Nagelhout Chapter 21 Flashcards
(373 cards)
1
Q
What is the primary purpose of perioperative fluid therapy?
A
To maintain physiological stability during surgery.
2
Q
What are the key objectives of perioperative fluid management?
A
- Maintaining intravascular volume. 2. Augmenting cardiac output. 3. Preserving tissue perfusion and oxygenation. 4. Correcting and maintaining electrolyte balance. 5. Enhancing microcirculatory flow. 6. Facilitating waste clearance.
3
Q
Why is targeted fluid administration necessary during surgery?
A
To counteract intraoperative losses and compensate for increased oxygen demands.
4
Q
What are the potential long-term effects of inappropriate fluid management?
A
Delayed wound healing, infections, and organ dysfunction.
5
Q
What percentage of lean body mass does total body water (TBW) account for in an average adult?
A
Approximately 60%.
6
Q
How is total body water (TBW) divided?
A
Into Intracellular Volume (ICV) and Extracellular Volume (ECV).
7
Q
What is the approximate proportion of Intracellular Volume (ICV) to total body water (TBW)?
A
~2/3 of TBW.
8
Q
What is the approximate proportion of Extracellular Volume (ECV) to total body water (TBW)?
A
~1/3 of TBW.
9
Q
What are the subdivisions of Extracellular Volume (ECV)?
A
- Intravascular compartment (plasma). 2. Interstitial compartment. 3. Transcellular fluids.
10
Q
What is the electrolyte composition of Extracellular Volume (ECV)?
A
High in sodium (Na⁺) and chloride (Cl⁻).
11
Q
What is the electrolyte composition of Intracellular Volume (ICV)?
A
High in potassium (K⁺) and phosphate (PO₄³⁻).
12
Q
What maintains the gradients of electrolytes in the body?
A
The sodium-potassium ATPase pump.
13
Q
What is the daily maintenance fluid requirement for a normothermic, metabolically stable adult?
A
Approximately 25–35 mL/kg/day (~2–3 liters per day).
14
Q
What governs fluid exchange across capillary membranes?
A
The balance of four key pressures.
**Footnote
Capillary, Interstitial fluid, plasma oncotic, interstitial oncotic
15
Q
What is Capillary Hydrostatic Pressure (Pc)?
A
It pushes fluid out of capillaries into the interstitium.
16
Q
What is Interstitial Fluid Pressure (Pif)?
A
Generally slightly negative, drawing fluid from capillaries; may be positive in encapsulated tissues like the brain or muscle.
17
Q
What is Plasma Oncotic Pressure (πp)?
A
Generated by plasma proteins (primarily albumin) retaining water within the vasculature.
18
Q
What is Interstitial Oncotic Pressure (πif)?
A
It pulls fluid into the interstitial space.
19
Q
What is the Starling Equation (Traditional)?
A
Net Filtration (Jv) = Kf ([Pc - Pif] - σ[πp - πif])
20
Q
What does Jv represent in the Starling Equation?
A
Net fluid movement.
21
Q
What does Kf represent in the Starling Equation?
A
Filtration coefficient (depends on capillary permeability and surface area).
22
Q
What does σ (sigma) represent in the Starling Equation?
A
Reflection coefficient (0 to 1) for macromolecules like albumin.
σ = 1: Completely impermeable to proteins.
σ = 0: Freely permeable.
23
Q
What does a positive Jv indicate?
A
Filtration into tissues.
24
Q
What does a negative Jv indicate?
A
Absorption into capillaries.
25
What occurs under normal physiology regarding fluid movement?
Slight net filtration (~2 mL/min) occurs across systemic capillaries, returned to circulation via the lymphatic system.
26
What is the glycocalyx?
The glycocalyx is a gel-like matrix lining the inner surface of the vascular endothelium.
27
What are the components of the glycocalyx?
It is composed of glycoproteins, proteoglycans, and hyaluronic acid.
28
What role does the glycocalyx play in vascular permeability?
It maintains the vascular permeability barrier.
29
How does the glycocalyx preserve plasma oncotic pressure?
It limits albumin leakage.
30
What effect does the glycocalyx have on leukocytes?
It prevents leukocyte adhesion and modulates immune response.
31
What is a mechanosensor?
The glycocalyx acts as a mechanosensor for shear stress and regulates vasoactive signals.
32
How does the glycocalyx contribute to blood flow?
It contributes to laminar blood flow and anticoagulation.
33
What is the Revised Starling Equation?
Net Filtration (Jv) = Kf ([Pc - Pif] - σ[πp - πsg])
34
What does πsg represent in the Revised Starling Equation?
πsg is the oncotic pressure within the subglycocalyx space, which more accurately reflects fluid exchange.
35
What can glycocalyx disruption lead to?
It can lead to excess capillary leak, edema, and worsened outcomes.
36
What activates the Renin-Angiotensin-Aldosterone System (RAAS)?
Hypotension (detected by baroreceptors in heart and kidneys) and sympathetic stimulation.
37
What is the role of renin in RAAS?
Renin converts angiotensinogen to angiotensin I.
38
What does ACE do in the RAAS?
ACE converts angiotensin I to angiotensin II.
39
What are the effects of angiotensin II?
It causes vasoconstriction and stimulates aldosterone release from the adrenal cortex.
40
What is the primary trigger for the release of Antidiuretic Hormone (ADH)?
Increased serum osmolality.
41
What does ADH promote in the kidneys?
It promotes water reabsorption in renal collecting ducts via aquaporin channels.
42
What additional role does ADH have?
ADH also acts as a vasoconstrictor.
43
What triggers the release of Atrial Natriuretic Peptide (ANP)?
Volume overload or increased atrial stretch.
44
What are the effects of ANP?
It promotes natriuresis (sodium excretion) and diuresis (water excretion).
45
How does ANP affect renin and ADH?
It inhibits renin and ADH.
46
What effect does ANP have on glomerular filtration rate (GFR)?
It increases GFR by vasodilating afferent and constricting efferent renal arterioles.
47
What are crystalloids?
Crystalloids are commonly used IV fluids that differ based on electrolyte composition and buffering agents.
48
What are some examples of crystalloids?
Examples include Lactated Ringer's (LR), PlasmaLyte-A, Normosol-R, and 0.9% Normal Saline.
49
What key variables are considered in crystalloids?
Key variables include concentrations of Sodium (Na⁺), Potassium (K⁺), Chloride (Cl⁻), Calcium (Ca²⁺), Magnesium (Mg²⁺), buffer agents (lactate, acetate, gluconate), pH, and osmolality.
50
What factors should be considered when choosing intravenous fluids?
Choice of fluid should consider electrolyte status, acid-base balance, type of surgery, and patient comorbidities.
51
What is the clinical importance of fluid selection in anesthesia?
The choice of intravenous (IV) fluids is critical for perioperative management, aiming to restore and maintain intravascular volume, enhance microvascular blood flow, and ensure adequate tissue perfusion.
52
What are the main goals of perioperative fluid resuscitation?
