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OCN Study > Oncogic Emergencies > Flashcards

Oncogic Emergencies Flashcards

1
Q

the inappropriate, systemic activation of the regulation Cascade that results in thrombosis and bleeding / hemorrhage is what oncologic emergency

A

disseminated intravascular coagulation

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2
Q

clot formation is also known as

A

thrombosis

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3
Q

clot breakdown is also known as

A

fibrinolysis

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4
Q

how is the process of thrombosis initiated?

A

through the destruction of the endothelial membrane and tissue injury.

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5
Q

tissue injury causes the release of_______ _______ into the circulation which leads to coagulation

A

tissue thromboplastin

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6
Q

what enzyme digests the components of a fibrin clot?

A

plasmin

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7
Q

what is the proteolytic enzyme that is responsible for both coagulation and fibrinolysis?

A

thrombin

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8
Q

what underlying conditions in the oncology patient may lead to excess circulating thrombin?

A

infection, malignancy, or trauma

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9
Q

excess thrombin results in what problem in the circulation?

A

multiple fibrin clots

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10
Q

excess clots in the circulatory system results in platelet traps which then causes what condition?

A

microvascular and macrovascular thrombosis

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11
Q

clot lodged in the vascular system leads to what problem?

A

ischemia, impaired organ perfusion, end-organ damage

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12
Q

the excess use of the coagulation factors in DIC is unable to be replaced which then leads to what problem?

A

excessive bleeding

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13
Q

excess plasmin in the circulatory system leads to what symptoms in DIC

A

shock, hypotension, increased vascular permeability

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14
Q

what diagnostic tests are done to diagnose disseminated intravascular coagulation,?

A

platelet count, fibrinogen level, D-dimer assay, FDP ( fibrin degradation products) titer

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15
Q

what tests are done to determine if accelerated quag ulation is a problem?

A

antithrombin III level, fibrinopeptide A level, prothrombin activation peptides, thronbin- antithrombin complexes

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16
Q

what tests are done to determine if accelerated fibrinolysis is a problem?

A

plasminogen level, plasmon Alpha 2 anti plasmin complex levels

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17
Q

what is the main goal of treatment related to DIC?

A

treatment of the underlying condition causing DIC, supporting the hemodynamics, manage the bleeding or thrombosis

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18
Q

how is the underlying condition for DIC typically treated?

A

chemotherapy for malignancy, antibiotics for infection

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19
Q

what hemodynamic support is often used in the patient with the DIC?

A

fluid replacement, oxygen therapy, administration of platelets, red blood cells, fresh frozen plasma, fibrinogen, cyroprecipitate

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20
Q

what treatment is used to replace quag ulation factors?

A

plasmapheresis

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21
Q

what does plasmapheresis do to help the patient with DIC?

A

it removes the triggers of coagulation

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22
Q

what lab values are decreased in the patient with DIC?

A

platelet count, fibrinogen level, antithrombin 3 level, plasminogen level, plasmon Alpha 2 antiplasmin complex

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23
Q

what lab values are increased in the patient with DIC?

A

D-dimer assay, fdp tighter, fibrinopeptide A, prothrombin activation peptides, thrombin antithrombin complex

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24
Q

What patients are at increased risk for developing DIC?

A

acute leukemia, mucin producing solid tumors, infection and sepsis, liver disease, hemolytic transfusion reactions, transplant reactions, Burns, trauma, pregnancy and obstetric complications, peritoneovenous shunts

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25
Q

what is the most common cause of DIC?

A

sepsis / infection

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26
Q

what are the early signs and symptoms of DIC in the skin?

A

pallor, petechiae, jaundice, ecchymosis, hematomas, bleeding, acral cyanosis

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27
Q

what are the early signs and symptoms of DIC in the GI system?

A

tarry stools, hematemesis, abdominal pain, abdominal distension

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28
Q

what are the early signs and symptoms of DIC in the GU system?

A

hematuria, decreased urinary output

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29
Q

what are the early signs and symptoms of DIC in the respiratory system?

A

dyspnea, tachypnea, hypoxia, hemoptysis, cyanosis

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30
Q

what are the early signs and symptoms of DIC in the neurological system?

A

headache, restlessness, confusion, lethargy, altered level of consciousness, obtundation, seizures, coma

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31
Q

what are the early signs and symptoms of DIC in the musculoskeletal system?

A

joint pain and stiffness

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32
Q

what are the early signs and symptoms of DIC in the cardiovascular system?

