Critical Care Flashcards
ARDS leads to
acute resp failure
what is ARDS
inadequate exchange of o2 and carbon
there is increased permeability which leads to fluid buildup in the alveoli which furthers the interference with gas exchange
what are initial manifstions of ARDS
nonspecific
XR initially of ards
normal
s/s of ARDS
refractory hypoxemia, dyspnea, bilateral pul edema, infiltrates (white out)
what to do before ABG
allens test
early s/s of any shock
agitation
restlessness
- due to cerebral hypoxia
all types of shock can lead to
SIRS
and MODS
which one first
- fluids
- pressors
fluids
drugs that increase preload
crystollids
blood products
drugs that decrease preload
morphine
nitrates
diuretics
drugs that increase after load
vasopressors
dopamine
drugs that decrease afterload
nitroprusside
ACEI
ARB
drugs that decrease contractility
beta blockers
CCB
drugs that increase contractility
dig
dobutamine
neurogenic shock HR
bradycardia
what position for cariogenic shock with pulmonary edema and why
high fowler to decrease venous return to left ventricle
when does the intraortic ballon inflate
diastole
DIC blood values
PT (increased), PTT (increased), fibrinogen (decreased), platelets (decreased), fibrin degradation/split products (increased)
S/S of dic
petechiae, purpura, bleeding from IV sites, hemoptysis, mental status change, hypotension
nursing considerations for DIC
minimize needle sticks, gentle oral care with swabs, turn frequently, minimize BP readings taken by cuff
DIC tx
heparin and blood products
s/s preceding a MI
chest pain usually described by crushing, change in stable angina, not relieved by nitro
when there is acidosis what is a nursing consideration
reduce PCO2 by increasing ventilation
what can exacerbate acidosis by producing CO2
bicarb
when do we use bicarb
hyperkalemia, TCA overdose, or pre-existing metabolic acidosis
H and T’s
hypovolemia, hypoxia, hydrogen ion acidosis, hypokalemia, hyperkalemia, hypoglycemia, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis, and trauma
what systemic change can occur with kidney damage
- blood
will result in decreased erythropoietin production and then reduced number of RBC and ultimately reduced O2
dehiscence
muscle
eviseration
organs
NSAID action
Inhibiting prostaglandins and other chemical mediator synthesis involved in pain (ibuprofen)
se of morphine
resp depression
stages of grief
Denial, anger, bargaining, depression, acceptance
hemorrhage results in
fall in blood pressure; elevated heart and respiratory rates; thready pulse; cool, clammy, pale skin; and restlessness
stages of shock
initial
nonprogressive
progressive
refractory
inital
- map decreased by
10
inital
- are there compensatory mechanisms
yes
inital
- lactic acid present? why if yes
yes, oxygenaition to vital organs is maintained but some tissues move into anaerobic metabolism leading to the production of lactic acid
inital
- HR and RR
increased
inital
- diastole increase or decreased
increase
NP
- MAP
decrease by 10-15
NP
- what happens in non vital organs
hypoxia
NP
- ph and electrolyte
acidosis
hyperkalemia
s/s of NP
thirst
anxiety
restlessness
tachycardia
increase RR
decerase UO
falling systolic and diasoltic
progressive
- MAP
decrease of 20 or more
progressive
- vital organs
hypoxic
progressive
- non vital organs
anoxic and ischemic
progressive
- blood level
low pH
rising lactic
rising potassium
what is happening in refractory
too much cell damage causes massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome
S/s of refractory
rapid loss of cons.
nonpalabale pulse
cold
dusky
slow and shallow reps
unmeasurable o2
the stress of severe sepsis can cause adrenal insufficiency so what drug may be given
IV hydrocortisone
oral fludrocortisone
1st line pressor
neorepi
- levo
what med given as continuous infusion of 200mg per day is recommended only for the patient in septic shock who remained hypotensive despite adequate fluid resuscitation and pressors
hydrocortisone
primary MODS
results from a well-defined insult in which organ dysfunction occurs early and is directly attributed to the insult itself. Direct insults initially cause localized inflammatory responses. Primary MODS accounts for only a small percentage of MODS cases. Examples of Primary MODS include the immediate consequences of posttraumatic pulmonary failure, thermal injuries, AKI, or invasive infections.
secondary MODS
consequence of widespread sustained systemic inflammation that results in dysfunction of organs not involved in the initial insult. Secondary MODS develops latently after an initial insult. The early impairment of organs normally involved in immunoregulatory function, such as the liver and the GI tract, intensifies the host response to the insult. The initial insult may prime the inflammatory system in such a way that even a mild second insult (hit) may perpetuate a sustained hyperinflammatory response. This “two-hit hypothesis” has been increasingly recognized as an important contributor to morbidity and mortality in patients with Secondary MODS.
what are the most common events in the development of 2ndary mods
SIRS and sepsis
hyperkalemia EKG
peaked T waves, a widening of the QRS interval, and, ultimately, ventricular tachycardia or fibrillation
diagnosis for DKA
Blood glucose greater than 250 mg/dL,
pH less than 7.3
Serum bicarbonate less than 18 mEq/L
Moderate or severe ketonemia or ketonuria
why do ketoacidosis occur
free fatty acids are metabolized into ketones and acetone
what causes the fruity odor of DKA
acetone
when is DKA resolved
blood and urine free from ketones
DKA presentation
complaints of malaise, headache, polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive hunger). Nausea, vomiting, extreme fatigue, dehydration, and weight loss follow. Central nervous system depression, with changes in the level of consciousness, can lead quickly to coma. The patient with DKA may be stuporous or unresponsive, depending on the degree of fluid-balance disturbance. The physical examination reveals evidence of dehydration, including flushed dry skin, dry buccal membranes, and skin turgor that takes longer than 3 seconds to return to its original position after the skin has been lifted. Often, “sunken eyeballs,” resulting from lack of fluid in the interstitium of the eyeball, are observed. Tachycardia and hypotension may signal profound fluid losses. Kussmaul respirations are present, and the fruity odor of acetone may be detected.
why do low K with DKA
occurs as insulin promotes the return of potassium into the cell and metabolic acidosis is reversed
Hypokalemia can occur within the first hours of rehydration and insulin treatment. Continuous cardiac monitoring is required because low serum potassium (hypokalemia) can cause ventricular dysrhythmias.
why do DKA get hyperkalemia
acidosis
what do nitrates and nitrites do
cause relaxation of the muscle fibers in the walls of the blood vessels. The relaxation increases the width of the vessels and reduces the pressure of the blood flow through the mucous membranes of the mouth, stomach, or lungs.
s/s of diabetic retinopathy
loaters, loss of vision, and difficulty with color perception
glargine
long acting
no peak
s/s of diabetic neuropathy
educed ability to feel pain or sense temperatures, muscle weakness and difficulty walking, and extreme sensitivity to touch
alkaline urine cause
infection
alt meds for penicillin
mycin
what can low albumin levels do to drugs
can result in toxic effects, this affects the distribution of drugs and influence of drug to drug interactions
how can decrease CO affect medication half life/excretion
Decreasing cardiac function is responsible for about 50% of blood flow to the kidneys, leading to reduced kidney efficiency. Drugs are not filtered as quickly from the bloodstream, which increases their half-life and leads to toxicity.
normal phos levels
2.4-4.4
pernicious anemia nursing consideration
require B12 IM injections
what is the purpose of epi in code situations
increase CO
