NOTES #4 Hemodynamic Monitoring Lab CMJ

Lab #4: Hemodynamic Monitoring (refer also to Module 4: Heart Failure)

Hemodynamic Monitoring

Hemodynamics: pressures of cardiovascular and circulatory system measured by

invasive methods (ICU setting):
• direct arterial BP monitoring (“A” lines)
• CVP (central venous pressure )
• Indirect measurement of left ventricular pressures by flow directed,
balloon-tipped catheter (PA catheter/Swan-Ganz catheter)
• *Measurements within vessels walls converted into signals then
into electrical wave forms graphically amplified/displayed
• For critically ill, unstable patients (ie patients with acute MI,
cardiomyopathy, right/left ventricular failure, etc.)

Information from hemodynamic monitoring

1. Heart parameters
a. Heart rate
b. Arterial blood pressure
c. Central venous pressure (CVP)
d. Pulmonary pressures
e. Cardiac output
2. Direct parameters: heart rate, arterial and venous pressures
3. Indirect or derived measurements: calculated from direct data
a. Cardiac output/cardiac index
b. Mean arterial blood pressure (MAP) (*What is significance of MAP? P.
877)
c. Stroke volume/SVR (Systemic Vascular Resistance) (What is SVR?
What factors evvect SVR and how would aan elevated SVR affect afterload?) p. 877;

Critical Concepts for review: (see text p. 870-871 and online Hemodynamic
reference )
Heart:
a. Two upper chambers-atria-two lower called ventricles, main pumping
chambers of the heart
b. Atria separated from ventricles by AV valves; tricuspid separates
right atrium from right ventricle; mitral separates left atrium from
left ventricle; pulmonic semilunar and the aortic semilunar help
control flow of blood from ventricle to lungs and systemic circulation;
pulmonic semilunar valve controls flow of blood from right ventricle
to lungs; aortic semilunar valve controls flow of blood from left
ventricle to the aorta.
1. Cardiac cycle: Electrical conduction system; specialized cells, electrical
impulses travel from atria to ventricles
a. Depolarization and replorization (Review definitions p.840)
b. Right atrium- receive venous blood from systemic circulation; left
atrium receives reoxyenated blood from lungs

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c. Atriums filling with blood, SA node in electrical conduction system
fires; starts process of depolarization
d. Atria fill with blood; pressure within atria increases, forces AV valves
open. (Most ventricular filling (diastole) passively occurs when AV valves
open)
e. After atrial depolarization, atria contract, forcing remaining atrial
blood into ventricles (atrial kick). *30% more blood into ventricles
f. Post atrial contraction; atria begin to relax, atrial pressure decreases;
electrical impulse from atria travels through rest of conduction system > ventricular
depolarization and onset ventricular contraction
g. Ventricular pressure exceeds atrial pressure; AV valves close and
semilunar open
h. Desaturated blood ejected from right ventricle into the lungs, CO2
dropped off and oxygen picked up. Oxygenated blood from the left ventricle is
ejected into the systemic circulation via the aorta (systole).

2. Preload *Understand significance of preload & afterload! P. 840

a. Filling volume of ventricles at end of diastole; reflects amount of
cardiac muscle stretch at end-diastole just before contraction; (pre-before=the
load or volume that stretches the LV or RV just prior to ejection/contraction)

b. Measured by
• Pulmonary Artery (PA) catheter for left ventricular pre-load, also
called Pulmonary artery occlusion pressure/pulmonary artery
wedge pressure or PAWP
*Preload of left ventricle= LVEDP (left ventricular end-diastolic pressure)
=PAWP.
• CVP for right ventricular pre-load)

c. Determined by
• Volume of blood returning to the heart
• Venous tone and actual amount of blood in venous system
• Directly related to force of myocardial contraction
d. Increased preload> greater the stroke volume (SV) and the greater
the CO (usually);
• What disease process/medication(s), etc. would increase preload?
How would that be managed? (p.798, 799)
e. Decreased preload> decreased stroke volume (SV) and decreased
cardiac output (CO)
• What disease process/medication(s) would decrease preload? How
would that be managed? (p. 798, 799)

3. Afterload

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a. Amount of resistance against which left and or right ventricle pumps
b. Measured by pulmonary vascular resistance (PVR) of systemic vascular
resistance (SVR)
c. Affected mostly by blood vessel compliance, blood viscosity, flow
patterns; valves also have effect
• Greater the resistance, harder myocardium has to work
determined by BP and arterial tone
• Vasoconstriction from increase in systemic arterial tone >increases
BP >increases afterload.

