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Week 41: > Shock > Flashcards

Shock Flashcards

1
Q

Shock

A
  • inability to maintain minimum perfusion (Flow) leads to hypoxia and impaired organ function
  • caused by a Cardiac Output that can’t maintain arterial pressure for perfusion
  • Leads to low BP in most cases except:
    • when your in shock and heart is overpumping to compensate: Normotensive hyperdyanmic shock states
      • early septicemia
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2
Q

Shock occurs because:

A
  • Cardiogenic Shock
    • pump fails
    • heart isn’t generating enough contraction
  • Hypovolemic Shock
    • pump is normal, but has nothing to pump
  • Neurogenic/septic/Anaphylactic shock
    • pump is normal, has something to pump, VASCULAR TONE IS ABSENT
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3
Q

Vasoconstriction or Vasodilation of Body in general:

A

have to have vasoconstriciton in parts of your body at all times to maintain adequate BP

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4
Q

Hypovolemic Shock

  • primary lesion
  • cause
  • example
A
  • Primary lesion:
    • losing blood volume
    • PUMP IS normal
  • Cause–>example
    • Loss of Whole blood- Hemorrhage/trauma
    • Loss of plasma- Burns/dehydration
    • Loss of GI Secretions-Vomitting/diarrhea
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5
Q

Cardiogenic Shock

  • Primary Lesion
  • Causes
  • Example
A
  • Primary lesion:
    • Disturbances in cardiac pumping
      • something wrong with heart
  • Causes-Example
    • Disturbances in filling-Pericardial Tamponade
    • Disturbances in emptying-MI/Acute heart failure
    • Disturbances in BOTH-Pulmonary embolism
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6
Q

Neurogenic/Anaphylactic/Septic Shock

  • primary lesion
  • causes
  • example
A
  • Primary lesion:
    • alterions in blood vessels–Vasodilation
  • Causes:
    • neural influneces on blood vessels
      • Neurogenic shock
      • Anesthesia
      • loss sympathetics constrictor tone
    • Humoral influences on Blood vessels
      • anaphylactic shock
      • septic shock
      • chemical or circulating influence
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7
Q

Trauma

A
  • Any trauma has the potential to cause shock
    • bleeding=internal or external hypovolemia
    • infection=potential for sepsis
    • Fear/pain=potenital for neurogenic shock
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8
Q

Surgery

A

All surgery is intentional trauma–>therefore any surgery has the potential to cause shock and

  • Treatment=potential for anaphylactic shock
  • Anesthesia=potential for neurogneic shock
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9
Q

General Features of Shock

A
  • Low BP
    • if vasoconstriction compensates for Low Cardiac Output, BP may not fall and shock is compensated
  • Cold Clammy Skin
    • Classical signa of Increase sympathetic outflow
    • Increase vasoconstriciton and sympathetic stimulation of sweat glands
  • Warm Skin
    • Due to opening of arterio-venous shunts in the skin
    • consequence of severe septic shock
    • poor prognosis
  • Rapid Thready Pulse
    • Hypotension reflexively activates sympathtic nervous system, and casues tachycardia
    • Thready nature associated with reduced Stroke volume and weaker pulse pressures
  • Peripheral Cyanosis: Blue tissue
    • causes include: (or simply reflex)
      • lactic acidosis
      • pain
      • anxiety
      • decreased oxygenation
    • Decreased cardiac output and vasoconstriction cause poor tissue flow, hypoxia, anerobic metobllism, and lactic acid production
  • Mental Confusion/CNS depressoin
    • poor cerebral perfusion
  • Renal Failure
    • Low renal blood flow
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10
Q

Classificaitn of shock due to volume loss:

