Pathophysiology 2 > Shock > Flashcards

Shock Flashcards

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1
Q

Shock: Defined

A

Lack of oxygen to the tissues that results in cells using anaerobic metabolism resulting in production of lactic acid (higher lactic high probability of mortality)

Lactic acid will also be produce with hypoxemia

When this state persists there will be an impaired organ function, irreversiable cell damage and death, hypotension, and oliguria (decreased urine output)

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2
Q

Classificiations of Shock

A

Hypovolemic

  • Decreased BP caused by a decrease of blood volume
  • Can be due to loss of blood or loss of fluid in general.

Cardiogenic

  • Decreased BP caused by failure of the heart’s ability to pump blood forward

Distributive

  • Widespread vasodilation( Decreased SVR) resulting in a relative hypovolemia
  • Can be septic, anaphylactic or neurogenicin origin

Obstructive

  • Decreased BP caused by an impedance to the filling of the heart or an obstruction to blood leaving the heart
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3
Q

Hypovolemic Shock Defintiion

A

The state where inadequate tissue perfusion results from lack of blood volume and corresponding decreased CO

Very common in COPD Exasterbationdue to the decrease appeities

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4
Q

Hypovolemic Shock Etiology

A

Can be due to acute blood loss or signifiant fluid loss

  • Acute Blood Loss (can be internal or external)
    • Trauma
    • GI bleed-Internal so it is easy to miss at first
    • Vascular (ruptured AAA)
    • Pregnancy related-placenta previa, ruptured ectopic pregnancy
    • Most hypovolemic shock is due to this “hemorrhagic shock”
  • Significant fluid loss
    • Extensive burns​
    • Inadequate fluid intake
    • Excessive diarrhea
    • Excessive vomiting
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5
Q

Hypovolemic Stage One

A
  • Blood loss < 10% Circulating blood volume is decreased but not enough to cause serious effects
  • Signs & Symptoms:
    • None; comparable to a blood donation
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6
Q

Hypovolemic Stage Two

A
  • Blood loss ~ 10-25%
    • Compensatory mechanisms maintain BP (increase HR and SVR)
    • Tissue perfusion is maintained at an adequate level to prevent cell damage
  • Signs & Symptoms:
    • Minimal increase in HR but < 100 bpm
    • Slightly ¯BP (but still in normal range)
    • Mild evidence of peripheral vasoconstriction (Cool hands/feet)
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7
Q

Hypovolemic Stage Three

A
  • Blood loss ~25 – 35%
    • Unfavorable signs appear as compensatory mechanisms can no longer maintain BP
    • Impaired blood flow to the vital organs
    • Cells and their enzyme systems are damaged
    • Capillary permeability

Signs & Symptoms:

  • Tachycardia
  • Decrease in pulse pressure
  • BP low to low/normal
  • Lactic acidosis
  • Altered LOC
  • Diaphoretic
  • Pallor
  • Oliguria
  • Extreme thirst
  • Rapid deep respirations
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8
Q

Hypovolemic Stage Four

A

Irreversible stage

Sustained hypoperfusion leads to irreversible multi-system organ failure

Even if blood volume is restored and vital signs stabilized, death will likely ensue due to MSOF

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9
Q

Hypovolemic Shock

Lab Findings

A
  • Hemoglobinand hematocrit
    • If due to blood loss: decreased Hbg, and possibly Hctif the patient has been fluid resuscitated
    • If due to fluid loss: Increased Hbg and Hctdue to hemoconcentration(same # of cells in a ¯volume)
  • Increased lactate levels
    • Due to poor peripheral circulation
    • Cells are not receiving oxygen and \using anaerobic metabolism
    • pH will correlate with the severity of the acidosis
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10
Q

Hypovolemic Shock

Management

A

Main goal = Fluid Resuscitation!!

  • Blood or blood products
  • Administered based on Hbgand Hctlevels
  • IV fluids
  • Crystalloids (e.g., NS, Ringer’s lactate)
  • Colloids (e.g., Pentaspan, albumin)

Supportive Care

  • Oxygen and/or mechanical ventilation as required
  • Frequent monitoring of:
  • Vital signs: especially HR and BP
  • Urine output
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11
Q

Cardiogenic Shock Definition

A

The state where inadequate tissue perfusion results from cardiac dysfunction/failure and the resultant decrease in CO.