d. *Left ventricular afterload measured by assessment of the SVR

(systemic vascular resistance); Pulmonary vascular resistance PVR
measures resistance against which right ventricle works (understand this
concept) (p. 871)
• *Greater the afterload, less the cardiac output
• Arterial BP: indirect measurement of afterload for LV
• What decreases afterload? (arterial vasodilation as in sepsis,
hyperthermia, use of nitrates)
• What increases afterload? (vasoconstriction. hypovolemia,
hypothermia, aortic stenosis, hypertension; medications
(catecholamines/inotropic drugs like norepinephrine/epinephrine
and intropin), pulmonary hypertension)

4. Heart Rate

a. Tachycardia above 120 > decreased CO due to decreased ventricular

filling Do you understand why?
b. Caused by: hypoxia, fear, anxiety, hypovolemia, catecholamines, pain,
exercise
c. Bradycardia: sudden bradycardia > decreased CO; athletes
compensate with increased SV
d. Caused by: vagal stimulation, heart blocks, drugs
e. Dysrhythmia: result in decreased CO > loss of synchronized atrial and
ventricular filling and ejection

5. Cardiac Output
a. Volume of blood pumped by heart in one minute; SV X HR; usual is 4-
8 L/min. (*adjusted for body size by calculation of cardiac index; normal 2.8-
4.2Lmin/m2) Define cardiac index. (p. 878)
b. Urine output: indirect measurement of CO
c. How does the body compensate for decreased CO (cardiac
dysfunction)? (p. 871-872: Frank Starling mechanism & neuroendocrine response)

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d. Decreased CO due to :
• poor ventricular filling, hypovolemia, poor emptying, decreased
myocardial contractility (infarct, ischemia, arrhythmias);
vasodilatation due to sepsis and drugs and increased SVR as
hypertension, aortic stenosis is, etc
e. Increased CO due to:
• increased O2 demand, effect of sympathetic nervous system (fear,
anxiety

6. Stroke volume
a. Amount of blood ejected with each heartbeat

• Normal SV=60-130cc/beat; factors that determine SV

include preload, afterload and contractility *Keep concept in
mind!

7. Contractility
a. Ability of cardiac muscle to contract
b. Starling’s Law= greater the stretch of muscle fibers, the
greater the force of contraction and volume of blood ejected.
• increased contractility due to sympathetic stimulation ie drugs
(dig, dopamine, dobutamine, epinephrine, calcium)
• decreased contractility due to loss of myocardial function as acute
MI, cardiomyopathy; hypoxemia; electrolyte imbalance (K,Ca, Mg);
drugs (lidocaine, calcium channel blockers, beta blockers)
c. Contractility not measured directly; determined by SV and ejection
fraction (EF) calculated by Echocardiogram

• EF: how much blood pumped with each contraction in

relation to how much blood available to be pumped. Normal 55-
65% (*understand this concept) *critical to heart failure

• Systolic blood pressure (normal 120 mm Hg): pressure

generated during ventricular systole; diastolic blood pressure
(normal 90 mm Hg)

• **Mean arterial blood pressure (desirable: 70 – 90 mm

Hg);*less than 60 danger area (may read slightly different
values)> inadequate perfusion to vital organs
• Formula: MAP = CO X SVR
*MAP < 60: severely jeopardizes perfusion to vital organs

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 MAP> 105: indicates hypertension or severe
vasoconstriction (**Know formula & how to calculate &
will see again!) Often calculated automatically on BP
machines!
**MAP = systolic BP+2(diastolic BP)
3

8. **General factors effecting hemodynamic findings: (know these

definitions)

a. Heart function
b. Intravascular volume (amount of blood in vasculature)
c. Intropy (strength of myocardial contractions)
d. Vasoactivity (expanding and contracting of blood vessels to
accommodate variations in blood flow, regulate arterial pressure, etc)
e. Chronotropy (timing and rate of heart contraction)

Hemodynamic Monitoring Systems **know/understand hemodynamic values &

MAP!!

A. Monitoring systems
1. Intra-arterial pressure monitoring
a. Indwelling arterial line (art line, “A line”): direct, continuous
monitoring of systolic, diastolic and mean arterial blood pressure
(MAP), easy access for arterial blood samples

Arterial line
b. Arterial blood pressure: direct reflection of cardiac output and
resistance to flow by arterial walls (Systemic Vascular
Resistance or SVR)
c. Allen test: performed prior to insertion “A” line to assess patency
radial/ulnar artery (see online reference)

2. Central venous pressure (CVP)

a. Measure of blood volume and venous return

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 b. *Right heart filling pressures; monitors fluid volume status
• Catheter inserted into internal jugular or subclavian vein; distal
end positioned in superior vena cava just above right atrium

