Module 13 - Circulatory Shock Flashcards

1
Q

Shock

A

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

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2
Q

Other than organs, what else can deteriorate in shock?

A

Heart muscle, walls of blood vessels and other circulatory parts

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3
Q

Shock usually results from …

A

inadequate cardiac output in relation to the needs of tissue metabolism

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4
Q

Stages of Shock

A
  1. Compensated
  2. Progressive
  3. Irreversible
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5
Q

Compensated Shocvk

A

first stage

tissue perfusion is deficient, but not to the degree that the cardiovascular system begins to deteriorate yet

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6
Q

Progressive Shock

A

second stage

circulatory system begins to deteriorate leading to a cycle ending in death unless appropriate treatment is started

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7
Q

Irreversible Shock

A

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

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8
Q

3 Major Types of Shock

A

Hypovolemic Shock

Obstructive Shock

Distributive Shock

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9
Q

Hypovolemic Shock

A

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

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10
Q

Obstructive Shock

A

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

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11
Q

Distributive Shock

A

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

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12
Q

What is the most common reason for Hypovolemic Shock?

A

Hemorrhage (massive volume loss)

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13
Q

What are some causes of Hypovolemic Shock

A

severe dehydration

severe burns

GI ulcers

Diarrhea

Vomiting

Sweating

Excess loss of fluid by the kidneys

Adrenal Insufficiency

Hemorrhaging (#1)

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14
Q

Why can adrenal insufficiency cause hypovolemic shock?

A

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

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15
Q

S/S of Hypovolemic Shock

A

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

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16
Q

What is a very early sign of hypovolemic shock and how can we tell?

A

Orthostatic Hypotension

A drop in blood pressure from a BASELINE that we know of at least 15 mmHg

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17
Q

Why is collapse of neck veins concerning in hypovolemic shock

A

decreased venous return to the heart

Central venous pressure will be below normal

however this is hard to assess

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18
Q

Why is Anxiety a symptom of hypovolemic shock

A

there is hyperactivity of the SNS from EP being released

This occurs due to decreased O2 in the brain for circulation

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19
Q

Pulse Pressure Equation

A

Systolic - Diastolic

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20
Q

Cardiac Output Equation

A

SV x Pulse

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21
Q

Why does pulse pressure decrease in hypovolemic shock

A

Blood volume loss causes systolic pressure to decline more rapidly than diastolic