The main goals are to restore and maintain intravascular volume, enhance microvascular blood flow, and ensure adequate tissue perfusion.
53
What are crystalloids?
Crystalloids are aqueous electrolyte solutions used for over a century, preferred for resuscitating dehydration-related volume losses.
54
What conditions are crystalloids preferred for?
Crystalloids are preferred for resuscitating volume losses caused by total body water loss, prolonged fasting, GI losses, polyuria, and hypermetabolic conditions.
55
What are the benefits of crystalloids in surgery?
Benefits include immediate restoration of plasma volume, microcirculatory support, reduction in vasoconstriction, and correction of plasma hyperviscosity from hemorrhage.
56
What are the preferred characteristics of crystalloids?
Crystalloids are preferred for their ease of metabolism and renal clearance, low allergenic potential, and preservation of electrolyte balance with proper administration.
57
What are the limitations of crystalloids?
Limitations include rapid exit from the intravascular space, causing only 25-30% to remain intravascular, potential hemodilution, decreased oncotic pressure, and possible edema with excessive volumes.
58
What is Normal Saline (0.9% NaCl)?
Most common crystalloid, historically considered 'physiologic'.
59
What ions does Normal Saline contain?
Contains equal Na⁺ and Cl⁻, but plasma Na⁺ > Cl⁻, resulting in a high chloride load.
60
What are the problems associated with high chloride in Normal Saline?
Hyperchloremic metabolic acidosis, impaired renal perfusion and GFR, risk of fluid overload, hemodilution, and interstitial edema.
61
What do studies suggest about Normal Saline?
NS alters acid-base balance, may require 2+ days for volume normalization, and increases postoperative risks.
62
What are Balanced Crystalloids?
Examples include PlasmaLyte-A, Normosol-R, and Lactated Ringer’s (LR).
63
How do Balanced Crystalloids compare to Normal Saline?
More physiologic, with closer pH and electrolyte profiles to plasma.
64
What is unique about Lactated Ringer’s (LR)?
Contains lactate as a buffer, which is converted to bicarbonate, resulting in less acidosis than NS. Contains calcium, contraindicated with blood products due to clotting risk.
65
What do PlasmaLyte-A and Normosol-R contain?
Do not contain calcium; use acetate and gluconate as buffers; safe with blood products.
66
What are the clinical outcomes associated with Balanced Crystalloids?
Show lower risk of AKI, metabolic derangements, and post-op complications.
67
What studies support the use of Balanced Crystalloids?
Studies such as SALT-ED, SMART, and SPLIT showed improved outcomes in critically ill patients.
68
What are hypertonic crystalloids used for?
They are used in neurosurgical, trauma, or head-injured patients.
69
What is the concentration of hypertonic crystalloids?
Concentrations are ≥ 3% NaCl.
70
What are the benefits of hypertonic crystalloids?
They help reduce cerebral edema and expand intravascular volume.
71
What caution should be taken with hypertonic crystalloids?
There is a risk of vascular irritation and osmotic demyelination.
72
What are colloids?
Colloids contain high-molecular-weight molecules that remain within the intravascular space, exerting oncotic pressure.
73
How do colloids function?
Colloids work by drawing water into the vessels, reducing transcapillary fluid loss, and decreasing endothelial permeability.
74
What are common types of colloids?
Common types of colloids include Albumin, Hydroxyethyl starch (HES), Dextrans, and Gelatins.
75
What are the advantages of colloids?
Colloids require smaller volumes to expand plasma volume, remain intravascular longer than crystalloids, and may reduce the risk of edema formation.
76
What are the disadvantages and safety concerns of colloids?
Disadvantages include high cost, allergic reactions (especially with synthetic colloids), and adverse outcomes associated with Hydroxyethyl starch (HES), including AKI and increased mortality.
77
In which situations are colloids not recommended?
Colloids are not recommended for sepsis, kidney injury, or critically ill populations.
78
When might colloids be appropriate to use?
Colloids may be appropriate in patients at risk of fluid overload or in need of rapid plasma expansion.
79
What is the first-line treatment for fluid resuscitation?
Crystalloids remain the first-line treatment, with colloids used selectively and cautiously.
80
What are Dextrans?
Dextrans are manufactured since the 1940s, derived from sucrose metabolism, and are hyperosmolar with short half-lives (6–12 hours).
81
What are the adverse effects of Dextrans?
Adverse effects include renal failure, coagulopathy, anaphylaxis, and interference with blood crossmatching.
82
Are Dextrans still used in clinical practice?
Dextrans are no longer used in clinical practice due to safety concerns.
83
What are Gelatins?
Gelatins are derived from bovine collagen, have a lower molecular weight (30–35 kDa), and a shorter half-life (~2–4 hours).
84
What are the limitations of Gelatins?
Limitations include interference with platelets, coagulopathy, nephrotoxicity, increased risk of allergic reactions, and concerns regarding prion disease transmission.
85
What do meta-analyses show about Gelatins?
Meta-analyses show increased adverse events with gelatin compared to albumin or crystalloids.
86
What are Hydroxyethyl Starches (HES)?
Synthetic colloids with various generations.
87
What are the characteristics of first-generation HES?
High MW: >450 kDa, substitution ratio 0.6–0.7.
## Footnote
Strongly associated with coagulopathy, renal injury, tissue storage.
88
What are the characteristics of second-generation HES?
Medium MW: 200–260 kDa.
89
What are the characteristics of third-generation HES?
Low MW: 70–130 kDa, substitution ratio 0.4–0.5.
## Footnote
Still associated with increased AKI, coagulopathy, sepsis.
90
What regulatory actions have been taken regarding HES?
FDA black box warning (2013): HES linked to renal failure and increased mortality.
## Footnote
EMA recommendation (2013 & 2018): Avoid HES in critically ill and surgical patients.
91
What is Albumin?
Human plasma-derived protein solution (MW ~65–69 kDa).
92
What are the uses of Albumin?
Used in sepsis, cirrhosis, trauma, and volume resuscitation; scenarios where transfusion is not possible or not ideal.
93
What are the effects of Albumin?
Increases oncotic pressure, pulls fluid into vasculature.
## Footnote
Associated with negative circulatory effects: 'dilutional anemia' due to expanded plasma volume.
94
What are the risks associated with Albumin?
Anaphylaxis (rare) and expensive.
95
What did the SAFE study conclude about Albumin?
Albumin vs. NS showed no difference in mortality or outcomes.
96
What potential benefits does Albumin have in early sepsis?
Possible benefit in preserving endothelial glycocalyx and may help reduce vascular leak and organ dysfunction in specific subgroups.
97
What is the current view on risk-benefit considerations in critically ill patients?
No clear mortality benefit for colloids over crystalloids; Albumin may be safer than synthetic colloids in sepsis.
98
What do the Surviving Sepsis Campaign guidelines recommend regarding Albumin?
Albumin as second-line fluid if large-volume crystalloids are inadequate.
99
What does NICE (UK) recommend for Albumin in sepsis?
