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CHAPTER 31: The Pathophysiology of the Circulation in Critical Illness 237

increased by this intervention, and the risk of pulmonary edema is can be initiated. The response to the initial therapy confirms or chal-
increased. When signs of pulmonary edema are present on clinical and lenges the working diagnosis. When features of the initial clinical
radiologic examinations of the thorax, diuretics, morphine, and nitro- presentation or the response of the patient to appropriate management
glycerin often reduce preload by relaxing the capacitance veins, associ- challenges the working diagnosis, early acquisition of more objective
ated with an increase in LV systolic performance. However, about 10% of hemodynamic data is appropriate. In the interim, other features of the
patients with myocardial ischemia present with significant hypovolemia. clinical presentation often suggest a cause of shock that falls outside
Accordingly, the clinical assessment of hemodynamics should be supple- this simplistic schema, or the possibility of overlapping or concurrent
mented as soon as possible with other means to exclude hypovolemia causes expands. This section briefly reviews several important differ-
(eg, echocardiography, dynamic tests of the adequacy of circulating ential diagnostic conditions for cardiogenic shock (eg, tamponade or
volume, right heart catheterization, or empiric volume challenge) so that acute right heart syndromes) and hypovolemic shock (eg, anaphylactic,
appropriate volume infusion or reduction can be titrated. When these neurogenic, or adrenal shock); see Table 31-2.
measures are addressed adequately but the hypoperfusion state persists,
early movement toward arteriolar vasodilator therapy or a balloon-assist Cardiac Tamponade: Pericardial effusion is often suggested early by the
device is indicated to reduce LV afterload and preserve coronary perfu- clinical setting (eg, renal failure, malignancy, or chest pain), physical exa-
sion pressure (see Chap. 37). These latter interventions are not relegated mination (eg, elevated neck veins, systolic BP that decreases >10 mm Hg
to the last resort but are considered early in this initial stabilization of on inspiration, or distant heart sounds), or routine investigations
cardiogenic shock. Similarly, early elective intubation and mechanical (eg, chest radiograph with “water bottle” heart, low voltage on the
ventilation allow effective sedation and reduce O consumption, and ECG, or electrical alternans). Such a constellation of clinical data
51
2
PEEP improves arterial oxygenation, often without reducing VR and requires early echocardiographic confirmation of pericardial effusion,
with improvement of pumping function in the damaged left ventricle by and tamponade is signaled by right ventricular and right atrial collapse
reducing preload and afterload. 54 that worsens with inspiration, with a relatively small left ventricle
(see Chap. 40). Tamponade requires urgent pericardiocentesis or
56
Hypovolemic Shock: Beyond the absence of clinical features suggesting operative drainage by pericardiostomy. While deciding on definitive
that the heart is too full in the hypotensive patient who is presenting treatment, one should remember that intravenous expansion of the
with reduced Q ˙ t (see Table 31-2), hypovolemic shock is distinguished circulating volume may produce small increases in BP, whereas reduc-
from cardiogenic shock by several positive clinical features. Often there tions in circulating volume (eg, diuretics, nitroglycerin, morphine,
is an obvious source of external bleeding (eg, multiple trauma, hemop- or intercurrent hemodialysis) are often associated with catastrophic
tysis, hematemesis, hematochezia, or melena); internal bleeding is often reduction in Q ˙ t by reducing the venous tone and volume necessary to
signaled by blood aspirated from the nasogastric tube or on rectal exam- maintain the Pms required to drive VR back to high Pra.
