Module 13 - Circulatory Shock Flashcards
Shock
Generalized inadequacy of blood flow throughout the body to the extent that the tissues are damaged
Can lead to every organ having no blood flow and leading to organ death ultimately
Other than organs, what else can deteriorate in shock?
Heart muscle, walls of blood vessels and other circulatory parts
Shock usually results from …
inadequate cardiac output in relation to the needs of tissue metabolism
Stages of Shock
- Compensated
- Progressive
- Irreversible
Compensated Shocvk
first stage
tissue perfusion is deficient, but not to the degree that the cardiovascular system begins to deteriorate yet
Progressive Shock
second stage
circulatory system begins to deteriorate leading to a cycle ending in death unless appropriate treatment is started
Irreversible Shock
third stage
shock has progressed to the point where all forms of therapy will be inadequate to save a person’s life
this is the point where the heart cannot pump effectively causing a decrease in CO, and this CO will continue to drop until a point of no return
3 Major Types of Shock
Hypovolemic Shock
Obstructive Shock
Distributive Shock
Hypovolemic Shock
Shock from loss of whole blood, plasma, or ECF
It comes from a lack of circulating volume which causes a lack of perfusion
ex: Burns causing plasma loss
Obstructive Shock
Inability of the heart to fill properly (cardiogenic shock including cardiac tamponade)
Obstruction to outflow from the heart occurs (PE, pneumothorax, etc)
It is a difficulty against pumping
Distributive Shock
Loss of sympathetic vasomotor tone (Neurogenic shock)
Presence of vasodilating substances in the blood (anaphylactic shock)
Presence of inflammatory mediators in the systemic circulation (septic shock)
You have enough blood and volume in the system, but so much vasodilation occurs so it is stretched thin across the body so not enough gets to the organs - anything causing massive VASODILATION can cause this if the blood is heading to the periphery
What is the most common reason for Hypovolemic Shock?
Hemorrhage (massive volume loss)
What are some causes of Hypovolemic Shock
severe dehydration
severe burns
GI ulcers
Diarrhea
Vomiting
Sweating
Excess loss of fluid by the kidneys
Adrenal Insufficiency
Hemorrhaging (#1)
Why can adrenal insufficiency cause hypovolemic shock?
Not enough ADH means increased UO causing hypovolemia (like in diabetes)
Decrease in aldosterone means the body will not hold sodium so water won’t be held either
S/S of Hypovolemic Shock
Hypotension
Collapse of neck Veins
Poor Capillary Refill time
Anxiety
Tachycardia, Increased RR, Weak Thready Pulse
Decreased Pulse Pressure
Brief Initial rise in BP
Respiratory Alkalosis Early in Shock
Orthostatic Hypotension
Decreased UO
Pale cool moist skin
Sustained low blood pressure
Metabolic Acidosis later on
What is a very early sign of hypovolemic shock and how can we tell?
Orthostatic Hypotension
A drop in blood pressure from a BASELINE that we know of at least 15 mmHg
Why is collapse of neck veins concerning in hypovolemic shock
decreased venous return to the heart
Central venous pressure will be below normal
however this is hard to assess
Why is Anxiety a symptom of hypovolemic shock
there is hyperactivity of the SNS from EP being released
This occurs due to decreased O2 in the brain for circulation
Pulse Pressure Equation
Systolic - Diastolic
Cardiac Output Equation
SV x Pulse
Why does pulse pressure decrease in hypovolemic shock
Blood volume loss causes systolic pressure to decline more rapidly than diastolic
We may not see a diastolic change
How much does pulse pressure change as it drops with hypovolemic shock
20 mmHg potentially
Why is there a brief initial rise in BP in hypovolemic shock
EP was released from the SNS response
But it will eventually drop from loss of blood
Blood vessels of the brain and coronary arteries are not affected by the generalized vasoconstriction either so it will drop
Why does Respiratory Alkalosis occur early in hypovolemic shock
hyperventilation (increased RR) from trying to fix tissue hypoxia
What can occur after Respiratory Alkalosis in hypovolemic shock
Metabolic Acidosis from lactic acid buildup when tissues are forced to switch from aerobic (oxidative) metabolism to anaerobic metabolism
The breathing ends up depressed later on as well which contributes too
Orthostatic Hypotension
