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High Acuity > Shock > Flashcards

Shock Flashcards

1
Q

Oxygen delivery is dependent on what 2 factors

A
  1. Cardiac Output
  2. Oxygen Content in blood
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2
Q

Cardiac output is dependent on what 2 things

A

HR + SV

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3
Q

SV is dependent on what 3 things

A

Preload
Contractility
Afterload

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4
Q

Oxygen content in blood is dependent on what 2 things

A

Oxygen saturation

HgB

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5
Q

Define shock

A

“Widespread abnormal cellular metabolism that occurs when gas exchange with oxygenation and tissue perfusion needs are not met sufficiently to maintain cell function”

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6
Q

Shock affects _____ body systems

A

all

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7
Q

Shock is an imbalance in ____________ for ___________

A

Supply and demand

O2 and nutrients

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8
Q

Shock is ___________ leading to decreased tissue perfusion

A

Circulatory insufficiency

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9
Q

In shock, cells revert to ___________

A

Anaerobic metabolism

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10
Q

Describe aerobic vs anaerobic metabolism

A
  1. Aerobic
    * Efficient production of ATP
    * ATP (energy) maintains normal cellular metabolic function
  2. Anaerobic
    * Inefficient ATP production
    * Lactate is by-product  metabolic acidosis
    * Cellular dysfunction  cell death
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11
Q

4 Stages of shock

A
  1. Initial
  2. Compensatory
  3. Progressive

4, Refractory (irreversible)

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12
Q

Initial stage of shock

A
  • Some anaerobic metabolism; overall metabolism still aerobic
  • baseline MAP decreased by <10 mmHg
  • No obvious clinical signs of shock
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13
Q

Compensatory stage of shock

A
  • Compensatory mechanisms triggered: SNS, RAAS
  • Vital organ function not disrupted
  • Reversible! – if cause is treated
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14
Q

Progressive stage of shock

A
  • Compensatory mechanisms ongoing, but not sufficient to perfuse vital organs
  • Anaerobic metabolism =
  • Rising lactic acid (>2)
  • K+ (cell death releasing intracellular products)
  • Low pH
  • Severe hypotension and hypoxemia  ischemia
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15
Q

Refractory stage of shock

A
  • Extensive damage to vital organs; continues despite interventions
  • Massive release of toxic metabolites and enzymes > vicious cycle > MODS
  • Liver, heart, brain, and kidney functions lost
  • Death imminent
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16
Q

Compensated vs Decompensated Shock and what BP changes do we see?

A

Compensated Shock: Stage 1 and 2 (normal/elevated BP)

Decompensated Shock: Stage 3 and 4 (decreased BP)

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17
Q

Describe the initial systemic compensatory mechanisms that occur with shock and what do we see with our pulse pressure

A

Compensation = SNS and RAAS systems

  1. SNS System: Baroreceptors in carotid and aortic bodies activate SNS in response to decreased BP
    * Vasoconstriction while blood to vital organs maintained
  2. RAAS System: Kidney’s sense decreased perfusion… activate RAAS

As a result - Narrowing Pulse Pressure:
- Difference between SBP and DBP
- Vasoconstriction (without substantial additional fluids) causes increased DBP, with little change in SBP

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18
Q

How well compensation happens depends on what 4 things?

A
  1. Extent of injury
  2. Age
  3. General state of health
  4. Amount of blood/volume loss
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19
Q

Respiratory Compensation that occurs with shock

A
  1. Respiratory rate increases to try to bring in more oxygen to send to the tissues, as well as to blow of C02 (to compensate for rising lactic acidosis)
  2. Smooth muscle relaxation (SNS activation) to increase air flow = increase oxygen exchange = decreased CO2
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20
Q

Renal Compensation that occurs with shock

A
  1. Renal hypoperfusion  activation of RAAS
  2. Increase Na+ and water reabsorption (lower urinary output: <30ml/hr) = try increase CO

> Hypoxia to kidneys puts them at risk for AKI/kidney failure

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21
Q

Vascular Compensation that occurs with shock

A
  1. Vessel constriction, allowing increased blood flow to vital organs
    > Cool, pale skin = Alpha receptors produce peripheral vasoconstriction to shunt blood to more vital organs
    > Cap refill >2 seconds
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22
Q

GI Compensation that occurs with shock

A
  1. Blood shunted away from splanchnic circulation (GI tract, spleen, liver, pancreas) = Allow more blood flow to more vital organs (i.e. heart, brain lungs)
  2. Decreased intestinal peristalsis = bowel sounds
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23
Q

Why does diaphoresis occur as compensatory mechanism with shock?

