This document discusses isotonic fluid imbalance, also known as hypovolemia. Hypovolemia occurs when water and electrolytes are lost in equal proportions, keeping sodium levels normal. It can result from extra-renal losses like vomiting, diarrhea, burns, or third spacing of fluids. It can also occur due to renal losses from conditions like renal disease or diuretic use. When fluid volume is depleted, the body activates compensatory mechanisms like increasing antidiuretic hormone and renin-angiotensin-aldosterone system to conserve water and sodium. This helps maintain blood pressure and cardiac output. Symptoms of hypovolemia include thirst, fatigue, dizziness, decreased skin turgidity,

1. Isotonic Fluid Imbalance
Hypovolemia:
Mehmood ul hassan
Assistant Head Nurse SICU

2. Objectives
 Describe the isotonic volume deficit
 Discuss the pathophysiology of isotonic volume deficit
 Enlist the clinical manifestation of isotonic volume deficit

3. Isotonic Fluid Volume Deficit
 It result when water and electrolytes are lost in an isotonic fashion
 Sodium level remain normal in this imbalance
 It may occur alone or in combination with other imbalances

4. causes
Extra-Renal Loss Renal loss

5. Extra-Renal Loss
Gastrointestinal (GI) Loss
Gastric:
 vomiting
Gastrointestinal suctioning
Intestinal:
Diarrhea
Ileostomies
Pancreatic or Biliary fistula
Drainage bags
Bleeding
Daily volumes of fluid ingested, secreted,
absorbed, and excreted from the GI tract
Figure 24.21, page 958

6. Skin losses
Diaphoresis (sweat can vary from 0 to
1000ml/hr )
Extensive burn (loss by evaporation)
Fever (increase sweating and respiration)
Third space
Ascites
Hypoalbuminemia
Intestinal obstruction
Decrease intake
NPO (nothing per oral)
Decrease GCS, comatose

7. Renal loss
Cause intrinsic to kidney injury
Renal disease
Salt wasting nephritis
Diuretic phase of acute renal failure
Cause extrinsic to kidney injury
Diuretic excess
Osmotic diuresis
Diabetic glycosuria
Enteral or parenteral hyper-alimentation
Mannitol therapy

8. Aldosterone deficiency
Addison disease
hypoaldosteronism

9. Hemodynamic Response to Fluid volume Deficit
 Volume depletion result in decrease Cardiac output (CO)
 Decrease cardiac output result in
Decrease blood pressure
 hypo-perfusion to vital organ
 Compensatory mechanism activate
To maintain cardiac output
To maintain adequate vital organs perfusion

10. Compensatory Mechanism
Neural compensation
Baroreceptor Reflexes
Chemoreceptor Reflexes
 Hormonal compensation
Renin–angiotensin–aldosterone
Epinephrine and norepinephrine
 Antidiuretic hormone (ADH)

11. Neural compensation
Baroreceptor Reflexes
Pressure sensed receptor present in carotid artery and aorta
They sensed fall in blood pressure
Send signal to vasomotor center in brain
Brain activate sympathetic response that cause
Peripheral vasoconstriction
Increased heart rate
Increase cardiac contractility
Increase cardiac output
Increase blood pressure and perfusion to vital organ

12. Regulation of blood pressure
via baroreceptor reflexes
Figure 21.14, pg, 778

13. Chemoreceptor Reflexes
 Chemoreceptors are located close to the baroreceptors
 They detect changes in blood level of O2 (Hypoxia), CO2 (hypercapnia), and
H (acidosis)
 Send impulses to the cardiovascular center
 In response, the cardiovascular center increases sympathetic stimulation
Vasoconstriction of arterioles and veins
 Increase blood pressure
 These chemoreceptors also provide input to the respiratory center in the brain
stem to adjust the rate of breathing

14. Hormonal compensation
 Lowered blood pressure stimulates the kidneys cells to secrete the enzyme renin
 Renin converts angiotensinogen, into angiotensin I
 angiotensin-converting enzyme (ACE) converts angiotensin I into the hormone
angiotensin II, which raises blood pressure in two ways
First, angiotensin II is a potent vasoconstrictor; it raises blood pressure by
increasing systemic vascular resistance
Second, it stimulates secretion of aldosterone, which increases reabsorption
of sodium ions (Na) and water by the kidney
The water reabsorption increases total blood volume, which increases blood
pressure
Renin–angiotensin–aldosterone (RAA) system.

15. Renin–angiotensin–aldosterone (RAA) system
F.g 18.16 pg, 667

16. Epinephrine and norepinephrine
 In response to sympathetic stimulation, the adrenal medulla releases
epinephrine and norepinephrine
 These hormones increase cardiac output by:
Increasing the rate
Increase force of heart contractions
Vasoconstriction of arterioles and veins in the skin and
abdominal organs

17. Antidiuretic hormone (ADH)
 ADH is produced by the hypothalamus and released from the
posterior pituitary in response to dehydration or decreased blood
volume.
 ADH causes vasoconstriction, which increases blood pressure. For
this reason ADH is also called vasopressin

18. Regulation of secretion and actions of
antidiuretic hormone (ADH)
Figure 18.9 pg, 657

19. Sign and Symptoms
 Lassitude, weakness and
fatigue
 Anorexia
 Thirst
 Orthostatic hypotension
 Tachycardia
 Dizziness, syncope
 Poor skin turgor
 Altered level of consciousness
 Cold extremities
 Increase capillary filling time (
more then 3-5 sec)
 Sticky oral mucosa
 Dry tongue
 Oliguria
 Rapid loss of body weight

20. References:
 Tortora, G. J., Derrickson, B., Kuwaki, T., Kurosawa, M., & Takahashi, K. (2010). Tōtora jintai
no kōzō to kinō. Tōkyō: Maruzen.
 Porth, C., & Hannon, R. A. (2010). Porth pathophysiology: Concepts of altered health states.
Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.
 Scales, K. (2005). Vascular access: A guide to peripheral venous cannulation. Nursing
Standard, 19(49), 48-52.