Hypovolemia

Isotonic fluid imbalance

1. Isotonic Fluid I mbalance Hypovolemia: Mehmood ul hassan Assistant Head N urse SICU

2. O bjectives 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) S end 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: I ncreasing the rate I ncrease force of heart contractions V asoconstriction 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 kōzo ̄ to kino ̄ . Tōkyo ̄: 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.