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Tintinalli's Emergency Medicine > Section 4: Shock > Chapter 30. Approach to the Patient in
Shock >
Epidemiology
More than 1 million cases of shock are estimated to present to U.S. hospital EDs each year.1 The
presentation may be cryptic, as in the patient with compensated heart failure, or obvious as in the
ultimate shock state of cardiac arrest. Despite aggressive treatment, mortality from shock
remains high. Approximately 30 to 45 percent of patients in septic shock, and 60 to 90 percent
for those with cardiogenic shock, die within 1 month of presentation.2,3 The definition and
treatment of shock continues to evolve. With a contemporary understanding of the disease and
new evolving technology, the emergency physician can recognize shock at an earlier stage and
initiate expert, timely intervention. The general approach to a patient in the initial stages of shock
follows similar principles regardless of the inciting factors or etiology.
Pathophysiology
Shock is defined as circulatory insufficiency that creates an imbalance between tissue oxygen
supply and oxygen demand. The result of shock is global tissue hypoperfusion and is associated
with a decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is
classified into four categories by etiology: (1) hypovolemic (caused by inadequate circulating
volume), (2) cardiogenic (caused by inadequate cardiac pump function), (3) distributive (caused
by peripheral vasodilatation and maldistribution of blood flow), and (4) obstructive (caused by
extra cardiac obstruction to blood flow). Clinically, shock may have a predominant cause, but as
the shock state persists or progresses to irreversible end organ damage, other pathophysiologic
mechanisms become operative.
Knowledge of the principles of oxygen delivery and consumption is important to the
understanding of shock. A maximum of four molecules of oxygen is loaded onto each molecule
of hemoglobin as it passes through the lungs. If all available oxygen sites are occupied (four per
molecule of hemoglobin), arterial oxygen saturation (SaO2) is 100 percent (Table 30-1). Arterial
oxygen content (CaO2) is the amount of oxygen bound to hemoglobin plus the amount dissolved
in plasma (Table 30-2). Oxygen is delivered to the tissues by the pumping function (cardiac
output) of the heart.
Table 30-1 Definitions of Abbreviations
(a-v)CO2
Arterial-central venous carbon dioxide difference
CaO2
Arterial oxygen content
CmvO2
Mixed venous oxygen content
CI Cardiac index (cardiac output/body surface area)
CO Cardiac output
CPP Coronary perfusion pressure
CVP Central venous pressure
DO2
Systemic oxygen delivery
DBP Diastolic blood pressure
Hb Hemoglobin
MAP Mean arterial pressure
MODS Multiorgan dysfunction syndrome
OER Oxygen extraction ratio
PaCO2
Arterial carbon dioxide pressure
PaO2
Arterial oxygen pressure
PAOP Pulmonary artery occlusion (wedge) pressure
SaO2
Arterial oxygen saturation
ScvO2
Central venous oxygen saturation
SmvO2
Mixed venous oxygen saturation (pulmonary artery)
SrvO2
Retinal venous oxygen saturation
SIRS Systemic inflammatory response syndrome
SVR Systemic vascular resistance
VO2
Systemic oxygen consumption
Table 30-2 Oxygen Transport and Utilization Components
Arterial oxygen content CaO2= 0.0031 x PaO2+ 1.38 x Hb x Sao2
CaO2 is the amount of O2 within 100 mL blood. Oxygen is contained within blood in two
forms: dissolved in plasma and chemically combined with hemoglobin. Assuming 15 g
hemoglobin per 100 mL blood and an oxygen saturation of 97%, the representative normal value
of CaO2 is 20.1 mL/100 mL blood (vol%).
Central venous/mixed venous oxygen saturation ScvO2 or SmvO2
SmvO2 reflects physiologic efforts to meet tissue O2 demands. Normal SmvO2 is 65 to 75%.
When the SmvO2 falls below 50%, the body's limits to compensate have been reached and O2
availability for tissue metabolism will be compromised, leading to lactic acidosis.
Central venous/mixed venous oxygen content CmvO2= 0.0031 x PmvO2+ 1.38 x Hb x SmvO2
CmvO2 is the amount of oxygen content returning to the heart. Normal CmvO2 is 15 mL/100
mL blood (vol%).
Systemic oxygen extraction ratio (OER) OER = C(a – v)O2/CaO2
The amount of O2 taken out of the blood by the tissues is the systemic OER. It is described as a
percentage. Normal OER is about 25%. Lactic acid production, an indicator of anaerobic
metabolism, usually accompanies an OER of greater than 50%.
Oxygen delivery DO2= CO x CaO2x 10
DO2 is the amount of O2 delivered to the tissues per minute. Assuming a normal cardiac output
of 5 L per min and a CaO2 of 20.1 vol%; a normal value for O2 delivery would be 1000 mL O2
per min.
Oxygen consumption VO2= CO x Hb x 1.38 x (SaO2– SmvO2) x 10
The amount of O2 consumed by tissues each minute and is equal to the difference in O2
delivered to tissues and the O2 returning from tissues. The normal value is about 250 mL O2 per
min. Note that this formula ignores the small contribution from dissolved oxygen.
