Caring for Clients in Shock Flashcards
adenosine triphosphate (ATP)
energy source for operating sodium and potassium pumps on cellular membrane
adrenocorticotropic hormone (ACTH)
substance secreted by the pituitary that stimulates the adrenal glands to secrete corticosteroid hormones
anaerobic metabolism
inefficient mechanism for meeting energy requirements used when the amount of oxygen reaching the cells decreases
anaphylactic shock
severe allergic reaction that occurs after exposure to a substance to which a person is extremely sensitive
antidiuretic hormone (ADH)
substance secreted by the pituitary in response to low blood volume that promotes reabsorption of water that the kidneys would ordinarily excrete
cardiac output
volume of blood ejected from the left ventricle per minute
cardiogenic shock
shock that occurs when contraction of the heart is ineffective and cardiac output is reduced
catecholamines
neurotransmitters that stimulate responses by the sympathetic nervous system
compensation stage
first stage of shock, during which several physiologic mechanisms attempt to stabilize the spiraling consequences of shock
corticosteroid hormones
chemicals secreted by the adrenal cortex
decompensation stage
stage in shock that occurs as compensatory mechanisms fail and the client’s condition spirals downward into cellular hypoxia, coagulation defects, and cardiovascular changes
distributive shock
shock that occurs when fluid in the circulatory system does not facilitate effective perfusion of the tissue; sometimes called normovolemic shock
endotoxins
harmful chemicals released from within a bacterial cell; probably the major cause of toxic shock
hypovolemic shock
condition that occurs when the volume of extracellular fluid is significantly diminished, primarily because of a loss or reduction in blood or plasma
hypoxia
decrease in the amount of oxygen reaching the cells
irreversible stage
stage in shock that occurs when significant numbers of cells and organ systems become damaged, and the client no longer responds to medical interventions
ischemia
impaired oxygenation of cells and tissues
multiple organ dysfunction syndrome
complication of overwhelming inflammation that results in massive cellular, tissue, and organ injury
neurogenic shock
shock that results from an insult to the vasomotor center in the medulla of the brain or to the peripheral nerves that extend from the spinal cord to the blood vessels
obstructive shock
shock that occurs when the heart or great vessels are compressed
oliguria
low urine output of less than 500 mL/day
positive inotropic agents
drugs with beta-adrenergic activity that increase the heart rate and improve the force of heart contraction
septic shock
shock associated with overwhelming bacterial infections; also called toxic shock
shock
life-threatening condition that occurs when arterial blood flow and oxygen delivery to tissues and cells are inadequate
systemic inflammatory response syndrome (SIRS)
inflammatory state without a proven source of infection
vasopressors
drugs that increase peripheral vascular resistance and raise blood pressure
Older adults, especially those with cardiac disease, are prone to:
cardiogenic shock
Older adults also have a decreased percentage of body water and are more likely to develop:
hypovolemic shock
Owing to a decreased immune response, which hinders the body’s ability to fight infection, older adults may be at higher risk for developing:
septic shock
Shock develops as a consequence of one of three events:
- blood volume decreases
- the heart fails as an effective pump
- peripheral blood vessels massively dilate
Four main categories of shock
- hypovolemic
- distributive
- obstructive
- cardiogenic
Distributive shock is subdivided into:
- neurogenic
- septic (toxic)
- anaphylactic
What is the most common type of shock?
hypovolemic (hemorrhagic) shock
What happens in hypovolemic (hemorrhagic) shock?
The volume of extracellular fluid is significantly diminished, primarily because of lost or reduced blood or plasma. Because the intravascular, interstitial, and intracellular fluid volume are interdependent, a loss from one location results in a similar depletion in the others. Thus, a deficit of intravascular volume (plasma) reduces the net circulating volume. Hypovolemic shock can develop when overall fluid volume is depleted from significant bleeding, such as during surgery, after trauma, or after delivery of an infant.
Hypovolemic shock class I
FLUID VOLUME LOSS: 0-15% (less than or equal to 750 mL)
SIGNS & SYMPTOMS: stable blood pressure; slight tachycardia; sudden anxiety.
