Pathology - University of Arizona



Pathology

Lecture 7 Shock and Heart Failure

1) To understand the mechanisms/classification and hemodynamic elements of various types of shock.

|Type |Classification/Mechanism |Examples |

|Hypovolemic |Blood volume loss |Hemorrhage, diarrhea, inflammation, burns |

|Cardiogenic |Pump Failure |MI, arrhythmias, CHF |

|Septic |Peripheral vasodilation; venous pooling |Overwhelming infection (more often Gram-negative, |

| | |endotoxin-producing bacteria) |

|Neuropathic |Loss of autonomic control |Anesthesia, spinal cord injury drugs |

|Anaphylaxis |Vasodilation and vascular leakage |Heterologous protein, drugs |

|Endocrine failure |Hyponatremia, volume loss |Addison’s disease |

2) To know the cellular and biochemical mediators of shock. Endotoxins (bacterial wall lipopolysaccharides-LPS) mediate the pathogenic events of septic shock – directly by cell injury or indirectly via mediators. Endotoxins act through mononuclear phagocyte system to release interleukin-1 (IL-1) and tumor necrosis factor (TNF), which are critical to the development of septic shock.

3) To be familiar with the clinical features of the various stages of shock.

1. Early, nonprogressive, “compensated”: Neurohumoral mechanisms respond to maintain cardiac output and blood pressure through tachycardia, peripheral vasoconstriction and renal fluid retention.

2. Progressive, “uncompensated”: significant tissue hypoxia causing lactic acidosis, impaired vasomotor response causing peripheral blood pooling. Features include: CNS deterioration; decreased urine output.

3. Irreversible: Generalized cell injury; lysosomal enzyme leakage. Features include: further decline of cardiac function (myocardial depressant factor); renal failure.

4) To recognize the gross and histologic changes of organs and tissues principally affected by shock.

|Organ/Tissue |Gross Changes |Histologic Changes |

|CNS |Infarction, Cerebral edema |Neuronal and cortical necrosis |

|Heart |Full-blown infarction |Localized necrosis – “zonal lesions” |

|Lungs |Pulmonary edema |Diffuse alveolar damage (clinical ARDS) |

|Kidneys |Severe functional impairment |Patchy necrosis of renal tubules |

|Intestine |Endotoxic shock starting at gut |Mucosal necrosis: patchy → generalized |

|Liver |Impaired clotting factor production |Centrilobular necrosis to confluent areas of necrosis |

|Adrenal |Focal cortical lipid depletion |Hemorrhagic necrosis |

|Pancreas |Unusual |Focal microscopic necrosis |

|Microcirculation |Thrombotic and/or bleeding complications |Disseminated intravascular coagulation, more likely form |

| | |septic shock |

5) To be aware of the differencecs in heart failure resulting from systolic versus diastolic dysfunction. Intrinsic myocardial dysfunction (failure of the heart as a pump) – systolic failure (e.g., ischemic heart disease). Impaired cardiac filling – diastolic failure (e.g., myocardial fibrosis). Systolic dysfunction results from insufficient ejection due to damaged myocardium or increased resistance (e.g., aortic stenosis). Diastolic dysfunction results form decreased compliance.

6) To relate the events of cardiac hypertrophy to cardiac failure as a tenuous balance. Cardiac hypertrophy is an adaptive response to accommodate increasing demand where myocytes increase in size, diameter, and DNA content to increase cardiac work. However, the thickening of the myocardium causes increased intercapillary distance, decreased ratio of capillary to myofiber volume, deposition of fibrous connective tissue, and abnormal, possibly dysfunctional, protein isoforms (altered gene expression). These limitations make it such that the increased workload cannot be supported and thus the heart is unable to maintain adequate circulation to meet the body’s needs, which is the definition of cardiac failure.

7) To know the causes and manifestations of left-sided and right-sided heart failure.

| |Left-sided heart failure |Right-sided heart failure |

|Causes|Ischemic heart disease, hypertension, valvular heart|Intrinsic lung disease (cor pulmonale); may be simulated by |

| |disease, other “primary” myocardial disease |constrictive pericarditis. |

|Manife|Pulmonary edema and capillary congestion. |Increased resistance of pulmonary vascular circulation makes right |

|statio|Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, |ventricle work harder |

|ns |Decreased renal perfusion with activation of |Congestion of systemic and portal venous systems prominent |

| |reninangiotensin system, |Chronic passive congestion of liver; may progress to centrilobular |

| |inadequate CNS perfusion. |necrosis |

| | |Congestive splenomegaly |

| | |Ascites |

| | |Peripheral edema |

8) To be responsible for all handout materials on Shock and Heart Failure. Review handout.

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