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NURS361 - Pathophysiology II > Module 13 - Circulatory Shock > Flashcards

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
Q

What can occur after Respiratory Alkalosis in hypovolemic shock

A

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

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26
Q

Orthostatic Hypotension

A

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

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27
Q

How does orthostatic hypotension progress in hypovolemic shock

A

eventually the pulse will remain rapid and thready regardless of position

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28
Q

Why is there decreased UO in hypovolemic shock

A

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

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29
Q

Why is the skin pale, cool, and moist in hypovolemic shock

A

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

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30
Q

At what point of blood volume loss is systolic blood pressure dropped significantly and sustained low blood pressure begins

A

when 15-20% of the blood volume is lost (that’s 15-20% of 5 Liters)

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31
Q

Treatments for Hypovolemic Shock

A

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

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32
Q

Why do we give hypovolemic shock patients whole or packed blood, normal saline, dextran solutions and salt poor albumin?

A

To give circulating volume for some

To increase osmotic pressure to maintain fluid in vascular spaces to increase volume and expansion for others

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33
Q

Burns cause loss of ___ so ___ may be used as a replacement

A

plasma; albumin

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34
Q

Why do we give hypovolemic shock patients Lactated Ringer’s Solution?

A

it becomes bicarbonate in the body which can buffer the acids of metabolic acidosis

also, it has K and Ca available to them

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35
Q

NS and LR are __ solutions

A

isotonic (stay where they are placed)

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36
Q

Why monitor hypovolemic shock patient urinary output?

A

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

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37
Q

Why elevate hypovolemic shock patient’s legs 45 degrees?

A

It can act like an autotransfusion that releases 500 ccs from the legs to go to the heart

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38
Q

What position can hypovolemic shock patients go in?

A

Modified Trendelenburg (laying flat with legs up 45 degrees) NOT trendelenburg

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39
Q

Why do we not place hypovolemic shock patients in Trendelenburg position?

A

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

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40
Q

What are the effects of blood flow for hypovolemic shock patients in the following positions: Standing, Lying, Trendelenburg, Modified Trendelenburg

A

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

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41
Q

Why is oxygen given to hypovolemic shock patients

A

to improve hypoxia!

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42
Q

Why is sodium bicarbonate given to hypovolemic shock patients

A

to correct severe metabolic acidosis when the pH is less than 7.2

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43
Q

Why is it very important to remain a calm atmosphere and watch what you say during a shock situation

A

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

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44
Q

Why are hypovolemic shock patients kept covered but not too warm or too cold

A

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

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45
Q

What is the worst type of shock

A

cardiogenic shock

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46
Q

why is cardiogenic shock the worst type

A

because it has the worst prognosis as it involved pump failure and cardiac tamponade

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47
Q

Compensated Shock

A

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

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48
Q

What does compensated shock look like?

A

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

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49
Q

What does uncompensated shock leading to cardiovascular deterioration look like

A

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

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50
Q

Eventually all forms of shock lead to ___ ___

A

heart damage

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51
Q

Neurogenic Shock

A

Normal amount of blood but extensive dilation of blood vessels d/t loss of sympathetic tone occurs

Vasodilation from lack of SNS tone

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52
Q

What has most input into the tone of the vasculature

A

SNS not PNS

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53
Q

Causes of Neurogenic Shock

A

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
Q

Spinal cord injury leading to neurogenic shock is also known as…

A

AUTONOMIC DYSREFLEXIA (vasoconstriction above injury level leading to massive vasodilation below injury level)

55
Q

Is fainting neurogenic shock

A

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
Q

Anaphylactic Shock

A

increase in the size and permeability of the vascular bed

massive vasodilation occurs with adequate blood volume due to vasoactive substances like histamine

57
Q

Anaphylactic is what kind of hypersensitivity reaction

A

A Type I Hypersensitivity Reaction

58
Q

Type 1 Hypersensitivity Reaction

A

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
Q

SRS-A

A

slow acting substances of anaphylaxis that move fluid into tissues

60
Q

Symptoms of Anaphylactic Shock

A

wheezing

sniffing

laryngeal edema

bronchial edema

suffocation

severe allergies

61
Q

Treatments for Anaphylactic Shock

A

Epinephrine (EP)

