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488 > Class 11: Multisystem dysfunction > Flashcards

Class 11: Multisystem dysfunction Flashcards

1
Q

Tonicity + isotonic solution

A

-Fluid that has same osmolality as normal plasma: NS, D5W (hypotonic in body), RL
-Used to replace fluid loss

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2
Q

Tonicity + hypertonic solution

A

Fluid that has a higher osmolality than normal plasma: Admixed solutions e.g. TPN; 3% saline; mannitol; & D50S

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3
Q

Tonicity + hypotonic solutions

A

-Fluid that has a lower osmolality than normal plasma: 0.45% saline
-Used to replace fluid without giving electrolytes

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4
Q

Tonicity + isotonic

A

Placing a cell into an isotonic solution will have no net effect on the cell as the tonicity (osmolality) of the cell equals to the fluid

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5
Q

Tonicity + hypertonic

A

Placing a cell into a hypertonic solution will draw water out on the cell and the cell will shrink

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6
Q

Tonicity + hypotonic

A

Placing a cell into a hypotonic solution will shift fluid into the cell and the cell will swell & possibly burst

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7
Q

Anything other than a isotonic solution can…

A

-Cause fluid shifts in the vein used for infusion & consequently, the vessel may become more easily damaged and inflamed

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8
Q

Hypertonic cells..

A

Shrink and are damaged. (That’s why hypertonic solutions are generally infused through a central venous catheter)

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9
Q

Hypotonic cells…

A

Swell and infusion may infiltrate

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10
Q

Slide 5

A
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11
Q

Fluid shifts & edema + osmotic pressure GOES w/ card 1

A

-Power of the solution to draw water across a semi permeable membrane
-Isotonic crystalloid solution (NS & RL)

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12
Q

Fluid shifts & edema + oncotic pressure

A

-Plasma proteins exert this pressure and as a result pull water from the interstitial space into the vascular system
-Colloid solution (large proteins: albumin, globulin, fibrinogen)

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13
Q

Fluid shifts & edema + hydrostatic pressure…

A

-In the arterial (30-40 mmHg) and venous (10-15 mmHg) ends of capillary
-Force blood exerts against vascular walls

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14
Q

Fluid shifts & edema + capillary permeability

A

Is increased for pts with burns, or allergic inflammatory reactions

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15
Q

Oral fluid and electrolyte replacement in acid-base imbalances + isotonic solutions (D5W)

A

0.9% NS, RL, & D5W in 0.225% saline

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16
Q

Oral fluid and electrolyte replacement in acid-base imbalances + hypotonic solutions (0.45% saline)

A

D5W (physiologically)

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17
Q

Oral fluid and electrolyte replacement in acid-base imbalances + hypertonic solutions (D10W)

A

3.0% saline , D5W in 0.45% saline, & D5W in 0.9% NS

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18
Q

Edema + peripheral vs local

A

-Peripheral– Systemic swelling & pitting edema
-Local e.g. Ascites

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19
Q

Systemic signs of edema

A

BP & CVP alterations occur

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20
Q

Fluid shifts + serum osmolality

A

Measure of solute concentration of the blood [sodium, glucose and urea] (↑ = fluid volume deficit, ↓ = fluid volume excess)

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21
Q

Fluid shift + urine osmolality

A

Measure of solute concentration of urine [nitrogenous wastes – creatinine, urea, and uric acid] (↑ = fluid volume deficit, ↓ = fluid volume excess)

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22
Q

Risk of fluid shifts in infants

A

Infants have proportionately more body water, a lot of which is in the extracellular space. This is more easily lost from the body so infants can become dehydrated easily

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23
Q

Others at risk for fluid shifts

A

-Elderly, who can’t compensate for fluid shifts
-Anyone with GI problems

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24
Q

Sodium & volume imbalances nursing diagnosis + ECF volume excess

A

-Ineffective airway clearance r/t Na+ & H2O retention
-Risk for impaired skin integrity r/t edema
-Disturbed body image & altered body appearance r/t edema
-(P) complication of pulmonary edema or ascites

