CNUR823 - Module 12

CNUR823, Module 12 - Introduction 2014-03-26, 9:32 AM
Developed by Beth Swart and Charene Wood
Introduction
Shock is a complex clinical systemic syndrome that results from inadequate tissue perfusion that results in
inadequate cellular oxygenation and anerobic metabolism (Gaieski, 2011). This leads to an imbalance between
oxygen delivery and oxygen consumption. Prolonged oxygen deprivation leads to hypoxia and alteration of cellular
processes (Wilmot, 2010). Shock states can be caused by decreased circulating blood volume (hypovolemic),
impaired heart function or failure (cardiogenic), abnormalities in vascular resistance (distributive), and mechanical
obstruction that interferes with cardiac output (obstructive). Early recognition of shock based on manifestations and
appropriate management is critical to avoid further progression of shock and survival.
Definition of Shock
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OBJECTIVES
1. Define shock.
2. Identify the stages of shock and the signs and symptoms found in each stage.
3. Explain how each stage of shock impairs and damages cellular perfusion and energy production.
4. Outline the various types of shock including their causes and pathophysiology.
5. Discuss the general treatment strategies for shock.
Determinants of Shock
Determinants of Shock
Source: Jones & Kline (2006)
Review
In order to understand the ramifications of hypoperfusion, a review of aerobic and anaerobic metabolism is
necessary.
Aerobic Metabolism
Anerobic Metabolism
What happens to the cell without adequate oxygen?
Why Anerobic Metabolism of Course!!!
Overview of Cellular Homeostasis and

Hemodynamics
Adequate blood flow to the tissues and cells requires the following components: adequate cardiac pump, effective
vasculature or circulatory system (peripheral vascular resistance), and adequate blood volume. Conditions that
significantly impact on any of these parameters will result in inadequate tissue perfusion.
Recall the basic hemodynamics:
The blood pressure is maintained through the balance of the autonomic nervous system, heart contractility, preload,
and afterload. There must be adequate intravascular volume and sufficient hemoglobulin. When preload or afterload
are altered, the following occurs:
AFTERLOAD IMPACT
BUT…when altered
PRELOAD IMPACT
BUT…when altered
The body mounts a complex physiological response to hypoperfusion in an effort to maintain homeostasis and
perfuse the most vital organs such as the brain, heart, and lungs.
Circulatory reflexes are triggered in an effort to restore the MAP as a consequence of hypoperfusion (decrease in
mean arterial filling pressure). Baroreceptors, volume receptors, and chemoreceptors sense changes to
hypoperfusion and respond via the hypothalamic-pituitary-adrenal axis and the autonomic nervous system to begin
compensatory mechanisms.
The baroreceptors (in carotid sinus and aortic arch) are sensory nerve endings that respond to pressure changes by
initiating sympathetic responses via the vasomotor and cardiac centres in the medulla resulting in vasoconstriction
and increased heart rate and contractility. Remember though that the cerebral and coronary arteries are not affected
by the sympathetic response unless the MAP falls to below 70 mm Hg.
A low pH and elevated pCO2 activate chemoreceptors in the carotid artery that also stimulates the vasomotor
centre.
Reduced blood flow to the kidney results in the stimulation of the renin-angiotensin-aldosterone system (see figure).
Angiotension II results in the production of aldosterone from the adrenal medulla, peripheral vasoconstriction, and
thirst. Aldosterone along with antidiuretic hormone (ADH) from the posterior pituitary (produced following receptor
stimulation of the hypothalamus) act on the kidney distal tubules and collecting ducts to retain sodium and water.
This increases venous return, peripheral resistance, cardiac output combined with the retention of water to increase
MAP.
Source: Wikipedia Commons
Pathophysiology of Shock
Shock affects the mitochondria first; without oxygen the mitochondria convert fuels to lactate or lactic acid and other
waste products. As these toxins accumulate, cell injury, inflammation and death occurs (Wilmot, 2010).
Decreased vascular wall tension increases sympathetic stimulation (this is blocked in sepsis) with increased
production of epinephrine, norepinephrine, cortisol, renin, and glucagon. Increased glycogenolysis and lipolysis
occurs producing glucose and free fatty acids which convert to tricarboxylic acid. Reduction in capillary hydrostatic
pressure allows movement of protein-free fluid from the interstitium to the vascular space, increasing intravascular
volume and reducing interstitial volume.
Neutrophil and macrophage activation occurs due to hypoxia resulting in enzymatic organ damage and
microischemia from capillary plugs. Tumour necrosis factor (TNF) and interleukins are released.
Stages of Shock
The Case of Fred

