Ch 5 Fluids Flashcards

1
Q

what are % total body water Int’s and extracellular compartnebts?

A

Water constitutes approximately 60% of body weight

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2
Q

Na+-K+/ATPase;

Which direction Intra/extracell,
Which high, low intracellular?

A

Na+ OUT
K+ IN
to the cell, consuming adenosine triphosphate (ATP)

Na+ concentration is very high in the extracellular fluid and very low in the intracellular fluid, and K+ is very high in the intracellular fluid and very low in the extracellular fluid

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3
Q

Movement of fluid from the intravascular to extravascular (interstitial and intracellular) space occurs at the level of the capillary.

A

endothelial barrier is a layer of glycoproteins and proteoglycans produced by the endothelium called the glycocalyx.

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4
Q

reabsorption of fluid requires what intravascular pressure?

A

increased intravascular oncotic pressure or decreased intravascular hydrostatic pressure

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5
Q

fluid filtration

A

decreased intravascular oncotic pressure or increased intravascular hydrostatic pressure

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6
Q

What is Oncotic pressure ?

Hydrostatic pressure?

A

osmotic pressure
(globulins, fibrinogen, and albumin)

intravascular blood pressures and vascular resistance.

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7
Q

increased fluid losses (hypotonic, isotonic, and/or hypertonic) and decreased intake may lead to dehydration

losses can also result in decreased effective circulating volume

A

losses can also result in decreased effective circulating volume

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8
Q

5-12% dehydration signs

A
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9
Q

how calculate fluid required

A
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10
Q

Treatment of shock

Important to deliver what to tissue?
Normalises what to ensure tissue perfusion? (5)

requires restoration of organ perfusion

A

Oxygen delivery to tissue DO2

Normalization:
- intravascular volume
- preload
- MAP
- cardiac output
- oxygen content
are crucial in supporting tissue perfusion

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11
Q

decrease in production of ATP. This energy deficit compromises the function of the Na+-K+/ATPase membrane pumps and causes

A

disruption of the cell membrane

exposure of subendothelial > activation of the platelets, clotting cascade

bacterial translocation in the intestinal tract.

SIRS, sepsis, and multiple organ dysfunction commonly result.

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12
Q

Perioperative Fluid Therapy

anesthetic drugs commonly have negative effects on the heart, blood pressure, and baroreceptor response

A

Tissue ischemia can interfere with wound healing and normal tissue defenses

dogs 5 mL/kg/h of crystalloids and cats started at 3 mL/kg/h

Close monitoring of the animal’s vital signs, blood pressure, and pulse oximetry reading

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13
Q

(goal-directed) approach for resuscitation
Aim to achieve (5)?

A

aimed to achieve:
- central venous pressure >8 to 12 mm Hg
- mean arterial pressure >65 mm Hg
- urine output >0.5 mL/kg/h
- arterial oxygen saturation [SaO2] >93%
- hematocrit >30%) within 6 hours.

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14
Q

Fluid/product types and uses (5) for shock

A

Isotonic crystalloids
(replacement fluids) are electrolyte-containing fluids with a composition similar to that of extracellular fluid

“Maintenance” crystalloid
hypotonic and contain less sodium

hypertonic crystalloids,

synthetic colloids

blood products

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15
Q

isotonic crystalloid

A

used to expand the intravascular and interstitial spaces and to maintain hydration

extracellular-expanding fluids,” and 75% of the volume redistributed to interstitial space

NaCl, LRS, Plasmalyte

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16
Q

Excessive fluid administration

A

lead to
interstitial edema, pulmonary edema, and cerebral edema, all of which will decrease oxygen delivery and organ function.

increased risk:
low colloid osmotic pressure, pulmonary contusions, cerebral trauma, renal disease, or cardiac disease, substantial hemodilution of red blood cells, plasma proteins, clotting factors, and platelets can occur.