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25
Q

Sodium & volume imbalances nursing diagnosis + ECF volume deficit

A

-Deficient fluid volume r/t ↑ECF losses or ↓ fluid intake
-Decreased CO r/t ↑ECF losses or ↓ fluid intake
-(P) complication of hypovolemic shock

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26
Q

Sodium & volume imbalances nursing diagnosis + hypernatremia

A

Risk for injury r/t to altered sensorium/seizures & abnormal CNS function

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27
Q

Sodium & volume imbalances nursing diagnosis + hyponatremia

A

Risk for injury r/t to altered sensorium/↓LOC & abnormal CNS function

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28
Q

ABG values

A

pH, CO2, HCO3-, & PaO2

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29
Q

Normal PaO2

A

80-110mmHg

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30
Q

Mild hypoxemia

A

60-79mmHg

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31
Q

Moderate hypoxemia

A

40-59mmHg

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32
Q

Severe hypoxemia

A

<39mmHg

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33
Q

Slide 15

A
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34
Q

Electrolyte imbalances

A

Abnormalities, causes and consequences associated with three critical electrolytes: Sodium, potassium, & calcium

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35
Q

Slide 17

A
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36
Q

Na+ is a major

A

Cation of ECF

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37
Q

Na+ has a

A

Water retaining effect; take caution with CHF & MI pts

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38
Q

Na+ is responsible for

A

Conduction of neuromuscular impulses via the sodium/potassium pump

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39
Q

Na+ is involved in

A

Enzymatic activity

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40
Q

Na+ regulates

A

Acid-base balance by combining with chloride or bicarbonate ions

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41
Q

Hyponatremia causes

A

Vomitting/diarrhea

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42
Q

Etiology of hyponatremia

A

Burns, inflammation, vomiting/diarrhea, gastric suction, perspiration, continuous D5W IV & SIADH

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43
Q

Drugs that cause hyponatremia

A

Lasix, mannitol & thiazides

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44
Q

Hypernatremia is caused by

A

CHF, cushing’s disease, hepatic failure, dehydration & vomiting/diarrhea

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45
Q

Drugs causing hypernatremia

A

Cough medicines, cortisone, antibiotics, laxatives, methyldopa & hydralazine

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46
Q

Consequences of hyponatremia

A

-Edema, confusion and giddiness leading to coma
-If water retention occurs rapidly it can lead to HF or pulmonary edema
-Hyponatremia with fluid loss will cause hypotension & tachycardia

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47
Q

Consequences of hypernatremia

A

CNS: Lethargy & confusion progressing to coma. Increased neuromuscular irritability which can progress to convulsions

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48
Q

Nursing interventions of aNa+

A

-Monitor serum sodium levels, for S&S of hyponatremia, VS & ins/outs
-Recognize symptoms of SIADH after surgery
-Educate your patient on the DASH diet

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49
Q

K+

A

-Found most abundantly in ICF
-Narrow range and cardiac arrest could occur if serum level is too high or too low
-80-90% is excreted by the kidneys; therefore kidney function very important

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50
Q

Etiology of hypokalemia

A

Vomitting/diarrhea, malnutrition, stress, gastric suctioning & burns

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51
Q

Drugs that cause hypokalemia

A

Lasix, cortisone, estrogen, gentamicin, bicarbonate, insulin, laxatives, kayexalate & ASA

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52
Q

Etiology of hyperkalemia

A

Reduced U/O, acute renal failure, Addison’s disease & metabolic acidosis

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53
Q

Addisons disease

A

Adrenal insufficiency, decreased steroid production of cortisol

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54
Q

Drugs that cause hyperkalemia

A

Spironolactone, Penicillin G potassium, heparin, epinephrine & histamine

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55
Q

Consequences of hypokalemia

A

Alkalosis, hypoventilation, muscle weakness, arrhythmias & possibility of cardiac arrest

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56
Q

Consequences of hyperkalemia

A

Skeletal muscle weakness, flaccid paralysis, bradycardia, arrhythmias and cardiac arrest

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57
Q

Nursing interventions with aK+

A

-Monitor trends of serum levels, VS, ins/outs
-Assess medications for addition or depletion of potassium
-Ask your patient about their diet

