Test 1 Flashcards

(246 cards)

1
Q

Secondary renal Na retention results from?

A

enhanced sympathetic activity, RAAS activation
CHF (from low CO)
Cirrhosis synthetic dysfunction & hypoalbuminemia

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2
Q

Hypervolemia/Na retention clinical presentation

A

Edema
effusions
rales
elevated JVP/CVP
hepatojugular reflux
S3
HTN
Low urine Na (<15mEq/L

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3
Q

Hypervolemia/Na retention symptoms

A

dypnea
abd distention
edema

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4
Q

Management of Hypervolemia/Na retention primary goals?

A

address underlying problem
limit Na intake (20-40mmol/d)

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5
Q

Management of Hypervolemia/Na retention
What medication should be used?

A

Diuretics

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6
Q

Proxmial tubule diuretic to use in management of Hypervolemia/Na retention?

A

Diamox

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7
Q

Loop Diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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8
Q

Distal tubule diuretic to use in management of Hypervolemia/Na retention

A

HCTZ

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9
Q

Collecting duct diuretic to use in management of Hypervolemia/Na retention?

A

Spironolactone

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10
Q

Which is the most potent diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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11
Q

How does spironolactone work?

A

competes with aldosterone

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12
Q

Antidiuretic hormone secretion leads to hyponatremia how?

A

either appropriate secretion in response to low circulating volume or inappropriate d/t neuro d/o, pulmonary disease, malignancy

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13
Q

Hyperosmolar hyponatremia is d/t?

A

hyperglycemia

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14
Q

Hyperosmolar hyponatremia causes increased ECF resulting in?

A

dilution of Na content

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15
Q

Hyperosmolar hyponatremia
For every 100 mg/dL rise in plasma glucose Na falls by?

A

1.6-2.4 mEq/L

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16
Q

Diagnostic approach to hyponatremia
Hypertonic Hyponatremia >295 mOsm/kg

A

Hyperglycemia
Hypertonic fluid admin

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17
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg first step?

Second step?

A

Assessment of volume status
hypovolemic
euvolemic
hypervolemic

Check urine sodium

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18
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium > 20 mEq/L

A

Renal solute loss

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19
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium </= 20 mEq/L

A

Extrarenal solute loss

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20
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Euvolemic: urine sodium always >20 mEq/L

A

SIADH
Endocrinopathies (Glucocorticoid deficiency)
Potassium depletion (diuretic use)

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21
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium > 20 mEq/L

A

Renal failure

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22
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium </= 20 mEq/L

A

Edematous d/o’s
Heart failure
Cirrhosis
Nephrotic Syndrome

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23
Q

Hyponatremic Clinical presentation

A

Neurologic abnormalities d/t cerebral edema from shifting of H2O from ECF to ICF

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24
Q

Hyponatremic Clinical Presentation
neurologic abnormalities severity depends on?