a pulse rate increase greater than 20 bpm when position changes from lying to sitting or sitting to standing as well as a drop in BP
How does orthostatic hypotension progress in hypovolemic shock
eventually the pulse will remain rapid and thready regardless of position
Why is there decreased UO in hypovolemic shock
there is decreased blood flow to the kidneys
This causes ADH and renin secretion to increase blood volume which also helps retain fluids instead of losing it
eventually this will lead to pre renal failure though
Why is the skin pale, cool, and moist in hypovolemic shock
there is vasoconstriction leading to decreased skin perfusion - so blood is being shunted to central circulation from the periphery
They may feel clammy skin the skin has lost the ability to hold back water and fluid can ooze through the capillaries as a result
At what point of blood volume loss is systolic blood pressure dropped significantly and sustained low blood pressure begins
when 15-20% of the blood volume is lost (that’s 15-20% of 5 Liters)
Treatments for Hypovolemic Shock
Replacement of Fluids
Blood transfusions
Dextran solutions, salt poor albumin solutions
normal saline and lactated ringers solution
monitor UO
elevate legs to 45 degrees
oxygen
sodium bicarbonate IV
maintaining a calm atmosphere
keep covered but not warm
Why do we give hypovolemic shock patients whole or packed blood, normal saline, dextran solutions and salt poor albumin?
To give circulating volume for some
To increase osmotic pressure to maintain fluid in vascular spaces to increase volume and expansion for others
Burns cause loss of ___ so ___ may be used as a replacement
plasma; albumin
Why do we give hypovolemic shock patients Lactated Ringer’s Solution?
it becomes bicarbonate in the body which can buffer the acids of metabolic acidosis
also, it has K and Ca available to them
NS and LR are __ solutions
isotonic (stay where they are placed)
Why monitor hypovolemic shock patient urinary output?
Because it is critical to assess renal perfusion and the effect of fluid replacement
It tells us if the kidney is being perfused and also if fluid replacement is working - more urine means kidneys are getting the blood volume they need to make urine
Why elevate hypovolemic shock patient’s legs 45 degrees?
It can act like an autotransfusion that releases 500 ccs from the legs to go to the heart
What position can hypovolemic shock patients go in?
Modified Trendelenburg (laying flat with legs up 45 degrees) NOT trendelenburg
Why do we not place hypovolemic shock patients in Trendelenburg position?
It makes abdominal contents press against the diaphragm and vena cava which interferes with ventilation and venous return to the heart
This blood will bypass the heart and head for the brain
What are the effects of blood flow for hypovolemic shock patients in the following positions: Standing, Lying, Trendelenburg, Modified Trendelenburg
Standing: Decreased blood volume and decreased brain perfusion available - its in the legs
Lying: Blood distributed throughout the body so there is decreased brain perfusion
Trendelenburg: Increased flow the brain but it can bypass the heart and have abdominal contents put pressure on the diaphragm and vena cava
Modified Trendelenburg: Allows blood flow back to the heart at a 45 degree angle of the legs
Why is oxygen given to hypovolemic shock patients
to improve hypoxia!
Why is sodium bicarbonate given to hypovolemic shock patients
to correct severe metabolic acidosis when the pH is less than 7.2
Why is it very important to remain a calm atmosphere and watch what you say during a shock situation
we do not want to cause unneeded anxiety
also, smell and hearing are the last senses to go so someone appearing catatonic can still here what you say
Why are hypovolemic shock patients kept covered but not too warm or too cold
because we do not want to counteract peripheral vasoconstriction and cause vasodilation which will drop pressure
we also do not want them shivering since the O2 and metabolism demand will increase
What is the worst type of shock
cardiogenic shock
why is cardiogenic shock the worst type
because it has the worst prognosis as it involved pump failure and cardiac tamponade
Compensated Shock
When the corrective measures are working in the body
Low Blood volume is sensed by baroreceptors that send messages to the brain and SNS (GAS) occurs leading to compensation
What does compensated shock look like?
