7 shock
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7 shock
- 2. DEFINITION Shock: It’s a Clinical state of Inadequate perfusion resulting in O2 debt at cellular level
- 3. Common Pathophysiology Cellular dysfunction DO2 and energy substrate reduction anaerobic metabolism systemic acidosis (myocardial, smooth muscle depressant), organ failure Marked decrease VO2, may indicate irreversible shock
- 4. Hemodynamic Classification of Shock Type PAP CO SVR hemorrhagic decr decr incr cardiogenic incr decr incr distributive nl, nl, decr decr incr, decr obstructive incr decr incr
- 5. Etiologic Classification of Shock • Cardiogenic • Hemorrhagic / Hypovolemic • Distributive (SIRS, septic, high output failure, spinal cord injury, anaphylactic)
- 7. Etiologic Classification of Shock Cardiogenic - causes • Myocardial Infarction • Ventricular Arrhythmia • Cardiac tamponade • Pulmonary embolism Basic mechanism: Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow
- 8. Pulmonary embolism – obstruction to out flow - failure
- 9. Myocardial infarction – pump failure
- 10. Myocardial infarction – pump failure
- 11. Myocardial infarction – pump failure
- 12. Myocardial infarction – Rupture of ventricle – External compression
- 13. Myocardial infarction – Rupture of ventricle – External compression Cardiac tamponade
- 14. Etiologic Classification of Shock Hypovolemic: • Hemorrhage • Fluid loss, e.g., vomiting, diarrhea, burns, or trauma Basic mechanism: Inadequate blood or plasma volume
- 15. Etiologic Classification of Shock Distributive: Increased vascular volume • SIRS - septic • high output failure • spinal cord injury • Anaphylactic • Superantigens Basic mechanism: Peripheral vasodilation and pooling of blood; endothelial activation / injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades
- 17. Septic shock Septic shock results from spread and expansion of an initially localized infection (e.g., abscess, peritonitis, pneumonia) into the bloodstream
- 18. Septic shock • 25-50% mortality in ICUs • 70% are due to endotoxins
- 19. Septic shock • ~ 70%) are caused by endotoxin- producing GNB • Endotoxins are bacterial wall lipopolysaccharides (LPSs)
- 21. Septic shock
- 22. Septic shock
- 23. Effects of LPSs • At low doses - activate monocytes and macrophages, with effects intended to enhance their ability to eliminate invading bacteria. • with higher levels of LPS cytokine-induced secondary effectors (e.g., nitric oxide become significant. In addition, systemic effects of the cytokines such as TNF and IL-1 may begin to be seen; these include fever and increased synthesis of acute phase reactants. • LPS at higher doses also results in diminished endothelial cell production of thrombomodulin and TFPI, tipping the coagulation cascade toward thrombosis. • Finally, at still higher levels of LPS, the syndrome of septic shock supervenes • Systemic vasodilation (hypotension) • Diminished myocardial contractility • Widespread endothelial injury and activation - acute respiratory distress syndrome. • Activation of the coagulation system, culminating in DIC
- 24. Septic shock
- 25. Septic shock
- 26. Stages of Shock • Initial nonprogressive phase: during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained • A progressive stage: characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis • An irreversible stage: severe tissue damage -- even with the correction of hemodynamic defects survival is not possible
- 27. Morphology • Hypoxic injury • Failure of multiple organ systems brain heart lungs kidneys adrenals & GIT
- 28. Morphology – Multi Organ Failure • Brain: Ischemic encephalopathy • Heart: Subendocardial necrosis and contraction bands • Kidneys: Acute tubular necrosis • Lungs: Shock lung • Adrenals: Cortical cell lipid depletion • GIT: Hemorrhagic enteropathy • Liver: Centrilobular necrosis
- 46. Clinical course The clinical manifestations depend on the precipitating insult. • In hypovolemic and cardiogenic shock, the patient presents with hypotension; a weak, rapid pulse; tachypnea; and cool, clammy, cyanotic skin. • In septic shock, however, the skin may initially be warm and flushed because of peripheral vasodilation. • The original threat to life stems from the underlying catastrophe that precipitated the shock state (e.g., myocardial infarct, severe hemorrhage, or uncontrolled bacterial infection). • Duration of shock: the cardiac, cerebral, and pulmonary changes secondary to the shock state may worsen the problem.