A

magnitude & rapidity of fall

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25
Hyponatremic Clinical Presentation Acute: timeframe? symptoms?
<2 days nausea malaise H/A lethargy confusion obtundation
26
Hyponatremic Clinical Presentation Na 115 mEq/L results in?
stupor seizures coma
27
Hyponatremic Clinical Presentation Chronic: timeframe? symptoms?
>3 days minimization of increased ICF/symptoms
28
Management of Hyponatremia is determined by?
ECV (extracellular volume): low, normal, high Presence of neuro symptoms
29
Symptomatic hyponatremia requires more rapid correction, however no greater increase in plasma Na than what rate? not to exceed what level? or how much Na mEq/L/d? why?
0.5mEq/L/hr 130 mEq/L >12 mEq/L/d possible occurrence of central pontine myelinolysis (CPM) from neuronal damage from rapid osmotic shifts
30
Management of Hyponatremia for low ECV?
hypertonic saline 3% if symptomatic NS if asymptomatic
31
Management of Hyponatremia for normal ECV?
lasix hypertonic saline if symptomatic NS if asymptomatic
32
Management of Hyponatremia for high ECV?
lasix hypertonic saline if symptomatic lasix if asymptomatic water restriction
33
SIADH is what?
inappropriate levels of ADH are secreted despite absence of osmotic or volume related stimuli
34
SIADH is a dysregulation of what?
cells secreting ADH or in feedback mechanisms responsible for release
35
SIADH causes CNS disease
tumor trauma infection CVA SAH GBS DTs MS
36
SIADH causes pulmonary disease
tumor pneumonia COPD PPV
37
SIADH causes malignancies
lung pancreas ovarian lymphoma
38
SIADH causes meds
NSAIDs narcotics diuretics antidepressants haldol !
39
SIADH other causes?
surgery idopathic
40
SIADH labratory volume status? Sodium status? Urine osmolality? Urine Na? Serum osmolality?
euvolemia hyponatremia secondary to H2O excess Elevated urine osmolality (>200 mOsm/kg) elevated urine Na (> 20mEq/L) decreased serum osmolality (<280 mOsm/kg)
41
Hypernatremia H2O deficit comes from?
diaphoresis diarrhea osmotic diuresis (hyperglycemia) diabetes insipidus
42
Hypernatremia Clinical Presentation symptoms
altered MS weakness neuromuscular irritability focal deficits coma seizures occasionally thirst polyuria if DI
43
Diabetes insipidus r/t ADH Central DI causes?
trauma anoxic encephalopathy surgery meningitis brain death ethanol neoplastic idiopathic
44
Diabetes insipidus r/t ADH Nephrogenic DI is d/t?
defective end-organ responsiveness to ADH
45
Diabetes insipidus r/t ADH Nephrogenic DI causes?
ampho lithium dye hypokalemia
46
Diabetes insipidus hallmark is what? urine osmolarity in central is? urine osmolarity in nephrogenic is?
dilute urine <200 mOsm/L 200-500 mOsm/L
47
Diabetes insipidus causes what Na balance?
hypernatremia
48
Diabetes insipidus serum osmolality is?
> 290 mOsm/kg
49
Diabetes insipidus dx is confirmed by?
response to fluid restriction failure of urine osmolarity to increase by >30 mOsm/L in initial hours is diagnositc
50
How to distinguish central DI from nephrogenic DI?Q
Response to vasopressin/dDAVP (1mcg SQ or IV)
51
Diagnostic Approach to Hypernatremia Urine Output is low?
Urine Osmolality will be high Was there hypotonic fluid loss? insensible losses GI losses Prior Renal Losses from Diuretics
52
Diagnostic Approach to Hypernatremia Urine Output is High; Urine Osmolality is Low
Diabetes Insipidus Response to DDAVP indicates Central No Response to DDAVP indicates Neprhogenic
53
Diagnostic Approach to Hypernatremia Urine Output is High; Urine Osmolality is High
Osmotic Diuresis?
54
DI H2O deficit should not be corrected more rapid than?
10-12 mEq/L/d less if chronic state
55
Management of Diabetes Insipidus free H2O admin should be done how?
calculate free H2O deficit Correct H2O deficit over 2-3 days to reduce risk of cerebral edema
56
Management of Diabetes Insipidus if central?
DDAVP 2-5 u SQ q 4-6hrs
57
Management of Diabetes Insipidus if neprhogenic?
low Na diet thiazide diuretic
58
A-fib anticoagulation/antiplatelet therapy Scores to calculate when patient has CHF, HTN, AGE, sex, DM, Prior stroke TIA, Vascular disease?
CHADS2 score CHA2DS2-VASc Score
59
A-fib anticoagulation/antiplatelet therapy Scores to calculate when patient has HTN, abnormal renal function, abnormal liver function, stroke, bleeding, labile INR, elderly >65, alcohol or drug use?
HAS-BLED
60
Possible Differential Diagnosis for pts experiencing stroke like symptoms
Tumors SDH Cerebral abscess Todd's paresis or paralysis Hypoglycemia Encephalitis Conversion D/O Migrainous aura focal seizure periveral nerve lesions
61
Clinical Manifestations for MCA stroke
Hemiparesis Hemiplegia Hemianesthesia Hemianopia Aphasia Neglect Gaze deviation !
62
Clinical Manifestations for Anterior Cerebral artery stroke
Lower extremity hemiplegia Primitive reflexes confusion abulia behavioral changes disturbance in memory
63
Clinical Manifestations for Vertebral and basilar artery stroke
Decreased LOC Vertigo Dysphagia Diplopia Ipsilateral CN findings Contralateral (or bilateral) sensory and motor deficits
64
Initial Evaluation 10 min or sooner from arrival
Evaluation by physician
65
Initial Evaluation
Stroke or neurologic expertise contacted
66
Initial Evaluation
NCCT or MRI
67
Initial Evaluation
interpretation of neuroimaging
68
Initial Evaluation
initiation of IV alteplase
69
Initial Evaluation What should be assessed?
ABCs Time of Onset Circumstances surrounding onset of neuro symptoms Hx Neuro eval (NIHSS) Labs and ECG STAT Head CT Vascular imaging
70
Initial Evaluation Exclude stroke mimics such as
Psychogenic Seizures Hypoglycemia Migraine HTN encephalopathy Wernicke's encephalopathy CNS abscess CNS tumor Drug toxicity
71
Initial Evaluation All patients need
Non-Con CT (NCCT) MRI Blood glucose Cardiac monitoring EKG Troponin BMP, CBC, PT/INR/aPTT Maintain O2 sats > 94%
