concepts of normal hemodynamics and shock
DESCRIPTION
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: - PowerPoint PPT PresentationTRANSCRIPT
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CONCEPTS OF NORMAL HEMODYNAMICS AND SHOCKAt the end of this self study the participant will:
1. Define the terms: stroke volume, cardiac output, preload, afterload, contractility,
2. Describe the difference between early and late cardiac compensation
3. Differentiate between three types of shock:a. Hypovolemicb. Cardiogenicc. Septic
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Normal Hemodynamics
Blood PressureRegulated by cardiac output
and resistanceNot an indicator of blood
flowPressure of force that blood
exerts against walls of blood vessels
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Stroke Volume (SV)Amount of blood ejected from the left ventricle
with each heart beat
Components of SV Preload Contractility
Afterload
Normal Hemodynamics
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Normal Hemodynamics
Preload Amount of stretch experienced by the ventricle during
diastole Directly related to the volume of blood filling the
chamberAfterload
Force within the vessels which oppose the ventricleA function of vessel constriction of the pulmonary artery
(RV) and the aorta (LV)
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ContractilityForce of recoil from
the myocardium in systole
Starling’s Law states that the greater the stretch, the more forceful the contraction
Normal Hemodynamics
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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
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Hemodynamic Compensation
Ability of the body to alter components of hemodynamic regulation to maintain homeostasis in periods of low blood flow
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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
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Late CompensationThere 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
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Shock
Shock is a progressive, widespread reduction in tissue perfusion that results from a decrease in effective circulating blood volume.
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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
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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
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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
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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
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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
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Hypovolemic Shock
Assessment findings / Signs and Symptoms Skin pale and cool Distant heart sounds Low BP Low CO and CVP Clear breath sounds
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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 lossReplace volume
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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
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Cardiogenic Shock assessment 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
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Cardiogenic Shock Treatment options
Goal is PRELOAD REDUCTION Diuretics such as furosemide
with ENHANCEMENT of CONTRACTILITY positive inotropic medications such as
dobutamine or milrinoneand careful management of AFTERLOAD
Vasoconstructors such as norepinephrine
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Septic Shock Heart pump and blood volume usually normal
Progressive syndrome
Early identification critical
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Septic Shock Cause
severe, overwhelming infection Mortality
40-90% Treatment options
Goal is AFTERLOAD enhancementVasopressors such as norepinephrineInotropes such as dobutamine
Find and appropriately treat the infection
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Differentiating Shock States
Decreased Volume: HYPOVOLEMIC
LV Failure: CARDIOGENIC
Decreased SVR: SEPTIC
LOC Urine Output VS
Unable to differentiate forms of shock based upon these parameters
Pulmonary Clear Orthopnea Dyspnea Crackles Decreased SpO2
Clear unless lung involvement
Cardiovascular Distant HS Preload low CO low BP low
S3 , S4
Systolic murmur Preload high CO low
CO high BP low or normal
Skin Cool Cool Warm (early)
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Next: Heart Failure