Acceptable strategies for administering additional fluid challenges to hypovolemic
patients are based on the direction and degree of change in the various hemodynamic
parameters in response to a fluid load rather than to their absolute values. CVP has a
poor correlation with RV end-diastolic volume because it can be affected by changes
in intrathoracic pressure, venous tone, and ventricular compliance (distensibility of
the relaxed ventricle or stiffness of the myocardial wall).
variation are more predictable markers of fluid status. Left ventricular SV (and thus
pulse pressure) is inversely related to intrathoracic pressures during respiration; SV
is maximally affected at lower filling pressures when the ventricles are operating on
the steepest portion of the Frank–Starling curve. A SV that varies at least 12% during
a respiratory cycle (between end inspiration and expiration) is highly predictive of a
positive response to fluid challenge.
Some practitioners argue that CVP is still an acceptable gauge of fluid
responsiveness when used in conjunction with other parameters, including CO, BP,
urine output, and tissue perfusion. Using CVP as a guide, an increase in the CVP of 5
mm Hg after a 250- to 500-mL fluid challenge in 10 minutes implies the LV is still
functioning on the steep portion of the volume–pressure curve. If the CVP rises
abruptly as fluid is given, with a small change in CO, the flat portion of the
ventricular function curve has been reached and the IV infusion rate should be
slowed. If signs and symptoms of inadequate tissue perfusion worsen or fail to
improve and if the CVP remains greater than 10 to 14 mm Hg, fluid challenges should
be stopped and inotropic therapy initiated.
Most critically ill patients require a CI above 2.5 L/minute/m2 and a PCWP of 12
to 18 mm Hg, or a CVP of 8 to 14 mm Hg to maintain an acceptable MAP of 65 to 75
mm Hg. A downward trend in the lactate and base deficit and the change in
hemodynamic parameters as well as vital signs and urine output should serve as
indicators for whether additional fluid is required.
CASE 17-2, QUESTION 6: P.T. has received a total of 3.5 L of NS boluses during the past 6 hours and
expander for P.T., and which agent should be used?
Albumin, the predominant protein in the plasma, accounts for approximately 80%
of the COP, the force that maintains fluid in the intravascular space.
heat-treated to eliminate the potential for disease transmission. Albumin 5% solution
increases plasma volume by approximately 80% to 100% of the volume infused, with
an initial duration of action of 16 hours.
39 At steady state (3–5 days), approximately
40% of albumin remains in the intravascular compartment while the rest is in the
interstitial compartment. Side effects involve transient clotting abnormalities and
anaphylactic reactions (0.5%), both of which are rare.
is caused by the pasteurization process, causing albumin to polymerize, which
produces an antigenic macromolecule. Albumin solutions also contain citrate, which
can lower serum calcium concentrations and theoretically lead to decreased LV
function. The effects on coagulation and serum calcium are possibly related to the
volume of fluid infused rather than albumin administration.
a 5% solution that is iso-oncotic with the plasma and as a 25% solution that is
hyperoncotic. The 5% solution is generally preferred for routine volume expansion,
whereas the 25% solution is most useful in correcting hypoproteinemia or
intravascular hypovolemia in patients with excess interstitial water. Albumin is
subject to availability, as approximately 1 L of pooled donor plasma is required to
produce 20 to 25 g of albumin.
Hydroxyethyl starch (HES) is a synthetic colloid made from amylopectin, which
closely resembles human serum albumin but is less expensive. Available as a 6%
solution, HES expands the plasma volume by an amount greater than the volume
infused because the high oncotic pressure draws water from the interstitial spaces.
HES solutions have varying locations and degrees of substitutions on the glucose
molecules, which slow enzymatic degradation and confer greater hydrolysis
resistance (Table 17-5). HES solutions have complex pharmacokinetics because of
their wide range of molecular weights; with an average molecular weight of 69,000
Da and a range of 1,000 to 3,000,000 Da. Numerous clinical studies have compared
albumin and hetastarch for fluid resuscitation in patients with and without shock.
However, most of these trials were underpowered and there were no significant
41,42 Although HES has comparable efficacy to albumin,
controversy exists regarding the use of HES owing to adverse effects seen with its
use. These adverse effects include severe pruritus, coagulopathy, and renal
dysfunction and appear to be class-related effects because the newer lower
molecular weight and substitution products are similar.
Dose-related reductions in platelet count and transient increases in PT, and PTT
have been reported with moderate infusions of HES (up to 1,500 mL/day), and
coagulopathies persist for up to 7 days with larger volumes.
