Disturbances of fluid and electrolyte balance

1. DISTURBANCES OF FLUID AND
ELECTROLYTE IMBALANCE
NURSING 2nd YEAR

2. • Homeostasis- the mechanism by which constancy of
the internal environment is ensured.
• Cell wall and vascular endothelium play important
role in exchanges of fluid, electrolytes, nutrients and
metabolites.

3. NORMAL COMPOSITION OF BODY
• Water(50-70%); Intracellular and extracellular
• Electrolytes(Potassium, Sodium, Magnesium,
Phosphates)
• Function of electrolytes
• Maintenance of acid base balance
• Maintain proper osmolality and volume of body
fluids
• Determines specific physiologic functions.

4. PRESSURE GRADIENTS
• Osmotic Pressure/Oncotic pressure- Pressure exerted
by the chemical constituents of the body
fluids(electrolytes and proteins).
• Hydrostatic pressure- Pressure exerted by the blood
flowing through the capillaries.

5. • Therefore, under normal circumstances, the outflow
of fluid at the arteriolar end is balanced by the inflow
at the venular end and the minimal residual fluid in
the interstitial space is cleared by the lymphatic
channels.

6. At the arteriolar end of capillary, the hydrostatic pressure is slightly more than
the plasma oncotic pressure there is net outward movement of fluid at the
arteriolar end. At the venular end, the plasma oncotic pressure is higher than
hydrostatic pressure  inward movement of fluid and solutes

7. DISORDERS OF HEMODYNAMIC
SYSTEM

8. • Disturbances of body fluid and electrolytes- Edema
• Disturbances in the volume of circulating blood-
hyperemia, congestion, hemorrhage, shock.
• Disturbances of hemodynamic system of obstructive
nature- thrombosis, embolism, infarction.

9. EDEMA
• Abnormal and excessive fluid accumulation in the
interstitial space(between the cells).

10. Pathophysiologic Categories
of Edema

11. • Caused by mechanism that interfere with the normal
balance of the intravascular and extravascular fluid
transfer.
• The 2 main driving forces for transfer of fluid in and
out of the vessels are the intravascular hydrostatic
pressure and colloid osmotic pressure.
• Increased hydrostatic pressure
• Decreased Plasma osmotic pressure.

12. DECREASED PLASMA ONCOTIC
PRESSURE
• Plasma oncotic pressure exerted by the total amount
of plasma proteins tends to draw fluid into the
vessels normally.
• Fall in plasma protein level lowering of plasma
oncotic pressure cannot counteract the effect of
hydrostatic pressure of blood increased outward
fluid movement from capillary wall and decreased
inward fluid movement from interstitial space
EDEMA

13. INCREASED CAPILLARY HYDROSTATIC
PRESSURE
• The hydrostatic pressure of the capillary is the force
that normally tends to drive fluid through the
capillary wall into the interstitial space by
counteracting the force of plasma oncotic pressure.
• Increase in hydrostatic pressure minimal or no
reabsorption of fluid at the venular end EDEMA

14. • Sodium and water retention-  causes both
increased hydrostatic pressure and decreased plasma
osmotic pressure
• Lymphatic obstruction- Normally, the interstitial fluid
in tissue spaces escapes via lymphatics. Obstruction
to outflow of these channels EDEMA

15. INCREASED CAPILLARY PERMEABILITY
• Intact capillary endothelium is a semipermeable
membrane; permits free flow of water and
crystalloids and minimal passage of plasma proteins.
• Permeability increased leakage of plasma proteins
into interstitial fluid reduced plasma oncotic
pressure and increased oncotic pressure of
interstitial fluid EDEMA

16. HYPEREMIA AND CONGESTION
• Increased blood volumes within tissues.
• Hyperemia is an active process; arteriolar dilatation
leads to increased blood flow.
• Congestion is a passive process; reduced outflow of
blood from a tissue.

17. SHOCK
• Shock is a state in which diminished cardiac output
or reduced effective circulating blood volume impairs
tissue perfusion and leads to cellular hypoxia.