- 47. Hemorrhagic Shock Pathophysiology Volume deficit - decr. BP, CO Compensatory Mechanisms Catecholamine, sympathetic stimulation Interstitial fluid entry into intravascular compartment
- 48. Hemorrhagic Shock Clinical Presentation Early Phase Tachycardia, narrow pulse pressure, may exhibit orthostatic changes in HR/AP Healthy patient with 25-30% loss may exhibit only these signs
- 49. Hemorrhagic Shock Less healthy patients will exhibit rapid decompensation with this magnitude of volume loss Later Phase Cool moist skin, hypotensive, anxious, disoriented, oliguric KEY: EARLY RECOGNITION
- 50. Hemorrhagic Shock Management Therapeutic Goals Correct Hypotension, thereby normalizing cellular perfusion, reducing acidemia Increase SaO2, thereby increasing DO2
- 51. Hemorrhagic Shock Restoration of intravascular volume Fluid administered should replace fluid lost Initial Management: Crystalloids,N.S./ Ringer’s Colloids ( 5% alb., hetastarch) do not increase survival and are costly W.B. PRBC, when indicated
- 52. Parameters of Adequate Resuscitation Urine output (0.5 - 1.0 ml/kg/hr) acceptable renal perfusion Reversal of lactic acidosis (nl. pH) improved tissue perfusion Normal mental status adequate cerebral perfusion
- 53. Cardiogenic Shock Pathophysiology AMI- 10-15% cardiogenic shock Mortality > 80% Decreased CO, AP Neurohumoral compensatory mechanisms can be deleterious: > venoconstriction - >preload
- 54. Cardiogenic Shock Clinical Presentation Hypotension - < 80 syst., decr. of 90 mm Hg in patient with HTN Cool diaphoretic skin, dyspnea, disorientation, oliguria
- 55. Cardiogenic Shock > SVR > afterload > HR > VO2 < AP < coronary perfusion All contribute to extension of infarct and morbid progression of cardiogenic shock
- 56. Cardiogenic Shock Prognostic Parameters Group PAEDP CI Mortality I > 29 100% II < 29 ->15 < 2 92% III < 29 < 2 63% IV < 15 > 2 13% PAEDP=mm Hg, CI=L/M2/min.
- 57. Cardiogenic Shock Management Principles Primary Goal: Improve myocardial function Decrease O2 consumption (VO2) Intubation, sedation, analgesia Increase O2 delivery (DO2) Optimize CI, Hgb., Hgb. sat. (SaO2)
- 58. Cardiogenic Shock Management Methods Pharmacologic Manipulation Preload (RAP,PAP) - morphine, nitro, lasix, volume Cardiac contractility - inotropes, chronotropes, vasopressors Afterload (PVR,SVR) - nitro, beta-blockers
- 59. Cardiogenic Shock Interventional Therapy Intraaortic Balloon Pump (IABP) or Counterpulsation IABP + Early CABG (12-16 hr. post AMI) Left Ventricular Assist Device (LVAD)
- 60. Septic Shock Clinical Presentation Early Phase Vasodilatation CO normal or high fever Agitation / confusion hyperventilation Often, fever and hyperventilation are the earliest signs Hypotension may not be present
- 61. Septic Shock Late Phase CO decreased, hypotension, vasoconstriction, impaired perfusion, decreased level of consciousness, oliguria, DIC Atypical Presentation Elderly/debilitated – Fever, respiratory alkalosis, confusion, hypotension
- 62. Septic Shock Etiology Gram neg bacteria (gm. neg rods) Most common (E. coli, 31% all cases) Incidence - 12.8%/1000 hosp. adm. Mortality 25%; 30-50% if shock present 30% if Resp./GI/unkn. Source 15% if Biliary/GU/GYN source
- 63. Septic Shock Management Fluid resuscitation Pressor support After adequate volume restored Dopamine (5-10 ug/kg/min) Dobutamine (5-20ug/kg/min) Airway management
- 64. Septic Shock Management cont… Surgical drainage (abscess, infected organ (gangrenous gallbladder, bowel) Antibiotics Site established, consider organisms known to occur in such sites Unknown site in 30% of patients
- 65. Distributive Shock Pathophysiology Peripheral vascular dilatation disproportionate to existing intravascular volume Septic/Systemic inflammatory shock(SIRS), anaphylaxis, spinal shock
- 66. Summary - Shock • Shock is a clinical state of decreased BP with O2 debt at cellular level • If prolonged it may result in multiorgan failure • Septic shock has cytokine basis – TNF, IL1, DIC
- 67. E N D
Editor's Notes
- NT = Normotensive, HT = Hypertensive.
