Download 9 Critical Care Shock

CRITICAL CARE. SHOCK
1 ЯНВАРЯ 2016 Г.
VITEBSK STATE MEDICAL UNIVERSITY
Content
Shock. General consideration.................................................................................................................. 2
Pathophysiology .................................................................................................................................. 2
Etiology and Classification ................................................................................................................... 5
Symptoms and Signs............................................................................................................................ 7
Diagnosis ............................................................................................................................................. 7
Prognosis and Treatment .................................................................................................................... 9
General management...................................................................................................................... 9
Hemorrhagic shock ........................................................................................................................ 11
Distributive shock .......................................................................................................................... 11
Cardiogenic shock.......................................................................................................................... 12
Anaphylaxis............................................................................................................................................ 14
Spinal shock and Neurogenic Shock ...................................................................................................... 18
Sepsis and Septic Shock ......................................................................................................................... 22
Cardiogenic Shock ................................................................................................................................. 29
Bradycardia and atrioventricular block ................................................................................................. 36
Tachycardias .......................................................................................................................................... 44
Sources .................................................................................................................................................. 48
1
Shock. General consideration.
Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death.
Mechanisms may involve decreased circulating volume, decreased cardiac output, and
vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. Symptoms
include altered mental status, tachycardia, hypotension, and oliguria. Diagnosis is clinical,
including BP measurement and sometimes markers of tissue hypoperfusion (eg, blood lactate,
base deficit). Treatment is with fluid resuscitation, including blood products if necessary,
correction of the underlying disorder, and sometimes vasopressors.
Pathophysiology
The fundamental defect in shock is reduced perfusion of vital tissues. Once perfusion
declines and O2 delivery to cells is inadequate for aerobic metabolism, cells shift to anaerobic
metabolism with increased production of CO2 and accumulation of lactic acid. Cellular function
declines, and if shock persists, irreversible cell damage and death occur.
During shock, both the inflammatory and clotting cascades may be triggered in areas
of hypoperfusion. Hypoxic vascular endothelial cells activate WBCs, which bind to the
endothelium and release directly damaging substances (eg, reactive O2 species, proteolytic
enzymes) and inflammatory mediators (eg, cytokines, leukotrienes, tumor necrosis factor
[TNF]). Some of these mediators bind to cell surface receptors and activate nuclear factor
kappa B (NFκB), which leads to production of additional cytokines and nitric oxide (NO), a
potent vasodilator. Septic shock may be more proinflammatory than other forms of shock
because of the actions of bacterial toxins, especially endotoxin.
In septic shock, vasodilation of capacitance vessels leads to pooling of blood and
hypotension because of “relative” hypovolemia (ie, too much volume to be filled by the
existing amount of blood). Localized vasodilation may shunt blood past the capillary exchange
beds, causing focal hypoperfusion despite normal cardiac output and BP. Additionally, excess
NO is converted to peroxynitrite, a free radical that damages mitochondria and decreases ATP
production.
Blood flow to microvessels including capillaries is reduced even though large-vessel
blood flow is preserved in settings of septic shock. Mechanical microvascular obstruction may,
at least in part, account for such limiting of substrate delivery. Leukocytes and platelets adhere
to the endothelium, and the clotting system is activated with fibrin deposition.
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Multiple mediators, along with endothelial cell dysfunction, markedly increase microvascular
permeability, allowing fluid and sometimes plasma proteins to escape into the interstitial
space. In the GI tract, increased permeability possibly allows translocation of the enteric
bacteria from the lumen, potentially leading to sepsis or metastatic infection.
Neutrophil apoptosis may be inhibited, enhancing the release of inflammatory
mediators. In other cells, apoptosis may be augmented, increasing cell death and thus
worsening organ function.
BP is not always low in the early stages of shock (although hypotension eventually
occurs if shock is not reversed). Similarly, not all patients with “low” BP have shock. The degree
and consequences of hypotension vary with the adequacy of physiologic compensation and
the patient’s underlying diseases. Thus, a modest degree of hypotension that is well tolerated
by a young, relatively healthy person might result in severe cerebral, cardiac, or renal
dysfunction in an older person with significant arteriosclerosis.
Compensation
Initially, when O2 delivery (DO2) is decreased, tissues compensate by extracting a
greater percentage of delivered O2. Low arterial pressure triggers an adrenergic response with
sympathetic-mediated vasoconstriction
and often
increased heart
rate. Initially,
vasoconstriction is selective, shunting blood to the heart and brain and away from the
splanchnic circulation. Circulating β-adrenergic amines (epinephrine, norepinephrine) also
increase cardiac contractility and trigger release of corticosteroids from the adrenal gland,
renin from the kidneys, and glucose from the liver. Increased glucose may overwhelm ailing
mitochondria, causing further lactate production.
Reperfusion
Reperfusion of ischemic cells can cause further injury. As substrate is reintroduced,
neutrophil activity may increase, increasing production of damaging superoxide and hydroxyl
radicals. After blood flow is restored, inflammatory mediators may be circulated to other
organs.
Multiple organ dysfunction syndrome (MODS)
The combination of direct and reperfusion injury may cause MODS—the progressive
dysfunction of ≥ 2 organs consequent to life-threatening illness or injury. MODS can follow
any type of shock but is most common when infection is involved; organ failure is one of the
defining features of septic shock. MODS also occurs in > 10% of patients with severe traumatic
injury and is the primary cause of death in those surviving > 24 h.
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Any organ system can be affected, but the most frequent target organ is the lung, in
which increased membrane permeability leads to flooding of alveoli and further inflammation.
Progressive hypoxia may be increasingly resistant to supplemental O2 therapy. This condition
is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS—
see Acute Hypoxemic Respiratory Failure (AHRF, ARDS)).
The kidneys are injured when renal perfusion is critically reduced, leading to acute
tubular necrosis and renal insufficiency manifested by oliguria and progressive rise in serum
creatinine.
In the heart, reduced coronary perfusion and increased mediators (including TNF and
IL-1) may depress contractility, worsen myocardial compliance, and down-regulate βreceptors. These factors decrease cardiac output, further worsening both myocardial and
systemic perfusion and causing a vicious circle often culminating in death. Arrhythmias may
occur.
In the GI tract, ileus and submucosal hemorrhage can develop. Liver hypoperfusion can
cause focal or extensive hepatocellular necrosis, transaminase and bilirubin elevation, and
decreased production of clotting factors.
Figure 1. Compensation in shock
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Etiology and Classification
There are several mechanisms of organ hypoperfusion and shock. Shock may be due
to a low circulating volume (hypovolemic shock), vasodilation (distributive shock), a primary
decrease in cardiac output (both cardiogenic and obstructive shock), or a combination.
Hypovolemic shock
Hypovolemic shock is caused by a critical decrease in intravascular volume. Diminished
venous return (preload) results in decreased ventricular filling and reduced stroke volume.
Unless compensated for by increased heart rate, cardiac output decreases.
A common cause is bleeding (hemorrhagic shock), typically due to trauma, surgical
interventions, peptic ulcer, esophageal varices, or ruptured aortic aneurysm. Bleeding may be
overt (eg, hematemesis, melena) or concealed (eg, ruptured ectopic pregnancy).
Hypovolemic shock may also follow increased losses of body fluids other than blood
(Hypovolemic Shock Caused by Body Fluid Loss).
Hypovolemic Shock Caused by Body Fluid Loss
Site of Fluid Loss
Mechanism of Loss
Skin
Thermal or chemical burn, sweating due to excessive heat
exposure
GI tract
Vomiting, diarrhea
Kidneys
Diabetes mellitus or insipidus, adrenal insufficiency, salt-losing
nephritis, the polyuric phase after acute tubular damage, use of
potent diuretics
Intravascular fluid lost Increased capillary permeability secondary to inflammation or
to the extravascular traumatic injury (eg, crush), anoxia, cardiac arrest, sepsis, bowel
space
ischemia, acute pancreatitis
Hypovolemic shock may be due to inadequate fluid intake (with or without increased
fluid loss). Water may be unavailable, neurologic disability may impair the thirst mechanism,
or physical disability may impair access.
In hospitalized patients, hypovolemia can be compounded if early signs of circulatory
insufficiency are incorrectly ascribed to heart failure and fluids are withheld or diuretics are
given.
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Distributive shock
Distributive shock results from a relative inadequacy of intravascular volume caused
by arterial or venous vasodilation; circulating blood volume is normal. In some cases, cardiac
output (and DO2) is high, but increased blood flow through arteriovenous shunts bypasses
capillary beds; this bypass plus uncoupled cellular O2 transport cause cellular hypoperfusion
(shown by decreased O2 consumption). In other situations, blood pools in venous capacitance
beds and cardiac output falls.
Distributive shock may be caused by anaphylaxis (anaphylactic shock); bacterial
