SHOCK Flashcards

1
Q

Types of Shock

A

-Hypovolemic
-Obstructive
-Cardiogenic
-Distributive

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2
Q

Hypovolemic Shock

A

-Hemorrhage, GI losses, Third spacing of fluids
-Decreased preload, diastolic filling, CO, increased SVR, decreased MAP, Shock/MODS
-Cool extremities, dry mucous membranes, flat neck veins, decreased CO, PAWP, SvO2 <65%, Increased SVR. Elevated lactate

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3
Q

Obstructive Shock

A

-Cardiac tamponade, tension ptx, PE
-Cool
-Decreased diastolic filling > decreased diastolic function > decreased CO > decreased MAP > Shock +/- MODS
-Increased ventricular afterload > decreased systolic function > decreased CO > Decreased MAP > Shock +/- MODS
-Impede venous return: Tension PTX, tamponade, restrictive pericarditis, auto-peep
–Obstruct cardiac outflow: PE, venous air embolism, aortic dissection
-TTE is the standard for dx
-Beck’s triad: Hotn, muffled heart tones, JVD
-Cool extremities, diminished breath sounds
-Decreased CO, PAWP, increased SVR, <65% Svo2, elevated lactate

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4
Q

Cardiogenic Shock

A

-MI, Stress cardiomyopathy, myocardial depression
-Parameters: persistent hotn SBP <80-90 or MAP 30 lower than baseline. CI <1.8 w/out support, or <2-2.2 with support. adequate and elevated filling pressures. End organ hypoperfusion (Urine output < 30 mL/h or cool extremities)
-ACS is still the most common etiology and accounts for ~80% of cardiogenic shock

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5
Q

Distributive Shock

A

-Sepsis, neurogenic, anaphylactic
-Decreased SVR, preload, diastolic filling, CO, decreased MAP, Shock/MODS
-Distributive shock is secondary to another process
-Warm extremities, dry mucous membranes, flat neck veins, febrile, decreased CO, PAWP, SVR. Svo2 >65%. Elevated lactate, leukocytosis, cultures positive

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6
Q

Neurogenic Shock (vasogenic shock)

A

-Combo of primary and secondary injuries that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the vagus nerve.
-Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation.
-symptoms: hotn, bradyarrhythmia’s, temp dysregulation

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7
Q

Prognosis of Neurogenic Shock

A

Prognosis: depends on the extent of spinal cord injury (ASIA) and response to treatment. Those associated with neurological deficits tend to have poor outcomes.

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8
Q

Neurogenic Shock Management

A

-Management of hemodynamics w/ fluids and pressors
-Recommend MAP 85-90 for first 7 days to improve spinal cord perfusion
-Phenylephrine is commonly used as its pure alpha 1 agonist that causes peripheral vasoconstriction to counteract the loss of sympathetic tone. —-lack of beta activity leads to reflex bradycardia
-Norepinephrine (both alpha and beta)
-Tx of bradycardia is atropine and glycopyrrolate to oppose vagal tone.
-Isoproterenol is considered for pure chronotropic effect
-Methylxanthines (theophylline and aminophylline) have been cited for refractory bradycardia
-Methylprednisolone and corticosteroids showed promised in animal modes
-Symptoms of neurogenic shock can persist for 4-5 weeks

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9
Q

Definition of severe sepsis

A

-Severe sepsis: Sepsis definition plus any evidence of organ dysfunction including altered mental status (brain hypoperfusion), renal failure, liver dysfunction, tissue hypoperfusion (diminished capillary refill), and/or lactic acid level >4.0

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10
Q

Definition of septic shock

A

-persistent hypotension despite adequate fluid resuscitation + sepsis + end-organ hypoperfusion/dysfunction

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11
Q

Management of Obstructive Shock

A

-Pericardial effusion: IV fluids, vasopressor, pericardiocentesis, pericardiostomy
-PE: IV fluids, AC, massive versus submassive (systemic lysis, surgical embolectomy, catheter directed thrombolysis), risk stratification

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12
Q

Which Fluid?

