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
2
Q
What are 4 types of Shock?
A
- Hypovolemic
- Cardiogenic
- Distrubutive
- Obstructive
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
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)
5
Q
What are key features of Distributive Shock
A
Widespread vasodilation (decreased SVR)
- Resulting in relative hypovolemia
- Can be Septic, Anaphylactic, or Neurogenic in origin
6
Q
What are key features of Obstructive Shock
A
Decreased BP caused by an impedance to the filling of the heart or an obstruction to blood leaving the heart
7
Q
What is the Etiology of Hypovolemic Shock
- What is the most common cause of hypovolemic shock?
A
Acute blood loss (internal or external) and Significant blood loss.
- Hemorrhagic shock
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)
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
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
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.
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)
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?
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
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)
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)
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)
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.
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
20
Q
Lab Findings for Hypovolemic Shock?
A
- Hemoglobin and Hematocrit abnormalities
- Increased Lactate levels
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
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
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
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)
25
What is admin of blood products based on?
Based on Hbg and Hct levels
26
What IV fluids would you give for treatment of Hypovolemic shock?
- Crystalloids (NS, Ringers Lactate)
- Colloids (Pentaspan, albumin)
27
What should you monitor during the treatment of hypovolemic shock?
Vital signs **(HR and BP)** and Urine Output (U/O)
28
What is Cardiogenic Shock?
The state where Inadequate tissue perfusion results from Cardiac dysfunction/failure and the resultant decrease in CO
29
What is the origin of Cardiogenic Shock?
**Myocardial Infarction** (MI)
- myocardial contusion
- myocarditis
- End stage cardiomyopathy
- Prolonged cardiopulmonary bypass
- Valvular dysfunction
- Cardiac arrhythmias
- CAD
30
What are contusions?
Bruises/Trauma
31
What is myocarditis?
Inflammation of myometrium (or myocardium) layer of the heart (middle layer)
32
What Cardiac Arrhythmias could lead to Cardiogenic Shock?
Vtach, Bradyarrhythmias, Tachyarrhymias
33
Pathophysiology of Cardiogenic shock?
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
34
Clinical manifestations of shock?
The "classic" shock symptoms:
- Thirst
- Hypotension
- Cool and clammy skin
- Cyanosis
- Poor mentation
- Oliguria/anuria
And the **Signs+Symptoms related to heart failure**
35
What are the signs and symptoms related to heart failure?
- Peripheral edema, Increased JVD, hepatomegaly, ascites
- Pulmonary edema, frothy pink secretions, tachypnea
36
Lab Findings of Cardiogenic Shock?
- Increased Lactate and corresponding decreased pH
- Increased Cardiac enzymes (Troponin, Creatnine, and CK-MB)
- **Don't worry about the following, but be mindful of them** : Natriuretic peptides (NPs), creatnine (CPK), and myoglobin could increase as well if heart dysfunction occurs such as in heart attacks).
37
Normal Lactate Values?
**4.5 to 19.8 mg/dL** or **0.5 to 2.2 mmol/L** depending on the units
- High and increasing level of lactate are a poor prognostic factor.
- High lactate indicates hypoxia and will correlate with acidosis (anaerobic glycolysis)
38
What are causes of increasing lactate?
Hypoperfusion and cells using Anaerobic metabolism as a result of hypoxia
- The body switches from anerobic processes because they're inefficient and the tissue/body is hypoxic for whatever reason.
- Common causes are Heart failure, sepsis, DKA, shock, and seizures. Anything that increases anaerobic demand/gylcoysis.
39
Why do cardiac enzymes increase as a reaction to Cardiogenic Shock?
**Ischemia or an MI has occurred**
How it works:
- Compromised CO reduces coronary blood flow leading to oxygen deprivatiation of the heart (MI)
- Enzyme release is due to the breakdown of cardiac myocytes (heart muscle cells) during prolonged ischemia aka release of cardiac enzymes into the blood stream
- Common are Troponin, Creatinine (CK-MB), and Lactate
40
What is the prognosis for a Pt with high and increasing levels of lactate?
