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Patho 2 (Path 311) > Mod 6 Shocks > Flashcards

Mod 6 Shocks Flashcards

1
Q

What is Shock?

A

Lack of oxygen to tissues resulting in cells using anaerobic metabolism (compensation mech)

  • Results in production of lactic acid
  • if persistent, impaired organ function followed by irreversible cell damage and death
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2
Q

What are 4 types of Shock?

A
  • Hypovolemic
  • Cardiogenic
  • Distrubutive
  • Obstructive
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3
Q

What are key features of Hypovolemic Shock?

A

Decreased BP caused by a decrease in blood volume (and corresponding decreased CO)

  • can be due to loss of blood or loss of fluids in general
  • Has 4 stages
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4
Q

What is a key feature of Cardiogenic Shock?

A

Decreased BP caused by failure of hearts ability to pump blood forward (or not as effectively)

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5
Q

What is a key feature of Distributive Shock

A

Widespread vasodilation (decreased SVR)

  • Resulting in relative hypovolemia
  • Can be Septic, Anaphylactic, or Neurogenic in origin
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6
Q

What is key feature of Obstructive Shock

A

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

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7
Q

What is the Etiology of Hypovolemic Shock

  • What is the most cause of most hypovolemic shock?
A

Acute blood loss (internal or external) and Significant blood loss.

  • Hemorrhagic shock
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8
Q

What are some causes of acute blood loss that would lead to Hypovolemic shock?

A
  • Trauma
  • GI bleed
  • vascular (ruptured AAA)
  • Pregnancy related (i.e placental aburption)
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9
Q

What are examples of fluid loss that can lead to Hypovolemic shock if left untreated?

A
  • Extensive burns (fluids literally evaporate at skin)
  • Inadequate fluid intake
  • Excessive diarrhea
  • Excessive vomiting
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10
Q

What does Stage 1 of Hypovolemic Shock involve?

  • Signs and Symptoms?
A

Blood loss < 10%

  • circulating blood volume is decreased but not enough to cause serious effect
  • No signs and symptoms
  • Comparable to a blood donation
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11
Q

What does Stage 2 of Hypovolemic Shock involve?

A

Blood loss 10-25%

  • Compenatory mechs for volume loss (increased HR and SVR) to maintain BP
  • Tissue perfusion is maintained at an adequate level to prevent cell damage.
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12
Q

What are the Signs and Symptoms of Stage 2 Hypovolemic shock?

A

Compensatory stage, so…

  • min increase in HR but < 100 bpm
  • Slightly decreased BP (but still normal range)
  • Mild evidence of peripheral vasoconstriction (Cold hands/Feet)
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13
Q

What does Stage 3 of Hypovolemic Shock involve?

A

Blood loss 25-35% = Decompensated shock

  • unfavourable signs appear as compensatory mechanisms fail to maintain BP
  • Impaired blood flow to vital organs
  • Cells and their enzyme systems are damaged
  • Increased capillary permeability?
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14
Q

Signs and symptoms of stage 3 Decompensated Shock

A
  • Tachycardia
  • Decrease in pulse pressure
  • BP low to low/normal
  • Lactic acidosis
  • Altered LOC
  • Diaphoretic
  • Oliguira
  • Extreme thirst
  • rapid deep respirations
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15
Q

What does Stage 4 of Hypovolemic Shock involve?

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 Multiple Organ System Failure (MOSF)
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16
Q

What is the pathophysiology of Hypovolemic shock?

A

A decrease in blood volume, causes Cardiac output to drop. Attempts to correct drops lead to the following snowball affect:

  • Decrease tissue Perfusion
  • Decrease systemic and pulmonary pressures
  • Stimulation of SNS (attempt to increase CO)
  • Decreased Blood flow (engages RAA system)
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17
Q

Why does decreased tissue perfusion produce lactic acidosis and organ dysfunction?

A

Tissues will have impaired cellular metabolism.

  • When Hypovolemic shock occurs, the body attempts to correct aerobic failure anabolically.
  • It may work for a bit, but will fail at some point (and produce lactic acid)
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18
Q

When the RAA system activates as a response to low urine output and blood flow to the kidneys, why doesn’t the increase in blood volume correct the affects of shock?

A

It does increase blood volume temporally but ultimately fails because it is inefficient and causes other problems.

  • Most likely leading to further blood loss.
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19
Q

What does RAA system activation and increased HR reflect in cases of shock?

A

An attempt to increase Cardiac Output (CO).

  • Can further aggravate blood loss
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20
Q

Lab Findings for Hypovolemic Shock?

