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
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?
**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
26
What is the 2nd line of defense?
Inflammation and phagocytosis -Help rid invading microoraganisms
27
What is 3rd line of defense?
**Specific immune response and Natural killer cells** -Very specific to an organism. Have to have exposure first
28
What are 5 types of WBC
Neutrophils Macrophages Monocytes Basophils Eosinophils
29
Neutrophils
Largest portion of WBC First line of defense Fight bacteria, infection, inflammation Short life - 12-18hrs
30
Macrophages
From stem cells in bone marrow Turn into matures monocytes Surrounds and kills organisms, removes dead cells, stimulates action of other cells
31
Monocytes
Can last months to years / largest WBC Protect against invasion and tissue injury Phagocytosis repair injured tissues
32
Basophils
Initiate inflammatory response release histamine defense against allergens, parasites, and pathogens: 0.5-1% of WBC
33
Eosinophils
Releases in allergic reactions help the body fight infections, parasites, allergens, and other foreign organisms
34
ANTIGENS
Any substances capable of stimulating a response from immune system (usually foregin)
35
Antibodies
Aka immunoglobin Proteins created in response to antigens so next time ready to fight
36
Steps of phagocytosis
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)
37
Humoral immunity
**-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.
38
IgG
in **serum** and **tissues** (interstitial fluid) role in **blood borne and tissue infections** Activates the **complement system** **phagocytosis** Crosses **placenta**
39
IgE
in **serum** **allergic** and **hypersensitivity** reactions **parasitic** infections
40
Natural Active immunity
Natural contact with antigen through infection "Happens naturally, you just get sick" Chicken pox, mumps, measles
41
Natural passive immunity
Passed through placenta to unborn infant or through breast milk (igA) "Happens naturally"
42
Artifical Active immunity
Immunization with antigen Given an immunization body has to look at antigen and CREATE antibodies aka ACTIVE
43
Artifical passive immunity
Injection or infusion of human immune globulin Body given antibody so no real work = passive
44
Inflammatory process Means? Causes: Physical Chemical Biological
Means "the fire within" / inflammed **Causes**: Physical - sunlight, xrays Chemical - venom, other chemicals Biological - bacterial, viruses
45
Signs of inflammation (5) Process of inflammation
**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.
46
Inflammation vs infection
**Inflammation** - nonspecific reaction to injury **Infection** - specific cause to tissue injury, usually bacterial organism
47
Autoimmune disease
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
48
Autoimmune disease Treatment
Corticosteroids, NSAIDS, immunosupressive therapy Adequate rest, hydration, nutrition, prevent infection
49
Systemic Lupus Erythematosus Symptoms
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
50
If you run a CBC on a pt with systemic lupus erythematosus what would you see?
Pancytopenia - decrease in all types of cells
51
SLE - treatments
Immunosuppressants Steroids - bad side effects (look them up) Suppress tissue inflammation
52
Acid
Substance that releases hydrogen iron when dissolved in water
53
Base
Substance that binds with hydrogen when released in water
54
Acidic Neutral Alkaline
Acidic 1-6.9 Neutral 7 Alkaline 7.1-14
55
What is our bodies natural pH level?
7.35-7.45
56
**Buffer system ** Lungs
RESPIRATORY BUFFER SYSTEM Lungs - retain Carbonic acid in form ofCo2 or by rapid respirations excreting CO2 Can be quick to change respirations
57
**Buffer system** Kidneys
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
58
# MUST KNOW!!!! **NORMAL VALUES** pH pCO2 HCO3 PaO2
pH - 7.35-7.45 pCO2 - 35-45mmHg HCO3 22-26mEq/L PaO2 - 80-100mmhg
59
What do ABGs tell us
Acid base balance Oxygenation status * usually from an artery, typically from wrist, usually done by respiratory therapist
60
**PaO2** Mild hypoxemia? Moderate Severe?
Normal - 80-100mmhg Mild - less than 80 Moderate - less than 60 Severe - less than 40
61
How to remember Alkalosis Acidosis
Alkalosis - KICKING up the pH = greater than 7.4 Acidosis - Down = less than 7.4
62
Causes of acidosis?
**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
63
Causes of Alkalosis?
**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
SYMPTOMS of RESPIRATORY ACIDOSIS
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
What is a late sign of hypoxia What are earlier signs?