Hypovolemic shock class II
FLUID VOLUME LOSS: 15-30% (750-1000 mL)
SIGNS & SYMPTOMS: tachycardia; tachypnea; stable blood pressure; increased diastolic pressure; cool clammy skin; decreased urine output; delayed capillary refill.
Hypovolemic shock class III
FLUID VOLUME LOSS: 30-40% (1500-2000 mL)
SIGNS & SYMPTOMS: Marked tachycardia ( more than 120 beats/min); marked tachypnea (more than 30 breaths/min); decreased systolic blood pressure (less than 100 mm Hg); oliguria ( less than 20 mL); confusion or agitation; skin pale, cold, and sweating noted.
Hypovolemic shock class IV
FLUID VOLUME LOSS: Greater than 40% (greater than 2000 mL)
SIGNS & SYMPTOMS: systolic blood pressure less than 70 mm Hg; weak pulse; marked oliguria; cold, pale skin; extreme sweating; unconscious.
Distributive shock
normovolemic shock; the amount of fluid in the circulatory system is not reduced, yet the fluid circulation does not permit effective tissue perfusion.
Vasodilatation, a prominent characteristic of distributive shock, increases the space in the vascular bed.
Central blood flow is reduced because peripheral vascular or interstitial areas exceed their usual capacity.
What is the rarest type of shock?
neurogenic shock
Neurogenic shock
results from injury that affects the vasomotor center in the medulla of the brain or to the peripheral nerves that extend from the spinal cord to the blood vessels. Injury to the spinal cord or head or overdoses of opioids, tranquilizers, or general anesthetics can cause neurogenic shock.
The tone of the sympathetic nervous system is impaired, resulting in decreased arterial vascular resistance, vasodilatation, and hypotension.
Because blood remains distributed in the periphery, the heart does not fill adequately, cardiac output is reduced, tissue perfusion is compromised, cells are deprived of oxygen and switch to anaerobic metabolism, and metabolic acidosis develops from an increase in lactic acid.
Which shock has the highest mortality rate?
septic shock
Septic shock
Client deaths occur in ____% to ____% of those who develop septic shock despite aggressive treatment.
40; 60
Systemic inflammatory response syndrome (SIRS)
an inflammatory state without a proven source of infection; progresses to sepsis when symptoms of SIRS are present and an infection is proven.
Septic shock occurs most commonly in clients with:
gram-negative bacteremia caused by such pathogens as Escherichia coli, species of Pseudomonas, and gram-positive drug-resistant Staphylococcus aureus and streptococcal species.
Endotoxins trigger an immune response in which:
vasoactive chemicals, such as cytokines, dilate the blood vessels and increase capillary permeability, causing vascular fluid to shift to the interstitium.
What is a characteristic of septic shock that other shocks do not have?
elevation of leukocytes
initial manifestation of fever
Systemic inflammatory response syndrome (SIRS) is diagnose when two or more of the following are present and there is a strong suspicion of inflammation such as microbial infection, pancreatitis, and multiple trauma:
- heart rate greater than 90 bpm
- body temperature less than 36C (96.8F) or greater than 38C (100.8F)
- respiratory rate over 20 breaths/min or blood gas measurement of carbon dioxide (PaCO2) of less than 32 mm Hg (normal is 35 - 45 mm Hg)
- white blood cell count less than 4000 cells/mm3 or greater than 12,000 cells/mm3 or the presence of more than 10% immature neutrophils
Anaphylactic shock
a severe allergic reaction that follows exposure to a substance to which a person is extremely sensitive.
The body’s immune response to the allergic substance causes mast cells in the connective tissues, bronchi, and GI tract to release histamine and other chemicals. The results are vasodilatation, increased capillary permeability accompanied by swelling of the airway and subcutaneous tissues, hypotension, and hives or an itchy rash.
Common allergic substances
bee venom
latex
fish
nuts
penicillin
Obstructive shock
occurs when there is interference with the circulation of blood into and out of the heart, compromising the volume of blood that enters and leaves the heart en route to the lungs and tissues.
Any condition that fills the thoracic cavity with fluid, air, or tissue can lead to obstructive shock.
Examples of causes of obstructive shock
increased fluid or blood in the pericardial sac (cardiac tamponade)
air that accumulates between the layers of pleura (tension pneumothorax)
abdominal tissue, fluid, or air that crowds the diaphragm, as in an enlarged liver and ascites, thus reducing the size of the thorax.
