1
Q
What does perioperative fluid management involve?
A
Maintaining intravascular volume, augementing CO, maintaining tissue perfusion, promoting oxygen delivery and maintaining electrolyte balance
1
Q
Total body water =
A
60% of lean body mass (42L)
2
Q
What adds into total body water:
A
ICV + ECV
ICV = 2/3 of TBW - 28L
ECV = 1/3 of TBW - 14L
3
Q
ICF fluid’s primary cation/anion
A
Cation - potassium
Anion - phosphate
4
Q
ECT primary cation/antion
A
Cation - sodium
Anion - chloride
5
Q
ECF is split into 2 compartments:
A
Intravascular (25%) - plasma (3L)
Interstitial (75%) - in tissue spaces (11L)
6
Q
_____ pressures in the extracellular compartment dictate direction of fluid movement across the capillary epithelium
A
4
7
Q
Intravascular pressures:
A
Capillary hydrostatic pressure (Pc) is the intravascular blood pressure driven by CO and impacted by vascular tone
Plasma oncotic pressure (๐p) is the osmotic force of colloidal proteins in the vascular space
8
Q
Interstitial pressures:
A
Interstitial fluid pressure (Pif) is the hydrostatic pressure of the interstitial space
Interstitial oncotic pressure (๐if) is the osmotic force of colloidal proteins within the interstitial space
9
Q
Increases in capillary hydrostatic pressure (Pc) + interstitial oncotic pressure (nIF) cause fluid to______ interstital space:
A
FILTER into
Positive net filtration = fluid exudation into the tissues aka fluid exits the capillary
10
Q
Net filtration pressure equation =
A
(Pc - Pif) - (np - nif)
11
Q
Increases in plasma oncotic pressure (np) + interstitial fluid pressure (Pif) cause fluid to be______ into intravascular space
A
ABSORBED
Negative net filtration = fluid is absorbed into the vasculature
12
Q
What is the glycocalyx:
A
Gel layer on the LUMINAL (interior) surface of the vascular endothelium
13
Q
what is the glycocalyx composed of:
A
Glycoproteins, polysaccharides, and hyaluronic acid that bind to ionic side chains and proteins to create an active barrier within the vascular space
14
Q
What does the glycocalyx repel?
A
Blood products but binds to plasma albumin to preserve capillary oncotic pressure
15
Q
Disruption of the glycocalyx creates what?
A
Capillary leak which causes accumulation of fluid and debris in the interstitial space and reduces tissue oxygenation (Damaged by sepsis, ischemia, diabetes, major vascular surgery.
16
Q
RAAS system renin release causes:
A
hypotension –> reacts with angiotensinogen –> forms angiotensin I
17
Q
What is angtioensin-converting-enzyme?
A
Released by the lungs and converts angiotensin I to angiotensin II
18
Q
what is angiotensin II?
A
Acts directly on blood vessels to cause vasoconstriction + causes release of aldosterone
19
Q
What does aldosterone stimulate?
A
Reabsorption of water and salt in the kidenys, increased PVR, and increased CO
20
Q
When is ADH released?
A
In response to increased serum osmolality
Posterior pituitary gland releases ADH which causes kidney to absorb water
Preserves circulating volume and increases urine concentration and osmolality (on V2 receptor)
21
Q
What does ADH also act as?
A
Potent arterial vasoconstrictor on V1 receptors
22
Q
Function of ANP?
A
Released from increased preload causing stretch receptors within the heart release ANP
STIMULATES the kidney to release sodium and water to reduce circulating blood volume and offload the heart
Can also inhibit release of renin and ADH
23
Q
Plasma osmolarty is normally:
A
280-290mOsm/L
24
What is the primary electrolyte that controls osmolarity;
Sodium
25
What is preferrable to give for resusciation of dehydration such as prolonged fasting states, active GI losses, polyuria and hypermetabolic conditions:
Crystalloids
26
What do isotonic crystalloids do?
