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Sem2: MDSA30160: Cardiorespiratory Disease > L10 Shock and Burns > Flashcards

L10 Shock and Burns Flashcards

1
Q

Cardiovascular collapse with reduced cardiac output & reduced circulating blood volume?

What does this lead to?

A

SHOCK = Cardiovascular collapse with reduced cardiac output & reduced circulating blood volume

Leads to:

Systemic hypotension => Hypoperfusion => Tissue hypoxia

Initially, tissue hypoxia/injury is reversible but w/ persistence tissue injury becomes irreversible (hypoxic effects)

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2
Q

Typical signs of Shock?

A

Typical signs of shock are low blood pressure, rapid heart rate

Also:

weak pulse,

low urine output,

confusion/ loss of consciousness

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3
Q

Causes of Hypovolemic Shock?

A
  1. Hemorrage
  2. Fluid Loss
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4
Q

Causes of Cardiogenic Shock?

A
  1. Cardiac Muscle Damage
  2. Arrythmias
  3. Mechanical Abnormalities
  4. Extra-Cardiac Abnormalities
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5
Q

Causes of Distributive Shock?

A
  1. Septic Shock (overwhelming Infection)
  2. Toxic Shock Syndrome (Superantigens from Strep. Pyogenes / Staph Aureus)
  3. Anaphylactic Shock (IgE Mediated Hypersenentivity Reaction)
  4. Neurogenic Shock (CNS or Spinal Injury)
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6
Q

What occurs during the First Stage of Shock?

A
  1. Non-progressive stage (compensatory)
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7
Q

What occurs during the Progressive (2nd Stage) of Shock?

A

Progressive stage: compensatory mechanisms overwhelmed =>Widespread tissue hypoxia

Due to persistent oxygen deficit => aerobic respiration replaced by Anaerobic glycolysis → excess production of LACTIC ACID => METABOLIC LACTIC ACIDOSIS

Lowers tissue pH => Impaired Vasomotor Repsonse

=> arteriolar dilatation & pooling of blood in the peripheral circulation

=>Decreases CO

=> Widespread tissue hypoxia

=>Vital organs begin to fail

Worsening hypoxia puts the vascular endothelial cells at risk of developing an anoxic injury

→ development of DIC –Disseminated Intravascular Coagulation.

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8
Q

What does hypoxia during Shock put the vascular endothelial cells at risk of developing?

A

anoxic injury → development of DIC –Disseminated Intravascular Coagulation.

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9
Q

What occurs during the Irreversible (3rd Stage) of Shock?

A

Irreversible stage (end organ Disfunction): Hypoxic → Cells begin to die

Widespread cell injury => lysosomal enzyme leakage => worsens shock

Reduced myocardial contractility (in part due to nitric oxide synthesis)

Coma/ Death

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10
Q

____________________:

Destruction of tubular epithelial cells with acute suppression of renal function.

The most common cause of acute renal failure

Causes?

A

Acute Tubular Necrosis (ATN):

Destruction of tubular epithelial cells with acute suppression of renal function.

Most common cause of acute renal failure

Causes:

Ischemic: As seen w/ shock

Due to inadequate renal blood flow (hypotension and shock)

Ischemia => vasoconstriction => reduced glomerular filtration rate

Nephrotoxic:

Due to:

Drugs (cisplatin, methotrexate, gentamycin)

Hemoglobin (transfusion reaction, malaria)

Myoglobin (from crush injury, myositis, muscle toxins)

Ig light chains (myeloma)

Ethylene glycol, mercury, lead, radiographic contrast agents

Greatest injury is to p_roximal convoluted tubule_s

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11
Q

Examples of Shock Lung?

How does it manifest?

A

Diffuse Alveolar Damage (DAD)

Adult Respiratory Distress Syndrome (ARDS)

Manifestation:

Rapid onset of severe, life-threatening respiratory insufficiency

Cyanosis

Severe arterial hypoxemia refractory to oxygen therapy

Severe pulmonary edema

Diffuse alveolar infiltration on x-ray

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12
Q

Shock Lung

Causes?

Pathophysiology/Gross?

Microscopy?

A

Causes: Sepsis, aspiration, diffuse pulmonary infections, mechanical trauma,; also other injury, inhaled irritants, chemical injury, radiation, amiodarone, chemotherapy, acute pancreatitis, burns or uremia

Pathophysiology: Diffuse damage to alveolar capillary walls in both lungs

Gross: Heavy, firm, red, and boggy lung

Microscopy: Congestion and hemorrhage, interstitial and intra-alveolar edema, fibrin deposition, hyaline membrane (composed of edema fluid and cellular debris) foam-like substance inhibiting gas exchange

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13
Q

Cardinal Findings Common to all types of shock? (5)

A

Clinical/Cardinal Findings Common to all types of shock

Hypotension

  • Absolute: systolic BP <90mmHg
  • Relative: drop in systolic BP of >40mmHg

Oliguria (Decreases in Urine Production

Altered mental status

Agitation → confusion/delirium → coma

Cool, clammy skin

Metabolic acidosis (LACTATE LEVELS!!!)

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14
Q

____________ Levels are an important indicator of shock

A

Lactate Levels are an important indicator of shock

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15
Q

Symptoms/Signs of Hypovolemic Shock?

