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

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

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

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)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Differentiating Shock States abcdefg

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