HYDRATE the entire ECV restoring water and electrolyte to intravascular and interstitial spaces
27
Advantages of crystalloids:
-LACK allergic potential
-Provide immediate resoration of circulating vascular volume
-preserve microcirculatory flow
-Decrease in hormone mediated vasoconstriciton
-Lower cost
28
Disadvantages of crystalloids:
75-80% will transfer into interspitial space due to hemodilution of plasma proteins and loss of capillary oncotic pressure
DILUTIONAL EFFECT on coagulation factors
29
Crystalloids Normal saline contents:
equal concentration of sodium and chloride
Sodium is higher in plasma than chloride, SO EXCESSIVE ADMINISTRATION of NS can cause hyperchloremia and hyperchloremic metabolic acidosis
30
What can hyperchloremia cause?
Decrease in GFR and renal handling of bicarbonate
31
What is Sodium chloride used for?
Neurosurgical patients due to hyperosmolality
And in PATIENTS who have anuria and end stage renal disease due to less potassium in fluid than other isotonic fluids
32
33
What is 3% saline used for?
Low doses for trauma and head-injury patients since they promote volume expansion that mobilizes intracellular AND interstitial fluid into the vasculature
34
Lactated Ringers contents:
Sodium lactate - acts as a buffering agent to maintain electrochemical balance and neutral pH of the solution
35
Advantages of LR
Better at preserving intravascular fluid than NS
36
Disadvantages of LR
LACTATE can cause gluconeogenesis (avoid large amounts in diabetics)
May contribute to ALKALOSIS due to alkalinizing effect of lactate
Mildly hypotonic, MAY cause transient serum hypoosmolality (avoid in traumatic brain injury or other neurovascular insults)
CONTAINS calcium - contraindicated for infusion with citrate (preservative in blood products)
37
Dextrans (Colloids) properties
Oldest artificial colloids
Have HIGH MOLECULAR WEIGHT (40-70 kDa) polymers derived from bacterial metabolism of sucrose
HYPEROSMOLAR and have half life of 6-12 hours
38
Disadvantages of Dextrans:
Can cause acute renal failure
COAGULOPATHIC effects due to impairment of von Willebrand factor, activation of plasminogen, and interference with platelet aggregation
NO LONGER USED
39
Gelatins (Colloids)
Synthetic colloids derived from bovine components
MOLECULAR weight of 30-35 kDa (Shorter half life of 2-4 hours)
40
Disadvantages of gelatins:
Interfere with PLATELET function
cause nephrotoxicity
Have high PROPENSITY to cause ANAPHYLAXIS
Use of them is CAUTIONED
41
Hydroxyethyl starches (HES)
SYNTHETIC macromolecules derived from starchy plants
Widely used in the EU
42
Disadvantages of HES
CAN CAUSE allergic reaction to those alleric to the starchy plants they are derived from (Potatoes, maize, sorghum)
FIRST GENERATION HES are associated with coagulopathy, pruritis and nephrotoxicity
SECOND GEN are associated with kidney injury, coagulopathy and sepsis
BLACK BOX WARNING
43
Albumin (colloids)
FRACTIONED blood product produced from pooled human plasma
Has a molecular weight of 65-69 kDa
Used as a volume expander due to small volumes providing greater degree of INTRAVASCULAR resuscitation as compared to equal or greater amounts of crystalloids
44
Disadvantages of albumin:
Costly
Anaphylaxis
45
Incisions trigger the following (starting at HPA)
Hypothalamus pituitary axis --> Hypothalamus releases corticotropin-releasing hormone --> anterior pituitary releases adrenocorticotropic hormone (ACTH) --> creation and RELEASE of cortisol from adrenal cortex
46
Incision and Cortisol:
Cortisol stimulates protein catabolism, hepatic gluconeogenesis, and glycogenolysis and release of plasma proteins
- HELPS maintain an increased plasma oncotic pressure which causes preservation of intravascular volume
47
Incision and catecholamine release:
From adrenal medulla causes increased HR, SVR, and microcirculatory vasoconstriction
- causes increase in BMR and O2 demand
- causes release of ADH which causes vasoconstriction, reabsorption of water and potassium EXCRETION
48
Local endothelial release of cytokines causes what?
