Renal/Electrolytes Flashcards
1
Q
Main functions of the kidneys:
- Cleanse and detoxify blood
- Filtration
- Reabsorption of water, electrolytes, amino acids
A
- Secretes water and wastes
- Acid/base balance
- BP regulation
- Erythropoietin production
- Electrolyte embalance
2
Q
Approximately, what percent of cardiac output goes to the kidneys?
A
~ 20%
3
Q
Name the 5 parts of the nephron:
A
- Glomerulus: the major filter of the nephron, the workhorse
- Proximal convoluted tubule: Reabsorption
- Loop of Henle: Job is to concentrate urine
- Distal convoluted tubule: “Fine tunes” by regulating pH, Na, K, Ca, and amino acids
- Collecting duct:
4
Q
The glomerulus is a network of capillaries that does what?
A
Filters blood.
“Workhorse” of the nephron
5
Q
The Proximal Convoluted Tubule reabsorbs what 4 things?
A
Reabsorbs water, sodium, amino acids and glucose.
6
Q
The Loop of Henle reabsorbs what 2 things?
A
Concentrates urine.
Reabsorbs water and sodium.
Where loop diuretics work (Lasix) by preventing urine concentration, thus diuresing… also, leading to loss of electrolytes
7
Q
What 4 things are regulated in the Distal Convoluted Tubule?
A
“Fine tunes.”
Regulates pH, K, Na and Calcium
8
Q
What is collected in the collecting duct?
A
Collects urine from the nephrons.
9
Q
The two major hormones involved in fluid balance?
A
ADH and Aldosterone
10
Q
Thirst, ANP, RAAS, ADH and &Aldosterone all help regulate what?
A
Fluid balance
11
Q
What hormone causes retention of Na and H2O?
( It is also released if hyperkalemic )
A
Aldosterone
Again, hyperkalemia leads to aldosterone excretion. The aldosterone triggers potassium excretion via the kidneys.
12
Q
This peptide triggers the kidneys to excrete water when the atria are overstretched:
A
Atria-natriuretic peptide (ANP)
13
Q
When this system is triggered, it leads to the kidneys to hold onto water:
A
Renin Angiotensin Aldosterone System (RAAS)
14
Q
Where is aldosterone synthesized?
What 2 triggers cause adrenal gland to make aldosterone?
A
Cortex portion of adrenal gland on top of kidneys; aldosterone is made from cholesterol.
Triggers:
1. When angiotensin II comes around (The conversion of angiotensin I to angiotensin II is catalyzed by an enzyme called angiotensin-converting enzyme (ACE). ACE is found primarily in the vascular endothelium of the lungs and kidneys. [To start the system or cycle, when blood pressure falls, your kidneys release the enzyme renin into your bloodstream. Renin splits angiotensinogen, a protein made in your liver and releases the pieces. One piece is the hormone angiotensin I.])
- When an elevated level of potassium ions are detected
15
Q
What do we call it when urine output is less than 100 mLs a day?
A
Anuria
16
Q
What is it called when urine output is between 100-400 mL/day?
A
Oliguria
17
Q
What is it called when urine output is about 1500 mLs per day?
A
Normal
0.5 mL/kg/hr
Ex 1: 45 kg/ 100 lbs ~ 23 mL/hr
Ex 2: 82 kg/ 180 lbs ~ 41 mL/hr
18
Q
If someone puts out >2500 mL/day, what is it called?
A
Polyuria
19
Q
What is azotemia?
A
Acute rise in BUN (blood urea nitrogen)
(BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body
Will cause altered mental status if it gets too high (~90 peds, 150 adults? not hard # out there)
20
Q
What (r/t kidneys) is used to evaluate kidneys’ ability to remove waste products?
A
GFR: Glomerular Filtration Rate
- Measurement of how much filtrate is made by the kidney (mL/min)
- Estimated by assessing creatinine clearance. (males have slightly higher creatinine clearance than females)
- Isolated plasma creatinine is NOT a sensitive marker for GFR in early stages of kidney injury
21
Q
What are the cylindrical structures formed by the kidneys in certain disease states, such as ?
Where are they released from?
How are they detected, diagnosed?
A
- Urine casts. Sign of tubular distress/damage.
- Distal tubules and collecting ducts.
