145 terms

Step Up to Medicine: Chapter 08 Fluids, Acid-Base Disorders

What is the treatment of hypokalemia?
Treat underlying cause
-d/c any meds that aggravate hypokalemia
-oral KCl (Klorcon) safest method of replacement-test always post admin
-10 mEq of Kcl inc K+ levels by 0.1 mEq / L
-slow acting/fast acting
-IV Kcl can be admin if severe hypK (< 2.5)
-admin slowly to avoid hyperK
Hormone maintaining sodium homeostatis? H20 homeostasis?
What is the treatment for hypercalcemia?
Increase urinary secretion
-IV fluids (normal saline)
-diuretics (ferosemide) - inhibits ca2+ resorption LOOSE CALCIUM

Inhibit bone resorption in patients with osteoclastic disease
-bisphosphonates (pamidronate)

Administer glucocorticoids if vitamin D mechanism (intoxications, granulomatous d/o) + multiple myeloma
HTN plus hypokalemia =
No HTN with hypokalemia =
1. excessive aldosterone activity (bind to aldo R and inc sodium resorption which results in water retention and increase HTN

2. GI or renal loss of K+ likely
Kcl IV infusion pearls to replenish if patient is severely hypokalemic?
1. Max infusion rate of 10 mEq/hr in peripheral IV line
2. Max infusion rate of 20 mEq/hr in central IV line
3. May add 1% lidocaine to bag to decrease the pain; potassium burns by IV

Normal values:
Locations in body:
Potassium secretion
-3.5-5.0 mEq/L
-most of the potassium (98%) intracellular
hypo = elevated pH, alkalosis, insulin administratino (becuase if alkalotic then cells will push OUT H+ to decrease pH and thus decrease serum K+)
-hyper = dec pH, acidosis, cell lysis, increased serum k+ (both force K+ out of cells into the ECF)
-K+ secretion: most occurs through kidneys (80%); remainder by GI. Aldosterone role in K+ secretion
What causes an elevation in serum K+ > 5.0meq/L

A. Increased TOTAL BODY K+ due to:
1. RF
2. Addisons disease (inc primary secretion of cortisol
3. K+ sparing diuretics (spironolactone and epleronone)
4. Hyporeninemic, hypoaldosteronism
5. ACEi
6. Iatrogenic OD - exercise cause with KCl in patients with ARF
7. Blood transfusion
What is the interpretation of urine potassium in hypokalemia?
Low with GI loss (<20mEq)
High with renal losses (>20mEq/L)
Most dangerous complication of hypokalemia?
-flattened t wave +/- inversion
-U-wave appears
Increased PTH, Increased urinary cAMP, increased Ca2+
Primary hyperparathyroidism with secondary hypercalcemia
Three reasons for oligourina
1. Low blood flow to kidney (assess heart - CHF)
2. Kidney problem (ARF)
3. Postrenal obstruction
-Placement of foley catheder
Patients with sepsis, fever, burns, open wounds, have high insensible losses and due to _____ _______ demand
HIGH METABOLIC demans. Increase in insensible losses (>600-900mL)/day due to
Normal output due to:
1. Urine =
2. Feces =
3. Insensible losses =
1. Urine 800-1500 mL/day
2. Stool 250 mL/day
3. Insensible losses 600-900 mL/day by sweat, hyperventilation and trachiostomies
Patients with liver failure, nephrotic syndrome, any condition causing hypoalbuminemia tends to ______-________ fluid out of the vasculature and may be totoal body hypervolemic but intravascularly depleted
Third space
For each degree of atmostpheric temp > 37 degrees C - bodys water loss increases by ___ mL/day
100 mL/day
Any disorder that decreases Co2 clearance (adequeate ventilation) can lead to?
Respiratory acidosis
If change in anion gap is ? than the change in HCO3-, then:
Metabolic alkalosis and high AG acidodid
-when AG increases, the acid must be bufferent by HCO3-, so HCO3- will dec. If HCO3- doesnt decrease, then you started at a high HCO3- (THUS must have been alkalosis meta)
With metabolic acidosis
-PaCO2 =

With metabolic alkalosis
-PaCO2 =

Failure of respiratory compensation indicates an additional primary respiratory AB disorder
PaCO2 decreases
PaCO2 increases
most common cause of hypophosphatemia?
alcohol abuse
What is the normal body fluid compartment for men? for women?
Men TBW = 60% body wt
Women TBW = 50% body wt
Metabolic acidosis
1. characteristics
dec pH (<735) with a bicarb (<22 mm Hg)

goal to idenify cause
When pH is elevated (alkalotic), calcium bound to albumin will ____. Thus serum or total calcium will be ____ but ionized calcium will be low.
increased ca2+ with albumin, decreased ionized ca2+, resembles signs of hypocalcemia
#1 way to distinguish b/t metabolic acidosis with volume contraction v. volume expansion
Cl- concentration by UA - contraction if LO urine CL and expansion if elevated urine CL
Pathophysiology of metabolic acidosis
1. fixed acid (lactate) is added, H+ from fixed acid is buffernd by bicarbonate system
2. CO2 formed and removed by lungs - HCO3- levels decreased in ECF therefore kidneys reabsorb more HCO3- *new- to maintain pH
Causes of proximal RTA:

Causes of distal RTA:
Proximal RTA - decreased bicarbonate resorption = MM, cystinosis, Wilsons disease
-carbonic anhydrase inhibitors or acetozolamide

Distal RTA - make HCO3- = SLE, Sjogrens, AMP B
Plasma phosphate concentration:

What is winters formula?
1.5(measured HCO3-) + 8 (+/-) 2

If PaCO2 doesnt fall within acceptable range: another prim AB d/o
If PaCO2 falls in predicted range: simple metabolic acidosis with appropriate 2ary hypercapnea.
If actual PaCO2 is higher than measured/calculated PaCO2: sign of impending respiratory failure to compensate
If PaCO2 is lower than calculated: then metabolic acidosis with primary respiratory alkalosis
Treatment if low phos?
If mild - >1mg/DL admin oral supplement
-neutra phos capsules
-K+ phos tablets