Recommend albumin in sepsis.
100
What did the Cochrane meta-analysis find regarding Albumin and crystalloids?
No difference in mortality between albumin and crystalloids.
101
What is the current approach to fluid management in critically ill patients?
Crystalloids first, albumin selectively, synthetic colloids largely avoided.
102
What activates the hypothalamic-pituitary-adrenal axis (HPA) during surgical stress?
The hypothalamus releases CRH, stimulating ACTH release from the pituitary.
103
What does ACTH stimulate?
ACTH stimulates cortisol production by the adrenal glands.
104
What are the effects of cortisol?
Cortisol promotes gluconeogenesis, protein catabolism, lipolysis, increases sympathetic tone, ADH, aldosterone, and causes water/sodium retention.
105
What are the effects of sympathetic activation during surgery?
Increased systemic vascular resistance (SVR), elevated heart rate, oxygen demand, blood pressure, and ADH release leading to water retention.
106
What may develop postoperatively due to surgical stress?
Hypervolemia may develop postoperatively.
107
What can cause hypovolemia after surgery?
Hypovolemia may occur from hemorrhage or fluid loss into interstitial/third spaces.
108
What is the inflammatory response to surgical trauma?
Cytokines and inflammatory mediators cause capillary leak, endothelial dysfunction, decreased regional perfusion, and tissue edema.
109
What role does cortisol play in inflammation?
Cortisol is an endogenous anti-inflammatory steroid that promotes vascular tone and mitigates cytokine-induced vasodilation.
110
What is the impact of laparoscopy on hemodynamics?
Laparoscopy is less invasive but still impacts hemodynamics, particularly through pneumoperitoneum which increases intra-abdominal pressure (IAP).
111
What are the effects of increased intra-abdominal pressure (IAP)?
Increased IAP may compress IVC, decrease venous return, increase SVR, MAP, and ADH release, and may impair renal and splanchnic perfusion.
112
What can high IAP (>12–15 mm Hg) lead to?
High IAP may reduce cardiac output and cause reflex bradycardia.
113
How can pneumoperitoneum affect patients with pre-existing cardiac disease?
It can decrease ejection fraction and cardiac performance.
114
How does the body attempt to maintain cardiac output (CO) during surgical stress?
By increasing heart rate (tachycardia) and enhancing left ventricular stroke work.
115
What is the goal of the body's compensatory mechanisms during surgical stress?
To preserve systemic perfusion and oxygen delivery.
116
What are the limitations of hemodynamic compensation?
Increased myocardial oxygen consumption, potential failure in patients with volume overload or impaired ventricular function, leading to acute cardiac decompensation and heart failure.
117
What pharmacologic strategies are effective in blunting the HPA axis activation?
Opioids and dexmedetomidine are effective in blunting the hypothalamic-pituitary-adrenal (HPA) axis activation.
118
What are the effects of opioids and dexmedetomidine on the neuroendocrine stress response?
They reduce the neuroendocrine stress response to surgery.
119
Why are large-dose opioids discouraged in ERAS protocols?
Due to side effects such as ileus, sedation, and nausea.
120
What are the uses of dexmedetomidine?
Can be used as an adjunct or premedication, provides analgesia and sympatholytic effects, offers opioid-sparing benefits, and helps attenuate hemodynamic stress of procedures like laparoscopy.
121
What can spinal or epidural anesthesia block?
Block afferent autonomic signals at the spinal cord level.
122
How does neuraxial anesthesia affect the HPA axis?
It diminishes HPA axis activation.
123
In which surgeries is neuraxial anesthesia most effective?
Most effective in lower body surgeries such as pelvis and lower extremities.
124
What is Goal-Directed Fluid Management (GDFM)?
A physiologically based approach to fluid therapy that tailors fluid and vasoactive interventions to real-time perfusion goals.
125
What are the key benefits of GDFM?
Supports oxygen delivery and tissue perfusion, prevents over-resuscitation, limits under-resuscitation, and helps attenuate the body’s neuroendocrine stress response.
126
What techniques are often included in GDFM?
Dynamic hemodynamic monitoring and target-driven fluid boluses combined with vasoactive agents.
127
What is essential to maintain throughout the perioperative period?
Maintaining euvolemia.
128
How does avoiding fluid overload help?
Protects the endothelial glycocalyx, preserves microvascular integrity, maintains capillary barrier function, and limits inflammatory response and edema.
129
What are traditional fluid management approaches based on?
Historically, fluid management used fixed, formulaic strategies applied uniformly to all surgical patients, regardless of preexisting volume status, cardiac and renal function, and vascular tone.
130
What is the 4-2-1 Rule for maintenance fluid requirements?
0–10 kg: 4 mL/kg/hr; 11–20 kg: Add 2 mL/kg/hr; 20 kg: Add 1 mL/kg/hr.
131
What additional factors are combined with the 4-2-1 Rule?
Fasting deficit replacement, surgical loss estimates (e.g., 2–8 mL/kg/hr depending on trauma level), and blood loss replacement.
132
What is the blood loss replacement ratio for crystalloids?
3 mL per 1 mL of estimated blood loss (EBL).
133
What is the blood loss replacement ratio for colloids or blood?
1 mL per 1 mL of estimated blood loss (EBL).
134
What does the Fasting Deficit Theory suggest?
It is based on the belief that preoperative fasting causes significant 'fluid debt' that must be corrected with preloading.
135
What does current evidence show about preoperative fasting?
Minimal true fluid loss from short-term fasting in elective surgeries; preloading in euvolemic patients leads to fluid overload and endothelial glycocalyx disruption.
136
What are the risks of preemptive fluid administration?
Increases the risk of interstitial edema, impaired microcirculation, organ dysfunction, and delayed recovery.
137
What are the effects of bowel preparation with hypertonic agents?
Causes fluid and electrolyte loss; Enhanced Recovery After Surgery (ERAS) protocols discourage routine bowel prep.
138
What is recommended regarding bowel prep and surgical site infections?
Combined oral antibiotics + bowel prep may reduce surgical site infections, but bowel prep alone does not.
139
What type of solutions are preferred to minimize fluid loss?
Isotonic solutions.
140
What is the 'third space' concept?
Introduced in the 1960s, the 'third space' referred to a nonfunctional fluid compartment where ECF supposedly redistributed postoperatively.
141
What did modern studies find about the 'third space'?
Modern studies refute the existence of a measurable 'third space'.
142
What are the consequences of liberal fluid replacement based on the 'third space' concept?
Liberal fluid replacement can lead to weight gain of up to 10 kg and poor outcomes.
143
What is a limitation of Mean Arterial Pressure (MAP) as a hemodynamic marker?
MAP is a poor indicator of volume status; patients may be normotensive but hypovolemic or vice versa.
144
What influences Central Venous Pressure (CVP)?
CVP is influenced by many variables, such as RV dysfunction and lung disease.
145
What percentage of patients with low CVP are actually fluid responsive?
Studies show only ~50% of patients with low CVP are actually fluid responsive.