Cyanosis Earlier - tachycardia/tachypnea
66
Nursing interventions for respiratory acidosis
Maintain patent airway - if OD narcan, intubate Encourage fluids to decrease secretions chest physiotherapy
67
Symptoms of RESPIRATORY ALKALOSIS
Seizures, deep rapid breathing, hyperventilation, tachycardia, decreased for normal bp Hypokalemia Numbness and tingling of extremities Lethargy and confusion Light headedness Nausea/vomit
68
Symptoms of METABOLIC ACIDOSIS
Headache Decreased BP Hyperkalemia Muscle twitching Warm flushed skin Nausea, vomit, diarrhea Changes in LOC Kussmaul respirations
69
**METABOLIC ACIDOSIS** Treat the cause DKA Hypovolemia Lactic acidosis Renal
DKA - treat hyper/hypo glycemia Hypovolemia - volume expanders, blood transfusions lactic acidosis - oxygen and bicarb Renal - treat renal failure
70
Metabolic alkalosis symptoms
Restlessness followed by lethargy Dysrhythmias Compensatory hypoventilation confusions Nausea, vomitting, diarrhea Tremors, muscle creamps, tingling of fingers and toes hypokalemia
71
Metabolic alkalosis Treatement
Check labs, admin potassium, observe for disrythmias, monitor I&O, monitor neurologic changes, treat cause
72
How do you know if you have an acid or base with normal value of 7.35-7.45 pH
Less than 7.4 = acid Greater than 7.4 = base
73
How to know if acid or base of HCO3?
Less than 22 = acid Greater than 26 = base
74
How to know if its an acid or base for pCO2
Less than 35 = base Greater than 45 = Acid
75
Symptoms of Air Embolism
Chest pain, shortness of breath
76
Symptoms of circulatory overload
Shortness of breath, crackles, chest pain/hyper/hypotension
77
Symptoms of Sepsis
Malaise, fever, neutrophilia
78
Signs of hyperglycemia
Polyuria, blurred vision , headache
79
Signs of hypoglycemia from abrupt stopping of TPN
Tremors, abrupt discontinuation from TPN
80
**Pernicious amenia B!2** -How ppl get it -How its treated -Acute/chronic? -Why need B12
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
Difference between antiplatelets and anticoagulants?
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
What are antiplatelet drugs?
Ticlopidine HCL / Ticlid Clopidogrel bisulfate / Plavix Aspirin prevent formation of platelet plugs - plavis ticlid / used for heart disease
83
What are anticoagulant drugs:?
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
Metabolic acidosis
Low pH due to increased H+ and low bicarb -gain of H+ or loss of bicarb
85
In what ways can body lose Bicarb?
Diarrhea, Lower intestinal fistula, diuretics, renal insuff, excessive chlorid, TPN w/o bicarb
86
In what ways does body excessively accumulate acids?
Lactic acidosis, salicylate poisioning, renal failure, DKA, starvation
87
Bodys 3 main means of defense?
Phagocytoic immune response Humoral / antibody response Cellular response
88
Stages of a response to an invasion
**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
Role of antibodies
Agglutionation - Clumping together Opsionization - removal of offending organisms Also release of vasoactive substances - histamine, and slow reacting substances
90
Types of T lymphocytes
Effector T - Helper T (stim rest of immune) & cytotoxic (lysis) Suppressor T - decrease B cell productions Memory T- recognize antigen from previous exposure
91
What cells are apart of humoral?
B lymphocyte - produces antibodies
92
What cells are apart of cellular immunity
T lymphocytes Helper T Supressor T Memory T Cytoxic T
93
Thermal burns
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
Chemical burns
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
Electrical burns
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
What tissues offer the most resistances against burns?
Fat and Bone Nerve and muscles offer least resistance
97
Electrical injury puts pt at risk for
dysrythmia, cardiac arrest, severe metabolic acidosis, myglobulinuria which can lead to kidney prob *watch for dysrythmias!! can be delayed up to 24 hours
98
Smoke inhalation S/S
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
Metabolic asphyxiation
Carbon monoxide poisioning Causes hypoxemia and death
100
How to treat carbon monoxide inhalation?
100% humidified oxygen
101
**Superficial partial thickness 1st degree** Causes Layer affects S/S Appearance
Sunburn, blanching, Epidermis S/S - Tingling, pain, peeling, itching Red, blanches w/ pressure, dry, minimal edema, possible blisters
102
**Partial thickness 2nd degree burn** Causes Layer affects S/S Appearance
From flames, flash and scoulds Epidermis and portion of dermis S/S pain, hyperesthesia, sensitive to air Blistered, mottled, red, weeping surface, edema
103
**Full thickness - 3rd degree** Causes Layer affected S/S Appearance
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
**Full thickness - 4th degree** Causes Layer affected S/S Appearance
Prolonged exposure or high voltage electrical injury Deep tissue, muscle and bone S/S shock, myoglobinuria and hemolysis Charred appearance
105
**Burns phases** Immediate Emergent Acute Rehab
**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
Capillary leak syndrome
capillaries become more permeable and fluids leak out Greatest fluid leak occurs in 24-36hr after injury
107
**BURNS labs** K+ HCT BUN/CR ABG
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
Rule of 9's
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
The parkland formula
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
Escharotomies
Cut with scalpal bc skin gets so tight
111
Burn shock
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
**Shock** - define failure of what 4 things?
Inadequate tissue perfusion Cardiovascular system failure: circulating blood volume, myocardial contractility, blood flow, vascular resistance
113
Without perfusion, oxygenattion is compromised and what takes place?