A
  • Hemoglobin and Hematocrit abnormalities
  • Increased Lactate levels
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21
Q

How would Hemoglobin and Hematocrit respond to Hypovolemic shock if caused by blood loss?

A
  • Decrease in Hbg
  • Decrease in Hct if the patient has been fluid resuscitated
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22
Q

How would Hemoglobin and Hematocrit respond to Hypovolemic shock if caused by fluid loss?

A

Hgb and Hct would increase due to hemoconcentration (same # of cells in a decreased volume)

  • i.e there would be less plasma but the same HgB
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23
Q

How are Lactate levels affected by Hypovolemic shock?

A

They are increased due to poor peripheral circulation.

  • Cells are not receiving oxygen and switching to anaerobic metabolism (most likely bc of tissue hypoxia)
  • pH will correlate w/severity of acidosis
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24
Q

Treatments for Hypovolemic Shock?

A

Fluid Resusctation and correction of the cause of volume loss must be corrected

  • Give blood or blood products
  • IV fluids
  • Supportive care (O2/Mech vents)
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25
Q

What is admin of blood products based on?

A

Based on Hbg and Hct levels

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26
Q

What IV fluids would you give for treatment of Hypovolemic shock?

A
  • Crystalloids (NS, Ringers Lactate)
  • Colloids (Pentaspan, albumin)
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27
Q

What should you monitor during the treatment of hypovolemic shock?

A

Vital signs (HR and BP) and Urine Output (U/O)

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28
Q

What is Cardiogenic Shock?

A

The state where Inadequate tissue perfusion results from Cardiac dysfunction/failure and the resultant decrease in CO

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29
Q

What is the origin of Cardiogenic Shock?

A

Myocardial Infarction (MI)

  • myocardial contusion
  • myocarditis
  • End stage cardiomyopathy
  • Prolonged cardiopulmonary bypass
  • Valvular dysfunction
  • Cardiac arrhythmias
  • CAD
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30
Q

What are contusions?

A

Bruises/Trauma

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31
Q

What is myocarditis?

A

Inflammation of myometrium (or myocardium) layer of the heart (middle layer)

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32
Q

What Cardiac Arrhythmias could lead to Cardiogenic Shock?

A

Vtach, Bradyarrhythmias, Tachyarrhymias

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33
Q

Pathophysiology of Cardiogenic shock?

A

Originates as cardiac dysfunctions that decrease Cardiac output, The snowball affect progresses much like other types of shock.

  • Myocardial demand increases as a the body attempts to compensate for inefficiencies and eventually fails.
  • Leads to further reduction in CO
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34
Q

Clinical manifestations of shock?

A

The “classic” shock symptoms:

  • Thirst
  • Hypotension
  • Cool and clammy skin
  • Cyanosis

-Poor mentation

  • Oliguria/anuria

And the Signs+Symptoms related to heart failure

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35
Q

What are the signs and symptoms related to heart failure?

A
  • Peripheral edema, Increased JVD, hepatomegaly, ascites
  • Pulmonary edema, frothy pink secretions, tachypnea
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36
Q

Lab Findings of Cardiogenic Shock?

A
  • Increased Lactate and corresponding decreased pH
  • Increased Cardiac enzymes
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37
Q

Normal Lactate Values?

A
  • 4.5 to 19.8 mg/dL

or

  • 0.5 to 2.2 mmol/L
  • High and increasing level of lactate are a poor prognostic factor.
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38
Q

What are causes of increasing lactate?

A

Hypoperfusion and cells using Anaerobic metabolism as a result.

  • The body switches from anerobic processes because they’re inefficient and the tissue/body is hypoxic for whatever reason.
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39
Q

Why do cardiac enzymes increase as a reaction to Cardiogenic Shock?

A

If an MI has occurred

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40
Q

What is the prognosis for a Pt with high and increasing levels of lactate?

A

Poor

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41
Q

Treatment for Cardiogenic Shock?

A

Same management for Heart Failure

  • Reduce preload (optimize fluid volume)
  • Reduce afterload
  • Inotropic drugs
  • Assist the heart (IABP or ventricular assist device)
42
Q

What drugs would you give to reduce preload?

A
  • Diuretics
  • Nitroglycerin
  • Morphine
43
Q

What drugs would you give to reduce afterload?

A
  • Beta blockers
  • ACE inhibitors
  • Nitroglycerin
44
Q

Why are Inodilators a better choice for Cardiogenic shock in comparison to Inotropic drugs?