A

tachycardia, hypotension, diminished peripheral pulses, changes in color and temperature of extremities

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33
Q

What nursing interventions will help maximize patient safety in the diagnosis of DIC?

A

fall precautions, assistance for adl’s, bleeding precautions, discourage dangling feet and pressure causing devices

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34
Q

what are the signs and symptoms of progressing DIC?

A

septic shock symptoms, proteinuria, anuria, decreased mental status, changes in breathing, bleeding

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35
Q

what important patient education should take place in the patient with known or suspected DIC?

A

signs and symptoms of DIC, report new bleeding, save all urine, emesis and stool for the nurse to check, bleeding precautions

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36
Q

the systemic inflammatory response to a documented infection is known as

A

sepsis

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37
Q

sepsis is the inflammatory response to what in the blood?

A

pathogenic microorganisms and associated endotoxins

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38
Q

sepsis usually presents with two or more of what signs and symptoms?

A

temperature greater than 100.4, heart rate greater than 90 BPM, respiration rate greater than 20 breaths / minutes, WBC greater than 12000 or less than 4000, or greater than 10% bands

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39
Q

sepsis results when the body fails to initiate an adequate___________ to an infection.

A

immune response

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40
Q

what are the signs and symptoms of septic shock?

A

fever, chills, tachycardia, tachypnea, mental status changes, hypotension

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41
Q

what are the phases of septic shock?

A

infection, bacteremia, systemic inflammatory response syndrome, sepsis, severe sepsis, septic shock, multiple organ dysfunction syndrome

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42
Q

what is the most common source of infection related sepsis?

A

bacterial organisms

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43
Q

which gram-negative organisms are common in septic shock cases?

A

e-coli,klebsiella pneumonia, pseudomonas aeruginosa

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44
Q

which gram-positive bacteria are most commonly associated with septic shock cases?

A

streptococcus pneumonia, staphylococcus aureus

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45
Q

which patients are at increased risk for gram-positive bacterial infections?

A

patients with vascular access devices, and those with a lack of mucosal integrity

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46
Q

patients with fungal infection related sepsis are at an increased risk for what problems?

A

increased length of hospitalization and death

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47
Q

where do most infections arise in the oncology patient?

A

endogenous Flora

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48
Q

mortality from sepsis is associated with what three factors?

A

causative organism, site of infection, level of duration of neutropenia

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49
Q

what are the basic infection control precautions?

A

good hand-washing, oral and perianal care, identification of patients at risk for infection, avoidance of invasive procedures

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50
Q

what diagnostic procedures are done to diagnose and treat sepsis?

A

blood cultures, chest x-ray, cultures of erudite, CBC, electrolytes,LFTs, PTL, PTT, ABGs, EKG

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51
Q

what tests are done to diagnose the degree of organ failure in a patient with sepsis?

A

echocardiogram, CT scans, ventilation perfusion scan, angiography

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52
Q

what is done to maintain hemodynamic support in the patient with sepsis?

A

administration of fluids, blood transfusions, vasopressors, oxygen therapy

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53
Q

what base oppressors are used to combat hypotension in the patient with sepsis?

A

dopamine, norepinephrine, dobutamine

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54
Q

what is the treatment recommendations for the patient with sepsis?

A

empiric antibiotics started at the first sign of sepsis

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55
Q

when is empiric antifungal therapy started in the patient with sepsis?

A

five to seven days after empiric antibiotic therapy has been started and the patient continues a fever

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56
Q

what are the risk factors for sepsis?

A

immunosuppression either from therapy or malignancy, comorbidities, age greater than 65, invasive devices, loss of skin or mucosal integrity

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57
Q

what comorbidities put a patient at increased risk for sepsis?

A

diabetes, renal, hepatic, cardiovascular, and / or pulmonary disease, GI abnormalities

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58
Q

a life-threatening metabolic imbalance that occurs with a rapid release of potassium, phosphorus, and nucleic acid into the bloodstream due to tumor cell kill is known as

A

tumor lysis syndrome

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59
Q

what electrolyte abnormalities are present in tumor lysis syndrome?

A

hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia

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60
Q

why is the calcium decreased in tumor lysis syndrome?

A

increased phosphorus binding to the calcium to form phosphatase salts

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61
Q

what does tumor lysis syndrome lead to in the cancer patient?