Oxygen affinity
Shifts in the oxyhemoglobin dissociation curve affect the release of O2 in the peripheral
circulation. Increased pH, decreased temperature, decreased carbon dioxide concentration
(PcO2) and decreases in 2,3-DPG levels all result in a shift of the oxyhemoglobin curve to the
left. Thus, for any particular value of PaO2, the O2 saturation will be higher. This increased
affinity of hemoglobin for O2 makes O2 loading easier, but release of O2 in the peripheral
tissues is impaired. The reverse is true with a decreased pH, increased temperature, increased
PcO2, and increased 2,3-DPG: there is a shift of the oxyhemoglobin dissociation curve to the
right resulting in a decreased affinity of hemoglobin for O2.
Note: See Table 30-1 for abbreviation definitions.
Systemic oxygen delivery (DO2) is the product of the CaO2 and cardiac output (CO). Systemic
oxygen consumption (VO2) comprises a sensitive balance between supply and demand.
Normally, the tissues consume approximately 25 percent of the oxygen carried on hemoglobin,
and venous blood returning to the right heart is approximately 75 percent saturated [mixed
venous oxygen saturation (pulmonary artery) (SmvO2)]. When oxygen supply is insufficient to
meet demand, the first compensatory mechanism is an increase in CO. If the increase in CO is
inadequate, the amount of oxygen extracted from hemoglobin by the tissues increases, which
decreases SmvO2.
When compensatory mechanisms fail to correct the imbalance between tissue supply and
demand, anaerobic metabolism occurs, resulting in the formation of lactic acid. Lactic acid is
rapidly buffered, resulting in the formation of measured lactate; normally between 0.5 and 1.5
mM/L. An elevated lactate level is associated with an SmvO2 <50 percent. Most cases of lactic
acidosis are a result of inadequate oxygen delivery, but lactic acidosis occasionally can develop
from an excessively high oxygen demand, for example, in status epilepticus. In other cases, lactic
acidosis occurs because of an impairment in tissue oxygen utilization, as in septic shock and
postresuscitation from cardiac arrest; a normal SmvO2 with an elevated lactate indicates such an
impairment. Elevated lactate is a marker of impaired oxygen delivery and/or utilization and
correlates with short-term prognosis of critically ill patients in the ED.
SmvO2 can also be used as a measure of the balance between tissue oxygen supply and demand.
SmvO2 is obtained from the pulmonary artery catheter, but similar information can be obtained
by central venous blood cannulation (ScvO2). ScvO2 correlates well with SmvO2 and can be
more easily obtained in the ED setting.4
Shock is usually, but not always, associated with systemic arterial hypotension; i.e., systolic
blood pressure less than 90 mm Hg. Pressure is the product of flow and resistance [mean arterial
pressure (MAP) = CO x systemic vascular resistance (SVR)]. Blood pressure may not fall if
there is increase in peripheral vascular resistance in the presence of decreased cardiac output,
resulting in inadequate flow to the tissue or global tissue hypoperfusion. The insensitivity of
blood pressure to detect global tissue hypoperfusion has been repeatedly confirmed. Thus, shock
may occur with a normal blood pressure, and hypotension may occur without shock.
The onset of shock provokes a myriad of autonomic responses, many of which serve to maintain
perfusion pressure to vital organs. Stimulation of the carotid baroreceptor stretch reflex activates
the sympathetic nervous system leading to (1) arteriolar vasoconstriction, resulting in
redistribution of blood flow from the skin, skeletal muscle, kidneys, and splanchnic viscera; (2)
an increase in heart rate and contractility that increases cardiac output; (3) constriction of venous
capacitance vessels, which augments venous return; (4) release of the vasoactive hormones
epinephrine, norepinephrine, dopamine, and cortisol to increase arteriolar and venous tone; and
(5) release of antidiuretic hormone and activation of the renin-angiotensin axis to enhance water
and sodium conservation to maintain intravascular volume. These compensatory mechanisms
attempt to maintain DO2 to the most critical organs—the coronary and cerebral circulation.
During this process, blood flow to other organs such as the kidneys and gastrointestinal tract may
be compromised.
The cellular response to decreased DO2 is adenosine triphosphate depletion leading to ion-pump
dysfunction, influx of sodium, efflux of potassium, and reduction in membrane resting potential.
Cellular edema occurs secondary to increased intracellular sodium, while cellular membrane
receptors become poorly responsive to the stress hormones insulin, glucagon, cortisol, and
catecholamines. As shock progresses, lysosomal enzymes are released into the cells with
subsequent hydrolysis of membranes, deoxyribonucleic acid, ribonucleic acid, and phosphate
esters. As the cascade of shock continues, the loss of cellular integrity and the breakdown in
cellular homeostasis result in cellular death. These pathologic events give rise to the metabolic
features of hemoconcentration, hyperkalemia, hyponatremia, prerenal azotemia, hyper- or
hypoglycemia, and lactic acidosis.
