test 2 Flashcards
PaO2
partial pressure of o2
Normal level is 80-100
PaCO2
partial pressure of CO 2
normal level is 35-45
lower is basic, higher is acidic
hypoxemic failure
problem with oxygenation. o2 is low
hypercapnic failure
problem with ventilation, leads to acidosis. CO2 will be high, pH will be low
pulmonary causes of hypoxemia
hypoventilation
collapsed alveolus
blood clot
interstitial fluid
hypoventilation
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
intrapulmonary shunting
alveoli not open, gas exchange can’t occur
maybe from pneumonia, atelactis
VQ mismatch
problem with o2 or perfusion. if O2 can’t get in, CO2 can’t get out
may be from pulm embolism
normal VQ ratio
0.8
rate at which O2 move in and out of the alveoli compared to rate of perfusion of blood through pulmonary capillaries
diffusion defect
diffusion of gas is slow due to increased space between alveolar membrane and cap beds
caused by COPD, and interstitial fluid
how does cardiac output and hgb affect tissue oxygenation
decreased cardio output leads to decreased hgb causing lower tissue oxygenation
what is resp failure
lack of O2 or increase In CO2
Neuro assessment findings in resp failure
first sign- confusion, restlessness, agitation
Resp assessment findings in resp failure
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
Cardio assessment findings in resp failure
tachycardia initially as its trying to increase cardiac output.
Later we will see decreased BP, HR, chest pain, and dysthymia’s
goals for ARF
- maintain patent airway (bronchodilators, suction, sitting up)
- optimize o2 delivery (limit secretions, right o2 mask)
- minimize o2 demand (rest periods, meds)
acute resp failure patho
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
criteria for ARDS
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
ARDS acute exudation
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
ARDS Fibroproliferation
fibrin matrix begins forming after 48 hours, fibrosis destroys alveoli and bronchioles
leads to decreased function and inflammation
ARDS interventions/treatments
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
ARF in COPD
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
ARF in asthma
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.
Ventilator associated pneumonia (VAP) bundle- prevention
HOB 30-45
Sedation vacation to assess readiness to wean
DVT prophylaxis
PUD prophylaxis
Daily oral care
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
Normal pH
7.35 - 7.45
lower is acidic, higher is basic
HCO3
bicarbonate
normal level is 22-26
lower is acidic, higher is basic
blood pH level that is deadly
acidic is 6.90 or below
basic is 7.80 and above
causes of resp acidosis- retention of co2
hypoventilation
CNS depression
restrictive lung issue
COPD
trauma
causes of resp alkalosis- loss of co2
hyperventilation
anxiety
pain
fever
causes of metabolic acidosis- increased blood acid
DKA
renal failure
Lactic acidosis
OD (salicylates)
causes of metabolic acidosis- too much acid loss or too much base
ingestion of antacids
admin of HCO3
blood transfusion
vomiting
NG suction
Diuretics
Tidal Volume
volume of normal breath
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
expiratory volume reserve (ERV)
Max amount of gas that can be forcefully expired at the end of a normal breath - extra pushed out
residual volume (RV)
Amount of air remaining in the lungs after max expiration - the air in luns at all times
inspiratory capacity (IC)
max volume of gas that can be inspired at normal resting expiration. this distends the lungs to the max amount
functional residual capacity (FRC)
volume of gas remaining in the lungs at normal resting expiration
vital capacity (VC)
Max volume of gas that can be forcefully expired after max inspiration
total lung capacity (TLC)
volume of gas in the lungs at the end of max inspiration
when to treat PaO2
if the value is less than 60
hypoxemia vs hypoxia
hypoxemia- decreased o2 of arterial blood
hypoxia- decreased o2 at tissue level
oxyhemoglobin dissociation left curve
Hgb clings to oxygen. o2 sat increases. we want this if pt is hyperthermic
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
how does oxyhemoglobin dissociation occur
when the PaO2 falls below 60 mmhg, changes reflect in the oxygen saturation
intubation position
sniffing position- high shoulders, head back
airway management position
high fowlers
devices for airway management
oral airway
nasopharyngeal airway
endotracheal intubation
endotracheal suction uses
maintain a airway
remove secretions
prevent aspirations (cuff pressure 20-30)
provide mechanical ventilation
steps to verify placement of endotracheal intubation
- Auscultate the lungs- bilateral equal breath sounds
- Auscultate stomach
- ETCOx detector
- Chest x-ray
record cm ay lip line
secure tube once verified
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
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
what to do if ET tube is in the esophagus
take it out and redo it
tracheostomy indications
long term mechanical ventilation
frequent suctioning
protecting the airway
bypass an airway obstruction
reduce work of breathing
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
when to suction ET tube
visible secretions
coughing
rhonchi
high PIP
ventilator alarm
don’t use saline
indications for ventilation
hypoxemia
hypercapnia
progressive deterioration
positive pressure ventilation
movement of gases into lungs through positive pressure.
