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LEC notes Flashcards

1
Q

What are 4 functions of blood?

A

Oxygenation
Hemostasis
Immune function
Transport

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2
Q

How does Oxygenation happen in blood?
Hemoglobin?

A

RBC transport oxygen from lungs to tissues and CO from tissues back to lungs for excretion.

Hemoglobin contains iron which allows it to pick up oxygen. “Heme” - iron, “globin” - oxygen transport protein

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3
Q

Hemostasis

A

Balance between clot formation and clot dissolution

*blood vessels will constrict to reduce bleeding, platelets form platelet plug and coagulation is initiated.

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4
Q

What is transportation function of blood

A

blood carries, oxygen, nutrients, hormones and waste products

Made possible by pumping of heart

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5
Q

Function of bone marrow?

Majority are produced in?

A

Spongy center of bones where RBC , platelets and WBC’s are made and stored

Majority are produced in vertebrae, ribs, sternum, skull, pelvis, long bones of legs

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6
Q

What is the function of the liver?

A

Manufacturer clotting factors, albumin, bile (critical in absorption in fat soluable vitamins K, A, E, D).
Cleans and removes dead RBC
Stores large quantities of blood and extra iron

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7
Q

Purpose of vitamin K

A

produces blood clotting factors.

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8
Q

What is the function of the spleen?

A

Removes old RBC from circulation,
Helps make RBC,
Filters bacteria,
Stores RBC and platelets

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9
Q

What is the purpose of clotting factors?

A

Form fiber matrix around wound to protect site while healing / scab

essential for preventing excessive bleeding and forming clots

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10
Q

What is Plasma

A

Carry RBC, platelets and clotting factors

Contains primary water, plamas protein and globuins, albumin

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11
Q

What are 3 types of blood cells?

A

Erythrocytes
Leukocytes
Thrombocytes

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12
Q

a single erythrocytes can carry how many hemoglobin modules?

A

1 can carry 300 hemoglobin modules

*hemoglobin gives blood its red color

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13
Q

What

Thrombocytosis

A

too many platelets

Body clots alot. RISK for stroke, heart attack, PE

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14
Q

What are neutropenic precautions?

A

Set of guidelines to prevent infection in people with low neutrophils

Diet, handwashing, PPE, room restrictions, avoid rectal procedures

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15
Q

Thrombocytopenia

A

Too few platelets in blood which can lead to excessive bleeding

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16
Q

BLOOD TRANSFUSION
5 important things

A
  1. Need to have a type and cross match
  2. Usually good for about 3 days
  3. Have consent and patient ID
  4. two nurses MUST verify
  5. Vitals before, during and after. Nurses stay 1st 15 mins after blood hits
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17
Q

What is the universal donor blood

A

O-

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18
Q

What is your universal recipent blood?

A

AB+

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19
Q

PRBCS

A

Packed reb blood cells
Transfuse over 2-4hours
4hr for pt who are worried about circulatory overload
Trauma - super fast even rapid transfusion

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20
Q

Hemolytic reaction to blood transfusion
Type of reaction
S/S
Time frame
Intervention

A

Antigen-antibody reaction
S/S: Fever, chills, nausea, dyspnea, chest pain, back pain
Happens shortly after starting
Stop transfusion and notify MD

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21
Q

Anaphylactic reaction to blood
Type of reaction
S/S
Time frame
Intervention

A

Hypersensitivity reaction
S/S urticaria, wheezing, dyspnea, hypotension
Within 30 mins of start
Stop transfusion, notify MD, prepare epi & steroids

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22
Q

Febrile reaction to blood
Type of reaction
S/S
Time frame
Intervention

A

Recipients antibodies react to donors leukocytes
S/S fever, chills
within 30-90 mins of starting
Stop transfusion, notify MD

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23
Q

Circulatory overload reaction to blood
Type of reaction
S/S -4
Time frame
Intervention - 4

A

CV system unable to manage fluid
S/S cough, frothy sputum, cyanosis, hypotension
Anytime during and several hours after
Stop transfusion, get help, prepare to admin O2 and lasix

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24
Q

Hemolytic and Febrile reactions to blood will both be shown with

A

Increase in temp

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25
Q

What is the 1st line of defense in immune system?
Sweat glands?
Sebacous glands?
Skin and GI tract?
Mammary glands, GI and resp?
Normal flora?
Silia, motility and slough?

