Shock Syndromes

Dr. McMath

How is shock characterized?

Inadequate global tissue perfusion

Is the presence of hypotension required to define shock?

Nope!!

What are the 4 etiologic mechanisms of shock?

• Hypovolemic

• Cardiogenic

• Obstructive

• Vasodilatory/Distributive

What should be measured in all patients in whom shock is suspected?

Blood lactate

Why should blood lactate be measured when shock is suspected?

Lactate increases in shock primarily due to reduced O₂ delivery to the tissues, leading to anaerobic metabolism and increased lactate production

For circulatory insufficiency associated with hemodynamic instability, what is the first-line fluid of choice?

Crystalloid solutions

When volume resuscitation fails in patients with shock, in order to maintain adequate blood pressure and hypoperfused tissues, what therapy is required?

Vasopressors and inotropes

What is the preferred initial vasopressor for shock?

Norepinephrine

In terms of SBP and MAP, what is the defining values that determine diagnosis of shock?

SBP < 90 mmHg, MAP <70 mmHg with tachycardia and organ perfusion abnormalities

Preload

All factors that contribute to passive ventricular wall stress (or tension) at the end of diastole

• Volume of blood in the ventricles at the end of diastole

Afterload

All the factors that contribute to total myocardial wall stress (or tension) during systolic ejection

• Pressure that must be overcome by the ventricles during systole

When does circulatory shock develop?

When cardiovascular system is unable to deliver an adequate oxygen supply to meet tissue oxygen demands resulting in cellular dysfunction

What are the two main consistencies throughout all shock syndromes?

Inadequate tissue and organ perfusion

When is lactate considered evidence of end organ dysfunction in shock?

> 2 mmol/L

When is INR / aPTT considered evidence of end organ dysfunction in shock?

INR > 1.5

aPTT > 60 seconds

When is platelet count considered evidence of end organ dysfunction in shock?

< 100,000

When is bilirubin considered evidence of end organ dysfunction in shock?

> 2 mg/dL

When is creatinine considered evidence of end organ dysfunction in shock?

> 2 mg/dL (damage to the kidneys)

When is urine output considered evidence of end organ dysfunction in shock?

< 0.5 mL/kg/hour x 2 hours

When is SBP and MAP considered evidence of end organ dysfunction in shock?

SBP < 90 mmHg, or decreased more than 40 mmHg from previously recorded patient normal

MAP < 70 mmHg

Vasodilatory/distributive shock

Tissue hypoperfusion resulting from decreased systemic vascular resistance (SVR)

What is the most common type of shock?

Distributive shock

Cardiogenic shock

Results from a loss in pump function, through decreased cardiac contractility (e.g., MI), acute valvular abnormality, or an arrhythmia (e.g., ventricular tachycardia)

• heart is not pumping correctly

Hypovolemic shock

Inadequate venous return, from internal or external loss of intravascular fluids (e.g., trauma, surgery, or hemorrhage), resulting in insufficient cardiac preload and decreased stroke volume

• not enough blood to go around

Obstructive shock

Extracardiac obstruction to blood flow into or out of the heart, such as tension pneumothorax, cardiac tamponade, or pulmonary embolism

How does hypovolemic shock affect Preload, CO, and Afterload?

• Preload ↓

• CO ↓

• Afterload ↑

How does cardiogenic shock affect Preload, CO, and Afterload?

• Preload ↑

• CO ↓

• Afterload ↑

How does obstructive shock affect Preload, CO, and Afterload?

• Preload ↑

• CO ↓

• Afterload ↑

How does vasodilatory/distributive shock affect Preload, CO, and Afterload in pre-resuscitation?

• Preload ↓

• CO ↓

• Afterload ↓

How does vasodilatory/distributive shock affect Preload, CO, and Afterload in post-resuscitation?

• Preload ↑

• CO ↑

• Afterload ↓

In hypovolemic shock, what is the target?

Preload

In cardiogenic shock, what is the target?

Inotrope

In obstructive shock, what is the target?

Not specific, pharmacotherapy is limited (e.g., surgery, fibrinolytic)

In vasodilatory/distributive shock, what is the target?

Afterload

What is afterload?