- D = decreased availability of O2 and energy substrates. VO2 = utilization of O2.
- SVR=Systemic venous resistance CO=Cardiac out put PAP=
- SIRS: Systemic inflammatory response syndrome. Septic shock: Overwhelming microbial Endotoxic shock Gram-positive septicemia, Fungal sepsis. Shock may occur in the setting of anesthetic accident or spinal cord injury (neurogenic shock), owing to loss of vascular tone and peripheral pooling of blood. Anaphylactic shock, initiated by a generalized IgE-mediated hypersensitivity response, is associated with systemic vasodilation and increased vascular permeability ( Chapter 6 ). In these instances, widespread vasodilation causes a sudden increase in the vascular bed capacitance, which is not adequately filled by the normal circulating blood volume. Thus, hypotension, tissue hypoperfusion, and cellular anoxia result.
- Bacteremia: presence of bacteria in the blood stream Septicemia: Multiplication of bacteria in the blood stream. It’s a clinical state.
- Most cases of septic shock (approximately 70%) are caused by endotoxin-producing gram-negative bacilli ( Chapter 8 ), hence the term endotoxic shock. Endotoxins are bacterial wall lipopolysaccharides (LPSs) that are released when the cell walls are degraded (e.g., in an inflammatory response). LPS consists of a toxic fatty acid (lipid A) core and a complex polysaccharide coat (including O antigens) unique to each bacterial species. Analogous molecules in the walls of gram-positive bacteria and fungi can also elicit septic shock.
- Endotoxins are bacterial wall lipopolysaccharides (LPSs) that are released when the cell walls are degraded (e.g., in an inflammatory response). LPS consists of a toxic fatty acid (lipid A) core and a complex polysaccharide coat (including O antigens) unique to each bacterial species. Analogous molecules in the walls of gram-positive bacteria and fungi can also elicit septic shock.
- mammalian Toll-like receptor protein 4 (TLR-4).
