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 parametersa. Heart rateb. Arterial blood pressure c. Central venous pressure (CVP)d. Pulmonary pressurese. Cardiac output

2. Direct parameters: heart rate, arterial and venous pressures3. Indirect or derived measurements: calculated from direct data

a. Cardiac output/cardiac indexb. 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 heartb. 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 ventriclesa. Depolarization and replorization (Review definitions p.840)b. Right atrium- receive venous blood from systemic circulation; left

atrium receives reoxyenated blood from lungsc. Atriums filling with blood, SA node in electrical conduction system

fires; starts process of depolarization

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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. I ncreased 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. Afterloada. Amount of resistance against which left and or right ventricle pumps b. Measured by pulmonary vascular resistance (PVR) of systemic vascular

resistance (SVR)

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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, drugse. Dysrhythmia: result in decreased CO > loss of synchronized atrial and

ventricular filling and ejection

5. Cardiac Outputa. 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 COc. How does the body compensate for decreased CO (cardiac

dysfunction)? (p. 871-872: Frank Starling mechanism & neuroendocrine response)

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:

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increased O2 demand, effect of sympathetic nervous system (fear, anxiety

6. Stroke volumea. 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. Contractilitya. Ability of cardiac muscle to contractb. 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 organsMAP> 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

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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 systems1. 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 returnb. *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

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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. Hypervolemiaii. Increased venous returniii. Right sided heart failrue, pulmonary hypertensioniv. Tricuspid stenosis and regurgitationv. 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)

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

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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 failureo Mitral valve problemso Hypervolemia and pericardial tamponade

Decreased PAWPo Low stroke volumeo 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 responsibilitiesa. Knowledge of catheters/management issuesb. Recognition of dyrhythmiasc. Monitoring device; treat entire client, not just monitoring deviced. 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 Atrial Pressure (RA))

2-6 mmHg2-8mm H2O

Pulmonary Artery Pressure (PA)

Systolic 20-30 mmHg (PAS)Diastolic 8-12 mmHg (PAD)Mean 15-25 mmHg

Pulmonary Capillary Wedge Pressure (PWCP) 8-12 mmHg

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