477 final exam

s/s of compensated shock

narrow pulse pressure, tachycardia, cool pale skin

weak peripheral pulses, slow cap refill, decreased urine output

s/s of decompensated shock

hypotension

organ dysfunction: such as confusion, no bowel sounds and ileus, decreased renal function, oxygenation issues

initiation shock fluid

isotonic fluid resuscitation (NS or LR)

vasoactive drips, positive inotropes, or blood

first hours tx of sepsis

fluid bolus, cultures, antibiotics, and lactic acid

what to know about fluid with shock

improves CO in pt with low preload

use caution with cardiogenic shock (they already have high preload)

RSI

done to decrease risk of aspiration during intubation

SEDATE FIRST

paralytic and sedation administration prior to intubation

indirect ARDS causes

sepsis-most common

pancreatitis

massive transfusion reaction

direct causes of ARDS

pulmonary trauma and pulmonary infectione

s/s tension pnuemo

hemodynamic instability

tracheal shifting

absent or referred breath sounds on effected side

JVD (due to torquing of heart on great vessels= decreased blood return to right atrium)

causes for high pressure alarm on vent

asynchrony with ventilator

needs suctioning

water in ventilator circuit

patient bitinf vent

low pressure alarm cause on vent

disconnected circuit

cardiac diagnostic test

BNP = HF

troponin= MI

post cardiac arrest syndrome

decrease in CNS function after cardiac arrest

results in decrease LOC: restlessness → irritability → and as high as a coma and death

T’s of causes of PEA

tension pneumothorax, tamponade, toxins, thrombosis, trauma

H’s of causes of PEA

hypoxia

hydrogen ion

hyper/hypokalemia

hypovolemia

risk factors for CV surgery

smoker

diabetic

hypertension

COPD → #1 pt who cannot come off the vent

other organ disease such as renal disease

CPP calculation

MAP-ICP= CPP

if less than 70 the brain isn’t perfused

post subarachnoid hemorrhage complications

rebleed is highest mortality rate, global s/s

vasospasm focal s/s

-nifedipine; hypervolemia, hemodilution, hypertensive

hydrocephalus

salt wasting

moderate TBI manifestations, concussion

headache, confusion (brief), amnesia for event, n/v

global s/s of TBI

decreased LOC (confusion → coma)

seizures

n/v

altered cognition

epidural hematona s/s pattern

usually arterial bleed

s/s of injury: unconscious, lucid period, then rapid neurological deterioration

treatment: surgery evacuation if determined to be arterial bleed

bowl shaped of CT

Cushing Triad

occurs to prevent brain stem ischemia

elevated systolic pressure = widened pulse pressure

bradycardia

irregular respirations

treatment elevated ICP

nursing interventions: quiet environment, HOB elevated, head midline

CSF drain if intraventricular drain present, mannitol, watch CO2 and don’t let it get high

advanced treatments for refractory ICP

DKA

presenting condition” metabolic acidosis and dehydration; acidosis brings them n

occurs in Type 1 diabetes

ketosis develops uncontrolled due to lack of sufficient insulin, labs show metabolic acidosis

treatment: NS and insulin infusion (after sugar is below 250 add K to fluids)

hyperosmolar hyperglycemic syndrome

occurs in type 2 diabetes due to insulin resistance

elevated serum glucose freq over 1000; dehydration brings them in

does not ketosis, normal blood gases

severe dehydration due to elevated glucose levels

treatment: fluids and insulin infusion

DIC treament

heparin: to decrease clotting (usually not used bc conditions must be identified early for it to be used)

clotting factor infusion: fresh frozen plasma, platelets, cryoprecipitate

types of renal injury and tx

prerenal, intrarenal, postrenal

IV and oral fluids intake based on amount of urine output

prerenal injury

anything causing sudden disruption of perfusion to kidneys

anoxic renal injury

caused by quick BP drop, sepsis, artery clamping

intrarenal injury

direct injury to renal cells= decreased GFR

causes: toxins, drugs, inflammation, dye

postrenal injury

decreased ability to filter blood due to obstruction of both ureters

remove obstruction

SAH complications

rebleed, vasospasms and hydrocephalus

treatment for SAH

specific to plan of care

frequent neuro checks, HOB elevated, permissive HTN (130s-140s systolic) and if there are vasospasms then BP 140s-150s

