Technology 1 Flashcards
Hypernatremia
Na > 142, (severe = Na > 160)
Causes: fluid restriction, excess free water loss
Abnormalities cause: AMS, focal neuro deficits, seizures
Tx: Give free water (slowly)
Hyponatremia
Na < 129
Abnormalities cause: AMS, focal neuro deficits, seizures
Causes:
–Pseudohyponatremia (elevated BG, TG, TSH)
–Hypervolemic : diurese
–Euvolemic: fluid restrict
–Hypovolemic : fluids w/ lytes
Hypervolemic hyponatremia
Ex: HF, Cirrhosis, Nephrotic Syndrome
Increased total body water but decreased intravascular volume
Brain releases ADH to retain fluid, diluting Na
Assessment: JVD, LE edema
Tx: Diurese
Euvolemic hyponatremia
Ex: SIADH (lung cancer, PNA)
ADH secretion outside of posterior pituitary (often by the lung), not responding to negative feedback increased fluid retention and dilutional hypoNa
Tx: Fluid restriction
Hypovolemic hyponatremia
Ex: Endurance athletes
Sweating increased ADH stimulates thirst free water intake w/o repleting electrolytes dilutional hyponatremia
Assessment: Mucus membranes
Tx: Give fluids w/ lytes
Hyperkelamia
> 5.5
Causes:
AKI,
Hyperaldosteronism (Spironolactone, ACE-Is, prolonged SQ heparin)
Hypoinsulinemia (DKA)
Acidosis
Cellular injury (bones, crush, TLS, rhabdo)
Symptoms: muscle weakness, peaked T waves, arrhythmias
Acute: Insulin +D50, CaGlu, Kayexalate
Subacute: Indication for dialysis
Hypokalemia
<3.5
Symptoms: muscle cramps, ECG changes
Causes:
GI loss (diarrhea)
GU loss (diuretics, hyperaldosteronism)
Hypomagnesemia (EtOH, tacrolimus)
Repletion: (4.0–actual K) x 100
replete primarily PO (up to 60 mEq, rest slowly IV)
Anion Gap Acidosis
16 +/-4
Addition of an unmeasured acid in blood causes acidosis
o Methanol
o Uremia/AKI (uric acid)
o DKA (ketones)
o Polyethylene glycol
o Isoniazid
o Lactate
o Ethylene glycol
o Salicylates
Non-AG Acidosis
Loss of HCO3
Diarrhea
Dehydration/fluid resuscitation w/ NSS
Hyperchloremia
Renal tubular acidosis
Creatinine
0.8-1.2
Muscle breakdown product, released into plasma at fairly steady rate –> marker of renal function, used to calculate GFR
Trends more important than individual numbers, view in context of broader clinical picture (ex: UO, s/sx fluid overload)
High–AKI
Low–poor nutritional status
BUN
6-20
Biproduct of protein degradation, marker of renal function
High: prerenal AKI (esp if elevated out of proportion to cr), GIb, TPN
Low: Poor nutritional status
Hypomagnesemia
<1.7
Can lead to hypocalcemia, hypokalemia, arrhythmias
Causes: K wasting diuretics, chronic etoh use
Tx 1 G IV to raise serum level by 0.1
Usually IV because PO causes severe GI ADEs (diarrhea)
Hypercalcemia
> 10.7
Slows smooth muscle cells, nerve cells
Stones (renal), bones (reabsorption), moans (joint pain), groans (constipation) and psychiatric overtones
Primary hyperparathyroidism
Adenoma in PT gland overproduces PTH
Slight increase in Ca (<11), Phos within normal range
Tx: remove PTH gland. Major head/neck surgery. Complications of not treating = bone loss
Secondary hyperparathyroidism
In the setting of CKD, elevated Phos signals PT to release PTH
Normal Ca, elevated Phos, elevated PTH
Risk = damage to bone health
Tx: low phosphate diet, phosphate binders with meals
Hyperparathyroidism of malignancy
Especially common in lung cancer
Ca extremely high (13-14), Phos low, PTH low
Tx: fluids
Hypocalcemia
Pretty rare
S/sx: easy excitement of electrical cells (Chvostek, Trousseau), prolonged QT, R on T phenomenon, seizures
Causes: pseudo/lab error (in setting of low albumin), sepsis, TLS, eating disorders, post blood transfusion
Leukocytosis
> 11,000
Infection/Inflammation: Will see increase in % neutrophils (shift to the Left)
Demargination: movement of WBC from peripheral tissue into circulation by exogenous steroids (Mechanism by which steroids can cause elevated WBC and immunosuppression)//Will also see shift to the Left
