Fluid Therapy - Exam 4 Flashcards
Total body water (TBW) represents about _% of lean body mass
60%
_ volume represents about 2/3 of TBW and _ volume represents about 1/3 of TBW.
Intracellular
Extracellular
ECV
-primary cation
-primary anion
Sodium
Chloride
ICV
-primary cation
-primary anion
Potassium
Phosphate
Resting membrane gradient of electrolytes in the ECV and ICV are maintained by the ++_ pump in the cell membrane which actively brings Na+ into the cell.
Na, K, ATPase pump
Under normal circumstances, the daily fluid volume needed to maintain TBW homeostasis is:
25-35mL/kg per day
(~2-3L/day)
1/4 of the ECV is made up of the _ compartment while the other 3/4 is made up of the _ compartment
Intravascular
Interstitial
_ _ _ (Pc) is the intravascular blood pressure, driven by the force of the _ and impacted by the _ tone
Capillary hydrostatic pressure
CO
vascular
_ _ _ (Pif) is the hydrostatic pressure of the interstitial space.
Interstitial fluid pressure
The Pif of most tissues is _ (positive/negative) likely from the effects of the lymph vessels in the interstitium. However, the tissues of the kidneys, brain, skeletal muscle, and bone marrow are _ (positive/negative)
negative
positive
_ _ _ (πp) is the osmotic force of _ proteins within the vascular space
Plasma oncotic pressure
colloidal
_ _ _ (πif) is the osmotic force of _ proteins within the interstitial space
Interstitial oncotic pressure
colloidal
_ is the primary determinant of plasma and interstitial oncotic pressures.
Albumin
-bc of its low molecular wt and high concentration
Increasing πif and Pc favor fluid filtration into the _ space whereas increasing πp and Pif favor fluid absorption into the _ space.
interstitial
intravascular
What equation is this?
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
Starling Equation
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-What does Jv represent?
Net fluid movement between compartments
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-What does Kf represent?
filtration coefficient accounting for capillary surface area and endothelial permeability to water (or capillary hydraulic conductivity)
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-What does [Pc-Pif]- σ[πp-πif] represent?
net driving force
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-What does σ represent?
reflection coefficient ranging from 0-1accounting for different degrees of endothelial permeability to different substances like albumin and large polar molecules
-σ = 0 = endothelium is freely permeable
-σ = 1 = it’s completely impermeable
-during capillary filtration, 100% of substance is reflected back into the vascular lumen
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
Increasing the Kf favors _ (filtration/absorption)
filtration
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-When net filtration (Jv) is positive, fluid moves towards the _ and is _.
tissues
filtered
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πif])
-When net filtration (Jv) is negative, fluid moves towards the _ and is _.
vasculature
absorbed
At the arterial end of the capillaries, the net filtration is slightly _ (+/-) and the venous end is slightly _ (+/-)
arterial- positive
venous - negative
Normally, the overall balance of filtration pressures in capillaries in the whole body is slightly _ (+/-), so a small % of intravascular volume is constantly filtered into interstitial space at _mL/min.
positive
2mL/min
-this volume is sent back intravascular via the lymphatic system
When euvolemic, net filtration is ~ _ (>,<, = ) lymphatic flow.
equal
The _ is the gel layer on the luminal surface of the vascular endothelium and plays a major role in the _ _ effect.
glycocalyx
double barrier
Processes supported by the glycocalyx:
-transcapillary fluid exchange
-microcirculatory flow
-blood component rheology
-plasma oncotic pressure
-signal transduction
-immune modulation
-vascular tone
The glycocalyx is about _ to _ mcM in diameter.
0.1-1.2mcM
The glycocalyx is composed of a matrix of _, _, and _ acid.
glycoproteins
polysaccharides
hyaluronic acid
The glycocalyx binds to _ _ _ and _ _, creating a physiologically active barrier in the vascular space.
ionic side chains
plasma proteins
The barrier created by the glycocalyx repels _ charged polar compounds and _ _ , preventing adhesion to the wall and augmenting laminar flow.
negatively charges
blood components
The glycocalyx binds to _ which helps preserve capillary oncotic pressure and _ its permeability to water. This modulates the impact of plasma _ pressure on net filtration. This is called the _ _ effect.
albumin
decreases
hydrostatic
double barrier
Net filtration (Jv) = Kf ([Pc-Pif]- σ[πp-πsg])
-What is this equation?
REVISED Starling Equation
-accounts for the double barrier effect
-πsg represents the oncotic pressure in the subglycocalyx space between the glycocalyx and endothelium
How does the glycocalyx affect the inflammatory process?
-contains inflammatory mediators whose binding sites are within its matrix, preventing leukocyte adhesion except when acute inflammation occurs or the endothelium is damaged
Beyond preventing unwanted adhesions to the vessel wall, facilitating the double barrier effect, and immune modulation, the glycocalyx also scavenges for _ _, binds to and activates _ _, and regulates _ _ from local vasoactive responses to mechanical stress.
free radicals
ANTIcoagulation factors
signal transduction
Normal minute daily alterations in TBW are regulated by _, _, and _ pathways.