72
Emergent Management of Ischemic Strokes ABCs
avoid hypotension, hypoxia and hypovolemia
73
Emergent Management of Ischemic Strokes Supplemental O2 for sats of?
>94%
74
Emergent Management of Ischemic Strokes Antipyretic medications for temp of?
> 38 C
75
Emergent Management of Ischemic Strokes Fluid resuscitation w/?
isotonic fluids
76
Management of Ischemic Strokes includes?
Thrombolytic therapy Mechanical thrombectomy Antiplatelet therapy BP management
77
Contraindications for IV Alteplase Presentation to GI
Presentation outside window (>4.5 hrs) Mild, nondisabling stroke (NIHSS 0-5) HCT w/ extensive areas of hypoattenuation or frank hypodensity ICH AIS w/n 3 mo Severe Head Trauma w/n 3 mo Acute head trauma Intracranial or intraspinal surgery w/n 3 mo symptoms suggestive of SAH GI malignancy or GI bleed w/n 21 days
78
Contraindications for IV Alteplase Infective to Concomitant
Infective endocarditis Aortic arch dissection intra-axial intracranial neoplasm coagulopathy (plt count < 100,000/mm3, aPTT > 40 sec, INR >1.7 or PT > 15 sec) LMWH - therapeutic dose in last 24 hrs Thrombin or Factor Xa inhibitors w/ elevated sensitive lab test (aPTT, INR, plt count, ECT; TT; appropriate factor Xa activity assays) Concomitant Abciximab Concomitant IV Aspirin
79
BP requirements for pts that are candidates for reperfusion therapy Systolic and diastolic prior to infusion? IVP medications that can be given to control BP? Dose? Frequency? (2) IV infusions that can be given to control BP? Initial dose, titration parameters, max dose? (2) Systolic and diastolic following infusion? for how long?
SBP
80
Alteplase Admin Dose (max dose) infusion time
0.9mg/kg (max dose 90mg) over 60 min w/ 10% of dose given as bolus over 1 min
81
Alteplase Admin What would require the discontinuation of infusion and obtaining an emergency head CT scan?
if the patient develops severe HA acute hypertension nausea or vomiting worsening neuro exam
82
Alteplase Admin What would be an indication for increasing frequency of BP measurements? How to manage this?
if SBP > 180 mmHg or DBP > 105 mmHg administer antihypertensive medications to maintain BP at or below these levels
83
Alteplase Admin Before starting anticoagulants or antiplatelet what needs to be done?
Obtain a follow up CT or MRI scan at 24 hr after IV alteplase
84
Tenectaplase Admin dose and infusion time?
Single IV bolus of 0.25mg/kg (max of 25mg) over 10 sec
85
Tenectaplase Admin Must be given where? Not compatible with? What must be administered before and after?
dedicated IV dextrose containing IVF NS 0.9% flush
86
Management of ICH occurring w/n 24 hrs of IV alteplase or tenecteplase Initial action? Labs to get? Imaging?
Stop infusion CBC, PT(INR), aPTT, fibrinogen, type and cross Emergency non-con head CT
87
Management of ICH occurring w/n 24 hrs of IV alteplase or tenecteplase Blood products? Medications? Consults? Anything else?
Cryoprecipitate 10 u infused over 10-30 min Tranexamic acid 1000mg (over 10 min) or Aminocaproic acid 4-5 gm over 1 hr Hematology and Neurosurgery Supportive therapy
88
Mechanical Thrombectomy Criteria Prestroke mRS score? Occlusion of? Age? NIHSS socre >/=? Alberta Stroke Program Early Computed Tomography Score (ASPECTS)? Treatment can be initiated via groin w/n?
0-1 ICA or MCA >/= 18 >/= 6 6 hrs
89
Mechanical Thrombectomy Selected pt further criteria Occlusion? Mismatch between? Age? No what on Head CT or MRI? No evidence of infarct involving? Presentation?
LVO severity of clinical deficit and infarct volume >/= 18 ICH more than 1/3 of the territory of the MCA Late
90
BP management for Ischemic Stroke patient Excessive BP lowering can have what effect?
worsen cerebral ischemia
91
Post stroke management admit where? neuro monitoring for? antiplatelet agents? consider dual antiplatelet therapy for? early what? continue/start what? (check what)
stroke unit hemorrhagic transformation or edema ASA 24-48 hrs post tPA/TNK; minor noncardioembolic (NIHSS
92
Post stroke management Glycemic management? treat BG of? mental health? Avoid what? Skin protection includes? Assessment of? Education? Evaluation of? Treatment of?
normoglycemia (140-180), treat BG <60mg/dL, Check HgbA1c Depression screening indwelling catheters turning, good skin hygeine, specialized mattress, wheelchair cushions functional assessment Smoking cessation; stroke education Cardiac evaluation Recurrent seizures
93
Meningitis Clinical Presentation Classic Triad?
Fever Nuchal rigidity AMS
94
Meningitis Clinical Presentation Symptoms outside of the classic triad include?
HA Photophobia Vomiting Lethargy Myalgia Seizures Skin manifestations Symptoms progress hours to days
95
Meningitis Clinical Presentation Clinical findings are often overlooked in?
infants obtunded patients elderly patients w/ heart failure elderly patients w/ pneumonia Immunocompromised individuals
96
Clinical Signs Brudzinski's Sign
Spontaneous flexion of the hips during attempted passive flexion of the neck
97
Clinical Signs Kerning's Sign
Inability or reluctance to allow full extension of the knee when the hip is flexed 90 degrees
98
Meningitis Diagnosis Hx will include
recent illness or sick exposure change in mental status focal deficit cranial nerve palsy
99
Meningitis Diagnosis Physical should include?
inspection of skin otoscopic exam inspect oral cavity/throat CSF otorrhea or rhinorrhea
100
Meningitis Diagnosis Imaging?
Head CT Exclude mass lesion or elevated ICP Prevent herniation d/t CSF removal
101
Algorithm With suspicion for bacterial meningitis, ask if the patient is/has
Immunocompromised hx of CNS disease new onset seizure papilledema altered consciousness focal neruo deficit delay in performatnce of diagnostic procedures
102