If severe or NPO = parenteral supplement
Hypocalcemia causes:
1. Hypoparathyroidism (due to surgical disturance on parotid gland with damage to nearby PTH)
2. Acute pancreatitis - deposition of Ca2+ deposits that lowers serum Ca2+ levels
3. Renal insufficiency - mainly due to decreased products of 1,25-dihydroxy vitaD
4. Hyperphosphatemia - PO4 precipitates with Ca2+ resulting in Ca2+ Po04 deposition
Bicarbonate level obtained in a serum chemistry panel v that in an ABG?
serum chem panel (venous CO2) is amesured value and more reliable
-abg level of HCO3- is calculated
Clinical features and diagnosis of metabolic alkalosis
1. asymptomatic
2. pts medical therapy/history (vomiting, gastric drain)
3. Diagnosis:
-pH inc
-HCO3- inc
-hypoK is common
-PaCO2 is HI as compensatory mechanism due to hypoventilation
-PaCO2 exceeds 50-55 mmHg is rare, if higher indicates resp acidosis
-urine cl (SS v. SR)

Treatment: NS and Klorcon (K+) if saline sensitive; address cause or give spironolactone if vol expanded (urine cl > 20 or saline R)
Three situations that can arise from met acidosis
1. A change in ANION GAP is equal to change in HCO3- = simple MA
-addition of acid causes anion gap to increase proportionally
2. the change in anion gap is less than change in HCO3-
-normal AG acidosis plus high AG acidodid (if after addtion of acid, the HCO3- is < calculated preidction, then started with decreased HCO30)
3, a change in AG > change in HCO3- then MA with HI AG
Clinical features of metabolic acidosis
1. Hyperventilation to breathe off excess CO2 produced from buffered HCO3- + H+ yielding H20 and CO2
-deep rhythmic breathing
-Kussmaul's respirations
-compensatory response to m. acidosis

2. Decreased cardiac output and decreased tissue perfusion
-acidosis decreases tissue responsivity to NE, E, DA leading to decreased perfusion, lactic acidosis, cardiac output, hypotension, tissue perfusion
Hypophosphatemia causes:
1. decreased intestional absorption due to alcohol abuse, vitamin D deficiency, malabsorption of phos; excessive use of phosphate binding antacids, hyperalimentation (TPN) and/or starvation

2. elevated renal excretion (excess PTH hormone) states if itamin D def or primary hyperparathroid)

4. Inc renal excretion with HYPERGLYCEMIA
5. Respiratory alkalosis, seteroids, hyperthermia, DKA, hungry bones syndrome
Treatment for metabolic acidosis
1. Sodium bicarb (esp for normal AG)
-takes HCO3- 24 hours to get to brain
-hyperventilation will continue until reaches brain - thus PaCO2 gets/stays low while HCO3- increases - danger combo --> [H+] = 24 (PaCO2/HCO3)

2. Mechanican ventilation may be required if patient fatigued from prolonged hyperventilation especially in DKA
Hyperphosphatemia (> 5mg/DL)
1. Renal insufficiency
2. bisphosphonates; hypoPTH, VitD intox or tumor calcinosis
3. rhabdo, cell lysis/acidosis (releases P04 into ECF)

1. met calcification
2. hypocalcemia can lead to neuro change

1. Phosphate binding antactids with AI-oh or carbonate; hemodialysis
Other causes of hypocalcemia?
-vitamin D deficiency
-malabsorption - SB syndome
-blood transfusions with citrated blood (ca2+ binds to citrate)
-osteoblastic metastasis
-hypoalbuminemia by IONIZED is normal so hypoalb is clinically irrelevant
Causes of MAcidosis
1. Increased AG
2. Normal AG
AG: Methanol, urea, DKA, paraldehyde, iron/isonizid, lactiv acidosis (los tissue perfusoin, shock state, excessive energy loss), ethanol/ethlyene glycol, salisylic acid

2. hyperchloremic metabolic acidosis - dec HCO3 associated with inc Cl- so that AG = normal. Renal loss of HCO3 - protimal tubular acidosis, DTA OR

-hypercholremic MA - RTA I or RTA IV
-GI loss of HCO3 (diarrhea, pancreatic fisutla, SBO, uterosignmoidostomy
The USPSTP does not have a formal recommentation for prostate cancer in patients less than 75 years of age, as there is no evidence demonstrating that screening improves mortality.

Therefore - when should a physciain discuss possible PSA screening?
If > 75 or if case/case basis
Metabolic alkalosis characteristics
increase blood pH and plasma HCO3-

uncomplicated Malkalosis typically transient because kidneys can normally excrete excess HCO3-

2 events of metabolic alk
1. Loss of H+ via gastric drainage/vomit or increased HCO3- due to ECF volume contraction
2. Mechanism that maintains m. alkalosis due to kidneys inability to excrete
54 YO M with abdominal distention. SOB, Hodgkin lymphoma dz. Alcohol use. Normal temp, BP 120/76, pulse 80/min RR 20. JVD of 7; dullness to percussion and decreased breath sounds in RL base. Abdomen distened with flui wave. Hepatomegaly present. Extremities have 2+ lower edema.

Labs: serum cr = normal (0.8); Albumin (4) = normal; BRtotal = 1 = normal; PT time normal at 11.

UA within normal limits - most likely cause of conditions?
Labs involved reveal normal hepatic functon and renal functoin. JVD and peripheral edema usually occurs 2/2 RVHF or RVinfarction. Dullness to percussion and SOB indicates LSHF - therefore what would cause both LH and RH failure?


-condition where pericardium is thickened or scarred resulting in restriction of diastolic filling. Because the heart cannot fill properly during diastole, CO is compromsied and venous pressures become crhonically elevated resulting in increased JVD, severes ascites and hepatic congeston and dyspnea and weakness On exam, KUSMAULS sin, failure of JVP to decrease on inspiration. Most common causes of constrictive pericarditis are cardiat surgery, VIRAL pericarditis, and RADIATION THERAPY.

-ddx made by calcified pericardium on CXR revealing a thickened pericardium on CT or MRI scanning or by measuring pressures during cardiac catherterization. Rx with either diuretics OR pericardiectomy.
Phosphate overview
influence on phos absorp:
Normal: 3-4.5 mg/DL
location: phosphorus in bones (85%); phosphorus in intracellular soft tissues (15%) with <0.1% ECF
influ: VitaminD controls phos absption in GI; PTH controls phos excetion in kidney, PTH inc renal ohos excretion by no allowing reabsorption. Function of kidney in maintaining PO4
ALL women who are > 65 YO per the USPSTF recommends?
A one time screening of ALL women who are 65 years and older with a DEXA SCAN of the spine and pelvis. Osteoporosis refers to decreased BONE MASS and increased fragility .