Fred is a 26-year-old healthy male with no significant medical history. He is outside the club “Fluid” on Richmond
and is caught in a gun fight. He takes a “45 to his right femur.” It takes a minute till he notices the blood.
What is happening?
What would his vitals be?
What stage of shock is he in?
Initial StageThis is the theoretical stage. There are no observable symptoms. Believed changes are occurring at the
cellular level so oxygen delivery and and/or uptake is compromised with anerobic metabolism, and production of
lactic acid.
No one has noticed Fred…and he left his cell phone at home.
Stages of Blood Loss
Fred has now moved into the next stage of shock. What is it called?
Compensated Shock
The compensatory mechanism improves perfusion to vital organs and tissues (heart and brain) at the expense of
the gastrointestinal tract, the skin, and skeletal muscle. The body is working harder to compensate for the volume
loss resulting in a change in vital signs to show a clear reflection of fluid volume deficit. The prognosis is certainly
improved if volume resuscitation is initiated and further volume loss is prevented.
Fred’s Presentation:
Tachycardia (pulse rate?) => Body is attempting to compensate for the decrease in circulating volume by
pumping faster to circulate the volume left as fast as possible. Remember, HR X SV = CO. If SV is reduced
with blood loss, the HR increases to maintain CO.
Decreased stroke volume and cardiac output ==> as the blood leaves the intravascular space there is less
to pump (decreased SV) and less blood results in decreased CO.
Rapid, thready peripheral pulses ==> consequence of tachycardia; thready pulse as blood is shunted away
from the peripheral vasculature to maintain perfusion of vital organs (brain, heart, lungs).
Normal blood pressure (hypotension begins at greater than 1500 mL blood loss).
Tachypnea ==> Hyperventilation is a result of the stimulation of the aortic and carotid chemoreceptors to
pain.Decreased pulmonary blood flow impairs gas exchange.

Decreased skin perfusion (assessment findings?) ==> blood is shunted away from the skin leading too poor
perfusion and cool, clammy extremities. Increased capillary refill time.
Decreased urine output (under 30 mL/h) ==>decreased blood flow to the kidneys causing poor kidney
perfusion and decreased urinary output.
Thirst ==>increased serum osmolarity and stimulation of the osmoreceptors in hypothalamus and antidiuretic
hormone from posterior pituitary
Altered mental status (observations?) ==> result of poor perfusion of the brain/CNS or hypoxia. Hypoxic
patients are likely to be restless, confused, agitated. Loss of consciousness occurs when more than 2 L of
blood is lost. Able to respond to verbal commands.
Fred has been there now for 15 minutes. Someone called 911. What will they see? This is a “scoop and run”
(severely injured patients are transported to a high-level trauma facility to reduce mortality).
Where did Fred get hit? Does it matter where he got shot? Why? What is the body doing physiologically
while he waits? What is the next stage of shock?
Progressive Stage
During the progressive stage, the body’s compensatory mechanisms begin to fail and the patient is in a state of
sustained hypotension resulting in decreased perfusion to the vital organs (multiorgan system failure).
Fred’s Presentation:
Hypotension (measurement?) ==> decreased preload from loss of autoregulation. CO continues to fall with
resultant reduction in BP, and coronary artery, cerebral, and peripheral perfusion. Potential for dysrhythmias
even myocardial infarction.
Prolonged capillary refill (normal?) ==>as a consequence of peripheral vasoconstriction
Marked increase in heart rate
Weak, rapid, thready pulse ==> extremities are probably cyanotic and cool. As a consequence of sustained
hypoperfusion.
Also:
Altered capillary permeability ==> due to continued reduction in cellular perfusion (lack of ATP availability
for transmembrane potential (Pearson, Round, & Ingram, 2011), fluid and protein moves from the vascular
space to the interstitial space resulting in edema. Also results in sluggish blood flow. Continued hypoperfusion
results in production of lactate and oxygen-free radicals initiating the inflammatory cascade (Pearson et al.).
Inflammatory hypoxic vascular endothelial cells activate neutrophils, which bind to the endothelium and
release directly damaging substances (e.g., reactive oxygen species, proteolytic enzymes) and inflammatory
mediators (e.g., cytokines, leukotrienes, tumor necrosis factor [TNF]). Some of these mediators bind to cell
surface receptors which leads to production of additional cytokines and nitric oxide (NO), a potent vasodilator.
Metabolic acidosis ==> progressive anaerobic metabolism.

