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671A - Anesthesia I > Week 10 - Fluids, Electrolytes, and Goal-Directed Therapy > Flashcards

Week 10 - Fluids, Electrolytes, and Goal-Directed Therapy Flashcards

1
Q

Total body water represents ________ of lean body mass

A

60%

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2
Q

How is intracellular volume and extracellular volume distributed in the body?

A

2/3 of TBW –> Intracellular
1/3 of TBW –> Extracellular

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3
Q

What are the primary cations and anions in the ICV and ECV?

A

ICV –> K+ and PO4-
ECV –> Na+ and Cl-

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4
Q

What is the importance of the Na+/K- pump?

A

Maintains the resting membrane gradient –> Moves Na+ into the ECV and K+ into the ICV

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5
Q

Cell membranes are permeable to water, what does this mean?

A

Maintains a state of osmotic equilibrium. Water will “follow the party” –> More solutes on one side causes water to go to that side

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6
Q

What is the daily fluid requirement of a healthy adult to maintain total body water homeostasis?

A

25-35 ml per kg –> 2-3 liters per day

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7
Q

What are the two sub compartments of the ECV?

A

Interstitial compartment –> 3/4 of the 1/3 of ECV
Intravascular compartment –> 1/4 of the 1/3 of ECV

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8
Q

What are some of the non-functional fluids of the ECV that generally aren’t considered due to being anatomically isolated from the ECV?

A

Trans-cellular fluids –> CSF, synovial fluid, GI secretions, and intra-ocular fluid

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9
Q

What is capillary hydrostatic pressure (Pc)?

A

Pc –> Intravascular fluid pressure, increased by increasing CO and impacted by vascular tone.

Increased Pc favors pushing fluid into the interstitial space

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10
Q

What is interstitial fluid pressure (Pif)?

A

Pif –> Hydrostatic pressure in the interstitial space –> This is generally negative due to the lymphatic system pulling fluid from here.
Rigid or encapsulated tissues have a slightly positive pressure –> kidneys, brain, bone marrow, and skeletal muscle

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11
Q

What is plasma oncotic pressure (pieP)?

A

pieP –> Osmotic force of the colloids in the vasculature
Increased pieP = Absorbing fluid into the vascular system –> Albumin is the primary colloid in the plasma and interstitial

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12
Q

What is interstitial oncotic pressure (pieIF)

A

pieIF –> Osmotic force of colloidal proteins in the interstitial space.
Increased pieIF –> Increased fluids in the interstitial space
Albumin is the primary colloid in the interstitial and plasma
Can cause excessive reactions if albumin is given to a patient with a damaged glycocalyx –> Edema

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13
Q

What is the net filtration formula?

A
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14
Q

What does an increased Kf in the net filtration formula mean?

A

Favors filtration –> Kf is a filtration coefficient that accounts for capillary surface area and endothelial permeability to water

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15
Q

In the net filtration formula, what does a positive number mean? What does a negative number mean?

A

Positive –> favors fluid exudation into the tissues
Negative –> favors fluid exudation into the vascular system

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16
Q

Where does net filtration tend to be slightly positive? Slightly negative?

A

Slightly positive on the arterial end and slightly negative on the venous end

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17
Q

What is the overall balance of the net filtration system?

A

Slightly negative –> Pushing fluids into the interstitial space, lymphatic system accounts for this and takes these fluids out of this space at an equal rate of approximately 2 mL per min.
Net fluid filtration = lymphatic flow (2 mL per min)

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18
Q

What is the gel layer on the endothelium that is responsible for maintaining fluid homeostasis?

A

Glycocalyx –> composed of primarily glycoproteins, polysaccharides, and hyaluronic acid –> These bind to ionic side chains and plasma proteins which form a physical barrier within the vascular space.

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19
Q

How does the glycocalyx aid in the prevention of blood component adhesion and augments laminar flow?

A

Repels negatively charged polar compounds as well as blood

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20
Q

What does the glycocalyx preserve and decreased? 2 things

A
  1. Preserves capillary oncotic pressure –> Keeps vascular albumin in the vascular system
  2. Decreases capillary permeability to water
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21
Q

True or false
The glycocalyx also serves to scavenge free radicals, bind and activation of clotting factors, signal transduction that helps regulate local vasoactive responses to mechanical stress, and regulates immune response.

A

True

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22
Q

How are normal alterations in total body water regulated and compensated for?

