Week 7 Hemodynamics Flashcards
Hemodynamics is
The study of the motion of blood through the body.
Fundamental Concepts of hemodynamics
Cardiac Output
Preload
Afterload
Contractility
Normal Hemodynamic Values SVO2
60-75%
Normal Hemodynamic Values Stroke Volume
50-100ML
Normal Hemodynamic Values Stroke Index
25-45mL/M2
Normal Hemodynamic Values Cardiac Output
4-8 L/min
Normal Hemodynamic Values MAP
60-100mm Hg
Normal Hemodynamic Values CVP
1-7mm Hg
Normal Hemodynamic Values PAP systolic
20-30mm Hg
Normal Hemodynamic Values PAP Diastolic
5-15 mm Hg
Normal Hemodynamic Values PAOP (wedge)
8-12 mm Hg
Normal Hemodynamic Values SVR
900-1300 dynes.sec.com
Cardiac Output
The cardiac output pushes the blood through the vascular system.
Cardiac output (CO) is calculated by multiplying the heart rate (HR) by the stroke volume (SV).
Stroke volume is the volume of blood pumped out of the heart with each heartbeat.
If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
This is known as compensatory tachycardia.
heart rates greater than 150 bpm actually drop stroke volume
Cardiac Index =
CO/BSA=2.4 - 4.0L/min/m2
BSA = height in c weight in k divide by 360 then divide all that by 2
Stroke volume is affected by three factors:
preload, afterload, and contractility
Compensatory tachycardia
If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
Preload
the amount of stretch on the cardiac myofibril at the end of diastole.
When the ventricle is at its fullest
Preload is most directly related to:
Fluid volume
Starling’s curve:
describes the relationship of preload to cardiac output As preload (fluid volume) increases, cardiac output will also increase until the cardiac output levels off. If additional fluid is added after this point, cardiac output begins to fall.
Preload Measurement
Not measured directly…instead measured by physical assessment of fluid volume
Signs of inadequate preload include:
Poor skin turgor Dry mucous membranes Low urine output Tachycardia Thirst Weak pulses Flat neck
Signs of excess preload in a patient with:
distended neck veins
crackles in the lungs
Bounding pulses
Increased preload in a patient with poor cardiac function presents with
crackles in the lungs S3 heart sound, low urine output Tachycardia cold clammy skin with weak pulses edema
Preload
Insufficient preload is commonly called hypovolemia or dehydration.
Insufficient volume is present in the vascular tree, the sympathetic nervous system is stimulated to release the atecholamines, epinephrine and norepinephrine.
These hormones cause increased heart rate and arterial vasoconstriction.
The increased heart rate produces a compensatory tachycardia while the vasoconstriction helps maintain an adequate blood pressure.
If these patients are treated with catecholamine drugs rather than receiving volume infusions, the tachycardia becomes very pronounced and the vasoconstriction can become severe enough that the organs fail and the distal extremities become ischemic.
The first step in treating any form of hemodynamic instability is:
to assess the patient for signs of insufficient preload (e g volume or blood loss)
Afterload is:
the resistance that the ventricle must overcome to eject its volume of blood.
The most important determinant of afterload is
vascular resistance
Other factors affecting afterload include:
blood viscosity
aortic compliance
valvular disease.
As arterial vessels constrict, what happens to afterload?
the afterload increases
As arterial vessels dilate, what happens to afterload?
the afterload decreases
Increased CO
higher volumes
Decreased CO
decreased volumes
In general, when you have someone with signs of low preload treat with
volume, until you know if its a stretch issue
High Afterload:
increases myocardial work and decreases stroke volume.
Patients with high afterload present with signs and symptoms of arterial vasoconstriction including
cool clammy skin
capillary refill greater than 5 seconds
narrow pulse pressure.
Pulse pressure is calculated by:
subtracting the diastolic blood pressure (DBP) from the systolic blood pressure (SBP).
What is normal pulse pressure at the brachial artery
40 mm Hg
Low afterload:
myocardial work and results in increased stroke volume.
Patients with low afterload present with symptoms of arterial dilation
warm flushed skin
Bounding pulses
wide pulse pressure
If the afterload is too low, what may result?
hypotension
Points to ponder for afterload:
A key component of treatment for heart failure is afterload reduction using beta-blockers and ACE inhibitors.
By decreasing the resistance to ventricular ejection the cardiac output is increased and myocardial workload is decreased.
The increase in cardiac output frequently improves the functional status of these patients.
ACE inhibitors
Beta blockers
Contractility refers to
the inherent ability of the cardiac muscle to contract regardless of preload or afterload status.
Contractility is enhanced by
exercise, catecholamines, and positive inotropic drugs.
Contractility is decreased by
by hypothermia, hypoxemia, acidosis, and negative inotropic drugs.
Myocardial compliance refers to
the ventricle’s ability to stretch to receive a given volume of blood.
Normally the ventricle is very compliant so large changes in volume will produce small changes in pressure.
If compliance is low, small changes in volume will result in large changes in pressure within the ventricle.
If the ventricle cannot stretch, it will be unable to increase cardiac output with increased preload.
Tissue perfusion is the
transfer of oxygen and nutrients from the blood to the tissues.
When performing interventions designed to improve hemodynamics
valuation of effectivess is whether or not the intervention was successful in improving tissue perfusion.
Many of the signs of inadequate preload, afterload and contractility also reflect poor tissue perfusion.
Cool clammy skin Cyanosis Low urine output Decreased level of consciousness Metabolic acidosis Tachycardia Tachypnea Hypoxemia
Labs and diagnostic testing that are used to evaluate tissue perfusion include
Arterial blood gases
Arterial lactate levels
Pulse oximetry.
Poor tissue perfusion is reflected by a low pH, low base excess and elevated lactate level.
Pulse oximetry readings are typically low when tissue perfusion is compromised to a significant degree.
Methods of Hemodynamic Monitoring
Arterial Blood Pressure Central Venous Pressure/ Right Atrial Pressure The Pulmonary Artery Catheter Cardiac Output Measurement Tissue Oxygenation
Arterial Blood Pressure
Non-invasive
MAP most accurate
Direct arterial pressure measurement
Reasons for Hemodynamic Monitoring
Assessment of cardiovascular function (complicated MI, Cardiogenic shock, papillary muscle rupture)
Peri-operative monitoring of surgical patients with major systems dysfunction
Shock of all type (septic, hypovolemic, any shock that is prolonged or origin is unknown)
Assessment of pulmonary status
Assessment of fluid status (dehydration, hemorrhage, GI bleed, burns)
Therapeutic indications (cardiac pacing )
Diagnostic indications (pulmonary hypertension)
Arterial Blood Pressure Site Selection; The most preferred insertion site
is the radial artery
alternate Arterial blood pressure sites include
the femoral and brachial arteries.
The femoral artery is not a preferred site due to its anatomic location.
if the radial artery is used
Assess site with modified Allen test
performed prior to cannulation to ensure that the ulnar artery provides adequate circulation to the hand to prevent tissue ischemia or necrosis.
Indications for Arterial Catheterization Need for continuous blood pressure measurement
Hemodynamic instability
Vasopressor requirement
MAP should be 60-100mm/Hg
Indications for arterial catheterization Respiratory failure
Frequent arterial blood gas assessments
Indications for Arterial Catheterization most common locations
radial, femoral, axillary, and dorsalis pedis
