Luis D. Pacheco
Antonio F. Saad
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Shock is a condition in which circulation fails to meet the nutritional needs of the cell and remove metabolic wastes.1
Shock may be further divided into four types: hypovolemic, distributive, cardiogenic, and obstructive. Table 25.1
summarizes the characteristics of the most common forms of shock. Table 25.2
describes the most significant pregnancy-induced changes in hemodynamic variables that need to be considered when making the diagnosis of shock in the pregnant patient.
Hypovolemic shock, the most common form seen in obstetrics, is due to excessive blood loss. When the circulating blood volume is less than the capacity of its vascular bed, hypotension with diminished tissue perfusion results, leading to cellular hypoxia, acidosis, and cell death.2
Depending on the duration and severity of the insult, irreversible organ damage or even death may occur. Distributive shock occurs in the setting of pathogenic peripheral vasodilation, resulting in decreased systemic vascular resistance (SVR). Vasodilation occurs typically in septic shock, anaphylactic shock, and neurogenic shock following spinal cord injury. Obstructive shock is characterized by an acute obstruction of blood flow and may be secondary to acute decreases in preload from a tension pneumothorax, cardiac tamponade, or pulmonary embolism. Cardiogenic shock is due to failure of either the right or left ventricle, resulting in inadequate cardiac output. The latter may be secondary to coronary ischemia, acute myocarditis, and nonischemic cardiomyopathies such as peripartum cardiomyopathy.
Table 25.1 Clinical Characteristics of Shock
Most common cause of shock in obstetrics. Decreased preload results in decreased cardiac output and compensatory increase in systemic vascular resistances. Transthoracic echocardiography reveals a hyperdynamic “empty” left ventricle.
Characterized by peripheral vasodilation with low systemic vascular resistances. The decreased afterload commonly results in an increased cardiac output. Sepsis and anaphylaxis are typical forms of distributive shock.
Shock secondary to acute obstruction of blood flow with decreased preload to the heart. Commonly seen with massive pulmonary embolism, cardiac tamponade, and tension pneumothorax.
“Pump” failure resulting in decreased heart contractility as seen in acute systolic dysfunction from peripartum cardiomyopathy or myocardial, myocardial infarction, or viral myocarditis.
Initial General Management of Shock in Pregnancy
summarizes the initial basic management of patients in shock. Several important initial steps should be performed when the diagnosis of shock is made in the obstetric patient. First, two large-bore intravenous (IV) lines, preferably 16-gauge, are placed for rapid expansion of intravascular volume. The use of fluids is usually discouraged in patients with shock due to acute right or left ventricular failures (cardiogenic shock) because it may result in overdistention of a failing right ventricle, and, in cases of a failing left ventricle, fluid will result in pulmonary edema. An indwelling bladder catheter is placed for hourly determination of urine output. An arterial line
allows continuous measurement of systemic blood pressure, as well as easy access for laboratory investigations. Oxygen may be administered via a face mask at 8 to 10 L/min, and the inspired oxygen concentration adjusted according to arterial blood gas results. Inability to protect the airway, poor arterial oxygenation, and airway obstruction may require early endotracheal intubation and mechanical ventilation. In viable pregnancies, electronic fetal monitoring and ultrasound examination are recommended. Importantly, during the initial phase of shock resuscitation, maternal care should not be interrupted or delayed due to fetal concerns.
Table 25.2 Hemodynamic Indices in Nonpregnant and Normal Third-Trimester Pregnant Women Measured by Pulmonary Artery Catheter
Normal Nonpregnant (n = 10)a
Normal Third Trimester (n = 10)a
Severe Preeclampsia (n = 45)b
Amniotic Fluid Embolism (n = 15)c
Cardiac output (L/min)
4.3 ± 0.9
6.2 ± 1.0
7.5 ± 0.2
Heart rate (bpm)
71 ± 10
83 ± 10
95 ± 2
Systemic vascular resistance (dyne/m/s−5)
1530 ± 520
1.210 ± 266
1496 ± 64
Pulmonary vascular resistance (dyne/cm/s−5)
119 ± 47
78 ± 22
70 ± 5
176 ± 72
Colloid osmotic pressure (mm Hg)
20.8 ± 1.0
18.0 ± 1.5
19.0 ± 0.5
Mean arterial pressure (mm Hg)
86 ± 8
90 ± 6
138 ± 3
Pulmonary capillary wedge pressure (mm Hg)
6.3 ± 2.1
7.5 ± 1.8
10 ± 1
18.9 ± 9.2
Central venous pressure (mm Hg)
3.7 ± 2.6
3.6 ± 2.5
4 ± 1
Left ventricular stroke work index (g/m/m−2)
41 ± 8
48 ± 6
81 ± 2
26 ± 19
Mean pulmonary artery pressure (mm Hg)
11.9 ± 2.0
12.5 ± 2.0
17 ± 1
26.2 ± 15.7
All data are presented as mean ± SD; bpm = beats per minute; SD = standard deviation.
