1. Low blood pressure
2. Inadequate tissu perfusion

**Shock is the result of inadequate cardiac output**

Cardiac output = SV * HR 

1. End diastolic volume (preload)
2. Myocardial contractility
3. Systemic vascular resistance (afterload) 

These factors are important because these are the factors that can be used to help treat shock

Why do you not want to treat shock by increasing HR?

So what factor will you use to help manage shock?

• Increased HR = Decreased preload
• During shock HR is already increased b/c increased sympathetic tone
• Increased HR = Increased likelihood of dysrhythmias 

**This is why you usually address SV during shock**

• O2: B/c one of the defining characteristics of shock is perfusion of tissue.  So this is a cornerstone therapy.  Establish an airway and provide supplemental O2
• Fluids:  use this aggressively to expand the fluid volume.  This is used to combat low BP and to increase preload.  This is the KEY therpy for increased SV. This is necessary in almost all cases of shock.  Keep in mind that if fluid therapy is prlonged, packed red blood cells might need to be given to keep hematocrit levels in within an APPROPRIATE range (mid 20%-this is low but you do NOT want to expose the patient to more transfusion product than necessary) 
• Correct acidemia: Inadequate tissue perfusion = lactic acidosis. Give bicarbonate. 

Describe the management of low BP during shock?

• Only treating low BP aggressively can be DELETERIOUS during shock
• During shock there is low BP + increased vascular resistance + increased sympathetic tone + increased HR
• Immediate + aggressive attention to increasing BP = FURTHER increases the peripheral resisance and can actually FURTHER decrease the tissue perfusion (lead to kidney damage is frequent in this senario).  
• Give fluids FIRST (slowly) and provide dopamine as the first DRUG:  As volume starts to increase, keep the BP elevated.  Dopamine prevents CV collapse by increasing systemic pressure (via alpha 1 receptors) and in the kidneys causes vasodilation via dopamine receptors.  Elevated systemic pressure w/o increase in resistance in the kidneys is the outcome. 

1. Early + adequate antibiotic therapy
2. Early BP support via NE (maybe DA) 

• Septic shock is due to sepsis which causes profound vasodilation and shock 
• Initial anti-biotic therapy is often empiric for both gram-negative bacilli and gram-positive cocci. Drugs often are aminoglycosides and carbapenem drugs.  More often carbapenems are used b/c broad spectrum.  
• Also literature says do NOT use older beta-lactam agents b/c cause release of endotoxins from bacteria and can actually make the shock worse 

• Normally in shock, vascular resistance is actually increased b/c BP is low causing an increase in vascular resistance
• In septic shock, bacterial products (lipopolysaccharides) cause vasodilation that causes a PROFOUND decrease in BP that causes decreases organ perfusion.  IF THE PATIENT DOES NOT RESPOND ADEQUATELY TO FLUIDS ALONE, THEN VASCULAR SUPPORT VIA NE OR DOPAMINE SHOULD BE STARTED.  

• What is the DOC in anaphylaxis shock and why? 
• What other drugs are going to be used during anaphylaxis shock? 

• DOC is Epinephrine:  IgE response causes anaphylaxis which leads to degranulation of mast cells which causes edema, bronchospasm, and vasodilation.  NE relieves the edema by constricting the vasculature via alpha-1 receptors and directly counteracts the bronochospam via a beta-2 receptor effect
• Anti-histamine (H1-blockers):  Onset is slower than NE and do not reverse the effects of histamine nearly as quickly as NE. But can still be used.
• Corticosteroids:  They have NO EFFICACY IN REVERSING THE LIFE-THREATENING EFFECTS OF MAST CELL DEGRANULATION and are slow on onset.  They are administered to prevent delayed reactions.  

• During hypovolemic shock, vascular resistance is high b/c of activated sympathetics.  
• Fluid replacement is critical
• To increase BP if it does not respond to fluids:

• Intrinsic cause of cardiogenic shock (e.g. MI): 

-Restore blood to the heart + all MI treatments

-Do NOT use NE because this increases afterload 

• Outflow cardiogenic shock (E.g. aortic valve stenosis): 

• Dopamine or other alpha-agonists if there is no response to DA
• Vasopressin 
• Atropine: This is to help with bradycardia which is often a componenet of neurogenic shock b/c the sympathetic system is inactivated which leaves the parasympathetic tone unopposed and activated above baseline levels.  This causes increased vagal tone to the SA node causing a decrease in BP.  Atropine blocks the bradycardia but requires high doses that will cause urinary retention and oter signs of muscarinic receptor blockade.