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58
Q

Etiology of hypercalcemia

A

Hyperparathyroidism, excessive vitamin D ingestion, prolonged immobilization (or weightlessness), renal disease preventing excretion, malignancies, and Cushing’s disease accompanied by osteoporosis

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59
Q

Consequences of hypercalcemia

A

Bone wasting, pathological fractures, kidney stones, deep muscle pain, N/V, arrhythmias/arrest, respiratory depression and coma

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60
Q

Etiology of hypocalcemia

A

Vitamin D deficiency, increased excretion in stress and increased protein intake, diarrhea & burns

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61
Q

Consequences of hypocalcemia

A

Tingling of fingers, tremors, tetany, convulsions, and depressed excitability of myocardial muscle

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62
Q

Slide 29-31 lab values

A
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63
Q

Hemoglobin

A

Protein found in red blood cells, gives blood its red colour, O2 carrier & is composed of iron

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64
Q

Low hemoglobin is caused by

A

Anemia, hemorrhage, leukemias, excess fluids, thalassemia & kidney disease

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65
Q

Drugs causing low hemoglobin

A

Penicillin, ASA, antineoplastic drugs, hydralazine & MAO inhibitors

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66
Q

High hemoglobin is caused by

A

Dehydration, hemoconcentration, polycythemia, high altitude, COPD, CHF & severe burns

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67
Q

Drugs that cause high hemoglobin

A

Gentamicin & methyldopa

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68
Q

Nursing interventions of aHemoglobin

A

Monitor VS especially if patient hemorrhaging, trends of hemoglobin, for signs of anemia, S&S of dehydration

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69
Q

Tx of aHemoglobin

A

Iron supplement or dietary modification to increase iron

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70
Q

Slide 35

A
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71
Q

Hematocrit

A

-Percentage of the blood volume occupied by red blood cells
-Indicator of hydration status

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72
Q

Low hematocrit is caused by

A

Acute blood loss, anemia, leukemia, protein malnutrition, vitamin deficiencies & RA

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73
Q

Drugs causing low hematocrit

A

Antineoplastic agents, penicillin & radioactive agents

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74
Q

Etiology of high hematocrit

A

Hemoconcentration, dehydration/hypovolemia, severe diarrhea, polycythemia vera, diabetic acidosis, surgery & burns

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75
Q

Nursing interventions of aHematocrit

A

Monitor VS for signs of shock, may require blood transfusion, may require fluid administration d/t dehydration & hypovolemia

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76
Q

Platelets

A

-AKA thrombocytes
-Help in the clotting process by gathering at a bleeding site and clumping together to form a plug

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77
Q

Low platelets (thrombocytopenia) causes

A

Bruising, aBleeding, purpura & petechiae

78
Q

Etiology of low platelets (thrombocytopenia)

A

Bleeding, Von Willebrand’s disease, leukemia & liver cirrhosis

79
Q

Drugs causing low platelet levels

A

Aspirin, ibuprofen, indocin, valium & theophylline

80
Q

High platelets (thrombocythemia) causes

A

Hypercoagulability, DM & increases the risk for CVA and MI

81
Q

Nursing interventions of aPlatelets

A

-May require transfusion, check for bleeding tendencies and assess for petechiae/purpura
-Educate your patient on impact of medications such as aspirin and coumadin and side effects such as decreased platelets and clotting time

82
Q

WBC

A

-Part of the body’s defense system
-Help determine the presence of an infection or blood cancer such as leukemia

83
Q

WBC + neutrophils

A

-Most abundant WBC’s
-First line of defence againts infection

84
Q

WBC + band neutrophils

A

Immature neutrophils that indicate new infection

85
Q

WBC + basophils

A

Increase during the healing process and allergic response

86
Q

WBC + eosinophils

A

Increase during an allergic and parasitic condition

87
Q

WBC + lymphocytes

A

-Occurs in chronic and acute viral infections
-Play a major role in B and T cells
-Decrease in numbers during steroid therapy

88
Q

WBC + monocytes

A

-Second line of defense against bacterial infections and foreign substances (macrophages)
-Stronger than neutrophils and can ingest larger particles of debris

89
Q

Monocytes respond..