- Urinalysis
22
Q
What is the following a definition of:
an abrupt decrease in the GFR?
A
Acute Kidney Injury (AKI)
Pt will begin to experience metabolic acidosis r/t build up of waste… may also have accompanying respiratory acidosis r/t pulmonary edema 2/2 to fluid overload.
23
Q
What % of hospitalized pts have some degree of AKI?
What % of ICU pts have some degree of AKI?
Avg hosp cost of AKI event?
A
~5%
~30%
17K
24
Q
What is the mortality rate for those who develop ATN?
A
~50%
Drops to 30% if they survive the first year.
25
Classic sign of ATN in the hospital?
acute tubular necrosis
Someone who gets hemodialysis for the first time.
26
What are the following risk factors for?
Elderly
Female > Male
HF
Existing renal insufficiency
Elevated BMI (>32)
COPD
Liver disease (HRS: hepatorenal syndrome)
Sepsis
GI Bleeding
Burns
Medications (vanco, Gent, antivirals)
AKI
Also:
Multi-system organ dysfunction
Hypotension
Trauma injury
Rhabdomyolysis
Contrast
kidneys and liver works side by side, if one fails, the other may start to fail.
27
RIFLE Criteria. What does RIFLE stand for?
FYI: This criteria can assist with preventing further kidney injury by assessing Cr levels prior to giving nephrotoxic Rx such as contrast... as well as diligent prevention of hypotension that decrease perfusion, etc.
Risk: Is the pt oliguric x 6 hr ( <0.5mg/kg/hr)? If not, 1-7 day decrease >25% in GFR, or serum creatinine x 1.5 sustained.
Injury: Oliguric x 12 hr OR GFR decrease >50% serum creatinine x 2
Failure: Adjust Cr or GFR decrease >75% or Anuric x 12 hr
Loss: Irreversible AKI or persistent AKI >4 wks
ESRD: > 3 months
28
Normal creatinine clearance?
80-120 ml/min
Note: Creatinine level has up to a 12 hr lag time.
29
Normal BUN/Creatinine ratio?
What is the most sensitive indicator of kidney function?
10:1 to 15:1
Urine output. BUN levels increase for quite a few reasons, Cr has the 12 hr lag time so we just track trends... urine output will be most accurate assessment.
30
What 3 main things are needed for treating AKI pts? (and protecting their kidneys)
1. Adequate hydration
2. Adequate perfusion
3. Stop nephrotoxic meds
31
Common labs for AKI evaluation?
- BUN
- Creatinine
- BUN/Cr ratio (normal 10:1)
- GFR
- UA --- casts (tubular cell death)
- Urine electrolytes
- Urine glucose
32
Causes of post-renal AKI?
OBSTRUCTION
1. Stone
2. Prostate
3. Infection
4. Neurogenic bladder
Can have a normal BUN/Cr ratio but will be elevated, ex: BUN 80, Cr 7.
33
Causes of PRE-renal AKI?
PERFUSION
1. Sepsis
2. HF
3. Trauma
4. Severe hypovolemia
34
BUN/Cr ratio in pre-renal AKI?
25:1
BUN elevates quicker than the Creatinine. If it isn't properly address, the Cr will continue to rise and may lead to ATN.
35
In early AKI, what will the urine sodium levels be?
What would their urine osmolality and specific gravity be like?
Low; < 10 mEq/L
(This is bc kidney's are holding onto Na and H2O)
Osmo and specific gravity will be high, urine will be concentrated.
36
Acute Tubular Necrosis (ATN), aka?
What are some causes?
Intrarenal Kidney Injury: damage w/in the nephron
mostly will always need some form of dialysis
Causes:
1. Hypotension
2. Glomerulonephritis
3. Diabetes
4. Rhabdomyolysis
5. Nephrotoxic medications
6. Shock states
37
What would BUN, Cr, BUN/Cr ratio, and treatment look like in ATN?
BUN: > 25 mg/dL
Cr: > 1.2 mg/dL
BUN/Cr ratio: Both elevated but still 10:1
* Treatment often requires renal replacement therapy (almost always need some form of dialysis).
* Prevent acidosis.
* Prevent electrolyte imbalances and uremia
* Stop nephrotoxic meds
38
What are the 2 types of ATN?
Causes of each?
