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Shock
Shock
Management of shock.
Volemic therapy in shock.
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 may be more proinflammatory than other forms of shock because of the actions of bacterial
toxins, especially endotoxin.
Pathophysiology
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.
Pathophysiology
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.
Pathophysiology
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)
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.
Multiple organ dysfunction syndrome
(MODS)
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
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.
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.
Diagnosis of cause
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