Malignancy
Leukopenia
Sepsis/infection
Malignancy
Marrow suppressive drugs: chemo, immunosuppressants, Abx (cephalosporins, PCN)
Platelet lifecycle
Thrombopoietin produced by liver and stimulates production of plt by megakaryocytes in bone marrow
Up to 1/3 platelets sequestered in spleen, the rest circulate in blood and form plugs at the sites of vessel injury then are cleared
Actively bleeding = clearing platelets
Thrombocytosis
Acute phase reaction
Anemia (esp. Fe deficiency anemia)
Essential thrombocytosis in malignancy
Post splenectomy (leave it alone)
Anterior Septal wall
Left Anterior Descending
V1-V4
Inferior wall
Right Coronary Artery
II, III, aVF
Lateral wall
Left Circumflex Artery
I, aVL, V5, V6
Posterior wall
Posterior descending artry
V1-V2 mirror image changes
Thrombocytopenia
10-50K
Decreased production: malignancy, bone marrow disorder, B12/folate deficiency, myelosuppression, Drugs (linezolid, Bactrim, PCN)
Splenic sequestration
Increased destruction: mechanical device destruction, ITP, Drug induced
Increased consumption: DIC, Heparin induced, TTP
ITP
Diagnosis of exclusion
Autoantibodies form to platelets
CBC otherwise normal, +compensatory megakaryocytes on bone marrow biopsy
TX: corticosteroids, IVIG, may req splenectomy
TTP
Extremely rare and life threatening
ADAMTS13 deficiency –> platelet clumping
CBC: decreased plt, anemia, +schistocytes on smear
Sx: seizures, AMS, stroke, MI, renal failure
Tx: plasma exchange apheresis
DIC
Etiology: cancer, sepsis, trauma, obstetrical complications
Thrombosis and bleeding
Low fibrinogen, elevated D-dimer, prolonged PT/PTT, thrombocytopenia
Tx: Address underlying cause, give blood products if bleeding
Normocytic anemia (MCV WNL)
Acute bleed
Nutritional (check ferririn and homocysteine)
Renal insufficiency (check Cr)
Hemolytic anemia (increased LDH/I. Bili/haptoglobin/reticulocyte count)
Microcytic anemia
Iron deficiency anemia: low serum ferritin
Anemia of chronic disease: normal ferritin in new/acquired microcytosis
*Consider Thalassemia and Heme Cons for chronic microcytic anemia w/ normal ferritin
Iron deficiency anemia
Microcytic anemia: low Hgb, low MCV, low serum ferritin
Paradoxical increase in transferrin so will see high total iron binding capacity (TIBC)
Macrocytic anemia
B12/Folate deficiency– (MMA for B12, homocysteine for both)
Drugs (hydroxyurea, alcohol)
hypothyroid
MDS
PR interval
0.12–0.20 seconds
Interval between beginning of P wave to the appearance of the next wave (Q or R)
Q-T interval
The interval between the first wave in the QRS complex and the end of the T wave
Prolongation = Torsades de pointes
Prolonged by various medications
Varies with heart rate, so must used adjusted QT (QTc) <350
Left Axis Deviation
–90-0
+I, –aVF
Can be normal variant
L BBB
LVH
Inferior wall MI
Cardiomyopathy
Congenital heart disease
Severe pulmonary disease
Right axis deviation
90-180
–I, +aVF
*Can be normal variant
R BBB
RVH
Anterolateral MI
Severe pulmonary disease
Reversal of R and L limb leads
R BBB
QRS> 0.12 = complete block
V1: rSR
V6: Slurred/sloped S wave
Causes:
Normal variant, rate related
CAD, CHD
Ventricular hypertrophy
Aberrant ventricular conduction
RV dilation
MI
Conduction system disease
L BBB
Impulse from ventricles completely messed up. Cannot look for injury/ischemia/infarct
QRS>0.12 = complete
V1: small R, large S (rS)
V6: Tall, slurred, or notched R wave
New L BBB + angina = cath alert
Causes:
MI, ischemia
CHF, cardiomyopathy
HTN
Conduction system disease
Severe AS
LVH
Left axis deviation
S V1/V2 + R V5/V6 >/= 35
Repolarization changes: T wave inversion (often in lateral leads 2/2 ischemia)
Causes:
Chronic HTN, cardiomyopathy, CHF
Mitral regurg, aortic stenosis/regurg
VSD w/ pulm HTN
Obesity
Cocaine
Anabolic steroids
Extreme athletic conditioning
RVH
Right axis deviation
V1: Tall/large R wave
ST depressions?