A

Inotropic drugs (epi, amiodarone, digoxin) can result in increased afterload and tachycardia (increased demand on the heart)

  • Inodilators decrease the demand on the heart with the desired affect of increasing the strength of contractions.
45
Q

What Inodilator drugs are used for Cardiogenic shock (or hearts in general)?

A

Inodilators are a class of medications that combine inotropic (increasing contractility) and vasodilator (relaxing blood vessels) effects.

  • Dobutamine (beta agonists)
  • Dopamine (domainergics)
  • Milirone (phosphodiesterase inhibtors) used freq in CVICU
46
Q

What is distributive shock and what is it generally characterized by?

A

Inadequate tissue perfusion results from a “maldistribution” of blood due to a reduced SVR

  • loss of blood vessel tone resulting in relative hypovolemia
  • Widespread vasodilation
47
Q

What is relative Hypovolemia?

A

When total volume of blood in the body is insufficient to maintain normal circulation, perfusion, and oxygen delivery to tissues, but the issue is not primarily due to a loss of blood from the circulatory system

  • Occurs when the distribution of blood within the body is uneven, leading to an effective decrease in blood volume in critical areas
  • Tx often involves addressing the underlying cause. (i.e vasoconstrictor medications to reduce vasodilation)
48
Q

What is the general snowball affect distributive shock (and relative hypovolemia) can result in?

A

Widespread vasodilation that increases the amount of blood the vasculature can hold (especially the venous system)

  • Causing pooling of blood away from the heart and central circulation, reducing venous return
  • The circulating blood volume is normal, but is insufficient to provide adequate cardiac filling
49
Q

What are 3 types of Distributive Shock?

A
  • Neurogenic shock
  • Anaphylactic shock
  • Septic Shock
50
Q

What are the primary mechanisms that lead to decreased in vessel tone in Distributive Shock?

A
  1. Decreased sympathetic control over vessel tone
  2. Presence of vasodilatory substances in the blood
51
Q

What is etiology of Neurogenic Shock?

A

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

  • Rarest form of shock and most often transient (short?(
52
Q

What are causes of Neurogenic Shock?

A
  • Head injury
  • Spinal cord injuries
  • Spinal anesthesia
  • General anesthesia]
  • Depressant drugs
53
Q

What are the clinical manifestations of Neurogenic Shock?

A
  • Bradycardia
  • Skin is usually warm and dry
  • Unstable Hemodynamic parameters: Decreased SVR, CVP, PAWP as blood pools w/decreasing venous return
  • Decreased CO2, HR, and Venous return.
54
Q

Why does Neurogenic Shock cause bradycardia?

A

Due to imbalance between SNS and PNS stimulation

55
Q

What shock is the skin warm and dry?

  • and why is it different from other forms of shock?
A

Neurogenic Shock presents as warm and dry because it causes vasodilation.

  • Other forms of shock tend to be cool and clammy because of peripheral vasoconstriction, meaning less circulation to the peripherals.
56
Q

What Hemodynamic parameters should you expect to see for neurogenic shock?

A
  • Decreased SVR
  • Decreased CVP (and subsequent PAP and PAWP) bc of decreased venous return
  • Decreased CO2, HR, and venous return
57
Q

Lab Findings for Neurogenic Shock?

A

If prolonged Lactic acidosis and corresponding decrease in pH

58
Q

Treatment for Neurogenic Shock

A
  • Fluid managment
  • Sympathomimetic agents
59
Q

Why are Sympathomimetic agents used to treat Neurogenic Shock? (2)

A
  1. For vasoconstricting effects; goal is to increase SVR
  2. For positive chronotropic effects to increase HR
60
Q

What is the Etiology of Anaphylactic Shock?

  • Snowball affect?
A

Immune mediated reaction to an antigen.

  • Causes widespread mast cell degranulation.
  • Releases vasodilator substances into the blood (histamines, leukotrienes and others ).
61
Q

In Anaphylactic shock, what is the end outcome of widespread mast cell degrenulation?

A

It results in massive vasodilation, leading to:

  • Pooling of the blood in the peripheral vessels
  • Increased permeability of the capillaries
62
Q

What are triggers of Anaphylactic Shock?

  • There’s a lot, generally categorize 6.
  • Don’t spend too much time on this.
A

Potential Allergens include:

  • Drugs
  • Foods
  • Venoms
  • Animal antigens
  • Blood products
  • Latex
63
Q

Clinical Manifestations of Shock

A
  • Itching, Urticaria (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 (bowel issues more common w/food allergies)
64
Q

Treatment for Anaphylactic Shock?