infection with endotoxin release (septic shock); severe injury to the spinal cord, usually above
T4 (neurogenic shock); and ingestion of certain drugs or poisons, such as nitrates, opioids, and
adrenergic blockers. Anaphylactic shock and septic shock often have a component of
hypovolemia as well.
Cardiogenic and obstructive shock
Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary
cardiac disorder. Obstructive shock is caused by mechanical factors that interfere with filling
or emptying of the heart or great vessels. Causes are listed in Mechanisms of Cardiogenic and
Obstructive Shock.
Mechanisms of Cardiogenic and Obstructive Shock
Type
Mechanism
Obstructive
Mechanical
Cause
interference Tension pneumothorax, cava compression,
with ventricular filling
Interference
cardiac tamponade, atrial tumor or clot
with Pulmonary embolism
ventricular emptying
Cardiogenic
Impaired
myocardial Myocardial ischemia or MI, myocarditis,
contractility
Abnormalities
drugs
of
cardiac Tachycardia, bradycardia
rhythm
Cardiac structural disorder
Acute
mitral
or
aortic
regurgitation,
ruptured interventricular septum, prosthetic
valve malfunction
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Symptoms and Signs
Lethargy, confusion, and somnolence are common. The hands and feet are pale, cool,
clammy, and often cyanotic, as are the earlobes, nose, and nail beds. Capillary filling time is
prolonged, and, except in distributive shock, the skin appears grayish or dusky and moist.
Overt diaphoresis may occur. Peripheral pulses are weak and typically rapid; often, only
femoral or carotid pulses are palpable. Tachypnea and hyperventilation may be present. BP
tends to be low (< 90 mm Hg systolic) or unobtainable; direct measurement by intra-arterial
catheter, if done, often gives higher and more accurate values. Urine output is low.
Distributive shock causes similar symptoms, except the skin may appear warm or
flushed, especially during sepsis. The pulse may be bounding rather than weak. In septic shock,
fever, usually preceded by chills, is typically present. Some patients with anaphylactic shock
have urticaria or wheezing.
Numerous other symptoms (eg, chest pain, dyspnea, abdominal pain) may be due to
the underlying disease or secondary organ failure.
Diagnosis
Diagnosis is mostly clinical, based on evidence of insufficient tissue perfusion
(obtundation, oliguria, peripheral cyanosis) and signs of compensatory mechanisms
(tachycardia, tachypnea, diaphoresis). Specific criteria include obtundation, heart rate > 100,
respiratory rate > 22, hypotension (systolic BP < 90 mm Hg) or a 30-mm Hg fall in baseline BP,
and urine output < 0.5 mL/kg/h.
Laboratory findings that support the diagnosis include lactate > 3 mmol/L, base
deficit < −4 mEq/L, and PaCO2< 32 mm Hg. However, none of these findings alone is diagnostic,
and each is evaluated by its trend (ie, worsening or improving) and in the overall clinical
context, including physical signs. Recently, measurement of sublingual PCO2 and near-infrared
spectroscopy have been introduced as noninvasive and rapid techniques that may measure
the degree of shock; however, these techniques have yet to be validated on a larger scale.
Diagnosis of cause
Recognizing the cause of shock is more important than categorizing the type. Often,
the cause is obvious or can be recognized quickly based on the history and physical
examination, aided by simple testing.
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Chest pain (with or without dyspnea) suggests MI, aortic dissection, or pulmonary
embolism. A systolic murmur may indicate ventricular septal rupture or mitral insufficiency
due to acute MI. A diastolic murmur may indicate aortic regurgitation due to aortic dissection
involving the aortic root. Cardiac tamponade is suggested by jugular venous distention,
muffled heart sounds, and a paradoxical pulse. Pulmonary embolism severe enough to cause
shock typically produces decreased O2 saturation and occurs more often in special settings,
including prolonged bed rest and after a surgical procedure. Tests include ECG, troponin I,
chest x-ray, ABGs, lung scan, helical CT, and echocardiography.
Abdominal or back pain or a tender abdomen suggests pancreatitis, ruptured
abdominal aortic aneurysm, peritonitis, and, in women of childbearing age, ruptured ectopic
pregnancy. A pulsatile midline mass suggests ruptured abdominal aortic aneurysm. A tender
adnexal mass suggests ectopic pregnancy. Testing typically includes abdominal CT (if the
patient is unstable, bedside ultrasound can be helpful), CBC, amylase, lipase, and, for women
of childbearing age, urine pregnancy test.
Fever, chills, and focal signs of infection suggest septic shock, particularly in
immunocompromised patients. Isolated fever, contingent on history and clinical settings, may
point to heatstroke. Tests include chest x-ray; urinalysis; CBC; and cultures of wounds, blood,
urine, and other relevant body fluids.
In a few patients, the cause is occult. Patients with no focal symptoms or signs
indicative of cause should have ECG, cardiac enzymes, chest x-ray, and ABGs. If results of these
tests are normal, the most likely causes include drug overdose, occult infection (including toxic
shock), anaphylaxis, and obstructive shock.
Ancillary testing
If not already done, ECG, chest x-ray, CBC, serum electrolytes, BUN, creatinine, PT, PTT,
liver function tests, and fibrinogen and fibrin split products are done to monitor patient status
and serve as a baseline. If the patient’s volume status is difficult to determine, monitoring of
central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) may be useful.
CVP < 5 mm Hg (< 7 cm H2O) or PAOP < 8 mm Hg may indicate hypovolemia, although CVP
may be greater in hypovolemic patients with preexisting pulmonary hypertension. Rapid
bedside echocardiography (done by the treating physician) to assess adequacy of cardiac
filling and function is being increasingly used to assess shock.
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Prognosis and Treatment
Untreated shock is usually fatal. Even with treatment, mortality from cardiogenic shock
after MI (60 to 65%) and septic shock (30 to 40%) is high. Prognosis depends on the cause,
preexisting or complicating illness, time between onset and diagnosis, and promptness and
adequacy of therapy.
General management
First aid involves keeping the patient warm. External hemorrhage is controlled, airway
and ventilation are checked, and respiratory assistance is given if necessary. Nothing is given
by mouth, and the patient’s head is turned to one side to avoid aspiration if emesis occurs.
Treatment begins simultaneously with evaluation. Supplemental O2 by face mask is
provided. If shock is severe or if ventilation is inadequate, airway intubation with mechanical
ventilation is necessary. Two large (14- to 16-gauge) IV catheters are inserted into separate
peripheral veins. A central venous line or an intraosseous needle, especially in children,
provides an alternative when peripheral veins cannot promptly be accessed.
Typically, 1 L (or 20 mL/kg in children) of 0.9% saline is infused over 15 min. In major
hemorrhage, Ringer’s lactate is commonly used. Unless clinical parameters return to normal,
the infusion is repeated. Smaller volumes (eg, 250 to 500 mL) are used for patients with signs
of high right-sided pressure (eg, distention of neck veins) or acute MI. A fluid challenge should
probably not be done in a patient with signs of pulmonary edema. Further fluid therapy is
based on the underlying condition and may require monitoring of CVP or PAOP. Bedside
cardiac ultrasonography to assess contractility and vena cava respiratory variability may help
determine the need for additional fluid vs the need for inotropic support.
Patients in shock are critically ill and should be admitted to an ICU. Monitoring includes
ECG; systolic, diastolic, and mean BP, preferably by intra-arterial catheter; respiratory rate and
depth; pulse oximetry; urine flow by indwelling bladder catheter; body temperature; and
clinical status, including sensorium (eg, Glasgow Coma Scale), pulse volume, skin temperature,
and color. Measurement of CVP, PAOP, and thermodilution cardiac output using a balloontipped pulmonary arterial catheter may be helpful for diagnosis and initial management of
patients with shock of uncertain or mixed etiology or with severe shock, especially when
accompanied
by
oliguria
or
pulmonary
edema.
Echocardiography
(bedside
or
transesophageal) is a less invasive alternative. Serial measurements of ABGs, Hct, electrolytes,
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serum creatinine, and blood lactate are obtained. Sublingual CO2 measurement, if available,
is a noninvasive monitor of visceral perfusion. A well-designed flow sheet is helpful.
Because tissue hypoperfusion makes intramuscular absorption, unreliable, all
parenteral drugs are given IV. Opioids generally are avoided because they may cause
vasodilation, but severe pain may be treated with morphine 1 to 4 mg IV given over 2 min and
repeated q 10 to 15 min if necessary. Although cerebral hypoperfusion may cause anxiety,
sedatives or tranquilizers are not routinely given.
After initial resuscitation, specific treatment is directed at the underlying condition.
Additional supportive care is guided by the type of shock.
Figure 2. General managment
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Hemorrhagic shock
In hemorrhagic shock, surgical control of bleeding is the first priority. Volume
replacement (see also Intravenous Fluid Resuscitation) accompanies rather than precedes
surgical control. Blood products and crystalloid solutions are used for resuscitation; however,
packed RBCs and plasma are being considered earlier and in a ratio of 1:1 in patients likely to
require massive transfusion. Failure to respond usually indicates insufficient volume
administration or unrecognized ongoing hemorrhage. Vasopressor agents are not indicated
for treatment of hemorrhagic shock unless cardiogenic, obstructive, or distributive causes are
also present.
Distributive shock
Distributive shock with profound hypotension after initial fluid replacement with 0.9%
saline
may
be
treated
with
inotropic
or
vasopressor
agents
(eg, dopamine, norepinephrine— Inotropic and Vasoactive Catecholamines). Patients with
septic shock also receive broad-spectrum antibiotics (see later). Patients with anaphylactic
shock unresponsive to fluid challenge (especially if accompanied by bronchoconstriction)
receive epinephrine 0.05 to 0.1 mg IV, followed by epinephrine infusion of 5 mg in 500 mL 5%
D/W at 10 mL/h or 0.02 mcg/kg/min (see later).
Inotropic and Vasoactive Catecholamines
Drug
Dosage
Hemodynamic Actions
Norepinephrine 4 mg/250 mL or 500 mL 5% D/W α-Adrenergic: Vasoconstriction
continuous IV infusion at 8–12 β-Adrenergic:
mcg/min
initially,
then
at
Inotropic
and
2–4 chronotropic effects*
mcg/min as maintenance, with wide
variations
Dopamine
400 mg/500 mL 5% D/W continuous α-Adrenergic: Vasoconstriction
IV infusion at 0.3–1.25 mL (250–1000 βAdrenergic:
Inotropic
and
mcg)/min 2–10 mcg/kg/min for low chronotropic
effects
and
dose 20 mcg/kg/min for high dose
Nonadrenergic:
vasodilation
Renal
and
splanchnic
vasodilation
Dobutamine
250 mg/250 mL 5% D/W continuous β-Adrenergic: Inotropic effects
IV infusion at 2.5–10 mcg/kg/min
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***
*Effects are not apparent if arterial pressure is elevated too much.