A

RAAS, ADH, and ANP

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23
Q

What is the primary electrolyte responsible for serum osmolality and water transport?

A

Na+

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24
Q

Explain the RAAS pathway

A

RAAS –> In response to hypotension via baroreceptors, the kidneys release renin. Renin can activate angiotensinogen which now becomes angiotensin I.
Angiotensin I can act like a mild vasoconstrictor now, but more importantly can be activated into angiotensin II via ACE which is made in the lungs.
Angiotensin II now acts as a POTENT vasoconstrictor, stimulates the renal tubules to reabsorb sodium and water AND activates aldosterone which causes further reabsorption of sodium and water.

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25
Q

Explain the ADH pathway

A

Posterior pituitary gland release ADH in increases of serum osmolality detected by osmo-receptors in the hypothalamus or decreases in blood pressure detected by baroreceptors –> This causes potent vasoconstriction and reabsorption of large amounts of water in the kidneys.

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26
Q

Explain the ANP pathway

A

Respond due to stretch within the cardiac atrial walls, this causes a release of ANP –> This causes the kidneys to excrete sodium and water, DECREASING fluid volume in the body. It also INCREASES glomerular filtration and inhibits the release of renin and ADH

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27
Q

In healthy adults, fluid intake and output are closely monitored to such a degree that only ________ represents TBW daily fluctuations.

A

0.2%

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28
Q

When are crystalloids preferred?

A

For resuscitation of dehydration –> Prolonged fasting, GI losses, polyuria, and hyper metabolic conditions

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29
Q

Why are crystalloids generally safer over colloids?

A

They lack allergenic components and are easily metabolized and cleared by the kidneys.

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30
Q

What happens with crystalloid infusion due to their low molecular weight?

A

75-80% end up in the interstitial space due to in hemodilution of the plasma

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31
Q

Although NS (0.9% NaCl) is the most common IV fluid administered worldwide, it is the least __________

A

Physiologic –> Components in NaCl do not represent the plasma components as well as other IV fluids.

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32
Q

Why can infusing too much NS cause hyper cholremic metabolic acidosis?

A

NS contains equal concentration of Na to Cl (154 mEq per L) –> Plasma consists of 142 mEq per L of Na and 108 mEq per L of Cl, Cl concentrations being much lower.
This increases the serum chloride level over time

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33
Q

0.9% NaCl is actually slightly _________osmolar

A

hyper

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34
Q

What effect does high chloride levels have on the body?

A

Causes decreased renal filtration as well mishandling of bicarbonate.

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35
Q

Large dose of 0.9% NS is known to cause hyperchloremia, what else is it known to do?

A

Increased sodium levels –> This leads to salt and water retention, hemodilution, and interstitial edema well into the post-operative period

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36
Q

Giving a healthy adult 2 liters of NS can take them ____ ________ to excrete

A

2 days

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37
Q

Enhanced recovery after surgery (ERAS) suggests using what type of fluids in peri-operative fluid management and high volume fluid resuscitation?

A

Balanced crystalloid solutions

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38
Q

Why are small volumes of NS in neurosurgical populations preferred?

A

Because NS is SLIGHTLY hypertonic to blood plasma, it can reduce cerebral edema.

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39
Q

What crystalloid solution is ideal from patients with anuria or end stage renal disease? Why?

A

0.9% NS –> Doesn’t contain potassium like other balanced crystalloids do, which is hard to the kidneys to excrete in these populations.

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40
Q

When would 3% saline be utilized?

A

Used in low dose infusions in trauma and head injury patients by promoting vascular expansion that moves fluid from the interstitial and intracellular space into the vascular space.

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41
Q

What are some complications associated with 3% saline infusions?

A

Vascular irritation, sudden and pronounced fluid shifts, and potential dehydration of neural cells leading to osmotic demyelination syndrome.

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42
Q

As you age, what happens to total body water percentage?

A

Decreases

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43
Q

True or False
An obese individual will have a higher body water percentage than a muscular individual?

A

False –> Obese individuals have a LOWER percentage of body water to that of a muscular individual

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44
Q

Lactated ringers is more effective than NS in doing what?

A

Preserving intravascular volume –> Used as a resuscitation fluid because it is much more balanced than NS and lower cost

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45
Q

What patient populations is Lactated ringers not suggested in and why?

A

Diabetic patients –> Sodium lactate is used as the buffering agent. When lactate is metabolized by the body is can result in gluconeogensis.

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46
Q

What surgical patient population is LR contraindicated in?