18. • Cardiogenic shock results from low cardiac output
due to myocardial pump failure.
• Hypovolemic shock results from low cardiac output
due to low blood volume, such as can occur with
massive hemorrhage or fluid loss from severe burns.
• Shock associated with systemic inflammation may be
triggered by a variety of insults, particularly microbial
infections, burns, trauma and pancreatitis

19. PATHOGENESIS OF SHOCK

20. STAGES OF SHOCK
• An initial nonprogressive phase during which reflex
compensatory mechanisms are activated and
perfusion of vital organs is maintained
• A progressive stage characterized by tissue
hypoperfusion and onset of worsening circulatory
and metabolic imbalances.
• An irreversible stage that sets in after the body has
incurred cellular and tissue injury so severe that even
if the hemodynamic defects are corrected, survival is
not possible

22. MORPHOLOGICAL CHANGES IN SHOCK
• The cellular and tissue changes are particularly evident
in brain, heart, lungs, kidneys, adrenals and
gastrointestinal tract.
• The kidneys typically exhibit acute tubular necrosis .
• In septic shock, the development of disseminated
intravascular coagulation leads to widespread
deposition of fibrin-rich microthrombi, particularly in
the brain, heart, lungs, kidney, adrenal glands, and
gastrointestinal tract.
• The consumption of platelets and coagulation factors
also often leads to the appearance of petechial
hemorrhages on serosal surface and the skin.

23. THROMBOSIS
• Process of formation of solid mass in circulation from
constituents of flowing blood.
• Causes- (Virchow’s Triad)
• 1. Endothelial Injury
• 2. Stasis or turbulent blood flow
• 3. Hypercoagulability of blood

24. VIRCHOW’S TRIAD

25. ENDOTHELIAL INJURY
• Intact endothelium is important for maintaining
normal blood flow.
• Endothelial injury leading to platelet activation
underlies thrombus formation in the heart and the
arterial circulation, where the high rates of blood
flow block clot formation.

26. ALTERATIONS IN BLOOD FLOW
• Normal blood flow is laminar such that the platelets
(and other blood cellular elements) flow centrally in
the vessel lumen, separated from endothelium by a
slower moving layer of plasma.
• Normal axial blood flow disturbed Stasis or
turbulence

27. • Turbulence contributes to arterial and cardiac
thrombosis by causing endothelial injury or
dysfunction, as well as by forming countercurrents
that contribute to local pockets of stasis.
• Stasis is a major contributor in the development of
venous thrombi.

28. Stasis and turbulence lead to…..
• Promote endothelial activation, enhancing
procoagulant activity and leukocyte adhesion, in part
through flow-induced changes in the expression of
adhesion molecules and pro-inflammatory factors
• Disrupt laminar flow and bring platelets into contact
with the endothelium
• Prevent washout and dilution of activated clotting
factors by fresh flowing blood and the inflow of
clotting factor inhibitors

29. A, Endothelial injury exposes
subendothelial matrix to
circulating blood. B, This triggers
three platelet steps involving
platelet
activation: adhesion, release and
aggregation. Platelet release is
associated with release of
granules (alpha granules and
dense bodies).
C, Concurrent activation of
coagulation cascade generates
fibrin strands
and thrombin forming a tight
meshwork called thrombus.

31. HYPERCOAGULABILITY OF BLOOD
• Increased risk to
develop venous
thrombosis.

32. MORPHOLOGY
Thrombus in an artery. The thrombus is adherent to the arterial
wall and is seen occluding most of the lumen. It shows lines of Zahn
composed of granular-looking platelets and fibrin meshwork with
entangled red cells and leucocytes.

33. FATE OF THROMBUS
• Resolution
• Organisation
• Propagation
• Thromboembolism

34. EMBOLISM
• An embolus is a detached intravascular solid, liquid,
or gaseous mass that is carried by the blood from its
point of origin to a distant site, where it often causes
tissue dysfunction or infarction.
Embolus from a lower extremity deep
venous thrombosis,
lodged at a pulmonary artery branchpoint.

35. TYPES OF EMBOLI

36. THROMBOEMBOLISM
• Detached thrombus or part of thrombus constitutes
the most common type of embolism.

37. • Pulmonary embolism
• Systemic embolism
• Fat embolism
• Air embolism
• Amniotic fluid embolism

38. INFARCTION
• An infarct is an area of ischemic necrosis caused by
occlusion of either the arterial supply or the venous
drainage

39. RED INFARCT
• Venous occlusions (testicular torsion)
• Loose, spongy tissues (lung) where blood can collect
in the infarcted zone
• Tissues with dual circulations (lung and small
intestine) that allow blood to flow from an
unobstructed parallel supply into a necrotic zone
• Tissues previously congested by sluggish venous
outflow

40. WHITE INFARCT
• solid organs with end-arterial circulation (e.g. heart,
spleen and kidney)
• where tissue density limits the seepage of blood
from adjoining capillary beds into the necrotic area

41. RED AND WHITE INFARCT

42. RENAL INFARCT

43. THANK YOU