**Effects depend on dosage and underlying pathophysiology.
***Chronotropic, arrhythmogenic, and direct vascular effects are minimal at lower doses.
Cardiogenic shock
In cardiogenic shock, structural disorders (eg, valvular dysfunction, septal rupture) are
repaired surgically. Coronary thrombosis is treated either by percutaneous interventions
(angioplasty, stenting), coronary artery bypass surgery, or thrombolysis. Tachydysrhythmia
(eg, rapid atrial fibrillation, ventricular tachycardia) is slowed by cardioversion or with drugs.
Bradycardia is treated with a transcutaneous or transvenous pacemaker; atropine 0.5 mg IV
up to 4 doses q 5 min may be given pending pacemaker placement. Isoproterenol (2 mg/500
mL 5% D/W at 1 to 4 mcg/min [0.25 to 1 mL/min]) is occasionally useful if atropine is
ineffective, but it is not advised in patients with myocardial ischemia due to coronary artery
disease.
Shock after acute MI is treated with volume expansion if PAOP is low or normal; 15 to
18 mm Hg is considered optimal. If a pulmonary artery catheter is not in place, cautious
volume infusion (250- to 500-mL bolus of 0.9% saline) may be tried while auscultating the
chest frequently for signs of fluid overload. Shock after right ventricular MI usually responds
partially to volume expansion; however, vasopressor agents may be needed. Bedside cardiac
ultrasonography to assess contractility and vena caval respiratory variability can help
determine the need for additional fluid vs vasopressors; inotropic support is a better approach
for patients with normal or above-normal filling.
If hypotension is moderate (eg, mean arterial pressure [MAP] 70 to 90 mm
Hg), dobutamine infusion may be used to improve cardiac output and reduce left ventricular
filling
pressure.
Tachycardia
and
arrhythmias
occasionally
occur
during dobutamine administration, particularly at higher doses, necessitating dose reduction.
Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacitance or lower
systemic vascular resistance, reduce the workload on the damaged myocardium and may
increase cardiac output in patients without severe hypotension. Combination therapy
(eg, dopamine or dobutamine with nitroprusside or nitroglycerin) may be particularly useful
but requires close ECG and pulmonary and systemic hemodynamic monitoring.
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For more serious hypotension (MAP < 70 mm Hg), norepinephrine or dopamine may
be given, with a target systolic pressure of 80 to 90 mm Hg (and not > 110 mm Hg). Intra-aortic
balloon counterpulsation is valuable for temporarily reversing shock in patients with acute MI.
This procedure should be considered as a bridge to permit cardiac catheterization and
coronary angiography before possible surgical intervention in patients with acute MI
complicated by ventricular septal rupture or severe acute mitral regurgitation who require
vasopressor support for >30 min.
In obstructive shock, nontraumatic cardiac tamponade requires immediate
pericardiocentesis, which can be done at the bedside. Trauma-related cardiac tamponade
requires surgical decompression and repair. Tension pneumothorax should be immediately
decompressed with a catheter inserted into the 2nd intercostal space, midclavicular line; a
chest tube is then inserted. Massive pulmonary embolism resulting in shock is treated with
anticoagulation and thrombolysis, surgical embolectomy, or extracorporeal membrane
oxygenation in select cases.
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Anaphylaxis
Anaphylaxis is an acute, potentially life-threatening, IgE-mediated allergic reaction that
occurs in previously sensitized people when they are reexposed to the sensitizing antigen.
Symptoms can include stridor, dyspnea, wheezing, and hypotension. Diagnosis is clinical.
Treatment is with epinephrine. Bronchospasm and upper airway edema may require inhaled
or injected β-agonists and sometimes endotracheal intubation. Persistent hypotension
requires IV-fluids and sometimes vasopressors.
Etiology
Anaphylaxis is typically triggered by
 Drugs (eg, β-lactam antibiotics, insulin, streptokinase, allergen extracts)
 Foods (eg, nuts, eggs, seafood)
 Proteins (eg, tetanus antitoxin, blood transfusions)
 Animal venoms
 Latex
Peanut and latex allergens may be airborne. Occasionally, exercise or cold exposure
(eg, in patients with cryoglobulinemia) can trigger or contribute to an anaphylactic reaction.
History of atopy does not increase risk of anaphylaxis but increases risk of death when
anaphylaxis occurs.
Pathophysiology
Interaction of antigen with IgE on basophils and mast cells triggers release of
histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction
(eg, resulting in bronchoconstriction, vomiting, or diarrhea) and vasodilation with plasma
leakage (eg, resulting in urticaria or angioedema).
Anaphylactoid reactions
These reactions are clinically indistinguishable from anaphylaxis but do not involve IgE
and do not require prior sensitization. They occur via direct stimulation of mast cells or via
immune complexes that activate complement. The most common triggers are iodinated
radiopaque dye, aspirin, other NSAIDs, opioids, blood transfusions, Ig, and exercise.
Symptoms and Signs
Symptoms typically begin within 15 min of exposure and involve the skin, upper or
lower airways, cardiovascular system, or GI tract. One or more areas may be affected, and
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symptoms do not necessarily progress from mild (eg, urticaria) to severe (eg, airway
obstruction, refractory shock), although each patient typically manifests the same reaction to
subsequent exposure. Symptoms range from mild to severe and include flushing, pruritus,
urticaria, sneezing, rhinorrhea, nausea, abdominal cramps, diarrhea, a sense of choking or
dyspnea, palpitations, and dizziness. Signs include hypotension, tachycardia, urticaria,
angioedema, wheezing, stridor, cyanosis, and syncope.
Shock can develop within minutes, and patients may have seizures, become
unresponsive, and die. Cardiovascular collapse can occur without respiratory or other
symptoms. Late-phase reactions may occur 4 to 8 h after the exposure or later. Symptoms and
signs are usually less severe than they were initially and may be limited to urticaria; however,
they may be more severe or fatal.
Diagnosis
Diagnosis is clinical. Anaphylaxis should be suspected if any of the following suddenly
occur without explanation:
 Shock
 Respiratory symptoms (eg, dyspnea, stridor, wheezing)
 Two or more other manifestations of possible anaphylaxis (eg, angioedema,
rhinorrhea, GI symptoms)
Risk of rapid progression to shock leaves no time for testing, although mild equivocal
cases can be confirmed by measuring 24-h urinary levels of N -methylhistamine or serum
levels of tryptase. The cause is usually easily recognized based on history.
Treatment
 Epinephrine given immediately
 Sometimes intubation IV fluids and sometimes vasopressors for persistent
hypotension
 Antihistamines
 Inhaled β-agonists for bronchoconstriction
Epinephrine is the cornerstone of treatment; it may help relieve all symptoms and
signs and should be given immediately. It can be given sc or IM (usual dose is 0.3 to 0.5 mL of
a 1:1000 [0.1%] solution in adults or 0.01 mL/kg in children, repeated every 10 to 30 min).
Maximal absorption occurs when the drug is given IM in the lateral thigh. Patients with
cardiovascular collapse or severe airway obstruction may be given epinephrine IV in a single
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dose (3 to 5 mL of a 1:10,000 [0.01%] solution over 5 min) or by continuous drip (1 mg in 250
mL 5% D/W for a concentration of 4 mcg/mL, starting at 1 mcg/min and titrated up to 4
mcg/min [15 to 60 mL/h]). Epinephrine may also be given by sublingual injection (0.5 mL of
1:1000 solution) or through an endotracheal tube (3 to 5 mL of a 1:10,000 solution diluted to
10 mL with saline). A second injection of epinephrine sc may be needed.
Glucagon 1-mg bolus (20 to 30 mcg/kg in children) followed by 1-mg/h infusion should
be used in patients taking oral β-blockers, which attenuate the effect of epinephrine.
Patients who have stridor and wheezing unresponsive to epinephrine should be given
O2 and be intubated. Early intubation is recommended because waiting for a response to
epinephrine may allow upper airway edema to progress sufficiently to prevent endotracheal
intubation and require cricothyrotomy.
Hypotension often resolves after epinephrine is given. Persistent hypotension can
usually be treated with 1 to 2 L (20 to 40 mL/kg in children) of isotonic IV fluids (eg, 0.9%
saline). Hypotension refractory to fluids and IV epinephrine may require vasopressors (eg,
dopamine 5 mcg/kg/min).
Antihistamines—both H1 blockers (eg, diphenhydramine 50 to 100 mg IV) and H2
blockers (eg, cimetidine 300 mg IV)—should be given q 6 h until symptoms resolve. Inhaled βagonists are useful for managing bronchoconstriction that persists after treatment with
epinephrine; albuterol 5 to 10 mg by continuous nebulization can be given.
Corticosteroids have no proven role but may help prevent a late-phase reaction;
methylprednisolone 125 mg IV initially is adequate.
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Figure 3. Poster Anaphylaxis Treatment. ERC
17
Spinal shock and Neurogenic Shock
Neurogenic shock is a type of distributive shock that describes the sudden loss of
autonomic tone due to spinal cord injury often characterized by hypotension and relative
bradycardia. Loss of sympathetic tone occurs with injuries above T6 and results in decreased
systemic vascular resistance. Peripheral vasoconstrictors, chronotropes, and inotropes may
be needed in cases of neurogenic shock. Autonomic instability may develop and often persists
several weeks after the injury. Aggressive management is imperative in the initial phases of
neurogenic shock to avoid further secondary ischemic injury to the cord.
Neurogenic shock describes the sudden loss of autonomic tone due to spinal cord
injury (SCI). Disruption of the descending sympathetic pathways results in unopposed vagal
tone in the vascular smooth muscle, causing decreased systemic vascular resistance and
vasodilation. The hypotension that results from neurogenic shock places patients at increased
risk of secondary spinal cord ischemia due to impairment of autoregulation. Though the terms
are sometimes used interchangeably, neurogenic shock describes the hemodynamic changes
following SCI, whereas spinal shock is characterized by a reversible reduction of sensory,
motor, or reflex function of the spinal cord below the level of injury(see later).
Neurogenic shock is a type of distributive shock, but should be a diagnosis of exclusion
in the early phases of traumatic resuscitation after hemorrhagic shock is ruled out. There is
no definitive diagnostic test, but classically patients exhibit hypotension and relative
bradycardia. The bradycardia is often exacerbated by suctioning, defecation, turning, and
hypoxia. The skin is often warm and flushed initially. Hypothermia may develop because of
profound vasodilation and heat loss. Often the central venous pressure is low due to
decreased systemic vascular resistance. Thus, patients with SCI must be monitored closely for
the development of neurogenic shock even if it is not present on presentation.
The loss of sympathetic tone, and thus neurogenic shock, is most common when the
