all exam 1 stuff

types of IV access

\-peripheral line

\-central venous catheter

enteral access

safest and most convenient way

-if given oral med achieves tissue and blood concs to the same extent as IV, there is little difference in uses

feeding routes through the nose

\-nasogastric

\-nasoduodenal

-nasojejunal

nasogastric

nose → stomach

nasoduodenal

nose → small intestine

nasojejunal

nose → jejenum (farther down in small intestine)

is gastrostomy or jejunostomy preferred? why?

gastrostomy

\-G clogs less than J

\-Food only through J, can give meds through G

nasogastric tube -use -pros -cons

short-term use

Pros : easy to place variety of sizes

Cons: not indicated if bleeding or esophageal disorder

orogastric tube -use -pros -cons

short-term use

Pros : lower incidence of sinusitis

Cons : not tolerated for long periods of time in alert patients tube may damage teeth

nasoenteric tube -use -pros -cons

short-term use

Pros : smaller diameter than NGT less pt discomfort can be used in delayed gastric emptying

Cons : difficult to position smaller tubes make admin difficult infusion pump needed

oroenteric tube -use -pros -cons

short-term use

Pros : same as orogastric tubes

Cons : same as orogastric tubes

gastrostomy tube -use -pros -cons

short and long-term use

Pros : easily cared for and replaceable large tube=bolus feeds

Cons : more invasive

jejunostomy tube

\-use

\-pros

\-cons

long-term use

Pros : decreases risk of rood and fluids passing into lungs allows for early post-op feeding

Cons : harder to place infusion pump needed

sequential therapy

replacing parenteral with oral counterpart of same compound

levetiracetam 100 mg IV → 100 mg PO

levothyroxine 80 mcg IV →100 mcg PO

switch therapy

IV → PO equivalent within same class and same potency, but is a different compound

-will say equivalent dose

morphine 2.5 IV → oxycodone 5 mg PO

methylpred 40 mg IV → prednisone 50 mg PO

step down therapy

inj → oral in another class or to a different med within the same class where the frequency, dose, and spectrum of activity may not be the same -

not equivalent dose

nicardipine → amlodipine

heparin → warfarin

FASTHUG MAIDENS

Feeding

Analgesia

Sedation

Thromboprophylaxis

Hyperactive or hypoactive delirium

U stress ulcer prophylaxis

Glucose control

\
Med rec

ABX or anti-infectives

Indications for meds

Drug dosing

Electrolytes and lab results

No drug interactions, allergies …

Stop dates

pathophysiology of VTE

virchow’s triad

components of virchow’s triad

stasis

vascular injury

hypercoagulable state

\-ICU patient have all 3 of these

formation of VTE

VTE starts as DVT usually starts in legs due to decreased movement=decreased blood flow from lack of movement -DVT can turn into PE

risk factors for VTE (5)

cancer

previous VTE

obesity

trauma

surgery

drug options for VTE prophylaxis

heparin

LMWH

fondaparinux

DOACs

heparin for VTE prophylaxis

most common agent

\-5000 units SQ Q24H or 5000 units SQ Q8H

\-no renal dose adjustment required

examples of LMWH

* enoxaparin
* dalteparin

enoxaparin and dalteparin dosing for VTE prophylaxis

* enoxaparin: requires renal adjustment 40 mg Q24H or 30 mg Q12H
* CrCl

fondaparinux for VTE prophylaxis

* the only synthetic agent
* not routinely used in critically ill patients
* CI in CrCl < 30

DOACs in VTE prophylaxis

no role in ICU patients

mechanical methods for VTE prophylaxis

sequential compression devices

use:

* combination with prophylaxis for increased risk monotherapy for patients with increased bleed risk

when can you not use mechanical methods for VTE prophylaxis

* if pt has injury to leg
* if pt has an ACTIVE DVT (could break off)

how to treat patients with multiple risk factors for VTE

should get pharmacologic and mechanical interventions

major effects of VTE prophylaxis

* bleeding
* heparin-induced TCP

who should not receive pharmacologic VTE prophylaxis

patients with platelets

bleeding due to VTE prophylaxis

prophylaxis does not cause major VTE bleeding

heparin-induced TCP due to VTE prophy

immune mediated disorder

* presents as low platelets in the presence of heparin or LMWH leads to thrombosis (stroke, MI, VTE)

dosing of VTE prophylaxis drugs in obesity/edema

obesity raises risk of VTE, but could also cause patients to be under-dosed \= more risk

stress ulcer

stress-related mucosal damage can develop 24 hours after ICU admission

pathophys of stress ulcers

acid hypersecretion in response to gastrin stimulation of parietal cells

independent risk factors for stress ulcers

need ONE to qualify for prophylaxis:

