Class 11: Multi-system dysfunction Flashcards
1
Q
Types of shock
A
Hypovolemic, cardiogenic & distributive
2
Q
Types of distributive shock
A
Sepsis, anaphylaxis & neurogenic
3
Q
Assess what in all types of shock
A
Acid-base analysis, especially in septic shock
4
Q
Types of cardiogenic shock
A
Obstructive
5
Q
Definition of shock
A
-A clinical syndrome resulting in cellular hypoxia, accumulation of cellular metabolic wastes, cellular destruction, and organ & system failure
6
Q
Shock begins as an…
A
Adaptive response, progressing to multi-system organ failure
7
Q
Interactive mechanisms of shock lead to…
A
-Decreased intravascular volume & myocardial contractility
-Increased venous capacitance
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
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
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
11
Q
Impaired glucose use is caused by…
A
Either impaired glucose delivery to the cells or uptake by the cells
12
Q
When glucose is impaired, cells perform…
A
Glycogenolysis, gluconeogenesis, and lipolysis to generate fuel for survival
13
Q
Gluconeogenesis causes…
A
A depletion of protein & subsequent muscle wasting that weakens skeletal & cardiac muscles
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)
15
Q
Slide 9
A
16
Q
Normal compensatory mechanisms
A
Normal BP, >100HR, >20breaths/min, cold/clammy skin, decreased urine output, confusion & respiratory alkalosis
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
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
19
Q
Hypovolemia
A
-Insufficient volume within the vascular space
-Decreased perfusion to tissues leading to hypoxia
20
Q
Etiology of hypovolemia
A
-Loss of whole blood
-Loss of plasma, fluid and interstitial fluid
21
Q
Pathophysiology of hypovolemic shock
A
Decreased blood volume; decreased venous return; decreased SV; decreased CO; decreased tissue perfusion
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
23
Q
Manifestations of hypovolemia
A
-Low systemic and pulmonary preloads & high afterload (SVR)
-Poor skin turgor, thirst, oliguria
-High HR & low BP
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
25
Etiology of decreased contractility in cardiogenic shock
AMI, cardiomyopathy, dysrhythmias, myocarditis, metabolic abnormalities, sepsis and papillary muscle rupture
26
Cardiogenic shock + etiology for pump failure
-Impaired diastolic filling arrhythmias is caused by obstructions such as:
-PE, cardiac tamponade, valvular disorders & wall rupture or defects
27
Cardiogenic shock pathophysiology
-Decreased contractility & SV leading to pulmonary congestion, decreased tissue perfusion & coronary artery perfusion
28
Slide 21
29
Subjective cardiogenic shock manifestations
-Chest pain, dyspnea
-Feeling faint & impending doom
30
Classic cardiogenic shock objective manifestations
-Tachycardia, tachypnea & JVD
-Hypotension, low CO & dysrhythmia
31
Additional signs of cardiogenic shock
-Cyanosis & mottling
-Rapid, faint or irregular pulses
-Low U/O, peripheral edema
-Symptoms of end organ failure
32
Pathophysiology of distributive shock
-Vasodilation & maldistribution of blood volume
-Decreased venous return, SV, CO & tissue perfusion
33
How distributive septic shock begins
-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
34
Inflammatory response of distributive shock
-Vasodilation
-Increased microvascular permeability
-Cellular activation
-Coagulation
35
Inflammatory response of distributive shock + vasodilation
Nutrient delivery & cellular access
36
Inflammatory response of distributive shock + increased microvascular permeability
Nutrient transport & cellular access
37
Inflammatory response of distributive shock + cellular activation
Phagocytosis, host protection, wound healing, further mediator stimulation (histamine, kinins, & prostaglandins)
38
Inflammatory response of distributive shock + coagulation
Prevents blood loss and walls off the injury
39
SIRS in distributive shock
-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
40
Manifestations of SIRS
-General non-specific symptoms
-Fever, malaise, weakness, aching & loss of appetite
41
Definition of septic shock
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
42
Progression of septic shock
-Sepsis: SIRS + infection
-Septic shock: Sepsis with profound hypotension and perfusion abnormalities despite fluid resuscitation
-Multi-organ dysfunction syndrome
43
Slide 34`
44
Common sources of sepsis you will encounter in acute care
-UTIs leading to urosepsis
-Pneumonia leading to full systemic sepsis
-Integumentary; necrotizing fasciitis
45
What a pt with septic shock looks like
-Hypotensive, tachycardic, febrile, decreased SVR, depressed myocardial function & lactic acidosis
-Leukopenia or leukocytosis, thrombocytopenia
-Vascular leakage, pulmonary congestion, tissue necrosis & organ failure
46
Distributive anaphylactic shock
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
47
An antigen-antibody reaction causes..