Hyperthermia, increased oxygen demands, and regional alterations in microcirculatory flow
49
50
Maximum allowable blood loss formula (Lowest acceptable HCT):
MABL = EBV x (Hct - lowest acceptable hct) /. Initial Hct
51
Estimation of blood loss is both ____ and ____
Objective and subjective
Must visually look at different sponges, drapes, gowns, gloves and suction canisters
52
Fully soaked surgical sponge:
10mL of blood
53
Fully soaked lap sponge:
100-150mL
54
1g of blood =
1mL
55
Most common approach of fluid management was:
4-2-1 rules
56
Maintanence fluid 4-2-1 for 70kg:
10 kg x 4mL/hr + 10kg x 2ml/hr + 50kg x 1ml/hr = 110ml/hr
Estimated fluid deficit: 110 x 8 = 880
Surgical losses: 4-6ml/kg/hr x 70 = 280-420
Total fluids (1160-1300)
57
Deficit of fluid given over 3 hours:
50% over 1st hour
25 over 2nd
25 over 3rd
58
What is the problem with the historical approach 4-2-1
DOES NOT account for cardiovascular and renal function in patients + does not consider the impact of true fasting in elective surgical patients
If euvolemic, giving too much fluid could impair glycocalyx and cause fluid overload
59
Over resusciation could cause:
Acute CHF
Decrease tissue oxygenation
Hemodilution - anemia
Decreased gut motility
Hepatic congestion and dysfunction
Increased infection rates
60
Under-resusciatation could cause:
Hypovolemia
Decreased oxygen delivery
Reduced tissue perfusion
PONV
Increased blood viscosity
61
Targets of fluid replacement used to be:
MAP, CVP, UO but they are unreliable predictors of volume responsiveness
62
Initial research showed that patients with PA catheters who were given goal directed fluid therapy had highter ____ and ____ than those who were forced _____ amounts of fluids
DO2 and CI
Standard
Concerns about needing invasive monitors such as PA catheters in ALL patients
63
Newer protocols of GDFT include what?
BASELINE assessment of target hemodynamic values followed by SMALL boluses (200-250ml) of fluid to assess patient's position along frank starling curve
64
Frank starling mechanism assesses the relationship between
LVEDV and Myocardial contractility (measured by SV)
65
As fluid is increased (Increase in LVEDV) the myocardial contractility will increase and cause____
Optimized overlap of the actin and myosin filaments to create a stronger cardiac force
66
Ascending is preload dependent
Plateau is preload independent
67
What do dilution techniques involve:
Introduction of a fixed volume of injectate into the vascular system and the consequent measure of CO and other hemodynamic values based on the area under a time - temperature or a concentration-time curve
68
What is the classic PAC measurement device?
Thermodilution
Chilled volume of injectate (10cc) is injected via RA port on PA catheter
Blood temp is measured in PA
-CO is measured based on time it takes the injectate to get to the pulmonary artery
-Low CO = larger area under curve d/t taking longer to get from RA to PA
-High CO = smaller area under the curve d/t taking shorter time to get from RA to PA
69
What does pulse contour analysis provide?
DYNAMIC measures of preload responsiveness by quantifying the degree of change of arterial, capnography or pulse oximetry waveforms associated with cyclic respiratory variations
70
In mechanically vented patients, during inspiration the compression of the pulmonary veins and pleural restrictions augments ____ leading to _____
LV filling --> increase in SV
Expiration - SV falls d/t reduced RV preload
71
The degree of SV variation is more prominent during_____
hypovolemia
1. Increased intrathoracic pressure from PPV decreases RV filling
2. Greater inspiratory impact on RV afterload if alveolar pressure exceedds pulmonary arterial and venous pressures impeding RV ejection
3. Greater ventricular contractility inresponse to LV preload (bolus)
72
To perform SVV via pulse contour analysis, patients must be:
-Mechanically ventilated with 7-8ml/kg tidal volumes
-No arrhythmias
-PEEP <15
If SVV is > 13% the patient may benefit from fluid bolus
73
What are ERAS protocols aimed at?
