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CV487 > Class 11: Multi-system dysfunction > Flashcards

Class 11: Multi-system dysfunction Flashcards

1
Q

Types of shock

A

Hypovolemic, cardiogenic & distributive

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2
Q

Types of distributive shock

A

Sepsis, anaphylaxis & neurogenic

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3
Q

Assess what in all types of shock

A

Acid-base analysis, especially in septic shock

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4
Q

Types of cardiogenic shock

A

Obstructive

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5
Q

Definition of shock

A

-A clinical syndrome resulting in cellular hypoxia, accumulation of cellular metabolic wastes, cellular destruction, and organ & system failure

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6
Q

Shock begins as an…

A

Adaptive response, progressing to multi-system organ failure

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7
Q

Interactive mechanisms of shock lead to…

A

-Decreased intravascular volume & myocardial contractility
-Increased venous capacitance

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8
Q

Shock occurs when…

A

The CVS fails to perfuse tissues, cells, and organs resulting in widespread impairment of cellular metabolism and tissue function

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9
Q

What happens to Na+ when there is reduced tissue oxygenation

A

Sodium moves into the cell & water follows; fluid is drawn out of the intravascular space decreasing circulatory volume and causing edema

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10
Q

Impaired O2 use & ATP

A

Low ATP stores cause metabolic acidosis to occur causing cardiac and skeletal muscles to use lactic acid as a fuel source

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11
Q

Impaired glucose use is caused by…

A

Either impaired glucose delivery to the cells or uptake by the cells

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12
Q

When glucose is impaired, cells perform…

A

Glycogenolysis, gluconeogenesis, and lipolysis to generate fuel for survival

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13
Q

Gluconeogenesis causes…

A

A depletion of protein & subsequent muscle wasting that weakens skeletal & cardiac muscles

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14
Q

Process of shock

A

-Inadequate tissue perfusion leading to anaerobic metabolism
-If left untreated will result in cell death
-Can lead to irreversible Multi-Organ Dysfunction Syndrome (MODS)

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15
Q

Slide 9

A
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16
Q

Normal compensatory mechanisms

A

Normal BP, >100HR, >20breaths/min, cold/clammy skin, decreased urine output, confusion & respiratory alkalosis

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17
Q

Progressive compensatory mechanisms

A

Systolic<80-90mmHg, HR>150, and rapid & shallow breaths with crackles
-Mottled/petechiae, 0.5mL/kg/hr, lethargy and metabolic acidosis

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18
Q

Irreversible compensatory mechanisms

A

-BP requires mechanical or pharmacological support, aneuric (dialysis required) and intubation
-Erratic or asystolic HR, jaundiced, unconscious and profound acidosis

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19
Q

Hypovolemia

A

-Insufficient volume within the vascular space
-Decreased perfusion to tissues leading to hypoxia

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20
Q

Etiology of hypovolemia

A

-Loss of whole blood
-Loss of plasma, fluid and interstitial fluid

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21
Q

Pathophysiology of hypovolemic shock

A

Decreased blood volume; decreased venous return; decreased SV; decreased CO; decreased tissue perfusion

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22
Q

Compensatory mechanism of hypovolemia

A

-Increased HR & afterload, vasoconstriction, decreased capillary hydrostatic pressure
-Liver & spleen add blood
-Renin is activated, aldosterone is released, Na+ retention and ADH increases water retention

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23
Q

Manifestations of hypovolemia

A

-Low systemic and pulmonary preloads & high afterload (SVR)
-Poor skin turgor, thirst, oliguria
-High HR & low BP

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24
Q

Cardiogenic shock

A

-Inability of the heart to pump enough blood to tissues and end organs
-Persistent hypotension and tissue hypo-perfusion
-Reduced contractility & impaired diastolic filling

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25
Q

Etiology of decreased contractility in cardiogenic shock

A

AMI, cardiomyopathy, dysrhythmias, myocarditis, metabolic abnormalities, sepsis and papillary muscle rupture

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26
Q

Cardiogenic shock + etiology for pump failure

A

-Impaired diastolic filling arrhythmias is caused by obstructions such as:
-PE, cardiac tamponade, valvular disorders & wall rupture or defects

