1. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 19 Heart Failure and Circulatory Shock

2. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Types of Heart Failure High-output versus low-output failure –Is cardiac output high or low? Systolic or diastolic failure –Is the heart failing to pump out enough blood, or failing to accept enough blood from the body and lungs? Right-sided or left-sided failure –Is the right or left side of the heart failing?

3. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Manifestations of Heart Failure Effects of impaired pumping Effects of decreased renal blood flow  RAA pathway Effects of the sympathetic nervous system

4. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario Mr. M has heart failure and he complains of severe shortness of breath, and has fluid in his lungs. He has tachycardia; increased diastolic blood pressure; pale, moist skin; and says he feels weak, dizzy, and anxious all the time. Questions: Which of these signs and symptoms are due to decreased renal blood flow? Which are due to the sympathetic nervous system? Which side of his heart do you think is failing?

5. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Left-sided Heart Failure Systolic: LV does not pump enough blood to body Diastolic: LV does not accept enough blood from lungs Body lacks blood Lungs fill with fluid right heart lungs left heart body

6. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Right-sided Heart Failure Systolic: RV does not pump enough blood to lungs Diastolic: RV does not accept enough blood from body Body fills with blood Lungs do not oxygenate enough blood right heart lungs left heart body

7. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins

8. Pulmonary Edema Capillary fluid moves into alveoli –Lung becomes stiffer –Harder to inhale –Less gas exchange in alveoli –Crackles –Frothy pink sputum Hemoglobin not completely oxygenated

9. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Tell whether the following statement is true or false. The characteristic pink sputum produced in pulmonary edema is tinged with blood.

10. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer True Rationale: In pulmonary edema, the alveolar capillary membrane is damaged, and blood from the capillaries moves into the alveoli. The blood from the capillaries causes the sputum (produced from the lower respiratory tract) to appear pink or light red.

11. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Cardiogenic Shock Heart fails to pump blood adequately –Decreased cardiac output lowers BP –Sympathetic system responds –Vasoconstriction increases resistance to blood flow –Increased workload on heart worsens heart failure

12. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Types of Shock Cardiogenic Hypovolemic Obstructive Distributive Septic

13. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Blood Pressure BP = CO x PR Which of the following affect CO, and which affect PR? Why? –Blood volume –Heart rate –Vasoconstriction –Angiotensin II –Aldosterone –Epinephrine –Histamine

14. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario Mr. M was injured in a motorcycle accident. On his arrival at the hospital he presented with bleeding from the right leg, restlessness, pallor, sweating, elevated heart rate, weak pulse, rapid breathing, and lack of bowel sounds; his blood pressure was slightly elevated. Question: What has happened to this patient’s: –Stroke volume –Cardiac output –Sympathetic nervous system

15. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario (cont.) Although he was given 6 units of blood, Mr. M got worse. He became lethargic and his blood pressure began to fall; he still had no bowel sounds or urine production. Questions: The intern ordered epinephrine, and Mr. M’s blood pressure increased. Why? Later, you overhear the resident telling the intern that was not the best treatment. Why not, if it raised Mr. M’s blood pressure?

16. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario (cont.) Mr. M’s blood pressure went up a bit. He has been moved out of the ICU. Question: His chart says you should do a 24-hour urine collection. Why?

17. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario (cont.) Mr. M appears to be improving. He sleeps quite a lot, but his blood pressure has remained stable; he had a little urine production; and he did not eat his supper. Checking on him in the evening, you notice that he is slightly flushed, his respiration rate is a little high, and his temperature is elevated. Questions: What is happening to his peripheral resistance? What do you expect his heart rate to be like? Why?

18. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Distributive or Vasodilatory Shock Blood vessels dilate There is not enough blood to fill the circulatory system Blood flow decreases Less blood is returned to the heart Less blood is circulated to the body

19. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which type of shock is caused by low blood volume? a.Cardiogenic b.Hypovolemic c.Distributive d.Septic

20. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer b.Hypovolemic Rationale: Hypo (low) volemia (blood volume) occurs when a patient has lost blood due to trauma, surgery, or third-space fluid loss.

21. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Causes of Distributive Shock Decreased sympathetic activity: neurogenic –Brain or spine injury; anesthetics; insulin shock; emotion Vasodilator substances in blood –Type I hypersensitivity (anaphylactic shock) –Inflammatory response to infection (sepsis) Vessel damage from severe hypovolemia

22. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Mechanism of Type I Hypersensitivity Mast cell Mast cell degranulates Sensitized mast cell IgE attaches to mast cell Allergen attaches to IgE

23. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Anaphylaxis Systemic response to the inflammatory mediators released in type I hypersensitivity –Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation ºWhat will happen when arterioles vasodilate throughout the body? –Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction ºWhat will happen when the bronchioles constrict?

24. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Sepsis or Systemic Inflammatory Response Syndrome (SIRS) Inflammatory mediators released into the circulation –Tumor necrosis factor –Interleukins –Prostaglandins Cause systemic signs of inflammation –Fever and increased respiration; respiratory alkalosis; vasodilation; warm, flushed skin Activate inflammatory pathways –Coagulation, complement

25. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Discussion: Why is septic shock called distributive? In the later phases of septic shock, blood volume decreases. What part of the inflammatory process explains this? Sepsis or Systemic Inflammatory Response Syndrome (SIRS) (cont.)

26. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Gut Barrier Failure decreased perfusion of the gut bacteria and toxins escape inflammatory response bacterial endotoxins in blood and lymph inflammatory mediators in blood and lymph vasodilation

27. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Septic Shock vasodilation decreased peripheral resistance decreased blood pressure SEPTIC SHOCK 40% mortality Also called systemic inflammatory response syndrome (SIRS) Inflammatory mediators also increase the metabolic rate of tissues, so they need more oxygen

28. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins “Despite the prompt implementation of appropriate antibiotic therapy, sepsis mortality remains high, in the range of 28% to 50%.” (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0) Septic Shock (cont.)

29. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins “Second, patients with culture-positive and culture-negative sepsis or septic shock have comparable mortality rates.” (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0).. Septic Shock (cont.)

30. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins “Third, administration of anti-endotoxin antibodies in large, clinical trials did not improve survival.” (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0) Septic Shock (cont.)

31. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0) inflammatory mediators vascular endothelial cells respond and: promote clot formation create adhesive molecules more WBCs move out into the tissues and release more inflammatory mediators produce more vasodilation substances (NO) more vasodilation

32. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0) blocking these does not improve survival inflammatory mediators vascular endothelial cells respond and…

33. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins (Aird, W. C. [2003.] The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 101[10],3765-3777. Retrieved February 10, 2004, from http://www.blood journal.org/cgi/content/full/101/10/3765.0) blocking this with ACTIVATED PROTEIN C improves survival in human tests blocking this is still under study blocking this works in some studies, not in others vascular endothelial cells respond and… promote clot formation create adhesive molecules produce more vasodilation substances (NO)

34. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which type of shock is the result of a severe allergic reaction? a.Cardiogenic b.Obstructive c.Anaphylactic d.Septic

35. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer c.Anaphylactic Rationale: Anaphylactic shock is caused when inflammatory mediators are released (type I hypersensitivity reaction). The mediators include histamine, acetylcholine, kinins, leukotrienes, and prostaglandins, all of which cause vasodilation.

36. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Activated Protein C Drotrecogin alfa Blocks clotting Blocks inflammation Increases survival of the most seriously ill sepsis patients May cause bleeding!

37. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Complications of Shock Scenario: A doctor has been called in to treat Mr. M and has started him on fluid and antibiotics You are warned to watch him carefully for any signs of respiratory distress Question: Why would blood pressure imbalances cause respiratory distress?

38. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Complications of Shock (cont.) Acute respiratory distress syndrome Acute renal failure Gastrointestinal complications Disseminated intravascular coagulation Multiple organ dysfunction syndrome

39. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Acute Respiratory Distress Syndrome (ARDS) Exudate enters alveoli –Blocks gas exchange –Makes inhaling more difficult Neutrophils enter alveoli –Release inflammatory mediators –Release proteolytic enzymes

40. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Acute Renal Failure (ARF) Renal vasoconstriction cuts off urine production –Acute renal failure Continued vasoconstriction cuts off renal oxygen supply Renal tubular cells die –Acute tubular necrosis

41. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Disseminated Intravascular Coagulation (DIC) coagulation pathways activated clots in many small blood vessels microinfarcts, ischemia platelets and clotting proteins used up bleeding problems

42. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Multiple Organ Dysfunction Syndrome (MODS) The most frequent cause of death in the noncoronary intensive care unit Mortality rates vary from 30% to 100% Mechanism not known

43. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Tell whether the following statement is true or false. Treatment for ARDS often includes breathing assistance using mechanical ventilation.

44. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer True Rationale: Because alveoli are filled with exudate and blood that has leaked from the capillary, the surface area available for gas exchange is greatly reduced. Most patients will require ventilatory support until the process reverses. ARDS has a high mortality rate because it is difficult to ventilate these patients.