A

Skin and mucous membranes
Sweat glands that secrete lysosomes
Sebacous glands that secrete sebum
acid secretions from skin and GI tract - inhibits pathogens from growting
Secretions from mammory glands and respiratory and GI - contain immunoglobin
Normal flora that helps to keep pathogens from entering
Silia in resp tract and motility in GI. Slough dead skin

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26
Q

What is the 2nd line of defense?

A

Inflammation and phagocytosis

-Help rid invading microoraganisms

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27
Q

What is 3rd line of defense?

A

Specific immune response and Natural killer cells

-Very specific to an organism. Have to have exposure first

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28
Q

What are 5 types of WBC

A

Neutrophils
Macrophages
Monocytes
Basophils
Eosinophils

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29
Q

Neutrophils

A

Largest portion of WBC
First line of defense
Fight bacteria, infection, inflammation
Short life - 12-18hrs

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30
Q

Macrophages

A

From stem cells in bone marrow
Turn into matures monocytes
Surrounds and kills organisms, removes dead cells, stimulates action of other cells

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31
Q

Monocytes

A

Can last months to years / largest WBC
Protect against invasion and tissue injury
Phagocytosis
repair injured tissues

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32
Q

Basophils

A

Initiate inflammatory response release histamine

defense against allergens, parasites, and pathogens:

0.5-1% of WBC

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33
Q

Eosinophils

A

Releases in allergic reactions
help the body fight infections, parasites, allergens, and other foreign organisms

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34
Q

ANTIGENS

A

Any substances capable of stimulating a response from immune system (usually foregin)

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35
Q

Antibodies

A

Aka immunoglobin
Proteins created in response to antigens so next time ready to fight

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36
Q

Steps of phagocytosis

A
  1. Exposure
  2. Attract forgein
  3. Adhere (stick to cell)
  4. Recognition (realize its forgein)
  5. Cellular ingestion (eat cell)
  6. Phagosome formation
  7. Degradation (break into pieces)
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37
Q

Humoral immunity

A

-Antibody response-
Exposure to foregin invader - B cells lymphocytes turn into plasma cells which manufacture antibodies and release. Antigen antibody binding = agglutination & opsonization, promote release of histamine and other substances in inflamm response. . Get rid of antigen and remember.

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38
Q

IgG

A

in serum and tissues (interstitial fluid)
role in blood borne and tissue infections
Activates the complement system
phagocytosis
Crosses placenta

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39
Q

IgE

A

in serum
allergic and hypersensitivity reactions
parasitic infections

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40
Q

Natural Active immunity

A

Natural contact with antigen through infection
“Happens naturally, you just get sick”
Chicken pox, mumps, measles

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41
Q

Natural passive immunity

A

Passed through placenta to unborn infant or through breast milk (igA)
“Happens naturally”

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42
Q

Artifical Active immunity

A

Immunization with antigen
Given an immunization body has to look at antigen and CREATE antibodies aka ACTIVE

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43
Q

Artifical passive immunity

A

Injection or infusion of human immune globulin
Body given antibody so no real work = passive

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44
Q

Inflammatory process
Means?
Causes:
Physical
Chemical
Biological

A

Means “the fire within” / inflammed
Causes:
Physical - sunlight, xrays
Chemical - venom, other chemicals
Biological - bacterial, viruses

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45
Q

Signs of inflammation
(5)
Process of inflammation

A

Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain
Decrease function

Hemodynamic changes, dilation of cap bed = increase blood flow to area = cause warmth and redness. Increased permeability = things flow in and out of vessels. Chemical mediators cause leukocytes to line blood vessels walls near injured site. WBC inhibit area. Permeability cause fluid to flow into intersitial space = swelling. Prostaglandins, histamins and leukotrines, cytokins, kinin, complement system, - released.