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27
Q

Cardiogenic shock pathophysiology

A

-Decreased contractility & SV leading to pulmonary congestion, decreased tissue perfusion & coronary artery perfusion

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28
Q

Slide 21

A
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29
Q

Subjective cardiogenic shock manifestations

A

-Chest pain, dyspnea
-Feeling faint & impending doom

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30
Q

Classic cardiogenic shock objective manifestations

A

-Tachycardia, tachypnea & JVD
-Hypotension, low CO & dysrhythmia

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31
Q

Additional signs of cardiogenic shock

A

-Cyanosis & mottling
-Rapid, faint or irregular pulses
-Low U/O, peripheral edema
-Symptoms of end organ failure

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32
Q

Pathophysiology of distributive shock

A

-Vasodilation & maldistribution of blood volume
-Decreased venous return, SV, CO & tissue perfusion

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33
Q

How distributive septic shock begins

A

-Difficult to locate infection
-Bacteria enters the bloodstream either directly or through toxic substances released by bacteria
-Toxic substances act as triggering molecules in the septic syndrome leading to a pro inflammatory response of septic mediators

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34
Q

Inflammatory response of distributive shock

A

-Vasodilation
-Increased microvascular permeability
-Cellular activation
-Coagulation

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35
Q

Inflammatory response of distributive shock + vasodilation

A

Nutrient delivery & cellular access

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36
Q

Inflammatory response of distributive shock + increased microvascular permeability

A

Nutrient transport & cellular access

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37
Q

Inflammatory response of distributive shock + cellular activation

A

Phagocytosis, host protection, wound healing, further mediator stimulation (histamine, kinins, & prostaglandins)

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38
Q

Inflammatory response of distributive shock + coagulation

A

Prevents blood loss and walls off the injury

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39
Q

SIRS in distributive shock

A

-Systemic Inflammatory Response Syndrome (SIRS); meets more than one of the following:
-Temp <36 OR >38
-HR >90
-RR >20 OR PaCO2<32 mmHg
-WBC <4 OR >12 x 10 9/L OR >10% bands

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40
Q

Manifestations of SIRS

A

-General non-specific symptoms
-Fever, malaise, weakness, aching & loss of appetite

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41
Q

Definition of septic shock

A

Seen in patients with sepsis who develop underlying circulatory and metabolic abnormalities resulting in hypotension that require vasopressors to maintain a MAP of > 65 mmHg and having a serum lactate level of > 2 mmol/L despite adequate volume resuscitation, resulting in a higher risk of mortality

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42
Q

Progression of septic shock

A

-Sepsis: SIRS + infection
-Septic shock: Sepsis with profound hypotension and perfusion abnormalities despite fluid resuscitation
-Multi-organ dysfunction syndrome

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43
Q

Slide 34`

A
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44
Q

Common sources of sepsis you will encounter in acute care

A

-UTIs leading to urosepsis
-Pneumonia leading to full systemic sepsis
-Integumentary; necrotizing fasciitis

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45
Q

What a pt with septic shock looks like

A

-Hypotensive, tachycardic, febrile, decreased SVR, depressed myocardial function & lactic acidosis
-Leukopenia or leukocytosis, thrombocytopenia
-Vascular leakage, pulmonary congestion, tissue necrosis & organ failure

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46
Q

Distributive anaphylactic shock

A

Caused by a severe allergic reaction when a patient who has already produced antibodies to a foreign substance (antigen) develops a systemic antigen-antibody reaction

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47
Q

An antigen-antibody reaction causes..

