Fluid Therapy Recap Flashcards
(89 cards)
1
Q
Primary Extracellular Cations
A
Na+
1
Q
Primary Extracellular Anions
A
Cl-
HCO3-
2
Q
Primary Intracellular Cations
A
K+
Mg+
3
Q
Primary Intracellular Anions
A
Phos
Proteins
4
Q
Define Osmolality
A
particles/molecules (osmoles) / kg
5
Q
Define Osmolarity
A
particles/molecules (osmoles) / L
6
Q
Equation for calculated osmolarity
A
Calculated osmolarity = 2 (Na+K) + glucose/18 + BUN/2.8
7
Q
Equation for effective osmolarity
A
Effective osmolarity = 2 (Na+K) + glucose/18
8
Q
What is the difference between calculated and effective osmolarity/osmolality?
A
BUN distributes equally between intracellular/extracellular space (freely diffusible), so is not effective at being an osmole (draws water equally to both places). However, the brain has relatively low urea permeability (BBB), so BUN is a more effective osmole in the brain.
9
Q
Write out and explain Starling’s Equation (traditional).
A
Net filtration = Kf [(Pcap-Pif) – σ (πp –πif)]
- Kf: Net permeability of the capillary wall (leaky or not leaky to water).
- Pcap: Pressure in capillary (generated by heart/BP)
- Pif: Pressure of interstitial fluid.
- πp: Oncotic pressure (pull) of plasma
- πif: Oncotic pressure (pull) of interstitial fluid
- σ : “reflection coefficient” for a particular solute (permeability of that capillary to that solute)
10
Q
Explain the modifications/revisions to Starling’s Law taking into account our more current knowledge of vascular fluid dynamics.
A
- Revised law replaces (πif) with the subglycocalyx space (πg)- oncotic pressure gradient is between the plasma and the space between the endothelial cell wall and the endothelial surface layer (glycocalyx)
- This space is nearly protein free (so interstitial protein content doesn’t matter much in reality)
- The glycocalyx is the semi-permeable membrane (rather than the endothelium)
- Different products have a different ability to move through the glycocalyx due to charge, so have different physiologic effects despite a similar COP (hetastarch moves easily, Albumin doesn’t)
11
Q
What factors can damage the glycocalyx?
A
- Ischemia/Reperfusion/Oxidant injury
- Inflammation
- Cytokines
- Hyperglycemia
- Hypercholesterolemia
- Hypervolemia/excessive fluid therapy
- Hypoalbuminemia
12
Q
Name 10-12 negative effects of excessive fluid therapy (positive fluid balance)
A
- Tissue and interstitial edema → poor oxygen diffusion, tissue distortion, obstructed capillary flow/drainage → organ dysfunction
- Increased duration of ICU stay
- Increased mortality
- Increased ICU infections (including lungs)
- Impaired tissue healing
- Compromised gas exchange in lungs
- Increased post operative ileus/delayed gastric emptying
- Impaired healing of GI anastamosis
- Impaired renal function and blood flow (encapsulated), decreased urine output
- Impaired hepatic function and blood flow (encapsulated)
- Decreased cardiac function including decreased contractility, impaired myocardial oxygenation, impaired conduction, increased cardiac morbidity
- Impaired neurologic function
13
Q
Explain how Aldosterone affects sodium/water regulation:
A
Increases Na reabsorption by increasing # and activity of open Na channels in collecting ducts, increases synthesis of Na+/K+ ATPase for insertion into basal membranes
14
Q
Explain how Catecholamines affect sodium/water regulation:
A
vasoconstriction of efferent > afferent arterioles → increased filtration fraction → increased water and Na reabsorption. Directly stimulate Na reabsorption in proximal tubule.