A

release heat as a by-product of metabolism (high metabolic rate/demand)

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24
Q

What hepatic compensatory mechanisms occur with shock?

A

increased glycolysis, gluconeogenesis, mobilization of free fatty acids (increase availability of glucose for energy due to increased metabolic rate – patients can be hyperglycemic)

does not help - oxygen problem not glucose

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25
Q

What CNS compensatory mechanisms occur with shock?

A
  1. Thirst d/t stimulation of brain in response to decreased blood volume
  2. Decreased LOC, restlessness, agitation (from cerebral hypoxia) - occurs when autoregulation fails
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26
Q

2 Hallmarks of Progressive Stage of Shock

A
  1. Decreased Cellular Perfusion + Altered Capillary Permeability
  2. Anasarca: full body edema because of vasodilation and increased permeability of vasculature throughout the body
    > Fluid leakage affects solid organs and peripheral tissues
    > Decrease blood flow to pulmonary capillaries
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27
Q

What respiratory changes are seen as a result of the progressive stage of shock

A

Fluid moves into alveoli
* Edema
* V/Q Mismatch
* Tachypnea
* Crackles
* Increased work of breathing
* Low Oxygenation

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28
Q

What myocardial changes are seen as a result of the progressive stage of shock?

A

Myocardial Dysfunction results in (what happens when heart is ischemic… loss of fxns)
* Dysrhythmias
* Ischemia/Infarction

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29
Q

What GI changes are seen as a result of the progressive stage of shock?

A

Mucosal Barrier of GI system becomes Ischemic (what happens when GI is ischemic… loss of fxns)
* Ulcers
* Bleeding
* Risk for translocation of bacteria
* Decreased ability to absorb nutrients

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30
Q

What hepatic changes are seen as result of the progressive stage of shock?

A

Liver fails to metabolize drugs and waste (what happens when liver is ischemic… loss of fxns)
* Jaundice
* Elevated enzymes
* Loss of immune function
* Risk for DIC = bleedings

> Increased waste products always lead to increased vasodilation (inflammatory response)

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31
Q

What occurs in the irreversible stage of shock?

A
  • Ischemia and necrosis is profound
  • Lost all blood volume to third spaces due to increased permeability and dilation of vessels
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32
Q

Cues of irreversible stage of shock

A
  • Rapid loss of consciousness
  • Nonpalpable pulse
  • Cold, dusky extremities
  • Slow, shallow resps; unmeasurable Sp02
  • Profound hypotension
  • Bradycardia
  • Coagulopathies
  • Signs of multiple organs failing (MODS)
  • Worsening metabolic acidosis (increasing lactate)
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33
Q

What is MODS

A
  • Progressive organ dysfunction in 2 or more separate organ systems
  • Homeostasis can’t be maintained without intervention
  • Both infectious (i.e. sepsis) and non-infectious (i.e. pancreatitis) etiology
  • Occurs in end-stage shock
    >Uncontrolled systemic inflammation
    > Global tissue hypoxia
    > Unregulated apoptosis
    > Microvascular coagulopathy
34
Q

What is hypovolemic shock?

A
  • Loss of vascular volume (blood or plasma)
  • Volume is insufficient to fill the tank
  • Results in decreased cardiac output = low perfusion
  • Most common type

(hemorrhage of hypovolemia)

35
Q

Common causes of blood loss in hypovolemic shock?

