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Technology 1 Flashcards

1
Q

Hypernatremia

A

Na > 142, (severe = Na > 160)

Causes: fluid restriction, excess free water loss

Abnormalities cause: AMS, focal neuro deficits, seizures

Tx: Give free water (slowly)

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2
Q

Hyponatremia

A

Na < 129

Abnormalities cause: AMS, focal neuro deficits, seizures

Causes:
–Pseudohyponatremia (elevated BG, TG, TSH)
–Hypervolemic : diurese
–Euvolemic: fluid restrict
–Hypovolemic : fluids w/ lytes

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3
Q

Hypervolemic hyponatremia

A

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

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4
Q

Euvolemic hyponatremia

A

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

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5
Q

Hypovolemic hyponatremia

A

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

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6
Q

Hyperkelamia

A

> 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

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7
Q

Hypokalemia

A

<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)

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8
Q

Anion Gap Acidosis

A

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

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9
Q

Non-AG Acidosis

A

Loss of HCO3

Diarrhea
Dehydration/fluid resuscitation w/ NSS
Hyperchloremia
Renal tubular acidosis

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10
Q

Creatinine

A

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

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11
Q

BUN

A

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

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12
Q

Hypomagnesemia

A

<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)

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13
Q

Hypercalcemia

A

> 10.7

Slows smooth muscle cells, nerve cells

Stones (renal), bones (reabsorption), moans (joint pain), groans (constipation) and psychiatric overtones

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14
Q

Primary hyperparathyroidism

A

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

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15
Q

Secondary hyperparathyroidism

A

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

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16
Q

Hyperparathyroidism of malignancy

A

Especially common in lung cancer

Ca extremely high (13-14), Phos low, PTH low
Tx: fluids

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17
Q

Hypocalcemia

A

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

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18
Q

Leukocytosis

A

> 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

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19
Q

Leukopenia

A

Sepsis/infection

Malignancy

Marrow suppressive drugs: chemo, immunosuppressants, Abx (cephalosporins, PCN)

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20
Q

Platelet lifecycle

A

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

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21
Q

Thrombocytosis

A

Acute phase reaction
Anemia (esp. Fe deficiency anemia)
Essential thrombocytosis in malignancy
Post splenectomy (leave it alone)

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22
Q

Anterior Septal wall

A

Left Anterior Descending

V1-V4

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23
Q

Inferior wall

A

Right Coronary Artery

II, III, aVF

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24
Q

Lateral wall

A

Left Circumflex Artery

I, aVL, V5, V6

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25
Q

Posterior wall

A

Posterior descending artry

V1-V2 mirror image changes

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26
Q

Thrombocytopenia

A

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

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27
Q

ITP

A

Diagnosis of exclusion
Autoantibodies form to platelets

CBC otherwise normal, +compensatory megakaryocytes on bone marrow biopsy

TX: corticosteroids, IVIG, may req splenectomy

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28
Q

TTP

A

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

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29
Q

DIC

A

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

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30
Q

Normocytic anemia (MCV WNL)

A

Acute bleed

Nutritional (check ferririn and homocysteine)

Renal insufficiency (check Cr)

Hemolytic anemia (increased LDH/I. Bili/haptoglobin/reticulocyte count)

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31
Q

Microcytic anemia

A

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

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32
Q

Iron deficiency anemia

A

Microcytic anemia: low Hgb, low MCV, low serum ferritin

Paradoxical increase in transferrin so will see high total iron binding capacity (TIBC)

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33
Q

Macrocytic anemia

A

B12/Folate deficiency– (MMA for B12, homocysteine for both)

Drugs (hydroxyurea, alcohol)

hypothyroid

MDS

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34
Q

PR interval

A

0.12–0.20 seconds

Interval between beginning of P wave to the appearance of the next wave (Q or R)

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35
Q

Q-T interval

A

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

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36
Q

Left Axis Deviation

A

–90-0
+I, –aVF

Can be normal variant

L BBB
LVH
Inferior wall MI
Cardiomyopathy
Congenital heart disease
Severe pulmonary disease

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37
Q

Right axis deviation

A

90-180
–I, +aVF

*Can be normal variant

R BBB
RVH
Anterolateral MI
Severe pulmonary disease
Reversal of R and L limb leads

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38
Q

R BBB

A

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

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39
Q

L BBB

A

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

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40
Q

LVH

A

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

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41
Q

RVH

A

Right axis deviation
V1: Tall/large R wave

ST depressions?

