SI Flashcards
4 Key interventions for sepsisw
Lab Diagnositics (Serum lactate and blood culture)
IV Fluids (Bolus isotonic fluid through large IV Port)
Antibiotics (Broad spectruum at first then narrow once result of blood culture are back)
Moniter: VS QH x6 hours, then Q4 for 12 hours
How often do you moniter as a sepsis intervention
VS QH x6 hours, then Q4 for 12 hours
And SPO2
LOC (GCS)
Urinary output (Catheter) - at least 25/30mL per hour
T1 vs T2 DM
T1: NO insulin; Early start (Non mod risk factors)
T2: SOME insulin production; not enough insulin or it’s ineffective
Diagnosis of DM
A1C > 6.5%; FBG> 7mmol/L, RBG > 11.1mmol/L
Recognizing the difference bw T1 vs T2
T1; Early onset, often w/ polyuria, polydipsia, polyuria cachexia (Starved) appearance
T2: Late onset normally, P neuropathy, fatigue, decreased cisual acuity, slow wound healing
Treatment for T1DM
Insulin
Treatment for T2DM
First lifestyle changes, second antihyperglycemic third insulin
Prediabetes
Disease process trending towards diabetees (IFTG 6.1-6.9mmol/L)
Secondary DM
Those with schizo, Cushings, Cystific Fibrosis etc.
Dyslipidemia
Abnormal Cholesterol
Most modifiable risk factor for DM
Abdom obesity
Type 2 DM is basically caused by an issue with which process
Insufficent insulin
Insulin resitance
Tired pancreas
Liver makes too much glucose hormones
ABCDESSS for DM
A1C - ideally less than 7%
BP less 130/80
Choleterol : LDL < 2.0 mmol
Drugs to protect the heart (Statin, ACE inhibitors)
Exercise and diet
Screening
Smoking cessation
Self management
Alpha cells produce
How to differntiate bw DKA and HSS
DKA happens bc NO insulin in the body (Therefore usually DMT1)
- Very easy to recognize
- Very sudden onset
- Breaks down ketones
- Ketones drop blood pH (Metabolic acidosis)
- Fast breathing (tachypnea)
- Fruity Breath
- Polyuria (Body excreting glucose + Blood volume increase)
- Fluid deficit causing polydipsia
HSS pts has SOME insulin - very high BG
- Slowly symptoms get more severe
- Super dehydrated (Water ism oving out of cells into blood to dilute all the glucose)
- No ketones
- No blood pH changes (NO acidosis)
Know hypoglycemic protocols
What to do first when you have a DKA pt
Stablize ABCs
Call MD
Check V/S
O2 infusion
Fluids
Correct electrolytes
Check BG QH
Check electrolytes
Macrovascular Complications
R/t development. of atherosclerosis on large BVs
- Increase risk for thrombus formation etc.
Microvascular complications pathoology
Thickining of cap basement membrane, capillaries harden adn ischemia of the rest
Retinopathy ID/treatment
Best treatment is prevention
Do regular eye exames BIY
Nephropathy ID/treatment
Good glycemic and BP control, annual screening for microalbuminuria
Neuropathy ID/Treatment
Sensory: Distal symmetrical neuropaty: Paresthesia, numgess, tingling
Tx for HHS
Slow fluid replacement
Insulin bolus
Electorlytes as needed
Chronic Stable Angina
Predictable (It’s happened before)
Same precipitating fcators
Relieved when precipitating factor is releived (Nitro or at rest)
Pain lasts 3-5 minutes
(COnstrictive, squeezing, heavy, choking pain)
Unstable Angina
New in onset
Occuring at rest or as a worsening pattern
Medical Emergency
No tissue death, no ECG chnges
NSTEMI
Partial thickness blockage MI
leads to thrombus formation
Occluded vessel = Where muscel will die
Less dramatic manifestation than STEMI
STEMI
Full thickness blockage MI
Same s/s as NSTEMI but faster onset + Progression
Usually look shocky/impending doom
Goal: Angiogram in 90 minutes (Only at RCH)
Heart attack pain
Heaviness, pressure, squeezing
Mneumonic if someone has chest pain
Precipiating
Quality of pain
Radiate
Severity (1-10)
Tining (Come and go, happening all the time)
If there are signs of a heart attack, what is the next step
Call MD
Order ECG
After MD has been called, ECG has been done, what nexted
Full CV assessment + VS
After assessment, what is the last thing to do
Check labs
Looking for treponin changes and ECG changes
Side effect of beta blocker
Drops BP
Heparin does what
Prevents clots from forming
Nitro would be effective if the patient was
Relieved of pain
Which ECG change is most importnat?