Causes:
Chronic pulmonic stenosis/regurg, tricuspid regurg
Pulm HTN
COPD
VSD
Chronic volume overload
Ischemia
least acute phase of tissue hypoxia – from decreased blood flow, often reversible
T wave flattening, inversion, ST depression
Injury
severe anoxia to the myocardium and necrosis (infarction) will occur if not reversed
ST elevation (>1 mm in two contiguous leads)
Infarction
Infarction = irreversible cell death to the myocardium
Pathologic Q waves
*Any Q wave in V2-V3 = pathologic. Should never see Q wave in V1-V4, okay to see small Q waves in V5-V6
*Increase size of prior seen Q waves or new Q waves
*1/4-1/3 height of R wave and 0.04 seconds or greater
Mallampati view
Assessment tool to determine difficult intubation status
PUSH:
Class I: Pillars, uvula, soft palate, hard palate
Class II: Uvula, SP, HP
Class III: SP, HP
Class IV: HP only
Thyromental distance
Measurement from upper edge of thyroid cartilage to the chin when neck hyperextended.
> 7 cm associated w/ easy intubation
<6 cm associated w/ difficult intubation
Airway assessment
Length of upper incisors
Presence of overbite
Mandibular mobility
Thickness and length of neck
Thyromental distance
Mallampati view
Laryngoscopy airway assessment
Grade 1 – vocal cords are visible
Grade 2 – vocal cords are partially visible
Grade 3 – only the epiglottis is visible
Grade 4 – epiglottis is not visible
Upper airway
Nose
Mouth
Pharynx
Hypopharynx
Larynx
Lower airway
Trachea
Bronchi
Bronchioles
Alveoli
Nasopharynx
@ C1
Humidifies air
Connects base of the skull to soft palate
Adenoids and eustachian tubes present
Blood supply – maxillary, ophthalmic and facial arteries
Motor innervation from facial nerve (CN VII) Sensory innervation from trigeminal nerve (V)
Oropharynx
Lies at C2-C3
Tongue, uvula and tonsils
Connection between soft palate and epiglottis
Motor innervation from vagus nerve (CN X)
Sensory innervation from glossopharyngeal (CN IX) , accessory (CN XI) and vagus nerve
Hypopharynx
Lies at C4-C6, Posterior to the larynx
Cricopharyngeal muscle – protection from regurgitation
Nerve innervation same as oropharynx
Larynx
Lies at C3-C6. Anterior to the esophagus.