Corticosteroids

62
Q

How does EP treat Anaphylactic Shock

A

increases vasoconstriction

63
Q

How does Corticosteroids treat anaphylactic shock

A

Decreases capillary permeability

stabilizes capillary membrane to prevent leakage from massive fluid shifts that occur

given after EP

64
Q

Bacteremia

A

bacteria in the blood

the immune system takes care of it though

65
Q

Septicemia

A

bacterial infection in the blood that causes sickness that cannot be fought off

66
Q

Septic Shock

A

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
Q

What is the causative agent of septic shock

A

Gram Negative Bacteria and products!!!

ex: E Coli (40%), Pseudomonas, Proteus, Klebsiella, Enterobacter, Serratia

68
Q

Risk Factors for Septic Shock

A

Very young (<1) or Very Old (>65)

Malnutrition or Physical Debilitation

Chronic Diseases

UTI

cholecystitis

obstruction and ruptured appendix

invasive procedures

immunosuppression

ventilators

69
Q

Why can UTI cause septic shock

A

E Coli often cause UTI and they can get into the kidneys and then the blood to cause septicemia

70
Q

How can appendicitis and obstruction/rupturing cause Septic shock?

A

the peritoneum is usually a sterile cavity and this can make it unsterile by spilling contents into it and getting into the blood

71
Q

What sort of chronic diseases are at risk for septic shock

A

DM

ETOH use

Ca

Liver issues

CV

renal issues

72
Q

Why can ventilators cause septic shock?

A

usually the lower lungs are sterile, but Iatrogenically bacteria could get in

73
Q

Progression of Septic Shock

A
  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
Q

Arachidonic Acid from gram negative bacteria that are lysed will turn into ___

A

prostaglandins

75
Q

Stages of Septic Shock

A

Warm Shock

Cold Shock

76
Q

Warm Shock

A

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
Q

What occurs with hyperdynamics of warm shock

A

increased CO from low peripheral vascular resistance

Vasodilation from histamines, bradykinins, and serotonin

Increased capillary permeability

Fluids shift into tissues and third spaces

78
Q

What causes Fever in warm shock

A

endogenous pyrogens from WBCs that work on the hypothalamus thermostat which resets causing fever, increased metabolic rate, and increased respiration rate

79
Q

What causes profound diuresis in warm shock

A

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
Q

What causes the increased RR in warm shock

A

effect of endotoxins on the respiratory center in the medulla

81
Q

What causes activation of clotting in warm shock and what can it lead to

A

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
Q

Hageman Factor

A

clotting factor 12(XII)

plasma protein that works to accelerate clotting in the capillaries when there is damage

83
Q

What occurs as a result of decreased cerebral perfusion in warm shock

A

slow responses, restlessness, confusion, thrashing

They often feel okay though they are not cognitively aware of what is happening due to endorphin release

84
Q

Cold Shock

A

second stage of septic shock - associated with hypodynamic states

it causes hypodynamics, subnormal body temperature, ABG changes, ARDS, and ARF

85
Q

What occurs with the hypodynamics of cold shock

A

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
Q

Why is there subnormal body temperature in cold shock

A

from peripheral vasoconstriction in a generalized fashion

they are cold, clammy, pale skin, mottled skin generalized

87
Q

What do ABGs show in cold shock

A

Hypoxemia and Metabolic Acidosis

88
Q

ARDS as a result of Cold Shock

A

Acute Respiratory Distress Syndrome - “wet lungs”

it is respiratory failure from accumulation of fluid in the lungs

89
Q

What causes ARDS and why is this important to note

A

It is often from inadequate perfusion to the kidneys and is a pre renal cause of renal failure since its a hypovolemic issue

90
Q

Treatments for Septic Shock

A

IV Fluids (fluid expanders, balanced electrolyte solutions, FFP)

