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 RCA- RA, RV&LV Inf, Inf Septum SA node 65% AV node 80% PDA 80-90% CX- LA,LV ( side/back) SA node 40% AV node 20% LAD – LV (front/bottom) Septum Bundle branches Left Main
Cardiac Cycle Diastole Phase SA node contracts. Atria contract. Ventricles fill with more blood. Contraction reaches AV node . Late Diastole Atria and Ventricles are relaxed. Semilunar valves are closed. Atrioventricular valves are open. Ventricles continue to fill with blood. Mid Diastole Ventricles relax. Semilunar valves close. Atrioventricular valves open. Ventricles fill with blood. Early Diastole Cardiac Cycle Systole Phase 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. Systole
Electrical Conduction system
right and left
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
Coronary Arteries Fill
The Cardiac Cycle
The Cardiac Cycle
The Cardiac Cycle
Normal CO 4-8 liters Normal Cardiac Index is 2.5 to 4.5 liters
Works with Stroke Volume
Factors Causing Low Cardiac Output
Inadequate Left Ventricular Filling
Mitral or tricuspid stenosis
Constrictive pericarditis or tamponade
Inadequate Left Ventricular Ejection
Coronary artery disease causing LV ischemia or infarction
Drugs that are negative inotropes
Preload - Stretch of ventricular wall. Usually related to volume. (how full is the tank?)
How well does the ventricular walls move? How good is the pump?
Decreased due to
Drugs – certain drugs will decrease contractility
Lido, Barbiturates, CCB, Beta-blockers
Positive inotropic drugs
Dobutamine, Digoxin, Epinephrine
Hypercalcemia ( high calcium)
CONTRACTILITY - PRECAUTIONS
Do Not use Inotropes until volume deficiency is corrected
Correct Hypoxemia and electrolyte imbalance.
– resistance the blood in the ventricle must overcome to force the valves open and eject contents to circulation.
Factors that increase afterload are
Systemic resistance or High Blood pressure
Myocardial Infarcts / Cardiomyopathy
Polycythemia – Increased blood viscosity
Factors that decrease Afterload
Septic shock- warm phase
End stage cirrhosis
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
1. PRELOAD- venous blood return to the heart
♥ .Blood Volume
♥ . Venous Dilation
Ca+ channel blockers
2. CONTRACTILITY - forcefulness of contractility Ca+ channel blockers Digoxin Dopamine/Dobutamine Milrinone/amrinone 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 blockers Labetalol Drugs of Hemodynamics
4. HEART RATE –
Calcium channel blockers
O2 O2 O2 O2 O2 O2 O2 To BODY From Body
O2 O2 O2
Factors that make up SVO 2 are
VO 2 (oxygen consumption)
Work of Breathing
Suctioning, bathing, repositioning
- LV dysfunction (cardiac disease, drugs)
- Shock – cardiac/septic (late)
- Anemia - Hemorrhage
Clinical Conditions Causative Factors
Increased SVO 2
Most common cause is - Sepsis
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).
PA Catheter KEEP COVERED KEEP LOCKED YELLOW Clear BLUE RED 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 SVO 2 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
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
♥ Re-level the transducer with any change in the patient’s 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 Angles 45° 30° 0 °
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
A B C
Thermodilution Cardiac Outputs
C ardiac O utputs 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)
C ardiac O utputs should be obtained at the end of respiration - at the same point each time
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
RV WAVEFORM 22 4
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
Don’t keep balloon inflated longer than 15 seconds
When completed - Allow air to passively exit the balloon
Dissection or Laceration of subclavian artery or vein
Pulmonary artery injury or rupture
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
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