In the early phases of septic shock, these physiologic changes produce a clinical syndrome called
the systemic inflammatory response syndrome or SIRS, defined as the presence of two or more
of the following features: (1) temperature greater than 38°C (100.4°F) or less than 36°C
(96.8°F); (2) heart rate faster than 90 beats/min; (3) respiratory rate faster than 20 breaths/min;
and (4) white blood cell count greater than 12.0 x 109/L, less than 4.0 x 109/L, or with greater
than 10 percent immature forms or bands.5 As SIRS progresses, shock ensues, followed by
multiorgan dysfunction syndrome (MODS) manifested by myocardial depression, adult
respiratory distress syndrome, disseminated intravascular coagulation, hepatic failure, or renal
failure. The fulminate progression from SIRS to MODS is determined by the balance of antiinflammatory and proinflammatory mediators or cytokines that are released from endothelial cell
disruption (Figure 30-1).
Fig. 30-1.
The pathophysiology of shock, SIRS, and MODS.
Global tissue hypoperfusion alone can independently activate the inflammatory response and
serve as a comorbid variable in the pathogenesis of all forms of shock.6 The failure to diagnose
and treat global tissue hypoperfusion in a timely manner leads to an accumulation of an oxygen
debt, the magnitude of which correlates with increased mortality.
Clinical Features
History
Often, the presence of shock will be instantly apparent along with the underlying cause, such as
acute myocardial infarction, anaphylaxis, or hemorrhage. Some patients may be in shock with
few symptoms other than generalized weakness, lethargy, or altered mental status. Symptoms
that suggest volume depletion include bleeding, vomiting, diarrhea, excessive urination,
insensible losses because of fever, or orthostatic light-headedness. A history of cardiovascular
disease is important, particularly episodes of chest pain or symptoms of congestive heart failure.
Prior neurologic diseases can render patients more susceptible to complications from
hypovolemia. Medication use, both prescribed and nonprescribed, is important. Some medication
will cause volume depletion (e.g., diuretics) whereas others depress myocardial contractility
(e.g., -blockers and calcium channel blockers). The possibility of an anaphylactic reaction to a
new medication, or cardiovascular depression as a consequence of drug toxicity should be
considered.
Physical Examination
The clinical presentation of shock can be dramatic, as in profound hypotension caused by
hemorrhage from a gunshot wound. On the other hand, shock can be subtle, as in heart failure,
or, paradoxically, with hypertension. No single vital sign or value is diagnostic of shock as vital
signs are insensitive in detecting and assessing the severity of tissue hypoperfusion.
Measurement of blood pressure can be particularly difficult because of peripheral vascular
disease, tachycardia with a small pulse pressure, and arrhythmias such as atrial fibrillation.
Although not specific, physical findings taken as a composite may be useful in the assessment of
patients in shock (Table 30-3).
Table 30-3 Physical Examination
Temperature Hyperthermia or hypothermia may be present. It is important to distinguish
endogenous hypothermia (hypometabolic shock) from exogenous hypothermia secondary to
environmental exposure. The treatment is obviously aggressive resuscitation in the former and
exogenous heat application in the latter.
Heart rate Usually elevated. However, paradoxical bradycardia can be seen in shock states such
as hemorrhagic shock (up to 30%), hypoglycemia, -blocker use, and preexisting cardiac disease.
Systolic blood pressure May actually increase slightly when cardiac contractility increases in
early shock and then fall as shock advances.
Diastolic blood pressure Correlates with arteriolar vasoconstriction and may rise early in shock
and then fall when cardiovascular compensation fails.
Pulse pressure Systolic minus diastolic pressure and related to stroke volume and rigidity of the
aorta. Increases early in shock and decreases before systolic pressure.
Pulsus paradoxus The change in systolic blood pressure with respiration. The rise and fall in
intrathoracic pressure affects cardiac output. This can be seen in asthma, cardiac tamponade, and
severe cardiac decompensation.
Mean arterial blood pressure Diastolic blood pressure +[pulse pressure/3]. The relationship
between cardiac output and vascular resistance determines can be seen in asthma, cardiac
tamponade, and severe cardiac decompensation.
Shock index Shock index = heart rate/systolic blood pressure. Normal = 0.5 to 0.7. The shock
index is related to left ventricular stroke work in acute circulatory failure. A persistent elevation
of the shock index (>1.0) indicates an impaired left ventricular function (as a result of blood loss
and/or cardiac depression) and carries a high mortality rate.15
Central nervous system Acute delirium or brain failure; restlessness, disorientation, confusion,
and coma secondary to decrease in cerebral perfusion pressure (mean arterial pressure –
intracranial pressure). Patients with chronic hypertension may be symptomatic at normal blood
pressures.
Skin Pallor, pale, dusky, clammy, cyanosis, sweating, altered temperature, and decreased
capillary refill.
Cardiovascular Neck vein distention or flattening, tachycardia, and arrhythmias. An S3 may
result from high-output states. Decreased coronary perfusion pressures can lead to ischemia,
decreased ventricular compliance, increased left ventricular diastolic pressure, and pulmonary
edema.