1. Toxic ATN: better to have toxic than ischemic.
Causes:
* Drugs, bacteria
(Vanco, Gent, Aminoglycosides, antivirals)
2. Ischemic ATN
Causes: low perfusion
39
Differences between toxic and ischemic ATN?
Toxic is uniform and widespread damage. Recovery is quicker ( < 8 days) and is REVERSIBLE (as long as the cause is ID'd and stopped).
Ischemic has irregular damage along tubular membranes, tubular damage and cast formation. Cause: poor to no kidney perfusion. Recovery is longer ( >8 days ).
40
Which medication should an AKI pt avoid?
- NSAIDS
- Acetaminophen
- ACE inhibitors
- Opioids
NSAIDS
They have an affect on prostaglandins which control renal perfusion. NSAIDS big no no in setting of renal dysfunction.
Prostaglandins (PGs) with best-defined renal functions are PGE2 and prostacyclin (PGI2). These vasodilatory PGs increase renal blood flow and glomerular filtration rate under conditions associated with decreased actual or effective circulating volume, resulting in greater tubular flow and secretion of potassium. They’re, otherwise, part of the inflammatory response system and are synthesized at sites of injury.
41
What are the most nephrotoxic medications?
(There are 16 listed)
1. Acyclovir
2. Aminoglycoside abx: Gentamycin
3. Amphotericin B (antifungal)
4. ACE Inhibitors (Angiotensin-Converting-Enzyme Inhibitor... for tx of HTN & HF): most end in -pril: Lisinopril
5. ARBs (Angiotensin II Receptor Blockers... for HTN) Similar effect as ACE. Angiotensin is a chemical that constricts vessels. Ex: Ending in -sartan; Cozaar (losartan)
6. Beta lactam abx (named for beta-lactam ring in their chemical structure): PCNs, cephalosporins.
7. Cisplatin (chemotherapy Rx)
8. Contrast dye (IV, not oral)
9. Ciprofloxacin (abx; Cipro)
10. Immunoglobulins. An antibody. A large Y-shaped protein used by immune system to target bacteria/viruses
11. Methotrexate. Chemo and immunosuppressant.
12. NSAIDs (reduced renal plasma perfusion 2/2 affect on prostaglandins)
13. Rifampicin
14. Sulphonamides: broad-spectrum abx/antiviral
15. Triamterene: diuretic
16. Vancomycin
42
3 Phases of ATN?
Of those who survive (50% mortality), 62% will recover most of their renal function; 33% will have CKD; 5% require long-term dialysis.
1. OLIGURIC phase: insult to injury w/in 48 hrs, inability to excrete fluid/waste = sig increase in BUN/Cr, acidosis. Fluid overload; S3 heart sound. Elevated K, Mg, Phos. Calcium low. Urine Na low bc holding onto Na & H2O; specific gravity high.
2. DIURETIC phase: Lasts 7-14 days. Must watch potassium levels & Na. Will see gradual improvement in renal function. Increase in GFR & often develop polyuria; urine output 2-5 L/day; kidneys can often clear volume but not solute or waste. Urine spec grav low, urine osmo < 350, Na 20-40. Monitor for fluid deficit (they can get a secondary injury).
3. RECOVERY phase: Can progress to CKD (5 stages), GFR returns to < 80% of w/in 1-2 yrs
43
What are some pt factors/characteristics for highest risk of contrast-induced nephropathy (CIN)?
* DM, HTN, HF
* Pre-existing renal insufficiency
* Dehydrated
* Concurrent use of nephrotoxic meds (NSAIDs & abx)
* High volume of IV contrast (10% receiving dye=CIN)
44
How to prevent contrast-induced nephropathy (CIN)?
FLUIDS!!! "Key to pollution is dilution." Flush kidneys!
* NaHCO3
* Mucomyst
Not a lot of evidence to support *
45
When is dialysis indicated?
(AEIOU)
A: Acid/base imbalance
E: Electrolyte imbalance (hyperkalemia/mg/phos)
I: Intoxications (ODs/toxins) Ex. Acetaminophen, ASA
O: Overload (fluid)
U: Uremic symptoms (fatigue, nausea, loss of appetite, a metallic taste in the mouth, and mental confusion)
46
Lab findings in pts needing RRT (renal replacement therapy)?