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46
Q

Inflammation vs infection

A

Inflammation - nonspecific reaction to injury
Infection - specific cause to tissue injury, usually bacterial organism

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47
Q

Autoimmune disease

A

Immune system reacts against & destroys itself
Genetic factor: tends to be familial
Can involve tissue or organ system
Causes injury in 3 ways:
-Effect of antibodies on cell surfaces
-Deposit of antigen-antibody complexes
- Through action of senitized T cells

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48
Q

Autoimmune disease
Treatment

A

Corticosteroids, NSAIDS, immunosupressive therapy

Adequate rest, hydration, nutrition, prevent infection

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49
Q

Systemic Lupus Erythematosus
Symptoms

A

Tachypnea, cough, pleural inflam/effusion
Photosensitivty -rash to areas exposed to sun
Weight loss, fatique, fever, arthritis
Emotional liability,
Butterfly rash over cheeks
Raynauds phenomenon, pericarditis, vascular inflamm
Lupus nephritis - protein uria, hematuria

avoid harsh soaps and substances

*affect women more in childbearing years 20-40

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50
Q

If you run a CBC on a pt with systemic lupus erythematosus what would you see?

A

Pancytopenia - decrease in all types of cells

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51
Q

SLE - treatments

A

Immunosuppressants
Steroids - bad side effects (look them up)
Suppress tissue inflammation

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52
Q

Acid

A

Substance that releases hydrogen iron when dissolved in water

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53
Q

Base

A

Substance that binds with hydrogen when released in water

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54
Q

Acidic
Neutral
Alkaline

A

Acidic 1-6.9
Neutral 7
Alkaline 7.1-14

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55
Q

What is our bodies natural pH level?

A

7.35-7.45

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56
Q

**Buffer system **
Lungs

A

RESPIRATORY BUFFER SYSTEM
Lungs - retain Carbonic acid in form ofCo2 or by rapid respirations excreting CO2

Can be quick to change respirations

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57
Q

Buffer system
Kidneys

A

METABOLIC BUFFER SYSTEM
-Retain or excreting NaHCO3
Excreting acidic or alkaline urine
Reabsorbing NaHCO3- or secreting free H+ ions

*Slower than lungs. Can take hours to days

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58
Q

MUST KNOW!!!!

NORMAL VALUES
pH
pCO2
HCO3
PaO2

A

pH - 7.35-7.45
pCO2 - 35-45mmHg
HCO3 22-26mEq/L
PaO2 - 80-100mmhg

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59
Q

What do ABGs tell us

A

Acid base balance
Oxygenation status

  • usually from an artery, typically from wrist, usually done by respiratory therapist
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60
Q

PaO2
Mild hypoxemia?
Moderate
Severe?

A

Normal - 80-100mmhg
Mild - less than 80
Moderate - less than 60
Severe - less than 40

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61
Q

How to remember Alkalosis
Acidosis

A

Alkalosis - KICKING up the pH = greater than 7.4
Acidosis - Down = less than 7.4

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62
Q

Causes of acidosis?

A

**Respiratory causes ** -HYPOVENTILATION- Things that make them not breathe as well (drug OD, Pulmonary edema, chest trauma, COPD, airway obstruction, over sedation- narcotics)

**Metabolid causes ** - DKA, Salicylate oD, Shock, sepsis, severe diarrhea, renal failure

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63
Q

Causes of Alkalosis?

A

Respiratory causes: HYPERVENTILATION = Anxiety, high altitudes, pregnancy, fever, hypoixa, initial stages of pulmonary emboli

**Metabolic causes: **loss of gastric jucies, potassium wasting diuretics, overuse of antacids

64
Q

SYMPTOMS of
RESPIRATORY ACIDOSIS

A

LUNGS CANNOT GET RID OF ACID (CO2)

Rapid shallow respirations
Decreased bp with vasodialtion
Dyspnea (SOB)
Headache
Hyperkalemia
Dysrhythmias
Drowiness, dizzy, disorientation
Muscle weakness

65
Q

What is a late sign of hypoxia
What are earlier signs?

