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Pathophysiology > Chapter 20 > Flashcards

Chapter 20 Flashcards

1
Q

Tissue Perfusion

A
  • tissue not being oxygenated
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2
Q

Causes of Shock

A
  • cardiogenic (inadequate cardiac output despite sufficient vascular volume)
  • obstructive (circulatory blockage, such as a large pulmonary embolus or cardiac tamponade, disrupts cardiac output)
  • hypovolemic (loss of blood volume as a result of hemorrhage or excessive loss of extracellular fluids) (dehydration or blood loss from trauma)
  • distributive (greatly expanded vascular space because of inappropriate vasodilation) (anaphylaxis)
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3
Q

Pathogenesis of Shock

A
  • common factor among all types of shock is hypoperfusion amd impaired cellular oxygen utilization
  • inadequate cellular oxygenation may result from decreased cardiac output, maldistribution of blood flow, and reduced blood oxygen content
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4
Q

Impaired tissue oxygenation

impaired oxygen utilization by cells

A
  • disrupts function and, if ongoing or severe, may lead to cell death, organ dysfunction, and stimulation of inflammatory reactions
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5
Q

Impaired tissue oxygenation (outcomes of lack of oxygen)

A
  • product of lactate
  • failure of ion pumps leads to sodium and water accumulation in the cell (hydropic swelling which leads to tissue necrosis or any shock)
  • formation of oxygen radicals
  • induction of inflammatory cytokines
  • cellular hypoxia, which causes anaerobic metabolism, free radical production, and macrophage induction
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6
Q

Reperfusion Injury

A
  • ischemic cells may produce oxygen-free radicals when oxygen supplies are restored, causing cells to die
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7
Q

Impaired Tissue Oxygenation (TNF-alpha, IL-1, and failure of microcirculaiton)

A
  • Tumor necrosis factor alpha and interlukin 1 cytokines increase during septic shock and are thought to be important mediators of vascular failure and progressive organ damage
  • increased activity of inducible nitric oxide (NO) synthase leading to excess NO (is a massive vasodilator that causes vasodilation of brain)
  • failure of microcirculation to autoregulate (tissue adjusts for BP change) bloodflow leads to activation of coagulation (leads to oxygen debt in tissues)
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8
Q

Compensatory Mechanisms and Stages of Shock

A
  • three clinical stages including compensated shock, progressive shock, and refactory shock
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9
Q

Compensatory Stage of Shock

A
  • homeostatic mechanisms are sufficient to maintain adequate tissue perfusion despite a reducction in CO, happens initially (good vital signs)
  • SNS activation attempts to maintatin blood pressure even though CO has fallen, increased CO and vascular resistance (result of release of dopamine, etc.)
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10
Q

Progressive Stage of Shock

A
  • marked by hypotension and marked tissue hypoxia
  • lactate production increases with anaerobic metabolism
  • lack of ATP leads to cellular swelling, dysfunction, and death
  • cellular and organ dysfunction result from oxygen free radicals, release of inflammatory cytokines, and activation of the clotting cascade (can get organ failure)
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11
Q

Clinical Manifestations of Shock

A
  • decreased levels of consciousness
  • Thirst
  • restlessness
  • dilated pupils
  • release of ADH
  • Increased Heart Rate
  • Increased Respiratory Rate
  • decreased urine output
  • increased specific gravity
  • cool, clammy, blush, or gray color in the legs
  • decreased capillary refill
  • constriction of splanchnic vessels
  • release of aldosterone and cortisol
  • Hypotension
  • Decreased pulse pressure
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12
Q

Clinical Manifestations of Cardiogenic Shock

A
  • Hypotension
  • High systemic vascular resistance
  • low cardiac output
  • High Cardiac Preload
  • Low Venous ocygen saturation
  • low urine output
  • cool skin temp
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13
Q

Clinical manifestations of Hypovolemic Shock

A
  • hypotension
  • High systemic vascular resistance
  • Low cardiac output
  • Low cardiac preload
  • Low venous oxygen saturation
  • low urine output
  • cool temp
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14
Q

Clinical Manifestations of Septic Shock

A
  • Hypotension
  • Low systemic vascular resistance
  • High Cardiac Output
  • Low cardiac preload
  • High venous oxygen saturation
  • low urine output
  • warm temp
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15
Q