RAAS
ADH
ANP
T/F Regulation of the ECV is largely dependent on potassium homeostasis
false
RAAS process
1._and _ afferent arteriole baroreceptors detect hypotension and _ (PNS/SNS) activation
2. The _ cells of the kidney release renin
3. Renin circulates and meets circulating angiotensinogen, cleaving it so it becomes active as _.
4. Angiotensin I causes _ vasoconstriction until it reaches the _.
5. In the , angiotensin I is converted to angiotensin II via _ _ _ ().
6. Angiotensin II is a potent _ and directly acts on the _ _ to reabsorb Na+ and water
7. Angiotensin II also makes the adrenal cortex release _, which increases Na+ and water _ by the kidneys.
- Intracardiac and renal
- juxtaglomerular
- angiotensin I
- local; lungs
- lungs; angiotensin-converting enzyme (ACE)
- vasoconstrictor; renal tubules
- aldosterone; retention
ADH process
1. _ in the hypothalamus detects minor increases in serum osmolality.
2. The _ _ _ releases ADH and the hypothalamus stimulates _.
3. ADH causes _ channels in the kidneys to absorb large amounts of water.
4. This causes preserved volume and drastically _ urine concentration and osmolality.
5. ADH also works as a potent _ _.
6. _ blood volume detected by baroreceptors in the _, _ body and aorta also can stimulate the release of ADH.
- Osmoreceptors
- Posterior Pituitary Gland; thirst
- aquaporin
- increasing
- ARTERIAL vasoconstrictor
- Decreased; atria, carotid body
ANP process
1. _ receptors in the cardiac atrial walls detect -volemia ( preload).
2. This stimulates the release of ANP from cardiac _.
3. ANP released causes the kidney to _ Na+ and water, _ the blood volume and _-loads the heart.
4. ANP also produces specific vasoactive responses in the afferent and efferent renal _ to _ the GFR.
5. This _ in GFR _ the release of renin and ADH.
6. Alternatively, when the preload is _, atrial receptors inhibit the release of ANP.
- Stretch; hypervolemia/ increased preload
2.myocytes - release; reducing; off
- arterioles; increase
- increase; decreases
- low
Daily water fluctuation represents only _% of TBW
0.2%
-bc of regulatory mechanisms maintaining fluid/lyte status
_ are preferred for resuscitation of dehydration conditions such as prolonged fasting, active GI losses, polyuria, and hypermetabolic states.
Crystalloids
-all of those conditions cause a hypertonic state of the plasma
When trying to fix hypertonicity from dehydration conditions, crystalloids can hydrate the entire _, restoring water/lyte homeostasis in both the _ and _ spaces.
ECV
intravascular and interstitial
In dehydration states, crystalloid admin is useful for:
-immediate restoration of circulating vascular volume
-preserving microcirculatory flow
-decreasing hormone-mediated vasoconstriction
-correcting plasma hyperviscosity from hemorrhage states
T/F Compared to colloids, crystalloids have a high allergenic potential compared to colloids, metabolize poorly, and have poor renal clearance.
false
-less allergy potential, better metabolized and excreted
T/F Because crystalloids are distributed in the ECV evenly, they expand plasma volume very well
-false
Due to _ molecular wt, crystalloids contribute to _ of plasma proteins and loss of capillary oncotic pressure, causing filtration of _ to _% of volume given into the interstitial space.
low
hemodilution
75-80%
The original and most commonly given crystalloid is:
0.9
Of all the isotonic crystalloids, _ is the least physiologic.
0.9
T/F There is more sodium than chloride in 0.9.
false, they are about equal
-there is more sodium than chloride in normal human plasma
Hyper-_ from high amounts of 0.9 administration could cause acid/base imbalance, leading to dose-dependent metabolic _.
Hyperchloremia
metabolic acidosis
Even with compensatory mechanisms to regulate pH, using 0.9 for volume resuscitation causes marked changes in _ excess from _ load. This can _ volume overload if a _ base excess was the infusion trigger.
base
chloride
worsen
negative
Excess renal absorption of chloride from excessive 0.9 admin can cause a _ in GFR and impair renal handling of _.
decrease
bicarbonate
Increased sodium load from excess 0.9 admin can cause increased sodium and water _, _, and _ edema.
retention
hemodilution
interstitial
Giving _L of 0.9 to healthy pts causes a positive sodium and water balance that takes up to _ days to excrete.
2L
2 days
ERAS strongly recommends the use of _ _ solutions for periop fluid management in the setting of high-volume fluid resuscitation.
balanced crystalloid
Which fluid is preferred for pts AT RISK for cerebral edema?
0.9
-mild hyperosmolality
Why is 0.9 preferred for fluid admin in pts that are anuric and ESRD?
-they would have a harder time excreting the potassium from more balanced crystalloids
3% saline solutions are indicated for:
trauma
head injuries
severe hyponatremia
-can help with intracranial hypertension
Hypertonic saline (3% +) promote volume expansion, pulling fluid from _ and _ spaces into the intravascular space.
intercellular
interstitial
Potential risks of hypertonic saline solutions:
vascular irritation
sudden massive fluid shift into intravascular space
dehydration of neural cells resulting in osmotic demyelination syndrome
The buffering agent (bicarbonate substrate) in LR is:
sodium lactate
T/F 0.9 is more effective in preserving intravascular volume than LR
false
The sodium lactate in LR maintains the electrochemical balance and _ pH while decreasing the anionic requirement for _.
neutral
chloride
Large volumes of LR aren’t recommended for diabetic pts because the byproduct from the _ metabolism can increase the rate of _.
hepatic
gluconeogenesis
T/F LR’s byproduct can increase the rate of glycogenesis and, therefore, isn’t recommended in large volumes to diabetic pts.
false
increases the rate of gluconeogenesis, not glycogenesis
The lactate metabolism pathway found in LR can have an _ effect and cause mild metabolic _.
alkalizing
alkalosis
How can LR contribute to cerebral edema?
it is mildly hypotonic and can cause transient serum hypoosmolality, leading to cerebral edema
T/F LR is the preferred solution to infuse blood products.