146
What is a risk of overreliance on CVP monitoring?
Overreliance on CVP may lead to fluid overload.
147
Why is urine output not a reliable measure of intravascular volume?
Urine output can be reduced due to ADH elevation from surgical stress, anesthesia, or pain.
148
What happens to volume loading in oliguric patients?
Volume loading in oliguric patients often expands interstitial rather than intravascular space.
149
What do restrictive fluid strategies show regarding renal outcomes?
Restrictive fluid strategies show no increased risk of oliguria or renal failure.
150
What is a finding about excess fluids in resuscitation?
Excess fluids are not always filtered effectively.
151
Is high-volume resuscitation nephroprotective?
High-volume resuscitation is not nephroprotective as once believed.
152
What are the characteristics of intraoperative fluid administration?
Intraoperative fluid administration has indications, therapeutic benefits, and potential side effects, particularly in a dose-dependent fashion.
153
What has the field shifted away from?
Uniform, liberal fluid strategies, static markers of volume status, and assumptions like third-space loss.
154
What has the field shifted toward?
Goal-Directed Fluid Therapy (GDFT) using dynamic measurements and individualized targets, and enhanced recovery protocols.
155
What are some components of enhanced recovery protocols?
Reduced pre-op fasting, selective use of bowel prep, and maintenance of euvolemia, not hypervolemia.
156
What is a key takeaway regarding intravenous fluid?
Intravenous fluid is a potent intervention with both benefits and risks. Its administration should be tailored, data-driven, and patient-specific.
157
What did Shoemaker’s studies in the 1980s focus on?
First trials using pulmonary artery catheters (PACs) to target supernormal hemodynamic parameters.
158
What were the results of Shoemaker's studies?
Improved survival, fewer complications, and reduced ICU length of stay.
159
What did the Svo₂ collaborative and meta-analyses conclude?
Normal oxygen delivery targets were as effective as supernormal ones.
160
What benefits were associated with GDFT?
Reduced complications, improved survival in surgical and critically ill patients, reduced incidence of acute kidney injury (AKI), and shortened hospital length of stay.
161
What techniques were originally used in GDFT?
Original GDFT relied on invasive PACs.
162
What are some minimally invasive/noninvasive methods used in GDFT?
Pulse pressure variation (PPV), stroke volume variation (SVV), dynamic arterial waveform analysis, and plethysmographic variability index (PVI).
163
What did Cannesson’s work demonstrate?
Respiratory variation in arterial pressure correlates with volume responsiveness, forming the basis for many noninvasive monitors used today.
164
What did recent sepsis trials show about GDFT?
No significant mortality benefit for GDFT compared to standard care, but acknowledged that modern standard care incorporates elements of GDFT.
165
What do the Surviving Sepsis Campaign Guidelines recommend?
MAP and CVP as dynamic variables, but GDFT is not universally mandated.
166
What are the consequences of liberal fluid strategies?
Liberal fluid strategies lead to increased morbidity, mortality, costs, and hospital stay.
167
What is the aim of the Zero-Balance Fluid Strategy?
The Zero-Balance Fluid Strategy aims to maintain preoperative weight by avoiding excess fluid.
168
What does the Zero-Balance Fluid Strategy involve?
It involves basal fluids and 1:1 replacement of measurable losses.
169
How does the Zero-Balance Fluid Strategy compare to liberal strategies?
It has been shown to reduce postoperative morbidity compared to liberal strategies.
170
What did some trials find about the difference between liberal and restrictive fluid strategies?
Some trials found little difference due to inconsistencies in definitions, such as only a 10 mL difference between groups.
171
What did a U-shaped curve in a registry study reveal?
It showed that both liberal and restrictive extremes worsened outcomes, with moderate, optimized fluid management being ideal.
172
What is the combined approach used in modern ERAS protocols?
It uses a zero-balance (weight-based) strategy to prevent overload and GDFT (dynamic monitoring) to ensure adequate perfusion.
173
What is GDFT sometimes referred to as?
GDFT is sometimes referred to as 'goal-directed fluid restriction.'
174
What do the ASER/POQI Guidelines recommend for colorectal surgery?
They recommend GDFT as the preferred strategy and accept zero-balance as an alternative for low-risk patients.
175
What are the steps involved in GDFT protocols?
GDFT protocols involve baseline hemodynamic assessment, fluid challenge, decision point, and reassessment every 5–10 minutes.
176
What is the fluid challenge volume in GDFT?
The fluid challenge typically involves a 200–250 mL bolus.
177
What are the goals of GDFT?
The goals are to optimize oxygen delivery, maintain euvolemia, preserve endothelial glycocalyx, and improve organ perfusion and recovery.
178
What does GDFT represent in fluid administration?
GDFT represents a major shift from static, uniform fluid administration to dynamic, individualized care.
179
What benefits has GDFT proven to provide?
GDFT has proven to reduce complications, improve bowel function recovery, shorten ICU/hospital stay, and support end-organ perfusion.
180
In which surgeries are the best results of GDFT seen?
The best results are seen in high-risk surgeries, with promising evidence for broader use, especially when integrated with ERAS pathways.
181
What is Goal-Directed Fluid Therapy (GDFT)?
GDFT uses real-time hemodynamic data to guide fluid administration, vasopressor use, and inotropy.
182
What does GDFT replace?
GDFT replaces reliance on static indicators (e.g., MAP, CVP, urine output) with dynamic, individualized targets.
183
What are the goals of GDFT?
The goal is to maintain euvolemia while avoiding both hypovolemia and fluid overload.
184
What does the Frank-Starling curve describe?
It describes the relationship between Left Ventricular End-Diastolic Volume (LVEDV) and Stroke Volume (SV).
185
What is preload dependence in the Frank-Starling mechanism?
Increased volume leads to increased Stroke Volume (SV).
186
What is preload independence in the Frank-Starling mechanism?
Further fluid yields no improvement in Stroke Volume (SV), leading to a risk of overload.
187
Why is the Frank-Starling mechanism clinically important?
It helps tailor fluid interventions based on the patient's position on the curve.
188
What is a recommended method to assess fluid responsiveness?
Use small-volume boluses (200–250 mL) to assess fluid responsiveness.
189
What should be avoided in preload-independent states?
Avoid fluid administration in conditions like heart failure.
190
What is thermodilution via PAC?
It involves introducing a chilled injectate in the right atrium and measuring temperature in the pulmonary artery.
191
What does thermodilution assess?
It assesses Cardiac Output (CO), Pulmonary Artery Occlusion Pressure (PAOP), and pulmonary edema.
192
What are the risks of thermodilution via PAC?
Risks include bleeding, infection, arrhythmias, and pulmonary artery rupture.
193
What does Pulse Contour Analysis analyze?
It analyzes arterial pressure waveform changes during respiratory cycles.
194
What are dynamic indices in Pulse Contour Analysis?
Dynamic indices include Stroke Volume Variation (SVV), Pulse Pressure Variation (PPV), Systolic Pressure Variation, and Plethysmography Variability Index (PVI).