A

Traumatic brain injury patients or other neurovascular procedures –> LR is slightly HYPOtonic and will cause a fluid shift into these spaces.

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47
Q

What are the crystalloids that represent the body plasma the best?

A

Plasmalyte-A, Normosol-R, and Isolyte S –> They preserve physiologic pH and renal perfusion!
They can also be administered with blood because they don’t contain calcium. (LR can’t be given with blood due to this)

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48
Q

How would you describe colloids and what is the only naturally occurring colloid aside from RBC’s?

A

High molecular weight molecules that increase plasma oncotic pressure –> albumin is the only naturally occurring colloid, used for active blood loss not requiring transfusion.
These are heat treated to eliminate pathogens but still carry allergenic components

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49
Q

What is the benefit of colloids over crystalloids?

A

Colloids have a fluid sparing effect.
Can give much less volume by pulling fluid from the interstitial space into the vascular system by increasing oncotic pressure in the plasma.

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50
Q

What are dextrans?

A

Oldest artificial colloid derived from bacterial metabolism of sucrose.
No longer used due to causing renal failure, anaphylaxis (HIGHLY allergenic), and coagulopathy (by impairing vWF, activating plasminogen, and interference with platelet aggregation)

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51
Q

What are gelatins?

A

Synthetic colloids derived from bovine components.
Like dextrans these are no longer used due to –>
Causing renal failure, anaphylaxis (HIGHLY allergenic), coagulopathy and histamine release

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52
Q

Which synthetic colloid has a black box warning?

A

Hydroxyethyl starches (HES) –> These are derived from starchy plants.
3 generations of these –> 1st was very big (>450 kDa) and progressively got smaller with 3rd being 70 - 130 kDa
Not used much due to reasons like the other synthetic colloids –> Causing renal failure, can cause allergic reactions and coagulopathy

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53
Q

What is the molecular weight of albumin?

A

65-69 kDa

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54
Q

What happens if colloids are administered in patients with endothelial glycocalyx injuries?

A

If these are used in glycocalyx injuries, the colloids can escape in the interstitial causing pulmonary edema and end organ complications.

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55
Q

What patient populations are colloids contraindicated in?

A

Conditions that like cause endothelial glycocalyx injuries –> Hyperglycemia and sepsis

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56
Q

What happens if colloids are administered in euvolemic patients?

A

Fluid volume overload can occur causing the body to secrete ANP

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57
Q

What does surgical incision stimulate?

A

Somatic and autonomic afferent pathways –> Triggers Hypothalamic pituitary axis (HPA)
H - Corticotropin releasing hormone (CRH)
P - Adrenocorticotropic hormone (ACTH)
A - Cortisol release from adrenal cortex

Cortisol causes protein catabolism, hepatic gluconeogensis and glycogenolysis, and increased release of plasma proteins from the liver.

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58
Q

What does the activation of the hypothalmic pituitary axis (HPA) cause within the body? When can this be bad?

A

Causes retention of intravascular plasma to preserve fluid via release of plasma proteins from the liver.
This can be maladaptive in patients with hyperglycemia (destructive to the glycocalyx which will lead to pulmonary edema and end organ complications) or vascular overload.

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59
Q

Surgical stimulation also causes the release of catecholamines, what effect does this have on the body?

A

Adrenal medulla releases these –> Causes SNS effects (Increased HR, increased SVR, vasoconstriction, increased O2 demand)
Also triggers the release of ADH –> Vasoconstriction and reabsorption which may continue for hours into the postoperative period.

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60
Q

What does surgical trauma cause local endothelial tissue to do?

A

Release cytokines and other inflammatory mediators –> This can contribute to hyperthemia, increased O2 demands, and regional alterations in microcirculation

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61
Q

During surgical stimulation, what is low level cytokine release associated with?

A

Hemostasis

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62
Q

What is prolonged surgeries associated with severe tissue damage associated with?

A

May promote inflammatory loss of GI endothelial integrity leading to translocation of bacteria and systemic inflammatory responses

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63
Q

What is one of the most beneficial effects of cortisol released from the body?

A

Anti-inflammatory effect

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64
Q

During hemorrhage or hypovolemia, Pc (capillary hydrostatic pressure) is decreased. What happens?

A

This favors absorption into the vascular space –> Auto transfusion of interstitial fluid into the vascular space

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65
Q

Hypervolemia can be marked as an increase in _______ but a dilution decrease in __________

A

Pc (Capillary hydrostatic pressure), pieP (Oncotic plasma pressure) –> This would push fluid into the interstitial space causing the lymphatic system to become overwhelmed.