Anaerobic metabolim = lactic acid = metabolic acidosis
114
**Hypovolemic** Define Causes
Low blood flow - inadequate circulating blood volume which leads to decreased 02 to tissues Hemmorage, severe diarrhea/vomit, excessive perisperation, intake fluid inadequate
115
**Hypovolemic shock** Absolute Relative -Causes of relative
**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
**Cardiogenic shock** Define Causes
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
**Obstructive Shock ** Define Causes
Mechanical obstruction to blood flow reducing cardiac output Tension pneumothorax, cardiac tamponade, pulmonary embolism, things that cause a blockage
118
**Vasogenic (distributive) shock ** Define 3 types
Vessels, how vessels are reacting Anaphylaic Septic Neurogenic
119
Symptoms of hypovolemic shock Diagnosis made when
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
**Vasogenic shock - Anaphylactic shock ** Process
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
**Vasogenic Shock - Septic shock** Define Process
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
Septic shock treatment
Give fluids first, vasopressors
123
Septic shock symptoms
Metabolic acidosis Oliguria acute enchepalophy coag disorders
124
Vasogenic shock - Neurologic shock
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
Causes of neurogenic shock
Spinal cord injury above T5 Spinal anesthesia Vasomotor center depression - severe pain, drugs, hypoglycemia
126
**Shock effects on body systems** Respiratory Acid-base balance
**Respiratory** - tissue hypoxia and anoxia, resp failure, ARDS **Acid**-**base** - Metabolic acidosis
127
**Shock effects on body systems ** Immune GI Renal
**Immune** - depressed immune system **GI** - decreased peristalisis, ischemia or intestinal submucosa, impaired liver function **Renal** - decreased GFR, inadequate perfusion, tubular necrosis
128
**Shock affects on body systems** CV Neurondocrine
**CV** - myocardial depression, DIC **Neuro** - release of catecholamines, mineralcorticoids, glucocorticodis, ADH Decreased LOC when cerebral blood flow falls
129
Stages of shock
Initial Compensatory Progressive Refractory
130
Initial stage of shock
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
Compensatory stage of shock
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
Compensatory stage symptoms
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
Progressive stage of shock
Compensatory mech function independently instead of cooperatively Sluggish blood flow, clumping of cells, deprived of O2, increase in lactic acid and metabolic acidosis
134
# ** Progressive shock symptoms
Listless confusion BP drop (indication from compensated to decomp) **Pulse** - weak, thready, tachycardia, dysrhythmias **Resp** - increased, deep, crackles **Temp** - subnormal
135
Irreversible (refractory) stage
Tissue perfusion deteriorates Coronary artery perfusion reduced Ischemia and dysrhythmias Cerebral ischemia
136
Shock treatment basics
Airway Breathing Circulation
137
Airway basics
Intubation / ariway protection Watch LOC, loss of gag reflex, severe bronchospasm
138
Breathing basics
Adequate 02 Mechanical vent Watch for hypoventilation, hypoxia, pulm edema
139
Circulation basics
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
What do Colloids do Crystalloids?
Colloids - remain in vascular system and draw fluid INTO blood stream Crystalloids - replace fluid and electrolytes
141
Pharamcologic agents used to increase BP
Dopamine Dobutamine Norepinephrine Epinerphrine Vasopressin
142
Meds used to decrease BP during shock
Nitroglycerin Nitroprusside
143
Interventions - pt in shock with decrease C/O
Hemodynamic monitoring - vitals Inotropic and antidysrhythmic agents Reduce 02 consumption - gentle handling and coordinating care Maintain adequate body heat; prevent shivering
144
Central venous pressure
The pressure created by volume in the right atrium
145
**Preload** Define Measured as Increased in:
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
**Afterload** Define Increased in
**Resistance** left ventricle must overcome to circulate blood Increased in: hypertension, vasoconstriction Increased AFTERLOAD = increased CARDIAC WORKLOAD
147
How can we influence afterload?
Dilating vessels Constriction of vessels
148
What does it mean when afterload is high? low?
Resistance is high and the heart works harder to pump Resistance is low and heart is not working heard to eject blood
149
In septic shock, its all about vessles so we can use things like ____to increase afterload and bp?
vasopressors
150
Why would you want to increase afterload?
Septic shock
151
Stroke volume
Amount of blood ejected by ventricles with each systole
152
**Cardiac output** Define Normal
Amount of blood in liters / minutes pumped by ventriles Normal - 4-8 L /min
153
Mean Arterial Pressure Define Formula Goal
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
Pulmonary Capillary Wedge Pressure
Indirect measure of volume in left ventricle
155
**Contractility** Define Drug to increase?
Hearts ability to produce force during contraction May use dobutamine to increase contractility