Podcast
Questions and Answers
Systemic Inflammatory Response Syndrome (SIRS) triggers which initial bodily response?
Systemic Inflammatory Response Syndrome (SIRS) triggers which initial bodily response?
- Decreased heart rate and increased urine output.
- Increased GI activity and decreased respiratory rate.
- Activation of the parasympathetic nervous system.
- Increased heart rate and decreased GI activity. (correct)
Which of the following compensatory mechanisms is associated with SIRS (Systemic Inflammatory Response Syndrome)?
Which of the following compensatory mechanisms is associated with SIRS (Systemic Inflammatory Response Syndrome)?
- Increased risk of infection due to immunosuppression. (correct)
- Elevated body temperature above 38°C.
- Decreased respiratory rate below 20 breaths per minute.
- Decreased risk of hospital-acquired infections (HAIs).
What diagnostic criteria is NOT typically associated with Systemic Inflammatory Response Syndrome (SIRS)?
What diagnostic criteria is NOT typically associated with Systemic Inflammatory Response Syndrome (SIRS)?
- Hypothermia with a body temperature lower than 36°C.
- Tachypnea with a respiratory rate greater than 20/min.
- Tachycardia with a heart rate greater than 90/min.
- Bradycardia with a heart rate less than 60/min. (correct)
A patient with sepsis exhibits altered mental status, hypoxemia, and oliguria. Which of the following conditions is most likely developing?
A patient with sepsis exhibits altered mental status, hypoxemia, and oliguria. Which of the following conditions is most likely developing?
A patient in the ICU is diagnosed with Multiple Organ Dysfunction Syndrome (MODS). Which of the following systems is typically affected first?
A patient in the ICU is diagnosed with Multiple Organ Dysfunction Syndrome (MODS). Which of the following systems is typically affected first?
Which of the following is a potential outcome of the "gut theory" in the progression of Multiple Organ Dysfunction Syndrome (MODS)?
Which of the following is a potential outcome of the "gut theory" in the progression of Multiple Organ Dysfunction Syndrome (MODS)?
A patient with ARDS is showing decreasing $O_2$ levels, but normal carbon dioxide levels. What pathological process is likely causing the patients condition?
A patient with ARDS is showing decreasing $O_2$ levels, but normal carbon dioxide levels. What pathological process is likely causing the patients condition?
Which of the following is the most common cause of ARDS (Adult Respiratory Distress Syndrome)?
Which of the following is the most common cause of ARDS (Adult Respiratory Distress Syndrome)?
A patient with acute kidney injury (AKI) is experiencing oliguria. What is the most appropriate intervention to support kidney function?
A patient with acute kidney injury (AKI) is experiencing oliguria. What is the most appropriate intervention to support kidney function?
What formula defines abdominal perfusion pressure (APP) in the context of abdominal compartment syndrome (ACS)?
What formula defines abdominal perfusion pressure (APP) in the context of abdominal compartment syndrome (ACS)?
In abdominal compartment syndrome (ACS), increased intra-abdominal pressure leads to:?
In abdominal compartment syndrome (ACS), increased intra-abdominal pressure leads to:?
Which of the following is a common early sign of disseminated intravascular coagulation (DIC)?
Which of the following is a common early sign of disseminated intravascular coagulation (DIC)?
A patient is suspected of having DIC. Several sites are exhibiting what symptom that indicates the need for further investigation?
A patient is suspected of having DIC. Several sites are exhibiting what symptom that indicates the need for further investigation?
After ruling out other morbid conditions, what physical exam findings would be most important in order to determine brain death?
After ruling out other morbid conditions, what physical exam findings would be most important in order to determine brain death?
During the compensatory stage of shock, what is the primary mechanism by which the body attempts to maintain cardiac output?
During the compensatory stage of shock, what is the primary mechanism by which the body attempts to maintain cardiac output?
In the progressive stage of shock, decreased perfusion to the kidneys, gut, pancreas, and liver primarily results in:
In the progressive stage of shock, decreased perfusion to the kidneys, gut, pancreas, and liver primarily results in:
What is a common endocrine response that counteracts hypoglycemia?
What is a common endocrine response that counteracts hypoglycemia?
Why do lactic acid levels build up during instances of shock?
Why do lactic acid levels build up during instances of shock?
Which hormone is released during shock to inhibit insulin activity and cause increased glucose levels?
Which hormone is released during shock to inhibit insulin activity and cause increased glucose levels?
Increased levels of thromboxane A2 & thromboplastin can have what impact on the endothelium?
