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Research in Progress - PACCM @ PittResearch in Progress Author Jason Stamm Created Date 6/24/2015 3:36:20 PM

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  • Case 1

    65 year old female nursing home

    resident with a hx CAD, PUD, recent hip

    fracture

    Transferred to ED with decreased

    mental status

    BP in ED 80/50

  • Case 1

    65 year old female nursing home

    resident with a hx CAD, PUD, recent hip

    fracture

    Transferred to ED with decreased

    mental status

    BP in ED 80/50

    This case demonstrates some common risk factors for causes of shock

    (ACS from CAD?, bleeding from a peptic ulcer?, PE from immobility?)

    and common manifestations of shock (altered mental status, hypotension)

  • Shock

    • Definition

    • Physiology of shock

    • Types of shock

    • Stages of shock

    • Clinical presentation of shock

    • A bit on vasopressors, inotropes

  • Definition

    Inadequate perfusion of tissues which is

    insufficient to meet cellular metabolic

    needs

    There is no set blood pressure, cardiac

    output, CVP, urine output, or etc that

    defines shock.

  • Mechanisms of Hypotension

    MAP – mean arterial pressure

    Cardiac Output

    Stroke Volume

    Preload Contractility

    SVR

    Heart Rate

    Dr. Kreit circa 2010

  • Mechanisms of Hypotension

    Hypotension

    Cardiac Output

    Stroke Volume

    Preload Contractility

    SVR

    Heart Rate

    Dr. Kreit circa 2010

  • Compensatory Mechanisms that

    maintain MAPLV Preload

    Stroke Volume

    Cardiac Output

    Arterial Pressure

    Baroreceptors Sympathetic activity

    Heart Rate Contractility

    +

    +

    Arterial constriction

    Venous constriction

    +

    SVR+

    Adapted from Dr. Kreit circa 2010

    Renin

    Angiotensin II

    Aldosterone

    VasopressinNa and H2O

    Retention

    +

    +

    +

  • Systemic O2 Delivery

    • Regulation of O2 delivery (DO2)

    – Normally, via cardiac output (CO) and tissue

    extraction

    – There is no “normal” cardiac output

    – Only adequate or inadequate cardiac output

    for given metabolic conditions

    Pinsky Chest 2007; 132: 2020

    http://www.ncbi.nlm.nih.gov/pubmed/18079239

  • Shock Physiology

    • Imbalance of O2 delivery and

    consumption

    • Shock results in inadequate O2 delivery

    – Cellular hypoxia → anaerobic metabolism

    – ↓ ATP generation

    – ↓ ion pumps, membrane function

    • Initially, damage is reversible →

    eventually there is irreversible injury

    – Cell death, organ failure, MOSF, death

  • Types of Shock

    • 4 major categories – Hinshaw and Cox

    • “Volume, pump, container”

    – Hypovolemic- volume

    • Fluid losses (fistulas, burns), hemorrhage

    – Cardiogenic- pump

    • Myopathic, arrhythmic, mechanical, thyroid

    – Distributive- container

    • Sepsis/SIRS, anaphylaxis, neurogenic, adrenal

    • Obstructive

    • PE, Aortic stenosis, tamponade, tension pneumo

  • Types of Shock

    Shock Type COCardiac output

    PCWPpulmonary capillary

    wedge pressure

    SVRsystemic vascular

    resistance

    Hypovolemic ↓ ↓ ↑

    Cardiogenic ↓ ↑ ↑

    Obstructive ↓ NL or ↑ ↑

    Distributive ↑ ↓ or NL ↓

  • Septic shock

    SIRS HR, WBC (↑,↓), RR (PaCO2), Temp (↑,↓)

    Sepsis SIRS with culture+ infection or identified infection

    Severe Sepsis Sepsis with organ hypoperfusion or dysfunction

    Septic Shock Severe sepsis with hypotension after volume

    Refractory Septic Shock Shock requiring high dose pressors after

    resuscitation

  • Stages of Shock

    • Pre-shock (“compensated shock”)– Homeostatic mechanisms are sufficient

    – You may see:

    – ↑ HR

    – peripheral vasoconstriction

    – BP remains nearly normal

    • Shock– Homeostatic mechanisms are overwhelmed

    – Organ dysfunction first appears

    • End organ dysfunction

  • Case 2

    You are call by a nurse:

    “Mrs. Jones is hypotensive”

    Step #1 – ?