  • Blood loss (mL)
  • Blood loss (%BV)
  • Pulse rate
  • BP
  • Pulse Pressure
  • Respiratory Rate
  • Urine output (mL/hr)
  • CNS/Mental Status
  • Fluid Replacement
A
  • Blood loss(mL):
    • Class I-Up to 750 mL
    • Class II-750-1500mL
    • Class III-1500-2000mL
    • Class IV- >2000mL
  • Blood loss (%BV)
    • Class I- <15%
    • Class II- 15-30%
    • Class III: 30-40%
    • Class IV: >40%
  • Pulse rate (Heart rate)
    • Class I: <100 (normal)
    • Class II: >100 (Tachy)
    • Class III: >120
    • Class IV: > 140
  • BP:
    • Class I: Normal
    • Class II: Normal
    • Class III: Decreased
    • Class IV: Decreased
  • Pulse Pressure: (SBP-DBP)
    • Class I: Normal
    • Class II: decreased
    • Class III: Decreased (<40)
    • Class IV: Decreased
  • Respiratory Rate
    • Class I: 14-20
    • Class II: 20-30
    • Class III: 30-40
    • Class IV: >35
  • Urine output: (ml/hr)
    • Class I: >30
    • Class II: 20-30
    • Class III: 5-15
    • Class IV: None
  • CNS/Mental Status:
    • Class I: Slightly Anxious
    • Class II: Mildly Anxious
    • Class III: Anxious and Confused
    • Class IV: Confused and Lethargic=unresponsive
  • Fluid Replacment: (Tx)
    • Class I: Crystalloid
    • Class II: Crystalloid
    • Class III: Crystalloid and blood
    • Class IV: Crystalloid and blood
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11
Q

Crystalloid

A
  • Natural fluid replacment
  • Ex: Normal Saline
  • No blood or blood products
  • does not restore ability of blood to carry oxygen, only restores volume to help BP
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12
Q

Normal Blood Volume % of body weight

A
  • 8% of body weight; 5-6L
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13
Q

What happens to our body when Cardiogenic/Hemorrhagic/Anaphylactic/Neurogenic shock occurs in our body

A
  • Cost of Compensating=Increased SVR (resistance)
    • shuts down organ perfusion
    • hypoxia of tissues
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14
Q

When your body responds to low BP for extended period of times what happens?

A
  • Autonomic nervous system exhausted and all reflexes fail–makes the BP workse overall
  • more decrease in CO and TPR=Decreased BP even more
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15
Q

When to intervene for patient in shock?

A
  • Compensatory portion=Treat
    • survival rate=85%
  • Decompensating portion
    • survival rate=30%
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16
Q

Hypotension must be caused by one of the following:

A
  • Decrease fluid volume
  • Decrease cardiac output
  • Decrease vascular resistance
17
Q

Managing Hypotension must include at least one of the following:

A

Something to:

  • Increase Fluid Volume
    • Fluids, transfusions
    • Increase preload
  • Increase Cardiac Output
    • Increase contractility
    • Beta agonists, sympathomimetics (dopamine and epinephrine), Positive Inotrope drugs
    • If hypotension is cardiac origin (Cardiogenic shock), try to avoid Increase HR
  • Increase Resistance:
    • Vasoconstrictors
    • alpha agonsists
    • If hypotension is cardiac in origin (Cardiogenic shock), try to avoid Increasing resistance
  • Activating reflexes in cardiogenic shock=makes hypotension worse, every other shock is fine
18
Q

Cardiogenic Shock is as clinical syndrome associated with:

A
  • systolic arterial BP less than 90mmHg or 30mmHg less than the previous basal level (if chronic HTN patient)
  • Evidence of reduced blow flows, shown by:
    • Urine output <20mL/hr
    • impaired mental fxn
    • peripheral vasoconstrction (Cold, clammy skin)
19
Q

Primary cause of Cardiogenic Shock

A
  • Complete infarction of >40% of the L ventricle
20
Q

Factors that may precipitate symptoms of decompensaition in patients with compensated Heart Failure:

A
  • Increased metabolic products
    • Fever
    • Tachycardia
    • Infection
    • Hyperthyroidism
    • Anemia
    • Pregnancy
  • Increased Circulatory Volume (Preload)
    • Excess Na+ content in diet
    • Excess fluid administration
    • Renal Faiure
  • Conditions that increase afterload
    • uncontrolled hypertension
    • Pulmonary embolism (increased R ventricualr afterload)
  • Conditions that impair contractility:
    • negative inotrope drug
    • myocardial ischemia of infarction
    • ethanol ingestion
  • failure to take prescribed HF medication
  • Excessively slow HR
21
Q

Heart Failure:

A
  • weakened heart muscle w/limited contractility
  • maintain BP by Increase Resistance or CO
    • Increase in resistance is work against CO
  • Decreased CO–>limits BP–>reflexes activate SNS
  • SNS–>vasoconstriction
    • Arteriolar tree inhibit heart SNS stimulation
    • Venous-venoconstriction–>decrease capacitance–>Increase Venous Return
      • promotes preload and supports CO
22
Q

Cardiac Index:

A
  • how we compare CO b/w people
  • CO/Body surface area
23
Q

How do you increase SV in setting of decrease Ejection Fraction due to decreased coronary flow?