Observations in pathophysiologic states (severe preeclampsia and amniotic fluid embolism) are shown for comparison.
Data from a Clark SL, Cotton DB, Gonik B, Greenspoon J, Phelan JP. Central hemodynamic alterations in amniotic fluid embolism. Am J Obstet Gynecol. 1988;158(5):1124-1126;
b Clark SL, Cotton DB, Lee W, et al. Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol. 1989;161(6 pt 1):1439-1442;
c Cotton DB, Benedetti TJ. Use of the Swan-Ganz catheter in obstetrics and gynecology. Obstet Gynecol. 1980;56:641; and unpublished data from the National Amniotic Fluid Embolism Registry.
Initial laboratory investigation usually includes blood type and cross-match, complete blood count, platelets, fibrinogen, electrolytes, blood urea nitrogen, creatinine, and arterial blood gas. Urine should be sent for analysis and microscopic evaluation as indicated. In cases of suspected sepsis, early cultures (blood, urine, respiratory, genital tract) and serum lactate levels should be obtained without delay.3
An ultrasound-focused initial assessment may easily identify the cause of shock in cases of hypovolemia, left ventricular failure, right ventricular failure, cardiac tamponade, and tension pneumothorax. Hypovolemia is usually suspected in the presence of a collapsed inferior vena cava (IVC) and a “hyperdynamic” appearance of the left ventricle (ie, empty cavity with complete obliteration during systole). Shock from a pulmonary embolism may be suspected with a dilated hypokinetic right ventricle (right ventricle larger than the left ventricle on a four-chamber view) and a distended IVC. Similarly, cardiogenic shock may be diagnosed in a patient with hypotension and pulmonary edema whose imaging reveals a severely dilated and hypokinetic left ventricle.
Hemorrhagic (Hypovolemic) Shock
Hemorrhagic shock is the most common form of shock in obstetrics. Most cases occur secondary to postpartum hemorrhage due to uterine atony and abnormal placentation.
Management of Hemorrhagic Shock in Pregnancy
The obstetrical management of bleeding is beyond the scope of this chapter; however, medical and surgical treatments usually involve administration of uterotonics; repair of genital lacerations as indicated; and a variety of surgical procedures, including uterine artery ligation, B-Lynch stitches, placement of intrauterine balloons, and hysterectomy. The latter interventions constitute the mainstay of treatment. From a critical care point of view, the most important intervention is to maintain hemodynamic stability until the bleeding is controlled (usually surgically).
Anaphylactic reactions are rare events but may be fatal in as many as 10% of cases.28
Antibiotics, anti-inflammatory agents, oxytocin, anesthetic agents, blood products, colloid solutions, and latex exposures are some of the most common causes of anaphylaxis during pregnancy. Anaphylaxis is a series of events that occur in a sensitized individual on subsequent exposure to a specific antigen. It classically refers to an immunoglobulin (Ig) E-mediated, type I hypersensitivity response, produced by the release of antigen-stimulated mast cells and basophil mediators (eg, prostaglandins, leukotrienes, histamine, tumor necrosis factor alpha). The latter may result in a life-threatening systemic reaction with urticaria, angioedema, hypotension from severe vasodilation, increased vascular permeability with third spacing, airway obstruction from edema, and multiorgan system failure. Anaphylactic reactions may also be non-IgE-mediated responses (ie, reactions to IV immunoglobulins, dialysis circuit membranes, dextrans, and iron). In the past, the latter were referred as anaphylactoid reactions; however, this term is no longer recommended.29
Clinical Assessment and Management of Anaphylactic Shock in Pregnancy
Early recognition and management of anaphylactic reactions is essential. Risk factors, including a prior history of anaphylaxis, should be noted carefully at admission. Anaphylaxis usually presents with acute onset of urticaria, hypotension, bronchospasm, angioedema, and cardiovascular collapse. Cardiac output may be decreased due to cytokine-mediated cardiac depression.30
Acute management of anaphylaxis in the obstetrical patient should not differ from that in the nonpregnant patient. A stepwise approach has been suggested and consists of first assessing the airway and supplementing oxygen. Early tracheal intubation is recommended in the setting of significant airway edema.
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