hypovolemia –> sensed by baroreceptors –> SNS reflex compensation (GAS) –> kidney renin –> RAA to Angiotensin II
Angiotensin II –> adrenal cortex secretes aldosterone –> Na and Water retention –> Vasoconstriction
Vasoconstriction –> sustained vasoconstriction and readjustment of blood volume
What does uncompensated shock leading to cardiovascular deterioration look like
further uncompensated loss of blood volume –> arterial pressure decreases –> decreased O2 and nutrients to cardiac muscles –> weak heart muscles –> further drop in arterial pressure –> baroreceptors fail –> vasodilation –> further BP and CO drop –> ARDS-ARF –>
ARDS-ARF–> sludge blood full of lactic acid, carbonic acid and metabolic acidosis begins –> intravascular clotting begins and DIC starts –> tissues release substances toxic to the myocardium - myocardial depressant factors –> generalized myocardial and body cell deterioration –> irreversible shock starts –> death
Eventually all forms of shock lead to ___ ___
heart damage
Neurogenic Shock
Normal amount of blood but extensive dilation of blood vessels d/t loss of sympathetic tone occurs
Vasodilation from lack of SNS tone
What has most input into the tone of the vasculature
SNS not PNS
Causes of Neurogenic Shock
Deep General Anesthesia (depresses baroreceptors)
Spinal Anesthesia (blocks SNS)
Brain Damage (destroys vasomotor receptors)
Spinal Cord Injury (vasodilation below level of damage)
Severe Hypoglycemia (starvation of brain cells)
Spinal cord injury leading to neurogenic shock is also known as…
AUTONOMIC DYSREFLEXIA (vasoconstriction above injury level leading to massive vasodilation below injury level)
Is fainting neurogenic shock
NO
It is a severe PNS RESPONSE
Dilation of peripheral blood vessels and decreased heart rate occurs
This is a large vagal response = PNS
Anaphylactic Shock
increase in the size and permeability of the vascular bed
massive vasodilation occurs with adequate blood volume due to vasoactive substances like histamine
Anaphylactic is what kind of hypersensitivity reaction
A Type I Hypersensitivity Reaction
Type 1 Hypersensitivity Reaction
release of vasodilating histamine and SRS-A which also increase capillary permeability which allows for massive fluid shifts into the tissues
fluid in these tissues are then not available for circulation
SRS-A
slow acting substances of anaphylaxis that move fluid into tissues
Symptoms of Anaphylactic Shock
wheezing
sniffing
laryngeal edema
bronchial edema
suffocation
severe allergies
Treatments for Anaphylactic Shock
Epinephrine (EP)
Corticosteroids
How does EP treat Anaphylactic Shock
increases vasoconstriction
How does Corticosteroids treat anaphylactic shock
Decreases capillary permeability
stabilizes capillary membrane to prevent leakage from massive fluid shifts that occur
given after EP
Bacteremia
bacteria in the blood
the immune system takes care of it though
Septicemia
bacterial infection in the blood that causes sickness that cannot be fought off
Septic Shock
Septicemia caused by gram negative sepsis or endotoxic shock
These gram negative products are vasoactive (cause vasodilation) and overwhelming shock can occur as a result
What is the causative agent of septic shock
Gram Negative Bacteria and products!!!
ex: E Coli (40%), Pseudomonas, Proteus, Klebsiella, Enterobacter, Serratia
Risk Factors for Septic Shock
Very young (<1) or Very Old (>65)
Malnutrition or Physical Debilitation
Chronic Diseases
UTI
cholecystitis
obstruction and ruptured appendix
invasive procedures
immunosuppression
ventilators
Why can UTI cause septic shock
E Coli often cause UTI and they can get into the kidneys and then the blood to cause septicemia
How can appendicitis and obstruction/rupturing cause Septic shock?
the peritoneum is usually a sterile cavity and this can make it unsterile by spilling contents into it and getting into the blood
What sort of chronic diseases are at risk for septic shock
DM
ETOH use
Ca
Liver issues
CV
renal issues
Why can ventilators cause septic shock?
