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test 2 Flashcards

1
Q

PaO2

A

partial pressure of o2

Normal level is 80-100

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2
Q

PaCO2

A

partial pressure of CO 2

normal level is 35-45

lower is basic, higher is acidic

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3
Q

hypoxemic failure

A

problem with oxygenation. o2 is low

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4
Q

hypercapnic failure

A

problem with ventilation, leads to acidosis. CO2 will be high, pH will be low

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5
Q

pulmonary causes of hypoxemia

A

hypoventilation
collapsed alveolus
blood clot
interstitial fluid

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6
Q

hypoventilation

A

occurs when alveoli don’t receive O2, and cannot participate in gas exchange. Air movement lacks but bloodflow is fine

clinical presentations- OD/sedation, shallow respirations, decreased rest rate, pain on inspiration

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7
Q

intrapulmonary shunting

A

alveoli not open, gas exchange can’t occur

maybe from pneumonia, atelactis

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8
Q

VQ mismatch

A

problem with o2 or perfusion. if O2 can’t get in, CO2 can’t get out

may be from pulm embolism

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9
Q

normal VQ ratio

A

0.8
rate at which O2 move in and out of the alveoli compared to rate of perfusion of blood through pulmonary capillaries

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10
Q

diffusion defect

A

diffusion of gas is slow due to increased space between alveolar membrane and cap beds

caused by COPD, and interstitial fluid

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11
Q

how does cardiac output and hgb affect tissue oxygenation

A

decreased cardio output leads to decreased hgb causing lower tissue oxygenation

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12
Q

what is resp failure

A

lack of O2 or increase In CO2

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13
Q

Neuro assessment findings in resp failure

A

first sign- confusion, restlessness, agitation

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14
Q

Resp assessment findings in resp failure

A

tachypnea at first - trying to blow off CO2 and bring in O2.
Later on we will see decreased shallow respirations,

auscultation will show coarse, wheezes
edema in alveoli will cause increased peak inspiratory pressure

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15
Q

Cardio assessment findings in resp failure

A

tachycardia initially as its trying to increase cardiac output.
Later we will see decreased BP, HR, chest pain, and dysthymia’s

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16
Q

goals for ARF

A
  1. maintain patent airway (bronchodilators, suction, sitting up)
  2. optimize o2 delivery (limit secretions, right o2 mask)
  3. minimize o2 demand (rest periods, meds)
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17
Q

acute resp failure patho

A

lung injury characterized by inflammation, edema, and loss of compliance. Damage to alv-cap membrane

2 phases: acute exudation and fibroproliferation

NONCARDIOGENIC pulmonary edema

caused by flu, pneumonia, aspiration of gastric contents chest trauma

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18
Q

criteria for ARDS

A

acute onset - within a week of insult
bilateral pulmonary opacities
altered PaO2/FiO2 ratio- O2 continuously goes down no matter how much o2 we give them

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19
Q

ARDS acute exudation

A

systemic inflammation. alveoli fill with exudate, protein and blood. Pulmonary Htn occurs

Can lead to platelet aggregation and thrombus formation
Ultimately leads to VQ mismatch

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20
Q

ARDS Fibroproliferation

A

fibrin matrix begins forming after 48 hours, fibrosis destroys alveoli and bronchioles

leads to decreased function and inflammation

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21
Q

ARDS interventions/treatments

A

we want a low tidal volume and low end inspiratory pressure because pressure is already high.

we want the FiO2 at about 60% or lower (<.60)

PEEP of 5 or less to recruit more alveoli to participate in oxygenation.

sedation- so they don’t exert energy

prone positioning

be conservative with fluids

nutrition and psychosocial support

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22
Q

ARF in COPD

A

we need to correct hypoxemia with supplemental o2. Ventilator is last resort for these patients. Try NPPV first (a mask)

COPD is chronic obstruction of airways. poor gas exchange and decreased ability to clear airway

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23
Q

ARF in asthma

A

Chronic inflammatory disorder of airways – causes bronchoconstriction, edema, increased mucous production, prolonged exhalation

Status asthmaticus – fails to respond to bronchodilators

try Bronchodilators/anticholinergics, and Steroids. Intubation may be needed if they don’t work.