ST elevation
You conduct an assessmnt on a patentient who expereienced STEMI 2 previously, what is a VERY concerning sign
Crackles bilaterally in mid lobe of lungs
ASA does what
Dissolves thrombus formation, does not remove plaque
Troponin panel tells
How much/fast is the heart dying
IV NacCL is given to a MI pt
To increase BP
Angina vs MI
Chest pain vs heart attack
Pathological basic for clinical manifestations
Ischemia causing pain
Backflow of blood into lungs causing crackles
Why wouldnt nitro or morphine be given for an MI?
If it is an inferior MI it could cause a sudden drop in BP
When is PCI indicatied for a STEMI versus “fibrinolysis”
Increased SNS in CHF
Increased HR and myocardial contractiltiy
Will not last forever, 1st mech, BUT probably LEAST effective
Neurohormonal response to CHF
RAAS system
Release of aldosterone to retain NA and H2O thus increasing preload
Eventually wil lead to systemic congestion and pripheral edema
Cardiac decomp response to CHF
Can’t maintain adequate cardiac output therefore insuffiecnt perfusion
Ventircular remodelling/hypertorphy repsonse to CHF
Larger, less efective pump
Increaed muscle mass r/t increased workload
Conutnererulatory ANP and BNP released wh4en too much blood volume in the heart
Ventricular Dilation response to CHF
Enlargemengt of the heart chambers and elevated rpressue increase force of contraction
Overtime decreased elasticity leading to decreased cardiac output
L Sided HF
Backup of blood atrium and pilmonary veins
Pulmonare yedema, lung crckles, SOB, paroxysmal dsypnea, cough with frothy blood tinged spututm
R Sided CHF
Backwards flow of blood into the right atrium and venous circulation
JVD, peripheral edema, spleen and liver enlargement
Nursing implications for CHF
Diuretics decrease fluid (venous returen
Ace inhibs- decrease vasc ressistance
Beta blockers- decrease HR and BP
Vsodilators - increases O2 supply to heart
Digoxin - increaes CO and contractiituy *toxicity
Acute Decompensated HF
The worst
Wjhen compensatory mechs failm it will manifest and PE often caused by an MI
S/S: SOB etc
Nursing implicaitons of nutritional therapy
Na resticitoin,
Fluid restiriction
Report weight gains
ACE inhibs end in
-PRIL
What causes a TIA
Caused by a microemboli
Symptoms of TIA
Same symptoms of normal stroke, temporary altered LOC lasting LESS than 24hr
It is different because it resolves on it’s own
Thrombotic stroke symptoms
Slow and progresseive, mane not have altered LOC in first 24hr
Embolic stroke sympomts
Suden, no chance for collateral circulation to form
Often emoblic strokes are r/t which condition
Afib
Intracerebral brain patho
Bleeding into the brain that occurs during activity
Sudden onset
Subarachnoid stroke patho and s/s
Intracranial bleeding into the CSF “silent killer”
Projectile vomiting
Headache
N/V
Manifestatoins of stroke depend on whether it is hem or ischemic
No, depends on where the stroke occurs
R side stroke
Paralyzed on L side
Spatial deficiets
Spontaneous, impaired judgement
Deny/miniize problems
L side stroke
Opposite soide stroke
Aphasias
Impaired R and L discriminations
Knowledge of deficits (depressions)
Impaired language and math abillities
Is a TIA a stroke?