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66
Q

Although laparoscopic procedures are minimally invasive, what 2 risks do these surgeries carry?

A

Increases in abdominal pressure –>
- This can suppress splanchnic blood flow leading to ischemia (Predisposing the GI endothelium to ischemia - reperfusion injury when blood flow is restored.)
- Can stimulate a vagal response via peritoneal and mesenteric afferent receptors (Being done rapidly or high pressures of 12-15 mmHg)

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67
Q

How does abdominal insufflation cause the body to release ANP?

A

High pressures can increase pressure on the SVC which will cause the atria to stretch releasing ANP (Increasing preload)
Too high of pressures in hypovolemic patients can cause cardiac collapse due to complete closure of the SVC

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68
Q

What effects to abdominal insufflation have on SVR, MAP, and SV?

A

SVR and MAP are increased due to the increased pressure
SV is decreased due to this increased pressure

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69
Q

Abdominal insufflation pressures of _______ - _______ mmHg has shown significant decreases in both RV and LV ejection fractions

A

10 - 15 –> Healthy patients can compensate for this with tachycardia and increased LV stroke work, this is at the expense of increased O2 demand

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70
Q

What drugs are known to be effective at suppressing the HPA mediated stress response to surgery?

A

Opioids and dexmedatomidine
Neuraxial blocks
Low dose clonidine
Propofol and volatile agents
Goal directed fluid therapy

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71
Q

Decreased renal perfusion activates what system?

A

RAAS

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72
Q

What is the historical approach to fluid management? What did this often lead to?

A

4 - 2 - 1 method, fluid overload

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73
Q

What GI preoperative medication leads to dehydration?

A

Bowel prep –> Need to consider this for this surgical population by administering more fluids and maintaining euvolemia

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74
Q

What is the “third space”?

A

Non functional component of the ECV –> Became a justification for a liberal fluid approach, this is NOT a good approach as this space doesn’t really exist. Liberal fluids causes damage and is associated with poor patient outcomes

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75
Q

What are some limitations of the 4 - 2 - 1 historical fluid management approach?

A

It relies on static and nonspecific indicators of fluid balance –> MAP, CVP, and urine output
These values do not predict volume responsiveness

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76
Q

What can be the problem with relying on urine output as a measurement of fluid volume?

A

If the patient has decreased urine output, the patients body will respond with ADH to reabsorb water. Giving too much fluid can cause the patient to become hypervolemic as this ADH secretion can continue well into the post operative period.

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77
Q

Survivors of high risk surgeries all had what in common?

A

Greater O2 delivery (DO2), arterial oxygen content (CaO2), and cardiac indexes (CI) than non survivors

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78
Q

What minimally/non invasive method has been developed to guide goal directed fluid therapy?

A

Pulse contour analysis –> Relationship between respiratory variation in plethysmography and arterial pressure
PAC is also used to guide this but is much more invasive and isn’t implemented in the majority of surgeries.

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79
Q

Goal directed fluid therapy has more __________ standards than traditional approaches

A

restrictive

80
Q

What is the “zero balance” approach?

A

Avoids surplus fluid admin –> Generally involves a basal fluid infusion with a 1:1 fluid/blood replacement

81
Q

What is the currently practiced fluid strategy of choice?

A

Goal directed fluid therapy, although zero balance approach is also acceptable.

82
Q

How do Patient Goal Directed Therapy (PGDT) protocols begin?

A

Baseline assessment of patients hemodynamic status, followed by a small volume bolus of 200-250 mL to assess the patients position on the Frank Starling curve.
Monitor preload responsiveness and oxygen delivery (every 5-10 minutes)
Prevent fluid OVERLOAD

83
Q

How do you interpret the Frank Starling curve?

A

If the patient is on the ascending portion –> they WILL respond to fluid (increased LVEDP = increased SV)
If the patient is on the plateau portion –> they WILL NOT respond to fluid (increased LVEDP = no change or decrease in SV)

84
Q

What is the shape of the curve on the Frank Starling curve determined by?

A

Myocardial fitness

85
Q

True or False
GDFT protocols relies on fluid administration triggers, and prompt consideration of vasoactive or inotropic support.

A

True

86
Q

What do most GDFT protocols promote constant reassessment of?

A

Preload responsiveness and oxygen delivery (every 5-10 minutes)

87
Q

What outcomes have been improved in high risk surgical patients due to implementing GDFT?

