Flashcards in Vascular and Fluid Balance Deck (44):
How is water distributed?
Total body water is the sum of all the water contained in different body compartments- transport of metabolites and waste.
2/3 in the ICF and 1/3 in the ECF: made of ISF, intravascular fluid (plasma), transcellular fluid (CSF). TBW is 60-70% lean weight.
What is the function of electrolytes and what are their functions?
Stability of the cellular environment.
K, Mg, Ca- normal cell function
Na, Cl- maintenance of extracellular osmotic pressure
HCO3- control of extracellular pH
What are the 5 main ways that body fluids and electrolytes are regulated?
1) GFR 2) RAAS 3) ADH 4) ANP 5) Thirst
How is GFR maintained?
By maintaining ECV by varying vascular resistance, CO, renal Na and water excretion
What does a lowered ECV result in and what does it lead to?
decreased venous return, decreased CO and decreased BP which leads to decreased GFR so less Na is excreted= increased water reabsorption and increased ECV.
How are volume and pressure detected and what happens if there is a drop in either?
By receptors in the cardiopulmonary system and kidneys: increased sympathetic tone and increased vasoconstriction, increased cardiac contractility and HR= inc CO and BP.
Activation of the RAAS system= aldosterone = enhanced renal absorption.
What is the function of the RAAS systems and how does it work?
It maintains ECV. Renin is produced in juxtaglomerular cells in the afferent arteriole. It is released in response to decreased perfusion and it converts angiotensinogen to angiotensin I which converts to angiotensin II. Angiotensin II increases aldosterone production by the adrenal cortex which enhances Na reabsorption.
What is the role of ADH and when is it secreted?
It controls the permeability of distal tubules and collecting ducts. It can be released from the hypothalamus when the osmoreceptors are stimulated by increased osmolarity or when decreased blood volume= decreased blood pressure which is picked up by baroreceptors in the atrium of the heart.
What happens if ADH is present or absent?
1) water permeability will be high which allows water to follow Na into the bloodstream so that urine vol is low.
2) water permeability is low, preventing water from following Na into the bloodstream so that urine vol is high.
How can ADH release be stimulated by pressure?
Baroreceptors in the left atrium are stimulated by increased blood volume, impulses pass to the neurones in the hypothalamus where they inhibit ADH release so that urine vol is high and pressure will drop.
Low BP leads to decreased firing of baroreceptors and increased ADH secretion so urine volume is low and pressure will increase.
How does ANP release regulate water balance?
ANP is released on response to stretching of the heart, they reduce CO and blood pressure by promoting the loss of Na and water from the kidneys and through vasodilation.
What is the ultimate compensation for water loss?
Thirst which is driven by low ECV, high plasma osmolarity and the osmoreceptors and baroreceptors seen before.
How is ISF composition controlled?
It requires control of fluid movement across capillaries which depends on:
1) hydrostatic pressure at the arteriolar end of the vascular network
2) osmotic pressure exerted by plasma proteins relative to interstitial proteins at the venous end.
Give four examples of how abnormal plasma concentrations can occur.
1) decreased or increased intake
2) shifts to and from the ICF
3) increased renal retention
4) increased loss via usual routes
What are the two ways that hypernatraemia can occur and what does it do to the cell?
Water deficiency due to decreased intake (throat abscess) or uncontrolled loss (renal disease) or water loss > Na loss (osmotic diuresis/ diarrhoea
Sodium excess- excess dietary (salt poisoning) or decreased renal excretion of Na (hyperaldosteronism-rare)
Cell dehydrates and dies when water moves to the ECF because Na is high there.
What are the two ways that hyponatraemia can occur and what are its effects?
Sodium deficit- Alimentary loss (excess salivation), renal loss, prolonged diuresis (furusomide), sweating.
Loss of Na and Cl= depletion of ECF osmolarity and water loss= moves into cells= over hydration and rupture. Also= ECF vol drop=haemoconcentration and circulatory failure.
Water excess- oedema (CHF), too much fluid therapy= water into cells (ECF osmol red)=intracellular oedema=CNS convulsions
Give a cause of hyperkalaemia and hypokalaemia internally and externally?
1)Addition of K from the environment- high fluid therapy or internal add of K shift from ICF to ECF due to diabetes mellitus.
2)decrease in total body K=profuse sweating in horses or shift from ECF to ICF due to high insulin levels.
Give two causes of hypomagnesaemia and hypermagnesaemia?