Respiratory Tachypnea, increased minute ventilation, increased dead space, bronchospasm,
hypocapnia with progression to respiratory failure, and adult respiratory distress syndrome.
Splanchnic organs Ileus, gastrointestinal bleeding, pancreatitis, acalculous cholecystitis, and
mesenteric ischemia can occur from low flow states.
Renal Reduced glomerular filtration rate, renal blood flow redistributes from the renal cortex
toward the renal medulla leading to oliguria. Paradoxical polyuria can occur in sepsis, which
may be confused with adequate hydration status.
Metabolic Respiratory alkalosis is the first acid–base abnormality, as shock progresses metabolic
acidosis occurs. Hyperglycemia, hypoglycemia, and hyperkalemia.
Diagnosis
Ancillary Studies
The clinical presentation and the presumptive etiology of shock will dictate the use of ancillary
studies. A battery of standard hematologic, coagulation, and biochemical tests usually provides
an assessment of the patient's general physiologic condition and occasionally detects an
abnormality that requires specific treatment (Table 30-4). A wide range of laboratory
abnormalities may be encountered in shock, but most abnormal values merely point to the
particular organ system that is either contributing to or being affected by the shock state. No
single laboratory value is sensitive or specific for shock.
Table 30-4 Ancillary Studies
Basic evaluation
Hemogram: white blood cell count and differential, hemoglobin and hematocrit, platelet count
Electrolytes, glucose, calcium, magnesium, phosphorus
Blood urea nitrogen, creatinine
Prothrombin time, partial thromboplastin time
Urinalysis
Chest radiograph
Electrocardiogram
Moderate physiologic assessment
Arterial blood gas (measured oxygen saturation)
Serum lactate
Fibrinogen, fibrin split products, d-dimer
Hepatic function panel
Noninvasive hemodynamic assessment
End-tidal carbon dioxide
Noninvasive cardiac output measurement
Echocardiogram
Invasive hemodynamic assessment
Filling pressures: CVP or PAOP
Cardiac output
Central venous oxygen saturation: SmvO2
Calculation of hemodynamic values: SVR, CO, DO2, VO2
As clinically indicated to define etiology or detect complications
Blood, sputum, urine, and pelvic cultures
CT of head and sinuses
Lumbar puncture
Culture suspicious wounds
Cortisol level
Pregnancy test
Acute abdominal series
Abdominal or pelvic ultrasound
Abdominal or pelvic CT
Note: See Table 30-1 for abbreviation definitions.
Hemodynamic monitoring is important in the assessment of patients in shock and evaluation of
response to treatment. Monitoring capabilities will vary from institution to institution, but should
include pulse oximetry, electrocardiographic monitoring, continuous noninvasive but preferably
intraarterial blood pressure monitoring, end-tidal CO2 monitoring, and central venous pressure
(CVP) monitoring.7 Because hemodynamic measurements are physiologic values, they should
be used to answer specific physiologic questions rather than to serve as therapeutic end points.
Treatment
The Rationale for Early Intervention
The tenet of trauma resuscitation is to initiate care within the "golden hour" of disease
presentation. A similar principle applies to patients with nonsurgical causes of shock. Current
national increases in ED patient acuity and overcrowding have resulted in extending the golden
hour into hours and even days, consequently requiring the provision of critical care in the ED.
The benefit of timely ED intervention in nontraumatic critical illness is significant; standard ED
care can significantly decrease the predicted mortality of critically ill patients in as little as 6 h of
treatment.8 Application of an algorithmic approach to optimize hemodynamic endpoints with
early goal-directed therapy in the ED reduces mortality by 16 percent in patients with severe
sepsis or septic shock.9 The ABCDE tenets of shock resuscitation are establishing Airway,
controlling the work of Breathing, optimizing the Circulation, assuring adequate oxygen
Delivery, and achieving End points of resuscitation.
Establishing Airway
Airway control is best obtained through endotracheal intubation for airway protection, positive
pressure ventilation (oxygenation), and pulmonary toilet. Sedatives, which are frequently used to
facilitate intubation, can exacerbate hypotension through arterial vasodilatation, venodilation,
and myocardial suppression. Furthermore, positive pressure ventilation reduces preload and
cardiac output. The combination of these interventions can lead to hemodynamic collapse.
Volume resuscitation or application of vasoactive agents may be required prior to intubation and
positive pressure ventilation.
Controlling the Work of Breathing
Control of breathing is required when tachypnea accompanies shock. Respiratory muscles are
significant consumers of oxygen during shock and contribute to lactate production. Mechanical
ventilation and sedation decrease the work of breathing and have been shown to improve
survival. SaO2 should be restored to greater than 93 percent and ventilation controlled to
maintain a PaCO2 35 to 40 mm Hg. Attempts to normalize pH above 7.3 by hyperventilation are
not beneficial. Mechanical ventilation not only provides oxygenation and corrects hypercapnia
but assists, controls, and synchronizes ventilation, which ultimately decreases the work of
breathing. Neuromuscular blocking agents are used as adjuncts to further decrease respiratory
muscle, oxygen consumption and preserve DO2 to vital organs.
