4 - Shock/Trauma Phys Flashcards
How do endotoxins contribute to end stage shock?
Gram negative Bacteria in the intestines release endotoxin when the gut begins to die
causes increased cellular metabolism despite inadequate oxygen delivery, leading to cardiac exhaustion
Why is the liver particularly effected by shock?
Has a high metabolic rate
AND
the liver is the first-line recipient of toxins in the blood from ischemia
What are four cellular effects of shock?
- Sodium and Potassium transport halts. Na accumulates in the cell and K can’t get into the cell
- Mitochondrial activity is depressed
- lysosomes break open and release hydrolases
- glucose metabolism stops
What happens to adenosine once it’s stripped of all phosphates?
It diffuses out of the cell and is converted to uric acid
Once it’s converted, it can’t re-enter the cell, so that adenosine is permanently lost and the body has to form new adenosine
How difficult is it to produce more adenosine?
Extremely
the body can produce about 2% per hour
Depletion of high-energy phosphate is a primary killer in shock states
An intestinal obstruction may cause what kind of shock?
Hypovolemic
blocked venous flow leads to increased hydrostatic pressure in the capillaries, and fluid flows out of the vasculature into the gut
To make matters worse, a lot of that fluid is proteinaceous, so you get hypoproteinemia and hypovolemia
How does hemorrhagic hypovolemic shock differ from hypovolemia caused by plasma loss?
When just plasma is lost, the blood becomes much more viscous
exacerbates the sluggishness of blood flow
In anaphylaxis, where is histamine released from?
Basophils in the blood
mast cells in the tissues
What are the effects of histamine during an anaphylactic reaction?
- Venous dilation → Decreased venous return
- Arteriolar dilation → decreased arterial blood pressure
- Increased capillary permeability
Most cases of septic shock are caused by _____ bacteria
gram positive
What % total heat loss occurs via radiation?
60%
Convective heat loss results from:
air movement
The cooling effect of wind at low velocities is about proportional to:
the square root of the wind velocity
a wind of 4 miles per hour is about twice as effective for cooling as a wind of 1 mile per hour.
Why is being submerged in cold water so much worse than being exposed to cold air?
Water has a specific heat thousands of times greater than air, meaning it can absorb way more heat from the skin
Since water’s heat conductivity is so high, it’s impossible for the body to heat a thin layer of water like it does when creating an “insulator zone” in air
When water evaporates from the body, how much heat is lost?
58 kCal/1 g of water
(600-700 ml/day)
Why does the body sweat in high temperatures?
when the temperature of the surroundings are higher than body temperature, it will cause body temp to rise
the only way for the body to counteract this is to get rid of heat via evaporation
hence, sweat
sweat glands are innervated by ____ nerve fibers
cholinergic
(secrete acetylcholine but run in sympathetic nerves)
why is a high rate of sweating less dangerous in someone who is accustomed to heat?
the body learns to reabsorb higher levels of sodium as the precursor secretion moves from the gland to the pore
The main determinant in amount of salt loss through sweating is:
the rate of sweating, not the amount
at a slow rate, almost all of the sodium is reabsorbed between the gland and the pore
A person who is accustomed to high heat will produce more or less sweat?
More! Their rate of sweating will increase from 1 L/hr to 2-3 L/hr
In an acclimatized individual, why do they sweat more but lose less salt?
secretion of aldosterone causes salt retention
Pretty much all temperature regulating centers are located in the:
hypthalamus
deep body temperature receptors are located in: (3)
Spinal Cord
Abdominal Viscera
Great veins of the upper abdomen and thorax
both skin and deep body receptors are primarily designed to detect:
HYPOthermia
What are three important mechanisms to reduce body heat?
- Vasodilation
- Sweating
- Inhibition of shivering and chemical thermogenesis
Why do we get goosebumps?
Not helpful in humans, but in animals with fur, it allows them to entrap a thick layer of insulating air
If the body is cold, will thyroxine secretion be elevated or decreased?
What if the body is hot?