Algorithm If pt has any of the following what are the next steps? Immunocompromised hx of CNS disease new onset seizure papilledema altered consciousness focal neruo deficit delay in performatnce of diagnostic procedures
Blood cultures STAT Dexamethasone (b) + empirical antimicrobial therapy(c) Negative CT scan of the head Perform LP CSF findings c/w bacterial meningitis Perform Gram Stain
103
Algorithm If pt does not have any of the following, what are the next steps? Immunocompromised hx of CNS disease new onset seizure papilledema altered consciousness focal neruo deficit delay in performatnce of diagnostic procedures
BC and LP STAT Dexamethasone (b) + empirical antimicrobial therapy CSF findings c/w bacterial meningitis Perform CSF gram stain
104
Algorithm Positive CSF Gram Stain Yes? No?
Yes - Dexamethasone (b) + targeted antimicrobial therapy No - Dexamethasone (b) + empirical antimicrobial therapy
105
When to Order a Head CT for suspected meningitis
Immunocompromised CNS disease New onset seizure Papilledema Altered LOC Focal Neuro deficit
106
LP contraindications
Coagulopathy/thrombocytopenia Clinical signs of impending herniation Infection at LP site
107
CSF analysis should include?
Color/clarity cell count protein glucose gram stain culture PCR and viral studies CSF to plasma glucose is about 2/3
108
CSF Characteristics in Bacterial vs. Viral Meningitis Bacterial: Color Cell count Glucose Protein Opening pressure
cloudy 200-20,000 PMN <40 >50-100 Markedly high
109
Most common organisms and treatment Age 2-50 Common bacterial pathogens? Antimicrobial therapy
N. meningitidis, S pneumoniae Vancomycin plus a third gen cephalosporin
110
Most common organisms and treatment Age > 50 years Common bacterial pathogens? Antimicrobial therapy
S. Pneumoniae, N. meningitidis, L. monocyotogenes, aerobic gram-negative bacilli Vancomycin plus ampicillin plus a third gen cephalosporin
111
Most common organisms and treatment Head trauma (Basilar Skull Fx) Common bacterial pathogens? Antimicrobial therapy
S. pneumoniae, H. influenzae, group A Beta-hemolytic streptococci Vancomycin plus a third gen cephalosporin
112
Most common organisms and treatment Head Trauma (Penetrating Trauma) Common bacterial pathogens? Antimicrobial therapy
Staphylococcus aureus, coagulase-negative staphylococci (especially Stahpylococcus epidermidis), aerobic gram-negative bacilli (including Pseudomonas aeruginosa) Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
113
Most common organisms and treatment Postneurosurgery Common bacterial pathogens? Antimicrobial therapy
Aerobic gram-negative bacilli (including p. aeruginosa), S. aureus, coagulase-negative staphylococci (especially S. epidermidis) Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
114
Most common organisms and treatment CSF shunt Common bacterial pathogens? Antimicrobial therapy
Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionbacterium acnes Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
115
Antibiotics Third Gen Cephalosporine/dose/frequency?
Ceftriaxone 2g q12hr Cefotaxime 2g q4-6hr
116
Antibiotics Glycopeptide/dose/frequency?
Vancomycin 15-20mg/kg q8-12hrs
117
Antibiotics PCN/dose/frequency?
Ampicillin 2g q4hrs (in adults > 50y/o)
118
Antibiotics In immunocompromised patients add what? Instead of ceftriaxone or cefotaxime use what?
pseudomonal coverage cefepime 2g q8hr or meropenem 2g q8hr
119
Antibiotics Antiviral for HSV meningitis/dose/frequency?
Acyclovir 5-10 mg/kg TID
120
Steroids steroid/dose/frequency/duration
dexamethasone 0.15mg/kg IV q6 hr for 2-4 days
121
Steroids Reduces risk of poor neurological outcome in pt with? Must be given when? Believed to minimize?
S. pneumoniae early inflammatory cascade
122
What are the 6 herniation syndromes?
Uncal Central Subfalcine Transcalvarial Infratentorial Tonsillar
123
Indications for ICP monitoring include?
GCS <9 and w/ an abnormal CT Comatose pts w/ normal CT scan and two or more of the following 1. Age > 40 2. Posturing 3. SBP < 90 mmHg
124
Elevated ICP treatments include?
Resuscitation Positioning Sedation BP control Fever Control Hyperventilation Osmotic Therapy Surgical Intervention Hypothermia
125
Positioning should be focused on?
HOB Elevated Head in neutral position Avoid tight c-collars
126
Acute Hyperventilation causes?
Cerebral vasoconstriction Decreased CBF Decreased CBV Decreased ICP Effects are temporary Should only be used as a temporizing measure
127
Osmotic Therapy includes what? What are it's effects?
Mannitol and hypertonic saline Reverse clinical herniation, even w/ normal ICP Reduces ICP Effects are due to osmotically induced fluid shifts
128
Mannitol Therapy Rapidly deteriorating patients require what dose for bolus? What are the maintenance doses? Labs required?
1g/kg IV 0.25-1g/kg q6hrs BMP and serum osmolality q12hrs (baseline required prior to 1st mannitol dose)
129
Hypertonic Saline - 23.4% Effectiveness compared to Mannitol? What kind of access can it be administered through? How much is equiosmolar to 1g of Mannitol?
Equally as effective Requires Central Access 0.686 ml of 23.4%
130
Hypertonic Saline - 5% How to dose it? What kind of access can it be administered through?
3.2mL/kg Dose not require a central line for bolus dose
131
Hypertonic Saline - 3% How to dose it? What kind of access can it be administered through?
5.3mL/kg Dose not require a central line for bolus dose
132
Clinical Manifestations of DVT include
May be asymptomatic, nonspecific Leg Edema Tenderness Discoloration/erythema Difficulty walking
133
Diagnosing DVT DVT unlikely what test? Positive? Negative?
D-DImers Positive complete venous US Negative = no DVT
134
Diagnosing DVT DVT likely what test?
complete venous US
135
Treatment for Proximal DVT
At least 3 mo AC; DOAC in noncancer pts if no contraindications
136
Reassessment of Proximal DVT occurs when? may extend for how long? and why?
