1. CONCEPTS OF NORMAL HEMODYNAMICS AND SHOCK
At the end of this self study the participant will:
Define the terms: stroke volume, cardiac output, preload, afterload, contractility,
Describe the difference between early and late cardiac compensation
Differentiate between three types of shock:
Hypovolemic
Cardiogenic
Septic

2. Normal Hemodynamics Blood Pressure
Regulated by cardiac output and resistance
Not an indicator of blood flow
Pressure of force that blood exerts against walls of blood vessels

3. Normal Hemodynamics Stroke Volume (SV)
Amount of blood ejected from the left ventricle with each heart beat
Components of SV
 Preload  Contractility  Afterload

4. Normal Hemodynamics Preload Afterload
Amount of stretch experienced by the ventricle during diastole
Directly related to the volume of blood filling the chamber
Afterload
Force within the vessels which oppose the ventricle
A function of vessel constriction of the pulmonary artery (RV) and the aorta (LV)

5. Normal Hemodynamics Contractility
Force of recoil from the myocardium in systole
Starling’s Law states that the greater the stretch, the more forceful the contraction

6. Cardiac Output (CO) HR X SV = CO
Amount of blood ejected from the left ventricle within one minute
Equal to heart rate times stroke volume
HR X SV = CO

7. Hemodynamic Compensation
Ability of the body to alter components of hemodynamic regulation to maintain homeostasis in periods of low blood flow

8. Early Compensation
Preload  increases to improve contractility (increased CO)
Heart rate  increase to improve CO (sympathetic stimulation)
Afterload (resistance)  constriction of the vessels to improve BP and blood flow
Autoregulation of individual organs

9. Late Compensation
There is inadequate preload to offset changes in contractility
Declining SV is no longer offset by increase in HR
BP continues to fall and vessels are unable to vasoconstrict any further
Autoregulatory mechanisms fail
Shock symptoms

10. Shock
Shock is a progressive, widespread reduction in tissue perfusion that results from a decrease in effective circulating blood volume.

11. Initial Stages of Shock
No signs or symptoms may be present
Decreased cellular perfusion is present
Decreased cardiac output has started
Reduced blood flow secondary to reduced intercellular volume
Peripheral vasoconstriction

12. Compensation Begins
Body attempts to maintain hemodynamic stability - homeostatic mechanisms activated
Increased total peripheral vascular resistance (PVR) and heart rate/ contractility results in increased cardiac output, BP, tissue perfusion
Increased Renal blood flow leads to vasoconstriction and H2O retention
Peripheral vasoconstriction increases central volume and vital organ blood supply

13. Progressive Stage of Shock
Compensatory mechanisms begin to fail
Blood vessels vasodilate reducing total peripheral resistance and BP
Perfusion now very poor leading to anaerobic metabolism and acidosis
ACID  signals the beginning of vasodilatation
Poor blood flow and agglutination - microclots - DIC

14. Refractory Stage of Shock
No response to any form of therapy; Death is likely to occur
Loss of autoregulation in micro-circulation
Capillary permeability changes and fluid shifts into interstitial space
Venous return and cardiac output almost negligible
Reduced cardiac output leads to severely impaired tissue perfusion

15. Types of Shock Hypovolemic Shock
PRELOAD failure due to loss of circulating volume / intravascular volume
Cardiogenic Shock
Primary failure of CONTRACTILITY due to ischemic insult
Septic Shock
Primary failure of AFTERLOAD

16. Hypovolemic Shock Assessment findings / Signs and Symptoms
Skin pale and cool
Distant heart sounds
Low BP
Low CO and CVP
Clear breath sounds

17. Hypovolemic Shock Causes Internal and External fluid shifts like:
Allergic, toxins, trauma, diuretics, gastric suction
Treatment options
Goal is PRELOAD enhancement
Restore fluid balance
Prevent further loss
Replace volume

18. Cardiogenic Shock Causes Pump failure Coronary and non-coronary
Ventricular dysfunction affects the forward flow of blood into the systemic circulation
Assessment findings / Signs and symptoms
Depends on Right vs. Left heart failure

19. Cardiogenic Shock assessment
LV failure: PULMONARY
Cool skin
S3 and S4, Systolic murmur
Increased Preload
Decreased CO and BP
Orthopnea, Dyspnea, Crackles
Decreased SpO2
RV failure: SYSTEMIC
Edema and weight gain
Distended neck veins
Low BP
Low CO

20. Cardiogenic Shock Treatment options Goal is PRELOAD REDUCTION
Diuretics such as furosemide
with ENHANCEMENT of CONTRACTILITY
positive inotropic medications such as dobutamine or milrinone
and careful management of AFTERLOAD
Vasoconstructors such as norepinephrine

21. Septic Shock Heart pump and blood volume usually normal
Progressive syndrome
Early identification critical

22. Septic Shock abcdefg Cause severe, overwhelming infection Mortality
40-90%
Treatment options
Goal is AFTERLOAD enhancement
Vasopressors such as norepinephrine
Inotropes such as dobutamine
Find and appropriately treat the infection
abcdefg

23. Differentiating Shock States
abcdefg

24. Next: Heart Failure