A

Late during the acute phase of infection and inflammatory process and continue to function during the chronic phase of phagocytosis

90
Q

Nursing interventions of aWBC

A

-Monitor trends of values, S&S of an infection such as increased temperature, tachycardia, edema, redness or wound drainage
-Monitor for S&S of allergies, such as tearing, runny nose or rash
-Monitor for S&S of healing

91
Q

Coagulation

A

Determines blood viscosity

92
Q

Prothrombin time (INR)

A

0.9-1.1

93
Q

Activated partial prothromboplastin time (PTT)

A

Lab value is specific to the area of intervention

94
Q

D-dimer

A

<0.3mmol/L

95
Q

PT/INR

A

-Taken pre-op to identify coagulation levels
-If the pt is taking coumadin, they will require routine blood levels to maintain blood consistency

96
Q

PTT

A

Blood test used to monitor PTT levels for IV heparin therapy

97
Q

D-dimer

A

-Occurs through fibrinolysis
-Measures the amount of fibrin degradation and confirms the presents of fibrin
-Used to diagnose PE, DIC and DVT

98
Q

Nursing interventions for aCoagulation

A

-Monitor for of bleeding
-Educate your pt on bleeding risks, bruising and petechiae associated with medication therapy such as coumadin
-Educate your patients on the rationale for frequent blood work

99
Q

Kidney function + Cr

A

-By-product of muscle catabolism
-Filtered by the glomeruli and excreted in the urine
-Indicator of renal disease
-Not influenced by diet or fluid intake

100
Q

Low levels of Cr indicate…

A

Pregnancy, eclampsia or small muscle mass

101
Q

High levels of Cr indicate…

A

RF, CHF, shock, SLE, cancer, leukemias, diabetic neuropathy, rhabdomyelosis, HTN & AMI

102
Q

Drugs influencing Cr levels

A

Ancef, gentamicin, barbituates & amphotericin B

103
Q

BUN

A

-End product of protein metabolism
-Excreted by the kidneys
-Correlates with Cr increase or decrease

104
Q

Etiology of decreased BUN levels

A

Severe liver damage, low-protein diet, overhydration, malnutrition (-ve nitrogen balance) & IV fluids (glucose)

105
Q

Drugs that cause decreased BUN levels

A

Phenothiazines

106
Q

Etiology of elevated BUN

A

Dehydration, high protein intake, DM, GI bleed, low renal blood supply & licorice

107
Q

Drugs that cause elevated BUN

A

-Nephrotoxic drugs
-Hydrochlorothiazide, edecrin, lasix, abx, gentamicin, methicillin, vancomycin, methyldopa, propranolol, morphine & lithum

108
Q

GFR

A

-Estimation of how well blood passes through the filters in the kidney
-Calculated value is based on the age & Cr level
-<60 ml/min indicates kidney damage

109
Q

Diabetes (hemoglobin A1C)

A

-Glucose molecule is attached to hemoglobin A1
-Calcultates the average blood glucose level within last 3 months
-Elevated levels above 8% indicate uncontrolled diabetes

110
Q

Slide 56&57

A
111
Q

Thyroid stimulating hormones (T3)

A

-More short acting and more potent than T4
-Secreted in response to thyroid- stimulating hormone from the pituitary gland and the thyroid-releasing hormone from hypothalamus
-Used for diagnosing hyperthyroidism

112
Q

Thyroid stimulating hormone (T4)

A

-Secreted by the thyroid gland
-More concentrated than T3
-PKU test in newborns
-Used to measure how well the thyroid gland is functioning and if tumors are present

113
Q

Nursing diagnosis of shock

A

-Ineffective peripheral tissue perfusion, risk for decreased cardiac tissue perfusion, ineffective cerebral tissue perfusion, and risk for impaired liver function
-Anxiety r/t threat of death & threat to current status

114
Q

Planning stage of shock + goals

A

-Restoration of adequate tissue perfusion
-Normal BP >65 mm Hg
-Return/recovery of organ function
-Progression toward further complications r/t prolonged states of hypoperfusion