A
  • External: scalp lacerations can cause significant blood loss
  • Chest: 2.5L in each hemothorax
  • Abdomen: Up to 6L from intraperitoneal bleedings
  • Pelvis and Retroperitoneum: Unstable pelvic fracturs can lose several liters
  • Femur fracture: 500-1000ml blood per femur
36
Q

4 Types of Shock

A
  1. Hypovolemic: lack of blood
  2. Cardiogenic: heart problem
  3. Obstructive: non-direct heart problem
  4. Distributive: systemic vasodilation problem
37
Q

Hemodynamic Cues in Hypovolemic Shock

(BP, HR, RR, Preload, Afterload, Contractility)

A
  • Low BP
  • High HR (low HR late sign)
  • High RR
  • Low preload (low return)
  • High afterload (compensatory squeezing down vasculature)
  • No change in contractility
38
Q

Lab Cues in hypovolemic shock

(Hgb, HcT, BUN/Creatinine, NA, ABG)

A
  • Hbg (can be decreased due to hemorrhage) + Elevate r/t to low blood volume
  • Hct (increased because low volume state, ratio of RBC is elevated) Elevate r/t to low blood volume
  • BUN elevates, creatinine normal as a sign of dehydration (hypovolemia).
    > However, can lead to acute renal failure if not corrected (creatinine will rise).
  • Increased Na due to compensation of aldosterone release (RAAS compensation)
  • ABGs can show a respiratory alkalosis (increased RR as compensation for metabolic acidosis – early/compensated shock.. later states metabolic acidosis will overtake)
39
Q

Physical cues in hypovolemic shock

A

signs of low circulating volumes/hypoxia
* Obvious external bleeding
* Decreased urine output
* Pallor, cool, clammy skin; weak peripheral pulses, slow cap refill
* Changes in mental status

40
Q

3 Priority Actions in Hypovolemic Shock

A
  1. Restore intravascular volume
    * Blood products
    * IV fluids - will not help oxygen carrying capacity with hemorrhagic loss – need to restore HgB
  2. Improve CO and tissue perfusion
    * Oxygen
    * Medication
  3. Correct cause of hypovolemia- bleeding, dehydration, heat stroke, interstitial losses
    * Tourniquet – external
    * Always note time it was applied
    * Never remove dressings from active bleeds, continue to add dressings and pressure
    * Damage-control surgery - internal
41
Q

Causes of Cardiogenic Shock

A
  • Arrhythmia
  • MI
  • Heart (pump) failure
42
Q

Hemodynamics of Cardiogenic Shock

(BP, HR, RR, Preload, Afterload, Contractility)

A
  • Low BP
  • High HR – compensatory
  • High RR – compensatory
  • Variable preload – dependent on patient factors/compensation
  • Variable afterload – dependent on patient factors/compensation
  • Low contractility – pump problem
43
Q

Diagnostics for Cardiogenic Shock

A

Signs of myocardial damage!!

  • Elevated cardiac markers: trop/CK/BNP for MI or HF
  • Changes in ECG – arrhythmias/ischemia location
  • CXR- pulmonary infiltrates, enlarged heart with HF), fluid back-up into lungs

Other Cues: Signs of heart ischemia, decreased CO and fluid back up in lungs
> chest pain, SOB, dysrhythmias, elevated trop, skin pale, cool, moist, cyanosis, decreased urine output
> Tachypnea, cyanosis, pulmonary crackles and wheezes (resp distress as fluid overload occurs)

44
Q

Patho of cardiogenic shock

A
  1. decreased contractility leads to decreased stroke volume leads to decreased CO
  2. Pulmonary congestion
  3. Decreased systemic tissue perfusion
  4. Coronary artery perfusion leading to further decreased contratility
45
Q

Priorities for cardiogenic shock

A
  1. limit myocardial damage
    - restore perfusion
    - reduce workload
  2. improve cardiac function to improve CO
    - control dysrhythmias
  3. Decrease pulmonary complications
    - oxygen
    - ventilation (PEEP)
    - positioning (upright)
    - diuretics
46
Q

