Renal approach to CP, SOB/DOE, Palpitations Flashcards
how is hyponatremia defined?
< 135 mEq/L
mild hyponatremia: 130-134
moderate hyponatremia: 120-129
severe hyponatremia: <120
what patient are common for Hyponatremia? and what are some risk factors
Very common electrolyte disorder
-more common in hospitilized patients especially in the ICU
Risk factors:
- CHF
- Cirrhosis
- Nephrotic syndrome
- Pneumonia (legionella especially)
- Postop state
- ICU
- Geriatric
- Medications
what is the normal Serum Osmolarity
what are the 2 systems that regulate?
280-290 mOsm/L
ADH system
thirst mechanism
what are the two stimuli that cause the release of ADH
Osmotic stimuli: from increases in serum osmolarity detected by osmoreceptors in the anterior hypothalamus
Non-osmotic stimuli: from decreases in blood pressure or blood volume detected by blood baroreceptors
- also: Nausea, Hypoxia, Pain (especially post op)
- medications (opiates, antidepressantss (SSRI’s))
- PRegnancy
what is the pathogenesis of Hyoponatremia
Results primarily from increases in TBW and less from changes in total body sodium
Increases in TBW results from either
- excessive intake of water (oral or IV)
- decreased renal excretion of water (usually from inability to suppress ADH release)
when do symptoms appear for Hyponatremia and what are those symptoms?
<125
- HA
- Fatigue/lethragy
- dizziness
- Nausea
- Gait instabillity/falls
- Confusion
- psychosis
- seizures
- coma from cerebral edema
what is considered Acute vs Chronic Hyponatremia
Acute Hyponatremia: < 48 hours
Chronic hyponatremia: >48 hours or unknown duration
what is the systemic approach to Hyponatremia?
First measure Serum Osmolarity:
-determine if hypotonic, isotonic, or hypertonic hyponatremia is present
if patient hasHypotonic hyponatremia then assess volume status of the patient
- measure random urine sodium level and urine osmolarity
- consider a serum uric acid to determine SIADH
Should you draw labs first or treat first?
Best to avoid treatment until labs are drawn so it is important to draw all labs simultaneously
Hypovolemia exam findings
- Hypotension
- orthostatic vital signs
- tachycardia
- Poor capillary refill
- Increased skin tugor
- Dry oral mucosa or tongue fissuring
- Flat JV
- Hx of decreased urine output
- > 50% collapse of IVC during inspiration on ECHO
Hypervolemic exam findings
Hypertension
- sacral or LE edema
- JVD
- Dilated IVC on ECHO
after assessing the ECF VOlume status as Hypovolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx
Renal fluid losses
- Diuretic excess
- adrenal insufficiency
- Osmotic diuresis
- post-obstructive diuresis
- RTA
- Cerebral salt wasting
- salt losing nephropathy
after assessing the ECF VOlume status as Hypovolemic Hyponatremia, Urine osm >300 and urine Na+ is <20 mEq/L what is the DDx
Extrarenal fluid loss
- vomiting
- diarrhea
- third spacing of fluids (burns, pancreatitis)
- blood excess
- excessive sweating
- lung losses
after assessing the ECF VOlume status as Euvolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx
SIADH -tumor -CNS or pulmonary disorder -drugs -nausea -pain hypoxia
Hypothyroidism
Adrenal insufficiency
thiazides
after assessing the ECF VOlume status as Euvolemic Hyponatremia, Urine osm <100 what is the DDx
Primary polydipsia
after assessing the ECF VOlume status as Hypervolemic Hyponatremia, Urine osm >300 and urine Na+ is <20 mEq/L what is the DDx
Nephrotic syndrome
Heart failure
Cirrhosis
after assessing the ECF VOlume status as Hypervolemic Hyponatremia, Urine osm >300 and urine Na+ is >20 mEq/L what is the DDx
Acute or chronic kidney failure (Low GFR)
after assessing the serum osmolarity it is >305 but the patient is hyponatremia what is the DDx
Hyperglycemia Hypertonic infusions -Glucose -Glycerol -Mannitol -Sorbitol -Glyceine -Ethanol
how is the diagnosis of SIADH (syndrome of inappropriate antidiuretic hormone) made
Diagnosis of exclusion
