860c EXAM 3

shock

an imbalance between O2 demand and O2 supply characterized by end organ dysfunction, altered hemodynamic parameters, altered O2 metabolism

what are some clinical signs and symptoms of shock?

1) altered mental status

2) tachycardia and loe BP

3) cool clammy skin

4) reduced urine output

5) increased lactate

how to calculate MAP

SBP + 2(DBP)/3

what is the MAP goal for a shock patient?

> 65

what are the 4 general types of shock?

1) hypovolemic

2) distributive

3) cardiogenic

4) obstructive

hypovolemic shock

shock resulting from blood or fluid loss

- hemorrhagic

- dehydration (vomiting/diarrhea)

- burns

distributive shock

A condition that occurs when there is widespread vasodilation

- sepsis

- anaphylaxis

- neurogenic

cariogenic shock

shock that results from

inadequate pumping of heart

- heart failure

- arrhythmias

obstructive shock

shock that results from decreased CO or venous return due to blockage

- tension pneumothorax

- pulmonary embolism

what are the two main fluid compartments in the body?

1) intracellular space

2) extracellular space (intravascular and interstitial)

ICF is _____ TBW and ECF is ______ TBW (ECF is further broken down into interstitial which is _____ of ECF and intravascular which is ____ of ECF space)

2/3

1/3

3/4

1/4

isotonic

stay in the ECF -> no effect on ICF

example of isotonic fluids 1

1) NS

2) balanced crystalloids (LR, plasmalyte)

hypotonic

increase the ICF -> distributed throughout ICF and ECF

examples of hypotonic solutions

1) D5W

2) 1/2 NS

3) 1/4 NS

hypertonic

can decrease ICF since they stay in the ECF and can even pull water out of the ICF

hypertonic solution example

3% NaCl

what is a risk factor with using NS over balanced crystalloids?

NS can cause hyperchloremic metabolic acidosis -> Na and Cl usually increase and decrease together but in this case Cl concentration goes up

what is a concern with using balanced crystalloids

compatibility issues but usually use these over NS

what are two myths about balanced crystalloids?

1) since they contain lactate and the patient has elevated lactate, we cant give

2) since they contain K+ we cant use if the patient is hyperkalemic

colloids

large molecules that remain in the intravascular space and give oncotic force to pull fluid into the intravascular space

3 examples of colloids

1) starches (hydroxyethyl starch)

2) dextrans

3) albumin

albumin

100% stays in the intravascular space

- costs alot of money and doesnt work too well

ADRs with hydroxyethyl starch

increase AKI and mortality risk -> dont use

ADRs with dextrans

renal dysfunction and anaphylaxis -> dont use

what are some ADRs with albumin

can leak into extravascular space and cause fluid accumulation and edema

what is the issue with compounding 5% albumin from 25% albumin by using sterile water for injection to dilute it?

you cant do this because it will create a HYPOTONIC solution which can put the patient at risk for hemolysis and hypotension -> must dilute with D5W only

what is the 1st line treatment for hemorrhagic hypovolemic shock?

blood products -> PRBCs because we want to replace the blood that the patient is losing

what is 1st line therapy for hypovolemic shock?

FLUIDS -> LR/plasmalyte or NS (never give D5W for fluid resuscitation)

what are the 7 vasopressor agents in shock treatment?

1) norepinephrine

2) vasopressin

3) epinephrine

4) dopamine

5) phenylephrine

6) isoproterenol

7) dobutamine

norepinephrine

alpha 1 agonist (increases SVR) and B1 agonist (increases HR) and B2 agonist (slightly decreases SVR)

vasopressin

V1 agonist to increase SVR

epinephrine

alpha 1 agonist (increases SVR) and B1 agonist (increases HR) and B2 agonist (slightly decreases SVR and bronchodialate)

Does epi or NE have a greater effect on HR?