Functionally protects the airway
Airflow for phonation
Blood supply–Thyroid and laryngeal arteries
Comprised of 3 anatomic subunits: supraglottis, glottis, subglottis
Recurrent Laryngeal Nerve Damage (RLN)
Unilateral
–paralyzed cord assumes intermediate position
–hoarseness
–common after subtotal thyroidectomy
Bilateral
–rare condition
–stridor, resp distress, aphonia
–paralyzed cord assumes midway position
–during inhalation, paralyzed cords come together causing obstruction
–intubation required
Laryngeal mask airway
Supraglottic airway device. Not a secured airway
General anesthetic delivery or rescue for difficult airway, or can be used for bronchoscopy
Does not req laryngoscope
Does not require muscle relaxant, lighter sedation needed
Spontaneous breathing and controlled ventilation
Not for use in pharyngeal obstruction, full stomach contents, low pulmonary compliance, obesity, surgical procedures
Benzodiazepines
Activation of the GABA receptor complex, results in hyperpolarization of neurons and reduction of excitability
Ex: Versed (Midazolam)
Metabolism: Liver
Retrograde/anterograde amnesia
Minimal resp depression
Antagonized by flumazenil
Hypnotics
Potentiation of the chloride current, mediated through the GABA receptor complex
Ex: propofol
Metabolism: liver
Supports bacterial growth, toss w/in 6 hr of vial opening
Notable decrease of systolic BP
Antiemetic
Burning on injection
Dissociative
non-competitive antagonist of N-methyl D-aspartate (NMDA) receptor
Ex: Ketamine (chemically related to PCP)
Also interacts with opioid receptors
Anticholinergic effects, bronchodilator
Metabolism: liver
Opioids
interaction with opioid receptors, inhibit the release of substance P from spinal cord
Ex: fentanyl (related to meperidine)
Metabolism: liver
Neuromuscular transmission
Nerve impulses produce influx of calcium in nerve vesicle
–>
Vesicles at nerve end release (ACH) into synaptic cleft
–>
ACH diffuses across synaptic cleft to nicotinic receptor (cholinergic receptor) on post synaptic membrane
–>
ACH binds to 2 alpha sub units on muscle, Causes sodium channels to open
–>
Influx of sodium and efflux of potassium occurs resulting in depolarization of muscle cells. Causes paralysis of muscle
Depolarizers
Succinylcholine (only drug on the market)
Mimics the action of acetylcholine to depolarize the muscle
Contracts the muscle, may see muscle fasciculations. WAIT to see fasciculations before preceding with intubation
Can see myalgia post procedure in muscular patients
Succinylcholine
*Only depolarizer in clinical practice
Dose : 1-1.5mg/kg
Rapid onset – 60 seconds. Short duration of action - up to 10 minutes
Causes fasciculation of muscles
ADE– cardiac dysrhythmias, hyperkalemia, myalgia, increase in close space pressures
Metabolism : plasma cholinesterase
Rocuronium
Non-depolarizer, aminosteroid neuromuscular blocking agent
Dose: 0.6-1.2mg/kg
Onset 1.5 -3 min. Duration of action 20-35 min (Resembles onset of succ. w/ increased doses)
Lacks potency
With renal disease, may have longer duration of action
Cisatracurium (Nimbex)
Non-depolarizer, Classified as a benzylisoquinolinium neuromuscular blocking agent
Onset of action - 3-5 minutes. Duration of action - 20-35 minutes
Undergoes Hoffman elimination and ester hydrolysis– temperature and pH dependent
Great for patients with significant renal disease or renal failure
Cholinesterase inhibitors
For reversal of neuromuscular blocking–Blocks action of acetylcholinesterase so more acetylcholine present for muscle contraction
Neostigmine – quaternary amine
Physostigmine – tertiary amine
Edrophonium – quaternary amine
Sugammadex
Reversal of NMB
Actively binds to rocuronium and vecuronium, forms a complex which inactivates the drug
ASA: Pt physical status
ASA PS 1 – A normal healthy patient
ASA PS 2 – A patients with mild systemic disease: No functional limitations; well-controlled disease of one body system
Mild obesity, Pregnancy
ASA PS 3 – A patients with severe systemic disease: Some functional limitation
No immediate danger of death
ASA PS 4 - A patients with severe systemic disease that is a constant threat to life
Has at least one severe disease that is poorly controlled or at end stage;
Possible risk of death