Cardiogenic Shock

A
  • usually result of a severe ventricular dysfunction associated with MI
  • Diagnostic features include decreased CO, Elevated left ventricular end-diastolic pressure (preload), S3 heart sounds (indication of volume overload), Pulmonary edema, Narrow pulse pressure
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16
Q

Results of Cardiogenic Shock

A
  • Low CO = reduced oxygen delivery to tissues = higher oxygen extraction = low SvO2
17
Q

Cardiogenic Shock Treatments

A
  • therapy is aimed at improving CO and myocardial oxygen delivery, decreasing workload
  • inotropic (gives heart nice squeez), preload reducing, and afterload reducing agents
  • intraaortic balloon conterpulsation (catheter is threaded through groin to aorta)
  • ventricular assist devices
  • heart transplantation (only after many times)
18
Q

Obstructive Shock

A
  • results from mechanical obstructions that prevent effective cardiac filling and stroke volume
  • common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax
  • manifests as right sided heart failure
  • rapid management of underlying obstruction is required to prevent cardiovascular collapse
19
Q

Hypovolemic Shock

A
  • Results from inadequate circulation blood volume precipitated by hemorrhage, burns, dehydration, or leakage of fluid into interstitial spaces (external hemorrhage is most common cause)
  • Low CO and intracardiac pressures (low preload) lead to SNS activation = elevated HR (tachycardia), vasoconstriction, and increased contractility
  • result of epinephrine & dopamine
  • Severity of symptoms correlates with amt of blood loss
20
Q

Treatment of Hypovolemic Shock

A
  • Therapy is aimed at fluid replacements and controlling the source of volume loss
  • Colloids: increase serum colloid osmotic pressure (RBC)
  • Crystalloids: solutions that contain elecctrolytes (IV fluids, Saline, dextrose)
  • Blood products
21
Q

Distributive Shock

A
  • characterized by excessive vasodialtion and peripheral pooling of blood
  • CO inadequate due to reduced preload
  • Types include anaphylactic shock, neurogenic shock (bad communication between CNS and receptors), and septic shock
22
Q

Anaphylactic Shock

A
  • result of excessive mast cell degranulation mediated by IgE antibodies in response to antigen
  • Mast cells release vasodilatory mediators (histamine) resulting in severe hypotension
  • causes include antibiotic therapy, in particular Beta lactams, peanuts and tree nuts, insect stings, and snake bites
23
Q

Clinical Symptoms and treatment of Anaphylactic shock

A
  • symptoms include urticaria (hives), bronchoconstriction, stridor (noise made from air trying to escape from lungs), Angioedema (subcutaneous swelling in the lips), wheezing (air trying to move through constricted airways), and itching (prutitis)
  • Treatment includes maintenance of airway patency, , use of epinephrine (causes bronchodilation), bronchodilators, antihistamines, vasorepressors, and IV fluids
24
Q

Neurogenic Shock

A
  • results from loss of sympathetic activation of arteriolar smooth muscle
  • causes include medullary depression (brain injury, drug overdose), or lesions of sympathetic nerve fibers (spinal cord injury)
  • treatment includes vasorepressors, fluids, elevation of the legs, slow position changes, and the use of pressure stockings on the legs
25
Q

Septic Shock: Causes

A
  • results from severe systemic inflammatory response to infection (body’s response to infection or other insults results in systemic signs and symptoms of widespread inflammation: systemic inflammatory response syndrome (SIRS))
  • common causes include gram negative and gram positive bacteria, as well as fungal infections
26
Q

Septic Shock: Gram Negative Shock

A
  • endotoxins in bacterial cell walls stimulate massive immune system activation
27
Q

Characteristics of Septic Shock

A
  • characterized by release of immune mediators resulting in widespread inflammation
  • Clotting cascade, complement system, and kinin system are activated
  • widespread inflammation then leads to profound peripheral vasodilation with hypotension, maldistribution of blood flow with cellular hypoxia, and increased capilllary permeability with edema formation
  • initially characterized by high CO due to sympathetic activation of the heart and warm extremities
  • even though CO is high, cellular hypoxia is present
28
Q