usually the lower lungs are sterile, but Iatrogenically bacteria could get in
Progression of Septic Shock
- bacteria enter blood and are destroyed by macrophages and other immune cells and complement systems
- Releases gram negative endotoxins
- Release of chemical mediators (complement, kinins, histamines, prostaglandins)
- Widespread vasodilation and increased vascular permeability
Arachidonic Acid from gram negative bacteria that are lysed will turn into ___
prostaglandins
Stages of Septic Shock
Warm Shock
Cold Shock
Warm Shock
stage 1 of septic shock - only applies to this shock not hypovolemic or anaphylactic shock - associated with hyperdynamic states
leads to hyperdynamics, fever, and profound diuresis, increased RR, activation of clotting, and decreased cerebral perfusion
What occurs with hyperdynamics of warm shock
increased CO from low peripheral vascular resistance
Vasodilation from histamines, bradykinins, and serotonin
Increased capillary permeability
Fluids shift into tissues and third spaces
What causes Fever in warm shock
endogenous pyrogens from WBCs that work on the hypothalamus thermostat which resets causing fever, increased metabolic rate, and increased respiration rate
What causes profound diuresis in warm shock
Debris in the blood causing high osmotic load for kidneys - dead bacteria, dead phagocytes, waste products of cellular metabolism
The hyperdynamic state makes a lot of waste products causing a load on the kidney and increased diuresis - the glomerulus will become leaky and allow RBC and proteins filter through which also increases osmotic gradient pulling more fluid in and increasing UO
What causes the increased RR in warm shock
effect of endotoxins on the respiratory center in the medulla
What causes activation of clotting in warm shock and what can it lead to
complement damage (any damage) to the vascular endothelium and Hageman factor accelerates clotting in the capillaries
uses up the clotting factors
this leads to petechiae and mottling below the knees
Hageman Factor
clotting factor 12(XII)
plasma protein that works to accelerate clotting in the capillaries when there is damage
What occurs as a result of decreased cerebral perfusion in warm shock
slow responses, restlessness, confusion, thrashing
They often feel okay though they are not cognitively aware of what is happening due to endorphin release
Cold Shock
second stage of septic shock - associated with hypodynamic states
it causes hypodynamics, subnormal body temperature, ABG changes, ARDS, and ARF
What occurs with the hypodynamics of cold shock
Decreased CO occurring 6-72 hours after warm shock started
Selective vasoconstriction of renal, splanchnic, and pulmonary arteries
DIC in warm shock leads to MDF from the pancreas to release and endorphins which depresses myocardium
Overall heart slows down and is less efficient
Why is there subnormal body temperature in cold shock
from peripheral vasoconstriction in a generalized fashion
they are cold, clammy, pale skin, mottled skin generalized
What do ABGs show in cold shock
Hypoxemia and Metabolic Acidosis
ARDS as a result of Cold Shock
Acute Respiratory Distress Syndrome - “wet lungs”
it is respiratory failure from accumulation of fluid in the lungs
What causes ARDS and why is this important to note
It is often from inadequate perfusion to the kidneys and is a pre renal cause of renal failure since its a hypovolemic issue
Treatments for Septic Shock
IV Fluids (fluid expanders, balanced electrolyte solutions, FFP)
Swanz Ganz Monitoring
Antibiotics
IV Dopamine
Nitroprusside
IV Nitroglycerine
Steroids
Benadryl
IV Indomethacin
Why give septic shock pts IV fluids
to increase circulating volume
Swans Ganz Monitoring
can monitor central venous pressure
Why give antibiotics to septic shock pts and why can it be a problem
treats underlying cause of infection, but giving it increases osmotic load for the kidneys which can precipitate a turn of events
despite this we need to treat it with broad spectrum then specific antibiotics after C&S
Death of bacteria can make a person worse via endotoxin release
ex: Cephalosporins, Aminoglycosides, Penicillin derivatives
Why give Dopamine to a Septic Shock pt
Dilates splanchnic and renal vesselqs and increased myocardial contractility of the heart –> this increases CO and decreases peripheral vascular resistance (TPR)
Nitroprusside
medicine given to septic shock patients
Dilates veins and arteries to decrease total peripheral resistance (TPR)
IV Nitroglycerine and Septic Shock
given to increase CO and decrease TPR
Why give steroids in septic shock and anaphylactic shock but NOT hypovolemic shock?