Epi -> has slightly more affinity for beta receptors than alpha receptors

dopamine

low dose = dopamine agonist

medium dose = B1 agonist & dopamine agonist

high dose = a1 agonist, B1 agonist, & dopamine agonist

T/F: dopamine has a high incidence of arrhythmias compared to the other vasopressors

TRUE

phenylephrine

pure a1 agonist to increase SVR -> not really used though because can cause reflex bradycardia

isoproterenol & dobutamine

B1 agonists (positive chronotropes and inotropes) that are useful in cardiogenic shock

neurogenic shock

a type of distributive shock in which there is a dysregulation of the NS due to injury at or above T6 vertebra

sepsis

life threatening organ dysfunction and dysregulated host response to infection

septic shock

patients with sepsis who require vasopressors to maintain MAP > 65 and have a serum lactate >/= 2 mmol/L despite adequate volume resuscitation

what are the 3 components of the qSOFA score?

respiratory rate, blood pressure, and altered mental status

qSOFA score

if a patient has >/= 2 of RR >/= 22, SBP

T/F: Fluid resuscitation of crystalloid fluids MUST occur in the setting of septic shock B4 initiation of vasopressors

TRUE because vasopressors need adequate preload/volume in order to be effective

abx therapy in a septic patient

broad spectrum abx for MRSA or pseudomonas coverage

broad spectrum gram -

1) cefepime

2) piperacilin-tazobactram

3) carbapenems

broad spectrum gram +

1) vancomycin

2) linezolid

3) daptomycin

T/F: bacterial cultures MUST BE DONE FIRST in a septic patient BEFORE the initiation of abx

TRUE

when should abx be started in a patient suspected of sepsis?

within 1 hr (& after bacterial culture)

what is the infusion rate of crystalloid fluids in septic shock?

30 mL/kg IV within the first 3 hours with a MAP goal of > 65

- if not met, then give adjunct vasopressor

T/F: want to give patients with HF, kidney impatient, pulmonary edema less than 30 ml/kg or fluids due to risk of fluid overload

TRUE

what is a dynamic fluid response assessment?

passive leg rise (45 degree angle with change in BP = pt responsive to fluids)

which vasopressor is first line in septic shock & hypotensive/normal HR neurogenic shock?

norepinephrine

which vasopressor is 2nd line in septic shock?

vasopressin then epi

when to initiate corticosteroids in a patient with septic shock?

if the MAP is < 65 still with adequate fluids and vasopressors (aka pressor resistant septic shock)

what corticosteroid is used in the setting of septic shock?

IV hydrocortisone (max 200 mg/day)

what is the benefit of using steroids in septic shock?

reduce ICU length of stay, time on mechanical vent, and shock duration/time on vasopressors

- no effect on mortality

- did no increase risk of new infection

what vasopressor is first line for neurogenic shock in hypotensive & bradycardic patient with neurogenic shock?

epi or dopamine

anaphylaxis is likely when:

1) involvement of skin/mucosal (rash, hives, itching) + at least one of sudden respiratory symptoms or collapse (decrease in BP)

2) two or more of: involvement of skin/mucosal (rash, hives, itching), sudden respiratory symptoms, hemodynamic instability/collapse (decrease in BP), sudden GI symptoms (cramping, pain, vomiting)

3) reduced BP when exposed to known allergen

what vasopressor is first line in anaphylaxis?

epinephrine

what is the dosing for epinephrine in anaphylaxis?

0.3-0.5 mg IM Q5-15 min with max 3 doses

- give in anterolateral portion of thigh; give continuous epi infusion once maxed on 3 doses of 1 mcg/min

T/F: there are no contraindications to the use of Epi in anaphylaxis

TRUE

what are some examples of how a lab value in critical care may leas to inappropriate clinical action

1) mild hyponatremia may be rapidly corrected and lead to osmotic demyelination

2) elevated K+ may occur from damaged RBC but lead to unnecessary hyperkalemia tx

3) elevated BUN may be mistaken for kidney dysfunction

4) increase in WBC after major surgery may be mistaken for an infection

5) high blood glucose due to infection/inflammation may be mistaken as DM

T/F: Na and Cl tend to increase and decrease together

TRUE and if they dont there is likely an acid base disturbance like hyperchloremic metabolic acidosis

example of when NaCl values aren't changing but their concentration relative to fluid increase or they decrease

they can increase when the patient is hypovolemic and decrease when patient is in volume overload

T/F: Na concentrations may be higher than normal in patients with dehydration

TRUE

T/F: hyponatremia can result from fluid overload (from fluid diluting the Na concentration) or fluid loss (executive vomiting/diarrhea like in hypovolemic hyponatremia)

TRUE

what is the most common intracellular ion?