A

Mast cells to release vasodilators such as histamine and bradykinin causing increased capillary permeability

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48
Q

Slide 39&40

A
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49
Q

Anaphylaxis clinical manifestations

A

-Dyspnea, wheezing, hoarseness, choking, drooling, sneezing, bronchospasm, stridor, feeling of “lump in throat” and can’t swallow
-Dizziness, nausea, headache & throbbing ears
-Tingling in throat, chest, tongue, mouth, face, increased HR and chest pain

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50
Q

Distributive neurogenic shock

A

-Vasodilation occurs as a result of a loss of sympathetic tone
-Bradycardia is a specific characteristic vs. tachycardia as seen in other shock states

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51
Q

Distributive neurogenic shock can be caused by

A

A spinal cord injury, spinal anesthesia, or nervous system damage

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52
Q

Progression of distributive neurogenic shock

A

Imbalance between sympathetic & parasympathetic stimulation; vasodilation; decreased vascular tone, SVR, CO & tissue perfusion; impaired cellular metabolism

53
Q

Multiple organ dysfunction syndrome

A

-Progressive process that involves the failure of two or more organ systems after a severe illness of injury

54
Q

Multiple organ dysfunction is initiated & perpetuated by an…

A

Uncontrolled system inflammatory and stress responses

55
Q

Multiple organ dysfunction is characterized by…

A

Hypermetabolic & hyperdynamic state that persists as organ dysfunction develops

56
Q

Slide 46

A
57
Q

Pathophysiology of COVID-19 + SARS-CoV-2 (step 1)

A

SARS-CoV-2 enters the host cell by binding to ACE2 receptors in the lung; membrane fusion of the virus and the host cell is activated after the binding, viral RNA is released into the cytoplasm establishing an infection

58
Q

Pathophysiology of COVID-19 + ACE-2 (step 2)

A

ACE-2 is expressed on the type II alveolar epithelial cells, and is weakly expressed on the surface of the epithelial cells, proximal tubule cells of the kidney and bladder urothelial cells, as well as the enterocytes of the small intestine, especially in the ileum

59
Q

Pathophysiology of COVID-19 + RAS (step 3)

A

RAS plays a significant role in COVID-19 infections

60
Q

Post-COVID-19: Long haulers

A

-People showing S&S weeks or months after recovery
-Occurs in some people after infection when they:
-Were hospitalized or needed intensive care during recovery OR
-Had asymptomatic, mild, or severe infection with symptoms

61
Q

Post-COVID-19: Long haulers + adult manifestations

A

-Fatigue, SOB, memory problems, sleep disturbances, difficulty thinking or concentrating
-Anxiety & depression, PTSD and general pain & discomfort

62
Q

Post-COVID-19: Long haulers + child manifestations

A

Fatigue, headaches, sleep disturbances, difficulty thinking or concentrating
-Stuffy or runny nose, weight loss & muscle pain

63
Q

COVID-19 + pediatrics

A

Multisystem Inflammatory Disease:
-Inflammation of the: Heart, lungs, kidneys, brain, skin, eyes and GI
-Increase in children with symptoms of Kawasaki disease

64
Q

Kawasaki disease is an

A

Acute febrile illness of unknown cause that primarily affects children younger than 5 years of age

65
Q

Manifestations of COVID-19 in pediatrics (similar to that of Kawasaki disease)

A

-Fever, vomiting, diarrhea, abdominal & neck pain
-Rash, bloodshot eyes & exhaustion

66
Q

Slide 51

A
67
Q

Physiological consequences of shock in a pediatric patient

A

Hypotension, tissue hypoxia & metabolic acidosis

68
Q

Shock in a pediatric pt results in…

A

Hypovolemia, aPVR or pump failure

69
Q

Slide 54

A
70
Q

Compensated manifestations of shock in pediatrics

A

-Apprehensiveness, irritability, unexplained tachycardia, narrowing pulse pressure
-Thirst, pallor, decreased urinary output and peripheral perfusion

71
Q

Decompensated manifestations of shock in pediatrics

A

-Confusion and somnolence, metabolic acidosis, tachypnea & oliguria
-Cool, pale extremities, decreased skin turgor & poor cap refill

72
Q

Irreversible manifestations of shock in pediatrics

A

Weak & thready pulse, hypotension, periodic breathing or apnea, anuria and stupor/coma

73
Q

Key differentiating signs of the stages of shock in pediatrics are observed in the…

A

Degree of tachycardia, perfusion to extremities, LOC and BP

74
Q

Hypovolemic shock in a pediatric patient

A

-Increase in the force and rate of the cardiac contraction and constriction of arterioles and veins to increase PVR
-Diminished venous return to the heart, low CVP, low CO and hypotension