15
Q
Explain how Angiotensin II affects sodium/water regulation:
A
vasoconstriction of efferent > afferent similar to catecholamines → increased water/Na reabsorption, directly stimulates Na/H antiporter in proximal tubules, stimulates aldosterone release
16
Q
Explain how ANP affects sodium/water regulation:
A
dilates afferent and constricts efferent arterioles to increase GFR, inhibits Na reabsorption in CD, inhibits renin and aldosterone secretion 🡪 increased Na/H20 excretion
17
Q
Explain how ADH/Vasopressin affects sodium/water regulation:
A
increases water reabsorption in collecting ducts by insertion of aquaporins into luminal membrane of principal cells
18
Q
What are the 3 broad causes of hypernatremia? Give an example of each.
A
1) Pure water deficit
Example: hypodypsia, diabetes insipidus, fever, inadequate access to water
2) Hypotonic fluid loss
Example: GI losses, 3rd space losses, cutaneous losses (burns), renal losses
3) Salt gain
Example: Salt ingestion, cathartic administration, hyperosmolar fluid administration, hyperaldosteronism,
19
Q
What are the 3 main categories of hyponatremia? Give an example of a cause of each.
A
1) Normal plasma osmolality
Example: pseudohyponatremia (not clinically relevant)
2) Increased plasma osmolality
Example: hyperglycemia, mannitol administration
3) Decreased plasma osmolality (“true” hyponatremia)
Example: Loss of higher sodium fluids (hypovolemic)- ie Addison’s, GI; CHF with RAAS activation (hypervolemic); psychogenic polydipsia (normovolemic)
20
Q
What effect would Acute hypernatremia have on the brain?
A
cerebral dehydration, hemorrhage +/- demyelination
21
Q
What effect would Acute hyponatremia have on the brain?
A
cerebral edema
22
Q
What effect would rapid correction of hypernatremia have on the brain?
A
Cerebral edema
23
Q
What effect would rapid correction of hyponatremia have on the brain?
A
cerebral dehydration, demyelination +/-hemorrhage
24
How would you treat this patient:
2.3 kg, 17yo FS DSH who has been eating less for a few weeks and losing weight, presents obtunded, 10% dehydrated. Na is 173
Chronic hypernatremia (symptomatic):
If hypotensive- bolus 0.9% saline until BP corrected. 7-10 ml/kg/hr D5W for the first 2-3 hrs until neuro improves. Then slow correction of free water deficit over 48 hours, dropping Na by no more than 0.5-1 mEq/L/hr to avoid cerebral edema, monitor Na q 4 hours.
7ml/kg/hr = 16ml/hr D5W x 2-3 hrs
FWD = 0.6 x 2.3kg x [(173/150) – 1] = 0.2 L / 48 hrs = 4ml/hr D5W
+ maintenance fluids
25
How would you treat this patient:
32kg ,4yo MN Lab, vomiting, ataxic, very mentally inappropriate, was playing at the beach 1 hour earlier. Na is 165.
Acute hypernatremia- can correct more rapidly with combination of D5W + furosemide (likely to be hypervolemic, increases Na excretion). Can correct as fast as possible.
10ml/kg/hr = 320ml/hr D5W
Furosemide 2mg/kg
Or
FWD = 0.6 x 32 x [(165/140) -1] = 3.4 liters
26
Would you give mannitol to an acute or chronic hypernatremic mentally inappropriate patient? Explain.
NO!!! Hypernatremia leads to cerebral dehydration- giving mannitol would make this worse!
27
What is SIADH?
Syndrome of inappropriate antidiuretic hormone secretion.
ADH secretion is inappropriate because it occurs in a situation of decreased plasma osmolality.
Patient is hyponatremic and euvolemic with high urine osmolality.
28
Explain & Draw the basic mechanisms of electrolyte reabsorption/secretion in the kidneys. This does not have to be a specific site or electrolyte.
