1. SHOCK: Classification, Pathophysiology and Approach to Management
Darin Stettler D.O.
Millcreek Community Hospital
Internal Medicine Resident Lectures

2. SHOCK: Classification, Pathophysiology and Approach to Management
Goal:
The resident will gain a basic understanding of the shock syndromes and their Management

3. SHOCK: Classification, Pathophysiology and Approach to Management
Objectives:
The resident will:
Identify the various classifications of shock.
Describe the hemodynamic profile associated with each class of shock.
Explain the Pathophysiology and mechanisms of cellular injury associated with shock.
Discuss the Management and therapy involved in the treatment of shock.

4. Background
Shock is one of the most frequent physiologic entities encountered by intensive care physicians.
Despite continued investigation into the syndrome, mortality from the shock states remains high (35%).

5. Definition
The appropriate definition varies with the context of its use.

6. Definition Emergency medical personnel
A definition that incorporates the typical clinical signs of shock, i.e.
Arterial hypotension,
Tachycardia,
Tachypnea,
Altered MS,
Decreased UOP.

7. Definition Physiologist
Shock may be defined by specific hemodynamic criteria involving ventricular filling pressures,
Venous pressures,
Arterial pressures,
CO,
SVR.

8. Definition
Physician
A syndrome in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.

9. Determinants of Effective Tissue Perfusion
Cardiac Function Local Oxygen unloading and Diffusion
Preload Oxyhemoglobin affinity
Afterload RBC 2,3 DPG
Contractility pH
Heart rate Temperature
Venous return (RAP)
Vascular compliance
Distribution of CO Cellular Energy Generation & Use
Intrinsic/ extrinsic regulation Citric acid Cycle
Autonomic Vascular resistance Oxidative phosphorylation pathway
Exogenous vasoactive agents Other energy metabolism pathways– ATP utilization
Microvascular Function
Pre/post capillary sphincter function
Capillary endothelial integrity
Microvascular obstruction (fibrin, platelets, WBC)

10. Classification

11. Obstructive Cardiogenic Hypovolemic Distributive
MI hemorrhage sepsis
Diastolic vs Systolic myocardial damage preload myocardial
Function depression
Systolic & Diastolic diastolic filling S & D
Function function
CO SVR
SVR CO
MAP
Maldistribution
SHOCK of flow
MODS

12. Hypovolemic Shock
Due to a decreased circulating blood volume in relation to total vascular capacity.
May be due to dehydration, internal/external hemorrhage, GI fluid losses (D/V), urinary losses (diuretics, renal dysfunction), decreased vascular permeability (sepsis), venodilation (drugs, spinal).

13. Hypovolemic Shock
NOTE: significant blood volume may be shed in the absence of any clinical sings
General manifestations include cold, clammy skin from SNS stimulation and peripheral hypoperfusion.
Decreased UOP and Tachycardia may be the only objective clinical abnormality.

14. Hypovolemic Shock Class I Class II Class III Class IV
Blood loss ml < , ,500-2, >2,000
Blood loss % <15% % % >40%
Pulse rate < > > >140
BP nml nml decreased decreased
Pulse Pressure nml/Inc decreased decreased decreased
CRT nml decreased decreased decreased
Respiratory rate >35
UOP ml/hr negligible
Mental Status sl anxious anxious confused lethargic
Fluid Replacement crystalloid crystalloid crystalloid +blood

15. Hypovolemic Shock Hemodynamic Profile Diagnosis CO SVR PWP CVP MVO2
Note: Filling pressures appear normal if hypovolemia occurs in the setting of base line myocardial compromise.

16. Hypovolemic Shock
Hypovolemic shock is more than a simple mechanical response to loss of volume.
It involves a dynamic process of competing adaptive and maladaptive responses at each stage of development.
While volume replacement is always a necessary component of treatment, a series of inflammatory mediators, CV, and organ responses are initiated that supersede the initial insult in driving further injury.