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24
Q

Ventilator associated pneumonia (VAP) bundle- prevention

A

HOB 30-45
Sedation vacation to assess readiness to wean
DVT prophylaxis
PUD prophylaxis
Daily oral care

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25
ARF with PE
Etiology – venous stasis, altered coagulability, damage to vessel walls Pathophysiology – clot reaches pulmonary vasculatoure – leads to VQ mismatch because it stops perfusion = no gas exchange Diagnostics – D dimer (positive means possible PE, negative means no PE), VQ scan, CT
26
Normal pH
7.35 - 7.45 lower is acidic, higher is basic
27
HCO3
bicarbonate normal level is 22-26 lower is acidic, higher is basic
28
blood pH level that is deadly
acidic is 6.90 or below basic is 7.80 and above
29
causes of resp acidosis- retention of co2
hypoventilation CNS depression restrictive lung issue COPD trauma
30
causes of resp alkalosis- loss of co2
hyperventilation anxiety pain fever
31
causes of metabolic acidosis- increased blood acid
DKA renal failure Lactic acidosis OD (salicylates)
32
causes of metabolic acidosis- too much acid loss or too much base
ingestion of antacids admin of HCO3 blood transfusion vomiting NG suction Diuretics
33
Tidal Volume
volume of normal breath
34
inspiratory reserve volume (IRV)
Max amount of gas that can be inspired at the end of a normal breath - deep breath - over and above the tidal volume
35
expiratory volume reserve (ERV)
Max amount of gas that can be forcefully expired at the end of a normal breath - extra pushed out
36
residual volume (RV)
Amount of air remaining in the lungs after max expiration - the air in luns at all times
37
inspiratory capacity (IC)
max volume of gas that can be inspired at normal resting expiration. this distends the lungs to the max amount
38
functional residual capacity (FRC)
volume of gas remaining in the lungs at normal resting expiration
39
vital capacity (VC)
Max volume of gas that can be forcefully expired after max inspiration
40
total lung capacity (TLC)
volume of gas in the lungs at the end of max inspiration
41
when to treat PaO2
if the value is less than 60
42
hypoxemia vs hypoxia
hypoxemia- decreased o2 of arterial blood hypoxia- decreased o2 at tissue level
43
oxyhemoglobin dissociation left curve
Hgb clings to oxygen. o2 sat increases. we want this if pt is hyperthermic
44
oxyhemoglobin dissociation right curve
releases o2 from hgb to tissues. o2 sat decreases. we want this for burn patients so they can heal their tissues
45
how does oxyhemoglobin dissociation occur
when the PaO2 falls below 60 mmhg, changes reflect in the oxygen saturation
46
intubation position
sniffing position- high shoulders, head back
47
airway management position
high fowlers
48
devices for airway management
oral airway nasopharyngeal airway endotracheal intubation
49
endotracheal suction uses
maintain a airway remove secretions prevent aspirations (cuff pressure 20-30) provide mechanical ventilation
50
steps to verify placement of endotracheal intubation
1. Auscultate the lungs- bilateral equal breath sounds 2. Auscultate stomach 3. ETCOx detector 4. Chest x-ray record cm ay lip line secure tube once verified
51
what to do if pt desats with endotracheal intubation
**Immediately notify RT to obtain a vent **Bedside suction **Vitals signs **Hyperoxygenating client with 100% oxygen **Ensuring bedside access to a rigid tonsil tip suction cathether
52
how to tell if ET tube is in the right mainstream bronchus
we would only hear right breath sounds this placement is wrong, it should be in the middle 2-3 inches above carina
53
what to do if ET tube is in the esophagus
take it out and redo it
54
tracheostomy indications
long term mechanical ventilation frequent suctioning protecting the airway bypass an airway obstruction reduce work of breathing
55
cuffed vs uncuffed trach
Mechanical ventilation will always be cuffed. Uncuffed is if you are trying to wean the patient, or if they are speaking
56
when to suction ET tube
visible secretions coughing rhonchi high PIP ventilator alarm don't use saline
57
indications for ventilation
hypoxemia hypercapnia progressive deterioration
58
positive pressure ventilation
movement of gases into lungs through positive pressure. we are shoving air into the lungs
59
positive end expiratory pressure (PEEP)
keeps the alveoli open, reducing need for FiO2. Can cause reduced cardiac output, hypotension and impede venous return if too high
60
vent settings