A
  • Airway (intubate if impending loss of airway)
  • Epi
  • Oxygen
  • Bronchodilators
  • Antihistamines
  • Corticosteroids
  • Fluid resuscitation
65
Q

What is the most common distributive shock?

A

Septic Shock

66
Q

What is MODS or MOFS?

A

Multi-organ dysfunction syndrome

  • Altered organ function; homeostasis cannot be maintained without intervention
  • Can also refer to organ failure
67
Q

What is Septic Shock?

A

Sepsis with hypotension despite fluid resuscitation

68
Q

What is Sepsis?

  • what is severe sepsis associated with?
A

Systemic inflammatory response syndrome (SIRS) caused by infection

  • Severe sepsis is associated w/organ dysfunction
69
Q

What is Systemic inflammatory response syndrome (SIRS)

A

Systemic hyperinflammatory response to a variety of severe clinical insults

Google Def:

  • An exaggerated defense response of the body to a noxious stressor (infection, trauma, surgery, acute inflammation, ischemia or reperfusion, or malignancy, to name a few) to localize and then eliminate the endogenous or exogenous source of the insult.
70
Q

What is Bacteremia?

A

Presence of bacteria in blood stream

71
Q

Pathophysiology of sepsis:

What are 5 core components to how Sepsis as a condition worsens over time?

  • Snowball affect/cascade?
A
  1. Amplified Immune Response aka SIRS
  2. Activation of the hypercoagulation Cascade
  3. Endothelial dysfunction aka overproduction and inappropriate systemic compensation
  4. Microcirculatory damage
  5. Altered hemodynamics
72
Q

Why is the immune response problematic when responding to Sepsis?

A

The immune response becomes amplified and generalized

  • Generalized = Not limited to the site of infection
  • Systemic response is to release inflammatory mediators SIRS
73
Q

Why is activation of the coagulation cascade problematic?

  • Hint think sepsis?
A

A Hypercoagulable state increases the risk of developing DIC

74
Q

What is Disseminated Intravascular Coagulation (DIC)

A

Widespread activation of the bloods clotting system and simultaneous breakdown of blood clots. (hemostasis is disrupted)

  • A secondary condition caused by a underlying condition w/varying triggers.
  • results in the formation of numerous microthrombi (small blood clots) throughout the body’s small blood vessels that can impede blood flow.
75
Q

What are the consequences of Disseminated Intravascular Coagulation (DIC)?

A
  • The body uses up clotting factors causing a low platelet count which can lead to excessive bleeding
  • Clotting in small blood vessels = reduced blood flow and tissue damage
  • organ dysfunction
76
Q

In the pathophysiology of Sepsis, what issues are caused by endothelial dysfunction? (3)

  • how do they happen?
  • Snowball affect?
A
  • Overproduction of nitric oxide, resulting in vasodilation
  • Hypotension results due to decreased SVR
  • Damage to microvasculature and tissues, leading organ dysfunction
77
Q

For Sepsis, what does microcirculatory damage typically entail?

  • Snowball affect?
A

Tissue hypoxia despite adequate fluid resuscitation.

  • Results in lactic acidosis and metabolic acidosis
  • Leads to organ dysfunction
78
Q

What Hemodynamic parameters should you expect to see for sepsis?

A
  • Increased HR and Cardiac output
  • Decreased SVR (assuming adequate fluid loading, meaning its variable, SVR could also be increased)
  • Reduced O2 extraction due to damage in the microvasculature
  • Increased O2 consumption due to high metabolic needs
79
Q

Why might Cardiac output increase during sepsis?

A

Early stages of sepsis are characterized by elevated catecholamine levels as a compensatory adrenergic response that is inefficient and eventually fails. You get a brief increase.

  • Aims to augment cardiac contractility and HR
  • Aim is to compensate for intravascular volume and inefficient heart?
80
Q

In early septic shock, why can’t cardiac output be sustained as a response to sepsis?

  • edit may be a poorly written question
A

The rise in CO is often limited by hypovolemia and a fall in preload because of low cardiac filling pressures.

  • When intravascular volume is augmented, the cardiac output usually is elevated (hyperdynamic phase of sepsis and shock).
  • Remember, CO is trying to compensate for a low SVR
81
Q

What is the expected end stage of symptoms for Septic shock?

  • What are the underlying issues caused by?
A

Progression of severe sepsis leading to:

  • Persistent hypotension despite fluid resuscitation
  • Presence of perfusion abnormalities (oliguria, altered mental status, altered skin perfusion)
  • **Increased Cardiac Output (CO is a compensatory response)
  • Half of hospital cases are nosocomial
82
Q

Clinical Manifestations of Septic Shock?