17. Cardiogenic Shock The underlying defect is PUMP Failure.
Most commonly due to ischemic myocardial injury- requires 40% nonfunctional myocardium.
Usually involves Anterior MI with Left Main or proximal LAD occlusion.

18. Cardiogenic Shock Incidence of shock after AWMI is 8-20%.
Unless the lesion is amenable to surgical correction, mortality rates can exceed 75%.
Other causes: cardiomyopathy, AS, aortic dissection, MS, AR/MR, VSD, Atrial Myxoma, dysrhythmias.

19. Cardiogenic Shock
Clinical signs: peripheral vasoconstriction, oliguria, +JVD, S3 and evidence of pulmonary edema.
The Hemodynamic profile includes CO, PAWP, and systemic hypotension.

20. Cardiogenic Shock Dx CO SVR PWP CVP MVO2 LVMI VSD LVCO nl MVR/ RVMI
(Mechanical) RVCO>LVCO
MVR/
RVMI

21. Cardiogenic Shock
Optimal cardiac performance in pt’s with impaired myocardium may occur at higher than normal PWP (20-24)
Pt’s should not be Dx with Cardiogenic Shock unless hypotension (MAP<65), and CI < 2.2, coexist with a PWP of > 18.

22. Cardiogenic Shock Tx
Stabilize BP with vasopressors (LV), Inotropes (RV), and fluids as tolerated.
Tx pulmonary congestion with diuretics and venodilators.
Institute mechanical ventilation, if needed.
Place IABP.
Restore NSR.
Assess candidacy for angioplasty/bypass or other surgical repair.

23. Obstruction to normal CO and diminished system perfusion
Obstructive Shock
Obstruction to normal CO and diminished system perfusion
Directly impair diastolic filling of the RV.
Indirectly impair RV filling by obstructing venous return.
Increased ventricular afterload.
Pericardial Tamponade, constrictive pericarditis.
Tension Pneumothorax Intrathoracic tumors.
Massive PE (> 2 lobar arteries with > 50% occlusion), acute P-HTN, aortic dissection & saddle embolus.

24. Obstructive Shock Hemodynamic Profile
Similar to other low output shocks with decreased CI, SVI, MVO2, Lactate.
Tension Pneumothorax, Intrathoracic tumors.
Cardiac Tamponade.
Constrictive pericarditis.
Massive PE.
Saddle embolus/aortic dissection.
CI, SVR +JVD.
Increased and equalized RV & LV diastolic pressures, PAD, CVP, PWP .
RV & LV diastolic pressures and within 5 mmHg of each other.
RV failure with PA & CVP and normal PWP.
PWP, BP signs of LVF.

25. Distributive Shock
The defining feature is loss of peripheral vascular resistance, characterized by SVR or Capacitance.
Septic shock---most common form.
Anaphylactic shock---IgE mediated release of mediators from tissue mast/basophils.
Neurogenic Shock---loss of peripheral vasomotor control, from spinal injury, or similar phenomenon of vasovagal syncope sometimes associated with SAB.

26. Septic Shock
Septic shock is an immediate life-threatening syndrome initiated by microorganisms, their toxins, or both, that have invaded the bloodstream.
Septic shock is the most common cause of non cardiac death in ICU’s across the country 25%-60%. It is primarily nosocomial.
Thought to be initiated by an exaggerated host inflammatory response to certain pathogens.