* coagulopathy: platelets

drugs that can be used for stress ulcer prophylaxis

* antacids
* sucralfate
* H2 receptor antagonists
* PPIs

antacids for stress ulcer prophy

not effective and associated with higher mortality

sucralfate for stress ulcer prophy

don’t work as well and have increased risk of toxicity

what do H2 receptor antagonists for stress ulcer prophy require

renal dosing

what occurs over time with H2 antagonists

tachyphylaxis

* drug stops working

dosage forms of H2 antagonists for stress ulcer prophy

IV and enteral

ADRs of H2 antagonists

1. TCP
2. mental status changes
3. nosocomial pneumonia

dosing of H2 antagonists for stress ulcer prophy

famotidine 20 mg IV or PO Q12H

ADRs of PPIs

* GI
* nosocomial pneumonia
* C.diff
* fractures
* electrolyte disturbances

effects of hyperglycemia

* dysregulation of NO function
* impaired neutrophil fxn
* increase production of pro-inflammatory cytokines

target glucose range

140-180 mg/dL

what is the main risk of acute glucose control

hypoglycemia

* it is easy to overshoot, and hypoglycemia is a much more acute risk of poor outcomes/mortality

level to treat hypoglycemia

treatment for hypoglycemia

1. discontinue insulin
2. administer dextrose: 25 g IV
3. re-evaluate insulin/glucose control

what to do if a patient’s glucose begins to trend under goal but patient is not hypoglycemic

decrease insulin dose or re-evaluate need for insulin

oral antidiabetic agents for glucose control

not routinely used

slinding/correctional scale for glucose control

most common initial method of ICU glucose control

* use short/rapid acting insulin
* short: 0-18 units Q4H
* rapid: 0-6 units TID

how to treat patients with high insulin requirements

basal alone

* started as a low dose and increased carefully as needed
* not used as routine control

3 uses of IV fluids

* providing hydration
* fluid resuscitation
* treating specific fluid-related issues

3 fluid spaces

* intracellular
* extracellular-intravascular
* extracellular-interstitial (extravascular)

third spacing

when fluid shifts from plasma to interstitial fluids \= accumulation of fluid in interstitial peripheral space BAD!!

how does third spacing happen

patients leak albumin and oncotic pressure lowers \= promotes fluid movement out of vasculature \= increases tendency for fluids to build up where it shouldn’t

effect of meds on third spaced fluids

therapies that increase fluid excretion remove fluid from the bloodstream, third spaced fluid remains in extravascular space

osmolarity

property of a solution that is independent of any membrane osmoles of solute/L of solvent

osmolality

number of osmoles / kg solvent -usually equal

osmolarity and osmolarity are usually considered \_______

equivalent

range for normal serum osmolality

275-300 mOsm/kg

tonicity

property of a solution that is in reference to a membrane

range for isotonic solutions

250-375 mOsm/L

when do tonicity/osmolarity of fluid matter

at 2 points in time during the infusion after the fluid has caused systemic effects

mEq in 0.9% NaCl

154 mEq Na

properties of 0.9% NaCl

purely isotonic

amount of dextrose in D5W

252 mOsm/L

properties of D5W

begins isotonic, then becomes hypotonic

properties of D5NS

purely isotonic -initi 560 isn’t hypertonic enough to have a significant effect, DON’T need a central line for admin

properties of D5 1/2 NS

begins isotonic, then becomes hypotonic

mOsm/L of lactated ringer’s

273 mOsm/L

properties of lactated ringers solution

purely isotonic

value for 3% NaCl

1027 mOsm/L

properties of 3% NaCl

purely hypertonic

caution with 3% NaCl

use central line

\-anything over 900 mOsm/L should be given centrally

uses for isotonic solutions

* fluid resuscitation
* maintenance fluids

uses for hypotonic solutions

* correcting sodium abnormalities
* treating conditions with intracellular dehydration

caution for hypotonic fluids

do not use hypotonic fluids in head injury patients

\-causes increased peripheral cerebral edema

use for hypertonic solutions

* correcting sodium abnormalities
* decreasing cerebral edema

amount of sodium in lactated ringer’s

130

crystalloids

fluids that contain water, electrolytes, and small molecules

\-cross cell membranes = useful for treating imbalances

\-bad in critically ill patients bc fluid diffuses into peripheral space = vol overload

colloids

fluids made up of large molecules

* -increase oncotic pressure and don’t redistribute into EV space
* benefits: smaller volume needed to correct losses bad: expensive and human product

common colloid solutions

* albumin 5%
* albumin 25%-won’t raise blood pressure, takes too long

normal sodium range

135-145 mEq/L

normal chloride range

97-107 mEq/L

what does treatment and maintenance of hyponatremia depend on

associated with decreased serum osmolality causes neurologic effects (fluid goes into cells, brain cell swell)

* treatment depends on serum osmolality
* maintenance depends on volume status

treatment for hypervolemia hyponatremia

* fluid/water restriction
* change fluids (if fluid induced)

treatment for euvolemic hyponatremia

due to SIADH

\-water restriction

when treating hyponatremia, do not increase plasma sodium faster than \_______

6-12 mEq/L/dy

maximum increase of plasma sodium rate if patients are acutely symptomatic

\
1-2 mEq/L/hr -still adhering to above 6-12 mEq/L/dy

treatment of hypovolemic hypernatremia

hypo or iso fluids

treatment for euvolemic hypernatremia

water replacement

most common cause of hyponatremia

* excess (hypotonic) fluid
* SIADH-can be induced by meds

treatment of hyponatremia

stop/change fluid

most common cause of hypernatremia

* dehydration
* diabetes insipidus

treatment of hypernatremia

hypotonic fluids

\-use carefully

\-don’t want to overcorrect sodium