Transcript Hemodynamics

CONCEPTS OF NORMAL
HEMODYNAMICS AND SHOCK
At 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. Hypovolemic
b. Cardiogenic
c. Septic
1
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
2
Normal Hemodynamics
Stroke Volume (SV)
Amount of blood ejected from the left ventricle
with each heart beat
Components of SV

Preload

Contractility

Afterload
3
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)
4
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
5
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
6
Hemodynamic Compensation
Ability of the body to alter
components of
hemodynamic regulation to
maintain homeostasis in
periods of low blood flow
7
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
8
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
Shock symptoms
Autoregulatory mechanisms fail
9
Shock

10
Shock is a progressive, widespread reduction in
tissue perfusion that results from a decrease in
effective circulating blood volume.
Initial Stages of Shock



11
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
12
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
13
Refractory Stage of Shock

14
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



15
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

16
Assessment findings / Signs and Symptoms
 Skin pale and cool
 Distant heart sounds
 Low BP
 Low CO and CVP
 Clear breath sounds
Hypovolemic Shock


17
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
18
Cardiogenic Shock assessment

LV failure: PULMONARY
 Cool skin
 S3 and S4, Systolic
murmur
 Increased Preload
 Decreased CO and BP
 Orthopnea, Dyspnea,
Crackles
 Decreased SpO2
19

RV failure: SYSTEMIC
 Edema and weight
gain
 Distended neck
veins
 Low BP
 Low CO
Cardiogenic Shock

20
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


21
pump and blood volume usually normal
Progressive
syndrome
Early identification
critical
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
22
Differentiating Shock States
LOC
Urine Output
VS
Pulmonary
Cardiovascular
Skin
Decreased
LV Failure:
Decreased
Volume:
SVR:
HYPOVOLEMIC CARDIOGENIC
SEPTIC
Unable to differentiate forms of shock based upon these
parameters
Clear
Distant HS
Preload low
CO low
BP low
Cool
Orthopnea
Dyspnea
Crackles
Decreased SpO2
S3 , S4
Systolic murmur
Preload high
CO low
Cool
Clear unless
lung
involvement
CO high
BP low or
normal
Warm (early)
abcdefg
23
Next: Heart Failure
24