Optimal fluid therapy, reduction of profound stress response attributed to sx, promote non-opioid postoperative pain modalities, and maintain baseline organ function post procedure
74
Fluid management in ERAS allows patients to have a _______
Carbohydrate clear liquid drink up to 2 hours PRIOR to surgery and eliminating mechanical bowel prep for colorectal surgeries
-Liquid decreases hypovolemia and hypotension
-carbs maintain adequate glucose and insulin lvls, thereby reducing preoperative thirst, hunger and anxiety levels experienced
75
Fluid administration by anesthetist via____ boluses to treat hypotension
250-500mL
76
Sodium is the main electrolyte in the ECV and is responsible for______
REFLECTS osmotic activity of the ECV
Concentration: 135-140 mEq/L
77
Concentration gradient between the ECF and ICF is maintained by what?
Na-K-ATPase pump
Exports 3Na into ECF for 2k cations into the cell
78
When a sodium imbalance occurs it reflects both what?
Sodium content AND water content
79
Treatment of sodium imbalance can include:
Restriction or expansion of water volume OR enhanced elmination or supplementation of sodium
80
Hyponatremia results in a condition where:
Intracellular environment is HYPEROSMOLAR relative to the ECV which leads ot an influx of water into the ICV
Major problem in brain due to confines of skull
If intracellular space becomes hyperosmolar, water from ECV will move into the brain and cause cerebral edema
81
Treatment for hyponatremia:
FLUID RESTRICTION and diuresis but needs to be done slowly
- rapid correction of sodium can cause OSMOTIC demyelination or myelinolysis --> cause spastic quadriparesis, mental disorders, and pseudobulbar palsy
DO NOT increase sodium more than 1-2mEq/L per hour
Can give 3% saline at a rate of 1-2mg/kg/hr
82
83
3 different types based on osmolality.
Normal osmolality โ pseudohyponatremia
Elevated osmolality โ hypertonic hyponatremia
Low osmolality โ evaluate ECV
- Hypovolemic hypotonic (treat with fluid)
Isovolemic hypotonic โ depends on urine sodium
Hypervolemic hypotonic โ sodium and water restrictions + diuretics
84
Why does hypernatremia occur?
Due to impaired water intake*
The brain adapts to slow onset hypernatremia by conserving intracellular solutes
85
What can rapid onset hypernatremia be accomanied by?
RAPID shrinking of the brain and traction on intracranial veins and venous sinuses
86
Causes of hypernatremia:
Vomiting, diarrhea, GI suctioning, burns
Excessive sodium intake
Increased renal lossess
87
Treatment of hyperantremia:
Replacement of water deficit
88
Hypernatremia - shrinkage
Hyponatremia - swelling
89
What is diabetes insipidus?
Lack of ADH, which causes lots of loss, can be seen after pituitary surgery, subarachnoid hemorrhage, and TBI
90
What is the princiipal intracellular electrolyte?
K+
Intracellular conc. - 150-160 mEq/L
Extra conc. - 3.5-5mEq/L
91
How is potassium maintained?
Na+/K+ pump
- insulin can stimulate this pump
- Catecholamines can stimulate this pump
Absorption of K+ from GI tract
Renal excretion or reabsorption into the peritubular capillary network
- REGULATED mainly by aldosterone
92
What is hypokalemia and what can it result from?
K+ <3.5mEq/L
Can result from GI LOSS, RENAL LOSS, INTRACELLULAR shift, increased non renal losses (Sweating, diarrhea, vomiting), endocrinopathies, and poor intake (malnutrition)
93
Why does intracellular shift of K occur?