Pressure that the ventricles must overcome in order to eject the blood into circulation

Symptoms seen in shock syndromes

Not very profound

• Dizziness

• Light-headedness

• Confusion

• Low urine output

Signs seen in shock syndromes

• Tachycardia (e.g., HR > 120 bpm) — heart trying to compensate for poor CO

• Tachypnea (e.g., RR > 30 rpm)

• Hypotension (not always diagnostic)

• Body temperature abnormalities

• Impaired capillary refill time (e.g., > 3 seconds) — low fill state

• AMS up to obtundation — decline in mental state

Laboratory tests for shock diagnoses

• Blood lactate (e.g., > 2 mmol/L)

  • Serial lactate concentrations are recommended in the early phases of shock treatment because lactate clearance and normalization correspond with improved global tissue perfusion

• Evidence of end-organ hypoperfusion — ↑ bilirubin, ↑ creatinine, ↑ INR

• Anemias in bleeding

• Positive cardiac troponin with acute MI — cardiogenic shock

MAP

Average pressure throughout one cardiac cycle → one cardiac cycle = systole & diastole

• Functions to perfuse blood to all the tissues of the body to keep them functional

• Should remain at least 60 mmHg so that blood can effectively reach all tissues

• Measured via usage of an arterial line

MAP = [SBP + (2 x DBP)] / 3

What is the MAP goal when treating patients with shock?

≥ 65 mmHg

Treatment algorithm for shock syndromes

What are blood products used for in the treatment of shock?

Predominantly associated with acute large volume blood loss

What is the goal of administering IV fluids when treating shock?

• ↑ SV

  • ↑ CO

• ↑ DO₂

• ↑ BP

Passive Leg Raise (PLR)

Transiently increases venous return in patients who are preload responsive, as such it is a diagnostic test not a treatment

• Predictor of fluid responsiveness (i.e., helps identify patients who are on the ascending portion of their starting curve and will have an increase in SV in response to fluid administration)

When using crystalloid solutions such as NS or LR, how much fluid should there be in the interstitial and intravascular compartments?

• Interstitial: 750 mL

• Intravascular: 250 mL

What is the major indication for using NS or LR?

Intravascular volume expansion

In distributive (septic) shock, what is the dose for fluid resuscitation?

Start with 30 mL/kg IV crystalloid (based on ABW)

• > 30 mL/kg in total may be needed to obtain goal MAP, reverse global hypoperfusion, or achieve clinical indication of regional organ-specific perfusion

What has been known to occur with excess fluid administration in septic shock?

Higher mortality, especially in patients with heart failure or impending pulmonary edema

Why is it harmful to give fluid resuscitation beyond minimal levels in patients with penetrating abdominal trauma?

Hemodilution and clot destabilization (risk of bleeding to death)

T/F: In hemorrhagic/traumatic shock, fluids should be given in small aliquots to yield a palpable pulse and to maintain MAP no more than 60 mmHg and SBP no more than 90 mmHg based on accurate measurements (e.g., arterial monitoring).

True

What is the fluid of choice in hemorrhagic/traumatic shock therapy, due to being associated with a lower risk of adverse effects?

Isotonic crystalloids

What solutions should be avoided in patients with severe TBI as it may worsen cerebral edema?

Balanced salts solutions

What causes an increase in sympathetic tone in hypovolemic shock?

Decreased preload directly reduces cardiac output, which activates baroreceptors

If hypovolemic shock is left untreated, what will happen?

Circulatory shock will continue

Complications associated with hypovolemic (hemorrhagic) shock

• Loss of RBCs may further ischemic damage to vital organs (i.e., end organ damage)

• Clotting factors and platelet counts may also be reduced in presence of hemorrhage

• Dilutional effect with crystalloid resuscitation can further decrease clotting activity

• Coagulopathy persists and is often accompanied by acidosis and hypothermia, leading to the “lethal triad”

What 2 pharmacotherapy options are required in patients with shock, when volume resuscitation is not indicated or fails to maintain adequate BP (MAP ≥ 65 mmHg) and organs and tissues remain hypoperfused?

Vasopressors and Inotropes

What can be used to temporarily treat life-threatening hypotension when tissue perfusion is inadequate despite ongoing aggressive fluid resuscitation?

Vasopressors

Norepinephrine as pharmacotherapy for shock

Combined strong α₁ activity and less potent β₁ agonist effects; Weak vasodilatory effects of β₂ stimulation

• ↑ MAP, ↑ SVR

• ↓ HR due to reflex bradycardia from ↑ SVR

• ↑ Cardiac filling pressure by ↑ venous return through via vasoconstriction (i.e., its more prominent α effects on all vascular beds)

  • Inconsistent effect!

Dosing of Norepinephrine IV for shock therapy

Start when MAP ≤ 65 mmHg and/or adequate tissue perfusion is not achieved with fluid resuscitation

• Initial → 0.05 to 0.1 mcg/kg/min (titrate to goal MAP)

• Usual range → 0.025 to 1 mcg/kg/min

• Max. (for refractory shock) → 1 to 3.3 mcg/kg/min

What is the absolute maximum dose for IV norepinephrine?