Diagnosed by omparies the bone density T score of a pateint that that of a younger individual of same gender and race. (if t score of 1.5-2.5 then osteopenia) - if score less than (-2.5) then osteoporosis. Increased fracture risk.
CLinical features of decreased < 2.5 mg/dL of phosphorus
None if mild

If severe then will have:
1. Neuro-encephalopathy, confusion, numbeness
2. MUS-weakness, bone pain, ricketts
3. HEME-hemolysis; RBC/WBC dysfunctoinand platelet dys
4. CARDIAC: cardiomyo, myo depression 2/2 low ATP
5. rhabdo
-difficulty with vent weaning
Skin rash - erythema multiforme

Doesnt gram stain.
Metabolic acidosis with anion gap?
1. Anion gap = Na - (Cl- + HCO3-)
-reflrects ion in serum but unmeausred (proteins, phosphates, organic acids, sulfates)
-normals = 8-15 mEQ/L
Multiple liver masses are much more liekly to be the result of a ______ disease rather than that of and infectious causes or primary liver malignncy. Primary tumors of the ____ tract, the _____, and the _____ are the top most common diseasses that cause liver mets.
GI tract, lungs, breast
effects of acidosis v. alkalosis
1. right shift O2 -hgb curce that diminishes O2 affinitiy to Hb and drops off thus inc delivery to tissues
2. decrease CNS
3. decrease pulmonary blood flow
4. arrhythmias
-no myoardial functoin
hyperkalemic present

1. decreased cerebral flow
2. left shift O2 hgb so dec O2 delivery
3. arrhythmias
4. tetany, seizures
ABS interpretation
CO2 level
-if elevated, think -
-if decreased, think -

-if elevated think
-if dec think
elevated CO@ - rep acidosis or compensation for metabolic alkalosis (inc HCO3)
low CO2 - resp alkalosis or copensation for MA (dec HCO3)

If hih tihnk MAlk or comp with respiratory acidosis
If lo think m acidosis or r. alkalosis with compensation if excess base/deficient base values in ABG indicate amt of a/b needed to titrate plasmat pH to 7.4
Diagnosis of metabolic acidosis
get patient history
calculate the AG (8-15) is normal
winters formula: expected PaCo2 = 1.5 (measured HCO3) + 8 (+/-)2
-predicts the expected resp compensation of Paco2 level to metabolic acidosis
-if PaCO2 doesnt fall within acceptable range, then patient has another primary AB disorder
Why might bolus fluids be combined with dextrose or K+ for fluid replenishment?
Leads to hyperglycemia
Leads to hyperkalemia
Causes of metabolic alkalosis
1. Saline sensitive
2. Saline resistant
Saline sensitive:
1. Urine Cl- <10mEq/L with ECF contraction and hypokalemia
2. Vomiting/NG suction
3. Patient loses Hcl, gastric HCO3- generation occurs causing alkalosis
4. Diurectics = dec ecf. Because HCO33- content remains the same, but plasma HCO3- increases because ECF contraction
5. Villous adenoma of colon, diarrhea with elevated Cl-

Saline R
1. Urine Cl- >20mEq/L ECF expansion and HTN due to increased mineralocorticoids
2. 2ndary to adrenal disorder like conn's
3. Inc aldosterone, Inc resorption of Na+ and HCO3- and an excessive loss of Cl- in urine
4. expansion secondary to increased sodium
5. Cushings; severe k+ def, Barterrs syndrome; diuretic abuse
Clinical findings of hypovolemia:
1. CNS findings: AMS, sleepiness, apathy, coma
2. CV findings: due to decreased plasma volume; ortho hypotension tachycardia,decreased pulse pressure, decrease CVP and decreased PCWP
3. SKIN: poor skin turger, hypothermia, pale, dry tongue
4. Oligourina
5. Ileus, weakness
6. ARF d/t prerenal azotemia
constrictive pericarditis -->
decreased diastolic filling and impairment of CO. Causes include VIRAL pericarditis, radiathion therapy, and cardiac surgery.
Treatment for hypovolemia?
1. Correct volume deficit
a. Bolus to get euvolemia
b. Start with isotonic solution
c. maintain urine output @ 0.5-1.0 mL/kg/day
2. Maintainence fluid
a. D51/2NS solution with 20mEq KCl/L most common adult maintenance fluid (dextros is added to decrease muscle breakdown)
How do we know how to calculate maintenance fluid dose in patients with hypovolemia?

2 ways: 100:50:20 v. 4:2:1
100:50:20 RULE
-100mL/kg for the 1st 10kg
-50mL/kg for the 2nd 10 kg
-20mg/kg for every other 1 kg over 20kg
-divide the total by 24 for the hourly rate of fluid replenishment
If 70 kg man = 100mL (x) 10kg + 50 mL (x) 10 kg + 50kg (x) 20 mL/kg =2500mL
-2500mL/24hr = 104 mL/hr of D51/2NS

4:2:1 RULE
-4mL/kg for the first 10 kg
-2mL/kg for the 2nd 10 kg
-1mL/kg for every other 1 kg over the first 20 kg
If 70 kg man = 4mL/kg (x) 10 kg + 2mL/kg (x) 10 kg + 1mL/kg (x) 50kg =110mL
-thus 110mL/hr
Causes of hypovolemia:
1. Losses due to vomiting, diarrhea, fistula damage
2. 3rd space asites, effusion, SBO, crush injury
3. Inadequate intake
4. Polyuria (DKA)
5. Sepsis, intraabdominal and retroperitoneal inflammatory process
6. Trauma, open wounds
7. Insensible losses = 75% by skin; 25% by respiratory tract
What is the diagnosis of hypovolemia
1. Monitor urine output and daily wt (if ill and cardiac/renal dys) - then start SWAN GANZ CATHEDER (check CVP and PCWP)
2. Increased serum sodium and decreased urine sodium
3. BUN:Cr ratio > 20:1 suggests hypoperfused kidneys and thus hypovolemia
4. Increased hematocrit
5. RBC/WBC/platelets and increased ECF deficits and decreased with ECF excess
What are the causes of hypervolemia
1. Iatrogenic (parenteral over hydration)
2. Fluid retaining status: CHF, nephrotic syndrome, cirrhosis, ESRD
15 YO males comes to office within one week history of fever, nonproductive cough, sore thraot and ehadaches. Today presents with skin rash. Temp 101.3, pulse 90/min. BP 115/78 and respirations are 16.min. Throat hyperemic, but there is no cervial LAD. CTAB. Note dusky red, target shaped skin leison over all four extremities. CAR reveals itnerstitial infrilates of LLL. Sputum gram stain = PMNs but no organisms. Most likely organism?
Atypical pneumonia - M. pneumo, C. pneumo, Legionella pneumophilia, coxiella, influenza