Medications used in management of cardiogenic shock

A
  1. Nitrates (nitroglycerin): dilation of coronary vessels
  2. Inotropes (dobutamine + inotrope): improves force of contraction
  3. Diuretics (furosemide): pull fluid build-up off lungs with pump failure
  4. B-adrenergic blockers (Metoprolol- B1 primarily): decrease workload/SNS activation (frank starling mechanism – if going faster, it isn’t able to fill)
  5. Labetalol (IV)  B-1 & a-1 receptor blocker:
  6. Analgesia: chest pain
  7. Antiplatelets: major cause of cardiogenic shock is clot in coronary vasculature
  8. Antiarrhythmics: if cause, or secondary to MI
47
Q

Causes of obstructive shock

A
  • Pericardial tamponade
  • Tension pneumothorax
48
Q

Hemodynamics of obstructive shock

(BP, HR, RR, Preload, Afterload, Contractility)

A
  • Low BP – unable to fill
  • High HR - compensatory
  • High RR – compensatory
  • Low preload – not filling/something compressing (could also compress IVC)
  • High afterload – SNS activation
  • Low contractility
49
Q

Signs and symptoms of obstructive shock

A

related to cause: anxious, muffled heart sounds (pericardial tamponade), JVD (backup if unable to enter heart/VC), chest pain, difficulty breathing

50
Q

Treatment of obstructive shock

A

relieve the obstruction! (pericardiocentesis, needle decompression, tumor debulk)

51
Q

Causes of distributive shock

A
  • Spinal cord injury (neurogenic)
  • Anaphylaxis
  • Sepsis
52
Q

Hemodynamics of distributive shock

(BP, HR, RR, Preload, Afterload, Contractility)

A
  • Low BP - vasodilation
  • High or Low HR – neurogenic has low (loss of SNS) - others will comp
  • High or Low RR – neurogenic has low (loss of SNS) - others will comp
  • Low preload – dilation makes it hard to return blood
  • Low afterload – dilation
  • No change in contractility
53
Q

Patho of neurogenic shock

What symptoms are seen

A

Caused by damage to the spinal cord – T6 or above (the part of the spine that innervates SNS)

Absolute loss of sympathetic tone/innervation > parasympathetic nervous system response

Vasodilation and blood pools (cold core and warm skin), decreased HR

**Hypotension, bradycardia, hypothermia

54
Q

Treatment of neurogenic shock

A

BP:
1. Vasopressors (to reduce pooling of blood)
2. Fluid resuscitation = careful; no large bolus needed! – do not have a fluid volume issue.. possibly some loss to interstitial but more so vasodilation

HR:
1. Atropine = block PNS (raise HR)

55
Q

5 Cues of Anaphylactic Shock

A
  1. Airway obstruction from bronchial constriction
  2. Resp distress due to laryngeal edema, bronchospasm
    > Wheezing, stridor, coughing, hoarseness
  3. Cardio collapse
    > Dizziness, chest pain, facial swelling
  4. Vascular collapse/fluid shifts due to local inflammation, vasodilation, and increased vascular permeability
    > Pruritis, urticaria, angioedema
    > Histamine as vasodilator
  5. Anxiety
56
Q

Action against anaphylactic shock

A
  1. ABC’S first!
  2. Bolus fluids for fluid leakage
  3. Epinephrine IM
    > **4hrs cardiac monitoring post-epi
    > Catecholamine of SNS – drastic HR increase
  4. Bronchodilators (albuterol, ipratropium, magnesium)
  5. Antihistamine (Benadryl)
  6. Corticosteroids (decrease inflammation/histamine response)
  7. Find cause/eliminate
  8. Treat signs of shock due to circulatory collapse
    > Fluid & vasopressors if needed
57
Q

Sepsis

A

Life-threatening organ dysfunction brought on by a dysregulated response to infection; bacteremia

58
Q

Septic Shock

A

a subset of sepsis in which circulatory, cellular, and metabolic abnormalities substantially increase the risk of death over that associated with sepsis alone. Decompensation and abnormal coagulation (WBC, platelets, and coagulation factors secondary to inflammatory response) occurs.