  • Case 2

    You are call by a nurse:

    “Mrs. Jones is hypotensive”

    Step #1 – Go See Patient –

    Assess and Treat simultaneously

    ○ ABCs

    IV access, crystalloid volume early

    Pulse ox, UOP, central venous and arterial lines

    ○ H&P clues

    Comorbidities, localizing sxs, etc.

    Bleeding, cardiac exam, JVP, infection, etc

  • Clinical Presentation of Shock

    • Signs and symptoms

    – Anxiousness, altered mental status

    – Tachycardia, tachypnea

    – Cool extremities (±in early distributive shock)

    – Weak pulses

    – ↓ urine output, acidemia (lactate)

    – eventually you will see ↓SBP (a late sign)

  • Shock Management

    • Improve DO2 to “adequate level”

    – There are no static values

    – It requires a knowledge of CO, vascular tone

    – Are they fluid (pre-load) responsive?

    – Can assess with:

    • Traditional parameters/methods:

    • CVP/Fluid challenge) - not always reliable

    • Pulse Pressure Variation, Passive leg raising

    – If pre-load optimized → is CO adequate?

    • Assess SvO2 for tissue oxygenation

  • Early Goal Directed

    Therapy

    “Functional Hemodynamic

    Monitoring”

    - early aggressive

    resuscitation

    - end point of improved

    tissue oxygenation

    - multicenter trials

    ongoing

    Rivers et al. NEJM 2001; 345:1368

    http://www.ncbi.nlm.nih.gov/pubmed/11794169

  • A bit on vasopressors and

    inotropes:

  • Adrenergic receptors

    ADRENOCEPTORS

    α1

    - Vasoconstriction

    - Increased peripheral resistance

    - Increased blood pressure

    α2

    - Inhibition of norepinephrinerelease

    β1

    - Tachycardia

    - Increased myocardial contractility

    β2

    - Vasodilation

    - Decreased peripheral resistance

    - Bronchodialation

  • Vasopressor parmacology

    α1 β1 β2 DA MAP PCWP CO SVR HR

    Dopamine

    10 mcg/kg/min +++ ++++ + 0 ↑↑ ↑ ↑ ↑ ↑↑

    Norepinephrine

    0.01-3 mcg/kg/min +++++ ++ 0 0 ↑↑↑ ↑↑ ↑↓ ↑↑↑ ↑↑

    Phenylephrine

    0.5-9 mcg/kg/min +++++ 0 0 0 ↑ ↑ ↑↓ ↑ NA

    Vasopressin

  • Inotrope pharmacology

    α1 β1 β2 MAP PAP CO SVR HR MOC

    Dopamine

    3-10 mcg/kg/min 0/+ ++++ ++ ↑ ↔↑ ↑ ↔↓ ↑ ↑

    >10 mcg/kg/min +++ ++++ + ↑↑ ↑ ↑ ↑ ↑↑ ↑

    Dobutamine

    2-20 mcg/kg/min + ++++ +++ ↓ ↓ ↑↑ ↓ ↑↑ ↑

    Epinephrine

    0.01-0.1 mcg/kg/min +++++ ++++ +++ ↑↑ ↑↑ ↑↑ ↑ ↑↑ ↑

    Milrinone

    0.125-0.75 mcg/kg/min

    PDE-3 inhibitor ↓↓ ↓↓ ↑↑ ↓↓ ↑ ↔↑

    Circulation 2008;118:1047-56

    Crit Care Med 2008;36:S106-11

    MOC; myocardial oxygen consumption

  • What pressor to chose?

    De Backer D. NEJM 2010

    http://www.ncbi.nlm.nih.gov/pubmed/20200382

  • More adverse events with

    dopamine

    De Backer D. NEJM 2010

    http://www.ncbi.nlm.nih.gov/pubmed/20200382

  • Vasopressors and Inotropes

    • Clinical considerations with pressors

    – Ensure fluid replete

    – Treating people with pressors who are

    hypovolemic can cause digital and organ

    ischemia

    – pH ≥ 7.0 to 7.1

    – Pressor-receptor interaction is poor with

    acidosis. May need to give buffer to get pH

    up.

    – Central line preferable

  • Take Home Messages

    Shock = inadequate tissue oxygen delivery

    Cardiogenic, hypovolemic, distributive, obstructive

    Treat patient at the bedside

    Treat underlying cause, make sure volume replete, and use pressorsjudiciously