A

Cyanosis
Earlier - tachycardia/tachypnea

66
Q

Nursing interventions for respiratory acidosis

A

Maintain patent airway - if OD narcan, intubate
Encourage fluids to decrease secretions
chest physiotherapy

67
Q

Symptoms of RESPIRATORY ALKALOSIS

A

Seizures, deep rapid breathing, hyperventilation, tachycardia, decreased for normal bp
Hypokalemia
Numbness and tingling of extremities
Lethargy and confusion
Light headedness
Nausea/vomit

68
Q

Symptoms of METABOLIC ACIDOSIS

A

Headache
Decreased BP
Hyperkalemia
Muscle twitching
Warm flushed skin
Nausea, vomit, diarrhea
Changes in LOC
Kussmaul respirations

69
Q

METABOLIC ACIDOSIS
Treat the cause
DKA
Hypovolemia
Lactic acidosis
Renal

A

DKA - treat hyper/hypo glycemia
Hypovolemia - volume expanders, blood transfusions
lactic acidosis - oxygen and bicarb
Renal - treat renal failure

70
Q

Metabolic alkalosis
symptoms

A

Restlessness followed by lethargy
Dysrhythmias
Compensatory hypoventilation
confusions
Nausea, vomitting, diarrhea
Tremors, muscle creamps, tingling of fingers and toes
hypokalemia

71
Q

Metabolic alkalosis
Treatement

A

Check labs, admin potassium, observe for disrythmias, monitor I&O, monitor neurologic changes, treat cause

72
Q

How do you know if you have an acid or base with normal value of 7.35-7.45 pH

A

Less than 7.4 = acid
Greater than 7.4 = base

73
Q

How to know if acid or base of HCO3?

A

Less than 22 = acid
Greater than 26 = base

74
Q

How to know if its an acid or base for pCO2

A

Less than 35 = base
Greater than 45 = Acid

75
Q

Symptoms of Air Embolism

A

Chest pain, shortness of
breath

76
Q

Symptoms of circulatory overload

A

Shortness of breath, crackles,
chest pain/hyper/hypotension

77
Q

Symptoms of Sepsis

A

Malaise, fever, neutrophilia

78
Q

Signs of hyperglycemia

A

Polyuria, blurred vision ,
headache

79
Q

Signs of hypoglycemia from abrupt stopping of TPN

A

Tremors, abrupt
discontinuation from TPN

80
Q

Pernicious amenia B!2
-How ppl get it
-How its treated
-Acute/chronic?
-Why need B12

A

Not absorbed from stomach. Lack of intrinsic factor needed for b12 to be absorbed. Weight loss surgery can take it away or ppl are born without it.

IM injection of Vit 12 (cyanocobalamin) for rest of life

Acute or chronic - body compensates - increase respiratory or circulatory rate to try and circulate more RBCs, tries to increase erythproesis to increase more RBC.

Need b12 to move folicate acid into cell for DNA synthesis and RBC production.

81
Q

Difference between antiplatelets and anticoagulants?

A

Antiplatelets - Prevent platelets from clumping together
Anticoagulants - Slow down bodys process of making clots but interfereing with proteins involved in process of making clots

82
Q

What are antiplatelet drugs?

A

Ticlopidine HCL / Ticlid
Clopidogrel bisulfate / Plavix
Aspirin

prevent formation of platelet plugs - plavis ticlid / used for heart disease

83
Q

What are anticoagulant drugs:?

A

Coumodin / warfarin
Enoxaparin sodium / levonox
Heparin

do not dissolve clots / inhibit new clot formation in venous system and inhibit further growth of existing clots / used in heart disease and stroke prevention

84
Q

Metabolic acidosis

A

Low pH due to increased H+ and low bicarb
-gain of H+ or loss of bicarb

85
Q

In what ways can body lose Bicarb?

A

Diarrhea, Lower intestinal fistula, diuretics, renal insuff, excessive chlorid, TPN w/o bicarb

86
Q

In what ways does body excessively accumulate acids?

A

Lactic acidosis, salicylate poisioning, renal failure, DKA, starvation

87
Q

Bodys 3 main means of defense?

A

Phagocytoic immune response
Humoral / antibody response
Cellular response

88
Q

Stages of a response to an invasion

A

Recognition stage - lymph nodes or lymphocytes
Proliferation - T and B enlarge and proliferate (T=cytotoxic, B=antibodies)
Response - Function in either humoral or cellular response
Effector - Antibody of humoral response or cytotoxic of cellular response connects with anitgen

89
Q

Role of antibodies

A

Agglutionation - Clumping together
Opsionization - removal of offending organisms
Also release of vasoactive substances - histamine, and slow reacting substances

90
Q

Types of T lymphocytes

A

Effector T - Helper T (stim rest of immune) & cytotoxic (lysis)
Suppressor T - decrease B cell productions
Memory T- recognize antigen from previous exposure

91
Q

What cells are apart of humoral?