FALSE!!!!!!
-it contains citrate which increases the risk of coagulation with calcium!!!!!!
-DO NOT INFUSE BLOOD PRODUCTS WITH LR; CONTRAINDICATED!!!
LR contraindications:
-blood product admin
-pts with TBI, other neurovascular insults
-not CI, but avoid large volumes in diabetic pts (increases gluconeogenesis)
The most isotonic balanced crystalloid solutions are:
-Plasmalyte-A
-Normosol-R
-Isolyte S
T/F 0.9 preserves physiologic pH and renal perfusion better than balanced salt solutions like plasmalyte.
False
-they have a better acid/base profile as well
Pros of plamalyte-a, isolyte s, and normosol-r:
-most isotonic of balanced solutions
-most favorable acid/base profile
-preserve pH better than 0.9
-preserve renal function better than 0.9
-use sodium gluconate and sodium acetate as buffers instead of lactate like LR
-no calcium, able to use with blood products
Composition of Plasma:
-all lytes in mEq/L
Na+ = 142
K+ = 4
Cl- = 103
Phosphate = 1.4
Mag = 2
Ca++ = 5
Composition of Plasma:
-pH and osmolality (mOsm/L)
pH =7.4
291 mOsm/L
Composition of Plasmalyte-A/Normosol-R/ Isolyte-S
-all lytes (in mEq/L)
Na+ = 140-141
K+ = 5
Cl- = 98
Phosphate = 1 (only in isolyte)
Mag = 3
Acetate = 27
Gluconate = 23
-no calcium!
Composition of Plasmalyte-A/Normosol-R/ Isolyte-S
-pH and osmolality (mOsm/L)
pH = 7.4
294-295 mOsm/L
Composition of LR
-lytes (mEq/L)
Na+ = 130
K+ = 4
Cl- = 110
Ca++ = 3
Lactate = 28
Composition of LR
-pH and osmolality (mOsm/L)
pH = 6.2
275 mOsm/L
Composition of 0.9%
-lytes (mEq/L)
Na+ = 154
Cl- = 154
Composition of 0.9%
-pH and osmolality (mOsm/L)
pH = 5.6
310 mOsm/L
T/F Crystalloids are high molecular weight molecules and colloids are typically low molecular weight molecules.
False
Colloids DIRECTLY increase plasma oncotic pressure (πp) by causing the endothelial glycocalyx to _ transcapillary filtration
decrease
T/F A fluid sparing method of increasing intravascular volume is giving crystalloids
false,
giving colloids
Only 2 naturally occurring colloids available for infusion:
-albumin
-PRBC
Which 3 ways are colloids classified by?
-molecular wt
-concentration
- half life
Dextran
-molecular wt
-1/2 life
40-70kDa
6-12 hr
Dextrans are derived from _ metabolism of sucrose
bacterial
-not used anymore due to renal and coag issues and anaphylaxis
Dextrans cause acute renal failure in 2 ways:
-INDIRECT hyperosmotic renal injury
-DIRECT renal tubular damage from accumulation
Dextrans cause coagulopathic effects in 4 ways:
-impairs von Willebrand factor
-activates plasminogen
-interferes with platelet aggregation
-adheres to the surface of platelets and RBCs interfering with crossmatching of blood products
T/F Gelatins are derived from porcine components
false
bovine
Gelatin
-molecular wt
-1/2 life
30-35kDa
2-4hr
-limited duration of plasma expansion
Cons of gelatins:
-interferes with platelet function
-cause nephrotoxicity
-high risk for anaphylaxis with urea-based formulations
-concern for bovine spongiform encephalitis (BSE)
Hydroxyethyl starches (HES) are made from starchy plants like _, _, and _.
potatoes
maize
sorghum
-can cause allergies if ppl are allergic to these !
HES are created by substituting hydroxyl groups at the _, _, and _ carbon atoms.
2nd, 3rd, and 6th
HES are classified by:
-molecular wt
-substitution ratios
C2/C6 ratio compares the degree of substitution at the 2nd carbon atom to the 6th and if the ratio is _, the HES will be more difficult to metabolize
high
1st gen HES:
Hetastarches
Hexastarches
1st gen HES
-molecular wt
-sub ratio
Highest molecular wts
>450kDa
0.6-0.7 ratio
1st gen HES
-a/e
-dose-dependent coag issues
-nephrotoxic (interstitial deposits accumulate in tissues/organs)
-pruritis
How do 1st gen HES contribute to dose-dependent coagulopathies?