M pneumo is the msot common atypical in amualtory setting. Distinguish from progenic penumo by indolent course, nonproductive cough and higher incidence of DPS. Low grade fever and weeks worth of symptoms are consistent with indolent course. Headache, sore throat, and skin rash = EPS.

Why might someone recovering from a MVA with head trauma and on a mechanical ventilator have an ABG of 7.54/124/20/17? (pH/Pao2/Pco2/hco3-) with HIGH URINE pH?
Mechanical ventilation can force hyper or hypoventilaton. Ventilation = TV x RR. Hyperventilation caused by increased TV and or RR results in excessive CO2 lsoses and repiratory alkalosis while hyPOventilation caused by decreased TV or decreased RR results in CO2 retentionand respiratory acidosis. The patient has respiratory alkalosis as evidenced of pH value and pCO2 value and low bicarb. The low bicarb is decreased 2/2 attempted renal compensation for respiratory alkalosis - therefore the kidneys will retain increased amounts of protons (H+) and secrete excessive amounts of HCO3- in attempt to normalie serum pH. This results in an alkalotic urine
What are the basic pathophysiologic mechanisms of syncope? What are the various types?
1. Vasovagal: common fainting spell precipitated by an emotional reaction and is preceded by presyncopal dizziness and weakness and nausea

2. Autonomic dysfcn/DI-postural HypoTN: orthostatic in nature in that it occurs on standing when blood is redistributed to the dependent parts of body. When syncopye occurs without preceding change in body position (standing) then likely to NOT be orthostatic

3. Seizure: clonic jerks may occur during syncopy if it is prolong and are due to brain hypoxia. Absense of a preivous history of seizure and the description of syncope make the diagnosis of seizure LESS common.

4. Arrhythmia: onset of syncope WITHOUT warning signs, positive presense of structual heart disease (POST MI, MVR because of characteristic murmur), and frequent ectopic beats. Another clue is HcTZ in the med list that can cause electrlyte disturbance and ventricular arrhythmias.
Which situations require intubation?
1. severe acidosis
2. PaCO2 > 60 mmHg or inabiltiy to increase PaO2 with suplemental O2
3. If patient is obtunded/deteriorated mental status
4. Impending respiratory fatigue (ensures with prolonged labored breathing)
Use of NIPPV v. Mechanical ventilation and/or intubation
NIPPV should be considered in patients with COPD exacerbation ahead of intubation. NIPPV is associated with decrease complications that are a hallmark of itubation which include infections.

1. NIPPV is recommended in a patient of respiratory distress with ABGs of pH< 7.35 or PaCO2 >45mmHg or RR > 25/min
2. If pt already
Causes of respiratory alkalosis
1. anxiety
2. PE, pneumonia, asthma
3. sepsis
4. hypoxia (inc RR)
5. mechanical ventilation
6. pregnancy inc serum progesterone levels, increase hyperventilation
7. Liver dz
8. Medication (ASA tox)
9. Hyperventilation syndrome
A 20YO female presents to office for a routine check up. No complaints and PMH insignificant. Not taking any medications and denies drug abuse. Her BP is 125/65 and HR is 80. Cardiac auscultation reveals early DIASTOLIC murmur at the left sternal border. What is the next best step in management of this patient?

Diastolic and continuous murmurs revelaed on CAuscultation should always be investigated because the probability that an organic cause is present is high. Midsystolic soft murmurs (grade 1-II/IV) in an asymptomatic pt are usually benign and need no further workup. However because this was a DIASTOLIC murmur, this should be investigated by TTE.
What is the distribution of TBW (60% of body weight)
TBW = 60% body weight - 40% body weight is intracellular fluid
ICF = 2/3 of 60% = 0.40 or 40%
TBW = 60% body weight - 40% body weight is extracellular fluid
ECF = 1/3 of 60% = 0.20 or 20%

Plasma is 1/3 ECF, 1/12 of TBW, 5% body weight
Interstitial fluid is 2/3 of ECF, 1/4 TBW, 15% body weight
Causes of respiratory acidosis
Alveolar hypoventilation
-prmary pulmonary disease = COPD, airway obstruction
-NM diseases = MG
-CNS malfun = brainstem
-drug induced hypoventilation = morphine, sedatives, narcotics in postop patients possibility (pinpoint)
-respiratory muscle fatigue
Clinical features of hyponatremia include
#1 Neurological symptoms:
a. H20 intoxication - osmotic water shifts, increased ICF volume, brain cell swelling or cerebral edema
b. headache, delirium, irritability
c. Muscle twitching, weakness
d. Hyperactive DTR

#2 Elevated ICP; Increased seizures, coma
#3 GI/nausea, vomiting, ileus, watery diarrhea
Why would administering O2 elevated by NC in patients with O2 therapy/hypercapnic/acidosis further impede the treatment of a COPD exacerbation?
Increasing O2 alone will reduce the respiratory drive. In COPD patients, PCO2 is elevated at bareline and it doesnt stimulate the respiratory ceter, unlike in formal individuals ("AIR TRAPPING" - cannot get air out). The only drive to increase the RR is that of hypoxia therefore if you just provide O2, it will WORSEN situation because will no longer have a respiratory drive 2/2 hypoxia and the baseline PaCO2 has already been compensated for. Always provide NIPPV to provide more O2 and to washout the CO2.
Venous insufficiency results from incompetent _____ within the lower extrmeity veins. Complications include ______ _ _____ _____. Therapies for such?
chronic edema, stasis dermatitis, ulceration

leg elevation, compression stocking and wound care
42 YO patient with depression, modd swings and poor sleep. Mild headaches and muscle weakness. Has two ER visits for kidney stones over past year. she denies drug use. Her BP is 160/105 and her heart rate was 85/min. Her lab findings reveal
a CBC WNL with CMP indicative of elevated serum Ca2+. Most likely cause of patients HTN?
Parathyroid gland DZ - why?

