Understanding Adult

Hemodynamics
Theory, Monitoring,
Waveforms and
Medications
Vicki Clavir RN

Purpose
The

primary purpose of invasive

hemodynamic monitoring is the early
detection, identification, and treatment of
life-threatening conditions such as heart
failure and cardiac tamponade. By using
invasive hemodynamic monitoring the
nurse is able to evaluate the patient's
immediate response to treatment such as
drugs and mechanical support. The nurse
can evaluate the effectiveness of
cardiovascular function such as cardiac
output, and cardiac index.

Objectives
Understands basic cardiac anatomy
Verbalizes determinates of Cardiac Output and their
relationships to each other
List indications for hemodynamic monitoring
Demonstrates monitor system and set up
Describe pharmacologic strategies that manipulate
the determinates of cardiac output

Indications for Hemodynamic

Monitoring:
One of the obvious indications for
hemodynamic monitoring is decreased
cardiac output. This could be from
dehydration, hemorrhage, G. I. bleed,
Burns, or surgery. All types of shock,
septic, cardiogenic, neurogenic, or
anaphylactic may require invasive
hemodynamic monitoring. Any deficit or
loss of cardiac function: such as acute
MI, cardiomyopathy and congestive
heart failure may require invasive
hemodynamic monitoring.

Coronary Arteries

Left Main

RCARA, RV&LV Inf,

Inf Septum
SA node 65%
AV node 80%
PDA 80-90%

CXLA,LV (side/back)
SA node 40%
AV node 20%

LAD
LV (front/bottom)
Septum
Bundle branches

Cardiac Cycle
Diastole Phase
Early Diastole

Ventricles relax.
Semilunar valves close.
Atrioventricular valves
open.
Ventricles fill with blood.

Mid Diastole

Atria and Ventricles are

relaxed.
Semilunar valves are
closed.
Atrioventricular valves
are open.
Ventricles continue to fill
with blood.

Late Diastole

SA node contracts.
Atria contract.
Ventricles fill with more
blood.
Contraction reaches AV
node.

Cardiac Cycle
Systole Phase
Systole

Contraction
passes from AV
node to
Purkinje fibers
and ventricular
cells.
Ventricles
contract.
Atrioventricular
valves close.
Semilunar
valves open.
Blood is
pumped from
the ventricles
to the arteries.

Cardiac Cycle

Electrical Conduction system

SA node
Atrial muscle
Internodal fibers
AV node
AV bundle
right and left
bundle branches

Ventricular muscle

Autonomic Nervous System

The

autonomic nervous system

stimulates the heart through a
balance of sympathetic nervous
system and parasympathetic nervous
system innervations.
The sympathetic nervous system plays a
role in speeding up impulse formation,
thus increasing the heart rate
The parasympathetic nervous system
slows the heart rate.

The Cardiac Cycle

The Cardiac Cycle

Coronary Arteries Fill

The Cardiac Cycle

The Cardiac Cycle

Normal CO 4-8 liters

Normal Cardiac Index is 2.5 to 4.5 liters

Heart Rate
Works with Stroke Volume
Compensatory
Tachycardia
Bradycardia
Dysrhythmias

Factors Causing Low Cardiac

Output

Inadequate Left
Ventricular Filling
Tachycardia
Rhythm disturbance
Hypovolemia
Mitral or tricuspid
stenosis
Pulmonic stenosis
Constrictive
pericarditis or
tamponade
Restrictive
cardiomyopathy

Inadequate Left
Ventricular Ejection
Coronary artery
disease causing LV
ischemia or infarction
Myocarditis,
cardiomyopathy
Hypertension
Aortic stenosis
Mitral regurgitation
Drugs that are
negative inotropes
Metabolic disorders

Hemodynamic terms
Preload-

Stretch of ventricular
wall. Usually related to
volume. (how full is the tank?)
Frank Starlings Law

Hemodynamic terms

Increased preload seen in

Increased circulating volume (too much

volume)
Mitral insufficiency
Aortic insufficiency
Heart Failure
Vasoconstrictor use- (dopamine)

Decreased Preload seen in

Decreased circulating volume (bleeding,3rd

spacing)
Mitral stenosis
Vasodilator use ( NTG)
Asynchrony of atria and ventricles