- TFPI Tissue factor pathway inhibitor
- At low doses, LPS predominantly serves to activate monocytes and macrophages, with effects intended to enhance their ability to eliminate invading bacteria. LPS can also directly activate complement, which likewise contributes to local bacterial eradication. The mononuclear phagocytes respond to LPS by producing cytokines, mainly TNF, IL-1, IL-6, and chemokines. TNF and IL-1 both act on endothelial cells to stimulate the expression of adhesion molecules ( Chapter 2 ; Fig. 4-21 ) and the production of other cytokines and chemokines. Thus, the initial release of LPS results in a circumscribed cytokine cascade doubtless intended to enhance the local acute inflammatory response and improve clearance of the infection. • With moderately severe infections, and therefore with higher levels of LPS (and a consequent augmentation of the cytokine cascade), cytokine-induced secondary effectors (e.g., nitric oxide; Chapter 2 ) become significant. In addition, systemic effects of the cytokines such as TNF and IL-1 may begin to be seen; these include fever and increased synthesis of acute phase reactants ( Chapter 2 ; Fig. 4-21 ). LPS at higher doses also results in diminished endothelial cell production of thrombomodulin and TFPI, tipping the coagulation cascade toward thrombosis. • Finally, at still higher levels of LPS, the syndrome of septic shock supervenes ( Fig. 4-22 ); the same cytokines and secondary mediators, now at high levels, result in: • Systemic vasodilation (hypotension) • Diminished myocardial contractility • Widespread endothelial injury and activation, causing systemic leukocyte adhesion and pulmonary alveolar capillary damage (acute respiratory distress syndrome; Chapter 15 ) • Activation of the coagulation system, culminating in DIC
- Shock is a progressive disorder that, if uncorrected, leads to death. Unless the insult is massive and rapidly lethal (e.g., a massive hemorrhage from a ruptured aortic aneurysm), shock tends to evolve through three general (albeit somewhat artificial) phases. A brief discussion here can help to integrate the sequential pathophysiologic and clinical events in the progression of shock. These have been documented most clearly in hypovolemic shock but are common to other forms as well: An initial nonprogressive phase during which reflex compensatory mechanisms are activated and perfusion of vital organs is maintained A progressive stage characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis An irreversible stage that sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible. In the early nonprogressive phase of shock, a variety of neurohumoral mechanisms help maintain cardiac output and blood pressure. These include baroreceptor reflexes, release of catecholamines, activation of the renin-angiotensin axis, antidiuretic hormone release, and generalized sympathetic stimulation. The net effect is tachycardia, peripheral vasoconstriction, and renal conservation of fluid. Cutaneous vasoconstriction, for example, is responsible for the characteristic coolness and pallor of skin in well-developed shock (although septic shock may initially cause cutaneous vasodilation and thus present with warm, flushed skin). Coronary and cerebral vessels are less sensitive to this compensatory sympathetic response and thus maintain relatively normal caliber, blood flow, and oxygen delivery to their respective vital organs. If the underlying causes are not corrected, shock passes imperceptibly to the progressive phase, during which there is widespread tissue hypoxia. In the setting of persistent oxygen deficit, intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. The resultant metabolic lactic acidosis lowers the tissue pH and blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculation. Peripheral pooling not only worsens the cardiac output, but also puts endothelial cells at risk for developing anoxic injury with subsequent DIC. With widespread tissue hypoxia, vital organs are affected and begin to fail; clinically the patient may become confused, and the urine output declines. Unless there is intervention, the process eventually enters an irreversible stage. Widespread cell injury is reflected in lysosomal enzyme leakage, further aggravating the shock state. Myocardial contractile function worsens in part because of nitric oxide synthesis. If ischemic bowel allows intestinal flora to enter the circulation, endotoxic shock may be superimposed. At this point, the patient has complete renal shutdown owing to acute tubular necrosis ( Chapter 20 ), and despite heroic measures, the downward clinical spiral almost inevitably culminates in death.
- Laminar necrosis.
- Hypoxic ischemic changes of neurons. Discussion: This picture shows features of hypoxic/ischemic changes of neurons. The neurons have smudged and pyknotic nuclei, collapsed and flame-shaped eosinophilic cytoplasm with accentuated (artificial) pericellular space. This type of neuronal death characteristically seen in adults and older infants or children. In contrast, apoptotic cell death caused by hypoxic/ischemic injury is seen most commonly in premature infants and, less commonly, term neonates. ---- Red Neuron: Note the spaces in the cerebral cortex tissue representing cerebral edema. The neurons are the cells with the eosinophilic staining cytoplasm and pyknotic nuclei (see arrow). The pathologic process causing the changes in the neurons is calledapoptosis. Recall that apoptosis refers to activation of programmed cell death with individual cell necrosis. The cytoplasm of apoptotic cells becomes intensely eosinophilic and the nucleus condensed. Neurons, which are permanent types of cells that can no longer divide, are extremely sensitive to injury in tissue hypoxia. When they die, they undergo apoptosis and produce these “red neurons”.