ASA PS 5 – Patients who are not expected to survive without the operation Multi-system organ failure
ASA PS 6 - A declared brain-dead patient
Patient’s organs are being removed for donor purposes
E – If the procedure is an emergency, the physical status is followed by “E”
Subfalcine herniation (cingulate herniation)
initially asymptomatic
HA, loss of attention, contralateral leg weakness
Descending central herniation
DI, cortical blindness, bleeding in midbrain and pons, irregular RR
Ascending central herniation
posturing, acute hydrocephalus, unequal pupils
Trans-calvarial herniation
Penetrating wounds, sx vary based on location of inury
Uncal herniation
Ipsilateral dilated pupils, down and outward gaze, contralateral then ipsilateral weakness, contralateral homonymous hemianopsia (often cannot assess because of decreased LOC), flexor posturing
Tonsillar/downward cerebellar herniation
Resp arrest, Cushing’s triad,
Intraventricular (EVD)
Gold standard of ICP monitoring, monitors and drains (but not at the same time)
Cons: risk of infection, hemorrhage, malpositioning, can be difficult to access ventricle in setting of cerebral edema, occlusion from blood/brain tissue
Intraparenchymal (Bolt)
Electric/fiberoptic
Sits in brain tissue, provides continuous ICP monitoring with low risk of infection/bleeding
Cons: no ability to drain, often has mechanical failure
Quad-lumen bolt: icp, microdialysis, seizure monitoring, cerebral blood flow
Subarachnoid ICP monitoring
low hemorrhage rates but clots frequently
Cerebral perfusion pressure
MAP-ICP
Goal > 60
P1 percussion wave
Arterial pressure from choroid plexus (what creates CSF in ventricles)
Should be taller than P2 and P3
P2 Tidal wave
Reflection wave influenced by intracranial compliance
Reflects venous compartments
Poor Compliance: P2>P1
P3 Dicrotic wave
Reflects aortic valve closure
ICP crisis tier 1 universal measures
Optimize outflow drainage. HOB 30, keep head aligned, minimizing intra thoracic/intra abdominal pressures
Prevent/treat seizures (Keppra)
Normothermia: arctic sun, tylenol
Treat storming
Short acting sedation
Storming
diaphoresis, tachycardia/tachypnea, hyperthermia + motor symptoms (rigidity, hypertonia)
ICP Crisis Tier 2 Acute strategies
Slight hyperventilation for short time: goal PaCO2 30-35 –>arterial vasoconstriction and reduced cerebral bloodflow
CSF diversion (EVD)
Hyperosmolar therapy: mannitol, hypertonic saline
Mannitol
sugar alcohol. 1g/kg bolus Q6 to reduce ICP
Total body dehydration: filtered in kidneys –> salt/water follow
Replete UO 1:1 for 2 hours after each dose
Monitor renal function and BMP prior to each dose. Not for use in renal failure
Caution in hypotension
Hyperosmolar therapy
2%-23.4% saline
No diuretic effect, safe in renal disease
Expands intravascular volume and increases cardiac output
Trend Na, Stop before reaches >160
Continuous infusions require central line
ICP Crisis Tier 3 salvage therapies
Compressive craniectomy
Neuromuscular paralysis with sedation (will lose neuro exam)
Laparotomy to decrease intraabdominal pressure (if >20)
Barbiturate or propofol coma
Barbiturate or propofol coma
ADE:
Hypotension
Immunosuppresive (pentobarb)
propofol infusion syndrome
Hypertriglyceridemia
Pancreatitis
tonicity
refers to the fluid “tension” within the ICF or ECF to generate a driving force that causes fluid movement and is determined by fluid osmolality
osmolality
total # of osmoles (solute) in a given volume of water
osmolality : # solute per kg of solvent
osmolaRity: # solute per liteR of solvent
NSS
Crystalloid, isotonic solution
Na: 154
Cl: 154 (much higher than plasma)
K: 0
Ca: 0
Lactate: 0
Osmo: 308
pH: 5.6
Large volume resuscitation =
–hyperchloremic metabolic acidosis (non AG gap)
–hyperchloremia induced uremia/kidney injury
–increased K through extracellular shifts
LR
Crystalloid, isotonic solution
Na: 130
Cl: 109 (closer to plasma)
K: 4 (doesn’t significantly increase plasma K)
Ca: 3
Lactate: 28
Osmo: 273
pH: 6.6
Tx of metabolic acidosis and GI loss
Sodium lactate reduces acidity as converted into bicab
Incompatible w/ blood products d/t calcium content
1/2 NaCl
Crystalloid, hypotonic solution
Na: 77
Cl: 77
K: 0
Ca: 0
Lactate: 0
Osmo: 154
pH: 5.6
For hypovolemic hypernatremia.