A

cardiac arrhythmias, renal failure, multi-system organ dysfunction

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62
Q

why do cancer patients with tumor lysis syndrome develop renal failure?

A

kidneys are the primary route of excretion of phosphatase salts, uric acid, and potassium and they become over taxed

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63
Q

what tests are done to diagnose and monitor for tumor lysis syndrome?

A

LDH, bun, creatinine, serum electrolytes

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64
Q

what is the treatment for tumor lysis syndrome?

A

IV hydration, alkalinization of urine, decrease the production of uric acid with medication, diuretics, manage electrolyte imbalances

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65
Q

what type of diet would be recommended in a patient with tumor lysis syndrome?

A

low potassium and low phosphorus

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66
Q

what foods are high in potassium?

A

bananas, oranges, orange juice, tomatoes

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67
Q

what foods are high in phosphorus?

A

eggs, meat, fish, nuts, cheese, bread, poultry, legumes, cereal, carbonated drinks

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68
Q

What patients are at the highest risk for developing tumor lysis syndrome?

A

patients with bulky or high-growth fraction hematologic tumors, recent chemotherapy, recent RT or surgery, comorbid renal and cardiac disease

69
Q

which cancers are generally known to have a higher risk for being a large, bulky tumor?

A

lymphoma, small cell lung cancer, breast cancer, neuroblastoma

70
Q

what level do patients have signs and symptoms related to hyperkalemia

A

serum levels exceed 6.5 mil mEq / L

71
Q

what are the signs and symptoms of hyperkalemia?

A

EKG changes, nausea, vomiting, diarrhea, muscle weakness, cramps, tingling, twitching, paresthesia, paralysis

72
Q

what are the signs and symptoms of hyperphosphatemia?

A

edema, oliguria, anuria, renal insufficiency, azotemia, acute renal failure

73
Q

what are the signs and symptoms of hypocalcemia?

A

hypotension, EKG changes, muscle cramps, twitching, paresthesias, seizures, tetany, altered mental status

74
Q

what are the signs and symptoms of hyper uricemia?

A

oliguria, anuria, azotemia, edema, neuropathy, flank, nausea, vomiting, diarrhea, hematuria, lethargy, somnolence, seizure

75
Q

what safety precautions may need to be initiated in the acute tumor lysis syndrome patient?

A

Fallen seizure precautions, intake and output, dietary modifications

76
Q

what types of problems in the cancer patient can lead to hypercalcemia?

A

increased bone resorption or bone destruction, increased level of parathyroid hormone or protogladin produced by the cancer

77
Q

what is calcium necessary for in the human body?

A

maintenance of bones and teeth, muscle contraction, nerve impulse transmission, normal clotting maintenance

78
Q

what hormonal substances help regulate calcium levels?

A

parathyroid, vitamin D, calcitonin

79
Q

what is the most common metabolic complication in the cancer patient?

A

hypercalcemia

80
Q

what are the most common cancers associated with hypercalcemia

A

breast, lung, head and neck, multiple myeloma, renal, lymphoma

81
Q

what is considered in the correction of calcium levels?

A

the effect of altered albumin concentration on the calcium levels

82
Q

what non- pharmacologic treatments are recommended for hypercalcemia?

A

weight bearing exercise, active or passive range of motion

83
Q

what are the pharmacologic treatments that are frequently used for hypercalcemia?

A

hydration, diuresis, antineoplastic therapy for primary and metastatic tumors, antiresoorptive therapy with biophosphonates, steroids

84
Q

what are the contributing factors for hypercalcemia?

A

immobility, dehydration, Advanced age, renal dysfunction, tpn, vitamin A and D intoxication, lithium, thiazide, and anti acid use

85
Q

what signs and symptoms of hypercalcemia should the patient and or caregivers be instructed to report?

A

nausea and vomiting, constipation, fatigue, weakness, changes in mental status or personality

86
Q

what safety precautions should be initiated in the patient with hypercalcemia?

A

fall precautions, seizure precautions, patient may have mental confusion so may need to keep close observation

87
Q

what is the name of an endocrine paraneoplastic syndrome resulting from the non physiologic release of antidiuretic hormone?

A

syndrome of inappropriate secretion of antidiuretic hormone

88
Q

where is the antidiuretic hormone synthesized and secreted from in the body?

A

synthesized in the hypothalamus, secreted from the pituitary gland

89
Q

ADH regulates water re-absorption in the renal tubules based on what factors?