Poor
41
Treatment for Cardiogenic Shock?
Same management for Heart Failure
- Reduce preload (optimize fluid volume)
- Reduce afterload
- Inotropic drugs
- Assist the heart (IABP or ventricular assist device)
42
What drugs would you give to reduce preload (venodilation)?
Preload is volume of blood returning to the heart (end diastolic volume). **Venodilators reduce preload by decreasing venous return**
- **Diuretics**
- **Nitroglycerin**: Nitrates dilate veins by pooling blood in the periphery reducing venous return.
- Morphine
- ACE inhibitors (indirect, reduce blood volume via aldosterone)
43
What drugs would you give to reduce afterload (arterial dilation)?
Afterload refers to the resistance the heart must pump against to eject blood. **Arterial vasodilators reduce SVR, improving CO**
- Beta blockers (Indirect)
- ACE inhibitors (block Angiotensin II -> reduce vasoconstriction and lower SVR)
- Nitroglycerin (reduce afterload and preload)
44
Why are Inodilators a better choice for Cardiogenic shock in comparison to Inotropic drugs?
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
What Inodilator drugs are used for Cardiogenic shock (or hearts in general)?
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
What is distributive shock and what is it generally characterized by?
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
What is relative Hypovolemia?
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
What is the general snowball affect distributive shock (and relative hypovolemia) can result in?
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
What are 3 types of Distributive Shock?
- Neurogenic shock
- Anaphylactic shock
- Septic Shock
50
What are the primary mechanisms that lead to decreased in vessel tone in Distributive Shock?
1. Decreased sympathetic control over vessel tone
2. Presence of vasodilatory substances in the blood
51
What is etiology of Neurogenic Shock?
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
What are causes of Neurogenic Shock?
- Head injury
- Spinal cord injuries
- Spinal anesthesia
- General anesthesia]
- Depressant drugs
53
What are the clinical manifestations of Neurogenic Shock?
- 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
Why does Neurogenic Shock cause bradycardia?
Due to imbalance between SNS and PNS stimulation
55
What shock is the skin warm and dry?
- and why is it different from other forms of shock?
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
What Hemodynamic parameters should you expect to see for neurogenic shock?
- Decreased SVR
- Decreased CVP (and subsequent PAP and PAWP) bc of decreased venous return
- Decreased CO2, HR, and venous return
57
Lab Findings for Neurogenic Shock?
If prolonged **Lactic acidosis** and corresponding decrease in pH
58
Treatment for Neurogenic Shock
- Fluid managment
- Sympathomimetic agents
59
Why are Sympathomimetic agents used to treat Neurogenic Shock? (2)
1. For vasoconstricting effects; **goal is to increase SVR**
2. For positive chronotropic effects to **increase HR**
60
What is the Etiology of Anaphylactic Shock?
- Snowball affect?
Immune mediated reaction to an antigen.
- Causes **widespread** mast cell degranulation.
- Releases vasodilator substances into the blood (histamines, leukotrienes and others ).
61
In Anaphylactic shock, what is the end outcome of widespread mast cell degrenulation?
It results in **massive vasodilation**, leading to:
- Pooling of the blood in the peripheral vessels
- Increased permeability of the capillaries
62
What are triggers of Anaphylactic Shock?
- There's a lot, generally categorize 6.
- Don't spend too much time on this.
Potential Allergens include:
- Drugs
- Foods
- Venoms
- Animal antigens
- Blood products
- Latex
63
Clinical Manifestations of Shock
- **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
Treatment for Anaphylactic Shock?
- **Airway** (intubate if impending loss of airway)
- **Epi**
- Oxygen
- Bronchodilators
- Antihistamines
- Corticosteroids
- Fluid resuscitation
65
What is the most common distributive shock?
Septic Shock
66
What is MODS or MOFS?
Multi-organ dysfunction syndrome
- Altered organ function; homeostasis cannot be maintained without intervention
- Can also refer to organ failure
67
What is Septic Shock?