Can lower Na (dilutional), especially in pt prone to fluid retention
3% NaCl
Hypertonic crystalloid
Na: 513
Cl: 513
K: 0
Ca: 0
Lactate: 0
Osmo: 1030
pH: 5
Good volume expander, pulls from ICF into intravascular spaces
Infuse SLOWLY
Some patients may need diuresis
Risk of cell dehydration
D5% W
Na: 0
Cl: 0
K: 0
Ca: 0
Lactate: 0
Osmo: 252
pH: 4.3
Calories: 170 kcal/L
Glucose: 50 gm/L
Initially isotonic, becomes hypotonic w/ metabolism
Cerebral edema in patients with increased ICP
Normosol, Plasmalyte
Isotonic crystalloid, closest to serum concentrations
Na: 140
Cl: 98
K: 5
Mag: 3
Acetate: 27
Gluconate: 23
Osmo: 295
pH: 7.4
Contain Acetate and Gluconate –> metabolized into Bicarbonate
Albumin
Serum protein, accounts for 75% plasma COP
5% 25g/500 mL –> COP 20 (similar to plasma)
25% 25 g/100 mL (COP 70)
Effects last 12-18 hours
Fluid creep
Additional fluids given in IV meds (Abx, electrolytes, IV push meds) contribute to intake
Orthostatic hypotension
20 mm Hg decrease in SBP or a 10 mm Hg decrease in DBP 3 minutes after rising from supine to standing
CVP
Approximates right atrial pressure and therefore RV end-diastolic volume –>
Further extrapolated to estimate LV end-diastolic pressure and volume
Ultimately estimates the LV stroke volume, which is the closest approximation of the overall intravascular volume state
Highly flawed, not recommended for use as a static value
Stroke Volume Variation
Based on the difference in intrathoracic pressure between insp. and exp. in patients on positive pressure ventilation
The larger the difference, the more likely the patient will respond favorably to a fluid bolus
Can be measured with arterial line or esophageal doppler
Inaccurate with patients spontaneously breathing, low tidal volumes (< 8 ml/kg), or with irregular heart rhythms
Passive Leg Raise
Induces a rapid and reversible increase in cardiac preload through an increase in venous return mimicking fluid administration (~300-500ml)
If CO (or BP) increases 10% within 60 seconds, the patient will most likely respond favorably to a fluid bolus
Contraindicated in TBI, leg fx, amputation
POCUS
Inferior vena cava diameter variation (IVCDV) throughout the respiratory cycle – similar to SVV and PPV – the greater the variability the more likely to be fluid responsive
Ventricular size and function – a hyperdynamic LV (kissing ventricles) is strongly indicative of hypovolemia
TRICC Trial
Transfusion Requirements in Critical Care (TRICC)
Randomized 838 euvolemic patients admitted to the ICU without evidence of active bleeding to either a:
Restrictive transfusion strategy (hgb 7-9 g/dL)
Liberal transfusion strategy (hgb 10-12 g/dL)
Primary outcome: Indicates similar 30-day mortality between the groups
EGDT (Rivers et al)
EGDT is a 6-hour resuscitation protocol for the administration of IVFs, vasopressors, inotropes, and RBC transfusion to achieve prespecified targets for BP, CVP, ScVo2, and hgb level
Not superior to current standards of practice
Transfusion complications
Hyperkalemia
hypocalcemia
Coagulopathy
TRALI
TRIM
TACO
Allergic reactions
Infection
TRALI
Dspnea, cough, hypoxia, diffuse pulmonary infiltrates, fever, hypotension during or within 6 hours of transfusion
Usually transient, treatment is supportive
Can happen with all products but most common with FFP
TACO: transfusion associated circulatory overload
during infusion–6 hours after
dyspnea, cyanosis, tachy, JVD, HTN w/ widening pulse pressures
Transfusion related immunomodulation (TRIM)
Down regulation of patient’s immune system
increased chances of post-operative infections and cancer recurrence, and possibly a transfusion-related multiple organ dysfunction syndrome
Acute hemolytic transfusion reaction
Rapid destruction (within minutes) of donor RBCs by recipient antibodies
Usually from ABO incompatibility
Fever, hypotension, tachycardia, myalgia, headache, anxiety, flushing, nausea, DIC