Treatment of Septic Shock

A
  • therapy aimed at improving distribution of blood flow and managing infection with antibiotics
  • administration of fluids and drugs to improve distribution of blood flow
29
Q

Assessment and Hemodynamic Monitoring

A
  • helpful for assessing CO, volume status, and oxygen delivery and consumption
  • right atrial pressure, pulmonary artery pressure, and left atrial pressure monitored
  • used to guide management of cardiac preload, afterload, and contractility to optimize, CO and minimize work load
30
Q

Assesment and Hemodynamic Monitoring (Cardiac Output)

A
  • preload: amount of blood in the ventricle at the end of diastole
  • Afterload: aortic impedance that the left ventricle must overcome to eject blood during systole
  • contractility: inherent state of activation of cardiac muscle fibers
31
Q

Assessement and Hemodynamic Monitoring (Arterial Oxygen Content)

A
  • oxygen delivery (DO2)
  • Oxygen consumption (VO2)
  • Normally 25% of oxygen in arterial blood is extracted from tissues, so mixed venous oxygen saturation is 75% (normal)
  • Low CO results in greater oxygen extraction and lower SVO2
  • Maldistribution of flow results in less oxygen extraction and higher SVO2
32
Q

Hemodynamic Monitoring

A
  • pulmonary artery catheter inserted via jugular or subclavian vein allows measurement of intracardiac pressures, CO, and SVO2
  • Right atrial pressure used to manage blood volume (right preload)
  • left atrial pressure is important because it indicates left ventricular preload (will be high)
33
Q

Complications of Shock

A
  • shock states result in reduced or inadequate cellular oxygen consumption and may affect all organs and systems of the body
  • complications are inflammatory in nature (due to tissue hypoxia and necrosis)
  • inflammation triggered by hypoxic injury to cells, by antigen or endotoxin
  • excessive immune response leads to leaking capillaries, damage from proteolytic enzymes, and systemic activation of the clotting, complement, and kinin systems
34
Q

Complications of Shock (Imflammatory Cytokines)

A
  • mediate organ damage by altering metabolism, recruiting neutrophils, initiating the coagulation cascade, and altering capillary permeability
35
Q

Complications of shock (Acute Respiratory Distress Syndrome (ARDS))

A
  • most commonly associated with septic shock
  • Development of refractory hypoxemia, decreased pulmonary compliance, and radiographic evidence of pulmonary edema
  • Primary cause of death in ARDS: multiple organ failure, not severe hypoxemia
  • doesnt respond well to O2 therapy
  • usually a result of something triggering it
36
Q

Acute Respiratory Distress Syndrome (ARDS) Causes and treatments

A
  • neutrophils release protelytic enzymes, produce oxygen free radicals, and secrete inflammatory chemicals that make pulmonary capillaries leaky (forms exudate)
  • exudate leaks into the interstital spaces and alveoli of the lung, where it interferes with pulmonary gas exchange
  • inflammation may also damage type II pneumocytes, which normally produce surfactant
  • Treatment: lots of O2, breathing tubes, ventilators deliver 100% of O2, Positive End Expitory Pressure, alveoli will remain distended
37
Q

Dissemenated Intravascular Coagulation (DIC)

A
  • usually occurs with septic shock
  • immune activation of the clotting cascade
  • microcirculation obstructions lead to ischemic tissue damage
  • widespread clot formation consumes platelets and clotting factors
  • Platelet count and fibrinogen levels are low, fibrin degredation products (d-dimer) are elevated
  • Test for D Dimers to look for development of DIC
  • usually a result of something triggering it
38
Q

Acute Renal Failure

A
  • kidneys undergo long periods of hypoperfusion
  • Vasoconstriction causes decreased glomerular blood flow which leads to reduced hydrostatic pressure and filtration rates
  • acute tubular necrosis (ATN) associated with decreased urinary excretion of waste products (elevated levels of creatine and urea)
  • may need dialysis
39
Q

Multiple Organ Dysfunction Syndrome (MODS)

A
  • when 2 or more systems are affected
  • most common causes of secondary MODS: sepsis and septic shock
  • initiated by immune mechanisms that are overactive and destructive
  • Cytokines affect endothelium, recruit neutrophils, and activate inflammation in vascular beds leading to tissue destruction and organ dysfinction

Pathophysiology (34 decks)

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