Causes:
Chronic pulmonic stenosis/regurg, tricuspid regurg
Pulm HTN
COPD
VSD
Chronic volume overload

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42
Q

Ischemia

A

least acute phase of tissue hypoxia – from decreased blood flow, often reversible

T wave flattening, inversion, ST depression

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43
Q

Injury

A

severe anoxia to the myocardium and necrosis (infarction) will occur if not reversed

ST elevation (>1 mm in two contiguous leads)

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44
Q

Infarction

A

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

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45
Q

Mallampati view

A

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

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46
Q

Thyromental distance

A

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

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47
Q

Airway assessment

A

Length of upper incisors
Presence of overbite
Mandibular mobility
Thickness and length of neck
Thyromental distance
Mallampati view

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48
Q

Laryngoscopy airway assessment

A

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

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49
Q

Upper airway

A

Nose
Mouth
Pharynx
Hypopharynx
Larynx

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50
Q

Lower airway

A

Trachea
Bronchi
Bronchioles
Alveoli

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51
Q

Nasopharynx

A

@ 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)

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52
Q

Oropharynx

A

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

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53
Q

Hypopharynx

A

Lies at C4-C6, Posterior to the larynx

Cricopharyngeal muscle – protection from regurgitation
Nerve innervation same as oropharynx

54
Q

Larynx

A

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

55
Q

Recurrent Laryngeal Nerve Damage (RLN)

A

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

56
Q

Laryngeal mask airway

A

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

57
Q

Benzodiazepines

A

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

58
Q

Hypnotics

A

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

59
Q

Dissociative

A

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

60
Q

Opioids

A

interaction with opioid receptors, inhibit the release of substance P from spinal cord
Ex: fentanyl (related to meperidine)

Metabolism: liver

61
Q

Neuromuscular transmission

A

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

62
Q

Depolarizers

A

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

63
Q

Succinylcholine

A

*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

64
Q

Rocuronium

A

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

65
Q

Cisatracurium (Nimbex)

A

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

66
Q

Cholinesterase inhibitors

A

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

67
Q

Sugammadex

A

Reversal of NMB

Actively binds to rocuronium and vecuronium, forms a complex which inactivates the drug

68
Q

ASA: Pt physical status

A

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”

69
Q

Subfalcine herniation (cingulate herniation)

A

initially asymptomatic
HA, loss of attention, contralateral leg weakness

70
Q

Descending central herniation

A

DI, cortical blindness, bleeding in midbrain and pons, irregular RR

71
Q

Ascending central herniation

A

posturing, acute hydrocephalus, unequal pupils

72
Q

Trans-calvarial herniation

A

Penetrating wounds, sx vary based on location of inury

73
Q

Uncal herniation

A

Ipsilateral dilated pupils, down and outward gaze, contralateral then ipsilateral weakness, contralateral homonymous hemianopsia (often cannot assess because of decreased LOC), flexor posturing

74
Q

Tonsillar/downward cerebellar herniation

A

Resp arrest, Cushing’s triad,

75
Q

Intraventricular (EVD)

A

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

76
Q

Intraparenchymal (Bolt)

A

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

77
Q

Subarachnoid ICP monitoring

A

low hemorrhage rates but clots frequently

78
Q

Cerebral perfusion pressure

A

MAP-ICP

Goal > 60

79
Q

P1 percussion wave

A

Arterial pressure from choroid plexus (what creates CSF in ventricles)

Should be taller than P2 and P3

80
Q

P2 Tidal wave

A

Reflection wave influenced by intracranial compliance

Reflects venous compartments

Poor Compliance: P2>P1

81
Q

P3 Dicrotic wave

A

Reflects aortic valve closure

82
Q

ICP crisis tier 1 universal measures

A

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

83
Q

Storming

A

diaphoresis, tachycardia/tachypnea, hyperthermia + motor symptoms (rigidity, hypertonia)

84
Q

ICP Crisis Tier 2 Acute strategies

A

Slight hyperventilation for short time: goal PaCO2 30-35 –>arterial vasoconstriction and reduced cerebral bloodflow