pathphys of tension pneumothorax

tracheal shift leading to

frank sterling law

frank sterling: how well a muscle contracts is dependent on the stretch of the fibers

preload: amount of stretch in fibers; too much or too little and you don’t get good contraction

mild TBI s/s

concussion

n/v, amnesia from event, headache, confusion (pt is not aggressive)

what to watch for in a post op patient that tells you they may be going into shock

decreased urine output, increase HR, cool and pale skin

tx for PEA

CPR, epi, look at H & T

focal SAH symptoms

vasospasms → give nimodipine to treat

HHH- hypervolemia, hemodilation, hypertension

tx for neurogenic hyperventilation

paralyze pt to stop them from breathing on thier own

make sure you sedate patient and give pain meds

arterial blood gases look at what

venous blood gases look at what

arterial: O2 delivery

venous: O2 consumption

signs of DIC

oozing at IV site, pink tinged endotracheal sputum, blood in urine or tears

number 1 shock tx

isotonic fluid

what type of fluid is blod

colloid

first thing to do if there is a change in cardiac rhythm

go and assess the pt first

all renal injuries cause what

decrease GFR

renal failure TX

strict I/O, fluid restriction, avoid K, possible diuretic use

case study:

Pt with PA catheter: low CVP, low PAD, SVR high, CI low, urine output low; no improve after 2 fluid bolus, hbg of 6.2

what is the tx

give blood

what to know how to see on EKG

the rhythms we have learned (no HB)

pacemaker → failure to sense, failure to capture

early signs of elevated ICP

mental status changes

irregular breathing

optic nerve swelling

Acute renal injury diagnosis and tx

look at labs, will have increased Creatinine, creatinine clearance, BUN, and K

loop diuretic is patient is still having output to force fluid through kidneys, CRRT, kidney rest

causes: renal toxic agents, dye, IV antibiotics

adverse effects of TPA

hemorrhage

assessment findings for a CVA

focal symptoms that affect the side opposite of the brain damage

difficulty swallowing, slurred speech, facial droop, aphasia, double vision or any visual changes, numbness and tingling

clinical findings and tx for critical illness induced adrenal insufficiency

liable glucose with no apparent cause on a patient not receiving external insulin

tx: give steroids

P/F ratio calculation

pO2/FiO2 (FiO2 as a decimal not a percent)

R HF s/s

L HF s/s

R= rest of body → edema, cool pale skin

L= lung → fluid backing into lung, increase work of breathing, sputum, chronic cough

both patients will have fatigue and poor exercise tolerance

diastolic HF

normal EF but low CO

causes: LV hypertrophy (heart stiffening and cannot relax to fill) or aortic stenosis

typically from uncontrolled HTN

tx: antihypertensives

systolic HF

low EF

causes: multiple MIs leading to stiffening of tissue and aortic insufficiency (regurg)

the heart fills with blood but cannot pump it out

tx: optimize preload and contractility

A fib symptoms

hypotension r/t loss of atrial kick, SOB, palpitations

metabolic acidosis

pH less than 7.35

HCO3 less than 22

caused by diarrhea, compensating will see a decrease in CO2

metabolic alkalosis

pH greater than 7.45

HCO3 greater than 28

caused by vomiting or pumping stomach

respiratory acidosis

pH less than 7.35

CO2 greater than 45

caused by hypoventilation

respiratory alkalosis

pH greater than 7.45

CO2 less than 35

caused by hyperventilation

hypovolemic shock s/s

weak thready pulse and tachycardia

decrease CO, CVP, and urine output

hypotension and poor oxygenation

increase SVR

cool pale skin with poor cap refill

septic shock pt

increase CO and low SVR

bounding pulse, hypotension, tachycardia

warm and pin initially but as they get worse they become cool and pale

increased O2 levels r/t cellular dysfunction

fever, increased RR, WBC and C reactive

cardiogenic shock

pump failure, heart cannot pump enough to meet perfusion demands

pulmonary edema, JVD

weak pulses, hypotension, increase HR, cool and clammy skin

increase CVP and SVR and decrease CO

distributive shock

damage to blood vessels causing them to be leaky

low SVR and extreme vasodilation

at first high CO but it will decrease as fluids move into interstitials spaces

warm and pink pt

obstructive

something is preventing blood from going in or out of heart

remove obstruction