A
88
Q

What two variables make up the Frank Starling mechanism?

A

Left ventricular end diastolic pressure (LVEDP) and strove volume (SV)

89
Q

What is the pathophysiologic curve of the Frank Starling mechanism?

A

Represents patients with heart failure or ventricular dysfunction. They have a long plateau indicating they can only tolerate small volumes of fluid before they become unable to increase contractility

90
Q

What is the most commonly used dilution monitoring device? How does this work?

A

Thermodilution PAC –> Measures CO , works by injecting chilled fluid into the RA. This chilled fluid is then measured how long it takes it to transit though the heart via a temperature probe.
Low CO coincides with a large area under the curve because it takes longer for this chilled fluid to transit through the heart.

91
Q

What measurement determines preload responsiveness by quantifying the degree of change of arterial, capnography, or pulse oximetry waveforms associated with cyclic respiratory variations and the resulting pleural pressure?

A

Pulse contour analysis

92
Q

What are some methods used to guide Patient Goal Directed Therapy? What is gold standard?

A

Small fixed volume boluses (assessed on Frank Starling curve), dilution techniques (CO), pulse contour analysis, Esophageal doppler/Echocardiography, and measures of tissue oxygenation
Transesophageal Echocardiography –> Gold standard for direct evaluation of cardiac function

93
Q

What value is predictive of fluid responsiveness in pulse contour analysis?

A

If the calculated value is greater than 13%

94
Q

How does an esophageal doppler work?

A

Assesses thoracic aortic blood flow velocity and provides real time LV function and measures of preload responsiveness

95
Q

What is ERAS?

A

Early recovery after surgery –> Multimodal patient management pathway to improve surgical outcomes, utilized patient goal directed therapy

96
Q

What 4 things do ERAS protocols aim to do?

A
  • Promote optimal fluid therapy
  • Reduce the profound stress response attributed to surgery
  • Promote non opioid postoperative pain modalities
  • Maintain baseline organ function post procedure
97
Q

ERAS goal during the preoperative period?

A

For the patient to arrive in the OR in a euvolemic state
Traditional 6-8 hour clear liquid fasting guidelines have been changed to 2 hours –> Helps patient remain in a euvolemic state

98
Q

ASA guidelines for fasting from a heavy meal prior to surgery?

A

8 hours

99
Q

ASA fasting guidelines from a light meal prior to surgery?

A

6 hours

100
Q

Why should mechanical bowel preparations be avoided if possible?

A

Leads to dehydration and fluid shifts that increase postoperative morbidity

101
Q

Reducing NPO time prior to surgery reduces what? What are these patients less likely to respond to?

A

Less likely to be dehydration which decreases peri operative hypotension
These patients are less likely to respond to fluids as they are generally already in a euvolemic state –> May need pressors or inotropic support for hypotension

102
Q

Drinking a carbohydrate drink 2 hours prior to surgery has been associated with what?

A

Maintaining adequate glucose and insulin levels in the preoperative period –> Decreasing post op thirst, hunger, and anxiety.

103
Q

What are some intra operative ERAS components?

A
104
Q

Liberal fluid administration can cause post operative complications, even a modest 3 kg weight gain can is associated with _____________

A

Delayed GI function recovery, increased rates of complications, and prolonged hospital stay

105
Q

The strategies of peri operative fluid management in PGDT for fluid management can decrease complications by ________

A

50%

106
Q

What should be encouraged in the post operative period early on according to ERAS?

A

Early discontinuation of IV fluids and encouraging oral intake of fluids –> Serval literals of IV crystalloids can cause postoperative ileus and delay hospital stay

107
Q

What is primary cellular injury in relation to surgical stimulation?

A

Direct surgical trauma from incisions, heating elements… –> Can impair oxygen and nutrient delivery to vital organs

108
Q

What is secondary cellular injury in relation to surgical stimulation?

A

Indirect physiologic response to the stress of surgery –> The body releases local inflammatory mediators such as cytokines.

109
Q

Primary and secondary cellular injury during surgical stimulation has been associated with _______________

A

delayed wound healing and gut dysfunction, as well as post surgical complications

110
Q

Two fundamental elements to effect post surgical outcomes

A

Effective fluid therapy and pain management

111
Q

What are the electrolytes in the ECV?

A

Na+ and Cl-

112
Q

What electrolyte in the ECV is mainly responsible for serum osmolarity and fluid shifts?