A

increased plasma osmolality, decreased plasma volume

90
Q

what signs and symptoms are present in the patient with SIADH?

A

hyponatremia, concentrated urine, elevated urine sodium concentration, intracellular edema, cerebral edema

91
Q

what cancer is associated with the highest number of SIADH cases?

A

small cell lung cancer

92
Q

what diagnostic tests are recommended to diagnose and monitor the patient with SIADH?

A

serum: sodium, plasma osmolality
urine: osmolality, specific gravity,
sodium: electrolytes, thyroid, adrenal, cardiac, hepatic, renal function tests, chest x-ray, CT scan of the head

93
Q

what are the nonpharmacologic treatments for SIADH?

A

fluid restriction to 500-1000 ml per day

94
Q

why is it important to correct sodium levels over time instead of immediately?

A

correcting sodium levels to rapidly may cause brain damage from brain cell dehydration

95
Q

what medications may increase the risk for SIADH?

A

morphine, diuretics, antidepressants

96
Q

what medications can be used to help correct SIADH?

A

demeclocycline, urea, lithium, hypertonic saline solutions

97
Q

what are the early signs and symptoms of SIADH?

A

nausea, anorexia, malaise, fatigue, weakness, muscle cramps, thirst, headache, confusion, vomiting, lethargy, weight gain, psychotic behavior

98
Q

what are the late signs and symptoms of SIADH?

A

delirium, obtundation refractory seizures, coma, and death

99
Q

and immediate, systemic hypersensitivity reaction that usually occurs within seconds to minutes after the administration of a foreign protein and can be life-threatening is known as

A

anaphylaxis

100
Q

anaphylactic reactions are predictable true or false

A

false, they are unpredictable. Anaphylaxis can result in respiratory failure, cardiovascular collapse, and possibly death.

101
Q

which classes of chemotherapy are more commonly associated with hypersensitivity reactions?

A

taxanes, Platinum compounds, monoclonal antibodies, biotherapy

102
Q

immediate hypersensitivity reactions are Medicated by what protein?

A

immunoglobulin E (igE)

103
Q

what factors influence the development of anaphylaxis?

A

route of Entry, amount, and absorption rate of the antigen and the patients degree of hypersensitivity to the antigen

104
Q

what systemic effects occur as a result of the release of mediators of hypersensitivity such as histamine and leukotrienes?

A

bronchospasm, inflammation, smooth muscle spasm, increased capillary leak, and mucosal edema

105
Q

what are the early signs and symptoms of an anaphylactic reaction?

A

Purists, urticaria, erythema, anfioedema, dyspnea, wheezibg, warmth, flushing, dizziness, hypertension, chest tightness, nausea, vomiting, diarrhea, abdominal discomfort, anxiety, dizziness, agitation, feeling of Doom

106
Q

what are the late signs and symptoms of an anaphylactic reaction?

A

Strider, bronchospasm, laryngeal edema, hypotension, tachycardia, arrhythmias, chest pain, loss of consciousness

107
Q

what medication is most commonly used for prophylaxis of an anaphylactic reaction?

A

epinephrine 1:1000, corticosteroids, H1 blockers, H2 blockers, acetaminophen

108
Q

What nursing measures can increase the safety of patients with an anaphylactic reaction?

A

Baseline vital signs, verified and documented allergy history, maintain IV access during administration of potential allergen, have Emergency agents available at all times

109
Q

at the first sign of an anaphylactic reaction, the nurse should do what?

A

stop the flow of the offending agent, maintain IV infusion, maintain patent Airway, administer emergency medications for protocol

110
Q

what are the symptoms of respiratory distress?

A

adventitous breath sounds, increased respiratory rate, Rhythm and effort, changes in ABGs

111
Q

what are the signs of fluid overload?

A

jugular neck vein distention, changes in intake / output ratio, changes and weight greater than 5 pounds per day

112
Q

what does the inter-cranial cavity contain?

A

brain tissue, vascular tissue, cerebral spinal fluid

113
Q

an increase in intracranial pressure can result because of what?

A

displacement of brain tissue, edema of brain tissue, obstruction of CSF flow, increased vascularity because of tumor growth

114
Q

what diagnostic test should be done to assess for increased ICP?

A

CT scan, MRI, cerebral angiography, Myla graphy, biopsy, pet, spect

115
Q

what nonpharmacologic interventions are available to treat increased intracranial pressure?