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17
Q

Surgical patients with head trauma
- Periop patients with severe hypoNa or hyperNa
- Surgical patients with hypoCl metabolic alkalosis
- Surgical patints with severe metabolic acidosis, not due to lactate

A

Head trauma –> 0.9%NaCl. Has the highest Na conc and therefore is least likely to cause a drop in osmolality and cerebral oedema
Hypo/hyperNa –> Choose the fluid which most closely matches their Na. Too rapid a drop can cause cerebral oedema. To rapid an increase can cause central pontine myelinolysis
HypoCl met alkalosis –> 0.9%NaCl as it is the highest in Cl and will help normalise the pH
Metabolic acidosis –> Crystallois with a buffer (lactate, acetate, gluconate). NOT NaCl

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18
Q

hypotonic fluids

maintenance fluids

A

0.45% NaCl
0.45%NaCl with 2.5% dextrose
Plastalyte 56
Plasmalyte M with 5% dextrose
Normosol M with 5% dextrose
5% Dextrose in water (D5W)
Dextrose is rapidly metabolised to H2O and CO2 (good source of free water)

Maintenance fluids low in sodium, chloride, and osmolarity

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19
Q

hypotonic fluids

maintenance fluids

A

Contraindicated as bolus therapy in animals with hypovolemia

Large volumes can lead to a rapid decrease in osmolarity and subsequent cerebral edema

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20
Q

Hypertonic (7.0% to 7.5%) sodium chlorid

A

transient osmotic shift of water from the extravascular to the intravascular

4 to 6 mL/kg over 10 to 20 minute,
transient (<30 minutes),.

Rates exceeding 1 mL/kg/min leads to vagally mediated hypotension, bradycardia, and bronchoconstriction and should be avoided

treatment of head trauma or cardiovascular shock in animals >30 kg

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21
Q

Synthetic colloid solutions

0.5 to 2 mL/kg/day.

total dose of <20 mL/kg/day is advised to avoid side effects.

treatment of ? (2)

A

carge molecules (molecular weight >20,000 daltons

increase the colloid osmotic pressure of the plasma > pull fluid into the intravascular space.

colloid particles help to retain this fluid in the intravascular space in the animal with normal capillary permeability

Treats: shock and hypoproteinemia

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22
Q

What are potential side effects of colloids? (4)

Hydroxyethyl starches

A

Disruption of normal coagulation
(depletion of VIII and vWB),
impaired platelet function,
interference of stability of fibrin clots

Anaphylaxis

Volume Overload

Renal impariment

difficult to predict which animals will develop clinical bleeding

23
Q

low colloid osmotic pressure

negatively affect wound healing

predispose to bacterial translocation from GIT into the bloodstream.

A

low oncotic pressure

lead to interstitial edema

decreased tissue perfusion

increased distance for the diffusion of oxygen and nutrients.

24
Q

Hemoglobin-Based Oxygen-Carrying Fluids

Oxyglobin

A

sterile, ultrapurified, stroma-free, polymerized bovine hemoglobin solution.
nonantigenic (typing or cross-matching not required)

an cause marked vasoconstriction through its nitric oxide–scavenging effect

25
Q

Q
How much blood loss requires a transfusion?

A

Can usually tolerate 10-15% blood loss but 20% often requires transfusion

hematocrit target may be increased to >30% to maximize oxygen-carrying capacity.

elective sx > donate blood in advance to have autologous blood available

26
Q

blood loss requiring transfusion

A

fresh whole blood or packed red blood cells and fresh frozen plasma should be used to stabilize clinical signs of shock

27
Q

Whole blood

A

All of the components present in blood.

clotting factors and platelets, but platelets are best administered within 8 hours

28
Q

Packed red blood cells

A

typically have a hematocrit of approximately 80%.