Sepsis with hypotension despite fluid resuscitation
68
What is Sepsis?
- what is severe sepsis associated with?
Systemic inflammatory response syndrome (SIRS) caused by infection
- Severe sepsis is associated w/organ dysfunction
69
What is Systemic inflammatory response syndrome (SIRS)
**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
What is Bacteremia?
Presence of bacteria in blood stream
71
Pathophysiology of sepsis:
What are 5 core components to how Sepsis as a condition worsens over time?
- Snowball affect/cascade?
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
Why is the immune response problematic when responding to Sepsis?
The immune response becomes amplified and generalized
- Generalized = Not limited to the site of infection
- Systemic response is to release inflammatory mediators SIRS
73
Why is activation of the coagulation cascade problematic?
- Hint think sepsis?
A Hypercoagulable state **increases the risk of developing DIC**
74
What is Disseminated Intravascular Coagulation (DIC)
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
What are the consequences of Disseminated Intravascular Coagulation (DIC)?
- 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
In the pathophysiology of Sepsis, what issues are caused by endothelial dysfunction? (3)
- how do they happen?
- Snowball affect?
- Overproduction of nitric oxide, resulting in vasodilation
- Hypotension results due to decreased SVR
- Damage to microvasculature and tissues, leading organ dysfunction
77
For Sepsis, what does microcirculatory damage typically entail?
- Snowball affect?
Tissue hypoxia despite adequate fluid resuscitation.
- Results in lactic acidosis and metabolic acidosis
- Leads to organ dysfunction
78
What Hemodynamic parameters should you expect to see for sepsis?
- 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
Why might Cardiac output increase during sepsis?
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
In early septic shock, why can't cardiac output be sustained as a response to sepsis?
- **edit** may be a poorly written question
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
What is the expected end stage of symptoms for Septic shock?
- What are the underlying issues caused by?
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
Clinical Manifestations of Septic Shock?
- 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
Lab Findings for Septic Shock?
- **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
What is Thrombocytopenia?
Platelet deficiency
85
What paremeters should you expect for ABGS for a Pt. going into Septic shock and in Septic Shock?
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
Treatment for Septic Shock? (4)
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
What is Immunomodulation?
- How does it relate to septic shock?
- Drugs that limit the pro-inflammatory cytokines
- Possibly corticosteroids (new evidence pending)
88
What would Circulatory support be for Septic Shock?
- Fluid resuscitation
- Vasopressors (compensate for decreased SVR)
- Positive inotropes (to help w/cardiac dysfunction)
89
What is Obstructive Shock?
State where inadequate cardiac output results from an impedance to either cardiac filling or an obstruction to emptying
90
Etiology of Obstructive Shock? (2)
1. Impedance to heart filling (cardiac tamponade)
2. Obstruction to heart emptying (PE, Tension Pneumothorax, diaphragmatic hernia)
91
Clinical manifestations of shock?
**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
What are the "classic" signs of shock?
- Thirst
- hypotension
- cool and clammy skin
- Cyanosis
- Poor mentation
- Oliguria/anuria
93
Oligura vs Anuria?
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
Treatment for Obstructive Shock?
**Treat the problem**
- Pericardiocentesis
- Thoracentesis and chest tube
- Thrombolytics for PE
- Surgery for diaphragmatic hernia
- Finding the causative agent is important for treatment
95
What is typically the primary treatment for pulmonary embolisms (PE)?
Thrombolytics
96
Hemodynamic parameters for: Hypovolemic shock
- What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
97
Hemodynamic parameters for: Cardiogenic shock
- What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
98
Hemodynamic parameters for: Septic shock
- What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
99
Hemodynamic parameters for: Neurogenic/spinal shock
- What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
100
Hemodynamic parameters for: Obstructive shock
- What would CVP, PAP, PAWP, BP, CO, HR, and SVR be?
101
Hemodynamic parameters: what are your normal values for adults:
- CVP
- PAP
- PAWP
- BP
- HR
- CO
- 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
Spinal vs Neurogenic Shock?
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