BUN
Cr
Acidosis
Electrolytes
BUN > 35
Cr > 4 or increasing by 1 per day
Uncompensated metabolic acidosis
K+ > 6.5 (mag and phos also high)
Decreased Ca, HCO3
Abnormal urine electrolytes
47
Characteristics of Uremic Syndrome?
Neurological
Cardiovascular
Hematological
Pulmonary
GI
Neuro: lethargy/fatigue, seizures, coma
Cardio: EKG changes (hyperK), signs of fluid overload (tachy, S3 heart sound)
Heme: Anemia
Pulmonary: Crackles/Pulmonary edema, SOB/edema/effusions, pleuritis from uremia
GI: Decreased appetite, N/V, Ascites - fluid overload
* Time for dialysis
48
General treatment goals for AKI:
* Hemodynamic stability
* Improve renal perfusion
* Correct chemistry (Lytes/BUN/Cr)
* Electrolyte imbalance
* Adequate hydration/ careful use of diuretics
- Accurate, meticulous daily weights
* Aggressive dialysis
* Monitor drug levels (dilantin, dig, Gent, vanco...)
* Monitor coags (possible coagulopathy)
* Minimize nephrotoxin exposure
* Prevent infection
* Maintain nutritional state
49
Lab findings in CKD?
Hgb
BUN/Cr/PO4
Ca/HCO3/Protein
* Anemia
* BUN/Cr/PO4 all increased
* Ca/HCO3/Protein decreased
50
What are the biggest RISK FACTORS for CKD?
(there are 10 listed)
1/2: DM, HTN. Together = 70% chronic renal failure cases.
3: Autoimmune diseases
4. Systemic infection
5. Urinary stones/lower urinary tract obstructions
6. Prolonged exposure to nephrotoxic Rx's
7. Increasing in age
8. Race/ethnic background (AfricanAmerican, American Indians, Hispanic all r/t DM and HTN)
9. Exposure to chemicals or environmental toxins
10. Family history
51
What persistent GFR value indicates CKD?
< 60 mL/min/1.73 m squared
CKD is a slow, progressive deterioration of renal function,
evidenced by low GFR and/or albuminuria.
GFR is estimated by creatinine clearance.
Normal creatinine clearance 80-120 mL's/min
52
Around what GFR value would we start seeing clinical signs of toxins and electrolyte imbalance?
What stage of CKD would you need dialysis?
What stage of CKD are you considered for transplant?
In stage 4: GFR 15-29 mL/min/1.73m squared
Stage 5 (last stage). GFR < 15
Stage 4/5 - qualify for transplant
53
What meds are removed by dialysis?
BLIST MED
** Hold BP meds until after dialysis bc one of the major side affects of HD is hypotension.
B - Barbiturates (phenobarbitol, etc
L - Lithium
I - Isoniazid
S - Salicylates
T - Theophyline/Caffeine (both are methylxanthines-used for pulmonary airway obstruction: asthma, chronic bronchitis, emphysema)
M - Methanol
E - Ethylene Glycol
D - Depakote (treats sz, bipolar, migraines)
54
What is one of the most common complications of intermittent Hemodialysis?
a. hypokalemia
b. hypotension
c. chest pain
d. anemia
b. hypotension
r/t connecting them to the machine, there is about 150 mL's in the circuitry... plus the waste/fluid being dialyzed off.
55
What is the most likely cause of confusion/agitation after Hemodialysis?
Dialysis Disequilibrium Syndrome
Caused by the rapid removal of urea nitrogen from the bloodstream having an affect on the blood brain barrier. It develops primarily from an osmotic gradient that develops between the brain and the plasma as a result of rapid hemodialysis.
usu confusion clears w/time but sometimes cerebral edema can occur.
56
Complications of Hemodialysis?
(8 of them)
1. Hypotension
2. Angina
3. Dysrhythmias (usu r/t K+/electrolytes)
4. Fever/ pyrogenic reaction (to the semipermeable membrane/ circuit - not as common anymore)
5. Coagulopathy/ thrombocytopenia (anytime your blood comes in contact with a foreign substance, plts will drop)
6. Disequalibrium Syndrome
7. Exsanguination
8. Air embolus
57
VENOUS signs of air embolus?
Treatment?