level of the injury is above T6. Moreover, neurogenic shock may occur anytime after the onset
of injury or illness, ranging from the time of presentation to several weeks after presentation.
However, reports indicate anywhere from 50-90% of adults with cervical SCI require fluid
resuscitation and vasoactive infusions to achieve the adult parameters recommended (MAP
>85-90 mm Hg for 7 days) by the Congress of Neurological Surgeons’ guidelines for
management of SCI.
18
Adults with higher SCI (C1-C5) may be more likely to require cardiovascular
interventions, such as vasoactive agents or cardiac pacing, than lower (C6-C7) SCI.
Decreased systemic vascular resistance results in a relative hypovolemia due to
increased venous capacity, and isotonic fluid administration is often necessary. However,
hypotension due to neurogenic shock is often refractory to fluid resuscitation. Nevertheless,
hypotension in a trauma patient cannot be assumed to be due to neurogenic shock initially,
and could be a sign of hemorrhagic shock. Thus, trauma victims with hypotension should be
treated initially with crystalloid (0.9% sodium chloride, ringer’s lactate) or colloid (albumin,
blood products) fluids and evaluated for any ongoing blood loss. Patients should be
adequately resuscitated from a hemodynamic perspective before undergoing operative spinal
cord decompression. Hypotension must be treated immediately in order to avoid secondary
ischemic SCI. Cervical SCI is often seen in patients who also have traumatic brain injury and
hypotension cannot be tolerated in the setting of traumatic brain injury either.
Mannitol should be avoided if shock is present in patients with suspected traumatic
brain and spinal cord injury, as hypertonic saline is now recommended as first-line
osmotherapy agent in pediatric severe traumatic brain injury. If hypotensive patients have
normal chronotropy and inotropy, then a α1-agonist acting as a peripheral vasoconstrictor
such as phenylephrine is indicated. Norepinephrine may also be considered, as it has α1- and
β1-agonistic activity. Epinephrine and vasopressin infusions may be used in refractory cases
of hypotension. The evidence for the elevated MAP goal (MAP >85-90 mm Hg for 7 days) in
adults published by the Congress of Neurological Surgeons is weak.
If bradycardia is present, patients may respond to atropine, glycopyrrolate, or
vasoactive infusions with chronotropic, vasoconstrictor, and inotropic properties such as
dopamine or norepinephrine. Also, isoproterenol may be considered if a strictly chronotropic
agent is needed. Phenylephrine can potentially cause reflex bradycardia, as there is no β
agonist activity, and should be used with caution in patients with bradycardia as part of their
neurogenic shock presentation. In rare cases, cardiac pacing has been successful however
since the cause of the bradycardia is neurochemical rather than electrophysiological, it may
be more prudent to use pharmacological treatments. If patients demonstrate particular
sensitivity to suctioning or positioning, one may consider giving atropine or glycopyrrolate
prior to manipulation.
19
Methylxanthines (theophylline, aminophylline) and propantheline have also been used
for refractory bradycardia. Sinus bradycardia is most common in patients with severe cervical
SCI, but patients may develop other dysrhythmias, including AV block, atrial fibrillation, or
even cardiac arrest.
Spinal Shock
Spinal shock following a spinal cord injury (SCI) is a specific term that relates to the loss
of all neurological activity below the level of injury. This loss of neurological activity include
loss of motor, sensory, reflex and autonomic function. Spinal shock is a short-term temporary
physiologic disorganisation of spinal cord function that can start between 30-60 minutes
following a spinal cord injury. Spinal shock can last up to six weeks post injury. Note that the
'shock' in spinal shock does not refer to circulatory collapse, and should not be confused
with neurogenic shock, which is life-threatening.
Mechanism for Spinal Shock
The mechanism for spinal shock involves the sudden loss of conduction in the spinal
cord as a result of the migration of potassium ions from the intracellular to extracellular
spaces. This is associated with a transient loss of somatic and automatic reflex activity below
the level of spinal cord segment damage. The spinal cord reflex arcs that are immediately
above the injury may also be severely disrupted.
Early Stages of Spinal Shock
Spinal shock following a spinal cord injury results in flaccid paralysis, areflexia and
anaesthesia below the level of injury. The return of the reflexes indicates the end of spinal
shock. Assessment of the end of spinal shock is based on the return of reflexes, with the
bulbocavernosus reflex typically being the first to return. However, some clinicians may
classify the end of spinal shock as the return of deep tendon reflexes or the return of reflexive
detrusor function, which may be months after injury.
Return of Reflexes Following Spinal Shock
Return of reflexes between 4-6 weeks post injury are characterised by hyper-reflexia,
or abnormally strong reflexes usually produced with minimal stimulation. Inter neurons and
lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The
first synapses to form are from shorter axons, usually from inter neurons - later changes are
soma-mediated, and will take longer for the soma to transport various growth factors,
including proteins, to the end of the axon.
20
Autonomic Effects of Spinal Shock. In spinal cord injuries in the thoracic spinal
segments of T6 and above, autonomic dysreflexia may occur, from the loss of autonomic
innervation from the brain. Sacral parasympathetics (S2-S4) are lost, as are many sympathetic
levels, depending on the level of the spinal cord injury. Cervical lesions cause total loss of
sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias – which
resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs with the return of
reflexes. Autonomic dysreflexia is characterised by unchecked sympathetic stimulation below
the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of
bladder/bowel control, sweating, headaches, and other sympathetic effects.
Updated guidelines issued in 2013 by the CNS and the American Association of
Neurological Surgeons (AANS) recommend against the use of steroids early after an acute SCI.
The guidelines recommend that methylprednisolone not be used for the treatment of acute
SCI within the first 24-48 hours following injury. The previous standard was revised because
of a lack of medical evidence supporting the benefits of steroids in clinical settings and
evidence that high-dose steroids are associated with harmful adverse effects. Nevertheless,
the administration of high-dose steroids within 8 hours of injury for all patients with acute
spinal cord injury is practiced by most physicians. The current recommendation is to treat all
patients with spinal cord injury according to the local/regional protocol. If steroids are
recommended, they should be initiated within 8 hours of injury with the following steroid
protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of
methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus.
21
Sepsis and Septic Shock
Sepsis is a systemic, deleterious host response to infection leading to severe sepsis
(acute organ dysfunction secondary to documented or suspected infection) and septic shock
(severe sepsis plus hypotension not reversed with fluid resuscitation). Severe sepsis and septic
shock are major healthcare problems, affecting millions of people around the world each year,
killing one in four (and often more), and increasing in incidence.
Sepsis is defined as the presence (probable or documented) of infection together with
systemic manifestations of infection. Severe sepsis is defined as sepsis plus sepsis-induced
organ dysfunction or tissue hypoperfusion. Sepsis-induced hypotension is defined as a systolic
blood pressure (SBP) < 90 mm Hg or mean arterial pressure (MAP) < 70 mm Hg or a SBP
decrease > 40 mm Hg or less than two standard deviations below normal for age in the
absence of other causes of hypotension. Septic shock is defined as sepsis-induced hypotension
persisting despite adequate fluid resuscitation. Sepsis-induced tissue hypoperfusion is defined
as infection-induced hypotension, elevated lactate, or oliguria.
Figure 4. Sepsis. Definitions and Criteria.
22
Pathophysiology of Sepsis
Sepsis is induced by an invasion of microorganisms or their toxins into the
bloodstream, together with the host response to this invasion.
Any infection may be complicated by sepsis. The innate immune system recognizes
specific molecular patterns associated with microorganisms called pathogen-associated
molecular patterns (PAMPs) that include cell wall products, exotoxins, bacterial DNA, and viral
RNA. The host’s innate immune system senses
the presence of microbial molecules by
specific receptors called pattern-recognition proteins (PRP), such as Toll-like receptors. An
excessive inflammatory response early in sepsis
is counteracted by an antiinflammatory
response, which may then result in hypoinflammation.
Hemostatic balance is shifted to a procoagulant state in sepsis due
to activation
of tissue factor and attenuation of natural anticoagulants. Sepsis causes endothelial
dysfunction. Cardiac dysfunction in sepsis is mainly due to intramyocardial nitric oxide
production and perhaps cardiac ischemia resulting in left ventricular diastolic dilatation and a
rightward shift of the Frank-Starling curve. Capillary leakage causes a large amount of
intravascular fluid to be shifted into the extravascular space resulting in significant
hypovolemia. Sepsis is accompanied by profound arterial hypotension due to massive
endothelial nitric oxide production. Microcirculatory dysfunction associated with sepsis is a
result of intravascular coagulation, endothelial cell swelling, activated leukocytes, and stiff
red blood cells.
23
Figure 5. Pathophysiology of Sepsis.
Treatment (Surviving Sepsis Campaign. International guidelines for management of severe sepsis and
septic shock. 2012)
A. Initial Resuscitation
1. Protocolized, quantitative resuscitation of patients with sepsis-induced tissue
hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge
or blood lactate concentration ≥ 4 mmol/L). Goals during the first 6 hrs of resuscitation:
a) Central venous pressure 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%,
respectively (grade 1C).
2. In patients with elevated lactate levels targeting resuscitation to normalize lactate.
B. Screening for Sepsis and Performance Improvement
1. Routine screening of potentially infected seriously ill patients for severe sepsis to allow
earlier implementation of therapy.
24
2. Hospital–based performance improvement efforts in severe sepsis.
C. Diagnosis
1. Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45
mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic
and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn
percutaneously and 1 drawn through each vascular access device, unless the device was
recently (<48 hrs) inserted.
2. Use of the 1,3 beta-D-glucan assay (grade 2B), mannan and anti-mannan antibody assays
(2C), if available, and invasive candidiasis is in differential diagnosis of cause of infection.
3. Imaging studies performed promptly to confirm a potential source of infection.