-hemodilution
-binding up clotting factors
-interfering with platelet adhesion
-inhibiting fibrin polymerization
-alter plasma viscosity
2nd gen HES:
Pentastarches
2nd gen HES
-mol wt
-sub ratio
Medium wt
200-260kDa
sub ratio 0.5
3rd gen HES:
Tetrastarches
3rd gen HES
-mol wt
-sub ratio
low molecular wt
70-130kDa
sub ratio 0.4
HES’ in general are associated with risks such as:
-kidney injury
-dialysis
-coagulopathy
-sepsis
-increased mortality
-FDA black box warning for renal issues and increased mortality
Adverse effects associated with HES’ can last up to _ days
90
_ is a fractionated blood product made from pooled human plasma
albumin
Albumin
-mol wt
65-69kDa
T/F Albumin has a high risk of transferring diseases as it is a blood product.
false,
it is heat treated to inactivate pathogens and eliminate risk of disease transmission
Which circumstances are ideal for admin of albumin?
-volume expansion in the setting of active loss NOT requiring transfusion
-helping reduce tissue edema
-hypoalbuminemia
T/F Albumin requires a lot of volume to see an effect but is cheaper than crystalloids.
false
-small volume = larger effect than crystalloids
-more expensive than crystalloids
T/F Because albumin is heat treated, it doesn’t run the risk of transmitting diseases and causing immune reactions.
false
-it doesn’t transmit diseases BUT it does have an anaphylactic and immune-mediated reaction risk
_ is a carrier for a number of protein-bound ionic substances, including drugs and their metabolites, electrolytes, enzymes, and hormones
albumin
Albumin carries a _ charge and binds ions which _ plasma osmolality and intravascular volume. This is called the _ Effect.
negative
increase
Donnan
_ are preferred for replacing circulating blood volume in pts with intact endothelial glycocalyx undergoing acute volume loss.
Colloids
What can occur if giving albumin or colloids to a pt with endothelial injuries?
Pulmonary edema and other end organ complications
-hyperglycemic pt may have endothelial injuies!
What may occur when giving a euvolemic pt a colloid?
ANP-mediated HYPERvolemic endothelial disruption
Avoid giving colloids to pts who are _-glycemic to prevent worsening endothelial injuries
hyper
Albumin is _ likely to cause nephrotoxicity and disrupt vascular endothelium, and can _ renal perfusion in septic patients.
less
preserve
Which colloid solution can help preserve the glycocalyx in early sepsis?
albumin
Biological processes from surgery that increase plasma oncotic pressure (πp) and preserve intravascular volume:
1. Surgical incision stimulates somatic and autonomic _ nerves which activate the _ _ _ (HPA)
2. HPA activation causes the _ to release corticotropin-releasing hormone
3. This causes the _ _ gland to release _ hormone (ACTH)
4. ACTH causes the creation and release of _ from the adrenal cortex
5. This stimulates _ catabolism, hepatic gluconeogenesis and _, increased hepatic creation and release of _ _
- afferent, hypothalamus-pituitary axis
- hypothalamus
- ANTERIOR pituitary gland, adrenocorticotropic
- cortisol
- protein, glycogenolysis, plasma proteins
-this all results in increased energy substrates which helps keep plasma oncotic pressure and intravasc volume stable
-cortisol is bad if pt is hyperglycemic or vascular overloaded
Hyperglycemia risks regarding organ perfusion/vascular flow:
-MAJOR risk factor for the damage/destruction of endothelial glycocalyx
-impaired wound healing
-osmotic diuresis
-impaired immune response
Physical stimulus from surgery directly stimulates sympathetic nerves causing release of _ from the adrenal _.
catecholamines
medulla
Catecholamine release from direct surgical stimulation of SNS causes increased:
-HR
-SVR
-microcirculatory vasoconstriction
-basal metabolic rate
-O2 demand
if in setting of hyperosmolar conditions too:
-release of ADH (more vasoconstriction)
-reabsorption of water
-K+ excretion
Surgical trauma/ tissue injury stimulates local endothelial release of _ and other inflammatory mediators.
cytokines
Release of cytokines and inflammatory mediators from surgical trauma cause:
-hyperthermia
-increased O2 demands
-regional changes in microcirculatory flow
LOW level cytokine release from surgical trauma is beneficial because:
-promotes local hemostasis
-migration of neutrophils to injured site
Cortisol release from surgery is beneficial because:
-has profound anti-inflammatory effects, inhibiting the production, release, and accumulation of inflammatory mediators
-preserves intravascular volume from increased plasma oncotic pressure
Unrestricted/ prolonged release of cytokines from surgical trauma cause:
-vasodilation
-endothelial damage
-increased filtration
-tissue edema
-insulin resistance
-intravascular loss
-HoTN
-poor organ transfusion
Severe tissue damage from prolonged surgery, especially in open abdominal cases, can cause _ loss of GI endothelial integrity which causes translocation of _ and _ inflammatory responses
inflammatory
bacteria
systemic
During hypovolemia or hemorrhage, decreased _ favors absorption and supplies an _ of fluid volume from the interstitial space into the intravascular space.
Pc (capillary hydrostatic pressure)
autotransfusion
During hypervolemia or vascular overload, increased _ and dilutional decreases in _ favor filtration, overfilling the interstitial space and overwhelming the _ system.
Pc (capillary hydrostatic pressure)
πp (plasma oncotic pressure)
lymphatic
Main cause of tissue congestion, capillary collapse, loss of waste removal and nutrient exchange, decreased microcirculatory flow, and tissue ischemia is:
Interstitial edema
Laparoscopic surgical technique benefits:
-less invasive
-reduced tissue damage, blood loss, and inflammatory release
Abdominal insufflation/pneumoperitoneum causes direct mechanical suppression of _ blood flow, causing transient _ ischemia and _ changes.
splanchnic
splanchnic
microcirculatory
Insufflation of the abdomen during lap cases causes SNS mediated _ of splanchnic circulation, sacrificing gut mucosal tissue _ and predisposes the GI epithelium to _ injury when flow is restored.
vasoconstriction
perfusion
reperfusion
During insufflation of the abdomen, especially when done rapidly or with high pressures or _-_mmHg, peritoneal and mesenteric _ receptors can cause a _ response.