A
  • Fever, usually preceded by chills
    (15-20% of patient present with hypothermia)
  • Warm, flushed skin which change to cool and clammy at end stage
  • Tachypnea +/- hyperventilation
  • Hypotension (due to decreased SVR)
  • Altered mental status
  • Oliguria
83
Q

Lab Findings for Septic Shock?

A
  • Increased WBC (often, but can be decreased)
  • Altered Blood gases (another slide will be more specific)
  • Positive blood cultures
  • Clotting abnormalities (Increased clotting time)
  • Thrombocytopenia
84
Q

What is Thrombocytopenia?

A

Platelet deficiency

85
Q

What paremeters should you expect for ABGS for a Pt. going into Septic shock and in Septic Shock?

A
  1. Precursor: Increased pH due decreased PaCO2 secondary to hyperventilation
  2. Once in shock: decreased pH due to Increased lactate levels
  • Mixed venous: Increase or decrease PvO2 or SvO2
86
Q

Treatment for Septic Shock? (4)

A
  1. Treat the infection w/antibiotics specific to infectious agent
  2. Circulatory support (Fluid resus, vasopressors, (+) inotropes)
  3. Respiratory support (oxygenation and mech vent prn)
  4. Immunomodulation
87
Q

What is Immunomodulation?

  • How does it relate to septic shock?
A
  • Drugs that limit the pro-inflammatory cytokines
  • Possibly corticosteroids (new evidence pending)
88
Q

What would Circulatory support be for Septic Shock?

A
  • Fluid resuscitation
  • Vasopressors (compensate for decreased SVR)
  • Positive inotropes (to help w/cardiac dysfunction)
89
Q

What is Obstructive Shock?

A

State where inadequate cardiac output results from an impedance to either cardiac filling or an obstruction to emptying

90
Q

Etiology of Obstructive Shock? (2)

A
  1. Impedance to heart filling (cardiac tamponade)
  2. Obstruction to heart emptying (PE, Tension Pneumothorax, diaphragmatic hernia)
91
Q

Clinical manifestations of shock?

A

Increased JVD due to blood backing up as well as the “Classic” shock symptoms aka:

  • Thirst
  • hypotension
  • cool and clammy skin
  • Cyanosis
  • Poor mentation
  • Oliguria/anuria
92
Q

What are the “classic” signs of shock?

A
  • Thirst
  • hypotension
  • cool and clammy skin
  • Cyanosis
  • Poor mentation
  • Oliguria/anuria
93
Q

Oligura vs Anuria?

A

Both are conditions where you have low urine output (u/o)

  • Oliguria is defined as having only 100 mL to 400 mL (3.3 to 13.5 oz) of urine per day (moderate severity)
  • Anuria (the most extreme of all of these) is defined as urine production of zero to 100 mL (0 to 3.3 oz) per day (high severity)
94
Q

Treatment for Obstructive Shock?

A

Treat the problem

  • Pericardiocentesis
  • Thoracentesis and chest tube
  • Thrombolytics for PE
  • Surgery for diaphragmatic hernia
  • Finding the causative agent is important for treatment
95
Q

What is typically the primary treatment for pulmonary embolisms (PE)?

A

Thrombolytics

96
Q

Hemodynamic parameters for: Hypovolemic shock

  • What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
A
97
Q

Hemodynamic parameters for: Cardiogenic shock

  • What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
A
98
Q

Hemodynamic parameters for: Septic shock

  • What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
A
99
Q

Hemodynamic parameters for: Neurogenic/spinal shock

  • What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
A
100
Q

Hemodynamic parameters for: Obstructive shock

  • What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
A
101
Q

Hemodynamic parameters: what are your normal values for adults:

  • CVP
  • PAP
  • PAWP
  • BP
  • HR
  • CO
A
  • CVP 2-6 mmHg
  • PAP 25/8 mmHg
  • PAWP 4-12 mmHg
  • BP 90-140/60-90 mmHg
  • HR 60-80 bpm
  • CO 4-8 L/min
102
Q

Spinal vs Neurogenic Shock?

A

Spinal shock occurs in phases that are temporally distributed over a period of weeks to months, whereas neurogenic shock tends to have sudden onset that requires more urgent management.

  • Spinal shock involves large set of injuries involving various parts of the spinal cord.
  • Neurogenic shock tends to be a result of spinal injuries above the T6 level

Patho 2 (Path 311) (15 decks)

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