemic dilated cardiomyopathy
Myocardial infarction
Myocardial ischemia
Chronic pressure overload Toxic/drug-induced damage
Hypertension
Obstructive valvular disease
Chronic volume overload Chagas disease
Regurgitant valvular disease Disorders of rate and rhythm
Intracardiac (left-to-right) shunting Chronic bradyarrhythmias
Extracardiac shunting Chronic tachyarrhythmias
Heart Failure With Preserved Ejection Fraction (≥ 50%)
Pathologic hypertrophy Restrictive cardiomyopathy
Primary (hypertrophic cardiomyopathies) Infiltrative disorders (amyloidosis, sarcoidosis)
Secondary (hypertension) Storage diseases (hemochromatosis)
Aging Fibrosis
Endomyocardial disorders
Pulmonary Heart Disease
Cor pulmonale
Pulmonary vascular disorders
High-Output States
Metabolic disorders Excessive blood flow requirements
Thyrotoxicosis Systemic arteriovenous shunting
Nutritional disorders (beriberi) Chronic anemia
a
Indicates disease process that can lead to HFpEF as well.
Reproduced with permission, from Longo DL, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine. 18th ed.
2012. http://accessmedicine.mhmedical.com. Copyright © McGraw Hill LLC. All rights reserved.
a
a
a
a
Familial/genetic disorders
Infiltrative disorders
Metabolic disorder
Viral etiologies
a
a
the most common valvular cause of HF; in the developing world, rheumatic valvular disease is more common. Other contributors to HF include smoking, obesity,
lower socioeconomic status, and sedentary life style.
Evaluation. Patients presenting with symptoms suggestive of HF should be evaluated with a history, physical examination, and focused testing. Diagnosis of HF is
clinical, and there is no single test that can determine its presence or absence. Testing should be designed to confirm HF (or lead to an alternate diagnosis), identify
a cause, and assess the severity of the disease. Initial blood tests should generally
include a CBC, serum electrolytes, magnesium, calcium, renal function tests, urinalysis, hepatic function tests, lipid panel, thyroid-stimulating hormone, cardiac
enzymes, and BNP. Other initial tests should include radiographic studies, electrocardiography, and echocardiography.
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Clinical Presentation
Presentation of Right-Sided Heart Failure. The symptoms and signs that occur are
characteristic of the alterations to the normal physiologic function of the heart.
Signs and symptoms of right-sided HF stem from increased pressure in the systemic veins, causing hepatic congestion, venous engorgement, and visceral edema.
Symptoms include nausea, vomiting, abdominal distension or bloating, diminished appetite, early satiety, and abdominal pain, particularly in the right upper
quadrant (due to hepatic congestion and stretching of the liver capsule). Signs of
right-sided HF are jugular venous distension, peripheral edema, hepatomegaly,
right upper quadrant tenderness, hepatojugular reflux, abdominal ascites, and
jaundice.
Presentation of Left-Sided Heart Failure. Left-sided HF manifests with elevated
pressure in the pulmonary veins, resulting in symptoms of dyspnea on exertion,
paroxysmal nocturnal dyspnea, orthopnea, wheezing, tachypnea, and cough. The
signs of pulmonary congestion are bilateral pulmonary rales, S3 gallop rhythm,
Cheyne-Stokes respirations (which are associated with low cardiac output), pleural
effusion, and pulmonary edema. Pulmonary edema is often the first manifestation of
HF, but it can also be caused by a variety of noncardiac conditions.
Presentation of Both Right- and Left-Sided Heart Failure. Dyspnea on exertion
is the most sensitive symptom for the diagnosis of HF, but its specificity is much
lower. Orthopnea and paroxysmal nocturnal dyspnea are more specific for HF,
but they are not as sensitive. Symptoms seen in both right- and left-sided HF
include weakness, fatigue, nocturia due to increased cardiac preload and decreased
renal vasoconstriction in the recumbent position, memory impairment, insomnia,
decreased exercise tolerance, headache, stupor, coma, paroxysmal nocturnal dyspnea, and declining functional status. Signs found in both left- and right-sided HF
are tachycardia, displaced point of maximal impulse, systolic murmur (mitral or
tricuspid), third heart sound (S3, ventricular filling gallop) associated with volume
overload, fourth heart sound (S4, atrial gallop) associated with diastolic dysfunction, pulsus alternans, diminished pulse pressure, cyanosis, oliguria, dependent
peripheral edema, and cardiac cachexia.
Complete Blood Count. A high white blood cell count can help to identify
the presence of an underlying infection, which is a common triggering event
of HF. Anemia is another common trigger of HF. In an anemic patient, the
oxygen-carrying ability of the blood is reduced, and cardiac output must increase
to compensate for this. If the anemia is mild or if the heart is normal, this compensation may occur without producing symptoms; if the anemia is severe or if there
is underlying cardiac abnormality (from previous ischemia, hypertension, valvular
abnormality, etc), HF may occur. Diabetes and hypo- or hyperthyroidism can also
precipitate HF.
Electrolyte Values. Electrolyte abnormalities are common in the presence of HF.
Neurohumoral responses to a failing heart result in water and sodium retention
and potassium excretion. Hyponatremia is a poor prognostic indicator, signifying activation of the renin-aldosterone-angiotensin system. Medications used by
patients with chronic heart disease (diuretics, ACEIs, ARBs, and aldosterone antagonists) also can lead to electrolyte abnormalities. Some electrolyte abnormalities,
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specifically hypo- or hyperkalemia, hypomagnesemia, and hypocalcemia, can lead to
arrhythmias, which could incite HF or cause significant morbidity in HF patients.