12-15mmHg
AFFERENT
vagal
Abdominal insufflation affects on CVP:
-can increase it from shunting splanchnic blood to thorax, this releases ANP
-can decrease it from decreased venous return from increased intraabdominal pressure
-if pt is hypovolemic, can cause cardiac collapse if pressures are high enough to compress the IVC
Adominal insufflation affects on SVR:
-significant compensatory increase in SVR from increased intrathoracic pressure
Abdominal insufflation causes SV to _
decrease
-due to compensatory increase of SVR from intrathoracic pressure
Abdominal insufflation causes MAP to _
increase
-this is from increased SVR despite the vascular flow being decreased
Insufflation to pressures of _-_mmHg decreases both R and L ejection fractions
10-15mmHg
-healthy hearts compensate by increasing HR and SV at the cost of increased O2 demand but heart failure pts cannot
Anesthetic interventions that can mitigate body’s responses of surgical trauma:
-opioids and precedex can reduce HPA stress response
-neuraxial anesthetics reduce spinal cord transmission of afferent impulses to decrease HPA response
-precedex can assist with analgesic effects and attenuate hemodynamic changes during lap cases
T/F Pts should have prophylactic volume admin even if they are euvolemic due to surgical losses
false,
don’t prophylactically hydrate the pt
ERAS strategies include _ fasting times and evaluating the need for _ bowel prep and trying to eliminate it if possible.
decreasing
hypertonic
-more isotonic bowel preps are better
T/F fluid management should account for the 3rd space volume deficits.
-false
-replacing fluid in accordance to 3rd space can cause up to 10kg wt gain
Why are MAP, CVP, and urine output not good indicators of fluid responsiveness?
-CVP depends on venous return, not just volume. Can be affected by R heart/ pulmonary function too.
-urine output if impacted by a million factors, including enhanced neuroendocrine responses, increased ADH with anesthesia too
-if MAP is low, they could also have altered vascular tone, not hypovolemia
How can MAP and CVP help determine fluid responsiveness?
-trending data
-useful as factors in a dynamic setting of multiple other factors measuring responsiveness
Perioperative GDFT is beneficial in reducing complications, supporting a timely recovery of _ function in major abdominal surgeries and improving overall survival rates
bowel
GDFT helps achieve targeted hemodynamic _ and _ _ optimization
interventions
oxygen delivery (DO2)
“Zero balance” strategy for intraop fluid management:
avoid surplus fluid to strictly maintain preop body wt
-basal fluid infusion with 1:1 fluid/blood replacement of losses
ERAS protocols combine both _ _ and _ _ _ _ strategies to manage fluid. This is called _ _ _ _.
zero balance
GDFT
goal directed fluid restriction
T/F Periop Quality Institute (POQI) recommends zero balance as fluid strategy of choice but GDFT is an ok alternative.
False
GDFT is strategy of choice and zero balance is ok alternative
Main goal of GDFT is to use individualized hemodynamic end points to support O2 transport balance by:
-minimizing: O2 demand
-optimizing: CO, tissue oxygenation, capillary and MACROvasc flow, O2 and nutrient delivery, and end-organ perfusion
GDFT protocols begin with _ _ _ measures then a small fluid challenge of _-_mL to see where pt is on the Starling curve
baseline target hemodynamic
200-250mL
Most GDFT protocols promote constant reassessment of factors such as _ responsiveness and _ _ every - minutes.
preload
O2 delivery
5-10min
The Frank-Starling mechanism is the relationship between _ and _.
LVEDV
SV
T/F Increased R ventricular preload will (to an extent) increase myocardial contractility and CO
False
-LEFT ventricular preload, not right. A lot can happen between those 2 structures affecting SV/CO
Increased L vent preload increases myocardial contractility (to a point) by stretching cardiac _ and optimizing the overlap of _ and _ filaments to generate greater force
sarcomeres
actin
myosin
Frank-Starling curve
-Ascending portion represents
preload dependence
-pts with normal heart WILL respond to fluid here and have higher SV
Frank-Starling curve
-Plateau portion represents
preload independence
-normal hearts will not compensate for extra volume and SV will no longer increase
Frank-Starling curve
-longer plateau of the pathophysiologic curve represents
sick heart (HF or vent dysfunction) can only tolerate small volumes of fluid before its SV stops increasing
-pts with poor ventricular compliance may move from being preload dependent to volume overloaded very quickly with minute increases in fluid
Thermodilution
-CO is calculated as area:
under curve
For thermodilution CO measurements, a lower CO would have a _ area under the curve
larger
-bc time needed for fluid to return to same temp will take longer
PAC is the most invasive method of hemodynamic monitoring used in GDFT but can measure:
-comprehensive assessment of cardiac function
-PAWP
-pulm edema
PAC hemodynamic monitoring risks:
-thrombus
-arrhythmias
-bleeding
-PA rupture
-infection
Devices used in GDFT that are less invasive than PAC:
-PiCCO (waveform analysis, injectate)
-VolumeView (injectate, integrates invasive and noninvasive data)
-LiDCOplus/PulseOCO (has attachments to monitor anesthesia depth)
-Pulse contour analysis (Flotrac, Hemosphere, ProAQT, Pulsioflex)
Dynamic measures from pulse contour analysis are predictive of fluid responsiveness only if the calculated value is > _ %
> 13%
NONinvasive systems for hemodynamic monitoring:
-ClearSight (finger cuff for a brachial art waveform)
-CNAP (double finger system)
T/F Gold standard for direct eval of cardiac function and volume status is Thoracic Impedance Cardiography (ICG)
False
-TEE
Information gained from a TEE:
-thoracic blood velocity
-real time LV function and aortic compliance
-real time preload responsiveness
-corrected flow time (FTc)
-SV
-change in peak aortic pulse wave velocity
-vent size
-systolic/diastolic function
-valve and wall abnormalities
-volume status
-cardiac handling of fluid admin
Drawbacks/limitations of thoracic electrical bioimpedance (TEB) for hemodynamic measurement:
-interference from pleural and pericardial effusions
-arrhtyhmias
-AV insufficiency
-aortic aneurism
-morbid obesity
-movement artifact
Measures of tissue oxygenation assess global tissue O2 balance with measuring _, _ _, and _ _ blood gases along with calculations of O2 consumption (VO2) and O2 delivery (DO2).