WHEN K+ shifts from ECV to ICV caused by BETA ADRENERGIC stimulation, INSULIN, and ALKALOSIS
94
What can levels of <2.5mEq/L K+ cause?
Paresthesia
depressed deep tendon reflexes
Muscle weakness
fasciculations
95
What EKG changes with hypo K?
ST SEGMENT depression
Flattened T wave
Presence of u wave
96
Treatment of hypo K?
IV ADMIN of K+ (IF DUE TO WHOLE BODY K+ losses
DO NOT administer if there was just a shift from ECV into the ICV
Must monitor EKG
97
Dose of K+
10-20mEq per hour is recommended to avoid iatrogenic hyperkalemia
10mEq per hour in a peripheral line
20mEq per hour in a central line
Should be mixed in a dextrose free solution to prevent stiulation of insulin (leads to K+ redistributing to the intracellular space)
98
What does Hyper K mostly manifest as?
EKG CHANGES
98
Define hyper k and what are the causes?
K+ >5.0 bEq
Causes include:
- Impaired renal excretion
- burns
-high intake of K+
Shift of K+ from ICV to ECV
-Meds - ACE inhibitors + ARBs decrease angiotensina nd cause hyperkalemia
-Beta 1 blockers - inhibit renin release which de creases aldosterone and causes hyper K
-Succ
99
Treatment of Hyper K
first assess PSEUDOHYPERKALEMIA - occurs due to hemolysis of blood sample, leukocytosis, thrombosis
Once assessed - calcium to stabilize cardiac membrane excitability, shift, eliminate!
100
101
Where is calcium found and what is the normal amount?
99% FOUND IN BONES - 1% is found in the plasma and body cells
Normal value IN THE BLOOD - 9.0-10.5mg/dL
102
1% of calcium is found in the ECV and exists in 3 fractions:
Ionized calcium 50%
Bound to anions 10%
Bound to albumin 40%
103
Calciums role :
Important action as a second messenger that couples the cell membrane receptors to cellular responses
- Muscle contractions (INcluding cardiac)
- release of hormones and neurotransmitters
- blood coag
104
105
How are serum calcium levels maintained?
PRIMARILY BY release or the inhibition of parathyroid hormone, but also by vitamin D and calcitonin
During periods of hypo/hypercalcemia, levels of PTH decrease or increase to normalize serum calcium
106
Hypocalcemia causes:
Hyperventilation (Causes increased pH which facilitates increased protein binding of Ca2+)
MASSIVE rapid transfusion (Citrate binds to calcium)
PARATHYROID hormone deficiency
VITAMIN D deficiency (Malnutrition, malabsorption, sepsis, anticonvulsants)
MEDICATIONS - phenobarbitol, phenytoin, carbamazepine
107
Treatment of hypocalcemia?
INFUSION OF CALCIUM
- CALCIUM chloride - 500-1000mg q6-8 hours (272mg of elemental calcium)
- can cause venous irritation and tissue necrosis
CALCIUM GLUCONATE - 10 mL of 10% over 5-10min, FOLLOWED by an infusion at 0.5-1.5 mg/kg/hr (contains 90mg of elemental calcium
108
Symptoms of hypocalcemia:
CHVOSTEK sign - provoked facial spasms with tapping of the facial nerve
Trousseau sign - provoked carpal spasm after inflation of BP cuff
EKG: Prolonged QT
109
Causes of hypercalcemia:
Movement of calcium from bone to ECV
PRIMARY HYPERPARATHYROIDISM (>50%)
MALIGNANCY
110
What is mild hypercalcemia:
- Serum Ca2+: 10.5-11.9
111
What is moderate hypercalcemia:
Serum Ca2+: 12-13.9 mg/dL
112
Hypercalcemic crisis:
Serum Ca2+: 14-16mg/dL
113
Symptoms of hypercalcemia:
SHORTENED QTc
Hypertension
CONFUSION, SOMNOLENCE, LETHARGY, SEIZURES
N/V, constipation
114
Treatment of hypercalcemia:
VOLUME EXPANSION WITH NS
Loop diuretics (Support in literature varies)
115
Magnesium is the ____ most abundant intracellular cation
SECOND
40-60% stored in muscle
30% in cells
1% in serum
116
How is magnesium regulated?