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12
Q

Cardiogenic Shock Etiology

A
  • Myocardial infarction**
    • Cardiogenicshock is most often associated with anterior MI
  • Myocardial contusion
  • Myocarditis
  • End-stage cardiomyopathy
  • Prolonged cardiopulmonary bypass
  • Valvular dysfunction
  • Cardiac arrhythmias
    • Vtach, bradyarrhythmias, tachyarrhythmias
  • CAD
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13
Q

Cardiogenic Shock Clinical Manifestations

A

The “classic” shock symptoms:

  • Thirst
  • Hypotension
  • Cool and clammy skin
  • Cyanosis
  • Poor mentation
  • Oliguria/anuria

Also the S & S related to heart failure:

  • Peripheral edema, JVD, hepatomegaly, ascites…
  • Pulmonary edema, frothy pink secretions, tachypnea…
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14
Q

Cardiogenic Shock Lab Findings

A
  • Increased lactate will correspond with a decreased pH
    • Due to the hypoperfusion of cells using anaerobic metabolism
  • Increase cardiac enzyme
    • if MI occuring
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15
Q

Normal Lactate

A
  1. 5 to 19.8 mg/dL
  2. 5 to 2.2 mmol/L
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16
Q

Cardiogenic Shock

Management

A

Reduced preload but optimizing fluid volume

  • Diuretics, nitroglycerin, morphie

Reduce afterload

  • B-blockers, ACE inhibitors, nitroglycerin

Inotropic Drugs (Ex. Epi, Aminodarone, dig)

  • Used with caution as result in increased afterload and tachycardia (both which increase demand on the heart!)
  • “Inodilators” a better choice as also decrease demand
  • Some Beta agonists (dobutamine), dopaminergics(dopamine), phosphodiesteraseinhibitors (milrinone).

Assisting the heart

  • IABP or ventricular assist device
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17
Q

Distributive Shock Definition

A

The state where inadequate tissue perfusion results from a “maldistribution” of blood due to a reduced SVR.

Characterized by loss of blood vessel tone resulting in a relative hypovolemia

Widespread vasodilation results in an increase in the amount of blood the vasculature can hold (especially the venous system)

This causes pooling of the blood away from the heart and central circulation and reduced venous return

While the circulating blood volume is normal it is insufficient to provide adequate cardiac filling

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18
Q

Types of Distributive Shock

A

There is three types of distributive shock

  1. Neurogenic shock
  2. Anaphylactic shock
  3. Septic Shock - Infection in the blood and can lead to ARDS
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19
Q

Distributive Shock

Loss of Vessel Tone

A

The loss of vessel tone is from one of two mechanisms:

  1. Decreased sympathetic control over vessel tone
  2. Presence of vasodilatorysubstances in the blood
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20
Q

Distributive Shock-Neurogenic Shock

Etiology

A

Due to defect in the vasomotor center of the brain or blockage of the sympathetic impulses

Caused by:

  • Head injury
  • Spinal cord injuries
  • Spinal anesthesia
  • General anesthesia
  • Depressant drugs
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21
Q

Distributive Shock-Neurogenic Shock

Hemodynamic Parameters

A

Decreased SVR

Decreased CVP

Decreased PAP and PAWP as blood pools in periphery decreasing venous return

Decreased CO 2°to Decreased HR and Decreased venous return

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22
Q

Distributive Shock-Neurogenic Shock

Clinical Manifestations

A

Bradycardia

  • Due to imbalance between S and PS stimulation

Skin is usually warm and dry

  • With other shock types it tends to be cool and clammy 2° to peripheral vasoconstriction—here we have vasodilation