We may not see a diastolic change

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22
Q

How much does pulse pressure change as it drops with hypovolemic shock

A

20 mmHg potentially

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23
Q

Why is there a brief initial rise in BP in hypovolemic shock

A

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

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24
Q

Why does Respiratory Alkalosis occur early in hypovolemic shock

A

hyperventilation (increased RR) from trying to fix tissue hypoxia

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25
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
26
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
27
How does orthostatic hypotension progress in hypovolemic shock
eventually the pulse will remain rapid and thready regardless of position
28
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
29
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
30
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)
31
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
32
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
33
Burns cause loss of ___ so ___ may be used as a replacement
plasma; albumin
34
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
35
NS and LR are __ solutions
isotonic (stay where they are placed)
36
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
37
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
38
What position can hypovolemic shock patients go in?
Modified Trendelenburg (laying flat with legs up 45 degrees) NOT trendelenburg
39
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
40
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
41
Why is oxygen given to hypovolemic shock patients
to improve hypoxia!
42
Why is sodium bicarbonate given to hypovolemic shock patients
to correct severe metabolic acidosis when the pH is less than 7.2
43
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
44
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
45
What is the worst type of shock
cardiogenic shock
46
why is cardiogenic shock the worst type
because it has the worst prognosis as it involved pump failure and cardiac tamponade
47
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
48
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
49
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
50
Eventually all forms of shock lead to ___ ___
heart damage
51
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
52
What has most input into the tone of the vasculature
SNS not PNS
53
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)
54
Spinal cord injury leading to neurogenic shock is also known as...
AUTONOMIC DYSREFLEXIA (vasoconstriction above injury level leading to massive vasodilation below injury level)
55
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
56
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
57
Anaphylactic is what kind of hypersensitivity reaction
A Type I Hypersensitivity Reaction
58
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
59
SRS-A
slow acting substances of anaphylaxis that move fluid into tissues
60
Symptoms of Anaphylactic Shock
wheezing sniffing laryngeal edema bronchial edema suffocation severe allergies
61
Treatments for Anaphylactic Shock
Epinephrine (EP) Corticosteroids
62
How does EP treat Anaphylactic Shock
increases vasoconstriction
63
How does Corticosteroids treat anaphylactic shock
Decreases capillary permeability stabilizes capillary membrane to prevent leakage from massive fluid shifts that occur given after EP
64
Bacteremia
bacteria in the blood the immune system takes care of it though
65
Septicemia
bacterial infection in the blood that causes sickness that cannot be fought off
66
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
67
What is the causative agent of septic shock
Gram Negative Bacteria and products!!! ex: E Coli (40%), Pseudomonas, Proteus, Klebsiella, Enterobacter, Serratia
68
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
69
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
70
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
71
What sort of chronic diseases are at risk for septic shock
DM ETOH use Ca Liver issues CV renal issues
72
Why can ventilators cause septic shock?
usually the lower lungs are sterile, but Iatrogenically bacteria could get in
73
Progression of Septic Shock
1. bacteria enter blood and are destroyed by macrophages and other immune cells and complement systems 2. Releases gram negative endotoxins 3. Release of chemical mediators (complement, kinins, histamines, prostaglandins) 4. Widespread vasodilation and increased vascular permeability
74
Arachidonic Acid from gram negative bacteria that are lysed will turn into ___
prostaglandins
75
Stages of Septic Shock
Warm Shock Cold Shock
76
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
77
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
78
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
79
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
80
What causes the increased RR in warm shock
effect of endotoxins on the respiratory center in the medulla
81
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
82
Hageman Factor
clotting factor 12(XII) plasma protein that works to accelerate clotting in the capillaries when there is damage
83
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
84
Cold Shock
second stage of septic shock - associated with hypodynamic states it causes hypodynamics, subnormal body temperature, ABG changes, ARDS, and ARF
85
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
86
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
87
What do ABGs show in cold shock
Hypoxemia and Metabolic Acidosis
88
ARDS as a result of Cold Shock
Acute Respiratory Distress Syndrome - "wet lungs" it is respiratory failure from accumulation of fluid in the lungs
89
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
90
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
91
Why give septic shock pts IV fluids
to increase circulating volume
92
Swans Ganz Monitoring
can monitor central venous pressure
93
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
94
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)
95
Nitroprusside
medicine given to septic shock patients Dilates veins and arteries to decrease total peripheral resistance (TPR)
96
IV Nitroglycerine and Septic Shock
given to increase CO and decrease TPR
97
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
98
Benadryl and Septic Shock
can block histamine release
99
IV Indomethacin
blocks the synthesis of prostaglandins - a major mediator of inflammation NSAID given to septic shock patients
100
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
101
All forms of untreated shock will turn into...
cardiogenic shock
102
Survival rate of cardiogenic shock
15-20% worst prognosis of all shock
103
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)
104
We monitor Cardiogenic shock...
invasively with a pump that is inserted in the periphery to increase aortic pressure
105
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
106
Treatments for Cardiogenic Shock
Swan Ganz Catheter Intra-Aortic Balloon Pump Drugs like Dopamine and Dobutamine
107
What does Dopamine and Dobutamine do for Cardiogenic Shock
it improves CO and decreases TPR
108
What are some complications that can occur d/t shock?
ARDS ARF GI Complications DIC MODS
109
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
110
When can ARDS set in after shock?
24-48 hours after injury occurs
111
What would an ABG show if someone has ARDS
hypoxemia and hypercapnia
112
Impaired diffusion across thickened alveolar-capillary membranes in ARDS causes what
a V/Q Mismatch
113
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
114
What is an important late cause of death in severe shock
ARF
115
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
116
What determines degree of renal damage in shock?
severity and duration of shock
117
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
118
When monitoring for shock related ARF what should you monitor
UO during shock serum creatinine and BUN
119
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
120
___ is a common symptom of GI ulceration with onset in __ to __ days
bleeding; 2; 10
121
GI lesions provide what?
a portal of entry for bacteria leading to sepsis and shock
122
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
123
What leads to the increased risk of bleeding in DIC
the depletion of PLTs and coagulation factors
124
DIC occurs in how many persons with sepsis or septic shock
30-50%
125
What is DIC thought to be caused by from shock?
The presence of inflammatory mediators
126
Occurrence of DIC is...
an independent predictor of mortality (it has a very low survival rate)
127
MODS
Multiple organ dysfunction syndrome presence of altered organ function such that homeostasis cannot be maintained and multiple organs die as a result
128
What organs are commonly impacted by MODS
kidneys lungs liver brain heart
129
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
130
Risk factors for MODS development
sepsis shock prolonged periods of HTN hepatic dysfunction trauma infarcted bowel advanced age alcohol abuse (fragile vessels bleed easily)
131
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