1) decreased absorption (staggers) or excess urinary excretion
2) decreased renal excretion or Increased PTH (milk fever)
Give two causes of Hypocalcaemia and hypercalcaemia?
1) milk fever in cows/eclampsia in bitches (dec PTH so dec Ca released) or hypoproteinaemia
2) malignant neoplasia or renal failure in horses.
What is the definition of oedema and what does it indicate?
An increased accumulation of fluid. It is not a disease itself but it acts as an indicator of diseased state when the fluid balance has gone awry.
Where does extra fluid accumulate?
In the interstitial space mainly but it can accumulate in other body cavities.
What is dependant oedema?
The fluid tends to sink with gravity so that the ventral abdomen and limbs are mainly affected.
What is pitting oedema?
With severe subcutaneous oedema a finger pressed into the expanded interstitium will leave an indentation.
What is hydrothorax?
Accumulation of fluid in the pleural cavity
What is Hydropericardium?
accumulation of fluid in the pericardial sac
What is ascites?
Accumulation of fluid in the peritoneal cavity
What is anasarca?
severe, generalised oedema involving the cavities and subcutis.
What does Starling equilibrium state?
That at rest, hydrostatic pressure forces fluid out of the arteriolar end of the capillary network and into the tissue spaces. At the venous end, the hydrostatic pressure has decreased and the osmotic pressure of plasma proteins exceeds venous hydrostatic pressure do fluid is reabsorbed.
What are the three major factors that control reabsorption of fluid?
1) a functioning circulatory system, including an intact endothelial barrier.
2) A functioning lymphatic system
3) serum albumin levels
What are the four main mechanisms that underpin oedema?
1) increased blood hydrostatic pressure
2) increased vascular permeability
3) decreased plasma colloidal-osmotic pressure
4) lymphatic obstruction
What are the two types of oedema that can occur as a result of increased blood hydrostatic pressure?
(oncotic pressure> hydrostatic pressure)
Generalised oedema- cardiac failure=inc venous pressure. RS=systemic congestion= systemic oedema, LS=pulmonary congestion=pulmonary oedema.
Localised e.g. thrombus, vascular torsion
What type of pathology is associated with increased vascular permability?
Oedema of inflammation- opening of interendothelial gaps allows leakage of plasma proteins and inflammatory cells. This oedema has a higher protein content.
What is oncotic pressure?
The measure of the ability of osmotic solutes to draw water towards them. The most important group of proteins are the plasma proteins and in particular albumin.
How are oedema and oncotic pressure connected?
A decrease in plasma oncotic pressure will cause an oedema. This is usually due to a hypoalbuminaemia.
What are the two causes of hypoalbuminaemia?
1) inadequate albumin production e.g. starvation, chronic liver disease.
2) net loss of albumin from either then kidney (glomerulonephritis) or the GIT (haemoncus parasitism- whole blood lost)
These are examples of generalised oedema.
How can lymphatic obstruction cause an oedema?
The drainage mechanism is blocked by trauma, surgery, inflammation or neoplasia. It is a localised oedema because the underlying lesion is localised- torsion of the testes.
What are the two causes of pulmonary oedema?
Haemodynamic and Microvascular injury.
due to damage of:
alveolar BM, lymphatic drainage and fluid dynamics
How does haemodynamic pulmonary oedema occur?
Due to increased hydrostatic pressure, secondary to Left heart failure and backing up of blood into the pulmonary system.
Or pulm v obstruction, lymphatic obstruction and causes of lowered oncotic pressure.
How does microvascular injury occur?
Capillaries in the pulmonary vascular bed are damaged- endothelial cells are damaged and hydrostatic pressure is normal.
What is the pathogenesis of pulmonary oedema?
1) fluid exceeds capacity of lymphatic drainage
2) fluid accumulates in the interlobar septa, perivascular and peri-airway CT
3) alveolar walls fill with fluid
4) alveolar spaces fill with fluid
5) grossly the lungs become heavy and wet, exuding red-tinged fluid on cut section
What are the clinical consequences of oedema?
Outcome depends on extent, location and duration of oedema. In the brain and lungs it can be fatal. Cerebral oedema which results in cerebellar herniation= suppression of respiratory centres.
Pulmonary oedema impedes gas exchange potentially leading to hypoxia.
What is the difference between transudate and exudate?
1) due to inc hydrostatic pressure or decreased oncotic pressure
2) an acute inflammatory response and show the presence of cells
What are the characteristics of transudate?
Colour- pale, clear, straw
Consistency- thin and serous
protein- 0.5% albumin
Specific gravity- low
underlying cause- all but inflammation