HTN, psychatric symptoms, recurrent kidney stones, and hypercalcemia

-presentation is concerning for hyperPTH. The parathyroid gland produces PTH which acts to increase serum calcium levels and decrease serum phosphate.
-stones bones mones and groans are common with hypercalcemia
-often have increased incidence of HTN although uncommon cause
Wha are the clinical factors of respiratory acidosis
1. solmnence, confusoion, myoclonus, asterixis,
2. headaches, confusion, papilledema are signs of acute O2 retention

1. varify patent airway
2. If low PaO2 (<60) initiate supplemental O2 (if CO2 retainers like COPD patients, O2 can exacerbate acidosis)
3. Correct reversible causes
4. Improve alveolar ventilation
5. Intubation and mechan ventilation may be necessary for relief of acidemia and hypoxia from decreased ventilation
What are the characteristics of a COPD exacerbation and how is this managed?
COPD exacerpation occurs in pts with prior DX of COPD.
-sudden loss of breath
-no fevers, chills, sweating, n/v or hemoptysis
-meds used ipratropium albuterol MC and o2 nc
-temp WNL, BP 110.65, pulse 110 and RR = 28
-ABGs show respiratory acidosis

If the patient is having acute exacerbtaiton of COPD in the refractory phase which doenst respond to standard initial management of corticosteroids and aerosolized BDilators then use NON-invasive PPV (NIPPV) ahead of intubation. This is associated with decreased complications that are hallmark of intubation (infections).

If the patient is crashing - then intubation and mechanically ventilation should be performed.
Characteristics of metabolic alkalosis
Inc pH and dec PaCO2

to maintain pH within normal limits: HCO3- must dec so renal compensation occurs (HCO3- excretion increases). Takes hours

Acute: for each 10mmHg drop in PaCO2, HCO3- decreases by 2 mEQ/L and blood pH in by 0.08

Chroni: decrease in 10mmHg in PaCO2, HCO3- decreases 5-6 and pH decreases by 0.02
When should a VENOUS blood gas be ordered?
Venous blood gas should differ very little from arterial blood gas except for the decrease in O2 levels seen in venous blood compared to arterial blood. Venous blood that contains a similar O2 content as arterial blood may indicate a disorder of respiratory metabolism such as CYANIDE poisoning.
Respiratory acidosis defined as a pH decreased 7.35 and PaCO2 > ___.

How long might renal cmpensation take to occur?

Acute v. Chronic?
> 40 mmHg

starts 12-24 hours and takes 5 days or so to complete

Acute respiratory = immediate inc in HCO3-/inc 1 mmol/L for every 10 mmHg increase PaCO2

Chronic respiratory acidosis
-renal adaptation occurs, HCO3- increases by 4 mmol/L per 10mmHg increases PaCO2
-seen in COPD patients
How does TBW change with age and obesity?
1. TBW decreases with age
2. TBW decreases with obestity because fat contains very LITTLE H2O
Neurological symptoms + ^ ICP + Nausea + HTN (d/t ICP^) + Salivation and ^ lacrimation + oligouria (may or may not be reversible) =
Hormonal control of Ca2+
PTH: inc plasma Ca2+ - inc in bone resorption
dec plasma Phos - decrease phos resorption and increase ca2+ resorption

Calcitonin: decreases plasma Ca2+; decreases plasma PO4 but acting on BONE, GUT, KIDNEY

Vitamin D: increase plasma Ca2+/increase plasma PO4
Hypernatremia and the clinical features
1. Neurologic symtoms predominante
A. AMS, restlessness, weakness, focal neurologic deficits
B. Can lead to confusion, seizure, COMA

2. TIssues and mucous membranes are dry; salivation decreases
causes of serum ca2+ > 10.5 due to malignancy
....metastatic cancer due tomprostate, kidney, lung (osteolytic), bony mets result in bone destruction by osteoclastic activity

...multiple myeloma loss of bone by tumor cells release of osteoclast activity, tumors that release pthrh

pharmacologic ... vitamin d intoxication, milk alkali syndrome, drugs hctz, lithium

...other includes sarcoid, inc gi absorption of ca2+, familial hypercalciuric hypercalcemia
Causes of hyponatremia
1. Hypotonic hyponatremia (TRUE)
a. Serum osmo < 280 mOSM/kg
b. Low urine sodium (<10 meq/L) - implies sodium retention by kidneys to compensate for extra renal loss (diarrhea, vomiting, diaphoresis, burns, third spacing (ascites/pacreatitis)
c. High urine sodium (>20mEq/L) - renal salt loss due to diuretics or decrease ACEi/ATN

2. Euvolemia hyponatremia - no change in ECF expansion/contraction on PE
b. Psychogenic polydypsia
c. Postop hyponatremia
d. Hypothyroidism
e. Admin/intake of relative excess, free H2O- if patient is given D5W
f. Haloperidol, cyclophosphamide, antineoplastic drugs
Calcium metabolism
1. Normal serum Ca2+
Ranges from 8.5-10.5
-Ca2+ balance is regulated by hormonal control but levels are also affected by albumin and platelets
Characteristics of hypernatremia
Defined as a plasma Na+ concentration >145mmol/L

-refers to excess Na+ in relation to h2o can result from H2O loss or sodium infusion
-assess ECF volume clinically
A. Hypovolemic hypernatremia
B. Isovolemic hypernatremia
C. Hypervolemia hypernatremia
CLinical features of serum calcium < 8.5?
1. asymptomatic
2. rickets, osteomalacia
3. increased NM irritability
-numbness/tingling - circumorol, in fingers, in toes
-tetany (hyperactive DTR, chovosteks sign, trousseaus sign)
4. Grand mal serizures
Isotonic hyponatremia (pseudohyponatremia)
Increased plasma solid lowers plasma sodium concentration but the amount of sodium in plasma is normal