Mast cells to release vasodilators such as histamine and bradykinin causing increased capillary permeability
48
Slide 39&40
49
Anaphylaxis clinical manifestations
-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
50
Distributive neurogenic shock
-Vasodilation occurs as a result of a loss of sympathetic tone
-Bradycardia is a specific characteristic vs. tachycardia as seen in other shock states
51
Distributive neurogenic shock can be caused by
A spinal cord injury, spinal anesthesia, or nervous system damage
52
Progression of distributive neurogenic shock
Imbalance between sympathetic & parasympathetic stimulation; vasodilation; decreased vascular tone, SVR, CO & tissue perfusion; impaired cellular metabolism
53
Multiple organ dysfunction syndrome
-Progressive process that involves the failure of two or more organ systems after a severe illness of injury
54
Multiple organ dysfunction is initiated & perpetuated by an...
Uncontrolled system inflammatory and stress responses
55
Multiple organ dysfunction is characterized by...
Hypermetabolic & hyperdynamic state that persists as organ dysfunction develops
56
Slide 46
57
Pathophysiology of COVID-19 + SARS-CoV-2 (step 1)
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
Pathophysiology of COVID-19 + ACE-2 (step 2)
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
Pathophysiology of COVID-19 + RAS (step 3)
RAS plays a significant role in COVID-19 infections
60
Post-COVID-19: Long haulers
-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
Post-COVID-19: Long haulers + adult manifestations
-Fatigue, SOB, memory problems, sleep disturbances, difficulty thinking or concentrating
-Anxiety & depression, PTSD and general pain & discomfort
62
Post-COVID-19: Long haulers + child manifestations
Fatigue, headaches, sleep disturbances, difficulty thinking or concentrating
-Stuffy or runny nose, weight loss & muscle pain
63
COVID-19 + pediatrics
Multisystem Inflammatory Disease:
-Inflammation of the: Heart, lungs, kidneys, brain, skin, eyes and GI
-Increase in children with symptoms of Kawasaki disease
64
Kawasaki disease is an
Acute febrile illness of unknown cause that primarily affects children younger than 5 years of age
65
Manifestations of COVID-19 in pediatrics (similar to that of Kawasaki disease)
-Fever, vomiting, diarrhea, abdominal & neck pain
-Rash, bloodshot eyes & exhaustion
66
Slide 51
67
Physiological consequences of shock in a pediatric patient
Hypotension, tissue hypoxia & metabolic acidosis
68
Shock in a pediatric pt results in...
Hypovolemia, aPVR or pump failure
69
Slide 54
70
Compensated manifestations of shock in pediatrics
-Apprehensiveness, irritability, unexplained tachycardia, narrowing pulse pressure
-Thirst, pallor, decreased urinary output and peripheral perfusion
71
Decompensated manifestations of shock in pediatrics
-Confusion and somnolence, metabolic acidosis, tachypnea & oliguria
-Cool, pale extremities, decreased skin turgor & poor cap refill
72
Irreversible manifestations of shock in pediatrics
Weak & thready pulse, hypotension, periodic breathing or apnea, anuria and stupor/coma
73
Key differentiating signs of the stages of shock in pediatrics are observed in the...
Degree of tachycardia, perfusion to extremities, LOC and BP
74
Hypovolemic shock in a pediatric patient
-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
Low volume + hypovolemic shock in a pediatric patient
-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
Impaired perfusion + hypovolemic shock in a pediatric patient
Leads to hypoxemia producing lactic acidosis
77
Complications of hypovolemic shock in pediatric patients
-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
Electrolye complications in hypovolemic shock in pediatrics
Hypoglycemia, hypocalcemia and other electrolyte disturbances
79
Manifestations of anaphylaxis in pediatrics
Uneasiness, restlessness, irritability, severe anxiety, headache, dizziness, disorientation, paresthesia
80
Progression of manifestations of anaphylaxis in pediatrics (1)
Cutaneous signs of flushing & urticaria are common early signs, followed by angioedema in the eye lids, lips, tongue, hands, feet and genitalia
81
Progression of manifestations of anaphylaxis in pediatrics (2)
Bronchiolar constriction, pulmonary edema & hemorrhage, laryngeal edema with acute upper airway obstruction
82
Progression of manifestations of anaphylaxis in pediatrics (3)
-Vasodilation, capillary permeability and loss of intravascular fluid
-Sudden hypotension and impaired CO with poor perfusion
83
Please review the Table: Age Specific VS and Laboratory Variables in Septic Shock [Table 47.7, pg. 1276, Keenan-Lindsay et al. (2023)]
84
Early septic shock in pediatric patients
Chills, fever and vasodilation with increased CO that results in a hyperdynamic phase *
85
Second stage of shock in pediatric patients
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
Late sepsis in septic shock in pediatric patients
DIC, signs of circulatory collapse, hypodynamic, hypotension, hypothermia, cold extremities, weak pulses, oliguria or anuria, and severe lethargy or comatose
87
Shock summary
-Hypovolemic shock; blood VOLUME problem
-Cardiogenic shock; blood PUMP problem
-Distributive shock; blood VESSEL problem
88
Homeostasis maintains what balances in the body?