115
Q

Collaborative care & successful management of shock includes

A

-Identification of patients at risk for shock
-Integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis
-Interventions to control or eliminate the cause of decreased perfusion
-Protection of target and distal organs from dysfunction
-Provision of multisystem supportive care

116
Q

Emergency management of shock

A

Patent airway & O2 delivery

117
Q

Cornerstoe of therapy for septic, hypovolemic & anaphylactic shock is…

A

-Volume expansion; isotonic crystalloids (NS) for fluid resuscitation

118
Q

Volume expansion

A

If the patient does not respond to 2 to 3L of crystalloids, blood administration and central venous monitoring may be instituted

119
Q

Complications of fluid resuscitation

A

-Hypothermia & coagulopathy

120
Q

Fluid resuscitation in pediatrics

A

Fluid resuscitation= 20 mL/kg of isotonic crystalloid/bolus

121
Q

Primary goal of drug therapy in shock is

A

-Correction of decreased tissue perfusion

122
Q

Adrenergic drugs for increasing tissue perfusion

A

Dobutamine, dopamine, E & NE

123
Q

Vasodilator goal & drugs in increasing tissue perfusion

A

-Achieve/maintain a MAP of >65mmHg
-Alpha-adrenergic agonists & nitroglycerin

124
Q

Vasoactive medications (adrenergic-agonists) effects

A

-Have a variety of effects on the alpha- and beta-adrenergic receptors
-Effects are related to the specific dose of the adrenergic drug

125
Q

Common vasoactive medications (adrenergic-agonists)

A

Dobutamine, dopamine, E & NE, midodrine hydrochloride and phenylephrine hydrochloride

126
Q

Maintenance dose of dobutamine hydrochloride

A

-2-15mcg/kg/min; acts on B1 more than B2

127
Q

High dose of dobutamine hydrochloride

A

40mcg/kg/min; acts on B2 more than A1

128
Q

Dopamine hydrochloride low dosage

A

0.5-3mcg/kg/min; dopaminergic

129
Q

Dopamine hydrochloride moderate dose

A

3-10mcg/kg/min; B1 &A1

130
Q

High dose of dopamine hydrochloride

A

> 10mcg/kg/min

131
Q

Epinephrine hydrochloride (adrenalin chloride) low drug dose

A

1-4mcg/min; B1 more than B2 and A1

132
Q

Epinephrine hydrochloride (adrenalin chloride) high dose

A

4-40mcg/min; A1 more than or equal to B1

133
Q

Slide 69

A
134
Q

Vasoactive drugs adverse effects + CNS

A

Headache, restlessness, tremors, nervousness, dizziness and insomnia

135
Q

Vasoactive drugs adverse effects +CV

A

Chest pain, vasoconstriction, HTN, tachycardia (positive chronotropy), fluctuations in BP, and palpitations or dysrhythmias

136
Q

Vasoactive drugs adverse effects +GI

A

Anorexia, dry mouth, N/V

137
Q

Vasoactive drug nursing considerations

A

-Ideally, administer through a central line rather than a peripheral IV
-High rate of extravasation
-Carefully monitor VS, pt will typically be in the ICU

138
Q

Nutrition + shock

A

-Enteral nutrition within the first 24 hours
-Initiate parenteral nutrition if enteral feedings contraindicated or fail to meet at least 80% of caloric requirements
-Monitor protein, nitrogen, BUN, glucose & electrolytes

139
Q

Health promotion in shock management

A

-Identify pt at risk

140
Q

Health promotion in shock management

A

-Identify pt at risk: Elderly, debilitating illness, immunocompromised & surgical or trauma pts
-Preventing shock: Monitor fluid balance to prevent hypovolemia and handwashing to prevent infection

141
Q

Nursing role with patients in shock

A

-Monitor ongoing physical & emotional status
-Planning & quickly implementing nursing interventions
-Evaluate the pt response to therapy
-Provide emotional support
-Collaborating with other members of the health team