arterial
mixed venous
central venous
Primary goal for GDFT for tissue oxygenation is to maintain O2 transport balance by optimizing _ and minimizing _.
DO2 (optimizing fluid, preserving CO and microcirculatory flow, and transfusions)
VO2 (minimizing opioids, beta-blockers, and maintaining normothermia)
What are 2 ways blood loss from surgery causes imbalance in O2 transport?
-loss of circulating volume
-loss of O2 carrying capacity
ERAS goals for major surgeries:
-decrease postop complications
-accelerate recovery after surgery
-promote early mobilization and discharge
ERAS preop goal for fluids:
pt arrive in OR in euvolemic state
ERAS fasting guidelines
clear liq
breast milk
formula/nonhuman milk/ lite meal
heavy meal (fried food, fatty food, meat)
clear liq= 2hrs
breast milk=4hr
lite meal/ non human milk/ formula = 6hr
heavy meal = 8hr
Carb drink 2hr preop can cause:
-improved pt optimization in preop phase
-maintains glucose/ insulin
-reduce thirst/hunger/ dry mouth/ anxiety
-less likely to have HoTN
-less likely to be fluid responsive intraop
T/F mechanical bowel prep is part of the ERAS preoperative protocol.
false
-avoid these if possible, dehydrates pt
Preop ERAS components:
-preadmission counseling
-fluid/ carb loading
-no prolonged fasting
-no/selective bowel prep
-Abx proph
-thromboprophylaxis
-no premedication
Intraop ERAS components:
-short acting anesthetics
-mid-thoracic epidurals for anesthesia/analgesia
-no drains
-avoid salt/water overload
-maintain normothermia
Postop ERAS components:
-mid-thoracic epidural anesthesia/analgesia
-no NG tubes
-prevent N/V
-avoid salt/water overload
-early catheter removal
-early PO nutrition
-non-opioids PO analgesia/NSAIDs
-early mobility
-stimulating gut mobility
-audit of compliance/outcomes
Surgical pt can receive fluid based on 4 concepts of fluid deficit:
-NPO fluid deficit
-maintenance fluid requirements
-3rd space fluid shifts/losses
-EBL
Excessive fluid admin intraop can cause edema of the _ _ and prolonged _.
gut wall
ileus
GDFT as an ERAS protocol can _ variations in practice such as 2 different providers choosing different treatments for intraop HoTN (fluid challenge and vasopressors)
reduce
1st line treatment for hemodynamic support during surgery:
fluids
Direct surgical trauma from incisions, heating elements like cautery, and retractions of organs can lead to _ cell injury.
primary
Primary cellular injury can impair _ and _ delivery to organs from global and local _ changes
O2 and nutrient
perfusion
Secondary cellular injury is caused by the _ _ from surgery that causes a release in local _ _ or the systemic effects of _, _ _, or hormones.
stress response
inflammatory mediators
cytokines, inflammatory mediators,
Both primary and secondary cellular injuries are attributed to delayed _ _ and _ dysfunction, and can cause postop complications.
wound healing
gut dysfunction
2 fundamental elements that affect postop outcomes are attributed to _ _ and effective _ _.
fluid therapy
pain management
Ratio of replacing blood loss with crystalloids intraop:
3:1
Electrolyte levels in different compartments
-Na+
ECV = 145mEq/L
ICV = 25mEq/L
Electrolyte levels in different compartments
-K+
ECV= 3.5-4.5mEq/L
ICV= 150-160mEq/L
Electrolyte levels in different compartments
-Ca++
IONIZED: 4.4-5.4mg/dL
SERUM: 1.0-10.5mg/dL
DIFFERENT UNTIS!!! NOT mEq/L!!!
*total intracellular level of calcium can be as high as extracellular levels, but it is largely sequestered or buffered so that cytoplasmic IONIZED calcium levels are about 1000x lower than extracellular fluid **0.3-2.6 microEq/L
Electrolyte levels in different compartments
-Mg++
1.5-3.0mEq/L serum
intracellular 20
intravasc 0.8
interstitial 0.7
What damages the glycocalyx?