Temperature, oxygen, carbon dioxide & pH
89
Relationships between pH/hydrogen/buffer systems
-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
Most important parts of the body that maintain the acid/base balance
Lungs, kidneys and bones
91
Body acids come in two forms
-Volatile acid; respiratory acid (CO2)
-Non-volatile; metabolic acids that are eliminated by kidneys or metabolized by liver
92
Buffers react to changes in the acid-base balance, they are located in the and include
-Located in ICF and ECF compartments
-Carbonic acid (H2CO3-), hemoglobin and bicarbonate
93
Finding balance equation
pH=Base/Acid = Renal regulation/pulmonary regulation
94
Finding balance
-Respiratory compensates for changes in pH by increasing or decreasing ventilation
-Renal system compensates by producing more acidic or more alkaline urine
95
Normal acid-base balances
-pH= 7.35-7.45
-CO2= 35-45mmHg (respiratory)
-HCO3-= 22-26mmol/L (kidneys)
96
Metabolic acidosis=
-pH<7.35 and HCO3-<22mmol/L
97
In metabolic acidosis...
-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
Anion gap is used to distinguish...
The different types of metabolic acidosis
99
Metabolic alkalosis=
pH>7.45 and HCO3->26mmol/L
100
Metabolic alkalosis
-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
Respiratory acidosis=
pH<7.35 and CO2>45mmHg
102
Respiratory acidosis
-Caused by hypoventilation
-CO2 is retained increasing hydrogen ions
103
Respiratory acidosis is caused by...
Respiratory depression, respiratory muscle paralysis, disorders of the chest wall and disorders of the lung parenchyma
104
Respiratory alkalosis=
pH>7.45 and CO2<35mmHg
105
Respiratory alkalosis
Occurs when there is alveolar hyperventilation and decreased plasma carbon dioxide
106
Respiratory alkalosis is caused by...
-Pulmonary disease, CHF, high altitudes and hysteria
-Hypermetabolic states such as fever, anemia or thyrotoxicosis
107
ABG analysis
-What direction is the pH moving in?
-What is the CO2 & HCO3-?
-Is the condition uncompensated, partially compensated or fully compensated?
108
Cellular metabolism
-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
Impaired O2 use & lactic acid
Lactice acid use increases and pts go into acidosis. Less O2 carrying capacity, heart works harder & less O2 is delivered (hypoxia to hypoxemia).
110
Decreased blood volume...
Increases its viscosity
111
Prevention of muscle wasting in pt with shock
Mobilize pts that are in shock to prevent muscle wasting (includes lungs)
112
Etiology of hypovolemia + plasma
Burns or insensible losses of plasma (3rd spacing)
113
Cardiogenic shock + HF
Caused by right ventricular failure
114
Cardiogenic shock results in...
-Vtach or Vfib
-Vfib can be a result of cause of AMI
115
Etiology of cardiogenic shock + AMI
-Anterior AMI (involves LAD & circumflex)
116
Hypovolemic shock is a...
Type II MI
117
In sepsis...
O2 demands cannot be met
118
Histamine & kinins...
Increase coagulability
119
SIRS is the...
First sign of septic shock/inflammatory response
120
SIRS leads to..
Sepsis (SIRS + infection) which leads to septic shock
121
Septic shock is...
Sepsis with arterial hypotension despite adequate fluid replacement
122
qSOFA
-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
Early septic shock is & late septic shock is...
Early; vasodilation, late; vasoconstriction
124
Order of organ failure
GI then GU then intubation then brain and then the heart
125
ACEII is in the...
Heart & lungs
126
Hypocalcemia triad
CATS; convulsion, arrhythmias (vtach, R on T), tetany & stridor
127
Bicarb is a...
Base
128
CO2 >45mmHg indicates...
Hypoxemia
129
ROME
Respiratory opposite, metabolic equal