A
  • Increase contractility of residual myocardium (nonischemic myocardium-not injured) but causes increased MVO2 (O2 consumption) wout ability to increase flow
  • Increase EDV (preload), but causes Increased wall tension, Increased MVO2, and preload needed to increase SV may be beyond limits
  • Decrease Afterload, but causes decrease in BP which may limit coronary flow
    • can’t maintain BP if CO doesn’t Increase
24
Q

Anaphylactic shock:

A
  • No Vascular Tone
  • Acute hyper-reaction to an ingested or injected antigen in a sensitized person
  • Mast cell degranulation occurs, releasing: Potent vasodilators
    • histamine
    • Serotonin
    • Bradykinin
  • Histamine:
    • also causes bronchial constriction and hypovolemia due to capillary dilation and loss of intravascular fluid
    • drives majority of anaphylactic shock
  • Intense vasodilation, BP can’t be maintained
  • 2 hallmark features:
    • Hypotension due to no vascular tone
    • Bronchial constriction (respiratory distress)
      • difficulty breathing
  • Treatment: ANtihistamines and epinephrine via IV
    • pressors and Inotropes
25
Q

Septic Shock:

A
  • Bacterial infection in blood produces endotoxin
  • Endotoxin acts as a antigen
    • activates the complement sequence
    • stimulates the release of vasoactive substances including serotonin
  • Vasoactive substances damage the microcirculation leading to:
    • Increased permeability of capilaries
    • Loss of protein from the plasma space, therefore
    • loss of reabsorption capability leading to loss of plasma volume and producing extravascular edema
  • 2 forms:
    • Hypodynamic sepsis
      • low output/high resistance form
      • late stage
      • vasoconstriction keeps up and heart loses pumping ability bc sepsis in heart
    • Hyperdyanimc sepsis:
      • high outputlow resistance form
      • early stage
      • also see in anaphylaxis
      • Better prognosis
26
Q

What is the better prognosis to support BP:

A
  • Support BP with a high CO better prognosis than supported with High resistance to offset low outputs
27
Q

Maintaining Normal Intracranial Pressure:

A
  • ICP is based on:
    • Brain tissue (80%)
    • CSF (10%)
    • Blood Volume (10%)
  • Pressure of these must remain balanced to maintain ICP
  • Volume changes in Brain tissue, cerebral blood flow, or CSF causes changes in ICP
  • Monro-Kelli Doctrine
    • To maintain normal ICP:
      • an increase in the volume of one of these must be compensated for b a decrease in volume of another
28
Q

Increase in ICP:

A
  • Provoke a Cushings Response
    • AKA: Cushing Reflex, CNS ischemic response
  • Brain thinks:
    • all cerebral ischemia is from reduced flow.
    • All reduced cerebral flow is due to inadequate systemic BP
  • Brain reponds by generating large CNS increase in sympathetic outflow (and a reflex bradycardia)
  • If cerebral ischemia is from:
    • true systemic decrease in blood volume
      • cushing response is last gasp effort by brain to raise BP
    • Increase ICP
      • secondary to intracranial injury and bleeding
      • provoking the response will make the problem worse
    • Cerebral vasodilation
      • causing cerebral swelling due to excessive hemodilation
      • makes problem worse
29
Q

How to decrease ICP?

A
  • Decreasing the volume of:
    • Brain tissue
    • CSF
    • circulation
  • CSF
    • Externally draining CSF via catheter place in ventricles
  • Circulation
    • Blood volume reduced by lowering BP
    • Low CO2 level will vasoconstrict cerebral arteries
      • reduces the volume of blood delivered to brain
  • Brain tissue:
    • Lobectomy
      • remove brain tissue
      • decresae volume and ICP
    • Decompreessive craniectomy
      • section of skull removed
      • allow expansion of the brain
      • allows ICP to increase without the danger of compressing brain tissue
30
Q

Respiratory failure

A
  • Terminal event in 30-50% of all shock related death
  • early ventilator support is critical in shock management
  • more oxygen available for other tissue

Week 41: (8 decks)

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