Caused by any condition leading to increased protein lipid levels (TG elevated; FLP elevated)
If hypoalbuminemia, the total Ca2+ is low, but the ionized Ca2+ is normal

How is ionized Ca2+ calculated:
Ionized Ca2+ = total Ca2+ - (serum albumin x 0.8)
1. Step 1, measure ______ to determine if HI, NOR, LO
2. Step 2, if < 280, LO serum OsMo; asscess ECF volume status. Then -
2. Step 2a, if HI (>295), then -
2. Step 2b, if normal (280-295), then -
If measure SERUM OSMOLARITY and normal:
-pseudohyponatremia (elevated proteins, elevated TG); confirm with FLP
If meansure serum osmolarity and HI:
-hypertonic hyponatremia (presense of osmotic substances -elevated glu, man, glycerol)
if measure serum osmolarity and low:
-THEN assess the volume status ECF
-LOW total body sodium, and HYPOVOLEMIA:
a. Measure urine Na+
b. Lo (<10) -diarrhea, diaphoresis, 3rd spacing ascites or nephrotic syn
c. Hi (>20) - renal salt loss, diurentics, decreased aldosterone, ATN
-NORMAL volume status, and EUVOLEMIA:
b. Psychogenic dyspnea
c. Postop hypothy
-HIGH volume status and HYPERVOLEMIA:
a. CHF
b. Nephrotic syn
c. Liver disease
Most cases of hypernatremia are due to which types of water loss:
1. Nonrenal loss = insensible loss, GI tract (diarrhea)
2. Renal loss = osmotic diuresis, diabetes insipidis
Treatment of hypernatremia
a. Hypovolemia
b. Isovolumic
c. Hypervolemia
1. Hypo - give isotonic NaCl to restore hemodynamics
2. Patients with DI require vasopressin thus prescribe oral fluids/if cannot drink admin D5W
3. Give diuretics (ferosemid and D5W to remove excess sodium) Dialyze patients with renal FAILURE
Causes of serum calcium levels < 8.5 mg/dL
TOtal Ca2+ (serum alb x 0.8) = ionized Ca2+

1. HypoPTH
2. Acute pancreatitis
3. Renal insufficiency
4. Hyperphosphatemia
5. PseudohypPTH
6. Hypomagnesemia (dec PTH)
7. Vitamin D deficiency
8. Malabsorption GI
9. Transfusions
Treatment of hyponatremia
ISOTONIC and hypertonic hyponatremia:
1. Treat the underlying cause
2. Hyperglycemia, mannitol, glycerol
HYPOTONIC hyponatremia
1. Mild (Na+ 12-0-130) withhold free H2O and allow patient to requilibrate spontaneously
2. Moderate (110-120) - loop diuratics
3. Severe (<110 or symp) - give hypertonic saline
SYmptoms of elevated magnesium >2.5?
ecg change = prolonged QT, T wave flattened, torsades
^ NM and CNS hyperirritability
-muscle twitching, weakness, tremors
-hyperrefllexia, seizures
-mental status change
-coexist with hypocalcemia bc of decrease release of PTH and bone resistance when MG is low.
-effect on K+ levels - hypokalemia in 50%
Treatment for hypocalcemia
-provide emergency treatment - IV calcium gluconate. Make sure mag2+ is replaced (if mag down, then Ca2+ is down)

LONGTERM managment
-oral ca2+ supplements (ca carbonate) and vitD

PTH deficiency
-replacement with vitamin D plus high oral Ca2+
-thiazide diuretics plus lower urinary Ca2+ and prevents urolithiasis
Redistribution leading to secondary hyperkalemia?
translocation of K+ from intra to extracellular space (metabolic acidosis)
1. MA
2. GI bleeding
3. Tissue breakdown-rhabdo, hemolysis, burns
4. Insulin def
5. BB administration
Hypertonic hyponatremia
1. Osmotic substances that cause osmotic shift of H2O out of cells
2. Substances do not cross cell membrane and create gradients
3. Causes
a. glucose hyperglycemia
b. hyperglycemia increases osmotic pressure, water shifts from cells into ECF and dilution hyponatremia in ECY
c. For every 100mg/dL increase in blood glucose - serum sodium decreases ~3mEq/L

ex; Mannitol, sorbitol, glycol, maltose
If K+ and ECG change, admin ____
If shift/redistribute K+ into cells: ____, ____
Remove excess from body: ____, ____, _____
IV calcium
glucose, insulin
kayexalate, hemodialysis, diuretics
Hyponatremia characteristics:
1. TOo much H2o v Na in serum
2. {PLASMA} < 135 mmol/L
3. Symp when <120mmol/L; increased ICP post head injury. As ECF osm decreases, H20 shifts into brain. Increased in ICP more; thus must keep serum Na+ normal or slightly elevated
How might TZDs cause > 10.5 mg/dL Ca2+

How does lithium increase calcium?
inhibits renal secretion

increases pTH levels in some patients (SQUAA CC)
NS v. D51/2NS v. D5W
NS : increases intravascular volume if pt is dehydrated or lost blood; DO NOT USE IN PATIENTS WITH CHF

D51/2NS: Standard maintainence fluid (with 20 mEq) of KCl/L of fluid; glucose is contained in it so decrease muscle breakdown and H2O for insensible loss

D5W: Dilute powdered medication; corrects hypernatremia; only 1/12 remains intravascular bc goes into TBW compartment
Treatment of severe hyponatremia (<Na+ <110 mmol/L) must be done with caution = why?
Hypertonic saline rapidly increases the tonicity of ECF (increases serum Na+ by 1-2 mEw/L per hour until symptoms improve)

DO NOT increase sodium more than 8 mmol/L per hour until symptoms improve
Overly rapid increase in serium concentration may cause central pontine demyelination
Excessivelyy rapid correction of hypernatremia can lead to _____ _______. Why?
Excessively rapid correction of hyponatremia can lead to?
1. Cerebral EDEMA - as H2O shifts into brain cells, therefore the rate of correction shuld not exceed 12mEw/L/day (<8 mEq/L in the 24 hours)

2. Central pontine demyelination - does not increase 8 mmol/L during first 24 hours
Dx of dec serum Ca2+?
Rx if serum Ca2+ is low?
1. Get bun, cr, mag, alb, ionized ca2+
2. Obtain amylase/lipases (pancreas)
3. obtain ALTS/ASTS
4. Serum phos; HIGH RENAL INSUFFICIENCY in hypoparathyroid; low if primary vitD def
5. PTH (low if primary hypoPTH)
If patient is hypovolemic hypernatremia - admin NaCl to restore hemodynamics.