Increased Preload

Decreased preload

Normal Value - 2-8 mm Hg

Or LVEDP
PAOP = 8-12 mm Hg
PAD = 10-15 mm Hg

Hemodynamic terms
Contractility-

How well does the ventricular walls

move? How good is the pump?
Decreased due to
Drugs certain drugs will decrease
contractility
Lido, Barbiturates, CCB, Betablockers
Infarction, Cardiomyopathy
Vagal stimulation
Hypoxia

Hemodynamic terms
Contractility-

Increased
Positive inotropic drugs
Dobutamine, Digoxin, Epinephrine
Sympathetic stimulation
Fear, anxiety
Hypercalcemia ( high calcium)

CONTRACTILITY PRECAUTIONS
Do

Not use Inotropes until

volume deficiency is corrected

Correct

Hypoxemia and
electrolyte imbalance.

Hemodynamic terms
Afterload

resistance the blood in the

ventricle must overcome to
force the valves open and eject
contents to circulation.

Hemodynamic terms
Factors

that increase afterload are

Systemic resistance or High Blood
pressure
Aortic stenosis
Myocardial Infarcts /
Cardiomyopathy
Polycythemia Increased blood
viscosity

Hemodynamic terms
Factors

that decrease Afterload

Decreased volume
Septic shock- warm phase
End stage cirrhosis
Vasodilators

Normal PVR is 120 to 200 dynes

Normal SVR - 800-1200 dynes

Mean Arterial Pressure

MAP is considered to be the perfusion
pressure seen by organs in the body.
It is believed that a MAP of greater than 60
mmHg is enough to sustain the organs of
the average person under most conditions.
If the MAP falls significantly below this
number for an appreciable time, the end
organ will not get enough blood flow, and
will become ischemic.
Calculated MAP = 2x diastolic + systolic
3

EKG

1.PRELOADvenous blood
return to the heart
Controlled by;
.Blood Volume
PRBCs
Albumin
Normal Saline
Diureticslasix,bumex
Thiazides
Ace inhibitors
. Venous Dilation
Nitroglycerine
Ca+ channel
blockers
clonidine
(Catapress)
methyldopa
trimethaphan
(arfonad)
Dobutamine

Morphine

Drugs of Hemodynamics

3.AFTERLOAD work
required to open
aortic valve and
eject blood
resistance to flow in
arteries
Dopamine (at
higher doses)
Ace inhibitors
Nipride/lesser
extent Nitro
Calcium channel

Labetalol

2. CONTRACTILITYforcefulness of contractility
Ca+ channel blockers
Digoxin
Dopamine/Dobutamine
Milrinone/amrinone

blockers

4. HEART RATE
Beta blockers
Calcium
channel blockers
Atropine
Dopamine
Dobutamine

O2

O2

To

O2

O2

Y
BOD

O2

O2
From

O2

Body

O2

O2

O2

Factors that make up SVO2 are

Cardiac output
SaO2
VO 2 (oxygen consumption)
Hemoglobin

Causative Factors

O2 Delivery
Hb concentration
Oxygen saturation
(SaO2)
Cardiac Output

Clinical Conditions
- Anemia
- Hemorrhage

- Hypoxemia
-

Lung disease
Low FIO2

- LV dysfunction (cardiac
disease, drugs)

- Shock cardiac/septic (late)

-

Oxygen consumption

Hypovolemia
Cardiac Dysrhythmias
Fever, infection
Seizures, agitation
Shivering
Work of Breathing

Suctioning, bathing,
repositioning
-

Increased SVO2
Most

common cause is - Sepsis

Or

Wedged

PA catheter

 Functions

of PA Catheter

Allows for continuous bedside monitoring of the

following

Vascular tone, myocardial contractility, and

fluid balance can be correctly assessed and
managed.
Measures Pulmonary Artery Pressures, CVP, and
allows for hemodynamic calculated values.
Measures Cardiac Output. (Thermodilution)
SvO2 monitoring (Fiber optic).
Transvenous pacing.
Fluid administration.

PA Catheter
RED
KEEP
COVERED

KEEP LOCKED

BLUE
Clear
YELLOW

Markings on catheter.
1. Each thin line= 10 cm.
2. Each thick line= 50 cm.

Description of PA Catheter
Ports/lumens.