Optimizing the Circulation
Circulatory or hemodynamic stabilization begins with intravascular access through large-bore
peripheral venous lines. Trendelenburg positioning, historically considered necessary for
maintaining perfusion in the hypotensive patient, does not improve cardiopulmonary
performance compared with the supine position. It may worsen pulmonary gas exchange and
predispose to aspiration. If a volume challenge is urgently required, rather than using the
Trendelenburg position, an alternative is to raise the patient's legs above the level of the heart
with the patient supine. Central venous access will aid in assessing volume status (preload) and
monitoring ScvO2. It is the preferred route for the long-term administration of vasopressor
therapy, and provides rapid access to the heart if pacemaker placement is required.
Fluid resuscitation begins with isotonic crystalloid; the amount and rate are determined by an
estimate of the hemodynamic abnormality. Most patients in shock have either an absolute or
relative volume deficit, except the patient in cardiogenic shock with pulmonary edema. Fluid is
given rapidly, in set quantities (e.g., 500 or 1000 mL), with reassessment of the patient after each
amount. Patients with modest degree of hypovolemia usually require an initial 20 mL/kg of
isotonic crystalloid. More fluids may be necessary with profound volume deficits.
The colloid-versus-crystalloid resuscitation controversy remains despite evidence that there is a
slight increase in mortality when colloids are used for volume replacement in critically ill
patients.10 Some studies have found a lower incidence of pulmonary edema, and possibly
greater benefit, in elderly patients with colloid resuscitation, although survival is not statistically
improved. In the acute situation with severe shock, colloids may be considered to achieve rapid
plasma expansion using less volume compared to crystalloids.
Without invasive hemodynamic monitoring, noncardiogenic pulmonary edema may be difficult
to differentiate from cardiogenic pulmonary edema in the ED. Even though the former may
respond to fluids, fluids should be minimized in a patient with clinical or radiographic evidence
of pulmonary edema until appropriate monitoring is established.
Vasopressor agents are used when there has been an inadequate response to volume resuscitation
or when a patient has contraindications to volume infusion.11 They are most effective when the
vascular space is "full" and least effective when the vascular space is depleted. However,
vasopressors may be necessary early in the treatment of shock, before volume resuscitation is
complete, in order to prevent potentially lethal consequences of prolonged systemic arterial
hypotension. This is especially important in elderly patients with significant coronary and
cerebrovascular disease. Rapidly restoring the MAP to 60 mm Hg or systolic pressure to 90 mm
Hg may avoid the coronary and cerebral complications of decreased blood flow. Vasopressor
agents are based on the catecholamine molecule and have variable effects on the -adrenergic, adrenergic, and dopaminergic receptors (Table 30-5).11,12
Table 30-5 Commonly Used Vasoactive Agents
Drug Dose/Mixture* Action Cardiac Stimulation Vasoconstriction Vasodilation Cardiac Output
Side Effects and Comments
Dopamine 0.5–25 g/kg per min
400 mg/250 mL , , and dopaminergic ++ at 2–10 g/kg per min ++ at 7 g/kg per min + at 0.5–5.0
g/kg per min Usually increases Tachydysrhythmias, increases myocardial O2 consumption, a
cerebral, mesenteric, coronary and renal vasodilator at low doses
Norepinephrine 0.01–0.5 g/kg per min
4 mg/250 mL Primarily 1, some 1
++ ++++ 0 Slight decrease Dose related, reflex bradycardia; useful when loss of venous tone
predominates, spares the coronary circulation
Phenylephrine 0.15–0.75 g/kg per min
10 mg/250 mL Pure 0 ++++ 0 Decrease Reflex bradycardia, headache, restlessness, excitability,
rarely arrhythmias; ideal for patients in shock with tachycardia or supraventricular arrhythmias
Ephedrine 5–25 mg and +++ ++ + Increases Causes palpitations, hypertension, cardiac
arrhythmias, an indirect-acting CNS stimulant; limited long-term value as therapy for shock.
Vasopressin 0.01–0.04 units per min
200 units/250 mL ++++ Primarily vasoconstriction, outcome data from its use is lacking;
infusions of 0.04 units per min may lead to adverse, vasoconstriction-mediated events
Epinephrine 0.01–0.75 g/kg per min
1 mg/250 mL and ++++ at 0.03–0.15 g/kg per min ++++ at 0.15–0.30 g/kg per min +++
Increases Causes tachydysrhythmia, leukocytosis, increases myocardial oxygen consumption
Dobutamine 2.0–20 g/kg per min
250 mg/250 mL 1, some 2 and 1 in large dosages
++++ + ++ Increase Causes tachydysrhythmia, occasional GI distress, increases myocardial
oxygen consumption, hypotension in volume depleted patient; has less peripheral
vasoconstriction than dopamine, can cause fewer arrhythmias than isoproterenol
Isoproterenol 0.01–0.05 g/kg per min
1 mg/250 mL 1 and some 2
++++ 0 ++++ Increases Causes tachydysrhythmia, facial flushing, hypotension in hypovolemic
patients; increases myocardial oxygen consumption; never use alone in shock.