A

surgery, radiation therapy, shunt placement, hyperventilation, fluid restriction

116
Q

which chemotherapy cross the blood-brain barrier, therefore may help with increased intracranial pressure?

A

nitrosoureas and procarbazine

117
Q

which route of administration of chemotherapy may help decrease increased intracranial pressure?

A

intra-arterial, intrathecal, intraventricular, intra tumor

118
Q

what what medication is typically the first medication started when symptoms of increased intracranial pressure are present?

A

corticosteroids

119
Q

what hyperosmotic agent reduces intracellular water of the brain?

A

Mannitol

120
Q

anticonvulsant may need to be started when a patient has what structural emergency?

A

increased intracranial pressure

121
Q

which cancers put patients at a higher risk of developing increased intracranial pressure?

A

cancers of the lung, breast, testes, thyroid, stomach, kidney or melanoma, brain or spinal cord

122
Q

what problems associated with cancer but not specifically tumors of the brain can cause an increase in intracranial pressure?

A

thrombocytopenia or platelet dysfunction may lead to bleeding in the brain

123
Q

what types of headaches an early sign and symptom of increased intracranial pressure?

A

headache, worse in the morning, aggravated by coughing, bending over, valsalva maneuver

124
Q

what neurological symptoms are an early sign and symptoms of increased intracranial pressure?

A

blurred vision, diplopia, decreased visual fields, extremity drifts, lethargy, apathy, confusion, restlessness

125
Q

what what neurological symptoms are a late sign of increased intracranial pressure?

A

decreased ability to concentrate, decreased level of consciousness, personality changes, hemiplegia, hemiparesis, seizures, pupillary changes, papilledema

126
Q

what is the Cushing’s Triad?

A

hypertension, bradycardia, abnormal respirations, a very late sign of increased ICP, the patient is usually comatose

127
Q

what activities should be discouraged in order to minimize increased ICP?

A

isometric muscle contractions, valsalva maneuver, external stimulation, stress, rotating the head or flexing the neck, lying in prone position

128
Q

what should be regularly assessed in a patient with increased ICP?

A

blood pressure, pulse, respiration, level of Consciousness, sensory or motor changes, nausea, vomiting, headache

129
Q

what structural emergency has occurred when a tumor compresses neural tissue and compromised the blood supply?

A

spinal cord compression

130
Q

the spinal cord has what three functions?

A

motor, sensory, and autonomic

131
Q

what diagnostic tests are done in order to determine if there is a spinal cord compression?

A

x-rays, bone scan, MRI, CT scan, myelogram, pet

132
Q

what are the nonpharmacologic interventions for spinal cord compression?

A

radiation therapy, surgery

133
Q

what pharmacologic interventions are used to treat spinal cord compression?

A

corticosteroids, chemotherapy, pain medications, anticonvulsant, antidepressants

134
Q

which cancers have a higher risk for metastasizing to the Bone?

A

breast, long, prostate, renal, melanoma, myeloma

135
Q

which cancers have a higher risk for metastasizing to the spinal cord?

A

lymphoma, seminoma, neuroblastoma

136
Q

what are the primary cancers of the spinal cord?

A

ependymoma, astrocytoma, glioma

137
Q

what are the early signs and symptoms of spinal cord compression?

A

neck or back pain, worse in supine position, local, radicular, worse with straining, coughing or flexion, motor weakness, sensory loss

138
Q

what are the late signs and symptoms of spinal cord compression?

A

loss of sensation for deep pressure, vibrations, position, incontinence of stool or urine, sexual impotence, paralysis, muscle atrophy

139
Q

what are the goals for treatment related to spinal cord compression?

A

acceptable pain control, Optimum level of physical Mobility, bowel and bladder control

140
Q

what structural emergency is a result of compromised venous drainage of the head, neck, upper extremities and thorax because of compression or obstruction?

A

superior vena cava syndrome

141
Q

compression that causes superior vena cava syndrome can be from what sources?

A

direct tumor invasion, enlarged lymph nodes, thrombus

142
Q

venous pressure ____________and cardiac output ________ when obstruction of the SVC occurs.

A

venous pressure increases and cardiac output decreases

143
Q

what is the goal of treatment in SVCS?

A

decreasing or eliminating the underlying cause and presenting symptoms

144
Q

what diagnostic tests are used to determine the cause and extent of SVCS?

A

chest x-ray, CT scan of the thorax, biopsy

145
Q

what nonpharmacologic interventions are commonly used for SVCS?