Hypothermia==> anaerobic metabolism prevents endogenous heat production (Pearson et al.) and
stimulates vasoconstriction which also worsens the hypoperfusion.
Coagulopathy ==> multifactorial. May be related to consumption of coagulation factors, acidosis,
hypothermia, and the inflammatory process with the coagulation cascade triggered.. The potential for
developing disseminated intravascular coagulation exists resulting in significant bleeding (Murthi et al., 2011).
Acute tubular necrosis and acute kidney injury ==> from prolonged ischemia to kidneys. Reduced urine
output and elevated blood urea and creatinine result. Metabolic acidosis increases as kidney is unable to
excrete hydrogen ion (acid) and reabsorb bicarbonate.
Respiratory failure ==> from ischemic alveolar cells there is increased pulmonary capillary permeability and
movement of fluid to the interstitial spaces. Eventually fluid moves into the alveoli leading to alveolar edema
and reduced surfactant production. Impaired gas exchange and a reduction in compliance occur with
increased work of breathing and crackles.
Liver ==> Reduced blood flow to liver results in elevation of liver enzymes, bilirubin, and loss of immune
function.
Bacteremia ==> develop ischemic “gut” syndrome from prolonged hypoperfusion and vasoconstriction in the
visceral and splanchnic circulation. The mucosa erodes with the possibility of bleeding. As well, gut bacteria
will be released into lymph or visceral circulation (translocation).
Source: Pearson, Round, & Ingram (2011)
Back to Fred
Despite receiving 10 litres of crystalloid and 6 units of packed red blood cells (PRBCs) and the
surgeons finding and stopping the bleeding from his right femur.
Fred died in the recovery room.
Refractory Stage
This stage involves complete failure of compensatory mechanisms. Death occurs even in presence of resuscitation.
Despite all efforts, organs have been overwhelmed with the inflammatory response, profound hypoperfusion, and
acidosis.
Types of Shock
Hypovolemic Shock
The most common cause of hypovolemic shock is acute hemorrhage that results in decreased circulating blood
volume. Other causes include fluid sequestration within the abdominal viscera or peritoneal cavity. The amount of
volume loss, the time frame from fluid loss to resuscitation, age, and co-morbid illnesses influence the severity of
shock.
The causes of hypovolemic shock can be either through internal or external losses. Internal losses include pooling
of fluid in third spaces (e.g. ascites), fractures of long bones, and internal hemorrhage (hemothorax). External
losses include whole blood loss (trauma or surgery), coagulation disorders (hemophilia), plasma (burns), and fluid
loss (severe vomiting, diarrhea).
Management is, of course, fluid replacement: hypovolemia with isotonic crystalloids and colloids; hemorrhage with
whole blood, packed red blood cells, hemoglobulin-based oxygen carriers, and isotonic crystalloids. Oygen support
and administration of vasoactive drugs are also used.
Pathophysiology of Hypovolemic Shock
Cardiogenic Shock
When the heart fails or develops impaired pump function, it is unable to maintain adequate tissue perfusion causing
cardiogenic shock. Acute myocardial injury, pulmonary edema, cardiomyopathies, dysrhythmias, and valvular
regurgitation are causes of cardiogenic shock. Signs are similar to hypovolemic shock with additional distension of
jugular veins due to increased jugular venous pressure.
Neurogenic Shock
Neurogenic shock occurs as a result of unopposed parasympathetic stimulation that suppresses vasoconstriction.
Warm skin, hypotension, and bradycardia are manifestations of loss of arterial tone and peripheral vasodilation.
Anaphylactic Shock
Anaphylactic shock is “container failure” usually as a result of massive and systemic allergic reaction with the
massive release of histamine that decreases peripheral resistance, increases capillary membrane permeability and
vasodilation.
consciousness
Septic Shock
In septic shock, endotoxins initiate the inflammatory process that results in systemic vasodilation. In gram-negative
shock, patients will first go through warm shock and then cold shock. Despite the increase in cardiac output
secondary to low vascular resistance, blood flow stagnates and tissue perfusion becomes inadequate. Increased
capillary permeability, altered coagulation and impaired fibrinolysis are other abnormalities in septic shock. In late
septic shock, cardiac output decreases.
In anaphylactic shock, the activation of mast cells and histamine release secondary to IgE cause systemic
vasodilation., increased vascular permeability, and bronchoconstriction with airway compromise.
Treatment Priorities
Airway, breathing and circulation are priorities in management. Sources of bleeding are continually assessed.
Admission in a critical care unit is necessary for frequent assessment and reassessment. Hemodynamic monitoring
is initiated and maintained. This monitoring includes ongoing BP monitoring, pulse oximetry, core body temperature,
and fluid balance. Cardiac monitoring may reveal persistent tachycardia despite resuscitation secondary to
ongoing hemorrhage. Rhythm disturbances may reflect a progressive shock state. A urine output of less than 1
mL/kg/h suggests inadequate resuscitation and poor kidney perfusion.
Oxygen saturation is ideally maintained above 96%. Hypoxia can also be monitored with changes in level of
consciousness.
Crystalloids (normal saline, lactated Ringer’s) and colloids (hetastarch), and blood products are used in fluid
resuscitation. Crystalloids expand intravascular volume and interstitial fluid while colloids expand the intravascular
volume by pulling the fluid from the interstitial spaces. Transfusion of packed red cells is indicated for a hematocrit
less than 0.28 and ongoing bleeding. Fluid balance must be monitored. Effects of management and complications
of shock are deliberately minimized.
Activity: This is a video that you may find helpful to understand shock:
//http://www.youtube.com/watch?v=Eipht99mh0g
References
Berry, R. D. (2008). Management of shock in trauma. Anesthesia and Intensive Care Medicine,
9(9), 390-393. http://dx.doi.org/10.1016/j.mpaic.2008.07.006
Bonanno, F. G. (2011). Clinical pathology of the shock syndromes. Journal of Emergencies,