NO
A patient experiencing TIAs is scheduled for a carotid endarterectomy.
The nurse explains that this procedure is done to:
To prevent a stroke by removing atherosclerotic plaques blocking cerebral blood flow.
When monitoring a patient post-hemorrhagic stroke, which of the following identify that the patient is demonstrating signs of increased ICP
a) Increased Systolic Blood Pressure
c) Bradycardia
d) Bradypnea
In the care of a patient with a post-hemorrhagic stroke, which of the following are applicable interventions in cases of increased ICP due to cerebral edema? Select all that
Administration of Mannitol
c) Neurological Assessment as per protocol.
d) Elevating HOB > 30°
Best intervention for acute peripeheral ischemia
Pt to remain lying supine as to not change pressure on thrombus clot
Which topic should the nurse include in patient teaching for a patient with a venous stasis ulcer on the left lower leg?
Which topic should the nurse include in patient teaching for a patient with a venous stasis ulcer on the left lower leg?
What type of wound dressing promtoes healing in venous stasis ulcers
Clean but moist environment
“I can’t get my shoes on at the end of the day.” Aligns best with what diagosis
PVD
A 45-year-old patient is admitted to the hospital complaining of a new “sharp, tearing” pain to her chest.
Based on the quality of her pain, what do you initially suspect?
The patient may be having an aortic dissection
Role of K+ and why it shifts
Too much glucose
Water moves into bloodstream to dilute
When cells are dehydrated they die
Releasing potassium into bloodstream
Why does hyperkalmeia occur in DKA
H+ ions that are in bloodstream from acidosis are moved into cells to try to decrease acidioty, kicking K+ ions into bloodstream
Hyperglycemia causes hyperKalemia
Tx (Fluids and insulin) can cause hypokalmeia as it moves back into cells
Therefore Potassium might need K+ supplements
Which blood tests indicate a positive diagnosis of DKA?
a) Blood test positive for beta hydroxybutyrate
c) RBG = 20mmol/L
d) K+ = 5.8
Cheyne stokes resps
Very shallow spread out
Most significant risk factor for DMT2
Abdom obesity
The nurse is caring for a patient who is hospitalized with diabetes mellitus. Which of the following laboratory test results would provide information related to the patient’s past glucose control?
c) glycated hemoglobin
Which of the following laboratory results follows the expected pattern accompanying macrovascular disease as a complication of diabetes?
Increased triglyceride levels (low density lipoprotieins
HF simply means
Fluid overload
Acute decompensated HF interventions
Often caused by an MI. Happens FAST
GET HELP AND ECG. CALL A DOCTOR.
IV diuretics and fluid restriction. Fix the cause (if NSTEMI or STEMI). 02 therapy prn, high positioning, deep breathing. Manage BP.
Interventions should occur RIGHT NOW.
the time She has hen a Exerdered that sining fargement ore al patient displaying flect
ventricular hypertrophy
c) Cardiac decompensation
For which of the following conditions is percutaneous coronary intervention (PCI) most clearly indicated?
Acute MI
Your patient has +2 pitting edema to lower calfs, weight gain, and paroxysmal nocturnal dyspnea. How would you classify their HF?
left and right sided
Is flushing a symptom of an MI?
No
For your preceptorship, you decide to go work for northern health where you work at the only hospital in a 300 km radius. A patient presents to you with crushing and heavy chest pain. An ECG shows that the patient is having a STEMI.
Give pt TNKase (Clot buster)
Intreventions for chest pain
PQRST (Hx is most important)
Order ECG
Full CV assessment w/ VS
Blood test (troponins)