3mo May extend AC to yearly evaluation d/t risk/benefit, compliance, and patients preference
137
Treatment of Isolated Distal DVT with High risk recurrence?
3 mo AC
138
Treatment/Surveillance options of Isolated Distal DVT with High risk recurrence?
Treatment AC (full or lower dose) or surveillance 4-6 wk venous US surveillance
139
Prox DVT/PE, no cancer can be treated w/ what? For how long?
Dabigatran Rivaroxaban Apixaban Edoxaban 3mo
140
DVT provoked by surgery can be treated w/ what? For how long?
Dabigatran Rivaroxaban Apixaban Edoxaban 3mo
141
DVT with no surgery can be treated w/ what? For how long?
Dabigatran Rivaroxaban Apixaban Edoxaban 3mo
142
1st unprovoked DVT can be treated with? for how long?
Rivaroxaban - reduced dose Apixaban - reduced dose Extended treatment
143
Active CA & + VTE/PE can be treated with? GI? for how long?
Rivaroxaban Apixaban Edoxaban LMWH - may be preferred if luminal GI malignancy Extended treatment
144
If unprovoked DVT & DCing anticoag use what?
ASA
145
Drugs that are Factor Xa inhibitors?
Rivaroxaban Apixaban Edoxaban
146
Drugs that are Thrombin inhibitors?
Dabigatran
147
Drugs that are Factor Xa/Thrombin Inhibitors?
LMWH
148
Complications of DVT: Post-thrombotic syndrome Occurs in up to what % of patients with proximal DVT, within how long, despite anticoagulation? Results from? Duration? Symptoms?
50% ~ 1-2yrs valvular incompetence &/or residual obstruction Chronic & progressive Pain, edema, sometimes ulcerations
149
Complications of DVT: Venous Ulceration From what? Usually appears where? Prevent by use of?
post-thrombotic syndrome usually appear perimalleolar area compression stockings
150
What type of PE can be life-threatening in normal persons? What type of PE can be life-threatening in person with impaired physiologic reserves?
Massive emboli Submassive
151
In those with HD instability, mortality from PE increases by how much?
7 fold
152
Heart Failure d/t PE results from?
Vascular resistance leading to decreased RV output to increased RV pressure leading to ventricular wall stress increase leading to cardiac ischemia.
153
In early phase of Heart Failure d/t PE what compensatory mechanisms maintain flow? Which leads to?
Tachycardia & RV dilation RV output falls d/t wall stress & ischemia leading to decreased LV preload
154
RV dilation causes interventricular septal shift leading to?
decreased LV compliance leading to decreased LV output leading to hypotension
155
Increased pulmonary vascular resistance is d/t?
thrombus itself & neural reflexes, humoral factor release from platelets/endothelium, & hypoxia
156
S&S of PE
Non-specific/asymptomatic Dyspnea Tachypnea Pleuritic pain Pre-syncope/sycope Cough Orthopnea Wheezing Tachycardia/afib Crackles on lung exam (21%) Hypoxemia Hypocapnia
157
PE may lead to acute cor pulmonale which is shown by?
distended neck veins, prominent component of 2nd heard sound
158
PE may cause EKG changes such as?
signs of R heart strain (New R axis deviation or new RBBB) or ST
159
PE may cause CXR changes such as?
elevated R diaphragm Pleural based opacities, Westermark's sign (dilation of pulm. vessels & sharp cutoff)
160
EKG suspicious for PE will Show S1Q3T3 meaning?
S-waves in lead I Q-waves in lead III Inverted T-waves in lead III
161
Differential Dx of PE can include?
MI Pericarditis Heart Failure Pneumonia Asthma COPD PTX Rib Fx Musculoskeletal pain Intrathoracic CA Sepsis
162
Diagnosing PE Need what? May Utilize objective clinical assessments such as?
Clinical suspicion Wells, Geneva, revised Geneva
163
Diagnosing PE Why use CXR? may have nonspecific findings of?
utilized in general evaluation of pts w/ possible PE to exclude other causes of clinical presentation Elevated diaphragm, pleural based infiltrates, focal oligemia (Westermark's sign), hypovascularity
164
Echocardiography (TTE) may show?
greater RV diameter & evidence of RV strain & failure McConnell's sign: regional RV dysfunction w/ akinesia of mid free wall but normal motion May actually identify PE Echo does not r/o presence of PE
165
Suspected PE in patient w/o hemodynamic instability Assess clinical probability of PE Low or intermediate clinical probaility or PE unlikely what test(s)?
D-dimer: if negative no treatment D-dimer: If positive CTPA CTPA: no PE no treatment CTPA: PE confirmed treatment
166
Suspected PE in patient w/o hemodynamic instability Assess clinical probability of PE High clinical probability or PE likely what test(s)?
CTPA: no PE no treatment or investigate further CTPA: PE confirmed Treatment
167
Suspected PE in a patient w/ hemodynamic instability Perform what test? If signs of PE are present, what test(s)?
Bedside TTE looking for RV dysfunction CTPA if immediately available. If not initiate treatment of high-risk PE CTPA if positive initiate treatment of high-risk PE CTPA if negative investigate other causes of shock or instability
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Risk Stratification PE Lab indicators
troponin BNP Lactate hyponatremia
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Risk Stratification PE Clinical findings?
RV failure (TTE, CT) tachycardia hypotension respiratory insufficiency syncope
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Tx of RV failure Volume optimization Dose? Properties and use? Caveats?
Cautious volume loading use NS or LR
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Tx of RV failure Vasopressors and inotropes Norepi Dose? Properties and use? Caveats
0.2-1.0 nanogram/kg/min Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and restores coronary perfusion gradient Excessive vasoconstriction may worsen tissue perfusion
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Tx of RV failure Mechanical circulatory support Strategy? Properties and use? Caveats?
