Patho Ch 20

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Patho Ch 20
2014-11-11 20:22:49

Exam #5
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  1. Heart Failure

    -What is it?
    -What does it lead to?
    -What are some compensatory mechanisms?
    •Inadequate pumping

    •Leads to decreased cardiac output, increased preload, and increased afterload

    •Compensatory mechanisms activated

    • –Activation of the sympathetic nervous system
    • –Activation of the renin-angiotensin-aldosterone system
    • –Ventricular hypertrophy
  2. 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?

    Systolic dysfunction

    –Decreased contractility

    Diastolic dysfunction

    –Decreased filling

    Right-sided or left-sided failure

    –Is the right or left side of the heart failing?

    –Mixed dysfunction : Both
  3. Manifestations of Heart Failure
    •Effects of impaired pumping

    •Effects of decreased renal blood flow ⇢ RAA pathway

    •Effects of the sympathetic nervous system
  4. Left-sided Heart Failure
    Cardiac output falls

    •Blood backs up to the pulmonary circulation

    •Causes: left ventricular infarction, hypertension, and aortic and mitral valve stenosis (narrowing)

    •Manifestations: pulmonary congestion, dyspnea, and activity intolerance
  5. Right-sided Heart Failure
    •Blood backs up to the systemic circulation

    •Causes: pulmonary disease, left-sided failure, and pulmonic and tricuspid valve stenosis

    •Manifestations: edema and weight gain
  6. Heart Failure
    •May be acute or chronic


    • –Depend on type
    • –Symptoms fluctuate
    • –Symptoms appear when body is not able to compensate.
    • –Include systemic and pulmonary fluid congestion

    •DX: HX, exam , Chest XR, ABGs, echocardiogram, ECG, and atrial & brain natriuretic peptide

    •TX: Identify and manage underlying cause

    –Include: lifestyle changes, diuretics, blood pressure meds, biventricular pacemaker, intraaortic balloon pump, and heart transplant
  7. Heart Failure: What to look for…
    •Fluid retention


    •Respiratory problems



    •Mental confusion




    •Sudden cardiac death
  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. Shock
    •Decreased blood volume or circulatory stagnation.

    •Results in inadequate tissue & organ perfusion

    •The most frequent cause of death in the noncoronary intensive care unit 

    •Mortality rates vary from 30% to 100% 

    •Mechanism not known
  10. Stages of Shock

    –Sympathetic nervous system and renin-angiotensin-aldosterone system are activated 


    • –Compensatory mechanisms fail
    • –Tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops


    –Organ damage occurs
  11. Types of Shock



    •Distributive (Neurogenic, Anaphalactic, Septic)
  12. Cardiogenic Shock
    •Left ventricle cannot maintain adequate cardiac output  (Heart fails to pump blood adequately)

    –Decreased cardiac output lowers BP

    –Sympathetic system responds

    –Vasoconstriction > resistance to blood flow

    –Increased workload on heart worsens heart failure
  13. Hypovolemic Shock
    •Hypovolemic shock

    –Venous return reduces because of external blood volume losses
  14. Obstructive Shock
    •Circulatory shock caused by mechanical obstruction of the flow of blood through great veins, heart, and lungs.

    •Causes: dissecting aortic aneurism, cardiac tamponade, pneumothorax, ruptured diaphram

    •Common cause: pulmonary embolism

    •S/Sx: elevated r-heart blood pressure; jugular venous distention
  15. Distributive Shock (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
  16. 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
  17. Types of Distributive Shock


    •Sepsis/Septic Shock
  18. Neurogenic Shock
    •Loss of vascular sympathetic tone and autonomic function lead to massive vasodilatation 

    •Often associated with spinal cord injury (spinal shock)

    •Can be from brain injury, depressant action of drugs, anesthesia, hypoxia, reduced glucose

    •Heart rate may be slower than normal and skin warm and dry.

    More rare form of shock.
  19. Anaphalaxis
    •Excessive allergic reaction

    •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?
  20. 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
  21. Septic Shock
    •Also called systemic inflammatory response syndrome (SIRS)

    •Inflammatory mediators also increase the metabolic rate of tissues, so they need more oxygen

    •Refer to FIGURE 20-10
  22. Septic Shock
    •“Despite the prompt implementation of appropriate antibiotic therapy, sepsis mortality remains high, in the range of 28% to 50%.”

    •Second, patients with culture-positive and culture-negative sepsis or septic shock have comparable mortality rates.”

    •Third, administration of anti-endotoxin antibodies in large, clinical trials did not improve survival.”
  23. Activated Protein C
    •Drotrecogin alpha

    •Blocks clotting

    •Blocks inflammation

    •Increases survival of the most seriously ill sepsis patients

    •May cause bleeding!
  24. Complication of Shock
    •Complications: acute respiratory distress syndrome, renal failure, disseminated intravascular coagulation, cerebral hypoxia, and death


    –Varies depending on type

    –Include: thirst, tachycardia, restlessness, irritability, tachypnea progressing to Cheyne-Stokes respiration, cool and pale skin, hypotension, cyanosis, and decreasing urinary output
  25. Complications of Shock
    •Acute respiratory distress syndrome

    •Acute renal failure

    •Gastrointestinal complications

    •Disseminated intravascular coagulation

    •Multiple organ dysfunction syndrome
  26. Acute Respiratory Distress Syndrome (ARDS)
    •Exudate enters alveoli

    –Blocks gas exchange

    –Makes inhaling more difficult

    •Neutrophils enter alveoli

    –Release inflammatory mediators

    –Release proteolytic enzymes
  27. 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
  28. 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