If patient is unstable, what is the first step?
Correct the hypernatremia; can wait until pt is hemodynamically stable = then replace free H2o deficiency

Water def = TBW (1 - actual Na+ (+) desired Na+)
What is milk alkali syndrome?
elevated calcium, elevated pH, renal impairment d/t increased calcium intake and absorbable antacids (calcium carbonate, milk)
Causes of pseudohyperkalemia?
Artificially increased plasma K+ due to K+ movement before venipuncture (or after). Prolonged use of tournaquit +/- repeated fist clenching. Causes acidosis and K+ loss from cells, plasma (not serum) K+ is normal

Leukocytosis, hemolysis, thrombocytosis
How might changes in pH change ratio of calcium binding?
elevated pH increased binding of Ca2+ to albumin. Thus in alkaemic states (acute resp alk), total Ca2+ is normal, but ionized Ca2+ is low and the patient manifests signs and symptoms of hypocalcemia.
Location in body:
Influences on mg secretion:
Mg abs and secretion:
1.8-2.5 mg/dL
-2/3 body mg in bone; 1/3 intracellular 1% mg is extracellular
-insulin/glucagons, PTH, calcitonins, ADH, steroids influence
-30-40% dietary mg absorbed in GI but inc when Mg levels fall
-kidney can resorb Mg and is major regulation of Mg balance
Post parathyroidectomy, DKA, thyrotoxicosis, lactation or burns, pancreatitis can decrease levels of ?
D5W is not effective to maintain _____ volume. Lactated ringers solution is indicated for?
Intravascular (only 1/12 will remain within compartment - used for medication like insulin)

Lactated ringers solution is excellent replacement of intravascular vol. It is not a amaintaining fluid. It is the most common trauma resusscitation fluid. Do NOT use if hyperkalemia is a concern (contains K+)
Hospitalized patients usually have LOW serum albumin concentrations thus patients will concomitatntly hanve decreased ____. Always look at albumin lelvels in relation to decreased serum CA and adjust.
Decreased magnesium with ____ serum Ca2+ and _____ serum K+
decrease ca2+ d/t dec PTH when Mg low
decrease in 50% in muscle and myocardium, when intracellular (1/3) total Mg or K+ decreases, corresponding decrease in other cation takes place.
Water exchange: What is normal intake? Normal output?
Normal intake = 1500 mL in fluids taken PO/day; 500 mL solids or product of oxidation

Normal output = from 800-1500 mL urine/day minimum urine output to excrete products of catabolism = 500-600mL per day

250 mL from stool and 600-900 mL/day from insensible losses
causes of hypercalcemia >10 mg/dL due to endocrine
...renal failure that results in hypocalcemia but hyperpth can inc pth high enough to cause hypercalcemia
...pagets disease of the bone due to osteoclastic bone resorption
...hyperparathyroidism, acromegaly, addisons disease
CLinical features of hypercalcemia
1. Stones - nephrolithiasis, nephrocalcinosis
2. Bones - bones/ascited/pains/osteitis fibrosa cystica (brown tumors)
3. Grunts/groans-muscle pains, pancreatitis, PUD, GOUT, constipation
4. Psychiatric overtones-depression/fatigue, anorexia
5. Polydipsia, polyurea
6. HTN
7. Wt loss
8. ECG - short QT if hypercalcemia
most important effect of hyperkalemia is on the heart

Elevated or peaked T waves by 10 mm
prolonged PR
widened QRS and merged QRS with T
vFIBB cardiac arrest
Causes of hypomag
GI: malabsorption, steatorrheic states, prolonged fasting, fistulas, pt on TPN without MG2+ supplementation

Alcoholism: common cause
Renal causes: SIADH, Diuretics, Bartters syn, renal xplant, drugs like gentamycin, AMPB, cisplatin
Hypervolemia with hypotonic hyponatremia
Low urine sodium due to H2O retention status. Excess H2O>Na+

B. Nephrotic syndrome
C. Cirrhosis/liver disease
Treatment of mild hypomag (<1.8)?

Treatment if severe?
Oral mag (magnesium oxide)
prenteral mg2+ (mag sulfate)
How might hyponatremia be diagnosed?
1. PLasma osmolarity will be LOW in a patient with true hyponatremia

2. Urine osmolarity will be elevated if increased levels of ADH (SIADH, CHF, hypothyroidism); or urine osmolarity will be LOW if kidneys are responding appropriately by diluting the urine and retaining the sodium via aldosterone

3. Urine sodium concentration will be low in a setting of decreased sodium serum. Urine sodium concentration > 20 mmol/L is consistant at salt wasting/diuretics
Urina [Na]>40 is consisitance with SIADH
Hypercalcemia v. Hypocalcemia on ECG?
If > 10.5 mg/dL then will have shortened QT interval

If < 10.5 mg/dL then prolonged QT interval
Method of fluid replacement therapy
1. normal saline
2. D51/2NS
3. D5W
4. Lactated ringers solution
Hypovolemic hypernatremia:
Isovolemic hypernatremia:
Hypervolemic hypernatremia:
1. Sodium stores are depleted, but more water loss than Na+ loss; renal loss from diuretics osmotic diuresis (due to glycosuria in DM type I), renal failure. Extrarenal loss from diarrhea, diaphoresis, resp losses

2. Isovolemic hypernatremia sodium stores normal H2O lost; diabetes insipidis; insensible losses respiratory (tachypnea)

3. Iatrogenic (most common) cause of hypervolemia hypernatremia; large amounts of parenteral sodium-bicarb, TPN. Cushings or saltwater drowning.
Diagnosis of hypernatremia
1. Urine volume should be low if kidneys are responding approprately to hypernatremia (want to dilute)
2. Urine osMo > 800 mOsm/kg
3. desmopresion should be given to differentiate nephrogenic from central diabetes insipidis if diabetes insipidis is suspected
How might fluid volume be assessed?
1. Tracking input and output is not an exact method bc cannot accurately calculate insensible losses = monitor urine output is VERY important becase normal URINE OUTPUT is greater than 1 mL/kg/hr.
2. Low urine output = volume depletion

**Daily weights can get an accurate assessment as well
How does albumin and pH affect Ca2+?
1. Albumin = Ca2+ in plasma exists in 2 forms
a. Protein bound
b. Free ionized form

A. Protein bound = most ca2+ ions bound to albumin so total ca2+ flux with protein (albumin) concentration.
B. Free ionized = physiological active fraction under tight control (PTH) independent of alb levels.