FiO2 (0.21-1.0) tidal volume 6-8 mL/kg PIP less than 40 cm resp rate 14-20 (look at ABG- pH, CO2)
61
why may peep be above 40
Vent circuit disconnection, suction, bronchospasm, biting tube, kink
61
what should the exhaled tidal volume not be more than
50 mL
62
2 types volume ventilation
volume assist/control (V-A/C) synchronized intermittent mandatory ventilation (SIMV)
63
volume assist/control (V-A/C)
Assist control always gets set tidal volume. Spontaneous breathing may be there too but it doesn’t have to be. Risk for hyperventilation is present with assist- resp alkalosis Ventilator performs most of work of breathing still even if person has spontaneous breaths
64
synchronized intermittent mandatory ventilation (SIMV)
vent delivers a mandatory set rate, but spontaneous breaths may occur in between. the ventilator attempt to synchronize the spontaneous breaths with the preset rate. this is used to wean patients from mechanical ventilation because patient contributes more to work of breathing.
65
pressure ventilation types
CPAP, Pressure support (PSV), Pressure A/C, inverse ratio ventilation, airway pressure release (APRV)
66
pressure A/C
Vent pressure will always be there, spontaneous breaths may or may not be there. You will always get the set pressure no matter what because vent kicks in
67
Pressure support
spontaneous effort is assisted by preset of positive pressure. This is the most common mode when pt is going to get extubated to wean them. You must be able to spontaneously breathe with this, but if you don’t the vent will alarm and you will be switched to a different setting
68
CPAP
continuous positive airway pressure throughout resp cycle to pt who is spontaneously breathing can be used to prevent re-intubation The patient performs all the WOB. CPAP provides pressure at end-expiration, which prevents alveolar collapse and improves the functional residual capacity and oxygenation
69
noninvasive positive pressure ventilation (NPPV)
he delivery of mechanical ventilation without an ETT or tracheostomy tube Delivers via face mask, nasal pillow/mask ***Pt must be able to spontaneously breathe for this People with this can eat and not be in discomfort this is only intended for acute exacerbations
70
types of vent alarms
high peek pressure low pressure; low PEEP/CPAP low exhaled tidal volume low minute ventilation high exhaled tidal volume high minute ventilation apnea
71
barotrauma
trauma with pressure could cause pneumothorax monitor for subcutaneous crepitus, high PAP, tracheal shift, hypoxemia
72
volutrauma
trauma from volume- overexpanding alveoli damages the lung similar to early ARDS
73
vent bundle
HOB at 30 degrees awaken daily and assess readiness to wean stress ulcer prophylaxis DVT prophylaxis oral care
74
how to know when a vent pt is ready to wean
Stable, alert and oriented, not resp distressed. IF NEGATIVE SYMPTOMS OCCUR WHEN WEANING STOP THE PROCESS AND PUT BACK ON VENT
75
extubation
removing the ET tube
76
functions of the kidney
regulation of: Fluid volume electrolyte balance acid base balance BP erythropoiesis excretion of nitrogenous waste metabolism of vitamin D
77
What is considered oliguria
urine output less than 0.5 ml/kg/hr
78
what is azotemia
accumulation of nitrogenous wastes (bun and creatine)
79
pre renal AKI
low bp, hypovolemia, dehydration like symptoms ex that may cause- hemorrhage, sepsis, heart failure, DI, burns, diuretics, etc
80
meds for prerenal AKI
norepinephrine- helps BP go up
81
intrarenal AKI
acute tubular necrosis- lack of blood flow and o2 to the kidneys examples that may cause this- ischemia, DM, htn, glomerulonephritis, thrombosis, etc
82
post renal AKI
obstruction of urine flow ex caused by- BPH, clots, renal stones, meds, foley Cath obstruction, etc
83
initiation phase of AKI
phase spans several hours to 2 days, during which time the normal renal processes begin to deteriorate, but kidney cell death has not yet occurred. The patient is unable to compensate for the diminished renal function and exhibits clinical signs and symptoms of AKI. Kidney injury is potentially reversible during the initiation phase.
84
maintenance phase AKI
phase last 1-2 weeks, but could last months renal damage occurs in this stage complications can be uremia, hyperkalemia and infection
85
recovery phase AKI
recovery may take as long as 4-6 months this is when renal tissue recovers and repairs itself
86
normal creatine
around 1.0
87
normal BUN
Around 20
88
AKI diagnostics