75
Q

Low volume + hypovolemic shock in a pediatric patient

A

-Low volume releases catecholamines, ADH, adrenocorticosteroids, and aldosterone to conserve volume
-Reduces flow to the skin, kidneys, muscles, and viscera leaving the skin cold and clammy, poor cap refill, and significantly reduced U/O

76
Q

Impaired perfusion + hypovolemic shock in a pediatric patient

A

Leads to hypoxemia producing lactic acidosis

77
Q

Complications of hypovolemic shock in pediatric patients

A

-Cerebral edema, cortical infarction, intraventricular hemorrhage, renal ischemia with tubular or glomerular necrosis and renal vein thrombosis
-ARDS, GIB and perforation associated with splanchnic ischemia and necrosis of intestinal mucosa

78
Q

Electrolye complications in hypovolemic shock in pediatrics

A

Hypoglycemia, hypocalcemia and other electrolyte disturbances

79
Q

Manifestations of anaphylaxis in pediatrics

A

Uneasiness, restlessness, irritability, severe anxiety, headache, dizziness, disorientation, paresthesia

80
Q

Progression of manifestations of anaphylaxis in pediatrics (1)

A

Cutaneous signs of flushing & urticaria are common early signs, followed by angioedema in the eye lids, lips, tongue, hands, feet and genitalia

81
Q

Progression of manifestations of anaphylaxis in pediatrics (2)

A

Bronchiolar constriction, pulmonary edema & hemorrhage, laryngeal edema with acute upper airway obstruction

82
Q

Progression of manifestations of anaphylaxis in pediatrics (3)

A

-Vasodilation, capillary permeability and loss of intravascular fluid
-Sudden hypotension and impaired CO with poor perfusion

83
Q

Please review the Table: Age Specific VS and Laboratory Variables in Septic Shock [Table 47.7, pg. 1276, Keenan-Lindsay et al. (2023)]

A
84
Q

Early septic shock in pediatric patients

A

Chills, fever and vasodilation with increased CO that results in a hyperdynamic phase *

85
Q

Second stage of shock in pediatric patients

A

Normodynamic, cool or hyperdynamic-decompensated stage (lasts only a few hours), skin is cool, but pulses and BP are still normal, U/O diminishes and mental state becomes depressed

86
Q

Late sepsis in septic shock in pediatric patients

A

DIC, signs of circulatory collapse, hypodynamic, hypotension, hypothermia, cold extremities, weak pulses, oliguria or anuria, and severe lethargy or comatose

87
Q

Shock summary

A

-Hypovolemic shock; blood VOLUME problem
-Cardiogenic shock; blood PUMP problem
-Distributive shock; blood VESSEL problem

88
Q

Homeostasis maintains what balances in the body?

A

Temperature, oxygen, carbon dioxide & pH

89
Q

Relationships between pH/hydrogen/buffer systems

A

-Hydrogen is necessary to maintain membrane integrity and speed of enzymatic reactions
-When the balance is disturbed, a severe reaction may occur
-Increased H+ ion causes a decrease in pH

90
Q

Most important parts of the body that maintain the acid/base balance

A

Lungs, kidneys and bones

91
Q

Body acids come in two forms

A

-Volatile acid; respiratory acid (CO2)
-Non-volatile; metabolic acids that are eliminated by kidneys or metabolized by liver

92
Q

Buffers react to changes in the acid-base balance, they are located in the and include

A

-Located in ICF and ECF compartments
-Carbonic acid (H2CO3-), hemoglobin and bicarbonate

93
Q

Finding balance equation

A

pH=Base/Acid = Renal regulation/pulmonary regulation

94
Q

Finding balance

A

-Respiratory compensates for changes in pH by increasing or decreasing ventilation
-Renal system compensates by producing more acidic or more alkaline urine

95
Q

Normal acid-base balances

A

-pH= 7.35-7.45
-CO2= 35-45mmHg (respiratory)
-HCO3-= 22-26mmol/L (kidneys)