Veno-arterial ECMO/extracorporeal life support Rapid short-term support combined w/ oxygenator Complications w/ use over longer periods (>5-10 days), including bleeding and infections; no clinical benefit unless combined with surgical embolectomy; requires an experienced team
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Anticoagulation for high or intermediate probability includes?
LMWH, fondaparinux, UFH, NOACs
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If anticoagulation is initiated parenterally, what is recommended for most patients?
LMWH or fondaparinux over UFH
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Rescue thrombolytic therapy is recommended for patients with what?
hemodynamic deterioration or anticoagulation treatment
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Anticoagulation dosing Enoxaparin
1mg/kg q12 hr 1.5mg/kg once daily
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Thrombolytic dosing rtPA
100 mg over 2 hr 0.6 mg/kg over 15 min (max dose of 50 mg)
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Medication tips LMWH dosing in obesity VKA monitoring after adjustment VKA monitoring stable dose No anti Xa levels in which patients No monitoring of DOACs when?
use actual body weight
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Medication tips INR w/ VKA 4.5-10 & no bleeding Elevated INR + life-threatening bleeding Bleeding on Xa inhibitor Bleeding on dabigatran Bleeding on LMWH or UFH Resume anticoagulation w/n how long of bleed?
no intervention PCC + vit K +/- PCC or Xa (recombinant), inactivated-zhzo idarucizumab protamine 90 days
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VS findings in Asthma
RR often 25-40 breaths/min tachycardia pulsus paradoxus SpO2 near 90% on RA
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What is Pulsus Paradoxus? What value suggests moderate severity of exacerbation?
Exaggerated inspiratory decrease in systolic BP 15mmHg
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What inspection finding may suggest respiratory muscle fatigue in patients w/ COPD?
paradoxical abdominal wall motion w/ inspiration
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Thoracic Exam findings in COPD Auscultation
Rhonchi w/ inspiration Wheezes ww/ forced exhalation decreased breath sounds in those w/ emphysema asymmetry raises possibility of pneumothorax
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Diagnostic requirements for asthma
Positive post-bronchodilator response defined as 12% and at least 200 ml increase in FEV1
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ABG findings in patients w/ asthma
PAO2 at sea level is 55-70 mmHg usually PaCO2 usually between 25-35 mmHg
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What is concerning when a patient w/ a hx of several days of moderate to severe airflow obstruction has a normal PaCO2?
It may indicate the mechanical load on the respiratory system is greater than can be sustained by the ventilatory muscles and that respiratory failure is imminent.
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Diagnostic criteria for COPD
Post-Bronchodilator ratio of FEV1/FVC < 0.7
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Patients w/ suspected COPD exacerbation may show evidence of what on CXR?
infiltrate suggestive of pneumonia
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What type of imaging is more sensitive in demonstrating parenchymal loss c/w emphysema, bullae, and pulmonary vascular changes suggestive of pulmonary HTN?
Chest CT
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ABG findings c/w COPD
Chronic hypercarbia typically accompanied by a respiratory acidosis w/ a compensatory elevation in the serum pH d/t elevated serum bicarbonate level that incompletely corrects the acidemia
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Asthma Pharmacologic Management (non-exacerbation) Track 1 Symptoms per step Step 1 Step 2 Step 3 Step 4 Step 5
1. infrequent asthma symptoms (1-2 d/wk w/ normal or mildly reduced lung function) 2. asthma symptoms < 3-5 d/wk w/ normal or mildly reduced lung function 3. asthma symptoms most days (4-5 d/wk or more); waking d/t asthma once a week or more, or low lung funciton 4. Daily asthma symptoms, waking at night w/ asthma once a wk or more w/ low lung volumes 5. Initial asthma presentation is during an acute exacerbation
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Pharmacologic Management (non-exacerbation) Track 1 Medications per step Step 1 Step 2 Step 3 Step 4 Step 5
1-2: As needed-only low dose ICS-formoterol (budesonide-formoterol) 3. Low dose maintenance ICS-formoterol w/ reliever ICS-formoterol 4. Medium dose maintenance ICS-formoterol 5. Add on LAMA (like glycopyrolate) Refer for assessment of phenotype. consider high dose maintenance ICS-formoterol. +/- anti-IgE, anti-IL5/5R, anti-IL4Ra, anti-TSLR
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Group A requirements and med management for COPD
mMRC 0-1, CAT < 10 0-1 moderate exacerbations (not leading to hospital admission) Should be prescribed a bronchodilator (albuterol - SABA) (salmeterol - LABA)
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Group B requirements and med management for COPD
mMRC >/= 2, CAT >/= 10, 0-1 moderate exacerbations (not leading to hospital admission) / year LABA + LAMA (Vilanterol/Umeclidinium)
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Group E requirements and med management for COPD
>/= 2 exacerbations or >/= 1 leading to hospitalization should be prescribed LABA + LAMA (Olodaterol/tiotropium)
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What to prescribe Group E if eos >/= 300
LABA + LAMA + ICS (Fluticasone/umeclidinium/vilanterol)