- Active transport at the basolateral membrane (3Na/2K/ATPase pump) creates a gradient (Na out of cell into interstitium, K into cell)
- Passive transcellular transport at the luminal membrane driven by concentration gradient, partially created by the active pump (cotransporters, antitransporters) and partially created due to lower concentration of electrolytes in blood (highly filtered at glomerulus)
- Paracellular transport driven by transepithelial (transmembrane) potential difference (electrical charge)- lumen positive or lumen negative
- Paracellular solute drag along with water (aids with reabsorption)
- “Sink” effect from rapid tubular flow (aids excretion)
29
Label the following diagram with the diuretic that acts at each site. Explain the net effect of each diuretic (inhibition, stimulation, electrolyte changes in the patient). Which is the most potent and why?
1. Diuretic: Furosemide (loop)
Net effect: inhibits Na/K/2Cl cotransporter, leading to increased loss of Na/K/Cl in urine 🡪 increased water loss. **MOST POTENT- loop of henle is the main site of creation of the urine concentration gradient**
2. Diuretic: Thiazides
Net effect: inhibits Na/Cl cotransporter leading to increased Na/Cl and water loss in the urine. Less potent because the DCT is mostly for fine tuning (not large volume of electrolyte movement).
3. Diuretic: K sparing (Amiloride, triamterene)
Net effect: block Na channels in the CD, so less Na reabsorption. Aldosterone antagonists (like spironolactone) antagonize the effect of aldosterone on these channels. Loss of Na and water, but not K.
30
Explain the effect of hypochloremia on acid-base status.
Chloride and HCO3 are both negatively charged and must be kept in balance. Decreased Cl → Increased HCO3. Hypochloremia increases the strong ion difference and causes a metabolic alkalosis that cannot be corrected without providing chloride.
31
Name 3 causes of Corrected hypochloremia:
1. GI losses
2. Renal losses (ie thiazide/loop diuretics)
3. Hyperadrenocorticism, chronic resp acidosis, administration of high Na/low Cl solution
32
Name 3 causes of Corrected hyperchloremia:
1. Pseudohyperchlormemia: bromide, hemolysis, lipemia, high bili
2. High Cl administration
3. Renal Cl retention (Addison’s)
33
Name 3 causes of hypokalemia:
1. Decreased intake
2. Translocation: alkalemia, insulin/glucose, albuterol, catecholamines, refeeding syndrome
3. Increased renal or GI losses
33
Name 4 causes of hyperkalemia:
1. Pseudohyperkalemia: thrombocytosis, hemolysis
2. Increased intake or oversupplementation (unlikely)
3. Translocation: acidosis, tumor lysis syndrome, reperfusion injury
4. DECREASED URINARY EXCRETION!!!
34
Name 3 causes of hypomagnesemia:
1. Decreased intake
2. Increased losses (GI or renal)
3. Altered distribution (glucose/insulin admin, increased catecholamines, sequestration in pancreatitis)
35
Name 3 causes of hypermagnesemia:
1. Decreased renal excretion (ie ARF)
2. Iatrogenic overdose
3. Endocrinopathies (Addison’s, hyperparathyroid, hypothyroid)
36
Draw a diagram to explain the resting membrane potential/threshold membrane potential and the effects of K and Ca abnormalities on cell excitability.
37
Explain the effects of hypokalemia on cell excitability.
decreases resting potential, making it more negative, hyperpolarizes the cell
38
Explain the effects of hyperkalemia on cell excitability.
increases the resting potential, making it less negative, cell more excitable
39
Explain the effects of ionized hypocalcemia on cell excitability.
lowers threshold potential, making cell more excitable
40
Explain the effects of ionized hypercalcemia on cell excitability.
increases threshold potential, making cell less excitable
41
Draw/explain the progressive effects of hyperkalemia on the EKG
42
Explain the key roles of magnesium in the body
- Cellular metabolism: mitochondria- oxidative phosphorylation, cofactor with ATP for ion pumps
- Muscle: cycling of calcium in muscle cells, muscle conduction
- Vasculature: aids in smooth muscle relaxation (vasodilation)
- Neuromuscular: deficiency leads to increased neuronal excitability
- Electrolyte balance: Cofactor with electrolyte transporters- deficiency can worsen potassium depletion, hypocalcemia
43
Explain the key roles of calcium in the body
- Enzymatic reactions
- Membrane transport and stability
- Blood coagulation
- Nerve conduction
- Vascular smooth muscle tone
- Hormone secretion
- Bone formation and resorption, skeletal support
- Control of hepatic glycogen metabolism
- Cell growth and division
- Primary intracellular messenger
44
How does parathyroid hormone effect calcium and phosphorus? What are the sites of action?