ination, by increasing abdominal girth, or by clinical and radiologic Right heart catheterization typically shows a Pra increased to about
examinations of the thoracic cavity for pleural, alveolar, retroperitoneal, 16 to 20 mm Hg and equal to pulmonary arterial DP and the Pwp; Q ˙ t and
or periaortic blood. Each of these signals is often associated with a new SV are much reduced (see Chap. 40). This hemodynamic subset resembles
reduction in the hematocrit. Nonhemorrhagic hypovolemia often pres- that of cardiogenic shock (high Ppw and low SV). However, in the case
ents with recognizable excess gastrointestinal fluid losses (eg, vomiting, of pericardial tamponade, Ppw is increased because pericardial pressure
diarrhea, suctioning, and stomas), excess renal losses (eg, osmotic or is increased, so the transmural pressure of the left ventricle approaches
drug diuresis and diabetes insipidus), or third-space losses as in exten- zero, a value consistent with the very low LVEDV accounting for the low
sive burns. Physical examination may show dry mucous membranes SV. Other etiologies of hypotension associated with high cardiac pressures
with decreased tissue turgor, and routine laboratory tests often show and small ventricular volumes include constrictive pericarditis, tension
increased serum urea nitrogen out of proportion to a relatively normal pneumothorax, massive pleural effusion, positive-pressure ventilation
creatinine level and increased hematocrit due to hemoconcentration. with high PEEP, and very high intra-abdominal pressure. Up to 33% of
The initial management of patients with presumed hypovolemic patients presenting with cardiac tamponade have increased BP despite low
shock necessitates early vascular access with two large-bore (14-gauge) Q ˙ t; this subset of patients has a high incidence of hypertension preceding
peripheral intravenous catheters for rapid infusion of large volumes of the onset of tamponade. 57
warmed blood and fluids for hemorrhagic shock and the appropriate Treatment of cardiac tamponade involves needle pericardiocentesis
crystalloid solution for dehydration. Central venous access ensures or the opening of a pericardial window (see Chap. 40). Careful observa-
adequate volume resuscitation and allows early measurement of CVP. tion postprocedure to watch for pulmonary edema is indicated. 58
An immediate response of increased BP and pulse volume supports the
presumed diagnosis, whereas no improvement in these hemodynamic Right Ventricular Overload and Infarction: Another clinical presentation
measurements necessitates emergent repair of the site of blood loss that may fall outside the simplest scheme presented in Table 31-2 is
or a reevaluation of the working diagnosis. Achieving hemostasis in the hypotension associated with acute or acute-on-chronic pulmonary
hemorrhagic shock is a prerequisite for adequate volume resuscitation: hypertension. Shock after acute pulmonary embolism is often signaled by
urgent and simultaneous pursuit of hemostasis and fluid resuscitation the clinical setting including risk factors (eg, perioperative, immobilized,
is encouraged. Vasoconstricting drugs such as norepinephrine should thrombophilia, or prior pulmonary embolisms); symptoms of acute dys-
55
be used only as short-term antihypotensives to mobilize endogenous pnea, chest pain, or hemoptysis; physical examination showing a loud P
2
unstressed volume or enhance arteriolar vasoconstriction until the with a widened and fixed split of the second heart sound; new hypoxemia
circulating volume is restored by transfusion; prolonged use of these without obvious radiologic explanation; and acute right heart strain
drugs confounds the physician’s assessment of the end point of volume on the ECG (see Chap. 38). Noninvasive Doppler studies of the veins in
resuscitation. Early endotracheal intubation and mechanical ventila- the lower extremities and helical computed tomographic angiography
tion reduce the patient’s work of breathing and allow respiratory confirm the diagnosis. Anticoagulation or placement of a filter in the
compensation for lactic acidosis during volume resuscitation; warming inferior vena cava reduces the incidence of subsequent emboli, and there
the fluids and covering the patient with warm dry blankets prevent may be some success with thrombolytic therapy (or, in some centers, sur-
the complication of hypothermia, including cold coagulopathy and gical removal of the embolus) in patients with shock due to pulmonary
further bleeding. embolism. Acute-on-chronic pulmonary hyper tension causes shock in
the setting of prior primary pulmonary hypertension, recurrent pul-
Other Common Causes of Shock: A Short Differential Diagnosis: The pur- monary emboli, progression of collagen vascular disease, acute hypoxic
pose of this initial schema is to formulate a working diagnosis for the respiratory failure, or chronic respiratory failure (eg, chronic obstructive
most common presentations of shock so that early and rapid therapy pulmonary disease or pulmonary fibrosis) aggravated in part by hypoxic

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