195
What is the physiologic basis for dynamic indices?
Mechanical ventilation alters pleural pressures, exaggerating preload variation in hypovolemia.
196
What does a dynamic index >13% indicate?
It is predictive of fluid responsiveness.
197
What does a dynamic index of 9–13% indicate?
It is considered the 'gray zone' where additional monitoring is needed.
198
What are minimally invasive and noninvasive platforms used for?
These systems offer safer, continuous monitoring and are integrated into GDFT protocols.
199
What does FloTrac/EV1000 & Hemosphere measure?
Uses a sensor-based pressure transducer and algorithm to measure CO and SVV.
200
What does ProAQT/PulsioFlex provide?
Provides real-time dynamic measures using arterial line inputs.
201
What technology does LiDCOrapid/PulseCO & LiDCOplus use?
Uses arterial waveform analysis.
## Footnote
LiDCOplus also uses lithium dilution for calibration and integrates blood gas data for oxygenation assessment.
202
What is the ClearSight System?
A noninvasive finger cuff using volume clamp technology that reconstructs brachial arterial waveform and calculates CO, SVV, MAP, and oxygen transport metrics.
203
What does PiCCO combine?
Combines pulse contour analysis and transpulmonary thermodilution.
## Footnote
Requires central arterial (femoral) and venous access and measures CO, SV, preload, afterload, extravascular lung water, SCVO₂, and organ function.
204
What does the VolumeView Set with EV1000 provide?
A femoral arterial catheter with integrated thermistor that provides dynamic data and tissue oxygenation metrics.
205
What does CNAP measure?
Uses double finger sensors to measure continuous arterial pressure and hemodynamic parameters.
206
What is the structured approach of GDFT protocols?
1. Baseline assessment of hemodynamic targets 2. Small-volume fluid challenge (200–250 mL) 3. Reassessment of fluid responsiveness (every 5–10 min) 4. Use of vasoactive/inotropic support if fluid nonresponsive.
207
What are the goals of GDFT protocols?
Ensures avoidance of unnecessary fluids, timely support of oxygen delivery and CO, protection of endothelial glycocalyx, and enhanced postoperative recovery.
208
What is Esophageal Doppler Monitoring (EDM)?
EDM uses Doppler ultrasound to measure thoracic aortic flow, corrected flow time (FTc), stroke volume (SV), and aortic compliance.
209
What are the benefits of Esophageal Doppler Monitoring (EDM)?
EDM provides dynamic, real-time assessments of preload responsiveness and left ventricular (LV) function. It is widely accepted in the UK as standard of care.
210
What does Transesophageal Echocardiography (TEE) evaluate?
TEE offers comprehensive evaluation of cardiac function, chamber sizes, wall motion, valve abnormalities, and fluid responsiveness.
211
What are the requirements for performing Transesophageal Echocardiography (TEE)?
TEE requires board certification to perform; it is more invasive but highly accurate.
212
What is Thoracic Electrical Bioimpedance (TEB)?
TEB is a noninvasive method of hemodynamic monitoring using paired surface electrodes at the neck and diaphragm.
213
How does Thoracic Electrical Bioimpedance (TEB) work?
TEB transmits low-level electrical currents across the chest and measures impedance changes related to cardiac output (CO) and blood flow.
214
What is the purpose of waveform mapping in TEB?
Waveform mapping is integrated with ECG signals to calculate hemodynamic parameters in real time.
215
What are the limitations of TEB?
TEB measurements can be affected by pleural/pericardial effusions, arrhythmias, aortic valve disease, aortic aneurysm, morbid obesity, and patient movement.
216
What are some common TEB devices?
Common TEB devices include Aesculon, BioZ, NICaS, Starling SV, and Task Force.
217
What measures are used to assess tissue oxygenation in GDFT?
Measures include arterial, venous, and mixed venous blood gases, oxygen delivery (DO₂), and oxygen consumption (VO₂).
218
What does GDFT focus on?
GDFT focuses on maximizing DO₂ through fluid optimization, CO support, microcirculatory flow, and transfusion, while minimizing VO₂ using opioids, β-blockers, and normothermia.
219
How is GDFT integrated into Enhanced Recovery After Surgery (ERAS)?
GDFT is a key element of ERAS protocols designed to improve surgical outcomes, decrease postoperative complications, accelerate recovery, minimize opioid use, and preserve organ function.
220
What is the origin of ERAS?
The concept of ERAS originated in the 1990s by Danish surgeon Henrik Kehlet, who identified delayed gut function and physical mobility as reasons for extended hospitalization.
221
What are the goals of ERAS?
ERAS aims to optimize perioperative care by standardizing best practices, emphasizing patient-specific strategies, integrating GDFT and non-opioid pain control, reducing unnecessary fasting, and encouraging early ambulation.
222
What evidence supports the integration of ERAS and GDFT?
Integration is associated with shorter hospital stays, fewer complications, decreased healthcare costs, and faster return of GI function and mobility.
223
What is a clinical takeaway regarding GDFT?
GDFT relies on various invasive, minimally invasive, and noninvasive technologies to assess volume status, fluid responsiveness, and tissue oxygenation.
224
Why is patient-specific selection critical in monitoring methods?
Not all monitoring methods are appropriate in every clinical scenario; patient-specific selection is critical to optimize outcomes.
225
How does combining GDFT principles with ERAS protocols benefit patients?
Combining GDFT with ERAS enhances recovery, optimizes fluid balance, and improves short- and long-term outcomes.
226
What is the origin of Enhanced Recovery After Surgery (ERAS)?
Originally developed for colon resection surgery.
227
In which types of surgeries is ERAS now widely applied?
Abdominal vascular, esophagectomy, gastrectomy, pancreatectomy, colorectal, gynecologic, orthopedic, and bariatric procedures.
228
How many treatment items does the ERAS Society outline under the ERAS protocol?
22 treatment items.
229
What did Lassen et al. find in their review of ERAS treatment elements?
15 supported by strong evidence; ERAS protocols improve postoperative outcomes, reduce complications, accelerate recovery, and support early discharge.
230
What are the three phases of the ERAS protocol?
Preoperative Phase, Intraoperative Phase, Postoperative Phase.
231
What are some key interventions in the Preoperative Phase of ERAS?
No routine bowel prep, short fasting periods, clear fluids allowed up to 2 hours pre-op, carbohydrate drinks 2 hours before surgery, preadmission counseling, thromboprophylaxis, antibiotic prophylaxis, no routine premedication.
232
What are some key interventions in the Intraoperative Phase of ERAS?
Maintenance of normothermia, short-acting anesthetics, mid-thoracic epidural or anesthesia/analgesia, avoidance of salt and water overload, no nasogastric tubes, no drains (if possible).
233
What are some key interventions in the Postoperative Phase of ERAS?
Early removal of catheters, early oral nutrition, early mobilization, non-opioid analgesia, prevention of nausea and vomiting, monitoring and compliance audits.
234
What are the new guidelines for preoperative fluid management in ERAS?