It stabilizes capillary membranes and decreases release of MDF and complement activation
Benadryl and Septic Shock
can block histamine release
IV Indomethacin
blocks the synthesis of prostaglandins - a major mediator of inflammation
NSAID
given to septic shock patients
Cardiogenic Shock
Worst Shock caused by the heart failing as a pump due to decreased contractility (ex: Cardiac Tamponade)
Decreased perfusion through the coronary arteries means extensive damage and this continues to get worse and worse
All forms of untreated shock will turn into…
cardiogenic shock
Survival rate of cardiogenic shock
15-20%
worst prognosis of all shock
When does Cardiogenic Shock occur
10% of all AMI with loss of 40% of more of the myocardium
Cardiac Tamponade patients
Pulmonary Embolism Patients
(Stuff that stops pumping)
We monitor Cardiogenic shock…
invasively with a pump that is inserted in the periphery to increase aortic pressure
Causes for Cardiogenic Shock
Heart failure as a pump d/t decreased contractility –> decreased coronary circulation –> myocardium damaged further –> more pump failure
some event that occurs in late stages of other types of circulatory shock
Treatments for Cardiogenic Shock
Swan Ganz Catheter
Intra-Aortic Balloon Pump
Drugs like Dopamine and Dobutamine
What does Dopamine and Dobutamine do for Cardiogenic Shock
it improves CO and decreases TPR
What are some complications that can occur d/t shock?
ARDS
ARF
GI Complications
DIC
MODS
ARDS
acute respiratory distress syndrome
lethal form of respiratory failure with a higher than 50% mortality
Results in stiff lungs that are difficult to inflate
“Wet Lungs” because fluid in the alveolar space cause stiff lungs
When can ARDS set in after shock?
24-48 hours after injury occurs
What would an ABG show if someone has ARDS
hypoxemia and hypercapnia
Impaired diffusion across thickened alveolar-capillary membranes in ARDS causes what
a V/Q Mismatch
What is ARDS thought to result from
neutrophil activity and endothelial injury with leakage of fluid and plasma proteins into the interstitium and alveolar spaces
Abnormalities in production, composition, and function of surfactant as well
What is an important late cause of death in severe shock
ARF
What is the primary underlying cause of Shock related ARF
septic shock - endotoxins acting as potent vasoconstrictors capable of activating SNS and causing intravascular clotting
trauma
What determines degree of renal damage in shock?
severity and duration of shock
The most common ARF lesion…
acute tubular necrosis
usually reversible although function may take weeks or months to return to normal
pre renal issues cause this intra renal issue which is the most common cause of intra renal failure
When monitoring for shock related ARF what should you monitor
UO during shock
serum creatinine and BUN
Why are there GI complications with shock?
In shock, there is widespread vasoconstriction to blood vessels supplying the GI tract
The GI tract is particularly vulnerable to ischemia and there is decreased mucosal perfusion due to the widespread vasoconstriction
As a result superficial mucosal lesions of the stomach and duodenum can develop in hours
___ is a common symptom of GI ulceration with onset in __ to __ days
bleeding; 2; 10
GI lesions provide what?
a portal of entry for bacteria leading to sepsis and shock
DIC
Disseminated Intravascular Coagulation
widespread activation of the coagulation system with formation of fibrin clots and thrombotic occlusion of small and midsized vessels –> leads to ischemic damage and organ failure
What leads to the increased risk of bleeding in DIC
the depletion of PLTs and coagulation factors
DIC occurs in how many persons with sepsis or septic shock
30-50%
What is DIC thought to be caused by from shock?
The presence of inflammatory mediators
Occurrence of DIC is…
an independent predictor of mortality (it has a very low survival rate)
MODS
Multiple organ dysfunction syndrome
presence of altered organ function such that homeostasis cannot be maintained and multiple organs die as a result
What organs are commonly impacted by MODS
kidneys
lungs
liver
brain
heart
Why is MODS life threatening
It is the most frequent cause of death in non coronary ICUs
mortality varies from 30-100% depending on the number of organs involved
Risk factors for MODS development
sepsis
shock
prolonged periods of HTN
hepatic dysfunction
trauma
infarcted bowel
advanced age
alcohol abuse (fragile vessels bleed easily)
Management of MODS depends on what
what organs and how many organs are dysfunctioning
this can make it hard to manage if many are dysfunctioning, which also causes a higher mortality rate
