CONCEPTS OF NORMAL HEMODYNAMICS AND SHOCK

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

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

22. Septic Shock • 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