A

Na+ –> Also most abundant

113
Q

What pump maintains cation ionic neutrality between the ECV and ICV?

A

Na/K ATPase pump –> Pumps Na in the ECV and K in the ICV

114
Q

What is a normal Na level in the ECV? ICV?

A

EVC –> 140 (135-145)
ICV –> 25

115
Q

Where does ionic osmotic equilibration not occur in the body due to limited permeability?

A

Blood brain barrier –> Prevents ionic equilibrium between the ICV and ECV due to limited permeability

116
Q

What electrolyte over plasma proteins is most influential on water content of the brain tissue?

A

Na+

117
Q

What are some manifestations of hyponatremia?

A
118
Q

What do the treatments of sodium imbalances generally include?

A

Expansion or restriction of fluids and enhanced elimination or supplementation of sodium

119
Q

How can dilution hyponatremia occur during surgery?

A

When the surgeon uses a hypotonic solution for irrigation, the ECV can absorb this causing hyponatremia

120
Q

Hyponatremia correlation between ECV and ICV?

A

ECV is hypotonic to the hypertonic ICV –> Water moves into the ICV.
The most significant complication of this is cerebral edema

121
Q

What compensatory mechanisms can brain cells use to maintain osmotic equilibrium?

A

In states of a hypotonic ECV and hypertonic ICV –> Brain cells can compensate by extruding solutes in the ICV to the ECV
If the hypotonic ECV is too much though, brain cells won’t be able to compensate for this change leading to cerebral edema neuronal cell death

122
Q

What patient population is at an increased risk of brain damage resulting from hyponatremia? Why?

A

Menstruating women –> Estrogen and progesterone are thought to inhibit the efficacy of the Na/K ATPase pump, which is essential to try to compensate for sodium imbalances

123
Q

What is the most common electrolyte imbalance in hospitalized patients?

A

Hyponatremia

124
Q

What can rapid correction of hyponatremia place a patient at an increased risk for?

A

Osmotic demyelination –> seizures, spastic quadriparesis, and coma

125
Q

What electrolyte imbalance would you use the “vaptan” drug class?

A

Hyponatermia –> Vaptan’s are vasopressin receptor antagonists, which causes increased free water excretion
Inhibit endogenous vasopressin by blocking renal receptors V1a, V1RA, V2, and V3RA

126
Q

How do the “vaptan” (vasopressin receptor antagonists) drugs work?

A

Inhibit endogenous vasopressin by blocking renal receptors V1a, V1RA, V2, and V3RA

127
Q

If the ECV is hypertonic to the ICV, what will happen?

A

Cells will shrink

128
Q

What is myelinolysis?

A

Same as Osmotic demyelination syndrome –> disorders of the upper neurons, spastic quadriparesis, and even death due to rapid correction of serum sodium

129
Q

How can the risk of myelinolysis (osmotic demyelination syndrome) be decreased?

A

Serum Na shouldn’t be corrected more than 1 to 2 mEq per L per hour. Once the patient is stable, this should be slowed to not raise the serum Na more than 10 to 15 mmol per L in 24 hours
Use 3% saline in symptomatic patients following these guidelines

130
Q

What is generally the cause of hypernatremia?

A

Dehydration –> Inadequate fluid admin of free water to hospitalized patients can cause this

131
Q

What is the dangers of rapidly occurring hypernatremia?

A

Rapid shrinking of the brain and veins –> Intracranial hemmorhage

132
Q

What can occur from rapid treatment of hypernatremia?

A

Cerebral edema

133
Q

What happens to the brain in slowly developed hypernatremia?

A

Nothing –> In cases of slowly developed hypernatremia, the brain can adequately equilibrate maintaining fairly normal Na ICV values

134
Q

How do you treat acute hypernatremia? (Develops in less than 24 hours)

A

Relative rapid correction with hypotonic solution

135
Q

How do you treat chronic hypernatremia with volume depletion?

A

Volume correction FIRST with isotonic solution –> Once circulating volumes have been restored, SECOND is hypotonic fluid for correction of Na+ excess

136
Q

How should chronic hypernatremia due to volume depletion be corrected?

A

Hypernatremia correction protocol –> Serum Na shouldn’t be decreased more than 1 to 2 mEq per L per hour. Once the patient is stable, levels should gradually correct over the next 24 hours.

137
Q

What is the primary electrolyte within the ICV?

A

K+

138
Q

What electrolyte is responsible for the resting membrane potential of the cell?

