Lecture 10

Shock- ethiology, criteria of treatment function etiology. Management of

shock. Volemic therapy in shock.

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 (see Sepsis and 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.
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.
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 β-receptors. 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.
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

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,

Site of Fluid Loss Mechanism of Loss

salt-losing nephritis, the polyuric phase after acute

tubular damage, use of potent diuretics

Intravascular fluid lost Increased capillary permeability secondary to

to the extravascular inflammation or traumatic injury (eg, crush),
space anoxia, cardiac arrest, sepsis, bowel 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.
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 bacterial infection with
endotoxin release; 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 Cause

Obstructive Mechanical Tension pneumothorax, cava

interference with compression, cardiac tamponade,
ventricular filling atrial tumor or clot

Interference with Pulmonary embolism

ventricular emptying

Cardiogeni Impaired myocardial Myocardial ischemia or MI,

c contractility myocarditis, drugs

Abnormalities of Tachycardia, bradycardia

cardiac rhythm

Cardiac structural Acute mitral or aortic regurgitation,

disorder ruptured interventricular septum,
prosthetic valve malfunction
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
 Clinical evaluation
 Test result trends
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.
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.
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 O 2 by face
mask is provided. If shock is severe or if ventilation is inadequate, airway
intubation with mechanical ventilation (see Airway Establishment and Control :
Tracheal Intubation) 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 caval
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
pulse volume, skin temperature, and color. Measurement of CVP, PAOP, and
thermodilution cardiac output using a balloon-tipped 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, serum creatinine, and blood lactate are obtained. Sublingual
CO2measurement, if available, is a noninvasive monitor of visceral perfusion. A
well-designed flow sheet is helpful.
Clinical Calculator:; Mean Vascular Pressure (systemic or pulmonary)
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.
Hemorrhagic shock
In hemorrhagic shock, surgical control of bleeding is the first priority. Volume
replacement 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 Patients
with septic shock also receive broad-spectrum antibiotics 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
Inotropic and Vasoactive Catecholamines
Drug Dosage Hemodynamic Actions

Norepinephrin 4 mg/250 mL or 500 mL 5% α-Adrenergic:

e D/W continuous IV infusion at Vasoconstriction
8–12 mcg/min initially, then at
β-Adrenergic:
2–4 mcg/min as maintenance,
Inotropic and
with wide variations
chronotropic effects*

Dopamine 400 mg/500 mL 5% D/W α-Adrenergic:

continuous IV infusion at 0.3– Vasoconstriction
1.25 mL (250–1000 mcg)/min
β-Adrenergic:
2–10 mcg/kg/min for low dose Inotropic and
chronotropic effects
20 mcg/kg/min for high dose
and vasodilation
Nonadrenergic: Renal
and splanchnic
vasodilation

Dobutamine 250 mg/250 mL 5% D/W β-Adrenergic:

continuous IV infusion at 2.5– Inotropic effects‡
10 mcg/kg/min

*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 (see also Overview of Coronary Artery Disease).
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.
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.