must rule out cortisol deficiency, hypothyroidism, and other causes
what are the two causes of SIADH that I need to be aware of
Postoperative state
Small cell lung cancer: most common malignancy associated with ectopic ADH production
what are some drug classes that are associated with SIADH
Antidepressants Anticonvulsants Antipsycotics Anticancer drugs: cyclophosphamide Misc: opiates, MDMA(extasy)
what is the rate of sodium correction in acute vs chronic hyponatremia
General rule of thumb is serum Na+ should be corrected over the same period for the time it took to get low
Acute <48 hours
-can have rapid correction little risk
Chronic: >48hrs
- must be careful due to osmotic demyelination syndrome (ODS)
- raise serum sodium 8-10 mEq/L a day and no more than 18 in first 48 hrs
what to give symptomatic patients who are hyponatremic
Give hypertonic saline (3%) to quickly raise sodiume
-3-4 mEq/L raise just to stop seizures then continue to raise slowly
what to do if you over correct the sodium
raise to fast, lower back down with:
- 5% dextrose in water aka free water
- DDAVP
- D5W and DDAVP
- discontinue some therapies that are raising sodiums
how to treat Hypovolemic Hyponatremia: Renal fluid losses or extrarenal fluid losses
Isotonic saline (no symptoms) Hypertonic saline (symptoms)
How to treat Primary Polydipsia
Water restriction
Hypertonic saline (symptoms)
How to treat SIADH
Hypertonic saline for symptoms
SIADH:
- Water restriction!
- furosemide!
- salt or urea tablets!
- vaptans
- Demeclocycline
How to treat Hypervolemic Hyponatremia
Water restriction
Furosemide
What are the major complications of Hyponatremia
Osteoprosis falls Seizures Coma Death from brain herniation Osmotic demylination syndrome (ODS) -occurring with rapid Na serum correction
how does Osmotic demyelination syndrome (ODS)
present and what are its diagnosis
demyleination occurs in the pontine and extrapontine neurons
Clinical manifestations occur 2-6 days after Na correction:
- dysarthria
- dysphagia
- Paraparesis
- behavioral disturbances
- Pseudobulbar palsy
- seizures
- coma
- locked in syndrome
- death
Diagnosis: Head MRI but can be negative up to 4 weeks
what happens in the brain when given NA too quickly ffor ODS
initially brain swells due to decrease of osm and then will adapt by losing organic osmolytes and electrolytes
-if correction is too fast brain cells will shrink and axonal shear damage occurs and there is disruption of blood brain barrier
how is Hypernatremia characterized? what patients is this common i? and what are some risk factors?
Hypernatremia: serum sodium is >145 mEq/L
seen in infants and elderly
risk factors:
- trauma
- burns
- ICU
- Dementia
- Uncontrolled diabetes
what re the 2 processes that the indivdual becomes hypernatremia:
Unreplaced water loss (dehydration)
- most common cause
- Gastrointestinal water loss (vomiting, diarrhea)
- renal water loss (DI, diuretics)
- Insensible water loss (excessive sweating or in burn patients, respiratory loss)
- impaired thirst mechanism
Sodium overload
- less common
- Hypertonic saline infusion, hemodialysis, sodium bicarbonate infusion
what are the differences between acute and chronic hypernatremia and what are the clinical manifestation of hypernatremia?
acute: <48 hrs
chronic: >48 hrs duration
Hypernatremia results in cellular shrinkage since ther is an osmotic gradient for H20 to move out of the cells
- irritabillity
- altered mental status
- letharagy
- ataxia
- seizures
- hyperreflexia
- intracerebral hemorrhages, subarachnoid, or subdural hematomas
what is the rate sodium correction of acute and chronic hypernatremia
acute: can have rapid correction of serum sodium with little risk of cerebral edema
chronic: must be careful of rapid correction of serum sodium as patient is at higher risk for cerebral edema
- goal is to lower serum sodium by 10-12 mEq/day
what are the 2 steps in treatment of hypernatremia?