Hypoalbuminema = total Ca2+ low but ionized calcium is normal
Treatment of hyperkalemia
1. If severe or ecg change = IV CALCIUM
-stabilized resting membrane potentioal of myocardial membrane and dec excitatbility


2. Shift K+ into intracellular compartment my admin
-glucose and insulin - glucose stimulaties insulin from b cells but exogenoush more rapid. Admin both and prevent hypoglycemia

3. Sodium bicarbonate - to increase pH level to force K+ into cells; used in emergency for severe hyperkalemia


4. Removed K+ from body
-Kayexalate - GI potassium exchange resin (Na/K+) exchange absorbs K+ in colon and prevents reabsorption in stool.

5. Hemodialysis
-most rapid and effectivel way to lower K+ in plasma; reserved for intractible hyperK and those with RF

6. Diuretics furosemide
Which three organs are responsible for calcium balance (PTH, Calcitonin, and vitamin D)?
1. Parathyroid, GUT, KIDNEY
Features of hyperMAG
nausea, weakness, facial paresthesias, loss of DTR, ecg resembles that of hyperK with increased PR and wide QRS with elevated T waves.

-death usualy caused by resp failure or cardia arrest
Treatment of hypermag
do not admin exogenous mag
-IV calcium gluconate for emergent symptoms for cardioprotection
-admin saline and furosemide
-order dialysis in RF patients
Water homeostasis
1. OsmoR in hypothalamus stimulated if plasma hypertonicity (normal >295). Activation of stimulators produces thirst

2. Hypertonic plasma increases ADH release from posterior pituitary gland to dilute the plasma. Thus ADH --> V2R --> AQP2 at collecting duct --> H2O retention

3. ADH decreases as osmolarity of plasma decreases
PTH v. Calcitonin v. Vitamin D
-PTH: high calcium resorp, dec phos resorp
-Calcitonin: dec calcium absorp; increase po resorption
-VitaminD: increase ca2+ resorp and dec phos
-PTH: vitamin d resorp
-Calcitonin: decreased postprandial o2 absorption
-VitaminD: inc Ca2+ absorption, inc po43-
-increased Ca2+ breakdown, increased po43- breakdown
-Calcitonin: dec bone turnover, inc bone breakdown
Salt and water regulation
Sodium regulation is intimately associated with H2o homeostasis; yet it is regulated by independent mechanism

1. Change in sodium concentration reflects that of water homeostasis
2. Change in sodium content reflects that of sodium homeostasis

1. Change in sodium balance = hypo/hypervolemia
2. Change in water balance = hypo/hypernatremia
Hypermagnesemia causes:
1. RF (most common)
2. Early stage burns, massive traumas, surgical stress, severe ECF volume deficit, severe acidosis
3. Excessive intake of magnesium-containing laxatives or antacids combined with renal insufficiency
4. Adrenal insufficiecy
5. Rhabdo
6. Iatrogenic-preeclam[sia or ecclampsia
Diuretics action on sodium homeostasis
Inhibits Na resorption in renal tubular system.
1. Ferosemide and other loop diuretics inhibit the Na-K-CL cotransporter in TALH;
2. HcTZ inhibits Na-Cl cotransporter at the early distal tubule.
What are the features of hypovolemia?
1. Weight gain
2. Peripheral edema
3. JVD
4. Elevated CVP and PCWP
5. Pulmonary edema/rales
6. Low HCT and albumin concentration
Decreased renal perfusion pressure results in activation of RAAS:

Aldosterone with bind to ______ receptor and result in an increase in ______ retention and ____ excretion. Also acts?
Aldosterone R
sodium retention
potassium excretion (hypokalemia)

Type A intercalated cells to retain H+ ions
Diagnosis of increased Ca2+
Same labs as if hypocalcemia: BUN, Cr, CO2, Cl-, K+, amylases, lipases, LFTs
-radioimmunoassay of PTH = inc if primary hyperPTH (low in malig)
-radioimmunoassay of PTHrP = inc if malig
-Bone scan/survey to identify lytic lesions
-inc urinary cAMP = inc if hyperPTH
Features of hypokalemia?
Arrhythmias - prolongs normal cardiac conduction with muscular weakness, fatigue and paralysis, muscle cramps.
Decreased DTR-
Paralytic ileus
Makes digitalis tox worse
Why must K+ levels be monitored in patients with hypocalemia or on digoxin?
bc likely to be on diuretics as well for CHF. Thus this would cause decrease in K+ thus hypo K predisposes patients to digoxin tox
Treatment of hypervolemia
1. Fluid restriction
2. Judicious use of diuretics
3. Monitor urine output and daily weights and consider swan ganz catheder placement depending upon patients condition
Cause of hypokalemia? < 3.5 mg/L
1. GI loss
-vomiting/NG drainage (decreased vol; metabolic acidosis)
-intestinal fistulas

2. Renal losses
-renal tubular/parenchymal disease
-Mg2+ def
-primary and secondary hypoaldosteronsim
What is the homeostasis of Na+
1. Sodum actively pumped out of cells is decreased and restricted to extracellular space. Osmotically active cation of the ECF

2. Increased sodium intake results in inscreased ECF volume and elevated GFR and elevated sodium exretion

3 If ECF decreases, ECF decreases, and there is a decrease in sodium excretion with an increase in sodium retention
What is Bartters syndrome?
Chronic volume depletion secondary to an AR defect in sodium reabsorption in the TALH leading to hyperplasia of JGA; increases renin secondary to increase in aldosterone