Will look like a PE:
* SOB
* Chest pain
* Severe case: Acute right heart failure (if obstructs flow from right heart from the lungs) R ventric dilation = compresses L ventric
TREATMENT:
- Lay on left side, trendelenburg position (using gravity to keep from going to lungs)
- Oxygenate with 100% FiO2 - accelerates removal of nitrogen in the air embolism.
- Hyperbaric oxygen therapy
58
ARTERIAL signs of air embolus?
Treatment?
Can be pretty fatal.
If it goes to the head = change in mentation
to the heart = looks like MI
- 2 mLs in the artery to be fatal
- 0.5 mL fatal in coronary artery
to the periphery = looks like a clot; obstruction to perfusion
TREATMENT
100% O2
59
What type of dialysate is used in peritoneal dialysis?
What is used as the semi-permeable membrane?
A glucose based solution (1.5%, 2.5%, 4.25%) is instilled (hypertonic - pulls fluid toward it) for about 3-4 hours. Then it's drained; has waste and electrolytes in it. Should look like urine. If it's cloudy - possible infection. If bloody - internal bleeding.
Semi-permeable membrane (SPM) is the abdominal mesenteric capillary bed
Usu 2 L exchanges Q 3-4 hours.
Advantages: pt can do, cost effective, no need for anticoag or vascular access
60
Complications of peritoneal dialysis (5):
Contraindications:
1. Peritonitis (the dialysate is glucose - food for bacteria)
2. Hyperglycemia. Systemic.
3. Diaphragmatic pressure/ respiratory compromise
4. Pleural effusion
5. Visceral herniation/ perforation (rare. surgical emergency)
Contraindications: recent abdominal surgery, abdominal adhesions, need for emergent dialysis.
61
Normal lab values for:
BUN
Creatinine
Urine Specific Gravity
Urine Osmolality
Urine Sodium
Urine Creatinine
Urine Urea
Urine Protein
BUN: 5 - 20 mg/dL
Creatinine: 0.6 - 1.2 mg/dL
Urine Specific Gravity: 1.010 - 1.020
Urine Osmolality: 500 - 800 mOsm/L
Urine Sodium: 40 - 100 mEq/ 24H
Urine Creatinine: 1 - 2 G/ 24H
Urine Urea: 6 - 17 G/ 24H
Urine Protein: 30 - 150 mg/ 24H
62
You need to know how electrolytes affect acidosis vs alkalosis. What's the “rhyme” to help you remember this?
"If your electrolytes are low, that's associated with alkaLOWsis."
"If you 'drop' acid, you'll get HIGH."
63
Which electrolyte regulates total body water and transmission of nerve impulses?
Sodium.
Also: regulation of acid-base balance; muscle contraction/cellular depolarization.
64
What are some causes of hypernatremia?
> 145 mEq/L
Symptoms?
Treatment?
- Dehydration
- Excess administration of NaCl or NaHCO3
- Hypertonic enteral feedings
- Burn injury
SYMPTOMS
- Thirst, tachycardia, hypotension, restless, irritable, lethargy, muscle weakness, flushed skin, oliguria (w/dehydration)
- May also see increased hematocrit (hemo-concentrated)
- Increased chloride (often > 106 mEq/L)
- Increased serum osmolality
- Increased urine specific gravity d/t concentrated urine in dehydration (often > 1.025)
- Decreased urine Na (in absence of dehydration, may see an increase)
TREATMENT
- Hydration, free H2O
- Diuretics (to remove Na) - NOT if dehydrated though.
65
What are the causes of Hyponatremia?
< 130 mEq/L
Symptoms? Treatment?
- Excess H2O or Na depletion
- Water retention
- Dehydration
- NG tube suction
- SIADH (dilutional hyponatremia)
- Diarrhea
- Intestinal surgery
- DKA
SYMPTOMS
- Neuro changes, headache, confusion, coma, death
- Anxiety, weakness, abdominal cramping, seizures, hypotension, tachycardia, shock
TREATMENT
** First you need to identify their intravascular volume status **
- If hypervolemic = diuretics and Na replacement
- If euvolemic = may only need to replace Na
- If hypovolemic = may only need to replace Na
66
What do you need to worry about with sodium replacement?
"Low to high, the brain will die."