CSF diversion (EVD)

Hyperosmolar therapy: mannitol, hypertonic saline

85
Q

Mannitol

A

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

86
Q

Hyperosmolar therapy

A

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

87
Q

ICP Crisis Tier 3 salvage therapies

A

Compressive craniectomy

Neuromuscular paralysis with sedation (will lose neuro exam)

Laparotomy to decrease intraabdominal pressure (if >20)

Barbiturate or propofol coma

88
Q

Barbiturate or propofol coma

A

ADE:
Hypotension
Immunosuppresive (pentobarb)
propofol infusion syndrome
Hypertriglyceridemia
Pancreatitis

89
Q

tonicity

A

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

90
Q

osmolality

A

total # of osmoles (solute) in a given volume of water

osmolality : # solute per kg of solvent
osmolaRity: # solute per liteR of solvent

91
Q

NSS

A

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

92
Q

LR

A

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

93
Q

1/2 NaCl

A

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

94
Q

3% NaCl

A

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

95
Q

D5% W

A

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

96
Q

Normosol, Plasmalyte

A

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

97
Q

Albumin

A

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

98
Q

Fluid creep

A

Additional fluids given in IV meds (Abx, electrolytes, IV push meds) contribute to intake

99
Q

Orthostatic hypotension

A

20 mm Hg decrease in SBP or a 10 mm Hg decrease in DBP 3 minutes after rising from supine to standing

100
Q

CVP

A

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

101
Q

Stroke Volume Variation

A

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

102
Q

Passive Leg Raise

A

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

103
Q

POCUS

A

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

104
Q

TRICC Trial

A

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

105
Q

EGDT (Rivers et al)

A

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

106
Q

Transfusion complications

A

Hyperkalemia
hypocalcemia
Coagulopathy
TRALI
TRIM
TACO
Allergic reactions
Infection

107
Q

TRALI

A

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

108
Q

TACO: transfusion associated circulatory overload

A

during infusion–6 hours after

dyspnea, cyanosis, tachy, JVD, HTN w/ widening pulse pressures

109
Q

Transfusion related immunomodulation (TRIM)

A

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

110
Q

Acute hemolytic transfusion reaction

A

Rapid destruction (within minutes) of donor RBCs by recipient antibodies
Usually from ABO incompatibility
Fever, hypotension, tachycardia, myalgia, headache, anxiety, flushing, nausea, DIC

111
Q

Febrile nonhemolytic transfusion reaction

A

Most common, occurs with all products but most commonly plt

Fever, chills, rigor, mild dyspnea

Cytokine mediated inflammatory response

Differentiate hemolytic vs bacterial contamination

112
Q

Allergic rxn

A

Most common w/ FFP and plt

Urticaria, pruritis, bronchospasm, angioedema

Give antihistamines, steroids

113
Q

Nitrogen washout

A

Room air: 21% FiO2, 78% Nitrogen

Nitrogen is nonabsorbable gas, prevent alveoli from passive atelectasis

Ventilating w/ 100% FiO2 for prolonged time = O2 toxicity

114
Q

ACVC

A

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

115
Q

V trig

A

Flow pt must generate to get a breath (typically 2L/min)

116
Q

V max

A

Flow delivered to the patient (start at 40-50 L/min)

117
Q

ACPC

A

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

118
Q

APRV

A

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

118
Q

Bilevel ventilation

A

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

118
Q

PSV

A

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

118
Q

E-sense

A

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

119
Q

SIMV

A

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

119
Q

Plateau pressure

A

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

119
Q

auto PEEP

A

Air trapping that occurs when expiration is shorter than the amount of time it takes for patient to fully exhale air out of lungs

119
Q

Driving pressures

A

Pplat–PEEP
Goal <14

120
Q

Atelectasis

A

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

121
Q

Pleural effusion

A

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

122
Q

All diffuse alveolar disease is _______ until proven otherwise

All diffuse alveolar disease that is not _______ is ________ or ____________

A

CHF

Multifocal pneumonia, ARDS

123
Q

Alveolar processes

A

Acute
Fluffy, cloud like, diffuse

124
Q

All diffuse interstitial disease is _______ until proven otherwise

A

CHF

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