27. Microbial Factors Gram-Positive Gram-Negative Fungal P. Aeruginosa
S. Aureus
Peptidoglycans of cw
Endotoxin (LPS)
Mennan from cw
Exotoxin A
TSST

28. Inflammatory Mediators
TNF
Stimulates IL-1,6,8, PAF, Prostaglandin's
Activates coagulation pathway and compliment system
Increases permeability
Produces fever
Depresses cardiac myocyte contractility
Decreases arterial pressure, SVR, EF, Increases CO

29. Inflammatory Mediators
Stimulates TNF, IL-6,8, PAF, Leukotrienes, T-A2, prostaglandin’s,
Promotes PMN cell activation and accumulation
Increased endothelial procoagulant activity
Depresses cardiac myocyte contractility.
Produces fever.
Promotes adhesion of endothelial cells
Activates T & B cells
IL-1

30. Hemodynamic Profile Dx CO SVR PWP CVP MVO2 Septic Shock
The hyperdynamic circulatory state ( CO and SVR) is dependant on fluid resuscitation. Prior to giving fluids, a hypodynamic circulation is typical.

31. Organ System Dysfunction
CNS
Heart
Pulmonary
Renal GI
Hepatic
Hematological
Metabolic
Encephalopathy (ischemic or septic) Cortical necrosis
Tachy/Bradycardia, SVT, Ventricular ectopy, Myocardial ischemia
Acute Respiratory Failure, ARDS.
Pre-renal failure, ATN
Ileus, Erosive gastritis, Pancreatitis, Acalculous cholecystitis, Transluminal translocation of bacteria/Endotoxin
Ischemic hepatitis, Shock Liver
DIC, dilutional thrombocytopenia
Hyperglycemia early, Hyopglycemia late hypertriglyceridemia

32. Septic Shock

33. Treatment
To effectively combat septic shock, clinicians should use an integrated treatment approach
Eradicate the microorganism
Provide ICU life support
Neutralize microbiological toxins
Modulate host inflammatory response

34. Immediate Goals Hemodynamic Support ** Optimization of O2 Delivery
Reversal of Organ System Dysfunction
MAP > 60mmhg, PWP=15-18 (inc. with Cardiogenic shock) CI>2.1L/m, (cardiac & Obstructive) CI>4.0L/m, (septic & hemorrhagic)
Hgb > 10, SaO2 > 92%, MVO2>60mmHg
Normalization of lactate (<2.2)
Reverse Encephalopathy Maintain UOP > 0.5cc/kg/hr
** Although CI is increased, perfusion may not be effective if it does not reach the tissue, or there is a defect in substrate utilization at the subcellular level

35. Vasopressors & Inotropic Support
Pressor Dose B A B Dopa Indicaiton
mcg/kg/min MAP<60, PWP>12-15
Dopamine or normal CO
NorEpi Dopamine failure
Phenylephrine Dysrhythmias
EPI CO, NorEpi Failure
Dobutamine CO, & NE Tx

36. Additional Points
New therapies for septic shock have been directed at specific bacterial toxins (endotoxin), and endogenous proinflamatory mediators like TNF, IL-1.
However, clinical trials have not established additional safety of better outcomes with this therapy.

37. Case One
A 66 y/o white male, who was diagnosed with a myocardial infarction 4 days ago suddenly develops dyspnea, fatigue, and orthopnea. You notice he has marked JVD and pulses paradoxus on exam. Which Hemodynamic profile would you expect to see in this patient?
Increased and equalized right and left ventricular diastolic pressures, PADP, CVP, and PWP.
Decreased SVR with an increased CO.
Increased SVR with an Increased CO.
Decreased PWP and a Decreased CVP.

38. Case Two
A 32 y/o white female recently had a subarachnoid block in the O.R. prior to having a total knee replacement. She suddenly becomes confused, anxious and vomits prior to passing out. Her BP is found to be 56/28 manually. Which classification of shock would best describe this event?
Hypovolemic
Cardiogenic
Obstructive
Distributive

39. Case Three
A 19 y/o male arrives in the Emergency Department following a auto-pedestrian accident. He is anxious and confused. Heart rate is 125, BP 84/60. Respirations are 30. His skin is cool and clammy with CRT>5 seconds. You diagnose him with Hypovolemic shock. Which class of Hypovolemic shock would best explain his situation?
Class I
Class II
Class III
Class IV
Class V