Note: 0 = no effect, += mild effect, ++= moderate effect, +++= marked effect, ++++= very
marked effect.
Abbreviations: CNS = central nervous system; GI = gastrointestinal.
*Individual drugs may be diluted in D5W or NS, and may be diluted in larger volumes or
concentrated into smaller volumes according to the fluid needs of the individual patient.
The use of vasopressors is accompanied with potential pitfalls. While improving perfusion
pressure in the large vessels, they may decrease capillary blood flow in certain tissue beds,
especially the bowel. Vasopressors also may alter the relationship between volume and pressure
measurements through their effect on the pulmonary and peripheral vascular beds. In other
words, vasopressors will falsely elevate intracardiac filling pressures (i.e., CVP). They should be
used judiciously, generally only after volume resuscitation. When multiple vasopressors are
used, they should be simplified as soon as the best therapeutic agent is identified.
Assuring Adequate Oxygen Delivery
Once blood pressure is stabilized through optimization of preload and afterload, DO2 can be
assessed and further manipulated. Arterial oxygen saturation should be returned to physiologic
levels (93 to 95 percent) and hemoglobin maintained above 10 g/dL.13 If cardiac output can be
assessed, it should be increased by using volume infusion and inotropic agents in incremental
amounts until venous oxygen saturation (SmvO2 or ScvO2) and lactate are normalized.
The control of VO2 is important in restoring the balance of oxygen supply and demand to
tissues. A hyperadrenergic state results from the compensatory response to shock, physiologic
stress, pain, and anxiety. Shivering frequently results when a patient is unclothed for examination
and then left inadequately covered in a cold resuscitation room. The combination of these
variables increases systemic oxygen consumption. Pain further suppresses myocardial function,
thus impairing DO2 and VO2. Providing analgesia, muscle relaxation, warm covering,
anxiolytics, and even paralytic agents, when appropriate, decreases this inappropriate VO2.
Tissue oxygen extraction assesses adequacy of the resuscitation in meeting the oxygen needs of
the tissues. Sequential examination of lactate and SmvO2 or ScvO2 is a method to assess
adequacy of tissue oxygen extraction. Continuous measurement of SmvO2 or ScvO2 through
fiberoptic technology can be used in the ED.4 A variety of other technologies have potential to
assess tissue perfusion during resuscitation (Table 30-6).14–17
Table 30-6 Adjuncts in Assessing Tissue Perfusion
Base deficit Base deficit is an indicator of metabolic acidosis and is an index of hemodynamic
and tissue perfusion changes in shock. Predicts illness severity in intraabdominal hemorrhage
and blunt trauma.
Invasive blood pressure monitoring Intensive vasoconstriction caused by sympathetic activity or
vasopressors given will cause the cuff pressure to underestimate true blood pressure. A Doppler
may be used in conjunction with a sphygmomanometer may enable more accurate measure of
systolic blood pressure once Korotkoff sound are no longer audible. Intra-arterial pressure
measurement is preferable because vasoactive drugs may cause rapid swings in blood pressure
and multiple blood samplings will typically be required.
Central venous pressure (CVP) Aids in assessing volume status. Preferred for the long-term
administration of vasopressor therapy and provides rapid access to the heart if pacemaker
placement is required. May not reliably reflect the left ventricular filling pressure in clinical
states such as pulmonary embolus, obstructive airway disease, right ventricular infarction, and
pericardial effusion. Common iliac venous pressure can approximate CVP.
Central venous oximetry (ScvO2)
ScvO2 closely approximates mixed venous O2 saturation (SmVO2) and can be monitored
continuously using infrared oximetry. This technology enables the clinician to detect clinically
unrecognized tissue global tissue hypoperfusion in the treatment of myocardial infarction,
general medical shock, trauma, hemorrhage, septic, hypovolemic, end-stage heart failure, and
cardiogenic shock during and after cardiopulmonary arrest.
Arterial-central venous CO2 difference
Increased arterial-mixed venous carbon dioxide gradients or (a-v)CO2 are seen in acute
circulatory failure, and inversely correlate with the cardiac index (CI).
Pulmonary artery catheterization The standard of care for assessing cardiac status. Valuable in
determining left-sided heart filling, pulmonary artery pressure, and assessing the cause of
pulmonary edema. Can obtain cardiac output and mixed venous oxygen saturation. Will be able
to calculate hemodynamic (i.e., SVR) and oxygen transport variables (VO2 and DO2). The
effectiveness of this monitoring technique on improving outcome is challenged.
Noninvasive cardiac output Cardiac output can be measured by transesophageal Doppler,
cutaneous bioimpedance, and lithium dilution.
Gastric tonometry and sublingual capnography Serial measurements of gastric and sublingual
mucosal blood flow are based on hydrogen ion diffusion and carbon dioxide elimination.