CVP Proximal (pressure line - injectate port

for CO)-BLUE
PA Distal (Pressure line hook up)- Yellow
Extra port - usually- Clear
Thermistor Red Cap

Continuous Cardiac Output and

SVO2 monitoring

Indications for PA catheter

The

pulmonary artery catheter is indicated

in patients whose cardiopulmonary
pressures, flows, and circulating volume
require precise, intensive management.
MI

cardiogenic shock - CHF

Shock - all types
Valvular dysfunction
Preoperative, Intraoperative, and Postoperative
Monitoring
ARDS, Burns, Trauma, Renal Failure

PRESSURE TRANSDUCER
SYSTEMS SET UP

500 ml Premixed Heparinized bag of NS

PHLEBOSTATIC REFERENCE
POINT

Angles 45
30

Re-level the transducer

with any change in the
patients position
Referencing the system 1
cm above the left atrium
decreases the pressure by
0.73 mm Hg
Referencing the system 1
cm below the left atrium
increases the pressure by
0.73 mm Hg

Remove cap and

keep sterile
Turn stopcock
towards
pressure bag
Zero monitor
Replace cap

SQUARE WAVE TEST

- Determines the
ability of the
transducer to
correctly
reflect
pressures.
- Perform at the
beginning of
each shift

Thermodilution Cardiac
Outputs

Cardiac Outputs reading should be within .5 of

each other for averaging purposes.

Except in patients with atrial fibrillation- just

average 3 to 4 readings. (due to loss of atrial
kick output changes from minute to minute)

Cardiac Outputs should be obtained at the end

of respiration - at the same point each time

ARTERIAL WAVEFORM

RN magazine April, 2003 - PA

catheter refresher course.

ALL PA measurements are calculated at end expiration

because the lungs are at their most equal (negative vs. positive pressures)

a, c,& v Waves and their Timing to the ECG tracing

RA WAVEFORM

RV WAVEFORM

22

Ventricular

PAP DOCUMENTATION
Measure at end expiration
Measure pressures from a
graphic tracing
Measure pulmonary capillary
wedge pressure at end-expiration
using the mean of the a wave
a wave indicates atrial contraction and
falls within the P QRS interval of the
corresponding ECG complex

PAW WAVEFORM WITH

MECHANICAL VENTILATION

PAOP/PAWP Pressure Safety

Points
Watch

monitor during inflation and

stop when you see PAOP waveform
Never inject more than 1.5 ml of air
or any fluid into PA port
Dont keep balloon inflated longer
than 15 seconds
When completed - Allow air to
passively exit the balloon

OVERWEDGE

COMPLICATIONS OF PA
CATHETER
Infection
Electrocution (Microshock)
Ventricular Arrhythmias

(Vtach.,Vfib., Cardiac Arrest)

Atrial Dysrhythmias, RBBB

Knotting and misplacement

Hemo or Pneumothorax
Cardiac valve trauma

COMPLICATIONS OF PA
CATHETER

Catheter
thromboembolism or
air embolism
Dissection or
Laceration of
subclavian artery or
vein
Cardiac Tamponade

Pulmonary
infarction
Pulmonary artery
injury or rupture
Balloon rupture

Hematoma

Trouble Shooting
Dampened

Waveform

Flush catheter
Check transducer system for air bubbles
Blood

in Tubing

Look for open Stopcock

Put 300mgHg pressure in pressure bag
Stuck

in Wedge /PWP

Very slowly and gently pull back

catheter until you see PA waveform

References

Pulmonary Artery Catheter Education Project @

www.pacep.org sponsored by

American Association of Critical Care Nurses

American Association of Nurse Anesthetists
American College of Chest Physicians
American Society of Anesthesiologists
American Thoracic Society
National Heart Lung Blood Institute
Society of Cardiovascular Anesthesiologists
Society of Critical Care Medicine

Hemodynamics Made Incredibly Visual LWW publishing

2007
AACN practice alert Pulmonary Artery Pressure Monitoring
- Issued 5/2004
Handbook of Hemodynamic Monitoring G Darovic 2 nd ed.
TCHP Education Consortium 2005 A Primer for
Cardiovascular Surgery and Hemodynamic Monitoring
Nursebob's MICU/CCU Survival Guide-Hemodynamics in
Critical Care -Hemodynamic Monitoring Overview
12/04/00