Elevated
Depressed
How does chemical thermogenesis release body heat?
norepinephrine and epinephrine are able to uncouple oxidation and phosphorylation
foodstuffs are oxidized and release heat instead of forming ATP
The degree of chemical thermogenesis that can occur in an animal is almost entirely dependent on:
the amount of brown fat
Why is brown fat optimal for chemical thermogenesis?
Contains lots of sympathetic nerve receptors, so its very sensitive to stimulation
contains large numbers of mitochondria capable of thermogenesis
How effective is chemical thermogenesis in adults?
In neonates?
10-15% increase in heat production
100% increase in heat production
Why are thyroid goiters more common in people living in cold climates?
Thyroxine production is increased by cold, leading to thyroid growth
What is the only really effective mechanism for preventing heat loss?
Behavioral control (putting on a coat, or going inside etc)
What happens to body temperature control when the spinal cord is severed?
It is severely impaired
Even though there are reflexes, the are very ineffective in comparison to hypothalamic control
Which cytokine is most important in causing fevers?
IL-1
Once bacteria begin to be broken down by macrophages, how long does it take for a fever to develop?
Often as little as 8-10 minutes
Why is aspirin antipyretic
It stops development of prostaglandin from arachidonic acid
Why is protein metabolism elevated in shock?
Widespread gluconeogenesis in response to the cell’s inability to uptake glucose begins to break down cellular structures
How does protein metabolism contribute to organ failure?
In anaerobic metabolism, protein breakdown liberates alanine, which is converted to pyruvate, which is is changed to lactic acid
lactic acid increases hemoglobin’s affinity for oxygen, resulting in tissue hypoxia and metabolic acidosis
Why are serum albumin levels low in patients with shock?
proteins are metabolized preferentially, starting with albumin and other plasma proteins
decreases capillary osmotic pressure and contributes to third spacing
why do patients in shock have hyperglycemia?
insulin resistance in the liver and muscles
adaptive response intended to ensure that glucose is available for the brain, cell nourishment and production, and wound healing
Neurogenic shock is caused by an imbalance between:
parasympathetic and sympathetic
Can be parasympathetic overstimulation
OR sympathetic understimulation
Neurogenic shock can be caused by any factor that stimulates _____ or inhibits _____
parasympathetic
sympathetic
Fainting can prevent someone from going into neurogenic shock. Why?
It puts them in a prone position, which equalizes BP from head to toe and actually prevents progression to a shock state
What are the six most commonly identified infections associated with sepsis in the ICU?
pneumonia
bloodstream
IVC
Intraabdominal
urosepsis
surgical wounds
What is the best definition of sepsis?
life-threatening organ dysfunction resulting from dysregulated host responses to infection
What are the two causes of lactic acidosis in septic shock?
tissue hypoxia
epinephrine-induced stimulation of aerobic glycolysis
What are the cellular effects of prolonged shock that causes lactic acidosis?
Increased NO synthesis
Activated K channels in vascular smooth muscle (hyperpolarized)
depletion of ADH
What molecules do gram-positive organisms release that trigger an inflammatory reaction?
Exotoxins:
Peptidoglycans
Lipoteichoic acids
Superantigens
What molecules do gram-negative organism release to trigger an inflammatory response?
Endotoxins:
LPS containing toxic lipid-A moiety
What are the three main proinflammatory cytokines that are released in response to bacterial toxins?
TNF- Alpha
IL1 alpha and Beta
IL6
A release of proinflammatory cytokines results in the activation of which systems?
Complement
Coagulation
Kinin
Monocyte-macrophage/Neutrophil
Name four anti-inflammatory cytokines
LPS binding protein
IL-1 receptor antagonist
IL10
Nitric oxide
A p/f ratio less than _____ is consistent with respiratory failure
300
What four things should be done with 3 hours of a patient presenting with sepsis-like symptoms?
- Measure lactate level
- Blood cultures
- Broad-spectrum antibiotics
- Fluid challenge of 30ml/kg crystalloid for hypotension OR lactate > 4
When should IV steroids be considered in a septic patient?