Inadequate visceral perfusion as evidenced by persistently low intramucosal pH or increased
sublingual carbon dioxide concentration after resuscitation is associated with subsequent organ
dysfunction and death.
Retinal venous O2 saturation
Retinal venous O2 saturation (SrvO2) correlates with blood volume, central venous O2
saturation and arterial O2 saturation.
Metabolic cart Directly measured VO2 without a pulmonary artery catheter. A reduction in VO2
(after acute myocardial infarction) predicts cardiogenic shock and mortality after human cardiac
arrest.
Achieving End Points of Resuscitation
Traditional end points have been normalization of blood pressure, heart rate, and urine output.
Because these underestimate the degree of remaining hypoperfusion and oxygen debt, more
physiologic end points have been investigated (Tables 30-7 and 30-8).18 No therapeutic end
point is universally effective, and only a few have been tested in prospective trials, with mixed
results.18 The goal of resuscitation is to maximize survival and minimize morbidity using
objective hemodynamic and physiologic values to guide therapy. A goal-directed approach at
achieving urine output >0.5 mL/kg per h, CVP 8 to12 mm Hg, MAP 65 to 90 mm Hg, and
ScvO2 >70 percent during ED resuscitation of septic shock significantly decreases mortality.9
Table 30-7 End Points of Resuscitation
Traditional: normalization of blood pressure, pulse, and urine output
Restoration of circulating volume
Restoration of all fluid compartments
Vascular space is "full"
Hemodynamic parameters are "normalized"
Tissue oxygen delivery is maximized
Restoration of aerobic metabolism, elimination of tissue acidosis, and repayment of oxygen debt
Table 30-8 Hemodynamic Resuscitation End Points
Modality Goals
Preload CVP 10–12 mm Hg
PAOP 12–18 mm Hg
Afterload MAP 90–100 mm Hg
SVR = (MAP – CVP/CO)(80) 800–1400 dyne s/cm5
Contractility CO 5.0 L/min
CI 2.5–4.5 L per min m2
SV = CO/heart rate 50–60 mL per min
Heart rate 60–100 bpm Avoid >100 bpm; this will decrease SV and increase myocardial oxygen
consumption
Coronary perfusion pressure CPP = DBP – CVP (or PAOP) >60 mm Hg
Tissue oxygenation ScvO2 or SmvO2
>70%
Serum lactate <2 mM/L
Note: See Table 30-1 for abbreviation definitions.
Abbreviation: bpm = beats per min.
Troubleshooting a Persistently Hypotensive Patient
Treatment of a persistently hypotensive patient after maximal therapy can be a harrowing
experience. Similar principles apply to both the trauma patient with ongoing hemorrhage and the
persistently hypotensive medical patient. Issues to keep in mind include the following:(1) Is the
patient appropriately monitored?7 (2) Is there malfunctioning arterial blood pressure monitoring,
such as dampening of the arterial line or disconnection from the transducer? (3) Is the patient
adequately volume resuscitated? (4) Does the early use of vasopressor falsely elevate CVP and
disguise hypovolemia? (5) Is the intravenous tubing into which the vasopressors are running
connected appropriately? (6) Are the vasopressor infusion pumps working? (7) Are the
vasopressors mixed adequately? (8) Does the patient have a pneumothorax after placement of
central venous access? (9) Has the patient been adequately assessed for an occult penetrating
injury (a bullet hole or stab wound)? (10) Is there hidden bleeding from a ruptured spleen or
ectopic pregnancy? (11) Does the patient have adrenal insufficiency? The incidence of adrenal
dysfunction can be as high as 30 percent in this subset of patients.19 (12) Is the patient allergic to
the medication just given (e.g., penicillin) or taken before arrival? (13) Is there cardiac
tamponade in the chronic renal failure patient on dialysis or cancer patient?
Bicarbonate Use in Shock
The primary treatment of acidosis in shock is to reverse the underlying cause. Because this goal
is not rapidly attainable, intravenous bicarbonate is often administered. The rationale for giving
bicarbonate is that it will diminish myocardial depression and counteract the insensitivity to
endogenous catecholamines attributed to acidosis, but experimental data indicate that exogenous
bicarbonate can actually worsen intracellular acidosis, and prospective studies have not shown
benefit. Bicarbonate also shifts the oxygen-hemoglobin dissociation curve to the left and impairs
tissue unloading of hemoglobin-bound oxygen. However, many clinicians remain uncomfortable
withholding bicarbonate, which has created disparate opinions in the medical literature. A
compromise is to partially correct the metabolic acidosis over time. The bicarbonate deficit is
determined, which is equal to (normal HCO3 minus the patient's HCO3) x 0.5 x body weight
(kilograms). One-half of this amount is infused slowly and the remainder over 6 to 8 h.
Additional bicarbonate should be withheld once arterial pH is 7.25 or greater.