Swanz Ganz Monitoring

Antibiotics

IV Dopamine

Nitroprusside

IV Nitroglycerine

Steroids

Benadryl

IV Indomethacin

91
Q

Why give septic shock pts IV fluids

A

to increase circulating volume

92
Q

Swans Ganz Monitoring

A

can monitor central venous pressure

93
Q

Why give antibiotics to septic shock pts and why can it be a problem

A

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
Q

Why give Dopamine to a Septic Shock pt

A

Dilates splanchnic and renal vesselqs and increased myocardial contractility of the heart –> this increases CO and decreases peripheral vascular resistance (TPR)

95
Q

Nitroprusside

A

medicine given to septic shock patients

Dilates veins and arteries to decrease total peripheral resistance (TPR)

96
Q

IV Nitroglycerine and Septic Shock

A

given to increase CO and decrease TPR

97
Q

Why give steroids in septic shock and anaphylactic shock but NOT hypovolemic shock?

A

It stabilizes capillary membranes and decreases release of MDF and complement activation

98
Q

Benadryl and Septic Shock

A

can block histamine release

99
Q

IV Indomethacin

A

blocks the synthesis of prostaglandins - a major mediator of inflammation

NSAID

given to septic shock patients

100
Q

Cardiogenic Shock

A

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
Q

All forms of untreated shock will turn into…

A

cardiogenic shock

102
Q

Survival rate of cardiogenic shock

A

15-20%

worst prognosis of all shock

103
Q

When does Cardiogenic Shock occur

A

10% of all AMI with loss of 40% of more of the myocardium

Cardiac Tamponade patients

Pulmonary Embolism Patients

(Stuff that stops pumping)

104
Q

We monitor Cardiogenic shock…

A

invasively with a pump that is inserted in the periphery to increase aortic pressure

105
Q

Causes for Cardiogenic Shock

A

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
Q

Treatments for Cardiogenic Shock

A

Swan Ganz Catheter

Intra-Aortic Balloon Pump

Drugs like Dopamine and Dobutamine

107
Q

What does Dopamine and Dobutamine do for Cardiogenic Shock

A

it improves CO and decreases TPR

108
Q

What are some complications that can occur d/t shock?

A

ARDS

ARF

GI Complications

DIC

MODS

109
Q

ARDS

A

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
Q

When can ARDS set in after shock?

A

24-48 hours after injury occurs

111
Q

What would an ABG show if someone has ARDS

A

hypoxemia and hypercapnia

112
Q

Impaired diffusion across thickened alveolar-capillary membranes in ARDS causes what

A

a V/Q Mismatch

113
Q

What is ARDS thought to result from

A

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
Q

What is an important late cause of death in severe shock

A

ARF

115
Q

What is the primary underlying cause of Shock related ARF

A

septic shock - endotoxins acting as potent vasoconstrictors capable of activating SNS and causing intravascular clotting

trauma

116
Q

What determines degree of renal damage in shock?

A

severity and duration of shock

117
Q

The most common ARF lesion…

A

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
Q

When monitoring for shock related ARF what should you monitor

A

UO during shock

serum creatinine and BUN

119
Q

Why are there GI complications with shock?

A

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
Q

___ is a common symptom of GI ulceration with onset in __ to __ days

A

bleeding; 2; 10

121
Q

GI lesions provide what?

A

a portal of entry for bacteria leading to sepsis and shock

122
Q

DIC

A

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
Q

What leads to the increased risk of bleeding in DIC

A

the depletion of PLTs and coagulation factors

124
Q

DIC occurs in how many persons with sepsis or septic shock

A

30-50%

125
Q

What is DIC thought to be caused by from shock?

A

The presence of inflammatory mediators

126
Q

Occurrence of DIC is…

A

an independent predictor of mortality (it has a very low survival rate)

127
Q

MODS

A

Multiple organ dysfunction syndrome

presence of altered organ function such that homeostasis cannot be maintained and multiple organs die as a result

128
Q

What organs are commonly impacted by MODS

A

kidneys

lungs

liver

brain

heart

129
Q

Why is MODS life threatening

A

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
Q

Risk factors for MODS development

A

sepsis

shock

prolonged periods of HTN

hepatic dysfunction

trauma

infarcted bowel

advanced age

alcohol abuse (fragile vessels bleed easily)

131
Q

Management of MODS depends on what

A

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

NURS361 - Pathophysiology II (20 decks)

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