If BP is unresponsive to fluid resuscitation
In an intubated septic patient, plateau pressures should be less than
30 cmH20
When are CRP and PCT levels useful?
In trending the degree of inflammation, especially in infections that are occult (like osteomyelitis)
A drop in either can also be an indication that antibiotics are no longer needed
Which is only present in bacterial inflammation: CRP or PCT?
PCT
CRP is produced in the liver in response to IL-6 inflammation of any type
What’s the difference between primary and secondary MODS?
Primary MODS is organ failure as a direct result of a shock state
Secondary MODS happens when the body is recovering from a shock state and the primed inflammatory system receives a second postinjury insult, dramatically overreacting and leading to a SIRS state
Which two mediators are primarily responsible for secondary MODS?
IL-1 and TNF
Why do release of TNF and IL1 cause endothelial damage?
When stimulated by TNF or IL1, endothelial cells change to a pro-inflammatory state and express adhesion molecules, attracting and adhering neutrophils
The injured endothelium also produced NO, leading to a loss of tone
The endothelium loses its ability to express thrombomodulin, leading to clotting
it also becomes more permeable
What effect does kinin activation have on SVR?
Produces bradykinin, which reduces SVR
What is the respiratory burst?
When neutrophils adhere to the endothelium, they undergo a respiratory burst, releasing large amounts of ROS
These ROS are extremely damaging to the endothelium and the tissue cells, attacking DNA and leading to tissue necrosis
What are the three arachidonic acid metabolites?
Prostaglandins
Thromboxanes
Leukotrienes
What effect does TXA2 have on vasculature?
PGI2?
Powerful vasoconstrictor
Powerful vasodilator
Overall, the inflammatory processes at work in MODS cause ____ and _____
maldistribution of blood flow
hypermetabolism
In septic shock/MODS, why is oxygen uptake so low, despite adequate oxygen delivery?
- Autoregulation is lost in the capillary beds, because TXA2 causes selective vasoconstriction
Also, injured endothelial cells lose the ability to respond to normal vasodilators
- interstitial edema from increased permeability increases the distance between cells and capillaries
- Capillaries get clogged d/t thrombi and WBC clumps
What causes the hypermetabolism associated with sepsis?
Stress response from catecholamines and cortisol
TNG and IL-1
What is supply-dependent oxygen consumption
The combined decrease in oxygen delivery and increase in oxygen consumption cause an imbalance
Normally oxygen consumption is dependent on cellular needs, since more oxygen is delivered than is needed
In MODS, the amount of oxygen consumed is completely dependent on the amount the circulation is able to deliver
What causes reperfusion injury?
during ischemic episodes, xanthine dehydrogenase (an enzyme that combines xanthine and NAD to form NADH) is converted to xanthine oxidase (an enzyme that combines xanthine and O2 to form superoxide ROS)
During reperfusion of ischemic tissue, XOD is released en masse into the blood stream and attacks vulnerable tissues
What is capillary seal?
the term use to indicate that burn shock from increased permeability has ended
In addition to loss of the skin layer, why are burn victims so prone to infection?
WBCs are altered
Decreased opsonization and phagocytosis
What is endotoxemia?
translocation of bacteria from the gut into the bloodstream d/t altered gut perfusion
What is the minimum acceptable urine output in an infant?
A Child?
An Adolescent?
2 ml/kg/hr
1ml/kg/hr
0.5ml/kg/hr
What is the most common type of shock in children?
Hypovolemic
What usually causes hypovolemic shock in children?
Dehydration and trauma
What is the most common terminal cardiac rhythm in children?
Bradycardia
Signals impending collapse
When do children with shock become hypotensive?
Only when the shock is very, very severe
What is the most sensitive indicator of inadequate systemic perfusion in children?
lactate
Why are children < 2 at increased risk for dehydration?
They lack the ability to concentrate urine AND have a larger body surface area in relation to weight