Disposition and Transition to the Intensive Care Unit
Documentation and communication are important. Resuscitation in the ED is commonly
performed in "ordered chaos." Even though resuscitation is systematic and thoughtful,
miscommunication with the intensivist or subspecialist accepting the patient can undo the
benefits of initial treatment. A system-oriented problem list with an assessment and plan,
including all procedures and complications, should be verbally communicated and written or
dictated prior to transfer. For prolonged ED stays, notations regarding patient status, diagnostic
and therapeutic intervention, and sentinel events should be provided frequently.
Prognosis
Outcome prediction at ED disposition has not been fully studied; however, some clinical
variables are associated with poor outcome, such as severity of shock, temporal duration,
underlying cause, preexisting vital organ dysfunction and reversibility. Direct noninvasive
measurement of VO2 is predictive of outcome in patients who developed cardiogenic shock
secondary to myocardial infarction and after cardiac arrest.8 Persistent elevated lactate levels are
prognostic in trauma, septic shock, and after cardiac arrest.8 Base deficit is also correlated with
the development of multisystem organ failure in trauma.20 Elevated sublingual partial pressure
of carbon dioxide (PCO2) is associated with increased mortality.14 Outcome predictions using
physiologic scoring systems in the ED are also being studied.8
References
1. McCaig LF, Ly N: National hospital ambulatory medical care survey: 2000 emergency
department summary. Advance Data from Vital and Health Statistics; No. 326. Hyattsville, MD,
National Center for Health Statistics, April 22, 2002.
2. Moscucci M, Bates ER: Cardiogenic shock. Cardiol Clin 13:391, 1995. [PMID: 7585775]
3. Angus DC, Linde-Zwirble WT, Lidicker J, et al: Epidemiology of severe sepsis in the United
States: Analysis of incidence, outcome, and associated costs of care. Crit Care Med 29:1303,
2001. [PMID: 11445675]
4. Rivers EP, Ander DS, Powell D: Central venous oxygen saturation monitoring in the critically
ill patient. Curr Opin Crit Care 7:204, 2001. [PMID: 11436529]
5. American College of Chest Physicians/Society of Critical Care Medicine consensus
conference: Definitions for sepsis and organ failure and guidelines for the use of innovative
therapies in sepsis. Crit Care Med 20:864, 1992.
6. Karimova A, Pinsky DJ: The endothelial response to oxygen deprivation: Biology and clinical
implications. Intensive Care Med 27:19, 2001. [PMID: 11280633]
7. Boldt J: Clinical review: Hemodynamic monitoring in the intensive care unit. Crit Care 6:52,
2002. [PMID: 11940266]
8. Nguyen HB, Rivers EP, Havstad S, et al: Critical care in the emergency department: A
physiologic assessment and outcome evaluation. Acad Emerg Med 7:1354, 2000. [PMID:
11099425]
9. Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of severe
sepsis and septic shock. New Engl J Med 345:1368, 2001. [PMID: 11794169]
10. Webb AR: The appropriate role of colloids in managing fluid imbalance: A critical review of
recent meta-analytic findings. Crit Care 4(suppl 2):S26, 2000.
11. Reinhart K, Sakka SG, Meier-Hellmann A: Haemodynamic management of a patient with
septic shock. Eur J Anaesthesiol 17:6, 2000. [PMID: 10758438]
12. Forrest P: Vasopressin and shock. Anaesth Intensive Care 29:463, 2001. [PMID: 11669425]
13. Hebert PC, Wells G, Tweeddale M, et al: Does transfusion practice affect mortality in
critically ill patients? Transfusion Requirements in Critical Care (TRICC) Investigators and the
Canadian Critical Care Trials Group. Am J Respir Crit Care Med 155:1618, 1997. [PMID:
9154866]
14. Rackow EC, O'Neil P, Astiz ME, Carpati CM: Sublingual capnometry and indexes of tissue
perfusion in patients with circulatory failure. Chest 120:1633, 2001. [PMID: 11713146]
15. Rady MY, Rivers EP, Nowak RM: Resuscitation of the critically ill in the ED: Responses of
blood pressure, heart rate, shock index, central venous oxygen saturation and lactate. Ann Emerg
Med 14:218, 1996. [PMID: 8924150]
16. Lind L: Veno-arterial carbon dioxide and pH gradients and survival in critical illness. Eur J
Clin Invest 25:201, 1995. [PMID: 7781668]
17. Denninghoff KR, Smith MH, Hillman LW, et al: Retinal venous oxygen saturation correlates
with blood volume. Acad Emerg Med 5:577, 1998. [PMID: 9660283]
18. Porter JM, Ivatury RR: In search of the optimal end points of resuscitation in trauma patients:
A review. J Trauma 44:908, 1998. [PMID: 9603098]
19. Rivers EP, Blake HC, Dereczyk B, et al: Adrenal dysfunction in hemodynamically unstable
patients in the emergency department. Acad Emerg Med 6:626, 1999. [PMID: 10386680]
20. Rutherford EJ, Morris JA Jr, Reed GW, Hall KS: Base deficit stratifies mortality and
determines therapy. J Trauma 33:417, 1992. [PMID: 1404512]
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