A

radiation therapy, removal of the central venous catheter, oxygen, angioplasty, stents, surgical reconstruction

146
Q

what pharmacologic interventions are commonly used for SVCS?

A

chemotherapy, corticosteroids, diuretics, thrombolytics

147
Q

which clients are at an increased risk for developing SVCS?

A

lymphoma, lung and breast cancer, patients with Central lines and pacemakers, previous RT to mediastinum

148
Q

what are the early signs and symptoms of svcs?

A

facial swelling worse in the morning, redness and edema around the eyes, swelling of the neck, arms and hands, neck and through a sick vein distention, dyspnea, cyanosis of upper torso, facial erythema, visible collateral veins of the chest and / or breasts

149
Q

what are the late symptoms of svcs?

A

severe headache, irritability, visual disturbances, dizziness, syncope, changes in mental status, stridor, tachycardia, CHF, decreased blood pressure, Horner’s syndrome, dysphasia, hemoptysis

150
Q

what laboratory tests should be considered when evaluating a patient with SVCS?

A

abg’s, electrolytes, kidney function, CBC, coagulation studies

151
Q

what interventions are important to decrease the severity of symptoms associated with SVCS?

A

Elevate the head of bed, avoid valsalva maneuver, maintain lower extremities in dependent position, remove rings and restrictive clothing around arms and neck, avoid pressure in the upper extremities

152
Q

what are the signs and symptoms of progressive respiratory distress in SVCS?

A

increased respiratory rate, anxiety, stridor, adventitious breath sounds, difficulty breathing

153
Q

what are the signs and symptoms of progressive edema and SVCS?

A

increase swelling in the face, arms, or neck, venous distention of the neck or thorax

154
Q

what are the signs and symptoms of changes in tissue perfusion related to SVCS?

A

decreased or absent peripheral pulses, decrease in blood pressure, pallor

155
Q

what are the adverse effects of long-term steroid therapy?

A

weakness of involuntary muscles, mood swings, hyperglycemia, dyspepsia, insomnia

156
Q

the excess accumulation of fluid in the pericardial Sac is known as what structural emergency?

A

cardiac tamponade

157
Q

what is the pericardial cavity?

A

the space between the two-layered sac known as the pericardium that surrounds the heart

158
Q

intracardiac pressure occurs because of what oncologic reasons?

A

fluid accumulation, direct or metastatic tumor Invasion, or fibrosis from radiation in the pericardial sac

159
Q

an increase in intrapericardiac pressure results in what changes in the circulatory system?

A

decrease left ventricular filling, decreased ability for the heart to pump, decreased cardiac output, impaired systemic perfusion

160
Q

what diagnostic can be done to determine if a patient has cardiac tamponade?

A

chest x-ray, CT scan, echocardiogram(most reliable), EKG, pericardiocentesis and cytology if fluid is found

161
Q

what are the nonpharmacologic interventions for cardiac tamponade?

A

pericardiocentesis, pericardial window, radiation therapy

162
Q

what are the pharmacologic interventions for cardiac tamponade?

A

pericardial sclerosis, chemotherapy, steroids

163
Q

how is pericardial sclerosis done?

A

installation of a chemical agent through a pericardial catheter, common agents are doxycycline, thiotepa, bleomycin, mitomycin C sterile talc

164
Q

what increases the risk for cardiac tamponade?

A

primary tumors of the heart (mesothelioma, sarcoma), metastatic tumors to the pericardium, > 4000 cGy of RT to the heart

165
Q

what are the early signs and symptoms of cardiac tamponade?

A

retrosternal chest pain relieved with leaning forward, dyspnea, cough, muffled heart sounds, weak or absent apical pulse, anxiety, hiccups

166
Q

what are the late signs and symptoms of cardiac tamponade?

A

tachycardia, tachypnea, narrowing pulse pressure, pulsus paradoxus greater than 10 mm HG classic, increased CVP, oliguria, peripheral edema, diaphoresis, cyanosis, altered Loc, Beck’s Triad

167
Q

a classic sign of cardiac tamponade is Becks Triad, what is it?

A

elevated central venous pressure (CVP), hypertension, distant heart sounds

168
Q

what interventions should be done for cardiac tamponade to monitor response to therapy?

A

Vital Signs evaluation, monitor Beck’s Triad, input and outtake, Loc, edema

OCN Study (11 decks)

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