A

B lymphocyte - produces antibodies

92
Q

What cells are apart of cellular immunity

A

T lymphocytes
Helper T
Supressor T
Memory T
Cytoxic T

93
Q

Thermal burns

A

most common type
Causes by flame, flash, scould or contact with hot objects
Severity depends on temp and duration of contact time

**Too hot water, stove / often with children

94
Q

Chemical burns

A

Result of a contact with acids, alkalids and organic compounds

Acids can be found in many household cleaners

*dont add water could make worse!! / quickly remove chemical and clothing. Can have tissue destruction up to 72 hours

95
Q

Electrical burns

A

Necrosis caused by intense heat generated by electric current

Damage to nerve, vessels, tissue anoxia and death

Enters, goes through body and comes out somewhere else

96
Q

What tissues offer the most resistances against burns?

A

Fat and Bone
Nerve and muscles offer least resistance

97
Q

Electrical injury puts pt at risk for

A

dysrythmia, cardiac arrest, severe metabolic acidosis, myglobulinuria which can lead to kidney prob

*watch for dysrythmias!! can be delayed up to 24 hours

98
Q

Smoke inhalation S/S

A

Soot stinged sputum
Singed nasal hairs
Facial burns blisters
Redness of airway and edema

  • can cause damage to rr tract. Major predictor of morality
99
Q

Metabolic asphyxiation

A

Carbon monoxide poisioning
Causes hypoxemia and death

100
Q

How to treat carbon monoxide inhalation?

A

100% humidified oxygen

101
Q

Superficial partial thickness
1st degree
Causes
Layer affects
S/S
Appearance

A

Sunburn, blanching,
Epidermis
S/S - Tingling, pain, peeling, itching
Red, blanches w/ pressure, dry, minimal edema, possible blisters

102
Q

Partial thickness 2nd degree burn
Causes
Layer affects
S/S
Appearance

A

From flames, flash and scoulds
Epidermis and portion of dermis
S/S pain, hyperesthesia, sensitive to air
Blistered, mottled, red, weeping surface, edema

103
Q

Full thickness - 3rd degree
Causes
Layer affected
S/S
Appearance

A

Flame, prolonged exposure, electric current, chemical, contact
Epidermis, dermis and sometimes subq; may involve connective tissue and muscle
S/S Shock, myoglobinuria (red pigment in urine), and hemolysis, possible entrance and exit wounds
Dry, pale, white, red, brown ,leathery, edema

104
Q

Full thickness - 4th degree
Causes
Layer affected
S/S
Appearance

A

Prolonged exposure or high voltage electrical injury
Deep tissue, muscle and bone
S/S shock, myoglobinuria and hemolysis
Charred appearance

105
Q

Burns phases
Immediate
Emergent
Acute
Rehab

A

Immediate - at scene
Emergent - 1st 36-48hrs until capillaries heal & fluid resuscitation is complete
Acute - 48-72 hours / diuresis occurs
Rehab- Grafting, PT, OT

106
Q

Capillary leak syndrome

A

capillaries become more permeable and fluids leak out
Greatest fluid leak occurs in 24-36hr after injury

107
Q

BURNS labs
K+
HCT
BUN/CR
ABG

A

K+ - elevated bc of hemoconcentration and fluid shifts. Possible to see low but typically elevated
HCT -increased due to hemoconcentration
BUN/CR -Elevated
ABG - imbalances

108
Q

Rule of 9’s

A

Whole head is 9 - front and back = 4.5%
Torso = 18% each side
Arms = each arm is 9, each side 4.5%
Each leg is 18, 9 for each side
Genitals 1%

109
Q

The parkland formula

A

Used for 1st 24 hour after burn injury / fluid replacment

Use Kg X % of TBSA X (2-4ml/per doc) = TOTAL. GIve 1/2 in first 8 hours give the rest in the next 16 hours

110
Q

Escharotomies

A

Cut with scalpal bc skin gets so tight

111
Q

Burn shock

A

if a burn injury over 20% = a lot of cap permeability
Fluids shift into intersitital = edema and decreased blood volume
Hematocrit increases and blood viscous = peripheral resistanace
Hypovolemic shock / happen rapidly

112
Q

Shock - define
failure of what 4 things?