-hyperglycemia
-hyperlipidemia
-sepsis
-smoking
-aggressive fluid resusc
repaired by albumin, normal amounts of fluid, steroids, and normal BG
Which IV fluids are hypertonic?
-dextran 10%
-NaCl 3%
Which IV fluids are isotonic?
-Albumin
-Plasmalyte
Is LR hyper, hypo, or isotonic?
hypotonic
SVV in a spont breathing pt, what happens on inspiration and expiration to ABP?
Inspiration - ABP decreases
Expiration - ABP increases
-opposite for vented pt
-pt must be in NSR
How to determine if pt is fluid responsive?
If after challenge, SBP, SV, CO increase, pt is responsive, repeat until pt is not.
USE SVI IF PT IS SPONT BREATHING, HAS LOW TV, OR HAS ARRHYTHMIAS:
-if SVI increases by 10%, pt is fluid responsive, if not, they are not responsive.
HypoK+
-ekg changes
-Short PR
-ST depression (<2.0)
-long QT (<2.5-2.8)
-flat T wave
-U wave (<1.7)
HyperK+
-ekg changes
V fib rhythm, arrhtyhmias, arrest
-flat P wave (6.5-7.5) or none (>6.0-late sign)
-PR long (6.5-7.5)
-QRS wide (7.0-8.0) or sine wave :( (>8.5)
-QT short
-T wave peaked (5.5-6.5)
HypoCa++
-ekg changes
Bradycardia, angina, CHF, HoTN, arrest
-long QT
HyperCa++
-ekg changes
Bradycardia, HB, BBB, HTN, ventricular dysrhythmias, arrest
-ST elevation
-QT short (plateaued)
HypoMag
-ekg changes
Torsades, A+V arrhythmias
-wide QRS
-long QT (very low levels)
-flat T wave
-U wave
HyperMag
-ekg changes
HB (10-15) or arrest (10-24), HoTN (5-7)
-PR prolongation
-QT short (very high)
Hypophosphatemia
-ekg changes
HB, Bradycardia, asystole
Function of electrolytes:
-Na+
Osmotic activity of ECF
most important osmotically active substance influencing water in the brain
Function of electrolytes:
-K+
responsible for RMP of the cell
Function of electrolytes:
-Ca++
Most important 2nd messenger in body
-Releases hormones and NTs
-Muscle contraction
-Helps with clotting
Function of electrolytes
-Mag
Function of the Na/K ATPase pump
-energy metabolism
-protein synth
-NM excitability
Function of electrolytes:
-Phosphorus
Component of ATP and 2,3 DPG
-functions as a buffer
Most common imbalance of electrolytes:
hypokalemia
How does magnesium affect NMBA, why?
it potentiates them by inhibiting prejunctional ACh release
How does phosphate level affect Ca++ levels?
Conc of phosphate is INVERSELY proportional to Ca++ levels
Normal level of phosphate
2.0-4.7mg/dL
***NOT MEQ/L
How is calcium found in the body?
99% in bones
1% in plasma and body cells
-ionized Ca accounts for 50% of calcium in ECV and is ACTIVE calcium
-remaining calcium is bound to anions (10%) or plasma proteins like albumin (40%)
How does acidosis affect calcium stores?
Acidosis increases amount of ionized Ca bc acidic environment pulls Ca off albumin in ECF
-may see hypercalcemia (short QT, ST elevation, bradycardia, BBB, vent arrhythmias, HB)
Lyte imbalances s/s
-HypoNa+
<135
AMS
-lethargic (115-124)
-seizure/coma (<115)
Cerebral edema
Muscle weakness
N/V (125-129)
Lyte imbalance s/s
-HyperNa+
> 145
AMS
-seizure/coma (>430)
Cerebral dehydration
Ataxia, tremors, weakness (376-400)
Hyperreflexia/ spasms (401-430)
Thirst
Lyte imbalance s/s
-HypoK+
<3.5
Altered LOC (<2.5)
Cramps
Weakness (2.5-3.5)
Depressed DTR (<2.5)
know EKG changes: flat/ inverted T, short PR, long QT, ST depression, U wave
Lyte imbalance s/s
-Hyper K+
> 5.5
EKG: flat p wave, long PR, wide QRS, short WT, peak T, arrhythmias
Lyte imblance s/s
-HypoCa++
<8.5 or <4.0
Nerve irritability (parasthesia)
Confusion/ psychosis
Seizures
Cramps
Tetanic spasms
Hyperreflexia
Chvosteks sign (eye)
Trousseau’s (wrist)
Laryngospasm
Lyte imbalance s/s
-Hyper Ca++
> 10.5 or >5.5
Psychosis
AMS
Seizures
N
Abd pain
Polyuria/Polydipsia
Lyte imbalance s/s
-Hypomag
<1.3
muscle weakness
spasm
EKG: wide QRS, long QT, flat T, U wave
Lyte imbalance s/s
-HyperMag
> 2.5
Coma (10)
Loss of DTR (4-5)
Potentiates NMB
Resp Paralysis (10)
Lyte imbalance s/s
-Hypophosphatemia
<2.0
Confusion
Coma
Seizure
Altered nerve/ muscle function
Bone reabsorption
Weakness
Decreased ATP
Platelet dysfunction
Resp Failure
Lyte imblance s/s
-Hyper phosphatemia
> 4.7
same as hypocalcemia!