Replace the water deficit
- 5% dectrose in water (D5W)
- other hypotonic solutions (1/2NS)
Correct underlying cause leading to water loss
how does cerebral edema occur in hypernatremia rapid correction
due to the high osmolarity water leaves the brain and it rapidly adapts by accumulating electrolytes and organic osmolytes
if rapid water enters and sodium the brain will rush with fluid and cause a hypertonic state and swell leading to cerebral edema
what are the primary regulators of the serum potassium (what cells, and what do they do) and how are immediate and long term responses controlled
THe kidney is the primary regulator of serum potassium
‘-principle cells (secretion)
-a-intercalated cells (reabsorption)
immediate response: transcellular shift
long term control: renal excretion
what part of the nephron regulates urinary K+ secretion?
distal part of the nephron
how is hyperkalemia described and what are some risk factors?
Hyperkalemia is defined as serum potassium of >5.0 or 5.5 mEq/L
risk factors:
- AKI
- CKD
- DM
- Medications(NSAIDS, ACE/ARB, aldosterone antagonists, heparin, etc)
- Malignancy
- Rhabdomyolysis
- older age
- acidosis
Clinical Manifestations of Hyperkalemia
Can range from asymptomatic to mild symptoms to life threatening
Cardiac Arrhythmia
- high enough potassium can lead to ventricular fibrillation
- bradycardia from AV block
- Asystole
Skeletal muscle weakness
-severe hyperkalemia can lead to respiratory failure from diaphragm weakness
Metabolic acidosis
- K+ ions enter the cells and H+ exit the cells to maintain electroneutrality
- decreases ammoniagenesis and thus decreases ammonium chloride excretion in the kidneys therefore less net acid excretion
what is the effect of K+ on resting Membrane Potential?
High K+ concentration makes membrane potential less negative
- initially increase excitabillity
- however long term persistent depolarization leads to inactivation of sodium channels and cause decrease in membrane excitability leading to impaired cardiac conduction and or neuromuscular weakness/paralysis
what are some ECG changes in Hyperkalemia
6-7: peaked T waves
7-8: Flattened P wave, prolonged PR interval, depressed ST segment, peaked T waves
8-9: atrial standstill, prolonged QRS duration, further peaking T waves
> 9: sinusoid wave pattern = ventricular fibrillation
what are the two main reasons for hyperkalemia
Transcellular shift (increased K+ release from cells)
Decreased Renal K+ excretion
what can cause a Transcellular shift causing increased K+ release from cells
- Pseudohyperkalemia
- Metabolic acidosis
- Insulin deficiency, hyperglycemia, hyperosmolality
- increased tissue catabolism
- Medications: B2 blockers, a1 adrenergic agonist, digoxin, succinylcholine, minoxidil
- Exercise
- Blood transfusions
what are some examples of Pseudohyperkalemia?
Results from an artificial increase in serum K+ due to K+ release from cells
- RBC hemolysis
- serum blood samples: due to clotting released from cells
- leukocytosis
what are some of the causes for decreased renal K+ excretion?
Low aldosterone secretion
-medications (ACEi, ARBs, Renin inhibitors, NSAIDS, Heparin, Ketoconazole) adrenal insufficiency
Aldosterone resistance:
- Potassium sparing diuretics (aldosterone receptor blockers, spironolactone or eplerenone)
- sodium channel blockers (amiloride or triamterene) or antibiotics like trimethoprim
AKI or CKD
-Low GFR
Hypovolemia
Ureterojejunostomy
Intrinsic renal defect
how is the diagnosis of Hyperkalemia made?