VIII and von Willebrand factor levels to be lowered beyond that which can be
attributed to hemodilution and also increases fibrinolysis.
von Willebrand disease at greater risk of bleeding. In critically ill patients,
particularly those with sepsis, HES is also associated with a dose-related increased
risk of acute kidney injury and greater probability of needing renal replacement
20,21,44–46 HES now includes warnings of excessive bleeding when used in
patients undergoing cardiopulmonary bypass as well as a boxed warning that states
these products are contraindicated in critically ill patients. Experts argue that HES
should not be used because of the potential adverse effects and that other alternatives
Dextrans are colloidal solutions that are synthesized by bacteria from sucrose and
are available in 40,000 and 70,000 Da average molecular weight solutions. These
products lack adequately powered randomized trials to adequately examine their
42 Like HES, dextrans can cause renal dysfunction, bleeding, and
anaphylactic reactions. Dextrans can cause acute kidney injury, possibly because of
accumulation of dextran molecules within the renal tubules. They increase bleeding
by causing dose-related decreased platelet adhesion, increased fibrinolysis, and
decreased levels of factor VIII. Dextran solutions are associated with the highest
incidence of anaphylactic reactions among all of the colloids.
Because of the lack of superior clinically important outcomes and less favorable
safety profiles for HES and dextrans compared to albumin, it is decided to use
albumin for further volume expansion in P.T.
Shock arising primarily from an abnormality of cardiac function constitutes
cardiogenic shock. The causes of cardiogenic shock can be separated largely into
cardiomyopathic, arrhythmogenic, and mechanical (Table 17-1), although
occasionally patients may have a combination of causes. Regardless of the source,
the underlying problem in cardiogenic shock is a decrease in CO that is not caused by
a reduction in circulating blood volume. This decrease in CO results in the syndrome
of shock, organ dysfunction, and death if measures to restore perfusion are not
The most common cause of cardiogenic shock is LV dysfunction and necrosis as a
result of acute myocardial infarction (AMI) (see Chapter 13, Acute Coronary
Syndrome). Necrosis of the left ventricle can be the result of a single massive
myocardial infarction (MI), numerous smaller events, or severe global cardiac
ischemia. Increases in sympathetic tone—seen clinically as increased HR and
peripheral vasoconstriction—initially serve to increase CO and maintain arterial
pressure. When necrosis exceeds approximately 40% of the LV, normal
compensatory responses can no longer maintain CO, and hypotension and
hypoperfusion results. In addition to decreased perfusion to vital tissues and organs,
the decrease in CO leads to a reduction in the flow of blood through the coronary
arteries, which can lead to infarct extension and a further worsening of cardiac
Cardiogenic shock is the leading cause of death in patients hospitalized with AMI.
It occurs in 5% to 10% of AMI cases and is more common with ST-elevation versus
incidence was higher in patients at least 75 years of age, women, and Asian/Pacific
Islanders versus less than 75 years of age, men, and other racial/ethnic groups,
respectively. Patients with end-stage renal disease appear to be at a higher risk of
cardiogenic shock and among those with ST-elevation MI that incidence increased
49 The in-hospital mortality for patients experiencing
shock decreased 29% from 2003 to 2010, most likely because of coronary
48 The overall mortality rate, however, has remained high
Infarction involving the RV can cause cardiogenic shock, even with normal LV
systolic function. In this situation, the volume of blood reaching the LV (preload) is
reduced because of the inability of the RV to move blood to the left side of the heart.
In most patients with cardiogenic shock and RV infarction, significant LV dysfunction
is present as well. Arrhythmias are often associated with worsening perfusion,
causing or worsening cardiogenic shock, and poor outcomes.
Patients with chronic heart failure (HF) (see Chapter 14, Heart Failure) usually
compensate for their poor cardiac function, but acute exacerbations can cause
cardiogenic shock with hypotension, hypoperfusion, and organ dysfunction. Cardiac
dysfunction occasionally can be seen with severe sepsis because of increases in the
production of inflammatory cytokines that have a depressant effect on the
myocardium. However, the cytokine-mediated vasodilation and reduction in
afterload usually negates the ability to detect the cardiac dysfunction. A similar
picture occurs after cardiopulmonary bypass with heart surgery through activation of
Cardiogenic shock caused by mechanical problems occurs relatively infrequently.