Parasthesia
Confusion
Psychosis
Seizures
Cramps
Spasm
Hyperreflexia (Chvostek -eye, Trousseau-wrist, L spasm)
Chronic calcification of soft tissue
Lyte storage and regulation
-Na+
Stored: ECF
Reg: Na/K ATPase pump
Lyte storage and regulation
-K+
Stored: ICF
Reg:
-absorbed: GI tract
-excreted: renal
Lyte storage and regulation
-Ca++
Stored:
-99% bone
-1% plasma (50% ionized, 40% on albumin, 10% on anions)
Reg: PTH, Vit D, Calcitonin
Lyte storage and regulation
-Mag
Storage: 40-60% muscle
30% intercellular
1% serum (intestines and kidneys)
Lyte storage and regulation
-Phosphate
Stored: 85% bone, small amt in plasma
Reg: PTH, Vit D, Calcitonin
Causes of lyte imbalances
-HypoNa+
overhydration
TRUP syndrome
SIADH
Cushings
CHF
Cirrhosis
Causes of lyte imbalances
-Hyper Na
Impaired thirst (elderly)
DI
Bicarb admin
Causes of lyte imbalances
-HypoK
Renal loss (diuretics, alkalosis, licorice)
GI loss (NG, N/V, diarrhea, kayexalate)
Poor PO intake
INTRAcellular shift (albuterol, insulin, alkalosis)
Endocrinopathy (cushing, Bartter syndrome, insulin therapy)
Causes of lyte imbalances
-Hyper K
Hemolyzed sample?
Poor excretion (ESRD, K sparing diuretics)
EXTRAcellular shift (acidosis)
Sux
Dig, Angiotensin, ACE-I, ARBs, Bblockers
Tumor lysis
Causes of lyte imbalances
-HypoCa
DIRECT RELATIONSHIP WITH PTH AND VIT D
Decreased PTH (pancreatitis, burns)
Decreased Vit D (liver disease, malnutrition)
Sepsis
Calcium chelation (citrate, alkalosis)
Hyperphosphatemia
Causes of lyte imbalances
-HyperCa
Hyperparathyroidism (most common)
Malignant diseases (CA)
Hyperthyroidism or Adrenal insufficiency
Thiazide diuretics
Immobilization
Causes of lyte imbalances
-HypoMag
Poor intake
Alcoholism (30%)
Diuretics ( or PPI and B agonists)
Critical illness (common)
Common with Hyperkalemia
Pregnancy
Endocrine Disorders
Causes of lyte imbalances
-HyperMag
Iatrogenic Admin (most common)
Tx of pre-eclampsia, preterm labor, ischemic heart disease, or arrhythmias
ESRD
Adrenal insufficiency
Causes of lyte imbalances
-Hypophosphatemia
INVERSE RELATIONSHIP WITH PTH AND CALCIUM
VIT D IS NEEDED FOR ABSORPTION (DIRECT)
Vit D deficiency
Hyperparathyroidism
Increased renal excretion
Antacids (magnesium)
Causes of lyte imbalances
-Hyperphosphatemia
Metastatic disease(common)
Acute renal failure
Long term laxative use
Hypoparathyroidism
Treatment of lyte imbalances
-HypoNa
IF SERUM OSMOLALITY IS LOW (<280 mOsm)
-hypovolemic too = give 0.9/ isotonic fluids
-euvolemic = FR, and or loop diuretic and or Hypertonic saline 1-2mL/kg/ hr
-hypervolemic = FR and sodium restriction, loop diuretic
Treatment of lyte imbalances
-Hyper Na
-hypovolemic = loopdiuretic
-euvolemic= fix water deficit (0.45%, D5W or po water)
-hypervolemic= isotonic fluids to fix volume deficit until hemodynamically stable
treatment of lyte imbalance
-HypoK
KCl
<2.0 = 40mEq/hr
Max= 10-20mEq/hr rec
Treatment of lyte imbalances
-HyperK
Calcium (stabilizes heart membrane)
10 unit IV insulin + 50% dextrose
Hyperventilate (induce alkalosis)
bicarb admin
albuterol (beta agonist)
K wasting diuretics or dialysis
Treatment of lyte imbalance
-HypoCa
272mg CaCl (via central line only) most rapid correction is 1.35mEq/mL
Ca Gluconate (PIV ok) 10mL 10% calcium gluconate over 10 min THEN
0.3-2mg/kg/hr of elemental calcium
vit D
Treatment of lyte imbalance
-Hyper Ca
Volume expansion to increase renal excretion
0.9 + lasix
Biphosphates, calcitonin, glucocorticoids
HD
Treatment of lyte imbalances
-HypoMag
Mag Sulf- rapid is ok
1-2g over 5 min with EKG THEN 1-2g/hr
Treatment of lyte imbalances
-HyperMag
DC admin
Calcium Chloride (urgent)
Treatment of lyte imbalance
-Hypophosphatemia
sodium phosphate
Treatment of lyte imbalance
-Hyperphosphatemia
Aluminum hydroxide (Antacids)
HD
What happens if hypoNa is fixed too quickly?
seziures
spastis quadresis
coma (due to osmotic demyelination)
-esp avoid rapid treatment if pt has been low for >48hr
What happens if hyperNa is fixed too quickly?
Can cause intracranial hemorrhage bc brain shrinks and pulls on intracranial veins and venous sinuses :(