3.3 mcg/kg/min

Epinephrine as pharmacotherapy for shock

Adjunctive therapy to Norepinephrine

• Associated with tachydysrhythmias and lactate elevation

• Combined α and β effects

What pharmacotherapy would be preferred if a patient has anaphylactic shock requiring β stimulation for opening the airways?

Epinephrine, due to β effects

Dosing of Epinephrine IV for cardiogenic shock therapy

0.01 to 0.5 mcg/kg/min; titrate based on clinical end point (e.g., BP, end-organ perfusion)

Dosing of Epinephrine IV for post-cardiac arrest shock therapy

0.01 to 1 mcg/kg/min; titrate based on clinical end points (e.g., MAP, end-organ perfusion)

Max. (for refractory shock) → 2 mcg/kg/min

Dosing of Epinephrine IV for septic shock & other vasodilatory shock states (adjunctive agent) therapy

0.01 to 0.2 mcg/kg/min; titrate to goal MAP or end-organ perfusion

• Usual range → 0.01 to 0.5 mcg/kg/min

• Max. (for refractory shock) → 0.5 to 2 mcg/kg/min

Phenylephrine as pharmacotherapy for shock

Should not be used as an initial vasopressor in shock patients with impaired myocardial performance

• A pure α₁ agonist; increases blood pressure primarily through vasoconstriction (via IV)

Dosing of Phenylephrine IV for septic shock & other vasodilatory shock states (adjunctive agent) therapy

0.5 to 2 mcg/kg/min; titrate to desired MAP

• Usual range → 0.25 to 5 mcg/kg/min

Dosing of Phenylephrine IV for cardiogenic shock therapy

Not ideal — concern for issues in the myocardium

• 0.1 to 10 mcg/kg/min; titrate to clinical end point

Dobutamine as pharmacotherapy for shock

Selective β₁ agonist with mild β₂ and α activity

• Strong inotropic activity without concomitant vasoconstriction

• Greater increase in CO compared to dopamine and is less arrhythmogenic

What are optimal uses of Dobutamine in shock therapy?

In patients with low CO and high filling pressures (e.g., left ventricular dysfunction demonstrated with echocardiography) or ongoing signs of global/regional hypoperfusion despite adequate resuscitation

What types of shock is Dobutamine primarily used?

Septic and cardiogenic shock; ↑ CO

What is the typical increase range for CO with Dobutamine treatment in septic/cardiogenic shock?

25% to 50%

Dosing of Dobutamine for inotropic support

• Initial: 2 to 5 mcg/kg/min; titrate based on clinical endpoint (e.g., BP, end-organ perfusion)

• Usual range → 2 to 10 mcg/kg/min

• Max. dose → 20 mcg/kg/min

Vasopressin as pharmacotherapy in vasodilatory/distributive shock

• Increases SVR and arterial blood pressure in patients with vasodilatory/distributive shock

• Reduction in dosage requirements of catecholamine adrenergic agents (e.g., NE)

• Enhances urine production

Dosing of Vasopressin IV for septic shock & other vasodilatory shock states (adjunctive agent)

0.03 units/minute (0.04 units/minute) added to norepinephrine as a fixed dose (not titrated)

• Usual range → 0.01 to 0.04 units/minute

• >0.04 units/minute for salvage therapy due to potential risk for ischemic complications

What is Angiotensin II?

Naturally occurring peptide hormone of RAAS that causes vasoconstriction and increases aldosterone release, which raises blood pressure and ↑ SVR

When should Angiotensin II be used with extreme caution?

In patients with impaired left ventricular systolic function

What adverse effects are commonly reported with Angiotensin II?

Delirium and lactic acidosis

Dosing of Angiotensin II IV for septic shock & other vasodilatory shock states (adjunctive agent)

10 to 20 ng/kg/minute; titrate by up to 10-15 ng/kg/minute every 5 minutes based on goal MAP

• Decrease dose by ≤ 15 ng/kg/minute every 5-15 minutes based on response ONCE SHOCK HAS IMPROVED

Corticosteroids as pharmacotherapy in shock

Improves arterial pressure while minimizing the dosage of catecholamine vasopressors

• Use is controversial — optimal dosing ~260 mg/day of hydrocortisone or equivalent

Dosing of Hydrocortisone IV for septic shock, inadequate response to fluid resuscitation and vasopressor therapy

50 mg bolus every 6 hours OR 100 mg every 8 hours for 5-7 days