Cardiogenic shock
heart contraction is ineffective, which reduces cardiac output.
What is the leading cause of cardiogenic shock?
myocardial infarction (MI)
Three progressing stages of shock
- compensation
- decompensation
- irreversible
Compensation stage of shock
first stage of shock; during which several physiologic mechanisms attempt to stabilize the spiraling consequences.
If these mechanisms are successful, homeostatic stability may be achieved.
If natural or medical means can reverse shock, the chances of uncomplicated recovered are greatly improved.
As shock progresses, positive outcomes are less predictable.
Compensatory mechanisms in the compensation stage
the release of catecholamines
activation of the renin-angiotensin-aldosterone system
production of antidiuretic and corticosteroid hormones
catecholamines
neurotransmitters that stimulate responses via the sympathetic nervous system.
To compensate in shock, the sympathetic nervous system releases endogenous catecholamines, epinephrine and norepinephrine, into the circulation.
The adrenal medulla secretes epinephrine, whereas the endings of sympathetic nerve fibers secrete norepinephrine.
Epinephrine and norepinephrine increase heart rate and myocardial contractility, which may be counterproductive in cardiogenic shock because it increases a demand for oxygen by an already compromised heart.
Venous return to the right atrium subsequently increases, as does blood sent to the lungs.
Bronchial dilatation increases the amount of oxygenated air entering the lungs, followed by a more efficient exchange of oxygen and carbon dioxide (CO2).
Renin-angiotensin-aldosterone system
a mechanism that restores blood pressure (BP) when circulating volume is diminished.
In response to low renal blood perfusion, the juxtaglomerular cells release renin, an enzymatic hormone in the nephrons of the kidneys. Release of renin causes a series of chemical reactions that eventually produce angiotensin II, a potent vasoconstrictor that raises BP. Angiotensin II also stimulates the hypothalamus to signal the adrenal cortex via the pituitary gland to release aldosterone, a mineralocorticoid that promotes reabsorption of sodium and water by the kidneys, which serves to increase blood volume.
Antidiuretic hormone (ADH) (vasopressin) and adrenocorticotropic hormone (ACTH) are secreted when blood volume is low…
ADH promotes reabsorption of water that the kidneys would ordinarily excrete.
ACTH stimulates the adrenal glands to secrete corticosteroid hormones, which include glucocorticoids and mineralcorticoids.
Glucocorticoids
help the body respond to stress
Mineralocorticoids
conserve sodium and promote potassium excretion
Decompensation Stage
occurs as compensatory mechanisms fail. The client’s condition spirals into cellular hypoxia, coagulation defects, and cardiovascular changes.
Hypoxic cells are forced to:
switch from aerobic metabolism to anaerobic metabolism.
As the energy supply falls below the demand, pyruvic and lactic acids increase, causing metabolic acidosis.
The structural integrity of cells is impaired because without sufficient adenosine triphosphate (ATP), sodium and water enter the cell, and potassium exits into the extracellular fluid.
Eventually, the cells swell and rupture, disrupting their ability to carry out electrochemical processes.
Lysosomes leak enzymatic fluid and contribute to further cellular destruction.
Gradually, significant numbers of cells are damaged.
Effects of endogenous catecholamines
constriction of arterioles of skin, mucous membranes, subcutaneous tissues || sends blood to larger blood vessels supplying vital organs
dilatation of arterioles of skeletal muscles || increases blood supply to skeletal muscles
dilatation of coronary arteries || increases oxygen to myocardium
increased contractility of myocardium || increases amount of blood leaving the left ventricle each time ventricle contracts
increased heart rate || increases blood supply to body, especially vital organs
bronchial dilatation || increases amount of air entering the lungs on inspiration
release of glycogen stored in the liver || provides energy
As cells become damaged from hypoxia, an inflammatory response ensues.
Platelets become sticky and accumulate in the blood vessels of the volume-depleted client, predisposing him or her to the formation of microemboli. Clots further compromise the ability of the red blood cells (RBCs) to deliver oxygen throughout the body. Cell and organ death are potentiated.