- You need to correct slowly: no more than 8 - 12 mEq/day
- NaPhos 1 - 2 mmol/hr over 3 - 4 hours
- Hypertonic saline; 2% or 3%
- Na tabs
67
If your electrolytes are LOW, that's associated w/alkaLOsis.
If you drop acid, you'll be high... electrolytes are HIGH = acidosis.
68
Possible causes of hypernatremia:
S/S of hypernatremia?
Treatment:
1. Dehydration
2. Over correction; excess NaCl (bag after bag of NS); NaHCO3 gtt for too long.
3. Hypertonic enteral feeding (not enough water boluses)
S/S
Same as dehydration: thirst, tachycardia, hypotension, restless, irritable, lethargy, muscle weakness, flushed skin, oliguria (w/dehydration)
Maybe see:
* Increased hematocrit (hemo-concentrated)
* Increased chloride (often > 106 mEq/L) r/t too much NS
* Increased serum osmolality
* Increased urine specific gravity (often > 1.025)
* Decreased urine sodium
TREATMENT: what is the patient's fluid status? will determine treatment plan.
1. Fluid hydration
2. Free H2O
3. Diuretics (to remove Na)
69
What do you need to think of/consider for treatment options in relation to sodium imbalances?
"What is their fluid status?"
Are they hypovolemic/ euvolemic/ hypervolemic? This determines treatment plan...
Hypovolemic:
- hyponatremic : fluid and sodium
- hypernatremic : fluid
Euvolemic:
- hyponatremic : sodium replacement
- hypernatremic : diuretic & maybe fluid
Hypervolemic:
- hyponatremic : diuretic & Na
- hypernatremic: diuretic
70
Potential causes of hyponatremia:
Treatment:
1. Heart failure
2. Loop diuretics
3. SIADH
4. NG tube suction
5. Diarrhea
6. Intestinal surgery
7. Liver or renal disease
TREATMENT: SUPER SLOW CORRECTION (low to high, the brain will die)
Na-Phos: 1-2 mmol/hr for first 3-4 hrs
Hypertonic saline
Na tabs
71
What is refeeding syndrome? What causes it? What electrolyte disturbance will you see?
Refeeding syndrome occurs after someone has been NPO for an extended amount of time and then nutrition is restarted...
What happens?
In refeeding syndrome, chronic whole body depletion of phosphorus occurs. Also, the insulin surge causes a greatly increased uptake and use of phosphate in the cells. These changes lead to a deficit in intracellular as well as extracellular phosphorus.
72
Regarding potassium, what % is intracellular vs extracellular?
90% intracellular.
The sodium-potassium pump is a vital transmembrane ATPase found in animal cells. It moves sodium ions out of cells & potassium ions into cells against steep conc. gradients. It maintains normal cell volume and electro-neutrality of the cell membrane.
73
Uses for potassium (purposes)?
(There are 5 of them)
1. Transmission of nerve impulses
2. Intracellular osmolality
3. Enzymatic reactions
4. Acid-base balance
5. Myocardial, skeletal, & smooth muscle contractility
74
Which ORGAN is primarily responsible for potassium excretion?
Which HORMONE is responsible?
Kidneys.
- Intestines play a role as well.
Aldosterone hormone. In setting of hyperkalemia, aldosterone will be excreted which triggers excretion of potassium through renal tubules.
75
What does a "U" wave on an ECG indicate?
a. Hypokalemia
b. Hypermagnesemia
c. Hypophosphatemia
d. Hypercalcemia
HYPOKALEMIA
Usu d/t:
- GI : NG suction, vomiting, diarrhea, fistula, ileostomy
- Accessive urinary losses: Hyperaldosterone states, thiazide diuretics, amphotericin, gentamycin, cisplatin
- Inadequate intake: anorexia, ETOH, magnesium depletion
- Intracellular shift: AlkaLOsis, DKA, insulin
76
If you see:
- PVCs
- Depressed ST segment
- U-wave
- Prolonged QT interval
- Vfib (severe)
... what electrolyte imbalance may be occurring?
HYPOKALEMIA
FYI: Hypokalemia can potentiate digoxin toxicity.
S/S:
a) Constipation
b) Heart palpitations
c) Fatigue
d) Muscle weakness/ spasms (muscles get irritated)
e) Tingling & numbness
TREATMENT:
Replace!
Oral is best.