59
Q

Normal response to infection

A

Infectious Organism > helpful, local inflammatory response to contain and eliminate infection

  1. WBC secrete cytokines  trigger local inflammation, bring more WBCs
  2. Causes constriction of small veins, dilation of arterioles (increases perfusion to locally infected tissues)
  3. Capillary leak/swelling = plasma can leak into tissues (edema)
    > Limited to the area of infection
60
Q

Define sepsis

A
  1. immune dysfunction
  2. systemic response as bacteria enters blood
  3. widespread inflammation
  4. no longer limited to area of infection - widespread vasodilation and increased vessel permeability
  5. entire body undergoing inflammatory response = coagulation factor consumption = DIC
61
Q

qSOFA criteria

A

Hypotension: SBP < 100mmHg

Tachypnea > 22

Altered Mental Status GCS < 15

2 or 3 points = higher risk of poor outcomes

62
Q

What is SIRS and the criteria

A

Widespread inflammation of INFECTIOUS or NONINFECTIOUS pathology

Temperature: >38 or <36
Heart Rate: > 90
Respiratory Rate: > 20
PaCO2: <32mmHg
WBC: > 12 or < 4 or >10% (immature WBC)

> For Sepsis Diagnosis: need 2 of these criteria AND documented infection

63
Q

Diagnosis of Septic Shock

A

Sepsis + 2 additional symptoms:

> Persisting hypotension; requiring vasopressors to reach a MAP of ＞65 mmHg
AND
Serum lactate ＞2 mmol/L despite adequate fluid resuscitation

64
Q

Compare infection, sepsis, septic shock, and MODS

A

Infection: reaction of host tissues and innate immune system to the invasion of an infectious agent and/or its toxins +/- nonspecific SIRS criteria

Sepsis: confirmed or suspected infection AND aberrant or dysregulated host response leading to an organ dysfunction

Septic Shock: sepsis AND persisting hypotension requiring vasopressors to maintain MAP > or = to 65mmHg AND serum lactate > 2mmol/L

MODS: septic shock AND multiple organ dysfunction syndrome

65
Q

Labs seen in sepsis

A
  1. Rising serum procalcitonin
    > Early detection of bacterial infection
  2. High lactate
    > Anaerobic metabolism
  3. Normal or low WBC
    > Initially high in sepsis to fight infection. Once progressed to shock, have used them up.
  4. Decreased segmented neutrophil level with rising band neutrophils (LEFT SHIFT)
    > Bone marrow sending out immature WBC
  5. Documented infection (i.e. bacteria in blood, UTI, etc.)
    > 48 hours for blood cultures to return; may not have information available
  6. DIC may cause low Hgb, Hct, fibrinogen, and platelet counts
    > aPTT, PT, INR changes
    > Bone marrow focussed on producing WBC/no focus on RBC causing low Hgb
  7. Low bicarb
  8. High creatinine
  9. High bilirubin
  10. Hyperglycemia (plasma glucose > 140mg/dL or 7.7 mmol/L) in the absence of diabetes
    > liver tries to give energy but primary issue is oxygen
66
Q

Initial resuscitation for sepsis/septic shock

A

Early recognition and treatment > within one hour
1. Measure lactate level
2. Obtain blood cultures before administering antibiotics
3. Administer broad-spectrum antibiotics
4. Begin rapid administration of 30ml/kg crystalloid for hypotension or lactate > 4mmol/L
5. Apply vasopressors if hypotensive during or after fluid resuscitation to main a MAP > 65mmHG
* Remeasure lactate if initial lactate elevated (>2mmol/L)