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Mild or Moderate Exacerbation presentation for Asthma
Talks in phrases Prefers sitting to lying not agitated RR increased No accessory muscle use HR 100-120 SpO2 on RA 90-95% PEF > 50% predicted or best
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Severe Exacerbation presentation for Asthma
Talks in words sits hunched forward agitated RR > 30/min Accessory muscle use HR > 120bpm SpO2 on RA < 90% PEF
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Exacerbation presentation requirements for COPD
Worsening dyspnea, and/or cough and sputum in < 14 days Often associated w/ increased local and systemic inflammation caused by airway infection, pollution, or other insults to lungs
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Exacerbation presentation w/ no respiratory failure
RR
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Exacerbation presentation w/ non-life-threatening acute respiratory failure
RR >24 breaths/min Using Accessory muscles no change in mental status hypoxemia improved w/ supplemental O2 via venti mask > 35% FiO2 Hypercarbia PaCO2 increased compared w/ baseline or elevated between 50-60 mmHg
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Exacerbation presentation w/ life-threatening acute respiratory failure
RR > 24 breaths/min using accessory muscles acute mental status changes hypoxemia not improved w/ supplemental O2 via venti mask or requiring > 40% FiO2 Hypercarbia PaCO2 increased compared w/ baseline or elevated > 60 mmHg or the presence of acidosis
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Exacerbation diagnosis for asthma
decrease in airflow quantified by PEF or FEV1 compared w/ previous lung function values
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Mild COPD Exacerbation diagnosis requirements
Dyspnea Visual Analog Scale < 5 RR< 24 breaths/min HR < 95bpm Resting Spo2 >/= 92% on RA CRP < 10 mg/L
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Moderate COPD Exacerbation diagnosis requirements
Dyspnea Visual Analog Scale >/= 5 RR >/= 24 breaths/min HR >/= 95 bpm Resting SpO2 < 92% on RA and/or change >3% of previous CRP >/= 10mg/L ABG may show hypoxemia (PaO2 45 mmHg) but no acidosis
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Severe COPD Exacerbation diagnosis requirements
Dyspnea Visual Analog Scale >/= 5 RR >/= 24 breaths/min HR >/= 95 bpm Resting SpO2 < 92% on RA and/or change >3% of previous CRP >/= 10mg/L ABG shows new onset/worsening hypercapnia and acidosis (PaCO2 > 45 mmHg and pH < 7.35)
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Exacerbation management for Asthma
Assess exacerbation severity from the degree of dyspnea, RR, HR, SpO2 and lung function while starting SABA and O2 therapy Infection control procedures should be followed
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When and where to transfer a patient w/ asthma exacerbation?
Immediate transfer to acute care facility or ICU for signs of severe exacerbation or the patient is drowsy, confused or has silent chest.
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What to prescribe asthma exacerbatio patients during transfer?
SABA (albuterol) and Ipratropium bromide controlled O2 systemic corticosteroids (prednisone 50mg PO 5-7 day course)
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What to do after 1 hr from interventions to treat asthma severe asthma exacerbations?
Reassess response of symptoms O2 saturation and lung function
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Only give ipratropium bromide for what? What to consider for patients w/ severe exacerbation not responding to initial treatment?
Severe exacerbations IV Mag Sulfate
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Exacerbation management for Severe but not life-threatening COPD Exacerbation?
Assess severity of symptoms, blood gases, chest radiograph Increase doses and/or frequency of SABA Combine SABA and anticholinergics (Salbutamol/ipratropium) Consider use of LABA (Salmeterol) when patient becomes stable Use spacers or air-driven nebulizers when appropriate Consider systemic corticosteroids (PO prednisone 40 mg for 5 days Consider ABx when signs of infection are present
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Classes of abx to use during COPD exacerbation w/ signs of infection?
aminopenicillin w/ clauvanic acid (augmentin, Unasyn) macrolide (azithromycin, Clarithromycin, erythromycin, fidoxomicin, telithromycin) tetracycline quinolone (Ciprofloxacin, norfloxacin, ofloxacin, levofloxacin, moxifloxacin)
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Considerations during management of COPD Exacerbations at all times?
monitor IVF balance consider SQH or LMWH for DVT prophylaxis ID and treat associated conditions (e.g. heart failure, arrhythmias, PE etc.)
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Indications for transfer to Respiratory or Medical ICU for COPD exacerbation
Severe dyspnea that responds inadequately to initial emergency therapy. Changes in mental status Persistent or worsening hypoxemia (PaO2 < 40mmHg) and/or severe/worsening respiratory acidosis (pH < 7.25) despite supplemental O2 and NIV Need for invasive mechanical ventilation Hemodynamic instability - need for vasopressors
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Indications for NIV include at least one of the following
1.Respiratory Acidosis (PaCO2 >/= 45 mmHg and arterial pH
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Indications for Invasive MV
Unable to tolerate NIV or NIV failure S/p respiratory or cardiac arrest Diminished consciousness, psychomotor agitation inadequately controlled by sedation Massive aspiration or persistent vomiting Persistent inability to remove respiratory secretions Severe hemodynamic instability w/o response to fluids and vasoactive drugs. Severe ventricular or supraventricular arrhythmias Life-threatening hypoxemia in patients unable to tolerate NIV