When stored at 4°C, the standard shelf life is 20 days,

no clotting factors or platelets

ready availability, low risk for volume overload, and reduced exposure to plasma antigens

29
Q

Plasma

Animals with vWD

A

clotting factors but also proteins, albumin, and globulins

Fresh frozen plasma is defined as plasma that is frozen within 6 hours

profound blood loss, a coagulopathy, or severe hypoalbuminemia. The ability of plasma products to increase colloid osmotic pressure is limited

dministered through a filter over at least 1 to 2 hours to monitor for a transfusion reaction and avoid volume overload,

thrombocytopenia or thrombocytopathia may require platelet-rich transfusion products

30
Q

blood types

A

blood donors should be dog erythrocyte antigen 1 and 7 negative if possible. In vitro cross-matching is also recommended if time allows.

feline are known: A and B.
ype B cats do often have strong naturally occurring anti-A antibodies.

Administration through a microfilter with 170-µm pores is commonly used to remove clots and larger red cell and platelet aggregate

31
Q

reaction (both immune-mediated and non–immune-mediated reactions),

patients should be monitored closely

A

Transfusion-associated circulatory overload (TACO)

nonhemolytic febrile reactions (1C within 30-60min)

Transfusion-related acute lung injury (TRALI)

igns of a transfusion reaction include fever, restlessness, vomiting or diarrhea, acute collapse, wheezing, dyspnea, urticaria, hemoglobinemia or hemoglobinuria, and/or hypotension.

32
Q

autotransfusion of whole blood

ministered through a blood filter to the patient.

A

recent (<24 hours), large-volume hemorrhage into the pleural or peritoneal cavity,

not a dependable source of clotting factors because depletion of fibrin

possible inflammatory response syndromes

Hemorrhage due to neoplastic or septic processes should not be autotransfused to prevent systemic circulation of these pathologic cells and organisms.

33
Q

Administration of 25% human albumin

A
34
Q

Sodium

primary extracellular cation

A

Na-K ATP pump

regulated by free water balance. Vasopressin (antidiuretic hormone) release and thirst are the primary mechanisms responsible for free water balance

Renal sodium retention or excretion regulates extracellular fluid volume > releasing renin, which ultimately results in increased serum aldosterone levels (via RAAS)

aldosterone > reabsorption of Na and H2O

35
Q

Causes of Hyponatremia

CS: depression, ataxia, coma, seizures secondary to cerebral edema

less than 140 mEq/L

A
  • Hypervolemia
    heart failure
    liver disease
    kidney failure / nephrotic syndrome
  • Normovolemia
    Psychogenic polydipsia
    Antidiuretic drugs
  • Hypovolemia
    Gastrointestinal loss (V+/D+)

Third-spacing loss
Peritonitis
Uroabdomen

Burns

Hypoadrenocorticism

Tx: slowly, no more quickly than 0.5 mEq/L/h

36
Q

Hypernatremia

CS: due to rapid increase, CNS signs

greater than 150 mEq/L

A

Hypovolemic
* Gastrointestinal loss (V+/D+, obstructions)
* Third-spacing loss (Peritonitis)
Burns
Renal failure
Diabetes mellitus

Postobstructive diuresis

Normovolemic Hypernatremia
* Diabetes insipidus
* Inadequate water intake

Hypervolemia
* Excessive salt ingestion
* Hypertonic fluid administration
* Hyperadrenocorticism
* Hyperaldosteronism

slowly to prevent cerebral edema, Tx isotonic crystallaoid 0.5meq/l/h

37
Q

Potassium

major intracellular cation

A

critical to cell resting membrane potential and neuromuscular transmission, particularly in excitable muscle and cardiac cells.

potassium moves down the concentration gradient across the cell membrane

negative charge inside the cell relative to the outside = resting membrane potential −90 mV.

balance > function of intake through the GIT, excretion via the kidneys (aldosterone)

outside > inside: glucose, insulin, catecholamines, metabolic alkaloses

38
Q

Hypokalaemia

CS: muscle weakness, cardiac arrhythmias, cervical flexion and pelvic limb weakness

less than 5.0 mEq/L

A

Decreased Intake
diet
fluids

Increased Loss
Chronic renal failure
Postobstructive diuresis
Loop diuretics

  • Mineralocorticoid excess
    Hyperadrenocorticism
    Hyperaldosteronism
  • GIT loss
    V+ gastric contents
    Diarrhea