In this setting, the systolic function (contractility) of the heart may be normal, but
other defects render the heart unable to eject a normal volume of blood. Pericardial
tamponade (bleeding into the pericardial sac) and tension pneumothorax (air leakage
from the lung into the chest) cause cardiogenic shock by compressing the heart and
decreasing the diastolic filling. [Pericardial tamponade and tension pneumothorax
are technically obstructive forms of shock as there is an extracardiac process that is
impeding forward circulatory flow.] Acute valvular insufficiency or stenosis
prevents the normal ejection of blood. Ventricular septal or free wall rupture can
occur, often in the setting of AMI, with the reduction in CO related to the inability of
the LV to eject a normal volume of blood during systole.
The symptoms of cardiogenic shock are largely the same as for other types of
shock. Hypotension and signs of inadequate tissue perfusion, such as confusion,
oliguria, tachycardia, and cutaneous vasoconstriction, are present in many patients.
Differentiating cardiogenic shock from distributive or hypovolemic shock requires
further examination. A history of coronary artery disease or symptoms of MI are
important findings. Hypovolemia occurs in up to 20% of patients in cardiogenic
shock, but patients frequently have signs of volume overload because the heart cannot
move blood through the circulation. Peripheral edema can be seen in the extremities;
lung sounds are diminished, and rales may be present as pulmonary edema develops
with LV dysfunction. These findings are particularly evident in patients with severe
Because the distinction between cardiogenic and other forms of shock can be
difficult to make based on physical examination alone, further testing with invasive
hemodynamic monitoring may be required to establish the diagnosis and guide
therapy. Table 17-6 lists the common laboratory, electrocardiogram (ECG), and
chest radiograph findings, and Table 17-3 lists the common hemodynamic findings in
cardiogenic shock. CVP may be easily attained, particularly if the patient already has
a central line; other hemodynamic findings will require further monitoring tools (e.g.,
PA catheter, echocardiography).
Typical Findings of Early Cardiogenic Shock
Hypoxemia secondary to pulmonary congestion with ventilation–perfusion abnormalities
Anion gap metabolic acidosis with a compensatory respiratory alkalosis
Elevated blood lactate levels (which contributes to the acidosis)
Thrombocytopenia (if disseminated intravascular coagulation is present)
Elevated cardiac enzymes if myocardial infarction is present
Electrocardiogram (ECG)–one or more of the following
T-wave changes indicating infarction
Pulmonary edema or evidence of adult respiratory distress syndrome (ARDS)
Valvular or mechanical problems if present
Normal or decreased ejection fraction
Hemodynamic monitoring—one or more of the following:
Elevated pulmonary capillary wedge pressure (PCWP) and central venous pressure (CVP)
Elevated pulmonary artery pressure (PAP)
Elevated systemic vascular resistance (SVR)
IMMEDIATE GOALS OF THERAPY AND GENERAL CONSIDERATIONS
shallow. Heart sounds include S3
gallops, but no murmurs are heard. The jugular venous pulse is normal. He
4 L/minute oxygen via nasal cannula, are the following:
What immediate goals of therapy are necessary to stabilize and treat J.S.?
J.S. has signs of cardiogenic shock with decreased systemic perfusion. His BP is
low, HR is elevated, and respiratory status is compromised. J.S. is restless, anxious,
and confused, indicating poor cerebral perfusion. His ABG results indicate a
As discussed in Chapter 13, Acute Coronary Syndrome, most patients presenting
with STEMI are routinely treated with aspirin, a β-blocker, and immediate
percutaneous coronary intervention (PCI) if available or, if not, thrombolytic therapy
50 The presence of cardiogenic shock can alter the
interventional strategy, however. Patients presenting in cardiogenic shock after MI
may progress rapidly to irreversible organ system dysfunction as the compensatory
mechanisms fail to maintain tissue perfusion. Treatment of these critically ill patients
involves two components: stabilization and definitive treatment. Initial stabilization
of the patient must be attained before further evaluation and treatment of the cause of
cardiogenic shock can proceed. The goals are to maintain adequate ḊO2
and to prevent further hemodynamic compromise. Stabilization includes (a)
establishing ventilation and oxygenation (arterial PO2 should be greater than 70 mm
Hg); (b) restoring arterial BP and CO with vasopressors and inotropic agents, if
needed; (c) infusing fluids, if hypovolemic; and (d) treating pain, arrhythmias, and
acid–base abnormalities, if present.
Administration of oxygen is appropriate for patients who have severe dyspnea,
hypoxemia (oxygen saturation below 90%), or persistent or worsening acidemia (pH
Improving oxygenation may contribute to improved ventricular
performance; however, supplemental oxygen could potentially be harmful by causing
increased coronary vascular resistance and infarct size, particularly in normoxic
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