A

K+

139
Q

How is K+ homeostasis maintained?

A

Absorption of K from the GI tract
Excretion or reabsorption via kidneys

140
Q

What does aldosterone do in regard to K+?

A

In states of hyperkalemia, the body releases aldosterone to promote K excretion from the distal tubules

141
Q

What can cause the plasma K+ (ECV) to be shifted into cells (ICV)?

A

Beta adrenergic stimulation, insulin, and alkalosis

142
Q

Thiazide diuretics effects of K+

A

Increases renal excretion of K+ –> Can lead to hypokalemia
Patients are 11x more likely to experience hypokalemia is using thiazide diuretics and men are 2x more likely to experience this than women

143
Q

What is the most common electrolyte abnormality encountered during clinical practice?

A

Hypokalemia

144
Q

What ECG changes would you expect in a patient experiencing hypokalemia?

A
145
Q

What are the five most common causes of hypokalemia?

A
146
Q

What are some patient manifestations that may occur with a serum K+ of less than 2.5 mEq per L?

A

Paresthesia, depressed deep tendon reflexes, fasciculations, muscle weakness, altered LOC

147
Q

What are common cardiac manifestations with hypokalemia?

A

First and second degree heart block, atrial and ventricular fibrillation, and asystole

148
Q

How should hypokalemia be corrected?

A

Give K+, patient needs to be under constant EKG monitoring –> Can give as much as 40 mEq per hour but 10-20 mEq per hour is recommended

149
Q

Why do chloride levels need to be replaced as well with patients who are hypokalemic?

A

Because if patients have low chloride levels with hypokalemia, the kidneys have a hard time retaining the supplemented K –> So chloride is generally given prophylactically with potassium

150
Q

Why should potassium chloride be mixed in a dextrose free mixture?

A

To prevent the stimulation of insulin which will shift the supplemented K into the ICV

151
Q

What are some causes of hyperkalemia?

A

Kidney injuries/failure, high K intake, shift of K in the ICV to the ECV –> This can lead to lactic acid production

152
Q

What common medications can increase serum K?

A

Digoxin, ACE inhibitors, ARBs, B blockers

153
Q

What are some causes of pseudohyperkalemia?

A

AND prolonged fist clenching during blood drawing

154
Q

What are the three physiologic events that must occur to correcting hyperkalemia?

A
  1. Stabilize cardiac membrane
  2. Driving K from ECV to ICV
  3. Removal of K from the body
155
Q

What is the standard treatment of hyperkalemia?

A

10 units of insulin IV with one ampule of D50 –> 5 units of insulin IV has been suggested to minimize hypoglycemia.

156
Q

What are some EKG changes associated with hyperkalemia?

A
157
Q

What is the importance of calcium in the body?

A

Role as a second messenger that couples cell membrane receptors to cellular responses –> Also important in coagulation, myocardial contraction, and muscle function

158
Q

What is the physiologically active calcium in the body?

A

Ionized calcium –> Accounts for 50% of the calcium in the ECV
Normal values = 4.6 - 5.2 mg per dL or 1.1 - 1.3 mmol per L
Remaining calcium is bound to anions (10%) or plasma proteins mainly being albumin (40%)

159
Q

What effect does acidosis or a decreased pH have on ionized calcium?

A

Causes it to increase while decreasing the protein bound calcium

160
Q

How are serum calcium levels primarily maintained?

A

release or inhibition of parathyroid hormone (PTH) and also vitamin D and calcitonin

161
Q

What is total serum calcium largely dependent on?

A

Albumin concentration

162
Q

What are the most likely causes of hypocalcemia?

A

Hyperventilation and massive blood transfusions

Hyperventilation leads to an increases pH –> This causes ionized calcium to decrease as protein bound calcium (inactive) increases

163
Q

What is the treatment of hypocalcemia?

A

Infusion of calcium salts –> CaCl (272 mg elemental calcium) is the most bioavailable parenteral preparation resulting in most rapid correction
Cons –> Can cause significant venous irritation and tissue necrosis compared to calcium gluconate (93 mg of elemental calcium)

164
Q

What can decrease the negative side effects associated with correcting hypocalcemia with CaCl?

A

Administer via central line

165
Q

How do you correct hypocalcemia with calcium gluconate?

A

10 mL of 10% calcium gluconate (93 mg of elemental calcium) over 10 minutes –> Followed by infusion of elemental calcium of 0.3 - 2 mg per kg per hour

166
Q

What should guide correction of hypocalcemia?