Translocation Into Intracellular
* Alkalemia
* Insulin
* Glucose

Tx: correct underlying disorder and supplementation K+, 0.5mEq/kg/hr

39
Q

Hyperkalaemia

CS: dysrythmia dt resting membrane potential chnage of cardiac myocytes

bradycardia, wide QRS, peaked T- wave

TX: potassium-deficient fluids.

Calcium gluconate (10%) 0.5 to 1 mL/kg over 10 to 20 minutes (TO ALTER CARDIAC MYOCYTE POTENITAL)

dextrose 0.5 to 1 g/kg with or without insulin 0.5 to 1 IU/kg (IV or IM) (DRIVE INTRACELLULAR)

peritoneal dialysis

greater than 5 mEq/L

A

Decreased Urinary Excretion
* Urethral or bilateral ureteral obstruction
* Uroabdomen
* renal failure
* Hypoadrenocorticism

  • Chylothorax with repeated thoracocentesis
  • Drugs
    Potassium-sparing diuretics
    Heparin
  • Translocation
    metabolic acidosis
    Tissue trauma
  • Insulin deficiency

Increased Intake
* Iatrogenic

Pseudohyperkalemia
* Thrombocytosis
* Marked elevations WBC

Tx: underlying cause + Ca + glucose/insluin

40
Q

Calcium

A

roles in neural excitability, muscle contraction, and blood coagulation.

99% bone, 1+ intra.extracell

ionized (active form), protein bound, and chelated.

Three hormones: parathyroid hormone, vitamin D (cholecalciferol), and calcitonin.

act at the kidney, intestine, and bone to regulate calcium balance.

Calcitonin inhibit bone resorption

41
Q

Hypocalcaemia

CS: tremors, restlessness, facial rubbing, seizures, ataxia, inappetence, vomiting,

ionised lower than 5.0 mg/dL (1.2 mmol/L)

A

Decreased PTH
1 or 2nd hypoparathyroidism
Post thyroidectomy
Post parathyroidectomy

renal failure
* Nutritional 2nd hyperparathyroidism
* Malabsorptive syndromes

  • Urinary tract obstruction
  • Ethylene glycol toxicosis
  • Peritonitis/sepsis

Hypoalbuminemia (Will Decrease Total Calcium but Not Ionized Calcium)

Tx: 10% calcium gluconate (0.5-1.5 mL/kg IV), monitor 4 bradycardia

42
Q

Hypercalcaemia

CS:
CNS (depression,lethargy, seizures)
weakness, decreased tendon reflexes
PUPD, vomiting, and anorexia
cardiac (short QT, prolonged PR, wide QRS)

ionized calcium 1.5 mmol/L dogs and 1.4 mmol/L cats.

A

HARDIONS

Hyperparathyroidism
Addisons
Renal Failure
Hypervitaminosis D
iatrogenic
Osteolytic
Neoplasia (Lymphosarcoma, OSA, AGASACA, mammary)
Spurious

Tx: cause, IVFT,frusemide, CCS, calcitonin, diet

43
Q

Glucose

A

principal substrate for energy in the brain

beta cells (pancreas) secrete insulin, movement of glucose into the cell

stored as glycogen or fat.

liver converts glycogen into glucose via glycogenolysis
forms glucose from lactate and amino acids via gluconeogenesis

Glucagon (alpha pancreatic cells) stimulates glycogenolysis and the release of glucose

44
Q

Hypoglycemia

Whipple’s triad (low blood glucose with concurrent clinical signs > resolution when level is normalized)