96
Q

Metabolic acidosis=

A

-pH<7.35 and HCO3-<22mmol/L

97
Q

In metabolic acidosis…

A

-Noncarbonic acids increase OR bicarbonate base is lost from ECF and cannot be regenerated by the kidneys
-HCO3- lowers the serum value of H+ ions to increase pH
-Respiratory attempts to compensate by increasing ventilation to blow off CO2

98
Q

Anion gap is used to distinguish…

A

The different types of metabolic acidosis

99
Q

Metabolic alkalosis=

A

pH>7.45 and HCO3->26mmol/L

100
Q

Metabolic alkalosis

A

-Occurs when bicarbonate increases or there is a loss of metabolic acids
-Kidneys attempt to hold onto hydrogen acids and reduce urine output
-Respiratory system attempts to hypoventilate

101
Q

Respiratory acidosis=

A

pH<7.35 and CO2>45mmHg

102
Q

Respiratory acidosis

A

-Caused by hypoventilation
-CO2 is retained increasing hydrogen ions

103
Q

Respiratory acidosis is caused by…

A

Respiratory depression, respiratory muscle paralysis, disorders of the chest wall and disorders of the lung parenchyma

104
Q

Respiratory alkalosis=

A

pH>7.45 and CO2<35mmHg

105
Q

Respiratory alkalosis

A

Occurs when there is alveolar hyperventilation and decreased plasma carbon dioxide

106
Q

Respiratory alkalosis is caused by…

A

-Pulmonary disease, CHF, high altitudes and hysteria
-Hypermetabolic states such as fever, anemia or thyrotoxicosis

107
Q

ABG analysis

A

-What direction is the pH moving in?
-What is the CO2 & HCO3-?
-Is the condition uncompensated, partially compensated or fully compensated?

108
Q

Cellular metabolism

A

-Impairment of O2 USE (cells shift to anaerobic metabolism) & glucose use: Cells use ATP (krebs cycle) for energy, without it cells lose the Na+/K+ pump

109
Q

Impaired O2 use & lactic acid

A

Lactice acid use increases and pts go into acidosis. Less O2 carrying capacity, heart works harder & less O2 is delivered (hypoxia to hypoxemia).

110
Q

Decreased blood volume…

A

Increases its viscosity

111
Q

Prevention of muscle wasting in pt with shock

A

Mobilize pts that are in shock to prevent muscle wasting (includes lungs)

112
Q

Etiology of hypovolemia + plasma

A

Burns or insensible losses of plasma (3rd spacing)

113
Q

Cardiogenic shock + HF

A

Caused by right ventricular failure

114
Q

Cardiogenic shock results in…

A

-Vtach or Vfib
-Vfib can be a result of cause of AMI

115
Q

Etiology of cardiogenic shock + AMI

A

-Anterior AMI (involves LAD & circumflex)

116
Q

Hypovolemic shock is a…

A

Type II MI

117
Q

In sepsis…

A

O2 demands cannot be met

118
Q

Histamine & kinins…

A

Increase coagulability

119
Q

SIRS is the…

A

First sign of septic shock/inflammatory response

120
Q

SIRS leads to..

A

Sepsis (SIRS + infection) which leads to septic shock

121
Q

Septic shock is…

A

Sepsis with arterial hypotension despite adequate fluid replacement

122
Q

qSOFA

A

-aMental status (GCS<13), tachypnea (>=22) & low systolic BP (<=100)
-qSOFA is met if you have 2 or more of these
-Used to inform a patients prognosis associated with infection and the level of tx required

123
Q

Early septic shock is & late septic shock is…

A

Early; vasodilation, late; vasoconstriction

124
Q

Order of organ failure

A

GI then GU then intubation then brain and then the heart

125
Q

ACEII is in the…

A

Heart & lungs

126
Q

Hypocalcemia triad

A

CATS; convulsion, arrhythmias (vtach, R on T), tetany & stridor

127
Q

Bicarb is a…

A

Base

128
Q

CO2 >45mmHg indicates…

A

Hypoxemia

129
Q

ROME

A

Respiratory opposite, metabolic equal

CV487 (15 decks)

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