Febrile nonhemolytic transfusion reaction
Most common, occurs with all products but most commonly plt
Fever, chills, rigor, mild dyspnea
Cytokine mediated inflammatory response
Differentiate hemolytic vs bacterial contamination
Allergic rxn
Most common w/ FFP and plt
Urticaria, pruritis, bronchospasm, angioedema
Give antihistamines, steroids
Nitrogen washout
Room air: 21% FiO2, 78% Nitrogen
Nitrogen is nonabsorbable gas, prevent alveoli from passive atelectasis
Ventilating w/ 100% FiO2 for prolonged time = O2 toxicity
ACVC
Set RR, volume, PEEP, FiO2
Most controlled, typical starting point
TV set @ 6-8 mL/kg ideal body weight
RR: start at 12-18 then think about obtaining minute ventilation of 5-8L/min (TV xRR = MV)
–Faster RR for ARDS, acidosis, increased ICP
PEEP: Start at 5, increase by 2.5
FiO2: typically start at 100%, rapidly titrate down as pt tolerates
V trig
Flow pt must generate to get a breath (typically 2L/min)
V max
Flow delivered to the patient (start at 40-50 L/min)
ACPC
Set RR, Pressure, PEEP, FiO2
Also need to set inspiration time (0.8)
Guarantees set pressure at expense of volume (so requires close monitoring and frequent adjustments)
Superior for pt at risk of volutrauma/barotrauma
Secretions/mucus plugging can contribute to pressures and lower volumes will be delivered to patient
MV hard to predict
APRV
Uses long periods of high pressure (inspiration) with very short periods of release (exhalation)
It is all about preventing atelectasis and increasing recruitment.
Patient may become hypercarbic, may have initially worsening hypoxia, may become hypotensive
Bilevel ventilation
Very similar to APRV, Main difference is that in BiLevel your Tlow is greater than 1sec
Also need to set a low peep to prevent derecruitment, 5-10 to start
PSV
Spontaneous mode of breathing: patient must be able to generate a breath
Flow triggered cycle
More comfy for pt
Considered weaning mode
BiPAP: Set PS (12-15), PEEP, FiO2
CPAP: No pressure support. Just set PEEP and FiO2
E-sense
Used in pressure support mode
Tells machine when to transition to exhalation, typically set at 25%
When flow decreases to 25% of peak
flow, then transition to exhalation
May be helpful in restrictive vs.
obstructive disease
SIMV
synchronized intermittent mandatory ventilation
Combo of ACVC and PSV
Bridge for patients not ready for full PSV
Allows patient to take spontaneous breaths with variable TVs while at the same time still getting guaranteed breaths and TVs
Limited use in practice, but helpful for oversedated post OP pt
Set RR (lower), TV, PEEP, FiO2, PS
–minimum # respirations at set rate
–Spontaneous respirations at set PS
Plateau pressure
the pressure in the lungs during mechanical ventilation that can be measured by performing an inspiratory pause at the end of inspiration. It is also known as the peak alveolar pressure
auto PEEP
Air trapping that occurs when expiration is shorter than the amount of time it takes for patient to fully exhale air out of lungs
Driving pressures
Pplat–PEEP
Goal <14
Atelectasis
Passive: Pain, neuromuscular disease, space occupying lesions (pneumothorax, pleural effusions), deep sedation
–Diffuse, fluffy (alveolar) white, thick bands, sub-segmental atelectasis
Obstructive (resorptive): Blockage of an airway –> lobar collapse
plates and discs. fissure pulled TOWARDS obstruction
Pleural effusion
Upright pt
Focal homogenous white
Lost costophrenic angle (or blunting)
Meniscus sign
150 CCs fluid needed to visualize on AP film
500 CCs correspond to portion of lung field whited out
All diffuse alveolar disease is _______ until proven otherwise
All diffuse alveolar disease that is not _______ is ________ or ____________
CHF
Multifocal pneumonia, ARDS
Alveolar processes
Acute
Fluffy, cloud like, diffuse
All diffuse interstitial disease is _______ until proven otherwise
CHF