based on history and exam
Laboratory tests are guided by suspected cause per history
Fractional excretion of K+ (FEK)
how to interpret Fractional excretion of K+ (FEK)
< 10 percent indicates renal etiology
> 10% indicates extrarenal etiology
Hyperkalemia treatment for peaked T waves
Calcium gluconate which stabilizes cardiac membrane
Hyperkalemia treatment for transcellular shift
Insulin and dextrose
B2 agonist (albuterol nebuilzer)
Bicarbonate infusion
Hyperkalemia treatment for Potassium removal
Loop diuretic or thiazide
Exchange resins:
- Sodium polystyrene sulfonate (kayexalate) which exchanges Na+ ions for potassium primarily in the colon
- zirconium cycloslicate (exchanges Na+ and H+ ions for ppotassium throughout intestines
- Patiromer (exchanges Ca+ for potassium primarily in the colon
Hemodialysis
Low K+ diet
discontinue medications that increase K+ (ACEi, ARB, ALdosterone blockers, potassium supplements, etc)
what is the characteristic of Hypokalemia and what are the risk factors?
Hypokalemia is defined by a serum potassium < 3.5 mEq/L
risk factors include:
- diarrhea
- viomiting
- medications: diuretics, insulin
Clinical Manifestations of Hypokalemia
usually not symptomatic until serum K< 3.0 mEq/L
Cardiac Arrhythmias
- Premature atrial contractions (PAC)
- Premature ventricular contractions (PVC)
- Tachycardia
- Brady cardia
- Ventricular fibrillation
Skeletal muscle weakness
-including diaphragmatic weakness
Rhabdomyolysis
Metabolic alkalosis
Nephrogenic diabetes insipidous
what are the effects of K+ on resting Membrane potential
Low K+ concentration makes membrane more negative
what are ECG changes in hypokalemia
- 5: low T wave
3: Low t wave and high U wave - 5: Low T wave, high U wave, low ST segment
3 main reasons for hypokalemia?
Transcellular shift (increased K+ uptake by cells)
Extrarenal loss (GI loss, sweat, etc)
Renal loss
what are the most common causes of hypokalemia via a Transcellular shuft
increased K+ uptake by cells
Insulin
-DM treatment or refeeding syndrome
B2 agonist
-Albuterol, catecholamines, etc
Metabolic alkalosis
Pseudohypokalemia
Hypokalemic periodic paralysis
barium toxicity
causes of Hypokalemia via extrarenal loss
Gastrointestinal loss:
- Upper GI losses (vomiting, NG suctioning both leading to volume depletion leading to activation of RAAS thus aldosterone leads to Na+ reabsorption and secondarily increases K + secretion
- Lower GI losses (intestinal K+ concentration is higher so diarrhea, laxatives, drains, fistulas
Cutaneous loss
-sweating
Plasmapheresis
Dialysis
causes of Hypokalemia via renal loss
Diuretics
Increased mineralcorticoid activity
- primary hyperaldosteronism (conns syndrome), hypercortisolism (cushing syndrome)
- aldosterone increases Na+ reabsorption via ENaC that makes the lumen more negative and more K+ secreted by ROMK
Hypomagnesemia
Increased distal delivery of Na+ and water
- nonreasorbable anions (bicarbonate, DKA, Hippurate toluene glue sniffing, penicillin derivative
- polyuria
RTA type 1 or 2
Intrinsic renal defect (bartter, gitleman, lpiddle syndrome
what are the diagnostic measures of Hypokalemia
laboratory tests per suspected history
- Primary hyperaldosteronism
- Hypercortisolism
- Renal artery stenosis
- RTA
- ABG
- Serum magnesium
- Hypokalemic periodic paralysis
Urinary K+ excretion:
- 24 hour urine potassium
- Urine K/Cr ratio
what does values on a 24 hour urine potassium test tell you that is below 25-30 mEq/day
> 25-30 mEq/day suggest renal K+ wasting
what is considered K renal wasting in urine K/Cr ratio
Urine K/Cr ratio is normally below 13 mEq/g
higher values seen in renal K wasting
what is the treatment for Hypokalemia?
Treat the underlying cause
Replace the potassium deficit
- give Potassium chloride
- general rule is K level increases 0.1 mEq/L for every 10 mEq of KCl given
Replace magnesium if low
- magnesium sulfate
- magnesium oxide