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Evaluation of Acute Hyperkalemia includes?
ECG re-send unclotted blood sample for electrolytes, glucose, BUN, Cr, CBC assess urine for heme to exclude rhabdo/hemolysis review med list and diet
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Management of acute hyperkalemia most exhibit ECG changes with what K level?
>6.7 mEq/L
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Management of acute hyperkalemia tx should be immediate for what K level?
> 6.5 mEq/L
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Management of acute hyperkalemia tx should be immediate regardless of levels when?
ECG changes
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Management of acute hyperkalemia Membrane stabilization includes?
CaGluconate (1g IV over 10 min) onset is immediate
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Management of acute hyperkalemia Redistribution of K into cells includes?
insulin (10u IVP + 1 amp D50 IV) albuterol (20mg/4mL) Bicarb 150 mEq/L
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Management of acute hyperkalemia insulin admin lowers K by how much? Onset is how long? when to not give D50?
approx. 1 mEq/L 20 min if patient is already hyperglycemic
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Management of acute hyperkalemia albuterol lowers K by how much? drawback of albuterol?
approx 1 mEq/L some may be resistant to albuterol; use as adjunct
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Management of acute hyperkalemia Elimination of K includes?
diuretics (lasix 40-80 mg IV) kayexalate - 15-30 g/ 15-30ml or lokelma hemodialysis
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Management of acute hyperkalemia onset for... diuretics sodium bicarb sodium polystyrene sulfonate (kayexalate)
15 min 1 hr > 2 hr
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Management of acute hyperkalemia How does sodium polystyrene sulfonate work? what are the effects? what adverse reaction is potential?
exchanges Na for K in colon variable intestinal necrosis
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ARDS Patho Overall occurrence is?
Diffuse alveolar damage & lung capillary endothelial injury
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ARDS Patho (early phase) is? includes: Increased? Influx of?
Exudative permeability of alveolar-capillary barrier protein-rich fluid into alveoli
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ARDS Patho Exudative (early phase) includes injury to?
alveolar epithelial cells promoting pulmonary edema formation, decreased clearance from alveoli, & may decrease surfactant production causing decreased compliance and alveolar collapse
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ARDS Patho Exudative (early phase) includes what sells are sequestered/activated? Leads to an imbalance between?
neutrophils, cytokines & platelets pro-inflammatory & anti-inflammatory cytokines after inciting event
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ARDS Patho Later phase is?
fibroproliferative
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Diagnosis of ARDS is?
Clinical diagnosis Acute onset (w/n 7 days of defined event) BL opacities on CXR or CT No need to exclude HF
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ARDS severity Mild P/F ratio is? Mortality? Moderate P/F ratio is? Mortality? Severe P/F ratio is? Mortality?
200-300; 27% 100-200; 32% <100; 45%
236
ARDS Management Primary goal?
treat underlying cause
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ARDS Management Lung Protective Strategies include?
low TV (4-8ml/kg PBW) Peep (>5 cm H2O) for O2 say 85-90% Lower FiO2 to minimize O2 toxicity (DAD, hyaline membrane formation, fibrosis)
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ARDS Management Lung Protective Strategies allow for?
permissive hypercapnia Caution for increased end-inspiratory volume (volutrauma), decreased preload, increased RV afterload
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ARDS Management Proning provides what? is done for how long/day? Is used in what classification of ARDS
mortality benefit > 12 hrs/day mod - severe ARDS
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ARDS Management ECMO is considered for?
P/F ratio < 80 mmHg High plateau pressures despite other strategies
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ARDS Management IVF? how do we feed them? DVT propylaxis? yes no?
conservative fluids enteral nutrition yes
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Early Management of ARDS Confirmed ARDS
VT about 6ml/kg of PBW Plateau pressue < 30 cmH2O PEEP > 5 cmH2O Check for hypercapnia
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Early Management of ARDS P/F ratio < 200
High level of PEEP if improves oxygenation
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Early Management of ARDS P/F ratio < 150
NMB Proning
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Early Management of ARDS P/F ratio < 80
discuss VV-ECMO
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ARDS Prognosis Mortality rate is about? & increases w/? Failure of pulmonary function to improve in 1st week is? Hospital course is? Development of what? The patient will lose? Muscle weakness/functional impairment lasts for how long? Disease severity & duration of MV are predictors of? HRQOL significantly < normal @?
~30-40%; age poor prognostic factor prolonged HAIs Weight months persistent abnormalities in pulm. function; may have significant impairment for years 6mo