Ca: Increased
Phos: Decreased
SOA: kidney, bone
45
How does PTH-rp effect calcium and phosphorus? What are the sites of action?
Ca: Increased
Phos: Decreased
SOA: kidney, bone
46
How does Vitamin D effect calcium and phosphorus? What are the sites of action?
Ca: Increased
Phos: Increased
SOA: GIT (#1), minor kidney/bone effects
47
How does Calcitonin effect calcium and phosphorus? What are the sites of action?
Ca: Decreased
Phos: Decreased
SOA: Bone, kidney
48
List the most common causes of hypercalcemia.
Hyperparathyroidism
Osteolysis
Granulomatous disease
Idiopathic (cats)
Neoplasia (#1)
Young/growing animal
Addison’s disease
Renal disease
Vitamin D toxicity
(HOGS IN YARD)
49
Why are hypercalcemic dogs often azotemic?
Impaired renal concentrating ability due to inhibition of ADH. Polyuria + anorexia + nausea → prerenal azotemia. Tissue mineralization occurs with very prolonged or severe hypercalcemia 🡪 renal azotemia (this is less likely).
Azotemia and significant systemic illness are less common with primary hyperparathyroidism.
50
What are possible treatment options for hypercalcemia?
- Treat underlying disease if present (ie chemo, parathyroidectomy)
- Diuresis: 0.9% saline is preferred, furosemide
- Steroid therapy (except in granulomatous disease)
- Calcitonin: short term only
- Bisphosphonates (ie pamidronate)
- EDTA: only as a last resort/rescue
- Dialysis: if renal failure or other methods fail
51
List possible causes of hypophosphatemia
- Translocation from ECF to ICF: DKA treatment, refeeding syndrome, respiratory alkalosis/hyperventilation, hypothermia
- Renal losses
- Primary hyperparathyroidism
- Decreased intake/absorption: dietary deficiency, phosphate binders, vitamin D deficiency
52
Explain renal secondary hyperparathyroidism
- Hyperphosphatemia inhibits calcitriol synthesis (also kidneys not making it appropriately) → inhibits Ca absorption in intestines
- Mass law effect: Ca x Phos = constant (so increased Phos → decreased Ca)
- Hypocalcemia → PTH secretion → mobilization of Ca from bone. PTH should also increase Phos excretion, but this is not effective if in renal failure.
- Further hyperphosphatemia contributes to renal injury
53
Explain the difference between perfusion and hydration.
Perfusion: delivery of blood to the capillary bed and tissues (generally reflective of intravascular compartment only)
Hydration: amount of water present in the body (includes intracellular and interstitial compartments)
54
Name 10 ways to assess/monitor hydration status
1. Skin turgor
2. Mucous membrane moisture
3. PCV
4. Total protein
5. Urine specific gravity
6. Serial body weight measurement
7. Urine output
8. Jugular vein distensibility
9. Peripheral or pulmonary edema/fluid buildup in body cavities
10. Sunken eyes vs chemosis
11. Renal values
55
Name at least 15 (-21) ways to assess/monitor perfusion and intravascular volume status
1. Pulse quality
2. Heart rate
3. Limb temperature
4. Mentation
5. Blood pressure
6. Lactate
7. Base excess and other acid-base status parameters
8. Jugular vein distensibility
9. Capillary refill time
10. Echocardiography
11. Caudal vena cava/pulmonary vessel size on radiographs
12. Caudal vena cava or arterial pulse pressure variation with respiration
13. Central venous pressure
14. ScvO2/SvO2
15. Cardiac output measurement
16. DO2/VO2
17. Systemic vascular resistance measurement
18. Microvascular imaging or tissue oxygenation measurements
19. Pulmonary capillary wedge pressure
20. Bloodwork indicators of end-organ perfusion and function (ALT, renal values)
21. Colloid osmotic pressure
56
What is Poiseuille’s law for flow? What does this mean for us clinically when administering fluids?
