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Alkalosis/Acidosis:
o Metabolic alkalosis: vomiting, nasogastric suction
o Respiratory alkalosis: hyperventilation
o Metabolic acidosis: diabetes
o Respiratory acidosis: respiratory failure
ABG values:
o pH: 7.35-7.45
o CO2: 35-45 respiratory
o HCO3: 22-26 metabolic
o PaO2: 80-100
o O2 sat: >92%
Heart failure
Every one of these patients will have diuretic, oxygen, continuous heart monitoring
Need to know:
Vascular
PAD:
ABI
Ankle/brachial index-- shows that what percentage of blood flow is flowing through
the ankle and arm, must be supine, 100% means no disease, if they are less than
<0.8 they must be seen for that
Ankle pressure: 50, brachial: 100, 50/100 x 100 this means you have 50%
blood flow impairment in your leg
You can teach about what the percentage means, it is in accordance to
nursing practice
If we want to prevent it from getting worse, and it asymptomatic, treat the
risk factors (smoking, HTN, etc.)
<0.7 start to have symptoms
<0.3 this is considered acute ischemia
- Claudication is specific for PAD, decreased blood flow to the leg, they start to
have pain when they walk and limp but is relieved with rest (on test 2/3), it is
reproducible pain
- Thrombosis: acute ischemia
o Clot in major arteries
o Acute ischemia is more emergent than PAD
o Cause of acute ischemia: platelet aggregation injury, underlying
disease, underlying PAD, acute injury (to the lumen of the vessel)
o Assessment Symptoms: cold, severe acute pain, pallor, paresthesia,
paralysis, pulselessness [report these five symptoms: rush to surgery]
o Treatment: no lifestyle modifications surgery is the only option
[angioplasty or bypass] (within 24 hours, hopefully within 12: because
there will be tissue death, losing toes)
Anyone with PAD should be taking an antiplatelet
-
5 P’s
- The five P’s: pain, pallor, paresthesia, paralysis, pulselessness, poikilothermia
- Vasospasm: Reynaud’s
o More often in women
o Predisposed from cold environment (exposure to cold)
o Occurs in small capillaries typically in the hand
o It does not stay in this state long enough to turn black
o Vasospasm of the capillary beds in the hands
o Assessment symptoms: hands, pain, pallor
o Treatment: wear gloves/protective clothing, avoid cold
(winter/freezer), avoid triggers, Med: CCB (prevent vasospasms)
- Inflammation: Beurger’s
o Acute inflammation in small capillaries
o More often in men
o Predisposed by smoking this does not go away until you stop
smoking
o This one will slough off tissue, kill tissue
o Assessment symptoms: pain, necrosis, gangrene, any extremity
o Treatment: quit smoking
- edema
- pain/tenderness
- warm skin
- erythema/redness
- sense of fullness
- paresthesias
- dilated superficial veins
- slight temperature over 100.4
- duplex ultrasound.
- Based on the dose, some of these medications can also be used to prevent VTE
in at-risk patients. When you give 5,000 units of Heparin in clinical (or 40mg
Fragmin) for example, you are most likely administering the prophylactic
dose, NOT a treatment dose.
o Heparin: Serious side effect – HIT (Heparin Induced
Thrombocytopenia),
o IV Heparin: What lab do you monitor? – aPTT,
o tPA: Class – thrombolytic,
o Lovenox: Class – Low molecular weight heparin,
o warfarin (Coumadin): Class – Vitamin K antagonists,
o warfarin (Coumadin): What lab do you monitor? – PT/INR,
o Heparin: Class – thrombin inhibitor,
o rivaroxaban (Xarelto): Class – Factor Xa inhibitor
- In chronic venous insufficiency there is long-term vascular abnormalities and
impaired blood flow. This can eventually lead to changes in the skin, venous
leg ulcers, and long-standing pain.
- On the left is a picture of a venous leg ulcer, on the right is a picture of
vascular browning (the skin of the lower leg becomes leathery with a
characteristic browning color from hemosiderin deposits).
- Need to know:
o Warmth and palpable cord over vein venous thromboembolism
o If giving vitamin K, you must know the prothrombin time because it
what is affected by coumadin
o VTE diagnosed by duplex ultrasound
o If patient has phlebitis Remove IV
o Daily enoxaparin is for preventing blood clots
o If patient is taking Cardizem for Raynaud’s phenomenon, it will show
improvement by improving finger perfusion
o Compression stockings are not for PAD (rest pain)
o Venous insufficiency dry itchy flaky skin
o PAD assist to walk after surgery
o Lovenox leave air bubble
o Enoxaparin is low weight use for DVT ineffective is leg swelling
ARTERIAL VENOUS
Kidneys
- Creatinine- More reliable than BUN as a determinant of renal function. Creatinine is end
product of muscle and protein metabolism and is released at a constant rate. Reference
interval: 0.6-1.3 mg/dL (53-115 μmol/L).
- BUN: 6-20
- BUN/Cr ratio: 12:1
- Uric acid: 2.3-6.6
- Sodium 135-145
- Potassium: 3.5-5
- Calcium: 8.6-10.2
- Phosphorus: 2.4-4.4
-
UTI:
Clinical Manifestations: dysuria, frequent urination, urgency, hesitancy, post void dribbling,
and suprapubic discomfort or pressure. The urine may be discolored and/or cloudy.