A

Inadequate tissue perfusion

Cardiovascular system failure: circulating blood volume, myocardial contractility, blood flow, vascular resistance

113
Q

Without perfusion, oxygenattion is compromised and what takes place?

A

Anaerobic metabolim = lactic acid = metabolic acidosis

114
Q

Hypovolemic
Define
Causes

A

Low blood flow - inadequate circulating blood volume which leads to decreased 02 to tissues

Hemmorage, severe diarrhea/vomit, excessive perisperation, intake fluid inadequate

115
Q

Hypovolemic shock
Absolute
Relative
-Causes of relative

A

Absolute - circulating blood volume = lost volume
Relative - circulating volume = vessels dilated so not effectively getting around body
Causes = burns, peritonitis, intestional obstruction causes plasma shifting into body tissues = relative

116
Q

Cardiogenic shock
Define
Causes

A

Low blood flow due to pump failure
Decreased C/O and Decreased tissue perfusion

Ex. Heart attack, dysrhythmias, valvular disease, myocarditis, cardiomyopathy, structural disorders

117
Q

**Obstructive Shock **
Define
Causes

A

Mechanical obstruction to blood flow reducing cardiac output

Tension pneumothorax, cardiac tamponade, pulmonary embolism, things that cause a blockage

118
Q

**Vasogenic (distributive) shock **
Define
3 types

A

Vessels, how vessels are reacting
Anaphylaic
Septic
Neurogenic

119
Q

Symptoms of hypovolemic shock

Diagnosis made when

A

Increased systemic vascular resistance, poor skin tugor, thirst, oliguria, low systemic and pulmonary preloads, rapid heart rates

Diagnosis made after a loss of 15% intravascular volume

120
Q

**Vasogenic shock - Anaphylactic shock **
Process

A

In reaction to something! Chemical mediators dilate blood vessels & increase capillary permeability
Fluid leaks out of caps into tissues
Decreased venous return & c/o
Bronchi constrict/airway obstruction
**Sudden and dramatic **

121
Q

Vasogenic Shock - Septic shock

Define
Process

A

Systemic inflammatory reaction to infection

Pathogens release toxins = dilate blood vessels, decrease vascular resistance, increase cap permeability = inadequate tissue perfusion & oxygenation

Results in circulatory collapse

122
Q

Septic shock treatment

A

Give fluids first, vasopressors

123
Q

Septic shock symptoms

A

Metabolic acidosis
Oliguria
acute enchepalophy
coag disorders

124
Q

Vasogenic shock - Neurologic shock

A

Sever brain damage results in collapse of body functions

Usually from brain stem, increase in ICP, cerebral herniation

Causes decrease in venous return and C/O

Bradycardia

125
Q

Causes of neurogenic shock

A

Spinal cord injury above T5
Spinal anesthesia
Vasomotor center depression - severe pain, drugs, hypoglycemia

126
Q

Shock effects on body systems
Respiratory
Acid-base balance

A

Respiratory - tissue hypoxia and anoxia, resp failure, ARDS

Acid-base - Metabolic acidosis

127
Q

**Shock effects on body systems **

Immune
GI
Renal

A

Immune - depressed immune system

GI - decreased peristalisis, ischemia or intestinal submucosa, impaired liver function

Renal - decreased GFR, inadequate perfusion, tubular necrosis

128
Q

Shock affects on body systems
CV
Neurondocrine

A

CV - myocardial depression, DIC

Neuro - release of catecholamines, mineralcorticoids, glucocorticodis, ADH

Decreased LOC when cerebral blood flow falls

129
Q

Stages of shock

A

Initial
Compensatory
Progressive
Refractory

130
Q

Initial stage of shock

A

Pt may not have clinical manifestations of decreased tissue perfusion

Lack of O2 occuring at cellular level

May have a decreas in MAP 5-10mmhh

HR will increase

131
Q

Compensatory stage of shock

A

Decreased CO2 triggers neural, endocrine & chemical compensatory responses to overcome anerobic metabolism & maintain blood flow to vital organs