Flow = π Δ P r4 /8 η L
Δ P = Pressure differential
r = radius
η = viscosity of fluid
L = length
- This law affects flow through any tube (catheters, trachea, vessels, etc).
- Radius of the tube is significantly more important than the other factors (to the 4th power!).
- Increased pressure gradient increases flow, increased viscosity or length of the tube decreases flow.
57
What are the basic composition of 0.9% NaCl?
Na (meq/L)
K (meq/L)
Other lytes?
Buffer?
Na (meq/L): 154
K (meq/L):0
Other lytes? Cl
Buffer? None
58
What are the basic composition of Norm-R (P-lyte?
Na (meq/L)
K (meq/L)
Other lytes?
Buffer?
Na (meq/L): 140
K (meq/L): 5
Other lytes? Cl, Mg
Buffer? Acetate/gluconate
59
What are the basic composition of LRS?
Na (meq/L)
K (meq/L)
Other lytes?
Buffer?
Na (meq/L): 130
K (meq/L): 4
Other lytes? Cl, Ca
Buffer? Lactate
60
What are the basic composition of Norm-M?
Na (meq/L)
K (meq/L)
Other lytes?
Buffer?
Na (meq/L): 40
K (meq/L): 13
Other lytes? Cl, Mg, dextrose
Buffer? Acetate
61
Why do most “maintenance” fluids contain dextrose?
To make the fluid iso-osmolar to plasma (they contain less Na and would otherwise be very hypo-osmolar).
62
Explain the major differences between the different hetastarch products and how these affect the action of the product.
- Concentration in solution: % starch in the crystalloid
- Molecular weight: mean molecular weight of the starch molecules (although all have a range of molecular weights- they are not all the same weight). Higher MW lasts longer in circulation. Lower MW has more molecules, so more “pull”
- Degree of substitution (0-1): higher degree of substitution lasts longer in circulation
- Ratio of C2 vs C6 substitutions: higher ratio (more C2) lasts longer in circulation
63
What are the values for “Vetstarch”?
VES: 6%, 130/0.4, 9:1. Overall, more molecules (higher pull) and doesn’t last as long in circulation as previous HES products.
64
Explain the controversy/risks of giving human albumin products to animals
- Possibility of reactions on first administration (ie anaphylaxis)- higher risk in healthy patients, some animals have detectable antibodies to human albumin without known prior exposure
- Possibility of delayed reactions (as the patient develops antibodies and the albumin is still in the system)- usually manifest as hives, edema, fever up to 3-4 weeks after administration
- Extremely high risk of anaphylactic reaction after repeat administration when antibodies have developed (significant increase in antibodies within 10 days in 1 study)
65
Explain how to calculate a fluid plan for a patient (including all phases of fluid therapy).
- Administer shock fluids if needed
- Calculate level of dehydration and replace over a predetermined period of time. Reassess this periodically, as estimates are often wrong.
- Calculate maintenance fluid needs (variety of equations)
- Replace ongoing losses in addition to the above
- Once rehydrated, periodically assess maintenance needs for supplementation versus patient intake and discontinue when appropriate
- Determine type of fluid to administer based on patient’s overall status (electrolytes, concurrent illnesses, acid-base status, etc).