Clear liquids up to 2 hours pre-op, breast milk up to 4 hours, light meals up to 6 hours.
235
What does traditional fasting cause according to ERAS?
Dehydration and metabolic stress.
236
What is the goal of preoperative fluid management in ERAS?
Ensure euvolemia on arrival to the OR.
237
What is the current stance on Mechanical Bowel Preparation (MBP) in ERAS?
Routine MBP is no longer supported for all patients.
238
What are the effects of hypertonic MBP?
Dehydration, fluid shifts, increased morbidity.
239
How do carbohydrate drinks before surgery help?
Reduce hunger, thirst, anxiety, and improve preoperative glucose and hydration status.
240
What does MBP with carbohydrate loading reduce?
Pre-op dehydration, intra-op fluid overload, post-op ileus risk.
241
What are the problems with traditional intraoperative fluid management methods?
Overhydration and wide practice variability.
242
What is the ERAS approach to intraoperative fluid management?
Replace only measurable losses, use Goal-Directed Fluid Therapy (GDFT), avoid routine correction of fasting deficit.
243
What does perioperative GDFT reduce?
Variability in fluid practice and post-op complications (e.g., ileus, edema, delayed recovery).
244
What are the components of GDFT?
Predefined bolus volumes, hemodynamic triggers (e.g., SVV, PPV), use of vasopressors as needed.
245
What is the focus of postoperative fluid management in ERAS?
Early discontinuation of IV fluids and early oral intake.
246
What are the benefits of early oral intake postoperatively?
Decreased risk of delayed gut recovery, fluid overload, pulmonary edema, prolonged hospital stay.
247
What is the new paradigm in perioperative fluid therapy?
Focus on physiologic changes from surgery, prevent organ injury from both under- and overhydration.
248
What is emphasized in the new paradigm of perioperative fluid therapy?
Targeted, responsive fluid administration over formulas.
249
What is the association between post-op complications and fluid management?
Strong association between post-op complications and fluid mismanagement.
250
What are the clinical implications of integrating ERAS and GDFT?
Improves outcomes, reduces costs, and shortens recovery.
251
What does avoidance of unnecessary fasting and bowel prep preserve?
Volume status.
252
What does GDFT allow for in fluid management?
Individualized, real-time fluid titration.
253
What is prioritized over IV fluid continuation postoperatively?
Post-op oral rehydration.
254
What is crucial for successful ERAS implementation?
A multidisciplinary team.
255
What is the role of sodium in the extracellular fluid (ECF)?
Sodium is the most abundant ECF electrolyte and plays a central role in osmotic activity, determining ECF volume, and maintaining water balance between compartments (ECF ↔ ICF).
256
What does the Na⁺-K⁺ ATPase pump do?
The Na⁺-K⁺ ATPase pump maintains the sodium gradient with ECF Na⁺ ≈ 140 mEq/L and ICF Na⁺ ≈ 25 mEq/L.
257
How does sodium concentration affect water movement?
Water movement across membranes is influenced by sodium concentration to achieve osmotic equilibrium.
258
What is the permeability of the blood-brain barrier (BBB) to sodium?
The blood-brain barrier (BBB) has limited permeability to sodium, preventing equilibration between compartments.
259
What is the primary osmotically active substance influencing brain water content?
Sodium is the primary osmotically active substance influencing brain water content, more so than plasma proteins.
260
What can sodium imbalances cause in the brain?
Imbalances can cause cerebral edema (especially in hyponatremia) and brain injury, particularly if shifts occur rapidly.
261
What is hyponatremia?
Low serum sodium due to dilutional effects or loss of sodium.
262
What can cause hyponatremia?
Excess water intake, SIADH, surgical irrigation with hypotonic solutions, CHF or cirrhosis (hypervolemic hyponatremia).
263
In surgical settings, what procedures are associated with hyponatremia?
Endometrial ablation and TURP (Transurethral Resection of the Prostate).
264
What can lead to acute dilutional hyponatremia?
Use of hypotonic fluids.
265
What happens at the cellular level in hyponatremia?
Water shifts into cells, leading to cellular swelling.
266
What are the brain-related consequences of cellular swelling due to hyponatremia?
Cerebral edema, increased intracranial pressure, and neuron death.
267
What compensatory mechanisms does the brain use in response to hyponatremia?
The brain attempts to adapt by extruding solutes to reduce intracellular osmolality.
268
What populations are at higher risk for brain damage from hyponatremia?
Menstruating women, patients with orthotopic liver transplant, chronic alcohol abuse, and hyponatremia duration > 48 hours.
269
What are the clinical manifestations of hyponatremia?
Range from asymptomatic to life-threatening, including mild symptoms like nausea and confusion, and severe symptoms like seizures and coma.
270
What does SIADH cause in terms of fluid balance?
Euvolemic hyponatremia, with water retention and no significant sodium loss.
271
What can chronic hyponatremia result in?
Cognitive impairment, gait disturbances, and increased mortality in patients with CHF and cirrhosis.
272
What is the initial management for hyponatremia?
Fluid restriction and diuresis for hypervolemic states; treat underlying causes.
273
What pharmacologic treatments are used for hyponatremia?
Vaptans (vasopressin antagonists) like Tolvaptan (oral) for euvolemic/hypervolemic hyponatremia and Conivaptan (IV) for short-term use.
274
What is the effect of vaptans on water and sodium?
They promote free water excretion without sodium loss.
275
Have vaptans been shown to reduce mortality?
No, they have not been shown to reduce mortality.
276
What is Osmotic Demyelination Syndrome (ODS) also known as?
Central pontine myelinolysis.
277
What are the neurologic symptoms of ODS?
Spastic quadriparesis, pseudobulbar palsy, seizures, coma, and death.
278
How can ODS be prevented?
Avoid raising serum Na⁺ >10–15 mEq/L in 24 hrs and limit to 1–2 mEq/L per hour. Use 3% hypertonic saline cautiously in symptomatic patients.
279
What is the most common electrolyte abnormality in hospitalized patients?
Hyponatremia.
280
What should anesthetists recognize regarding hyponatremia?
Perioperative risk, monitor neurologic status, be cautious with fluid administration, and consider vasopressin antagonists if SIADH is suspected.
281
How is hypernatremia defined?
An elevated serum sodium level (>145 mEq/L), typically due to a relative deficit of free water.
282
What is the most frequent cause of hypernatremia?
Impaired water intake, especially in elderly, debilitated, or intubated patients.
283
What are some causes of excessive water loss leading to hypernatremia?
GI losses (diarrhea, vomiting), renal losses (diuretics, osmotic diuresis, diabetes insipidus), and insensible losses (fever, burns).
284
What happens to cells in serum hyperosmolality?
Water shifts out of cells, leading to cellular shrinkage.
285
What are the risks associated with rapid-onset hypernatremia?
Brain shrinkage, tearing/traction of bridging veins, and risk of intracranial hemorrhage.
286
How do brain cells adapt in chronic hypernatremia?