D. Antimicrobial Therapy
1. Administration of effective intravenous antimicrobials within the first hour of recognition
of septic shock and severe sepsis without septic shock as the goal of therapy.
2a. Initial empiric anti-infective therapy of one or more drugs that have activity against all
likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate
concentrations into tissues presumed to be the source of sepsis (grade 1B).
2b. Antimicrobial regimen should be reassessed daily for potential deescalation (grade 1B).
3. Use of low procalcitonin levels or similar biomarkers to assist the clinician in the
discontinuation of empiric antibiotics in patients who initially appeared septic, but have no
subsequent evidence of infection (grade 2C).
4a. Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and
for patients with difficult-to-treat, multidrug-resistant bacterial pathogens such as
Acinetobacter and Pseudomonas spp. (grade 2B). For patients with severe infections
associated with respiratory failure and septic shock, combination therapy with an extended
spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa
bacteremia (grade 2B). A combination of beta-lactam and macrolide for patients with septic
shock from bacteremic Streptococcus pneumoniae infections (grade 2B).
4b. Empiric combination therapy should not be administered for more than 3–5 days.
Deescalation to the most appropriate single therapy should be performed as soon as the
susceptibility profile is known (grade 2B).
25
5. Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who
have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some
fungal and viral infections or immunologic deficiencies, including neutropenia (grade 2C).
6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock
of viral origin (grade 2C).
7. Antimicrobial agents should not be used in patients with severe inflammatory states
determined to be of noninfectious cause (UG).
E. Source Control
1. A specific anatomical diagnosis of infection requiring consideration for emergent source
control be sought and diagnosed or excluded as rapidly as possible, and intervention be
undertaken for source control within the first 12 hr after the diagnosis is made, if feasible
(grade 1C).
2. When infected peripancreatic necrosis is identified as a potential source of infection,
definitive intervention is best delayed until adequate demarcation of viable and nonviable
tissues has occurred (grade 2B).
3. When source control in a severely septic patient is required, the effective intervention
associated with the least physiologic insult should be used (eg, percutaneous rather than
surgical drainage of an abscess) (UG).
4. If intravascular access devices are a possible source of severe sepsis or septic shock, they
should be removed promptly after other vascular access has been established (UG).
F. Infection Prevention
1a. Selective oral decontamination and selective digestive decontamination should be
introduced and investigated as a method to reduce the incidence of ventilator-associated
pneumonia; this infection control measure can then be instituted in health care settings and
regions where this methodology is found to be effective (grade 2B).
1b. Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to
reduce the risk of ventilator-associated pneumonia in ICU patients with severe sepsis (grade
2B).
Recommendations: Hemodynamic Support and Adjunctive Therapy*
G. Fluid Therapy of Severe Sepsis
1. Crystalloids as the initial fluid of choice in the resuscitation of severe sepsis and septic shock
(grade 1B).
26
2. Against the use of hydroxyethyl starches for fluid resuscitation of severe sepsis and septic
shock (grade 1B).
3. Albumin in the fluid resuscitation of severe sepsis and septic shock when patients require
substantial amounts of crystalloids (grade 2C).
4. Initial fluid challenge in patients with sepsis-induced tissue hypoperfusion with suspicion of
hypovolemia to achieve a minimum of 30 mL/kg of crystalloids (a portion of this may be
albumin equivalent). More rapid administration and greater amounts of fluid may be needed
in some patients (grade 1C).
5. Fluid challenge technique be applied wherein fluid administration is continued as long as
there is hemodynamic improvement either based on dynamic (eg, change in pulse pressure,
stroke volume variation) or static (eg, arterial pressure, heart rate) variables (UG).
H. Vasopressors
1. Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg (grade
1C).
2. Norepinephrine as the first choice vasopressor (grade 1B).
3. Epinephrine (added to and potentially substituted for norepinephrine) when an additional
agent is needed to maintain adequate blood pressure (grade 2B).
4. Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either
raising MAP or decreasing NE dosage (UG).
5. Low dose vasopressin is not recommended as the single initial vasopressor for treatment of
sepsis-induced hypotension and vasopressin doses higher than 0.03-0.04 units/minute should
be reserved for salvage therapy (failure to achieve adequate MAP with other vasopressor
agents) (UG).
6. Dopamine as an alternative vasopressor agent to norepinephrine only in highly selected
patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia)
(grade 2C).
7. Phenylephrine is not recommended in the treatment of septic shock except in
circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac
output is known to be high and blood pressure persistently low or (c) as salvage therapy when
combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP
target (grade 1C).
27
8. Low-dose dopamine should not be used for renal protection (grade 1A). 9. All patients
requiring vasopressors have an arterial catheter placed as soon as practical if resources are
available (UG).
I. Inotropic Therapy
1. A trial of dobutamine infusion up to 20 micrograms/kg/min be administered or added to
vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated
cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite
achieving adequate intravascular volume and adequate MAP (grade 1C).
2. Not using a strategy to increase cardiac index to predetermined supranormal levels (grade
1B).
J. Corticosteroids
1. Not using intravenous hydrocortisone to treat adult septic shock patients if adequate fluid
resuscitation and vasopressor therapy are able to restore hemodynamic stability (see goals
for Initial Resuscitation). In case this is not achievable, we suggest intravenous hydrocortisone
alone at a dose of 200 mg per day (grade 2C).
2. Not using the ACTH stimulation test to identify adults with septic shock who should receive
hydrocortisone (grade 2B).
3. In treated patients hydrocortisone tapered when vasopressors are no longer required
(grade 2D).
4. Corticosteroids not be administered for the treatment of sepsis in the absence of shock
(grade 1D).
28
Cardiogenic Shock
The clinical definition of cardiogenic shock includes decreased cardiac output and
evidence of tissue hypoxia in the presence of adequate intravascular volume. The
diagnosis of circulatory shock is made at the bedside by the presence of hypotension
along with a combination of clinical signs indicative of poor tissue perfusion, including
oliguria, clouded sensorium, and cool, mottled extremities. Hemodynamic criteria include
sustained hypotension (systolic blood pressure <90 mm Hg for at least 30 minutes) and
a reduced cardiac index (<2.2 L /min/m2 ) in the presence of elevated filling pressures
(pulmonary capillary occlusion pressure >15 mm H g). Cardiogenic shock is diagnosed
after documentation of myocardial dysfunction and exclusion or correct ion of factors
such as hypovolemia, hypoxia, and acidosis.
Etiology
The most common cause of cardiogenic shock is left ventricular failure in the
setting of an extensive acute MI , although a smaller infarct ion in a patient with
previously compromised left ventricular function may also precipitate shock. Cardiogenic
shock can also be caused by mechanical complications such as acute mitral regurgitation,
rupture of the interventricular septum, or rupture of the free wall—or by large right
ventricular infarctions.
Causes of Cardiogenic Shock
Acute Myocardial Infarction
Pump failure
Large infarction
Smaller infarction with preexisting left ventricular dysfunction
Infarct extension
Reinfarction
Infarct expansion
Mechanical complications
Acute mitral regurgitation due to papillary muscle rupture
Ventricular septal defect
Free wall rupture
Pericardial tamponade
Right ventricular infarction
Other Conditions
End- stage cardiomyopathy
29
Myocarditis
Myocardial contusion
Prolonged cardiopulmonary bypass
Septic shock with severe myocardial depression
Left ventricular out flow tract obstruct ion
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Obstruction to left ventricular filling
Mitral stenosis
Left atrial myxoma
Acute mitral regurgitation (chordal rupture)
Acute aortic insufficiency
Patients may have cardiogenic shock at initial presentation, but most do not;
shock usually
evolves over several hours, suggesting that
early
treatment
may
potentially prevent shock. In fact , some data indicate that early thrombolytic therapy
may decrease the incidence of cardiogenic shock. Risk factors for the development of
cardiogenic shock in MI generally parallel those for left ventricular dysfunction and the
severity of coronary artery disease. Shock is more likely to develop in patients who are
elderly , are diabetic, and have anterior MI .
Pathophysiology
Cardiac dysfunction in patients with cardiogenic shock is usually initiated by MI
or ischemia. The myocardial dysfunction resulting from ischemia worsens that ischemia,
creating a downward spiral (see Figure). When a critical mass of ischemic or necrotic left
ventricular myocardium fails to pump, stroke volume and cardiac output decrease.
Myocardial perfusion, which depends on the pressure gradient between the coronary arterial
system and the left ventricle and on the duration of diastole, is compromised by
hypotension and tachycardia, exacerbating ischemia. The increased ventricular diastolic
pressures caused by pump failure reduce coronary perfusion pressure, and the additional
wall stress elevates myocardial oxygen requirements, further worsening ischemia.
Decreased cardiac output also compromises systemic perfusion. When myocardial function is
depressed, several compensatory
mechanisms are activated, including sympathetic
stimulation to increase heart rate and contractility and renal fluid retention to increase
preload. These compensatory mechanisms may become maladaptive and can actually
worsen the situation when cardiogenic shock develops. Increased heart rate and
30
contractility increase myocardial oxygen demand and exacerbate ischemia. Fluid retention
and impaired diastolic filling caused by
tachycardia and ischemia may
result
in
pulmonary congestion and hypoxia. Vasoconstriction to maintain blood pressure increases
myocardial afterload, further impairing cardiac performance and increasing myocardial
oxygen demand. This increased demand, in the face of inadequate perfusion, worsens
ischemia and begins a vicious cycle that will end in death if not interrupted. The
interruption of this cycle of myocardial dysfunction and ischemia forms the basis for the
therapeutic regimens for cardiogenic shock.
Figure 6. The "downward spiral" in cardiogenic shock. LVEDP - left ventricular end-diastolic pressure.
Treatment
Cardiogenic shock is an emergency requiring the following:

Fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is
present

Prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac output

Admission to an intensive care setting (eg, cardiac catheterization suite or ICU or critical care
transport to a tertiary care center)

Early and definitive restoration of coronary blood flow; at present, this represents standard
therapy for patients with cardiogenic shock due to myocardial ischemia
31

Correction of electrolyte and acid-base abnormalities (eg, hypokalemia, hypomagnesemia,
acidosis)
Invasive procedures include the following:

Placement of a central line may facilitate volume resuscitation, provide vascular access for
multiple infusions, and allow invasive monitoring of central venous pressure

An arterial line may be placed to provide continuous blood pressure monitoring

An intra-aortic balloon pump may be placed as a bridge to percutaneous coronary
intervention (PCI, see later) or coronary artery bypass grafting (CABG, see later)
Pharmacologic therapy

Patients with MI or acute coronary syndrome are given aspirin and heparin

Inotropic and/or vasopressor drug therapy may be necessary in patients with inadequate
tissue perfusion and adequate intravascular volume, so as to maintain mean arterial
pressure (MAP) of 60 or 65 mm Hg

Diuretics are used to decrease plasma volume and peripheral edema
Features of dopamine are as follows:

Dopamine is the drug of choice to improve cardiac contractility in patients with hypotension

Dopamine may increase myocardial oxygen demand

Dopamine is usually initiated at a rate of 5-10 mcg/kg/min IV

The infusion rate is adjusted according to the blood pressure and other hemodynamic
parameters

Often, patients may require doses as high as 20 mcg/kg/min
Features of dobutamine are as follows:

Dobutamine may be preferable to dopamine if the systolic blood pressure is higher than 80
mm Hg

Compared with dopamine, dobutamine has less effect on myocardial oxygen demand

Tachycardia from dobutamine may preclude its use in some patients
If the patient remains hypotensive despite moderate doses of dopamine, a direct
vasoconstrictor may be administered, as follows:

Norepinephrine is started at a dose of 0.5 mcg/kg/min and titrated to maintain an MAP of
60 mm Hg

The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min

Doses as high as 3.3 mcg/kg/min have been used
32
Phosphodiesterase inhibitors (eg, inamrinone [formerly amrinone], milrinone) are
inotropic agents with vasodilating properties and long half-lives that are beneficial in patients
with cardiac pump failure, but they may require concomitant vasopressor administration
PCI and CABG (see below)

Either PCI or CABG is the treatment of choice for cardiogenic shock

PCI should be initiated within 90 minutes after presentation

PCI remains helpful, as an acute intervention, within 12 hours after presentation