66
Name reasons you would pick LRS over Norm-R.
neuromuscular blockade (want to avoid Mg), desire for lower sodium replacement fluid
67
Name reasons you would pick Norm-R over LRS.
concurrent administration of blood products, severe liver dysfunction or DKA or lymphoma (do not metabolize lactate as well), myocardial damage/arrhythmias/brain injury (no calcium)
68
Name reasons you would pick 0.9% Saline over LRS or Norm-R.
hypercalcemia, metabolic alkalosis, hypochloremia, desire for higher sodium replacement fluid (correction of hypo/hypernatremia)
69
Name reasons you would pick Norm-M over Norm-R.
long-term maintenance fluid therapy, correction of hypernatremia
70
Name reasons you would pick Norm-R over Norm-M.
replacement fluid therapy (boluses)
71
Briefly define an acid.
Proton donor (HA)
72
Briefly define a base
Proton acceptor (A-)
73
Briefly define pH
exponential expression of the concentration of H+, in the body it is a function of the log of the ratio between CO2 and HCO3
74
Briefly define pKa
the pH at which the acid is equally dissociated/associated [HA] = [A-]
75
Explain how the bicarbonate-carbonic acid system works as a buffer in the body
- Dissolved CO2 + H20 < -- > H2CO3 < -- > H+ + HCO3-
- When an acid is added, the equation is pushed to the left (CO2 is produced, HCO3 decreases), which is then breathed off (increased RR). The kidneys then regenerate HCO3 to correct the imbalance.
- In alkalosis, the equation is pushed to the right. The respiratory rate decreases to elevate the CO2 to replace the H+. Kidneys also secrete extra HCO3 and regenerate H+ to correct the imbalance.
76
List the expected compensations for metabolic acidosis:
respiratory compensation- 0.7 decrease in pCO2 for every 2mEq decrease in HCO3
77
List the expected compensations for respiratory acidosis (acute and chronic)
metabolic compensation
Acute: 0.15 increase HCO3 for 1mmHg pCO2
Chronic: 0.35 increase HCO3 for 1mmHg pCO2
78
List the expected compensations for respiratory alkalosis (acute and chronic)
metabolic compensation
Acute: 0.25 decrease HCO3 for 1mmHg pCO2
Chronic: 0.55 decrease HCO3 for 1mmHg pCO2
79
Write the equation for anion gap.
AG= Measured Cations – Anions = (Na + K) – (Cl + HCO3)-
80
List 10 potential unmeasured acids (anions).
Methanol, Ethylene Glycol, Salicylates, Lactic Acid, Renal failure, DKA (MEGS LARD)
Sulfuric acid, propylene glycol, metaldehyde, D-lactate, ethanol
81
In the Strong Ion approach to acid-base analysis, what are the independent variables?
- pCO2
- Strong ion difference (SID): Na – (Cl + organic anions or sulfate)
- Total concentration of weak acid (Atot): weak acids/bases in plasma that are not fully dissociated at physiologic pH (Phosphate, Albumin, Globulin).
82
In the Strong Ion approach to acid-base analysis, what are the dependent variables?
HCO3 (up to 50% of daily variability in HCO3 is attributed to changes in pCO2)
83
What is the expected acid-base effect for Hypernatremia? Write the short Fencl-Stewart equation
alkalosis.
Free water effect = (Measured Na-Normal Na)/4
84
What is the expected acid-base effect for hypochloremia? Write the short Fencl-Stewart equation
alkalosis.
Chloride effect: Normal Cl – Corrected Cl
85
What is the expected acid-base effect for Hyperphosphatemia? Write the short Fencl-Stewart equation
acidosis.
Phosphate effect= (Normal Phos – measured Phos)/2
86
What is the expected acid-base effect for hypoalbuminemia? Write the short Fencl-Stewart equation
alkalosis.
Albumin effect =(Normal albumin – measured albumin) x 4
87
What is the expected acid-base effect for hyperlactatemia? Write the short Fencl-Stewart equation
acidosis.
Lactate effect = - 1 x lactate