142
Q

Acute intervention of pt in shock

A

Neuro, CV, resp, renal, temperature & skin changes, GI, hygiene and emotional support/comfort

143
Q

Cardiogenic shock oxygenation

A

Supplemental O2, intubation

144
Q

Cardiogenic shock circulation

A

Blood flow restored with thrombolytics, angioplasty with stent implantation, coronary revascularization, decreased workload of the heart with circulatory devices such as IABP & VAD

145
Q

Cardiogenic shock drug therapies

A

Nitrates, inotropes (dobutamine), diuretics (furosemide), B-adrenergic blockers (contraindicated with rEF)

146
Q

Cardiogenic shock supportive therapies

A

Correction of dysrhythmias

147
Q

Hypovolemic shock oxygenation

A

Supplemental O2

148
Q

Hypovolemic shock circulation

A

Fluid volume restored, rapid fluid replacement with large-bore IV, peripheral IV, end points of fluid resuscitation such as CVP of 15mmHg & PAOP of 10-12mmHg

149
Q

Hypovolemic shock drug therapies

A

No specific drug therapies

150
Q

Hypovolemic shock supportive therapies

A

-Cause corrected (ie. Bleeding or GI losses)
-Warmed fluids used

151
Q

Septic shock oxygenation

A

Supplemental O2 or intubation

152
Q

Septic shock circulation

A

Aggressive fluid resuscitation, end points of fluid resuscitation accomplished such as CVP of 15mmHg and PAOP of 10-12mmHg

153
Q

Septic shock drug therapies
GOES w/ card 168

A

Antibiotics, vasopressors (dopamine), inotropes (dobutamine), anticoagulants (LMWH)

154
Q

Septic shock supportive therapies

A

Cultures before antibiotics, monitor temperature, maintain glucose, stress ulcer prevention

155
Q

Neurogenic shock oxygenation

A

Patency of airway, supplemental O2 & intubation

156
Q

Neurogenic shock circulation

A

Fluids administered with caution

157
Q

Neurogenic shock drug therapies

A

Vasopressors (phenylephrine), atropine (for bradycardia)

158
Q

Neurogenic shock supportive therapies

A

Minimize spinal cord trauma & monitor temperature

159
Q

Anaphylactic shock oxygenation

A

Patent airway, supplemental O2 & intubation

160
Q

Anaphylactic shock circulation

A

Aggressive fluid resuscitation with colloids

161
Q

Anaphylactic shock drug therapies

A

Antihistamine (diphenhydramine), epinephrine with nebulizer, bronchodilators with nebulizer (albuterol), and corticosteroids if hypotension persists

162
Q

Anaphylactic shock supportive therapies

A

Remove noxious stimuli, avoid known allergens, premedicate according to prior hx of sensitivity

163
Q

Collaborative care of cardiogenic shock

A

-Restore blood flow to the myocardium by restoring the balance between 02 supply & demand
-Thrombolytic therapy, angioplasty with stenting, emergency revascularization and valve replacement

164
Q

Collaborative care of cardiogenic shock cont’d

A

-Hemodynamic monitoring drug therapy (e.g., diuretics to reduce preload)
-Circulatory assist devices (e.g., intra-aortic balloon pump or ventricular assist device)

165
Q

Collaborative care of hypovolemic shock

A

-Management focuses on stopping the loss of fluid and restoring the circulating volume
-Fluid replacement is calculated using a 3: 1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)

166
Q

Collaborative care of septic shock

A

-Fluid replacement to restore perfusion; hemodynamic monitoring
-Vasopressors (NE)
-Vasopressin (ADH) for patients resistant to vasopressor therapy

167
Q

Collaborative care of septic shock cont’d

A

-IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP
-Antibiotics after cultures are obtained

168
Q

Collaborative care of septic shock cont’d (2)

A

-Glucose levels <10 mmol/L
-Stress ulcer prophylaxis with histamine (H2)-receptor blockers
-DVT prophylaxis with low-dose unfractionated heparin or LMWH