CS: mental depression, syncope, ataxia, blindness, seizures, or coma

less than 3.3 mmol/l

A
  • Insulin overdose
  • Insulinoma
  • Paraneoplastic syndrome
    (hepatocellular carcinoma, Pulmonary, mammary, Lymphoma)
  • Toxins and medications

Excess Glucose Utilization
(Infection, pregnancy, polycythaemia)

  • Neonatal
  • Hepatic dysfunction (PSS)
  • Hypocortisolism

Tx: dextrose (0.5 g/kg) bolus, CRI 2.5% to 5% dextrose

insulin-like peptides, increased glucose utilization by the neoplasm

45
Q

hyperglycaemia

> 10 mmol/l

A

Postprandial

  • Diabetes mellitus
  • Pancreatitis
  • Glucocorticoids
    Stress
    Hyperadrenocorticism
    Exogenous steroids
  • Catecholamines
    Pheochromocytoma
  • Growth hormone–secreting neoplasms
  • Glucose- or dextrose-containing fluids

Tx: short-acting insulin 0.1 - 0.25 unit/kg IM or CRI 1.1- 2.2 units/kg

46
Q

Acid-BAse

A

buffers play an important role in acid-base homeostasis in the body

bicarbonate, proteins, and phosphate

regulation of PaCO2 through alveolar ventilation in the lungs and maintenance of normal [HCO3−] in the extracellular fluid by the kidneys

chemoreceptors that sense changes in blood pH

95% of filtered HCO3− is reabsorbed in the proximal tubule

47
Q

base excess

+

ANion gap

−4 to +4 mEq/L

A

assess the metabolic component of acid-base disturbances.

negative = nonrespiratory acidosis, and positive = nonrespiratory alkalosis.

Electrolyte derangements are often the first sign of an acid-base disorder
electroneutrality. increased anion gap acidoses include ketoacidosis, lactic acidosis, ethylene glycol toxicosis, salicylate toxicosis, and uremic states.

in dogs 11 to 26 mEq/L, and in cats 13 to 27 mEq/L.

48
Q

metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis

A

Primary disorders are accompanied by secondary adaptive compensation by the opposing system of acid-base regulation.

49
Q

Respiratory Acidosis

hypoventilation causes hypercapnia

increase blood PaCO2 + decreased pH

A

Hypoventilation due to neuromuscular or structural/airway conditions

  Central respiratory depression
  Drugs (eg, opioids)
  Brain disease
  Cervical spinal cord injury
  Neuromuscular disease
  Respiratory muscle fatigue
  Airway obstruction

Anesthetized patient
  Increased inspired CO2
  Increased apparatus dead space
  Malignant hyperthermia

Tx: correct underlying and improve ventilation

50
Q

Respiratory Alkalosis

when hyperventilation results in hypocapnia

low PaCO2 with an elevated pH

A

brain disease
Drugs
Sepsis

Pulmonary disease

  Pain, anxiety, stress

Low CO > Hypovolemic shock

no specific therapy

51
Q

Metabolic Acidosis

loss of HCO3− via the kidney or gastrointestinal tract or increase in nonvolatile acids

low [HCO3−] with a low pH

A

Bicarbonate loss (hyperchloremic)
  Renal tubular acidosis
  Intestinal loss
  Saline administration

Acid gain (Increased anion gap)
D—Diabetic ketoacidosis
U—Uremia
E—Ethylene glycol toxicity
L—Lactic acidosis

Tx: underlying, Sodium bicarbonate

52
Q

bicarbonate therapy,
adverse effects

A

hypernatremia, hypervolemia, ionized hypocalcemia, hypokalemia, and
respiratory acidosis

53
Q

Metabolic Alkalosis

gain of bicarbonate or the loss of acid

increased [HCO3] and increased pH

A

Bicarbonate gain
sodium bicarbonate admin
Acetate, citrate

Acid loss
 Vomiting with proximal GIT obstruction
  Nasogastric tube suctioning
  Renal acid loss

tx: underlying, fluid and electrolyte (hypokalemia and hypochloremia)