we are shoving air into the lungs
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
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)
why may peep be above 40
Vent circuit disconnection, suction, bronchospasm, biting tube, kink
what should the exhaled tidal volume not be more than
50 mL
2 types volume ventilation
volume assist/control (V-A/C)
synchronized intermittent mandatory ventilation (SIMV)
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
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.
pressure ventilation types
CPAP, Pressure support (PSV), Pressure A/C, inverse ratio ventilation, airway pressure release (APRV)
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
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
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
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
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
barotrauma
trauma with pressure
could cause pneumothorax
monitor for subcutaneous crepitus, high PAP, tracheal shift, hypoxemia
volutrauma
trauma from volume- overexpanding alveoli
damages the lung similar to early ARDS
vent bundle
HOB at 30 degrees
awaken daily and assess readiness to wean
stress ulcer prophylaxis
DVT prophylaxis
oral care
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
extubation
removing the ET tube
functions of the kidney
regulation of:
Fluid volume
electrolyte balance
acid base balance
BP
erythropoiesis
excretion of nitrogenous waste
metabolism of vitamin D
What is considered oliguria
urine output less than 0.5 ml/kg/hr
what is azotemia
accumulation of nitrogenous wastes (bun and creatine)
pre renal AKI
low bp, hypovolemia, dehydration like symptoms
ex that may cause- hemorrhage, sepsis, heart failure, DI, burns, diuretics, etc
meds for prerenal AKI
norepinephrine- helps BP go up
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
post renal AKI
obstruction of urine flow
ex caused by- BPH, clots, renal stones, meds, foley Cath obstruction, etc
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.
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
recovery phase AKI
recovery may take as long as 4-6 months
this is when renal tissue recovers and repairs itself
normal creatine
around 1.0
normal BUN
Around 20
AKI diagnostics
KUB xray
renal ultrasound
MRI
IV pyelogram
computed tomography
renal angiography
renal scan
renal biopsy
AKI interventions
I/o
daily weights
IV fluids
prevent infection
monitor electrolytes
pre renal AKI med management
volume replacement
maintain perfusion
early recognition=better outcome
intrarenal AKI med management
drug therapy
diet restriction
manage f&e
CRRT/dialysis
post renal AKI med management
alleviate obstruction
what does decreased GFR lead to
hyperkalemia
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
potassium 6-7 EKG change
peaked T wave
potassium 7-8 EKG change
peaked T wave
flattened p wave
prolonged PR interval
depressed ST segment
potassium 8-9 EKG
atrial standstill
prolonged QRS duration
further peaking T wave
potassium above 9 ekg changes
wave pattern. possible vtach
why does hyponatremia happen in AKI
nephrons are damaged, they can’t conserve sodium
types of dialysis
hemodialysis
continuous renal replacement therapy- CRRT
Peritoneal
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
CRRT
like hemodialysis but slower
these pts need to be on bed rest
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
normal output ml/kg/hr
0.5-1 ml/kg/hr
where does acid base regulation occur
proximal and distal tubules in nephron
what influences glomerular filt rate
mean arterial pressure
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
Hematopoiesis
formation and maturation of RBC
primary site of hematopoietic production
bone marrow
secondary hematopoietic organs
spleen, liver, thymus, lymphatic system, lymphoid tissue
erythrocytes
RBC- function to deliver hemoglobin throughout the body
platelets
first responders for clotting
granulocytes
neutrophils, basophils, and eosinophils, all of which function in phagocytosis
agranulocytes
monocytes and lymphocytes
function of neutrophils
bacterial infection
function of eosinophils
parasites
skin, lung, GI tract
basophils function
inflammatory/allergic response
monocyte function
mature into macrophage then do phagocytosis- attack foreign bodies and remove dead cells
lymphocyte function
humoral immunity- B lymphocytes (antibody prod)
cellular immunity- T lymphocytes (long term immunity)
what mechanisms trigger clotting
tissue injury
vessel injury
foreign body in the bloodstream
symptoms of all anemia types
fatigue, weakness, short of breath
aplastic anemia s/s
bruising
nosebleeds
petechiae
hemolytic anemia s/s
jaundice, abd pain, liver/spleen enlargement
sickle cell anemia s/s
joint swelling, pain
How does HIV lead to AIDS
by depleting helper T cells, CD4 cells, and macrophages
AIDS CD4 count
less than 200/microliter and presence of indicator of condition
HIV treatment
antiretroviral therapy
thrombocytopenia
low platelets under 150k
risk for bleeding
treated by platelets (depending on type)
heparin induced thrombocytopenia (HIT)
Adverse reaction to heparin
it causes hypercoagulability and thrombus
treatment- stop heparin, admin drugs that inhibit thrombin (bivalirudin)
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
DIC diagnosis
elevated fibrin degradation products
increased d-dimer
decreased antithrombin III
treatment of DIC
treat underlying cause
platelet transfusion
FFP transfusion
RBC for hemorrhage
heparin
cryoprecipitate