A

-Crystalloid: LR, NS -30 mls/kg
-Colloid: Albumin, RBC
-Semisynthetic colloids: Hetastarch, Succinylated gelatin

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13
Q

Toxic Shock Syndrome

A

“Toxic shock syndrome is a rare, life-threatening complication of certain types of bacterial infections.”
-Staphylococcus aureus–Treated w/ combo of antistaphylococcal penicillin plus clindamycin
-Streptococcus pyogenes (group A)-treated with a combination of penicillin plus clindamycin
-Rapid recognition and medical/surgical therapy is required
-Rapid progression, especially streptococcal disease
-80% of streptococcal-caused infections have soft tissue involvement
-IV immunoglobulin may improve outcomes

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14
Q

Surviving Sepsis Campaign

A
  1. EARLY IDENTIFICATION IS KEY!
    qSOFA is out. SIRS/NEWS/MEWS are in!
    Measure a lactate on those suspected of having sepsis.
  2. EARLY TREATMENT IS KEY!
    For those with hypoperfusion or shock, at least 30 ml/kg of crystalloid should be given within the first three hours of resuscitation. Resuscitation to be guided by decrease in serum lactate versus. not using a serum lactate
  3. Main pts of treatment
    “Balanced” crystalloid over normal saline.
    Norepinephrine, vasopressin, and epinephrine
    Broad spectrum antibiotics based on risk factors
    Source control
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15
Q

Cardiogenic Shock: Cold and Wet

A

-Classic cardiogenic shock
-decreased CI
-Increased PCWP, SVRI
-Levophed, Dopamine
-Iontropes only after revascularization

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16
Q

Cardiogenic Shock: Dry and cold

A

-Euvolemic cardiogenic shock
-decreased CI
-Increased SVRI, PCWP
-Fluid boluses 250-500 mL
-Norepinephrine or Dopamine
-Inotropes – Dobutamine, Milrinone, Epinephrine

17
Q

Cardiogenic Shock Wet and Warm

A

-Vasodilatory cardiogenic shock or mixed shock
-decreased CI, SVRI
-Increased PCWP
-Norepinephrine or Dopamine
-PA catheter guided therapy

18
Q

Cardiogenic Shock Warm and Dry

A

-Vasodilatory shock (non-cardiogenic shock)
-increased CI
-Decreased SVRI, PCWP

19
Q

Neurogenic Shock Etiology

A

-Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock
-Sudden loss of sympathetic tone: hotn, temperature dysregulation, bradyarrhythmias

20
Q

Colloid Albumin

A

Suggested in Liver Disease, but still suggest 30 mls/kg of crystalloid first.
Consider 7 mls/kg of 5% after 30 mls/kg of crystaloid

21
Q

Fluid Resuscitation: Vasopressors

A

-Norepinephrine 0.05 mcg/kg/min Recommended
-Vasopressin 0.03 units/min
-Phenylephrine 0.5 mcg/kg/min
-Epinephrine 0.05 mcg/kg/min

For pressor resistant hypotension start Hydrocortisone 50 mg IV q6h STAT

22
Q

Monitoring During Shock with Fluid Resuscitation

A

-Monitor urine output every hour
-Trend 3 Lactates the first 6 hours
Initial
-After 30 mls/kg
-2nd bolus and or pressors
-Consider monitoring CVP
-Eary abx is essential

23
Q

Abx Pneumonia

A

CAP
-Rocephin, Levaquin
-Ceftriaxone, Azithromycin
-MRSA Concern? Add vancomycin
Healthcare Associated
-Vancomycin, Zosyn, Atypical coverage
-Cefepime/Flagyl are replacing Zosyn in many Kidney Injury/CKD patients

24
Q

Intra-abdominal Abx

A

Community Acquired
-Rocephin and Flagyl
Healthcare Associated
-Zosyn or Ceftriaxone
-Hx MRSA? Add Vancomycin

25
Q

Urinary Abx

A

-Urosepsis is no longer used.
Community Acquired
-Zosyn
Healthcare Associated
-Zosyn
Hx MRSA? Vancomycin

26
Q

Soft Tissue Abx

A

Necrotizing
-Zosyn, Clindamycin, and Vancomycin
-Cefepime/Flagyl are replacing Zosyn in many Kidney Injury/CKD patients

Non-surgical wounds
-Zosyn and Vancomycin
-Cefepime/Flagyl are replacing Zosyn in many Kidney Injury/CKD patients

Cellulitis
-Vancomycin

27
Q

Goals of Cardiogenic Shock Management

A

-Address the etiology
-Preload reduction
-Afterload reduction
-Ionotropic support
-Mechanical support

28
Q

Management of cardiogenic shock

A

-Preload: Gentle 250-500 mL fluid bolus with careful hemodynamic monitoring
-Oxygenation: Goal saturation >92%, consider early intubation to decrease work of breathing
-Arrhythmias
-DC cardioversion of tachyarrhythmias
-Transvenous pacing of bradyarrhythmias
-Discontinue anti-hypertensives
-Usually avoid vasopressin and phenylephrine unless vasodilatory shock, outflow obstruction or pure RV failure
-Caution with rate-control in regurgitant lesions
-Consider pacing/cardioversion as a hemodynamic stabilization adjunct