In older adults, the only s/s of a UTI is often confusion. They frequently do NOT have fevers
with a UTI.
Treatment/Nsg Interventions:
As nurses, we always want to care for the immediate needs of the patient. However, we also
are thinking ahead to prevent any complications of the pathological process occurring in the
body.
There are 2 main complications of UTI's that you need to be aware
of - pyelonephritis and urosepsis.
Pyelonephritis is a severe upper urinary tract inflammation, caused when the organism
(bacterial, viral, fungal..) has ascended through the bladder and up into the kidney itself. In
addition to the s/s of a UTI, patients with pyelonephritis also have flank pain (CVA
tenderness), fever, and chills. These patients can have fevers for days, even with
improvement.
Nursing Interventions: You'll get a UA and a urine culture, and expect to see orders for a
CBC (monitoring white count) and even blood cultures (to see if the infection has spread
into the blood stream). Antibiotics are needed, as well as fluids (IV and PO), close
monitoring of I &O and vitals, monitor urine characteristics, administer NSAIDs for pain and
fever, and monitor for sepsis (remember, sepsis is NOT the same as an infection in the
blood).
Urosepsis: You'll cover sepsis senior year, but for now I want you to know that sepsis
is systemic inflammation, often caused by a bacterial or viral organisms. When named
urosepsis, the sepsis is caused by a urinary source (i.e. a UTI or pyelo). Urosepsis can be
fatal, so monitoring for this complication is crucial.
Nephrotic syndrome
Clinical Manifestations:
ascites
anasarca
hyperlipidemia (decreased serum proteins stimulates the liver to undergo lipoprotein
synthesis (as body is searching for way to get protein) --> hyperlipidemia)
massive proteinuria
hypoalbuminemia
Fun fact: hypercoagulability is common, because the anticoagulant proteins are lost in
the urine)
Nursing Interventions: We'll focus on the ones that deal with the edema:
daily weights
accurate I & O
grading of edema
replace protein by diet (you can give IV albumin, but it's debated on if this really helps.
The best way to increase albumin levels is by diet, but it takes TIME)
Also you'll want to monitor for infections (as the immune system is weakened).
Bladder outlet obstruction - often in men this obstruction is an enlarged prostate. Any male
that is voided small amounts frequently should be bladder scanned to determine their post-
void residual (PVR).
Surgical interventions (TURP) to help treat prostatic enlargement and/or urethral strictures if
the cause of the retention is an obstruction
• Arteriovenous Fistula- feel turbulence, there is a thrill, use bell because it’s a high-
pitched noise, assess access site: palpate & auscultate AVF, Check Distal pulses and
Circulation
Pre/Intra/Post renal causes of AKI
- Prerenal. Prerenal causes of AKI are factors external to the kidneys. These factors reduce
systemic circulation, causing a reduction in renal blood flow. The decrease in blood flow leads
to decreased glomerular perfusion and filtration of the kidneys. Although kidney tubular and
glomerular function is preserved, glomerular filtration is reduced as a result of decreased
perfusion. LOW CO, hypovolemia
- Intrarenal. Intrarenal causes of AKI (see Table 47-2) include conditions that cause direct
damage to the kidney tissue, result- ing in impaired nephron function. The damage from
intrarenal causes usually results from prolonged ischemia, nephrotoxins (e.g., aminoglycoside
antibiotics, contrast media), hemoglobin released from hemolyzed red blood cells (RBCs), or
myoglobin released from necrotic muscle cells. ATN
- Postrenal. Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As
the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function.
The most common causes are benign prostatic hyper- plasia, prostate cancer, calculi, trauma,
and extrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis (kidney
dilation), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive
decline in kidney function. Hyperplasia calculi
A dissecting abdominal aortic aneurysm is a prerenal cause of AKI because it can
decrease renal artery perfusion and therefore the glomerular filtrate rate.
Remember how preload is almost synonymous with volume? The same is true
with prerenal causes of AKI - prerenal causes are almost always due to
a hypovolemic state. In a dissecting AAA, the patient is losing volume.
Aminoglycoside antibiotic administration, a hemolytic blood transfusion
reaction, and post-streptococcal glomerulonephritis are all intrarenal causes of
AKI. This is because these items all cause direct damage to the kidney tissue.
Aminoglycosides
Aminoglycosides: “a mean-old-mycin”
- Mean: treat serious illnesses, significant side effects/toxicity issues
- Mycin: all end in -mycin or -micin
- Used for resistant infections: MRSA, VRE, MDR,
- Used for systemic infection: multi-lobed pneumonia leading to sepsis (not for ear infection or
UTI)
- Toxicity: these meds cause ototoxicity (causes ear damage)
o assess for hearing, balance, dizziness
- Toxicity: these meds also cause kidney damage
o assess creatinine lab, GFR
- Toxicity: these meds cause damage to cranial nerve 8 (ear nerve), and should not be given more
than every 8 hours
There are 3-4 questions about Heparin/Coumadin. This table helps compare/contrast them
Heparin Coumadin
Prevents clots from forming (does not break up
Prevents clots from forming (does not break up clots)
clots)
Lovenox is a viable alternative (low molecular weight
apixaban (Eliquis) is a viable alternative
heparin)
Works immediately Takes days to reach therapeutic level
Used short-term (days/weeks) Used long-term (may be lifelong)