169
Q

1 hour bundle for initial resuscitation for sepsis & septic shock

A

-Initiate bundle
1. Measure lactate level (remeasure if it is >2mmol/L)
2. Obtain blood cultures
3. Administer broad-spectrum antibiotics
4. Begin rapid administration of 30ml/kg crystalloid for hypotension or lactate >=4mmol/L
5. Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP of >=65mmHg

170
Q

Vasoactive agent management

A

-Use NE as first-line vasopressor
-Target MAP of 65mmHG (for pt w septic shock)

171
Q

Slide 86&87

A
172
Q

Collaborative care of neurogenic shock in a spinal cord injury

A

-Spinal stability
-Tx of the hypotension & bradycardia with vasopressors & atropine
-Fluids used cautiously as hypotension generally is not r/t fluid loss
-Monitor for hypothermia

173
Q

Collaborative care of anaphylactic shock

A

-Epinephrine & diphenhydramine
-Maintain patent airway with nebulized bronchodilators & endotracheal tube OR cricothyroidotomy if necessary

174
Q

Collaborative care for anaphylactic shock cont’d

A

-Priority is airway
-Aggressive fluid replacement
-IV corticosteroids if significant hypotension persists after 1 to 2 hours of aggressive therapy

175
Q

Disseminated intravascular coagulation (DIC) is always caused by…

A

-An underlying disease or condition which must be tx for it to be resolved

176
Q

Rapidly occuring DIC

A

-DIC that evolves rapidly (over hours/days) causes primarily bleeding
-Diagnosed by demonstrating thrombocytopenia, an elevated PTT, PT & d-dimer (or serum fibrin degradation products), and a decreasing plasma fibrinogen level

177
Q

Tx of DIC

A

Correction of the cause and replacement of platelets, coagulation factors (in FFP), and fibrinogen (in cryoprecipitate) to control severe bleeding

178
Q

Expected outcomes of DIC includes

A

Verbalization of fears or anxiety

179
Q

Tx of systemic inflammatory response syndrome (SIRS)

A

-Prevention & tx of infection
-Maintenance of tissue oxygenation
-Nutritional & metabolic needs
-Support of failing organs (ARDS, DIC, RF)

180
Q

ARF

A

Acute respiratory failure

181
Q

ARF & ARDS

A

Pt requires intubation with PEEP

182
Q

Nursing diagnosis of ARF/ARDS

A

-Impaired gas exchange
-Ineffective airway clearance

183
Q

Respiratory failure diagnostic studies

A

-Hx & physical assessment
-ABG analysis, chest x-ray, CBC, sputum/blood cultures, electrolytes, ECG, urinalysis
-Ventilation/perfusion (V/Q) lung scan
-Pulmonary artery catheter in severe cases

184
Q

ARF nursing diagnosis

A

-Impaired gas exchange
-Ineffective airway clearance
-Ineffective breathing pattern
-Risk for fluid volume imbalance

185
Q

Planning/goals of ARF tx

A

-ABG values within patient’s baseline
-Breath sounds within patient’s baseline
-No dyspnea or breathing patterns within patient’s baseline
-Effective cough and ability to clear secretions

186
Q

ARF prevention

A

-Thorough hx & physical assessment to identify at-risk patients
-Early recognition of respiratory distress

187
Q

ARF respiratory therapy

A

-O2 to correct hypoxemia
-Mobilization of secretions
-Positive-pressure ventilation (PPV)
-Non-invasive PPV: Bi-PAP or CPAP

188
Q

ARF drug therapy

A

-Bronchodilators -Relief of bronchospasm
-Corticosteroids -Reduction in airway inflammation
-Diuretics, nitrates if HF present -Reduction in pulmonary congestion

189
Q

Diuretics, nitrates if HF present -Reduction in pulmonary congestion
+ ARF

A

-IV antibiotics
-Benzodiazepines +/or narcotics

190
Q

ARF + medical supportive therapy

A

-Tx the underlying cause
-Maintain adequate CO & hemoglobin concentration

191
Q

ARF + nutritional therapy

A

-Maintain protein and energy stores
-Enteral or parenteral nutrition
-Nutritional supplements

192
Q

ARDS + COVID

A

Prone positioning

488 (16 decks)

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