A

Ionized calcium –> Normal is 4.6 - 5.2 mg per dL

167
Q

What is the most common cause of hypercalcemia?

A

Primary hyperparathyroidism, followed by malignancy

168
Q

What occurs when the movement of calcium from the bone to the ECV exceeds the ability of the kidney to excrete the calcium?

A

Hypercalcemia

169
Q

What is the typical treatment of hypercalcemia?

A

Volume expansion with NS which aids in increased excretion of calcium
A loop diuretic can be added to enhance this more

Biphosphonates, calcitonin, glucocorticoids, and phosphate salts can also be used

170
Q

What is the treatment of rapidly developing hypercalcemia?

A

Hemodialysis –> Needs to be quickly treated as this can cause arrythmias

171
Q

What normally occurs in states of hypercalcemia with parathyroid hormone?

A

It decreases to decrease production

172
Q

What electrolyte ensures proper function of the Na/K ATPase pump?

A

Mg

173
Q

Two things IV magnesium can do

A

Relieve severe bronchospasm
Decrease pain

174
Q

Normal magnesium levels

A

1.5 - 3.0

175
Q

Hypomagnesemia has an inhibitory effect on the ________________. This can cause __________________

A

Na/K ATPase pump, decreased ICV potassium –> This can alter the resting membrane potential, specifically phase 4

176
Q

Excessive alcohol consumption can result in which electrolyte abnormality?

A

Hypomagnesemia –> 30% of alcoholics because of poor intake and increased excretion

177
Q

How is severe hypomagnesemia treated?

A

Treated with 1-2 g of mag sulfate over 5 minutes WITH EKG monitoring –> followed by admin of 1-2 g of mag sulfate per hour

178
Q

What are the usual causes of hypermagnesemia?

A

Iatrogenic causes –> Usually due to treatment of preeclampsia, preterm labor, ischemic heart disease, and cardiac dysrhythmias

179
Q

What symptoms are associated with hypermagnesemia?

A

Depression of the PNS/CNS, hypotension, QRS widening, PR and QT prolonged, heart blocks, and cardiac arrest

180
Q

What is magnesiums effect on non-depolarizing muscle relaxants?

A

POTENTIATES them! Patients with hypermagnesemia may need careful monitoring if they are used

181
Q

What is the treatment of hypermagnesemia?

A

Stopping administration of magnesium –> If acute and severe, CaCl should be used as an antagonist

182
Q

Where is the majority of phosphate stored?

A

In the bone –> 85%
Calcium in 99% in the bone

183
Q

Functions of phosphate in the body

A

Acid base buffer, intracellular component of ATP and 2,3 DPG

184
Q

Concentration of phosphate in the plasma in ____________ proportional to that of calcium

A

inversely –> Phosphate levels are regulated by the same things that regulate calcium levels –> PTH, vitamin D, and calcitonin

185
Q

Normal phosphate levels

A

3 - 4.5 mg per dL

186
Q

What level is considered hypophosphatemia

A

2.0 mg per dL or less

187
Q

Why does respiratory alkalosis contribute to hypophosphatemia?

A

Causes accelerated use of ATP by cells

188
Q

Does hypophosphatemia cause a left or right shift? What happens?

A

Left shift –> Because O2 has greater affinity for Hgb, less O2 will be delivered to the body. This causes anaerobic metabolism, decreased ATP production, and acidosis

189
Q

Decreased ATP production due to hypophosphatemia include what consequences?

A

Hypoxia, heart block, bradycardia, and asystole

190
Q

What levels are considered hyperphosphatemia?

A

4.7 mg per dL or greater

191
Q

What is the leading cause of hyperphophatemia?

A

Cellular destruction caused by metastatic disease

192
Q

Treatment for mild hyperphosphatemia

A

Aluminum hydroxide (antacids) –> Decrease serum phosphate by binding within the GI tract

193
Q

Treatment for severe hyperphosphatemia?

A

Dialysis

194
Q

A patient presents with hyperphosphatemia, what other electrolyte imbalance would you suspect?

A

Hypocalcemia

195
Q

What symptoms would be associated with a magnesium level of 4.8 mg per dL?

A

Decreased deep tendon reflexes

196
Q

A patient presents with facial and eye muscle twitching along with carpopedal spasms, what electrolyte imbalance do you suspect?

A

Hypocalcemia

671A - Anesthesia I (22 decks)

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