- Neuronal death due to hypoxic/ischemic damage. Discussion: At the center of the photograph is an apoptotic cell that is characterized by multiple, dark, densely packed dense nuclear bodies that is rimmed by a small amount of eosinophilic cytoplasm. Hypoxic/ischemic changes in fetal immature neurons are characterized by apoptotic cell death as illustrated here. The other cells lack the characteristic features of Alzheimer type II astrocytes, namely enlarged, pale nucleus with an irregular contour, cloud like clear or “watery” nucleoplasm, and one or more small nucleoli. There is no large inclusion body to suggestive cytomegalovirus infection. The dense nuclear bodies are too big to suggest toxoplasmosis. There is no features of HIV infection such as microglial nodule associated with multinucleated giant cells being shown here
- Fig. 1. Hyperemia of capillaries of pulmonary alveoli and mononuclear infiltration were shown. Fibrin and red blood cells could be found inside the alveolar spaces. (HE staining, original magnification¡Á200).Fig. 2. Thickened basement membranes of capillaries and widened walls of pulmonary alveoli with fibrinous deposition were detected. (HE staining, original magnification¡Á200).Fig. 3. Hyaline-membrane formation was observed. (HE staining, original magnification¡Á200).Fig. 4. Epithelium desquamation of bronchioles mucosa could be detected, together with neutrophils and some fibrous thrombosis in the accompanied vessels. (HE staining, original magnification¡Á200).
- Acute Tubular Necrosis Ischemic injury to the donor organ during harvesting and subsequent transplantation into the patient, is a common cause of oliguria/anuria in the immediate post-transplant period. The clinical course is usually self-limited, and recovery ensues within a few weeks. Biopsies of the allograft during the ischemic phase show coarse irregular cytoplasmic vacuoles in the renal tubular epithelium and focal coagulative necrosis. During the resolution phase of the injury, the tubules may only show non-specific dilatation, cast formation, and regeneration. The peri-tubular capillaries sometimes show extra-medullary hematopoiesis. In the glomeruli, severe ischemic injury may result in capillary thrombi and neutrophilic infiltration
- Acute Tubular Necrosis Ischemic injury to the donor organ during harvesting and subsequent transplantation into the patient, is a common cause of oliguria/anuria in the immediate post-transplant period. The clinical course is usually self-limited, and recovery ensues within a few weeks. Biopsies of the allograft during the ischemic phase show coarse irregular cytoplasmic vacuoles in the renal tubular epithelium and focal coagulative necrosis. During the resolution phase of the injury, the tubules may only show non-specific dilatation, cast formation, and regeneration. The peri-tubular capillaries sometimes show extra-medullary hematopoiesis. In the glomeruli, severe ischemic injury may result in capillary thrombi and neutrophilic infiltration
- Acute Tubular Necrosis Ischemic injury to the donor organ during harvesting and subsequent transplantation into the patient, is a common cause of oliguria/anuria in the immediate post-transplant period. The clinical course is usually self-limited, and recovery ensues within a few weeks. Biopsies of the allograft during the ischemic phase show coarse irregular cytoplasmic vacuoles in the renal tubular epithelium and focal coagulative necrosis. During the resolution phase of the injury, the tubules may only show non-specific dilatation, cast formation, and regeneration. The peri-tubular capillaries sometimes show extra-medullary hematopoiesis. In the glomeruli, severe ischemic injury may result in capillary thrombi and neutrophilic infiltration
- Acute Tubular Necrosis Ischemic injury to the donor organ during harvesting and subsequent transplantation into the patient, is a common cause of oliguria/anuria in the immediate post-transplant period. The clinical course is usually self-limited, and recovery ensues within a few weeks. Biopsies of the allograft during the ischemic phase show coarse irregular cytoplasmic vacuoles in the renal tubular epithelium and focal coagulative necrosis. During the resolution phase of the injury, the tubules may only show non-specific dilatation, cast formation, and regeneration. The peri-tubular capillaries sometimes show extra-medullary hematopoiesis. In the glomeruli, severe ischemic injury may result in capillary thrombi and neutrophilic infiltration
- CO = Cardiac out put.