K+ -> 98% of total K+ is inside the cell (> 3000 mEq)

serum K+ and pH have an _____ proportional relationship

inversely -> so K+ will increase when pH decreases (each 0.1 increase in pH will cause 0.6 mEq decrease in K+)

T/F: K+ can be given as an IV push

FALSE

what 2 lab values and 3 electroplates tend to increase with renal dysfunction?

Scr, BUN

K+, Mg, Phos

which lab value will decrease with renal dysfunction?

bicarb (can't be as easily reabsorbed)

what is one situation in which a high bicarb does not need to be treated to normalize it?

chronic compensated respiratory acidosis -> COPD

what is BUN?

a measure of nitrogen in the blood

T/F: BUN and Scr often increase together in the case of a kidney impairment

TRUE

what may be the reason that BUN is increasing but Scr is not?

BUN is increasing on its own this may indicate GI bleed/dehydration

what does it mean with the BUN:SCR ratio is >20:1?

PRERENAL AKI (azonatremia)

T/F: hematocrit is 3X the hemoglobin level

TRUE

what does a decreased H/H indicate?

anemia or blood loss

what is the bodies physiologic response to laryngeal manipulation?

sympathetic stimulation -> HR, BP increases, ICP and IOP increases

what is unusual about the response to laryngeal manipulation that can occur in children <1?

the can have a parasympathetic (vagal nerve) response

what are the 3 major roles of sedatives in intubation?

1) induces unconsciousness rapidly to prevent awareness of paralysis

2) blunts the sympathetic response to laryngeal manipulation

3) enhance the effects of neuromuscular blockers

what are the 4 common induction (sedatives) agents used in RSI?

1) etomidate

2) ketamine

3) propofol

4) midazolam

when is etomidate typically first line induction agent for RSI?

1) hemodynamic instability (hypotension or hypertension)

2) head injury or ICP

etomidate is hemodynamically neutral

when might ketamine be a more useful induction agent?

the the setting of RSI for asthma/bronchospasm since it has bronchodilator effects

when to avoid ketamine as inaction agent in RSI

critically ill or septic patients that may have catecholamine depletion such ketamine can actually tank the BP in these patients

3 ADRs of propofol

1) elevated triglyceride levels

2) hypotension

3) PRIS (when used long term and at high doses)

which sedative has a long DOA and typically produces deeper sedation?

midazolam

which sedatives for RSI have shorter DOAs?

1) etomidate (3-5 min)

2) propofol (3-6 min)

3) ketamine (10-20 min)

what is the rationale for NMBAs in RSI?

NMBAs paralyze the patient to facilitate endotracheal intubation

what are the two types of paralytic agents used in RSI?

1) depolarizing NMB -> succinylcholine

2) non depolarizing NMB -> rocuronium

what are 8 major CI to using succinylcholine in a patient that needs RSI?

1) end stage real disease (ESRD)

2) hyperkalemia

3) malignant hyperthermia

4) Increased IOP or ICP

5) neuromuscular diseases

5) muscular dystrophy

6) multiple sclerosis

what is an important thing to consider regarding the duration of sedatives and paralytics in RSI?

rocuronium DOA will outlast many of the induction agents so if using this one, it is important that we immediately start post intubation sedation protocols to maintain adequate sedation

traumatic brain injury

alteration in brain function or evidence of brain pathology caused by external force

primary brain injury

the initial insult -> the immediate damage caused by head trauma due to direct mechanical impact or penetration

secondary brain injury

subsequent damage that develops overtime after the initial impact (reduced blood flow, swelling, inflammation)

what are the 5 predictors of poor outcomes in patients with TBI?

1) elevated ICP

2) herniation

3) low GCS score (the lower = the more traumatic the injury is)

4) absent cough/gag reflex

5) over breathing the ventilator

Cerebral perfusion pressure (CPP)

what ensures that adequate blood flow is going to the brain

CPP equation

MAP - ICP

what are two ways to increase the CPP?

increase MAP

decrease ICP