KUB xray renal ultrasound MRI IV pyelogram computed tomography renal angiography renal scan renal biopsy
89
AKI interventions
I/o daily weights IV fluids prevent infection monitor electrolytes
90
pre renal AKI med management
volume replacement maintain perfusion early recognition=better outcome
91
intrarenal AKI med management
drug therapy diet restriction manage f&e CRRT/dialysis
92
post renal AKI med management
alleviate obstruction
93
what does decreased GFR lead to
hyperkalemia
94
treating elevated potassium
meds to lower- kayaxelate (sodium poly sulfonate) shift potassium from outside cell to inside- insulin. must also give dextrose calcium given to help protect the cardiac cell membrane - it doesn't lower k
95
potassium 6-7 EKG change
peaked T wave
96
potassium 7-8 EKG change
peaked T wave flattened p wave prolonged PR interval depressed ST segment
97
potassium 8-9 EKG
atrial standstill prolonged QRS duration further peaking T wave
98
potassium above 9 ekg changes
wave pattern. possible vtach
99
why does hyponatremia happen in AKI
nephrons are damaged, they can't conserve sodium
100
types of dialysis
hemodialysis continuous renal replacement therapy- CRRT Peritoneal
101
Interventions for patients with dialysis graft/shunt
monitor labs weight pt daily don't admin water soluble meds avoid antihyp before hand assess bruit and thrill
102
CRRT
like hemodialysis but slower these pts need to be on bed rest
103
4 types of CRRT
Slow continuous ultrafiltration (SCUF)- Used to remove plasma / water in case of fluid overload. Continuous venovenous hemofiltration (CVVH)-Removes fluids and solutes across a hemofilter. Continuous venonvenous hemodialysis (CVVHD)- Similar to CVVH except that instead of replacement fluid, dialysate is added around then hemofilter and causes increased removal of solutes and fluid. Continuous venovenous hemodiafiltration (CVVHDF)- Maximum removal of fluid and uremic wastes ASSESS HEMOFILTER every 2-4 hours for clotting
104
normal output ml/kg/hr
0.5-1 ml/kg/hr
105
where does acid base regulation occur
proximal and distal tubules in nephron
106
what influences glomerular filt rate
mean arterial pressure
107
if potassium is high and EKG shows abnormal rhythm what is the priority first step
calcium chloride- it will protect heart after this give kayexelate to lower k
108
Hematopoiesis
formation and maturation of RBC
109
primary site of hematopoietic production
bone marrow
110
secondary hematopoietic organs
spleen, liver, thymus, lymphatic system, lymphoid tissue
111
erythrocytes
RBC- function to deliver hemoglobin throughout the body
112
platelets
first responders for clotting
113
granulocytes
neutrophils, basophils, and eosinophils, all of which function in phagocytosis
114
agranulocytes
monocytes and lymphocytes
115
function of neutrophils
bacterial infection
116
function of eosinophils
parasites skin, lung, GI tract
117
basophils function
inflammatory/allergic response
118
monocyte function
mature into macrophage then do phagocytosis- attack foreign bodies and remove dead cells
119
lymphocyte function
humoral immunity- B lymphocytes (antibody prod) cellular immunity- T lymphocytes (long term immunity)
120
what mechanisms trigger clotting
tissue injury vessel injury foreign body in the bloodstream
121
symptoms of all anemia types
fatigue, weakness, short of breath
122
aplastic anemia s/s
bruising nosebleeds petechiae
123
hemolytic anemia s/s
jaundice, abd pain, liver/spleen enlargement
124
sickle cell anemia s/s
joint swelling, pain
125
How does HIV lead to AIDS
by depleting helper T cells, CD4 cells, and macrophages
126
AIDS CD4 count
less than 200/microliter and presence of indicator of condition
127
HIV treatment
antiretroviral therapy
128
thrombocytopenia
low platelets under 150k risk for bleeding treated by platelets (depending on type)
129
heparin induced thrombocytopenia (HIT)
Adverse reaction to heparin it causes hypercoagulability and thrombus treatment- stop heparin, admin drugs that inhibit thrombin (bivalirudin)
130
Disseminated intravascular coagulation (DIC)
Increased microvascular clotting, depletion of clotting factors and subsequent bleeding most common cause is sepsis. after thrombotic phase, clots begin to lyse and excessive bleeding occurs
131
DIC diagnosis
elevated fibrin degradation products increased d-dimer decreased antithrombin III
132
treatment of DIC
treat underlying cause platelet transfusion FFP transfusion RBC for hemorrhage heparin cryoprecipitate

critical care (4 decks)

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