Increase in sympathetic nervous system = increase hr, constriction of peripheral vessels, decreased flow to kidneys, lungs, skin, muscles and GI tract, increased water and sodium retention, decrease blood pH and increase arterial Co2 = **resp increase resp rate and depth. **

132
Q

Compensatory stage symptoms

A

Anxiety, restlessness, BP can remain normal, may decrease, pulse increases, tachycardia (unless in neuro). increase rr, decreased urine, skin cool and pale (warm and dry with septic) decrease bowel sounds, blood glucose increase, thirst

133
Q

Progressive stage of shock

A

Compensatory mech function independently instead of cooperatively

Sluggish blood flow, clumping of cells, deprived of O2, increase in lactic acid and metabolic acidosis

134
Q

**

Progressive shock symptoms

A

Listless confusion
BP drop (indication from compensated to decomp)
Pulse - weak, thready, tachycardia, dysrhythmias
Resp - increased, deep, crackles
Temp - subnormal

135
Q

Irreversible (refractory) stage

A

Tissue perfusion deteriorates
Coronary artery perfusion reduced
Ischemia and dysrhythmias
Cerebral ischemia

136
Q

Shock treatment basics

A

Airway
Breathing
Circulation

137
Q

Airway basics

A

Intubation / ariway protection
Watch LOC, loss of gag reflex, severe bronchospasm

138
Q

Breathing basics

A

Adequate 02
Mechanical vent
Watch for hypoventilation, hypoxia, pulm edema

139
Q

Circulation basics

A

Main issue poor perfusion

Hypovolemia - IV fluids that increase vascular spaces
Vasopressers will not work without IV fluids
Watch for Arrythmias

Generally, in cardiogenic or neurogenic may not give fluids

140
Q

What do Colloids do
Crystalloids?

A

Colloids - remain in vascular system and draw fluid INTO blood stream
Crystalloids - replace fluid and electrolytes

141
Q

Pharamcologic agents used to increase BP

A

Dopamine
Dobutamine
Norepinephrine
Epinerphrine
Vasopressin

142
Q

Meds used to decrease BP during shock

A

Nitroglycerin
Nitroprusside

143
Q

Interventions - pt in shock with decrease C/O

A

Hemodynamic monitoring - vitals
Inotropic and antidysrhythmic agents
Reduce 02 consumption - gentle handling and coordinating care
Maintain adequate body heat; prevent shivering

144
Q

Central venous pressure

A

The pressure created by volume in the right atrium

145
Q

Preload
Define
Measured as
Increased in:

A

The amount of blood in ventricles at end of diastole

Measured as a / volume indicator

increased in: hypervolemia, regurgitation of cardiac valves, heart failure

146
Q

Afterload
Define
Increased in

A

Resistance left ventricle must overcome to circulate blood

Increased in: hypertension, vasoconstriction

Increased AFTERLOAD = increased CARDIAC WORKLOAD

147
Q

How can we influence afterload?

A

Dilating vessels
Constriction of vessels

148
Q

What does it mean when afterload is high?
low?

A

Resistance is high and the heart works harder to pump

Resistance is low and heart is not working heard to eject blood

149
Q

In septic shock, its all about vessles so we can use things like ____to increase afterload and bp?

A

vasopressors

150
Q

Why would you want to increase afterload?

A

Septic shock

151
Q

Stroke volume

A

Amount of blood ejected by ventricles with each systole

152
Q

Cardiac output
Define
Normal

A

Amount of blood in liters / minutes pumped by ventriles

Normal - 4-8 L /min

153
Q

Mean Arterial Pressure
Define
Formula
Goal

A

The average pressure in a pt arteries during one cardiac cycle

*Considered better indicator of perfusion to vital organs than BP

MAP = SBP + 2 (DBP) /
3

						 *usually 65
154
Q

Pulmonary Capillary Wedge Pressure

A

Indirect measure of volume in left ventricle

155
Q

Contractility
Define
Drug to increase?

A

Hearts ability to produce force during contraction

May use dobutamine to increase contractility

211 (9 decks)

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