Inside of intestines and kidneys
Cofactor in many enzymatic reactions including energy metabolism, protein synthesis, neuromuscular excitability and function of Na-K-ATPase pump
117
Normal range of mag:
1.7-2.1mg/dL
118
Magnesium is an antagonist to waht?
Ca2+
119
What can magnesium block?
NMDA receptor helping with pain
Used for torsades and pre-eclampsia
120
Hypomagnesemia causes:
<1.8mg/dL
-Excessive alcohol intake
-PREGNANCY
-Renal losses
-GI LOSSES
-Medications
121
Symptoms of hypomag?
Fatigue, muscle weakness/spasms, depression
122
EKG changes with hypomag?
Flat T wave
PRESENCE of U wave
PROLONGED QT interval
WIDENED QRS
123
Treatment of hypomag?
1-2g mag sulfate over 5 mins, followed by 1-2g per hour
124
Hypermag causes:
>2.5mg/dL
Mainly from iatrogenic causes (IV admin)
125
Symptoms of hypermag
Depression of peripheral and CNS - Starts as diminished DTR's --> loss of reflexes --> resp depression
126
EKG changes with hypermag:
Prolonged PR
Prolonged QT interval
Widened QRS
Potentiation of NM blockade
127
Treatment of hypermag:
D/C of mag infusion
CALCIUM CHLORIDE can be used as an agonist
128
129
Where is majority of phosphate and what is the primary component?
Phosphate is located in bone (85%) - small amount in plasma exists as phosphoipids, phosphate esters and inorganic phosphate
PRIMARY component of ATP and 2,3 DIPHHOSPHOGLYCERATE (2-3DPG)
130
Concentration of phosphate in the plasma is inversely proportional to:
Calcium
Tightly controlled by same mechanisms (PTH, Vitamin D and calcitonin
131
Hypophosphatemia level and causes:
<2mg/dL
Causes - increased renal excretion and intestinal malabsorption
132
S/s of hypophos
Left shift oxyhemoglobin DC due to low 2-3DPG --> causes increased affinity between Hgb and oxygen and results in anaerobic metabolism, decreased ATP formation and acidosis
Hypoxia, Heart blocks, bradycardia, Asystole
Seizures
Coma
133
Treatment of hypophos?
1-3mEq/hr slowly (to avoid inducing hypocalcemia
134
Hyperphos causes and level
>4.7mg/dL
Causes
- Cellular destruction
- CKD
135
S/S of hyperphos
Hypocalcemia (SAME SYMPTOMS)
Bradycardia
QT prolongation
Chvostek's
Trousseau's
Tetany
Muscle weakness/spasm
136
Treatment of hyperphos:
Dietary restrictions
Increasing phosphate excretion via phosphate binders (Calcium carbonate)
NA 1
flashcards
Decks in class (27)
# Cards
-
infection control49
-
Table top80
-
Preop eval Pt 1105
-
Basic monitoring141
-
Preop eval Pt 2167
-
airway163
-
ABG22
-
General Anesthesia74
-
Fluid management138
-
Positioning106
-
Monitored anesthesia Care110
-
Oxygenation and mechanical vent pt 148
-
Tables Exam 210
-
Oxygen therapy/mechanical vent Part 2121
-
Hemorrhage/transfusion148
-
Regional Anesthesia187
-
Allergic response127
-
PACU care115
-
MH51
-
Review exam 316
-
Opthalmic sx75
-
Geriatrics/obesity136
-
Orthopedics121
-
Lap/ROBO49
-
NORA162
-
GYN153
-
GI diseases159