• Reading approximates right ventricular end diastolic pressure

or right ventricular function and general fluid status (pre-load)
• Measured in cm of water with manometer (normal: 2 – 8 cm) or
mm Hg if connected to transducer (normal: 2 – 6 mm HG)
• What causes a decreased CVP? (**p. 878)
• Increased CVP
i. Hypervolemia
ii. Increased venous return
iii. Right sided heart failrue, pulmonary hypertension
iv. Tricuspid stenosis and regurgitation
v. Vsoconstriction, cardiac tamponade

3. Pulmonary artery (PA) pressure monitoring (*continuous monitoring

as catheter advanced)
a. Pulmonary artery (PA) catheter (Swan Ganz catheter);flow-directed,
balloon tipped catheter; evaluate left ventricular and overall
cardiac function (has access ports for CVP, CO, PAP, PCWP, balloon
inflation, some for fluid/medication administration)

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 • Catheter into central vein, threaded into right atrium
• Balloon inflated, floats into right ventricle and into
pulmonary artery
• Carried forward until wedges in small branch of pulmonary
vasculature *gives information on LVEDP (left ventricular
end diastolic pressure (*when inflated…or wedged, blocks
pressure from behind balloon-right side-gives pressure reading
from left ventricle)
• Balloon deflated, multiple lumens of catheter allow for pressure
readings in right atrium, pulmonary artery (PA), left ventricle

* Patient monitored continuously during passage of PA catheter, characteristic

changes in ECG waveform determine location of catheter; balloon inflated during
passage (floats through), then wedges in pulmonary capillary, reading taken, then
deflated..; *Potential for dysrhythmia as catheter is advanced

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 b. Normal PA (pulmonary artery pressure- PAP) pressure: **20-
30 mmHg systolic and 8-12 diastolic usual is 25/10
• Mean is 15 mm Hg
• Increased systolic in pulmonary HTN
• Increased diastolic from ventricular failure
• Decreased PAP with hypovolemia, shock

c. ***As above inflation of balloon blocks pressure from behind

(wedging) allows measurement of pressure generated by left
ventricle= Pulmonary Artery Wedge Pressure (PAWP)
• Assesses left ventricular function
• Normal PAWP: 8–12 mm Hg (*slightly different values various
sources; average value)
• **Reflects preload of the LV or LVEDP; equal to PA diastolic
if no pulmonary problems
• Increased PAWP
o Left ventricular failure
o Mitral valve problems
o Hypervolemia and pericardial tamponade
• Decreased PAWP
o Low stroke volume
o Hypovolemia, shock

d. Cardiac output measurement

• Measured with PA catheter, separate lumen on catheter, use
thermodilution (change in water temperature as goes through
heart). What is normal CO?
• Cardiac index: calculation of cardiac output per square meter
of body surface area) is calculated
• Normal Cardiac index is 2.8 – 4.2 L/mn/m2

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B. Complications/Nursing responsibilities

1. Complications related to catheter

a. Arterial line, CVP and/or PA catheter
• Infection, occlusion
• Air embolism due to central line or arterial line placement and use
of pressurized bag (Art line and PA catheter)
• Bleeding potential
b. PA/Swan Ganz catheter specific problems
• Thrombosis from rupture of balloon or persistent wedging of Swan
Ganz catheter
• Occluded ports, balloon rupture due to overinflation of balloon or
frequent use of the balloon
• Pneumothorax: during initial placement
• Dysrhythmias: catheter migration
• Air embolism from balloon rupture or air in infusion line
• Pulmonary thromboembolism: improper flushing technique, non-
heparinized flush solution
• Pulmonary artery rupture/injury: perforation during placement,
overinflation of balloon, overuse of balloon, pulmonary infarction -
caused by the catheter migrating into the wedge position, the
balloon left inflated, or thrombus formation around the catheter
which causes an occlusion

2. Nursing responsibilities
a. Knowledge of catheters/management issues
b. Recognition of dyrhythmias
c. Monitoring device; treat entire client, not just monitoring device
d. Use as a tool for determining client cardiac function/status, fluid balance

Hemodynamics: Basics
Parameter Normal value
Mean Arterial Pressure (MAP) 70 -90 mm Hg
Cardiac Index (CI) 2.8-4.2 L/min/m2
Cardiac Output (CO) 4-8 L/min
Central Venous Pressure (CVP) (also known as Right 2-6 mmHg
Atrial Pressure (RA)) 2-8mm H2O
Systolic 20-30 mmHg
(PAS)
Pulmonary Artery Pressure (PA) Diastolic 8-12 mmHg
(PAD)
Mean 15-25 mmHg
Pulmonary Capillary Wedge Pressure (PWCP) 8-12 mmHg

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