By accumulating intracellular solutes to preserve ICV volume, delaying symptoms but increasing the risk of cerebral edema if corrected too rapidly.
287
What are the neurologic symptoms of hypernatremia?
Lethargy, confusion, seizures, and coma.
288
What complications can arise from severe or rapid hypernatremia?
Intracranial hemorrhage, especially in pediatric and elderly populations.
289
What is the first step in treating hypernatremia?
Assess duration and volume status.
290
How should acute hypernatremia (<24 hrs) be corrected?
Can be corrected more quickly using hypotonic solutions (e.g., D5W or 0.45% NaCl).
291
How should chronic hypernatremia (>24 hrs) be corrected?
Must be corrected slowly; first correct volume depletion with isotonic fluids (e.g., 0.9% NaCl), then administer hypotonic fluids to correct free water deficit.
292
What is the recommended rate of correction for serum Na⁺?
Should be decreased by 1–2 mEq/L per hour, with total sodium correction not exceeding 10–12 mEq/L in 24 hours.
293
What is the risk of rapid overcorrection of hypernatremia?
Cerebral edema.
294
What is the treatment strategy for Acute Hypernatremia (<24h)?
Rapid correction with hypotonic fluids (e.g., D5W)
295
What is the treatment strategy for Chronic Hypernatremia with hypovolemia?
First: Isotonic fluid resuscitation (e.g., NS)
Then: Gradual correction with hypotonic fluids
296
What is the target correction rate for sodium in hypernatremia?
Decrease Na⁺ by 1–2 mEq/L per hour until stable
297
What is the maximum 24-hour correction for sodium to prevent cerebral edema?
10–12 mEq/L
298
What is a key clinical point regarding hypernatremia in hospitalized patients?
Hypernatremia is often iatrogenic—monitor fluid orders carefully.
299
What should be evaluated before correcting serum sodium?
Evaluate volume status and duration
300
What should be avoided to prevent rebound cerebral edema?
Avoid overcorrection, particularly in chronic cases.
301
What neurologic symptoms can result from hypernatremia or its correction?
Confusion, lethargy, seizures
302
What is the primary intracellular electrolyte?
Potassium (K⁺) is the primary intracellular electrolyte, with 98% of total body K⁺ located inside cells.
303
What are the normal ranges for intracellular and extracellular potassium?
Intracellular K⁺: 150–160 mEq/L
Extracellular K⁺: 3.5–5.0 mEq/L
304
Why is the potassium concentration gradient critical?
It is critical for maintaining resting membrane potential, neuromuscular excitability, and cardiac electrical conduction.
305
What is the primary means of potassium balance?
Renal excretion is the primary means of potassium balance.
306
What factors influence renal potassium excretion?
1. Concentration gradient between distal tubule and peritubular capillaries
2. Tubular flow rate and sodium concentration
3. Aldosterone levels
4. Acid-base balance (acidosis/alkalosis)
307
How does aldosterone respond to hyperkalemia?
Aldosterone promotes renal excretion of K⁺ and enhances potassium secretion in the distal tubules.
308
What are the causes of potassium imbalances?
K⁺ disturbances may arise from a shift between ECF and ICF (distributional) or true body store depletion or excess.
309
What is hypokalemia?
Hypokalemia is defined as serum K⁺ < 3.5 mEq/L.
310
What are the etiologies of hypokalemia?
1. Absolute K⁺ loss: GI loss (vomiting, diarrhea), renal loss (diuretics, hyperaldosteronism), poor intake.
2. Intracellular shift: β-adrenergic stimulation, insulin, alkalosis.
311
Which diuretics are strongly associated with hypokalemia?
Thiazide diuretics are strongly associated with hypokalemia, with an 11x increased risk.
312
Who is more commonly affected by hypokalemia?
Hypokalemia is more common in men.
313
What are the clinical manifestations of mild hypokalemia?
Mild hypokalemia is often asymptomatic or may include palpitations, muscle weakness, and myalgia.
314
What are the symptoms of severe hypokalemia?
Severe hypokalemia (<2.5 mEq/L) may include paresthesia, muscle fasciculations, weakness, hyporeflexia, and altered mental status.
315
What cardiac effects are associated with severe hypokalemia?
Increased risk of dysrhythmias, particularly in patients with ischemic heart disease or CHF, including first/second-degree heart block, atrial or ventricular fibrillation, and asystole.
316
What ECG changes are seen in hypokalemia?
ECG changes include ST segment depression, flattened T waves, prominent U waves, and prolonged QT interval.
317
What factors determine the clinical management of hypokalemia?
Treatment depends on severity, presence of symptoms, and cardiac risks.
318
When is IV potassium replacement used?
IV potassium replacement is used when symptoms are severe or dysrhythmias are present, at a rate of no more than 10–20 mEq/hr unless in a monitored setting.
319
What is the preferred method for oral potassium supplementation?
Oral supplementation is appropriate for mild-moderate cases, with KCl preferred; potassium phosphate may be used if hypophosphatemia coexists.
320
How should potassium be mixed for administration?
Mix K⁺ in dextrose-free solution (e.g., normal saline) to avoid further intracellular shifts from insulin stimulation.
321
What are the risks associated with preoperative potassium levels?
Both hypokalemia (K⁺ < 4.0 mEq/L) and hyperkalemia (K⁺ > 5.5 mEq/L) significantly increase the risk of 30-day postoperative mortality and Major Adverse Cardiovascular Events (MACE).
322
Why is preoperative electrolyte optimization important?
Preoperative electrolyte optimization, particularly potassium, is critical for perioperative risk reduction.
323
What is hyperkalemia?
Serum K⁺ > 5.0 mEq/L
324
What are the causes of hyperkalemia?
Impaired renal excretion, high K⁺ intake (uncommon unless renal impairment exists), shift of K⁺ from ICF to ECF due to tissue breakdown, acidosis, ACE inhibitors, ARBs, NSAIDs, beta-blockers, and pseudohyperkalemia (e.g., hemolysis during phlebotomy).
325
What are the pathophysiological effects of hyperkalemia?
Leads to membrane depolarization, lactic acidosis, and apoptosis.
326
What ECG abnormalities can result from hyperkalemia?
Progress with severity and can result in muscle weakness and lethal arrhythmias.
327
What is the clinical risk associated with preoperative hyperkalemia?
K⁺ > 5.5 mEq/L is associated with higher 30-day mortality and increased cardiovascular events after surgery.
328
What is the first step in the management of hyperkalemia?
Verify it’s not pseudohyperkalemia.
329
How do you stabilize the myocardium in hyperkalemia?
Administer IV calcium gluconate or chloride.
330
What is a method to shift K⁺ intracellularly?
IV insulin + dextrose (D50).
## Footnote
Recommended: 5 units regular insulin + D50; lower risk of hypoglycemia vs. traditional 10 units.
331
What are other methods to shift K⁺ intracellularly?
Beta-agonists (albuterol) and sodium bicarbonate (if acidosis present).
332
What are the methods to enhance elimination of potassium?