Thrombolytic therapy is second best but should be considered if PCI and CABG are not
immediately available.
Percutaneous coronary intervention
PCI (percutaneous coronary intervention) - commonly known as coronary
angioplasty or simply angioplasty, is a non-surgical procedure used to treat
the stenotic(narrowed) coronary arteries of the heart found in coronary heart disease. These
stenotic segments are due to the buildup of the cholesterol-laden plaques that form due
to atherosclerosis. PCI is usually performed by an interventional cardiologist, though it was
developed and originally performed by interventional radiologists.
During PCI, a cardiologist feeds a deflated balloon or other device on a catheter from
the inguinal femoral artery or radial artery up through blood vessels until they reach the site
of blockage in the heart. X-ray imaging is used to guide the catheter threading. Angioplasty
usually involves inflating a balloon to open the artery and allow blood flow. Stents or scaffolds
may be placed at the site of the blockage to hold the artery open. Current concepts recognize
that after three months the artery has adapted and healed and no longer needs the stent,
which is the premise for developing stents that dissolve naturally after they are no longer
necessary.
33
Figure 7. Percutaneous coronary intervention
Coronary artery bypass graft
Coronary artery bypass surgery, also known as coronary artery bypass graft (CABG,
pronounced "cabbage") surgery, and colloquially heart bypass or bypass surgery, is a surgical
procedure consisting of either diverting the left internal thoracic artery (left internal
mammary artery or "LIMA") to the left anterior descending (LAD) branch of the left main
coronary artery; or a harvested great saphenous vein of the leg, attaching the proximal end to
the aorta or one of its major branches, and the distal end to immediately beyond a partially
obstructed coronary artery (the "target vessel") - usually a 50% to 99% obstruction.
The purpose is to restore normal blood flow to that partially obstructed coronary
artery. It is performed to relieve angina unsatisfactorily controlled by maximum tolerated antiischemic medication, prevent or relieve left ventricular dysfunction, and/or reduce the risk of
death. It does not prevent heart attacks.
This surgery is usually performed with the heart stopped, necessitating the usage
of cardiopulmonary bypass; however, two alternative techniques are also available allowing
CABG to be performed on a beating heart either without using the cardiopulmonary bypass
deemed as "off-pump" surgery or performing beating surgery using partial assistance of the
cardiopulmonary bypass called as "on-pump beating" surgery. The latter gathers the
advantages of the on-pump stopped and off-pump while minimizing their respective side
effects.
34
Figure 8. Coronary artery bypass surgery
Intra-aortic balloon pump
The
Intra-aortic
balloon
pump
(IABP)
is
a
mechanical
device
that
increases myocardial oxygen perfusion while at the same time increasing cardiac output.
Increasing cardiac output increases coronary blood flow and therefore myocardial oxygen
delivery. It consists of a cylindrical polyethylene balloon that sits in the aorta, approximately
2 centimeters (0.79 in) from the left subclavia artery and counterpulsates. That is, it actively
deflates in systole, increasing forward blood flow by reducing afterload through a vacuum
effect. It actively inflates in diastole, increasing blood flow to the coronary arteries via
retrograde flow. These actions combine to decrease myocardial oxygen demand and increase
myocardial oxygen supply.
Figure 9. Intra-aortic balloon pump
35
Bradycardia and atrioventricular block
Classification of bradycardia and atrioventricular (AV) block
Bradycardia
 Sinus bradycardia
 Junctional bradycardia
 Slow atrial fibrillation (distinguished from atrial fibrillation with complete AV block by
variability in RR interval)
 Atrial flutter/atrial tachycardia with 4 : 1 AV block
 Complete AV block with junctional or ventricular escape rhythm
Atrioventricular block
 First degree AV block (constant PR interval >200 ms)
 Second degree AV block, Mobitz type 1 (Wenckebach)
 Second degree AV block, Mobitz type 2
 Third degree/complete AV block
Causes of sinus bradycardia
Cardiovascular
 Chronic sinus node dysfunction (due to idiopathic degenerative/fibrotic change in
sinus node)
 Acute sinus node dysfunction due to ischemia (typically in inferior myocardial
infarction; sinus node artery arises from right coronary artery in ∼90%)
 Maneuvers triggering high vagal tone, e.g. suctioning of airway
 Vasovagal syncope
 Carotid sinus hypersensitivity
Systemic
 Drugs (beta-blockers, digoxin, diltiazem, verapamil, other antiarrhythmic drugs)
 Hypothermia
 Hypothyroidism
 Hypokalemia, hyperkalemia
 Raised intracranial pressure
36
Causes of atrioventricular (AV) block
Acute
 High vagal tone (may cause Mobitz type 1 second-degree AV block, but not Mobitz
type 2 or complete AV block)
 Myocardial ischemia/infarction
 Drugs (beta-blockers, digoxin, diltiazem, verapamil, other antiarrhythmic drugs)
 Hyperkalemia
 Infections: Lyme disease
 Myocarditis
 Endocarditis with abscess formation
Chronic
 Idiopathic conducting system fibrosis
 Congenital complete AV block
 Cardiomyopathy
Signs and symptoms
Signs and symptoms of atrioventricular (AV) block include the following:

First-degree AV block: Generally not associated with any symptoms; it is usually an incidental
finding on electrocardiography

Second-degree AV block: Usually is asymptomatic, but in some patients, sensed irregularities
of the heartbeat, presyncope, or syncope may occur; may manifest on physical examination
as bradycardia (especially Mobitz II) and/or irregularity of heart rate (especially Mobitz I
[Wenckebach])

Third-degree AV block: Frequently associated with symptoms such as fatigue, dizziness, lightheadedness, presyncope, and syncope; associated with profound bradycardia unless the site
of the block is located in the proximal portion of the atrioventricular node (AVN)
In third-degree AV block, exacerbation of ischemic heart disease or congestive heart failure
caused by AV block–related bradycardia and reduced cardiac output may lead to specific,
clinically recognizable symptoms, such as the following:

Chest pain

Dyspnea

Confusion
37

Pulmonary edema
Sinus bradycardia is most often asymptomatic. However, symptoms may include the
following:

Syncope

Dizziness

Lightheadedness

Chest pain

Shortness of breath

Exercise intolerance
Treatment
See Algorithm below.
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Figure 10. Treatment of Bradycardia
Transvenous and Transcutaneous Cardiac Pacing
An artificial pacemaker is an electronic device that provides an electrical signal to make
the heart beat when the heart's own built-in pacemaker, or conduction system, fails. The
body’s anatomical, built-in pacemaker, known as the SAN (Sinoatrial) node is made up of
specialized nervous tissue at the junction of the superior vena cava and the right atrium. When
the SA node generates an electrical impulse, it causes the heart to contract, and the right and
left atria carry the signal on to the atrioventricular (AV) node. The AV node then carries the
impulse through the wiring in the ventricles, thus causing the lower chambers of the heart to
39
contract. The anatomical pacemaker provides what is called the heart’s “intrinsic” rhythm.
When the internal pacemaker fails or is compromised, artificial pacemakers are appropriate
therapy.
There are two types of artificial pacemaker: temporary and permanent. Permanent
(epicardial) pacemakers are implanted by means of a surgical procedure and are used to treat
permanent conduction problems. Temporary pacemakers are used in emergency situations
for transient conduction disturbances or prophylactically for anticipated dysrhythmias.
Temporary pacemakers may be invasive (transvenous) or non-invasive (transthoracic).
Temporary non-invasive pacemakers are typically available to clinicians as part of a cardiac
resuscitation system, complete with defibrillation, cardioversion and monitoring capabilities.
The two most common reasons for using temporary pacing to maintain an optimal
cardiac output are when the patient has developed a symptomatic bradycardia or is asystolic.
The cause for this is frequently due to impairment within the conduction system in the
heart. The problem may be located within the atrioventricular (AV) node or below, within the
bundle branches coursing through the ventricles. Patients can experience bradycardia as a
result of several types of AV blocks. This, in turn, frequently causes decreased cardiac output.
Permanent pacemakers can be implanted into these individuals to increase and maintain
adequate heart rate.
A second reason patients may require temporary pacing is because they are
experiencing fast heart rates. Symptomatic tachycardias (rates greater than 180) may produce
inadequate ventricular filling with inadequate perfusion. Some very chaotic rhythms, like
ventricular fibrillation, require defibrillation. Some fast rhythms (tachycardia) are amenable
to overdrive pacing by a pacemaker. These may be atrial tachydysrhythmias (atrial flutter,
atrial fibrillation or atrial tachycardia) or ventricular tachycardia. This rapid rate may impair
the ability of the heart to eject an adequate stroke volume. A temporary non-invasive
pacemaker can be used to pace the atria at a rapid rate. If one of the pacer stimuli falls at the
right time, it gains the responsibility for pacing the heart. This is known as overdrive pacing,
and it either stops the tachydysrhythmia or converts the patient to a sinus rhythm.
Temporary pacing can be used either on an emergency basis or to support and/or
maintain an adequate heart rate for several hours or days. In some cases, the clinician uses a
temporary pacemaker until the patient is stabilized and definitive care, such as a permanent
implanted pacemaker, is available.
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Non-invasive Pacemaker Functionality
The non-invasive pacemaker does two things: it monitors the patient’s own intrinsic
rhythm using a “sensing circuit,” and it delivers an electrical signal using an “output circuit.” If
the patient’s own intrinsic rhythm becomes too slow or disappears completely, the pacemaker
senses the reduction in the signal or the rate and initiates pacing through the combination
pads on the patient’s chest wall. The output signals provide a regular electrical stimulus to the
heart’s conduction system, signaling the heart to contract at a rate determined by the
pacemaker.
Pulse duration
Pulse duration is the time of impulse stimulation. Early non-invasive pacemakers used
short-duration (1-2 milliseconds) impulses. The action potential (electrical impulse including
depolarization and repolarization) of cardiac muscle cells is longer than that for skeletal
muscle, requiring 20-40 milliseconds to reach maximum effect. ZOLL found that increasing the
duration from 1 to 4 milliseconds resulted in a 3-fold reduction in threshold (the current
required for stimulation) to produce capture. Increasing the current from 4 to 40 milliseconds
further halves the threshold. Longer durations produced no further advantage. Current ZOLL
non-invasive pacemakers deliver a 40-millisecond impulse for each paced beat. This 40millisecond impulse is patented by ZOLL.
Synchronous/asynchronous modes
Most defibrillators have both fixed rate and synchronous pacing. Synchronous pacing
is a demand mode, in which the pacer fires only when no complex is sensed for a
predetermined amount of time. Pacing generally should be started in the synchronous mode
to coordinate the efforts of the cardiac resuscitation system’s pacemaker with the patient’s
own cardiac electrical activity. In the fixed rate (asynchronous) mode, the non-invasive
pacemaker delivers an electrical stimulus at preset intervals, independent of intrinsic cardiac
activity.
Asynchronous pacing mode
Human studies have shown that the average current necessary for external pacing is
about 65-100 milliamperes (mA) in unstable bradycardias and about 50-70 mA in
hemodynamically stable patients and volunteers. The clinician increases the current until the
pacemaker “captures” the myocardium, taking over the pacemaker functions of the heart and
resulting in a characteristic pacemaker rhythm. The clinician then confirms the presence of a
41
pulse following each pacemaker spike. The force of skeletal muscle contraction, not the
electrical current, determines the patient’s level of discomfort during non-invasive pacing.
Electrodes
Non-invasive pacing can cause discomfort for patients and can be quite painful. Pain is a
function of the current delivered per unit of skin surface area. Electrodes with a large surface
area minimize pain sensation. Most commercially available electrodes are 80-100 cm2.Proper
application of the external pacemaker electrodes is simple but critical. Proper skin contact is
an important factor in reducing resistance and improving capture. Electrodes can be placed
on the anterior chest wall,
with one electrode below the right clavicle lateral to the sternum
and the other electrode below the breast tissue along the midaxillary
line. Electrodes can
also be placed in an anteroposterior configuration with the anterior electrode placed over
the precordium and the posterior electrode at the right infrascapular location.
For transvenous pacing, the pacing catheter can be advanced through the brachial
(antecubital), femoral, internal jugular (preferable right), subclavian
(preferable
left),
or the right subclavian via supraclavicular access (experienced practitioner). The ECG can
guide blind placement using a balloon-tipped catheter. A V1 lead of a conventional ECG is
connected to the distal pole (cathode) of the pacing catheter and used to monitor a unipolar
intracavitary electrogram. The catheter is floated, seeking display of
intracavitary
a
right
ventricular
electrogram point at which the balloon can be deflated and the catheter
advanced a few centimeters to position its tip in the right ventricular apex. Endocardial contact
is confirmed by development of an “injury” current characterized by prominent ST-segment
elevation. The pacing electrode is connected to the pulse generator and used in unipolar or
bipolar configuration. In emergency situations when pacing is immediately required, the
pacing lead may be advanced with the pulse generator on, set to its maximum output, and
in the asynchronous mode at a rate of 70 to 100 ppm.
Mechanical capture manifests with signs of improving cardiac output such as an
increased level of consciousness or blood pressure. The clinician must monitor and assess for
both electrical and mechanical capture of the myocardium. The electrical activity of the
external pacer shows up clearly on the monitor as large complexes at the rate you have
selected. While pacing capture on the monitor is an important sign, the appearance of these
complexes does not mean that the patient’s myocardium is mechanically captured and cardiac
output is occurring.
42
Skeletal muscle contraction can be uncomfortable and is often the limiting factor in
non-invasive pacing use. Placing electrodes over areas of least skeletal muscle can minimize
discomfort. The clinician should consider sedation if these measures are inadequate.
43
Tachycardias
Vagal maneuvers to terminate tachycardia.
Carotid Sinus Massage
 Ensure that there is no significant carotid artery disease (carotid bruits).
 Monitor the electrocardiogram continuously.
 Place the patient in the supine position with the head slightly extended.
44
 Start with right carotid sinus massage.
 Apply firm rotatory or steady pressure to the carotid artery at the level of the third
cervical vertebra for 5 sec.
 If no response, massage the left carotid sinus.
 Generally, right carotid sinus massage decreases sinus node discharge, and left carotid
sinus massage slows atrioventricular conduction.
 Do not massage both carotids at the same time.
 A single application of carotid sinus pressure is effective in about 20% to 30% of
patients with paroxysmal supraventricular tachycardias; multiple applications
terminate tachycardia in about 50% of patients.
 Asystole is a potential but rare complication.
Valsalva Maneuver
 Valsalva maneuver involves an abrupt voluntary increase in intrathoracic and
intraabdominal pressures by straining.
 Monitor the electrocardiogram continuously.
 Place the patient in the supine position.
 The patient should not take a deep inspiration before straining.
 Ideally, the patient blows into a mouthpiece of a manometer against the pressure of
30-40 mm Hg for 15 sec.
 Alternatively, the patient strains for 15 sec while breath-holding.
 Transient acceleration of tachycardia usually occurs during the strain phase as a result
of sympathetic excess.
 On release of strain, the rate of tachycardia slows because of the compensatory
increase in vagal tone (baroreceptor reflex); it may terminate in about 50% of patients.
 Termination of tachycardia may be followed by pauses and ventricular ectopics.
45
Cardioversion
DC-cardioversion (DCC)
Cardioversion is a synchronized administration of shock during the R waves or QRS
complex of a cardiac cycle. During defibrillation and cardioversion, electrical current travels
from the negative to the positive electrode by traversing myocardium. It causes all of the heart
cells to contract simultaneously. This interrupts and terminates abnormal electrical rhythm.
This, in turn, allows the sinus node to resume normal pacemaker activity.
Tachyarrhythmias that do not respond to medical treatment or that are associated with
hemodynamics compromise (e.g. hypotension, worsening heart failure) may be converted
to sinus rhythm by the use of
a transthoracic electric shock. A short-acting general
anaesthetic is used. Musclerelaxants are not usually given. When the arrhythmia has
definite QRS complexes,
the delivery
of the shock should be timed to occur with the
downstroke of the QRS complex (synchronization). The machine being used to perform the
cardioversion will do this automatically if the appropriate button is pressed. There is a crucial
46
difference between defibrillation and cardioversion: a non-synchronized shock is used to
defibrillate. Accidental defibrillation of a patient who does not require it may itself precipitate
ventricular fibrillation. Typical indications for cardioversion include:
 atrial fibrillation
 atrial flutter
 sustained ventricular tachycardia
 junctional tachyarrhythmias.
If atrial
necessary
fibrillation or flutter has been present for more than a few days, it
to anticoagulate
is
the patient adequately for 3 weeks before elective
cardioversion to reduce the risk of embolization. The
duration of anticoagulation after
successful
cardioversion for atrial fibrillation is a complex issue and depends on a number
of factors:
it should be for at least 4
weeks after the procedure and may well befor
much longer.
Digoxin toxicity may lead to ventricular arrhythmias or asystole following
cardioversion. Therapeutic digitalization does not increase the risks of cardioversion, but it
is conventional to omit digoxin several days prior to elective cardioversion in order to be
sure that toxicity is not present. Cardiac enzyme levels may rise after a cardioversion.
Cardioversion
Defibrillation
Elective planned procedure
Emergency life-saving procedure
Synchronized Shock
UN-Synchronized Shock
Low energy shock
High energy shock
There can be some delay
No delay, immediate
Anti-coagulation needed
No anti-coagulation needed
Less damage to myocardium
More damage to myocardium
Used in most of the arrhythmias except Used in VT/VF
VT/VF
47
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John F. Butterworth IV, David C. Mackey, John D. Wasnick - Morgan & Mikhail’s Clinical
Anesthesiology. 5th Edition - Copyright © 2013, 2006, 2002 by McGraw-Hill Education, LLC.
2.
Agamemnon Despopoulos, Stefan Silbernagl - Color Atlas of Physiology -
© 2003 Thieme
3.
C.A. Vacanti - Essential clinical anesthesia - © 2011 - Cambridge University Press
4.
Joseph E. Parrillo, R. Phillip Dellinger - Critical Care Medicine. Principles of Diagnosis and
Management in the Adult. 4th Edition. - © 2014 by Saunders, an imprint of Elsevier Inc
5.
International Guidelines for Management of Severe Sepsis and Septic Shock: 2012
6.
Parveen Kumar - Clinical Medicine. Seventh Edition.- © 2009, Elsevier Limited.
48