A

Hypovolemic Shock

Symptoms:

  • vomiting*
  • diarrhea*
  • hematemesis*
  • hematochezia*
  • trauma*

Signs:

  • dry skin/tongue/oral mucosa*
  • decreased skin turgor*
  • postural hypotension*
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16
Q

Symptoms/Signs of Cardiogenic shock?

A

Cardiogenic shock

Symptoms:

  • dyspnea*
  • chest pain*
  • palpitations*

Signs:

  • murmur*
  • muffled heart sounds*
  • diminished peripheral pulses*
  • diffuse crepitations*
17
Q

Symptoms/Signs of Distributive Shock?

A

Distributive (Septic /Anaphylactic/ Neurogenic) Shock Manifests as

Symptoms

  • chills*
  • headache*
  • photophobia*
  • cough*
  • dyspnea*
  • dysuria*
  • hematuria*
  • abdominal pain*
  • rash*

Signs:

  • fever*
  • tachypnoea*
  • tachycardia*
  • abnormal mental state*
  • meningism*
18
Q

__________ =Presence of bacteria within the bloodstream

A

Bacteremia =Presence of bacteria within the bloodstream

19
Q

___________= Microorganisms (bacteria, viruses, fungi) in the blood stream

A

Septicemia= Microorganisms (bacteria, viruses, fungi) in the blood stream

20
Q

What is Systemic Inflammatory Response Syndrome (SIRS)?

A

Systemic Inflammatory Response Syndrome (SIRS): clinical response to an infectious or non-infectious origin (surgical procedures, trauma, medications, and therapies)

Defined as 2 or more of the following variables:

Fever or hypothermia

Tachycardia

Increased blood pressure

Raised WCC

21
Q

What is Sepsis/ How does it occur?

A

Sepsis: systemic response to infection and is defined as the presence of SIRS in addition to a documented or presumed infection.

Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body => triggers a cascade of changes damaging organ systems, causing them to fail

22
Q

What is Septic Shock?

What is its predominant cause?

A

Septic Shock: results from the spread/expansion of an initially localized infection (abscess, pneumonia/peritonitis) into the bloodstream (septicemia)

70% cases due to Endotoxin-producing gram-negative bacteria (endotoxin shock)

Endotoxin = Lipopolysaccharides (LPS) in walls of bacteria

23
Q

4 Effects of the Cytokines and Secondary mediators in Septic Shock?

A

Effects of the cytokines and secondary mediators:

  1. Systemic vasodilation & hypotension
  2. Decreased myocardial contractility & decreased CO
  3. Widespread endothelial injury & activation resulting in:
    - Systemic leukocyte adhesion
    - Pulmonary alveolar-capillary damage (DAD/ARDS)
    - Activation of the coagulation cascade
  4. Multiorgan failure and Death
24
Q

3 Cardinal signs of Inflammation?

A

Cardinal signs of inflammation:

  1. Leucocyte accumulation (WBC)
  2. Vasodilation
  3. Vascular permeability
25
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

DIC is a systemic process producing both thrombosis and hemorrhage

An acquired/secondary syndrome characterized by excessive activation of coagulation

=> eventual overwhelming of anticoagulant and fibrinolytic systems

=> Tissue ischemia

26
Q

What does excessive free, circulating, unopposed thrombin and plasmin as seen in DIC result in?

A

Excessive free, circulating, unopposed thrombin and plasmin results in:

=> Activation and consumption of platelets, coagulation factors, fibrinogen and fibrin

=> Depletion of anticoagulant proteins (protein C, protein S and antithrombin)

=> Generation of D-dimers and fibrin degradation products

27
Q

Disseminated Intravascular Coagulation is often associated with ___________

A

DIC is often associated w/ Obstetric complications (abruption placenta, retained fetus, septic abortion)

28
Q

Clinical Features of Disseminated Intravascular Coagulation (DIC)? Bloods?

A

Clinical Features of Disseminated Intravascular Coagulation (DIC)?

Bleeding, Thrombosis or both

BLOODS:

↓Platelets

↓Fibrinogen

↑Prothrombin time (PT)

↑Activated partial thromboplastin time (PTT)

↑D-dimers

29
Q

Classification of Burns?

A

1st degree: s_uperficial epithelium_

erythematous w/pain, edema, skin peeling; does not scar

2nd degree: full-thickness epidermis and superficial dermis

skin appendages are spared; blistering, painful; usually do not scar

3rd degree: involves all skin layers, including full-thickness dermis and skin appendages

no pain due to nerve injury; appears white; severe scarring

4th degree: complete destruction of skin, subcutaneous tissue and possibly bone

30
Q

Guidelines for Documenting Thermal Injury?

A

Documenting Thermal Injury:

Rule of 9’s (Adults)

Rule of 5’s (Infants)

31
Q

Mechanism of Death in Thermal Injuries?

A

Delayed mechanism of death due to thermal injury

–Delayed hypovolemic shock with renal failure

–ARDS

–Infection (pneumonia, sepsis/septic shock, cutaneous)

–Pulmonary embolus due to immobilization

Immediate mechanism of death due to thermal injury

–Neurogenic shock secondary to severe pain

–Hypovolemic shock and acute renal failure due to loss of fluid from skin

–Toxic gas inhalation –Carbon monoxide/CO (most common), cyanide, acrolein, nitrogen dioxide, hydrochloric acid - Often see soot in nose/mouth

Sem2: MDSA30160: Cardiorespiratory Disease (24 decks)

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