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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