Loop diuretics, Kayexalate, patiromer, sodium zirconium cyclosilicate, and dialysis (in severe/refractory cases).
333
What is the normal total serum calcium level?
9.0–10.5 mg/dL.
334
What forms does plasma calcium exist in?
Ionized (active), bound to plasma proteins (mainly albumin), and bound to anions (e.g., phosphate).
335
What is the clinically active form of calcium?
Ionized calcium.
336
How does acid-base status affect calcium levels?
Acidemia → ↓ protein binding → ↑ ionized calcium; alkalemia → ↑ protein binding → ↓ ionized calcium.
337
What are the regulatory hormones for calcium?
Parathyroid hormone (PTH) – raises serum calcium, Vitamin D – increases GI absorption of calcium, Calcitonin – lowers serum calcium (minor effect).
338
What are intraoperative causes of hypocalcemia?
Hyperventilation (alkalosis → increased protein binding → ↓ ionized Ca²⁺) and massive rapid blood transfusion (due to citrate, which binds calcium).
339
What are the clinical consequences of hypocalcemia?
Neuromuscular irritability (tetany, muscle cramps, paresthesias, seizures) and cardiovascular effects (QT prolongation, ventricular arrhythmias, hypotension).
340
What is the treatment for hypocalcemia?
IV calcium salts based on severity and IV access: Calcium chloride (272 mg elemental Ca²⁺) or calcium gluconate (93 mg elemental Ca²⁺ per 10 mL of 10% solution).
341
What is a typical regimen for IV calcium gluconate?
10 mL of 10% calcium gluconate IV over 10 minutes, followed by continuous infusion (0.3–2 mg/kg/hr) based on ionized calcium levels.
342
What is hypercalcemia?
Hypercalcemia is a condition resulting from excessive calcium mobilization from bone or inadequate renal excretion.
343
What are the common causes of hypercalcemia?
Common causes include primary hyperparathyroidism, malignancy, vitamin D toxicity, sarcoidosis, immobilization, and certain medications (thiazides, lithium).
344
What are the clinical signs of hypercalcemia?
"Stones, bones, groans, and psychiatric overtones": kidney stones, bone pain, abdominal pain, constipation, confusion, fatigue, lethargy.
345
What severe complications can arise from hypercalcemia?
Severe hypercalcemia may cause life-threatening dysrhythmias.
346
What is the first treatment step for hypercalcemia?
Volume expansion with normal saline (NS) promotes renal calcium excretion.
347
What pharmacologic agents are used to treat hypercalcemia?
Agents include bisphosphonates, calcitonin, glucocorticoids, phosphate salts, and mithramycin.
348
When is hemodialysis indicated in hypercalcemia?
Hemodialysis is indicated for acute, severe cases or renal failure.
349
What is the normal serum range for magnesium?
The normal serum range for magnesium is 1.5–3.0 mEq/L.
350
What are the key physiological roles of magnesium?
Magnesium is a cofactor in over 300 enzymatic reactions, regulates neuromuscular excitability and myocardial function, and stabilizes Na⁺/K⁺-ATPase pump, calcium channels, and intracellular K⁺ levels.
351
What are common causes of hypomagnesemia?
Common causes include GI losses, renal losses, poor intake, endocrine/metabolic issues, and certain medications.
352
What are the clinical features of hypomagnesemia?
Clinical features include neuromuscular symptoms (tremors, tetany, seizures) and cardiovascular dysrhythmias.
353
What ECG findings are associated with hypomagnesemia?
ECG findings include flat T waves, prominent U waves, prolonged QT interval, and widened QRS.
354
How is mild hypomagnesemia treated?
Mild or asymptomatic cases are treated with oral magnesium (e.g., Mg oxide).
355
What is the treatment for severe hypomagnesemia?
Severe or symptomatic cases are treated with IV magnesium sulfate.
356
What are common causes of hypermagnesemia?
Common causes include excessive magnesium administration, renal insufficiency, excessive antacid/laxative use, and tumor lysis syndrome.
357
What are the clinical features of hypermagnesemia?
Clinical features include nausea, flushing, hypotension, lethargy, and severe cases can lead to complete heart block and respiratory depression.
358
What is the initial treatment for hypermagnesemia?
The initial treatment involves stopping magnesium intake.
359
How is cardiac membrane stabilized in hypermagnesemia?
Cardiac membrane stabilization is achieved with IV calcium gluconate.
360
What is the treatment for enhancing magnesium elimination in hypermagnesemia?
Enhancing magnesium elimination can be done with loop diuretics and hydration, or dialysis if renal failure or magnesium levels exceed 10 mEq/L.
361
What is the normal range of serum phosphate?
2.5–4.7 mg/dL
362
In what forms does phosphate exist?
1. Phospholipids
2. Phosphate esters (e.g., ATP, 2,3-DPG)
3. Inorganic phosphate (ionized, active)
363
What are the critical functions of phosphate?
1. ATP production
2. Oxygen delivery (via 2,3-DPG in RBCs)
3. Acid-base buffering
4. Skeletal mineralization
364
What defines hypophosphatemia?
Serum phosphate < 2.0 mg/dL
365
What are some causes of hypophosphatemia?
1. GI losses/malabsorption
2. Respiratory alkalosis
3. Refeeding syndrome
4. Alcoholism, DKA recovery, burns
5. Diuretics, antacids
366
What is the pathophysiology of hypophosphatemia?
↓ Phosphate → ↓ 2,3-DPG → ↑ O₂ affinity of hemoglobin → ↓ oxygen unloading → tissue hypoxia
367
What are the clinical features of hypophosphatemia?
1. Neuromuscular: weakness, paresthesias, confusion, seizures
2. Cardiac: bradycardia, decreased contractility, asystole
3. Hematologic: hemolysis, impaired leukocyte function
4. Respiratory: diaphragmatic weakness, failure to wean from ventilator
368
What is the treatment for mild/moderate hypophosphatemia?
Oral phosphate
369
What is the treatment for severe hypophosphatemia?
IV phosphate (sodium or potassium phosphate)
## Footnote
Monitor calcium (risk of hypocalcemia and precipitation)
370
What defines hyperphosphatemia?
Serum phosphate > 4.7 mg/dL
371
What are some causes of hyperphosphatemia?
1. Renal failure (most common)
2. Cell lysis: tumor lysis syndrome, rhabdomyolysis, trauma
3. Vitamin D toxicity, acidosis
4. Excess phosphate intake (e.g., laxatives, phosphate enemas)
372
What are the clinical features of hyperphosphatemia?
Often asymptomatic, but can cause:
1. Calcium-phosphate precipitation in soft tissues
2. Hypocalcemia symptoms: tetany, muscle cramps, seizures
3. Long-term: vascular calcification, nephrocalcinosis
373
What is the treatment for hyperphosphatemia?
1. Phosphate binders: calcium acetate, sevelamer, lanthanum
2. Low-phosphate diet
3. Dialysis (in renal failure or severe hyperphosphatemia)
