L10 Shock and Burns Flashcards by Jackson Barrett

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

What does this lead to?

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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Typical signs of Shock?

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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Causes of Hypovolemic Shock?

Hemorrage
Fluid Loss

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Causes of Cardiogenic Shock?

Cardiac Muscle Damage
Arrythmias
Mechanical Abnormalities
Extra-Cardiac Abnormalities

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Causes of Distributive Shock?

Septic Shock (overwhelming Infection)
Toxic Shock Syndrome (Superantigens from Strep. Pyogenes / Staph Aureus)
Anaphylactic Shock (IgE Mediated Hypersenentivity Reaction)
Neurogenic Shock (CNS or Spinal Injury)

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What occurs during the First Stage of Shock?

Non-progressive stage (compensatory)

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

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

anoxic injury → development of DIC –Disseminated Intravascular Coagulation.

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

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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____________________:

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

The most common cause of acute renal failure

Causes?

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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Examples of Shock Lung?

How does it manifest?

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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Shock Lung

Causes?

Pathophysiology/Gross?

Microscopy?

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

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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____________ Levels are an important indicator of shock

Lactate Levels are an important indicator of shock

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Symptoms/Signs of Hypovolemic Shock?

Hypovolemic Shock

Symptoms:

vomiting*
diarrhea*
hematemesis*
hematochezia*
trauma*

Signs:

dry skin/tongue/oral mucosa*
decreased skin turgor*
postural hypotension*

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Symptoms/Signs of Cardiogenic shock?

Cardiogenic shock

Symptoms:

dyspnea*
chest pain*
palpitations*

Signs:

murmur*
muffled heart sounds*
diminished peripheral pulses*
diffuse crepitations*

Symptoms/Signs of Distributive Shock?

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*

__________ =Presence of bacteria within the bloodstream

Bacteremia =Presence of bacteria within the bloodstream

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

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

What is Systemic Inflammatory Response Syndrome (SIRS)?

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

What is Sepsis/ How does it occur?

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

What is Septic Shock?

What is its predominant cause?

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

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

Effects of the cytokines and secondary mediators:

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

3 Cardinal signs of Inflammation?

Cardinal signs of inflammation:

Leucocyte accumulation (WBC)
Vasodilation
Vascular permeability

What is Disseminated Intravascular Coagulation (DIC)?

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**

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

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

Disseminated Intravascular Coagulation is often associated with \_\_\_\_\_\_\_\_\_\_\_

DIC is often associated w/ **_Obstetric complications_** (abruption placenta, retained fetus, septic abortion)

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

Clinical Features of Disseminated Intravascular Coagulation (DIC)? **Bleeding**, **Thrombosis** or **both** _BLOODS:_ ↓Platelets ↓Fibrinogen ↑Prothrombin time (PT) ↑Activated partial thromboplastin time (PTT) ↑D-dimers

Classification of Burns?

**1st degree**: s_uperficial epithelium_ erythematous w/pain, edema, skin peeling; does not scar **2nd degre**e: _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

Guidelines for Documenting Thermal Injury?

Documenting Thermal Injury: Rule of 9's (Adults) Rule of 5's (Infants)

Mechanism of Death in Thermal Injuries?

_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