•Hemodynamic parameters

§¯¯SVR

§¯CVP (and ¯PAPs, ¯PAWP) as blood pools in periphery decreasing venous return

¯CO 2°to¯HR and ¯venous return

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23
Q

Distributive Shock-Neurogenic Shock

Lab Findings

Study These Flashcards
A

If prolonged

  • Lactic acidosis and corresponding¯pH
24
Q

Distributive Shock-Neurogenic Shock

Management

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A

Fluid management

Sympathomimetic agents

For vasoconstricting effects to increase SVR

For positive chronotropic effects to increase HR

25
Distributive Shock-Anaphylactic Shock Etiology
Immune mediated reaction to an antigen * The allergen triggers WIDESPREAD mast cell degranulation which releases vasodilator substances into the blood (histamine, leukotrienes and others) * Result is massive vasodilation, pooling of the blood in the peripheral vessels and increased permeability of the capillaries
26
Distributive Shock-Anaphylactic Shock Potential Allergens
* Drugs * Penicillin, cephalosporins * Foods * Nuts, shellfish, eggs * Venoms * Insects: bees, wasps, fire ants, spiders * Animals: snakes, jellyfish, lizards * Animal antigens * Blood products * Latex
27
Distributive Shock-Anaphylactic Shock Clinical Maniestations
* Itching, urticarial (Hives, pale red rash, itchy) * Choking * Wheezing * Chest tightness * Dyspnea * General edema, swollen tongue/throat * Decreased BP, and thus weak pulses * Tachycardia * Cyanosis * Nausea, vomiting, abdominal cramping * GI symptoms more common with food allergy reactions
28
Distributive Shock-Anaphylactic Shock Management
* **AIRWAY\*\*** * Intubate if impending loss of airway * Oxygen * Bronchodilators * Epinephrine * Antihistamines * Corticosteroids * Fluid resuscitation
29
Distributive Shock-Septic Shock
Most common type of distributive shock ## Footnote Sepsis with hypotension despite fluid resuscitation
30
Bacteremia
Presence of bacteria in blood stream
31
SIRS
Systemic hyperinflammatory response to a variety of severe clinical insults
32
Sepsis
SIRS caused by infection
33
Severe Sepsis
Sepsis associated with organ dysfunction
34
Multi-organ dysfunction syndrome (MODS)
Altered organ function; homeostasis cannot be maintained without intervention
35
Sepsis Pathophysiology
Microcirculatory damage * Tissue hypoxia despite adequate fluid resuscitation * Results in lactic acidosis and metabolic acidosis * Leads to organ dysfunction
36
Sepsis Hemodynamics
Increased HR, increased CO, decreased SVR (assuming adequate fluid loading) Reduced oxygen extraction due to damage in the microvasculature Increased oxygen consumption due to high metabolic needs Thus, SVO2can be increased or decreased!
37
Severe Sepsis Pathophysiology
* Persistent hypotension despite fluid resuscitation * Presence of perfusion abnormalities * e.g., oliguria, altered mental status, altered skin perfusion * Increased CO * Affects 10-15 % of ICU patients and has a mortality rate of 50-60%. * One half of the infections were nosocomial!
38
Spetic Shock Clinical Manifestations
* Fever, usually preceded by chills * 15-20% of patient present with hypothermia * Skin is warm, flushed * Cool, clammy extremities in end-stage * Tachypnea +/- hyperventilation * Tachycardia * Hypotension (due to the ¯SVR) * Altered mental status * Oliguria
39
Spetic Shock Lab Findings
* Increased WBC (often; but can be decreased!) * Blood gases * Precursor: Increased pH due to Decreased PaCO2 2°to hyperventilation * Once in shock: decrerased pH due to lactate levels * Mixed venous: decreased or increased PvO2 or SvO2 * Positive blood cultures * Clotting abnormalities (­clotting time) * Thrombocytopenia
40
Spetic Shock Mangement for the infection
* Treat the infection, if there is one! * Antibiotic agents specific to the infectious agent
41
Spetic Shock Mangement - Circulatory support
* Fluid resuscitation * Vasopressors (compensate for the decreased SVR * Positive Inotropes (to help with the cardiac dysfunction)
42
Spetic Shock Mangement - Immunomodulation
* Drugs that limit the pro-inflammatory cytokines * Possibly corticosteroids (new evidence pending
43
Spetic Shock Mangement - Respiratory Support
* Oxygenation and mechanical ventilation as required
44
Obstructive Shock Definition
The state where inadequate cardiac output results from an impedance to either cardiac filling or an obstruction to emptying.
45
Obstructive Shock Etiology
* Impedance to heart filling * Cardiac tamponade * Obstruction to heart emptying * PE * Tension pneumothorax * Diaphragmatic hernia
46
Obstructive Shock Clinical Manifestations
There will also be the S & S of the underlying cause!! The “classic” shock symptoms: * Thirst * Hypotension * Tachycardia * Cool and clammy skin * Cyanosis * Poor mentation * Oliguria/anuria Also JVD due to blood backing up
47
Obstructive Shock Management
Treat the problem! Pericardiocentesis Thoracentesisand chest tube Thrombolyticsfor PE Sx (surgery)for diaphragmatic hernia If the causative agent is not quickly diagnosed then prognosis is very poor!
48
Cardiac Output
The amount of blood that is pumped out of each ventricle. 4-6 L/min
49
Systemic Vascular Resistance (SVR) Normal
1200-1600 dynes.sec.cm^ -5
50
Central Venous Pressure
Reflects the preload on the right side of the heart CVP 2-8 mmHg
51
Pulmonary Artery Pressure (PAP)
(20-30)/(6-15) mmHg
52
Pulmonary wedge Pressure (PAWP)
4-12
53
Obstructive Shock Hemodynamic Parameters
**CVP:** Big Increase **PAP:** Big Increase **PAWP:** Can increase or decrease **BP:** Decrease **CO:** Decrease **HR:** Incraese **SVR:** Increase
54
Neurogenic Shock Hemodynamic Parameters
**CVP:** Decrease **PAP:** Decrease **PAWP:** Decrease **BP:** Decrease **CO:** Decrease **HR:** Decrease **SVR:** decrease
55
Septic Shock Hemodynamic Parameters
**CVP:** Decrease **PAP:** Decrease **PAWP:** Dcrease **BP:** Decrease **CO:** Increase **HR:** Increase **SVR:** Big decrease
56
Cardiogenic Shock Hemodynamic Parameters
**CVP:** Increase **PAP:** Big Increase **PAWP:** Big Increase **BP:** Decrease **CO:** Decrease **HR:** Increase **SVR:** Big increase
57
Hypovolemic Shock Hemodynamic Parameters
**CVP:** Big Decrease **PAP:** Big Decrease **PAWP:** Big Decrease **BP:** Decrease **CO:** Decrease **HR:** Increase **SVR:** Big increase
Pathophysiology 2
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