Standard dose 10-20 mEq over an hour (central line is best; monitor IV site for irritation)
77
What will you see on an ECG in the setting of hyperkalemia?
Tall peaked T waves.
78
Causes of hyperkalemia?
(> 5.5 mEq)
-There are 8 of them listed-
1. Renal failure = 75% of all cases. Inability for renal tubules to excrete K+
2. Acidosis r/t intracellular shifting or DKA
3. Decreased cardiac output
4. Elderly taking potassium sparing diuretics
5. Severe trauma and burns
6. Infection
7. Addison's disease
8. Too much consumption of substitute table salt or antacids.
79
S/S of hyperkalemia:
1. N/V (classic sign) - if a dialysis pt - let them vomit!
2. Diarrhea
3. Tingling skin
4. Numbness in hands and feet
5. Flaccid paralysis
6. Cardiac signs (as K+ increases: T wave peaks peaks peaks, QRS widens widens widens, asystole)
7. Apathy
8. Confusion
80
Treatment of hyperkalemia?
1. Regular insulin, to shift K+ into cells
2. Dextrose if BG normal or low
3. Calcium chloride (cardio protectant; no affect on K+): theoretically stabilizes action potential membrane of the resting cells
4. NaHCO3 (causes minor transcellular shift of K+)
5. Nebulized albuterol (speeds up the Na-K+ pumps, pushing K+ into cell)
-- onset ~ 15 min, duration 15-90 min
6. Dialysis
7. If pt has working kidneys - sodium polystyrene sulfonate (Kayexalate)
-- dose 15 g, 1-4 doses/day, 24 hrs to correct (not an emergent Rx)
81
Normal Magnesium levels?
What are the (5) functions of mag?
1.5 - 2.5 mEq/L
1. Neuromuscular transmission
2. Cardiac contraction
3. Activation of enzymes for cellular metabolism
4. Active transport at the cellular level
5. Transmission of hereditary information
82
Hypomagnesemia < 1.3 mEq/L
Causes (5)?
1. Increased excretion:
-- NG suction, diarrhea, fistulas
-- Diuretic; blocks Na reabsorption
-- Osmotic diuresis
-- Abx and antineoplastics
-- Hypercalcemia
2. Decreased intake
3. Chronic alcoholism - classic pt.
4. Malabsorption
5. Acute pancreatitis
83
S/S of hypomagnesemia:
CV: Tachycardia, depressed ST segment, prolonged QT
- PACs and PVCs
-- Increased risk for digoxin toxicity
-- Hypotension
-- Coronary artery spasm (low K/ Mg = irritability)
Neuromuscular
- Twitching, paresthesias, cramps, muscle tremors (irritability)
CNS
- Mentation changes and seizures
Hypokalemia
84
Emergency management of hypomagnesemia ("1-2 over 1-2")
Other management aspects/considerations?
1-2 grams over 1-2 minutes (for an EMERGENCY [symptomatic torsades], otherwise over an hour)
Considerations:
1. Renal function
2. Increase intake
3. Monitor BP and airway (vasodilates)
4. Monitor neuro status
5. Monitor K+ and Ca++
6. Serial magnesium levels
85
What is the "Mag drag?"
Hypermagnesemia - muscle weakness and fatigue.
> 2.5 mEq/L -- Very rare
Etiology: Decreased excretion - renal failure (most common); acidosis DKA; given too much Mg.
86
What is the antidote/reversal given for hypermagnesemia?
Calcium gluconate
87
S/S of hypermagnesemia?
Treatment?
Vasodilator...
Flushing, hypotension
TREATMENT:
-- Increase excretion
-- Fluids and diuretics
88
What is the "active" form of calcium called?
Ionized calcium.
Ionized calcium is calcium in your blood that is not attached to proteins. It is also called free calcium. All cells need calcium in order to work. Calcium helps build strong bones and teeth.
89
Normal level of ionized calcium?
What is more common hypercalcemia or hypocalcemia?
NORMAL: 1.1 - 1.35 mmol/L
Hypocalcemia is more common. Treatment involves replacement
Causes: Renal failure, Diarrhea, Diuretics, Malabsorption, Alkalosis (Ca++ bound to albumin & is inactive) - alkalotic from the low levels or transcellular shifting is occurring - leading to the hypocalcemia.
Hyper is rare and treated with fluids.