Increased levels of thromboxane A2 & thromboplastin can have what impact on the endothelium?
What is the most common cause of cardiogenic shock?
What is the most common cause of cardiogenic shock?
What is a clinical finding described for cardiac tamponade?
What is a clinical finding described for cardiac tamponade?
Disruption of the sympathetic nervous system is the usual cause of this type of shock:
Disruption of the sympathetic nervous system is the usual cause of this type of shock:
Why would blood sugar levels often be elevated in septic shock?
Why would blood sugar levels often be elevated in septic shock?
Flashcards
Systemic Inflammatory Response Syndrome (SIRS)
Systemic Inflammatory Response Syndrome (SIRS)
Overwhelming inflammatory reaction, develops from significant damage to the body
SIRS Clinical Manifestations
SIRS Clinical Manifestations
↑ HR, cardiac output, and RR, ↓ Gl activity and urine output
Compensatory Anti-inflammatory Response Syndrome (CARS)
Compensatory Anti-inflammatory Response Syndrome (CARS)
Immunosuppression after SIRS, can lead to increased infection risk
SIRS Diagnosis
SIRS Diagnosis
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Sepsis or Septicemia
Sepsis or Septicemia
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Sepsis key signs
Sepsis key signs
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Severe Sepsis
Severe Sepsis
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Multiple Organ Dysfunction Syndrome (MODS)
Multiple Organ Dysfunction Syndrome (MODS)
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Most common cause of MODS
Most common cause of MODS
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MODS Clinical Manifestations
MODS Clinical Manifestations
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Clinical Phases of MODS: Stage 1
Clinical Phases of MODS: Stage 1
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Clinical Phases of MODS: Stage 2
Clinical Phases of MODS: Stage 2
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Clinical Phases of MODS: Stage 3
Clinical Phases of MODS: Stage 3
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Clinical Phases of MODS: Stage 4
Clinical Phases of MODS: Stage 4
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ARDS
ARDS
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Indications of ARDS
Indications of ARDS
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Acute Kidney Injury (AKI)
Acute Kidney Injury (AKI)
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AKI Diagnosis
AKI Diagnosis
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Abdominal Compartment Syndrome (ACS)
Abdominal Compartment Syndrome (ACS)
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ACS Clinical Manifestations
ACS Clinical Manifestations
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AKI Diagnosis
AKI Diagnosis
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Treatment of AKI
Treatment of AKI
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Disseminated Intravascular Coagulation (DIC)
Disseminated Intravascular Coagulation (DIC)
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DIC Manifestations
DIC Manifestations
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Treatment of Neurogenic Shock
Treatment of Neurogenic Shock
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Study Notes
Systemic Inflammatory Response Syndrome (SIRS)
- It is an overwhelming inflammatory reaction harming the body
- Sympathetic nervous (SNS) and endocrine responses are similar to the alarm stage of the stress response
- Catecholamines, glucocorticoids, mineralocorticoids, antidiuretic hormone (ADH), and angiotensin II increase
- Results in increased HR, cardiac output, and RR
- Results in decreased GI activity and urine output
Clinical Manifestations
- Increased HR, cardiac output, and RR
- Decreased GI activity and urine output
Diagnosis
- Must have two of the following:
- Tachycardia (HR greater than 90/min)
- Tachypnea (RR greater than 20/min)
- Hyperthermia (higher than 38C) or hypothermia (lower than 36C)
- Leukocytosis (greater than 12,000/m m3)
- Leukopenia (lower than 4,000/m m3)
- Greater than 10% immature forms
Compensatory Anti-inflammatory Response Syndrome (CARS)
- Immunosuppression after SIRS
- Concomitant (associated) with SIRS which leads to increased infection risk (i.e., sepsis)
- Patients become susceptible to HAIs
Possible Progression
- SIRS leads to CARS
- CARS leads to sepsis
- Septic shock may develop
- MODS may develop
- Death
Sepsis or Septicemia
- A body wide infection
- "Bloodstream infection"
- Considered a life-threatening condition where the immune system is overwhelmed
Clinical Manifestations
- Altered mental state
- Hypoxemia (Arterial O2 < 72 mm Hg)
