Ch 5 Fluids Flashcards
what are % total body water Int’s and extracellular compartnebts?
Water constitutes approximately 60% of body weight
Na+-K+/ATPase;
Which direction Intra/extracell,
Which high, low intracellular?
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
Movement of fluid from the intravascular to extravascular (interstitial and intracellular) space occurs at the level of the capillary.
endothelial barrier is a layer of glycoproteins and proteoglycans produced by the endothelium called the glycocalyx.
reabsorption of fluid requires what intravascular pressure?
increased intravascular oncotic pressure or decreased intravascular hydrostatic pressure
fluid filtration
decreased intravascular oncotic pressure or increased intravascular hydrostatic pressure
What is Oncotic pressure ?
Hydrostatic pressure?
osmotic pressure
(globulins, fibrinogen, and albumin)
intravascular blood pressures and vascular resistance.
increased fluid losses (hypotonic, isotonic, and/or hypertonic) and decreased intake may lead to dehydration
losses can also result in decreased effective circulating volume
losses can also result in decreased effective circulating volume
5-12% dehydration signs
how calculate fluid required
Treatment of shock
Important to deliver what to tissue?
Normalises what to ensure tissue perfusion? (5)
requires restoration of organ perfusion
Oxygen delivery to tissue DO2
Normalization:
- intravascular volume
- preload
- MAP
- cardiac output
- oxygen content
are crucial in supporting tissue perfusion
decrease in production of ATP. This energy deficit compromises the function of the Na+-K+/ATPase membrane pumps and causes
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.
Perioperative Fluid Therapy
anesthetic drugs commonly have negative effects on the heart, blood pressure, and baroreceptor response
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
(goal-directed) approach for resuscitation
Aim to achieve (5)?
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.
Fluid/product types and uses (5) for shock
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
isotonic crystalloid
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
Excessive fluid administration
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.
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
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
hypotonic fluids
maintenance fluids
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
hypotonic fluids
maintenance fluids
Contraindicated as bolus therapy in animals with hypovolemia
Large volumes can lead to a rapid decrease in osmolarity and subsequent cerebral edema
Hypertonic (7.0% to 7.5%) sodium chlorid
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
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)
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
What are potential side effects of colloids? (4)
Hydroxyethyl starches
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
low colloid osmotic pressure
negatively affect wound healing
predispose to bacterial translocation from GIT into the bloodstream.
low oncotic pressure
lead to interstitial edema
decreased tissue perfusion
increased distance for the diffusion of oxygen and nutrients.
Hemoglobin-Based Oxygen-Carrying Fluids
Oxyglobin
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
Q
How much blood loss requires a transfusion?
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
blood loss requiring transfusion
fresh whole blood or packed red blood cells and fresh frozen plasma should be used to stabilize clinical signs of shock
Whole blood
All of the components present in blood.
clotting factors and platelets, but platelets are best administered within 8 hours
Packed red blood cells
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
Plasma
Animals with vWD
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
blood types
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
reaction (both immune-mediated and non–immune-mediated reactions),
patients should be monitored closely
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.
autotransfusion of whole blood
ministered through a blood filter to the patient.
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.
Administration of 25% human albumin
Sodium
primary extracellular cation
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
Causes of Hyponatremia
CS: depression, ataxia, coma, seizures secondary to cerebral edema
less than 140 mEq/L
- 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
Hypernatremia
CS: due to rapid increase, CNS signs
greater than 150 mEq/L
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
Potassium
major intracellular cation
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
Hypokalaemia
CS: muscle weakness, cardiac arrhythmias, cervical flexion and pelvic limb weakness
less than 5.0 mEq/L
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
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
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
Calcium
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
Hypocalcaemia
CS: tremors, restlessness, facial rubbing, seizures, ataxia, inappetence, vomiting,
ionised lower than 5.0 mg/dL (1.2 mmol/L)
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
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.
HARDIONS
Hyperparathyroidism
Addisons
Renal Failure
Hypervitaminosis D
iatrogenic
Osteolytic
Neoplasia (Lymphosarcoma, OSA, AGASACA, mammary)
Spurious
Tx: cause, IVFT,frusemide, CCS, calcitonin, diet
Glucose
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
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
- 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
hyperglycaemia
> 10 mmol/l
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
Acid-BAse
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
base excess
+
ANion gap
−4 to +4 mEq/L
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.
metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis
Primary disorders are accompanied by secondary adaptive compensation by the opposing system of acid-base regulation.
Respiratory Acidosis
hypoventilation causes hypercapnia
increase blood PaCO2 + decreased pH
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
Respiratory Alkalosis
when hyperventilation results in hypocapnia
low PaCO2 with an elevated pH
brain disease
Drugs
Sepsis
Pulmonary disease
Pain, anxiety, stress
Low CO > Hypovolemic shock
no specific therapy
Metabolic Acidosis
loss of HCO3− via the kidney or gastrointestinal tract or increase in nonvolatile acids
low [HCO3−] with a low pH
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
bicarbonate therapy,
adverse effects
hypernatremia, hypervolemia, ionized hypocalcemia, hypokalemia, and
respiratory acidosis
Metabolic Alkalosis
gain of bicarbonate or the loss of acid
increased [HCO3] and increased pH
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)
