By:Dawit Ayele MD,Internist
Definition Epidemiology Physiology Classes of Shock Clinical Presentation Management Controversies
A physiologic state characterized by ◦ Inadequate tissue perfusion Clinically manifested by ◦ Hemodynamic disturbances ◦ Organ dysfunction
Mortality ◦ Septic shock – 35-40% (1 month mortality) ◦ Cardiogenic shock – 60-90% ◦ Hypovolemic shock – variable/mechanism
Imbalance in oxygen supply and demand Conversion from aerobic to anaerobic metabolism Appropriate and inappropriate metabolic and physiologic responses Resultant systemic physiology:- ◦ Cell death and end organ dysfunction ◦ MSOF and death
Characterized by three stages ◦ Preshock (warm shock, compensated shock) ◦ Shock ◦ End organ dysfunction
Compensated shock ◦ Low preload shock – tachycardia, vasoconstriction, mildly decreased BP ◦ Low afterload (distributive) shock – peripheral vasodilation, hyperdynamic state
Shock ◦ Initial signs of end organ dysfunction: ◦ Tachycardia ◦ Tachypnea ◦ Metabolic acidosis ◦ Oliguria ◦ Cool and clammy skin
End Organ Dysfunction ◦ Progressive irreversible dysfunction ◦ Oliguria or anuria ◦ Progressive acidosis and decreased CO ◦ Agitation, obtundation, and coma ◦ Patient death
Schemes are designed to simplify complex physiology Major classes of shock ◦ Hypovolemic ◦ Cardiogenic ◦ Distributive
Results from decreased preload Etiologic classes ◦ Hemorrhage - e.g. trauma, GI bleed, ruptured aneurysm ◦ Fluid loss - e.g. diarrhea, vomiting, burns, third spacing, iatrogenic
Hemorrhagic Shock ParameterIIIIIIIV Blood loss (ml)<750750– –2000>2000 Blood loss (%)<15%15–30%30–40%>40% Pulse rate (beats/min)<100>100>120>140 Blood pressureNormalDecreased Respiratory rate (bpm)14–2020–3030–40>35 Urine output (ml/hour)>3020–305–15Negligible CNS symptomsNormalAnxiousConfusedLethargic Crit Care. 2004; 8(5): 373–381.
Results from pump failure ◦ Decreased systolic function ◦ Resultant decreased cardiac output Etiologic categories ◦ Myopathic ◦ Arrhythmic ◦ Mechanical ◦ Extracardiac (obstructive)
Results from a severe decrease in SVR ◦ Vasodilation reduces afterload ◦ May be associated with increased CO Etiologic categories ◦ *Sepsis ◦ *Neurogenic / spinal ◦ Other (next page)
Other causes ◦ Systemic inflammation – pancreatitis, burns ◦ Toxic shock syndrome ◦ Anaphylaxis and anaphylactoid reactions ◦ Toxin reactions – drugs, transfusions ◦ Addisonian crisis ◦ Myxedema coma
Septic Shock
Clinical presentation varies with type and cause, but there are features in common:- Hypotension (SBP 40) Cool, clammy skin (exceptions – early distributive, terminal shock) Oliguria Change in mental status Metabolic acidosis
Done in parallel with treatment! Hx&P/E – helpful to distinguish type of shock Full laboratory evaluation (including H&H, cardiac enzymes, ABG) Basic studies – CxR, EKG, U/A Basic monitoring – V/S, UOP, CVP, A-line Imaging if appropriate – FAST, CT Echo vs. P/A catheterization ◦ CO, PAS/PAD/PAW, SVR, SvO2
Manage the emergency Determine the underlying cause Definitive management or support
Your patient is in extremis – tachycardic, hypotensive, obtunded How long do you have to manage this? Suggests that many things must be done at once Draw in ancillary staff for support! What must be done?
One person runs the code! Control airway and breathing Maximize oxygen delivery Place lines, tubes, and monitors Get and run IVF on a pressure bag Get and run blood (if appropriate) Get and hang pressors & Call your senior /fellow/ attending
Often obvious based on history Trauma most often hypovolemic (hemorrhagic) Postoperative most often hypovolemic (hemorrhagic or third spacing) Debilitated hospitalized pts most often septic Must evaluate all pts for risk factors for MI and consider cardiogenic Consider distributive (spinal) shock in trauma