- Elevated plasma lactate level
- Oliguria
Risk Factors
- Immunosuppression
- Older age
Multiple Organ Dysfunction Syndrome (MODS)
- It is a progressive and potentially reversible dysfunction of two or more organs
- Variety of causes; sepsis is the most common
- Leading cause of death in ICU
- Respiratory system is the first system affected, which is a frequent cause of death for many COVID patients
Theories
- Hypoxia- microvascular theory: Microvascular injury prevents O2 delivery
- Gut theory: Decreased blood flow to GI tract, which increases permeability and the GI contents are released
- Endotoxin theory: Endotoxins release from gram-negative bacteria causing widespread inflammation & circulatory collapse
Clinical Manifestations
- Altered LOC, confusion, and psychosis
- Hypoxia
- Tachypnea
- Jaundice
- Increased bili & liver enzymes
- Decreased albumin
- Tachycardia
- HOTN
- Increased lactate
- Oliguria
- Increased Cr
- Petechiae
Clinical Phases
- Stage 1: Increased volume requirements and mild respiratory alkalosis
- Oliguria, hyperglycemia, and increased insulin requirements
- Stage 2: Tachypnic, hypocapnic (low CO2), and hypoxemic with moderate liver dysfunction
- Stage 3: Shock with azotemia (excess urea and creatinine) and acid-base disturbances that include significant coagulation abnormalities
- Stage 4: Vasopressor dependent, oliguric or anuric leading to ischemic colitis and lactic acidosis
ARDS (Adult Respiratory Distress Syndrome)
- Characterized by the widespread injury of alveoli with severe hypoxemia and acute dyspnea
- Considered severe acute lung injury
- Pulmonary artery vasoconstriction is related to hypoxemia, which causes a ventilation-perfusion mismatch
- There is decreased O2 exchange, but carbon dioxide exchange is less affected because carbon dioxide is more soluble
Pathology
- Direct lung injury
- Indirect lung injury
- Injury to lungs causes secretion of cytokines
- Type I epithelial cells have increased alveolar permeability and fluid in alveoli
- Type II epithelial cells are affected and have decreased surfactant
Clinical Manifestations
- Shortness of breath & tachypnea
- Bilateral crackles
- Hypoxia & cyanosis
- HOTN
- Peripheral vasoconstriction with cold extremities
- Muscle fatigue
- General weakness
Diagnosis
- Must differentiate from HF via echocardiogram and BNP levels (helps differentiate from pulmonary edema)
- Chest X-ray
- Arterial blood gases
- Initially hypoxemia drives ventilation & reduces CO2
- Over time, CO2 levels elevate as O2 levels fall
####Treatment
- Treatment of etiology is the most important
- Mechanical ventilation
- Medically induced coma
- Antibiotics often needed
- Prone positioning can be helpful
- ECMO may be helpful
Acute Kidney Injury (AKI)
- Hypotension often leads to hypoperfusion which can result in renal ischemia
- Can be caused by Nephrotoxic drugs which result in renal toxicity
- Nephrons are sensitive to hypoperfusion
- Comorbidities increase risk for AKI
Clinical Manifestations
- U/O needs to be at least 400/day
- Oliguria is < 400 mL/day
- Anuria is less than 100mL a day
Diagnosis
- Elevated serum BUN & Cr
- Brown cast in urinalysis indicating tubular necrosis
####Treatment
- Dialysis
- AKI in ICU patients increases risk of death
Thrombus
- It can occur in response to injury or sluggish/ stagnant blood flow
- Thrombosis is defined as the generation of an occlusive clot
- Clot formation is balanced by process of clot dissolution (fibrinolysis)
Intrinsic Pathway (APTT)
- Injury to vessel, can also be activated by stasis of blood (as occurs in afib) leading to eventual activation of factor X
- Clotting time of intrinsic pathway can be measured by ACTIVATE PARTIAL THROMBOPLASTIN TIME (aPTT)
Extrinsic Pathway (PT AND INR)
- Activation of factor VII comes into contact w/ tissue factor (TF) to form TF-factor VII which eventually leads to activation of factor X
- Clotting time of extrinsic pathway can be measured by PROTHROMBIN TIME (PT) & INTERNATIONAL NORMALIZED RATIO (INR)
Clotting
- Disorders are caused by:
- Increased platelet number and activity
- Increased coagulation activity
Bleeding
- Disorders are caused by:
- Decreased platelet number & activity
- Severely depleted (>20,000 results in with spontaneous bleeding)
- Impaired platelet activity
- Defective coagulation (impaired synthesis of coagulation factors)
Drug-Induced Thrombocytopenia
- Over 1,500 medications, herbal, and OTC meds may be to blame, and misdiagnosed as platelet autoimmune destruction
Heparin-Induced Thrombocytopenia (HIT)
- HIT, on the other hand, involves clot formation
- An antibody to heparin
Intrinsic & Extrinsic Pathways of the Clotting Cascade
- KNOW WHAT'S IN RED!! ​
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