67
Q

Collaborative Interventions for Shock

A
  1. Fluids
    > Use balanced crystalloid (RL or plasmalyte) instead of NS for fluid resuscitation
    > Blood products (albumin)
  2. Drugs:
    > Vasopressors: Norepinephrine 1st line
    > Arterial line: continuous BP monitoring, frequent blood draws/ABGs (high risk for bleeding, limit pokes)
    > Recommended to start peripherally rather than delaying until central access; central line is best practice
    > Vasoconstrict and decrease permeability
    > Antibiotics: treatment of cause
    > IV corticosteroids: suppress inflammatory reaction
    > Clotting issues: dependent on issue (heparin, protamine sulfate, vitamin k, FFP for factor)
    > Stress-ulcer/GI prophylaxis: PPI IV
    > DVT prophylaxis– LMWH
    > Insulin (for glucose >10mmol/L): liver releasing all glucose stores; often hyperglycemic
    > Sodium bicarbonate: treatment of acidosis - temporizing measure
  3. Source control
    > Drain abscess, remove infected device, debride, etc.
  4. Maintain normothermia
  5. Oxygenation support
  6. Nutritional support
    > Enteral feeding within 72hrs
68
Q

Who is at greatest risk for sepsis?

A
  1. immunocompromised
    2.Other chronic diseases
    > DM – bacteria feeds on glucose
    > CKD – body already using compensatory mechanisms at baseline
  2. malnutrition, wounds, etc.
69
Q

Cardiovascular complications of shock

A
  • Ventricular failure
  • Microvascular thrombosis
70
Q

Neurologic complications of shock

A
  • Sympathetic nervous system dysfunction
  • Cardiac & resp depression
  • Thermoregulatory failure
  • Coma
71
Q

Pulmonary complications of shock

A
  • Acute lung failure
  • Acute resp distress syndrome (ARDS)
72
Q

Renal complications of shock

A

Acute Kidney Injury

73
Q

Hematologic complications of shock

A

Disseminated intravascular coagulation (DIC)

74
Q

Trauma triad of death + why they occur in shock

A
  1. Coagulopathy
    * Trauma-induced
    * Resuscitation-related (giving fluids/PRBC only)
  2. Acidosis
    * Elevated lactate (anaerobic metabolism)
    * Excessive fluids
  3. Hypothermia
    * Exposure
    * Excessive bleeding
    * Worsening acidosis
75
Q

Patho of DIC as shock complication

A

Result of excessive clotting; in small capillaries of liver, kidney, brain, and heart

leads to ++ clots use up clotting factors & fibrinogen faster than they’re made
> Leads to poor clotting = hemorrhage

We see:
* Petechia
* Ecchymosis
* Bleeding from phlebotomy sites, nose, gums, etc.

Result = decreased perfusion and gas exchange = hypoxia & ischemia

76
Q

Patho of ARDS as shock complication

A

NOT a primary lung disease

> Caused by SIRS, increasing formation of oxygen free-radicals, which damage lung cells
Damaged alveolar-capillary membranes

> Septic shock + ARDS = HIGH MORTALITY RATE

> Increased vasodilation and permeability = fluid shifts into lungs

> Pulmonary edema not originated from cardiac source; bilateral

77
Q

Fluid replacement for shock

A

> Isotonic crystalloids - not NS

> Blood components (PRBCs, FFP, albumin)

78
Q

Vasoactive medications for shock

A
  • Used to increase myocardial contractility, regulate HR, reduce myocardial resistance, and initiate vasoconstriction to increase blood flow
  • First line: Norepinephrine (Levophed)*
  • First line cardiogenic shock: Dobutamine
  • Dopamine, Phenylephrine
  • Drugs to improve cardiac contractility & coronary artery perfusion (Inotropes, nitro)
79
Q

How is total body work decreased in shock

A

decrease metabolic rate
>Mechanical ventilation
> Sedation/paralysis = propofol
> Neuromuscular blocking agents (NMBAs)
> Reduce anxiety & pain

80
Q

ABG of shock

A
  • Decreased pH
  • Decreased PaO2
  • Increased PaCO2
  • Base deficit
81
Q

Lactate of shock

A
  • Increased (normal <2 mmol/L)
82
Q

CBC/lytes/creatinine in shock

A
  • Incr OR decr Hgb
  • Incr OR decr Hct
  • Increased K+
  • Increased creatinine

High Acuity (20 decks)

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