90
Does calcium have an inverse relationship or a positive correlation relationship with phosphorus?
INVERSE
When phos is high = low calcium; & vice versa
91
What do we call the clinical sign referring to a twitch of the facial muscles that occur when gently tapping an individual's cheek, in front of the ear?
What does it mean?
Chvostek's Sign
Associated with hypocalcemia.
92
What do we call the clinical sign referring to the carpopedal spasm induced by ischemia through inflation of a sphygmomanometer? What does this suggest?
Trousseau's Sign
Associated with hypocalcemia. When the blood flow is restricted while the brachial artery is occluded, this further exacerbates the calcium deficiency in the distal arm, causing spasms in the hand and forearm muscles.
93
What electrolyte imbalance could present with the following s/s?
Low BP, CO
Prolonged QTc
Ventricular ectopy/ Fibrillation
Tingling/ tetany/ spasms/ seizures
Bronchospasms/ labored shallow breathing
GI: Smooth muscle hyperactivity
Bleeding prolonged/ not clotting
HYPOCALCEMIA
V fib in severe cases
Ca++ is needed to clot
Safety concern: confusion, seizures, bleeding
-- Muscle cramps can precede tetany
-- Monitor airway (bronchospasms)
94
Reasons/causes for hypophosphatemia: < 2.5 mg/dL
Decreased intake:
- ETOH/ small bowel dz
Increased elimination:
- V/D
- Use of phosphate binding antacids
- Increased urinary losses: osmotic diuresis, thiazide diuretics
and/or...
Increased utilization:
- Necessary for cellular energy
- Tissue catabolism -- increased use in tissue repair
Intracellular shifts:
- Alkalosis (respiratory)
- Refeeding syndrome
95
CHRONICally low levels of which electrolyte can result in the following symptoms?
Memory loss
lethargy
Bone pain
Hypomagnesemia
HYPOPHOSPHATEMIA
Symptoms are 2/2 to decreases in ATP and 2,3 DPG (diphosphoglyceric acid). 2,3-DPG levels in the erythrocytes help regulate hemoglobin oxygenation. Unloading of oxygen in tissue capillaries is increased by 2,3-DPG, and small changes in its concentration can have significant effects on oxygen release.
96
Acutely low levels of this electrolyte can present with the following symptoms:
Chest pain
Confusion
Seizures
Tingling
Trouble breathing
Coma
Speech difficulty
HYPOPHOSPHATEMIA
Chest pain d/t poor oxygenation of the myocardium (ATP & 2,3 DPG)
Numbness/tingling of fingers; circumoral region
Incoordination/ speech difficulty
Trouble breathing r/t weakness of respiratory muscles
Management:
1) ID & eliminate the cause.
2) Increase dietary intake: Seafood, Dairy, Lentils, Poultry, Peas
3) Oral phosphate supplements
4) IV replacement
97
What electrolyte imbalance could have the clinical manifestations of:
Rebound hypocalcemia
Ectopic disposition of Ca-PO4
Anorexia, N/V
Muscle weakness/ hyper-reflexia/ tetany
Tachycardia
HYPERPHOSPHOTEMIA
Rebound hypocalcemia: Phosphate binds with free calcium and ionized serum calcium falls.
Remember PO4's relationship w/Ca++
High PO4 = Low Ca++
MANAGEMENT
1) ID & eliminate cause.
2) Use of aluminum, magnesium, or calcium gels or antacids - binds phosphorus in the gut.
3) Diet low in PO4: Avoid meats, poultry, fish, dairy, beans, seeds, nuts, eggs.
4) Dialysis therapy
5) Acetazolamide stimulated urinary excretion.
98
Which electrolyte has a normal level of 98 - 106 mg/ dL?
Hint: Too much of this is associated w/a non gap metabolic acidosis.
CHLORIDE
Metabolic acidosis from excessive NS administration. This is hard to correct.
Hypochloremia: Metabolic alkalosis ("if your electrolytes are LOW = AlkaLOsis")
- Excess serum HCO3 displaces Cl in ECF (extracellular fluid compartment) resulting in hypochloremia
- Decreased Cl- delivery to nephron
- Volume-sensing cells in distal tubules are chloride dependent.
- Interpret hypochloremia as volume depleted
- RAA system activated = Na & HCO3 reabsorbed