Trauma, and Shock, 4(2), 233-243. doi: 10.4103/0974-2700.82211
Erstad, B. (2011). Hypovolemic shock, In J. Dipiro, R. Talbert, C. Yee, G. Matzke, B. Wells, and
M. Posey (Eds.). Pharmacotherapy: A pathophysiological approach (8th ed., pp. 421-435).
Toronto, ON: McGraw Hill.
Jones, A.E. & Kline, J. A. (2006). Shock. In J. A. Marx, R. S. Hockberger, and R. M. Walls. (Eds.),
Rosen's emergency medicine: Concepts and clinical practice (6th ed., pp. 41-56. St. Louis,
MO:Mosby Elsevier.
Lustenberger, T., Turina, M., Seifert, B., Mica, L.& Keel, M. (2009). The severity of injury and the
extent of hemorrhagic shock predict the incidence of infectious complications in trauma
patients. European Journal of Trauma and Emergency Surgery, 6,: 538-546.
doi: 10.1007/s00068-009-8128-y
Maier, R. (2011). Approach to the patient with shock. In D. Longo, A. Fauci, D. Kasper, S. Hauser,
J. L. Jameson, and J. Loscaizo, Harrison’s principles of internal medicine (18th ed., pp.
2215-2222). Toronto, ON: McGraw Hill.
Murthi, S. B., Stansbury, L. G., Durron, R. P., Edelman, B. B., Scalea, T. M., & Heiss, J. R. (2011).
Transfusion medicine for trauma patients: An update: The acute coagulopathy of trauma &
shock. Retrieved from http://www.medscape.org/viewarticle/749747_4
Pearson, J. D., Round, J. A., & Ingram, M. (2011). Management of shock in trauma. Anesthesia
and Intensive Care Medicine, 12(9), 387-389.
Spaniol, J. R., Knight, A. R., Zebley, J. L., Anderson, D., & Pierce, J. D. (2007). Fluid resuscitation
therapy for hemorrhagic shock. Journal of Trauma Nursing, 14(3), 152-160.
Strickler, J. (2010). Traumatic hypovolemic shock: Halt the downward spiral. Nursing, 40(10, 34-
39.

CNUR823 - Module 12

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CNUR823, Module 12 - Introduction 2014-03-26, 9:32 AM

Developed by Beth Swart and Charene Wood

What happens to the cell without adequate oxygen?

Why Anerobic Metabolism of Course!!!

Overview of Cellular Homeostasis and

Source: Wikipedia Commons

The Case of Fred

No one has noticed Fred…and he left his cell phone at home.

Stages of Blood Loss

pain.Decreased pulmonary blood flow impairs gas exchange.

Metabolic acidosis ==> progressive anaerobic metabolism.

Source: Pearson, Round, & Ingram (2011)

Pathophysiology of Hypovolemic Shock

jugular veins due to increased jugular venous pressure.

Bonanno, F. G. (2011). Clinical pathology of the shock syndromes. Journal of Emergencies,

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