Increased venous pressure can lead to passive congestion of the liver, resulting in
elevated serum transaminases. Severe HF can lead to jaundice as a consequence of
impaired hepatic function caused by congestion.
Cardiac Enzymes. Measurement of cardiac enzymes is necessary to evaluate for
the presence of acute myocardial infarction as the inciting event. Elevated cardiac
enzymes that do not reach levels consistent with acute myocardial infarction are
seen in about half of patients with systolic HF and indicate elevated left ventricular
filling pressure due to volume overload.
B-Type Natriuretic Peptide Values. One of the neurohumoral responses to the
presence of a failing ventricle is release of BNP. BNP and its prohormone (proBNP) can be used to assist in the diagnosis of HF as a cause of acute dyspnea.
Elevated levels of BNP and pro-BNP are sensitive and specific markers for the
diagnosis of HF. However, BNP is not recommended as a screening test or as a
method of monitoring progression of HF, as the level can be increased by advancing
age, renal failure, cardiac ischemia, and pulmonary embolism and can be decreased
by acute pulmonary edema, acute mitral regurgitation, and mitral stenosis.
Electrocardiographic Findings. Electrocardiographic findings in HF are variable
but can help determine the cause of HF. An ECG is useful to evaluate for evidence of acute ischemia or arrhythmia as a cause of the HF and can also reveal
the presence of ventricular hypertrophy, often seen in chronic hypertension. Left
bundle branch block seen in the setting of HF indicates higher 1-year all-cause
mortality.
Chest X-ray. Chest x-ray can help to evaluate for other causes of dyspnea, such
as pneumonia, chronic obstructive pulmonary disease, pneumothorax, or lung cancer. A chest x-ray showing cardiomegaly, pulmonary venous congestion, pulmonary
edema, or pleural effusion increases the likelihood of HF in a dyspneic patient.
A cardiothoracic ratio greater than 50% indicates systolic dysfunction. One of the
earliest chest x-ray findings in HF is cephalization of the pulmonary vasculature
(upper lobe pulmonary vein dilation with lower lobe pulmonary vein constriction),
which indicates increased preload. As the failure progresses, interstitial pulmonary
edema can be seen as perihilar infiltrates, often in a butterfly pattern. Kerley lines,
which are spindle-shaped linear opacities in the periphery of the lung bases, appear
in later HF as well. Pleural effusions can also be found. Effusions are usually bilateral, but if they are unilateral, they are more often seen on the right hemithorax
than the left.
Echocardiography. Echocardiography is the gold standard diagnostic modality in
the presence of HF. It can evaluate left ventricular ejection fraction, ventricle size,
wall thickness, ventricular filling pressures, valve function, wall motion abnormalities due to ischemic heart disease, and cardiomyopathy. It can also find pericardial effusion, pericardial constriction, or tamponade. Echocardiography is useful
in identifying valvular stenosis or regurgitation, either of which can lead to HF.
These findings aid in the determination of whether the HF has a preserved ejection fraction or reduced ejection fraction, critical distinctions when deciding the
appropriate treatment.
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Table 27–2 • CLASSIFICATION OF SEVERITY OF CONGESTIVE
HEART FAILURE
American
Heart
Association
A I None with normal activities;
B II Mild symptoms and slight
C III Marked limitation in activity
D IV Severe limitations; experiences
New York
Heart
Association Objective Assessment Patient Symptoms
No limitation of physical
no objective evidence of
cardiovascular disease
limitation during ordinary
activity; comfortable at rest;
objective evidence of minimal
cardiovascular disease
due to symptoms, even
during less-than-ordinary
activity; comfortable only at
rest; objective evidence of
moderately severe cardiovascular disease
symptoms even while at rest;
objective evidence of severe
cardiovascular disease
activity; ordinary physical
activity does not cause undue
fatigue, palpitation, dyspnea
(shortness of breath)
Slight limitation of physical
activity; comfortable at rest;
ordinary physical activity
results in fatigue, palpitation,
dyspnea
Marked limitation of physical
activity; comfortable at rest;
less than ordinary activity
causes fatigue, palpitation, or
dyspnea
Symptoms of heart failure
at rest
Treatment Principles
Classification of Heart Failure. Heart failure severity is characterized by the symptoms a patient has and the degree that the symptoms limit a patient’s lifestyle.
There are several classification systems in use; two of the most widely used are
the New York Heart Association (NYHA) and the American Heart Association
(AHA) classifications. Table 27–2 summarizes these systems. The classification of
HF is important in determining the appropriate treatment and prognosis for the
patient.
Prevention. Prevention is the most important part of managing HF. The AHA
classification system helps clinicians identify patients at risk so that preventive
strategies may be implemented early. Aggressive control of hypertension has been
shown to reduce incidence of HF by up to 50%. Treating patients who have CAD or
who have had a myocardial infarction with ACEIs, ARBs, beta-blockers, and aldosterone antagonists reduces the risk of progression to symptomatic HF. Treating
dyslipidemia with statin therapy can also reduce incidence of HF by 20%.
Controlling other risk factors, such as diabetes mellitus, atherosclerotic vascular
disease, and thyroid disease and avoidance of cardiotoxic drugs such as tobacco,
alcohol, cocaine, and amphetamines, are important for reducing risk as well. Some
patients may need cardiac catheterization if CAD is thought to be a significant
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